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Pathology > Inflammation & Tissue Repair > Flashcards

Inflammation & Tissue Repair Flashcards

1
Q

process of removing harmful agents and beginning repair process

A

Inflammation

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2
Q

Acute inflammation is part of _____ immunity

A

Innate

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3
Q

PAMPs are recognized by these receptors on endothelium, dendritic cells, macrophages, and WBCs

A

Toll-like receptors

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4
Q

Necrotic tissue is recognized by these

A

Damage-associated molecular patterns (DAMPs)
Examples: uric acid, free DNA, low K+

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5
Q

DAMPs are recognized by these receptors present on all cells

A

NOD-like receptors

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6
Q

DAMPs are recognized by NOD-like receptor to produce ________

A

Inflammasome

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7
Q

Inflammasome activates this enzyme

A

Caspase 1
(which activates IL-1 –> fever and leukocyte recruitment)

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8
Q

Caspase 1 activates this

A

IL-1 –> fever and leukocyte recruitment

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9
Q

Caspase 1 is involved in this process

A

DAMPs are recognized by NOD-like receptor to produce inflammasome, which then activates caspase 1 to activate IL-1 –> fever and leukocyte recruitment

= Recognition of threat; begins process of acute inflammatory response

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10
Q

Dilation of small arterioles during acute inflammation is mediated by these

A

Histamines

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11
Q

Dilation of small arterioles increases or decreases capillary blood flow?

A

Increases
Increased blood flow leads to redness (rubor) and warmth (color)

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12
Q

____ blood flow allows leukocytes to leave circulation

A

Slow

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13
Q

Leukocyte margination occurs during acute inflammation due to this

A

Stasis (slow blood flow)

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14
Q

Leukocyte rolling is mediated by these

A

Selectins

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15
Q

Leukocyte adhesion to endothelium is mediated by this interaction

A

Integrin : adhesion molecule interaction

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16
Q

Leukocyte migration across vessel wall occurs in venules toward ______ gradient

A

Chemokine

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17
Q

Increased vascular permeability occurs via these 2 mechanisms

A

Endothelial contraction (mediated by histamines, leukotrienes, bradykinins)
Endothelial damage (detachment from basement membrane)

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18
Q

Endothelial contraction causes increased vascular permeability is mediated by these 3 things, and is rapid and short-lived

A

Histamines, Leukotrienes, Bradykinins

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19
Q

Mechanism of increased vascular permeability that is rapid and short-lived (minutes)

A

Endothelial contraction

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20
Q

Mechanism of increased vascular permeability that may be long-lived (hours to days); caused by thermal burns, some microbial toxins

A

Endothelial damage

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21
Q

Increased vascular permeability allows _____ rich exudate to flow into tissues, causing swelling

A

Protein and cell-rich

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22
Q

Key cell types recruited to site of acute inflammation are:

A

Phagocytes (neutrophil and macrophage)

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23
Q

Earliest cell to arrive in acute inflammation

A

Neutrophils

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24
Q

Main cell that arrives at site of acute inflammation

A

Macrophage

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25
Q

Neutrophils arrive at site of acute inflammation after _____ hours

A

6-24 hours
Earliest cell

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26
Q

Macrophages arrive at site of acute inflammation after _____ hours

A

24-48
(later; after neutrophils)

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27
Q

Step of acute inflammation that involves innate anti-inflammatory processes

A

Regulation

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28
Q

Membrane bound threat destruction can involve either of these

A

Phagolysosome / inflammasome

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29
Q

_______ apoptosis immediately after phagolysosome destruction is involved in the regulation step of acute inflammation

A

Neutrophil

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30
Q

2 Anti-inflammatory mediators involved in the regulation step of acute inflammation

A

IL-1:IL-1 receptor antagonist
Bradykinin (kinases)

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31
Q

2 protease inhibitors involved in the regulation step of acute inflammation

A

Serum alpha-1 antitrypsin
Neutrophil elastase

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32
Q

Excess tissue liquefaction is a possible outcome of acute inflammation that leads to this

A

Abscess

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33
Q

Liquefaction necrosis is a possible outcome of acute inflammation that involves _____ surrounded by fibrosis

A

PMNs (polymorphonuclear leukocytes = neutrophils, basophils, eosinophils)

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34
Q

Term that describes excess tissue liquefaction (pus forming)

A

Suppuration

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35
Q

Early repaired tissue; early scar

A

Granulation tissue

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36
Q

Cells that lay down collagen in scar formation

A

Fibroblasts

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37
Q

Immunodeficiency due to defective Beta chain of neutrophil integrins
Prevents WBC:endothelial adhesion and tissue migration
Delayed umbilical cord separation, followed by omphalitis
Elevated WBC count
Frequent/recurrent indolent bacterial infection
May have skin/other sites necrotizing infection/abscess without pus

A

Leukocyte adhesion deficiency-1

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38
Q

Elevated WBC count and chronic skin infections with no pus are indicative of this condition

A

Leukocyte adhesion deficiency-1

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39
Q

3 clinical signs of Leukocyte adhesion deficiency-1

A

Delayed umbilican cord separation, followed by omphalitis
Elevated WBC count
Frequent/recurrent skin (or other sites) infections without pus

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40
Q

Leukocyte adhesion deficiency-1 is due to defective this

A

Defective Beta chain of neutrophil integrins

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41
Q

Leukocyte adhesion deficiency-1 prevents this

A

WBC:endothelial adhesion and tissue migration
(due to defective beta chain of neutrophil integrins)

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42
Q

During phagocytosis, these structures surround and engulf particles into phagosome

A

Pseudopods

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43
Q

Organelle that produces materials to kill/digest offending agent

A

Lysosome

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44
Q

These are produced after phagolysosome fusion and during respiratory burst of neutrophils

A

ROS

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45
Q

How many components does NADPH oxidase have?

A

7; some in membrane, some in cytoplasm

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46
Q

This process results in the NADPH oxidase components being brought together to form active enzyme

A

Phagocytosis

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47
Q

Reactive nitrogen and reactive oxygen species are produced during this step in phagocytosis

A

Phagolysosome fusion

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48
Q

Immune deficiency due to defective phagosome-lysosome fusion
Autosomal recessive mutation of LYST gene
Affects neutrophil granules, melanocyte granules (partial albinism), neuronal axonal vesicle transport (peripheral neuropathy), platelet granules (bleeding disorder)
Neutropenia
Neutrophils and lymphocytes with LARGE fused granules
Delayed microbial killing
Mostly skin/mucosal infections
Bleeding diathesis

A

Chediak-Higashi Syndrome

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49
Q

Chediak-Higashi Syndrome is due to defective this

A

Phagosome-lysosome fusion

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50
Q

Chediak-Higashi Syndrome
is caused by an autosomal recessive mutation of this

A

LYST gene (LYSosomal Traffic regulator)

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51
Q

Chediak-Higashi Syndrome affects these 4 cells

A

Neutrophil granules (innate immune deficiency)
Melanocyte granules (partial albinism)
Neuronal axonal vesicle transport (peripheral neuropathy)
Platelet granules (bleeding disorder)

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52
Q

Condition characterized by neutrophils and lymphocytes with LARGE fused granules

A

Chediak-Higashi Syndrome

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53
Q

Condition that can involve albinism, bleeding diathesis, peripheral neuropathy, delayed microbial killing

A

Chediak-Higashi Syndrome

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54
Q

Mediator of acute inflammation:
Vasoactive amine released by mast cells (preformed and stored in granules)
Released by various stimuli
Causes vasodilation and venule permeability

A

Histamine

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55
Q

Histamine is released by these cells

A

Mast cells

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56
Q

2 actions of histamine

A

Vasodilation and Venule permeability

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57
Q

Mediator of acute inflammation:
Arachidonic acid metabolite
Produced by lipooxygenase in mast cells, other WBCs (preformed and stored in granules)
Causes neutrophil chemotaxis and activation, smooth muscle contraction

A

Leukotrienes

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58
Q

Leukotrienes are a metabolite of this

A

Arachidonic acid

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59
Q

Leukotrienes are produced by this enzyme in mast cells and other WBCs

A

Lipooxygenase

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60
Q

3 actions of leukotrienes

A

Neutrophil chemotaxis
Neutrophil activation
Smooth muscle contraction

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61
Q

Mediator of acute inflammation:
Arachidonic acid metabolite
Produced by cyclo-oxygenase in mast cells, endothelium, platelets, other WBCs (preformed and stored in granules)
Causes neutrophil chemotaxis and vascular permeability

A

Prostaglandins

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62
Q

Prostaglandins are metabolites of this

A

Arachidonic acid

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63
Q

Prostaglandins are produced by this enzyme in mast cells, endothelium, platelets, other WBCs

A

Cyclo-oxygenase

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64
Q

2 actions of prostaglandins

A

Neutrophil chemotaxis
Vascular permeability

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65
Q

Lipooxygenase in mast cells and other WBCs produce this mediator of acute inflammation

A

Leukotrienes

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66
Q

Cyclo-oxygenase in mast cells, endothelium, platelets and other WBCs produces this mediator of acute inflammation

A

Prostaglandins

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67
Q

Mediator of acute inflammation that causes vasodilation and venule permeability

A

Histamine

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68
Q

Mediator of acute inflammation that causes neutrophil chemotaxis and activation, and smooth muscle contraction
(Bronchus = bronchoconstriction)
(Arterioles = Vasoconstriction)

A

Leukotrienes

69
Q

Mediator of acute inflammation that causes neutrophil chemotaxis and vascular permeability

A

Prostaglandins

70
Q

Endogenous pyrogen that sets thermoregulation at higher set-point

A

IL-2

71
Q

Complement factors that induce histamine release, leading to vasodilation and permeability

A

C3a and C5a

72
Q

C5a activates this enzyme, which produces leukotrienes and thromboxanes

A

Lipooxygenase

73
Q

5 cardinal signs of acute inflammation

A

Rubor: tissue erythema
Calor: tissue warmth
Tumor: tissue swelling
Dolor: tenderness/pain
Functio laesa (loss of function)

74
Q

Cardinal sign of acute inflammation that describes tissue erythema

A

Rubor

75
Q

Cardinal sign of acute inflammation that describes tissue warmth

A

Calor

76
Q

Cardinal sign of acute inflammation that describes tissue swelling

A

Tumor

77
Q

Cardinal sign of acute inflammation that describes tendernoss/pain

A

Dolor

78
Q

prolonged inflammatory response with co-existing tissue injury and repair attempts

A

Chronic inflammation

79
Q

2 main cells of chronic inflammation

A

Macrophage > lymphocytes (mononuclear cells)

80
Q

Macrophage becomes M1 cell when T cells secrete this

A

gamma IFN

81
Q

Macrophage becomes M2 cell when T cells secrete this

A

IL-4 and IL-13

82
Q

When T cells secrete gamma IFN, macrophages become this

A

M1 cell

83
Q

When T cells secrete IL-4 and IL-13, macrophages become this

A

M2 cell

84
Q

M1 cell produces these

A

NO and ROS, lysosomal enzymes (innate immunity)

85
Q

M2 cell produces these

A

PDGF, FGF (initiates repair process)

86
Q

2 morphological forms of macrophages

A

Mononuclear cell (kidney bean shaped nucleus)
Multinucleated forms called Giant Cells

87
Q

Type of T cells that secrete gamma interferon, activating M1 cells

A

Th1

88
Q

Type of T cells that secrete IL-4, IL-5, and IL-13, activating M2 cells (tissue repair) and recruiting eosinophils

A

Th2

89
Q

Type of T cells that secrete IL-17, recruiting neutrophils

A

Th17

90
Q

Th17 cells secrete IL-17, recruiting these

A

Neutrophils

91
Q

Type of T cells involved in bacteria, viruses, and autoimmune diseases

A

Th1 and Th17

92
Q

Type of T cells involved with helminths and allergy

A

Th2

93
Q

Type of cells that morphologically have small round nuclei, usually scant cytoplasm
Activated forms have more cytoplasm

A

Lymphocytes

94
Q

Type of cell that morphologically looks like “glass slippers”

A

Plasma cells

95
Q

Type of chronic inflammation against persistent stimuli

A

Granulomatous inflammation

96
Q

Granulomatous inflammation is a type of chronic inflammation against this

A

Persistent stimuli

97
Q

Cell type involved in granulomatous inflammation

A

Macrophages

98
Q

Change in macrophage morphology to epitheliod histiocyte (“banana shape”) occurs during this
May form multinucleated giant cells

A

Granulomatous inflammation

99
Q

Released by macrophages and has elevated serum levels granulomatous inflammation

A

ACE

100
Q

Released by macrophages during granulomatous inflammation and increases Ca absorption (hypercalcemia)

A

Vitamin D

101
Q

How does granulomatous inflammation act to eliminate threats?

A

Walls off threats

102
Q

2 typical persistent infections eliminated by granulomatous inflammation

A

Tuberculosis and Fungi

103
Q

Granulomatous inflammation often contains this which appears morphologically pink/glassy

A

Fibrous/hyalinized material

104
Q

Granulomatous inflammation that is caseating is seen in this infection

A

Tuberculosis

105
Q

Immunodeficiency due to NADPH oxidase deficiency
Results in inability to generate superoxide from NADPH
Cannot generate ROS to kill microorganisms
Poor fungal and bacterial killing by neutrophils
Monocytes/macrophages are recruited
Attempt to wall off infection with granulomas
Early childhood onset
Recurrent infections with catalase positive organisms
Pneumonia
Osteomyelitis
Skin infections
Lymphadenitis (lymph node enlargement)
Ineffective phagocyte killing → attempt to contain with granulomas
Also with draining skin nodules

A

Chronic granulomatous disease

106
Q

Chronic granulomatous disease is due to a deficiency in this

A

NADPH oxidase
Cannot generate ROS to kill microorganisms

107
Q

Condition characterized by ineffective phagocyte killing; attempt to contain with granulomas

A

Chronic granulomatous disease

108
Q

In Chronic granulomatous disease, there is ineffective phagocyte killing, so the body compensates by doing this

A

Attempt to contain infection with granulomas

109
Q

Condition characterized by early childhood onset, recurrent infections with catalase positive organisms, skin infections, lymphadenitis

A

Chronic granulomatous disease

110
Q

3 key cells in tissue repair

A

Macrophages (M2), fibroblast (collagen), endothelial cell (angiogenesis)

111
Q

2 processes by which tissue repair occurs

A

Regeneration
Connective tissue deposition

112
Q

Describes tissues that are normally continuously regenerating
Surface epithelium, bone marrow

A

Labile tissues

113
Q

Tissues that are not dividing but able to stimulate cells to divide
Stem cells, mature cells can re-enter cell cycle

A

Stable tissues

114
Q

Tissues that are unable to divide and have no ability to regenerate
Nervous, cardiac muscle

A

Permanent tissues

115
Q

2 types of permanent tissues

A

Nervous and cardiac muscle

116
Q

2 examples of labile tissues

A

Surface epithelium and bone marrow

117
Q

Example of stable tissue

A

Stem cells

118
Q

This process of tissue repair depends on proliferative potential of tissue (labile, stable, permanent)

A

Regeneration

119
Q

Connective tissue deposition occurs during tissue repair in these 2 settings

A

Damage is too severe to restore with cellular regeneration
Damage to organ incapable of regeneration (e.g. cardiac)

120
Q

Connective tissue deposition produces this type of tissue

A

Granulation tissue - scar/fibrosis

121
Q

3 components of connective tissue deposition during tissue repair

A

Angiogenesis (vessels)
Connective fiber deposition
Connective tissue remodeling

122
Q

During angiogenesis, vasodilation occurs due to these 2 molecules

A

NO and VEGF
Produces increased vascular permeability

123
Q

NO and VEGF lead to this

A

Vasodilation; angiogenesis

124
Q

Cells that separate from vessel and breakdown the basement membrane during angiogenesis

A

Pericytes

125
Q

Family of enzymes that digest the basement membrane

A

MMPs (matrix matelloproteinases)

126
Q

Cells that separate from vessel and breakdown basement membrane during angiogenesis

A

Pericytes

127
Q

M2 cells produce TGF beta, which recruits these cells during connective tissue deposition

A

Fibroblasts

128
Q

M2 cells produce this which recruits fibroblasts during connective tissue deposition

A

TGF beta

129
Q

Cells which produce TGF beta, recruiting fibroblasts during connective tissue deposition

A

M2 cells

130
Q

Granulation tissue that is diffuse or parenchymal

A

Fibrosis

131
Q

Granulation tissue that is localized/defined

A

Scar

132
Q

M2 cells produce this during connective tissue deposition, which recruits fibroblasts, stimulates collagen and fibronectin production, inhibits MMPs, and inhibits lymphocyte and other WBC activity

A

TGF beta

133
Q

M2 cells produce TGF beta during connective tissue deposition, which stimulates the production of these

A

Collagen and fibronectin

134
Q

M2 cells produce TGF beta during connective tissue deposition, which inhibits these enzymes

A

MMPs

135
Q

M2 cells produce TGF beta during connective tissue deposition, which inhibits these cells

A

Lymphocytes and other WBC activity

136
Q

At what point during connective tissue deposition in tissue repair is there granulation tissue?

A

After connective tissue fiber deposition; where M2 cells have produced TGF beta

137
Q

Enzymes that are important during connective tissue remodeling of connective tissue deposition in tissue repair and allow collagen turnover

A

MMPs (matrix metalloproteases)

138
Q

Type of fibroblasts that produce actin filaments

A

Myofibroblasts

139
Q

Cells that are able to contract and reapproximate wound edges togethers during collagen tissue deposition of tissue repair

A

Myofibroblasts

140
Q

At what point of collagen tissue deposition of tissue repair is there a mature scar? (dense collagen, mature vessels that are not leaky and have thicker walls)

A

After connective tissue remodeling

141
Q

During this part of tissue repair, vessel number decreases, collagen density increases, myofibroblasts produce actin filaments, and WBCs depart

A

Connective tissue remodeling

142
Q

Repair process for small wound and minimal separation

A

First intention tissue repair

143
Q

Formation of this during first intention tissue repair provides scaffold for repair

A

Clot formation
Attracts WBCs, fibroblasts, and endothelium

144
Q

What happens <24 hours during first intention tissue repair?

A

Neutrophils begin removing necrotic tissue
Epithelium at base begin proliferating

145
Q

What happens day 3 during first intention tissue repair?

A

Surface covered by epithelium
Macrophages replace neutrophils

146
Q

What happens day 5 during first intention tissue repair?

A

Fibroblasts proliferate and begin type I collagen production

147
Q

What happens week 2 during first intention tissue repair?

A

Scar is maturing

148
Q

What happens at 1 month during first intention tissue repair?

A

Mature scar without WBCs, tensile strength ~70% of original

149
Q

At what time of first intention tissue repair does:
Neutrophils begin removing necrotic tissue
Epithelium at base begins proliferating

A

<24 hours

150
Q

At what time of first intention tissue repair does:
Surface covered by epithelium
Macrophages replace neutrophils

A

Day 3

151
Q

At what time of first intention tissue repair does:
Fibroblasts proliferate and begin producing collagen

A

Day 5

152
Q

At what time of first intention tissue repair does:
Scar is maturing

A

Week 2

153
Q

At what time of first intention tissue repair does:
Mature scar without WBCs; tensile strength ~70% of original

A

1 month

154
Q

Repair process for wound without approximation (i.e. gaping wound; edges are not brought together)

A

Second intention

155
Q

Type of collagen that forms provisional matrix during second intention tissue repair

A

Collegen type III

156
Q

Type of collagen that replaces the provisional matrix during first intention tissue repair

A

Type I collagen

157
Q

Why does second intention tissue repair have higher potential for inflammation-mediated damage and infection?

A

Gap is filled with larger volume of clot and necrotic material

158
Q

Healing by second intention often produces this type of scar

A

Hypertrophic scar
Raised above surrounding tissue

159
Q

Tissue repair abnormality of excessive fibrous tissue where certain people are predisposed to this

A

Keloid formation (greatly raised about surrounding tissue)

160
Q

Keloid formation is more common in people of this origin

A

African origin

161
Q

Tissue repair abnormality of excessive fibrous tissue that disturbs organ function

A

Parenchymal fibrosis

162
Q

Two cytokines that can lead to production of PG-E2 during fever

A

IL-1 and TNF

163
Q

Compound that leads to increased preoptic nucleus set point during systemic inflammatory response syndrome

A

PG-E2

164
Q

Occurs when WBCs are released from storage pools and increased production

A

Leukocytosis

165
Q

Immune cells elevated in bacterial infection

A

Neutrophils

166
Q

Immune cells elevated in viral infection

A

Lymphocytes

167
Q

Immune cells elevated in bacterial parasitic infection and allergy

A

Eosinophils

168
Q

C-reactive protein, erythrocyte sedimentation rate (ESR), serum amyloid A, hepcidin, and fibrinogen are examples of acute phase reactants that are seen in these states

A

Inflammatory states

Pathology (3 decks)

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