Physiology & Pathophysiology - 2000

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Q0001:In a ventricular pacemaker cell; what phase of theaction potential is affected by NE?


Phase 4; NE increases the slope of the prepotential; allowingthreshold to be reached sooner; and increases the rate of firing.


Q0002:Anatomical and alveolar dead spaces togetherconstitute what space?


Physiologic dead space is the total dead space of therespiratory system.


Q0003:What three organs are necessary for the production ofvitamin D3(cholecalciferol)?


Skin; liver; and kidneys


Q0004:What is the effect of LH on the production of adrenalandrogens?


LH has no effect on the production of adrenal androgens;ACTH stimulates adrenal androgen production.


Q0005:What four conditions result in secondaryhyperaldosteronism?


1. CHF ;2. Vena caval obstruction or constriction ;3. Hepaticcirrhosis ;4. Renal artery stenosis


Q0006:What are the five hormones produced by Sertoli cells?


1. Inhibin ;2. Estradiol (E2) ;3. Androgen-binding protein ;4.Meiosis inhibiting factor (in fetal tissue) ;5. Antimüullerian

hormone


Q0007:What is the term for the negative resting membranepotential moving toward threshold?


Depolarization (i.e; Na+ influx)


Q0008:Does the left or right vagus nerve innervate the SAnode?


Right vagus innervates the SA node and the left vagusinnervates the AV node


Q0009:How does ventricular repolarization take place; baseto apex or vice versa?


Repolarization is from base to apex and from epicardium toendocardium.


Q0010:What is the term for any region of the respiratorysystem that is incapable of gas exchange?


Anatomical dead space; which ends at the level of the terminalbronchioles.


Q0011:What four factors shift the Hgb-O2 dissociation curveto the right? What is the consequence of this shift?


Increased CO2; H+; temperature; and 2; 3-BPG levels all shiftthe curve to the right; thereby making the O2 easier to remove

(decreased affinity) from the Hgb molecule.


Q0012:What two factors result in the apex of the lung beinghypoperfused?


Decreased pulmonary arterial pressure (low perfusion) andless-distensible vessels (high resistance) result in decreased

blood flow at the apex.


Q0013:What is the ratio of pulmonary to systemic bloodflow?


1:1. Remember; the flow through the pulmonary circuit andthe systemic circuit are equal.


Q0014:To differentiate central from nephrogenic diabetesinsipidus; after an injection of ADH; which will show a

decreased urine flow?


Central. Remember; there is a deficiency in ADH productionin the central form.


Q0015:In what area of the GI tract are water-soluble vitaminsabsorbed?


Duodenum


Q0016:What wave is the cause of the following venous pulsedeflections?;? The rise in right atrial pressure secondary to

blood filling and terminating when the tricuspid valves opens


V wave


Q0017:What wave is the cause of the following venous pulsedeflections?;? The bulging of the tricuspid valve into the right

atrium


C wave


Q0018:What wave is the cause of the following venous pulsedeflections?;? The contraction of the right atrium


A wave


Q0019:What are the four functions of saliva?


1. Provide antibacterial action ;2. Lubricate ;3. Begin CHOdigestion ;4. Begin fat digestion


Q0020:When a person goes from supine to standing; whathappens to the following?;? Dependent venous pressure


Increases;Remember; the carotid sinus reflex attempts tocompensate by increasing both TPR and heart rate;;------------

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Q0021:When a person goes from supine to standing; whathappens to the following?;? Dependent venous blood volume


Increases;Remember; the carotid sinus reflex attempts tocompensate by increasing both TPR and heart rate;;------------

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Q0022:When a person goes from supine to standing; whathappens to the following?;? Cardiac output


Decreases;Remember; the carotid sinus reflex attempts tocompensate by increasing both TPR and heart rate.


Q0023:When a person goes from supine to standing; whathappens to the following?;? BP


Decreases;Remember; the carotid sinus reflex attempts tocompensate by increasing both TPR and heart rate;;------------

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Q0024:When does the hydrostatic pressure in Bowman'scapsule play a role in opposing filtration?


It normally does not play a role in filtration but becomesimportant when there is an obstruction downstream.


Q0025:What happens to intrapleural pressure when thediaphragm is ontracted during inspiration?


Intrapleural pressure decreases (becomes more negative).


Q0026:What is used as an index of cortisol secretion?


Urinary 17-OH steroids


Q0027:If the pH is low with increased CO2 levels anddecreased HCO3- levels; what is the acid-base disturbance?


Combined metabolic and respiratory acidosis


Q0028:What is the term that refers to the number of channelsopen in a cell membrane?


Membrane conductance (think conductance = channels open)


Q0029:What are the five tissues in which glucose uptake isinsulin independent?


1. CNS ;2. Renal tubules ;3. Beta Islet cells of the pancreas ;4.RBCs ;5. GI mucosa


Q0030:Place in order from fastest to slowest the rate ofgastric emptying for CHO; fat; liquids; and proteins.


Liquids; CHO; protein; fat


Q0031:Is most of the coronary artery blood flow duringsystole or diastole?


Diastole. During systole the left ventricle contracts; resultingin intramyocardial vessel compression and therefore very little

blood flow in the coronary circulation.


Q0032:What modified smooth muscle cells of the kidneymonitor BP in the afferent arteriole?


The JG cells


Q0033:What are the three functions of surfactant?


1. Increase compliance ;2. Decrease surface tension ;3.Decrease probability of pulmonary edema formation


Q0034:Name the hormone—glucagon; insulin; orepinephrine;? Glycogenolytic; gluconeogenic; lipolytic;

glycolytic; and stimulated by hypoglycemia


Epinephrine


Q0035:Name the hormone—glucagon; insulin; orepinephrine;? Glycogenolytic; gluconeogenic; lipolytic;

glycolytic; proteolytic; and stimulated by hypoglycemia andAAs


Glucagon


Q0036:Name the hormone—glucagon; insulin; orepinephrine;? Glycogenic; gluconeogenic; lipogenic;

proteogenic; glycolytic; and stimulated by hyperglycemia;AAs; fatty acids; ketosis; ACh; GH; and Beta-agonist


Insulin


Q0037:Is the hydrophobic or hydrophilic end of thephospholipids of the cell membrane facing the aqueous

environment?


Hydrophilic (water-soluble) end faces the aqueousenvironment and the hydrophobic (water-insoluble) end faces

the interior of the cell.


Q0038:What type of muscle is characterized by nomyoglobin; anaerobic glycolysis; high ATPase activity; and

large muscle mass?


White muscle; short term too


Q0039:What percentage of CO2 is carried in the plasma asHCO3- ?


90% as HCO3-; 5% as carbamino compounds; and 5% asdissolved CO2


Q0040:What is the most potent male sex hormone?


Dihydrotestosterone

Q0041:With a decrease in arterial diastolic pressure; whathappens to;? Stroke volume?

Decreases

Q0042:With a decrease in arterial diastolic pressure; whathappens to;? TPR?

Decreases

Q0043:With a decrease in arterial diastolic pressure; whathappens to;? Heart rate?

Decreases

Q0044:What linkage of complex CHOs does pancreaticamylase hydrolyze? What three complexes are formed?

Amylase hydrolyzes alpha-1; 4-glucoside linkages; formingalpha-limit dextrins; maltotriose; and maltose.

Q0045:Does the heart rate determine the diastolic or systolicinterval?

Heart rate determines the diastolic interval; and contractilitydetermines the systolic interval.

Q0046:On a graphical representation of filtration;reabsorption; and excretion; when does glucose first appear in

the urine?

At the beginning of splay is when the renal threshold forglucose occurs and the excess begins to spill over into the

urine.

Q0047:What is the relationship between preload and thepassive tension in a muscle?

They are directly related; the greater the preload; the greaterthe passive tension in the muscle and the greater the

prestretch of a sarcomere.

Q0048:What is the rate-limiting step in the syntheticpathway of NE at the adrenergic nerve terminal?

The conversion of tyrosine to dopamine in the cytoplasm

Q0049:How many days prior to ovulation does LH surgeoccur in the menstrual cycle?

1 day prior to ovulation

Q0050:How are flow through the loop of Henle andconcentration of urine related?

As flow increases; the urine becomes more dilute because ofdecreased time for H2O reabsorption.

Q0051:What is the PO2 of aortic blood in fetal circulation?

60%

Q0052:How do elevated blood glucose levels decrease GHsecretion? (Hint: what inhibitory hypothalamic hormone is

stimulated by IGF-1?)

Somatotrophins are stimulated by IGF-1; and they inhibit GHsecretion. GHRH stimulates GH secretion.

Q0053:What segment of the nephron has the highestconcentration of inulin? Lowest concentration of inulin?

Terminal collecting duct has the highest concentration andBowman's capsule has the lowest concentration of inulin.

Q0054:What type of resistance system; high or low; isformed when resistors are added in a series?

A high-resistance system is formed when resistors are addedin a series.

Q0055:What hormones; secreted in proportion to the size ofthe placenta; are an index of fetal well-being?

hCS and serum estriol; which are produced by the fetal liverand placenta; respectively; are used as estimates of fetal well-

being.

Q0056:What primary acid-base disturbance is caused by anincrease in alveolar ventilation (decreasing CO2 levels)

resulting in the reaction shifting to the left and decreasing bothH+ and HCO3- levels?

Respiratory alkalosis (summary: low CO2; low H+; slightlylow HCO3-)

Q0057:What respiratory center in the caudal pons is thecenter for rhythm promoting prolonged inspirations?

Apneustic center (deep breathing place)

Q0058:What area of the GI tract has the highest activity ofbrush border enzymes?

Jejunum (upper)

Q0059:What is the term to describe the increased rate ofsecretion of adrenal androgens at the onset of puberty?

Adrenarche

Q0060:What period is described when a larger-than-normalstimulus is needed to produce an action potential?

Relative refractory period

Q0061:Does T3 or T4 have a greater affinity for its nuclearreceptor?

T3 has a greater affinity for the nuclear receptor and thereforeis considered the active form.

Q0062:What are the three main functions of surfactant?

1. Lowers surface tension; so it decreases recoil and increasescompliance ;2. Reduces capillary filtration ;3. Promotes

stability in small alveoli by lowering surface tension

Q0063:What is the only important physiological signalregulating the release of PTH?

Low interstitial free Ca2+ concentrations

Q0064:What endocrine abnormality is characterized by thefollowing changes in PTH; Ca2+; and inorganic phosphate

(Pi)? ;? PTH decreased; Ca2+ increased; Pi increased

Secondary hypoparathyroidism (vitamin D toxicity)


(Pi)? ;? PTH increased; Ca2+ decreased; Pi decreased

Secondary hyperparathyroidism (vitamin D deficiency; renaldisease)


(Pi)? ;? PTH decreased; Ca2+ decreased; Pi increased

Primary hypoparathyroidism


(Pi)? ;? PTH increased; Ca2+ increased; Pi decreased

Primary hyperparathyroidism

Q0068:What is the amount in liters and percent body weightfor the following compartments? ;? ECF

14 L; 33% of body weight

Q0069:What is the amount in liters and percent body weightfor the following compartments? ;? Interstitial fluid

9.3 L; 15% of body weight

Q0070:What is the amount in liters and percent body weightfor the following compartments? ;? ICF


Q0071:What is the amount in liters and percent body weightfor the following compartments? ;? Vascular fluid

4.7 L; 5% of body weight

Q0072:What is the amount in liters and percent body weightfor the following compartments? ;? Total body water


Q0073:What hormone is secreted by the placenta late inpregnancy; stimulates mammary growth during pregnancy;

mobilizes energy stores from the mother so that the fetus canuse them; and has an amino acid sequence like GH?

Human chorionic somatomammotropin (hCS) or humanplacental lactogen (hPL)

Q0074:What thyroid abnormality has the following?;? TRHdecreased; TSH decreased; T4 increased

Graves disease (Increased T4 decreases TRH and TSHthrough negative feedback.)

Q0075:What thyroid abnormality has the following?;? TRHincreased; TSH decreased; T4 decreased

Secondary hypothyroidism/pituitary (Low TSH results inlow T4 and increased TRH because of lack of a negative

feedback loop.)

Q0076:What thyroid abnormality has the following?;? TRHdecreased; TSH decreased; T4 decreased

Tertiary hypothyroidism/hypothalamic (Low TRH causes allthe rest to be decreased because of decreased stimulation.)

Q0077:What thyroid abnormality has the following?;? TRHincreased; TSH increased; T4 decreased

Primary hypothyroidism (Low T4 has a decreased negativefeedback loop; resulting in both the hypothalamus and theanterior pituitary gland to increase TRH and TSH release;

respectively.)

Q0078:What thyroid abnormality has the following?;? TRHdecreased; TSH decreased; T4 increased

Secondary hyperthyroidism (Increased TSH results inincreased T4 production and increased negative feedback on to

hypothalamus and decreased release of TRH.)

Q0079:What two stress hormones are under the permissiveaction of cortisol?

Glucagon and epinephrine

Q0080:If the radius of a vessel doubles; what happens toresistance?

The resistance will decrease one-sixteenth of the originalresistance.

Q0081:What prevents the down-regulation of the receptorson the gonadotrophs of the anterior pituitary gland?

The pulsatile release of GnRH

Q0082:True or false? Epinephrine has proteolytic metaboliceffects.

False. It has glycogenolytic and lipolytic actions but notproteolytic.

Q0083:What is the only 17-hydroxysteroid with hormonalactivity?

Cortisol; a 21-carbon steroid; has a -OH group at position 17.

Q0084:Does the oncotic pressure of plasma promotefiltration or reabsorption?

The oncotic pressure of plasma promotes reabsorption and isdirectly proportional to the filtration fraction.

Q0085:Why is the base of the lung hyperventilated when aperson is standing upright?

The alveoli at the base are small and very compliant; so thereis a large change in their size and volume and therefore a high

level of alveolar ventilation.

Q0086:By removing Na+ from the renal tubule and pumpingit back into the ECF compartment; what does aldosterone do

to the body's acid-base stores?

The removal of Na+ results in the renal tubule becomingnegatively charged. The negative luminal charge attracts both

K+ and H+ into the renal tubule and promotes HCO3- toenter the ECF and results in hypokalemic alkalosis.

Q0087:What hormone causes contractions of smooth muscle;regulates interdigestive motility; and prepares the intestine for

the next meal?

Motilin

Q0088:What two vessels in fetal circulation have the highestPO2 levels?

Umbilical vein and ductus venosus (80%)

Q0089:How many days prior to ovulation does estradiol peakin the menstrual cycle?

2 days prior to ovulation

Q0090:What serves as a marker of endogenous insulinsecretion?

C-peptide levels

Q0091:What is the term for the total volume of air moved inand out of the respiratory system per minute?

Total ventilation (minute ventilation or minute volume)

Q0092:What is the renal compensation mechanism foralkalosis?

Increase in urinary excretion of HCO3-; shifting the reactionto the right and increasing H+

Q0093:What is a sign of a Sertoli cell tumor in a man?

Excess estradiol in the blood

Q0094:In the systemic circulation; what blood vessels havethe largest pressure drop? Smallest pressure drop?

Arterioles have the largest drop; whereas the vena cava hasthe smallest pressure drop in systemic circulation.

Q0095:What is the major stimulus for cell division inchondroblasts?

IGF-1

Q0096:What are two causes of diffusion impairment in thelungs?

Decrease in surface area and increase in membrane thickness(Palv O2 > PaO2)

Q0097:What are the four effects of suckling on the mother?

1. Increased synthesis and secretion of oxytocin ;2. Increasedrelease of PIF by the hypothalamus ;3. Inhibition of GnRH

(suppressing FSH/LH) ;4. Milk secretion

Q0098:A migrating myoelectric complex is a propulsivemovement of undigested material of undigested material fromthe stomach to the small intestine to the colon. During a fast;

what is the time interval of its repeats?

It repeats every 90 to 120 minutes and correlates withelevated levels of motilin.

Q0099:With an increase in arterial systolic pressure; whathappens to;? Stroke volume?

Increases

Q0100:With an increase in arterial systolic pressure; whathappens to;? Vessel compliance?

Decreases

Q0101:With an increase in arterial systolic pressure; whathappens to;? Heart rate?

Decreases

Q0102:What enzyme is needed to activate the followingreactions?;? Trypsinogen to trypsin

Enterokinase

Q0103:What enzyme is needed to activate the followingreactions?;? Chymotrypsinogen to chymotrypsin

Trypsin

Q0104:What enzyme is needed to activate the followingreactions?;? Procarboxypeptidase to carboxypeptidase

Trypsin

Q0105:In a ventricular pacemaker cell; what phase of theaction potential is affected by ACh?

Phase 4; ACh hyperpolarizes the cell via increasing potassiumconductance; taking longer to reach threshold and slowing the

rate of firing.

Q0106:What is the most potent stimulus for glucagonsecretion? Inhibition?

Hypoglycemia for secretion and hyperglycemia for inhibition

Q0107:What is the term for the summation of mechanicalstimuli due to the skeletal muscle contractile unit becoming

saturated with calcium?

Tetany

Q0108:What form of renal tubular reabsorption ischaracterized by low back leaks; high affinity of a substance;and easy saturation? It is surmised that the entire filtered loadis reabsorbed until the carriers are saturated; and then the rest

is excreted.

A transport maximum (Tm) system

Q0109:In an adrenergic nerve terminal; where is dopamineconverted to NE? By what enzyme?

Dopamine is converted into NE in the vesicle via the enzymedopamine-Beta-hydroxylase.

Q0110:Is the clearance for a substance greater than or lessthan for inulin if it is freely filtered and secreted? If it is freely

filtered and reabsorbed?

Filtered and secreted: Cx > Cin (i.e; PAH). Filtered andreabsorbed: Cx < Cin (i.e; glucose); where Cx = clearance of a

substance and Cin = clearance of inulin.

Q0111:What is the term for the load on a muscle in the relaxedstate?

Preload. It is the load on a muscle Prior to contraction.

Q0112:The surge of what hormone induces ovulation?

LH

Q0113:What are the two best indices of left ventricularpreload?

LVEDV and LVEDP (left ventricular end-diastolic volume andend-diastolic pressure; respectively)

Q0114:What stage of male development is characterized bythe following LH and testosterone levels?;? LH pulsatileamplitude and levels increase; with increased testosterone

production.

Puberty

Q0115:What stage of male development is characterized bythe following LH and testosterone levels?;? Both LH and

testosterone levels drop and remain low.

Childhood

Q0116:What stage of male development is characterized bythe following LH and testosterone levels?;? LH secretion

drives testosterone production; with both levels parallelingeach other.

Adulthood

Q0117:What stage of male development is characterized bythe following LH and testosterone levels?;? Decreased

testosterone production is accompanied by an increase in LHproduction.

Aged adult

Q0118:What primary acid-base disturbance is caused by aloss in fixed acid forcing the reaction to shift to the right;

thereby increasing HCO3- levels?

Metabolic alkalosis (summary: high pH; low H+ and highHCO3-)

Q0119:When referring to a series circuit; what happens toresistance when a resistor is added?

Resistance increases as resistors are added to the circuit.

Q0120:Why is there an increase in prolactin if thehypothalamic-pituitary axis was severed?

Because the chronic inhibition of dopamine (PIF) on therelease of prolactin from the anterior pituitary gland isremoved; thereby increasing the secretion of prolactin.

Q0121:Why is the clearance of creatinine always slightlygreater than the clearance of inulin and GFR?

Because creatinine is filtered and a small amount is secreted

Q0122:What acid form of H+ in the urine cannot be titrated?

NH4+(ammonium)

Q0123:Regarding the venous system; what happens to bloodvolume if there is a small change in pressure?

Because the venous system is more compliant than the arterialvessels; small changes in pressure result in large changes in

blood volume.

Q0124:In what stage of sleep is GH secreted?

Stages 3 and 4 (NREM)

Q0125:Where does the conversion of CO2 into HCO3- takeplace?

In the RBC; remember; you need carbonic anhydrase for theconversion; and plasma does not have this enzyme.

Q0126:From the fourth month of fetal life to term; whatsecretes the progesterone and estrogen to maintains the

uterus?

The placenta

Q0127:What two factors are required for effective exocytosis?

Calcium and ATP are required for packaged macromoleculesto be extruded from the cell.

Q0128:What is the best measure of total body vitamin D ifyou suspect a deficiency?

Serum 25-hydroxy-vitamin D (25-OH-D)

Q0129:What hormone is required for 1; 25-dihydroxy-vitaminD (1; 25-diOH-D) to have bone resorbing effects?

PTH

Q0130:Is bone deposition or resorption due to increasedinterstitial Ca2+concentrations?

Bone deposition increases with increased Ca2+ or PO 4-concentrations; whereas resorption (breakdown) is increased

when there are low levels of Ca2+ or PO4-.

Q0131:The opening of what valve indicates the termination ofisovolumetric relaxation phase of the cardiac cycle?

Opening of the mitral valve indicates the termination of theisovolumetric relaxation phase and the beginning of the

ventricular filling phase.

Q0132:Why is there a decrease in the production inepinephrine when the anterior pituitary gland is removed?

The enzyme phenyl ethanolamine N-methyltransferase(PNMT); used in the conversion of epinephrine; is regulatedby cortisol. Removing the anterior pituitary gland decreases

ACTH and therefore cortisol.

Q0133:Name the period described by the following statement:no matter how strong a stimulus is; no further action

potentials can be stimulated.

Absolute refractory period is due to voltage inactivation ofsodium channels.

Q0134:How many carbons do estrogens have?

Estrogens are 18-carbon steroids. (Removal of one carbonfrom an androgen produces an estrogen.)

Q0135:True or false? The alveolar PO2 and PCO2 levelsmatch the pulmonary end capillary blood levels.

True. Because of intrapulmonary shunting; there is a slightdecrease in PO2 and increase in PCO2 between the

pulmonary end capillary blood and the systemic arterialblood.

Q0136:In high altitudes; what is the main drive forventilation?

The main drive shifts from central chemoreceptors (CSF H+)to peripheral chemoreceptors monitoring low PO2 levels.

Q0137:Describe what type of fluid is either gained or lostwith the following changes in body hydration for the ECFvolume; ICF volume; and body osmolarity; respectively;?

ECF; decrease; ICF; no change; body; no change

Loss of isotonic fluid (diarrhea; vomiting; hemorrhage)


ECF; increase; ICF; increase; body; decrease

Gain of hypotonic fluid (water intoxication or hypotonicsaline)


ECF; decrease; ICF; decrease; body: increase

Loss of hypotonic fluid (alcohol; diabetes insipidus;dehydration)


ECF: increase; ICF: no change; body: no change

Gain of isotonic fluid (isotonic saline)


ECF; increase; ICF; decrease; body; increase

Gain of hypertonic fluid (mannitol or hypertonic saline)

Q0142:What hormone excess produces adrenal hyperplasia?

ACTH

Q0143:Is there more circulating T3 or T4 in plasma?

T4; because of the greater affinity for the binding protein; T4has a significantly (nearly fifty times) longer half-life than T3.

Q0144:Why is the cell's resting membrane potential negative?

The resting membrane potential of the cell is -90 mV becauseof the intracellular proteins.

Q0145:True or false? Thyroid size is a measure of itsfunction.

False. Thyroid size is a measure of TSH levels (which aregoitrogenic).

Q0146:If the radius of a vessel is decreased by half; whathappens to the resistance?

The resistance increases 16-fold.

Q0147:What neurotransmitter is essential for maintaining anormal BP when an individual is standing?

NE; via its vasoconstrictive action on blood vessels

Q0148:What form of diabetes insipidus is due to aninsufficient amount of ADH for the renal collecting ducts?

Central/neurogenic diabetes insipidus; in the nephrogenic formthere is sufficient ADH available; but the renal collecting

ducts are impermeable to its actions.

Q0149:Name the three methods of vasodilation via thesympathetic nervous system.

1. Decrease alpha-1 activity ;2. Increase Beta-2 activity ;3.Increase ACh levels

Q0150:What hormone is characterized by the following renaleffects?;? Calcium reabsorption; phosphate excretion

PTH

Q0151:What hormone is characterized by the following renaleffects?;? Calcium excretion; phosphate excretion

Calcitriol

Q0152:What hormone is characterized by the following renaleffects?;? Calcium reabsorption; phosphate reabsorption

Vitamin D3

Q0153:True or false? Progesterone has thermogenic activities.

True. Elevated plasma levels of progesterone can raise thebody temperature 0.5° to 1.0°F.

Q0154:How long is the transit time through the smallintestine?

2 to 4 hours

Q0155:Where is the last conducting zone of the lungs?

Terminal bronchioles. (No gas exchange occurs here.)

Q0156:True or false? Cortisol inhibits glucose uptake inskeletal muscle.

True; cortisol inhibits glucose uptake in most tissue; making itavailable for neural tissue use.

Q0157:What percentage of cardiac output flows through thepulmonary circuit?

100%; the percentage of blood flow through the pulmonaryand systemic circulations are equal.

Q0158:Name the Hgb-O2 binding site based on the followinginformation;? Least affinity for O2; requires the highest PO 2

levels for attachment (approx. 100 mm Hg)

Site 4

Q0159:Name the Hgb-O2 binding site based on the followinginformation;? Greatest affinity of the three remaining sites for

attachment; requires PO2 levels of 26 mm Hg to remainattached

Site 2

Q0160:Name the Hgb-O2 binding site based on the followinginformation;? Remains attached under most physiologic

conditions

Site 1

Q0161:Name the Hgb-O2 binding site based on the followinginformation;? Requires a PO2 level of 40 mm Hg to remain

attached

Site 3

Q0162:Which three factors cause the release of epinephrinefrom the adrenal medulla?

1. Exercise ;2. Emergencies (stress) ;3. Exposure to cold ;;(Thethree Es)

Q0163:How many ATPs are hydrolyzed every time a skeletalmuscle cross-bridge completes a single cycle?

One; and it provides the energy for mechanical contraction.

Q0164:Why would a puncture to a vein above the heart havethe potential to introduce air into the vascular system?

Venous pressure above the heart is subatmospheric; so apuncture there has the potential to introduce air into the

system.

Q0165:What type of saliva is produced underparasympathetic stimulation?

High volume; watery solution; sympathetic stimulationresults in thick; mucoid saliva.

Q0166:In what area of the GI tract does iron get absorbed?

Duodenum

Q0167:Why is the apex of the lung hypoventilated when aperson is standing upright?

The alveoli at the apex are almost completely inflated prior toinflation; and although they are large; they receive low levels

of alveolar ventilation.

Q0168:What pancreatic islet cell secretes glucagons?

alpha-Cells; glucagon has stimulatory effects on -cells andinhibitory effects on -cells.

Q0169:What are the four characteristics of all protein-mediated transportation?

1. Competition for carrier with similar chemical substances ;2.Chemical specificity needed for transportation ;3. Zero-order

saturation kinetics (Transportation is maximal when alltransporters are saturated.) ;4. Rate of transportation faster

than if by simple diffusion

Q0170:What is secretin's pancreatic action?

Secretin stimulates the pancreas to secrete a HCO3--richsolution to neutralize the acidity of the chyme entering the

duodenum.

Q0171:Why is there an increase in FF if the GFR is decreasedunder sympathetic stimulation?

Because RPF is markedly decreased; while GFR is onlyminimally diminished; this results in an increase in FF

(remember FF = GFR/RPF).

Q0172:What triggers phase 3 of the action potential in aventricular pacemaker cell?

Rapid efflux of potassium

Q0173:What is the primary target for the action of glucagon?

Liver (hepatocytes)

Q0174:What is the renal compensation mechanism foracidosis?

Production of HCO3-; shifting the reaction to the left andthereby decreasing H+

Q0175:What enzyme found in a cholinergic synapse breaksdown ACh? What are the byproducts?

Acetylcholinesterase breaks ACh into acetate and choline(which gets resorbed by the presynaptic nerve terminal).

Q0176:What hormone; produced by Sertoli cells; if absentwould result in the formation of internal female structures?

MIF

Q0177:What happens to the lung if the intrapleural pressureexceeds lung recoil?

The lung will expand; also the opposite is true.

Q0178:What two factors determine the clearance of asubstance?

Plasma concentration and excretion rate

Q0179:What type of muscle contraction occurs when themuscle shortens and lifts the load placed on it?

Isotonic contraction

Q0180:What type of potential is characterized as being an all-or-none response; propagated and not summated?

Action potential

Q0181:What primary acid-base disturbance is caused by again in fixed acid forcing the reaction to shift to the left;

decreasing HCO3- and slightly increasing CO2?

Metabolic acidosis (summary: low pH; high H+; and lowHCO3-)

Q0182:What two pituitary hormones are produced byacidophils?

GH and prolactin are produced by acidophils; all others areby basophils.

Q0183:What organ of the body has the smallest AV oxygendifference?

The renal circulation has the smallest AV O2 (high venousPO2) difference in the body because of the overperfusion of

the kidneys resulting from filtration.

Q0184:What is the titratable acid form of H+ in the urine?

H2PO4- (dihydrogen phosphate)

Q0185:What hypothalamic hormone is synthesized in thepreoptic nucleus?

GnRH

Q0186:What five factors promote turbulent flow?

1. Increased tube radius ;2. Increased velocity ;3. Decreasedviscosity ;4. Increased number of branches ;5. Narrowing of

an orifice

Q0187:What is the major hormone produced in the followingareas of the adrenal cortex?;? Zona glomerulosa

Aldosterone;Remember; from the outer cortex to the innerlayer; Salt; Sugar; Sex. The adrenal cortex gets sweeter as you

go deeper.

Q0188:What is the major hormone produced in the followingareas of the adrenal cortex?;? Zona fasciculata

Cortisol;Remember; from the outer cortex to the inner layer;Salt; Sugar; Sex. The adrenal cortex gets sweeter as you go

deeper.

Q0189:What is the major hormone produced in the followingareas of the adrenal cortex?;? Zona reticularis

DHEA (androgens);Remember; from the outer cortex to theinner layer; Salt; Sugar; Sex. The adrenal cortex gets sweeter as

you go deeper.

Q0190:Where is most of the body's Ca2+ stored?

In bone; nearly 99% of Ca2+ is stored in the bone ashydroxyapatite.

Q0191:What is the relationship between ventilation andPCO2 levels?

They are inversely related. If ventilation increases; there willbe a decrease in PCO2 levels and vice versa.

Q0192:Is T3 or T4 responsible for the negative feedback loopon to the hypothalamus and anterior pituitary gland?

T4; as long as T4 levels remain constant; TSH will beminimally effected by T3.

Q0193:What is the signal to open the voltage-gatedtransmembrane potassium channels?

Membrane depolarization is the stimulus to open these slowchannels; and if they are prevented from opening; it will slow

down the repolarization phase.

Q0194:Increased urinary excretion of what substance is usedto detect excess bone demineralization?

Hydroxyproline

Q0195:What is the term to describe how easily a vesselstretches?

Compliance (think of it as distensibility)

Q0196:What is the ratio of T4:T3 secretion from the thyroidgland?

20:1T4T3. There is an increase in the production of T3 wheniodine becomes deficient.

Q0197:Do the PO2 peripheral chemoreceptors of the carotidbody contribute to the normal drive for ventilation?

Under normal resting conditions no; but they are stronglystimulated when PO2 arterial levels decrease to 50 to 60 mm

Hg; resulting in increased ventilatory drive.

Q0198:What determines the overall force generated by theventricular muscle during systole?

The number of cross-bridges cycling during contraction: thegreater the number; the greater the force of contraction.

Q0199:Where does most circulating plasma epinephrineoriginate?

From the adrenal medulla; NE is mainly derived from thepostsynaptic sympathetic neurons.

Q0200:What causes a skeletal muscle contraction toterminate?

When calcium is removed from troponin and pumped backinto the SR; skeletal muscle contraction stops.

Q0201:What happens to intracellular volume when there is anincrease in osmolarity?

ICF volume decreases when there is an increase in osmolarityand vice versa.

Q0202:Which CHO is independently absorbed from the smallintestine?

Fructose; both glucose and galactose are actively absorbed viasecondary active transport.

Q0203:When is the surface tension the greatest in therespiratory cycle?

Surface tension; the force to collapse the lung; is greatest atthe end of inspiration.

Q0204:What adrenal enzyme deficiency results inhypertension; hypernatremia; increased ECF volume; and

decreased adrenal androgen production?

17-alpha-Hydroxylase deficiency

Q0205:In reference to membrane potential (Em) andequilibrium potential (Ex); which way do ions diffuse?

Ions diffuse in the direction to bring the membrane potentialtoward the equilibrium potential.

Q0206:Under normal conditions; what is the main factor thatdetermines GFR?

Hydrostatic pressure of the glomerular capillaries (promotesfiltration)

Q0207:The closure of what valve indicates the beginning ofthe isovolumetric relaxation phase of the cardiac cycle?

Closure of the aortic valve indicates the termination of theejection phase and the beginning of the isovolumetric

relaxation phase of the cardiac cycle.

Q0208:What vessels in the systemic circulation have thegreatest and slowest velocity?

The aorta has the greatest velocity and the capillaries have theslowest velocity.

Q0209:Thin extremities; fat collection on the upper back andabdomen; hypertension; hypokalemic alkalosis; acne;

hirsutism; wide purple striae; osteoporosis; hyperlipidemia;hyperglycemia with insulin resistance; and protein depletion

are all characteristics of what disorder?

Hypercortisolism (Cushing syndrome)

Q0210:What enzyme is essential for the conversion of CO2to HCO3-?

Carbonic anhydrase

Q0211:True or false? The parasympathetic nervous systemhas very little effect on arteriolar dilation or constriction.

True

Q0212:What three lung measurements must be calculatedbecause they cannot be measured by simple spirometry?

TLC; FRC; and RV have to be calculated. (Remember; anyvolume that has RV as a component has be calculated.)

Q0213:What is the venous and arterial stretch receptors'function regarding the secretion of ADH?

They chronically inhibit ADH secretion; when there is adecrease in the blood volume; the stretch receptors send fewer

signals; and ADH is secreted.

Q0214:What cell converts androgens to estrogens?

Granulosa cell

Q0215:What hormone acts on Granulosa cells?

FSH

Q0216:How long is the transit time through the largeintestine?

3 to 4 days

Q0217:Does subatmospheric pressure act to expand orcollapse the lung?

Subatmospheric pressure acts to expand the lung; positivepressure acts to collapse the lung.

Q0218:What hormone constricts afferent and efferentarterioles (efferent more so) in an effort to preserve glomerular

capillary pressure as the renal blood flow decreases?

AT II

Q0219:Why is there a minimal change in BP during exercise ifthere is a large drop in TPR?

Because the large drop in TPR is accompanied by a largeincrease in cardiac output; resulting in a minimal change in BP.

Q0220:What is the effect of insulin on protein storage?

Insulin increases total body stores of protein; fat; and CHOs.When you think insulin; you think storage.

Q0221:What is the term for an inhibitory interneuron?

Renshaw neuron


Calcium influx secondary to slow channel opening

Q0223:What are the following changes seen in the luminalfluid by the time it leaves the PCT of the nephron?;?Percentage of original filtered volume left in the lumen

At the end of the PCT 25% of the original volume is left

Q0224:What are the following changes seen in the luminalfluid by the time it leaves the PCT of the nephron?;?

Percentage of Na+; Cl-; K+ left in the lumen

At the end of the PCT 25% of Na+; Cl-; K+ is left


Osmolarity

300 mOsm/L


Concentration of CHO; AA; ketones; peptides

No CHO; AA; ketones; or peptides are left in the tubularlumen.

Q0227:True or false? Enterokinase is a brush border enzyme.

False. It is an enzyme secreted by the lining of the smallintestine.

Q0228:Where does the synthesis of ACh occur?

In the cytoplasm of the presynaptic nerve terminal; it iscatalyzed by choline acetyltransferase.

Q0229:What pancreatic islet cell secretes somatostatin?

delta-Cells; somatostatin has an inhibitory effect on alpha-and Beta-islet cells.

Q0230:Why is O2 content depressed in anemic patients?

Anemic patients have a depressed O2 content because of thereduced concentration of Hgb in the blood. As for

polycythemic patients; their O2 content is increased becauseof the excess Hgb concentrations.

Q0231:What term describes the volume of plasma from whicha substance is removed over time?

Clearance

Q0232:If capillary hydrostatic pressure is greater than oncoticpressure; is filtration or reabsorption promoted?

Filtration; if hydrostatic pressure is less than oncoticpressure; reabsorption is promoted.

Q0233:What cells of the parathyroid gland are simulated inresponse to hypocalcemia?

The chief cells of the parathyroid gland release PTH inresponse to hypocalcemia.

Q0234:At the base of the lung; what is the baselineintrapleural pressure; and what force does it exert on the

alveoli?

Intrapleural pressure at the base is -2.5 cm H2O (morepositive than the mean); resulting in a force to collapse the

alveoli.

Q0235:What hormone is necessary for normal GH secretion?

Normal thyroid hormones levels in the plasma are necessaryfor proper secretion of GH. Hypothyroid patients have

decreased GH secretions.

Q0236:What is the signal to open the voltage-gatedtransmembrane sodium channels?

Membrane depolarization is the stimulus to open thesechannels; which are closed in resting conditions.

Q0237:What hormones are produced in the median eminenceregion of the hypothalamus and the posterior pituitary gland?

None; they are the storage sites for ADH and oxytocin.

Q0238:What is the most energy-demanding phase of thecardiac cycle?

Isovolumetric contraction

Q0239:What presynaptic receptor does NE use to terminatefurther neurotransmitter release?

alpha2-Receptors

Q0240:Are salivary secretions hypertonic; hypotonic; orisotonic?

Hypotonic; because NaCl is reabsorbed in the salivary ducts

Q0241:What is the effect of T3 on heart rate and cardiacoutput?

T3 increases both heart rate and cardiac output by increasingthe number of Beta-receptors and their sensitivity to

catecholamines.

Q0242:Why will turbulence first appear in the aorta inpatients with anemia?

Because it is the largest vessel and has the highest velocity insystemic circulation

Q0243:What is the origin of the polyuria if a patient isdehydrated and electrolyte depleted?

If the polyuria begins before the collecting ducts; the patientis dehydrated and electrolyte depleted. If the polyuria

originates from the collecting ducts; the patient is dehydratedwith normal electrolytes.

Q0244:What is the physiologically active form of Ca2+?

Free ionized Ca2+

Q0245:What are the two factors that affect alveolar PCO2levels?

Metabolic rate and alveolar ventilation (main factor)

Q0246:Why is spermatogenesis decreased with anabolicsteroid therapy?

Exogenous steroids suppress LH release and result in Leydigcell atrophy. Testosterone; produced by Leydig cells; is

needed for spermatogenesis.

Q0247:What type of membrane is characterized as beingpermeable to water only?

Semipermeable membrane; a selectively permeable membraneallows both water and small solutes to pass through its

membrane.

Q0248:What thyroid enzyme is needed for oxidation of I– toI'?

Peroxidase; which is also needed for iodination and couplinginside the follicular cell

Q0249:What is the most important stimulus for the secretionof insulin?

An increase in serum glucose levels

Q0250:What term is described as the prestretch on theventricular muscle at the end of diastole?

Preload (the load on the muscle in the relaxed state)

Q0251:What peripheral chemoreceptor receives the mostblood per gram of weight in the body?

The carotid body; which monitors arterial blood directly

Q0252:What adrenal enzyme deficiency results inhypertension; hypernatremia; and virilization?

11-Beta-Hydroxylase deficiency results in excess productionof 11-deoxycorticosterone; a weak mineralocorticoid. It

increases BP; Na+; and ECF volume along with production ofadrenal androgens.

Q0253:What is the term for diffusion of water across asemipermeable or selectively permeable membrane?

Osmosis; water will diffuse from higher to lower waterconcentrations.

Q0254:When do hCG concentrations peak in pregnancy?

In the first 3 months

Q0255:How many milliliters of O2 per milliliter of blood?

0.2

Q0256:What type of cell is surrounded by mineralized bone?

Osteocyte

Q0257:What two forces affect movement of ions across amembrane?

Concentration force and electrical force

Q0258:What happens to the resistance of the system when aresistor is added in a series?

Resistance of the system increases. (Remember; whenresistors are connected in a series; the total of the resistance is

the sum of the individual resistances.)

Q0259:What is the greatest component of lung recoil?

Surface tension; in the alveoli; it is a force that acts to collapsethe lung.

Q0260:Where is ADH synthesized?

In the supraoptic nuclei of the hypothalamus; it is stored inthe posterior pituitary gland.

Q0261:How is velocity related to the total cross-sectionalarea of a blood vessel?

Velocity is inversely related to cross-sectional area.

Q0262:True or false? Aldosterone has a sodium-conservingaction in the distal colon.

True. In the distal colon; sweat glands; and salivary ducts;aldosterone has sodium-conserving effects.

Q0263:What form of hormone is described as havingmembrane-bound receptors that are stored in vesicles; using

second messengers; and having its activity determined by freehormone levels.

Water-soluble hormones are considered fast-acting hormones.

Q0264:What forms of fatty acids are absorbed from the smallintestine mucosa by simple diffusion?

Short-chain fatty acids

Q0265:What is the term for the day after the LH surge in thefemale cycle?

Ovulation

Q0266:The opening of what valve indicates the beginning ofthe ejection phase of the cardiac cycle?

Opening of the aortic valve terminates the isovolumetricphase and begins the ejection phase of the cardiac cycle.

Q0267:What is the region of an axon where no myelin isfound?

Nodes of Ranvier

Q0268:What disorder of aldosterone secretion is characterizedby;? Increased total body sodium; ECF volume; plasma

volume; BP; and pH; decreased potassium; renin and AT IIactivity; no edema?

Primary hyperaldosteronism (Conn syndrome)

Q0269:What disorder of aldosterone secretion is characterizedby;? Decreased total body sodium; ECF volume; plasma

volume; BP; and pH; increased potassium; renin; and AT IIactivity; no edema?

Primary hypoaldosteronism (Addison's disease)

Q0270:What four factors affect diffusion rate?

1. Concentration (greater concentration gradient; greaterdiffusion rate) ;2. Surface area (greater surface area; greater

diffusion rate) ;3. Solubility (greater solubility; greaterdiffusion rate) ;4. Membrane thickness (thicker the membrane;

slower the diffusion rate) ;;Molecular weight is clinicallyunimportant

Q0271:How long after ovulation does fertilization occur?

8 to 25 hours

Q0272:What is the name of the force that develops in the wallof the lungs as they expand?

Lung recoil; being a force to collapse the lung; increases as thelung enlarges during inspiration.

Q0273:What day of the menstrual cycle does ovulation takeplace?

Day 14

Q0274:How does sympathetic stimulation to the skin resultin decreased blood flow and decreased blood volume? (Hint:

what vessels are stimulated; and how?)

A decrease in cutaneous blood flow results from constrictionof the arterioles; and decreased cutaneous blood volume

results from constriction of the venous plexus.

Q0275:What two compensatory mechanisms occur to reversehypoxia at high altitudes?

Increase in erythropoietin and increase in 2; 3-BPG; alsocalled 2; 3-diphosphoglycerate (2; 3-P2Gri) (increase in

glycolysis)

Q0276:What female follicular cell is under LH stimulation andproduces androgens from cholesterol?

Theca cell

Q0277:What is the main factor determining FF?

Renal plasma flow (decrease flow; increase FF)

Q0278:Where is the action potential generated on a neuron?

Axon hillock

Q0279:If free water clearance (CH2O) is positive; what typeof urine is formed? And if it is negative?

If positive; hypotonic urine (osmolarity <300 mOsm/L); ifnegative; hypertonic urine (osmolarity > 300 mOsm/L)>>

Q0280:What cell in the heart has the highest rate ofautomaticity?

SA node; it is the reason it is the primary pacemaker of theheart.

Q0281:What is pumped from the lumen of the ascending loopof Henle to decrease the osmolarity?

NaCl is removed from the lumen to dilute the fluid leaving theloop of Henle.

Q0282:True or false? In skeletal muscle relaxation is an activeevent.

True. Sarcoplasmic calcium-dependent ATPase supplies theenergy to terminate contraction; and therefore it is an active

process.

Q0283:What three factors increase simple diffusion?

1. Increased solubility ;2. Increased concentration gradient ;3.Decreased thickness of the membrane

Q0284:What is the pancreatic action of CCK?

CCK stimulates the pancreas to release amylase; lipase; andproteases for digestion.

Q0285:What is the rate-limiting step in a conduction of aNMJ?

The time it takes ACh to diffuse to the postjunctionalmembrane

Q0286:Is excretion greater than or less than filtration for netsecretion to occur?

Excretion is greater than filtration for net secretion to occur.

Q0287:What acid-base disturbance is produced fromvomiting?

Hypokalemic metabolic alkalosis occurs from vomitingbecause of the loss of H+; K+; and Cl-.

Q0288:What phase of the menstrual cycle is dominated byestrogen? Progesterone?

Follicular phase is estrogen-dependent with increased FSHlevels; while the luteal phase is progesterone-dependent.

Q0289:Name the lung measurement based on the followingdescriptions;? The amount of air that enters or leaves the lung

system in a single breath

Tidal volume (VT)

Q0290:Name the lung measurement based on the followingdescriptions;? The maximal volume inspired from FRC

Inspiratory capacity

Q0291:Name the lung measurement based on the followingdescriptions;? Additional volume that can be expired after

normal expiration

Expiratory reserve volume (ERV)

Q0292:Name the lung measurement based on the followingdescriptions;? Maximal volume that can be expired after

maximal inspiration

Vital capacity (VC)

Q0293:Name the lung measurement based on the followingdescriptions;? Volume in the lungs at the end of passive

expiration

Functional residual capacity (FRC)

Q0294:Name the lung measurement based on the followingdescriptions;? Additional air that can be taken in after normal

inspiration

Inspiratory reserve volume (IRV)

Q0295:Name the lung measurement based on the followingdescriptions;? Amount of air in the lungs after maximal

expiration

Residual volume (RV)

Q0296:Name the lung measurement based on the followingdescriptions;? Amount of air in the lungs after maximal

inspiration

Total lung capacity (TLC)

Q0297:What growth factors are chondrogenic; working on theepiphyseal end plates of bone?

Somatomedins (IGF-1)

Q0298:What determines the Vmax of skeletal muscle?

The muscle's ATPase activity

Q0299:True or false? All of the hormones in thehypothalamus and anterior pituitary gland are water soluble.

True

Q0300:What is the effect of T3 on the glucose absorption inthe small intestine?

Thyroid hormones increase serum glucose levels by increasingthe absorption of glucose from the small intestine.

Q0301:Is the bound form or free form of a lipid-solublehormone responsible for the negative feedback activity?

Free form determines hormone activity and is responsible forthe negative feedback loop.

Q0302:What region or regions of the adrenal cortex arestimulated by ACTH?

Zona fasciculata and zona reticularis

Q0303:Are the following parameters associated with anobstructive or restrictive lung disorder: decreased FEV1; FVC;

peak flow; and FEV1/FVC; increased TLC; FRC; and RV?

Obstructive lung disorders. The opposite changes (where yousee decrease exchange it for increase and vice versa) are seen in

a restrictive pattern.

Q0304:What is the respiratory compensation mechanism formetabolic alkalosis?

Hypoventilation; which increases CO2; shifting the reactionto the right and increasing H+

Q0305:During puberty; what is the main drive for theincreased GH secretion?

Increased androgen secretion at puberty drives the increasedGH secretion.

Q0306:What type of potential is characterized as graded;decremental; and exhibiting summation?

Subthreshold potential

Q0307:What three organs are responsible for peripheralconversion of T4 to T3?

Liver; kidneys; and pituitary gland via 5' deiodinase enzyme

Q0308:The closure of what valve indicates the beginning ofisovolumetric contraction?

Mitral valve closure indicates the termination of theventricular filling phase and beginning of isovolumetric

contraction.

Q0309:How many carbons do androgens have?

Androgens are 19-carbon steroids.

Q0310:At the apex of the lung; what is the baselineintrapleural pressure; and what force does it exert on the

alveoli?

Baseline apical intrapleural pressure is -10 cm H2O (morenegative than the mean) resulting in a force to expand the

alveoli.

Q0311:True or false? Renin secretion is increased in 21-beta-hydroxylase deficiency.

True. Increased renin and AT II levels occur as a result of thedecreased production of aldosterone.

Q0312:What are the four ways to increase TPR?

1. Decrease the radius of the vessel ;2. Increase the length ofthe vessel ;3. Increase the viscosity ;4. Decrease the number

of parallel channels

Q0313:What form of estrogen is of placental origin?

Estriol

Q0314:What term is an index of the effort needed to expandthe lungs (i.e; overcomes recoil)?

Compliance; the more compliant a lung is; the easier it is toinflate.

Q0315:At which three sites in the body is T4 converted toT3?

1. Liver ;2. Kidney ;3. Pituitary gland (via 5'-deiodinaseenzyme)

Q0316:Using Laplace's relationship regarding wall tension;why is the wall tension in an aneurysm greater than in the

surrounding normal blood vessel's wall?

The wall tension is greater because the aneurysm has a greaterradius than the surrounding vessel.

Q0317:What percentage of nephrons is cortical?

Seven-eighths of nephrons are cortical; with the remainderjuxtamedullary.

Q0318:To what is the diffusion rate indirectly proportional?

Diffusion rate is indirectly proportional to membranethickness and is directly proportional to membranes surface

area.

Q0319:ADH is secreted in response to what two stimuli?

ADH is secreted in response to increased plasma osmolarityand decreased blood volume.

Q0320:What vessels have the largest total cross-sectional areain systemic circulation?

Capillaries

Q0321:How many days before the first day of menstrualbleeding is ovulation?

14 days in most women (Remember; the luteal phase isalways constant.)

Q0322:What is the major muscle used in the relaxed state ofexpiration?

Under resting conditions expiration is considered a passiveprocess; therefore; no muscles are used. In the active state the

abdominal muscles can be considered the major muscle ofexpiration.

Q0323:What subunit of hCG is used to detect whether apatient is pregnant?

The beta-subunit; remember; the alpha-subunit is nonspecific.

Q0324:What happens to capillary oncotic pressure withdehydration?

Oncotic pressure increases because of the removal of water.

Q0325:What cells of the kidney are extravascularchemoreceptors for decreased Na+; Cl-; and NaCl?

Macula densa

Q0326:What is the effect of insulin on intracellular K+ stores?

Insulin increases intracellular K+ stores while decreasingserum K+ levels.


Decreasing potassium conductance; which results in increasedexcitability

Q0328:What is it called when levels of sex steroids increase;LH increases; and FSH increases?

GnRH pulsatile infusion

Q0329:What parasympathetic neurotransmitter of the GItract stimulates the release of gastrin?

Gastrin-releasing peptide (GRP) stimulates G cells to releaseGastrin. (All G's)

Q0330:What reflex increases TPR in an attempt to maintainBP during a hemorrhage?

The carotid sinus reflex

Q0331:What is the name of the regulatory protein that coversthe attachment site on actin in resting skeletal muscle?

Tropomyosin

Q0332:Which way does the Hgb-O2 dissociation curve shiftin patients with CO poisoning?

The pathologic problem with CO poisoning is that CO has240 times as much affinity for Hgb molecule as does O2;

reducing the carrying capacity and shifting the curve to theleft; making it difficult to remove the CO molecule from Hgb.

Q0333:What is the main factor determining GFR?

Glomerular capillary pressure (increased glomerular capillarypressure; increased GFR and vice versa)

Q0334:What is the effect of hypoventilation on cerebral bloodflow?

Hypoventilation results in an increase in PCO2 levels andtherefore an increase in blood flow.

Q0335:What cells of the thyroid gland are stimulated inresponse to hypercalcemia?

The parafollicular cells of the thyroid (C cells) releasecalcitonin in response to hypercalcemia.

Q0336:What is the term for the amount of blood in theventricle after maximal contraction?

Residual volume

Q0337:What does failure of PaO2 to increase withsupplemental O2 indicate?

Pulmonary shunt (i.e; pulmonary embolism)

Q0338:What two substances stimulate Sertoli cells?

FSH and testosterone

Q0339:The clearance of what substance is the gold standardof renal plasma flow?

Para-aminohippurate (PAH)

Q0340:What bile pigment is formed by the metabolism ofbilirubin by intestinal bacteria; giving stool its brown color?

Stercobilin

Q0341:Is ACh associated with bronchoconstriction orbronchodilation?

Bronchoconstriction is associated with parasympatheticstimulation (ACh); and catecholamine stimulation is

associated with bronchodilation (why epinephrine is used inemergency treatment of bronchial asthma.)

Q0342:What are the growth factors released from the livercalled?

Somatomedins

Q0343:Regarding skeletal muscle mechanics; what is therelationship between velocity and afterload?

An increase in the afterload decreases velocity; they areinversely related. (V equals 1 divided by afterload.)

Q0344:What happens to extracellular volume with a net gainin body fluid?

The ECF compartment always enlarges when there is a netgain in total body water and decreases when there is a loss oftotal body water. Hydration status is named in terms of the

ECF compartment.

Q0345:What are the six substances that promote the secretionof insulin?

1. Glucose ;2. Amino acid (arginine) ;3. Gastrin inhibitorypeptide (GIP) ;4. Glucagon ;5. beta-Agonists ;6. ACh

Q0346:Does O2 or CO2 have a higher driving force across thealveolar membrane?

O2 has a higher driving force but is only one-twenty-fourth assoluble as CO2. CO 2 has a very small partial pressure

difference across the alveolar membrane (47-40 = 7 mmHg);but it is extremely soluble and therefore diffuses readily

across the membrane.

Q0347:What is used as an index for both adrenal and testicularandrogens?

Urinary 17-ketosteroids

Q0348:How are resistance and length related regarding flow?

Resistance and vessel length are proportionally related. Thegreater the length of the vessel; the greater the resistance is on

the vessel.

Q0349:Is filtration greater than or less than excretion for netreabsorption to occur?

Filtration is greater than excretion for net reabsorption tooccur.

Q0350:What hormone; stimulated by epinephrine; results inan increase in lipolysis?

Hormone-sensitive lipase; which breaks down triglycerideinto glycerol and free fatty acid

Q0351:True or false? Miniature end-plate potentials(MEPPs) generate action potentials.

False

Q0352:Is GH considered a gluconeogenic hormone?

Yes; it decreases fat and muscle uptake of glucose; therebyincreasing blood glucose levels.

Q0353:True or false? Somatic motor neurons innervate thestriated muscle of the bulbospongiosus and ischiocavernous

muscles and result in ejaculation of semen.

True

Q0354:What happens to intraventricular pressure and volumeduring isovolumetric contraction?

As the name indicates; there is no change in volume but thereis an increase in pressure.

Q0355:Do high levels of estrogen and progesterone block milksynthesis?

Yes; they stimulate the growth of mammary tissue but blockmilk synthesis. At parturition; the decrease in estrogen lifts

the block on milk production.

Q0356:What two factors lead to the development of thebends (caisson disease)?

Breathing high-pressure nitrogen over a long time and suddendecompression result in the bends.

Q0357:In what type of circuit is the total resistance alwaysless than that of the individual resistors?

Parallel circuit

Q0358:What is the term for days 15 to 28 in the female cycle?

Luteal phase

Q0359:What happens to total and alveolar ventilation with;?Increased rate of breathing?

With an increased rate of breathing the total ventilation isgreater than the alveolar ventilation. Rapid; shallow breathingincreases dead space ventilation with little change in alveolar

ventilation. (This is hypoventilation).

Q0360:What happens to total and alveolar ventilation with;?Increased depth of breathing?

With an increased depth of breathing both the total andalveolar ventilation increase;This concept is always tested on

the boards; so remember it.

Q0361:What pathophysiologic disorder is characterized bythe following changes in cortisol and ACTH?;? Cortisol

decreased; ACTH increased

Primary hypocortisolism (Addison's disease)


increased; ACTH increased

Secondary hypercortisolism (pituitary)


increased; ACTH decreased

Primary hypercortisolism


decreased; ACTH decreased

Secondary hypocortisolism (pituitary)

Q0365:What happens to flow and pressure in capillaries witharteriolar dilation? Arteriolar constriction?

Capillary flow and pressure increase with arteriolar dilationand decrease with arteriolar constriction.

Q0366:What has occurred to the renal arterioles based on thefollowing changes in the GFR; RPF; FF; and glomerular

capillary pressure?;? GFR increased ; RPF increased ; FFnormal; capillary pressure increased

Dilation of afferent arteriole


capillary pressure?;? GFR increased ; RPF decreased ; FFincreased ; capillary pressure increased

Constriction of efferent arteriole


capillary pressure?;? GFR decreased ; RPF increased ; FFdecreased ; capillary pressure decreased

Dilation of efferent arteriole


capillary pressure?;? GFR decreased ; RPF decreased ; FFnormal; capillary pressure decreased

Constriction of afferent arteriole

Q0370:Which direction is air flowing when the intra-alveolarpressure is zero?

When the intra-alveolar pressure equals zero; there is noairflow.

Q0371:What phase of the female cycle occurs during days 1to 15?

Follicular phase

Q0372:What determines the effective osmolarity of the ICFand the ECF compartments?

The concentration of plasma proteins determines effectiveosmolarity because capillary membranes are freely permeable

to all substances except proteins.

Q0373:What region of the brain houses the centralchemoreceptors responsible for control of ventilation?

The surface of the medulla

Q0374:What is the site of action of cholera toxin?

Cholera toxin irreversibly activates the cAMP-dependentchloride pumps of the small and large intestine; producing a

large volume of chloride-rich diarrhea.

Q0375:Name the phase of the ventricular muscle actionpotential based on the following information;? Slow channels

open; allowing calcium influx; voltage-gated potassiumchannels closed; potassium efflux through ungated channels;

plateau stage

Phase 2

Q0376:Name the phase of the ventricular muscle actionpotential based on the following information;? Slight

repolarization secondary to potassium and closure of thesodium channels

Phase 1

Q0377:Name the phase of the ventricular muscle actionpotential based on the following information;? Fast channels

open; then quickly close; and sodium influx results indepolarization

Phase 0

Q0378:Name the phase of the ventricular muscle actionpotential based on the following information;? Slow channelsclose; voltage-gated potassium channels reopen with a large

influx of potassium; and the cell quickly repolarizes

Phase 3

Q0379:Where in the kidney are the long loops of Henle andthe terminal regions of the collecting ducts?

In the medulla; all the other structures are cortical.

Q0380:What is absorbed in the gallbladder to concentrate bile?

Water

Q0381:What type of hormone is described as havingintracellular receptors; being synthesized as needed; mostlybound to proteins; and having its activity determined by free

hormone levels?

Lipid-soluble hormones are considered slow-acting hormones.

Q0382:What are the three stimuli that result in thereninangiotensin-aldosterone secretion?

1. Low pressure in the afferent renal arteriole ;2. Low sodiumsensed by the macula densa ;3. Increased beta-1-sympathetic

stimulation of the JG cells

Q0383:Is there a shift in p50 values with anemia?Polycythemia?

The p50 value does not change in either anemia orpolycythemia; the main change is the carrying capacity of the

blood.

Q0384:What hormone level peaks 1 day before the surge ofLH and FSH in the female cycle?

Estradiol

Q0385:True or false? Active protein transport requires aconcentration gradient.

True; it requires both a concentration gradient and ATP towork.

Q0386:Up to how many hours post ejaculation do spermretain their ability to fertilize the ovum?

Up to 72 hours; the ovum losses its ability to be fertilized 8to 25 hours after release.

Q0387:What type of membrane channel opens in response todepolarization?

Voltage-gated channel

Q0388:What are the five effects of insulin on fat metabolism?

1. Increased glucose uptake by fat cells ;2. Increasedtriglyceride uptake by fat cells ;3. Increased conversion of

CHOs into fat ;4. Decreased lipolysis in fat tissue ;5.Decreased ketone body formation

Q0389:True or false? In a skeletal muscle fiber; the interior ofthe T-tubule is extracellular.

True. They are evaginations of the surface membranes andtherefore extracellular.

Q0390:Under resting conditions; what is the main determinantof cerebral blood flow?

Arterial PCO2 levels are proportional to cerebral blood flow.

Q0391:On the venous pressure curve; what do the followingwaves represent?;? A wave?

Atrial contraction;Atrial; Contraction; Venous

Q0392:On the venous pressure curve; what do the followingwaves represent?;? C wave?

Ventricular contraction;Atrial; Contraction; Venous

Q0393:On the venous pressure curve; what do the followingwaves represent?;? V wave?

Atrial filling (venous filling);Atrial; Contraction; Venous

Q0394:What cell type in the bone is responsible for bonedeposition?

Osteoblast (Remember; blasts make; clasts take)

Q0395:True or false? The blood stored in the systemic veinsand the pulmonary circuit are considered part of the cardiac

output.

False. Cardiac output refers to circulating blood volume. Theblood in the systemic veins and the pulmonary circuits arestorage reserves and therefore are not considered in cardiac

output.

Q0396:What hormone disorder is characterized by thefollowing abnormalities in sex steroidsdecreased ;

LHdecreased ; and FSHdecreased ?;? Sex steroids ; LH ; FSH

Pituitary hypogonadism

Q0397:What hormone disorder is characterized by thefollowing abnormalities in sex steroids; LH; and FSH?;? Sex

steroids increased ; LH decreased ; FSH decreased ?

GnRH constant infusion

Q0398:What hormone disorder is characterized by thefollowing abnormalities in sex steroidsdecreased ; LHincreased

; and FSHincreased ?;? Sex steroids ; LH ; FSH ?

Primary hypogonadism (postmenopausal women)

Q0399:What are the three characteristics of autoregulation?

1. Flow independent of BP ;2. Flow proportional to localmetabolism ;3. Flow independent of nervous reflexes

Q0400:What is the fastest-conducting fiber of the heart?Slowest conduction fiber in the heart?

Purkinje cell is the fastest; and the AV node is the slowest.

Q0401:What equals the total tension on a muscle minus thepreload?

Afterload

Q0402:What follicular cell possesses FSH receptors andconverts androgens into estradiol?

Granulosa cells

Q0403:What are the primary neurotransmitters at thefollowing sites?;? Postganglionic sympathetic neurons

NE

Q0404:What are the primary neurotransmitters at thefollowing sites?;? Chromaffin cells of the adrenal medulla

Epinephrine

Q0405:What are the primary neurotransmitters at thefollowing sites?;? Brainstem cells

Serotonin

Q0406:What are the primary neurotransmitters at thefollowing sites?;? The hypothalamus

Histamine

Q0407:What are the primary neurotransmitters at thefollowing sites?;? All motor neurons; postganglionic

parasympathetic neurons

ACh

Q0408:What are the primary neurotransmitters at thefollowing sites?;? Autonomic preganglionic neurons

ACh

Q0409:What region of the nephron has the highestosmolarity?

Tip of the loop of Henle (1200 mOsm/L)

Q0410:What pH (acidotic or alkalotic) is needed forpepsinogen to pepsin conversion?

Acid is needed for the activation of pepsin and thereforeneeded for protein digestion.

Q0411:What is the term for the amount of blood expelledfrom the ventricle per beat?

Stroke volume

Q0412:True or false? Oxytocin initiates rhythmiccontractions associated with labor.

False. It does increase uterine synthesis of prostaglandins;which increase uterine contractions.

Q0413:Why does carbon monoxide diffusion in the lung(DLCO) decrease in emphysema and fibrosis but increase

during exercise?

DLCO; an index of lung surface area and membrane thickness;is decreased in fibrosis because of increased membrane

thickness and decreased in emphysema because of increasedsurface area without increase in capillary recruitment; in

exercise there is an increase in surface area due to capillaryrecruitment.

Q0414:What enzyme converts androgens to estrogens?

Aromatase

Q0415:The clearance of what substance is the gold standardof GFR?

Inulin

Q0416:How does myelination affect conduction velocity ofan action potential?

The greater the myelination; the greater the conductionvelocity.

Q0417:What are the three end products of amylase digestion?

1. Maltose ;2. Maltotetrose ;3. alpha-Limit dextrans (alpha-1;6 binding)

Q0418:Where is most of the airway resistance in therespiratory system?

In the first and second bronchi

Q0419:What is the respiratory compensation mechanism formetabolic acidosis?

Hyperventilation; which decreases CO2; shifting the reactionto the left and decreasing H+

Q0420:How are resistance and viscosity related regardingflow?

Viscosity and resistance are proportionally related. Thegreater the viscosity; the greater the resistance is on the

vessel.

Q0421:T3 increases bone ossification through synergisticeffect with what hormone?

GH

Q0422:Name the ventricular muscle membrane channel;?Closed at rest; depolarization causes channels to open slowly

Voltage-gated calcium channel

Q0423:Name the ventricular muscle membrane channel;?Always open

Ungated potassium channel

Q0424:Name the ventricular muscle membrane channel;?Closed at rest; depolarization causes channels to open

quickly; will not respond to a second stimulus until cell isrepolarized.

Voltage-gated sodium channel

Q0425:Name the ventricular muscle membrane channel;?Open at rest; depolarization is stimulus to close; begin toreopen during the plateau phase and during repolarization

Voltage-gated potassium channels

Q0426:What are the three glycogenic organs?

Liver; kidney; and GI epithelium

Q0427:Is CO2 a perfusion-or diffusion-limited O2 gas?

Since CO2 is 24 times as soluble as O2; the rate at which CO2is brought to the membrane determines its rate of exchange;

making it perfusion-limited a gas. For O2 the more time it is incontact with the membrane; the more likely it will diffuse;

making it diffusion-limited.

Q0428:What is the term for the potential difference across acell membrane?

Transmembrane potential (an absolute number)

Q0429:What adrenal enzyme deficiency can be summed up asa mineralocorticoid deficiency; glucocorticoid deficiency; and

an excess of adrenal androgens?

21-beta-Hydroxylase deficiency leads to hypotension;hyponatremia; and virilization.

Q0430:When the ECF osmolarity increases; what happens tocell size?

Increase in ECF osmolarity means a decrease in ICFosmolarity; so cells shrink.

Q0431:When does cortisol secretion peak?

In early-morning sleep; usually between the sixth and eighthhours

Q0432:What is the term for ventilation of unperfused alveoli?

Alveolar dead space

Q0433:What is the bioactive form of thyroid hormone?

T3

Q0434:What acid-base disturbance occurs in colonic diarrhea

Hypokalemic metabolic acidosis occurs in colonic diarrheabecause of the net secretion of HCO3- and potassium into the

colonic lumen.

Q0435:What two AAs act as excitatory transmitters in theCNS; generating EPSPs?

Glutamine and aspartate

Q0436:What are the three mechanisms of action for atrialnatriuretic peptide's diuretic and natriuretic affects?

1. Dilation of the afferent arteriole ;2. Constriction of theefferent arteriole ;3. Inhibition of reabsorption of sodium and

water in the collecting ducts

Q0437:In a parallel circuit; what happens to resistance when aresistor is added in parallel

Resistance decreases as resistors are added in parallel.

Q0438:What component of the ANS is responsible formovement of semen from the epididymis to the ejaculatory

ducts?

Sympathetic nervous system

Q0439:What happens to O2 affinity with a decrease in p50?

O2 affinity increases with a decrease in the p50; making O2more difficult to remove from the Hgb molecule.

Q0440:If the ratio of a substance's filtrate and plasmaconcentrations are equal; what is that substance's affect on the

kidney?

If the ratio of the filtrate to plasma concentration of asubstance is equal; the substance is freely filtered by the

kidney.

Q0441:What does a loss of afferent activity from the carotidsinus onto the medulla signal?

A loss of afferent activity indicates a decrease in BP; and anincrease in afferent activity indicates an increase in BP.

Q0442:What are the five F's associated with gallstones?

1. Fat ;2. Forty ;3. Female ;4. Familial ;5. Fertile

Q0443:True or false? Menstruation is an active process dueto increased gonadal sex hormones?

False. It is a passive process due to decreased sex hormones.

Q0444:What happens to the intrapleural pressure when thediaphragm relaxes?

Relaxation of the diaphragm increases the intrapleuralpressure (becomes more positive).

Q0445:What component of the renin-angiotensin-aldosteroneaxis increases sodium reabsorption in the proximal convoluted

tubules and increases thirst drive?

AT II

Q0446:What large-diameter vessel has the smallest cross-sectional area in systemic circulation?

The aorta

Q0447:Excess bone demineralization and remodeling can bedetected by checking urine levels of what substance?

Hydroxyproline (breakdown product of collagen)

Q0448:What happens to the following during skeletal musclecontraction?;? A band

No change in length

Q0449:What happens to the following during skeletal musclecontraction?;? I band

Shortens

Q0450:What happens to the following during skeletal musclecontraction?;? H zone

Shortens

Q0451:What happens to the following during skeletal musclecontraction?;? Sarcomere

Shortens

Q0452:What happens to the following during skeletal musclecontraction?;? Actin and myosin lengths

No change in length

Q0453:What are the three effects of insulin on proteinmetabolism?

1. Increased amino acid uptake by muscles ;2. Decreasedprotein breakdown ;3. Increased protein synthesis

Q0454:What is the main mechanism for exchange of nutrientsand gases across a capillary membrane?

Simple diffusion; it does not use protein-mediated transport

Q0455:What event signifies the first day of the menstrualcycle?

Onset of bleeding

Q0456:Name the muscle type based on the histologicalfeatures;? Actin and myosin in sarcomeres; striated;

uninuclear; gap junctions; troponin:calcium binding complex;T tubules and SR forming dyadic contacts; voltage-gated

calcium channels

Cardiac muscle

Q0457:Name the muscle type based on the histologicalfeatures;? Actin and myosin in sarcomeres; striated;

multinuclear; lacks gap junctions; troponin:calcium binding; Ttubules and SR forming triadic contacts; highest ATPase

activity; no calcium channels

Skeletal muscle

Q0458:Name the muscle type based on the histologicalfeatures;? Actin and myosin not in sarcomeres; nonstriated;

uninuclear; gap junctions; calmodulin:calcium binding; lacks Ttubules; voltage-gated calcium channels

Smooth muscle

Q0459:Name the valve abnormality based on the followingcriteria;? Back-filling into the left atrium during systole;

increased v-wave; preload; left atrial volume; and leftventricular filling

Mitral insufficiency

Q0460:Name the valve abnormality based on the followingcriteria;? Systolic murmur; increased preload and afterload;decreased aortic pulse pressure and coronary blood flow

Aortic stenosis

Q0461:Name the valve abnormality based on the followingcriteria;? Diastolic murmur; increased right ventricular

pressure; left atrial pressure; and atrial to ventricular pressuregradient; decreased left ventricular filling pressure

Mitral stenosis

Q0462:Name the valve abnormality based on the followingcriteria;? Diastolic murmur; increased preload; stroke volume;and aortic pulse pressure; decreased coronary blood flow; no

incisura; and peripheral vasodilation

Aortic insufficiency

Q0463:Circulating levels of what hormone cause the cervicalmucus to be thin and watery; allowing sperm an easier entry

into the uterus?

Estrogen

Q0464:What hormone controls relaxation of the loweresophageal sphincter during swallowing?

VIP is an inhibitory parasympathetic neurotransmitter thatresults in relaxation of the lower esophageal sphincter.

Q0465:What is the term for the difference between systolicand diastolic pressures?

Pulse pressure

Q0466:What hormone; produced by the Sertoli cells; isresponsible for keeping testosterone levels in the seminiferous

tubules nearly 50 times that of the serum?

Androgen-binding protein

Q0467:True or false? There are no central O2 receptors.

True

Q0468:What cell type of the bone has PTH receptors?

Osteoblasts; which in turn stimulate osteoclasts to breakdown bone; releasing Ca2+ into the interstitium. (Remember;

blasts make; clasts take.)

Q0469:What substance is secreted by parietal glands and isrequired for life?

Intrinsic factor (IF)

Q0470:What is the only way to increase O2 delivery in thecoronary circulation?

Increasing blood flow is the only way to increase O2 deliveryin the coronary circulation because extraction is nearly

maximal during resting conditions.

Q0471:What is the term for the load a muscle is trying tomove during stimulation?

Afterload

Q0472:What is the term for days 1 to 7 of the female cycle?

Menses

Q0473:What is the term for the force the ventricular musclemust generate to expel the blood into the aorta?

Afterload

Q0474:What happens to the tonicity of the urine withincreased ADH secretion?

The urine becomes hypertonic because of water reabsorptionin the collecting duct.

Q0475:What form of renal tubular reabsorption ischaracterized by high back leak; low affinity for substance;and absence of saturation and is surmised to be a constant

percentage of a reabsorbed filtered substance?

Gradient-time system

Q0476:What type of circuit is described when the totalresistance is always greater than the sums of the individual

resistors?

Series circuit

Q0477:What hormone excess brings about abnormal glucosetolerance testing; impaired cardiac function; decreased body

fat; increased body protein; prognathism; coarse facialfeatures; and enlargements of the hands and feet?

Increased secretion of GH postpuberty leading to acromegaly.

Q0478:What happens to V/Q ratio if a thrombus is lodged inthe pulmonary artery?

The V/Q ratio increases; since the area is ventilated buthypoperfused as a result of the occlusion.

Q0479:What hormone has the following effects: chondrogenicin the epiphyseal end plates of bones; increases AA transport

for protein synthesis; increases hydroxyproline (collagen);and increases chondroitin sulfate synthesis?

GH; especially IGF-1. GH also increases the incorporation ofthymidine in DNA synthesis and uridine in RNA synthesis.

Q0480:True or false? Bile pigments and bile salts arereabsorbed in the gallbladder.

False

Q0481:What component of an ECG is associated with thefollowing?;? Conduction delay in the AV node

PR interval

Q0482:What component of an ECG is associated with thefollowing?;? Ventricular depolarization

QRS complex

Q0483:What component of an ECG is associated with thefollowing?;? Atrial depolarization

P wave

Q0484:What component of an ECG is associated with thefollowing?;? Ventricular repolarization

T wave

Q0485:Where is the greatest venous PO2 in resting tissue?

Renal circulation

Q0486:Near the end of pregnancy; what hormone's receptorsincrease in the myometrium because of elevated plasma

estrogen levels?

Oxytocin

Q0487:What respiratory center in the rostral pons has aninhibitory affect on the apneustic center?

Pneumotaxic center (short; fast breaths)

Q0488:For what hormone do Leydig cells have receptors?

LH

Q0489:What primary acid-base disturbance is cause by adecrease in alveolar ventilation (increasing CO2 levels)

resulting in the reaction shifting to the right and increasing H+and HCO3- levels?

Respiratory acidosis (summary: high CO2; high H+; slightlyhigh HCO3-)

Q0490:What lecithin: sphingomyelin ratio indicates lungmaturity?

2.0 or greater

Q0491:What is the term for the negative resting membranepotential becoming more negative?

Hyperpolarization (i.e; K+ influx)

Q0492:What type of resistance system (i.e; high or low) isformed when resistors are added in parallel?

A low-resistance system is formed by resistors added inparallel.

Q0493:Why is hypothyroidism associated with nightblindness?

Thyroid hormones are necessary for conversion of carotene tovitamin A.

Q0494:What is the FiO2 of room air?

0.21; it is a fancy way of saying 21% of the air is O2.

Q0495:Where are the lowest resting PO2 levels in a restingindividual?

Coronary circulation

Q0496:What is the rate-limiting step in the production ofsteroids?

The conversion of CHO to pregnenolone via the enzymedesmolase

Q0497:In the water deprivation test; does a patient withreduced urine flow have primary polydipsia or diabetes

insipidus?

Primary polydipsia; patients with diabetes insipidus willcontinue to produce large volumes of dilute urine.

Q0498:True or false? There is an inverse relationship betweenfat content and total body water.

True; the greater the fat; the less the total body water.

Q0499:What is the role of the negative charge on the filteringmembrane of the glomerular capillaries?

The negative charge inhibits the filtration of protein anions.

Q0500:What cardiac reflex is characterized by stretchreceptors in the right atrium; afferent and efferent limbs via

the vagus nerve; and increased stretch leading to an increase inheart rate via inhibition of parasympathetic stimulation?

Bainbridge reflex

Q0501:Where in the GI tract does the reabsorption of bilesalts take place?

Bile salts are actively reabsorbed in the distal ileum.

Q0502:What three structures increase the surface area of theGI tract?

1. Plicae circularis (3 times) ;2. Villi (30 times) ;3. Microvilli(600 times)

Q0503:Does physiologic splitting of the first heart soundoccur during inspiration or expiration? Why?

Splitting of the first heart sound occurs during inspirationbecause of the increased output of the right ventricle; delaying

the closure of the pulmonic valve.

Q0504:How much dietary iodine is necessary to maintainnormal thyroid hormone secretion?

150 mcg/day is the minimal daily intake needed. Most peopleingest 500 mcg/day.

Q0505:What is the central chemoreceptor's main drive forventilation?

CSF H+ levels; with acidosis being the main central drive;resulting in hyperventilation (the opposite being true with

alkalosis)

Q0506:What result occurs because of the negative alveolarpressure generated during inspiration?

Air flows into the respiratory system.

Q0507:Corticotropin-releasing hormone promotes thesynthesis and release of what prohormone?

Pro-opiomelanocortin (POMC) is cleaved into ACTH andbeta-lipotropin.

Q0508:What happens to free hormone levels when the liverdecreases production and release of binding proteins?

Free hormone levels remain constant; and the bound hormonelevel changes with a decrease in binding hormones.

Q0509:What type of estrogen is produced in peripheraltissues from androgens?

Estrone

Q0510:What changes does more negative intrathoracicpressure cause to systemic venous return and to the

pulmonary vessels?

Promotes systemic venous return into the chest and increasesthe caliber and volume of the pulmonary vessels

Q0511:Where is renin produced?

In the JG cells of the kidney

Q0512:True or false? Right-sided valves close before thevalves on the left side of the heart.

False. Right-sided valves are the first to open and last toclose.

Q0513:What enzyme is associated with osteoblastic activity?

Alkaline phosphatase

Q0514:What is the order of attachment of O2 to Hgb-bindingsites in the lung? Order of release from the binding sites in the

tissue?

Order of attachment is site 1; 2; 3; 4; and for release is 4; 3; 2;1.

Q0515:What hormone is secreted into the plasma in responseto a meal rich in protein or CHO?

Insulin

Q0516:What happens to blood flow and pressuredownstream with local arteriolar constriction?

With arteriolar constriction both the flow and pressuredownstream decrease.

Q0517:What occurs when the lower esophageal sphincter failsto relax during swallowing due to abnormalities of the enteric

nervous plexus?

Achalasia

Q0518:True or false? Ungated channels are always open.

True. They have no gates; so by definition they are alwaysopen.

Q0519:What component of the ANS is responsible fordilation of the blood vessels in the erectile tissue of the penis;

resulting in an erection?

Parasympathetics (parasympathetics point; sympatheticsshoot)

Q0520:What muscle type is characterized by low ATPaseactivity; aerobic metabolism; myoglobin; association with

endurance; and small muscle mass?

Red muscle

Q0521:What happens to diastolic and systolic intervals withan increase in sympathetic activity?

Systolic interval decreases secondary to increasedcontractility; diastolic interval decreases secondary to an

increase in heart rate.

Q0522:Circulating levels of what hormone in men isresponsible for the negative feedback loop to the

hypothalamus and the anterior pituitary gland regulating therelease of LH?

Testosterone

Q0523:How are pulse pressure and compliance related?

They are inversely proportional to each other; as pulsepressure increases; compliance decreases.

Q0524:What three substances stimulate parietal cells?

ACh; histamine; and gastrin

Q0525:What two factors result in the base of the lung beinghyperperfused?

Increased pulmonary arterial pressure (high perfusion) andmore distensible vessels (low resistance) result in increased

blood flow at the base.

Q0526:True or false? Without ADH the collecting duct wouldbe impermeable to water.

True. Without ADH hypotonic urine would be formed.

Q0527:How does ventricular depolarization take place; baseto apex or vice versa?

Depolarization is from apex to base and from endocardium toepicardium.

Q0528:What are effects of PTH in the kidney?

PTH increases Ca2+ reabsorption in the DCT of the kidneyand decreases PO4- reabsorption in the PCT.

Q0529:Regarding muscle mechanics; how is passive tensionproduced?

It is produced by the preload on the muscle prior tocontraction.

Q0530:Insulin-induced hypoglycemia is the most reliable (byfar not the safest) test for what hormone deficiency?

GH deficiency

Q0531:In regards to solute concentration; how does waterflow?

Water flows from a low-solute to high-solute concentrations.

Q0532:Which extravascular chemoreceptor detects low NaClconcentrations?

Macula densa

Q0533:If the AV difference is positive; is the substanceextracted or produced by the organ?

A positive AV difference indicates that a substance isextracted by the organ; and a negative difference indicates that

it is produced by the organ.

Q0534:What is used as an index of the number of functioningcarriers for a substance in active reabsorption in the kidney?

Transport maximum (Tm) occurs when all function carriersare saturated and therefore is an index of the number of

functioning carriers.

Q0535:Why is there a transcellular shift in K+ levels in adiabetic patient who becomes acidotic?

The increased H+ moves intracellularly and is buffered by K+leaving the cells; resulting in intracellular depletion and serum

excess. (Intracellular hypokalemia is the reason yousupplement potassium in diabetic ketoacidosis; even though

the serum levels are elevated.)

Q0536:True or false? Catechol-O-methyl transferase(COMT) is not found in smooth muscle; liver; and the

kidneys.

False. That is precisely where COMT is found; it is notfound in adrenergic nerve terminals.

Q0537:What somatomedin serves as a 24-hour marker of GHsecretion?

IGF-1 (somatomedin C)

Q0538:What receptor is in the smooth muscle cells of thesmall bronchi; is stimulated during inflation; and inhibits

inspiration?

Stretch receptors prevent overdistension of the lungs duringinspiration.

Q0539:True or false? Thyroid hormones are necessary fornormal menstrual cycles.

True. They are also necessary for normal brain maturation.

Q0540:What component of the cardiovascular system has thelargest blood volume? Second largest blood volume?

The systemic veins have the largest blood volume; and thepulmonary veins have the second largest blood volume in the

cardiovascular system. They represent the reservoirs ofcirculation.

Q0541:Serum concentration of what substance is used as aclinical measure of a patient's GFR?

Creatinine

Q0542:Where does CHO digestion begin?

In the mouth with salivary alpha-amylase (ptyalin)

Q0543:How does the sympathetic nervous system affectinsulin secretion?

It decreases insulin secretion.

Q0544:How does cell diameter affect the conduction velocityof an action potential?

The greater the cell diameter; the greater the conductionvelocity.

Q0545:in a ventricular pacemaker cell; what phase of theaction potential is effected by NE

phase 4

Q0546:anatomical and alveolar dead spaces togetherconstitute...

physiologic dead space;= total dead space of resp system

Q0547:what three organs are necessary for the production ofvitamin D3 (cholecalciferol)

skin;liver;kidney

Q0548:what is the effect of LH on the production of adrenalandrogens

no effect;ACTH stimulates adrenal androgen production

Q0549:what four conditions result in secondaryhyperaldosteronism

CHF;vena calval obstruction;hepatic cirrhosis;renal arterystenosis

Q0550:what are the five hormones made by sertoli cells

inhibin;estradiol;androgen-binding protein;meiosis inhibitingfactor ;antimullerian hormone

Q0551:does the left or right vagus innervate the SA node

Right vagus innervates SA node (*need the right nerve tocontrol the important node*);Left vagus innervates AV node

Q0552:how does ventricular repolarization take place; base toapex or vice versa

base to apex ;and;epicardium to endocardium

Q0553:what is the term for any region of the respiratorysystem that is incapable of gas exchange

anatomical dead space (ends at terminal bronchioles)

Q0554:what four factors shift the Hgb-O2 curve to the right?

inc CO2;inc H;inc temp;inc 2;3-BPG;FACILITATEOFFLOADING O2

Q0555:what two factors result in the apex of the lung beinghypoperfused

decreased pulmonary arterial pressure and less distensablevessels

Q0556:what is the ratio of pulmonary to systemic blood flow

1:01

Q0557:to differentiate central from nephrogenic diabetesinsipidus; after an injection of ADH; which will show

decreased urine flow

central

Q0558:in what area of the GI tract are water-soluble vitaminsabsorbed

duodenum

Q0559:what wave is the cause of the following venous pulsedeflection: rise in right atrial pressure secondary to bloodfilling and terminating when the tricuspid valve opens?;the

bulging of the tricuspid valve into the right atrium?;thecontraction of the right atrium?

v wave;C wave;A wave

Q0560:what are the four functions of saliva

antibacterial;lubricate;CHO digestion;fat digestion

Q0561:supine to standing..;dependent venous press?;depvenous blood volume?;CO?;BP?

inc;inc;dec;dec;**carotid sinus reflex attempts toCOMPENSATE by increasing TPR and heart rate

Q0562:when does the hydrostatic pressure in Bowman'scapsule play a role in opposing filtration

when there is an obstruction downstream

Q0563:what happens to intrapleural pressure when thediaphragm is contracted during inspiration

intrapleural pressure decreases

Q0564:what is used as an index of cortisol secretion

urinary 17-OH steroids

Q0565:what is used as an index of cortisol secretion

urinary 17-OH steroids

Q0566:if the pH is low with increased CO2 levels anddecreased HCO3 levels; what is the acid-base disturbance

combined respiratory acidosis and metabolic acidosis

Q0567:what is the term that refers to the number of channelsopen in a cell membrane

conductance

Q0568:what are the five tissues in which glucose uptake isinsulin dependent

CNS;renal tubules;beta islet cells;RBCs;GI mucosa

Q0569:place in order from fastest to slowest the rate ofgastric emptying for CHO; fat; liquids; proteins

liquids;CHO;protein;fat

Q0570:is most of the coronary artery blood flow duringsystole or diastole

diastole

Q0571:what modified smooth muscle cell of the kidneymonitors BP in the afferent arteriole

juxtaglomerular cells

Q0572:what are the three functions of surfactant

decrease surface tension;increase compliance;decreaseprobability of pulmonary edema formation

Q0573:glycogenolytic;gluoneogenic;lipolytic;glycolytic;andstimulated by hypoglycemia

epi

Q0574:glycogenolytic;gluconeogenic;lipolytic;glycolytic;proteolytic;and stimulated by hypoglycemia and aa

glucagon

Q0575:glycogenic;gluconeogenic;lipogenic;proteogenic;glycolytic;and stimulated hy hyperglycemia; aa's; fatty acids; ketosis;

ACh; GH; and beta agonists

insulin

Q0576:what type of muscle is characterized by nomyoglobin; anaerobic glycolysis; high ATPase activity; and

large muscle mass

white muscle; short term too

Q0577:what percentage of CO2 is carried in the plasma asHCO3?;as carbamino compounds?;as dissolved CO2?

90%;5%;5%

Q0578:what is the most potent male sex hormone

dihydrotestosterone

Q0579:with a decreased arterial diastolic pressure; whathappens to stroke volume?;TPR?;heart rate?

all decrease

Q0580:what linkage of complex CHOs does pancreaticamylase hydrolyze? What three complexes are formed?

alpha-1;4-glucoside linkages; forming alpha-limit dextrins;maltotriose; and maltose

Q0581:does the heart rate determine the diastolic or systolicinterval

diastolic;contractility determines systolic interval

Q0582:on a graphical representation of filtration;reabsorption; and excretion; when does glucose first appear in

urine

at the beginning of splay (about 250)

Q0583:what is the relationship between preload and passivetension in a muscle

direct;the greater the preload; the greater the passive tensionand the greater the prestretch of a sarcomere

Q0584:what is the rate-limiting step in the synthetic pathwayof NE at the adrenergic nerve terminal

conversion of tyrosine to dopamine by tyrosine hydroxylase

Q0585:how many days prior to ovulation does LH surgeoccur

1 day prior

Q0586:how are flow through the loop of Henle andconcentration of urine related

as flow increases; the urine becomes more dilute because ofdecreased time for H2O reabsorption

Q0587:what is the PO2 of aortic blood in fetal circulation

60%

Q0588:how do elevated blood glucose levels decrease GHsecretion

somatotrophins are stimulated by IGF-1 and they inhibit GHsecretion;GHRH stimulates GH secretion

Q0589:what segment of the nephron has the highestconcentration of inulin?;lowest conc?

terminal collecting duct has highest concentration;Bowman'scapsule has lowest?

Q0590:what type of resistance system; high or low; is formedwhen resistors are added in series

high

Q0591:what hormones; secreted in proportion to the size ofthe placenta; are an index of fetal well being

hCS and serum estriol; which are produced by the fetal liverand placenta; respectively; are used as estimates of FETAL

well being

Q0592:what primary acid-base disturbance is caused by anincrease in alveoloar ventilation (decreasing CO2 levels)

resulting in the reaction shifting to the left and decreasing boththe H and HCO3 levels

respiratory alkalosis;(low CO2;low H;slightly low HCO3)

Q0593:what respiratory center in the caudal pons is thecenter for rhythm promoting prolonged inspirations

apneustic center (deep breathing place)

Q0594:what area of the GI tract has the highest activity ofbrush border enzymes

jejunum

Q0595:does T3 or T4 have greater affinity for nuclearreceptors

T3

Q0596:what is the only signal regulating release of PTH

low interstitial free Ca

Q0597:1. PTH dec; Ca inc; Pi inc;2. PTH inc; Ca dec; Pidec;3. PTH dec; Ca dec; Pi inc;4. PTH inc; Ca inc; Pi dec

1. secondary hypo;2. secondary hyper;3. primary hypo;4.primary hyper

Q0598:1. TRH dec; TSH dec; T4 inc;2. TRH inc; TSH dec;T4 dec;3. TRH dec; TSH dec; T4 dec;4. TRH inc; TSH inc;

T4 dec;5. TRH dec; TSH inc; T4 inc

1. graves;2. secondary hypo (pituitary);3. tertiary hypo(hypothalamic);4. primary hypo;5. secondary hyper

Q0599:what two stress hormones are under the permissiveaction of cortisol

glucagon and epi

Q0600:if radius of a vessle doubles; what happens toresistance

dec 1/16

Q0601:what preventgs the down regulation of the recptors onthe gonadotrophos of the anterior pituitary

pulatile release of GnRH

Q0602:does epi have proteolytic action

no- only glycogenolytic and lipolytic

Q0603:what is the only 17-hydroxysteroid with hormonalactivity

cortisol

Q0604:does the oncotic pressure of plasma promote filtrationor reabsorption

reabsorption

Q0605:why is the baes of the lung hyperventialted when aperson is standing upright

alveoli are small and very compliant; so there is a large changein their size and volume and therefore a high level of alveolar

ventilation

Q0606:by removing Na from the renal tubule and pumping itback into the ECF compartment; what does aldosterone do to

the body's acid base stores

removal of Na creates a net negative charge in the renal tubule-> promotes entry of K and H and promotes HCO3 to go to

plasma -> produces hypokalemic alkalosis

Q0607:what hormone causes contraction of smooth mucle;regulates interdigestive motility; and prepares intestine for

next meal

motilin

Q0608:what two vessels in fetal circulatin have the highestPO2 levles

umbilical vein and ductus venosus

Q0609:how many days prior to ovulation does estradiol peakin the menstrual cycle

2 days prior

Q0610:what serves as a marker of endogenous insulinsecretion

C-peptide

Q0611:what is the term for the total volume of air moved inand out of the respiratry system per minute

total ventilation;= minute ventilation;= minute volume

Q0612:what is the renal compensation mechanism foralkalosis

increase urinary excretion of HCO3;shifts reaction to right andincreasing H

Q0613:what is a sign of a sertoli cell tumor in a man

excess estradiol in blood

Q0614:in the systemic circulation; what blood vessels havethe largest pressure drop?;smallest pressure drop?

arterioles;vena cava

Q0615:what is the major stimulus for cell division inchondroblasts

IGF-1

Q0616:what are two causes of diffusion impairment in thelungs

decrease in surface area and increase in membrane thickness

Q0617:what are four effects of suckling on the mother

increased synthesis and secretion of oxytocin;increased releaseof PIF from hypothalamus;inhibition of GnRH;milk secretion

Q0618:a MMC is a propulsive mov't of undigested materialfrom the stomach to the small intestine; to the colon. during a

fast; what is the time interval of its repeats

90 to 120 minutes;correlates with levels of motilin

Q0619:increasing arterial systolic pressure..;strokevolume?;vessel compliance?;heart rate?

inc;dec;dec

Q0620:what enzyme is needed to activate trypsinogen totrypsin?;chymotrypsinogen to

chymotrypsin?;procarboxypeptidase to carboxypeptidase?

enterokinase;trypsin;trypsin

Q0621:in a ventricular pacemaker cell; what phase of theaction potential is affected by ACh

phase 4

Q0622:what is the most potent stimulus for glucagonsecretion? inhibition?

hypoglycemia -> secretion;hyperglycemia -> inhibition

Q0623:what is the term for the summation of mechanicalstimuli due to the skeletal muscle contractile unit becoming

saturated with calcium

tetany

Q0624:what form of renal tubular reabsorption ischaracterized by low back leaks; high affinity of a substance;and easy saturation? It is surmised that the entire filtered loadis reabsorbed until the carriers are saturated; and then the rest

is excreted

a transport maxium (Tm) system

Q0625:in an adrenergic nerve terminal; where is DA convertedto Nepi?

in the vesicle by dopamine-beta-hydroxylase

Q0626:is the clearance for a substance greater than or lessthan for inulin if it is freely filtered and secreted? if it is freely

filtered and reabsorbed?

greater (ex PAH);less (ex glucose)

Q0627:what is the term for the load on a muscle in the relaxedstate

preload is load Prior to contraction

Q0628:what are the two best indices of left ventricularpreload

LVEDV and LVEDP

Q0629:in males..;1. LH pulsatile amplitude and levelsincrease; with increased testosterone?;2. both LH and

testosterone levels drop and remain low?;3. LH secretiondrives testosterone production; with both paralleling

eachother?;4. decreased testosterone and increased LH?

1. puberty;2. childhood;3. adulthood;4. aged adult

Q0630:why is the clearance of creatinine always slightlygreater than the clearance of inulin and GFR?

because creatinine is freely filtered and slightly secreted

Q0631:what primary acid-base disturbace is caused by a lossin fixed acid forcing the reaction to shift to the left; thereby

increasing HCO3 levels

metabolic alkalosis;(high PH; low H; high HCO3)

Q0632:when referring to a series circuit; what happens toresistance when a resistor is added

increases

Q0633:why is there an increase in prolactin if thehypothalamic pituitary axis is severed

the chronic inhibition of dopamine (PIF) on the release ofprolactin from the anterior pituitary gland is removed; thereby

increasing the release of prolactin

Q0634:what acid form of H in the urine cannot be titrated

NH4

Q0635:regarding the venous system; what happens to bloodvolume if there is a small change in pressure

venous system is more compliant -> small changes in pressureresult in large changes in blood volume

Q0636:in what stage of sleep is GH secreted

3 and 4

Q0637:where does the conversion of CO2 into HCO3 takeplace

RBC

Q0638:from the fourth month of fetal life to term; whatsecretes the progesterone and estrogen to maintain the uterus

placenta

Q0639:what two factors are required for exocytosis

Ca and ATP

Q0640:what is the best measure of total body vitamin D ifyou suspect a deficiency

serum 25-OH-D

Q0641:what hormone is required for 1;25-dihydroxy-D tohave bone resorbing effects

PTH

Q0642:is bone deposition or resorption due to increasedinterstitial Ca concentration

deposition

Q0643:the opening of what valve indicates the terminatino ofisovolumetric relaxation of the cardiac cycle

mitral valve

Q0644:why is there a decrease in the production in epi whenthe anterior pituitary gland is removed

PNMT used in the conversion of epi; is regulated by cortisol;removing the anterior pituitary gland decreases ACTH and

therefor cortisol

Q0645:name the period described by the following: no matterhow strong a stimulus; no further action potentials can be

stimulated

absolute refractory period (voltage inactivation of Nachannels)

Q0646:how many carbons do estrogens have

18;(remove one C from an androgen makes an estrogen)

Q0647:T or F? the alveolar PO2 and PCO2 levels match thepumonary end capillary blood levels

true- because of intrapulmonary shunting; there is a slightdecrease in PO2 and increase in PCO2 between the

pulmonary end capillary blood and the systemic arterial blood

Q0648:in high altitudes; what is the main drive for ventilation

shifts from central chemoreceptors (CSF H) to periopheralchemoreceptors monitoring O2

Q0649:1. ECF dec; ICF no change; body no change;2. ECFinc; ICF inc; body dec;3. ECF dec; ICF dec; body inc;4. ECF

inc; ICF no change; body no change;5. ECF inc; ICF dec; bodyinc

1. loss of isotonic fluid (diarrhea; hemorrhage);2. gain ofhypotonic fluid (water intoxication);3. loss of hypotonic fluid(dehydration);4. gain of isotonic saline;5. gain of hypertonic

fluid

Q0650:what hormone excess produces adrenal hyperplasia

ACTH

Q0651:is there more circulating T3 or T4

T4- because the greater affinity for the binding protein; T4has a significantly longer half life than T3 (50x)

Q0652:why is the cells resting membrane potential negative

intracellular proteins

Q0653:is thyroid size a measure of its function

no!;TSH is a measure of its function

Q0654:if the radius of a vessel is decreased by half; whathappens to resistance

increased 16x

Q0655:what neurotransmitter is essential for maintaining anormal BP when an individual is standing

NE

Q0656:what form of diabetes insipidus is due to aninsufficient amount of ADH

central/neurogenic

Q0657:three methods of vasodilation via the sympatheticnervous system

decreased alpha 1;increased beta 2;increased ACh

Q0658:1. Ca reabsorption and phosphate excretion;2. Caexcretion and phosphate excretion;3. Ca reabsortpion and

phosphate reabsorption

1. PTH;2. calcitriol;3. vitamin D3

Q0659:does progesterone have thermogenic activities

yes

Q0660:how long is the transit time through the small intestine

2-4 hours

Q0661:where is the last conducting zone of the lungs

terminal bronchioles (no gas exchange)

Q0662:does cortisol inhibit glucose uptake in skeletal muscle

yes- makes it available for neural tissue

Q0663:what percentage of cardiac output flows through thepulmonary circuit

100%

Q0664:HGb binding site?;1. least affinity for O2; requireshighest PO2 (100);2. greatest affinity for attachment; requires

PO2 of 26;3. remains attached under most conditions;4.requires a PO2 of 40

1. site 4;2. site 2;3. site 1;4. site 3

Q0665:which three factors cause the release of epi fromadrenal medulla

1. exercise;2. emergencies;3. exposure to cold

Q0666:how many ATPs are hydrolyzed every time a skeletalmuscle cross-bridge completes a single cycle

one

Q0667:why would a puncture to a vein above the heart havethe potential to introduce air into the vascular system

venous pressure above the heart is subatmospheric

Q0668:what type of saliva is produced underparasympathetic stimulation

high volume;watery

Q0669:in what area of the gI tract does iron get absorbed

duodenum

Q0670:why is the apex of the lung hypoventilaged when aperson is standing

alveli at apex are almost completely inflated prior to inflation-> they receive low levels of alveolar ventilation

Q0671:what pancreatic islet cell secretes glucagon

alpha;glucagon has stimulatory affects on beta cells andinhibitory effects on delta cells

Q0672:what are the four characteristics of protein mediatedtransport

1. comp for carrier;2. chemic specificity;3. zero-ordersaturation;4. rate of transportation faster than if by simple

diffusion

Q0673:what is secretin's pancreatic action

stimulates HCO3 rich solution release

Q0674:why is there an increase in FF if the GFR is decreasedunder sympathetic stimulation

because RPF is markedly decreased; while GFR is only;minimally dec --> inc FF (=GFR/RPF)

Q0675:what triggers phase 3 of action potential in ventricularpace maker cell

efflux of potassium

Q0676:what is the primary target for glucagon

liver

Q0677:what is the renal compensation for acidosis

makes HCO3; shifting reaction to left and decreasing H

Q0678:what enzyme found in a cholinergic synapse breaksdown ACh?

acetylcholinesterase;-> acetate and choline

Q0679:what hormone; produced by sertoli cells; if absentwould result in the formation of internal female structures

MIF

Q0680:what happens to the lung if the intrapleural pressureexceeds lung recoil

lung will expand

Q0681:what two factors determine the clearance of asubstance

plasma concentration and excretio rate;= U/V

Q0682:what type of muscle contraction occurs when themsucle shortens and lifts the load placed on it

isotonic

Q0683:what type of potential is characterized as being an allor none; propagated and not summated

action potential

Q0684:what primary acid-base disturbace is cuased by a gainin fixed acid forcing the reaction to shift to the left; decreasing

HCO3 and inc CO2

metabolic acidosis (low pH; high H; low HCO3)

Q0685:pregnant woman in 3rd trimester has normal BP whenstanding and sitting. When supine BP drops to 90/50;what is

the dx?

compression of the IVC

Q0686:35 y/o man has high BP in arms and lowBP in hislegs;what is the dx

coarction of teh aorta

Q0687:5 y/o boy presents weith a systolic murmur and awide fixed split S2. what is the dx

ASD

Q0688:During a game a young football player collapses anddies immediately. What is the most likely type of cardiac dz

hypoertrophic cardiomyopathy

Q0689:pt has a stroke after incurring multiple long bonefractures in trauma stemming from a MVA. What caused the

infarct

fat emboli

Q0690:elderly woman presents with a headache and jaw pain.labs show elevated ESR. what is teh dx

temporal arteritis

Q0691:80 y/o man presents w/ systolic crescendo-decrescendo murmur. What is the most likely cause?

aortic stenosis

Q0692:Man starts a medication for hyperlipidemia. He thendevelops a rash; pruritis; and GI upset. What drug was it

Niacin

Q0693:Pt developes a cough and must discontinue captopril.What is a good replacement drug and why doesn't it have the

same side effects?

losartan; an angiotensin II receptor antagonist; does notincrease bradykinin as captopril does.

Q0694:What are the 3 sx inside the carotid sheath

1) Internal jugular Vein (lateral);2) Common carotid Artery(medial);3) Vagus Nerve (posterior);mneu: VAN

Q0695:In the majority of cases; the SA and AV nodes aresupplied by this carotid artery?

Right coronary artery

Q0696:80% of the time the Right coronary artery is"dominant"; suppplying the left ventricle via the _________

branch

Posterior descending artery

Q0697:cardiac output =

SVxHR

Q0698:During exercise; CO increased as a result of anincreased in _____. After prolonged exercise; CO increased

as a result of an increased in ____

SV;HR

Q0699:cardiac output =

SVxHR

Q0700:During exercise; CO increased initially as a result ofan increased in ____. After prolonged exercise; CO increased

as a result of an increased in ____.

SV;HR

Q0701:Mean argerial Pressure (MAP)=;give 2 equasions;1)CO; TPR;2) systolic; diastolic

1) CO x TPR;2)1/3 systolic +2/3 diastolic

Q0702:CO=;rate of O2 consumption; aa O2 content; vv O2content

rate of O2 consumption / (aa O2 content-vv O2 content)

Q0703:Pulse pressure =;systolic; diastolic

systolic-diastolic

Q0704:pulse pressure ≈

stroke volume

Q0705:SV=;(2 equasions);1) CO; HR;2)EDV;ESV

1)=CO/HR;2)=EDV-ESV

Q0706:Coronary Artery Anatomy [pic]

1)Right Coronary aa (RCA);2)Left main coronary aa(LCA);3)Circumflex artery (CFX);4) Left anterior descendingaa (LAD;5) Posterior descending aa (PD);6) Acute marginal aa

Q0707:Stroke volume is affected by what 3 things ;mneu: SVCAP

Contractility; Afterload; and Preload;mneu: SV CAP

Q0708:increased Preload →__SV

increased

Q0709:increased Afterload→ __SV

decreased

Q0710:increased contractility→ __SV

increased

Q0711:SV ___ in anxiety; exercise; & pregnancy

increased

Q0712:a failing heart has a ___ SV

decreased

Q0713:Contractality (and SV); ____ with catecholemines

increased

Q0714:Contractality (and SV); ____ with increasedintracellular Ca++

increased

Q0715:Contractality (and SV); ____ with decreasedextracellular sodium

increased

Q0716:Contractality (and SV); ____ with digitalis

increased

Q0717:Contractality (and SV); ____ with beta1 blockade

decreased

Q0718:Contractality (and SV); ____ with heart failure

decreased

Q0719:Contractality (and SV); ____ with acidosis

decreased

Q0720:Contractality (and SV); ____ withhypoxia/hypercapnea

decreased

Q0721:Contractality (and SV); ____ with Ca++ channelblockers

decreased

Q0722:Myocardial demand is ___ by increased afterload(diastolic BP)

increased

Q0723:Myocardial demand is ___ by increased contractility

increased

Q0724:Myocardial demand is ___ by increased heart rate

increased

Q0725:Myocardial demand is ___ by increased heart size

increased

Q0726:ventricular EDV

Preload

Q0727:Systolic arterial pressure

afterload

Q0728:proportional to peripheral resistance

afterload

Q0729:venous dialators (e.g. nitroglycerine) decreased_______;(preload or afterload)

preload

Q0730:vaso dialators (e.g. hydralazine) decreased_______;(preload or afterload)

afterload

Q0731:______ increased w/ exercise; increased bloodvolume; exitement (sympathetics);(preload or afterload)

Preload

Q0732:Starling Curve: Force of _______ is proportional toinitial length of cardiac mm fiber (preload)

contraction

Q0733:contraction state of the myocardium is ____ bycirculating catecholamines;(+;-)

+

Q0734:contraction state of the myocardium is ____ bydigitalis;(+;-)

+

Q0735:contraction state of the myocardium is ____ bysympathetic stimulation;(+;-)

+

Q0736:contraction state of the myocardium is ____ bypharmacologic depressants;(+;-)

-

Q0737:contraction state of the myocardium is ____ by loss ofmyocardium (MI);(+;-)

-

Q0738:EF=;(give 2 equasions);1) SV; EDV;2) EDV; ESV;EDV

1) SV/EDV;2) EDV-ESV/EDV

Q0739:this is an index of ventricular contractility

EF

Q0740:EF is normally > ___%

55

Q0741:Place condition on the Starling curve [pic p.219]

1)exercise;2)CHF + digitalis;3)CHF

Q0742:(driving Pressure)ΔP=;Q (flow) ;R (resistance)

Q x R

Q0743:Resisitance (R) =;Give 2 equasions;1)ΔP(drivingpressure);flow(Q) ;2)n(viscosity); length(l); radius (r)

1)=ΔP/Q;2)8nxl/Πr(^4)

Q0744:viscosity depends mostly on _______

hematocrit

Q0745:increased ______ in;1) Polycythemia;2)Hyperproteinemic states (e.g; multiple myeloma);3)

hereditary spherocytosis

viscosity

Q0746:resistance is ________ to viscosity ;(proportional orinversely proportional)

proportional

Q0747:resistance is ________ to the radius to the 4thpower;(proportional or inversely proportional)

inversely proportional

Q0748:cardiac and vascular fx curves [pic p.219]

1) (+) inotropy;2) (-) inotropy;3) (increased ) bloodvolume;4) (decreased ) blood volume

Q0749:cardiac cycle image [p. 220]

1)isovolumetric contraction;2) aortic valve opens;3)ejection;4) aortic valve closes;5) isovolumetric relaxation;6)mitral valve opens;7)ventricular filling;8) mitral valve closes

Q0750:Name the phase of the cardiac cycle;period betweenmitral valve closure and aortic valve opening.

isovolumetric contraction

Q0751:Name the phase of the cardiac cycle: period of highestO2 consumption

isovolumetric contraction

Q0752:Name the phase of the cardiac cycle: period betweenaortic valve opening and closing

systolic ejection

Q0753:Name the phase of the cardiac cycle: period betweenaortic valve closing and mitral valve opening

isovolumetric relaxation

Q0754:Name the phase of the cardiac cycle: period just aftermitral valve opening

rapid filling

Q0755:Name the phase of the cardiac cycle: period just beforemitral valve closure

slow filling

Q0756:name the heart sound: mitral and tricuspid valveclosure

S1

Q0757:name the heart sound: aortic and pulmonary valveclosure

S2

Q0758:name the heart sound: at the end of rapid ventricularfilling

S3

Q0759:name the heart sound: high atrial pressure/stiffventricle

S4

Q0760:this heart sound is associated w/ dilated CHF

S3

Q0761:this heart sound AKA "atrial kick" is associated with ahypertrophic ventricle

S4

Q0762:Jugular venous pulse waves;a wave

Atrial contraction

Q0763:Jugular venous pulse waves: c wave

RV Contraction (tricuspid valve bulging into atrium)

Q0764:Jugular venous pulse waves: v wave

increaseed atrial pressure due to filling against closed tricuspidValve

Q0765:jugular venous distention is seen in ___________

right heart failure

Q0766:when the aortic valve closes before the pulmonic thisheart sound abnormality results

S2 splitting

Q0767:S2 splitting is increased upon ________

inspiration

Q0768:Paradoxical splitting (S2 split increasd upon expirationis associated with what?

aortic stenosis

Q0769:pressure volume relationship [pic p. 221]

--

Q0770:cardiac mm contraction is dependent on extracellular________; which enters the cells during plateau of action

potential and stimulates ______ release from the cardiac mmsarcoplasm reticulum.

calcium;calcium;calcium induced calcium release

Q0771:In contrast to skeletal mm; cardiac mm action potentialhas a plateau; which is due to ____ influx.

Ca+

Q0772:In contrast to skeletal mm; cardiac nodal cells________ depolarize; resulting in automaticity

spontaneously

Q0773:In contrast to skeletal mm; cardiac myocytes areelectrically coupled to each other by ________

gap junctions

Q0774:myocardial action potential occurs in atrial andventricular myocytes and ________

perkinje fibers

Q0775:In a myocardial action potential; this phase is therapid upstroke; when voltage gated Na+ channels open

phase 0

Q0776:In a myocardial action potential; this phase is theinitial repolarization-inactivation of voltage0gated Na+

channels. Voltage gated K+ channels begin to open

Phase 1

Q0777:In a myocardial action potential; this phase is theplateu--Ca++ influx through voltage-gated Ca++ channels

balances K+ efflux. Ca++ influx triggers another Ca++ releasefrom sarcoplasmic reticulum and myocyte contraction.

phase 2

Q0778:In a myocardial action potential; this phase is therapid repolarization--massive K+ efflux due to opening of

voltage-gated slow K_ channels and closure of voltage gatedCa++ channels.

Phase 3

Q0779:In a myocardial action potential; this phase is theresting potential--high K+ permeability through K+ channels.

phase 4

Q0780:Pacemaker action potentials occur where

SA & AV nodes

Q0781:In a pacemaker action potential this phase is theupstroke phase--it involves opening of voltage-gated Ca++channels. These cells lack fast voltage-gated Na+ channels.

Results in a slow conduction velocity that is used by the AVnode to prolong transmission from the atria to ventricles.

phase 0

Q0782:In a pacemaker action potential this phase; the plateauis absent.

phase 2

Q0783:In a pacemaker action potential this phase; the slowdiastolic depololarization results in membrane potential

spontaneously depolarizing as Na+ conductance increases.This accounts for automaticity of SA and AV nodes. The

slope of this phase in the SA node determines the heart rate.ACh decreases and catecholamines increasee the rate of

diastolic depolarization decreasing or increasing heart raterespectively.

phase 4

Q0784:electrocardiogram: atrial depolarization

P wave

Q0785:electrocardiogram: conduction delay through AV node(normally <200 msec)

PR segment

Q0786:electrocardiogram: vetricular depolarization (normally< 120 msec)

QRS complex

Q0787:electrocardiogram: mechanical contraction of theventricles

QT interval

Q0788:electrocardiogram: ventricular repolarization

T wave

Q0789:electrocardiogram;atrial repolarization is masked by_______

QRS complex

Q0790:electrocardiogram: isoelectric; ventricles depolarized

ST segment

Q0791:electrocardiogram: These waves caused byhypokalemia

U wave

Q0792:this syndrome is caused by an accessory conductionpathway from atria to vetricle (bundle of kent); bypassing AV

node. As a result; ventricles begin to partially depolarizeearlier; giving rise to characteristic delta wave on ECG. May

result in reentry current leading to supraventriculartachycardia [image p.223]

Wolff-Parkinson-White syndrome

Q0793:This ECG tracing has a chaotic and erratic baseline(irregularly irregular) with no discrete P waves in between

irregularly spaced QRS complexes (pic. p 224)

Atrial fibrillation

Q0794:This ECG tracing has a rapid succession of identical;back to back atrial depolarization waves. The identical

appearance accounts for the "sawtooth" appearance of theflutter waves. (pic. p 224)

Atrial flutter

Q0795:In this condition PR interval is prolonged (>200msec). Asymptomatic;(pic. p 224)

1st degree AV block.

Q0796:Progressive lenthening of the PR interval until a beat is"dropped" (a P wave not followed by a QRS complex).

Usually asymptomatic. (pic. p 224)

2nd degree AV block;Mobitz type I (Wenckebach)

Q0797:On ECG shows dropped beats that are not precededby a change in the length of the PR interval. These abrupt;nonconducted P waves result in a pathologic condition. It isoften found as a 2:1 block; where there are 2 P waves to 1

QRS response. May progress to 3rd degree block.(pic. p 225)

Mobitz type II AV block

Q0798:In this condition; the atria and ventricles beatindependently of each other. Both P waves and QRS

complexes are present; although the P waves bear no relationto the QRS complexes. The atrial rate is faster than the

ventricular rate. Usually treat with pacemaker.

3rd degree AV block (complete)

Q0799:completely erratic rhythm with no identifiable waves.Fatal arrhythmia without immediate CPR and defibrillation.

(pic. p 225)

Ventricular Fibrillation

Q0800:________receptor transmits via vagus nn to medulla(responds only to increase blood pressure)

aortic arch receptor

Q0801:________ receptor transmits via glossopharyngeal nnto medulla

carotid sinus

Q0802:decreased firing by aroreceptors during hypotensionresults in an increase in efferent ________ firing

sympathetic

Q0803:In a carotid massage; the increased pressure on carotidaa results in increased stretch and ____ in heart rate

decrease

Q0804:Peripheral chemoreceptors in the carotid and aorticbodies respond to (3 things)

decreased PO2 (<60mmHg); increased PCO2 and decreasedpH of blood

Q0805:Central chemoreceptors respond to what changes (2)

changes in pH and Pco2 (not Po2)

Q0806:This chemoreceptor is responsible for Cushingreaction; response to cerebral ischemia; response to increase

intracranial pressure leads to hypertension (sympatheticresponse) and bradycardia (parasympathetic response)

Central chemoreceptor

Q0807:This orgen gets the largest share of systemic cardiacoutput

liver

Q0808:this organ gets the highest blood flow per gram oftissue

kidney

Q0809:this orgen has a large arteriovenous O2 differnece.Increased O2 demand is met by increased coronary blood

flow; not by increased extraction of O2.

heart

Q0810:this is a good approximation of L atrial pressure andmeasured with a Swan-Ganz catheter

Pulmonary capillary wedge pressure

Q0811:blood flow is altered to meet demands of tissue

autoregulation

Q0812:Name the organ regulated by the local metabolites;O2adenosine; NO

heart

Q0813:Name the organ regulated by the localmetabolites;CO2 (pH)

brain

Q0814:Name the organ regulated by the local metabolites:Myogenic and tubuloglomerular feedback

kidneys

Q0815:Name the organ regulated by the local metabolites:hypoxia causes vasoconstriction

lungs

Q0816:_______ vasculature is unique in that hypoxia causesvasoconstriction (in other organs hypoxia causes vasodilation)

pulmonary

Q0817:Name the organ regulated by the local metabolites:lactate; adenosine; K+

skeletal mm

Q0818:Name the organ regulated by the local metabolites:sympathetic stimulation most important mechanism--temp

control

skin

Q0819:______ forces determine fluid movement by osmosisthroug capillary membranes

starling

Q0820:moves fluid out of capillary

P(c) capillary pressure

Q0821:moves fluid into capillary

P(i) interstitial fluid pressue

Q0822:moves fluid into capillary

π(c) plasma colloid osmotic pressure

Q0823:moves fluid out of capillary

π(i) interstitial fluid colloid osmotic pressure

Q0824:net filtration pressure=Pnet=

[Pc-Pi)-(πc-πi)];capillary pressure -interstitial pressure ;-;plasma colloid osmotic presure - interstitual fluid colloid

osmotic pressures

Q0825:Kf=

filtration constant (capillary permeability)

Q0826:excess fluid outflow into interstitium

edema

Q0827:edema is commonly caued by ___ capillary pressure(give example)

increased P(c);Heart failure

Q0828:edema is commonly caued by ___ plasmaprotiens(give example)

decreased π(c) plasma proteins ;(nephrotic syndrome; liverfailure)

Q0829:edema is commonly caused by ___ capillarypermeability (give example)

increased Kf;infections; burns

Q0830:edema is commonly caued by ___ interstitial fluidcolloid osmotic pressure;(give example)

increased πi;lymphatic blockage

Q0831:right-to-left shunts (early cyanoisis) "blue babies"

3 Ts;Tetrology;Transposition;Truncus

Q0832:Children with this type of shunt may squat to increasevenous return

right to left shunts

Q0833:Right-to Left shunts (early cyanosis) - "blue babies"

1) Tetrology of fallot;2) Transposition of great vessels;3)Truncus arteriosis;The 3 Ts

Q0834:children with this type of shunt may squat to increasevenous return.

right to left shunt

Q0835:Left to right shunts (late cyanosis) - "blue kids"

1) VSD;2) ASD;3) PDA

Q0836:this is the most common cause of early cyanosis

tetralogy of fallot

Q0837:this is the most common congenital cardiac anomaly

VSD

Q0838:this congenital heart dz manifests itself with a loud S1and a wide; fixed split S2

ASD

Q0839:this congenital heart defect is closed withindomethacin

PDA

Q0840:give the frequency of occurance with;PDA;VSD;ASD

VSD>ASD>PDA

Q0841:Uncorrected VSD; ASD or PDA leads to progressivepulmonary hypertension. As pulmonary resistance increases;the shunt reverses from L to R to R to L; which causes late

cyanosis (clubbing & polycythemia). [pic p. 228]

eisenmenger's syndrome

Q0842:Tetrology of Fallot [pic. p 228]

1) Pulmonary stenosis ;2)RVH;3) Overiding aorta (overidesVSD);4) VSD;mneu: PROVe

Q0843:most important determinant for prognosis of tetrologyof fallot

pulmonary stenosis

Q0844:ON x-ray TOF looks ________

boot shaped

Q0845:give the frequency of occurance with;PDA;VSD;ASD

VSD>ASD>PDA

Q0846:Aorta leaves RV (anterior) and pulmonary trunkleaves LV (posterior)leading to separation of systemic and

pulmonary circulations.

Transposition of great vessels

Q0847:Transposition is not compatable with life unless a_____is present to allow adequate mixing of blood;[pic p.

229]

shunt (e.g. VSD; PDA or patent foramen ovale)

Q0848:transposition of great vessels is due to failure of the_________ septum to spiral

aorticopulmonary

Q0849:this type of coarction of aorta is aortic stenosisproximal to insertion of ductus arteriosus (preductal)

infantile;INfantile: IN close to the heart

Q0850:this type of coarction of aorta is aortic stenosis isdistal to ductus arteriosus (postductal) it is associated with

notching of the ribs; hypertension in upper extremities; weakpulses in lower extremities.

adult type;aDult: Distal to Ductus

Q0851:Coarction of aorta has a male: female ratio of ____

3:01

Q0852:what is best way to diagnose coartation of aorta

femoral pulses on pysical exam

Q0853:In fetal period; shunt is right to left. In neonatalperiod; lung resistance decreases and shunt becomes L to R w/

subsequent RVH and failure. [pic p. 229]

patent ductus arteriosis

Q0854:______ is used to closed a PDA

indomethacin

Q0855:______ is used to keep a PDA open; which may benecessary to sustain life in conditions such as transposition of

the great vessels

PGE

Q0856:Congenital cardiac defect associations;22q11

truncus arteriosus; tetralogy of Fallot

Q0857:Congenital cardiac defect associations;Downsyndrome

ASD; VSD

Q0858:Congenital cardiac defect associations;Congenitalrubella

septal defects; PDA

Q0859:Congenital cardiac defect associations;Turnerssyndrome

coarctation of aorta

Q0860:Congenital cardiac defect associations;Marfan'ssyndrome

aortic insufficiency

Q0861:Congenital cardiac defect associations: Offspring ofdiabetic mother

transposition of great vessels

Q0862:Hypertension

BP >140/90

Q0863:HTN risk factors

increase age; obesity; diabetes; smoing; genetics;blck>white>asians

Q0864:90% of hypertension is this kind

essential

Q0865:essentail hypertention is related to either one of thesetwo factors

increased CO or TPR

Q0866:10% of HTN is mostly secondary to ______ dz

renal

Q0867:this type of HTN is severe and rapidly progressing

malignant

Q0868:HTN predisposes pts to (give 3)

athrosclerosis; stroke; CHF; renal failure; retinopathy; &aortic dissection

Q0869:Hyperlipidemia signs;Plaques in blood vessel walls

Atheromata

Q0870:Hyperlipidemia signs;plaques or nodules composed oflipid-laden histocytes in the skin; especially the eyelids

Xanthoma

Q0871:Hyperlipidemia signs: lipid deposits in the tendon;esp. the achilles

Tendinous xanthoma

Q0872:Hyperlipidemia signs: lipid deposit in cornea;nonspecific (arcus senilis)

corneal arcus

Q0873:This type of arteriosclerosis is in the media of thearteries; esp radial or ulnar. Usually benign.

Monckeberg

Q0874:This type of arteriosclerosis is hyalin thickening ofsmall arteries in essential hypertension. Hyperplastic "onion

skinning" in malignant hypertension.

Arteriolosclerosis

Q0875:This type of arteriosclerosis is when fibrous plaquesand atheromas form in intima of arteries

atherosclerosis

Q0876:risk factors for atherosclerosis

smoking; hypertension; dbts; hyperlipidemia; family hx

Q0877:progression of atherosclerosis;complex atheromas;fatty streaks; proliferative plaque

fatty streaks to proliferative plaque to complex atheromas

Q0878:complications of atherosclerosis (give 3)

aneurisms; ischemia; infarcts; peripheral vascular dz;thrombus; emboli

Q0879:most common location of atherosclerosis

abdominal aorta> coronary artery>popliteal artery>carotidartery

Q0880:symptoms of atherosclerosis

angina; claudication; but can be asymptomatic

Q0881:CAD narrowing >75%

angina

Q0882:retrosternal chest pain with exertion ; mostlysecondary to atherosclerosis

stable angina

Q0883:chest pain occurring at rest secondary to corony arteryspasm

prinzmetal's variant (unstable angina)

Q0884:worsening of chest paiin due to thrombosis but nonecrosis

unstable/crescendo angina

Q0885:most often acute thrombosis due to coronary arteryatherosclerosis. Results in myocyte necrosis

myocardial infarction

Q0886:death from cardiac causes within 1 hour of onset ofsymptoms; most commonly due to a lethal arrythmia

sudden cardiac death

Q0887:progressive onset of CHF over many years due tochronic ischemic myocardial damage

chronic ischemic heart dz

Q0888:infarcts occuring in loose tissues with collaterals; suchas lungs; intestine; or follwing reperfusion

red (hemorrhagic) infarcts;REd=REperfusion

Q0889:infarcts occur in solid tissues with single bloodsupply; such as brain; heart; kidney and spleen.

pale infacts

Q0890:give order of highest frequency of coronary arteryocclusion ;CFX; LAD; RCA

LAD>RCA>CFX

Q0891:symptoms of MI (give 4)

diaphoresis; nausea; vomiting; severe retrosternal pain; pain inleft arm or jaw; shortness of breath; fatigue; adrenergic

symptoms.

Q0892:How long ago did the MI occur?;Occluded artery butno visable change by light microscopy

2-4 hours

Q0893:How long ago did the MI occur?;Gross: dark mottling;pale with tetrazolium stain;Micro: coagulative nocrosis.

coagulation bands visable. release of contents of necrotic cellsinto bloodstream and the begining of neutrophil emigration.

after 4 hrs. 1st day

Q0894:How long ago did the MI occur?;Gross: hyperemicborder; central yellow-brown softening;Micro: outer zone

(ingrowth of granulation tissue); macrophages; & neutrophils

5-10 D

Q0895:How long ago did the MI occur?;Gross: grey-white;Micro: scar complete

7 weeks

Q0896:dx of MI what is gold standard in the 1st 6 hrs

ECG

Q0897:This lab test rises after 4 hours and is elevated for 7-10D.

troponin I

Q0898:this lab test is more specific than other proteinmarkers

troponin I

Q0899:This is predominantly found in myocardium but canalso be relased from skeletal mm

CK-MB

Q0900:This is nonspecific and can be found in cardiac; liverand skeletal mm cells

AST

Q0901:ECG changes include ST elevation which indicates

transmural infarct

Q0902:ECG changes include ST depression which indicates

subendocardial infarct

Q0903:ECG changes include pathological Q waves

transmural infact

Q0904:This MI complication is the most important cause ofdeath before reaching hosptial; it is common in the 1st few

days

cardiac arrhythmia

Q0905:This MI complication results in pulmonary edema

LV failure

Q0906:This MI complication has a high risk of mortaniltyand occurs when there is a large infarct

cardiogenic shock

Q0907:Rupture of ventricular free wall; interventricularseptum; or paillary mm; usually occurs _____ post MI

4-10D

Q0908:This MI complication of an MI results in decreasedCO; a risk of arrythmia; and embolus from mural thrombus

aneurism formation

Q0909:this MI complication is also known as a friction ruband occurs 3-5 D post MI

fibrinous pericarditis

Q0910:This MI complication is an autoimmune phenomenonresulting in fibrinous pericarditis; several weeks post-MI

dresslers syndrome

Q0911:This is the most common cardiomyopathy (90%)

dialated (congestive) cardiomyopathy

Q0912:In dialated (congestive) cardiomyopathy ________dysfunction ensues

systolic

Q0913:In this type of cardiomyopathy; the heart looks like abaloon on chest x-ray

dialated (congestive) cardiomyopathy

Q0914:etiology of dialated (congestive) cardiomyopathy

Alcohol ;Beriberi;Coxsackie B;Cocaine;Chagasdz;Doxorubicin;peripartum;hemochromatosis

Q0915:this type of cardiomyopathy often involves anasymetric enlargement of the intraventricular septum

hypertrophic cardiomyopathy

Q0916:In hypertrophic cardiomyopathy ______ disfunctionoccurs

diastolic

Q0917:hypertrophic cardiomyopathy is a __________ trait;and 50% are familial

autosomal dominant

Q0918:This is a very common cause of sudden death in youngathletes.

hypertrophic cardiomyopathy

Q0919:What are the heart sound findings with hypertrophiccardiomyopathy

loud S4; apical impulses; systolic murmur

Q0920:How do you tx hypertrophic cardiomyopathy

Beta blocker

Q0921:major causes of this type of cardiomyopathy includesarcoidosis; amyloidoss; postratdiation fibrosis; endocarrdial

fibroelastosis; and endomyocardial fibrosis (Loffler's)

restrictive/obliterative cardiomyopathy

Q0922:Heart Murmurs;holostolic; high piched "blowingmurmur" loudest at apex

mitral regurgitation

Q0923:Heart Murmurs: crecendo-decrescendo systolicejection murmur following ejection click. radiates to

carotids/apesx. "pulsus parvus et tardus" pulses weakcompared to heart sounds

aortic stenosis

Q0924:Heart Murmurs;holosystolic murmur

VSD

Q0925:Heart Murmurs;Late systolic murmur withmidsystolic click. Most frequent valvular lesion

mitral prolapse

Q0926:Heart Murmurs;immediate high-pitched "blowing"diastolic murmur. Wide puse pressure

aortic regurgitation

Q0927:Heart Murmurs: follows opening snap. delayedrumbling late diastolic murmur.

mitral stenosis

Q0928:Heart Murmurs: Continuous machine like murmur.Loudest at time of S2

PDA

Q0929:most common primary cardiac tumor in adults.Usually described as a "ball-valve" obstruction in the LA

myxomas.

Q0930:90% of myxomas occur in the _____

atria (mostly LA)

Q0931:Most frequent primary cardiac tumor in children;associated with tuberous sclerosis

rhabdomyomas

Q0932:Most common heat tumor (see color image 88)

metasteses

Q0933:Given the pathophysiology tell me the symptom ofCHF;failure of LV output to increase during exercise

dyspnea on exertion

Q0934:Given the pathophysiology tell me the symptom ofCHF: greater ventricular end-diastolic volume

cardiac dilation

Q0935:Given the pathophysiology tell me the symptom ofCHF;Lv ventrical failure leads to increased pulmonary venous

pressure which leads to pulmonary venous distention andtransudation of fluid.

pulmonary edema (paroxysmal nocturnal dyspnea)

Q0936:this CHF abnormality is associated with presence ofhemosiderin-laden macrophages

pulmonary edema

Q0937:Given the pathophysiology tell me the symptom ofCHF: increase venous return in supine position exacerbates

pulmonary vascular congestion

orthopnea (shortness of breath when supine)

Q0938:Given the pathophysiology tell me the symptom ofCHF: increased central venous pressure leading to increased

resistance to portal flow.

hepatomegaly (nutmeg liver)

Q0939:Given the pathophysiology tell me the symptom ofCHF: RV failure leads to increased venous pressure which

leads to fluid transudation

ankle ; sacral edema

Q0940:embolus types

Fat; Air; Thrombus; Bacteria; Amniotic fluid; Tumor;mneu:an embolus moves like a a FAT BAT

Q0941:this type of emboli are associated with long bonefractures and liposuction.

fat

Q0942:approximately 95% of pulmonary emboli arise fromwhere?

deep leg veins

Q0943:this type of emboli can lead to DIC; especiallypostpartum

amniotic fluid

Q0944:this type of embolus is associated with chest pain;tachypnea; and dyspnea

pulmoary embolus

Q0945:compression of heart by fluid (i.e;blood) inpericardium; leading to decreased cardiac output and

equilibration of pressures in all four chambers.

cardiac tamponade

Q0946:youre pt presents with hypotension; JVD; and distantheart sounds. He shows pulsus paradoxus and ECG shows

electrical alternans

cardiac tampanad

Q0947:pulsus paradoxus

(exaggeration of nml variation in the systemic arterial pulsevolume with respiration-- becoming weaker with inspiration

and stronger with expiration)

Q0948:electrical alternans

(beat to beat alterations in QRS complex height)

Q0949:Symptoms of bacterial endocarditis

Fever;Roth spots;osler nodes;Murmur (new);Janewaylesions;Anemia;Nail-bed hemorrhage;Emboli;;mneu: bacteria

FROM JANE

Q0950:osler nodes

tender raised lesions on finger or toe pads

Q0951:Roth's spots

round white spotss on retina surrounded by hemorrhage

Q0952:Janeway lesions

small erythematous lesions on palm or sole

Q0953:What is the most frequently involved valve in bacterialendocarditis

mitral valve

Q0954:What valve is associated with endocarditis associatedwith IV drug abuse

tricuspid valce

Q0955:what are some of the complications associated withbacterial endocartitis (give 2)

chordae rupture;glomerulonephritis;supportivepericarditis;emboli

Q0956:acute endocarditis has a rapid onset. It results fromlarge vegetations on previously normal valves. It is most often

caused by this bug.

S. aureus (high virulence)

Q0957:Subacute bacterial endocarditis has a more insidiousonset. It consists of smaller vegetations on congentitallyabnormal or diseased valves. It can be a sequela of dental

procedures. Often caused by this bug

viridans streptococcus (low virulence)

Q0958:endocarditis may also be nonbacterial and secondaryto these 2 conditions

metastasis or renal failure (marantic/ thrombotic endocarditis)

Q0959:In this condition; associated with lupus; vegetationsdevelop on both sides of valve leading to mitral valve stenosis

but do not embolize

libman-sacks endocarditis;mneu: SLE causes LSE

Q0960:Rhematic heart dz is a late consequence of pharyngealinfection with this organism

a beta hemolytic streptococci

Q0961:rhematic heart dz affects heart valves in this order

mitral>aortic>>tricuspid;mneu: high pressure valvesassociated most.

Q0962:Give the symptoms of rheumatic heart dz

Fever;Erythema marginatum;Valvular damage;ESR (high);Red-hot joints (polyartheritis);Subcutaneous nodules;St. Vitus'

dance (chorea);mneu: FEVERSS

Q0963:This is associated with Aschoff bodies; migratorypolyarthritis; erythema marginatum; elevated ASO titers.

Rheumatic heart dz

Q0964:is rheumatic heart dz immune mediated or the directeffect of bacteria

immune mediated

Q0965:Associated ith Aschoff bodies and Anitschkow's cells

rheumatic heart dz;mneu: think of 2 RHussians withRHeumatic heart dz (Aschoff & Anischkow)

Q0966:Aschoff bodies

granuloma with giant cell

Q0967:Anitschkow's cells

activated histiocytes

Q0968:This condition presents with pericardial pain; frictionrub; ECG changes (diffuse ST elevation in all leads) pulsus

paradoxus; distant heart sounds

pericarditis

Q0969:pericarditis can resolve without scarring however;scarring can lead to this

chronic adhesive or chronic constrictive pericarditis

Q0970:this type of pericarditis is caused by SLE; rheumatoidarthritis; infection; or uremia

serous pericarditis

Q0971:this type of pericarditis is caused by uremia; MI;rheumatic fever

fibrinous pericarditis

Q0972:this type of pericarditis is caused by TB ormalignancy (e.g; melanoma)

hemorrhagic

Q0973:this dz disrupts the vasa vasora of the aorta withconsequent dilation of the aorta and valve ring. It often effectsthe aortic root and results in calcification of ascending arch of

the aorta

syphalitic heart dz (tertiary syphalis)

Q0974:This dz can result in aneurism of the ascending aortaor aortic arch and aortic valve incompetence.

syphalitic heart dz (tertiary syphalis)

Q0975:This Rx used for HTN has the adverse effect ofHYPOKALEMIA; slight hyperlipidemia; hyperuricemia;

lassitude; hypercalcemia; hyperglycemia

hydrochlorothiazide (diuretic)

Q0976:This Rx used for HTN has the adverse effect ofpotassium wasting; metabolic alkalosis; hypotension;

ototoxicity

loop diuretics

Q0977:This sympathoplegic used in the tx of HTN has theadverse effect of dry mouth; sedation; severe rebound HTN

clonidine

Q0978:This sympathoplegic used in the tx of HTN has theadverse effect of sedation; positive Coomb's test

methyldopa

Q0979:This sympathoplegic used in the tx of HTN has theadverse effect of severe orthostatic hypotension; blurred

vision; constipation; sexual disfunction

hexamethonium

Q0980:This sympathoplegic used in the tx of HTN has theadverse effect of sedation; depression; nasal stuffiness;

diarrhea

reserpine

Q0981:This sympathoplegic used in the tx of HTN has theadverse effect of orthostatic and exercise hypotension; sexual

dysfunction; diarrhea

Guanethidie

Q0982:This sympathoplegic used in the tx of HTN has theadverse effect of 1st dose orthostatic hypotension; dizziness;

headache

Prazosin

Q0983:This sympathoplegic used in the tx of HTN has theadverse effect of impotence; asthma; bradycardia; CHF; AV

block; sedation & sleep alterations

B blockers

Q0984:This vasodialator used in the tx of HTN has theadverse effect of nausea; headache; lupus-like syndrome;

reflex tachycardia; angina; salt retension

hydralazine

Q0985:This vasodialator used in the tx of HTN has theadverse effect of hypertrichosis; pericardial effusion; reflex

tachycardia; angina; salt retension

minoxidil

Q0986:This vasodialator used in the tx of HTN has theadverse effect of dizziness; flushing; constipation; nausea

nifidipine; veripamil (constipation)

Q0987:This vasodialator used in the tx of HTN has theadverse effect of cyaide toxicity (releases CN)

nitroprusside

Q0988:This ACE inhibitor used in the tx of HTN has theadverse effect of;Hyperkalemia; Cough; Angioedema;Proteinuria; Taste changes; hypOtension; Pregnancy

problems (fetal renal damage); Rash; Increased renin; Lowerangiotensin II

Captopril;mneu:CAPTOPRIL-Cough; Angioedema;Proteinuria; Taste changes; hypOtension; Pregnancy


Q0989:This angiotensin II receptor inhibitor has theadverseeffect of fetal renal toxicity; hyperkalemia

Losartan

Q0990:This vasodialator used in the tx of HTN has theadverse effect of hypertrichosis; pericardial effusion; reflex

tachycardia; angina; salt retension

minoxidil

Q0991:This vasodialator used in the tx of HTN has theadverse effect of dizziness; flushing; constipation; nausea

nifidipine; veripamil (constipation)

Q0992:This vasodialator used in the tx of HTN has theadverse effect of cyaide toxicity (releases CN)

nitroprusside

Q0993:This ACE inhibitor used in the tx of HTN has theadverse effect of;Hyperkalemia; Cough; Angioedema;Proteinuria; Taste changes; hypOtension; Pregnancy


Captopril;mneu:CAPTOPRIL-Cough; Angioedema;Proteinuria; Taste changes; hypOtension; Pregnancy


Q0994:The MOA of this drug used for severe HTN & CHFis that it increases cGMP leading to smooth mm relaxation. It

vasodilates arterioles > veins resulting in a reduction ofafterload

hydralazine

Q0995:Toxicity of this drug for severe HTN & CHF includecompensitory tachycardia; fluid retension; & lupus like

syndrome

hydralazine

Q0996:The druges Nifedipine; verapamil & diltiazem belongto this category

calcium channel blockers

Q0997:The MOA of these drugs is that they block voltage-dependent L-type calcium channels of cardiac and smooth

muscle and thereby reduce mm contractilty

calcium channel blockers

Q0998:give the order of potency of the 3 CCBs (nifedipine;verapamil; diltiazem) in;1) the heart;2)vascular smooth mm

heart-verapamil>diltiazem>nifedipine;vascular sm mm--;nifedipine>diltiazem>verapamil

Q0999:CCBs are used in hypertension but also in these 2conditions

angina; arrythymias (not nifedipine)

Q1000:These drugs produce a toxicity of cardiac depression;peripheral edema; flushing; dizziness; & constipation

CCBs

Q1001:These 2 drugs used for angina; pulmonary edema; andas an erection enhancer have a MOA of vasodilating by

releasing NO in smooth mm; causing an increase in cGMP andsmooth mm relaxation. They dialate vv>>arteries resulting in

a decrease in preload

nitroglycerine; isosorbide dinitrate

Q1002:toxicity of these drugs include tachycardia;hypotension; headache; "Monday dz" in industrial exposure;

development of tolerance for the vasodilating action during thework week and loss of tolerance over the weekend; resulting

intahycardia; dizziness; and headache.

nitroglycerin; isosorbide dinitrate

Q1003:What are the 2 major Rxs used in the tx of antianginaltherapy

nitrates & B blockers

Q1004:In antianginal therapy the goal is to do what?

reduce myocardial O2 consumption.

Q1005:In order to reduce myocardial O2 consumption youneed to decrease 1 or more of the determinants of MVO2

which are give 2(5)

1)EDV;2)BP;3)HR;4) contractility;5) ejection time

Q1006:Used for antianginal therapy Nitrates reduce _______(preload or afterload)

preload

Q1007:Used for antianginal therapy B-blockers reduce_______ (preload or afterload)

afterload

Q1008:For each of the determinants of myocardial O2consumption (MVO2). 1) Give the effect that Nitrates have.

2) that B-blockers have.3) And that Nitrates + B-blockrshave;EDV

N (preload):decreased ;BB (afternoad):increased ;C: no effector decreased


2) that B-blockers have.3) And that Nitrates + B-blockrshave;BP

N (preload):decreased ;BB (afternoad):decreased ;C:decreased


2) that B-blockers have.3) And that Nitrates + B-blockrshave;Contractility

N (preload):increased (reflex response);BB(afternoad):decreased ;C:little or no effect


2) that B-blockers have.3) And that Nitrates + B-blockrshave;HR

N (preload):increased reflex response;BB(afternoad):decreased ;C:decreased


2) that B-blockers have.3) And that Nitrates + B-blockrshave;Ejection time

N (preload):decreased ;BB (afternoad):increased ;C:little or noeffect


2) that B-blockers have.3) And that Nitrates + B-blockrshave;MVO2

N (preload): decreased ;BB (afternoad): decreased ;C:decreased decreased

Q1014:CCBs: Nifedipine is similar to ________ (nitrates or Bblockers); Verapamil is similar to ________nitrates or B

blockers)

Nitrates ;B blockers

Q1015:Cardiac drugs: sites of action

1) Digitalis (-);2) CCB (-);3) B blockers;4) Ryanodine (+);5)Ca++ sensitizers

Q1016:This cardiac drug inhibits Na+/K+ ATP ase

digitalis

Q1017:These 2 cardiac drugs inhibit on voltage gated Ca++channels

CCBs;B blockers

Q1018:This cardiac drug sensitizes Ca++ release channel inthe SR

Ryanodine

Q1019:These cardiac drug is a site of Ca+ interaction withtroponin-tropomyosin system

Ca++ sensitizers

Q1020:This cardiac glycoside has 75% bioavalibility; is 20-40% protein bound; has a half life of 40 hours and is excreted

in the urine

digoxin

Q1021:the MOA of this drug is that it inhibits the Na+/K+ATPase of the cardiac sarcomere; causing an increase in

intracellular Na+. Na+-Ca++antiport does not function asefficiently; casing an increase in intracellular Ca++; leading to

positive inotropy.

digoxin

Q1022:this drug may cause an elevated PR; a depressed QT; ascooping of ST segment; and a T-wave inversion on ECG

digoxin

Q1023:The clinical uses for this drug include 1) ________ dueto increased contractility 2) _______ due to decreased

conduction at AV node

1) CHF;3) atrial fibrillation

Q1024:toxicity of this drug includes N/V/D. Blurry yellowvision. Arrhythmia.

digoxin

Q1025:Digoxins toxicities are increased by_________(decreased excretion); _______(potentiates drug's

effects) ; and _________ (decreases digoxin clearance anddisplaces dignoxin from tissue binding sites

renal failure ;hypokalemia ;quinidine

Q1026:What is the treatment for digoxin toxicity

slowly normalize K+;lidocaine;cardiac pacer;anti-dig Fabfragments

Q1027:antiarrythmics (Class I) are _____ channel blockers

Na+

Q1028:antiarrythmics (Class II) are _____ blockers

Beta

Q1029:antiarrythmics (Class III) are _____ channel blockers

K+

Q1030:Thhs class of antiarrhthmics are local anesthetics.They act by slow or decreasd conduction. They decrese theslope of phase 4 ddepolarization and increase threshhold for

firing in abnormal pacemaker cells.

antiarrhythmics-Na+ channel blockers (class I)

Q1031:antiarrhythmics-Na+ channel blockers (class I) arestate dependent meaning what

they selectively depress tissue that is frequently depolarized(e.g; tachycardia

Q1032:this class of antiarrhythmics has 3 subcategories A; B;& C

antiarrhythmics-Na+channel blockers (class I)

Q1033:this class of antiarrythmics includes Quinidine;Amiodarone; Procainamide; Disopyramide.

Class IA;mneu: Queen Amy Proclaims Diso's PYRAMID

Q1034:This class of antiarrhytmics has an increased APduration; increased effective refractory period (EERP;

increased QT interval. It can affect both atrial and ventriculararrhythmias

IA

Q1035:This member of class IA antiarrhytmics has toxicitiesthat include (cinchonism-headache; tinnitis;

thrombocytopenia; torsades de pointes due to prolonged QTinterva)

quinidine

Q1036:This member of class IA antiarrhytmics has toxicitiesthat include reverible SLE-like syndrome

procainamide

Q1037:This class of antiarrythmics include lidocainemexiletine; tocainide

IB (Na+ channel blockers)

Q1038:this class of antiarrythmics acts to decrease APduration. It effects ischemic or depolarized purkinje and

ventricular tussue. It is useful in acute ventricular arrhytmias(especially post-MI) and i digitalis-induced arrhythmias.


Q1039:This class of antiarrhytmics has toxicities that includelocal anesthetic effects; CNS stimulation/depression;

cardiovascular depression


Q1040:This class of antiarrhythmics includes flecainide;encainide; propafenone.

class IC (Na+ channel blockers.

Q1041:This class of antiarrhythmics has no effect on APduration. It is useful in V-tachs that progress to VF and

intractable SVT. Usually used only as last result in refractorytachyarrythmias.


Q1042:Toxicities of this class of antiarrhythmics includesarrythmias; especially post MI (CONTRAINDICATED)


Q1043:picture p. 242 Class I antiarrythmics (Na+ channelblockers)

1) IA;2) IB;3) IC

Q1044:This clas of antiarrythmics includes propanolol;esmolol; metroprolol; atenolol; timool.

Beta Blockers (Class II)

Q1045:This class of antiarrythmics acts by decreased cAMP;decreased Ca+ currents; and by supressing abnormal

pacemakers by decreased slope of phase 4. The AV node isparticularly sensitive resulting in increaed PR interval

B-blockers (Class II antiarrythmics)

Q1046:this is the shortest acting B blocker

esmolol

Q1047:Toxicities of this class of antiarrythmics includeimpotence; exacerbation of asthma; CV effects (bradycardia;AV block; CHF); CNS effects (sedation; sleep alterations). It

may mask signs of hypoglycemia.

B-blockers (Class II antiarrythmics)

Q1048:This class of antiarrythmics includes Sotalol; ibutilide;bretylium; & amiodarone

K+ channel blockers (class III)

Q1049:This class of antiarrythmics acts by increased APduration; increased ERP. It thends to increased QT interval.

It is used when other antiarrhythmics fail.

K+ channel blockers (class III)

Q1050:This class III antiarrythmic has toxicities whichinclude torsades de pointes and excessive beta block

sotalol

Q1051:This class III antiarrythmic has toxicities whichinclude new arrhytmias& hypotension

bretylium

Q1052:This class III antiarrythmic has toxicities whichinclude PULMONARY FIBROSIS; HEPATOTOXICITY;

HYPOTHYROIDSIM/HYPERTHYROIDISM; cornealdeposits; skin depsits resulting in photodermatiitis; neurologic

effects; constipation; CV effects (bradycardia; heart block;CHF

amiodarone;mneu: remember to check PFTs; LFTs; and TFTswhen using amiodarone.

Q1053:This class of antiarrythmics include the drugsverapamil; and diltiazem.

Ca++ channel blockers (class IV)

Q1054:The MOA of this class of antiarrythmics is primarilyon AV nodal cells. They decreased conduction velocity;

increased ERP; increased PR interval.


Q1055:this class of antiarrythmics is used in prevention ofnodal arrhythmias (e.g; SVT)


Q1056:Toxicity of this class of antiarrythmics can includeconstipation; flushing; edema; CV effects (CHF; AV block;

sinus node depression; & torsades de pointes.


Q1057:Other antiarrythmics: this antiarrhythmic is the drugof choice in diagnosing/abolishing AV nodal arrhythmias

adenosine

Q1058:Other antiarrythmics: this antiarrhythmic depressesectopic pacemakers; especially in digoxin doxicity

K+

Q1059:Other antiarrythmics: this antiarrhythmic is effectivein torsades de pointes and digoxin toxiciity

Mg+

Q1060:cardiac output(CO) formula

rate of O2 consumption/;(arterial O2 content - venous)

Q1061:mean arterial pressure (MAP) formula

MAP = CO - TPR;MAP also = 1/3 systolic + 2/3 diastolic

Q1062:stroke volume (SV) formula

SV = CO/ HR;SV also = EDV-ESV

Q1063:cardiac output variables

SV CAP ;->SV is affected by Contractility; Afterload andPreload

Q1064:contractility/SV increases due to

increased catecholamines (high activity of Ca pump inSR);increased [Ca]i;decreased [Na]e;digitalis admin (increases

intracellular Na which leads to increased [Ca]i)

Q1065:contractility/SV decreases due to

B1 blockers;heart failure;acidosis;hypoxia/hypercapnea;Cachannel blockers

Q1066:force of contraction [starling curve

is proportional to the initial length of cardiac muscle fiber[PRELOAD]

Q1067:ejection fraction (EF) formula

EF = SV/EDV = (EDV-ESV)/EDV;EF is an index ofventricular contractility;EF should be >/= 55%

Q1068:resistance/pressure/flow formula

change in P = Q x R;Q = flow; R = resistance;R= 8 x viscosityx length/;pi radius ^4;*viscostity increased in;polycythemia;

high protein and hereditary spherocytosis

Q1069:JVP waves

a: atrial contraction;c: RV contraction(when tricuspid bulgesback into RA);v: increased atrial pressure due to atrial filling

against closed tricuspid valve

Q1070:cardiac myocyte vs skeletal myocytes

cardiac muscle;-> AP has a plateau ;-> nodal cellsSPONTANEOUSLY depolarize [automaticity];-> myocytesare electrically coupled via gap jxns;**contraction is due to

extracellular Ca

Q1071:AP in atrial/ventricular myocytes and purkinje fibers

phase O: rapid upstroke (Na);1: intial repol (inactivation ofNa channels);2: plateau (Ca influx balances slowly increasing

K efflux);3: rapid repol (massive K efflux due to slow Kchannels and closure of Ca channels);4: resting potential (Kand Ca leak currents + Na/K ATPase and Na/Ca exchanger)

Q1072:AP in pacemaker cells

phase 0: upstroke due to Ca channels; NO fast Na channels;2:no plateau (pointy);4: slow diastolic depol (I-f accounts for

automaticity of SA/AV nodes);**slope of phase 4 in SA nodedetermines heart rate**

Q1073:wolf parkinson white syndrome

accessory conduction pathway from atria toventricle;bypasses the AV node;**see a DELTA WAVE

before QRS complex;can lead to SVTs

Q1074:1st degree AV block

PR interval prolonged (>200 msec);is asymptomatic

Q1075:2nd degree AV block

mobitz type 1;->progressive lengthening of PR until a beat isdropped. asymptomatic;mobitz type 2;->dropped beats not

proceeded by change in PR length. is symptomatic: 2 P wavesto 1 QRS

Q1076:3rd degree AV block [complete heart block]

atria and ventricles beat independantly;P waves have norelation to QRS;atrial rate > ventricular;*Tx = pacemaker;rate

of ventricular beat: 30-45;stroke volume is increased (highpulse pressure)

Q1077:O2 demand in heart

high O2 demand drives increased blood flow; NOT increasedextraction of O2

Q1078:fluid pressure [hydrostatic] starling forces

Pc = capillary fluid pressure;-> fluid out of capillary;Pi =interstitial fluid pressure;-> fluid into capillary

Q1079:colloid pressure starling forces

pi-c: plasma colloid osmotic p;-> moves fluid intocapillary;pi-i: interstitial colloid p;-> moves fluid out of

capillary

Q1080:right to left shunts

=early cyanosis (blue babies);Teratology ofFallot;Transposition of great arteries;Truncus arteriosus

Q1081:left to right shunts

VSD (#1 congenital anomaly);ASD (loud S1; fixed splitS2);PDA (close w/indomethacin)

Q1082:teratology of Fallot

PROVe;Pulmonary a. stenosis (Px feature);RVH;Overridingaorta (overrides VSD);VSD;*pts suffer 'cyanotic

spells';caused by anteriosuperior displacement of aorta

Q1083:transposition of great vessels

aorta leavse RV and pulm trunk leaves LV (posterior);notcompatible with life unless shunt is present to mix systemic

and pulm circulations (VSD; pDA or pFO)

Q1084:coarctation of aorta

infants: aortic stenosis proximal to insertion of DA;adults:distal to DA;-> notching of ribs; HTN in upper extremities;

weak pulses in lower extremities;-> 3:1 male to femaleratio;**ass'd with Turner Syndrome

Q1085:patent DA

in fetal pd; shunt R to L (bypasses pulmonarycirculation);birth = lung resistance drops and shut becomes L

to R which causes RVH and R heart failure;*continuousmachine like murmur;patency = low O2 tension; PGE

Q1086:congenital cardiac defects

22q11: truncus arteriosus; teratology of fallot;Ts21: ASD orVSD;rubella: septal defects; pDA;turner's: coarctation of

aorta;marfan's: aortic insufficiency;mom w/DM: transpositionof great vessels

Q1087:monckeburg arteriosclerosis

calcification of arteries; especially radial or ulnar;usuallybenign

Q1088:arteriolosclerosis

hyaline thickening of small arteries due to essentialhypertension;ONION SKINNING in malignant HTN

Q1089:cardiovascular system is derived from which celllayer?

mesoderm;paired endocardial heart tubes from in cephalicregion

Q1090:primitive embryonic heard dilates into five areas(starting at weeks 5-8):

from cranial to caudal;-truncus arteriosus: proximal aorta andproximal pulm artery;-bulbus cordis: smooth parts of rightventricle and LV;-primitive ventricle: RV; LV;-primitive

atrium: RA and LA;-sinus venosus (R and L): smooth part ofRA; coronary sinus; oblique vein

Q1091:pathophysiology of teratology of Fallot

aberrant development of aortico-pulmonary septum [whichshould normally divide aorta and pulmonary trunk]

Q1092:development of aortic arches

6 paired aortic arches at 1st;->arch 3: common carotids;->4:aorta and proximal subclavian artery;->6: DA and pulmonary

trunk

Q1093:developent of veins

vitelline veins: ductus venosus carries O2 blood from placentato fetus;L umbilical vein: ligamentum teres hepatis;R umbilical

vein: regresses

Q1094:paradoxical emboli

originate in the venous circulation and pass through pFO orASD to produce symptoms on arterial side

Q1095:situs inversus

all body's organs are transposed ;associated with Kartagener'ssyndrome [immotile cilia]

Q1096:Eisenmerger's syndrome

change of L to R to R to L shunt secondary to increasingpulmonary HTN;often result of chronic response to VSD

Q1097:acquired arteriovenous fistula

decreased TPR leads to increased CO (increased HR andSV);diastolic bp falls b/c blood rapidly exits arterial

system;but mean bp is relatively normal b/c regulatingmechanisms are normal

Q1098:change in pulse pressure with arteriosclerosis

increases (b/c arteries have hardened; need to push harder[higher systolic bp] to get the blood out)

Q1099:type of endocarditis in pts with SLE

Libman-Sacks;->small granular vegetations consisting of fibrindevelop on mitral and aortic valves;->leads to aortic stenosis

Q1100:premortum thrombus

look for Lines of Zahn (composed of platelets);->b/c hasformed over a period of time;often due to atrial fibrillation

Q1101:pathology of repeated episodes of stable angina

gradual loss of myocytes;->small patches of fibrosis andvacuolization;->usually in subendocardial area (poorly

perfused)

Q1102:thoracic outlet syndrome with the presence of acervical rib

subclavian artery compressed btwn scalenus anterior and therib;=pain and tingling on affected side

Q1103:effect of severe anemia

wide pulse pressure;->resting CO is increased due toincreased SV and HR;also see tachycardia

Q1104:causes of decreased pulse pressure

aortic valve obstruction;cardiac tamponade;heart failure;mitralvalve obstruction

Q1105:effect of malignant hypertension on arteriole structure

arteriolar rarefaction;=dissolution and loss of arterioles;-due tolong term over-perfusion of tissues;also; arteriolar wall to

lumen ratio INCREASES (thicker wall)

Q1106:syphilitic aneurysm

massive dilation of aortic root with absence ofatherosclerosis;histo = plasma cell lesion in vasa vasorum thatsupply the aorta [eventually obliterate it and cause aneurysm]

Q1107:cyanosis

only from R-L shunt

Q1108:signs of cardiac tamponade

decreased arterial pressure;small; quiet heart;hypotension;tachypnea; tachycardia; increased JVP;*pulsus paradoxus

Q1109:signs of pericarditis

sharp; knife like pain;->usually related to breathing;diffuseSTEs and upright T waves;pericardial rub MAY be present

Q1110:location of femoral vein on CT

medial to femoral artery;('venous toward the penis')

Q1111:typical bp of someone with aortic regurgitation

wide pulse pressure (160/80);systemic pressure drops duringdiastole b/c blood flows back thru aorta into LV

Q1112:most common cause of sudden cardiac death (SCD)

ischemic heart disease;*in younger patients; the non-atherosclerotic causes are more common;->hypertrophy;

MVP; myocarditis; dilated cardiomyopathy; etc

Q1113:Kawasaki disease

'mucocutaneous lymph node syndrome';leading cause ofacquired heart disease in kids in the US;all sizes of arteries

affected;*risk of coronary artery aneurysm

Q1114:positive result in starling equation

=net fluid leaving capillaries;(Pc-Pi) - (pi c - pi i)

Q1115:Dressler's syndrome

autoimmune phenomenon several weeks post-MI;->fibrinouspericarditis

Q1116:dilated cardiomopathy

90% of all cardiomyopathies;Alcohol; Beriberi; Coxsackie B;Cocaine; Chagas'; Doxorubicin toxicity [chemo]; peripartum;

hemochromatosis;-> SYSTOLIC dysfunction

Q1117:hypertrophic cardiomyopathy

often asymmetric; involves intraventricular septum;50%familial (AD);sudden death in young athletes;loud S4**;

strong apical impulse; systolic murmur;treat with B-blockers;-> DIASTOLIC dysfunction

Q1118:restrictive/obliterative cardiomyopathy

sarcoidosis; amyloidosis; postradiation; Loffler's

Q1119:MR

holosystolic;high pitched; 'blowing';loudest at apex

Q1120:AS

crescendo-decrescendo systolic; following an ejection click;LV>> aortic pressure in systole;radiates to carotids;

apex;*pulsus parvus et tardus*

Q1121:VSD

holosystolic

Q1122:MVP

late systolic murmur;midsystolic click;#1 valvular lesion

Q1123:AR

high pitched blowing diastolic;associated with wide pulsepressure

Q1124:MS

delayed rumbling late diastolic;follows opening snap;LA >>LV during diastole (takes a lot to open the stenoticMV);**tricuspid stenosis murmur gets louder with

INSPIRATION** (b/c more blood to lungs)

Q1125:pDA murmur

continuous; machine like;throughout systole anddiastole;loudest at S2 (aortic/pulmonic close)

Q1126:'heart failure cells'

hemosiderin laded macrophages

Q1127:cause of orthopnea in CHF

increased venous return in supine position;exacerbatespulmonary vascular congestion (= SOB)

Q1128:virchow's triad

stasis;hypercoagulability;endothelial damage;leads to DVTs

Q1129:features of cardiac tamponade

compression of heart by fluid leads to low CO;equilibration ofpressures in all 4 chambers**;hypotension; high JVP; pulsus

paradoxus

Q1130:Aschoff bodies

=granulomas with giant cells;found in rheumatic heartdisease;also see Anitschkow's cells (activated histiocytes)

Q1131:hydralazine

increases cGMP: sm musc relaxation;vasodilates arterioles >veins;REDUCED AFTERLOAD;SEs: tachycardia; fluid

retention; lupus like syndrome

Q1132:CCBs

block L-type Ca channels;->reduced cardiaccontractility;nifedipine better vascular sm muscle;verapamilbetter heart muscle;SEs: cardiac depression; edema; flushing;

constipation

Q1133:nitroglycerine; isosoribde dinitrate

release NO in smooth muscle: increased cGMP ;veins >>arteries;REDUCED PRELOAD;for angina; pulmonary edema

Q1134:digoxin

inhibits Na/K/ATPase;->increased Na-i leads to increased Ca-i(b/c Na won't come in using Na/Ca antiport);EKG changes;->low QT; scooping of ST; T wave inversion*;used for CHF;

a-fib (low AV);SEs;-> n/v; van gogh vision; arrhymthmias

Q1135:Digoxin drug interaction

increased [ ] with renal failure;hypokaleima potentiates effects(low K = more K out; Na in);quinidine decreases

clearance;*treat Dig toxicity with K+ admin (or Mg+)

Q1136:beta blockers with intrinsic sympathomimetic activity

acebutolol and pindolol;not recommended for pts with angina(can exacerbate)

Q1137:CCBs to avoid in those with CHF

verapamil;->1st gen CCB that has strong negative inotropiceffect;dilitiazem;->mild to mod negative inotrope;*amlodipine

and felodipine are used in CHF pts (can actually increasecontractility)

Q1138:treatment of WPW

don't use an agent that slows AV node conduction (willincrease propensity to go to bypass tract);DO use ibutilide(K channel blocker);->disrupts reentry circuits and increases

refractory period of the bypass tract

Q1139:acute treatment of atrial fibrillation

dilitiazem (IV);-inhibits Ca into vascular sm muscle andmyocardium;-AV node blocker;*amiodarine takes 1-3 weeks

to work properly

Q1140:most common cardiac anomaly in Ts21

endocardial cushion defect (??);or maybe ASD/VSD;20% havecongenital cardiac abnormalities

Q1141:mean linear velocity of a RBC is lowest in whatvessels?

capillaries (have the largest cross-sectional area);velocity fromhighest to lowest;aorta > vena cavae > large veins > smallarteries > arterioles > small veins > venules > capillaries

Q1142:Churg-Strauss syndrome

aka allergic granulomatosis and angiitis;variant of PAN-->ass'd with asthma and eosinophilia;vascular lesions;

granulomas; GI vasculitis

Q1143:polyarteritis nodosa (PAN)

affects small/med arteries;->esp GI tract and kidneys;fibrinoidnecrosis of vessels w/ polys; eos; monos;often young adult

males;Tx: steroids; cyclophosphamide

Q1144:severe anemia's affects on vessels

hypoxia causes dilation of small arterioles and arteries;also:low blood viscosity; decreased PVR; low splanchnic blood

flow

Q1145:most common primary cardiac tumor in children

rhabdomyoma;composed of cells that resemble skeletalmuscle;**common in kids with tuberous sclerosis

Q1146:mechanism of cocaine-induced hypertension

blocks re-uptake of NE

Q1147:arterioles account for ___% of total peripheralresistance

50% (greatest fall in bp occurs as blood goes thru arterioles);-highest ratio of wall to cross-sectional area to lumen cross-

sectional area

Q1148:leukocytoclastic angiitis

=microscopic PAN;smaller affected vessels;vasculitisw/hemorrhage to skin (palpable purpura);many fragmented

neutrophils;*penicillin is a common trigger

Q1149:vascular structures that contain the greatest % of totalblood volume

venules and veins (64%)

Q1150:week of gestation when heart forms

4th week;(heart forms and starts beating almostimmediately);6th week = heart is fully formed (so difficult to

prevent congenital malformations b/c heart forms so early)

Q1151:alpha1 agonists act on;

smooth muscle cells in media of arterioles;leads to increase inintracellular Ca [smooth muscle contraction]

Q1152:ASD found in Down's syndrome

ostium primum (most common type in general is the ostiumsecundum);can also be associated with tricuspid and mitralvalve abnormalities;*L-R shunts with late cyanosis (when

reversal occurs)

Q1153:mean systemic filling pressure (MSFP)

pressure that exists when heart has been stopped and bloodhas been redistribuited equally;as MSFP increases; there ismore venous return to heart;**venous system is importantblood reservoir (normal fxn can be resored w/20% of blood

loss)

Q1154:when O2 consumption of the heart increases; thisbuilds up in heart muscle

adenosine;(ATP degrades to adenosine);adenosine then dilatesvessels allowing increased coronary blood flow

Q1155:graft vascular disease (aka graft arteriosclerosis)

develops years after transplant;intimal thickening of coronaryarteries w/out atheroma formation or inflammation;leads toprogressive stenosis;chest pain DOES NOT accompany theischemia--> sudden death;**can't be prevented with current

immunosuppresive Tx

Q1156:this decreases in old age and causes widened pulsepressure

arterial compliance (usually due to hardening byarteriosclerosis)

Q1157:cardiac complications of fragile X syndrome

mitral valve prolapse and aortic root dilatation ;[occur late inadolescence or adulthood]

Q1158:___% of those with ischemic heart disease will presentwith death

25%

Q1159:Beta-1 selective beta blockers

A BEAM;atenolol; betaxolol; esmolol; acebutalol;metroprolol;non-selective: labetalol (also adds alpha 1);

timolol; nadolol

Q1160:individual cardiac muscles are joined together at

intercalated disks (that contain gap jxns)

Q1161:fetal umbilical arteries arise from

the fetal iliac arteries (supply unoxygenated blood to theplacenta);umbilical vein takes newly oxygenated blood from

placenta to fetal liver then to IVC via the ductus venosus

Q1162:fibrinous and serofibrionous pericarditis

= Dresseler's syndrome (when following an acute MI)

Q1163:why is atenolol contra-indicated in DM pts?

b/c it can block the 'warning signs' of hypoglycemia

Q1164:what is a cystic hygroma??

lymphatic malformations resembling hemangiomas;-->afeature of Turner syndrome that contributes to the 'webbed

neck';(and remember; Turner is associated with coarctation ofthe aorta)

Q1165:side effect of metroprolol

dyslipidemia

Q1166:ovary drainage

R ovary = ovarian vein to IVC;L ovary = ovarian vein toRENAL VEIN to IVC

Q1167:best drug for initial treatment of hypertrophiccardiomyopathy

beta blocker (metoprolol);Sx: sustained apical impulse; loudS4; systolic ejection murmur;echo = systolic anterior motionof mitral valve; assymetic LVH; early closing of aortic valve

Q1168:appearance of amyloidosis

waxy texture of affected organs;histo = positive Congo redstaining

Q1169:TPR

(MAP-RAP) / CO;pressure = flow x resistance;(P = Q x R)

Q1170:removing an organ will ___ the TPR

INCREASE;(organs are in parallel; and adding parallelresistances = lower total)

Q1171:fully compensated aortic coarctation

blood flow normal in upper and lower body ;but there isincreased arterial pressure in upper body;->lower vascularresistance in lower body (b/c resistance = pressure / flow)

Q1172:possible finding at autopsy of a SIDS baby

RVH

Q1173:endocardial fibroelastosis

probably related to intrauterine viral infection(mumps);thickened endocardium w/fibrous and elastic

tissue;LV is most commonly involved;other findings = muralthrombi; flattened trabeculae and stenosed valves;*infantile

and adolescent forms

Q1174:artery commonly damaged in knee dislocations

popliteal artery;-divides into anterior tibial; posterior tibialand peroneal;-emerges from superficial femoral artery

Q1175:classical findings in ASD

prominent RV impulse;systolic ejection murmur heard inpulmonic area;fixed split S2;*due to abnormal L-R shunt

[creates volume overload on R side]

Q1176:massive PE affects which part of the heart first?

RV ;[a saddle PE causes acute cor pulmonale with abrupt RVdilation];*acute cor pulmonale is a surgical emergency

Q1177:cardiac tamponade causes build up of fluid in whichspace?

between the epicardium [visceral pericardium] and parietalpericardium;(aka the pericardial space)

Q1178:PO agent similar to lidocaine

mexiletine;(class IB anti-arrhythmic for treatment of VT);Nachannel blocker and shortens AP duration

Q1179:Which hormone increases HCl secretion by parietalcells; pepsinogen secretion by chief cells?

Gastrin

Q1180:What are the actions of CCK?

Stimulates gall bladder contraction and relaxes sphincter ofOddi to allow pancreatic enzyme secretion.

Q1181:Which hormone increases blood flow to the intestines?

CCK

Q1182:Which hormone is stimulated by low pH to increasepancreatic bicarb secretion and increase bile production (and

decrease gastric H production?)

Secretin

Q1183:Which hormone increases insulin release and decreasesgastric H+ secretion?

GIP

Q1184:Which hormone is turned on in the fasting state toinitiate the MMC?

Motolin

Q1185:Which hormone is turned on when the acid in thestomach is below pH3 to inhibit basically everything?

Somatostatin

Q1186:Which other two hormones in the pituitary doessomatostatin inhibit?

TSH and GH

Q1187:Action of Histamin?

increase gastric acid secretion.

Q1188:Tumor of non alpha and non beta islet cells of thepancrease that causes watery diarrhea secretes this:

VIP (VIPoma)

Q1189:Which hormone relaxes intestinal sm mm; increasespancreatic bicarb secretion; and stimulates intestinal secretion

of electrolytes and water?

VIP

Q1190:This hormone is released from vagal nerve endings tomediate the release of gastrin.

GRP

Q1191:Somatostatin is released from these cells in the GItract.

Delta (D) cells

Q1192:CCK is released from these cells in the duodenum andjejunum.

I cells

Q1193:Secretin does what to the rate of stomach emptying?

decreases it.

Q1194:What is the effect of GIP on pancreatic beta cells?

stimulates the release of insulin

Q1195:Region of stomach parietal and chief cells are located

body/corpus

Q1196:region of stomach G cells are located?

antrum (G cells secrete gastrin)

Q1197:Which gland produces 70% of total salivarysecretions?

submandibular

Q1198:Which hormone is the primary regulator of bicarbsecretion from the pancreas?

secret

Q1199:Which pancreatic cells secrete somatostatin

alpha

Q1200:actions of gastrin?

(G cells of antrum) inc'd gastric H+; stim growth of gastricmucosa

Q1201:what stimulates release of gastrin?

sm peptides; amino acids in stomach lumen; stomachdistention; vagus (via GRP)

Q1202:where is CCK from?

I cells of duodenum

Q1203:5 actions of CCK

1. stim gallbladder contraction and Oddi relaxation; 2) stimpancreatic enzyme secretion; 3) potentiates secretin-inducedstim of pancreatic bicarb secretion; 4) stim growth of exocrine

pancrease; 5) inhibits gastric empyting

Q1204:what stimulates release of CCK from duodenum?

small peptides; amino acids; fatty acids and monoglycerides(not TGs b/c can't cross intestinal membrane)

Q1205:actions of secretin?

1. stim pancreatic bicarb (potentiated by CCK) and inc'dgrowth of exocrine pancrease; 2) stim bicarb and H2O

secretion by liver and inc'd bile production; 3) inhibits H+ bygastric parietal cells

Q1206:what stimulates release of secretin from S cells ofduodenum?

H+ and fatty acids in duodenum

Q1207:actions of GIP (gastric inhibitory peptide)

1. stimulates insulin release (this is why oral glucose better!)2. inhibits H+ secretion

Q1208:what stimulates release of GIP from K cells?

fatty acids; amino acids; oral glucose (only GI hormone thatresponds to fat; protein; and carbs!)

Q1209:what inhibits release of somatostatin?

vagal stimulation

Q1210:effect of His on GI

increased H+ secretion directly and indirectly by potentiatingeffects of gastrin and vagal stim

Q1211:actions of VIP?

relaxation of GI smooth mm (LES!); stimulate pancreaticbicarb; inhibits H+

Q1212:basal electric rhythm of a) stomach b) duodenum c)ileum

a) 3 Hz; b) 12 Hz; c) 8-9 Hz

Q1213:gastroileal reflex?

food in stomach--> increased peristalsis in ileum andrelaxation of ileocecal sphincter

Q1214:gastrocolic reflex?

food in stomach--> increased colon motility and frequency ofmass movements

Q1215:composition of saliva

high K+; HCO3-; low NaCl (hypotonic; unless made rapidly);alpha amylase; lingual lipase; kallikrein

Q1216:parasympathetic regulation of saliva production?

CN VII; IX (via muscarinic R IP3 or Ca); inc'd production

Q1217:sympathetic regulation of saliva production

increased production; via beta adrenergic stim (cAMP)

Q1218:composition of aq part of pancreatic secretions?

always ISOTONIC; more bicarb than in plasma; if low flowrate--high Na Cl; if high flow rate--high Na HCO3-

Q1219:what does sucrase do?

degrades sucrose to glucose and fructose

Q1220:what does SLGT 1 in intestine do?

transports glucose and galactose into cells; Na+-dependent

Q1221:how is fructose transported into intestinal cells?

facilitated diffusion

Q1222:optimum pH for pepsin activity?

1-3 (in pH>5; denatures)

Q1223:(hypothetical) deficiency of enterokinase--> ?

no activation of pancreatic proteases b/c it convertstyrpsinogen into trypsin and tryspin then cleaves all the

others

Q1224:why might hypersecretion of gastrin causesteatorrhea?

low duodenal pH inactivates pancreatic lipase

Q1225:what would a lack of apoprotein B do in intestine?

cause steatorrhea b/c apo B necessary for transportingchylomicrons out of intestinal cells

Q1226:what happens to K+ in GI?

dietary K+ absorbed paracellularly; activly secreted in colon(similar to in kidney)

Q1227:how does Vibrio Cholerae cause diarrhea?

toxin binds R in luminal membrane; activates AC whichcauses increase cAMP--> lumenal Cl- channels open. Na and

H2O follow Cl--> secretory diarrhea!!

Q1228:Effect of sympathetic stimulation in the GI tract

decreased motility; decreased secretions; increasedcontraction of sphincters

Q1229:Effect of parasympathetic stimulation in GI tract

increased motility; increased secretions; increased relaxationof sphincters (except LES which contracts); increased gastrin

release

Q1230:Hormones of the GI system

Gastrin; CCK; secretin; GIP

Q1231:Stimulus for gastrin secretion

Stomach distension. Stomach acid in the duodenum inhibitsgastrin release

Q1232:Sources of gastrin

G cells of the stomach anthrum; duodenum

Q1233:Actions of gastrin

Stimulates acid secretion by parietal cells; increases motilityand secretions.

Q1234:Source of secretin

S cells of the duodenum

Q1235:Stimulus for secretin release

Acid entering the duodenum

Q1236:Actions of secretin

Stimulates HCO3 secretion by pancreas to neutralize acidentering duodenum

Q1237:Source of CCK

Cells lining the duodenum

Q1238:Stimulus for CCK secretion

Fat and amino acids entering duodenum

Q1239:Actions of CCK

Inhibits gastric emptying; stimulates pancreatic enzymesecretion; stimulates contraction of the gallbladder and

relaxation of sphincter of Oddi.

Q1240:Source of GIP

Duodenum

Q1241:Stimulus for GIP secretion

Fat; carbs and amino acids

Q1242:Actions of GIP

Inhibits stomach motility and secretion

Q1243:Properties of GI smooth muscle

Stretch stimulates contraction; electrical syncytium with gapjunctions; pacemaker activity

Q1244:Factors that inhibit gastric motility

Acid in the duodenum (secretin); fat in the duodenum (CCK);hypoerosmolarity in duodenum; distension of duodenum

Q1245:Factors that stimulate gastric motility

Distension of the stomach and ACh

Q1246:What are the different contractions of the intestines?

Segmentation contractions (mixing); peristaltic movements(propulsive).

Q1247:What factors control the ileocecal sphincter?

Distension of the ileum relaxes; distension of the coloncontracts

Q1248:What are the different contractions of the colon

Segmentation contractions (haustrations); peristalsis and massmovements

Q1249:Composition of salivary secretions

Low in NaCl because of reabsorption; High in K and HCO3because of secretion; alpha-amylase begins digestion of carbs;

fluid is hypotonic due to NaCl reabsorption andimpermeability of ducts to water

Q1250:Parietal cells

Located in the middle part of the gastric glands. Secrete HCland intrinsic factor.

Q1251:Chief cells

Located in the deep part of the gastric glands. Secretepepsinogen which is converted to pepsin by acid medium.

Pepsin begins digestion of proteins to peptides

Q1252:Mucous cells of the stomach

Located in the superficial part if the gastric glands (gastricpits). Secrete mucus and HCO3. Secretion is stimulated by

PGE2

Q1253:Ionic composition of gastric secretions

High in H+; K+ and Cl-; low in Na+. Vomiting producesmetabolic alkalosis and hypokalemia.

Q1254:Control of acid secretion

Acetylcholine; histamine and gastrin stimulate parietal cells tosecrete acid.

Q1255:Secretion of acid by parietal cells

CO2 is extracted from the blood and combined into H2CO3by carbonic anhydrase. H+ ions are exchanged by the proton

pump for K+ ions (active antitransport)

Q1256:Pancreatic amylase

Hydrolyzes alpha-1;4-glucoside bonds forming alpha-limitdextrins; maltotriose and maltose

Q1257:Pancreatic lipase

Needs colipase which displaces bile from surface of micelles.Lipase digests triglycerides to two free fatty acids and one 2-

monoglyceride

Q1258:Cholesterol esterase

Hydrolizes cholesterol esters to yield cholesterol and freefatty acids

Q1259:Pancreatic proteases

Trypsinogen is converted to trypsin by enterokinase -->chymotrypsinogen is converted to chymotrypsin by trypsin --> procarboxypeptidase is converted to carboxypeptidase by

trypsin

Q1260:Ionic composition of pancreatic secretions

Isotonic due to permeability of ducts to water and high inHCO3. Stimulated by CCK and secretin.

Q1261:What are the primary bile acids?

Cholic acid and chenodeoxycolic acid. Synthesized in the liverfrom cholesterol.

Q1262:How are bile salts formed?

Bile acids (cholic and deoxycholic) are conjugated with glycineand taurine which mix with cations to form salts.

Q1263:What are the secondary bile acids?

Formed by deconjugation of bile salts by enteric bacteria -deoxycholic acid (from cholic acid) and lithocolic acid (from

chenodeoxycholic acid). Lithocholic acid is hepatotoxic and isexcreted.

Q1264:Enterohepatic circulation

Bile acids are reabsorbed only in the distal ileum. Resection ormalabsoption syndromes lead to steatorrhea and cholesterol

gallstones.

Q1265:What are the components of bile?

Conjugated bile acids (cholic and chenodeoxycholic);billirubin; lecithin and cholesterol.

Q1266:How are carbohydrates absorbed?

Glucose and galactose via active secondary Na cotransporter.Fructose is absorbed independently

Q1267:How are amino acids absorbed?

Secondary active transport linked to Na and receptor-mediated endocytosis.

Q1268:How are lipids absorbed?

Micelles diffuse to the brush border then digested lipids (2-monoglycerides; fatty acids; cholesterol and ADEK vitamins)diffuse into enterocytes. Triglycerides are resynthesized andpackaged as chylomicrons with apoB48. Leave the intestine

via lymphatics to thoracic duct.

Q1269:source of gastrin

G cells in antrum of stomach

Q1270:source of CCK

I cells in duo and jejunum

Q1271:source of secretin

s cells; duodenum

Q1272:action of gastrin

increased H+ in stomach ;increased growth of gatric mucosa;increased gastric motility

Q1273:action of CCK

increases pancreatic secretions ;increases gallbladdercontraction ;slows gastric emptying

Q1274:action of secretin

release of HCO3-;decreased gastric acid secretion

Q1275:regulation of gastrin

decreased when stomach pH <1.5;increased when stomach isdistended; presence of AA and peptides;increased in vagal

stimulation

Q1276:regulation of CCK

decreased if stomach pH<1.5;decreased by secretin ;increasedby fatty acids and AA

Q1277:regulation of secretin

increased by acid; FA in lumen of duo

Q1278:source of somatostatin

D cells of pancreatic islets and GI mucosa

Q1279:what regulates somatostatin

increased by acid ;decreased by vagal stimulation

Q1280:what is somatostatin used to treat

VIPoma ;carcinoid tumors

Q1281:what releases GIP?

K cells in duo and jejunum

Q1282:what does GIP do?

exocrine fxn of decreasing H secretion ;endocrine fxn ofincreasing insulin release

Q1283:regulation of GIP

increased by fatty acids; AA; oral glucose

Q1284:which is used more rapidly: oral or IV glucose?

oral

Q1285:source of VIP

parasympathetic ganglia in sphincters; gallbladder and smallintestines

Q1286:action of VIP

increases intestinal water absorption ;relaxation of intestinalsmooth muscle and sphincters

Q1287:regulation of VIP

increased by distention and vagal stimulation ;decreased byadrenergic imput

Q1288:what is VIPoma

non-alpha; non-beta islet cell pancreatic tumor that secreteVIP --> copious watery diarrhea

Q1289:action of NO on GI tract

increased smooth muscle relaxation; (NB: lower P in LES)

Q1290:what is implicated in decreased NO secretion

accounts for incresed LES tone seen in achalasia

Q1291:where is HCO3- released from?

mucosal cells;stomach;duo

Q1292:where is pepsin released from?

chief cells of stomach

Q1293:what controls gastric acid release

increased by histamine and ACh;decreased by somatostatin;GIP; PG; secretin

Q1294:fxn of salivary amylase

hydrolyzes alpha-1;4 linkages --> disaccharides

Q1295:fxn of pancreatic amylase

hydrolyzes starch to oligosaccharides and disaccharides

Q1296:where is pancreatic amylase found

highest [] in duo lumen

Q1297:fxn of oligosaccharide hydrolase

hydrolyzes oligosaccharidses --> monosaccharides ;RL step incarb digestion

Q1298:What cells are the source of GASTRIN?

G cells (antrum)

Q1299:What cells are the source of CCK?

I cells (duodenum; jejunum)

Q1300:What cells are the source of SECRETIN?

S cells (duodenum)

Q1301:What cells are the source of SOMATOSTATIN?

D cells (pancreatic islets; GI mucosa)

Q1302:What cells are the source of GIP?

K cells (duodenum; jejunum)

Q1303:What cells are the source of INTRINSIC FACTOR?

Parietal cells (body; fundus)

Q1304:What cells are the source of HCL?

Parietal cells (body; fundus)

Q1305:What cells are the source of PEPSIN?

Chief cells (stomach)

Q1306:What cells are the source of HCO3-?

Mucosal cells (stomach; duodenum)

Q1307:What is the function of GASTRIN?

increased gastric H+ secretion;increased gastric mucosa

Q1308:What is the function of CCK?

increased pancreatic secretions;Stimulates gallbladdercontraction;Inhibits gastric emptying

Q1309:What is the function of SECRETIN?

increased pancreatic HCO3- secretion ;Inhibits HCl secretion

Q1310:What is the function of SOMATOSTATIN?

Inhibits everything;Inhibits gallbladder contraction;Inhibitsrelease of both insulin and glucagon

Q1311:What is the function of GIP?

Exocrine: decreased gastric H+ secretion;Endocrine: increasedinsulin release

Q1312:What is the function of INTRINSIC FACTOR

Binds B12

Q1313:What is the function of HCL?

decreased stomach pH

Q1314:What is the function of PEPSIN?

Protein digestion at pH of 1.0-3.0

Q1315:What is the function of HCO3-?

Neutralizes acid;Prevents autodigestion

Q1316:What stimulates gastrin release?

Stomach distention;Amino acids;Vagal stimulation

Q1317:What inhibits gastrin release?

H+ secretion;pH < 1.5

Q1318:What stimulates CCK release?

Fatty acids;Amino acids

Q1319:What inhibits CCK release?

Secretin;pH < 1.5

Q1320:What stimulates secretin release?

Low duodenal pH;Fatty acids in lumen of duodenum

Q1321:What stimulates somatostatin release?

Low pH

Q1322:What inhibits somatostatin release?

Vagal input

Q1323:What stimulates HCl secretion?

Histamine;ACh;Gastrin

Q1324:What inhibits HCl secretion?

Somatostatin;GIP;Prostaglandins

Q1325:What stimulates pepsin secretion?

Vagal input;Local acid

Q1326:What stimulates HCO3- secretion?

Secretin

Q1327:What is the function of VIP?

Relaxes intestinal smooth muscle;Stimulates pancreaticHCO3- secretion;Inhibits gastric H+ secretion

Q1328:What is the source of VIP?

Smooth muscle and nerves of intestines

Q1329:Where does TRYPSIN cleave?

Carboxy side of ARG and LYS

Q1330:Where does CHYMOTRYPSIN cleave?

Carboxy side of aromatic amino acids (PHE; TYR; TRP)

Q1331:Where does ELASTASE cleave?

Carboxy side of ALA; GLY; and SER

Q1332:What is the function of SALIVARY AMYLASE?

Starts digestion;Hydrolyzes alpha-1;4 linkages to givemaltose; maltotriose; and alpha-limit dextrans

Q1333:What is the function of PANCREATIC AMYLASE?

Hydrolyzes starch to oligosaccharides; maltose; andmaltotriose

Q1334:Where is the highest concentration of PANCREATICAMYLASE?

Duodenal lumen

Q1335:Where are lipids digested?

Duodenum

Q1336:Where are lipids absorbed?

Jejunum

Q1337:major cations/anions of ICF?

cations--K+; Mg2+; anions--protein; organic phosphates (egATP)

Q1338:markers for measuring TBW

D2O; tritiated H2O

Q1339:markers for measuring ECF?

mannitol; sulfate; inulin

Q1340:markers for measuring plasma?

RISA; Evan's blue

Q1341:markers for measuring interstitial fluid?

indirect: ECF - plasma (mannitol - Evan's blue)

Q1342:markers for measuring ICF?

do indirectly: TBW - ECF (D2O - mannitol)

Q1343:What happens if isotonic NaCl is infused?

isosmotic volume expansion

Q1344:What happens to fluid volumes if you have diarrhea?

loss of isotonic fluid-->isometric volume contraction

Q1345:what happens to fluid volumes if excessive NaClintake?

hyperosmotic vol expansion

Q1346:what happens to fluid volumes if you get lost in adesert? (dehydration)

hyperosmotic vol contractino

Q1347:what happens to fluid volumes in SIADH?

hyposmotic volume expansion

Q1348:what happens to fluid volumes if adrenocorticalinsufficiency?

hyposmotic volume contraction

Q1349:treatment of SIADH?

demeclocyclene; water restriction

Q1350:renal blood flow is what % of CO?

~25%

Q1351:at low [ang II]; what effect on renal arterioles?

preferential dilation of efferent arteriole--> protects GFR

Q1352:over what range of pressures does renal blood flowremain constant (autoregulation)

80-200mmHg (thanks to myogenic mech and tubuloglomerularfeedback)

Q1353:How measure renal plasma flow?

use PAH; which is both filtered and secreted by renal tubules(so that~none in renal veins); this is the effective RPF

Q1354:filtration fraction?

GFR/RPF (normal~0.20)

Q1355:where does acetozolamide work in kidney?

(carbonic anhydrase inhibitor) works in PCT to inhibitresorption of HCO3- (w/o bicarb; don't have H+ needed forNa-H antiport) (N.B. can also tx acute mountain sickness)

Q1356:middle/late PCT vs. early PCT?

early PCT--Na resorb.coupled with glucose; aa; phosphate;etc; mid/late PCT--Na resorb.w/ Cl-

Q1357:where do K+sparing diuretics work?

in CCD

Q1358:role of alpha intercalated cells?

secrete H+ and resorb. K+ if hypokalemic (or acidic?)

Q1359:what cell is responsible for excreting K+ inhyperkalemia?

principal cell (via Na-K ATPase and K channels)

Q1360:where is phosphate resorbed?

only in PCT. ~15% of filtered phosphate excreted (imp forbuffering later on)

Q1361:effect of PTH on phosphate in kidney?

PTH inhibits phosphate resorb. in PCt via inc'd AC-->cAMP. (get phosphaturia and inc'd urinary cAMP)

Q1362:which diuretics can be used to treat hypercalcemia?

loop diuretics

Q1363:which diuretics can be used to treat hypercalciURIA

thiazides (increase Ca resorb.)

Q1364:relationship of K+ and NH3?

hyperkalemia inhibits NH3 synthesis (RTA type 4); dec'dH+ excretion; hyPOkalemia--stim NH3 synthesis

Q1365:ECF volume contraction and acid/base balance?

ECF volume contraction-->HCO3- resorb; contractionalkalosis (N.B. in vomiting; met alk made worse if ECF vol

contracts!)

Q1366:why might you get tingling; numbness; muscle spasmsin respiratory alkalosis?

signs/symptoms of hypocalcemia; b/c H+ and Ca2+ competefor protein binding sites and dec'd H+ means more bound Ca

and less free Ca (~hypocalc.)

Q1367:effect of insulin on K+?

insulin deficiency--> shift of K+ out of cells; hyperkalemia;insulin-->shift of K+ into cells; hypokalemia

Q1368:what happens to osmolarity of ECF if person isinfused with isotonic saline solution?

stays the same

Q1369:what happens to osmolarity of ECF if person has lossof isotonic fluid? (example)

diarrhea;stays the same

Q1370:what happens to osmolarity of ECF if person has highNaCl intake?

incresaes

Q1371:what happens to ECF osmolarity if person is sweatingin the desert?

increases (sweat is hyposmotic; more water than salt is lost)

Q1372:what happens to ECF osmolarity in SIADH?

decreases

Q1373:what happens to ECF osmolarity in adrenocorticalinsufficiency (NaCl loss)?

decreases (lack of aldosterone); kidneys excrete more NaClthan water

Q1374:what happens to plasma protein [] and hematocrit ininfusion of isotonic NaCl?

decreases (overall increase in fluid)

Q1375:what happens to plasma protein [] and hct in diarrhea?

increases (from volume contraction)

Q1376:what happens to plasma protein [] and hct in highNaCl consumption?

decrease (ICF shrinks to accomodate the increased osmolarityin ECF; this dilutes out the plasma protein)

Q1377:what happens to plasma protein [] and hct whenswaeting in desert?

protein increases;hct stays same b/c fluid leaves rbcs to offsetfuid loss

Q1378:what happens to plasma protein [ ] and hct in siadh

decreases;stays same

Q1379:what happens to plasma protein [] and hct in adrenalinsuff?

plasma protein increases;hct increases (from decreased ECFvolume and rbc swelling from water entry)

Q1380:how does vasoconstriction of renal arterioles affectRBF? how is this achieved?

decreases RBF;SNS

Q1381:how does AII affect renal arterioles

preferentially constricts efferent arterioles unless it is asituation where there is a massive hemorrhage. then; so much

AII is released that it constricts both efferent and afferentarterioles

Q1382:how does ACE affect renal arterioles

preferentially constricts efferent arterioles

Q1383:what effects does AII have on GFR?

increases it

Q1384:what effect do ACE-I have on GFR

decreass it by dilating efferent arterioles

Q1385:what does afferent arteriole constriction do to RPF?

decreases

Q1386:what does efferent artiorole constriction do to GFR?

increases (by increasing Pgc)

Q1387:what does increased plasma protein do to GFR?

decreases it by increasing osmotic pressure in GC

Q1388:what does decreased plasma protein do to GFR?

increases it by decreasing osmotic pressure in GC

Q1389:what does increased plasma protein do to RBF?

nothing

Q1390:what does decreased plasma protein [] do to RBF?

nothing

Q1391:what does efferent arteriole constriction do to RBF?

decreases it

Q1392:what happens to the filtration fraction in afferentarteriole constriction?

(GFR/RBF);GFR decreases; RBF decreases;FF no change

Q1393:what happens to FF in efferent arteriole constriction

GFR/RBF;GFR increases; RBF decreases ;FF increases

Q1394:what happens to FF in increased plasma proteinconcentraton

GFR/RBF;GFR decreases; RBF no change;FF decreases

Q1395:what happens to FF in decreased plasma protein []

GFR/RBF;GFR increases; RBF no change;FF increases

Q1396:what happens to FF when ureter is constricted?

GFR/RBF ;GFR decreases; RBF no change;FF decreases

Q1397:what things are reabsorbed in the PCT?

glucose;AA's;most of the HCO3

Q1398:describe how HCO3 is handled in PCT

HCO3 is in the lumen and combines with H that is secretedinto the lumen --> H2CO3;Carbonic anhydrase --> H20 +

CO2 ;which re-enters the tubule and reforms as H2CO3 withCA ;the H is then secreted into the lumen and the HCO3 is

reabsorbed

Q1399:what happens in the TAL?

NKCC pump (blocked by furosemide): aids in reabsorbingNa; Cl; K ;K flows back out into lumen and the gradient

drives the absorption of Mg and Ca ;also aids in the runningof the NKCC pump

Q1400:is the TAL permeable to water

no

Q1401:what is the thin descending loop permeable to?

water; but not Na

Q1402:what is happens in the early distal convaluted tubule

actively reabsorbs Na; Cl ;Ca absorption is controlled byPTH receptors found here

Q1403:what happens in the collecting tubules

Na is reabsorbed in exchange for K/H (regulated byALDOSTERONE!!!) ;reabsorption of water regulated by

ADH (aquaporins)

Q1404:which part of the nephron is impermeable to water?

TAL (and collecting tubule if there is no ADH)

Q1405:where in kidney is EPO released from

endo cells of peritubular capillaries

Q1406:what enzyme converts 25-OH vitamin D to its activeform?

1-alpha hydroxylase

Q1407:what do JG cells do?

secrete renin in response to low renal blood pressure

Q1408:what does the macula densa do?

senses the amt of Na

Q1409:where is the macula densa

part of the DCT

Q1410:what do PGs do to the kidney

vasodilate the afferent arterioles (that's why NSAIDS can -->ARF by inhibiting PG)

Q1411:what effect does aldosterone have on H

more H is secreted

Q1412:where does aldosterone work in kidney?

DCT

Q1413:where does PTH work?

PCT to decrease PO4 reabsorption ;DCT to increase Careabsorption ;stimulates 1-alpha hydroxylase in PCT

Q1414:where is ACE released from?

lung

Q1415:increased glomerular pressure; decreased peritulbuarpressure; decreased RPF

Efferent arteriole constriction

Q1416:decreased glomerular pressure; increased peritubularpressure; increased RPF

Efferent arteriole dilation

Q1417:decreased glomerular pressure; decreased peritulbuarpressure; decreased RPF

Afferent arteriole constriction

Q1418:increased glomerular pressure; increased peritulbuarpressure; increased RPF

Afferent arteriole dilation

Q1419:Afferent arteriole dilation

increased glomerular pressure; increased peritulbuarpressure; increased RPF; increased GFR

Q1420:Afferent arteriole constriction

decreased glomerular pressure; decreased peritulbuarpressure; decreased RPF; decreased GFR

Q1421:Efferent arteriole dilation

decreased glomerular pressure; increased peritubularpressure; increased RPF; decreased GFR

Q1422:Efferent arteriole constriction

increased glomerular pressure; decreased peritulbuarpressure; decreased RPF; increased GFR; increased FF

Q1423:Plasma oncotic pressure changes as blood flowsthrough the nephron

Oncotic pressure increases because filtered fluid increasesprotein concentration. Oncotic pressure is resposible for

peritubular reabsorption

Q1424:Normal capillary hydrostatic pressure of theglomerulus

45 mmHg

Q1425:Normal capillary oncotic pressure of the glomerulus

27 mmHg

Q1426:Normal hydrostatic pressure of bowman's capsule

10 mmHg

Q1427:Normal GFR value

120 ml/min

Q1428:Normal RPF value

600 ml/min

Q1429:Normal filtration fraction value

FF = GFR/RPF = 120mi/min / 600ml/min = 0.20

Q1430:Effect of sympathetic stimulation in the nephron

decreased GFR; increased FF; increased peritubularreabsoption

Q1431:Effect of angiotensin II in the kidney

Vasoconstriction of the efferent arteriole more than afferent --> maintains GFR

Q1432:Filtered load

Rate at which a substance filters into Bowman's capsule = FL= GFR x Free plasma concentration

Q1433:Excretion of a substance in the urine

Excretion = filtered load + (amount secreted - amountreabsorbed) = filtered load + transport OR urine concentration

X urine flow rate

Q1434:Characteristics of a Tm system

Carriers become saturated; carriers have high affinity; lowback leak. The filtered load is reabsorbed until carriers are

saturated - the excess is excreted.

Q1435:Renal treshold for glucose

180 mg/dl or 1.8 mg/ml. Represents the beginning of splay.

Q1436:Tm rate of reabsorption of glucose

375 mg/min. Represents the maximum filtered load that can bereabsorbed when all carriers in the kidney are saturated (end

of splay region).

Q1437:Glucose reabsorption graph

At normal glucose levels; the amount filtered is the same asthe amount reabsorbed. At threshold (beginning of splay); the

excretion curve starts to ascend and the amount filteredexceeds the amount reabsorbed.

Q1438:Substances that are reabsorbed using a Tm system

Glucose; amino acids; small peptides; myoglobin; ketones;calcium; phosphate.

Q1439:Characteristics of a gradient-time system

Carriers are not saturated; carriers have low affinity; high backleak

Q1440:Substances that are reabsorbed using a gradient-timesystem

Sodium; potassium; chloride and water

Q1441:Substances secreted using a Tm system

PAH. 20% filtered; 80% secreted.

Q1442:Graph for PAH secretion

At low plasma concentration secretion is 4 times the filteredload. When carriers become saturated; secretion reaches a

plateau and the amount excreted is proportional to the amountfiltered.

Q1443:How is the net transport rate for a substancecalculated?

Net transport rate = filtered load - excretion rate = (GFR XPx) - (Ux X V)

Q1444:Effects of blood pressure changes in the kidney

GFR and RBF are maintained constant within theautoregulatory range. Urine flow is directly proportional to

blood pressure due to pressure natriuresis and pressurediuresis.

Q1445:What is clearance and how is it calculated?

It's the volume of plasma cleared of a substance over time.Clearance = excretion / Px = Ux X V / Px

Q1446:Characteristics of glucose clearance

At normal glucose levels; clearance is zero. Above tresholdlevels; clearance increases as plasma concentration increases

but never reaches GFR as there's always glucose reabsorption.

Q1447:Characteristics of inulin clearance

A constant amount of inulin is cleared regardless of plasmaconcentration (parallel line to x axis). Inulin clearance is equal

to GFR because it's not secreted nor reabsorbed. If GFRincreases; clearance increases (line shifts upward); and vice

versa.

Q1448:Characteristics of creatinine clearance

A constant amount of creatinine is cleared regardless ofplasma concentration; but creatinine clearance is more than

GFR because some is always secreted.

Q1449:Characterisics of PAH clearance

As plasma concentration increases; clearance decreasesbecause carriers that mediate active secretion become

saturated. At normal levels; PAH clearance = RPF because allis excreted.

Q1450:How is GFR calculated using inulin?

GFR is equal to inulin clearance because it's only filtered andnone is secreted nor reabsorbed. Cin = GFR = Uin X V / Pin

Q1451:How is creatinine production calculated?

Creatinine production = creatinine excretion = filtered load ofcreatinine = [Cr]p X GFR. Creatinine is filtered and secreted;

not reabsorbed.

Q1452:How does inulin concentration change as it passesthrough the nephron?

Inulin becomes more concentrated as it passes through thetubules because water is being reabsorbed and not inulin.

Q1453:Gold standard to measure GFR

Inulin clearance because it's filtered but not secreted norreabsorbed.

Q1454:Gold standard to measure RPF

PAH clearance because some is filtered and the remaining is allsecreted.

Q1455:How is effective RPF calculated?

PAH clearance = RPF = Upah X V / Ppah

Q1456:How is renal blood flow calculated?

ERPF / 1-Hct; ERPF = Upah X V / Ppah

Q1457:What does positive free water clearance mean?

Water is being eliminated. Hypotonic urine is being formed toincrease plasma osmolarity.

Q1458:What does negative free water clearance mean?

Water is being conserved. Hypertonic urine is being formed tolower plasma osmolarity.

Q1459:How is free water clearance calculated?

V - (Uosm(V) / Posm)

Q1460:Which substance is cleared the most: PAH; inulin;glucose; creatinine

PAH

Q1461:Which substances are cleared more than glucose?

Sodium; inulin; creatinine; PAH

Q1462:Which substance is cleared the least: PAH; inulin;glucose; creatinine

Glucose

Q1463:Which substances are cleared more than inulin?

Creatinine; PAH

Q1464:Which substances are cleared less than creatinine?

Inulin; glucose; sodium

Q1465:Transporters in the luminal membrane of the proximaltubule

Secondary Na/glucose cotransporter; secondary Na/amino acidcotransporter; secondary Na/H countertransporter

Q1466:What substances are reabsorbed in the proximal tubuleand how much?

Na (2/3 of filtered load); glucose (100%); amino acids (100%);HCO3 (indirectly; 80%); H20 (2/3); K (2/3); Cl (2/3)

Q1467:Tubular osmolarity at beginning and end of proximaltubule

At the beginning and end is isotonic with plasma but only 1/3of the filtered load.

Q1468:Transporters in the basal membrane of proximal tubule

Na/K ATPase - luminal membrane secondary Na transportersdepend on this.

Q1469:Transporters in the basolateral membrane of proximaltubule

Na/K ATPase - luminal membrane secondary Na transportersdepend on this.

Q1470:Most energy-dependant process in the nephron

Active reabsorption of Na by the basal and basolateral Na/KATPase

Q1471:Characteristics of the loop of henle

Descending limb is permeable to water so water difuses outand intraluminal osmolarity increases to 1;200mOsm

Ascending limb is impermeable to water and Na is activelypumped out by Na/K/2Cl pump so fluid becomes hypotonic.Flow is slow; anything that increases flow; decreases capacity

to concentrate urine.

Q1472:Characteristics of the collecting duct

Impermeable to water unless ADH is present. ADH increasespermeability to H20 and urea to concentrate urine. Tight

junctions with little back-leak.

Q1473:Specialized cells of the distal tubule and collecting duct

Principal cells (aldosterone) and intercalated cells (createHCO3)

Q1474:Actions of principal cells of the distal tubule andcollecting duct

Aldosterone increases Na receptors in the membrane andincreases primary transport by Na/K ATPase. Secondary

transport of Na and secretion of K.

Q1475:Actions of intercalated cells of the distal tubule andcollecting duct

Acidify the urine and produce new bicarbonate

Q1476:Actions of the distal tubule and collecting duct

Reabsorption of Na and secretion of K (stimulated byaldosterone); acidification of the urine (secretion of H and

creation of HCO3)

Q1477:Urine buffer systems

H2PO4- (dihydrogen phosphate) (tritratable acid) buffers33% of secreted H. NH4+ (amonium) (nontritratable acid)

buffers the remaining secreted H.

Q1478:How is potassium affected by acidosis?

High concentration of ECF H --> H diffuses to ICF --> Kdiffuses to ECF --> hyperkalemia

Q1479:How is potassium affected by alkalosis?

Low concentration of ECF H --> H diffuses to ECF --> Kdiffuses to ICF --> hypokalemia

Q1480:Potassium dynamics in acute alkalosis

Hypokalemia; increased intracellular K; increased renal Kexcretion; negative K balance

Q1481:Potassium dynamics in chronic alkalosis

Hypokalemia; decreased intrecellular K; increased renal Kexcretion; negative K balance

Q1482:Potassium dynamics in acute acidosis

Hyperkalemia; decreased intracellular K; decreased renal Kexcretion; positive K balance

Q1483:Potassium dynamics in chronic acidosis

Hyperkalemia; decreased intracellular K; increased renal Kexcretion; negative K balance

Q1484:How is potassium balance in acute acidosis?

Positive (potassium is reabsorbed)

Q1485:How is potassium balance in acute alkalosis?

Negative (potassium is excreted)

Q1486:How is potassium balance in chronic alkalosis?


Q1487:How is potassium balance in chronic acidosis?


Q1488:How is plasma potassium concentration in alkalosis?

Hypokalemia

Q1489:How is plasma potassium concentration in acidosis?

Hyperkalemia

Q1490:What is the difference in potassium dynamics betweenacute and chronic alkalosis?

Acute alkalosis --> increased intracellular K; Chronicalkalosis --> decreased intracellular K

Q1491:What is the difference in potassium dynamics betweenacute and chronic acidosis?

Acute acidosis --> decreased renal K excretion; positive Kbalance; Chronic acidosis --> increased renal K excretion;

negative K balance

Q1492:Changes in respiratory acidosis

Hypoventilation --> increased PaCO2 --> increased H andslight increased in HCO3 --> decreased pH

Q1493:Changes in respiratory alkalosis

Hyperventilation --> decreased PaCO2 --> decreased H andHCO3 --> increased pH

Q1494:Changes in metabolic acidosis

Gain of H or loss of HCO3 --> decreased HCO3 -->decreased pH. To see if gain of H or loss of HCO3 check

anion gap.

Q1495:Changes in metabolic alkalosis

Loss of H or gain in HCO3 --> increased HCO3 --> increasedpH. To see if gain of H or loss of HCO3 check anion gap.

Q1496:Normal values of PCO2; HCO3 and pH

pH = 7.4; PCO2 = 40mmHg; HCO3 = 24mmol/L

Q1497:increased pH; increased HCO3; increased PCO2;decreased PO2; alkaline urine

Partially compensated metabolic alkalosis

Q1498:decreased pH; increased PCO2; increased HCO3;decreased PO2; acid urine

Partially compensated respiratory acidosis

Q1499:increased pH; decreased PCO2; decreased HCO3;normal PO2; alkaline urine

Partially compensated respiratory alkalosis

Q1500:decreased pH; decreased PCO2; decreased HCO3;normal PO2; acid urine

Partially compensated metabolic acidosis

Q1501:Normal plasma anion gap value

PAG = 12

Q1502:Conditions that increase plasma anion gap

Lactic acidosis; ketoacidosis; ingestion of salicylate

Q1503:Hyperchloremic non-anion gap metabolic acidosis

Loss of HCO3 (as in diarrhea) causes increases absorption ofsolutes and water; increasing Cl. Therefore decreased HCO3

and increased Cl with a plasma anion gap of 12.

Q1504:Equation to measure body fluid volumes

V= Q/C;V= body fluid volume;Q= indicatoradministered;C=concentration of indicator

Q1505:TBW indicators

D20; H20; antipyrine

Q1506:ECF indicators

Na; inulin; mannitol

Q1507:PV indicators

Albumin; Evans blue; Cr red blood cells

Q1508:100 mM glucose =

100 osm

Q1509:100 nM NACL

200 mOsm/L

Q1510:Filtered Load =

GFR * Solute (plasma)

Q1511:Excretion:

Volume Urine Flow * Urine concentration

Q1512:Clearance Concept

Related the excretion of a substance to its concentration inplasma

Q1513:Clearance Calculation

C= U*V/Ps;Cs: Clearance of substance;U: urine concetrationof substance;V: Urine flow;P: Plasma concentration

Q1514:Applying Clearance to GFR

Inulin Clearance used to measure GFR

Q1515:Best clinical measure of GFR

Creatinine

Q1516:Clearance to Renal Plasma Flow and RBF

PAH clearance = RBF ;PAH measures PLASMA FLOWONLY

Q1517:RBF using REnal plasma flow =

RBF=RPF (1- hematocrit);*Hct: 0.40

Q1518:Specialized portion of capillaries that perfuse medilla

vasa recta

Q1519:Filtration fraction

GFR/RBF

Q1520:Filtration

GFR= KF (Pgc-Pbc) - ;(TT gc-TTbc)

Q1521:Myogenic autoregulation

Increase in arterial pressure; stretches vessel wall leading to anicnrease in calcium movement and contraction

Q1522:Tubuloglomerular feedback

decrease in arterial pressure causes decrease in GFR;decreasing NACL to macula densa; Therefore efferentarteriolar resistnace Increases in response to HIGH

angiotensin II.

Q1523:Regulation of filtration of AFFERENT Arteriole;CONSTRICTION (Dilation is opposite)

Pcap: D;GFR: D;RBF: D

Q1524:Regulation of filtration of EFFERENTArteriole;CONSTRICTION ;(Dilation is opposite)

Pcap: U;GFR: U;RBF: D

Q1525:T Max or GLucose is

300 mg/min reabsorption

Q1526:REABSORPTION AND SECRETION

REABSORPTION AND SECRETION

Q1527:Proximal Tubule

NAHCO3 reabsoprtion;NACL ;Water;Glucose

Q1528:How are ions absorbed

Na/H antiport;Cl/Anion antiport ;Na/K Atpase;*Waterfollows non Cl reabsorption and icnreases tubular fluid of Cl.

Q1529:H= in proximal tubule is

Secreted

Q1530:Descending Thin Limb

Reabsorbs 15% GFR;Tbublular fluid volume DECREASES;Tubular fluid osmolarity INCREASES

Q1531:Thick Ascending Loop of Henle

break

Q1532:Reabsorption of Na

Symport with Cl/ K;Antiport with H

Q1533:Reabsorption of K

Symport with Na and Cl-

Q1534:Reabsorption of Ca

Ca Atpase; Na/Ca exchange;2G/Ca Atpase antiport;PTHstimulates

Q1535:Reabsorption of MG

active and electrical force

Q1536:SECRETION of H

Na/H exchange/ NH4+

Q1537:Early Distal tubulue

REabsorbs NACL via Na-Cl symoporter;REabsorbs Ca viaPTH

Q1538:What inhibits NA/CL symporter and PTH

Thiazide diuretics

Q1539:LAte Tubule

H20 reabsorbed by ADH;NACL REab byAldosterone;HCO# reab vy aldosterone;SECRETION Of K=

Aldosterone

Q1540:Secretion of K determines

total excretion

Q1541:Collecting Duct

Reabsorbs H20 by ADH;Reab. UREA via ADH

Q1542:PTH acts on ? for Ca reabsorption

DCT

Q1543:ADH receptor complex activates

adenylate cyclase. CAMP activates a kinase andphosphorylates proteins

Q1544:In Normal system; Urine flow and osmolarity are

inversely related

Q1545:In the presence of ADH

Water is reabsorbed;Urine volume is Small;Urineconcentration is same in MEdulla = HYPEROSMOTIC

Q1546:In the absence of ADH

No Water reabsorbed;Urine flow is high/dilute;Medullaryosmoloarty if low.

Q1547:REgulation of Plama osmoloarity by ADH

see page 300

Q1548:ADH secretion is increased my

elevated plasma sodium or osmolarity

Q1549:ADH secretion is decresed by

High blood volume or pressure

Q1550:Glucose in a DM patietn causes

opsmotic diuresis

Q1551:ANP will

Increase GFR;Decrease REnin; angio II; aldosterone; NACLand H2o reapbsortopn; ADH secretion

Q1552:ADH will

Increase H20 reabsorption; decrease urine flow and Increaseurine osmolarity

Q1553:Henderson Hasselbach equation

ph=6.1 log (HCO3) / 0.03 PCO2

Q1554:Increase in ventilation will

decrease PCO@ (Alkalosis)

Q1555:Decrease in Ventilation

Increases PCO2 (acidosis)

Q1556:Cahnge in renal acid excretion and HCO3 production is

Metabolic response

Q1557:Standard Values of ;HCO3 = 24 mEq/L;PCO2= 40mm HG

Just know

Q1558:Acidosis due to loss of HCO3 or DIARRHEA

Hyperchloremic Acidosis (because kdineys reabosrb CL sinceno HCO3)

Q1559:Conducting zone ;Consists of

nose; pharynx; trachea; bronchi; bronchioles; and terminalbronchioles.

Q1560:Respiratory zone ;Consists of

respiratory bronchioles; alveolar ducts; and alveoli.

Q1561:Pneumocytes;Pseudocolumnar ciliated cells extend tothe

respiratory bronchioles;

Q1562:Pneumocytes;extend to the respiratory bronchioles

Pseudocolumnar ciliated cells

Q1563:Pneumocytes;goblet cells extend to the

terminal bronchioles.

Q1564:Pneumocytes;extend to the terminal bronchioles.

goblet cells

Q1565:Pneumocytes;%'s

Type I cells (97% of alveolar surfaces);Type II cells (3%)

Q1566:role of;Type I cells

line the alveoli.

Q1567:role of;Type II cells

-secrete pulmonary surfactant;-serve as precursors to type Icells and other type II cells. Type II cells

Q1568:role of;clara cells

secrete a component of surfactant - degrade toxins - act asreserve cells

Q1569:ratio of in amniotic ;?uid is indicative of fetal ;lungmaturity.

A lecithin-to-sphingomyelin ;ratio of > 2.0

Q1570:bronchopulmonary segment ;structure

3°(segmental) bronchus ;- 2 arteries (bronchial ;andpulmonary) in the center - veins and lymphatics drain along

the borders.

Q1571:what is described by RALS––

the heart. The relation of the ;pulmonary artery to the;bronchus at each lung hilus ;is described by RALS–– ;Right

Anterior; Left ;Superior.

Q1572:Structures perforating diaphragm;what and levels

-T8: IVC;-T10: esophagus; vagus (2 trunks);-At T12: aorta(red); thoracic duct (white); azygous vein (blue).

Q1573:Pain from the diaphragm can be referred to

the shoulder.

Q1574:Muscles of respiration;in exercise

Inspiration––external intercostals; scalene muscles;sternomastoids;Expiration––rectus abdominis; internal and

external obliques; transversus abdominis;internal intercostals.

Q1575:5 Important lung products

-Surfactant;-ACE;-Prostaglandins;-histamine;-Kallikrein

Q1576:Surfactant;aka

dipalmitoyl phosphatidylcholine ;or ;lecithin

Q1577:Collapsing pressure =

2T/R;T=tension;R= radius

Q1578:what activates bradykinin

Kallikrein

Q1579:role of Kallikrein

activates bradykinin

Q1580:role of ACE in lung

angiotensin I → angiotensin II; inactivates bradykinin

Q1581:lung effects of ACE inhibitors and other effect

ACE inhibitors increased bradykinin and ;cause cough;angioedema)

Q1582:role of surfactant/mech

decreased alveolar surface tension;increased compliance

Q1583:TLC =

IRV + TV + ERV + RV

Q1584:VC =

TV + IRV + ERV

Q1585:TV + IRV + ERV

VC

Q1586:IRV + TV + ERV + RV

TLC

Q1587:what causes a shift of the curve ;to the right.

An increased in all factors (except pH)

Q1588:what causes a shift of the curve to the left.

A decreased in all factors (except pH)

Q1589:Pulmonary circulation;;normal resistnace andcompliance

Normally a low-resistance; high-compliance system.

Q1590:Pulmonary circulation;;A decreased in PaO2 causes

a hypoxic vasoconstriction that shifts blood away from;poorly ventilated regions of lung to well-ventilated regions of

lung.

Q1591:Pulmonary circulation;;Perfusion limited;whatmolecules / when / describe / how to change

O2 (normal health);-CO2;-N2O;Gas equilibrates early alongthe length of the capillary. Diffusion can be increased only if

blood ?ow increased .

Q1592:Pulmonary circulation;;Diffusion limited;whatmolecules / when / describe

–O2 (exercise; emphysema;?brosis);-CO;-Gas does notequilibrate by the time blood reaches the end of the capillary.

Q1593:Normal pulmonary artery pressure =;and when is itchanges

Normal pulmonary artery pressure = 10–14 mm Hg; or >35mm Hg during exercise;-pulmonary HTN ≥25 mm Hg

Q1594:Pulmonary hypertension;primary vs secondary

Primary––unknown etiology; poor prognosis;;Secondary––usually caused by COPD; also can be caused by L → R

shunt.

Q1595:O2 content =

(O2 binding capacity × % saturation) + dissolved O2.

Q1596:O2 changes as Hb falls

O2 content of arterial blood decreased as [Hgb] falls;but O2saturation and arterial PO2 do not.

Q1597:Arterial PO2 decreased with

chronic lung disease; physiologic shunt decreased O2extraction ratio;not decrease in Hb

Q1598:-Normally 1 g Hgb can bind;-normal Hgb amount inblood;-Normal O2 binding capacity

-1 g Hgb can bind 1.34 mL O2;-Hgb amount in blood is 15g/dL;-O2 binding capacity ≈ 20.1 mL O2 / dL.

Q1599:increased A-a gradient may occur in

-hypoxemia; causes include ;shunting; high V/Q mismatch;?brosis (diffusion block)

Q1600:CO2 transport forms

1. Bicarbonate (90%);2. Bound to hemoglobin ascarbaminohemoglobin (5%);3. Dissolved CO2 (5%)

Q1601:Haldane effect

In lungs; oxygenation of hemoglobin promotes dissociation ofCO2 from hemoglobin

Q1602:Bohr effect

In peripheral tissue; increased H+ shifts curve to right;unloading O2

Q1603:7 Response to high altitude

1. Acute increased in ventilation;2. Chronic increased inventilation;3. increased erythropoietin ;4. increased 2;3-DPG

;5. Cellular changes (increased mitochondria);6. increasedrenal excretion of bicarbonate to ;compensate for therespiratory alkalosis;7. Chronic hypoxic pulmonary

vasoconstriction results in RVH

Q1604:Emphysema ;types with causes

Centriacinar: caused by smoking;Panacinar: alpha 1-antitrypsin de?ciency

Q1605:alpha 1-antitrypsin de?ciency leads to

Panacinar Emphysema and liver cirrhosis

Q1606:Paraseptal emphysema: what and who

associated with bullae →can rupture →pneumothorax;often inyoung; otherwise healthy males.

Q1607:associated with bullae →can rupture →pneumothorax;often in young; otherwise healthy males.

Paraseptal emphysema

Q1608:Emphysema ;pathology

increased elastase activity;Enlargement of air spaces anddecreased recoil resulting from destruction of alveolar ;walls.

Q1609:Chronic Bronchitis ;pathology

Hypertrophy of mucus glands in the bronchioles →Reid index= gland depth / total thickness of bronchial wall; in COPD;

Reid index > 50%.

Q1610:Reid index

gland depth / total thickness of bronchial wall; in COPD; Reidindex > 50%.

Q1611:Bronchiectasis ;pathology

Chronic necrotizing infection of ;bronchi →permanentlydilated airways;

Q1612:Bronchiectasis ;complications

purulent sputum; recurrent infections; hemoptysis.

Q1613:causes of Bronchiectasis

Associated with bronchial obstruction; CF; poor ciliarymotility; Kartagener’s ;syndrome.

Q1614:Asthma triggers

Can be triggered by viral URIs; allergens; and stress.

Q1615:Restrictive lung;disease causes ;Poor breathingmechanics (extrapulmonary):

a. Poor muscular effort––polio; myasthenia gravis;b. Poorstructural apparatus––scoliosis; morbid obesity

Q1616:Restrictive lung;disease 8 types;Interstitial lungdiseases (pulmonary):

1. (ARDS) 2. Neonatal RDS ;3. Pneumoconioses ;4.Sarcoidosis;5. Idiopathic pulmonary ?brosis;6. Goodpasture’s

syndrome;7. Wegener’s granulomatosis;8. Eosinophilicgranuloma

Q1617:Pneumoconioses ;name some

coal miner’s silicosis; asbestosis

Q1618:Neonatal respiratory distress ;syndrome;Tx

maternal steroids before birth;arti?cial surfactant for infant.

Q1619:Adult acute respiratory distress syndrome(ARDS);pathophys

Diffuse alveolar damage →increased alveolar capillarypermeability →protein-rich leakage into alveoli. Results in

formation of intra-alveolar hyaline membrane.

Q1620:Adult acute respiratory distress syndrome(ARDS);initial damage due to

-neutrophilic substances toxic to alveolar wall;-activation ofcoagulation cascade;-oxygen-derived free radicals.

Q1621:Sleep apnea;types

Central sleep apnea––no respiratory effort;Obstructive sleepapnea––respiratory effort ;against airway obstruction.

Q1622:Sleep apnea;define

Person stops breathing for at least 10 seconds ;repeatedlyduring sleep.

Q1623:Sleep apnea;complications

- systemic/pulmonary hypertension;-arrhythmias;-possiblysudden death;-chronic fatigue

Q1624:Asbestosis;mech

Diffuse pulmonary interstitial ?brosis caused by inhaledasbestos ?bers.

Q1625:asbestos;wrt malignancy

increased risk of;pleural mesothelioma ;bronchogeniccarcinoma.

Q1626:pneumoconioses ;where in lungs

Asbestosis Mainly affects lower lobes. Otherpneumoconioses ;affect upper lobes (e.g; coal worker's lung).

Q1627:Asbestos and smoking

Asbestosis and smoking greatly;increased risk ofbronchogenic cancer (smoking not additive with

mesothelioma).

Q1628:Asbestosis;histo

Ferruginous bodies in lung (asbestos ?bers coated withhemosiderin). Ivory-white pleural plaques

Q1629:Bronchial obstruction ;-Breath Sounds ;-Resonance ;-Fremitus ;-Tracheal Deviation

-Absent/decreased over affected area ;-decreased ;-decreased;-Toward side of lesion

Q1630:Pleural effusion;-Breath Sounds ;-Resonance ;-Fremitus ;-Tracheal Deviation

-decreased over effusion ;-Dullness ;-decreased ;- NC

Q1631:Pneumonia (lobar) ;-Breath Sounds ;-Resonance ;-Fremitus ;-Tracheal Deviation

-May have bronchial ;breath sounds over lesion;-Dullness ;-increased ;-NC

Q1632:Pneumothorax;-Breath Sounds ;-Resonance ;-Fremitus;-Tracheal Deviation

-decreased ;-Hyperresonant ;-Absent ;-Away from side oflesion

Q1633:Breath Sounds; Resonance; Fremitus; TrachealDeviation;-Absent/decreased over affected area ;-decreased ;-

decreased ;-Toward side of lesion

Bronchial obstruction

Q1634:Breath Sounds; Resonance; Fremitus; TrachealDeviation;-decreased over effusion ;-Dullness ;-decreased ;-

NC

Pleural effusion

Q1635:Breath Sounds; Resonance; Fremitus; TrachealDeviation;-May have bronchial ;breath sounds over lesion;-

Dullness ;-increased ;-NC

Pneumonia (lobar)

Q1636:Breath Sounds; Resonance; Fremitus; TrachealDeviation;-decreased ;-Hyperresonant ;-Absent ;-Away from

side of lesion

Pneumothorax

Q1637:Lung cancer;complications

SPHERE of complications;-Superior vena cava syndrome;-Pancoast’s tumor;-Horner’s syndrome;-Endocrine

(paraneoplastic);-Recurrent laryngealsymptoms;(hoarseness);-Effusions (pleural or ;pericardial)

Q1638:Lung cancer;which types are central

-Squamous cell carcinoma;-Small-cell

Q1639:Lung cancer;which types are peripheral

Adenocarcinoma;Bronchial ;Bronchoalveolar ;Large cellcarcinoma

Q1640:Lung cancer;describe Squamous cell ;carcinoma (gross)

Hilar mass arising from bronchus; Cavitation;

Q1641:Lung cancer;which have strong smoking association

-Squamous cell carcinoma;-Small-cell

Q1642:Lung cancer;Undifferentiated → very aggressive

Small-cell (oat-cell) carcinoma

Q1643:Lung cancer;ectopic production of ACTH or ADH


Q1644:Lung cancer;Lambert-Eaton syndrome.


Q1645:Lung cancer histology;Small-cell (oat-cell) carcinoma

Neoplasm of neuroendocrine ;Kulchitsky cells → small dark;blue cells.

Q1646:Lung cancer histology;Squamous cell carcinoma

Keratin pearls and intercellular ;bridges.

Q1647:Lung cancer histology;Neoplasm of neuroendocrine;Kulchitsky cells → small dark ;blue cells


Q1648:Lung cancer histology;Keratin pearls and intercellularbridges

Squamous cell carcinoma

Q1649:Lung cancer histology;Clara cells → type IIpneumocytes multiple densities on x-ray of chest.

both types of Adenocarcinoma;Bronchial;and;Bronchoalveolar

Q1650:Lung cancer histology;Pleomorphic giant cells with;leukocyte fragments in ;cytoplasm.

Large cell carcinoma

Q1651:Lung cancer histology;Adenocarcinoma

Both Types: Clara cells → type II pneumocytes multipledensities on x-ray of chest.

Q1652:Lung cancer histology;Large cell carcinoma

Pleomorphic giant cells with ;leukocyte fragments in;cytoplasm.

Q1653:Lung cancer characteristics;Adenocarcinoma: Bronchial

Develops in site of prior pulmonary in?ammation or injury

Q1654:Lung cancer characteristics;most common lung CA innon-smokers

Adenocarcinoma: Bronchial

Q1655:Lung cancer characteristics;Develops in site of priorpulmonary in?ammation or injury

Adenocarcinoma: Bronchial

Q1656:Lung cancer characteristics;Not linked to smoking.

Adenocarcinoma: Bronchoalveolar

Q1657:Lung cancer characteristics;parathyroid-like activity→ PTHrP


Q1658:Lung cancer characteristics;Hilar mass arising frombronchus; Cavitation


Q1659:Lung cancer characteristics;Highly anaplasticundifferentiated tumor; poor prognosis.

Large cell carcinoma

Q1660:Lung cancer characteristics;Large cell carcinoma

Highly anaplastic undifferentiated tumor; poor prognosis.

Q1661:Lung cancer characteristics;Carcinoid tumor

Secretes serotonin; can cause carcinoid ;syndrome (?ushing;diarrhea; wheezing;salivation).

Q1662:Lung cancer characteristics;?ushing; diarrhea;wheezing;salivation

Carcinoid tumor

Q1663:Lung cancer characteristics;most common. Brain(epilepsy); bone (pathologic fracture); and liver

(jaundice;hepatomegaly).

Metastases

Q1664:Lung cancer common presentation features

cough; hemoptysis; bronchial ;obstruction; wheezing;pneumonic “coin” lesion on x-ray ?lm.

Q1665:cough; hemoptysis; bronchial ;obstruction; wheezing;pneumonic “coin” lesion on x-ray ?lm.

Lung cancer

Q1666:Pancoast’s tumor;where and findings

Carcinoma that occurs in apex of lung and may affect cervicalsympathetic plexus; causing ;Horner’s syndrome.

Q1667:Carcinoma that occurs in apex of lung and may affectcervical sympathetic plexus; causing ;Horner’s syndrome.

Pancoast’s tumor

Q1668:Kulchitsky cells

Enterochromaffin (EC) cells (Kulchitsky cells) are a type ofenteroendocrine cell[1] occurring in the epithelia lining the

lumen of the gastrointestinal tract. also implicated in the originof small cell lung cancer.

Q1669:Lambert-Eaton syndrome;findings

progressive weakness that does not usually involve therespiratory muscles and the muscles of face. In patients withaffected ocular and respiratory muscles; the involvement is

not as severe as myasthenia gravis. The proximal parts of thelegs and arms are predominantly affected.

Q1670:Lambert-Eaton syndrome;causes

small-cell lung cancer; lymphoma; non-Hodgkin's lymphoma

Q1671:progressive weakness that does not usually involvethe respiratory muscles and the muscles of face. In patients

with affected ocular and respiratory muscles; the involvementis not as severe as myasthenia gravis. The proximal parts of

the legs and arms are predominantly affected.

Lambert-Eaton syndrome

Q1672:Small-cell carcinoma ;aka

oat-cell carcinoma

Q1673:oat-cell carcinoma ;aka

Small-cell carcinoma

Q1674:Pneumonia types with different organism causes

Lobar - Pneumococcus usually;Bronchopneumonia - S.aureus; H. ?u; Klebsiella; S. pyogenes;Interstitial (atypical)

pneumonia - viruses (RSV; adenoviruses);Mycoplasma;Legionella; Chlamydia

Q1675:Lobar pneumonia Characteristics

Intra-alveolar exudate → consolidation; may involve entirelung

Q1676:Bronchopneumonia Characteristics

Acute in?ammatory in?ltrates ;from bronchioles into ;adjacentalveoli; patchy ;distribution involving ≥ 1 ;lobes

Q1677:Interstitial (atypical) ;pneumonia Characteristics

Diffuse patchy in?ammation ;localized to interstitial areas ;atalveolar walls; distribution involving ≥ 1 lobes

Q1678:Which type of pneumona;Intra-alveolar exudate →consolidation; may involve entire lung

Lobar

Q1679:Which type of pneumona;Acute in?ammatoryin?ltrates ;from bronchioles into ;adjacent alveoli; patchy

;distribution involving ≥ 1 ;lobes

Bronchopneumonia

Q1680:Which type of pneumona;Diffuse patchy in?ammation;localized to interstitial areas at alveolar walls; distribution

involving ≥ 1 lobes

Interstitial (atypical);pneumonia

Q1681:Which type of pneumona;Pneumococcus mostfrequently

Lobar

Q1682:Which type of pneumona;S. aureus

Bronchopneumonia

Q1683:Which type of pneumona;Viruses (RSV; adenoviruses)

Interstitial (atypical) ;pneumonia

Q1684:Which type of pneumona;Mycoplasma; Chlamydia


Q1685:Which type of pneumona;Legionella


Q1686:Interstitial pneumonia;aka

atypical pneumonia

Q1687:atypical pneumonia;aka

Interstitial ;pneumonia

Q1688:Which type of pneumona;S. aureus

Bronchopneumonia

Q1689:Which type of pneumona;H. ?u

Bronchopneumonia

Q1690:Which type of pneumona;Klebsiella

Bronchopneumonia

Q1691:Which type of pneumona;S. pyogenes

Bronchopneumonia

Q1692:what are Lung abscess and who gets them

Localized collection of pus within parenchyma; usuallyresulting from bronchial ;obstruction (e.g; cancer) or aspirationof gastric contents (especially in patients ;predisposed to loss

of consciousness; e.g; alcoholics or epileptics).

Q1693:Pleural effusions what and causes of;Transudate

decreased protein content;Due to CHF; nephrotic syndrome;or hepatic cirrhosis.

Q1694:Pleural effusions what and causes of;Exudate

increased protein content; cloudy. Due to malignancy;pneumonia; collagen vascular disease;trauma.

Q1695:Which type of Pleural effusion;decreased proteincontent

Transudate

Q1696:Which type of Pleural effusion;CHF

Transudate

Q1697:Which type of Pleural effusion;nephrotic syndrome

Transudate

Q1698:Which type of Pleural effusion;hepatic cirrhosis

Transudate

Q1699:Which type of Pleural effusion;increased proteincontent; cloudy

Exudate

Q1700:Which type of Pleural effusion;malignancy

Exudate

Q1701:Which type of Pleural effusion;pneumonia;

Exudate

Q1702:Which type of Pleural effusion;collagen vasculardisease

Exudate

Q1703:Which type of Pleural effusion;increased proteincontent

Exudate

Q1704:Which type of Pleural effusion;cloudy

Exudate

Q1705:Which type of Pleural effusion;trauma

Exudate

Q1706:1st generation H1 blockers;names

Diphenhydramine; dimenhydrinate; chlorpheniramine.

Q1707:1st generation H1 blockers;Clinical uses

Allergy; motion sickness; sleep aid.

Q1708:1st generation H1 blockers;Toxicity

Sedation; antimuscarinic; anti-alpha -adrenergic.

Q1709:1st generation H1 blockers;mech

Reversible inhibitors of H1 histamine receptors.

Q1710:2nd generation H1 blockers;mech

Reversible inhibitors of H1 histamine receptors.

Q1711:2nd generation H1 blockers;names

Loratadine; fexofenadine; desloratadine.


Allergy.


Far less sedating than 1st generation.

Q1714:Asthma drugs;name the Nonspeci?c beta -agonists

Isoproterenol

Q1715:Asthma drugs;Isoproterenol;mech and uses

Nonspeci?c beta -agonists relaxes bronchial smooth muscle(beta 2).

Q1716:Asthma drugs;Isoproterenol;toxicity

Nonspeci?c beta -agonists Adverse effect is tachycardia (beta1).

Q1717:Asthma drugs;name the beta 2 agonists

Albuterol and Salmeterol

Q1718:Asthma drugs;Albuterol;mech and uses

beta 2 agonist relaxes bronchial smooth muscle (beta 2). Useduring acute exacerbation.

Q1719:Asthma drugs;Salmeterol;mech and uses

beta 2 agonist long-acting agent for prophylaxis.

Q1720:Asthma drugs;Salmeterol;toxicity

Adverse effects are tremor and arrhythmia.

Q1721:asthma drug;Adverse effects are tremor andarrhythmia.

Salmeterol

Q1722:Asthma drugs;;name the Methylxanthines

Theophylline

Q1723:Asthma drugs;Theophylline;mech and uses

Methylxanthine - likely causes bronchodilation by inhibitingphosphodiesterase; thereby decreased ;cAMP hydrolysis.

Q1724:Asthma drugs;Theophylline;tioxicity

Usage is limited because ;of narrow therapeutic index(cardiotoxicity;neurotoxicity).

Q1725:Asthma drugs;Usage is limited because ;of narrowtherapeutic index (cardio and neuro toxicity).

Methylxanthines: Theophylline

Q1726:Asthma drugs;name the muscarinic antagonists

Ipratropium

Q1727:Asthma drugs;Ipratropium;mech and uses

competitive block of muscarinic ;receptors; preventingbronchoconstriction.

Q1728:Cromolyn ;mech and uses

Prevents release of mediators from mast cells. Effective;onlyfor the prophylaxis of asthma. Not effective ;during an acute

asthmatic attack.

Q1729:Asthma drugs;7 different Tx drug classes

1. Nonspeci?c beta -agonists ;2.beta 2 agonists ;3.Methylxanthines;4. Muscarinic antagonists ;5. Cromolyn ;6.

Corticosteroids;7. Antileukotrienes

Q1730:Cromolyn ;toxicity

Toxicity is rare.

Q1731:Asthma drugs;name the corticosteroids

Beclomethasone; prednisone

Q1732:Asthma drugs;Beclomethasone; prednisone;mech

inhibit the synthesis ;of virtually all cytokines. Inactivate NF-κB; the ;transcription factor that induces the production of

;TNF-alpha ; among other in?ammatory agents.

Q1733:1st-line therapy for chronic asthma.

Beclomethasone; prednisone

Q1734:name the Antileukotrienes

Zileuton;Za?rlukast; montelukast

Q1735:Zileuton;mech and uses

A 5-lipoxygenase pathway inhibitor. Blocks conversion ofarachidonic acid to leukotrienes;asthma

Q1736:A 5-lipoxygenase pathway inhibitor. Blocksconversion of arachidonic acid to leukotrienes.

Zileuton

Q1737:Za?rlukast; montelukast;mech and uses

Za?rlukast; montelukast––block leukotrienereceptors;Especially good for aspirin induced asthma.

Q1738:block leukotriene receptors.

Za?rlukast; montelukast

Q1739:Especially good for aspirin induced asthma.

Za?rlukast; montelukast

Q1740:Expectorants;names

-Guaifenesin (Robitussin);;-N-acetylcystine

Q1741:Guaifenesin;aka

Robitussin

Q1742:Robitussin;aka

Guaifenesin

Q1743:Guaifenesin ;mech and uses

Removes excess sputum but large doses necessary; does notsuppress cough re?ex;Expectorants

Q1744:Removes excess sputum but large doses necessary

Guaifenesin

Q1745:Mucolytic → can loosen mucus plugs in CF patients.

N-acetylcystine

Q1746:N-acetylcystine ;mech and uses

Mucolytic → can loosen mucus plugs in CF patients;alsoused as an antidote for acetaminophen overdose

Q1747:antidote for acetaminophen overdose

N-acetylcystine

Q1748:What is the epithelium of the bronchi? What are somecauses of ciliary dyskinesia?

Pseudostratisfied ciliated columnar cells with goblet (mucussecreting) cells;Primary ciliary dyskinesia: AR disorder that

renders cilia unable to beat;Secondary ciliary dyskinesia:cigarette smoking.

Q1749:Describe the differences between bronchi andconducting bronchioles.

Bronchi: many layers of SMCs; cartilage is present;pseudostratified columnar; densely ciliated; diameter is

independent on lung volume;Bronchioles: 1-3 layers of SMCs;no cartilage; simple columnar with few ciliated cells; diameter

depends on lung volume.

Q1750:Where is resistance the greatest in the lung airways?

Conducting bronchioles because they are arranged in series.Small airways are aligned in parallel; which reduces resistance

greatly (1/= 1/R1+ 1/R2;).

Q1751:What are the layers of the pulmonary membrane?

Surfactant; alveolar epithelium (mostly type I pneumocytes);BM; and capillary epithelium.

Q1752:What vertebral level does the trachea begin? Whatvertebral level does the trachea bifurcate?

The trachea begins just inferior to the cricoid cartilage; C6; andends at the sternal angle (T4) level where it bifurcates.

Q1753:What equation is used to calculate physiological deadspace?

Vd = Vt * ((PACO2 - PECO2)/PACO2) ;Vt = tidalvolume;PACO2 = PCO2 of alveolar gas;PECO2 = PCO2 of

expired air

Q1754:How is alveolar ventilation calculated?

Alveolar ventilation = (tidal volume - dead space) *breaths/min

Q1755:Which of the following can be measured byspirometry?;Tidal volume; total lung capacity; functional

residual capacity; residual volume; vital capacity?

Tidal volume and vital capacity. All other volumes listedcontain residual volume which cannot be measured.

Q1756:Use boyles law to explain inspiration of air?

PV= k. Increasing lung volume decreases the pressure whichallows atmospheric air to flow in the lungs (down a pressure

gradient).

Q1757:What muscles are used in inspiration? Expiration?

Inspiration: diaphragm and during exercise or respiratorydistress: external intercostals; scalenes;

sternocleidomastoids;Expiration: normally expiration ispassive; but during exercise: internal intercostal; innermost

intercostal; and abdominal muscles

Q1758:What are the sources of resistance during inspiration?

Airway resistance: air molecules colliding with wall =friction;Compliance resistance: expansion of alveolar andparanchyma tissue;Tissue resistance: parietal and visceral

pleura friction

Q1759:What are the sources of resistance during expiration?

Intrathoracic pressure increases which compresses airwaysand reduces airway diameter. Reduced airway diameter is the

primary source of resistance.

Q1760:Compliance work (resistance) is the energy required toovercome the intrinsic elastic recoil of the lungs. It accountsfor 75% of the total work in breathing. Is compliance work

increased or decreased in emphysema?

Emphysema destroys lung paranchyma. Compliance work isdecreases and inspiration is easy. Expiration is difficult.

Q1761:Does elastance increase or decreased in restrictive lungdisease?

Elastance will increase in restrictive lung diseases. Elastance =resist deformation. Is is inversely proportional to compliance.

E = change in P/change in V.

Q1762:Explain how emphysema changes the functionalresidual capacity.

Lung compliance (distensibility) is increased in emphysemaand the tendency of the lungs to collapse decreases. The lung-

chest wall system will seek a higher FRC until the twoopposing forces (tendency of the chest wall to expand and

collapsing force of lung) reach a new equilibrium.

Q1763:What is LaPlace's law? What decreases the collapsingforce on alveoli?

P = 2T/r;P = collapsing pressure on alveolus;T = surfacetension;r = radius of alveolus;Surfactant.

Q1764:Describe surfactant and its function.

Phophatidylcholine (phospholipid) synthesized by type IIalveolar cells and reduces surface tension by disrupting the

intermolecular forces between liquid molecules.Lecithin:sphingomyelin ratio greater than 2:1 reflects mature

levels of surfactant in the fetus.

Q1765:What is Dalton's law of partial pressure? What is thepartial pressure of oxygen in dry air; inspired air; alveolar air;

systemic arterial blood; and venous blood?

Partial pressure = total pressure * concentration of gas;O2:160; 150; 100; 100; 40;CO2: 0; 0; 40; 40; 46

Q1766:What is Fick's law of diffusion?

D = change in P * A * S / T;A = surface area;S = solubilitycoeff. of oxygen;T = distant oxygen must diffuse across

pulmonary membrane

Q1767:How is V/Q optimized for the most efficient gasexchange (ventilation matches perfusion)?

Hypoxia-induced vasoconstriction. Paradoxicalvasoconstriction in response to hypoxia.

Q1768:How does V/Q ratio change in exercise?

V/Q at rest is 0.8. During exercise; V/Q approaches 1.0 and ismore efficient. Under perfused areas become more perfuseddue to increased PA blood pressures and under ventilated

areas become more ventilated (apices).

Q1769:In terms of V/Q; whats the difference between a shuntand dead space?

In a shunt V/Q approaches 0; e.g. airway obstructions;In deadspace V/Q approaches infinity; e.g. pulmonary embolism

occluding a pulmonary artery.

Q1770:An A-a gradient greater than ____ mmHg indicates apathological condition. How are both PAO2 and PaO2

calculated?

30 mmHg;PAO2 = PiO2 - PACO2/R;PaO2 is measured witharterial blood gas labs.

Q1771:What is the oxygen saturation in arterial blood?Venous blood?

Arterial partial pressure of oxygen in arterial blood isapproximately 100 mmHg. At this PP; Hb is 100% bound. Invenous blood; the PP of oxygen is 40 mmHg. At this PP; Hb

is 75% bound to hemoglobin.

Q1772:What are some causes of hypoxia with an increase inA-a gradient? Normal A-a gradient?

Increased A-a: ventillation; perfusion; or diffusion defects; R-L shunts;Normal A-a: CNS depression; phrenic nerve lesion;

upper airway obstruction (?)

Q1773:How come the pH of venous blood only drops to 7.26(from 7.4) despite the large offloading of H+ (via CO2 + H20yielding H + HCO3)? (In other words; who is buffering the

H+ so efficiently)

Deoxyhemoglobin buffers H+ inside the RBCs.

Q1774:What is the chloride shift?

Cl ions are taken up by RBCs in exchange for HCO3. HCO3is transported to the lungs via plasma. This is how CO2 is

transported to the lungs.

Q1775:20% of CO2 is transported in the blood by Hb. Whatis the Bohr effect?

Binding of CO2 to Hb decreases the O2 affinity of Hb(facilitates offloading of oxygen).

Q1776:Where in the medulla is the respiratory center located?What part controls inspiration? Expiration?

Reticular formation. Inspiration and the basic rhythm forbreathing is controlled by the dorsal respiratory group.

Expiration (not active in normal breathing) is controlled by theventral respiratory group.

Q1777:What two centers in the pons help to controlbreathing?

Apneustic center: lower pons; stimulates deep and prolongedinspiratory gasp;Pneumotaxic center: upper pons; inhibits

inspiration; thus; regulating volume and rate

Q1778:What do central chemoreceptors in the medullarespond to?

Central chemoreceptors respond to acidosis (high CO2 levels)in the CSF and in response they increase ventilation

(breathing rate).

Q1779:What do peripheral chemoreceptors in the carotid (viaCNIX) and aortic (via CNX) bodies respond to?

Decreased PaO2 ( < 60 mmHg); decrease pH; and increasePaCO2.

Q1780:What is Ondine's curse?

Impaired autonomic control of breathing.

Q1781:What receptors are responsible for Hering-Breuerreflex?

Lung stretch receptors. When stimulated by distention of thelungs they produce a reflex decrease in breathing frequency.

Q1782:Explain why climbers must ascend mountains slowly.

Initially; decrease PaO2 stimulates hyperventilation viaperipheral chemoreceptors. This causes respiratory alkalosis.The increase pH inhibits the central chemoreceptor inductionof hyperventilation. Meanwhile; the kidney excretes HCO3 in

response to resp. alkalosis (1-3 days). When pH returns tonormal; peripheral chemoreceptors can again stimulate

hyperventilation.

Q1783:What stimulates the J receptors?

Engorgement of the pulmonary capillaries stimulate the Jreceptors which then cause rapid; shallow breathing.

Q1784:A claustrophobic girl is stuck in an elevator. Hervision becomes blurry and she feels dizzy; why?

Hyperventilation decreases PaCO2. PaCO2 is a potentvasodilator for cerebral arteries. The decrease in oxygen

delivery to the brain causes these symptoms.

Q1785:Where are irritant receptors located?

Large-diameter airways. Mediate cough; sneeze andbronchoconstriction in response to noxious substances.

Q1786:What is histotoxic hypoxia? Does supplementaloxygen alleviate symptoms?

Inability of cells to us O2 effectively (cyanide poisoning). No.

Q1787:What are some physiological responses to highaltitude (4)?

1) Hyperventilation;2) Renal hypoxia induces EPO =polycythmemia;3) Increased anaerobic metabolism increases2;3-BPG production = right shift of Hb dissociation curve;4)

Pulmonary hypoxic vasoconstriction = pulmonaryhypertension

Q1788:What is and what causes Biot's breathing?

Is: abnormal pattern of breathing characterized by groups ofquick; shallow inspirations followed by regular or irregular

periods of apnea;Cause: damage to the medulla oblongata dueto strokes or trauma or by pressure on the medulla due to

uncal or tentorial herniation. Or opioid use.

Q1789:What is and what causes Cheyne-Stokes breathing?

Is: periodic breathing amid higher PaCO2 to stimulatebreathing. Characterized by oscillation of ventilation between

apnea and tachypnea;Causes: head trauma.

Q1790:What is Kussmaul's breathing?

Bodies response to metabolic acidosis. Rapid; deep breathingto expire CO2. Often occurs in type I diabetic patients

experiencing ketoacidosis.

Q1791:How is FEV1; FVC; and FEV1/FVC affected inasthma and COPD? How about in fibrosis?

FEV1 is greatly reduced. FVC is reduced. FEV1/FVC isreduced;Fibrosis: FEV1 is reduced. FVC is greatly reduced.

FEV1/FVC is either normal or increased.

Q1792:What are Clara cells?

Clara cells are located in the bronchioles and they secrete acomponent of surfactant; metabolize toxins; and release Clions into the lumen (cGMP-guanylate cyclase ion channel).

Q1793:What are type I pneumocytes? Type II pneumocytes?

Type I pneumocytes are simple squamous epithelium joinedby tight junctions (zonula occludens) that line alveoli and have

no mitotic capacity;Type II pneumocytes are large andcuboidal shaped cells. They secrete surfactant (stored in

lamellar bodies). They are stem cells that regenerate type Iand type II pneumocytes.

Q1794:What is the function of the pores of Kohn?

These alveolar pores are found within interalveolar septae andequalize pressure within alveoli.

Q1795:Name some bronchoconstrictors;Name somebronchodilators:

BCs: LTC4; LTD4; PGF; TxA2; and parasympatheticstimulation;BDs: PGE2; sympathetic stimulation (Beta-2

agonists).

Q1796:Describe the clinical features of pink puffers(emphysema).

Thin; barrel-shaped chest; tachypneic; mild hypoxemia;hypocapnia or normocapnia.

Q1797:Describe the clinical features of blue bloaters (chronicbronchitis).

Muscular; barrel-shaped chest; severe hypoxemia withcyanosis; hypercapnia leading to respiratory acidosis; RV

failure; and systemic edema.

Q1798:Tidal volume

Volume of air that enters and leaves the lung in a single cycle.500ml

Q1799:Functional residual capacity

Amount of air in the lungs after passive expiration. 2;700ml

Q1800:Inspiratory capacity

Maximal volume of gas inspired from FRC. 4;000ml

Q1801:Inspiratory reserve volume

Air that can be inhaled after normal inspiration. 3;500ml

Q1802:Expiratory reserve volume

Air that can be expired after a normal expiration. 1;500ml

Q1803:Residual volume

Air in the lungs after maximal expiration. 1;200ml

Q1804:Vital capacity

Maximal air that can expired after maximal inspiration.5;500ml

Q1805:Total lung capacity

Air in the lungs after maximal inspiration. 6;700ml

Q1806:Total ventilation

Total ventilation = Tidal volume X respiratory rate.

Q1807:Dead space

Regions that contain air but do not exchange O2 and CO2

Q1808:Anatomic dead space

Conducting zones. Approximately equal to person't weight inpounds.

Q1809:Alveolar dead space

Alveoli with air but without blood flow

Q1810:Physiologic dead space

Anatomic dead space plus alveolar dead space

Q1811:Alveolar ventilation

Tidal volume - anatomic dead space X respiratory rate.

Q1812:Lung recoil

Force that collapses the lung. As the lung enlarges; recoilincreases and vice versa.

Q1813:Intrapleural pressure

Normally -5 cmH2O. Force that expands the lung. The morenegative; the more lung expansion.

Q1814:Lung mechanics before inspiration

Glotis is open but no air is flowing - alveolar pressure = 0.Intrapleural pressure and lung recoil are equal but opposite.

Gravity decreases intrapleural pressure at the apex andincreases it at the bases. Apex alveoli are more distended.

Q1815:Lung mechanics during inspiration

Diaphragm contracts; intrapleural pressure becomes morenegative. Expansion of alveoli makes alveolar pressure

negative causing air to flow into the lungs.

Q1816:Lung mechanics at the end of inspiration

Intrapleural pressure and recoil are the same but opposite.Alveolar pressure returns to zero and air stops flowing in.

Q1817:Lung mechanics during expiration

Diaphragm relaxes; intrapleural pressure increases; lung recoilcollpases the lung. Alveoli compress tha air and alveolar

pressure becomes positive and air flows out of the lungs untilalveolar pressure is back to zero. Lung recoil and intrapleural

pressure become equal but opposite.

Q1818:Assisted control mode ventilation

Inspiration is initiated by the patient or the machine if nosignal is detected.

Q1819:Positive end-expiratory pressure

Does not allow intraalveolar pressure to return to zero at theend of expiration. The larger lung volume prevents atelectasis.

Q1820:What is lung compliacnce?

It's the change in volume with a change in pressure. Increasedcompliance means more air flows in with a given change inpressure. Decreased compliance means the opposite. Thesteeper the slope of the lung inflation curve; the greater thecompliance. Emphysema = very compliant; fibrosis = not

compliant.

Q1821:Components of lung recoil

1) the tissue's collagen and elastin fibers and 2) the surfacetension (greatest component)

Q1822:Functions of surfactant

Lowers lung recoil and increases compliance (decreasedsurface tension) more in small alveoli than large alveoli;reduces capillary filtration forces reducing tendency to

develop edema.

Q1823:Pathophysiology of respiratory distress syndrome

Low surfactant --> increased recoil; decreased compliance (agreater change in intrapleural pressure is necessary to inflate

the lungs); alveoli collapse (atelectasis); more negativeintrapleural pressures promote capillary filtration (pulmonary

edema)

Q1824:Airway resistance

R = 1/r4; first and second bronchi have less radius thanalveoli; therefore more resistance. Ach increases resistance(bronchoconstriction); catecholamines decrease resistance

(bronchodilation)

Q1825:Effect of lung volume on airway resistance

increased lung volume --> increased radius --> decreasedresistance. The more negative the intrapleural pressure; the

less resistance

Q1826:Lung volumes in obstructive disease

increased TLC; increased RV; increased FRC; decreasedFEV1; decreased FVC; decreased FEV1/FVC

Q1827:Lung volumes in restrictive disease

decreased TLC; decreased RV; decreased FRC; decreasedFEV1; decreased FEV; increased FEV1/FVC

Q1828:Pressure of alveolar O2 and CO2

PAO2 = 100mmHg; PACO2 = 40mmHg

Q1829:Pressure of venous pulmonary capillary O2 and CO2

PvO2 = 40mmHg; PvCO2 = 47mmHg

Q1830:Pressure of arterial pulmonary capillary O2 and CO2

PO2 = 100mmHg; PCO2 = 40mmHg

Q1831:Which factors affect PCO2?

Metabolic CO2 production and alveolar ventilation

Q1832:Relationship between alveolar ventilation and PACO2

Inversely proportional. Hyperventilation decreases PACO2;hypoventilation increases PACO2.

Q1833:Relationship between PAO2 and PACO2

decreased PACO2 --> increased PAO2 (hyperventilation);increased PACO2 --> decreased PAO2 (hypoventilation)

Q1834:Which factors affect PAO2?

Atmospheric pressure; oxygen concentration of inspired airand PACO2

Q1835:What determines oxygen content?

Hemoglobin concentration. 1.34ml O2 combines with eachgram of hemoglobin.

Q1836:Amount of dissolved oxygen in the blood

0.3 volumes %; 0.3ml per 100ml of blood. Determines PO2which acts to keep oxygen bound to Hb

Q1837:What determines oxygen attachment to hemoglobin?

PO2 and the affinity of the individual attachment sites. Thehigher the affinity; the less PO2 is needed to keep it attached

Q1838:What determines PO2?

Amount of oxygen dissolved in plasma. Normally 0.3volumes %.

Q1839:Site 4 of hemoglobin

Oxygen is attached at 100mmHg. Least affinity; last site to besaturated.


Oxygen is attached at 40mmHg. More affinity than site 4; lessaffinity than site 2.


Oxygen is attached at 26mmHg which is p50. More affinity;second site to be saturated.


Oxygen remains attached under physiologic conditions.Highest affinity; first site to be saturated.

Q1843:Factors that shift oxygen dissociation curve to theright

increased CO2; increased 2;3BPG; fever; acidosis

Q1844:Factors that shift oxygen dissociation curve to the left

decreased CO2; decreased 2;3BPG; hypothermia; alkalosis;HbF; methemoglobin; carbon monoxide; stored blood

Q1845:How is CO2 carried in the blood?

5% dissolved; 5% attached to Hb (carbamino compounds);90% as bicarbonate.

Q1846:Main drive for ventilation

H+ ions from dissociated H2CO3 which stimulate centralchemoreceptors. H2CO3 is proportional to PCO2 of CSF

Q1847:Central chemoreceptors

Sense [H+] which is proportional to PCO2 and H2CO3 of theCSF (not systemic)

Q1848:Peripheral chemoreceptors

Carotid bodies (afferents via IX); aortic bodies (afferents viaX). Monitor PO2 and [H+/CO2]

Q1849:Main drive for ventilation in severe hypoxemia

Peripheral chemoreceptors sense PaO2 (dissolved oxygen)once PaO2 falls to 50-60mmHg.

Q1850:Ventilatory response to chronic hypoventilation

Peripheral chemoreceptors are the main drive for ventilationeventhough PaCO2 is increased.

Q1851:Ventilatory response to anemia

PaO2 and PACO2 are normal; therefore neither peripheral norcentral chemoreceptors respond.

Q1852:Central control of ventilation

Apneustic center in the caudal pons promotes prolongedinspiration. Pneumotaxic center in the rostral pons inhibits

apneustic center. Efferents are from the medulla to the phrenicnerve (C1-C3) to the diaphragm

Q1853:Differences in ventilation between the base and theapex of the lung

Base intrapleural pressure is -2.5; alveoli are compliant andsmall with a small volume of air but are underventilated due to

too much blood flow; Apex pressure is -10; alveoli are largeand stiff and contain a large volume of air but are

overventilated due to limited blood flow

Q1854:Differences in blood flow between the base and theapex of the lung

Blood vessels of the apex are less distended; have moreresistance and receive less blood flow. Blood vessels of the

base are more distended; have less resistance and receive moreblood flow

Q1855:Ventilation/perfussion relationship at the base of thelungs

Blood flow is higher than ventilation; the relationship is lessthan 0.8; the bases are underventilated; increased shunts

Q1856:Ventilation/perfussion relationship at the apex of thelungs

Blood flow is lower than ventilation; the relationship is morethan 0.8; the apex are overventilated; increased dead space

Q1857:What does a ventilation/perfussion relationship underand over 0.8 mean?

Under 0.8 (at the bases) lungs are underventilated and less gasexchange takes place; therefore PACO2 and end-capillary

PCO2 will be higher and PAO2 and end-capillary PO2 will belower.

Q1858:What is hypoxic vasoconstriction?

A decrease in PAO2 causes vasoconstriction and shunting ofblood through that segment.

Q1859:What is the effect of a thrombus in a pulmonaryartery?

Blood flow decreases; therefore increased Va/Q --> decreasedPACO2; increased PAO2

Q1860:What is the effect of a foreign object occluding aterminal bronchi?

Ventilation decreases; therefore decreased Va/Q --> increasedPACO2; decreased PAO2

Q1861:What constitutes a pulmonary shunt?

Regions of the lung where blood is not ventilated. Low Va/Qrelationship.

Q1862:What constitutes alveolar dead space?

Regions of the lung where there's no blood flow in spite ofventilation. High Va/Q relantionship

Q1863:Va/Q > 0.8

Represents alveolar dead space. Can be reversed withsupplemental O2

Q1864:Va/Q < 0.8

Represents a pulmonary shunt. Cannot be reversed withsupplemental O2

Q1865:What is the normal A-a gradient?

5-10 mmHg

Q1866:Hypoventilation

decreased PAO2 but diffusion and A-a gradient are normal.Perfusion-limited defect.

Q1867:What is a perfussion-limited defect?

There's a lung problem but A-a gradient is normal

Q1868:What is a diffusion-limited defect?

There's a lung problem where A-a gradient is below normal;therefore diffusion isn't normal

Q1869:Diffusion impairment lung defect

Due to structural problem (increased thickness or decreasedsurface area). A-a gradient is more than normal. Supplemental

oxygen compensates structural deficit but increased A-agradient remains. Fibrosis; emphysema.

Q1870:Diffusion capacity of the lung

Its measured with CO because it's a diffusion-limited gas.Structural problems decrease CO uptake. It's an index of

surface area and membrane thickness.

Q1871:Pulmonary right-left shunt

decreased Va/Q. Ther is an increased A-a gradient that isunresponsive to supplemental O2. Atelectasis or ARDS.

Q1872:PO2 in atrial septal defect

increased Right atrial PO2; increased right ventricular PO2;increased pulmonary artery PO2; increased pulmonary blood

flow and pressure

Q1873:PO2 in ventricular septal defect

No change in right atrial PO2; increased right ventricular PO2;increased pulmonary artery PO2; increased pulmonary flow

and pressure

Q1874:PO2 in patent ductus arteriosus

No change in right atrial PO2 nor right ventricular PO2;increased pulmonary artery PO2; increased pulmonary flow

and pressure

Q1875:Factor XII;Intrinsic; extrinsic or common?

intrinsic

Q1876:Factor XII;PTT or PT?

PTT

Q1877:Factor XII;activates?

XI

Q1878:Factor XI;Intrinsic; extrinsic; or common?

Intrinsic

Q1879:Factor XI;PTT or PT?

PTT

Q1880:Factor XI;activates?

IX;***requires Ca++ and platelet phospholipid

Q1881:Factor IX;Intrinsic; extrinsic; or common?

intrinsic

Q1882:Factor IX;PTT or PT

PTT

Q1883:Factor IX;activates?

X;**requires Ca++ and platelet phospholipid

Q1884:Factor VII;intrinsic; extrinsic; or common?

extrinsic

Q1885:Factor VII;PTT or PT?

PT

Q1886:Factor VIIa;Activates?

X;**requires Ca++ and platelet phospholipid

Q1887:Tissue factor;activates?

VII;**requires Ca++ and platelet phospholipid

Q1888:Xa and Va;Activate?

Prothrombin;**requires Ca++ and platelet phospholipid

Q1889:factor X;intrinsic; extrinsic; or common?

common

Q1890:Thrombin;activates?

Fibrinogen

Q1891:Factor which crosslinks fibrin

XIIIa

Q1892:inactivate Va and VIIIa

Protein C;Protein S;**Vitamin K dependent

Q1893:inactivates;thrombin;IXa;Xa;XIa

Antithrombin III

Q1894:activated by heparin

Antithrombin III

Q1895:generates plasmin; which cleaves fibrin

tPA

Q1896:fibrinolytic system link to complement cascade?

plasminogen activates C3

Q1897:Clotting link to kallikrein-kinin system

XIIa activates Prekallikrein ;->kallikrein

Q1898:Kallikrein link to kinin system?

kallikrein activates HMWK;-->Bradykinin

Q1899:Kinin link to Clotting system

HMWK activates Factor XII

Q1900:Kallikrein link to fibrinolytic system

Kallikrein activates Plasminogen;-->Plasmin

Q1901:Microcytic anemias: Definition

Mean Corpuscular Volume less than 80 cubic micrometers

Q1902:Macrocytic anemias: Definition

Mean Corpuscular Volume more than 100 cubic micrometers

Q1903:Normocytic anemias: Definition

Mean Corpuscular Volume between 80 and 100 cubicmicrometers

Q1904:Corrected reticulocyte count less than 3%: Bonemarrow status

Ineffective erythropoiesis

Q1905:Corrected reticulocyte count greater than or equal to3%: Bone marrow status

Effective erythropoiesis

Q1906:Regular hematocrit level

45%

Q1907:Stimuli for erythropoietin

-hypoxemia;-left-shifted oxygen binding curve;-high altitude

Q1908:Where is erythropoietin made?

Endothelial cells of peritubular capillaries

Q1909:Corrected reticulocyte count: Definition

(Actual hematocrit/45) * reticulocyte count;If polychromasia;divide by 2.

Q1910:Reticulocyte count: What does it measure?

-Effective erythropoiesis;-Must be corrected for degree ofanemia

Q1911:How long does it take for reticulocyte count toincrease after blood loss?

5-7 days.

Q1912:Microcytic (less than 80 cubic micrometers) anemias:List

-Iron deficiency;-Anemia of chronic disease;-Thalassemia(alpha and beta);-Sideroblastic anemia

Q1913:Sideroblastic anemias: List

-Chronic alcoholism (most common);-Pyridoxine (B6)deficiency;-Lead poisoning

Q1914:Anemias of chronic disease: List

-Chronic inflammation (eg rheumatoid arthritis; TB);-Alcoholism;-Malignancy

Q1915:Type of anemia: Iron deficiency

Early-stage: Normocytic with a low reticulocyte count;Later-stage: Microcytic

Q1916:Type of anemia: Anemia of chronic disease

Early-stage: Normocytic with a low reticulocyte count;Later-stage: Microcytic

Q1917:Type of anemia: Thalassemia

Microcytic

Q1918:Sign: Dark blue iron granules around the nucleus ofdeveloping normoblasts

Ringed sideroblasts; indicating sideroblastic anemia

Q1919:Type of anemia: Sideroblastic

Microcytic

Q1920:Type of anemia: Pyridoxine deficiency

Sideroblastic; so Microcytic

Q1921:Type of anemia: Lead poisoning

Sideroblastic; so microcytic

Q1922:Type of anemia: Alcoholism

Either sideroblastic; or anemia of chronic disease. Either way;microcytic.

Q1923:Type of anemia: Rheumatoid arthritis

Chronic inflammation; so anemia of chronic disease; somicrocytic

Q1924:Type of anemia: TB

Chronic inflammation; so anemia of chronic disease; so;Early:Normocytic with low reticulocyte count;Later: Microcytic

Q1925:Type of anemia: Malignancy

Anemia of chronic disease; so microcytic

Q1926:Type of anemia: Vitamin B12 deficiency

B12 deficiency or metabolism defect means megaloblasticmacrocytic

Q1927:Type of anemia: Vitamin B12 metabolism defect

B12 deficiency or metabolism defect means megaloblasticmacrocytic

Q1928:Type of anemia: Folate deficiency

Folate deficiency or metabolism defect means megaloblasticmacrocytic

Q1929:Type of anemia: Folate metabolism defect

Folate deficiency or metabolism defect means megaloblasticmacrocytic

Q1930:Type of anemia: DNA synthesis defect

Macrocytic megaloblastic

Q1931:Type of anemia: Liver disease

non-megaloblastic macrocytic;or ;normocytic with a normalreticulocyte count and an extrinsic RBC defect

Q1932:Type of anemia: Cytotoxic drugs

Macrocytic non-megaloblastic

Q1933:Type of anemia: Hypothyroidism


Q1934:Type of anemia: Stress erythropoiesis


Q1935:Type of anemia: Blood loss

Normocytic;Reticulocyte count;-Less than one week: low;-More than one week: normal

Q1936:Type of anemia: Aplastic anemia

Normocytic with a low reticulocyte count

Q1937:Type of anemia: Renal disease

Normocytic;Reticulocyte count;-low;-normal: extrinsic defecthemolytic anemia

Q1938:Type of anemia: Absence of erythropoietin


Q1939:Type of anemia: Replacement of bone marrow


Q1940:Type of anemia: Hereditary spherocytosis

Membrane defect; so;Normocytic hemolytic anemia withnormal reticulocyte count

Q1941:Type of anemia: Hereditary elliptocytosis

Membrane defect; so;Normocytic with normal reticulocytecount

Q1942:Type of anemia: South-East Asian Ovalocytosis


Q1943:Type of anemia: Paroxysmal NocturnalHemoglobinuria


Q1944:Type of anemia: G6PD deficiency

Metabolism defect so;Normocytic hemolytic anemia withnormal reticulocyte count

Q1945:Type of anemia: Glutathione deficiency


Q1946:Type of anemia: Pyruvate kinase deficiency


Q1947:Type of anemia: Sickle cell disease

Hemoglobin defect so;Normocytic hemolytic anemia withnormal reticulocyte count

Q1948:Type of anemia: Drugs

Normocytic hemolytic anemia with normal reticulocyte count

Q1949:Type of anemia: Chemical/Physical agents


Q1950:Type of anemia: Snake bite venom

Toxin so;Normocytic hemolytic anemia with normalreticulocyte count

Q1951:Type of anemia: Clostridial toxin

Toxin so;Normocytic hemolytic anemia with normalreticulocyte count

Q1952:Type of anemia: Burns

Injury so;Normocytic hemolytic anemia with normalreticulocyte count

Q1953:Type of anemia: Fresh water drowning

Injury so;Normocytic hemolytic anemia with normalreticulocyte count

Q1954:Type of anemia: Hypersplenism


Q1955:Type of anemia: Cold antibody type

Autoimmune so;Normocytic hemolytic anemia with normalreticulocyte count

Q1956:Type of anemia: Warm antibody type

Autoimmune so;Normocytic hemolytic anemia with normalreticulocyte count

Q1957:Type of anemia: Alloimmune

Immune so;Normocytic hemolytic anemia with normalreticulocyte count

Q1958:Type of anemia: Drug induced immune hemolyticanemia

Drug-induced and/or immune so;Normocytic hemolyticanemia with normal reticulocyte count

Q1959:Type of anemia: Vasculitis

Red cell fragmentation syndrome so;Normocytic hemolyticanemia with normal reticulocyte count

Q1960:Type of anemia: Mechanical devices


Q1961:Type of anemia: Microangiopathic hemolytic anemia


Q1962:Type of anemia: Macroangiopathic hemolytic anemia


Q1963:Type of anemia: March hemoglobinuria


Q1964:How do you identify a reticulocyte?

-Supravital stain (new methylene blue);-RNA filaments

Q1965:How do you get hemoglobin from hematocrit?

hb = (1/3)hct

Q1966:For every unit of packed red blood cells; you increase:

hemoblobin by 1;hematocrit by 3

Q1967:Most common cause of anemia in the world

iron deficiency

Q1968:Most common cause of iron deficiency

GI bleed

Q1969:RDW: Definition

RBC Distribution Width;Checks uniformity of size.

Q1970:Low MCV with Increased RDW

-Increases variation in size: Mixture of normocytic andmicrocytic RBCs;-Iron deficiency

Q1971:Spherocyte: membrane defect

Too little membrane

Q1972:Target cell: membrane defect

Too much membrane so more hemoglobin can collect in themiddle

Q1973:Target cell: markers for what?

-Alcoholism;-Hemoglobinopathy

Q1974:How to identify a microcytic cell

Too much central pallor

Q1975:How to identify a spherocyte

-No central pallor;-Small and red

Q1976:Spoon nails: Sign of?

Iron deficiency

Q1977:Cheilosis: Sign of?

-Iron deficiency;-Riboflavin deficiency

Q1978:Pale conjunctiva: Sign of?

Low hemoglobin

Q1979:No red in palmar creases: Sign of?

Iron deficiency

Q1980:Discoloration of gum margin: Sign of?

Known as "lead lines". A sign of lead poisoning.

Q1981:Normal serum iron

About a 100 (like the alveolar oxygen)

Q1982:Serum ferritin: what is it?

Soluble circulating form of iron storage

Q1983:Serum ferritin: what does it represent?

Amount of iron in bone marrow;-Best overall screening test

Q1984:Carrying protein for iron

Transferrin (Carries iron)

Q1985:TIBC: What does it measure?

Transferrin

Q1986:What does increased TIBC indicate?

Increased transferrin synthesis by liver; so decreased ironstores in the bone marrow.

Q1987:What does decreased TIBC indicate?

Decreased transferrin synthesis by liver; so increased ironstores in the bone marrow.

Q1988:Define: % iron saturation

Serum iron/TIBC

Q1989:Normal TIBC

300

Q1990:Normal % iron saturation

33%;=normal serum iron/ normal TIBC = 100/300

Q1991:Hemoglobin type: 2 alpha chains and 2 beta chains

HbA

Q1992:Hemoglobin type: 2 alpha chains and 2 delta chains

HbA2

Q1993:Hemoglobin type: 2 alpha chains and 2 gamma chains

HbF

Q1994:Mechanism of pathogenesis in Anemia of ChronicDisease

Bugs increase reproduction with iron; so body assumes thereis a bacterial infection; and keeps iron away from bacteria;Ironis normally stored in macrophages in bone marrow. It's kept

away from RBCs.

Q1995:Where does Hemoglobin synthesis begin?

Mitochondria of RBC

Q1996:First reaction of Hemoglobin synthesis

Succinyl CoA + Glycine (catalyzed by ALA synthetase)yields delta-ALA;all in the mitochondria

Q1997:What kind of neurotransmitter: Glycine

Inhibitor of muscle.

Q1998:What toxin blocks glycine?

Tetanus

Q1999:Rate limiting step in Heme synthesis

delta-ALA synthesis

Q2000:What enzyme does heme inhibit?

ALA synthase

Q2001:Why does alcoholism cause sideroblastic anemia?

Alcohol is a mitochondrial toxin.

Q2002:What are sideroblasts?

Overloaded mitochondria

Q2003:Why does B6 deficiency cause sideroblastic anemia?

Can't form CoA; so can't form succinyl CoA; so can't do firstreaction of heme synthesis.

Q2004:Mechanism of lead poisoning

Lead denatures ferrochelatase --> Can't form heme

Q2005:Test for lead poisoning

Blood lead levels

Q2006:What are the main groups that we see alpha-thalassemia?

-Southeast asians;-Black Americans

Q2007:What are the main populations we see beta-thalassemia in?

-black Americans;-Greeks;-Italians

Q2008:% of Hb that is: HbA

95%

Q2009:% of Hb that is: HbA2

2%

Q2010:% of Hb that is: HbF

1%

Q2011:alpha-thalassemia: mode of inheritance

Autosomal recessive

Q2012:alpha-thalassemia: pathogenesis

problem making alpha chains

Q2013:alpha-thalassemia: electropheresis results

all normal proportions (all Hbs decreased)

Q2014:alpha-thalassemia: one gene deletion

Silent carrier

Q2015:alpha-thalassemia: two gene deletions

alpha-thalassemia minor;-mild anemia (microcytic becauseglobin is decreased)

Q2016:alpha-thalassemia: three gene deletions

Four beta chains form making HbH. Found inelectropheresis;Called HbH disease

Q2017:alpha-thalassemia: four gene deletions

Four gamma chains form making Hb Bart. Found inelectropheresis. Called hydrops fetalis.

Q2018:Why is choriocarcinoma increased in far east?

1. Increased alpha thalassemia rates;2. Increased spontaneousabortions due to Hb Bart;3. Increased choriocarcinoma

Q2019:alpha-thalassemia: treatment

Q2020:beta-thalassemia: permutations of problems

beta by itself: normal number of beta chains;beta with a +sign: not making enough; but are making;beta with a 0: not

making it at all

Q2021:beta-thalassemia: mode of inheritance

autosomal recessive

Q2022:beta-thalassemia: what is the genetic association withsevere anemia?

Nonsense mutation with formation of a stop codon

Q2023:beta-thalassemia: what hemoglobin will decrease

HbA

Q2024:beta-thalassemia: what hemoglobins will increase

HbA2 and HbF

Q2025:beta-thalassemia: electropheresis results

Will show increased HbA2 and HbF with decreased HbA

Q2026:beta-thalassemia: treatment

none

Q2027:Cooley's anemia: disease type

Not making any beta chains (beta 0)

Q2028:Cooley's anemia: Prognosis

Will not live past 30

Q2029:Main way to tell Anemia of chronic disease from Irondeficiency

Ferritin levels;Low: Iron deficiency;High: Anemia of chronicdisease

Q2030:Stain used to find Ringed Sideroblasts

Prussian Blue

Q2031:Histologic sign associated with Lead poisoning

Coarse basophilic stippling

Q2032:Where does stippling come from?

Inability to break down ribosomes.

Q2033:Classic presentation of lead poisoning in children

-Severe abdominal colic;-Cerebral edema (convulsions; etc);-Severe microcytic anemia;-Failure to thrive

Q2034:What is seen on a flat plate?

-Iron (if kid took iron tablets);-Lead (from intestine);-Mercury

Q2035:Mechanism of lead poisoning

Buildup of delta-ALA; leading to neuronal toxicity

Q2036:Presentation of lead poisoning in adults

-Workers from automobile factory or moonshine makers orpottery painters;-Abdominal colic;-Diarrhea;-Neuropathy

(slapping gait; drops (radial; ulnar palsies); claw hand

Q2037:What is the disease: Serum Iron (low); TIBC (high); %iron saturation (low); Serum ferritin (low)

Iron deficiency

Q2038:What is the disease: Serum Iron (low); TIBC (low); %iron saturation (low); Serum ferritin (high)

Anemia of Chronic Disease

Q2039:What is the disease: Serum Iron (normal); TIBC(normal); % iron saturation (normal); Serum ferritin (normal)

Thalassemia

Q2040:Sideroblastic anemias: Iron status

Iron overload

Q2041:Hemochromatosis: Iron status

Iron overload

Q2042:Hemosiderosis: Iron status

Iron overload

Q2043:What is the disease: Serum Iron (high); TIBC (low); %iron saturation (high); Serum ferritin (high)

Iron overload (Sideroblastic anemia; hemochromatosis;hemosiderosis)

Q2044:What do B12 and folate deficiencies most immediatelynot allow production of?

dTMP (using Thymidylate synthase) leading to lack of DNAproduction

Q2045:What is the size of immature nuclei?

Nucleus gets smaller and more condensed due to increasedDNA?

Q2046:What are cells called with immature nuclei?

Megaloblasts

Q2047:Why is B12 called Cobalamin?

It has cobalt in it.

Q2048:What is the circulating form of Folate?

N5-methyl-Tetrahydrofolate

Q2049:What does B12 do in folate metabolism?

B12 removes methyl group from N5-methyl-THF to makeTHF

Q2050:What happens when you add a methyl group tohomocysteine?

Methionine

Q2051:Which amino acid is used for one-carbon transfers?

Methionine

Q2052:What are serum homocysteine levels in B12 or THFdeficiency?

High

Q2053:Why do high homocysteine levels producethromboses?

It damages endothelial cells predisposing them to thrombosis.

Q2054:What is the most common cause of high homocysteinelevels?

Folate deficiency

Q2055:Drugs which inhibit folate metabolism

5-fluorouracil (which inhibits thymidylatesynthase);Methotrexate and TMP-SMX (which both inhibit

DHF reductase); Phenytoin (which inhibits intestinalconjugase); Oral contraceptives and alcohol (which both

inhibit of uptake of monoglutamate in jejunum; but alcoholalso inhibits the release of folate from the liver)

Q2056:What happens if B12 is missing to Methylmalonyl-CoA?

It builds up; because it cannot form succinyl-coA

Q2057:Sensitive test for B12 deficiency

Methylmalonic acid

Q2058:What is methylmalonic acid level a test for?

B12 deficiency

Q2059:What is the mechanism of B12 deficiency leading toneurologic deficiencies?

Propionyl CoA builds up; and myelin production is deficient.

Q2060:What are the neurologic effects of B12 deficiency?

Dementia; demyelination of posterior columns(proprioception and vibratory sensation) and lateralcorticospinal tract (upper motor neuron problems)

Q2061:Serum levels to order in dementia

TSH to rule out hypothyroidism and B12 to rule out B12deficiency

Q2062:Where is B12 gotten from?

Animal products

Q2063:What is the first factor B12 binds to?

R factor

Q2064:What does R factor do?

It protects B12 from being destroyed?

Q2065:Where does intrinsic factor come from?

Parietal cells in the gastric body and fundus.

Q2066:Where is vitamin B12 absorbed?

Terminal ileum

Q2067:What deficiencies are found in Crohn's disease?

Bile salts and vitamin B12 (both due to reabsorptionproblems in terminal ileum)

Q2068:Most common cause of B12 deficiency

Pernicious anemia

Q2069:What is the mechanism in pernicious anemia?

Autoimmune destruction of parietal cells and intrinsic factor

Q2070:What is achlorhydria?

Atrophic gastritis of the body and fundus leading to ;lack ofacid which leads to gastric adenocarcinoma;AND;bacterial

overgrowth from stasis

Q2071:Causes for achlorhydria

Tapeworms; pernicious anemia; folate deficiency

Q2072:Eaten form of folate

Polyglutamate

Q2073:What converts polyglutamate to monoglutamate?

Intestinal conjugase

Q2074:What drug blocks intestinal conjugase?

Phenytoin

Q2075:What is the mechanism of Phenytoin?

Blocks intestinal conjugase

Q2076:What blocks absorption of monoglutamate fromjejunum?

Alcohol and oral contraceptives

Q2077:What are hypersegmented neutrophils with neurologicdeficiency diagnostic for?

Vitamin B12 deficiency

Q2078:What are hypersegmented neutrophils withoutneurologic deficiency diagnostic for?

Folate deficiency

Q2079:What is a characteristic CBC finding in macrocyticanemia?

Pancytopenia

Q2080:Schilling's test

1. Give radioactive B12 by mouth;2. 24 hour urinecollection;3. If nothing comes out; can't reabsorb B12;4. Thengive radioactive B12 and intrinsic factor together by mouth;5.

24 hour urine collection. If something comes out; it'spernicious anemia. If not; go to step 6;6. Give broad-spectrum

anti-biotic. If you see B12 in the urine; you have bacterialovergrowth. If not; go to step 7;7. Take pancreatic extract

with radioactive B12. If you get B12 in the urine; they havechronic pancreatitis. If not; it could be Crohn's disease; a

worm; or some other cause.

Q2081:Stages of iron deficiency

1. Ferritin goes down;2. Iron decreases; TIBC increases; %iron sat decreases;3. Mild normocytic anemia;4. Microcytic

anemia

Q2082:What test must be ordered to confirm aplastic anemia?

Bone marrow study

Q2083:Most common cause of aplastic anemia

Idiopathic

Q2084:Most common known cause of aplastic anemia

Drugs (Indomethacin; Phenylbutazone; Thyroid-related drugs;Chloramphenicol)

Q2085:Second most common known cause of aplastic anemia

Hepatitis C

Q2086:Most common infective cause of pure RBC aplasia

Parvovirus

Q2087:Mechanisms of hemolysis

1) Intravascular hemolysis;2) Extravascular hemolysis whichis more common

Q2088:What is the mechanism of extravascular hemolysis?

Macrophages kill them at the Cords of Bilroth

Q2089:What are some causes of RBCs being phagocytosed atthe cords of Bilroth?

IgG or c3b on the surface;or Howell-Jolly bodies inside; or anabnormal shape (such as spherical or sickle cell)

Q2090:End product of phagocytosing an RBC

Unconjugated bilirubin

Q2091:Clinical finding in extravascular hemolysis

Jaundice; which is due to unconjugated bilirubin due tomacrophages phagocytosing red blood cells.

Q2092:Causes of intravascular hemolysis

1) Congenital bicuspid aortic valve;2) IgM binding to surfaceand activating complement system

Q2093:End product of intravascular hemolysis

Hemoglobin

Q2094:Name of protein which binds free hemoglobin in blood

Haptoglobin

Q2095:Clinical findings in intravascular hemolysis

1) Hemoglobinuria;2) Low haptoglobin levels

Q2096:general steps in hormone synthesis

1. preprohormone synthesized in rER; 2. signal peptidescleaved--> prohormone transported to Golgi; 3. more cleavagein golgi and HORMONE then packaged in secretory granules

Q2097:amine hormones

derivates of TYROSINE; include thyroid hormone; Epi; NE

Q2098:active form of G protein?

ATP-bound to alpha subunit

Q2099:how does caffeine work?

inhibits phosphodiesterase which degrades cAMP (get morecAMP)

Q2100:IP3 signalling mech

hormone + R--> Gq --> PLC --> DAG and IP3 --> PKC

Q2101:which hormones of anterior pituitary mosthomologous to TSH?

FSH; LH (identical alpah subunits)

Q2102:"children" of POMC

ACTH; MSH; beta-lipotropin; beta-endorphin

Q2103:which hormone of anterior pituitary most related toGH?

prolactin

Q2104:what increases the pulsatile secretion of GH?

sleep; stress; puberty; starvation; exercise; hypoglycemia

Q2105:what decreases GH secretion?

somatostatin; somatomedins; obesity; hyperglycemia;preggers

Q2106:what does GH do in liver?

causes production of somatomedins (insulin-life growthfactors)

Q2107:4 direct actions of GH

1. dec'd glucose uptake into cells; 2. inc'd lipolysis; 3. inc'dprotein synthesis in mm; 4. inc'd production of IGF

Q2108:actions of GH via IGF

inc'd protein synthesis! In chondrocytes--> growth spurt; inmm-->inc'd lean body mass; inc'd organ size

Q2109:how is prolactin secretion regulated?

tonic inhibition by dopamine (which is stimulated by PRL);TRH increases PRL secretion

Q2110:4 actions of PRL

1. stim milk production; 2. stim breast development(w/estrogen); 3. inhibits ovulation via GnRH inhibition; 4.

inhibits spermatogenesis

Q2111:how treat PRL excess?

bromocriptine (DA agonists)

Q2112:hormones of the posterior pituitary?

ADH (supraoptic hypothal); oxytocin (paraventricularhypothal)

Q2113:what inhibits the iodide pump/trap in thyroidfollicular epithelial cells?

thiocyanate and perchlorate anions

Q2114:Wolff-Chaikoff effect?

high levels of I- inhibit I- pump

Q2115:significance of propylthiouracil?

inhibits peroxidase enzyme (which first catalyzes oxidation ofI- to I2;and then other steps); used for treatment of

hyperthyroidism

Q2116:what happens when TSh stimulates thyroid?

iodinated thyroglobulin is taken back into follicular cells;digested and T3; T4 released into circulation. Leftover MIT;

DIT deiodinated by thyroid deiodinase

Q2117:what happens to T3; T4 in circulation?

mostly bound to TBG (inc'd in preggers); peripherally; T4-->T3 or rT3

Q2118:bone manifestation of thyroid deficiency?

bone age < chronologic age; b/c TH stimulates bonematurations

Q2119:effect of TH on heart?

upregulates beta 1 R

Q2120:effect of TH on O2 consumption?

increases b/c of upregulation of Na-K ATPase (which usesATP;which comes from O2;kinda)

Q2121:which part of adrenal cortex makes mineralocorticoids?

(outermost) zona glomerulosa (works on kidneys;which haveglomeruli)

Q2122:which part of adrenal cortex makes glucocorticoids?

(middle) zona fasciculata

Q2123:which part of adrenal cortex makes androgens (DHEA;androstenedione)

(innermost) zona reticularis (b/c you should be reallyparticularis of your sex partners)

Q2124:effect of ACTH on adrenal cortex?

stimulates cholesterol desmolase thereby increasing steroidsynthesis; also upregulates own R

Q2125:control of aldosterone secretion?

tonically--ACTH; also Ang II stimulates aldosterone synthase(corticosterone--> aldosterone)

Q2126:4 actions of glucocorticoids

1. stim gluconeogenesis; 2. anti inflamm; 3.immunosuppressive; 4. upregulate alpha 1 R on arterioles

Q2127:how do glucocorticoids stimulate gluconeogenesis?

1. increase protein catabolism in mm (more aa available);2)decrease glucose utilization and insulin sensitivty of fat; 3)

increase lipolysis (more glycerol available)

Q2128:how are glucocorticoids anti-inflammatory?

induce synthesis of lipocortin (inhibits PLA2); inhibitproduction of IL-2; thereby inhibit proliferation of T cells;inhibit relase of His and serotonin from mast cells; platelets

Q2129:Name the dz: Increased ACTH; hypoglycemia;hyperpigmentation; ECF volume contraction

Addison's disease

Q2130:how is secondary adrenocortical insufficiency differentfrom Addison's?

no hyperpigmentation; no volume contraxn ;hyperKalemia;metab acidosis

Q2131:Conn's syndrome leads to?

HTN; hypokalemia; metab alkalosis; dec'd renin

Q2132:name the dz: decreased cortisol and aldosterone;increased adrenal androgens; virilization; suppression of gonad

function

21 hydroxylase deficiency

Q2133:name the dz: decreased androgen and glucocorticoidlevels; increased aldosterone; hypoglycemia; lack of pubes

17 hydroxylase deficiency

Q2134:3 major cell types and their main export in islets ofLangerhans?

alpha--glucagon; beta--insulin; delta--somatostatin; gastrin

Q2135:what do delta cells islets of Langerhans secrete?

somatostatin; gastrin

Q2136:what stimulates glucagon release from alpha cells?

decreased blood glucose

Q2137:3 actions of glucagon

1. increase blood glucose; 2. increase blood FA; ketoacids; 3.increase urea production

Q2138:mechanism of insulin secretion?

glucose binds GLUT 2 on beta cell membrane-->depolarization of membrane--> Ca channel opens; influx -->

insulin secretion

Q2139:why get hyPOtension in uncontrolled DM?

high [glucose] exceeds Tm in kidney so urine is very sugary-->osmotic diuretic

Q2140:what stimulates secretion of PTH?

dec'd Ca; mildly dec'd Mg (severe hypoMg inhibits PTHsecretion!)

Q2141:"goal" of PTH

increase calcium; decrease phosphate

Q2142:4 actions of PTH

1. increase bone reabsorp; 2 inhibit renal phosphatereabsorp.(PCT); 3. increase renal Ca reabsorp; 4. stimulate

production of active vit D

Q2143:Albright's hereditary osteodystrophy

pseudohypoparathyroidism cause by defective Gs in kidenyand bone-->end organ resistance to PTH

Q2144:how does chronic renal failure lead to hypocalcemia?

increased GFR--> increased sr phosphate which complexeswith Calcium; thereby decreasing free Ca; also decreased vit D

Q2145:"goal" of vit D

increase calcium and phosphate in ECF for bonemineralization

Q2146:Calcitonin: a) where b)stim'd by c)action

a)parafollicular thyroid cells; b) increased sr Ca; c) inhibitbone reabsorp.

Q2147:what do Leydig cells make?

testosterone

Q2148:why can't Leydig cells make glucocorticoids andmineralocorticoids?

no 21 beta hydroxylase or 11 beta hydroxylase

Q2149:significance of 5 alpha reductase?

enzyme that converts testosterone to DHT; found inaccessory sex organs like the prostate

Q2150:significance of finasteride?

inhibits 5alpha reductase (can tx BPH)

Q2151:FSH acts on Sertoli cells to?

stimulate production of inhibin which has negative feedbackeffect on FSH

Q2152:what do theca cells make?

androgens which are converted to estrogens by aromatase ingranulosa cells

Q2153:2 causes of end organ ADH resistance

1. drugs (Li!!! Inhibits Gs); 2. severe hypercalcemia (inhibitsAC)

Q2154:which diuretics can also be used for treatment of acutemountain sickness?

carbonic anhydrase inhibitors like acetazolamide (metabolicacidosis to combat respiratory alkalosis)

Q2155:why get HTN in 11beta hydroxylase deficiency?

the precursor that the enzyme would act on is a weakmineralocorticoid

Q2156:Factors that affect hormone binding protein synthesis

Estrogen increases binding proteins; androgens decreasebinding proteins. In pregnancy there's increased total

hormones with normal levels of free hormone.

Q2157:Site of synthesis of CRH

Paraventricular nucleus

Q2158:Site of synthesis of TRH

Paraventricular nucleus

Q2159:Site of synthesis of PIF

Arcuate nucleus

Q2160:Site of synthesis of GHRH

Arcuate nucleus

Q2161:Site of synthesis of GnRH

Preoptic region

Q2162:Site of synthesis of ADH

Supraoptic and paraventricular nuclei

Q2163:How do hypothalamic hormones reach the anteriorpituitary?

Hormones are released in the hypophyseal-portal system

Q2164:Hypothalamic hormones

GHRH; GnRH; PIF (dopamine); TRH; CRH; Somatostatin;ADH; prolactin

Q2165:Anterior pituitary hormones

ACTH; TSH; LH; FSH; GH; prolactin

Q2166:Sheehan syndrome

Ischemic necrosis of the pituitary due to severe blood lossduring delivery. Causes hypopituitarism.

Q2167:Obstruction of pituitary stalk

Adenoma compresses pituitary stalk and decreases secretionof anterior pituitary hormones except prolactin.

Q2168:What prevents downregulation of pituitary receptors?

Pulsatile release of hypothalamic hormones.

Q2169:Hyperprolactinemia

Results from dopamine antagonists or pituitary adenomasthat compress the pituitary stalk. Amenorrhea; galactorrhea;

decreased libido; impotence; hypogonadism

Q2170:What hormone controls release of cortisol and adrenalandrogens?

ACTH

Q2171:What hormone regulates release of aldosterone?

Angiotensin II and also potassium in hyperkalemia

Q2172:Layers of the adrenal cortex

From external to internal: glomerulosa (aldosterone);fasciculata (cortisol); reticularis (androgens)

Q2173:Consequences of loss of zona glomerulosa

No aldosterone: loss of Na; decreased ECF; decreased bloodpressure; circulatory shock; death

Q2174:Consequences of loss of zona fasciculata

No cortisol: circulatory failure (cortisol is permissive forcathecolamine vasoconstriction); can't mobilize energy stores

during exercise or cold (hypoglycemia)

Q2175:Consequences of loss of adrenal medulla

No epinephrine: decreased capacity to mobilize fat andglycogen during stress. Not necessary for survival.

Q2176:What are the 17-OH steroids?

17OHpregnenolone; 17OHprogesterone; 11-deoxycortisol;cortisol. Urinary 17OH steroids are an index of cortisol

secretion.

Q2177:What is the rate-limiting enzyme for steroid hormonesynthesis?

Desmolase - converts cholesterol into pregnenolone

Q2178:What are the 17-ketosteroids?

DHEA and androstenidione

Q2179:DHEA

Weak androgen 17-ketosteroid conjugated with sulfateto makeit water-soluble

Q2180:What is measured as an index of androgen production?

Urinary 17-ketosteroids. In females and prepubertal males isan index of adrenal 17-ketosteroids. In postpubertal males is

an index of 2/3 adrenal androgens and 1/3 testicular androgens.

Q2181:Stimulus for the zona glomerulosa

Angiotensin II and potassium in hyperkalemia stimulateproduction of aldosterone

Q2182:Hormone responsible for negative feedback for ACTHrelease

Cortisol

Q2183:Enzyme deficiencies that produce congenital adrenalhyperplasia and low cortisol levels

21beta -OH; 11beta -OH and 17alpha -OH all result in lowcortisol levels.

Q2184:21beta -OH deficiency

No aldosterone: loss of Na; decreased ECF; decreased bloodpressure in spite of high renin and angiotensin II; circulatory

shock; death. No cortisol (low 17OH steroids): skinhyperpigmentation (due to excess ACTH); adrenal

hyperplasia; hypotension (persmissive for catecholamines);fasting hypoglycemia. Excess androgens (17-ketosteroids):

female pseudohermaphrodite; hirsutism

Q2185:11beta -OH deficiency

Excess 11-deoxycorticosterone: Na and water retention; low-renin hypertension. No cortisol (low 17OH steroids): skin

hyperpigmentation (due to excess ACTH); adrenalhyperplasia; fasting hypoglycemia. Excess androgens (17-

ketosteroids): female pseudohermaphrodite; hirsutism

Q2186:17alpha -OH deficiency

Excess 11-deoxycorticosterone and low aldosterone (no AII):Na and water retention; low-renin hypertension. No cortisol:

skin hyperpigmentation (due to excess ACTH); adrenalhyperplasia; corticosterone partially compensates low

cortisol levels. No 17-ketosteroids: malepseudohermaphrodite; no testosterone; no estrogen.

Q2187:decreased 17OH-steroids increased ACTH; decreasedblood pressure; decreased mineralocorticoids; increased 17-

ketosteroids

21beta -OH deficiency

Q2188:decreased 17OH-steroids increased ACTH; increasedblood pressure; decreased aldosterone; increased 11-

deoxycorticosterone; increased 17-ketosteroids

11beta -OH deficiency

Q2189:decreased 17OH-steroids increased ACTH; increasedblood pressure; decreased aldosterone; increased 11-

deoxycorticosterone; decreased 17-ketosteroids

17alpha -OH deficiency

Q2190:Stress hormones

GH; Glucagon; cortisol; epinephrine

Q2191:Actions of GH in stress situations

Mobilizes fatty acids by increasing lipolysis in adipose tissue

Q2192:Actions of glucagon in stress situations

Mobilizes glucose by increasing liver glycogenolysis

Q2193:Actions of cortisol in stress situations

Mobilizes fat; carbs and proteins

Q2194:Actions of epinephrine in stress

Mobilizes glucose via glycogenolysis and fat via lipolysis.

Q2195:Metabolic actions of cortisol

1) Protein catabolism and delivery of amino acids; 2) lipolysisand delivery of fatty acids and glycerol 3) gluconeogenesis

raises glycemia; also inhibits glucose uptake.

Q2196:Permissive actions of cortisol

Enhances glucagon (without cortisol --> fastinghypoglycemia); enhances epinephrine (without cortisol --

>hypotension)

Q2197:alpha -MSH

Stimulates melanocytes and causes darkening of skin.Synthesized along with ACTH from pro-opiomelanocortin.

Q2198:increased cortisol; decreased CRH; decreased ACTH;no hyperpigmentation

Primary hypercortisolism

Q2199:decreased cortisol; increased CRH; increased ACTH;hyperpigmentation

Addison disease - primary hypocortisolism

Q2200:increased cortisol; decreased CRH; increased ACTH;hyperpigmentation

Secondary hypercortisolism

Q2201:decreased cortisol; increased CRH; decreased ACTH;no hyperpigmentation

Secondary hypocortisolism

Q2202:decreased cortisol; decreased CRH; decreased ACTH;no hyperpigmentation; symptoms of excess cortisol

Steroid administration

Q2203:Cushing syndrome

Protein depletion; weak inflammatory response; poor woundhealing; hyperglycemia; hyperinsulinemia; insulin resistance;

hyperlipidemia; osteoporosis; purple striae; hirsutism;hypertension; hypokalemic alkalosis; buffalo hump

Q2204:Actions of aldosterone

increased Na channels in lumen of principal cells; increasedactivity of Na/K ATPase of principal cells --> increases Na

reabsorption. Also increased secretion of K and H leading tohypokalemic metabolic alkalosis.

Q2205:Addison disease

increased ACTH; hyperpigmentation; hypotension (noaldosterone; no cortisol); hyperkalemic metabolic acidosis (noaldosterone); loss of body hair (no androgens); hypoglycemia;

increased ADH secretion

Q2206:Causes of secondary hyperaldosteronism

CHF; vena cava constriction; cirrhosis; renal artery stenosis

Q2207:Primary hyperaldosteronism

Na and water retention; hypertension; hypokalemic metabolicalkalosis; decreased renin and angiotensin; no edema due to

pressure diuresis and natriuresis.

Q2208:Primary hypoaldosteronism

Na and water loss; hypotension; hyperkalemic metabolicacidosis; increased renin and angiotensin II; no edema

Q2209:Secondary hyperaldosteronism

increased renin and angiotensin II; increased Na and waterretention in venous circulation; edema

Q2210:Factors that influence ADH secretion

increased osmolarity --> increased ADH secretion; decreasedblood volume --> baroreceptors --> medulla --> increased

ADH secretion

Q2211:Actions of ADH

Inserts water channels in luminal membrane of collectingducts; increases reabsorption of water.

Q2212:Central diabetes insipidus

Not enough ADH secreted. Dilute urine is formed in spite ofwater deprivation. Responds to injected ADH.

Q2213:Nephrogenic diabetes insipidus

ADH is secreted but ducts are unresponsive to it. Dilute urineis formed in spite of water deprivation or injected ADH.

Q2214:SIADH

Excessive secretion of ADH in spite of low osmolarity.Concentrated urine is formed.

Q2215:decreased permeability of collecting ducts; increasedurine; decreased urine osmolarity; decreased ECF; increased

osmolarity

Diabetes insipidus

Q2216:increased permeability of collecting ducts; decreasedurine; increased urine osmolarity; decreased ECF; increased

osmolarity

Dehydration

Q2217:increased permeability of collecting ducts; decreasedurine; increased urine osmolarity; increased ECF; decreased

osmolarity

SIADH

Q2218:decreased permeability of collecting ducts; increasedurine; decreased urine osmolarity; increased ECF; decreased

osmolarity

Primary polydipsia

Q2219:Actions of ANP

Atrial stretch or increased osmolarity --> ANP secretion -->dilation of afferent; constriction of efferent --> increased

GFR --> natriuresis; also decreases permeability of collectingducts to water.

Q2220:Delta cells of the pancreas

Between alpha and beta cells; represent 5% of islets. Secretesomatostatin.

Q2221:Alpha cells of the pancreas

Near the periphery of the islets; represent 20%. Secreteglucagon.

Q2222:Beta cells of the pancreas

In the center of the islets; represent 60-75%. Secrete insulinand C peptide.

Q2223:Insulin receptor

Has intrinsic tyrosine kinasae activity. Insulin receptorsubstrate binds tyrosine kinase; activates SH2 domain

proteins: PI-3 kinase (translocation of GLUT-4); p21RAS.

Q2224:Tissues that require insulin for glucose uptake

Resting skeletal muscle and adipose tissue

Q2225:Tissues independent of insulin for glucose uptake

Brain; kidneys; intestinal mucosa; red blood cells; beta cells ofthe pancreas.

Q2226:Anabolic hormones

Insulin; GH/IGF-1; androgens; T3/T4; IGF-1 (somatomedinC)

Q2227:Effects of insulin on potassium

Increases Na/K ATPase uptake of K. Insulin + glucose usedto treat hyperkalemia.

Q2228:Mechanism of insulin release

Glucose enters beta cells and is metabolized --> increasedATP --> closes K channels --> increased depolarization -->

increased Ca influx --> exocytosis of insulin.

Q2229:Factors that stimulate secretion of insulin

Glucose; arginine; GIP; glucagon

Q2230:Factors that inhibit insulin release

Somatostatin; norepinephrine via alpha 1 receptors

Q2231:increased glucose; increased insulin; increased Cpeptide

Type 2 diabetes

Q2232:increased glucose; decreased insulin; decreased Cpeptide

Type 1 diabetes

Q2233:decreased glucose; increased insulin; increased Cpeptide

Insulinoma

Q2234:decreased glucose; increased insulin; decreased Cpeptide

Factitious hypoglycemia (insulin injection)

Q2235:Actions of somatomedin C

Increases cartilage synthesis at epiphyseal plates (increasedbone length). Also increased lean body mass. Protein-boundand long half-life correlates with GH secretion. Also called

IGF-1.

Q2236:Secretion of GH

Pulsatile during non-REM sleep; more frequent in pubertydue to increased androgens; requires thyroid hormones;

decreases in the elderly.

Q2237:Factors that stimulate GH secretion

Deep sleep; hypoglycemia; exercise; arginine; GHRH; lowsomatostatin

Q2238:Factors that inhibit GH secretion

Negative feedback by GH on GHRH; positive feedback onsomatostatin by IGF-1

Q2239:Dwarfism

Due to GH insensitivity during prepuberty

Q2240:Acromegaly

Due to excess GH in postpuberty. Enlargement of hands; feetand lower jaw; increased proteins; decreased fat;

visceromegaly; cardiac insuficiency.

Q2241:Composition of bone

Phosphate and calcium precipitate forming hydroxyapatite inosteoid matrix.

Q2242:Actions of PTH

Rapid actions: increases Ca reabsorption in distal tubules anddecreases phosphate reabsorption in proximal tubules; thuslowering blood phosphate and lowering solubility productwhich leads to bone resorption and raises plasma Ca. Slowactions: increases number and activity of osteoclasts (via

osteoclast activating factor released by osteoblasts); increasesactivity of alpha-1 hydroxylase in the proximal tubules which

increases active vitamin D and absorption of Ca andphosphate in the instetines.

Q2243:Clinical features of primary hyperparathyroidism

increased plasma Ca and decreased plasma phosphate;phosphaturia; polyuria; calciuria (filtered load of Ca exceeds

Tm); increased serum alkaline phosphatase; increasedurinary hydroxyproline; muscle weakness; easy fatigability.

Q2244:Clinical features of primary hypoparathyroidism

decreased plasma Ca and increased plasma phosphate;hypocalcemic tetany due to increased excitability of motor

neurons.

Q2245:increased PTH; increased Ca; decreased phosphate

Primary hyperparathyroidism. Causes: parathyroid adenoma(MEN I and II); ectopic PTH tumor (lung squamous CA)

Q2246:decreased PTH; decreased Ca; increased phosphate

Primary hypoparathyroidism. Cause: surgical removal ofparathyroid.

Q2247:increased PTH; decreased Ca; increased phosphate

Secondary hyperparathyroidism due to renal failure (no activevitamin D; decreased GFR)

Q2248:increased PTH; decreased Ca; decreased phosphate

Secondary hyperparathyroidism. Causes: deficiency ofvitamin D due to bad diet or fat malabsorption.

Q2249:decreased PTH; increased Ca; increased phosphate

Secondary hypoparathyroidism due to excess vitamin D.

Q2250:Vitamin D synthesis

Dietary and skin cholecalciferol is hydroxylated by 25-hydroxylase in the liver and activated to 1;25 di-OH

cholecalciferol by 1-alpha hydroxylase in the proximaltubules.

Q2251:Actions of 1;25 di-OH cholecalciferol

Increases Ca binding proteins by intestinal cells whichincreases intestinal reabsorption of Ca and phosphate. Alsoincreases reabsorption of Ca in the distal tubules. Increased

serum Ca promotes bone deposition.

Q2252:Osteomalacia

Underminerilized bone in adults due to vitamin D deficiencyleads to bone deformation and fractures. Low calcium leads to

secondary hyperparathyroidism.

Q2253:Rickets

Underminerilized bone in children due to vitamin D deficiencyleads to bone deformation and fractures. Low calcium leads to

secondary hyperparathyroidism.

Q2254:Excess vitamin D

Leads to bone reosprtion and demineralization

Q2255:Synthesis of thyroid hormones

1) Iodine is actively transported into follicle cell; 2)thyroglobulin is synthesized in the RER; glycosylated in theSER and packaged in the GA; 3) Peroxidase is found in the

luminal membrane and catalizes oxidation of I-; iodination ofthyroglobulin and coupling to form MITs and DITs; 4)iodinated thyroglobulin is stored in the follicle lumen.

Q2256:Structure of thyroid hormones

T4 has iodine attached to carbons 3 and 5 of both fenol rings;T3 has iodide attached to carbons 3 and 5 of the amino

terminal fenol ring and the 3 prime carbon of the hydroxyl endfenol ring; reverse T3 has iodide in carbon 3 of the amino

terminal fenol ring but not carbon 5.

Q2257:Secretion of thyroid hormones

Iodinated thyroglobulin is endocytosed from the lumen of thefollicles into lysosomes. Thyroglobulin is degraded into amino

acids; T3; T4; DITs and MITs. T4 and T3 are secreted in a20:1 ratio. DITs and MITs are deiodinated and iodine is

recycled.

Q2258:Transport of thyroid hormones

99% is bound to TBG; 1% is free. T4 has greater affinity forTBG and a half-life of 6 days. T3 has greater affinity for

nuclear receptor and is the active form with a 1 day half-life.50:1 T4/T3 ratio in periphery.

Q2259:Activation and degradation of thyroid hormones

5' monodeiodinase activates T4 into T3. 5-monodeiodinaseinactivates T4 into reverse T3.

Q2260:Actions of thyroid hormones

increased metabolic rate by increased Na/K ATPase exceptin brain; uterus and testes; essential for brain maturation andmenstrual cycle; permissive for bone growth; permissive for

GH synthesis and secretion; increased clearance ofcholesterol; required for activation of carotene; increased

intestinal glucose absorption; increased affinity and numberof beta 1 receptros in the heart.

Q2261:Effects of hypothyroidism in newborns

decreased dendritic branching and myelination lead to mentalretardation.

Q2262:Effects of hypothyroidism in juveniles

Cretinism results in decreased bone growth and ossification --> dwarfism. Due to lack of permissive action on GH.

Q2263:Control of thyroid hormone secretion

Circulating T4 is responsible for negative feedback of TSH bydecreasing sensitivity to TRH. T4 is converted to T3 in the

thyrotroph to induce negative feedback.

Q2264:Effects of TSH

Rapid actions: increased iodide trapping; increased synthesisof thyroglobulin; increased reuptake of iodinated

thyroglobulin; increased secretion of T4; late effects:increased blood flow to thyroid gland; increased

hypertrophy of follicles and goiter.

Q2265:decreased T4; increased TSH; increased TRH

Primary hypothyroidism; increased TSH is the more sensibleindex

Q2266:decreased T4; decreased TSH; increased TRH

Pituitary (secondary) hypothyroidism

Q2267:decreased T4; decreased TSH; decreased TRH

Hypothalamic (tertiary) hypothyroidism

Q2268:increased T4; increased TSH; decreased TRH

Pituitary (secondary) hyperthyroidism

Q2269:increased T4; decreased TSH; decreased TRH

Graves disease

Q2270:Pathophysiology of iodine deficiency

Thyroid makes less T4 and more T3 so actions of T3 may benormal but low levels of T4 stimulate TSH secretion with

development of goiter. Thus euthyroid with goiter.

Q2271:Clinical features of hypothyroidism

decreased basal metabolic rate with cold intolerance;decreased cognition; hyperlipidemia; nonpitting myxedema

(mucopolysacchride accumulation around eyes retains water);physiologic jaundice (increased carotene); hoarse voice;

constipation; anemia; lethargy

Q2272:Clinical features of hyperthyroidism

increased metabolic rate with heat intolerance and sweating;increased apetite with weight loss; muscle weakness; tremor;

irritability; tachycardia; exophthalmos.

Q2273:Leydig cells

Stimulated by LH; produce testosterone for peripheral tissuesand Sertoli cells. Testosterone provides negative feedback for

LH secretion by pituitary.

Q2274:Sertoli cells

Stimulated by FSH; produce inhibins (inhibits secretion ofFSH); estradiol (testosterone is converted by aromatase);androgen binding proteins and growth factors for sperm.

Responsible for development of sperm in males. Also MIH inmale fetus.

Q2275:decreased sex steroids; increased LH; increased FSH

Primary hypogonadism or postmenopause.

Q2276:decreased sex steroids; decreased LH; decreased FSH

Pituitary hypogonadism or constant GnRH infusion(downregulates GnRH receptors of pituitary.

Q2277:increased sex steroids; decreased LH; decreased FSH

Anabolic steroid therapy. LH supression causes Leydig cellatrophy with decreased Leydig testosterone which

suppresses spermatogenesis.

Q2278:increased sex steroids; increased LH; increased FSH

Pulsatile infusion of GnRH

Q2279:Fetal development of male structures

LH --> Leydig cells --> testosterone --> Wolffian ducts(internal male structures: epididymis; vasa deferentia andseminal vesicles). Testosterone + 5-alpha reductase -->

dihydrotestosterone --> urogenital sinus and external organs.MIH by Sertoli cells --> regression of Mullerian ducts and

female structures.

Q2280:Characteristics of sub-threshold potentials

Proportional to stimulus strength; not propagated;decremental with distance; summation

Q2281:Characteristics of action potentials

Independent of stimulus strength; propagated unchanged inmagnitude; summation not possible

Q2282:Factors that affect conduction velocity of the actionpotential

Cell diameter and amount of myelination are directlyproportional to conduction velocity

Q2283:Absolute refractory period

No stimulus can depolarize the cell

Q2284:Relative refractory period

A large stimulus can depolarize the cell

Q2285:Neuromuscular transmission

Action potential travels down axon and opens pre-synapticCa channels --> calcium influx --> release Ach vesicles -->

Ach diffuses and attaches to nicotinic ion channels -->increased gNa --> end-plate depolarization (local) spreads toareas with voltage-gated Na channels --> depolarization of

muscle fiber

Q2286:Excitatory postsynaptic potentials

Transient subtreshold depolarizations due to increased gNa --> summation reaches axon hillock at the junction of cell bodyand axon --> voltage-gated Na channels depolarize the axon

Q2287:Inhibitory postsynaptic potentials

increased gCl or increased gK hyperpolarize the cell and lowerthreshold for depolarization

Q2288:Electrical synapse

Action potential transmitted from one cell to the next via gapjunctions; without synaptic delay and in both directions.

Cardiac muscle; smooth muscle.

Q2289:Sarcomere A band

Contains overlapping actin and myosin. Does not shortenduring contraction.

Q2290:Sarcomere H zone

Contains thick myosin filaments. Shortens during contraction.

Q2291:Sarcomere I band

Contains thin actin filaments. Shortens during contraction.

Q2292:Sarcomere Z line

Within the I band.

Q2293:Sarcomere M line

Within the H zone.

Q2294:Actin

Structural protein of the thin filaments; contains attachmentsites for myosin cross-bridges.

Q2295:Myosin

Structural protein of the thick filaments; contains cross-bridges that attach to actin. Has ATPase activity to terminate

actin-myosin cross-bridges. ATP decreases actin-myosinaffinity.

Q2296:Tropomyosin

Part of thin filaments. Covers the actin attachment sites forthe myosin cross-bridges

Q2297:Troponin

Part of thin filaments; binds calcium; which movestropomyosin out of the way exposing actin binding sites for

cross-bridges.

Q2298:What happens if calcium is removed to thesarcoplasmic reticulum?

Muscle goes back to resting state. Removal of calciumrequires ATP.

Q2299:Rigor mortis

Depletion of ATP - cycling stops with myosin attached toactin - (muscle contracted).

Q2300:Muscle contraction steps

Action potential travels down T-tubules --> activatesdihydropiridine voltage sensors --> foot processes are pulled

aways from ryanodine calcium release channels ofsarcoplasmic reticulum --> calcium is released --> calcium

attaches to troponin --> tropomyosin moves exposing actinbinding sites for myosin cross-bridges --> myosin binds actin

--> myosin ATPase breaks down cross bridges producingactive tension and shortening --> contraction terminated by

active pumping of Ca into the sarcoplasmic reticulum.

Q2301:Myosin ATPase

Hydrolizes ATP to supply energy for active tension andshortening. ATP decreases myosin-actin affinity

Q2302:Sarcoplasmic calcium-dependent ATPase

Supplies energy to terminate contraction and pump Ca backinto sarcoplasmic reticulum.

Q2303:Source of calcium for skeletal muscle contraction

Sarcoplasmic reticulum. No extracellular calcium is involvedbecause it doesn’t have voltage-gated Ca channels.

Q2304:Source of calcium for heart and smooth musclecontraction

Sarcoplasmic reticulum and extracellular. Cardiac and smoothmuscle have voltage-gated calcium channels.

Q2305:Tetanus

Multiple action potentials increase release of calcium thusincreasing contraction. Muscle cells have a short refractory

period.

Q2306:Preload

Stretch prior to contraction. increased preload --> increasedprestretch of the sarcomere --> increased passive tension

Q2307:Afterload

The load the muscle is working against. increased afterload --> increased cross-bridge cycling --> increased active tension

Q2308:What is the best measure of preload?

Sarcomere length

Q2309:Preload-length tension curve

It’s a function of the legth of the relaxed muscle. A positiveparabola.

Q2310:Isomertric contraction

Active tension is produced but length stays the same.Afterload is greater than active tension; load not moved.

Q2311:How is active tension produced?

Calcium binds troponin --> tropomysion exposes actin sites --> myosin cross-bridges bond to actin --> myosin ATPase

generates energy to break cross-bridge link --> cycle repeats --> active tension. The more cross-bridges that cycle; the

greater the active tension.

Q2312:Total tension

Passive (preload) tension + active (afterload) tension

Q2313:Active tension curve

It's a function of the number of cross-bridges capable of cross-linking with actin. Negative parabola.

Q2314:What is L0?

The optimum length to produce maximum active tension.Beyond L0; muscle is overstretched; below L0; it's

understretched.

Q2315:Isotonic contraction

Muscle contracts and shortens to move the load. Occurs whentotal tension equals the load.

Q2316:Most energy demanding phase of cardiac cycle

Isovolumetric contraction. Active tension is generated.Equivalent to isometric contraction of skeletal muscle.

Q2317:Relationship between load; muscle force and musclevelocity

increased ATPase activity --> increased velocity; increasedmuscle mass --> increased force generated; increased

afterload --> decreased velocity

Q2318:Regulation of skeletal muscle force and work

increased frequency of action potentials; increasedrecruitment; increased preload and increased afterload -->

increased force and work

Q2319:Regulation of cardiac and smooth muscle force andwork

Factors that regulate force and work are preload; afterload andcontractility (which is altered by hormones). No summation

nor recruitment.

Q2320:Characteristics of white muscle

Large mass; high ATPase activity (fast muscle); anaerobicglycolysis; low myoglobin

Q2321:Characteristics of red muscle

Small mass; low ATPase activity (slower muscle); aerobicmetabolism (mitochondria); high myoglobin.

Q2322:Characteristics of skeletal muscle

Actin and myosin form sarcomeres; sarcolema lacks junctionalcomplexes; each fiber innervated; troponin binds calcium; high

ATPase activity; triadic contacts by T-tubules at A-Ijunctions; no calcium channels on membrane

Q2323:Characteristics of cardiac muscle

Actin and myosin form sarcomeres; gap junctions; electricalsyncytium; troponin binds calcium; intermediate ATPase

activity; dyadic contacts by T-tubules near Z-lines; voltage-gate calcium channels.

Q2324:Characteristics of smooth muscle

Actin and myosin not organized in sarcomeres; gap junctions;electrical syncytium; calmodulin binds calcium; low ATPase

activity; lacks T-tubules; voltage-gated calcium channels.

Documents

Physiology & Pathophysiology - 2000