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inflammation
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- 1what is inflammationa non-specific localised reaction to many kinds of insults - vascular, metabolic and cellular changes occur.
it is a dynamic response of tissue to injury; it is intended to be protective, servicing to bring defence and healing mechanisms to site of injury. - 2exogenous causes of inflammationphysical agents
mechanical agents (fractures, foreign objects)
thermal agents (burns, freezing)
chemical agents (toxic gasses, acids, bases)
biological agents (bacteria, parasites, viruses) - 3endogenous causes of inflammationcirculation disorders, thrombosis, infarction, haemorrhage, enzyme activation (pancreatitis) accumulation of metabolic products, such as urea or uric acid.
- 44 signs of inflammationredness (due to local vessel dilation)
heat (due to local vessel dilation)
swelling (due to influx of plasma proteins and phagocytic cells into the tissue)
pain (due to local release of enzymes and increased tissue pressure) - 5mechanisms of inflammation1) vasodilation - increases delivery of mediators, increases temperature
2) exudation (edema) - delivers immunoglobulins and dilutes toxins, delivers fibrinogen increases lymphatic drainage
3) emigration of cells - white blood cells are able to move through the vessel wall and mediators call more
4) chemotaxis - 6specific vs nonspecific inflammationnon specific inflammation occurs from an external
specific inflammation is an immune response and involves antigen - antibody - 7production of inflammatory mediators: vasoactive mediatorsDAF
Leukotrines
bradykinin
histamine
prostaglandins
anaphylaktoxins
serotonin
= incased vascular permeability
= oedema - 8production of inflammatory mediators: chemotactic factorsC5a
lipoxygenase products (LTB4)
formylated peptides
lympokines
monotones
= recruitment and stimulation of inflammatory cells
acute inflammation- PMNs and platelets
chronic = macrophages, lymphocytes and plasma cells - 9inflammatory mediators: TNF- alpha and IL-1TNF-alpha and IL-1 are responsible for fever, and release of stress hormones (noradrenaline and vasopressin) and activation of RAAS.
they are also responsible for then synthesis of IL-6, IL-8, and IFN-gamma - 10inflammatory mediators: cytokines (especially IL-6)stimulates the release of acute phase reactants such as C-Reactive Protein (CRP)
- 11Pro-Inflammatory InterleukinsFunction either directly on tissue, or, by secondary mediators, to activate the coagulation cascade, complement cascade. and, release of nitric oxide, histamine, bradykinin, platelet activating factor, prostaglandins and leukotrienes
- 12bacterial lipopolysaccharideslipopolysaccharides are a major constituent of the outer cell membrane of gram-negative bacteria.
bacterial lipopolysaccharides induce an inflammatory response through a complex mechanism involving cytokines and effector molecules. - 13leukocyte exudation1) margination (rolling and adhesion to endothelium)
2) diapedis (trans-migration of WBC across epithelium)
3) migration towards chemotactic stimuli from source of tissue injury - movement into tissue spaces
4) phagocytosis (chomp chomp chomp) - 14emigration and chemotaxisonce WBCs have exited capillary through diapedis the leukocytes move through tissue, guided by secreted cytokines and bacterial and cellular debris.
chemotaxis is the process by which leukocytes migrate in response to a chemical signal. - 15outcomes of inflammationresolved
fibrosis
unresolved: access, ulcer, fistula-sinus
unresolved = chronic inflammation - 16resolution of inflammationnormal restoration of the inflamed tissue back to normal status, inflammatory measures such as vasodilation, chemical production and leukocyte infiltration cease, damaged parenchyma cells regenerate. in situations where limited or short inflammation has occurred, this is usually the outcome.
- 17fibrosis following inflammationwhere large amounts of tissue experiences destruction, or damage in tissues is unable to regenerate, fibrous scarring can occur. the scar is mostly comprised of collagen. because there are no parenchyma cells there may be functional impairment.
- 18abscess formation following inflammationa cavity containing pus (opaque fluid containing dead WBCs and bacteria with general debris from destroyed cell) is formed
- 19chronic inflammationif the injurious agent persists, or the reaction persists, we will see chronic inflammation. this process is marked by inflammation lasting from days to years. chronic inflammation may lead to formation of a chronic wounds. it is characterised by the dominating presence of macrophages in the injured tissue; consequently chronic inflammation is almost always accompanied by tissue destruction.
- 20anti-inflammatory drugs + targetsglucocorticoids: target membrane lipids (phospholipase C and A2)
Lipoxygenase inhibitors + NSAIDs: free arachidonic acid; prostaglandin's and TXAs
Leukotrienes - 21—
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- (Fundamental Fundamentals) pharmacology Fichas sobre inflammation, creado por Amelia Claire el 17/06/2017.
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- Amelia Claire
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