Darrow Bullshit Flashcards
hypokalemia
produces glucose intolerance
insulin secretion depends on potassium
hypokalemia in kidney
produces defective activation of renal adenylyl cyclase and thus - nephrogenic DI
polyuria occurs
alkalosis
hypokalemia
albuterol
lower serum K concentrations
-by stimulating release of insulin
shifts insulin into cells - lowering serum potassium levels
insulin
causes glucose and potassium to enter cell
no edema in conns
overactive aldosteron
- retention of sodium
- with volume expansion - have production of ANP - counteracts the aldosterone effect
glomerulosa drive
ANG II and K - ANP blocks
fasciculata drive
ACTH
reticularis drive
ACTH
aldosterone
sodium reabsorption in cortical collecting tubule
for each 2 Na reabsorbed - loss of K and H
hypokalemic alkalosis
conns syndrome
primary hyperaldosteronism
can cause HTN
genetic defect with glomerulosa
under control of ACTH
diagnosis of primary hyperaldosteronism
sodium loading
high urine aldosterone and low plasma renin
postural stimulation test
for determine if primary hyperaldosteronism is bilateral hyperplasia or adenoma
post supine elevation of aldosterone - shows b/l adrenal hyperplasia
no response - adenoma
adenoma vs. b/l adrenal hyperplasia tx
adenoma - surgery
adrenal hyperplasia - medical - spironolactone
licorice
inhibits HSD2 - allowing cortisol to drive mineralocorticoid receptor
resultant HTN
-with low aldosterone and renin
pseudohyperaldosteronism
low renin and low aldosterone
liddles, CAH, licorice, cushings, exogenous steroids
primary vs. secondary aldosteronism
primary - high aldosterone, low renin
secondary - high renin, high aldosterone
liddles
GOF mutation of sodium channel
-hyperactive
low renin and low aldosterone
gitelmans
thiazide diuretic effect
don’t reabsorb sodium - goes to collecting duct - turns on sodium reabsorption pathway
bartters syndrome
from loop diuretic
hirsutism due to
decreased sex hormone binding globulin
and excessive 5 alpha reductase activity
decreased sex hormone binding globulin with
decreased estrogen insulin GH obesity hypothyroid glucocorticoids
LH/FSH ration >2 and decreased E/T
polycystic ovarian syndrome
leads to hirsutism
lab test for hirsutism
testosterone
DHEAS
17-hydroxy
ovarian neoplasm
testosterone increase
adrenal neoplasm
DHEAS increase
CAH
17-hydroxy increased
congenital adrenal hyperplasia
virilization with low BP
21 hydroxy
virliation with high BP
11 hydroxy
NE, E and hyperglycemia
alpha 2 - decreased insulin
beta 2 - increased liver gluconeogenesis
NE tumor
paraganglion chain
E tumor
adrenal tumor
incidentalomas
60% associated with some degree of CAH
