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MSK > Rheumatoid Arthritis > Flashcards

Rheumatoid Arthritis Flashcards

1
Q

what is RA

A

symmetrical inflammatory arthritis affecting mainly the peripheral joints

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2
Q

if untreated what can RA lead to

A

joint damage, irreverisble deformities, loss of function, increased morbidity and mortality

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3
Q

who is more likely to get it men or women

A

women (x3)

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4
Q

what age group can be affected by RA

A

any

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5
Q

what part of spine can be affected

A

just C1 and C2

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6
Q

what gene mediates RA

A

HLA-DR4

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7
Q

what are the potential triggers for RA

A

smoking, infections, stress

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8
Q

what do the severity and course of RA depend on

A

genetic factors and presence of auto antibodies

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9
Q

what is the link to smoking

A

smoking cause proteins in the lungs to become citrullinated (irreversible) and antobodies are created against these which also target the joints

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10
Q

what is the main structure involved in RA and how is it affected

A

synovium- gets thickened and inflammed

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11
Q

what is the synovium

A

lines the inside of joint capsules and tendon sheaths

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12
Q

what joints are synovial

A

C1,C2, hand, wrists, elbows, shoulders, TMJs, knees, ankles, feet, hips

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13
Q

what is a pannus and how is it formed in RA

A

an abnormal layer of fibrovascular tissue or granulation tissue

Inflammation and exuberant proliferation of the synovium leads to formation of pannus and destruction of cartilage, bone, tendons, ligaments, and blood vessels. Pannus= the hypertrophied (enlarged) synovium

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14
Q

how is the inflammatory cascade perpetuated

A

inflamed synovium caused increased blood flow- more antibodies and inflammatory cells

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15
Q

how does bone erosion occur in RA

A

as osteoclasts activated by proinflammatory cytokines

cartilage cells are prevented from being regenerated

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16
Q

describe the immune pathogenesis of RA

A

antigen (unknown) presented to niave T cells which is activated and stimulates B cells to produce rheumatoid factor and IL-6 and macrophages to produces IL-1 and 6 and TNF alpha

net result is osteoclast stimulation, hypervascular pannus and destruction of cartilage and joint

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17
Q

what is the theraputic window for rheumatoid arthritis

A

when it is in early stages (first three months)

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18
Q

what defines early RA

A

less than two years since symptom onset

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19
Q

what is tendonsynovium

A

the synovium surrounding a tendon, can be affected by RA

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20
Q

the involvement of larger or smaller joints produces a higher ECR/EULAR score

A

smaller joints

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21
Q

what are the symptoms of RA

A

will be fit and well then joints will start to be sore

early morning stiffness lasting 30-hour or even until lunchtime

swelling of the joints that is symmetrical and tender

involvement of small joints of hands and feet

positive compression tests of metacarpophalangeal (MCP) and metatarsalangeal (MTP) joints

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22
Q

why do you get early morning stiffness

A

as synovial fluid gets thicker overnight due to lack of movement

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23
Q

what diagnostic tests can be done

A

mostly history and clinical exam

blood tests- anaemia of chronic disease, raised platelets

inflammatory markers (CRP, ESR, plasma viscosity)

autoantibodies (seen in 70% of cases)

imaging (x rays of hands, feet and chest as a baseline)

systemic exam- listen for involvement of the lungs, test reflexes and sensations

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24
Q

what does RA in the feet feel like

A

walking on pebbles

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25
Q

what is monoarthritis

A

rare- when one joint in inflamed

26
Q

what is tenosynovitis

A

inflammation of tendons (rare)

27
Q

what is trigger finger

A

clinical presentation of RA, when finger gets stuck in flexed position then extends with a click

28
Q

how many patients with RA have bilateral carpal tunnel syndrome

A

15%

29
Q

what is polymyalgia pheumatica

A

muscle pain, stiffness and inflammation in the muscles surrounding the neck, shoulder and hips

30
Q

what is palindromic rheumatism

A

variant of RA that comes and goes- usually progresses to complete RA

31
Q

how is grip affected in RA patients

A

reduced- many unable to make a fist

32
Q

what is extensor tenosynovitis

A

swelling in the extensor tendons

tendons flare and tear

33
Q

what is synovitis

A

inflammation of the synovial membrane

34
Q

what happens to the muscles in synovitis

A

waste due to the inflammation

35
Q

what autoantibodies are associated with RA

A

rheumatoid factor (rheumatoid IgM)

antibodies to cyclic citrullinated peptide (anti-ccp antibodies)

anti-ccp antibodes have higher sensitivity and specificity

36
Q

describe the link between RA and anti-ccp antibodies and what they are associated with

A

can be present for several years prior to articular symptoms

associated with erosive damage

remain positive despite treatment

associated with smoking

37
Q

what does the low sensitivity of antibodies mean

A

absence does not exclude the disease

38
Q

what imaging can be done for RA

A

x rays

ultrasound

MRI scans

39
Q

what do xrays show

A

soft tissue swelling

periartiuclar osteopaenia

erosions

OR nothing in early stages

40
Q

what do ultrasound scans show

A

increased sensitivity for synovitis in early disease

erosions

increased blood flow to inflamed synovium

41
Q

what do MRI scans show

A

bone marrow oedema (associated with inflammatory joint disease and possible precursor to erosions)

integrity of tendons

can distinguish synovitis from effusions

detects erosions earlier

can monitor disease activity

(most sensitive but limited by cost)

42
Q

what and how many joints are affected by RA

A 
28 in total
10 PIPs
10 MCPs
2 wrists 
2 elbow
2 shoulders
43
Q

what are the DAS288 scoring parameters

A

> 5.1 active disease

  1. 2-5.1 moderate
  2. 6-3.2 low disease activity

<2.6 remission

44
Q

what is the treatment for RA

A

disease modifying anti rheumatic drugs

NSAIDs and steriods only s adjuncts (steroids bridge until effect of DMARDs starts)

45
Q

what treatments when remission is achieved

A

gradually withdraw treatments

46
Q

what is the management pathway for RA

A 
aspirin/ NSAIDs
\+ steriods
\+DMARD 1
\+DMARD 2
\+DMARD 3
47
Q

why is aggressive treatment of RA important

A

stops disease progression- why its essential to diagnose and treat early

48
Q

how can steroids be given in RA

A

orally, IA (intra articular) or IM

49
Q

when steroids be given IA

A

if fewer than 5 joints involved

50
Q

name three DMARDs

A

methotrexate (main one)
sulfasalazine
hydroxycholoquine

(combo therapy with all three)

also have leflunomide, gold injection, penicillamine, azathioprine

51
Q

what must be give 24 hours after methotrexate

A

folic acid

52
Q

what is the route of methotrexate

A

parenteral

53
Q

what dosage of methotrexate

A

start at 15mg/ week then increase

max dose 25mg/week

54
Q

what precautions should be made when on DMARDs

A

regularly monitor LFTs and FBCs

teratogenic effects- advise contraception

55
Q

what are the risks of DMARDs

A

pneumonitis (methotrexate)

bone marrow suppression

live function derangement

infection

56
Q

what are biologic agents and when are they used in RA

A

e.g. anti TNF agents (-mabs), t cell blocker, B cell depletor, IL-6 blocker, JAK 2 inhibitor

dont give to patients already prone in to infection

rationed as very expensive

only when no response to DMARDs and DAS28 score greater that 5.1 on two occasions 4 weeks apart

57
Q

what is co prescribed by biological agents

A

methotrexate

58
Q

what should you screen for and avoid when using biological agents

A

latent/ active TB, hep B and C, HIV, varicella zoster

avoid live attenuated vaccines

59
Q

what are the complications of untreated RA

A

joint damage and deformities

60
Q

how is cardiovascular disease risk affected by RA

A

accelerated (risk decreased with DMARDs)

61
Q

what should be screened for (bone wise) in RA patients

A

osteoporosis (osteoclasts, post menopausal)

MSK (71 decks)

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