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16 Cards in this Set
- Front
- Back
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5 Clinical Signs of Inflammation.
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Redness (color)
Swelling Loss of Function Pain (dolor) Increased Temperature |
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Processes involved in inflammation.
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Changes in Blood Vessels.
Migration of Leukocytes - Neutrophils. Chemical Mediator control. |
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Calibre of blood vessels?
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Transient vasoconstriction.
Then Vasodilation. Relaxation of Pre-Capillary Sphincters opens new routes to capillary bed. Increases the blood supply. |
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Vascular Permeability?
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Increases.
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Causes of Vascular Permeability changes?
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Mediators: Vasoactive Amines, NO
- Destruction of tight junctions. - Vesicles carrying fluid form new channels. - Chemicals sereted from leukocytes. - New blood vessels form with NO tight junctions. |
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What is Oedema?
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An increase in fluid in the extravascular spaces.
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How is inflammatory oedema formed?
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Increase in vascular permeability.
Proteins released (not normally). No osmotic pressure difference at venule end to transport fluid back. Increase in interstitium. Protein rich EXUDATE. |
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Exudate
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Inflammatory Fluid.
Protein-rich Sp. Gravity <1.020 |
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Transudate
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Cardiac damage.
Ultra-filtrate of the blood. Few proteins. Sp. Gravity >1.012 |
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Why is rate of blood flow reduced?
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Loss of protein-rich fluid and products means only Blood Cells remain. Fluid is more viscous. Hence slowed blood flow.
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Cellular events - IN ORDER
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Margination
Rolling Adhesion Diapedesis Chemotaxis Phagocytosis |
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Margination
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Blood cells lie in central axial column normally.
Reduced blood flow causes them to fall to the periphery of the blood vessel. |
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Rolling
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Weak bonds form between the leukocyte selectins and the integrin molecules on the endothelial surface.
Flow of blood pushes them along the vessel, rotating around. |
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Adhesion
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Increased affinity of LFA-1 (Beta 2 integrin) for ICAM-1 on the endothelial surface causes strong bonds to form.
Also known as Pavementation. |
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Diapedesis
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Is migration of the leukocytes (mostly neutrophils) accross the endothelia.
Mediated by PECAM-1/CD-31 Collagenase breaks down the basement membrane to allow passage of the neutrophils into extravascular spaces. |
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Chemotaxis
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Chemoattractants attract neutrophils to the site of the injury. These may be:
Exogenous - produced by bacteria. Endogenous: - Complement C5a - AA Metabolites - Leukotriene B4 - Cytokines - IL-8 |
