Diabetes

Written by Megan Boucher

Last updated 23rd December 2025
5 Revisions

Diabetes mellitus is caused by a deficiency in insulin secretion or by insulin resistance, leading to persistent hyperglycaemia. The pancreas produces the hormones insulin and glucagon, both of which help to control blood glucose. 

This article describes the different types of diabetes, signs and symptoms, hypoglycaemia, hyperglycaemia, and associated disease states.

Types Of Diabetes

There are several different types of diabetes, the most common are type 1 diabetes and type 2 diabetes. Other types include gestational diabetes and secondary diabetes (can be caused by pancreatic damage, drug therapy such as antipsychotics, hepatic cirrhosis or endocrine disease)

  • Type 1 diabetes: pancreatic beta cells are attacked by the body’s immune system, leaving the body unable to produce sufficient insulin. It generally presents earlier in life (often in childhood) but can occur at any age.
    • Treatment: insulin therapy alongside active management of cardiovascular risk factors. 
  • Type 2 diabetes: the body becomes resistant to insulin, therefore more insulin is required to shift glucose into cells and reduce blood glucose levels. 
    • Treatment: multiple options exist, including oral antidiabetic therapy such as GLP-1 agonists, biguanide, SGLT-2 inhibitors, sulfonylureas, DPP-4 inhibitors and thiazolidinediones. Insulin therapy can also be used.

Fig. 1: the pancreas and insulin secretion in type 1 and type 2 diabetes.

Signs And Symptoms

Common symptoms of diabetes include thirst, frequent urination, thrush, fatigue, weight loss, blurred vision and delayed wound healing. 

Diabetes is usually diagnosed with the laboratory markers HbA1c and blood glucose. 

  • HbA1c is glycated haemoglobin which forms when red blood cells are exposed to glucose. Since red blood cells have a 2-3 month lifespan, HbA1c reflects average plasma glucose over this period.  
    • Common treatment target in type 1 and 2 diabetes: <48mmol/mol 
  • Blood glucose concentrations: a random blood glucose of >11mmol/L is typical in patients presenting with newly diagnosed type 1 diabetes.

Complications

Chronic complications

Microvascular complications affecting small blood vessels including retinopathy, neuropathy and nephropathy

Macrovascular complications affect larger blood vessels and include cardiovascular disease, cerebrovascular disease and peripheral vascular disease

Other important complications include diabetic foot ulcers which can lead to infection and amputation, increased risk of infection and erectile dysfunction.

Fig 2: Long-term complications of diabetes

Acute complications

Acute complications of diabetes include hypoglycaemia, diabetic ketoacidosis (DKA) and hyperosmolar hyperglycaemic state (HHS). These need to be treated as an emergency and are short term complications.

Hypoglycaemia

Patients taking antidiabetic therapy, especially insulin and/or sulfonylureas, may experience hypoglycaemia (blood glucose <4mmol/L). It is unlikely without such treatment.

Symptoms include: headache, hunger, nausea and vomiting, aggression, confusion, visual and speech disorders, tremor, delirium, convulsions and coma.

Risk factors include:

  • Malnutrition
  • Irregular carbohydrate intake
  • Renal/hepatic insufficiency 
  • Overdose of sulfonylurea
  • Thyroid disorders
  • Hypopituitarism
  • Adrenal insufficiency 
  • Alcohol intake 
  • Medications that increase risk: antidiabetic agents, testosterone, anabolic steroids, beta blockers, fluconazole, MAOIs, trimethoprim, clarithromycin, NSAIDs, H2-receptor antagonists 

Treatment: 

  • If the patient is conscious and able to swallow: oral fast acting carbohydrate (e.g. glucose tablets)
    • Repeat after 15 minutes if blood glucose remains <4 mmol/L, up to a maximum of 3 doses.
    • Follow up with long-acting carbohydrate once recovered.
  • If oral glucose is ineffective or consciousness is impaired:
    • IM Glucagon: glucagon is produced by the alpha cells of the islets of Langerhans, and released when blood sugars are low. It stimulates glycogenolysis (glycogen breakdown into glucose in the liver which raises blood sugar).
      • Ineffective if liver glycogen is depleted (e.g., prolonged fasting, adrenal insufficiency, chronic hypoglycaemia, alcohol-induced hypoglycaemia).
  • IV glucose infusion if no response to glucagon after 10 minutes. 

Hyperglycaemia 

Hyperglycaemia can lead to diabetic ketoacidosis (DKA) and hyperosmolar hyperglyceamic state (HHS); both with high morbidity and mortality. The major precipitating factor for both conditions is infection, however can also be caused by inadequate insulin therapy and stress. 

General symptoms of hyperglycaemia include thirst, increased urination, nausea, vomiting, drowsiness, flushed dry skin, dry mouth, loss of appetite and a pear drop smell on breath (acetone).

The table below describes the key characteristics and treatment of DKA and HHS.

Condition  DKA HHS
Onset  Few hours Days
Laboratory signs  Blood glucose >11mmol/L

Blood ketone >3mmol/L / ketonuria of >2+

Acidosis: Bicarbonate <15mmol/L and/or venous pH <7.3

Blood glucose >30mmol/L

Osmolarity >320mOsm/kg

Symptoms  Polydipsia and polyuria, weight loss, excessive tiredness, nausea, vomiting, abdominal pain, Kussmaul respiration (rapid and deep respiration) with acetone breath, and reduced consciousness. Dehydration due to polyuria and polydipsia, weakness, weight loss, tachycardia, dry mucous membranes, poor skin turgor, hypotension, acute cognitive impairment, and in severe cases, shock.
Treatment IV fluids followed by IV insulin

Potassium replacement and glucose may be required to prevent subsequent hypokaleamia and hypoglycaemia

IV fluids followed by IV insulin

+/- potassium if required

References

  1. Hypoglycaemia | Treatment summaries | BNF | NICE
  2. Diabetic hyperglycaemic emergencies | Treatment summaries | BNF | NICE
  3. Diabetes | Treatment summaries | BNF | NICE

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