Chapter 13 - Inflammation and Cytokines Flashcards

1
Q

Injury to the epithelium causes:

A

exposure of collagen, platelet-activating factor release, tissue factor release from endothelium.

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2
Q

When platelets bind to exposed collagen matrix, they release________ which leads to _________ recruitment

A

platelet derived growth factor; PMN and Macrophage

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3
Q

______ are the dominant cells in wound healing. They release_________.

A

Macrophages. PDGF, IL-1 and TNF-alpha

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4
Q

Actions of PDGF:

A
  • chemotactic and activates PMNs and Macros
  • Chemotactic and activates fibroblasts
  • Angiogenesis
  • Epithelialization
  • Chemotactic for smooth muscle
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5
Q

Actions of EGF:

A
  • chemotactic and activates fibroblasts
  • Angiogenesis
  • Epithelialization
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6
Q

Actions of FGF (Fibroblastic growth factor):

A
  • Chemotactic and activates fibroblasts
  • Angiogenesis
  • Epithelialization
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7
Q

Platelet Activating factor generated where? does what?

A

Generated by phospholipase in endothelium

-Stimulates inflammatory cells, chemotactic, increases adhesion molecules

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8
Q

These cytokines are chemotactic for inflammatory cells:

A
  • TGF beta
  • PDGF
  • IL-8
  • LTB-4
  • C5a and C3a
  • PAF
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9
Q

These cytokines are chemotactic for Fibroblasts:

A
  • TGF-beta
  • PDGF
  • EGF
  • FGF
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10
Q

These cytokines cause angiogenesis:

A
  • TGF-beta
  • EGF
  • FGF
  • TGF-alpha
  • IL-8
  • Hypoxia
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11
Q

These cytokines cause epithelialization:

A
  • TGF-beta
  • PDGF
  • EGF
  • FGF
  • TGF-alpha
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12
Q

How long do PMN’s last in tissue? in blood?

A

1-2 days in tissue, 7 days in blood

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13
Q

How long to Platelets last?

A

7-10 days

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14
Q

How are eosinophils involved in type I hypersensitivity reactions?

A
  • Have IgE receptors for allergen

- Release major basic protein- stimulates basophils and mast cells to release histamine

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15
Q

How are Basophils involved in type I hypersensitivity reactions?

A
  • Have IgE receptors

- Main source of histamine in blood

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16
Q

How are Mast cells involved in type I hypersensitivity reactions?

A

Primary cell in type I hypersensitivity reactions. Main source of histamine in tissues other than stomach.

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17
Q

What does Histamine do?

A
  • Vasodilation
  • Tissue edema
  • Postcapillary leakage
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18
Q

What does Bradykinin do?

A
  • Vasodilation
  • Increased Permeability
  • Pain
  • Contraction of Pulmonary Arterioles
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19
Q

The two main initial cytokines released in response to injury and infection are?

A

TNF alpha and IL-1

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20
Q

This cell type is the major producer of TNF

A

Macrophages

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21
Q

Cachexia is mediated by this cytokine

A

TNF

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22
Q

TNF’s main functions are?

A
  • Increases adhesion molecules
  • Procoagulant
  • Activates neutrophils and macrophages
  • Fever, hypothermia, tachycardia, ^ Icardiac output, decrease SVRI
  • (high doses cause circulatory collapse and multisystem organ failure)
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23
Q

This cell is the main source for IL-1

A

Macrophages

24
Q

IL-1 causes fever through this mechanism

A

PGE-2 Mediated increased thermal set point (NSAIDS block PGE2)

25
How does fever occur in atelectasis?
Alveolar macrophages release IL-1
26
What does IL-1 do to IL-6 production?
increases it.
27
What does IL-6 do?
- Increases Hepatic acute phase proteins (C-reactive protein, amyloid A) - Lymphocyte activation
28
What cells release interferons?
Lymphocytes in response to viral infections
29
What doe interferons do?
Activate macrophages, natural killer cells, cytotoxic T cells -Inhibit viral replication
30
What is the most important stimulator for hepatic acute phase proteins?
IL-6
31
These proteins are increased in Hepatic Acute Phase Response:
- C-reactive protein (opsonin, ^ complement) - Amyloid A and P - Fibrinogen - Haptoglobin - Ceruloplasmin - Alpha 1 antitrypsin - alpha 1 chymotrypsin - Complement
32
These proteins are decreased in the hepatic acute phase response:
Albumin, transferrin
33
The first step in cell adhesion:
Rolling; L-selectins on leukocytes bind to E and P selectins
34
Second step in cell adhesion:
Anchoring; Beta 2 Integrans (CD11/18 molecules) in leukocytes bin ICAMs
35
Where are ICAM, VCAM, PECAM, FLAM located and what do they do?
Endothelial cells. Bind Beta 2 Integrins. Also help with transendothelial migration
36
The classic complement pathway is activated by what?
Antigen-Antibody Complex (IgG or IgM)
37
These factors are found only in the classic pathway:
C1, C2, C4
38
The alternative pathway is activated by what?
endotoxin, bacteria
39
These factors are found only in the alternative pathway:
B, D, and P (Properdin)
40
This is factor is common to both and is the convergence point:
C3
41
This electrolyte is needed for both pathways
Mg
42
These are the Anaphylatoxins of the complement, they do what?
C3a, C4a, C5a; increase vascular permeability, smooth muscle contraction, activate mast cells and basophils.
43
This is the membrane attack complex of complement
C5b-9b
44
Complement Opsonization is caused by:
C3b
45
Complement Chemotaxis is caused by:
C3a and C5a
46
PGI2 and PGE2 cause what?
- Vasodilation, - bronchodilation - vascular permeability - Inhibit platelets
47
PGD2 causes what?
- Vasodilation - Bronchoconstriction - Increased vascular permeability
48
NSAIDs do what?
Inhibit cyclooxygenase reversibly
49
Aspirin does what?
- Inhibits cyclooxygenase irreversibly | - Inhibits platelet adhesion by decreasing TXA2
50
Steroids do what to eicosanoid production?
Inhibit phospholipase which converts phospholipids to arachidonic acid.
51
What are LTC4, LTD4, LTE4?
Leukotrienes; slow reacting substances of anaphylaxix. Bronchoconstriction, vasoconstriction, increased permeability
52
What is LTB4
Chemotactic leukotriene
53
How long before catecholamines peak after injury?
24-48 hours
54
Where is Norepinephrine released from?
Sympathetic postganglionic neurons and Adrenal Medulla
55
Where is Epinephrine released from?
Adrenal Medulla
56
What are the neuroendocrine responses to injury?
Afferent nerves from injury site stimulate CRF, ACTH, ADH, Growth Hormone, Epi, Nor-Epi