Thread by @mghmedres

Recap of noon conference today with Dr. Nancy Wei on every intern’s favorite call admission aka DKA!!

Here’s a framework to think about the different types of ketosis-prone diabetes subgroups!

Remember to think about beta-cell function and auto-antibody status to beta-cells!

How does DKA happen?

Not via hyperglycemia.

It is from high glucagon and NO insulin. This leads to a release of glucose from glycogen stores, then subsequently a release of fatty acids from fat cells leading to ketone production, and ultimately, ketoacidosis.

The key to preventing DKA is thus having BASAL INSULIN 🙌

As an FYI: the concentration of insulin needed to suppress lipolysis is about 1/10 that is needed to suppress gluconeogenesis!

So...what are the presenting sxs of DKA?

Vomiting, polyuria, polydipsia, weakness, weight loss, abdominal pain, visual changes, leg cramps 🤢

Remember: when you start an insulin gtt, you want to consider:
-blood sugar measurement 🍲
-the trajectory of blood sugar change 📊
-magnitude of blood sugar change 📏

BTW, IV insulin has a half life of ~10 minutes

Work-up of DKA?
The five I’s:
-infection
-infarction
-infant (pregnancy)
-indiscretion/intoxication (cocaine, EtOH)
-insulin omission

*in new diagnoses, consider anti-GAD65 and anti-IA2 antibodies