IM11.1-6 | Diabetes Foundations — Summary & Reflection

KEY TAKEAWAYS

Diabetes mellitus is a syndrome of chronic hyperglycaemia caused by defects in insulin secretion, insulin action, or both. The major types are T1DM (autoimmune beta-cell destruction, absolute insulin deficiency, ketosis-prone), T2DM (insulin resistance + progressive beta-cell failure, the dominant form globally and in India), GDM, MODY, and secondary forms.

Diagnostic thresholds (ADA): Fasting glucose ≥126 mg/dL; 2-h OGTT ≥200 mg/dL; HbA1c ≥6.5%; random glucose ≥200 mg/dL with symptoms — any one of these, confirmed on repeat (except unequivocal hyperglycaemia with symptoms).

T1DM pathogenesis: HLA-DR3/DR4 genetic susceptibility + environmental trigger → autoimmune beta-cell destruction (GAD65, IA-2, ICA, IAA autoantibodies) → absolute insulin deficiency → DKA risk.

T2DM pathogenesis: Insulin resistance (visceral adiposity, FFA excess, GLUT-4 defect, ectopic fat) + progressive beta-cell failure (glucotoxicity, lipotoxicity, IAPP amyloid) → chronic hyperglycaemia. Indians have a 'thin-fat' phenotype with higher visceral adiposity at lower BMI.

Complications: Microvascular — retinopathy (NPDR → PDR, neovascularisation), nephropathy (microalbuminuria → macroalbuminuria → ESRD, Kimmelstiel-Wilson nodules), neuropathy (stocking-glove polyneuropathy, autonomic). Macrovascular — CAD, stroke, PAD, diabetic foot.

Emergencies: DKA (T1DM, ketonaemia, metabolic acidosis, pH <7.3, Kussmaul breathing); HHS (elderly T2DM, glucose >600, osmolality >320, no significant ketosis); hypoglycaemia (glucose <70 mg/dL, adrenergic + neuroglycopenic features).

REFLECT

Suresh and Kavitha — from the opening hook — represent two faces of the same diagnosis separated by mechanism, age, and clinical urgency. Think about how the pathogenetic framework you have now built helps you understand why Suresh was asymptomatic for years (the gradual insulin resistance and progressive beta-cell failure of T2DM allows partial compensation to continue for a long time) while Kavitha deteriorated over weeks (absolute insulin deficiency leaves no compensatory reserve). Now consider your future clinical practice: if you screen 100 patients in an urban Indian outpatient clinic aged 45–65 with overweight and a family history of diabetes, how would you estimate how many are likely to have undiagnosed prediabetes or diabetes? And if you could intervene at the prediabetes stage with lifestyle modification — what would that mean for their 10-year trajectory of retinopathy, nephropathy, and cardiovascular risk? The foundation you have built here is not merely examination knowledge; it is the basis for preventive medicine practice that can meaningfully alter the health trajectory of millions.