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:


Diabetic Ketoacidosis

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[1].

– Plasma glucose or HbA1c must show evidence of diabetes of two separate occasions if asymptomatic:


  1. Fasting glucose > 7.0 mmol/L
  2. Random glucose/OGTT > 11.1mmol/L
  3. 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

Gestational diabetes

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

Secondary diabetes

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