Pharmaceutical Chemistry and Pharmacology Flashcards

Which antifungal drug inhibits ergosterol synthesis by targeting lanosterol 14-alpha demethylase (CYP51)?

Answer: Fluconazole (azole class)

Azole antifungals (fluconazole, itraconazole, voriconazole) inhibit fungal CYP51 (lanosterol 14α-demethylase), blocking ergosterol synthesis. Ergosterol is essential for fungal membrane integrity. Amphotericin B binds ergosterol directly; caspofungin inhibits glucan synthase; terbinafine inhibits squalene epoxidase.

A pharmacist is reviewing the pharmacokinetics of gentamicin. Why are aminoglycosides dosed once daily rather than multiple times daily?

Answer: Concentration-dependent killing and post-antibiotic effect allow once-daily dosing with equivalent/better efficacy and less nephrotoxicity

Aminoglycosides exhibit concentration-dependent killing — their bactericidal activity correlates with the peak:MIC ratio. They also have a prolonged post-antibiotic effect (PAE). Once-daily dosing achieves high peaks (maximizing killing) and allows low trough periods (reducing nephrotoxicity from tubular accumulation).

Which class of antihypertensive is preferred in a patient with diabetes and chronic kidney disease to slow renal progression?

Answer: ACE inhibitors (e.g., ramipril) or ARBs (e.g., losartan)

ACE inhibitors and ARBs reduce intraglomerular pressure by dilating the efferent arteriole, decreasing proteinuria and slowing progression of diabetic nephropathy. They are recommended as first-line in diabetic CKD (unless bilateral RAS or pregnancy). Both are equivalent in this indication.

What is the mechanism by which metronidazole kills anaerobic bacteria?

Answer: Reduced to reactive nitro radical intermediates that damage DNA

Metronidazole is reduced by bacterial ferredoxin (in anaerobes) to nitro radical anions that cause DNA strand breaks and inhibit DNA synthesis. Because aerobic bacteria lack the ferredoxin electron transport system, they cannot activate metronidazole — explaining its selective activity against anaerobes and protozoa.

A pharmacist is counseling a patient on ibuprofen. Which mechanism explains ibuprofen's analgesic and anti-inflammatory effects?

Answer: Reversible competitive inhibition of both COX-1 and COX-2, reducing prostaglandin synthesis

Ibuprofen (non-selective NSAID) reversibly inhibits both COX-1 and COX-2, reducing prostaglandin (PGE2, PGI2) and thromboxane synthesis. This reduces inflammation, pain sensitization, and fever. Unlike aspirin, the inhibition is reversible. COX-1 inhibition causes GI side effects; COX-2 inhibition provides the therapeutic benefit.

A pharmacist notes a patient's prescription includes both sildenafil and a nitrate for chest pain. What is the danger of this combination?

Answer: Severe life-threatening hypotension — both cause vasodilation by potentiating cGMP-mediated smooth muscle relaxation

Both sildenafil (PDE5 inhibitor, prevents cGMP breakdown) and nitrates (increase cGMP via cGMP synthesis) cause vasodilation through cGMP. Combined, they cause synergistic, potentially fatal hypotension. Sildenafil is absolutely contraindicated with all organic nitrates.