Potassium Flashcards
N/K ATPase
stimulated by insulin, aldosterone, and B agonists
pumps K into cells
where is K reabsorbed first
Ascending LOH by Na/K/2Cl
first line tx in hyperkalrmia
inject Ca2+
medications that cause hyperkalemia
k sparing diuretics
NSAIDs via 1) direct tubular damage (interstital nephritis)–>TG feedback–>dec renin production 2) blocks PG–>vascon on afferent arterial–>ischemia and dec tubular flow–>dec gradient
cyclosporine
bactrim
Na/K ATPase dec activity due to
ATP depletion (exercise, ischemia-reperfusion) direct blockage via digitalis
how does hyperosmolarity affect K
ICF shifts to ECF and squeezes K out
ways to get hypoaldosteronism
PRIMARY
adrenal gland damage
congenital (21 alpha hydroxylase def)
heparin
SECONDARY
JGA Damage (diabetes, obstructibe uropathy)
ACEi/ARB- directly and via efferent dilation
acute hyperkalmia management
IV Ca
insulin/glucose
albuterol
bicarb
buy time but eventuallt need to remove k
how to get K out of body
Kayexalate
Familial Hyperkalemic HTN/Gordon’s Syndrome genes
WNK4 inact, WNK1 act
renal losses leading to hypokalemia
diuretic use
hyperaldo
anion excess
hypomagnesiemia (dysfunctioning Na/K ATPase)
GI losses leading to hypokalemia
massive diarrhea/laxative
gastric losses–>decrease H+–>alkalosis–>excrete HCO3- pulling K with it
*both of these have volume depletion aspect too
rapid cell growth
consumes a lot of K (tumors n stuff)
Bartter’s syndrome
defective Na/K/2Cl-- chronic look hypokalemia hypomag volume dep alkalosis
Gitelman’s
defective Na/Cl cotransporter at DCT–stimulates chronic thiazide
less severe than barterrs
hypokal/meta alk