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BDS1 BAMS pathology and immunity > chronic inflammation > Flashcards

chronic inflammation Flashcards

1
Q

what is chronic inflammation associated with?

A

greater tissue destruction

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2
Q

what is inflammatory infiltrate in chronic inflammation?

A

mixture of macrophages and B cells/Tcells

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3
Q

what is the time period for chronic inflammation?

A

persistent- occurs over months, years an possibly forever

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4
Q

what are the three main classes of chronic inflammation?

A
  • non-specific chronic
  • specific (primary) chronic
  • chronic granulomatous
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5
Q

what is non-specific chronic inflammation?

A

Failure to resolve acute inflammation
Persistent bouts of acute inflammation
Excessive suppuration

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6
Q

what is specific chronic inflammation?

A

Arises de novo
Persistent exposure to agent

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7
Q

what is chronic granulomatous inflammation?

A

subset of specific chronic inflammation

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8
Q

what is an example of acute inflammation progressing into chronic inflammation?

A

gingivitis to periodontitis

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9
Q

what type of chronic inflammation do autoimmune diseases come under?

A

specific

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10
Q

when does chronic inflammation normally arise?

A

from acute inflammatory disease when the immune system not sufficient to eradicate stimulus

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11
Q

what is the infiltrate in non-specific chronic inflammation?

A

tissue macrophages, T cells and B cells

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12
Q

what is non- specific chronic inflammation characterised by?

A

a dynamic balance between tissue destruction and repair

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13
Q

what are the subcategories within specific chronic inflammation?

A

non-granulomatous or granulomatous

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14
Q

what is specific chronic inflammation characterised by?

A

excessively activated macrophages

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15
Q

non-immunological specific chronic inflammation induced by?

A
  • foreign body reactions
  • inert noxious material eg silica
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16
Q

immunological specific chronic inflammation induced by?

A

Infective organisms that grow in cells
Hypersensitivity reactions
Autoimmune reactions
Infection by fungi, protozoa or parasites

17
Q

what is an autoimmune diease?

A
  • Examples of specific chronic inflammation
  • Unwanted response to body’s own cells and tissues or commensal bacteria
  • Loss of tolerance to self antigens or commensal bacteria
  • Multiple mechanisms of tolerance usually prevent autoimmunity
  • Recall the positive and negative selection
  • Sustained immune response (chronic inflammation) generates cells and molecules that destroy tissues
18
Q

rheumatoid arthritis

A

production of PAD and protease enzymes which drive peptide citrullination leading to loss of tolerance

19
Q

what are the predominant cell types in chronic granulomatous inflammation?

A

modified activated macrophages (epitheloid macrophages)
- giant cells
- B and T cells

20
Q

what are the immunological causes of chronic granulomatous inflammation?

A

delayed hypersensitivity type reaction or invading pathogens

21
Q

what are the non-immunological causes of chronic granulomatous inflammation?

A

foreign body in tissue

22
Q

what are the ways in which macrophages cause tissue injury?

A

Toxic oxygen metabolites
Proteases
Neutrophil chemotactic factors
Coagulation factors
AA metabolites
Nitric oxide

23
Q

what are the ways in which macrophages cause tissue repair?

A

Process of fibrosis
Growth factors
(PDGF,FGF,TGF beta)
Fibrogenic cytokines
Angiogenesis factors (FGF)
Remodelling collagenases

24
Q

what is orofacial granulomatosis?

A
  • an example of chronic granulomatous inflammation
  • granulomas in soft tissue of oral cavity
  • if intestinal crohns it is termed oral crohns
  • no intestinal crohns- termed orofacial granulomatosis
25
Q

does M1 injure or repair?

A

injures

26
Q

MMPs

A

matrix metalloproteinases
- enzymes which help degrade the extra-cellular matrix (remodel the collagen)

27
Q

why do MMPs remodel the ECM?

A
  • help cells migrate
  • drives angiogenesis (formation of new blood vessels)
28
Q

what is osteoblastogeneis?

A

formation of bone

29
Q

what is osteoclastogenesis?

A

bone resorption
- RANKL produced by osteoblasts activates RANK (the receptor) on osteoclasts
- RANKL production controlled – no bone resorption

30
Q

how often do adults ‘get a new skeleton’?

A

every 10 years

31
Q

where do osteoclasts differentiate from?

A

macrophages

32
Q

where do osteoclasts differentiate from?

A

macrophages

33
Q

what do osteoblasts secrete?

A

osteoprotogerin (OPG)

34
Q

what is the function of OPG?

A

inhibits RANKL function
- therefore controlls bone resorption

35
Q

what is critical to balance?

A

RANKL and OPG ratio

BDS1 BAMS pathology and immunity (12 decks)

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