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USMLE fluids, vit2

QuestionAnswer
% body wgt that's total body water, intracell, extracell, plasma, interstitial? TBW=60% (50% in women), ICF=40%, ECF=20% (incl 15% interstitial, 5% plasma)
how does Hct change in hypovol for ea 1L deficit: Hct incrsd 3%
algorithm of tests for management of low serum Na 1) measure serum osmolality (to determine if true hypoNa (hypotonic), or hypertonic, or isotonic (pseudohypoNa); 2) if hypotonic measure volume status; 3) if hypovol hypotonic hypoNa measure Urine Na to see if renal Na loss or extrarenal
Serum osmolality cut off for hypotonic, hypertonic hypoNa >295=hypertonic, 280-295=nml, <280=hypotonic
in hypotonic hypoNa, how differentiate extrarenal Na loss and renal Na loss <10=extrarenal loss, >20=renal Na loss
causes of hypertonic hypoNa? isotonic HypoNa? hypertonic=osmotic substances ie hyperGlu; isotonic=other particles, ie fat and protein
causes of hypovol hypotonic hypoNa (divided by renal and extrarenal) extrarenal: 3rd space, diarrhea, vomit; renal: diuretic, low aldos, ATN
causes of euvol hypotonic hypoNa SIADH, polydipsia, postop, hypothyroid
causes of hypervol hypotonic hypoNa CHF, nephrotic, liver dz
how treat hypovol hyperNa give isotonic NaCl to restore hemodynamics, then correct Na
how treat hypervol hyperNa furosemide
describe pseudohypoparathroid AR where end organs not responsive to PTH (so PTH levels are very high); also MR and short metacarpals
how differentiate renal and GI losses in causing hypoK GI=urine K<20, renal >20
clinical features of hypoK arrhythmias (flatten/inversion T wave, appearance U wave), i DTR, fatigue, musc wknss, digitalis toxicity, N/V paralytic ileus
when evaluating hypoK: causes K nml but redistributed metabolic alkalosis, insulin, epi
treatment of hypoK oral KCl, but if <2.5 or arrhythm use IV KCl; max 10mEq/hr by peripheral IV, 20mEq/hr by central lines; add 1% lidocaine bc it burns
how much KCl treatment raises serum K? 10mEq KCl incrs 0.1mEq/L
hyperK and how affects ammonia in kidney hyperK inihibits renal ammonia synthesis and reabsorb->met acidosis->more hyperK
causes of hyperK (grpd by incrsd total body K, redistrib, spurious) incrsd total body K:RF, spironolactone, ACEI, blood transfusion; redistrib: acidosis, tissue/cell breakdown (rhabdomyolysis, hemolysis, burn), GI bleed, insulin defic; spurious: using tourniquet too long w/o rept fist clench
clinical features of hyperK arrhythmias, esp>6 (peaked T, long PR, widen QRS, V fib and cardiac arrest); decrsd DTR& N/V (same as hypoK)
2 MC causes severe hypophosphate EtOH, DKA
MC cause hyperphosphate renal insuffic
causes of metabolic acidosis w incrsd anion gap MUDPILES=MeTOH, uremia (CRF), DKA, Paraldehyde, Infxn/Iron/INH, Lactic acidosis (incl hypoxic tissues, shock, hypovol, sepsis), Ethylene glycol/EtOH (although EtOH lactic acid causes AG), Salicylates
respiratory compensation for metabolic acidosis CO2=1.5(HCO3)+8 +/-2 -->if not in that range, need to look for another acid-base problem.
what does it mean if CO2 is higher than what calculated for respir compensation for metabol acidosis respir acidosis--which can indicate impending respi failure
what 2 events are needed for metabolic alk 1) an initial event that causes loss of H+ or incrsd HCO3, 2) inability to excrete xtra HCO3
what's the algorithm for categories of metabol alk ECF contraction and hypoK (urine Cl<10 saline responsive) and ECF expansion w HTN (urine Cl>20, saline resistant)
what are the causes of metabol alk (categorized by Urine Cl) 1) ECF contraction, urine Cl<10: vomitting (loss H+), diuretics; 2) ECF expansion, urine Cl>20: primary hyperaldost (Na and HCO3 reabsorb, Cl lost), Cushings
tx for 2 grps of metabol alk 1) ECF contraction: NS + K; 2) ECF expansion: underlying cause or spironolactone
compensation amts for respir acidosis acute: HCO3 incrses 1 mmol/L per 10 CO2, chronic: 4 mmol/L per 10 CO2
compensation amts for respir alk acute: HCO3 decrses 2 mmol/L per 10 CO2, chronic: 5-6 mmol/L per 10 CO2
how do PTH, calcitonin, and vit D ea act on bone PTH and vit D incrs Ca, P reabsorb, calcitonin decrses
how do PTH, calcitonin, and vit D ea act on GI PTH activ vitD, calcitonin decrs Ca, vit incrses Ca
how do PTH, calcitonin, and vit D ea act on renals PTH and vitD incrs Ca, decrses P; calcitonin does the opposite
ECG changes QT assoc w metabolites QT: long=hypoCa or Mg, short=hyperCa;
ECG changes PR assoc w metabolites PR: long=hyperK or Mg, short=hypoK;
ECG changes T wave and QRS wave assoc w metabolites T: peaked=hyperK or Mg, flattened=hypoK or Mg; QRS: long=hyperK
ECG changes assoc w Mag hyper Mag: long QT, flat T; hypo Mag: short PR, pkd T
what happens to electrolytes in RF hypoCa (not making 1,25 vitD), Hyper K, Mg, and P, Hypovol Hypotonic HyperNa
defic vit A causes night blindness, dry eyes, scaly rash, spots (Bitot's debris) on conjunctiva, repeated infxns
defic vit C causes scurvy (hemorrhages/skin petechia, bone (causing bone pain), gums; loose teeth/gingivitis); poor wound healing, hyperkeratotic hair follicles
too much vit A causes pseudotumor cerebri (incr intercranial pressure), bone thickening, teratogen
defic vit D causes rickets, osteomalacia, hypocalcemia
too much vit D causes hyper Ca++, nausea, renal toxicity
defic vit E causes anemia, peripheral neuro, ataxia
too much vit E causes necrotizing enterocolitis in infants
defic vit K causes hemorrhage, incrsd PT
too much vit K causes hemolysis/kernicterus
defic B1 (aka) thiamine defic, Wet beriberi=high output cardiac failure; dry beriberi=peripheral neuropathy; Wernicke and Korsakoff syndromes
defic B2 (aka) riboflavin; cheilosis, angular stomatitis, dermatitis
defic B3 (aka) niacin; pellagra=dementia, dermatitis, diarrhea; stomatitis
defic B6 (aka) pyridoxine; peripheral neuropathy, cheilosis, stomatitis, convulsions in infants, microcytic anemia, seborrheic dermatitis
too much B6 peripheral neuropathy (note, only B vitamin w toxicity)
defic B12 (aka) cobalamin, megaloblastic anemia w neuro symptoms [v Folic acid]
describe Wernicke-Korsakoff defi B1, usu in alcoholic: Wernicke encephal: nystag, ophthalmople, ataxia; Korsakoff: confabulations, amnesia
diff bw B2 and B6 defic both have cheilosis, dermatitis, stomatitis, but B6 also has anemia and peripheral neuropathy
iodine defic gotier, cretinism, hypothyroid
iodine toxicity myxedema
Created by: ehstephns on 2011-01-24



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