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26 Cards in this Set

  • Front
  • Back
Normal K levels
98% intracellular (mostly muscle)
120-150 meq/L
Nernst Equation
balance between electric and chemical forces across a membrane
E=-RT/F*ln(Ki/Ko)
decr K incr electric gradient --> incr excitability
incr K decr electric gradient
Acid-Base affect on K
Acidemia --> K out/H out --> HyperK
inhibit distal tubular secretion of K
0.1 decr in pH incr serum K 0.5
Alkamemia --> K in/H out --> HypoK
enhances renal excr of K
0.1 incr in pH decr K 0.1 to 0.4
Hypertonicity affect on K
incr serum glucose w/o insulin shifts H2O and K out of cells --> hyperK

worse in HHNK than DKA b/c of K deficiency associated w/ DKA
Insulin affect on K
insulin stimulates Na-K-ATPase shifting K into cells
insulin administered in cases of life-threatening hyperK
beta2 agonists
shift K from extracell to intracell by increasing cAMP which stimulates Na-K-ATPase
beta blockers incr serum K by 0.5 meq/L
Renal excretion/reabsorption
88% reabsorbed
50-70% in proximal tubule
15-20% in loop of henle
enhanced secretion: incr K intake, incr Na delivery, mineralocorticoids, incr urine flow, alkalosis
Factitious hyperK
incr WBCs in sample lyse before analysis leading to factitious hyperK
Increased K load
exogenous, endogenous (rhabdomyolysis, trauma, burns, tumor lysis, hemorrhage), intra to extracell shift (acidosis, insulin def, hyperosm, dig overdose, succinylcholine, arginine or lysine infuse), hyperkalemic periodic paralysis
Hyperkalemic Periodic Paralysis
AD w/ 100% penetrance
mutated non-inactivating Na channel
onset in 1st year of life
attacks precipitated by EtOH, mental stress K intake, glucocorticoids, exercise
prophylax w/ thiazide diuretics, carbonic anhydrase inhibitors, mineralocorticoids
Impaired K secretion
acute or chronic renal fail (GFR<15)
K spareing diuretics
mineralocorticoid deficiency - addisons, idiopathic, hyporeninemic hypoaldosteronism (DM, interstitial nephritis, obstructive uropathy), adrenogenital syndrome, ACEi
Calcineurin inhibitors (cyclosporine, tacrolimus)
clinical manifestations of hyperK
peaked T waves, widened QRS
ascending flacid paralysis (K>7.0)
hyperchloremic acidosis
management of acute hyperK
Ca gluconate - antagonizes membrane affect of hyperK (never w/ dig tox)
Glucose-insulin - stimulates Na-K-ATPase
NaHCO3
Kayexalate - K binding resin
dialysis
HypoK
inadequate dietary intake (EtOH, anorexia)'
GI loss
extracell to intracell shift (insulin, alkalosis)
hypoK periodic paralysis
Renal K wasting w/ HTN
high plasma renin - incr aldo, incr renal K secretion, DDX: renal a. stenosis, malignant HTN, renin producing tumor
Low plasma renin - primary hyperaldo, exogenous mineralocorticoid, liddle's syndrome, adrenogenital syndrome, glucocorticoid excess
Renal K wasting (normotensive)
diuretics
RTA I/II
Mg def
DKA
non absorbing anions
Rx
Bartter's syndrome
Liddle's syndrome
mutation in beta-subunit of ENaC causing constitutve activation of the amiloride sensitive distal renal Na channel
AD
causes HTN, hypoK, met alk, decr renin & aldo
Tx: Na restrict or triamterene
Bartter's syndrome
like endogenous lasix
thick ascending limp mutations to Na-K-2Cl txp, or type II K channel, or Cl channel, or barttin
causes proximal muscle weakness, polyuria, growth retardation
Tx: K replace, K sparing diuretic
Gitelman's syndrome
like constitutive HCTZ
inactivating mutation in Na-Cl cotxp in DCT
present in adolescence w/ hypoK, met alk, hypoMg, hypoCa
may have intermittent cramps and muscle weakness
clinical manifestations of hypoK
cardiac - U waves (arrhythmia risk as T wave encroaches on QRS complex)
neuromusc - ascending muscle weak, resp fail, rhabdomyolysis, paralytic ileus
renal - polyuria, hypoK, intertitial nephritis, chronic renal insufficiency
acid-base - cannot correct met alk w/o correcting K depletion
Osmotic Diuretic
Mannitol
MOA - causes water to be retained in tubules promoting diuresis (opposes action of ADH)
*Na sparing (long term)
Uses - tx elevated ICP, reduce intraocular pressure, promotion of toxin excretion
AE - rapid H2O move from intra to extracellular causes acute transient ECF expand and hyponatremia --> n/v/headache, CHF complication, incr intracellular K
carbonic anhydrase inhibitors
Acetazolamid (Dichlophenamid, methazolamide)
MOA - inhibits CA and decr bicarb reabsorb leading to bicarb diuresis
*may cause met acid, alkalinizes urine
Uses - prophylax AMS, glaucoma (CA in eye)
AE - met acid, phosphaturia and hypercalciuria --> stone, K wasting, drowsiness (CA in CNS), paresthesias, contraindicated in liver dz (worsen hepatic encephalopathy)
Loop diuretics
furosemide (bumetanide, torsemide, ehtyacrynic acid)
MOA - inhibits Na-K-Cl txper in cortical and medullary thick ascending limb of loop of henle (RAPID onset)
*also have ceiling dose
Uses - first line for acute pulm edema, CHF, combo w/ HCTZ for HTN, K excrete, edema
AE - hypoK, hypoMg, hyperuricemia, incr delivery of Na to DCT --> incre K & H excrete --> met alk, hearing loss, sulfa allergy cross react, incr LDL decr HDL
Thiazide Diuretics
HCTZ (chlorothiazide, chlorthalidone, metolazone)
MOA - inhibits Na-Cl txper in DCT causing contraction of ECF volume
*"ceiling" diuretic
Uses - HTN, mild CHF, edema, Ca urinary stones, osteoporosis, nephrogenic DI (COUNTERINTUITIVE)
AE - Na/K/Cl/Mg depletion, uric acid retention, Ca retention, impaired insulin release, incr LDL, photosensitivity, sulfa allergy cross rxn, ineffective for GFR<40 (except metazolone (GFR<20))
K sparing diuretics
Spironolactone (Eplerenone) - aldo antagonists
Triamterene (Amiloride) - interferes w/ Na influx in CD
Uses - hyperaldo, HTN, diuretic induced hypoK
AE - hyperK, hyperchloremic met acid, Spironolactone: endocrine AE
Diuretic Uses
edema
CHF - reduce symptoms, improve exercise tolerance, no effect on dz progression
Cirrhosis - tx edema and ascites (spironolactone and furosemide)
Kidney Dz - mild dz
HTN - HCTZ 1st line
Nephrolithiasis - HCTZ
HyperCa - loop
DI - HCTZ