Electrolyte and acid/base disorders Flashcards
Hormones affecting kidney
PTH: increased Ca2+ reabsorption, decrease reabsorption of phosphate, activate Via D
RAAS
Atrial natriuretic peptide: constrict efferent a, dilates afferent -> increased GFR -> diuresis
ADH: vasopressin - water reabsorption, urine concentration
SIADH
too much ADH
absorbing too much H2O -> low serum osmolarity, low serum Na+
excessive concentration of urine
High ADH from: small cell lung CA lung pathology head trauma, stroke, CNS infections drugs - cyclophophamide idiopathic
Central pontine myelinolysis
replace Na+ too quickly -> locked in sn
Excessive thirst + polyuria workup for DI
check glucose to r/o DM
check osmolality - low urine and high serum
water deprivation test - (normal -> concentrated urine) - urine osmolality stays low in DI
Central vs nephrogenic:
Desmopressin challenge (ADH analog)
-Central DI: increase urine concentration by 50%
-nephrogenic DI: no change or less than 50% if rises
Diabetic insipidus
too little ADH
increased urine volume
dilute urine
high serum osmolarity
low urine specific gravity
Central DI
abnl ADH production by hypothalamus
complete - no ADH
partial - insufficient ADH
Tx: intranasal desmopressin
Nephrogenic DI
kidney unresponsive to ADH
Lithium
Demeclocycline - tx SIADH
hypercalcemia
mutation of ADH receptor gene
Tx:
HCTZ - causes slight dehydration -> increased H2O absorption in proximal tubule -> more concentrated urine downstream
indomethacin - decreases RBF -> lower urine output
Amiloride for Lithium induced
Causes of K+ shifts out of cell -> hyperkalemia
low insulin b-blockers acidosis digoxin cell lysis - leukemia
Causes of K+ shift into cells -> hypokalemia
Ways to Correct hyperkalemia:
insulin: IV insulin + dextrose
b-agonist: albuterol
Alkalosis : IV bicarb
Cell creation/proliferation - cancer
Hyponatremia sx
confusion altered mental status - esp elderly seizures stupor coma
Hypercalcemia sx
“stone, bones, abdominal growns and psychiatric overtones”
confusion, delirium
hypocalcemia sx
tetany
+ Troussea/Chvostek signs
Hypomagnesemia sx
tetany
EKG abnl - arrhythmias -> prolonged QT
-VT, torsades
Hypermagnesemia sx
low reflexes
serial neuro exams
hypokalemia sx
prolonged QT -> VT, torsades
flat T wave, U wave
Hyperkalemia sx
VT
Tall peaked T waves
MUDPILES
high anion gap
Methanol uremia DKA propylene glycol Iron tables/ INH Lactic acid Ethylene glycol Salicylates – late
Respiratory acidosis
hypoventilation: airway obstruction and air trapping lung dz weak respiratory m. opioids
Respiratory alkalosis
hyperventilation: psychogenic high altitude PE aspirin toxicity – early
Metabolic acidosis
adding acid -> high anion gap
losing bicarb: -> normal anion gap D renal tubular acidosis spironolactone acetazolamide
Metabolic alkalosis
lose H+:
excessive V
diruetics
hyperaldosteronism - hyperkalemia, htn, metabolic alkalosis
Renal tubular acidosis - non-anion gap Type I
Type I (distal) - CT: alpha intercalated cells unable to secrete H+ -> acidotic Urine pH >5.5 ** hypokalemia assoc w/ stones
H+ - 1
Renal tubular acidosis - non-anion gap Type IV
hypoaldosteroneism - not putting K+ into urine
Hyperkalemia - prevents PCT from generating NH4+
urine pH less than 5.5
NHIV
Renal tubular acidosis - non-anion gap Type 2
Proximal tubule defect of HCO3- reabsorption
hypokalemia
hypophosphatemia
urine pH less than 5.5
pH calculation
HCO3-/PCO2
Compensatory mechanism
should never bring pH all the way back to normal range
if pCO2 and HCO3- out of whack w/ normal pH = mixed disorder
Calculate expected PCO2
1.5 (HCO3) +8 +/- 2
Work through example ABG values to determine acid base disorder
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