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Diabetes - type 1

SNOMED: 1290118005881 words•Updated 03/03/2026
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Exam Tips

  • In symptomatic adults, do not delay treatment waiting for HbA1c; random plasma glucose >11 mmol/L plus ketosis/weight loss strongly suggests type 1 diabetes.
  • Older age or BMI >=25 kg/m2 does not exclude type 1 diabetes; use clinical judgement and early specialist referral.
  • Know DKA triad for OSCE/viva: hyperglycaemia, ketonaemia, metabolic acidosis; initial management is fixed-rate IV insulin plus fluids and potassium monitoring.
  • State key safety warning explicitly: never stop basal insulin in type 1 diabetes, even when not eating.
  • For visual recognition practice, review a retinal image set showing non-proliferative vs proliferative diabetic retinopathy and a DKA pathophysiology flow diagram (see standard UK undergraduate diabetes chapter figures).

Definition

Type 1 diabetes mellitus is a chronic autoimmune metabolic disorder in which pancreatic beta-cell destruction causes absolute endogenous insulin deficiency and persistent hyperglycaemia. It often presents rapidly (especially in children and young adults), but can occur at any age, and untreated insulin deficiency can progress to life-threatening diabetic ketoacidosis within days to weeks.

Pathophysiology

Genetically susceptible individuals develop immune-mediated destruction of pancreatic islet beta cells (classically involving islet autoantibodies such as GAD, IA-2, and ZnT8), leading to near-complete loss of insulin secretion. Absolute insulin deficiency impairs peripheral glucose uptake and increases hepatic gluconeogenesis/glycogenolysis, causing hyperglycaemia with osmotic diuresis and dehydration. Low insulin with relative glucagon excess accelerates lipolysis and hepatic ketogenesis, producing ketonaemia and metabolic acidosis (DKA). Chronic hyperglycaemia drives advanced glycation, oxidative stress, and endothelial injury, underlying microvascular disease (retina, kidney, nerves) and accelerated atherosclerotic cardiovascular disease.

Risk Factors

  • Family history of type 1 diabetes (higher risk in siblings and offspring of affected parents; highest in monozygotic twins)
  • Polygenic susceptibility (especially HLA-associated risk haplotypes)
  • Personal or family history of other autoimmune disease (for example autoimmune thyroid disease or coeliac disease)
  • Possible environmental triggers in susceptible people (for example enteroviral exposure, microbiome changes, nutritional/vitamin D-related factors)

Clinical Features

Symptoms

  • Polyuria, polydipsia, and nocturia
  • Unintentional weight loss over weeks
  • Fatigue/lethargy and reduced exercise tolerance
  • Blurred vision
  • Recurrent infections (including skin/oral/genitourinary)
  • Abdominal pain, nausea, vomiting, and drowsiness if DKA develops

Signs

  • Random plasma glucose usually >11 mmol/L in symptomatic presentation
  • Dehydration (dry mucosa, tachycardia, postural symptoms)
  • Ketosis (urine ketones >=2+ or blood ketones >=3 mmol/L)
  • Kussmaul respiration and acetone breath in DKA
  • Lower BMI is common at onset, but normal/high BMI does not exclude type 1 diabetes

Investigations

Capillary/venous glucose:Hyperglycaemia; random plasma glucose >11 mmol/L with typical symptoms supports diagnosis
Blood ketones (preferred) or urine ketones:Blood ketones >=3 mmol/L (or urine ketones >=2+) suggests significant ketosis and possible DKA
Venous blood gas and bicarbonate (if acutely unwell):Metabolic acidosis in DKA (low pH and low bicarbonate)
Urea/electrolytes/creatinine:Dehydration-related AKI, sodium disturbance, and potassium abnormalities (total body K+ deficit may coexist with normal/high serum K+)
Diabetes autoantibodies (for example GAD, IA-2, ZnT8):At least one positive autoantibody supports type 1 diabetes classification
Non-fasting serum C-peptide (selected cases):Low C-peptide supports severe insulin deficiency when diagnosis remains uncertain and autoantibodies are negative
HbA1c:Usually elevated; useful for baseline and follow-up glycaemic control, but treatment of suspected type 1/DKA should not be delayed awaiting HbA1c
Screening for associated autoimmunity:TFTs/thyroid antibodies and coeliac serology may identify comorbid autoimmune disease

Management

Lifestyle Modifications

  • Same-day referral to specialist diabetes team at diagnosis for structured education and individual care plan
  • Carbohydrate counting with dose adjustment of prandial insulin
  • Frequent glucose monitoring (capillary or CGM) and ketone testing during illness
  • Sick-day rules: maintain hydration, continue basal insulin, increase monitoring, seek urgent review for persistent ketones/vomiting
  • Cardiovascular risk reduction: smoking cessation, BP/lipid management, regular exercise, weight optimisation, and annual complication screening (eyes, feet, kidneys)

Pharmacological Treatment

Basal-bolus insulin replacement (first-line long-term)

  • Insulin detemir (basal) typically once or twice daily, dose individualised
  • Insulin glargine U100/U300 (basal) once daily, dose individualised
  • Insulin degludec (basal) once daily, dose individualised
  • Rapid-acting mealtime insulin: insulin aspart, insulin lispro, or insulin glulisine before meals (dose individualised to carbohydrate intake and glucose)

Typical total daily insulin requirement is often around 0.4-1.0 units/kg/day in adults, split between basal and bolus, then titrated to glucose targets. Never omit basal insulin in type 1 diabetes due to DKA risk.

Continuous subcutaneous insulin infusion (CSII) / hybrid closed-loop

  • Rapid-acting insulin analogue in pump reservoir (for example insulin aspart or lispro), continuously infused with programmable boluses

Consider in appropriate patients via specialist services; if pump failure occurs, urgent backup injected insulin is required to prevent rapid ketosis.

DKA emergency insulin therapy

  • Soluble insulin (for example Actrapid) IV fixed-rate infusion 0.1 units/kg/hour

Use alongside IV 0.9% sodium chloride and potassium replacement per protocol; continue background long-acting basal insulin where local protocol advises. Requires close monitoring for hypokalaemia, fluid overload, and cerebral oedema risk (especially in children).

Hypoglycaemia rescue

  • Oral glucose 15-20 g fast-acting carbohydrate if conscious
  • Glucagon 1 mg IM (adult and child >25 kg), 500 micrograms IM (child <25 kg)
  • IV glucose in severe hypoglycaemia if unable to take oral treatment

Recheck glucose after 10-15 minutes and follow with longer-acting carbohydrate once recovered; review precipitating factors and insulin dosing.

Complications

  • Diabetic ketoacidosis (including risk of cerebral oedema, especially in children)
  • Hypoglycaemia (including severe episodes and mortality risk in younger adults)
  • Diabetic kidney disease (microalbuminuria progressing in a subset to end-stage kidney disease)
  • Diabetic retinopathy (non-proliferative/proliferative disease, maculopathy, potential vision loss)
  • Peripheral and autonomic neuropathy (painful neuropathy, gastroparesis, orthostatic hypotension, bladder/sexual dysfunction)
  • Diabetic foot disease (ulceration, infection, ischaemia, amputation risk)
  • Accelerated macrovascular disease (ischaemic heart disease, stroke, peripheral arterial disease, heart failure)
  • Associated autoimmune disease (especially autoimmune thyroid disease and coeliac disease)
  • Skin and oral complications (for example necrobiosis lipoidica, vitiligo, periodontitis)

Prognosis

Without insulin therapy, type 1 diabetes is rapidly fatal. With modern insulin replacement and structured multidisciplinary care, most people can live long, active lives, but lifetime risk of microvascular and macrovascular complications remains substantial. Tight glycaemic and blood pressure control, early detection, and proactive complication management significantly improve long-term outcomes.

Sources & References

💊BNF Drug References(2)

✅NICE Guidelines(1)

📖Textbook References(20)

  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1148)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1276)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1243)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1275)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1266, 1267)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1197)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1197, 1198)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1148)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 296)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1268, 1269)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1264)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 973, 974)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 973)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 973)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 847)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 977)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 847)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 974)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 977)[context]
  • [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 238)[context]

Sources

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