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11 Cards in this Set
- Front
- Back
Define chronic inflammation
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can follow acute inflammation
begin insidiously involves lymphocytes, macrophages, and plasma cells involves tissue destruction and repair (as well as ganulomas) |
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List several broad causes of chronic inflammation
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persistent infection
immune mediated inflammatory disease (autoimmune, unregulated immune response against microbes, asthma) prolonged exposure to toxic agents (ie silica) |
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Describe the morphologic features and types of cells seen in chronic inflammation
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collagenous tissue replacing normal tissue
infiltration of lymphocytes & fibrosis |
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Describe the role of the macrophage in chronic inflammation including its activation as well as it’s secreted products
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macrophage is key component of chronic inflammation
monocytes recruited from blood to site then transformed into macrophages activated by microbial products, cytokines macrophages attempt to destroy injurious agent, initiate repair, recurit other cells, induce fibroblast proliferation, angiogenesis, collagen deposition activated macrophages release TNF and IL-1 which recruits lymphocytes (are t cells in blood stream at all?). macrophages display antigens to T cells and stimulate T cells via IL12. Activated T cells recruit monocytes. INF-gamma = strong activator of macrophages. SLIDE 29 |
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Describe granulomatous inflammation including its morphologic appearance as well as etiologies.
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Generations of granulomas. Granulomas are focal accumulations of macrophages that have transformed into epithelium like cells called epitheliod macrophages.These cells are surrounded by a collar of mononuclear leukocytes which are mostly lymphocytes and some plasma cells.Granuloma formation attempts to contain a difficult to eradicate agent.
Giant cells represent the fusion of epithelioid cells foreign ganulomas vs immune granulomas |
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Define acute phase response and describe its physical manifestations.
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fever, leukocytosis, tachycardia, blood pressure increase, malaise, chills
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Describe the pathophysiology of fever and list the cytokines and prostaglandins involved in this process.
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prominent clinical expression of acute phase reponse
pyrogens stimulate the synthesis of prostaglandins in vascular and preivascular cells of hypothalamus endogenous cytokines: IL-1 and TNF - increase cyclooxygenases (convert AA->prostaglandin) prostaglandins (especially PGE2) stimulate the production of neurotransmitters that reset temperature set point purpose of fever? |
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Define and know the significance of the acute phase reactants discussed in the reading.
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Acute phase proteins - proteins made in liver that increase in production by inflammation
C reactive protein serum amyloid protein fibrinogen may act as opsonins and assist in clearance of necrotic cell nuclei |
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Describe the basis for the erythrocyte sedimentation rate and give examples of its use in diagnostic evaluations.
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erythrocyte sedimentation rate- fibrinogen is an acute phase reactant that coats RBCs blunting their surface charge and causes them to rouleaux (physiologic purpose?)
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Understand the importance of leukocytosis and describe its pathophysiology.
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release of white blood cells from post mitotic reserve in bone marrow
left shift = more immature forms of neutrophils in blood (sign of inflammation) 5k-10k/uL = normal Bacterial infections cause neutrophilia, viral cause lymphocytosis, parasitic/allergic cause eosinophilia) |
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Briefly outline the pathophysiology of sepsis as described in the reading assignment and describe some of the clinical consequences.
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Sepsis is the condition that results when the body responds to a severe infection with the production of a very large amount of cytokines including TNF and IL1
This can result in DIC, metabolic changes, and cardiovascular failure otherwise known as septic shock |