Internal Diseases · MU Sofia

Theory · 58 & 59. Diabetes mellitus - etiology, pathogenesis & complication

Covers diabetes mellitus as a chronic hyperglycaemic disorder, moving from definition to classification and aetiology in a table of type 1A, type 1B, type 2, gestational and secondary forms. It then outlines the pathogenesis of type 1 and type 2 disease, clinical features of each, and diagnostic thresholds for glucose, OGTT and HbA1c in a summary table. The second half addresses acute complications such as ketoacidosis and hyperosmolar states, microvascular, macrovascular and infectious complications, and prevention with management points.

Inside: 10 sections · 5 labelled pictures · 3 tables · 15 flashcards · 4 min

Topic 55 of 88 in the MU Sofia syllabus for Internal Diseases (Dental Medicine, Year 4). The free AceMed note covers it in 10 sections, about 407 words (4 min of reading), with 15 flashcards.

In this note

  1. Diabetes Mellitus – Etiology, Pathogenesis, Clinical Features, Diagnosis
  2. Definition
  3. Classification & Etiology
  4. Pathogenesis
  5. Clinical Features
  6. Diagnosis
  7. Diabetes Mellitus – Complications
  8. Overview
  9. I. Acute Complications
  10. II. Chronic Complications

Definition

Diabetes mellitus (DM) is a chronic metabolic disorder characterized by hyperglycemia due to a deficiency of insulin secretion, insulin action, or both. It leads to disturbances in the metabolism of carbohydrates, fats, and proteins.

Pathogenesis

Type 1 DM (T1DM)

  • T-cell-mediated autoimmune destruction of β-cells → ↓ insulin production.
  • Often triggered in genetically predisposed individuals by environmental factors (e.g., viral infections like coxsackie B).
  • Insulin deficiency leads to increased lipolysis, ketone production → risk of diabetic ketoacidosis (DKA).

Type 2 DM (T2DM)

  • Insulin resistance (↓ cellular response to insulin) + β-cell dysfunction.
  • Obesity (especially visceral) plays a major role by secreting inflammatory cytokines → worsens insulin resistance.
  • Initially compensated by ↑ insulin secretion, but later β-cell exhaustion leads to hyperglycemia.

Clinical Features

T1DM (often acute onset in youth)

  • Polyuria, Polydipsia, Polyphagia
  • Weight loss despite increased appetite
  • Fatigue
  • Acetone breath (from ketosis)
  • DKA in severe cases

T2DM (often insidious in adults)

  • Gradual onset
  • Fatigue, blurred vision, poor wound healing
  • Recurrent infections
  • May be asymptomatic, discovered incidentally via routine labs

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