AceMed Universities MU Sofia Medicine Year 3 Pathophysiology Topic 72
Pathophysiology · MU Sofia
72. Disorders in sodium, potassium and magnesium metabolism - etiology, pathogenesis, clinical manifestations.
Inside: 1 section · 1 table · 16 flashcards · 2 min
Topic 72 of 168 in the MU Sofia syllabus for Pathophysiology (Medicine, Year 3). The free AceMed note covers it in 1 section, about 281 words (2 min of reading), with 16 flashcards .
In this note Disorders in sodium, potassium, and magnesium metabolism – etiology, pathogenesis, and clinical manifestations.
Disorders in sodium, potassium, and magnesium metabolism – etiology, pathogenesis, and clinical manifestations. Sodium metabolism disorders Hyponatremia (Na <135 mmol/L) Etiology Hypovolemic hyponatremia: diarrhea, vomiting, diuretics, burns. Euvolemic hyponatremia: SIADH, hypothyroidism, adrenal insufficiency. Hypervolemic hyponatremia: heart failure, cirrhosis, nephrotic syndrome. Pathogenesis Dilutional (excess water relative to sodium). Sodium loss exceeding water loss. Clinical manifestations Headache, nausea, vomiting. Muscle cramps. Confusion, lethargy. Seizures, coma (severe cases). Hypernatremia (Na >145 mmol/L) Etiology Water loss (dehydration): fever, sweating, diarrhea. Diabetes insipidus (central or nephrogenic). Excessive sodium intake (rare). Pathogenesis Cellular dehydration due to hyperosmolarity → water shifts from cells to ECF. Clinical manifestations Thirst. Weakness, irritability. Neurological signs: confusion, seizures, coma. Potassium metabolism disorders Hypokalemia (K <3.5 mmol/L) Etiology GI losses: vomiting, diarrhea. Renal losses: hyperaldosteronism, diuretics. Shift into cells: insulin excess, alkalosis. Pathogenesis Reduced extracellular K → hyperpolarization of cell membranes → decreased excitability. Clinical manifestations Muscle weakness, fatigue. Hyporeflexia, cramps. Cardiac arrhythmias (flattened T waves, U waves). Constipation, ileus. Hyperkalemia (K >5.5 mmol/L) Etiology Renal failure (most common). Hypoaldosteronism (Addison’s). Cell lysis (hemolysis, rhabdomyolysis, tumor lysis). Acidosis (shift from cells to plasma). Pathogenesis Depolarization of cell membranes → increased excitability initially, then reduced as levels rise further. Clinical manifestations Muscle weakness, paralysis. Cardiac arrhythmias (peaked T waves, widened QRS, sine-wave pattern). Paresthesias. Magnesium metabolism disorders Hypomagnesemia (Mg² <0.7 mmol/L) Etiology Malnutrition, alcoholism. Diarrhea, malabsorption. Diuretics. Pathogenesis Mg² deficiency → impaired PTH secretion and action → secondary hypocalcemia. Affects K handling → often associated with hypokalemia. Clinical manifestations Neuromuscular: tremor, tetany, muscle weakness, hyperreflexia. CNS: confusion, seizures. Cardiac: arrhythmias (similar to hypokalemia). Hypermagnesemia (Mg² >1.1 mmol/L) Etiology Renal failure. Excessive intake (antacids, laxatives containing Mg² ). Pathogenesis Depresses neuromuscular and cardiac conduction. Clinical manifestations Lethargy, weakness. Hyporeflexia. Hypotension, bradycardia. Severe: respiratory paralysis, cardiac arrest. Summary Table
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