What is hyperaldosteronism?

Hyperaldosteronism is a condition characterized by excessive secretion of aldosterone from the adrenal cortex, leading to sodium and water retention, potassium loss, metabolic alkalosis, and hypertension.

What are the main types of hyperaldosteronism?

The main types are primary hyperaldosteronism (autonomous aldosterone secretion with low renin), secondary hyperaldosteronism (renin-mediated aldosterone excess), and pseudohyperaldosteronism (aldosterone-like effects without high aldosterone).

What is primary hyperaldosteronism?

Primary hyperaldosteronism is caused by autonomous aldosterone production from the adrenal glands, most commonly due to aldosterone-producing adenoma or bilateral adrenal hyperplasia, with suppressed renin levels.

What causes secondary hyperaldosteronism?

Secondary hyperaldosteronism results from increased renin secretion due to conditions such as renal artery stenosis, heart failure, cirrhosis, nephrotic syndrome, diuretic use, or pregnancy.

What is Conn syndrome?

Conn syndrome refers to primary hyperaldosteronism caused by an aldosterone-producing adrenal adenoma.

What are the common clinical features of hyperaldosteronism?

Common features include resistant hypertension, hypokalemia, muscle weakness, fatigue, polyuria, polydipsia, metabolic alkalosis, and increased cardiovascular risk.

Is hypokalemia always present in hyperaldosteronism?

No, hypokalemia is not mandatory. Many patients with primary hyperaldosteronism have normal serum potassium levels, especially in early or mild disease.

When should patients be screened for primary hyperaldosteronism?

Screening is recommended in resistant hypertension, hypertension with hypokalemia, adrenal incidentaloma with hypertension, early-onset hypertension, or family history of early stroke or hyperaldosteronism.

What is the best initial screening test for primary hyperaldosteronism?

The plasma aldosterone–renin ratio (ARR) is the preferred initial screening test.

How is primary hyperaldosteronism confirmed?

Confirmation is done using suppression tests such as saline infusion test, oral sodium loading test, fludrocortisone suppression test, or captopril challenge test.

What is the role of adrenal venous sampling?

Adrenal venous sampling is the gold standard to differentiate unilateral from bilateral aldosterone secretion and is required before surgical intervention.

How is unilateral primary hyperaldosteronism treated?

Unilateral disease is treated with laparoscopic adrenalectomy, which often normalizes potassium levels and improves or cures hypertension.

How is bilateral adrenal hyperplasia managed?

Bilateral disease is managed medically using mineralocorticoid receptor antagonists such as spironolactone or eplerenone.

What drugs are used to treat hyperaldosteronism?

Common drugs include spironolactone, eplerenone, and amiloride, depending on the cause and patient tolerance.

What are the major complications of untreated hyperaldosteronism?

Complications include stroke, myocardial infarction, atrial fibrillation, left ventricular hypertrophy, chronic kidney disease, and increased cardiovascular mortality.

Why does hyperaldosteronism not usually cause edema?

Aldosterone escape occurs due to pressure natriuresis and atrial natriuretic peptide, preventing persistent edema despite sodium retention.

What acid–base abnormality is seen in hyperaldosteronism?

Metabolic alkalosis occurs due to increased hydrogen ion secretion in the renal tubules.

What is familial hyperaldosteronism type I?

It is a glucocorticoid-remediable form of hyperaldosteronism caused by a genetic defect, where aldosterone secretion is regulated by ACTH and suppressed by low-dose glucocorticoids.

What is the prognosis of hyperaldosteronism?

With early diagnosis and appropriate treatment, prognosis is excellent, with significant reduction in cardiovascular and renal complications.

Can hyperaldosteronism be cured?

Yes, unilateral primary hyperaldosteronism can often be cured with adrenalectomy, while bilateral disease can be effectively controlled with medical therapy.

ACROMEGALY

1. Definition

Acromegaly is a chronic endocrine disorder caused by excess growth hormone (GH) secretion after epiphyseal closure, leading to progressive enlargement of hands, feet, face, and internal organs with severe cardiometabolic and musculoskeletal complications.

(If excess GH occurs before epiphyseal closure → Gigantism)

2. Pathophysiology

Normal Physiology

Hypothalamus → GHRH ↑ → Pituitary → GH ↑ → Liver → IGF-1 ↑ → Tissue growth

Somatostatin inhibits GH.

In Acromegaly

Most commonly:

> Pituitary somatotroph adenoma → Excess GH → Excess IGF-1

IGF-1 causes:

Bone overgrowth (mandible, hands, feet)
Organomegaly
Insulin resistance
Cardiomyopathy
Soft tissue hypertrophy

GH causes:

Lipolysis
Anti-insulin effect
Sodium retention
Increased cardiac output

3. Causes

A. Pituitary (95%)

GH-secreting pituitary adenoma

B. Ectopic (rare)

GHRH-secreting tumors

(Bronchial carcinoid, pancreatic NET)

4. Clinical Features

A. Skeletal

Enlarged hands and feet (rings no longer fit)
Prognathism (jaw protrusion)
Frontal bossing
Spade-like hands
Increased shoe size
Kyphosis

B. Soft Tissue

Thick oily skin
Enlarged tongue (macroglossia)
Coarse facial features
Deep voice
Snoring, obstructive sleep apnea

C. Joint and Muscle

Arthralgia
Proximal myopathy
Carpal tunnel syndrome

D. Cardiovascular (Major cause of death)

Hypertension
Cardiomegaly
Concentric LV hypertrophy
Diastolic dysfunction
Heart failure
Arrhythmias

E. Metabolic

Diabetes mellitus
Insulin resistance
Hypertriglyceridemia

F. Neurological

Headache
Visual field defects (bitemporal hemianopia)

G. Reproductive

Amenorrhea
Erectile dysfunction
Infertility

(due to ↑ prolactin or pituitary compression)

5. Investigations

A. Screening Test

Serum IGF-1 (best test)

Always elevated
Age-adjusted

B. Confirmatory Test

Oral Glucose Tolerance Test (OGTT)

Normal: GH suppresses to <1 ng/mL

Acromegaly: GH fails to suppress

C. Localization

MRI pituitary with contrast

D. Complication Workup

ECG, Echo
Fasting glucose / HbA1c
Lipids
Colonoscopy (↑ colon cancer risk)
Sleep study

6. Differential Diagnosis

Gigantism
Hypothyroidism (coarse face)
Paget disease
Pseudoacromegaly (insulin resistance syndromes)

7. Management

Goal

Normalize IGF-1 & GH, remove tumor, prevent complications

A. Surgery (First line)

Trans-sphenoidal pituitary surgery

Indication:

Pituitary adenoma

B. Medical Therapy

Used if:

Surgery fails
Patient unfit
Residual tumor

1. Somatostatin Analogs

| Drug | Octreotide, Lanreotide |

| ---- | ---------------------- |

Mechanism

Inhibit GH secretion from pituitary tumor

Dose

Octreotide LAR 20–30 mg IM monthly
Lanreotide 60–120 mg deep SC monthly

Adverse effects

Gallstones
Diarrhea
Abdominal cramps
Bradycardia
Hypothyroidism

Monitoring

IGF-1
Gallbladder USG
LFTs

2. Dopamine Agonists

| Drug | Cabergoline, Bromocriptine |

Mechanism

Suppress GH in some tumors (especially with ↑ prolactin)

Dose

Cabergoline 0.5–1 mg twice weekly

Side effects

Nausea
Orthostatic hypotension
Valvular heart disease (high dose)

3. GH Receptor Blocker

| Drug | Pegvisomant |

Mechanism

Blocks GH receptor → ↓ IGF-1

Dose

10–30 mg SC daily

Side effects

LFT elevation
Injection site reaction

C. Radiotherapy

For persistent disease after surgery + drugs

8. Complications

Cardiomyopathy (most common cause of death)
Hypertension
Diabetes mellitus
Sleep apnea
Colon cancer
Arthritis
Visual loss

9. Prognosis

If untreated:

Reduced life expectancy by 10–15 years

If treated early:

Near-normal lifespan

10. High-Yield Exam Points

Best screening test → IGF-1
Best confirmatory test → OGTT with GH
Cause → Pituitary adenoma
Most common death → Cardiac disease
Treatment of choice → Transsphenoidal surgery

Acromegaly Complete Clinical Guide With Diagnosis Management Pathophysiology Complications

ACROMEGALY

1. Definition