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Pain > Rheumatoid Arthritits > Flashcards

Rheumatoid Arthritits Flashcards

1
Q

what is RA

A

Autoimmune attack on joints

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2
Q

Drugs and supplements for RA

A
  • NSAIDs
  • Glucocorticoid
  • csDMARDs: Methotrexate, Sulfasalazine Hydroxychloroquine, Leflunomide
  • tsDMARDs: Tofacitinib
  • bDMARDs: TNF-alpha blockers, IL1 blocker, IL6 blocker
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3
Q

factors increasing risk of RA

A
  • female (3:1 compared to male)
  • Genetic (HLA-DR4 related antigen)
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4
Q

primary target area of RA

A

synovial tissues, bone erosion, joint deformity

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5
Q

MOA of methotrexate

A

folic acid analogue that has anti-proliferative effect on T cells that inhibits macrophage functions decreasing cytokines and other pro-inflammatory mediators due to:

  1. [major] increased adenosine levels due to 5-aminoimidazole 4 carboxamide ribonucleotide (AICAR) transformylase / IMP cyclohydrolase (ATIC) inhibition
  2. [minor] decrease pyrimidines due to inhibition of dihydrofolate reductase and hence thymidylate synthase
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6
Q

ADR of methotrexate

A
  • N&V, GI and mouth ulcers
  • hair thinning (minimise folinic acid)
  • Myelosuppression, hepatotoxicity, pneumonitis, pulmonary fibrosis
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7
Q

who should avoid methotrexate

A

impaired renal function

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8
Q

MOA of sulfasalazine

A
  • decrease IgA and IgM rheumatoid factors
  • suppression of T and B cells and macrophages
  • decreases inflammatory cytokines (IL-1beta, TNF-alpha, IL-6)
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9
Q

ADR of sulfasalazine

A
  • N&V, GI discomfort
  • cytopenia/ neutropenia
  • oligospermia in men (reversible)
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10
Q

MOA of Leflunomide

A
  • inhibit dihydroorotate dehydrogenase (decrease pyrimidine synthesis)
  • anti-proliferative effects on T cells and inhibits B cell autoantibody production
  • inhibits NF-kappaB activation of pro-inflammatory pathways
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11
Q

ADR of leflunomide

A
  • N&V, GI discomfort
  • myelosuppression, hepatotoxicity, pulmonary fibrosis
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12
Q

what should pre-pregnancy female do if they used to take leflunomide

A

wash out with cholestyramine 11 days before starting due to very long half life (detectable even years after last dose)

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13
Q

MOA of Tofacitinib

A
  • Janus kinase (JAK) pathway inhibitor
  • Blocks cytokine production by blocking JAK/STAT activation
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14
Q

ADR of Tofacitinib

A
  • immunosuppression and hence opportunistic infections
  • N&V, diarrhea
  • dyslipidaemia, hyperlipidaemia, increase blood cholesterol, venous thromboembolism
  • insomnia, HA
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15
Q

what should Tofacitinib avoid giving with

A

biological DMARDs (eg. TNF-alpha blockers, IL-1 blockers, IL-6 blockers)

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16
Q

MOA of hydroxychloroquine

A
  • increase pH of intracellular vesicles (interferes with garbage processing and loading of antigens on to MHC II receptors for antigen presentation)
  • Blocks toll-like receptor 9 (TRL9)
  • shields endothelial annexing V, blocks anti-phospholipid antibodies
17
Q

ADR of hydroxychloroquine

A
  • N&V
  • ocular toxicity (Bull’s eye maculopathy)
  • cardiomyopathy
18
Q

examples of TNF-alpha blockers

A

infliximab, adalimumab

19
Q

examples of IL1 blockers

A

Anakinra

20
Q

example of IL6 blockers

A

Tocilixumab

21
Q

ADR of TNF- alpha blockers

A
  • infection (hep B, TB)
  • increased risk of lymphoma
  • optic neuritis
  • Leukopenia, aplastic anaemia
  • exacerbation of multiple sclerosis
  • drug induced lupus
  • live vaccination CI
22
Q

ADR of Anakinra

A
  • injection site reactions
  • infections due to immunosuppression
23
Q

MOA of Tocilizumab

A

humanised chimeric mAb IgG1 directed against IL6R alpha chain, prevents binding of IL6 to IL6 alpha and IL6 signalling

24
Q

ADR of tocilizumab

A
  • immunosuppression resulting in risk in infections (esp URTI), leucopenia, neutropenia, fever
  • skin eruptions, rashes, stomatitis (inflammation of mucous membrane of mouth)
  • hypercholesterolaemia, HA, dizziness
25
Q

DI of tocilizumab

A
  • interacts with CYP450 34A, 1A2, 2C9
    eg. Atorvastatin, CCB, theophylline, warfarin, phenytoin, BZD

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