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Pathology > Test 1: 06-07 Acute Inflammation > Flashcards

Test 1: 06-07 Acute Inflammation Flashcards

1
Q
  1. Give five signs of inflammation and briefly their causes
A

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

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2
Q
  1. Give four patterns of acute inflammation
A

<br></br>i. Serous inflammation
<br></br>ii. Fibrinous inflammation
<br></br>iii. Suppurative or Purulent inflammation
<br></br>iv. Ulcers

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3
Q
  1. What is serous inflammation marked by? Name the cutaneous injury and its cause, associated with this step.
A

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

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4
Q
  1. What is suppurative or purulent inflammation characterized by? What does this consist of?
A

Pus (neutrophils, necrotic cells and edema fluid)

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5
Q
  1. What is an abscess? Produced by?
A

Focal localized collections of purulent tissue produced by pyogenic bacteria

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6
Q
  1. Describe an ulcer including its cause. When does it only exist?
A

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

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7
Q
  1. Over what occurs in the margins and base of the ulcer?
A

Fibroblastic proliferation with scarring

<br></br>Accumulation of lymphocytes, macrophages, and plasma cells

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8
Q
  1. Give the three inflammatory time periods
A

<br></br>i. Acute: 0-2 days
<br></br>ii. Subacute: 2-10 days
<br></br>iii. Greater than 2 weeks

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9
Q
  1. What inflammatory cells/elements are associated inflammation cell show below?<br></br>
    <br></br>i. neutrophils
    <br></br>ii. neutrophils, monocytes, lymphocytes, plasma cells, fibroblastic elements, angioblastic elements
    <br></br>iii. monocytes, lymphocytes, plasma cells, <br></br>macrophages, granuloma cells (epithelioid cells and giant cells)
    <br></br>
A

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

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10
Q
  1. What other four cells are associated with inflammation?
A

i. Basophils <br></br>
ii. Fibroblasts <br></br>
iii. Mast cells <br></br>
iv. Platelets <br></br>

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11
Q
  1. What five cell/tissue derived molecular systems are there in inflammation?
A

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

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12
Q
  1. Give the 6 sequential steps of hemodynamic changes in vasculature due to inflammation
    <br></br>
    hint: 2,2,3 items
A

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

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13
Q
  1. Difference between normal, transudation, and exudation
A
  1. Normal capillary <br></br>
    a. Lots of proteins in blood keeps fluid in vasculature <br></br>
    i. Known as colloid osmotic pressure, pulling in <br></br>
    i. Hydrostatic and colloid osmotic pressures nearly the same. Net effect= no fluid in/out

<br></br><br></br>

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

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14
Q
  1. Name the 5 steps of leukocyte exudation. What three cell types are included in all 5 steps?
A

Cells include neutrophils, macrophages, and lymphocytes <br></br>

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

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15
Q
  1. What are three members of the cell adhesion molecules family Selectin? <br></br>What are they dependent upon?
A

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

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16
Q
  1. What is the Selectin family’s role and where are they found?
A

a. Homing receptors and mediate rolling of leukocytes along endothelium <br></br>
b. Surface of endothelium, platelets, and leukocytes

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17
Q

What stimulates their transport?

A

a. TNF or IL-1 <br></br>

18
Q
  1. Role of intercellular adhesion molecule-1 (ICAM-1)? Expressed on? Binds to?
A

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

19
Q
  1. Vascular adhesion molecule binds to?
A

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

20
Q
  1. Platelet endothelial cell adhesion molecule (PECAM-1) is also called? Binds in what way? Role?
A

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

21
Q
  1. The most notable of the ß1 integrins is? Where is it expressed and what does it bind to?
A

a. VLA-4 <br></br>
b. Leukocytes <br></br>
c. VCAM-1 (on endothelium)

22
Q
  1. In the phagocytosis of an organism, the recognition and attachment step is enhanced by? What does bind to? Give examples of each
A 
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>
23
Q
  1. What are the three pathways of the killing/degradation stage of the phagocytosis? Describe
A

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

24
Q
  1. The cell-derived mediators vasoactive amines have what as their mediators? Causes?
A

a. Histamine and serotonin <br></br>

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

25
Q
  1. Give 2 kinds of leukotrienes and one kind of Lipozin
A

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

26
Q
  1. What role do cytokines stimulate do? Classified by?
A

Chemokines stimulate leukocyte recruitment in inflammation. These small proteins (8-10 kD) are classified according to conserved cysteine residues in the protein: <br></br>

i. C-X-C or β-chemokines: Act primarily on neutrophils. Best example is IL-8. <br></br>
ii. C-C or β-chemokines: Attract monocytes, eosinophils, basophils, and <br></br>

27
Q
  1. Nitric oxide is a soluble free radical gas. It acts in a paracrine way on target though cGMP. Role in septic shock. Effects include:
A

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

28
Q
  1. Oxygen derived Free molecules (Reactive Oxygen Species, ROS) <br></br>
    Extracellularly cause?
A

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

29
Q
  1. What is the critical step in the activation of complement? <br></br> Name four pathways
A

b. Pathways <br></br>
i. Classic pathway (initiated by binding of antigen-antibody complex to C1) <br></br>
ii. Alternate pathway (C3 directly activated by bacterial endotoxins, complex polysaccharides, aggregated globulins, e.g., IgA) <br></br>
<br></br>iii. Lectin pathway (C1 activation by binding of plasma mannose-binding lectin to carbohydrates on microbes)
<br></br>iv. Cleavage by proteolytic enzymes ( Plasmin and lysosomal enzymes in inflammatory exudates)

30
Q
  1. What are the specific protein fragments made during complement activation in inflammation? <br></br>What do they stimulate? W <br></br>hat kind of toxins are they?
A

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

31
Q
  1. What purpose does C5a have?
A

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

32
Q
  1. C3b’s role?
A

Oponization by receptors on neutrophils, macrophages, eosinophils

33
Q
  1. C5-9’s role?
A

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

34
Q
  1. The Kinin System deals with what conversion?
A

<br></br>Activated Hagerman Factor converts prekallibrein into kallikrein

35
Q
  1. Give 6 roles for Kalikrein
A

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

36
Q
  1. Factor XII of the intrinsic clotting system, is activated by direct contact with endotoxins, collagen, or basement membrane. This triggers?
A

the kinin system and the clotting cascade.

37
Q
  1. Most likely mediators in Inflammation for vascular permeability are?
A

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

38
Q
  1. Most likely mediators in Inflammation for chemotaxis and leukocyte activation are?
A

C5a, Leukotriene B4, Chemokines

39
Q
  1. Most likely mediators in Inflammation for Pain are?
A

Prostaglandins, Bradykinin

40
Q
  1. Most likely mediators in Inflammation for Tissue damage are?
A

Lysosomal enzymes, oxygen metabolites, NO

Pathology (6 decks)

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