Mechanisms of action — candesartan, dexamethasone, rivaroxaban

Correct answer: A. Blocks angiotensin II at the AT1 receptor

• A. Correct. Candesartan is an ANGIOTENSIN II RECEPTOR BLOCKER (ARB). It competitively blocks angiotensin II at the AT1 receptor, preventing vasoconstriction and aldosterone release. Because it acts downstream of ACE, it does NOT cause the bradykinin accumulation responsible for the ACE-inhibitor cough.
• B. Beta-1 blockade is the mechanism of metoprolol and atenolol.
• C. Calcium channel blockade is the mechanism of amlodipine and nifedipine — dentally important because the dihydropyridines cause GINGIVAL ENLARGEMENT.
• D. ACE inhibition is the mechanism of the '-pril' drugs — lisinopril, enalapril, ramipril — which prevent the CONVERSION of angiotensin I to angiotensin II.

Note: Suffix shortcut: '-SARTAN' = ARB (blocks the RECEPTOR); '-PRIL' = ACE inhibitor (blocks the ENZYME/conversion). This file tests ACE inhibitor MOA repeatedly with slightly different wording — learn both precisely.

Correct answer: C. Agonist at glucocorticoid receptors

• A. Dexamethasone has minimal MINERALOCORTICOID activity — this is precisely why it is preferred when sodium and water retention must be avoided.
• B. It is an agonist, not an antagonist. (Mifepristone is an example of a glucocorticoid receptor antagonist.)
• C. Correct. Dexamethasone is a synthetic corticosteroid that acts as an AGONIST at intracellular GLUCOCORTICOID receptors. The receptor-ligand complex translocates to the nucleus and alters gene transcription — suppressing phospholipase A2 (blocking both the cyclooxygenase and lipoxygenase pathways), reducing cytokine production and inhibiting leukocyte migration.
• D. Spironolactone is the mineralocorticoid receptor antagonist.

Note: DENTAL RELEVANCE: dexamethasone is used to reduce post-operative oedema after third molar surgery. In patients on long-term steroids, consider ADRENAL SUPPRESSION and the potential need for supplementation before major procedures, and remember the increased risk of infection and delayed healing.

Correct answer: D. Direct factor Xa inhibitor

• A. Aspirin is the irreversible COX inhibitor, acting on platelet function rather than the coagulation cascade.
• B. Dabigatran is the direct THROMBIN (factor IIa) inhibitor.
• C. Warfarin is the vitamin K antagonist; it inhibits vitamin K epoxide reductase and reduces synthesis of factors II, VII, IX and X, and is monitored by INR.
• D. Correct. Rivaroxaban is a DIRECT ORAL ANTICOAGULANT (DOAC) that directly and reversibly inhibits FACTOR Xa, the convergence point of the intrinsic and extrinsic pathways, thereby preventing the conversion of prothrombin to thrombin.

Note: The '-XA-BAN' drugs inhibit factor XA: riva-ROXA-ban, apiXAban, edoXAban. DENTAL MANAGEMENT: for routine procedures, DO NOT stop the DOAC. Use local haemostatic measures — sutures, oxidised cellulose, tranexamic acid mouthwash — and where possible schedule so that the procedure occurs at the TROUGH level, before the next dose. Note also that INR does NOT monitor DOACs.