Endocrine Disorders

6 min read Updated Mar 26, 2026

The MCAT does not ask you to diagnose patients, but it regularly presents endocrine disorders in passage-based questions to test whether you understand the underlying physiology. The strategy is always the same: identify which hormone is too high or too low, then reason through the feedback loop to predict the consequences.

Every disorder in this section can be understood by asking three questions:

Which hormone is abnormal?
Is it too much (hyper) or too little (hypo)?
Where in the axis is the problem - gland, pituitary, or hypothalamus?

Growth Hormone Disorders

Gigantism - GH excess before epiphyseal plate closure (in children). Excess GH/IGF-1 drives excessive linear growth.

Acromegaly - GH excess after plate closure (in adults). Long bones can no longer lengthen, so bones thicken instead (hands, feet, face).

Dwarfism - GH deficiency (or GH-receptor insensitivity) in childhood. Produces proportional short stature, unlike the disproportionate short stature of achondroplasia.

Adrenal Disorders

Cushing Syndrome - cortisol excess. Predictable from cortisol’s actions: hyperglycemia (gluconeogenesis), central fat deposition, muscle wasting (protein catabolism), hypertension, and immunosuppression. Causes include a pituitary adenoma (high ACTH), an autonomous adrenal tumor (low ACTH), or exogenous steroids.

Addison Disease - primary adrenal insufficiency. The adrenal cortex is destroyed, so both cortisol and aldosterone drop. Loss of cortisol feedback drives ACTH very high, which also drives hyperpigmentation (ACTH and MSH share a precursor). Expect low Na⁺, high K⁺ (no aldosterone), low glucose, and low blood pressure.

Thyroid Disorders (Detailed)

Diagram of the hypothalamus-pituitary-thyroid axis showing TRH, TSH, and T3/T4 feedback pathways — The HPT axis. Understanding this feedback loop is key to predicting lab values in thyroid disorders: Graves disease (high T3/T4, low TSH) vs. Hashimoto's (low T3/T4, high TSH). *Credit: Wikimedia Commons, CC0 Public Domain*

Graves Disease - autoimmune hyperthyroidism. Antibodies mimic TSH and continuously stimulate the thyroid. Labs: high T3/T4, LOW TSH (suppressed by feedback, but the antibodies bypass that control).

Hashimoto Thyroiditis - autoimmune destruction of the thyroid. Labs: low T3/T4, HIGH TSH (pituitary trying to rescue a damaged gland).

Iodine Deficiency Goiter - no iodine means no T3/T4. TSH stays elevated, chronically stimulating the thyroid, which enlarges into a visible goiter.

Water Balance Disorders

SIADH (Syndrome of Inappropriate ADH Secretion) - too much ADH. The kidneys reabsorb too much water, diluting the blood. Result: hyponatremia (dangerously low sodium from dilution), concentrated urine, water retention. Can be caused by certain tumors, drugs, or CNS disorders.

Diabetes Insipidus - too little ADH effect. Two types:

Central DI: hypothalamus/posterior pituitary does not produce enough ADH
Nephrogenic DI: kidneys do not respond to ADH (receptor or aquaporin defect)

Both produce the same symptoms: enormous volumes of very dilute urine (the patient “insipidly” wastes water), extreme thirst, and risk of dehydration. Note: “diabetes” here means “excessive urination” (from Greek “to pass through”) - this has nothing to do with blood sugar or insulin.

Aldosterone Disorders

Hypoaldosteronism - aldosterone deficiency. Causes sodium loss, potassium retention (hyperkalemia), low blood volume, and hypotension. Often seen as part of Addison disease.

Catecholamine Disorder

Master Disorder Table

Disorder	Hormone Problem	Key Lab Findings	Key Symptoms
Cushing Syndrome	Cortisol excess	High cortisol, variable ACTH	Moon face, central obesity, hyperglycemia
Addison Disease	Cortisol + aldosterone deficiency	Low cortisol, HIGH ACTH	Hypotension, hyperpigmentation, fatigue
Graves Disease	T3/T4 excess	High T3/T4, LOW TSH	Weight loss, tachycardia, exophthalmos
Hashimoto Thyroiditis	T3/T4 deficiency	Low T3/T4, HIGH TSH	Weight gain, fatigue, cold intolerance
Acromegaly/Gigantism	GH excess	High GH, high IGF-1	Enlarged extremities (acromegaly) or tall stature (gigantism)
Type 1 Diabetes	Insulin deficiency	High glucose, low insulin, low C-peptide	Polyuria, polydipsia, weight loss
Type 2 Diabetes	Insulin resistance	High glucose, high insulin (early)	Polyuria, polydipsia, obesity
SIADH	ADH excess	Low serum Na+, concentrated urine	Water retention, hyponatremia
Diabetes Insipidus	ADH deficiency/resistance	High serum Na+, dilute urine	Massive urine output, extreme thirst
Conn Syndrome	Aldosterone excess	Low K+, high Na+	Hypertension, hypokalemia
Pheochromocytoma	Catecholamine excess	High catecholamines/metabolites	Episodic hypertension, tachycardia

A patient has high cortisol, low ACTH, and a mass on the adrenal gland. What is the diagnosis and why is ACTH low?

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This is Cushing syndrome caused by an adrenal tumor autonomously producing cortisol. ACTH is low because the excess cortisol suppresses CRH and ACTH via negative feedback. The pituitary is functioning normally - it is responding appropriately to high cortisol by reducing ACTH. The problem is at the adrenal gland level.

A patient produces enormous volumes of dilute urine. Administration of exogenous ADH concentrates the urine normally. Is this central or nephrogenic diabetes insipidus?

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Central diabetes insipidus. The kidneys responded normally to exogenous ADH, meaning the receptors and aquaporin channels work fine - the problem is that the body is not producing enough ADH. In nephrogenic DI, the kidneys would NOT respond to exogenous ADH because the defect is in the kidney's ADH receptors or aquaporin channels.