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12 Cards in this Set

  • Front
  • Back
Chronic inflammation definiton
1. Inflammation for prolonged period of time

2. Associated with immunoligical response and breakdown and repair with fibrosis

3. Progressive and extensive tissue necrosis
T/F: Chronic inflammation always precededs acute inflammation
FALSE: Chronic inflammation can occur de novo without the an acute phase
Origins of chronic inflammation
Chronic inflammation following acute inflammation is due to:

1. Persistent injury

2. Interference with healing process
Characteristics of injurious agents of chronic inflammation
1. Endogenous - "self-antigens" exposed to tissue damage

2. Exogenous - virues, bacteris, microbes

3. Less toxic but more persistent and difficult to eliminate then acute inflammatory agents
Effector cells of immunological reactions in chronic inflammation
1. Lymphocytes - T cells consist of cytotoxic CD8+ cells and CD4+ helper cells; B-cells become plasma cells

2. Plasa cells - produce Ab

3. Eosinophils - involved in IgE mediated immune resposes and against parasites

4. Macrophages - involved in healing, inflammatory, and immunological responses; belongs to mononuclear-phagocyte system (MPS)
MPS cells morphological features
1. Abundant cytoplasm and many organelles
2. "Kidney shaped" nucleus
3. Complex membrane with pinocytotic vesicles, ruffles, flanges, and psuedopods

4. Well-developed cytoskeleton
MPS functional characteristics
1. Mobility
2. Endocytose - phagocytosis and pinocytosis
3. Intracellular killing and sequestering of injurious agents
4. Synthesis and secretion like

- Cytokines (IL-1, TNF)
- Growth factors (VE-, F-, E-, P-GF)
- Reactive O2 metabolites
- Arachadonic acid metabolites
- Plasma proteins (C' proteins, clotting factors)
- Enzymes (collagense, elastase)
How do macrophages accumulate at the site of injury?
1. Margination
2. Chemotaxis
3. Susceptibility of inflammatory macrophages to be activated
4. Local proliferation
4. Prolonged survival
5. Immobilization

- Monocytes are known as macrophages once outside of the blood vessel
Macrophage activation
1. basal activity altered in activation

2. Actvated through IL-1 and TNF

3. Number of organelles are increased

4. Metabolism increased
5. Synthesis and secretion increased

6. Activated macrophages changed to EPITHELOID CELLS and multinucleated GIANT CELLS in GRANULOMATOUS DISEASES

7. Released products defend against microorganisms but also cause tissue destruction and fibrosis
Two types of injurious agents that case granulomatous inflammation
1. Antigenic agents that incite immune response

- Macrophage phagocytose injurious agent but it still survives within them

- T-cell mediated immune response involved

- Example is TB which causes caseous necrosis

- Granulomas in this case are called IMMUNE GRANULOMAS

2. Non-antigenic agents that incite nonimmune response

- Occurs when foregin bodies introduced into body like suture material, talc, and dental amalgams

- Macrophages fuse to become multinucleated giant cell to phagocytose large injurious agents

- Granulomas in this case as called FOREIGN BODY GRANULOMAS
Role of T-cell mediated immunity in granulomatous inflammation
1. T-cells release cytokine INF-gamma to recruit macrophages ⇒ which become epitheloid cells ⇒ which become giant multinucleated cells

2. Epitheloid cells are less mobile, have increased phagocytotic ability, and synthesize and secrete more

3. Granuloma may cause central necrosis through hypoxia and free radicals. (e.g. caseous necrosis in TB)
Histologic characterisitics of granulomatous inflammation
1. Activated macrophage resembles epithelial cell ⇒ thus EPITHELOID CELL

2. GRANULOMAS - aggregates of epitheloid cells that isolate injurious agent away from surrounding normal tissue

3. Granulomas surrounded by rim of LYMPHOCYTES and FIBROUS CT

4. Epitheloid cells may fust to form mulitnucleated giant cell (Langhans giant cells or foreign body giant cells)

6. Older granulomas may become fibrotic or calcify