11 - Ca, PO4, Mg Flashcards
electrolyte rule of 3s
Ca, P, Mg
controlled by PTH, VitD, phosphatonins
affect bone, intestine, kidney
PTH - stimulated by, inhibited by
stim: low ionized Ca (inactivation of Ca Sensing Receptor)
inc serum phosphate, low serum Mg
inhib: inc ionized Ca levels
calcitriol
how are hypomagnesemia and hypocalcemia associated with each other?
hypomagnesemia affects cGMP signaling > PTH unable to work at bone / release Ca
how does PTH inc serum Ca?
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
Ca sensing receptor - location
kidney, parathyroid gland, intestine
action of Ca sensing receptor (CaSR) in parathyroid gland
less PTH produced
action of CaSR in kidney
thick ascending loop
when activated, inhibits apical K channel
Ca absorption stops
end result is like furosemide > calciuresis
treating hyperPTH
cinacalcet - binds to CaSR
also can try calcitriol (form of vit D) for feedback inhibition, or surgical parathyroidectomy
activation of Vit D
first by 25-hydroxylase in liver
then 1-alpha hydroxylase in kidney
another name for activated vit d
calcitriol
what stimulates activation of vit d?
PTH (feedback)
low PO4, low Ca
estrogen, prolactin, calcitonin, growth hormone
actions of calcitriol
inc Ca, Mg, PO4 abs in intestine
inhibit PTH secretion
phosphatonins - example, where made, what is main message
FGF23
bone
tells kidneys to dump PO4
what hormone is high in CKD due to PO4 retention?
phosphatonins
calcitonin
minor role in Ca reg
opposite of PTH
lowers serum Ca
nl serum Ca
9-10.4 mg/dl
serum Ca distribution and how it is affected by change in acid base state
nl - 45% protein bound, 45% ionized, 10% complexed
acidosis - inc ionized Ca
alkalosis - dec ionized Ca
where in the nephron is Ca transport hormone regulated?
DCT
how to correct serum Ca for albumin
corrected = Ca + (4-albumin)*0.8
etiologies of hypocalcemia
absence of PTH gland/function
hypomagnesemia
ineffective PTH - vit D def, malabsorption of Ca
PTH overwhelmed - hyperphosphatemia causes Ca PO4 complexing
presentation of hypocalcemia
tetany, Trousseau and Chvostek signs
seizures, neuropsych changes
prolonged QT, arrhythmias, hypotension, HF
coarse scaly skin, cataracts
tx of hypocalcemia
correct underlying dz
give Ca and/or vit D
causes of hypercalcemia
hyperPTH acidemia immobilization (>breakdown of bone) vit D and Ca abs in GI, lots of milk thiazide diuretics familial hypercalcemia granulomatous production and calictriol
presentation of hypercalcemia
“bones stones groans abd moans”
vasoconstriction, HTN, short QT
ulcers, constipation, pancreatitis
lethargy, obtundation, psychosis, weakness
extraskeletal calcifications - dermal, ocular, vascular, visceral organs
how can hypercalcemia affect kidney?
AKI
nephrogenic DI
stones
calicifications
tx for hypercalcemia
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
MCC hypercalcemia (2)
primary hyperPTH and malignancy
how is GI abs of PO4 regulated?
inc by calcitriol
no way to reduce it though - kidneys must remove excess absorbed
how is PO4 reabs in the kidney handled?
most reabs in PCT
inhib by PTH and FGF23 via reducing transporter expression
causes of hypoPO4
severe alcoholism gluc infusion after starvation elevated PTH Fanconi syndrome PO4 binding antacids vit D deficiency > dec GI abs certain tumors / neoplastic syndrome
presentation of hypoPO4
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
tx of hypophosphatemia
milk, cheese, eggs, supplements
IV in emergencies, but can cause severe hypocalcemia by complexing w/ Ca
causes of hyperPO4
tumor lysis
rhabdomyolysis (also trauma/crush)
kidney dz
consequences of hyperPO4
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
tx of hyperPO4
correct underlying problem
3 d’s: diet, dietary binders (PO4 binders like Mg, Al, Ca, etc), dialysis
causes of Mg cell efflux and influx
efflux - beta stim
influx - insulin, calcitriol, vit B6
role of Mg in body
DNA/protein synth
neuronal activity, cardiac excitability, vasomotor tone / BP
cofactor for transport of K and Ca
where is most Mg reabs in kidney?
thick ascending limb
hypomagnesemia cause
malnutrition, alcoholism, malabsorption
renal wasting after nephrotoxic drugs
hypomagnesemia presentation
muscle weakness, tremors, fasciculations, arrhythmias
neuro/psych changes
hypocalcemia, hypokalemia
hypermagnesemia causes
iatrogenic (use as tocolytic)
Mg containing antacids
presentation of hypermagnesemia
thirst, nausea, vomiting
drowsiness, hypotension, depressed DTR
coma, resp paralysis, cardiac arrest
tx of hypermagnesemia
initial - IV Ca - stabilize heart
loop diuretics
dialysis
