Pathophysiology · MU Sofia

72. Disorders in sodium, potassium and magnesium metabolism - etiology, pathogenesis, clinical manifestations.

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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.

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  1. 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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