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llms.txtPsychiatry LLM catalogSitemap

Phys Topicsendocrine

Phys · endocrine

Diabetes Mellitus

Also known as type 1 diabetes · type 2 diabetes · T1DM · T2DM · diabetes mellitus · insulin-dependent diabetes · non-insulin-dependent diabetes · LADA · MODY · latent autoimmune diabetes in adults · maturity-onset diabetes of the young · gestational diabetes · diabetic nephropathy · diabetic retinopathy · diabetic neuropathy · diabetic foot

Consultant-physician-depth guide to diabetes mellitus — pathophysiology, classification, diagnosis, glycaemic target individualisation, the modern pharmacological hierarchy for type 2, insulin therapy, microvascular and macrovascular complications, diabetic foot, glycaemic emergencies, diabetes in pregnancy, and diabetes technology — structured for FRACP DWE and DCE preparation.

high12 referencesUpdated 26 July 202612 min readSource-verified · Sept 2026

Checked against its sources on 13 Sept 2026

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FRACP DWEFRACP DCEMRCP Part 1MRCP Part 2MRCP PACESABIM Internal Medicine

Red flags

  • Diabetic ketoacidosis — ketonaemia, metabolic acidosis, Kussmaul breathing
  • Hyperosmolar hyperglycaemic state — marked hyperglycaemia, profound dehydration, altered consciousness
  • Severe hypoglycaemia — blood glucose below 3.0 mmol/L with impaired consciousness
  • Severe hyperkalaemia with diabetic nephropathy and RAAS blockade
  • Limb-threatening diabetic foot infection — deep ulcer with abscess, osteomyelitis, or wet gangrene
  • Sudden vision loss — vitreous haemorrhage or retinal detachment from proliferative retinopathy
  • Rapid decline in eGFR — suggests superimposed renovascular disease or acute interstitial nephropathy
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Target exams

FRACP DWEFRACP DCEMRCP Part 1MRCP Part 2MRCP PACESABIM Internal Medicine

Red flags

  • Diabetic ketoacidosis — ketonaemia, metabolic acidosis, Kussmaul breathing
  • Hyperosmolar hyperglycaemic state — marked hyperglycaemia, profound dehydration, altered consciousness
  • Severe hypoglycaemia — blood glucose below 3.0 mmol/L with impaired consciousness
  • Severe hyperkalaemia with diabetic nephropathy and RAAS blockade
  • Limb-threatening diabetic foot infection — deep ulcer with abscess, osteomyelitis, or wet gangrene
  • Sudden vision loss — vitreous haemorrhage or retinal detachment from proliferative retinopathy
  • Rapid decline in eGFR — suggests superimposed renovascular disease or acute interstitial nephropathy

Diabetes Mellitus

The answer first

Diabetes is defined by chronic hyperglycaemia from defects in insulin secretion, action, or both. The binary classification — type 1 (absolute insulin deficiency from autoimmune beta-cell destruction) and type 2 (insulin resistance with progressive beta-cell failure) — covers more than 95 per cent of cases. The remainder (MODY, type 3c, LADA, gestational) must not be missed because they change treatment.[1]

The management logic for type 2 has been rewritten by the cardiovascular and renal outcome trials. The modern hierarchy: lifestyle plus metformin, then add an SGLT2 inhibitor or GLP-1 receptor agonist chosen for the patient's cardiorenal profile — before escalating through insulin or sulphonylureas. Glucose-lowering is no longer the sole goal.[6][7][10]

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References12ShowHide
  1. [1]Nathan DM, Genuth S, Lachin J, et al. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus N Engl J Med, 1993.PMID 8366922
  2. [2]UK Prospective Diabetes Study (UKPDS) Group Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). UK Prospective Diabetes Study (UKPDS) Group Lancet, 1998.PMID 9742976
  3. [3]Holman RR, Paul SK, Bethel MA, Matthews DR, Neil HAW 10-year follow-up of intensive glucose control in type 2 diabetes N Engl J Med, 2008.PMID 18784090
  4. [4]Gerstein HC, Miller ME, Byington RP, et al. Effects of intensive glucose lowering in type 2 diabetes N Engl J Med, 2008.PMID 18539917
  5. [5]Gaede P, Lund-Andersen H, Parving HH, Pedersen O Effect of a multifactorial intervention on mortality in type 2 diabetes N Engl J Med, 2008.PMID 18256393
  6. [6]Zinman B, Wanner C, Lachin JM, et al. Empagliflozin, Cardiovascular Outcomes, and Mortality in Type 2 Diabetes N Engl J Med, 2015.PMID 26378978
  7. [7]Marso SP, Daniels GH, Brown-Frandsen K, et al. Liraglutide and Cardiovascular Outcomes in Type 2 Diabetes N Engl J Med, 2016.PMID 27295427
  8. [8]Marso SP, Bain SC, Consoli A, et al. Semaglutide and Cardiovascular Outcomes in Patients with Type 2 Diabetes N Engl J Med, 2016.PMID 27633186
  9. [9]Norhammar A, Bodegård J, Nyström T, et al. Dapagliflozin and cardiovascular mortality and disease outcomes in a population with type 2 diabetes similar to that of the DECLARE-TIMI 58 trial: A nationwide observational study Diabetes Obes Metab, 2019.PMID 30609272
  10. [10]Heerspink HJL, Stefánsson BV, Correa-Rotter R, et al. Dapagliflozin in Patients with Chronic Kidney Disease N Engl J Med, 2020.PMID 32970396
  11. [11]Frías JP, Davies MJ, Rosenstock J, et al. Tirzepatide versus Semaglutide Once Weekly in Patients with Type 2 Diabetes N Engl J Med, 2021.PMID 34170647
  12. [12]McMurray JJV, Solomon SD, Inzucchi SE, et al. Dapagliflozin in Patients with Heart Failure and Reduced Ejection Fraction N Engl J Med, 2019.PMID 31535829

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