Affects mostly Type 1, result of total lack of insulin and increase in counter regulatory hormones that allows hepatic FA oxidation in liver to make 3 main ketone body production, leads to ketoacidosis
Acetoacetic acid
Beta-hydroxybutyric Acid (from reduction of acetoacetic acid, can measure in blood)
Acetone (from decarboxylation of acetoacetic acid, can vaporize and gives "acetone" smell associated with DKA)
What is HHS
Mostly type 2, result of relative lack of insulin that causes hyperosmolality, ketones may spill into urine, not enough ketone production to cause ketoacidosis
Patient becomes more volume depleted and hyperglycemic
Difference between DKA and HHS presentation
DKA: pt usually presents earlier b/c of sx so less dehydration and glucose not as high (<800, usually 350-450)
HHS: Greater dehydration d/t osmotic diuresis, high glucose (~1000), ketones in urine, enough insulin to prevent lipolysis
DKA patient findings
Tend to be younger and have better kidney function, RAPID development, neuro sx, abd pain, dehydration, tachycardia, hypotension, hyperventilation (Kussmaul), fruity breath
HHS patient findings
Develop over a longer time period, polyuria/-dipsia, weight loss, neuro sx, dehydration, tachycardia, hypotension