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Acid-Base and Nutrition > Potassium and Calcium Disorders > Flashcards

Potassium and Calcium Disorders Flashcards

1
Q

What are the physiological functions of K?

A

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)

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2
Q

How long does it take to excrete acute K load?

A

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

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3
Q

How do the kidneys handle K?

A

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)

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4
Q

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

A

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

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5
Q

How does aldosterone effect K secretion?

A

directly increase the activity of Na/K ATPase in CD

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6
Q

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

A

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

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7
Q

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

A

primary aldosteronism, secondary aldosteronism: diuretics, vomiting

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8
Q

What causes shifts of K from IC to EC?

A

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

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9
Q

How does exercise effect K regulation?

A

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

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10
Q

Laboratory tests for differential diagnosis for K?

A

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

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11
Q

What is TTKG?

A

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

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12
Q

Causes of hypokalemia with high TTKG? low TTKG?

A

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

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13
Q

Causes of hyperkalemia with high TTKG? low TTKG?

A

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

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14
Q

What are the signs and symptoms of hypokalemia?

A

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)

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15
Q

What areas of interest are there for assessment of hypokalemia?

A

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

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16
Q

What are the extra-renal causes of hypokalemia?

A

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

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17
Q

What are the renal causes of hypokalemia?

A

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

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18
Q

What is pseudohypokalemia?

A

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

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19
Q

What are the two mechanisms of redistribution hypokalemia?

A

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

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20
Q

What are sources of extrarenal K loss?

A

skin (sweat), GI tract losses

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21
Q

What are causes of renal K loss hypokalemia?

A

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

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22
Q

what are the clinical features of apparent mineralocorticoid excess?

A

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!

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23
Q

What are the features of glucocorticoid-remediable aldosteronism?

A

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

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24
Q

What are causes of secondary aldosteronism?

A

diuretics, vomiting, disorders of decreased EABV

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25
Q

What is cushings? How does it effect K?

A

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

26
Q

How do you treat hypokalemia?

A

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

27
Q

what are the clinical manifestations of hyperkalemia?

A

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
Q

What are some extrarenal causes of hyperkalemia?

A

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

29
Q

What are some renal causes of hyperkalemia?

A

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

30
Q

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

A

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

31
Q

What conditions impair aldosterone production?

A

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

32
Q

How do you treat hyperkalemia?

A

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
Q

What is the function of PTH?

A

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
Q

What triggers PTH secretion?

A

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

35
Q

What can reduce PTH release?

A

profound hypomagnesemia

36
Q

How is vitamin D synthesized?

A

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
Q

What are the major functions of calcitriol?

A

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

38
Q

What is FGF23? function?

A

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

39
Q

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

A

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

40
Q

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

A

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
Q

What are the clinical manifestations of hypocalcinemia?

A

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
Q

What is Chvostek’s sign?

A

tapping of facial nerve branches leads to twitching of facial muscle

43
Q

What is Trousseau’s sign?

A

carpal spasm in reponse to forearm ischemia (tourniquet)

44
Q

What are some causes of hypocalcemia?

A

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

45
Q

What are some causes of lack of PTH induced hypocalcemia?

A

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

46
Q

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

A

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

47
Q

What are some causes of increased Ca complexation induced hypocalcemia?

A

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

48
Q

How do you treat hypomagnesemia induced hypocalcemia differently?

A

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

49
Q

How do you treat hypocalcemia?

A

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
Q

What is hypercalcemia? clinical consequences?

A

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

51
Q

What are the 2 main causes of hypercalcemia?

A

hyperparathyroidism or malignancy

52
Q

What is primary hyperparathyroidism?

A

PTH secreted autonomously from adenomatous glands without regard to physiological stimuli

53
Q

What is secondary hyperparathyroidism?

A

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

54
Q

What to conditions does secondary hyperparathyroidism cause? TReatment?

A

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
Q

How does hyperthyroidism cause hypercalcemia?

A

increased bone turnover

56
Q

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

A

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

57
Q

What is milk alkali syndrome?

A

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
Q

What are the main categories of causes of hypercalcemia?

A

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

59
Q

What labs help with diagnosis of hypercalcemia?

A

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

60
Q

What imaging is important in diagnosing hypercalcemia?

A

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

61
Q

How do you treat hypercalcemia?

A

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

Acid-Base and Nutrition (6 decks)

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