Review of Pharmacology - 9E (2015)

Review of Pharmacology
166. Ans. (d) Verapamil (Ref: Katzung. 11/e p181)
167. Ans. (d) Productive cough (Ref: Katzung 11/e p241; Harrison 17/e p1953)
‘Liver toxicity caused by amiodarone is also called ‘pseudoalcoholic liver injury’ and can range from fatty liver to hepatitis
to cirrhosis’. It can also result in pulmonary fibrosis and corneal microdeposits.
Cardiovascular System
206
168. Ans. (a)It increases effective refractory period; (c) Causes paradoxical tachycardia; (e) Cinchonism is seen (Ref: KDT 6/e
p511-512)
Quinidine has following properties:
– Class I A and III antiarrythmic properties
– Increases the ERP (effective refractory period).
– Antivagal action, causing tachycadia. This tachycardia is paradoxical, because quinidine is a cardiac depressant and
thus not expected to increase the heart rate.
– Some a-blocking properties and its use can cause hypotension, but not used as antihypertensive agent.
– At higher doses, cinchonism occurs, characterized by ringing in ear, deafness, vertigo, headache, visual disturbances,
mental changes and delirium.
– Antimalarial action is poorer than quinine.
– ECG changes: ↑ PR and QT interval and broadens QRS complex and change the shape of T wave.
169. Ans. (a) Verapamil (Ref: Katzung 11/e p243-244, KDT 6/e p517-518)
• Adenosine is DOC for PSVT termination.
• Verapamil is DOC for prophylaxis of PSVT and for management of sustained supraventricular tachycardia.
170. Ans. (a) Quinidine (Ref: Katzung 10/e p224; KDT 6/e p510)
• Torsades’de pointes is a polymorphic ventricular tachycardia that is usually caused due to blockade of delayed rectifier
K + channels in the heart.
• It manifests in the ECG as QTc prolongation.
• Drugs having cardiac K + channel blocking activities can cause this arrhythmia. These include:
––
Class Ia antiarrhythmics -Quinidine, Procainamide (Na + and K + channel blockers)
––
Class III antiarrhythmics -Bretylium, sotalol, dofetilide, ibutilide and amiodarone (K + channel
blockers)
––
Other drugs like Terfenadine, Cisapride, Astemizole, Sparfloxacin, Gatifloxacin, Grepafloxacin,
Mefloquine, Pentamidine, Thioridazine, Ziprasidone etc.
171. Ans. (d) Systemic lupus erythematosis (Ref: KDT 6/e p516)
172. Ans. (a) Tocainide (Ref: KK Sharma/307, G & G, 10/e p962)
• Althrough the name is similiar to class Ic agents (like flecainide, encanide), tocainide comes under class Ib.
173. Ans. (c) It is excreted through bile following hepatic metabolism (Ref: KDT 6/e p140, 515)
Sotalol is a non-selective β-blocker having class III (K + channel blocking) anti-arrhythmic property. It prolongs APD by
blocking cardiac K + channels. Therefore, it can prolong QT interval and result in torsades de pointes (polymorphic ventricular
tachycardia). It is a lipid insoluble beta blocker that is excreted predominantly by kidney.
174. Ans. (a) Magnesium sulphate (Ref: Goodman & Gilman 11/e p929, 930)
• Magnesium is the agent of choice for the immediate treatment of torsades associated with both congenital and acquired
long QT syndrome. Use of i.v. isoproternol is limited only to acquired long QT syndrome. Long term treatment
with oral beta blockers is required only for congenital disease.
175. Ans. (a) Quinidine; (b) Disopyramide; (c) Procainamide (Ref: KDT 6/e p510)
• Torsades de pointes is seen with K + channel blockers (class Ia and class III antiarrhythmic drugs), e.g. quinidine, disopyramide,
procainamide, bretylium, ibutilide, etc.
176. Ans. (d) Sodium lactate (Ref: CMDT -2010/1445)
Pressor agents (to reverse hypotension) and sodium lactate (to reverse arrhythmias) are indicated for the treatment of
procainamide toxicity.
177. Ans. (b) Esmolol (Ref: KDT 6/e p515)
It is a very short acting b-blocker. It has to be administered i.v. for acute therapy of arrhythmias. Amiodarone, verapamil
and quinidine can be used for chronic oral treatment of arrhythmias.
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