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26 Cards in this Set
- Front
- Back
Normal K levels
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98% intracellular (mostly muscle)
120-150 meq/L |
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Nernst Equation
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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 |
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Acid-Base affect on K
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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 |
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Hypertonicity affect on K
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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 |
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Insulin affect on K
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insulin stimulates Na-K-ATPase shifting K into cells
insulin administered in cases of life-threatening hyperK |
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beta2 agonists
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shift K from extracell to intracell by increasing cAMP which stimulates Na-K-ATPase
beta blockers incr serum K by 0.5 meq/L |
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Renal excretion/reabsorption
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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 |
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Factitious hyperK
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incr WBCs in sample lyse before analysis leading to factitious hyperK
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Increased K load
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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
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Hyperkalemic Periodic Paralysis
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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 |
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Impaired K secretion
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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) |
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clinical manifestations of hyperK
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peaked T waves, widened QRS
ascending flacid paralysis (K>7.0) hyperchloremic acidosis |
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management of acute hyperK
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Ca gluconate - antagonizes membrane affect of hyperK (never w/ dig tox)
Glucose-insulin - stimulates Na-K-ATPase NaHCO3 Kayexalate - K binding resin dialysis |
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HypoK
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inadequate dietary intake (EtOH, anorexia)'
GI loss extracell to intracell shift (insulin, alkalosis) hypoK periodic paralysis |
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Renal K wasting w/ HTN
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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 |
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Renal K wasting (normotensive)
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diuretics
RTA I/II Mg def DKA non absorbing anions Rx Bartter's syndrome |
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Liddle's syndrome
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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 |
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Bartter's syndrome
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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 |
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Gitelman's syndrome
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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 |
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clinical manifestations of hypoK
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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 |
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Osmotic Diuretic
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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 |
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carbonic anhydrase inhibitors
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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) |
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Loop diuretics
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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 |
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Thiazide Diuretics
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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)) |
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K sparing diuretics
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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 |
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Diuretic Uses
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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 |