Chapter 13 - Inflammation and Cytokines Flashcards Preview

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Flashcards in Chapter 13 - Inflammation and Cytokines Deck (56):
1

Injury to the epithelium causes:

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

2

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

platelet derived growth factor; PMN and Macrophage

3

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

Macrophages. PDGF, IL-1 and TNF-alpha

4

Actions of PDGF:

-chemotactic and activates PMNs and Macros
-Chemotactic and activates fibroblasts
-Angiogenesis
-Epithelialization
-Chemotactic for smooth muscle

5

Actions of EGF:

-chemotactic and activates fibroblasts
-Angiogenesis
-Epithelialization

6

Actions of FGF (Fibroblastic growth factor):

-Chemotactic and activates fibroblasts
-Angiogenesis
-Epithelialization

7

Platelet Activating factor generated where? does what?

Generated by phospholipase in endothelium
-Stimulates inflammatory cells, chemotactic, increases adhesion molecules

8

These cytokines are chemotactic for inflammatory cells:

-TGF beta
-PDGF
-IL-8
-LTB-4
-C5a and C3a
-PAF

9

These cytokines are chemotactic for Fibroblasts:

-TGF-beta
-PDGF
-EGF
-FGF

10

These cytokines cause angiogenesis:

-TGF-beta
-EGF
-FGF
-TGF-alpha
-IL-8
-Hypoxia

11

These cytokines cause epithelialization:

-TGF-beta
-PDGF
-EGF
-FGF
-TGF-alpha

12

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

1-2 days in tissue, 7 days in blood

13

How long to Platelets last?

7-10 days

14

How are eosinophils involved in type I hypersensitivity reactions?

-Have IgE receptors for allergen
-Release major basic protein- stimulates basophils and mast cells to release histamine

15

How are Basophils involved in type I hypersensitivity reactions?

-Have IgE receptors
-Main source of histamine in blood

16

How are Mast cells involved in type I hypersensitivity reactions?

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

17

What does Histamine do?

-Vasodilation
-Tissue edema
-Postcapillary leakage

18

What does Bradykinin do?

-Vasodilation
-Increased Permeability
-Pain
-Contraction of Pulmonary Arterioles

19

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

TNF alpha and IL-1

20

This cell type is the major producer of TNF

Macrophages

21

Cachexia is mediated by this cytokine

TNF

22

TNF's main functions are?

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

23

This cell is the main source for IL-1

Macrophages

24

IL-1 causes fever through this mechanism

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