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Pathology I Test I > Inflammation and Repair > Flashcards

Inflammation and Repair Flashcards

1
Q

What is inflammation?

A

The reaction of the blood vessels, leading to the accumulation of fluid and leukocytes in the extravascular tissues

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2
Q

What is the function of inflammation?

A

A protective response

  • eliminate microbes and toxins
  • eliminate necrotic cells and tissues
  • prepare for tissue repair
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3
Q

What do neutrophils do?

A

First responder (acute inflammation) bacterial or fungal infection

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4
Q

What forms pus?

A

Increased activity and death of neutrophils

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5
Q

What general percentage of WBC’s do neutrophils make up?

A

60%

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6
Q

What do lymphocytes do?

A

Chronic inflammation

- T cell and B cell response/activation

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7
Q

What general percentage of WBC’s do lymphocytes make up?

A

30%

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8
Q

What do monocytes do?

A

Long lived Phagocyte that present pathogen parts to T cells

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9
Q

What are monocytes when they are in tissue?

A

Macrophages

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10
Q

What general percentage of WBC’s do monocytes make up?

A

5-6%

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11
Q

What do eosinophils do?

A

Parasite and Allergic response

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12
Q

What general percentage of WBC’s do eosinophils make up?

A

2-3%

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13
Q

What do basophils do?

A

Allergic and antigen response and releasing the chemical histamine

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14
Q

What are basophils when they are in tissue?

A

Mast Cells

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15
Q

What general percentage of WBC’s do basophils make up?

A

<1%

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16
Q

What is the order from largest to smallest of the WBC’s?

A 
Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
(Never Let Monkeys Eat Bananas)
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17
Q

Where do T lymphocytes mature?

A

Thymus

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18
Q

Where do B lymphocytes mature?

A

Bone maroow

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19
Q

Are thrombocytes WBCs?

A

No they are platelets

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20
Q

What is the function of thrombocytes?

A

To plug up holes

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21
Q

What is the life span of an RBC?

A

120 days

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22
Q

What is the life span of WBC?

A

days to years

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23
Q

What is the life span of a platelet?

A

8 days

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24
Q

What are the two types of inflammation?

A

Acute and Chronic

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25
Q

What is the duration and onset speed of acute inflammation?

A

Rapid onset and short duration (min/hours/days)

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26
Q

Is there edema with acute inflammation?

A

Yes

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27
Q

What type of leukocyte is predominantly present with acute inflammation?

A

Predominantly neutrophils, but also eosinophils and antibody mediated

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28
Q

What is the duration and onset speed of chronic inflammation?

A 
Slower onset
Long duration (wks, months, years)
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29
Q

What are some characteristic appearances of chronic inflammation?

A

Presence of new blood vessels, fibrosis, and tissue necrosis

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30
Q

What type of leukocyte is predominantly present with chronic inflammation?

A

Predominantly macrophages and lymphocytes

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31
Q

What are the key signs and symptoms of acute inflammation?

A

1) Redness
2) Heat
3) Swelling
4) Pain
5) Loss of function

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32
Q

What is the Latin term for redness?

A

Rubor

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33
Q

What is the Latin term for heat?

A

Calor

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34
Q

What is the Latin term for swelling?

A

Tumor

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35
Q

What is the Latin term for Pain?

A

Dolor

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36
Q

What is the Latin term for Loss of function?

A

Functio laesa

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37
Q

What vascular changes occur with inflammation?

A

1) Vascular dilation and increased blood flow (causing erythema and warmth)
2) Extravasation and deposition of plasma fluid and proteins (edema)
3) Leukocyte emigration and accumulation in the site of injury

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38
Q

What is the net flow of fluid of microvasculature in normal circulation?

A

Small flow out of the precapillary arteriole but returned in the precapillary venuole

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39
Q

What happens to the net flow of the microvasculature with acute inflammation?

A

Arteriole pressure is increased and the mean capillary pressure is increased due to arteriolar dilation. The venous pressure increases and the osmotic colloidal pressure is reduced due to protein leakage across the venule which results in an excess of extravasated tissue

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40
Q

What is oncotic pressure?

A

Pressure bringing in fluid into vasculature from tissue due to albumin concentration

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41
Q

What causes oncotic pressure?

A

Albumin concentration

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42
Q

What controls arteriole pressure?

A

Sphincters of muscles that clamp off blood flow

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43
Q

What collects the small flow out of the capillary bed?

A

Lymphatic system

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44
Q

What is hyperemia?

A

Increased blood flow

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45
Q

What occurs with the precapillary sphincter during normal circumstances?

A

The precapillary sphincters are closed

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46
Q

What occurs with the precapillary sphincter during acute inflammation?

A

The precapillary sphincters are open

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47
Q

During normal flow how are the RBC’s and platelets and neutrophils distributed?

A

Scattered

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48
Q

Where in a circulatory vessel is the flow the fastest?

A

The middle because of laminar flow

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49
Q

What is the term for the stacking of RBCs as they move towards laminar flow?

A

Rouleaux of RBC

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50
Q

What does marginalization of neutrophils refer to?

A

When the neutrophils are pushed aside and moving towards the endothelium

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51
Q

What is the rouleaux relation to erythrocyte sedimentation rate?

A

It elevates the ESR

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52
Q

What are the steps of leukocyte extravasation?

A

1) Margination
2) Pavementing
3) Extravascular migration

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53
Q

What is the main leukocyte of margination?

A

Neutrophils

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54
Q

What are the parts of the pavementing stage of leukocyte extravasation?

A

1) rolling
2) tight binding
3) diapedesis/migration

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55
Q

What are some parts of tight binding of the pavementing stage of leukocyte extravasation?

A

1) integrin activation

2) stable adhesion

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56
Q

What occurs in extravascular migration?

A

Chemokines and cytokines direct the leukocyte to go to specific area

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57
Q

What are the 3 steps of phagocytosis of a particle?

A

1) recognition and attachment
- microbes bind to phagocyte receptors
2) engulfment
- phagocyte membrane zips up around microbe
3) killing and degradation
- fusion of phagosome with lysosome
- killing of microbes by lysosomal enzymes in phagolysosome

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58
Q

What 2 groups are the mediators of inflammation divided into?

A

1) plasma derived

2) cell derived

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59
Q

Do mediators of inflammation act only on a single cell?

A

No, they are multifunctional and act on many cells and tissues

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60
Q

Are mediators of inflammation biochemically the same or diverse?

A

Biochemically diverse including biogenic amines, peptides and arachidonic acid derivatives

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61
Q

What is a histamine?

A

Biogenic amine that is from a cell derived source (stored in cell)

62
Q

Where histamines released from?

A

Platelets and mast cells

63
Q

What is the function of histamine?

A

Stimulates retraction of endothelial cells of the venules and leads to gaps therefore increased permeability

64
Q

Is the action of histamine short or long and why?

A

The action of histamine is short because it is inactivated by histaminase

65
Q

What vitamin stabilizes mast cells?

A

Vitamin C, during an acute response

66
Q

What is bradykinin?

A

Plasma protein in the liver that is derived from kininogen through the enzymatic action of kallikrein?

67
Q

what is Kallikrein do and what is it activated by?

A

Kallikrein acts on the clotting and fibrinolytic systems of the blood and activated by Hageman factor

68
Q

What does bradykinin induce?

A

Pain

69
Q

What is the relationship between bradykinin and histamine?

A

They both have a similar action

70
Q

What were the mast cells called before they exited the blood vessel?

A

Basophils

71
Q

What is a complement system?

A

A group of plasma proteins produced by the liver

72
Q

Does the complement system circulate in an active form?

A

No, it circulates in an inactive form

73
Q

How is the complement system activated?

A

Through a classical or alternative pathways

74
Q

What does the activation of the complement system lead to?

A

The formation of biologically active fragments, intermediate complexes and terminal membrane attack complexes

75
Q

What are the main function of activated complement derivatives?

A

1) Opsonization
2) Anaphylaxis
3) Chemotaxis
4) Cell lysis

76
Q

What is opsonization

A

Facilitated phagocytosis of bacteria

77
Q

What is anaphylaxis/

A

Histamine release with increased vessel wall permeability

78
Q

What is the function of chemotaxis by activated complement derivaties?

A

migration of leukocytes

79
Q

Through what complex does the activated complement derivatives cause cell lysis?

A

Through the action of Membrane attack complex (MAC)

80
Q

What 3 pathways can activate the complement system?

A

1) Alternative pathway
2) Classical pathway
3) Lectin pathway

81
Q

What stimulus activates the alternative pathway of the complement system?

A

Microbes

82
Q

What stimulus activates the classical pathway of the complement system?

A

Antibodies

83
Q

What stimulus activates the lectin pathway of the complement system?

A

mannose binding lectin

84
Q

What do all the Complement pathways do after being initiated

A

C3b is deposited on the microbe and C3a is released

85
Q

What does C3a function as?

A

it initiates inflammation via recruitment and activation of leukocytes

86
Q

What does C3b of the activated complement system do/

A

1) Initiates phagocytosis via allowing recognition of the microbe by binding the C3b to the phagocyte C3b receptor
2) Causes formation of membrane attack complex and causes lysis of microbes

87
Q

What are the 3 steps of phagocytosis of bacteria?

A

1) Attachment of the opsonized bacterium to the polymorphonuclear leukocytes
2) Engulfment of the bacterium
3) Formation of the phagocytic vacuole

88
Q

What is the common, final pathway for the classical, mannose binding lectin and alternative pathways of the complement pathways?

A

When the C3 convertase (C3 con) cleaves C3 into C3a and C3b

89
Q

What is arachidonic acid?

A

Arachidonic acid is derived from phospholipids through the action of phospholipases

90
Q

How is arachidonic acid metabolized?

A

1) Lipoxygenase pathway

2) Cyclooxygenase pathway

91
Q

What are the 5 arachidonic acid derivatives?

A

1) Leukotrienes
2) Lipoxins
3) Thromboxane
4) Prostacyclin
5) Prostaglandins

92
Q

What is the function of leukotrienes?

A

Chemoxtaxis, vascular permeability and bronchospasm

93
Q

What is the function of lipoxins?

A

vasodilatation, inhibition of neutrophil chemotaxis, and monocyte adhesion

94
Q

What is the function of thromboxane?

A

Platelet aggregation, thrombosis

95
Q

What is the function of Prostacyclin?

A

Opposes the effects of thromboxane

96
Q

What is the function of Prostaglandins?

A

Smooth muscle contraction

97
Q

Is Omega 3 fatty acids (fish oil) a good substrate for conversion?

A

No it is a poor substrate

98
Q

Are animal fats good for conversion to substrate?

A

Yes, animal fat is a good substrate

99
Q

Generally, what lymphokines are released with macrophage activation and lead to inflammation?

A

Interleukin-1 and Tumor Necrosis factor

100
Q

What are the acute-phase reactions activated by interleukin-1 and tumor necrosis factor?

A

1) Fever
2) increased sleep need
3) decreased appetite
4) Increased acute-phase proteins
5) hemodynamic effects (shock)
6) Neutrophilia (attract neutrophils)

101
Q

What are the endothelial effects activated by interleukin-1 and tumor necrosis factor?

A

1) increased leukocyte adherence
2) Increased prostacyclin synthesis
3) Increased procoagulant activity
4) decreased anticoagulant activity
5) Increased Interleukin and platelet derived growth factor

102
Q

What are the fibroblast effects activated by interleukin-1 and tumor necrosis factor?

A

1) increased proliferation
2) increased collagen synthesis
3) increased collagenase
4) increased protease
5) increased prostaglandin synthesis

103
Q

What are the leukocyte effects activated by interleukin-1 and tumor necrosis factor?

A

Increased cytokine secretion (interleukin 6 and 8)

104
Q

What does long term tumor necrotic factor production lead to?

A

Cachexia (wasting away syndrome)

105
Q

What leads to the pathogenesis of fever?

A

TNF and IL-1 that changes the set point of internal temperature in the hypothalamus

106
Q

What are the different types of nitrous oxide synthase?

A

1) endothelial
2) neuronal
3) inducible

107
Q

Where does endothelial nitrous oxide synthase have effects on?

A

Affects the smooth muscle of vessel walls

108
Q

Where does neuronal nitrous oxide synthase have effects on?

A

effects within the macrophage

109
Q

Is a morning erection a good or bad sign?

A

Good sign as it reflects cardiovascular health)

110
Q

What can the urea cycle create?

A

Arginine

111
Q

What is the effect of arginine of vessels?

A

It causes the relax of vessels to promote vessels so that increased blood flow occurs (good for athletes and asthmatics as it relaxes the smooth muscle of the trachea as well)

112
Q

what are the two types of neutrophil granuoles?

A

primary and secondary granules

113
Q

What is another name for secondary granules?

A

Specific granules

114
Q

What is another name for primary granules?

A

Azurophil

115
Q

What is the difference between azurophil and specific granules?

A

Azurophils are larger than specific granules

116
Q

What causes the injury for acute inflammation?

A

1) infarction
2) bacterial infections
3) toxins
4) trauma

117
Q

What are some of the outcomes of acute inflammation?

A

1) vascular changes
2) neutrophil recruitment
3) mediators

118
Q

What happens if acute inflammation progresses?

A

It becomes chronic inflammation

119
Q

What causes the injury directly for chronic inflammation?

A

1) viral infections
2) chronic infections
3) persistent injury
4) autoimmune diseases

120
Q

What are some of the outcomes of chronic inflammation?

A

1) angiogenesis via platelet derived growth factor
2) mononuclear cell infiltrate
3) fibrosis (scar)

121
Q

What does the healing of both acute and chronic inflammation lead to?

A

Fibrosis

122
Q

What does fibrosis do?

A

Causes loss of function

123
Q

What are the three possible outcomes of acute inflammation?

A

1) Resolution
2) Pus formation
3) Fibrosis

124
Q

With resolution of an acute inflammation what occurs?

A

1) clearance of injurious stimuli
2) clearance of mediators and acute inflammatory cells
3) replacement of injured cells
4) normal function

125
Q

What occurs with pus formation?

A

abcesses

126
Q

What does pus formation eventually lead to?

A

Fibrosis

127
Q

What are the events in the resolution of inflammation?

A

1) return to normal vascular permeability
2) drainage of edema fluid and proteins into lymphatics or 3) by pinocytosis into macrophages
4) phagocytosis of apoptotic neutrophils
5) phagocytosis of necrotic debris
6) disposal of macrophages

128
Q

What are the different types of morphologic patterns of inflammation?

A

1) serous inflammation
2) Fibrinous inflammation
3) purulent inflammation
4) ulcerative inflammation
5) psedomembranous inflammation
6) chronic inflammation
7) granulomatous inflammation

129
Q

What is serous inflammation?

A

Early stage of most inflammation

130
Q

What are some examples of causes of serous inflammation?

A

1) Viral infection of skin vesicles in herpesvirus infection
2) joint swelling in rheumatoid arthritis
3) Eczema
4) Skin Burn (blister)

131
Q

What is effusion?

A

secretion from lining of peritoneal, pleural or pericardial cavities. (fluid between tissue)

132
Q

What is an abscess?

A

A capsulated collection of fluid (pus) within the tissue that cannot escape

133
Q

What is a sinus?

A

a collection of fluid within the tissue that has an escape

134
Q

What is a fistula?

A

A connection between two organs or connecting from an abscess may or may not be open to the surface

135
Q

What does a granuloma consist of?

A

1) lymphocytes
2) epithelioid cells
3) multinucleated giant cells

136
Q

Why does a granuloma become a multinucleated giant cells?

A

Cells fusing together (strength in numbers) to wall off/surround the infectious agent

137
Q

What is a suppurative inflammation?

A

Inflammation with pus

138
Q

What is the progression from stem cell to activated macrophage?

A

Stem cell -> monoblast -> monocyte -> macrophage -> activated macrophage

139
Q

What are macrophages in the CNS?

A

microglia cells

140
Q

What are macrophages in the liver?

A

Kupffer cells

141
Q

What are macrophages in the lung?

A

Alveolar macrophages

142
Q

What are macrophages in the bone?

A

Osteoclasts

143
Q

What are macrophages in the lymph nodes?

A

Sinus histocytes

144
Q

At what point does a monocyte become a macrophage?

A

When the monocyte moves from blood to tissue

145
Q

What are some chemotactic stimuli to cause monocytes to become macrophage?

A

1) chemokines
2) C5a
3) Growth factors
4) collagen & fibronectin fragments
5) Fibrinopeptides

146
Q

What are the two outcomes of activated macrophage?

A

1) Tissue Injury/ Destruction (ROS)

2) Fibrosis

147
Q

What are some hallmarks and signs of chronic inflammation / tissue injury or destruction?

A

1) Toxic oxygen metabolites
2) Proteases
3) Neutrophil chemotactic factors
4) Coagulation factors
5) Amino acid metabolites
6) nitric oxide

148
Q

What are some signs and effects of fibrosis due to activated macrophages?

A

1) growth factors
2) fibrogenic cytokines
3) angiogenesis factors (FGF)
4) Remodeling collagenesis

149
Q

How does an activated macrophage recruit leukocytes?

A

TNF

IL-1

150
Q

What do activated macrophages do?

A

Present antigen to T cells and uses cytokines to stimulate T cell response

151
Q

What occurs when a T lymphocyte is activated?

A

TNF and other inflammatory mediators recuit Leukocytes and cause inflammation

Pathology I Test I (5 decks)

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