Acute Inflammation Ii

Front 1

What are the two phases following cellular or tissue injury?

Back 1

1.) Vascular Phase
2.) Cellular Phase

Front 2

Describe what happens during the vascular phase.

Back 2

1.) Fleeting vasoconstriction (neuro-mediated) -- lasts only a few seconds.
2.) Lasting Vasodilation

Front 3

What are the five cardinal signs of acute inflammation, and what causes them?

Back 3

1.) Rubor (redness) -- b/c vasodilation and inc. blood flow.
2.) Tumor (swelling) -- b/c increased vascular permeability and resulting edema.
3.) Calor (warmth) -- b/c increased blood flow and resetting of hypothalamic temperature center by PGE2.
4.) Dolor (pain) -- b/c fluid entry into extracellular space impinges on nerve endings.
5.) Functio Laesa (loss of function) -- for all the above reasons.

Front 4

Describe the three subsets if increased vascular permeability ... where they occur and what causes them.

Back 4

1.) Immediate Transient Response -- happens ONLY in venules, due to presence of Histamine, Bradykinin, and Leukotrienes.
2.) Immediate Sustained Response -- affects everything: arterioles, capillary bed, and venules. This is very bad -- can be caused by radiation burn.
3.) Delayed Prolonged Leakage -- Only affects the capillary bed and venules, classic example is sunburn (it takes a while for the redness to show up after UV damage).

Front 5

What is transudate v. exudate?

Back 5

Transudate: extacellular fluid leakage, fluid comes out b/c hydrostatic pressure increase. NO cells or proteins in fluid. Ex: congestive heart failure.

Exudate: Fluid includes proteins and cells. This is a reaction to injury.

Front 6

What are the initial four stages in the cellular response in acute inflammation.

Back 6

1.) Margination of WBC's
2.) Rolling with transient adnesions
3.) Firm ahesion
4.) Transmigration (diapedesis)

Front 7

Describe Margination.

Back 7

Increase blood flow due to injury. PMNs are larger, and with central laminar flow of RBCs ("axial column"), the PMNs get pushed to the sides, which is a good thing because they need to get in contact with the endothelial cell wall. Chemotaxis is also a factor in drawing the PMNs to the endothelial surface.

Front 8

What are the key players in Rolling with transient adhesion?

Back 8

Selectins on the endothelial surface bind to Siayl-Lewis X oligosaccharides on the PMN surface.

Front 9

What are selectins, what are the two types involved, and what promotes their up-regulation?

Back 9

Selectins are receptors on endothelial cells that transiently bind to S-L-X oligosaccharides on PMN surfaces. Part of the Lectin family.

P-selectins (his mnemonic is that they come from Weibel-Pilade bodies in the cell, which also store Von Willebrand factor) ... are up-regulated via Histamine and Thrombin.

E-selectin (E for endothelial), is up-regulated via TNF and IL-1.

Front 10

What are the key players in Firm Adhesion? Be specific about types of each.

Back 10

Intigrins, on PMN surface, bind to Cell Adhesion Molecules on endothelial surface.

LFA-1 (Leukocyte Function Associated Integrin) binds to ICAM (Intercellular Adhesion Molecule)

VLA-4 (Very Late Antigen) binds to VCAM (Vascular Adhesion Molecule)

Front 11

What factor aids in Diapedisis?

Back 11

PECAM-1 (Platelet/Endothelial Cell Adhesion Molecule) ... also known as CD31 (Cluster Density 31)

Front 12

What are some examples of opsonins, and what do they bind to?

Back 12

Antibodies (IgG) --> binds Fc receptors on PMNs

C3 (3rd fraction of complement proteins) --> bind to Complement Receptors CR1 and CR3 on PMNs

Collectins (Plasma carbohydrate-binding lectins) --> Bind to C1q on PMNs.

Front 13

What binds to LPS. What is another term for LPS?

Back 13

LPS = lipopolysaccharaide, present on Gm neg. bacteria. AKA Endotoxin.

Toll-like receptor 4, a recognition factor on PMNs binds to this.

Front 14

What are some reactive oxygen species generated in the "Respiration Burst"? What are three enzymes responsible for their generation?

Back 14

Myloperoxidase (MPO) + Cl- = Hypochlorous radical

Nitric oxide (via iNOS ... inducible NO synthase)

Superoxide (Via NADPH oxidase) --> which leads to hydrogen peroxide and then Hydroxyl radical (via Fenton reduction)

Front 15

Describe four inherited Leukocyte Deficiency diseases.

Back 15

1.) Chronic granulomatous disease, results from a defect in NADPH oxidase, leads to excess macrophage recruitment and granuloma formation.

2.) Leukocyte Adhesion Deficiency, type I -- due to lack of LFA-1, and therefore no adhesion.

3.) Leukocyte adhesion deficiency, type II, Problem with the S-L-X (b/c cell cannot metabolize fucose), therefore cannot bind with selectins and so no rolling phase.

4.) Chediak-Higashi syndrome -- results impaired fusion of phagosome and lysosome, so no phagocytosis.