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CVS-Diabetes
 

CVS-Diabetes

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    CVS-Diabetes CVS-Diabetes Document Transcript

    • Cardiovascular المعلومات بالداخل موثوق بها لأنها مراجعه و معتمده من Certified from Pharmacists_coffee magazine
      • 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
      • 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).
      • Mode of action of diuretics:
        • Thiazides (e.g. HCTZ) inhibit Na + reabsorption at distal tubules
        • Loop diuretics (e.g. bumetanide inhibit Na + / Cl - exchange at the ascending limb frusimide Lasix) of the Loop of Henle
        • K sparing diuretics (amiloride inhibit the effects of aldosterone hormone on spironolactone & triametrene) distal tubules
        • Carbonic anhydrase inhibitors inhibit carbonic anhydrase enzyme & this (e.g. acetazolamide) inhibits Na + / H + exchange at proximal tubules decreasing its reabsorption
        • Osmotic diuretics (e.g. urea & increase osmolarity of glomerular filtrate, mannitol) (thus decrease reabsorption of water & increase urination)
      • Thiazide diuretics:  uric acid excretion  hyperuricemia; except for Ticrynofen which has a uricosuric effect. Hypokalemia & hypercalcemia (NSAIDs  efficacy of thiazides).
      • Mercurial diuretics: are given IM. They are not absorbed from GIT, thus not given orally.
      • Ethacrynic acid (Edecrine): is a loop diuretic capable of producing ototoxicity & may aggravate ototoxicity of aminoglycosides. (NSAIDs  efficacy of loop diuretics).
      • Diuretics enhance proximal tubular reabsorption of solutes including uric acid.
      • Acetazolamide leads to hyperchloremic metabolic alkalosis as a result of  loss of water coupled with  distal Na reabsorption in exchange for K & …
      • Thiazides  hypercalcemia Loop diuretics  hypocalcemia (Hypercalciurea)
      • The antidiuretic hormone (ADH or Vasopressin): is secreted from the posterior pituitary & acts on the distal tubules to enhance the reabsorption of water & salt.
      • General Notes:
      • In complete heart block: beats of the atria & ventricles are both blocked.
      • In acute asthma & in anaphylactic shock adrenaline is used.
      • The highest BP is in the pulmonary artery, the lowest BP is in the vena cavae.
      • CNS reaction towards increased arterial pressure  peripheral vasodilatation.
      • In moderate exercise, the HR increases because the sympathetic stimulation of  -receptors in arterioles causes vasodilatation   TPR  leading to reflex  in HR.
      • When venous return is increased to the right atrium, consequently:
        • Tachycardia occurs.
        • Increased oxygen consumption (OC).
      • Organ ischemia: can result from organ-turnicate.
      • Bed sores: are caused by body weight pressure in patients laying in 1 position for long time.
      • 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).
      • Organ Receptor 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.
      • 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.
      • 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).
      • 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.
      • 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.
      • 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.
      • 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.
        • 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  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
        • Anticoagulants
        • Heparin Caumarine (Warfarin)
        • Onset of action Immediate Gradual
        • Duration 4 hrs 2-5 days
        • Used in Emergency & prophylaxis Prophylaxis
        • Route of administration IV or SC Oral
        • Lab control of dose APTT Prothrombin time
        • Treatment of overdose Protamine SO 4 Fresh blood &/or Vitamin K
        • Use in pregnancy Can be given Contraindicated
        • Drug interactions Few Many
        • Effect of antacids No effect  its effect
        • Pharmacologic action Anticoag. in vivo & in vitro Anticoagulant in vivo
        • Cost Expensive Cheap
        • The anticoagulant effect of heparin: is quantitated by the “Active Partial Thromboplastin Time” (APTT) & the “Activated Coagulation Time” (ACT) which is 3-5 min.
        •  Normally, APTT is from 30-45 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).
        • Angina Types Angina Pectoris (strangling of the chest)
          • Beta Blockers
          • Methyl dopa. (Use)
          • Antihyperlipidemic
          • Hydralazine (vasodilator)
        • Beta Blockers
          • Non Selective (B 1 + B 2 ) Propranolol Pindolol Nadolol
        • Sotalol Timolol
          • Cardio Selective (B 1 ) Acebutolol Atenolol Metoprolol
          • 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
          • Proximal Tubule: Osmotic Diuretics: e.g. Mannitol.
          • Loop of Henele: Reduction of Na + re-absorption  leads to K + loss at site 4; e.g. Frusemide.
          • Cortical diluting segment: Reduction of Na + re-absorption  leads to K + loss at site 4; e.g. Thiazides.
          • Distal tubule: inhibition of Na + exchange for K + / H + ; e.g. K + sparing diuretics (aldosterone, spironolactone, triametrene, Amiloride).
      • Heparin is:
        • Like coumarine c. Acts on certain steps of coagulation system
        • Oral d. Of benefit in arterial blood clot as prophylaxis
      • In left ventricular failure the blood pools in:
        • Lungs c. Vena cavae
        • Liver
      • Patients with moderate HT & a history of heart disease (CHF) are treated with:
        • Propranolol c. Hydrochlorothiazide
        • Methyl dopa d. Reserpine
      • An important advantage of using dopamine (inotropic sympathomemetic) in cardiac shock is:
        • It will not cross the BBB & will not cause CNS side effects.
        • It produces a dose dependant increase in CO & renal perfusion
        • It will not increase the blood pressure
        • It has no effect on  &  receptors.
        • It can be given orally
      • For a sympathomimetic drug to be effective it should be:
        • Able to fit in receptors
        • Bound to plasma proteins
        • Compete at the site of release of the transmitter
      • A HT patient suffering from depression should not be given all of the following EXCEPT:
        • Reserpine (depletes NE stores)
        • Clonidine (  2 agonist  negative feedback  E & NE)
        • Methyl dopa (False methylation  methyl NE   2 agonist)
        • Guanithidine
        • Hydralazine (direct vasodilatation)
      • Vasodilators cause:
        • Reflex bradycardia b. Reflex tachycardia
      • In an ischemic myocardium, which is released & causes coronary vasodilatation:
        • Adrenaline c. Serotonin
        • Acetylcholine d. Adenosine
      • Which hormone increases water reabsorption from distal tubules:
        • Aldosterone (also vasopressin – ADH) c. Acetylcholine
        • Adrenaline d. Adenosine
        • N.B. Vasopressin acts on distal tubules to  water re-absorption
      • At rest (or during sleep), which organ receives the richest blood supply:
        • Lungs c. Heart
        • Liver (27%) d. Kidneys (22%)
      • Which drug, although increasing the heart rate, causes vasodilatation (  BP):
        • Adrenaline d. Propranolol
        • Carbacol e. Phenylephrine
        • Ephedrine f. Isoproterenol (more  stimulant than  )
      • The highest blood pressure is in the:
        • Veins c. Arteries (pulmonary artery)
        • Venules d. Arterioles
      • Diuretics are most likely to produce:
        • Hyperkalemia. c. Hypokalemia. e. Hyperuricemia
        • Hypercalcemia. d. Hypocalcemia f. Urinary alkalosis
      • Digitalis toxicity does not cause:
        • Nausea, vomiting, fatigue d. Vision change g. Anorexia
        • Dysrhythmia e. AV block
        • Ventricular tachycardia f. Constipation (it causes diarrhea)
      • Which of the following clotting factors is normally found in circulating blood:
        • Thrombin c. Prothrombin
        • Thromboplastin
      • Which of the following drugs  the sympathetic stimulation of the adrenal medulla:
        • Nicotine (in small doses) b. Acetylcholine (in large doses)
      • Blood going to the branches of the coronary artery has just passed the:
        • Aortic valve c. Inferior vena cava
        • Right atrium d. Superior vena cava
      • In HT of renal origin, which antihypertensive is used:
        • Clonidine b. Hydralazine c. Captopril
      • Which of the following vasodilators cause venous pooling:
        • Sodium nitroprusside c. Hydralazine
        • Nitroglycerine d. Isosorbid dinitrate
        • Methyldopa
      • Which of the following is an  -agonist:
        • Clonidine b.  -methyl dopa
      • In an acute anginal attack, which drug can be given:
        • Propranolol c. Nitroglycerine (Short acting)
        • Isosorbid dinitrate
      • Which drug is used in prophylaxis of angina:
        • Nifedipine
        • Diltiazem
      • A person with fever has:
        • Paroxysmal tachycardia c. Sinus tachycardia
        • Bradycardia d. SA arrhythmia
      • Following moderate exercise, BP is usually higher than normal because:
        • Release of acetylcholine.
        • Activation of the RAA system
        • Increased venous return.
      • Repeated arrhythmia means:
        • Paroxysmal arrhythmia c. Tachy arrhythmia
        • Ventricular arrhythmia
      • Which of the following drugs causes rebound HT:
        • Clonidine c. Hydralazine
        • Guanithedine
      • Prolonged use of diuretics causes all of the following except:
        • Hypoglycemia d. Hyperuricemia
        • Hypokalemia e. Alkalosis of urine
        • Sexual dysfunction
      • During the absolute refractory period, if you apply another stimulus, the muscle will:
        • Contract c. Relax
        • Remain in its existing state (no response to stimuli)
      • Aldosterone is secreted from the:
        • Adrenal medulla c. Kidney
        • Adrenal cortex
      • During rest (or inspiration), BP is lowest in:
        • Venules c. Arterioles
        • Vena cavae d. Capillaries
      • Which of the following is an  -blocker:
        • Prazocin b. Doxazocin c. Terazocin
      • What is true about the hypophyseal portal system:
        • It begins & ends in capillaries c. None
        • It begins with capillaries & ends with veins
      • Which drug is used in mild to moderate HT:
        • Captopril c. Propranolol
        • Lasix
      • Which drug is used in mild HT:
        • HCTZ c. Prazocin
        • Clonidine
      • Arterial dilators include:
        • Diazoxide. c. Hydralazine.
        • Minoxidil d. Sodium nitroprusside (arteriolar & venous)
      • Which antihypertensive is used in diabetic patients:
        • Captopril (ACEIs) c. Prazocin (  -blocker) e. CCBs
        • HCTZ d. Atenolol
      • In angina pectoris, propranolol is used as:
        • Treatment c. Acute attacks
        • Prophylactic (  O 2 consumption)
      • The outer layer of the adrenal cortex secretes:
        • Aldosterone c. Norepinephrine
        • Cortisone
      • The middle layer of the adrenal cortex secretes:
        • Aldosterone c. Norepinephrine
        • Cortisone
      • The adrenal medulla secretes:
        • Aldosterone c. Norepinephrine & epinephrine
        • Cortisone
      • In complete heart block (AV block):
        • No arterial impulses reach the ventricles c. Ventricles beat slower
        • Atria & ventricles contract independently. d. Ventricles beat irregularly
      • What is the mechanism by which chenodioxycholic acid dissolves gall stones: ???
        • Reduces cholesterol synthesis c. Increases bile acid production
        • Increases phospholipids
      • Arrhythmias may be caused by:
        • Catecholamines
      • The anti-coaggulant effect of warfarin increases in:
        • Vitamin K deficiency.
      • What is the side effect of minoxidil:
        • Hirsutism c. Weight gain
        • Fluid retention d. Tachycardia
      • Heparin is used for:
        • Prophylaxis & treatment of venous thrombosis
        • Prophylaxis & treatment of pulmonary (or peripheral arterial) embolism.
        • Prevent clotting during surgery (arterial or cardiac)
        • Fibrillation with embolization
      • Which is true about heparin:
        • Works in vivo & in vitro d. Inactive orally
        • Has anti-thrombin / anti-thromboplastin effects
        • Prevents arterial thrombosis e. Safe in pregnancy
      • Which is true about warfarin:
        • Decrease platelet aggregation d. Works in vivo & in vitro
        • Activity  in vit K deficiency e. Decreases hepatic fibrinogen synthesis
        • Produces prompt action if given IV
      • Which diuretics cause urinary alkalosis:
        • Thiazides c. Carbonic anhydrase inhibitors
        • Loop diuretics d. K + sparing diuretics
      • Which diuretic acts on proximal tubules:
        • Acetazolamide b. HCTZ
      • Which diuretics  water excretion at distal tubules:
        • Triametrene c. Amiloride e. Frusimide
        • Spironolactone d. Thiazide f. Acetazolamide
      • The use of  -blockers in HT is limited to:
        • Patients who can not take diuretics or beta-blockers.
      • Which drug is contra-indicated in CHF & HT:
        • NSAIDs
      • The major side effects of nitrates is:
        • Headache (lasts for > 12 hrs)
      • Nifedipine is:
        • 1,4 dihydropyridine b. pyrimidine
      • Respiratory acidosis means:
        • Increase in PCO 2 in the brain
      • Hyperchloremic acidosis is caused by:
        • Acetazolamide (carbonic anhydrase inhib.) b. Aceterol (diamox) ???
      • SMZ, TMP & Miconazole,  warfarin efficacy through:
        • Decreasing hapatic metabolism
        • Inhibiting bacterial flora   vit. K synthesis  potentiates warfarin
        • Displacing warfarin from plasma protein binding sites.
      • Nifedipine is used in:
        • Angina b. CHF
      • Acute pre-renal failure results in:
        • Azotemia b. Uremia
      • Which diuretic decreases Ca excretion & leads to hypercalcemia:
        • Loop diuretics b. Thiazide diuretics
      • Metabolic acidosis is caused by:
        • Acetazolamide c. Methyl alcohol e. Starvation
        • Renal falure d. Ethylene glycol
      • Which agent  water excretion at (  permiability of) collecting tubules:
        • Triametrene b. Amiloride c. Ethacrinic acid
      • Parathyroid hormone promotes Ca excretion by action on:
        • Proximal tubules. c. Distal tubules
        • Glomerulus d. Renal tubules
      • What is true about ACE:
        • Natural substrate is A I b. Normal alternative for A I
      • Nephrotic syndrome is characterized by:
        • Proteinuria b. Hypoalbuminuria
      • Which CCB causes MI:
        • Diltiazem b. Verapamil c. Nifedipine
      • The tension in blood vessels depends on:
        • Radius of blood vessel b. Pressure created on blood vessel
        • Length of blood vessel
      • What is common in thiazides & sulphonamides:
        • The sulpha group
      • A drug which inhibits aldosterone secretion (e.g. ACEIs) will:
        • Cause hyperkalemia b.  effect of spironolactone
      • Compared to sublingual nitroglycerine, transdermal patches have:
        • Prolonged effect b. Rapid effect
      • Which is used as a voltage dependant Na + channel blocker:
        • Tetraiodoxine  Na + channel blocker but toxic  not used
        • Benzodiazepine  Cl - channel opener   GABA
        • Digitalis  Ca ++ channel opener
        • Verapamil  Ca ++ channel blocker
        • Phenytoin (& lidocaine)  Na + channel blockers
      • Which is a Na + channel blocker:
        • Phenytoin b. Lidocaine c. Triametrene
      • Which drugs act through lipoprotein activation:
        • Clofibrate c. Gemfebrozil e. Nicotinic acid
        • Atrovastatin d. Cholistyramine
      • Edema occurs in cases of:
        • Hypervolemia c. Na + loss e. Liver chirrosis
        • Right side CHF d. Hypovolemia f. Hyperthyroidism
      • Edema occurs in all except:
        • Ascitis c. Glomerular damage
        • Hyperthyroidism d. Excess corticosteroid usage
      • Which is not a symptom associated with MI:
        • Arrhythmia c. AV block e. Headache
        • Heart burn d. diarrhea
      • Acetazolamide & sulphonamides are both: (carbonic anhydrase inhibitors are aromatic or heterocyclic sulphonamides with prominent thiadiazole gp)
        • Sulphonamides b. Anti-microbials
      • What is azotemia:
        • Synonymous to uremia b.  SrCr c.  NH 3 & urea in blood (  BUN)
      • Digoxin is affected by:
        • Erythromycin b. Cholistyramine c. Primaquine
      • Hypovolemia causes all except:
        • Pulmonary edema b. Oliguria
      • Renal failureis associated with:
        • Hyperphosphatemia
      • Side effects of atenolol include:
        • Hypotension b. Tremors c. Visual disturbances
      • Fibrinolytic agents cannot be given post-op. if:
        • Patient had gastric bleeding within the past 6 months
        • Patient > 65 yrs c. Patient is hypertensive
      • Osmotic dialysis is effective with:
        • Low mol. wt. substance c. Large volume of distribution
        • High plasma protein binding
      • Bile acids (bile salts) are:
        • Hydrophilic c. Steroid in nature (not absorbed)
        • Prepare O/W emulsions ???
      • Which drugs is most effective in decreasing LDL & VLDL:
        • Clofibrate c. Nicotinic acid
        • Atrovastatin d. Cholistyramine
      • Vasodilators may cause:
        • Orthostatic hypotension b. Tachycardia
      • The dose of warfarin could be adjusted by measuring:
        • APTT c. Warfarin conc. in blood
        • PT (prothrombin time) d. Coagulation time
      • Which is true about pulmonary thrombotic disease:
        • Fatal b. Mainly due to varicose (starting in the legs)
      • Injection of high dose of K+ may cause:
        • Cardiac arrest
      • Side effects of thiazides include:
        • Hyperglycemia b. Hyperuricemia c. Alkalosis
      • Streptokinase is used for:
        • Deep venous thrombosis
      • Which of the following anti-arrhythmics can be used orally:
        • Mexiliten ???
      • Digitalis consists of digitalide plus:
        • Sugar b. Amino acid c. Alkaloid
      • Which diuretic decreases Na, K, & Cl & causes mild urinary alkalosis:
        • Thiazides b. Loop diuretics c. Amiloride
      • Which diuretic increases Ca excretion:
        • Thiazides b. Laxis c. Amiloride
      • Triametrene:
        • Acts on distal & collecting tubules
        • Distrupts the exchange with K+ & H+ b blocking sodium channels & decreasing the driving force for the excretion of H+ & K+
      • Which agent increases the water permiability of renal tubules (Increases reabsorption):
        • ADH c. Amiloride
        • Lasix
      • Which is used in arterial thrombosis:
        • Asprin b. Clofibrate
      • Probucol: ????
        • Is used to decrease serum cholesterol
        • Does not affect the later stages of cholesterol synthesis (HDL & LDL)
      • Any drug given in CHF may be nephrotoxic because:
        • Blood flow to the kidney is not sufficient
      • Infarction results because of:
        • Blood cannot reach the right & left carotids ???
      • Ouabin in the treatment of CHF (similar to digitalis) is:
        • Of rapid onset c. Not absorbed from GIT
        • Of short duration d. Given IM (it is given IV only)
      • Digitalis alkaloid is:
        • Highly water soluble b. Water insoluble
      • In acute renal failure, CrCl over estimates glomerular filtration because:
        • Cr is less synthesized d. Cr is highly metabolized in liver
        • Cr is bound to plasma proteins e. Cr is secreted by renal tubules
        • Cr is reabsorbed
      • The best time to give an anti-hyperlipidemic drug like Atrovastatin is at:
        • night c. morning
        • Afternoon ( at night synthesis of lipids increase)
      • Which of the following anti-arrhythmics can be used orally:
        • Mexiliten ???
      • Digitalis consists of digitalide plus:
        • Sugar b. Amino acid c. Alkaloid
      • Which diuretic decreases Na, K, & Cl & causes mild urinary alkalosis:
        • Thiazides b. Loop diuretics c. Amiloride
      • Which diuretic increases Ca excretion:
        • Thiazides b. Laxis c. Amiloride
    • Diabetes
      • Diabetes
      • There are 3 significant parameters in a glucose tolerance curve (blood-glucose vs. time curve)
        • The peak conc. of the glucose in blood.
        • The time required to achieve peak serum level.
        • The rate at which blood glucose level declines with time.
      • In diabetes mellitus the blood glucose peak is higher, occurs later, & declines more slowly than a corresponding glucose tolerance curve of a normal individual.
      • In the glucose tolerance curve:
        • The normal fasting glucose level is 90-120 mg /100 ml of blood.
        • Diabetic patients have fasting blood sugar curve higher than 120 mg / 100 ml of blood.
      • Ketone bodies (acetone  -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 about 4 Kcal.
        • Each gram of carbohydrates supplies about 4 Kcal.
        • Each gram of dextrose supplies about 4 Kcal.
        • Each gram of fats supplies about 9 Kcal.
        • Each gram of ethanol supplies about 7 Kcal.
        • 1 Kcal = 1,000 calories
      • 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
      • 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
      • Classification of Insulin: insulin can be classified according to onset & duration of action.
        • Class Onset Duration Examples
        • Fast acting 0.5-1 hr 6-8 hrs Crystalline or Soluble insulin
        • Acid regular insulin
        • Neutral regular insulin
        • Semi-lent (susp. small particles)
        • Intermediate 2 hrs 24 hrs Isophane insulin suspension
        • Insulin Zn suspension
        • Globin Zn insulin
        • NPH & Lent
        • (lent = 30% semilent + 70% ultralent)
        • Long acting 4 hrs 36 hrs Protamine Zn Insulin
        • 6-8 hrs Ultralent (extended Insulin Zn)
        • (a suspension of large particles)
      • Mechanism of action of insulin:
        • Enhances glucose utilization in peripheral tissues.
        • Increases glucose storage in form of glycogen in liver & skeletal muscles, through enhancing the hexokinase enzyme  glucose-6-phosphate formation.
        • It is anabolic, enhancing protein synthesis.
        • Decreases fat catabolism & enhances lipogenesis.
        • It decreases gluconeogenesis (i.e.  conversion of amino-acids  glucose)
      • Insulin degradation: occurs in the liver as well as the kidneys.
      • Insulin when injected IV has a short plasma t 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.
      • Which of the following causes hypoglycemia:
        • Insulin c. Sulphonylurea drugs (e.g.Daonil)
        • Biguanides (e.g. metformine “Glucophage”)
      • Which of the following gives +ve reducing results with Cu salts in testing glucose in urine:
        • Testape d. Clinistix
        • Diastix e. Benedict’s solution (Cu reduction method)
        • Clinitest (Cu reduction method)
      • Which of the following agents interferes with glucose test in urine:
        • Vitamin C c. Cephalosporins
        • Methyl Dopa d. Ampicillin
      • In juvenile diabetes, the patient should be treated with:
        • Insulin b. Fasting
        • Eating frequent meals (many times a day).
      • Which agent causes hypoglycemia:
        • Corticosteroids (  glucose) b. Adrenaline (  glucose)
        • Sulfonylurea.
      • What is specific for a fasting glucose test:
        • Glucose levels will be high but not more than 120 mg / 100 ml.
        • There will be ketosis.
        • There will be glucose urea as in diabetics
      • In which of the following physiologic conditions do ketone bodies accumulate:
        • Juvenile diabetes c. Diabetes mellitus
        • Starvation d. All of the above
      • Which of the following insulin prep. is expected to have the longest duration of action:
        • Semilent insulin. d. Globin insulin.
        • NPH insulin. e. Regular insulin.
        • Protamine Zn insulin.
      • Which hormone acts on the surface of the cell:
        • Adrenaline b. Gastrine c. Insulin
      • Carbose decreases blood glucose level through:
        • Decreasing GIT absorption of carbohydrates
        • Blunting the post brandial blood glucose curve
      • Which anti-diabetic agent cannot be used for lactic acid acidosis:
        • Metformie c. Tolbutamide
        • Clorpropamide d. Glyberide
      • What causes Juvenile onset (Type I – IDDM) diabetes & what is used for its treatment:
        • It is caused by degeneration of  cells of islets of langerhans & is treated with insulin
      • Why is insulin injected in SC tissue:
        • To avoid tissue damage b. To control the dose
      • Insulin shock in an unconscious patient is treated by:
        • Glucagon injection b. Glucose IV
      • Which is true about SC insulin therapy:
        • Lipodistrophy (SC fat at site of injection).
      • For ketoacidosis we use:
        • Zn insulin (regular) IV
      • In which of the following conditions does insulin requirements increase:
        • Stress c. Bacterial infection
        • Pregnancy d. Surgery
      • Alcohol is contraindicated with:
        • Metformine c. Gliburide
        • Metronidazole (disulfuram like reactions)
      • After opening an insulin injection, how many days can it be kept :
        • At room temp  30 days
        • Under refrigeration  till expiry date
      • Longstanding diabetes leads to:
        • Retinopathy c. Nephropathy e. CAD
        • Neuropathy d. Diabetic foot (ulcer or gangrene)
      • Which of the following is specific for measuring glucose:
        • Tes-tape
      • Clopropamide should not be given with:
        • Alcohol b. Antacids
      • The threshold of glucose is:
        • 3.5 L / min
      • Ketoacidosis is determined by all except:
        • B-hydroxy buteric acid c. Acetone
        • Acetic acid d. Lactic acid
      • To monitor compliance in diabetes, we monitor:
        • Glucosuria c. Glycemia
        • Proteinuria d. Ketonuria
      • Ketoacidosis may result from:
        • Diabetes b. Insulin deficiency
      • When administered IV, insulin has:
        • Short t ½ b. Large volume of distribution
      • Which is true about insulin pump:
        • Gives regular insulin all night
        • Supposed to be the most similar to physiologic
      • Human insulin: ???
        • Can be frozen b. Cannot be easily replaced by other forms
      • In a healthy adult person, after a meal blood glucose will:
        • Increase above 200 then decrease rapidly
      • Acrabose is: ????
        • A basic tetra-saccharide laxative
        •  glucosidase inhibitor (inhibits the enzyme responsible for hydrolysis of sucrose)
        • Inhibits absorption of glucose in the small intestine   glucose levels
        • Blunts post brandial glucose curve
      • What is true about sulphonyl ureas:
        • Acidic products
        • Stimulate  cells to release insulin
        • Cause lactic acidosis
      • Longstanding diabetes leads to:
        • Retinopathy c. Nephropathy e. CAD
        • Neuropathy d. Diabetic foot (ulcer or gangrene)
      • Which of the following is specific for measuring glucose:
        • Tes-tape
      • Clopropamide should not be given with:
        • Alcohol b. Antacids
      • The threshold of glucose is:
        • 3.5 L / min
      • Ketoacidosis is determined by all except:
        • B-hydroxy buteric acid c. Acetone
        • Acetic acid d. Lactic acid