approach to the patient with electrolyte disorders hypokalemia-hyperkalemia zehra eren, m.d
DESCRIPTION
POTASSİUM DİSTRİBUTİON Gastrointestinal absorption → %98 intracellular %2 extracellular NA + K + ATPase → transports two K + into cell three Na + out cellTRANSCRIPT
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Approach to the patient with electrolyte disorders
Hypokalemia-Hyperkalemia
Zehra Eren, M.D.
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LEARNING OBJECTIVES• recall potassium distribution• recall etiology of hypokalemia and hyperkalemia
• describe sing and symptoms of hypokalemia and hyperkalemia
• describe laboratory findings of hypokalemia and hyperkalemia
• explane treatment of hypokalemia and hyperkalemia
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POTASSİUM DİSTRİBUTİON
•Gastrointestinal absorption→%98 intracellular%2 extracellular
•NA+K+ ATPase → transports two K+ into cell three Na+ out cell
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Hypokalemia
•Serum K+ < 3.5 mEq/L (mmol/L)
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Causes of Hypokalemia • Pseudohypokalemia
-Extreme leukocytosis
• Decreased K intake
• Increased K losses -Nonrenal (skin, gastrointestinal)-Renal
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RENAL POTASSİUM LOSS1. Increased distal flow and distal Na+ delivery
-diuretics -osmotic diuresis -salt-wasting nephropathies
2. Increased secretion of potassium - Mineralocorticoid excess: primary
hyperaldosteronism [aldosterone-producing adenomas (APAs)], primary or unilateral adrenal hyperplasia (PAH), idiopathic hyperaldosteronism (IHA) due to bilateral adrenal hyperplasia, and adrenal carcinoma], familial hyperaldosteronism (FH-I, FH-II, congenital adrenal hyperplasias), secondary hyperaldosteronism (malignant hypertension, renin-secreting tumors, renal arterystenosis, hypovolemia), Cushing's syndrome, Bartter's syndrome, Gitelman's syndrome
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RENAL POTASSİUM LOSS-Apparent mineralocorticoid excess: genetic
deficiency of 11β-dehydrogenase-2 (syndrome of apparent mineralocorticoid excess), inhibition of 11β-dehydrogenase-2 (glycyrrhetinic/glycyrrhizinic acid and/or carbenoxolone; licorice, food products, drugs), Liddle's syndrome [genetic activation of epithelial Na+ channels (ENaC)]
-Distal delivery of nonreabsorbed anions: vomiting, nasogastric suction, proximal renal tubular acidosis, diabetic ketoacidosis, glue sniffing (toluene abuse), penicillin derivatives (penicillin, nafcillin, dicloxacillin, ticarcillin,oxacillin and carbenicillin)
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Causes of Hypokalemia• Redistribution (increased entry into cell)
-Insulin excess-Alkalemia-“Stress” [β2 adrenergic sympathetic activityꜛ: asthma attack,
acute coronary syndrome, trauma, drug intoxication (cocaine) or alcohol withdrawal, B2 adrenergic drugs ]
-α-adrenergic antagonists-Hypokalemic periodic paralysis-Thyrotoxicosis-Barium, Cesium -Hypothermia-Downstream stimulation of NA+/K+ ATPase: theophyline, cafferine
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DİAGNOSİS
• Rule out -pseudohypokalemia-redistribution
• Potassium deplettion-renal-gastrointestinal-skin
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Clinical manifestations • Cardiovascular:
-Hypertansion (↑BP 5-10mmHg )-Arrhythmias-Digitalis toxicity
• Neuromuscular: 1.Smooth muscle:
-Ileus2.Skeletal muscle:
-Weakness-Paralysis-Rhabdomyolysis
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Clinical manifestations• Endocrine:
-Glucose intolerance (↓insulin release and sensitivity)
• Renal: ↓blood flow,↑vascular resistance-Vasopressin resistance-Increased ammonia production-Metabolic alkalosis (retention of Na, Cl, HCO3)-Polyuria, phosphaturia, hypocitraturia
Structural changes: Renal cystsInterstitial changesPT dilation, vacuolization
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TREATMENT GOALS
• prevent life-threatening and/or chronic consequences
• replace the associated K+ deficit
• correct the underlying cause and/or mitigate future hypokalemia
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TREATMENT
Urgency of therapy depends on -the severity of hypokalemia -associated clinical factors (cardiac disease,digoxin therapy, etc.) -rate of decline in serum K+
Cautions-severe redistributive hypokalemia -concomitant Mg2+ deficiency
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TREATMENT•Oral
• İntravenousSafely at a rate of 10 mmol/h
20mmol KCL →↑serum K + ~ 0.25 mmol/L
↑20mmol/h replacement → central venous catheter
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Hyperkalemia
•Serum K ≥5.0 mEq/L (mmol/L)
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Causes of Hyperkalemia • Pseudohyperkalemia
-Thrombocytosis-Leukocytosis-Ischemic blood draw
• Redistibution (increased K release from cells)-Exercise, especially in setting of β adrenergic receptor blockage and mineral acidosis-Hyperchloremic metabolic acidosis-Insulin deficiency-Hypertonicity-α adrenergic receptor stimulation
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Causes of Hyperkalemia • Excessive intake: rare as sole cause
• Impeared renal K+ excretionGFR <20 mL/min:
-Endogenous or exogenous K+
-Drugs that impair K+ excretion
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Clinical manifestations
• May be disproportionately greater than level of serum K• Cardiovascular
-T-wave abnormalities-Bradyarrhythmias
• Neuromuscular-Ileus-Paresthesias-Weakness-Paralysis
• Renal/electrolyte-Decreased ammonia production-Metabolic acidosis
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Case1• A 70-year-old man with advanced prostate cancer develops
bilateral ureteral obstruction and acute on chronic renal failure.
His potassium rises to 7.7 mEq/L with peaked T-waves on electrocardiogram. His medications include digoxin.
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Case2• A 72 year old male found collapsed at home on floor of his
bedroom, incontinent of urine and faeces. He complained of significant pain in his right hip with shortening and rotation. His family last had contact with him 3 days prior to his collapse.
• Medical History:CCF , Hypertension , Type 2 DM, Osteoarthritis
• Medication History:His is taking enlapril for hypertension; spironolactone & metoprolol for his CCF and celebrex for his osteoarthritis.His diabetes is diet controlled.
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