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week 2- acute inflammation Flashcards

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
Q

what happens during chronic inflammation?

A

-infiltration with mononuclear cells
-tissue destruction
-attempts at healing
-days to years

26
Q

what are cardinal signs of inflammation?

A

-rubor
-tumor
-calor
-dolor
-functio laesa

27
Q

what part of acute inflammation is the fluidic phase

A
  1. dilation of small blood vessels
  2. increased vascular permeability
28
Q

what part of acute inflammation is the cellular phase

A
  1. emigration of leukocytes from vasculature
29
Q

what happens during dilation of small blood vessels?

A

-changes in blood
-vasodilation (involves arterioles, opening of new capillary beds)
-results in increased blood flow (erythema)

30
Q

what happens during increased vascular permeability?

A

-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
Q

what are mechanisms of vascular permeability

A

retraction of endothelial cells
endothelial injury
leukocyte mediated vascular injury
increased transcytosis

32
Q

what happens during vasodilation microvascular permeability

A

-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
Q

what causes redness and heat in acute inflammation?

A

vasodilation, stasis, hemoconcentration

34
Q

what is transudate?

A

-extravascular fluid with low protein content, low SG, and few cells
-clear, thin, effusions, and edema

35
Q

what causes transudate fluid leakage?

A

leaky vessels
retraction of endothelial cells
due to increased histamines

36
Q

what is exudate protein leakage?

A

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
Q

what is fibrin?

A

-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
Q

how is fibrin formed

A

thrombin cleaves fibrinogen to fibrin

39
Q

what components occur during the cellular phase of acute inflammation (recruitment) ?

A

-deliver leukocytes to site of injury
-allows for removal
-leukocyte adhesion cascade

40
Q

what is involved in leukocyte adhesion cascade

A

margination
rolling
stable (tight) adhesions
transmigration

41
Q

what is cellular exudate?

A

-viscous, opaque
-may have flecks of fibrin, pockets of fluid
-cells recruited to site of injury
-can remove damage
-neutrophils=pus, suppurative

42
Q

what causes redness

A

increased blood flow and vascular permeability

43
Q

what causes heat

A

increased blood flow

44
Q

what causes swelling

A

edema, and cell accumulation

45
Q

what causes pain

A

damage to tissue, release of mediators of inflammation

46
Q

what causes loss of function

A

due to pain and tissue damage

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