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Molecules and cells in human disease > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

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1
Q

what’s an infectious inflammatory disease?

A

inflammation caused by an infectious disease

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2
Q

what’s a sterile infectious disease?

A

inflammation without an infectious cause

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3
Q

what’s the overarching aim of inflammation?

A

to remove damaged tissue/pathogen in order to allow repair

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4
Q

which immune system plays a central role in inflammatory line of defense?

A

Innate Immune system

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5
Q

What is acute inflammation?

A

rapid inflammatory response to infection/injury

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6
Q

how long does acute inflammation last?

A

hours-days

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7
Q

what are the 6 causes of acute inflammation?

A

microbial infections
hypersensitivity reactions- e.g. nickel allergy
chemical injury- e.g. burn
physical injury
tissue necrosis-e.g. during/after a stroke
autoimmune diseases- directed against a self-antigen

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8
Q

when does acute inflammation cease?

A

once the cause has been removed (pathogen/damaged tissue)

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9
Q

what is suppurative (purulent) inflammation?

A

macroscopic appearance of inflammation
large amounts of pus containing dying/dead neutrophils, microorganisms and oedema fluid. (may be walled off by tissue causes abscess)

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10
Q

what is fibrinous inflammation?

A

macroscopic appearance of inflammation

lots of fibrinogen which polymerises to form a thick fibrin coating

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11
Q

what’s pseudomembranous inflammation?

A

macroscopic appearance of inflammation

growth of surface layer made of disrupted mucosa, fibrin, mucus and inflammatory cells (often caused by antibiotics)

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12
Q

what is serous inflammation?

A

macroscopic appearance of inflammation

lots of protein-rich fluid exudate

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13
Q

what is cattarhal inflammation?

A

macroscopic appearance of inflammation

hypersecretion/ inflammation of mucous membrane

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14
Q

what’s hemorrhagic inflammation?

A

macroscopic appearance of inflammation

inflammation caused by severe vascular injury

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15
Q

what’s membranous inflammation?

A

macroscopic appearance of inflammation

epitheilium coated with fibrin, desquamated epithelial cells and inflammatory cells

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16
Q

what’s necrotising inflammation?

A

macroscopic appearance of inflammation
high tissue pressure (from oedema) leads to vascular occlusion and thrombosis, leading to widespread septic necrosis of affected organ

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17
Q

what are the vascular (on site) characteristics of inflammation? (5) (more prevalent in acute inflammation)

A
  • heat
  • soreness
  • redness
  • swelling
  • loss of function
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18
Q

What are the systemic characteristics of inflammation? (tend to be more prominent in chronic inflammation)

A
  • fever
  • lethargy
  • loss of appetite
  • leukocytosis (increased leukocytes)
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19
Q

what’s the overall process of acute inflammation?

A
  • recognition of damaged tissue/ pathogens
  • release of chemical mediators
  • recruitment of leukocytes and plasma proteins
  • increased blood flow and permeability allow them to reach site
  • they enter tissues and release chemical mediatiators (e.g. phagocytes) to eliminate pathogen/ necrotic tissue
  • tissue can then repair
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20
Q

what are PRRs?

A

Pattern Recognition Receptors

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21
Q

What to PRRs recognise?

A

PAMPs and DAMPs

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22
Q

What are PAMPs?

A

Pathogen Associated Molecular Patterns

- highly conserved structures in bacteria, fungus and viruses

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23
Q

What are DAMPs?

A

Danger/ Damage associated Molecular Patterns

- released by necrotic cells

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24
Q

what are TLRs?

A

Toll Like Receptors

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25
Q

Where are TLRs found?

A

cell/ endosome membranes

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26
Q

what do TLRs detect?

A

both DAMPs and PAMPs

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27
Q

which PAMPs do TLRs detect?

A

microbial RNA/DNA, flagellin and LPS

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28
Q

what is LPS?

A

Lipopolysaccharides - a major component of gram-negative bacteria

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29
Q

which DAMPs do TLRs detect?

A

heat shock proteins, ECM components, oxidised LDL

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30
Q

What is Pentaxin?

A

A PRR

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31
Q

where is Pentaxin found?

A

extracullularly (in blood stream)

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32
Q

What does Pentaxin detect?

A

PAMPs- phosphocholine in microbial membranes

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33
Q

How many TLR types are there?

A

13

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34
Q

How many TLRs are there in humans?

A

10

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35
Q

Are TLRs membrane spanning?

A

yes

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36
Q

what do TLRs do after detecting PAMPs/DAMPs?

A

induce inflammatory genes

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37
Q

What does the extracellular region of TLRs contain?

A

leucine-rich repeats to form a ligand bidning domain (horseshoe shaped) which dimerises upon ligand binding

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38
Q

what do endothelial cells secrete in acute inflammation?

A

NO (nitric oxide)

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39
Q

what does NO do?

A

vasodilation

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40
Q

what does vasodilation do?

A

increases delivery of plasma and blood cells to site of inflammation

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41
Q

which cells enter the site first in acute inflammation?

A

neutrophils

42
Q

which immune cells are the most numerous in the blood stream?

A

neutrophils

43
Q

which immune cells are fastest to respond to chemokine release?

A

neutrophils

44
Q

how do neutrophils attach to endothelial cells?

A

using adhesion molecules

45
Q

what do neutrophils generate?

A

reactive oxygen and nitrogen species

46
Q

what’s the difference between monocytes and macrophages?

A

they’re monocytes when in blood stream

they’re macrophages in the tissue

47
Q

what’s the main, immune property of macrophages?

A

they’re phagocytic

48
Q

what do macrophages generate?

A

cytokines

reactive oxygen species

49
Q

what do mast cells produce?

A

histamine and other enzymes involved in allergies

50
Q

what does histamine do?

A

causes dilation and permeability of BVs

51
Q

what do platelets do in an inflammatory response?

A

blood clotting

synthesise serotonin

52
Q

what is meant by a vasoactive chemical mediator?

A

chemical that’s active on blood vessels

53
Q

give 4 examples of vasoactive chemical mediators

A

histamine
serotonin
lomoms
eicosanoids

54
Q

generally, what are eicosanoids?

A

signaling molecules

55
Q

what are the 2 main examples of eicosanoids?

A

Prostaglandins (PGs)

Leukotrienes (LTs)

56
Q

what produces prostaglandins?

A

mast cells, macrophages, endothelial cells

57
Q

which parts of inflammation are prostaglandins involved in?

A

systemic and vascular reactions

58
Q

what secretes leukotrienes?

A

leukocytes

59
Q

what are leukotrienes made from?

A

12- lipoxygenase

60
Q

what’s the difference between lipoxins and leukotrienes?

A

lipoxins are anti-inflammatory

leukotrienes are inflammatory

61
Q

where at PGs and LTs derived from?

A

phospholipid bilayer

62
Q

what are cytokines?

A

protein/polypeptide mediators synthesised and released by cells of the immune system during inflammation
they aid in the coordination of the inflammatory response
act locally by autocrine or paracrine mechanisms

63
Q

what are chemokines?

A

a type of cytokine that control the migration of leukocytes and mediate their activity by binding to GPCRs

64
Q

what are the 2 important chemokines to remember?

A

TNF-a and IL-1B

65
Q

what are TNF-a and IL-1B?

A

interleukins

66
Q

other than chemokines, what receptors do most cytokines act on?

A

kinase-linked receptors

67
Q

what vascular inflammatory actions do TNF and IL-1 have? (5)

A
  • increase leukocyte adhesion molecules
  • increase pro-coagulant activity
  • reduce anti-coagulant activity
  • activate leukocytes
  • produce other cytokines
68
Q

what repair actions do TNF and IL-1 have?

A
  • increase fibroblast proliferation

- increase collagen synthesis

69
Q

what systemic inflammatory actions do TNF and IL-1 have?

A
  • fever
  • leukocytosis
  • increase acute phase proteins
  • reduce appetite
  • increase sleep
70
Q

what makes phagocytosis more effiecient?

A

opsonization

71
Q

how are complement proteins activated?

A

by proteolytic cleavage when they leave blood plasma

72
Q

what’s the critical step of the complement cascade?

A

cleavage of C3

73
Q

how many pathways can cause cleavage of C3?

A

3

74
Q

what are the 3 pathways that cause cleavage of C3?

A

classical
lectin
alternative

75
Q

what happens in the classical pathway?

A

fixation of C1 to antibody combined with antigen

76
Q

what happens in the lectin pathway?

A

triggered by binding of mannose lectin

77
Q

what happens in the alternative pathway?

A

triggered by microbial surface particles

78
Q

what’s the general process/ order of complement proteins?

A

C3 (activated)–> C3a –> C3b –> C5a–> C 5,6,7,8,9 (membrane attack complex)

79
Q

what are reactive oxygen species involved in?

A

phagocytosis

80
Q

what are 2 important reactive oxygen species?

A

super oxide

hydrogen peroxide

81
Q

what is Nitric Oxide (NO)?

A

soluble gas produced from arginine by the action of NOS

82
Q

What’s NOS?

A

Nitric Oxide Synthase

83
Q

how many isoforms of NOS?

A

3

84
Q

what are the 3 isoforms of NOS?

A

nNOS, eNOS, iNOS

85
Q

what is nNOS?

A

localised primarily in CNS+ PNS

acts as neurotransmitter

86
Q

where’s eNOS found?

A

endothelial cells, epithelial cells etc.

87
Q

What’s iNOS?

A

the only calcium independent NOS

controls vascular tone

88
Q

what inflammatory responses do histamine and serotonin give? (2)

A

vasodilation

vascular permeability

89
Q

what inflammatory responses do prostaglandins give? (3)

A

vasodilation
fever
pain

90
Q

what inflammatory responses does NO give? (1)

A

vasodilation

91
Q

what inflammatory response do complement proteins give? (3)

A

vascular permeability
chemotaxis
leukocyte recruitment/activation

92
Q

what inflammatory response do leukotrienes give? (3)

A

vascular permeability
chemotaxis
leukocyte recruitment/activation

93
Q

what inflammatory response do interleukins give? (3)

A
  • chemotaxis
  • leukocyte recruitment/activation
  • fever
94
Q

what inflammatory response do chemokines give? (2)

A

chemotaxis

leukocyte recruitment/activation

95
Q

what inflammatory response do leukotrienes give? (2)

A

chemotaxis

leukocyte recruitment/activation

96
Q

what inflammatory response do bradykinins give? (1)

A

fever

97
Q

what inflammatory response do lysosomal enzymes give? (1)

A

tissue damage

98
Q

what inflammatory response do ROSes give? (1)

A

tissue damage

99
Q

what inflammatory response does LTB4 give? (1)

A

tissue damage

100
Q

give a very general summary of acute inflammation (4 steps)

A

recognise PAMPs/DAMPs
vascular changes- increased BF and permeability
attracting phagocytes and leukocytes
wide range of chemical mediators

Molecules and cells in human disease (7 decks)

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