Q- A patient treated with gentamicin develops renal impairment. What is the primary mechanism of this adverse effect?
A- Accumulation in proximal tubule cells
B- Acute interstitial nephritis
C- Decreased renal blood flow
D- Immune-mediated glomerulonephritis
A- Accumulation in proximal tubule cells- Aminoglycosides concentrate in proximal tubular epithelial cells, causing cellular damage and acute tubular necrosis, leading to nephrotoxicity.
Q- A patient on long-term NSAID therapy develops gastric ulcers. Which mechanism is responsible?
A- Decreased leukotriene production
B- Direct bacterial injury
C- Increased gastric acid secretion
D- Inhibition of prostaglandin synthesis
D- Inhibition of prostaglandin synthesis- NSAIDs inhibit COX enzymes, reducing prostaglandins that normally protect the gastric mucosa by increasing mucus, bicarbonate secretion, and mucosal blood flow.
Q- A patient with chronic obstructive pulmonary disease (COPD) is prescribed tiotropium. What is the mechanism of action of this drug?
A- β₂-adrenergic agonism
B- Leukotriene receptor blocker
C- Muscarinic receptor antagonism
D- Phosphodiesterase inhibition
C- Muscarinic receptor antagonism- Tiotropium blocks M3 receptors in airway smooth muscle, reducing bronchoconstriction and mucus secretion, leading to long-acting bronchodilation in COPD.
Q- Which drug is most appropriate for the acute management of anaphylaxis?
A- Albuterol
B- Diphenhydramine
C- Epinephrine
D- Hydrocortisone
C- Epinephrine- Epinephrine is first-line therapy for anaphylaxis because it causes rapid vasoconstriction (α₁), bronchodilation (β₂), and increased cardiac output (β₁), reversing life-threatening hypotension and airway compromise.
Q- Which antiarrhythmic drug is classified as a Class III agent?
A- Amiodarone
B- Lidocaine
C- Propranolol
D- Verapamil
A- Amiodarone- Class III antiarrhythmics block potassium channels, prolonging repolarization and action potential duration, making them effective in treating both atrial and ventricular arrhythmias.