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Lytes, Vit USMLE

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)
nml water intake per day 1500mL/d in fluids, 500mL/d in solids
nml water output (urine, stools) per day and per hr urine: 800-1500 (min is 500), stools: 250; nml urine 1.0ml/kg/hr
insensible losses per d 600-900
cases when insensible losses are incrsd sepsis, F, burns, open wounds, higher atmospheric temp
cases when 3rd spacing of fluids any condition low albumin (liver failure, nephrotic), CHF
name 4 and describe use of major fluids used in resuscitation NS (incrses intravasc vol, but don't use in CHF), D5 1/2 NS (std maintenance, often w 20mEq KCl), D5W (used to dilute powder meds, 1/12 goes intravasc), Lactated ringers (good intravasc used in trauma, but don't use if concern hi K)
calculation of maintenance fluids for pt's wgt 4/2/1 rule: 4ml/kg/hr for first 10kg, 2ml/kg/hr for next 10kg, 1ml/kg/hr for rest
lab values suggestive of hypovol low FeNa (incrsd serum Na, decrsd urine Na), BUN:Cr >20
how does Hct change in hypovol for ea 1L deficit: Hct incrsd 3%
causes of hypovol GI, 3rd spacing, DKA (polyuria), sepsis, trauma, wounds
management of hypovol 1) bolus w LR or NS, maintenance w D5 1/2NS w 20mEq KCl/L; 2) replace blood loss w crystalloid 3:1 ratio
causes of hypervol iatrogenic, fluid retaining states CHF, ESRD, liver cirrhosis, nephrotic states
management of hypervol diuretics and fluid restriction
how manage Na in head injury keep Na nml to high bc when ECF osmolality decrsd, water goes to brain cells and incrses ICP
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
what value Urine Na would be consistent w SIADH >40
how correct hypoNa incrs 1-2mEq/L/hr, but not >8mmol/L over 1st 24hr (can cause central pontine demyel)
features of central pontine demyelination dysphagia, dyarthria (diff speaking) and acute paralysis
how subdivide HyperNa, and what has happened to Na and water in ea condition hypovol ( where descrd water>decrsd Na, incl renal and extrarenal), euvol (decrsd Water), hypervol (incrsd Na>incrsd water)
causes of hyperNa euvol diabetes insipidus, tachypnea
what are 2 types of diabetes insipidus, describe pathophysiol and how to differentiate central DI=no ADH produced, will correct w desmopresin (vasopresin); nephrogenic DI=kidney not responding to ADH
causes of hyperNa hypervol TPN, steroids, Cushings, primary hyperaldost
causes of hyperNa hypovol (renal and extrarenal) renal=diuretic (?? Which--can't find), DM glycosuria, renal failure; extra renal=diarrhea, diaphoresis, respir losses
how correct hyperNa not >8mmol/L over 1st 24hr (can cause cerebral edema)
how treat hypovol hyperNa give isotonic NaCl to restore hemodynamics, then correct Na
how treat hypervol hyperNa furosemide
forms of Ca in body, which active most Ca is bound to albumin, physiol active form is unbound form [which is tightly regul by PTH]
how PTH affects Ca and phosphate levels net: incrsd Ca, decrsd P; bone: incrsd reabsorb of Ca and P; renal: incrsd Ca, decrsd P; GI activate vit D
how calcitonin affects Ca and phosphate levels net: decrsd Ca, P; bone decrsd Ca, P; renal: decrsd Ca, incrsd P; GI: decrsd Ca
how vitD affects Ca and phosphate levels net: incrsd Ca, P; bone: incrsd Ca, P; renal: incrsd Ca, decrsd P; GI: incrsd Ca, P
causes of hypoCa by grp (electrolyte, hormone, other) lyte: incrsd P (ppts Ca), decrsd Mg (decrsd PTH), citrate in blood transfusions; horm: hypoparathyroid (MC, thyr sx), pseudohypoparathyr (organs resist PTH), renal insuff (decrsd 1,25 vitD); acute pancreat (Ca deposits); misc: malabsorb, osteoblastic mets
describe pseudohypoparathroid AR where end organs not responsive to PTH (so PTH levels are very high); also MR and short metacarpals
clinical features of hypoCa 1) rickets and osteomalacia, 2) neuromusc: numbness, tetany (h DTR, Chvosteks sign-tap facial n causes twitch, Trousseau-inflate BP cuff over SBP for 3 min causes carpal twitch), grand mal sz; long QT
how use PTH levels in diagnosing causes of hypoCa decrsd PTH in hypoparathyroid, very incrs in pseudohypoparathyroid, incrs in vit D defic
how use P levels in diagnosing causes of hypoCa incrsd P in hypoparathyroid and renal insuffic, decrsd in vit D defic
treatment of hypoCa IV Ca gluconate + Mg if symptomatic, long term Ca carbonate oral + vit D [and treat PTH defic if applicable]
causes of hyperCa hyperparathyr, Pagets, cancers (mets, depending on if osteoblastic or osteoclastic, mltpl myeloma, lung cancer producting PTH), sarcoid, vitD intox, milk-alkali syn, thiazide, lithium
clinical features of hyperCa stones, bones (bone aches), grunts&groans (mscl pain, wknss, PUD, gout, constipation, pancreatitis), psych overtones (depression, fatigue) + short QT
special tests for diagnosing hyperCa radioimmunoassay of PTH: incrsd primary hyperparathyroid, decrsd occult cancer; urinary cAMP (very incrsd primary hyperparathyroid)
treatment of hyperCa incrsd urinary excretion: IV NS, furosemide; inhibit bone reasborb w bisphosphamides (pamidronate) & calcitonin; steroids if vitD intox, granulomatous dz, mltpl myeloma
location of K, key processes that incrs or decrs K almost all intracell, insulin and alkalosis decrs K, acidosis and cell lysis incrs K
causes of hypoK GI: vomitting, diarrhea; Renal: diuretics, hyperaldosterone (primary, secondary, Bartter's), Rx: insulin, epinephrine/b2 agonists, steroids, lytes: low Mg, alk
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), decrsd DTR, fatigue, musc wknss, digitalis toxicity, N/V paralytic ileus
when evaluating hypoK: causes K nml but redistributed metabolic alkalosis, insulin, epi
K depleted hypoK divided by renal/extrarenal and alk/acidosis Extrarenal nml acid/base: laxatives, sweating; extrarenal met alk: GI losses; renal met acidosis: renal tub acidosis, thiazide, DKA
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)
treatment of hyperK 1) if severe or ECG changes give IV Ca++ first (stabilizes mem, but also predisposses to dig toxicity), 2) shift K intracell (insulin, Glu, NaHCO3 for acidosis); 3) remove K (kayecelate, GI K/Na exchange resin) hemodialysis, furosemide
regulators of phosphate levels vit D in GI, PTH in kidney
MC cause sever hypophosphate EtOH, DKA
causes hypophosphate (grpd by decrsd GI absorb, incrsd renal excretion, other) decrsd GI absorb: EtOH, vitD defic, phosphate-binding antacids, TPN; incrsd renal excretion: incrsd PTH, hypergly, hypoK or Mg; other: respir alk steroids, DKA
MC cause hyperphosphate renal insuffic
clinical features (relates to Ca) calcifications (esp if serum_Ca x serum_phosphate > 70)
when will see metastatic calcification due to high Ca and phosphate? esp if serum_Ca x serum_phosphate > 70
treatment of hyperphosphate phosphate-binding antacids
how analyze ABG to determine acid-base disorders 1) pH (tells whether primarily acidosis or alkalosis), 2) CO2 (if respir process CO2 will be hi with acidosis, low alk), 3) HCO3 (if metabolic process HCO3 will be hi with alk, low acidosis),
pH <7.4, hi CO2 indicates respir acidosis (if also hi HCO3 then metabolic compensation)
pH <7.4, low CO2 indicates metabolic acidosis w respir compensation (so HCO3 also low)
pH >7.4, hi CO2 indicates metabolic alkalosis w respir compensation (so HCO3 also high)
pH >7.4, low CO2 indicates respiratory acidosis (if also low HCO3 then metabolic compensation)
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
primary acid/base disorder from salicylate OD BOTH primary respir alkalosis and metabolic acidosis
causes of nml AG metabolic acidosis loss of HCO3: 1) renal: proximal tubule acidosis can't reabsorb HCO3, distal tubule acidosis can't make HCO3; 2) GI: MC diarrhea
clinical features of metabolic acidosis hyperventilation (Kussmaul deep rhythmic breathing, esp pH<7.2), decrsd CO and tissue perfusion
nml anion gap ~8-15
general effects of acidosis HbO2 h delivery O2 to tissues, hyperK, arrhyth, depress myocard, depress CNS, i pul BF
general effects of alkalosis HbO2 i delivery O2 to tissues, i cerebral BF, arrhyth, tetany, szs
hi CO2 indicates either respir acidosis or compensation for metabol alk
low CO2 indicates either respir alk or compensation for metabol acid
hi HCO3 indicates either metabol alk or compensation for respir acidosis
low HCO3 indicates either metabol acidosis or compensation for respir alk
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 h 1 mmol/L per 10 CO2, chronic: 4 mmol/L per 10 CO2
cut off for respir acidosis pH<7.4, CO2>40
causes of respir acidosis unable to clear CO2, respir: COPD, airway obstruction, neurmusc: MG, CNS injury brainstem, Rx: morphine, anesthetic, sedative, narcotic OD (pinpt pupils)
compensation amts for respir alk acute: HCO3 decrs 2 mmol/L per 10 CO2, chronic: 5-6 mmol/L per 10 CO2
what are main det of CO2 in respir alk RR and tidal vol
causes of respir alk alveolar hypervent: anxiety, PE, PNA, asthma, sepsis, hypoxia (incrs RR), preg progest (incrs RR), salicylate toxicity
clinical features of respir alk decrsd cerebral BF can cause dizziness, tetany
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&P
how do PTH, calcitonin, and vit D ea act on renals PTH and vitD incrs Ca, decrs P; calcitonin does the opposite (decrs Ca, incrs P)
in HyperCa how differentiate bw hyperparathyroidism and occult cancer hyperparathyroid has high radioimmunoassay PTH and very high urinary cAMP; occult cancer has low radioimmunoassay PTH
ECG changes assoc w metabolites QT: long=hypoCa or Mg, short=hyperCa; PR: long=hyperK or Mg, short=hypoK; 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
how treat electrolyte abnmlties in CRF 1) hyper P-give calcium citrate (binds phosphate), 2) prevent 2ry hyperparathyroid by Ca and vit D (also helps uremic osteodystrophy), 3) acidosis-oral bicarb
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
defic folic acid megaloblastic anemia w/o neuro symptoms [v B12]; neural tube defects if pregnant
ID vit or min: pellagra (&symptoms) B3 (niacin)=dementia, dermatitis, diarrhea [also see stomatitis with B3 defic]
ID vit or min: beriber (&symptoms) B1 (thiamine): Wet beriberi=high output cardiac failure; dry beriberi=peripheral neuropathy; [also see w B1 defic: Wernicke and Korsakoff syndromes]
iodine defic gotier, cretinism, hypothyroid
iodine toxicity myxedema
fat soluble vit A, D, E, K
cause of defic in fat sol vitamins malabsorb (celiac, CF, bile duct obstruct, pancreatitis, cirrhosis)
cause B12 defic pernicious anemia, gastrectomy, ileal abnormality
Wernicke syndrome acute encephalopathy w opthalmoplegia, nystagmus, ataxia and/or confusion. Reverse with thiamine [if you give an alcoholic glu w/o giving thiamine first you can cause this]
korsakoff chronic anterograde amnesia (can't form new memories), confabulation (lying). Irreversible (damage to mamillary bodies and thalamic nuclei). Also thiamine defic
how treat alcoholic w hypoglycemia? give thiamine before glu; if you give an alcoholic glu w/o giving thiamine first you can cause Wernicke
Created by: ehstephns on 2010-12-06



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