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Cardiovascular المعلومات بالداخل موثوق بها لأنها مراجعه و معتمده من Certified from Pharmacists_coffee magazine
<ul><li>Hypertension </li></ul><ul><li>Cardiac Output (CO)  =  Heart Rate (HR)  X  Stroke Volume (SV) </li></ul><ul><li>Bl...
<ul><li>Mechanism of action of antihypertensives: </li></ul><ul><ul><li>I - Sympatholytics:  these include: </li></ul></ul...
<ul><li>Mode of action of diuretics: </li></ul><ul><ul><li>Thiazides  (e.g. HCTZ) inhibit Na +  reabsorption at  distal tu...
<ul><li>Selectivity of   -blockers: </li></ul><ul><ul><li>Propranolol (Inderal)    Non selective (  1  +   2 ) </li></...
<ul><li>HT patients with concomitant diseases can be treated by: </li></ul><ul><ul><li>Patients with renal failure:  the s...
<ul><li>Arrhythmia:   is any deviation from the normal heart beat pattern. </li></ul><ul><li>Myocardial action potential: ...
<ul><li>Anti-arrhythmic Drugs </li></ul><ul><li>Can be classified according to their ability to alter the action potential...
<ul><li>Quinidine:  </li></ul><ul><ul><li>It is used for supraventricular arrhythmias. </li></ul></ul><ul><ul><li>It is th...
<ul><li>Congestive Heart Failure </li></ul><ul><li>In right-side CHF:  blood accumulates in liver, kidney, vena cavae, low...
<ul><li>Hypercholesterolemia </li></ul><ul><li>Cholestyramine resin (Questran):  is an anion exchange resin  used to treat...
<ul><ul><li>Normal Coagulation of Blood:   entails the formation of fibrin by the interaction of more than a dozen protein...
<ul><ul><li>Anticoagulants </li></ul></ul><ul><ul><li>  Heparin   Caumarine (Warfarin) </li></ul></ul><ul><ul><li>Onset of...
<ul><ul><li>Angina Types Angina Pectoris (strangling of the chest) </li></ul></ul><ul><ul><ul><li>Beta Blockers </li></ul>...
<ul><li>Heparin is: </li></ul><ul><ul><li>Like coumarine c.  Acts on certain steps of coagulation system </li></ul></ul><u...
<ul><li>At rest (or during sleep), which organ receives the richest blood supply: </li></ul><ul><ul><li>Lungs  c.  Heart <...
<ul><li>In an acute anginal attack, which drug can be given: </li></ul><ul><ul><li>Propranolol c.  Nitroglycerine  (Short ...
<ul><li>What is true about the hypophyseal portal system: </li></ul><ul><ul><li>It begins & ends in capillaries c.  None <...
<ul><li>Arrhythmias may be caused by: </li></ul><ul><ul><li>Catecholamines </li></ul></ul><ul><li>The anti-coaggulant effe...
<ul><li>Nifedipine is: </li></ul><ul><ul><li>1,4 dihydropyridine b.  pyrimidine </li></ul></ul><ul><li>Respiratory acidosi...
<ul><li>A drug which inhibits aldosterone secretion (e.g. ACEIs) will: </li></ul><ul><ul><li>Cause hyperkalemia b.    eff...
<ul><li>Side effects of atenolol include: </li></ul><ul><ul><li>Hypotension b.  Tremors c.  Visual disturbances </li></ul>...
<ul><li>Triametrene: </li></ul><ul><ul><li>Acts on distal & collecting tubules </li></ul></ul><ul><ul><li>Distrupts the ex...
Diabetes
<ul><li>Diabetes </li></ul><ul><li>There are 3 significant parameters in a glucose tolerance curve (blood-glucose vs. time...
<ul><li>Oral Hypoglycemic Drugs </li></ul><ul><li>Oral Hypoglycemic Drugs:  They are classified in 2 groups: </li></ul><ul...
<ul><li>Oral anti-diabetics: </li></ul><ul><li>Sulphonyl ureas:  activate receptors on B-islets cells of pancrease    Rel...
<ul><li>Classification of Insulin:   insulin can be classified according to onset & duration of action. </li></ul><ul><ul>...
<ul><li>Which of the following causes hypoglycemia: </li></ul><ul><ul><li>Insulin c.  Sulphonylurea drugs (e.g.Daonil) </l...
<ul><li>Which anti-diabetic agent cannot be used for lactic acid acidosis: </li></ul><ul><ul><li>Metformie c.  Tolbutamide...
<ul><li>To monitor compliance in diabetes, we monitor: </li></ul><ul><ul><li>Glucosuria c.  Glycemia </li></ul></ul><ul><u...
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CVS-Diabetes

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CVS-Diabetes

  1. 1. Cardiovascular المعلومات بالداخل موثوق بها لأنها مراجعه و معتمده من Certified from Pharmacists_coffee magazine
  2. 2. <ul><li>Hypertension </li></ul><ul><li>Cardiac Output (CO) = Heart Rate (HR) X Stroke Volume (SV) </li></ul><ul><li>Blood Pressure (BP) = Cardiac Output (CO) X Total Peripheral Resistance (TPR). </li></ul><ul><li>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. </li></ul><ul><li>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. </li></ul><ul><li>Additionally, ACEIs prevent the degradation of bradykinin (vasodilator) to inactive kinins. </li></ul><ul><li>Members include: Captopril, Enalapril, Lisinopril, Fosinopril, Benzapril, Quinapril & Ramipril. They are used in mild to moderate hypertension, proteinuria & in CHF. </li></ul><ul><li>NSAIDs inhibit the activity of ACEIs. </li></ul><ul><li>Side effects of ACEIs include: </li></ul><ul><ul><li>Proteinurea – Hypogasia/dysgasia (temporary loss of taste). </li></ul></ul><ul><ul><li>Renal insufficiency – Hyperkalemia (not used with K sparing diuretics). </li></ul></ul><ul><ul><li> neutrophils (neutropenia). – Rash, headache, dizziness, fatigue, cough. </li></ul></ul><ul><ul><li>1 st dose hypotension. </li></ul></ul><ul><li>Mechanism of action of ACEIs: </li></ul>Angiotensinogen Renin Angiotensin I Angiotensin II Aldosterone Production Sodium & Water Retention ACEIs Angiotensin Converting Enzyme Vasoconstriction Blood Pressure Bradykinin (Vasodilator) Inactive kinins
  3. 3. <ul><li>Mechanism of action of antihypertensives: </li></ul><ul><ul><li>I - Sympatholytics: these include: </li></ul></ul><ul><ul><ul><li>BBs  block  -1 receptors (heart)   cardiac contractility & HR   CO. </li></ul></ul></ul><ul><ul><ul><li>E.g. propranolol, pindolol, atenolol, acebutolol, nadolol, timolol </li></ul></ul></ul><ul><ul><ul><li>Post-synaptic   - blockers: block a receptors in vasculature  vasodilatation   TPR. E.g.: Prazocin, terazocin, doxazocin </li></ul></ul></ul><ul><ul><ul><li>Prazocin (Minipress)   blocker & direct vasodilator  syncope,1 st dose hypo-tension, possibly tachycardia (sudden discontinuation  rebound HT ). Not used. </li></ul></ul></ul><ul><ul><ul><li>Centrally acting  2 stimulants: </li></ul></ul></ul><ul><ul><ul><li>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. </li></ul></ul></ul><ul><ul><ul><li>Methyldopa (Aldomet)  false neurotransmitter. Postural hypoten. , rebound HT . </li></ul></ul></ul><ul><ul><ul><li>Adrenergic neuron blockers: </li></ul></ul></ul><ul><ul><ul><li>Reserpine  Catecholamine depletor (depletes epinephrine & NE stores). </li></ul></ul></ul><ul><ul><ul><li>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. </li></ul></ul></ul><ul><ul><li>II - Direct vasodilators:  direct peripheral vasodilator (direct action on arterioles). </li></ul></ul><ul><ul><ul><li>Hydralazine (SLE, postural hypoten.) Minoxidil (Hirsutism) </li></ul></ul></ul><ul><ul><ul><li>Diazoxide (Na retention) Na nitroprusside </li></ul></ul></ul><ul><ul><li>III - ACEIs  Inhibit the conversion of A-I to A-II   TPR & salt & water retention. </li></ul></ul><ul><ul><ul><li>E.g. Captopril, fosinopril, benzapril, enalapril, lisinopril, ramipril, quinapril </li></ul></ul></ul><ul><ul><li>IV- CCBs  inhibit influx of Ca through slow channels in vascular smooth muscle  relaxation   TPR </li></ul></ul><ul><ul><ul><li>E.g. Verapamil, diltiazem, dihydropyredines (flodipen, amlodipine, isradipine). </li></ul></ul></ul><ul><ul><ul><li>Nifedipine (Adalat): CCB used in angina & heart failure; causes ankle edema. </li></ul></ul></ul><ul><ul><li>V- Angiotensin II receptor antagonists: Block A-II receptors   TPR &  aldosterone </li></ul></ul><ul><ul><ul><li>E.g. Irbesartan, eprosartan, losartan, candesartan, valsartan, telmisartan. </li></ul></ul></ul><ul><ul><li>N.B. </li></ul></ul><ul><ul><li>Veratrum alkaloids  Direct action on the CNS. </li></ul></ul><ul><ul><li>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). </li></ul></ul>
  4. 4. <ul><li>Mode of action of diuretics: </li></ul><ul><ul><li>Thiazides (e.g. HCTZ) inhibit Na + reabsorption at distal tubules </li></ul></ul><ul><ul><li>Loop diuretics (e.g. bumetanide inhibit Na + / Cl - exchange at the ascending limb frusimide Lasix) of the Loop of Henle </li></ul></ul><ul><ul><li>K sparing diuretics (amiloride inhibit the effects of aldosterone hormone on spironolactone & triametrene) distal tubules </li></ul></ul><ul><ul><li>Carbonic anhydrase inhibitors inhibit carbonic anhydrase enzyme & this (e.g. acetazolamide) inhibits Na + / H + exchange at proximal tubules decreasing its reabsorption </li></ul></ul><ul><ul><li>Osmotic diuretics (e.g. urea & increase osmolarity of glomerular filtrate, mannitol) (thus decrease reabsorption of water & increase urination) </li></ul></ul><ul><li>Thiazide diuretics:  uric acid excretion  hyperuricemia; except for Ticrynofen which has a uricosuric effect. Hypokalemia & hypercalcemia (NSAIDs  efficacy of thiazides). </li></ul><ul><li>Mercurial diuretics: are given IM. They are not absorbed from GIT, thus not given orally. </li></ul><ul><li>Ethacrynic acid (Edecrine): is a loop diuretic capable of producing ototoxicity & may aggravate ototoxicity of aminoglycosides. (NSAIDs  efficacy of loop diuretics). </li></ul><ul><li>Diuretics enhance proximal tubular reabsorption of solutes including uric acid. </li></ul><ul><li>Acetazolamide leads to hyperchloremic metabolic alkalosis as a result of  loss of water coupled with  distal Na reabsorption in exchange for K & … </li></ul><ul><li>Thiazides  hypercalcemia Loop diuretics  hypocalcemia (Hypercalciurea) </li></ul><ul><li>The antidiuretic hormone (ADH or Vasopressin): is secreted from the posterior pituitary & acts on the distal tubules to enhance the reabsorption of water & salt. </li></ul><ul><li>General Notes: </li></ul><ul><li>In complete heart block: beats of the atria & ventricles are both blocked. </li></ul><ul><li>In acute asthma & in anaphylactic shock adrenaline is used. </li></ul><ul><li>The highest BP is in the pulmonary artery, the lowest BP is in the vena cavae. </li></ul><ul><li>CNS reaction towards increased arterial pressure  peripheral vasodilatation. </li></ul><ul><li>In moderate exercise, the HR increases because the sympathetic stimulation of  -receptors in arterioles causes vasodilatation   TPR  leading to reflex  in HR. </li></ul><ul><li>When venous return is increased to the right atrium, consequently: </li></ul><ul><ul><li>Tachycardia occurs. </li></ul></ul><ul><ul><li>Increased oxygen consumption (OC). </li></ul></ul><ul><li>Organ ischemia: can result from organ-turnicate. </li></ul><ul><li>Bed sores: are caused by body weight pressure in patients laying in 1 position for long time. </li></ul>
  5. 5. <ul><li>Selectivity of  -blockers: </li></ul><ul><ul><li>Propranolol (Inderal)  Non selective (  1 +  2 ) </li></ul></ul><ul><ul><li>Pindolol (Visken)  Non selective (  1 +  2 ) + ISA </li></ul></ul><ul><ul><li>Nadolol (Corgard)  Non selective (  1 –  2 ) + OD </li></ul></ul><ul><ul><li>Timolol (Timoptic)  Non selective (glucoma) </li></ul></ul><ul><ul><li>Labetalol (Trandate)  Non-Selective (  1 +  2 +  blocker) </li></ul></ul><ul><ul><li>Atenolol (Tenormin)  Selective (  1 >  2 ) + OD </li></ul></ul><ul><ul><li>Metoprolol (Lopressor)  Selective (  1 >  2 ) </li></ul></ul><ul><ul><li>Acebutolol (Sectral)  Selective (  1 >  2 ) + ISA + OD </li></ul></ul><ul><ul><li>Esmolol  Short acting, given IV </li></ul></ul><ul><li>B-Blocker terms </li></ul><ul><ul><li>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. </li></ul></ul><ul><ul><li>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. </li></ul></ul><ul><li>Selectivity is dose dependent: there is no selectivity at high doses even with selective BBs. </li></ul><ul><li>Nonselective BB are contraindicated in patients with bronchial asthma, as these precipitate bronchospasm . </li></ul><ul><li>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 . </li></ul><ul><li>Sudden withdrawal of BBs  MI, angina & rebound HT. </li></ul><ul><li>Peyronie’s disease: is reported with metoprolol (p.253). </li></ul><ul><li>Organ Receptor Response </li></ul><ul><li>Heart  1 Stimulation  increased contraction & HR </li></ul><ul><li>Arterioles  1 Stimulation  vasoconstriction </li></ul><ul><li>  2 Stimulation  vasodilatation </li></ul><ul><li>GIT  1 Stimulation  decreased contraction </li></ul><ul><li>Bronchi  2 Stimulation  bronchodilatation </li></ul><ul><li>Uterus  2 Stimulation  Relaxation </li></ul><ul><li>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. </li></ul>
  6. 6. <ul><li>HT patients with concomitant diseases can be treated by: </li></ul><ul><ul><li>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). </li></ul></ul><ul><ul><li>Patients with hepatic failure: can be treated with a polar  -blocker (e.g. pindolol, nadolol or atenolol). These are excreted mainly via the kidney. </li></ul></ul><ul><ul><li>Patients with bronchial asthma: can be treated with a selective  -blocker (e.g. metoprolol or atenolol). Better agents might be ACEI / CCBs / AIIRAs. </li></ul></ul><ul><ul><li>Patients with CHF: can be treated with captopril & / or prazocin. </li></ul></ul><ul><ul><li>Patients with tachycardia: can be treated with a non-selective  -blocker (e.g. nadolol or propranolol). (BB without ISA ) </li></ul></ul><ul><ul><li>Patients with depression: hydralazine is the drug of choice (reserpine, guanithidine, methyl dopa & clonidine can cause depression). </li></ul></ul><ul><li>Hypertensive crisis is treated by sodium nitroprusside & diazoxide (given by IV infusion or injection) as they have a direct vasodilating effect on blood vessels. </li></ul><ul><li>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. </li></ul><ul><li>Metyrosine (Demiser): is an antihypertensive used in pheochromocytoma . </li></ul><ul><li>Papaverine: is used primarily for its ability to produce vasodilatation. It causes relaxation of arteriolar smooth muscles. </li></ul><ul><li>A sudden increase in blood pressure will cause reflex bradycardia. </li></ul><ul><li>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. </li></ul><ul><li>Orthostatic hypotension, either due to direct action on arterioles or via CNS, is caused by: </li></ul><ul><ul><li>Vasodilators – Guanithidine –  1 - blockers. – MAO-Is (antidepressants) </li></ul></ul><ul><li>Acetylcholine: has a direct effect on the heart  coronary vasodilatation. </li></ul><ul><li>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. </li></ul><ul><li>Hydergine is claimed to be a mood elevator is also available as sublingual tablets. </li></ul><ul><li>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. </li></ul><ul><li>Compared to nitroglycerine tablets , nitroglycerine ointment provides a prolonged effect. </li></ul>
  7. 7. <ul><li>Arrhythmia: is any deviation from the normal heart beat pattern. </li></ul><ul><li>Myocardial action potential: is the cardiac depolarization & repolarization necessary for myocardial contraction. </li></ul><ul><li>Depolarization & repolarization result from changes in electrical potential across cell membrane, caused by exchange of Na & K ions. This occurs in 5 phases: </li></ul><ul><ul><li>Phase 0  Rapid depolarization . Takes place as Na + enters the cell; cell membrane's electrical charge changes from negative to positive. </li></ul></ul><ul><ul><li>Phase 1  Early rapid repolarization . As fast Na channels close & K + leaves the cell, the cell rapidly repolarizes. </li></ul></ul><ul><ul><li>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. </li></ul></ul><ul><ul><li>Phase 3  Final rapid repolarization . K + is pumped out of the cell as the cell rapidly completes repolarization & resumes its initial negativity. </li></ul></ul><ul><ul><li>Phase 4  Slow depolarization . The cell returns to its resting state with K + inside the cell & Na & Ca ions outside. </li></ul></ul><ul><ul><li>During depolarization & repolarization, a cell's ability to initiate an action potential varies. </li></ul></ul><ul><ul><li>The cell cannot respond to any stimulus during the absolute refractory period (beginning during phase 1 & ending at the start of phase 3). </li></ul></ul><ul><ul><li>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. </li></ul></ul><ul><ul><li>When the cell has been completely repolarized, it can again respond fully to stimuli. </li></ul></ul><ul><li>The action potential of the heart (tone of the heart muscle) is 95 – 105 millivolt. (90–105) </li></ul><ul><li>Anti-arrhythmic Drugs: </li></ul><ul><li>These are classified in 8 groups: </li></ul><ul><li>Cinchona alkaloids: (Quinidine, an optical isomer of quinine). </li></ul><ul><li>Amides: Procainamide (Pronestyl) & desopyramide (Rhythmadon). </li></ul><ul><li>Xylyl derivatives: Lidocaine (Xylocaine). </li></ul><ul><li>4ry ammonium salts: Bretylium (Bretylol). </li></ul><ul><li>Amiodarone (Cordarone) </li></ul><ul><li>Beta blockers . </li></ul><ul><li>CCBs: Verapamil (Isopten) & diltiazem (Cardiazem). </li></ul><ul><li>Hydantoins: Phenytoin (Dilantin). </li></ul>
  8. 8. <ul><li>Anti-arrhythmic Drugs </li></ul><ul><li>Can be classified according to their ability to alter the action potential of cardiac cells. </li></ul><ul><li>Class I: This class includes: </li></ul><ul><ul><li>Quinidine – Lidocain – Procainamide (Pronestyl), </li></ul></ul><ul><ul><li>Phenytoin (Dilantin) – Disopyramide (Rythmadon) </li></ul></ul><ul><li> These are used for ventricular & supraventricular arrhythmias </li></ul><ul><li> They decrease the rate of rise of phase 0; i.e. slow the rate of conduction, excitation & spontaneous repolarization. </li></ul><ul><li> They decrease the slope of phase 1  prolong the effective refractory period. </li></ul><ul><li>Class II: It includes  -antagonists (  -blockers), e.g. propranolol. </li></ul><ul><li> They are used in atrial arrhythmias . </li></ul><ul><li> They depress phase 4 depolarization. </li></ul><ul><li> They competitively inhibit  receptor sites. </li></ul><ul><li>Class III: these include: – Bretylium – Amiodaron (Cordaron). </li></ul><ul><li> These are used in ventricular fibrillations . </li></ul><ul><li> They prolong the duration of the action potential. </li></ul><ul><li> They  the absolute refractory period (prolongation of repolarization). </li></ul><ul><li>Class IV: these include CCBs e.g. verapamil (Isopten), nifedipine, diltiazem (cardiazem). </li></ul><ul><li> These are used in atrial fibrillation & flutter supraventricular tachycardia . </li></ul><ul><li> They decrease the amount of Ca ions available for displacement from the cell membrane, i.e. decrease the inward current carried by Ca. </li></ul><ul><li> They prolong the absolute refractory period. </li></ul><ul><li> They depress phase 4 spontaneous depolarization. </li></ul><ul><li> Verapamil (5-10 mg over 1-2 min) used to treat paroxysmal ventricular tachycardia. </li></ul><ul><li>Tachycardia: means faster heart beats (usually > 100 beat / min); this may be due to: </li></ul><ul><li>  body temp. (~ HR  by 10 beats / min for every 1 o F rise in temp.) </li></ul><ul><li> Toxic condition. </li></ul><ul><li> Autonomic sympathetic stimulation. </li></ul><ul><li>Bradycardia: means slower heart beats (usually < 60 beat / min); Any circulatory reflex that stimulates the vagus nerve (parasympathetic) causes a considerable  in HR. </li></ul>
  9. 9. <ul><li>Quinidine: </li></ul><ul><ul><li>It is used for supraventricular arrhythmias. </li></ul></ul><ul><ul><li>It is the drug of choice in atrial premature contractions. </li></ul></ul><ul><ul><li>It is used in ventricular premature contractions (VPC). </li></ul></ul><ul><ul><li>It is given orally or IV. </li></ul></ul><ul><ul><li>Quinidine should not be used without prior degitalization, because it may increase the frequency of impulse transmission. </li></ul></ul><ul><li>Procainamide (Pronestyl): </li></ul><ul><ul><li>It is used in VPC & ventricular tachycardia. </li></ul></ul><ul><ul><li>It is contraindicated in CHF as it causes Lupus like reactions (SLE). </li></ul></ul><ul><li>Disopyramide (Rhythmadon): </li></ul><ul><ul><li>Used in the treatment of VPC & repetitions. </li></ul></ul><ul><ul><li>Used in ventricular arrhythmias. </li></ul></ul><ul><li>Lidocaine (Xylocaine): </li></ul><ul><ul><li>It is used in the treatment of ventricular arrhythmias (  HR). </li></ul></ul><ul><ul><li>It is the drug of choice in arrhythmias associated with emergencies (MI, open heart surgery, digitalis intoxication…) </li></ul></ul><ul><ul><li>The anti-arrhythmic effect of lidocaine is: </li></ul></ul><ul><ul><li> No effect on SA node (unlike quinidine). </li></ul></ul><ul><ul><li> Suppress automacity in Purkinje fibers & atrium. </li></ul></ul><ul><ul><li> Depression of phase 0 depolarization (  Na influx) (it is depressant but not like procainamide/quinidine). </li></ul></ul><ul><ul><li> It  the effective refractory period on Purkinje fibers & inhibit the duration of action potential . </li></ul></ul><ul><ul><li> Show very little changes of ECG. </li></ul></ul><ul><li>Phenytoin (Dilantin): </li></ul><ul><ul><li>It alters Na + conc. by promoting Na + influx. </li></ul></ul><ul><ul><li>It is used in the both ventricular & supraventricular arrhythmias. </li></ul></ul><ul><ul><li>It is also used in digitalis induced arrhythmias. </li></ul></ul><ul><li>Propranolol (Inderal): is most valuable in atrial arrhythmias (tachycardia). </li></ul><ul><li>N.B: Proximal sinus arrhythmia: may result from an increase in temp. </li></ul><ul><li>N.B: Catecholamines may cause arrhythmias. </li></ul>
  10. 10. <ul><li>Congestive Heart Failure </li></ul><ul><li>In right-side CHF: blood accumulates in liver, kidney, vena cavae, lower extremities  edema </li></ul><ul><li>In left-side CHF: blood accumulates in lungs  pulmonary edema </li></ul><ul><li>Digitalis glycosides: are used to treat CHF. </li></ul><ul><li>Digoxin is the primary active constituent of digitalis. </li></ul><ul><li>The Pharmacological action of digoxin is: </li></ul><ul><ul><li>It  myocardial contractility through direct stimulation of the ventricular muscle & through enhancing Ca availability to the contractile proteins (+ve inotropic). </li></ul></ul><ul><ul><li>Reduce conductivity (  conduction velocity in the atrial muscle). This effect predominates over its vagotonic effect (  conduction) (-ve chronotropic) </li></ul></ul><ul><ul><li>Slow the cardiac pace maker (SA node) (-ve chronotropic) </li></ul></ul><ul><ul><li>Prolong the refractory period (-ve chronotropic) </li></ul></ul><ul><ul><li>Does not increase oxygen consumption. </li></ul></ul><ul><li>Digitalis toxicity results in: </li></ul><ul><ul><li>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: </li></ul></ul><ul><ul><ul><li>Premature ventricular fibrillation (treated with xylocain or phenytoin). </li></ul></ul></ul><ul><ul><ul><li>Premature atrial fibrillation </li></ul></ul></ul><ul><ul><ul><li>AV block </li></ul></ul></ul><ul><ul><ul><li>Paroxysmal atrial tachycardia </li></ul></ul></ul><ul><ul><ul><li>Ventricular tachycardia </li></ul></ul></ul><ul><ul><li>Extra-cardiac effect: </li></ul></ul><ul><ul><ul><li>Vomiting, diarrhea, anorexia </li></ul></ul></ul><ul><ul><ul><li>Weakness, fatigue, headache, dizziness </li></ul></ul></ul><ul><ul><ul><li>Photophobia & hazy vision </li></ul></ul></ul><ul><ul><ul><li>Massive over doses cause delusions & coma. </li></ul></ul></ul><ul><ul><li>Does not cause constipation, anemia nor vagal arrest. </li></ul></ul><ul><li>The official bioassay of digitalis leaf utilizes pigeon. </li></ul>
  11. 11. <ul><li>Hypercholesterolemia </li></ul><ul><li>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. </li></ul><ul><ul><li>Cholestyramine & Colestipol: increase the efficiency of lipoprotein removal. </li></ul></ul><ul><ul><li>It is the drug of choice in pregnancy (it is not absorbed  has no systemic effect). </li></ul></ul><ul><li>Because cholestyramine is an anionic surfactant, it will interfere with the GI absorption of penicillin, tetracyclines, phenobarbital, phenyl butazone, warfarin & chlorthiazide. </li></ul><ul><li>Fibrates: Clofibrate (Atromid S), Bezafibrate (Bezalip), Gemfebrozil (Lopid) </li></ul><ul><ul><li>Interfere with cholesterol synthesis. </li></ul></ul><ul><ul><li>They  lipoprotein lipase activity  enhance breakdown of TG   VLDL & LDL. </li></ul></ul><ul><ul><li>They lower the cholesterol & TG levels. </li></ul></ul><ul><ul><li>Can not be given for long time. </li></ul></ul><ul><li>Niacin:  lipolysis in adipose tissue   free fatty a formation   TG   VLDL & LDL </li></ul><ul><li>Statins: inhibit the HMG-CoA reductase enzyme   cholesterol synthesis. </li></ul><ul><li>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. </li></ul>
  12. 12. <ul><ul><li>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. </li></ul></ul><ul><ul><li>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. </li></ul></ul><ul><ul><li>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. </li></ul></ul><ul><ul><li> Warfarin is used as an antidote for vitamin K. </li></ul></ul>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
  13. 13. <ul><ul><li>Anticoagulants </li></ul></ul><ul><ul><li> Heparin Caumarine (Warfarin) </li></ul></ul><ul><ul><li>Onset of action Immediate Gradual </li></ul></ul><ul><ul><li>Duration 4 hrs 2-5 days </li></ul></ul><ul><ul><li>Used in Emergency & prophylaxis Prophylaxis </li></ul></ul><ul><ul><li>Route of administration IV or SC Oral </li></ul></ul><ul><ul><li>Lab control of dose APTT Prothrombin time </li></ul></ul><ul><ul><li>Treatment of overdose Protamine SO 4 Fresh blood &/or Vitamin K </li></ul></ul><ul><ul><li>Use in pregnancy Can be given Contraindicated </li></ul></ul><ul><ul><li>Drug interactions Few Many </li></ul></ul><ul><ul><li>Effect of antacids No effect  its effect </li></ul></ul><ul><ul><li>Pharmacologic action Anticoag. in vivo & in vitro Anticoagulant in vivo </li></ul></ul><ul><ul><li>Cost Expensive Cheap </li></ul></ul><ul><ul><li>The anticoagulant effect of heparin: is quantitated by the “Active Partial Thromboplastin Time” (APTT) & the “Activated Coagulation Time” (ACT) which is 3-5 min. </li></ul></ul><ul><ul><li>  Normally, APTT is from 30-45 sec; on using an anticoagulant it should be 45 – 60 sec. </li></ul></ul><ul><ul><li>The anticoagulant effect of warfarin: is quantitated by the “Prothrombin Time” (PT). </li></ul></ul><ul><ul><li>  Normally, PT is 12 sec; on adequate anticoagulant control it should be 24 – 30 sec. </li></ul></ul><ul><ul><li>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). </li></ul></ul><ul><ul><li>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. </li></ul></ul><ul><ul><li>Drugs that induce the liver microsomal enzyme system (barbiturates, phenytoin) may accelerate the metabolism of warfarin   serum levels  subtherapeutic levels. </li></ul></ul><ul><ul><li>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). </li></ul></ul><ul><ul><li>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). </li></ul></ul>
  14. 14. <ul><ul><li>Angina Types Angina Pectoris (strangling of the chest) </li></ul></ul><ul><ul><ul><li>Beta Blockers </li></ul></ul></ul><ul><ul><ul><li>Methyl dopa. (Use) </li></ul></ul></ul><ul><ul><ul><li>Antihyperlipidemic </li></ul></ul></ul><ul><ul><ul><li>Hydralazine (vasodilator) </li></ul></ul></ul><ul><ul><li>Beta Blockers </li></ul></ul><ul><ul><ul><li>Non Selective (B 1 + B 2 ) Propranolol Pindolol Nadolol </li></ul></ul></ul><ul><ul><li>Sotalol Timolol </li></ul></ul><ul><ul><ul><li>Cardio Selective (B 1 ) Acebutolol Atenolol Metoprolol </li></ul></ul></ul><ul><ul><ul><li>Non Selective (B +  ) Labetalol </li></ul></ul></ul><ul><ul><li>Methyl Dopa (Aldomet): Interfere with synthesis of dopamine   Me-dopamine ?????   Sympathetic outflow   peripheral vascular resistance + slight reduction in CO & BP. </li></ul></ul><ul><ul><li>Diuretics </li></ul></ul><ul><ul><ul><li>Proximal Tubule: Osmotic Diuretics: e.g. Mannitol. </li></ul></ul></ul><ul><ul><ul><li>Loop of Henele: Reduction of Na + re-absorption  leads to K + loss at site 4; e.g. Frusemide. </li></ul></ul></ul><ul><ul><ul><li>Cortical diluting segment: Reduction of Na + re-absorption  leads to K + loss at site 4; e.g. Thiazides. </li></ul></ul></ul><ul><ul><ul><li>Distal tubule: inhibition of Na + exchange for K + / H + ; e.g. K + sparing diuretics (aldosterone, spironolactone, triametrene, Amiloride). </li></ul></ul></ul>
  15. 15. <ul><li>Heparin is: </li></ul><ul><ul><li>Like coumarine c. Acts on certain steps of coagulation system </li></ul></ul><ul><ul><li>Oral d. Of benefit in arterial blood clot as prophylaxis </li></ul></ul><ul><li>In left ventricular failure the blood pools in: </li></ul><ul><ul><li>Lungs c. Vena cavae </li></ul></ul><ul><ul><li>Liver </li></ul></ul><ul><li>Patients with moderate HT & a history of heart disease (CHF) are treated with: </li></ul><ul><ul><li>Propranolol c. Hydrochlorothiazide </li></ul></ul><ul><ul><li>Methyl dopa d. Reserpine </li></ul></ul><ul><li>An important advantage of using dopamine (inotropic sympathomemetic) in cardiac shock is: </li></ul><ul><ul><li>It will not cross the BBB & will not cause CNS side effects. </li></ul></ul><ul><ul><li>It produces a dose dependant increase in CO & renal perfusion </li></ul></ul><ul><ul><li>It will not increase the blood pressure </li></ul></ul><ul><ul><li>It has no effect on  &  receptors. </li></ul></ul><ul><ul><li>It can be given orally </li></ul></ul><ul><li>For a sympathomimetic drug to be effective it should be: </li></ul><ul><ul><li>Able to fit in receptors </li></ul></ul><ul><ul><li>Bound to plasma proteins </li></ul></ul><ul><ul><li>Compete at the site of release of the transmitter </li></ul></ul><ul><li>A HT patient suffering from depression should not be given all of the following EXCEPT: </li></ul><ul><ul><li>Reserpine (depletes NE stores) </li></ul></ul><ul><ul><li>Clonidine (  2 agonist  negative feedback  E & NE) </li></ul></ul><ul><ul><li>Methyl dopa (False methylation  methyl NE   2 agonist) </li></ul></ul><ul><ul><li>Guanithidine </li></ul></ul><ul><ul><li>Hydralazine (direct vasodilatation) </li></ul></ul><ul><li>Vasodilators cause: </li></ul><ul><ul><li>Reflex bradycardia b. Reflex tachycardia </li></ul></ul><ul><li>In an ischemic myocardium, which is released & causes coronary vasodilatation: </li></ul><ul><ul><li>Adrenaline c. Serotonin </li></ul></ul><ul><ul><li>Acetylcholine d. Adenosine </li></ul></ul><ul><li>Which hormone increases water reabsorption from distal tubules: </li></ul><ul><ul><li>Aldosterone (also vasopressin – ADH) c. Acetylcholine </li></ul></ul><ul><ul><li>Adrenaline d. Adenosine </li></ul></ul><ul><ul><li>N.B. Vasopressin acts on distal tubules to  water re-absorption </li></ul></ul>
  16. 16. <ul><li>At rest (or during sleep), which organ receives the richest blood supply: </li></ul><ul><ul><li>Lungs c. Heart </li></ul></ul><ul><ul><li>Liver (27%) d. Kidneys (22%) </li></ul></ul><ul><li>Which drug, although increasing the heart rate, causes vasodilatation (  BP): </li></ul><ul><ul><li>Adrenaline d. Propranolol </li></ul></ul><ul><ul><li>Carbacol e. Phenylephrine </li></ul></ul><ul><ul><li>Ephedrine f. Isoproterenol (more  stimulant than  ) </li></ul></ul><ul><li>The highest blood pressure is in the: </li></ul><ul><ul><li>Veins c. Arteries (pulmonary artery) </li></ul></ul><ul><ul><li>Venules d. Arterioles </li></ul></ul><ul><li>Diuretics are most likely to produce: </li></ul><ul><ul><li>Hyperkalemia. c. Hypokalemia. e. Hyperuricemia </li></ul></ul><ul><ul><li>Hypercalcemia. d. Hypocalcemia f. Urinary alkalosis </li></ul></ul><ul><li>Digitalis toxicity does not cause: </li></ul><ul><ul><li>Nausea, vomiting, fatigue d. Vision change g. Anorexia </li></ul></ul><ul><ul><li>Dysrhythmia e. AV block </li></ul></ul><ul><ul><li>Ventricular tachycardia f. Constipation (it causes diarrhea) </li></ul></ul><ul><li>Which of the following clotting factors is normally found in circulating blood: </li></ul><ul><ul><li>Thrombin c. Prothrombin </li></ul></ul><ul><ul><li>Thromboplastin </li></ul></ul><ul><li>Which of the following drugs  the sympathetic stimulation of the adrenal medulla: </li></ul><ul><ul><li>Nicotine (in small doses) b. Acetylcholine (in large doses) </li></ul></ul><ul><li>Blood going to the branches of the coronary artery has just passed the: </li></ul><ul><ul><li>Aortic valve c. Inferior vena cava </li></ul></ul><ul><ul><li>Right atrium d. Superior vena cava </li></ul></ul><ul><li>In HT of renal origin, which antihypertensive is used: </li></ul><ul><ul><li>Clonidine b. Hydralazine c. Captopril </li></ul></ul><ul><li>Which of the following vasodilators cause venous pooling: </li></ul><ul><ul><li>Sodium nitroprusside c. Hydralazine </li></ul></ul><ul><ul><li>Nitroglycerine d. Isosorbid dinitrate </li></ul></ul><ul><ul><li>Methyldopa </li></ul></ul><ul><li>Which of the following is an  -agonist: </li></ul><ul><ul><li>Clonidine b.  -methyl dopa </li></ul></ul>
  17. 17. <ul><li>In an acute anginal attack, which drug can be given: </li></ul><ul><ul><li>Propranolol c. Nitroglycerine (Short acting) </li></ul></ul><ul><ul><li>Isosorbid dinitrate </li></ul></ul><ul><li>Which drug is used in prophylaxis of angina: </li></ul><ul><ul><li>Nifedipine </li></ul></ul><ul><ul><li>Diltiazem </li></ul></ul><ul><li>A person with fever has: </li></ul><ul><ul><li>Paroxysmal tachycardia c. Sinus tachycardia </li></ul></ul><ul><ul><li>Bradycardia d. SA arrhythmia </li></ul></ul><ul><li>Following moderate exercise, BP is usually higher than normal because: </li></ul><ul><ul><li>Release of acetylcholine. </li></ul></ul><ul><ul><li>Activation of the RAA system </li></ul></ul><ul><ul><li>Increased venous return. </li></ul></ul><ul><li>Repeated arrhythmia means: </li></ul><ul><ul><li>Paroxysmal arrhythmia c. Tachy arrhythmia </li></ul></ul><ul><ul><li>Ventricular arrhythmia </li></ul></ul><ul><li>Which of the following drugs causes rebound HT: </li></ul><ul><ul><li>Clonidine c. Hydralazine </li></ul></ul><ul><ul><li>Guanithedine </li></ul></ul><ul><li>Prolonged use of diuretics causes all of the following except: </li></ul><ul><ul><li>Hypoglycemia d. Hyperuricemia </li></ul></ul><ul><ul><li>Hypokalemia e. Alkalosis of urine </li></ul></ul><ul><ul><li>Sexual dysfunction </li></ul></ul><ul><li>During the absolute refractory period, if you apply another stimulus, the muscle will: </li></ul><ul><ul><li>Contract c. Relax </li></ul></ul><ul><ul><li>Remain in its existing state (no response to stimuli) </li></ul></ul><ul><li>Aldosterone is secreted from the: </li></ul><ul><ul><li>Adrenal medulla c. Kidney </li></ul></ul><ul><ul><li>Adrenal cortex </li></ul></ul><ul><li>During rest (or inspiration), BP is lowest in: </li></ul><ul><ul><li>Venules c. Arterioles </li></ul></ul><ul><ul><li>Vena cavae d. Capillaries </li></ul></ul><ul><li>Which of the following is an  -blocker: </li></ul><ul><ul><li>Prazocin b. Doxazocin c. Terazocin </li></ul></ul>
  18. 18. <ul><li>What is true about the hypophyseal portal system: </li></ul><ul><ul><li>It begins & ends in capillaries c. None </li></ul></ul><ul><ul><li>It begins with capillaries & ends with veins </li></ul></ul><ul><li>Which drug is used in mild to moderate HT: </li></ul><ul><ul><li>Captopril c. Propranolol </li></ul></ul><ul><ul><li>Lasix </li></ul></ul><ul><li>Which drug is used in mild HT: </li></ul><ul><ul><li>HCTZ c. Prazocin </li></ul></ul><ul><ul><li>Clonidine </li></ul></ul><ul><li>Arterial dilators include: </li></ul><ul><ul><li>Diazoxide. c. Hydralazine. </li></ul></ul><ul><ul><li>Minoxidil d. Sodium nitroprusside (arteriolar & venous) </li></ul></ul><ul><li>Which antihypertensive is used in diabetic patients: </li></ul><ul><ul><li>Captopril (ACEIs) c. Prazocin (  -blocker) e. CCBs </li></ul></ul><ul><ul><li>HCTZ d. Atenolol </li></ul></ul><ul><li>In angina pectoris, propranolol is used as: </li></ul><ul><ul><li>Treatment c. Acute attacks </li></ul></ul><ul><ul><li>Prophylactic (  O 2 consumption) </li></ul></ul><ul><li>The outer layer of the adrenal cortex secretes: </li></ul><ul><ul><li>Aldosterone c. Norepinephrine </li></ul></ul><ul><ul><li>Cortisone </li></ul></ul><ul><li>The middle layer of the adrenal cortex secretes: </li></ul><ul><ul><li>Aldosterone c. Norepinephrine </li></ul></ul><ul><ul><li>Cortisone </li></ul></ul><ul><li>The adrenal medulla secretes: </li></ul><ul><ul><li>Aldosterone c. Norepinephrine & epinephrine </li></ul></ul><ul><ul><li>Cortisone </li></ul></ul><ul><li>In complete heart block (AV block): </li></ul><ul><ul><li>No arterial impulses reach the ventricles c. Ventricles beat slower </li></ul></ul><ul><ul><li>Atria & ventricles contract independently. d. Ventricles beat irregularly </li></ul></ul><ul><li>What is the mechanism by which chenodioxycholic acid dissolves gall stones: ??? </li></ul><ul><ul><li>Reduces cholesterol synthesis c. Increases bile acid production </li></ul></ul><ul><ul><li>Increases phospholipids </li></ul></ul>
  19. 19. <ul><li>Arrhythmias may be caused by: </li></ul><ul><ul><li>Catecholamines </li></ul></ul><ul><li>The anti-coaggulant effect of warfarin increases in: </li></ul><ul><ul><li>Vitamin K deficiency. </li></ul></ul><ul><li>What is the side effect of minoxidil: </li></ul><ul><ul><li>Hirsutism c. Weight gain </li></ul></ul><ul><ul><li>Fluid retention d. Tachycardia </li></ul></ul><ul><li>Heparin is used for: </li></ul><ul><ul><li>Prophylaxis & treatment of venous thrombosis </li></ul></ul><ul><ul><li>Prophylaxis & treatment of pulmonary (or peripheral arterial) embolism. </li></ul></ul><ul><ul><li>Prevent clotting during surgery (arterial or cardiac) </li></ul></ul><ul><ul><li>Fibrillation with embolization </li></ul></ul><ul><li>Which is true about heparin: </li></ul><ul><ul><li>Works in vivo & in vitro d. Inactive orally </li></ul></ul><ul><ul><li>Has anti-thrombin / anti-thromboplastin effects </li></ul></ul><ul><ul><li>Prevents arterial thrombosis e. Safe in pregnancy </li></ul></ul><ul><li>Which is true about warfarin: </li></ul><ul><ul><li>Decrease platelet aggregation d. Works in vivo & in vitro </li></ul></ul><ul><ul><li>Activity  in vit K deficiency e. Decreases hepatic fibrinogen synthesis </li></ul></ul><ul><ul><li>Produces prompt action if given IV </li></ul></ul><ul><li>Which diuretics cause urinary alkalosis: </li></ul><ul><ul><li>Thiazides c. Carbonic anhydrase inhibitors </li></ul></ul><ul><ul><li>Loop diuretics d. K + sparing diuretics </li></ul></ul><ul><li>Which diuretic acts on proximal tubules: </li></ul><ul><ul><li>Acetazolamide b. HCTZ </li></ul></ul><ul><li>Which diuretics  water excretion at distal tubules: </li></ul><ul><ul><li>Triametrene c. Amiloride e. Frusimide </li></ul></ul><ul><ul><li>Spironolactone d. Thiazide f. Acetazolamide </li></ul></ul><ul><li>The use of  -blockers in HT is limited to: </li></ul><ul><ul><li>Patients who can not take diuretics or beta-blockers. </li></ul></ul><ul><li>Which drug is contra-indicated in CHF & HT: </li></ul><ul><ul><li>NSAIDs </li></ul></ul><ul><li>The major side effects of nitrates is: </li></ul><ul><ul><li>Headache (lasts for > 12 hrs) </li></ul></ul>
  20. 20. <ul><li>Nifedipine is: </li></ul><ul><ul><li>1,4 dihydropyridine b. pyrimidine </li></ul></ul><ul><li>Respiratory acidosis means: </li></ul><ul><ul><li>Increase in PCO 2 in the brain </li></ul></ul><ul><li>Hyperchloremic acidosis is caused by: </li></ul><ul><ul><li>Acetazolamide (carbonic anhydrase inhib.) b. Aceterol (diamox) ??? </li></ul></ul><ul><li>SMZ, TMP & Miconazole,  warfarin efficacy through: </li></ul><ul><ul><li>Decreasing hapatic metabolism </li></ul></ul><ul><ul><li>Inhibiting bacterial flora   vit. K synthesis  potentiates warfarin </li></ul></ul><ul><ul><li>Displacing warfarin from plasma protein binding sites. </li></ul></ul><ul><li>Nifedipine is used in: </li></ul><ul><ul><li>Angina b. CHF </li></ul></ul><ul><li>Acute pre-renal failure results in: </li></ul><ul><ul><li>Azotemia b. Uremia </li></ul></ul><ul><li>Which diuretic decreases Ca excretion & leads to hypercalcemia: </li></ul><ul><ul><li>Loop diuretics b. Thiazide diuretics </li></ul></ul><ul><li>Metabolic acidosis is caused by: </li></ul><ul><ul><li>Acetazolamide c. Methyl alcohol e. Starvation </li></ul></ul><ul><ul><li>Renal falure d. Ethylene glycol </li></ul></ul><ul><li>Which agent  water excretion at (  permiability of) collecting tubules: </li></ul><ul><ul><li>Triametrene b. Amiloride c. Ethacrinic acid </li></ul></ul><ul><li>Parathyroid hormone promotes Ca excretion by action on: </li></ul><ul><ul><li>Proximal tubules. c. Distal tubules </li></ul></ul><ul><ul><li>Glomerulus d. Renal tubules </li></ul></ul><ul><li>What is true about ACE: </li></ul><ul><ul><li>Natural substrate is A I b. Normal alternative for A I </li></ul></ul><ul><li>Nephrotic syndrome is characterized by: </li></ul><ul><ul><li>Proteinuria b. Hypoalbuminuria </li></ul></ul><ul><li>Which CCB causes MI: </li></ul><ul><ul><li>Diltiazem b. Verapamil c. Nifedipine </li></ul></ul><ul><li>The tension in blood vessels depends on: </li></ul><ul><ul><li>Radius of blood vessel b. Pressure created on blood vessel </li></ul></ul><ul><ul><li>Length of blood vessel </li></ul></ul><ul><li>What is common in thiazides & sulphonamides: </li></ul><ul><ul><li>The sulpha group </li></ul></ul>
  21. 21. <ul><li>A drug which inhibits aldosterone secretion (e.g. ACEIs) will: </li></ul><ul><ul><li>Cause hyperkalemia b.  effect of spironolactone </li></ul></ul><ul><li>Compared to sublingual nitroglycerine, transdermal patches have: </li></ul><ul><ul><li>Prolonged effect b. Rapid effect </li></ul></ul><ul><li>Which is used as a voltage dependant Na + channel blocker: </li></ul><ul><ul><li>Tetraiodoxine  Na + channel blocker but toxic  not used </li></ul></ul><ul><ul><li>Benzodiazepine  Cl - channel opener   GABA </li></ul></ul><ul><ul><li>Digitalis  Ca ++ channel opener </li></ul></ul><ul><ul><li>Verapamil  Ca ++ channel blocker </li></ul></ul><ul><ul><li>Phenytoin (& lidocaine)  Na + channel blockers </li></ul></ul><ul><li>Which is a Na + channel blocker: </li></ul><ul><ul><li>Phenytoin b. Lidocaine c. Triametrene </li></ul></ul><ul><li>Which drugs act through lipoprotein activation: </li></ul><ul><ul><li>Clofibrate c. Gemfebrozil e. Nicotinic acid </li></ul></ul><ul><ul><li>Atrovastatin d. Cholistyramine </li></ul></ul><ul><li>Edema occurs in cases of: </li></ul><ul><ul><li>Hypervolemia c. Na + loss e. Liver chirrosis </li></ul></ul><ul><ul><li>Right side CHF d. Hypovolemia f. Hyperthyroidism </li></ul></ul><ul><li>Edema occurs in all except: </li></ul><ul><ul><li>Ascitis c. Glomerular damage </li></ul></ul><ul><ul><li>Hyperthyroidism d. Excess corticosteroid usage </li></ul></ul><ul><li>Which is not a symptom associated with MI: </li></ul><ul><ul><li>Arrhythmia c. AV block e. Headache </li></ul></ul><ul><ul><li>Heart burn d. diarrhea </li></ul></ul><ul><li>Acetazolamide & sulphonamides are both: (carbonic anhydrase inhibitors are aromatic or heterocyclic sulphonamides with prominent thiadiazole gp) </li></ul><ul><ul><li>Sulphonamides b. Anti-microbials </li></ul></ul><ul><li>What is azotemia: </li></ul><ul><ul><li>Synonymous to uremia b.  SrCr c.  NH 3 & urea in blood (  BUN) </li></ul></ul><ul><li>Digoxin is affected by: </li></ul><ul><ul><li>Erythromycin b. Cholistyramine c. Primaquine </li></ul></ul><ul><li>Hypovolemia causes all except: </li></ul><ul><ul><li>Pulmonary edema b. Oliguria </li></ul></ul><ul><li>Renal failureis associated with: </li></ul><ul><ul><li>Hyperphosphatemia </li></ul></ul>
  22. 22. <ul><li>Side effects of atenolol include: </li></ul><ul><ul><li>Hypotension b. Tremors c. Visual disturbances </li></ul></ul><ul><li>Fibrinolytic agents cannot be given post-op. if: </li></ul><ul><ul><li>Patient had gastric bleeding within the past 6 months </li></ul></ul><ul><ul><li>Patient > 65 yrs c. Patient is hypertensive </li></ul></ul><ul><li>Osmotic dialysis is effective with: </li></ul><ul><ul><li>Low mol. wt. substance c. Large volume of distribution </li></ul></ul><ul><ul><li>High plasma protein binding </li></ul></ul><ul><li>Bile acids (bile salts) are: </li></ul><ul><ul><li>Hydrophilic c. Steroid in nature (not absorbed) </li></ul></ul><ul><ul><li>Prepare O/W emulsions ??? </li></ul></ul><ul><li>Which drugs is most effective in decreasing LDL & VLDL: </li></ul><ul><ul><li>Clofibrate c. Nicotinic acid </li></ul></ul><ul><ul><li>Atrovastatin d. Cholistyramine </li></ul></ul><ul><li>Vasodilators may cause: </li></ul><ul><ul><li>Orthostatic hypotension b. Tachycardia </li></ul></ul><ul><li>The dose of warfarin could be adjusted by measuring: </li></ul><ul><ul><li>APTT c. Warfarin conc. in blood </li></ul></ul><ul><ul><li>PT (prothrombin time) d. Coagulation time </li></ul></ul><ul><li>Which is true about pulmonary thrombotic disease: </li></ul><ul><ul><li>Fatal b. Mainly due to varicose (starting in the legs) </li></ul></ul><ul><li>Injection of high dose of K+ may cause: </li></ul><ul><ul><li>Cardiac arrest </li></ul></ul><ul><li>Side effects of thiazides include: </li></ul><ul><ul><li>Hyperglycemia b. Hyperuricemia c. Alkalosis </li></ul></ul><ul><li>Streptokinase is used for: </li></ul><ul><ul><li>Deep venous thrombosis </li></ul></ul><ul><li>Which of the following anti-arrhythmics can be used orally: </li></ul><ul><ul><li>Mexiliten ??? </li></ul></ul><ul><li>Digitalis consists of digitalide plus: </li></ul><ul><ul><li>Sugar b. Amino acid c. Alkaloid </li></ul></ul><ul><li>Which diuretic decreases Na, K, & Cl & causes mild urinary alkalosis: </li></ul><ul><ul><li>Thiazides b. Loop diuretics c. Amiloride </li></ul></ul><ul><li>Which diuretic increases Ca excretion: </li></ul><ul><ul><li>Thiazides b. Laxis c. Amiloride </li></ul></ul>
  23. 23. <ul><li>Triametrene: </li></ul><ul><ul><li>Acts on distal & collecting tubules </li></ul></ul><ul><ul><li>Distrupts the exchange with K+ & H+ b blocking sodium channels & decreasing the driving force for the excretion of H+ & K+ </li></ul></ul><ul><li>Which agent increases the water permiability of renal tubules (Increases reabsorption): </li></ul><ul><ul><li>ADH c. Amiloride </li></ul></ul><ul><ul><li>Lasix </li></ul></ul><ul><li>Which is used in arterial thrombosis: </li></ul><ul><ul><li>Asprin b. Clofibrate </li></ul></ul><ul><li>Probucol: ???? </li></ul><ul><ul><li>Is used to decrease serum cholesterol </li></ul></ul><ul><ul><li>Does not affect the later stages of cholesterol synthesis (HDL & LDL) </li></ul></ul><ul><li>Any drug given in CHF may be nephrotoxic because: </li></ul><ul><ul><li>Blood flow to the kidney is not sufficient </li></ul></ul><ul><li>Infarction results because of: </li></ul><ul><ul><li>Blood cannot reach the right & left carotids ??? </li></ul></ul><ul><li>Ouabin in the treatment of CHF (similar to digitalis) is: </li></ul><ul><ul><li>Of rapid onset c. Not absorbed from GIT </li></ul></ul><ul><ul><li>Of short duration d. Given IM (it is given IV only) </li></ul></ul><ul><li>Digitalis alkaloid is: </li></ul><ul><ul><li>Highly water soluble b. Water insoluble </li></ul></ul><ul><li>In acute renal failure, CrCl over estimates glomerular filtration because: </li></ul><ul><ul><li>Cr is less synthesized d. Cr is highly metabolized in liver </li></ul></ul><ul><ul><li>Cr is bound to plasma proteins e. Cr is secreted by renal tubules </li></ul></ul><ul><ul><li>Cr is reabsorbed </li></ul></ul><ul><li>The best time to give an anti-hyperlipidemic drug like Atrovastatin is at: </li></ul><ul><ul><li>night c. morning </li></ul></ul><ul><ul><li>Afternoon ( at night synthesis of lipids increase) </li></ul></ul><ul><li>Which of the following anti-arrhythmics can be used orally: </li></ul><ul><ul><li>Mexiliten ??? </li></ul></ul><ul><li>Digitalis consists of digitalide plus: </li></ul><ul><ul><li>Sugar b. Amino acid c. Alkaloid </li></ul></ul><ul><li>Which diuretic decreases Na, K, & Cl & causes mild urinary alkalosis: </li></ul><ul><ul><li>Thiazides b. Loop diuretics c. Amiloride </li></ul></ul><ul><li>Which diuretic increases Ca excretion: </li></ul><ul><ul><li>Thiazides b. Laxis c. Amiloride </li></ul></ul>
  24. 24. Diabetes
  25. 25. <ul><li>Diabetes </li></ul><ul><li>There are 3 significant parameters in a glucose tolerance curve (blood-glucose vs. time curve) </li></ul><ul><ul><li>The peak conc. of the glucose in blood. </li></ul></ul><ul><ul><li>The time required to achieve peak serum level. </li></ul></ul><ul><ul><li>The rate at which blood glucose level declines with time. </li></ul></ul><ul><li>In diabetes mellitus the blood glucose peak is higher, occurs later, & declines more slowly than a corresponding glucose tolerance curve of a normal individual. </li></ul><ul><li>In the glucose tolerance curve: </li></ul><ul><ul><li>The normal fasting glucose level is 90-120 mg /100 ml of blood. </li></ul></ul><ul><ul><li>Diabetic patients have fasting blood sugar curve higher than 120 mg / 100 ml of blood. </li></ul></ul><ul><li>Ketone bodies (acetone  -hydroxy butyric acid) are caused by starvation & diabetes (hyperglycemia) & are characterized by the acetone odor of mouth. </li></ul><ul><li>Test for ketones in urine: (specific for ketone bodies & acetone) </li></ul><ul><ul><li>Acetest – Ketostix </li></ul></ul><ul><li>Tests for glucose in urine: (specific for glucose) </li></ul><ul><ul><li>Testape, Clinistix & Diastix: contain glucose oxidase </li></ul></ul><ul><ul><li>Benedict solution, Fehling’s solution & Clinitest: based on copper reduction method </li></ul></ul><ul><li>Ascorbic acid, L-dopa, salicylates, phenazopyridine, penicillins & cephalosporins may give false +ve test with Benedict & Clinitest. </li></ul><ul><li>Fehling’s solution gives red color with glucose & acetaldehyde. </li></ul><ul><li>After an insulin injection: hypoglycemia may occur because of a low carbohydrate diet. </li></ul><ul><li>Alcoholic beverages: are contra-indicated in patients taking oral hypoglycemics. </li></ul><ul><li>Juvenile diabetes patients should receive insulin therapy & eat according to a caloric diet. </li></ul><ul><li>Insulin: is the hormone that acts on the cell membrane. </li></ul><ul><li>Insulin shock: in an unconscious patient is treated with glucagon injection. </li></ul><ul><li>Adrenaline causes hyperglycemia </li></ul><ul><li>Calories: </li></ul><ul><ul><li>Each gram of protein supplies about 4 Kcal. </li></ul></ul><ul><ul><li>Each gram of carbohydrates supplies about 4 Kcal. </li></ul></ul><ul><ul><li>Each gram of dextrose supplies about 4 Kcal. </li></ul></ul><ul><ul><li>Each gram of fats supplies about 9 Kcal. </li></ul></ul><ul><ul><li>Each gram of ethanol supplies about 7 Kcal. </li></ul></ul><ul><ul><li>1 Kcal = 1,000 calories </li></ul></ul>
  26. 26. <ul><li>Oral Hypoglycemic Drugs </li></ul><ul><li>Oral Hypoglycemic Drugs: They are classified in 2 groups: </li></ul><ul><ul><li>Sulfonylurea derivatives. </li></ul></ul><ul><ul><li>Biguanides. </li></ul></ul><ul><li>Sulfonylurea derivatives: are used to treat type II diabetes. </li></ul><ul><ul><li>Mechanism of action: </li></ul></ul><ul><ul><li> These stimulate the  -cells of the pancreas to secrete insulin. </li></ul></ul><ul><ul><li> They also decrease glycogenolysis. </li></ul></ul><ul><ul><li> May cause hypoglycemia. </li></ul></ul><ul><ul><li>Acetohexamide (Demilor): is reported to have a uricosuric effect </li></ul></ul><ul><ul><li> It is metabolized to a compound having equal or greater hypoglycemic activity. </li></ul></ul><ul><ul><li>Chlopropamide: has an antidiuretic effect which may be useful in diabetes insipidus. </li></ul></ul><ul><ul><li> 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). </li></ul></ul><ul><ul><li>Tolbutamide (Rastinon): is totally metabolized to the inactive form. </li></ul></ul><ul><ul><li>Tolazamide (Tolinase): is more slowly absorbed from the GIT than other compounds. </li></ul></ul><ul><ul><li>Glipizide (Amaryl): Excreted via the liver. </li></ul></ul><ul><li>Biguanide derivatives: </li></ul><ul><ul><li>Mechanism: potentiate action of insulin on glucose (activate pancreatic insulin). </li></ul></ul><ul><ul><li>Metformin (Glucophage): Excreted via the kidney </li></ul></ul><ul><ul><li> Indicated in obese diabetics, where hyperglycemia is due to ineffective insulin. </li></ul></ul><ul><ul><li> Side effects: weight loss, lactic acidosis, metallic taste, GIT upset. </li></ul></ul><ul><ul><li>Phenformin </li></ul></ul><ul><li>Diabetes insipidus: </li></ul><ul><ul><li>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 </li></ul></ul><ul><ul><li>Treated with lypressin (vasopressin analogue) </li></ul></ul><ul><ul><li>Increased urinary output in DM: is due to the osmotic pressure of glucose in urine </li></ul></ul><ul><li>Oral anti-diabetics: </li></ul><ul><li>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 </li></ul><ul><li>Biguanides: reduce production of glucose in liver. Used for obese patients; e.g. Metformin </li></ul><ul><li>Glucosidase Inhibitor: ↓ breakdown and absorption of carbohydrates; e.g. Acarbose </li></ul>
  27. 27. <ul><li>Oral anti-diabetics: </li></ul><ul><li>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 </li></ul><ul><li>Biguanides: reduce production of glucose in liver. Used for obese patients; e.g. Metformin </li></ul><ul><li> -Glucosidase Inhibitor: ↓ breakdown and absorption of carbohydrates; e.g. Acarbose </li></ul>
  28. 28. <ul><li>Classification of Insulin: insulin can be classified according to onset & duration of action. </li></ul><ul><ul><li>Class Onset Duration Examples </li></ul></ul><ul><ul><li>Fast acting 0.5-1 hr 6-8 hrs Crystalline or Soluble insulin </li></ul></ul><ul><ul><li>Acid regular insulin </li></ul></ul><ul><ul><li>Neutral regular insulin </li></ul></ul><ul><ul><li>Semi-lent (susp. small particles) </li></ul></ul><ul><ul><li>Intermediate 2 hrs 24 hrs Isophane insulin suspension </li></ul></ul><ul><ul><li>Insulin Zn suspension </li></ul></ul><ul><ul><li>Globin Zn insulin </li></ul></ul><ul><ul><li>NPH & Lent </li></ul></ul><ul><ul><li> (lent = 30% semilent + 70% ultralent) </li></ul></ul><ul><ul><li>Long acting 4 hrs 36 hrs Protamine Zn Insulin </li></ul></ul><ul><ul><li>6-8 hrs Ultralent (extended Insulin Zn) </li></ul></ul><ul><ul><li>(a suspension of large particles) </li></ul></ul><ul><li>Mechanism of action of insulin: </li></ul><ul><ul><li>Enhances glucose utilization in peripheral tissues. </li></ul></ul><ul><ul><li>Increases glucose storage in form of glycogen in liver & skeletal muscles, through enhancing the hexokinase enzyme  glucose-6-phosphate formation. </li></ul></ul><ul><ul><li>It is anabolic, enhancing protein synthesis. </li></ul></ul><ul><ul><li>Decreases fat catabolism & enhances lipogenesis. </li></ul></ul><ul><ul><li>It decreases gluconeogenesis (i.e.  conversion of amino-acids  glucose) </li></ul></ul><ul><li>Insulin degradation: occurs in the liver as well as the kidneys. </li></ul><ul><li>Insulin when injected IV has a short plasma t ½ of 9 min. </li></ul><ul><li>Crystalline Zn insulin: is the only insulin (regular intermediate acting) that can be used IV in case of diabetes ketoacidosis </li></ul><ul><li>Insulin has a large volume of distribution which approximates that of extracellular fluids. </li></ul><ul><li>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). </li></ul><ul><li>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. </li></ul><ul><li>Most insulin preparations used in USA are single peak, i.e. single component. </li></ul><ul><li>Single component insulin: means from 1 source only (pork or beef). </li></ul><ul><li>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. </li></ul>
  29. 29. <ul><li>Which of the following causes hypoglycemia: </li></ul><ul><ul><li>Insulin c. Sulphonylurea drugs (e.g.Daonil) </li></ul></ul><ul><ul><li>Biguanides (e.g. metformine “Glucophage”) </li></ul></ul><ul><li>Which of the following gives +ve reducing results with Cu salts in testing glucose in urine: </li></ul><ul><ul><li>Testape d. Clinistix </li></ul></ul><ul><ul><li>Diastix e. Benedict’s solution (Cu reduction method) </li></ul></ul><ul><ul><li>Clinitest (Cu reduction method) </li></ul></ul><ul><li>Which of the following agents interferes with glucose test in urine: </li></ul><ul><ul><li>Vitamin C c. Cephalosporins </li></ul></ul><ul><ul><li>Methyl Dopa d. Ampicillin </li></ul></ul><ul><li>In juvenile diabetes, the patient should be treated with: </li></ul><ul><ul><li>Insulin b. Fasting </li></ul></ul><ul><ul><li>Eating frequent meals (many times a day). </li></ul></ul><ul><li>Which agent causes hypoglycemia: </li></ul><ul><ul><li>Corticosteroids (  glucose) b. Adrenaline (  glucose) </li></ul></ul><ul><ul><li>Sulfonylurea. </li></ul></ul><ul><li>What is specific for a fasting glucose test: </li></ul><ul><ul><li>Glucose levels will be high but not more than 120 mg / 100 ml. </li></ul></ul><ul><ul><li>There will be ketosis. </li></ul></ul><ul><ul><li>There will be glucose urea as in diabetics </li></ul></ul><ul><li>In which of the following physiologic conditions do ketone bodies accumulate: </li></ul><ul><ul><li>Juvenile diabetes c. Diabetes mellitus </li></ul></ul><ul><ul><li>Starvation d. All of the above </li></ul></ul><ul><li>Which of the following insulin prep. is expected to have the longest duration of action: </li></ul><ul><ul><li>Semilent insulin. d. Globin insulin. </li></ul></ul><ul><ul><li>NPH insulin. e. Regular insulin. </li></ul></ul><ul><ul><li>Protamine Zn insulin. </li></ul></ul><ul><li>Which hormone acts on the surface of the cell: </li></ul><ul><ul><li>Adrenaline b. Gastrine c. Insulin </li></ul></ul><ul><li>Carbose decreases blood glucose level through: </li></ul><ul><ul><li>Decreasing GIT absorption of carbohydrates </li></ul></ul><ul><ul><li>Blunting the post brandial blood glucose curve </li></ul></ul>
  30. 30. <ul><li>Which anti-diabetic agent cannot be used for lactic acid acidosis: </li></ul><ul><ul><li>Metformie c. Tolbutamide </li></ul></ul><ul><ul><li>Clorpropamide d. Glyberide </li></ul></ul><ul><li>What causes Juvenile onset (Type I – IDDM) diabetes & what is used for its treatment: </li></ul><ul><ul><li>It is caused by degeneration of  cells of islets of langerhans & is treated with insulin </li></ul></ul><ul><li>Why is insulin injected in SC tissue: </li></ul><ul><ul><li>To avoid tissue damage b. To control the dose </li></ul></ul><ul><li>Insulin shock in an unconscious patient is treated by: </li></ul><ul><ul><li>Glucagon injection b. Glucose IV </li></ul></ul><ul><li>Which is true about SC insulin therapy: </li></ul><ul><ul><li>Lipodistrophy (SC fat at site of injection). </li></ul></ul><ul><li>For ketoacidosis we use: </li></ul><ul><ul><li>Zn insulin (regular) IV </li></ul></ul><ul><li>In which of the following conditions does insulin requirements increase: </li></ul><ul><ul><li>Stress c. Bacterial infection </li></ul></ul><ul><ul><li>Pregnancy d. Surgery </li></ul></ul><ul><li>Alcohol is contraindicated with: </li></ul><ul><ul><li>Metformine c. Gliburide </li></ul></ul><ul><ul><li>Metronidazole (disulfuram like reactions) </li></ul></ul><ul><li>After opening an insulin injection, how many days can it be kept : </li></ul><ul><ul><li>At room temp  30 days </li></ul></ul><ul><ul><li>Under refrigeration  till expiry date </li></ul></ul><ul><li>Longstanding diabetes leads to: </li></ul><ul><ul><li>Retinopathy c. Nephropathy e. CAD </li></ul></ul><ul><ul><li>Neuropathy d. Diabetic foot (ulcer or gangrene) </li></ul></ul><ul><li>Which of the following is specific for measuring glucose: </li></ul><ul><ul><li>Tes-tape </li></ul></ul><ul><li>Clopropamide should not be given with: </li></ul><ul><ul><li>Alcohol b. Antacids </li></ul></ul><ul><li>The threshold of glucose is: </li></ul><ul><ul><li>3.5 L / min </li></ul></ul><ul><li>Ketoacidosis is determined by all except: </li></ul><ul><ul><li>B-hydroxy buteric acid c. Acetone </li></ul></ul><ul><ul><li>Acetic acid d. Lactic acid </li></ul></ul>
  31. 31. <ul><li>To monitor compliance in diabetes, we monitor: </li></ul><ul><ul><li>Glucosuria c. Glycemia </li></ul></ul><ul><ul><li>Proteinuria d. Ketonuria </li></ul></ul><ul><li>Ketoacidosis may result from: </li></ul><ul><ul><li>Diabetes b. Insulin deficiency </li></ul></ul><ul><li>When administered IV, insulin has: </li></ul><ul><ul><li>Short t ½ b. Large volume of distribution </li></ul></ul><ul><li>Which is true about insulin pump: </li></ul><ul><ul><li>Gives regular insulin all night </li></ul></ul><ul><ul><li>Supposed to be the most similar to physiologic </li></ul></ul><ul><li>Human insulin: ??? </li></ul><ul><ul><li>Can be frozen b. Cannot be easily replaced by other forms </li></ul></ul><ul><li>In a healthy adult person, after a meal blood glucose will: </li></ul><ul><ul><li>Increase above 200 then decrease rapidly </li></ul></ul><ul><li>Acrabose is: ???? </li></ul><ul><ul><li>A basic tetra-saccharide laxative </li></ul></ul><ul><ul><li> glucosidase inhibitor (inhibits the enzyme responsible for hydrolysis of sucrose) </li></ul></ul><ul><ul><li>Inhibits absorption of glucose in the small intestine   glucose levels </li></ul></ul><ul><ul><li>Blunts post brandial glucose curve </li></ul></ul><ul><li>What is true about sulphonyl ureas: </li></ul><ul><ul><li>Acidic products </li></ul></ul><ul><ul><li>Stimulate  cells to release insulin </li></ul></ul><ul><ul><li>Cause lactic acidosis </li></ul></ul><ul><li>Longstanding diabetes leads to: </li></ul><ul><ul><li>Retinopathy c. Nephropathy e. CAD </li></ul></ul><ul><ul><li>Neuropathy d. Diabetic foot (ulcer or gangrene) </li></ul></ul><ul><li>Which of the following is specific for measuring glucose: </li></ul><ul><ul><li>Tes-tape </li></ul></ul><ul><li>Clopropamide should not be given with: </li></ul><ul><ul><li>Alcohol b. Antacids </li></ul></ul><ul><li>The threshold of glucose is: </li></ul><ul><ul><li>3.5 L / min </li></ul></ul><ul><li>Ketoacidosis is determined by all except: </li></ul><ul><ul><li>B-hydroxy buteric acid c. Acetone </li></ul></ul><ul><ul><li>Acetic acid d. Lactic acid </li></ul></ul>

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