Which of the following is NOT a criterion for the diagnosis of Primary Hyperaldosteronism?

Diastolic Hypertension without edema

Hyperaldosteronism which is not suppressed by volume expansion

Which of the following is the most prominent clinical manifestation of primary hyperaldosteronism (Conn's syndrome)?

Expansion of Extracellular and Plasma volume

Which of the following statements about pheochromocytoma is true?

Arises from chromaffin cells of adrenal medulla

Hypotension rules out pheochromocytoma

Almost always a malignant tumor

What is the primary effect of beta blockers in the management of thyroid storm?

Provides rapid relief of symptoms

Increases metabolism of thyroxine

Decreases synthesis of thyroxine

Endocrine Hypertension for FMGE: High-Yield Internal Medicine Lessons

Endo HTN Overview - Suspect & Screen

Secondary HTN from hormone excess. Affects 5-10% of hypertensive patients. Early identification crucial.

Clinical Clues:

Resistant HTN (≥3 drugs, or controlled on ≥4)
Severe HTN (BP >180/110 mmHg) or abrupt onset
Young age (<30 yrs) without family history/obesity
HTN with hypokalemia (unprovoked/diuretic-induced)
Adrenal incidentaloma
Paroxysmal HTN, palpitations, pallor, perspiration (Pheochromocytoma - 📌 4 P's)
Cushingoid features, striae, easy bruising

Initial Screening Approach:

Endocrine Hypertension: Suspecting, Screening, Diagnosis

⭐ Primary Aldosteronism (PA) is the most common cause of endocrine hypertension, accounting for ~50-60% of cases.

Primary Aldosteronism - Salty Spies

Pathophysiology: Autonomous aldosterone secretion → Na⁺ retention, K⁺ excretion, ↓renin, HTN.
Causes:
- Bilateral Idiopathic Hyperplasia (IHA, ~60%)
- Aldosterone-Producing Adenoma (APA/Conn's, ~35%)
Clinical: Resistant HTN, ± hypokalemia (muscle weakness), metabolic alkalosis.
Diagnosis:
- Screening: ↑Aldosterone-Renin Ratio ($ARR$) > 20-30 (Plasma Aldosterone Concentration [PAC] > 10-15 ng/dL, Plasma Renin Activity [PRA] < 1 ng/mL/hr).
- Confirmatory: Saline suppression test (post-saline aldosterone > 5-10 ng/dL).
- Localization: Adrenal CT. Adrenal Vein Sampling (AVS) for lateralization (APA vs IHA).
Management:
- APA: Unilateral adrenalectomy.
- IHA: Mineralocorticoid Receptor Antagonists (MRAs) e.g., Spironolactone, Eplerenone.

📌 Mnemonic - CONN'S: Causes HTN, Out K⁺, Na⁺ retention, No Renin, Spironolactone/Surgery.

⭐ Despite classic teaching, hypokalemia is present in only ~30-50% of primary aldosteronism cases.

CT scan showing adrenal adenoma

Pheochromocytoma/PGL - Adrenaline Attack

Catecholamine-secreting tumors: Pheo (adrenal medulla), PGL (extra-adrenal).
Classic 5 P's: Pressure (HTN), Pain (headache), Perspiration, Palpitations, Pallor.
📌 Rule of 10s (approximate): 10% bilateral, 10% extra-adrenal (PGL), 10% malignant, 10% familial (now ~25-40%), 10% in children.
Diagnosis:
- Best initial: ↑ 24hr urinary fractionated metanephrines & normetanephrines; or plasma free metanephrines.
- Localization: CT/MRI; MIBG scan for PGL/metastasis.
Management:
- Pre-op (crucial):
  - Alpha-blockade (e.g., phenoxybenzamine) FIRST for 10-14 days (BP control).
  - THEN Beta-blockade (e.g., propranolol) if tachycardia (⚠️ NEVER beta-blocker first).
  - Saline for volume expansion.
- Surgery: Definitive.

⭐ Unopposed beta-blockade (without prior alpha-blockade) can precipitate a hypertensive crisis.

MIBG and CT scans of pheochromocytoma

Cushing's, Thyroid & More - Diverse Disruptors

Diverse endocrine conditions beyond primary aldosteronism and pheochromocytoma cause secondary HTN. Compare key differentiating features:

Feature	Cushing's Syndrome	Thyroid Disorders (Hyper/Hypo)	Acromegaly	CAH (11β/17α def.)
HTN Patho.	↑Cortisol (MC effect), ↑SNS	Hyper: ↑CO; Hypo: ↑SVR, Na+ ret.	↑GH/IGF-1 → Na+ ret., vol. exp.	↑DOC (mineralocorticoid)
Key Clues	Striae, moon facies, central obesity	Hyper: Tachy; Hypo: Brady, fatigue	Coarse facies, big hands/feet	Virilization (11β), Ambiguous gen. (17α), HypoK+
HTN Type	Systolic/Diastolic	Hyper: Systolic; Hypo: Diastolic	Systolic/Diastolic	Volume, low renin
Dx Tests	Dexa supp., 24h UFC, LNSC	TSH, fT3, fT4	IGF-1, GH supp. (OGTT)	Serum DOC, 17-OHP
%%{init: {'flowchart': {'htmlLabels': true}}}%%
flowchart TD

PC["🏠 Primary Care
• Early onset HTN• Resistant HTN"]

BIS["🔬 Baseline Labs
• U+Es and TFTs• HbA1c and Lipids"]

SC["🏥 Secondary Care
• Aldosterone-Renin• Metanephrines"]

SI["🖥️ Specialist Imaging
• Adrenal CT/MRI• Pituitary MRI"]

TC["🏛️ Tertiary Care
• Venous Sampling• Genetic Testing"]

OP["💊 Management
• Adrenalectomy• Renal Angioplasty"]

PC --> BIS BIS --> SC SC --> SI SI --> TC TC --> OP

style PC fill:#F7F5FD, stroke:#F0EDFA, stroke-width:1.5px, rx:12, ry:12, color:#6B21A8 style BIS fill:#FFF7ED, stroke:#FFEED5, stroke-width:1.5px, rx:12, ry:12, color:#C2410C style SC fill:#FEF8EC, stroke:#FBECCA, stroke-width:1.5px, rx:12, ry:12, color:#854D0E style SI fill:#FFF7ED, stroke:#FFEED5, stroke-width:1.5px, rx:12, ry:12, color:#C2410C style TC fill:#EEFAFF, stroke:#DAF3FF, stroke-width:1.5px, rx:12, ry:12, color:#0369A1 style OP fill:#F1FCF5, stroke:#BEF4D8, stroke-width:1.5px, rx:12, ry:12, color:#166534


> ⭐ In **11β**-hydroxylase deficiency (CAH), ↑DOC leads to HTN & hypokalemia, while ↑androgens cause virilization.

##  High‑Yield Points - ⚡ Biggest Takeaways

> * **Primary aldosteronism**: Most common secondary HTN; screen with **aldosterone-renin ratio (ARR)**.
> * **Pheochromocytoma**: **Episodic HTN**, palpitations, headache, sweating; test **urinary/plasma metanephrines**.
> * **Cushing's syndrome**: HTN from **cortisol excess**; screen with **24-hr UFC** or **dexamethasone suppression**.
> * **CAH**: **11β-hydroxylase** & **17α-hydroxylase deficiencies** cause HTN.
> * **Hyperthyroidism**: Causes **systolic HTN** and **widened pulse pressure**.
> * **Hypothyroidism**: May cause **diastolic HTN**.
> * Evaluate for endocrine causes in **resistant HTN** or **young hypertensives**.

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