Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

musculoskeletal RDT > Rheumatoid arthritis > Flashcards

Rheumatoid arthritis Flashcards

1
Q

What is rheumatoid arthritis?

A

Chronic autoimmune disease characterised by pain, stiffness and symmetrical synovitis (inflammation of the synovial membrane) of synovial (diarthrodial) joints

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the features of chronic arthritis?

A

Polyarthritis - swelling of the small joints of the hand and wrists is common Symmetrical Early morning stiffness in and around joints May lead to joint damage and destruction - ‘joint erosions’ on radiographs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the features of extra-articular disease?

A

Rheumatoid nodules and other rarer features like vasculitis and episcleritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the rheumatoid factor that can be detected in blood?

A

Rheumatoid ‘factor’ may be detected in blood IgM autoantibody against IgG - should really call this rheumatoid ‘antibody’ not ‘factor’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What percentage of the population has rheumatoid arthritis?

A

1% it is a common cause of significant disability in young adults

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the gender ratio?

A

F:M=3:1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the genetic component of rheumatoid arthritis in twins and family

A

disease concordance rates for twins are 15-30% (monozytic) and 5% (dizygotic). Heritability estimates 60%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the specific genes involved with rheumatoid arthritis?

A

Specific HLA-DRB genes variants mapping to amino acids 70-74 of the BRbeta-chains are strongly associated with rheumatoid arthritis. Ther region encodes conserved amino acid sequence in the HLA-DR antigen-binding groovewhich is common to rheumatoid arthritis-associated DR alleles – termed ‘shared epitope’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe the environmental component of rheumatoid arthritis

A

Smoking- contributes 25% if population attributable risk and interacts with shared epitope to increase risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the most comments effected joints in RA?

A

Metacarpophalangeal joints (MCP) Proximal interphalangeal joints (PIP) Wrists Knees Ankles Metatarsophalangeal joints (MTP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What the significance of callous formation under metatarsals?

A

Callous formation under heads of metatarsals due to joint deformity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what are some of the features of joint deformity and destruction

A

Swan neck deformity Boutonniere deformity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is meant by symmetrical polyarthritis?

A

Damage and destruction tends to occur symmetrically. E.g. symmetrical involvement of the metacarpo-phalangeal joints and the bilateral ulnar deviation of the fingers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is meant by swan-neck deformity?

A

there is hyper-extension at the PIP (proximal interphalangeal) joint and hyperflexion and the DIP (distal interphalangeal) joint

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is meant by a Boutonniere deformity?

A

There is hyperflexion at the PIP joint

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the primary site of pathology for RA?

A

synovium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are some examples of synovium?

A
  • Synovial joints (proximal inter-phalangeal joints)
  • Tenosynovium surrounding tendons
  • Bursa
18
Q

What is proximal inter-phalangeal joint synovitis?

A
19
Q

What is extensor tenosynovitis?

A
20
Q

What are subcutaneous nodules?

A

Central area of fibrinoid necrosis surrounded by histiocytes and peripheral layer of connective tissue.

21
Q

What are sub-cutaneous nodules associated with?

A
  • Severe disease
  • Extra-articular manifestations
  • Rheumatoid factor
22
Q

Where are subcutanous nodules normally located?

A
  • In the hands- e.g. around the PIP joint
  • Rheumatoid nodule- e.g in the ulnar
23
Q

What are rheumatoid factors?

A
  • Antibodies that recognize the Fc portion of IgG as their target antigen
  • Typically IgM antibodies i.e. IgM anti-IgG antibody!

This test is positive in 70% at disease onset and further 10-15% become positive over the first 2 years of diagnosis

24
Q

What are antibodies to citrullinated protein antigens?

A

Antibodies to citrullinated peptides are highly specific for rheumatoid arthritis.

25
Q

What are some of the common extra-articular features?

A

Common

  • Fever, weight loss
  • Subcutaneous nodules
26
Q

What are some uncommon extra-articular features?

A

Uncommon

  • vasculitis (inflammation of blood vessels)
  • Ocular inflammation e.g. episcleritis
  • Neuropathies
  • Amyloidosis
  • Lung disease – nodules, fibrosis, pleuritis
  • Felty’s syndrome – triad of splenomegaly, leukopenia and rheumatoid arthritis
27
Q

What does the synovitis cause?

A

Bone erosion, pannus (abnormal layer of fibrovascular tissue) and cartilage degradation (joint space narrowing)

28
Q

What can be found inside the synovial joint?

A
  1. Synovium
  2. Synovial fluid
  3. Articular cartilage
29
Q

What is in the synovium?

A

it is 1-3 cells thin

It contains type-A synoviocyte (phagocytic), type-B synoviocytes (producing hyaluronic acid) and Type 1 collagen

30
Q

What is in synovial fluid?

A

Hyaluronic acid

31
Q

What is in articular cartilage?

A

Type 2 collagen

Proteoglycan- mainly aggrecan

32
Q

Describe the synovial membrane in rheumatoid arthritis

A

Synovium beocmes proliferated mass of tissue (pannus) due to:

  • Neovascularisation
  • Lymphangiogenesis
  • inflammatory cells- B/T cells, plasma cells, mast cells and activated macrophages
33
Q

Why are there so many inflammatory cells in RA?

A

Due to excess pro-inflammatory cytokine imbalance

Mainly due to actions of TNF-alpha Therapy for rheumatoid arthritis can be inhibited by antibodies and fusion proteins.

34
Q

What is TNF-alpha?

A

The cytokine tumour necrosis factor-alpha (TNFα) is the dominant pro-inflammatory cytokine in the rheumatoid synovium and its pleotropic actions are detrimental in this setting

35
Q

What is TNF alpha inhibition?

A

TNFα in rheumatoid arthritis validated by the therapeutic success of TNFα inhibition in this condition.

TNFα inhibition is achieved through parenteral administration (most commonly sub-cutaneous injection) of antibodies or fusion proteins

36
Q

Describe other biological therapy apart form TNF-alpha blockade

A

Il-6 and IL-1 can also be blockaded

In addition to cytokine blockade, we can also deplete B cells in rheumatoid arthritis by parenteral (intravenous) administration of an antibody against a B cell surface antigen, CD20

37
Q

What is the management of RA?

Describe the three therapies

A

Multidisciplinary approach – physio, occupational therapy, hydrotherapy, surgery.

Medication including:

  • Drugs – DMARDs – Disease-Modifying Anti-Rheumatic Drugs. Started early in the disease – joint destruction = inflammation x time. DMARDs (“steroid-sparing agents”) are safer and more effective in the long term than steroids since they avoid the long-term side-effects of steroids.
  • Biological therapy.
  • Glucocorticoid therapy – e.g. prednisolone.

· Avoid long-term use due to side effects but useful in the short term for symtpom relief.

38
Q

What are DMARDs?

A

They are disease-modifying anti-rheumatic drugs.

Drugs that induce remission and prevent joint damage- they do not cure.

They do this by reducing inflammation in synovium and slowing/ preventing structural joint damage.

It has a slow onset

39
Q

Give some examples of DMARDs?

A
  • Methotrexate
  • Sulphasalazine
  • Hydrochloroquine

Leflunomide, gold and penicillamine (are rarely used)

Everything has signifcant side effects so bloods need to be monitored.

40
Q

What are the Rituximab and Infliximab management techniques for RA?

A

Rituximab & Infliximab are chimeric antibodies with Fab mouse regions and human constant regions.

Adalimumab & Golimumab are full human antibodies.

TNFR-Fc is a fusion protein example of TNF-a.

–>Etanercept.

41
Q

What are the side effects/ cons of biological treatment?

A

These treatments (including the ones above) are very expensive and limited by NICE.

o Biological therapy involves all the antibody treatments.

o Methotrexate (not biological therapy) is used first and then if this is ineffective, biological therapy is used.

Side effects from biological therapy include an increased infection risk chance.

o TNF-a inhibition =increased susceptibility to mycobacterial infections (screen patients for TB).

o B-cell depletion=(can) to hepatitis B reactivation (so screen patients for Hep B).

o B-cell depletion =(can) to JC virus infection and progressive multifocal leukoencephalopathy (PML).

musculoskeletal RDT (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions