Inflammation Async (1) PDF
Document Details
Uploaded by SafeWillow7496
Tags
Summary
This presentation covers inflammatory mediators, including histamine, prostaglandins, plasma proteins, clotting systems, leukotrienes, platelet-activating factor, and cytokines. It also distinguishes between acute and chronic inflammation, highlighting the differences in exudates and cell types involved. Various examples of chronic inflammatory conditions are given.
Full Transcript
Chemical mediators Exudates Acute vs Chronic INFLAMMATION INFLAMMATORY MEDIATORS Histamine: found in granules in platelets, basophils and mast cells causes vasodilation and increased permeability of capillaries; one of the first mediators of inflamma...
Chemical mediators Exudates Acute vs Chronic INFLAMMATION INFLAMMATORY MEDIATORS Histamine: found in granules in platelets, basophils and mast cells causes vasodilation and increased permeability of capillaries; one of the first mediators of inflammatory response INFLAMMATORY MEDIATORS Prostaglandins: are ubiquitous, lipid‐soluble molecules derived form arachidonic acid, a fatty acid liberated from cell membrane phospholipids (and contained in foods like poultry, animal organs and meat, fish, seafood, and eggs) contribute to vasodilation, capillary permeability, pain and fever aspirin reduces inflammation by inhibiting the production of prostaglandins glucocorticoids reduces the availability of arachidonic acid INFLAMMATORY MEDIATORS Plasma Proteins: include kinins, activated complement proteins, & clotting factors bradykinin causes dilation of vessels, increased capillary permeability and pain complement consists of at least 10 (named C1, C2, C3, C4, C4a, C4b etc.) proteins that take part in every part of inflammatory response including killing microorganisms directly INFLAMMATORY MEDIATORS Clotting system: forms a fibrinous meshwork at the inflamed site to trap exudates, microorganisms, and foreign bodies, which: prevents the spread of infection and inflammation to adjacent tissues, keeps microorganisms close to an area of greatest This Photo by Unknown Author is licensed under CC BY-NC-ND amount of phagocytes, forms a clot that stops bleeding and provides a framework for future repair and healing INFLAMMATORY MEDIATORS Leukotrienes: produced from arachidonic acid in leukocytes and mast cells promotes margination and chemotaxis of leukocytes some cause vasodilation INFLAMMATORY MEDIATORS Platelet‐Activating Factor: induces platelet aggregation (sticking together) during clotting activates neutrophils and provides chemotactic signals to eosinophils We look INFLAMMATORY at these more in MEDIATORS a few weeks Cytokines: produced by several cells including lymphocytes, macrophages, and other cells Includes: Interleukins, (some are pyrogens) Interferons (interfere with viruses infecting nearby cells) and other related proteins ACUTE INFLAMMATION Has a rapid onset with minimal damage and rapid resolution Is often characterized by the formation of different types of exudates Serous exudate – watery, with low protein; usually seen with mild inflammation Hemorrhagic exudate – when there is severe tissue and blood vessel damage with leakage of RBCs from capillaries Fibrinous exudate – contains large amount of fibrinogen and form a thick and sticky meshwork Purulent exudate – contains pus (degraded white blood cells, proteins and tissue debris); caused by certain microorganisms Which one of these is a serous exudate? What’s an example of where you find this? Which one is purulent? What’s an example of where you find this? INFLAMMATION CHRONIC INFLAMMATION inflammation that may last for weeks, months, or years may develop during recurrent or progressive acute inflammatory responses or from low‐grade, responses that fail to evoke an acute response macrophages and lymphocytes instead of neutrophils are the major WBC moving to the site proliferation of fibroblasts also occurs, which can lead to scarring and deformity can be caused by talc, asbestos, silica, and surgical suture materials; several viruses, bacteria (e.g. tubercle bacillus) and fungi can also elicit chronic inflammation two patterns of chronic inflammation are possible: nonspecific chronic inflammation and granulomatous inflammation INFLAMMATIO N Nonspecific Chronic Inflammation: involves a diffuse accumulation of macrophages and lymphocytes at the site of injury fibroblast proliferation occurs and leads to scar formation that replaces the normal CT or parenchymal tissues CHRONIC INFLAMMATION GRANULOMATOUS LESION: granuloma is a small (1 ‐2mm) lesion where infiltration of macrophages is surrounded by lymphocytes occurs as a result of contact with: splinters, sutures, silica and asbestos, and microorganisms that cause tuberculosis, syphilis these substances are poorly digested and therefore hard to control; a mass of macrophages (sometimes called epithelioid cells) surrounds the foreign substance; a dense membrane of connective tissue eventually encapsulates the lesion and isolates it A tubercle is a granulatomous inflammatory response to Mycobacterium tuberculosis infection