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Q0001:Bioavailability
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- Measure of absorption;- F = AUC oral/AUC injected x100;AUC = Area Under the Curve of;[Plasma] vs. Time
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Q0002:Volume of Distribution
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- Vd = D/C (mL);D = amount of drug in body;C = [plasma];-Low Vd -> drug in plasma;- Med Vd -> in p & interstitium;-
High Vd -> in p; i; & tissues/cells
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Q0003:Drug Metabolism: Phase I v II
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Phase I;-Converts lipophilic into slightly polar; water-solublemetabolites;- Cytochrome P-450;Phase II;-Yields very polar;
inactive metabolites that the kidneys can excrete;- Conjugationreactions
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Q0004:Clearance (CL)
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CL = rate of drug elimination/[plasma];= rate at which avolume of fluid is cleared of drug;= blood flow x extraction
rate;= Vd x Ke (L/hr)
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Q0005:Elimination constant (Ke)
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Ke gives information about the amount of time to reach asteady state or wash-out;Ke = CL/Vd (1/hr);*independent of
drug dose.
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Q0006:Half-life (t1/2)
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Time required to change amount of drug in body by 1/2;t1/2 =ln(0.5)/-Ke = 0.693Vd/CL;Infusion: 94%Css - 4 t1/2;87.5% -
3;75% - 2;50% - 1
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Q0007:Stead State Plasma Concentration (Css)
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elimination = rate of administration;Css = R/(Vd x Ke) =R/CL;R = infusion rate (amount/time)
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Q0008:Loading & Maintenances doses
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Loading dose = Vd x Cp/F;Maintenance = Cp x CL/F;Cp =target plasma Css
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Q0009:Pharmacodynamics: Efficacy v. Potency
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Efficacy = maximal response produced by a drug (~Vmax);Potency = amount required to elicit a response;
expressed as ED50=EC50= dose causing 50% max effect
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Q0010:Pharmacodynamics: antagonists and partial agonists
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Competitive ant: decreases potency;Noncompetitive ant:decreases efficacy;Partical ag: lower max. efficacy than full;
(potency is independent of efficacy)
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Q0011:Urine pH - fx on drug elimination
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Weak acids: pH = pKa + log(A-/HA);-Digested in acidicenvironments (<pKa);-Trapped in basic environment (A-);-
Treat overdose with bicarbonate;Weak bases: pH = pKa + log(B/BH+);-Digested in basic environments (>pKa);-Trapped inacidic environment (BH+);-Treat overdose with ammonium Cl
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Q0012:Therapeutic index
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TD50/ED50 = median toxic dose/median effectivedose;Measure of drug safety (higher # is more safe)
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Q0013:Maximum dosing interval (tau-max)
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Concentration constrained dosing;tau-max = ln(Cmax/Cmin)/k
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Q0014:(amount of drug)/(fluid compartment concentration)
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Vd
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Q0015:protein bound drugs;liver and kidneydisease;pharmacodynamic variable altered?
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Vd
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Q0016:Vd eq
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Vd = drug amount/drug concentration
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Q0017:Cl eq
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Cl = elimination rate/[drug]
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Q0018:t1/2 eq
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t1/2 = .7*Vd/Cl
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Q0019:10% remaining concentration;# half lives?
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3.3
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Q0020:12.5% remaining concentration;# half lives?
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3
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Q0021:25% remaining concentration;# half lives?
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2
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Q0022:Loading dose eq
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Loading dose = Cp*Vd/F
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Q0023:Maintenance dose eq
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Maintanence Dose = Cp*CL/F;Cp= target [drug];F =bioavailability
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Q0024:change in loading dose with renal/hepatic disease
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Unchanged
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Q0025:change in maintanence dose with renal/hepatic disease
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lower
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Q0026:zero order elimination;constant __ of drug eliminatedper time
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amount
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Q0027:first order elimination;constant __ of drug eliminatedper time
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fraction
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Q0028:zero order elimitation;Cp decreaseslinearly/exponentially?
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linearly
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Q0029:first order elimination;Cp decreaseslinearly/exponentially?
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exponentially
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Q0030:Phase I metabolism;resulting metabolite characteritics
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slightly polar;water soluble;often still active
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Q0031:Phase I metabolism reactions
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oxidation;reduction;hydrolysis
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Q0032:oxidation;reduction;hydrolysis;Phase?
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Phase I
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Q0033:cytochrome P-450;phase?
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Phase I
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Q0034:Phase II metabolism;resulting metabolitecharacteristics
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very polar;inactive;*renally excreted
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Q0035:Phase II metabolism reactions
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acetylation;glucuronidation;sulfanation
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Q0036:acetylation;glucuronidation;sulfanation;Phase?
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Phase II
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Q0037:conjugation;Phase?
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Phase II
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Q0038:Phase metabolism lost in geriatrics
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Phase I
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Q0039:competitive antagonist effect on agonist dose curve
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shift to right;**decreased potency
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Q0040:noncompetitive antagonist effect on agonist dose curve
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shifts downward;**decreased efficacy
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Q0041:EC50 vs Kd in system w/ spare receptors
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Q0042:partial agonist vs full agonist
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Q0043:phase 1 clinical trial questions
Page 86
is it safe?;pharmacokinetics?
Page 87
Q0044:Phase 2 clinical trial questions?
Page 88
does it work in patients?
Page 89
Q0045:Phase 3 clinical trial questions?
Page 90
Does it work double blind?
Page 91
Q0046:Phase 4 clinical trial questions?
Page 92
Postmarketing is it safe?
Page 93
Q0047:amount of drug in body/_______ = Vd
Page 94
plasma drug concentration ;;(Vd is Volume of Distribution)
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Q0048:rate of elimination of drug/[plasma drug] = ?
Page 97
Q0049:(.7)(Vd)/CL = ?
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Q0050:A drug infused at a constant rate reaches about 94% ofsteady state after _______ t 1/2s.
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Q0051:A loading dose is calculated using this formula.
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Loading Dose = (Cp)(Vd)/F ;(Cp = target plasma conc; F =bioavailability)
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Q0052:A maintenance dose is calculated using this formula.
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(Cp)(CL)/F;(CL = Clearance)
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Q0053:Rate of elimination is proportional to _______ ______in 1st order elimination.
Page 106
drug concentration
Page 107
Q0054:In the case of EtOH; which is elimated by _____ orderelimination; a constant amount of drug is eliminated per unit
time.
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Q0055:Phase ____ (I or II) reactions yield slightly polarmetabolites that are often _____ (active or inactive)
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Q0056:Phase ____ (I or II) reactions yield very polarmetabolites that are often _____ (active or inactive) and are
excreted by the _______.
Page 112
II; inactive; kidney
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Q0057:Phase II reactions are often of this type.
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Q0058:Cytochrome P-450 is involved in _____ phase (I or II)reactions.
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Q0059:A drug patent lasts for _____ years after filing forapplication.
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Q0060:How many phases are there in drug development?
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Q0061:Drugs are first tested in patients in phase _____ ofclinical testing; pharmacokinetic safety is determined in phase______ of clinical testing; double blind tests are done in phase
____ and post-market surveillance is done in phase _____.
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Q0062:In a dose response curve; a competitive antagonistshifts the curve _____;a non-competitive antagonist shifts the
curve ______.
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Q0063:What pharmacologic relationship would determine theexistence of spare receptors?
Page 126
EC50 is lower then Kd (EC50 is more to the left)
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Q0064:What does it mean if EC50 and Kd are equal?
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The system does not have spare receptors
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Q0065:A partial agonist acts on the same receptor system asa full agonist? T/F
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Q0066:What's the main difference between a partial agonistand a full agonist?
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A partial agonist has a lower maximal efficacy.
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Q0067:Is a partial agonist less potent than a full agonist?
Page 134
Not necessarily. It can be less; more or equally potent as a fullagonist.
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Q0068:Equation for Half Life
Page 136
T 1/2 = (0.7 x Vd)/CL
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Q0069:Percent of concentration in the following number ofhalf lives;1;2;3;3.3
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1 = 50%;2 = 75%;3 = 87.5%;3.3 = 90%
Page 139
Q0070:How do the Loading and Maintenance doses change ina patient w/ Renal or Hepatic dysfunction?
Page 140
Loading - unchanged;;Maintenance - Decreased
Page 141
Q0071:Equation for Theraputic Index
Page 142
TI = Toxic dose/Effective dose
Page 143
Q0072:Phase in clinical drug testing;safety; pharmacokinetics
Page 145
Q0073:Phase in clinical drug testing;Protocol; dose level; workon patients
Page 147
Q0074:Phase in clinical drug testing;double blind study;efficacy; adverse effects
Page 149
Q0075:(3) drugs that use Zero-order elimination
Page 150
Alcohol;;Aspirin;;Phenytoin
Page 151
Q0076:What phase of a reaction uses cytP-450?;What is thepurpose of this phase?
Page 152
Phase I;converts lipophilic to polar
Page 153
Q0077:What is the main focus of Phase II reactions?
Page 155
Q0078:When pH < pKa; what is more common?;(2);whichcan pass through the membrane?
Page 156
HA and BH+;;HA passes thru the membrane (uncharged)
Page 157
Q0079:Definition;Amount of the drug required for a givenresponse
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Q0080:what is the first NT to everything?;the first receptor?
Page 160
NT: ACh;Receptor: Nicotinic
Page 161
Q0081:what system does not have a synapse from the spinalcord to the tissue?
Page 162
Somatic NS;(skeletal muscle);ACh to Nicotinic receptor
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Q0082:what is the only sympathetic ACh?;what is thereceptor?
Page 164
Sweat gland;;receptor: Muscarinic
Page 165
Q0083:what is the receptor for the Parasympathetic systemat the tissue?
Page 167
Q0084:what are the Adverse Effects of Acetylcholine?;whichis the only Nicotinic receptor response?
Page 168
DUMBBELSS;Diarrhea; Urination;Miosis;Bradycardia;Bronchoconstriction;Excite skeletal muscle
(N);Lacrimation;Sweat; Salivation
Page 169
Q0085:what receptors use Gq as their second messenger?;(5)
Page 170
HAVe 1 M&M;H1;Alpha1;V1;M1;M3
Page 171
Q0086:what G-protein uses Phospholipase C?
Page 173
Q0087:what receptors use Gi as their secondmessenger?;action?
Page 174
MAD 2s;M2;Alpha2;D2;inhibits Adenylyl Cyclase
Page 175
Q0088:what receptor increases gastric acid secretion?
Page 177
Q0089:Inhibits choline re-entering the presynaptic terminal
Page 179
Q0090:Inhibits ACh into vesicles
Page 181
Q0091:Inhibits NE into vesicles
Page 183
Q0092:Inhibits release of ACh into synaptic membrane
Page 185
Q0093:Inhibits release of NE into synaptic membrane
Page 187
Q0094:Promotes release of NE into synaptic membrane
Page 189
Q0095:Inhibits reuptake of NE into presynaptic nerve;(2)
Page 191
Q0096:what receptor does NE act on in the presynapticneuron as neg feedback to inhibit its release?
Page 193
Q0097:(3) Cholinomimetrics and use of each
Page 194
Bethanechol - post-OP activates GI/GU;Carbachol -Glaucoma;Pilocarpine - Glaucoma
Page 195
Q0098:Anticholinesterase used for post-OP activation ofGI/GU; myasthinia gravis;what is it an antidote for?
Page 196
Neostigmine;;antidote: Curarae (NMJ block)
Page 197
Q0099:Anticholinesterase used for glaucoma and crossesBBB;what is it an Antidote for?
Page 198
Physostigmine;;antidote: Atropine overdose
Page 199
Q0100:(3) ACh receptor blockers
Page 200
Atropine;;Scopalamine;;Ipratropium
Page 201
Q0101:ACh receptor blocker used for Motion Sickness
Page 202
Scopolamine;(DOC)
Page 203
Q0102:ACh receptor blocker used for Asthma/COPD
Page 205
Q0103:what drug slows the HR at 0.5mg and increases it at>1.0mg?
Page 206
Atropine;(muscarinic antagonist)
Page 207
Q0104:what are the AE of Atropine?
Page 208
Opposite of DUMBBELSS;Hot as hare;Dry as bone;Red asbeet;Blind as Bat;Mad as hatter
Page 209
Q0105:Insecticide antidote
Page 211
Q0106:Nicotinic ACh receptor antagonist;use?
Page 212
Hexamethonium;use;prevents reflex bradycardia caused byNE
Page 213
Q0107:drug used for intubation for its rapid onset and quickduration in causing flaccid paralysis
Page 215
Q0108:which NMJ (nicotinic) blocker also releaseshistamine?
Page 217
Q0109:Epinepherine effects on;1. BP;2. HR;3. TPR
Page 218
Epinepherine;BP: Inc Systolic; Dec Diastolic;HR: Inc(tachycardia);TPR: Dec
Page 219
Q0110:NE effects on;1. BP;2. HR;3. TPR
Page 220
NE;BP: BIG INC in systolic and diastolic;HR:DECREASES;TPR: BIG INCREASE
Page 221
Q0111:Isoproterenol effects on;1. BP;2. HR;3. TPR
Page 222
Isproterenol;BP: Decrease in systolic and diastolic;HR: BIGINCREASE;TPR: BIG DECREASE
Page 223
Q0112:DOC for Shock to increase renal perfusion and forCHF to increase CO
Page 225
Q0113:DOC for CHF to increase CO w/o increasing oxygendemand
Page 227
Q0114:Alpha agonist that is used for HTN w/ renal Dz
Page 229
Q0115:what occurs if atropine is given before NE?
Page 230
Heart rate increases instead of decreases
Page 231
Q0116:a1-blocker for urinary retention in BPH and HTN
Page 233
Q0117:a2-blocker for depression
Page 235
Q0118:what occurs w/ BP if a-blocker is given beforeIsoproterenol?
Page 237
Q0119:what occurs w/ BP if a-blocker is given beforeEpinepherine?
Page 238
Reverses the vasoconstriction effect of Epi and Decreases BP
Page 239
Q0120:which beta-blockers are beta1 selective?
Page 240
if they start w/ A-M in alphabet;(except Labetalol - partialagonist)
Page 241
Q0121:what glaucoma drug should not be used in closed-angleglaucoma?
Page 243
Q0122:Antidote/Tx for;Salicylates
Page 244
Alkalinize urine
Page 245
Q0123:Antidote/Txfor;Anticholinesterases;Organophosphates;(2)
Page 246
Atropine;;Pralidoxime
Page 247
Q0124:Antidote/Tx for;Antimuscarinic;Anticholinergic agents
Page 249
Q0125:Antidote/Tx for;beta-blockers
Page 251
Q0126:Antidote/Tx for;Digitalis;(4)
Page 252
Stop Dig;;normalize K;;Lidocaine;;Magnesium
Page 253
Q0127:Antidote/Tx for;Iron
Page 255
Q0128:Antidote/Tx for;Lead;(3)
Page 256
CaEDTA;;Dimercaprol;;Succimer (kids)
Page 257
Q0129:Antidote/Tx for;Arsenic; gold; mercury;(2)
Page 258
Dimercaprol;;Succimer (kids)
Page 259
Q0130:Antidote/Tx for;Copper
Page 261
Q0131:Antidote/Tx for;Cyanide;(3)
Page 262
Nitrite;;Hydrocobalamin;;Thiosulfate
Page 263
Q0132:Antidote/Tx for;Methemoglobin
Page 265
Q0133:Antidote/Tx for;Carbon Monoxide
Page 266
100% O2;(or hyperbaric O2)
Page 267
Q0134:Antidote/Tx for;Methanol;Ethylene glycol(antifreeze);(2)
Page 268
Ethanol;;Fomepizole
Page 269
Q0135:Antidote/Tx for;Opioids;(2)
Page 270
Naloxone;;Naltrexone
Page 271
Q0136:Antidote/Tx for;Benzodiazepines
Page 273
Q0137:Antidote/Tx for;TCAs
Page 275
Q0138:Antidote/Tx for;Heparin
Page 277
Q0139:Antidote/Tx for;Warfarin;(2)
Page 279
Q0140:Antidote/Tx for;tPA; Streptokinase
Page 280
Aminocaproic acid
Page 281
Q0141:Urine pH and drug elimination for;Weak acids
Page 282
alkalinize urine w/ Bicarb
Page 283
Q0142:Urine pH and drug elimination for;Weak bases
Page 284
Acidify urine w/ NH4Cl
Page 285
Q0143:What is the reversible cholinesterase inhibitorindicated for the Tx of Alzheimer's Dz?
Page 287
Q0144:what is the skeletal muscle relaxant that acts directlyon the contractile mechanism of the muscle fiber?
Page 289
Q0145:which Glaucoma agent acts by decreaseing productionof aqueous humor?
Page 291
Q0146:why is Epi mixed w/ anesthetics?
Page 292
to retard the systemic absorption
Page 293
Q0147:which muscles are most affected by tubocurarine?
Page 294
fine movement muscles (head; neck; face)
Page 295
Q0148:what is the alpha receptor-assoc eye muscle?
Page 297
Q0149:what agent for bronchial asthma causes tremor?
Page 298
Salmeterol;(b-agonist)
Page 299
Q0150:what ANS drug class masks hypoglycemia in treateddiabetics?;how?
Page 300
b-blockers;;blocks catecholamines; which stimulateGlyconeogenesis
Page 301
Q0151:(2) MAO inhibitors that are used for depression
Page 302
Tranylclpromine;;Phenelzine sulfate
Page 303
Q0152:DOC for thyroid storm
Page 305
Q0153:Definition;two drugs act on the same tissue viaindependent receptors resulting in effects in the opposite
direction
Page 306
Physiologic antagonist
Page 307
Q0154:Definition;when two drugs combine and the activity ofone or both drugs is blocked
Page 308
Chemical antagonist
Page 309
Q0155:equation for the Elimination constant;(2)
Page 310
Ke = 0.7/half-life = CL/Vd
Page 311
Q0156:when calculating an IV dosage; what needs to beremembered?
Page 312
multiply drug (mg/kg) by weight (kg)
Page 313
Q0157:(2) equations for Extraction ratio
Page 314
ER = (Ci-Co)/Ci = CL/Q
Page 315
Q0158:Which is not absorbed well in the stomach;Aspirin(pKa = 3) or Propranolol (pka = 9.4)?
Page 317
Q0159:the AE of convulsions are MC w/ what drug?
Page 319
Q0160:what drug can cause Hypocalemic Tetany?
Page 320
Edetate Disodium (Na-EDTA)
Page 321
Q0161:what mineral toxicity can decrease Amylase secretion?
Page 323
Q0162:AE of drug is Congenital goiter; Hypothyroidism
Page 325
Q0163:AE of drug is Agenesis of fetal kidneys
Page 327
Q0164:Km: Definition
Page 328
Km = Substrate at 0.5*Vmax;Km reflects the affinity of theenzyme for its substrate
Page 329
Q0165:Vmax indicates what?
Page 330
Vmax is directly proportional to the enzyme concentration.
Page 331
Q0166:Relationship between Km and affinity
Page 332
-The lower the Km; the higher the affinity;-Smaller Km meansenzyme is saturated earlier; which means that small amounts
of substrate are picked up by the enzyme.
Page 333
Q0167:Reading an inverse curve: Y-intercept equals ?
Page 334
1/Vmax;The higher the Y-intercept the lower the Vmax
Page 335
Q0168:Reading an inverse curve: X-intercept equals ?
Page 336
(1/-Km);The further to the right the x-intercept; the greaterthe Km
Page 337
Q0169:Reading an inverse curve: Slope equals ?
Page 339
Q0170:Reading an inverse curve: Effect of a competitiveinhibitor
Page 340
X-intercept farther to the right; meaning Km is greater;because you need more substrate to get the same effect as thecompetitive inhibitor is hogging the enzyme;The y-interceptis the same; meaning Vmax hasn't changed; because there isn't
any more enzyme;;The slope is greater; because Km hasincreased while Vmax has stayed the same.
Page 341
Q0171:Reading an inverse curve: Effect of a noncompetitiveinhibitor
Page 342
The x-intercept is the same; meaning Km is the same; becausethe affinity for the enzyme hasn't changed; there's just less of
it;;The y intercept has increased; meaning Vmax hasdecreased; because enzyme has been inactivated by the
noncompetitive inhibitor;The slope is greater; because Vmaxhas decreased while Km has stayed the same.
Page 343
Q0172:Competitive inhibitor: Resemble substrate
Page 345
Q0173:Competitive inhibitor: Overcome by increasedsubstrate?
Page 347
Q0174:Competitive inhibitor: Binds active site?
Page 349
Q0175:Competitive inhibitor: Effect on Vmax
Page 350
Unchanged. The amount of enzyme has not changed.
Page 351
Q0176:Competitive inhibitor: Effect on Km
Page 352
Increased. A lot more substrate needs to be available to seizethe active sites.
Page 353
Q0177:Noncompetitive inhibitor: Resemble substrate?
Page 355
Q0178:Noncompetitive inhibitor: Overcome by increasedsubstrate?
Page 357
Q0179:Noncompetitive inhibitor: Binds active site?
Page 359
Q0180:Noncompetitive inhibitor: Effect on Vmax
Page 360
Decreased. Takes the enzyme out.
Page 361
Q0181:Noncompetitive inhibitor: Effect on Km
Page 362
Unchanged. Does not change the affinity for the enzyme.
Page 363
Q0182:Volume of distribution: Abbreviation
Page 365
Q0183:Vd: Stands for what?
Page 366
Volume of distribution
Page 367
Q0184:Volume of distribution: definition
Page 368
Vd = (amount of drug in the body)/(plasma drugconcentration)
Page 369
Q0185:Volume of distribution: What alters it?
Page 370
Liver and kidney disease
Page 371
Q0186:Where are drugs with a low Vd distributed?
Page 373
Q0187:Where are drugs with a medium Vd distributed?
Page 374
extracellular space
Page 375
Q0188:Where are drugs with a high Vd distributed?
Page 377
Q0189:Clearance: definition
Page 378
=(rate of elimination of drug)/(plasma drugconcentration);=Vd x Ke where Ke=elimination constant
Page 379
Q0190:Half life: definition
Page 380
The time required to change the amount of drug in the bodyby 1/2 during elimination (or during a constant infusion).
Page 381
Q0191:What percentage of steady state is a drug at after: 1half life
Page 383
Q0192:What percentage of steady state is a drug at after: 2half lives
Page 385
Q0193:What percentage of steady state is a drug at after: 3half lives
Page 387
Q0194:What percentage of steady state is a drug at after: 3.3half lives
Page 389
Q0195:What percentage of steady state is a drug at after: 4half lives
Page 391
Q0196:How many half lives does it take for a drug to reachthe following percentage of steady state: 50%
Page 393
Q0197:How many half lives does it take for a drug to reachthe following percentage of steady state: 75%
Page 395
Q0198:How many half lives does it take for a drug to reachthe following percentage of steady state: 87.5%
Page 397
Q0199:How many half lives does it take for a drug to reachthe following percentage of steady state: 90%
Page 399
Q0200:How many half lives does it take for a drug to reachthe following percentage of steady state: 94%
Page 401
Q0201:Cp stands for what?
Page 402
target plasma concentration
Page 403
Q0202:What is the abbreviation for target plasmaconcentration?
Page 405
Q0203:In pharmacology; what is F an abbreviation for?
Page 407
Q0204:What is the abbreviation in pharmacology forbioavailability?
Page 409
Q0205:Loading dose: Definition
Page 410
Loading dose = (Cp * Vd)/F (where Cp equals the targetplasma concentration; Vd equals volume of distribution; and F
equals bioavailability)
Page 411
Q0206:Maintenance dose: Definition
Page 412
Maintenance dose = (Cp * CL)/F (where Cp is the targetplasma concentration and CL is clearance and F is
bioavailability)
Page 413
Q0207:Zero-order elimination: definition
Page 414
Constant elimination over time regardless of drug.
Page 415
Q0208:How does Cp vary with time during zero-orderelimination?
Page 416
Cp decreases linearly with time.
Page 417
Q0209:Zero-order elimination: Drug examples
Page 418
-Ethanol;-Phenytoin;-Aspirin (at high concentrations)
Page 419
Q0210:First-order elimination: definition
Page 420
Rate of elimination is proportional to drug concentration
Page 421
Q0211:Zero-order elimination vs First-order elimination:Comparison
Page 422
Zero-order: Constant amount of drug eliminated per unittime;1st-order: Constant fraction of drug eliminated per unit
time
Page 423
Q0212:How does Cp vary with time during first-orderelimination?
Page 424
Cp decreases exponentially with time.
Page 425
Q0213:Urine: Which species get trapped in urine?
Page 427
Q0214:In what kind of environment is the following trapped?:Weak acids
Page 428
Basic environments
Page 429
Q0215:In what kind of environment is the following trapped?:Weak bases
Page 430
Acidic environments
Page 431
Q0216:In what kind of environment is the followingdigested?: Weak acids
Page 432
Acidic environments (below pKa)
Page 433
Q0217:In what kind of environment is the followingdigested?: Weak bases
Page 434
Basic environments (above pKa)
Page 435
Q0218:How do you treat an overdose of the following?: Weakacids
Page 437
Q0219:How do you treat an overdose of the following?: Weakbases
Page 438
Ammonium chloride
Page 439
Q0220:Phase I metabolism: Processes
Page 440
Cytochrome P450;-reduction;-oxidation;-hydrolysis
Page 441
Q0221:Phase II metabolism: Processes
Page 442
Conjugation;-acetylation;-glucuronidation;-sulfation
Page 443
Q0222:Phase I metabolism: Metabolites
Page 444
-slightly polar;-water-soluble;-often still active
Page 445
Q0223:Phase II metabolism: Metabolites
Page 446
-very polar;-renally excreted;-inactive
Page 447
Q0224:What phase of metabolism do geriatric patients losefirst?
Page 449
Q0225:Effect on dose/effect curve of: competitive antagonist
Page 450
Shifts curve to the right; decreasing potency and increasingEC50.
Page 451
Q0226:Effect on dose/effect curve of: noncompetitiveantagonist
Page 452
Shifts curve downward; decreasing efficacy
Page 453
Q0227:What is EC50?
Page 454
Dose causing 50% of maximal effect
Page 455
Q0228:What is Kd?
Page 456
Concentration of drug required to bind 50% of receptor sites
Page 457
Q0229:How many half lives does it take for a drug to reachthe following percentage of steady state: 97%
Page 459
Q0230:What percentage of steady state is a drug at after: 5half lives
Page 461
Q0231:Effect on dose/effect curve: Spare receptors
Page 462
The drug binding and drug effect are independent of each otherwith effect to the left of binding;This means that EC50 is
lower than Kd; so very little drug needs to bind to get 50% ofthe effect.
Page 463
Q0232:Effect on dose/effect curve: Partial agonist
Page 464
-Lower maximal efficacy;-Potency independent (amount ofdose to get to maximum effect)
Page 465
Q0233:Therapeutic Index: Definition
Page 466
=(TD50)/(ED50);where TD50 equals median toxic dose; andED50 equals median effective dose.
Page 467
Q0234:blocks cell wall synthesis by inhibition ofpeptidoglycan cross-linking
Page 468
penicillin;ampicillin;tiracillin;piperacillin;imipenem;aztrenam;cephalosporins
Page 469
Q0235:block peptidoglycan synthesis
Page 470
bacitracin; vancomycin; cycloserine
Page 471
Q0236:disrupt bacterial/fungal cell membranes
Page 473
Q0237:block nucleotide synthesis
Page 474
sulfonamides; trimethoprim
Page 475
Q0238:block fungal cell memebranes
Page 476
amphotericin B;nystatin;fluconazole/azoles
Page 477
Q0239:block nuecliotide synthesis
Page 478
sulfonamides; trimethoprim
Page 479
Q0240:block DNA topoisomerases
Page 481
Q0241:red orange body fluids
Page 483
Q0242:Block Protein synthesis at 50S ribosomal subunit
Page 484
chlorophenicol; erythromycin/macrolides; lincomycin;clindamycin; streptogramins (quinupristin; dalfopristin);
linezolid
Page 485
Q0243:block protein synthesis at 30S ribosomal subunit
Page 486
Aminoglycosides ; tetracylins
Page 487
Q0244:bactericidal antibiotics
Page 488
penicillin; cephalosporins; vancomycin; aminoglycosides;floroquines; metronidazole
Page 489
Q0245:penicillin G
Page 490
IV form of penicillin
Page 491
Q0246:penicillin V
Page 492
oral form of penicillin
Page 493
Q0247:MOA of penicillin
Page 494
1. bind penicillin binding protein (aka tranpepsidase);2. blocktranspepsidase cross-lining of cell wall;3. activate autolytic
enzymes;(works on dividing bacteria)
Page 495
Q0248:clinical use of penicillin?
Page 496
bactericidal ;for gram-positive cocci/rods;gram-negativecocci;spirochetes
Page 497
Q0249:is penicillin penicillinase resistant?
Page 499
Q0250:toxisity of penicillin
Page 500
hypersensitivity reactions; drug-induced coombs positive-hemolytic anemia
Page 501
Q0251:how do gram negative bacteria protect themselvesfrom penicillin?
Page 502
1.prvent peniciiln from penetrating cell layers by alteringporins;2. beta-lactase enzyme;3.alter molecular structure of
transpepsidase so beta-lactam antibiotic (penicillin) no bind toit
Page 503
Q0252:example of a bacteria that uses: altered molecularstructure of transpepsidase so beta-lactam antibiotic
(penicillin) no bind to it
Page 505
Q0253:how do gram positive bacteria protect themselvesfrom penicillin?
Page 506
1. secrete beta-lactamase = penicillinase(S aureus) and try tointercept antibiotic outside the cell wall
Page 507
Q0254:name the penicillinase resistant penicillin?
Page 508
methicillin; nafcillin;dicloxacillin
Page 509
Q0255:clinical use of penicillinase resistant penicillin?whysuch narrow spectrum?
Page 510
s. Aureus - but not MRSA;B/C HAVE BULKIER r GROUP
Page 511
Q0256:TOXICITY of penicillinase resistant penicillin
Page 512
HYPERSENSITIVITY reactions
Page 513
Q0257:which penicillinase resistant penicillin causesintersitial nephritis?
Page 515
Q0258:aminopenicillins - names?
Page 516
ampicillin; amoxicillin
Page 517
Q0259:MOA of aminopenicillins diff than penicillins?
Page 518
wider specturm b/c better penitration through gram negativeouter membrane and better binding to transpepsidase
Page 519
Q0260:are aminopenicillins penicillinase sensitive?
Page 521
Q0261:clinical use of aminopenicillins?
Page 522
extended-spectrum penicillin;gram-poitive and gram negrods(H.influenza;E coli;listeria monocytes; proteus mirabilis;salmoella; enterococci;note: they are one of few drugs against
gram-positive enterococcus
Page 523
Q0262:toxicity of aminopenicillins?
Page 524
hypersensitivity reactions ;ampicillin rash;psuedomembranous colitis
Page 525
Q0263:anti-pseudomonals?
Page 526
ticarcillin; carbeicillin; pipercillin
Page 527
Q0264:diff in MOA of anti-pseudomonals and penicillin?
Page 528
nothing but extensed spectrum
Page 529
Q0265:clinical use of anti-pseudomonals?
Page 530
psudomonas spp. and gram negative rods ;anerobes(bacteroides fragalis)
Page 531
Q0266:are anti-pseudomonals susceptible to penillinase?what can use to help with?
Page 532
yes;give wiht clavulanic acid - which is a beta-lactamaseinhibitor
Page 533
Q0267:toxicity of anti-pseudomonals?
Page 534
hypersensitivity reactions
Page 535
Q0268:B lactamdrugs that inhibit cel wall synthesis but areless susceptible to penicilinase. and a bactericidal
Page 537
Q0269:what are the first generation cephalosporins?
Page 538
cefazolin; cephalexin;cef with lin xin
Page 539
Q0270:clinical use of 1st generation cephalosporins?
Page 540
gram positive cocci; proteus mirabilis; ecoil; klebsiellapneumoniae;pek
Page 541
Q0271:what are the 2nd generation cephalosporins?
Page 542
cefoxitin; cefaclor;cefuroxime;furry fox is fat
Page 543
Q0272:clinical use of 2nd generation cephalosporins?
Page 544
gram positive cocci;h. influenza; enterobacter aerogenes;neiseseria spp;proteus mirabilis; ecoil; klebsiella
pneumoniae;hen peks
Page 545
Q0273:what are the 3rd generation cephalosporins?
Page 546
cetriaxone; cefotaxime; ceftazidime
Page 547
Q0274:clinical use of 3rd generation cephalosporins?
Page 548
serious gram negative infections resistant to oteher Blactams;meningitis (most penetrate BBB)
Page 549
Q0275:ceftazidime used for what?
Page 551
Q0276:ceftriaxone used for what?
Page 553
Q0277:what are 4th generation cephs?
Page 554
cefepime and cefpiramide;pime mide
Page 555
Q0278:clinical use of 4th generation cephalosporins?
Page 556
increased activity against pseudomonas and gram positiveorganisms
Page 557
Q0279:toxicities of all cephs?
Page 558
hypersensitivity reactions;cross hypersensitivity wihtpenicillins;increased nephro tox of aminoglycosides;disuliram
like reaciton w/ ethanol
Page 559
Q0280:what is aztreonam?
Page 560
a monobactam resistan to Beta lactamase
Page 561
Q0281:what is the mOA of aztreonam?
Page 562
inhibits cell wall synthesis ( binds to PBP3) synergistic withaminoglycosides ;no cross-allergy with penicillin
Page 563
Q0282:what is the clinical use of aztreonam?
Page 564
gram negative rods;klebiella spp;pseudomonas spp; serratiaspp;NO activity against gram positive gram positives or
anerobes
Page 565
Q0283:toxicity of aztreonam?
Page 566
usually nontoxic; occasional GI upset
Page 567
Q0284:what drugs avoid during preg?
Page 568
SAFE Moms Take Really GoodCare;Sulfonamides;Aminoglycosides
;Fluoroquinolone;Erythromycin;Metronidazole;Tetracyclins;Ribavirin;Griseoulvin;Chloamphenicol
Page 569
Q0285:what birth defect sulfonamides cause?
Page 571
Q0286:what birth defect aminoglycosides cause?
Page 573
Q0287:what birth defect Fluoroquinolones cause?
Page 574
Cartilage damage
Page 575
Q0288:what birth defect erthyromycin cause?
Page 576
acute cholestatic hepatitis in mom
Page 577
Q0289:what birth defect clarithromycin cause?
Page 579
Q0290:what birth defect metronidazole cause?
Page 581
Q0291:what birth defect tetracylines cause?
Page 582
discolored teeth; inhibition of bone growth
Page 583
Q0292:what birth defect ribavirin cause?
Page 585
Q0293:what birth defect griseofulvin cause?
Page 587
Q0294:what birth defect choloramphenicol cause?
Page 589
Q0295:treat onchoceriasis
Page 590
Ivermectin (rIVER blindness treated wiht IVERmectin)
Page 591
Q0296:treat nemaode/ roundworm (pinworm;whipforminfections
Page 592
mebendazole/thiabendazole
Page 593
Q0297:used to treat;giant worm - ascaris;Hookworm-nectar/ancylostoma;pinworm-enterobius
Page 594
pyrantel pamoate
Page 595
Q0298:used to treat ;trematode/fluke-schistosomes;paragonimus;clonochis;and ;cyticercosis
Page 597
Q0299:treat cestode/tapeworm-diphyllobothriumlatum;taenia;x-cept cysticercosis
Page 599
Q0300:RX leishmaniasis
Page 600
pentavalent antimony
Page 601
Q0301:Rx Malaria
Page 602
Chloroquine;quinine;meloquine;atovaquone;proguanil
Page 603
Q0302:Rx Latent hypnozoite(liver) forms of malaria(P.vivax;P.Ovale)
Page 605
Q0303:RX giardiasis ;amebic dysentry(e. histolytica);bacterial vaginitis (gardnerella vavginalis; Trichomonas
Page 607
Q0304:RX pneumocystis carnii pneumonia prophylaxis
Page 608
TMP-SMX; pentamindine
Page 609
Q0305:RX chagas disease; american typanosomiasis (T.cruzi)
Page 611
Q0306:RX African trypanocomiasis (sleeping sickness)
Page 613
Q0307:what is imipenem/cilastratin. meropenem?
Page 614
broad spectrum ; B lactamase resistant carbenem-alwaysadministered with cilastatin
Page 615
Q0308:what is cilastatin and why is it administered withimipenem?
Page 616
it is a renal dihydropeptidase inhibitor to decease theinactivation of renal tubules
Page 617
Q0309:clinical use of imipenem/cilastatin; meropenem
Page 618
gram poitive cocci; gram negative rods; and anerobes;enterobactor- drug of choice
Page 619
Q0310:drug of choice for enteobacter ?
Page 620
imipenem/cilastatin; meropenem
Page 621
Q0311:what is tox of imipenem/cilastatin; meropenem?
Page 622
GI distress ; skin rash; CNS tox(seizures)@ high plasmalevels
Page 623
Q0312:what drung inhibits cell wall mucopeptide formationby binding D-ala D ala of cell wall precursors.
Page 625
Q0313:how does vancomycin resistance occur?
Page 626
D-ALA D-ALA TO D-ALA D-LAC
Page 627
Q0314:is vacomycin bactericidal or static?
Page 629
Q0315:what is the clinical use of vancomycin?
Page 630
gram positive multidrug resistant organisms includ S. aureusand C. difficile
Page 631
Q0316:what causes nephrotox; ototox; thrombophlebitis anddiffuse flusing
Page 633
Q0317:what causes red man syndrome
Page 635
Q0318:how prevent red man syndrom
Page 636
pretraeat with antihistamines and slow inusion rate
Page 637
Q0319:30 s inhibitors
Page 638
AT 30 ;Aminoglycosides - bacteriocidal;Tetracyclines -bacteristatic
Page 639
Q0320:50 s inhibitors
Page 640
cell at50;Chloamphenicol;erythromycin;lincomycin;cLindamycin;all
bacterio static
Page 641
Q0321:examples of aminoglycosides
Page 642
streptomycin; gentamycin;tobramycin; amikacin
Page 643
Q0322:they are bactericidal ;inhibit ormaltion of initiationcomplex and cause misrading of mrna ;require o2 for uptake
;therfore ineffective angainst anaerobes
Page 645
Q0323:severe gram negative infections ;synergistic with B -lactam antibiotics
Page 647
Q0324:used for bowel surgery
Page 649
Q0325:cause neph tox-es used wiht cephalosporins;ototox -espec with loop diuretics;teratogen
Page 651
Q0326:B lactamase clevage of B lactam ring ;resistance againstwhat?
Page 652
penicillins/cepalosporins
Page 653
Q0327:Modification via acetylation; adenylation; orphosporylation;resistance against what
Page 655
Q0328:terminal D alla of cell wall component with D LACdecreased affinity of drug;resistance against what
Page 657
Q0329:mod via acetylaion;resistance against what
Page 658
choloramphenicol;aminoglycosides
Page 659
Q0330:methylation of rRNA near erythromycin's ribosome-binding site;resistance against what
Page 661
Q0331:increased transport out of cell;resistance against what
Page 663
Q0332:altered enzyme (bacterial dihydropteroate synthetase)or resistance against what
Page 665
Q0333:increased paba synthesis
Page 667
Q0334:decreased uptake
Page 668
tetracyclin and sulfonamides
Page 669
Q0335:antimirobial prophylaxis;meningococcal
Page 670
riampin(drug o choice);minocyclin
Page 671
Q0336:antimirobial prophylaxis;gonorrhea
Page 673
Q0337:antimirobial prophylaxis;syphillis
Page 674
Benzathine penicillin G
Page 675
Q0338:antimirobial prophylaxis;history recurrent UTI's
Page 677
Q0339:antimirobial prophylaxis;pneumocytis cariniipneumonia
Page 678
TMP-SMX (drug of choice);aerosolized pentamidine
Page 679
Q0340:antimirobial prophylaxis;endocarditis with surgical ordental procedures
Page 681
Q0341:inhibits cell wall synthesis ;used for fungus
Page 683
Q0342:clinical use invasive aspergillos
Page 685
Q0343:GI upset and flushing
Page 687
Q0344:inhibits fungal enzyme squalene epoxidase
Page 689
Q0345:used to treat dermatophytoses;esceciallyonychomycosis
Page 691
Q0346:inhibits DNA synthesis by conversion to luorouracil;which completes wiht uracil
Page 693
Q0347:used in systemic fungal infections (candida;cryptococcus)
Page 695
Q0348:causes nausea; vomiting; diarrhea; bone marrowsuppression
Page 697
Q0349:interferes wiht micotubule funtion; disrupts mitosis
Page 699
Q0350:deposits in keratin-containing tissues (nails)
Page 701
Q0351:used for oral treatmetn of superficial infections
Page 703
Q0352:inhibits growth of dermatophytes (tinea andringworm)
Page 705
Q0353:is a teratogenic; carcinogenic; causes confusion;headaches; increased p-450 and warfarin metabolism
Page 707
Q0354:binds to ergosterol ;disrupting ungal membranes ;tootoxic for systemic use
Page 709
Q0355:forms membrane pores that allow leakage ofelectrolyrtes and distrupts homeostatis;bind ergosterol
Page 711
Q0356:causes fever/chills (shake and bake) ; hypotention;neph tox; arrythmias; anemia; IV phlebiis (amphoterrible)
;hydration reduces nephrotox
Page 713
Q0357:used for wide specturm of systemic mycosis;cryptococcus; blastomyces; coccidiodies; aspergillus;
histoplasma; candida; mucor(systemic mycoses);intathecallyfor fungal memingitis; no cross BBB
Page 715
Q0358:swish and swallow or oral candidiasis(thrush);topicalor diaper rash or vaginal candidiasis
Page 717
Q0359:inhibit fungal steroid ergosterol synthesis
Page 718
fluconazol; kepconazole; clotrimazole; itaconazole;voricconazole
Page 719
Q0360:systemic mycosis
Page 720
fluconazol; kepconazole; clotrimazole; itaconazole;voricconazole
Page 721
Q0361:used ofr cytptococcial meningitis in AIDS patinetsand candidal infections of all types -yeast infections
Page 723
Q0362:blastomyces; coccidiodies; histoplasma; candidaalbicans ;
Page 725
Q0363:hormone inhibition (gynecomastia); liver disfunciton(inhibit cytochrome p-450) fever and chills
Page 726
fluconazol; kepconazole; clotrimazole; itaconazole;voricconazole
Page 727
Q0364:inhibits bacterial dihydrofolate reductase;bacteriostatic
Page 729
Q0365:causes megaloblastic anemia; leukopenia;granulocytopenia ;(may alleviate wiht supplimental folinic
acid)
Page 731
Q0366:used in combination wiht sulfonamides (TMP-SMX)causeing sequential block o folate sntheiss ;-combo used in for
what organisms?
Page 732
trimethoprim;used or UTI'S shegella; salmoella; pneumocystiscarinii pneumonia
Page 733
Q0367:What are the Macrolides:
Page 734
Erythromycin; azithromycin; clarithromycin
Page 735
Q0368:Inhibit protein synthesis by blocking translocation;bind to the 23S rRNA of the 50S ribosomal subunit;
bacteriostatic
Page 737
Q0369:Clinical use of macrolides
Page 738
URIs; pneumonias; STDs-- gram positive cocci (streptococcalinfections in patients allegic to penicillin); Mycoplasma;
Legionella; Chlamydia; Neisseria
Page 739
Q0370:GI discomfort (most common cause ofnoncompliance); acute cholestatic hepatitis; eosinophilia; skin
rashes.
Page 740
Macrolides toxicity
Page 741
Q0371:Increases serum concentration of theophyllines; oralanticoagulants
Page 742
Macrolides toxicity
Page 743
Q0372:Chloamphenicol mechanism
Page 744
Inhibits 50S peptidyltransferase; bacteriostatic
Page 745
Q0373:Meningitis (Haemophilus influenzae;Neisseriameningitidis; Streptococcus pneumoniae
Page 746
clinical use of chlorophenicol
Page 747
Q0374:tox chloroamphenicol
Page 748
anemia(doe dependent); aplastic anemia(does independnet);gray abby syndrome (in premature infants b/c they lack liver
udp-glycuronyl transferase
Page 749
Q0375:clocks peptide bond formation at 50s ribosomalsubunit . bacteriostatic
Page 751
Q0376:treats anaerobes above the diaphram
Page 753
Q0377:treat anaerobic infections (Bacteroides fragalis;clostridium perfringens)
Page 755
Q0378:pseudomembranous colitis (C. difficile overgrowth.fever ; diarrhea
Page 757
Q0379:types of sulfonamides
Page 758
sulfamethoxazole (SMX) sulfisoxazole; triple sulfas;sulfadiazine
Page 759
Q0380:PABA antimetabolites inhibit dihydropteroatesynthase. bacteriostatic
Page 760
sulfonamides MOA
Page 761
Q0381:clinical use of sulfonamides
Page 762
gram-positive; gram-negative; Nocaria; Chlamydia. Triplesulfas or SMX for simple UTI
Page 763
Q0382:Hypersensitivity reactions; hemolysis if G6PDdeficient; nephrotoxicity (tubulointerstitial nephritis)
Page 765
Q0383:kernicterus in infacnts
Page 767
Q0384:displace other drugs from albumin (e.g. warfarin)
Page 769
Q0385:What are the fluoroquinolones
Page 770
ciprofloxacin; norfloxacin; ofloxacin; sparfloxacin;moxifloxacin; gatifloxacin; enoxacin; nalidixic acid (a
quinolone)
Page 771
Q0386:inhibit DNA gyrase (topoisomerase II); bacericidal
Page 772
fluoroquinolones' mechanism
Page 773
Q0387:clinical use of fluoroquinolones
Page 774
gram-negative rods or urinary and GI tracts (includingPesudonomas); Neisseria; some gram-positive organisms
Page 775
Q0388:GI upset; superinfections; skin rashes; headache;dizziness.
Page 776
fluoroquinolones tox
Page 777
Q0389:Contradicted in pregnant women and children becauseanimal studies show damage to cartilage.
Page 778
fluoroquinolones tox
Page 779
Q0390:Tendonitis and tendon rupture in adults; leg crampsand myalgias in kids.
Page 780
fluoroquinolones tox
Page 781
Q0391:Metronidazole mechanism
Page 782
forms metabolites in the bacterial cell; bactericidal
Page 783
Q0392:Antiprotozoal
Page 784
Metronidazole clinical use
Page 785
Q0393:Giardia; Entamoeba; Trichomonas; Gardnerellavaginalis; anaerobes (bacteriodes; clostridium)
Page 786
Metronidazole clinical use
Page 787
Q0394:used with bismuth and amoxicillim (or tetracycline) for"triple therapy" against H. pylori
Page 788
Metronidazole clinical use
Page 789
Q0395:polymixin B and polymixin E are examples of what?
Page 791
Q0396:bind to cell membranes of bacteria and distrupt theirosmotic properties ;care cationic;basic ;act like detergents
Page 792
polymixins;-myxins mix up membranes
Page 793
Q0397:resistant to grm negative infections
Page 795
Q0398:neurotox; acute renal tubular necrosis
Page 797
Q0399:streptomycin;pyrazinamide;isoniazid(INH);rifampin;ethambutol;cycloserin
e (2nd line therapy)
Page 799
Q0400:tb prophylazxis?
Page 801
Q0401:deacerased synthesis of mycolic acid
Page 803
Q0402:hemolysis if G6PD deficincy ; enurotox; hepatotox;SLE ;
Page 805
Q0403:what can prevent neurotox in INH
Page 806
pyridoxine vit b6
Page 807
Q0404:common tox to all anti-tb drugs
Page 809
Q0405:inhibits DNA- dependent RNA polymerase
Page 811
Q0406:used against TB delays reasistance to dapsone whenused for leprosy ;used for meningococcal prophylaxis in
contacts of childeren with H. influenza type B
Page 813
Q0407:causes minor heptotox and drug interaction (increasedP 450)
Page 815
Q0408:inhibits influenza neuroaminidase. so release ofprogeny virus is decreased
Page 816
Zanamivir; oseltamivir
Page 817
Q0409:influeza A and B
Page 818
Zanamivir; oseltamivir
Page 819
Q0410:inhibits synthesos o guanine nucleotides bycompetivitly inhibiting IMP dehydrogenase
Page 821
Q0411:RSV; chronic hepatitis C
Page 822
Clinical use of ribavirin
Page 823
Q0412:hemolytic anemia; sever teratogen
Page 825
Q0413:preferentially inhibits viral DNA polymerase whenphosphorylates by viral thymidine kinase
Page 827
Q0414:HSV;VZV;EBV;mucocutaneous and genital herpeslesions. prophylaxis in immunocompromised patients
Page 829
Q0415:delirium; tremor; nephrotox
Page 831
Q0416:lack of thymidine kinase
Page 833
Q0417:phosphorylation by viral kinas preferentially inhibitsCMV DNA polymerase
Page 835
Q0418:CMV ; esecially in immunocompromised patients
Page 837
Q0419:leukopenia; neutropenia; thrombocytopenia; renal tox.MOre tox to host enzymes than acyclovir
Page 839
Q0420:Mutated CMV DNA polymerase or lack of thymidinekinase
Page 841
Q0421:blocks viral penetration/uncoating(M2 protein) maybuffer pH o endosome. also caus the release of dopamine rom
intact nerve terminals
Page 843
Q0422:prophylaxis and treatmetn for influenza A;parkinson's disease
Page 844
Clinical use of amantadine
Page 845
Q0423:ataxia; dizziness; slurred speech
Page 846
tox of amantadine
Page 847
Q0424:Mutated M2 protein. In 2006 ; 90% of influenza Awere resistant to amantadine
Page 849
Q0425:is a derivative with fewer Cns side effects . does notcross the BBB
Page 851
Q0426:Viral DNA polymerase inhibitor that binds to thepyroposphate binding site o the enzyme . does not require
activatiation by viral kinase
Page 855
Q0428:mutated DNA Polymerase
Page 856
mechanism of resistance of foscarnet
Page 857
Q0429:glycoproteins from human leukocytes that blockvarious various stages of RNA and DNA syntheiss. Induce
ribonuclease that degrades viral mRNA
Page 859
Q0430:pyrofosphate analog
Page 861
Q0431:IFN alpha used for what
Page 862
chronic hep B and C;KAPOSi's sarcoma
Page 866
NADPH; OXIDASE DEFICIENCY
Page 867
Q0434:NEUTROPENIA
Page 868
tox or interferone
Page 869
Q0435:plioconanl
Page 870
for poliovirus inhibits penetration of picornavirus into cell
Page 871
Q0436:saquinavir ; ritonavir ; indinavir nelfinacir amprenavirused for what?are what>
Page 872
HIV THERAPY ;are protease inhibitors;NAVIR tease a pro-tease inhibitor
Page 873
Q0437:what inhibits assembly of new virus by blockingprotease in progency virons
Page 874
protease inhibitors for HIV therapy;saquinavir ; ritonavir ;indinavir nelfinacir amprenavir
Page 875
Q0438:cause GI intolerance (N; dia); hyperglycemia;lipodystrophy; thrombocytopenia(indinavir)
Page 877
Q0439:ZIDOVUDINE(AZT); didanosine (ddI);zalcitabine(ddC); stavudine(d4T); lamivudine(3TC);abacavir
Page 878
nucleosides - reverse transcriptase inhibitores for HIV
Page 879
Q0440:nin nucleoside reverse transcriptase inhibitors for HIV
Page 880
Nevirapine; efavirenz;delavirdine
Page 881
Q0441:prefeentially inhibit reverse transcriptase of HIV;incorporation of viral genome into ost DNA
Page 882
reverse transcriptase inhibitors both types
Page 883
Q0442:cause bone marrow suppression (neutropenia andanemia); peripheral neuropathy; lactic ascisoiss(neucleosides)
rash (non-nucleaosides); megaloblastic anemia(AZT)
Page 884
TOX of reverse transcriptase inhibitors both types
Page 885
Q0443:highly active antiretroviral therapy
Page 887
Q0444:what is HAART
Page 888
combo therapy o protease inhibitos reverse transcriptaseinhibitors
Page 889
Q0445:at what cell count is HAART INDICATED
Page 890
<500cells/mm3 of CD4; or high viral load
Page 891
Q0446:is AZT USED during preg why?
Page 892
yes - to reduce risk o etal transmission
Page 893
Q0447:Clinical use of tetracyclines:
Page 894
Vibrio cholerae; Acne; Chlamydia; Ureaplasma; Urealyticum;Mycoplasma pneumoniae; Tularemia; H. pylori; Borrelia
burgdorferi (Lyme Disease); Rickettsia;Vaccum the Bedroom
Page 895
Q0448:GI distress; discoloration of teeth and inhibition ofbone growth in children; photosensitivity; contradiction in
pregnancy
Page 896
Tetracycline toxicity
Page 897
Q0449:Tetracyclines
Page 898
Bacteriostatic; bind to 30S and prevent attachment ofaminoacyl-tRNA; limited to CNS penetration
Page 899
Q0450:This is fecally eliminated and can be used in patientswith renal failure
Page 900
Doxycycline ;(must not take with milk; antacids; or iron-containtaing preparations because divalent cations inhibit its
absorbtion in the gut)
Page 901
Q0451:What are the tetracyclines?
Page 902
Tetracyclines; doxycycline; demeclocycline; minocycline
Page 903
Q0452:block mRNA synthesis
Page 905
Q0453:penicillin;blocks ___ (1.) cross-linking of cell wall bybinding PBP's;activates ___ (2.) enzymes;and is
bacteriCIDAL for ___(3; 4; 5; 6.)
Page 906
1. transpeptidase;2. autolytic;3. gram pos cocci;4. gram posrods;5. gram neg cocci;6. spirochetes
Page 907
Q0454:methicillin; nafcillin; dicoxacillin;are penicillinase __(1);have ___ (2) spectrum due to ___ (3);tx: (4)
Page 908
1. resistant;2. narrow;3. bulkier R group;4. staph a
Page 909
Q0455:ampicillin and amoxacillin;penicillinase __ (1);whichhas greater oral bioavailabiliity? (2);tx: (3-8)
Page 910
1. sensitive;2. amOxacillin;3. Haemophilus;4. E. coli;5.listeria;6. proteus;7. salmonella;8. enterococci;(HELPS kill
Enterococci)
Page 911
Q0456:carbenicillin; piperacillin; ticarcilin;penicillinase __(1);tx: (2; 3)
Page 912
1. sensitive;2. pseudomonas;3. gram neg rods
Page 913
Q0457:cephalosporins inhibit __ (1);1st gen tx (2-4);2nd gentx (5-10);3rd gen tx (11-12);(13) for pseduomonas;(14) for
gonorrhea;4th gen tx (15-16)
Page 914
1. Proteus 2. E coli 3. Klebsiella (PEcK);4. Haemophilus 5.Enterobacter aerogenes 6. Neisseria 7. Proteus 8. E coli 9.
Klebsiella 10. Serratia (HEN PEcKS);11. serious gram neg and12. meningitis;13. ceftazidime;14. ceftriaxone;15.
pseudomonas and gram pos
Page 915
Q0458:aztreonam;beta lactamase __(1);inhibits cell wallsynthesis by binding __(2);synergistic w/ __ (3);tx: (4-6);used
for patients;(7)
Page 916
1. resistant;2. PBP3;3. aminoglycosides;4. Klebsiella;5.pseudomonas;6. serratia;7. with penicillin allergy and thosewith renal insufficiency who can't tolerate aminoglycosides
Page 917
Q0459:impipenem;the kill is lastin w/ ; (1.)because (1)inhibits (2)to dec inactivation in renal tubules;beta lactamase
(3);tx (4-6);drug of choice for (7)
Page 918
1. cilastatin;2. renal dihydropeptidase I;3. resistant;4. grampos cocci;5. gram neg rods;6. anaerobes;7. enterobacter
Page 919
Q0460:vancomycin;inhibits cell wall mucopeptide formationby binding (1);tx: serious gram pos MDR organisms including;(2-3);it is generally well tolerated but side effects include (4-7)
Page 920
1. D-ala-D-ala;2. staph a;3. C. difficille;4. Nephrotoxicity;5.Ototoxicity;6. Thrombophlebitis;7. red man syndrome
(minimized w/ HA)
Page 921
Q0461:mnemonic for protein synthesis inhibitors;
Page 922
buy AT 30; CELL at 50;Aminoglycosides -bacteriCIDAL;Tetracyclines;Chloramphenicol;Erythromycin;
Lincomycin;cLindamycin
Page 923
Q0462:aminoglycosides;require _(1) for uptake;tx(2);synergistic w/ (3);use (4) for bowel surgery;toxicity (5; 6)
Page 924
1. O2 (-> innefective against anaerobes);2. severe gram neg rodinf;3. beta lactams;4. neomycin;5. nephrotoxicity;6.
otoxicity;(amiNOglycosides)
Page 925
Q0463:testracyclines;(1) is fecally eliminated -> can be usedw/ renal failure;must not take w/ (2) because divalent cations
inhibit absorption;tx (3-10)
Page 926
1. doxycyclin;2. milk; anatids; Fe;3. vibrio 4. acne 5.chlamydia 6. ureaplasma urealyticum 7. mycoplasma
pneumonia 8. borellia 9. rickettsia 10. tularemia;(VACUUMyour Bed Room Tetracyclines)
Page 927
Q0464:macrolides;tx generally (1-3);specifically- (4-8)
Page 928
1. URI;2. pneumonia;3. STDs;4. gram pos cocci;5.mycoplasma;6. legionella;7. chlamydia;8. neisseria
Page 929
Q0465:chloramphenicol;tx (1);limit use because of (2);causesGray baby syndrome because they lack (3)
Page 930
1. meningitis;2. toxicities- dose dependent anemia; doseindependent aplastic anemia;3. UDP-glucuronyl transferase
Page 931
Q0466:clindamycin;tx (1)
Page 932
anaerobes above the diaphragm
Page 933
Q0467:sulfonamides;inhibit (1);tx (2-5);toxicity (6-9)
Page 934
dihydropteroate synthase;2. gram pos;3. gram neg;4.nocardia;5. chlamydia;6. hemolysis of G6pD;7.
nephrotoxicity;8. kernicterus in infants;9. displace drugs fromalbumin
Page 935
Q0468:simple UTIs;recurrent UTIs
Page 936
triple sulfas or SMX;TMP-SMX
Page 937
Q0469:trimethoprim inhibits (1);toxicity (2);may alleviate w/supplemental (3)
Page 938
1. DHF reductase;2. TMP- treats marrow badly(megaloblastic anemia; leukopenia; granulocytopenia);3.
folinic acid
Page 939
Q0470:TMP/SMX combo used for;(1-4)
Page 940
recurrent UTIs;salmonella;PCP;shigella;(USPS)
Page 941
Q0471:fluoroquinolones;inhibit (1);tx: (2);toxicity (3)
Page 942
1. DNA topoisomerase I (gyrase);2. gram neg rods of UTtract and GI tract;3. damage to cartilage; tendonitis; tendonrupture;(Fluoroquinolones hurt attachments to your bones)
Page 943
Q0472:metronidazole tx (1-3);toxicity: (4)
Page 944
1. giardia;2. entamoeba;3. trichomonas;(GET on the metro);4.disulfiram like effect w/ alcohol
Page 945
Q0473:polymyxins are cationic basic proteins that act like(1);tx (2);toxicity (3-4)
Page 946
1. detergents;2. res gram neg inf;3. neurotoxicity;4. acute renaltubular necrosis
Page 947
Q0474:isoniazid;dec synthesis of;(1);only agent used as soloprophylaxis for (2);toxicity (3-6);different half-lives in (7)
Page 948
1. mycolic acids;2. mycobacterium TB;3. hemolysis if G6PDdef;4. SLE-like syndrome;5. neurotoxicity (can prevent with
B6);6. hepatotoxicity;(INH Injures Neurons andHepatocytes);7. slow vs fast acetylators
Page 949
Q0475:rifampin;inhibits (1);tx (2-5);6. Four R's of rifampin;
Page 950
1. DNA dep RNA pol;2. TB;3. delays resistance to dapsonefor leprosy;4. meningococcal prophylaxis;5. H. influenze Bprphylaxis;6. RNA pol inhibitor;Revs up P450;Red/orange
body fluids;Rapid resistance if used alone
Page 951
Q0476:1. name the five anti-TB drugs;2. which is used alonefor prophylaxis;3. all are ;
Page 952
1. Rifampin; Ethambutol; Streptomycin; Pyrazinamide; INH(RESPIre);2. INH;3. hepatotoxic
Page 953
Q0477:aminoglycoside resistance
Page 954
modification via;acetylation;adenylation;phosphorylation
Page 955
Q0478:vancomycin resistance
Page 956
replace terminal D-Ala w/ D-lac to dec affinity
Page 957
Q0479:macrolide resistance
Page 958
methylation of rRNA near erythromycin's ribosome bindingsite
Page 959
Q0480:tetracycline resistance
Page 960
dec uptake or inc transport out of cell
Page 961
Q0481:sulfonamide resistance
Page 962
altered enzyme;dec uptake;inc PABA
Page 963
Q0482:prophylaxis for;1. meningococcus;2. gonorrhea;3.syphilis;4. recurrent UTI;5. PCP
Page 964
1. rifampin;2. ceftriaxone;3. benzathine penicillin G;4. TMP-SMX;5. TMP-SMX
Page 965
Q0483:amphotericin;binds (1);tx (2);cross the bbb?(3);toxicity (4)
Page 966
1. ergosterol - tears holes in wall;2. systemic mycoses;3.doesn't cross BBB- use intrathecaly for fungal meningitis;4.
"shake and bake" fevers and chills; arrhythmias(amphoterrible)
Page 967
Q0484:nystatin;binds (1);tx (2)
Page 968
1. ergosterol;2. swish and swallow for thrush
Page 969
Q0485:azoles;inhibit (1);tx (2);(3) for cryptococcal meningitisand candida;(4) for blasto; coccidioides; histo; candida;also
used to tx (5);toxicity (6-7)
Page 970
1. ergosterol synthesis;2. systemic mycoses;3. fluconazole;4.ketoconazole;5. hypercortisolism;6. gynecomastia;7. inh P450
Page 971
Q0486:flucytosine;inhibits (1);tx (2)
Page 972
1. DNA synthesis by conversion to FU which competes w/uracil;2. systemic fungal infections
Page 973
Q0487:caspofungin ;inhibits (1);tx (2)
Page 974
1. cell wall synthesis;2. invasive aspergillosis
Page 975
Q0488:terbinafine;inhibits (1);tx (2)
Page 976
1. squalene epoxidase which converts squalene to lanosterol;2.dermatoophytoses
Page 977
Q0489:griseofulvin;inhibits (1);tx (2);toxicity (3)
Page 978
1. microtubules fx;2. oral tx of superficial infections;3. incwarfarin metabolism
Page 979
Q0490:amantadine;blocks (1);causes release of (2);tx (3-5);amantadine mnemonic (6)
Page 980
1. uncoating;2. DA;3. influenza A;4. rubellA;5. Parkinson's;6.Amantadine blocks influenza A and rubellA and causes
problems with the cerebellA
Page 981
Q0491:rimantadine has (1) CNS side effects than amantadine
Page 983
Q0492:zanamivir inhibits (1);tx (2-3)
Page 984
1. neuramidase;2. influenza A;3. influenza B
Page 985
Q0493:ribavirin inhibits (1);tx (2);toxicities (3-4)
Page 986
1. IMP dehydrogenase -> no guanine;2. CMV;3. hemolyticanemia;4. teratogenic!
Page 987
Q0494:acyclovir;MOA (1)
Page 988
inhibits DNA pol when phosphorylated by viral thymidinekinase
Page 989
Q0495:DHPG (dihydroxy-2-propoxymethyl guanine);=(1);MOA (2);tx (3);toxicities (4-7)
Page 990
1. ganciclovir;2. phosphorylation by viral kinase ->preferential inhibition of CMV DNA pol;3. CMV;4.
thrombocytopenia;5. leukopenia;6. neutropenia;7. renaltoxicity
Page 991
Q0496:foscarnet;MOA (1);tx (2);toxicity (3)
Page 992
1. binds to pyrophosphate binding site of DNA pol ->inhibition;(FOScarnet - pyroFOSphate analog);2. CMV
retinitis if ganciclovir fails;3. renal toxicity
Page 993
Q0497:"-navir" drug;MOA
Page 994
protease inhibitor
Page 995
Q0498:Rerverse transcriptase inhibitors;(6)
Page 996
abacavir;lamivudine;didanosine;stavudine;zidovudine(AZT);zalcitabine;(AL DiSsed ZZ and
NED);nevirapine;efavirenz;delavirdine;(NED is a non-nucleoside)
Page 997
Q0499:interferons;tx (3);toxicity (4)
Page 998
chronic HBV;HCV;kaposi sarcoma;neutropenia
Page 999
Q0500:tx for onchocerciasis
Page 1000
ivermectin;(tx rIVER blindness with IVERmectin)
Page 1001
Q0501:taenia solium;transmission;tx
Page 1002
undercooked pork tapewom;praziquantel;albendazole forcysticercosis
Page 1003
Q0502:echinococcus granulosus;transmission;tx
Page 1004
dog feces -> cysts in liver;albendazole
Page 1005
Q0503:trematodes;tx
Page 1007
Q0504:schistosoma;transmission;tx
Page 1008
from snails -> granulomas and fibrosis of spleen andliver;praziquantel
Page 1009
Q0505:clonorchis sinensis;transmission;tx
Page 1010
undercooked fish -> biliary tract inflammation;praziquantel
Page 1011
Q0506:paragonimus westernami;transmission;tx
Page 1012
undercooked crab meat -> inflammation of lung;praziquantel
Page 1013
Q0507:ancylcostomal duodenale
Page 1014
hookworm;mebendazole
Page 1015
Q0508:ascaris lumbricoides
Page 1017
Q0509:enterobius vermicularis
Page 1018
pinworm;mebendazole
Page 1019
Q0510:strongyloids stercoralis
Page 1021
Q0511:trichinella spiralis
Page 1023
Q0512:dracuncullus medinensis
Page 1024
nitridazole;(Dracula comes out at Night)
Page 1026
transmitted by deer fly;can see worm crawling inconjunctiva;tx diethylcarbamazine
Page 1027
Q0514:toxocara canis
Page 1028
diethylcabamazine
Page 1029
Q0515:wucheria bancrofit
Page 1030
diethycarbamazine;(can cause elephantiasis)
Page 1031
Q0516:Imipenem/cilastatin What is imipenem?
Page 1032
broad spectrum beta-lactamase-resistant carbapenem
Page 1033
Q0517:Imipenem What do you always administer it with andwhy?
Page 1034
cilastatin -- it decreases inactivation of imipenem in renaltubules
Page 1035
Q0518:Imipenem/cilastatin What do you use it for?
Page 1036
Gram pos cocci; gram neg rods and anaerobes (broadspectrum); drug o' choice for Enterobacter;the girl from
Ipanema was a Broad; y era Enterita
Page 1037
Q0519:Imipenem/cilastatin What bug is it the drug of choicefor?
Page 1039
Q0520:Imipenem/cilastatin What are its side-effects
Page 1040
GI distress; skin rash; seizures at high conc;kid with skinproblems getting nervous (upset stomach; shaking) when
talking to girl from Ipanema
Page 1041
Q0521:Vancomycin Is it bactericidal or bacteriastatic andwhy?
Page 1042
Bactericidal because it blocks cross linkage and elongation ofpeptidoglycan by binding D-ala D-ala protion of cell wall.
Page 1043
Q0522:Vancomycin How does resistance to Vanco occur?
Page 1044
D-ala D-ala is replaced with D-ala D-lactate which vanco doesnot block
Page 1045
Q0523:Vancomycin What is it used for?
Page 1046
Used for serious infection that is resistant to other drugs (e.g.gram pos multi-drug resistant organisms like S. aureus and C.
difficile; methicillin resistant staph (MRSA))
Page 1047
Q0524:Vancomycin What are the important toxicities ofvanco?
Page 1048
generally NOT many problems except; Nephrotoxicity;Ototoxicity and Thrombophlebitis;*also red man syndrome;
give with histamine to prevent
Page 1049
Q0525:Vancomycin What can happen with rapid infusion ofvanco?
Page 1050
Red man's syndrome. Diffuse flushing which can be controlledby pretreatment with anti-histamines and with slow infusion
rate
Page 1051
Q0526:Protein Synthesis Inhibitors Which drugs targetbacterial protein synthesis by blocking the 30S unit vs 50S
unit?
Page 1052
Buy AT 30; CELL at 50
Page 1053
Q0527:Protein Synthesis Inhibitors What does AT stand for?
Page 1054
A = Aminoglycosides (streptomycin; gentamicin; tobramycinan damikacin. And T = Tetracyclines
Page 1055
Q0528:Protein Synthesis Inhibitors What does CELL standfor?
Page 1056
C = Chloramphenicol; E= Erythromycin; L= Lincomycin andL= cLindamycin
Page 1057
Q0529:Which of the Protein Synthesis Inhibitors arebactericidal?
Page 1058
Only the aminoglycosides are; the rest are bacteriostatic
Page 1059
Q0530:Aminoglycosides Name some aminoglycosides?
Page 1060
Gentamicin; neomycin; amikacin; tobramycin andstreptomycin;mean GNATS
Page 1061
Q0531:Aminoglycosides How do these drugs work?
Page 1062
They inhibit formation of the initiation complex in mRNAtranslation
Page 1063
Q0532:Aminoglycosides Why are they ineffective againstanaerobes?
Page 1064
They require oxygen for uptake into bacteria
Page 1065
Q0533:Aminoglycosides When would you useaminoglycosides?
Page 1066
against severe gram-negative rod infections
Page 1067
Q0534:Aminoglycosides What drugs can you useaminoglycosides with for synergy?
Page 1068
the drugs that inhibit cell wall synthesis (e.g. penicillin andcephalosporins -- the beta-lactam antibiotics). Presumablythis allows the drug to get in with out reliance on oxygen
transport
Page 1069
Q0535:Aminoglycosides What drug in this class is commonlyused for bowel surgery?
Page 1071
Q0536:Aminoglycosides What are the major toxicities?
Page 1072
Nephrotoxicity (esp w/ cephalosporins); Ototoxicity (esp w/loop diuretics); Teratogen;mean GNATS canNOT kill
anaerobes
Page 1073
Q0537:Tetracyclines Name some tetracylcines
Page 1074
Tetracycline; doxycycline; demeclocycline; minocycline
Page 1075
Q0538:Tetracyclines How does it work?
Page 1076
Blocks t-RNA attachment to 30S subunit
Page 1077
Q0539:Tetracyclines Which tetracycline can you use inpatients with renal failure and why?
Page 1078
Can use doxycycline because its elimination is fecal
Page 1079
Q0540:Tetracyclines Should you take these drugs with a glassof milk?
Page 1080
NO; because it intereferes with absorption in the gut as doesantacids and iron-containing preparations; or any divalent
cations
Page 1081
Q0541:Tetracyclines What are tetracyclines used for?
Page 1082
Toby; VACUUM THe Bed Room-- Vibrio cholerae; Acne;Chlamydia; Ureaplasma; Urealyticum; Mycoplasma
pneumoniae; Tularemia; H pylori; Borrelia burgdorferi;Rickettsia
Page 1083
Q0542:Tetracyclines What are the common toxicities
Page 1084
GI distress; teeth discoloration; inhibition of bone growth inchildren; Fanconi's syndrome and photosensitivity.
Contraindicated in pregnancy
Page 1085
Q0543:Macrolides Name some macrolides?
Page 1086
Erythromycin; azithromycin; Clarithromycin;EaZy was aCrip Mac
Page 1087
Q0544:Macrolides How do these drugs work?
Page 1088
bind to 23S rRNA of 50S and inhibit translocation;bacteriostatic
Page 1089
Q0545:Macrolides What are they used for?
Page 1090
URIs; pneumonias; STDs -- streptococcal in patients that areallergic to PNC --- Mycoplasm; Legionella; Chlamydia;
Neisseria;Eryc's Nipple's at the Mid Clavicular Line
Page 1091
Q0546:Macrolides Pneumonic for macrolide use?
Page 1092
Eryc's Nipple is at his Mid Clavicular Line (Eryc is brandname for erythromycin; and eazy e's real name). Neisseria;
Mycoplasm; Chlamydia; Legionella.
Page 1093
Q0547:Macrolides What are the major toxicities?
Page 1094
GI discomfort; acute Cholestatic hepatitis; Eosinophilia; skinrashes;increases serum theophylines and oral
anticoagulants;the Mac eazy E was a Gangsta Crip with badSkin
Page 1095
Q0548:Macrolides What is the most common cause for non-compliance to macrolides?
Page 1097
Q0549:Chloramphenicol How does this drug work?
Page 1098
inhibits 50S peptidyltransferase
Page 1099
Q0550:Chloramphenicol Main use?
Page 1100
Meningitis (H. influenzae; N. meningitides; S. pneumo). Usedconservatively b/c of toxicity
Page 1101
Q0551:Chloramphenicol What are the main toxicities?
Page 1102
Anemia and aplastic anemia (both dose dependent); gray babysyndrome (in premes b/c they lack UDP-glucoronyl
transferase)
Page 1103
Q0552:Clindamycin How does it work?
Page 1104
blocks peptide bond formation at 50S;with CLINdamycin; theamino acids don't CLINk together
Page 1105
Q0553:Clindamycin When do you use it?
Page 1106
Anaerobic infections (e.g. Bacteroides fragilis andC.perfringens)
Page 1107
Q0554:Clindamycin Toxicities?
Page 1108
Pseudomembranous colitis; fever; diarrhea
Page 1109
Q0555:Sulfonamides Name some sulfonamides
Page 1110
Sulfamethoxazole (SMX); sulfisoxazole; triple sulfa andsulfadiazine
Page 1111
Q0556:Sulfonamides How does it work?
Page 1112
Inhibits bacterial folic acid synthesis from PABA by blockingdihydropteroate synthase.
Page 1113
Q0557:Sulfonamides What are its uses?
Page 1114
Gram-positive; gram-negative; Nocardia; Chlamydia. Triplesulfas and SMX for simple UTIs
Page 1115
Q0558:Sulfonamides Toxicities?
Page 1116
hypersensitivity rxn; hemolysis if G6PD deficient;nephorotoxicity (tubulointerstitial nephritis); kernicterus in
infants; displace other drugs from albumin (e.g. warfarin)
Page 1117
Q0559:Trimethoprim How does it work?
Page 1118
inhibits folic acid pathway by blocking dihydrofolatereductase which humans have as well
Page 1119
Q0560:Trimethoprim What are its uses?
Page 1120
used in combo with Sulfamethoxazole (TMP-SMX) causing asequential block of folate synthesis. Used for recurrent UTIs;
Shigella; Salmonella; and prophylaxis for PCP in AIDSpatients
Page 1121
Q0561:Trimethoprim Toxicities?
Page 1122
Megaloblastic anemia; pancytopenia (may be alleviated withsupplemental folinic acid)
Page 1123
Q0562:Fluoroquinolones What the most famousfloroquinolone?
Page 1124
Ciprofloxacin (treatment for Anthrax)
Page 1125
Q0563:Fluoroquinolones How does it work?
Page 1126
inhibits DNA gyrase (topoisomerase II)
Page 1127
Q0564:Fluoroquinolones What are its uses?
Page 1128
Gram neg rods or urinary and GI tract (incl. pseudomonas);Neisseria; some gram pos spp
Page 1129
Q0565:Fluoroquinolones What population is contraindicatedfor use?
Page 1130
pregnancy and children
Page 1131
Q0566:Fluoroquinolones What are its toxicities?
Page 1132
GI upset; superinfection; skin rashes; headache; dizziness andtendonitis and tendon rupture in adults. FluoroquinoLONES
hurt attachment to BONES.
Page 1133
Q0567:Metronidazole How does it work?
Page 1134
forms toxic metabolites in the bacteria. Bactericidal.
Page 1135
Q0568:Metronidazole What are its uses?
Page 1136
antiprotazoal;Giardia; Entamoeba; Trichomonas;GET on theMetro;anaerobes;gardnerella vaginalis; Bacteroides;clostridium;Used with bismuth and amoxicillin (or
tetracycline) for triple therapy against H pylori;BAM!
Page 1137
Q0569:What is the role of Metronidazole in H. pyloriinfection?
Page 1138
Used as part of triple therapy: bismuth; amoxicillin andmetronidazole;BAM!
Page 1139
Q0570:Metronidazole Main toxicity?
Page 1140
disulfiram-like (antabuse) reaction to alcohol and headache
Page 1141
Q0571:Which drug do you use to treat anaerobic infectionsabove the diaphram and which for below the diaphram
Page 1142
anaerobes above diaphram: Clindamycin; and anaerobes belowdiaphram: metronidazole
Page 1143
Q0572:Polymyxins How does it work?
Page 1144
disrupts osmotic properties of bacteria; acts like a detergent
Page 1145
Q0573:Polymyxins What is it used for?
Page 1146
resistant gram negative infections
Page 1147
Q0574:Polymyxins Toxicities?
Page 1148
neurotoxicity; acute renal tubular necrosis
Page 1149
Q0575:Isoniazid How does it work?
Page 1150
decreases synthesis of mycolic acid
Page 1151
Q0576:Isoniazid What is it used for?
Page 1152
MTB (mycobacterium tuberculosis). The only agent used assolo prophylaxis against TB
Page 1153
Q0577:Isoniazid Toxicities?
Page 1154
Hemolysis if G6PD deficient; neurotoxicity; hepatotoxicitiy;drug induced SLE. INH; Injures Neurons and Hepatocytes
Page 1155
Q0578:Isoniazid What vitamin prevents neurotoxicity
Page 1156
Vitamin B6 (pyridoxine)
Page 1157
Q0579:Isoniazid Why are toxicities particularly important tomonitor in patients taking INH?
Page 1158
INH half-lives are different in fast versus slow acetylators!
Page 1159
Q0580:Rifampin How does it work?
Page 1160
inhibits DNA-dependent RNA polymerase
Page 1161
Q0581:Rifampin What is it used for?
Page 1162
Mycobacterium tuberculosis; delays resistance to dapsonewhen used for leprosy; meningococcal prophylaxis
Page 1163
Q0582:Rifampin Toxicities?
Page 1164
Minor hepatotoxicity and increases P-450
Page 1165
Q0583:Rifampin How can it be used for leprosy?
Page 1166
rifampin delays resistance to dapsone when used for leprosy
Page 1167
Q0584:Rifampin What would happen if you used rifampinalone?
Page 1168
get rapid resistance
Page 1169
Q0585:Rifampin What does it do to bodily fluids?
Page 1170
makes them red/orange in color
Page 1171
Q0586:Rifampin What are the 4 R's of Rifampin
Page 1172
RNA polymerase inhibitor; Revs up microsomal p-450;Red/Orange body fluids; Resistance is rapid if used alone
Page 1173
Q0587:Anti-TB Drugs What are the anti-TB drugs?
Page 1174
Rifampin; Ethambutol; Streptomycin; Pyrazinamide;Isoniazid (INH) -- RESPIre
Page 1175
Q0588:Anti-TB Drugs What do you use for TB prophylaxis?
Page 1177
Q0589:Anti-TB Drugs What toxicity is common to all?
Page 1179
Q0590:Most common resistance mechanism for penicillins /cephalosporins.
Page 1180
Beta-lactamase cleavage of beta-lactam ring.
Page 1181
Q0591:Most common resistance mechanism foraminoglycosides.
Page 1182
Modification via acetylation; adenylation; orphosphorylation.
Page 1183
Q0592:Most common resistance mechanism for vancomycin.
Page 1184
Terminal D-ala of cell wall component replaced with D-lac;decrease affinity.
Page 1185
Q0593:Most common resistance mechanism forChlorampenicol.
Page 1186
Modification via acetylation.
Page 1187
Q0594:Most common resistance mechanism for macrolides.
Page 1188
Methylation of rRNA near erythromycin's ribosome-bindingsite.
Page 1189
Q0595:Most common resistance mechanism for tetracycline.
Page 1190
Decrease uptake or increase transport out of cell.
Page 1191
Q0596:Most common resistance mechanism for sulfonamides.
Page 1192
Altered enzyme (bacterial dihydropteroate synthetase);decrease uptake; or increase PABA synthesis.
Page 1193
Q0597:drug of choice for prophylaxis of meningococcalinfection.
Page 1194
Rifampin (drug of choice)
Page 1195
Q0598:Drug of choice for gonorrhea.
Page 1196
Ceftriaxone. 3rd generation cephalosporin.
Page 1197
Q0599:Drug of choice for syphilis.
Page 1198
Benzathine penicillin G.
Page 1199
Q0600:Drug of choice for meningococcal infection. Drug ofchoice for history of recurrent UTIs.
Page 1201
Q0601:Drug of choice for Pneumocystis carinii pneumonia.
Page 1202
TMP-SMX (drug of choice); aerosolized pentamindine
Page 1203
Q0602:Viral adsorption and penetration into the cell isblocked by ---------.
Page 1204
Gama-globulins (non-specific).
Page 1205
Q0603:Uncoating of the virus after its penetration into thecell is blocked by --------.
Page 1206
Amantadine (influenza A).
Page 1207
Q0604:Antiviral chemotherapy: Early viral protein synthesisis blocked by --------.
Page 1208
Fomivirsen (CMV).
Page 1209
Q0605:Antiviral chemotherapy: Viral nuclei acid synthesis isblocked by --------.
Page 1210
Purine; pyrimidine analogs; reverse transcriptase inhibitors.
Page 1211
Q0606:Late viral protein synthesis and processing is blockedby --------.
Page 1212
Methimazole (variola); protease inhibitors.
Page 1213
Q0607:Antiviral chemotherapy: Packaging and assembly ofnew viron is blocked by --------.
Page 1214
Rifampin (vaccinia).
Page 1215
Q0608:Mechanism of action of Amantadine.
Page 1216
Blocks viral penetration/uncoating; may buffer pH ofendosome. Also causes the release of dopamine from intact
nerve terminals. "Amantadine blocks influenza A and rubellAand causes problems with the cerebellA."
Page 1217
Q0609:Clinical uses of Amantadine.
Page 1218
Prophylaxis for influenza A; Parkinson's disease.
Page 1219
Q0610:Symptoms of Amantadine toxicity.
Page 1220
Ataxia; dizziness; slurred speech. (Rimantidine is a derivativewith fewer CNS side effects.) "Amantadine blocks influenza
A and rubellA and causes problems with the cerebellA."
Page 1221
Q0611:Mechanism of action of Zanamivir.
Page 1222
Inhibits influenza neuraminidase.
Page 1223
Q0612:Clinical use of Zanamivir.
Page 1224
Both influenza A and B.
Page 1225
Q0613:Mechanism of action of Ribavirin.
Page 1226
Inhibits synthesis of guanine nucleotides by competitivelyinhibiting IMP dehydrogenase.
Page 1227
Q0614:Clinical use of Ribavirin.
Page 1228
RSV (respiratory syncytial virus).
Page 1229
Q0615:Symptoms of Ribavirin toxicity.
Page 1230
Hemolytic anemia. Severe teratogen.
Page 1231
Q0616:Mechanism of aciton of Acyclovir.
Page 1232
Perferentially inhibits viral DNA polymerase whenphosphorylated by viral thymidine kinase.
Page 1233
Q0617:Clinical use of Acyclovir.
Page 1234
HSV; VZV; EBV. Mucocutaneous and genital herpes lesions.Prophylaxis in immunocompromised patients.
Page 1235
Q0618:Symptoms of Acyclovir toxicity.
Page 1236
Delirium; tremor; nephrotoxicity.
Page 1237
Q0619:Mechanism of action of Ganciclovir.
Page 1238
Phosphorlation by viral kinase; perferentially inhibits CMVDNA polymerase.
Page 1239
Q0620:Clinical use of Ganciclovir.
Page 1240
CMV; especially in immunocompromised patients.
Page 1241
Q0621:Symptoms of Ganciclovir toxicity.
Page 1242
Leukopenia; neutropenia; thrombocytopenia; renal toxicity.More toxic to host enzymes than acyclovir.
Page 1243
Q0622:Mechanism of action of Foscarnet.
Page 1244
Viral DNA polymerase inhibitor that binds to thepyrophophate binding site of the enzyme. Does not require
activation by viral kinase. "FOScarnet = pyroFOSphateanalog."
Page 1245
Q0623:Clinical use of Foscarnet.
Page 1246
CMV retinitis in immunocompromised patients whenganciclovir fails.
Page 1247
Q0624:Foscarnet toxicity.
Page 1248
Nephrotoxicity.
Page 1249
Q0625:Saquinavir; ritonavir; indinavir; nelfinavir; amprenavirare example of this type of anti-HIV drug.
Page 1250
Protease inhibitor.
Page 1251
Q0626:Mechanism of action of protease inhibitors.
Page 1252
Inhibit assembly of new virus by blocking protease enzyme.
Page 1253
Q0627:Symptoms of protease inhibitor toxicity.
Page 1254
GI intolerance (nausea; diarrhea); hyperglycemia; lipidabnormalities; thrombocytopenia (indinavir).
Page 1255
Q0628:Zidovudine (AZT); didanosine (ddI); zalcitabine(ddC); stavudine (d4T); lamivudine (3TC); and abacavir are
examples of --------- reverse transcriptase inhibitors.
Page 1257
Q0629:Nevirapine; delavirdine; and efavirenz are examples of--------- reverse transcriptase inhibitors.
Page 1258
Non-nucleoside.
Page 1259
Q0630:Mechanism of action of reverse transcriptaseinhibitors.
Page 1260
Preferentially inhibit reverse transcriptase of HIV; preventincorporation of viral genome into host DNA.
Page 1261
Q0631:Symptoms of reverse transcriptase inhibitor toxicity.
Page 1262
Bone marrow supression (neutropenia; anemia); periphralneuropathy; lactic acidosis (nucleosides); rash (non-
nucleosides); megaloblastic anemia (AZT).
Page 1263
Q0632:Highly active antiretroviral therapy (HAART)generally entails combination therapy with ---------- and -------
----.
Page 1264
Protease inhibitors; reverse transcriptase inhibitors.
Page 1265
Q0633:When should HIV therapy be initiated?
Page 1266
When patients have low CD4 counts (<500 cells/mm3) orhigh viral load.
Page 1267
Q0634:Mechanism of action of Interferons.
Page 1268
Glycoproteins from human leukocytes that block variousstages of viral RNA and DNA synthesis.
Page 1269
Q0635:Clinical use of Interferons.
Page 1270
Chronic hepatitis B and C; Kaposi's sarcoma.
Page 1271
Q0636:Symptoms of Interferon toxicity.
Page 1273
Q0637:protease inhibitors name them
Page 1274
never (NAVIR) tease a pro-tease inhibitor. All end in "navir"
Page 1275
Q0638:protease inhibitor MOA
Page 1276
inhibits assembly of new virus by inhibiting protease inprogeny virus
Page 1277
Q0639:protease inhibitor toxicity
Page 1278
GI intolerance (nausea; diarhea); hyperglycemia;lipodystrophy; thrombocytopenia (indinavir)… metabolic
syndrome
Page 1279
Q0640:reverse transcriptase inhibitors
Page 1280
nucleoside: zidoVUDINE (AZT); staVUDINE (d4T);lamiVUDINE; abacavir; zalcitabine (ddC); didanosine (3TC).
Non-nucleosides: Never deliver nucleosides. Nevirapine;efavirenz; delavirdine
Page 1281
Q0641:reverse transcriptase inhibitors MOA
Page 1282
preferentially inhibits HIV reverse transcriptase. Preventsincorporation of viral genome into host DNA
Page 1283
Q0642:reverse transcriptase toxicity
Page 1284
BM supression (neutropenia; anemia); peripheral neuropathy;LACTIC ACIDOSIS (nucleosides); rash (non nucleosides);
megaloblastic anemia (didovudine
Page 1285
Q0643:reverse transcriptase inhib clinical use
Page 1286
HAART. Combination tx w/ protease inhibitors and reversetranscriptase inhibitors. Started when pts have CD4<500 orhigh viral load. AZT used in preg to reduce transmission risk
Page 1287
Q0644:interferons mechanism
Page 1288
block various stages of viral RNA and DNA syn. Inducesribonuclease that degrades viral mRNA.
Page 1289
Q0645:interferon clinical use
Page 1290
IFN alpha. Chronic hepatitis B and C; Kaposi sarcoma. IFNbeta - MS. IFN gamma - NADPH oxiodase deficiency
Page 1291
Q0646:interferon toxicity
Page 1292
neutropenia; depression
Page 1293
Q0647:pleconaril MOA
Page 1294
prevents attachment of poliovirus to cell
Page 1295
Q0648:Sulfamethoxazole (SMX);sulfisoxizole;triplesulfas;sulfadiazine
Page 1296
MECH: bacteriostatic; inhibits dihydropterate synthasewhich bac need to make folate;USE: Gm+; Gm-; Nocardia;
Chlamydia; PCP; UTIs;TOX;Cystalluria (tubulo-interstitialnephritis);hypersensitivity;hemolytic anemia (G6PD
deficiency);Kernicterus;drug potentiation (warfarin; displacesother drugs from albumin)
Page 1297
Q0649:Trimethoprim (TMP)
Page 1298
MECH: bacteriostatic; inhibits bac dihydrofolate reductaseinterfering with folate production. Folate is needed for nucleicacids; cell growth;USE: With sulfas; Gm-s are resistant;TOX:
folate deficiency → megaloblastic anemia; leukopenia;granulocytopenia (reversed with folinic acid - bac can't use)
Page 1299
Q0650:Co-Trimoxazole;Bactrim
Page 1300
MECH: inhibits two sequential steps of folate production inbac;USE: UTI (recurrent/chronic); PCP; Shigella; Salmonella;gonococcal urethritis; oropharyngeal gonorrhea;TOX: derm;
GI; heme (megaloblastic anemia; leukopenia;thrombocytopenia - reversed by folinic acid); HIV drug-
induced fever; drug interactions (warfarin)
Page 1301
Q0651:Penicillin G
Page 1302
IV form;MECH;1. Bind penicillin-binding proteins;2. Blocktranspeptidase cross-linking of cell wall;3. Activate autolytic
enzymes;USE: bateriocidal for gm+ cocci (esp.pneumococcus); gm+ rods (listeria); gm- cocci (gonococcus);
spirochetes (syphillis);TOX: Hypersensitivity rxn(sometimes causing hemolytic anemia via haptens associated
with RBC); diarrhea (imbalance of gut flora)
Page 1303
Q0652:Penicillin V
Page 1304
Oral form;MECH;1. Bind penicillin-binding proteins;2. Blocktranspeptidase cross-linking of cell wall;3. Activate autolytic
enzymes;USE: bateriocidal for gm+ cocci (esp.pneumococcus); gm+ rods (listeria); gm- cocci (gonococcus);
spirochetes (syphillis);TOX: Hypersensitivity rxn(sometimes causing hemolytic anemia via haptens associated
with RBC); diarrhea (imbalance of gut flora)
Page 1305
Q0653:Methicillin
Page 1306
Penicillinase-resistant penicillin;MECH;1. Bind penicillin-binding proteins;2. Block transpeptidase cross-linking of cellwall;3. Activate autolytic enzymes;USE: S. aureus (except
MRSA);TOX: Hypersensitivity rxn; *interstitial nephritis*
Page 1307
Q0654:Nafcillin
Page 1308
Penicillinase-resistant penicillin;MECH;1. Bind penicillin-binding proteins;2. Block transpeptidase cross-linking of cellwall;3. Activate autolytic enzymes;USE: S. aureus (except
MRSA);TOX: Hypersensitivity rxn
Page 1309
Q0655:Oxacillin
Page 1310
Penicillinase-resistant penicillin;MECH;1. Bind penicillin-binding proteins;2. Block transpeptidase cross-linking of cellwall;3. Activate autolytic enzymes;USE: S. aureus (except
MRSA);TOX: Hypersensitivity rxn
Page 1311
Q0656:Cloxacillin; dicloxacillin
Page 1312
Penicillinase-resistant penicillin;MECH;1. Bind penicillin-binding proteins;2. Block transpeptidase cross-linking of cellwall;3. Activate autolytic enzymes;USE: S. aureus (except
MRSA);TOX: Hypersensitivity rxn
Page 1313
Q0657:Ampicillin
Page 1314
Aminopenicillin;MECH;1. Bind penicillin-binding proteins;2.Block transpeptidase cross-linking of cell wall;3. Activate
autolytic enzymes;USE: penicillin + more gm- enterobac;H.flu;E. coli;Listeria;Proteus;Salmonella;*combine with beta -
lactamase inhibitors (clavulanic acid) to extend;TOX:Hypersensitivity rxn; rash; pseudomembranous colitis
Page 1315
Q0658:Amoxicillin
Page 1316
Aminopenicillin (more orally bioavailable thanAmp);MECH;1. Bind penicillin-binding proteins;2. Block
transpeptidase cross-linking of cell wall;3. Activate autolyticenzymes;USE: penicillin + more gm- enterobac;H. flu;E.
coli;Listeria;Proteus;Salmonella;*combine with beta -lactamase inhibitors (clavulanic acid) to extend;TOX:Hypersensitivity rxn; rash; pseudomembranous colitis
Page 1317
Q0659:Clavulanic acid;Sulbactam;Tazobactam
Page 1318
beta -lactamase inhibitors;-Competitive inhibitor;-Combinewith penicillinase-sensitive penicillins
Page 1319
Q0660:Ticarcillin
Page 1320
Anti-pseudomonal;MECH;1. Bind penicillin-bindingproteins;2. Block transpeptidase cross-linking of cell wall;3.
Activate autolytic enzymes;USE: Pseudomonas aeruginosa &gm- rods (H. flu; enterobactor; E. coli; Proteus);*combine
with beta -lactamase inhibitors (clavulanic acid) to extend toKlebsiella;TOX: Hypersensitivity rxn
Page 1321
Q0661:Carbenicillin
Page 1322
Anti-pseudomonal;MECH;1. Bind penicillin-bindingproteins;2. Block transpeptidase cross-linking of cell wall;3.
Activate autolytic enzymes;USE: Pseudomonas aeruginosa &gm- rods (H. flu; enterobactor; E. coli; Proteus);*combine
with beta -lactamase inhibitors (clavulanic acid) to extend toKlebsiella;TOX: Hypersensitivity rxn
Page 1323
Q0662:Piperacillin
Page 1324
Anti-pseudomonal;MECH;1. Bind penicillin-bindingproteins;2. Block transpeptidase cross-linking of cell wall;3.
Activate autolytic enzymes;USE: Pseudomonas aeruginosa &gm- rods (H. flu; enterobactor; E. coli; Proteus);*combine
with beta -lactamase inhibitors (clavulanic acid) to extend toKlebsiella;TOX: Hypersensitivity rxn
Page 1325
Q0663:Cefazolin
Page 1326
1st Gen Cephalosporin w/ bone penetration;MECH: beta -lactam; inhibits cell wall synthesis (like penicillins);USE: gm+
cocci &;Proteus;E. coli;Klebsiella;TOX: Hypersensitivityreactions; disulfiram-like rxn
Page 1327
Q0664:Cephalexin
Page 1328
1st Gen Cephalosporin w/oral admin;MECH: beta -lactam;inhibits cell wall synthesis (like penicillins);USE: gm+ cocci
&;Proteus;E. coli;Klebsiella;TOX: Hypersensitivity reactions;disulfiram-like rxn
Page 1329
Q0665:Cefotoxitin
Page 1330
2nd Gen Cephalosporin ;MECH: beta -lactam; inhibits cellwall synthesis (like penicillins);USE: gm+ cocci & Bacteroides
fragilis;H. flu;Enterobactor;Neisseria;Proteus;E.coli;Klebsiella;Serratia;TOX: Hypersensitivity reactions;
disulfiram-like rxn
Page 1332
2nd Gen Cephalosporin (oral);MECH: beta -lactam; inhibitscell wall synthesis (like penicillins);USE: gm+ cocci &;H.
flu;Enterobactor;Neisseria;Proteus;E.coli;Klebsiella;Serratia;TOX: Hypersensitivity reactions;
disulfiram-like rxn; *serum sickness*
Page 1333
Q0667:Cefuroxime
Page 1334
2nd Gen Cephalosporin (oral);MECH: beta -lactam; inhibitscell wall synthesis (like penicillins);USE: gm+ cocci &;H.
flu;Enterobactor;Neisseria;Proteus;E.coli;Klebsiella;Serratia;TOX: Hypersensitivity reactions;
disulfiram-like rxn
Page 1335
Q0668:Ceftriaxone
Page 1336
3rd Gen Cephalosporin w/ long t1/2 and good CSFpenetration;MECH: beta -lactam; inhibits cell wall synthesis
(like penicillins);USE: gm- HEN PEcKS +; esp. Neisseriagonorrhea;TOX: Hypersensitivity reactions; disulfiram-like
rxn
Page 1337
Q0669:Cefotaxime
Page 1338
3rd Gen Cephalosporin w/ good CSF penetration;MECH:beta -lactam; inhibits cell wall synthesis (like penicillins);USE:
gm- HEN PEcKS +;TOX: Hypersensitivity reactions;disulfiram-like rxn
Page 1339
Q0670:Ceftazidime
Page 1340
3rd Gen Cephalosporin ;MECH: beta -lactam; inhibits cellwall synthesis (like penicillins);USE: gm- HEN PEcKS +; esp.
P. aeruginosa;TOX: Hypersensitivity reactions; disulfiram-like rxn
Page 1342
4th Gen Cephalosporin w/ good CSF penetration;MECH:beta -lactam; inhibits cell wall synthesis (like penicillins);USE:
gm+ & P. aeruginosa; E. coli; Klebsiella; Proteus;TOX:Hypersensitivity reactions; disulfiram-like rxn
Page 1343
Q0672:Aztreonam
Page 1344
Monobactam;MECH: Inhibits cell wall synthesis; resistant tobeta -lactamase;USE: Gm- rods: Klebsiella; Pseudomonas;
Serratia;*No activity against gm+ or anaerobes;TOX: usuallynone
Page 1345
Q0673:Imipenam/cilastatin
Page 1346
Carbapenam;MECH: Inhibits cell wall synthesis; resistant tobeta -lactamase;*cilastatin protects imapenam from cleavage
which creates a nephrotoxic metabolite;USE: very broadspectrum: gm+ cocci; gm- rods; anaerobes; esp.
Enterobacter;TOX: GI; rash; seizures (at high plasma levels)
Page 1347
Q0674:Vancomycin
Page 1348
MECH: bactericidal; inhibits cell wall formation by bindin D-ala D-ala portion of cell wall precursors;USE: gm+ MDR
organisms - S. aureus; C. diff;TOX: Fever; chills; phlebitis;red man syndrome (fast infusion); nephrotox; ototox
Page 1349
Q0675:Tetracycline
Page 1350
MECH: Bacteriostatic; binds 30S and prevents aminoacyl-tRNA attachment to inhibit protein synthesis;USE: V.cholera; Acne; Chlamydia; Ureaplasma; Mycoplasma
pneumo; Tularemia; H. pylori; Borrelia burdorferi;Rickettsia;TOX: GI distress; binds calcifying tissue → teeth
discoloration & disrupted growth;photosensitivity;Contraindicated in preg and renal failure;
don't take with milk
Page 1351
Q0676:Doxycycline
Page 1352
MECH: Bacteriostatic; binds 30S and prevents aminoacyl-tRNA attachment to inhibit protein synthesis;USE: V.cholera; Acne; Chlamydia; Ureaplasma; Mycoplasma
pneumo; Tularemia; H. pylori; Borrelia burdorferi;Rickettsia;TOX: GI distress; binds calcifying tissue → teethdiscoloration & disrupted growth; photosensitivity;*Can be
used in pts with renal failure
Page 1353
Q0677:Demeclocycline
Page 1354
MECH: Bacteriostatic; binds 30S and prevents aminoacyl-tRNA attachment to inhibit protein synthesis; *antagonized
ADH;USE: SIADH; V. cholera; Acne; Chlamydia;Ureaplasma; Mycoplasma pneumo; Tularemia; H. pylori;
Borrelia burdorferi; Rickettsia;TOX: GI distress; bindscalcifying tissue → teeth discoloration & disrupted growth;photosensitivity;Contraindicated in preg and renal failure;
don't take with milk
Page 1355
Q0678:Minocycline
Page 1356
MECH: Bacteriostatic; binds 30S and prevents aminoacyl-tRNA attachment to inhibit protein synthesis;USE: V.cholera; Acne; Chlamydia; Ureaplasma; Mycoplasma
pneumo; Tularemia; H. pylori; Borrelia burdorferi; Rickettsia;*can cross BBB to eradicate carrier state;TOX: GI distress;binds calcifying tissue → teeth discoloration & disrupted
growth; photosensitivity; *vestibularproblems;Contraindicated in preg and renal failure; don't take
with milk
Page 1357
Q0679:Gentamicin
Page 1358
MECH: bactericidal; binds 30S inhibiting formation ofinitiation complex and causing mRNA misreading. Requires
O2 for uptake;USE: only aerobic; gm- rods;TOX: Nephrotox(dose-related); Ototox; teratogen
Page 1360
Topical;MECH: bactericidal; binds 30S inhibiting formationof initiation complex and causing mRNA misreading. RequiresO2 for uptake;USE: only aerobic; gm- rods;TOX: Nephrotox
(dose-related); Ototox; teratogen
Page 1362
MECH: bactericidal; binds 30S inhibiting formation ofinitiation complex and causing mRNA misreading. Requires
O2 for uptake;USE: only aerobic; gm- rods;TOX: Nephrotox(dose-related); Ototox; teratogen
Page 1363
Q0682:Tobramycin
Page 1364
MECH: bactericidal; binds 30S inhibiting formation ofinitiation complex and causing mRNA misreading. Requires
O2 for uptake;USE: only aerobic; gm- rods;TOX: Nephrotox(dose-related); Ototox; teratogen
Page 1365
Q0683:Streptomycin
Page 1366
MECH: bactericidal; binds 30S inhibiting formation ofinitiation complex and causing mRNA misreading. Requires
O2 for uptake;USE: only aerobic; gm- rods;TOX: Nephrotox(dose-related); Ototox; teratogen
Page 1367
Q0684:Erythromycin
Page 1368
MECH: binds 50S inhibiting translocation step;USE: same asPenG (good for pts with PEN allergies); URIs; pneumonias;STDs; Mycoplasma; Legionella; Chlamydia; Neisseria;TOX:
GI; acute cholestatic hepatitis; eosinophila; skin rash;metabolized in liver and interferes with warfarin; theophyline
leading to accumulation
Page 1369
Q0685:Clarithromycin
Page 1370
MECH: binds 50S inhibiting translocation step;USE: same asPenG (good for pts with PEN allergies); URIs; pneumonias;STDs; Mycoplasma; Legionella; Chlamydia; Neisseria;TOX:
GI; acute cholestatic hepatitis; eosinophila; skin rash;metabolized in liver and interferes with warfarin; theophyline
leading to accumulation
Page 1371
Q0686:Azithromycin
Page 1372
MECH: binds 50S inhibiting translocation step;USE: same asPenG (good for pts with PEN allergies); URIs; pneumonias;
STDs; Mycoplasma; Legionella; Chlamydia; Neisseria; H. flu;Moraxella; MAI;TOX: GI; acute cholestatic hepatitis;
eosinophila; skin rash; metabolized in liver and interferes withwarfarin; theophyline leading to accumulation
Page 1373
Q0687:Chloramphenicol
Page 1374
MECH: bacteriostatic; inhibits 50S peptidyltransferase;USE:Broad spectrum; but nasty toxicities limit use. Enters CNSreadily: H. flu; N. meningitidis; S. pneumo;TOX: hemolytic
anemis (G6PD deficiency); aplastic anemia; gray babysyndrome (UDP-glucuronyl transferase deficiency in
newborn)
Page 1375
Q0688:Clindamycin
Page 1376
MECH: blocks peptide bond formation at 50S;USE:Anaerobes above the diaphragm: B. frag; C. perf;TOX:
pseudomembranous colitis; diarrhea; fever
Page 1377
Q0689:-floxacin;Cipro-; moxi-; gati-; nor-; o-; spar-;
Page 1378
MECH: bactericidal; inhibit DNA gyrase → DNAcleavage;USE;- gm- rods of GI;Klebsiella;Enterobacter;E.
coli;Proteus;Serratia;Shigella;- gm- rods of urinarytract;KEEPSS + P. aeruginosa;- Resistant respiratory
infections: pneumococcus;- Neisseria;TOX: GI; CNS (HA;N/V; dizziness); skin
rash/photosensitivity;*Tendonitis/rupture in adults; crampsand myalgias in kids
Page 1379
Q0690:Isoniazid
Page 1380
MECH: inhibits synthesis of mycolic acids;USE:Mycobacterium Tuberculosis;TOX: Neurotox (peripheralneuritis; B6/pyridoxine can prevent); hepatotox; hemolysis
(G6PD deficient); SLE-like syndrome
Page 1382
MECH: inhibits DNA dependent RNA polyerase;USE:Mycobacterium Tuberculosis; M. leprae; prophylaxis of
meningococcus and H. flu contacts;TOX: minor; druginteractions (increased P450); rapid resistance if used alone
Page 1383
Q0692:Pyrazinamide
Page 1384
USE: Mycobacterium Tuberculosis
Page 1385
Q0693:Ethambutol
Page 1386
USE: Mycobacterium Tuberculosis
Page 1389
Q0695:Amphotericin B
Page 1390
Polyene antifungal;MECH: binds ergosterol which disruptsfungal membrane → leakage;USE: wide spectrum for systemicinfections - Blasto; Histo; Cocci; Crypto; Aspergillus; Mucor;
Candida;*intrathecally for meningitis (doesn't crossBBB);TOX: highly toxic - fever/chills; hypotension;
nephrotox (hydration reduces); arrhythmias; anemia; phlebitis
Page 1392
Polyene antifungal;MECH: binds ergosterol which disruptsfungal membrane → leakage;USE: Too toxic for systemic use -
oral thrush; diaper rash; vaginal candidiasis;TOX: same asamphotericin
Page 1393
Q0697:Azoles;Floconazole; ketoconazole; itraconazle;voriconazole
Page 1394
MECH: Inhibits ergosterol synthesis → disrupting membrane(don't use with ampho);USE: Systemic mycoses - ;Flucon forcrypto;Keto for blasto; cocci; histo; candida;TOX: Hormonesynthesis inhibition → endocrine abnormalities; liver dysfxn
(inhibits cytP-450); fever; chills
Page 1395
Q0698:Flucytosine
Page 1396
MECH: inhibits DNA synthesis;USE: systemic candida;crypto;*resistance develops - use with ampho;TOX: N/V;
dairrhea; bone marrow suppression; hepatotox
Page 1397
Q0699:Caspofungin
Page 1398
MECH: inhibits cell wall synthesis;USE: invasiveaspergilloss;TOX: GI; flushing
Page 1399
Q0700:Terbinafine
Page 1400
MECH: inhibits fungal enzyme squalene epoxidase;USE:dermatophytoses
Page 1401
Q0701:Griseofulvin
Page 1402
MECH: interferes with microtubules → disruptsmitosis;USE: dermatophytosis - oral treatment of superficialinfxns;TOX: teratogenic; carcinogenic; HA; increased P-450
and warfarin metabolism
Page 1403
Q0702:Metronidazole
Page 1404
MECH: nitro group serves as an electron-acceptor; formingreduced cytotoxic compounds that bind proteins and DNA →
cell death;USE;anaerobic protazoa: E. histolytica; Giardia;Trichomonas;anaerobic bac: Bacteroides; C. difficile;
Gardnerella;TOX: GI; metallic taste; oral yeast infection;disulfiram-like effect; neurotox (rarely)
Page 1405
Q0703:Primaquine
Page 1406
MECH: not understood - oxidants kill schizonts;USE: P.vivax and P. ovale (liver stage);TOX: Hemolytic anemia
(G6PD deficient)
Page 1407
Q0704:Chloraquine
Page 1408
MECH: inhibits schizont's ability to break down heme →build up; also kills RBC; alkalinization of food vacuole;
decreased DNA synthesis;USE: Plasmodium sporozites in theblood;TOX: GI; pruritis; HA
Page 1410
MECH: effects DNA synthesis;USE: chloraquine-resistantPlasmodium;TOX: cinchonism - N/V; tinnitus; vertigo;
hemolytic anemia
Page 1411
Q0706:Mefloquine
Page 1412
MECH: effects DNA synthesis;USE: choraquine-resistantPlasmodium;TOX: cinchonism - N/V; tinnitus; vertigo;
disorientaiton
Page 1413
Q0707:Pyrimethamine
Page 1414
MECH: inhibits plasmodial dihydrofolate reductase → blockof DNA synthesis;USE: sporonticide; P. falciparum; with
sulfonamide treats P. malariae and Toxoplasma gondii
Page 1415
Q0708:Melarsoprol
Page 1416
MECH: reacts with enzymes;USE: african sleeping sickness -trypanosoma brucei;TOX: CNS; hypersensitivity; GI
Page 1417
Q0709:Nifurtimox
Page 1418
MECH: oxygen radicals;USE: Trypanosoma cruzi(American);TOX: hypersensitivity; GI
Page 1419
Q0710:Stibugluconate
Page 1420
USE: Leishmania
Page 1421
Q0711:Albendazole; Mebendazole; Thiabendazole
Page 1422
MECH: inhibits microtubules → paralysis → passing ofworms in stool;USE: intestinal nematodes;Ancyclostoma
(hookworm);Ascaris(roundworm);Enterobius;Strongyloides;Trichinella;TOX: GI;
teratogenic
Page 1423
Q0712:Pyrantel pomoate
Page 1424
MECH: depolarizing neuromuscular blockingagent;USE;Ancyclostoma (hookworm);Ascaris(roundworm);Enterobius;TOX: N/V; HA; rash
Page 1425
Q0713:Diethylcarbamazine
Page 1426
MECH: increased phagocytosis of fillaria;USE;Wuchereriabancrofti (elephantitis);Loa loa (skin swelling);Onchocerca
volvulus (river blindness);TOX: reaction caused by death ofparasites
Page 1427
Q0714:Ivermectin
Page 1428
MECH: targets GABA → paralysis;USE: Onchocercavolvulus (river blindness);TOX: contraindicated with other
GABA agonists
Page 1429
Q0715:Praziquantel
Page 1430
MECH: increased calcium permeability →paralysis;USE;Trematodes - Schistosoma; Clonorchis;
Paragonimus westermani;Cestodes - Taenia; Echinococcus
Page 1431
Q0716:Niclosamide
Page 1432
MECH: inhibits ADP phosporylation → death of scolex(head);USE: Cestodes - Taenia; Echinococcus
Page 1433
Q0717:Amantadine
Page 1434
MECH: Blocks viral penetration/uncoating (M2); causesrelease of DA;USE: influenza A prophylaxis and treatment;Parkinson's dz;TOX: cerebellar (ataxia; dizziness; slurred
speech)
Page 1435
Q0718:Rimantidine
Page 1436
MECH: Blocks viral penetration/uncoating (M2);USE:influenza A prophylaxis and treatment;TOX: doesn't cross
BBB (fewer side fx than amantadine)
Page 1437
Q0719:Ribavarin
Page 1438
MECH: inhibits viral mRNA synthesis ;USE: RSV; HepC;Influenza A & B;TOX: hemolytic anemia; teratogen
Page 1439
Q0720:Acyclovir
Page 1440
MECH: preferentially inhibits viral DNA polymerase whenphosphorylated by viral thymidine kinase;USE: HSV
(mucocutaneous and genital lesions); VZV; EBV; prophylaxisin immunocompromised;TOX: delirium; tremor; nephrotox (in
dehydrated);RESISTANCE: lack of thymidine kinase
Page 1441
Q0721:Gancyclovir
Page 1442
MECH: preferentially inhibits CMV DNA polymerase whenphosphorylated by viral thymidine kinase;USE: CMV; esp. in
immunocompromised;TOX: leukopenia; neutropenia;thrombocytopenia; delirium; tremor; nephrotox
;RESISTANCE: lack of thymidine kinase or mutated DNApol
Page 1443
Q0722:Foscarnet
Page 1444
MECH: Binds pyrophosphate site of viral DNA polymerasecausing inhibition;USE: CMV retinitis in
immunocompromised after gancyclovir failure (IVonly);TOX: nephrotox;RESISTANCE: mutated DNA pol
(does not require kinase activation)
Page 1445
Q0723:Zidovudine (AZT);didanosine (ddI);zalcitabine(ddC);stavudne(d4T);lamivudine (3TC);abacavir
Page 1446
Reverse transcriptase inhibitors - nucleosides;MECH: inhibitRT; prevent viral incorporation;USE: HIV with HAART;reduce maternal-to-infant transmission;TOX: bone marrow
suppression; peripheral neuropathy; lactic acidosis;megaloblastic anemia(AZT)
Page 1447
Q0724:Nevirapine;efavirenz;delavirdine
Page 1448
Reverse transcriptase inhibitors - non-nucleosides;MECH:inhibit RT; prevent viral incorporation;USE: HIV with
HAART; reduce maternal-to-infant transmission;TOX: bonemarrow suppression; rash; elev liver enzymes
Page 1449
Q0725:Saquinavir;ritonavir;indinavir;nelfinavir
Page 1450
Protease inhibitors;MECH: block protease to inhibitassembly of new virions;USE: HIV with HAART;TOX:
dyslipidemia; insulin resistance/hyperglycemia;lipodystrophy
Page 1451
Q0726:Enfuviritide
Page 1452
MECH: binds gp41 preventing HIV fusion with targetcell;USE: salvage regimen
Page 1453
Q0727:Interferons (alpha; beta; gamma)
Page 1454
MECH: glycoproteins from human leukocytes that blockvarious stages of viral RNA and DNA synthesis; induce
ribunuclease to degrade viral mRNA;USE;IFNalpha - chronichepB and hepC; karposi's saroma;IFNbeta - MS;IFNγ -
NADPH oxidase deficiency;TOX: Neutropenia
Page 1455
Q0728:Mechanism of action of the anti-fungal therapypolyenes.
Page 1456
Form artificial pores in the cytoplasmic membrane.
Page 1457
Q0729:Mechanism of action of the anti-fungal therapiesterbinafine and azoles.
Page 1458
Terbinafine blocks the conversion of squalene to lanosterol.Azoles block the conversion of lanosterol to ergosterol.
Page 1459
Q0730:Mechanism of action of the anti-fungal therapyflucytosine.
Page 1460
Inhibits DNA synthesis by conversion to fluorouracil; whichcompetes with uracil.
Page 1461
Q0731:Mechanism of action of the anti-fungal therapygriseofulvin.
Page 1462
Disrupts microtubles. Deposits in keratin-containing tissues.
Page 1463
Q0732:Mechanism of action of Amphotericin B.
Page 1464
Binds ergosterol (unique to fungi); forms membrane pores thatallow leakage of electrolytes and disrupt homeostasis."Amphotericin 'tears' holes in the fungal membrane by
forming pores."
Page 1465
Q0733:Clinical uses of Amphotericin B.
Page 1466
Used for a wide spectrum of sytemic mycoses.Cryptococcus; Blastomyces; Coccidioides; Aspergillus;
Histoplasma; Candida; Mucor (systemic mycoses).Intrathecally for fungal meningitis; does not cross blood-brain
barrier.
Page 1467
Q0734:Symptoms of Amphotericin B toxicity.
Page 1468
Fever/chills ("shake and bake"); hypotension; nephrotoxicity;arrhythmias ("amphoterrible").
Page 1469
Q0735:Mechanism of action of Nystatin.
Page 1470
Binds to ergosterol; disrupting fungal membranes.
Page 1471
Q0736:Clinical use of Nystatin.
Page 1472
Swish and swallow for oral candidiasis (thrush). Topical fordiaper rash or vaginal candidiasis.
Page 1473
Q0737:Mechanism of action for fluconazole; ketoconazole;clotrimazole; miconazole; itraconazole; voriconazole.
Page 1474
Inhibits fungal steroid (ergosterol) synthesis. Blocks:lanosterol -> ergosterol
Page 1475
Q0738:Clinical uses of fluconazole; ketoconazole;clotrimazole; miconazole; itraconazole; voriconazole.
Page 1476
Systemic mycoses. Fluconazole for cryptococcal meningitis inAIDS patients and candidal infections of all types (i.e; yeast
infections). Ketoconazole for Blastomyces; coccidioides;Histoplasma; Candida albicans; hypercortisolism.
Page 1477
Q0739:Symptoms of fluconazole; ketoconazole; clotrimazole;miconazole; itraconazole; voriconazole toxicity.
Page 1478
Hormone synthesis inhibition (gynecomastia); liverdysfunction (inhibits cytochrome P-450); fever; chills.
Page 1479
Q0740:Mechanism of action of Flucytosine.
Page 1480
Inhibits DNA synthesis byconversion to fluorouracil; whichcompetes with uracil.
Page 1481
Q0741:Clinical uses of Flucytosine.
Page 1482
Used in sytemic fungal infections (e.g. Candida;Cryptococcus).
Page 1483
Q0742:Flucytosine toxicity.
Page 1484
Nausea; vomitting; diarrhea; bone marrow suppression.
Page 1485
Q0743:Mechanism of action for Caspofungin.
Page 1486
Inhibits cell wall synthesis.
Page 1487
Q0744:Clinical use of Caspofungin.
Page 1488
Invasive aepergillosis.
Page 1489
Q0745:Symptoms of Caspofungin toxicity.
Page 1490
GI upset; flushing.
Page 1491
Q0746:Mechanism of action of Terbinafine.
Page 1492
Inhibits the fungal enzyme squalene epoxidase. Inhibitssqualene -> lanosterol
Page 1493
Q0747:Clinical use of Terbinafine.
Page 1494
Used to treat dermatophytoses (especially onychomycosis).
Page 1495
Q0748:Mechanism of action of Griseofulvin.
Page 1496
Interfers with microtubule function; disrupts mitosis.Deposits in keratin-contianing tissues (e.g. nails).
Page 1497
Q0749:Clinical use of Griseofulvin.
Page 1498
Oral treatment of superficial infections; inhibits growth ofdermatophytes (tinea; ringworm).
Page 1499
Q0750:Symptoms of Griseofulvin toxicity.
Page 1500
Teratogenic; carcinogenic; confusion; headaches; increasewarfarin metabolism.
Page 1501
Q0751:opioid receptors that may be involved in alteringreactivity to pain are located in these regions of the brain?
Page 1502
basal ganglia; hypothalamus; limbic structures; and cerebralcortex
Page 1503
Q0752:what are the types of opioid receptors?
Page 1504
mu; delta; and kappa
Page 1505
Q0753:this opioid receptor plays a major role in therespiratory depressant actions of opioids?
Page 1507
Q0754:activation of this receptor is involved in the sedativeactions of opioids?
Page 1509
Q0755:all 3 major opioid receptors are coupled to theireffector by these things?
Page 1510
G proteins and activate phospholipase C or inhibit adenylylcyclase
Page 1511
Q0756:at the postsynaptic level activation of the opioidreceptors causes this to occur?
Page 1512
opening of K+ channels to cause hyperpolarization (IPSP)
Page 1513
Q0757:at the presynaptic evel opioid receptor activation canclose these ion channels?
Page 1514
voltage gated Ca2+ channels to inhibit neurotransmitterrelease
Page 1515
Q0758:examples of strong opioids?
Page 1516
morphine; methadone; meperidine; fentanyl; levorphanol; andheroin
Page 1517
Q0759:these opioid are partial agonists and have mild tomoderate analgesic efficacy?
Page 1518
Codeine; hydrocodone and oxycodone
Page 1519
Q0760:this agent is a very weak opioid agonist?
Page 1521
Q0761:pupillary constriction is characteristic effect of allopioids except this one; which has a muscarinic blocking
action?
Page 1523
Q0762:this condition includes rhinorrhea; lacrimation chills;gooseflesh; muscle aches; diarrhea; yawning; anxiety and
hostility?
Page 1524
abstinenece syndrome
Page 1525
Q0763:which opioids are useful cough suppressants?
Page 1526
Codeine and detromethorphan
Page 1527
Q0764:opioids used to treat diarrhea?
Page 1528
loperamide and diphenoxylate
Page 1529
Q0765:this opioid may be useful in acute pulmonary edemabecause of its hemodynamic actions?
Page 1531
Q0766:what is the triad of opioid overdose signs?
Page 1532
pupillary constriction; comatose state; and respiratorydepression
Page 1533
Q0767:diagnosis of opioid overdose is confirmed by thisaction?
Page 1534
IV injection of Naloxone (opioid antagonist)--->prompt signsof recovery
Page 1535
Q0768:concomitant use of certain opioid like meperidine withMAOIs can result in this condition?
Page 1536
hyperpyrexic coma
Page 1537
Q0769:meperidine has also been implicated in serotoninsyndrome when used with this antidepressant class?
Page 1539
Q0770:the prolonged activity of Buprenorphine is clinicallyuseful to suppress withdrawal signs in dependency
states;how does this property affect Naloxone reversalefforts?
Page 1540
Buprenorphine is resistant to naloxone reversal due to itsprolonged activity
Page 1541
Q0771:this drug decreases the craving for Alcohol and isapproved for adjunctive use in alcohol dependency programs?
Page 1543
Q0772:Effects of H1 receptor activation
Page 1544
Increased capillary dilation and permeability (hypotension;edema); bronchoconstriction; activation of nociceptive
receptors (pain; pruritus)
Page 1545
Q0773:Effects of H2 receptor activation
Page 1546
Increased gastric acid secretion (ulcers); positive inotropism
Page 1547
Q0774:H1 antagonist drugs
Page 1548
Diphenhydramine; promethazine; chlorpheniramine;meclizine; hydroxyzine; loratadine; fexofenadine
Page 1549
Q0775:Uses of H1 antagonists
Page 1550
Hay fever; rhinitis; urticaria; motion sickness and vertigo(meclizine); nausea in pregnancy
Page 1551
Q0776:Adverse effects of H1 antagonists
Page 1552
M block and sedation; GI distress; allergic reactions.
Page 1553
Q0777:Substances that increase proton pump activity
Page 1554
ACh; gastrin; histamine (H2 receptors)
Page 1555
Q0778:H2 antagonist drugs
Page 1556
Cimetidine; ranitidine
Page 1557
Q0779:MOA of H2 antagonists
Page 1558
Indirectly decrease proton pump activity (histamine increasesproton pump activity)
Page 1559
Q0780:Uses of H2 antagonists
Page 1560
Peptic ulcer disease; GERD; Zollinger-Ellison
Page 1561
Q0781:Side effects of H2 antagonists
Page 1562
GI distress; dizziness; sommnolence; Cimetidine: inhibitsP450 --> increases effects of quinidine; phenytoin; TCAs;
warfarin; also decreases androgens --> gynecomastia
Page 1563
Q0782:Omeprazole
Page 1564
Direct; irreversible proton pump inhibitor. Uses: PUD;GERD; Zollinger-Ellison; H. pylori. Side effects: decreases
bioavailability of weak acids (fluoroquinolones;ketoconazole); inhibits P450
Page 1565
Q0783:Misoprostol
Page 1566
PGE1 analog; increases mucus and bicarbinote; decreases HCLsecretion. Use: NSAID-induced ulcers.
Page 1567
Q0784:Sulcralfate
Page 1568
Polymerizes in stomach to coat ulcers. Increases healing anddecreases ulcer recurrence.
Page 1569
Q0785:Drugs that require acid stomach pH to be absorbed
Page 1570
Azoles; fluoroquinolones; warfarin
Page 1571
Q0786:Drugs used as antiemetics
Page 1572
5HT3 antagonists (ondansetron); DA antagonists(metoclopramide); H1 blockers (diphenhydramine; meclizine);
muscarinic blockers (scopolamine)
Page 1573
Q0787:Metabolism of serotonin
Page 1574
5HT is metabolized by MAOa to 5-hydroxyinolacetic acid(marker for carcinoid)
Page 1575
Q0788:Buspirone
Page 1576
Partial 5HT1a agonist used for generalized anxiety disorder
Page 1577
Q0789:Sumatriptan
Page 1578
5HT1d agonist in cerebral vessels; used for migraine
Page 1579
Q0790:Olanzapine
Page 1580
Atypical antipsychotic; 5HT2a receptor antagonist; decreasespsychosis
Page 1581
Q0791:Cyproheptadine
Page 1582
5HT2 antagonist used in carcinoid
Page 1583
Q0792:Ondansetron
Page 1584
5HT3 antagonist; used as antiemetic in chemotherapy;radiation and post-op. 5HT3 receptors are found in area
postrema
Page 1585
Q0793:Ergonovine
Page 1586
Uterine muscle contraction after placental delivery
Page 1587
Q0794:Ergotamine
Page 1588
Partial 5HT2 and alpha agonist causes vasoconstriction todecrease pulsation in migraine acute attack. Side effect is
vasoconstriction (prinzmetal)
Page 1589
Q0795:Prophylaxis of migraine headaches
Page 1590
Propranolol; verapamil; amitriptyline; valproic acid
Page 1592
Vasodilation in kidneys; increases renal blood flow; increasesgastric mucosal blood flow (mucoprotection); activates
osteoclasts; fever; pain; maintains ductus arteriosus
Page 1593
Q0797:Prostacyclin (PGI2)
Page 1594
Vasodilation and inhibits platelet aggregation
Page 1596
Constitutive enzyme synthesizes GI PGs and TxA2
Page 1598
Inducible enzyme synthesizes PGs involved in inflammation;fever and pain.
Page 1600
Lipoxygenase inhibtor used in asthma
Page 1601
Q0801:Zafirlukast and -lukasts
Page 1602
Leukotriene receptor antagonist used in asthma
Page 1603
Q0802:MOA of aspirin
Page 1604
Nonselective; irreversible COX inhibitor via acetylation ofserine near active site
Page 1605
Q0803:Actions of aspirin
Page 1606
Low dose: antiplatelet aggregation (post-MI); moderate dose:analgesia; antipyeresis; hyperuricemia; High dose:
antiinflammatory; uricosuria
Page 1607
Q0804:Effects of aspirin on acid-base and electrolytes
Page 1608
Antiinflammatory doses: uncoupling of ETC --> increasesrespiration --> decreased pCO2 --> resp. alkalosis --> renal
compensation via HCO3 excretion --> compensatedrespiratory alkalosis. Toxic doses: inhibits respiratory center -
-> decreases respiration --> resp. acidosis plus ETCuncoupling --> metabolic acidosis; decreases ATP;
hyperthermia; hypokalemia
Page 1609
Q0805:Side effects of aspirin
Page 1610
Gastritis; ulcers; bleeding; tinnitus; vertigo; decreased hearing;bronchoconstriction; hypersensitivity (asthma; nasal polyps;
rhinitis); Reye syndrome; increased bleeding time; renaldysfunction at high doses
Page 1611
Q0806:Aspirin overdose management
Page 1612
Gastric lavage; alkalinization of urine (zero-order kinetics attoxic doses)
Page 1613
Q0807:Celecoxib
Page 1614
Selective COX-2 inhibitor. Antiinflammatory. Increases PTwhen used with warfarin; prothrombotic. Cross
hypersensitivity with sulfonamides. Potential cardiotoxicityresulted in withdrawal of rofecoxib.
Page 1615
Q0808:Acetaminophen
Page 1616
Inhibits COX in CNS only. No antiplatelet activity; notimplicated in Reye syndrome; no effects on uric acid; no
bonchoconstriction. Metabolized via P450. Hepatotoxic dueto reactive metabolite N-acetylbenzoquinonemine; which is
inactivated by GSH. Upon GSH depletion; metabolitedamages hepatocytes; nausea; vomiting; abdominal pain;centrilobular necrosis. Inducers of P450 enhance toxicity.
Management of hepatotoxicity: N-acetylcysteine.
Page 1617
Q0809:Hydroxychloroquine
Page 1618
Used for rheumatoid arthritis. Stabilizes lysosomes anddecreases chemotaxis. Side effects: GI distress; visual
dysfunction; hemolysis in G6PDH deficiency
Page 1619
Q0810:Methotrexate
Page 1620
Used for rheumatoid arthritis. Cytotoxic to lymphocytes.Side effects: hematotoxicity; mucositis; crystalluria
Page 1621
Q0811:Sulfasalazine
Page 1622
Used for rheumatoid arthritis. Decreases B cell function;possibly inhibits COX. Side effects: GI distress; rash;hemolysis in G6PDH deficiency; drug-induced lupus
Page 1623
Q0812:Glucocorticoids
Page 1624
Used in rheumatoid arthritis. Decrease LTs and plateletactivating factor (PAF). Side effects: ACTH suppression;
Cushingoid state; osteoporosis; GI distress; glaucoma
Page 1625
Q0813:Gold salts
Page 1626
Used in rheumatoid arthritis. Decreases lysosomal andmacrophage functions. Side effects: dermatitis;
hematotoxicity; nephrotoxicity
Page 1627
Q0814:Penicillamine
Page 1628
Used in rheumatoid arthritis. Suppresses T cells andcirculating rheumatoid factor. Side effects: proteinuria;
hematotoxicity; autoimmune disease.
Page 1629
Q0815:Etanercept
Page 1630
Used in rheumatoid arthritis. Binds TNF. Side effects:hypersensitivity; injection site reactions; infections
Page 1631
Q0816:Infliximab
Page 1632
Used in rheumatoid arthritis. Monoclonal antibody to TNF.Side effects: infusion reactions; infections
Page 1634
Used in rheumatoid arthritis. IL-1 receptor antagonist. Sideeffects: infections; injection site reactions
Page 1635
Q0818:Colchicine
Page 1636
Used in acute gout. Binds tubulin --> decreases microtubularpolymerization ; decreases LTB4 and leukocyte/granulocyte
migration. Side effects: diarrhea; GI pain; hematuria;myelosuppression; neuropathy
Page 1637
Q0819:Allopurinol
Page 1638
Prodrug converted by xanthine osidase into alloxanthine whichinhibits the enzyme --> decreases purine metabolism -->
decreases uric acid. Side effects: GI distress; neuropathy; rash;vasculitis; stones.
Page 1639
Q0820:Probenecid
Page 1640
Inhibits tubular reabsorption of urate. Interactions: inhibitssecretion of acidic drugs (cephalosporins; fluoroquinolones).
Side effects: GI distress; rash; nephrotic syndrome;crystallization
Page 1641
Q0821:Glucocorticoid drugs
Page 1642
Cortisol; prednisone; triamcinolone; betamethasone;dexamethasone
Page 1643
Q0822:MOA of glucocorticoids
Page 1644
Inhibits leukocyte migration; phagocytosis and capillarypermeability; decreases PGs; LTs; expression of COX2; PAF
and interleukins
Page 1645
Q0823:Uses of glucocorticoids
Page 1646
Antiinflammatory and immunosuppressive
Page 1647
Q0824:Side effects of glucocorticoids
Page 1648
Suppression of ACTH --> cortical atrophy; shock if abruptlywithdrawn; cushingoid syndrome; hyperglycemia (increased
gluconeogenesis); osteoporosis with vertebral fractures;gastric acid secretion (ulcers); Na+ and H2O retention with
edema and hypertension; hypokalemic alkalosis;hypocalcemia; inhibits bone growth in children; decreaseswound healing (infections); increased sorbitol (glaucoma;
cataracts); mental dysfunction.
Page 1649
Q0825:Role of beta agonists in asthma
Page 1650
Selective beta 2 agonists: Relief of acute bronchoconstriction(albuterol; metaproterenol; terbutaline) and prophylaxis ofnightime attacks (salmeterol). Side effects include anxiety;
tremors and CV toxicity
Page 1651
Q0826:Ipratropium
Page 1652
Muscarinic blocker causes bronchodilation in acute asthma.Safer than beta 2 agonists in patients with cardiovascular
disease. DOC in bronchospasm induced by beta -blockers.
Page 1653
Q0827:Theophylline
Page 1654
Inhibits phosphodiesterase --> increases cAMP -->bronchodilation. Also antagonizes adenosine
(broncoconstrictor). Narrow therapeutic index. Side effects:nausea; diarrhea; increases HR; arrhythmias. Increased
toxicity with erythromycin; cimetidine and fluoroquinolones.
Page 1655
Q0828:Role of glucocorticoids in asthma
Page 1656
Decreases reactivity by decreasing PGs; LTs and Ils; Maycause oropharyngeal candidiasis and retarded bon growth with
chronic use; low doses prevent desensitization of betareceptors.
Page 1657
Q0829:Zafirlukast; mentelukast
Page 1658
LTD4 antagonists with slow onset. Used prophylactically forantigen; exercise or drug-induced asthma.
Page 1660
Selective inhibitor of lypoxygenases --> decreased Ils. Rapidonset; adjunct to steroids.
Page 1661
Q0831:MOA of NSAIDS
Page 1662
inhibit prostaglandin synthesis by inhibiting cyclo-oxygenase(cox)
Page 1663
Q0832:Difference between aspirin and other NSAIDS
Page 1664
Aspirin irreversibly inhibits cyclooxygenase
Page 1665
Q0833:Four main actions of NSAIDS
Page 1666
Anti-inflammatory; analgesia; antipyretic and antiplateletactivity
Page 1667
Q0834:Agent used for closure of patent ductus arteriosus
Page 1669
Q0835:Aspirin is contraindicated in children with viralinfection
Page 1670
Potential for development of Reye's syndrome
Page 1671
Q0836:SE of salicylates
Page 1672
Tinnitus; GI bleeding
Page 1673
Q0837:NSAID also available as an ophthalmic preparation
Page 1675
Q0838:NSAID available orally; IM and ophthalmically
Page 1677
Q0839:NSAID that is used for acute condition; such as pre-op anesthesia and has limited duration (<5 days) of use due to
nephrotoxicity
Page 1679
Q0840:Newer NSAIDs that selectively inhibit COX-2
Page 1680
Celecoxib and rofecoxib
Page 1681
Q0841:COX 2 inhibitors may have reduced risk of
Page 1682
Gastric ulcers and GI Bleeding
Page 1683
Q0842:COX 2 inhibitors should be used cautiously in ptswith
Page 1684
Pre-existing cardiac or renal disease
Page 1685
Q0843:Acetaminophen only has
Page 1686
Antipyretic and analgesic activity
Page 1687
Q0844:SE of acetaminophen
Page 1689
Q0845:Antidote for acetaminophen toxicity
Page 1690
N-acetylcysteine
Page 1691
Q0846:DMARDs are slow acting drugs for
Page 1692
Rheumatic disease
Page 1693
Q0847:MOA of gold salts
Page 1694
Alter activity of macrophages and suppress phagocyticactivity of PMNs
Page 1695
Q0848:SE of gold salts
Page 1696
Dermatitis of the mouth aplastic anemia and agranulocytosis
Page 1697
Q0849:Causes bone marrow suppression
Page 1699
Q0850:SE of penicillamine
Page 1700
Aplastic anemia and renal
Page 1701
Q0851:Interferes with activity of T-lymphocytes
Page 1702
Hydroxychloroquine
Page 1703
Q0852:Anti-malarial drug used in rheumatoid arthritis (RA)
Page 1704
Hydroxychloroquine
Page 1705
Q0853:SE of hydroxychloroquine
Page 1706
Retinal destruction and dermatitis
Page 1707
Q0854:MOA of Leflunomide (newer agent)
Page 1708
Inhibiting Dihydroorotate Dehydrogenase which leads todecreased pyrimidine synthesis
Page 1709
Q0855:Proteins that prevent action of tumor necrosis factoralpha (TNF-alpha)
Page 1710
Infliximab and etanercept
Page 1711
Q0856:Anti-rheumatic agent also used for ulcerative colitis
Page 1713
Q0857:NSAIDS used in gout
Page 1714
Indomethacin and phenylbutazone
Page 1715
Q0858:NSAID contraindicated in gout
Page 1717
Q0859:SE of phenylbutazone
Page 1718
Aplastic anemia and agranulocytosis
Page 1719
Q0860:MOA of Colchicine (used in acute gout)
Page 1720
Selective inhibitor of microtubule assembly
Page 1721
Q0861:SE of colchicine
Page 1722
Kidney and liver toxicity
Page 1723
Q0862:Agent used to treat chronic gout by increasing uric acidsecretion
Page 1724
Probenecid and sulfinpyrazone
Page 1725
Q0863:Allopurinol treats chronic gout by inhibiting
Page 1726
Xanthine oxidase
Page 1727
Q0864:Disease caused by excess ergot alkaloids
Page 1728
St. Anthony's Fire
Page 1729
Q0865:Endogenous substances commonly interpreted ashistamine; serotonin; prostaglandins; and vasoactive peptides
Page 1731
Q0866:Syndrome of hypersecretion of gastric acid and pepsinusually caused by gastrinoma; it is associated with severe
peptic ulceration and diarrhea
Page 1732
Zollinger-Ellison Syndrome
Page 1733
Q0867:Drug that causes contraction of the uterus
Page 1735
Q0868:Distribution of histamine receptors H1; H2; and H3
Page 1736
Smooth muscle; stomach; heart; and mast cells; nerve endings;CNS respectively
Page 1737
Q0869:Prototype antagonist of H1 and H2 receptors
Page 1738
Diphenhydramine and impromidine respectively
Page 1739
Q0870:1st generation antihistamine that is highly sedating
Page 1740
Diphendydramine
Page 1741
Q0871:1st generation antihistamine that is least sedating
Page 1742
Chlorpheniramine or cyclizine
Page 1743
Q0872:2nd generation antihistamines
Page 1744
Fexofenadine; loratadine; and cetirizine
Page 1745
Q0873:Generation of antihistamine that has the most CNSeffects
Page 1746
First generation due to being more lipid-soluble
Page 1747
Q0874:Major indication for H1 receptor antagonist
Page 1748
Use in IgE mediated allergic reaction
Page 1749
Q0875:Antihistamine that can be used for anxiety andinsomnia and is not addictive
Page 1750
hydroxyzine (Atarax)
Page 1751
Q0876:H1 antagonist used in motion sickness
Page 1752
Dimenhydrinate; meclizine; and other 1st generation
Page 1753
Q0877:Most common side effect of 1st generationantihistamines
Page 1755
Q0878:Lethal arrhythmias resulting from concurrent therapywith azole fungals (metabolized by CYP 3A4) and these
antihistamines which inhibit the 3A4 iso-enzyme.
Page 1756
Terfenadine and astemizole (have been removed from themarket)
Page 1757
Q0879:H2 blocker that causes the most interactions withother drugs
Page 1759
Q0880:Clinical use for H2 blockers
Page 1760
Acid reflux disease; duodenal ulcer and peptic ulcer disease
Page 1761
Q0881:Receptors for serotonin (5HT-1) are located
Page 1762
Mostly in the brain; and they mediate synaptic inhibition viaincreased K+ conductance
Page 1763
Q0882:5HT-1d agonist used for migraine headaches
Page 1764
Sumatriptan; naratriptan; and rizatriptan
Page 1765
Q0883:Triptan available in parenteral and nasal formulation
Page 1767
Q0884:H1 blocker that is also a serotonin antagonist
Page 1769
Q0885:5HT2 antagonist mediate synaptic excitation in theCNS and smooth muscle contraction
Page 1770
Ketanserin; cyproheptadine; and ergot alkaloids (partialagonist of alpha and serotonin receptors)
Page 1771
Q0886:Agents for reduction of postpartum bleeding
Page 1772
Ergonovine and ergotamine
Page 1773
Q0887:Agents used in treatment of carcinoid tumor
Page 1774
Ketanserin cyproheptadine; and phenoxybenzamine
Page 1775
Q0888:5HT-3 antagonist used in chemotherapeutic inducedemesis
Page 1776
Ondansetron; granisetron; dolasetron and alosetron
Page 1777
Q0889:5ht-3 antagonist that has been associated with QRSand QTc prolongation and should not be used in patients with
heart disease
Page 1779
Q0890:DOC of chemo induced nausea and vomiting
Page 1781
Q0891:Drug used in ergot alkaloids overdose; ischemia andgangrene
Page 1783
Q0892:Reason ergot alkaloids are contraindicated inpregnancy
Page 1784
Uterine contractions
Page 1785
Q0893:SE of ergot alkaloids
Page 1786
Hallucinations resembling psychosis
Page 1787
Q0894:Ergot alkaloid used as an illicit drug
Page 1789
Q0895:Dopamine agonist used in hyperprolactinemia
Page 1791
Q0896:Peptide causing increased capillary permeability andedema
Page 1792
Bradykinin and histamine
Page 1793
Q0897:Mediator of tissue pain; edema; inactivated by ACE;and may be a contributing factor to the development of
angioedema
Page 1795
Q0898:Drug causing depletion of substance P (vasodilator)
Page 1797
Q0899:Prostaglandins that cause abortions
Page 1798
Prostaglandin E1 (misoprostol) PGE2; and PGF2alpha
Page 1799
Q0900:Difference between COX 1 and COX 2
Page 1800
COX 1 is found throughout the body and COX 2 is only ininflammatory tissue
Page 1801
Q0901:Drug that selectively inhibits COX 2
Page 1802
Celecoxib; valdecoxib; and rofecoxib
Page 1803
Q0902:Inhibitor of lipoxygenase
Page 1805
Q0903:Major SE of zileuton
Page 1807
Q0904:Inhibitor of leukotrienes (LTD4) receptors and used inasthma
Page 1808
Zafirlukast and montelukast
Page 1809
Q0905:Used in pediatrics to maintain patency of ductusarteriosis
Page 1811
Q0906:Approved for use in severe pulmonary HTN
Page 1812
PGI2 (epoprostenol)
Page 1813
Q0907:Prostaglandin used in the treatment impotence
Page 1815
Q0908:Irreversible; nonselective COX inhibitor
Page 1817
Q0909:Class of drugs that reversibly inhibit COX
Page 1819
Q0910:Primary endogenous substrate for Nitric OxidaseSynthase
Page 1821
Q0911:MOA and effect of nitric oxide
Page 1822
Stimulates cGMP which leads to vascular smooth musclerelaxation
Page 1823
Q0912:Long acting beta 2 agonist used in asthma
Page 1825
Q0913:Muscarinic antagonist used in asthma
Page 1827
Q0914:MOA action of cromolyn
Page 1828
Mast cell stabilizer
Page 1829
Q0915:Enzyme which theophylline inhibits
Page 1830
Phosphodiesterase
Page 1831
Q0916:Methylxanthine derivative used as a remedy forintermittent claudication
Page 1833
Q0917:Antidote for severe CV toxicity of theophylline
Page 1835
Q0918:MOA of corticosteroids
Page 1836
inhibit phospholipase A2
Page 1837
Q0919:SE of long term (>5 days) corticosteroid therapy andremedy
Page 1838
Adrenal suppression and weaning slowly; respectively
Page 1839
Q0920:Parathyroid hormone (PTH) acts on these receptors toinc. cAMP in bone and renal tubular cells?
Page 1840
G-protein couples receptors
Page 1841
Q0921:Vit D is a derivative of this compound?
Page 1842
7-dehydrocholesterol
Page 1843
Q0922:the actions of Vit D are mediated through receptors inthis location?
Page 1844
nuclear receptors (which regulate gene expression)
Page 1845
Q0923:Bone formation may be increased by theadministration of this form of Vit D?
Page 1846
24;25-dihydroxyvitamin D (secalcifediol)
Page 1847
Q0924:Vit D supplements and synthetic derivatives are usedin these conditions?
Page 1848
deficiency states such as: chronic renal failure; intestinalosteodystrophy; & nutritional rickets
Page 1849
Q0925:this hormone has been used in conditions in which anacute reduction of serum calcium is needed (eg Paget's disease
and hypercalcemia)?
Page 1851
Q0926:what is the benefit of using salmon calcitonin overhuman calcitonin?
Page 1852
Salmon Calcitonin has a longer half life and greater potency
Page 1853
Q0927:these drugs can prevent or delay bone loss inpostmenopausal women through inhibition of PTH-
stimulated bone resorption?
Page 1854
Estrogens and SERMS (tamoxifen and Raloxifen)
Page 1855
Q0928:chronic systemic use of these drugs is a common causeof osteoporosis in adults?
Page 1856
Glucocorticoids
Page 1857
Q0929:these hormone are useful in the intermediate termtreatment of Hypercalcemia?
Page 1858
Glucocorticoids
Page 1859
Q0930:examples of bisphosphonates?
Page 1860
alendronate; etidronate; pamidronate; and risedronate (ALLEND IN -DRONATE)
Page 1861
Q0931:actions of bisphosphonates?
Page 1862
reduce both resorption and formation of bone; affect Vit Dproduciton; calcium absorption from GI tract; and direct
effects of OsteoClasts
Page 1863
Q0932:chronic therapy with this class of drugs can slow theprogress of postemenopausal osteoporosis and REDUCES
FRACTURES?
Page 1864
Bisphosphonates
Page 1865
Q0933:what is the oral bioavailability of bisphosphonates?
Page 1866
LOW <10% (and food impairs absorption)
Page 1867
Q0934:side effect of bisphosphonates?
Page 1868
Esophageal ulceration (so pts shoudl take with lots of H2O)
Page 1869
Q0935:acute toxicity of this compound (as would occur w/ingestion of Rat poison) results in GI and Neurologic
symptoms?
Page 1871
Q0936:what is seen with CHRONIC Fluoride toxicity(fluorosis)?
Page 1872
Ectopic bone formation and Bony Bumps on Bones(exostoses)
Page 1873
Q0937:antibiotic used to reduce serum calcium and boneresorption in Paget's disease and hypercalcemia?
Page 1874
Plicamycin (mithramycin)
Page 1875
Q0938:what are the serious toxicities of Plicamycin?
Page 1876
thrombocytopenia; hemorrhage; hepatic and renal damage (sonot used commonly; mainly restricted to short term treatment
of serious hypercalcemia)
Page 1877
Q0939:diuretics that can affect serum calcium levels?
Page 1878
Thiazides and Furosemide (Loop)
Page 1879
Q0940:(5) Parkinsons drugs
Page 1880
BALSA;Bromocriptine;Amantadine;Levodopa;Selegiline;Antimuscarinics
Page 1881
Q0941:Parkinson drug;agonized dopamine receptors
Page 1883
Q0942:Parkinson drug;Increases Dopamine;(2)
Page 1884
Amantidine;;L-Dopa
Page 1885
Q0943:Parkinson drug;selectively inhibits MAO-B; therebyincreasing availability of DA
Page 1887
Q0944:Parkinson drug;improves cholinergic activity (tremorand rigidity)
Page 1888
Benztropine;(anti-muscarinic)
Page 1889
Q0945:what coverts L-dopa to dopamine in the brain?;AE toperiphreal L-dopa/carbidpoa
Page 1890
Carboxylase;;AE;Arrthymias
Page 1891
Q0946:serotonin agonist causing vasoconstriction for Tx ofmigraine or cluster HA;what specific receptor?;AE
Page 1892
Sumatriptan;receptor: 5HT-1D;AE: Coronary vasospasm
Page 1893
Q0947:AE of Benzodiazepines
Page 1895
Q0948:(3) drugs that are first-line for Tonic-Clonic seizures
Page 1896
PVC;Phenytoin;;Valproic Acid;;Carbamazepine
Page 1897
Q0949:(2) drugs that are first-line for Absent seizures
Page 1898
Ethosuximide;;Valproic Acid
Page 1899
Q0950:MOA of Valproic Acid;(3) AE;Aside from Bipolard/o; what other psych Dx can it be used for?
Page 1900
MOA;Na-channel (and Ca-channel)blocker;AE;Hepatotoxicity;Neural tube defects infetus;Tremor;(also can be used for Schizophrenia)
Page 1901
Q0951:What are the (4) Tx for Status Epilepticus
Page 1902
Diazepam;;Lorazepam;;Phenytoin;;Phenobarbital
Page 1903
Q0952:DOC for seizures in pregnant women and children
Page 1905
Q0953:DOC for Trigeminal neuralgia; Tonic-Clonic seizures;schizophrenia and bipolar disorder;(2) AE;what monthly test
should be done to patient?
Page 1906
Carbamazepine;AE;Hepatotoxicity;Aplastic Anemia;monthlytest: LFTs
Page 1907
Q0954:(2) epilepsy drugs that can cause Stevens-Johnsonsyndrome
Page 1908
Ethosuximide;Lamotrigine
Page 1909
Q0955:MOA of Ethosuximide
Page 1910
Blocks T-type Ca-channels
Page 1911
Q0956:epileptic drug that blocks Na channels and inhibitsglutamate release from presynaptic neurons;AE (4)
Page 1912
Phenytoin;AE;Gingival hyperplasia;Hirsutism;SLE-likesyndrome;Nystagmus and ataxia
Page 1913
Q0957:drug class that facilitates GABA action by increasingthe duration of Cl- channel opening;contraindication?
Page 1914
Barbiturates;[barbiDURATes inc DURATion];CI: Porphyria
Page 1915
Q0958:Barbiturate that is used in ansthesia induction
Page 1917
Q0959:drug class that facilitates GABA action by increasingthe frequency of Cl- channel opening;use (4)*
Page 1918
Benzodiazepines;use (DumbASS);Detoxification;Anxiety;Status epilepticus;Sleep issues
(walking; terrors)
Page 1919
Q0960:(3) short-acting Benzos
Page 1920
short TOM thumb;Triazolam;Oxazepam;Midazolam
Page 1921
Q0961:DOC for Huntington's DZ;(3)*
Page 1922
Practice HuntingTrees;Phenothiazines;Haloperidol;Tetrabenazine
Page 1923
Q0962:DOC for Tourette's
Page 1925
Q0963:beta-blocker used to Tx tremor
Page 1927
Q0964:DOC in Wilson's Dz
Page 1929
Q0965:(3)* Neuroleptic Antipsychotics that block the D2receptors;main use?
Page 1930
THC;Thioridazine;;Haloperidol;;Chlorpromazine;use:Schizophrenia
Page 1931
Q0966:AE of Neuroleptics (antipsychotics);for each receptorblocked;1. DA;2. Muscarinic;3. Alpha;4. Histamine
Page 1932
DA: Hyperprolactinemia; gynecomastia;Muscarinic: drymouth; constipation;Alpha: Hypotension;;Histamine:
Sedation
Page 1933
Q0967:Dx;rigidity; myoglobinuria; autonomic instability;hyperpyrexia; recent Tx for schizophrenia;Tx?;(3 possible)
Page 1934
Neuroleptic Malignant syndrome;Tx;1. Bromocriptine;2.Amantidine;3. Dantrolene
Page 1935
Q0968:Dx;strange oral-facial movements; chorea; recentneuroleptic ingestion
Page 1936
Tardive Dyskinesia
Page 1937
Q0969:(3) Atypical Antipsychotics
Page 1938
OLanzapine; CLOZapine; RISPERidone;[its not ATYPICALfor OLd CLOZets to RISPER]
Page 1939
Q0970:MOA of Atypical antipsychotics;which is used to TxOCD?;which causes Agranulocytosis as an AE?
Page 1940
block Serotonin and Dopamine receptors;OLanzapine -OCD;CLOZapine - Agranulocytosis
Page 1941
Q0971:(4)* AE of Lithium;Use?
Page 1942
Lithium;LMNOP;Lithium AE =;Movement(tremor);Nephrogenic DI;hypOthyroidism;Pregnancy
problems;Use: Mood stabilizer for Bipolar disorder to blockmanic events
Page 1943
Q0972:(4)* SSRIs;;AE? (2)
Page 1944
"the CITy PAROt FLU downSERTRAIL";CITalopram;;PAROxetine;;FLUoxetine;;SERTR
ALine;AE: Sexual dysfunction and N/V
Page 1945
Q0973:(3) TCAs;MOA;Basic (not toxic) AE (2)
Page 1946
CIA;Clomipramine;Imipramine;Amitriptyline;MOA: blockreuptake of NE and Serotonin;AE;Sedation;anticholinergic
side effects
Page 1947
Q0974:TCA used for bedwetting
Page 1949
Q0975:TCA used for OCD
Page 1951
Q0976:Toxicity of TCA;(3)
Page 1952
("Tri-C");Convulsions;;Coma;;Cardiotoxicity
Page 1953
Q0977:(5)* Heterocyclic Antidepressants
Page 1954
"you need BUtane in your VEINs to MURder for a MAP ofalcaTRAZ";BUproprion;VENlafaxine;MIRtazapine;MAProti
line;TRAZodone
Page 1955
Q0978:heterocyclic that also Tx smoking
Page 1957
Q0979:heterocyclic that inhibits Serotonin; NE and DAreuptake
Page 1959
Q0980:heterocyclic that is an alpha2-blocker
Page 1961
Q0981:what (3) drugs can MAO-inhibitors not combinewith?;why?
Page 1962
Tyramine - HTN crisis;SSRI - Serotonin syndrome;B-agonist- Serotonin syndrome
Page 1963
Q0982:what does it mean if an anesthetic has a high solubilityin blood?;(2)
Page 1964
slower induction and slower recovery time;(Low bloodsolubility = rapid induction and recovery time)
Page 1965
Q0983:what does it mean if an anesthetic has a high solubilityin lipids?
Page 1966
Increased Potency;High lipid solubility = 1/MAC
Page 1967
Q0984:AE of Halothane
Page 1969
Q0985:(5)* types of IV anesthetics
Page 1970
B.B.King on OPIATES PROPOsesFOOLishly;Barbs;Benzos;Ketamine;Opiates;Propofol
Page 1971
Q0986:common Benzo used for endoscopy
Page 1973
Q0987:how can you tell Amide local anesthetics versusesters?;MOA of locals
Page 1974
AmIdes have 2 "I's" in the name;ex: LIdocaIne;MOA: Na-channel blockers
Page 1975
Q0988:which local anesthetic has cardiovascular toxicity?
Page 1977
Q0989:used to Tx hyperthermia caused by inhalationanesthetics and neuroleptic malignant syndrome;MOA
Page 1978
Dantrolene;;MOA;prevents release of Ca from SR of skeletalmuscles
Page 1979
Q0990:what mixed agonist/antagonist of opioid receptors canplace a person on Methadone back into withdrawal?
Page 1981
Q0991:what is the only opioid delivered parenterally?
Page 1983
Q0992:what is the only local anesthetic used topically?
Page 1985
Q0993:(2) MAO inhibitors
Page 1986
Phenelzine;;Tranylcypromine
Page 1987
Q0994:what NT does it block;Neuroleptics
Page 1989
Q0995:what NT does it block;Atypical antipsychotics
Page 1990
Serotonin;Dopamine
Page 1991
Q0996:what (2) NT does it block;TCAs
Page 1993
Q0997:what NT does it block;Heterocyclics
Page 1995
Q0998:which SSRI also inhibits NE?
Page 1997
Q0999:which opiate receptor has the majority of the AE andEuphoria?;which has Dysphoria?
Page 1998
U - Euphoria (and AE);;K - Dysphoria
Page 1999
Q1000:in addition to Tx schizo; what abdominal Sx doesChlorpromazine Tx?
Page 2000
Nausea and Vomiting
Page 2001
Q1001:what class of Antipsychotics have AE associated w/blocking Dopamine; Muscarinic; alpha and Histamine
receptors?
Page 2002
Neuroleptics;Chlorpromazine ("-AZINES") and Haloperidol
Page 2003
Q1002:Which Schizophrenic drug is also effective inminimizing the emotional bluntness and social withdrawal Sx?
Page 2005
Q1003:what "NSAID" does not inhibit prostaglandinsynthesis?
Page 2007
Q1004:general anesthetic that causes AE of Hyperthermia;HTN; HyperK; tachycardia; muscle rigidity and Metabolic
Acidosis?
Page 2009
Q1005:which Benzo is good for alcohol withdrawal?
Page 2011
Q1006:which anti-alcohol med causes nausea and vomiting w/alcohol consumption?
Page 2013
Q1007:what Benzo is good versus Agoraphobia and Panicdisorders?
Page 2015
Q1008:what anti-epileptic / anti-psychotic can induceseizures?
Page 2017
Q1009:AE of Propofol
Page 2018
Metabolic Acidosis
Page 2019
Q1010:list the progressive depression of the CNS;(5)
Page 2020
Sedation -> Hypnosis -> Anesthesia ->;Coma -> death
Page 2021
Q1011:what is the effect a local anesthetic has on nervefibers?
Page 2022
Pain -> Sensory -> Motor
Page 2023
Q1012:What is the underlying cause of Parkinson's?
Page 2024
loss of dopaminergic neurons and excess cholinergic activity
Page 2025
Q1013:Mneumonic for Parkinson's Disease drugs?
Page 2026
BALSA: Bromocriptine; Amantiadine; Levodopa(+carbidopa); Selegiline (+COMT inhibitors);
Antimuscarinics
Page 2027
Q1014:MOA of Bromocriptine?
Page 2028
agonize dopamine receptors (ergot alkaloid and partialdopamine agonist)
Page 2029
Q1015:Agents that increase dopamine?
Page 2030
Amantadine (increase dopamine release); L-dopa/carbidopa(converted to dopamine in CNS)
Page 2031
Q1016:MOA of Selegiline and entacapone/tolcapone?
Page 2032
Prevent dopamine breakdown (Selegiline=selective MAOtype B inhibitor)and (entacapone/tolcapone=COMT
inhibitors)
Page 2033
Q1017:MOA of Benztropine?
Page 2034
Curbs excess cholinergic activity (antimuscarinic)
Page 2035
Q1018:Antimuscarinic that improves tremor and rigidity buthas little effect on bradykinesia?
Page 2037
Q1019:Clinical use of L-dopa/carbidopa?
Page 2039
Q1020:MOA of L-dopa/carbidopa?
Page 2040
Increase dopamine levels in brain. Cross BBB and convertedby dopa decarboxylase in CNS to dopamine.
Page 2041
Q1021:Toxicity of L-dopa?
Page 2042
Arrhythmias from peripheral conversion to dopamine;dyskinesia after doses and akinesia between doses.
Page 2043
Q1022:How can you avoid L-dopa induced arrhythmias?
Page 2044
Give with carbidopa = a peripheral decarboxylase inhibitor
Page 2045
Q1023:Selegiline MOA?
Page 2046
Inhibits MAO-B; increase dopamine availability
Page 2047
Q1024:Selegiline toxicity?
Page 2048
enhance adverse effects of L-dopa
Page 2049
Q1025:Sumatriptin MOA?
Page 2050
5-HT1D agonist. Causes vasoconstriction.
Page 2051
Q1026:Clinical use of Sumatriptin?
Page 2052
acute migraine; cluster headaches
Page 2053
Q1027:Sumatriptin toxicity and contraindications?
Page 2054
coronary vasospasm; contraindicated in pts with CAD orangina
Page 2055
Q1028:Clinical use of phenytoin?
Page 2056
1st line for generalized tonic-clonic seizures and statusepilepticus prophylaxis. Also a class IB antiarrhythmic.
Page 2057
Q1029:MOA of phenytoin?
Page 2058
increase Na+ channel inactivation. Inhibits glutamate(excitatory) release.
Page 2059
Q1030:Clinical use of Carbamazepine?
Page 2060
1st line for generalized tonic-clonic seizures and trigeminalneuralgia. Also for simple and complex partial seizures.
Page 2061
Q1031:MOA of Carbamazepine?
Page 2062
increase Na+ channel inactivation
Page 2063
Q1032:Toxicity of Carbamazepine?
Page 2064
diplopia; atazia; agranulocytosis; aplastic anemia; livertoxicity; teratogenesis; induces cyto P-450
Page 2065
Q1033:Toxicity of phenytoin?
Page 2066
nystagmus; diplopia; ataxia; sedation; gingival hyperplasia;hirsutism; megaloblastic anemia; teratogenesis; malignanthyperthermia; SLE-like syndrome; induces cyto P-450
Page 2067
Q1034:Lamotrigine MOA?
Page 2068
blocks voltage-gaated Na+ channels
Page 2069
Q1035:Clinical use Gabapentin?
Page 2070
simple and complex partial seizures; generalized tonic-clonic.Also peripheral neuropathy.
Page 2071
Q1036:MOA of Gabapentin?
Page 2072
increase GABA release
Page 2073
Q1037:Topiramate MOA?
Page 2074
blocks Na+ channels; increase GABA action
Page 2075
Q1038:Gabapentin toxicity?
Page 2076
sedation; ataxia
Page 2077
Q1039:Lamotrigine toxicity?
Page 2078
Stevens-Johnson syndrome.
Page 2079
Q1040:Topiramete toxicity?
Page 2080
sedation; mental dulling; kidney stones; weight loss
Page 2081
Q1041:Phenobarbital clinical use?
Page 2082
1st line in preggers and kids. Generalized tonic-clonic andsimple and complex partial seizures.
Page 2083
Q1042:Barbituate toxicity?
Page 2084
sedation; tolerance; dependence; cyto P-450 induction;resp/CV depression; additive with alcohol
Page 2085
Q1043:Barbituate MOA?
Page 2086
increases GABA-A action by increase DURATION of Cl-channel opening; which decreases neuron firing.
[barbiDURATe=increased DURATion]
Page 2087
Q1044:Valproic acid clinical use?
Page 2088
1st line for generalized tonic-clonic seizures. Also formyoclonic and absence seizures.
Page 2089
Q1045:Valproic acid MOA?
Page 2090
increase Na+ channel inactivation. Increase GABAconcentration.
Page 2091
Q1046:Valproic acid toxicity?
Page 2092
GI distress; fatal hepatotoxicity; neural tube defects; tremor;weight gain
Page 2093
Q1047:Ethosuximide clinical use?
Page 2094
1st line for absence seizures.
Page 2095
Q1048:MOA ethosuximide?
Page 2096
blocks thalamice T-type Calcium channels
Page 2097
Q1049:Ethosuximide toxicity?
Page 2098
GI distress; lethargy; headache; urticaria; Stevens-Johnsonsyndrome
Page 2099
Q1050:Benzodiazepine clinical uses?
Page 2100
1st line for acute status epilepticus; also for seizures ofeclampsia
Page 2101
Q1051:Name 4 barbituates.
Page 2102
Phenobarbital; pentobarbital; thiopental; secobarbital
Page 2103
Q1052:Barbituate contraindication?
Page 2105
Q1053:Name some Benzodiazepines. (8)
Page 2106
diazepam; lorazepam; triaxolam; temazepam; oxazepam;midazolam; chlordiazepoxide; alpraxolam
Page 2107
Q1054:MOA of Benzos?
Page 2108
Facilitate GABA-A action by increse FREQUENCY of Cl-channel opening
Page 2109
Q1055:What drug class do you use for alcohol withdrawal-DTs?
Page 2111
Q1056:What are the 3 short-acting Benzos?
Page 2112
TOM thumb= Triazolam; Oxazepam; Midazolam
Page 2113
Q1057:Do benzos or barbituates have a higher risk of respdepression and coma?
Page 2115
Q1058:How do you treat a Benxo overdose?
Page 2116
Flumazenil (competitive antagonist at GABA receptor)
Page 2117
Q1059:Name 6 inhaled anesthetics
Page 2118
halothane; enflurane; isoflurane; sevoflurane; methoxyflurane;nitrous oxide
Page 2119
Q1060:Effects of inhaled anesthetics?
Page 2120
myocardial and resp depression; nausea/emesis; increasecerebral blood flow
Page 2121
Q1061:Toxicity of halothane; methoxyflurane; and enflurane?
Page 2122
hepatotoxicity (halothane); nephrotoxicity (methoxyflurane);proconvulsant (enflurane)
Page 2123
Q1062:Drug classes used as IV anesthetics? (5)
Page 2124
Barbiturates; Benzos; Ketamine; Opiates; Propofol
Page 2125
Q1063:Name the local anesthetics that are esters
Page 2126
procaine; cocaine; tetracaine; amides
Page 2127
Q1064:Name the local anesthetics that are amides
Page 2128
lidocaine; mepivacaine; bupivacaine
Page 2129
Q1065:barbiturate used as IV anesthetic?
Page 2130
thiopental - used for short surgical procedures and inductionof anesthesia
Page 2131
Q1066:drug used for endoscopy?
Page 2133
Q1067:Arrylcyclohexamine (ketamine) effects?
Page 2134
CV stimulant; disorientation; hallucination; bad dreams;increase cerebral blood flow
Page 2135
Q1068:Opeates used during general anesthesia?
Page 2136
morphine; fentanyl
Page 2137
Q1069:MOA of local anesthetics?
Page 2138
block Na+ channels. Tertiary amines penetrate membrane inuncharged form; then bind to ion channels as charged form.
Page 2139
Q1070:Order of nerve block?
Page 2140
small diameter>large diameter. Myelinated>unmyelinated.Size predominates over myelination.
Page 2141
Q1071:order of loss during nerve block?
Page 2142
pain(1st)>temp>touch>pressure
Page 2143
Q1072:how do you enhance local action?
Page 2144
give with vasoconstrictors (EPI)
Page 2145
Q1073:What happens to local anesthetics in infected tissues?
Page 2146
tissue is acidic; anesthetics are charged and can't penetratemembrane. More anesthetic is needed.
Page 2147
Q1074:What receptor do neuromuscular blocking drugs targetand what are they used for clinically?
Page 2148
motor (vs. autonomic) nicotinic receptor. Used for muscleparalysis in surgery or mechanical ventilation.
Page 2149
Q1075:Depolarizing neuromuscular blocking drug?
Page 2150
succinylcholine
Page 2151
Q1076:nondepolarizing neuromuscular blocking drugs?
Page 2152
tubocurarine; atracurium; mivacurium; pancuronium;vecuronium; rapacuronium
Page 2153
Q1077:What is dantrolene used for?
Page 2154
treatment of malignant hyperthermia and neurolepticmalignant syndrome
Page 2155
Q1078:MOA of dantrolene?
Page 2156
prevents release of calcium from the SR of skeletal muscle
Page 2157
Q1079:How do you reverse blockade of nondepolarizingneuromuscular blocking drugs?
Page 2158
neostigmine; edrophonium; and other cholinesterase inhibitors
Page 2159
Q1080:Name 4 antipsychotics (neuroleptics).
Page 2160
thioridazine; haloperidol; fluphenazine; chlorpromazine
Page 2161
Q1081:What is the MOS of antipsychotics?
Page 2162
block dopamine D2 receptors
Page 2163
Q1082:Drug class used to treat excess dopamine connectedwith schizophrenia?
Page 2165
Q1083:Adverse effects of antipsychotics?
Page 2166
extrapyramidal symptoms; gynacomastia; dry mouth;constipation; hypotension; sedation. Important: neuroleptic
malignant syndrome and tardive dyskinesia!
Page 2167
Q1084:Symptoms of neuroleptic malignant syndrome?
Page 2168
rigidity; myoglobinuria; autonomic instability; hyperpyrexia
Page 2169
Q1085:How do you treat neuroleptic malignant syndrom?
Page 2170
dantrolene and dopamine agonists
Page 2171
Q1086:What are EPS side effects?
Page 2172
acute dystonia; akinesia; akathisia; tardive dyskinesia (oftenirreversible)
Page 2173
Q1087:Name 3 atypical antipsychotics.
Page 2174
clozapine; olanzapine; riserperidone
Page 2175
Q1088:MOA of clozapine?
Page 2176
blocks 5-HT2 and dopamine receptors
Page 2177
Q1089:Clinical use of olanzapine?
Page 2178
schizo positive and neg. symptoms; OCD; anxiety disorder;depression; mania; tourettes
Page 2179
Q1090:Side effects of atypical antipsychotics?
Page 2180
fewer EPS and fewer anticholinergic side effects than typicalantipsychotics. Clozapine may cause agranulocytosis.
Page 2181
Q1091:Clinical use of lithium?
Page 2182
mood stabilizer for bipolar affective disorder; blocks relapseand acute mania events
Page 2183
Q1092:Side effects of lithium?
Page 2184
tremor; hypothyroidism; nephrogenic diabetes insipidus;teratogenesis. Narrow therapeautic window!!
Page 2185
Q1093:Buspirone MOA?
Page 2186
stimulates 5-HT1a receptors
Page 2187
Q1094:Buspirone clinical use?
Page 2188
generalized anxiety disorder
Page 2189
Q1095:Name the 4 main classes of antidepressants.
Page 2190
SSRIs; TCAs; Heterocyclic antidepressants; MAOIs
Page 2191
Q1096:Name 4 SSRIs.
Page 2192
fluoxetine; sertraline; paroxetine; citalopram
Page 2193
Q1097:Toxicity of SSRIs?
Page 2194
fewer side effects than TCAs. GI distress; sexual dysfunction;"serotonin syndrome" if used with MAOIs (= hyperthermia;
muscle rigidity; CV collapse)
Page 2195
Q1098:Do antidepressants work immediately?
Page 2196
No; usually takes 2-3 weeks
Page 2197
Q1099:What drug class do the following belong to:imipramine; amitriptyline; desipramine; nortriptyline;
clomipramine; doxepin?
Page 2199
Q1100:How do TCAs work?
Page 2200
block reuptake of NE and serotonin
Page 2201
Q1101:Which TCAs have more anticholinergic side effects?
Page 2202
tertiary TCAs (amitriptyline) have more than secondaryTCAs (nortriptyline)
Page 2203
Q1102:What are the major toxixities associated with TCAs?
Page 2204
"Tri-C's" = Convulsions; Coma; Cardiotoxicity (arrhythmias).Also resp. depression and hyperpyrexia (extremely high
fever)
Page 2205
Q1103:Name the 5 heterocyclic antidepressants.
Page 2206
Bupropion; Venlafaxine; Mirtazapine; Maprotiline;Trazodone
Page 2207
Q1104:Which antidepressant is also used for smokingcessation?
Page 2209
Q1105:MOA of Venlafaxine?
Page 2210
inhibits serotonin; NE; and dopamine reuptake
Page 2211
Q1106:MOA of Mirtazapine?
Page 2212
alpha-2 antagonist (increases release of NE and serotonin); 5-HTs and 5-HT3 receptor antagonist
Page 2213
Q1107:MOA of Maprotiline?
Page 2214
blocks NE reuptake
Page 2215
Q1108:MOA of trazodone?
Page 2216
inhibits serotonin reuptake
Page 2217
Q1109:Name 2 MAOIs
Page 2218
phenelzine; tranylcypromine
Page 2219
Q1110:Clinical use of MAOIs?
Page 2220
atypical depression with psychotic or phobic features;anxiety; hypochondriasis
Page 2221
Q1111:Important toxicity of MAOIs?
Page 2222
Hypertensive crisis with tyramine ingestion (red wine; cheese;fava beans) and meperidine.
Page 2223
Q1112:define dopamine hypothesis (& the disorder itreferences)?
Page 2224
hypothesis of schizophrenia proposes that disorder is causedby relative excess of function activity of the neurotransmitter
dopamine in specific neuronal tracts in the brain
Page 2225
Q1113:what type of dopamine receptor is found on thecaudate putamen; nucleus accumbens; cerebral cortex; and
hypothalamus that is negatively coupled to adenylyl cyclase?
Page 2227
Q1114:blockade of D2 receptors has this adverse effect?
Page 2228
extramyramidal dysfunction
Page 2229
Q1115:most of the newer atypical drugs (olanzapine;quetiapine; risperidone) have high affinity for this receptor?
Page 2230
5-HT 2A (although they may also interact with D2 and otherreceptors)
Page 2231
Q1116:with the exception of this drug all antipsychotic drugsblock H1 receptors to some degree?
Page 2233
Q1117:what is the function of the dopaminergic mesocortical-mesolimbic pathways?
Page 2234
regulates mentation and mood
Page 2235
Q1118:what is the function of the dopaminergic nigrostriataltract?
Page 2236
extrapyramidal function
Page 2237
Q1119:what is teh function of the dopaminergictuberoinfundibular pathway?
Page 2238
control of prolactin release
Page 2239
Q1120:what are the positive symptoms of psychophrenia?
Page 2240
hyperactivity; bizarre ideation; hallucinations; and delusions
Page 2241
Q1121:newer atypical durgs are reported to improve some ofthe negative symptoms of schizophrenia including?
Page 2242
emotional blunting and social withdrawl
Page 2243
Q1122:this drug has been sued as the sole agent in the manicphase and acts as mood stabilizer in bipolar disorder?
Page 2245
Q1123:this antipsychotic durg is used mainly in Tourette'ssyndrome?
Page 2247
Q1124:with the exception of this drug most phenothiazinehave antiemetic actions?
Page 2249
Q1125:this phenothiazine is used soley for its antiemeticproperties?
Page 2250
Prochlorperazine
Page 2251
Q1126:extrapyramidal toxicity occurs most frequently withthis drug?
Page 2252
Haloperidol (and the more potent piperazine side chainphenothiazines (eg fluphenazine; trifluoperazine)
Page 2253
Q1127:this toxicity includes choreoathetoid movements of themuscles of the lips and buccal cavity and may be irreversible?
Page 2254
Tardive dyskinesias
Page 2255
Q1128:which drug has the strongest autonomic effects?
Page 2257
Q1129:which drug has the weakest autonomic effects?
Page 2259
Q1130:all of the atypicals can cause this side effect?
Page 2260
orthostatic hypotension
Page 2261
Q1131:failure ot ejaculate is common in men treated withthese drugs?
Page 2263
Q1132:endocrine and metabolic side effects ofantipyschotics?
Page 2264
hyperprolactinemia; gynecomastia; and amenorrhea-galactorrhea syndrome and infertility; significant also {weightgain and hyperglycemia (diabetogenic action) w/ olanzapine
and clozapine}
Page 2265
Q1133:pts particularly sensitive to the extrapyramidal effectsof antipsychotics may develop this syndrome?
Page 2266
malignant hyperthermic syndrome
Page 2267
Q1134:what is the treatment for malignant hyperthermia?
Page 2268
Dantrolene (and perhaps dopamine agonists)
Page 2269
Q1135:sedation is a marked side effect with phenothiazinesespecially this one?
Page 2271
Q1136:what is the least sedating of the newer agents?
Page 2273
Q1137:visual impairment due to retinal deposits has occurredwith this drug
Page 2275
Q1138:at high doses this drug can cause severe conductiondefects in the heart resulting in fatal ventricular arrhythmias?
Page 2277
Q1139:this drug prolongs the QT interval of the ECG?
Page 2279
Q1140:this drug causes a small but important (1-2%)incidence of agranulocytosis and at high doses has caused
seizures?
Page 2281
Q1141:plasma levels of this drug may be altered by changes inbody water?
Page 2283
Q1142:dehydration of treatment with thiazide diuretics mayresult in an increase in levels of this drug that may reach toxic
levels?
Page 2285
Q1143:this drug increases the renal clearance of Lithium?
Page 2287
Q1144:MOA of lithium?
Page 2288
inhibits recycling of neuronal membrane phosphoinositidesinvolved in teh generation fo inositol triphosphate (IP3) and
DAG. these 2nd messengers are imp in amineneurotransmission
Page 2289
Q1145:what are the adverse neurologic symptoms ofLithium?
Page 2290
tremor; sedation; ataxia; & aphasia
Page 2291
Q1146:this renal condition occurs commonly at therapeuticdug levels of lithium?
Page 2292
Diabetes insipidus
Page 2293
Q1147:Edema is a frequent adverse effect of this drug?
Page 2295
Q1148:acneiform skin eruptions occur and leukocytosis isalways present when on this drug?
Page 2297
Q1149:the use of Lithium in prenancy may increase incidenceof this congenital defect?
Page 2298
Congentical Cardiac Anomalies (Ebstein's anomaly)
Page 2299
Q1150:Lithium is contraindicated in this group of people?
Page 2300
nursing mothers
Page 2301
Q1151:what is the amine hypothesis of mood?
Page 2302
postulates that brain amines; particularly NE and serotonin(5-HT) are neurotransmitters in pathways that function in the
expression of mood- a funcitonal decrease in the activity ofsuch amines -->depression and an increase --->mood elevation
Page 2303
Q1152:what is the acute effect of tricyclic drugs?
Page 2304
to inhibit the reuptake mechanisms (transporters) responsiblefor the termination of synaptic actions of both NE and
serotonin in the brain
Page 2305
Q1153:this drug has the unique action to increase aminerelease from nerve endings by antagonism of presynaptic
alpha2 adrenoceptors?
Page 2306
Mirtazapine (alpha2 receptors are involved in feedbackinhibition)
Page 2307
Q1154:this is a common CNS side effect of tricyclic drugs andsome heterocyclic agents?
Page 2309
Q1155:MAOIs; SSRIs; and bupropion are more likely tocause this CNS effect?
Page 2310
CNS stimulation
Page 2311
Q1156:antagonism of these receptors occurs with alltricylcics?
Page 2312
antagonism of muscarinic receptors (marked withamitriptyline and doxepin)
Page 2313
Q1157:what are the cardiovascular effects that occur mostcommonly with tricyclics?
Page 2314
hypotension from alpha blockade and depression of cardiacconduction (may lead to arrhytmias)
Page 2315
Q1158:what happens to the convulsive threshold when onTCAs and MAOIs?
Page 2316
lowers seizure threshold so seizures may occur (esp withoverdoses)
Page 2317
Q1159:MAOIs are most useful in patients with theseadditional symptoms to depression?
Page 2318
anxiety; phobic features; and hypochondriasis
Page 2319
Q1160:this class of drugs can also be used in the treatment ofbipolar disorder; acute panic attacks; phobic disorders;
enuresis; ADHD and chronic pain states
Page 2321
Q1161:high doses of this drug show efficacy in neuropathicpain?
Page 2323
Q1162:these drugs are effective in Obsessive compulsivedisorder?
Page 2324
Clomipramine and SSRIs
Page 2325
Q1163:this class of drugs is also approved for use in pts withgeneralized anxiety disorders; panic attacks; social phobias;
Bulemia; an dprementral dysphoric disorder and may beuseful in alcohol dependence treatment?
Page 2327
Q1164:this drug is used int eh management of patientsattemptins to withdraw from nicotine dependence?
Page 2329
Q1165:what are the 3 C's associated with TCA overdose?
Page 2330
coma; convulsions; and cardiotoxicity
Page 2331
Q1166:a withdrawal syndrome has been described for thisclass fo drugs that includes nausea; dizziness; anxiety; tremor
and palpitations?
Page 2333
Q1167:this class of drugs are inhibitors of P450 which leadsto increased activity of other drugs including TCAs and
Warfarin?
Page 2335
Q1168:this syndrome occurs with combo of fluoxetine andMAOI?
Page 2336
serotonin syndrome
Page 2337
Q1169:define serotonin syndrome?
Page 2338
life threatening syndrome includes severe muscle rigidity;myoclonus; hyperthermia; cardiovascualr instability; and
marked CNS stimulatory effects including seizures
Page 2339
Q1170:MAOIs administered with this class of drugs canresult in Serotonin syndrome?
Page 2341
Q1171:what are the low potency antipsychotics
Page 2342
chlorpromazine;thioridazine
Page 2343
Q1172:what are the side effects of thioridazine
Page 2344
most cardiotoxic in OD ;irreversible retinal pigmentation
Page 2345
Q1173:what are the side effects of chlorpromazine
Page 2346
hepatic toxicity ;derm problems (skin eruptions;discoloration);deposits in lens and cornea ;most sedating
Page 2347
Q1174:are low or high potency antipsychotics moreassociated with neurologic side effects?;non-neurologic?
Page 2348
high potency ;low potency
Page 2349
Q1175:examples of high potency antipsychotics
Page 2350
haloperidol;perphenazine ;fluphenazine
Page 2351
Q1176:what are EPS
Page 2352
pseudoparkinsonism ;akathisia ;acute dystonia
Page 2353
Q1177:aside from EPS what are other neurologic side effects
Page 2354
TD ;NMS ;decreased seizure threshold
Page 2355
Q1178:how to treat acute dystonia
Page 2356
anticholinergic ;antihistamine
Page 2357
Q1179:how to treat NMS
Page 2358
stop the offending drug immediately;give skeletal musclerelaxant;provide medical support;switch to low potency med
Page 2359
Q1180:how to treat TD
Page 2360
substitute low potency or atypical antipsychotic
Page 2361
Q1181:how to treat pseudoparkinsonism
Page 2362
anticholinergic (genztropine; ex) ;b/c DA normally suppressesACh activity; if you give anticholinergic it will cause increased
release of DA and relieve sx ;can also tx with antihistamine
Page 2363
Q1182:which neuro side effect takes >6mo to develop?
Page 2365
Q1183:Side effects of amitryptiline
Page 2366
sedation ;anticholinergic
Page 2367
Q1184:which HCA is most serotonin specific
Page 2369
Q1185:which HCA is least sedating
Page 2371
Q1186:which HCA has the least anticholinergic effects
Page 2373
Q1187:which HCA stimulates appetite
Page 2375
Q1188:what are the effects of desipramine
Page 2376
least sedating;stim appetite;least anticholinergic
Page 2377
Q1189:effets of doxepin
Page 2378
sedation ;antihistaminergic ;anticholinergic
Page 2379
Q1190:which HCA is likely to cause orthostatic hypotension
Page 2381
Q1191:which HCA may cause seizures
Page 2383
Q1192:which HCA has low cardiotoxicity
Page 2385
Q1193:which HCA is LEAST likely to cause orthostatichypotension
Page 2387
Q1194:other than depression; uses for amitryptiline
Page 2388
depresssion with insomnia ;chronic pain
Page 2389
Q1195:other than depression; uses for clomipramine
Page 2391
Q1196:other than depression; uses for desipramine
Page 2392
panic do ;depression in elderly ;eating DO ;(think of sideeffects)
Page 2393
Q1197:other than depression; uses for doxepine
Page 2395
Q1198:other than depression; uses for maprtoiltine
Page 2396
anxiety with depressive features
Page 2397
Q1199:other than depression; uses for nortriptyline
Page 2398
depression in elderly ;pruritus ;pts with cardiac dz
Page 2399
Q1200:which HCAs are good for treating depression inelderly?
Page 2400
nortriptyline ;desipramine
Page 2401
Q1201:General side effects from SSRIs?
Page 2402
SIG HAS ;Sexual side effects;Insomnia;GIprobs;HA;Anorexia;Serotonin syndrome (if given w MAOIs)
Page 2403
Q1202:What are SSRIs used to treat?
Page 2404
OCD (fluvoxamine);Premature ejac ;Panic d/o;PMDD(fluoxetine) ;Social phobia (paroxetine)
;Hypochondriasis;Chronic pain ;PTSD;paraphilias
Page 2405
Q1203:which SSRI --> weight loss
Page 2407
Q1204:which SSRI --> agitation and insomnia
Page 2408
fluoxetine;"one FLU over the cuckoo's nest"
Page 2409
Q1205:which SSRI is most sedating
Page 2411
Q1206:which SSRI is most anti-cholinergic
Page 2413
Q1207:which of sSRIs is most likely --> GI probs
Page 2415
Q1208:which SSRI is most cardiotoxic
Page 2418
Venlafaxine;duloxetine ;5HT and NorE reuptake inhib
Page 2420
buproprion ;norE/DA reuptake inhib
Page 2422
Nefazodone ;Trazodone ;5HT antagonist and reuptake inhib
Page 2424
Mirtazapine ;norE and 5HT antag
Page 2425
Q1213:advantage to SNRIs
Page 2426
rapid sx relief;few sexual side effects
Page 2427
Q1214:other than depression; uses of duloxetine
Page 2428
refractory depression ;urine stress incontinence
Page 2429
Q1215:other than depression; uses of venlafaxine
Page 2430
refractory depression ;GAD ;social phobia
Page 2431
Q1216:contradindications for buproprion
Page 2432
seizures ;eating d/o ;psychosis (at higher doses; high DAeffects) ;mania
Page 2433
Q1217:other than depression; uses of MAOIs
Page 2434
atypical depression;pain d/o ;eating d/o ;panic d/o ;socialphobia
Page 2435
Q1218:Pharmacological treatment for: Alcohol withdrawal
Page 2436
Benzodiazepines
Page 2437
Q1219:Pharmacological treatment for: Anorexia/bulimia
Page 2439
Q1220:Pharmacological treatment for: Anxiety
Page 2440
1. Barbiturates;2. Benzodiazepines;3. Buspirone (for GAD;does not cause sedation or addiction; and does not interactwith EtOH);4. MAO inhibitors;5. Venlafaxine (SNRI; for
GAD);6. Olanzapine (an atypical antipsychotic)
Page 2441
Q1221:Pharmacological treatment for: Atypical depression
Page 2443
Q1222:Pharmacological treatment for: Bipolar disorder
Page 2444
Mood stabilizers (Lithium; Valproic acid; Carbamazepines)
Page 2445
Q1223:Pharmacological treatment for: Depression
Page 2446
1. SSRIs (endogenous depression);2. SNRIs (when SSRIs areineffective or neuropathic pain);3. TCAs/Maprotiline (severemajor depression);4. MAO inhibitors (atypical depression or
inability to use TCAs);5. Bupropion;6. Mirtazapine;7.Trazodone/Nefazodone;8. Olanzapine (an atypical
antipsychotic)
Page 2447
Q1224:Pharmacological treatment for: Depression withinsomnia
Page 2448
Trazodone and Mirtazapine
Page 2449
Q1225:Pharmacological treatment for: OCD
Page 2450
1. Fluvoxamine (an SSRI);2. Olanzapine (an atypicalantipsychotic);3. Clomipramine (a TCA)
Page 2451
Q1226:Pharmacological treatment for: Panic disorder
Page 2452
TCAs and Buspirone
Page 2453
Q1227:Pharmacological treatment for: Schizophrenia
Page 2454
1. Typical Neuroleptics;2. Atypical neuroleptics (for positiveand negative symptoms)
Page 2455
Q1228:Mechanism of neuroleptics
Page 2456
Most block dopamine D2 receptors (as excess dopamineeffects are connected with schizophrenia)
Page 2457
Q1229:Mechanism of Venlafaxine
Page 2458
Inhibits reuptake of serotonin (at all doses); norepinephrine(athigh doses); and dopamine (mild)
Page 2459
Q1230:Mechanism of lithium
Page 2460
Not established; possibly related to inhibition of PIPresynthesis leading to its relative depletion in neurons
Page 2461
Q1231:Mechanism of buspirone
Page 2462
Stimulates 5-HT1A receptors
Page 2463
Q1232:Mechanism of SSRIs
Page 2464
Selective serotonin reuptake inhibition; leading to downregulation of presynaptic inhibitory receptors; leading to
increased release of neurotransmitter; leading to therapeuticresponse.
Page 2465
Q1233:Mechanism of tricyclic antidepressants
Page 2466
1. Nonselectively inhibit reuptake of norepinephrine andserotonin (beneficial);2. Block serotonergic; alpha-adrenergic;
histaminic; and muscarinic receptors (not beneficial)
Page 2467
Q1234:Mechanism of clozapine
Page 2468
Blocks D2 like normal neuroleptic; but also blocks 5HT2 aswell as D1; D4; muscarinic; and alpha-adrenergic receptors.
Page 2469
Q1235:Mechanism of risperidone
Page 2470
Blocks 5HT2 receptors more than D2 receptors
Page 2471
Q1236:Mechanism of aripiprazole
Page 2472
Partial agonist of D2 and 5HT1A receptors; and blocks5HT2A receptors.
Page 2473
Q1237:Mechanism of bupropion
Page 2475
Q1238:Mechanism of mirtazapine
Page 2476
Alpha2 antagonist (increasing release of NE and serotonin)and potent 5-HT2 and 5-HT3 receptor antagonist
Page 2477
Q1239:Mechanism of duloxetine
Page 2478
SNRI. Inhibits reuptake of serotonin and norepinephrine at alldose.
Page 2479
Q1240:Mechanism of nefazodone and trazodone
Page 2480
Block 5-HT1 presynaptic autoreceptors; thereby increasingserotonin release. Weak inhibitors of serotonin re-uptake.
Page 2481
Q1241:Mechanism of MAO inhibitors
Page 2482
Irreversibly inhibits monoamine oxidase which normallyinactivates monoamines such as NE; 5-HT; and DA that leak
out of presynaptic vesicles. MAO inhibitors allow theseleaky molecules to accumulate and activate post synaptic
response.
Page 2483
Q1242:Pharmacological treatment for: Psychosis
Page 2484
1. Typical neuroleptics
Page 2485
Q1243:Pharmacological treatment for: Acute mania
Page 2486
1. Typical neuroleptics;2. Olanzapine;3. Lithium (relapse andtreatment)
Page 2487
Q1244:Pharmacological treatment for: Tourette syndrome
Page 2488
1. Typical neuroleptics;2. Olanzapine
Page 2489
Q1245:Pharmacological treatment for: Bedwetting
Page 2490
1. Imipramine (a tricyclic antidepressant)
Page 2491
Q1246:Pharmacological treatment for: Hypochondriasis
Page 2492
1. MAO inhibitors
Page 2493
Q1247:Antidepressants which have adverse effect of GIdistress
Page 2494
SSRIs: all;SNRIs: all;Atypical: Nefazodone;Tricyclic:Clomipramine;MAO inhibitors: none
Page 2495
Q1248:Antidepressants which have adverse effect of sedation
Page 2496
Note: useful effect if agitated;SSRIs;1. Fluvoxamine;2.Paroxetine;SNRIs: none;Atypical: All except
bupropion;Tricyclic: All except desipramine andprotryptiline;MAO inhibitors: none
Page 2497
Q1249:Antidepressants which have high potential fororthostatic hypertension
Page 2498
SSRIs: none;SNRIs: none;Atypical: none;Tricyclic;1.Amitriptyline;2. doxepin;MAO inhibitors: All
Page 2499
Q1250:Antidepressants which have adverse effect of weightgain
Page 2500
SSRIs: none;SNRIs: none;Atypical: Mirtazapine;Tricyclic:(so big you need a DICTAphone to type);1. Doxepin;2.
Imipramine;3. Clomipramine;4. Trimipramine;5.Amitriptyline;MAO inhibitors: none
Page 2501
Q1251:Toxicities of typical neuroleptics
Page 2502
1. Extrapyramidal dopamine side effects;2. Endocrinedopamnine side effects (dopamine receptor antagonism
leading to hyperprolactinemia leading to gynecomastia);3.Blocking muscarinic receptors (dry mouth; constipation);4.
Blocking alpha-adrenergic receptors (hypotension);5.Blocking histamine receptors (sedation);6. Neuroleptic
malignant syndrome;7. Tardive dyskinesia
Page 2503
Q1252:Describe neuroleptic malignant syndrome.
Page 2504
Neuroleptic malignant syndrome can cause you HARM;1.Hyperpyrexia;2. Autonomic instability;3. Rigidity;4.
Myoglobinuria
Page 2505
Q1253:How is neuroleptic malignant syndrome treated?
Page 2506
Dantrolene or dopamine agonists (bromocriptine)
Page 2507
Q1254:Describe tardive dyskinesia and what causes it?
Page 2508
Long-term antipsychotic use leads to dopamine receptorsensitization which causes stereotypic oral-facial movements
Page 2509
Q1255:Mechanism and treatment for extrapyramidal sideeffects
Page 2510
Blocking of dopamine's inhibitory effects causes excessstimulation by acetylcholine. Treat wth anticholinergic drugs
like thioridazine.
Page 2511
Q1256:Toxicities of atypical neuroleptics
Page 2512
Weight gain. Clozapine may cause agranulocytosis. (Requiresweekly WBC monitoring.) Fewer extrapyramidal andanticholinergic side effects than typical neuroleptics.
Page 2513
Q1257:Which atypical neuroleptic can cause agranulocytosis?
Page 2514
Clozapine (requires weekly WBC monitoring)
Page 2515
Q1258:Toxicities of lithium
Page 2516
Mnemonic: LMNOPP (prounounced "pee-pee");Lithium sideeffects;1. Movement (Tremor);2. Narrow therapeuticwindow;3. hypOthyroidism;4. Pregnancy problems
(Teratogenesis);5. Polyuria as lithium is ADH antagonist;leading to nephrogenic diabetes insipidus
Page 2517
Q1259:Toxicities of SSRIs
Page 2518
1. GI distress;2. Sexual dysfunction (anorgasmia);3. Serotoninsyndrome (with MAO inhibitors)
Page 2519
Q1260:What is serotonin syndrome?
Page 2520
Excess serotonergic activity caused by use of both SSRIs andMAO inhibtiors;1. Hyperthermia;2. Muscle rigidity;3.
Cardiovascular collapse
Page 2521
Q1261:Side effects and toxicities of tricyclic antidepressants
Page 2522
TCAs mess you up. Make you a stuttering SHAARCCC;1.Sedation;2. Hyperpyrexia;3. alpha-blocking effects;4.
atropine-like (anticholinergic) effects (tachycardial; urinaryretention; confusion and hallucinations in elderly);5.
Respiratory depression;and the Tri-C's;6. Convulsions;7.Coma;8. Cardiotoxicity (arrhythmias)
Page 2523
Q1262:Treatment for confusion and hallucinations in elderlyon tricyclic antidepressants
Page 2524
Due to anticholinergic activity. Use nortriptyline instead.
Page 2525
Q1263:Toxicities of bupropion
Page 2526
1. Stimulant effects (tachycardia; insomnia);2. Headache;3.Seizure in bulimic patients
Page 2527
Q1264:Toxicities of venlafaxine
Page 2528
Things have trouble going down your SINCS (GI distress);1.Stimulant effects;2. Increased blood pressure;3. Nausea;4.
Constipation;5. Sedation
Page 2529
Q1265:Toxicities of mirtazapine
Page 2530
1. Sedation;2. Increased appetite;3. Weight gain;4. Dry mouth
Page 2531
Q1266:Toxicities of Maprotiline
Page 2532
1. Sedation;2. Orthostatic hypotension
Page 2533
Q1267:Toxicities of Trazodone
Page 2534
1. Sedation;2. Nausea;3. Priapism;4. Postural hypotension
Page 2535
Q1268:Toxicities of MAO inhibitors
Page 2536
1. Hypertensive crisis with tyramine ingestion andmeperidine;2. CNS stimulation;3. Serotonin syndrome (whencoadministered with SSRIs or beta-agonists);4. Increased risk
of orthostatic hypotension
Page 2537
Q1269:which lipid-lowering agent has best effect on HDL?
Page 2538
niacin (side effects: flushing which is dec'd by aspirin orlongterm use)
Page 2539
Q1270:which statin is NOT metabolized by P450 system?
Page 2541
Q1271:which lipid lowering agent causes a slight increase inTG?
Page 2542
bile acid resins (cholestyramine; colestipol)
Page 2543
Q1272:which lipid loweirng agents have biggest loweringeffect on TGs?
Page 2544
"fibrates"--gemfibrozil; clofibrate; bezafibrate; fenofibrate
Page 2545
Q1273:which lipid lowering agents work by decreasingproduction of VLDL?
Page 2547
Q1274:which lipid lowering agents work by stimulatingLPL/enhancing rate of catabolism of VLDL?
Page 2548
fibrates (gemfribrozil; clofibrate; bezafibrate; fenofibrate)
Page 2549
Q1275:which class of lipid lowering agents is safest and whatis the effect?
Page 2550
cholesterol absorption blockers (ezetimibe). only decreasesLDL. no effect on HDL or TGs
Page 2551
Q1276:which antihypertensive can cause a positive Coombstest?
Page 2552
methyldopa (cental acting alpha agonist; safe for preggers)
Page 2553
Q1277:which antiHTNives have sexual side effects?
Page 2554
hexamthonium (ganglionic blocker--sexual dysfxn);guanethidine (inhibits Mg-ATPase--sexual dysfxn); beta
blockers (impotence)
Page 2555
Q1278:which antiHTNive can cause hypertrichosis?
Page 2556
minodixil (a vasodilator; use with beta blocker to preventrelfex tachycardia and w/diuretic to block salt retention)
Page 2557
Q1279:which CCB should NOT be used for arrhythmias?
Page 2559
Q1280:MOA of nitroglycerin
Page 2560
vasodilate by releasing NO in smooth muscle--> increase incGMP and smooth muscle relaxation; dilates veins>> arteries
Page 2561
Q1281:which heart drug has "Monday dz" as a toxicity
Page 2562
(tolerance during the work week and loss of tolerance overweekend-> tachycardia; dizzinesss; headache); nitroglycerin
Page 2563
Q1282:half life of digoxin?
Page 2565
Q1283:MOA of cardiac glycosides
Page 2566
directly inhibit Na/K ATPase--> indirect inhibition of Na/Caexchanger leads to increased intracellular calcium
Page 2567
Q1284:clinical use of cardiac glycosides
Page 2568
CHF (to increase contractility); afib (decreases conduxn at AVnode; depresses SA node)
Page 2569
Q1285:what diuretics should go with digoxin?
Page 2570
spironolactone/K+ sparers b/c hypokalemia potentiates digtoxicity
Page 2571
Q1286:what increases toxicities of digoxin
Page 2572
renal failure; hypokalemia; quinidine (dec'd clearance;displaces dig from tissue binding sites)
Page 2573
Q1287:antidote to digoxin toxicity
Page 2574
slowly normalize K+; lidocaine; cardiac pacer; anti-dig Fabfragments
Page 2575
Q1288:name 4 Class IA antiarr
Page 2576
quinidine; amiodarone; procainamide; disopyramide (queenamy proclaims diso's pyramid)
Page 2577
Q1289:name 3 Class IB antiarr
Page 2578
lidocaine; mexiletine; tocainide
Page 2579
Q1290:name 3 Class IC antiarr
Page 2580
flecainide; encainide; propafenone
Page 2581
Q1291:very short acting class II antiarr?
Page 2582
esmolol (beta blocker(
Page 2583
Q1292:name 4 class III antiarr
Page 2584
sotalol; ibutilide; bretylium; amiodarone
Page 2585
Q1293:name 2 class IV antiarr
Page 2586
verapamil; diltiazem
Page 2587
Q1294:compare the class I antiarr in terms of effect on APduration
Page 2588
IA (Na; intermediate acting)--increase duration; IB (Na; fastacting)--decrease duration; IC (Na; slow acting)--no change in
AP
Page 2589
Q1295:usefulness of IA antiarr?
Page 2590
(quinidine; amiodarone; procainamide; disopyramide) affectboth ATRIAL and VENTRICULAR s; esp reenrant and
ectopic tachycardias
Page 2591
Q1296:which antiarrhythmics useful in acute ventriculararrhytmias; esp post MI?
Page 2592
IB (lidocaine; mexiletine; tocainide)
Page 2593
Q1297:drug of choice in diagnosing/abolishing AV nodalarrhythmias
Page 2594
adenosine (maybe cause flushing)
Page 2595
Q1298:which antiarr contraindicated post-MI?
Page 2596
class IC (flecainide; encainide; propafenone)
Page 2597
Q1299:when use class IC antiarr?
Page 2598
usually only as last resort in refractory tachyarrhythmias
Page 2599
Q1300:which antiarr only work on AV and SA nodes?
Page 2600
class II (beta blockers)
Page 2601
Q1301:which antiarr can cause dyslipidemia?
Page 2602
metoprolol (class II)
Page 2603
Q1302:amiodarone toxicities
Page 2604
pulmonary fibrosis; hepatotoxicity; thyroidisms; cornealdeposits; photodermatitis; neurologic effects; constipation;
check PFTs; LFTs; TFTs!!!
Page 2605
Q1303:use of class IV antiarr?
Page 2606
(nondihydropyridine CCBs; verpamil; diltiazem); primarilyaffect AV nodal cells--> good for prevention of nodal
arrhythmias
Page 2607
Q1304:antiarrhythmic effect of K+?
Page 2608
depresses ectopic pacemakers; esp in digoxin toxicity
Page 2609
Q1305:botulinum toxin mechanism
Page 2610
blocks ACh release
Page 2611
Q1306:choline acetyltransferase action
Page 2612
synthesizes ACh
Page 2613
Q1307:acetylcholinesterase
Page 2615
Q1308:rate-limiting step in NE synthesis
Page 2616
Tyrosine hydroxylase (tyrosine to dopa)
Page 2617
Q1309:metyrosine action
Page 2618
inhibits tyrosine hydroxylase
Page 2620
norepinephrine transporter into neuron
Page 2621
Q1311:uptake II
Page 2622
uptake by extraneuronal tissue
Page 2623
Q1312:Monoamine oxidase action
Page 2624
makes catecholamine aldehydes
Page 2625
Q1313:Catechol-o-methyltransferase (COMT) action
Page 2626
makes (nor)metanephrine
Page 2627
Q1314:physostigmine action
Page 2628
inhibits cholinesterase
Page 2629
Q1315:carbidopa action
Page 2630
dopa decarboxylase inhibition
Page 2631
Q1316:receptor type which stimulates adenylyl cyclase
Page 2633
Q1317:Gi receptor types
Page 2635
Q1318:receptor types stimulating PKC
Page 2637
Q1319:phenylephrine mechanism
Page 2639
Q1320:methoxamine mechanism
Page 2641
Q1321:mydriasis
Page 2643
Q1322:Phentolamine mechanism
Page 2644
competitive a1 antagonist;**short half life
Page 2645
Q1323:phentolamine uses
Page 2646
dx pheochromocytoma
Page 2647
Q1324:pphenoxybenzamine mechanism
Page 2648
noncompetitive a1 antagonist;*long acting
Page 2649
Q1325:phenoxybenzamine use
Page 2650
treat pheochromocytoma
Page 2651
Q1326:prazosin mechanism
Page 2652
alpha1 antagonist
Page 2653
Q1327:prazosin use
Page 2654
tx of hypertension and CHF
Page 2655
Q1328:prazosin risks
Page 2656
syncope after first oral dose;reduced efficacy with chronic use
Page 2657
Q1329:clonidine mechanism
Page 2658
a2 agonist--> reduced symp outflow
Page 2659
Q1330:clonidine use
Page 2660
tx of hypertension
Page 2661
Q1331:methyldopa mechanism
Page 2662
metabolite a-methyl*norepinephrine* is a2 agonist
Page 2663
Q1332:methyldopa use
Page 2664
tx of hypertension
Page 2665
Q1333:yohimbe mechanism
Page 2666
alpha 2 antagonist
Page 2667
Q1334:Isoproterenol mechanism
Page 2668
stimulates b1 and b2
Page 2669
Q1335:dobutamine mechanism
Page 2671
Q1336:uses of dobutamine
Page 2672
tx of pulmonary edema; coronary bypass post op
Page 2673
Q1337:Propranolol mechanism
Page 2674
competitive inhibitor of b1 and b2
Page 2675
Q1338:uses of propranolol
Page 2676
tx of angina;ventricular arrhythmia;htn *dec renin*;postmyocardial infarction
Page 2677
Q1339:propranolol side efx
Page 2678
worse heart failure;reduced AVconduction;nightmares;fatigue;cold extremities
Page 2679
Q1340:Metoprolol mechanism
Page 2681
Q1341:atenolol mechanism
Page 2682
b1 blocker; does not cross blood brain barrier.slow
Page 2683
Q1342:atenolol uses
Page 2684
htn (one a day);glaucoma
Page 2685
Q1343:bromocriptine mechanism
Page 2686
dopanergic agonist
Page 2687
Q1344:tyramine mechanism
Page 2688
displaces NE into synaptic cleft
Page 2689
Q1345:population vulnerable to tyramine relatedhypertension
Page 2690
pts on monoamine oxidase inhibitors
Page 2691
Q1346:Phenylpropanolamine mechanism
Page 2692
indirect sympathetic stim
Page 2693
Q1347:methacholine mechanism
Page 2695
Q1348:bethanachol mechanism
Page 2696
muscarinic agonist
Page 2697
Q1349:pilocarpine mechanism
Page 2698
muscarinic agonist
Page 2699
Q1350:bethanachol uses
Page 2700
improved gastric emptying;tx of urinary retension (if nophysical obstruction)
Page 2701
Q1351:pilocarpine uses
Page 2702
induce salivation;open angle glaucoma--constricts irissphincter (miosis)
Page 2703
Q1352:methacholine use
Page 2704
provoke bronchoconstriction for dx testing;(methacholinechallenge)
Page 2705
Q1353:atropine mechanism
Page 2706
muscarinic antagonist
Page 2707
Q1354:atropine use
Page 2708
raising heart rate when vagal activity is pronounced**vasovagal syncope;decreased respiratory secretions for
intubation
Page 2709
Q1355:Bezold-Jarisch reflex
Page 2710
bradyardia; hypotension; nausea from high nicotine dose
Page 2711
Q1356:ganglionic blocking agents mechanism
Page 2712
block Nn receptors
Page 2713
Q1357:insectiside mechanism
Page 2714
anticholinesterase
Page 2715
Q1358:physostigmine mechansim
Page 2716
"reversible" short acting cholinesterase inhibitor;enters CNS
Page 2717
Q1359:neostigmine mechanism
Page 2718
"reversible" short acting cholinesterase inhibitor;does notenter CNS
Page 2719
Q1360:physostigmine side effects
Page 2720
enters cns; restlessness; apprehension; hypertension;typicalmuscarinic/nicotinic efx
Page 2721
Q1361:why neostigmine no enter cns?
Page 2722
quaternary amine (charged)
Page 2723
Q1362:uses of neostigmine
Page 2724
myasthenia gravis;glaucoma
Page 2725
Q1363:propranolol "traditional" frequency of dosing
Page 2727
Q1364:atenolol mechanism
Page 2728
b1 selective blocker
Page 2729
Q1365:metroprolol mechanism
Page 2731
Q1366:metabolism of propranolol
Page 2732
heavily liver metabolized;protein bound;interindividualvariability
Page 2733
Q1367:atenolol metabilism
Page 2734
reduced hepatic metabolization (vis a vis propranolol)
Page 2735
Q1368:metroprolol metabolism
Page 2736
less hepaticlly metabolized (vis a vis propranolol)
Page 2737
Q1369:esmolol clinical use
Page 2738
b blocker for critical care
Page 2739
Q1370:esmolol metabolism
Page 2740
short half life; IV use only
Page 2741
Q1371:labetolol mechanism
Page 2742
b blocker with a1 effect
Page 2743
Q1372:carvedilol clinical use
Page 2745
Q1373:carvedilol mechanism
Page 2746
beta blocker with a1 blocking
Page 2747
Q1374:type of b blocker for treatment of portal hypertensivebleeding
Page 2748
non selective (propranolol in US)
Page 2749
Q1375:betablocker type for essential tremor
Page 2751
Q1376:vascular headache prophylaxis betablocker type
Page 2752
propranolol (non selective and more lipophilic)
Page 2753
Q1377:methyldopa side effects
Page 2754
sedation; depression; dry mouth
Page 2755
Q1378:special situations in which methyldopa is particularlysafe
Page 2756
for htn in pts with ischemic heart disease (no efx on CO);doesnot block baroreceper rflx;--safe for anti-htn in elective
surgery
Page 2757
Q1379:dosing of methyldopa
Page 2758
delayed onset of effect (needs to be metabolized to methyel-NE);twice a day for maintanence
Page 2759
Q1380:drug of choice for hypertensive pregnant pts
Page 2761
Q1381:why clonidine is poor choice in pts with *severe*HTN?
Page 2762
clonidine rebound. withdrawal syndrome w/ massive sympdischarge
Page 2763
Q1382:pharmacokinetics of prazosin
Page 2764
hepatic metabolism
Page 2765
Q1383:pharmacokinetics of terazosin and doxazosin
Page 2766
longer lasting than prazosin
Page 2767
Q1384:labetolol R R stereoisomer mechanism
Page 2768
b1 antagonist and partial b2 agonist
Page 2769
Q1385:labetalol SR stereoisomer mechanism
Page 2771
Q1386:S isomer of Carvedilol
Page 2772
b blocker (both isomers a1 blockers)
Page 2773
Q1387:The critical factor affecting the therapeutic utility ofnitrates
Page 2775
Q1388:what is given along with nitroprusside?
Page 2776
Na2S2O3 (Na thiosulfate);the antidote to CN
Page 2777
Q1389:pharmacokinetics of nitroprusside
Page 2778
infusion only--dissolved immediately prior to use inglucose/water;rapid/potent/fast half life
Page 2779
Q1390:nitroprusside clinical use
Page 2780
acute hypertensive crisis
Page 2781
Q1391:mechanism of hydralazine
Page 2782
who the fuck knows
Page 2783
Q1392:clinical utility of hydralazine
Page 2784
hypertension--use with beta blocker and diuretic;heart failure
Page 2785
Q1393:metabolism of hydralazine
Page 2786
acetylated (pt variability)
Page 2787
Q1394:hydralazine side effects
Page 2788
Na retention; coronary steal
Page 2789
Q1395:minoxidil mechanism
Page 2790
sulfate metabolite opens atp sensitive k channel;--hyperpolarizes cell;--arterial vasodilation
Page 2791
Q1396:chemical class: nifedipine
Page 2792
1;4 dihydropyridines
Page 2793
Q1397:chemical class: verapamil
Page 2794
phenylalkamines
Page 2795
Q1398:chemical class: diltiazem
Page 2796
benzothiazepines
Page 2797
Q1399:verapamil mechanism
Page 2798
L type calcium channel blocker;cardiac selective
Page 2799
Q1400:diltiazem mechanism
Page 2800
L type calcium channel blocker;intermediate cardiac/vascularselective
Page 2801
Q1401:nifedipine mechanism
Page 2802
L type calcium channel blocker;vascular selective
Page 2803
Q1402:diltiazem and verapamil tx for what arrythmia
Page 2804
supraventricular tachycardia
Page 2805
Q1403:CCB metabolism
Page 2806
protein bound and big first pass effect;low bioavailability
Page 2807
Q1404:CCBs inhibit what entity important for druginteractinos
Page 2809
Q1405:interaction of CCBs and beta blockers
Page 2810
profound conduction and contractile depression;decreasedliver flow (betas) less clearance of CCBs
Page 2811
Q1406:chemistry of captopril
Page 2812
contains a sulfhydryl group at zinc ligand site;--other ACEinhibs do not
Page 2813
Q1407:hyperkalemia in ace inhibitors???
Page 2814
decrease in aldosterone;**beware in pts with bad kidneys
Page 2815
Q1408:he "diluting segment" of the nephron.
Page 2816
thick ascending limb
Page 2817
Q1409:mannitol site of action
Page 2818
proximal tubule
Page 2819
Q1410:mannitol characteristics of diuresis
Page 2820
loss of H2O in excess of Na and Cl
Page 2821
Q1411:Acetazolamide site of action
Page 2822
proximal tubule; inhibits carbonic anhydrase
Page 2823
Q1412:acetazolamide characteristics of diuresis
Page 2824
loss of Na; HCO3; Cl; and K
Page 2825
Q1413:Furosemide site of action
Page 2826
thck ascending loop of henle
Page 2827
Q1414:furosemide characteristics of diuresis
Page 2828
loss of Na; Cl; K;Lose Mg and Ca;potentially loss of 50%filtered Na
Page 2829
Q1415:Thiazide like diuretics site of action
Page 2830
distal tubule +/- proximal tubule inner medullary collectingtubule
Page 2831
Q1416:thiazide like diuretics characteristics of diuresis
Page 2832
loss of Na; Cl and K;increase blood Ca and uricacid;**prevent kidney stones;**inhibit osteoporosis
Page 2833
Q1417:chemistry of carbonic anhydrase inhibitors
Page 2834
contain sulfamyl moiety;i.e. are sulfonamides
Page 2835
Q1418:acetazolamide mechanism
Page 2836
noncompetitive carbonic anhydrase inhibitor
Page 2837
Q1419:pharmacokinetics of acetazolamide
Page 2838
absorbed from GI;eliminated by kidney;actively secreted byorganic acid transport system
Page 2839
Q1420:clinical uses of carbonic anhydrase inhibitors
Page 2841
Q1421:toxicity of carbonic anhydrase inhibitors
Page 2842
metabolic acidosis;renal stone formation (renal stones fromalkaline pH);K+ wasting;decreased NH3 secretion
Page 2843
Q1422:furosemide mechanism
Page 2844
Na-K-Cl2 symport inhibitor
Page 2845
Q1423:ethacrynic acid mechanism
Page 2846
Na-K-Cl2 symport inhibitor
Page 2847
Q1424:ethacrynic acid chemistry
Page 2848
not a sulfonamide
Page 2849
Q1425:furosamide chemistry
Page 2850
contains sulfamyl moiety
Page 2851
Q1426:loop diuretics and mg++; ca++
Page 2852
substantial urinary loss of these divalent cations;**abolisheslumen positive potential
Page 2853
Q1427:pharmacokinetics of loop diuretics
Page 2854
absorved in GI;secretion via organic acid secretion;thresholdeffect--once at effective dosage; more wont help;**can
increase frequency for more urination
Page 2855
Q1428:toxicity of furosemide
Page 2856
K+ loss;ototoxicity;H loss with metabolic alkalosis
Page 2857
Q1429:hydrochlorothiazide chemistry
Page 2858
sulonamide (sulfamyl moiety)
Page 2859
Q1430:hydrochlorothiazide mechanism
Page 2860
inhibit Na trnasport in distal convoluted tubule
Page 2861
Q1431:pharmacokinetics of hydrochlorothiazide
Page 2862
rapidly absorbed from GI;filterd and secreted in proximaltubule;binds to plasma proteins
Page 2863
Q1432:thiazide diuretics and calcium
Page 2864
increase Ca++ reabsorption
Page 2865
Q1433:triamterene chemistry
Page 2866
organic base; not sulfonamide
Page 2867
Q1434:amiloride chemistry
Page 2868
organic base; not sulfonamide
Page 2869
Q1435:triamterene mechanism
Page 2870
inhibition of Na+ channel in collecting tubule;k sparing
Page 2871
Q1436:amiloride mechanism
Page 2872
inhibition of Na+ channel in collecting tubule;k sparing
Page 2873
Q1437:amiloride pharmacokinetics
Page 2874
partially absorbed from GI;completely eliminated in kidney
Page 2875
Q1438:triamterene pharmacokinetics
Page 2876
well absorbed from GI;elimenated by renal excretiona andmetabolism
Page 2877
Q1439:toxicity of amiloride and triamterene
Page 2878
do not combine with spironolactone;caution with aceinhibitors;do not combine with K+ supplements
Page 2879
Q1440:spironolactone mechanism
Page 2880
competitive aldosterone inhibitor
Page 2881
Q1441:Na+ channel blocking drugs terminate and preventarrhythmias by
Page 2882
· slowing conduction to interrupt a reentrant circuit;·increasing refractoriness to terminate functional reentry and so
that there is "less room" for premature beats (which causeslowed conduction ? reentry to occur)
Page 2883
Q1442:Tx of atrial flutter/fibrillation to slow ventricularresponse
Page 2884
AV nodal blockers;verapamil/diltiazem;beta blockers;digitalis
Page 2885
Q1443:tx of atrial flutter/fibrillation to maintain normal rythm
Page 2886
(increase refractoriness in fast respone tissue);class Ia;ClassIc;Class III
Page 2887
Q1444:tx of supraventricular reentrant tachycardias: Acute(IV);;***(Almost always; the reentrant loop involves the AV
node)
Page 2888
adenosine (drug of choice);verapamil or betablocker;digitalis;maneuvers to increase vagal tone: vasalva;
carotid massage
Page 2889
Q1445:txt of svt reentrant (assuming AV node) tachycardia:oral (chronic)
Page 2890
verapamil or diltiazem;beta blocker;digitalis;class Ic
Page 2891
Q1446:tx of svt using a bypass tract;(fast response tissue)
Page 2892
Class Ia;Class Ic;Class III;**avoid empiric tx with AV nodeblockers
Page 2893
Q1447:tx of ventricular arrhythmias: acute (IV);**(slowcondux; increase refractoriness in fast response tissue-
>ventricles)
Page 2894
lidocaine--Ib;procainamide--Ia;amiodarone--III
Page 2895
Q1448:tx of ventricular arrhythmia: chronic
Page 2896
class Ia;Class Ib;Class Ic;class III
Page 2897
Q1449:tx of undiagnosed wide complex tachycardia
Page 2898
could be PSVT or VT. "all bets are off";**avoid verapamil
Page 2899
Q1450:tx for narrow complex tachycardia
Page 2900
usually slow response=av node;adenosine;verapamil;esmolol
Page 2901
Q1451:tx of unstable rhythm causing hemodynamiccompromise
Page 2902
shock the muthafucka
Page 2903
Q1452:QUINIDINE class and mechanism
Page 2904
Ia;blocks Na+ and multiple K+ currents;a-receptor block andvagal inhibition
Page 2905
Q1453:Quinidine antiarrhythmic use
Page 2906
chronic therapy of atrial fib/flutter (and VT)
Page 2907
Q1454:Quinidine problems
Page 2908
diarrhea;more death in pts with a-fib?;torsade de pointes 2-5%
Page 2909
Q1455:procainamide class and mechanism
Page 2910
Ia;blocks Na and K+;metabolite N-acetylprocainamide blocksK+ channels
Page 2911
Q1456:procainamide use
Page 2912
IV for SVT adn ventricular arrhythmia
Page 2913
Q1457:procainamide things to look out for
Page 2914
dose adjustment in renal disease;lupus syndrome w/ chronictherapy
Page 2915
Q1458:LIDOCAINE class and use
Page 2916
Ib;decrease incidence of V fib;**mortality increase
Page 2917
Q1459:lidocaine dosage issues
Page 2918
rapid distribution half life;slow elimination half life;clearancereduced in CHF and liver disease
Page 2919
Q1460:Flecainide Class Ic use
Page 2920
effective at surpressing isolated PVC and reentrantSVT;*BUT INCREASED mortality in patients following
myocaridal infarction. wtf
Page 2921
Q1461:esmolol class and usage
Page 2922
Class II; beta blocker;short half life=9 min;useful for recklessbeta blockade
Page 2923
Q1462:why does bretylium (class III) suck?
Page 2924
due to hypotensive effect; bretylium can cause hemodynamiccollapse during previously well-tolerated VT (therefore use
lidocaine; procainamide first)
Page 2925
Q1463:amiodarone useage; but sucks b/c?;class?
Page 2926
Class I + II + III + IV action;· very effective for mostarrhythmias; but NOT first-line oral therapy because ;;·
multiple toxicities: eye; *lungs*; liver; skin; thyroid duringchronic treatment
Page 2927
Q1464:verapamil: NEVER USE WHEN
Page 2928
undiagnosed; wide complex tachycardia (? hemodynamiccollapse);· "preexcited" atrial fibrillation over an accessory
pathway in the Wolff-Parkinson-White syndrome (may cause? heart rate; VF);· heart failure;· sinus node dysfunction; AV
block (*caution: Class I + IV*)
Page 2929
Q1465:DILTIAZEM usefulness
Page 2930
· intravenous form: useful AV nodal blocker usually withouthypotension (especially for rate control of atrial fibrillation)
Page 2931
Q1466:ADENOSINE good for?
Page 2932
Acute therapy of choice for: supraventricular tachycardias;undiagnosed wide-complex tachycardia;**short acting--
seconds
Page 2933
Q1467:Quinidine; Verapamil; Amiodarone; (?Flecainide);interactinos with ;Digitalis
Page 2934
inc digitalis concentration and toxicity
Page 2935
Q1468:amiodarone interactions with ;warfarin; digoxin;procainamide; quinidine
Page 2936
decreased drug metabolism and excretion;increased drugeffects
Page 2937
Q1469:renal disease interaction wtih ;procainamide (Ia) anddofetilide (III)
Page 2938
decreased clearance
Page 2939
Q1470:liver disease interaction with lidocaine
Page 2940
decreased clearance
Page 2941
Q1471:heart failure interaction with lidocaine
Page 2942
decreased clearance;decreased central volume (lidocaine)whatever the fuck that means
Page 2943
Q1472:disopyramide; flecainide; beta blockers; verapamilinteraction with;heart failure
Page 2944
worsen heart failure
Page 2945
Q1473:dofetilide interaction with cimetidine and ketoconazole
Page 2946
increased dofetilide concentrations
Page 2947
Q1474:plasmin; enzyme type
Page 2949
Q1475:enzyme that dissolves clots
Page 2951
Q1476:what do kringle domains on plasminogen activatorsbind
Page 2953
Q1477:Streptokinase mechanism
Page 2954
indirect activator of plasminogen;helps one plasminogenactivate another
Page 2955
Q1478:streptokinase problems
Page 2956
allergic rx's ;bleeding; hypotension
Page 2957
Q1479:urokinase mechanism
Page 2958
direct activator of plasminogen
Page 2959
Q1480:urokinase metabolism
Page 2960
liver; short half life 15 min
Page 2961
Q1481:urokinase inactivation
Page 2962
inactivated by PAI-1
Page 2963
Q1482:second generation thrombolytic with long half life
Page 2964
APSAC;60 mins. given by bolus
Page 2965
Q1483:APSAC; what is it?
Page 2966
complex of streptokinase and plasminogen
Page 2967
Q1484:t-PA mechanism
Page 2968
binds to fibrin and activates plasmin **clot specific**
Page 2969
Q1485:pharmacokinetics of t-PA
Page 2970
PAI-1 irreversibly inhibits;cleared in liver;short half life; 6mins
Page 2971
Q1486:Reteplase; what is it?
Page 2972
genetically engineered derivative of t-PA;just the kringle andprotease; not glycosylated
Page 2973
Q1487:TNK-t-PA (tenecteplase); wtf is it?
Page 2974
t-PA with no glycosylation site
Page 2975
Q1488:the two antifibrinolytics?
Page 2976
Amicar (e-aminocaproic acid) or tranexamic acid
Page 2977
Q1489:digoxin effects at AV node
Page 2978
increased ERP; and decreased conduction;slower ventricularrate during atrial flutter/fib
Page 2979
Q1490:Digoxin effects at His-Purkinje fibers
Page 2980
increased automaticity;premature ectopic beats
Page 2981
Q1491:digitalis effect on PR interval
Page 2983
Q1492:digitalis effect on ST segment
Page 2985
Q1493:digitalis effect on amplituted of T waves
Page 2986
decreased;may invert
Page 2987
Q1494:digitalis effect on QT interval
Page 2989
Q1495:aspirin mechanism
Page 2990
blocks cyclooxegenase--> no thromboxane A2
Page 2991
Q1496:Dipyridamole action
Page 2992
Inhibits cyclic nucleotide phosphodiesterase to increaseintraplatelet accumulation of cAMP;¨ Blocks the uptake of
adenosine
Page 2993
Q1497:Ticlopidine and Clopidogrel mechanism
Page 2994
Metabolites Inhibit platelet activity via effects on;· Inhibitionof ADP induced platelet activation (primary);· Glycoprotein
IIb/IIIa receptor;· von Willebrand factor
Page 2995
Q1498:pharmacokinetics of ticlodipine and Clopidogrel
Page 2996
delay in onset;effects persist several days
Page 2997
Q1499:ticlodipine and Clopidogrel interactions
Page 2998
activated by CYP3A4;inhibitors of CYP3A4 may reduceactivation
Page 2999
Q1500:Adverse effects of Ticlodipine and Clopidogrel
Page 3000
neutropenia in 3% of pts. ticlodipine problem
Page 3001
Q1501:(Abciximab mechanism
Page 3002
antibody to the IIb/IIIa receptor;
Page 3003
Q1502:factors inactivated by heparin
Page 3004
thrombin (II);activated IX; X; XI; and XII;**inactivates freethrombin; thus best for preventing clots
Page 3005
Q1503:administration of heparin
Page 3006
IV; not absorbed thru GI
Page 3007
Q1504:never ever administer heparin this way
Page 3009
Q1505:Two forms of heparin-induced thrombocytopenia(HIT)
Page 3010
1 heparin induced platelet aggregation leading to decreasedplatelets;2 Rarer. b/t 7 and 11 days. immune response with
thrombotic complications
Page 3011
Q1506:what to do if in case of severe bleeding from heparinoverdose
Page 3012
discontinue infusion;protamine administration
Page 3013
Q1507:protamine mechanism
Page 3014
binds to and inactivates heparin;**possible allergic toxicity
Page 3015
Q1508:mechanism of low molecular weight heparin
Page 3016
bind antithrombin/factor Xa
Page 3017
Q1509:LMWH and PTT
Page 3018
b/c very little binds to AT-III/thrombin; little effect onPTT;NOT USED FOR MONITORING
Page 3019
Q1510:advantages of LMWH over regular heparin
Page 3020
less frequent administration;sub-q administration;morepredictable response to dose
Page 3021
Q1511:Direct Thrombin Inhibitors?
Page 3022
lepirudin; agatroban
Page 3023
Q1512:lepirudin; agatroban mechanism
Page 3024
directly inhibit binding of thrombin to fibrinogen
Page 3025
Q1513:warfarin action;which factors affected?
Page 3026
antagonist of vitamin K;affects synthesis of II; VII; IX; X;protein C; and protein S
Page 3027
Q1514:adverse effects of warfarin
Page 3028
bleeding; yo;paradoxical thrombis;--pretein C and S fucked upfirst
Page 3029
Q1515:beta blockers and hepatic metabolism
Page 3030
atenolol only beta blocker not metabolized in liver
Page 3031
Q1516:Bethanecol (class and application)
Page 3032
direct cholinomimetic; postop and neurogenic ileus andurinary retention;
Page 3033
Q1517:Bethanecol (class and action)
Page 3034
direct cholinomimetic; Activates Bowel and Bladder smoothmuscle; resistant to AChE
Page 3035
Q1518:Carbachol (class and application)
Page 3036
direct cholinomimetic; glaucoma;
Page 3037
Q1519:Carbachol (class and action)
Page 3038
direct cholinomimetic; activates ciliary muscle of the eye(open angle glaucoma); pupillary sphincter (narrow angle);
resistant to ACHE
Page 3039
Q1520:pilocarpine (class; application)
Page 3040
direct cholinomimetic; glaucoma;
Page 3041
Q1521:pilocarpine (class; action)
Page 3042
direct cholinomimetic; activates ciliary muscle of the eye(open angle glaucoma); pupillary sphincter (narrow angle);
resistant to ACHE
Page 3043
Q1522:Neostigmine (class; application)
Page 3044
indirect cholinomimetic (anticholinesterase); postop andnuerogenic ileus and urinary retention; myesthenia gravis;
reversal of neuromuscular junction blockade (postop)
Page 3045
Q1523:Neostigmine (class; action)
Page 3046
indirect cholinomimetic (anticholinesterase); increasedendogenous Ach
Page 3047
Q1524:Pyridostigmine (class; application)
Page 3048
indirect cholinomimetic (anticholinesterase); myestheniagravis
Page 3049
Q1525:Pyridostigmine (class; action)
Page 3050
indirect chlinomimetic (anticholinesterase); increasedendogenous Ach; increased strength
Page 3051
Q1526:Edrophonium (class; application)
Page 3052
indirect cholinomimetic (anticholinesterase); dx of myestheniagravis (very short acting)
Page 3053
Q1527:Edrophonium (class; action)
Page 3054
indirect cholinomimetic (anticholinesterase); increasedendogenous Ach
Page 3055
Q1528:Physostigmine (class; application)
Page 3056
indirect cholinomimetic (anticholinesterase); glaucoma(crosses BBB) and atropine overdose
Page 3057
Q1529:Physostigmine (class; action)
Page 3058
indirect cholinomimetic (anitcholinesterase); increasedendogenous Ach
Page 3059
Q1530:Echothiophate (class; application)
Page 3060
indirect cholinomimetic (anticholinesterase); glaucoma
Page 3061
Q1531:Echothiophate (class; action)
Page 3062
indirect cholinomimetic (anticholinesterase); increasedendogenous Ach
Page 3063
Q1532:Symptoms of Cholinesterase inhibitor poisoning
Page 3064
DUMB BELSS - Diarrhea; Urination; Miosis; Bronchospasm;Bradycardia; Excitation of skeletal muscle and CNS;Lacrimation; Sweating and Salivation (also abdominal
cramping)
Page 3065
Q1533:What are parathion and organophosphates?
Page 3066
cholinesterase inhibitors that are likely to poison you
Page 3067
Q1534:What is the antidote to cholinesterase inhibitorpoisoning?
Page 3068
atropine (muscarinic antag) plus pralidoxime (chem antagonistused to regenerate active cholinesterase)
Page 3069
Q1535:Atropine (class; site of action; application)
Page 3070
Cholinoreceptor blocker (muscarinic antag); Eye; producemydriasis and cycloplegia
Page 3071
Q1536:tropicamide (class; site of action; application)
Page 3072
Cholinoreceptor blocker; Eye; produce mydriasis andcycloplegia
Page 3073
Q1537:Benztropine (class; site of action; application)
Page 3074
cholinoreceptor blocker; CNS; Parkinson's
Page 3075
Q1538:Scopolamine (class; site of action; application)
Page 3076
Cholinoreceptor blocker; CNS; Motion Sickness
Page 3077
Q1539:Ipratropium (class; site of action; application)
Page 3078
Cholinoreceptor blocker; Respiratory; Asthma; COPD
Page 3079
Q1540:Methscopolamine (class; site of action; application)
Page 3080
Cholinoreceptor blocker; Genitourinary; Reduce urgency inmild cystitis and reduce bladder spasms
Page 3081
Q1541:oxbutin (class; site of action; application)
Page 3082
Cholinoreceptor blocker; Genitourinary; Reduce urgency inmild cystitis and reduce bladder spasms
Page 3083
Q1542:Glycopyrrolate (class; site of action; application)
Page 3084
Cholinoreceptor blocker; Genitourinary; Reduce urgency inmild cystitis and reduce bladder spasms
Page 3085
Q1543:Actions of Atropine
Page 3086
Blocks SLUD (Salivation; Lacrimation; Urination; Defecation)also pupil dilation and cycloplegia
Page 3087
Q1544:ADR of Atropine
Page 3088
hot as a hare; dry as a bone; red as a beet; blind as a bat; madas a hatter. Also rapid pulse; constipation. Can causeglaucoma in elderly; urinary retention in BPH pts; and
hyperthermia in infants
Page 3089
Q1545:Hexamethonium (MOA and application)
Page 3090
Nicotinic Ach receptor antagonist; ganglionic blocker;prevents vagal reflex responses to changes in BP (for
experimental models)
Page 3091
Q1546:Epinephrine (class; selectivity; applications)
Page 3092
catecholamine; direct general agonist (a1; a2; b1; b2);anaphylaxis; glaucoma (open angle); asthma; hypotension
Page 3093
Q1547:NE (class; selectivity; applications)
Page 3094
catecholamine; a1; a2; b1; hypotension (but decreased renalperfusion)
Page 3095
Q1548:Isoproterenol (class; selectivity; applications)
Page 3096
catecholamine; b1 = b2; AV block (rare)
Page 3097
Q1549:Dopamine (class; selectivity; applications)
Page 3098
catecholamine; D1 = D2 > b > a; shock (increased renalperfusion); heart failure
Page 3099
Q1550:Dobutamine (class; selectivity; applications)
Page 3100
catecholamine; b1 > b2; shock; heart failure
Page 3101
Q1551:Amphetamine (class; selectivity; applications)
Page 3102
sympathomimetic; indirect general agonist (releases storedcatecholamines); narcolepsy; obesity; ADD
Page 3103
Q1552:Ephedrine (class; selectivity; applications)
Page 3104
sympathomimetic; indirect general agonist (releases storedcatecholamines); nasal decongestion; urinary incontinence;
hypotension
Page 3105
Q1553:Phenylephrine (class; selectivity; applications)
Page 3106
sympathomimetic; a1 > a2; pupil dilator; vasoconstriction;nasal decongestion
Page 3107
Q1554:Albuterol (class; selectivity; applications)
Page 3108
sympathomimetic; b2 > b1; asthma
Page 3109
Q1555:Terbutaline (class; selectivity; applications)
Page 3110
sympathomimetic; b2 > b1; asthma
Page 3111
Q1556:Cocaine (class; selectivity; applications)
Page 3112
sympathomimetic; indirect general agonist (uptake inhibitor);causes vasoconstriction and local anesthesia
Page 3113
Q1557:Clonidine (class; selectivity; applications)
Page 3114
sympathomimetic; centrally acting a-agonist; decreased centraladrenergic outflow; hypertension; especially with renal dz (no
decreas in renal perfusion)
Page 3115
Q1558:a-methyldopa (class; selectivity; applications)
Page 3116
sympathomimetic; centrally acting a-agonist; decreased centraladrenergic outflow; hypertension; especially with renal dz (no
decreas in renal perfusion)
Page 3117
Q1559:Phenoxybenzamine (class; application; toxicity)
Page 3118
nonselective; irreversible a-blocker; pheochromocytoma; tox:orthostatic hypotension; reflex tachycardia
Page 3119
Q1560:Phentolamine (class; application; toxicity)
Page 3120
nonselective; reversible a-blocker; pheochromocytoma; tox:orthostatic hypotension; reflex tachycardia
Page 3121
Q1561:Prazosin (class; application; toxicity)
Page 3122
a1 blocker; HTN; urinary retention in BPH; tox: 1st doseorthostatic hypotension; dizziness; HA
Page 3123
Q1562:Terazosin (class; application; toxicity)
Page 3124
a1 blocker; HTN; urinary retention in BPH; tox: 1st doseorthostatic hypotension; dizziness; HA
Page 3125
Q1563:Doxazosin (class; application; toxicity)
Page 3126
a1 blocker; HTN; urinary retention in BPH; tox: 1st doseorthostatic hypotension; dizziness; HA
Page 3127
Q1564:Mirtazapine (class; application; toxicity)
Page 3128
a2 blocker; Depression; tox: sedation; increased serumcholesterol; increased appetite
Page 3129
Q1565:How do beta blockers work to treat HTN?
Page 3130
decreased cardiac output; decreased renin secretion
Page 3131
Q1566:5 major side effects for hydrochlorothiazide
Page 3132
hypokaleia; slight hyperlipidemia; hyperuricemia;hypercalcemia; hyperglycemia
Page 3133
Q1567:4 major side effects for loop diruetics
Page 3134
potassium wasting; metabolic alkalosis; ototoxicity;hypotension
Page 3135
Q1568:clonidine side effects (2)
Page 3136
dry mouth; severe rebound hypertension
Page 3137
Q1569:methyldopa side effects (2)
Page 3138
sedation; positive Coombs test
Page 3139
Q1570:hexamethonium side effects (4)
Page 3140
severe orthostatic hypotension; blurred vision; constipation;sexual dysfunction
Page 3141
Q1571:reserpine side effects (4)
Page 3142
sedation; depression; nasal stuffiness; diarrhea
Page 3143
Q1572:guanethidine side effects (4)
Page 3144
orstastic/exericse hypotension; sexual dysfunction; diarrhea
Page 3145
Q1573:prazosin side effects (3)
Page 3146
1st-dose orthostatic hypotensoin; dizziness; headache
Page 3147
Q1574:beta-blocker major side effects (6)
Page 3148
asthma; impotence; sleep problems; bradycardia; chf; av block
Page 3149
Q1575:hydralazine side effects (4)
Page 3150
lupus like snydrome; reflex tachycardia; angina; salt retention
Page 3151
Q1576:minoxidil side effets (5)
Page 3152
hair; pericardial effusion; reflex tachycardia; angina; saltretention
Page 3153
Q1577:vasodilator: calcium blocker side effects (3)
Page 3154
flushing; constipatipn; nausea
Page 3155
Q1578:nitroprusside major side efect
Page 3156
cyanodie toxicity
Page 3157
Q1579:captopril side effects (8)
Page 3158
hyperkalemia; cough; angioedema; proteinuria; taste changes;hypotension; pregnancy (fetal renal damage); rash
Page 3159
Q1580:ARB side effect (losartan)
Page 3160
fetal renal toxicity; hyperkalemia
Page 3161
Q1581:two drugs that cause hyperkalemia
Page 3162
losartan and captopril
Page 3163
Q1582:what do you have to do wit hhydralazine andminoxidil?
Page 3164
use beta blockers to treat reflex tachy; diuretic to block saltretention
Page 3165
Q1583:mechanism of hydralazine
Page 3166
increase cGMP; smooth muscle relaxation; vasodilatoin;afterload reduction
Page 3167
Q1584:what is dilation is hydralazine selective for
Page 3169
Q1585:clinical use for hydralazine (2)
Page 3170
severe hypertension; CHF
Page 3171
Q1586:mechanism for clonidine
Page 3173
Q1587:mechanism for methyldopa
Page 3175
Q1588:mechanism for prazosin
Page 3177
Q1589:mechanism for reserpine
Page 3178
decrease norepi
Page 3179
Q1590:mechanism for guanethidine
Page 3180
decrease norepi
Page 3181
Q1591:block ach receptor
Page 3183
Q1592:name 3 calcium channel blockers
Page 3184
nifedipine; verapamil; diltiazem
Page 3185
Q1593:mechanism of calcium blockers
Page 3186
block voltage-dependent calcium channels on cardiac/smoothmuscle and reducing muscle contractility
Page 3187
Q1594:rank vascular smooth muscle block by calcium blocker
Page 3188
nifedipine>diltiazem>verapamil
Page 3189
Q1595:rank heart smooth muscle block by calcium blocker
Page 3190
verapamil>diltiazem>nifedipine
Page 3191
Q1596:use for calcium blockers
Page 3192
hypertension; angina; arryhtmia (not nifedipine)
Page 3193
Q1597:calcium blocker toxicity (3)
Page 3194
cardiac depression; peripheral edema; flushing;
Page 3195
Q1598:mechanism for nitro drugs
Page 3196
vasodilate by releasing nitric oxide; increase cGMP; smoothmuscle relaxation; decrease preload
Page 3197
Q1599:rank the preference for dilation in nitro drugs
Page 3198
veins > arterioles
Page 3199
Q1600:clinical use for nitro drugs (4)
Page 3200
angina; pulmonary edema; aphrodisiac; erection enhancer
Page 3201
Q1601:name side effects for nitro (4)
Page 3202
tachycardia; hypotension; headache; monday disease
Page 3203
Q1602:define monday disease
Page 3204
build tolerance to nitro during work; resensitize on weekendand get tachy and dizziness
Page 3205
Q1603:goal of antianginal therapy
Page 3206
reduce myocardial oxygen consumption
Page 3207
Q1604:name 5 determinants of antianginal therapy
Page 3208
end diastolic volume; blood presure; heart rate; contractility;and ejection time
Page 3209
Q1605:how does nitro effect end diastolic volume; bloodpressure; contractility; heart rate; and ejection time
Page 3210
decrease; decrease; increase (reflex); increase (reflex); decrease
Page 3211
Q1606:how does beta-blocker affect diastolic volume; bloodpressure; contractility; heart rate; ejection time
Page 3212
increase; decrease; decrease; decrease; increase
Page 3213
Q1607:name 3 factors that combo beta-blockers + nitrateswill decrease
Page 3214
blood pressure; heart rate; and overall myocardial oxygenconsumption
Page 3215
Q1608:for calcium channel blockers; what drug is similar tonitro
Page 3217
Q1609:for calcium channel blockers; what durg is similar tobeta-blockers
Page 3219
Q1610:define bioavailability; protein bound percentage; whereecreted; and 1/2 life for digoxin
Page 3220
75%; 20-40%; kidney; 40 hours
Page 3221
Q1611:mechanism for digoxin
Page 3222
block na/k atpase; increase na; slow na/ca antiport; increaes ca;positive inotrope
Page 3223
Q1612:how does digoxin affect arryhtmia
Page 3224
vagal effects increase PR; decrease QT; T wave inversion onECG
Page 3225
Q1613:name 2 uses for digoxin
Page 3226
CHF (increase contractility) and a fib (decrease conduction atAV node)
Page 3227
Q1614:5 major general digoxin side efects
Page 3228
nausea; vomiting; diarrhea; blurry yellow vision; arryhtmia
Page 3229
Q1615:name 3 contraindications with digoxin
Page 3230
renal failure; quinidine (will displace dig on protein; potentiateeffect); hypokalemia (potentiate effect)
Page 3231
Q1616:what is the antidote for digoxin
Page 3232
slowly normalize K; lidocaine; cardiac pacer; anti-dig FABfragments
Page 3233
Q1617:describe function that all class I antiarryhtmics have
Page 3234
decrease slope of phase 4 depolarization
Page 3235
Q1618:define state dependency and state what drugs are statedependent
Page 3236
class I antiarryhtmics. selectively depress tissue what isdepolarized
Page 3237
Q1619:name 4 class Ia drugs
Page 3238
quinidine; amiodarone; procainamide; disopyramide
Page 3239
Q1620:name 3 mechanisms of class Ia
Page 3240
increase AP duratoin; increase ERP; increase QT interval
Page 3241
Q1621:what do you use class Ia for?
Page 3242
atrial and ventricular arryhtmias
Page 3243
Q1622:quinidine toxicities
Page 3244
cinchonism: headache; tinnitisum; thrombocytopenia plustorsades
Page 3245
Q1623:procainamide toxicity
Page 3246
reversible lupus like side effect
Page 3247
Q1624:name 3 class IB drugs
Page 3248
lidocaine; mexiletine; tocainide
Page 3249
Q1625:mechanism for class IB
Page 3250
decrease AP duration.
Page 3251
Q1626:where does class IB affect?
Page 3252
affect ischemic or depolarized purkinje ventricular tissue.
Page 3253
Q1627:what is class IB useful for?
Page 3254
acute ventricular arryhtmias (post-MI) and digitalis inducedarryhtmia
Page 3255
Q1628:name 4 side effects of class IB
Page 3256
local anesthetic; cns stimulation; cns depression;cardiovascular depression
Page 3257
Q1629:name 3 class IC drugs
Page 3258
flecainide; encainide; propafenone
Page 3259
Q1630:name mechanism of class IC
Page 3260
no effect on AP
Page 3261
Q1631:what is class IC sueful for?
Page 3262
v-tach that progress to V fib and also for SVT. usuaully onlygood for refractory tachyarryhtmias
Page 3263
Q1632:class IC toxicities
Page 3264
proarryhtmitic; especially post-mI (contraindiciated)
Page 3265
Q1633:name 5 class II antiarrythmiycs
Page 3266
propanolol; esmolol; metoprolol; atenolol; timolol
Page 3267
Q1634:mechanism of class II drugs
Page 3268
decrease camp; decrease CA; decrease slope phase 4; increasePR interval at AV node
Page 3269
Q1635:what is a short acting class II
Page 3271
Q1636:name 5 side effects of class II drugs
Page 3272
mask hypoglycema; impotence; asthma; CV effects(bradycardia; av block; chf). sleep
Page 3273
Q1637:name 4 class III drugs
Page 3274
sotalol; ibutilide; bretylium; amiodarone
Page 3275
Q1638:mehcanism of class III
Page 3276
increase AP duration; incrase ERP; increase QT; used whenothers fail
Page 3277
Q1639:sotalol toxicity
Page 3278
torsades; excessive beta-block
Page 3279
Q1640:ibutilide toxicity
Page 3281
Q1641:bretylium toxicity
Page 3282
new arrhythmias; hypotension
Page 3283
Q1642:amiodorone toxicity
Page 3284
hypothyrodism/hyperthyrodism; pulmonary fibrosis; hepatictoxicity; corneal deposits; skin deposits (photodermatitis);
neurologic defects; constipation; bradycardia; heart block; chf
Page 3285
Q1643:what 3 tests to do before using amiodarone?
Page 3287
Q1644:name 2 class IV antiarrhytmics
Page 3288
verapamil; diltiazem
Page 3289
Q1645:mechanism for class IV
Page 3290
affect AV nodal cells; decrease conduction velocity; incraseERP; increase PR.
Page 3291
Q1646:what is class IV used for
Page 3292
prevent nodal arryhtmias (SVT)
Page 3293
Q1647:what are 4 general side effects for class IV
Page 3294
constipation; flushing; edema; cv (chf; av block; sinus nodedepression)
Page 3295
Q1648:bepridil toxicity
Page 3297
Q1649:adenosine function
Page 3298
drug of choice in diagnosisng/abolishing AV nodal arryhtmias
Page 3299
Q1650:potassium function
Page 3300
depress ectopic pacemaker; esp in dig toxicity
Page 3301
Q1651:magnesium function
Page 3302
torsades and dig toxicity use
Page 3303
Q1652:Parasympathetic preganglionic neurons release theneurotransmitter -------- which act on -------- receptors.
Page 3304
Ach; nicotinic.
Page 3305
Q1653:Parasympathetic postganglionic neurons release theneurotransmitter -------- which act on ------- receptors.
Page 3306
Ach; muscarinic.
Page 3307
Q1654:Sympathetic preganglionic neurons to sweat glandsrelease the neurotransmitter ------- which act on -------
receptors.
Page 3308
Ach; muscarinic.
Page 3309
Q1655:Sympathetic postganglionic neurons to sweat glandsrelease the neurotransmitter ------- which act on -------
receptors.
Page 3310
Ach; muscarinic.
Page 3311
Q1656:Sympathetic preganglionic neurons to glands; cardiacand smooth muscles release the neurotransmitter ------- which
act on ------- receptors.
Page 3312
Ach; nicotinic.
Page 3313
Q1657:Sympathetic postganglionic neurons to glands; cardiacand smooth muscles release the neurotransmitter ------- which
act on ------- receptors.
Page 3314
NE; alpha and beta
Page 3315
Q1658:Sympathetic preganglionic neurons to renal vascularsmooth muscle release the neurotransmitter ------- which act
on ------- receptors.
Page 3317
Q1659:Sympathetic postganglionic neurons to renal vascularsmooth muscle release the neurotransmitter ------- which act
on ------- receptors.
Page 3319
Q1660:Sympathetic preganglionic neurons to the adrenalmedulla release the neurotransmitter ------- which act on -------
receptors.
Page 3320
Ach; nicotinic.
Page 3321
Q1661:Sympathetic preganglionic neurons to the adrenalmedulla synapse directly on ------- cells of the adrenal
medulla.
Page 3323
Q1662:Somatic neurons synapse directly on -------- muscleand release the neurotransmitter ------- which act on -------
receptors.
Page 3324
skeletal muscle; Ach; nicotinic.
Page 3325
Q1663:Ach is synthesized from acetyl-CoA and choline bythe enzyme ---------.
Page 3326
Choline acetyltransferase.
Page 3327
Q1664:The transport of choline into the nerve terminal can beinhibited by --------.
Page 3329
Q1665:The release of transmitter from vesicles in the nerveending require the entry of ------ into the neuron.
Page 3331
Q1666:The action of Ach in the synapse is terminated by itsmetabolism to acetate and choline by the enzyme ---------.
Page 3332
Acetylcholinesterase.
Page 3333
Q1667:In the noradrenergic nerve terminal; tyrosine ishydroxylated to -------; which is decarboxylated to --------;
which is finally hydroxylated to NE.
Page 3334
DOPA; dopamine.
Page 3335
Q1668:Dopamine is transported into vesicles forhydroxylation to NE. This transport can be blocked by the
drug --------.
Page 3337
Q1669:The action of NE and DA is terminated by ---------and ----------.
Page 3338
Reuptake; diffusion (different than for Ach).
Page 3339
Q1670:The --------- drugs promote catecholamine release.
Page 3341
Q1671:The drugs --------- and ---------- inhibit the reuptake ofNE.
Page 3343
Q1672:The release of NE from a sympathetic nerve ending ismodulated by ---------; --------- and ---------.
Page 3344
NE; Ach; angiotensin II.
Page 3345
Q1673:NE inhibits its own release at the noradrenergic nerveterminal through --------- receptors.
Page 3347
Q1674:Angiotensin II --------- (inhibits / stimulates) therelease of NE from the noradrenergic nerve terminal.
Page 3349
Q1675:Ach inhibits the release of NE from the noradrenergicnerve terminal by binding to --------- receptors.
Page 3351
Q1676:Clinical application and action of Bethanechol.
Page 3352
Postoperative and neurogenic ileus and urinary retention. /Activates bowel and bladder smooth muscle.
Page 3353
Q1677:Clinical application and action of Carbachol andPilocarpine.
Page 3354
Glaucoma. / Activates ciliary muscle of eye (open angle);pupillary sphincter (narrow angle).
Page 3355
Q1678:Clinical application / action of Neostigmine.
Page 3356
Postoperative and neurogenic ileus and urinary retention;myasthenia gravis; reversal of neuromuscular junctionblockade (postoperative). / Increase endogenous Ach.
Page 3357
Q1679:Clinical application / action of Pyridostigmine.
Page 3358
Myasthenia gravis. / Increase Ach; increase strength.
Page 3359
Q1680:Clinical application / action of Edrophonium.
Page 3360
Diagnosis of myasthenia gravis (extremely short acting). /Increase endogenous Ach.
Page 3361
Q1681:Clinical application / action of Physostigmine.
Page 3362
Glaucoma (crosses blood-brain barrier) and atropine overdose./ Increase endogenous Ach.
Page 3363
Q1682:Clinical application / action of Echothiophate.
Page 3364
Glaucoma. / Increase endogenous Ach.
Page 3365
Q1683:Symptoms of cholinesterase inhibitor poisoning.
Page 3366
Diarrhea; Urination; Miosis; Bronchospasm; Bradycardia;Excitation of skeletal muscle and CNS; Lacrimation; Sweating;
Salivation (also abdominal cramping). "DUMBBELSS".
Page 3367
Q1684:Cholinesterase inhibitor poisoning may be caused by ---------.
Page 3368
Parathion and other organophosphates.
Page 3369
Q1685:The cholinesterase regenerator ------- can be used as anantidote for cholinesterase inhibitor poisoning.
Page 3371
Q1686:Mechanism of action of Pralidoxime.
Page 3372
Regenerates active cholinesterase; chemical antagonist; used totreat organophosphate exposure.
Page 3373
Q1687:Clinical uses of the muscarinic antagonist Atropine.
Page 3374
Dilate pupils; decrease acid secretion in peptic ulcer disease;decrease urgency in mild cystitis; decrease GI motility; reduce
airway secretions; and treat organophosphate poisoning."Blocks SLUD: Salivation; Lacrimation; Urination;
Defecation."
Page 3375
Q1688:Side effects of Atropine.
Page 3376
Increase body temp; rapid pulse; dry mouth; dry/flushed skin;disorientation; mydriasis with cycloplegia; and constipation."Atropine parasympathetic block side effects: Blind as bat;
Red as a beet; Mad as a hatter; Hot as a hare; Dry as a bone."
Page 3377
Q1689:Hexamethonium (ganglionic blocker) blocks --------receptors.
Page 3379
Q1690:tropi are anti-muscarinic; mneumonic?
Page 3380
while vacationing in the tropics you lie on a beach and yourmuscles waste away!
Page 3381
Q1691:benztropine is used to treat
Page 3382
Parkinson's disease
Page 3383
Q1692:scopolamine is used to treat
Page 3384
motion sickness
Page 3385
Q1693:name 2 antimuscarinic drugs that act on the CNS
Page 3386
benztropine; scopolamine
Page 3387
Q1694:name a muscarinic used to treat motion sickness
Page 3389
Q1695:name a muscarinic used to treat Parkinson's disease
Page 3391
Q1696:mechanism of action of benztropine
Page 3393
Q1697:mechanism of action of scopolamine
Page 3395
Q1698:name three antimuscarinics that act on eye
Page 3396
atropine; homatropine; tropicamide
Page 3397
Q1699:the action of atropine is ______
Page 3398
produce mydriasis; cycloplegia
Page 3399
Q1700:mechanism of atropine is
Page 3401
Q1701:the action of homatropine is ______
Page 3402
produce mydriasis; cycloplegia
Page 3403
Q1702:mechanism of homatropine is
Page 3405
Q1703:the action of tropicamide is
Page 3406
produce mydriasis; cycloplegia
Page 3407
Q1704:mechanism of tropicamide is
Page 3409
Q1705:ipatropium is used to treat
Page 3411
Q1706:mechanism of ipatropium is
Page 3413
Q1707:name an antimuscarinic used to treat asthma andCOPD
Page 3415
Q1708:(2) diuretics used for HTN;;what do both lower as anAE?
Page 3416
Thiazides;Loops;;both lower K+
Page 3417
Q1709:Vasodilator used for severe HTN and CHF;AE?
Page 3418
Hydralazine;;AE: SLE-like effects
Page 3419
Q1710:Vasodilator used for emergency HTN situations;AE?
Page 3420
Nitroprusside;;AE: converts to cyanide
Page 3421
Q1711:Anti-HTN; anti-anginal and anti-arrhythmic class thatworks by reducing heart contractility;(2) AE
Page 3422
Calcium channel blockers;;AE: Cardiac depression; Edema
Page 3423
Q1712:which of the calcium channel blockers most specificfor;Vascular Smooth Muscle
Page 3425
Q1713:which of the calcium channel blockers most specificfor;Heart muscle
Page 3427
Q1714:Drug for angina that also is effective againstpulmonary edema
Page 3429
Q1715:what are the (5)* determinants of myocardial oxygenconsumption?
Page 3430
BEECH;BP;Ejection time;EDV;Contractility;HR
Page 3431
Q1716:Drug used for CHF and A-fib can causearrthymias;what are the ECG changes?;(3)
Page 3432
Digoxin;ECG;Inc PR;Dec QT;T-wave inversion
Page 3433
Q1717:MOA of digoxin;(2) AE?
Page 3434
Inhibit Na/K pump to indirectly inhibit Na/Ca antiport;causing Ca increase inside cell;AE;Yellow vision; Arrhythmias
Page 3435
Q1718:(4)* class IA antiarrhythmics
Page 3436
Queen Amy Proclaims Diso'sPYRAMID;Quinidine;Amiodarone;Procainamide;Disopyrami
de
Page 3437
Q1719:MOA of class IA Na-channel blockers;what type ofarrhythmias is it good for?
Page 3438
Inc action potential duration by Inc QRS (QT interval);Use:Ventricular Arrhythmia
Page 3439
Q1720:how do the Na-channel blockers affect HR; CO; BPand SV?
Page 3440
Dec HR -> Dec CO -> Dec BP -> Inc SV;(more time to fill)
Page 3441
Q1721:AE for Quinidine
Page 3442
Cinchonism;HA; Tinnitus; thrombocytopenia; Torsades dePointes
Page 3443
Q1722:why are Procainamide and Disopyamide successful atslowing the QT interval?
Page 3444
both are Amides; which are metabolized in the liver givingNH4 that can be converted to GLU -> GABA
Page 3445
Q1723:AE for Procainamide
Page 3446
SLE-like effects
Page 3447
Q1724:DOC for V-Tach
Page 3448
Lidocaine;(b/c it affects ischemic tissues and works quickly;IV only)
Page 3449
Q1725:what is the class and drug that is the last resort (V-fib)as a ;Na-channel blocker?;when is it contra-indicated?
Page 3450
Class IC: Flecainide;;CI;post-MI (leads to heart stopping)
Page 3451
Q1726:Na-channel blocker class/drug that decreases ActionPotential time
Page 3452
Class IB: Lidocaine
Page 3453
Q1727:(3) drugs that can block both Na and Ca channels;whatDx are they good for?
Page 3454
Procainamide;;Phenytoin;;Quinidine;use: Wolf ParkinsonWhite
Page 3455
Q1728:Class II antiarrhythmics class and MOA
Page 3456
Beta-blockers;MOA;Dec cAMP and Ca currents ->;Decslope of phase 4 and Inc PR interval
Page 3457
Q1729:(3) AE of Beta-blockers
Page 3458
blocking betas make me SICk;Sedation;;Impotence;;CV effects(bradycardia; CHF)
Page 3459
Q1730:B-blocker;Longest acting
Page 3461
Q1731:B-blocker;Shortest acting
Page 3463
Q1732:B-blocker;also blocks Alpha-receptors;(for Pheos andHTN crisis);(2)
Page 3464
Labetalol;;Carvedilol
Page 3465
Q1733:B-blocker;for Miosis
Page 3467
Q1734:B-blocker;also blocks K+ channels
Page 3469
Q1735:B-blocker;good for patient w/ DM; asthmatics; MIand elderly
Page 3471
Q1736:(3)* drugs in Class III anti-arrhythmics
Page 3472
BiAS to K-channel blockers;Bretylium;;Amiodarone;;Sotalol
Page 3473
Q1737:MOA of K-channel blockers
Page 3474
Inc AP by Inc QT interval
Page 3475
Q1738:AE of Amiodarone;(4)
Page 3476
Amy aught to run PFTs; LFTs and TFTs or you'll beBLUE;Pulmonary
fibrosis;Hepatotoxicity;Hyper/Hypothyroidism (containsiodine);turns skin Blue
Page 3477
Q1739:Class of choice for Atrial arrhythmias;MOA
Page 3478
Ca-Channel blockers;;For AV nodal cells; Inc ST segment andInc PR interval
Page 3479
Q1740:DOC for Digitalis-induced arrthymias
Page 3481
Q1741:drug that inhibits VLDL production; Dec TG and DecHDL breakdown;AE?
Page 3482
Niacin;;AE: Flushing
Page 3483
Q1742:class that increases the production of lipoproteinlipase to ;Inc breakdown of TG;(2) AE?
Page 3484
Fibrates;"-FIBR-" (Gemfibrozil; Fenofibrate);AE: GI upset;gall stones
Page 3485
Q1743:contraindication of Bile Acid Sequestrants?
Page 3486
High TG levels;BAS Increases TG
Page 3487
Q1744:DOC in AV nodal arrhythmias
Page 3489
Q1745:Antiarrhythmic that depresses ectopic pacemakers;(esp digoxin toxicity)
Page 3491
Q1746:(3) First generation H1 blockers
Page 3492
Diphenhydramine (Benadryl);;Chlorpheniramine (Chlor-trimeton);;Promethazine (Phenergan)
Page 3493
Q1747:Clinical uses (3) and AE (3) of First generation H1blockers
Page 3494
Uses;Motion sickness;Allergy (hives; itching; nasal);Sleepaid;AE;Sedation;Antimuscarinic;Anti-alpha-adrenergic
Page 3495
Q1748:(3) Second generation H1 blockers;Use?
Page 3496
Loratadine (Claritin);;Fexofenadine (Allegra);;Centirazine(Zyrtec);Use: Non-drowsy Allergic rhinitis; Hay fever
Page 3497
Q1749:Name and MOA of a Nasal Decongestant
Page 3498
Pseudoepherine (Sudafed);Alpha-agonist leading tovasoconstriction
Page 3499
Q1750:(2) Cough suppressants
Page 3500
Codeine;;Dextromethophan (DM)
Page 3501
Q1751:Name and MOA of expectorant
Page 3502
Guaifenesin;(Robitussin);;Inc. respiratory secretions andviscosity
Page 3503
Q1752:Long acting B2-agonist for Asthma Prophylaxis
Page 3505
Q1753:Methylxanthine used for Severe asthma;MOA?;(2)AE?
Page 3506
Theophylline;Bronchodilator by Inh Phosphodiesterase andDec cAMP hydrolysis;AE;Cardiotoxicity;Neurotoxicity
Page 3507
Q1754:Drug and MOA of Mast Cell Stabilizers;Use?
Page 3508
Cromolyn;causes Mast cells not to release histamine;use:Only for Prophylaxis
Page 3509
Q1755:what is the most potent anti-inflammatory agent thatis effective for mild; moderate and severe asthma ;(first line
for chronic asthma)?;MOA?
Page 3510
Glucocorticosteroids;;Inh NF-kB transcription factor thatinduces TNF-alpha; inhibiting formation of PGE and LTE
Page 3511
Q1756:(2) Adverse effects of Glucocorticoids?
Page 3512
Oral candidiasis;;bone demineralization
Page 3513
Q1757:Leukotriene effect modulator that inhibitslipoxygenase and leukotriene formation;AE?
Page 3514
Zileuton;;AE: Hepatotoxicity
Page 3515
Q1758:(2) Leukotriene effect Modulator that binds theleukotriene receptors;Use?
Page 3516
Zafirlukast;;Montelukast;;Use: Prophylaxis; mild/moderateasthma
Page 3517
Q1759:Muscarinic antagonist that preventsbronchoconstriction
Page 3519
Q1760:non-specific Beta-agonist that relaxes bronchialsmooth muscle;AE?
Page 3520
Isoproterenol;;AE: tachycardia
Page 3521
Q1761:What asthma agents deal with an early response(bronchoconstriction)?;(4)
Page 3522
My BLT;Muscarinic antagonist;;Beta-agonist;;Leukotrieneantagonist;;Theophylline
Page 3523
Q1762:what asthma agents deal w/ mast cells releasingmediators?;(2)
Page 3524
Cromolyn;;Steroids
Page 3525
Q1763:Ganglionic blocker (rarely used) for the rapidreduction of HTN
Page 3527
Q1764:only drug that reduces morbidity and mortality inheart failure
Page 3528
Spironoloactone
Page 3529
Q1765:drug given IV for severe acute heart failure
Page 3531
Q1766:what anti-HTN drug may ilicit a positive Coombs testand hemolytic anemia?
Page 3533
Q1767:DOC for variant angina
Page 3535
Q1768:what drug interaction w/ Digoxin increases its toxicity?
Page 3536
Thiazides;(Dec K+ -> Inc Dig toxicity)
Page 3537
Q1769:Anti-anginal Tx that has AE of severe constipation
Page 3539
Q1770:(2) AE of Adenosine
Page 3540
Burning sensation in chest;;SOB
Page 3541
Q1771:(2) AE of Dobutamine
Page 3543
Q1772:HTN medication that has AE of "Loss of taste"
Page 3545
Q1773:patient treated w/ anti-arrhythmic that causesrecurrent attacks of feeling faint and experiencing episodes of
loss of consciousness. what drug?
Page 3547
Q1774:Cardiac AP drug;affects Phase 4;(3)
Page 3548
Digoxin;;Verapamil ;(Ca-channel blockers);;Lidocaine
Page 3549
Q1775:Cardiac AP drug;affects Phase 0 to slow conductionand prolong repolarization
Page 3550
IA drugs;(All class I slow conduction; but only IA prolongsrepolarization)
Page 3551
Q1776:Cardiac AP drug;affects Phase 0 but causes no changein repolarization
Page 3552
Class IC - Flecainide
Page 3553
Q1777:Cardiac AP drug;blocks Na; Ca and K channels
Page 3555
Q1778:Drug that lowers HTN by inhibiting PeptidylDipeptidase
Page 3556
ACEi;(at biochemical level)
Page 3557
Q1779:drug class for CHF that decreases Preload and BV
Page 3559
Q1780:only Drug class that increases the survival rate in CHF
Page 3561
Q1781:Diuretics
Page 3562
Bumetanide (Bumex);furosemide (Lasix);HCTZ-hydrochlorothiazide (Microzide; Esidrix);spironolactone(Aldactone);triamterene (Dyrenium/ Maxide w/ HCTZ)
Page 3563
Q1782:Beta-Blockers
Page 3564
Atenolol (Tenormin);Labetolol (Normodyne;Trandate);metoprolol (Lopressor);nadolol
(Corgard);propranolol (Inderal);timolol (Timoptic)
Page 3565
Q1783:ACE Inhibitors
Page 3566
Benazepril (Lotensin);captopril (Capoten);enalapril(Vasotec);fosinopril (Monopril);lisinopril (Zestril);moexipril(Univasc/ Uniretic w/HCTZ);quinapril (Accupril);ramipril
(Altace)
Page 3567
Q1784:Angiotensin II Antagonist
Page 3568
Losartan (Cozaar; Hyzaar w/ HCTZ);valsartan (Diovan)
Page 3569
Q1785:Calcium channel blockers
Page 3570
Amlodipine (Norvasc; Lotrel w/ Benazepril);Diltiazem(Cardizem; Tiazac);felodipine (Plendil);isradipine
(Dynacirc);nicardipine (Cardene);nifedipine (Procardia;Adalat);nisoldipine (Sular; Nisocor);verapamil (Calan; Covera;
Isoptin)
Page 3571
Q1786:Alpha Blockers
Page 3572
Doxazosin (Cardura);Prazosin (Minipress);Terazosin(Hytrin)
Page 3574
Clonidine (Catapres);diazoxide (HyperstatIV);hydralazine;alpha-methyldopa (Aldomet?);minoxidil
(Loniten);sodium nitroprusside (Nipride)
Page 3575
Q1788:Class I Na+ Channel Blockers?;(1A)
Page 3576
Disopyramide (Norpace);Procainamide (Procan);Quinidine(Quinidex)
Page 3577
Q1789:Class I Na+ Channel Blockers (1b)?
Page 3578
Lidocaine (Elamax/Lidoderm);Mexiletine (Mexitil);Tocainide(Tonocard)
Page 3579
Q1790:Class I Na+ Channel Blockers (1c)?
Page 3580
Flecainide (Tambocor);Propafenone(Rhythmol);Others;Adenosine;Digoxin
Page 3581
Q1791:Class II B-Blockers
Page 3582
Esmolol (Brevibloc);Metoprolol (Lopressor;Toprol);Pindolol(Visken);Propranolol (Inderal)
Page 3583
Q1792:Class III K+ Channel Blockers
Page 3584
Amiodarone (Cordarone);Bretylium (Bretylol);Sotalol(Betapace)
Page 3585
Q1793:Class IV Ca++ Channel Blockers
Page 3586
Diltiazem (Cardizem; Tiazac);Verapamil (Calan; Covera;Isoptin)
Page 3587
Q1794:Mechanism of action of Class IA antiarrhytmics?
Page 3588
Na+ Channel Blockers;class 1A slows phase 0 depolarization
Page 3589
Q1795:Mechanism of action of Class IB antiarrhytmics?
Page 3590
Na+ Channel Blockers;Class 1B shortens phase 3repolarization
Page 3591
Q1796:Mechanism of action of Class IC antiarrhytmics?
Page 3592
Na+ Channel Blockers;Class 1C markedly slows phase 0depolarization
Page 3593
Q1797:Mechanism of action of Class 2 antiarrhytmics?
Page 3594
Class II B-Blockers (supresses phase 4 depolarization)
Page 3595
Q1798:Mechanism of action of Class 3 antiarrhytmics?
Page 3596
Class III K+ Channel Blockers (prolongs phase 3repolarizaion)
Page 3597
Q1799:Mechanism of action of Class 4 antiarrhythmics?
Page 3598
Class IV Ca++ Channel Blockers (shortens action potential)
Page 3599
Q1800:What are the clinical uses of the H1 blockers?
Page 3600
allergy; motion sickness; sleep aid
Page 3601
Q1801:Name the H1 blockers. (3 1st generation and 3 2ndgeneration).
Page 3602
1st = diphenhydramine; dimenhydrinate; chlorpheniramine.2nd = loratadine; fexofenadine; desloratadine
Page 3603
Q1802:The side effects of H1 blockers?
Page 3604
sedation; animuscarinic; anti-alpha-adrenergic. 2nd gen far lesssedating.
Page 3605
Q1803:What classes of drugs are used to treat asthma?
Page 3606
B-agonists; B2-agonists; methylxanthines; muscarinicantagonists; cromolyn; corticosteroids; antileukotrienes
Page 3607
Q1804:Name the nonspecific B-agonist that causes bronchialsmooth muscle relaxation and tachycardia.
Page 3609
Q1805:Name the B2 agonist used during acute asthmaexacerbations.
Page 3611
Q1806:What is Salmeterol used for?
Page 3612
long-acting B2-agonist used for prophylaxis
Page 3613
Q1807:What is the MOA of Theophylline (amethylxanthine)?
Page 3614
causes bronchodilation by inhibiting phosphodiesterase anddecreasing cAMP hydrolysis.
Page 3615
Q1808:Adverse effects of Theophylline?
Page 3616
Narrow therapeautic index! Limited use! Cardiotoxicity andneurotoxicity
Page 3617
Q1809:Which class of drugs does Ipratropium belong to?
Page 3618
Muscarinic antagonists
Page 3619
Q1810:What is the MOA of Cromolyn and what is its clinicaluse?
Page 3620
prevents degranulation of mast cells; therefore only effectivefor prophylaxis and not during and asthma attack.
Page 3621
Q1811:What is 1st line therapy for chronic asthma?
Page 3622
corticosteroids (beclomethasone and prednisone)
Page 3623
Q1812:What is the MOA of beclomethasone?
Page 3624
inhibit cytokine synthesis. Inactivate NF-kappaB; the tf thatinduces TNF-alpha
Page 3625
Q1813:What is the MOA of Zileuton?
Page 3626
5-lipoxygenase pathway inhibitor that blocks conversion ofarachidonic acid to leukotrienes
Page 3627
Q1814:What are Zafirlukast and montelukast especially goodat treating? (MOA?)
Page 3628
aspirin-induced asthma; b/c they block leukotriene receptors
Page 3629
Q1815:Do expectorants (Guaifenesin) suppress the coughreflex?
Page 3630
No; they only remove excess sputum
Page 3631
Q1816:What is N-acetylcystine?
Page 3632
a mucolytic that can loosen mucus plugs in CF patients
Page 3633
Q1817:Epinephrine
Page 3634
Properties - stimulates both α (vasoconstriction - esp skin;mucosa and kidneys) and β (bronchodilatation) receptors. β2
stimulation may also decrease mast cell secretions. vitalcapacity increases due to relief of bronchial mucosal
congestion. not effective orally; rapidly absorded IM orSQ;Indications - acute asthmatic attacks; hypersensitivity
reactions; prolongation of infiltration anesthetic action; topicalhemostatic effect;SE; Tox - anxiety; termor; palpitations;
tachycardia; headache; diaphoresis; pallor;CI - HTN;hyperthroid; ischemic heart disease; cerebrovascular
insufficiency. don't use if older than 60 unless asthma isintractable.
Page 3635
Q1818:Ephedrine
Page 3636
Properties - stimulates both α and β receptors and increasesthe release of NE. vasoconstriction/cardiac stimulation -->increase pulse pressure. CNS stimulant. Rapidly absorbed
PO. Compared to epi - longer duration of action; more centraleffects; lower potency;Indications - chronic asthma (rarely
used now); mydratic (aqueously);SE; Tox - CNS stimulation;increased PVR.
Page 3637
Q1819:Isoproterenol
Page 3638
Properties - stimulates β receptors. all smooth muscle isrelaxed and PVR is lowered in skeltal; renal; and mesentericvascular beds. rapidly absorded after inhalation;Indications -relieves respiratory distress in severe asthmatic attacks butrarely used now that there's more selective agents;SE; Tox -
acute toxicity less than with epi. tachycardia; headache;flushing; nausea; dizziness; diaphoresis. anginal pain/cardiac
arrhythmias. tolerance can occur.
Page 3639
Q1820:Metaproterenol
Page 3640
Properites - β2 selective. relaxes smooth muscle of bronchi;uterus; skeletal muscle vasculature; decreases airway
resistance. resistant to COMT methylation. PO or inhaled;duration up to 4 hours;Indications - bronchodilator in
treatment of asthma; reversible bronchospasm;SE; Tox -tachycardia; hypertension; nervousness; termor; palpitations;n/v. caution in pts with severe HTN; coronary artery disease;
CHF; hyperthroid. tolerance less like compared to inhaledisoproterenol.
Page 3641
Q1821:Terbutaline
Page 3642
Properties - β2 selective when given orally but causes cardioeffects similar to isoproterenol when given SQ. resistant to
COMT methylation;Indications - only β2 agonist usedparenterally for tx of status asthmaticus;SE; Tox - oral causestremor. dizziness; nervousness; fatigue; tinnitus; palpitations
rare. SQ causes same effects as epi.
Page 3643
Q1822:Salmeterol
Page 3644
Properties - β2 selective. longer actinging;Indications - asthmaprophylaxis.
Page 3645
Q1823:Albuterol
Page 3646
Properties - similar to terbutaline. β2 selective. aviable as oraland aersol preparation. peak effect 30-40 min with 3-4 hour
duration;Indications - reversible obsructive airway disease;SE;Tox - nervousness; termor; headache; insomnia; weakness;
dizziness; tachycardia; palpitations. use in caution in pts wtihcoronary artery insufficiency; HTN; hyperthroid; DM and
pts recieving MAO-I or TCAs.
Page 3647
Q1824:Theophylline
Page 3648
Properties - inhibits phosphodiesterase --> increased cAMP.relaxes bronchial smooth muscles --> increased VC; potent
CNS stimulant; imporves diaphragmatic contractility. positiveinotropic action. increases water and electrolyte excretion.oral; rectal; or parental. distributed into all compartments;
60% pro bound;Met/Excr- liver met; t1/2 = 8 hrs;Indications -bronchodilator in asthma and COPD; improve diaphragmatic
function in COPD; reduceds prolonged apnea in preterminfants;SE; Tox - oral causes headache; nervousness;
dizziness; n/v; epigastric pain. iv causes cardiac arrhythmias(blocks adenosine receptors which then increases AV nodal
conduction); hypotension; cardiac arrest and seizures;inchildren; CNS stimulation; diuresis; fevers;monitor serumm
levels (tox at >20 mg/L; benefit at 7 10)
Page 3649
Q1825:Cromolyn Sodium/Nedocromil
Page 3650
Properties - inhibits the degranulation of mast cells preventingthe realse of histamine and other autacoids after immunologicand nonimmunologic stimulation. inhaled because of low oralabsorption;Met/Excr - excreted unchanged within a few days.
maximal levels reached within minutes with t1/2 = 1 hr.response observed within weeks;Indications - prevent asthma
attacks esp. in cold and exercise induced asthma. mostprotective n kids with chronic unstable asthma. can also be
used as a nasal spray for allergic rhinitis;SE; Tox - seen in lessthan 5% of pts. sore thraot; cough; dry mouth most common.
urticaria; maculopapular dermatitis; gastroenteritis.
Page 3651
Q1826:Prednisone/Prednisolone
Page 3652
Class - corticosteroids. reduce inflammation and edema andpotentiate the bronchodilating effects of adrenergic agonists.inactivate NF-kB the transcription factor that induces the
production of TNF-α;Indications - severe chronic and acutebronchospasm;SE; Tox - suppression of growth;
osteoporosis; aggravation of diabetes; aseptic bone necrosis;adrenocortical suppresions.
Page 3653
Q1827:Beclomethasone dipropionate
Page 3654
Class - corticosteroids. reduces inflammation and edema nadpotentiates the bronchodilating effects of adrenergic
agonists;Properties - inhaled in metered doses. highly potent.only minor systemic absorption and rapid metabolism so it
has no effect on the HPA axis;Indications - substiute for oralpreparations in selected individuals with severe steroid-dependent asthma;SE; Tox - oropharyngeal and laryngeal
candidal infection. hoarseness; sore throat; dry mouth.
Page 3655
Q1828:Atropine/Ipratropium Bromide
Page 3656
Properties - block muscarinic receptors thereby inhibitingaceycholine-induced bronchoconstriction;Indications - in
asthma pts unresponsive to adrenergic agents andmethylxantihines. bromidey is often used in COPD because italso reduced secretions;SE; Tox - drowsiness; sedation; drymouth; blurred vision; urinary retenion; constipation. not aspronounced with ipratropium because it does not cross the
BBB.
Page 3658
Class - anitleukotriene;Properties - inhibits 5-lipoxygenasetherefore blocks synthesis of leukotrienes. use with
corticosteroids;Indications - prophylaxis of asthma;SE; Tox -diarrhea; headache; increased risk of infections.
Page 3659
Q1830:Zafirlukast
Page 3660
Blocks LTD4 leukotriene receptors. LTD4 is a receptorsfunction in bronchoconstriction; vasoconstriction; contraction
of smooth muscle and increased vascular permeability.
Page 3661
Q1831:First Generation H1 Blockers
Page 3662
Examples - Diphenhydramine; dimenhydrinate;chlorpheniramine;Indications - Allergy; motion sickness; sleep
aid;Toxicity - Sedation; antimuscarinic; anti-α-adrenergic.
Page 3663
Q1832:Second Generation Histamine Blockers
Page 3664
Examples - Loaratidine; fexofenadine;desloratadine;Indications - Allergy;Toxicity - far less sedating
than first generation.
Page 3665
Q1833:What are the short acting beta-2-adrenoreceptoragonists? What are they used to treat?
Page 3666
Albuterol; levalbuterol; metaproterenol; pirbuteol;These drugsare used for the treatment of the acute bronchoconstriction of
asthma by relaxing bronchial smooth muscle.
Page 3667
Q1834:What are the long acting beta-2-adrenoreceptoragonists? How are they chemically different than short acting
beta-2 adrenoreceptor agonists?
Page 3668
Salmeterol; formoterol;These drugs have lipophilic side chainsthat slow diffusion out of the airway.
Page 3669
Q1835:What is isoproterenol?
Page 3670
Nonselective beta-receptor agonists and a potentbronchodilator.
Page 3671
Q1836:What is the most common adverse effect of beta-2adrenoreceptor agonists?
Page 3672
Skeletal muscle tremor. Other: tachycardia; arrhythmias;exacerbation of angina.
Page 3673
Q1837:Theophylline; theobromine; and caffeine are part ofwhat drug family that is used to treat asthma? What are the
pharmacologic effects of theophylline?
Page 3674
Methylxanthines;Pharmacologic effects: relax bronchialsmooth muscle; decrease histamine release; stimulate ciliarytransport of mucus; stimulate medullary respiratory center.
Page 3675
Q1838:Name two anticholinergic drugs used to treat asthma.
Page 3676
Ipratropium bromide and atropine. They inhibit ACh-mediated constriction of bronchial airways and also decrease
vagal stimulated mucus secretion.
Page 3677
Q1839:How does cromolyn sodium treat asthma?
Page 3678
Cromolyn sodium inhibit the release of mediators from mastcells; suppress the activation of neutrophils; eosinophiles; and
monocytes and inhibit the cough reflex.
Page 3679
Q1840:How should cromolyn sodium be used in order toeffectively combat asthma?
Page 3680
Cromolyn sodium is used prophylactically. It does notreverse an established bronchospasm. It is also the only
antiasthmatic that inhibits both early and late phaseresponses.
Page 3681
Q1841:When is nedocromil sodium used in place of cromolynsodium?
Page 3682
Nedocromil is more effective in blocking bronchospasminduced by exercise or cold air.
Page 3683
Q1842:How does beclomethasone treat asthma?
Page 3684
It is a glucocorticoid that increases airway diameter byattenuating prostaglandin and leukotriene synthesis via
inhibition of phopholipase A2.
Page 3685
Q1843:What are the side effects of oral administration ofbudesoide and flunisolide?
Page 3686
These are glucocorticoids. Side effects include hoarseness andoral candidiasis. More serious adverse effects are adrenal
suppression and osteoporosis.
Page 3687
Q1844:The -lukast drugs are antagonists of the _______.
Page 3688
Montelukast and zafirlukast are antagonists of the leukotrienereceptor LT1. This blocks LTC; D; E4.
Page 3689
Q1845:Name the asthmatic drug that inhibits 5-lipoxygenase;the rate-limiting enzyme in leukotriene biosynthesis.
Page 3691
Q1846:What is omalizumab?
Page 3692
Omalizumab is an anit-IgE antibody that binds to IgE's Fcreceptors; blocking the binding of IgE to mast cells and
basophils.
Page 3693
Q1847:Allergic rhinitis; but not rhinitis associated with colds;can be effectively treated with antihistamines (H1-receptor
antagonists). Name a few.
Page 3694
Diphenhydramine; brompheniramine; chlorpheniramine; andloratadine.
Page 3695
Q1848:What is clemastine used to treat?
Page 3696
Rhinorrhea. It is a second generation H1-receptor antagonist.
Page 3697
Q1849:What is an antitussive?
Page 3698
Medicine used to inhibit or suppress coughing.
Page 3699
Q1850:Name the mucolytic drug used to reduce the viscosityof mucus and treat COPD exacerbations.
Page 3700
Acetylcysteine: cleaves disulfide bonds.
Page 3701
Q1851:An asthmatic female who is recovering from an MI ison several medications. She complains about bruising easily.Blood panel reveals elevated ALT. What antiasthmatic is she
on?
Page 3702
Zilueton - inhibits metabolism of warfarin and increases liverenzymes.
Page 3703
Q1852:Why are opiods effective in the suppression ofcoughing?
Page 3704
They act centrally to decrease sensitivity of the cough centerto peripheral stimuli.
Page 3705
Q1853:What initiates coughing?
Page 3706
Cough receptors; specialized stretch receptors in the tracheaand bronchial tree; send vagal afferents to the cough center.
Page 3707
Q1854:Theophylline has several mechanims; many which areunknown. What are two known moa's of this drug?
Page 3708
Adenosine-receptor antagonist activity and the inhibition ofphosphodiesterase.
Page 3709
Q1855:What drug is used to counter opioid overdose?
Page 3711
Q1856:Which drug is most contraindicated in patients withCOPD: acebutolol; nadolol; atenolol; esmolol; metoprolol?
Page 3712
Nadolol because it is a non-selective beta antagonist.
Page 3713
Q1857:What asthma drug can cause U-waves on ECG? How?
Page 3714
Albuterol may cause potassium to shift into cells; resulting inhypokalemia.
Page 3715
Q1858:What drug can be used to stop the bronchoconstrictionresulting from an asthmatic allergic reaction?
Page 3716
Zileuton. Asprin diverts the arachidonic acid pathway to theleukotrienes. Zileuton blocks 5-lipoxygenase which is the
enzyme that forms the LTs.
Page 3717
Q1859:4 H2 blockers
Page 3718
cimetidine; ranitidine; famotidine; nizatidine
Page 3719
Q1860:MOA of H2 blockers
Page 3720
reversibly block H2 receptors which causes decreased H+secretion by gastric parietal cells
Page 3721
Q1861:cimetidine toxicities
Page 3722
P450 inhibitor; antiandrogenic; crosses BBB (confusion; HAs;dizziness) and placenta
Page 3723
Q1862:2 proton pump inhibitors
Page 3724
omeprazole; lansoprazole
Page 3725
Q1863:MOA of PPIs
Page 3726
irreversibly bind H+/K+ ATPase in gastric parietal cells
Page 3727
Q1864:MOA of bismuth; sucralfate
Page 3728
bind to ulcer base and provide physical protection; allowbicarb secretion to reestablish pH gradient in mucous layer
Page 3729
Q1865:triple tx of H. pylori?
Page 3730
metronidazole + bismuth + amoxicilin/tetracycline
Page 3731
Q1866:MOA of misoprostol
Page 3732
PGE1 analog; that increases production and secretion ofgastric mucous barrier and decreases acid production
Page 3733
Q1867:toxicity/contraindications for misoprostol
Page 3734
(PGE1 analog) diarrhea; not for women of childbearingpotential
Page 3735
Q1868:which 2 muscarinic antagonists used for treatment ofpeptic ulcer?
Page 3736
pirenzepine; propantheline
Page 3737
Q1869:toxicities of pirenzepine and propantheline?
Page 3738
tachycardia; dry mouth; difficulty focusing eyes
Page 3739
Q1870:overuse of aluminum hydroxide can cause whatproblems?
Page 3740
(antacid) constipation; hypophosphatemia; proximal mmweakness; osteodystrophy; seizures
Page 3741
Q1871:overuse of magnesium hydroxide can cause whatproblems?
Page 3742
(antacid) diarrhea; hyporeflexia; hypotension; cardiac arrest
Page 3743
Q1872:overuse of calcium carbonate can cause whatproblems?
Page 3744
(antacid)hypercalcemia; rebound acid increase
Page 3745
Q1873:MOA of infliximab
Page 3746
monoclonal TNF-alpha ab
Page 3747
Q1874:clinical use of infliximab
Page 3748
Crohn's dz; rheumatoid arthritis
Page 3749
Q1875:infliximab toxicity
Page 3750
respiratory infection; fever; hypotension
Page 3751
Q1876:MOA sulfasalazine
Page 3752
combo antibacterial (sulfapyridine) and anti-inflammatory(mesalamine); activated by colonic bacteria
Page 3753
Q1877:clinical use of sulfasalazine
Page 3754
UC; Crohn's disease
Page 3755
Q1878:toxicity of sulfasalazine (5)
Page 3756
malaise; nausea; sulfonamide toxicity; reversible oligospermia
Page 3757
Q1879:MOA of ondansetron
Page 3758
5-HT3 antagonist (powerful central acting anti emetic)
Page 3759
Q1880:clinical use of ondansetron
Page 3760
antiemetic; to control vomiting post-op and in pts undergoingchemotherapy
Page 3761
Q1881:toxicity of ondansetron
Page 3762
headache; constipation
Page 3763
Q1882:MOA of cisapride
Page 3764
acts thru serotoni R to increase Ach release at myentericplexus; increases esophageal tone; increases gastric and
duodenal contracitlity and improves transit time (prokinetic)
Page 3765
Q1883:Clinical use of cisapride
Page 3766
prokinetic (on GIT) but no longer used because of seriousinteractions with erythromycin; ketoconazole; nefazodone;
fluconazole (-->torsades de pointes!)
Page 3767
Q1884:MOA of metoclopramide
Page 3768
D2 R antagonist; increases resting tone; contractility; LEStone; motility but does not increase transit time thru colon.
(pro-kinetic)
Page 3769
Q1885:clinical use of metoclopramide
Page 3770
diabetic and post-surgery gastroparesis
Page 3771
Q1886:toxicity of metoclopramide
Page 3772
(D2 R antag). Increased Parkinsonian effects; restlessness;drowsiness; fatigue; depression; nausea; constipation.
Page 3773
Q1887:drug interactions of metoclopramide
Page 3774
digoxin and diabetic agents
Page 3775
Q1888:contraindications for metoclopramide?
Page 3776
(D2 R antag) pts with small bowel obstruction
Page 3777
Q1889:Calcium carbonate
Page 3778
Class - nonsystemic Antacid;Indication - PUD; refluxesophagitis;SE; Tox - hypercalcemia (esp. with dairy
products); renal stones; Ca stimulates secretion of gastrin andHCl --> acid rebound
Page 3779
Q1890:Aluminum hydroxide
Page 3780
Class - nonsystemic Antacid;Indications - PUD;SE; Tox -*constipation*; hypophosphatemia; proximal myopathy;
encephalopathy in pts on dialysis
Page 3781
Q1891:Magnesium salts
Page 3782
Class - nonsystemic Antacid;Indication - PUD;SE; Tox -*diarrhea*; milk-alkali syndrome with dairy products;
metabolic *alkalosis* esp. in renal insufficiency. exacerbationof CHF; edema because of sodium intake;CI - HTN
Page 3784
All can cause hypokalemia.
Page 3785
Q1893:Cimetidine
Page 3786
Class - H2 blockers (block parietal cell histaminereceptors);Indications - Tx/prevent PUD; ZE; gastritis; mildGERD;Properties - acid secretion inhibited for 4 hours;SE;Tox - only H2 blocker to inhibit P450 system --> increase
serum levels of EtOH; warfarin; digitoxin; TCA; phenytoin;carbamazepine; beta -blockers; benzos. antiadrogenic;
decreased renal excretion of creatinine.
Page 3787
Q1894:Ranitidine
Page 3788
Class - H2 blockers (block parietal cell histaminereceptors);Indications - Tx/prevent PUD; ZE; gastritis; mild
GERD;Properties - more potent than cimetidine. 1-2xdaily;SE; Tox - less than cimetidine; doesn't penetrate CNS as
much; no P450 effect.
Page 3789
Q1895:H2 Blockers
Page 3790
cimetidine; ranitidine; famotidine; nizatidine
Page 3791
Q1896:Omeprazole; Lansoprazole
Page 3792
Class - PPI;Indications - GERD; PUD; ZE; gastritis. esp.when refractory to H2 blockers;Properties - irreversible
inhibition; prodrug that diffuses into acid space of secretorycanaliculus where it is protonated to active form;SE; Tox -
overgrowth of bacteria
Page 3793
Q1897:Sucralfate
Page 3794
Indications - PUD;Properties - activated in acid environment.negative charges bind to positively-charged proteins inulcerated tissue. Provides physical protection;SE; Tox -
minor. mostly constipation. decrased absoprtion ofciproflaxin; norflaxin. because it needs acid to be activated; do
not give with antacids; H2 blockers; PPIs.
Page 3796
Indications - PUD;Properties - binds to ulcerr providingphysical protection. possible antimicrobial activity against H.
pylori.
Page 3797
Q1899:Misoprostol
Page 3798
Class - PGE? analog;Indications - prevent gastric ulcerscaused by NSAIDS;SE; Tox - Diarrhea;CI - potentially
childbearing women (induces labor).
Page 3799
Q1900:Antibiotics for PUD
Page 3800
Tetracycline; Metronidazole; Clarithromycin; plus H2 blockerdrastically reduces recurrence compared to H2 blocker alone.
Page 3802
Class - Emetic;Properties - irritates GI tract; stimulateschemoreceptor zone. Onset = 15-30 min.
Page 3803
Q1902:Prochlorperazine; chlorpromazine; metoclopramide
Page 3804
Class - Dopamine receptor antagonists;Properties - Act at D2receptors at chemoreceptor trigger zone --> antiemesis.
Page 3805
Q1903:Ondansetron
Page 3806
Class - Antiemetic;Properties - 5-HT3 antagonist;Indications- control vomiting postop and during chemotherapy;SE; Tox -
headache; constipation.
Page 3807
Q1904:Bulk-forming Laxatives
Page 3808
Examples - dietary fiber; semisyntheticpolysaccharides/cellulose (methylcellulose);Properties -osmotic effect --> fluid/electrolyte renetion in intestinal
lumen. increased fecal mass/softness --> accelerated transit.Works within 1-3 days after PO administration;Indications -
diverticular disease; IBS;SE; Tox - flatulance; electrolyteimbalances; esophogeal/intestinal obstruction therefore take
with fluids
Page 3809
Q1905:Castor Oil
Page 3810
Class - Stimulant laxative;Properties - hydrolyzed in smallintestine to active ingredient --> decreased reabsorption of
electrolytes/fluids and stimulates peristalsis. works within 1-3hours after PO administration;SE; Tox - chronic use impairsabsorption of essential nutrients; excacerbates dehydration
and electrolyte disturbances.
Page 3811
Q1906:Bisacodyl
Page 3812
Class - Stimulant laxative;Properties - onset of action (oral) =6-12h; (rectal) = 1h;SE; Tox - fluid/electrolyte deficiencies;
rash; rectal burning
Page 3813
Q1907:Anthroquinones
Page 3814
Class - Stimulant Laxative. (cascara and senna; eg);Properties -effect at large intestine. Increase peristalsis.
Page 3815
Q1908:Docusates
Page 3816
Class - Stimulant Laxative;Properties - anionic surfactant.Softens stool by emulsifying water; fat; and feces. Onset ofaction = 1-3d;Indications - used after abdominal surgery andpostMI;SE; Tox - nausea; cramping. Don't use with mineral
oil.
Page 3817
Q1909:Salt-containing Osmotic Laxatives
Page 3818
Properties - contain Mg; phosphate; sulfate salts. fluidretention --> increased motility. Onset of action = 2h;semifluid stools;Indications - bowel evacuation prior to
surgery/imaging;SE; Tox - Mg salts --> hypermagnesemia inpts with renal insufficiency. Na salts exacerbate CHF; cause
dehydration.
Page 3819
Q1910:Lactulose
Page 3820
Class - nonsalt Osmotic Laxative;Properties - semisyntheticdisaccharide. Traps ammonia as NH4+; enhances excretion ofnitrogenous wastes in hepatic insuffiency. Onset of action =1-3d;Indications - laxative and in hepatic encephalopathy;SE;Tox - N/V; flatulence; diarrhea; dehydration; hypokalemia.
Page 3821
Q1911:Mineral Oil
Page 3822
Class - Surfactant Laxative;Properties - softens stool;SE; Tox- limiting. pneumonitis after aspiration; imparied absorption
of fat-soluble nutrients; pruritus ani (ew.)
Page 3823
Q1912:Loperamide
Page 3824
Class - Opiate;Indications - Diarrhea;Properties - since itpoorly crosses BBB; it has few side effects and low potential
for abuse. decreases GI motility.
Page 3825
Q1913:Infliximab
Page 3826
Class - monoclonal Ab to TNF-alpha (a proinflammatorycytokine);Indications - Crohn's Disease; rheumatoid
arthritis;SE; Tox - respiratory infection; fever; hypotension
Page 3827
Q1914:Sulfasalazine
Page 3828
Class - combo of sulfapyridine (antibacterial) and mesalamine(anti-inflmmatory);Indications - Ulcerative colitis; Crohn's
disease;SE; Tox - Malaise; nausea; sulfonamide toxicity(hypersensitivity rxn; hemolysis in G6PD deficient pts;
nephrotoxicity; kernicterus; displacing drugs (warfarin) fromalbumin)
Page 3829
Q1915:examples of H2 blockers
Page 3830
cimitidine ;ranitidine;famotidine;nizatidine;(-tidine)
Page 3831
Q1916:mechanism of H2 blockers
Page 3832
reversibly bind to H2 recetors; blocking H2 activation anddecreased H+ release by parietal cells
Page 3833
Q1917:toxicity of H2 blockers
Page 3834
cimitidine has the most: anti-androgenic effects; p450interactions; crosses BBB (--> dizziness; confusion; HA); can
cross placenta;rantidine and cimetidine decrease renalexcretion of creatinine
Page 3835
Q1918:examples of PPI
Page 3836
omeprazole ;lansoprazole ;(-prazole)
Page 3837
Q1919:MOA of PPI
Page 3838
irreversibly binds to H-K-ATPase pump in parietal cells
Page 3839
Q1920:clinical use for H2 inhibitor
Page 3840
peptic ulcers;gastritis ;mild GERD
Page 3841
Q1921:clinical uses for PPI
Page 3842
peptic ulcers; gastritis; GERD; Zollinger-Ellison syndrome
Page 3843
Q1922:MOA of bismuth
Page 3844
binds at the base of the ucler; giving physical protection;allows HCO3- secretion to re-establish pH gradient in mucus
layer
Page 3845
Q1923:clinical use of bismuth
Page 3846
ucler healing;traveller's diarrhea
Page 3847
Q1924:MOA sucralfate
Page 3848
binds at base of ulcer; giving physical protection ;allowsHCO3- secretion to re-establish pH gradient in mucus layer
Page 3849
Q1925:clinical use of sucralfate
Page 3850
increase ulcer healing ;traveller's diarrhea
Page 3851
Q1926:MOA of misoprostol
Page 3852
agonizes PGE1; increases production of mucous barrier;decreases acid production
Page 3853
Q1927:what is the triple therapy against HP?
Page 3854
metronidazole ;bismuth;amoxy (or tetracycline)
Page 3855
Q1928:clinical uses for misoprostol
Page 3856
prevention of NSAID induced ulcers ;maintain patent PDA;induce labor
Page 3857
Q1929:toxicity of misoprostol
Page 3859
Q1930:examples of muscarinic antagonists
Page 3860
pirenzepine ;propantheline
Page 3861
Q1931:MOA of muscarinic antagonists
Page 3862
blocks M1 receptors on ECL cells and M3 receptors onparietal cells (vagal stimulation goes ot M3) ;blocking M1
receptor decreases H2 secretion and blocking M3 decreasesH+ secretion
Page 3863
Q1932:clinical uses for muscarinic antagonists
Page 3865
Q1933:toxicity of muscarinic antagonist
Page 3866
tachycardia;dry mouth;difficulty focusing eyes
Page 3867
Q1934:toxicity associated with Al(OH)3
Page 3868
constipation (minimum amt of feces);muscleweakness;osteodystrophy ;seizures;hypokalemia
Page 3869
Q1935:toxicity associated with Mg(OH)2
Page 3870
diarrhea ;hyporeflexia;hypotension;cardiac arrest;hypokalemia
Page 3871
Q1936:toxicity associated with calcium carbonate
Page 3872
hypercalcemia;rebound acid increase;hypokalemia
Page 3873
Q1937:MOA of infliximab
Page 3874
mAB against TNF-alpha
Page 3875
Q1938:clinical uses of infliximab
Page 3876
Crohn's disease;RA
Page 3877
Q1939:toxicity assicated with infliximab
Page 3878
respiratory infx;hypotension ;fever
Page 3879
Q1940:MOA sulfasalazine
Page 3880
combo of sulfapyridine and mesalamine (antibacterial andanti-inflammatory) ;activated by colonic bacteria
Page 3881
Q1941:clinical use of sulfasalazine
Page 3883
Q1942:toxicity of sulfasalazine
Page 3884
malaise;nausea;sulfonamide toxicity ;reversible oligospermia
Page 3885
Q1943:MAO ondansetron
Page 3886
seratonin antagonist ;antiemetic
Page 3887
Q1944:clinical use for ondansetron
Page 3888
control vomiting post-op and in pts taking chemo
Page 3889
Q1945:toxicity associated with ondansetron
Page 3890
HA;constipation
Page 3891
Q1946:examples of pro-kinetic agents
Page 3892
cisapride ;metoclopramide
Page 3893
Q1947:MOA cisapride
Page 3894
increases ACh release at myenteric plexus ;increasesesophageal ton e;increases gastric and duo contractility
;improves transit time
Page 3895
Q1948:cisapride toxicity
Page 3896
NO LONGER USED b/c of interactions with erythromycin;ketoconazole; nefazodone; fluconazole
Page 3897
Q1949:MOA metoclopramide
Page 3898
D2 recepotr antagonist;increses resting tone; contractility;LES tone; motolity ;does not increase transit time through
colon
Page 3899
Q1950:which motility agent increases transit time throughcolon?
Page 3901
Q1951:clinical use of metoclopramide
Page 3902
diabetic and post-surggery gastroparesis
Page 3903
Q1952:toxicity of metoclopramide
Page 3904
increased parkinsonian effects;restlessness;drowsiness;fatigue;depression;nausea;constipation
Page 3905
Q1953:drug interactions with metoclopramide
Page 3906
digoxin ;DM meds
Page 3907
Q1954:when is metoclopramide contraindicated
Page 3908
pts with small bowel obstruction
Page 3909
Q1955:Cimetidine
Page 3910
Reversible H2 Blocker;AE: P450 Inhibitor;Anti-androgenic;Cross BBB (confusion; etc);Decrease Creatinine
excretion.
Page 3911
Q1956:Omeprazole
Page 3912
Irreversibly inhibts ACTIVE pumps;P450 clearance andINHIBITION;Prodrugs must be pronated in cells.
Page 3913
Q1957:Bismuth. Sucralafate.
Page 3914
Bind to ucler base; providing physical protrection. AllowHCO3 secretion to reestablish pH gradient in mucous;Also
anti-Diarrhea;Part of H. pylori triple therapy.
Page 3915
Q1958:Misoprostol
Page 3916
Prostaglandin analog;SE: Diarrhea;Contraindicated inchildbearing women.
Page 3917
Q1959:Pirenzepine; Propantheline.
Page 3918
Muscarinic antagonists (M1 on ECL cells and M3 on parietalcells);SE: Tachycardia; dry mouth; cycloplegia.
Page 3919
Q1960:Loperimide
Page 3920
Opioid anti-diarrheal;Excluded from CNS by mdrtransporter;SE: cIx in children.
Page 3921
Q1961:Sulfasalazine
Page 3922
Sulfapyridine (antibacterial) + Mesalanine (anti-inflammatory). Activated by colonic bacteria;SE: Malaise;
nausea; sulfonamide toxicity; oligospermia (reversible).
Page 3923
Q1962:Ondansetron
Page 3924
Antiemeic. 5HT3 antagonist;SE: Headache; Constiplation.
Page 3925
Q1963:Antacids in general
Page 3926
Can effect absorption; bioavailablity; urinary excretion ofother drugs by changing gastric pH or delaying gastric
emptying;Cause systemic alkalosis; hypokalemia.
Page 3927
Q1964:Aluminum Hydroxide
Page 3928
Antacid;SE: Constipation; hypophospahtemia; proximalmuscle weakness; osteodystrophy; seizures
Page 3929
Q1965:Magnesium Hydroxide
Page 3930
Antacid;SE: Diarrhea (osmotic); hyporeflexia; hypotension;cardiac arrest.
Page 3931
Q1966:Calcium Carbonate
Page 3932
Antacid;SE: Hypercalcemia; REBOUND ACIDINCREASE;Also; can chelate and decrease effectiveness of
other drugs (Tetracyclines).
Page 3933
Q1967:Cisapride
Page 3934
Prokinetic Agent;5HT receptors to increase ACh release atthe myenteric plexus. Increase esophageal tone; increasegastric/duodenal contractitlity;SE: NO LONGER USED.
TORSADES DES POINTES when given with erythromycin;ketoconazole; flucanazole; nefazodone.
Page 3935
Q1968:Metoclopramide
Page 3936
D2 receptor antagonist. Increases resting tone; contractility;LES tones; motility. DOES NOT influence colon transport
time;Used for gastroparesis (DM and post surgery);SE:Increases Parkinsonian effects. Interacts with digoxin and DM
agents. cIx if small bowel obstructed.
Page 3938
Properties - inhibits COX therefore preventing TXA2synthesis (irreversible inhibition at platelets - life long = 7-10days) but endo can continue to produce anticoagulant PGI2.
Can prolong bleeding time after one dose;Indications - preventreinfarct; prevent MI; prevent occlusion in coronary artery
bypass grafts. pts with TIAs to prevent stroke.
Page 3939
Q1970:Why is there a yellow jacket in here?
Page 3940
Cuz mom left the door open for no reason. If I get stung whilestudying; I'm just not taking the boards.
Page 3941
Q1971:Clopidogrel
Page 3942
Properties - inhibits plately aggrecation by irreversiblymodifying the platelt ADP receptor;Indications - reduction of
atherosclorotic events in pts with known atherosclorosis.
Page 3943
Q1972:Ticlopidine
Page 3944
Properties - inhibits expression of glycoprotein IIb/IIIAreceptors on platelets. GPIIb/IIIA has fibrinogen bindingsites;Indications - pts with stroke precursors who can't
tolerate aspirin;SE; Tox - life-threatening blood dyscrasia.
Page 3946
Properties - accelarates antithrombin III (heparin cofactor)binding to thrombin which then inactivates thrombin; Xa; XIa;
XIIa; and kallikrein. Given IV/SQ. Prolongs PTT; thrombintime; whole blood clotting time. only anticoagulate that workswithin minutes;Met/Excr - liver met by heparinase;Indications- sq in low doses to prevent clot for pts at high risk; used tostop ongoing thrombosis; in the acute phase of MI; safe in
pregnant women because doesn't cross the placenta;SE; Tox -bleeding - monitor PTT! protamine sulfate reverses theanticoag effect of heparin but too much causes its ownanticoagulant effect. so that's helpful. transient and mild
thrombocytopenia. hypersensitivity. chonically;osteoporosis. elevation of LFTs.
Page 3947
Q1974:Low Molecular Weight Heparins
Page 3948
Properties - have more antifactor Xa activity; less inactivationof thrombin; less inhibition of platelets. longer half life than
heparin. don't need to be monitored but are not easilyreversible;Indications - hip replacements.
Page 3950
Properties - a thrombin inhibitor - binds to the active site andfibrinogen recognition site of thrombing. little bleeding at
therapeutic doses. given IV or SQ.
Page 3951
Q1976:Streptokinase
Page 3952
Properties - produced by beta -hemolytic strep. formscomplexes with plasminogen which can then cleave free
plasminogen into plasmin. longest half life of the thrombolyticagents;Indications - AMI;SE; Tox - bleeding;
hypersensitivity-Ag reactions. rare anaphylaxis.
Page 3953
Q1977:Alteplase (tPA)
Page 3954
Properties - an endogenously produce serine protease. "fibrinselective" - activates only plasminogen bound to fibrin; so V;
VIII remain active. Half life of only 5 minutes;SE; Tox -Hemorrhage with no less incidence than streptokinase.
Page 3955
Q1978:E Aminocaproic Acid (anistreplase)
Page 3956
Properties - a lysine analog that binds to lysine-binding siteson plasminogen and plasmin to block plasmin's binding tofibrin; inhibiting fibrinolysis;Indications - Tx of systemichyperfibrinolysis with surgical commplications followingheart surgery and portocaval shunt. or cancer and blah. can
reverse the action of thrombolytic agents.
Page 3957
Q1979:Epoetin alpha
Page 3958
Properties - growth factor produced by the kidney thatstimulates RBC production. Given parenterally;Indications -
anemia secondary to renal failure and chemotherapy;secondary to AZT in AIDS pts. used prior to surgery to
alleviate potential surgical blood loss and to facilitateautologous blood donation.
Page 3959
Q1980:Sargramostim
Page 3960
Properties - recombinant granulocyte granulocyte-macrophagecolony-stimulating factor. Produced by T lymphocytes leadsto proliferation of granulocytes; monocytes; macrophages;
megakaryocytes;Indications - neutropenia;SE; Tox -induration; thrombophlebitis at site; bone pain; fever; rashes;myalgias. limit-dose if pleuritis; pleural effusions; pericarditis.
Page 3961
Q1981:Filgrastim
Page 3962
Properties - recombinant granulocyte colony-stimulatingfactor. produced by monocytes; fibroblasts; endothelial cells
and stimulates the production of neutrophils;Indications -chemotherapy-induced neutropenia and others;SE; Tox - less
severe than with GM-CSF. bone pain and vascultitis.
Page 3963
Q1982:Abciximab
Page 3964
Properties - binds to glycoprotein receptor IIb/IIIa onactivated platelets;Indications - acute coronary snydromes;
PTCA;SE; Tox - bleeding; thrombocytopenia.
Page 3965
Q1983:Name 4 antiplatelet drugs and their MOA
Page 3966
aspirin: inhibits CO dec. TXA2;clopidogrel: modifies ADPreceptor;Ticlopidine: inhibits GPIIb/IIIaexpression;Abciximab: binds GPIIb/IIIa
Page 3967
Q1984:Heparin MOA;lab?
Page 3968
activates antithrobin III;(thus decreases thrombin andinactivates IXa-XIIa);increase PTT
Page 3969
Q1985:Heparin use
Page 3970
immediate anticoag;(pulmonary embolism; stroke; angina; MI;DVT)
Page 3971
Q1986:What can you administer to reverse the heparineffects?
Page 3972
protamine sulfate;(binds neg. charged heparin)
Page 3973
Q1987:Low MX heparins;(enoxaprin);(used in hipreplacements);MOA;advantages
Page 3974
act more at Xa;;longer half-life;subQ administration;do nothave to monitor PTT
Page 3975
Q1988:Warfarin MOA (an oral agent);lab?
Page 3976
interferes w/ Vit K dep modification II; VII; IX; X; Protein Cand S;follow PT
Page 3977
Q1989:Warfarin use
Page 3978
chronic anticoag
Page 3979
Q1990:How do you treat warfarin overdose
Page 3980
IV of Vit K and fresh frozen plasma
Page 3981
Q1991:What drugs can increase the hepatic metab. of warfarin(3)
Page 3982
barbituates;glutethimide;rifampin
Page 3983
Q1992:what drugs can decrease the metabolism of warfarin(6);IMPORTANT
Page 3984
metronidazole;trimethoprim;disulfiram;cimetidine;phenylbutazone;sulfonamides;(influenza vaccine and acute alcohol intox)
Page 3985
Q1993:Heparin or warfarin; which crosses the placenta?
Page 3986
warfarin;(it is teratogenic)
Page 3987
Q1994:Name 4 thrombolytic agents and their use
Page 3988
streptokinase;anistrepelase (ASPAC);atelplase(tPA);urokinase;early MI
Page 3989
Q1995:Aminocaproic acid class;MOA
Page 3990
fibrinolytic inhibitor;blocks plasmin biding to fibrinogen andfibrin
Page 3991
Q1996:Name the follwing hematopoeitic growthfactors;RBC;GM-CSF;C-CSF;macrophage (2)
Page 3992
erythropoietin;Sargamostin (recombinant);Filgrastim(recombinant);Il-3 and M-CSF
Page 3994
Activates antithrombin III; decreases thrombin & factorXa;Intrinsic pathway inhibitor; increases PTT more thanPT;Short half-life. Does not cross placenta;Antidote =
protamine sulfate
Page 3996
Inhibits synthesis & gamma-carboxylation of vit K dependentfactors (II; VII; IX; X; prot C; prot S);Crosses placenta
(teratogen);Inhibits extrinsic pathway; increases PT;Antidote= vitamin K; fresh frozen plasma
Page 3998
Irreversibly inhibits COX-1 and COX-2;Increased bleedingtime. No change to PT; PTT;SE: ulcers; bleeding;
hyperventilation; Reye's syndrome; tinnitus (CN8)
Page 3999
Q2000:Clopidogrel; Ticlopidine
Page 4000
Inhibits platelet aggregation. Irreversibly blocks ADPreceptors; blocks GP IIb/IIIa expression;SE: ticlopidine =
neutropenia
Page 4001
Q2001:Abciximab
Page 4002
Inhibits platelet aggregation; antibody to GP IIb/IIIareceptors;SE: thrombocytopenia
Page 4003
Q2002:tPA; urokinase; streptokinase; anistreplase
Page 4004
Thrombolytics; aid conversion of plasminogen to plasmin andcleaves thrombin/fibrin clots;Antidote = aminocaproic acid
(fibrinolysis inhibitor)
Page 4006
Anticoagulant;MECH: increased activity of antithrombin(III) which inhibits thrombin (IIa); Xa; and IXa (given
parenterally; short t1/2; monitor PTT);USE: PE; MI; angina;stroke; DVT; can be used during preg (doesn't cross
placental);TOX: bleeding; thrombocytopenia; drug-druginteractions (very negative molecule); hypersensitivity; anti-
platelet antibodies
Page 4007
Q2004:Enoxaparin
Page 4008
LoAnticoagulant;MECH: increased activity of antithrombin(III) to inhibit Xa (can be given subcu; longer t1/2);USE: PE;MI; angina; stroke; DVT; can be used during preg (doesn't
cross placental);TOX: bleeding; thrombocytopenia; drug-druginteractions (very negative molecule); hypersensitivity; anti-
platelet antibodies
Page 4009
Q2005:Protamine sulfate
Page 4010
MECH: very positively charged molecule binds heparinwhich is negatively charged;USE: reversal of heparinization
Page 4011
Q2006:Warfarin/coumadin
Page 4012
Anticoagulant;MECH: interferes with normal synthesis andcarboxylation of vitamin-K dependent clotting factors - II;VII; IX; X; C; S (oral; long t1/2; several days to take effect;
monitor PT);USE: long term anticoagulation - DVT; PEprophylaxis;TOX: bleeding teratogenic; drug-drug interactions
(
Page 4013
Q2007:Alteplase / tPA (tissue plasminogen activator)
Page 4014
Thrombolytic;MECH: activates plasminogen bound to fibrinto plasmin which dissolves fibrin clots; recombinant humanprotein;USE: Acute MI and ischemic stroke (within 3-6 oursof the event); PE; DVT;TOX: bleeding (internal and external)
Page 4015
Q2008:Streptokinase
Page 4016
Thrombolytic;MECH: activates plasminogen (free and bound)to plasmin which dissolves fibrin clots; isolated from
streptococci;USE: Acute MI and ischemic stroke (within 3-6ours of the event); PE; DVT;TOX: bleeding (internal and
external); hypersensitivity rxn
Page 4017
Q2009:Urokinase
Page 4018
Thrombolytic;MECH: activates plasminogen (free and bound)to plasmin which dissolves fibrin clots; isolated from
streptococci;USE: PE;TOX: bleeding (internal and external);less antigenic than streptokinase
Page 4019
Q2010:APSAC (anistreplase)
Page 4020
Thrombolytic;MECH: lys-plasminogen/streptokinasecomplex which binds fibrin and becomes slowing
activated;TOX: non-selective; long lasting hypocoagulablestate
Page 4021
Q2011:Aminocaproic acid
Page 4022
Anti-thrombolytic;MECH: inhibits fibrinolysis;USE:thrombolytic toxicity
Page 4023
Q2012:Aspirin (ASA)
Page 4024
Antithrombotic;MECH: Acetylates and irreversibly inhibitscyclooxygenase (COX-1 and -2) to prevent conversion of
arachidonic acid to prostaglandins: (1) inhibition ofthromboxane (TxA2) → decreased activity and aggregation ofplatelets; (2) at high doses; it decreased synthesis of PGI2 byendothelial cells which reduces the antithrombotic action;USE:antipyretic; analgesic; anti-inflammatory; anti-platelet;TOX:
gastric ulceration; bleeding; hyperventilation; Reye'ssyndrome; tinnitus
Page 4025
Q2013:Dipyridamole
Page 4026
Antithrombotic;MECH: inhibits platelet uptake of adenosinewhich had vasodilatory and antiaggregating activity;USE:
prophylaxis in pts with prosthetic heart valves
Page 4027
Q2014:Clopidigrel (Plavix) & Ticlopidine
Page 4028
Antithrombotic;MECH: (1) irreversibly block ADP receptors→ decreased platelet aggregation; (2) prevent glycoprotein
IIb/IIIa expresion → decreased fibrinogen binding;USE: acutecoronary syndromes; percutaneous; transluminal coronary
angiography;TOX: bleeding; thrombocytopenia
Page 4029
Q2015:Abciximab; Eptifibatide & Tirofiban
Page 4030
Antithrombotic;MECH: chimeric monoclonal antibody;synthetic peptide; & peptide mimetic that bind IIb/IIIa →
decreased fibrinogen binding → decreased plateletaggregation;USE: MI; angina; percutaneous coronary
intervention;TOX: bleeding
Page 4031
Q2016:Mechlorethamine
Page 4032
Alkylating Agent;MECH: binds Ns and Os of purines andpyrimidines in DNA → abnl base pairing; depurination; ringcleavage and DNA strand crosslinks; acts in late G1 and S
phase;USE: IV route; MOPP regime for Hodgkins dz;TOX:leukopenia and thromboctyopenia
Page 4033
Q2017:Cyclophosphamide
Page 4034
Alkylating Agent;MECH: binds Ns and Os of purines andpyrimidines in DNA → abnl base pairing; depurination; ringcleavage and DNA strand crosslinks; acts in late G1 and Sphase; requires bioactivation by liver which also creates a
toxic metabolite (acrolein);USE: oral; IV; or IM; non-Hodgkin's lymphoma; breast & ovarian CA;
immunosuppressant;TOX: myelosuppression; hemorrhagiccystitis (Acrolein) can be prevented with MESNA
Page 4035
Q2018:Ifosfamide
Page 4036
Alkylating Agent;MECH: binds Ns and Os of purines andpyrimidines in DNA → abnl base pairing; depurination; ringcleavage and DNA strand crosslinks; acts in late G1 and Sphase; requires bioactivation by liver which also creates a
toxic metabolite (acrolein);USE: oral; IV; or IM; non-Hodgkin's lymphoma; breast & ovarian CA;
immunosuppressant;TOX: myelosuppression; hemorrhagiccystitis (less tox than cyclophosphamide)
Page 4037
Q2019:Chlorambucil
Page 4038
Alkylating Agent;MECH: binds Ns and Os of purines andpyrimidines in DNA → abnl base pairing; depurination; ringcleavage and DNA strand crosslinks; acts in late G1 and S
phase;USE: orally for CLL; some lymphomas; andHodgkins;TOX: less severe marrow suppression than other
nitrogen mustards
Page 4040
Alkylating Agent;MECH: binds Ns and Os of purines andpyrimidines in DNA → abnl base pairing; depurination; ringcleavage and DNA strand crosslinks; acts in late G1 and S
phase;USE: orally for CML;TOX: pulmonary fibrosis;hyperpigmentation
Page 4041
Q2021:Carmustine; lomustine; semustine
Page 4042
Alkylating Agent;MECH: binds Ns and Os of purines andpyrimidines in DNA → abnl base pairing; depurination; ringcleavage and DNA strand crosslinks; acts in late G1 and Sphase;USE: highly lipophillic → cross BBB → treat brain
tumors (including GBM); Hodgkin's dz;TOX:myelosuppression; renal failure; CNS tox (dizziness; ataxia)
Page 4043
Q2022:Streptozocin
Page 4044
Alkylating Agent;MECH: binds Ns and Os of purines andpyrimidines in DNA → abnl base pairing; depurination; ringcleavage and DNA strand crosslinks; acts in late G1 and S
phase;USE: pancreatic islet cell CA and carcinoid;TOX: NOTmyelosuppressive; renal tox is dose-limiting
Page 4045
Q2023:Cisplatin
Page 4046
Platinum compound;MECH: complexes with DNA to formcross-links (like alkylating agents);USE: testicular; ovarian;
and bladder CAs;TOX: nephrotox; ototox; peripheralneuropathy
Page 4047
Q2024:Carboplatin
Page 4048
Platinum compound;MECH: complexes with DNA to formcross-links (like alkylating agents);USE: testicular; ovarian;
bladder; transitional; NSC lung CA;TOX: myelosuppression;nephrotox; ototox; peripheral neuropathy
Page 4049
Q2025:Methotrexate
Page 4050
Antimetabolite;MECH: S-phase specific folic acid analoguethat inhibits dihydrofolate reductase → decreased DNA andprotein synthesis;USE: ALL; choriocarcinoma; trophoblastic
tumors; Burkitt and other non-Hodgkin's lymphoma;osteogenic sarcoma; abortion; ectopic pregnancy; RA;
psoriasis;TOX: myelosuppressive (treat withleucovorin/folinic acid); Gi; nephrotox
Page 4051
Q2026:Cytarabine
Page 4052
Antimetabolite;MECH: S-phase specific pyrimidineantagonist - metabolites inhibit DNA polyermase;USE: Acuteleukemias (esp. AML) and non-Hodgkin's lymphoma;TOX:
leukopenia; thrombocytopenia; megaloblastic anemia
Page 4053
Q2027:Flourouracil (5-FU)
Page 4054
Antimetabolite;MECH: S-phase specific pyrimidineantagonist; activated form complexes folic acid that inhibits
thymidilate synthase → decreased DNA and proteinsynthesis;USE: parenterally colon CA and other solid cancers;topically basal cell CA;TOX: myelosuppression (rescue with
thymidine); photosensitivity
Page 4055
Q2028:Mercaptopurine & Thioguanine
Page 4056
Antimetabolite;MECH: analogues of purines; activated byHGPRTase; block de novo purine synthesis;USE: leukemias;
lymphomas (not CLL or Hodgkins);TOX: bone marrowsuppression
Page 4057
Q2029:Fludararbine
Page 4058
Antimetabolite;MECH: analogues of purines; interferes withDNA synthesis;USE: CLL;TOX: bone marrow suppression
Page 4059
Q2030:Vincristine
Page 4060
Vinca alkaloid;MECH: M-phase specific; binds tubulin toprevent microtubule polymerization → mitotic spindle can't
form;USE: lymphoma (MOPP); Wilm's tumor;choriocarcinoma;TOX: neurotox (areflexia; peripheral
neuritis); paralytic ileus
Page 4061
Q2031:Vinblastine
Page 4062
Vinca alkaloid;MECH: M-phase specific; binds tubulin toprevent microtubule polymerization → mitotic spindle can't
form;USE: lymphoma (MOPP); Wilm's tumor;choriocarcinoma;TOX: bone marrow suppression
Page 4063
Q2032:Paclitaxel
Page 4064
MECH: M-phase specific; stabilizes microtubles so that themitotic spindle cannot break down in anaphase;USE: ovarian
& breast CA;TOX: myelosuppression; hypersensitivity
Page 4065
Q2033:Etoposide
Page 4066
MECH: G2-phase specific; inhibits topoisomerase II → dsDNA breaks;USE: SCLC; prostate and testicular CA;TOX:
leukopenia
Page 4067
Q2034:Dactinomycin (actinomycin D)
Page 4068
Antibiotic;MECH: intercalates into DNA; phase non-specific;USE: Wilm's tumor; Ewing's sarcoma;rhabdomyosarcoma;TOX: myelosuppression
Page 4069
Q2035:Doxorubicin (adriamycin); daunorubicin
Page 4070
Antibiotic;MECH: intercalate into DNA; generate freeradicals → DNA strand breaks;USE: part of many regimens
(ABVD); Hodgkin's; myelomas; sarcomas; solid tumors;TOX:cardiotoxicity; alopecia
Page 4071
Q2036:Bleomycin
Page 4072
MECH: induces formation of free radicals → DNA strandbreaks (G2 phase specific);USE: testicular CA; lymphomas
(ABVD);TOX: pulmonary fibrosis; skin changes
Page 4073
Q2037:Imatinib (Gleevec)
Page 4074
MECH: bcr-abl tyrosine kinase inhibitor ;USE: CML(Philadelphia chrom); GI stromal tumors;TOX: fluid retention
Page 4075
Q2038:Trastumab (Herceptin)
Page 4076
MECH: IgG against HER2 protein (erb-B2); cell death byantibody dependent cytotoxicity;USE: Metastatic breast
cancer;TOX: cardiotoxicity
Page 4077
Q2039:Tamoxifen; raloxifene
Page 4078
MECH: competitive antagonist of estrogen receptor → blockestrogen-dependent growth;USE: breast cancer;
osteoporosis;TOX: hot flashes; increased risk of endometrialcancer (not raloxifene)
Page 4079
Q2040:Prednisone
Page 4080
MECH: may trigger apoptosis (glucocorticoid);USE: CLL;Hodgkin's; autoimmune dzs;TOX: Cushing-like symptoms
Page 4081
Q2041:Rituximab
Page 4082
MECH: binds CD20 antigen on B-cells → cell lysis;USE:non-hodgkin's lymphoma; thrombocytopenic purpura;TOX:
derm and GI
Page 4083
Q2042:which cancer drugs are cell cycle specific (5)
Page 4084
antimetabolites (MTX; 5-FU; 6-MP); etoposide; bleomycin;vinca alkaloids; paclitaxel
Page 4085
Q2043:which cancer drugs are cell cycle nonspeficic (2)
Page 4086
alkylating agents; antibiotics
Page 4087
Q2044:MOA of MTX
Page 4088
S-phase specific antimetabolite. Inhibits duhydrofolatereductase (b/c is folate acid analog)
Page 4089
Q2045:Clinical uses of MTX
Page 4090
leukemias; lymphomas; choriocarcinomas; sarcomas; abortion;ectopic preggers; RA; psoriasis
Page 4091
Q2046:toxicities of MTX
Page 4092
myelosuppression (use leucovorin for "rescue");macrovesicular fatty change in liver
Page 4094
S-phase specific antimetabolite. Bioactivated form (5F-dUMPcomplexes with folic acid and inhits thymidylate synthase
Page 4095
Q2048:Clinical use of 5-FU
Page 4096
colon cancer and other solid tumors; basal cell carcinoma(topical). Synergy with MTX
Page 4097
Q2049:toxicity of 5-FU
Page 4098
myelosuppression which is NOT reversible with leucovorin(vs MTX); photosensitivity
Page 4100
blocks de novo purine synthesis
Page 4101
Q2051:what activates 6-MP?
Page 4103
Q2052:Toxicities of 6-MP
Page 4104
done marrow; GI; liver; metabolized by xanthine oxidase soincreased toxicity with allopurinol
Page 4105
Q2053:MOA cytarabine (ara-C)
Page 4106
inhibits DNA polymerase
Page 4107
Q2054:Clinical use of ara-C?
Page 4109
Q2055:toxicities of ara-C
Page 4110
leukopenia; thrombocytopenia; megaloblastic anemia
Page 4111
Q2056:MOA of cyclophosphamide/ifosfamide
Page 4112
(alkylaying agts) covalently x-link DNA at guanine N-7;require bioactivation by liver
Page 4113
Q2057:Clinical use of cyclophosphamide/ifosfamide
Page 4114
non-Hodgkin's lymphoma; breast and ovarian carcinomas
Page 4115
Q2058:toxicities of cyclophosphamide
Page 4116
myelosuppressin; hemorrhagic cystitis (use mesna!!)
Page 4117
Q2059:4 nitrosoureas
Page 4118
carmustine; lomustine; semustine; streptozocin
Page 4119
Q2060:MOA of nitrosoureas
Page 4120
(e.g. carmustine; steptozocin). Alkylate DNA; requirebioactivation; CROSS BBB!!
Page 4121
Q2061:toxicities of nitrosoureas
Page 4122
CNS (dizziness; ataxia)
Page 4123
Q2062:MOA of cisplatin; carboplatin
Page 4124
act like alkylating agents
Page 4125
Q2063:clinical uses of cisplatin?
Page 4126
testicular; bladder; ovary; and lung carcinomas
Page 4127
Q2064:toxicity of cisplatin?
Page 4128
nephrotoxicity and acoustic nerve damage
Page 4129
Q2065:MOA of busulfan
Page 4131
Q2066:clinical use of busulfan
Page 4133
Q2067:toxicities of busulfan
Page 4134
pulmonary fibrosis; hyperpigmentation
Page 4135
Q2068:MOA of doxorubucin; daunurubicin
Page 4136
generate free radicals and noncovalently intercalate into DNA
Page 4137
Q2069:Clinical uses of doxorubucin; daunorubicin
Page 4138
part of ABVD treatment for Hodgkin's; also for myelomas;sarcomas; solid tumors
Page 4139
Q2070:toxicities of doxorubicin; daunorubicin
Page 4140
cardiotoxic; myelosuppression; marked alopecia; toxicextravasation
Page 4141
Q2071:MOA dactinomycin
Page 4142
DNA intercalater
Page 4143
Q2072:clinical uses of dactinomycin
Page 4144
Wilm's tumor; Ewing's sarcoma; rhabdomyosarcoma (forchildhood tumors!)
Page 4145
Q2073:toxicity of dactinomycin
Page 4146
myelosuppression
Page 4147
Q2074:MOA of bleomycin
Page 4148
induces formation of free radicals-->DNA strand breaks
Page 4149
Q2075:Clinical uses of bleomycin
Page 4150
testicular cancer; part of ABVD for Hodgkin's (along withdoxorubicin/daunorubicin)
Page 4151
Q2076:toxicities of bleomycin
Page 4152
PULMONARY FIBROSIS; skin changes; MINIMALmyelosuppression
Page 4153
Q2077:MOA of etoposide
Page 4154
G2 phase specific agt; inhibits topoisomerase II
Page 4155
Q2078:Clinical uses of etoposide
Page 4156
small cell carcinoma of lung and prostate; testicular carcinoma
Page 4157
Q2079:Toxicities of etoposide
Page 4158
myelosuppression; GI irritation; alopecia
Page 4159
Q2080:MOA of prednisone
Page 4160
steroid; may trigger apoptosis?
Page 4161
Q2081:Clinical uses of prednisone
Page 4162
lots but spefically part of MOPP regimen for Hodgkin's ;CLL
Page 4163
Q2082:Toxicities of prednisone
Page 4164
Cushing-like sxs; immunosuppression; CATARACTS; acne;OSTEOPOROSIS; HTN; peptic ulcers; hyperglycemia;
psychosis
Page 4165
Q2083:MOA of tamoxifen; raloxifene
Page 4166
estrogen R antagonits in breasts; agonists in bone
Page 4167
Q2084:tamoxifen vs raloxifene
Page 4168
tamoxifen may increase risk of endometrial cancer butraloxifene is an endometrial ANTAGonist
Page 4169
Q2085:MOA of trastuzumab (herceptin)
Page 4170
monoclonal Ab against HER-2; helps kill breast cancer cellsthat overexpress HER-2
Page 4171
Q2086:Clinical use of trastuzumab
Page 4172
(herceptin) metastatic breast cancer
Page 4173
Q2087:toxicity of trastuzumab
Page 4175
Q2088:MOA of imatinib?
Page 4176
(Gleevec) Phl chromosome bcr-abl tyrosine kinase inhibitor
Page 4177
Q2089:Clinical uses of imatinib
Page 4178
(gleevec) CML; GI stromal tumors
Page 4179
Q2090:toxicity of imatinib
Page 4180
(gleevec) fluid retention
Page 4181
Q2091:MOA of vincristine; vinblastine
Page 4182
(vinca alkaloids) M phase specifics; bind tubulin and blockpolymerization of microtubules
Page 4183
Q2092:Clinical uses of vincristine; vinblastine
Page 4184
part of MOPP regimen (as is prednisone) for lymphoma;Wilms' tumor; choriocarcinoma
Page 4185
Q2093:toxicity of vincristine
Page 4186
neurotoxicity; paralytic ileus
Page 4187
Q2094:toxicity of vinblastine
Page 4188
myelosuppression (vinBLASTine BLASTS bone marrow)
Page 4189
Q2095:MOA of taxols
Page 4190
(e.g. paclitaxel) M phase specific agents to bind tubulin anddisallow microtubule breakdown
Page 4191
Q2096:clinical uses of taxols
Page 4192
ovarian and breast carcinomas
Page 4193
Q2097:toxicities of taxols
Page 4194
myelosuppression and hypersensitivity
Page 4195
Q2098:Which cancer drugs are M-phase specific?
Page 4196
taxols and vinca alkaloids
Page 4197
Q2099:protects against rejection from organ transplants. doesnot induce bone marrow depression.
Page 4199
Q2100:alkylating agent of both purine and pyrimidine basesof DNA. treatment for CLL.
Page 4200
Cyclophosphamide
Page 4201
Q2101:causes nepho and ototoxicity
Page 4203
Q2102:anti-metabolite of folic acid: inhibits dihydrofolatereductase
Page 4205
Q2103:this drug can block or reduce the host toxicity ofMethotrexate by providing a reduced folate to increase folic
acid
Page 4206
Leucovorin Rescue
Page 4207
Q2104:toxicity profile includes pneumonitis and pulmonaryfibrosis
Page 4209
Q2105:drug used in organ transplantation = kidney allografts.Allopurinol can inc. the activity by inhibiting its
biotransformation by xanthine oxidase
Page 4211
Q2106:chemotherapy regimen used in hodgkin's disease
Page 4212
MOPP = Mechlorethamine (nitrogen mustard); Oncovorin(aka Vincristine blocks microtubule assembly); Procarbazine;
Prednisone (glucocorticoid that induces apoptosis)
Page 4213
Q2107:estrogen receptor blocker used to treat breat tumors;can potentially result in endometrial cancer.
Page 4215
Q2108:antiandrogenic. used w/ Leuprolide (LHRH analog) totreat prostate cancer
Page 4217
Q2109:progesterone receptor inhibitor used to treatEndometrial cancer
Page 4219
Q2110:androgenic steroid used to treat mammary cancer inpostmenopausal women
Page 4220
Fluoxymesterone
Page 4221
Q2111:folic acid analog that inhibits tetrahydrofolatesynthesis by inhibiting dihydrofolate reductase. used to treat
ALL and Psoriasis
Page 4223
Q2112:treatment for Brain tumor
Page 4224
Lomustine and Carmustine
Page 4225
Q2113:side effect of carmustine
Page 4226
pulmonary fibrosis
Page 4227
Q2114:drug that attaches to beta cells and is used to treatpancreatic insulinomas
Page 4229
Q2115:pyrimidine analog that is DOC for AML
Page 4230
Cytarabine (AraC)
Page 4231
Q2116:used for Wilms tumor and rhabdomyosarcoma
Page 4233
Q2117:used for oat cell carcinoma
Page 4235
Q2118:used for Ovarian Cancer
Page 4237
Q2119:can decrease nephrotoxicity caused by chronic use ofCisplatin
Page 4239
Q2120:Catalyzes the activation of antithrombin III todecrease thrombin and Xa;Uses (2);site of action?
Page 4240
Heparin;;Uses;Immediate anticoagulation;(PE; MI; stroke;DVT);Used during pregnancy (does not cross);site: Blood
Page 4241
Q2121:Interferes w/ factors II; VII; IX and X and protein Cand S;Use;site of action?
Page 4242
Warfarin;use;Chronic coagulation;[the EX-PaTriot went toWAR];EXtrinsic-PT pathway;site: Liver
Page 4243
Q2122:drug class that aids in conversion of plasminogen toplasmin (which cleaves thrombin and fibrin clots);name (4)
Page 4244
Thrombolytics;Streptokinase;Urokinase;tPA(alteplase);Antistreplase
Page 4245
Q2123:what inhibits plasminogen to plasmin?
Page 4246
Aminocaproic acid
Page 4247
Q2124:what glycoprotein in platelet binds to exposedcollagen?;which bind together to aggregate?
Page 4248
to collagen: GP-1a;;together: GP-IIb/IIIa
Page 4249
Q2125:The only irreversible binder in the group to inhibitCOX-1 and COX-2
Page 4251
Q2126:drug inhibits platelet binding by irreversibly blockingADP receptors; thereby inhibiting fibrinogen binding by
preventing GP-IIb/IIIa expression;(2) uses;AE?
Page 4252
Clopidogrel;use;Acute Coronary syndrome;Coronarystenting;AE;Neutropenia;(tiCLOPidine)
Page 4253
Q2127:drug that binds directly to GP-IIb/IIIa on activatedplatelets; preventing aggregation;use?
Page 4254
Abciximab;;use;Angioplasty
Page 4255
Q2128:S-phase specific anti-cancer drugs;(5)
Page 4256
Methotrexate;5-FU;Cytarabine;6-MP;Hydroxyurea
Page 4257
Q2129:S-phase antimetabolite that inhibits DHF reductaseresulting in low dTMP;(2) AE?
Page 4258
Methotrexate;;AE;Myelosuppression;Macrovesicular fattyliver
Page 4259
Q2130:what reduces the myelosuppression toxicity inMethotrexate?
Page 4261
Q2131:S-phase pyrimidine analog that inhibits thymidylatesynthase; resulting in low dTMP;(3) uses;(2) AE
Page 4262
5-Fluorouricil (5-FU);uses;Colon CA;solid tumors;Basal cellCA;AE;Myelosuppression;photosensitivity
Page 4263
Q2132:S-phase that blocks Purine synthesis and is activatedby HGPRTase;(2) uses?;what can increase toxicity?
Page 4264
6-Mercaptopurine (6-MP);use;Leukemias (notCLL);Lymphomas (not Hodgkin);inc Toxicity:Allopurinol;(metabolized by Xanthine Oxidase)
Page 4265
Q2133:S-phase tha inhibits DNA polymerase to compete w/dCTP;use?;(3) AE
Page 4266
Cytarabine (ARA-C);use:AML;AE;Leukopenia;Thrombocytopenia;Megaloblastic
anemia
Page 4267
Q2134:Alkylating agent covalently x-link DNA at guanine N-7;use (3);AE
Page 4268
Cyclophosphamide;use;Non-Hodgkins lymphomas;BreastCA;Ovarian CA;AE;hemorrhagic CYSTITIS
Page 4269
Q2135:Alkylating agent class that crosses BBB;name drugs(2);AE
Page 4270
Nitrosoureas;drugs;"-MUSTINE";Streptozocin;AE;CNStoxicity (dizzy; ataxia)
Page 4271
Q2136:(2) anti-cancer drugs that act like Alkylating agentsand form free radicals; they cause AE of Ototoxicity and
Nephrotoxicity;use (4)
Page 4272
Cisplatin; Carboplatin;use (BOLT);Bladder CA;OvarianCA;Lung CA;Testicular CA;;[BOLT ON the PLAnTation]
Page 4273
Q2137:Alkalaying agent of DNA used as DOC for CML;(2)AE
Page 4274
Busulfan;AE;Pulmonary fibrosis;hyperpigmentation
Page 4275
Q2138:(2) anti-cancers that generates free radicals andnoncovalently intercalate in DNA (breaking strands); AE
include cardiotoxicity;(2) uses;another AE
Page 4276
Doxorubicin (Adriamycin);Danorubicin;use;Hodgkins (A inABVD combo);solid tumors;AE;Alopecia
Page 4277
Q2139:another name for;Doxorubicin
Page 4279
Q2140:what anti-cancer drug that intercalates in DNA; is usedfor childhood tumors?
Page 4280
ACTinomycin-D;[children ACT out]
Page 4281
Q2141:drug that induces formation of free radicals to causebreaks in DNA; AE is pulmonary fibrosis;(2) uses
Page 4282
Bleomycin;use;Testicular CA;Hodgkins (B in ABVD combo)
Page 4283
Q2142:G2-specific agent that inhibits Topoisomerase-II;(3)uses
Page 4284
EToPoSide (VP-16);uses;T: Testicular CA;P: Prostate CA;S:Small cell CA of lung
Page 4285
Q2143:MC glucocorticoid in cancer therapy;(2) uses;asidefrom usual corticoid AE (cushings; osteoporosis) what other
AE?
Page 4286
Prednisone;use;Hodgkins (P in MOPPcombo);CLL;AE;cataracts
Page 4287
Q2144:monoclonal Ab against HER-2 (erb-B2)--BreastCA;AE
Page 4288
Trastuzumab (HERceptin);AE;Cardiotoxicity
Page 4289
Q2145:monoclonal Ab against the Philadelphia chromosomebrc-abl tyrosine kinase
Page 4290
Gleecec (Imatinib)
Page 4291
Q2146:M-phase specific alkaloids that bind to tubulin andblock polymerization of microtubules so that spindle fibers
cannot form;use (3);AE (2)
Page 4292
Vincristine ("Oncovin"); Vinblastine;use;Hodgkins (O inMOPP combo);Wilm's
Tumor;Choriocarcinoma;AE;Vincristine -Neurotoxicity;Vinblastine - BLASTs bone marrow
Page 4293
Q2147:M-phase specific that bind to tubulin andhyperstabilize polymerized microtubules so that spindle
fibers cannot breakdown (anaphase cant occur);use (2);AE (2)
Page 4294
Taxols (Paclitaxel);use;Ovarian CA;BreastCA;AE;myelosuppression;Hypersensitivity
Page 4295
Q2148:what are the drugs in the ABVD Hodgkins combo?
Page 4296
Adriamycin(doxorubicin);Bleomycin;Vinblastine;Dacarabazine
Page 4297
Q2149:what are the drugs in the MOPP Hodgkins combo?
Page 4298
Mechlorethamine;Oncovoin(Vincristine);Prednisone;Procarbazine
Page 4299
Q2150:DOC for CLL
Page 4301
Q2151:DOC in CML;(2)
Page 4302
Gleevac;;Busulfan
Page 4303
Q2152:DOC in AML
Page 4305
Q2153:anti-cancer drug that causes Pancreatitis
Page 4307
Q2154:anti-cancer drug that causes oral and GI ulcers
Page 4309
Q2155:which ant-cancer drugs are clasified as Alkylatingagents?;(4)*
Page 4310
"at NITe the CYCLOne picked-up the BUS andCAR";NITrosureas;CYCLOphosphamide;BUSulfan;CARbop
latin; cisplatin
Page 4311
Q2156:what anti-cancer drug works in the G-0 phase?
Page 4313
Q2157:which anti-cancer drugs generate free radicals?;(3)*
Page 4314
BAD radicals;Bleomycin;Actinomycin-D;Doxorubicin;Daunorubicin
Page 4315
Q2158:(2) drugs that work in the G-2 phase
Page 4316
Bleomycin;;Etoposide (VP-16)
Page 4317
Q2159:Inhibit IL-2 production/secretion
Page 4318
Cyclosporine (calceneurin); Tacrolimus (FK506)
Page 4319
Q2160:IL-2 Inhibitors (downstream)
Page 4320
Sirolimus (mTOR inhibitor); Daclizumab (mAb against IL-2receptor)
Page 4321
Q2161:Antimetabolites
Page 4322
Azathioprine (6MP precursor; lymphtoxic); Mycophenolatemofetil (Inhibits de novo Guanine synethesis)
Page 4323
Q2162:Other Action
Page 4324
Muronomab-CD3 (OKT3)--mAb binds to CD-3 on T-cells
Page 4325
Q2163:activated T helper cells secrete this cytokine whichcauses proliferation and activation of two subsets of T helper
cells; TH1 & TH2
Page 4327
Q2164:function of TH1 cells?
Page 4328
cell mediated immunity and delayed hypersensitivityreactions
Page 4329
Q2165:what do TH1 cells produce?
Page 4330
IFN-gamma; IL-2 and TNF-B (which activate macrophages;CTLs; & NK cells.
Page 4331
Q2166:what do TH2 secrete when activated?
Page 4332
IL-4; IL-5; IL-6 (which promote B cell proliferation anddifferentiation)
Page 4333
Q2167:what is the action of IL-10?
Page 4334
down regulate the action of TH1 cells
Page 4335
Q2168:what is action of IFN-gamma on helper T cells?
Page 4336
down regulates TH2 response
Page 4337
Q2169:name an agent that acts at the step of antigenrecognition in the immune response?
Page 4338
antibodies including Rho(D) immune globulin;antilymphocyte globulin; and muromonab CD3.
Page 4339
Q2170:name an agent that acts at the step of differentiationand synthesis in the immune response?
Page 4340
cyclosporine; tacrolimus; dactinomycin; and antilymphocyticglobulin and monoclonal anti-T cell antibodies
Page 4341
Q2171:MOA of glucocorticoids?
Page 4342
decrease the synthesis of Prostaglandins; leukotrienes;cytokines; and other signaling molecules that participate inimmune responses (eg Platelet activating factor). They alsoinhibit proliferation of T cells and to a lesser degree dampenhumoral immunity. continuous therapy lowers IgG levels
through inc. catabolism
Page 4343
Q2172:what is the toxicity of corticosteroids?
Page 4344
adrenal suppression; growth inhibition; muscle wasting;osteoporosis; salt retention; diabetogenesis and possible
psychosis
Page 4345
Q2173:MOA of cyclosporine?
Page 4346
binds to cyclophilin to inhibit Calcineurin; a cytoplasmicphosphatase. which prevents T cell production of cytokines
that would be produced w/ TCR activation
Page 4347
Q2174:MOA of tacrolimus?
Page 4348
binds to FK-binding protein and inhibits calcineurin; aphosphatase that regulates the ability of activated T cells toproduce cytokines; thus inhibiting this cytokine production
(same action as cyclosporine but diff binding site)
Page 4349
Q2175:MOA of Sirolimus?
Page 4350
ALSO binds to FKBP however it inhibits T cell RESPONSEto Cytokines w/o affecting cytokine production (and potentinhibitor of B cell prolif. antibody product. and mononuclear
cell responses to colony stimulating factors as well)
Page 4351
Q2176:most frequent toxicities of Cyclosporine andTacrolimus?
Page 4352
renal dysfunction; hypertension and neurotoxicity
Page 4353
Q2177:sirolimus is more likely than cyclospoine or tacrolimusto induce this side effect?
Page 4354
HyperTriglyceridemia; hepatotoxicity; diarrhea andmyelosuppression
Page 4355
Q2178:MOA of Mycophenolate Mofetil?
Page 4356
rapidly converted to mycophenolic acid; which inhibitsinosine monophosphate dehydrogenase; an enzyme in the de
novo pathway of purine synthesis. SO this suppressesBOTH B & T cell ACTIVATION
Page 4357
Q2179:toxicity of Mycophenolate mofetil?
Page 4359
Q2180:MOA of Azathioprine?
Page 4360
prodrug transformed to antimetabolie mercaptopurine; whichinhibits enzymes in purine metabolism. It is cytotoxic to early
phase of lymphoid cell proliferation w/ greater effect onTcells than B cells
Page 4361
Q2181:toxicity of azathioprine?
Page 4362
associated with inc incidence of cancer. toxic effects inc byconcomitant use of allopurinol b/c azathio is metabolized by
xanthine oxidase
Page 4363
Q2182:MOA of cyclophosphamide?
Page 4364
transformed by liver enzymes to an alkylating agent that iscytotoxic to proliferating lymphoid cells. greater effect on BCELLS than T cells and will inhibit an estrablished immune
response
Page 4365
Q2183:MOA of etanercept?
Page 4366
recombinant form of TNF receptor that binds TNF-a; aproinflamm cytokine; thereby decreasing formation of IL and
adhesion molecules (used in RA)
Page 4367
Q2184:name two monoclonal antibodies that block the actionsof TNF-alpha?
Page 4368
Infliximab and adalimumab
Page 4369
Q2185:MOA of the RA drug Leflunomide?
Page 4370
arrests lymphocytes in the G1 phase of cell cycle
Page 4371
Q2186:what is thalidomide used for?
Page 4372
Leprosy; SLE; and as an anti-Cancer drug also aphthousulcers and the wasting syndrome in AIDS is treated with the
Rx
Page 4373
Q2187:MOA of thalidomide?
Page 4374
sedative drug notorious for teratogenic effects; ALSOsuppresses TNF production
Page 4375
Q2188:MOA Antilymphocyte globulin and AntithymocyteGlobulin?
Page 4376
selectively block cellular immunity rather than Antibodyformation; which account for their ability to suppress organ
graft rejection; a cell mediated process
Page 4377
Q2189:MOA of RhoD immune globulin?
Page 4378
feedback immunosuppression
Page 4379
Q2190:MOA Muromonab-CD3?
Page 4380
MAb binds to the CD3 antigen on surface of thymocytes andmature T cells and blocks the killing action of CTLs and other
T cell functions
Page 4381
Q2191:MOA of daclizumab?
Page 4382
highly specific MAb that binds to the alpha subunit of the IL-2 receptor expressed on T cells and prevents activation by IL-
2
Page 4383
Q2192:what is the drug that induces remission in treatment-resistant Crohn's disease?
Page 4384
Infliximab (targeted against TNF-alpha)
Page 4385
Q2193:MOA of Aldeslekin?
Page 4386
recombinant IL-2; that promotes production of cytoxic T cellsand activates NK cells - indicated for adjunctive trx of renal
cell carcinoma and malignant melanoma
Page 4387
Q2194:IFN-beta-1b has some beneficial effects in thisrelapsing disorder?
Page 4389
Q2195:what disease is IFN-alpha-2a used for?
Page 4390
hairy cell leukemia; chronic myelogenous leukemia; malignantmealnoma; Kaposi's sarcoma and hep B and C
Page 4391
Q2196:this drug is used for immunization against TB?
Page 4392
BCG (Bacille Calmette-Guerin) (it activates macrophages andresults in enhancement of immune responses)
Page 4393
Q2197:MOA thymosin?
Page 4394
stimulates maturation of pre-T cells in thymusand promotesformation of T cells from lymphoid stem cells (Used in
DiGeorge's syndrome; thymic aplasia)
Page 4395
Q2198:define mechanism of Type 2 hypersensitivity drugallergy?
Page 4396
involves IgG or IgM antibodies that are bound to circulatingblood cells.
Page 4397
Q2199:give examples of type 3 hypersensitivity reactions?
Page 4398
Drug induced serum sickness and vasculitis; stevens johnsonfrom sulfonamide therapy is another
Page 4399
Q2200:examples of type 4 hypersensitivity?
Page 4400
contact dermatitis (cell mediated injury)
Page 4401
Q2201:examples of drugs that commonly cause a type 1hypersens. rxn?
Page 4402
penicillins and sulfonamides
Page 4403
Q2202:DOC for long-term obesity management;MOA;(2) AE
Page 4404
Orlistat;(Inhibits pancreatic lipases);AE;Steatorrhea;GI pain
Page 4405
Q2203:Drug that acts as a short and long-term obesitymanagement;MOA;(2) AE
Page 4406
Sibutramine;(Serotonin and NE reuptakeinhibitor);AE;Tachycardia;HTN
Page 4407
Q2204:Inhibits thyroid hormone synthesis and decreasesperipheral conversion of T4 -> T3;(3) AE
Page 4408
Propylthiouracil (PTU);AE;Aplastic anemia;skinrash;Agranulocytosis (rare)
Page 4409
Q2205:DOC for Turner's syndrome
Page 4410
Somatostatin;(also GH deficiency)
Page 4411
Q2206:What (4) disorders does Octreotide (somatostatinanalog) treat?
Page 4412
"C 8 (Oct)GAG";Carcinoid;;Gastrinoma;;Acromegaly;;Glucagonoma
Page 4413
Q2207:Tx for Central DI
Page 4415
Q2208:Tx for Hypothyroidism;(3) AE
Page 4416
Levothyroxine; Triiodothyronine;AE;Tachycardia;Heatintolerance;Tremors
Page 4417
Q2209:(4) Dx that use Glucocorticoids as Tx;AE?
Page 4418
Addisons Dz;;Inflammation;;Immunesupression;;Asthma;AE: Iatrogenic Cushing's syndrome
Page 4419
Q2210:A 5-alpha-reductase inhibitor used to Tx BPH andpromote hair growth*
Page 4421
Q2211:a Non-steroidal competitive inhibitor of androgens atthe testosterone receptor to Tx prostate CA
Page 4424
Oral birth control
Page 4425
Q2213:(2) drugs that inhibit steroids and are used in PCOS totreat hirsutism
Page 4426
Ketoconazole;;Spironolactone
Page 4427
Q2214:Inhibits cGMP phosphodiesterase causing Inc cGMPand smooth muscle relaxation in corpus cavernosum;(2) AE?
Page 4428
Sildenafil (or Vardenafil);AE;headache;blue-green vision;(headthrobs w/ blue balls)
Page 4429
Q2215:what drug is both an agonist and antagonist toGnRH?;(explain);Use for each?
Page 4430
Leuprolide;Pulsitile fashion: Agonist;(Infertility);Continuous:Antagonist;(prostate cancer)
Page 4431
Q2216:Partial agonist at estrogen receptors in pituitarygland;Use?;AE?
Page 4432
Clomiphene;(prevents Neg feedback to increase LH andFSH);Use;Stimulate Ovulation (infertility Tx);AE;Ovarian
enlargement; multiple preg
Page 4433
Q2217:Competitive inhibitor of Progestins at progesteronereceptor;Use?;(2) AE?
Page 4434
Mifepristone (RU-486);Abortifacient (preventsimplantation);AE;Heavy bleeding;GI upset
Page 4435
Q2218:greatest AE of oral contraception
Page 4436
Hypercoagulable state
Page 4437
Q2219:Tx for hormone replacement therapy andOsteoporosis;(2)
Page 4438
Raloxifene;(SERM);;Estrogen/Progesterone therapy
Page 4439
Q2220:for contraception; what is in Oral; Depo and animplant?
Page 4440
Oral: E2/P4 combo;Depo: Medroxyprogesterone;Implant:Norgestrel
Page 4441
Q2221:DOC for Breast CA w/ estrogen receptors;AE?
Page 4442
Tamoxifen;(SERM);AE: Endometrial hyperplasia
Page 4443
Q2222:what drug class has AE of Acne; decreased HDL;depression; hirsutism; weight gain
Page 4445
Q2223:Drug that activates E2 receptors in Endometrium andblocks them in Breast
Page 4447
Q2224:Drug that activates E2 receptors in bone and blocksthem in Breast and Endometirum
Page 4449
Q2225:DOC for reduction of bone resorption and increasingnew bone formation
Page 4450
Alendronate;(bisphosphonate)
Page 4451
Q2226:MOA of Etidronate
Page 4452
Inhibition of the formation of Hydroxyapatite crystals
Page 4453
Q2227:DOC for Padget's Dz
Page 4455
Q2228:what is the treatment for Tetany following athyroidectomy?
Page 4456
Calcium gluconate
Page 4457
Q2229:What drug is useful in testing endocrinefunction?;How?;MOA
Page 4458
Metyrapone;Tests Pituitary-adrenal axis;Inhibits 11b-OH
Page 4459
Q2230:how do glucocorticoids work as anti-inflammatory andimmunosupressive drugs?
Page 4460
Reduce capillary permeability and edema at the inflam siteand prevent PMNs from entering interstitial space
Page 4461
Q2231:DOC to inhibit Prolactin release
Page 4463
Q2232:Rapid onset insulin form
Page 4465
Q2233:(2) Maintenance forms of insulin (peak 4 - 12 hrs)
Page 4467
Q2234:Longest acting insulin
Page 4469
Q2235:MOA of Sulfonylureas
Page 4470
blocks K+ channels in Beta cell causing opening of Cachannels; releasing insulin from storage vesicles
Page 4471
Q2236:DOC for Rickets or any Vit-D deficiency;MOA
Page 4472
Calcitrol;(enhances intestinal absorption of calcium)
Page 4473
Q2237:DOC androgen derivative for Endometriosis
Page 4474
Danazol;(monitor LFTs)
Page 4475
Q2238:Dx;postmenopausal female develops weakness;polyuria and polydipsia; also mild acidosis and
nephrocalcinosis
Page 4476
Hypervitaminosis D;(too much Vit-D)
Page 4477
Q2239:MOA of PTU
Page 4478
Inhibition of Thyroidal Peroxidase
Page 4479
Q2240:what drug inhibits; by acting as a competitor; theaccumulation of Iodide in thyroid follicular cells?
Page 4480
Potassium Perchlorate
Page 4481
Q2241:what is the Tx for Graves Dz in pregnent woman?
Page 4483
Q2242:Steroid derivative that promotes the synthesis offactors II; VII; IX and X and may interfere w/ effects of
Warfarin or result in thromboemboli?
Page 4484
Ethinyl Estradiol
Page 4485
Q2243:steroid to help promote lung maturity
Page 4487
Q2244:Drug that lowers serum calcium from cancers
Page 4489
Q2245:Octreotide
Page 4490
Properties - Synthetic somatostatin analog givenSQ;Indications - acromegaly; glucagonoma; insulinoma; GI
bleeding; intractable diarrhea
Page 4491
Q2246:Leuprolide
Page 4492
Properties - GnRH analog that inhibits gonadotropin releasewhen given in continuous doses. Given SQ or IM;Indications
- Prostate cancer; PCOS; uterine fibroids; endometriosis.
Page 4493
Q2247:Bromocriptine
Page 4494
Properties - Dopamine receptor agonist. Givenorally;Indications - hyperprolactinemia and associated
infertility and breast ingorgement; inhibit lacation postpartum.Can also be used with octreotide in acromegaly;SE; Tox - N/V;
arrhythmias; hypotension; paranoia/psychosis.
Page 4496
Properties - posterior pituitary hormone. Given IV toinduce/maintain labor; IM to control postpartum bleeding; as
a nasal spray to cause milk secretion.
Page 4497
Q2249:DDAVP (desmopressin)
Page 4498
Properties - analog of ADH with no V1 effects (so no smoothmuscle contraction --> HTN);Indications - central diabetes
insipidus
Page 4499
Q2250:Menotropins
Page 4500
Properties - partially degraded FSH and LH;Indications -induces ovulation in infertile women when followed by HCG.
induces spermatogenesis in infertile men when followingHCG;SE; Tox - overstimulation of ovaries --> multiple
pregnancies; ovarian cysts.
Page 4501
Q2251:Cosyntropin
Page 4502
Properties - a sythetic ACTH analog which is lessantigenic;Indications - Used in the diagnosis of adrenalfunction (failure to respond indicates primary adrenal
disorder).
Page 4503
Q2252:Levothroxine sodium
Page 4504
Properties - levo isomer of T4 given orally or IV. T4 hashalflife of 6-7 days;Indications - hypothyroidism. preferreddrug because cheaper; easier to monitor; and has longer half
life than synthetic T3 drug.
Page 4506
Properties - 50+mg/d will lead to autoinhibition of thyroidhormone production. Blocks uptake of iodide by the glandand diminishes vascularity. Given as Lugol solution (iodineand potassium iodide). Works within 24 hours;Indications -given preop to shrink the gland before surgical removal; as tx
for thyroid storm. NOT long term;SE; Tox - dose-related.hypersensitivity; head cold symptoms; gastric irritation;parotitis. long-term use --> sudden disinhibition --> acute
hyperparathyroidism.
Page 4507
Q2254:Propylthiouricil (PTU) and methimazole
Page 4508
Class - Thioamides;Properties - inhibit the peroxidaseenyzmes (oxidation of iodide and coupling of iodinatedtyrosyl groups) --> decreased hormone synthesis. Also
inhibits peripheral T4 --> T3. Onset of action after performedhormones have been metabolized;Indications - control of
hyperthyroidism until surgery; until the effect of radioactiveiodide begins; and long-term therapy for mild-moderate cases.
PO;SE; Tox - maculopapular rash; joint pain; headache;nausea; hair loss. Rare; serious agranulocytosis. Can crossplacenta and enter breast milk; PTU is more protein-bound
therefore less likely to do so.
Page 4509
Q2255:Radioactive Iodine
Page 4510
Properties - Either PO or IV; it is taken up rapidly by thethyroid --> thyroglobulin. Causes destruciton of the gland byemission of beta particles with minimal damage to surroundingtissue;Indications - hyperthyroidism;SE; Tox - overdosage -->
delayed hypothyroidism;CI - pregnancy.
Page 4511
Q2256:Calcitonin
Page 4512
Properties - lowers serum calcium; inhibits bone resorption;blocks Ca; phosphate release from bone;Indications -
hypercalcemia; hyperPTH; vitamin D toxicity; Paget disease;bone tumors; osteoporosis;SE; Tox - hypersensitivity rxns;
hypocalcemia
Page 4513
Q2257:Vitamin D
Page 4514
Indications - hypocalcemia due to rickets; hypoPTH;osteomalacia;SE; Tox - hypercalcemia
Page 4515
Q2258:Diphosphonates
Page 4516
Properties - analogs of pyrophosphate bind tohydroxyapatite crystals and reduce their formation; growth;
and dissolution --> less bone turnover;Indications -hypercalcemia of malignancy; Page disease; osteoporosis;
hyperPTH
Page 4517
Q2259:Sulfonylureas
Page 4518
Examples - Tolbutamide; chlorpropamide; glyburide;glipizide;Properties - stimulates insulin release by closing Kchannels in beta cell membrane --> depol --> Ca influx and
insulin release;Indications - NIDDM;SE; Tox - hypoglycemiaesp. with long-acting chlorpropamide and high-potency
glyburide and glipizide; skin rashes; GI upset;hypothyroidism; disulfiram-like reaction; esp with
chlorpropamide
Page 4519
Q2260:Metformin
Page 4520
Properties - mechanism unknown; possibly inhibitsgluconeoneogenesis; increases glycolysis --> decreased serum
glucose levels;Indications - NIDDM; don't need isletfunction;SE; Tox - NO hypoglycemia; can result in lactic
acidosis
Page 4521
Q2261:Glitazones or Thiazolidinediones (the longest nameEVER)
Page 4522
Examples - Pioglitazone; risiglitazone;Properties - increasetarget cell response to insulin. can be used alone or with other
agents;SE; Tox - weight gain; troglitazone is hepatotoxic
Page 4523
Q2262:Repaglinide
Page 4524
Properties - sulfonylurea-like; stimulates insulin release
Page 4526
Properties - inhibits alpha -glucosidase of brush border andprevents asorption of glucose;SE; Tox - GI discomfort
Page 4527
Q2264:Short acting insulins?
Page 4528
insulin; lispro
Page 4529
Q2265:intermediate insulins?
Page 4531
Q2266:long acting insulins?
Page 4532
lente; ultralente
Page 4533
Q2267:MOA of insulin?
Page 4534
liver (increased glucose stored as glycogen) Muscle (increasedglycogen and protein synth; K uptake) Fat (aids TG storage)
Page 4535
Q2268:Uses of insulin other than DM1?
Page 4536
life threatening hyperkalemia and stress inducedhyperglycemia
Page 4537
Q2269:Insulin toxicity?
Page 4538
hypoglycemi; hypersensitivity rxn (very rare)
Page 4539
Q2270:Name the first generation sulfonylureas.
Page 4540
tolbutamide; chlorpropamide
Page 4541
Q2271:name the second generation sulfonylureas.
Page 4542
glyburide; glimeperide; glipizide
Page 4543
Q2272:MOA of sulfonylureas.
Page 4544
close K channel in beta cell membrane so cell depolarizes…triggers insulin release via increased Ca influx
Page 4545
Q2273:Are sulfonylureas good for DM1; DM2 or both?
Page 4546
DM2. (useless in DM1 b/c needs some islet fxn)
Page 4547
Q2274:First generation sulfonylureas toxicities?
Page 4548
disulfiram-like effects
Page 4549
Q2275:Second generation sulfonylurea toxicity?
Page 4551
Q2276:What class of drugs is metformin?
Page 4553
Q2277:Probable MOA of metformin?
Page 4554
decreased GNG; increased glycolysis; decreased serumglucose
Page 4555
Q2278:Metformin for DM1; DM2 or both?
Page 4557
Q2279:Metformin toxicity?
Page 4558
lactic acidosis (contraindicated in renal insufficiency; CHF;elderly)
Page 4559
Q2280:MOA of glitazones?
Page 4560
increased target cell response to insulin
Page 4561
Q2281:Glitazones; DM1; DM2 or both?
Page 4563
Q2282:Glitazone toxicities/
Page 4564
weight gain; CHF (fluid retention); (troglitazone ishepatotoxic)
Page 4565
Q2283:name two alpha glucosidase inhibitors.
Page 4566
acarbose; miglitol
Page 4567
Q2284:alpha glucosidase inhibitor MOA?
Page 4568
inhibit intestinal brush border alpha glucosidases (delayedsugar hydrolysis and glucose absorption lead to decreased
postpradial hyperglycemia)
Page 4569
Q2285:alpha glucosidase inhibitor toxicity?
Page 4571
Q2286:Orlistat MOA?
Page 4572
alters fat metabolism by inhibiting pancreatic lipases
Page 4573
Q2287:Indications for orlistat?
Page 4574
long term obesity management
Page 4575
Q2288:Orlistat toxicities?
Page 4576
steatorrhea; GI discomfort; reduced absorption of fat solublevitamins; HA
Page 4577
Q2289:Sibutramine MOA?
Page 4578
sympathomimetic SNRI
Page 4579
Q2290:Indication for sibutramine?
Page 4580
short-term and long term obesity management
Page 4581
Q2291:Sibutramine toxicity?
Page 4582
HTN; tachycardia
Page 4583
Q2292:Propylthiouracil; methimazole MOA?
Page 4584
inhibit organification and coupling of thyroid hormonesynthesis. Propylthiouracil also decreases peripheral
conversion of T4 to T3
Page 4585
Q2293:Indications for propylthiouracil or methimazole?
Page 4586
hyperthyroidism
Page 4587
Q2294:Toxicities of propylthiouracil and methimazole?
Page 4588
skin rash; agranulocytosis (rare); aplastic anemia
Page 4589
Q2295:Indication for somatostatin?
Page 4590
GH deficiency; turner's syndrome
Page 4591
Q2296:Indication for octreotide?
Page 4592
acromegaly; carcinoid; gastrinoma; glucagonoma
Page 4593
Q2297:Indication for oxytocin?
Page 4594
stimulates labor; uterine contractions; milk let-down; controlsuterine hemorrhage
Page 4595
Q2298:Indication for desmopressin?
Page 4596
Central (not nephrogenic) DI
Page 4597
Q2299:Uses of levothyroxine; triiodothyroxine?
Page 4598
hypothyroidism; myxedema
Page 4599
Q2300:Levothyroxine; triiodothyroxine toxicity?
Page 4600
tachycardia; heat intolerance; tremors
Page 4601
Q2301:What kind of drug is triamcinolone?
Page 4603
Q2302:MOA of glucocorticoids?
Page 4604
decreased production of leukotrienes/prostaglandins byinhibiting PLA2 and COX-2 expression
Page 4605
Q2303:Uses of glucocorticoids?
Page 4606
addison's; inflammation; immune suppression; asthma
Page 4607
Q2304:Glucocorticoid toxicity?
Page 4608
iatrogenic cushings (buff hump; moon facies; truncal obesity;muscle wasting; thin skin; easy bruisability; osteoporosis;
adrenocortical atrophy; peptic ulcers)
Page 4609
Q2305:Action and use of Finasteride?
Page 4610
5alpha-reductase inhibitor (decreased conversion oftestosterone to dihydrotestosterone). Used for BPH and
baldness
Page 4611
Q2306:Action and use of Flutamide?
Page 4612
nonsteroidal competitive inhibitor of androgens at thetestosterone receptor. Used in prostate ca
Page 4613
Q2307:Action and use of ketoconazole?
Page 4614
inhibit steroid synth; used in polycystic ovarian syndrome toprevent hirsutism
Page 4615
Q2308:Action and use of spironolactone?
Page 4616
inhibit steroid synth; used in polycystic ovarian syndrome toprevent hirsutism
Page 4617
Q2309:MOA of sildenafil/vardenafil?
Page 4618
inhibit cGMP phosphodiesterase causing increased cGMP;smooth musc relax in corpus cavernosum; increased blood
flow and erection
Page 4619
Q2310:Use of sildenafil/vardenafil?
Page 4620
treatment of erectile dysfxn
Page 4621
Q2311:Toxicity of sildenafil/vardenafil?
Page 4622
HA; flushing; dyspepsia; blue-green color vision. Risk of life-threatening hypotension in pts taking nitrates
Page 4623
Q2312:MOA of leuprolide?
Page 4624
GnRH analog w/agonist properties when used in pulsatilefashion; antagonist properties when used in continuous
fashion (continous causes transient initial burst of LH andFSH)
Page 4625
Q2313:Use of leuprolide?
Page 4626
infertility (pulsatile); prostate ca (continuous w/flutamide);unterine fibroids
Page 4627
Q2314:Toxicity of leuprolide?
Page 4628
antiandrogen; N/V
Page 4629
Q2315:MOA of clomiphene?
Page 4630
partial agonist at estrogen receptors in pituitary gland.Prevents nrm feedback inhibition and increases release of LH
and FSH from pituitary…stimulates ovulation
Page 4631
Q2316:Use of clomiphene?
Page 4632
tx of infertility
Page 4633
Q2317:Toxicity of clomiphene?
Page 4634
hot flashes; ovarian enlargement; multiple simultaneouspregnancies; visual disturbances
Page 4635
Q2318:MOA of mifepristone (ru-486)?
Page 4636
competitive inhibitor of progestins at progesterone receptors
Page 4637
Q2319:Use of mifepristone?
Page 4638
abortifactant (prevents implantation)
Page 4639
Q2320:Toxicity of mifepristone (ru-486)?
Page 4640
heavy bleeding; GI effects (N/V; anorexia); ab pain
Page 4641
Q2321:Advantages of oral contraceptives (5)?
Page 4642
reliable; decreased risk of endometrial/ovarian ca; decreasedrisk ectopic preg; decreased pelvic infxn; regulation of menses
Page 4643
Q2322:Disadvantages of oral contraception (5)?
Page 4644
taken daily; no STD protection; increased triglycerides;depression/wt gain/nausea/HTN; hypercoaguable state
Page 4645
Q2323:Which drugs cause gynecomastia as a side effect?
Page 4646
Some Drugs Create Awesome Knockers! - Spironolactone;Digitalis; Cimetidine; Alcohol; Ketoconazole
Page 4647
Q2324:Finasteride use and mechanism
Page 4648
used for BPH and male-pattern baldness; blocks 5-alpha-reductase to prevent conversion of T to DHT
Page 4649
Q2325:Flutamide use and mechanism
Page 4650
nonsteroidal competitive inhibitor of androgens. blocks Treceptor. Used in prostate carcinoma
Page 4651
Q2326:Kotoconazole use and mechanism
Page 4652
inhibits steroid synthesis; used in treatment of polycysticovarian syndrome to prevent hirsutism
Page 4653
Q2327:Spironolactone use and mechanism
Page 4654
inhibits steroid binding; used in Polycystic ovarian syndrometo prevent hirsutism
Page 4655
Q2328:Mechanism of Leuprolide?
Page 4656
GnRH analog with agonist properties when used in pulsatilefashion. Antagonist when used continuously.
Page 4657
Q2329:Uses of Leuprolide?
Page 4658
Infertility (pulsatile); prostate cancer (continuous use withflutamide); uterine fibroids
Page 4659
Q2330:Toxicity of Leuprolide?
Page 4660
antiandrogen; nausea; vomiting
Page 4661
Q2331:Sildenafil; Vardenafil mechanism
Page 4662
Inhibits cGMP phosphodiesterase --> increased cGMP -->smooth muscle relaxation in corpus cavernosum --> increased
blood flow --> PENILE ERECTION!
Page 4663
Q2332:Toxicity of Sildenafil and Vardenafil?
Page 4664
HA; flushing; dyspepsia; impaired blue-green color vision.DO NOT USE WITH NITRATES!!! causes hypotension
Page 4665
Q2333:mechanism of Mifepristone (RU-486)?
Page 4666
competitive inhibitor of progestins at progesterone receptors
Page 4667
Q2334:clinical use of mifepristone
Page 4668
termination of pregnancy. used with misoprostol (PGE1)
Page 4669
Q2335:toxicity of mifepristone
Page 4670
heavy bleeding; GI effects (nausea; vomiting; anorerxia);abdominal pain
Page 4671
Q2336:advantages of OCPs?
Page 4672
decreased risk of endometrial and ovarian cancer; decreasedincidence of ectopic pregnancy; decreased pelvic infections;
regulation of menses
Page 4673
Q2337:disadvantages of OCPs?
Page 4674
no protection against STDs; increased triglycerides;depression; weight gain; nausea; hypertension;
hypercoagulable state
Page 4675
Q2338:What is Dinoprostone?
Page 4676
PGE2 analog causing cervical dilation and uterine contraction;inducing labor
Page 4677
Q2339:Ritodrine/Terbutaline are what?
Page 4678
B2 agonists that relax the uterus
Page 4679
Q2340:What is anastrozole?
Page 4680
aromatase inhibitor used in postmenopausal women withbreast cancer.
Page 4681
Q2341:What are the toxicities of estrogens (ethinyl estradiol;DES; mestranol)
Page 4682
increased risk of endometrial cancer; bleeding inpostmenopausal women; clear cell adenocarcinoma of vaginain females exposed to DES in utero; increased risk of thrombi
Page 4683
Q2342:What is the toxicity of testosterone?
Page 4684
masculinization in females; reduces intratesticular testosteronein males by inhibiting Leydig cells; leads to gonadal atrophy.
premature closure of epiphyseal plates. increased LDL;decreased HDL
Page 4685
Q2343:Mechanism of Clomiphene?
Page 4686
partial agonist at estrogen receptors in pituitary gland.prevents normal feedback inhibition and increased release of
LH and FSH from pituitary; which stimulates ovulation
Page 4687
Q2344:Uses of Clomiphene?
Page 4688
treat infertility and PCOS.
Page 4689
Q2345:toxicity of clomiphene?
Page 4690
hot flashes; ovarian enlargement; multiple pregnancies; visualdisturbances
Page 4691
Q2346:mechanism of Tamoxifen?
Page 4692
estrogen antagonist on breast tissue. used to preventrecurrence of ER-positive breast cancer
Page 4693
Q2347:mechanism and use of Raloxifene?
Page 4694
estrogen agonist on bone; reduces reabsorption of bone; usedto treat osteoporosis
Page 4695
Q2348:MOA of mannitol
Page 4696
(osmotic diuretic); increases tubular fluid osmolarity; therebyincreasing urine flow
Page 4697
Q2349:Clinical uses of mannitol
Page 4698
shock; drug OD; to decrease intracranial/intraocular P
Page 4699
Q2350:MOA acetazolamide
Page 4700
carbonic anhydrase inhibitor; causes self-limited NaHCO3diuresis and reduction in total-body bicarb stores
Page 4701
Q2351:Clinical uses of acetazolamide
Page 4702
glaucoma; urinary alkalinization; metabolis alkalosis; altitutesickness
Page 4703
Q2352:toxicities of acetazolamide
Page 4704
hyperchloremic metabolic acidosis; neuropathy; NH3toxicity; sulfa allergy
Page 4705
Q2353:MOA of ethacrynic acid
Page 4706
(diuretic); phenoxyacetic acid derivative--NOT sulfonamide--that works like furosemide (loop diuretic)
Page 4707
Q2354:Clinical use of ethacrynic acid
Page 4708
diuresis in pts with sulfa allergy (b/c NOT a sulfonamide)
Page 4709
Q2355:toxicity of ethacrynic acid
Page 4710
similar to furosemide (OH DANG) but can be used inhyperuricemia and no sulfa allergy
Page 4711
Q2356:MOA of furosemide
Page 4712
sulfonamide loop diuretic; inhibits Na-K-2Cl contransporterof thick ascending limb; abolishes hypertonicity of medulla
which prevents concentration of urine; increases Ca excretion
Page 4713
Q2357:toxicity of furosemide
Page 4714
OH DANG! Ototoxicty; Hypokalemia; Dehydration;Allergy; Nephritis (interstitial); Gout
Page 4715
Q2358:MOA hydrochlorothiazide
Page 4716
thiazide loop diuretic. Inhibits NaCl reabsorption in earlydistal tubule which reduces diluting capacity of nephron.
Page 4717
Q2359:thiazide diuretics vs. loop diuretics with respect tocalcium?
Page 4718
loop diuretics (furosemide; ethacrynic acid)--increase Caexcretion; thiazides DECREASE Ca excretion.
Page 4719
Q2360:4 K+ sparing diuretics
Page 4720
spironolactone; triamterene; amiloride; eplereone
Page 4721
Q2361:MOA of spironolactone
Page 4722
competitive aldosterone R antagonist in cortical collectingtubule
Page 4723
Q2362:MOA of triamterene
Page 4724
(K+sparer) block Na channels in CCT (same as amiloride)
Page 4725
Q2363:MOA of amiloride
Page 4726
(K+sparer) blocks Na channels in CCT (same as triameterene)
Page 4727
Q2364:Clinical use of K+ sparing diuretics
Page 4728
hyperaldosteronism; K+ depletion; CHF
Page 4729
Q2365:toxicity of K+ sparing diuretics
Page 4730
hyperkalemia; endocrine effects (eg. Spironolactone--gynecomastia; antiandrogenics)
Page 4731
Q2366:which diuretics decrease the blood pH (more acidic)
Page 4732
carbonic anhydrase inhibitors (acetazolamide); K+ sparers(spironolactone; triamterene; amiloride; eplererone)
Page 4733
Q2367:which diuretics increase blood pH (make more basic)
Page 4734
loop diuretics (furosemide; ethacrynic acid); thiazides
Page 4735
Q2368:3 AcE inhibitors
Page 4736
captopril; enalapril; lisinopril
Page 4737
Q2369:MOA of ACE inhibitors
Page 4738
inhibit angiotensin converting enzyme which reduces levels ofangiotensin II and prevents inacitvation of bradykinin (potent
vasodilator); renin release increased b/c of lack of feedbackinhibition
Page 4739
Q2370:effect of ACE inhibitors on renin release?
Page 4740
renin release increased due to loss of feedback inhibition
Page 4741
Q2371:Clinical uses of ACE inhibitors
Page 4742
HTN; CHF; diabetic renal disease
Page 4743
Q2372:toxicities of ACE inhibitors
Page 4744
CAPTOPRIL: cough; angioedema; proteinuria; taste changes;hypOtension; preggers problems; rash; increased renin; lower
angiotension II. Also hyperkalemia.
Page 4745
Q2373:can ACE inhibitors be used in bilateral renal arterystenosis?
Page 4747
Q2374:Why am I so frightened right now?
Page 4748
Cuz the man who lives in our fridge is making really angrynoises and there's a moth that keeps flying into my head.
Page 4749
Q2375:Democlocycline
Page 4750
Properties - antagonizes ADH ;Indications - SIADH.
Page 4751
Q2376:Drugs that cause SIADH
Page 4752
carbamazepine (seizures; manic) TCAs; thiazides;phenothiazines (neuroleptics?); chlorpropamide (sulfonylura
for DM); cisplatin (anti-neoplastic)
Page 4753
Q2377:Pulmonary infiltrations inducing drugs
Page 4754
"Go BAN Me!";Gold;Bleomycin/ Busulphan/BCNU;Amiodarone/ Acyclovir/
Azathioprine;Nitrofurantoin;Melphalan/ Methotrexate/Methysergide
Page 4755
Q2378:Respiratory depression inducing drugs
Page 4756
"STOP breathing";Sedatives andhypnotics;Trimethoprim;Opiates;Polymyxins
Page 4757
Q2379:Monoamine oxidase inhibitors: members
Page 4758
"PIT of despair";Phenelzine;Isocarboxazid;Tranylcypromine;·A pit of despair; since MAOs treat depression.
Page 4759
Q2380:Gynaecomastia-causing drugs
Page 4760
DISCOS;Digoxin;Isoniazid;Spironolactone;Cimetidine;Oestrogens;Stilboestrol
Page 4761
Q2381:Sulfonamides: common characteristics
Page 4762
SULFA;Steven-Johnson syndrome/ Skin rash / Solubilitylow;Urine precipitation/ Useful for UTI;Large spectrum (grampositives and negatives);Folic acids synthesis blocker (as well
as synthesis of nucleic acids);Analog of PABA
Page 4763
Q2382:Muscarinic effects
Page 4764
SLUG BAM;Salivation/ Secretions/Sweating;Lacrimation;Urination;Gastrointestinalupset;Bradycardia/ Bronchoconstriction/ Bowelmovement;Abdominal cramps/ Anorexia;Miosis
Page 4765
Q2383:Clopidogrel: use
Page 4766
CLOPIdogrel is a drug that prevents ;CLots; an Oral PlateletInhibitor (OPI).
Page 4767
Q2384:Morphine: side-effects
Page 4768
MORPHINE;Myosis;Out of it (sedation);Respiratorydepression;Pneumonia (aspiration);Hypotension;Infrequency
(constipation; urinary retention);Nausea;Emesis
Page 4769
Q2385:Methyldopa: side effects
Page 4770
METHYLDOPA;Mental retardation;Electrolyteimbalance;Tolerance;Headache/ Hepatotoxicity;psYcological
upset;Lactation in female;Drymouth;Oedema;Parkinsonism;Anaemia (haemolytic)
Page 4771
Q2386:4-Aminopyradine (4-AP) use
Page 4772
4-AP is For AP";For AP (action potential) propagation inMultiple Sclerosis
Page 4774
L- lithium intox;M-metallic taste; movement disorders;N-nephrogenic diabetes insipidus;O - hypothyroidism;P - contra
in pregnancy
Page 4775
Q2388:Calcium chelator
Page 4777
Q2389:Brown teeth
Page 4779
Q2390:Gray-baby syndrome
Page 4780
Chloramphenicol
Page 4781
Q2391:Oto- and nephrotoxicity
Page 4782
Vancomycin; aminoglycosides
Page 4783
Q2392:Optic neuritis
Page 4785
Q2393:Polyarthralgia
Page 4787
Q2394:Induces cytochrome P450
Page 4789
Q2395:Red-man syndrome
Page 4791
Q2396:Pseudomembranous colitis
Page 4793
Q2397:Kernicterus
Page 4795
Q2398:Megaloblastic anemia (supplement with vitamin B6)
Page 4796
Trimethoprim-sulfamethoxazole
Page 4797
Q2399:Cartilage damage; tendonitis
Page 4798
Fluoroquinolones
Page 4799
Q2400:Orange bodily fluids
Page 4801
Q2401:Fast vs. slow acetylators
Page 4803
Q2402:Infusion-related toxicity
Page 4805
Q2403:D-Ala-D-Ala
Page 4809
Q2405:Blocks peptidyltransferase
Page 4810
Chloramphenicol
Page 4811
Q2406:Blocks peptide bond formation
Page 4813
Q2407:Blocks ribosomal translocation by preventing exit oftRNA
Page 4815
Q2408:Inhibits initiation complex; causes mRNA misreading;blocks translocation
Page 4816
Aminoglycosides
Page 4817
Q2409:Blocks tRNA binding to ribosome
Page 4819
Q2410:Bactericidal for H. flu; S. pneumo; N. meningitidis
Page 4820
Chloramphenicol
Page 4821
Q2411:Blocks initiation step of protein synthesis
Page 4823
Q2412:PABA analogue
Page 4825
Q2413:Prevents synthesis of dihydrofolic acid
Page 4827
Q2414:Inhibits dihydropteroate synthetase
Page 4829
Q2415:Prevents synthesis of tetrahydrofolic acid
Page 4831
Q2416:Inhibits dihydrofolate reductase
Page 4833
Q2417:Resistance is due to rRNA methylation
Page 4834
Clindamycin; macrolides
Page 4835
Q2418:DNA gyrase; topoisomerase IV
Page 4836
Fluoroquinolones
Page 4837
Q2419:RNA polymerase
Page 4839
Q2420:Inhibits mycolic acid synthesis
Page 4841
Q2421:Inhibits arabinogalactan synthesis
Page 4843
Q2422:Inhibits microtubule function
Page 4845
Q2423:Inhibits beta(1;3)D-glucan synthetase
Page 4847
Q2424:Binds ergosterol
Page 4848
Amphotericin B; nystatin
Page 4849
Q2425:Inhibits lanosterol demethylation by cytochrome P450
Page 4851
Q2426:Inhibits thymidylate synthase
Page 4853
Q2427:Used to treat cryptococcal meningitis
Page 4855
Q2428:Used for meningococcal prophylaxis
Page 4857
Q2429:Used to treat Pseudomonas infection in CF patients
Page 4858
Fluoroquinolones
Page 4859
Q2430:Used to treat nocardiosis
Page 4861
Q2431:Used to treat VRE; MRSA; PRSP
Page 4863
Q2432:Used to treat C. perfringens and B. fragilis
Page 4865
Q2433:Used to treat Mycoplasma pneumoniae
Page 4867
Q2434:Used to treat chlamydia
Page 4869
Q2435:Used to treat Legionella
Page 4871
Q2436:Used to treat gonorrhea
Page 4873
Q2437:Used to treat H. flu meningitis
Page 4874
Chloramphenicol
Page 4875
Q2438:Agranulocytosis;(2)*
Page 4876
Clozapine;Carbamazepine;[AGRANny parked her CAR-BAM in the CLOZet]
Page 4877
Q2439:Aplastic Anemia;(3)
Page 4878
Chloramphenicol;NSAIDs;Benzene
Page 4879
Q2440:Atropine-like Side Effects;(sedation; seizures; coma;anticholinergic effects; arrhythmias)
Page 4881
Q2441:Cardiotoxicity;(2)
Page 4882
Doxorubicin;Daunorubicin;[double D "Rubis" are a "sin" forthe chest]
Page 4883
Q2442:Cartilage Damage in children
Page 4884
Fluoroquinolones (Ciprofloxacin)
Page 4885
Q2443:Cinchonism (HA; tinnitus);and;Torsades de pointes
Page 4889
Q2445:Diabetes Insipidus
Page 4891
Q2446:Disulfiram-like effect;and;Metallic taste
Page 4893
Q2447:Extrapyramidal Side Effects
Page 4894
Antipsychotics;Typical > Atypical;(Thioridazine;Haloperidol; Chlorpromazine)
Page 4895
Q2448:Fanconi’s Syndrome;(growth failure; rickets;dehydration)
Page 4897
Q2449:Gingival Hyperplasia
Page 4898
Phenytoin;;[PHEN he's TOYIN' w/ GINGer]
Page 4899
Q2450:Gray Baby Syndrome
Page 4900
Chloramphenicol
Page 4901
Q2451:Gynecomastia;(6)*
Page 4902
Some Excellent Drugs Create AwesomeKnockers;Spirolactone;Estrogens;Digitalis;Cimetidine;Alcohol
(chronic);Ketoconazole
Page 4903
Q2452:Hemolytic Anemia in G6PD-deficiency;(5)*
Page 4904
C'PISA;Chloramphenicol;Primaquine;Isoniazid;Sulfonamides;Aspirin;[AN ENEMIA (enemy) and 6 PDs knocked down
C'PISA]
Page 4905
Q2453:Hepatitis
Page 4907
Q2454:Hot Flashes; Flushing;(3)*
Page 4908
No Cold Temp;Niacin;Calcium Channel Blockers;Tamoxifen
Page 4909
Q2455:Induce CP450;(6)*
Page 4910
Queen Barb takes Phen-phen & Refuses Greasy Carbs;-Quinidine;- Barbiturates;- Phenytoin;- Rifampin;-
Griseofulvin;- Carbamazepine
Page 4911
Q2456:Inhibit CP450;(8)*
Page 4912
Inhibitors Stop Cyber Kids From Eating Grapefruit Salad;-Isoniazid;- Sulfonimides;- Cimetidine;- Ketoconazole;- FQ
(Ciprofloxacin);- Erythromycin;- Grapefruits/St. Johns Wort
Page 4913
Q2457:Interstitial Nephritis
Page 4915
Q2458:What is Monday Disease?;Cause?
Page 4916
- Nitroglycerin Industrial exposure -> tolerance during week -> loss of tolerance during weekend -> headache; tach;
dizziness upon re-exposure
Page 4917
Q2459:Orange Body Fluids
Page 4919
Q2460:Osteoporosis;(2)
Page 4920
Heparin;Corticosteroids
Page 4921
Q2461:Positive Coombs’ Test
Page 4923
Q2462:Pulmonary Fibrosis;(2)*
Page 4924
Amiodarone;Bleomycin;[AMY cant BLEOw anymore]
Page 4925
Q2463:Red Man Syndrome;(histamine release)*
Page 4926
Vancomycin;[red mAN vAN]
Page 4927
Q2464:Severe HTN with Tyramine;and;Serotonin syndrome(w/ meperidine)
Page 4929
Q2465:SLE-like Syndrome / Drug-induced Lupus;(7)*
Page 4930
Lupus Quickly Moaned In Pain - His Penis Cracked;-Quinidine;- Methyldopa;- INH;- Procainamide;-Hydralazine;- Penicillamine;- Chlorpromazine
Page 4931
Q2466:Tardive Dyskinesia
Page 4932
- Antipsychotics ;(Thioridazine; Haloperidol;Chlorpromazine)
Page 4933
Q2467:Tinnitus;(2)*
Page 4934
Aspirin;Quinidine;[ApirIN for QuIN-tIN Tinnitus]
Page 4935
Q2468:Torsades de pointes;(2 classes)
Page 4936
Class III;Class IA antiarrhythmics
Page 4937
Q2469:fetal Spina Bifida
Page 4938
Valproic Acid;[no folIC ACID or valproIC ACID]
Page 4939
Q2470:fetal Renal Dysgenesis -> death;(2)
Page 4940
ACE inhibitors;ARB
Page 4941
Q2471:Arrhythmias and Yellow visual changes
Page 4943
Q2472:Acute cholestatic Hepatitis
Page 4945
Q2473:Massive Hepatic Necrosis;(4)*
Page 4946
A Hepatic Ending Varies;- Acetaminophen;- Halothane;-Ethanol;- Valproic acid
Page 4947
Q2474:Livedo Reticularis;(patchy swollen blood vessels onlegs with cold)
Page 4949
Q2475:Thyroid toxicity;(2)
Page 4950
Lithium;Amiodarone
Page 4951
Q2476:Severe rebound HA and HTN;dry mouth
Page 4953
Q2477:Hemorrhagic Cystitis;Myelosuppression
Page 4954
Cyclophosphamide
Page 4955
Q2478:Photosensitivity;(3)*
Page 4956
SAT for a photo;- Sulfonamides;- Amiodarone;- Tetracycline
Page 4957
Q2479:Stevens-Johnson syndrome;(2)
Page 4958
Sulfonamides;Ethosuximide
Page 4959
Q2480:Seziures;(3)*
Page 4960
Impending Big Chills;- Imipenem;- Bupropion;- Cilastatin
Page 4961
Q2481:Retinal Toxicity
Page 4962
- Chloroquine;[CHLORine in pools hurts eyes]
Page 4963
Q2482:both Nephrotoxicity & Ototoxicity;(3)
Page 4964
Aminoglycosides;Loop diuretics;Cisplatin;[an ALCoholiccant hear well and urinates a lot]
Page 4965
Q2483:Priapism ;(prolonged erection w/o sexual stimulation)
Page 4966
Trazodone;(anti-depressant)
Page 4967
Q2484:Erectile dysfunction;(3 classes)*
Page 4968
No Tone Bone;- Neuroleptics;- TCAs;- Beta-blockers
Page 4969
Q2485:Malignant Hyperthermia
Page 4970
Succinylcholide
Page 4971
Q2486:Enhances erections
Page 4972
- Dopamine agonist;[it's DOPE AGain to get a big erection]
Page 4973
Q2487:atropine-like side effects
Page 4975
Q2488:cardiac toxicity
Page 4976
doxorubicin; daunorubicin
Page 4977
Q2489:coronary vasospasm
Page 4979
Q2490:cutaneous flushing
Page 4980
niacin (lipid lowerer; increases HDL); CCB; adenosine;vancomycin (red man syndrome!)
Page 4981
Q2491:torsades de pointes
Page 4982
class III antiarrythm (sotalol); class IA antiarrhythm.(quinidine); cisapride
Page 4983
Q2492:agranulocytosis (3)
Page 4984
clozapine (atypical antipsych; least EPS); carbamazepine(AED; mood stabilizer; P450 inducer); colchicine
Page 4985
Q2493:aplastic anemia
Page 4986
chloramphenicol; benzene; NSAIDs; also: propylthioracil;methimazole (inhibit organificatin and coupling of thyroid
hormone synth)
Page 4987
Q2494:gray baby syndrome
Page 4988
(ab distention; progressive pallid cyanosis; vasomotorcollapse) chloramphenicol (binds 50s; inhibits
peptidlytransferase)
Page 4989
Q2495:hemolysis in G6PD deficient pts
Page 4990
sulfonamides; INH; aspirin; ibuprofen; primaquine;nitrofurantoin (abx)
Page 4991
Q2496:thrombotic complications
Page 4994
ace inhibitors (bradykinin!)
Page 4995
Q2498:pulmonary fibrosis
Page 4996
bleomycin (induces free radical formation; for testicularcacner; lymphomas--ABVD regimen); amiodarone (class IAantiarrhthm); busulfan (alkylates DNA; CML; also causes
hyperpigmentation)
Page 4997
Q2499:acute cholestatic hepatitis
Page 4998
macrolides (dont give to preggers!)
Page 4999
Q2500:focal to massive hepatic necrosis
Page 5000
halothane (inhaled anesthetic); valproic acid; acetaminophen;Amanita phalloides (mushroom poison alpha amanitin--
>inhibits euk RNA pol)
Page 5001
Q2501:gynecomastia
Page 5002
Some Drugs Create AwesomE Knockers--Spironolactone;Digitalis; Cimetidine; Alcohol chronique; Estrogens;
Ketoconazole
Page 5003
Q2502:gingival hyperplasia
Page 5005
Q2503:osteoporosis
Page 5006
corticosteroids; heparin
Page 5007
Q2504:photosensitivity
Page 5008
sulfonamides; amiodarone; tetracycline; also 5-FU
Page 5009
Q2505:SLE-like syndrome
Page 5010
hydralazine (antiHTN for preggers; stim cGMP); INH;procainamide (Class IA antiarrh.); phenytoin
Page 5011
Q2506:Fanconi's syndrome
Page 5012
expired tetracycline
Page 5013
Q2507:interstitial nephritis
Page 5014
methicillin; also acute interstitial nephritis: NSAIDs; betalactams; sulfa diuretics; phenytoin; cimetidine; methyldopa
Page 5015
Q2508:hemorrhagic cystitis
Page 5016
cyclophosphamide; ifosfamide
Page 5017
Q2509:diabetes insipidus
Page 5018
lithium; demeclocycline
Page 5020
bupropion (heterocyclic antidepressant; no sexual sideeffects); imipenem/cilastin
Page 5021
Q2511:disulfiram-like reaction
Page 5022
metronidazole; some cephalosporins; procarbazine(antineoplastic alkylator); sulfonylureas
Page 5023
Q2512:nephrotoxicity/neurotoxicity
Page 5025
Q2513:nephrotoxicity/ototoxicty
Page 5026
aminoglycosides; loop diuretics; cisplatin
Page 5027
Q2514:Acetaminophen: Antidote
Page 5028
N-acetylcysteine
Page 5029
Q2515:Salicylates: Antidote
Page 5030
Alkalnize urine; dialysis
Page 5031
Q2516:Anticholinesterases; organophosphates: Antidote
Page 5032
Atropine; Pralidoxime
Page 5033
Q2517:Antimuscarinic (Atropine); anticholinergics: Antidote
Page 5034
Physostigmine (AChE inhibitors)
Page 5035
Q2518:B-blockers: Antidote
Page 5037
Q2519:Digitalis: Antidote
Page 5038
1. Stop digitalis;2. Normalize K+;3. Lidocaine;4. Mg2+;5.anti-dig Fab fragments
Page 5039
Q2520:Iron: Antidote
Page 5041
Q2521:Lead: Antidote
Page 5042
- CaEDTA; Dimercaprol (1st line for adults);- Succimer (kids- "sucks" to be a kid with lead poisoning);- Penicillamine
Page 5043
Q2522:Arsenic: Antidote
Page 5044
Dimercaprol; Succimer;Penicillamine
Page 5045
Q2523:Mercury: Antidote
Page 5046
Dimercaprol; Succimer
Page 5047
Q2524:Gold: Antidote
Page 5048
Dimercaprol; Succimer;Penicillamine
Page 5049
Q2525:Copper: Antidote
Page 5051
Q2526:Cyanide: Antidote
Page 5052
1. Nitrite - (oxidizes Hemoglobin to methemoglobin [Fe3+];which has high afinity for CN- but low affinity for O2);2.
Hydroxocobalamin;3. Thiosulfate
Page 5053
Q2527:Methanol; Ethylene glycol: Antidote
Page 5054
Ethanol; dialysis;- Fomepizole
Page 5055
Q2528:Methemoglobin: Antidote
Page 5057
Q2529:Carbon monoxide: Antidote
Page 5058
100% 02; hyperbaric O2
Page 5059
Q2530:Opioids: Antidote
Page 5060
Naloxone/Naltrexone
Page 5061
Q2531:Benzodiazepines: Antidote
Page 5063
Q2532:TCA's: Antidote
Page 5064
NaHCO3 (nonspecific) ??
Page 5065
Q2533:Heparin: Antidote
Page 5067
Q2534:Warfarin: Antidote
Page 5068
Vit K (hours); Fresh Frozen Plasma (instant)
Page 5069
Q2535:tPA; streptokinase: Antidote
Page 5070
Aminocaproic acid
Page 5071
Q2536:Lead poisoning: LLEEAADD
Page 5072
- Lead Lines on gingivae and long bone epiphyses (on xray);-Encephalopathy; Erythrocyte basophilic stippling;-
Abdominal colic; Anemia (sideroblastic);- Drops-wrist andfoot drop; Dimercaprol as antidote (Succimer for kids)
Page 5073
Q2537:Inducers of CYP450
Page 5074
Quinidine;Barbiturates(phenobarbitol);Phenytoin;Rifampin;Griseofulvin;Carbemaze
pine;St. Johns Wort
Page 5075
Q2538:Inhibitors of CYP450
Page 5076
Isoniazid(INH);Sulfonylureas;Cimetidine;Ketoconazole;Erythromycin;
Grapefruit Juice
Page 5077
Q2539:tx benzodiazepam overdose
Page 5079
Q2540:go from phospholipids in the cell membrane tolukotrienes and other products of arachidonic acid metabolism
Page 5080
1. phospholipid in cell membrane -> phospholipase A2 (+ bybradykinin and angiotensin; - by corticosteroids);2.
phospholipase A2 -> arachidonic acid;3a. arachidonic acidbecomes PGG2 via cyclooxygenase (- by NSAIDS) -> PGG2
broken down by hydroperoxidase to PGH2 -> PGH2becomes thromboxane A2 (inhibited by dipyridamole); PGE2;
PGF2; and PGI2 (aka prostacyclin);3b. arachidonic acidbecomes 5-HPETE via 5-lipoxygenase -> 5-HPETE becomes
leukotrienes
Page 5081
Q2541:what causes the cough and angioedema in patient on anACEI
Page 5083
Q2542:how much epinephrine do you use in shock
Page 5084
1:1000 dilution subcutaneously
Page 5085
Q2543:what is dantrolene used for
Page 5086
treatment of malignant hyperthermia after halothane
Page 5087
Q2544:treat acetaminophen overdose
Page 5088
acetylcysteine to replace used of GSH (neutralizesacetaminophen free readicals formed in the liver cytochrome
system)
Page 5089
Q2545:mechanism of a loop diuretic
Page 5090
blocks Na-K-2Cl cotransport in the thick ascending limb inthe renal medulla; also blocks Ca reabsorption
Page 5091
Q2546:treat cyanide poisoning (useful to know that takingnitropusside orally instead of IV gives cyanide poisoning)
Page 5092
infusion of sodium thiosulfate -> produce thiocyanate;alsouse amyl nitrite
Page 5093
Q2547:complication of corticosteroid inhaler
Page 5095
Q2548:isotretinoin given to a young woman requires;
Page 5096
pregnancy test; then put them on OCs
Page 5097
Q2549:mechanism of propylthiouracil
Page 5098
blocks iodinqation of the tyrosine residues of thyroglobulin;also blocks coupling of DIT an MIT; only drug that can be
used in pregnancy but may produce goiter in the newborn andnail defects
Page 5099
Q2550:what does the P450 in the liver do
Page 5100
makes drugs water soluble
Page 5101
Q2551:what do angioedema and renal failure have to do withone another
Page 5103
Q2552:MOA of retinoic acid
Page 5104
behaves like a steroid in that it binds to receptors in thenucleus w/ subsequent transcription of genes; proteins
produced by the action ar eimportant in growth;differentiation; reproduction; and embryonic development;
also used in treatment of acute progranuloctyic leukemia
Page 5105
Q2553:allopurinol MOA in purine synthesis
Page 5106
blocks xanthine oxidase (takes hypoxanthine to xanthine andxanthine to uric acid); mercaptopurine degradation is inhibited
also
Page 5107
Q2554:most common antibiotic used to prevent endocarditisin patients w/ valvular disease
Page 5108
amoxicillin (all vavlular diseases except asymptomatic MVPand all congential heart disease except asymptomatic ASD)
Page 5109
Q2555:drug that may cause yellow coloration of skin that canbe mistaken for jaundice
Page 5110
quinacrine;(chlorpromazine and arsenic produce blue-greycolor to the skin)
Page 5111
Q2556:diffuse erythema followed by separation of the skin(scalded skin syndrome or toxic epidermal necrolysis)- drug?
Page 5112
barbituates; sulfonamides; phenytoin; NSAIDS
Page 5113
Q2557:hair loss in a woman- drug?
Page 5114
oral contraceptives (predictable side effect- estrogen causeshair to be at same stage of development; may also occur after
delivery)
Page 5115
Q2558:erythematous; hyperpigmented plaque-like lesion thatrecurs at the same site every time?
Page 5116
fixed drug eruption (phenolphthalein; NSAIDS; tetracycline;Bactrim; and barbituates are the most common)
Page 5117
Q2559:group of drugs that has the highest association w.urticarial and maculopapular lesions
Page 5118
amoxicillin; TMP/SMX; ampicillin/penicllin (rashes are theMOST COMMON adverse reaction to drugs; with
maculopapular rashes leading the list; most drug reactionsinvolving the skin are NOT type I hypersensitivity related)
Page 5119
Q2560:elderly woman on thiazides is most at risk fordeveloping;
Page 5121
Q2561:tardive dyskinesia; malignant syndrome (sweating;hyperpyrexia; autonomic instability)
Page 5123
Q2562:antipsychotic drug requiring visual exam
Page 5124
thioridazine (also produces heart conduction defects)
Page 5125
Q2563:nephrogenic diabetes insipidus- drug?
Page 5126
lithium for bipolar disturbances
Page 5127
Q2564:drug contraindicated w/ MAOI
Page 5129
Q2565:use of phentolamine
Page 5130
non-selective alpha blocker that lowers blood pressure duringsurgery for a pheochromocytoma
Page 5131
Q2566:mechanism of AZT
Page 5132
inhibits reverse transcriptase; produces a macrocytic anemiaunrelated to folate/B12
Page 5133
Q2567:treatment of Pb poisoning
Page 5135
Q2568:drugs involved in folate metabolism
Page 5136
phenytoin blocks intestinal conjugase (polyglutamate tomonoglutamate); BCP blocks uptake of monoglutamate;methotrexate/TMP-SMX block dihydrofloate reductase
Page 5137
Q2569:MOA of cromolyn sodium
Page 5138
stabilizes mast cell membrane preventing release of preformedmediators and release of prostaglandins/leukotrienes after the
release reaction
Page 5139
Q2570:methotrexate MOA
Page 5140
blocks dihydrofolate reductase and the conversion ofdihydrofolate to tetrahydrofolate
Page 5141
Q2571:glucoronyl transferase in liver renders compounds;
Page 5143
Q2572:COX inhibitors
Page 5144
aspirin inhibits irreversible;NSAIDS reversible
Page 5145
Q2573:thromboxane A2
Page 5146
synthesized in platelet; vasoconstrictor and increases plateletaggregation; also a bronchoconstrictor
Page 5147
Q2574:effect of proton blockers
Page 5148
blocks H-K-ATPase proton pump in parietal cell; not areceptor mediated event
Page 5149
Q2575:H2 blockers
Page 5150
blocks H2 receptor; which normally activates adenylatecyclase producing cAMP which stimulates protein kinase
Page 5151
Q2576:misoprostol
Page 5152
blocks the prostaglandin receptor; which normally inhibitsadenylate cyclase and cAMP production
Page 5153
Q2577:treatment of schistosomiasis and clonorchiasis
Page 5155
Q2578:7-fold membrane spanning protein- drug?
Page 5157
Q2579:phase 3 clinical trials
Page 5159
Q2580:ticlopidine
Page 5160
substitute for aspirin in preventing strokes; CAD if thepatient is allergic to aspirin; causes neutropenia
Page 5161
Q2581:drug induced SLE
Page 5162
hydralazine;INh;procainamide;phenytoin
Page 5163
Q2582:overdose of succinylcholine
Page 5164
acetylcholine blocker
Page 5165
Q2583:finasteride
Page 5166
blocks 5-a-reductase which converts testosterone inodihydrotestosterone; hence testosterone would increase
proximal to the block and dihydrotestosterone would decrase-> increases hair growth
Page 5167
Q2584:flutamide; cyproterone and spironolactone
Page 5168
block androgen receptors; hencetestosterone/dihydrotestosterone increase byt have no
physiologic effect
Page 5169
Q2585:ketoconazole
Page 5170
inhibits testosterone synthesis (suppresses adrenal steroidsynthesis)
Page 5171
Q2586:leuprolide
Page 5172
GnRH analogue; which when given in sustained fashioninhibits FSH and LH; hence lowering testosterone and
estrogen levels
Page 5174
increase in renin and ATI; but a decrease in ATII andaldosterone; aldosterone eventually increases; hence the
addition of spironoladctone to keep aldosterone suppressed;increases longevity in CHF
Page 5175
Q2588:arsenic poisoning
Page 5177
Q2589:chloroquine in treatmento f malaria- malaria recurred;why?
Page 5178
exoerythrocytic/hepatic stage (P. vivax and P. ovale); drugkills active disease but does not eradicate hepatic stage
Page 5179
Q2590:primaquine in treatment of malaria
Page 5180
not good in active stage byt does kill the hepatic stage of p.vivax and p. ovale
Page 5181
Q2591:dantrolene MOA
Page 5182
reduces the release of Ca from the sarcoplasmic reticulum ofskeletal muscle; antispasmodic drug also used in treating
malignant hyperthermia
Page 5184
increased anion gap metabolic acidosis due to conversion ofmethanol into formic acid; optic nerve degeneration and
blindness; treat w/ alcohol infusion to block metabolism ofmethanol by alcohol dehydrogenase
Page 5185
Q2593:botulsim toxin
Page 5186
blocks the release of acetylcholine; used to treat LES spasm inachalasia
Page 5187
Q2594:ribavirin
Page 5188
used in severe RSV infection in kids
Page 5190
albuterol (b2 selective agonist); may cause hypokalemia-drives K into cells
Page 5191
Q2596:acetylcholine breakdown
Page 5192
occurs in the synapse into choline and acetate byacetylcholinesterase in the cleft; products are recycled and not
excreted
Page 5193
Q2597:know the graph of norepi/epi and isoproterenol andtheir effects on blood pressure and heart rate
Page 5194
plus the effect of alpha -1 blockers
Page 5195
Q2598:amphotericin
Page 5196
disrupts cell membrane permeability; binds to ergosterol inthe membrane
Page 5197
Q2599:ketoconazole
Page 5198
inhibits the metabolism of nosedating antihistamines likeSeldane leading to cardiac arrhytmias
Page 5199
Q2600:be very familiar w/ secondary messengers
Page 5200
IP3 DAG and on and on
Page 5201
Q2601:opiod toxicity tx
Page 5202
naloxone (opiod receptor antagonist)
Page 5204
metabolized into morphine in amall amounts owing tosignificant first pass metabolism of morphine in liver
Page 5205
Q2603:delirium trements tx
Page 5206
benzodiazepines
Page 5207
Q2604:lovastatine
Page 5208
HMG CoA reductase inhibitors
Page 5209
Q2605:patent ductus arteriosus- keep open w/ ?
Page 5211
Q2606:penicillin
Page 5212
beta lactam antibiotic that inhibits cell wall synthesis; binds tospecific receptors in cytoplasmic membrane; inhibits
transpeptidase enzymes that cross-link linear peptidoglycoanchains that form part of the cell wall; activate autolytic
enzymes in the cell wall
Page 5213
Q2607:cephalosporins + aminoglycosides
Page 5214
synergistic effect of enhancing nephrotoxicity
Page 5215
Q2608:erythromycin
Page 5216
interacts w/ 50S subunit of bacterial ribosomes leading toinhibition of protein synthesis;inhibits the formation of the
initiation complex and interferes w/ translocationreactions;resistance develops secondary to plasmid mediated
formation of enzymes that methylate reactions;resistancedevelops secondary to plasmid mediated formation of
enzymes that methylate the receptor that erythromycin bindswith;coliforms produce an transmissible plasmid that
produces an esterase that hydrolyzes the lactone ring oferythromycin
Page 5217
Q2609:chloramphenicol
Page 5218
gray baby syndrome (dose related aplastic anemia)
Page 5219
Q2610:sulfonamides; dapsone
Page 5220
may precipiate hemolysis in G6P deficiency
Page 5222
inhibits dihydrofolate reductase; plasmid mediated resistance;TMP + SMX has a synergistic effect from the sequential
blockade of folate synthesis; since SMX blocksdihydropterate synthase; which is an enzyme that converts
PABA into DHF
Page 5223
Q2612:metronidzole
Page 5224
produces a disulfiram like reaction
Page 5225
Q2613:fluconazole
Page 5226
tx of esophageal candidiasis
Page 5227
Q2614:ganciclovir
Page 5228
first drug used in treating CMV retinitis; the most commoncause of blindness in AIDS; foscarbet is used if ganciclovir
doesn't work
Page 5229
Q2615:clolinomimetic used in treating open angle glaucoma
Page 5230
pilocarpine;physostigmine
Page 5231
Q2616:dobutamine
Page 5232
inotropic (increase contractility) vasodilator (decreasesafterload) that activates alpha 1 and beta 1 > beta 2 activitywithout much chronotropic effect; used in the treatment ofshock (cardiogenic) associated w/ hypotension; hyptension
associated w/ renal failure of CHF
Page 5234
stimulates cardiac beta 1 receptors; peripheral alphareceptors; and dopaminergic receptors in vessels in the renaland splanchnic bed; at low doses it is primarily a vasodilator
that increases renal and splanchnic blood flow; at high doses itincreases cardiac contractility and cardiac output via its
activation of cardiac beta 1 receptors
Page 5235
Q2618:benzodiazepine MOA
Page 5236
via its own receptors in the thalamus; limbic structures; andcerebral cortex which are part of the GABA freceptgor-chloride ion channel macromolecular complex; benzo'dfacilitate the inhibitor action of GABA via increased
conductgance in the chloride ion channels (flumazenil blocksthis effect by blocking the receptor for benzos and is the
treatment of choice for benzo overdose)
Page 5237
Q2619:a child who ingests 30 adult aspirin is most likely todevelop;
Page 5238
increased anion gap metabolic acidosis ;(adults get mixedmetabolic acidosis and respiratory alkalosis);tx is to performgastric lavage and add activated charcoal and to produce an
alkalone urine for increased excretion
Page 5239
Q2620:open angle gaucoma is best treated w/
Page 5240
a beta blocker (timolol is good; pilocarpine may als be used;most common type of glaucoma; produces gradual loss of
peripheral vission (tunnel vision) and optic atrophy)
Page 5241
Q2621:trazodone
Page 5242
second degneration anti-depressant; inhibition of serotoninreuptake; sedation; may cause priapism
Page 5243
Q2622:thioridazine complication
Page 5244
retinitis pigmentosum
Page 5245
Q2623:tamoxifen
Page 5246
anti-estrogen; estrogen receptor partial agonist that blocks thebinding of estrogen to their redceptors in ERA-[os breast
cancer cells; also protects against osteoporosis and CAD; riskfactor for endometrial cancer; can be used in treating progestin
resistant endometrial cancer
Page 5247
Q2624:acetaminophen
Page 5248
analgesic and antipyrietic but not an anti-inflammatory agent;inhibiots prostaglandin synthesis in the CNS; very weak
COX inhibitor; most common drug causing acute fulminanthepatitis; converted into free readicals in the liver; glutathione
inactivates the FRs
Page 5249
Q2625:digitalis toxicity
Page 5250
tx w/ digoxin FAB antibodies
Page 5251
Q2626:cephalosporins
Page 5252
first generation: drug of choice for surgical prophylaxis inmany cases;second: sinusitis (cefuroxime); mixed anaerobic
infection;third: minigitis; GC (ceftriaxone)
Page 5253
Q2627:cromolyn sodium in asthma
Page 5254
only for prophylaxis; blocks early and late asthmaticresponses to allergens
Page 5255
Q2628:omeprazole
Page 5256
inhibits the proton pump located on the luminal membrane ofthe parietal cell; useful in the treatment of ZE syndrome;
GERD; and h. pylori infection
Page 5257
Q2629:clozapine
Page 5258
blocks D4 and 5-HT receptors more so than D2 receptors
Page 5259
Q2630:fever in a patient on a loop diuretic
Page 5260
do not use any type of NSAID (including aspirin) since itblocks renal synthesis of prostaglandin; which it does not
interfere with prostaglandin synthesis. Loop diuretics lead tovolume depletion; hence angiotensin II will be elevated
(vasoconstricts efferent arteriole);loss of prostaglandin effectpredisposes the patent to renal failure
Page 5261
Q2631:pathogenesis of cough and angioedema in ACEI
Page 5262
increase in bradykinin
Page 5263
Q2632:red man syndrome
Page 5265
Q2633:drug for bacterial carrier states (s. aureus; N.meningitidis; h. influenza)
Page 5267
Q2634:single dose drug for GC and chlamydia
Page 5269
Q2635:Rx of malignant hypertension
Page 5271
Q2636:patient on Lasix who develops fever and needsantipyrietic
Page 5272
use acetaminophen; do not use NSAIDs since they blockprostaglandin production in the kidneys
Page 5273
Q2637:antihypertensive and antiarrhtymic drug that lowersblood pressure and increases heart rate
Page 5274
Ca channel blocker (nifedipine)
Page 5275
Q2638:What drugs are Ototoxic; Auditory?
Page 5276
Loops (Ethacrynic Acid >Furosemide);VANCOMYCIN;Macrolides;Cisplatin
Page 5277
Q2639:What drugs are Ototoxic; Vestibular?
Page 5279
Q2640:What drugs are Ototoxic Auditory and Vestibular?
Page 5280
Aminoglycosides
Page 5281
Q2641:What drugs are Ototoxic causing Tinnitus?
Page 5282
Quinidine/Quinine (cinchonism);ASA (salicylism)
Page 5283
Q2642:What drugs are nephrotoxic?
Page 5284
Vancomycin;Aminoglycosides;Amphothericin B;Foscarnet(hypercalcemia);Cisplatin (minimized w/
Amifestine);Cyclosporine
Page 5285
Q2643:What drug causes causes SIADH?
Page 5286
Carbamazepine;Chlorpropamide
Page 5287
Q2644:What drug causes Nephrogenic DI?
Page 5288
Lithium;Demeclocycline
Page 5289
Q2645:What drug causes hemorrhagic cystitis?
Page 5290
Cylcophosphamide
Page 5291
Q2646:How do you prevent hemorrhagic cystitis w/cyclophosphamide?
Page 5293
Q2647:How do you minimize nephrotoxicity from Cisplatin?
Page 5295
Q2648:What are the hepatotoxic drugs?
Page 5296
AMIODARONE;STATINS;VALPROIC ACID(hepatitis);Felbamate;Tolcapone;TETRACYCLINE (in
pregnancy);RIPE TB therapy (Rifampin; Isoniazid;Pyrazinamide);ACETAMINOPHEN
Page 5297
Q2649:What do you give to OD w/ ACETAMINOPHEN?
Page 5299
Q2650:What drugs cause Blood dyscrasias?
Page 5301
Q2651:What drug causes Aplastic Anemia?
Page 5303
Q2652:What drug causes agranulocytosis?
Page 5305
Q2653:What drug causes aplastic anemia and is dosedependent and dose independent?
Page 5306
Chloramphenicol
Page 5307
Q2654:What HIV medication causes Blood dyscrasias(anemia/bone marrow suppresion)?
Page 5309
Q2655:What anticoagulant produces thrombocytopenia?
Page 5311
Q2656:What drug causes thrombotic thromocytopenia;purpura or TPP?
Page 5313
Q2657:Most Cancer chemotherapeutic drugs cause?
Page 5314
Blood Dyscrasias
Page 5315
Q2658:What drugs cause pancreatitis?
Page 5316
Valproic Acid;Didanosine/Zalcitabine;Sulindac;Asparaginase
Page 5317
Q2659:What drug used for seizures causes pancreatitis?
Page 5319
Q2660:What drug used for HIV cause pancreatitis?
Page 5320
Didanosine;Zalcitabine
Page 5321
Q2661:What NSAID causes pancreatitis?
Page 5323
Q2662:What drug used for ALL causes pancreatitis?
Page 5325
Q2663:What drugs produce gingival hyperplasia?
Page 5326
Phenytoin;Nifedipine;Cyclosporine
Page 5327
Q2664:What drugs cause SLE in SLOW acetylators?
Page 5328
Hydralazine;Isoniazid;Procainamide
Page 5329
Q2665:Drugs w/ problems with AtypicalPseudocholinesterase?
Page 5330
Succinylcholine (prolongs the activity)
Page 5331
Q2666:What drug causes malignant hyperthermia?
Page 5333
Q2667:What drug causes Hemolytic Anemia in G6PDdeficiency?
Page 5334
Sulfonamide;Primaquine;Quinidine
Page 5335
Q2668:What drugs cause disulfiram like reaction?
Page 5336
Metronidazole;Chlorpropamide;Griseofulvin;Cefamandole;Cefotetan;Cefoperazone
Page 5337
Q2669:What drug (combination) causes Serotonin Sx?
Page 5338
MAOIs; TCAs; SSRIs; Meperidine
Page 5339
Q2670:What drug causes acute hypertensive crisis?
Page 5340
Non-Selective MAOIs + Tyramine
Page 5341
Q2671:What are the non-selective MAOIs?
Page 5342
Phenelzine;Trancylpromine
Page 5343
Q2672:What contains Tyramine?
Page 5344
Aged Cheese;Red Wine
Page 5345
Q2673:What DDI (drug-drug interaction) causes decrease inB.P. and possible death?
Page 5346
Sildenafil + Nitroglycerin
Page 5347
Q2674:What two drugs in anti-cancer therapy you shouldnever mix?
Page 5348
6-MP (Azathioprine) + Allopurinol;precipitate gout
Page 5349
Q2675:DOC for Borrelia?
Page 5351
Q2676:DOC for Ricketssia?
Page 5353
Q2677:DOC for T. pallidum?
Page 5355
Q2678:DOC for gonorrhea?
Page 5356
Ceftriaxone;"Floxacins"
Page 5357
Q2679:DOC for Atypicals (Chlamydia; Mycoplasma)?
Page 5358
Doxycicline or ;Macrolide
Page 5359
Q2680:DOC listeria?
Page 5361
Q2681:DOC Legionella?
Page 5363
Q2682:DOC Step (Group A)?
Page 5365
Q2683:DOC C. difficile?
Page 5366
Metronidazole;or Vancomycin
Page 5367
Q2684:DOC enterococcus?
Page 5368
Penicillin + AG (Aminoglucoside)
Page 5369
Q2685:DOC P. areuginosa?
Page 5370
Ticarcillin + AG
Page 5371
Q2686:DOC for T. pallidum but penicillin allergy?
Page 5373
Q2687:DOC N. gonorreah but Penicillin Allergy?
Page 5375
Q2688:DOC for Listeria but penicillin allergy?
Page 5377
Q2689:DOC Strep (Group A) but penicillin allergy?
Page 5379
Q2690:DOC enterococcus but penicillin allergy?
Page 5381
Q2691:DOC P. areuginosa but penicillin allergy?
Page 5383
Q2692:DOC Borrelia in Pregnancy or Child?
Page 5385
Q2693:DOC Ricketssia in Pregnancy or Child?
Page 5386
Chloramphenicol
Page 5387
Q2694:DOC N. gonorrhea in Pregnancy or Child?
Page 5389
Q2695:DOC atypicals [chlamydia; Mycoplasma] inPregnancy or Child?
Page 5391
Q2696:DOC P. areuginosa w penicillin allergy?
Page 5392
Aztreonam; AG; Floxacin
Page 5393
Q2697:DOC for Borelia for a prenant woman?
Page 5395
Q2698:DOC N. gonorrhea for a prenant woman?
Page 5397
Q2699:DOC Atypicals [Chlamydia; Mycoplasma] for aprenant woman?
Page 5399
Q2700:DOC for Borrelia in Children?
Page 5401
Q2701:DOC N. gonorrhea in Children?
Page 5403
Q2702:DOC Atypicals in Children?
Page 5405
Q2703:What is the Serotonin Sx?
Page 5406
Hyperthermia;Rigidity;AutonomicInstability;Myoclonus;Kind of like when having sex!!!
Page 5407
Q2704:What causes Serotonin Sx in w/ Meperidine?
Page 5408
Combination w/ MAOIs; TCAs;but it is a metabolite callednormeperidine that acts like SSRI
Page 5409
Q2705:How do protease inhibitors work?
Page 5410
Inhibit Aspartate Protease
Page 5411
Q2706:Name two protein inhibitors?
Page 5412
Indinavir;RitonAVIR;gp120;gp41
Page 5413
Q2707:What happens to Uric Acid at high does Aspirin?
Page 5414
UA stays in the lumen and is peed out = uricosuric
Page 5415
Q2708:What happens to Uric acid w/ low dose Aspirin?
Page 5416
Transport of UA (Uric Acid) is blocked from the blood to thelumen so it causes hyperuricemia;Aspirin (low dose) blocks
secretion of Uric Acid
Page 5417
Q2709:What drug protects patient from nephrotoxicity takingcisplatin?
Page 5419
Q2710:What drug prevents cardiotoxicity w/ Doxorubicin?
Page 5421
Q2711:What drug prevents toxicity to epithelial; GI and bonemarrow in Methotrexate high dose anti-cancer tx?
Page 5422
Leucovorin;restores purines
Page 5423
Q2712:Where does Aspirin work?
Page 5424
COX-1;Cycloxygenase 1
Page 5425
Q2713:Where does abcximab work?
Page 5426
GP IIB/IIIA receptor on platelets. Can't join together
Page 5427
Q2714:Where does ticlopidine work? (Clopidrogel)
Page 5428
Blocks ADP release
Page 5429
Q2715:Where does propilthioracil and Methimazole work?
Page 5430
Peroxidase in thyroid synthessis
Page 5431
Q2716:Where does Iodide (high dose) work?
Page 5432
blocks release of proteolytic T3 ---> T4
Page 5433
Q2717:Where does Propilthioracil and Propanolol work?
Page 5434
inhibit deiodinase (liver) conversion of T4 to T3
Page 5435
Q2718:28 year old chemist presents with MPTPexposure;What NT is depleted?
Page 5437
Q2719:Woman taking tetracycline exhibitsphotosensitivity;What are the clinical manifestations?
Page 5438
Rash on sun-exposed regions of body
Page 5439
Q2720:Nondiabetic patient presents with hypoglycemia butlow levels of C peptide;What is the diagnosis
Page 5440
Surreptitious insulin injection
Page 5441
Q2721:African American male who goes to Africa developshemolytic anemia after taking malaria prophylaxis;What is the
enzyme defficiency
Page 5442
Glucose 6 phosphate dehydrogenase
Page 5443
Q2722:27 year old female with history of psychiatric illnessnow has urinary retention due to neuroleptic;What do you
treat it with?
Page 5445
Q2723:Farmer presents with dyspnea; salivation; miosis;diarrhea; cramping and blurry vision;What caused this and
what is the mechanism
Page 5446
Insecticide poisoning; inhibition of acetylcholinesterase
Page 5447
Q2724:Patient with recent kidney transplant is oncyclosporine for immunosuppresion; he requires antifungalagent for candidiasis;What antifungal drug would result in
cyclosporine toxicity?
Page 5449
Q2725:Man on several medications including antidepressantsand antihypertensives; has mydriasis and becomes
constipated;What is the cause of symptoms?
Page 5451
Q2726:55 year old postmenopausal woman on tamoxifentherapy;What is she at increased risk of acquiring?
Page 5452
Endometrial carcinoma
Page 5453
Q2727:Woman on MAO inhibitor has hypertensive crisisafter meal;What did she ingest?
Page 5454
Tyramine (wine or cheese)
Page 5455
Q2728:After taking clindamycin; patient develops toxicmegacolon and diarrhea;What is the mechanism of diarrhea?
Page 5456
Clostridium difficile overgrowth
Page 5457
Q2729:Man starts a medication for hyperlipidemia. He thendevelops rash; pruritus and GI upset;What drug was it?
Page 5459
Q2730:Patient is on carbamazepine;What routine workupshould be done?
Page 5461
Q2731:23 year old female who is on rifampin for TBprophylaxis and on birth control (estrogen) gets
pregnant;Why?
Page 5462
Rifampin augments estrogen metabolism in liver rendering itless effective
Page 5463
Q2732:Patient develops cough and must discontinuecaptopril;WHat is a good replacement drug and why doesnt it
have the same side effects?
Page 5464
Losartan - an angiotensin II receptor antagonist; does notincrease bradykinin as captopril does
Page 5465
Q2733:Relates the amount of drug in the body to plasmaconcentration
Page 5466
Vd - volume of distribution
Page 5467
Q2734:Formule for volume of distribution
Page 5468
Vd = amount of drug in the body/plasma drug concentration
Page 5469
Q2735:Vd of plasma protein-bound drugs can be altered bywhat disease?
Page 5470
Liver and kidney
Page 5471
Q2736:Relates the rate of elimination to plasma concentration
Page 5473
Q2737:Formula for clearance
Page 5474
Cl = rate of elimination of drug/plasma drug concentration
Page 5475
Q2738:The time required to change the amount of drug in thebody by 1/2 during elimination (or during constant infusion) is
called _
Page 5477
Q2739:After 1 half life concentration of drug equals _ %
Page 5479
Q2740:After 2 half lifes concentration of drug equals_
Page 5481
Q2741:A drug infused at constant rate reaches about _ % ofsteady state after 4 T1/2
Page 5483
Q2742:Formula for T1/2
Page 5484
T1/2 = 0.7 * Vd/CL
Page 5485
Q2743:Loading dose formula
Page 5486
Loading dose = Cp * Vd/F;Cp= target plasma concentration;F= bioavailibility
Page 5487
Q2744:Formula for maintenance dose
Page 5488
Cp * CL / F;Cp = target plasma concentration;F =bioavailibility
Page 5489
Q2745:In patients with impaired renal or hepatic function; theloading dose decreases; increases or remains unchanged?
;Maintenance dose?
Page 5490
Loading dose remains unchanged;Maintenance dose decreases
Page 5491
Q2746:Rate of elimination is constant (constant amount ofdrug is eliminated per unit time) - what order
elimination?;What happens to target plasma concentration?
Page 5492
Zero order elimination;Target plasma concentration decreaseslinearly with time
Page 5493
Q2747:Rate of elimination is proportional to drugconcentration (constant fraction of drug eliminated per unit
time) - what order elimination? ;What happens to targetplasma concentration?
Page 5494
First order elimination;Cp decreases exponentially with time
Page 5495
Q2748:Give examples of drugs with zero order elimination
Page 5496
Ethanol;Phenytoin;Aspirin (at high or toxic concentration)
Page 5497
Q2749:Phase I metabolism (reduction; oxidation; hydrolysis)yields _ metabolites (often still active)
Page 5498
Slightly polar; water soluble
Page 5499
Q2750:What phase of metabolism associated withcytochrome P450
Page 5501
Q2751:What phase of metabolism associated with conjugation
Page 5503
Q2752:Phase II metabolism (acetylation; glucoronidation;sulfation) yields _ metanolites (renally excreted)
Page 5504
Very polar; inactive
Page 5505
Q2753:Geriatric patients lose which phase of metabolismfirst?
Page 5507
Q2754:Is it safe? Pharmacokinetics? - which phase of clinicaltesting of the drug
Page 5509
Q2755:Does it work in patients?- which phase of clinicaltesting of the drug
Page 5511
Q2756:Does it work? Double blind - which phase of clinicaltesting of the drug
Page 5513
Q2757:What happens in phase IV of clinical testing of thedrug
Page 5514
Postmarketing surveillance
Page 5515
Q2758:A competitive antagonist shifts agonist curve where?
Page 5517
Q2759:A noncompetitive antagonist (irreversible) shiftsagonist curve where?
Page 5519
Q2760:Name antibiotics that block cell wall synthesis byinhibition of peptidoglycan cross linking
Page 5520
Penicillin;Ampicillin;Ticarcillin;Pipercarcillin;Imipenem;Aztreonam;Cephalosporins
Page 5521
Q2761:Name antibiotics that block peptidoglycan synthesis
Page 5522
Bacitracin;Vancomycin;Cycloserine
Page 5523
Q2762:Name antibiotics that block protein synthesis at 50Sribosomal unit
Page 5524
Chloramphenicol;Erythromycin/macrolides;Lincomycin;Clindamycin;Streptogramins (quinupristin; dalfopristin);Linezolid
Page 5525
Q2763:Name antibiotics that block protein synthesis at 30Sribosomal unit
Page 5526
Aminoglycosides;Tetracyclines
Page 5527
Q2764:Name antibiotics that block nucleotide synthesis
Page 5528
Sulfonamides;Trimethoprim
Page 5529
Q2765:Name antibiotics that block DNA topoisomerase
Page 5531
Q2766:Name antibiotic that blocks mRNA synthesis
Page 5533
Q2767:Name bactericidal antibiotics
Page 5534
Penicillin;Cephalosporins;Vancomycin;Aminoglycosides;Fluoroquinolones;Metronidazole
Page 5535
Q2768:Name drugs that disrupt bacterial/fungal cell membrane
Page 5537
Q2769:Name drugs that disrupt fungal cell membranes
Page 5538
Amphotericin B;Nystatin;Flucoconazole/azoles
Page 5539
Q2770:Oral form of penicillin is called _ ;IV form?
Page 5540
Penicillin V;Penicillin G
Page 5541
Q2771:Mechanism of penicillin
Page 5542
- Binds penicillin binding proteins;- Blocks transpeptidasecross linking of cell walls;- Activates autolytic enzymes
Page 5543
Q2772:This antibiotic is bactericidal for gram positive cocci;gram positive rods; gram negative cocci and spirochetes. Not
penicillinase resistant
Page 5545
Q2773:Toxicity of penicillin
Page 5546
Hypersensitivity reactions;Hemolytic anemia
Page 5547
Q2774:Methicillin; nafcillin; dicloxacillin - mechanism ofaction? ;Narrow or broad action? ;Penicillinase resistant or
not?
Page 5548
Same as penicillin;Narrow action;Penicillinase resistantbecause of bulkier R groups
Page 5549
Q2775:Methcillin; nafcillin and dicloxacillin are clinically usedfor treatment of what bug?
Page 5551
Q2776:Methicillin toxicity
Page 5552
Interstitial nephritis
Page 5553
Q2777:Methcillin; nafcillin; dicloxacillin toxicity
Page 5554
Hypersensitivity reactions
Page 5555
Q2778:Ampicillin; Amoxicillin- mechanism ofaction;Penicillinase sensitive or resistant? ;Spectrum narrow
or wide?
Page 5556
SAME AS PENICILLIN;Wide spectrum;Penicillinasesensitive
Page 5557
Q2779:Ampicillin; amoxicillin can be combined with _ toenhance spectrum
Page 5558
Clavulinic acid
Page 5559
Q2780:Which has greater oral bioavailibility - amoxicillin orampicillin
Page 5560
AmOxicillin has greater Oral bioavailibility
Page 5561
Q2781:Name antibiotics that are extended-spectrumpenicillins - against certain gram positive and gram negative
rods ;Name rods
Page 5562
HELPS kill enterococci - H influenzae; E.coli; Listeriamonocytogenes; Proteus mirabilis; Salmonella;
enterococci;Ampicillin; amoxicillin
Page 5563
Q2782:Toxicity for ampicillin and amoxicillin
Page 5564
Hypersensitivity reactions; ampicillin rash;pseudomembranous colitis
Page 5565
Q2783:Mechanism for carbenicillin; pipercillin;ticarcillin;Spectrum?
Page 5566
Same as penicillin; extended spectrum
Page 5567
Q2784:Name penicillins used for treatment of Pseudomonas;and gram negative rods;Is it penicillinase resistant or
sensitive;Can it be used with clavulinic acid
Page 5568
Carbencillin; Piperacillin; Ticarcillin;Penicillinasesensitive;Use with clavulinic acid
Page 5569
Q2785:Toxicity for carbencillin; piperacillin; ticarcillin
Page 5570
Hypersensitivity reactions
Page 5571
Q2786:Beta lactam drugs that inhibit cell wall synthesis butare less susceptible to penicillinases; bactericidal
Page 5573
Q2787:Which cephalosporins target gram positive cocci +Proteus ; E. coli;Klebsiella
Page 5575
Q2788:Which cephalosporins target gram positive cocci + H.flu; Enterobacter; Neisseria; Proteus; E coli Klebsiella; Serratia
Page 5577
Q2789:Which cephalosporins target serious gram negativeinfections resitant to other beta lactams; meningitis (most
penetrate BBB) - give examples
Page 5578
3d generation - ceftazidime; ceftriaxone
Page 5579
Q2790:3d generation cephalosporin used for treatment ofPseudomonas
Page 5581
Q2791:3d generation cephalosporin used for treatment ofgonorrhea
Page 5583
Q2792:Which cephalosporins have increased activity againsPsedudomonas and gram positive organisms
Page 5585
Q2793:Is there cross hypersensitivity betweencephalosporins and penicillin
Page 5587
Q2794:Toxicity for cephalosporins
Page 5588
Hypersensitivity reactions;Increase nephrotoxicity ofaminoglycosides;Disulfiram like reaction with ethanol (in
cephalosporins with methylthiotetrazole group) -cefamandole
Page 5589
Q2795:A monobactam resistant to beta lactamases. Inhibitscell wall synthesis (binds to PBP3); synergistic with
aminoglycosides; no cross allerginicity with penicillins
Page 5591
Q2796:This antibiotic is used for Gram negative rods(Klebsiella; Pseudomonas; Serratia); no activity agains gram
positives or anaerobes; for penicillin allergic patients andthose with renal insufficiency who cannot tolerate
aminoglycosides
Page 5593
Q2797:Is there any toxicity associated with AZTREONAM
Page 5594
Usually nontoxic; occasional GI upset
Page 5595
Q2798:Broad spectrum beta lactamase resistant carbapenem
Page 5597
Q2799:Imipenem is ALWAYS administered with _ ;WHY?
Page 5598
CILASTATIN;Inhibitor of renal dihydropeptidase I - todecrease inactivation of the drug in renal tubules
Page 5599
Q2800:Drug of choice for Enterobacter; also active againstgram positive cocci; gram negative rods and anaerobes
Page 5600
Imipenem + cilastatin
Page 5601
Q2801:Toxicity associated with Imipenem/cilastatin
Page 5602
GI distress; skin rash; CNS toxicity (seizures) at high plasmalevels
Page 5603
Q2802:Inhibits cell wall mucopeptide formation by binding Dala D ala portion of cell wall precursors. Resistance occurs
with amino acid change of D ala D ala to D ala D lac
Page 5605
Q2803:This antibiotic is used for serious gram positive multidrug resistant organisms; including S aureus; and Clostridium
difficile (pseudomembranous colitis)
Page 5607
Q2804:Diffuse flushing ("red man syndrome") associatedwith vancomycin can be largely prevented by?
Page 5608
Pretreatment with antihistamines and slow infusion rate
Page 5609
Q2805:Toxicity for Vancomycin
Page 5610
Nephrotoxicity;Ototoxicity;Thrombophlebitis;Well toleratedin general - does NOT have many problems
Page 5611
Q2806:Gentamicin; neomycin; amikacin; tobramycin;streptomycin - what class of antibiotics?
Page 5612
Aminoglycosides
Page 5613
Q2807:Bactericidal; inhibit formation of initiation complexand cause misreading of mRNA. Require O2 for uptake;
therefore ineffective against anaerobes
Page 5614
AMINOGLYCOSIDES
Page 5615
Q2808:Which aminoglycoside is used for bowel surgery
Page 5617
Q2809:Aminoglycosides are _ with beta lactams
Page 5619
Q2810:Aminoglycosides are clinically used for treatment of _
Page 5620
Severe gram negative rod infections
Page 5621
Q2811:Toxicity of aminoglycosides
Page 5622
Nephrotoxicity (especially with cephalosporins);Ototoxicity(especially with loop diuretics)
Page 5623
Q2812:Doxycycline; demeclocycline; minocycline - nameclass of antibiotics
Page 5625
Q2813:Bacteriostatic; bind to 30S and prevent attachment ofaminoacyl-tRNA; limited CNS penetration
Page 5627
Q2814:Which tetracycline is fecally eliminated and can beused in patients with renal failure
Page 5629
Q2815:Must NOT take tetracyclines with _ ;Why?
Page 5630
Milk;Antacids;Iron containing preparations;Divalent cationsinhibit its absorption in gut
Page 5631
Q2816:Clinical use of tetracyclines
Page 5632
Vibriocholerae;Acne;Chlamydia;Ureaplasma;Urealyticum;Mycoplas
ma pneumonia;Boreliaburgdorferi;Riccketsia;Tularemia;VACUUM your BedRoom
Tonight
Page 5633
Q2817:Toxicity of tetracyclines
Page 5634
GI distress; discoloration of teeth and inhibition of bonegrowh in children; photosensitivity
Page 5635
Q2818:Erythromycin; azithromycin; clarithromycin- nameclass of antibiotics
Page 5637
Q2819:Inhibit protein synthesis by blocking translocation -bind to 23S rRNA of 50S ribosomall subunit; bacteriostatic
Page 5639
Q2820:Clinical use macrolides
Page 5640
URI;Pneumonia;STD;gram positive cocci (streptococcalinfections in patients allergic to penicillin); Mycoplasma;
Legionella; Chlamydia; Neisseria
Page 5641
Q2821:Toxicity macrolids
Page 5642
GI discomfort; acute cholestatic hepatitis; eosinophilia; skinrashes
Page 5643
Q2822:Patient on antibiotic therapy develops acutecholestatic hepatitis - which clas of drug?
Page 5645
Q2823:Most common cause of non compliance withmacrolides
Page 5647
Q2824:Inhibits 50S peptidyltransferase; bacteriostatic
Page 5648
Chloramphenicol
Page 5649
Q2825:This drug is used for treatment of meningitis (H flu; Nmeningitidis; Strep pneumoniae) but conservatively used due
to toxicities
Page 5650
Chloramphenicol
Page 5651
Q2826:Toxicities with chloramphenicol
Page 5652
Anemia (dose dependent);Aplastic anemia (doseindependent);Gray baby syndrome
Page 5653
Q2827:Which drug causes gray baby syndrome and why
Page 5654
Chloramphenicol - premature infants because they lack liverUDP-glucuronyl transferase)
Page 5655
Q2828:Blocks peptide bond formation at 50S ribosomalsubunit; bacteriostatic
Page 5657
Q2829:Which antibiotic is used to treat anaerobic infections(Bacteroides fragilis; Clostridium perfringens)
Page 5659
Q2830:Toxicity associated with clindamycin
Page 5660
Pseudomembranous colitis (C. difficile overgrowth); fever;diarrhea
Page 5661
Q2831:PABA antimetabolites inhibit dehydropteoratesynthase; bacteriostatic
Page 5663
Q2832:Which sulfonamides are used for treatment of simpleUTI
Page 5664
Triple sulfas or SMX
Page 5665
Q2833:Clinical use of sulfonamides
Page 5666
Gram positive;Gram negative;Nocardia;Chlamydia
Page 5667
Q2834:Toxicity with sulfonamides
Page 5668
Hypersensitivity reactions;Hemolysis if G6PDdeficient;Nephrotoxicity (tubulointerstitial
nephritis);Kernicterus in infants;Displace other drugs fromalbumin (warfarin)
Page 5669
Q2835:Antibiotic inhibits dihydropteorate synthase
Page 5671
Q2836:Antibiotic inhibits dihydrofolate reductase
Page 5672
Trimethoprim; pyrimethamine
Page 5673
Q2837:Inhibits bacterial dihydrofolate reductse; bacteriostatic
Page 5675
Q2838:This drug is used in combination with sulfonamidescausing sequential block of folate synthesis
Page 5677
Q2839:This drug is used for recurrent UTI's; Shigella;Salmonella; Pneumocystis carinii pneumonia
Page 5679
Q2840:Toxicity of trimethoprim
Page 5680
Megaloblastic anemia;Leukopenia;Granulocytopenia;TMP -Treats Marrow Poorly
Page 5681
Q2841:Toxicity connected with trimethoprim can bealleviated by _
Page 5682
Supplemental folinic acid
Page 5683
Q2842:Ciprofloxacin; norfloxacin; ofloxacin; sparfloxacin;moxifloxacin; gatifloxacin; enoxacin - name class
Page 5684
Fluoroquinolones
Page 5685
Q2843:Antibiotics inhibit DNA gyrase (topoisomerase II);bactericidal
Page 5686
Fluoroquinolones
Page 5687
Q2844:Used clinically for treatment of gram negative rods ofurinary and GI tracts (including Pseudomonas); Neisseria;
some gram positive organisms
Page 5688
Fluoroquinolones
Page 5689
Q2845:Are fluoroquinolones safe in pregnant women
Page 5690
Contraindicated in pregnant women and in children becauseanimal studies show damage to cartilage.
Page 5691
Q2846:Fluoroquinolones toxicity
Page 5692
Tendonitis and tendon rupture in adults;GIupset;Superinfections;Skin
rashes;Headache;Dizziness;FluoroquinoLONES hurtattachments to your BONES
Page 5693
Q2847:Forms toxic metabolites in bacterial cells; bactericidal
Page 5695
Q2848:Antiprotozoal; Giardia; Entamoeba; Trichomonas;Gardenrella vaginalis; anearobes (bacteroides; clostridium) -
name drug
Page 5697
Q2849:This drug is used with bismuth and amoxicillin (ortetracycline) for "triple therapy" against H pylori
Page 5699
Q2850:Anaerobic infections above diaphragm - ?;Anaerobicinfections below diaphragm?
Page 5700
Above - clindamycin;Below - metronidazole
Page 5701
Q2851:Toxicity of metronidazole
Page 5702
Disulfiram like reaction with alcohol; headache
Page 5703
Q2852:Bind to cell membranes of bacteria and disrupt theirosmotic properties; cationic; basic proteins that act like
detergents - treat resistant gram negativ infections
Page 5705
Q2853:Toxicity for polymyxins
Page 5706
Neurotoxicity;Acute renal tubular necrosis
Page 5707
Q2854:Name anti TB drugs
Page 5708
RESPIre;Rifampin;Ethambutol;Streptomycin;Pyrazinamide;Isoniazid
Page 5709
Q2855:2nd line therapy for TB
Page 5711
Q2856:All anti TB drugs have same toxicity - name it
Page 5713
Q2857:Anti TB drug - decreases synthesis of mycolic acids
Page 5715
Q2858:The only agent used as solo prophylaxis against TB
Page 5717
Q2859:Toxicity for INH (Isoniazid)
Page 5718
Hemolysis if G6PDdefficient;Neurotoxicity;Hepatoxocitiy;SLE like
syndrome;INH - Injures Neurons and Hepatocytes
Page 5719
Q2860:_ can prevent neurotoxicity caused by isoniazid
Page 5720
Pyridoxine (B6)
Page 5721
Q2861:Which anti TB drug has different half lifes in fast vsslow acetylators
Page 5723
Q2862:Anti TB drug - inhibits DNA dependent RNApolymerase
Page 5725
Q2863:Delays resistance to dapsone when used for leprosy
Page 5727
Q2864:Used for meningococcal prophylaxis andchemoprophylaxis in contacts of children with H influenzae
type B
Page 5729
Q2865:Rifampin toxicity
Page 5730
Minor hepatoxicity and drug interactions (increases P450)
Page 5731
Q2866:Rifampin 4 R's
Page 5732
RNA polymerase inhibitos;Revs up P450;Red/orange bodyfluids;Rapid resistance if used alone
Page 5733
Q2867:Beta lactamase cleavage of beta lactam drug is aresistance mechanism against which drugs
Page 5734
Penicillins and cephalosporins
Page 5735
Q2868:Modification via acetylation; adenylation; orphosphorylation is resistance mechanism against which drugs
Page 5736
Aminoglycosides
Page 5737
Q2869:Terminal D ala component of cell wall replaced with Dlac; decreases affinity - resistance mechanism against which
drug
Page 5739
Q2870:Modification via acetylation - resistance mechanismagainst which drug
Page 5740
Chloramphenicol
Page 5741
Q2871:Decreased uptake or increased transport out of cell isresistance mechanism against which drugs
Page 5743
Q2872:Altered enzyme (bacterial dihdropteorate synthetase);decreased uptake or increased PABA synthesis is resistance
against which drugs
Page 5745
Q2873:Drug of choice for prophylaxis of meningococcalinfections;Alternative?
Page 5746
Rifampin;Minocyclin
Page 5747
Q2874:Prophylaxis of gonorrhea
Page 5749
Q2875:Prophylaxis of syphillis
Page 5750
Benzathine penicillin G
Page 5751
Q2876:Prophylaxis in patients with history of recurrent UTI
Page 5753
Q2877:Drug of choice for prophylaxis for pneumocysticcarinii pneumonia;Alternative
Page 5754
TMP-SMX;Aerosolized pentamidine
Page 5755
Q2878:Binds ergosterol (unique to fungi); forms membranepores that allow leakage of electrolytes and disrupt
homeostasis
Page 5757
Q2879:Used for wide spectrum of systemic mycoses(Cryptococcus; Blastomyces; Coccidioides; Aspergillus;Histoplasma; Candida; Mucor). Intrathecally for fungal
meningitis; does NOT cross BBB
Page 5759
Q2880:Toxicity of Amphotericin B
Page 5760
NEPHROTOXICITY;Arrhythmias(amphoterrible);Fever/chills (shake and bake);Hypotension
Page 5761
Q2881:Binds to ergosterol; disrupting fungal membranes; usedas "swish and swallow" for oral candidiasis (thrush)
Page 5763
Q2882:Inhibit fungal steroid (ergosterol) synthesis
Page 5765
Q2883:Drug of choice for cryptococcal meningitis in AIDSpatients and candidal infections of all types (i.e yeast
infections)
Page 5767
Q2884:Drug of choice for Blastomyces; Coccidioides;Histoplasma; Candida albicans; hypercortisolism
Page 5769
Q2885:Toxicity of azoles
Page 5770
Hormone synthesis inhibition (gynecomastia);Liverdysfuntion (inhibits cytochrome P450);Fever; chills
Page 5771
Q2886:Inhibits DNA synthesis by conversion to fluorouracilwhich competes with uracil; used in systemic fungal
infections (Candida; Cryptococcus); causes bone marrowsuppression; n/v/d
Page 5773
Q2887:Antifungal medication; inhibits cell wall synthesis;clinically used for invasive aspergillosis; can cause GI upset
and flushing
Page 5775
Q2888:Antifungal; inhibits fungal enzyme squalene epoxidase;used to treat dermatophytoses (especially onychomycosis)
Page 5777
Q2889:Anti fungal; interferes with microtubule function;disrupts mitosis; deposits in keratin containing tissues (nails)- oral treatment of superficial infections; inhibits growth of
dermatophytes (tinea; ringworm)
Page 5779
Q2890:Toxicity Griseofulvin
Page 5780
Teratogenic;Carcinogenic;Confusion';Headache;Increasedwarfarin metabolism
Page 5781
Q2891:Antiviral drug used for prophylaxis for influenza Aand treatment of Parkinsons
Page 5783
Q2892:Derivative of Amantadine with fewer CNS side effects
Page 5785
Q2893:Anti viral medication; blocks biralpenetration/uncoating; may buffer pH of endosome; alsocauses release of dopamine from intact nerve terminals
Page 5787
Q2894:Toxicity of amantadine
Page 5788
Ataxia + dizziness+ slurred speech;Amantadine causesproblems with cerebellA
Page 5789
Q2895:Two antiviral medications that inhibits influenzaneuraminidase; both used for influenza A and B
Page 5790
Zanamivir;Oseltamivir
Page 5791
Q2896:Antiviral - inhibits synthesis of guanine nucleotides bycompetitively inhibiting IMP dehydrogenase; used for
treatment of RSV and chronic hep C
Page 5793
Q2897:Toxicity for Ribavirin
Page 5794
Severe teratogen;Hemolytic anemia
Page 5795
Q2898:THis antiviral medication preferentially inhibits viralDNA polymerase when phosphorylated by viral thymidine
kinase
Page 5797
Q2899:Antiviral medication used for treatment of VZV; HSV;EBV; mucocutaneous and genital herpes lesions; prophylaxis
in immunocompromised patients
Page 5799
Q2900:Toxicity for acyclovir
Page 5800
Delirium;Tremor;Nephrotoxicity
Page 5801
Q2901:Antiviral drug - works by phosphorylation viralkinase; preferentially inhibits CMV DNA polymerase; drugof choice for CMV especialy in immunocopromised patients
Page 5803
Q2902:Which drug is more toxic - acyclovir or ganciclovir tohost enzymes
Page 5805
Q2903:Ganciclovir toxicity
Page 5806
Leukopenia;Neutropenia;Thrombocytopenia;Renal toxicity
Page 5807
Q2904:Viral DNA polymerase inhibitor that binds to thepyrophosphate binding site of the enzyme. Does not require
activation by viral kinase
Page 5808
FOSCARNET = pyroFOSphate analog
Page 5809
Q2905:Antiviral drug used for treatment of CMV retinitis inimmunocompromised patients when ganciclovir fails
Page 5811
Q2906:Patient is on foscarnet for CMV retinitis; whichtoxicity could be suspected?
Page 5813
Q2907:Saquinavir; ritonavir; indinavir; nelfinavir; aprenavir -class of drugs
Page 5814
HIV therapy; protease inhibitors - inhibit assembly of newvirus by blocking protease enzyme
Page 5815
Q2908:HIV patient is taking anti HIV drugs; develops GIintolerance - nausea; diarrhea; hyperglycemia; lipid
abnormalities; thrombocytopenia - which drugs was he taking
Page 5816
PROTEASE INHIBITORS
Page 5817
Q2909:Zidovudine (AZT); didanosine; zalcitobine; stavudine;lamivudine; abacavir - what class of drugs
Page 5818
Reverse transcriptase inhibitors; nucleosides
Page 5819
Q2910:Name non-nucleosides reverse transcriptase inhibitors
Page 5820
Nevirapine;Delavirdine;Efavirenz
Page 5821
Q2911:Toxicity associated with reverse transcriptaseinhibitors
Page 5822
Bone marrow suppression (neutropenia; anemia);Peripheralneuropathy;Lactic acidosis (nucleosides);Megaloblastic
anemia;Rash (non-nucleosides)
Page 5823
Q2912:Highly active antiretroviral therapy (HAART)generally entails combination of?
Page 5824
Protease inhibitors + reverse transcriptase inhibitors
Page 5825
Q2913:Which antiretroviral drug is used during pregnancy toreduce risk of fetal transmission
Page 5827
Q2914:Patient on anti HIV therapy develops megaloblasticanemia - which drug most likely caused it
Page 5829
Q2915:When is HAART initiated?
Page 5830
When patients have low CD4 counts (<500 cell/mm3) or highviral load
Page 5831
Q2916:Glycoproteins from human leukocytes that blockvarious stages of viral RNA and DNA synthesis; used fortreatment of chronic hep B and C; Kaposis sarcoma;Name
drug and what toxicity associated with it
Page 5832
Interferons;Neutropenia
Page 5833
Q2917:Antiparasitic drug from onchocerciasis
Page 5834
Ivermectin (rIVER blindness treated with IVERmectin)
Page 5835
Q2918:Antiparasitic drug used to treat nematode/roundworm(pinworm; whipworm) infections
Page 5836
Mebendazole/thiabendazole
Page 5837
Q2919:Antiparasitic drugs used to treat gian roundowrm(ascaris); hookworm (Necator/Ancylostoma) and pinworm
(Enterobius)
Page 5838
Pyrantel pamoate
Page 5839
Q2920:Antiparasitic used to treat trematode/fluke(shistosomes; Paragonimus; Clonorchis) and cysticercosis
Page 5841
Q2921:Niclosamide is used to treat?
Page 5842
Cestode/tapeworm infections except cysticercosis
Page 5843
Q2922:Drug of choice for leishmaniasis
Page 5844
Pentavalent antimony
Page 5845
Q2923:Name anti malaria drugs
Page 5846
Chloroquine;Quinine;Mefloquine;Atovaquone;Proguanil
Page 5847
Q2924:Name drug used for treatment of latent hypnozoite(liver) forms of malaria (Plasmodium vivax; P.ovale)
Page 5849
Q2925:Drug of choice agains giardiasis; amebic dysentery;bacteria vaginitis; Trichomonas
Page 5851
Q2926:Drug of choice for Chagas disease; Americantrypanosomiasis (trypanosoma cruzi)
Page 5853
Q2927:Drug of choice for African trypanosomiasis (sleepingsickness)
Page 5855
Q2928:Cholinomimetic used for postoperative and neurogenicileus and urinary retention - activates bowel and bladder
smooth muscle
Page 5857
Q2929:Direct agonist; cholinomimetic used for treatment ofglaucoma; activates ciliary muscle of eye (open angle);
pupillary sphincter (narrow angle)
Page 5858
Carbachol; pilocarpine
Page 5859
Q2930:Anticholinesterase; used in treatment of postoperativeand neurogenic ileus and urinary retention; myasthenia gravis;reversal of neuromuscular junction blockade (postoperative);
increases endogenous Ach
Page 5861
Q2931:Anticholinesterase used in treatment of myastheniagravis - increases endogenous Ach; increases strength
Page 5863
Q2932:This anticholinesterase is used for diagnosis ofmyasthenia gravis (extremely short acting); increases
endogenous Ach
Page 5865
Q2933:Anticholinesterase; used in treatment of glaucoma(crosses BBB to CNS) and atropine overdose; increases
endogenous Ach
Page 5867
Q2934:Anticholinergic; used for treatment of glaucoma;increases endogenous Ach
Page 5869
Q2935:Name symptoms of cholinesterase inhibitor poisoning
Page 5870
DUMBBELSS;Diarrhea;Urination;Miosis;Bronchospasm;Bradycardia;Excitation of skeletal muscle;Lacrimation;Sweating
;Salivation (also abdominal cramping)
Page 5871
Q2936:Name substances that can lead to cholinesteraseinhibitor poisoning
Page 5872
Parathion and other organophosphates
Page 5873
Q2937:Antidote used in treatment of organophosphatepoisoning
Page 5874
Atropine (muscarinic antagonist) plus pralidoxime (chemicalantagonist used to regenerate active cholinesterase)
Page 5875
Q2938:What do you develop w/ benzodiazepines use? Whatreceptors?
Page 5876
Tolerance;down-regulation of B2 receptors
Page 5877
Q2939:Initial Tx for Status Epilepticus?
Page 5878
1) Diazepam;2) Lorazepam
Page 5879
Q2940:What drug causes sedation; ataxia and diplopia?
Page 5880
Phenytoin;SAD Sx.
Page 5881
Q2941:What is SAD Sx and who produces it?
Page 5882
sedation; ataxia and diplopia;Phenytoin
Page 5883
Q2942:What drugs causes gingival hyperplasia?
Page 5884
1) Phenytoin;2) Nifedipine;3) Cyclosporin
Page 5885
Q2943:CNS drugs
Page 5887
Q2944:Name the anticonvulsant that is degraded in zero-order?
Page 5889
Q2945:What drug is used for tx of abscence seizure?
Page 5891
Q2946:What is the mechanism of action of ethosuximide?
Page 5892
blocks Ca+ in thalamic neurons
Page 5893
Q2947:What drug do you use for preop sedation i.v.? Itcauses amnesia;
Page 5895
Q2948:Name the drug that causes megaloblastic anemia anddecreases folic acid?
Page 5897
Q2949:What anticovulsant causes SIADH?
Page 5899
Q2950:What effect does carbamazepine have on the liver?
Page 5900
it induces cyt P450 (+)
Page 5901
Q2951:What is the formula for minimal alveolar anestheticconcentration?
Page 5902
MAC= 1/(potency[lipid solubility]);Lipid = potency =1/MAC
Page 5903
Q2952:What anticonvulsant causes drug induced Ricketts orostemalacia?
Page 5905
Q2953:DOC for trigeminal neuralgia?
Page 5907
Q2954:What are 3 Side/Effects (S/E)of Carbamazepine?
Page 5908
1) Cyt. P450 inducer (+);2) Hematotoxicity;3) increase ADH(retains water)
Page 5909
Q2955:What is the effect of carbamazepine and OralContraceptives?
Page 5910
inactivates sex steroids and O.C;lowers estriol
Page 5911
Q2956:What is carbamazepine the DOC for?
Page 5912
Trigeminal Neuralgia
Page 5913
Q2957:What effect does carbamazepine have on P450?
Page 5915
Q2958:Name two important Side/Effects (S/E) ofCarbamazepine?
Page 5916
1) hematotoxicity;2) SIADH
Page 5917
Q2959:Drug used for Anxiety/Panic?
Page 5919
Q2960:Patien w/ depression needs to be treated but has liverfailure? Tx pt. w/ which benzos;
Page 5920
1) Oxazepam;2) Temazepam;3) Lorazepam;Out The Liver
Page 5921
Q2961:What are the three OUT THE LIVERBenzodiazepines?
Page 5922
Oxazepam;Temazepam;Lorazepam
Page 5923
Q2962:Tx for Status Epilepticus (I.V.)?
Page 5925
Q2963:What drug is used for relaxation and detoxification forwithdrawal states?
Page 5927
Q2964:Antidote for Zolpidem overdose?
Page 5929
Q2965:Where do benzodiazepines work?
Page 5930
GABAa receptor;gama binding site;BZ1 hypnotic(sleep);increases frecuency of Cl- channel
Page 5931
Q2966:What site do benzodiazepines act in?
Page 5932
gama binding site;BZ 1
Page 5933
Q2967:What drug is antagonist at the BZ receptor?
Page 5935
Q2968:What drug acts in the BZ1 receptor but it's not abenzodiazepine?
Page 5937
Q2969:What is the action of barbiturates [high dose]?
Page 5938
increase duration Cl-;opens Cl- channels;blocks Na+channels;barbiDURATES;increases duration of Cl- open
Page 5939
Q2970:What is the mechanism of Buspirone?
Page 5940
- no gaba;- partial agonist at 5HT1a;-nonsedating
Page 5941
Q2971:What is the action of disulfiram? Whic cellcompartment does it work on?;Increase what?
Page 5942
inhibits acetaldehyde dehydrogenase;- mitochondria;-increases NADH
Page 5943
Q2972:What is Methanol used for? (Tx)
Page 5944
- Ehtanol intoxication;- fomepizole
Page 5945
Q2973:What is the definite Tx for ethanol/fomepizoleintoxication?
Page 5947
Q2974:What is methanol degraded to?;Enzyme?
Page 5948
formaldehyde;- alcohol dehydrogenase
Page 5949
Q2975:What is the lethal dose of methanol?
Page 5951
Q2976:What is the toxic retinal dose of methanol?
Page 5953
Q2977:What does the Disulfiram Reaction consists of?
Page 5954
1) Nausea;2) Vomiting;3) Vertigo;4) Hypotension/Shock
Page 5955
Q2978:What causes a 3/sec spike pattern on EEG?
Page 5956
Abscence seizure ;Petite Mal
Page 5957
Q2979:What is indicated in neuropathic pain?
Page 5958
1) Felbamate;2) Lamotrigine;3) Gabapentin
Page 5959
Q2980:What are the S/E of Felbamate?
Page 5960
Aplastic Anemia;Acute Liver Failure
Page 5961
Q2981:What are the S/E of Lamotrigine?
Page 5962
Steven-Jonhson Sx;Rash
Page 5963
Q2982:What are felbamate; lamotrigine and gabapentin usedfor?
Page 5964
Neuropathic pain
Page 5965
Q2983:Name the 3 new Anticovulsants?
Page 5966
Felbamate;Lamotrigine;Gabapentin
Page 5967
Q2984:Name 3 drugs used in complex seizure tx?
Page 5968
Valproic Acid;Phenytoin;Carbamazepine
Page 5969
Q2985:Tx for Generalized Anxiety States (GAS)?
Page 5971
Q2986:How long do you wait for buspirone to take effect?
Page 5973
Q2987:What is divalproex used for?
Page 5974
Bipolar Disorder (backup)
Page 5975
Q2988:What is the mech. of action (M/A) for Divalproex?
Page 5976
Ca+ block;inhibits GABA transaminase;axonal Na+ block
Page 5977
Q2989:What are the A/E of Valproic Acid?
Page 5978
1) hePAtotoxicity;2) PAncreatitis;3) aloPEcia;4) sPIna Bifida(Teratogenic);PA PE PI;VALPA PE PI
Page 5979
Q2990:What combination w/ anticonvulsants have additiveCNS depression?
Page 5980
1) antihistamines;2) ethanol;3) sedative-hypnotics;4) opioids
Page 5981
Q2991:What happens if you withdrawal anticonvulsantsabruptly?
Page 5982
Seizure might be precipitated
Page 5983
Q2992:What is the Tx for Tonic-clonic seizure?
Page 5984
- Valproic Acid;- Phenytoin;- Carbamazepine
Page 5985
Q2993:This is unique to collagen?
Page 5987
Q2994:What is the defect in Ehlers-Danlos? name the gene
Page 5988
mutation of collagen gene;- lysine hydroxylase gene
Page 5989
Q2995:What are the symptoms of Ehlers-Danlos
Page 5990
hyperextensible; hypermobile joints; dislocations
Page 5991
Q2996:What is the defect in Menkes Dz?
Page 5992
inhibition of lysyl oxidase;Copper (Cu+) deficiency
Page 5993
Q2997:What are the symptoms in Menkes Dz?
Page 5994
depigmented steely hair;decrease urinary Cu+
Page 5995
Q2998:What disease has mutation in collagen I?
Page 5996
Osteogenesis Imperfecta
Page 5997
Q2999:What are the symptoms for Osteogenesis Imperfecta?
Page 5998
Pathologic Fractures;blue sclera;collagen problems
Page 5999
Q3000:Patient with coarse facial features; gingival hyperplasiaand macroglosia? Dx?
Page 6001
Q3001:What enzyme is deficient in I-Cell Dz?
Page 6002
phosphotransferase
Page 6003
Q3002:Where in the cell is the problem in I-Cell Dz?
Page 6004
Golgi apparatus;Manose-6 Residues
Page 6005
Q3003:What are the symptoms of I-cell Dz?
Page 6006
coarse facial features;gingival hyperplasia;macroglosia
Page 6007
Q3004:Patient with deficiency in Leu; Ile and Val aminoacids?
Page 6009
Q3005:What type of amino acids are Leu; Ile and Val?
Page 6010
Branched Amino Acids
Page 6011
Q3006:What drug inhibits activation? binds to t-RNA withribosome?
Page 6012
blocks initiation;Aminoglycosdies;A first letter of thealphabet
Page 6013
Q3007:What drug has the mechanism of inhibiting peptidyltransferase?
Page 6014
Chloramphenicol
Page 6015
Q3008:What drug inhibits aminoacyl-tRNA binding to Asite?;Elongation
Page 6016
Tetracycline;t is for tRNA
Page 6017
Q3009:What drug inhibits the translocation of tRNA?;E.F.3
Page 6019
Q3010:What bacteria have the same mechanism of action asmacrolides?
Page 6020
diphtheria toxin;pseduomonas toxin
Page 6021
Q3011:What drug is an Angiotensin II blocker?
Page 6023
Q3012:What are the effects of Sartans on aldosterone;bradykinin; AT-1
Page 6024
decrease aldosterone;decrease bradykinin;increase AT-1
Page 6025
Q3013:What is the DOC (drug of choice) for CHF (CardiacHeart Failure)?
Page 6027
Q3014:What effect does ACE have on ATII; bradykinin;aldosterone; fluid; preload; afterload?
Page 6028
decrease ATII;increase bradykinin;decreasealdosterone;decrease fluid;increase vasodilation;decrease
preload;decrease afterload
Page 6029
Q3015:What it the drug used for HTN causes dry cough andangioedema?
Page 6031
Q3016:Why do ACE(-) cause cough?
Page 6032
increases bradykinin and causes edema in the pharynx
Page 6033
Q3017:What drug causes disorientation; visual effects (halos);hallucinations; SVTs; AV block?
Page 6034
Digitalis Toxicity
Page 6035
Q3018:What enzymes increase cAMP in cardiac cells?
Page 6036
(+) adenylyl cyclase;(-) phosphodiesterase III
Page 6037
Q3019:What is the mechanism of action of sildenafil?
Page 6038
blocks PDE V;(-) phosphodiesterase V;increases cGMP
Page 6039
Q3020:What drug interacts with sildenafil?
Page 6040
Nitrous Oxide;since NO also increases cGMP
Page 6041
Q3021:What is the mechanism of phosphodiesterase III?What cells are involved?
Page 6042
inhibits conversion of cAMP to AMP ;so increase incAMP;Cardiac Cell
Page 6043
Q3022:What two drugs inhibit PDE III?
Page 6044
theophylline;inamirone
Page 6045
Q3023:What is the mechanism of action of inamirone?
Page 6046
blocks cAMP to AMP;incrases cAMP inside cardiaccell;increases force of contractilily
Page 6047
Q3024:What enzymes are deficient in vitamin C def?
Page 6048
(-) prolyl and lysyl hydroxylase
Page 6049
Q3025:What part of the cell are prolyl and lysylhydroxylase?
Page 6050
inside the R.E.R.
Page 6051
Q3026:What is the mechanism of action of dobutamine anddopamine?
Page 6052
B1 receptor;increase adenylyl cyclase (+);ATP----> increasescAMP;cAMP---> Protein Kinase;Protein Kinase opens Ca2+
channels;increase in Ca2+
Page 6053
Q3027:What is the mechanism of action of digoxin?
Page 6054
inhibits Na+/K+ ATPase;decreases sodium/Ca+ exchange;Ca+stays inside the cell;to increase contraction force;inhibited by
K+ increase
Page 6055
Q3028:What 5 drugs/states cause digitalis toxicity?
Page 6056
1) quinidine;2) NSAIDS;3) Amiodarone;4) Verapamil;5)hypokalemia
Page 6057
Q3029:What is the mechanism of phosphodiesterase V?
Page 6058
increases cGMP;blocks breakdown of cGMP--> GMP
Page 6059
Q3030:What drugs/compounds stimulate Gq to IP3?
Page 6060
Acetylcholine (Ach);Bradykinin;5HT
Page 6061
Q3031:What happens to Gq after it is converted to IP3?
Page 6062
releases Calcium
Page 6063
Q3032:What is Calciums effect on Nitrous Oxide?
Page 6064
it stimulates the conversion of L-arg to NO
Page 6065
Q3033:What amino acid does Nitrous Oxide derive from?
Page 6067
Q3034:Where is does the reaction L-Arg to NO take place?
Page 6069
Q3035:What does NO do inside the smooth muscle?
Page 6070
stimulates guanylate cyclase
Page 6071
Q3036:What does guanulate cyclase stimulate?
Page 6072
Conversion of GTP to cGMP;so increase cGMP
Page 6073
Q3037:What other amino acid is involved in making NO?
Page 6075
Q3038:What does NO stimulate?
Page 6076
guanylate cyclase;and conversion of GTP to cGMP;increasescGMP
Page 6077
Q3039:Where in the nephron does acetazolamide act?
Page 6078
proximal convoluted tube
Page 6079
Q3040:What are the effects of acetazolamide?
Page 6080
decreases HCO3-
Page 6081
Q3041:What are the toxic effects of acetazolamide?
Page 6082
metabollic acidosis;neuropathy; sulfa allergy
Page 6083
Q3042:What happens to the urine with acetazolamide?
Page 6084
increase Na+ excresion;increases HCO3- excresion
Page 6085
Q3043:What diuretic works in the collecting ducts?
Page 6086
Potassium Sparing (K+) diuretics
Page 6087
Q3044:What are the K+ sparing diuretics?
Page 6088
Spirinolactone;Amiloride;Triamterene
Page 6089
Q3045:How is Spirinolactone different from Amiloride andtriamterene?
Page 6090
Spirinolactone is an Aldosterone receptor inhibitor;the othertwo are Na+ Channel blockers
Page 6091
Q3046:What drug blocks Na+/Cl- symport in the renalsystem?
Page 6093
Q3047:What part of the nephron do thiazides act in?
Page 6094
Distal Convoluted Tube;DCT
Page 6095
Q3048:What is used in HTN and Heart Failure (CHF)?
Page 6097
Q3049:What happens to ions in blood after thiazideadministration?
Page 6098
Hypokalemia;Alkalosis;HyperCAlcemia
Page 6099
Q3050:What are thiazides used for?
Page 6101
Q3051:What are the toxicities of hydrochorothiazides?
Page 6102
hyperGLUC;sulfa allergies
Page 6103
Q3052:What does hyperGLUC stand for?
Page 6104
hyperGlycemia;hyperLipidemia;hyperUricemia;hyperCalcemia;Sulfa Allergies
Page 6105
Q3053:What is the potential toxicity of K+-SparingDiuretics?
Page 6106
Hyperkalemia;endocrine effects likeGYNECOMASTIA!;Anti-Androgen
Page 6107
Q3054:Diuretic that causes hyperglycemia?
Page 6109
Q3055:What is the mechanism for thiazide acting ashyperglycemia?
Page 6110
blocks insulin release;opens K+ Channels;keeps insulin insideb-cells
Page 6111
Q3056:What diurectic causes alkalosis and hypoCalcemia?
Page 6113
Q3057:What diuretic causes alkalosis and hyperCalcemia?
Page 6115
Q3058:What diuretic causes acidosis and hyperKalemia?
Page 6117
Q3059:What diuretic causes acidosis and hypoKalemia?
Page 6118
Carbonic Anahydrase inhibitors
Page 6119
Q3060:All diuretics cause what?
Page 6120
hypokalemia to a degree;except K+ sparing
Page 6121
Q3061:What is the mechanism of CA(-) Carbonic anahydraseinhibitors?
Page 6122
NaHCO3 diuresis;HCO3- decreases in blood so causes H+ tobe unbalanced;Acidosis
Page 6123
Q3062:What is the only lipid friendly thiazide?
Page 6125
Q3063:What diuretics are in the sulfa family?
Page 6127
Q3064:What diuretic works on ATII? Aldosterone receptorblocker?
Page 6129
Q3065:What mechanism does Spirinolactone use? (protein)
Page 6130
acts via Zinc Finger Protein;increases geneexpression;increases Na+ Channels to open
Page 6131
Q3066:What diuretic causes ginecomastia?
Page 6133
Q3067:Diuretic that causes hypoCAlcemia?
Page 6134
Loops;Loops Loose Calcium;Tx malignancies with it!
Page 6135
Q3068:Diuretic that causes hyperCalcemia?
Page 6139
Q3070:Pharmacology Kaplan
Page 6141
Q3071:What drug do Loop diuretics interfere with?
Page 6142
Lithium decreases clearance and increases lithium in serum
Page 6143
Q3072:What drug potentiates OTOtoxicity w/ Loopdiuretics?
Page 6144
Aminoglycosides
Page 6145
Q3073:What drug interacts w/ Gemfibrozil?
Page 6146
HMG-coA reductase inhibitors (statin drugs)
Page 6147
Q3074:What is the result of the DDI (drug drug interaction)of Gemfibrozil and Statin drugs?
Page 6148
Rhabdomyolisis increases
Page 6149
Q3075:What drug potentiates Gemfibrozil?
Page 6150
Warfarin and Sulfonylurea
Page 6151
Q3076:What drugs inhibit HMG-coA reductase?
Page 6153
Q3077:What effect do statin drugs have on cytochrome p450?
Page 6154
increases p450 activity p450(+) inducer
Page 6155
Q3078:What is the effect of stain drugs on HDL and TGs?
Page 6156
HDL increase and decrease in TGs (triclyerides)
Page 6157
Q3079:What are the A/E (adverse/effects) of statin drugs?
Page 6158
myalgia/myopathy; rhabdomyolysis; p450(+) renal failure;death
Page 6159
Q3080:What antilipid drug causes flushing and pruritus(hepatotoxicity)?
Page 6161
Q3081:What is the mechanism of action of Cholestipol andCholestyramine?
Page 6162
they are bile acid sequestrants that prevent reabsorption ofbile salts in the GI tract
Page 6163
Q3082:What is the effect of decrease in bile acid?
Page 6164
increase synthesis of new bile salts; decrease liver cholesterol;increase LDL receptors; decrease plasma LDL
Page 6165
Q3083:What is contraindicated w/ bile acid sequestrants?
Page 6166
concomitant use with hypertriglyceridemias because theyincrease VLDL and TGs
Page 6167
Q3084:What do bile acid sequestrants DDI with?
Page 6168
DDI digoxin and warfarin; decrease their absorption
Page 6169
Q3085:Does HMG-coA reductase cause SLE Sx?
Page 6171
Q3086:What ist the mechanism of action of nicotinic acid?
Page 6172
inhibits VLDL synthesis and apoprotein synthesis
Page 6173
Q3087:What is good about nicotinic acid?
Page 6175
Q3088:How do you treat the flushing and pruritus w/nicotinic acid?
Page 6177
Q3089:What is another adverse effect of nicotinic acid?
Page 6179
Q3090:What drug causes flushing; sedation; dyspnea and onlyacts for t1/2 30 sec?
Page 6181
Q3091:Adenosine is antagonized by?
Page 6182
theophilline and caffeine
Page 6183
Q3092:Pharmacologist refer to adenosine as?
Page 6184
Reset Button Dead for 30 seconds and then heart starts again
Page 6185
Q3093:DOC for PSVTs?
Page 6187
Q3094:What are the effects of adenosine on SA and AV?
Page 6188
decrease SA and AV; increases AV refractory period
Page 6189
Q3095:What drug is an M blocker and is used for asthma andCOPD? It has no CNS entry
Page 6191
Q3096:It's a cholinomimetic; AchE inhibitor; contracts ciliarym; increases outflow?
Page 6192
Pilocarpine and ECHOthiopate
Page 6193
Q3097:What are Pilocarpine and Echothiopate used for?
Page 6195
Q3098:What are the three K+ channel blockers?
Page 6196
Amiodarone; Bretylium and Sotalol ABS system
Page 6197
Q3099:What do K+ channel blockers do?
Page 6198
slow phase 3; increase APD
Page 6199
Q3100:What is the mechanism of action of Quinidine?
Page 6200
blocks Na+ channels (decrease I Na); increase APD and ERP;M blocker; alpha block
Page 6201
Q3101:DOC for arrythmias following cardioversion? I.V. use
Page 6203
Q3102:What is amiodarone used for?
Page 6204
Atrial and Ventricular Arrythmias
Page 6205
Q3103:What are the S/E of Amiodarone?
Page 6206
hepatic necrosis; PULMONARY FIBROSIS; CornealDeposits; BLUE Pigmentation (SMURF) Skin; Photoxocity;
Thyroid Dysfunction
Page 6207
Q3104:What is the t1/2 life of Amiodarone?
Page 6208
40 days; Largest Vd
Page 6209
Q3105:What is Manitol used for?
Page 6210
1) maintain renal function; 2) close angle glaucoma; 3) decreaseintracraneal pressure (tumor; hematoma)
Page 6211
Q3106:Newborn w/ strabysmus; decrease growth; midfacilhypoplasia; microcephaly; CNS Dysfunction; Thin Upperlip
(Phyltrum)
Page 6212
Fetal Alcohol Syndrome
Page 6213
Q3107:What is Benztropine and Trihexyphenidyl used for?
Page 6214
Parkinson's; Drug-Induced Extrapyramidal Dysfunction
Page 6215
Q3108:Mechanism of action of Benztropine andTrixehyphenidyl?
Page 6217
Q3109:Drug used in organophosphate poisoning?
Page 6219
Q3110:What does Pralidoxime do w/ symptoms?
Page 6220
corrects patients labored breathing and decreases muscleweakness
Page 6221
Q3111:What is pralidoxime used for?
Page 6222
Organophosphate Poisoning
Page 6223
Q3112:What drug is used for Parkinson and Drug-InducedExtrapyramidal Dysfunction?
Page 6224
Benztropine and Trihexyphnidyl
Page 6225
Q3113:How does alcohol produce gout?
Page 6226
Alcohol decreases NADH and increases NAD; increasesconversion of reversible reaction pyr ---> Lactate; Lactateincreases and competes w/ uric acid excrecion causing gout
Page 6227
Q3114:What biochemical compound is increased inalcoholism?
Page 6229
Q3115:What 2 drugs interact with digoxin (DDI)?
Page 6230
Quinidine and Verapamil (the queen and the rapper alwaysinterfere)
Page 6231
Q3116:Drug that causes phototoxicity?
Page 6233
Q3117:Name 3 drugs used in AchE inhibitor poisoning?
Page 6234
Malathion; Parathion and Sarin (nerve gas)
Page 6235
Q3118:What is the MOA of Hydralazine?
Page 6236
increase NO;increase Guanylate Cyclase;increasecGMP;relaxes vascular musculature
Page 6237
Q3119:What is the effect of Hydralazine on TPR?
Page 6238
decreases TPR;involves NO/EDRF pathway;decreasesresistnace in coronary; renal and cerebral beds
Page 6239
Q3120:What is hydralazine used for?
Page 6240
Tx for moderate to severe HTN
Page 6241
Q3121:What is Hydralazine metabolized by?
Page 6242
N-acetyltransferase
Page 6243
Q3122:What are A/E of hydralazine?
Page 6244
headache; flushing; sweating and fluid retention;part of HIP;soSLE-like symptoms
Page 6245
Q3123:What is used in HT emergency?
Page 6247
Q3124:What is the effect of nitroprusside on TPR?
Page 6248
decrease TRP via dilation of arterioles and venules
Page 6249
Q3125:What happens when there is venule dilation afternitroprusside use?
Page 6250
Orthostatic Hypotension
Page 6251
Q3126:What are by-products of nitroprusside?
Page 6252
thiocyanate and cyanide ions
Page 6253
Q3127:What part of the mitochrondria is damaged withcyanide compounds?
Page 6254
Comple IV (looks like N);cyt. a/a3
Page 6255
Q3128:What is ethylene glycol?
Page 6257
Q3129:What happens to ethylene glycol once ingested?
Page 6258
it is degraded to gycoaldehyde;- Alcohol Dehydrogenase is theenzyme
Page 6259
Q3130:What comes after degradation of glycoaldehyde?
Page 6260
glycolic acid and oxalic acid;latter is nephrotoxic
Page 6261
Q3131:What causes drug induced SIADH?
Page 6262
1) Carbamazepine;2) Chlorpropamide
Page 6263
Q3132:What are the symptoms in Phenytoin Intoxication?
Page 6264
SAD Sx;;Sedation;Ataxia;Diplopia
Page 6265
Q3133:Name an anticonvulsant that is Zero-Order?
Page 6267
Q3134:What condition has an EEG with 3/sec spike pattern?
Page 6268
Generalized Abscence Seizure
Page 6269
Q3135:What is the Tx for Generalized Abscence Seizure?
Page 6271
Q3136:Name 4 drugs that block voltage gated axonal Na+influx of fast channels?
Page 6272
1) Carbamazepine;2) Phenytoin;high dose;3) Barbiturates;4)Valproic Acid
Page 6273
Q3137:What drug decreases Ca2+ influx through T channelsin thalamic neurons?
Page 6274
Ethosuximide;Valproic Acid
Page 6275
Q3138:What is the action on alpha 2 receptors?;1) NE;2)trasmitter release;3) platelets;4) Pancreas
Page 6276
1) decrease NE synthesis;2) decrease transmitter release atprejunctional nerve terminals;3) increase aggregation of
platelets;4) decrease insulin secretion;catabolism
Page 6277
Q3139:Effect of B1 receptors on renin?
Page 6278
increase renin release
Page 6279
Q3140:What adrenoreceptor increases insulin secretion?
Page 6280
beta 2 receptor stimulation
Page 6281
Q3141:What adrenoreceptor induces glycogenolysis?
Page 6283
Q3142:What adrenoreceptor causes uterine relaxation?
Page 6285
Q3143:amount of drug in body/_______ = Vd
Page 6286
plasma drug concentration (note: Vd is Volume ofDistribution)
Page 6287
Q3144:rate of elimination of drug/[plasma drug] = ?
Page 6289
Q3145:(.7)(Vd)/CL = ?
Page 6291
Q3146:A drug infused at a constant rate reaches about 94% ofsteady state after _______ t 1/2s.
Page 6293
Q3147:A loading dose is calculated using this formula.
Page 6294
(Cp)(Vd)/F (note: Cp = target plasma concentration; and F =bioavailability)
Page 6295
Q3148:A maintenance dose is calculated using this formula.
Page 6297
Q3149:Rate of elimination is proportional to _______ ______in 1st order elimination.
Page 6298
drug concentration
Page 6299
Q3150:In the case of EtOH; which is elimated by _____ orderelimination; a constant amount of drug is eliminated per unit
time.
Page 6301
Q3151:Phase ____ (I or II) reactions yield slightly polarmetabolites that are often _____ (active or inactive)
Page 6303
Q3152:Phase ____ (I or II) reactions yield very polarmetabolites that are often _____ (active or inactive) and are
excreted by the _______.
Page 6304
II; inactive; kidney
Page 6305
Q3153:Phase II reactions are often of this type.
Page 6307
Q3154:Cytochrome P-450 is involved in _____ phase (I or II)reactions.
Page 6309
Q3155:A patent lasts for _____ years after filing forapplication.
Page 6311
Q3156:How many phases are there in drug development?
Page 6313
Q3157:Drugs are first tested in patients in phase _____ ofclinical testing; pharmacokinetic safety is determined in phase______ of clinical testing; double blind tests are done in phase
____ and post-market surveillance is done in phase _____.
Page 6315
Q3158:In a dose response curve; a competitive antagonistshifts the curve _____; while a non-competitive antagonist
shifts the curve ______.
Page 6317
Q3159:What pharmacologic relationship would determine theexistence of spare receptors?
Page 6319
Q3160:What does it mean if EC50 and Kd are equal?
Page 6320
The system does not have spare receptors
Page 6321
Q3161:A partial agonist acts on the same receptor system asa full agonist? T/F
Page 6323
Q3162:What's the main difference between a partial agonistand a full agonist?
Page 6324
A partial agonist has a lower maximal efficacy.
Page 6325
Q3163:Is a partial agonist less potent than a full agonist?
Page 6326
Not necessarily. It can be less; more or equally potent as a fullagonist.
Page 6327
Q3164:The penicillin type drugs work by blocking ------synthesis; specifically by inhibiting this molecule from cross-
linking?
Page 6328
blocks bacterial cell wall synthesis by inhibition ofpeptidoglycan synthesis.
Page 6329
Q3165:Which other drugs (aside from penicillin) have thissame mechanism of action?
Page 6330
Imipenem; aztreonam and cephalosporins
Page 6331
Q3166:Bacitracin; vancomycin and cycloserine block thesynthesis of this molecule; preventing cell wall synthesis
Page 6333
Q3167:These drugs block the 50s ribosomal subunit
Page 6334
clindamycin; chloramphenicol; erythromycin; lincomycin;linezolid; streptogramins "Buy AT 30; CELL at
50"
Page 6335
Q3168:These drugs block the 30s ribosomal subunit
Page 6336
Aminoglycosides and tetracyclines "Buy AT 30; CELLat 50"
Page 6337
Q3169:These drugs block nucleotide synthesis by interferingwith the folate pathway
Page 6338
Sulfonamides (e.g. Bactrim); trimethoprim
Page 6339
Q3170:These drugs block DNA topoisomerases
Page 6340
Quinolones (e.g. Cipro)
Page 6341
Q3171:Which drug blocks mRNA synthesis
Page 6343
Q3172:Which are the bacteriacidal Abx
Page 6344
Penicillin; cephalosporin; vancomycin; aminoglycosides;fluoroquinolones; metronidazole
Page 6345
Q3173:These drugs disrupt the bacterial/fungal cellmembranes
Page 6347
Q3174:These specific disrupt fungal cell membranes
Page 6348
amphotericin B; nystatin; fluconazole/azoles (FAN the fungalcell membranes)
Page 6349
Q3175:What is the mechanism of action of Pentamidine
Page 6351
Q3176:Which is the IV form and which is the oral form
Page 6353
Q3177:Which of these is not a mechanism of penicillin action:(1) binds penicillin-binding protein; (2) blocks peptidoglycansynthesis; (3) blocks transpeptidase catalyzed cross-linking
of cell wall and (4) activates autolytic enzymes
Page 6354
Penicillin does not block peptioglycan synthesis; bacitracin;vancomycin and cycloserine do that
Page 6355
Q3178:T or F: penicillin is effective against gram pos andgram neg rods
Page 6356
False: penicillin is used to treat common streptococci (but notstaph); meningococci; gram pos bacilli and spirochetes (i.e.
syphilis; treponema). Not used to treat gram neg rods.
Page 6357
Q3179:What should you watch out for when giving penicillin?
Page 6358
Hypersensitivity rxn (urticaria;severe pruritus) and hemolyticanemia
Page 6359
Q3180:These drugs are used mainly for what type ofinfection
Page 6360
Staphlococcal infection (hence very narrow spectrum)
Page 6361
Q3181:T or F: these drugs have the same mechanism of actionas penicillin
Page 6363
Q3182:Are these drugs penicillinase resistant? If so why?
Page 6364
Bulkier R group makes these drugs resistant to penicillinase
Page 6365
Q3183:What should you watch out for when giving thesedrugs?
Page 6366
Hypersensitivity rxn (urticaria;severe pruritus); methicillincan cuase interstitial nephritis
Page 6367
Q3184:T or F: these drugs have the same mechanism of actionas penicillin
Page 6369
Q3185:Which has greater oral bioavailability?
Page 6370
amOxicillin (O for Oral)
Page 6371
Q3186:What do you use these for?
Page 6372
Ampicillin/amoxicillin HELPS to kill enterococci (H.influenzae; E. coli; Listeria monocytogenes; Proteus mirabilis;
Salmonella)
Page 6373
Q3187:Can penicillinase effect these drugs efficacy?
Page 6374
Yes; they are penicillinase sensitive
Page 6375
Q3188:Why not give these drugs with a penicillinaseinhibitor. Name one.
Page 6376
clavulanic acid
Page 6377
Q3189:What should you watch out for when giving thesedrugs?
Page 6378
Hypersensitivity rxn (ampicillin rash); pseudomembranouscolitis
Page 6379
Q3190:Why are these Carbenicillin; piperacillin; ticarcillinconsidered to have an extended spectrum?
Page 6380
Because they are effective against pseudomonas and othergram neg rods (enterobacter and some species of klebsiella)
Page 6381
Q3191:What should you watch out for when giving thesedrugs?
Page 6382
Hypersensitivity rxn
Page 6383
Q3192:Why does concomitant administration with clavulanicacid increase the efficacy of these drugs?
Page 6384
Because they are penicillinase sensitive. (only piperacillin andticarcillin)
Page 6385
Q3193:What is the mechanism of action of Cephalosporins?
Page 6386
inhibit cell wall synthesis
Page 6387
Q3194:How are they similar/different from penicillin?
Page 6388
both have a beta-lactam ring structure but cephalosporins areless susceptible to penicillinases
Page 6389
Q3195:What are the main similarities/difference between 1stand 2nd generation cephalosporins?
Page 6390
2nd gen has extensive gram neg coverage but weaker gram poscoverage
Page 6391
Q3196:1st gen covers what bugs?
Page 6392
gram positives (staph and strep); Proteus mirabilis; E. coli;Klebsiella (PEcK)
Page 6393
Q3197:2nd gen covers what bugs?
Page 6394
gram positives (staph and strep) though less so; H.influenzae; Enterobacter aerogenes; Neisseria; Proteus
mirabilis; E. coli; Klebsiella (HEN PEcK)
Page 6395
Q3198:What can 3rd generation drugs do that 1st and 2ndgeneration can't?
Page 6396
Cross the blood brain barrier
Page 6397
Q3199:What are some other benefits of 3rd gen?
Page 6398
better activity against gram neg bugs resistant to beta-lactamdrugs. Ceftazidime for Pseudomonas and ceftriaxone for N.
gonorrhea
Page 6399
Q3200:What are the benefits of 4th gen (e.g. Cefipime)?
Page 6400
increased activity against Pseudomonas; gram pos organismsand more beta-lactamase resistant (i.e. 4th gen combines 1st
gen and 3rd gen characteristics into super drug)
Page 6401
Q3201:What drugs should you avoid taking withcephalosporins?
Page 6402
Aminoglycosides (increases nephrotoxicity) and ethanol(causes a disulfiram-like rxn -- headache; nausea; flushing;
hypotension)
Page 6403
Q3202:When would you use aztreonam?
Page 6404
Only to treat Klebsiella; Pseudomonas and Serratia spp.
Page 6405
Q3203:Is it beta-lactamase resistant?
Page 6406
Yes; this is one of the huge benefits of the drug; and it is notcross-reactive with PCN!
Page 6407
Q3204:Which population of pt. is this drug good for?
Page 6408
The PCN-allergic patient that can't take aminoglycosides b/cof renal insufficiency
Page 6409
Q3205:Are there any toxicity issues with this drug?
Page 6410
Not really. Generally well tolerated with occasional GI upset.Vertigo; Headache and rare hepatotoxicity have been reported.
Page 6411
Q3206:What is imipenem?
Page 6412
broad spectrum beta-lactamase-resistant abx
Page 6413
Q3207:What do you always administer it with and why?
Page 6414
cilastatin -- it decreases inactivation of imipenem in renaltubules
Page 6415
Q3208:What do you use it for?
Page 6416
Gram pos cocci; gram neg rods and anaerobes (broadspectrum)
Page 6417
Q3209:What bug is it the drug of choice for?
Page 6419
Q3210:What are its side-effects
Page 6420
GI distress; skin rash; seizures at high conc.
Page 6421
Q3211:Is Vancomycin bactericidal or bacteriastatic and why?
Page 6422
Bactericidal because it blocks cross linkage and elongation ofpeptidoglycan by binding D-ala D-ala protion of cell wall.
Page 6423
Q3212:How does resistance to Vanco occur?
Page 6424
D-ala D-ala is replaced with D-ala D-lactate which vanco doesnot block
Page 6425
Q3213:What is it used for?
Page 6426
Used for serious infection that is resistant to other drugs (e.g.gram pos multi-drug resistant organisms like S. aureus and C.
difficile; methicillin resistant staph (MRSA))
Page 6427
Q3214:What are the important toxicities of vanco?
Page 6428
generally NOT many problems except; Nephrotoxicity;Ototoxicity and Thrombophlebitis
Page 6429
Q3215:What can happen with rapid infusion of vanco?
Page 6430
"Red man's" syndrome. Diffuse flushing whichcan be controlled by pretreatment with anti-histamines and
with slow infusion rate
Page 6431
Q3216:Which drugs target bacterial protein synthesis byblocking the 30S unit vs 50S unit?
Page 6432
Buy AT 30; CELL at 50
Page 6433
Q3217:What does AT stand for?
Page 6434
A = Aminoglycosides (streptomycin; gentamicin; tobramycinan damikacin. And T = Tetracyclines
Page 6435
Q3218:What does CELL stand for?
Page 6436
C = Chloramphenicol; E= Erythromycin; L= Lincomycin andL= cLindamycin
Page 6437
Q3219:Which of the above are bactericidal?
Page 6438
Only the aminoglycosides are; the rest are bacteriostatic
Page 6439
Q3220:Name some aminoglycosides?
Page 6440
Gentamicin; neomycin; amikacin; tobramycin andstreptomycin
Page 6441
Q3221:How do these drugs work?
Page 6442
They inhibit formation of the initiation complex in mRNAtranslation
Page 6443
Q3222:Why are they ineffective against anaerobes?
Page 6444
They require oxygen for uptake into bacteria
Page 6445
Q3223:When would you use aminoglycosides?
Page 6446
against severe gram-negative rod infections
Page 6447
Q3224:What drugs can you use aminoglycosides with forsynergy?
Page 6448
the drugs that inhibit cell wall synthesis (e.g. penicillin andcephalosporins -- the beta-lactam antibiotics). Presumablythis allows the drug to get in with out reliance on oxygen
transport
Page 6449
Q3225:What drug in this class is commonly used for bowelsurgery?
Page 6451
Q3226:What are the two major toxicities?
Page 6452
Nephrotoxicity (esp. when used with cephalosporins) andOtotoxicity (esp. when used with loop diuretics).
amiNOglycosides
Page 6453
Q3227:Name some tetracylcines
Page 6454
Tetracycline; doxycycline; demeclocycline; minocycline
Page 6455
Q3228:How does it work?
Page 6456
Blocks t-RNA attachment to 30S subunit
Page 6457
Q3229:Which tetracycline can you use in patients with renalfailure and why?
Page 6458
Can use doxycycline because its elimination is fecal
Page 6459
Q3230:Should you take these drugs with a glass of milk?
Page 6460
NO; because it intereferes with absorption in the gut as doesantacids and iron-containing preparations
Page 6461
Q3231:What are tetracyclines used for?
Page 6462
VACUUM your Bed Room -- Vibrio cholerae; Acne;Chlamydia; Ureaplasma; Urealyticum; Mycoplasma
pneumoniae; Borrelia burgdorferi; Rickettsia; tularemia
Page 6463
Q3232:What are the common toxicities
Page 6464
GI distress; teeth discoloration; inhibition of bone growth inchildren; Fanconi's syndrome and photosensitivity
Page 6465
Q3233:Name some macrolides?
Page 6466
Erythromycin; azithromycin; clarithromycin
Page 6467
Q3234:How do these drugs work?
Page 6468
inhibit protein synthesis
Page 6469
Q3235:What are they used for?
Page 6470
URIs; pneumonias; STDs -- gram pos cocci in patients thatare allergic to PNC --- Mycoplasm; Legionella; Chlamydia;
Neisseria.
Page 6471
Q3236:Pneumonic for macrolide use?
Page 6472
Eryc's Nipple is at his Mid Clavicular Line (Eryc is brandname for erythromycin). Mycoplasm; Legionella; Chlamydia;
Neisseria.
Page 6473
Q3237:What are the major toxicities?
Page 6474
GI discomfort; acute cholestatic hepatitis; eosinophilia; skinrashes
Page 6475
Q3238:What is the most common cause for non-complianceto macrolides?
Page 6477
Q3239:How does Chloramphenicol work?
Page 6478
inhibits 50S peptidyltransferase
Page 6479
Q3240:Main use?
Page 6480
Meningitis (H. influenzae; N. meningitides; S. pneumo). Usedconservatively b/c of toxicity
Page 6481
Q3241:What are the main toxicities?
Page 6482
Anemia and aplastic anemia (both dose dependent); gray babysyndrome (in premes b/c they lack UDP-glucoronyl
transferase)
Page 6483
Q3242:How does Clindamycin work?
Page 6484
blocks peptide bond formation at 50S
Page 6485
Q3243:When do you use it?
Page 6486
Anaerobic infections (e.g. Bacteroides fragilis andC.perfringens)
Page 6487
Q3244:Toxicities?
Page 6488
Pseudomembranous colitis; fever; diarrhea
Page 6489
Q3245:Name some sulfonamides
Page 6490
Sulfamethoxazole (SMX); sulfisoxazole; triple sulfa andsulfadiazine
Page 6491
Q3246:How does it work?
Page 6492
Inhibits bacterial folic acid synthesis from PABA by blockingdihydropteroate synthase.
Page 6493
Q3247:What are its uses?
Page 6494
Gram-positive; gram-negative; Nocardia; Chlamydia. Triplesulfas and SMX for simple UTIs
Page 6495
Q3248:Toxicities?
Page 6496
hypersensitivity rxn; hemolysis if G6PD deficient;nephorotoxicity (tubulointerstitial nephritis); kernicterus in
infants; displace other drugs from albumin (e.g. warfarin)
Page 6497
Q3249:How does Trimethoprim work?
Page 6498
inhibits folic acid pathway by blocking dihydrofolatereductase which humans have as well
Page 6499
Q3250:What are its uses?
Page 6500
used in combo with Sulfamethoxazole (TMP-SMX) causing asequential block of folate synthesis. Used for recurrent UTIs;
Shigella; Salmonella; and prophylaxis for PCP in AIDSpatients
Page 6501
Q3251:Toxicities?
Page 6502
Megaloblastic anemia; pancytopenia (may be alleviated withsupplemental folinic acid)
Page 6503
Q3252:What the most famous floroquinolone?
Page 6504
Ciprfloxacin (treatment for Anthrax)
Page 6505
Q3253:How does it work?
Page 6506
inhibits DNA gyrase (topoisomerase II)
Page 6507
Q3254:What are its uses?
Page 6508
Gram neg rods or urinary and GI tract (incl. pseudomonas);Neisseria; some gram pos spp
Page 6509
Q3255:What population is contraindicated for use?
Page 6510
pregnancy and children
Page 6511
Q3256:What are its toxicities?
Page 6512
GI upset; superinfection; skin rashes; headache; dizziness andtendonitis and tendon rupture in adults. FluoroquinoLONES
hurt attachment to BONES.
Page 6513
Q3257:How does Metronidazole work?
Page 6514
forms toxic metabolites in the bacteria. Bactericidal.
Page 6515
Q3258:What are its uses?
Page 6516
anti-protozoal: Giardia; Entamoeba; Trichomonas; Gardnerellavaginalis; anaerobes (bacteroides; clostridium)
Page 6517
Q3259:What is the role of Metronidazole in H. pyloriinfection?
Page 6518
Used as part of triple therapy: bismuth; amoxicillin andmetronidazole
Page 6519
Q3260:Main toxicity?
Page 6520
disulfiram-like (antabuse) reaction to alcohol and headache
Page 6521
Q3261:Which drug do you use to treat anaerobic infectionsabove the diaphram and below the diaphram
Page 6522
anaerobes above diaphram: Clindamycin; and anaerobes belowdiaphram: metronidazole
Page 6523
Q3262:How does polymyxin work?
Page 6524
disrupts osmotic properties of bacteria; acts like a detergent
Page 6525
Q3263:What is it used for?
Page 6526
resistant gram negative infections
Page 6527
Q3264:Toxicities?
Page 6528
neurotoxicity; ATN
Page 6529
Q3265:How does INH work?
Page 6530
decreases synthesis of mycolic acid
Page 6531
Q3266:What is it used for?
Page 6532
MTB (mycobacterium tuberculosis). The only agent used assolo prophylaxis against TB
Page 6533
Q3267:Toxicities?
Page 6534
Hemolysis if G6PD deficient; neurotoxicity; hepatotoxicitiy;drug induced SLE. INH; Injures Neurons and Hepatocytes
Page 6535
Q3268:What vitamin prevents neurotoxicity
Page 6536
Vitamin B6 (pyridoxine)
Page 6537
Q3269:Why are toxicities particularly important to monitor inpatients taking INH?
Page 6538
INH half-lives are different in fast versus slow acetylators!
Page 6539
Q3270:How does it work?
Page 6540
inhibits DNA-dependent RNA polymerase
Page 6541
Q3271:What is it used for?
Page 6542
MTB; meningococcal prophylaxis
Page 6543
Q3272:Toxicities?
Page 6544
Minor hepatotoxicity and increases P-450
Page 6545
Q3273:How can it be used for leprosy?
Page 6546
rifampin delays resistance to dapsone when used for leprosy
Page 6547
Q3274:What would happen if you used rifampin alone?
Page 6548
get rapid resistance
Page 6549
Q3275:What does it do to bodily fluids?
Page 6550
makes them red/orange in color
Page 6551
Q3276:What are the 4 R's of Rifampin
Page 6552
RNA polymerase inhibitor; Revs up microsomal p-450;Red/Orange body fluids; Resistance is rapid
Page 6553
Q3277:What are the anti-TB drugs?
Page 6554
Rifampin; Ethambutol; Streptomycin; Pyrazinamide;Isoniazid (INH) -- RESPIre
Page 6555
Q3278:What do you use for TB prophylaxis?
Page 6557
Q3279:What toxicity is common to all?
Page 6559
Q3280:name the enzyme that liberates AA from the cellmembrane
Page 6560
phospholipase A2
Page 6561
Q3281:what does the lipoxygenase pathway yield
Page 6562
leukotrienes (L for Lipoxygenase and Leukotrienes)
Page 6563
Q3282:LTB4 is a____
Page 6564
neutrophil chemotactic agent
Page 6565
Q3283:which leukotrienes are involved inbronchoconstriction; vasoconstriction; smooth muscle
contraction; and increased vascular permeability
Page 6566
LT C4; D4; E4 (SRS-A)
Page 6567
Q3284:what are the 3 products of the cyclooxygenasepathway?
Page 6568
thromboxane; prostacyclin; prostaglandin
Page 6569
Q3285:what are the 2 functions of TxA2
Page 6570
platelet aggregation; vasoconstricion
Page 6571
Q3286:what are the 2 functions of PGI2
Page 6572
inhibition of platelet aggregation; vasodilation (PlateletGathering Inhibitor)
Page 6573
Q3287:what are the shape and dimensions of a microtubule?
Page 6574
cylindrical; 24 nm in diameter; variable length.
Page 6575
Q3288:what are the components of a microtubule
Page 6576
polymerized dimers of alpha and beta tubulin (+2 GTPs perdimer)
Page 6577
Q3289:where are microtubules found
Page 6578
cilia; flagella; mitotic spindles; neuronal axons (slowaxoplasmic transport)
Page 6579
Q3290:antihelminthic drug that acts on microtubules
Page 6580
mebendazole/thiabendazole
Page 6581
Q3291:anti breast cancer drug that acts on microtubules(prevent disassembly)
Page 6583
Q3292:antifungal drug that acts on microtubules
Page 6585
Q3293:anti cancer drug that acts on microtubules (preventassembly)
Page 6586
vincristine/vinblastine
Page 6587
Q3294:anti gout drug that acts on microtubules
Page 6589
Q3295:Most common resistance mechanism for penicillins /cephalosporins.
Page 6590
Beta-lactamase cleavage of beta-lactam ring.
Page 6591
Q3296:Most common resistance mechanism foraminoglycosides.
Page 6592
Modification via acetylation; adenylation; orphosphorylation.
Page 6593
Q3297:Most common resistance mechanism for vancomycin.
Page 6594
Terminal D-ala of cell wall component replaced with D-lac;decrease affinity.
Page 6595
Q3298:Most common resistance mechanism forChlorampenicol.
Page 6596
Modification via acetylation.
Page 6597
Q3299:Most common resistance mechanism for macrolides.
Page 6598
Methylation of rRNA near erythromycin's ribosome-bindingsite.
Page 6599
Q3300:Most common resistance mechanism for tetracycline.
Page 6600
Decrease uptake or increase transport out of cell.
Page 6601
Q3301:Most common resistance mechanism for sulfonamides.
Page 6602
Altered enzyme (bacterial dihydropteroate synthetase);decrease uptake; or increase PABA synthesis.
Page 6603
Q3302:Drug of choice for meningococcal infection.
Page 6604
Rifampin (drug of choice); minocycline.
Page 6605
Q3303:Drug of choice for gonorrhea.
Page 6607
Q3304:Drug of choice for syphilis.
Page 6608
Benzathine penicillin G.
Page 6609
Q3305:Drug of choice for history of recurrent UTIs.
Page 6611
Q3306:Drug of choice for Pneumocystis carinii pneumonia.
Page 6612
TMP-SMX (drug of choice); aerosolized pentamindine.
Page 6613
Q3307:Mechanism of action of the anti-fungal therapypolyenes.
Page 6614
Form artificial pores in the cytoplasmic membrane.
Page 6615
Q3308:Mechanism of action of the anti-fungal therapiesterbinafine and azoles.
Page 6616
Terbinafine blocks the conversion of squalene to lanosterol.Azoles block the conversion of lanosterol to ergosterol.
Page 6617
Q3309:Mechanism of action of the anti-fungal therapyflucytosine.
Page 6618
Blocks the production of purines from the precurors.
Page 6619
Q3310:Mechanism of action of the anti-fungal therapygriseofulvin.
Page 6620
Disrupts microtubles.
Page 6621
Q3311:Mechanism of action of Amphotericin B.
Page 6622
Binds ergosterol (unique to fungi); forms membrane pores thatallow leakage of electrolytes and disrupt homeostasis.
"Amphotericin 'tears' holes in the fungal membrane byforming pores."
Page 6623
Q3312:Clinical uses of Amphotericin B.
Page 6624
Used for a wide spectrum of sytemic mycoses.Cryptococcus; Blastomyces; Coccidioides; Aspergillus;
Histoplasma; Candida; Mucor (systemic mycoses).Intrathecally for fungal meningitis; does not cross blood-brain
barrier.
Page 6625
Q3313:Symptoms of Amphotericin B toxicity.
Page 6626
Fever/chills ("shake and bake"); hypotension;nephrotoxicity; arrhythmias ("amphoterrible").
Page 6627
Q3314:Mechanism of action of Nystatin.
Page 6628
Binds to ergosterol; disrupting fungal membranes.
Page 6629
Q3315:Clinical use of Nystatin.
Page 6630
"Swish and swallow" for oral candidiasis (thrush).
Page 6631
Q3316:Mechanism of action for fluconazole; ketoconazole;clotrimazole; miconazole; itraconazole; voriconazole.
Page 6632
Inhibits fungal steroid (ergosterol) synthesis.
Page 6633
Q3317:Clinical uses of fluconazole; ketoconazole;clotrimazole; miconazole; itraconazole; voriconazole.
Page 6634
Systemic mycoses. Fluconazole for cryptococcal meningitis inAIDS patients and candidal infections of all types (i.e; yeast
infections). Ketoconazole for Blastomyces; coccidioides;Histoplasma; Candida albicans; hypercortisolism.
Page 6635
Q3318:Symptoms of fluconazole; ketoconazole; clotrimazole;miconazole; itraconazole; voriconazole toxicity.
Page 6636
Hormone synthesis inhibition (gynecomastia); liverdysfunction (inhibits cytochrome P-450); fever; chills.
Page 6637
Q3319:Mechanism of action of Flucytosine.
Page 6638
Inhibits DNA synthesis byconversion to fluorouracil; whichcompetes with uracil.
Page 6639
Q3320:Clinical uses of Flucytosine.
Page 6640
Used in sytemic fungal infections (e.g. Candida;Cryptococcus).
Page 6641
Q3321:Symptoms of Flucytosine toxicity.
Page 6642
Nausea; vomitting; diarrhea; bone marrow suppression.
Page 6643
Q3322:Mechanism of action for Caspofungin.
Page 6644
Inhibits cell wall synthesis.
Page 6645
Q3323:Clinical use of Caspofungin.
Page 6646
Invasive aepergillosis.
Page 6647
Q3324:Symptoms of Caspofungin toxicity.
Page 6648
GI upset; flushing.
Page 6649
Q3325:Mechanism of action of Terbinafine.
Page 6650
Inhibits the fungal enzyme squalene epoxidase.
Page 6651
Q3326:Clinical use of Terbinafinel.
Page 6652
Used to treat dermatophytoses (especially onychomycosis).
Page 6653
Q3327:Mechanism of action of Griseofulvin.
Page 6654
Interfers with microtubule function; disrupts mitosis.Deposits in keratin-contianing tissues (e.g. nails).
Page 6655
Q3328:Clinical use of Griseofulvin.
Page 6656
Oral treatment of superficial infections; inhibits growth ofdermatophytes (tinea; ringworm).
Page 6657
Q3329:Symptoms of Griseofulvin toxicity.
Page 6658
Teratogenic; carcinogenic; confusion; headaches; increasewarfarin metabolism.
Page 6659
Q3330:Viral adsorption and penetration into the cell isblocked by ---------.
Page 6660
Gama-globulins (non-specific).
Page 6661
Q3331:Uncoating of the virus after its penetration into thecell is blocked by --------.
Page 6662
Amantadine (influenza A).
Page 6663
Q3332:Early viral protein synthesis is blocked by --------.
Page 6664
Fomivirsen (CMV).
Page 6665
Q3333:Viral nuclei acid synthesis is blocked by --------.
Page 6666
Purine; pyrimidine analogs; reverse transcriptase inhibitors.
Page 6667
Q3334:Late viral protein synthesis and processing is blockedby --------.
Page 6668
Methimazole (variola); protease inhibitors.
Page 6669
Q3335:Packaging and assembly of new viron is blocked by --------.
Page 6670
Rifampin (vaccinia).
Page 6671
Q3336:Mechanism of action of Amantadine.
Page 6672
Blocks viral penetration/uncoating; may buffer pH ofendosome. Also causes the release of dopamine from intactnerve terminals. "Amantadine blocks influenza A and
rubellA and causes problems with the cerebellA."
Page 6673
Q3337:Clinical uses of Amantadine.
Page 6674
Prophylaxis for influenza A; Parkinson's disease.
Page 6675
Q3338:Symptoms of Amantadine toxicity.
Page 6676
Ataxia; dizziness; slurred speech. (Rimantidine is a derivativewith fewer CNS side effects.)
Page 6677
Q3339:Zanamivir
Page 6679
Q3340:Mechanism of action of Zanamivir.
Page 6680
Inhibits influenza neuraminidase.
Page 6681
Q3341:Clinical use of Zanamivir.
Page 6682
Both influenza A and B.
Page 6683
Q3342:Mechanism of action of Ribavirin.
Page 6684
Inhibits synthesis of guanine nucleotides by competitivelyinhibiting IMP dehydrogenase.
Page 6685
Q3343:Clinical use of Ribavirin.
Page 6686
RSV (respiratory syncytial virus).
Page 6687
Q3344:Symptoms of Ribavirin toxicity.
Page 6688
Hemolytic anemia. Severe teratogen.
Page 6689
Q3345:Mechanism of aciton of Acyclovir.
Page 6690
Perferentially inhibits viral DNA polymerase whenphosphorylated by viral thymidine kinase.
Page 6691
Q3346:Clinical use of Acyclovir.
Page 6692
HSV; VZV; EBV. Mucocutaneous and genital herpes lesions.Prophylaxis in immunocompromised patients.
Page 6693
Q3347:Symptoms of Acyclovir toxicity.
Page 6694
Delirium; tremor; nephrotoxicity.
Page 6695
Q3348:Mechanism of action of Ganciclovir.
Page 6696
Phosphorlation by viral kinase; perferentially inhibits CMVDNA polymerase.
Page 6697
Q3349:Clinical use of Ganciclovir.
Page 6698
CMV; especially in immunocompromised patients.
Page 6699
Q3350:Symptoms of Ganciclovir toxicity.
Page 6700
Leukopenia; neutropenia; thrombocytopenia; renal toxicity.More toxic to host enzymes than acyclovir.
Page 6701
Q3351:Mechanism of action of Foscarnet.
Page 6702
Viral DNA polymerase inhibitor that binds to thepyrophophate binding site of the enzyme. Does not require
activation by viral kinase. "FOScarnet = pyroFOSphateanalog."
Page 6703
Q3352:Clinical use of Foscarnet.
Page 6704
CMV retinitis in immunocompromised patients whenganciclovir fails.
Page 6705
Q3353:Symptoms of Foscarnet toxicity.
Page 6706
Nephrotoxicity.
Page 6707
Q3354:Saquinavir; ritonavir; indinavir; nelfinavir; amprenavirare example of this type of anti-HIV drug.
Page 6708
Protease inhibitor.
Page 6709
Q3355:Mechanism of action of protease inhibitors.
Page 6710
Inhibit assembly of new virus by blocking protease enzyme.
Page 6711
Q3356:Symptoms of protease inhibitor toxicity.
Page 6712
GI intolerance (nausea; diarrhea); hyperglycemia; lipidabnormalities; thrombocytopenia (indinavir).
Page 6713
Q3357:Zidovudine (AZT); didanosine (ddI); zalcitabine(ddC); stavudine (d4T); lamivudine (3TC); and abacavir are
examples of --------- reverse transcriptase inhibitors.
Page 6715
Q3358:Nevirapine; delavirdine; and efavirenz are examples of--------- reverse transcriptase inhibitors.
Page 6716
Non-nucleoside.
Page 6717
Q3359:Mechanism of action of reverse transcriptaseinhibitors.
Page 6718
Preferentially inhibit reverse transcriptase of HIV; preventincorporation of viral genome into host DNA.
Page 6719
Q3360:Symptoms of reverse transcriptase inhibitor toxicity.
Page 6720
Bone marrow supression (neutropenia; anemia); periphralneuropathy; lactic acidosis (nucleosides); rash (non-
nucleosides); megaloblastic anemia (AZT).
Page 6721
Q3361:Highly active antiretroviral therapy (HAART)generally entails combination therapy with ---------- and -------
----.
Page 6722
Protease inhibitors; reverse transcriptase inhibitors.
Page 6723
Q3362:When should HIV therapy be initiated?
Page 6724
When patients have low CD4 counts (<500 cells/mm3) orhigh viral load.
Page 6727
Q3364:Mechanism of action of Interferons.
Page 6728
Glycoproteins from human leukocytes that block variousstages of viral RNA and DNA synthesis.
Page 6729
Q3365:Clinical use of Interferons.
Page 6730
Chronic hepatitis B and C; Kaposi's sarcoma.
Page 6731
Q3366:Symptoms of Interferon toxicity.
Page 6733
Q3367:Clinical uses of Ivermectin.
Page 6734
Onchocerciasis "rIVER blindness treated withIVERmectin"
Page 6735
Q3368:Clinical uses of Mebendazole / thiabendazole.
Page 6736
Nematode/roundworm (e.g; pinworm; whipworm) infections.
Page 6737
Q3369:Clinical uses of Pyrantel pamoate.
Page 6738
Giant roundworm (Ascaris); hookworm(Necator/Ancylostoma); pinworm (Enterobius).
Page 6739
Q3370:Clinical uses of Praziquantel.
Page 6740
Trematode/fluke (e.g; schistosomes; Paragonimus; Clonorchis)and cysticercosis.
Page 6741
Q3371:Clinical uss of Niclosamide
Page 6742
Cestode/tapeworm (e.g; Diphyllobothrium latum; Taeniaspecies) infections except cysticercosis.
Page 6743
Q3372:Clinical uses of Pentavalent antimony.
Page 6745
Q3373:Clinical uses of Chloroquine; quinine; mefloquine;atovaquone; proguanil.
Page 6747
Q3374:Clinical uses of Primaquine.
Page 6748
Latent hypnozoite (liver) forms of malaria (Plasmodiumvivax; P.ovale).
Page 6749
Q3375:Clinical uses of Metronidazole.
Page 6750
Giardiasis; amebic dysentery (Entamoeba histolytica);bacterial vaginitis (Gardnerella vaginalis); Trichomonas.
Page 6751
Q3376:Clinical uses of Pentamidine.
Page 6752
Pneumocystis carinii pneumonia prophylaxis.
Page 6753
Q3377:Clinical uses of Nifurtimox.
Page 6754
Chagas' disease; American trypanosomiasis (Trypanosomacruzi).
Page 6755
Q3378:Clinical uses of Suramin.
Page 6756
African trypanosomiasis (sleeping sickness).
Page 6757
Q3379:Parasympathetic preganglionic neurons release theneurotransmitter -------- which act on -------- receptors.
Page 6758
Ach; nicotinic.
Page 6759
Q3380:Sympathetic preganglionic neurons to sweat glandsrelease the neurotransmitter ------- which act on -------
receptors.
Page 6760
Ach; nicotinic.
Page 6761
Q3381:Ach is synthesized from acetyl-CoA and choline bythe enzyme ---------.
Page 6762
Choline acetyltransferase.
Page 6763
Q3382:In the noradrenergic nerve terminal; tyrosine ishydroxylated to -------; which is decarboxylated to --------;
which is finally hydroxylated to NE.
Page 6764
DOPA; dopamine.
Page 6765
Q3383:The action of NE and DA is terminated by ---------and ----------.
Page 6766
Reuptake; diffusion (different than for Ach).
Page 6767
Q3384:The drugs --------- and ---------- inhibit the reuptake ofNE.
Page 6769
Q3385:Ach inhibits the release of NE from the noradrenergicnerve terminal by binding to --------- receptors.
Page 6771
Q3386:Clinical application and action of Carbachol andPilocarpine.
Page 6772
Glaucoma. / Activates ciliary muscle of eye (open angle);pupillary sphincter (narrow angle).
Page 6773
Q3387:Clinical application / action of Neostigmine.
Page 6774
Postoperative and neurogenic ileus and urinary retention;myasthenia gravis; reversal of neuromuscular junctionblockade (postoperative). / Increase endogenous Ach.
Page 6775
Q3388:Clinical application / action of Pyridostigmine.
Page 6776
Myasthenia gravis. / Increase Ach; increase strength.
Page 6777
Q3389:Clinical application / action of Physostigmine.
Page 6778
Glaucoma (crosses blood-brain barrier) and atropine overdose./ Increase endogenous Ach.
Page 6779
Q3390:Clinical application / action of Echothiophate.
Page 6780
Glaucoma. / Increase endogenous Ach.
Page 6781
Q3391:Symptoms of cholinesterase inhibitor poisoning.
Page 6782
Diarrhea; Urination; Miosis; Bronchospasm; Bradycardia;Excitation of skeletal muscle and CNS; Lacrimation; Sweating;
Salivation (also abdominal cramping)."DUMBBELSS"
Page 6783
Q3392:Cholinesterase inhibitor poisoning may be caused by ---------.
Page 6784
Parathion and other organophosphates.
Page 6785
Q3393:The cholinesterase regenerator ------- can be used as anantidote for cholinesterase inhibitor poisoning.
Page 6787
Q3394:Mechanism of action of Pralidoxime.
Page 6788
Regenerates active cholinesterase; chemical antagonist; used totreat organophosphate exposure.
Page 6789
Q3395:Clinical uses of the muscarinic antagonist Atropine.
Page 6790
Dilate pupils; decrease acid secretion in peptic ulcer disease;decrease urgency in mild cystitis; decrease GI motility; reduce
airway secretions; and treat organophosphate poisoning."Blocks SLUD: Salivation; Lacrimation; Urination;
Defecation."
Page 6791
Q3396:Side effects of Atropine.
Page 6792
Increase body temp; rapid pulse; dry mouth; dry/flushed skin;disorientation; mydriasis with cycloplegia; and constipation."Atropine parasympathetic block side effects: Blind asbat; Red as a beet; Mad as a hatter; Hot as a hare; Dry as a
bone."
Page 6793
Q3397:Hexamethonium (ganglionic blocker) blocks --------receptors.
Page 6795
Q3398:"tropi" are anti-muscarinic
Page 6796
while vacationing in the tropics you lie on a beach and yourmuscles waste away!
Page 6797
Q3399:benztropine is used to treat
Page 6798
Parkinson's disease
Page 6799
Q3400:scopolamine is used to treat
Page 6800
motion sickness
Page 6801
Q3401:name 2 antimuscarinic drugs that act on the CNS
Page 6802
benztropine; scopolamine
Page 6803
Q3402:name a muscarinic used to treat motion sickness
Page 6805
Q3403:name a muscarinic used to treat Parkinson's disease
Page 6807
Q3404:mechanism of action of benztropine
Page 6809
Q3405:mechanism of action of scopolamine
Page 6811
Q3406:name three antimuscarinics that act on eye
Page 6812
atropine; homatropine; tropicamide
Page 6813
Q3407:the action of atropine is ______
Page 6814
produce mydriasis; cycloplegia
Page 6815
Q3408:mechanism of atropine is
Page 6817
Q3409:the action of homatropine is ______
Page 6818
produce mydriasis; cycloplegia
Page 6819
Q3410:mechanism of homatropine is
Page 6821
Q3411:the action of tropicamide is
Page 6822
produce mydriasis; cycloplegia
Page 6823
Q3412:mechanism of tropicamide is
Page 6825
Q3413:ipatropium is used to treat
Page 6827
Q3414:mechanism of ipatropium is
Page 6829
Q3415:name an antimuscarinic used to treat asthma andCOPD
Page 6831
Q3416:neuromuscular blocking drugs are used for
Page 6832
muscle paralysis in surgery or mechanical ventilation
Page 6833
Q3417:name a depolarising neurmuscular blocking drug
Page 6834
succinylcholine
Page 6835
Q3418:name 6 nondepolarizing neuromuscular blocking drugs
Page 6837
Q3419:*mnemonic -- the "cur" drugs arenondepolarizing neuromuscular blocking agents
Page 6838
Atracurium; mivacurium; pancuronium; vecuronium;rapacuronium
Page 6839
Q3420:is succinylcholine depolarizing or nondepolarizing?
Page 6841
Q3421:is tubocurarine depolarizing or nondepolarizing?
Page 6842
nondepolarizing
Page 6843
Q3422:is atracurium depolarizing or nondepolarizing?
Page 6844
nondepolarizing
Page 6845
Q3423:is mivacurium depolarizing or nondepolarizing?
Page 6846
nondepolarizing
Page 6847
Q3424:is pancuronium depolarizing or nondepolarizing?
Page 6848
nondepolarizing
Page 6849
Q3425:is vacuronium depolarizing or nondepolarizing?
Page 6850
nondepolarizing
Page 6851
Q3426:is rapacuronium depolarizing or nondepolarizing?
Page 6852
nondepolarizing
Page 6853
Q3427:what is tubocurarine used for
Page 6854
nondepolarizing neuromuscular blockade
Page 6855
Q3428:what agents are used to reverse neuromuscularblockade by succinylcholine?
Page 6856
cholinesterase inhibitors in phase II (ex -- neostigmine)
Page 6857
Q3429:what phase of succinylcholine neuomuscularbloackade is reversible?
Page 6858
phase II (repolarized but blocked)
Page 6859
Q3430:what agents are used to reverse pahse I neuromuscularblockade by succinylcholine?
Page 6860
phase I Succinylcholine neuromuscular blockade cannot bereversed
Page 6861
Q3431:what phase of succinylcholine neuomuscularbloackade is irreversible?
Page 6862
phase I Succinylcholine neuromuscular blockade cannot bereversed
Page 6863
Q3432:what is atracurium used for
Page 6864
nondepolarizing neuromuscular blockade
Page 6865
Q3433:what is the effect of cholinesterase inhibitors onsuccinylcholine neuromuscular blockade?
Page 6866
phase I: cholinesterase inhibitors potentiates the blockadephase II: cholinesterase inhibitors reverse the blockade
Page 6867
Q3434:what cholinesterase inhibitor is used to reverse phaseII of succinylcholine neuromuscular blockade?
Page 6869
Q3435:what is mivacurium used for
Page 6870
nondepolarizing neuromuscular blockade
Page 6871
Q3436:what is dantrolene used for
Page 6872
treat malignant hyperthermia
Page 6873
Q3437:what causes malignant hyperthermia
Page 6874
use inhalation anesthetics and succinylcholine together
Page 6875
Q3438:what inhalation anesthetic DOES NOT causemalignanat hyperthermia?
Page 6877
Q3439:what is dantrolene used for
Page 6878
neuroleptic malignant syndrome
Page 6879
Q3440:what is neuroleptic malignant syndrome
Page 6880
a toxicity of antipsychotic drugs
Page 6881
Q3441:what drug is used to treat malignant hyperthermia
Page 6883
Q3442:what is the mechanism of dantrolene
Page 6884
prevents release of Ca++ from saarcoplasmic reticulum ofskeletal muscle
Page 6885
Q3443:epinephrine; NE; isoproterenol; dopamine; anddobutamine are all________________
Page 6887
Q3444:catecholamines are_____________________
Page 6888
sympathomimetics
Page 6889
Q3445:name 5 catecholamines
Page 6890
EPI; NE; Isoproterenol; dopamine; dobutamine
Page 6891
Q3446:what receptors does epinephrine act on?
Page 6892
alpha-1; alpha-2; beta-1; beta-2 adrenergics
Page 6893
Q3447:what receptors does NE work on?
Page 6894
alpha-1; alpha-2; beta-1 adrenergics
Page 6895
Q3448:what receptors does isoproterenol work on?
Page 6896
beta-1 = beta-2 adrenergics
Page 6897
Q3449:what receptors does dopamine work on?
Page 6898
D1 = D2; D1 and D2 more than beta; beta more than alpha
Page 6899
Q3450:what receptors does dobutamine work on?
Page 6900
beta-1 > beta-2
Page 6901
Q3451:which catecholamines are agonists to alpha-adrenergicreceptors
Page 6902
EPI; NE > dopamine
Page 6903
Q3452:which catecholamines are agonists to beta-1 adrenergicreceptors
Page 6904
EPI; NE; Isoproterenol; dopamine; dobutamine
Page 6905
Q3453:which catecholamines are agonists to beta-2 adrenergicreceptors
Page 6906
EPI; isoproterenol; dopamine and dobutamine (less)
Page 6907
Q3454:what is epinephrine used to treat?
Page 6908
anaphylaxis; open-angle glaucoma; asthma; hypotension
Page 6909
Q3455:what is norepinephrine used to treat?
Page 6910
hypotension (but decreases renal perfusion)
Page 6911
Q3456:what is isoproterenol used to treat?
Page 6913
Q3457:what is dopamine used to treat
Page 6914
shock with renal failure; heart failure
Page 6915
Q3458:what is dobutamine used to treat
Page 6916
shock; heart failure
Page 6917
Q3459:what catecholamine is used to treat anaphylaxis
Page 6918
epinephrine ("EPI-pen")
Page 6919
Q3460:what catecholamines are used to treat hypotension
Page 6921
Q3461:what catecholamine is used to treat asthma
Page 6923
Q3462:what catecholamine is used to treat AV block
Page 6925
Q3463:what catecholamines are used to treat shock
Page 6926
doapmine; dobutamine
Page 6927
Q3464:what is the action of amphetamine
Page 6928
indirect general adrenergic agonist; releases storedcatecholamines
Page 6929
Q3465:what is the action of ephedrine
Page 6930
indirect general adrenergic agonist; releases storedcatecholamines
Page 6931
Q3466:what is amphetamine used to treat
Page 6932
narcolepsy; obesity; attention deficit disorder
Page 6933
Q3467:what is ephedrine used to treat
Page 6934
nasal decongestion; urinary incontinence; hypotension
Page 6935
Q3468:name three sympathomimetic drugs used to treathypotension
Page 6936
epinephrine; norepinephrin; ephedrine
Page 6937
Q3469:what is the action of phenylephrine
Page 6938
adrenergic agonist; alpha-1 > alpha-2
Page 6939
Q3470:what is the action of albuterol
Page 6940
adrenergic agonist; beta-2 >beta-1
Page 6941
Q3471:what is the action of terbutaline
Page 6942
adrenergic agonist; beta-2 >beta-2
Page 6943
Q3472:what is phenylephrine used for?
Page 6944
pupil dilator; vasoconstriction; nasal decongestion
Page 6945
Q3473:what sympathomimetics are used to treat nasalcongestion
Page 6946
ephedrine; phenylephrine
Page 6947
Q3474:what is the mechanism of cocaine
Page 6948
indirect general adrenergic agonist; catecholamine uptakeinhibitor
Page 6949
Q3475:what is the action of cocaine
Page 6950
vasoconstriction; local anesthesia
Page 6951
Q3476:what is the mechanism of clonidine
Page 6952
centrally acting alpha-adrenergic agonist; decreases centraladrenergic outflow
Page 6953
Q3477:what drug has the same mechanism as amphetamine
Page 6955
Q3478:what is the mechanism of alpha-methyldopa
Page 6956
centrally acting alpha-adrenergic agonist; decreases centraladrenergic outflow
Page 6957
Q3479:what drug has the same mechanism as clonidine
Page 6958
alpha-methyldopa
Page 6959
Q3480:what are clonidine and alpha-methyldopa used to treat
Page 6960
hypertension; especially in renal disease because they do notdecreased blood flow to the kidney
Page 6961
Q3481:what sympathomimetic is used to treat urinaryincontinence
Page 6963
Q3482:what sympathomimetic is used to treat attentiondeficit disorder
Page 6965
Q3483:what sympathomimetic is used to treat narcolepsy
Page 6967
Q3484:name a nonselective irreversible alpha blocker
Page 6968
phenoxybenzamine
Page 6969
Q3485:name a nonselective reversible alpha blocker
Page 6971
Q3486:what is the mechanism of phenoxybenzamine
Page 6972
nonselective irreversible alpha blocker
Page 6973
Q3487:what is the mechanism of phentolamine
Page 6974
nonselective reversible alpha blocker
Page 6975
Q3488:what are phenoxybenzamine and phentolamine usedfor
Page 6976
pheochromocytoma
Page 6977
Q3489:what are the side effects of nonselective alpha blockers
Page 6978
orthostatic hypotension; reflex tachycardia
Page 6979
Q3490:name 3 alpha-1 selective adrenergic blockers
Page 6980
prazosin; terazosin; doxazosin
Page 6981
Q3491:what is the mechanism of prazosin
Page 6982
alpha-1 selective adrenergic blocker
Page 6983
Q3492:what is the mechanism of terazosin
Page 6984
alpha-1 selective adrenergic blocker
Page 6985
Q3493:what is the mechanism of doxazosin
Page 6986
alpha-1 selective adrenergic blocker
Page 6987
Q3494:what are alpha-1 selective adrenergic alpha blockersused for
Page 6988
hypertension; urinary retention in BPH
Page 6989
Q3495:what are the side effects of alpha-1 blockers
Page 6990
orthostatic hypotension; dizziness; headache
Page 6991
Q3496:what is prazosin used for?
Page 6992
hypertension; urinary retention in BPH
Page 6993
Q3497:what drugs have the same action as prazosin
Page 6994
terazosin; doxazosin
Page 6995
Q3498:what are the side effects of terazosin?
Page 6996
orthostatic hypotension; dizziness; headache
Page 6997
Q3499:what selective alpha blockers cause orthostatichypotension
Page 6998
phenoxybenzamine; phentolamine; terazosin; prazosin;doxazosin
Page 6999
Q3500:name an alpha-2 selective adrenergic blocker
Page 7001
Q3501:what is yohimbine used for
Page 7002
impotence (effectiveness controversial)
Page 7003
Q3502:what alpha blockers are used to treatpheochromocytoma
Page 7004
phenoxybenzamine; phentolamine
Page 7005
Q3503:name some beta-blockers
Page 7006
propranolol; metoprolol; atenolol; nadolol; timolol; pindolol;esmolol; labetalol
Page 7007
Q3504:what is the mechanism of propanolol
Page 7008
selective beta-adrenergic blocker
Page 7009
Q3505:what is the mechanism of metoprolol
Page 7010
selective beta-adrenergic blocker
Page 7011
Q3506:what is the mechanism of esmolol
Page 7012
selective beta-adrenergic blocker
Page 7013
Q3507:what is the mechanism of pindolol
Page 7014
selective beta-adrenergic blocker
Page 7015
Q3508:what are beta-blockers used to treat
Page 7016
hypertension; angina; MI; SVT; CHF; glaucoma
Page 7017
Q3509:how do beta blockers treat hypertension
Page 7018
decrease cardiac output; decrease renin secretion
Page 7019
Q3510:how do beta blockers treat angina
Page 7020
decrease heart rate; decrease cardiac contractility; decreasedO2 consumption
Page 7021
Q3511:why are beta blockers used to treat MI
Page 7022
decrease MI mortality
Page 7023
Q3512:which beta blockers are used to treat SVT
Page 7024
propanolol; esmolol
Page 7025
Q3513:how do propanolol and esmolol treat SVT
Page 7026
decrease AV conduction velocity
Page 7027
Q3514:how do beta blockers treat CHF
Page 7028
slow progression of chronic failure
Page 7029
Q3515:which beta blocker is used to treat glaucoma
Page 7031
Q3516:what is timolol used to treat glaucoma
Page 7032
decrease secretion of aqueous humor
Page 7033
Q3517:what are the toxic effects of beta blockers
Page 7034
impotence; exacerbation of asthma; caution in diabetes
Page 7035
Q3518:what are the cardiovascular toxic effects of betablockers
Page 7036
bradychardia; AV block; CHF
Page 7037
Q3519:what are the CNS adverse effects of beta blockers
Page 7038
sedation; sleep alterations
Page 7039
Q3520:which beta blockers are beta-1 selective
Page 7040
acebutolol; betaxolol; esmolol; atenolol; metaprolol (A BEAMof beta-1 blockers)
Page 7041
Q3521:which beta-1 blocker is short-acting
Page 7043
Q3522:which beta blockers are non-selective
Page 7044
propanolol; timolol; pindolol; nadolol; labetalol
Page 7045
Q3523:which beta blocker also blocks alpha receptors
Page 7046
labetalol (all others are spelled "olol")
Page 7047
Q3524:which alpha agonists are used to treat glaucoma
Page 7048
epinephrine; brimonidine
Page 7049
Q3525:which beta blockers are used to treat glaucoma
Page 7050
timolol; betxolol; carteolol
Page 7051
Q3526:which cholinomimetics are used to treat glaucoma
Page 7052
pilocarpine; carbachol; physostigmine; echothiophate
Page 7053
Q3527:which diuretics are used to treat glaucoma
Page 7054
acetazolamide; dorzolamide; brinzolamide
Page 7055
Q3528:which prostaglandin is used to treat glaucoma
Page 7057
Q3529:what classes of drugs are used to treat glaucoma
Page 7058
alpha agonists; beta blockers; cholinomimetics; diuretics;prostaglandins (*mnemonic -- treating glaucoma is easy as
ABCD)
Page 7059
Q3530:what is the effect of epinephrine in glaucoma
Page 7060
increase outflow of aqueous humor
Page 7061
Q3531:what are the side effects of epinephrine treatment inglaucoma
Page 7062
mydriasis; stinging
Page 7063
Q3532:what glaucoma should epinephrine NOT be used for
Page 7064
closed-angle glaucoma
Page 7065
Q3533:what is the effect of brimonidine in glaucoma
Page 7066
decreased aqueous humor synthesis
Page 7067
Q3534:what are the side effects of brimonidine treatment inglaucoma
Page 7068
no pupillary or vision changes
Page 7069
Q3535:what is the effect of beta-blocker treatment inglaucoma
Page 7070
decrease aqueous humor secretion
Page 7071
Q3536:what are the side effects of beta blocker treatment inglauzoma
Page 7072
no pupillary or vision changes
Page 7073
Q3537:what is the effect of cholinomimetics in glaucoma
Page 7074
ciliary muscle contraction; opening of trabecular meshwork;increase outflow of aqueous humor
Page 7075
Q3538:what are the side effects of cholinomimetics inglaucoma
Page 7076
miosis; cyclospasm
Page 7077
Q3539:what is the effect of diuretic treatment in glaucoma
Page 7078
inhibition of carbonic anhydrase --> decrease HCO3secretion --> decrease aqueous humor secretion
Page 7079
Q3540:what are the side effects of diuretics in glaucoma
Page 7080
no pupillary or vision changes
Page 7081
Q3541:what is the effect of prostaglandin (latanoprost)treatment in glaucoma
Page 7082
increase outflow of aqueous humor
Page 7083
Q3542:what is the side effect of prostaglandin treatment inglaucoma
Page 7084
darkens color of iris (browning)
Page 7085
Q3543:which drugs used to treat glaucoma increase outflow ofaqueous humor
Page 7086
cholinomimetics; prostaglandin; epinephrine
Page 7087
Q3544:can you use epinephrine in closed-angle glaucoma
Page 7089
Q3545:brimonidine is used to treat what eye disease
Page 7091
Q3546:what kind of drug is latanoprost
Page 7093
Q3547:latanoprost is used to treat what eye disease
Page 7095
Q3548:which glaucoma drugs decrease aqueous secretion
Page 7096
beta blockers; diuretics
Page 7097
Q3549:what does L-dopa stand for
Page 7099
Q3550:what is the mechanism of action of L-dopa/carbidopa
Page 7100
increase dopamine level in brain
Page 7101
Q3551:what is L-dopa/carbidopa used to treat
Page 7102
Parkinson's disease
Page 7103
Q3552:how is L-dopa different from dopamine
Page 7104
L-dopa can cross the blood-brain barrier; dopamine cannot
Page 7105
Q3553:what happens to L-dopa after it crosses the BBB
Page 7106
converted to dopamine by dopa decarboxylase
Page 7107
Q3554:what enzyme convertes L-dopa to dopamine
Page 7108
dopa decarboxylase
Page 7109
Q3555:what is the function of carbidopa
Page 7110
peripheral decarboxylase inhibitor
Page 7111
Q3556:why is carbidopa given with L-dopa
Page 7112
increase L-dopa availability in CNS by inhibitingdecarboxylase in periphery; also limits peripheral side effects
Page 7113
Q3557:what are the side effects of L-dopa.carbidopatreatment
Page 7114
arrhythmias; dyskinesias
Page 7115
Q3558:why do patients taking L-dopa get arrhythmias
Page 7116
peripheral effects of dopamine
Page 7117
Q3559:why do patients taking L-dopa get dyskinesias
Page 7118
excess dopamine stimulation in CNS
Page 7119
Q3560:what drugs are used to treat Parkinson's disease
Page 7120
dopamine agonists; MAO inhibitors; antimuscarinics
Page 7121
Q3561:specifically; which drugs are used to treat Parkinson's
Page 7122
Bromocriptine; Amantadine; Levodopa; Selegiline;Antimuscarinics (BALSA)
Page 7123
Q3562:which dopamine agosts are used to treat Parkinson's
Page 7124
L-dopa/carbidopa; bromocriptine; pramipexole; ropinirole;amantadine
Page 7125
Q3563:what is the action of bromocriptine in Parkinson's
Page 7126
ergot alkaloid; partial dopamine agonist
Page 7127
Q3564:what is the action of amantadine in Parkinson's
Page 7128
enhances dopamine release
Page 7129
Q3565:what MAOI is used to treat Parkinson's
Page 7131
Q3566:what is the mechanism of selegiline
Page 7132
selective MAO type B inhibitor
Page 7133
Q3567:what antimuscarinic is used to treat Parkinson's
Page 7135
Q3568:what is the effect of benztropine in Parkinson's
Page 7136
improves tremor; rigidity; little effect on bradykinesia
Page 7137
Q3569:what is sumatriptan used for
Page 7138
acute migraine; cluster headache attacks
Page 7139
Q3570:what is the mechanism of sumatriptan
Page 7141
Q3571:what is the half life of sumatriptan
Page 7142
less than 2 hours
Page 7143
Q3572:what are the side effects of sumatriptan
Page 7144
chest discomfort; mild tingling
Page 7145
Q3573:what are the contraindications for sumatriptan
Page 7146
patients with CAD or Prinzmetal's angina
Page 7147
Q3574:which drugs are used for simple and complex partialseizures
Page 7148
phenytoin; carbamazapine; lamotrigine; gabapentin;topiramate; phenobarbital
Page 7149
Q3575:what types of seizures is phenytoin indicated for
Page 7150
simple and complex partial; tonic-clonic; status epilepticus
Page 7151
Q3576:what types of seizures is carbamazepine indicated for
Page 7152
simple and complex partial; tonic-clonic
Page 7153
Q3577:what types of seizures is lamotrigine indicated for
Page 7154
simple and complex partial; tonic-clonic
Page 7155
Q3578:what types of seizures is gabapentin indicated for
Page 7156
simple and complex partial; tonic-clonic
Page 7157
Q3579:what types of seizures is topiramate indicated for
Page 7158
simple and complex partial
Page 7159
Q3580:what types of seizures is phenobarbital indicated for
Page 7160
simple and complex partial; tonic-clonic
Page 7161
Q3581:what drugs can be used for tonic-clonic seizures
Page 7162
phenytoin; carbamazapine; lamotrigine; gabapentin;phenobarbital; valproate
Page 7163
Q3582:what drugs can be used for absence seizures
Page 7164
valproate; ethosuximide
Page 7165
Q3583:what drugs can be used for status epilepticus
Page 7166
phenytoin; benzodiazapines (diazepam; lorazepam)
Page 7167
Q3584:what types of seizure is valproate indicated for
Page 7168
tonic-clonic; absence
Page 7169
Q3585:what types of seizure is ethosuximide inidcated for
Page 7171
Q3586:what type of seizure are benzodiazepines indicated for
Page 7172
status epilepticus
Page 7173
Q3587:other than anti-seizure; what else is phenytoin usedfor
Page 7174
class 1B anti-arrhythmic
Page 7175
Q3588:how should a patient taking carbamazepine befollowed
Page 7176
monitor LFT's weekly
Page 7177
Q3589:which seizure drugs have adjunct use
Page 7178
gabapentin; topiramate
Page 7179
Q3590:which seizure drug is safest in pregnant women
Page 7181
Q3591:which seizure drug is used in Crigler-Najjar II
Page 7183
Q3592:what are the advantages of phenobarbital
Page 7184
can be used in pregnant women; Crigler Najjar II
Page 7185
Q3593:what are the side effects of benzodiazepines
Page 7186
sedation; tolerance; dependence
Page 7187
Q3594:what are the side effects of carbamazepine
Page 7188
diplopia; ataxia; CYP induction; blood dyscrasias; livertoxicity
Page 7189
Q3595:what are the side effects of ethosuximide
Page 7190
GI distress; lethargy; headache; urticaria; Stevens-Johnsonsyndrome
Page 7191
Q3596:what are the side effects of phenobarbital
Page 7192
sedation; CYP induction; tolerance; dependence
Page 7193
Q3597:what are the side effects of phenytoin
Page 7194
nystagmus; diplopia; ataxia; sedation; ginigival hyperplasia;hirsutism; anemias; teratogenic
Page 7195
Q3598:what are the side effects of valproate
Page 7196
GI distress; rare by fatal hepatotoxicity; neural tube defects(spina bifida)
Page 7197
Q3599:what are the side effects of lamotrigine
Page 7198
life-threatening rash; Stevens-Johnson syndrome
Page 7199
Q3600:what are the side effects of gabapentin
Page 7200
sedation; movement disorders
Page 7201
Q3601:what are the side effects of topiramate
Page 7202
sedation; mental dulling; kidney stones; weight loss
Page 7203
Q3602:which anti-epileptic drug is teratogenic
Page 7205
Q3603:which anti-epileptic drug can cause dependence
Page 7206
benzodiazepines; phenobarbital
Page 7207
Q3604:which anti-epileptic drug can cause neural tube defects
Page 7209
Q3605:which anti-epileptic drugs can cause GI distress
Page 7210
valproate; ethosuximide
Page 7211
Q3606:it is necessary to check LFT's with which anti-epileptic drugs
Page 7212
carbamazepine; valproate
Page 7213
Q3607:which anti-epileptic drugs cause CYP induction
Page 7214
phenobarbital; carbamazepine
Page 7215
Q3608:which anti-epileptic drugs can cause blood problems
Page 7216
carbamazepine; phenytoin
Page 7217
Q3609:which anti-epileptic drugs can cause Stevens-Johnsonsyndrome
Page 7218
lamotrigine; ethosuximide
Page 7219
Q3610:which anti-epileptic drugs can cause diplopia
Page 7220
carbamazepine; phenytoin
Page 7221
Q3611:what is the mechanism of phenytoin action
Page 7222
use-dependent blockade of Na+ channels
Page 7223
Q3612:what is the clinical application of phenytoin
Page 7224
grand mal seizures
Page 7225
Q3613:what are the toxicities of phenytoin
Page 7226
nystagmus; ataxia; diplopia; lethargy
Page 7227
Q3614:what are the chronic toxicities of phenytoin
Page 7228
gingival hyperplasia in children; peripheral neuropathy;hirsutism; megaloblastic anemia; malignant hyperthermia
(rare)
Page 7229
Q3615:should pregnant women take phenytoin
Page 7230
NO -- teratogenic
Page 7231
Q3616:why does phenytoin cause megaloblastic anemia
Page 7232
causes decreased vitamin B-12
Page 7233
Q3617:name 4 barbiturates
Page 7234
phenobarbital; pentobarbital; thiopental; secobarbital
Page 7235
Q3618:what is the mechanism of barbiturate action
Page 7236
increase duration of Cl channel opening --> decreasedneuron firing --> facilitate GABA-A action
Page 7237
Q3619:how do barbiturates facilitate GABA-A action
Page 7238
increase duration of Cl channel opening which decreasesneuron firing (Barbidurate increases duration
Page 7239
Q3620:is barbiturate action on the CNS stimulatory orinhibitory
Page 7241
Q3621:what is the clinical application of barbiturates
Page 7242
sedative for anxiety; seizures; insomnia; anesthesia induction(thiopental)
Page 7243
Q3622:which barbiturate is used for anesthesia induction
Page 7245
Q3623:what are the side effects of barbiturates
Page 7246
dependence; additive CNS depression effects with alcohol;respiratory or CV depression (death); drug interactions due to
CYP induction
Page 7247
Q3624:what should you find out before giving a patientbarbiturates
Page 7248
what other medications they take; because of CYP inductionand many drug interactions
Page 7249
Q3625:what happens if you give barbiturates to a patient inalcohol-induced coma or DT's
Page 7250
they might DIE!! Because of additive effect of barbituratesand alcohol --> respiratory depression
Page 7251
Q3626:when are barbiturates contra-indicated
Page 7253
Q3627:can barbiturates cause dependence
Page 7255
Q3628:My friend Barb was very anxious so her doctor gaveher barbiturates to increase the duration of the time she couldspeak in public without freaking out and having a seizure. She
became so dependent on it that she recommended it to herfriend Portia who couldn't take it because of porphyria. Oneday Barb drank too much alcohol and took her barbiturates
and never woke up! THE END
Page 7256
clinical pharmacology made ridiculous. Period
Page 7257
Q3629:name a bunch of benzodiazepines
Page 7258
diazepam; lorazepam; triazolam; temazepam; oxazepam;midazolam; chlordiazepoxide (all have ZZZ in them)
Page 7259
Q3630:what is the mechanism of benzodiazepines
Page 7260
increase frequency of Cl channel opening --> facilitateGABA-A action (Frenzodiazepines increase frequency)
Page 7261
Q3631:which GABA receptors are facilitated by barbituratesand bezodiazepines
Page 7263
Q3632:what are the clinical applications of benzodiazepines
Page 7264
anxiety; spasticity; status epilepticus (diazepam);detoxification (alcohol withdrawal; DT's)
Page 7265
Q3633:which benzodiazepine can be used for statusepilepticus
Page 7267
Q3634:what drugs can be used to treat alcohol withdrawal
Page 7268
benzodiazepines
Page 7269
Q3635:which benzodiazepines are short-acting
Page 7270
TOM thumb: Triazolam; Oxazepam; Midazolam
Page 7271
Q3636:what are the toxic effects of benzos
Page 7272
dependence; additive CNS depression effects with alcohol
Page 7273
Q3637:how are benzos better than barbiturates
Page 7274
less respiratory depression and coma risk
Page 7275
Q3638:how do you treat benzo overdose
Page 7277
Q3639:what is flumzenil used for
Page 7279
Q3640:how does flumazenil work
Page 7280
competitive antagonist at GABA receptor
Page 7281
Q3641:can a patient become benzodiazepine dependent
Page 7283
Q3642:are barbiturates or benzodiazepines used for alcoholwithdrawal
Page 7284
benzodiazepines
Page 7285
Q3643:what is another name for antipsychotics
Page 7287
Q3644:name 4 antipsychotic drugs
Page 7288
thioridazine; haloperidol; fluphenazine; chlorpromazine
Page 7289
Q3645:how do you keep benzos straight from antipsychotics
Page 7290
Benzos help 3rd year Jon Kazam be less anxious aroundpatients: Shazam Kazam! Without antipsychotics patients
talk like a crazy 'zine (well; not perfect; but I'm working on it)
Page 7291
Q3646:what is the mechanism of most antipsychotics
Page 7292
block dopamine D2 receptors
Page 7293
Q3647:what is the clinical application of antipsychotics
Page 7294
schizophrenia; psychosis
Page 7295
Q3648:what are the side effects of antipsychotics
Page 7296
extrapyramidal side effects (EPS); sedation; endocrine;muscarinic blockade; alpha blockade; histamine blockade
Page 7297
Q3649:what is a long-term effect of antipsychotic use
Page 7298
tardive dyskinesia
Page 7299
Q3650:what is neuroleptic malignant syndrome
Page 7300
a side effect of antipsychotics; rigidity; autonomic instability;hyperpyrexia
Page 7301
Q3651:how do you treat neuroleptic malignant syndrome
Page 7302
dantrolene; dopamine agonists
Page 7303
Q3652:what is tardive dyskinesia
Page 7304
side effect of neuroleptics; stereotypic oral-facial movements;may be due to dopamine receptor sensitization
Page 7305
Q3653:what is the "rule of 4" with EPS sideeffects from antipsychotic drugs
Page 7306
evolution of EPS side effects: 4 hours -- acite dystonia; 4 days-- akinesia; 4 weeks -- akasthesia; 4 months -- tardvie
dyskinesia
Page 7307
Q3654:is tardvie dyskinesia reversible
Page 7308
often irreversible
Page 7309
Q3655:what is fluphenazine used for
Page 7310
schizophrenia; psychosis
Page 7311
Q3656:name 3 atypical antipsychotics
Page 7312
clozapine; olanzapine; risperidone
Page 7313
Q3657:what type of antipsychotic is clozapine
Page 7315
Q3658:what type of antipsychotic is olanzapine
Page 7317
Q3659:what type of antipsychotic is risperidone
Page 7319
Q3660:what is the mechanism of atypical antipsychotics
Page 7320
block 5-HT2 and dopamine receptors
Page 7321
Q3661:what is the mechanism of clozapine
Page 7322
block 5-HT2 and dopamine receptors
Page 7323
Q3662:what is the mechanism of olanzapine
Page 7324
block 5-HT2 and dopamine receptors
Page 7325
Q3663:what is the mechanism of risperidone
Page 7326
block 5-HT2 and dopamine receptors
Page 7327
Q3664:what is the clinical application of clozapine
Page 7328
schizophrenia positive and negative symptoms
Page 7329
Q3665:what is the clinical application of olanzapine
Page 7330
schizophrenia positive and negative symptoms; OCD; anxietydisorder; depression
Page 7331
Q3666:what is the clinical application of risperidone
Page 7332
schizophrenia positive and negative symptoms
Page 7333
Q3667:how are atypical antipsychotics different from classicones
Page 7334
atypicals treat positive and negative symptoms ofschizophrenia; fewer extrapyramidal and anticholinergic side
effects than classic antipsychotics
Page 7335
Q3668:which antipsychotics should be used to treat positiveand negative symptoms of schizophrenia
Page 7336
atypical ones -- clozapine; olanzapine; risperidone
Page 7337
Q3669:which antipsychotics should be used for fewer sideeffects
Page 7338
atypical ones -- clozapine; olanzapine; risperidone
Page 7339
Q3670:what is a potential toxicity of clozapine
Page 7340
agranulocytosis
Page 7341
Q3671:which antipsychotic drug can cause agranulocytosis
Page 7343
Q3672:what test must be done weekly on patients takingclozapine
Page 7344
WBC count because of potential agranulocytosis
Page 7345
Q3673:what is the mechanism of action of lithium
Page 7346
unknown; may be related to inhibition of phosphoinositolcascade
Page 7347
Q3674:what is the clinical application of lithium
Page 7348
mood stabilizer for bipolar disorder
Page 7349
Q3675:how does lithium help people with bipolar disorder
Page 7350
prevents relapse and acute manic episodes
Page 7351
Q3676:what are the side effects of lithium
Page 7352
tremor; hypothyroidism; polyuria; teratogenic
Page 7353
Q3677:is it OK for women taking lithium to get pregnant
Page 7354
NO -- teratogenic
Page 7355
Q3678:what does lithium cause polyuria
Page 7356
ADH antagonist --> nephrogenic diabetes insipidus
Page 7357
Q3679:What do the following drugs inhibit: 1. MAOinhibitors; 2. Desipramine/maprotilline; 3. Mirtazapine and 4.
Fluoxetine/trazodone?
Page 7358
1. MAO 2. NE reuptake 3. Alpha 2-R 4. 5HT reuptake
Page 7359
Q3680:All of the above actions are ------synaptic
Page 7361
Q3681:List the Tricyclic Antidepressants
Page 7362
pg 311 Imipramine; amitriptyline; desipramine; nortriptyline;clomipramine; doxepin
Page 7363
Q3682:What are the three C's of their toxicity?
Page 7364
Convulsions; Coma; Cardiotoxicity (arrythmias). Alsorespiratory depression; hypyrexia.
Page 7365
Q3683:How about toxicity in the eldery?
Page 7366
confusion and hallucinations due to anticholinergic SE
Page 7367
Q3684:What is the mechanism of TCA?
Page 7368
block reuptake of NE and 5HT
Page 7369
Q3685:What is the clinical uses of TCAs?
Page 7370
Endogenous depresion. Bed wetting - imipramine. OCD-clomipramine.
Page 7371
Q3686:How are tertiary TCA's different than secondary interms of side effects?
Page 7372
Amitriptyline (tertiary) has more anti-cholinergic effects thando secondary (nortriptyline). Desipramine is the least
sedating.
Page 7373
Q3687:what are the SE of TCAs?
Page 7374
sedation; alpha blocking effects; atropine-like anti cholinergicside effects (tachycardia; urinary retention)
Page 7375
Q3688:Fluoxetine; sertraline; paroxetine; citalopram are whatclass of drugs?
Page 7376
pg 311 SSRI's for endogenous depression
Page 7377
Q3689:How long does it take an anti-depressant to have aneffect?
Page 7379
Q3690:How does the toxicity differ fromTCA's and what arethey?
Page 7380
Fewer than TCA's. CNS stimulation - anxiety; insomnia;tremor; anorexia; nausea; and vomiting.
Page 7381
Q3691:What toxicity happens with SSRI's and MAOinhibitors given together?
Page 7382
Seratonin Syndrome! Hyperthermia; muscle rigidity;cardiovascular collapse
Page 7383
Q3692:What are heterocyclics?
Page 7384
pg 312 2nd and 3rd generation antidepressants with variedand mixed mechanisms of action. Used major depression.
Page 7385
Q3693:Examples of heterocyclics?
Page 7386
trazodone; buproprion; venlafaxine; mirtazapine; maprotiline
Page 7387
Q3694:Which one is used for smoking cessation?
Page 7388
Buproprion. Mechanism not known. Toxicity - stimulanteffects; dry mouth; aggrevation of pyschosis
Page 7389
Q3695:Which one used in GAD?
Page 7390
Venlafaxine - inhibits 5HT and DA reuptake. Toxicity -stimulant effects
Page 7391
Q3696:which one blocks NE reuptake
Page 7393
Q3697:Which one increases release of NE and 5HT via alpha2 antagonism?
Page 7394
mirtazapine. Also potent 5HT Rantagonist. Toxicity -sedation; increase serum cholesterol; increase appetite
Page 7395
Q3698:What is trazodone and it' SE?
Page 7396
primarily inhibits seratonin reuptake. Toxicity - sedation;nausea; priapism; postural hypotension
Page 7397
Q3699:Give 2 examples of MAO
Page 7398
pg 312 phenelzine. Tranylcypromine
Page 7399
Q3700:Mechanism and Clinical Uses?
Page 7400
non selevtive MAO inhibition. Atypical antidepressant;anxiety; hypochondriasis
Page 7401
Q3701:What is the toxicity with tyramine ingestion (in foods)and meperidine?
Page 7402
Hypertensive crisis
Page 7403
Q3702:Other toxicities?
Page 7404
CNS stimulation; contraindicated with SSRI's or B-agonists
Page 7405
Q3703:What is the mechanims of selgiline (deprenyl)?
Page 7406
pg 312 Selectively inhibits MAO-B; increasing DA
Page 7407
Q3704:what is the clinical use and toxicity?
Page 7408
adjunctive agent to L-dopa for Parkinsons. May enhanceadverse effects of L-dopa
Page 7409
Q3705:What is the significance of drugs with decreasedsolubility in blood?
Page 7410
rapid induction and recovery times . Ie. N20
Page 7411
Q3706:What is the significance of drugs with increasedsolubility in blood?
Page 7412
increased potency = I/ MAC. Ie. Halothane
Page 7413
Q3707:list Inhaled Anesthetics
Page 7414
halothane; enflurane; isoflurane; sevoflurane; methoxyflurane;nitrous oxide
Page 7415
Q3708:What is good about lower solubility?
Page 7416
the quicker the anesthetic response; and the quicker therecovery
Page 7417
Q3709:What are these drug's effects?
Page 7418
myocardial depression; respiratory depression; nausea/emesis;increase cerebral blood flow
Page 7419
Q3710:What toxicity mactches the following drugs 1.Halothane 2. Methoxyflurane 3. Enflurane 4. Rare
Page 7420
1. Hepatotoxcity 2. Nephrotoxicty 3. Proconvulsant 4.Malignant hyperthermia
Page 7421
Q3711:What do barbituates; benzodiazepines;arylcyclohexylamines and narcotic analgesics have in
common?
Page 7422
they are IV anesthetics
Page 7423
Q3712:What the pharmacokinetics and uses of thiopental?
Page 7424
high lipid solubility; rapid entry into brain. Used for inductionof anesthesia for short surgical procedures. Terminated byredistribution from brain. Decreased cerebral blood flow
Page 7425
Q3713:Give an example of a benzo and what is this class'sshortcoming?
Page 7426
midazolam used for endoscopy. Used with gaseousanesthetics and narcotics. May cause severe post-op
respiratory depressio and amnesia
Page 7427
Q3714:What does Ketamine (PCP analog and anarylcyclohexylamine) do?
Page 7428
dissociative anesthetic. Cardiovascular stimulant. Causesdisorientation; hallucination; bad dreams. Increases cerebral
blood flow.
Page 7429
Q3715:How are narcotic analgesics used? Examples?
Page 7430
Morphone and fentanyl are used with CNS depressant duringgeneral anesthesia.
Page 7431
Q3716:What is the advantage of propofol
Page 7432
used for rapid anesthesia induction and short procedures. Lesspost-op nausea than thiopental
Page 7433
Q3717:Name some Local ester anesthetics?
Page 7434
procaine; cocaine; tetracaine;
Page 7435
Q3718:Name some amides?
Page 7436
lidocaine; bupivacaine; (amides have two I's in name!)
Page 7437
Q3719:What is the mechanism and clinical use?
Page 7438
bind receptor and block Na channels. Tertiary amine localanesthetics penetrate membrane in uncharge form; then bind
charged form. Use for minor surgical procedures; spinalanesthesia.
Page 7439
Q3720:How do you decide to use ester or amides?
Page 7440
if allergic to esters; give amides
Page 7441
Q3721:what is the toxicity
Page 7442
CNS excitation; severe cardiovascular toxicity (bupivacaine);hypertension; arrhythmias (cocaine)
Page 7443
Q3722:In infected ________ tissue; anesthetics are chargedand cannot penetrate membrane. Therefore; ______
anesthetics are needed.
Page 7445
Q3723:What is the order of nerve blockade for size andmyelination? Which factor predominates?
Page 7446
small diameter> large diameter. Myelinated fibers>unmyelinated fibers. Size factor predominates
Page 7447
Q3724:what is the order of loss of sensation?
Page 7448
pain first; then temp; then touch; then pressure
Page 7449
Q3725:Why would you give these drugs withvasoconstrictors?
Page 7450
to enhance local action
Page 7451
Q3726:List as many Opiod analgesics as you can.
Page 7452
morphine; fentanyl; codeine; heroin; methadone; meperidine;dextromethorphan
Page 7453
Q3727:Mechanism: They act as _____ for opiod receptors tomodulate synaptic transmission
Page 7455
Q3728:which drugs act at the mu; delta; kappa receptors?
Page 7456
morphine enkephalin; dynorphin
Page 7457
Q3729:Clinical use?
Page 7458
pain; cough supression (dex); diarrhea (loperamide); acutepulmonary edema; methadone maintenance programs
Page 7459
Q3730:What are the major toxicities?
Page 7460
addiction; respiratory depression; constipation; miosis;additive CNS depression wth other drugs
Page 7461
Q3731:Tolerance does not develop to __________and______
Page 7462
miosis and constipation
Page 7463
Q3732:How would you treat toxicity?
Page 7464
naloxone; naltrexone (opiod R antagonist)
Page 7465
Q3733:List three NSAIDS?
Page 7466
ibuprofen; naproxen; indomethacin
Page 7467
Q3734:What is their mechanism?
Page 7468
reversibly inhibit COX 1 and 2. Blocks PG synthesis
Page 7469
Q3735:What is their clinical use (3As)?
Page 7470
Antipyretic; analgesic; anti-inflammatory. Indomethacin isused to close a PDA.
Page 7471
Q3736:What are common toxicities?
Page 7472
renal damage; aplastic anemia; GI distress; ulcers
Page 7473
Q3737:Where is cox2 found?
Page 7474
in inflammatory cells and mediates inflammation and pain
Page 7475
Q3738:Why is cox2 inhibition better than cox1?
Page 7476
cox1 helps to maintain gastric mucosa; thus; should not havethe corrosive effects of other NSAIDs on the GI lining (less
incidence of ulcers and bleeding)
Page 7477
Q3739:Clinical Use?
Page 7478
RA and osteoarthritis
Page 7479
Q3740:What is Acetaminophen mechanism and where does itwork?
Page 7480
reversibly inhibits cox; mostly in CNS. Inactivatedperipherally.
Page 7481
Q3741:What are its 2 As?
Page 7482
antipyretic; analgesic but NOT anti-inflammatory.
Page 7483
Q3742:Overdose effects?
Page 7484
hepatic necrosis; acetaminophen metabolites depletesglutathine and forms toxic tissue adducts in the liver
Page 7485
Q3743:Changes in CO affect two major cardiovascularpathways?
Page 7486
1. Carotid sinus firing; sympa discharge 2. Renal blood flow;renin-ang pathway
Page 7487
Q3744:What is the effect of the following drugs: 1. Positiveinotropic drugs 2. Beta blockers 3. Ace inhibitors 4. AII
antagonists 5. Vasodilators and 6. Diuretics
Page 7488
1. Increases cardiac output. 2. Inhibit renin release. 3. InhibitACE 4. Inhibits effects of AngII including increasing the
preload; increasing the afterload and remodelling. 5. Decreasethe preload and afterload. 6. Decrease the preload and
afterload
Page 7489
Q3745:What are the adverse effects of these two diueretics:hydrochlorothiazide; loop diuretics
Page 7490
1. Hypokalemia; hyperlipidemia; hyperuricemia; lassitude;hypercalcemia; hyperglycemia 2. Hypokalemia; met alk;
hypotension; ototoxicity
Page 7491
Q3746:These are what class of drugs: clonidine; methyldopa;ganglionic blockers; reserpine; guanethidine; prazosin; beta
blockers?
Page 7492
sympathoplegics
Page 7493
Q3747:Adverse effects of clonidine?
Page 7494
dry mouth; sedation; severe rebound HTN
Page 7495
Q3748:Adverse effects of methyldopa?
Page 7496
sedation; positive coombs test
Page 7497
Q3749:Adverse effects of ganglionic blockers?
Page 7498
orthostatic HTN; blurred vision; constitpation; sexualdysfuncction
Page 7499
Q3750:Adverse effects of reserpine?
Page 7500
sedation; depression; nasal stuffiness; diarrhea
Page 7501
Q3751:adverse effects of beta blockers?
Page 7502
impotence; asthma; cardiovascular; cns
Page 7503
Q3752:Adverse effects of guanethidine?
Page 7504
orthostatic and exercise Hypotension; sex dysfxn; diarrhea
Page 7505
Q3753:Adverse effects of prazosin?
Page 7506
1st dose orthostatic hypotension; dizzy; headache
Page 7507
Q3754:The following are what class: hydralazine; minoxidil;nifedipine; verapamil; nitroprusside
Page 7509
Q3755:which one causes lupus like syndrome? Othertoxicities?
Page 7510
hydralazine; nausea; headache; reflex tachycardia; angina; saltretention
Page 7511
Q3756:adverse effets of minoxidil?
Page 7512
hypertrichosis (hair growth - think Rogaine with minoxidil!);pericardial effusion; reflex tachycardia; angina; salt retention
Page 7513
Q3757:Side effects of nifedipine; verapamil?
Page 7514
dizziness; flushing; constipation; nausea
Page 7515
Q3758:which one causes cynide toxicity?
Page 7517
Q3759:Adverse effects of ACE-I Captorpil? ThinkCAPTOPRIL
Page 7518
C: cough; A: angioedema; P: proteinuria; T: taste changes; O:hypOtension; P: pregnancy problems like fetal renal damage;
R: rash; I: increased renin; L: lower angiotensin. Alsohyperkalemia.
Page 7519
Q3760:Losartan is a ----------- R-Inhibitor? With ____-toxicity and ____kalemia
Page 7520
angiotensin II; fetal renal; hyper
Page 7521
Q3761:Which two anti-HTN drugs do you use with Bblockers to prevent reflex tachycardia; diuretic to block salt
retention?
Page 7522
hydralizine; minoxidil
Page 7523
Q3762:What is hydralizine's mechanims and clinical use?
Page 7524
increase cGMP --> smooth muscle relaxation. Vasodilatesarteries > veins. Reduces afterload. Used for severe HTN
or CHF
Page 7525
Q3763:Calcium channel blockers; name three
Page 7526
pg. 315 - nifedipine; verapamil; diltiazem
Page 7527
Q3764:Mechanism: block _____ chanels of cardiac andsmooth muscles to reduce contractility
Page 7528
voltage dependednt L type Ca
Page 7529
Q3765:Rank their effects on vascular smooth muscle ad onthe heart.
Page 7530
smooth muscle nifed> diltia > verapamil heart: vera>diltia> nifedepine
Page 7531
Q3766:What is the calcium channel blockers use?
Page 7532
HTN; angina; arrythmias (not nifedipine)
Page 7533
Q3767:ACE -I; name three
Page 7534
pg 316 - captopril; enalapril; lisinopril
Page 7535
Q3768:Mechanim considering bradykinin and renin release?
Page 7536
reduce lvels of ang II; prevent inactivation of bradykinin; reninrelease is increased to to loss of feedback inhibition
Page 7537
Q3769:what is the clinical use of these?
Page 7538
HTN; CHF; diabetic renal disease
Page 7539
Q3770:What is the site of action of 1. Acetazolamide; 2.Osmotic agents; 3. Loop agents; 4. Thiazides; 5. Potassium
sparing; 6. ADH antagonists
Page 7540
1. PCT 2. PCT; thin desc limb; CD 3. Thick ascending limb 4.Distal conv tubule 5. DCT a bit later 6. CD in inner medulla
Page 7541
Q3771:How does mannitol an osmotic diuretic work?
Page 7542
increase tubular fluid osmolarity; producing increased urineflow
Page 7543
Q3772:what is the use and toxicity?
Page 7544
Use: shock; drug overdose; decrease intracranial pressure.Toxicity - pulmonary edema; dehydration. Contraindicated in
anuria; CHF
Page 7545
Q3773:Acetazolamide Is a ______inhibitor. Causes______diuresis and _____ in total body HC03 stores.
Page 7546
Carbonic anhydrase; self-limited NaHCO3; reduction.
Page 7547
Q3774:What electrolye disturbace does it treat? Does itcause?
Page 7548
treats met alk; causes in toxicity hyperchloremic met acidosis.ACIDazolamide caues ACIDosis.
Page 7549
Q3775:Other toxicity?
Page 7550
neuropathy; NH3 toxicity; sulfa allergy
Page 7552
glaucoma; urinary alk; met alk; altitude sickeness
Page 7553
Q3777:This sulfonamide loop diuretic Furosemide inhibits_______cotransport
Page 7555
Q3778:Furosemide also works by?
Page 7556
abolishes hypertonicit y of medulla; prevent concentration ofurine. Increase Caexcertion. Loops Lose calcium
Page 7557
Q3779:The three uses for this loop diuretic?
Page 7558
edematous states; htn; hypercalcemia
Page 7559
Q3780:Toxicity using the OH DANG?
Page 7560
ototoxicity; hypokalemia; dehydration; allergy; nephritisinterstitial; gout
Page 7561
Q3781:How is Ethacrynic Acid different from furosemide?And how does that affect its use?
Page 7562
Although both have the same action; ethacrynic is aphenoxyacetic acid derivative not a sulfonamide. Therefore
use this drug when you are allergic to sulfa.
Page 7563
Q3782:What drug can be used to treat acute gout?
Page 7564
ethacrynic acid
Page 7565
Q3783:Hydrochlorothiazide is a thiazide diuretic that inhibitsthe reabsorption of ----- in the ---- tubule
Page 7566
NaCl; early distal tubule
Page 7567
Q3784:Does hydrochlorothiazide increase or decrease theexcretion of calcium ion?
Page 7569
Q3785:A toxic dose of hydrochlorathiazide will do what tothe blood levels of these electrolites: potassium; sodium;
glucose; lipid; uric acid; calcium
Page 7570
hypokalemic metabolic alkalosis; hyponatremia;hyperGlycemia; hyperLipidemia; hyperUricemia;
hyperCalcemia (hyperGLUC)
Page 7571
Q3786:Spironolactone is a competitive antagonist to the ---receptor in the ---- tubule
Page 7572
aldosterone; cortical collecting tubule
Page 7573
Q3787:Name two K+-sparing diuretics that block Na+channels in the cortical collecting duct
Page 7574
Triamterine and amiloride
Page 7575
Q3788:Besides causing hyperkalemia; a toxic dose ofspironolactone will cause this endocrine effect
Page 7576
Gynecomastia (antiandrogen effect)
Page 7577
Q3789:Name three K+-sparing diuretics
Page 7578
Spironolactone; Triamterene; Amiloride (The K+ STAys.)
Page 7579
Q3790:Diuretics are classified as carbonic anhydraseinhibitors; loop diuretics; thiazides; and K+-sparing diuretics.
Which of these causes in increase in urine NaCl?
Page 7581
Q3791:Which types of diuretucs increase urine K+?
Page 7582
All except K+-sparing diuretics. Carbonic anhydraseinhibitors; loop diuretics; thiazides.
Page 7583
Q3792:Do carbonic anhydrase inhibitors increase or decreaseblood pH?
Page 7584
Decrease; cause acidosis
Page 7585
Q3793:Do K+-sparing diuretics cause acidosis or alkalosis?
Page 7586
Acidosis; decreases pH
Page 7587
Q3794:Do loop diuretics cause acidosis or alkalosis?
Page 7588
Alkalosis; increases pH
Page 7589
Q3795:Do thiazide diuretics cause an increase or decrease inblood pH?
Page 7590
Increase; cause alkalosis
Page 7591
Q3796:Do loop diuretics increase or decrease levels of urinecalcium ion?
Page 7593
Q3797:Do thiazide diuretics increase or decrease levels ofurine calcium ion?
Page 7595
Q3798:Name four determinants of the level of myocardialoxygen consumption
Page 7596
There are five: end diastolic volume; blood pressure; heartrate; contractility; ejection time
Page 7597
Q3799:Do nitrates affect preload or afterload?
Page 7599
Q3800:Do Beta-blockers affect preload or afterload?
Page 7601
Q3801:What is the effect of nitrates on: diastolic volume;blood pressure; contractility; heart rate; ejection time?
Page 7602
decrease EDV; decrease BP; increase contractility (reflexresponse); increase HR (reflex response); decrease ejection
time
Page 7603
Q3802:What is the effect of Beta-blockers on: diastolicvolume; blood pressure; contractility; heart rate; ejection
time?
Page 7604
increase EDV; decrease BP; decrease contractility; decreasedHR; increase ejection time
Page 7605
Q3803:The effects of using nitrates and Beta-blockerstogether will: a) decrease myocardial oxygen demands by the
same amount as using either alone; b) decrease myocardialoxygen demands by an amount greater than if each were used
alone; or c) have no effect on myocardial oxygen demand
Page 7606
b) Decrease myocardial oxygen demands by an amount greaterthat if each were used alone
Page 7607
Q3804:Nifedipine blocks -- channels
Page 7609
Q3805:In its effects on myocardial oxygen consumption; isNifedipine similar to Nitrates or B-blockers?
Page 7610
Nitrates (Nifedipine is similar to Nitrates)
Page 7611
Q3806:In its effects on myocardial oxygen consumption; isVerapamil similar to Nitrates or B-blockers?
Page 7613
Q3807:Dose nitroglycerin dilate arteries or veins more?
Page 7614
Veins>>arteries
Page 7615
Q3808:Does nitroglycerin increase or decrease cGMP insmooth muscle?
Page 7617
Q3809:In industrial exposure to nitroglycerine; weekendwithdrawal is characterized by which three symptoms?
Page 7618
Tachycardia; dizziness ; and headache ("Mondaydisease")
Page 7619
Q3810:Toxic dosage of nitroglycerine causes which threesymptoms?
Page 7620
Tachycardia; hypotension; headache
Page 7621
Q3811:Digitalis has its action on which cell membranetransporter?
Page 7623
Q3812:Ryanodine has its action on which channel?
Page 7624
Calcium release channel in the sarcoplasmic receptor
Page 7625
Q3813:Calcium enters cardiac cells through which channel?
Page 7626
Voltage-gated calcium channel
Page 7627
Q3814:Cytoplasmic calcium concentrations in cardiac cellscan be decreased by sequestering calcium in the sarcoplasmicreticulum. Calcium enters the SR through which transporter?
Page 7628
Calcium pump in the wall of the SR
Page 7629
Q3815:Calcium channel blockers have their effect on whichcalcium transporters?
Page 7630
Voltage-gated calcium channel
Page 7631
Q3816:What is digoxin's effect on the intracellular Na+ level?
Page 7633
Q3817:What is digoxin's effect on the intracellular calciumlevel?
Page 7635
Q3818:Name two ECG changes ellicited by digoxinadministration
Page 7636
There are 4: increase PR; decrease QT; scooping of STsegment; T-wave inversion
Page 7637
Q3819:Name three symptoms of digoxin toxicity
Page 7638
Nausea; vomiting; diarrhea; blurry vision; arrhythmia
Page 7639
Q3820:Which potentiates the effects of digoxin- hypo- orhyperkalemia?
Page 7641
Q3821:Which phase of the cardiac action potential doantiarrhythmics decrease the slope of?
Page 7642
Phase 4 depolarization
Page 7643
Q3822:What type of antiarrhythmic is Amiodarone?
Page 7644
Class 1A (Class 1A includes Quinidine; Amiodarone;Procainamide; Disopyramide; "Queen Amy Proclaims
Diso's pyramid."
Page 7645
Q3823:Do class 1A antiarrhythmics increase or decrease theeffective refractory period; AP duration; and QT interval?
Page 7646
Increase ERP; increase AP duration; increase QT interval
Page 7647
Q3824:What do class 1B antiarrhythmics do to the APduration?
Page 7648
Decrease AP duration
Page 7649
Q3825:What type of antiarrhythmic is mexiletine?
Page 7650
Class 1B (includes Lidocaine; mexiletine; tocainide)
Page 7651
Q3826:What type of antiarrhythmic is encainide?
Page 7652
Class IC (includes flecainide; encainide; propafenone)
Page 7653
Q3827:What effect do class 1C antiarrhythmics have on theAP duration?
Page 7655
Q3828:What does esmolol do to the cAMP in cardiac cells?
Page 7656
decreases cAMP (a beta-blocker)
Page 7657
Q3829:What does atenolol do the calcium currents in cardiaccells?
Page 7658
decreases calcium current (beta-blocker)
Page 7659
Q3830:Timolol decreases the slope of which phase of thecardiac AP cycle?
Page 7660
Phase 4 (a beta-blocker)
Page 7661
Q3831:What does propanolol do the the PR interval?
Page 7662
Increases interval (beta-blocker)
Page 7663
Q3832:Is esmolol a short- or long-acting beta blocker?
Page 7665
Q3833:Does amiodarone increase or decrease AP duration?
Page 7666
Increase (K+ channel blocker)
Page 7667
Q3834:Does sotalol increase or decrease the effectiverefractory period?
Page 7668
Increase (K+ channel blocker)
Page 7669
Q3835:Does bretylium increase or decrease the QT interval?
Page 7670
Increase (K+ channel blocker)
Page 7671
Q3836:Name a symptom of sotalol toxicity.
Page 7672
Torsades de pointes (K+ channel blocker)
Page 7673
Q3837:Name three of the symptoms of amiodarone toxicity.
Page 7674
Pulmonary fibrosis; corneal deposits; hepatoxicity; skindeposits resulting in photodermatitis; neurologic effects;
constipation; bradychardia; heart block; CHF;hypothyroidism/hyperthyroidism. (Therefore; should check
PFTs; LFTs; and TFTs)
Page 7675
Q3838:Does verapamil increase or decrease the conductionvelocity of the AV nodal cells?
Page 7676
Decrease (calcium channel blocker)
Page 7677
Q3839:How does diltiazem affect the effective refractoryperiod and the PR interval?
Page 7678
Increases ERP; increases PR (calcium channel blocker)
Page 7679
Q3840:Name a potential use of Mg+ to treat arrhythmias.
Page 7680
To treat torsades de pointes and digoxin toxicity
Page 7681
Q3841:Name a potential use of K+ to treat arrhythmias.
Page 7682
Depress ectopic pacemakers; especially in digoxin toxicity
Page 7683
Q3842:Name a use of adenosine in treating arrhythmias.
Page 7684
To diagnose and abolish AV nodal arrhythmias.
Page 7685
Q3843:What is the effect of cholestyramine on the serumtriglyceride level?
Page 7686
Slight increase (cholestyramine is a bile acid resin)
Page 7687
Q3844:What is the effect of colestipol on HDL?
Page 7688
No effect! (colestipol is a bile acid resin)
Page 7689
Q3845:What is the effect of lovastatin on HDL?
Page 7690
Increase (lovastatin is an HMG-CoA reductase inhibitor)
Page 7691
Q3846:Name 2 side effects of pravastatin.
Page 7692
Increase LFTs and cause myositis (prevastatin is an HMG-CoA reductase inhibitor)
Page 7693
Q3847:What is the effect of Niacin on HDL?
Page 7695
Q3848:What are the side effects of clofibrate?
Page 7696
Incease LFTs and cause myositis (Clofibrate is a"Fibrate")
Page 7697
Q3849:Which increases HDL most: simvastatin; niacin; orgemfibrozil?
Page 7699
Q3850:Which decreases triglyceride level most: colestipol;Atorvastatin; niacin; or bezafibrate?
Page 7701
Q3851:What is the main effect of ezetimibe?
Page 7702
decrease serum LDL (a cholesterol absorption inhibitor)
Page 7703
Q3852:Gemfibrozil increases the activity of which enzyme?
Page 7704
Lipoprotein lipase (which converts VLDL to IDL)
Page 7705
Q3853:What enzyme breaks down membrane lipid intoarachidonic acid?
Page 7706
Phospholipase A2
Page 7707
Q3854:What two enzymes are responsible for the productionof Hydroperoxides (HPETEs) and Endoperoxidases;
respectively from arachidonate?
Page 7708
Lipoxygenase= HPETE; Cyclooxygenases=endoperoxidases
Page 7709
Q3855:What major class of products do HPETEs give rise to?
Page 7711
Q3856:What are the 3 major products of Endoperoxidases?
Page 7712
Prostacyclin (PGI); Prostaglandins (PGE; PGF);Thromboxane (TXA)
Page 7713
Q3857:In general what effect do leukotrienes have onbronchial tone?
Page 7714
Leukotrienes in general increase bronchial tone
Page 7715
Q3858:In the arachodonic acid pathway; what two enzymesdo corticosteroids block?
Page 7716
Phospholipase A2; COX-2
Page 7717
Q3859:NSAIDs; Acetaminophen and COX-2 inhibitors blockwhich arachadonic acid pathway enzymes
Page 7718
NSAIDs-non-selectively block COX-1 and COX-2;acetaminophen doesn't block COX-1 or COX-2; but instead it
may block COX-3 in found in the brain; COX-2 inhibitorsblock COX-2
Page 7719
Q3860:What are the 4 major effects of Prostacyclin
Page 7720
decrease platelet aggregation; decrease vascular tone; decreasebronchial tone; decrease uterine tone
Page 7721
Q3861:What are the 3 major effects of Prostaglandins
Page 7722
increased uterine tone; decrease vascular tone; decreasebronchial tone
Page 7723
Q3862:What are the 3 major effects of Thromboxane
Page 7724
increase platelet aggregation; increase vascular tone; increasebronchial tone
Page 7725
Q3863:Zileuton is a ________ pathway inhibitor?
Page 7727
Q3864:Zariflukast is associated with what enzymes?
Page 7729
Q3865:Bronchodilation is mediated by what molecule
Page 7731
Q3866:Bronchoconstriction is mediated by _________ and___________
Page 7732
Ach and adenosine
Page 7733
Q3867:How many asthma drug categories are there?
Page 7734
7- (1) nonspecific B-agonists; (2) B2 agonists; (3)Methylxanthines; (4) muscarinic antagonist; (5) cromolyn; (6)
corticosteroids; (7) Antileukotrienes
Page 7735
Q3868:What is the only nonspecific B-agonist drug and whatare its effects?
Page 7736
Isoprotenerol-relaxes bronchial smooth muscle (B2) andtachycardia (B1) (adverse effect).
Page 7737
Q3869:What are the two B2 selective agonist asthma drugs?
Page 7738
Albuterol- relaxes bronchial smooth muscle (B2); Salmetrol
Page 7739
Q3870:What are the indications for Albuterol and Salmetrol;respectively?
Page 7740
Albuterol- use during acute exarcebation; Salmetrol- long-acting agent for prophylaxis
Page 7741
Q3871:what are the notable adverse effects of B2 agonist?
Page 7742
arythmias and tremor
Page 7743
Q3872:B2-agonists activate this enzyme in bronchial smoothmuscle that leads to an increase in ________ =
bronchodilation
Page 7744
B2 agonists activate adenylate cyclase and increase conversionof ATP to cAMP
Page 7745
Q3873:What are the likely mechanism of action theophylline?
Page 7746
bronchodialation by inhibition phosphodiesterase (PDE);decreasing cAMP hydrolysis and antagnonizing adenosine
action
Page 7747
Q3874:Why is usage of theophylline limited?
Page 7748
limited b/c narrow therapeutic index (cardiotoxicity;neurotxicity)
Page 7749
Q3875:What kind of drug is Ipratropium?
Page 7750
muscarinic antagonist
Page 7751
Q3876:How does mechanism of action of Ipratropium?
Page 7752
competitive block of muscarinic receptors= prevention ofbronchoconstriction
Page 7753
Q3877:cromolyn works by inhibiting the release of _______from ______ cell?
Page 7754
prevents release of medicators from mast cells
Page 7755
Q3878:Cromolyn is mainly used for the ______ of athsmaand it is not indicated for _______ treatment of athsma?
Page 7756
Used only for prophylaxis; not effective during acute episode.Also; toxicity rare
Page 7757
Q3879:__________and ________ are two majorcorticosteroids used for treatment of what kind of asthma?
Page 7758
Beclomethasone and prednisone are 1st line therapy forchronic asthma
Page 7759
Q3880:What is the mechanism of action of corticosteroids?
Page 7760
inhibits the synthesis of virtually of cytokines-->inactivates NF-KB; the transcription factor that inducesthe production of TNF-a; amonth other inflammatory agents.
Page 7761
Q3881:Zileuton blocks the conversion of _______ to________.
Page 7762
zileuton is a 5-lipoxygenase pathway inhibitior. Blocks theconversion of arachidonic acti to leukotrienes
Page 7763
Q3882:Zafirlukast works by_______ ________ ________
Page 7764
bloking leukotriene receptors
Page 7765
Q3883:What the most basic asthma treatment strategy?
Page 7766
avoidance of exposure to antingen (dust; pollen; etc)
Page 7767
Q3884:After exposure to antigen crosslinks IgE on mast cells.This is prevented by the following drugs: _________ and
________
Page 7768
cromolyn and steroids
Page 7769
Q3885:Following allergen exposure mediators are released (ex._______ and _________). This triggers an ______ asthmaticresponse characterized by ________ and may be treated with
the following 3 asthmatic drug categories to treat thesymptoms.
Page 7770
examples of mediators are leukotrienes and histamine.Following allergen exposure an early asthmatic response
characterized by bronchoconstriction that can be treated withB-agonsists; methylxanthines; and muscarinic antagonists.
Page 7771
Q3886:Also; mediators elicit a ________ response is whichleads to bronchial __________ and is treated with
__________.
Page 7772
mediators elicit a late response and this leads to bronchialhyperactivity. This is best treated with steroids.
Page 7773
Q3887:the following questions are from the diagram at the topof the page
Page 7775
Q3888:_____ cells are predominatly found in the antrum and_________ cells are predominatly found in the fundus.
Page 7776
Gastrin cells are predominant in the antrum and parietal cellsare predominant in the fundus.
Page 7777
Q3889:What are the 3 main stimuli of acid secretion?
Page 7778
Ach; histamine; gastrin
Page 7779
Q3890:Gastrin stimulates the ECL cells to secrete histaminethat stimulates ______ cells. Gastrin also activate the ______
cells to increase expression of _______ that increases______secretion.
Page 7780
Gastrin stimulates the ECL cells to secrese histamine thatstimulates parietal cells. Parietal cells are also activated bygastrin to increase the expression of the H;K ATPase that
increases acid secretion.
Page 7781
Q3891:This type of drug acts by inhibiting M1 and M3receptors on ECL cells and Parietal cells; respectively.
Page 7782
muscarinic antagonists block M1 receptors in ECL cells andM3 receptors in parietal cells.
Page 7783
Q3892:This type of drug inhibits the ability of the ECL cellto stimulate acid secretion by interfering with the _____
receptor.
Page 7784
H2 blocker inhibits the ability of the ECL cell to stimulateacid secretion by interfering with the parietal H2 receptor.
Page 7785
Q3893:The most direct way of inhibiting acid secretion is byusing this type of drug which acts on this enzyme.
Page 7786
the most direct way of inhibiting acid secretion is by usingproton pump blockers which inhibit the H;K ATPase on
parietal cells.
Page 7787
Q3894:____________ acts by binding to the ulcer andincreasing its healing. It may interfere with drug absorption in
the stomach.
Page 7788
sucralfate binds to the ulcer base and provides physicalprotection. It allows HCO3- secretion to reestablish pH
gradient in the mucus layer.
Page 7789
Q3895:What hormone binds ECL cells and decreases acidsecretion?
Page 7791
Q3896:These type of drugs used to decrease pH in thestomach.
Page 7792
antacids….duh….jk. (I was instructed to make a question ofevery word)
Page 7793
Q3897:____________; ___________; ___________; and___________ are examples of H2 blockers and they act by
(reversibly/irreversibly)
Page 7794
cimetedine; ranitidine; famotidine; nizatidine reversilbly blockH2 receptors.
Page 7795
Q3898:This H2 blocker is the only one that has many sideeffects which include potent inhibition of ______; _____
effects; and _____ renal excretion of creatinine.
Page 7796
cimetedine is a potent inhibitor of P450; it has antiandrogeniceffect and decrease renal excretion of creatinine. Other H2
blockers are relatively free of these effects.
Page 7797
Q3899:_________ and _________ (reversibly/irreversibly)inhibit the H/K ATPase in the stomach _______cells.
Page 7798
Omeprazole and Iansoprazole irreversibly inhibit the H/KATPase in stomach parietal cells
Page 7799
Q3900:Proton pump inhibitors are indicated for peptic ulcer;________; _______; and _________ syndrome
Page 7800
peptic ulcer; gastritis; esophageal reflux; and Zollinger-Ellisonsyndrome
Page 7801
Q3901:T/F: Bismuth and sucralfate allow HCO3- secretion.
Page 7802
True: bismuth and sucralfate bind to ulcer base and providephysical protection; and allow HCO3- secretion to reestablish
pH gradient in the mucus layer=increased ulcer healing
Page 7803
Q3902:T/F: misoprostol is a PGE2 analog and increases theproduction and secretion of gastric mucous barrier.
Page 7804
False: misoprostol is a PGE1 analog and it increases theproduction and secretion of gastric mucous barrier.
Page 7805
Q3903:What are the 3 indications for misoprosol?
Page 7806
prevention of NSAID-induced peptic ulcers; maintains a PDAand used to induce labor
Page 7807
Q3904:In what population is misoprostol contraindicated?
Page 7808
women of childbearing potential (abortifacient). It also casuesdiarrhea
Page 7809
Q3905:Infliximab is ___________ against ______.
Page 7810
monoclonal antibody to TNFa
Page 7811
Q3906:The clinical indication for Infliximab is:
Page 7812
Crohn's; along with fistula healing
Page 7813
Q3907:T/F: Infliximab can cause respiratory infection; fever;hypotension
Page 7815
Q3908:This drug offers both anitbacterial action and anti-inflamatory effects. It is used for 2 inflammatory GI diseases
______ and _______.
Page 7816
sulfasalazine: combination of sulfapyridine (antibacterial) andmesalamine (anti-inflammatory effects). It is used for
Ulcerative colitis and remission of Crohn's.
Page 7817
Q3909:T/F: Side effects of the above include: malaise;sulfonamide toxicity; neutropenia
Page 7818
false: side effects: malaise; nausea; sulfonamide toxicity
Page 7819
Q3910:___________ is a powerful central-acting antiemetic.It acts by antagonizing the______ receptor.
Page 7820
Ondansetron: is a powerful antiemetic. Think: you will notvomit with ondansetron; so you can go on dancing.
Page 7821
Q3911:T/F used to treat vomiting preoperatively and forcancer chemo therapy pts.
Page 7822
False: it is used to treat vomiting postoperatively.
Page 7823
Q3912:Headache and __________ are side effects
Page 7824
constipation (can't vomit or poop)
Page 7825
Q3913:Antacid overuse can affect:_________; __________;or ______ excretion of other drugs by altering ______ and
______ pH or by delaying gastric _________.
Page 7826
Antacid overuse can affect absorption; bioavailability; orurinary excretion of other drugs by altering gastric and urinary
pH or by delaying gastric emptying.
Page 7827
Q3914:Constipation and (hypo/hyper) phosphatemia is seenwith overuse of ________________
Page 7828
aluminum hydroxide - Aluminimum amt. of feces
Page 7829
Q3915:Magnesium hydroxide overuse = ___________
Page 7830
diarhea; Mg = Must go to the bathroom
Page 7831
Q3916:Calicium carbonate= hypercalcemia and(increase/decreased) acid
Page 7832
causes hypercalcemia and increased acid.
Page 7833
Q3917:T/F: hyperkalemia can be seen with AlOH; MgOH;CaCO2
Page 7834
False! hypokalemia
Page 7835
Q3918:heparin Catalyzes activation of ____________;decreases ________ and __________. It has a ____t1/2. check
PTT
Page 7836
catalyzes the activation of antithrombin III; decreasesthrombin and Xa. It has a short t1/2
Page 7837
Q3919:It is used for immediated anticoagulation forpulmonary embolism;_______; _______; MI; and ________.
Follow PTT
Page 7838
used for pulmonary embolism; stroke; angina; MI; and DVT.
Page 7839
Q3920:T/F: Is used during pregnancy
Page 7840
true: it is used during pregnancy because it does not cross theplacenta.
Page 7841
Q3921:It can cause bleeding;___________; and drug-druginteractions.
Page 7842
thrombocytopenia
Page 7843
Q3922:___________ is used for rapid reversal of heparization(it is a _______ charged molecule that binds the ________
charged heparin)
Page 7844
protamine sulfate is used for rapid reversal of heparinization(it is a positively charged molecule that binds the negatively
charged heparin).
Page 7845
Q3923:Newer________________ (enoxaparin) act more on_____; have better bioavailability and 2-4 times longer t1/2.
Can be administered subcut and (with/without) labmonitoring.
Page 7846
lower-molecular-weight heparins (enoxaparin) act more on Xa;have better bioavailabitlity and 2-4 times longer half-life. Can
be adm. Subcut and without lab monitoring.
Page 7847
Q3924:warfirin (coumandin) Interferes with normal synthesisand gamma-carboxylation of vitamin K-dependent factors
___; ___; ___; and ___; also; ___ and ___ via ______antagonism.
Page 7848
Interferes with normal synthesis and gamma-carboxylation ofvitamin K-dependent clotting factors II; VII; IX; and X;
protein C and S via vitamin K antagonism.
Page 7849
Q3925:t1/2 (short/long)
Page 7851
Q3926:Used for _______ anticoagulation. Follow PT
Page 7852
WEPT - Warfirin affects the Extrinsic pathway and prolongsPT
Page 7853
Q3927:T/F: is used during pregnacy
Page 7854
False! (warfarin; unlike heparin; can cross the placenta).
Page 7855
Q3928:Toxicity: bleeding; _________; drug-drug interactions
Page 7857
Q3929:Heparin is a (large/small) _____charged acicid polymerwhile Warfarin is (large/small) (charged/neutral) molecule
Page 7858
Heparin is a large negatively charged acidic polymer whileWarfarin is a small neutral charged lipid-soluble molecule
Page 7859
Q3930:T/F: Heparin is given orally while warfarin is givenSC/IV
Page 7860
False! Heparin is given IV/SC and warfarin is give oral
Page 7861
Q3931:Site of action: heparin _________; warfarin ______
Page 7862
heparin's site of action is the blood; warfarin's site of action isthe liver (synthesises clotting factors)
Page 7863
Q3932:Onset of action of _________ is slow; the onset ofaction of ______ is rapid
Page 7864
onset of action of heparin is rapid (secs) and the onset ofaction of warfarin is slow; limitd by t1/2 of normal clotting
factors.
Page 7865
Q3933:Warfarin works by imparing the synthesis of _______dependent factors __; ___; ___; and ___ also _____; and
____; heparin activates _____; ____ and ___
Page 7866
Warfarin works by imparing the synthesis of vitamin Kdependent factors II; VII; IX; and X also protein S and
protein C; heparin activates ATIII; Iia (thrombin) and Xa.
Page 7867
Q3934:Heparin 's duration of action is (acute/chronic);warfarin's duration of action is (actue/chronic)
Page 7868
Heparin's duration of action is actute and warfarin's durationof action is chronic.
Page 7869
Q3935:Tx of acute OD: Heparin = _________;warfarin=______
Page 7870
Tx of heparin OD is protamine sulfate; Tx of warfarin= IVvit. K and fresh frozen plasma.
Page 7871
Q3936:Warfarin is monitored by _________ while Heparin ismonitored by ___________.
Page 7872
Warfrin is monitored by PT (extrinsic pathway) (WEPT) andheparin is monitored by PTT (intrinsic pathway)
Page 7873
Q3937:plasmin is the major ___________ enzyme. It breaksdown both _______ and _______
Page 7874
fibrinolytic enzyme. It accelerates breaks down of both fribinand fibrinogen yielding fibrin splip products and degradation
products; respectively.
Page 7875
Q3938:Fibrinogen is converted to fibrin by _________
Page 7877
Q3939:tPA and urokinase promote the converson of ______to ________ thereby increasing fibrinolysis.
Page 7878
plasminogen to plasmin
Page 7879
Q3940:Various stimuli activate a blood proactivator to ablood activator that promotes conversion of _________ to
blank thereby increasing fibrinolysis
Page 7880
plasminogen to plasmin
Page 7881
Q3941:Aminocaproic acid:____________ fibrinolysis.
Page 7882
inhibits fibrinolysis by inhibition of plasminogen conversionto plasmin.
Page 7883
Q3942:4 examples of thrombolytics include: ________;_________; _____________; and ___________
Page 7884
Streptokinase; urokinase; tPA(altepalse); APSAC(anistreplase)
Page 7885
Q3943:work by directly or indirectly aiding the conversion of___________ to __________; which cleaves ______ and
________ clots. tPA specifically coverts _______________to plasmin
Page 7886
Directly or indirectly aid conversion of plaminogen toplasmin; which cleaves thrombin and fribrin clots. It is
claimed that tPA specifically coverts fribrin-boundplasminogen to plasmin.
Page 7887
Q3944:T/F: clinical use is for DVTs
Page 7888
False: used for early MI
Page 7889
Q3945:pts. receiving this medication are at most risk for:______
Page 7891
Q3946:When a break in the endothelium occurs _________and _________ are exposed.
Page 7892
collagen and vWF
Page 7893
Q3947:Platelets are activated by binding to the abovemacromolecules. The two structures expressed by theplatelets involved in this process are __________ and
_________ and they bind to _________ and __________;repectively
Page 7894
Platelets bind to collagen and vWF. The two structuresexpressed by platelets that are involved in this process are GP
1a and GP 1b. GP 1a and GP 1b bind to collagen and vWF;respectively.
Page 7895
Q3948:After platelet activation _________ is expressed ontheir surface. What is the role of this structure?
Page 7896
after platelets are activated they express GP IIb/IIIa. Thismolecule is important in platlelet-platelet aggregation.
Page 7897
Q3949:_________ and _________ interaction is needed inorder for platelet aggregation to occur.
Page 7898
GP IIb/IIIa and fribinogen
Page 7899
Q3950:5-HT; _______; and ________ are molecules that playa role in the glycoprotein expression of activated platelets.
Page 7900
5-HT; ADP; and TxA2 are molecules that play a role in theglycoprotein expression of activated platelets.
Page 7901
Q3951:Aspirin acts by inhibiting production of ________that in turn inhibits glycoprotein expression in activated
platelets.
Page 7903
Q3952:ADP production is inhibited by the drug _________.
Page 7905
Q3953:This antibody drug targets the _______ on platelets.
Page 7907
Q3954:Copidogrel; ticlopidine T/F: inhibits plateleaggregation by irreversibly inhibiting the ADP pathway
involved in the binding of fibrinogen
Page 7909
Q3955:It is used for ______ ________ syndrome; coronary_______; and it has been shown to decrease the incidence or
recurrence of___ ____.
Page 7910
it is used for acute coronary syndrome; coronary stenting.Decreases incidence or recurrence of thrombotic stroke
Page 7911
Q3956:Ticlopidine is associated with_________ as a sideeffect.
Page 7912
Ticlopidine causes neutropenia and it is reserved for thosewho cannot tolerate aspirin.
Page 7913
Q3957:Abciximab binds to __________ on activatedplatelets.
Page 7915
Q3958:It is used for ___________ and ________ ____________________ ___________
Page 7916
acute coronary syndromes and percutanous transluminalcoronary angioplasty
Page 7917
Q3959:toxiciites are _______ and ________
Page 7918
bleeding and thrombocytopenia
Page 7919
Q3960:It ________ and (reversibly/irreversibly) inhibitsCOX1 and COX2 to prevent the conversion of _______ to
prostaglandins.
Page 7920
acetilates and irreversably inhibits COX-1 and COX-2
Page 7921
Q3961:T/F: aspirin has an effect of PT; PTT
Page 7922
false it has no effect
Page 7923
Q3962:What are the 4 A's of aspirin and NSAIDS in general
Page 7924
Antipyretic; Analgesic; Anti-inflam; antiplatelet
Page 7925
Q3963:Important toxicities include _________; bleeding;hyperventilation; __________- in children; and CN ____
toxicity
Page 7926
gastric ulceration; bleeding; hyperventilation; Reyes syndromeand tinnitus (CNVIII).
Page 7927
Q3964:Hydrocortisone; prednisone; triamcinolone;dexamtasone; bleclomethasone are examples of what kind of
drugs?
Page 7929
Q3965:Glucocorticoids decrease the production of ___ and____
Page 7930
Leukotrienes and prostanglandins
Page 7931
Q3966:To treat Addison's disease; inflammation; immunesuppression; asthma; use ____
Page 7932
Glucocorticoids
Page 7933
Q3967:An important side-effect of Glucocortioid usage is____
Page 7934
Iatrogenic Cushing's Syndrome
Page 7935
Q3968:Buffalo hump; moon facies; truncal obesity; muscleswasting; thin skin; easy bruisability; osteoporosis;
adrenocortical atrophy; peptic ulcers characterize whatsyndrome?
Page 7936
Cushing's Syndrome
Page 7937
Q3969:Which two drugs inhibit cGMP phosphodiesterase;leading to smooth muscle relaxation in the corpus cavernosum
and penile erection?
Page 7938
Sildenafil and Verdenafil --they fill the penis
Page 7939
Q3970:What class of drugs are used tto treat erectiledysfunction
Page 7940
cGMP Inhibitors
Page 7941
Q3971:CGMP inibitors taken with ____have a high risk ofliofe-threeatening hypotension
Page 7943
Q3972:Which drugs is a partial agonist of estrogen recpetorsin the pituitary gland; stimulating increase in LH and FSH;
which stimulates ovulation to treat infertility
Page 7945
Q3973:Clomiphene's side effects include:
Page 7946
Hotflashes; ovarian enlargment; multiple simultaneouspregnancies; visual disturbances
Page 7947
Q3974:What abortifacient is a competitite inhibitor ofpreogestins at progesterone recpetor and may lead to heavy
menstrual-like bleeding?
Page 7948
Mifepristone (RU486)
Page 7949
Q3975:The advantage of this drug is that it is reliable;decreases incidence of ectopic pregnancy; decreases risk of
pelvic infections; and regulates menses; however it also putsyou in a hypercoagulable stat and may increase your
trigylcerides; weight; and blood pressure
Page 7950
Oral Contracpetices - syntheitc progestins/estrogen
Page 7951
Q3976:____is converted to uric acid which leads to gout
Page 7952
Xanthine (converted from excess purines)
Page 7953
Q3977:This drug depolymerizes microtubules; impairingleukocyte chemotaxis and degranulation; and used to treat
acute gout
Page 7955
Q3978:This drugs inhibits reabsorption of uric acid and usedto treat chronic gout
Page 7957
Q3979:This drug is used to treat chronic gout; but also inhbitssecretion of penicillin
Page 7959
Q3980:This drugs inhibits xanthine oxidase decreasing theconversion fo xanthine to uric acid
Page 7961
Q3981:What are the cell cycle specific oncologic drugs
Page 7962
antimetabolites; plant alkaloids; stroid hormones; bleomycin;paclitaxel; etoposide
Page 7963
Q3982:What are the cell cycle Nonspecific oncologic drugs?
Page 7964
alkylating agents and antibiotics
Page 7965
Q3983:____is an S-phase-specific anti-metabolite that is anfolic acid analog that inhibits dihydrofolate reducate
decreasing dTMP(thymidine and purines) and decreaingDNA/prtein synthesis.
Page 7967
Q3984:____is an S-phase-specific anti-metabolite that is apyrmidine analog which complexed to folic acid; inhibitingthymidylate synthase; decreasing dTMP and decreasing
DNA/protein synthesis
Page 7968
5-Fluorouracil (5-FU)
Page 7969
Q3985:Myelosuppression by methotrxate is reversible with____
Page 7970
leucovorin (folinic acid) rescue
Page 7971
Q3986:Which drug blocks purine synthesis and is used totreat leukemias; lymphomas (not CLL or Hodgkins)
Page 7972
6-mercaptopurine (6-MP)
Page 7973
Q3987:Which drug alkylates DNA and is used to treat CML?
Page 7975
Q3988:Which drug inhibits DNA polymerase and is used totreat AML?
Page 7977
Q3989:This drug used to treat Leukemias and Lymphomas ismetaboilized by xanthine oxidase
Page 7978
6-mercaptopurine (6-MP)
Page 7979
Q3990:Used to treat leukemias; lymphomas; choricarcinoma;sacromas; rheumatoid arthritis; psoriasis; and can be an
abortifacient; it may lead to myelosuppression
Page 7981
Q3991:Used to treat colon cancer and other solid tumors;basal cell carcinoma (topically)
Page 7982
5-Fluorouracil (5-FU)
Page 7983
Q3992:Myelosuppression by 5-FU is ______
Page 7985
Q3993:This drug used to treat AML may lead to leukopenia;thrombocytopenia; megaloblastic anemia?
Page 7987
Q3994:This drugs used to treat CML may lead to pulmonaryfibrosis and hyperpigmentation?
Page 7989
Q3995:____is an alkylating agent acivated by liver thatcovalently x-links DNA at guanine N-7; and is used to treat
non-hodgkin's lymphoma; breast/ovarian carcinomas
Page 7990
cyclophosphamides
Page 7991
Q3996:____ alkylates DNA after bioactivation and can crossthe BBB and treats brain tumors (glioblastoma multiforme)
Page 7992
Nitrosoureas (Carmustine; lomustine; semustine;streptozocin)
Page 7993
Q3997:____acts like an alkylating agent; x-linking viahyrdolysis of Cl and platinum; used to treat testicular;
bladder; lung carcinomas
Page 7995
Q3998:This alkylating agent can cause myelosuppression andhemorhagic cystitis
Page 7996
cyclophosphamides
Page 7997
Q3999:This combination of drugs is used to treat Hodgkin'sand myelomas; sarcomas; and solid tumors (breast; ovary;
lung)
Page 7998
ABVD: Adriamycin; Bleomycin; Vinblastine; Dacarbazine
Page 7999
Q4000:____noncovalently intercalates in DNA; creatingbreaks to decrease replication and transcription
Page 8000
Doxorubicin (adriamycin)
Page 8001
Q4001:____intercalates DNA strands and induces free radicalfromation which causes strand breaks
Page 8002
Bleomycin; Dactinomycin
Page 8003
Q4002:Which drugs causes cardiotoxicity; alopecia; andmyelosuppression?
Page 8004
Doxorubicin (adriamycin)
Page 8005
Q4003:Which drug is used to trat oat cell carcinoma of thelung and prostate/testicular carcinoma?
Page 8007
Q4004:This combination of drugs is used to treat lymphoma;CLL; Hodgkin's; Wilm's tumor; choriocarcinoma
Page 8008
MOPP (Mustargen; Oncovin (Vincristine); Procarbazine(Matulane); Prednisone)
Page 8009
Q4005:Which glucocorticoid may trigger apoptosis and mayeven work on nondividing cells
Page 8011
Q4006:This drug is a G2-phase specific inhibitor ofTopisiomerase II; leaving double strand breaks in DNA
following DNA replication
Page 8013
Q4007:This drug used to treat testicular cancer andlymphomas may cayse pulmonary fibrosis; skin chnages; and
myelosuppression
Page 8014
Bleomycin; Dactinomycin
Page 8015
Q4008:This drugs used as an immunosuppressant and inlymphomas may cause acne; osteoporosis; hypertension;
peptic ulcers; hyperglycemia; psychosis?
Page 8017
Q4009:____is an estrogen receptor mixed agonist/antagonistthat blocks the binding of estrogen to ER+ cells.
Page 8018
Tomoxifen/Raloxifene
Page 8019
Q4010:____is n M-phase-specific alkaloid that binds totubulin and blocks polymerization of microtubules;
preventing spindle formation
Page 8020
Vincristine and Vinblastine
Page 8021
Q4011:____is an M-phase-specific agen that binds to tubulinand hyperstabilizes the polymerized microtubules; so that the
mitotic spindle cannot break down
Page 8023
Q4012:What drugs is used to treat breast cancer; but mayincreas the risk of endometrial carcinomas and hot flashes
Page 8025
Q4013:Side-effects of Vinblastine include….
Page 8026
VinBASTine BLASTs Bone Morraow; causingmyelosuppression; as well as neurotoxicity and paralutic
ileus.
Page 8027
Q4014:Side effects of Paclitaxel include….
Page 8028
Myelosuppression and hypersensitivity
Page 8029
Q4015:Which drug binds to cyclophilins; blockingdifferentiation and activation of T cells mainly by inhibiting
IL2 production
Page 8031
Q4016:This antimetabolite derivative of 6-mercaptopurineinterferes with the metabolism and synthesis of nucleic acid;
therefore toxic to proliferating lymphocytes
Page 8033
Q4017:This potent immunosuppressive drug binds to theFK-binding protein and inhibits secretion of IL2 and other
cytokines
Page 8034
tacrolimus (FK506)
Page 8035
Q4018:This drug is used to suppress organ rejection aftertransplantation; but may predispose patient to viral infections
and lymphoma
Page 8037
Q4019:Azaothioprine is used to in what setting?
Page 8038
Kidney transplants; autoimmune disorders(glomerulonephritis; hemolytic anemia)
Page 8039
Q4020:Recombinant Cytokine- Aldesleukin (interleukin-2) isused for?
Page 8040
Renal cell carcinoma; metastatic melanoma
Page 8041
Q4021:Recombinant Cytokine- Erythropoietin (epoetin) isused for?
Page 8043
Q4022:Recombinant Cytokine- Filgrastim is used for?
Page 8044
Recovery of Bone Marrow; it is a granulocyte colonystimulating factor
Page 8045
Q4023:Recombinant Cytokine- alpha interferon is used for?
Page 8046
Hep B/C; Kaposi's sarcoma; leukemia; malgnant melanoma
Page 8047
Q4024:Recombinant Cytokine- beta interferon is used for?
Page 8048
Multiple Sclerosis
Page 8049
Q4025:Recombinant Cytokine- gamma interferon is used for?
Page 8050
Chronic Granulomatous disease
Page 8051
Q4026:Recombinant Cytokine- oprelvekin (interleukin2) isused for?
Page 8052
Thrombocytopenia
Page 8053
Q4027:Recombinant Cytokine- sargamostim is used for?
Page 8054
Recovery of Bone Marrow (it is a granulocyte-macrophagecolony stimulating factor)
Page 8055
Q4028:Recombinant Cytokine- thrombopoietin is used for?
Page 8056
Thrombocytopenia
Page 8057
Q4029:What is the antidote for acetaminophentoxicity/overdose
Page 8058
N-acetylcysteine
Page 8059
Q4030:What is the antidote for salicylates toxicity/overdose
Page 8060
Alkanize urine/dialysis
Page 8061
Q4031:What is the antidote for antichoinesterasetoxicity/overdose
Page 8062
Atropine; pralidoxime
Page 8063
Q4032:What is the antidote for antimuscarinic/anticholinergicagents toxicity/overdose
Page 8064
physostigimine salicylate
Page 8065
Q4033:What is the antidote for Beta-blockerstoxicity/overdose
Page 8067
Q4034:What is the antidote fordigitalis toxicity/overdose
Page 8068
Stop digitalis; Normalize K+; lodpcaine; anti-digitialis FabFragments; Magnesium
Page 8069
Q4035:What is the antidote for lead toxicity/overdose
Page 8070
CaEDTA; dimercaprol; succimer; penicillamine
Page 8071
Q4036:What is the antidote for iron toxicity/overdose
Page 8073
Q4037:What is the antidote for aresnic/mercury/goldtoxicity/overdose
Page 8074
Dimercaprol (BAL); succimer
Page 8075
Q4038:What is the antidote for copper; arsenic; goldtoxicity/overdose
Page 8077
Q4039:What is the antidote N-acetylcysteine used to treat?
Page 8078
Acetaminophen toxicity/overdose
Page 8079
Q4040:What is the antidote for cyanide toxicity/overdose
Page 8080
nitrite; hydroxocobalamin; thiosoulfate
Page 8081
Q4041:What is the antidote for methemoglobintoxicity/overdose
Page 8083
Q4042:What is the antidote glucagon used to treat?
Page 8084
Beta-blocker toxicity/overdose
Page 8085
Q4043:What is the antidote for carbon monoxidetoxicity/overdose
Page 8086
100% oxygen; hyperbaric oxygen
Page 8087
Q4044:What is the antidote atropine used to treat?
Page 8088
anticholinesterase toxicity/overdose
Page 8089
Q4045:What is the antidote for methanol toxicity/overdose
Page 8090
Ethanol; dialusis; fomepizole
Page 8091
Q4046:What is the antidote for opiods toxicity/overdose
Page 8092
Nalozone/naltrexone
Page 8093
Q4047:What is the antidote for ethylene glycoltoxicity/overdose
Page 8094
Ethanol; dialusis; fomepizole
Page 8095
Q4048:What is the antidote for benzodiazepinestoxicity/overdose
Page 8097
Q4049:What is the antidote for (TCA) TricyclicAntidepressants toxicity/overdose
Page 8099
Q4050:What is the antidote for Heparin toxicity/overdose
Page 8101
Q4051:What is the antidote Deferoxamine used to treat?
Page 8102
Iron toxicity/overdose
Page 8103
Q4052:What is the antidote for warfarin toxicity/overdose
Page 8104
vitamin K; fresh frozen plasma
Page 8105
Q4053:What is the antidote Naloxone/naltrexone used totreat?
Page 8106
opioid toxicity/overdose
Page 8107
Q4054:What is the antidote for tPA/streptokinasetoxicity/overdose
Page 8108
aminocaproic acid
Page 8109
Q4055:What is the antidote Physostigmine salicylate used totreat?
Page 8110
Antimuscarinic/anticholinergic agents toxicity/overdose
Page 8111
Q4056:What is the antidote Flumazenil used to treat?
Page 8112
Benzodiazepine toxicity/overdose
Page 8113
Q4057:What is the antidote Protamine used to treat
Page 8114
Heparin toxicity/overdose
Page 8115
Q4058:Children living in old houses might eat the paint chipswhich could cause ____
Page 8117
Q4059:Signs of Lead poisoning include:
Page 8118
Lead Lines on gingivae and epiphyses of Long bones;Encephalopathy and Erythrocyte Basophilic stippling;
Abdominal colic and sideroblastic Anemia; Wrist and FootDrop
Page 8119
Q4060:1st line of Treatment for Lead Poisoning include
Page 8120
Dimercaprol and EDTA
Page 8121
Q4061:Weak acids; such as phenobarbitol; methotreaxate;aspirin; alkanize urine with ____ to increase clearance
Page 8123
Q4062:Weak bases; such as amphetamines; acidify urine withNH4Cl to ____ clearance
Page 8127
Q4064:Drugs causing Pulmonary fibrosis (3)
Page 8128
bleomycin; amiodarone; busulfan
Page 8129
Q4065:Drugs causing Hepatitis (2)
Page 8130
isoniazid; halothane
Page 8131
Q4066:Drugs causing Focal to massive hepatic necrosis (4)
Page 8132
halothane; valproic acid; acetaminophen; amanita phalloides
Page 8133
Q4067:Drugs causing Anaphylaxis (1)
Page 8135
Q4068:Drugs causing SLE-like syndrome (4). [mnemonic: it'snot HIPP to have lupus]
Page 8136
hydralazine; INH; procainamide; phenytoin
Page 8137
Q4069:Drugs causing Hemolysis in G6PD-deficient patients(8)
Page 8138
sulfonamides; INH; aspirin; ibuprofen; primaquine;nitrofurantoin; pyrimethamine; chloramphenicol
Page 8139
Q4070:Drugs causing Thrombotic complications (1 class)
Page 8140
OCPs (e.g. estrogens and progestins)
Page 8141
Q4071:Drugs causing Adrenocortical insufficiency(withdrawal of what class of drugs causes adrenocortical
insufficiency?)
Page 8142
withdrawal of glucocorticoids causes hypothalamic-pituitary-axis suppression
Page 8143
Q4072:Drugs causing Photosensitivity reactions (3)[mnemonic: SAT for a photo]
Page 8144
Sulfonamides; amiodarone; tetracycline
Page 8145
Q4073:Drugs causing Induce P-450 system (6)
Page 8146
barbiturates; phenytoin; carbamazepine; rifampin;griseofulvin; quinidine
Page 8147
Q4074:Drugs causing Inhibit P-450 system (6; including onefruit)
Page 8148
cimetidine; ketoconazole; grapefruit; erythromycin; INH;sulfonamides
Page 8149
Q4075:Drugs causing Tubulointerstitial nephritis (5)
Page 8150
sulfonamides; furosemide; methicillin; rifampin; NSAIDs(except aspirin)
Page 8151
Q4076:Drugs causing Hot flashes (1)
Page 8153
Q4077:Drugs causing Cutaneous flushing (4)
Page 8154
niacin; Ca++ channel blockers; adenosine; vancomycin
Page 8155
Q4078:Drugs causing Cardiac toxicity (2)
Page 8156
doxorubicin (adriamycin); daunorubicin
Page 8157
Q4079:Drugs causing Agranulocytosis (3; all start with letterC)
Page 8158
clozapine; carbamazepine; colchicine
Page 8159
Q4080:Drugs causing Stevens-Johnson syndrome (3)
Page 8160
ethosuximide; sulfonamides; lamotrigine
Page 8161
Q4081:Drugs causing Cinchonism (2)
Page 8162
quinidine; quinine
Page 8163
Q4082:Drugs causing Tendonitis; tendon rupture and cartilagedamage (kids) (1)
Page 8164
fluoroquinolones
Page 8165
Q4083:Drugs causing Disulfiram-like reaction (4)
Page 8166
metronidazole; certain cephalosporins; procarbazine;sulfonylureas
Page 8167
Q4084:Drugs causing Otoxicity and nephrotoxicity (3)
Page 8168
aminoglycosides; loop diuretics; cisplatin
Page 8169
Q4085:Drugs causing Drug-induced Parkinson's (4)
Page 8170
haloperidol; chlorpromazine; resperine; MPTP
Page 8171
Q4086:Drugs causing Torsades de pointes (two subclasses ofantiarrhythmics)
Page 8172
Class III (sotalol); class IA (quinidine) antiarrhythmics
Page 8173
Q4087:Drugs causing Aplastic anemia (3)
Page 8174
chloramphenicol; benzene; NSAIDs
Page 8175
Q4088:Drugs causing Neuro/nephrotoxicity (1)
Page 8177
Q4089:Drugs causing Pseudomembranous colitis (2)
Page 8178
clindamycin; ampicillin
Page 8179
Q4090:Drugs causing Gynecomastia (5) [mnemonic: SomeDrugs Create Awesome Knockers]
Page 8180
spironolactone; digitalis; cimetidine; chronic Alcohol use;estrogens; ketoconazole
Page 8181
Q4091:Drugs causing Atropine-like side effects (1)
Page 8183
Q4092:Drugs causing Cough (1)
Page 8184
ACE inhibitors (losartan --> no cough)
Page 8185
Q4093:Drugs causing Gingival hyperplasia (1)
Page 8187
Q4094:Drugs causing Diabetes insipidus (1)
Page 8189
Q4095:Drugs causing Tardive dyskinesia (1)
Page 8191
Q4096:Drugs causing Fanconi's syndrome (1)
Page 8193
Q4097:Drugs causing Gray baby syndrome (1)
Page 8194
chloramphenicol
Page 8195
Q4098:Drugs causing Extrapyramidal side effects (3)
Page 8196
chlorpromazine; thioridazine; haloperidol
Page 8197
Q4099:Drugs causing Osteoporosis (2)
Page 8198
corticosteroids; heparin
Page 8199
Q4100:Ethylene glycol is converted to ------- ------ by alcoholdehydrogenase. This product can lead to acidosis and
nephrotoxicity.
Page 8201
Q4101:Alcohol dehyrogenase also converts methanol toformaldehyde and formic acid; which can cause severe -----
and damage to the -------.
Page 8202
acidosis. retina
Page 8203
Q4102:Ethanol competes with ethylene glycol and methanol(if present) for alcohol dehydrogenase. ADH action on EtOH
produces -------.
Page 8205
Q4103:What symptoms does acetaldehyde cause?
Page 8206
nausea; vomiting; headache; hypotension
Page 8207
Q4104:Acetaldehyde itself can be metabolized byacetaldehyde dehydrogenase to ----- -----.
Page 8209
Q4105:Acetaldehyde dehydrogenase is inhibited by whatdrug?
Page 8211
Q4106:Clinical use of echinacea
Page 8213
Q4107:Clinical use of ephedra
Page 8214
as for ephedrine
Page 8215
Q4108:Clinical use of feverfew
Page 8217
Q4109:Clinical use of ginko
Page 8218
intermittent claudication
Page 8219
Q4110:Clinical use of kava
Page 8220
chronic anxiety
Page 8221
Q4111:Clinical use of milk thistle
Page 8222
viral hepatitis
Page 8223
Q4112:Clinical use of saw palmetto
Page 8224
benign prostatic hyperplasia
Page 8225
Q4113:Clinical use of St. John's wort
Page 8226
mild to moderate depression
Page 8227
Q4114:Clinical use of dehyroepiandrosterone
Page 8228
symptomatic improvement in females with SLE or AIDS
Page 8229
Q4115:Clinical use of Melatonin
Page 8230
jet lag; insomnia
Page 8231
Q4116:echinacea toxicity
Page 8232
GI distress; dizziness; and headache
Page 8233
Q4117:ephedra toxicity
Page 8234
CNS and cardiovascular stimulation; arrhythmias; stroke andseizures at high doses.
Page 8235
Q4118:feverfew toxicity
Page 8236
GI distress; mouth ulcers; antiplatelet actions
Page 8237
Q4119:ginko toxicity
Page 8238
GI distress; anxiety; insomnia; headache; and antiplateletactions
Page 8239
Q4120:kava toxicity
Page 8240
GI distress; sedation; ataxia; hepatotoxicity; phototoxicity;dermatotoxicity
Page 8241
Q4121:milk thistle toxicity
Page 8243
Q4122:saw palmetto toxicity
Page 8244
GI distress; decreased libido; hypertension
Page 8245
Q4123:St. John's wort toxicity
Page 8246
GI distress and phototoxicity; serotonin syndrome withSSRIs
Page 8247
Q4124:dehyroepiandrosterone toxicity
Page 8248
Androgenization (premenopausal women); estrogenic effects(postmenopausal); feminization (young men)
Page 8249
Q4125:Melatonin toxicity
Page 8250
Sedation; suppresses midcycle LH; hypoprolactinemia