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Chapter 3 Part 1 Flashcards

1
Q

Major participants in inflammatory response

A

blood vessels and leukocytes

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2
Q

Mediators involved in ARDs

A

neutrophils

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3
Q

Mediators involved in asthma

A

eosinophils, IgE antibodies

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4
Q

Mediators of glomerulonephritis

A

antibodies and complement, neutrophils, monocytes

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5
Q

Mediators of septic shock

A

cytokines

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6
Q

Mediators of arthritis

A

lymphocytes, macrophages, antibodies

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7
Q

Mediators of asthma

A

eosinophils, IgE antibodies

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8
Q

Mediators of atherosclerosis

A

macrophages, lymphocytes

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9
Q

Mediators of pulmonary fibrosis

A

macrophages, fibroblasts

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10
Q

Features of acute inflammation

A

fast onset
mainly neutrophils
usually mild and self-limited injury
prominent local and systemic signs

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11
Q

Features of chronic inflammation

A

slow onset
monocytes, macrophages, and lymphocytes
often severe and progressive
less local and systemic signs

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12
Q

Causes of inflammation

A

Infections
Tissue Necrosis
Foreign Bodies
Immune Reactions

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13
Q

What are the steps of the inflammatory response?

A

1) recognition of the injurious agent
2) recruitment of leukocytes
3) removal of the agent
4) regulation (control) of the response
5) resolution (repair)

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14
Q

What are the 3 major components of acute inflammation?

A

1) dilation of small vessels leading to an increase in blood flow
2) increased permeability of the microvasculature enabling plasma proteins and leukocytes to leave the circulation
3) emigration of the leukocytes from the microcirculation, their accumulation in the focus of the injury, and their activation to eliminate the offending agent

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15
Q

Exudate

A

an extravascular fluid that has a high protein concentration and contains cellular debris; implies an increase in permeability of vessels triggered by injury

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16
Q

Transudate

A

fluid with low protein content, little or no cellular material, and low specific gravity; result of osmotic imbalance without an increase in vascular permeability

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17
Q

Edema

A

excess fluid in the interstitial tissue; exudate or transudate

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18
Q

Pus

A

purulent inflammatory exudate rich in leukocytes, the debris of dead cells, and microbes

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19
Q

What does vasodilation lead to?

A

increased blood flow, causing heat and redness to area of inflammation

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20
Q

What does increased permeability of microvasculature lead to?

A

loss of fluid leads to slower blood flow, concentration of RBC in small vessels and increased viscosity in blood (stasis)

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21
Q

What occurs as stasis develops?

A

blood leukocytes (neutrophils) accumulate along the vascular endothelium

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22
Q

What is the most common mechanism of vascular leakage?

A

contraction of endothelial cells resulting in increased inter endothelial spaces induced by histamine and short-lived

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23
Q

What occurs with endothelial injury?

A

vascular permeability caused by burns and some microbial toxins, may be long lived

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24
Q

What do the lymphatic vessels do during inflammation?

A

lymph flow is increased and helps drain edema fluid that accumulates because of increased vascular permeability

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25
Phases of leukocyte recruitment to site of injury
1) Margination, rolling, and adhesion to endothelium occurs in the lumen 2) migration across the endothelium and vessel wall 3) migration in the tissues toward a chemotactic stimulus
26
Define margination
leukocyte redistribution that occurs as the blood flow slows, stasis occurs, hemodynamic conditions change, and more white blood cells assume a peripheral position
27
What are the two major families of molecules involved in leukocyte adhesion and migration?
selectins and integrins
28
What do the weak rolling interactions allow?
slow down the leukocytes and give them the opportunity to bind more firmly to the endothelium
29
L-selectin
neutrophils and monocytes, T cells, B cells
30
E-selectin
endothelium activated by cytokine (TNF, IL-1)
31
P selectin
endothelium activated by cytokines (TNF, IL-1)
32
LFA-1 integrin
neutrophils, monocytes, T cells | binds to ICAM-1 and 2
33
MAC-1 integrin
monocytes, DCs | binds to ICAM 1 and 2
34
VLA-4 integrin
monocytes and T cells | binds to VCAM1
35
a4B7 integrin
monocytes and T cells | binds to VCAM-1 and MasCAM-1
36
CD31 (Ig family)
endothelial cells and leukocytes | CD31
37
Where does transmigration of leukocytes occur?
post capillary venules
38
Define chemotaxis
movement of leukocytes toward the site of injury by after exiting circulation along a chemical gradient
39
Most common exogenous chemoattractants
bacterial products (n-formylmethionine and lipids)
40
Examples of endogenous chemoattractants
cytokines, components of complement system, AA metabolites
41
What predominates in the inflammatory infiltrate during the first 6-24 hours
neutrophils
42
What replaces the neutrophils in the inflammatory infiltrate by 24-48 hours
monocytes
43
Why are neutrophils the first response
most numerous, respond more rapidly, attach more firmly on endothelial cells, short-lived
44
Why do monocytes predominate later
survive longer, proliferate in the tissues
45
What are agents that block TNF used as therapeutics for?
chronic inflammatory diseases
46
What leads to leukocyte activation
recognition of microbes, signaling pathways that increase cytosolic Ca2+, and activation of protein kinase C and phospholipase A
47
What are the steps of phagocytosis
1) recognition and attachment of the particle to be ingested by the leukocyte 2) engulfment with subsequent formation of a phagocytic vacuole 3) killing or degradation of ingested material
48
Why is the mannose receptor a good receptor to use for phagocytosis in humans?
recognizes microbes, but not host cells
49
What are the major opsonins for phagocytosis?
IgG antibodies, C3b, mannose-binding lectin
50
Describe the process of engulfment
1) particle bound to phagocytic receptor 2) pseudopods flow around and plasma membrane closes off to form phagosome 3) phagosome fuses with lysosomal granule
51
What are the agents that kill microbes?
ROS, nitric oxide
52
How are ROS produced?
rapid assembly and activation of NADPH oxidase, which oxidizes NADPH, and reduces oxygen to superoxide anion
53
Where are ROS produced?
phagolysosome and lysosome; they can act on ingested particles without damaging the host cell
54
What does the enzyme MPO do?
in the presence of a halide, converts H2O2 (byproduct of superoxide anion) to hypocrite which can destroy microbes by halogenation or oxidation
55
What are some of the antioxidant mechanisms to protect against ROS?
``` superoxide dismutase catalase- detoxifies H2O2 glutathione peroxidase- detoxifies H2O2 ceruloplasmin- copper containing serum protein transferrin- iron free fraction of serum ```
56
Which type of nitric oxide is involved in microbial killing and how is it activated?
iNOS, induced when macrophages and neutrophils are activated by cytokines
57
What does NO do within macrophages?
reacts with superoxide to generate peroxynitrite
58
Functions of NO
microbicidal substance, relaxes vascular smooth muscle, vasodilation
59
What are the two types of granules in neutrophils?
1) smaller specific- contain lysozyme, collagenase, gelatins, lactoferrin, plasminogen activator, histaminase, alkaline phosphatase 2) larger azurophil- contain myeloperoxidase, bactericidal factors, acid hydrolyses, neutral proteases
60
Function of acid proteases
degrade bacteria and debris within phagolysosomes
61
Function of neutral proteases
capable of degrading various extracellular components
62
What is the role of antiproteases?
control the destructive effects of lysosomal enzymes | ex) a1-antitrypsin
63
NETs
extracellular fibrillar networks that provide a high concentration of anti microbial substances at the site of infection and prevent the spread of microbes by trapping them in the fibrils

MOD (34 decks)

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