Chapter 2. Inflammation and Repair - Chronic Inflammation Flashcards
what is the definition of chronic inflammation?
inflammation of prolonged duration (weeks to years) that most often results from persistence of an injury-causing agent
what are 3 causes of chronic inflammation?
- infection (most common)
- autoimmune tisease
- sterile agents (silica, uric acid)
what are the cell types in chronic inflammation?
monocytes and macrophages (key cells), lymphocytes, plasma cells, eosinophils
is there necrosis in chronic inflammation?
not as prominent a feature as in acute inflammation
how is the parenchyma in chronic inflammation
destruction; loss of functional tissue with repair by fibrosis
how is granulation tissue formed in chronic inflammation?
- highly vascular tissue made of blood vessels and activated fibroblasts
- blood vessels derived from preexisting blood vessels
- essential for normal wound healing
- precursor for scar tissue - fibronectin is required for granulation tissue formation
- cell adhesion glycoprotein in ECM binds to collagen, fibrin, and cell surface receptors
- chemotactic factor that attracts fibroblasts and endothelial cells (form new blood vessels, angiogenesis)
- -VEGF and BFGF are important in angiogenesis
what is fibronectin?
key adhesion glycoprotein in ECM
what is granulomatous inflammation? what is it caused by?
specialized type of chronic inflammation
- from infectious (caseous necrosis due to lipid released from cell wall of dead pathogens) or noninfectious (noncaseating, hard granulomas) causes
- pale, white nodule with or without central caseation
- usually well circumscribed
what are cell types in granulomatous inflammation?
- epithelioid cells (activated macrophages), mononuclear (round) cell infiltrate (CD4 helper T cells, TH1 cells)
- multinucleated giant cells formed by fusion of epitheliold cells (nuclei at periphery)
what does TNF-alpha do in granulomatous inflammation?
important in formation and maintenance of TB and systemic fungal granulomas
- TNF-alpha and Y-interferon recruit cells for granuloma formation
- TNF-alpha inhibitors cause breakdown of granulomas leading to dissemination of disease
what is the sequence of events in formation of tuberculous granuloma?
- tubercle bacillus M. tuberculosis undergoes phagocytosis by alveolar macorphages (processing of bacterial Ag)
- macrophages present Ag to CD4 T cells in association with class II Ag sites
- macrophages release IL-12 (to stimulate naive TH cells to make TH1 memory cells) and IL-1 (cause fever, activate TH1 cells)
- TH1 cells release IL-2 (stimulates TH1 proliferation), Y-interferon (activates macrophages to kill tubercle bacillus, epithelioid cells), and migration inhibitory factor (causes macrophages to accumulate)
- lipids from killed tubercle bacillus lead to caseous necrosis
- activated macrophages fuse and become multinucleated giant cells
how to acute and chronic inflammation differ in terms of pathogenesis?
acute: microbial pathogens, trauma, and burns
chronic: persistent acute inflammation, foreign bodies, autoimmune disease, certain types of infection
how to acute and chronic inflammation differ in terms of primary cells involved?
acute: neutrophils
chronic: monocytes/macrophages (key cells), B and T lymphocytes, plasma cells, fibroblasts
how to acute and chronic inflammation differ in terms of primary mediators?
A: histamine (key), prostaglandins, leukotrienes
C: cytokines, growth factors
how to acute and chronic inflammation differ in terms of necrosis?
A: present
C: less prominent
