Brainscape's Knowledge GenomeTM

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


See full index

Pathology > Ch2: Acute and Chronic Inflammation > Flashcards

Ch2: Acute and Chronic Inflammation Flashcards

1
Q

Inflammation is fundamentally what type of response?

A

Protective

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

Two main components of inflammation?

A
  1. Blood vessels

2. Leukocytes

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

What triggers inflammation?

A

Soluble factors produced by cells or derived from plasma proteins

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

Is inflammation acute or chronic?

A

Both

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

Acute inflammation is due to what cells?

A

PMN’s

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

Chronic inflammation is due to what cells?

A

Lymphocytes

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

Subacute inflammation is due to what cells?

A

Eosinophils

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

When is inflammation terminated?

A

When offending agent is eliminated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are some harmful effects of inflammatory response? 2

A
  1. Anaphylactic response

2. Chronic disabling diseases

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

Anaphylactic shock can be induced by what?

A
  1. allergies
  2. bug bites
  3. certain drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the main component of bee venom?

A

Melittin

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

What does melittin stimulate?

A

Phospholipase A2

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

Five features of inflammation in latin and english

A
  1. Calor = heat
  2. Rubor = redness
  3. Tumor = swelling
  4. Dolor = pain
  5. functio laesa = loss of function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

3 main components of acute inflammation?

A
  1. Increased blood flow through change in vessel size (heat, redness)
  2. Leaky vessels (swelling)
  3. Recruitment of leukocytes to injury and their activation (pain, loss of function)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are 4 acute inflammation stimuli?

A
  1. Infections/toxins
  2. tissue necrosis
  3. Foreign bodies
  4. Immune reactions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What receptors recognize certain bacteria, viruses, and fungi?

A

Toll-like receptors

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

Tissue necrosis can be caused by what? 4

A
  1. ischemia
  2. trauma
  3. physical and chemical injury
  4. Hypoxia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is exudation?

A

Escape of fluids proteins and blood cells from vascular system into the interstitial tissue or body cavities

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

What is exudate?

A

High protein content (specific gravity greater than 1.020)

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

What is transudate?

A

Low protien condate (Specific gravity less than 1.012)

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

What is edema?

A

Excess fluid in interstitial tissue or body cavities

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

What is purulent exudate?

A

Exudate rich in neutrophils

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

Is edema transudate or exudate?

A

Transudate

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

What are the changes in pressure in transudate?

A
  1. increased hydrostatic pressure

2. Decreased colloid osmotic pressure

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

Main cause of transudate?

A
  1. increased hydrostatic pressure

2. Decreased colloid osmotic pressure

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

Main cause of exudate?

A

Inflammation

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

Compare transudate and exudate in terms of appearance?

A

Transudate: clear
Exudate: cloudy

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

Compare transudate and exudate in terms of fluid protein?

A

Transudate: less than 0.5
Exudate: greater than 0.5

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

Compare transudate and exudate in terms of fluid LDH?

A

Transudate: Less than 0.6
Exudate: Greater than 0.6

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

What is the earliest manifestation of acute inflammation?

A

Vasodilation

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

Vasodilation first involves what vessels?

A

Arterioles through opening of new capillary beds

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

Vasodilation causes what two things? (2)

A
  1. heat

2. redness

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

Vasodilation is induced by what?

Two examples?

A

Mediators of vascular smooth muscle

Histamine and NO

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

Vasodilation is followed by what in acute inflammation?

A

Increased permeability of microvasculature

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

Changes in vascular flow and caliber lead to what? (3)

All these combine for what state of flow?

A
  1. slower blood flow
  2. concentration of red blood cells in small vessels
  3. Increased viscosity

Stasis

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

Vascular leakage is normally due to what?
What is this called normally?
If it takes too long?

A

Contraction of endothelial cells resulting in increased interendothelial spaces

Immediate transient response (15-30 minutes)

Delayed prolonged leakage (2-12 hours)

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

Delayed prolonged leakage is seen when ? (3)

A
  1. burns
  2. UV
  3. bacterial toxins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Two other causes of vascular leakage?

A
  1. endothelial injury: loss of endothelial cells

2. Transcytosis

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

What is transcytosis?

A

Increased transport of fluids and proteins through endothelial cells

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

During inflammation, what changes in lymph flow?

A

It is increased due to edema

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

What is lymphangitis?

A

Inflammation of lymphatic vessels

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

What is reactive or inflammatory lymphadenitis?

A

Lymph node enlargement because of hyperplasia of the lymphoid follicles and increased numbers of lymphocytes and macrophages

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

Streaking near a skin wound follows what?

What is it diagnostic of?

A

Course of lymphatic channels

Diagnostic of lymphangitis

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

What is lymphadenitis?

A

Painful enlargement of draining lymph nodes

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

What are the four steps of recruitment of leukocytes to sites of injury and infection?

A
  1. Margination
  2. Rolling
  3. adhesion
  4. Diapedesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

In stasis, what do WBC’s do?

What is this process called?

A

WBC’s become more peripheral along endothelial surface

Margination

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

Rolling interactions are mediated by what proteins?

A

Selectins

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

What is rolling regulated by?

A

Cytokines

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

Selectins in leukocytes are called?

A

L-selectins

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

Selectins in endothelium are called what?

A

E-selectin

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

Selectins in platelets are called what?

A

P-selectin

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

Firm adhesion of leukocytes is mediated by what?

A

Integrins

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

What two cytokines induce endothelial expression of ligands for integrins?

A

TNF and IL-1

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

V-CAM is ligand for what?

A

VLA-4 integrin

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

ICAM1 is ligand for what?

A

LFA-1 and Mac-1

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

Leukocytes normally express integrins in what state?

What reverses this?

A

Low affinity

Chemokines

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

What conains P-selectin and vWF in endothelial cells and platelets?

A

Weibel Palade Bodies

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

What causes a cell to express P-selectin? 2

A

Histamine and thrombin

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

3 rolling endothelial molecules and their corresponding leukocyte molecule?

A
  1. P-selectin: Sialyl Lewis
  2. E-selectin: Sialyl Lewis
  3. Glycam-1/CD34: L-selectin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

2 adhesion endothelial molecules and corresponding leukocyte molecule?

A
  1. ICAM-1: LFA-1, MAC-1

2. VCAM-1: VLA-4

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

LAD-1 is a defect in what?

What is the functional result of this?

A

Defect in Beta2 chain of LFA-1 and Mac-1 integrins.

Neutrophils can’t adhere

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

Clinical manifestation of LAD-1? (3)

A
  1. Skin infections
  2. Inflammatory lesions without neutrophils
  3. Delayed separation of umbilical cord at birth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Treatment of LAD-1?

A

Granulocyte concentration with functional WBC’s.

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

LAD-2 is a defect in what?

What is functional result of this?

A

Absence of sialyl-lewis for E- and P- selectins

Rolling issue

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

Manifestations of LAD-2? 2

A

Skin infections

Mental retardation

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

Leukocyte migration across endothelial cells is called what?

A

Diapedesis or Transmigration

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

Where does diapedesis occur?

A

Post-capillary venules

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

What mediates diapedesis?

A

PECAM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What do leukocytes make to cross BM?

A

Collagenases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What is the most common exogenous agent for chemotaxis?

A

Bacterial products

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

endogenous chemoattracts include? 3

A
  1. Cytokines (IL-8)
  2. Components of complement (C5a and C3a)
  3. Arachidonic acid metabolites (leukotrieneB4)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

First cell on scene are what?

Why? (2)

A

neutrophils

  1. more present in blood
  2. Respond very rapidly to chemokines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

When do neutrophils dominate the inflammatory infiltrate?

A

6 to 24 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Monocytes predominate during when?

Why? 2

A

24-48 hours

  1. last longer
  2. proliferate in tissues
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Exceptions to when cells show up first (so not neutrophils first) 1

A
  1. Viral infections (lymphocytes first)

2. Hypersensitivity (eosinophils)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Responses of leukocytes consist of what two sets of events?

A
  1. Recognition of offending agents

2. Activation of leukocytes to ingest and destroy offending agents and amplify the inflammatory reaction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Leukocytes have what receptors (4)

A
  1. Toll-like receptors
  2. G-coupled receptors
  3. Receptors for opsonins
  4. Receptors for cytokines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

G-protein coupled receptors recognize what?

A

Bacterial peptide containing N-FM residues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Leukocyte receptors for cytokines include what main one?

A

IFN-gamma (macrophage activating cytokine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Three steps of phagocytosis?

A
  1. Recognition and attachment of particle
  2. Engulfment that forms a vacuole
  3. Killing or degradation of material
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Receptors for phagocytosis include? (3)

A
  1. mannose receptors
  2. scavenger receptors
  3. receptors for various opsonins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What are the three steps of engulfment?

A
  1. Extensions of cytoplasm (pseudopods) around material
  2. Plasma membrane pinches off to form phagosome
  3. phagosome fuses with lysosome to make phagolysosome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Microbial killing is accomplished by what? (2)

A
  1. ROS

2. reactive nitrogen species

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Substances in leukocyte granules for phagocytosis include? 7

A
  1. elastase
  2. defensins
  3. cathelicidins
  4. lysozyme
  5. lactoferrin
  6. major basic protein
  7. bactericidal/permeability increasing protein
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What is the most efficient bactericidal system in neutrophils?

A

H2O2-MPO halide system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What happens in H2O2-MPO-halide system? 3

A
  1. H2O2 generated by NADPH
  2. Myeloperoxidase in granules of PMN’s converts H2O2 to hypochlorite (bleach)
  3. killing by halogenation or lipid peroxidation
87
Q

The growth factors that activated leukocytes produce do what? (3)

A
  1. Stimulate proliferation of endothelial cells
  2. promote synthesis of collagen
  3. Promote enzymes that remodel CT
88
Q

Classically activated macrophage (M1) does what?

A

Microbicidal

89
Q

Alternatively activated macrophage is involved in what?

A

tissue repair and fibrosis

90
Q

Do activated leukocytes secrete mediators or inhibitors of inflammatory response?

91
Q

What are 3 situations in which leukocytes mediate tissue injury?

A
  1. Infection
  2. Autoimmune
  3. React excessively against environmental substances
92
Q

What is frustrated phagocytosis

A

Inability of leukocytes to surround and ingest activating substances with release of lysosomal enzymes extracellularly

93
Q

4 defects in leukocyte function

A
  1. leukocyte adhesion defect
  2. phagolysosome defect
  3. microbicidal activity defect
  4. acquired deficiencies
94
Q

The main leukocyte adhesion defect is what?
Clinical problem?
Classic example?

A

LAD1 and LAD2
recurrent bacterial infections
delayed umbilical cord separation

95
Q

What is main disease of phagolysosome function?

A

Chediak-Higashi syndrome

96
Q

Manifestations of Chediak-Higashi syndrome?

A
  1. Albinism (melanocyte problem)
  2. nerve defects
  3. bleeding
  4. Defective PMN’s
  5. Leukocytes with giant granules
  6. Delayed killing
97
Q

What is the genetic problem in chediak-higashi?

98
Q

What is the main defect in microbicidal activity in leukocytes?

A

Chronic granulomatous disease

99
Q

Chronic granulomatous disease is result of what mutation?

A

Defective genes encoding NADPH-oxidase either X-linked or autosomal recessive

100
Q

The variants of chronic granulomatous disease also differ in terms of location, what are they?

A
  1. X-linked: membrane

2. AR: cytosol

101
Q

Patients with granulomatous disease have what problem?

A

Recurrent bacterial infection (catalase positive)

102
Q

Test for chronic granulomatouse disease is what?

A

Nitroblue tetrazolium (yellow = disease)

103
Q

Most frequent cause of leukocyte defects is what?

A

Bone marrow suppression due to diabetes or steroids

104
Q

Mediators of inflammation are made when?

A

Long as the stimulus persists (rapid bursts)

105
Q

What are the anti-inflammatory cytokines? (2)

A
  1. TGF-beta

2. IL-10

106
Q

What are the anti-inflammatory lipid mediators called? (2)

A
  1. Resolvins

2. protectins

107
Q

What neural impulse inhibits production of TNF in macrophages?

A

Cholinergic discharge

108
Q

Mediators are generated from what?

A

Cells or plasma proteins

109
Q

What is the relative length of life of a mediator of inflammation?

110
Q

What are the two major vasoactive amines?

A

Histamine

Serotonin

111
Q

When are vasoactive amines released?

A

First to be released during inflammation

112
Q

Histamine is released by what cells? (3)

A
  1. mast cells
  2. basophils
  3. platelets
113
Q

Histamine is released to what stimuli? 6

A
  1. Physical injury
  2. binding of antibodies to mast cell
  3. anaphylatoxins (c3a c5a)
  4. histamine-releasing proteins from leukocytes
  5. neuropeptides
  6. Cytokines (IL-1, IL8)
114
Q

What neuropeptide modulates pain?

A

Substance P

115
Q

Histamine causes what? 2

A

Arterior dilation

Increases permeability of venules

116
Q

Histamine is the principal mediator of what?

A

Immediate phase of increased vascular pemerability

117
Q

Where does histamine bind?

A

H1 receptors in interendothelial gaps of venules

118
Q

Serotonin has what effects? 2

A

Arterior dilation

Increases permeability of venules

119
Q

Serotonin is found where?

When is it released?

A

Platelets

Platelet aggregation

120
Q

What cells have serotonin in GI?

A

Enterochromaffin

121
Q

Membrane derived arachidonic acid produces what?
Via what enzyme?
What initiates all this?

A

Prostaglandins and leukotrienes

Phospholipases

inflammatory mediators

122
Q

Steroids have what effects on phospholipases?

A

Inhibit them.

123
Q

COX converts what to what?

A

Arachidonic acid into prostaglandins, prostacyclin, and thromboxanes.

124
Q

12-lipoxygenase converts what to what?

A

5-HPETE into lipoxin

125
Q

Prostacyclin causes what? 2

A

Vasodilation

Inhibits platelet aggregation

126
Q

Thrombaxane A2 causes what? 2

A

Causes vasoconstriction

Promotes platelet aggregation

127
Q

PGD2 and PGE2 causes what? 2

A

Vasodilation

Increased vascular permeability

128
Q

Leukotrienes do what? 3

A

Vasoconstriction
Bronchospasm
Increased vascular permeability

129
Q

Lipoxins do what? 2

A

Inhibit neutrophil adhesion and chemotaxis

130
Q

5-lipoxygenase converts what to what?

A

Arachidonic acid into leukotriene and lipoxin

131
Q

Platelets contain what prostaglandin enzyme?

Which makes what?

A

Thromboxane synthetase

TxA2

132
Q

What prostglandin enzyme does vascular endothelium have?

A

Prostacyclin synthetase

133
Q

Aspirin and NSAIDS inhibit what enzymes?

A

COX-1 and COX-2

134
Q

COX-2 generates prostaglandins involved in what reactions?

A

Inflammatory reactions

135
Q

COX-1 generates prostaglandins involved in what?

A

Cytoprotective and inflammatory reactions

136
Q

LTB4 causes what?

A

Neutrophils to aggregate (chemotactic)

137
Q

LTC4, LTD4, LTE4 cause what? (3)

A

Vasoconstriction
Bronchospasm
Increased vascular permeability

138
Q

Which is more potent, leukotrienes or histamine?

A

Leukotrienes

139
Q

Lipoxin LxA4 causes what?

A
  1. vasodilation

2. antagonizes LTC4

140
Q

Lipoxins may have what relationship with leukotrienes?

A

Negative regulators of leukotriene actions

141
Q

What are the two COX inhibitors?

A

ASA and NSAIDS

142
Q

What are the two lipoxygenase inhibitors?

A

Zileuton

Montelukast

143
Q

Montelukast is used in treatment of what?

144
Q

Fish oil has what effect on eicosanoids synthesis? 2

A

Fish oils can be poorly converted into active metabolites by COX and LOX pathways.
Can be used to produce resolvins and protectins

145
Q

Platelet activating factor is generated from what?

A

Membrane phospholipids

146
Q

What does PAF do? 7

A
  1. leukocyte adhesion
  2. chemotaxis
  3. degranulation
  4. oxidative burst
  5. vasoconstriction
  6. bronchoconstriction
  7. increased vascular permeability
147
Q

Free radicals at low levels do what?

A

Increase cytokines

148
Q

Free radicals at high levels do what? (2)

A
  1. tissue damage

2. inactivate antiproteases

149
Q

Antioxidant protective mechanisms are include what? 5

A
  1. catalase
  2. superoxide dismutase
  3. glutathione peroxidase
  4. ceruloplasmin
  5. transferrin
150
Q

Nitric oxide factor is released from what cells?

Causes what?

A

Endothelial cells

Relax smooth muscle causing vasodilation

151
Q

NO in macrophages does what?

A

kills microbes

152
Q

What is NO’s role in inflammation? 3

A
  1. vasodilation
  2. antagonize platelet aggregation and adhesion
  3. Microbicidal agent
153
Q

Cytokines are defined how?

A

Peptides modulating functions of other cells

154
Q

TNF and IL-1 are produced by what cells?

A

Activated macrophages

155
Q

TNF and IL-1 have what effects? 2

A
  1. cause endothelial activation

2. Induce acute phase responses

156
Q

Production of IL-1 is called what?

A

Inflammasome

157
Q

What happens when IL-1 is mutated?

A

Cause inherited autoinflammatory syndromes (familial Mediterranean fever) (upregulated IL-1 production

158
Q

Sustained release of TNF causes what?

159
Q

C-X-C chemokines use what coreceptor for HIV?

160
Q

C-C chemokines use what coreceptor for HIV?

161
Q

What is the main C chemokine (gamma chemokine)

A

Lymphotactin

162
Q

What is the main CX3C chemokine?

A

Fractalkine

163
Q

Two main functions of chemokines?

A
  1. Recruit leukocytes

2. Control normal migration of cell through tissues

164
Q

IFN-gamma is released by what cells?

A

T lymphocytes and NK cells

165
Q

IFN-gamma activates what?

A

Macrophages

166
Q

What counteracts proteases?

Two examples?

A

Antiproteases

  1. alpha2-macroglobulin
  2. alpha1-antitrypsin
167
Q

Neuropeptides are secreted by who?

A

Sensory nerve fibers and leukocytes

168
Q

Neuropeptides have what role?

A

Initiate and propagate inflammatory response

169
Q

Nerve fibers containing substance P do what? (3)

A
  1. transmit pain signals
  2. regulate vessel tone
  3. modulate vascular permeability
170
Q

Is complement system innate or adaptive?

171
Q

What triggers classical complement pathway?

A

Fixation of C1 to IgM or IgG

172
Q

What triggers alternative pathway?

A

Microbial surface proteins

173
Q

C3a and C5a are called?

Because they do what?

A

Anaphylatoxins

Stimulate histamine release

174
Q

c5a acts as what agent as well?

What can it activate also?

A

Chemotactic for leukocytes

Activate lipoxygenase pathway

175
Q

C3b has what role in phagocytosis?

A

Act as opsonin

176
Q

MAC makes cells permeable to what?

A

Water and ions

177
Q

Intrinsic clotting pathway activated by what?

A

Hageman factor/Factor XII

178
Q

Thrombin promotes what?

A

Inflammation

179
Q

Describe the steps of Kinin system 2

A
  1. Factor XIIa converts prekallikrein into kallikrein

2. Kallikrein converts HMWK into bradykinin

180
Q

What are the precursors of vasoactive peptides called?

A

Kininogens

181
Q

Bradykinin has what functions? (3)

A
  1. Increase vascular permeability
  2. Smooth muscle contraction
  3. Dilation of blood vessels
182
Q

What inactivates bradykinin?

183
Q

Factor XIIa, induces what two pathways?

A
  1. fibrin clot formation

2. fibrinolytic system

184
Q

What other thing does kallikrein do besides kinin pathway? 2

A

Converts plasminogen to plasmin

Convert C5 to C5a

185
Q

Activated Hageman factor (factor XIIa) initiates what four pathways?

A

Kinin
Clotting
Fibrinolytic
Complement

186
Q

What does plasmin do?

A
  1. Cleaves fibrin

2. Converts C3 to C3a

187
Q

What are possible outcomes of inflammation? (2)

A
  1. Resolution and healing

2. progression to chronic inflammation

188
Q

Morphologic hallmarks of inflammation? (3)

A
  1. Dilation of small blood vessels
  2. slowing of blood flow
  3. accumulation of leukocytes and fluid in extravascular tissue
189
Q

What is serous inflammation?

Example?

A

Outpouring of thin fluid (effusion)

Skin blister

190
Q

What is fibrinous inflammation?

When is it seen?

A

Fibrin is formed and deposited in extracellular spaces. Exudate develops when leaks become large.
Common in lining of body cavities: meninges, pericardium, pleura

191
Q

Suppurative/purulent inflammation/abscess is due to what?

A

Production of large amounts of pus or purulent exudate.

192
Q

bacteria that cause pus formation are known as what?

193
Q

What is an ulcer?

A

Local defect on surface of organ or tissue produced by sloughing or inflamed necrotic tissue

194
Q

What is chronic inflammation?

A

Inflammation lasting weeks to months

195
Q

Chronic inflammation results from what? (3)

A
  1. persistent microbial infections
  2. prolonged exposure to toxic agents
  3. autoimmune diseases
196
Q

Silica in lungs leads to what?

197
Q

Plasma lipid toxicity is known as what?

A

Atherosclerosis

198
Q

Characteristic cells of chronic inflammation?

A

Macrophages
Lymphocytes
Plasma cells

199
Q

What shows up morphologically in chronic inflammation?

A

Tissue destruction

Attempts to heal by CT replacement of damaged tissue utilizing angiogenesis and fibrosis

200
Q

What is the dominant player in chronic inflammation?

A

Macrophages

201
Q

Macrophages in spleen and lymph nodes are known as what?

A

Sinus histiocytes

202
Q

macrophages in placenta?

A

Hofbauer cell

203
Q

Half life of blood monocyte?

204
Q

life span of tissue macrophage?

A

several months or years

205
Q

Macrophages secrete products to do what?

A
  1. eliminate agents (ROS, NO, enzymes)

2. initiate repair (growth factors)

206
Q

Plasma cells are involved in opsonization how?

207
Q

granules of eosinophils contain what?

A

Major basic protein

208
Q

Mast cells are found in what tissues mainly?

209
Q

Mast cells upon IgE activation do what?

A

Release histamines and prostaglandins

210
Q

What is chronic bacterial infection of bone?

A

Osteomyelitis

211
Q

What are two types of granulomas?

A

Foreign body

Immune granulomas

212
Q

What initiates a foreign body granuloma?

A

Inert foreign bodies like sutures

213
Q

What initiates immune granulomas?

Typical one

A

Something doesn’t degrade well.

Myobacterium tuberculosis

214
Q

What does defective inflammation result in?

Why?

A

Susceptibility to infections
And bad wound healing

Bad inflammation = bad innate immunity

Pathology (36 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions