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BDS1 Pathology > Chronic Inflammation > Flashcards

Chronic Inflammation Flashcards

1
Q

How does chronic inflammation differ from acute inflammation?

A
  • Greater tissue destruction
  • Inflammatory infiltrate is a mixture of macrophages, lymphocytes and plasma cells (neutrophils may be present)
  • The reaction is more productive than exudative (i.e. production of new fibrous tissue rather than exudation of fluid)
  • Chronic inflammation/healing often proceed in unison
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2
Q

What are the 3 main classes of chronic inflammation?

A
  • Non-specific
  • Specific
  • Granulomatous (subset of specific)
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3
Q

What is non-specific chronic inflammation?

A
  • Failure to resolve acute inflammation (need more armoury at site of infection)
  • Persistent bouts of acute inflammation
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4
Q

What is specific chronic inflammation?

A
  • Arises de novo (starts from the beginning) - something initiates immune response - goes straight to acute then straight to chronic
  • Persistent exposure to antigen
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5
Q

What is granulomatous chronic inflammation?

A
  • Subset of specific chronic inflammation characterised by presence of granulomas - seen in number of diseases such as Crohns’s disease
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6
Q

When does chronic inflammation occur?

A

When the acute inflammation response is not adequate to resolve completely

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7
Q

Describe the process of non-specific chronic inflammation?

A
  • Infiltrate is dominated by tissue macrophages, T cells and B cells
  • Non specific chronic inflammation is characterised by a dynamic between tissue destruction and repair
  • Disease pathogenesis may include repeated acute phases and chronic phases with ongoing repair
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8
Q

What are the subsets of specific chronic inflammation?

A

Can be granulomatous or non-granulomatous

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9
Q

What is specific chronic inflammation characterised by?

A

Excessively activated macrophages - driving force between acute and chronic inflammation

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10
Q

What non-immunological factors is specific chronic inflammation induced by?

A
  • Foreign body reactions

- Inert noxious material(non-moving poisonous material) (e.g. silica and asbestos)

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11
Q

What immunological factors is non-specific chronic inflammation induced by?

A
  • Infective organisms that grow in cells (viruses, mycobacteria)
  • Hypersensitive reactions
  • Autoimmune reactions
  • Infection by fungi, protozoa or parasites
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12
Q

What are the 2 subsets of macrophages?

A

Macrophages are central figures in chronic inflammation

  • M1: cause tissue destruction - they are great at fighting disease and produce lots of different molecules that can also cause tissue damage so have to be carefully regulated
  • M2: Produce a lot of molecules that can switch off M1 - also molecules that drive tissue repair

All about balance - want immune system to eradicate pathogen but then needs to switch to repairing damage caused to tissues

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13
Q

What can activated macrophage products result in?

A
  • Tissue injury

- Fibrosis

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14
Q

Activated macrophage products can result in tissue injury, by using what?

A
  • Toxic oxygen metabolites
  • Proteases
  • Neutrophil chemotactic factors
  • Coagulation factors
  • AA metabolites
  • Nitric oxide
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15
Q

Activated macrophage products can result in fibrosis, by using what?

A
  • Growth factors
  • Fibrogenic cytokines
  • Angiogenesis factors
  • Remodelling collagenases
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16
Q

How does chronic granulomatous inflammation differ from normal chronic inflammation?

A

As the predominant cell types are modified activated macrophages:

  • epithelioid macrophages
  • Giant cells (multi-nucleated: formed from fused epithelioid macrophages)
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17
Q

What are the causes of chronic granulomatous inflammation?

A

Immunological
- Invading pathogens which cannot be cleared (can avoid host immune system and persist in tissue) e.g. TB

Non-immunological
- Foreign body in tissue e.g. asbestos particles

Unknown
- Chronic inflammatory diseases such as Chron’s and sarcoidosis (no causes have been effectively proven)

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18
Q

What is the process of granuloma formation?

A
  1. Macrophages present antigen to lymphocytes
  2. T cells (lymphocytes) recognise antigen and produce cytokines
  3. Induces the formation of epithelioid macrophages
  4. Epithelioid macrophages fuse together to form giant cells
  5. Giant cells - macrophages engulf foreign material
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19
Q

What is oral Chron’s/orofacial granulomatosis?

A

Granulomas in soft tissues of oral cavity and swelling

Chron’s is an autoimmune reaction to commensal organisms in the GIT

20
Q

What is intestinal Chron’s called?

A

Oral Chron’s

21
Q

What is non-intestinal Chron’s called?

A

Orofacial granulomatosis

22
Q

What are the inciting causes and pathogenesis of oral Chron’s?

A

Relatively unknown

23
Q

What is an effective treatment for paediatric patients with orofacial granulomatosis?

A
  • Dietary restriction

2 common things patients with Chron’s may have hypersensitivity to is cinnamaldehyde and benzoates (benzoate found in fizzy drinks)

24
Q

What is an autoimmune disease?

A
  • Unwanted response to body’s own cells and tissues or commensal bacteria
  • Loss of tolerance to self antigens or commensal bacteria
25
Q

What in our body usually prevents autoimmunity?

A
  • Multiple mechanisms of tolerance

- Autoimmunity develops if these safeguards are overcome

26
Q

What does the sustained immune response do?

A

Generates cells and molecules that destroy tissues

27
Q

What is the disease mechanism and consequence of Psoriasis?

A
  • Psoriasis is one of the most common autoimmune diseases

Disease mechanism
- Autoreactive T cells against skin-associated antigens

Consequence
- Inflammation of skin with formation of scaly patches or plaques

28
Q

What is the disease mechanism and consequence of Sjogren’s syndrome?

A

This is an orally relevant autoimmune disease (of unknown cause)

Disease mechanism
- *Autoantibodies and autoreactive T cells against ‘self’ ribonucleoprotein antigens

Consequence
- Lymphocyte infiltration of exocrine glands, leading to dry eyes and/or dry mouth; other organs may be involved, leading to systemic disease

Chronic inflammation associated with glands

  • T cell infiltration ( greater than 75% of cells)
  • B cells
  • Auto-antibodies as above *
29
Q

What is the disease mechanism and consequence for Type 1 diabetes?

A

This is a chronic immune disease

Disease mechanism
- Autoreactive T cells against pancreatic islet cell antigens

Consequence
- Destruction of pancreatic islet beta cells leading to nonproduction of insulin

30
Q

Periodontal disease is a form of chronic inflammation and tissue destruction. What are the characteristics of this?

A
  • Soft tissue destruction

- Alveolar bone loss (hard tissue destruction) - losing the supporting structures of the teeth

31
Q

What is extracellular matrix?

A

A complex structure that supports cells

32
Q

What is extracellular matrix made of?

A

Protein fibres - mainly collagen

33
Q

What is extracellular matrix re-modelled by?

A

Matrix Metalloproteinases

34
Q

Why is extracellular matrix remodelled?

A

If cells need to move they need to make their way through the ECM they will break the fibres - so MMP’s in the ECM will help to repair this

35
Q

How are matrix metalloproteinases activated?

A
  • Start life as pro-MMP which is an active enzyme with a block on it
  • Cytokines can drive the production of these enzymes
  • Enzyme produced in safe form - plasmin can remove safety device to produce the active enzyme
  • Increased production of pro-MMP’s and plasmin results in loads of active MMP’s when you don’t really want them, however we do have molecules that can switch off MMP’s (TIMPS) - but, cytokines can switch off the production of TIMPS
36
Q

Matrix metalloproteinases are associated with tissue destruction in many pathologies. Name 3 of these pathologies?

A
  • Arthritis
  • Caries
  • Periodontal disease
37
Q

MMP’s are not the only factor that causes self-harm. What else does?

A

Numerous other proteins and chemical produced by host can cause ‘collateral damage’ if not regulated

38
Q

Dysregulation of the host response promotes excessive production of what mediators?

A
  • Constantly activated cell signalling pathways

- Recruitment/activation/ differentiation of immune cell subtypes

39
Q

What does ROS stand for?

A

Reactive oxygen species

40
Q

What does NOS stand for?

A

Reactive nitrogen species

41
Q

What is the term used for ‘bone formation’?

A

Osteoblastogenesis

42
Q

What is the term used for ‘bone resorption’?

A

Osteoclastogenesis

43
Q

Bone is constantly remodelled during adult life. How many years does it take to form a completely new skeleton?

A

Around every 10 years

44
Q

Why is there no net loss of bone in bone remodelling?

A

In general formation and resorption of bone are couples so there is a balance between osteoblastogenesis and osteoclastogenesis

45
Q

What is the process of osteoclastogenesis?

A
  • Activation of Receptor Activator of Nuclear Factor Kappa-B (RANK) by its ligand (RANKL)
  • RANKLY expressed by numerous immune cells (including macrophages)
  • If expression of RANKL not controlled then increased alveolar bone loss
46
Q

What is the process of osteoblastogenesis?

A
  • Osteoblasts secrete Osteoprotogerin (OPG)

- OPG inhibits RANKL therefore bone resorption

47
Q

In bone remodelling what is an excessive immune response associated with?

A

An increase in the RANKL/OPG ratio and ‘tips the balance’ towards bone loss

BDS1 Pathology (14 decks)

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