Metabolic Medicine
Showing 15 of 15 topics
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Alcoholic ketoacidosis is a high-anion-gap metabolic acidosis that usually follows heavy alcohol use, poor oral intake, vomiting, and abrupt reduction in alcohol consumption. Glucose may be low, normal, or only modestly elevated. Treatment centers on volume replacement, dextrose, thiamine, electrolyte repletion, and recognition of concurrent alcohol withdrawal or another dangerous cause of acidosis.
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Intercurrent illness can destabilize diabetes and kidney function at the same time. Sick-day management in CKD requires continued glucose and ketone surveillance, adequate hydration, individualized insulin adjustment, and temporary withholding of selected medications that can worsen dehydration, ketoacidosis, or kidney injury. Patients need explicit restart instructions rather than a vague order to stop medicines when sick.
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Most recurrent diabetic ketoacidosis is preventable when patients have reliable insulin access, a written sick-day plan, ketone testing, hydration guidance, and clear thresholds for contacting the diabetes team or seeking emergency care. People with type 1 diabetes should not stop basal insulin during illness even when oral intake is reduced.
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Sodium reduction is a practical treatment for hypertension and an important part of heart-failure and kidney-disease management. Most dietary sodium comes from packaged, prepared, and restaurant foods rather than the salt shaker. Counseling works best when it translates a daily target into label reading, meal choices, and realistic substitutions rather than simply telling patients to 'avoid salt.'
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Hyperkalemia is an electrolyte emergency when potassium is markedly elevated, rapidly rising, or associated with ECG changes. Management follows three simultaneous goals: stabilize the cardiac membrane with IV calcium when indicated, shift potassium into cells with insulin and beta-agonist therapy, and remove potassium from the body through renal excretion, gastrointestinal binders, or dialysis.
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Calculate free water deficit, correct chronic hypernatremia slowly, and choose enteral or IV hypotonic fluids with frequent sodium checks.
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Hypertriglyceridemia can precipitate acute pancreatitis, especially when triglycerides are markedly elevated, often above 1,000 mg/dL. Management combines standard pancreatitis care with rapid correction of metabolic drivers, glycemic control when needed, and a plan to prevent recurrence. IV insulin can accelerate triglyceride clearance in selected patients, while plasmapheresis is reserved for exceptional severe cases rather than routine use.
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Hypokalemia can cause weakness, ileus, rhabdomyolysis, atrial and ventricular arrhythmias, and respiratory failure when severe. Management requires confirmation, ECG assessment when clinically significant, identification of renal versus extrarenal loss, magnesium correction, and oral or IV potassium replacement selected according to severity, symptoms, route tolerance, and ongoing losses.
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Lactic acidosis is an elevated lactate associated with metabolic acidosis or physiologic stress and should prompt a search for impaired oxygen delivery, excessive metabolic demand, impaired clearance, or toxin/drug effects. Treatment is cause-directed: restore perfusion and oxygen delivery when deficient while rapidly addressing sepsis, seizure, ischemia, toxic exposure, thiamine deficiency, or other drivers.
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Metabolic acidosis is identified by reduced bicarbonate with an acidemic or compensating blood gas and should be classified by anion gap before treatment. The anion gap narrows the differential, while delta-gap analysis can reveal a second metabolic process hidden within a high-gap acidosis.
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Metabolic syndrome is a clustering of abdominal adiposity, elevated blood pressure, hyperglycemia, high triglycerides, and low HDL cholesterol that identifies increased cardiometabolic risk. Management is not a single-drug treatment for the syndrome itself; it is aggressive risk reduction through weight loss, physical activity, dietary quality, smoking cessation, and evidence-based treatment of each abnormal component.
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Metformin is effective and generally safe when renal function is adequate and acute hypoxic or hypoperfusion states are absent. It is contraindicated when eGFR is below 30 mL/min/1.73 m2 and should not be initiated at eGFR 30 to 44. The major safety concern is metformin-associated lactic acidosis, which is rare but can occur when drug accumulation coincides with kidney failure, shock, hypoxemia, sepsis, or severe hepatic dysfunction.
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Non-anion-gap metabolic acidosis results from bicarbonate loss or impaired renal acid excretion and is commonly caused by diarrhea, saline-associated hyperchloremia, or renal tubular acidosis. Urine studies, potassium pattern, kidney function, and clinical context distinguish gastrointestinal loss from renal acidification disorders.
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Modern obesity pharmacotherapy is chronic disease treatment, not a short course for cosmetic weight loss. GLP-1 receptor agonists and the dual GIP/GLP-1 agonist tirzepatide produce the largest average weight reductions among widely used medications, but selection must consider indications, contraindications, adverse effects, comorbid diabetes and cardiovascular disease, access, and the likelihood of weight regain after discontinuation.
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Recurrent hypoglycemia requires more than repeated carbohydrate administration. Determine whether episodes are medication related, fasting or postprandial, associated with critical illness or endocrine disease, and whether Whipple triad is documented in a patient without diabetes. Prevention relies on medication adjustment, CGM when appropriate, ready access to glucagon, and targeted evaluation of unexplained episodes.
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