Chronic inflammation

===Lecture Details===
Anthony Longano; Week 10 MED1011; Pathology
===Lecture Content===
Chronic inflammation can be primarily from transplant rejection, some autoimmune diseases, progression from acute to chronic eg abscess or effusion that cannot be drained, recurrent bouts of chronic can be from cholecystitis. Macroscopic appearance- chronic ulcer has granulated tissue base, abscess cavity has thickened walls, hollow viscus with walls thickened has chronic inflammatory cells and fibrosis, granulomatous inflammation has central caseous necrosis. Lymphocytes recruit and trap macrophages and activate them. They increase vascular permeability, directly destroy target cells and recruit more lymphocytes to the tissue site. Macrophages are longer lived than neutrophils, ingest microorganisms and cellular debris, and will harbor viable organisms intracellularly if they can't kill with lysosomal enzymes.
Granulomatous inflammation is characterised by the presence of granulomata (nodular collection of epithelioid histiocytes). There can be central necrosis and multi-nucleate giant cells. Can be from infection, reactions to foreign bodies, or idiopathic. Epithelioid histiocytes are generally arranged in clusters, not much phagocytic activity, adapted to a secretory function with unknown range and function.
Multinucleate giant cells form in the presence of matter which cannot be digested. Langhan's cells are horseshoe arrangement of nuclei, formed in tuberculosis. Foreign-body type have a random scattering of nuclei, made from foreign material. Touton have a central ring of nuclei with peripheral clear cytoplasm and are seen at sites of adipose tissue breakdown.
===Readings===
====JC Underwood Ch 10====