Flashcards in DKA Deck (15):
plasma glc to diagnose DKA
> 250 mg/dl
plasma glc to diagnose hyperglycemic hyperosmolar syndrome
> 600 mg/dl
How is mild, moderate, and severe DKA distingushed?
serum pH and bicarb
mild: 7.25-7.3 and **********
severe: < 7
preipitating factors for DKA and HHS
new onset DM
hormone of "fed state" vs "fasting state"
fed = insulin and fasting = glucagon
anything that causes stress produces (insulin or glucagon) secretion
how does acute insulin deficiency lead to circulatory failure?
↑blood glc → ↑urine glc → polyuria → dehydration and loss of electrolytes → circulatory failure
→ ↑glycogen breakdown + ↑ gluconeogenesis, further increases blood glc
→ ↑ protein breakdown for gluconeogenesis → further inc blood glc
why to pts with acute insulin def have ↑BUN
How does ↑ketone body production lead to acidosis
↑plasma ketones causes ↓alkali reserve (i.e. bicarb) → acidosis
how is the glucagon:insulin ratio changed in DKA
how does insulin def lead to ↑FA oxidation ∴ ↑KB production
↑protein kinase → activates lipase → ↑TG to FFA
TCA cycle is (on or off) in DKA. significance?
OFF → FFA are converted to glc to further ↑hyperglycemia ????
**FFA converted to citrate, ↑↑↑ citrate inhibit TCA, so FFA shunted into glc production???
What are the enzymes needed to convert FFA to glc?
Are these active or inactive in DKA?
F 1,6 bisphosphate
What inhibits the TCA cycle in DKA?