14146809
Description
Flashcards by Jennifer Huber, updated more than 1 year ago
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Created by Jennifer Huber
over 6 years ago
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| Question | Answer |
| Injury to endothelium causes what? | exposed collagen, platelet-activating factor release, and tissue factor release |
| Role of Platelet-Derived Growth Factor PDGF | chemotactic and activated inflammatory cells and fibroblasts Angiogenesis + Epithelialization |
| Role of Epidemal Growth Factor (EGF) | Chemotactic and activates fibroblasts Angiogenesis and Epithelialization |
| Role of Fibroblastic Growth Factor (FGF) | Chemotactic and activates fibroblasts Angiogenesis + Epithelialization |
| What is platelet-activating factor (PAF)? | generated by phospholipase in endothelium; its a phospholipid chemotactic for inflammatory cells, increases adhesion molecules activates platelets |
| Chemotactic Factors for Inflammatory cells | PDGF, IL-8, LTB-4, C5a, C3a, PAF, TNF-alpha, IL-1 |
| Chemotactic Factors for Fibroblasts | PDGF, EGF, FGF |
| Angiogenesis Factors | hypoxia, PDGF, EGF, FGF, IL-8 |
| Epithelialization factors | PDGF, EGF, FGF |
| PMNs lifespan in blood vs in tissue | Blood: 7days Tissues: 1-2days |
| Lifespan of Platelets | 7-10days |
| Mast Cells | Primary cell in Type I HS Main source of histamine in tissues |
| Basophils | in type I HS main source of histamine in blood not found in tissue |
| Histamine | causes vasodilation, tissue edema, postcapillary leakage primary effector in Type 1 HS rxns |
| Bradykinin | Causes peripheral vasodilation, increased permeability, pain, pulmonary vasoconstriction, bronchoconstriction, involved in angioedema |
| Enzyme that inactivates bradykinin in lung | ACE: angiotensin-converting enzyme |
| Precursor for Nitric Oxide | Arginine |
| How Nitric Oxide works | activates guanylate cyclase and increases cGMP, resulting in vascular smooth muscle dilation |
| Effects of Endothelin | causes vascular smooth muscle constriction |
| Main initial cytokine response to injury and infection are release of what? | TNF-alpha and IL-1 |
| Effects of TNF-alpha | increases adhesion molecules procoagulant cause cachexia in CA pts activate neutrophils and marophages high conc can cause SIRS |
| Main source for TNF-alpha | Macrophages |
| Effects of IL-1 | responsible for fever (PGE2 mediated in hypothalamus), by raising thermal set point |
| Why do you get a fever with atelectiasis? | alveolar macrophages release IL-1 resulting in fever |
| IL-6 | increases hepatic acute phase proteins CRP and amyloid A |
| IL-8 | PMN chemotaxis, angiogenesis |
| IL-10 | decreases the inflammatory response |
| Interferons | released by lymphocytes in response to viral infection activates: macrophages, NK cells and cytotoxic T cells inhibit viral replication |
| Selectins | L-selectins on leukocytes E - on endothelium P - on platelets rolling adhesion |
| Beta-2 integrins | CD11/18 molecules on leukocytes bind ICAMs achoring adhesion |
| What molecules are found on endothelial cells and involved with transendothelial migration (diapedesis)? | ICAM, VCAM, PECAM, ELAM |
| What activates the classic compliment pathway? | IgG/IgM, antigen-antibody complex |
| What activates the alternative complement pathway? | endotoxin, bacteria, other stimuli |
| Factors associated with the classic complement pathway | Factors C1, C2, and C4 |
| Factors associated with alternative complement pathway | Factors B, D, and P |
| What factor is common to and is the convergence point to both classic and alternative complement pathways? | C3 |
| Anaphylatoxins | C3a, C4a, C5a increase vascular permeability, bronchoconstriction, activate mast cells and basophils |
| What is the membrane attack complex (MAC)? | C5b-9b; causes cell lysis (usually bacteria) |
| Opsonization | targets antigen for immune response C3b and C4b |
| Complements associated with chemotaxis for inflammatory cells | C3a and C5a |
| Effects of PGI2 and PGE2 | vasodilation, bronchodilation, increased permeability; inhibits platelets |
| NSAIDs | inhibits cyclooxygenase (reversible) |
| Aspirin | inhibits cyclooxygenase (irreversible), inhibits platelet adhesion by decreasing TXA2 |
| Steroid MoA | inhibit phospholipase, which converts phospholipids to arachidonic acid Inhibits inflammation |
| Pathway that prostaglandins use | Cyclooxygenase |
| Pathway Leukotrienes Use | Lipoxygenase pathway (leukocyte derived) |
| What are the slow-reacting substances of anaphylaxis? | LTC4, D4, E4 |
| What are the effects of slow-reacting substances of anaphylaxis? | bronchoconstriction, vasoconstriction followed by increased permeability (wheal and flare) |
| Leukotriene that is chemotactic for inflammatory cells | LTB4 |
| Catecholamine peak after injury | 24-48hrs |
| Where is Norephinephrine released from? | sympathetic postganglionic neurons and adrenal medulla |
| Where is epinephrine release from? | adrenal medulla |
| Neuroendocrine response to injury | afferent nerves from site of injury stimulate CRF, ACTH, ADH, GH, Epi and NE |
| CXC chemokines | cysteine, amino acid, cysteine chemotaxis, angiogenesis, wound healing Ex: IL-8 and plt factor 4 |
| Oxidants | generated in inflammation superoxide anion radical, H2O2, NADPH oxidase, xanthine oxidase |
| Primary mediator of Reperfusion Injury | PMNs |
| Chronic Granulomatous Disease | NADPH-oxidase system enzyme defect in PMNs resulting in decreased superoxide radical formation |
| Primary Mechanism of Injury for oxygen radicals | DNA Damage |
| Respiratory Burst | rapid release of reactive oxygen species (superoxide anion and hydrogen peroxide) Macrophages and PMNs |
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