What is the pathophysiology of alcoholic ketoacidosis (AKA)?

Updated: Aug 27, 2020
  • Author: George Ansstas, MD; Chief Editor: Romesh Khardori, MD, PhD, FACP  more...
  • Print
Answer

During starvation there is decrease in insulin secretion and increases in production of counter-regulatory hormones such as glucagon, catecholamines, cortisol, and growth hormone. Hormone-sensitive lipase is normally inhibited by insulin, and, when insulin levels fall, lipolysis is up-regulated, causing release of free fatty acids from peripheral adipose tissue.

Free fatty acids are either oxidized to CO2 or ketone bodies (acetoacetate, hydroxybutyrate, and acetone), or they are esterified to triacylglycerol and phospholipid. Carnitine acyltransferase (CAT) transports free fatty acids into the mitochondria and therefore regulates their entry into the oxidative pathway. The decreased insulin-to-glucagon ratio that occurs in starvation indirectly reduces the inhibition on CAT activity, thereby allowing more free fatty acids to undergo oxidation and ketone body formation.

Prolonged vomiting leads to dehydration, which decreases renal perfusion, thereby limiting urinary excretion of ketoacids. Moreover, volume depletion increases the concentration of counter-regulatory hormones, further stimulating lipolysis and ketogenesis.


Did this answer your question?
Additional feedback? (Optional)
Thank you for your feedback!