IM8.{1-8,10-19} | Hypertension — Practice Quiz

Correct. ACC/AHA 2017 defines Stage 1 hypertension as systolic 130-139 mmHg or diastolic 80-89 mmHg. This patient has 135/85, which falls in Stage 1. Note: JNC 7 would classify this as prehypertension (120-139/80-89). Always specify which guideline you are citing when staging blood pressure.

ACC/AHA 2017: Normal <120/80; Elevated 120-129/<80; Stage 1 130-139/80-89; Stage 2 >=140/>=90. JNC 7: Normal <120/80; Prehypertension 120-139/80-89; Stage 1 140-159/90-99; Stage 2 >=160/>=100. Always state which classification system you are using.

ACC/AHA 2017 lowers the hypertension threshold compared with JNC 7. Stage 1 hypertension (ACC/AHA 2017) = systolic 130-139 OR diastolic 80-89 mmHg. JNC 7 would call 135/85 prehypertension, not hypertension. The patient's BP 135/85 meets ACC/AHA Stage 1 criteria.

Correct. This is a hypertensive emergency — severely elevated BP with acute end-organ damage (hypertensive retinopathy with papilloedema and acute kidney injury). IV antihypertensives are required. The target in most hypertensive emergencies is to reduce mean arterial pressure by no more than 20-25% in the first hour to avoid watershed ischaemia. Sublingual nifedipine causes unpredictable rapid drops and is contraindicated.

Hypertensive emergency = severe BP elevation + acute end-organ damage (encephalopathy, AKI, retinopathy with papilloedema, acute LVF, aortic dissection, eclampsia). Requires IV drugs and ICU. Target: reduce MAP by 20-25% in first hour; do not normalise BP acutely. Sublingual nifedipine is contraindicated — causes unpredictable precipitous drops.

Papilloedema, fundal haemorrhages, and a rising creatinine confirm hypertensive emergency — acute end-organ damage is present. This requires IV antihypertensives (labetalol, nitroprusside, or nicardipine) with controlled MAP reduction of 20-25% in the first hour, not rapid or oral treatment.

Correct. The triad of hypertension, hypokalaemia, and suppressed plasma renin with elevated aldosterone is the hallmark of primary hyperaldosteronism (Conn syndrome). Elevated aldosterone causes sodium and water retention (raising BP) and kalaemia wasting. The aldosterone-to-renin ratio is the screening test of choice. Renovascular HTN also suppresses renin but aldosterone is elevated secondarily — renin is not suppressed.

Primary hyperaldosteronism clues: hypertension + spontaneous hypokalaemia + suppressed plasma renin activity + elevated aldosterone. Screen with aldosterone-to-renin ratio (ARR >30 suggestive). Confirmed by saline suppression or fludrocortisone test. Causes: adrenal adenoma (unilateral, surgical cure) or bilateral hyperplasia (medical: spironolactone/eplerenone).

Hypokalaemia + hypertension + suppressed renin + high aldosterone = primary hyperaldosteronism. Renovascular HTN causes high renin and secondary high aldosterone. Cushing syndrome causes hypokalaemia but also hyperglycaemia and phenotypic features. Phaeochromocytoma causes episodic hypertension with normal or high renin.

Correct. ACE inhibitors and ARBs have a compelling indication in hypertension with diabetic nephropathy (proteinuria >300 mg/day or albumin-creatinine ratio >300 mg/g, or any CKD with proteinuria). They reduce intraglomerular pressure by dilating the efferent arteriole, independently slowing CKD progression beyond their BP-lowering effect. Do not combine ACE inhibitor with ARB — dual RAAS blockade increases adverse effects without additive renal benefit.

Compelling indications for specific drug classes: ACE inhibitor/ARB — heart failure, post-MI, diabetic nephropathy, CKD with proteinuria; beta-blocker — post-MI, heart failure with reduced EF, atrial fibrillation; CCB — isolated systolic hypertension in elderly, Raynaud phenomenon. Thiazides are first-line in uncomplicated HTN but not preferred first addition in CKD with proteinuria.

Diabetic nephropathy with significant albuminuria (ACR >300 mg/g here) is a compelling indication for RAAS blockade — ACE inhibitor or ARB. They reduce intraglomerular hypertension independently of systemic BP lowering and are the only class proven to slow CKD progression in this setting. Avoid dual ACE + ARB combination.

Correct. Elevated urinary metanephrines (or normetanephrines) biochemically confirm phaeochromocytoma. Anatomical localisation requires adrenal protocol MRI (preferred over CT because of radiation and the risk of contrast-induced catecholamine release), or 123I-MIBG scintigraphy for extraadrenal (paraganglioma) lesions. MIBG is especially useful for multiple or extraadrenal tumours.

Phaeochromocytoma: biochemical screen = 24-hour urine metanephrines/normetanephrines or plasma fractionated metanephrines. Localisation = adrenal MRI or MIBG scintigraphy (for ectopic). Pre-operative alpha-blockade is mandatory. 10% rule: 10% bilateral, 10% extraadrenal, 10% malignant, 10% in children.

Episodic hypertension + palpitations + sweating + elevated urinary metanephrines = phaeochromocytoma biochemically confirmed. Localisation = adrenal protocol MRI or 123I-MIBG scan. Always block alpha-adrenoceptors (phenoxybenzamine or doxazosin) BEFORE beta-blockade to prevent hypertensive crisis during preparation for surgery.

Correct. Standard triple therapy for uncontrolled hypertension is ACE inhibitor (or ARB) + CCB + thiazide-type diuretic. This is the evidence-based step-up from dual therapy. Chlorthalidone is preferred over hydrochlorothiazide in most guidelines because of its longer half-life and superior outcome data. Resistant hypertension is only defined when BP remains uncontrolled on three drugs at optimal doses including a diuretic.

Uncontrolled HTN on two agents: add thiazide diuretic (chlorthalidone preferred). Resistant HTN = uncontrolled on 3 drugs at optimal doses INCLUDING a diuretic; next step = check adherence, exclude secondary causes, add spironolactone (if potassium allows) or doxazosin. ASCOT-BPLA: ACE inhibitor + CCB superior to atenolol + thiazide in cardiovascular outcomes.

When BP is uncontrolled on two-drug therapy (ACE inhibitor + CCB at optimal doses), the evidence-based next step is to add a thiazide-type diuretic (chlorthalidone preferred) as the third agent. Resistant hypertension is defined as uncontrolled BP despite three drugs at optimal doses including a diuretic — this patient has not yet reached that threshold.

Correct. Renovascular hypertension is caused by reduced perfusion pressure distal to the stenosis, which activates the juxtaglomerular cells to release renin. Renin converts angiotensinogen to angiotensin I, which is converted to angiotensin II — a potent vasoconstrictor. Angiotensin II stimulates aldosterone release, causing sodium retention. This RAAS activation raises systemic BP. Plasma renin activity is high; aldosterone is elevated secondarily (unlike Conn syndrome where renin is suppressed).

Renovascular HTN: atherosclerotic (older men, ostial plaques) or fibromuscular dysplasia (young women, mid-renal artery beading). Screen with captopril-enhanced renal scintigraphy or renal Doppler. Plasma renin activity is high (unlike Conn where it is suppressed). ACE inhibitors are relatively contraindicated in bilateral RAS or solitary kidney RAS — can precipitate acute renal failure.

Renal artery stenosis reduces perfusion pressure to the ischaemic kidney. The juxtaglomerular apparatus responds by releasing excess renin, activating the RAAS — high renin, high angiotensin II (vasoconstriction), high aldosterone (sodium retention). This is the pathophysiology of renovascular (Goldblatt) hypertension.

Correct. Long-standing systemic hypertension causes pressure overload on the left ventricle, leading to concentric left ventricular hypertrophy (LVH) — wall thickening (>11 mm in women) with a normal or reduced cavity size. LVH causes diastolic dysfunction (impaired relaxation) even before systolic dysfunction appears. The result is heart failure with preserved ejection fraction (HFpEF, formerly diastolic heart failure). LVH on ECG (Sokolow-Lyon criteria) is also a marker of target organ damage.

Hypertensive target organ damage: Heart (LVH, diastolic dysfunction, HFpEF, CAD); Brain (lacunar infarcts, hypertensive encephalopathy, haemorrhagic stroke); Kidneys (nephrosclerosis, microalbuminuria, CKD); Retina (Keith-Wagener grades 1-4: arteriolar narrowing, AV nipping, flame haemorrhages, papilloedema); Vessels (aortic aneurysm, peripheral arterial disease). LVH regression with antihypertensive treatment is associated with CV risk reduction.

Concentric LVH + diastolic dysfunction + preserved EF from long-standing hypertension = hypertensive heart disease. LVH is the most important cardiac target organ damage marker. It independently increases risk of atrial fibrillation, sudden death, and heart failure. ECG detects LVH less sensitively than echocardiogram.

Correct. ACE inhibitors block the breakdown of bradykinin. Bradykinin accumulation in the airways causes a dry, irritating, non-productive cough in 10-15% of patients (higher rates in South Asian and East Asian populations — up to 30-40%). This is a class effect of all ACE inhibitors. The correct substitution is an ARB (e.g., losartan, telmisartan), which does not affect bradykinin metabolism and has equivalent BP-lowering efficacy without causing cough.

ACE inhibitor side effects: dry cough (10-15%, up to 30-40% in South Asians — switch to ARB); angioedema (rare, life-threatening — absolute contraindication to ACE inhibitor AND ARB); hyperkalaemia; acute kidney injury in bilateral RAS. ARB side effects: hyperkalaemia; no cough. Both ACE inhibitors and ARBs are contraindicated in pregnancy.

Dry, persistent, non-productive cough is the most common side effect of ACE inhibitors, caused by bradykinin accumulation. It is a class effect — switching to another ACE inhibitor does not help. Switch to an ARB, which blocks angiotensin II at its receptor without affecting bradykinin.

Correct. ACC/AHA 2017 recommends initiating pharmacological treatment for Stage 1 hypertension (130-139/80-89 mmHg) when the 10-year ASCVD risk is >=10%, or for ANY Stage 2 hypertension (>=140/>=90) regardless of risk. This patient has Stage 2 hypertension (152/98) AND high ASCVD risk (12%) — both criteria independently mandate immediate drug therapy alongside lifestyle modification.

ACC/AHA 2017 treatment thresholds: Stage 1 (130-139/80-89) + ASCVD risk <10%: lifestyle modification, reassess 3-6 months. Stage 1 + ASCVD risk >=10% or clinical CVD: start drugs + lifestyle. Stage 2 (>=140/>=90): start drugs + lifestyle regardless of ASCVD risk. Lifestyle benefits are quantified: DASH diet -11/-3 mmHg, sodium restriction -5/-3, weight loss 1 mmHg per kg, aerobic exercise -5/-3, alcohol moderation -4/-3.

ACC/AHA 2017: Stage 1 HTN + ASCVD risk <10% = lifestyle 3 months first; Stage 1 + ASCVD >=10% OR Stage 2 HTN = immediate drug therapy + lifestyle. This patient has Stage 2 HTN (152/98) — drug therapy is indicated now, not after a trial of lifestyle alone.