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
Wound contraction (3rd phase of wound healing) occurs from days ___ to \_\_\_
Days 3-30
26
The fourth and final phase of wound healing, collagen accumulation and remodelling, occurs from days ___ to \_\_\_
days 3-100, maybe even longer
27
What are the 3 possible outcomes following acute inflammation?
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
28
What are the 4 vascular events of an innate immune response?
1. coaggulation cascade 2. complement cascade 3. fibrinolytic cascade 4. kinin cascade
29
what 4 tissue cells are involved in innate cellular immune response?
1. endothelial cells 2. mast cells 3. macrophages 4. dendritic cells
30
what 4 blood cells are involved in the cellular events of the innate immune system?
1. neutrophils 2. monocytes 3. eosinophils 4. dendrocytes
31
The adaptive immune response can be ____ mediated or __ mediated.
Antibody, cell
32
what are the 4 macroscopic signs and symptoms of inflammation?
1. red 2. hot 3. swollen 4. painful
33
what is the difference in the onset and duration of acute vs chronic inflammation?
acute = rapid onset last for a few days chronic = delayed onset last for weeks to years
34
what are the cardinal signs of acute inflammation?
1. pain 2. heat 3. swelling 4. redness 5. loss of function
35
what is the cardinal sign of chronic inflammation?
loss of function
36
what is the specificity of response of acute vs chronic inflammation?
acute is not specific whereas chronic is specific to causative agent (involves acquired immunity)
37
what are the causative agents for acute inflammation?
1. pathogens 2. physical/chemical injury 3. tissue necrosis 4. immune response
38
what are the causative agents of chronic inflammation?
1. persistent infection 2. continued presence of foreign body 3. autoimmunity
39
what are the fundamental cells involved in acute inflammation?
neutrophils then macrophages
40
what are the fundamental cells involved in chronic inflammation?
1. macrophages 2. lymphocytes 3. plasma cells
41
What are the Latin words for the 5 cardinal signs of acute inflammation?
heat = calor redness = rubor swelling = tumor pain = dolor (like dolores umbridge was a fkn pain in the butt) loss of function = functio laesa
42
what causes heat, redness and swelling in acute inflammation?
increased blood supply and leakiness in the tissue
43
what causes pain in acute inflammation?
release of chemical mediators
44
what causes functional loss in acute inflammation?
tissue damage
45
what is exudation and when does it occur?
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.
46
when does neutrophil involvement begin in an acute inflammatory response? how long does it last?
about 1 hour in, subsides after about 1 day.
47
what is the onset and duration for apoptosis during the acute inflammatory response?
onset at 6 hours, finishes at around 2 days
48
when does mononuclear cell involvement begin and subside in acute inflammation?
begins after 1 day subsides at around 60 hours
49
List 4 exogenous inciting agents for acute inflammation
1. infections 2. trauma 3. physical 4. foreign body
50
List 2 endogenous inciting agents for acute inflammation
1. tissue necrosis 2. immune reaction
51
what is the difference between the responses of exogenous vs endogenous inciting agents of acute inflammation?
THERE IS NO DIFFERENCE AHAHAHA ha
52
what cells are primarily responsible for the recognition of tissue injury?
tissue macrophages and mast cells
53
what are the two vascular changes during acute inflammation?
vasodilation and increased permeability
54
What are the 3 cellular changes in acute inflammation?
1. leukocyte recruitment 2. leukocyte activation 3. destruction of pathogen by leukocytes (phagocytosis/degradation)
55
what causes the swelling in acute inflammation?
leakage of plasma proteins into the interstitial space
56
which chemical mediators cause contraction of endothelial cells in postcapillary venules during acute inflammation?
histamine, bradykinin, leukotrienes
57
Histamine: Source (3 cells) and action?
source = mast cells, platelets, basophils action = vasodilation, increased permeability
58
serotonin: source and action?
source = platelets action = vasodilation, increased permeability
59
prostaglandins: source and action?
source = mast cells and leukocytes action = increase permeability
60
Leukotrienes: source and action?
source = mast cells and leukocytes action = increased permeability
61
platelet activation factor: source and action?
source = leukocytes and mast cells action = vasodilation and increased permeability
62
kinins: source and action?
source = plasma (produced in the liver) action = vasodilation and increased permeability
63
which cells release cytokines and chemokines in the damaged tissue during acute inflammation?
macrophages
64
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.
selectins, integrins
65
in acute inflammation leukocyte recruitment, which leukocyte is recruited?
mainly neutrophils
66
the release of selectins and integrins causes what?
leukocyte adhesion to lumen walls
67
selectins are expressed from?
endothelial cells
68
integrins are expressed from?
leukocytes
69
which cells initially produce the chemotactic proteins?
the microbes themselves or macrophages
70
once leukocytes arrive, they also begin to produce _____ proteins (in addition to macrophages and the infecting microbes)
chemotactic
71
chemokines are also called _____ \_\_\_\_\_?
chemotactic proteins
72
chemotactic molecules bind to cell surface receptors on \_\_\_\_\_
leukocytes
73
once activated by a chemokine binding to its surface receptor, how does a leukocyte move?
by extending pseudopods containing contractile filaments
74
how long does it take for macrophages to migrate to a site of infection?
24-48 hours
75
Once neutrophils have been recruited, they must be activated to perform a specific function. What are the three specific functions?
1. phagocytosis 2. lysis/killing of engulfed pathogens (uses H2O2 to perforate cell membrane) 3. production of mediators that amplify the reaction
76
what does the neutrophil bind to on the microbe?
either the native receptor on microbe surface or opsonins (such as IgG antibody) bound to microbe.
77
what does the engulfment of a microbe by a neutrophil form?
a phagosome
78
what does the phagosome fuse with to kill/degrade the microbe?
a lysosome
79
once a phagosome has fused with a lysosome, the microbe is killed by 3 mechanisms, what are they?
1. enzymes (such as myeloperoxidase) 2. reactive oxygen species 3. nitric oxide
80
once a phagosome has fused with a lysosome, what is used to degrade the microbe?
lysosomal acid hydrolases
81
what are the 3 steps of phagocytosis?
1. recognition 2. engulfment 3. killing + degradation
82
cytokines: initial source and action?
source = macrophages, endothelial cells and mast cells action = endothelial activation (expression of selectins)
83
chemokines: initial source and action?
initial source = leukocytes and macrophages action = leukocyte activation and chemotaxis
84
prostaglandins: initial source and action?
initial source = mast cells and leukocytes action = leukocyte adhesion, chemotaxis and degranulation
85
leukotrienes: source and action?
initial source = mast cells and leukocytes action = leukocyte adhesion and activation, chemotaxis
86
nitric oxide: source and action?
initial source = endothelium and macrophages action = killing of microbes
87
reactive oxygen species: source and action?
initial source = leukocytes action = killing microbes
88
proteases: source and action?
initial source = plasma (liver) action = leukocyte chemotaxis and activation
89
complement: source and action?
initial source = plasma (liver) action = endothelial activation and WBC recruitment
90
what are the 3 possible outcomes of acute inflammation?
1. resolution 2. healing with scarring 3. progression to chronic inflammation.
91
chronic inflammation is characterised by a _______ cell infiltration
mononuclear
92
an example of chronic inflammation caused by persistent infection by microbes that are difficult to eradicate
Tuberculosis
93
an example of chronic inflammation caused by immune-mediated inflammatory diseases (hypersensitivity)
Rheumatoid arthritis
94
an example of chronic inflammation caused by prolonged exposure to potentially toxic agents
Silicosis (chronic lung disease caused by silica exposure)
95
there are 6 mononuclear cells involved in chronic inflammation, which are the 3 most important and which 3 play a more minor role?
Main bois: macrophages, lymphocytes, plasma cells Small timers: eosinophils, mast cells, neutrophils
96
what is the main activating chemical mediator for macrophages?
cytokines
97
what are activated macrophages called?
histiocytes
98
what attracts B and T cells to the site of injury?
chemokines
99
T cells secrete more _____ to help to activate macrophages
cytokines
100
what do mature B cells produce?
antibodies
101
which cells produce antibodies in chronic inflammation?
plasma cells/mature B cells
102
What does granulomatous inflammation indicate?
TB
103
what is a collection of epithelioid histiocytes (some of which fuse to form giant cells) known as?
Granulomatous inflammation
104
what causes granulomatous inflammation to form?
cytokine production by T cells in response to persistent inflammation
105
why would cytokine production by T cells in response to inflammation be ongoing?
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
what is the name of a granuloma caused by a foreign body (eg splinter) which the immune system cannot remove?
foreign body granuloma
107
Fever occurs in response to \_\_\_\_\_\_
pyrogens
108
examples of pyrogens
* 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
what causes sepsis?
severe pyrogenic infection
110
what happens during sepsis?
Hypotensive shock and disseminated intravascular coagulation
111
what is leukocytosis?
Elevated numbers of white blood cells in the blood
112
elevated plasma levels of acute-phase proteins are implicated in causing what?
chronic diease(e.g. cardiovascular disease)
113
Permanent tissues (e.g. neurons, cardiac muscle) cannot repair by ________ and must be healed by \_\_\_\_\_\_\_
regeneration, scarring
114
labile tissue (eg epithelium) repair by \_\_\_\_\_?
regeneration (occurs continuously)
115
4 steps of healing by scarring?
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
Healing with scarring is the outcome for what 5 things?
* Acute inflammation (when severe) * Chronic inflammation * Ischaemic necrosis * Wounds (e.g. skin) * Bone fractures
117
Repair is under the control of which 5 growth factors?
* 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
where are growth factors primarily produced?
produced primarily by macrophages and platelets in sites of injury
119
List 5 actions of growth factors
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
When damage is limited tissue can be repaired by \_\_\_\_\_\_\_?
regeneration
121
Scar formation begins with the formation of ______ \_\_\_\_\_, and culminates in laying down of mature fibrous tissue
granulation tissue
122
Healing with scar formation is under the control of ____ \_\_\_\_\_
growth factors
123
Acute inflammation is characterised by rapid early influx of _____ into injured tissue
neutrophils
124
Chronic inflammation is characterised by activated _____ and \_\_\_\_\_\_\_
macrophages, lymphocytes, dendrocytes and plasma cells