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11 Cards in this Set
- Front
- Back
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Acute Inflammation
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Initial tissue reaction to a large range of injurious agents.
Rubor Calor Tumor Dolor |
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Microscopic Changes: ACUTE
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Vascular Dilatation
- Increased Blood Flow -Increased Hydrostatic Pressure Increased Vascular Permeability -Loss of fluid, protein and cells to tissue. Increased lymphatic flow. -Stimulates Immunity -Dilutes toxins Leukocyte migration |
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Neutrophil
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Key Cell of acute inflammation
-polymorph -nuclear dust shows sign of neutrophil activity |
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Sequelae: ACUTE
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Resolution
-healing by first intention Repair -Large defect or debris can't be removed. -gap > loss of specialised tissue replaced by connective tissue. -scaring via granulation tissue. -endothelial cells (angiogenesis) -fibroblasts (> fibrous tissue) -macrophages (remove debris, co-ordinate) -healing by secondary intention. Suppuration - Pus formation PUS: Exudate, cells, debris, organisms, ABSCESS: Localised collection of pus. EMPYEMA: hollow viscus filled with pus |
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Chronic Inflammation
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Usually weeks +
-Persistent/Recurrent tissue injury and attempted repair. -causes: *chronic absess *resistent organism *autoimmune *unknown aetiology |
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Microscopic Changes: CHRONIC
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-Tissue Destruction
-Inflammation *lymphocytes *macrophages *plasma cells -Granulation tissue/repair |
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Macroscopic Changes: CHRONIC
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-Absess
-Fistula -Sinus -Chronic Ulcer -Fibrosis and Strictures -Caseation |
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Clinical effects: CHRONIC
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-Pain/Swelling
- Decreased Rubor and Calor -Swinging Fever -Malaise -Lymphadenopathy -Increased ESR and WBC -Fibrosis |
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Complications: CHRONIC
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-Amyloidosis
-Carcinogenesis -Hypersensitivity Type 3 and 4 |
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Macrophages
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-Phagocytes
-Present antigens -Release Inflammatory mediators *Tissue repair and damage |
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Granulomas
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-Collections of epitheliod macrophages
- Ball of macrophages which merge together. (secretion>phagocytes) -Giant cell -Angiotensin converting enzyme |
