USMLE fluids, vit2
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| % 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)
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| how does Hct change in hypovol | for ea 1L deficit: Hct incrsd 3%
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| 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
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| Serum osmolality cut off for hypotonic, hypertonic hypoNa | >295=hypertonic, 280-295=nml, <280=hypotonic
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| in hypotonic hypoNa, how differentiate extrarenal Na loss and renal Na loss | <10=extrarenal loss, >20=renal Na loss
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| causes of hypertonic hypoNa? isotonic HypoNa? | hypertonic=osmotic substances ie hyperGlu; isotonic=other particles, ie fat and protein
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| causes of hypovol hypotonic hypoNa (divided by renal and extrarenal) | extrarenal: 3rd space, diarrhea, vomit; renal: diuretic, low aldos, ATN
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| causes of euvol hypotonic hypoNa | SIADH, polydipsia, postop, hypothyroid
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| causes of hypervol hypotonic hypoNa | CHF, nephrotic, liver dz
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| how treat hypovol hyperNa | give isotonic NaCl to restore hemodynamics, then correct Na
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| how treat hypervol hyperNa | furosemide
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| describe pseudohypoparathroid | AR where end organs not responsive to PTH (so PTH levels are very high); also MR and short metacarpals
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| how differentiate renal and GI losses in causing hypoK | GI=urine K<20, renal >20
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| clinical features of hypoK | arrhythmias (flatten/inversion T wave, appearance U wave), i DTR, fatigue, musc wknss, digitalis toxicity, N/V paralytic ileus
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| when evaluating hypoK: causes K nml but redistributed | metabolic alkalosis, insulin, epi
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| 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
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| how much KCl treatment raises serum K? | 10mEq KCl incrs 0.1mEq/L
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| hyperK and how affects ammonia in kidney | hyperK inihibits renal ammonia synthesis and reabsorb->met acidosis->more hyperK
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| 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
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| 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)
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| 2 MC causes severe hypophosphate | EtOH, DKA
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| MC cause hyperphosphate | renal insuffic
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| 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
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| respiratory compensation for metabolic acidosis | CO2=1.5(HCO3)+8 +/-2 -->if not in that range, need to look for another acid-base problem.
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| 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
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| 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
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| 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)
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| 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
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| tx for 2 grps of metabol alk | 1) ECF contraction: NS + K; 2) ECF expansion: underlying cause or spironolactone
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| compensation amts for respir acidosis | acute: HCO3 incrses 1 mmol/L per 10 CO2, chronic: 4 mmol/L per 10 CO2
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| compensation amts for respir alk | acute: HCO3 decrses 2 mmol/L per 10 CO2, chronic: 5-6 mmol/L per 10 CO2
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| how do PTH, calcitonin, and vit D ea act on bone | PTH and vit D incrs Ca, P reabsorb, calcitonin decrses
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| how do PTH, calcitonin, and vit D ea act on GI | PTH activ vitD, calcitonin decrs Ca, vit incrses Ca
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| how do PTH, calcitonin, and vit D ea act on renals | PTH and vitD incrs Ca, decrses P; calcitonin does the opposite
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| ECG changes QT assoc w metabolites | QT: long=hypoCa or Mg, short=hyperCa;
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| ECG changes PR assoc w metabolites | PR: long=hyperK or Mg, short=hypoK;
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| ECG changes T wave and QRS wave assoc w metabolites | T: peaked=hyperK or Mg, flattened=hypoK or Mg; QRS: long=hyperK
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| ECG changes assoc w Mag | hyper Mag: long QT, flat T; hypo Mag: short PR, pkd T
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| what happens to electrolytes in RF | hypoCa (not making 1,25 vitD), Hyper K, Mg, and P, Hypovol Hypotonic HyperNa
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| defic vit A causes | night blindness, dry eyes, scaly rash, spots (Bitot's debris) on conjunctiva, repeated infxns
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| defic vit C causes | scurvy (hemorrhages/skin petechia, bone (causing bone pain), gums; loose teeth/gingivitis); poor wound healing, hyperkeratotic hair follicles
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| too much vit A causes | pseudotumor cerebri (incr intercranial pressure), bone thickening, teratogen
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| defic vit D causes | rickets, osteomalacia, hypocalcemia
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| too much vit D causes | hyper Ca++, nausea, renal toxicity
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| defic vit E causes | anemia, peripheral neuro, ataxia
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| too much vit E causes | necrotizing enterocolitis in infants
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| defic vit K causes | hemorrhage, incrsd PT
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| too much vit K causes | hemolysis/kernicterus
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| defic B1 (aka) | thiamine defic, Wet beriberi=high output cardiac failure; dry beriberi=peripheral neuropathy; Wernicke and Korsakoff syndromes
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| defic B2 (aka) | riboflavin; cheilosis, angular stomatitis, dermatitis
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| defic B3 (aka) | niacin; pellagra=dementia, dermatitis, diarrhea; stomatitis
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| defic B6 (aka) | pyridoxine; peripheral neuropathy, cheilosis, stomatitis, convulsions in infants, microcytic anemia, seborrheic dermatitis
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| too much B6 | peripheral neuropathy (note, only B vitamin w toxicity)
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| defic B12 (aka) | cobalamin, megaloblastic anemia w neuro symptoms [v Folic acid]
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| describe Wernicke-Korsakoff | defi B1, usu in alcoholic: Wernicke encephal: nystag, ophthalmople, ataxia; Korsakoff: confabulations, amnesia
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| diff bw B2 and B6 defic | both have cheilosis, dermatitis, stomatitis, but B6 also has anemia and peripheral neuropathy
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| iodine defic | gotier, cretinism, hypothyroid
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| iodine toxicity | myxedema
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