aldosteronism and phenochromocytomas Flashcards
complications of hypokalemia
glucose intolerance dt decreased insulin release
DI d/t defective vassopressin signaling
albuterol and K
lowers serum potassium by stimulating release of insulin which shifts K into cells
glomerulosa
aldosterone
fasiculata
cortisol
reticularis
Androgens
what is the ald>renin ratio in primary hyperaldosteronism
> 30
conns syndrome
primary hyperaldosteronism
5-10% of HTN patients
causes of conns
adrenal adenoma
unilateral or bilateral hyperplasia
genetic defect with overly strong effect of ACTH on aldosterone
workup for primary aldosteronism
- 8am renin (if high, not primary hyperaldosteronism)
- if renin low stand for 3 hours then take A/R ratio, if >30 they have primary hyperaldosteronism
- Confrim with Na loading and 24hr urin for aldosterone, if >20 confirmed
- adrenal CT or adrenal vv sampling, if both sides have = aldosterone secretion then they have b/l adrenal hyperplasia, if only unilateral they have adenoma
- if you can’t do imaging use postural stimulation test (if bl hyperplasia aldosterone will increase more)
Tx of adenoma
surgery
Tx of hyperplasia
spironolactone or eplerenone
licorice
inhibits 11beta hydroxysterioid dehydrogenase 2
secondary aldosteronism
high renin and aldosterone
diuretics (excluding K sparring)
vomiting
nasogastric suction
psudohyperaldosteronism
low renin and aldosterone liddles cushings exogenous steroids CAH licorice
bartters/gitelmans
syndromes which cause pt to present in childhood like they r on diuretics vomiting dehydrated increased renin hypotensive
Liddles
gain of fnx mutation, apical NaCh always open
HTN with low K, low R, and low A
pseudohyperaldosteronism
Hirsutism
usually dt decreased sex hormone binding globlin -> increased free T
causes of hirsutism
decreased E insulin GH obesity (PCOS) hypothyroidism glucocorticoids (cushings) androgens nephrotic syndrome excessive activity of 5-alpha reductase idiopathic/familial
PCOS
LH/FSH >2 -> decreased E/T
hypothyroidism
decreases SHGB and TRH induces prolactin
ovarian/adrenal tumors
LH/FSH -> hyperthecosis
arrested development w/luteinized thecal cells over producing T
drugs
pheytoin minoxidil anabolic steroid cyclosporine OCPs penicillin
CAH
deficiency of 21 hyroxylase
labs for hirsutism
TSH PRL IGF-1 24 hr cortisol T DHEA 17OHP
what will labs look like if idiopathic/hereditary
free and total T
DHEAS
17OHP
all normal
PCOS labs
T mildly increased
DHEAS and 17OHP normal
CAH labs
total T, DHEAS, 17OHP all increased
causes of virilization
ovarian tumor
adrenal tumor
CAH
labs for ovarian tumor
total T greatly increased with normal DHEAS and 17OHP
adrenal tumor labs
greatly increased DHEAS
CAH labs
total T, DHEAS, 17OHP all increased
Tx for hirsuitism
OCPs with progestins
antiandrogens: spironolactone, flutamide, dinasteride
metformin
GnRH agonists
causes of non-essential HTN
aldosteronism licorice myxedema and hypercalcemia pheochromocytoma steroid excess hyperthyroid
NE/epi can cause what
neutrophilia
hyperglycemia -> decreased insulin output and increased liver glucose production
hypotension
hypercalcemia
how does NE/epi cuase hypotension
down regulation of alpha R -> hypotension
Epi -> B2 -> vasodilate
how does NE/epi cause hypercalcemia
adrenergic stim of parathyroids or tumor itself releases PTH-rP
Epi producing tumor
must be in adrenals
NE producing tumor
anywhere in paraganglion chain
Dx of pheo
plasma metanephrine
24-hour urinary catecholamine
CT, MRI, MIBG
whole body scan for mets
when should u Bx an incidentaloma?
when >6cm
pre-op eval should include plasma metanephrines and dexamethazone supression test
causes of flushing
carcinoid
medullary carcinoma of thyroid
pheo
