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Pathology > Ch2: Acute and Chronic Inflammation > Flashcards

Ch2: Acute and Chronic Inflammation Flashcards

1
Q

Inflammation is fundamentally what type of response?

A

Protective

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2
Q

Two main components of inflammation?

A
  1. Blood vessels

2. Leukocytes

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3
Q

What triggers inflammation?

A

Soluble factors produced by cells or derived from plasma proteins

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4
Q

Is inflammation acute or chronic?

A

Both

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5
Q

Acute inflammation is due to what cells?

A

PMN’s

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6
Q

Chronic inflammation is due to what cells?

A

Lymphocytes

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7
Q

Subacute inflammation is due to what cells?

A

Eosinophils

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8
Q

When is inflammation terminated?

A

When offending agent is eliminated

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9
Q

What are some harmful effects of inflammatory response? 2

A
  1. Anaphylactic response

2. Chronic disabling diseases

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10
Q

Anaphylactic shock can be induced by what?

A
  1. allergies
  2. bug bites
  3. certain drugs
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11
Q

What is the main component of bee venom?

A

Melittin

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12
Q

What does melittin stimulate?

A

Phospholipase A2

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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
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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)
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15
Q

What are 4 acute inflammation stimuli?

A
  1. Infections/toxins
  2. tissue necrosis
  3. Foreign bodies
  4. Immune reactions
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16
Q

What receptors recognize certain bacteria, viruses, and fungi?

A

Toll-like receptors

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17
Q

Tissue necrosis can be caused by what? 4

A
  1. ischemia
  2. trauma
  3. physical and chemical injury
  4. Hypoxia
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18
Q

What is exudation?

A

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

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19
Q

What is exudate?

A

High protein content (specific gravity greater than 1.020)

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20
Q

What is transudate?

A

Low protien condate (Specific gravity less than 1.012)

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21
Q

What is edema?

A

Excess fluid in interstitial tissue or body cavities

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22
Q

What is purulent exudate?

A

Exudate rich in neutrophils

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23
Q

Is edema transudate or exudate?

A

Transudate

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24
Q

What are the changes in pressure in transudate?

A
  1. increased hydrostatic pressure

2. Decreased colloid osmotic pressure

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25
Q

Main cause of transudate?

A
  1. increased hydrostatic pressure

2. Decreased colloid osmotic pressure

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26
Q

Main cause of exudate?

A

Inflammation

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27
Q

Compare transudate and exudate in terms of appearance?

A

Transudate: clear
Exudate: cloudy

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28
Q

Compare transudate and exudate in terms of fluid protein?

A

Transudate: less than 0.5
Exudate: greater than 0.5

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29
Q

Compare transudate and exudate in terms of fluid LDH?

A

Transudate: Less than 0.6
Exudate: Greater than 0.6

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30
Q

What is the earliest manifestation of acute inflammation?

A

Vasodilation

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31
Q

Vasodilation first involves what vessels?

A

Arterioles through opening of new capillary beds

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32
Q

Vasodilation causes what two things? (2)

A
  1. heat

2. redness

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33
Q

Vasodilation is induced by what?

Two examples?

A

Mediators of vascular smooth muscle

Histamine and NO

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34
Q

Vasodilation is followed by what in acute inflammation?

A

Increased permeability of microvasculature

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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

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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)

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37
Q

Delayed prolonged leakage is seen when ? (3)

A
  1. burns
  2. UV
  3. bacterial toxins
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38
Q

Two other causes of vascular leakage?

A
  1. endothelial injury: loss of endothelial cells

2. Transcytosis

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39
Q

What is transcytosis?

A

Increased transport of fluids and proteins through endothelial cells

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40
Q

During inflammation, what changes in lymph flow?

A

It is increased due to edema

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41
Q

What is lymphangitis?

A

Inflammation of lymphatic vessels

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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

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43
Q

Streaking near a skin wound follows what?

What is it diagnostic of?

A

Course of lymphatic channels

Diagnostic of lymphangitis

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44
Q

What is lymphadenitis?

A

Painful enlargement of draining lymph nodes

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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
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46
Q

In stasis, what do WBC’s do?

What is this process called?

A

WBC’s become more peripheral along endothelial surface

Margination

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47
Q

Rolling interactions are mediated by what proteins?

A

Selectins

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48
Q

What is rolling regulated by?

A

Cytokines

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49
Q

Selectins in leukocytes are called?

A

L-selectins

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50
Q

Selectins in endothelium are called what?

A

E-selectin

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51
Q

Selectins in platelets are called what?

A

P-selectin

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52
Q

Firm adhesion of leukocytes is mediated by what?

A

Integrins

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53
Q

What two cytokines induce endothelial expression of ligands for integrins?

A

TNF and IL-1

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54
Q

V-CAM is ligand for what?

A

VLA-4 integrin

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55
Q

ICAM1 is ligand for what?

A

LFA-1 and Mac-1

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56
Q

Leukocytes normally express integrins in what state?

What reverses this?

A

Low affinity

Chemokines

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57
Q

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

A

Weibel Palade Bodies

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58
Q

What causes a cell to express P-selectin? 2

A

Histamine and thrombin

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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
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60
Q

2 adhesion endothelial molecules and corresponding leukocyte molecule?

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

2. VCAM-1: VLA-4

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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

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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
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63
Q

Treatment of LAD-1?

A

Granulocyte concentration with functional WBC’s.

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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

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65
Q

Manifestations of LAD-2? 2

A

Skin infections

Mental retardation

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66
Q

Leukocyte migration across endothelial cells is called what?

A

Diapedesis or Transmigration

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67
Q

Where does diapedesis occur?

A

Post-capillary venules

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68
Q

What mediates diapedesis?

A

PECAM

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69
Q

What do leukocytes make to cross BM?

A

Collagenases

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70
Q

What is the most common exogenous agent for chemotaxis?

A

Bacterial products

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71
Q

endogenous chemoattracts include? 3

A
  1. Cytokines (IL-8)
  2. Components of complement (C5a and C3a)
  3. Arachidonic acid metabolites (leukotrieneB4)
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72
Q

First cell on scene are what?

Why? (2)

A

neutrophils

  1. more present in blood
  2. Respond very rapidly to chemokines
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73
Q

When do neutrophils dominate the inflammatory infiltrate?

A

6 to 24 hours

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74
Q

Monocytes predominate during when?

Why? 2

A

24-48 hours

  1. last longer
  2. proliferate in tissues
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75
Q

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

A
  1. Viral infections (lymphocytes first)

2. Hypersensitivity (eosinophils)

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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

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77
Q

Leukocytes have what receptors (4)

A
  1. Toll-like receptors
  2. G-coupled receptors
  3. Receptors for opsonins
  4. Receptors for cytokines
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78
Q

G-protein coupled receptors recognize what?

A

Bacterial peptide containing N-FM residues

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79
Q

Leukocyte receptors for cytokines include what main one?

A

IFN-gamma (macrophage activating cytokine)

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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
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81
Q

Receptors for phagocytosis include? (3)

A
  1. mannose receptors
  2. scavenger receptors
  3. receptors for various opsonins
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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
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83
Q

Microbial killing is accomplished by what? (2)

A
  1. ROS

2. reactive nitrogen species

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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
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85
Q

What is the most efficient bactericidal system in neutrophils?

A

H2O2-MPO halide system

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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?

A

Both

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?

A

LYST gene

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?

A

Short

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?

A

Asthma

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?

A

Cachexia

159
Q

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

A

CXCR4

160
Q

C-C chemokines use what coreceptor for HIV?

A

CCR5

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?

A

Both

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?

A

Kininase

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?

A

Pyogenic

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?

A

Silicosis

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?

A

1 day

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?

A

Make IgG

207
Q

granules of eosinophils contain what?

A

Major basic protein

208
Q

Mast cells are found in what tissues mainly?

A

CT

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)

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