ACUTE AND CHRONIC INFLAMATION Neutralizing antibodies
INFLAMATION- body’s alert system
Elie Metchnikoff INFLAMMATION
- Describes phagocytosis A protective response involving host
- Noble Prize 1908 cells, blood vessels, and proteins o Eliminate initial course of cell Paul Erlich injury - Who recognized the role of serum o Remove necrotic cells and factors, mainly antibodies tissue o Initiate the process repair Granulocytes Also a potential harmful process Basophils – inflammation o Components of inflammation that are capable of destroying Eosinophils – parasitic infection microbes can alas injury Neutrophils – bacteria bystander normal tissue
Symptomatic treatment
Agranulocytes “itis” = inflammation
Lymphocyte “function aesa”
B – “Bursa of Fabricius” CARDINAL SIGNS OF INFLAMMATION
Plasma Cells Heat (calor) Produce antibodies Redness (rubor) IgG – genitalia, chronic Swelling (tumor) infections Pain (dolor) IgA – “asa labas” o Celsus, De Medecina section o IgM – “mauuna” Loss of function “Malaki”, Acute section o Rudolf Virchow “father of 5 IgG = 1 IgM modern pathology” IgD – “Di alam” ~to help~ Vascular Reactivity - involves blood vessels IgE – “Ellergy” “Parasitic infection” Vasoconstriction -blood vessels constrict and get T – “Thymus” narrower. T-Helper Vasodilation - blood vessels get wider. T-Killer T-Suppressor Endothelial cells - form a single cell layer that lines all blood vessels and regulates exchanges Monocytes between the bloodstream and the surrounding tissues. - Engulfing phagocyting CELLS
o Constriction of the blood vessels adhesion o Formation of a temporary “platelet plug” activation o Activation of the coagulation secretion o Formation of “fibrin plug” or the final clot aggregation Secondary (involves coagulation factors) o Stable clot