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year 3 exam 1 > rheumatoid arthritis > Flashcards

rheumatoid arthritis Flashcards

1
Q

epidemiology

A

0.3-1.5% of the population and 1% of the UK

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2
Q

aetiology

A
  • ages of 25-50 - 2-3:1 (F: M) - genetics with no racial or geographical significance
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3
Q

genetic factors in RA

A
  • HLA (human leukocyte antigen - 15-20% concordance in twins
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4
Q

environmental factors in RA

A
  • tobacco smoke, air pollution, mineral oil, female hormones, streoptoccocous
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5
Q

pathophysiology of RA

A

systemic, chronic autoimmune disease affecting the synovial joints, lungs, heart and eyes

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6
Q

what are the 4 phases of RA

A
  1. initiator phase 2. inflammation stage 3. self-perpetuating phase 4. destruction phase
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7
Q

what happens in the initiator phase

A

Event unknown, antigen presenting cells and citrillination of proteins - now seen as non-self

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8
Q

what happens in the inflammation stage

A

Self-antigens are presented causing clonal expansion of T/B cells insufficiently controlled by Tregs

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9
Q

what happens in the self perpetuating stage

A

Inflammatory damage in synovium causes self-antigens previously unseen by the immune system to be exposed

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10
Q

what happens in the destruction phase

A

Synovial fibroblasts and osteoclasts activated by cytokines (TNF, IL6)

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11
Q

cells involved in synovial inflammation

A

b cells, autoantibodies, t cells, mmps

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12
Q

role of b cells in synovial inflammation

A

produce autoantibodies, which can activate compliment and bind to activated macrophages in synovium, perpetuates inflammation

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13
Q

role of t cells in synovial inflammation

A

potentially activate monocytes, macrophages and synovial fibroblasts which produce TNFα, IL-1 and IL-6

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14
Q

role of autoantibodies in synovial inflammation

A

rheumatoid factor (RF) (directed against Fc fragment of IgG) and anti-citrullinated peptides (anti- CCP) are directed against antigens commonly present outside of the joint.

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15
Q

role of mmps in synovial inflammation

A

degrade the cartilage

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16
Q

role of IL6

A

iron redistribution in liver

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17
Q

Effects of excess TNF/RANKL

A

low bone mineral density/fractures

18
Q

role of TBFa/IL6/1

A

low stress tolerance, depression

19
Q

role of TNFa/IL6

A

free fatty acid adipocytes

20
Q

What can compliment immune complexes/IL6/TNFa cause

A

atherogenesis, MI, stroke

21
Q

signs/symptoms

A

varies and often insidious - fever, malaise, weakness, weight loss, fatigue, nodules, synovitis (symmetrical)

22
Q

co-morbidities

A

Increases CV, infection, respiratory, osteoporosis, malignancy, depression risk - Worse when treatment is delayed

23
Q

diagnosis

A
  • Erythrocyte sedimentation rate (ESR): quicker sedimentation means more inflammation * C-reactive protein (CRP): more inflammation means more inflammation * Rheumatoid factor (RF): not specific but indicative severe disease * Antinuclear antibody (ANA): uncommon (40%) indicative of severe disease * Anti-cyclic peptide (anti-CCP): more RA specific, not present in everyone ○ ANA and anti-CCP = 0 positive * Anaemia * Radiology - On examination * Limitation of movement and tenderness on palpation
24
Q

aims of treatment

A
  • To minimise pain and swelling - Prevent deformity - Maintain quality of life and control extra articular manifestations
25
Q

medications used for treatment

A
  • NSAIDS- pain management * Glucocorticoids - inflammation management * DMARDs- remission * Biologics
26
Q

what is ocilizumab/sarilumab

A

IL-6 receptor inhibitor

27
Q

what is Rituximab

A

anti B cell

28
Q

what is Abatacept

A

antibody blocking T cell simulation

29
Q

what is Anakina

A

IL-1 receptor inhibitor

30
Q

what are tofacitinib, baricitinib, filgotinib

A

targeted JAK inhibitors

31
Q

NICE guidelines 1st line

A
  1. Newly diagnosed - conventional DMARD monotherapy (mtx, slfs, lfl) AND short term steroid bridging
32
Q

NICE guidelines 2nd line

A
  1. Step up - additional cDMARD
33
Q

NICE guidelines 3rd line

A

urther management - biologics/targeted DMARD (cheapest) - For those with moderate disease - they must have a moderate response (DAS28 improvement of >0.6 and <1.2) at 6 months in order to continue - For those with severe disease - they must have a moderate response (DAS28 improvement of >1.2) at 6 months in order to continue

34
Q

NICE step down

A
  • If maintained for a year without need for corticosteroids - step down may be considered - Consider reducing or stopping - Return to previous DMARD regime if target no longer met
35
Q

flare management

A

short term steroids

36
Q

symptom control

A

NSAIDs (DMARD should control so should be short term - consider PPI)

37
Q

factors in DAS28 score

A

§ Number of swollen joints / 28 § Number of tender joints / 28 § ESR or CRP § Global assessment of health score

38
Q

DAS28 scores

A

§ >5.1: active disease § <3.2: low activity § <2.6: remission

39
Q

things to discuss at annual reviews

A
  • Assess disease activity, damage and functional ability (HAQ) - Check for development of co-morbidities - Organise cross-referral in multi-disciplinary team - Assess effect on personal life
40
Q

EULAR guidelines phase I

A
  • Methotrexate (or leflunomide/sulfasalazine if contraindicated) + short term glucocorticoids - If improvement is seen at 3 months and target achieved at 6 months continue - If not: step up
41
Q

EULAR guidelines phase II

A
  • Poor prognostic factors (high disease activity etc) present : bDMARD or JAK inhibitor - If no poor prognostic factors present: change DMARD or add DMARD - If improvement is seen at 3 months and target achieved at 6 months continue - If not: step up (DON’T NEED TO KNOW)

year 3 exam 1 (44 decks)

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