Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CRG RUSVM Immunology > Inflammation > Flashcards

Inflammation Flashcards

1
Q

-itis

A

suffix meaning inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is the general mechanical cause of inflammation

A

when the mechanical barrier of the innate immunity is breached tissue injury induces a complex cascade of events that constitute inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Definition of inflammation

A

Defense reaction of living tissue against damage, aimed at removing the cause of injury and repairing the tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

which immune response does inflammation play a role in

A

both innate and adaptive immunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are the types of inflammation

A
  • Acute

- chronic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

-Acute inflammation

A

fights the early stages of infection and prepares the process that leads to tissue repair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Chronic inflammation

A

is characterized by the dominating presence of macrophages in the injured tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the three main exogenous causes of inflammation

A
  • physical agent
  • chemical agents
  • Biological agents
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are the main endogenous causes of inflammation

A
  • Circulation disorders

- Metabolic products

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are the 5 hallmark signs of acute inflammation

A
  • calor
  • rubor
  • tumor
  • dolar
  • functio laesa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Calor:

A

heat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Rubar:

A

redness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Tumor:

A

swelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Dolar:

A

pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Functio laesa:

A

loss of function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how does vasodilation affect lead to inflammation

A

-vasodilation increases the blood flow to the injured area rising the temp (heat/calor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how does large volumes of blood contribute to inflammation

A

-large amounts of blood in the area of injury cause hyperaemia (redness/rubar) of the area of injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

how does vascular permeabiltiy increase lead to inbflammation

A

this leads to fluid leaking from the blood vessels into the area of injury.
- this fluid accumulation leads to oedema (swelling/tumor)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how do leukocytes contribute to inflammation

A
  • within a few hours leukocytes adhere to the endothelium in the injured area leading to extravasation
  • the leukocytes phagocytose invading pathogens and release mediators that further contribute to inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the mediators that are released by the leukocytes responsible for

A

they are responsible for such things as pain(Dola) in the area of injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Inherently with an injury the are affected losses _____

A

function/Functio Laesa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what are the pro-inflammatory cytokines

A
  • TNFalpha
  • IL-1
  • IL-6
  • IL-8
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

TNFalpha:

A

tumor necrosis factor alpha

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

TNFalpha and IL-1 induce

A
  • fever

- stress hormone production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what stress hormones do TNFalpha and IL-1 induce

A
  • norepinephrine

- vasopressin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what do norepinephrine vasopressin hormones induce

A

-activations of the RAAS system (Renin-angiotensin-aldosterone system)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what other signaling molecules does TNFalpha and IL-1 induce synthesis of

A
  • IL-6
  • IL-8
  • IFNy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

IL-6 stimulates the release of _____ such as

A
  • acute phase proteins

- C-reactive protein (CRP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

The proinflammatory cytokines activate the _______ cascade,release of _____, ____________, __________, and ________

A

The proinflammatory cytokines activate the coagulation cascade, release of nitric oxide, Platelet-activating factor, prostaglandins, and leukotrienes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

which interleukins promote chemotaxis, induce extravasation of granulocytes and degranulation of neutrophils

A
  • IL-1
  • IL-6
  • IL-8
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what complement components increase vascular permeabiltiy

A
  • C3a

- C5a

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Complement components C3a and C5a stimulate ______ of neutrophils, eosinophils, and monocytes

A

chemotaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what is prostaglandins

A

lipid soluble molecules derived from arachidonic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

________ contributes to vasodilation, capillary permeability, pain and fever during inflammation

A

Prostaglandins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

how do prostaglandins affect BP

A

it lowers BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

how do stable prostaglandins (PGE1 and PGE2) effect histamine and other inflammatory mediators

A

PGE1 and PGE2 potentiate the effects of histamine and other inflammatory mediators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Prostaglandin thromboxane A2 promotes___________ and __________

A
  • platelet aggregation

- vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what are leukotrienes

A

eicosanoid inflammatory mediators produced in leukocytes by the oxidation of arachidonic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what are the 4 leukotrienes we are concerned with

A
  • LTB4
  • LTC4
  • LTD4
  • LTE4
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

LTB4 is:

A

a potent chemoattractant of neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Vasoactive amines:

A

-histamines and serotonin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

where are vasoactive amines found in high conc.

A
  • in platelets
  • basophils
  • mast cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what do vasoactive amines cause

A

-dilation and increased permeability . of capillaries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

which receptors do the vasoactive amines act through

A
  • H1 (histamine)

- 5-HT (serotonin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

PAF:

A

Platelet-activating factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

PAF is generated from

A

-lipid complex stored in cell membranes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what is the function of PAF

A

it affects many cell types and induces platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what cells do PAF activate

A

neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

what cell treats PAF as a potent chemoattractant

A

eosinophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

how does PAF contribute to edema

A

-it contributes to exflux of plasma proteins leading to edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

what are the two main types of plasma proteases

A
  • Kinins

- Clotting factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what is the function of Kinins

A

-particularly bradykinin- increase capillary permeability (a role in hyperthermia and redness) and pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

what is the function of clotting factors

A

-Production of fibrin peptides during the final steps of the clotting process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What are the 2 important stages of inflammation

A
  • vascular

- cellular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

what triggers the vascular and cellular stages of inflammation

A

the entry of a pathogen in healthy tissues of the body

56
Q

the vascular response phase 1

A
  • vasoconstriction
  • momentary constriction of small blood vessels in the area
  • begins 30-sec post-injury and lasts a few mins.
57
Q

the vascular response phase 2

A
  • Active vasodilation
  • Dilation of arterioles and capillaries (redness=rubar)
  • increase in blood flow
  • Active hyperemia in inflamed region and increased cellular metabolism leading to higher local temp (heat=colar)
58
Q

the vascular response phase 3

A
  • passive vasodilation
  • bloodvessels stop reacting to nervous and humoral stimuli
  • increase in vascular permeability causes swelling (tumor), pain, and impaired function (functio laesa)
59
Q

what is the cellular response to an injury

A
  • marked by the movement of leukocytes into the area of injury
  • mainly granulocytes and monocytes
60
Q

The cellular response phase 1

A
  • chemotaxis

- Leukocytes migrate in response to a chemical signal

61
Q

The cellular response phase 2

A
  • Rolling

- leukocytes slow down and increase their epression of adhesion molecules

62
Q

The cellular response phase 3

A
  • Migration

- migrate into the tissue spaces

63
Q

The cellular response phase 4

A
  • Phagocytosis

- Neutrophils and macrophages engulf and degrade the bacteria and cellular debris

64
Q

what are the first cells to arrive at the site of injury

A
  • cells of innate immunity (granulocytes, neutrophils, M(phi), NK)
  • AKA Leukocytes
65
Q

how long does it take for the immune system to react after an injury

A

the immune system reacts immediately after an injury

66
Q

what is another name for the migration of leukocytes to sites of infection

A

Leukocyte trafficking

67
Q

migration of leukocytes to sites of infection is _____ regulated

A

-highly

68
Q

CAM:

A

cell adhesion molecules

69
Q

what is the function of CAM

A

cells of a given tissue are held together by CAM

70
Q

how are CAM important for immune cells

A

In order for cells of the immune system to participate in the inflammatory response, they need to use CAM to migrate to tissues where inflammation is taking place

71
Q

Extravasation of leukocytes from _______ into ______ or entrance of leukocytes int ______ requires adhesion to the endothelium

A

Extravasation of leukocytes from blood vessels into inflamed tissues or entrance of leukocytes into lymph nodes requires adhesion to the endothelium

72
Q

some of the _____ present on leukocytes are required for leukocyte-leukocyte interaction

A

CAM

73
Q

how are CAM typically expressed

A
  • Most are constitutively expressed

- some are expressed dependent on local conditions

74
Q

what are the 4 families of proteins that make up CAMs

A
  • selectin
  • Mucins
  • Integrins
  • Ig-superfamily CAM
75
Q

what are selectins

A

-membrane glycoproteins containing extracellular lectin domains bind carb moieties found on mucin like molecules

76
Q

what are the most important selectins

A

-Selectin-E,L,P

(CD62E, CD62L, and CD62P respectively

77
Q

where is selectin L expressed

A

on leukocytes

78
Q

where are selectin P and E expressed

A

on the endothelium during inflammation

79
Q

selectin P is contained in ______ found in ________ cells

A
  • granules

- endothelial

80
Q

selectin P is released when:

A

the granules fuse with the cell membrane

81
Q

Selectin E is synthesized ______ after stimulation by _____

A
  • De novo

- cytokines

82
Q

what are selectins responsible for during the initial vascular phase of inflammation

A

-leukocyte interaction with the endothelium during the initial vascular phase of inflammation

83
Q

What are mucins:

A

a group of heavily glycosylated, serine- and threonine-rich proteins that bind to selectins

84
Q

what are some examples of Mucines

A
  • CD34 or GlyCAM-1 on endothelial cells bind to CD62L on leukocytes
  • PSGL-1 on neutrophils binds to selectin E and P on endothelial cells
85
Q

what are integrins:

A

Heterodimeric proteins consisting of alpha and beta chains that are covalently joined at the cell surface

86
Q

what do the alpha and beta chains of integrins form

A

-the alpha and beta chains of the integrins form a binding site to which the Ig superfamily domains bind

87
Q

how are integrins divided into subgroups

A

integrins are divided into subgroups according to type of beta chain expressed (from beta 1 to beta 7)

88
Q

Leukocytes express integrins with which beta chain

A
  • beta2 chain

- CD18

89
Q

what does a deficiency in beta 2 integrin chains lead to

A
  • immunodeficiency called leukocyte adhesion deficiency (LAD)- and autosomal recessive disease
  • manifested by recurrent bacterial infections
90
Q

what is the primary problem associated with LAD

A
  • Leukocyte adhesion deficiency

- neutrophils are unable to extravasate

91
Q

CAM of the IG-superfamily contain

A
  • Ig like domains

- fibronectin domains

92
Q

Important representatives of CAM Ig-superfamily are:

A
  • ICAM-1 (CD154)
  • ICAM-2 (CD102)
  • ICAM-3 (CD50)
  • VCAM (CD106)
93
Q

Ig-superfamily CAMs bind to______

A

integrins

94
Q

where are Ig-superfamily CAMs expressed

A

on endothelial cells

95
Q

Endothelial cell activation:

A
  • during inflammation, cytokines and other mediators of inflammation stimulate the endothelial cells leading to increased expression of CAMs
  • leukocytes can now exit the blood vessels into the inflamed tissue
96
Q

Extravasation of leukocytes is divided in to _____ phases

A

4 phases

97
Q

what are the 4 phases of extravasation of leukocytes

A

1) rolling
2) activation
3) arrest/adhesion
4) transendothelial migration

98
Q

Rolling:

A

at the site of injury, leukocytes, with the aid of their mucin CAMs, loosely bind to selectin E and P on the endothelial cells, their movement slows down and they begin to roll on the endothelium

99
Q

Activation

A
  • increase in cytokine, particularly chemokine secretion by endothelial cells
  • Increase in chemokine receptor expression on leukocytes leading to activation of leukocytes
100
Q

Adhesion (strict adhesion)

A
  • Activation of the endothelium and leukocytes produces conformational changes in cells
  • Integrtins oin leukocytes can now bind firmly to the endothelium
101
Q

Diapedesis (transendothelial migration)

A
  • leukocytes squeeze in between two neighboring endothelial cells and pass into the inflamed tissue
  • Leukocytes use homotypic binding of platelet-endothel;ial cell adhesion molecule 1 (PECAM-1 (CD131)) on endothelium (self to self binding)
102
Q

T/F neutrophils are among the last cells to arrive at the site of inflammation

A

F neutrophils are among the first cells to arrive at the site of inflammation

103
Q

do neutrophils bind to endothelial cells under normal circumstances?

A

no neutrophils do not bind to endothelial cells under normal circumstances (i.e. without inflammation)

104
Q

neutrophils can not migrate (extravasation) without inflamation because

A
  • there is no expression of selectin E, P and other CAMs on the endothelium
  • the expression has to be induced
105
Q

which receptors are responsible for rolling of neutrphils

A
  • selectin L

- PSGL-1

106
Q

which receptors are responsible for activation of neutrophils during extravasation

A
  • IL-8

- MIP-1beta

107
Q

Activation also leads to increased expression of ICAM on the _________ and CD11a/CD18, CD11b/CD18(LFA-1 and MAC-1) on ________, leading to firm adhesion and finally diapedesis

A
  • endothelium

- Neutrophils

108
Q

after diapedesis, the chemokine _____ then leads the neutrophils to the focal pont of inflammation

A

gradient

109
Q

______ arrive slightly late at the site of inflammation, because high expression of _______ and ______ is possible only after the activation stage

A
  • Monocytes
  • VCAM-1
  • ICAM-1
110
Q

why might under normal circumstances might a monocyte extravasate

A

for the purpose of replenishing tissue macrophages and dendritic cells

111
Q

what regulates the homeostatic migration of monocytes

A

CXCL14

112
Q

what cell protein is responsible for monocyte cell rolling

A

CD63L

113
Q

What protein is responsible for the regulation of activation of monocytes

A

MCP-1

114
Q

what protein is responsible for diapedesis of monocytes

A

PECAM-1

115
Q

Complement receptors such as ______ and ______, bacterial peptides participate in _______ of monocytes into inflamed tissue

A
  • CR3
  • CR4
  • extravasation
116
Q

where is the typical migration of lymphocytes under normal conditions

A

-Lymphocytes are continuously circulating between blood and lymphatic tissues

117
Q

Extravasation of lymphocytes is similar to that of ________

A

neutrophils

118
Q

where will lymphocytes migrate to

A

-lymphocytes will migrate toward areas of infection

119
Q

lymphocytes use the same mechanism to extravasate into inflammatory sites or ____________

A

secondary lymphoid organs

120
Q

where do lymphocytes pass through when they extravasate

A
  • (HEV) high enothelial venules

- they pass through post capillary venules called HEV

121
Q

which receptors activate lymphocytes in HEV prior to extravasation

A

-Chemokines CCL19, CCL21, and CXCL12

122
Q

Under optimal conditions will the inflammation response become a systemic response

A

No the inflammatory response should remain confined to a localized area under optimal conditions

123
Q

in some cases of local injury what can cause the systemic manifestation of an systemic inflammatory response

A

–inflammatory mediators are released into the circulation

124
Q

what is the most prominent systemic manifestation of inflammation

A
  • the acute phase response
  • Alterations in white blood cell count (leukocytosis or leukopenia)
  • high fever
  • sepsis and septic shock also called the systemic inflammatory response
125
Q

APR

A

acute phase response

126
Q

APR definition

A

changes in serum proteins during infection is referred to as APR

127
Q

Proteins whose concentration increase or decrease during infection as referred to as

A

acute phase response protein (APP)

128
Q

what are some important examples of APP

A
  • some complement system proteins

- C-reactive proteins (CRP) are part of the innate immune response

129
Q

where are most APR proteins synthesized

A

in the liver

130
Q

synthesis of APR proteins are induced by _____________ produced by phagocytes (TNFalpha, IL-1, IL-6)

A

-pro-inflammatory cytokines

131
Q

CRP bound to the surface of microbe promotes uptake by phagocytes and activates ___________

A

-complement mediated attack

132
Q

Mannose-binding lectin is a APP that recognizes mannose on ________ and not on _______

A
  • microbes

- veterbrate cells

133
Q

what are other systemic effects of inflammation

A
  • anorexia
  • altered sleep patterns
  • lethargy
  • muscular wasting
  • metabolic acidosis (lowered blood pH)
134
Q

cachexia:

A

muscle wasting

135
Q

what is the main characteristic of inflammation mediators in vivo that ends the inflammation response

A

-short half-life

CRG RUSVM Immunology (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions