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24 Cards in this Set

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clues to identify mixed acid-base disorder
[HCO3−] and PCO2 move in opposite directions
pH changes in the direction opposite that expected from a known primary disorder.
An uncommon cause of elevated AG metabolic acidosis
phosphate intoxication. This can occur if NaH2PO4, present in some enemas and oral bowel cleansing prepar ations, is absorbed in excess of the kidney's ability to excrete phosphate. Dissociation into H+ and HPO42− results in markedly high phosphate levels and a proportionately elevated AG
When calculating the AG in the setting of marked hyperglycemia, there is ?
no need to correct sodium level for glucose.
Sepsis and salicylate intoxication both may present with
mixed respiratory alkalosis and elevated AG metabolic acidosis
contraction alkalosis is seen in
(in which volume depletion causes extracellular fluid to “contract” around a fixed quantity of bicarbonate, raising [HCO3−] and thus inducing a metabolic alkalosis.)
diuretics use
test done to differentiate various type of metabolic alkosis is?
urinary chloride
chronic respiratory acidosis, what happens to chloride levels?
chloride is excreted to neutralise bicarbonate absorption.
hypochloremia occurs.
correction equation for acute respiaratry acidosis is ?
for every 10mm of hg increase in pCO2, HCO3 increases by 1meq/l.
correction equation for chronic respiratory acidoisis is ?
for every 10mm of hg increase in pCO2 , HCO3 increases by 3.5meq/l
benzodiazepine toxicity causes?
acute respiratory acidosis.
acute respiratory alkalosis, correction is ?
for every 10mm of hg decrease in pCO2 , HCO3 decreases by 2 meq/l
chronic respiratory alkalosis correction is?
for every 10mm of hg decrease in pCO2 , HCO3 DECREASES by 5 meq/l
clinical features of hypocalcemia are seen in which acid base disorder?
respiratory alkalosis.
whats the mechanism for hypocalcemia in alkalosis?
in alkalosis, H+ is low, ca2+ takes the place of H+, lower free ca2+ ions.
what is the role of demeclocycline in SIADH?
demeclocycline is given in chronic symptomatic SIADH.
not responsive to fluid restriction.
it takes 1-3 days to inhibit the action of ADH on the kidney.
causes for pseudohyponatremia( isotonic)
hyperlipidemia
hyperprotenimia( multiple myeloma,waldenstorms macroglobulinimia)
causes for hypertonic hyponatremia
hyperglycemia
mannitol excess
urea
glycerol therapy
psychogenic polydipsia is an example for
hypotonic ,euvolemic hyponatremia.
hyponatremia is exacerbated by antidepressant and neuroleptic drugs.
calculation of plasma osmolality
all values in mmol/l
2Na+S.glucose+S.urea in mmol/l
correction of S.Na when there is hyperglycemia
corrected S.Na= observed S.Na +

1.4x{observed glucose-5}
---------------------------------------
5
what are the values for percentage of TBW., total body water in the following
percentage of TBW
in young men-------0.6
in young women and elderly men-----0.5
elderly women ---------0.4
calcualtion of free water deficit-
free water deficit = wt in kg x percentage of TBW x{S.Na/140) - 1}

to this value add insensible and ongoing losses.
this whole fluid is given in next 48 hrs.
infusion rate ---100ml/hr
calculation of sodium deficit-
Na+ deficit = { S.Na desired - S.Na observed} x ( body wt in kg x percentage of TBW)
what empiric replacement fluids can be used for fluid losses?
gastric----------D5 1/2 NS with 20-30KCL/L ( never give lactated ringer)

sweat------D5 1/4 NS with 5KCL/L

BILE, PANCREAS, SMALL BOWEL-------lactated ringers solution

colon------D5 1/2 NS with 30KCL/L

third space losses-----lactated ringers solution