Review of Pharmacology - 9E (2015)
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Review of Pharmacology - 9E (2015)

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Cardiovascular System<br />

188<br />

<strong>Review</strong> <strong>of</strong> <strong>Pharmacology</strong><br />

(c) Flecainide<br />

(d) Propanolol<br />

196. Which <strong>of</strong> the following anti-arrythmic drug decreases<br />

the action potential duration in purkinje fibers?<br />

(a) Quinidine<br />

(b) Flecainide<br />

(c) Amiodarone<br />

(d) Lignocaine<br />

197. All <strong>of</strong> the following decrease AV conduction EXCEPT:<br />

(a) Esmolol (Jharkhand 2003)<br />

(b) Digitalis<br />

(c) Lignocaine<br />

(d) Verapamil<br />

198. Class III anti arrythmic drug is: (Jharkhand 2005)<br />

(a) Amiodarone<br />

(b) Phenytoin<br />

(c) Propafenone<br />

(d) Pindolol<br />

199. A sixteen-year-old girl is found to have paroxysmal<br />

attacks <strong>of</strong> rapid heart rate. The antiarrhythmic <strong>of</strong> choice<br />

in most cases <strong>of</strong> acute AV nodal tachycardia is:<br />

(a) Adenosine (Karnataka 2006, Karnataka 2005)<br />

(b) Amiodarone<br />

(c) Propanolol<br />

(d) Quinidine<br />

200. Drug <strong>of</strong> choice for paroxysmal supraventricular<br />

tachycardia (PSVT) is: (Karnataka 2005)<br />

(a) Verapamil<br />

(b) Digitalis<br />

(c) Quinidine<br />

(d) Diphenylhydantoin<br />

201. Drug <strong>of</strong> choice for ventricular arrhythmias due to<br />

myocardial infarction (MI) is: (Karnataka 2005)<br />

(a) Quinidine<br />

(b) Amiodarone<br />

(c) Xylocaine<br />

(d) Diphenylhydantoin<br />

202. Drug <strong>of</strong> choice for ventricular premature beats (VPC)<br />

due to digitalis toxicity is: (Karnataka 2005)<br />

(a) Diphenylhydantoin<br />

(b) Quinidine<br />

(c) Amiodarone<br />

(d) Verapamil<br />

203. Arrhythmias refractory to the treatment <strong>of</strong> lignocaine<br />

can be treated by: (Karnataka 2002)<br />

(a) Sotalol<br />

(b) Diltiazem<br />

(c) Amiodarone<br />

(d) Quinidine<br />

204. Quinidine exerts its action on heart by:<br />

(a) Ca 2+ channel blockade (DPG 2008)<br />

(b) Na + channel blockade<br />

(c) K + channel opening<br />

(d) Cl – channel opening<br />

DYSLIPIDEMIA<br />

205. Ezetimibe acts by: (DPG 2009)<br />

(a) Enhancing excretion <strong>of</strong> bile acids<br />

(b) Decreasing absorption <strong>of</strong> cholesterol<br />

(c) Inhibiting HMG-CoA reductase<br />

(d) Inhibiting intracellular lipase<br />

206. True about fibrates is all except: (AIIMS Nov., 2007)<br />

(a) Drug <strong>of</strong> choice for Type III hyperlipoproteinemia<br />

and severe hypertriglyceremia<br />

(b) Activate PPAR to stimulate LPL<br />

(c) Absorbed good on empty stomach and absorption is<br />

delayed by fatty meals<br />

(d) Side effect are rash, urticaria, myalgia and impotence<br />

207. All <strong>of</strong> the following are true about HMG CoA reductase<br />

inhibitors except: (AIIMS May, 2002)<br />

(a) CNS accumulation <strong>of</strong> simvastatin and lovastatin<br />

is high and less for pravastatin and fluvastatin<br />

(b) Simvastatin is rapidly and pravastatin is least metabolized.<br />

(c) Bioavailability is minimally modified when pravastatin<br />

is taken with food<br />

(d) Fibrinogen levels are increased by pravastatin<br />

208. Mechanism <strong>of</strong> action <strong>of</strong> statins is:<br />

(a) Inhibition <strong>of</strong> HMG-CoA synthase<br />

(b) Stimulation <strong>of</strong> HMG-CoA reductase<br />

(c) Indirect increase <strong>of</strong> LDL receptors synthesis<br />

(d) Inhibition <strong>of</strong> intestinal cholesterol absorption<br />

209. Which hypolipidemic drug can exacerbate the symptoms<br />

<strong>of</strong> gout?<br />

(a) Ezetimibe<br />

(b) Gemfibrozil<br />

(c) Niacin<br />

(d) Simvastatin<br />

210. The rate-limiting step in cholesterol synthesis is<br />

inhibited by: (TN 2007)<br />

(a) Probucol<br />

(b) Cholestyramine<br />

(c) Statins<br />

(d) Gemfibrozil<br />

211. Lipid lowering drug that significantly reduces lipoprotein-a<br />

[Lp (a)] levels is? (MH 2008)<br />

(a) Fen<strong>of</strong>ibrate<br />

(b) Gemfibrosil<br />

(c) Rosuvastatin<br />

(d) Nicotinic acid<br />

212. Cl<strong>of</strong>ibrate, a lipid lowering agent inhibits both cholesterol<br />

and triglyceride synthesis by:<br />

(a) Inhibiting HMG CoA reductase (DPG 2001)<br />

(b) Binding to bile acids and preventing its reabsorption<br />

(c) Inhibiting VLDL production<br />

(d) Activating lipoprotein lipase, resulting in VLDL<br />

degradation<br />

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