Type 1 Diabetes
This is insulin deficiency due to an autoimmune destruction of pancreatic B-cells
– T lymphocytes attack islets, with autoantibodies against insulin present
– It is associated with HLA-DR3 and HLA-DR4
– The disease usually manifests in adolescence, sometimes after a viral infection.
– Hyperglycemia – low insulin leads to decreased glucose uptake by fat and muscle
– Weight loss, low muscle mass – unopposed glucagon leads to lipolysis and glycogenolysis
– Polyuria, polydipsia and glycosuria
1) Insulin therapy – twice-daily insulin detemir is a common regime, but depends on patient’s diet and compliance
2) Monitor HbA1c every 3-6months – target of <48mM
3) Self-monitoring glucose – test this 4 times/day, before and after each meal + before sleep
– More frequency monitoring in illness, sport, pregnancy and breastfeeding
– Target = 5-7mM (Waking) 4-7mM (before meals)
4) Metformin – consider adding if BMI > 25kg/m2
5) Glucagon kit – given to all patients in case of hypoglycaemic crisis
There are several complications which are associated with Type 1 diabetes, which can be life threatening:
This is an emergency which is characterized by severe hyperglycaemia and severe acidosis, seen in diabetes.
– Due to the body being in starvation like state and excessive ketone body production.
– Triad of drowsiness + dehydration + Unexplained vomiting
– Ketotic breath, coma
– Deep breathing (Kussmaul hyperventilation)
Diagnosis – Acidaemia (Venous pH <7.3 or HCO3– >15mM)
– Hyperglycaemia (glucose >11mM) or known diabetic
– Ketones >3mM or >2 on a urine dipstick
Management – Use the ABC approach
i) Start fluid infusion 1L 0.9% saline
ii) Add insulin – IV infusion at 0.1 unit/kg/hour
– If on insulin, continue long-acting insulin, stop short-acting
iii) Monitor blood glucose and ketones hourly
iv) Dextrose solution – once [glucose] < 15mM, add 5% dextrose to prevent hypoglycaemia
v) Monitor Potassium – insulin forces K+ into cells, so give potassium to reduce hypokalaemia
– Arrhythmias secondary to hyperkalaemia/iatrogenic hypokalaemia
– Cerebral oedema –> seen more in children/young adults, occurs 4-12 hours usually after treatment
–> Gives headache, confusion, visual disturbances due to raised ICP
Impaired Hypoglycaemia Awareness
Long standing hyperglycaemia can lead to neuropathy of the autonomic nervous system.
– This is the leading cause of impaired hypoglycaemic awareness in diabetic patients
– Awareness is also reduced by usage of b-blockers
Type 2 Diabetes
This is end-organ insulin resistance which is the most common form of diabetes.
– Arises in middle aged, obese adults due to decreased number insulin receptors.
– Later insulin deficiency develops due to b-cells exhaustion
Causes: Obesity, lack of excessive + alcohol excess
– Stronger genetic influence than type 1 – high in Asians, men and the elderly
Symptoms: Initially clinically silent, but then similar symptoms to Type 1 in later disease
The diagnosis of diabetes mellitus can be made using plasma glucose or a HbA1c sample.
– Plasma glucose or HbA1c must show evidence of diabetes of two separate occasions if asymptomatic:
- Fasting glucose > 7.0 mmol/L
- Random glucose/OGTT > 11.1mmol/L
- HbA1c > 48mmol/mol (6.5%)
Management: NICE 2015 guidelines for management.
1) If HbA1c rises to 48mM
– Lifestyle modifications – diet, weight control + exercise
2) If HbA1c stays above 48mM
– Commence Metformin – aim for HbA1c < 48mM
3) If HbA1c rises >58mM
– Add sulphonylurea or DPP–4 inhibitor or Thiazolidinedione or SGLT-2 inhibitor
4) If HbA1c stays >58mM
– Add 3rd drug (metformin + 2 of previous)
5) If not effective/tolerated and BMI>35 kg/m2
– Try metformin + Sulphonylurea + GLP1 mimic
6) If still not controlled –> commence insulin therapy (but continue metformin)
Other Diabetes Types
Latent autoimmune diabetes of adults (LADA)
This is a form of type 1 DM, but with slower progression to insulin dependence in later life.
Maturity Onset Diabetes of the Young
This is an autosomal dominant mutation in HNF1A gene
– Leads to poor production of insulin, causing T2DM symptoms in much younger patients
Treatment – Sulphonylureas
This is a transitory form caused by pregnancy associated hormonal changes
This is the term u sed for patients who do not meet the criteria but are likely to develop condition soon
– HbA1c of 42-47mmol/mol or Fasting Glucose of 6.1-69mM
This can be due to conditions that affect blood glucose and/or insulin:
– Pancreatitis – damage to insulin producing cells.
– Hyperthyroidism – thyroid hormone excess
– Acromegaly – GH excess
– Cushing’s disease – cortisol excess
Image 1: https://cks.nice.org.uk/diabetes-type-2#!diagnosisSub
Image 2: https://www.nice.org.uk/guidance/ng28/chapter/Key-priorities-for-implementation