DKA

Question 1

plasma glc to diagnose DKA

Answer 1

> 250 mg/dl

Question 2

plasma glc to diagnose hyperglycemic hyperosmolar syndrome

Answer 2

> 600 mg/dl

Question 3

How is mild, moderate, and severe DKA distingushed?

Answer 3

serum pH and bicarb

mild: 7.25-7.3 and **
moderate: 7-7.4
severe: < 7

Question 4

preipitating factors for DKA and HHS

Answer 4

infection
new onset DM
DC insulin
unknown

Question 5

hormone of “fed state” vs “fasting state”

Answer 5

fed = insulin and fasting = glucagon

Question 6

anything that causes stress produces (insulin or glucagon) secretion

Answer 6

glucagon

Question 7

how does acute insulin deficiency lead to circulatory failure?

Answer 7

↑blood glc → ↑urine glc → polyuria → dehydration and loss of electrolytes → circulatory failure

+ glucagon
→ ↑glycogen breakdown + ↑ gluconeogenesis, further increases blood glc
→ ↑ protein breakdown for gluconeogenesis → further inc blood glc

Question 8

why to pts with acute insulin def have ↑BUN

Answer 8

↓protein synthesis

Question 9

How does ↑ketone body production lead to acidosis

Answer 9

↑plasma ketones causes ↓alkali reserve (i.e. bicarb) → acidosis

Question 10

how is the glucagon:insulin ratio changed in DKA

Answer 10

↑glucagon:↓insulin

Question 11

how does insulin def lead to ↑FA oxidation ∴ ↑KB production

Answer 11

↑protein kinase → activates lipase → ↑TG to FFA

Question 12

TCA cycle is (on or off) in DKA. significance?

Answer 12

OFF → FFA are converted to glc to further ↑hyperglycemia ????

**FFA converted to citrate, ↑↑↑ citrate inhibit TCA, so FFA shunted into glc production???

Question 13

What are the enzymes needed to convert FFA to glc?

Are these active or inactive in DKA?

Answer 13

PC
PEPCK
F 1,6 bisphosphate
G-6-Phosphate

inactive??

Question 14

What inhibits the TCA cycle in DKA?

Answer 14

citrate

Question 15

In DKA anion gap is ↓ or ↑?

Answer 15

↑