Chronic Inflammation Tutorial Materials | Western Sydney University - Edubirdie

University:
Western Sydney University
Course:
MEDI 2003 | Clinical Sciences 2
Academic year:

2024
Views:

234

Pages:

1
Author:

Mariam A. A.

Chronic inflammation Types • • • Causes • • • ‘Non-specific’ – some acute inflammation, some proliferation of small blood vessels and fibrosis Granulomatous: aggregates of macrophages form granulomas, or macrophages will fuse into multinucleated giant cells E.g. tuberculosis Defined principally by duration – weeks, months, years May follows acute inflammation May be chronic from the outset arising from: o Persistent infections – low acute virulence e.g. Mycobacterium tuberculosis o Persistent toxins e.g. asbestos fibres in lung o Auto-immune diseases – inflammation against own antigens o Repetitive bouts of injury, inflammation and healing e.g. peptic ulcers Gross signs • Features of acute inflammation • Effects of scarring: o Deformity, contractures on skin e.g. after severe burns o Narrowing of hollow organs e.g. bowel in Crohn’s disease Microscopic • Mix of tissue destruction (necrosis) and healing (scar) physiology • Inflammatory cells mostly ‘mononuclear’ WBCs o Macrophages: ingest pathogen and dead tissue, secrete mediators o Others: lymphocytes and plasma cells (auto-immune), eosinophils (hypersensitivity, parasitic), mast cells o Neutrophils in acute flare ups Molecular • Complex interacting network of chemical mediators, many from macrophages or lymphocytes Outcomes Inactive • Acute elements subside • Affected area = scar Active • Persists and spreads – eventually may be fatal e.g. pulmonary tuberculosis inflammation extends progressively Persists but is limited • Chronic disability (e.g. osteoarthritis)

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