Integrative Physiology II- Renal Regulation of Potassium Secretion and Diuretics Flashcards
(51 cards)
what is the [K+]ECF
4.2 meq/L
what are the mechanisms controlling K+ homeostasis
-control of K+ distribution between ECF and ICF
- to keep [K]+ ECF constant, rate of K+ excretion=rate of K+ input
what are factors that shift K+ into cells thereby decreasing [K+]ECF
-insulin
-aldosterone
- beta2 adrenergic stimulation
- alkalosis
- low ECF Osm
- increased Na+/K+ ATPase activity
-dilute ICF
- low EC gradient for diffusion of K+ out of cell
what are factors that shift K+ out of cells thereby increasing [K+]ECF
-increased insulin deficiency in DM
- aldosterone deficiency in Addisons disease
-Beta2 adrenergic antagonists
-acidosis
-increased ECF Osm
-strenuous exercise
-Cell lysis
-decreased Na+/K+ ATPase activity
-concentrated ICF
- high EC gradient for diffusion out of cell
does acidosis cause hyperkalemia or hypokalemia
hyperkalemia
how does acidosis cause hyperkalemia
H+ inhibits Na+ K+ ATPase causing K+ to build up in the cell
what are the three factors in the tubular processing of K+
filtration, reabsorption and secretion
where is most K+ absorbed
in the PT
where is most K+ secreted
CD
what are the substances that go through all 3 processes in renal processing
urea and K+
what is day to day regulation of [K+] ECF a function of
late distal tubule/collecting duct
what does a high K+ intake cause
increased K+ secretion by principal cells
what does a low K+ intake cause
increased K+ reabsorption by alpha intercalated cells
what are the factors that determine rate of K+ secretion by principal cells
- Na+/K+ ATPase activity
- transepithelial potential difference (TEPD) between blood and lumen
- permeability of apical membrane for K+
what are factors that control prinicpal cell K+ secretion
- high [K+]ECF
- high aldosterone
-high distal tubule flow rate - acid/base status: if alkalosis: high K+ secretion and if acidosis: low K+ secretion
what are the mechanisms of how increased [K+]ECF increases K+ secretion
-increased Na+/K+ ATPase activity
-TEPD is more lumen negative due to increased Na+ reabsorption which favors K+ secretion
- increased number K+ channels in apical membrane
- stimulates aldosterone secretion
how does aldosterone increase K+ secretion
-increased K+ intake -> increased plasma K+ -> increased aldosterone secretion at the renal cortex -> increased plasma aldosterone -> increased K+ secretion at the CCD
-> K+ excretion
what causes increased distal tubule flow rate to increase K+ secretion
- increased ECF volume
-Na+ loading
-some diuretics
what are the mechanisms of increased distal tubule flow rate increasing K+ secretion
-increased tubule flow rate keeps luminal K+ lower, maintaining chemical gradient for secretion
- increases #BK channels in apical membrane
what are the causes of hyperkalemia
- renal failure
- decreased distal nephron flow (CHF, NSAID)
- decreased aldosterone or decreased effect of aldosterone (adrenal insufficiency, resistance to aldosterone, K+ sparing diuretics)
-metabolic acidosis - diabetes
what are the causes of hypokalemia
- very low intake of K+
- GI loss of K+ from diarrhea
- metabolic alkalosis
- excess insulin
- increased distal tubular flow: salt wasting nephropathies, osmotic diuretics, loop diuretics
- excess aldosterone
what are diuretics
drugs that increase urine volume output
what is the most common reason for diuretics
to reduce ECFV which reduces edema and MAP
what are the 2 mechanisms of action of diuretics and which is more common
-act by decreasing Na+ reabsorption from some part of the nephron - more common
- act by decreasing water reabsorption
