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Pathophysiology 2.0 > Week 3 lec - inflammation > Flashcards

Week 3 lec - inflammation Flashcards

1
Q

Name the white blood cells

A
  1. neutrophils
  2. lymphocyes
  3. monocytes
  4. basophils
  5. eosinophils
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2
Q

what do neutrophils fight against?

A

bacteria

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3
Q

B cells produce what?

A

antibodies

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4
Q

T cells can be divided into what 2 categories?

A

Killer and helper

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5
Q

TH1 and TH2 are a type of?

A

T helper cell

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6
Q

dendritic antigen presenting cells are derived from what type of cell?

A

monocytes

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7
Q

when a monocyte is in tissue it is called a?

A

macrophage

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8
Q

osteoclasts are specialised what?

A

macrophages

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9
Q

glial cells in the CNS (eg astrocytes) are specialised?

A

macrophages

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10
Q

eosinophils are involved in? (name 2 things)

A
  1. allergies
  2. fighting parasites
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11
Q

basophils

A
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12
Q

Haematoxylin stain:

  1. what is stained?
  2. what type of stain is it?
  3. what is it’s adjective?
A
  1. DNA
  2. basic
  3. basophilic
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13
Q

Eosin stain:

  1. what is stained?
  2. what type of stain is it?
  3. what is it’s adjective?
A
  1. cytoplasm, collagen, muscle fibres
  2. acidic stain
  3. eosinophilic
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14
Q

what shaped nucleus does a monocyte have?

A

kidney shaped

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15
Q

Kuppfer cells and sinus histocytes are types of specialised ____?

A

monocytes

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16
Q

______ are the principal cells involved in acute inflammation

A

neutrophils

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17
Q

what does infiltration of tissue by neutrophils indicate?

A

acute inflammation

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18
Q

what is pus made from?

A

a collection of neutrophils and necrotic cells

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19
Q

what is an abscess?

A

a walled-off collection of pus

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20
Q

Give an overview of the tissue’s response to injury (2 pathways)

A
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21
Q

what is the body’s most common response to substantial tissue damage?

A

healing by repair mechanisms, resulting in scar formation (fibrous repair) and loss of specialised function

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22
Q

what are the 4 phases of wound healing?

A
  1. inflammation
  2. granulation tissue
  3. wound contraction
  4. collagen accumulation and remodelling
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23
Q

What is the duration of the inflammation phase (1st phase) of wound healing?

A

Up to 3 days

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24
Q

The second phase of wound healing (granulation tissue) occurs from days ___ until ___

A

0.3 - 10 days

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25
Q

Wound contraction (3rd phase of wound healing) occurs from days ___ to ___

A

Days 3-30

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26
Q

The fourth and final phase of wound healing, collagen accumulation and remodelling, occurs from days ___ to ___

A

days 3-100, maybe even longer

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27
Q

What are the 3 possible outcomes following acute inflammation?

A
  1. damaging agent destroyed before tissue damage occurs
  2. tissue regeneration (repair without scarring) following chronic inflammation
  3. tissue healing (repair with scarring) following chronic inflammation
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28
Q

What are the 4 vascular events of an innate immune response?

A
  1. coaggulation cascade
  2. complement cascade
  3. fibrinolytic cascade
  4. kinin cascade
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29
Q

what 4 tissue cells are involved in innate cellular immune response?

A
  1. endothelial cells
  2. mast cells
  3. macrophages
  4. dendritic cells
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30
Q

what 4 blood cells are involved in the cellular events of the innate immune system?

A
  1. neutrophils
  2. monocytes
  3. eosinophils
  4. dendrocytes
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31
Q

The adaptive immune response can be ____ mediated or __ mediated.

A

Antibody, cell

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32
Q

what are the 4 macroscopic signs and symptoms of inflammation?

A
  1. red
  2. hot
  3. swollen
  4. painful
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33
Q

what is the difference in the onset and duration of acute vs chronic inflammation?

A

acute = rapid onset last for a few days

chronic = delayed onset last for weeks to years

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34
Q

what are the cardinal signs of acute inflammation?

A
  1. pain
  2. heat
  3. swelling
  4. redness
  5. loss of function
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35
Q

what is the cardinal sign of chronic inflammation?

A

loss of function

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36
Q

what is the specificity of response of acute vs chronic inflammation?

A

acute is not specific whereas chronic is specific to causative agent (involves acquired immunity)

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37
Q

what are the causative agents for acute inflammation?

A
  1. pathogens
  2. physical/chemical injury
  3. tissue necrosis
  4. immune response
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38
Q

what are the causative agents of chronic inflammation?

A
  1. persistent infection
  2. continued presence of foreign body
  3. autoimmunity
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39
Q

what are the fundamental cells involved in acute inflammation?

A

neutrophils then macrophages

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40
Q

what are the fundamental cells involved in chronic inflammation?

A
  1. macrophages
  2. lymphocytes
  3. plasma cells
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41
Q

What are the Latin words for the 5 cardinal signs of acute inflammation?

A

heat = calor

redness = rubor

swelling = tumor

pain = dolor (like dolores umbridge was a fkn pain in the butt)

loss of function = functio laesa

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42
Q

what causes heat, redness and swelling in acute inflammation?

A

increased blood supply and leakiness in the tissue

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43
Q

what causes pain in acute inflammation?

A

release of chemical mediators

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44
Q

what causes functional loss in acute inflammation?

A

tissue damage

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45
Q

what is exudation and when does it occur?

A

the leaking of plasma into tissues, onset begins about 30 minutes into the acute inflammatory response, peaks at about 3 hours and subsides at around 3 days.

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46
Q

when does neutrophil involvement begin in an acute inflammatory response? how long does it last?

A

about 1 hour in, subsides after about 1 day.

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47
Q

what is the onset and duration for apoptosis during the acute inflammatory response?

A

onset at 6 hours, finishes at around 2 days

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48
Q

when does mononuclear cell involvement begin and subside in acute inflammation?

A

begins after 1 day subsides at around 60 hours

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49
Q

List 4 exogenous inciting agents for acute inflammation

A
  1. infections
  2. trauma
  3. physical
  4. foreign body
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50
Q

List 2 endogenous inciting agents for acute inflammation

A
  1. tissue necrosis
  2. immune reaction
51
Q

what is the difference between the responses of exogenous vs endogenous inciting agents of acute inflammation?

A

THERE IS NO DIFFERENCE AHAHAHA

ha

52
Q

what cells are primarily responsible for the recognition of tissue injury?

A

tissue macrophages and mast cells

53
Q

what are the two vascular changes during acute inflammation?

A

vasodilation and increased permeability

54
Q

What are the 3 cellular changes in acute inflammation?

A
  1. leukocyte recruitment
  2. leukocyte activation
  3. destruction of pathogen by leukocytes (phagocytosis/degradation)
55
Q

what causes the swelling in acute inflammation?

A

leakage of plasma proteins into the interstitial space

56
Q

which chemical mediators cause contraction of endothelial cells in postcapillary venules during acute inflammation?

A

histamine, bradykinin, leukotrienes

57
Q

Histamine: Source (3 cells) and action?

A

source = mast cells, platelets, basophils

action = vasodilation, increased permeability

58
Q

serotonin: source and action?

A

source = platelets

action = vasodilation, increased permeability

59
Q

prostaglandins: source and action?

A

source = mast cells and leukocytes

action = increase permeability

60
Q

Leukotrienes: source and action?

A

source = mast cells and leukocytes

action = increased permeability

61
Q

platelet activation factor: source and action?

A

source = leukocytes and mast cells

action = vasodilation and increased permeability

62
Q

kinins: source and action?

A

source = plasma (produced in the liver)

action = vasodilation and increased permeability

63
Q

which cells release cytokines and chemokines in the damaged tissue during acute inflammation?

A

macrophages

64
Q

during acute inflammation, the release of cytokines and chemokines from macrophages causes expression of ______ on endothelial cells and _______ on leukocytes, allowing adhesion of leukocytes (neutrophils) to the vascular wall.

A

selectins, integrins

65
Q

in acute inflammation leukocyte recruitment, which leukocyte is recruited?

A

mainly neutrophils

66
Q

the release of selectins and integrins causes what?

A

leukocyte adhesion to lumen walls

67
Q

selectins are expressed from?

A

endothelial cells

68
Q

integrins are expressed from?

A

leukocytes

69
Q

which cells initially produce the chemotactic proteins?

A

the microbes themselves or macrophages

70
Q

once leukocytes arrive, they also begin to produce _____ proteins (in addition to macrophages and the infecting microbes)

A

chemotactic

71
Q

chemokines are also called _____ _____?

A

chemotactic proteins

72
Q

chemotactic molecules bind to cell surface receptors on _____

A

leukocytes

73
Q

once activated by a chemokine binding to its surface receptor, how does a leukocyte move?

A

by extending pseudopods containing contractile filaments

74
Q

how long does it take for macrophages to migrate to a site of infection?

A

24-48 hours

75
Q

Once neutrophils have been recruited, they must be activated to perform a specific function. What are the three specific functions?

A
  1. phagocytosis
  2. lysis/killing of engulfed pathogens (uses H2O2 to perforate cell membrane)
  3. production of mediators that amplify the reaction
76
Q

what does the neutrophil bind to on the microbe?

A

either the native receptor on microbe surface or opsonins (such as IgG antibody) bound to microbe.

77
Q

what does the engulfment of a microbe by a neutrophil form?

A

a phagosome

78
Q

what does the phagosome fuse with to kill/degrade the microbe?

A

a lysosome

79
Q

once a phagosome has fused with a lysosome, the microbe is killed by 3 mechanisms, what are they?

A
  1. enzymes (such as myeloperoxidase)
  2. reactive oxygen species
  3. nitric oxide
80
Q

once a phagosome has fused with a lysosome, what is used to degrade the microbe?

A

lysosomal acid hydrolases

81
Q

what are the 3 steps of phagocytosis?

A
  1. recognition
  2. engulfment
  3. killing + degradation
82
Q

cytokines: initial source and action?

A

source = macrophages, endothelial cells and mast cells

action = endothelial activation (expression of selectins)

83
Q

chemokines: initial source and action?

A

initial source = leukocytes and macrophages

action = leukocyte activation and chemotaxis

84
Q

prostaglandins: initial source and action?

A

initial source = mast cells and leukocytes

action = leukocyte adhesion, chemotaxis and degranulation

85
Q

leukotrienes: source and action?

A

initial source = mast cells and leukocytes

action = leukocyte adhesion and activation, chemotaxis

86
Q

nitric oxide: source and action?

A

initial source = endothelium and macrophages

action = killing of microbes

87
Q

reactive oxygen species: source and action?

A

initial source = leukocytes

action = killing microbes

88
Q

proteases: source and action?

A

initial source = plasma (liver)

action = leukocyte chemotaxis and activation

89
Q

complement: source and action?

A

initial source = plasma (liver)

action = endothelial activation and WBC recruitment

90
Q

what are the 3 possible outcomes of acute inflammation?

A
  1. resolution
  2. healing with scarring
  3. progression to chronic inflammation.
91
Q

chronic inflammation is characterised by a _______ cell infiltration

A

mononuclear

92
Q

an example of chronic inflammation caused by persistent infection by microbes that are difficult to eradicate

A

Tuberculosis

93
Q

an example of chronic inflammation caused by immune-mediated inflammatory diseases (hypersensitivity)

A

Rheumatoid arthritis

94
Q

an example of chronic inflammation caused by prolonged exposure to potentially toxic agents

A

Silicosis (chronic lung disease caused by silica exposure)

95
Q

there are 6 mononuclear cells involved in chronic inflammation, which are the 3 most important and which 3 play a more minor role?

A

Main bois: macrophages, lymphocytes, plasma cells

Small timers: eosinophils, mast cells, neutrophils

96
Q

what is the main activating chemical mediator for macrophages?

97
Q

what are activated macrophages called?

A

histiocytes

98
Q

what attracts B and T cells to the site of injury?

A

chemokines

99
Q

T cells secrete more _____ to help to activate macrophages

100
Q

what do mature B cells produce?

A

antibodies

101
Q

which cells produce antibodies in chronic inflammation?

A

plasma cells/mature B cells

102
Q

What does granulomatous inflammation indicate?

103
Q

what is a collection of epithelioid histiocytes (some of which fuse to form giant cells) known as?

A

Granulomatous inflammation

104
Q

what causes granulomatous inflammation to form?

A

cytokine production by T cells in response to persistent inflammation

105
Q

why would cytokine production by T cells in response to inflammation be ongoing?

A

because the infection organisms are resistant to phagolysosomal degradation (eg TB) or there is a foreign body (eg splinter) which the immune system cannot remove

106
Q

what is the name of a granuloma caused by a foreign body (eg splinter) which the immune system cannot remove?

A

foreign body granuloma

107
Q

Fever occurs in response to ______

108
Q

examples of pyrogens

A
  • Exogenous substances–e.g.bacteriallipopolysachharides
  • Endogenous substances–cytokines (e.g.TNF), prostaglandins (PGE2)
  • Prostaglandins exert their effect by resetting the hypothalamic thermostat
  • Elevated body temperature may help fight pathogens
109
Q

what causes sepsis?

A

severe pyrogenic infection

110
Q

what happens during sepsis?

A

Hypotensive shock and disseminated intravascular coagulation

111
Q

what is leukocytosis?

A

Elevated numbers of white blood cells in the blood

112
Q

elevated plasma levels of acute-phase proteins are implicated in causing what?

A

chronic diease(e.g. cardiovascular disease)

113
Q

Permanent tissues (e.g. neurons, cardiac muscle) cannot repair by ________ and must be healed by _______

A

regeneration, scarring

114
Q

labile tissue (eg epithelium) repair by _____?

A

regeneration (occurs continuously)

115
Q

4 steps of healing by scarring?

A
  1. formation of new blood vessels
  2. migration and proliferation of fibroblasts
  3. deposition of extracellular matrix
  4. maturation and organisation of fibrous tissue (remodelling)
116
Q

Healing with scarring is the outcome for what 5 things?

A
  • Acute inflammation (when severe)
  • Chronic inflammation
  • Ischaemic necrosis
  • Wounds (e.g. skin)
  • Bone fractures
117
Q

Repair is under the control of which 5 growth factors?

A
  • Transforming growth factor beta (TGF-B)
  • Vascular endothelial growth factor (VEGF)
  • Platelet-derived growth factor (PDGF)
  • Epidermal growth factor (EGF)
  • Fibroblast growth factor (FGF)
118
Q

where are growth factors primarily produced?

A

produced primarily by macrophages and platelets in sites of injury

119
Q

List 5 actions of growth factors

A
  1. Chemotaxis (attract more macrophages in chronic and late acute inflammation)
  2. Fibroblast migration and proliferation
  3. Angiogenesis
  4. Increase synthesis of extra-cellular matrix collagen
  5. Stimulate epithelial proliferation (e.g. in the skin)
120
Q

When damage is limited tissue can be repaired by _______?

A

regeneration

121
Q

Scar formation begins with the formation of ______ _____, and culminates in laying down of mature fibrous tissue

A

granulation tissue

122
Q

Healing with scar formation is under the control of ____ _____

A

growth factors

123
Q

Acute inflammation is characterised by rapid early influx of _____ into injured tissue

A

neutrophils

124
Q

Chronic inflammation is characterised by activated _____ and _______

A

macrophages, lymphocytes, dendrocytes and plasma cells

Pathophysiology 2.0 (19 decks)

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