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Copy ABSITE Review: Fiser, Decker, SCORE, UpToDate, TrueLearn > Chapter 13 - Inflammation and Cytokines > Flashcards

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
Q

How does fever occur in atelectasis?

A

Alveolar macrophages release IL-1

26
Q

What does IL-1 do to IL-6 production?

A

increases it

27
Q

What does IL-6 do?

A
  • Increases hepatic acute phase proteins (CRP, amyloid A)
  • Lymphocyte activation
28
Q

What cells release interferons?

A

Lymphocytes in response to viral infections

29
Q

What do interferons do?

A
  • Activate macs, natural killer cells, cytotoxic T cells
  • Inhibit viral replication
30
Q

These proteins are increased in Hepatic Acute Phase Response:

A
  • CRP (opsonin, ^ complement) - most important
  • Amyloid A and P
  • Fibrinogen
  • Haptoglobin
  • Ceruloplasmin
  • Alpha 1 antitrypsin
  • Alpha 1 chymotrypsin
  • Complement
31
Q

These proteins are decreased in the hepatic acute phase response:

A
  • Albumin
  • Transferrin
32
Q

The first step in cell adhesion:

A

Rolling; L-selectins on leukocytes bind to E and P selectins

33
Q

Second step in cell adhesion:

A

Anchoring; Beta 2 Integrans (CD11/18 molecules) in leukocytes bind ICAMs

34
Q

Where are ICAM, VCAM, PECAM, FLAM located and what do they do?

A
  • Endothelial cells
  • Bind Beta 2 Integrins
  • Also help with transendothelial migration
35
Q

The classic complement pathway is activated by what?

A

Antigen-Antibody Complex (IgG or IgM)

36
Q

These factors are found only in the classic pathway:

A
  • C1
  • C2
  • C4
37
Q

The alternative pathway is activated by what?

A
  • endotoxin
  • bacteria
38
Q

These factors are found only in the alternative pathway:

A

B, D, and P (Properdin)

39
Q

This factor is common to both classic and alternative pathways and is the convergence point:

A

C3

40
Q

This electrolyte is needed for both the classic and alternative pathways

A

Mg

41
Q

These are the anaphylatoxins of the complement, they do what?

A

C3a, C4a, C5a

increase vascular permeability, smooth muscle contraction, activate mast cells and basophils

42
Q

This is the membrane attack complex of complement

A

C5b-9b

43
Q

Complement Opsonization is caused by what complement component:

A

C3b

44
Q

Complement Chemotaxis is caused by what complement components:

A

C3a and C5a

45
Q

PGI2 and PGE2 cause what?

A
  • vasodilation
  • bronchodilation
  • vascular permeability
  • inhibit platelets
46
Q

PGD2 causes what?

A
  • Vasodilation
  • Bronchoconstriction
  • Increased vascular permeability
47
Q

NSAIDs do what?

A

Inhibit cyclooxygenase reversibly

48
Q

Aspirin does what?

A
  • Inhibits cyclooxygenase irreversibly
  • Inhibits platelet adhesion by decreasing TXA2
49
Q

Steroids do what to eicosanoid production?

A

Inhibit phospholipase which converts phospholipids to arachidonic acid.

50
Q

What are LTC4, LTD4, LTE4?

A

Leukotrienes - slow reacting substances of anaphylaxix

Bronchoconstriction, vasoconstriction, increased permeability

51
Q

What is LTB4

A

Chemotactic leukotriene

52
Q

How long before catecholamines peak after injury?

A

24-48 hours

53
Q

Where is Norepinephrine released from?

A

Sympathetic postganglionic neurons and Adrenal Medulla

54
Q

Where is Epinephrine released from?

A

Adrenal Medulla

55
Q

What are the neuroendocrine responses to injury?

A

Afferent nerves from injury site stimulate CRF, ACTH, ADH, Growth Hormone, Epi, Nor-Epi

Copy ABSITE Review: Fiser, Decker, SCORE, UpToDate, TrueLearn (50 decks)

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