rheumatoid arthritis Flashcards

1
Q

is RA seropositive or seronegative?

A

seropositive

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2
Q

what is inflammatory arthritis?

A

clearly defined group of conditions where the joint or tendon is inflamed

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3
Q

how does RA present?

A
  • morning stiffness in small joints (usually hands and feet)
  • reduction in grip strength
  • rapid onset
  • swelling of affected joints
  • usually symmetrical
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4
Q

who is more affected men or women?

A

women 3x more affected than men

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5
Q

what type of joints are usually affected by RA?

A

synovial joint

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6
Q

what are some triggers to RA?

A
  • smoking
  • stress
  • infection
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7
Q

how to diagnose RA?

A
  • clinical diagnosis (morning stiffness <30 mins)
  • 6 or >6= definite RA of 2010 ACR/EULAR
  • positive compression tests of MCP and MTP joints
  • anti CCP antibody (99%) or RF factor (70%)
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8
Q

what antibodies can be tested for in RA?

A

rheumatoid factor
Anti-CCP

however, not all patients with RA have this
RF 70% sensitive
Anti-CCP 99% sensitive

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9
Q

what antibody is more likely found in a patient who smoked and has RA?

A

Anti-CCP

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10
Q

What will be seen on an Xray of a patient with early RA?

A
  • can be normal
  • soft tissue swelling
  • periarticular osteopenia
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11
Q

what will be seen on an Xray of a patient with late RA?

A
  • erosions

- subluxation

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12
Q

what can be seen on an ultrasound of a patient with RA?

A
  • erosions in joint

- increased synovial fluid and thickening (dark)

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13
Q

what investigation is best for looking for erosions?

A

ultrasound

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14
Q

what is gold standard investigation for looking at joint pathology?

A

MRI scan

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15
Q

what are some extra-articular manifestations of RA?

A
  • dry eyes, dry mouth
  • lymphadenopathy
  • pericarditis, myocarditis
  • interstitial fibrosis, pleuritis
  • amyloidosis, renal failure
  • rheumatoid nodules in the skin
  • myositis
  • tenosynovitis
  • rheumatoid vasculitis
  • peripheral edema
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16
Q

what are some complications of RA?

A
  • increased cardiovascular risk

- osteopenia/ osteopeniasis

17
Q

what is the first line drug for RA?

A

methotrexate and short term glucocortisteroids

18
Q

what drugs should the patient use if they have contra indications to methotrexate?

A

-leflunomide or sulfasalazine

19
Q

what are the side effects of DMARDs?

A
  • bone marrow suppression
  • infection
  • liver function derangement
  • pneumonitis
  • nausea
20
Q

what is the RA scoring system?

A

DAS28

21
Q

what medication are patients put on if theyve already been on 2 DMARDs and have a DAS28 score >5.1?

A

Biologics

22
Q

what are examples of biologics?

A
  • Anti TNF agents (infliximab)
  • T cell recepto blocker (abatacept)
  • B cell depletor (rituximab)
  • IL 6 blocker (tocilizumab)
  • JAK inhibitor (tofacitinib)
23
Q

what alleles does RA have a strong connection with?

A

HLA-DRB1 alleles

24
Q

when should methotrexate not be taken?

A
  • when pregnant

- if trying to conceive the patient should remain on contraception for 3 months since stopping the methotrexate

25
Q

what type of hypersensitivity reaction is RA?

A

Type IV T cell mediated autoimmune reaction

26
Q

what type of joints does RA affect?

A

synovial joints

27
Q

what is the basic pathology of RA?

A

the mutation causes the immune cells to get confused causing the antigen-presenting cells to pick up self antigens and take them to the lymph nodes, activating CD4 T helper cells, causing B cells to proliferate and then differentiate into plasma cells to then go on to produce specific autoantibodies against these self antigens.

The CD4 T helper cells and autoantibodies enter the circulation and reach the joints. Once in the joints T. cells secrete cytokines such as IL- gamma and IL-17 to recruit macrophages into the joint, producing TNF alpha, IL-1 and IL-6 causing synovial cell proliferation.

The increase in synovial cells and immune cells causes a PANNUS (thick, swollen synovial membrane with granulation tissue).

Over time the pannus destroys the bone. Active Synovial cells also produce proteases which break down cartilage, meaning the bones from the synovial joint rub together.

Anti-CCP and RF form immune complexes and activate the complement system causing joint inflammation. Chronic inflammation causes angiogenesis (formation of new blood vessels) meaning more inflammatory proteins can reach and destroy the joint.

The cytokines dont only stay at the joint, they move through the blood stream and attack other organs.

28
Q

which joints are affected in the hands?

A

PIP and MCP

29
Q

why are DIP joints not affected by RA?

A

RA affects joints containing synovium so the joint must be

  1. large enough to contain enough synovium
  2. be a synovial joint

DIP is a synovial joint but it is too small

30
Q

how many patients experience rheumatoid nodules?

A

25%

31
Q

what lung involvement may occur to a patient with RA?

A

pleural effusion
interstitial fibrosis
pulmonary nodules

32
Q

what DAS 28 score suggests high level of disease?

A

> 5.1

33
Q

what DAS28 score means a patient is eligible for biological therapy ?

A

> 5.1

34
Q

what investigation does NICE always recommend for someone with suspected RA?

A

Xray

35
Q

what are some common side effects of hydroxychloroquine?

A
  • retinotherapy

- corneal deposits