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BPT Rheumatology > Rheumatoid Arthritis > Flashcards

Rheumatoid Arthritis Flashcards

1
Q

Prevalence of RA

A

0.5-1%

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2
Q

Age and gender of RA

A

30-60 years, female

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3
Q

What is the reduced life expectancy of RA?

A

7-10 years

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4
Q

Which environmental factors lead to the progression of RA?

A

smoking, periodontitis, gut microbiome

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5
Q

What is the shared epitope of RA?

A

The amino acid motif QKRAA in the HLA-DRB1 region

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6
Q

Which bacteria in periodontal disease is an environmental factor in RA?

A

prophyromonas gingivalis

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7
Q

When do anti CCP antibodies peak?

A

disease onset to first year of symptoms

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8
Q

What are the autoantibodies in RA?

A

RF, ACPA, anti-PAD4, AntiCarP, Anti-MDA, Anti-MMA

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9
Q

What are RF antibodies directed against?

A

Fc portion of human IgG

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10
Q

What percentage of patients with RA will have positive RF?

A

75%

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11
Q

Who has more severe disease seropositive or seronegaitve patients?

A

seropositive

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12
Q

Which other autoimmune diseases may have positive RF?

A

sjogrens, cryoglobulinaemia, SLE

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13
Q

Which non autoimmune diseases may have positive RF?

A

chronic infection (hep B, hep C), cancer

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14
Q

What is citrullination?

A

the post translational conversion of peptidylarginine to peptidylcitrulline

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15
Q

What are ACPAs associated with?

A

more severe disease, RA related lung disease, cardiovascular disease

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16
Q

What are the key cytokines in RA?

A

TNF, IL-17A, IL-17F, IL-1alpha, IL-1beta, IL-6

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17
Q

Which joints are spared in RA?

A

DIP

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18
Q

What is RS3PE syndrome?

A

Remitting, seronegative, symmetric synovitis with pitting edema syndrome:

  • oedema of dorsum of hand or foot
  • tenosynovitis
  • seronegative for RF and ACPA
  • responds well to glucocorticoids
  • can be paraneoplastic
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19
Q

Which direction does the wrist deviate?

A

radial

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20
Q

Which direction do the fingers deviate at the MCP?

A

ulnar

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21
Q

What are the dermatologic manifestations of RA?

A

rheumatoid nodules, vasculitis, ulcers, neutrophilic dermatoses, treatment related rashes

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22
Q

What are the opthalmologic manifestations of RA?

A

episcleritis, scleritis, perilimbic ischaemic ulcers, secondary sjogren’s syndrome

23
Q

What are the pulmonary manifestations of RA?

A

pleural effusions, nodules, cricoaretynoid arthritis, interstitial lung disease, bronchiectasis, cryptogenic organising pneumonia

24
Q

What are the cardiovascular manifestations of RA?

A

premature atherosclerosis, pericarditis, pericardial effusion, arrhythmias, myocarditis, heart failure, cardiac nodules

25
Q

What are the GI manifestations of RA?

A

xerostomia, gastritis (from NSAIDs), stomatitis, mucositis (from methotrexate)

26
Q

What are the renal manifestations of RA?

A

glomerulonephritis, proteinuria, treatment related kidney injury

27
Q

What are the hepatic manifestations of RA?

A

nodular regenerative hyperplasia, portal fibrosis, treatment related hepatitis/cirrhosis

28
Q

What are the haematological manifestations of RA?

A

lymphadenopathy, felty syndrome, lymphoma, amyloidosis, cryoglobulinaemia, large granular lymphocyte syndrome

29
Q

What are the radiographic characteristics of RA?

A 
Periarticular soft tissue swelling (joint effusion, tenosynovitis)
Juxta-articular osteoporosis
Marginal erosions
Joint space narrowing
Symmetric involvement
Deformities in advanced disease
30
Q

Which is the most important DMARD?

A

methotrexate

31
Q

What is the dose of methotrexate?

A

15-25mg weekly

32
Q

What are the adverse effects of methotrexate?

A

nausea, hair loss, stomatitis, hepatotoxicity, cytopaenias, pneumonitis, teratogenecity

33
Q

What is the efficacy (ACR70 response rate) of methotrexate?

34
Q

How is methotrexate excreted?

35
Q

What is the dose of sulfasalazine?

A

2-4g daily

36
Q

What is the efficacy (ACR70 response rate) of sulfasalazine?

A

8% at 2g/d

37
Q

What are the adverse effects of sulfasalazine?

A

hypersensitivity reactions, nausea, diarrhoea, agranulocytosis, drug induced lupus, azoospermia

38
Q

What are the adverse effects of hydroxychloroquine?

A

hyperpigmentation, retinopathy, myopathy, cardiomyopathy

39
Q

What is the mechanism of action of leflunomide?

A

inhibition of DHODH (dihydrooratedehydrogenase), an enzyme in de novo pyrimidine synthesis (required for T-cell activation)

40
Q

What is the dose of leflunomide?

A

10-20mg daily

41
Q

What are the adverse effects of leflunomide?

A 
Diarrhoea(~25%)
Hypertension
Hypersensitivity reactions
LFTs and pneumonitis (esp. if combined with methotrexate and b/g ILD)
Leukocytopenia
Teratogenicity
Peripheral neuropathy
42
Q

What are the different types of biologic DMARDs?

A

TNF inhibitors, Anti-CD20, IL-6R inhibitor, Jak inhibitors, T cell costimulation inhibitors

43
Q

What are the contraindications for TNF inhibitors?

A 
SLE
Demyelinating disorders
Current, active, serious infection
Recurrent or chronic infection
Untreated latent or active mycobacterial infection
Hepatitis B infection
Congestive heart failure
Pregnancy
44
Q

What are the adverse effects of TNF inhibitors?

A 
Infections (including serious infections)
Opportunistic infections (e.g., tuberculosis)
Malignancies (skin cancer, lymphoma [?])
Demyelinating conditions
Autoantibodies (ANA, anti–ds DNA)
Hepatotoxicity
Dermatologic reactions
Lupus-like syndromes
45
Q

What is abatacept?

A

A T-cell costimulation inhibitor

46
Q

What is tocilizumab?

A

An IL-6 receptor inhibitor

47
Q

Why can’t CRP be used as a measure of infection in patients on tocilizumab?

A

Because IL-6 is a driver of inflammation so CRP may be normal

48
Q

What are the adverse effects of tocilizumab?

A 
Infections
Deranged LFTs
Thrombocytopaenia
Neutropaenia
GI perforation
Anaphylaxis
49
Q

What is rituximab?

A

An anti CD-20 antibody that depletes B cells but spares plasma cells

50
Q

What are the adverse effects of rituximab?

A

Infections, infusion reactions, diminished response to vaccination, reactivation of hepatitis B, rarely: progressive multifocal leukoencephalopathy

51
Q

What are the adverse effects of jak inhibitors?

A

infections
herpes zoster
cytopaenias
hyperlipidaemia

52
Q

What is the standard strategy for RA treatment?

A

first line: start methotrexate plus short term glucocorticoids
second line: add a biologic DMARD or targeted synthetic DMARD
third line: use a different biologic or targeted synthetic
when in remission phase taper doses or increase time between treatment

53
Q

How should you manage cardiovascular risk in patients with RA?

A

measure lipids while in remission or low disease activity

BPT Rheumatology (8 decks)

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