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Primitive response = phagocytosis,hypertrophy/hyperplasia - inflammation - reaction of blood vessels - Repair |
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What happens when a local response can't maintain a infection -Whole body is affected |
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-Direct injury - Damage-associated molecular pattern (DAMPs) - Pathogen-associated molecular patterns (PAMPs) |
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inflammation of the liver |
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-inflammation dominated by vascular changes, accompanied by neurtophilis -minutes/days -plasma, neutrophils |
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- happens when initial doesn't fix the problem -uses mature/fibrous tissue to form a scar -weeks -Fibrous tissue, macrophages, lymphocytes, plasma cells |
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-red (hyperemia), swelling, heat (calor), pain(dolor), loss of function |
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-Neutralize the stimulus/agent -prepare for repair -essential for healing of that area -get plasma from the blood to increase healing process |
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life threatening to critical organs (lungs, brain) -Cause damage by itself |
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Vascular phase Cellular phase Reparitive phase |
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Vascular Phase (Plasma & Vascular phase) |
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Plasma, flows into tissue through gaps (leukotrienes) Endothelial cells contract becoming smaller, gaps between them open up Vasodilation opens capillaries increasing blood flow, circulation decreases due to increased permeability -Stasis develops, leukocytes migrate out of vessel |
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-leukocytes emigrate to tissues -leukocyte activation, -phagocytosis -release of leukocyte products |
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direct leukocytes to an area of injury, increase concentration of an enticing smell |
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Connective tissue cells and components fibroblasts |
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Specific Symptomatic Cost Benefit Analysis R.I.C.E |
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remove the cause e.x remove splinter from finger |
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makes you feel better until it heals itself e.x pain killers |
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Beneficial effect v.s Adverse reaction |
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rest, ice, compression, elevation |
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Targets for pharmaceuticals originate from plasma or cells Many act through receptors Many cause release of other mediators Most are short lived Most may have harmful effects |
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vasodilation and increase permeability |
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dilates arterioles (vasodilation) increase permeability of venules -produced by mast cells |
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Block receptors -Drying -Sedation |
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-Reduce blood flow -vasoconstriction (increase air flow in nose) -Steroids -Non steroidal |
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reduce side effects of inflammation by reducing blood flow |
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substances similar to what is produced by our own adrenal glands -Very effective (very potent) -reduce your ability to fight infection |
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original was aspirin (anti inflammatory drug) -same effects as steroids without adverse side effects |
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Cell membrane phospholipids |
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-Phospholipase A (breakdown cell membranes): Arachidonic Acid broke down in to Leukotrienes by lipoxygenase or Prostaglandins (important mediators of inflammation) by Cyclooxygenase |
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Maintains blood flow to kidney, stomach, and intestine |
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Cocaine, Procaine, Lidocaine -menthol (local anesthetic) - salicylic acid (part of the aspirin group) |
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Pain - systemic analgesics |
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Narcotics: heroin, morphine, opium Non-narcotics: tylenol, NSAIDS |
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Systemic Effect: Acute Phase Response |
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Fever, shivering, leucocytosis(dead tissue is removed), acute phase protein release |
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Cytokines Chemokines pro/anti-inflammatory cytokines |
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After Initial Phase Repeated bouts of inflammation Insidious smouldering reaction |
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neutrophilic Eosinophilic Lymphocytic plasmacytic Histiocytic and granulomatous |
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allergic hypersensitivity |
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Granulomatous Inflammation |
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bacteria, fungi, inorganic substances -Dominated by marcophages w/lymphocytes |
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monocytes have single nucleus & no prominent granules, go into tissue and reside -activated T cells produce lymphokines, influence monocytes to activate macrophages -T cell recognize antigens and fight disease w/ macrophages |
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