PMI03-2013 Flashcards

1
Q

When can chronic inflammation develop?

A

As progression from acute inflammation

Following repeated episodes of acute inflammation

“de novo” if the causative agent only produces a mild (undetected) acute response

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2
Q

What are the two main processes we should consider with chronic inflammation?

A

Healing/repair

Tissue damage

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3
Q

What are the general features of chronic inflammation?

A

Later onset and longer duration

More tissue destruction and ulceration than acute inflammation

Inflammatory infiltrate contains macroophages, plasma cells and lymphocytes (few PMNs)

Granulation tissue and fibrosis

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4
Q

Describe the general mechanism of chronic inflammation?

A

Continued recruitment of macrophages and lymphocytes to area then activation

Local proliferation

Enhanced survival and immobilisation of cells in inflamed area

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5
Q

Give examples of cellular mediators involved in inflammation.

A

Histamine

Prostaglandins

Leukotrienes

Cytokines

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6
Q

Give examples of plasma-derived mediators involved in inflammation.

A

Clotting factors

Complement

Kinins

Fibrinogen/fibrin

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7
Q

What process does hydrocortizone interfere with?

A

Protein/enzyme synthesis

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8
Q

What patterns of chronic inflammation are there?

A

Serous (watery, around jaws)

Fibrinous (blood clotting)

Suppurative/purulent (pus)

Granulomatous (granuloma)

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9
Q

What is a granuloma?

A

Collection of epithelioid cells (activated macrophages with abundant eosinophilic/pale-staining cytoplasm, spindle nuclei)

Also some Langhans Giant Cells

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10
Q

What is a Langhans Giant Cell?

A

Large multinucleated cell formed by fusion of macrophages

Crescent nucleus at periphery

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11
Q

When may solitary granulomas form?

A

In response to persistent local inflammatory stimuli (eg foreign body)

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12
Q

What are chronic granulomatous diseases? Give an example.

A

Diseases characterised by granuloma formation

Tuberculosis

Sarcoidosis

Crohn’s disease

Oro-facial granulomatosis

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13
Q

What causes tuberculosis?

A

Mycobacterium tuberculosis = intracellular bacteria

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14
Q

Describe the progression of tuberculosis.

A
  1. Primary lesions (Ghon Focus) - childhood, mainly lungs and may heal without symptoms
  2. Migration to regional lymph nodes (Ghon Complex) - primary lesions with hilar lymphadenopathy; may heal or be controlled
  3. Spread to bronchi and blood if immune system cannot control:
    - millary TB = widespread
    - organ TB = single organ
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15
Q

Describe how Mycobacterium tuberculosis causes damage.

A

Mycobacterium ingested into macrophages and excite a T cell response

Intracellular => protected from attack and reside in tissues

Macrophages containing M. tuberculosis continue to proliferate and secrete pro-inflammatory cytokines

Caseating granuloma forms and most damage/fibrosis is a result of host immune response (type IV sensitivity reaction)

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16
Q

What is a caseating granuloma?

A

Dense mass of epithelioid cells walled off with fibrous tissue (may have Langhans Giant Cells)

Caseous necrosis centrally

17
Q

What is rheumatoid arthritis?

A

Chronic systemic inflammatory disorder

Mainly affects joints symmetrically which become deformed and painful with loss of function

Unknown stimulus

18
Q

How many joints are involved in a “poly-arthritis”?

A

> 5

19
Q

How is arthritis relevant to dentistry?

A

TMJ

Hand joints = holding toothbrush/other dental aids

20
Q

Describe how the joints become deformed in rheumatoid arthritis.

A

Inflammation of synovium and inflammatory cells enter joint space

Synovium expands and fills joint space

Fibrous tissue forms to try and wall off inflammation/tissue damage

Fibrous tissue eventually ossifies causing loss of function, distortion and further tissue damage

21
Q

What can stimulate the formation of foreign body granulomas?

A

Lip filler

Sutures

22
Q

Why are granulomas harmful?

A

Continuous production of mediators = ongoing inflammation (usually requires surgery/therapy to remove)