急性炎症教学教材演示幻灯片.pptVIP

INFLAMMATION;Acute inflammation;“Inflame” – to set fire. Inflammation is “A dynamic response of vascularised tissue to injury.” It is a protective response. It serves to bring defense healing mechanisms to the site of injury.;What is Inflammation?;Reaction of tissues to injury, characterized clinically by: heat, swelling, redness, pain, and loss of function. Pathologically by : vasoconstriction followed by vasodilatation, stasis, hyperemia, accumulation of leukocytes, exudation of fluid, and deposition of fibrin.;How Does It Occur?;Etiologies;Cardinal Signs of Inflammation;Time course Acute inflammation: Less than 48 hours Chronic inflammation: Greater than 48 hours (weeks, months, years) Cell type Acute inflammation: Neutrophils Chronic inflammation: Mononuclear cells (Macrophages, Lymphocytes, Plasma cells).;Changes in vascular flow (hemodynamic changes) ;Time scale;Lymphatics in inflammation:;Transudate: An ultrafiltrate of blood plasma permeability of endothelium is usually normal. low protein content ( mostly albumin);Exudate: A filtrate of blood plasma mixed with inflammatory cells and cellular debris. permeability of endothelium is usually altered high protein content.;Pus: A purulent exudate: an inflammatory exudate rich in leukocytes (mostly neutrophils) and parenchymal cell debris.;Leukocyte exudation;Phagocytosis;Defects in leukocyte function:;Inflammation Outcome;Chemical Mediators:;Morphologic types of acute inflammation;Serous – excess clear fluid – Heart, lung Allergic inflammation Haemorrhagic – b.v. damage - anthrax. Necrotising inflammation. ;Acute inflammation has one of four outcomes:;Abscess formation:;Site: skin, subcutaneous tissue, internal organs like brain, lung, liver, kidney,……. Pathogenesis: the necrotic tissue is surrounded by pyogenic membrane, which is formed by fibrin and help in localize the infection.;Carbuncle;Furuncle or boil;Cellulitis