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25 Cards in this Set
- Front
- Back
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Inflammation definition |
-biological reaction to noxious (harmful) stimulus such as microbes, burns and trauma -fundamentally protective process but may potentially be harmful leading to tissue damage |
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5 signs of inflammation |
rubor- redness tumour- swelling -calor- heat -dolor- pain -functio laesa- loss of function |
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Acute inflammation definition purpose time frame |
Rapid host response to deliver leucocytes and plasma proteins such as antibodies to the sites of infection or tissue injury -protects the body from further injury in response to -infection, trauma, burns, allergic reaction, tissue necrosis -occurs immediatley and last hours- days |
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3 major components of acute inflammation |
-Vascular dilation to increase blood flow -Structure changes in the microvasculature to allow plasma proteins and leukocytes to leave the circulation -Emigration of leukocytes from the microvasculature, their accumulation in the injury site and their activation to eliminate the offending agent |
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Vascular reaction to acute inflammation |
-vessel dilation and increases blood flow -leakage of plasma fluid and protein -leukocyte emigration and accumulation in the site of injury |
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Vessel dilation -purpose -result -caused by |
-Earliest signs of acute inflammation -purpose to increase blood flow -results in heat and redness -induced by action of mediators- histamine, bradykinin and NO |
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Mediators of vascular reaction -name -source -function |
Histamine -Source- mast cells, basophiles, platlets -Function arteriole dilation, increased venous permeability Bradykinin -source- kinin system -function- vasodilation, increase vascular permeability, pain Nitric oxide - source- endothelial cells -Function- vasodilation |
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Increased vascular permeability -what is it -mechanism |
-hall mark of acute inflammation -allow plasma fluid and protein to escape from circulation into extracellul tissue -cause of oedema mech -endothelial cell contraction to increase intercellular spaces. Cells 'shrink' -endothelial cell injury and detachment -increase transport of fluid and protein through endothelial cells (recent finding, much slower) |
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Leukocyte recruitment - 3 stages |
1- leukocyte adhesion to endothelium 2- leukocyte migrate through endothelium- extravastion 3- chemotaxis of leukocytes |
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chemoattractants -2 types |
Exogenous - bacterial products Endogenous - complement components - cytokines -products of lipoxygenase pathway |
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Leucocyte recognition |
through leukocyte receptors Receptors for microbial products eg Toll-like receptors G protein couples receptors- recognise short bacterial peptide containing N-formylmethionyl residues receptors for opsonins- eg antibodies receptor for cytokines- IFN |
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Phagocytosis 3 stages |
-recognition and attachment -engulfment- engulfed particles fuses with lysosome to form phagolysosome, degranulation -killing- ROS and other lysosomal enzymes |
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Acute inflammatory cytokines (4) and source |
TNF-a- source- macrophages, mast cells, T cells IL-1- macrophages, endothelial cells, epithelial cells IL-6- macrophages, other cells chemokines- macrophages, endothelial cells, T cells, mast cell and others |
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Morphology patterns of acute inflammation |
Fibrinous- fibrinous exudate which can lead to scar formation and limited function Purulent- pus filled fluid made of neutraphils and dead cells. caused by staphylcoccal infections Serous- copious effusion of non-viscous serous fluid eg skin blister Ulcerative- necrotic loss of tissue from the surface, exposing layers leading to ulcer formation |
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Outcomes of acute inflammation (3) |
Complete resolution healing by connective tossue replacement (fibrous) Progression to chronic inflammation |
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Chronic- differences to acute |
-not characterised by 5 signs of acute inflammation -prolonged duration- months, years -simultaneous injury and healing -dominant cells type macrophage (where as neutraphil in acute) |
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causes of chronic inflammation |
-persistent infection -immune- mediated inflammatory disease eg autoimmune or allergic disease -prolonged exposure to toxic agents |
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Morphology of chronic inflammation |
-infiltration of mononuclear cells- macrophages, lymphocytes and plasma cells -tissue destruction -attempts at healing by connective tissue replacement- may loose epithelial function. forms fibrosis and new blood vessels generated- angiogenesis |
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Cells in chronic inflammation |
Macrophages - dominant cell type Lymphocytes -produces cytokines- interferon (IFN) Plasma cells from activated B cells Eosinophils Mast cells |
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Macrophage-lymphocyte interactions |
macrophages engulf pathogen, isolate antigen and present to T cells activating them -also release cytokines which also activate T cells -T cells release IFN which activates macrophages -activated T cells release factors to recruit more WBC |
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Changes in chronic inflammation |
-persistent inflammatory stimulus -absence of neutraphils -predominately lymphocytes -macrophages present to clear debris, present antigen and granuloma formation -Angiogenesis -proliferation of fibroblast- bibrosis |
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Granuloma formation |
-special type of chronic inflammation -cause by resistance to phagocytosis- when macrophages can't digest debris so they enlarge (can't complete phagocytosis) horse shoe shape - 2 types: Caseating- mycobacterial infection eg TB Non-caseating- autoimmune |
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3 ways body tries to treat chronic inflammation and consequence |
-Antobodies from plasma cells -direct killing by lymphocytes -phagocytosis by macrophages this can become harmful and result in tissue necrosis and fibrosis |
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Systemic effects of inflammation |
Fever -1-4 degrees higher -pathogens can be pyrogens (fever generating) Acute phase protein -increase conc indicative of chronic inflammation -C-creative protein (CRP), fibrogen and serum amyloid (SAA) Leukocytosis -increase in leukocytes -feature of bacterial infection -15k-20k but can be as hih at 100k Others -increase bp -decreases sweating and chills |
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Outcomes of chronic inflammation |
fibrosis- loss of function |
