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Flashcards in Inflammation 1 Deck (16):

What is inflammation?

inflammatory cells, like neutrophils and lymphocytes, move from the blood vessel to the tissue space. if neutrophils are the primary cells out, it is acute. if it is lymphocytes coming out, it is chronic inflammation.


What is actue inflammation

characterized by edema (fluid from blood vessels) and neutrophils in tissue


What stimuli cause acute inflammation? What is the goal?

infection or tissue necrosis
goal is to eliminate pathogen or clear necrotic debris
this is an immediate response that relies on innate immunity (limited specificity)



1. Toll like receptors. present on macrophages and dendritic cells. they recognize PAMPs (pathogen associated...). PAMPs are commonly shared by microbes.
Example: CD14 on macrophages recognizes LPS on the outer membrane of GN bacteria. TLR activation results in upregulation of NF-KB. this activates immune response genes that leads to the production of multiple immune mediators.
TLRs also important in chronic inflammation, because they are also seen on cells of adaptive immunity, like lymphocytes


Aracidonic acid and derivatives

released from phospholipid cell by phospholipase A.
2 pathways:
1. cyclooxygenase produces prostaglandin. PGI2, PGD2, PGE2 mediate vasodilation (at level of arteriole) and incr. vascular permeability (at the post-capillary venule). PGE3 also mediates fever and pain.
2. 5 lipooxygenase pathways: makes leukotrienes. LTB4: attracts and activates neutrophils.
LTC4, LTD4, and LTE4 mediate vasoconstriction, bronchospasm, and increased vascular permeability. Basically, they contract smooth muscle (pericytes contract too, which increases vascular permeability by pulling apart endothelial cells).


mediators that attract and activate neutrophils

leukotriene B4, IL-8, C5A, bacterial products


Mast cells. Where are they, how are they activated?

widely distributed throughout CT
activated by tissue trauma, complement proteins C3a and C5a, and cross linking of surface IgE by antigen.


What does the mast cell do once activated?

immediate response: release of preformed histamine granules. histamines cause vasodilation of arterioles and increased vascular permeability in the post-capillary venule.
delayed response: production of arachidonic acid metabolites, esp. leukotrienes. Leukotrienes are very important


Complement: what is it and what activates it

proinflammatory serum proteins. circulate as inactive precursors
1. classical pathway: C2 binds to IgG or IgM that is bound to antigen ("GM makes classic cars.")
2. Alternative pathway: microbial products directly activate complement
3. Mannose-binding lectin pathway: MBL binds mannose on microorganisms, and activates complement


What are the results of activation of complement? What are the key products

C3 convertase is generated. C3 convertase converts C3 to C3a and C3b. C3b helps generate C5 convertase. C5 convertase converts C5 to C5a and C5b. C5b complexes with C6-C9 to make membrane attack complex, which makes holes in the organism.
C3a and C5a: trigger mast cell degranulation
C5a: chemotactic for neutrophils
C3b: opsonin for phagocytosis
MAC: lyses microbes by creating holes in cell membrane.


What is hageman factor

inactive proinflammatory protein produced in the liver. activated upon exposure to subendothelial or tissue collagen.
implays an important role in DIC, esp. in gram neg sepsis.
Hagemen activates coagulation and fibrinolytic system (important for DIC), and complement and kinin system. Kinin system: cleaves HMW kinin to bradykinin. Bradykinin mediates vasodilation, incr. vascular permeability, and pain.


What are the cardinal signs of inflammation?

redness and warmth, swelling, pain, fever


What is the cause of redness and warmth in inflammation? What mediates this?

vasodilation, which results in incr. blood flow. occurs via relaxation of arteriolar smooth muscle. mediators are histamine, PGs (I2, E2 and D2), and bradykinin. histamine is similar.


What causes swelling in inflammation?

d/t leakage of fluid from postcapillary venules into the interstitial space.
mediated by histamine and tissue damage.


What causes pain in inflammation?

bradykinin and PGE2, which sensitize sensory nerve endings


What mediates fever?

macrophages release IL-1 and TNF
IL1 and TNF hit the perivascular cells of the hypothalamus and incr. COX activity in those cells. this increases PGE2, which raises the temperature set point in the hypothalamus.

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