USMLE/COMLEX 1 - Hypokalemia Management

Here are key facts for USMLE Step 1 & COMLEX-USA Level 1 from the Hypokalemia Management tutorial, as well as points of interest at the end of this document that are not directly addressed in this tutorial but should help you prepare for the boards. See the tutorial notes for further details and relevant links.
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VITAL FOR USMLE/COMLEX 1
Definition & Classification
1. Definition: K+ < 3.5 mEq/L. 2. Classification by Severity:
    • Mild/Moderate: K+ 3.0-3.4 mEq/L
    • Severe/Symptomatic: K+ < 3 mEq/L
Etiology
1. Major causes:
    • Gastrointestinal losses
    • Renal losses
    • Redistribution into cells
    • Inadequate intake
Clinical Manifestations
1. Muscle symptoms: Cramps, weakness, rhabdomyolysis 2. Cardiac manifestations: Premature beats, arrhythmias 3. Diagnostic ECG changes: U waves, flattened T waves
Hypokalemia
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HIGH YIELD
Management of Severe Hypokalemia (K+ < 3.0)
1. IV replacement: 20 to 60 mEq KCl in saline 2. Administration rate: Not more than 10-20 mEq/hr to avoid peripheral vein irritation 3. Monitoring requirements: Close monitoring, ECG monitoring if arrhythmias present
Management of Mild-Moderate Hypokalemia (K+ 3.0-3.4)
1. Oral replacement: K+ supplements – 10-20 mEq, 2-4× daily (max 80 mEq/day) 2. Dietary intervention: Increase intake of K+-rich foods
Monitoring Principles
1. Target range: Maintain K+ between 3.5-5 mEq/L 2. Adjustment goal: Avoid hyperkalemia and arrhythmias
Treatment of Underlying Causes
1. Address primary etiology: Gastrointestinal losses, diuretic therapy 2. Consider renal function: Important during replacement therapy
Critical Adjunctive Considerations
1. Magnesium status: Check for and correct magnesium deficiency 2. Pharmacologic intervention: Consider potassium-sparing diuretics in renal losses (e.g., amiloride) 3. Individualized approach: Based on comorbidities and clinical status
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Beyond the Tutorial
Below is additional information not explicitly contained within the tutorial but important for USMLE Step 1.
Pathophysiologic Considerations
1. Cellular membrane potential: Hypokalemia leads to hyperpolarization of cell membranes 2. Aldosterone effect: Promotes renal K+ excretion and Na+ retention 3. Acid-base disturbances: Metabolic alkalosis commonly coexists with hypokalemia
Specific Causes
1. Diuretics: Loop and thiazide diuretics are common iatrogenic causes 2. Endocrine disorders: Cushing's syndrome, hyperaldosteronism 3. Medications: Beta-agonists, insulin, and theophylline can cause redistribution 4. Renal tubular acidosis: Type 1 (distal) and Type 2 (proximal) RTA
Complications
1. Glucose metabolism: Impaired insulin release and glucose intolerance 2. Neurologic: Paresthesias, tetany, and in severe cases, ascending paralysis 3. Renal effects: Polyuria, polydipsia, and nephrogenic diabetes insipidus 4. Gastrointestinal: Ileus, constipation