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

Correct. Subarachnoid haemorrhage with hypertensive emergency requires careful BP control. Current evidence (including the INTERACT2 trial context applied to SAH) supports targeting systolic BP <160 mmHg to reduce rebleeding risk, using IV agents (nicardipine, labetalol) with careful titration. Aggressive lowering risks cerebral ischaemia due to impaired autoregulation. Sublingual nifedipine is contraindicated for all hypertensive emergencies. Withholding all antihypertensives is incorrect when BP is severely elevated in SAH.

Hypertensive emergency + SAH: target systolic <160 mmHg with IV nicardipine or labetalol; avoid >25% MAP reduction. Nimodipine (oral) is given for vasospasm prevention — not for acute BP control. Contrast with ischaemic stroke: do not treat unless BP >220/120 (or >185/110 if thrombolysis planned).

In subarachnoid haemorrhage with hypertension, the goal is systolic <160 mmHg using IV agents (nicardipine or labetalol) with gradual titration. Avoid excessive BP reduction — cerebral autoregulation is impaired in SAH, and MAP drops >25% can cause ischaemia in vulnerable penumbra. Sublingual nifedipine and furosemide are inappropriate.

Correct. Resistant hypertension is defined as BP uncontrolled despite three optimised drugs including a diuretic. The first step after confirming adherence (confirmed here) and excluding pseudoresistance (white coat, poor measurement, high sodium intake — urine sodium 210 mmol = excess intake, but BP still uncontrolled) is to screen for secondary causes. Primary hyperaldosteronism is the MOST COMMON secondary cause of resistant hypertension, affecting 15-20% of resistant HTN patients. The aldosterone-to-renin ratio is the recommended first-line screening test.

Resistant HTN protocol: (1) Confirm adherence and correct measurement technique; (2) Check 24-hr urine sodium (high = non-adherence to salt restriction — dietary counselling); (3) Screen for secondary causes: ARR first (primary hyperaldosteronism), then renal Doppler (RAS), urine metanephrines (phaeochromocytoma), overnight 1mg dexamethasone suppression (Cushing). Spironolactone is most effective 4th-line drug for resistant HTN in non-hypokalaemic patients.

Resistant hypertension (uncontrolled BP on three optimised drugs including a diuretic) must trigger secondary cause screen. Primary hyperaldosteronism is the single most common cause of resistant hypertension (15-20%). Screen first with aldosterone-to-renin ratio (ARR). Other secondary causes — renal artery stenosis, phaeochromocytoma, Cushing — are less common but should be assessed if ARR is normal.

Correct. Severe pre-eclampsia (BP >=160/110 with proteinuria, OR BP >=140/90 with severe features such as thrombocytopaenia, worsening renal/liver function, or neurological symptoms) requires: magnesium sulphate for seizure prophylaxis (Pritchard or Zuspan regimen), IV labetalol or hydralazine for acute BP control (target <160/105 to prevent maternal cerebrovascular accident), and planning for expedited delivery — the only cure. ACE inhibitors are absolutely contraindicated in pregnancy.

Hypertensive emergencies in pregnancy: pre-eclampsia (>20 weeks, HTN + proteinuria) vs eclampsia (with seizures) vs HELLP (haemolysis, elevated liver enzymes, low platelets). Treatment: MgSO4 (seizure prophylaxis and treatment), IV labetalol or hydralazine for acute BP control, oral nifedipine for maintenance. ACE inhibitors and ARBs are absolutely contraindicated in pregnancy. Delivery is the definitive treatment.

Severe pre-eclampsia with worsening features (thrombocytopaenia, rising uric acid, neurological symptoms) requires: magnesium sulphate (seizure prophylaxis), IV antihypertensives (labetalol or hydralazine — not ACE inhibitors, which are contraindicated in pregnancy), and delivery planning. Outpatient management is inappropriate with these features.

Correct. This is a hypertensive urgency — severely elevated BP (>=180/120) WITHOUT acute end-organ damage. Grade 2 retinopathy and mild LVH are CHRONIC changes, not acute end-organ damage. Creatinine is normal. There is no encephalopathy, no acute renal impairment, no pulmonary oedema, and no fundal haemorrhages or papilloedema. Management is oral antihypertensives with BP reduction over 24-48 hours. Sublingual captopril is inappropriate in any setting — the drop is unpredictable and can cause cerebral/coronary ischaemia.

Urgency vs Emergency: BP >=180/120 ALONE = urgency. BP >=180/120 + acute end-organ damage (encephalopathy, SAH/ICH, AKI, acute LVF/pulmonary oedema, aortic dissection, eclampsia, papilloedema) = emergency. Urgency: oral drugs, 24-48 hour reduction target. Emergency: IV drugs, ICU, 20-25% MAP reduction in first hour. Grade 1-2 retinopathy and LVH are chronic TOD, not acute emergency criteria.

Hypertensive urgency = severe BP elevation WITHOUT acute end-organ damage. Grade 2 retinopathy and LVH are chronic — not acute. Creatinine is normal. Treatment = oral antihypertensives, BP reduction over 24-48 hours, close outpatient follow-up. IV drugs and ICU are for hypertensive EMERGENCY (with acute end-organ damage). Sublingual captopril is never appropriate.

Correct. In significant unilateral renal artery stenosis, the ischaemic kidney maintains GFR by efferent arteriolar constriction driven by angiotensin II. ACE inhibitors and ARBs block angiotensin II, dilate the efferent arteriole, and can precipitate acute renal failure in the stenotic kidney. While contraindicated with absolute confidence in bilateral RAS or RAS in a solitary kidney, they must be used with extreme caution (if at all) in severe unilateral RAS with contralateral renal disease or risk. This patient has worsening renal function suggesting haemodynamically significant stenosis.

Renovascular HTN and ACE inhibitor risk: bilateral RAS = absolute contraindication; unilateral RAS (especially with contralateral dysfunction) = relative contraindication; use with caution and monitor creatinine/potassium at 1-2 weeks after starting. >30% creatinine rise = stop the drug. First-line in RAS: CCB (amlodipine). Revascularisation (angioplasty ± stent) for haemodynamically significant RAS with deteriorating renal function.

In significant renal artery stenosis, the ischaemic kidney depends on angiotensin II-mediated efferent arteriolar constriction to maintain GFR. ACE inhibitors or ARBs abolish this mechanism, precipitating acute-on-chronic kidney injury. Calcium channel blockers are safe and preferred. Beta-blockers are also safe. Monitor creatinine carefully if ACE/ARB used at all.

Correct. Dihydropyridine calcium channel blockers (amlodipine, nifedipine) cause selective precapillary arteriolar dilation without equivalent postcapillary venular dilation. This raises capillary hydrostatic pressure in dependent limbs, forcing fluid into interstitial tissues — a pharmacodynamic, not a cardiac or renal, mechanism. Cardiac failure is excluded by normal JVP and echo. Oedema from CCBs is typically positional, worse at the end of the day. Management: switch to ACE inhibitor or ARB, or add ACE inhibitor (also reduces CCB-induced oedema synergistically).

CCB-induced ankle oedema: class effect of dihydropyridines (amlodipine, nifedipine, felodipine); not heart failure; not fluid retention. Management: adding RAAS blocker reduces it (venoconstriction partially corrects the imbalance); alternatively switch to non-dihydropyridine CCB (diltiazem, verapamil) — but non-DHP CCBs are negative chronotropes and contraindicated with beta-blockers. Isolated systolic HTN in elderly: CCB or thiazide preferred (SHEP, Syst-Eur trials).

Dihydropyridine CCB oedema is not due to heart failure or renal retention — it is a direct vascular pharmacodynamic effect: precapillary dilation without postcapillary dilation increases capillary hydrostatic pressure, causing dependent oedema. It is not a sign of drug toxicity or therapy failure. Adding an ACE inhibitor/ARB can reduce CCB-associated oedema.

Correct. Sokolow-Lyon criteria for LVH: SV1 + RV5 (or RV6, whichever is larger) > 35 mm. Here: 28 + 22 = 50 mm, satisfying criteria. QRS duration 88 ms rules out bundle branch block (>120 ms). LVH on ECG is a marker of hypertensive cardiac target organ damage and is associated with increased risk of arrhythmias, sudden cardiac death, heart failure, and coronary events. ECG LVH has ~50% sensitivity but high specificity; echocardiogram is more sensitive. Cornell voltage criteria (RAVL + SV3 >20 mm in women or >28 mm in men) are an alternative.

ECG LVH criteria: Sokolow-Lyon (SV1 + RV5/6 >35 mm); Cornell voltage (RAVL + SV3 >28 mm men, >20 mm women); Cornell product (Cornell voltage × QRS duration >2440 mm.ms). Associated ECG changes: strain pattern = ST depression + T inversion in lateral leads (V5, V6, I, aVL) indicating pressure overload. ECG has ~50% sensitivity but high specificity for anatomical LVH. Echo is gold standard.

Sokolow-Lyon criterion: SV1 + RV5 > 35 mm = LVH. Normal QRS duration (88 ms) excludes bundle branch block. LVH on ECG signifies hypertensive cardiac target organ damage. ECG sensitivity for LVH is ~50%; echo is more sensitive. LVH regression with treatment is a surrogate for reduced cardiovascular risk.

Correct. The four lifestyle modifications with the highest evidence-based quantified BP-lowering effects are: DASH diet (rich in fruits, vegetables, low-fat dairy, reduced saturated fat — reduces BP 8-14 mmHg systolic); sodium restriction to <2.3 g/day (reduces BP 2-8 mmHg); aerobic physical activity 30+ minutes most days (reduces BP 4-9 mmHg); weight reduction of 10 kg (reduces BP 5-20 mmHg). These effects are additive. Smoking cessation is essential for cardiovascular risk reduction but does not reliably lower BP.

Lifestyle BP-lowering (approximate systolic reductions): DASH diet -8 to -14 mmHg; sodium <2.3g/day -2 to -8 mmHg; alcohol moderation -2 to -4 mmHg; aerobic exercise -4 to -9 mmHg; weight loss -5 to -20 mmHg per 10 kg. Potassium-rich diet (fruits, vegetables) additively lowers BP. These interventions are the foundation for all stages of hypertension management and can delay or eliminate need for pharmacotherapy in Stage 1 low-risk HTN.

The four evidence-based lifestyle interventions with quantified BP benefit are: DASH diet (-8 to -14 mmHg systolic), sodium restriction (<2.3 g/day, -2 to -8 mmHg), aerobic exercise (-4 to -9 mmHg), and weight loss (-5 to -20 mmHg per 10 kg lost). These are additive. Smoking cessation reduces overall CV risk enormously but does not directly lower BP.

Correct. Malignant hypertension (accelerated-phase hypertension) is defined by severely elevated BP with bilateral papilloedema (grade 4 retinopathy) and acute end-organ damage — specifically acute microangiopathic injury to the kidneys (granular casts, acute rise in creatinine) and brain (encephalopathy, confusion). This is not mere urgency (which by definition has no acute end-organ damage). Hypertensive encephalopathy is a subset of malignant HTN. The syndrome requires immediate IV antihypertensive therapy in ICU, with urgent renal protection.

Malignant hypertension: severe HTN + papilloedema (retinal grade 4) + microangiopathic haemolytic anaemia + AKI (fibrinoid necrosis of arterioles). Labs: thrombocytopaenia, haemolysis, rising creatinine, urinary granular/red cell casts. Treatment: ICU, IV labetalol or nitroprusside, target MAP reduction 20-25% in first hour. Renal prognosis depends on speed of BP control. Distinguish from TTP/HUS (also microangiopathic but not primarily HTN-driven).

Malignant (accelerated) hypertension = severely elevated BP + papilloedema (Keith-Wagener grade 4) + microangiopathic end-organ damage (AKI with casts, encephalopathy). It is a medical emergency requiring IV antihypertensives with careful titration. Untreated, 90% 1-year mortality. With treatment, prognosis has improved dramatically. Distinguish from urgency (no acute end-organ damage).

Correct. Obstructive sleep apnoea (OSA) is one of the most common reversible causes of secondary and treatment-resistant hypertension. Classic features — overweight middle-aged man, loud snoring, witnessed apnoeic episodes, morning headaches, daytime somnolence (Epworth score >=10 is significant) — strongly suggest OSA. OSA causes intermittent nocturnal hypoxia, sympathetic surges, and loss of normal nocturnal BP dipping, resulting in sustained hypertension. Polysomnography (sleep study) confirms the diagnosis. CPAP therapy reduces BP, particularly nocturnal BP.

OSA and hypertension: OSA present in up to 30% of hypertensive patients, 80% of resistant HTN patients. Mechanism: repetitive hypoxia → chemoreflex activation → sympathetic surges → sustained HTN + loss of nocturnal dipping. Diagnosis: polysomnography (AHI >=15/hr moderate-severe OSA). Treatment: CPAP reduces BP 2-10 mmHg, particularly nocturnal. Screen all resistant HTN patients with Epworth and clinical history.

Overweight man + snoring + witnessed apnoea + morning headaches + daytime sleepiness (Epworth >=10) = classic OSA presentation. OSA is a common reversible secondary cause of hypertension (especially resistant HTN). Nocturnal sympathetic surges and intermittent hypoxia sustain daytime BP elevation. Confirm with polysomnography; treat with CPAP.

Correct. Takayasu arteritis (pulseless disease) typically affects young women (age <40), causing granulomatous inflammation of the aorta and its major branches. Hallmarks include: unequal upper limb pulses or absent pulses (right arm unrecordable), BP discrepancy between arms >10 mmHg (which is actually the measured BP difference here), abdominal bruit from aortic/visceral involvement, and radiofemoral delay from aortic involvement. It is distinct from coarctation (which causes radiofemoral delay but bilateral arm hypertension) and from fibromuscular dysplasia (typically mid-renal artery, no limb pulse discrepancy).

Secondary HTN in young women: fibromuscular dysplasia (RAS, flank bruit, high renin) vs Takayasu arteritis (pulseless disease, unequal arm BPs, elevated ESR/CRP, aortic and branch vessel involvement on CT/MR angiography). Coarctation: radiofemoral delay, rib notching on CXR, equal arm BP. Phaeochromocytoma: paroxysmal symptoms, elevated urine metanephrines. These diagnoses are rare but yield in young hypertensives without family history.

Young woman + absent right arm pulse + asymmetric upper limb BP + abdominal bruit + radiofemoral delay = Takayasu arteritis. Coarctation causes equal arm BPs but radiofemoral delay. Renal artery FMD causes unilateral flank bruit but not limb pulse asymmetry. In Takayasu, measured BP is unreliable — toe-to-brachial index or imaging (CT angiography) guides assessment.

Correct. Hypertensive nephrosclerosis with CKD G3a and microalbuminuria requires: (1) BP target <130/80 mmHg (ACC/AHA, KDIGO); (2) RAAS blockade (ACE inhibitor or ARB) to reduce intraglomerular hypertension and proteinuria — even at low-grade albuminuria, RAAS blockers slow CKD progression; (3) Annual monitoring of eGFR and ACR. Dialysis is not the immediate priority (eGFR 55). ACE inhibitors are not contraindicated in CKD — they are the preferred agents. A transient 10-30% rise in creatinine on initiation is expected and acceptable (efferent arteriolar dilation reduces GFR slightly but is renoprotective long-term).

Hypertensive nephropathy and RAAS blockade: ACE inhibitors/ARBs reduce intraglomerular hypertension and proteinuria in CKD — renoprotective independent of BP. Acceptable creatinine rise on initiation: up to 30% (efferent vasodilation effect). Discontinue if rise >30%. BP target in CKD with albuminuria: <130/80 mmHg. Monitor potassium (risk of hyperkalaemia, especially with eGFR <45 or K >4.5). KDIGO 2021: RAAS blocker recommended for CKD with albuminuria regardless of diabetic status.

CKD G3a with microalbuminuria from hypertensive nephrosclerosis: BP target <130/80; RAAS blocker (ACE inhibitor or ARB) to reduce intraglomerular pressure even with low-grade albuminuria. A 10-30% creatinine rise on ACE inhibitor initiation is expected — only stop if rise >30%. Annual ACR and eGFR monitoring. This patient is NOT near dialysis (eGFR 55).