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Pathology > Exam 3: Acute Inflammation > Flashcards

Exam 3: Acute Inflammation Flashcards

1
Q

What is inflammation?

A

The response of living tissue of injury

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2
Q

What does inflammation involve?

A

A well-organized cascade of fluidic and cellular changes

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3
Q

Describe the process of inflammation

A

Process is redundant and complex

Process is continuous over a period of time

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4
Q

What is the primary delivery system for inflammatory components?

A

Blood

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5
Q

What is acute inflammation?

A

Standardized reaction, early response

Immediate vascular response

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6
Q

What is chronic inflammation?

A

Alteration of an inflammatory response

Weeks to years

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7
Q

What can both acute and chronic inflammation occur due to?

A

Microbes or non-infectious reasons

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8
Q

What is the goal of acute inflammation?

A

Dilute toxins
Isolate
Eliminate
Repair

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9
Q

Describe diluting toxins with acute inflammation

A

Biological and chemical

Add fluid to it

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10
Q

Describe isolation with acute inflammation

A

Sequester microbes, foreign material, dead tissue

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11
Q

Describe elimination with acute inflammation

A

Kill/remove inciting cause

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12
Q

Describe repair with acute inflammation

A

Remove necrotic cells, recruit reparative cells and factors

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13
Q

Is fibrin acute or chronic?

A

Acute

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14
Q

What are harmful effects of inflammation?

A

Persistent cytokine release
Destruction of normal tissue
Swelling
Inappropriate inflammatory response

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15
Q

What are systemic effects of inflammation?

A

Leukocytosis

Fever

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16
Q

What is leukocytosis?

A

An abnormally high number of circulating white blood cells

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17
Q

What do increased neutrophils often indicate?

A

A bacterial infection

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18
Q

What are increased lymphocytes associated with?

A

Viral infections

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19
Q

Describe fever

A

Coordinated by the hypothalamus and involves a wide range of factors

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20
Q

What is fever commonly associated with?

A

An infectious cause

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21
Q

What are the cardinal signs of inflammation?

A 
Heat
Redness
Swelling
Pain
Loss of function
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22
Q

What is heat?

A

Increase in temperature due to increased blood flow

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23
Q

What causes redness?

A

Dilation of small blood vessels within an area (hyperemia)

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24
Q

What is swelling a result of?

A

Edema

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25
Q

What is pain due to?

A

Stretching and distortion of tissues (due to edema and chemical mediators)

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26
Q

What is loss of function?

A

Movement inhibited by pain or swelling

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27
Q

What are exogenous stimuli of inflammation?

A

Microbes
Foreign bodies
Injury: chemical, thermal, heat, ischemia

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28
Q

What are endogenous stimuli of inflammation?

A

Autoreactive- newly developed antigens from degenerate or neoplastic cells
Hypersensitivity reactions

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29
Q

What do the stimuli of inflammation cause?

A

Activation of the innate immune response

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30
Q

Describe nonspecific defense of the innate immune response

A

Physical barriers: epithelial surfaces, ciliated cells, secretion
Molecular products: secreted by epithelial cells
Chemical mediators from effector cells within connective tissue of the barriers

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31
Q

What are the characteristics of acute inflammation?

A

Recognition of injury/pathogen
Send inflammatory cells: microvascular exudation of electrocytes, fluid, and plasma proteins (fluidic phase); leukocyte emigration (cellular phase)
Send effector molecules
Repair and heal (reparative phase)

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32
Q

How does the body recognize invaders (microbes and damaged cells)?

A

Cellular receptors
Cellular sensors
Circulating proteins

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33
Q

What are innate immune cells able to do?

A

Recognize certain components from microbes and from damaged/dead tissue

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34
Q

What are the different cellular receptors on immune cells?

A

Receptors on the plasma membrane
Cyctosolic receptors
Receptors on the endosome

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35
Q

What happens when TLRs recognize microbial molecules?

A

Induction of pro-inflammatory cytokines and type I interferons

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36
Q

What does TLR4 do?

A

Bind to LPS of gram-negative bacteria

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37
Q

What are pattern recognition receptors?

A

PAMPs

DAMPs

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38
Q

Describe PAMPs

A

Pathogen-associated molecular patterns

Microbial structures

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39
Q

Describe DAMPs

A

Danger-associated molecular patterns

Released from necrotic cells

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40
Q

What are NOD-like receptors?

A

Cytosolic receptors that recognize a diverse set of molecules

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41
Q

What do NOD-like receptors activate?

A

The inflammasome

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42
Q

Describe the inflammasome

A

A multiprotein complex

Induces production of IL-1

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43
Q

What does IL-1 do?

A

Recruit leukocytes

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44
Q

Describe C-type lecitn receptors

A

On the plasma membrane

Detect fungal glycans and elicit inflammation to fungi

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45
Q

Describe Fc

A

Leukocytes express the receptors for Fc tails of antibodies for complement proteins
Recognize opsonized material

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46
Q

Describe circulating proteins

A

Complement: reacts against microbes and produces mediators of inflammation

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47
Q

What are mediators of inflammation?

A

Substances secreted by cells that initiate and regulate inflammatory reactions

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48
Q

What are mediators of inflammation secreted by?

A

Primarily macrophages, dendritic cells, and mast cells

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49
Q

What can happen to mediators of inflammation?

A

Sequestered in intracellular granules for rapid secretion OR may be synthesized de novo

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50
Q

What are mediators of inflammation produced in response to?

A

Various stimuli

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51
Q

What do mediators of inflammation bind to and what do they do?

A

Bind to receptors on target cells to secrete additional inflammatory mediators

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52
Q

What are the checks and balances of mediators of inflammation?

A

Have short half-lives and quickly decay
Are enzymatically destroyed
Are scavenged by antioxidants

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53
Q

Describe inflammatory mediators from plasma proteins

A

They are constantly being secreteed by the liver as precursors
Activated via proteolytic cleavage in circulatory system

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54
Q

Look at inflammatory mediators chart

A

Look at inflammatory mediators chart

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55
Q

What are examples of preformed inflammatory proteins?

A

Histamine

Serotonin

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56
Q

What produces histamine?

A

Mast cells
Basophils
Platelets

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57
Q

What does histamine do?

A

Vasodilation

Increased vascular permeability

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58
Q

What produces serotonin?

A

Mast cells

Platelets

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59
Q

What are the functions of serotonin similar to?

A

Similar to histamine’s functions

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60
Q

What are the synthesized mediators?

A

Cytokines
Chemokines
Arachidonic acid metabolites

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61
Q

What are cytokines?

A

Proteins produced by many cell types (primarily macrophages, lymphocytes, dendritic cells)

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62
Q

What stimulates production of cytokines?

A

Extrinsic and intrinsic factors

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63
Q

What is the function of cytokines?

A

Regulate immune and inflammatory reactions

64
Q

What are the cytokines release with acute inflammation?

A

TNF, IL-1, IL-6

65
Q

What are the actions of cytokines?

A

Endothelial activation
Leukocyte recruitment
Leukocyte activation
Systemic acute phase response

66
Q

What are chemokines?

A

Cytokines that promote leukocyte chemotaxis and migration

67
Q

What is an example of a chemokine?

A

IL-8

68
Q

What does IL-8 do?

A

Chemotaxis of neutrophils

69
Q

What are arachidonic acid metabolites?

A

Lipid mediators, prostaglandins and leukotrienes, produced from arachidohic acid present in membrane phospholipids

70
Q

How are arachidonic acid metabolites released?

A

Mechanical, chemical, physical stimuli releases AA from the membrane

71
Q

What are arachidonic acid derived mediators?

A

Prostaglandins

Leukotrienes and lipoxins

72
Q

What is the function of arachidonic acid metabolites?

A

Mediate virtually every step of acute inflammation

73
Q

Which arachidonic acid metabolites cause vasodilation?

A

Prostaglandins

74
Q

Which arachidonic acid metabolites cause vasoconstriction?

A

Leukotrienes, thromboxane

75
Q

Which arachidonic acid metabolites cause increased vascular permeability?

A

Leukotrienes

76
Q

Which arachidonic acid metabolites cause chemotaxis and leukocyte adhesion?

A

Leukotrienes

77
Q

What is the complement system?

A

Collection of soluble proteins and membrane receptors that function in host defense

78
Q

Where are complement proteins present in their inactive forms?

A

Plasma

79
Q

What are the functions of the complement system?

A

Inflammation
Opsonization and phagocytosis
Cell lysis

80
Q

How does the complement system cause inflammation?

A

C3a and C5a are cleavage products
Stimulate histamine release (anaphylatoxins)
C5a: chemotactic for leukocytes

81
Q

How does the complement system cause opsonization and phagocytosis?

A

C3b: when fixed to microbial cell wall, acts as opsonin and promotes phagocytosis

82
Q

How does the complement system cause cell lysis?

A

Deposition of the membrane attack complex

Kills by making cells permeable to water—> lysis

83
Q

What does activated factor XII do?

A

Activates the intrinsic coagulation and catalyzes the formation of kallikrein

84
Q

Describe Bradykinin

A

Short lived
Increased vascular permeability
Vasodilation
Pain

85
Q

What does Kallikrein do?

A

Acts on plasminogen to form plasmin and cleaves C3

86
Q

What do fibrin polymers do?

A

Provide a surface or network to facilitate phagocytosis and prevent spread of infectious agents

87
Q

What does excessive fibrin do?

A

Obstructs the microvasculature resulting in ischemic injury

88
Q

What does excessive activation of the fibrinolytic system do?

A

Leads to depletion of fibrinogen and possibly hemorrhage

89
Q

What are oxygen-derived free radicals released from?

A

Neutrophils and macrophages following exposure to chemokines and after phagocytosis

90
Q

What can oxygen-derived free radicals do?

A

Alter signaling molecules

91
Q

What is nitric oxide synthesized by?

A

Endothelial cells and macrophages

92
Q

What does nitric oxide do?

A

Vasodilation
Inhibits platelet aggregation and adhesion
Oxidizes lipids

93
Q

Describe platelet-activating factor

A

Phospholipid derived mediator
Many cells can elaborate the factor
Vasoconstriction and bronchoconstriction

94
Q

Know role of mediators in different reactions of inflammation

A

Know role of mediators in different reactions of inflammation

95
Q

What is the function of the fluidic phase?

A

Dilute and localize the stimulus

96
Q

What is the sequence of vascular events in the fluidic phase?

A

Increased blood flow:
—Mediators- several but most notably histamine
—Vasodilation of arterioles leads to opening of capillary beds—> increased blood flow
Heat and redness
Increased permebaility of capillaries and postcapillary venules:
—Loss of fluid increased vessel diameter—> slower blood flow, concentration or red cells and increased blood vicosity
Swelling

97
Q

What is the mechanism of increased vascular permeability?

A

Retraction by contraction of actin/myosin filaments or reorganization of the cytoskeletal microtubule and proteins
Endothelial cell necrosis and detachment
Activates platelets, clotting, and complement

98
Q

Describe serous fluid

A

Clear watery fluid

Low concentration of plasma proteins with no or low number of leukocytes

99
Q

What does serous fluid result from?

A

Increased vascular permeability

100
Q

What does serous fluid suggest about the injury?

A

That is rather mild or peracute

101
Q

How does serous fluid look histologically?

A

Affected tissues are spread apart by the watery fluid

102
Q

What is fibrinous inflammation?

A

Term used to describe a pattern of acute inflammation

103
Q

What is fibrinous inflammation caused by?

A

Infectious etiologies

104
Q

What happens in fibrinous inflammation?

A

Accumulation of fluid with a high concentration of plasma protein (exudate)
Leakage of large molecular weight proteins (fibrinogen)
Fibrinogen polymerizes to form fibrin

105
Q

What is seen grossly with fibrinous exudate?

A

Surface of affected tissue is often red
Early- surface may be granular and dull
Surface covered with a thick, stringy, white-gray to yellow material that can be easily removed

106
Q

What is seen microscopically with fibrinous exudate?

A

Eosinophilic proteinaceous material- often fibrillary

In many cases, rapidly becomes infiltrated by neutrophils—> fibrinosupparative exudate

107
Q

What is the consequence of fibrinous inflammation?

A

May resolve without any sequelae

If extensive, fibroblasts may migrate in and being organizing exudate—> fibrous adhesions

108
Q

What is the function of cellular phase?

A

Deliver leukocytes to the site in order to kill and/or digest the stimulus

109
Q

Describe the leukocyte adhesion cascade

A

Movement of leukocytes from vessel into the connective tissue
Driven by chemokines, cytokines, and chemoattractant substances

110
Q

When is the leukocyte adhesion cascade initiated?

A

During the fluidic phase

111
Q

What occurs during the cellular phase?

A

Margination
Rolling
Adhesion to endothelium
Migration

112
Q

What is margination?

A

Leukocytes move to periphery of the vascular lumen in apposition with endothelial cell

113
Q

What is pavementing?

A

When the surface of the endothelium becomes line by leukocytes

114
Q

What is rolling?

A

Leukocytes adhere transiently to endothelium

115
Q

What is adhesion to endothelium?

A

Firm adhesion

116
Q

What is migration?

A

Migration through the endothelium and then to the stimulus

117
Q

What is rolling and adhesion mediated by?

A

Adhesion molecules expressed on leukocytes and endothelial cells

118
Q

What is the expression of rolling and adhesion enhanced by?

A

Cytokines

119
Q

Where does leukocyte migration through endothelium occur?

A

Mainly in post-capillary venules

120
Q

What stimulates cells to migrate?

A

Chemokines

121
Q

What causes cell to migrate towards a stimulus?

A

Chemical concentration gradient (chemotaxis)

122
Q

What happens during chemotaxis?

A

Leukocytes move toward the site of injury

Exogenous and endogenous substances act as chemoattractants

123
Q

What are common exogenous substances?

A

Bacterial products and some lipids

124
Q

What are common endogenous substances?

A

Cytokines (IL-8), components of complement system, arachidonic acid metabolits

125
Q

What determines which cells are the first to arrive?

A

The stimulus

126
Q

When are neutrophils the first cells to arrive?

A

In bacterial infection

127
Q

When are lymphocytes and plasma cells the first to arrive?

A

In some hypersensitivity reactions

Lymphocytes are also the first with viral infections

128
Q

When are eosinophils the first cells to arrive?

A

In allergic reactions

129
Q

What is purulent inflammation?

A

Term used to describe a pattern of acute inflammation

130
Q

What does the response of purulent inflammation consist of?

A

Accumulation of fluid with high concentration of plasma protein and high number of neutrophils

131
Q

What is pus?

A

An accumulation of dead neutrophils

132
Q

What is plegmon?

A

Pus distributed in tissue layers or along tissue layers

Also called cellulitis

133
Q

What dpes purulent inflammation look like grossly?

A

Surface or connective tissue is hyperemic with thick white to gray to yellow material

134
Q

When is purulent inflammation white?

A

If neutrophils are the predominant component

135
Q

When is purulent inflammation yellow?

A

If there is a lot of necrotic debris

136
Q

What is the consistency of purulent inflammation?

A

May be watery, creamy, or firm depending on the species and the inciting agent

137
Q

What is fibrinopurulent?

A

When purulent inflammation is mixed with fibrin

138
Q

What is seen microscopically with purulent inflammation?

A

Large numbers of neutrophils

May degenerate neutrophils and mixed with necrotic debris, tissue debris, plasma proteins, and fibrin

139
Q

What is the significance of purulent inflammation?

A

Neutrophils are there to neutralize the offending agent

140
Q

What is the outcome of purulent inflammation?

A

Neutralize
Form pus—> resorption of pus
May progress to chronic inflammation

141
Q

What is an abscess?

A

A circumscribed collection of pus surrounded by connective tissue capsule

142
Q

What is a systemic acute phase response with TNF, IL-1, and IL-6?

A

Fever

Increase production of leukocytes by the bone marrow

143
Q

What is fever mediated by?

A

Prostaglandins that are increased int the hypothalamus

144
Q

How does fever occur?

A

Cytokines increase cyclooxygenases that convert AA to prostaglandins

145
Q

How do NSAIDs reduce fever?

A

By inhibiting prostaglandin synthesis

146
Q

What does increased production of leukocytes by the bone marrow result from?

A

Mobilization of neutrophils from storage pools in bone marrow

147
Q

What is the systemic acute phase response with TNF?

A

Energy balance

148
Q

What is the systemic acute phase response with IL-1 and IL-6?

A

Stimulate acute phase protein production by the liver

149
Q

What are the acute phase proteins?

A

C-reactive protein
Serum amyloid A
Fibrinogen

150
Q

What do C-reactive protein and serum amyloid A do?

A

Bind to microbial cells walls

Activate complement

151
Q

What is septiciemia?

A

Clinically significant form of bacteremia complicated by toxemia, fever, malaise, and often shock

152
Q

What results in sepsis or shock?

A

Systemic interaction of microorganisms and their products with hist cells and chemical mediators

153
Q

What are the clinical manifestations of shock?

A

DIC
Hypotension and metabolic disturbances
Multiple organ failure and death

154
Q

What are the gross findings with septicemia?

A

Fluid body cavity, pulmonary edema, petechial hemorrhages, congestion of the liver and intestine

155
Q

What are the histology findings with septicemia?

A

Acute necrosis of renal tubules, centrolobular hepatocytes and cardiac myocytes

156
Q

What are the 4 types of pneumonia?

A

Bronchopneumonia
Interstitial pneumonia
Granulomatous pneumonia
Embolic pneumonia

Pathology (16 decks)

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