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16 Cards in this Set
- Front
- Back
1. What are the inflam. mediators for the:
a. plasma b. complement system c. Mast Cells |
a. complement, kinin, and clotting system
b. C3a, C5a c. Histamine, Herapin, eiocosanoids, cytokines, chemokines |
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2. What are the inflam. mediators for the:
a. Leukocytes b. Fever / endothelial cells c. Pain d. Vasodilation |
a. eiocosanoids, cytokines, chemokines
b. IL-1, TNF, prostaglandins c. Kinins d. Histamine, prostaglandins |
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3. What are the inflam. mediators for the:
a. increased vascular permeability b. Attraction of leukocytes c. Activation of endothelium |
a. TNF, leukotrienes, c3a, c5a
b. chemokines, leukotrienes c. TNF, IL-1, chemokines |
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4. Cytokines and Chemokines
a. Two most important Pro Inflam cytoks b. Three most important anti inflam cytoks c. This Chemokine recruits neutrophils |
a. IL-1 and TNF-alpha
b. IL-6, 10, TGF-b (transformer growht factor) c. cxcl-8 |
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5. There are 5 important actions of Eicosanoids. What are they?
E's are lipid mediators of inflammation |
Vasoconstriction
Vasodilation Increased Vascular Permeability Chemitaxis, and Leukocyte adhesion Know they include prostoglandins, Platlett Aggregating factors (PAF), Leukotrienes, Asprins work on cyclooxygenase, and corticosteroids inhibit phospholipase |
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6. Where do the Alternative, Classical, and Lactin Comlement pathway's merge into one step?
Describe unbound IgG and where C1 binds? |
C3 is broken down to C3A and B. A mediates inflam. B stays to create MAC
upside down Y. Flips up to Y and C1 binds in the pits |
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What effect does C3a and C5a have on mast cells?
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induced degranulation, release histamines, and increase vascular permeability.
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What if C3B lands on an innocent bistander?
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Neutrophil's will still attack it and cause tissue damage
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10. Which is an adaptive defense and which is an innate defense (alternative and classic)
What creates inflammation in both? |
Classic is adaptive (IgG) and alternative in innate.
C3a and C5a |
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12. The second most abundant (and unstable) protein in the body.
In Alternative Pathway, what is the role of the properdin? |
12. 3a.
Stabalizes the complex |
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13. List the three parts of the complement system?
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Opsinization, Inflammation, and Cell Lysis
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14. In terms of cellular inflammatory mediators, list three that come from Arachadonic acid
Where are mast cells found |
Prostoglandins, Leukotrienes, and Platelet Activating Factor
Skin and Mucus Membranes |
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15. What is the entrance of leukocytes into Connective tissue called?
Name the two endothelial molecules that aid in rolling, tight adhesions for leuk and the endothelial, and the one that aids migration though the endothelial cell at the end |
Diapedesis
P and E selectin, VLA4 and VCAM, and CD31 |
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16. This is a hallmark of acute inflammation that forms gaps between endo. cells
What can cause this? |
Increased Vasular Permeability
Vasoactive mediators, and injury to endothelium |
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17. Describe Changes in vasular flow and calaber in acute inflammation?
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Increased net flow out into tissue at both ends from increased hydrostatic pressure and decreases coloid osmotic pressire.
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18. Define inflammation?
shorter duration and NEUTROPHILS here |
A complex reaction to tissue injury following infection, trauma or noxious agents involving vascular alterations, migration of leukocytes from blood into tissues and possibly systemic effects. Inflammation is usually liked with repair. Can lead to excessive tissue damage
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