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Pathophysiology. Acute Cholangitis. Host antibacterial defenses. Immune dysfunction. Biliary obstruction. bacteria. bacteria. bacteria. bacteria. bacteria. bacteria. bacteria. bacteria. bacteria. bacteria. bacteria. bacteria. bacteria. bacteria. bacteria. bacteria.

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Pathophysiology


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    1. Pathophysiology

    2. Acute Cholangitis Host antibacterial defenses Immune dysfunction Biliary obstruction bacteria bacteria bacteria bacteria bacteria bacteria bacteria bacteria bacteria bacteria bacteria bacteria bacteria bacteria bacteria bacteria

    3. Acute Cholangitis Hepatic Ducts Biliary Tree Duodenum bacteria Portal venous blood bacteria

    4. Septic Shock Monocytes Peptidoglycan Bacteria LPS macrophages Host binding protein CD 14 fimbriae DNA Neutrophils Lipoteichoic acid Cytokines TLR chemokines leukotriens prostanoids

    5. Septic Shock Inc. Blood flow IL-6 Enhance vessel permeability Recruit neutrophils monocytes Endothelial cells Elicit pain Coagulation! Cytokines chemokines leukotriens prostanoids

    6. Septic Shock • Control Mechanisms • Prevent inflammation within organs distant from infection site • Work of anti-inflammatory molecules

    7. Septic Shock • Organ dysfunction and shock • Prevalence of anti-inflammatory molecules • Blood leukocytes often HYPOresponsive to agonists such as LPS • Increases risk of mortality

    8. Septic Shock • Vascular injury • Endothelial injury Vascular injury Leukokcyte-derived mediators Platelet-leukocyte-fibrin thrombi SHOCK!!! Inc. vascular resistance Nitric oxide Procoagulant molecules PAF Vascular endothelial cells cytokines TNFa Microvascular thrombosis hypotension DIC