week 2- acute inflammation Flashcards

(46 cards)

1
Q

2 types of immune responses

A

innate, adaptive

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2
Q

main differences between innate and adaptive

A

innate: always ready, recognizes broad group of threats, does not have memory
adaptive: highly specific, recognize specific molecules, memory

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3
Q

players involved in innate immunity

A

macrophage, dendritic cell, neutrophil, eosinophil, mast cell, NKC

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4
Q

what are the 5 R’s

A
  1. recognition
  2. recruitment
  3. removal
  4. regulation
  5. resolution
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5
Q

c3 of the complement system results in what 3 actions?

A
  1. recruitment of neutrophils and monocytes
  2. opsonization for phagocytosis
  3. membrane attack complex
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6
Q

What is involved in recognition in innate immunity

A

PRR and PAMPs/DAMPs

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7
Q

What do PRR bind to ?

A

PAMPs/DAMPs

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8
Q

Where are PRR located

A

surface of cell, inside cell membrane, or soluble

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9
Q

How does Recognition of innate immunity work?

A

If pathogen sensed, PRR binds to it and produces cytokines and interferons which tell the body to produce immunity/reaction

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10
Q

an example of innate immunity recruitment

A

neutrophil recruitment

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11
Q

how does recruitment of innate immunity work?

A

-the cytokines will act on the endothelium of blood vessel and inflammatory cells.
-mast cells will release granules and histamine when sense danger or bind complement
-histamine stimulates inflam cells which react and allow the appropriate cells to move to the site of insult

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12
Q

4 steps of neutrophil recruitment

A
  1. margination
  2. rolling
  3. firm adhesion
  4. transmigration
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13
Q

3 main killing mechanisms of innate immunity removal?

A

intracellular killing
extracellular secretion and effectors
direct cell mediated killing of damaged/infected cells

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14
Q

example of intracellular killing

A

phagocytosis

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15
Q

4 steps of phagocytosis

A

1.detect
2. receptor signaling
3. internalization
4. destruction

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16
Q

3 parts of extracellular secretion and effectors

A
  1. degranulation
  2. contents of granules released into extracellular space
  3. neutrophil extracellular traps
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17
Q

what is involved in degranulation

A

neutrophils, eosinophils, mast cells

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18
Q

what is involved when the contents of granules are released into extracellular space?

A

-defensins
-proteolytic enzymes
-deployed inside PMN by fusion with phagosomes
-deploy extracellularly as well

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19
Q

what is involved in a Neutrophil extracellular trap?

A

-composed primarily of neutrophil DNA
-binds pathogens
-disarm them with antimicrobial proteins
-physical barrier
-minimize damage to host cells

20
Q

what is involved in direct cell mediated killing of damaged/infected cells?

A

control of natural killer cells

21
Q

what are natural killer cells

A

-perforin forms pores in plasma membrane
-granzyme enters via perforin pores
-activates apoptosis, cleaves many things
-very controlled

22
Q

how do we control NKCs

A

remove the inhibitor and bind the activator to release killing enzymes

23
Q

2 categories of inflammation

A

acute, chronic

24
Q

what happens during acute inflammation

A

-dilation of small blood vessels
-increase vascular permeability
-emigration of leukocytes
-minutes to days

25
what happens during chronic inflammation?
-infiltration with mononuclear cells -tissue destruction -attempts at healing -days to years
26
what are cardinal signs of inflammation?
-rubor -tumor -calor -dolor -functio laesa
27
what part of acute inflammation is the fluidic phase
1. dilation of small blood vessels 2. increased vascular permeability
28
what part of acute inflammation is the cellular phase
3. emigration of leukocytes from vasculature
29
what happens during dilation of small blood vessels?
-changes in blood -vasodilation (involves arterioles, opening of new capillary beds) -results in increased blood flow (erythema)
30
what happens during increased vascular permeability?
-hallmark of acute inflammation -post capillary venules -allows plasma proteins and leukocytes to reach sites of infection -early fluid leakage is low protein, low cellularity -both increase as response increases
31
what are mechanisms of vascular permeability
retraction of endothelial cells endothelial injury leukocyte mediated vascular injury increased transcytosis
32
what happens during vasodilation microvascular permeability
-loss of fluid and increased vessel diameter (-results in slower blood flow -conc of red cells -increased blood viscosity) -leads to venous stasis -congestion (redness) -leukocytes come out of laminar flow to contact endothelium
33
what causes redness and heat in acute inflammation?
vasodilation, stasis, hemoconcentration
34
what is transudate?
-extravascular fluid with low protein content, low SG, and few cells -clear, thin, effusions, and edema
35
what causes transudate fluid leakage?
leaky vessels retraction of endothelial cells due to increased histamines
36
what is exudate protein leakage?
endothelial gaps get bigger and more proteins and cells leak out making the fluid more cloudy and viscous -low protein, SG, and increased cells
37
what is fibrin?
-an insoluble protein formed from fibrinogen during the clotting of blood, it forms a fibrous mesh that impedes the flow of blood -made in liver -forms friable, threads, and plaques during acute inflammations
38
how is fibrin formed
thrombin cleaves fibrinogen to fibrin
39
what components occur during the cellular phase of acute inflammation (recruitment) ?
-deliver leukocytes to site of injury -allows for removal -leukocyte adhesion cascade
40
what is involved in leukocyte adhesion cascade
margination rolling stable (tight) adhesions transmigration
41
what is cellular exudate?
-viscous, opaque -may have flecks of fibrin, pockets of fluid -cells recruited to site of injury -can remove damage -neutrophils=pus, suppurative
42
what causes redness
increased blood flow and vascular permeability
43
what causes heat
increased blood flow
44
what causes swelling
edema, and cell accumulation
45
what causes pain
damage to tissue, release of mediators of inflammation
46
what causes loss of function
due to pain and tissue damage