# Clinical Cases: Hypertension

## Case 1: Hypertensive Emergency with End-Organ Damage

### Clinical Image
![Hypertensive Retinopathy](case_01_image.jpg)
*Source: [Wikimedia Commons - Hypertensive retinopathy](https://commons.wikimedia.org/wiki/File:Hypertensive_retinopathy.jpg) - CC BY-SA 3.0*

### Patient Presentation
A 52-year-old man is brought to the emergency department by his wife after he developed a severe headache, blurred vision, and confusion over the past 6 hours. He was diagnosed with hypertension 5 years ago but stopped taking his medications 8 months ago because he "felt fine." He has not seen a doctor since then.

### Demographics
- Age: 52 years
- Sex: Male
- Past Medical History: Hypertension (untreated for 8 months), hyperlipidemia
- Medications: None (non-adherent)
- Social History: Occasional alcohol, no smoking

### Chief Complaint
Severe headache, visual changes, and confusion

### Physical Examination
- Blood pressure: 248/142 mmHg (repeated, confirmed in both arms)
- Heart rate: 102 bpm
- Temperature: 37.1°C
- Respiratory rate: 22/min
- Oxygen saturation: 96% on room air
- General: Appears distressed, confused, oriented to person only
- Cardiovascular: S4 gallop, laterally displaced PMI, grade 2/6 systolic murmur
- Respiratory: Bibasilar crackles
- Neurological: No focal deficits, confusion
- Fundoscopy: Grade IV hypertensive retinopathy - bilateral papilledema, flame hemorrhages, cotton-wool spots, arteriovenous nicking

### Workup
- Basic metabolic panel: Creatinine 2.8 mg/dL (elevated from baseline 1.0)
- Urinalysis: 3+ protein, RBC casts (suggests glomerular injury)
- Troponin: Mildly elevated
- BNP: 890 pg/mL (heart failure)
- ECG: Left ventricular hypertrophy with strain pattern, sinus tachycardia
- Chest X-ray: Cardiomegaly, pulmonary vascular congestion
- CT head: No acute intracranial hemorrhage or infarct
- Echocardiography: LVH with diastolic dysfunction, EF 45%

### Diagnosis
Hypertensive Emergency with:
- Hypertensive encephalopathy
- Acute kidney injury (hypertensive nephrosclerosis)
- Acute heart failure
- Grade IV hypertensive retinopathy

### Treatment
1. **ICU admission** with continuous blood pressure monitoring
2. **IV antihypertensive therapy**:
   - Nicardipine infusion (titratable, predictable)
   - Target: Reduce MAP by 20-25% in first hour, then gradually to 160/100 over 2-6 hours
3. **Avoid rapid BP reduction** (risk of watershed infarcts)
4. Loop diuretic for pulmonary congestion if needed
5. Hold nephrotoxic agents; monitor renal function
6. Transition to oral antihypertensives when stable
7. Long-term: Multi-drug regimen, adherence counseling, address barriers to care

### Physiological Principles Demonstrated
- **Hypertensive emergency definition**: Severely elevated BP with acute end-organ damage (brain, heart, kidneys, eyes) - this distinguishes emergency from urgency.
- **Autoregulation failure**: Normally, cerebral blood flow is autoregulated across a range of pressures. In hypertensive encephalopathy, pressure exceeds the upper limit of autoregulation, causing hyperperfusion, blood-brain barrier breakdown, and cerebral edema.
- **Gradual BP reduction**: The autoregulatory curve shifts rightward in chronic hypertension. Rapid normalization of BP can cause watershed ischemia because the brain cannot autoregulate at "normal" pressures.
- **End-organ vulnerability**: The brain, heart, kidneys, and eyes are particularly vulnerable to hypertensive damage due to their high metabolic demands and microvascular architecture.

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## Case 2: Primary Aldosteronism - Secondary Hypertension

### Clinical Image
![Primary Aldosteronism CT](case_01_image.jpg)
*Source: [Radiopaedia - Adrenal adenoma](https://radiopaedia.org/articles/adrenal-adenoma) - Educational use*

### Patient Presentation
A 38-year-old woman is referred to endocrinology for evaluation of resistant hypertension. Despite taking three antihypertensive medications at maximum doses (including a diuretic), her blood pressure remains elevated. She has been experiencing muscle cramps, weakness, and fatigue. Her primary care physician noted that her potassium has been persistently low despite potassium supplementation.

### Demographics
- Age: 38 years
- Sex: Female
- Past Medical History: Hypertension diagnosed at age 32 (young-onset)
- Medications: Amlodipine 10 mg, lisinopril 40 mg, chlorthalidone 25 mg, potassium chloride 40 mEq daily
- Family History: No hypertension in immediate family

### Chief Complaint
Resistant hypertension and recurrent hypokalemia despite supplementation

### Physical Examination
- Blood pressure: 168/102 mmHg (despite three medications)
- Heart rate: 78 bpm
- BMI: 26 kg/m2
- General: Well-appearing
- Cardiovascular: Normal S1/S2, no murmurs
- Neurological: Proximal muscle weakness (difficulty rising from squat)
- No cushingoid features, no abdominal bruit

### Workup
- Serum potassium: 2.9 mEq/L (low despite supplementation)
- Serum sodium: 144 mEq/L (high-normal)
- Plasma aldosterone concentration (PAC): 28 ng/dL (elevated)
- Plasma renin activity (PRA): 0.2 ng/mL/hr (suppressed)
- Aldosterone-to-renin ratio (ARR): 140 (elevated; >30 suggests primary aldosteronism)
- Confirmatory test: Oral sodium loading - aldosterone remains elevated (not suppressed)
- CT adrenal: 1.8 cm left adrenal adenoma, right adrenal normal
- Adrenal vein sampling: Lateralizes to left adrenal gland

### Diagnosis
Primary Aldosteronism (Conn Syndrome) due to Left Adrenal Aldosterone-Producing Adenoma

### Treatment
1. Hold interfering medications before testing (MRA, diuretics if possible)
2. Preoperative preparation:
   - Spironolactone or eplerenone to control BP and correct hypokalemia
   - Potassium supplementation
3. **Laparoscopic left adrenalectomy** (curative for unilateral adenoma)
4. Postoperative monitoring:
   - BP typically normalizes or improves significantly
   - Monitor for transient hypoaldosteronism
5. Long-term: If bilateral disease or surgery not pursued, medical therapy with mineralocorticoid receptor antagonist

### Physiological Principles Demonstrated
- **Primary vs. secondary aldosteronism**: In primary aldosteronism, the adrenal gland produces excess aldosterone autonomously. Renin is suppressed due to volume expansion and sodium retention. In secondary hyperaldosteronism (e.g., renal artery stenosis), renin is elevated.
- **Aldosterone effects**: Aldosterone acts on the distal nephron to promote sodium reabsorption and potassium/hydrogen secretion. Excess aldosterone causes hypertension (volume expansion) and hypokalemia.
- **Resistant hypertension clues**: Young onset, hypokalemia, and failure of multiple antihypertensives should raise suspicion for secondary causes.
- **Aldosterone-to-renin ratio**: The ARR exploits the expected reciprocal relationship between aldosterone and renin to screen for autonomous aldosterone production.

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## Case 3: Renovascular Hypertension - Fibromuscular Dysplasia

### Clinical Image
![Fibromuscular Dysplasia](case_01_image.jpg)
*Source: [Wikimedia Commons - FMD angiography](https://commons.wikimedia.org/wiki/File:Fibromuscular_dysplasia_-_string_of_beads.jpg) - CC BY-SA 3.0*

### Patient Presentation
A 28-year-old woman presents to her primary care physician after being told her blood pressure was elevated at a routine gynecology visit. She has no symptoms and was previously healthy. Her mother has hypertension but developed it in her 50s. On review of systems, she mentions occasional unilateral headaches and a "whooshing" sound in her ears.

### Demographics
- Age: 28 years
- Sex: Female
- Past Medical History: None
- Medications: None
- Family History: Maternal hypertension (age 50s)
- Social History: Non-smoker, occasional alcohol

### Chief Complaint
Newly discovered hypertension at age 28

### Physical Examination
- Blood pressure: 162/98 mmHg (right arm), 158/96 mmHg (left arm)
- Heart rate: 74 bpm
- BMI: 22 kg/m2
- General: Healthy appearing young woman
- Cardiovascular: Normal heart sounds, grade 2/6 systolic bruit heard in right upper quadrant/flank
- Peripheral pulses: Normal and symmetric

### Workup
- Basic metabolic panel: Normal creatinine, potassium normal
- Plasma renin activity: Elevated
- Plasma aldosterone: Elevated (secondary to elevated renin)
- Renal duplex ultrasound: Elevated velocities in right renal artery suggestive of stenosis
- CT angiography: "String of beads" appearance in mid-portion of right renal artery, consistent with fibromuscular dysplasia (medial fibroplasia subtype)
- Evaluation for FMD in other vascular beds:
  - CTA head/neck: No carotid or intracranial FMD
  - Normal abdominal aorta

### Diagnosis
Renovascular Hypertension due to Fibromuscular Dysplasia of Right Renal Artery

### Treatment
1. Blood pressure control with ACE inhibitor (if tolerated with close creatinine monitoring)
2. **Percutaneous transluminal renal angioplasty (PTRA)**:
   - First-line treatment for FMD
   - High success rate (cure or improvement in 80-90%)
   - Stenting usually not required for FMD
3. Post-procedure BP monitoring
4. Screening for FMD in other vascular territories
5. Family screening not routinely recommended (low familial occurrence)
6. Avoid oral contraceptives (thrombotic risk with hypertension)

### Physiological Principles Demonstrated
- **Renovascular hypertension mechanism**: Renal artery stenosis reduces renal perfusion pressure, activating the renin-angiotensin-aldosterone system. Angiotensin II causes systemic vasoconstriction, and aldosterone causes sodium retention, together elevating blood pressure.
- **FMD vs. atherosclerotic renal artery stenosis**: FMD affects the middle and distal renal artery with characteristic "string of beads" appearance; it typically occurs in young women. Atherosclerotic disease affects the ostium and proximal renal artery, typically in older patients with cardiovascular risk factors.
- **Renin-angiotensin feedback**: The elevated renin and aldosterone in this case represent an appropriate physiological response to reduced renal perfusion, unlike primary aldosteronism where renin is suppressed.
- **ACE inhibitor considerations**: ACE inhibitors can be used but require monitoring; in bilateral disease or solitary kidney, they can cause AKI by removing the efferent arteriolar tone needed to maintain GFR.