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GPAT > inflammation and repair > Flashcards

inflammation and repair Flashcards

1
Q

inflammation

A

a complex reaction important in the process of repair that leads to the accumulation of fluid and leukocytes (white blood cells) in vascularized tissue. it is fundamentally a protective response that, if dysregulated, can cause harm

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2
Q

acute

A

short duration, most characterized by vascularized tissue. it is fundamentally a protective response that, if dysregulated, can cause harm

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3
Q

acute

A

short duration, mostly characterized by vascular changes that lead to edema of surrounding tissues and infiltration by neutrophils (also called polymorphonuclear leukocytes (PMNLs) or polys

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4
Q

chronic

A

longer duration, characterized by lymphocytes and macrophages (monocytes), tissue destruction by these cells and an attempt at at tissue repair via proliferation of blood vessels (angiogenesis) and connective tissue (fibrosis and scarring)

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5
Q

classic local signs of inflammation

A

rubor (redness)
swelling (tumor)
pain (dolor)
warmth (calor)

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6
Q

systemic signs of inflammation

A

fever
increased white cell count
enlargement of lymph nodes

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7
Q

associated microscopic events of redness & heat

A

dilation of microcirculation

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8
Q

associated microscopic events of swelling

A

permeability of vessels leads to exudate formation in tissues

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9
Q

associated microscopic events of pain

A

pressure on nerves by exudate, release of chemical mediators inducing pain

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10
Q

associated microscopic events of loss of normal tissue function

A

the result of swelling and pain

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11
Q

inflammatory response

A

1) injury
2) constriction of the microcirculation
3) dilation of small blood vessels
4) increase in permeability of small blood vessels
5) exudate leaves small blood vessels

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12
Q

hyperemia

A

increased blood flow that floods the capillary beds in the injured tissue

responsible for redness (erythema) and heat

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13
Q

exudate

A

inflammatory fluid formed as a reaction to injury of tissues and blood vessels

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14
Q

serous exudate

A

composed mainly of plasma fluids and proteins with a few white blood cells

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15
Q

purulent exudate (supparation)

A

contains tissue debris and many white blood cells, in additon to plasma fluids and proteins

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16
Q

fistula

A

a passage through the tissues which allows the excess exudate to drain

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17
Q

incision and drainage

A

surgical procedure for the removal of the excessive exudate

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18
Q

vasoactive factors

A 
histamine
seratonin
bradykinin
LTs/PGs
PAF
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19
Q

chemotactic factors

A 
C5a
LTB
formylated peptides
lymphokines
monokines
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20
Q

increase vascular permeability

A

edema

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21
Q

margination

A

the movement of the white blood cells to the periphery of the blood vessel walls

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22
Q

adhesion or pavementing

A

the adherence of white blood cells to the blood vessel walls

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23
Q

chemotaxis and emigration

A

the directed movement of white blood cells to the area of injury by chemical mediators which are called chemotactic factors (chemotaxis) and then the passage of white blood cells through the endothelium and wall of the microciruclation into the injured tissue (emigration)

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24
Q

phagocytosis and intracellular degradation

A

white blood cells ingest foreign material

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25
Q

extraceullar release of leukocyte producets

A

granules can release their contents into the tissue causing tissue damage

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26
Q

cellular events in acuste inflammation

A

1) margination
2) adhesion or pavementing
3) chemotaxis and emigration
4) phagocytosis and intracellular degradation
5) extracellular release of leukocyte products

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27
Q

exudation

A

neutrophils are the most prominent inflammatory cell in the first few hours (acute inflammation)

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28
Q

cytokines

A

activator; must be made in the cell –> further inflammation (attracting more cells); systemic effects like fever

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29
Q

prostaglandins

A

activator; must be made in the cell –> further inflammation; pain (aspirin)

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30
Q

histamine

A

activator; released from granules –> vasodilation and increased vascular perm. (anti-histamines)

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31
Q

complement

A

activator; increase in vascular perm.; attacts inflammatory cells; attacks microorganisms

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32
Q

kinins

A

activator; increase in vascular perm; pain

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33
Q

clotting

A

activator; coagulation

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34
Q

resolution

A

involves neutralization or removal of the chemical mediators of actue inflammation with subsequent normalization of vascular permeabiltiy and halting of leukocyte emigration; the combined efforts of lymphatic drainage and macrophage digestion lead to clearance of edema fluid, inflammatory cells and enecrotic debirs, resulting in the restoration of the inflammatory site to histologic and functional normalcy

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35
Q

when does resolution occur

A

1) the injury is limited or short lived
2) there has been minimal tissue destruction
3) the tissue is capable of regeneration

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36
Q

scarring (fibrosis)

A

extensive fibrinous exudates that cannot be absorbed are instead organized by ingrowth of connective tissue elements, resulting in a mass of fibrous scar tissue

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37
Q

scarring occurs when

A

1) inflammation affects tissues that cannot regenerate

2) there has been substantial tissue destruction

38
Q

abscess formation

A

occurs in the setting of certain pyogenic bacterial or fungal infections

39
Q

chronic inflammation

A

1) infiltration with mononuclear “chronic inflammatory” cells which include macrophages, T lymphocytes, and plasma cells
2) tissue destruction, largely due to the inflammatory cells themselves
3) repair involving new vessel proliferation (angiogenesis) and scarring (fibrosis)

40
Q

chronic inflammation

A

inflammation of prolonged duration (months to years) in which active inflammation, tissue injury and healing proceed simultaneously

41
Q

persistent infections

A

by a select of microorganisms including mycobacteria (tuberculosis bacilli), trepponema pallidum (syphilis) and some fungi; these are generally organisms of low pathogenicity that evoke delayed hypersensitivity reactions in the host (sometimes leading to a granulomatous reaction)

42
Q

settings where chronic inflammation arises

A

1) persistent infections
2) prolonged exposure to toxic agents
3) autoimmune diseases

43
Q

chronic inflammatory cells

A

1) tissue macrophages
2) t lymphocytes
3) plasma cells
4) eosinophils

44
Q

tissue macrophages

A

originate as monocytes in the blood; they will migrate out to the site of injury 24-48 hours after the onset of acute inflammation, where they are then called tissue macrophages. macrophages specialize in ingesting debris and microorganisms and producing cytokines, important inflammatory mediators that recruit and activate T lymphocytes

45
Q

T lymphocytes

A

in turn, will stimulate macrophage activity by producing their own cytokines

46
Q

plasma cells

A

B lymphocytes that make antibodies

47
Q

eosinophils

A

associated with allergic reactions and parasites

48
Q

macrophage activation

A

chemokines, especially RANTES, MCP-1 and MIP-1 are secreted by monocytes, smooth muscle cells and fibroblasts in damagedtissue, which then recruit and activate monocytes and changes their integrin configuration, allowing them to bind VCAMs and ICAms on endothelium and migrate out into the tissues in a manner analagous to neutrophils

lymphokines from T lymphocytes recruit and activate macrophages; activated macrophages increase in size and produce more lysosomal enzymes as well as cytokines and growth factors of their own that influence blood vessel and smooth muscle cell growth; these factors regulate local healing and formation of the final scar

49
Q

fibrosis

A

GFs (PDGF, FGF, TGFB)
fibrogenic cytokines
angiogenesis factors (FGF)
remodeling (collagenases)

50
Q

tissue injury

A 
toxic oxygen metabolites
proteases
neutrophil chemotractic factors
coagulation factors
A.A. metabolites
nitric oxide
51
Q

IL-1, TNF-apha acute phase reaction

A 
fever (via PGE)
increase sleep
decrease appetite, muscle wasting
increase acute phase proteins
hemodynamic effects (shock)
neutrophilia
52
Q

IL-1, TNF-alpha endothelial effects

A 
increase luekocyte adherence
increase PGI synthesis
increase PAG
increase pro-coagulant activity
decrease anti-coagulant acitivyt
53
Q

IL-1, TNFalpha fibroblast effects

A

increase proliferation
increase collagenase
increase protease
increase pGE sythesis

54
Q

systemic manifestations of chronic inflammation

A

fever
leukocytosis
acute phase response

55
Q

fever

A

endogenous pyrogens (IL-1, TNFalpha0

56
Q

luekocytosis

A

an increase in the numbers of circulating leukocytes due to release of IL-1, TNFalpha

57
Q

acute phase response

A

fever, leukocytosis, decreased appetite, altered sleep patterns, acute phase proteins; increase erythrocyte sedimentation (ESR) reflects higher plasma levels of acute phase proteins

58
Q

b lymphocytes

A

terminally differentiate into plasma cells and eisinophils

59
Q

non-specific inflammation

A

mononuclear cell infiltrate with a proliferation of fibroblasts and new blood vessels; chronic inflammation can be the initial response in viral infections, parasitic infections, autoimmune disease and malignancy

60
Q

granulomatous inflammation

A

characterized by granulomas (collections of activated macrophages called “epithelial cells” surrounded by a rim of lymphocytes, +/- gaint cells); IFNgamma and IL_4 released by T lymphocytes modified macrophages, sometimes resulting in their fusion to form multinucleated giant cells. granulomatous ifnlammation occurs in response to bacterial infections fungal infections, parasitic infections, inorganic metals or dusts, forign body reactions, diseases of uknown cause

61
Q

stable cells

A

form tissues that normally are renewed very slowly but are capable of rapid renewal after tissue loss (liver, proximal renal tubules, endocrine glands, endothelium); in these tissues the ability to regenerate depends on the potential to replicate, not the actual number of steady-state mitoses

62
Q

permanent cells

A

permanent cells are terminally differentiated and have lost all capacity for regeneration (neurons, cardiac monocytes, cells of the lens)

63
Q

EGF

A

mitogenic for epithelial cells and fibroblasts

64
Q

PDGF

A

released from platelet alpha granules but is also produced by activated macrophages, endothelial cells, smooth muscle cells and a variety of transformed cells; it induces fibroblast, smooth muscle cell and monocyte migration and proliferation

65
Q

FGF

A

made by active macrophages and binds to heparin and other anionic ECM components, so it has a strong affinity for the basement membrane. it strongly promotes angiogenesis.

66
Q

TGF-beta

A

made by a many cell types in an active form that needs to be proteolytically cleaved to become functional; it has a variety of effects but generally is growth inhibitory for epithelial cells and promotes fibrinogenesis and scarring - it stimulate fibroblast chemotais and production of collagen and fibronectin and inhibits digestion of the ECM by metalloproteinases

67
Q

VEGF

A

there are many isoforms; it is made by tumor cells and promotes angiogenesis and vascular permeability; increased vessel leakiness leads to deposition of plasma proteins, such as fibrinogen, out in the tissues, which provides a provisional stroma for fibroblast and endothelial cell ingrowth

68
Q

cytokines (IL-1, TNF-aplpha)

A

chemotactic and mitogenic for fibroblasts, an also induces synthesis of collagen and collagenases

69
Q

basement membrane

A

structures that separate epithelial and endothelial cells, schwann cells in the PNS and adipocytes and all types of muscle cellsm from the stroma; it provides polarity and is required for orderly renewal of tissue, particularly epithelieum

70
Q

collagen

A

widely represented in the body and has mainly mechanical functions; collagen fibers provide strength and support; there are many types, most of which form strong, triple helical fibers

71
Q

type I

A

collagen is the principle collagen of bone, skin, and tendons and the predominant collagen in mature scars

72
Q

type II

A

collagen is the major collagen in cartilage

73
Q

type III

A

collagen is adbundant in embryonic tissues, blood vessels, uterus and GI tract

74
Q

type IV

A

collage in found exclusively in basement membranes

75
Q

type V-XXII

A

basement membranes

76
Q

glycoproteins

A

a structurally diverse group of proteins whose role is to link ECM components to cells and to one another; these include fibronectin (which binds integrins), laminin (the most abundant protein in the BM), and thrombospondins

77
Q

proteoglycans

A

includes glycosaminoglycans like dermatan sulfate and heaprin sulfate that help maintan ECM structure and permeability

78
Q

fibrosis steps

A

1) angiogenesis
2) migration and proliferation of fibroblasts
3) deposition of Ecm
4) maturation and organization of the scar

79
Q

events that occur during healing

A

induction of acute inflammation following initial injury –> parenchymal cell regeneration (if possible) –> migration and proliferation of parenchyma an connective tissue cells –> synthesis of ECM components –> remodeling of parenchyma and ECM to restore function and increase wound strenght

80
Q

events that occur during healing day of injury

A

clot formation

fibrin+
RBCs+
platelets

81
Q

events that occur during healing day 1

A

neutrophils

phagocytosis

82
Q

events that occur during healing day 2

A 
macrophages
lymphocytes
plasma cells
fibroblasts
epitheliial cells
granulation tissue formation
epithelial proliferation and migration
83
Q

events that occur during healing one week

A 
fibrin digestion
initial repair complete
inflammation complete
granulation tissue formation
epithelial proliferation and migration
84
Q

events that occur during two weeks

A

scar

85
Q

healing by primary intention

A

a clean incision with approximal ends; as a result, epithelial regneration predomintes over fibrosis. little granulation tissue forms and less scar tissue resutls

86
Q

healing by secondary intention

A

where cell or tissue loss is extensive (large, ulcer, abscess or open wound); there can be extensive granulation tissue and scarring with a great deal of wound contraction (due to myofibroblasts)

87
Q

healing by tertiary intention

A

waiting until an infection is resolved before performing tissue repeair

88
Q

local factors that influence healing

A

wound type, size and location
vascular supply
infection
movement

89
Q

systemic factors that influence helaing

A

circulatory status
infection
metabloic status
malnutrition

90
Q

complications of wound healing

A

deficient scar formation (dehiscence and incisional, hearnias, ulceration); extensive scar formation (hypertrophic scar formation); exxcessive contraction (contractures)

GPAT (3 decks)

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