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Cardiovascular المعلومات بالداخل موثوق بها لأنها مراجعه و معتمده من Certified from Pharmacists_coffee magazine.

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Presentation on theme: "Cardiovascular المعلومات بالداخل موثوق بها لأنها مراجعه و معتمده من Certified from Pharmacists_coffee magazine."— Presentation transcript:

1 Cardiovascular المعلومات بالداخل موثوق بها لأنها مراجعه و معتمده من Certified from Pharmacists_coffee magazine

2 Hypertension Cardiac Output (CO) = Heart Rate (HR) X Stroke Volume (SV) Blood Pressure (BP) = Cardiac Output (CO) X Total Peripheral Resistance (TPR). The Renin - Angiotensin – Aldosterone 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. –1 st dose hypotension. Mechanism of action of ACEIs: Angiotensinogen Renin Angiotensin I Angiotensin II Aldosterone Production Sodium & Water Retention ACEIs Angiotensin Converting Enzyme Vasoconstriction Blood Pressure Bradykinin (Vasodilator) Inactive kinins

3 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,1 st 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 endings – storage 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 as they block neurotransmission at both sympathetic & PS ganglia  many side effects (dry mouth, constipation, impaired visual accommodation, urine retention).

4 Mode of action of diuretics: –Thiazides (e.g. HCTZ)inhibit Na + reabsorption at distal tubules –Loop diuretics (e.g. bumetanideinhibit Na + / Cl - exchange at the ascending limb frusimide Lasix) of the Loop of Henle –K sparing diuretics (amilorideinhibit the effects of aldosterone hormone on spironolactone & triametrene)distal tubules –Carbonic anhydrase inhibitorsinhibit 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.

5 Selectivity of  -blockers: –Propranolol (Inderal)  Non selective (  1 +  2 ) –Pindolol (Visken)  Non selective (  1 +  2 ) + ISA –Nadolol (Corgard)  Non selective (  1 –  2 ) + OD –Timolol (Timoptic)  Non selective (glucoma) –Labetalol (Trandate)  Non-Selective (  1 +  2 +  blocker) –Atenolol (Tenormin)  Selective (  1 >  2 ) + OD –Metoprolol (Lopressor)  Selective (  1 >  2 ) –Acebutolol (Sectral)  Selective (  1 >  2 ) + 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 BBs  MI, angina & rebound HT. Peyronie’s disease: is reported with metoprolol (p.253). OrganReceptor Response Heart  1 Stimulation  increased contraction & HR Arterioles  1 Stimulation  vasoconstriction  2 Stimulation  vasodilatation GIT  1 Stimulation  decreased contraction Bronchi  2 Stimulation  bronchodilatation Uterus  2 Stimulation  Relaxation N.B: Reserpine causes CNS depression (as it  the conc. of dopamine). It also causes lethargy sedation & night-mares. It is a post-ganglionic neuron blocker causing depletion of catecholamine stores in the brain & the peripheral adrenergic system.

6 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  -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  -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.

7 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 (beginning during 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 95 – 105 millivolt. (90–105) 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).

8 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)  These are used for ventricular & supraventricular arrhythmias  They decrease the rate of rise of phase 0; i.e. slow the rate of conduction, excitation & spontaneous repolarization.  They decrease the slope of phase 1  prolong the effective refractory period. Class II: It includes  -antagonists (  -blockers), e.g. propranolol.  They are used in atrial arrhythmias.  They depress phase 4 depolarization.  They competitively inhibit  receptor sites. Class III: these include: – Bretylium – Amiodaron (Cordaron).  These are used in ventricular fibrillations.  They prolong the duration of the action potential.  They  the absolute refractory period (prolongation of repolarization). Class IV: these include CCBs e.g. verapamil (Isopten), nifedipine, diltiazem (cardiazem).  These are used in atrial fibrillation & flutter supraventricular tachycardia.  They decrease the amount of Ca ions available for displacement from the cell membrane, i.e. decrease the inward current carried by Ca.  They prolong the absolute refractory period.  They depress phase 4 spontaneous depolarization.  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:   body temp. (~ HR  by 10 beats / min for every 1 o F rise in temp.)  Toxic condition.  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.

9 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 lidocaine is:  No effect on SA node (unlike quinidine).  Suppress automacity in Purkinje fibers & atrium.  Depression of phase 0 depolarization (  Na influx) (it is depressant but not like procainamide/quinidine).  It  the effective refractory period on Purkinje fibers & inhibit the duration of action potential.  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.

10 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 leaf utilizes pigeon.

11 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 of the 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.

12 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 heparin’s 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.  Warfarin is used as an antidote for vitamin K. Ca ++ Soluble Fibrin + XIII* Stabilized Fibrin * Denotes the activated forms of coagulation factors Factor I  FibrinogenFactor VIII  Antihemophilic globulin (AHG) Factor II  ProthrombinFactor IX  Christruns Factor III  Tissue thromboplastinFactor X  Stuart power factor Factor IV  Ionic CalciumFactor XI  Plasma thromboplastin Factor V  labile factor AG, proaccelerinFactor XII  Hageman factor Factor VI  No factorFactor XIII  Fibrin stabilizing Factor VII  Proconvertin, autothrombin IPF-3  Platelet factor PF-3 (II) (II*) (I) (II*) XIII

13 Anticoagulants Heparin Caumarine (Warfarin) Onset of actionImmediateGradual Duration4 hrs2-5 days Used inEmergency & prophylaxisProphylaxis Route of administrationIV or SCOral Lab control of doseAPTTProthrombin time Treatment of overdoseProtamine SO 4 Fresh blood &/or Vitamin K Use in pregnancyCan be givenContraindicated Drug interactionsFewMany Effect of antacidsNo effect  its effect Pharmacologic actionAnticoag. in vivo & in vitroAnticoagulant in vivo CostExpensiveCheap The anticoagulant effect of heparin: is quantitated by the “Active Partial Thromboplastin Time” (APTT) & the “Activated Coagulation Time” (ACT) which is 3-5 min.  Normally, APTT is from sec; on using an anticoagulant it should be 45 – 60 sec. The anticoagulant effect of warfarin: is quantitated by the “Prothrombin Time” (PT).  Normally, PT is 12 sec; on adequate anticoagulant control it should be 24 – 30 sec. Hypoprothrombinemia induced by oral anticoagulants: is most rapidly offset by fresh blood or plasma. If not, by vitamin K 3 (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).

14 Angina TypesAngina Pectoris (strangling of the chest)  Beta Blockers  Methyl dopa. (Use)  Antihyperlipidemic  Hydralazine (vasodilator) Beta Blockers  Non Selective (B 1 + B 2 )PropranololPindolol Nadolol SotalolTimolol  Cardio Selective (B 1 )AcebutololAtenololMetoprolol  Non Selective (B +  )Labetalol Methyl Dopa (Aldomet): Interfere with synthesis of dopamine   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).

15 1.Heparin is: a.Like coumarinec. Acts on certain steps of coagulation system b.Orald. Of benefit in arterial blood clot as prophylaxis 2.In left ventricular failure the blood pools in: a.Lungsc. Vena cavae b.Liver 3.Patients with moderate HT & a history of heart disease (CHF) are treated with: a.Propranololc. Hydrochlorothiazide b.Methyl dopad. 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  &  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 (  2 agonist  negative feedback  E & NE) c.Methyl dopa (False methylation  methyl NE   2 agonist) d.Guanithidine e.Hydralazine (direct vasodilatation) 7.Vasodilators cause: a.Reflex bradycardiab. Reflex tachycardia 8.In an ischemic myocardium, which is released & causes coronary vasodilatation: a.Adrenalinec. Serotonin b.Acetylcholined. Adenosine 9.Which hormone increases water reabsorption from distal tubules: a.Aldosterone (also vasopressin – ADH)c. Acetylcholine b.Adrenalined. Adenosine N.B. Vasopressin acts on distal tubules to  water re-absorption

16 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.Adrenalined. Propranolol b.Carbacole. Phenylephrine c.Ephedrinef. Isoproterenol (more  stimulant than  ) 12.The highest blood pressure is in the: a.Veinsc. Arteries (pulmonary artery) b.Venulesd. Arterioles 13.Diuretics are most likely to produce: a.Hyperkalemia.c. Hypokalemia.e. Hyperuricemia b.Hypercalcemia.d. Hypocalcemiaf. Urinary alkalosis 14.Digitalis toxicity does not cause: a.Nausea, vomiting, fatigued. Vision changeg. Anorexia b.Dysrhythmiae. AV block c.Ventricular tachycardiaf. Constipation (it causes diarrhea) 15.Which of the following clotting factors is normally found in circulating blood: a.Thrombinc. 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 valvec. Inferior vena cava b.Right atriumd. Superior vena cava 18.In HT of renal origin, which antihypertensive is used: a.Clonidineb. Hydralazinec. Captopril 19.Which of the following vasodilators cause venous pooling: a.Sodium nitroprussidec. Hydralazine b.Nitroglycerined. Isosorbid dinitrate c.Methyldopa 20.Which of the following is an  -agonist: a.Clonidineb.  -methyl dopa

17 21.In an acute anginal attack, which drug can be given: a.Propranololc. 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 tachycardiac. Sinus tachycardia b.Bradycardiad. 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 arrhythmiac. Tachy arrhythmia b.Ventricular arrhythmia 26.Which of the following drugs causes rebound HT: a.Clonidinec. 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.Contractc. Relax b.Remain in its existing state (no response to stimuli) 29.Aldosterone is secreted from the: a.Adrenal medullac. Kidney b.Adrenal cortex 30.During rest (or inspiration), BP is lowest in: a.Venulesc. Arterioles b.Vena cavaed. Capillaries 31.Which of the following is an  -blocker: a.Prazocinb. Doxazocinc. Terazocin

18 32.What is true about the hypophyseal portal system: a.It begins & ends in capillariesc. None b.It begins with capillaries & ends with veins 33.Which drug is used in mild to moderate HT: a.Captoprilc. Propranolol b.Lasix 34.Which drug is used in mild HT: a.HCTZc. Prazocin b.Clonidine 35.Arterial dilators include: a.Diazoxide.c. Hydralazine. b.Minoxidild. Sodium nitroprusside (arteriolar & venous) 36.Which antihypertensive is used in diabetic patients: a.Captopril (ACEIs)c. Prazocin (  -blocker)e. CCBs b.HCTZd. Atenolol 37.In angina pectoris, propranolol is used as: a.Treatmentc. Acute attacks b.Prophylactic (  O 2 consumption) 38.The outer layer of the adrenal cortex secretes: a.Aldosteronec. Norepinephrine b.Cortisone 39.The middle layer of the adrenal cortex secretes: a.Aldosteronec. Norepinephrine b.Cortisone 40.The adrenal medulla secretes: a.Aldosteronec. Norepinephrine & epinephrine b.Cortisone 41.In complete heart block (AV block): a.No arterial impulses reach the ventriclesc. Ventricles beat slower b.Atria & ventricles contract independently.d. Ventricles beat irregularly 42.What is the mechanism by which chenodioxycholic acid dissolves gall stones: ??? a.Reduces cholesterol synthesisc. Increases bile acid production b.Increases phospholipids

19 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.Hirsutismc. Weight gain b.Fluid retentiond. 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 vitrod. Inactive orally b.Has anti-thrombin / anti-thromboplastin effects c.Prevents arterial thrombosise. Safe in pregnancy 48.Which is true about warfarin: a.Decrease platelet aggregationd. Works in vivo & in vitro b.Activity  in vit K deficiencye. Decreases hepatic fibrinogen synthesis c.Produces prompt action if given IV 49.Which diuretics cause urinary alkalosis: a.Thiazidesc. Carbonic anhydrase inhibitors b.Loop diureticsd. K + sparing diuretics 50.Which diuretic acts on proximal tubules: a.Acetazolamideb. HCTZ 51.Which diuretics  water excretion at distal tubules: a.Triametrenec. Amiloridee. Frusimide b.Spironolactoned. Thiazidef. Acetazolamide 52.The use of  -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)

20 55.Nifedipine is: a.1,4 dihydropyridineb. pyrimidine 56.Respiratory acidosis means: a.Increase in PCO 2 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.Anginab. CHF 60.Acute pre-renal failure results in: a.Azotemiab. Uremia 61.Which diuretic decreases Ca excretion & leads to hypercalcemia: a.Loop diureticsb. Thiazide diuretics 62.Metabolic acidosis is caused by: a.Acetazolamidec. Methyl alcohole. Starvation b.Renal falured. Ethylene glycol 63.Which agent  water excretion at (  permiability of) collecting tubules: a.Triametreneb. Amiloridec. Ethacrinic acid 64.Parathyroid hormone promotes Ca excretion by action on: a.Proximal tubules.c. Distal tubules b.Glomerulusd. Renal tubules 65.What is true about ACE: a.Natural substrate is A Ib. Normal alternative for A I 66.Nephrotic syndrome is characterized by: a.Proteinuriab. Hypoalbuminuria 67.Which CCB causes MI: a.Diltiazemb. Verapamilc. Nifedipine 68.The tension in blood vessels depends on: a.Radius of blood vesselb. Pressure created on blood vessel b.Length of blood vessel 69.What is common in thiazides & sulphonamides: a.The sulpha group

21 70.A drug which inhibits aldosterone secretion (e.g. ACEIs) will: a.Cause hyperkalemiab.  effect of spironolactone 71.Compared to sublingual nitroglycerine, transdermal patches have: a.Prolonged effectb. 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.Phenytoinb. Lidocainec. Triametrene 74.Which drugs act through lipoprotein activation: a.Clofibratec. Gemfebrozile. Nicotinic acid b.Atrovastatind. Cholistyramine 75.Edema occurs in cases of: a.Hypervolemiac. Na + losse. Liver chirrosis b.Right side CHFd. Hypovolemiaf. Hyperthyroidism 76.Edema occurs in all except: a.Ascitisc. Glomerular damage b.Hyperthyroidism d. Excess corticosteroid usage 77.Which is not a symptom associated with MI: a.Arrhythmiac. AV blocke. Headache b.Heart burnd. diarrhea 78.Acetazolamide & sulphonamides are both: (carbonic anhydrase inhibitors are aromatic or heterocyclic sulphonamides with prominent thiadiazole gp) a.Sulphonamidesb. Anti-microbials 79.What is azotemia: a. Synonymous to uremiab.  SrCrc.  NH 3 & urea in blood (  BUN) 80.Digoxin is affected by: a.Erythromycinb. Cholistyraminec. Primaquine 81.Hypovolemia causes all except: a.Pulmonary edemab. Oliguria 82.Renal failureis associated with: a.Hyperphosphatemia

22 83.Side effects of atenolol include: a.Hypotensionb. Tremorsc. 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. substancec. Large volume of distribution b.High plasma protein binding 86.Bile acids (bile salts) are: a.Hydrophilicc. Steroid in nature (not absorbed) b.Prepare O/W emulsions ??? 87.Which drugs is most effective in decreasing LDL & VLDL: a.Clofibratec. Nicotinic acid b.Atrovastatind. Cholistyramine 88.Vasodilators may cause: a.Orthostatic hypotensionb. Tachycardia 89.The dose of warfarin could be adjusted by measuring: a.APTTc. Warfarin conc. in blood b.PT (prothrombin time)d. Coagulation time 90.Which is true about pulmonary thrombotic disease: a.Fatalb. 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.Hyperglycemiab. Hyperuricemiac. 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.Sugarb. Amino acidc. Alkaloid 96.Which diuretic decreases Na, K, & Cl & causes mild urinary alkalosis: a.Thiazidesb. Loop diureticsc. Amiloride 97.Which diuretic increases Ca excretion: a.Thiazidesb. Laxisc. Amiloride

23 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.ADHc. Amiloride b.Lasix 100.Which is used in arterial thrombosis: a.Asprinb. 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 onsetc. Not absorbed from GIT b.Of short durationd. Given IM (it is given IV only) 105.Digitalis alkaloid is: a.Highly water solubleb. 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.nightc. 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.Sugarb. Amino acidc. Alkaloid 110.Which diuretic decreases Na, K, & Cl & causes mild urinary alkalosis: a.Thiazidesb. Loop diureticsc. Amiloride 111.Which diuretic increases Ca excretion: a.Thiazidesb. Laxisc. Amiloride

24 Diabetes

25 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 mg /100 ml of blood. –Diabetic patients have fasting blood sugar curve higher than 120 mg / 100 ml of blood. Ketone bodies (acetone  -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, Fehling’s solution & Clinitest: based on copper reduction method Ascorbic acid, L-dopa, salicylates, phenazopyridine, penicillins & cephalosporins may give false +ve test with Benedict & Clinitest. Fehling’s 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 about4 Kcal. –Each gram of carbohydrates supplies about4 Kcal. –Each gram of dextrose supplies about4 Kcal. –Each gram of fats supplies about9 Kcal. –Each gram of ethanol supplies about7 Kcal. –1 Kcal = 1,000 calories

26 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:  These stimulate the  -cells of the pancreas to secrete insulin.  They also decrease glycogenolysis.  May cause hypoglycemia. –Acetohexamide (Demilor): is reported to have a uricosuric effect  It is metabolized to a compound having equal or greater hypoglycemic activity. –Chlopropamide: has an antidiuretic effect which may be useful in diabetes insipidus.  It has the longest duration of action (t ½) of all oral hypoglycemics (require several weeks 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  Indicated in obese diabetics, where hyperglycemia is due to ineffective insulin.  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

27 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

28 Classification of Insulin: insulin can be classified according to onset & duration of action. ClassOnsetDurationExamples –Fast acting0.5-1 hr6-8 hrsCrystalline or Soluble insulin Acid regular insulin Neutral regular insulin Semi-lent (susp. small particles) –Intermediate2 hrs24 hrsIsophane insulin suspension Insulin Zn suspension Globin Zn insulin NPH & Lent (lent = 30% semilent + 70% ultralent) –Long acting4 hrs36 hrsProtamine Zn Insulin 6-8 hrsUltralent (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 ½ 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.

29 1.Which of the following causes hypoglycemia: a.Insulinc. 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.Testaped. Clinistix b.Diastixe. Benedict’s solution (Cu reduction method) c.Clinitest (Cu reduction method) 3.Which of the following agents interferes with glucose test in urine: a.Vitamin Cc. Cephalosporins b.Methyl Dopad. Ampicillin 4.In juvenile diabetes, the patient should be treated with: a.Insulinb. Fasting b.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 diabetesc. Diabetes mellitus b.Starvationd. 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.Adrenalineb. Gastrinec. Insulin 10.Carbose decreases blood glucose level through: a.Decreasing GIT absorption of carbohydrates b.Blunting the post brandial blood glucose curve

30 11.Which anti-diabetic agent cannot be used for lactic acid acidosis: a.Metformiec. Tolbutamide b.Clorpropamided. Glyberide 12.What causes Juvenile onset (Type I – IDDM) 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 damageb. To control the dose 14.Insulin shock in an unconscious patient is treated by: a.Glucagon injectionb. 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.Stressc. Bacterial infection b.Pregnancyd. Surgery 18.Alcohol is contraindicated with: a.Metforminec. 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.Retinopathyc. Nephropathye. CAD b.Neuropathyd. 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.Alcoholb. Antacids 23.The threshold of glucose is: a.3.5 L / min 24.Ketoacidosis is determined by all except: a.B-hydroxy buteric acidc. Acetone b.Acetic acidd. Lactic acid

31 25.To monitor compliance in diabetes, we monitor: a.Glucosuriac. Glycemia b.Proteinuriad. Ketonuria 26.Ketoacidosis may result from: a.Diabetesb. Insulin deficiency 27.When administered IV, insulin has: a.Short t ½ 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 frozenb. 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.  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.Retinopathyc. Nephropathye. CAD b.Neuropathyd. 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.Alcoholb. Antacids 36.The threshold of glucose is: a.3.5 L / min 37.Ketoacidosis is determined by all except: a.B-hydroxy buteric acidc. Acetone b.Acetic acidd. Lactic acid


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