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
  • Activates PMNs and Macros
  • Activates fibroblasts
  • Angiogenesis
  • Epithelialization
  • Chemotactic for smooth muscle
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5
Q

Actions of EGF:

A
  • Chemotactic
  • Activates fibroblasts
  • Angiogenesis
  • Epithelialization
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6
Q

Actions of FGF (Fibroblastic growth factor):

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