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19 Cards in this Set
- Front
- Back
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potassium is mainly located in which cellular comparment
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intracellular
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cellular functions of K+
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regulate protein and glycogen synth
resting membrane potential hyperkalemia - initally see increased membrane excitability, then ultimately decreased membrane excitability hypokalemia - increased neuromuscular excitability |
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intercalated cell secretes or reabsorbs K+
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reabsorbs
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principle cell secretes or reabsorbs K+
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secretes (especially under aldosterone influence)
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hypokalemia etiology
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mainily due to increased cellular uptake or excretion
cellular uptake seen in alkalosis - H+ goes out, K+ goes into cell ---see increased cellular uptake with high insulin, high catecholamines ---hypokalemic periodic paralysis, treatment of anemia, hypothermia, barium, pseudohypokalemia excretion ---vomiting, N-G suction induces aldosterone -> secrete K+ into urine ---diarrhea, villous adenoma, laxitives ----urine loss through increased Na+, mineralocorticoid, nonreabsorbable anions, nephrotoxin |
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T/F more potassium is lost as more Na+ is delivered to distal nephron
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True
increased Na+ delivery to distal nephron can cause hypokalemia diuretics bartter syndrome gitelman's syndrome |
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bartter syndrome
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defect in Na-K-2Cl transporter usually (defect is like being on furosomide)
in thick ascending limb |
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gitelman's syndrome
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defect in NaCl co transporter (like being on a thiazide diuretic)
in distal convoluted tubules |
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mineralocorticoid excess states
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primary hyperalodsteronism due to adrenal adenoma, bilateral adrenal hyperplasia
glucocorticoid suppressible hyperaldosteronism - chimeric gene for aldosterone contians ACTH responsive unit cushings ectopic ACTH congenital adrenal hyperplasia hyperrennism - renal artery stenosis syndrome of apparently mineralocorticoid excess (licorice) |
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nonreabsorbable anions to distal nephron
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can cause hypokalemia
HCO3- will draw out K+ ketoacids hippurates penicillin derivatives |
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nephrotoxins
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amphotericin B interacts with membrane sterols -> K+ loss across membrane
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liddle's syndrome
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activated Na+ channels of principle cells (independent of aldosterone) - stuck on
auto dom |
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hypomagnesmia
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often see with hypokalemia
need to correct Mg++ |
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hypokalemia manifestation
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muscle weakness
ileus re-entrant arrhythmias EKG: ST depression, U waves, QT prolonged nephrogenic DI rhabdomyolysis |
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hyperkalemia
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some defect in excretion
and high intake |
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hyperkalemia cellular shift
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pseudohyperkalemia - K+ movement out of cells during or after blood drawn - due to leukocytosis, thrombocytosis, trauma
metabolic acidosis - cells buffer H+ by cellular uptake and K+ moves OUT insulin deficiency - decreases Na+ K+ ATPase activity cell death - tumor lysis, rhabomyolysis - releases K+ beta blockers digoxin - inhibits Na/K ATPase exercise sucinylcholine, arginine cardiac bypass |
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hyperkalemia inpaired excretion
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renal failure
volume depletion hypoaldosteronism - due to decreased activity (hyporeninemic hypoaldosteronism, ACEI, NSAIDS) or decreased synthesis (primary adrenal insufficiency, enzyme defect, heparin) aldosterone resistance - K+ sparing diuretics, trimepthoprim, pseudohypoaldosteronism type II) |
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assessing hypoaldosteronism
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asses hypoaldosteronism with plasma renin to plasma aldo - look a transtubular K+ gradient
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hyperkalemia sympoms
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arryhthmias
ekg findings: peaked T waves short Q-T interval but longer later widened QRS decreased P wave sinewave sorry if potassium > 7.5 mEq/L |
