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Inflammation Flashcards

1
Q

What are the three functions of inflammation/

A

remove pathogenic insults

remove injured tissue

institute wound healing

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2
Q

What are the four cardial signs of inflammation

A

Erythema
Edema
Heat
Pain

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3
Q

What are the three major components of acute inflammation?

A
  1. Dilation of smal lblood vessels
  2. Inreased vascular permeability
  3. Accumulation/activation of leukocytes at the site in infection/injury
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4
Q

What are the four possible outcomes of inflammation?

A
  1. Resolution
  2. Abscess
  3. scarring
  4. chronic inflammation
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5
Q

What is chronic inflammation?

A

a prolonged response (weeks or months) in which inflammation, tissue injury and attempts at repair coexist.

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6
Q

What are the leukocytes that are at epithelial barriers?

A

macrophages
dendritic cells
mast cells
innate lymphoid cells

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7
Q

What are the mediators of vasodilation? (3)

A

Protaglandins
Nitric oxide
Histamine

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8
Q

What are the mediators of increased vascular permeability? (4)

A

Histamine
Bradykinin
Leukotrienes
PAF

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9
Q

What are the mediatiors of chemotaxis and leukocyte recruitment/activation? (3)

A

IL-1
TNF
Prostaglandins

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10
Q

What are the mediators of fever?

A

IL-1
TNF
Prostaglandins

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11
Q

What are the mediators of pain? (2)

A

Prostaglandins

Bradykinin

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12
Q

What are the mediators of tissue damage? (3)

A

Lysosomal enzymes of leukocytes

ROS

NO

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13
Q

What is the first step (in inflammation) that the macrophages/mast cells/dendritic cells/innate lymphoid cells take when the encounter an antigen?

A

Release inflammatory mediators

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14
Q

Mast cells are activated by C5a to produce what?

A

Histamine and prostaglandins

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15
Q

What is histamine? How is it released so quickly?

A

It is a vasoactive amine that is preformed and stored in mast cell granules, and therefore it is released immediately following mast cell activation

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16
Q

What is histamine the principle mediator of?

A

Vascular permeability

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17
Q

What do anti-histamines block?

A

H1 receptors located on mast cells which, when activated, would release histamine

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18
Q

What does histamine stimulate?

A

It stimulate the EC to synthesize NO, which cause vasodilation and subsequent increased blood flow

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19
Q

What are prostaglandins? What specific chemical are they produced from?

A

Lipid mediators (like PGD2) that are produced from arachiodonic acid

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20
Q

What produced prostaglandins?

A

Mast cells

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21
Q

What are the two effects of prostaglandins?

A

vasoilation (edema)

Pain

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22
Q

What is Hageman factor (factor XII) and what activates it?

A

A protein that leads to the activation of anaphylatoxins and the clotting cascade, including bradykinin

Injury to the basement membrane activates it

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23
Q

What is bradykinin?

A

It is an inflammatory mediator (specifically a vasoactive peptide) that is generated by a protease called kallikrein (which is activated by Hageman factor).

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24
Q

What is the effect of bradykinin?

A

It increases vascular permeability and causes contraction of smooth muscle, dilation of blood vessels, and pain (same thing as histamine)

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25
What are the three major proinflammatory cytokines of acute inflammation?
TNFα IL-1 IL-6
26
What activates TNFα, IL-1 and IL-6?
monocytes/macrophages/dendritic cells following activation with pathogen associated molecular patterns (PAMPS) that bind to PRR (pattern recognition receptors).
27
What is the effect of TNF, IL1, (and also histamine) on epithelial cells?
upregulate expression of adhesion molecules
28
What is the effect of the upregulation of adhesion molecules by TNF, IL1, and histamine?
Adhesion molecules act as stop signs for circulating leukocytes and allow them to slow down, roll, adhere and extravasate
29
What are the chemokines that promote leukocyte migration to the site of injury/infection?
C5a and C3a
30
How do chemokines lead leukocytes to were they need to go?
Complement cascade starts on the surface of microbe, and gradient is produced
31
What are the three major chemical that are released by lyososomes that are toxic to both microbe and host?
Lysosomal enzymes ROS NO
32
What are the first leukocytes to migrate out to the site of infection/injury? What is the time scale of this?
PMN (neutrophils) arrived within hours
33
How do neutrophils localize to the sites of injury?
Adhesion molecules expressed by epithelial cells cause rolling
34
What are the five steps of leukocyte extravasation?
1. Rolling or tethering via selectins and selectin ligands 2. Leukocyte activation via chemokines 3. Tight adhesion via integrins and integrin ligands 4. Transendothelial migration (mediated by PECAM and others) 5. Migration along a chemokine gradient
35
What are addressins, and what are the three cell types that use them?
Cell adhesion molecules that direct either lymphocytes, monocytes, or neutrophils to extravasate
36
What is the chemical that causes neutrophil extravasation? How is it release so quickly?
P-selectin, which is stored in Weibel-Palade bodies
37
What does P-selectin bind to on the surface of neutrophils? When is this expressed?
P selection glycolipid 1 (PSGL-1), which is constitutively expressed by neutrophils
38
What is the effect of P-selectin/PSGL-1 binding?
Rolling and extravasation of neutrophils
39
Is the affinity between P-selectin and PSGL-1 high or low?
Low (relatively)
40
What is the next chemical to be upregulated on the surface of epithelial cells after neutrophils have bound to P-selectin? What does it do?
ICAM-1, which binds to LFA-1 o the surface of neutrophils
41
What state is LFA-1? What is the different between its active state and inactive state? What activates it?
LFA-1 is an integrin consisting of an α and β chain that is found in a low affinity state until the cell is activated by a chemokine such as C5a
42
What is the chemical interaction between epithelium and neutrophils that stop the rolling process?
ICAM-1 on epithelial surface LFA-1 on neutrophil
43
Is the affinity between LFA and ICAM-1 high or low?
High
44
What is the chemical that is constitutively expressed by neutrophils and the tight junctions of epithelial cells? What does this do?
PECAM-1, which allows neutrophils to squeeze between epithelial cells and basement membrane
45
How are neutrophils influenced to migrate toward the site of inflammation?
By a gradient of chemotactic substances
46
What are the chemcials released by neutrophils that kill bacteria? What else do they do to bacteria?
ROS Enzymes They also phagocytose them
47
What is the cell type that replaced neutrophils/come in next? When does this occur?
Monocytes (macrophages), which come in 24-48 hours after infection
48
What are M1 and M2 macrophages?
M1-classically induced macrophages that produce proinflammatory ROS and NO M2- produce anti-inflammatory cytokines (IL-10 and TGFβ)
49
What is the function of the TGFβ produced by M2 macrophages?
Initiate the process of wound healing by stimulating fibroblasts and collagen synthesis
50
What are the systemic effects of inflammation?
Fever Neutrophilia Acute phase response Shock
51
What are the two routes by which a systemic infection may be initiated?
1. Pathogen gains entry into blood | 2. Inflammatory mediators released into blood
52
What are the chemicals that initiate the fever response? How do they exert their effects?
Pyrogens, which stimulate prostaglandin synthesis in the vascular and perivascular cells of the hypothalamus
53
What is the effect of upregulation of PGE2 by pyrogens and leukocytes on the hypothalamus?
Upregulate neurotransmitters, like cAMP, which will reset the temperature base point
54
What is the mechanism by which NSAIDs reduce fever?
Inhibit prostaglandin synthesis
55
What is neutrophilia?
Increased peripheral blood neutrophils that commonly accompanies acute inflammation
56
What are the two specific chemicals that bring about neutrophilia?
Proinflammatory cytokines IL-1 and TNF stimulate accelerated release of PMN’s from the bone marrow
57
What is the form of neutrophils that are released from granulocyte colony stimulating factor.
Band form
58
What are band cells?
Immature leukocytes
59
What is the acute phase response?
Increase in CRP and ESR due to the release of interleukin 6
60
What is interleukin-6, and what are its effects?
It is a chemical released by macrophages that acs on hepatocytes to synthesize and release acute phase proteins (like CRP)
61
What CRP and what are its effects?
C-reactive protein which acts as an opsonin to facilitate phagocytosis
62
What is the chemical that causes septic shock? How does this work?
TNF, which stimulates vasodilation and low heart output
63
Systemic activation of the coagulation system (“DIC”) resulting from systemic inflammation leads to what?
a cut-off of blood supply to organs and organ failure

Immuno (16 decks)

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