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MOD-E1 > Chapter 3: inflammation and repair > Flashcards

Chapter 3: inflammation and repair Flashcards

1
Q

in acute respiratory distress syndrome which immune cells are most involved

A

neutrophils

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2
Q

in asthma, which immune cells are most involved

A

Eosinophils, IgE ab

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3
Q

in glomerulonephritis which immune cells are most involved

A

Ab and complement; neutrophils monocytes

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4
Q

in septic shock which immune components are most involved

A

cytokines

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5
Q

in arthritis which immune cells are most involved

A

lymphocytes macrophages; ab?

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6
Q

in atherosclerosis which immune cells are most involved

A

macrophages; lymphocytes

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7
Q

in pulmonary fibrosis which immune cells are most involved

A

macrophages; fibroblasts

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8
Q

five R’s of inflammatory response

A 
recognition
recruitment
removal 
regulation
resolution
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9
Q

cardinal signs of inflammation

A 
rubor 
tumor
calor
dolor
functio laesa (loss of fxn)
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10
Q

what can trigger inflammatory responses

A

infection***
tissue necrosis
foreign bodies
immune reactions

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11
Q

three major components of acute inflammation

A

dilation of small vessels –> increase flow, but slow (stasis)
increasaed dpermeability
emigration of leukocytes

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12
Q

what is exudation

what is an exudate and what does it indicate

A

escape of fluid proteins and blood cells from vascular system into interstitial tissue or body cavities

exudate – high protein
indication of increased permeability triggered by some sort of injury and ongoing inflammatory rxn

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13
Q 
define
exudate
transudate
edema
pus
A

exudate - high protein
transudate - low protein
edema - excess fluid in interstitial tissue or serous cavity
pus - purulent exudate w/ neutrophils, debris of dead cells, microbes

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14
Q

what induces increased vascular permeability

A

histamine

kinins

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15
Q 
key players in the steps of leukocyte recruitment
rolling
activation
adhesion
transmigration
A

rolling- selectins (P, E, L – on leukocytes)
activation - chemokines/cytokines – increase affinity of integrins (TNF?, IL-1?)
adhesion - integrins (ICAM-1, VCAM-1)
transmigration - PECAM-1 (CD31)

chemokines usually presented bound to proteoglycans

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16
Q

what causes margination

A

in early inflammation, blood flow increases, but is slow (stasis)
wall shear stress dereases
more white blood cells assume positions closer to walls of endothelium

leads to rolling

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17
Q

where does transmigration of leukocytes mainly occur

A

post capillary venules

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18
Q

what is the main exogenous chemoattractant

A

N-formylmethionine (start codon for bacterial DNA)

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19
Q

what are some endogenous chemoattractants (3)

A

cytokines
complement
arachidonic acid metabolites (LTB4)

all bind to specific GPCRs

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20
Q

what is one of the most successful therapies for treating chronic inflammatory diseases

A

agents that block TNF

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21
Q

steps of phagocytosis

A

recognition and attachment
engulfment
killing or degradation

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22
Q

types of phagocytic receptors

ligand?

A

mannose-binding – mannose sugar on microbial cell walls
scavenger – usually acetylated LDL molecules
opsonin binding – c3b, IgG

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23
Q

describe engulfment

A

after recognition, phagocyte’s pseudopodia surround the particle and pinches off part of its PM to form a phagosome

phagosomes fuse with lysosomes to form phagolysosomes

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24
Q

where are ROS produced

A

within the lysosome/phagolysosome

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25
Q

what ROS do neutrophils utilize

A

myeloperoxidase (MPO)

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26
Q

which type of NOS is used in the killing of microbes

A

iNOS by M0 and N0

activated by cytokines

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27
Q

effects of NO on cells

A

damages lipids, proteins, and nucleic acids of microbes and host cells

also relaxes vascular smooth m and promotes vasodilation

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28
Q

what two main types of granules do N0 have

A 
smaller specific (secondary) granules 
azurophil (primary) granules

primary includes the MPO

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29
Q

what regulates lysosomal enzymes

what are some examples

A

antiproteases

a1-antitrypsin
a2-macroglobulin

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30
Q

what microbicidal granule content is utilized by eosinophils to combat multicell. ags

A

major basic protein

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31
Q

what are NETs

A

extracellular fibril network w/ high concentration of antimicrobial substances at sites of infection and prevent the spread of microbes by trapping them

produced by neutrophils

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32
Q

which T cells are most important in the contribution to acute inflammation

A

Th17

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33
Q

absence of effective Th17 responses can result in what

A

increased susceptibility to fungal and bacterial infections

“cold abscesses”

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34
Q

in the termination of acute inflammatory responses, what occurs with active termination mechanism

A

switches arachidonic acid metabolite produced from proinflammatory leukotrienes (LTB4) to anti-inflammatory cytokines (TGF-b, IL-10)

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35
Q

most important mediators of acute inflammation

A

vasoactive amines, lipid products (prostaglandins and leukotrienes), cyto/chemokines, products of complement activation

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36
Q

examples of vasoactive amines (2)

A

histamine
serotonin

stored as preformed molecules in cells
among first to be released in inflammation

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37
Q

primary f(x) of serotonin as a vasoactive amine

A

vasoconstrictor in GI

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38
Q

arachidonic acid metabolites (2)

A

leukotrienes

prostaglandins

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39
Q

what GPCR ligand can mediate virtually every step of inflammation

A

eicosanoids (leukotrienes and prostaglandins)

lipoxins

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40
Q

actions of what enzymes generate prostaglandins

A

cyclooxygenases

COX-1 and COX-2

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41
Q

which prostaglandins are involved in vasodilation?

vasoconstriction?

A

dilation: prostacyclin, PGE1/2, PGD2
constriction: thromboxane A2 (TxA2)

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42
Q

which prostaglandin is a potent inhibitor of platelet aggregation

A

prostacyclin (PGI2)

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43
Q

leukotrienes are produced by the actions of which enzymes?

what processes are they involved in

A

lipoxygenase

involved in vascular and smooth m reactions and leukocyte recruitment

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44
Q

which leukotriene is involved in chemotaxis and leukocyte adhesion

A

LTB4

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45
Q

what are the functions of LTC4, LTD4, LTE4

A

vasoconstriction, increased vascular permeability of venules, bronchospasm

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46
Q

f(x) of lipoxins

A

suppress inflammation by inhibiting the recruitment of leukocytes

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47
Q

what do platelets do in the process of lipoxin synthesis

A

convert intermediates created by neutrophils into lipoxins

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48
Q

which chemokine receptors act as coreceptors for HIV and thus are involved in binding and entry of the virus into cells

A

CXCR-4 and CCR-5

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49
Q

three main functions of complement

A

inflammation
opsonization and phagocytosis
cell lysis

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50
Q

of the inflammation mediators in the complement pathway, which is strongest

A

C3a>C5a>C4a

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51
Q

what is another function of C5a that will further increase inflammatory responses

A

activates lipoxygenase pathway of AA metabolism –> leukotrienes in N0 and monocytes

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52
Q

important regulatory proteins for the complement pathway

A

C1 INH - blocks C1 activation

DAF - prevents formation of C3 convertases (C4b2a, C3bBb)
CD59 - prevents formation of MAC

DAF and CD59 are linked by a glycophosphatidyl (GPI) anchor

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53
Q

hereditary angioedema

A

inherited deficiency of C1 INH

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54
Q

paroxysmal nocturnal hemoglobinuria

A

acquired deficiency of enzyme that creates GPI anchors btw DAF and CD59

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55
Q

functions of PAF

A

platelet aggregation
vasoconstriction bronchospasm

in low concentrations induces vasodilation and increased venular permeability

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56
Q

how are bradykinins produced

A

cleavage of kininogen by kallikrein

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57
Q

effects of bradykinin

A

increase vascular permeability, contraction of smooth m, vasodilation, pain when injected into the skin

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58
Q

morphologic patterns of acute inflammation and examples

A

serous inflammation - skin blister from burn
fibrous inflammation - fibrinous pericarditis
purulent inflammation - acute appendicitis/abscess
ulcers - bed sores

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59
Q

pyogenic definition

A

pus producing

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60
Q

most frequent cause of purulent inflammation

A

bacterial infections that cause liquefactive necrosis – staph

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61
Q

most common sites to encounter ulcers

A

mucosa of mouth, stomach, intestines, or genitourinary tract

skin and subQ tissue of LE in older pts w/ circulatory disturbances

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62
Q

ulcers definition

A

local defect or excavation of the surface of an organ or tissue that is produced by sloughing of inflamed necrotic tissue

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63
Q

acute stage of ulcer

A

polymorphonuclear infiltration and vascular dilation

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64
Q

chronic stage of ulcer

A

margin and base develop fibroblastic prolif, scarring, and accumulation of lymphocytes, m0, and plasma cells

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65
Q

outcomes of acute inflammation (3)

A

complete resolution
healing by CT replacement
chronic inflammation

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66
Q

when does scarring or fibrosis occur (3)

outcome of acute inflammation

A

after substantial tissue destruction

when tissues injured are incapable of regen

abundant fibrin exudation in tissue or serous cavities that cannot be adequately cleared

67
Q

what is organization

scarring or fibrosis

A

CT growing into the area of damage or exudate and converting it into a mass of fibrous tissue

68
Q

what accounts for the signs and symptoms of the inflammatory response

A

vascular and cellular reactions

69
Q

causes of chronic inflammation (3)

A

persistent infections

hypersensitivity diseases

prolonged exposure to potentially toxic agents, endogenous or exogenous

70
Q

morphologic features of chronic inflammation

A

infiltration with mononuclear cells - m0, lymphocytes, plasma cells

tissue destruction - induced by persistent offending agent or by inflammatory cells

attempts at healing - by CT replacement of damaged tissue, accomplished by angiogenesis and fibrosis

71
Q

dominant cell type in most chronic inflammatory reaction

A

macrophages

72
Q

specific macrophages

A

liver - kuppfer
spleen and LNs - sinus histiocytes
CNS - microglial
lungs - alveolar macrophages

73
Q

where do macrophages develop from

A

bone marrow, fetal liver, yolk sac

74
Q

half-life of tissue macrophage

A

several months or years

75
Q

half-life of blood monocytes

A

~1 day

76
Q

what stimulates classical macrophage activation

A

microbes, IFN-gamma

77
Q

what do M1 macrophages produce

A

ROS, NO, inflammatory cytokines (1, 12, 23)

78
Q

what stimulates alternatively activated macrophages

A

IL-4, IL-13

79
Q

principal function of M2 macrophages

A

tissue repair

80
Q

what do M2 macrophages produce

A

GFs, TGF-beta, IL-10

81
Q

functions of macrophages in general (4)

A

phagocytose

tissue repair (scar formation and fibrosis)

secrete mediators of inflammation (TNF, IL-1, eicosanoids)

APC to T-cells and respond to signals from T-cells

82
Q

what does each type of T-cell secrete

A

Th1 - IFN-gamma –> classical M0 activation
Th2 - IL-4, 5, 13 –> alternative M0 activation
Th17 - IL-17 –> N0 and monocyte recruitment

83
Q

which T-cell helps in defense against helminths

A

Th2 –> IL-4, 5, 13 –> IgE and Eosinophil recruitment

84
Q

which T-cells are involved in defense against virus/bacteria

A

Th1, Th17

85
Q

what is responsible for granulomatous inflammation

A

T and B lymphocytes

86
Q

what are tertiary lymph nodes

A

clusters of accumulated lymphocytes, APCs, and plasma cells

87
Q

in which conditions can tertiary LNs be seen

A

some chronic inflammatory rxns
long-standing RA
hashimoto thyroiditis

88
Q

which cell type binds to IgE in allergic responses

A

Mast cells
have FceRI
release histamine and prostaglandins

89
Q

what is granuloma formation

A

a cellular attempt to contain an offending agent that is difficult to eradicate

90
Q

what is a granulomatous inflammation

A

form of chronic inflammation characterized by collections of activated M0, often with T lymphocytes, and sometimes associated with central necrosis

91
Q

what are epithelioid cells

A

activated M0s that develop abundant cytoplasm and begin to resemble epithelial cells (granulomatous inflammation)

92
Q

what are giant cells

A

fused activated M0

multinuclear

93
Q

two types of granulomas

A

foreign body granuloma

immune granuloma

94
Q

foreign body granuloma

A

caused by foreign body
can form around talc (IVD use), sutures, other large fibers
do NOT produce inflammatory or immune response

95
Q

immune granuloma

A

caused by variety of agents capable of inducing persistent T cell-mediated immune response
occurs with microbes particularly hard to kill

96
Q

when looking at a granuloma, what is the first disease you need to rule out

A

TB

97
Q

diseases with granulomatous inflammation

A 
TB
leprosy
syphilis
cat-scratch disease
sarcoidosis
crohn disease - U.S!!
98
Q

TB

A 
caused by mycobacterium tuberculosis
caseating granuloma (tubercle)
99
Q

leprosy

A

mycobacterium leprae

noncaseating granuloma

100
Q

Syphilis

A

treponema pallidum

gumma: microscopic to grossly visible lesion, enclosing wall of histiocytes

101
Q

cat-scratch disease

A

gram-negative bacillus

rounded or stellate granuloma central granular debris and recognizable N0; giant cells uncommon

102
Q

sarcoidosis

A

unknown etiology

noncaseating granuloma w/ abundant activate M0

103
Q

Crohn disease

A

immune reaction against intestinal bacteria, possibly self Ags
occasional noncaseating granulomas in the wall of the intestine, with dense chronic inflammatory infiltrate

104
Q

important mediators of the acute-phase reaction

A

IL-1, IL-6, TNF

105
Q

exogenous pyrogen

A

bacterial products (LPS)

106
Q

endogenous pyrogens

A

IL-1, TNF –> increase COX –> increase in prostaglandins

107
Q

what can stimulate the production of neurotransmitters that reset the temperature set point at a higher level

A

prostaglandins (PGE2)

108
Q

how do NSAIDs (aspirin) reduce fever

A

inhibit production of prostaglandins

109
Q

examples of acute-phase proteins (3)

A

C-reactive protein (CRP)
fibrinogen
serum amyloid A (SAA)

110
Q

what is the basis for the erythrocyte sedimentation rate

A

fibrinogen binds to red cells and causes them to form stacks (rouleaux) that sediment more quickly than RBCs at unit gravity

111
Q

what can cause secondary amyloidosis

A

prolonged production of acute-phase proteins (especially SAA) in states of chronic inflammation

112
Q

how does CRP and SAA work

A

attaches to cell walls

opsonize and fix complement

113
Q

what should you think about if you see increased serum levels of CRP

A

increased risk of a MI in pts w/ coronary artery disease

114
Q

what does chronically elevated levels of hepcidin do to the body

A

reduces amount of iron available

responsible for anemia associated with chronic inflammation

115
Q

what are leukemoid reactions

A

extreme elevations of leukocytes

116
Q

what is important to distinguish from when a pt presents with a leukemoid reaction

A

leukemia

blood counts are similar in both

117
Q

what is leukocytosis

A

increased leukocyte count (–> 15,000 or 20,000; can get to 40,000-100,000)

118
Q

initial source of elevated leukocytes in leukocytosis

A

bone marrow postmitotic reserve pool

associated with rise of more immature neutrophils known as left shift

119
Q

what is left shift

A

presence of more immature neutrophils responding to inflammatory events?

120
Q

other manifestations of acute-phase response

A

increased P and BP
decreased sweating

rigors
chills
anorexia
somnolence
malaise
probably bc of actions of cytokines on the brain
121
Q

clinical triad of septic shock

A
  • disseminated intravascular coagulation
  • hypotensive shock
  • metabolic disturbances including insulin resistance and hyperglycemia
122
Q

what happens in sepsis

A

production of enormous amounts of several cytokines (TNF and IL-1 most notably)

123
Q

two reactions of repair

A

regeneration by proliferation of residual cells and maturation of tissue stem cells

deposition of CT to form a scar

124
Q

what is it called if extensive deposition of collagen occurs in an area with inflammatory exudate

A

organization

125
Q

what determines a tissue’s ability to repair themselves

A

their intrinsic proliferative capacity

126
Q

types of proliferative tissue (3)

A

labile - continuously dividing
stabile - quiescent; minimally proliferative
permanent - terminally differentiated; nonproliferative

127
Q

what drives cell proliferation

A

growth factors and extracellular matrix signals

128
Q

in terms of cell proliferation and repair, what is the f(x) of satellite cells

A

helps skeletal m regenerative ability

129
Q

sources of the growth factors for cell proliferation

A

M0** activated by tissue injury
epithelial
stromal cells

130
Q

two major mechanisms of liver regeneration

A

proliferation of remaining hepatocytes

repopulation from progenitor cells

131
Q

what triggers hepatocyte proliferation in a regenerating liver

A

cytokines and polypeptide growth factors

132
Q

stages of hepatocyte proliferation

description

A

priming phase - IL-6 secreted mainly by kuppfer (resident M0) make hepatocytes more receptive to GFs

growth factor stage - HGF and TGF-alpha act on primed cells to mmove them out of G0 –> G1 (takes several hours bc hepatocytes are quiescent)

termination stage - cells return to their quiescent states

133
Q

when is regeneration from progenitor cells the dominant form of liver regeneration

A

in times where liver hepatocyte proliferation capabilities are limited
ex. chronic liver injury

134
Q

steps in scar formation

A

angiogenesis
formation of granulation tissue
remodeling of connective tissue

135
Q

what growth factor drives angiogenesis

what is its f(x)

A

VEGF – formation of blood vessels from pre-existing vessels also increases vascular permeability

stimulates both migration and proliferation of endothelial cells – initiating capillary sprouting
stimulates NO production

136
Q

what is granulation tissue formed by

A

migration and proliferation of fibroblasts and deposition of loose CT together w/ vessels and interspersed leukocytes

appears in about 3-5 days

137
Q

histological appearance of granulation tissue

A

characterized by proliferation of fibroblasts and new thin-walled, delicate capillaries, in a loose CT matrix often w/ inflammatory cells, mainly M0

138
Q

f(x) of FGFs

A

stimulates the proliferation of endothelial cells

139
Q

f(x) of PDGF

A

recruitment of smooth m cells

140
Q

f(x) of angiopoietins 1 and 2

A

ang1 interacts with TKRs on endothelial cells called Tie2

play role in angiogenesis and structural maturation of new vessels
recruitment of pericytes and smooth m cells

141
Q

notch signaling

A

works w/ VEGF through cross-talk – regulates sprouting and branching of new vessels and ensures that new vessels have enough spacing to effectively supply healing tissue w/ blood

142
Q

2 steps to deposition of connective tissue

A

migration and proliferation of fibroblasts into the site of injury

deposition of ECM proteins produced by these cells

143
Q

what orchestrates the deposition of CT

A

cytokines and GFs

PDGF, FGF-2, TGF-beta

144
Q

what is the most important cytokine for deposition of CT

A

TGF-beta

145
Q

how is TGF-beta regulated

A

post-transcriptional activation

rate of secretion

factors in the ECM (integrins) that enhance or diminish TGF-beta activity

146
Q

f(x)s of TGF-beta

A

stimulate fibroblastmigration and proliferation
increased synthesis of collagen and fibronectin
decreases degradation of ECM due to inhibition of MMPs
plays role in fibrosis in lung, liver and kidneys following chronic inflammation
anti-inflammatory cytokine

147
Q

what contributes to the contraction of a scar over time

A

myofibroblasts

148
Q

what influences the outcome of the repair process

A

balance between synthesis and degradation of ECM proteins

149
Q

f(x) of MMPs

A

degradation of collagens and other ECM components

150
Q

f(x) of TIMPs

A

during scar formation, shuts down MMPs

151
Q

factors that influence tissue repair

A 
infection
diabetes
nutritional status
glucocorticoids (steroids) - weakness in scar due to inhibition of TGF-beta production = decreased fibrosis (not always a bad thing - corneal infections)
mechanical factors
poor perfusion
foreign bodies
type and extent of injury - types of cells involved (stabile/labile/ permanent)
location of injury
152
Q

when does healing by first intention occur

A

when injury involves only epithelial layer (ex. healing of clean uninfected surgical incision approximated by sutures)

153
Q

three connected processes of healing by first intention

A

inflammation
proliferation
maturation

154
Q

when does healing by second intention occur

A

with more extensive tissue or cell loss – large wounds, abscesses, ischemic necrosis, ulcerations

155
Q

healing by first intention vs second intention

whats different about the mechanisms

A

first intention - epithelial regen
second intention - combo of regen and scarring; inflammatory rxn is more intense, abundant granulation tissue, accumulation of ECM, wound contraction (myofibroblasts)

156
Q

what is an important feature of healing by secondary intention

A

wound contraction

157
Q

what causes the recovery of tensile strength of a wound

A

result of excess of collagen synthesis over degradation during first two months of healing
later, from cross-linking and increased fiber size after collagen synthesis stops

158
Q

in lung kidney and liver, what are the main source of collagen

A

lung and kidney - myofibroblasts

liver - stellate cells (liver cirrhosis)

159
Q

wound dehiscence and ulceration are complications that arise due to what

A

inadequate formation of granulation tissue or formation of a scar

occurs most frequently in abdominal surgery – due to incrased abd pressure

160
Q

what can give rise to hypertrophic scars and keloids

A

excessive formation of the components of the repair process

161
Q

keloid definition

A

if scar tissue grows beyond the boundaries of the original wound and does not regress

more common in african-americans

162
Q

what is proud flesh

A

extra granulation

must be removed by cautery or surgical excision to allow for continuity of epithelium

163
Q

what is it called if exuberant granulation occurs after removal of proud flesh

A

desmoid or aggressive fibromatoses (low grade neoplasms that lie btw malignant and benign)

164
Q

most likely areas for contracture to occur

A

palms, soles, anterior aspect of the thorax

commonly seen after burns, can affect joint mobility

MOD-E1 (3 decks)

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