Endocrine - Hyper and Hypo- glycaemia

Question 1

What are the criteria for DKA?

Answer 1

Glucose >11 OR known diabetes

Bicarb <15 OR pH <7.3

Ketones >3mmol/L OR urine ketones >+++
(ketones >1.5mmol/L is Mod-Large, 0.6-1.5 is small-mod)

Question 2

How does DKA get precipitated and start?

Answer 2

Stress/infection in absolute insulin deficiency
with increased counter-regulatory hormones
- glucagon
- catecholamines
- cortisol
- growth hormone

Question 3

How does ketoacidosis happen?

Answer 3

Increased lipolysis –> FFAs are oxidised by ACETYLCOENZYME A in liver from acetoacetate to ACETONE and BETA-HYDROXYBUTYRATE

–> reduced alkali reserve and decreased bicarb

–> ketoacidosis:
acetate gives fruity breath
beta-hydroxybutyrate stimulates nausea and vomiting

Question 4

What does acetylcoenzyme A do?

Answer 4

In the liver oxidises free fatty acetates from acetoacetate to acetone and beta-hydroxybutyrate

Question 5

How does hyperglycaemia and glucosuria form in DKA?

Answer 5

increased proteolysis with decreased protein synthesis
AND increased glycogenolysis

–> substrates for gluconeogenesis (with increased gluconeogenesis)

BUT there is decreased glucose utilisation

–> hyperglycaemia and glucosuria

Question 6

What is the diagnostic criteria for HHS?

Answer 6

Serum Osm >320
Serum glucose >33
Profound dehydration
NO ketoacidosis

Question 7

What are the most common underlying causes of DKA in diabetes?

Answer 7

25% are NEW T1DM

25% are poor insulin compliance / missed doses

40% are infection

Other:

• brittle diabetes
• medical or surgical stress
• insulin infusion blockage/failure
• medications

Question 8

What medications can precipitate DKA?

Answer 8

Corticosteroids
Thiazides
Sympathomimetics
Pentamidine
Clozapine and new antipsychotics
SGLT2 inhibitors

Question 9

What is the leading bacterial cause of DKA?

Answer 9

Klebsiella

Question 10

Physiological response to hypoglycaemia?

Answer 10

1) decreased insulin secretion from pancreatic beta cells
- -> increased hepatic glygogenolysis
- -> increased renal and hepatic gluconeogenesis
- -> increased lipolysis and proteolysis
- -> reduced peripheral glucose utilisation

2) Increased glucagon secretion from pancreatic alpha-cells
- -> increased hepatic glycogenolysis

3) Increased adrenaline release from adrenal medulla
- -> increased hepatic glycogenolysis
- -> increased hepatic and renal gluconeogenesis

4) increased cortisol and growth hormone if PROLONGED HYPOGLYCAEMIA