3 - Anterior Pituitary 2

Question 1

why is dexamethasone nice for endocrinologists?

Answer 1

doesnt show up on cortisol assay so you can still measure pt’s endogenous production of cortisol while they are on it

Question 2

basic derangement in cushing’s

Answer 2

glucocorticoid (cortisol) excess

Question 3

signs/sx of cushing’s

Answer 3

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

Question 4

mech for HTN in cushing’s

Answer 4

cortisol can activate aldosterone receptor

can also have assoc hypokalemia, hypernatremia, metab alkalosis

Question 5

mech for osteoporosis / avascular necrosis in cushing’s / steroid use

Answer 5

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

Question 6

3 problems caused by long term glucocorticoid excess

Answer 6

cataracts, glaucoma, gastritis/PUD

Question 7

common sources of ectopic ACTH for ACTH dependent Cushing’s

Answer 7

Neuroendocrine tumors - carcinoid, small cell lung CA, medullary thyroid CA, pheo, pancreatic islet tumor, gastrinoma

Question 8

main cause of ACTH independent Cushing’s

Answer 8

adrenal adenoma

Question 9

order of diagnostics in Cushing’s

Answer 9

biochemical first (find out if ACTH (in)dependent etc), then you can do imaging

Question 10

biochemical tests to confirm Cushing’s

Answer 10

dexamethasone suppression test
24 hr urine free cortisol
midnight serum cortisol

*random serum cortisol is not helpful!!

Question 11

causes of pseudo-Cushing’s

Answer 11

depression, obesity, alcohol

Question 12

test to best distinguish cushing’s from pseudo-cushing’s

Answer 12

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

Question 13

determining primary vs ectopic ACTH

Answer 13

MRI - if >5mm adenoma in pituitary, likely to be primary. if not, need to keep investigating w/

Question 14

is this primary or ectopic ACTH Cushing’s? ACTH stimulates w/ CRH and suppresses w/ high dose dex

Answer 14

primary

Question 15

is this primary or ectopic ACTH Cushing’s? ACTH doesn’t stimulate w/ CRH and doesn’t suppress w/ high dose dex

Answer 15

ectopic

Question 16

inferior petrosal sinus sampling

Answer 16

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!

Question 17

tx of primary ACTH Cushing’s

Answer 17

surgical removal - transsphenoidal
drugs - ketoconazole, metyrapone, mitotane (destroys adrenal tissue - adrenocortical CA), mifipristone (RU486 - glucocorticoid receptor antagonist
radiation
adrenalectomy - risk for Nelson’s dz

Question 18

Nelson’s dz

Answer 18

uncontrolled growth of residual ACTH producing pituitary tumor due to lack of feedback control by cortisol following adrenalectomy > extreme hyperpigmentation and muscle weakness

Question 19

pituitary apoplexy - what is it and presentation

Answer 19

bleeding into pituitary > leads to hypopituitarism
30% cases - acute event w/ HA and visual disturbances, N/V
70% - silent asymptomatic

Question 20

genetic cause of hypopituitarism

Answer 20

PROP-1 mutation - dont make enough pituitary neurons

Question 21

tx of pituitary apoplexy

Answer 21

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

Question 22

insulin tolerance test

Answer 22

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