Questions

         

DRUG THERAPY OF HYPERTENSION   1) RAAS INHIBITORS (MOST IMPORTANT HTN SYSTEM TARGET) Blоcking RAAS → ↓ Angiоtensin II → ↓ vаsоconstriction + ↓ аldosterone ↓ Nа⁺/H₂O retention → ↓ volume ↓ sympathetic activity ↓ cardiac remodeling (HF benefit)   A. ACE Inhibitors (ACEIs): Lisinopril, Enalapril, Captopril, Fosinopril, Benazepril MOA ACE inhibition → ↓ Angiotensin II ↑ Bradykinin → ↑ NO + PGI₂ → vasodilation Major physiologic effects ↓ SVR (vasodilation) ↓ aldosterone → ↓ Na⁺/H₂O retention Efferent arteriole dilation → ↓ intraglomerular pressure → ↓ proteinuria Uses (very high yield) First-line HTN (esp. DM, CKD) HFrEF (mortality benefit) Post-MI Proteinuric CKD Hypertensive urgency Adverse Effects (classic exam set) Dry cough (↑ bradykinin) Angioedema (dangerous) Hyperkalemia Hypotension (first dose) ↓ GFR in bilateral renal artery stenosis Teratogenic (fetal renal failure, oligohydramnios) Key interactions NSAIDs ↓ effect (↓ prostaglandins → afferent constriction) K⁺ supplements / K-sparing diuretics → severe hyperkalemia   B. Angiotensin II Receptor Blockers (ARBs): Losartan, Valsartan, Candesartan, Telmisartan MOA Block AT1 receptor → inhibit Ang II actions directly Key differences vs ACEIs ❌ No bradykinin effect → NO cough ❌ No angioedema Uses ACEI intolerance (cough/angioedema) HTN, CKD, HFrEF AEs Hyperkalemia Hypotension Teratogenic Same renal risk in bilateral renal artery stenosis   C. Renin Inhibitors: Aliskiren MOA Directly inhibits renin → ↓ Ang I → ↓ Ang II Uses Resistant HTN (limited clinical use) AEs Hyperkalemia Hypotension Renal dysfunction Avoid with ACEI/ARB (↑ renal + K⁺ toxicity)   D. Aldosterone Receptor Antagonists (ARAs): Spironolactone, Eplerenone MOA Block aldosterone in collecting duct → ↓ Na⁺/H₂O retention + ↑ K⁺ retention Uses (VERY HIGH YIELD) Resistant HTN (key drug!) HFrEF (mortality benefit) Primary hyperaldosteronism Post-MI HF Hypokalemia Spironolactone: hirsutism, PCOS AEs Hyperkalemia (major) Metabolic acidosis Gynecomastia (spironolactone) Impotence, menstrual irregularities Contraindicated in pregnancy (spironolactone)   2) DIURETICS (↓ Na⁺ → ↓ volume + long-term ↓ SVR) A. Thiazides / Thiazide-like: Hydrochlorothiazide, Chlorthalidone, Indapamide MOA Block Na⁺/Cl⁻ cotransporter in DCT Uses (first-line HTN) Mild–moderate HTN Elderly Stroke prevention (very high yield) Calcium stone prevention (↓ urinary Ca²⁺) Nephrogenic DI AEs (“hyper” mnemonic) HyperGLUC: Hyperglycemia Hyperlipidemia Hyperuricemia (gout) Hypercalcemia Hypokalemia Hyponatremia Metabolic alkalosis   B. Loop Diuretics: Furosemide, Bumetanide, Torsemide, Ethacrynic acid MOA Block Na⁺/K⁺/2Cl⁻ in thick ascending limb Uses HTN with CKD Pulmonary edema (HF) Edema (HF, liver, renal failure) Hypercalcemia (treatment) AEs (important distinctions) Ototoxicity Hypokalemia Hypocalcemia Hypomagnesemia Dehydration Interstitial nephritis Ethacrynic acid = safe in sulfa allergy   C. K⁺-sparing diuretics 1. Aldosterone antagonist: Spironolactone, Eplerenone MOA Block aldosterone in collecting duct → ↓ Na⁺/H₂O retention + ↑ K⁺ retention Uses (VERY HIGH YIELD) Resistant HTN (key drug!) HFrEF (mortality benefit) Primary hyperaldosteronism Post-MI HF Hypokalemia Spironolactone: hirsutism, PCOS AEs Hyperkalemia (major) Metabolic acidosis Gynecomastia (spironolactone) Impotence, menstrual irregularities Contraindicated in pregnancy (spironolactone)   2. ENaC blockers: Amiloride, Triamterene MOA Block epithelial Na⁺ channels in collecting duct Uses Same as ARAs (adjunct HTN, hypokalemia prevention) AEs Hyperkalemia Amiloride: ↑ BUN Triamterene: Kidney stones Crystalluria AKI Megaloblastic anemia   Question: A 62-year-old man with type 2 diabetes mellitus and chronic kidney disease is started on lisinopril for blood pressure control and renal protection. One week later, he returns with fatigue. Labs show: Serum potassium: 5.8 mEq/L (ref: 3.5–5.1 mEq/L) Serum creatinine increased from baseline Which of the following best explains this patient’s change in renal function?

Which оf the fоllоwing projections will best demonstrаte the olecrаnon process of the ulnа in profile?