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MOD > Chapter 3 Part 4 > Flashcards

Chapter 3 Part 4 Flashcards

1
Q

What are the mediators of vasodilation?

A

histamine and prostaglandins

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2
Q

What are the mediators of increased vascular permiability?

A

histamine, serotonin, C3a and C5a, leukotrienes (C, D, and E)

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3
Q

What are the mediators of chemotaxis?

A

TNF, IL-1, chemokines, C3a, C5a, leukotriene B

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4
Q

What are the mediators of a fever?

A

IL-1, TNF, prostaglandins

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5
Q

What are the mediators of pain?

A

prostaglandins and bradykinin

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6
Q

What are the mediators of tissue damage?

A

lysosomal enzymes of leukocytes and ROS

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7
Q

Definition of repair

A

restoration of tissue architecture and function after an injury

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8
Q

What two reactions must occur to repair damaged tissues?

A

regeneration/proliferation by residual cells and maturation of tissue stem cells; formation of a connective tissue scar

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9
Q

What is tissue regeneration dependent on?

A

The ability of tissues to intrinsically proliferate, a process driven by growth factors

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10
Q

What cell types proliferate during tissue repair?

A

remnants of injured tissue, vascular endothelial cells, fibroblasts

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11
Q

Define labile cells

A

Cells that continuously divide, are lost and replaced by maturation of stem cells; examples include surface epithelia, hematopoietic cells, cuboidal epithelia of exocrine glands, columnar epithelium of GI,etc.

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12
Q

Define stable tissues

A

Quiescent cells in G0 that have minimally proliferative activity; examples include liver, kidney, pancreas

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13
Q

Define permanent tissues

A

cells that are terminally differentiated and nonproliferative; examples include neurons and cardiac muscle cells

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14
Q

What is the mechanism of tissue regeneration in labile tissues?

A

Injured cells are rapidly replaced by proliferation of residual cells and differentiation of stem cells on an intact basement membrane

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15
Q

What are the two cell types responsible for liver regeneration?

A

proliferation of hepatocytes and repopulation from progenitor cells

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16
Q

What is the first stage of hepatocyte proliferation in liver regeneration?

A

Priming; Kupffer cells release IL-6 to make hepatocytes competent to respond to growth factor

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17
Q

What is the second stage of hepatocyte proliferation in liver regeneration?

A

Growth factor; HGF and TGF-alpha stimulate hepatocyte metabolism, triggering the differentiation of almost all parenchymal and nonparenchymal hepatocytes

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18
Q

What is the third stage of hepatocyte proliferation in liver regeneration?

A

Termination; hepatocytes return to quiescence, mechanism unknown (possibly TGF-B)

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19
Q

Where do liver progenitor cells reside?

A

Canals of Hering

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20
Q

What are the steps of scar formation?

A

Angiogenesis, formation of granulation tissue, remodeling of connective tissue

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21
Q

What role do macrophages play in scar formation?

A

Clear dead tissue and offending agent, provide growth factors for cell proliferation, secrete cytokines that stimulate fibroblast proliferation and connective tissue synthesis

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22
Q

Definition of angiogenesis

A

Process of new blood vessel development from existing blood vessels

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23
Q

What is the first step of angiogenesis?

A

Vasodilation in response to nitric oxide and increased permeability by VEGF

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24
Q

What is the second step of angiogenesis?

A

Separation of pericytes from albuminal surface and breakdown of basement membrane to allow for vessel sprouting

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25
Q

What is the third step of angiogenesis?

A

Migration of endothelial cells toward area of tissue injury

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26
Q

What is the fourth step of angiogenesis?

A

Proliferation of endothelial cells just behind the tip of migrating cells

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27
Q

What is the fifth step of angiogenesis?

A

Remodeling capillary tubes

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28
Q

What is the sixth step of angiogenesis?

A

Recruitment of pericytes to form mature vessel

29
Q

What is the seventh step of angiogenesis?

A

Suppression of endothelial proliferation and migration and deposition of basement membrane

30
Q

What are the prominent growth factors involved in angiogenesis?

A

VEGF-A, FGF-2, Angiopoietins 1 and 2, PDGF, TGF-B

31
Q

What is the function of VEGF in angiogenesis?

A

Stimulates endothelial cell proliferation and migration, promotes vasodilation and formation of vascular lumen

32
Q

What is the function of FGF-2 in angiogenesis?

A

stimulates proliferation of endothelial cells and promotes migration of macrophages and fibroblasts

33
Q

What is the function of angiopoietins in angiogenesis?

A

Structural maturation of blood vessels by the recruitment of pericytes and smooth muscle

34
Q

What is the function of PDGF in angiogenesis?

A

recruitment of smooth muscle cells

35
Q

What is the function of TGF-B inangiogenesis?

A

suppresses endothelial proliferation and migration

36
Q

What is the notch signaling pathway?

A

regulates the sprouting and branching of new vessels

37
Q

What role do ECM proteins play in angiogenesis?

A

Form interactions with integrin receptors on endothelial cells and provide a scaffold for vessel growth

38
Q

What is the role of metalloproteinases in angiogenesis?

A

ECM degradation to permit remodeling and extension of vascular tube

39
Q

What two steps are involved in the deposition of connective tissue during scar formation?

A

migration and proliferation of fibroblasts to injury, deposition of ECM proteins produced by cells

40
Q

What are the main cell types involved in deposition of connective tissue?

A

M2 macrophages, mast cells, lymphocytes

41
Q

What is the most important cytokine for deposition of connective tissue in scar formation?

A

TGF-B

42
Q

What is the role of TGF-B in tissue deposition?

A

stimulates fibroblast migration and proliferation, increases synthesis of collagen and fibronectin, and decreases degradation of ECM by inhibiting metalloproteinases

43
Q

What are the levels of TGF-B regulated by?

A

Activation of latent TGF-B, rate of secretion of active molecule and ECM factors that enhance or diminish activity of TGF

44
Q

What components does scar tissue consist of?

A

fibroblasts, dense collagen, fragments of elastic tisue and other ECM components

45
Q

What cells contribute to scar contraction?

A

myofibroblasts

46
Q

What enzymes are primarily responsible for the remodeling of connective tissue?

A

matrix metalloproteinases

47
Q

What are the functions of matrix metalloproteinases?

A

cleavage of fibrillar collagen, amorphous collagen and fibronectin, degradation of proteoglycans and laminin

48
Q

What factors regulate matrix metalloproteinase functions?

A

Proteases activate, TIMPs inhibit

49
Q

What are key factors that can alter tissue repair?

A

infection, diabetes, nutritional status, glucocorticoids, mechanical factors, poor perfusion, foreign bodies, type and extent of injury, location of injury

50
Q

What defines healing by first intention?

A

injury involves only epithelial layer and requires epithelial regeneration

51
Q

What are the three steps of healing by first intention?

A

inflammation, proliferation, and maturation

52
Q

What initially happens when a wound occurs?

A

rapid activation of coagulation pathways and formation of a blood clot on the surface, acts as a scaffold for migrating cells

53
Q

What happens within the first 24 hours of a wound during healing by first intention?

A

Neutrophils migrate towards the fibrin clot and clear debris, basal cells at the edge of the debris begin to undergo mitosis and deposit components of basement membrane

54
Q

What should occur by day three during healing by first intention?

A

Neutrophils are replaced by macrophages and granulation tissue begins to invade the wound, collagen fibers begin to form

55
Q

What should occur by day five of healing by first intention?

A

Neovascularization and migration of fibroblasts (driven by TNF, TGF-B and FGF from macrophages)

56
Q

What occurs during the second week of healing by first intention>

A

Continued collagen accumulation and fibroblast proliferation, regression of vascular channels

57
Q

What defines healing by second intention?

A

extensive tissue loss involving a combination of regeneration and scarring

58
Q

What are some key differences between primary and secondary healing?

A

Secondary healing involves larger clot layers, exudate, and necrotic debris and larger amounts of granulation tissue, involves wound contraction

59
Q

What is the initial provisional matrix formed from in healing by second intention?

A

fibrin, plasma, fibronectin, type III collagen

60
Q

What is the second provisional matrix formed from in healing by second intention?

A

Type I collagen

61
Q

What is primarily responsible for the recovery of tensile strength after a wound?

A

excess collagen synthesis

62
Q

Define fibrosis

A

excessive deposition of collagen and other ECM components, often refers to abnormal development of collagen in damaged organs

63
Q

What are two complications of inadequate formation of granulation tissue?

A

wound dehiscence (wound rupture) and ulceration

64
Q

What causes keloid and hypertrophic scar formation?

A

Excessive formation of components of the repair process

65
Q

What is the difference between a keloid and a hypertrophic scar?

A

Hypertrophic scars occur due to excessive amounts of collagen within the boundary of the wound, Keloid formation occurs when the scar tissue grows beyond boundaries of the wound

66
Q

What is exuberant granulation?

A

Formation of excessive amounts of granulation tissue

67
Q

What is a desmoid or aggressive fibromatoses?

A

neoplasms that occur due to exuberant fibroblast proliferation and other connective tissue elements

68
Q

What is the result of abnormal wound contraction?

A

Contracture leading to wound deformities, commonly seen after serious burns and most commonly occur on palms, soles and anterior thorax

MOD (34 decks)

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