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31 Cards in this Set

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depressed ST & U wave on EKG
hypokalemia
hypokalemia effect on EKG
ST depression & U wave
location of K in body
3000-4000 meq/l

incracellular
-muscle
-liver
-RBC
increased if large muscle mass
Na/K ATPase
ion exchange w/ATPase
2 K for 3 Na
extracellular location of K
bone
ISF
plasma

(readily absorbed from gastrointestinal tract)
daily requirement for K
.3-.4 mEq/kg
depressed ST & U wave on EKG
hypokalemia
hypokalemia effect on EKG
ST depression & U wave
-ventricular repol delay
-hyperpol
-decrease k channel activity
location of K in body
3000-4000 meq/l

incracellular
-muscle
-liver
-RBC
increased if large muscle mass
Na/K ATPase
ion exchange w/ATPase
2 K for 3 Na
extracellular location of K
bone
ISF
plasma

(readily absorbed from gastrointestinal tract)
daily requirement for K
.3-.4 mEq/kg
depressed ST & U wave on EKG
hypokalemia
hypokalemia effect on EKG
ST depression & U wave
location of K in body
3000-4000 meq/l

incracellular
-muscle
-liver
-RBC
increased if large muscle mass
Na/K ATPase
ion exchange w/ATPase
2 K for 3 Na
extracellular location of K
bone
ISF
plasma

(readily absorbed from gastrointestinal tract)
daily requirement for K
.3-.4 mEq/kg
excretion of K
95% is at kidney
principal cells in CD
-high Na into principal via ROMK
-high flow in lumen via MaxiK
-low Cl in lumen via Cl/K costransport
drug inhibiting Na/K ATPase
Digoxin
(can cause hyperK)
factors affecting K excretion
aldosterone
(increase excretion K, lower Na)
Na delivery & flow rate
plasma concentration K
pH (Cl delivery & anion effect)
Na intake
diuretics

ADH (minimal)
insulin affect on K
can treat hyperK
intracellular shift
major causes of hypokalemia
GI loss
-vomit, diarrhea, tube drainage

urinary loss
-loop & thiazide diuretics
-primary mineralcorticoid excess (aldost b/c adrenal adenoma)
-secondary hyperaldost (renal artery stenosis)
-renal tube acidosis

decreased intake (rare as single cause)

increased cell entry (temporary)
-metabolic alkalosis
-beta adrenergic response
treatment for hypoK
replacement
KCl or KHCO3

NOT KSO4 (b/c anion)
cell membrane effect of hypoK
hyperpolarize membrane
inactivation of Na channel causes muscle weakness (Na in K out)
pseudo-hyperkalemia caused by
hemolysis of blood sample (in tube)

hyperleukocytosis
-WBC >100,000
-plts >400,000

check w/EKG
causes of hyperK
high glucose
-extracellular shift

Acidosis
-organic not effect
-nonorganic increases

Drugs

Renal failure
-urine output <600 ml/day
-GFR <10 ml/min
(b/c decreased Na delivery to CD)

Volume depletion
Tissue breakdown (rhabdomyolysis)
meds causing HyperK
ACE inhibitors & ARBs
NSAIDs (b/c block PGs rls renin)
K sparing
-spironalactone (Ald antag)
-amileride & triamterone

beta blockers
trimethoprim (increases charge in tubules)
cyclosporin
musc depol agents (for intubation)
digoxin
beta blockers
EKG w/peaked T
hyperK

flat P & wide QRS with very high

finally a sign wave
EKG effects of hyperK
peaked T

-increased K channel conductance

flat P & wide QRS if very high
-delay in depol
treatment for hyperK
Ca immed to stabilize memb

NaHCO3 to internalize K into cell

insulin & glucose
beta 2 agonist (albuterol)
kayexalate (cation exchange resin)
hemodialysis