0521779407-09 CUNY1086/Karliner 0 521 77940 7 June 4, 2007 21:13
748 Hyperkalemia■excess intake
➣intravenous fluids containing K
➣increased dietary K important only with defect in renal K excre-
tion
■cell shift
➣cell damage: rhabdomyolysis, tumor lysis, tissue ischemia, mas-
sive hemolysis
➣insulin deficiency: diabetic ketoacidosis
➣hyperosmolality: diabetic ketoacidosis, nonketotic hyperosmo-
lar coma
➣metabolic acidosis: only with mineral acidosis (hyperchloremic
acidosis) and not organic acidosis
increased K in diabetic ketoacidosis due to insulin deficiency
and hyperosmolality, not metabolic acidosis
increased K in lactic acidosis due to inhibition of Na/K ATPase
and cell leakage from injury or ischemia
➣drugs: beta blockers in setting of exercise, neuromuscular block-
ade with succinylcholine
➣toxin: digoxin overdose
➣familial hyperkalemic periodic paralysis: recurrent episodes of
flaccid paralysis precipitated by cold or exercise; mutation in
voltage activated Na channel decreased renal K excretion respon-
sible for sustained hyperkalemia
➣often accompanied by normal gap metabolic acidosis (type IV
RTA)
➣due to one or more of several abnormalities: renal insufficiency,
decreased mineralocorticoid activity, or a distal tubular defect
renal insufficiency
GFR <10 ml/min: end stage renal disease from any cause
GFR >10 ml/min: tubulointerstitial renal disease
decreased mineralocorticoid activity
decreased renin, decreased aldosterone
mild to moderate diabetic nephropathy
drugs
nonsteroidal antiinflammatory agents
beta-blockers
cyclosporine
increased renin, decreased aldosterone
adrenal destruction (Addison’s disease)
angiotensin converting enzyme inhibitors
angiotensin receptor blockers