(059) Autoimmune disease and the musculoskeletal system Flashcards

1
Q

How can leukocytic tolerance be broken ?

A

• Microbial/Self antigen cross-reaction (molecular mimicry)

• Pathogen alters structure or presentation of self antigen

• Regulatory T cell failure

• Cytokine dis regulation

• Thymic defect

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2
Q

Rheumatoid arthritis prevalence ?

A

common (1% of population)

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3
Q

cytokines related to RA ?

A

-TNF alpha

  • IL-1

-IL-6

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4
Q

….. is a protein that can be altered to contain citrulline residues during inflammation

A

vimentin

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5
Q

“During inflammation, arginine amino acid residues can be enzymatically converted into citrulline residues in proteins such as vimentin”

This process is called :

A

citrullination

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6
Q

…… have proved to be powerful biomarkers (highly specific) that allow the diagnosis of rheumatoid arthritis (RA) to be made at a very early stage.

A

Anti-citrullinated protein antibodies (ACPAs)

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7
Q

TNF Alpha activates ….. (Cells) in RA , leading to bone resorption

A

Osteoclasts (bone macrophages)

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8
Q

TNF Alpha leads to leukocyte accumulation at site of RA through the process of :

A

Upregulating E-selectin and VCAM-1 (Vascular Cell Adhesion protein 1)

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9
Q

Chondrocytes are activated by the action of ….. (Immune mediator)

A

TNF Alpha

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10
Q

…. (Immune mediator) is responsible for the extensive angiogenesis in RA

A

TNF Alpha

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11
Q

Diagnosis of RA by Blood tests ?

A
  • CBC : Elevated erythrocyte sedimentation rate (ESR) or C-reactiVe protein (CRP) ; indicating inflammation
  • Rheumatoid factor ,, and cyclic citrullinated peptide (anti-CCP) antibodies.
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12
Q

Imaging diagnosis of RA ?

A
  • X-rays to help track the progression of rheumatoid arthritis in your joints over time.
  • MRI and ultrasound tests can help in early diagnosis of inflammation and to detect severity of the disease in your body.
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13
Q

List methods of treating RA

A

1- Nonsteroidal anti-inflammatory drugs (NSAIDs)

2- Steroids

3- Disease-modifying antirheumatic drugs (DMARDs)

4- Biologic agents

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14
Q

Role of NSAIDs in RA treatment ?

A

relieve pain and reduce inflammation

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15
Q

Role of Steroids in RA treatment ?

And give an example

A
  • reduce inflammation and pain and slow joint damage
  • Example : prednisone
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16
Q

Side effects of steroidal treatment of RA ?

A

Side effects may include thinning of bones, weight gain and diabetes

17
Q

How are steroids often used in the treatment of RA ?

A

Doctors often prescribe a corticosteroid to relieve acute symptoms, with the goal of gradually tapering off the medication

18
Q

Disease-modifying antirheumatic drugs (DMARDs) ?

A

These drugs can slow the progression of rheumatoid arthritis and save the joints and other tissues from permanent damage.

Common DMARDs include methotrexate, hydroxychloroquine (Plaquenil) and sulfasalazine (Salazopyrine)

19
Q

Famous synthetic DMARDs ?

A

-methotrexate

-hydroxychloroquine (Plaquenil)

-sulfasalazine (Salazopyrine)

20
Q

Biological DMARDs that inhibit TNF-Alpha ?

A

-Infliximab

-Etanercept

-Adalimumab

21
Q

Biological DMARDs that inhibit IL-1 ?

A

Anakinra

22
Q

Biological DMARDs that inhibit IL-6 ?

A

Tocilizumab

23
Q

Biological DMARDs that inhibit B Cell depletion ?

A

Rituximab

24
Q

Biological DMARDs that inhibit co-stimulation?

A

Abatacept

25
Q

Prevalence of Polymyositis/dermatomyositis ?

A

Fairly rare (prevalence 1 in 20,000)

26
Q

What is Polymyositis/dermatomyositis ?

A

Muscle disease associated with inflammation and autoantibodies to histidyl-tRNA synthetase

27
Q

the auto-antigen of Polymyositis/dermatomyositis ?

A

histidyl-tRNA synthetase

28
Q

In polymyositis ; associated skin involvement occurs in …..% of cases

A

50-60%

29
Q

This a microscopy of polymyositis : explain the found abnormality

A
30
Q

Describe the microscopical abnormality ,, and give your diagnosis

A
31
Q

Treatment options in polymyositis/dermatomyositis ?

A

-Corticosteroids

  • synthetic DMARDs (Methotrexate)
  • Azathioprine
  • Intravenous immunoglobulin
32
Q

Commonest treatment for MG ?

A

Acetylcholinesterase inhibitors