5. Give five signs of inflammation and briefly their causes

i. Heat/sweat (increased blood flow) ii. Swelling and induration (accumulation of water and cells) iii. Pain (pressure of fluid, inflammatory mediators) iv. Loss of function v. Systemic changes (humoral factors)

8. Give four patterns of acute inflammation

i. Serous inflammation ii. Fibrinous inflammation iii. Suppurative or Purulent inflammation iv. Ulcers

21. Describe an ulcer including its cause. When does it only exist?

Local defect or excavation made by shedding of inflammatory necrosis Only exists when necrosis is on or near surface

25. Over what occurs in the margins and base of the ulcer?

Fibroblastic proliferation with scarring Accumulation of lymphocytes, macrophages, and plasma cells

26. Give the three inflammatory time periods

i. Acute: 0-2 days ii. Subacute: 2-10 days iii. Greater than 2 weeks

28. What other four cells are associated with inflammation?

i. Basophils ii. Fibroblasts iii. Mast cells iv. Platelets

30. What five cell/tissue derived molecular systems are there in inflammation?

i. Vasoactive amines (histamine, serotonin) ii. Acidic lipids (prostaglandins, leukotrienes, lipoxins) iii. Cytokines (IL-1, TNF) and chemokines (IL-8, MCP-1, MIP-1a, lymphotactin) v. Others (PAF, nitric oxide, free radicals, lysosomal enzymes)

31. Give the 6 sequential steps of hemodynamic changes in vasculature due to inflammation hint: 2,2,3 items

i. Vasoconstriction Vasodilation ii. Increased permeability Increased permeability iii. Leakage of fluid and cells to interstitial space Stasis of circulation results in increased blood viscosity Decreased absorption from interstitial space

34. Name the 5 steps of leukocyte exudation. What three cell types are included in all 5 steps?

Cells include neutrophils, macrophages, and lymphocytes i. Marginiation ii. Adhesion (pull to EC surface) iii. Emigration iv. Chemotaxis v. Chemokinesis/Chemotaxis

36. What are three members of the cell adhesion molecules family Selectin? What are they dependent upon?

a. Selectin family: i. P-Selectin (CD62P) ii. E-Selectin (CD62E) iii. L-Selectin(CD62L) b. Calcium

37. What is the Selectin family’s role and where are they found?

a. Homing receptors and mediate rolling of leukocytes along endothelium b. Surface of endothelium, platelets, and leukocytes

Test 1: 06-07 Acute Inflammation Flashcards by Matthew DuPhénix

Give five signs of inflammation and briefly their causes

i. Heat/sweat (increased blood flow) 
ii. Swelling and induration (accumulation of water and cells)
 iii. Pain (pressure of fluid, inflammatory mediators)
 iv. Loss of function
 v. Systemic changes (humoral factors)

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Give four patterns of acute inflammation

i. Serous inflammation
 ii. Fibrinous inflammation
 iii. Suppurative or Purulent inflammation
 iv. Ulcers

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What is serous inflammation marked by? Name the cutaneous injury and its cause, associated with this step.

Outpour of protein-poor, thin fluid from blood serum or secretions of mesothelial cells of the peritoneal, pleural, and pericardial cavities (effusion)
 Skin blisters (virus or burns)

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What is suppurative or purulent inflammation characterized by? What does this consist of?

Pus (neutrophils, necrotic cells and edema fluid)

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What is an abscess? Produced by?

Focal localized collections of purulent tissue produced by pyogenic bacteria

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Describe an ulcer including its cause. When does it only exist?

Local defect or excavation made by shedding of inflammatory necrosis
 Only exists when necrosis is on or near surface

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Over what occurs in the margins and base of the ulcer?

Fibroblastic proliferation with scarring

Accumulation of lymphocytes, macrophages, and plasma cells

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Give the three inflammatory time periods

i. Acute: 0-2 days
 ii. Subacute: 2-10 days
 iii. Greater than 2 weeks

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What inflammatory cells/elements are associated inflammation cell show below? 
 i. neutrophils
 ii. neutrophils, monocytes, lymphocytes, plasma cells, fibroblastic elements, angioblastic elements
 iii. monocytes, lymphocytes, plasma cells, macrophages, granuloma cells (epithelioid cells and giant cells)

i. Acute: neutrophils
 ii. Subacute: neutrophils, monocytes, lymphocytes, plasma cells, fibroblastic elements, angioblastic elements
 iii. Chronic: monocytes, lymphocytes, plasma cells, macrophages, granuloma cells (epithelioid cells and giant cells)
 (iv. Eosinophils: predominant inflammatory cells in allergic reactions and parasitic infestations)

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What other four cells are associated with inflammation?

i. Basophils 
ii. Fibroblasts 
iii. Mast cells 
iv. Platelets

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What five cell/tissue derived molecular systems are there in inflammation?

i. Vasoactive amines (histamine, serotonin) 
ii. Acidic lipids (prostaglandins, leukotrienes, lipoxins) 
iii. Cytokines (IL-1, TNF) and chemokines (IL-8, MCP-1, MIP-1a, lymphotactin) 
v. Others (PAF, nitric oxide, free radicals, lysosomal enzymes)

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Give the 6 sequential steps of hemodynamic changes in vasculature due to inflammation
 
hint: 2,2,3 items

i. Vasoconstriction 
Vasodilation
 ii. Increased permeability 
Increased permeability
 iii. Leakage of fluid and cells to interstitial space 
Stasis of circulation results in increased blood viscosity 
Decreased absorption from interstitial space

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Difference between normal, transudation, and exudation

Normal capillary 
a. Lots of proteins in blood keeps fluid in vasculature 
i. Known as colloid osmotic pressure, pulling in 
i. Hydrostatic and colloid osmotic pressures nearly the same. Net effect= no fluid in/out

Transudate 
a. Ex. congestive heart failure 
i. See increased hydrostatic pressure due to backup of blood 
a. Net pressure change, not inflammatory mediators, is what causes fluid movemen 
 
1. Exudate 
a. Inflammation involved here 
i. Endothelial cells contract 
1. Spaces between them open up so that proteins can flow out 
2. Once proteins are out of vasculature, fluid follows

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Name the 5 steps of leukocyte exudation. What three cell types are included in all 5 steps?

Cells include neutrophils, macrophages, and lymphocytes

i. Marginiation 
ii. Adhesion (pull to EC surface) 
iii. Emigration 
iv. Chemotaxis 
v. Chemokinesis/Chemotaxis

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What are three members of the cell adhesion molecules family Selectin? What are they dependent upon?

a. Selectin family: 
i. P-Selectin (CD62P) 
ii. E-Selectin (CD62E) 
iii. L-Selectin(CD62L) 
b. Calcium

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What is the Selectin family’s role and where are they found?

a. Homing receptors and mediate rolling of leukocytes along endothelium 
b. Surface of endothelium, platelets, and leukocytes

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What stimulates their transport?

a. TNF or IL-1

Role of intercellular adhesion molecule-1 (ICAM-1)? Expressed on? Binds to?

a. Assist localization of leukocytes to tissue injury 
b. Surface of cytokine stimulated endothelium 
c. LFA-1 and Mac-1

Vascular adhesion molecule binds to?

VLA-4 leukocyte receptor on lymphocytes, monocytes, eosinophils, basophils

Platelet endothelial cell adhesion molecule (PECAM-1) is also called? Binds in what way? Role?

a. CD31 
b. Hemophilic (CD3 binds CD3) 
c. Diapedesis step of leukocyte emigration in inflammation

The most notable of the ß1 integrins is? Where is it expressed and what does it bind to?

a. VLA-4 
b. Leukocytes 
c. VCAM-1 (on endothelium)

In the phagocytosis of an organism, the recognition and attachment step is enhanced by? What does bind to? Give examples of each

1.	In the phagocytosis of an organism, the recognition and attachment step is enhanced by? What does bind to?  <br>Give examples of each <br>
Opsonin <br>
i.	Complement C3 <br>
i.	Fc <br>
ii.	C3 <br>
a.	Leukocyte opsonin receptors  <br>

What are the three pathways of the killing/degradation stage of the phagocytosis? Describe

i. Oxygen-dependent: Oxygen reduced to superoxide ion (O2) via NADPH oxidase Superoxide converted to H2O2. 
ii. H2O2-Myeloperoxidase-Halide system: Myeloperoxidase from neutrophilic granules catalyzes reactions between Cl- and H2O2 forming HOCL (hypochlorous acid)
 iii. Oxygen-Independent: leukocyte granule products: leukocyte granule products

The cell-derived mediators vasoactive amines have what as their mediators? Causes?

a. Histamine and serotonin

b. Anterior dilation (but constrict large arteries) and increase permeability of postcapillary venules

61. Give 2 kinds of leukotrienes and one kind of Lipozin

i. Leukotrienes B4 (neutrophil aggregation/adhesion to endothelium)
ii. Leukotrienes C4, D4, E4
(vasoconstriction/bronchospasm/permeability)
iii. Lipoxin A4 and B4 (formed on neutrophil-derived LTA4, inhibit neutrophil chemotaxis, adhesion; inverse b/n lipoxin and leukotrienes

69. What role do cytokines stimulate do? Classified by?

Chemokines stimulate leukocyte recruitment in inflammation. These small proteins (8-10 kD) are classified according to conserved cysteine residues in the protein:
i. C-X-C or β-chemokines: Act primarily on neutrophils. Best example is IL-8.
ii. C-C or β-chemokines: Attract monocytes, eosinophils, basophils, and

70. Nitric oxide is a soluble free radical gas. It acts in a paracrine way on target though cGMP. Role in septic shock. Effects include:

i. Strong vasodilation/smooth muscle relaxation
ii. Reduces platelet aggregation and adhesion, leukocyte recruitment (reducing inflame)
iii. Host defense against infection

72. Oxygen derived Free molecules (Reactive Oxygen Species, ROS)
Extracellularly cause?

Endothelial cell damage (increased vascular permeability)
Inactivation of antiproteases (oxidation of methionyl resideues on α-1-antitrypsin
Injury to other cells

75. What is the critical step in the activation of complement?
Name four pathways

b. Pathways
i. Classic pathway (initiated by binding of antigen-antibody complex to C1)
ii. Alternate pathway (C3 directly activated by bacterial endotoxins, complex polysaccharides, aggregated globulins, e.g., IgA)

iii. Lectin pathway (C1 activation by binding of plasma mannose-binding lectin to carbohydrates on microbes)
iv. Cleavage by proteolytic enzymes ( Plasmin and lysosomal enzymes in inflammatory exudates)

76. What are the specific protein fragments made during complement activation in inflammation?
What do they stimulate? W
hat kind of toxins are they?

a. C3a, C4a, C5a
b. Stimulate histamine release from mast cells leading to increased vascular permeability and vasodilation
c. Anaphylatoxins

77. What purpose does C5a have?

i. Chemotaxis
ii. Increase leukocyte adhesion molecules on surface
iii. Activates lipooxygenase pathway in neutrophils and monocytes

78. C3b’s role?

Oponization by receptors on neutrophils, macrophages, eosinophils

79. C5-9’s role?

Complex attacks membrane, inserts into lipid bilayer forming macropores which increase permeability and lysis

80. The Kinin System deals with what conversion?

Activated Hagerman Factor converts prekallibrein into kallikrein

81. Give 6 roles for Kalikrein

i. Amplify activation of Hagerman Factor
ii. Convert plasminogen to plasmin
iii. Chemattractant for neutrophils
iv. Cleaves kininogen foams bradykinin
v. Brief vasoactive peptide
vi. Increases cell adhesion molecule expression on endothelium

89. Factor XII of the intrinsic clotting system, is activated by direct contact with endotoxins, collagen, or basement membrane. This triggers?

the kinin system and the clotting cascade.

91. Most likely mediators in Inflammation for vascular permeability are?

Vasoactive amines, C3a and C5a (via histamine),
Bradykinin, Leukotrienes (C4, D4, E4), PAF, Substance P

92. Most likely mediators in Inflammation for chemotaxis and leukocyte activation are?

C5a, Leukotriene B4, Chemokines

94. Most likely mediators in Inflammation for Pain are?

Prostaglandins, Bradykinin

95. Most likely mediators in Inflammation for Tissue damage are?

Lysosomal enzymes, oxygen metabolites, NO