primarily from anterior pituitary, 3rd-4th decades, M=F
incidence in autopsy studies approximately 20%
Classification
microadenoma <1 cm; macroadenoma ≥1 cm
endocrine active (functional/secretory) vs. inactive (non-functional)
differential: parasellar tumours (e.g. craniopharyngioma, tuberculum sellae meningioma), carotid aneurysm
Clinical Features
mass effects
H/A
bitemporal hemianopsia (compression of optic chiasm)
CN III, IV, V1, V2, VI palsy (compression of cavernous sinus)
endocrine effects
hyperprolactinemia (prolactinoma): infertility, amenorrhea, galactorrhea, decreased libido
ACTH production: Cushing’s disease, hyperpigmentation
GH production: acromegaly/gigantism
panhypopituitarism (hypothyroidism, hypoadrenalism, hypogonadism)
associated MEN-1 syndrome
diabetes insipidus
Go Look For The Adenoma Please – GH, LH, FSH, TSH, ACTH, Prolactin
A compressive adenoma in the pituitary will impair hormone production in this order (i.e. GH-secreting cells are most sensitive to compression).
pituitary apoplexy (sudden expansion of mass due to hemorrhage or necrosis)
abrupt onset H/A, visual disturbances, ophthalmoplegia, reduced mental status, and panhypopituitarism
CSF rhinorrhea and seizures (rare)
signs and symptoms of subarachnoid hemorrhage (rare)
Investigations
formal visual fields, CN testing
endocrine tests (prolactin level, TSH, 8 AM cortisol, fasting glucose, FSH/LH, IGF-1), electrolytes, urine electrolytes, and osmolarity
imaging (MRI with and without contrast)
Treatment
Medical
for apoplexy: rapid corticosteroid administration ± surgical decompression
for prolactinoma: dopamine agonists (e.g. bromocriptine)
for Cushing's: serotonin antagonist (cyproheptadine), inhibition of cortisol production (ketoconazole)
for acromegaly: somatostatin analogue (octreotide) ± bromocriptine
endocrine replacement therapy
Surgical
trans-sphenoidal, trans-ethmoidal, trans-cranial approaches for non-secreting adenomas causing mass effect and Cushing/acromegaly (50% cure rate)