see also:

• diabetes mellitus
• diabetic ketoacidosis (DKA)
• hyperosmolar hyperglycaemic state (HSS or HONK)

• blood glucose levels are normally kept within strict limits to prevent hypoglycaemia or dehydration from osmotic diuresis resulting from high levels of glucose in the blood with resultant glycosuria
• temporary high levels of blood glucose are common in non-diabetics as part of the acute stress response

• check urine for ketones
• consider arterial or venous blood gas to exclude evidence of acidosis
• if glucose > 13.8 AND raised ketones AND pH < 7.30 AND Bicarb < 15 then Mx as for diabetic ketoacidosis (DKA)
• otherwise, if glucose > 32 AND serum osmolarity > 320 then Mx as for hyperosmolar hyperglycaemic state (HSS or HONK)
• if neither of the above are present Mx as for unstable diabetes:
  • look for cause such as infection, AMI, acute limb thrombosis, etc
  • Rx any dehydration
  • stabilise blood glucose levels with sub-cut insulin (insulin infusion is NOT usually indicated)

• add the following FASTING blood tests:
  • HbA1c
  • lipids, c peptide, glucose, TSH, Anti-GAD Anti -IA2
• Urine - Albumin/Creatinine Ratio
• diabetic education

• caused by insulin deficiency
• account for 5-10% of cases of diabetes mellitus
• most are autoimmune and onset is rapid with presentation usually before age 30 yrs
• some have a slower rate of pancreatic beta cell destruction and present as latent autoimmune diabetes in adults (accounts for ~5% of “type 2 diabetics”)
• require life long insulin replacement Rx otherwise will develop diabetic ketoacidosis (DKA) within hours or days

• predominantly caused by insulin resistance with relative insulin deficiency
• accounts for 90-95% of cases of diabetes mellitus
• usually occurs in adults with obesity or central obesity

• impaired glucose tolerance during pregnancy

• NB. this does not include type 2 DM occurring in obese children
• see MODY probability calculator
• these are due to genetic mutations:
  • MODY 1:
    • HNF-4 alpha gene on chromosome 20
    • can be mistaken for type 1 DM but do not become totally insulin deficient
    • associated with microvascular complications
    • very sensitive to Rx with sulphonylureas
  • MODY 2:
    • gluockinase gene on chromosome 7
    • causes fasting hyperglycaemia but little post-prandial hyperglycaemia (<3 mmol/L rise after glucose load)
    • does not require Rx unless:
      • during pregnancy and fetus does not have the mutation (risk of macrosomia)
      • patient develops type 2 DM as indicated by deteriorating HbA1c
  • MODY 3:
    • due to HNF-1 alpha gene on chromosome 12
    • see as for MODY 1
  • MODY 4:
    • IPF-1 gene on chromosome 13
  • MODY 5:
    • due to HNF-1 alpha gene on chromosome 17
  • MODY 6:
    • due to NeuroD1 gene on chromosome 2

• inherited from the mother
• usually associated with hearing impairment
• gradual functional decline in pancreatic beta cells

• pancreatic diseases eg. pancreatitis
• endocrinopathies eg. Cushing's disease
• drugs eg. corticosteroids, olanzapine