3 - Anterior Pituitary 2 Flashcards
why is dexamethasone nice for endocrinologists?
doesnt show up on cortisol assay so you can still measure pt’s endogenous production of cortisol while they are on it
basic derangement in cushing’s
glucocorticoid (cortisol) excess
signs/sx of cushing’s
truncal obesity moon facies diabetes / glucose intolerance gonadal dysfunction hirsutism/acne (hyperandrogenism) HTN weakness/muscle atrophy skin atrophy > striae, bruising fat pads psychiatric disturbance (hallucinations, emotional lability) hyperpigmentation acanthosis
mech for HTN in cushing’s
cortisol can activate aldosterone receptor
can also have assoc hypokalemia, hypernatremia, metab alkalosis
mech for osteoporosis / avascular necrosis in cushing’s / steroid use
inc bone resorption - pos effects on osteoclasts, dec gonadal hormones
dec bone formation - inhib osteoblasts, apoptosis, muscle weakness
dec intestinal Ca absorption
inc renal Ca excretion
3 problems caused by long term glucocorticoid excess
cataracts, glaucoma, gastritis/PUD
common sources of ectopic ACTH for ACTH dependent Cushing’s
Neuroendocrine tumors - carcinoid, small cell lung CA, medullary thyroid CA, pheo, pancreatic islet tumor, gastrinoma
main cause of ACTH independent Cushing’s
adrenal adenoma
order of diagnostics in Cushing’s
biochemical first (find out if ACTH (in)dependent etc), then you can do imaging
biochemical tests to confirm Cushing’s
dexamethasone suppression test
24 hr urine free cortisol
midnight serum cortisol
*random serum cortisol is not helpful!!
causes of pseudo-Cushing’s
depression, obesity, alcohol
test to best distinguish cushing’s from pseudo-cushing’s
dexamethasone suppressed CRH stimulation test - 48 hrs of dex will suppress normally in most pseudo pts, so no stimulation w/ CRH. Cushing’s pt will still respond to CRH b/c aberrant feedback inhibition
determining primary vs ectopic ACTH
MRI - if >5mm adenoma in pituitary, likely to be primary. if not, need to keep investigating w/
is this primary or ectopic ACTH Cushing’s? ACTH stimulates w/ CRH and suppresses w/ high dose dex
primary
is this primary or ectopic ACTH Cushing’s? ACTH doesn’t stimulate w/ CRH and doesn’t suppress w/ high dose dex
ectopic
inferior petrosal sinus sampling
very invasive technique to determine primary vs ectopic ACTH Cushing’s
measure ratio of central ACTH to peripheral - high indicates primary
**only useful if hypercotisolism is already proven! a normal person will respond like a primary Cushing’s pt on this test!
tx of primary ACTH Cushing’s
surgical removal - transsphenoidal
drugs - ketoconazole, metyrapone, mitotane (destroys adrenal tissue - adrenocortical CA), mifipristone (RU486 - glucocorticoid receptor antagonist
radiation
adrenalectomy - risk for Nelson’s dz
Nelson’s dz
uncontrolled growth of residual ACTH producing pituitary tumor due to lack of feedback control by cortisol following adrenalectomy > extreme hyperpigmentation and muscle weakness
pituitary apoplexy - what is it and presentation
bleeding into pituitary > leads to hypopituitarism
30% cases - acute event w/ HA and visual disturbances, N/V
70% - silent asymptomatic
genetic cause of hypopituitarism
PROP-1 mutation - dont make enough pituitary neurons
tx of pituitary apoplexy
ICU care, IV fluids
high dose IV corticosteroids (assumed adrenal insufficiency)
craniotomy / decompression of pituitary fossa
post op evaluation for pituitary hormone deficiencies > hormone replacment
insulin tolerance test
gold standard for assessing pituitary hormone secretion. based on opposing roles of insulin vs cortisol and GH. cortisol and GH should increase to stabilize plasma glucose after insulin load
