Pituitary Disorders for NEET PG — Complete Guide 2026

Version 1.0 — Published January 2026

Pituitary disorders are high-yield NEET PG vignettes — the post-partum woman who cannot lactate, the 35-year-old with widening shoe size, the headache with bitemporal visual loss — and recognising the pattern plus the first-line drug separates marks. This guide covers pituitary anatomy and the HPA axis, hypopituitarism, pituitary adenoma subtypes and management, diabetes insipidus, and SIADH. Pair it with the medicine subject hub, the thyroid disorders guide, and the common mistakes in medicine NEET PG article for endocrine integration.

Anatomy and the hypothalamic–pituitary axis

The pituitary gland is a pea-sized endocrine organ sitting in the sella turcica of the sphenoid bone, connected to the hypothalamus by the infundibulum — and its two lobes have distinct embryological origins and secretory control.

Anatomy overview:

• Anterior pituitary (adenohypophysis) — from Rathke's pouch (ectoderm of oral cavity); ~80% of gland mass; secretes six trophic hormones
• Posterior pituitary (neurohypophysis) — neural tissue from the diencephalon; stores ADH and oxytocin synthesised in the hypothalamus (supraoptic and paraventricular nuclei)
• Blood supply — hypothalamic–hypophyseal portal system carries releasing hormones from the median eminence to the anterior pituitary; the posterior pituitary is supplied directly by the inferior hypophyseal artery
• Neighbours — optic chiasm superiorly (bitemporal hemianopia on expansion), cavernous sinus laterally (cranial nerves III, IV, V1, V2, VI — ophthalmoplegia and facial sensation), sphenoid sinus inferiorly (transsphenoidal surgical route)

Hypothalamic releasing and inhibiting hormones:

Anterior pituitary hormones and targets:

Posterior pituitary hormones:

• ADH (vasopressin) — water reabsorption via V2 receptors on collecting duct (aquaporin-2 insertion); vasoconstriction via V1a
• Oxytocin — uterine contraction, milk ejection, social bonding

Clinical anchor: stalk compression from a pituitary macroadenoma disconnects dopamine inhibition → mild prolactin elevation (usually <150 ng/mL). A prolactin level >200 ng/mL in the setting of a sellar mass strongly suggests a true prolactinoma, not stalk effect.

Hypopituitarism

Hypopituitarism is partial or complete deficiency of anterior pituitary hormones — its sequence of hormone loss, causes, and hormone-replacement order are high-yield.

Causes:

Sequence of anterior pituitary hormone loss (mnemonic Go Look For The Adenoma):

1. GH — earliest; short stature in children, central adiposity in adults
2. LH / FSH — amenorrhoea, erectile dysfunction, infertility, loss of libido
3. TSH — cold intolerance, fatigue, weight gain, hyponatraemia
4. ACTH — fatigue, hypoglycaemia, hypotension (latest and most dangerous)
5. Prolactin — failure of lactation (earliest in Sheehan)

Sheehan syndrome — post-partum pituitary necrosis:

• Pathophysiology — pregnancy enlarges the pituitary; postpartum haemorrhage causes hypotension and ischaemic necrosis
• Earliest clue — failure to lactate
• Next features — amenorrhoea, loss of pubic/axillary hair, fatigue, hypothyroid features, adrenal crisis months to years later
• MRI — empty sella
• Replace cortisol FIRST, then thyroxine (giving T4 first precipitates adrenal crisis)

Pituitary apoplexy — haemorrhagic infarction of an adenoma:

• Presentation — sudden thunderclap headache, bitemporal hemianopia, ophthalmoplegia (III > IV, VI from cavernous sinus), altered sensorium, acute adrenal crisis
• MRI — haemorrhage within the adenoma
• Management — IV hydrocortisone 100 mg immediately, stabilise, urgent transsphenoidal decompression for visual compromise

Craniopharyngioma:

• Arises from Rathke pouch remnants; bimodal age (5–15 y and 50–75 y)
• Calcified suprasellar cystic mass on imaging; motor oil-like cyst fluid
• Compresses optic chiasm (bitemporal hemianopia) and pituitary (hypopituitarism, DI in ~30%)
• Surgery ± radiation

Hormone replacement rules:

• Cortisol first (hydrocortisone 15–25 mg/day split dose) — always before starting thyroxine
• Thyroxine (levothyroxine titrated to mid-normal free T4, NOT TSH-based)
• Sex steroids — testosterone in men, oestrogen-progesterone in women
• GH — consider in symptomatic adults and children
• Desmopressin — for coexisting central DI
• Stress dose steroids — triple oral dose or IV hydrocortisone 50–100 mg every 6–8 h for illness, surgery, or trauma

Pituitary adenomas — classification and approach

Pituitary adenomas are benign monoclonal tumours of adenohypophysis cells — classified by size and hormone secretion, and both axes shape management.

By size:

• Microadenoma — <10 mm
• Macroadenoma — >=10 mm (more likely to cause mass effect: visual loss, hypopituitarism, headache)
• Giant — >=40 mm

By hormone secretion and frequency:

Work-up:

• Hormonal screen — prolactin, IGF-1, 8 am cortisol + ACTH, TSH + free T4, LH/FSH + testosterone/oestradiol
• MRI pituitary with gadolinium
• Visual fields (Humphrey or Goldmann perimetry) if macroadenoma or close to chiasm
• Dynamic testing as indicated — OGTT (acromegaly), dexamethasone suppression (Cushing), water deprivation (DI)

Prolactinoma

Prolactinoma is the most common functioning pituitary adenoma — dopamine agonists are first-line for both micro- and macroadenomas, including most visual-field defects.

Clinical features:

• Women (usually micro) — amenorrhoea, galactorrhoea, infertility, low libido
• Men (usually macro) — low libido, erectile dysfunction, infertility, mass effect (headache, bitemporal hemianopia), gynaecomastia
• Bone loss — from hypogonadism (oestrogen/testosterone deficiency)

Prolactin levels and interpretation:

• Normal: <20 ng/mL (women), <15 ng/mL (men)
• >200 ng/mL → strongly suggests prolactinoma (macro usually >250 ng/mL)
• 25–100 ng/mL → overlap with stalk effect, drugs, hypothyroidism, pregnancy, stress, PCOS, CKD
• Hook effect — very large prolactinomas with extremely high prolactin can falsely read low on immunoassay; dilute sample if big tumour but mildly elevated level
• Always exclude pregnancy before work-up

Secondary causes of hyperprolactinaemia:

• Drugs — antipsychotics (risperidone most potent), metoclopramide, methyldopa, verapamil, SSRIs, opiates, H2 blockers
• Hypothyroidism (TRH stimulates prolactin)
• Pregnancy and lactation, nipple stimulation
• Chronic kidney disease, liver disease
• PCOS (mild elevation)
• Macroprolactinoma stalk compression (mild elevation <150 ng/mL)

Management:

Pregnancy:

• Microadenoma — stop DA once pregnancy confirmed (tumour enlargement risk very low)
• Macroadenoma — continue DA or switch to bromocriptine; serial visual fields; do NOT do routine prolactin levels during pregnancy
• Breastfeeding safe if tumour stable

Acromegaly and gigantism

Acromegaly is GH excess in adults (after epiphyseal closure) presenting with coarsened features and organomegaly, while gigantism is GH excess in children with open epiphyses — both are almost always from a somatotroph adenoma.

Clinical features of acromegaly:

• Coarse facies — prominent supraorbital ridges, enlarged nose, macroglossia, spaced teeth (interdental spacing), prognathism
• Hands and feet — spade-like hands, increasing ring/shoe size, doughy skin
• Systemic — HTN (~30%), diabetes/IGT (30–50%), cardiomyopathy (biventricular hypertrophy), obstructive sleep apnoea, carpal tunnel syndrome, colon polyps / colorectal cancer (increased risk), skin tags
• Hypogonadism, galactorrhoea — stalk effect or co-secretion
• Mass effect — bitemporal hemianopia in macroadenoma

Diagnosis:

1. IGF-1 — age and sex matched; screening test of choice (single random level reliable, unlike GH)
2. OGTT with GH — confirmatory: 75 g oral glucose; failure of GH to suppress below 1 ng/mL (0.4 ng/mL sensitive assay) at 2 h confirms acromegaly
3. MRI pituitary with gadolinium — localises adenoma
4. Complications screen — HbA1c, fasting glucose, echocardiogram, colonoscopy, sleep study, visual fields

Management:

Follow-up goal — IGF-1 normalisation; random GH <1 ng/mL; post-op OGTT to confirm cure.

Cushing disease workflow

Cushing disease is ACTH-secreting pituitary adenoma — distinguishing it from ectopic ACTH and adrenal causes requires a strict three-step workflow.

Step 1 — SCREEN (confirm hypercortisolism): use any two of:

• 24-hour urinary free cortisol (UFC) — >3× upper limit highly suggestive
• Late-night salivary cortisol — loss of diurnal variation
• 1 mg overnight dexamethasone suppression test — cortisol >1.8 mcg/dL next morning = positive
• Exclude pseudo-Cushing (alcohol, depression, obesity) and exogenous steroid use first

Step 2 — ACTH-dependent vs independent:

• ACTH-dependent (high/normal ACTH >10–20 pg/mL) → Cushing disease or ectopic ACTH
• ACTH-independent (suppressed ACTH <5 pg/mL) → adrenal source (adenoma, carcinoma, bilateral macronodular hyperplasia, PPNAD) — proceed to CT adrenals

Step 3 — LOCALISE ACTH-dependent:

• High-dose dexamethasone suppression (8 mg) — Cushing disease usually suppresses >50%, ectopic does not (not absolute)
• CRH stimulation — Cushing disease responds, ectopic does not
• MRI pituitary — identifies adenoma in ~60–70% (may miss microadenomas)
• Inferior petrosal sinus sampling (IPSS) — gold standard when MRI negative or discordant biochemistry; central-to-peripheral ACTH gradient >2 (basal) or >3 (post-CRH) confirms pituitary source
• CT chest/abdomen — if ectopic suspected (small cell lung, bronchial carcinoid, medullary thyroid, pheo)

Management:

• First-line — transsphenoidal surgery (remission 70–90% microadenoma, 50% macroadenoma)
• Medical — ketoconazole, metyrapone, mitotane, osilodrostat (cortisol synthesis inhibitors); pasireotide (somatostatin analogue acting on pituitary); mifepristone (glucocorticoid-receptor antagonist, for steroid-induced diabetes)
• Bilateral adrenalectomy — refractory cases; risk of Nelson syndrome (ACTH tumour enlargement post-adrenalectomy)
• Radiotherapy — adjunct if surgery fails

Diabetes insipidus and SIADH

Diabetes insipidus (DI) and SIADH are posterior-pituitary disorders of ADH — DI causes dilute polyuria, SIADH causes euvolaemic hyponatraemia — and both are classic NEET PG scenarios.

Diabetes insipidus — central vs nephrogenic:

Water deprivation test protocol:

• Patient fasts fluids; hourly weight, urine volume, urine osmolality, serum osmolality/sodium
• Stop if >3% body weight loss, thirst, or Na >145
• Measure plasma ADH at end (or copeptin)
• Give 2 mcg desmopressin IM and recheck urine osmolality at 1 and 2 h

Clinical clues:

• Polyuria (>3 L/day), polydipsia, nocturia, hypernatraemic dehydration if access to water is impaired
• Primary (psychogenic) polydipsia — low baseline serum osmolality, dilute urine that concentrates with water deprivation

SIADH — features:

SIADH causes (mnemonic: SIADH):

• Small cell lung cancer (classic ectopic ADH source)
• Intracranial pathology — meningitis, encephalitis, haemorrhage, trauma
• Alveolar — pneumonia, TB, aspergillosis
• Drugs — SSRIs, carbamazepine, cyclophosphamide, vincristine, desmopressin, MDMA ("ecstasy")
• Hereditary gain-of-function V2 receptor mutations

Management:

1. Mild/asymptomatic — fluid restriction <800–1000 mL/day; salt tabs ± loop diuretic
2. Severe symptomatic hyponatraemia (seizures, coma, Na <120) — hypertonic 3% saline 100–150 mL bolus(es); target Na rise 4–6 mEq/L in first 6 h
3. Correction speed — do NOT exceed 8–10 mEq/L per 24 h (osmotic demyelination / central pontine myelinolysis risk, especially in chronic hyponatraemia, alcoholism, malnutrition)
4. Chronic SIADH — tolvaptan (vasopressin V2 antagonist), demeclocycline
5. Treat underlying cause — SCLC chemotherapy, drug withdrawal, infection treatment

Cerebral salt wasting (CSW) differential: similar labs to SIADH but hypovolaemic (raised urea, low CVP, weight loss, orthostasis). Treat with salt and fluid replacement (opposite of SIADH fluid restriction). Seen in SAH, neurosurgery.

Sources and references

1. Harrison's Principles of Internal Medicine, 21st Edition (Loscalzo, Fauci, Kasper, Hauser, Longo, Jameson, Eds., 2022) — Chapters on pituitary disorders, hyponatraemia, and diabetes insipidus.
2. Williams Textbook of Endocrinology, 14th Edition (Melmed, Auchus, Goldfine, Koenig, Rosen, Eds., 2019) — Chapters on anterior and posterior pituitary physiology and disease.
3. Melmed S et al. Diagnosis and Treatment of Hyperprolactinemia: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2011; 96:273-288.
4. Katznelson L et al. Acromegaly: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2014; 99:3933-3951.
5. Nieman LK et al. Treatment of Cushing's Syndrome: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab 2015; 100:2807-2831.
6. Fleseriu M et al. Consensus on diagnosis and management of Cushing's disease: a guideline update. Lancet Diabetes Endocrinol 2021; 9:847-875.
7. Verbalis JG et al. Diagnosis, evaluation, and treatment of hyponatremia: expert panel recommendations. Am J Med 2013; 126(10 Suppl 1):S1-S42.

Frequently asked questions

How many pituitary disorder questions appear in NEET PG?

Pituitary disorders contribute 2-3 direct questions per NEET PG paper, mostly from medicine and endocrinology. High-yield subtopics include prolactinoma first-line therapy, acromegaly diagnostic test (OGTT suppression of GH), Sheehan syndrome in a post-partum woman with failure of lactation, central vs nephrogenic diabetes insipidus, and the sequence of hormone loss in hypopituitarism (GH first, ACTH last).

What is the sequence of hormone loss in hypopituitarism?

The classic sequence of anterior pituitary hormone loss is GH first, then gonadotropins (LH, FSH), then TSH, then ACTH, and finally prolactin. The mnemonic Go Look For The Adenoma captures it. ACTH loss is the most life-threatening (adrenal crisis) and is the last axis to fail — making GH deficiency and hypogonadism the earliest clinical clues in slowly progressive pituitary disease.

What is the first-line therapy for prolactinoma?

Dopamine agonists are first-line for prolactinomas of all sizes, including macroadenomas. Cabergoline 0.25-0.5 mg twice weekly is preferred over bromocriptine because it is longer-acting, more effective at normalising prolactin, better tolerated, and causes tumour shrinkage in up to 80-90 percent. Bromocriptine is used in pregnancy-related prolactinoma. Transsphenoidal surgery is reserved for dopamine-agonist intolerance, resistance, CSF leak, or visual compromise not improving on medical therapy.

How is acromegaly diagnosed?

Acromegaly is diagnosed by elevated serum IGF-1 (age and sex matched) as the screening test, confirmed by failure of GH to suppress below 1 ng/mL (0.4 ng/mL by sensitive assay) during a 75 g oral glucose tolerance test. MRI pituitary localises the adenoma. Random GH is unreliable due to pulsatile secretion. Adjuncts include colonoscopy (colon polyp risk), echo (cardiomyopathy), sleep study (OSA), and fasting glucose (diabetes).

What is Sheehan syndrome?

Sheehan syndrome is post-partum pituitary necrosis from hypotension and infarction of an enlarged gravid pituitary, usually after obstetric haemorrhage. Failure of lactation is the earliest and most classic feature (prolactin loss), followed by amenorrhoea and loss of pubic and axillary hair. Later features include hypothyroidism, adrenal insufficiency, and GH deficiency. MRI shows empty sella. Replace hormones in order — cortisol FIRST, then thyroxine — to avoid precipitating adrenal crisis.

How do you distinguish central from nephrogenic diabetes insipidus?

The water deprivation test followed by desmopressin is diagnostic. In central DI, urine osmolality fails to concentrate with dehydration but rises by greater than 50 percent after desmopressin. In nephrogenic DI, urine osmolality fails to rise despite desmopressin (less than 10 percent rise) because the kidney is unresponsive. Causes of central DI include trauma, surgery, tumour, Sheehan, autoimmune; nephrogenic causes include lithium, hypercalcaemia, hypokalaemia, and congenital AVPR2/AQP2 defects.

What is the workflow for Cushing disease?

Workflow has three steps: SCREEN, CONFIRM, LOCALISE. Screening uses any two of — 24-hour urinary free cortisol, late-night salivary cortisol, or 1 mg overnight dexamethasone suppression test. Confirm hypercortisolism if two abnormal. Measure ACTH to split ACTH-dependent (Cushing disease, ectopic ACTH) from ACTH-independent (adrenal). For ACTH-dependent, high-dose dexamethasone suppression and MRI pituitary separate Cushing disease from ectopic; inferior petrosal sinus sampling is confirmatory when imaging is equivocal.

What is pituitary apoplexy?

Pituitary apoplexy is acute haemorrhagic infarction of a pituitary adenoma presenting with sudden severe headache, visual field loss (classically bitemporal hemianopia), ophthalmoplegia (cranial nerves III, IV, VI in cavernous sinus), and acute adrenal insufficiency. It is a neuroendocrine emergency — give IV hydrocortisone 100 mg immediately (before confirmatory imaging), stabilise haemodynamics, and do urgent MRI. Transsphenoidal decompression is indicated for visual compromise or depressed consciousness.

What are the features of SIADH?

SIADH is hyponatraemia with euvolaemia, inappropriately concentrated urine (urine osmolality greater than 100 mOsm/kg), urine sodium greater than 40 mEq/L, low serum uric acid, and normal adrenal and thyroid function. Causes include small cell lung cancer, CNS disorders, drugs (SSRIs, carbamazepine, cyclophosphamide), and pulmonary infections. Treatment is fluid restriction (first-line), hypertonic saline for severe symptomatic hyponatraemia (correct less than 8-10 mEq/L per 24 h to avoid osmotic demyelination), tolvaptan for chronic cases.

When is transsphenoidal surgery indicated for pituitary adenoma?

Transsphenoidal surgery is first-line for all pituitary adenomas EXCEPT prolactinoma (which is medical). Indications include GH-secreting adenoma (acromegaly), ACTH-secreting adenoma (Cushing disease), TSH-secreting adenoma, non-functioning macroadenoma with visual compromise, pituitary apoplexy with vision loss, dopamine-agonist resistant or intolerant prolactinoma, and CSF leak. Remission rates are 80-90 percent for microadenomas and 50-70 percent for macroadenomas. Complications include hypopituitarism, diabetes insipidus, CSF leak, and meningitis.

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Written by: NEETPGAI Editorial Team Reviewed by: Pending SME Review Last reviewed: January 2026

This article is reviewed by qualified medical professionals for clinical accuracy and exam relevance. For corrections or updates, contact the editorial team.