Fichas
Inflammation and Cytokines - Absite
Fichas del conjunto (59)
- 1Injury to endothelium causes what?exposed collagen, platelet-activating factor release, and tissue factor release
- 2Role of Platelet-Derived Growth Factor PDGFchemotactic and activated inflammatory cells and fibroblasts
Angiogenesis + Epithelialization - 3Role of Epidemal Growth Factor (EGF)Chemotactic and activates fibroblasts
Angiogenesis and Epithelialization - 4Role of Fibroblastic Growth Factor (FGF)Chemotactic and activates fibroblasts
Angiogenesis + Epithelialization - 5What is platelet-activating factor (PAF)?generated by phospholipase in endothelium; its a phospholipid
chemotactic for inflammatory cells, increases adhesion molecules
activates platelets - 6Chemotactic Factors for Inflammatory cellsPDGF, IL-8, LTB-4, C5a, C3a, PAF, TNF-alpha, IL-1
- 7Chemotactic Factors for FibroblastsPDGF, EGF, FGF
- 8Angiogenesis Factorshypoxia, PDGF, EGF, FGF, IL-8
- 9Epithelialization factorsPDGF, EGF, FGF
- 10PMNs lifespan in blood vs in tissueBlood: 7days
Tissues: 1-2days - 11Lifespan of Platelets7-10days
- 12Mast CellsPrimary cell in Type I HS
Main source of histamine in tissues - 13Basophilsin type I HS
main source of histamine in blood
not found in tissue - 14Histaminecauses vasodilation, tissue edema, postcapillary leakage
primary effector in Type 1 HS rxns - 15BradykininCauses peripheral vasodilation, increased permeability, pain, pulmonary vasoconstriction, bronchoconstriction, involved in angioedema
- 16Enzyme that inactivates bradykinin in lungACE: angiotensin-converting enzyme
- 17Precursor for Nitric OxideArginine
- 18How Nitric Oxide worksactivates guanylate cyclase and increases cGMP, resulting in vascular smooth muscle dilation
- 19Effects of Endothelincauses vascular smooth muscle constriction
- 20Main initial cytokine response to injury and infection are release of what?TNF-alpha and IL-1
- 21Effects of TNF-alphaincreases adhesion molecules
procoagulant
cause cachexia in CA pts
activate neutrophils and marophages
high conc can cause SIRS - 22Main source for TNF-alphaMacrophages
- 23Effects of IL-1responsible for fever (PGE2 mediated
in hypothalamus), by
raising thermal set point - 24Why do you get a fever with atelectiasis?alveolar macrophages release IL-1 resulting in fever
- 25IL-6increases hepatic acute phase proteins
CRP and amyloid A - 26IL-8PMN chemotaxis, angiogenesis
- 27IL-10decreases the inflammatory response
- 28Interferonsreleased by lymphocytes in response to viral infection
activates: macrophages, NK cells and cytotoxic T cells
inhibit viral replication - 29SelectinsL-selectins on leukocytes
E - on endothelium
P - on platelets
rolling adhesion - 30Beta-2 integrinsCD11/18 molecules
on leukocytes
bind ICAMs
achoring adhesion - 31What molecules are found on endothelial cells and involved with transendothelial migration (diapedesis)?ICAM, VCAM, PECAM, ELAM
- 32What activates the classic compliment pathway?IgG/IgM, antigen-antibody complex
- 33What activates the alternative complement pathway?endotoxin, bacteria, other stimuli
- 34Factors associated with the classic complement pathwayFactors C1, C2, and C4
- 35Factors associated with alternative complement pathwayFactors B, D, and P
- 36What factor is common to and is the convergence point to both classic and alternative complement pathways?C3
- 37AnaphylatoxinsC3a, C4a, C5a
increase vascular permeability, bronchoconstriction, activate mast cells and basophils - 38What is the membrane attack complex (MAC)?C5b-9b; causes cell lysis (usually bacteria)
- 39Opsonizationtargets antigen for immune response
C3b and C4b - 40Complements associated with chemotaxis for inflammatory cellsC3a and C5a
- 41Effects of PGI2 and PGE2vasodilation, bronchodilation, increased permeability; inhibits platelets
- 42NSAIDsinhibits cyclooxygenase (reversible)
- 43Aspirininhibits cyclooxygenase (irreversible), inhibits platelet adhesion by decreasing TXA2
- 44Steroid MoAinhibit phospholipase, which converts phospholipids to arachidonic acid
Inhibits inflammation - 45Pathway that prostaglandins useCyclooxygenase
- 46Pathway Leukotrienes UseLipoxygenase pathway (leukocyte derived)
- 47What are the slow-reacting substances of anaphylaxis?LTC4, D4, E4
- 48What are the effects of slow-reacting substances of anaphylaxis?bronchoconstriction, vasoconstriction followed by increased permeability (wheal and flare)
- 49Leukotriene that is chemotactic for inflammatory cellsLTB4
- 50Catecholamine peak after injury24-48hrs
- 51Where is Norephinephrine released from?sympathetic postganglionic neurons and adrenal medulla
- 52Where is epinephrine release from?adrenal medulla
- 53Neuroendocrine response to injuryafferent nerves from site of injury stimulate CRF, ACTH, ADH, GH, Epi and NE
- 54CXC chemokinescysteine, amino acid, cysteine
chemotaxis, angiogenesis, wound healing
Ex: IL-8 and plt factor 4 - 55Oxidantsgenerated in inflammation
superoxide anion radical, H2O2, NADPH oxidase, xanthine oxidase - 56Primary mediator of Reperfusion InjuryPMNs
- 57Chronic Granulomatous DiseaseNADPH-oxidase system enzyme defect in PMNs resulting in decreased superoxide radical formation
- 58Primary Mechanism of Injury for oxygen radicalsDNA Damage
- 59Respiratory Burstrapid release of reactive oxygen species (superoxide anion and hydrogen peroxide)
Macrophages and PMNs
Información
- Descripción
- Surgery - Absite Review Fichas sobre Inflammation and Cytokines - Absite, creado por Jennifer Huber el 12/06/2018.
- Creado por
- Jennifer Huber · jun 2018
- Actualizado
- 12 jun 2018
- Visitas
- 19
- Valoración