rheumatoid arthritis Flashcards

1
Q

what type of disorder is rheumatoid arthritis

A

it is a Chronic systemic inflammatory auto-immune disorder

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2
Q

what are some symptoms of rheumatoid arthritis

A

Joint inflammation, synovial proliferation, destruction of articular cartilage

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3
Q

what is the pathogenesis of rheumatoid arthritis

A

immune complexes activate complement which in turn releases cytokines. the cytokines release one of the two

  1. TNF-a, IL-1
  2. prostaglandins
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4
Q

what would DMARDs (disease modifying anti-rheumatic drugs) do to a patient suffering with rheumatoid arthritis

A

To inhibit / halt the underlying immune process /prevent the long-term damage (articular cartilage damage, bone erosions)

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5
Q

what are some side effects of taking methrotrexate

A

Oral ulcerations, Nodulosis, nausea, GI upset, cytopenias, liver damage, chest infection

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6
Q

how does cyclosporine treat RA

A

inhibits IL-1 and IL-2 receptor production. Its major adverse effect is nephrotoxicity, which gets attenuated with NSAIDs, enzyme inhibitors.
NOTE ( NOT IN USE CURRENTLY)

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7
Q

why is azathioprine not used frequently in the medical field

A

Use in RA is declined due to toxicity (BM depression, leukopenia, thrombocytopenia, alopecia, increased risk of infections etc)

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8
Q

what is the advantage of using hydroxychloroquine instead of other DMARDS

A

has less effects on the liver and immune system than other DMARDs

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9
Q

what are some mechanisms of action of leflunomide

A

It reduces DNA / RNA synthesis, hence lymphocyte proliferation

Antibody production by B-cells may be depressed.

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10
Q

what are some side effects of leflunomide

A

diarrhoea, headache, rashes, loss of hair, thrombocytopenia, liver damage, increased chances of chest infections

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11
Q

what is the mechanism of action of sulfasalazine

A

Sulfapyridine- active moiety, suppress the generation of superoxide free radicals and cytokine release by inflammatory cells
Also used for early, mild R.A in combination with methotrexate and / or hydroxychloroquine.

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12
Q

what do TNF-a inhibitors do to reduce effects of RA

A

Shown to decrease signs and symptoms of R.A, reduce progression of structural damage, and improve physical function.
by inhibiting the TNF-a

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13
Q

what are the risks of using TNF-a inhibitors

A

increased risk for infections (tuberculosis, sepsis), fungal opportunistic infections, and pancytopenia.

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14
Q

what is the mechanism of action of adalimumab

A

antibody that binds to TNF-α, thereby interfering with endogenous TNF-α activity by blocking its interaction with cell surface receptors

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15
Q

what is the mechanism of action of etanercept

A

Genetically engineered, soluble, recombinant, fully human receptor fusion protein that binds to TNF-α, thereby blocking its interaction with cell surface TNF-α receptors.

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16
Q

what is the mechanism of action of golimumab

A

neutralizes the biological activity of TNF-α by binding to it and blocking its interaction with cell surface receptors.

17
Q

what is the mechanism of action of infliximab

A

binds specifically to human TNF-α and inhibits binding with its receptors. Approved for use in combination with methotrexate in patients with RA who have had inadequate response to methotrexate monotherapy.

18
Q

what is the mechanism of action of Anakinra which is a IL-1 receptor antagonist

A

Anakinra treatment leads to a modest reduction in the signs and symptoms of moderate to severe R.A in patients, Used in DMARDs failure cases, Less clinically effective than TNFα inhibitor

19
Q

why are corticosteroids used to treat RA

A

Can be inducted at any stage in R.A along with first / second line drugs

Commonly used in patients with R.A to provide symptomatic relief and bridge the time until DMARDs are effective

20
Q

how are corticosteroids administered

A

In case of single/few joint involvement with severe symptoms, intra-articular injection of glucocorticoid afford relief for several weeks, joint damage may be slowed

21
Q

how do we choose which drug to use dependant of how far the patient is

A

In low disease activity: Monotherapy may be initiated with any of the DMARDs

In moderate to high disease: activity or inadequate response to monotherapy: combination DMARD therapy or use of anti-TNF drugs

For patients with more established disease, use of other biologic therapies (Non-TNF like abatacept, rituximab) can be considered.