🩺 HYPERTENSION: A Complete Medical Teaching Guide

Based on Harrison's 22E (2025), Davidson, Comprehensive Clinical Nephrology 7e, Katzung Pharmacology 16e, Symptom to Diagnosis 4e, Park's Preventive Medicine + 2025 AHA/ACC & 2024 ESC Guidelines

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Quick-start for interns: Hypertension is the world's #1 cardiovascular risk factor. It is usually silent, discovered on routine BP measurement. Most patients need lifelong treatment. Your job is to diagnose it correctly, rule out secondary causes, protect target organs, and get BP to goal.

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1. DEFINITION

Simple language first:

The formal definition (Harrison's 22E):

"Hypertension is defined as the presence of blood pressure elevation to a level that places patients at increased risk for target organ damage in several vascular beds including the retina, brain, heart, kidneys, and large conduit arteries."

• Washington Manual of Medical Therapeutics

Clinical pearl: When systolic and diastolic fall in different categories, use the higher category.

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2. CAUSES & RISK FACTORS

Two big types: Primary vs Secondary

HYPERTENSION
    │
    ├── PRIMARY (Essential) = 90-95% of all cases
    │   ├── No single identifiable cause
    │   └── Results from interaction of genes + environment
    │
    └── SECONDARY = 5-10% of cases
        ├── Renal causes (most common secondary cause)
        ├── Endocrine causes
        ├── Vascular causes
        └── Drug-induced

Risk Factors for Primary (Essential) Hypertension

• Age - BP rises with age; systolic rises throughout life, diastolic rises until ~50s then plateaus
• Family history / Genetics - Strong hereditary component
• Race - Higher prevalence and severity in Black populations
• Sex - More common in men before 50; women "catch up" after menopause

• Obesity / Overweight - Increases cardiac output and insulin resistance
• High sodium intake - Increases fluid retention (not everyone is "salt-sensitive")
• Low potassium intake - Impairs vasodilation
• Physical inactivity - Reduces arterial compliance
• Excessive alcohol - Directly raises BP; >2 drinks/day is an independent risk
• Smoking - Acutely raises BP and damages endothelium
• Stress - Activates sympathetic nervous system
• Sleep apnea - Intermittent hypoxia → sympathetic activation
• Diabetes mellitus - Metabolic syndrome overlap

• NSAIDs (very common - >26% of US adults take them regularly)
• Oral contraceptive pills
• Corticosteroids
• Sympathomimetics (nasal decongestants, cocaine, amphetamines)
• Antidepressants (SNRIs, MAOIs)
• Angiogenesis inhibitors (oncology drugs)
• Caffeine (acute, short-term)
• Herbal: ephedra (Ma-Huang), ginseng, licorice, St. John's Wort

Causes of Secondary Hypertension

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3. CLASSIFICATION / TYPES

By aetiology:

1. Primary (Essential) - 90-95%
2. Secondary - 5-10%

By degree (ESC 2024 / JNC 7):

• Grades 1, 2, 3 (see table above)

Special patterns:

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4. RELEVANT ANATOMY & PHYSIOLOGY

The Basic Formula (know this deeply):

Blood Pressure = Cardiac Output × Peripheral Vascular Resistance
      BP        =      CO        ×         PVR

CO = Heart Rate × Stroke Volume
PVR = controlled by arteriolar tone (smooth muscle)

1. Pump more water through (↑ CO) - like tachycardia or fluid overload
2. Narrow the nozzle (↑ PVR) - like vasoconstriction

The Renal Pressure-Natriuresis System (Guyton model):

Key Vasoreactive Systems:

1. Renin-Angiotensin-Aldosterone System (RAAS):
   • Low BP → Kidney releases renin
   • Renin cleaves angiotensinogen → Angiotensin I
   • ACE converts Ang I → Angiotensin II (powerful vasoconstrictor)
   • Ang II stimulates aldosterone → Na/water retention
   • Net effect: ↑ BP
2. Sympathetic Nervous System (SNS):
   • Stress, pain, fear → ↑ catecholamines (norepinephrine)
   • Heart rate ↑, vasoconstriction, renal sodium retention
   • Long-term SNS activation = sustained hypertension
3. Nitric Oxide (NO) system:
   • Endothelial cells produce NO → vasodilation
   • In hypertension: endothelial dysfunction → less NO → vasoconstriction
4. Endothelin:
   • Potent endothelium-derived vasoconstrictor
   • Role in hypertension especially with CKD

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5. PATHOPHYSIOLOGY

Step-by-Step: Cause → Disease Process → Symptoms → Complications

GENETIC + ENVIRONMENTAL FACTORS
           ↓
    DISRUPTION OF NORMAL BP REGULATION:
    • Renal pressure-natriuresis reset
    • RAAS overactivation
    • Excess sympathetic tone
    • Endothelial dysfunction (↓ NO)
    • Altered vascular smooth muscle tone
           ↓
    SUSTAINED HIGH BLOOD PRESSURE
           ↓
    MECHANICAL + BIOCHEMICAL INJURY TO VESSELS
    • Shear stress → endothelial damage
    • Vascular remodeling (hypertrophy of arteriolar walls)
    • Accelerated atherosclerosis
    • Small vessel arteriosclerosis (hyaline change)
    • Fibrinoid necrosis (in severe/malignant HTN)
           ↓
TARGET ORGAN DAMAGE (TOD)
    ↙        ↓        ↓       ↓        ↘
  HEART    BRAIN   KIDNEYS  EYES    ARTERIES
  LVH     Lacunar  Nephro-  Retino-  Peripheral
  HF      infarcts  sclerosis pathy   arterial
  IHD     Stroke   CKD/ESRD          disease
  AF      Dementia

Why does blood pressure damage organs?

• High pressure = constant mechanical stress on vessel walls
• The inner lining (endothelium) gets damaged → triggers inflammation
• Smooth muscle cells in vessel walls hypertrophy (thicken) → lumen narrows
• Narrowed vessels → less blood to organs → ischaemia
• In the heart: ventricle pumps harder against resistance → left ventricular hypertrophy (LVH)
• In the kidney: glomerular hypertension → protein leaks into urine → nephron loss → CKD (a vicious cycle)

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6. CLINICAL FEATURES

"The Silent Killer" - Why Most Patients Have NO Symptoms:

1. End-organ damage (complications)
2. Severely elevated BP (hypertensive crisis)

Symptoms (when present):

Mnemonic for complications/symptoms: "HEADACHES"

• H - Heart (LVH, IHD, HF, AF)
• E - Eyes (retinopathy)
• A - Arteries (PAD, aortic dissection)
• D - Dementia
• A - Aorta
• C - CKD/renal failure
• H - Hypertensive crisis
• E - Encephalopathy
• S - Stroke

Signs on Physical Examination:

Keith-Wagener-Barker Classification of Hypertensive Retinopathy:

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7. HISTORY TAKING

Key Questions and Why They Matter:

• "How long have you had high blood pressure?"
• "Where was it first measured? Has it been measured more than once?" (Avoid single-reading diagnosis)
• "Do you check your BP at home?"

• "What was your last BP reading?"
• "Are you on any BP medications? Are you taking them regularly?"

• "Any headaches, especially in the morning?" (Cerebral)
• "Any chest pain, breathlessness, palpitations?" (Cardiac)
• "Any visual changes?" (Retinal)
• "Any leg swelling, reduced exercise tolerance?" (HF)
• "Any weakness, slurred speech, or transient visual loss?" (TIA/Stroke)
• "Any change in urine output or frothy urine?" (Renal)

• "Any weight gain, stretch marks, bruising easily?" (Cushing's)
• "Episodes of severe headache + palpitations + sweating that come and go?" (Phaeochromocytoma)
• "Do you snore loudly or feel sleepy during the day?" (OSA)
• "Any flank pain or blood in urine?" (Renal disease)
• "Do you feel cold, constipated, tired all the time?" (Hypothyroidism)

• NSAIDs (even OTC ibuprofen)
• OCP / HRT
• Nasal decongestants
• Herbal supplements
• Alcohol, cocaine, amphetamines

• Diabetes, dyslipidaemia, smoking, family history of HTN / heart disease / stroke
• Dietary sodium and potassium intake; exercise habits; stress levels

• Prior CVD events, CKD, diabetes

• Hypertension, premature CVD, renal disease, PKD (autosomal dominant)

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8. DIFFERENTIAL DIAGNOSIS

"Is this truly hypertension, and is there a secondary cause?"

"ABCDE" mnemonic for secondary causes:

• A = Aldosterone excess (primary aldosteronism), Apnoea (OSA)
• B = Bruits (renovascular), Bad kidney
• C = Catecholamines (phaeochromocytoma), Coarctation, Cushing
• D = Drugs, Diet
• E = Endocrine (thyroid, parathyroid)

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9. INVESTIGATIONS

Basic Tests (ALL hypertensive patients):

For Assessment of Cardiovascular Risk:

• 10-year ASCVD risk score (ACC/AHA Pooled Cohort Equations)
• Echocardiogram if LVH suspected on ECG or symptoms

Specific Tests (when secondary HTN suspected):

Imaging:

How to Interpret ABPM:

• Normal ABPM: Daytime <135/85, Nighttime <120/70, 24h <130/80
• Non-dipper pattern (nocturnal BP doesn't fall >10%): higher stroke/renal risk
• Night-time HTN: worse prognosis than daytime HTN

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10. DIAGNOSIS

Diagnostic Approach (Harrison's 22E + 2025 AHA/ACC):

• Patient seated, 5 min rest, no caffeine/smoking for 30 min
• Appropriate cuff size (too small = overestimates)
• Two readings, averaged, in each arm
• Use validated oscillometric device

• Diagnosis requires ≥2 elevated readings on ≥2 separate visits
• Exception: if BP >180/120 with TOD - single reading sufficient for urgent action

Special diagnostic situations:

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11. COMPLICATIONS

Organised by Target Organ: "BRAIN-HEART-KIDNEY-EYE-ARTERY"

The "Risk Multiplier" effect:

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12. RED FLAGS & EMERGENCIES

Hypertensive Urgency vs Emergency

Critical clinical pearl (Symptom to Diagnosis 4e): "A hypertensive emergency is defined by the presence of TOD, not by the degree of BP elevation." A normotensive pregnant woman with eclampsia can have a hypertensive emergency at 160/100 mmHg, while a chronic hypertensive may be asymptomatic at 220/130 mmHg.

Signs of Hypertensive Emergency (must not miss):

• Severe headache + vomiting + visual changes → Hypertensive encephalopathy / ICH
• Chest pain radiating to back → Aortic dissection (control BP very rapidly, SBP <120 in 20 min)
• Chest pain + ST changes → ACS with hypertension
• Acute breathlessness + pulmonary oedema → Acute LV failure
• Focal neurological deficit → Stroke (careful BP management - don't lower unless >185/110 if tPA candidate)
• Papilloedema + renal failure → Malignant/Accelerated hypertension
• Pregnancy + proteinuria → Pre-eclampsia / Eclampsia
• Paroxysmal HTN + triad of headache/palpitations/sweating → Phaeochromocytoma crisis
• Haematuria + AKI → Hypertensive nephropathy

Admission Criteria:

• Hypertensive emergency (any)
• New end-organ damage
• BP >220/120 with any symptoms
• Aortic dissection (emergency surgery)
• Eclampsia / severe pre-eclampsia
• Hypertensive encephalopathy

When to Refer:

• Suspected secondary hypertension
• Resistant hypertension (BP not controlled on 3+ drugs)
• Young patient (<30 years) with HTN
• Hypertension in pregnancy
• Significant CKD (eGFR <30) - nephrology
• LV dysfunction / HF - cardiology

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13. MANAGEMENT

Treatment Goals (2025 AHA/ACC + Harrison's 22E):

A. Non-Drug Treatment (Lifestyle Modifications - MANDATORY for ALL patients)

Important: Lifestyle modification is the ONLY treatment for Elevated BP (120-129/<80) and Stage 1 HTN with low CVD risk. Drug therapy is added when lifestyle alone fails after 3-6 months or when risk is high.

B. Drug Treatment - Overview

First-line drug classes (2025 AHA/ACC):

• Thiazide/thiazide-like diuretics (chlorthalidone preferred over HCTZ)
• Calcium Channel Blockers (CCBs) - amlodipine, nifedipine
• ACE Inhibitors (ACEi) - lisinopril, enalapril, ramipril
• Angiotensin Receptor Blockers (ARBs) - losartan, valsartan, olmesartan

Beta-blockers are NOT first-line for uncomplicated HTN (inferior to other classes for stroke prevention), but ARE first-line when there are compelling indications (heart failure, post-MI, angina, AF rate control).

Compelling Indications - Drug selection by comorbidity:

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14. PHARMACOLOGY OF IMPORTANT DRUGS

CLASS 1: THIAZIDE/THIAZIDE-LIKE DIURETICS

CLASS 2: ACE INHIBITORS (ACEi)

CLASS 3: ANGIOTENSIN RECEPTOR BLOCKERS (ARBs)

CLASS 4: CALCIUM CHANNEL BLOCKERS (CCBs)

Dihydropyridines (vascular selective - use for HTN):

Non-dihydropyridines (cardiac effects - use for rate control):

CLASS 5: BETA-BLOCKERS

CLASS 6: ALDOSTERONE ANTAGONISTS

CLASS 7: DIRECT VASODILATORS

CLASS 8: CENTRALLY ACTING AGENTS

IV Drugs for Hypertensive Emergency (Harrison's 22E):

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15. TREATMENT ALGORITHM

STEP-BY-STEP FLOWCHART:

ELEVATED BP MEASURED
         ↓
CONFIRM: ≥2 readings, ≥2 visits
(or ABPM if white coat suspected)
         ↓
CLASSIFY BP + CALCULATE 10-year ASCVD RISK
         ↓
┌─────────────────────┬──────────────────────┬────────────────────────┐
│  ELEVATED BP        │   STAGE 1 HTN        │   STAGE 2 HTN         │
│  (120-129/<80)      │   (130-139/80-89)    │   (≥140/≥90)          │
├─────────────────────┼──────────────────────┼────────────────────────┤
│  Lifestyle mod only │ LOW CVD RISK (<10%): │  DRUG THERAPY         │
│  No drugs           │  Lifestyle x 3-6 mo  │  +  lifestyle         │
│                     │ HIGH CVD RISK (≥10%):│  from day 1           │
│                     │  Drug + lifestyle    │                        │
│                     │  from start          │  If SBP ≥160: usually │
│                     │                      │  need 2 drugs          │
└─────────────────────┴──────────────────────┴────────────────────────┘
         ↓
FIRST-LINE DRUG CHOICES (pick based on comorbidity/ethnicity):
─────────────────────────────────────────────────────────
 No compelling indication:
   → Thiazide diuretic (chlorthalidone) OR CCB (amlodipine)
     OR ACEi (lisinopril) OR ARB (losartan)
   → Black patients: CCB + thiazide preferred over ACEi/ARB alone

 STEP 2 (if BP not at goal in 1 month):
   → Add second drug from a different class
   → Preferred: CCB + ACEi/ARB; or Thiazide + CCB; or Thiazide + ACEi/ARB
   → Avoid: ACEi + ARB (double RAAS = ↑ harm, minimal benefit)

 STEP 3 (Triple therapy - if still not at goal):
   → CCB + ACEi/ARB + Thiazide diuretic (the "optimal triple")

 STEP 4 (Resistant HTN - confirmed on ABPM):
   → Add SPIRONOLACTONE 25 mg
   → Review adherence, white coat effect, secondary cause
─────────────────────────────────────────────────────────
         ↓
TARGET: BP <130/80 mmHg (most patients)
         ↓
MONITORING: Every 1-3 months until goal achieved, then every 3-6 months
Recheck eGFR and electrolytes 2-4 weeks after starting ACEi/ARB/diuretic

Algorithm for HYPERTENSIVE EMERGENCY:

SEVERE HTN + SYMPTOMS / SIGNS OF TOD
              ↓
IMMEDIATE ASSESSMENT: ABCs, IV access, cardiac monitoring
              ↓
IDENTIFY TYPE OF EMERGENCY:
    Neurological ─────→ CT brain (exclude ICH); BP control with labetalol or nicardipine
    ACS ───────────────→ GTN IV; avoid labetalol if HF present
    Acute pulmonary oedema → GTN IV + loop diuretic
    Aortic dissection ────→ Esmolol IV + nitroprusside; target SBP <120 in 20 min
    Eclampsia ────────────→ Labetalol IV / hydralazine IV / MgSO4 for seizures
    Phaeochromocytoma ────→ Phentolamine IV (alpha-blocker FIRST, then beta-blocker)
              ↓
GOAL: Reduce MAP by ≤25% in first hour
Do NOT normalise BP rapidly (causes cerebral, renal, coronary ischaemia)
              ↓
ORAL AGENTS over next 24-48h, then outpatient follow-up

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16. REAL-WORLD CLINICAL APPROACH

OPD Approach:

1. Don't panic, don't label immediately. Ask: was the patient anxious? Had they just rushed to clinic? Get at least 2 readings after 5 min rest.
2. Take a systematic history (duration, symptoms, family history, drugs, lifestyle)
3. Examine both arms, fundoscopy, listen for bruits, check for signs of TOD
4. Basic tests first - urinalysis, creatinine, electrolytes, fasting glucose, lipids, ECG
5. Calculate CVD risk - this determines whether to start drugs with Stage 1
6. Lifestyle counselling - always, for every patient
7. Start drug therapy if indicated; start low, titrate up
8. Review in 4-6 weeks - check BP, side effects, labs
9. Adjust, combine, optimise until target BP reached
10. Address all CVD risk factors - statin, aspirin (only if established CVD), smoking cessation, glucose control

Emergency Approach (BP >180/120 in ED):

1. Rule out emergency first - symptoms? TOD on examination (focal neurology, pulmonary oedema, papilloedema)?
2. If urgency (no TOD): Oral amlodipine 5-10 mg or oral labetalol; aim for 25-33% reduction over 24h; outpatient follow-up in 1 week
3. If emergency (TOD present): IV access, monitoring, identify specific emergency type, select targeted IV agent, admit to ICU/HDU
4. Do NOT lower BP too fast - autoregulation is set at a high level in chronic hypertensives; rapid drop → watershed infarcts

Common Mistakes to Avoid:

Clinical Pearls:

• "A BP cuff that's too small for the arm will overestimate BP - always use the right cuff size."
• "Chlorthalidone beats HCTZ - same thiazide class, much better evidence and duration of action."
• "Spironolactone is the most effective 4th-line agent for resistant hypertension (PATHWAY-2 trial)."
• "The best antihypertensive is the one the patient will take. Complexity kills adherence."
• "In CKD, creatinine rising by up to 30% after starting ACEi is acceptable and expected - this is haemodynamic, not nephrotoxic."
• "In aortic dissection: treat with beta-blocker FIRST, then vasodilator. If you give vasodilator alone, reflex tachycardia increases shear stress on the aortic wall."
• "Masked hypertension carries as much CVD risk as sustained hypertension - don't be falsely reassured by a normal clinic BP."
• "The 'J-curve' (excessive BP lowering causing harm) is most relevant in patients with coronary artery disease - don't lower DBP below 60-65 mmHg."

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17. PRESCRIPTION EXAMPLES

Example 1: Stage 1 HTN, Low CVD Risk, No Comorbidities

Rx:
1. Lifestyle modifications: DASH diet, sodium restriction, weight reduction, 
   30 min aerobic exercise daily, limit alcohol, stop smoking
2. Review in 3 months
3. If BP still ≥130/80 → start pharmacotherapy

Example 2: Stage 2 HTN, 55-year-old non-Black patient, no compelling indications

Rx:
1. Tab. Amlodipine 5 mg once daily (morning)
2. Tab. Lisinopril 5 mg once daily (can uptitrate to 10-20 mg)
   (OR: Amlodipine 5mg + Chlorthalidone 12.5mg as combination tablet)
3. DASH diet, sodium restriction (<2.3 g/day), exercise
4. Recheck BP, serum creatinine, K+, urine ACR in 4 weeks
5. Uptitrate to Amlodipine 10 mg and/or Lisinopril 10-20 mg if target not met
6. If BP still uncontrolled → add Chlorthalidone 12.5-25 mg

Example 3: Stage 2 HTN + Diabetes + Proteinuria (Diabetic nephropathy)

Rx:
1. Tab. Lisinopril 10 mg once daily (renoprotective - FIRST LINE)
   (OR Losartan 50-100 mg if ACEi-intolerant)
2. Tab. Amlodipine 5 mg once daily if additional BP lowering needed
3. Monitor: creatinine, K+, urine ACR, BP every 4-8 weeks
4. Target BP: <130/80 mmHg
5. Target urine ACR: reduction of ≥30%

Example 4: Hypertensive Emergency - Hypertensive Encephalopathy

EMERGENCY ORDERS:
1. Admit to HDU / ICU
2. IV access x 2, cardiac monitor, continuous BP monitoring (intra-arterial if possible)
3. Inj. Nicardipine 5 mg/hr IV infusion (titrate up by 2.5 mg/hr every 5 min to max 15 mg/hr)
   OR Inj. Labetalol 20 mg IV bolus over 2 min, repeat every 10 min (max 300 mg)
   OR Inj. Sodium Nitroprusside 0.3-0.5 mcg/kg/min IV infusion
4. TARGET: Reduce MAP by ≤25% in first hour (NOT to normal)
5. Then oral agents over 24-48 hours
6. CT brain to rule out ICH, call neurology

Example 5: Pregnancy-related hypertension (not eclampsia)

Rx:
1. Tab. Labetalol 100 mg twice daily (uptitrate to 200 mg twice daily if needed)
   OR Tab. Nifedipine LA 30 mg once daily
   OR Tab. Methyldopa 250 mg twice daily (older but safe)
2. AVOID: ACEi, ARBs, direct renin inhibitors (teratogenic)
3. Refer to obstetrics-maternal medicine
4. Watch for pre-eclampsia: protein in urine, headache, visual disturbance, 
   abdominal pain, rising creatinine

Common Prescribing Errors:

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18. PREVENTION

Primary Prevention (preventing HTN from occurring):

Secondary Prevention (in diagnosed hypertensives, prevent complications):

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19. PROGNOSIS

Prognostic Factors:

Outcome data (Harrison's 22E):

• BP lowering reduces stroke by 35-40%
• Reduces MI by 20-25%
• Reduces HF by up to 50%
• Every 10 mmHg SBP reduction = ~13% reduction in major CV events
• An increase in SBP of 20 mmHg or DBP of 10 mmHg doubles mortality from heart disease or stroke

The "Rule of Halves" (still relevant globally):

• Of all hypertensives: only ~50% are aware
• Of those aware: only ~50% are on treatment
• Of those on treatment: only ~50% are well controlled
• This means only ~12.5% of all hypertensives globally are at target BP

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20. PATIENT COUNSELING

Key Messages to Give Patients (in simple language):

"Your blood pressure is like pressure in a water pipe. If the pressure is too high for too long, the pipes can burst or get blocked. In your body, those 'pipes' are your blood vessels - and when they get damaged, you can have a stroke, heart attack, kidney damage, or loss of vision."

"That's exactly what makes high blood pressure dangerous - it often has no symptoms until it's already caused serious damage. We call it the 'silent killer'. Feeling well doesn't mean your blood pressure is normal."

"These tablets don't cure hypertension - they control it, like glasses correct vision. You will likely need them long-term. Don't stop them just because you feel better - stopping abruptly can be dangerous."

"Medicines work better when you support them with a healthy lifestyle. If you cut your salt intake, lose some weight, and exercise regularly, you may be able to reduce your tablet dose over time."

"Measure your BP at home (mornings and evenings, 2-3 minutes after sitting quietly). Keep a diary. Bring it to every visit."

• Sudden severe headache (worst of life)
• Sudden weakness or numbness (one side)
• Sudden difficulty speaking or understanding speech
• Sudden blurred or loss of vision
• Chest pain or severe breathlessness
• "These symptoms with high BP are medical emergencies."

"Missing doses is the most common reason BP goes out of control. Try to link taking your tablet with a daily habit (breakfast, brushing teeth). Use a pill organiser if needed."

• A = Activity (exercise daily)
• B = Beverages (cut alcohol and caffeine)
• C = Cigarettes (stop completely)
• D = Diet (DASH diet - fruits, vegetables, low salt)
• E = Evaluation (regular BP monitoring and follow-up)

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SUMMARY TABLE: Quick Reference for Clinicians

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Key current evidence update (2025):

• The 2025 AHA/ACC Guideline [PMID: 40811516] confirms BP target <130/80 for most adults, with an emphasis on earlier intervention and combination therapy.
• The 2024 ESC Guidelines [PMID: 39210715] provide a slightly more conservative threshold (≥140/90 for initiating drug treatment) but converge on similar targets.
• Spironolactone remains the most effective add-on agent for resistant hypertension (PATHWAY-2 RCT evidence).
• Chlorthalidone is preferred over HCTZ as the thiazide diuretic of choice, given superior 24-hour BP coverage and outcomes data from landmark trials.
• Never use ACEi + ARB combination (ONTARGET trial showed no benefit, increased harm).

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What You Just Received

• Harrison's Principles of Internal Medicine 22e (2025) - definitions, physiology, pharmacology, treatment algorithms
• Comprehensive Clinical Nephrology 7e - classification, renal involvement, secondary causes
• Katzung Pharmacology 16e - drug mechanisms and side effects
• Symptom to Diagnosis 4e - emergency vs urgency distinction, clinical reasoning
• Park's Preventive & Social Medicine - ESC classification table, epidemiology
• 2025 AHA/ACC Guidelines [PMID: 40811516] and 2024 ESC Guidelines [PMID: 39210715] - most current evidence

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Most Important Things to Internalize

1. Hypertension is a clinical diagnosis confirmed by repeat measurements - never label a patient on one reading.
2. Target BP is <130/80 for most adults (2025 AHA/ACC standard).
3. First-line drugs: Thiazide (chlorthalidone) / CCB (amlodipine) / ACEi (lisinopril) / ARB (losartan) - pick based on comorbidities. Beta-blockers are NOT first-line for uncomplicated HTN.
4. Never combine ACEi + ARB - hyperkalaemia, AKI, no added benefit.
5. Hypertensive emergency = TOD present, not just a BP number. Reduce MAP by ≤25% in first hour.
6. ACEi/ARB are contraindicated in pregnancy - use labetalol, methyldopa, or nifedipine.
7. Always screen for secondary causes in young patients (<30) and resistant hypertension.