hypertension and fever case viva questions
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Now I have enough information from the medical library to compile a thorough viva question-and-answer guide. Here it is:
Hypertension & Fever - Viva Questions & Answers
SECTION 1: HYPERTENSION
Basic Definitions & Classification
Q1. How is blood pressure classified in adults?
(ACC/AHA 2017 Guidelines - Fuster and Hurst's The Heart, 15th Ed)
| Category | SBP | DBP |
|---|---|---|
| Normal | <120 mmHg | and <80 mmHg |
| Elevated | 120-129 mmHg | and <80 mmHg |
| Stage 1 HTN | 130-139 mmHg | or 80-89 mmHg |
| Stage 2 HTN | ≥140 mmHg | or ≥90 mmHg |
In children <13 years, BP is classified using age-adjusted percentiles. Normal = <90th percentile.
Q2. What is the definition of hypertension in children?
- Children 1-12 years: ≥95th percentile (Stage 1) or ≥95th percentile + 12 mmHg (Stage 2)
- Children ≥13 years: same as adult criteria (130/80 mmHg)
Q3. What is the difference between primary and secondary hypertension?
- Primary (essential) hypertension: No identifiable cause; accounts for ~90-95% of cases. Family history, obesity, and lifestyle factors are major contributors.
- Secondary hypertension: Due to a specific identifiable cause (~5-10% of cases).
Q4. What are the causes of secondary hypertension?
(Symptom to Diagnosis, 4th Ed; Robbins & Kumar Pathologic Basis of Disease)
| Category | Causes |
|---|---|
| Endocrine | Primary hyperaldosteronism, pheochromocytoma, thyroid disease, hyperparathyroidism, Cushing syndrome |
| Renal | CKD, acute kidney injury |
| Vascular | Renovascular disease (renal artery stenosis), coarctation of the aorta |
| Pulmonary | Obstructive sleep apnea |
| GI/Metabolic | Obesity |
| Drug-induced | NSAIDs, COX-2 inhibitors, corticosteroids, OCPs, cocaine, alcohol, sympathomimetics, cyclosporine, tacrolimus, erythropoietin, amphetamines |
Q5. What clues suggest secondary hypertension?
- Young age at onset (<30 years)
- Resistant to 3 or more drugs
- Sudden onset or worsening of previously controlled HTN
- Hypokalemia (suggests primary hyperaldosteronism)
- Episodic headache, sweating, palpitations (pheochromocytoma triad)
- Abdominal bruit (renal artery stenosis)
- Truncal obesity, striae, moon face (Cushing's)
Pathophysiology
Q6. What is the RAAS and its role in hypertension?
Renin (from juxtaglomerular cells) converts angiotensinogen to angiotensin I → ACE converts it to angiotensin II → causes vasoconstriction + aldosterone release → sodium and water retention → increased BP.
Q7. What is the role of the sympathetic nervous system in hypertension?
Increased sympathetic activity raises heart rate, cardiac output, and peripheral vascular resistance. It also stimulates renin release from kidneys. This is why beta-blockers and alpha-blockers are used as antihypertensives.
Complications / Target Organ Damage
Q8. What are the target organ damages in hypertension?
| Organ | Damage |
|---|---|
| Heart | LVH, coronary artery disease, heart failure, arrhythmias |
| Brain | Stroke (hemorrhagic or ischemic), hypertensive encephalopathy, TIA |
| Kidney | Nephrosclerosis, CKD, proteinuria |
| Eyes | Hypertensive retinopathy (AV nicking, flame hemorrhages, papilledema) |
| Aorta | Aortic dissection, aneurysm |
Q9. What is a hypertensive emergency vs. urgency?
(Fuster and Hurst's The Heart, 15th Ed)
- Hypertensive urgency: BP >180/120 mmHg WITHOUT acute target organ damage. Treat with oral agents, gradual reduction over 24-48 hours.
- Hypertensive emergency: BP >180/120 mmHg WITH evidence of acute target organ damage (e.g., AKI, stroke, aortic dissection, pulmonary edema, hypertensive encephalopathy). Requires IV therapy with controlled BP reduction (max 25% in first hour).
Q10. What are the triggers of hypertensive emergencies?
- Withdrawal of antihypertensives (especially clonidine)
- Pain
- Sympathomimetics (cocaine, amphetamines)
- Pheochromocytoma with adrenergic storm
- Severe autonomic dysfunction
- Preeclampsia/eclampsia in women
Treatment
Q11. What are the 5 main classes of antihypertensive drugs?
(Katzung's Basic & Clinical Pharmacology, 16th Ed; Goodman & Gilman's)
- ACE inhibitors (e.g., enalapril, lisinopril) - block angiotensin II formation
- Angiotensin Receptor Blockers (ARBs) (e.g., losartan) - block AT1 receptor
- Calcium Channel Blockers (CCBs) (e.g., amlodipine) - vasodilation
- Thiazide diuretics (e.g., hydrochlorothiazide, chlorthalidone) - reduce volume
- Beta-blockers (e.g., metoprolol, atenolol) - reduce HR and CO
Q12. What is the preferred first-line regimen?
- For most patients: ACE inhibitor/ARB or CCB or thiazide diuretic
- If 3 drugs needed: combine diuretic + ACE-I/ARB + CCB
- If 4th drug needed: add mineralocorticoid receptor antagonist (spironolactone)
- ACE-I and ARB should NOT be combined (risk of hyperkalemia and AKI)
Q13. What is resistant hypertension?
BP that remains above goal despite 3 optimally dosed antihypertensives of different classes, including a diuretic. "Refractory HTN" = uncontrolled on 5+ agents including a thiazide-like diuretic and mineralocorticoid antagonist.
Q14. What is pseudoresistance?
Falsely elevated BP due to: white coat HTN, improper measurement technique, medication non-adherence, clinician inertia/undertreatment.
Q15. What BP target is recommended?
- General adults: <130/80 mmHg (ACC/AHA 2017)
- CKD with proteinuria: <130/80 mmHg
- Elderly (>65 years): SBP <130 mmHg if tolerated (per SPRINT trial showing benefit of intensive target ~121 mmHg SBP)
SECTION 2: FEVER
Definition & Mechanism
Q16. How is fever defined?
Fever = elevation of body temperature, usually by 1-4°C above normal (normal oral ~37°C / 98.6°F). Rectal >38°C (100.4°F) is commonly used clinically.
Q17. What is the mechanism of fever?
(Robbins & Kumar Basic Pathology)
- Exogenous pyrogens (e.g., bacterial LPS) or endogenous stimuli activate leukocytes
- Leukocytes release endogenous pyrogens: IL-1, TNF, IL-6
- These cytokines upregulate PGE2 synthesis in vascular and perivascular cells of the hypothalamus
- PGE2 acts on the preoptic nucleus of the hypothalamus → raises the thermoregulatory set point
- Body generates and conserves heat (shivering, vasoconstriction) to reach new set point
Q18. How do antipyretics work?
NSAIDs (including aspirin, paracetamol) inhibit cyclooxygenase (COX) → block prostaglandin synthesis → lower the hypothalamic set point → fever reduces.
Q19. What are exogenous vs. endogenous pyrogens?
| Type | Examples |
|---|---|
| Exogenous | Bacterial LPS (endotoxin), viral antigens, fungal cell wall components, drugs |
| Endogenous | IL-1, IL-6, TNF-alpha, interferon-gamma |
Q20. What is the difference between fever, hyperthermia, and hyperpyrexia?
| Term | Definition |
|---|---|
| Fever | Elevated set point due to pyrogens; body regulates to higher temp |
| Hyperthermia | Body temp exceeds thermoregulatory capacity (e.g., heat stroke, malignant hyperthermia) - set point is NORMAL |
| Hyperpyrexia | Fever >41.5°C (106.7°F) - indicates severe, dangerous fever (CNS hemorrhage, sepsis, heat stroke) |
Q21. What are the systemic effects of inflammation/fever?
(Robbins & Kumar Basic Pathology)
- Fever (IL-1, TNF, PGE2 mediated)
- Leukocytosis - WBC 15,000-20,000/μL; shift to the left (increased band cells); extreme elevations (40,000-100,000) = leukemoid reaction
- Acute phase proteins - CRP, fibrinogen, serum amyloid A (SAA) increased; albumin decreased
- Anorexia, somnolence, malaise
Causes of Fever
Q22. What are the common causes of fever?
| Category | Examples |
|---|---|
| Infectious | Bacterial (pneumonia, UTI, TB, sepsis), viral (influenza, COVID-19, dengue), parasitic (malaria), fungal |
| Inflammatory/Autoimmune | SLE, rheumatoid arthritis, vasculitis, adult-onset Still's disease |
| Neoplastic | Lymphoma, leukemia, renal cell carcinoma, hepatocellular carcinoma |
| Drug fever | Penicillins, cephalosporins, phenytoin, allopurinol |
| Miscellaneous | DVT/PE, tissue necrosis (MI, surgery), transfusion reaction |
Q23. What is Fever of Unknown Origin (FUO)?
Classic definition (Petersdorf & Beeson):
- Temperature >38.3°C (101°F) on multiple occasions
- Duration >3 weeks
- No diagnosis after 1 week of intensive inpatient investigation
Categories of FUO: Infections (~30%), Neoplasms (~20%), Autoimmune/inflammatory (~20%), Miscellaneous (~15%), Undiagnosed (~15%)
Q24. What is the workup for FUO?
- Detailed history and physical (travel, animal exposure, medications, family history)
- CBC with differential, ESR, CRP
- Blood cultures x3, urine culture
- LFTs, ANA, RF, ANCA
- CXR, CT chest/abdomen/pelvis
- Bone marrow biopsy if lymphoma suspected
- PET scan if no diagnosis after initial workup
Important Viva Points - Hypertension + Fever Together
Q25. What conditions cause BOTH hypertension and fever?
| Condition | Mechanism |
|---|---|
| Pheochromocytoma | Catecholamine surge → episodic severe HTN + diaphoresis + fever |
| Hypertensive encephalopathy | BP crisis can include fever, headache, altered sensorium |
| Preeclampsia/Eclampsia | HTN + fever may signal HELLP syndrome or infection |
| Vasculitis (e.g., polyarteritis nodosa) | Systemic inflammation causing HTN (renal) + fever |
| Malignant hypertension | May present with fever due to end-organ ischemia |
| Drug withdrawal (e.g., clonidine) | Rebound HTN + fever-like sympathetic storm |
| Sepsis | Can cause fever + hypertension before progressing to shock |
Q26. A patient presents with hypertension, fever, headache, and confusion - what is your differential?
- Hypertensive encephalopathy
- Meningitis/encephalitis (fever + HTN from intracranial pressure)
- Pheochromocytoma crisis
- Subarachnoid hemorrhage (sudden severe headache + HTN + fever)
- Posterior reversible encephalopathy syndrome (PRES) associated with severe HTN
Q27. How does NSAIDs use relate to hypertension?
NSAIDs are a well-documented cause of secondary or drug-induced hypertension. They inhibit prostaglandin synthesis → cause sodium and water retention → increased BP. They also blunt the effect of most antihypertensives (except CCBs). This is clinically important when NSAIDs are given for fever in a hypertensive patient.
Q28. What antipyretic is preferred in hypertensive patients?
Paracetamol (acetaminophen) is the preferred antipyretic. NSAIDs (including aspirin and ibuprofen) can raise BP and antagonize antihypertensive drugs, so they should be used with caution or avoided in hypertensive patients.
Quick Recall Summary
| Topic | Key Fact |
|---|---|
| HTN definition (adults) | ≥130/80 (Stage 1), ≥140/90 (Stage 2) per ACC/AHA 2017 |
| Most common type | Primary/essential (~90-95%) |
| Most common secondary cause | Renovascular disease / renal parenchymal disease |
| First-line drugs | ACE-I/ARB, CCB, thiazide diuretic |
| HTN emergency IV drug | Labetalol, nicardipine, nitroprusside (aortic dissection: target SBP <120 in 20 min) |
| Fever mechanism | Pyrogens → IL-1/TNF → PGE2 → hypothalamic set point raised |
| FUO definition | >38.3°C for >3 weeks, undiagnosed after 1 week investigation |
| NSAIDs and HTN | Raise BP; blunt antihypertensives; use paracetamol instead |
| Both HTN + fever | Think pheochromocytoma, vasculitis, HELLP, meningitis, PRES |
Sources: Fuster and Hurst's The Heart 15th Ed; Symptom to Diagnosis 4th Ed; Robbins & Kumar Basic Pathology; Katzung's Basic & Clinical Pharmacology 16th Ed; Goodman & Gilman's Pharmacological Basis of Therapeutics; Campbell-Walsh-Wein Urology; Robbins Cotran Kumar Pathologic Basis of Disease
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