penyakit jantung rematik anak

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1. Fibrin-platelet deposits provide a surface for adherence by bacteria 2. Fibrin cover adherence organisms and protect them from host defences by inhibiting chemotaxis and migration of phagocytes.

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Page 1: penyakit jantung rematik anak

1. Fibrin-platelet deposits provide a surface for adherence by bacteria

2. Fibrin cover adherence organisms and protect them from host defences by inhibiting chemotaxis and migration of phagocytes.

Page 2: penyakit jantung rematik anak

Three factor determine the ability of an organism to induce IE1. Access to the blood stream (dental desease/procedure,

intravenous drug use)2. Survival of organism in the circulation (90% gram

positive)3. Adherence of the bacteria to the endocardium

Bacterial endocarditis1. Mechanical cardiac injury (progresive valvular

damage, abscess formation, erosion into cardiac conduction system)

2. Thrombotic or septic emboli 3. Immune injury mediated by antigen antibody

deposition (glomerulonephritis, arhritis, or vasculitis)

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Kriteria klinis Dukes untuk EIEndokarditis Infektif definite

kriteria patologis mikroorganismelesi patologis

kriteria klinis 2 kriteria mayor 1 mayor + 3 minor 5 kriteria minor

Endokarditis Infektif possible temuan konsisten dengan EI, dibawah kriteria definite tapi tidak memenuhi kriteria rejected

Endokarditis Infektif rejected tidak memenuhi manifestasi endokarditis resolusi manifestasi endokarditis dengan terapi antibiotika selama ≤ 4 hari bukti patologis pada saat operasi atau autopsi (-) setelah terapi antibiotika

selama ≤ 4 hari

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Pathogenesis

Host-pathogen interaction• Infection by streptococci begins with the

binding of bacterial surface ligands to specific receptors on host cells, and subsequently involves specific processes of adherence, colonization and invasion

• Binding fibronectin, streptococcal fibronectin-binding proteins, Streptococcal lipoteichoic acid and M-protein

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Once valve leaflets are inflamed through the valvular surfaceendothelium and new vascularization occurs, the newly formed microvasculature allows T-cells to infiltrate and perpetuate the cycle of valvular damage.

The presence of T-cell infiltration, even in old mineralizedlesions, is indicative of persistent and progressive disease inthe valves.

Valvular interstitial cells and other valvular constituentsunder the influence of inflammatory cytokines perpetuate aberrant repair. valvular scarring

hubungannya dengan oral hygene:showed increased amounts of proinflammatory cytokines (IL-1, IL-6, TNF-a and IFN-g) severe valve scaring,

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