Diabetic Ketoacidosis (DKA) - Pathogenesis and Clinical ...

Diabetic Ketoacidosis (DKA) - Pathogenesis and Clinical Findings

 • Note: in DKA, body K+ is lost via osmotic diuresis & vomiting. But diffusion of K+ out of cells may cause serum [K+] to be falsely normal/elevated. To prevent hypokalemia, give IV KCI along with IV insulin as soon as serum <5.0 mmol/L. But ensure patient has good renal function/urine output first!

 • Due to neuronal metabolism, ketone bodies are the only other energy molecule besides glucose that can be used by the brain... thus, the body produces them when low on glucose.

Treating DKA: 1) +++ fluids. 2) Insulin + KCI. 3) Follow the anion gap until it closes. 4) Identify the precipitant. 5) treat low PO4 (typically occurs a few hours to a day after ketosis resolves due to ATP production.


 • Polydipsia

 • Polyphagia

 • Polyuria, Glucosuria, Ketouria

 • Severe Dehydration (up to 4-5L dry) - (Decr JVP, orthostasis: postural hypotension/postural tachycardia, Incr resting HR)

 • Abdominal pain, nausea, vomiting (Incr dehydration)

 • Kussmaul respiration (deep, fast breathing)

 • Ketone breath (fruity odor)

 • Weakness confusion coma

#DiabeticKetoacidosis #DKA #pathophysiology #endocrinology #diabetes
Contributed by

The Calgary Guide to Understanding Disease
Account created for The Calgary Guide to Understanding Disease - Linking pathophysiology to clinical presentation - http://calgaryguide.ucalgary.ca/

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