chronic inflammation Flashcards

(35 cards)

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
does M1 injure or repair?
injures
26
MMPs
matrix metalloproteinases - enzymes which help degrade the extra-cellular matrix (remodel the collagen)
27
why do MMPs remodel the ECM?
- help cells migrate - drives angiogenesis (formation of new blood vessels)
28
what is osteoblastogeneis?
formation of bone
29
what is osteoclastogenesis?
bone resorption - RANKL produced by osteoblasts activates RANK (the receptor) on osteoclasts - RANKL production controlled – no bone resorption
30
how often do adults 'get a new skeleton'?
every 10 years
31
where do osteoclasts differentiate from?
macrophages
32
where do osteoclasts differentiate from?
macrophages
33
what do osteoblasts secrete?
osteoprotogerin (OPG)
34
what is the function of OPG?
inhibits RANKL function - therefore controlls bone resorption
35
what is critical to balance?
RANKL and OPG ratio