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Renal > 11 - Ca, PO4, Mg > Flashcards

11 - Ca, PO4, Mg Flashcards

1
Q

electrolyte rule of 3s

A

Ca, P, Mg
controlled by PTH, VitD, phosphatonins
affect bone, intestine, kidney

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2
Q

PTH - stimulated by, inhibited by

A

stim: low ionized Ca (inactivation of Ca Sensing Receptor)
inc serum phosphate, low serum Mg

inhib: inc ionized Ca levels
calcitriol

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3
Q

how are hypomagnesemia and hypocalcemia associated with each other?

A

hypomagnesemia affects cGMP signaling > PTH unable to work at bone / release Ca

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4
Q

how does PTH inc serum Ca?

A

inc resorption of bone > release Ca and PO4
inhibit PO4 reabs in kidney in PCT (less PO4 to bind Ca > more free Ca)
inc reabs of Ca in DCT and stimulates renal 25(OH)D-1-hydroxylase > activation of vit D > abs of Ca from GI tract

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5
Q

Ca sensing receptor - location

A

kidney, parathyroid gland, intestine

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6
Q

action of Ca sensing receptor (CaSR) in parathyroid gland

A

less PTH produced

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7
Q

action of CaSR in kidney

A

thick ascending loop
when activated, inhibits apical K channel
Ca absorption stops
end result is like furosemide > calciuresis

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8
Q

treating hyperPTH

A

cinacalcet - binds to CaSR

also can try calcitriol (form of vit D) for feedback inhibition, or surgical parathyroidectomy

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9
Q

activation of Vit D

A

first by 25-hydroxylase in liver

then 1-alpha hydroxylase in kidney

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10
Q

another name for activated vit d

A

calcitriol

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11
Q

what stimulates activation of vit d?

A

PTH (feedback)
low PO4, low Ca
estrogen, prolactin, calcitonin, growth hormone

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12
Q

actions of calcitriol

A

inc Ca, Mg, PO4 abs in intestine

inhibit PTH secretion

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13
Q

phosphatonins - example, where made, what is main message

A

FGF23
bone
tells kidneys to dump PO4

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14
Q

what hormone is high in CKD due to PO4 retention?

A

phosphatonins

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15
Q

calcitonin

A

minor role in Ca reg
opposite of PTH
lowers serum Ca

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16
Q

nl serum Ca

A

9-10.4 mg/dl

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17
Q

serum Ca distribution and how it is affected by change in acid base state

A

nl - 45% protein bound, 45% ionized, 10% complexed
acidosis - inc ionized Ca
alkalosis - dec ionized Ca

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18
Q

where in the nephron is Ca transport hormone regulated?

A

DCT

19
Q

how to correct serum Ca for albumin

A

corrected = Ca + (4-albumin)*0.8

20
Q

etiologies of hypocalcemia

A

absence of PTH gland/function
hypomagnesemia
ineffective PTH - vit D def, malabsorption of Ca
PTH overwhelmed - hyperphosphatemia causes Ca PO4 complexing

21
Q

presentation of hypocalcemia

A

tetany, Trousseau and Chvostek signs
seizures, neuropsych changes
prolonged QT, arrhythmias, hypotension, HF
coarse scaly skin, cataracts

22
Q

tx of hypocalcemia

A

correct underlying dz

give Ca and/or vit D

23
Q

causes of hypercalcemia

A 
hyperPTH
acidemia
immobilization (>breakdown of bone)
vit D and Ca abs in GI, lots of milk
thiazide diuretics
familial hypercalcemia
granulomatous production and calictriol
24
Q

presentation of hypercalcemia

A

“bones stones groans abd moans”
vasoconstriction, HTN, short QT
ulcers, constipation, pancreatitis
lethargy, obtundation, psychosis, weakness
extraskeletal calcifications - dermal, ocular, vascular, visceral organs

25
Q

how can hypercalcemia affect kidney?

A

AKI
nephrogenic DI
stones
calicifications

26
Q

tx for hypercalcemia

A

optimize renal excretion by giving Na and water to lessen reabs in PCT, promote Ca loss at LoH w/ loop diuretics
inhibit bone resorption w/ calcitonin or bisphosphonates

** most important is aggressive volume replacement

27
Q

MCC hypercalcemia (2)

A

primary hyperPTH and malignancy

28
Q

how is GI abs of PO4 regulated?

A

inc by calcitriol

no way to reduce it though - kidneys must remove excess absorbed

29
Q

how is PO4 reabs in the kidney handled?

A

most reabs in PCT

inhib by PTH and FGF23 via reducing transporter expression

30
Q

causes of hypoPO4

A 
severe alcoholism
gluc infusion after starvation
elevated PTH
Fanconi syndrome
PO4 binding antacids
vit D deficiency > dec GI abs
certain tumors / neoplastic syndrome
31
Q

presentation of hypoPO4

A 
acute:
inadequate ATP production
muscle weakness/necrosis
cardiac failure, neurologic dysfunction
hemolysis, tissue hypoxia
impaired platelet and macrophage function

chronic - inc bone resorption - demineralization and pain

32
Q

tx of hypophosphatemia

A

milk, cheese, eggs, supplements

IV in emergencies, but can cause severe hypocalcemia by complexing w/ Ca

33
Q

causes of hyperPO4

A

tumor lysis
rhabdomyolysis (also trauma/crush)
kidney dz

34
Q

consequences of hyperPO4

A

complexes w/ Ca > deposits everywhere. Calciphylaxis has VERY high mortality

secondary hyperPTH:
hypocalcemia due to complexing > release of PTH
osteitis fibrosa cystica and metastatic califications

35
Q

tx of hyperPO4

A

correct underlying problem

3 d’s: diet, dietary binders (PO4 binders like Mg, Al, Ca, etc), dialysis

36
Q

causes of Mg cell efflux and influx

A

efflux - beta stim

influx - insulin, calcitriol, vit B6

37
Q

role of Mg in body

A

DNA/protein synth
neuronal activity, cardiac excitability, vasomotor tone / BP
cofactor for transport of K and Ca

38
Q

where is most Mg reabs in kidney?

A

thick ascending limb

39
Q

hypomagnesemia cause

A

malnutrition, alcoholism, malabsorption

renal wasting after nephrotoxic drugs

40
Q

hypomagnesemia presentation

A

muscle weakness, tremors, fasciculations, arrhythmias
neuro/psych changes
hypocalcemia, hypokalemia

41
Q

hypermagnesemia causes

A

iatrogenic (use as tocolytic)

Mg containing antacids

42
Q

presentation of hypermagnesemia

A

thirst, nausea, vomiting
drowsiness, hypotension, depressed DTR
coma, resp paralysis, cardiac arrest

43
Q

tx of hypermagnesemia

A

initial - IV Ca - stabilize heart
loop diuretics
dialysis

Renal (20 decks)

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