Kinin is turned into bradykinin which is responsible for pain chemotaxis

Kinin is turned into bradykinin which is responsible

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Kinin is turned into bradykinin which is responsible for: pain, chemotaxis, increase vascular permeability and vasodilation (sepsis*) Coagulation Cascade **Group of plasma protein in a system whose ultimate function is to form a fibrin mesh to stop bleeding and to trap microorganisms * The coagulation cascade has a role in activating the kinin system. Factor XII (Hageman factor) activates kinin.
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Analyze the steps of the arachidonic acid pathway and describe the implications for treatment of inflammation. The arachidonic pathway is the biochemical process which is responsible for the synthesis of prostaglandins. It is a separate arm of the inflammatory process & has a significant role in maintaining homeostasis. Arachidonic acid is made from linoleic acid which is part of the phospholipid cell membrane. *see algorithm page* This is on OBJECTIVES for Module#3 and appears Important. This is not a complete study guide, will need to look at it more in depth, maybe draw it out. The arachidonic pathway is the biochemical process which is responsible for the synthesis of prostaglandins. It is a separate arm of the inflammatory process and has a significant role in maintaining homeostasis. Arachidonic acid is made from linoleic acid which is part of the phospholipid cell membrane. The enzyme phospholipase A2 is responsible for the conversion of linoleic acid to arachidonic acid. Arachidonic acid is then converted by the COX 1 & COX2 enzymes to prostaglandin H2. Prostaglandin H2 undergoes further conversion to form prostaglandins, thromboxane A2, and prostacyclin. The prostaglandins formed by the COX1 pathway function to maintain homeostasis. They maintain the gastric mucosa, fluid and electrolyte balance, and platelet aggregation. The prostaglandins made from the COX2 pathway function mainly in the inflammatory process and produce pain and fever. However they too have a role in maintaining homeostasis (renal function, tissue repair, reproduction development). Because the prostaglandins made from the COX2 pathway function mainly in a pathologic manner drugs were developed to inhibit the action of COX2. COX2 inhibitors (NSAIDS) were developed to help preserve the gastric mucosa (prevent ulcers & bleeds) while at the same time inhibit the effects of inflammation. All of the COX2 inhibitors (except for one) have been removed from the market secondary to an increase in cardiac events which were associated with their use. Celebrex is the only COX2 inhibitor which is still available for use. A note of caution… while COX2 inhibitors block the inflammatory functions of prostaglandins, they can also impair renal function. There is a risk of renal impairment because those prostaglandins made from COX2 have a role in maintaining renal function. Non selective NSAIDS inhibit both COX1 and COX2 prostaglandin synthesis hence the risk of gastric ulcerations, GI bleeds, increased risk of bleeding and edema. These are common side effects of NSAIDS as is renal impairment. Aspirin blocks both COX1 and COX2 but its inhibition
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  • Fall '15
  • david,mary

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