Pathophysiology · MU Sofia

121. Infective endocarditis - classification, etiology, pathogenesis, clinical manifestations.

Inside: 6 sections · 2 tables · 16 flashcards · 2 min

Topic 121 of 168 in the MU Sofia syllabus for Pathophysiology (Medicine, Year 3). The free AceMed note covers it in 6 sections, about 271 words (2 min of reading), with 16 flashcards.

In this note

  1. Infective endocarditis – classification, etiology, pathogenesis, and clinical manifestations.
  2. Classification
  3. Etiology
  4. Predisposing factors
  5. Pathogenesis
  6. Clinical manifestations

Infective endocarditis – classification, etiology, pathogenesis, and clinical manifestations.

Infective endocarditis is an infection of the endocardial surface of the heart, most commonly affecting heart valves, characterized by formation of vegetations composed of fibrin, inflammatory cells, and microorganisms.

Classification

By clinical course

By valve type

  • Native valve endocarditis (NVE).
  • Prosthetic valve endocarditis (PVE).
  • Intravenous drug user (IVDU) endocarditis (often involves right heart valves, especially tricuspid).

Etiology

Common organisms

Predisposing factors

  • Rheumatic or degenerative valvular disease.
  • Congenital heart defects.
  • Prosthetic heart valves.
  • Intravenous drug use.
  • Poor dental hygiene or dental procedures.

Pathogenesis

  1. 1 Endothelial injury on valve surface
  • Can be from turbulent blood flow (e.g., in damaged or abnormal valves).
  1. 2 Platelet and fibrin deposition
  • Forms a sterile thrombotic vegetation (non- bacterial thrombotic endocarditis).
  1. 3 Bacteremia
  • Microorganisms enter bloodstream (via dental procedures, IV drug use, catheters).
  1. 4 Adhesion and colonization
  • Bacteria adhere to vegetations via surface adhesins.
  1. 5 Vegetation growth
  • Organisms proliferate within protective fibrin-platelet matrix → vegetations enlarge and become resistant to host defenses and antibiotics.
  1. 6 Complications
  • Local destruction: valve insufficiency, abscess formation.
  • Embolization: vegetations break off → infarcts or septic emboli in distant organs.
  • Immune complex deposition: leads to vasculitis and glomerulonephritis.

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