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23 Cards in this Set
- Front
- Back
Inflammation
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a protective response whose purpose is to eliminate the cause of cell injury and the necrotic cells resulting from the injury
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What are some examples of harmful or potentially fatal inflammatory responses?
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Asthma, atherosclerosis, anaphylaxis, pericarditis, RA
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What are the characteristics of acute inflammation?
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lasts minutes to days, fluid and protein from blood seep into tissue, neutrophils infiltrate the tissue, inflammation resolves with minimal or no damage
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What are the characteristics of chronic inflammation?
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lasts days to years, lymphocytes and macrophages infiltrate the tissue, they cause tissue destruction, tissue repair is by fibrosis and neovascularization.
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A critical function of the acute inflammatory response is to deliver ___________ to the site of cell injury.
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neutrophils
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Neutrophils may prolong inflammation and induce tissue damage by releasing _________.
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enzymes, chemical mediators, and free radicals
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What causes local hyperemia in acute inflammation?
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local arteriolar vasodilation, the site becomes red and warm. There is an increase in RBC's and neutrophils There is an increase in flow volume but a decrease in flow velocity.
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What causes vascular permeability in acute inflammation?
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Structural changes in local microvasculature permit leakage of water, plasma proteins, and neutrophils. The site becomes swollen and painful.
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What else can cause "leakiness"?
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direct injury from mechanical impact, burn or bacterial toxins, or endogenous factors like ischemia/hypoxia.
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What else can injury to a cell cause besides "leakiness"?
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release of histamines, bradykinin, leukotrienes, IL-1, TNF, all of which aggrevate the leakiness.
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What occurs in leukocyte emigration?
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as blood flow slows, laminar flow decreases, neutrophils have increased contact with epithelial cells, stick, roll along the endo. and finally adhere and emigrate by diapedesis.
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Binding of _____ factors enhances the neutrophils' mobility and initiates new neutrophil tricks.
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chemotactic
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What happens when chemotactic factors activate leukocytes?
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Arachidonic acid ->
1)cyclooxygenase -> prostaglandins 2)5-lipoxygenase -> Leukotrienes |
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What are the chemical mediators of inflammation?
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histamine, found in mast cells
eicosanoids (prostaglandins, leukotrienes) cytokines, Nitric oxide, lysosomal enzymes |
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What do NSAID's do?
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block the cyclooxygenase pathway that produces prostaglandins
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What diagnostic tools are used to detect inflammation?
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C-reactive protein (will be high)
esr, which will increase because of the increase in fibrinogen. |
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What are the outcomes of acute inflammation?
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complete resolution, scarring, abscess formation, progression to chronic inflammation.
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When is chronic inflammation seen?
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persistent infections, like syphilis and tuberculosis, prolonged exposure to toxic agents, autoimmune diseases, sarcoidosis
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What type of cells are involved in chronic inflammation?
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macrophages, lymphocytes, plasma cells, eosinophils
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This is a distinctive form of chronic inflammation, characterized by aggregation of activated macros that develop a squamous
"epithelioid" appearance. |
granulomatous inflammation
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What is the role of the lymphatics during inflammation?
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They remove inflammatory fluid and debris from the interstitial space.
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What is the Blood brain barrier and what is its use?
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The BBB is made up of capillaries with tighter epithelial cell junctions, making it harder for certain dangerous and helpful substances to get through.
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What are the morphologic patterns in acute and chronic inflammation?
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serus - i.e. skin blister
fibrinous - leads to scarring suppurative - exudate forms with an abcess ulceration - epit. surface becomes inflammed, necrotic, and eroded. |