JAWAHARLAL NEHRU TECHNOLOGICAL UNIVERSITY HYDERABAD B. Pharmacy III Year PHARMACOLOGY-II Previous Question Paper (September-2021 - R17)

Atorvastatin is a potent HMG-CoA reductase inhibitor (statin) used as the first-line therapy for hyperlipidaemia due to its ability to significantly lower low-density lipoprotein (LDL) cholesterol. By competitively inhibiting the rate-limiting enzyme HMG-CoA reductase, it reduces the hepatic synthesis of cholesterol. This depletion of intracellular cholesterol triggers a compensatory upregulation of LDL receptors on the surface of hepatocytes, which in turn increases the clearance of LDL-cholesterol from the plasma.

Beyond its lipid-lowering effects, atorvastatin exhibits pleiotropic effects that contribute to cardiovascular protection, including the stabilization of atherosclerotic plaques, reduction of vascular inflammation, improvement of endothelial function, and inhibition of platelet aggregation. These properties make it highly effective in both the primary and secondary prevention of coronary artery disease and myocardial infarction.

The Vaughan Williams classification categorizes anti-arrhythmic drugs based on their primary mechanism of action on cardiac ion channels:

• Class I: Sodium channel blockers (e.g., Quinidine, Lidocaine, Flecainide).
• Class II: Beta-adrenergic blockers (e.g., Propranolol, Metoprolol).
• Class III: Potassium channel blockers (e.g., Amiodarone, Sotalol).
• Class IV: Calcium channel blockers (e.g., Verapamil, Diltiazem).

Class I agents act by blocking voltage-gated sodium channels, thereby reducing the rate of rise of phase 0 depolarization in cardiac action potentials. They are further subdivided:

• Class IA: Moderate sodium channel blockade; also prolongs repolarization (e.g., Quinidine).
• Class IB: Weak sodium channel blockade; shortens repolarization (e.g., Lidocaine).
• Class IC: Potent sodium channel blockade; minimal effect on repolarization (e.g., Flecainide).

Pharmacologically, these agents decrease membrane excitability, slow conduction velocity, and increase the threshold for excitation, effectively suppressing ectopic pacemaker activity and re-entrant circuits in the myocardium.