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63 Cards in this Set
- Front
- Back
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What is the most abundant cation in the body?
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Potassium
50 Meq/Kg 98% intracellular |
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Avg dietary intake of potassium
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100-150 mEq/day
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How is K excreted
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Free kidney filtration in glomerulus
= 0.5 mEq/min 67% reabsorbed in PCT 20% is reabsorbed in loop DCT can absorb or secrete Collecting duct can absorb or secret Can excrete as little as 1% or as much as 80% of that based on regulatory factors |
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K and the distal nephron
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Absorption vs secretion is based on electrochemical gradient
Increased gradient for secretion from Aldosterone Increased tubular flow rate Increased distal Na delivery Increased urinary anions |
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Aldosterone and K
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Increases secretion
Aldo opens Na channels on principal cells Na absorption results in electronegative lumen K enters tubule in response Expands extracellular fluid vol, resulting in higher tubular filtration rate |
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Tubular flow rate a K
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High flow rate keep the K gradient high as secreted ions are swept out
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Cause/effect of increased distal tubule Na delivery
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Usually caused by diuretics
Higher Na gradient for reabsorption in distal nephron Electrochemical gradient for K increased K secretion increased |
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How does metabolic alkalosis cause hypokalemia
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Increased anions in tubular fluid of distal nephron
Increased K secretion |
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Metabolic response to hyperkalemia
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Insulin - shift K into cells
Epi via B adrenergic - shift K into cells Aldosterone - shift K into cells, increase renal K secretion All in place to avoid the shifts in plasma K that would result from normal dietary consumption |
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Potassium and acid
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Acidemia shifts K out of cells
Alkalemia shifts K into cells |
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Hyperkalemia
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K > 5
Rare May be asymptomatic or result in death |
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Clinical manifestation of hyperkalemia
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Muscle weakness
Cardiac arrythmias PR prolongation Peaked T waves QRS widening Sine wave/asystole Depend on rate of rise as well as degree |
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Etiology of hyperkalemia
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Increased intake
Decreased secretion Transcellular shifting Spurious |
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Where is K intake?
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Food: potatoes, tomatoes, citrus, melons, milk
Antibiotics, K supplements Salt substitutes |
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Causes of decreased K excreiton
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Low GFR
Hypoaldosteronism Meds |
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When does dietary K become a problem?
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When excretion is limited
If GFR falls to 30/L day, max excretion is 120 mEq |
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Causes of primary hypoaldosteronemia
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Adrenal insufficiency
Genetic - 21 hydroxylase Heparin - blocks aldosterone production |
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'Secondary' hypoaldosteronemia
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Hyporeninemic
Damage to JGA -- diabetic nephropathy, obstructive uropathy Iatrogenic |
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ACE/ARB therapy and K
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Hyperkalemic from low aldosterone
Decreased angiotensin II production = decreased aldo production Efferent arteriole dilate can lead to reduced GFR/low tubular flow rate NSAID use worsens |
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Aldosterone resistance
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Receptor defects
Aldosterone antagonists (K sparing diuretics) Pseudohypoaldosteronism -- post-receptor defects |
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K-sparing diuretics and K
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Block Na reabsorption in distal tubule
Unable to create negative electrochemical gradient in order to secrete K Amiloride, Triamterene, Spironolactone, Eplerenone |
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NSAIDs and renal K handling
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Hyperkalemia
Direct kidney damage - interstitial nephritis = decreased renin production Afferent arteriole constriciton reduces tubular flow rate |
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Cylcosporine and K
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Hyperkalemia
Immunosuppresive agent has SE of renal vasoconstriction --reduces GFR and flow rate Can also cause tubular ischemic damage |
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Trimethoprim and K
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Structurally similar to a K sparing diuretic
Blocks distal Na channel |
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What causes transcellular K shifting that can result in hyperkalemia?
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Acidemia
Insulin deficiency Beta blockade Hemolysis/rhabdomyolysis/tumor lysis Excercise Digitalis toxicity Hyperosmolarity |
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Mechanism of hyperkalemia in acidemia
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H+ enters cells by diffusion
K+ leaves cells to balance positive charge |
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Cellular dysfunction and hyperkalemia
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Reduced function of Na/K ATPase results in K leak out of cells
Can occurs from ATP depletion (excercise, ischemia/reperfusion) Digitialis inhibits directly |
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Succinylcholine and K
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Can cause massive K exodous from cells of patients with neuromuscular dysfunction
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Pseudohyperkalemia
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Severe leukocytosis/thrombocystosis = more K released from cells in tube
-- check plasma levels Hemolyzed blood sample Prolonged tourniquet time |
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Evaluation of hyperkalemia
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Establish cardiac stability -- ECG, telemetry
Confirm true hyperkalemia (reduce tourniquet time, larger bore needle) H/P, meds (ARBs, ACEI, diuretics, etc) Renal fnc 24 hr urine K/TTKG |
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Normal 24 urine K
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>500 mEq K per day is possible for a normal kidney
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TTKG
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Transtubular K gradient
Estimate of renal K excretion = (Urine K x serum osm)/ (serum K x urine osm) Typically 8-9 >11 in hyperkalemia |
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Low TTKG in hyperkalemia
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< 7 is highly suggestive of hypoaldosteronism
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Management of acute hyperkalemia
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IV calcium
Insulin/glucose Albuterol Bicarb Kayexalate |
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IV calcium in hyperkalemia
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Stabilizes myocardial membrane
Works in 5-10 Lasts 30 minutes to 2 hours May cause transient hyperacalcemia Does not change serum K 10cc of 10% over 2-3 minutes |
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Insulin/glucose treatment in hyperkalcemia
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Regular insulin IV
Glucose to prevent hypoglycemia Shifts K into cells Works in 30-60, lasts 4-6 hours 10 units insulin + 50cc D50 |
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Albuterol in treatment of hyperkalemia
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Shifts K into cells
Works in 30-60 Lasts 4-8 hours May cause tachycardia, agitation 10-20 puffs or 10-20mgs |
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Bicarbonate
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Idea is to drive K into cells
Really only works well with patients in metabolic alkalosis Works in 30-60 Lasts 4-6 50 mEq NaHCO3 over 5 minutes |
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General management of hyperkalemia
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Monitor heart
Use temporizing measures (calcium- ekg changes, albuterol, bicarb - alkalosis, insulin) to lower a few points for a few hours Increased excretion with kayexalate |
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Kayexalate
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Increases GI loss of K
Resin exchanges K for Na (cause in CHF, ESRD) Works in 2-4 hous 10 gs lower serum K b 0.1-0.2 mEq/L Give 30-60 g PO with sorbitol Risk of colonic necrosis in post surgical patients |
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Acute indications for dialysis
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K+ > 7
Widening QRS with inability to take kayexalate, renal failure Refractory hyperkalemia Ongoing K release -- bleed, lysis |
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Treatment of chronic hyperkalemia
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Usually hypoaldosteronism
Reduce K intake Fludricortisone to replace aldo if patient is not HTN or edematous Furosemide if they are Avoid meds which increase K |
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Hypokalemia
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Decrease in serum K
Considering the ratio of serum to intracellular K, changes to serum K represent a large loss of total K |
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Clinical manifestation of hypokalemia
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Muscle weakness
-- decreased membrane excitability Cardiac arrythmias -- altered membrane potential and repol Metabolic alkalosis -- hypokalemia increased tubular H secretion Nephrogenic diabetes insipidus |
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Dietary deficiency of K leading to hypokalemia?
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Rare
Typical intake is high and kidney can reabsorp most of it |
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Increased renal losses of K
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Diuretics -- loop and thiazide
Hyperaldosteronism Anion excess HCO3, ketones, penicillins, glue Polyuria Hypomagnesmia -- reduces pump effectiveness Genetic disease |
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Causes of hyperaldosteronism
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Primary overproduction by adrenal gland
Volume depletion Renal artery stenosis |
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Polyuria and K
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Can cause hypokalemia
Kidney can only dilute urine so much (K = 5-10 mEq) Intake restricted settings worsen effect |
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Hypomagnesemia and K
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Cause of renal K wasting
Often occurs with hypokalemia and needs to be corrected before K can be Both lost in vomit, diarrhea, diuretics |
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Bartter's Syndrome
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Inactivating mutation in Na/K/2Cl pump of loop
Hypokalemia, hypomagnesemia, vol depletion, metabolic alkalosis |
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Gitelman's syndrome
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Mutation in NaCl reabsorption in the distal tubule
Like being on a chronic thiazide Hypokalemia, metabolic alkalosis |
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Liddle's syndrome
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Aldo sensitive Na channel is distal tubule is constitutively activate
Pseudohyperaldosteronemia HTN and hypokalemia Low renin and aldo |
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Diarrhea and hypokalemia
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Direct loss -- intestinal fluids contain 20-50mEq/L
Resulting hypovolemia leads to increased aldo and more K loss |
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Vomiting and hypokalemia
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Little K is lost directly
Metabolic alkalosis increases bicarb in urine, an unabsorbed anion, which pulls K in Volume depletion leads to increased aldo and more K loss |
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Other ways to lose K
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Dialysis (periotoneal > hemo)
Plasmapheresis Excessive sweating High vol peritoneal drainage |
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What causes transcellular K shifting resulting in hypokalemia
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Hyperinsulinemia
Adrenergic excess - ie pheo Alkalemia Refeeding syndrome Increased blood cell production like when folate/b12 deficiency corrected Periodic paralysis |
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Alkalemia and K
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Shifts K into cells
Bicarb excretion results in K trapping in urine |
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Periodic paralysis
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Rare genetic disorder
Recurrent severe hypokalemia and resulting paralysis Associated with thyrotoxicosis in Asian males Often triggered by excercise, stress, eating |
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Spurious hypokalemia
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Severe leukocytosis
Cells can uptake K in tube Either refridgerate or process fast to avoid |
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HTN plus hypokalemia not on diuretics?
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Hyperaldosteronism
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Metabolic alkalosis + low urinary K + hypokalemia
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Vomiting or diuretic abuseI
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Urinary K in hypokalemia
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Normal kidney can dilute K to 5-10meq/L urine
>20 meq/day in hypokalemia is abnormal TTG >5 and hypokalemia suggest hyperaldosteronism |
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Managing hypokalemia
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Total body deficity is 100 x change in serum
KCl is preferred replacement Need central line because peripheral tolerance for K is 60 mEq/L Can go 10 mEq/hr on floor and 20 in ICU Need cardiac monitoring for >10 |
