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Questions and Answers
What is a key feature of granulation tissue?
What is a key feature of granulation tissue?
What is the main function of macrophages in granulation tissue?
What is the main function of macrophages in granulation tissue?
What is the role of Th1 response in tuberculosis?
What is the role of Th1 response in tuberculosis?
What type of cells have a good capacity to proliferate?
What type of cells have a good capacity to proliferate?
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What is the process of healing by primary intention?
What is the process of healing by primary intention?
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What is the process of repair by fibrosis?
What is the process of repair by fibrosis?
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What is the role of fibroblasts in granuloma formation?
What is the role of fibroblasts in granuloma formation?
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What is the outcome of delayed hypersensitivity to MT antigen?
What is the outcome of delayed hypersensitivity to MT antigen?
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What is the primary difference between acute and chronic inflammation in terms of time span?
What is the primary difference between acute and chronic inflammation in terms of time span?
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What type of cells are involved in chronic inflammation?
What type of cells are involved in chronic inflammation?
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What is the purpose of granulomas in chronic inflammation?
What is the purpose of granulomas in chronic inflammation?
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What is the mechanism of excessive macrophage accumulation in chronic inflammation?
What is the mechanism of excessive macrophage accumulation in chronic inflammation?
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What is the difference between necrotising and non-necrotising granuloma?
What is the difference between necrotising and non-necrotising granuloma?
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What is the purpose of granulation tissue in chronic inflammation?
What is the purpose of granulation tissue in chronic inflammation?
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What is the role of CRP in chronic inflammation?
What is the role of CRP in chronic inflammation?
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What is the characteristic of ESR in chronic inflammation?
What is the characteristic of ESR in chronic inflammation?
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Study Notes
Pathogenesis of Chronic Inflammation
- Progression from acute inflammation that is not totally resolved
- Involves macrophages, lymphocytes, and plasma cells
Mechanism of Chronic Inflammation
- Excessive macrophage accumulation due to continuous recruitment, local proliferation, and immobilization of peripheral macrophages
Morphology of Chronic Inflammation
- Granuloma: aggregation of macrophages that form in response to chronic inflammation
- Macrophages secrete IL-1, interferon alpha, and TNF
- Macrophage elongation leads to formation of epithelioid histiocytes
- Epithelioid histiocytes and macrophage accumulation leads to giant cell formation
- Types of granulomas: necrotising granuloma (central area of necrosis, occurs in TB) and non-necrotising granuloma (no necrosis, occurs in Sarcoidosis)
- Granulation tissue: new connective tissue and microscopic blood vessels that form during healing
Difference between Acute and Chronic Inflammation
- Longer time span
- Tissue destruction, inflammation, and healing all happen simultaneously
- Cells involved: polymorphonuclear cells in acute inflammation, macrophages, plasma cells, and lymphocytes in chronic inflammation
Diagnostic Laboratory Tests
- ESR (Erythrocyte Sedimentation Rate): measures rate at which RBC separate from plasma and fall to the bottom of the tube
- Quicker sedimentation rate means inflammation more likely
- CRP (C-Reactive Protein): CRP is produced by the liver and increases if there's inflammation
- PV (Plasma viscosity): more viscosity means inflammation more likely
Granulomatous Inflammation
- Purpose: granulation tissue repairs pre-existing defects, granulomas destroy foreign material but may destroy tissue as well
- Components: new vessel formation occurs in granulation tissue, no new vessels occur in granulomas
- Fibroblasts: play an essential role in granulation tissue formation, sometimes involved in the final stages of granuloma formation
- Activity of macrophages: in granulation tissue, macrophages clear debris and fibrin, direct new vessel formation and fibroblast accumulation through secretion of growth factors; in granulomas, macrophages try to kill foreign material through release of lysosomal content and cytokine secretion
Chronic Inflammation in Relation to Tuberculosis
- Mycobacterium TB (mt hominis or mt bovis)
- Pathogenesis:
- 0-3 weeks: MT enter macrophages via endocytosis, fever and malaise, nodule at site of infection or asymptomatic, delayed hypersensitivity to MT antigen (TM skin test)
- 4-6 weeks: Th1 response activates macrophages to become bactericidal, Th1 release IFN-gamma, stimulates macrophages to fuse with lysosome, Th1 stimulates formation of granulomas
Healing and Repair
- Regeneration: growth of cells and tissues to replace lost structures
- Repair by fibrosis/scarring: laying down of fibrous tissue
- Examples:
- Skin: labile cells with good capacity to proliferate, will regenerate and repair quickly
- Liver: stable cells with slow proliferative rate unless necessary, permanent cells with no effective regeneration
Process of Healing by Primary and Secondary Intention
- Primary Intention: healing of a clean, uninfected surgical incision
- Wound edges joined by fibrin
- Regrowth of basal layer of epidermis
- Lysis of fibrin and re-epithelialisation
- Restoration of skin
- Secondary Intention: more extensive loss of cells and tissue
- Large defect filled via blood clot
- Granulation tissue grows from dermis into fibrin
- Granulation tissue fibroblasts lay down collagen
- Maturation of collagen restores skin integrity and regrowth of epidermis
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Description
This quiz covers the progression of acute inflammation to chronic inflammation, the role of macrophages, lymphocytes, and plasma cells, and the formation of granulomas.