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pathology 1 > chronic inflammation > Flashcards

chronic inflammation Flashcards

1
Q

how does chronic inflammation differ from acute?

A
  • greater tissue destruction
  • reaction more productive rather than exudative
  • macrophages, lymphocytes and plasma cells prominent
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2
Q

what are the 2 classes based on how chronic inflammation arises?

A
  • non-specific chronic inflammation

- specific chronic inflammation

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3
Q

name a subset of specific chronic inflammation

A

granulomatous chronic inflammation

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4
Q

how does non-specific chronic inflammation occur ?

A

failure to resolve acute inflammation, persistent bouts of acute inflammation

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5
Q

how does specific (primary) chronic inflammation occur ?

A

arises from the beginning due to persistent exposure to agent

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6
Q

what is granulomatous chronic inflammation ?

A

subset of specific chronic inflammation characterised by the presence granulomas

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7
Q

non-specific chronic inflammation infiltrate is dominated by which cells?

A

t cells, macrophages, b cells

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8
Q

specific chronic inflammation is characterised by the excessive activation of what immune cell?

A

macrophage

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9
Q

specific chronic inflammation can be induced in 2 categorical ways, what are these?

A
  • non immunologically

- immunologically

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10
Q

give examples of non-immunological stimuli which may cause specific chronic inflammation

A

inert noxious material (silica, asbestos)

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11
Q

give examples of immunological stimuli which may cause specific chronic inflammation

A
  • virus, bacteria, fungi, parasite
  • hypersensitivity reaction
  • autoimmune reaction
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12
Q

macrophages are the central figure in chronic inflammation, what are the 2 subsets of macrophages?

A
  • M1

- M2

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13
Q

What is the function of M1 macrophages?

A
  • cytotoxicity
  • fight disease, phagocytose
  • produce proteins which cause tissue damage
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14
Q

What is the function of M2 macrophages?

A
  • immune suppression
  • produce molecules which switch off M1 and drive heading
  • anti-inflammatory
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15
Q

how does chronic granulomatous inflammation differ from normal chronic inflammation?

A

predominant cell type of granulomatous is modified activated macrophages (epitheliod macrophages form gaint cells)

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16
Q

give examples of modified activated macrophages

A
  • epitheliod macrophages

- giant cells (multi nucleated)

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17
Q

what may cause chronic granulomatous inflammation?

A
  • delayed hypersensitivity (immunological)

- foreign body in tissue (non-immunological)

18
Q

oral crohns/orofacial granulomatosis (OFG) is characterised by what?

A

granulomas in soft tissue and swelling

19
Q

what is crohns?

A

autoimmune reacyion to commensal organisms in GIT

20
Q

give examples of autoimmune diseases

A
  • rheumatoid arthritis
  • psoriasis
  • sjorens
  • MS
  • type 1 diabetes
21
Q

give two symptoms of sjorens?

A
  • xerostomia

- xerophthalmia (dry eyes)

22
Q

describe periodontal disease

A
  • chronic inflammation, soft and hard tissue destruction
23
Q

name the complex structure that supports cells in the gingivae?

A

ECM

24
Q

what is the ECM made from?

A

protein fibres (mainly collagen)

25
Q

the ECM is remodelled by which molecule?

A

MMPs (matrix metalloproteinases)

26
Q

what do MMPs do to the ECM once activated?

A

breakdown matrix

27
Q

which molecules inhibit MMPs?

A

Tissue inhibitors TIMPs

28
Q

why is remodelling of the ECM important?

A
  • path clearing
  • ECM proteolysis generates signalling molecules
  • angiogenesis (formation new BVs)
29
Q

which type of immune cell are TIMPs?

A

cytokines

30
Q

what does ROS stand for?

A

reactive oxygen species

31
Q

what does RNS stand for?

A

reactive nitrogen species

32
Q

RNS and NOS are byproducts of which process?

A

phagocytosis

33
Q

what may RNS and NOS cause?

A
  • cell membrane damage
  • mitochondria damage
  • DNA damage
34
Q

what is the name for the process of bone formation?

A

osteoblastogenesis

35
Q

what is the name for the process of bone resorption?

A

osteoclastogenesis

36
Q

which molecule drives osteoclastogenesis?

A

RANKL (receptor activator of nuclear factor kabob B ligand)

37
Q

what substance inhibits RANKL?

A

OPG (osteoprotogerin)

38
Q

what cell produces OPG?

A

osteoblasts

39
Q

excessive immune response has what effect on RANKL:OPG?

A

increased -tipping balance towards bone loss

40
Q

high RANKL:OPG in gingival crevicular fluid is associated with what disease?

A

periodontal

pathology 1 (13 decks)

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