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
what is monoarthritis
rare- when one joint in inflamed
26
what is tenosynovitis
inflammation of tendons (rare)
27
what is trigger finger
clinical presentation of RA, when finger gets stuck in flexed position then extends with a click
28
how many patients with RA have bilateral carpal tunnel syndrome
15%
29
what is polymyalgia pheumatica
muscle pain, stiffness and inflammation in the muscles surrounding the neck, shoulder and hips
30
what is palindromic rheumatism
variant of RA that comes and goes- usually progresses to complete RA
31
how is grip affected in RA patients
reduced- many unable to make a fist
32
what is extensor tenosynovitis
swelling in the extensor tendons | tendons flare and tear
33
what is synovitis
inflammation of the synovial membrane
34
what happens to the muscles in synovitis
waste due to the inflammation
35
what autoantibodies are associated with RA
rheumatoid factor (rheumatoid IgM) antibodies to cyclic citrullinated peptide (anti-ccp antibodies) anti-ccp antibodes have higher sensitivity and specificity
36
describe the link between RA and anti-ccp antibodies and what they are associated with
can be present for several years prior to articular symptoms associated with erosive damage remain positive despite treatment associated with smoking
37
what does the low sensitivity of antibodies mean
absence does not exclude the disease
38
what imaging can be done for RA
x rays ultrasound MRI scans
39
what do xrays show
soft tissue swelling periartiuclar osteopaenia erosions OR nothing in early stages
40
what do ultrasound scans show
increased sensitivity for synovitis in early disease erosions increased blood flow to inflamed synovium
41
what do MRI scans show
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
what and how many joints are affected by RA
``` 28 in total 10 PIPs 10 MCPs 2 wrists 2 elbow 2 shoulders ```
43
what are the DAS288 scoring parameters
>5.1 active disease 3. 2-5.1 moderate 2. 6-3.2 low disease activity <2.6 remission
44
what is the treatment for RA
disease modifying anti rheumatic drugs NSAIDs and steriods only s adjuncts (steroids bridge until effect of DMARDs starts)
45
what treatments when remission is achieved
gradually withdraw treatments
46
what is the management pathway for RA
``` aspirin/ NSAIDs + steriods +DMARD 1 +DMARD 2 +DMARD 3 ```
47
why is aggressive treatment of RA important
stops disease progression- why its essential to diagnose and treat early
48
how can steroids be given in RA
orally, IA (intra articular) or IM
49
when steroids be given IA
if fewer than 5 joints involved
50
name three DMARDs
methotrexate (main one) sulfasalazine hydroxycholoquine (combo therapy with all three) also have leflunomide, gold injection, penicillamine, azathioprine
51
what must be give 24 hours after methotrexate
folic acid
52
what is the route of methotrexate
parenteral
53
what dosage of methotrexate
start at 15mg/ week then increase | max dose 25mg/week
54
what precautions should be made when on DMARDs
regularly monitor LFTs and FBCs teratogenic effects- advise contraception
55
what are the risks of DMARDs
pneumonitis (methotrexate) bone marrow suppression live function derangement infection
56
what are biologic agents and when are they used in RA
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
what is co prescribed by biological agents
methotrexate
58
what should you screen for and avoid when using biological agents
latent/ active TB, hep B and C, HIV, varicella zoster avoid live attenuated vaccines
59
what are the complications of untreated RA
joint damage and deformities
60
how is cardiovascular disease risk affected by RA
accelerated (risk decreased with DMARDs)
61
what should be screened for (bone wise) in RA patients
osteoporosis (osteoclasts, post menopausal)