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11 Cards in this Set

  • Front
  • Back
Define chronic inflammation
can follow acute inflammation

begin insidiously

involves lymphocytes, macrophages, and plasma cells

involves tissue destruction and repair (as well as ganulomas)
List several broad causes of chronic inflammation
persistent infection

immune mediated inflammatory disease (autoimmune, unregulated immune response against microbes, asthma)

prolonged exposure to toxic agents (ie silica)
Describe the morphologic features and types of cells seen in chronic inflammation
collagenous tissue replacing normal tissue

infiltration of lymphocytes & fibrosis
Describe the role of the macrophage in chronic inflammation including its activation as well as it’s secreted products
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
Describe granulomatous inflammation including its morphologic appearance as well as etiologies.
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
Define acute phase response and describe its physical manifestations.
fever, leukocytosis, tachycardia, blood pressure increase, malaise, chills
Describe the pathophysiology of fever and list the cytokines and prostaglandins involved in this process.
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?
Define and know the significance of the acute phase reactants discussed in the reading.
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
Describe the basis for the erythrocyte sedimentation rate and give examples of its use in diagnostic evaluations.
erythrocyte sedimentation rate- fibrinogen is an acute phase reactant that coats RBCs blunting their surface charge and causes them to rouleaux (physiologic purpose?)
Understand the importance of leukocytosis and describe its pathophysiology.
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)
Briefly outline the pathophysiology of sepsis as described in the reading assignment and describe some of the clinical consequences.
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