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22 Cards in this Set
- Front
- Back
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What are the three major components of acute inflammation? |
Vasodilation - increased blood flow Increased vasc permeability - enables plasma proteins and leuc to leave circ Emigration of leucocytes from microcirculation to the site of injury |
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Describe the sequence of cellular events in acute inflammation |
leucocytes are the major cell type first 6 - 24hrs: neutrophils 24 - 48hrs: monocytes/macrophages First stasis blood -> increased leucocytes along endothelial wall Leucocyte margination + adhesion to vessel wall Migration + diapedesis across wall Migration to chemotactic stimuli |
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How are leucocytes delivered to the site of injury |
Margination of WCC in vessels w/ rolling and Adhesion to endothelium Migration + diapedesis across endothelium Migration towards chemotactic stimuli |
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What leucocyte types are characteristic of acute inflammation? |
Neutrophils (first 6 - 24hrs) Monocytes and macrophages 24 - 48hrs Lymphocytes in viral Eosinophils in hypersensitivity |
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Why do neutrophils predominate in the inflammatory response in the first 6 - 24 hrs? |
Largest number in the circulation Respond more rapidly to chemokines May attach more firmly to adhesion molecules shorter lifespan therefore disappear after 24 - 48hrs (monocytes live longer) |
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What is the role of leukocytes in acute inflammation? |
Opsonin: Recognition and attachment to materials Killing of microbes: phagocytosis, engulfment, killing/degradation Release of products: Amplify inflammatory reaction |
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What stimuli causes production of inflammatory mediators? |
Substances released from: - necrotic cells - microbial products - cell injury - mechanical irritation (2 to pass) |
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What are the chemical mediators of acute inflammation and what are their actions? |
Histamine/serotonin: Vasodilation, incr vasc perm PG: Vasodilation, incr vasc perm, pain/fever Cytokines (IL1/TNF): pain/fever, endo activation Chemokines: chemotaxis/ WC activation Kinin: Incr vasc perm, vasodilation, pain PAF: chemotaxis, vasodilation, incr vasc perm Leukotrienes: incr vasc perm + chemotaxis Complement: vasodilation, WC chemotaxis Pass: 4 to pass incl name and action |
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Name some of the chemoattractants responsible for chemotaxis? |
Exogenous: Bacterial products Endogenous: IL-8, C5a, Leukotriene 4 |
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Which mediators of inflammation are derived from cells? |
Vasoactive amines: histamine, serotonin Arachidonic acid metabolites: PG, Leukotrienes Reactive O2 species PAF NO Cytokines (TNF/IL1) Chemokines Pass: Bold + 1 other |
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Which cells release histamine? |
Mast cells Basophils Platelets Pass =/>2 |
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What are the effects of histamine in an inflammatory response? |
Vasodilation Incr vasc permeability Can cause constriction of large arteries |
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What chemical mediators are responsible for pain, fever and tissue damage? |
Prostaglandin Cytokines (IL-1/TNF) Bradykinin Reactive O2 species NO Neutrophil + macrophage lysosomal enzymes Bold + 1 |
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Describe the vascular changes that occur in acute inflammation |
Initial transient vasoconstriction, then vasodilation - increased blood flow - mediated by histamine and NO Increased vasc permeability Stasis blood flow Leucocytes accumulate at vasc endothelium, adhere to and then migrate across, then migrate to chemotactic stimuli |
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What are the mechanisms for the increased vascular permeability? |
Gaps due to endothelial cell contraction Direct injury to vessel Leucocyte mediated injury/leakage Increased transcytosis of fluids/proteins through endothelial cells |
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What are the different types of acute inflammation? (Promt: What are the morphological patterns of acute inflammation) |
Serous: burns/effusions Purulent: Bacterial inflam /necrotic cells Fibrinous: inflammation in body cavities i.e. pleural/meninges/pericardial sac Ulcers: Loacal defect in surface of organ/tissue Pass 2 with examples |
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What are the outcomes of acute inflammation? |
Complete resolution +/- scarring Abscess formation Fibrosis Chronic Pass 2/4 |
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What are the characteristics of chronic inflammation? |
Inflammation for a prolonged period (wk or more) Characterised by macrophages With simultaneous: - active inflammation - tissue destruction - attempts at repair 3/4 bold to pass |
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What are the causes of chronic inflammation? |
Persistant infection: TB/syphilis Autoimmune: RA/SLE/MS/IBD Prolonged exposure to toxic agents: silica/FB 2/3 bold w/ examples to pass |
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What cell types are present in chronic inflammation? |
Macrophages Lymphocytes Plasma cells Eosinophils Mast cells Neutrophils |
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Why does macrophage accumulation persist in chronic inflammation? |
Continued recruitment of monocytes - continued expression of adhesion molecules chemotactic factors Local proliferation of macrophages Immobilisation of macrophages |
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What products are released by activated macrophages in chronic inflammation? |
Products assoc with tissue injury:
- Toxic O2 metabolites, AA metabolites, NO, Coag Products associated with fibrosis: - Growth factos (PDGF, TGF) - Fibrogenic cytokines - Remodelling collagenases |
