Potassium and Calcium Disorders Flashcards Preview

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Flashcards in Potassium and Calcium Disorders Deck (61):

What are the physiological functions of K?

cell metabolism (regulation of protein and glycogen synth), ratio K IC:K EC is major determinant of RMP (low and high K can result in potentially fatal muscle paralysis and cardiac arrhythmias)


How long does it take to excrete acute K load?

6-12 hours, 90-95% of dietary potassium by kidneys, remaining by gut


How do the kidneys handle K?

freely filtered across glomerular capillary into PT, completely reabsorbed by PT and LOH, in DT and CD K secreted into tubular lumen (determinant of Uk excretion)


What are the 5 major factors that stimulate distal K secretion?

aldosterone, high distal Na delivery, high urine flow rate, high [K] in tubular cell, and metabolic alkalosis


How does aldosterone effect K secretion?

directly increase the activity of Na/K ATPase in CD


What are the causes of hyperkalemia due to impaired aldosterone production?

diabetic nephropathy, chronic interstitial nephritis, NSAIDs, ACE-inhibitors, ARBs, DRI, Heparin, Spironolactone


What are the causes of hypokalemia due to increased aldosterone levels?

primary aldosteronism, secondary aldosteronism: diuretics, vomiting


What causes shifts of K from IC to EC?

stimulation of Na/K ATPase by insulin and B2-adrenergic agonists or acid/base disorders (Alk-> K in, hypokalemia, Acid-> K out, hyperkalemia), hyperosmolality- H2O in and K out


How does exercise effect K regulation?

hypokalemia due to alpha-adrenergic receptor activation inhibits NaKATPase -> K out-> induces arterial dilation; B2 stimulates K uptake and minimizes severity of hyperkalemia


Laboratory tests for differential diagnosis for K?

spot urine K- >20 renal wasting, < 20 extrarenal cause; TTKG


What is TTKG?

index reflecting conservation of K in CD, estimates ratio of K in lumen to peritubular capillaries, valid only when Uosm >300 and Una >25


Causes of hypokalemia with high TTKG? low TTKG?

high- >7 high renal losses (hyperaldosteronism), low- extrarenal (<3 in hypo)


Causes of hyperkalemia with high TTKG? low TTKG?

high- consistent w/ extra-renal cause, low- renal cause, 10


What are the signs and symptoms of hypokalemia?

muscle weakness or paralysis, cardiac arrhythmias (esp. ventricular), Rhabdomyolysis, renal dysfunction (impaired conc. and acidification, abnormal NaCl reabsorption), hyperglycemia (impairs insulin release and tissue sensitivity)


What areas of interest are there for assessment of hypokalemia?

Hx- drug use, Vomit, diarrhea, Exam- hydration status, Lab- blood and urine electrolytes and osm, EKG


What are the extra-renal causes of hypokalemia?

lab error, decreased intake, increased loses from GI or skin, redistribution- alkalemia, insulin, B2 agonists


What are the renal causes of hypokalemia?

loop and thiazide diuretics, mineralocortiod excess, renal transport problems: liddle's, bartter's, gitelman's


What is pseudohypokalemia?

large numbers of WBC take up EC K if blood is stored for prolonged periods


What are the two mechanisms of redistribution hypokalemia?

hormones (insulin, aldosterone, B2 adrenergic) stimulate transcellular K uptake or hypokalemic periodic paralysisdue to genetic abnormalities in dihydropyridine sensitive Ca channel


What are sources of extrarenal K loss?

skin (sweat), GI tract losses


What are causes of renal K loss hypokalemia?

drugs (thiazide, loop diuretics, cisplatin, toluene), endogenous hormones (aldosterone), Magnesium depletion, intrinsic renal defect, bicarbonaturia


what are the clinical features of apparent mineralocorticoid excess?

11 B-hydroxysteroid dehydrogenase deficiency, defect in conversion of cortisol to cortisone, high tissue cortisol activates mineralocorticoid receptors producing HTN and hypokalemia, congenital adrenal hyperplasia; hypertension!


What are the features of glucocorticoid-remediable aldosteronism?

rare AD condition, fushion of 11B-hydroxylase and aldosterone synthase genes, aldosterone secretion stimulated by ACTH and suppressed by exogenous mineralocorticoid; HTN and hypokalemia


What are causes of secondary aldosteronism?

diuretics, vomiting, disorders of decreased EABV


What is cushings? How does it effect K?

cortisol weak mineralocorticoid, rapidly converted to cortisone usually in CD, production exceeds conversion in cushings producing aldosteronism effect, hypokalemia


How do you treat hypokalemia?

symptomatic- IV K (no more than 10mEq/hr), Asymptomatic- Oral K (20-40mEq), correct underlying medical problem


what are the clinical manifestations of hyperkalemia?

GI: anorexia, N/V, cramps, diarrhea; CV: Vfib, arrest, EKG changes (peaked T, flat/absent P, widened QRS, brady, pseudoinfarct, sine wave); NM: parethesias, weakness, muscle cramps; MSk: extreme paralysis and resp. failure


What are some extrarenal causes of hyperkalemia?

Spurious (pseudo or lysis), Excess intake, redistribution (acidosis, insulin def., B block, Exercise, Tissue lysis- rhabdo/tumor)


What are some renal causes of hyperkalemia?

Failure, insufficiency (obstruction, interstitial disorder), aldosterone deficiency (1, Type 4 RTA, antiangiotensin)


What is significant in history or physical/labs to consider for hyperkalemia?

drugs, diet and supplements, kidney disease, DM, BP, Edema, P and U osm and electrolyte, ABG, EKG


What conditions impair aldosterone production?

Disease- DM, chronic interstitial nephritis; Drugs: NSAIDs, ACE-1, ARB, DRI, Heparin, Spironalactone/amiloride/triamterene


How do you treat hyperkalemia?

Calcium gluconate if EKG changes to stabilize myocardium, insulin and glucose (cellular shift K, only hours), NaHCO3 (30 min, more effective in acidosis), B agonist (30 min, 2-4hours), kayexalate (oral- 2-4 hrs, rectal 1 hour), hemo or peritoneal dialysis


What is the function of PTH?

maintain Ca homeostasis by: inc. bone mineral dissolution to release Ca and P, increase renal reabsorption of Ca, enhance GI absorption Ca and P, (indirect effect on calcitriol synthesis)


What triggers PTH secretion?

hypocalcemia- EC ionized Ca, active secretion of PTH grannules controlled by CaSR in thyroid C-Cells and in kidney; hyperphosphatemia, calcitriol deficiency


What can reduce PTH release?

profound hypomagnesemia


How is vitamin D synthesized?

light + 7-dehyrocholesterol(skin) = calcidiol, calcidiol can also be ingested from plants, converted to caclitriol in kidney by 1ahydroxylase, calcitriol ingested from oily fish-> diol in liver


What are the major functions of calcitriol?

SI- regulate absorption of Ca, lesser degree (P and Mg), inhibits PTH synthesis, directly stimulates secretion of FGF23 from bone


What is FGF23? function?

made by osteocytes, inhibits conversion of calcidiol to calcitriol through down regulation of 1ahydroxylase, inhibits PTH (completing feedback, PTH stimulates FGF23)


Where and how much Ca is reabsorbed or secreted in the kidneys?

PT- passive reabsorption 60% filtered, TAL LOH- driven passive paracellular reabsorption 20%, DCT and CT- active transcellular transport 18% filtered load


What is hypocalcemia and what can skew the results? how?

Sca < 8.5md/dL, true= low ionized, hypoalbuminemia have decreased total but not necessarily inonized, excess citrate or acute HCO3 percent bound to these ions increases so less ionized available


What are the clinical manifestations of hypocalcinemia?

fatigue, muscular weakness, inc. irritability, loss of memory, confusion, hallucination, paranoia, depression; acute-parethesias of lips, extremeties and muscle cramps; Chvosteks and trousseau's


What is Chvostek's sign?

tapping of facial nerve branches leads to twitching of facial muscle


What is Trousseau's sign?

carpal spasm in reponse to forearm ischemia (tourniquet)


What are some causes of hypocalcemia?

lack of PTH or vitamin D, increased Ca complexation, or hypomagnesemia


What are some causes of lack of PTH induced hypocalcemia?

post thyroidectomy or parathyroidectomy, hereditary hypoparathyroidism, pseudohypoparathyroidism (lack effective PTH), hypomagnesemia (blocks secretion)


What are some causes of lack of vitamin D induced hypocalcemia?

dietary deficiency or malabsorption (osteomalacia), inadequate sunlight, defective metabolism (anitconvulsants, liver disease, renal disease, vitamin D resistant rickets)


What are some causes of increased Ca complexation induced hypocalcemia?

"bone hunger" after parathyroidectomy, rhabdomyolysis, acute pancreatitis, tumor lysis syndr. (hyperphosphatemia), malignancy (inc. osetoblastic activity)


How do you treat hypomagnesemia induced hypocalcemia differently?

need to fix Mg defecit before it will respond to D and Ca


How do you treat hypocalcemia?

Life threatening: seizures, tetany, hypotension or cardiac dysrhythmias- IV Ca 100-300 mg over 10-15 minutes; severe symptomatic IV Ca, mild- oral supplement possibly with D


What is hypercalcemia? clinical consequences?

Sca > 10.5 mg; CNS: confusion lethargy, Muscle: weak, constipation, Cardiac: delayed repolarization, skin: itching, renal: concentrating defect, vasculature: constriction, HBP


What are the 2 main causes of hypercalcemia?

hyperparathyroidism or malignancy


What is primary hyperparathyroidism?

PTH secreted autonomously from adenomatous glands without regard to physiological stimuli


What is secondary hyperparathyroidism?

PTH secreted as a normal response but to abnormal stimuli; prolonged period of CKD, hyperplastic glands become adenomatous and unresponsive to suppressive signals


What to conditions does secondary hyperparathyroidism cause? TReatment?

hyperphosphatemia, hypocalcemia, inc bone resorption, inc intestinal absorption of Ca and Pi, treat by diet, dialysis and meds- phosphate binders to prevent absorption, CaSR agonists, Caclitriol


How does hyperthyroidism cause hypercalcemia?

increased bone turnover


What are some endogenous sources of excess calcitriol seen with hypercalcemia?

lymphoma, granulomatous disease (sarcoidosis, tubercular disease- macrophage express 1a-hydroxylase which increase calcitriol production)


What is milk alkali syndrome?

hypercalcemia, metabolic alkalosis, and renal insufficiency; alkalosis augments hypercalcemia by directly stimulating Ca reabsorption in DT, Ca induced decline renal function- vasoconstriction, hypercalcemia, structural injury, can also contribute


What are the main categories of causes of hypercalcemia?

excess PTH production, excess calcitriol production, increased bone resorption, increased intestinal absorption, decreased renal secretion, and impaired bone formation and incorporation of Ca


What labs help with diagnosis of hypercalcemia?

total and ionized Ca, albumin, BUN/creatinine, PTH, PTHrP, levels of calcidiol and calcitriol, urinary excretion of Ca


What imaging is important in diagnosing hypercalcemia?

cervical US or SESTAMIBI (nuclear med scan) scan to locate PT adenoma


How do you treat hypercalcemia?

IV normal saline, loop diuretics (augment urinary Ca losses), calcitonin, bisphosphonates (malignancy and immobilaization), steroids (endogenous calcitriol prod.), Cinacalcet or parathyroidectomy (hyperparathyroidism)