Alcoholic ketoacidosis tins Flashcards
Anion gap
The difference in cations to anions, used to determine causes of metabolic acidosis
Alcoholic ketoacidosis
Often associated with acute cessation of ETOH
Alcoholic ketoacidosis signs
Nausea, vomiting, vague GI complaints. Metabolism of ETOH combined with little or no glycogen reserves results in elevated ketoacid levels.
Rare but has been described after binge drinking (usually alchies)
Metabolism of ETOH (important for understanding alchy ketoacidy)
ETOH metab requries NAD
and enzymes alcohol dehydrogenase and aldehyde dehydrogenase to convert ethanol to acetyl coenzyme A
Acetyl coA may be metabolized directly resulting in ketoacid production, used as a substrate for the Krebs cycle, or used for FFA synthesis
Alcoholic ketoacidosis pathology
Happens when NAD is depleted, resulting in inhibition of aerobic metabolism in krebs cycle, depletion of glycogen stores, ketone formation, and lipolysis stimulation
When glycogen stores are depleted in a pt with a stressor, insulin secretion is also supressed. Glucagon, catechols and gH are all secreted which inhibits aerobic in favor of anaerobic
Clinical features of alcoholic ketoacidosis
Nausea, vomiting, nonspecific abdo pain, gastritis or pancreatitis.
Mental status changes are typically secondary to other causes such as toxic ingestion, hypoglycemia, ETOH withdrawal, seizures, or unrecognized head injury
Diagnosis
Made with labs
Metabolic acidosis, positive serum ketones, elevated anion gap, low or mildly elevated glucose
TX for alcoholic ketoacidosis
Glucose and fluids. Insulin from glucose stops lipolysis and halts further ketone formation, Glucose also oxidizes from NADH to NAD, further stopping ketone production
Cerebral edema is of little concern as these pts are not hyperosmolar
Just feed the fucker if hes awake
Insulin doesn’t help, can be dangerous since they may be sugar depleted
No bicarb unless pH less than 7. Severe acidemia is probskis not from alcoholic ketoacidosis
Tx lytes, they’re probskis shitty