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27 Cards in this Set
- Front
- Back
Inflammtion
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protective response intended to eliminate the initial cause of cell injury as well as the necrotic cells and tissues resulting from the original insult
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Function of inflammation (3)
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1.To dilute/destroy/neutralize agents-microbes and toxins.
2. removal of dead and damaged tissue 3. initiate repair |
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3 ways in which inflammation may cause pathology
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1.reaction is very strong
2. reaction is prolonged 3. inappropriate reaction |
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goal of inflammation
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to bring cells and molecules of host defences from the blood stream to the site of infection or damage
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Acute inflammation characteristics
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rapid onset and duration
fluid and plasma protein exudate in tissue neutrophilic accumulation in the inflamed tissue |
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chronic inflammation characteristics
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longer duration
influx of lymphocytes and macrophages vascular proliferation occurring and fibrosis |
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hyperaemia
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increased blood flow to tissues
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margination of leukocytes
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leukocytes accumulate along the endothelial surface, pavementing- endothelium lined by leukocytes, blood vessel walls become sticky
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inflammatory stimuli (4)
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1. physical- cuts, burns, fractures
2. chemical- acid, alkali 3. microbial- bacteria, fungi, toxin, parasite 4. immunological (norm immune response/ hypersensitivity) |
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clinical signs of acute inflammation (5)
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1. Heat- vasodilation increased blood flow, increased metabolic rate
2.Redness- increased blood flow 3. Swelling- accumulation of exudate 4. Pain- tension in tissue, neerotransmitters of pain acting on nerves 5. Loss of function- due to pain, swelling |
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vasodilation
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arterioles dilate and capillary beds in damaged area expand in volume to accommodate increased blood flow (heat and redness)
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Reason for exudate formation in capillaries and venules
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high density of receptors on endothelial cells for histamine, serotonin, bradykinin trigger gap formation via reorganisation of endothelial cell cytoplasm
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exudate
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extracellular fluid rich in proteins and or cells
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Transudate
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extravascular fluid that is filtered so contains little or no protein or cells. fluid is glossy clear
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Tumor necrosis factor alpha in inflammation
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triggers inflammation, induces cardinal signs of inflammation, prolongs and amplifies it
produced by macrophages, mast cells, t and b cells, endothelial cells |
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Interleukin 1
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Responsible together with TNF-alpha for sickness, fever, lethargy, lack of appetite.
Macrophage cytokine |
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interleukin 6
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produced by innate immune cells after stimulation with il-1, TNF-alpha or PAMPS .
affects inflammation and acquired immunity. |
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The triple response (heat, redness and swelling) is biphasic, What occurs during the immediate phase?
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due to histamine granules in basophils, serotonin of platelets complement and blood clotting factors acting on the endothelial cells to cause vasodilation and increased permeability.
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Delayed phase of the triple response
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due to kinins and prostaglandins and leukotrienes,
Delayed as these are newly synthesised molecules which takes time. Affect vasodilation and increased permeability. |
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Types of exudate (6)
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1. serous- watery
2. fibrinous- fibrin content high 3. catarrhal- mucin 4. haemorrhagic- frank bleeding into tissues 5. suppurative- pus 6. necrotizing - cell death, ischemia |
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Lymphangitis
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virulent bacteria lodge in the lymphatics and causes inflammation in the lymphatic vessel walls
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Lymphadenitis
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acute inflammation in the lymph nodes
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Tissue cells associated with inflammation (4)
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1. mast cells
2. fibroblasts 3. macrophages 4. endothelial cells |
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Cells of the blood associated with inflammation (5)
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1. PMN
2. Monocytes 3. Eosinophils 4. Basophils 5. Platelets |
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Function of neutrophil in inflammation (3)
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1. Phagocytosis- of pathogen, Ag/Ab complexes via TLR's and FcR
2. Liquification- of tissue by lysosomal enzymes 3. Amplification- of inflam by production of PG, LT and PAF |
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Why is monocyte adherence and migration to injury sight slower?
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MCP-1 (monocyte chemoattractant protein-1) production is slower and there is more neutphils than monocytes in tissue
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Role of macrophages in acute inflammation
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1. phagcytosis of pathogens via TLP and FcR receptors
2. Secrete toxic factors (eg nitric oxide, proteases) 3. Secrete IL-1, TNF-alpha and IL-6- Promoting leukocyte adherence and migration, induces synthesis of PG and LT, induces acute phase response 4. Secrete Colony Stimulating Factor- promotes differentiation of immature granulocyte and monocyte |