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31 Cards in this Set

  • Front
  • Back
nl total serum Ca
8.5 - 10.5
nl ionized Ca
4.4 - 5.4
calc corrected calcium
(obs Ca + .8)*(4 - obs alb)
wat are the 3 main regulators of normal ca intake and maintence?
kidney
bone
intestines
____ is the most important hormone regulator of [Ca] in the serum
parathyroid hormone
important ions and parts of Ca reabsorption in the the nephron
-50-70% of Ca is reabsorbed in the proximal tubules that are NA-DEPENDENT DOE

-PTH reabsorbeds Ca in the DT and Collecting duct

-30-40% of Ca reabsorbed in the loop of henle. loop diuretics/furesomide prevent Ca reabsoption
what lab should order for a pt who is in an alkalotic / acidotic state?
ionized Ca lab

alkalosis - dec ionized Ca. more alb-ca

acidotic - inc ionized Ca. less Ca bound to alb
nl for vitamin 25(OH)D serum levels
nl 30-80 ng/mL
wat are the vitD conversions of calcitriol, doxeralciferol, paricalcitol
calcitriol - 1mcg
-2 to 1
doxercalciferol - 2mcg
-2 to 1
paricalcitol - 4mcg

paricalcitol or calcitriol 4:1
tx of acute hypocalcemia
-200-300mg elemental CaIV bolus over 5-10mins til stms resolve
-elemental Ca .5 - 2 mg/kg/hr until ionized Ca resolves
.3 - .5 mg/kg/hr infusion to maintain Ca

monitor ionized Ca until resolved
how much elemental Ca is in CaCO3 1250 mg
500mg, 40%
how much elemental Ca is in CaAcetate 667 mg
169mg, 25%

want to give 1-2 gm elemental Ca / day outside of meals in divided doses...at least 1.5 hrs
DI hypercalcemia causes
thiazides
lithium
anti-estrogens
vitD, A toxicity
tx hypercalcemia and when?
cincaclet to dec [PTH] and Ca when iPTH >300 pg/mL and corrected Ca >8.4 mg/dL
wat to expect and when to adjust cinacalcet?
anticipate 10% dec in [Ca]

-obtain 1-2 weeks after initiation or dose increase
tx for emergent hypercalcemia
-hydrate with NS
-furosemide
-monitor Ca, PTH, Na, Mg, K

-Calcitonin in CHF or non-responders to saline/furosemide
--must use test dose first doe
tx hypercalcemia bc of malignancy?
rehydrate
-use bisphosphonates
--monitor for nephrotoxictity; Scr, jaw osteonecrosis
--PO4, Mg, Ca
tx for chronic hypercalcemia
chronic hypercalcemia with corticosteroids by dec Ca, GI absorption by inhibiting vit D activation
minute shifts of organic P between ECF <--> inctracellular cause _______
profound changes in P levels
nl serum P
varying factors
2.5 - 4.5 mg/dL
-can vary diurnally through insulin and carbs
PO4 things need to look up frequently
-mmol conversion to meQ and elemental P
-administration of IV PO4 repletion
-PO replacement therapy with PO4
______ most important regulator of serum P
kidneys most important regulator of serum P
wat happens to PO4 in CKD / 2nd hyper-PTH
PTH not stimulating kidneys to excrete P by blocking reabsorption.

-have high Phosphate levels
wat happens to PO4 in primary hypo-PTH
dec PTH, not stimulating PO4 urinary excretion.

- have high phosphate levels
wat happens to PO4 in primary hyperparathyroidism
PTH causes inc in urinary P excretion and decreases P serum

- have low PO4 levels
wat conditions of hypophosphatemia, do not tx
diabetica ketoacidosis / DKA
nonketotic hyperglcemia NKH
wat level and usually see with cells with hypophosphohatemia
PO4 < 1 mg/dL

high turnover cells like RBC / WBC
administer caution with PO4 IV repletion
administer slow n low....over 6 hrs
when to lower / hold dose adjustments to PO4
Ca > 12 mg/dL. hold PO4 bc calcifications can occur
amt of PO4 to add to TPNs to prevent refeding syndrome
15mmol of PO4 / L OR per 1,000 calories of dextrose
goals of KDOQI P binder use
P < 5.5 mg / dL (stage 5).... want <5.5