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26 Cards in this Set
- Front
- Back
- 3rd side (hint)
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1. What are the possible harms of inflammation?
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1. Anaphylactic reaction, rheumatoid arthritis, pericarditis.
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2. What are components of inflammation?
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2. Vascular wall, circulating blood cells, connective tissue, proteins, tissue fibroblasts.
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3. What is the order of events?
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3. Stimulus activates plasma or connective tissue release soluble chemical mediators, causing a vascular and cellular response.
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4. How do we differentiate acute and chronic inflammation?
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4. Acute inflammation is over minutes to days, involves leukocytes along with fluid and plasma exudates. Chronic inflammation lasts days to years, involves monocytes, macrophages, and lymphocytes, with vascular proliferation and scarring.
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5. What are the 5 cardinal signs of inflammation? Which ones are related to vascular changes, and which are related to chemical mediators?
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5. Rubor, calor, tumor, by vascular changes, dolor, and function laesa due to chemical mediators.
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6. What is Sir Thomas Lewis’s triple response?
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6. Dull red line, red halo, wheal.
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7. What vascular changes are observed in inflammation?
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7. Transient vasoconstriction followed by arteriolar dilation (causing erythema and warmth), and increased permeability into interstitial space. Laminar flow slows and leukocytes marginate and may migrate.
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8. What is normal arterial end fluid migration in ml/min? Venous fluid return? Lymph load?
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8. 14 ml/min out, 12 ml/min in, 2 ml/min in lymph.
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9. Hydrostatic pressure increase will lead to transudate and exudates formation. What is the difference between the two? What will exudate formation cause?
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9. Transudate has no protein, exudates is similar to plasma, and causes a decrease in blood osmotic pressure, and decreased fluid return in the venous end.
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10. What is the effect of histamine on vascular endothelium?
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10. Histamine causes an immediate but transient endothelial constriction in venules, opening tight junctions, allowing leakage.
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11. Cytokines such as TNF and IL-1?
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11. After 4-6 hours venules and capillaries experience endothelial retraction, for up to 24 hours.
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12. Direct endothelial injury form UV light or mild thermal injury or bacterial toxins will cause what kind of endothelial changes? Extreme burns or infections?
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12. Apoptosis on mild injury, necrosis on extreme injury.
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13. Leukocytes cause endothelial injury through what mechanism?
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13. Leukocytes produce reactive oxygen species (ROS), and proteolytic enzymes which injury venules (esp. HEV), and pulmonary capillaries.
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14. What are the effects of vascular endothelial growth factors (VEGF) on endothelium?
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14. VEGF causes pinocytosis in venules, and angiogenesis, which is associated with blood loss because of incomple cell junctions.
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15. What are the 4 steps of leukocyte migration, and what molecules are involved?
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15. Margination, Rolling (selectins), Adhesion (Integrins), and Transmigration.
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16. What are the leukocyte and endothelial selectins involved in rolling? What is the origin of the endothelial selectins?
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16. L-selectin on the leukocyte associates with CD 34 on endothelial cells. Silalyl-Lewis X GPs on the leukocyte associate with P-selectins stored in Weibel-Palade bodies, and E-selectins, which are synthesized.
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17. What is the structure of integrins? What integrins are involved in adhesion?
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17. Integrins have 2α and 2β subunits with cytoskeletal and extracellular connections, in the immunoglobulin superfamily. Leukocyte to epithelial integrins are, CD11a/CD18 to ICAM-1, CD11b/CD18 to ICAM-1, and VLA-4 to VCAM-1, respectively.
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18. What molecules on both endothelial cells and leukocytes act in diapedesis?
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18. PECAM-1 (CD31)
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19. What are the chemotactic agents which act on leukocytes?
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19. Soluble bacterial products, C5a, Lipoxygenase metabolism of arachidonic acid, IL-8.
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20. What is the surface receptor for these agents? What are the 2nd messengers?
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20. G-protein (GTP for GDP exchange). PLC hydrolyses PIP2 to IP3 and DAG. IP3 causes Ca2+ release, allowing cytoskeletal changes for movement and phagocytosis. DAG activated PKC, allowing lysosomal degranulation and excretion, and oxidative bursts, as well as the activation of PLA (for arachidonic acid).
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21. What are the 3 steps in phagocytosis, and their subparts?
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21. Phagocytosis: stages: a) Recognition and attachment, with IgG Fc segment, C3b, and collectins, recognized by FcR, CR1,2,3, and C1q, respectively, on the leukocyte
b) Engulfement, c) Fusion with the lysosome, and degradation. |
None
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22. What are the steps in degranulation?
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22. Degradation has kill and digestion steps. Kill with free radicals: ●O2-, H2O2, and ●OCl. Digest with lysosomal acid hydrolases, bactericidal permeability increasing protein (BPI), major basic protein (eosinophils), and defensins (holes in bacterial proteins).
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23. What defect in leukocyte function is associated with Sialyl-Lewis X GP deficiency, and what is the effect?
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23. LAD 2 defect, decreased rolling, therefore decreased adhesion and transmigration.
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24. Integrin β defect?
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24. LAD 1 defect, decreased adhesion, therefore decreased transmigration.
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25. Lysosome phagosome union?
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25. Chediak Higashi syndrome, decreased phagosome formation and phagosome lysosome union.
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26. NADPH deficiency?
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26. Chronic Granulamotous Disease (CGD), decreased free radical production.
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