Pituitary Pathology
On this page
Direct answer
Three presentations cover nearly all pituitary disease: hormone excess, hormone deficiency, and mass effect on the optic chiasma. Overwhelmingly the lesions are benign adenomas — microadenomas under 10 millimetres, macroadenomas above — and prolactin-secreting adenomas are the commonest, followed by somatotroph, corticotroph and non-functioning tumours. Hypersecretion maps to the cell type: prolactinoma with amenorrhoea, galactorrhoea and infertility; growth-hormone excess producing gigantism before epiphyseal fusion and acromegaly after; ACTH excess causing Cushing disease. Hypopituitarism in Indian practice still classically follows postpartum haemorrhage — Sheehan syndrome, ischaemic necrosis of the pregnancy-enlarged pituitary whose first sign is failure of lactation — while pituitary apoplexy and childhood craniopharyngioma complete the high-yield list.
What you must remember
- Adenoma essentials: prolactinoma is the commonest functioning adenoma; non-functioning adenomas present latest, by mass effect; bitemporal hemianopia from chiasmal compression is the signature field defect; macroadenomas can present with headache, diplopia (cavernous sinus extension) or hypopituitarism from compression of normal gland.
- Prolactinoma rules: microadenomas in young women (amenorrhoea-galactorrhoea), macroadenomas in men (visual loss, hypogonadism); dopamine agonists — cabergoline preferred to bromocriptine — shrink the tumour and are first-line; surgery is for resistance or apoplexy.
- Acromegaly testing: random growth hormone is unreliable — measure IGF-1 as the screen and confirm with failure of growth hormone to suppress during a 75 g oral glucose load; trans-sphenoidal adenomectomy is first-line, with somatostatin analogues (octreotide, lanreotide), pegvisomant or cabergoline as adjuncts; diabetes, hypertension and cardiomyopathy drive mortality.
- Cushing disease: ACTH-secreting corticotroph microadenoma — the commonest cause of endogenous Cushing syndrome; confirm hypercortisolism first (overnight dexamethasone suppression, 24-hour urinary free cortisol, midnight salivary cortisol), then localise with ACTH and high-dose suppression.
- Sheehan syndrome: postpartum haemorrhage, failure of lactation, then sequential hormone loss (gonadotrophins and growth hormone before TSH and ACTH); in India, where postpartum haemorrhage remains a leading cause of maternal mortality and morbidity, Sheehan syndrome is still regularly encountered — hedge-free viva territory.
- Pituitary apoplexy: sudden haemorrhage into an adenoma — thunderclap headache, ophthalmoplegia, visual loss, meningism and acute adrenal insufficiency; give parenteral hydrocortisone before anything else.
- Childhood mass: craniopharyngioma, a Rathke-pouch remnant — suprasellar, calcified on imaging, adamantinomatous type in children; pressure causes growth failure, visual loss and hypothalamic dysfunction.
Worked example: a young woman with galactorrhoea
A 27-year-old reports amenorrhoea for ten months and milky nipple discharge; she takes an anti-emetic and is not pregnant. Step one excludes pregnancy and drugs — metoclopramide, antipsychotics and oestrogens raise prolactin pharmacologically. Step two checks thyroid function, because primary hypothyroidism increases TRH, which is prolactin-releasing. Step three sends serum prolactin: a level in thousands strongly suggests a macroprolactinoma, while a modest rise (say under 100 ng/mL) with a large tumour on MRI raises the alternative — the stalk effect, where any sellar mass compresses the pituitary stalk and removes dopamine's brake on lactotrophs. That distinction changes everything: a true macroprolactinoma is treated first with cabergoline and shrinks beautifully, whereas a non-functioning macroadenoma causing a stalk effect needs surgery. Visual field charting and pituitary profiling complete the work-up. This is the single most instructive pituitary algorithm, because the number alone misleads without the anatomy.
High-yield viva angles
Expect the sequential order of anterior pituitary hormone loss in compressive disease: gonadotrophins and growth hormone fall first, TSH next, ACTH and prolactin last — while in Sheehan syndrome lactation failure is the opening symptom because prolactin is the one hormone that is under tonic inhibition. The empty sella, once an incidental terror, is usually benign herniation of the arachnoid. And remember corticotroph hyperplasia after bilateral adrenalectomy — Nelson syndrome, with hyperpigmentation and an expanding sellar mass.
Frequently asked questions
What visual field defect does a pituitary macroadenoma cause?
Bitemporal hemianopia, from compression of decussating nasal retinal fibres at the optic chiasma.
Why does Sheehan syndrome present with failure of lactation?
The lactotrophs are among the cells lost in postpartum pituitary necrosis, so prolactin — required for milk production — fails first and lactation never establishes.
Which single drug class shrinks a prolactinoma?
Dopamine agonists — cabergoline or bromocriptine — which suppress prolactin secretion and prolactinoma cell growth, avoiding surgery in most patients.
How is acromegaly biochemically confirmed?
Elevated IGF-1 for age and sex, plus failure of growth hormone to suppress below 1 ng/mL during an oral glucose tolerance test.
What is the emergency drug in pituitary apoplexy?
Parenteral hydrocortisone — adrenal crisis from ACTH deficiency kills before the neurosurgical problem is addressed.