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USMLE STEP 2
HYPERMAGNESEMIA ETIOLOGY AND PATHOPHYSIOLOGY Hypermagnesemia is diagnosed by a serum magnesium titers greater than 2.3 mg / dL. It is typically due to renal failure with decreased excretion, abuse of antacids containing magnesium, tumor lysis syndrome or rhabdomyolysis, redistribution in DKA or pheochromocytoma, and toxicity from lithium.
PRESENTATION AND DIAGNOSIS Hypermagnesemia presents with decreased DTR, hypotension, paresthesia, coma, and specific EKG changes. EKG changes are opposite of those found with hypomagnesemia.
TREATMENT Treatment of hypermagnesemia is to treat the EKG changes with IV calcium and use dialysis to regain normal magnesium homeostasis. TABLE 554 HYPERMAGNESEMIA Hypermagnesemia Etiology
Due to renal failure with decreased excretion, abuse of antacids containing magnesium, tumor lysis syndrome or rhabdomyolysis, redistribution in DKA or pheochromocytoma, and toxicity from lithium.
Presentation
Decreased DTR, hypotension, paresthesia, coma, and specific EKG changes.
Diagnosis
EKG
Treatment
IV calcium and use dialysis to regain normal magnesium homeostasis.
ACID-BASE DISORDERS ANION GAP METABOLIC ACIDOSIS As discussed above, an anion gap metabolic acidosis is commonly due to lactic acidosis, ketoacidosis (but not ketone bodies), uremia in chronic renal failure, and ingestion of toxins such as aspirin, ethylene glycol, methanol, and paraldehyde. Anion gap metabolic acidosis is diagnosed by ketoacids being present (as in alcoholic ketoacidosis, diabetic ketoacidosis [DKA], paraldehyde poisoning, starvation, high-fat diet, and isopropyl alcohol poisoning) or ketoacids being absent (as in renal failure, lactic acidosis, methanol poisoning, ethylene glycol poisoning, and aspirin poisoning).
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