PAT 20A/B Study Guide - Midterm Guide: Oncotic Pressure, Hyperaemia, Cell Adhesion Molecule

• School: Ryerson University
• Department: Pathotherapeutics
• Course: PAT 20A/B
• Professor: Leo Michelis

Document Summary

Increase blood flow to the site of injury. Initially there is vasoconstriction ( neural reflex) to stop bleeding mediated by norepinephrine: platelets adhere to vessels and aggregate to seal the injured area forming a fibrin platelet clot. Injured cells release histamine from mast cells causes vasodilation ( hyperemic response) occurs b/c of histamine & no: dilates capillaries increases blood flow. Injured cells activate the plasma protein fibrinogen to become fibrin: the clot traps bacteria to prevent their spread. Alerts the products of healing to move to the site of injury leukocytes & neutrophils move to the site of injury. Cellular response: phagocytes produce nitric oxide (no) inhibits smooth muscle contraction inhibits platelet aggregation inhibits leukocyte adhesion to endothelium, macrophages release cytokines--- causes endothelial cells to express cellular adhesions ( selecti(cid:374)"s & i(cid:374)tegri(cid:374)"s(cid:895) Leukocytes & neutrophils move to the site of injury: activation of leukocytes, margination and adhesion to the endothelium. Early stages signaling between blood leukocytes and the vascular endothelium.