Brainscape's Knowledge GenomeTM

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


See full index

MF2 Final study > Inflammation & tissue repair > Flashcards

Inflammation & tissue repair Flashcards

1
Q

process of removing harmful agents and beginning repair process

A

Inflammation

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

Acute inflammation is part of _____ immunity

A

Innate

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

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

A

Toll-like receptors

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

Necrotic tissue is recognized by these

A

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

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

DAMPs are recognized by these receptors present on all cells

A

NOD-like receptors

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

DAMPs are recognized by NOD-like receptor to produce ________

A

Inflammasome

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

Inflammasome activates this enzyme

A

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

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

Caspase 1 activates this

A

IL-1 –> fever and leukocyte recruitment

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

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

3 main phases of leukocyte recruitment during acute inflammation

A

Dilation of small arterioles (increase blood flow)
Increased vascular permeability (leakage of protein rich fluid)
Emigration of leukocytes from vessel in tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Dilation of small arterioles during acute inflammation is mediated by these

A

Histamines

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

Dilation of small arterioles increases or decreases capillary blood flow?

A

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

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

____ blood flow allows leukocytes to leave circulation

A

Slow

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

Leukocyte margination occurs during acute inflammation due to this

A

Stasis (slow blood flow)

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

Leukocyte rolling is mediated by these

A

Selectins

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

Leukocyte adhesion to endothelium is mediated by this interaction

A

Integrin : adhesion molecule interaction

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

Leukocyte migration across vessel wall occurs in venules toward ______ gradient

A

Chemokine

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

Increased vascular permeability occurs via these 2 mechanisms

A

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

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

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

A

Histamines, Leukotrienes, Bradykinins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

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

A

Endothelial contraction

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

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

A

Endothelial damage

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

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

A

Protein and cell-rich

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Key cell types recruited to site of acute inflammation are:

A

Phagocytes (neutrophil and macrophage)

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

Earliest cell to arrive in acute inflammation

A

Neutrophils

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

Main cell that arrives at site of acute inflammation

A

Macrophage

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

Neutrophils arrive at site of acute inflammation after _____ hours

A

6-24 hours
Earliest cell

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

Macrophages arrive at site of acute inflammation after _____ hours

A

24-48
(later; after neutrophils)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Leukocytes are brought to site of acute inflammation via chemotaxis, mediated by these 4 things

A

Bacterial production (e.g. LPS)
Cytokines
Complement (especially C5a)
Arachidonic acid metabolites (e.g. leukotriene B4)

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

Step of acute inflammation that involves innate anti-inflammatory processes

A

Regulation

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

Membrane bound threat destruction can involve either of these

A

Phagolysosome / inflammasome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

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

A

Neutrophil

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

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

A

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

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

2 protease inhibitors involved in the regulation step of acute inflammation

A

Serum alpha-1 antitrypsin
Neutrophil elastase

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

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

A

Abscess

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

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

A

PMNs (polymorphonuclear leukocytes = neutrophils, basophils, eosinophils)

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

Term that describes excess tissue liquefaction (pus forming)

A

Suppuration

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

Early repaired tissue; early scar

A

Granulation tissue

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

Cells that lay down collagen in scar formation

A

Fibroblasts

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

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

A

Leukocyte adhesion deficiency-1

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

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

Leukocyte adhesion deficiency-1 is due to defective this

A

Defective Beta chain of neutrophil integrins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Leukocyte adhesion deficiency-1 prevents this

A

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

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

During phagocytosis, these structures surround and engulf particles into phagosome

A

Pseudopods

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

Organelle that produces materials to kill/digest offending agent

A

Lysosome

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

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

A

ROS

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

How many components does NADPH oxidase have?

A

7; some in membrane, some in cytoplasm

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

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

A

Phagocytosis

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

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

A

Phagolysosome fusion

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

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

Chediak-Higashi Syndrome is due to defective this

A

Phagosome-lysosome fusion

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

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

A

LYST gene (LYSosomal Traffic regulator)

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

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

Condition characterized by neutrophils and lymphocytes with LARGE fused granules

A

Chediak-Higashi Syndrome

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

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

A

Chediak-Higashi Syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Histamine is released by these cells

A

Mast cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

2 actions of histamine

A

Vasodilation and Venule permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Leukotrienes are a metabolite of this

A

Arachidonic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

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

A

Lipooxygenase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

3 actions of leukotrienes

A

Neutrophil chemotaxis
Neutrophil activation
Smooth muscle contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Prostaglandins are metabolites of this

A

Arachidonic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

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

A

Cyclo-oxygenase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

2 actions of prostaglandins

A

Neutrophil chemotaxis
Vascular permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

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

A

Leukotrienes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

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

A

Prostaglandins

69
Q

Mediator of acute inflammation that causes vasodilation and venule permeability

A

Histamine

70
Q

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

A

Leukotrienes

71
Q

Mediator of acute inflammation that causes neutrophil chemotaxis and vascular permeability

A

Prostaglandins

72
Q

Mediator of acute inflammation that cause:
Endothelial activation
WBC activation
Fibroblast activation
Acute phase response
Induce protein and lipid catabolism; suppress appetite

A

Cytokines, especially TNF, IL-2, and IL-1

73
Q

Endogenous pyrogen that sets thermoregulation at higher set-point

A

IL-2

74
Q

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

A

C3a and C5a

75
Q

Complement factor that leads to chemotaxis of neutrophils, monocytes, eosinophils, basophils

A

C5a

76
Q

Complement factor that activates lipooxygenase, which produces leukotrienes and thromboxanes

A

C5a

77
Q

C5a activates this enzyme, which produces leukotrienes and thromboxanes

A

Lipooxygenase

78
Q

Cardinal sign of acute inflammation that describes tissue erythema

A

Rubor

79
Q

Cardinal sign of acute inflammation that describes tissue warmth

A

Calor

80
Q

Cardinal sign of acute inflammation that describes tissue swelling

A

Tumor

81
Q

Cardinal sign of acute inflammation that describes tendernoss/pain

A

Dolor

82
Q

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

A

Chronic inflammation

83
Q

2 main cells of chronic inflammation

A

Macrophage > lymphocytes (mononuclear cells)

84
Q

Macrophage becomes M1 cell when T cells secrete this

A

gamma IFN

85
Q

Macrophage becomes M2 cell when T cells secrete this

A

IL-4 and IL-13

86
Q

When T cells secrete gamma IFN, macrophages become this

A

M1 cell

87
Q

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

A

M2 cell

88
Q

M1 cell produces these

A

NO and ROS, lysosomal enzymes (innate immunity)

89
Q

M2 cell produces these

A

PDGF, FGF (initiates repair process)

90
Q

2 morphological forms of macrophages

A

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

91
Q

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

A

Th1

92
Q

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

A

Th2

93
Q

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

A

Th17

94
Q

Th17 cells secrete IL-17, recruiting these

A

Neutrophils

95
Q

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

A

Th1 and Th17

96
Q

Type of T cells involved with helminths and allergy

A

Th2

97
Q

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

A

Lymphocytes

98
Q

Type of cell that morphologically looks like “glass slippers”

A

Plasma cells

99
Q

Type of chronic inflammation against persistent stimuli

A

Granulomatous inflammation

100
Q

Granulomatous inflammation is a type of chronic inflammation against this

A

Persistent stimuli

101
Q

Cell type involved in granulomatous inflammation

A

Macrophages

102
Q

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

A

Granulomatous inflammation

103
Q

Released by macrophages and has elevated serum levels granulomatous inflammation

A

ACE

104
Q

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

A

Vitamin D

105
Q

How does granulomatous inflammation act to eliminate threats?

A

Walls off threats

106
Q

2 typical persistent infections eliminated by granulomatous inflammation

A

Tuberculosis and Fungi

107
Q

Granulomatous inflammation often contains this which appears morphologically pink/glassy

A

Fibrous/hyalinized material

108
Q

Granulomatous inflammation that is caseating is seen in this infection

A

Tuberculosis

109
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

110
Q

Chronic granulomatous disease is due to a deficiency in this

A

NADPH oxidase
Cannot generate ROS to kill microorganisms

111
Q

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

A

Chronic granulomatous disease

112
Q

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

A

Attempt to contain infection with granulomas

113
Q

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

A

Chronic granulomatous disease

114
Q

3 key cells in tissue repair

A

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

115
Q

2 processes by which tissue repair occurs

A

Regeneration
Connective tissue deposition

116
Q

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

A

Labile tissues

117
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

118
Q

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

A

Permanent tissues

119
Q

2 types of permanent tissues

A

Nervous and cardiac muscle

120
Q

2 examples of labile tissues

A

Surface epithelium and bone marrow

121
Q

Example of stable tissue

A

Stem cells

122
Q

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

A

Regeneration

123
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)

124
Q

Connective tissue deposition produces this type of tissue

A

Granulation tissue - scar/fibrosis

125
Q

3 components of connective tissue deposition during tissue repair

A

Angiogenesis (vessels)
Connective fiber deposition
Connective tissue remodeling

126
Q

During angiogenesis, vasodilation occurs due to these 2 molecules

A

NO and VEGF
Produces increased vascular permeability

127
Q

NO and VEGF lead to this

A

Vasodilation; angiogenesis

128
Q

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

A

Pericytes

129
Q

Family of enzymes that digest the basement membrane

A

MMPs (matrix matelloproteinases)

130
Q

Cells that separate from vessel and breakdown basement membrane during angiogenesis

A

Pericytes

131
Q

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

A

Fibroblasts

132
Q

M2 cells produce this which recruits fibroblasts during connective tissue deposition

A

TGF beta

133
Q

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

A

M2 cells

134
Q

Granulation tissue that is diffuse or parenchymal

A

Fibrosis

135
Q

Granulation tissue that is localized/defined

A

Scar

136
Q

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

A

Collagen and fibronectin

137
Q

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

A

MMPs

138
Q

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

A

Lymphocytes and other WBC activity

139
Q

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

A

MMPs (matrix metalloproteases)

140
Q

Type of fibroblasts that produce actin filaments

A

Myofibroblasts

141
Q

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

A

Myofibroblasts

142
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

143
Q

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

A

Connective tissue remodeling

144
Q

Repair process for small wound and minimal separation

A

First intention tissue repair

145
Q

What happens <24 hours during first intention tissue repair?

A

Neutrophils begin removing necrotic tissue
Epithelium at base begin proliferating

146
Q

What happens day 3 during first intention tissue repair?

A

Surface covered by epithelium
Macrophages replace neutrophils

147
Q

What happens day 5 during first intention tissue repair?

A

Fibroblasts proliferate and begin type I collagen production

148
Q

What happens week 2 during first intention tissue repair?

A

Scar is maturing

149
Q

What happens at 1 month during first intention tissue repair?

A

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

150
Q

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

A

<24 hours

151
Q

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

A

Day 3

152
Q

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

A

Day 5

153
Q

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

A

Week 2

154
Q

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

A

1 month

155
Q

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

A

Second intention

156
Q

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

A

Collegen type III

157
Q

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

A

Type I collagen

158
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

159
Q

Healing by second intention often produces this type of scar

A

Hypertrophic scar
Raised above surrounding tissue

160
Q

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

A

Keloid formation (greatly raised about surrounding tissue)

161
Q

Keloid formation is more common in people of this origin

A

African origin

162
Q

Tissue repair abnormality of excessive fibrous tissue that disturbs organ function

A

Parenchymal fibrosis

163
Q

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

A

IL-1 and TNF

164
Q

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

A

PG-E2

165
Q

Occurs when WBCs are released from storage pools and increased production

A

Leukocytosis

166
Q

Immune cells elevated in bacterial infection

A

Neutrophils

167
Q

Immune cells elevated in viral infection

A

Lymphocytes

168
Q

Immune cells elevated in bacterial parasitic infection and allergy

A

Eosinophils

169
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

MF2 Final study (28 decks)

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