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General Pathology (Fall 2014) > Inflammation > Flashcards

Inflammation Flashcards

1
Q

inflammation

A

the process of rxn of living vascularized tissue to injury.

Is usually beneficial (destroy invaders, prepare injured tissue for repair) but sometimes induces tissue damage

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2
Q

central events in inflammation involve

A

blood vessels:

  1. increased blood flow
  2. increased vascular permeability
  3. leukocyte exudation through vessels
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3
Q

repair

A

process by which lost or necrotic cells are replaced by vital cells

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4
Q

regeneration

A

replacement by cells of the same type

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5
Q

scarring or fibrosis

A

replacement by connective tissue. Does not occur in brain

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6
Q

2 processes of repair

A

regeneration and scarring/fibrosis

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7
Q

5 signs of acute inflammation

A

1) rubor (redness)
2) tumor (swelling) (doesn’t refer to neoplasia)
3) calor (heat)
4) dolor (pain)
5) functio laesa (loss of function

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8
Q

hyperemic

A

increased blood flow to an area. Causes rubor

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9
Q

chemical mediators of inflammation from PLASMA

A

1) Kinins: bradykinin
2) Complement fragments: C5a
3) Coagulation/Fibrinolytic products

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10
Q

chemical mediators of inflamm. from CELLS AND TISSUE:

A

1) vasoactive amines: histamine, serotonin
2) prostaglandins and leukotrienes: PGE2, LTB4
3) cytokines/chemokines: TNF-a, IL-1,IL-8, MIP-1
4) nitric oxide

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11
Q

3 major components of acute inflammation

A

1) vascular changes in flow and caliber
2) increased vascular permeability
3) leukocytic events (margination, adhesion/migration, chemotaxis and activation)

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12
Q

steps in vascular changes in flow and caliber during inflamm.

A

1) transient vasoconstriction (neurally mediated, short term)
2) vasodilation (mediated by PGE2, histamine, NO; long term)

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13
Q

mechanism of increased vascular permeability during inflamm.

A
  1. endothelial contraction (most common and short-lived*)
  2. direct endothelial injury (i.e. toxins, burns)
  3. leukocyte-endothelial injury (i.e. during sepsis)
  4. increased transcytosis
  5. endothelial proliferation (angiogenesis) and leak (immature blood vessels are leaky)
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14
Q

gaps due to endothelial contraction affects venules or arterioles?

A

venules

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15
Q

increased transcytosis is mediated by what?

A

Vascular endothelial-derived growth factor (VEGF)

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16
Q

Which mechanism of increased vascular permeability is the only mech. to affect arterioles and capillaries in addition to venules?

A

direct injury (all others only affect venules)

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17
Q

Where in leukocyte movement out of blood vessel do selectins act? Integrins?

A
  • selectins help leukocytes roll along blood vessel

- integrins help leukocytes adhere and transmigrate through vessels

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18
Q

leukocytic margination and rolling is mediated by:

A

selectin molecules on endothelial cells and oligosaccharides on leukocytes

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19
Q

What mediators upregulate selectin?

A

TNF-a, IL-1

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20
Q

selectin is composed of?

A

single chain carb-binding glycoprotein

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21
Q

leukocyte adhesion is mediated by:

A

Endothelium: ICAM-1, VCAM-1 (adhesion moleucules)
Leukocytes: integrins (LFA-1, Mac-1, VLA-4)

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22
Q

What mediators upregulate integrin?

A

TNF-a, IL-1, IL-8

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23
Q

leukocytic transmigration is mediated by:

A

PECAM-1 (CD31) (a homophilic adhesion molecule expressed on both endothelium and leukocytes)

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24
Q

leukocyte adhesion deficiencys involves what in animals?

A

integrins (integrins AND selectins in humans)

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25
Q

Bovine Leukocyte adhesion deficiency (BLAD)

A
  • defect in CD18 expression on leukocytes due to homozygous D126G allele
  • causes poor neutrophil response to infection
  • decreased survival, enteritis, pneumonia
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26
Q

chemotaxis

A

cell migration along a concentration gradient of chemical mediator

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27
Q

chemokinesis

A

random migration stimulated by a mediator

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28
Q

first cells to respond to inflammation

A

neutrophils

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29
Q

what do neutrophils release?

A

-superoxide anion and lysosomal enzymes (which can induce tissue damage)

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30
Q

neutrophil half-life in circulation

A

6-7 hours

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31
Q

macrophage lifespan

A

30-60 days

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32
Q

what do macrophages release (among others)?

A
  • superoxide anion and lysosomal enzyme (can contribute to tissue damage)
  • IgA to recruit neutrophils
  • growth factors for scar formation
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33
Q

macrophages derive from

A

monocytes or local division

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34
Q

what do macrophages form?

A

epitheliod cells and multinucleated cells

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35
Q

what do macrophages modulate?

A

inflammatory, immune, and repair processes through mediators and cytokines

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36
Q

component of eosinophils that make it effective killer of helminths

A

major basic protein

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37
Q

eosinophils are component of many hypersensitivity diseases and mediate tissue damage in chronic rxns

A

:)

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38
Q

fx of IL-5

A

prolongs tissue survival

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39
Q

How is inflammation classified?

A

by:
duration (acute, subacute, chronic)
distribution (focal, multifocal, locally-extensive, diffuse)
type of exudate (serous, fibrinous, suppurative, etc…)
tissue involved (hepatitis, nephritis, encephalitis, etc…)

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40
Q

types of exudate

A 
serous
fibrinous
suppurative
eosinophilic
hemorrhagic
necrotizing
lymphocytic
proliferative
granulomatous
Mixed: fibrinonecrotic, fibrinopurulent
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41
Q

mast cells contain what preformed mediators?

A

histamine and serotonin

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42
Q

mast cells are a major source of:

A

leukotrienes, cytokines, chemokines

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43
Q

Fx of mast cells

A
  • bind IgE and other Ab –> degranulate and release mediators when Ag binds
  • mediate hypersensitivity disease
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44
Q

functions of all lymphocytes

A
  • regulator/effector of Ag-driven inflammatory processes

- produce cytokines that modulate inflammation and immunity (interleukins, gamma-interferon)

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45
Q

Which lymphocytes produce Ab?

A

B cells, plasma cells

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46
Q

Which lymphocytes mediate helper activity and cytotoxicity?

A

T cells

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47
Q

what do platelets release?

A

-release serotonin, PAF, growth factors (PDGF, TGF-beta, FGF)

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48
Q

morphologic diagnosis

A

diagnosis based solely on morphology (i.e. chronic diffuse granulomatous enteritis

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49
Q

etiologic diagnosis

A

dx including causative agent (i.e. - intestinal mycobacteriosis)

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50
Q

hallmark of chronic reaction

A

fibrosis/scarring

occurs beyond 10-14 days

51
Q

acute inflamm. char. by:

A
  • hours to days
  • changes in vessel permeability and flow
  • leukocyte exudation
52
Q

subacute inflamm. char. by:

A
  • several days to 7-10 days
  • tissue cell proliferation
  • NO fibrosis
53
Q

fibrinous responses are often char. by:

A
  • acute bacterial infection with marked increase in vascular permeability
  • clotting proteins leak out and initiate coag cascade and fibrin formation in large amounts
54
Q

fibrinopurulent = mix of:

A

fibrin and neutrophils

55
Q

erosion

A

defect assoc. with necrosis that goes down to level of basement membrane

56
Q

ulcer

A

defect assoc. with necrosis that goes down to level below BM into deep connective tissue (goes further than erosion!)

57
Q

what can cause granulomatous inlammatory response?

A

macrophage dominated inflammatory response results in thickening

58
Q

fungi usually induce what response?

A

necrosis, hemorrhage (granulomas if severe)

59
Q

nematodes usually induce what response?

A

granulomatous

60
Q

3 mediators of vasodilation*

A

PGE2, histamine, NO

61
Q

mediators of vascular permeability*

A 
histamine
C3a
C5a
bradykinin
leukotrienes C4, D4, E4, PAF
62
Q

mediators of chemotaxis/activation*

A 
IL-8
C5a
LTB4
microbial products
fibrinopeptides
63
Q

3 mediators of fever*

A

IL-1
TNF-alpha
PGE2

64
Q

2 mediators of pain*

A

bradykinin

PGE2

65
Q

2 mediators of tissue damage*

A

lysosomal enzymes

oxygen radicals

66
Q

Basic chars. of mediators of inflamm.

A
  • produced in response to stimuli
  • one mediator can stimulate release of others
  • short lived
  • functions overlap (redundancy)
67
Q

How is bradykinin formed?

A

Factor 12 activates prekallikrein –> kallikrein, which cleaves kinnogen to bradykinin

68
Q

bradykinin fx

A

vasodilation, increased vascular permeability, pain (via stimulation of free nerve endings), smooth m. contraction

69
Q

C5a effects

A
  • chemotactic for neutrophils
  • neutrophil activation
  • mast cell degranulation
  • increased vascular permeability
70
Q

C3a effects

A

-increased vascular permeability

71
Q

how does fibrinogen get cleaved?

A
  • by plasmin and streptokinase after activation of thrombin via intrinsic/extrinsic pathways
  • fibrin formed is chemotactic for neuts and macs
72
Q

Which chemokine attracts mainly neutrophils?**

A

IL-8

73
Q

Which chemokines attracts mainly monocyte/macrophages/T-lymphocytes?**

A

MIP-1a, RANTES, MCP-3

74
Q

Which chemokine attracts mainly eosinophils?**

A

Eotaxin

75
Q

2 vasoactive amines

A

histamine and serotonin

76
Q

sources of histamine

A

mast cells, basophils (platelets)

77
Q

histamine actions

A
  • vasodilation
  • increased vascular permeability
  • bronchial and other smooth m. contraction
78
Q

What do LTB4/C4/D4/E4 all have in common?

A
  • slow releasing substances of anaphylaxis
  • increase vascular permeability
  • chemotactic for neutrophils
79
Q

steroid down/upregulates arachidonic acid

A

downregulates

80
Q

what converts AA to prostaglandin? What inhibits this?

A

cyclooxygenase; inhibited by COX-1 and 2 inhibitors, aspirin

81
Q

what converts AA to leukotriene?

A

5-lipoxygenase

82
Q

cyclooxygenase source

A

resident cells, leukocytes, mast cells

83
Q

PGE2 action

A
  • increase vascular flow, permeability

- fever, pain

84
Q

PGD2 action

A
  • increase vascular flow, permeability

- smooth m. contraction in some tissues

85
Q

cyclooxygenase products

A

prostaglandins

86
Q

source of LTB4

A

neuts, macs, eos

87
Q

LTB4 action

A
  • chemotactic for neuts and eos

- chemokinesis for macs

88
Q

“big three” molecules that are chemotactic for neuts*

A

LTB4, C5a, IL-8

89
Q

source of LTC4/D4/E4

A

-neuts, macs, eos

90
Q

action of LTC4/D4/E4

A
  • increase vascular perm.

- smooth m. contraction

91
Q

Source of Lipoxin A4 and B4 (LXA4 and LXB4)

A

transcellular biosynthesis by neuts and platelets

92
Q

action of lipoxin A4 and B4

A

inhibit leukocyte adhesion and chemotaxis

93
Q

name 2 cytokines

A

IFN-y, TNF-a

94
Q

sources of IFN-y

A

T-cells, NK cells (stimulated by Ag, early immune response)

95
Q

IFN-y actions

A

UPREGULATE MAC FX:

  • increase superoxide production/killing capacity
  • induce IL-12 and Th1 shifted immune response
  • upreg. class II MHC: inc. Ag presentation
  • upreg. growth factors
  • giant cell formation
96
Q

sources of TNF-a

A

macs, fibroblasts, etc. (stim. by endotoxin, bacteria, virus, protozoa, toxins)

97
Q

actions of TNF-a

A

The primary role of TNF is in the regulation of immune cells

  • upreg. E-selectin and inc. thrombogenicity of endothelial cells
  • enhance mac interleukins and NO
  • induce acute phase rxn proteins
  • induce fibroblast proliferation and collagen synthesis
  • fever
  • cachexia by appetite suppression and lipoprotein lipase inhib.
  • apoptosis in selected cells
98
Q

source of chemokines

A

macs, stromal cells, epithelial cells

99
Q

chemokine stimuli

A

virus, bacteria, toxins, protozoa, cytokines

100
Q

name 4 potent mediators of increased vascular permeability*

A
  • bradykinin

- LTC4/D4/E4

101
Q

Name 2 things that mediate pain perception*

A

PGE2, bradykinin

102
Q

3 main mediators of vasodilation***

A

PGE2, histamine, NO

103
Q

main mediators of vascular permeability***

A 
histamine
C3a
C5a
bradykinin
leukotrienes C4,D4,E4
PAF
104
Q

main mediators of chemotaxis/activation***

A 
IL-8
C5a
LTB4
microbial products
fibrinopeptides
105
Q

3 main mediators of fever***

A

IL-1
TNF-a
PGE2

106
Q

2 main mediators of tissue damage***

A

lysosomal enzymes

oxygen radicals

107
Q

clinical/pathophysiologic systemic events of inflammation

A
  • loss of tissue fx
  • poor weight gain/weight loss
  • fever
  • leukocytosis
  • acute phase reactants via TNF, IL-1, IL-6
108
Q

sequelae of acute inflamm. if stimulus is REMOVED

A
  • resolution of inflamm.

- repair of tissue

109
Q

sequelae of acute inflamm. if stimulus PERSISTS

A
  • chronic inflamm.
  • repair and tissue damage
  • scarring
110
Q

chronic inflamm.

A

inflamm. that results from injurious stimuli that are persistent and leads to predominantly proliferative and scarring, rather than exudative, reaction. Hallmark = fibrosis or scarring

111
Q

what inflamm. cells predominate in chronic inflamm?

A

macs, lymphocytes, plasma cells. Neuts may continue to be present

112
Q

granulomatous inflamm.**

A

inflammatory process dominated by macrophages

113
Q

granuloma

A

compact and organized collection of mononuclear inflamm. cells dominated by macs

114
Q

Char. of stimuli of granulomatous inflamm.**

A

1) particulate substance resisting lysosomal degradation

2) induce T-cell hypersensitivity

115
Q

Types of stimuli for granulomatous inflamm.**

A
  • inert particles
  • lipids and waxes
  • resistant microbes
  • high MW polymers
  • Ag inducing T-cell hypersensitivity
116
Q

cells of the granulomatous inflamm. rxn

A
  • monocytes
  • macs
  • epitheliod cells (secrete lysosomal enzymes and toxic O radicals)
  • MNGCs
117
Q

3 types of granulomatous inflamm. rxns**

A

granulomatous: macs +/- epitheliod cells, giant cells
simple granuloma: compact inflamm. cell exudate
complex granuloma: granuloma w/ central necrosis +/- calcification

118
Q

granulomatous inflamm. is usually acute/chronic?**

A

chronic (unless there is pre-existing T cell hypersensitivity)

119
Q

Type I allergic rxn mediator/mech/dz ex.**

A

mediator: IgE, IgG
mech: mediator release
Dz: anaphylaxis

120
Q

Type II allergic rxn**

A

mediator: IgM, IgG
mech: cytotoxicity, dysfunction
dz: autoimmune, hemolytic anemia

121
Q

Type III allergic rxn**

A

mediator: IgM, IgG
mech: immune complex
dz: glomerulonephritis

122
Q

Type IV allergic rxn**

A

mediator: T cells, cell mediated
mech: contact dermatitis, immunity
dz: mycobacteriosis, TB, contact dermatitis, transplant reject,viral cytopathology

123
Q

what do activated T cells produce in type IV hypersensitivity rxn?

A

IFN-y to activate macs, which then differentiate into giant cells and epithelioid macs

General Pathology (Fall 2014) (6 decks)

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