Potassium and Calcium Disorders Flashcards Preview

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Flashcards in Potassium and Calcium Disorders Deck (61):
1

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)

2

How long does it take to excrete acute K load?

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

3

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)

4

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

5

How does aldosterone effect K secretion?

directly increase the activity of Na/K ATPase in CD

6

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

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

7

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

primary aldosteronism, secondary aldosteronism: diuretics, vomiting

8

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

9

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

10

Laboratory tests for differential diagnosis for K?

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

11

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

12

Causes of hypokalemia with high TTKG? low TTKG?

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

13

Causes of hyperkalemia with high TTKG? low TTKG?

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

14

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)

15

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

16

What are the extra-renal causes of hypokalemia?

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

17

What are the renal causes of hypokalemia?

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

18

What is pseudohypokalemia?

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

19

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

20

What are sources of extrarenal K loss?

skin (sweat), GI tract losses

21

What are causes of renal K loss hypokalemia?

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

22

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!

23

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

24

What are causes of secondary aldosteronism?

diuretics, vomiting, disorders of decreased EABV

25

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

26

How do you treat hypokalemia?

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

27

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

28

What are some extrarenal causes of hyperkalemia?

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

29

What are some renal causes of hyperkalemia?

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

30

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

31

What conditions impair aldosterone production?

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

32

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

33

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)

34

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

35

What can reduce PTH release?

profound hypomagnesemia

36

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

37

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

38

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)

39

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

40

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

41

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

42

What is Chvostek's sign?

tapping of facial nerve branches leads to twitching of facial muscle

43

What is Trousseau's sign?

carpal spasm in reponse to forearm ischemia (tourniquet)

44

What are some causes of hypocalcemia?

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

45

What are some causes of lack of PTH induced hypocalcemia?

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

46

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)

47

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)

48

How do you treat hypomagnesemia induced hypocalcemia differently?

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

49

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

50

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

51

What are the 2 main causes of hypercalcemia?

hyperparathyroidism or malignancy

52

What is primary hyperparathyroidism?

PTH secreted autonomously from adenomatous glands without regard to physiological stimuli

53

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

54

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

55

How does hyperthyroidism cause hypercalcemia?

increased bone turnover

56

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)

57

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

58

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

59

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

60

What imaging is important in diagnosing hypercalcemia?

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

61

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)