55. Chronic Inflammation Flashcards

1
Q

How long does acute inflammation take to present?

A

Days

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2
Q

How long is chronic inflammation present for?

A

Months or years

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3
Q

Name the 2 sub-sets of chronic inflammation

A
  1. Non-specific

2. Specific (primary)

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4
Q

To which subset of chronic inflammation does granulomatous inflammation derive?

A

specific chronic inflammation

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5
Q

Give a definition of non specific chronic inflammation.

A

A dynamic balance between tissue destruction and repair.

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6
Q

Periodontitis is a form of which type of chronic inflammation?

A

Periodontitis - non-specific chronic inflammation

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7
Q

Name the 4 stages of inflammation and give an example at each stage.

A
  1. Initiation (health)
  2. Progression (Mild gingivitis)
  3. Amplification (severe gingivitis)
  4. Resolution? (If no -> periodontitis)
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8
Q

Does specific chronic inflammation arise with or without warning?

A

Without warning

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9
Q

Give the 2 categories specific chronic inflammatory responses can be classed as.

A
  1. Granulomatous

2. Non granulomatous

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10
Q

Specific chronic inflammation is characterised by excessively activated __________________.

A

Macrophages

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11
Q

Specific chronic inflammatory responses can be induced by which 2 types of agents? Give examples of each.

A
  1. Non-immunological (foreign body reaction eg. grit in a wound).
  2. Immunological (eg. hypersensitivity reaction)
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12
Q

Which type of inflammation are autoimmune diseases examples of?

A

Specific chronic inflammation.

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13
Q

Give an example of an autoimmune disease.

A

Rheumatoid arthritis

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14
Q

Describe the process of “loss of tolerance” in autoimmune diseases, with reference to specific amino acids.

A

Due to infection, enzymes produced convert arginine to citrulline which is not recognised as a self-protein. The body has thus lost tolerance against its “self cells” and attacks the body’s own cells.

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15
Q

Describe the type and give the name of the most prominent cells in chronic granulomatous inflammation.

A

Modified activated macrophages called epithelioid cells.

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16
Q

Describe how “giant cells” are formed.

A

Fused epithelioid macrophages.

17
Q

Name and give examples of the 2 ways chronic granulomatous inflammation can be induced.

A

!. Non immunological (foreign particles)

2. Immunological (hypersensitivity)

18
Q

Briefly describe the transition from monocytes to macrophages.

A

Monocytes circulate in the blood, reach the tissue then differentiate into macrophages.

19
Q

Describe the main aim of macrophages.

A

To phagocytose and present the antigen.

20
Q

Name and describe the 2 types of macrophages.

A

M1 (Pro inflammatory) (injury)

M2 (anti inflammatory) (repair)

21
Q

Give 1 difference between tissue injury and repair.

A

Injury involves coagulation factors.

Repair uses the process of fibrosis.

22
Q

Describe steps 2 and 3 of granuloma formation :

  1. Macrophages present the antigen to lymphocytes.
  2. _____________
  3. _____________
  4. Giant cell macrophages engulf bacteria.
A
  1. Macrophages present the antigen to lymphocytes.
  2. Lymphocytes (T cells) produce interleukins.
  3. Induced formation of epithelioid macrophages (giant cells formation)
  4. Giant cell macrophages engulf bacteria
23
Q

What type of inflammation is orofacial granulomatosis?

A

Chronic granulomatous inflammation.

24
Q

On examination, oral granulomas would present as what?

A

Swellings of the oral soft tissues.

25
Q

Describe the 2 terms given to describe oral granulomas based on medical history.

A

If intestinal crohns is present, it is termed “oral crohns”.

If intestinal crohns is not present, it is termed “orofacial granulomatosis”.

26
Q

What type of cells does acute inflammation involve mostly?

A

Neutrophils

27
Q

What type of cells does chronic inflammation involve mostly?

A

Macrophages

28
Q

Name the cell type which predominantly makes up inflamed epithelial tissue in gingivitis.

A

Defence cells.

29
Q
Describe stages 2 and 3 of tissue destruction in periodontitis.
1. Initiation of immune response
   Recruitment of immune cells
   Immune cell activation
2. \_\_\_\_\_\_\_\_\_\_\_\_\_
3. \_\_\_\_\_\_\_\_\_\_\_\_\_
4. Activation of MMPs.
A
  1. Initiation of immune response
    Recruitment of immune cells
    Activation of immune cells
  2. RANKL production (apoptosis regulator)
  3. Activation of osteoclasts (resorb bone)
    Reduced function of osteoblasts
  4. Activation of MMPs.
30
Q

The ECM made up of many _____________ fibres.

31
Q

What can the ECM be remodelled by?

32
Q

What is angiogenesis?

A

The formation of new blood vessels.

33
Q

Name the process of :

  1. Bone formation
  2. Bone resorption
A
  1. Bone formation - osteoblastogenesis

2. Bone resorption - osteoclastogenesis

34
Q

How often do we get a new skeleton?

A

Every 10 years

35
Q

Which cell type do osteoclasts differentiate from?

A

Macrophages

36
Q

Which cell produced RANKL?

A

Osteoblasts

37
Q

Which receptor does RANKL activate? Where is it?

A

RANKL activates RANK (receptor) on osteoclasts.

38
Q

Why is RANKL production controlled?

A

If it were uncorntrolled, osteoclasts would constantly be activated so bone would always be resorbed. It prevents excessive bone resorption.

39
Q

What do osteoblasts also secrete in addition to RANKL? Why is this important?

A

Osteoblasts secrete osteoprotogerin (OPG) which inhibits RANKL.