Pharmacotherapy for RA and Gout Flashcards

1
Q

What are the five classes of disease-modifying antirheumatic drugs (DMARDs)?

A

Antineoplastic agents, antimalarial agents, chelating agents (don’t need to know this one), immunosuppressives, mechanism-targeted inhibitors

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2
Q

What antineoplastic agent is most commonly used in the treatment of RA?

A

Methotrexate

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3
Q

What is the mechanism of anti-inflammatory activity of methotrexate in RA?

A

Not fully understood; may inhibit T cell activation or suppress expression of adhesion molecules on T cells

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4
Q

What are the most common side effects of methotrexate at doses used to treat RA?

A

Nausea/vomiting, mouth sores, headache, fatigue, alopecia, rash; rarely life-threatening hepatotoxicity, pulmonary damage, and myelosuppression (usually not at this dose)

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5
Q

What antimalarial agent is used to treat RA?

A

Hydroxycholorquine

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6
Q

What is the mechanism of action of hydroxychloroquine in treating RA?

A

Not fully understood; may inhibit TLRs, block antigen processing in macrophages,, and/or block the presentation of antigen-MHC complex to CD4+ T cells

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7
Q

What are the most common side effects of hydroxychloroquine when used to treat MA?

A

Headache, dizziness, hair loss, nausea, muscle pain, worsening psoriasis; rarely causes leukopenia, thrombocytopenia, anemia, and retinal damage

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8
Q

Why is methotrexate contraindicated in patients with impaired kidney function?

A

80-90% is eliminated unchanged in the urine; impaired kidney function will increase serum half life and can cause toxicity

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9
Q

Why is hydroxychloroquine most frequently used in combination with other therapies for RA?

A

Onset of anti-rheumatic activity is relatively slow and has limited efficacy

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10
Q

What are the four most common cytokine blockers used to treat RA?

A

Infliximab, adalimumab, etanercept, and anakinra

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11
Q

What cytokine do infliximab, adalimumab, and etanercept inhibit?

A

TNF-α

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12
Q

What cytokine does anakinra inhibit?

A

IL-1

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13
Q

What is the molecular composition of infliximab?

A

Chimeric mouse/human anti-TNF-α monoclonal antibody

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14
Q

What is the molecular composition of etanercept?

A

Human TNF-α receptor linked to the Fc portion of human IgG1; soluble TNF-α receptor binds and inactivates TNF-α, recombinant degrades more slowly than naturally occurring soluble receptor

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15
Q

What is the molecular composition of adalimumab?

A

Human monoclonal anti-TNF-α antibody

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16
Q

What are the common side effects of anti-TNF-α agents?

A

Increased risk of infection, lupus-like syndrome, heart failure, exacerbation of demyelinating disease, headache, nausea; infliximab rarely causes a severe, potentally fatal infusion reaction

17
Q

What is the molecular composition of anakinra?

A

Recombinant, synthetic form of IL-1 receptor antagonist

18
Q

What are the common side effects of anakinra?

A

Headache, nausea, injection site reaction, increased risk of infection, increased risk of lymphoma

19
Q

What is the molecular composition of abatacept?

A

Fusion protein of the extracellular domain of the CTLA4 molecule and Fc domain of human IgG1

20
Q

What is the mechanism of action of abatacept in treating RA?

A

Abatacept is a soluble protien that binds to CD80/86 and blocks the binding of CD28, the costimulatory signal required for T-cell activation

21
Q

What are the common side effects of abatacept?

A

Headache, nausea, increased risk of infection

22
Q

What is the molecular composition of rituximab?

A

Mouse/human monoclonal antibody against CD20

23
Q

What is the mechanism of action of rituximab in treating RA?

A

Several proposed mechanisms, all involving depletion or inhibition of B cells

24
Q

What is the mechanism of action of tofacitinib in treating RA?

A

Blocks JAK1 and JAK3 (and JAK2 to a lesser extent), which blocks transcription of certain cytokines

25
Q

What are the side effects of tofacitinib?

A

Inflammation of nasal passages and upper pharynx, upper respiratory infections, increased risk of TB and lymphoma, headache