Polypharmacy — Cardiovascular & GI

Correct answer: D. Blocks angiotensin-converting enzyme, preventing conversion of angiotensin I to angiotensin II

• A. That describes an ARB such as losartan or valsartan. ARBs act downstream at the receptor and do not raise bradykinin, which is why they rarely cause the dry cough.
• B. That describes a thiazide diuretic such as hydrochlorothiazide.
• C. That describes a direct renin inhibitor such as aliskiren.
• D. Correct. Lisinopril is an ACE inhibitor. Blocking the conversion of angiotensin I to angiotensin II produces vasodilation and lowers peripheral resistance; renin and angiotensin I levels rise as a consequence.

Correct answer: C. Dry, persistent cough

• A. Reflex tachycardia is more typical of direct vasodilators such as hydralazine and of dihydropyridine calcium channel blockers.
• B. Gingival hyperplasia is associated with calcium channel blockers, phenytoin, and cyclosporine — not ACE inhibitors.
• C. Correct. ACE also degrades bradykinin. When ACE is inhibited, bradykinin accumulates and produces the classic dry cough; angioedema is the same mechanism in its severe form.
• D. ACE inhibitors cause hyper‑, not hypokalemia, because reduced aldosterone decreases potassium excretion.

Note: Long-term NSAID use blunts the antihypertensive effect of ACE inhibitors and raises the risk of renal injury — relevant when writing post-operative analgesia for this patient.

Correct answer: D. The H⁺/K⁺-ATPase proton pump of gastric parietal cells

• A. That is the mechanism of ranitidine and famotidine, which are H₂ blockers, not PPIs.
• B. Gastrin receptor antagonism is not a clinically used mechanism for this drug class.
• C. Anticholinergics reduce acid through M3 blockade, but that is not omeprazole.
• D. Correct. Omeprazole is a proton pump inhibitor; it irreversibly binds the H⁺/K⁺-ATPase, the final common step of acid secretion.

Note: Dental relevance: PPIs raise gastric pH and therefore reduce absorption of azole antifungals (ketoconazole, itraconazole) and ampicillin, and they increase serum levels of benzodiazepines, phenytoin, and warfarin.

Correct answer: D. Blocks voltage-dependent calcium channels, reducing calcium influx in cardiac muscle and decreasing workload

• A. Potassium channel opening describes minoxidil, a direct vasodilator.
• B. That is a beta blocker such as atenolol. Verapamil slows the heart, but through calcium channels, not adrenergic receptors.
• C. Sodium-potassium ATPase inhibition is the mechanism of digoxin.
• D. Correct. Verapamil is a non-dihydropyridine calcium channel blocker with strong cardiac selectivity; reduced calcium entry lowers contractility, heart rate, and myocardial workload.

Correct answer: D. Direct inhibition of factor Xa

• A. Direct thrombin inhibition is dabigatran.
• B. Potentiating antithrombin III by bringing it together with thrombin is heparin.
• C. Blocking vitamin K recycling — and therefore factors II, VII, IX, and X — is warfarin.
• D. Correct. Apixaban and rivaroxaban selectively bind the active site of factor Xa, preventing conversion of prothrombin to thrombin.

Correct answer: A. Discontinue it approximately 2 days before the surgical procedure, in consultation with the physician

• A. Correct. Apixaban has a short half-life, so a hold of roughly 2 days before an invasive procedure is the conventional recall answer. Any interruption of anticoagulation is a shared decision with the prescribing physician.
• B. A 7-day hold reflects the irreversible platelet inhibition of aspirin, not a direct oral anticoagulant.
• C. Bridging with warfarin would prolong, not shorten, the period of altered coagulation.
• D. Vitamin K reverses warfarin, not factor Xa inhibitors.

Note: For routine simple extractions many current protocols keep DOACs uninterrupted and rely on local hemostatic measures. Know both the recall answer and the modern trend.

Correct answer: A. Inhibition of HMG-CoA reductase, reducing hepatic cholesterol production

• A. Correct. Statins competitively inhibit HMG-CoA reductase, the rate-limiting enzyme of hepatic cholesterol synthesis.
• B. NPC1L1 inhibition describes ezetimibe.
• C. Bile acid sequestration describes cholestyramine.
• D. PPAR-alpha activation describes fibrates such as gemfibrozil.

Correct answer: B. Fluconazole, because of the risk of rhabdomyolysis

• A. Topical amphotericin B is not associated with this interaction.
• B. Correct. Azoles such as fluconazole inhibit CYP-mediated statin metabolism. Raised statin levels can produce myopathy and, at the extreme, rhabdomyolysis — the classic pairing tested with simvastatin.
• C. Clotrimazole troches are largely topical, with far less systemic azole exposure than fluconazole.
• D. Nystatin is essentially not absorbed from the gut, so systemic interaction is negligible. It is the safer choice here.

Correct answer: A. Inhibits xanthine oxidase, decreasing uric acid production

• A. Correct. Allopurinol blocks xanthine oxidase, the enzyme that converts hypoxanthine and xanthine to uric acid, so less urate is produced.
• B. Microtubule inhibition in leukocytes is colchicine, used for the acute gout attack.
• C. That is a uricosuric such as probenecid.
• D. Enzymatic conversion of urate to allantoin describes rasburicase/pegloticase.