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This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.
The Bottom Line
- Autoimmune destruction of pancreatic beta cells — presents acutely with polyuria, polydipsia, weight loss, and may present in DKA
- Diagnosis: hyperglycaemia + clinical features. GAD/IA-2 antibodies and low C-peptide confirm autoimmune aetiology
- First-line: basal-bolus insulin regimen (e.g. insulin detemir/glargine + rapid-acting analogue with meals)
- HbA1c target: 48 mmol/mol (6.5%) or lower — individualise to minimise hypoglycaemia risk
- All patients should be offered structured education (e.g. DAFNE) within 6–12 months of diagnosis
- Annual screening: retinopathy (digital photography), nephropathy (urine ACR), neuropathy (foot check), lipid profile, TFTs
Overview
Type 1 diabetes mellitus is an autoimmune condition characterised by T-cell-mediated destruction of the insulin-producing beta cells of the pancreatic islets, leading to absolute insulin deficiency. It accounts for approximately 8–10% of all diabetes in the UK. Patients require exogenous insulin from diagnosis for survival. The pathogenesis involves genetic susceptibility (HLA-DR3/DR4), environmental triggers (viral infections such as Coxsackie B, enterovirus), and autoimmune mechanisms. The condition is associated with other autoimmune diseases including autoimmune thyroiditis, coeliac disease, Addison disease, and pernicious anaemia (autoimmune polyglandular syndromes).
Epidemiology
Approximately 400,000 adults in the UK have type 1 diabetes. Peak incidence is in childhood (age 10–14 years) but it can present at any age — approximately 50% of cases present after age 18. It is more common in Northern European populations. The incidence has been increasing by approximately 3–4% per year in the UK. Males and females are equally affected. Family history confers increased risk (6% if father affected, 2% if mother affected, 30% if both parents). LADA (latent autoimmune diabetes of adults) is a slowly progressive form of autoimmune diabetes presenting in adults >30 years — often initially misclassified as type 2.
Clinical Features
Symptoms
Polyuria (osmotic diuresis from glycosuria)
Polydipsia (compensatory thirst)
Unintentional weight loss (often marked — catabolism of fat and muscle due to insulin deficiency)
Fatigue and lethargy
Blurred vision
Recurrent infections (candidiasis, UTI)
Presentation in DKA: nausea, vomiting, abdominal pain, Kussmaul breathing, reduced consciousness
Rapid onset of symptoms (days to weeks) — slower in LADA
Signs
Weight loss, dehydration
Ketotic breath (pear-drop/acetone smell) in DKA
Kussmaul (deep, sighing) respiration in DKA
Tachycardia, hypotension (if severely dehydrated)
No features of insulin resistance (typically normal/low BMI, no acanthosis)
Investigations
First-line
Random plasma glucose≥11.1 mmol/L with symptoms confirms diabetes. Fasting ≥7.0 mmol/L or HbA1c ≥48 mmol/mol also diagnostic
Blood ketonesElevated (≥3.0 mmol/L = significant ketosis) — supports T1DM over T2DM at presentation
ABG / VBGIf DKA suspected: pH <7.3 and/or bicarbonate <15 mmol/L with ketonaemia
Second-line
GAD and IA-2 antibodiesPositive in ~85–90% of T1DM. Confirm autoimmune aetiology. Useful when diagnosis uncertain (e.g. older patient, not clearly T2DM)
C-peptideLow or undetectable — indicates absolute insulin deficiency. Measured with concurrent glucose. Most useful ≥3 years post-diagnosis
TFTsScreen for autoimmune thyroid disease — check at diagnosis and annually
Coeliac screen (tTG-IgA)Check at diagnosis — ~4–9% of T1DM patients have coeliac disease
Specialist
HbA1c monitoringEvery 3–6 months. Target ≤48 mmol/mol. Use with CGM data for full picture
Annual complication screeningRetinal screening, urine ACR, foot check, lipids, BP, renal function — from 12 years of age or 5 years post-diagnosis
1
Insulin therapy — basal-bolus regimen
- Multiple daily injection (MDI) basal-bolus is the regimen of choice for all adults with T1DM
- Basal insulin: insulin detemir (Levemir) or insulin glargine (Lantus) — once or twice daily
- Bolus insulin: rapid-acting analogue (insulin lispro, aspart, or glulisine) before each meal
- Carbohydrate counting: teach all patients to match bolus doses to carbohydrate intake
- Consider continuous subcutaneous insulin infusion (CSII / insulin pump) if MDI inadequate or disabling hypoglycaemia
- Automated insulin delivery (AID) systems increasingly used — integrate CGM with pump for closed-loop control
2
Blood glucose monitoring
- Self-monitoring of blood glucose (SMBG): at least 4 times/day (before meals and before bed)
- Consider intermittently scanned CGM (isCGM e.g. FreeStyle Libre) if: recurrent/severe hypos, impaired hypo awareness, or inability to self-monitor
- Real-time CGM (rtCGM) for those with highest risk — impaired awareness of hypoglycaemia despite optimised MDI/pump
- HbA1c target: ≤48 mmol/mol — individualise; avoid problematic hypoglycaemia
3
Structured education
- Offer structured education (e.g. DAFNE — Dose Adjustment For Normal Eating) 6–12 months after diagnosis
- Covers insulin dose adjustment, carbohydrate counting, hypo management, sick-day rules
- Reduces HbA1c and severe hypoglycaemia events
4
Cardiovascular risk management
- Statin therapy: atorvastatin 20 mg if ≥40 years, or diabetes >10 years, or established nephropathy, or other CVD risk factors
- BP target: <135/85 mmHg (or <130/80 if kidney/eye/cerebrovascular disease)
- ACEi/ARB if microalbuminuria (ACR ≥3 mg/mmol) — even if normotensive
- Annual lipid and renal function monitoring
Complications
- DKA: Life-threatening emergency — most common cause of death in T1DM under 30. Triggered by missed insulin, infection, new diagnosis
- Hypoglycaemia: Common with insulin therapy. Impaired awareness of hypoglycaemia develops in ~25%. Managed with rapid glucose, glucagon for severe episodes
- Diabetic retinopathy: Leading cause of blindness in working-age adults — annual screening from diagnosis
- Diabetic nephropathy: Progresses from microalbuminuria to overt proteinuria to ESRD. ACEi/ARB slows progression
- Diabetic neuropathy: Peripheral sensory (glove-and-stocking) and autonomic (gastroparesis, postural hypotension, erectile dysfunction)
- Macrovascular: CVD risk 2–4× increased — accelerated atherosclerosis
- Associated autoimmune conditions: Thyroid disease (25%), coeliac disease (4–9%), Addison disease, pernicious anaemia
UKMLA Exam Tips
- 1T1DM = autoimmune beta-cell destruction = absolute insulin deficiency. T2DM = insulin resistance + relative deficiency. Know the differences
- 2Presentation: young, lean, acute onset, ketosis → think T1DM. Older, obese, gradual onset → think T2DM (but overlap exists — LADA)
- 3ALL T1DM patients need insulin from diagnosis. Never give metformin alone to a T1DM patient
- 4GAD antibodies confirm autoimmune cause. Low C-peptide confirms absolute insulin deficiency
- 5HbA1c target: ≤48 mmol/mol. Check every 3–6 months. If unreliable (haemoglobinopathy, anaemia), use fructosamine
- 6DKA triad: hyperglycaemia (>11 mmol/L) + ketosis (blood ketones ≥3.0) + acidosis (pH <7.3 / bicarb <15)
- 7DVLA: must notify. Must check glucose before driving and every 2 hours on long journeys
practicetest your knowledge on type 1 diabetesApply what you've learnt with UKMLA-style questions from the iatroX Q-Bank — endocrine and beyond.
open q-bank regional clinical guidance
Type 1 Diabetes Mellitus: guidance by region
Recommendations, thresholds and pathways can differ. Open the page written for the jurisdiction you need.