Oituitary Tumours Flashcards
pituitary tumour size and position classifications:
microadenoma if below 1cm, macroadenoma if above. sellar/suprasellar, whether or not it invades cavernous sinus/compresses optic chiasm
sellar vs suprasellar
whether or not it goes out past sella turcica
functional vs non functional:
whether or not there is excess secretion of a hormone e.g. prolactinoma
how to tell bw benign and malignant:
mitotic index measured w Ki67 index , benign = less than 3%. pituitary tumours can have benign histology but malignant behaviour
effect of hyperprolactinemia on gonads
inhibits kisspeptin release therefore less downstream GnRH, FSH, LH, test/est. leads to oligomenorrhea, low libido, infertility, osteoporosis
how do prolactin levels vary with prolactinoma
will be > 5000 usually. excess is proportional to prolactinoma size
other causes of elevated prolactin
physical e.g. nipple/chest stimulation, stress (includes venepuncture), pregnancy/breastfeeding.
pathological e.g. primary hypothyroidism, PCOS, chronic renal failure
iatrogenic e.g. antipsychotics, opiates, high dose estrogen
prolactinoma treatment:
mainly medical after confirmation by MRI. dopamine receptor agonists e.g. cabergoline, bromocriptine (older drug with lots of side effects) aim = normal serum prolactin, shrink prolactinoma.
where and how do dopamine receptors work in the pituitary gland?
D2 receptors on lactotrophs in anterior pituitary. when bound they inhibit the release of prolactin from the cell. medicine binds these and also tends to induce apoptosis
acromegaly vs gigantism
gigantism = GH excess in childhood, acromegaly = in adulthood
- insidious i.e. 10 years bw diagnosis and onset of symptoms. coarse facial features e.g. macroglossia, prognathism (large jaw), hand feet nose size up, hypertension, impaired glucose tolerance/diabetes
what factor accompanies GH and where is it produced
Insulin like growth factor 1 from liver
why is random GH measurement unhelpful for diagnosis
As it’s pulsatile
diagnostic tool for GH excess:
oral glucose load. normal should be drop in GH then return to baseline, GH excess is paradoxical rise of GH
IGF1 levels will be high
-
GH tumour treatment
surgical first line - trans-sphenoidal. medical options include somatostatin analogues eg octreotide (endocrine cyanide), dopamine receptor agonists (less effective) (GH tumour cells often have D2 receptors). aim: normalise serum GH and IGF-1
radiotherapy but its very slow
cushing’s syndrome vs cushing’s disease
syndrome = excess cortisol, disease = due to pituitary tumour secreting ACTH (disease is ACTH dependent). ACTH independent can be taking oral steroids, adrenal adenoma.
