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Pathology > Inflammation and Repair, TBP > Flashcards

Inflammation and Repair, TBP Flashcards

1
Q

Protective response to rid the body of the cause of cell injury its resultant necrotic cells

A

Inflammation

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2
Q

Process by which WBCs are drawn to the area where they are needed

A

Chemotaxis

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3
Q

Acute vs chronic inflammation: Tissue repair coexists with tissue destruction

A

Chronic

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4
Q

Acute inflammation: Stages (3)

A

1) Vasodilation (after a transient vasoconstriction)
2) Increased vascular permeability
3) Movement of WBCs from blood vessels into soft tissue at site of inflammation

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5
Q

Acute inflammation: Purpose of vasodilation (2)

A

1) Increases hydrostatic pressure

2) Facilitates margination of leukocytes

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6
Q

Acute inflammation: Mediators of increased vascular permeability (5)

A

1) Histamine
2) LTC4, D4, E4
3) Bradykinin
4) TNF
5) IL-1

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7
Q

Acute inflammation: Purpose of increased vascular permeability

A

Increase protein levels in interstitial tissue

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8
Q

Mechanisms of increase in vascular permeability (2)

A

1) Physiologic

2) Pathologic

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9
Q

Mechanisms of increase in vascular permeability: Physiologic (2)

A

1) Endothelial contraction

2) Endothelial retraction

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10
Q

Mechanisms of increase in vascular permeability: Referred to as immediate-transient response

A

Endothelial contraction

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11
Q

Endothelial contraction: Mediators (3)

A

1) Histamine
2) Bradykinin
3) Leukotrienes

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12
Q

Endothelial contraction: Vessels affected

A

Postcapillary venules

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13
Q

Endothelial contraction: Time course

A

Immediate and short-lived (up to 30 minutes)

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14
Q

Endothelial retraction: Mediators

A

1) TNF

2) IL-1

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15
Q

Endothelial retraction: How

A

Structural rearrangement of cytoskeleton

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16
Q

Endothelial retraction: Time course

A

4-6 hours hence referred to as delayed response, long-lived

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17
Q

Direct endothelial injury: Mediators

A

Bacterial enzymes

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18
Q

Direct endothelial injury: Vessels affected

A

All

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19
Q

Direct endothelial injury: How

A

Endothelial cell necrosis

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20
Q

Direct endothelial injury: Time course

A

Immediate hence referred to as immediate-sustained response

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21
Q

Mechanisms of increase in vascular permeability: Due to UV, x-ray, and mild thermal injury

A

Delayed prolonged response

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22
Q

Movement of WBCs from vessels to soft tissue: Steps

A

1) Rolling
2) Pavementing
3) Transmigration

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23
Q

Movement of WBCs from vessels to soft tissue: Loose, intermittent contact of WBCs with endothelium, partially due to margination of WBCs from stasis of blood

A

Rolling

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24
Q

Rolling: Mediator

A

1) Sialyl-Lewis X on WBCs

2) E-selectins on endothelial cells

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25
Q

Movement of WBCs from vessels to soft tissue: Tight, constant contact of WBCs with endothelium

A

Pavementing

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26
Q

Pavementing: Mediators

A

1) LFA-1 and MAC-1 on WBCs

2) ICAM-1 and VCAM-1 on endothelial cells

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27
Q

Movement of WBCs from vessels to soft tissue: WBCs crossing through endothelial layer

A

Transmigration

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28
Q

Transmigration: Mediators

A

CD31 or PECAM on both WBCs and endothelial cells

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29
Q

Chemotaxis: Exogenous mediators

A

Bacterial polysaccharides

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30
Q

Chemotaxis: Mechanism utilised by most endogenous mediators

A

Activation of G protein-activation of GTPases-Polymerization of actin

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31
Q

Opsonins: Recognized by Fc receptor on WBCs

A

IgG

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32
Q

Opsonins: REcognized bt C1q on leukocytes

A

Collectins

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33
Q

Methods of killing and/or degradation of foreign substances: Uses 2 O2 molecules to produce superoxide which is converted to H2O2

A

Reduced NADPH oxidase

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34
Q

Methods of killing and/or degradation of foreign substances: Converts H2O2 and halogen to HOCl causing halogenation or lipid peroxidation

A

Myeloperoxidase

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35
Q

Impaired inflammatory response: Loss of NADPH oxidase system

A

Chronic granulomatous disease

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36
Q

CGD: Components of NADPH oxidase system

A

1) Membrane

2) Cytoplasmic

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37
Q

CGD: Forms

A

1) Autosomal recessive

2) X-linked

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38
Q

CGD: Form that results in defective CYTOPLASMIC component

A

Autosomal recessive

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39
Q

CGD: Form that results in defective MEMBRANE component

A

X-linked

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40
Q

CGD: Effect of mutation

A

Inability to form H2O2

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41
Q

CGD: Particular organisms that cause infection

A

Catalase-producing

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42
Q

Impaired inflammatory response: Decreased cellular killing of bacteria due to reduced transfer of lysosomal enzymes to phagocytic vesicles

A

Chediak-Higashi syndrome

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43
Q

Chediak-Higashi: Autosomal vs X-linked

A

Autosomal recessive

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44
Q

Chediak-Higashi: Associated symptoms

A

1) Albinism
2) Nerve defects
3) Platelet disorders

45
Q

Acute inflammation: Types (3)

A

1) Serous
2) Fibrinous
3) Purulent

46
Q

Serous inflammation: Appearance

A

Watery fluid

47
Q

Serous inflammation: Contents of fluid

A

Transudative

48
Q

Serous inflammation: Seen in (2)

A

1) Viral infections

2) Burns

49
Q

Fibrinous inflammation: Appearance

A

Thick, finely particulate fluid

50
Q

Fibrinous inflammation: Contents

A

Exudative

51
Q

Fibrinous inflammation: Seen in

A

Uremic and post-MI pericarditis

52
Q

Purulent inflammation: Appearance

A

Pus

53
Q

Purulent inflammation: Contents

A

Neutrophils, protein, and necrotic cells

54
Q

Purulent inflammation: Seen in

A

Bacterial and fungal infections

55
Q

Light criteria, exudate: Fluid/serum protein ratio

A

> 0.5

56
Q

Light criteria, exudate: Fluid/serum LDH ratio

A

> 0.6

57
Q

Light criteria, exudate: Effusion LDH

A

Greater than 2/3 the upper limit of lab reference range

58
Q

Outcome of acute inflammation: Inciting agent is removed and all damage done by inciting ager and inflammatory cells repaired

A

Resolution

59
Q

1) Organ must be capable of regeneration

2) Body must be capable of completely dealing with the inciting agent

A

Resolution

60
Q

Resolution: Important for regeneration of epithelium

A

1) Intact basement membrane
2) Intact connective tissue scaffolding
3) Cells capable of cell division

61
Q

Outcome of acute inflammation: Walled off collection of pus

A

Abscess

62
Q

1) Body cannot rid itself of inciting agent

2) Repair and scarring is more rapid in tissue around site of abscess

A

Abscess: Requirements for formation

63
Q

Outcome of acute inflammation: Loss of mucosa

A

Erosion

64
Q

Outcome of acute inflammation: Loss of mucosa and deeper tissues

A

Ulcer

65
Q

Ulcer: Requirement

A

Body cannot rid itself of inciting agent

66
Q

Ulcer: Layers (superficial to deep)

A

1) Fibrin
2) Neutrophils
3) Granulation tissue
4) Fibrosis

67
Q

Ulcer: Most common location

A

GIT

68
Q

Outcome of acute inflammation: Anomalous connection between 2 organs

A

Fistula

69
Q

Fistula: Most common organs involved

A

Organs with a lumen

70
Q

1) Inflammatory process involving FULL-THICKNESS of wall of organ, duct, or vessel
2) Wall adheres to an adjacent wall

A

Fistula: Requirements

71
Q

Outcome of acute inflammation: T/F Acute inflammation can result in chronic inflammation

A

T

72
Q

Outcome of acute inflammation: Replacement of lost parenchyma with disorganised CT (e.g. collagen)

A

Scar formation

73
Q

1) Loss of tissue in an organ NOT CAPABLE of regeneration

2) Loss of basement membrane or other framework required for successful regeneration

A

Scar formation: Requirements

74
Q

Prolonged inflammation consisting of active inflammation and tissue destruction and repair, all occurring simultaneously

A

Chronic inflammation

75
Q

Chronic inflammation: Cells involved

A

Macrophages and lymphocytes

76
Q

Chronic inflammation: Products of activated macrophages that activate lymphocytes (2)

A

1) IL-1

2) TNF

77
Q

Chronic inflammation: Product of activated lymphocytes that activates macrophages

A

IF-γ

78
Q

Chronic inflammation: Collection of epithelia histiocytes

A

Granulomatous inflammation

79
Q

Chronic inflammation: Morphology of granuloma

A

Activated macrophages (epithelia histiocytes) and multinucleate giant cells

80
Q

Granulomatous inflammation: Causes

A

Mycobacteria, fungi, foreign materials, sarcoidosis, silica

81
Q

Regeneration of parenchyma or replacement of damaged tissue with a scar

A

Repair

82
Q

Healing vs regeneration: Complete replacement of damaged cells with no scar formation

A

Regeneration

83
Q

Healing vs regeneration: Regeneration of cells combined with scarring and fibrosis

A

Healing

84
Q

Tissues capable of regeneration (2)

A

1) Renewing tissues such as the GIT and skin

2) Stable tissues such as the liver and kidney

85
Q

Mediators of repair: Stimulates granulation tissue formation

A

EGF

86
Q

Mediators of repair: Induces blood vessel formation

A

VEGF

87
Q

Mediators of repair: Promotes migration and proliferation of FIBROBLASTS, smooth muscle cells, and monocytes

A

PDGF

88
Q

Mediators of repair: Stimulates blood vessel formation and wound repair through macrophages, fibroblasts, and endothelial cell migration

A

FGF

89
Q

Mediators of repair: Acts as growth inhibitor for epithelium

A

TGF-b

90
Q

Components of healing

A

1) Induction of inflammatory process to deal with source of injury
2) Angiogenesis
3) Production of extracellular matrix
4) Tissue remodelling
5) Wound contracture
6) Increasing wound strength

91
Q

T/F: Multinucleated giant cells are required for the formation of granuloma

A

F

92
Q

1) Angiogenesis
2) Migration and proliferation of fibroblasts
3) Deposition of extracellular matrix
4) Maturation and reorganisation of fibrous tissue

A

Replacement of wound by scar

93
Q

Tissue remodelling is a balance between

A

Extracellular matrix synthesis and degradation

94
Q

Extracellular matrix is degraded by

A

Metalloproteinases

95
Q

Timeframe of scarring: Begins

A

Within 24 hours of onset

96
Q

Timeframe of scarring: Granulation tissue is formed

A

3-5 days

97
Q

Timeframe of scarring: Collagen continues to be deposited and edema and inflammatory cells are almost entirely absent

A

Week 2

98
Q

Timeframe of scarring: Inflammatory infiltrate absent and scar consists of collagen

A

1 month

99
Q

Healing: Clean edges, close reapproximation of margins, minimal tissue disruption

A

Healing by first intention

100
Q

Healing: Unclean edges, extensive tissue disruption, tissue necrosis

A

Healing by second intention

101
Q

Wound contraction reduces wound size by

A

5-10%

102
Q

Wound contraction occurs due to these cells

A

Myofibroblasts

103
Q

Wound strength: 10% at

A

1 week

104
Q

Unintentional reopening of wound due to pressure or torsion

A

Dehiscence

105
Q

Hypertrophic scar vs keloid: Involve tissue beyond boundaries of wound

A

Keloid

106
Q

Hypertrophic scar vs keloid: May undergo spontaneous resolution

A

Hypertrophic scar

107
Q

Chemotaxis: Endogenous mediators (3)

A

1) C5a
2) LTB4
3) IL-8

108
Q

Opsonins

A

1) IgG
2) C3b
3) Collectins

109
Q

Opsonins: Recognized by CR 1,2,3 on leukocytes

A

C3b

Pathology (16 decks)

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