radang kronik

16
Outcomes of acute inflammation: 1.Resolution 2.Healing by fibrosis 3.Chronic inflammation

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Radang Kronik

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  • Outcomes of acute inflammation:ResolutionHealing by fibrosisChronic inflammation

  • Events in the resolution of inflammation

    Return to normal vascular permeability;Drainage of edema fluid and proteins into lymphatics or by pinocytosis into macrophages;Phagocytosis of apoptotic neutrophils and necrotic debris;Disposal of macrophages. Macrophages also produce growth factors that initiate the subsequent process of repair. Note the central role of macrophages in resolution.

  • Serous inflammation. A skin blister showing the epidermis separated from the dermis by a focal collection of serous effusion.

  • Fibrinous pericarditis. A, Deposits of fibrin on the pericardium. B, A pink meshwork of fibrin exudate (F) overlies the pericardial surface (P).

  • Suppurative inflammation. A, A subcutaneous bacterial abscess with collections of pus. B, The abscess contains neutrophils, edema fluid, and cellular debris.

  • The morphology of an ulcer. A, A chronic duodenal ulcer. B, Low-power cross-section of a duodenal ulcer crater with an acute inflammatory exudate in the base.

  • Maturation of mononuclear phagocytes.

  • The roles of activated macrophages in chronic inflammationMacrophages are activated by :Cytokines from immune-activated T cells (particularly IFN-gamma), Nonimmunologic stimuli such as endotoxin.

  • Chronic inflammation in the lung, showing all three characteristic histologic features: (1) collection of chronic inflammatory cells (*), (2) destruction of parenchyma (normal alveoli are replaced by spaces lined by cuboidal epithelium, arrowheads), and (3) replacement by connective tissue (fibrosis, arrows).

  • By contrast, in acute inflammation of the lung (acute bronchopneumonia), neutrophils fill the alveolar spaces and blood vessels are congested

  • Mechanisms of macrophage accumulation in tissues. The most important is continued recruitment from the microcirculation.

  • Macrophage-lymphocyte interactions in chronic inflammation. Activated lymphocytes and macrophages influence each other and also release inflammatory mediators that affect other cells.

  • Typical tuberculous granuloma showing an area of central necrosis, epithelioid cells, multiple Langhans-type giant cells, and lymphocytes.