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Cardiovascular

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Hypertension

Cardiac Output (CO) = Heart Rate (HR) X Stroke Volume (SV)

Blood Pressure (BP) = Cardiac Output (CO) X Total Peripheral Resistance (TPR).

The Renin - AngiotensinAldosterone System (RAAS): If BP falls (for any reason) the

kidney secretes renin which converts Angiotensinogen Angiotensin I (A-I) (a weak

vasoconstrictor). A-I, while passing through the lung, is converted to Angiotensin II (A-II) by

the Angiotensin converting Enzyme (ACE). A-II is a potent vasoconstictor TPR# BP.

Additionally, it stimulates the adrenal cortex to secrete aldosterone salt & water retention

# BP.

ACE Inhibitors: These inhibit the ACE, thus inhibit the conversion of A-I to A-II, thus $ the

TPR as well as $ aldosterone release ($ salt & water retention $ plasma volume)$ BP.

Additionally, ACEIs prevent the degradation of bradykinin (vasodilator) to inactive kinins.

Members include: Captopril, Enalapril, Lisinopril, Fosinopril, Benzapril, Quinapril &

Ramipril. They are used in mild to moderate hypertension, proteinuria & in CHF.

NSAIDs inhibit the activity of ACEIs.

Side effects of ACEIs include:

Proteinurea Hypogasia/dysgasia (temporary loss of taste).

Renal insufficiency Hyperkalemia (not used with K sparing diuretics). $ neutrophils (neutropenia). Rash, headache, dizziness, fatigue, cough.

1st dose hypotension.

Mechanism of action of ACEIs:

Angiotensinogen

Renin

Angiotensin I

Angiotensin II

Aldosterone Production

Sodium & WaterRetention

ACEIs

Angiotensin

Converting

Enzyme

Vasoconstriction

Blood Pressure

Bradykinin

(Vasodilator)

Inactive

kinins

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Mechanism of action of antihypertensives:

I - Sympatholytics: these include:

BBs block -1 receptors (heart)$ cardiac contractility & HR$ CO.

E.g. propranolol, pindolol, atenolol, acebutolol, nadolol, timolol

Post-synaptic - blockers: block a receptors in vasculature vasodilatation

$ TPR. E.g.: Prazocin, terazocin, doxazocin

Prazocin (Minipress) blocker &direct vasodilator syncope,1st dose hypo-

tension, possibly tachycardia (sudden discontinuation rebound HT). Not used.

Centrally acting 2 stimulants:

Clonidine (Catapress) inhibits vasomotor center (sympath. activity) vaso-

dilatation. Also acts peripherally $ NE release. Sudden withdrawal rebound

HT. It can cause depression. Not given with propranolol nor to noncompliant pts.

Methyldopa (Aldomet) false neurotransmitter. Postural hypoten., rebound HT.

Adrenergic neuron blockers:

Reserpine Catecholamine depletor (depletes epinephrine & NE stores).

Guanithidine Catecholamine depletor (replaces NE at nerve endingsstorage

site). [ tricyclic antidepressants $ uptake of guanithidine abolish anti HT effect]

Postural hypotension & $ ejaculation. Sympathomimetic use & pheocromocytoma

are contraindications.

II - Direct vasodilators: direct peripheral vasodilator (direct action on arterioles).

Hydralazine (SLE, postural hypoten.) Minoxidil (Hirsutism)

Diazoxide (Na retention) Na nitroprusside

III - ACEIs Inhibit the conversion of A-I to A-II$ TPR & salt & water retention.

E.g. Captopril, fosinopril, benzapril, enalapril, lisinopril, ramipril, quinapril

IV- CCBs inhibit influx of Ca through slow channels in vascular smooth muscle

relaxation$ TPR

E.g. Verapamil, diltiazem, dihydropyredines (flodipen, amlodipine, isradipine).

Nifedipine (Adalat): CCB used in angina & heart failure; causes ankle edema.

V- Angiotensin II receptor antagonists: Block A-II receptors$ TPR & $ aldosterone

E.g. Irbesartan, eprosartan, losartan, candesartan, valsartan, telmisartan.

N.B.

Veratrum alkaloids Direct action on the CNS.

Mecamylamine Ganglion blocker. These are not widely used as antihypertensives asthey block neurotransmission at both sympathetic & PS ganglia many side effects

(dry mouth, constipation, impaired visual accommodation, urine retention).

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Mode of action of diuretics:

Thiazides (e.g. HCTZ) inhibit Na+ reabsorption at distal tubules

Loop diuretics (e.g. bumetanide inhibit Na+ / Cl- exchange at the ascending limb

frusimide Lasix) of the Loop of Henle

K sparing diuretics (amiloride inhibit the effects of aldosterone hormone on

spironolactone & triametrene) distal tubules Carbonic anhydrase inhibitors inhibit carbonic anhydrase enzyme & this

(e.g. acetazolamide) inhibits Na+ / H+ exchange at proximal tubules

decreasing its reabsorption

Osmotic diuretics (e.g. urea & increase osmolarity of glomerular filtrate,

mannitol) (thus decrease reabsorption of water &

increase urination)

Thiazide diuretics: $ uric acid excretion hyperuricemia; except for Ticrynofen which has

a uricosuric effect. Hypokalemia & hypercalcemia (NSAIDs $ efficacy of thiazides).

Mercurial diuretics: are given IM. They are not absorbed from GIT, thus not given orally.

Ethacrynic acid (Edecrine): is a loop diuretic capable of producing ototoxicity & may

aggravate ototoxicity of aminoglycosides. (NSAIDs $ efficacy of loop diuretics).

Diuretics enhance proximal tubular reabsorption of solutes including uric acid.

Acetazolamide leads to hyperchloremic metabolic alkalosis as a result of# loss of water

coupled with $distal Na reabsorption in exchange for K &

Thiazides hypercalcemia Loop diuretics hypocalcemia (Hypercalciurea)

The antidiuretic hormone (ADH or Vasopressin): is secreted from the posterior pituitary &

acts on the distal tubules to enhance the reabsorption of water & salt.

General Notes:

In complete heart block: beats of the atria & ventricles are both blocked.

In acute asthma & in anaphylactic shock adrenaline is used.

The highest BP is in the pulmonary artery, the lowest BP is in the vena cavae.

CNS reaction towards increased arterial pressure peripheral vasodilatation.

In moderate exercise, the HR increases because the sympathetic stimulation of -receptors

in arterioles causes vasodilatation $ TPR leading to reflex # in HR.

When venous return is increased to the right atrium, consequently:

Tachycardia occurs.

Increased oxygen consumption (OC). Organ ischemia: can result from organ-turnicate.

Bed sores: are caused by body weight pressure in patients laying in 1 position for long time.

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Selectivity of -blockers:

Propranolol (Inderal) Non selective (b1 + b2)

Pindolol (Visken) Non selective (b1 + b2) + ISA

Nadolol (Corgard) Non selective (b1b2) + OD

Timolol (Timoptic) Non selective (glucoma)

Labetalol (Trandate) Non-Selective (b1 + b2 + a blocker)

Atenolol (Tenormin) Selective (b1 > b2) + OD

Metoprolol (Lopressor) Selective (b1 > b2)

Acebutolol (Sectral) Selective (b1 > b2) + ISA + OD

Esmolol Short acting, given IV

B-Blocker terms

Relative cardioselective activity. Relative to propranolol, BBs have a greater tendency

to occupy the 1-receptor in the heart, rather than the 2-receptors in the lungs.

Intrinsic sympathomimetic activity (ISA). These agents have the ability to release

catecholamines & to maintain a satisfactory HR. ISA may prevent bronchoconstriction

& other direct -blocking actions.

Selectivity is dose dependent: there is no selectivity at high doses even with selective BBs.

Nonselective BB are contraindicated in patients with bronchial asthma, as these

precipitate bronchospasm.

Propranolol is used to treat HT with tachycardia. Being non-polar, it is excreted via the

liver, it can be given to HT patients with renal failure.

Sudden withdrawal of BBsMI, angina & rebound HT.

Peyronies disease: is reported with metoprolol (p.253).

Organ Receptor Response

Heart b1 Stimulation increased contraction & HR

Arterioles a1 Stimulation vasoconstriction

b2 Stimulation vasodilatation

GIT b1 Stimulation decreased contraction

Bronchi b2 Stimulation bronchodilatation

Uterus b2 Stimulation Relaxation

N.B: Reserpine causes CNS depression (as it $ the conc. of dopamine). It also causes lethargysedation & night-mares. It is a post-ganglionic neuron blocker causing depletion of

catecholamine stores in the brain & the peripheral adrenergic system.

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HT patients with concomitant diseases can be treated by:

Patients with renal failure: the safest drug is hydralazine (it # renal blood flow). If not

active give Lasix + Aldomet. Alternatively a non-polar b-blocker (Inderal) or Clonidine

can be used. Inderal is excreted via the liver (& is contraindicated in hepatic failure).

Patients with hepatic failure: can be treated with a polar -blocker (e.g. pindolol,

nadolol or atenolol). These are excreted mainly via the kidney.

Patients with bronchial asthma: can be treated with a selective -blocker (e.g.

metoprolol or atenolol). Better agents might be ACEI / CCBs / AIIRAs.

Patients with CHF: can be treated with captopril & / or prazocin.

Patients with tachycardia: can be treated with a non-selective b-blocker (e.g. nadolol

or propranolol). (BB without ISA)

Patients with depression: hydralazine is the drug of choice (reserpine, guanithidine,

methyl dopa & clonidine can cause depression).

Hypertensive crisis is treated by sodium nitroprusside & diazoxide (given by IV infusion or

injection) as they have a direct vasodilating effect on blood vessels.

Diazoxide: is a direct vasodilator. If administered orally, it has a mild antihypertensive effect.

It is usually given by rapid IV infusion to $ BP rapidly in patients with hypertensive crisis.

Metyrosine (Demiser): is an antihypertensive used in pheochromocytoma.

Papaverine: is used primarily for its ability to produce vasodilatation. It causes relaxation of

arteriolar smooth muscles.

A sudden increase in blood pressure will cause reflex bradycardia.

Postural hypotension: response to drug is greater in the erect than in the supine position.

This is a characteristic effect of the drugs that block the sympathetic NS.

Orthostatic hypotension, either due to direct action on arterioles or via CNS, is caused by:

Vasodilators Guanithidine 1 - blockers. MAO-Is (antidepressants)

Acetylcholine: has a direct effect on the heart coronary vasodilatation.

Both nitroglycerine & isosorbide dinitrate (Isordil) are available in sublingual dosage

forms used as coronary vasodilators in the treatment &/or prophylaxis of anginal attacks.

Both agents are equally active.

Hydergine is claimed to be a mood elevator is also available as sublingual tablets.

Dopamine (Inotropine) in cardiogenic shock: is an inotropic sympathomimetic. it #

contractility with less effect on HR at low doses. It # vasodilatation & renal perfusion through

its action on 1 receptors. Its major advantage is that it produces dose dependant # in CO &renal perfusion.

Compared to nitroglycerine tablets, nitroglycerine ointment provides a prolonged effect.

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Arrhythmia:is any deviation from the normal heart beat pattern.

Myocardial action potential: is the cardiac depolarization

& repolarization necessary for myocardial contraction.

Depolarization & repolarization result from changes

in electrical potential across cell membrane, caused

by exchange of Na & K ions.This occurs in 5 phases: Phase 0 Rapid depolarization.

Takes place as Na+ enters the cell;

cell membrane's electrical charge

changes from negative to positive.

Phase 1 Early rapid repolarization.

As fast Na channels close & K+ leaves the

cell, the cell rapidly repolarizes.

Phase 2 Plateau. Ca++ enters the cell through slow channels while K+ exit. As cell

membrane's electrical activity temporarily stabilizes, action potential reaches a plateau.

Phase 3 Final rapid repolarization. K+ is pumped out of the cell as the cell rapidly

completes repolarization & resumes its initial negativity.

Phase 4 Slow depolarization. The cell returns to its resting state with K+ inside the

cell & Na & Ca ions outside.

During depolarization & repolarization, a cell's ability to initiate an action potential varies.

The cell cannot respond to any stimulus during the absolute refractory period (beginningduring phase 1 & ending at the start of phase 3).

A cell's ability to respond to stimuli increases as repolarization continues. During the

relative refractory period (during phase 3) the cell can respond to a strong stimulus.

When the cell has been completely repolarized, it can again respond fully to stimuli.

The action potential of the heart (tone of the heart muscle) is 95105 millivolt. (90105)

Anti-arrhythmic Drugs:

These are classified in 8 groups:

Cinchona alkaloids: (Quinidine, an optical isomer of quinine).

Amides: Procainamide (Pronestyl) & desopyramide (Rhythmadon).

Xylyl derivatives: Lidocaine (Xylocaine).

4ry ammonium salts: Bretylium (Bretylol).

Amiodarone (Cordarone)

Beta blockers.

CCBs: Verapamil (Isopten) & diltiazem (Cardiazem).

Hydantoins: Phenytoin (Dilantin).

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Anti-arrhythmic Drugs

Can be classified according to their ability to alter the action potential of cardiac cells.

Class I: This class includes:

Quinidine Lidocain Procainamide (Pronestyl),

Phenytoin (Dilantin) Disopyramide (Rythmadon)

d These are used for ventricular & supraventricular arrhythmias

d They decrease the rate of rise of phase 0; i.e. slow the rate of conduction,

excitation & spontaneous repolarization.

d They decrease the slope of phase 1 prolong the effective refractory period.

Class II: It includes -antagonists ( -blockers), e.g. propranolol.

d They are used in atrial arrhythmias.

d

They depress phase 4 depolarization.d They competitively inhibit receptor sites.

Class III: these include: Bretylium Amiodaron (Cordaron).

d These are used in ventricular fibrillations.

d They prolong the duration of the action potential.

d They # the absolute refractory period (prolongation of repolarization).

Class IV: these include CCBs e.g. verapamil (Isopten), nifedipine, diltiazem (cardiazem).

d These are used in atrial fibrillation & flutter supraventricular tachycardia.

d They decrease the amount of Ca ions available for displacement from the cell

membrane, i.e. decrease the inward current carried by Ca.

d They prolong the absolute refractory period.

d They depress phase 4 spontaneous depolarization.

d Verapamil (5-10 mg over 1-2 min) used to treat paroxysmal ventricular tachycardia.

Tachycardia: means faster heart beats (usually > 100 beat / min); this may be due to:

d # body temp. (~ HR # by 10 beats / min for every 1oF rise in temp.)

d Toxic condition.

d Autonomic sympathetic stimulation.

Bradycardia: means slower heart beats (usually < 60 beat / min); Any circulatory reflex that

stimulates the vagus nerve (parasympathetic) causes a considerable $ in HR.

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Quinidine:

It is used for supraventricular arrhythmias.

It is the drug of choice in atrial premature contractions.

It is used in ventricular premature contractions (VPC).

It is given orally or IV.

Quinidine should not be used without prior degitalization, because it may increase the

frequency of impulse transmission.

Procainamide (Pronestyl):

It is used in VPC & ventricular tachycardia.

It is contraindicated in CHF as it causes Lupus like reactions (SLE).

Disopyramide (Rhythmadon):

Used in the treatment of VPC & repetitions. Used in ventricular arrhythmias.

Lidocaine (Xylocaine):

It is used in the treatment of ventricular arrhythmias ($ HR).

It is the drug of choice in arrhythmias associated with emergencies (MI, open heart

surgery, digitalis intoxication)

The anti-arrhythmic effect of lidocaineis:

d No effect on SA node (unlike quinidine).

d Suppress automacity in Purkinje fibers & atrium.

d Depression of phase 0 depolarization ($ Na influx)

(it is depressant but not like procainamide/quinidine).

d It $ the effective refractory period on Purkinje

fibers & inhibit the duration of action potential.

d Show very little changes of ECG.

Phenytoin (Dilantin): It alters Na+ conc. by promoting Na+ influx.

It is used in the both ventricular & supraventricular arrhythmias.

It is also used in digitalis induced arrhythmias.

Propranolol (Inderal): is most valuable in atrial arrhythmias (tachycardia).

N.B: Proximal sinus arrhythmia: may result from an increase in temp.

N.B: Catecholamines may cause arrhythmias.

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Congestive Heart Failure

In right-side CHF: blood accumulates in liver, kidney, vena cavae, lower extremities

edema

In left-side CHF: blood accumulates in lungs pulmonary edema

Digitalis glycosides: are used to treat CHF. Digoxin is the primary active constituent of digitalis.

The Pharmacological action of digoxin is:

It # myocardial contractility through direct stimulation of the ventricular muscle &

through enhancing Ca availability to the contractile proteins (+ve inotropic).

Reduce conductivity ($ conduction velocity in the atrial muscle). This effect

predominates over its vagotonic effect (# conduction) (-ve chronotropic)

Slow the cardiac pace maker (SA node) (-ve chronotropic) Prolong the refractory period (-ve chronotropic)

Does not increase oxygen consumption.

Digitalis toxicity results in:

Cardiac effects: dose related disrhythmias terminating ventricular fibrillation. The

common predisposing factor is a $ in intracellular K+. This can be treated by K sparing

diuretics or corticosteroids. Cardiac irregularities e.g. coupled beats signal a need to $

digitalis dose. The cardiac symptoms of toxicity include:

Premature ventricular fibrillation (treated with xylocain or phenytoin).

Premature atrial fibrillation

AV block

Paroxysmal atrial tachycardia

Ventricular tachycardia

Extra-cardiac effect:

Vomiting, diarrhea, anorexia Weakness, fatigue, headache, dizziness

Photophobia & hazy vision

Massive over doses cause delusions & coma.

Does not cause constipation, anemia nor vagal arrest.

The official bioassay of digitalis leafutilizes pigeon.

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Hypercholesterolemia

Cholestyramine resin (Questran): is an anion exchange resin used to treat hypercholest-

erolemia. It is not absorbed from the GIT. It is a quaternary ammonium chloride compound

that binds to bile acids in the intestine preventing heir absorption. This results in increased

hepatic conversion of cholesterol to bile acids lowering cholesterol levels.

Cholestyramine & Colestipol: increase the efficiency of lipoprotein removal.

It is the drug of choice in pregnancy (it is not absorbed has no systemic effect).

Because cholestyramine is an anionic surfactant, it will interfere with the GI absorption of

penicillin, tetracyclines, phenobarbital, phenyl butazone, warfarin & chlorthiazide.

Fibrates: Clofibrate (Atromid S), Bezafibrate (Bezalip), Gemfebrozil (Lopid)

Interfere with cholesterol synthesis.

They # lipoprotein lipase activity enhance breakdown of TG$ VLDL & LDL.

They lower the cholesterol & TG levels.

Can not be given for long time.

Niacin:$ lipolysis in adipose tissue$ free fatty a formation$ TG$ VLDL & LDL

Statins: inhibit the HMG-CoA reductase enzyme$ cholesterol synthesis.

Chenodeoxycholine (Chendiol): it is a natural bile acid which can disintegrate (dissolve)

gall stones (cholelithiasis). Gall stones are formed due to failure to solubilize cholesterol

ppt. Chendiol $ cholesterol & replaces it (desaturation) & the result is gradual dissolution ofthe stone. However it is ineffective against calcified or pigment containing gall stones.

Cholesterol gall stones consist of a combination of bile acids, chenodeoxycholic acid, &

normal hepatic metabolites of cholesterol.

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Normal Coagulation of Blood: entails the formation of fibrin by the interaction of

more than a dozen proteins in a cascading series of proteolytic reactions.

Mechanism of Action of Heparin: it inhibits thromboplastin$ conversion of prothrombin to

thrombin$ the conversion of fibrinogen to fibrin, i.e. it has anti-thromboplastin & anti-

thrombin effect. These effects are related to heparins strong acidic (electronegative) nature.

Binds to antithrombin III & enhances its action (increase degradation of coagulation factors).

Factor X is the major factor inhibited by heparin following its binding with antithrombin III.

Mechanism of Action of Warfarin: it suppresses the formation of prothrombin & factors VII, IX

& X. These factors are synthesized by the liver & their production requires the presence of

vitamin K. Since caumarines resemble vitamin K, they interfere with its uptake by the liver cells

(competitive inhibition). Factors VII, IX, & X are dependant on Vitamin K for their action.

d Warfarin is used as an antidote for vitamin K.

Ca++Soluble Fibrin + XIII* Stabilized Fibrin

* Denotes the activated forms of coagulation factors

Factor I Fibrinogen Factor VIII Antihemophilic globulin (AHG)

Factor II Prothrombin Factor IX Christruns

Factor III Tissue thromboplastin Factor X Stuart power factor

Factor IV Ionic Calcium Factor XI Plasma thromboplastin

Factor V labile factor AG, proaccelerin Factor XII Hageman factor

Factor VI No factor Factor XIII Fibrin stabilizing

Factor VII Proconvertin, autothrombin I PF-3 Platelet factor - 3

+ PF-3

(II)(II*)

(I)

(II*)

XIII

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Anticoagulants

Heparin Caumarine (Warfarin)

Onset of action Immediate Gradual

Duration 4 hrs 2-5 days

Used in Emergency & prophylaxis Prophylaxis

Route of administration IV or SC Oral

Lab control of dose APTT Prothrombin time

Treatment of overdose Protamine SO4 Fresh blood &/or Vitamin K

Use in pregnancy Can be given Contraindicated

Drug interactions Few Many

Effect of antacids No effect # its effect

Pharmacologic action Anticoag. in vivo & in vitro Anticoagulant in vivo

Cost Expensive Cheap

The anticoagulant effect of heparin: is quantitated by the Active Partial Thromboplastin

Time (APTT) & the Activated Coagulation Time (ACT) which is 3-5 min.

d Normally, APTT is from 30-45 sec; on using an anticoagulant it should be 4560 sec.

The anticoagulant effect of warfarin: is quantitated by the Prothrombin Time (PT).

d Normally, PT is 12 sec; on adequate anticoagulant control it should be 2430 sec.

Hypoprothrombinemia induced by oral anticoagulants: is most rapidly offset by fresh

blood or plasma. If not, by vitamin K3 (menadione) as an antidote for warfarin (coumarine).

Warfarin is extensively bound to plasma proteins (90%). Certain drugs (e.g. salicylates,

diazoxide, phenyl butazone, sulfonamides, indomethacin & chloral hydrate) can displace

warfarin from its plasma protein binding sites # free warfarin in blood# bleeding.

Drugs that induce the liver microsomal enzyme system (barbiturates, phenytoin) may

accelerate the metabolism of warfarin$ serum levels subtherapeutic levels.

Drugs that inhibit the hepatic microsomal enzymes [cimetidine (Tagamet)], potentiate the

action of warfarin, causing reversible but significant increase in plasma warfarin levels & in

prothrombin time (prothrombin time is normally 11 sec).

Anticoagulants in peptic ulcer patients taking antacids: is warfarin the best choice, since

antacids do not affect warfarin absorption from the GIT? (No, antacids may increase the

absorption of warfarin).

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Angina Types Angina Pectoris (strangling of the chest)

Beta Blockers

Methyl dopa. (Use)

Antihyperlipidemic

Hydralazine (vasodilator)

Beta Blockers

Non Selective (B1 + B2) Propranolol Pindolol Nadolol

Sotalol Timolol

Cardio Selective (B1) Acebutolol Atenolol Metoprolol

Non Selective (B + a) Labetalol

Methyl Dopa (Aldomet): Interfere with synthesis of dopamine a Me-dopamine ?????

$ Sympathetic outflow$ peripheral vascular resistance + slight reduction in CO & BP.

Diuretics

1. Proximal Tubule: Osmotic Diuretics: e.g. Mannitol.

2. Loop of Henele: Reduction of Na+ re-absorption leads to K+ loss at site 4; e.g.

Frusemide.

3. Cortical diluting segment: Reduction of Na+ re-absorption leads to K+ loss at site 4;

e.g. Thiazides.

4. Distal tubule: inhibition of Na+ exchange for K+ / H+; e.g. K+ sparing diuretics

(aldosterone, spironolactone, triametrene, Amiloride).

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1. Heparin is:

a. Like coumarine c. Acts on certain steps of coagulation system

b. Oral d. Of benefit in arterial blood clot as prophylaxis

2. In left ventricular failure the blood pools in:

a. Lungs c. Vena cavae

b. Liver

3. Patients with moderate HT & a history of heart disease (CHF) are treated with:

a. Propranolol c. Hydrochlorothiazide

b. Methyl dopa d. Reserpine

4. An important advantage of using dopamine (inotropic sympathomemetic) in cardiac shock is:

a. It will not cross the BBB & will not cause CNS side effects.

b. It produces a dose dependant increase in CO & renal perfusion

c. It will not increase the blood pressure

d. It has no effect on a & b receptors.

e. It can be given orally

5. For a sympathomimetic drug to be effective it should be:

a. Able to fit in receptors

b. Bound to plasma proteins

c. Compete at the site of release of the transmitter

6. A HT patient suffering from depression should not be given all of the following EXCEPT:

a. Reserpine (depletes NE stores)

b. Clonidine (a2 agonistnegative feedbackE & NE)

c. Methyl dopa (False methylation methyl NEa2 agonist)

d. Guanithidine

e. Hydralazine (direct vasodilatation)

7. Vasodilators cause:a. Reflex bradycardia b. Reflex tachycardia

8. In an ischemic myocardium, which is released & causes coronary vasodilatation:

a. Adrenaline c. Serotonin

b. Acetylcholine d. Adenosine

9. Which hormone increases water reabsorption from distal tubules:

a. Aldosterone (also vasopressinADH) c. Acetylcholine

b. Adrenaline d. Adenosine

N.B. Vasopressin acts on distal tubules to # water re-absorption

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10. At rest (or during sleep), which organ receives the richest blood supply:

a. Lungs c. Heart

b. Liver (27%) d. Kidneys (22%)

11. Which drug, although increasing the heart rate, causes vasodilatation ($ BP):

a. Adrenaline d. Propranolol

b. Carbacol e. Phenylephrine

c. Ephedrine f. Isoproterenol (more stimulant than )

12. The highest blood pressure is in the:

a. Veins c. Arteries (pulmonary artery)

b. Venules d. Arterioles

13. Diuretics are most likely to produce:

a. Hyperkalemia. c. Hypokalemia. e. Hyperuricemiab. Hypercalcemia. d. Hypocalcemia f. Urinary alkalosis

14. Digitalis toxicity does not cause:

a. Nausea, vomiting, fatigue d. Vision change g. Anorexia

b. Dysrhythmia e. AV block

c. Ventricular tachycardia f. Constipation (it causes diarrhea)

15. Which of the following clotting factors is normally found in circulating blood:

a. Thrombin c. Prothrombin

b. Thromboplastin

16. Which of the following drugs # the sympathetic stimulation of the adrenal medulla:

a. Nicotine (in small doses) b. Acetylcholine (in large doses)

17. Blood going to the branches of the coronary artery has just passed the:

a. Aortic valve c. Inferior vena cava

b. Right atrium d. Superior vena cava

18. In HT of renal origin, which antihypertensive is used:

a. Clonidine b. Hydralazine c. Captopril

19. Which of the following vasodilators cause venous pooling:

a. Sodium nitroprusside c. Hydralazine

b. Nitroglycerine d. Isosorbid dinitrate

c. Methyldopa

20. Which of the following is an a-agonist:

a. Clonidine b. -methyl dopa

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21. In an acute anginal attack, which drug can be given:

a. Propranolol c. Nitroglycerine (Short acting)

b. Isosorbid dinitrate

22. Which drug is used in prophylaxis of angina:

a. Nifedipine

b. Diltiazem

23. A person with fever has:

a. Paroxysmal tachycardia c. Sinus tachycardia

b. Bradycardia d. SA arrhythmia

24. Following moderate exercise, BP is usually higher than normal because:

a. Release of acetylcholine.

b. Activation of the RAA system

c. Increased venous return.

25. Repeated arrhythmia means:

a. Paroxysmal arrhythmia c. Tachy arrhythmia

b. Ventricular arrhythmia

26. Which of the following drugs causes rebound HT:

a. Clonidine c. Hydralazine

b. Guanithedine

27. Prolonged use of diuretics causes all of the following except:

a. Hypoglycemia d. Hyperuricemia

b. Hypokalemia e. Alkalosis of urine

c. Sexual dysfunction

28. During the absolute refractory period, if you apply another stimulus, the muscle will:

a. Contract c. Relax

b. Remain in its existing state (no response to stimuli)

29. Aldosterone is secreted from the:

a. Adrenal medulla c. Kidney

b. Adrenal cortex

30. During rest (or inspiration), BP is lowest in:

a. Venules c. Arterioles

b. Vena cavae d. Capillaries31. Which of the following is an a-blocker:

a. Prazocin b. Doxazocin c. Terazocin

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43. Arrhythmias may be caused by:

a. Catecholamines

44. The anti-coaggulant effect of warfarin increases in:

a. Vitamin K deficiency.

45. What is the side effect of minoxidil:

a. Hirsutism c. Weight gain

b. Fluid retention d. Tachycardia

46. Heparin is used for:

a. Prophylaxis & treatment of venous thrombosis

b. Prophylaxis & treatment of pulmonary (or peripheral arterial) embolism.

c. Prevent clotting during surgery (arterial or cardiac)

d. Fibrillation with embolization

47. Which is true about heparin:

a. Works in vivo & in vitro d. Inactive orally

b. Has anti-thrombin / anti-thromboplastin effects

c. Prevents arterial thrombosis e. Safe in pregnancy

48. Which is true about warfarin:

a. Decrease platelet aggregation d. Works in vivo & in vitro

b. Activity in vit K deficiency e. Decreases hepatic fibrinogen synthesis

c. Produces prompt action if given IV

49. Which diuretics cause urinary alkalosis:

a. Thiazides c. Carbonic anhydrase inhibitors

b. Loop diuretics d. K+ sparing diuretics

50. Which diuretic acts on proximal tubules:

a. Acetazolamide b. HCTZ

51. Which diuretics # water excretion at distal tubules:

a. Triametrene c. Amiloride e. Frusimide

b. Spironolactone d. Thiazide f. Acetazolamide

52. The use ofa-blockers in HT is limited to:

a. Patients who can not take diuretics or beta-blockers.

53. Which drug is contra-indicated in CHF & HT:

a. NSAIDs

54. The major side effects of nitrates is:

a. Headache lasts for > 12 hrs

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55. Nifedipine is:

a. 1,4 dihydropyridine b. pyrimidine

56. Respiratory acidosis means:

a. Increase in PCO2 in the brain

57. Hyperchloremic acidosis is caused by:

a. Acetazolamide (carbonic anhydrase inhib.) b. Aceterol (diamox) ???

58. SMZ, TMP & Miconazole, # warfarin efficacy through:

a. Decreasing hapatic metabolism

b. Inhibiting bacterial flora$ vit. K synthesis potentiates warfarin

c. Displacing warfarin from plasma protein binding sites.

59. Nifedipine is used in:

a. Angina b. CHF

60. Acute pre-renal failure results in:

a. Azotemia b. Uremia

61. Which diuretic decreases Ca excretion & leads to hypercalcemia:

a. Loop diuretics b. Thiazide diuretics

62. Metabolic acidosis is caused by:

a. Acetazolamide c. Methyl alcohol e. Starvation

b. Renal falure d. Ethylene glycol

63. Which agent # water excretion at (# permiability of) collecting tubules:

a. Triametrene b. Amiloride c. Ethacrinic acid

64. Parathyroid hormone promotes Ca excretion by action on:

a. Proximal tubules. c. Distal tubules

b. Glomerulus d. Renal tubules

65. What is true about ACE:

a. Natural substrate is A I b. Normal alternative for A I

66. Nephrotic syndrome is characterized by:

a. Proteinuria b. Hypoalbuminuria

67. Which CCB causes MI:

a. Diltiazem b. Verapamil c. Nifedipine

68. The tension in blood vessels depends on:

a. Radius of blood vessel b. Pressure created on blood vessel

b. Length of blood vessel69. What is common in thiazides & sulphonamides:

a. The sulpha group

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70. A drug which inhibits aldosterone secretion (e.g. ACEIs) will:

a. Cause hyperkalemia b. effect of spironolactone

71. Compared to sublingual nitroglycerine, transdermal patches have:

a. Prolonged effect b. Rapid effect

72. Which is used as a voltage dependant Na+ channel blocker:

a. Tetraiodoxine Na+ channel blocker but toxic not used

b. Benzodiazepine Cl- channel opener# GABA

c. Digitalis Ca++ channel opener

d. Verapamil Ca++ channel blocker

e. Phenytoin (& lidocaine) Na+ channel blockers

73. Which is a Na+ channel blocker:

a. Phenytoin b. Lidocaine c. Triametrene

74. Which drugs act through lipoprotein activation:

a. Clofibrate c. Gemfebrozil e. Nicotinic acid

b. Atrovastatin d. Cholistyramine

75. Edema occurs in cases of:

a. Hypervolemia c. Na+ loss e. Liver chirrosis

b. Right side CHF d. Hypovolemia f. Hyperthyroidism

76. Edema occurs in all except:

a. Ascitis c. Glomerular damageb. Hyperthyroidism d. Excess corticosteroid usage

77. Which is not a symptom associated with MI:

a. Arrhythmia c. AV block e. Headache

b. Heart burn d. diarrhea

78. Acetazolamide & sulphonamides are both: (carbonic anhydrase inhibitors are aromatic or

heterocyclic sulphonamides with prominent thiadiazole gp)

a. Sulphonamides b. Anti-microbials

79. What is azotemia:

a. Synonymous to uremia b. SrCr c. NH3 & urea in blood ( BUN)

80. Digoxin is affected by:

a. Erythromycin b. Cholistyramine c. Primaquine

81. Hypovolemia causes all except:

a. Pulmonary edema b. Oliguria

82. Renal failureis associated with:

a. Hyperphosphatemia

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83. Side effects of atenolol include:

a. Hypotension b. Tremors c. Visual disturbances

84. Fibrinolytic agents cannot be given post-op. if:

a. Patient had gastric bleeding within the past 6 months

b. Patient > 65 yrs c. Patient is hypertensive

85. Osmotic dialysis is effective with:

a. Low mol. wt. substance c. Large volume of distribution

b. High plasma protein binding

86. Bile acids (bile salts) are:

a. Hydrophilic c. Steroid in nature (not absorbed)

b. Prepare O/W emulsions ???

87. Which drugs is most effective in decreasing LDL & VLDL:

a. Clofibrate c. Nicotinic acid

b. Atrovastatin d. Cholistyramine

88. Vasodilators may cause:

a. Orthostatic hypotension b. Tachycardia

89. The dose of warfarin could be adjusted by measuring:

a. APTT c. Warfarin conc. in blood

b. PT (prothrombin time) d. Coagulation time

90. Which is true about pulmonary thrombotic disease:

a. Fatal b. Mainly due to varicose (starting in the legs)

91. Injection of high dose of K+ may cause:

a. Cardiac arrest

92. Side effects of thiazides include:

a. Hyperglycemia b. Hyperuricemia c. Alkalosis

93. Streptokinase is used for:

a. Deep venous thrombosis

94. Which of the following anti-arrhythmics can be used orally:

a. Mexiliten ???

95. Digitalis consists of digitalide plus:

a. Sugar b. Amino acid c. Alkaloid

96. Which diuretic decreases Na, K, & Cl & causes mild urinary alkalosis:

a. Thiazides b. Loop diuretics c. Amiloride

97. Which diuretic increases Ca excretion:

a. Thiazides b. Laxis c. Amiloride

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98. Triametrene:

a. Acts on distal & collecting tubules

b. Distrupts the exchange with K+ & H+ b blocking sodium channels & decreasing

the driving force for the excretion of H+ & K+

99. Which agent increases the water permiability of renal tubules (Increases reabsorption):

a. ADH c. Amiloride

b. Lasix

100. Which is used in arterial thrombosis:

a. Asprin b. Clofibrate

101. Probucol: ????

a. Is used to decrease serum cholesterol

b. Does not affect the later stages of cholesterol synthesis (HDL & LDL)

102. Any drug given in CHF may be nephrotoxic because:

a. Blood flow to the kidney is not sufficient

103. Infarction results because of:

a. Blood cannot reach the right & left carotids ???

104. Ouabin in the treatment of CHF (similar to digitalis) is:

a. Of rapid onset c. Not absorbed from GIT

b. Of short duration d. Given IM (it is given IV only)

105. Digitalis alkaloid is:

a. Highly water soluble b. Water insoluble

106. In acute renal failure, CrCl over estimates glomerular filtration because:

a. Cr is less synthesized d. Cr is highly metabolized in liver

b. Cr is bound to plasma proteins e. Cr is secreted by renal tubules

c. Cr is reabsorbed

107. The best time to give an anti-hyperlipidemic drug like Atrovastatin is at:

a. night c. morning

b. Afternoon (at night synthesis of lipids increase)

108. Which of the following anti-arrhythmics can be used orally:

a. Mexiliten ???

109. Digitalis consists of digitalide plus:

a. Sugar b. Amino acid c. Alkaloid

110. Which diuretic decreases Na, K, & Cl & causes mild urinary alkalosis:

a. Thiazides b. Loop diuretics c. Amiloride

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Diabetes

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Diabetes

There are 3 significant parameters in a glucose tolerance curve (blood-glucose vs. time curve)

The peak conc. of the glucose in blood.

The time required to achieve peak serum level.

The rate at which blood glucose level declines with time.

In diabetes mellitus the blood glucose peak is higher, occurs later, & declines more slowly

than a corresponding glucose tolerance curve of a normal individual.

In the glucose tolerance curve:

The normal fasting glucose level is

90-120 mg /100 ml of blood.

Diabetic patients have fasting blood sugar

curve higher than 120 mg / 100 ml of blood.

Ketone bodies (acetone b-hydroxy butyric acid) are caused by starvation & diabetes(hyperglycemia) & are characterized by the acetone odor of mouth.

Test for ketones in urine: (specific for ketone bodies & acetone)

Acetest Ketostix

Tests for glucose in urine: (specific for glucose)

Testape, Clinistix & Diastix: contain glucose oxidase

Benedict solution, Fehlings solution & Clinitest: based on copper reduction method

Ascorbic acid, L-dopa, salicylates, phenazopyridine, penicillins & cephalosporins may

give false +ve test with Benedict & Clinitest.

Fehlings solution gives red color with glucose & acetaldehyde.

After an insulin injection: hypoglycemia may occur because of a low carbohydrate diet.

Alcoholic beverages: are contra-indicated in patients taking oral hypoglycemics.

Juvenile diabetes patients should receive insulin therapy & eat according to a caloric diet.

Insulin: is the hormone that acts on the cell membrane.

Insulin shock: in an unconscious patient is treated with glucagon injection.

Adrenaline causes hyperglycemia

Calories:

Each gram of protein supplies about 4 Kcal.

Each gram of carbohydrates supplies about 4 Kcal.

Each gram of dextrose supplies about 4 Kcal.

Each gram of fats supplies about 9 Kcal.

Each gram of ethanol supplies about 7 Kcal.

1 Kcal = 1,000 calories

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Oral Hypoglycemic Drugs

Oral Hypoglycemic Drugs: They are classified in 2 groups:

Sulfonylurea derivatives.

Biguanides.

Sulfonylurea derivatives: are used to treat type II diabetes.

Mechanism of action:d These stimulate the -cells of the pancreas to secrete insulin.

d They also decrease glycogenolysis.

d May cause hypoglycemia.

Acetohexamide (Demilor): is reported to have a uricosuric effect

d It is metabolized to a compound having equal or greater hypoglycemic activity.

Chlopropamide: has an antidiuretic effect which may be useful in diabetes insipidus.

d It has the longest duration of action (t ) of all oral hypoglycemics (require severalweeks to be completely eliminated from the body after discontinuation).

Tolbutamide (Rastinon): is totally metabolized to the inactive form.

Tolazamide (Tolinase): is more slowly absorbed from the GIT than other compounds.

Glipizide (Amaryl): Excreted via the liver.

Biguanide derivatives:

Mechanism: potentiate action of insulin on glucose (activate pancreatic insulin).

Metformin (Glucophage): Excreted via the kidney

d Indicated in obese diabetics, where hyperglycemia is due to ineffective insulin.

d Side effects: weight loss, lactic acidosis, metallic taste, GIT upset.

Phenformin

Diabetes insipidus:

Is a central endocrine disorder characterized by $ secretion of ADH from the pituitary

(hypothalamus) excessive urinary output (urine output # from 1.5 l 18 L) thirst

Treated with lypressin (vasopressin analogue)

Increased urinary output in DM: is due to the osmotic pressure of glucose in urine

Oral anti-diabetics:

Sulphonyl ureas: activate receptors on B-islets cells of pancreas Release more insulin in

response to glucose; they do not insulin formation and they may cause hypoglycemia, and

weight gain; e.g. Tolbutamide & Glipizide

Biguanides: reduce production of glucose in liver. Used for obese patients; e.g. Metformin

Glucosidase Inhibitor: breakdown and absorption of carbohydrates; e.g. Acarbose

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Oral anti-diabetics:

Sulphonyl ureas: activate receptors on B-islets cells of pancrease Release more insulin in

response to glucose; they do not insulin formation and they may cause hypoglycemia, and

weight gain; e.g. Tolbutamide & Glipizide

Biguanides: reduce production of glucose in liver. Used for obese patients; e.g. Metformin

-Glucosidase Inhibitor: breakdown and absorption of carbohydrates; e.g. Acarbose

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Classification of Insulin:insulin can be classified according to onset & duration of action.

Class Onset Duration Examples

Fast acting 0.5-1 hr 6-8 hrs Crystalline or Soluble insulin

Acid regular insulin

Neutral regular insulin

Semi-lent (susp. small particles)

Intermediate 2 hrs 24 hrs Isophane insulin suspension

Insulin Zn suspension

Globin Zn insulin

NPH & Lent

(lent = 30% semilent + 70% ultralent)

Long acting 4 hrs 36 hrs Protamine Zn Insulin

6-8 hrs Ultralent (extended Insulin Zn)

(a suspension of large particles)

Mechanism of action of insulin:

Enhances glucose utilization in peripheral tissues.

Increases glucose storage in form of glycogen in liver & skeletal muscles, through

enhancing the hexokinase enzyme glucose-6-phosphate formation.

It is anabolic, enhancing protein synthesis.

Decreases fat catabolism & enhances lipogenesis.

It decreases gluconeogenesis (i.e. $ conversion of amino-acids glucose)

Insulin degradation: occurs in the liver as well as the kidneys.

Insulin when injected IV has a short plasma t of 9 min.

Crystalline Zn insulin: is the only insulin (regular intermediate acting) that can be used IV

in case of diabetes ketoacidosis

Insulin has a large volume of distribution which approximates that of extracellular fluids.

When low conc. of insulin (20 units) is indicated in LVPs, only soluble insulin (not

suspension) can be used. Additionally, the % of insulin adsorbed on the walls of the container

or administration set is significant (not less than 50% loss).

Single peak insulin: means that it displays a single protein peak when assayed

chromatographically. (Not all antigenic components are removed ~99%). It has higher degree

of purity compared to older insulin preparations.

Most insulin preparations used in USA are single peak, i.e. single component.

Single component insulin: means from 1 source only (pork or beef).

Diabetic patients sensitive to foreign proteins: appear to tolerate pork insulin rather than

beef insulin. Tletin II is a single component, pork insulin, for highly sensitive diabetics.

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1. Which of the following causes hypoglycemia:

a. Insulin c. Sulphonylurea drugs (e.g.Daonil)

b. Biguanides (e.g. metformine Glucophage)

2. Which of the following gives +ve reducing results with Cu salts in testing glucose in urine:

a. Testape d. Clinistix

b. Diastix e. Benedicts solution(Cu reduction method)

c. Clinitest (Cu reduction method)

3. Which of the following agents interferes with glucose test in urine:

a. Vitamin C c. Cephalosporins

b. Methyl Dopa d. Ampicillin

4. In juvenile diabetes, the patient should be treated with:

a. Insulin b. Fastingb. Eating frequent meals (many times a day).

5. Which agent causes hypoglycemia:

a. Corticosteroids (#glucose) b. Adrenaline (#glucose)

b. Sulfonylurea.

6. What is specific for a fasting glucose test:

a. Glucose levels will be high but not more than 120 mg / 100 ml.

b. There will be ketosis.

c. There will be glucose urea as in diabetics

7. In which of the following physiologic conditions do ketone bodies accumulate:

a. Juvenile diabetes c. Diabetes mellitus

b. Starvation d. All of the above

8. Which of the following insulin prep. is expected to have the longest duration of action:

a. Semilent insulin. d. Globin insulin.

b. NPH insulin. e. Regular insulin.

c. Protamine Zn insulin.

9. Which hormone acts on the surface of the cell:

a. Adrenaline b. Gastrine c. Insulin

10. Carbose decreases blood glucose level through:

a. Decreasing GIT absorption of carbohydrates

b. Blunting the post brandial blood glucose curve

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11. Which anti-diabetic agent cannot be used for lactic acid acidosis:

a. Metformie c. Tolbutamide

b. Clorpropamide d. Glyberide

12. What causes Juvenile onset (Type IIDDM) diabetes & what is used for its treatment:

a. It is caused by degeneration of cells of islets of langerhans & is treated with insulin

13. Why is insulin injected in SC tissue:

a. To avoid tissue damage b. To control the dose

14. Insulin shock in an unconscious patient is treated by:

a. Glucagon injection b. Glucose IV

15. Which is true about SC insulin therapy:

a. Lipodistrophy (SC fat at site of injection).

16. For ketoacidosis we use:

a. Zn insulin (regular) IV

17. In which of the following conditions does insulin requirements increase:

a. Stress c. Bacterial infection

b. Pregnancy d. Surgery

18. Alcohol is contraindicated with:

a. Metformine c. Gliburide

b. Metronidazole (disulfuram like reactions)

19. After opening an insulin injection, how many days can it be kept :

a. At room temp 30 days

b. Under refrigeration till expiry date

20. Longstanding diabetes leads to:

a. Retinopathy c. Nephropathy e. CAD

b. Neuropathy d. Diabetic foot (ulcer or gangrene)

21. Which of the following is specific for measuring glucose:

a. Tes-tape

22. Clopropamide should not be given with:

a. Alcohol b. Antacids

23. The threshold of glucose is:

a. 3.5 L / min

24. Ketoacidosis is determined by all except:a. B-hydroxy buteric acid c. Acetone

b. Acetic acid d. Lactic acid

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25. To monitor compliance in diabetes, we monitor:

a. Glucosuria c. Glycemia

b. Proteinuria d. Ketonuria

26. Ketoacidosis may result from:

a. Diabetes b. Insulin deficiency

27. When administered IV, insulin has:

a. Short t b. Large volume of distribution

28. Which is true about insulin pump:

a. Gives regular insulin all night

b. Supposed to be the most similar to physiologic

29. Human insulin: ???

a. Can be frozen b. Cannot be easily replaced by other forms

30. In a healthy adult person, after a meal blood glucose will:

a. Increase above 200 then decrease rapidly

31. Acrabose is: ????

a. A basic tetra-saccharide laxative

b. a glucosidase inhibitor (inhibits the enzyme responsible for hydrolysis of sucrose)

c. Inhibits absorption of glucose in the small intestine$ glucose levels

d. Blunts post brandial glucose curve

32. What is true about sulphonyl ureas:

a. Acidic products

b. Stimulate cells to release insulin

c. Cause lactic acidosis

33. Longstanding diabetes leads to:

a. Retinopathy c. Nephropathy e. CAD

b. Neuropathy d. Diabetic foot (ulcer or gangrene)

34. Which of the following is specific for measuring glucose:

a. Tes-tape

35. Clopropamide should not be given with:

a. Alcohol b. Antacids