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Pharmacology > Osteoarthritis and Rheumatoid Arthritis > Flashcards

Osteoarthritis and Rheumatoid Arthritis Flashcards

1
Q

Difference between Bouchards and Herberdens Nodes

A

Bouchards - PIP joints

Herberdens- DIP joints

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2
Q

What are typical first line options for pain due Osteoarthritis?

What is this medication fails?

A

Acetaminophen

Topical or oral NSAIDS

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3
Q

What is the primary goal when treating Osteoarthritis?

A

Pain relief

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4
Q

What are contraindications of NSAIDS

A

Liver failure

Renal failure

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5
Q

What are some monitoring parameters of NSAIDS?

A

complete blood count
serum creatinine
hepatic transaminase levels

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6
Q

What are toxicities associated with NSAIDS

A

GI toxicity

Cardiovascular risk

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7
Q

When is topical NSAIDS recommended vs oral?

What topical is preferred

A

Recommended for patients older than 75 years to decrease the risks of systemic toxicity

Ketoprofen most common

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8
Q

How is Rheumatoid Arthritis defined?

A

Most common systemic inflammatory disease characterized by symmetrical joint involvement

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9
Q

What is the Goal of treatment for RA

A

Achieve remission or low disease activity referred to as “Treat to Target”

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10
Q

What are complications that can occur with Rheumatoid arthritis?

A

Marked ulnar deviation,
swan-neck deformity,
active synovitis,
nodules.

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11
Q

What are first line treatment options for RA?

A

Disease-modifying antirheumatic drugs (DMARDs) or biologic agents within the first 3 months diagnosis

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12
Q

What are first line treatment options for RA?

Which drug is most preferred?

A

Disease-modifying antirheumatic drugs (DMARDs)

Methotrexate

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13
Q

What treatment options can you use if one DMARDS doesn’t work?

A

Combo therapy with 2 DMARDS OR

DMARD plus biologic agent

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14
Q

What are the non-biological DMARD?

A 
Methotrexate
Leflunomide
Hydroxychloroquine
Sulfasalazine
Minocycline
Tofacitinib
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15
Q

MOA of Methotrexate

A

Inhibits cytokine production,
inhibits purine biosynthesis,
and may stimulate release of adenosine–leads to its antiinflammatory properties

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16
Q

Which nutrient does Methotrexate block the production of?

A

Folic acid antagonist—leading to deficiency

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17
Q

Contraindications for Methotrexate?

A 
Pregnancy-teratogenic and nursing women
Chronic liver disease
Immunodeficiency
Pleural or peritoneal effusions
Leukopenia, thrombocytopenia,
CrCl <40ml/min
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18
Q

What are toxicities of Methotrexate

A

Stomatitis—may see first (sores in the mouth)
hematologic-thrombocytopenia
pulmonary fibrosis and pneumonitis
hepatic-elevated liver enzymes

19
Q

What should be monitored when taking Methotrexate

A

CBC
LFT
CXR

20
Q

What is the MOA of non-biological Leflunomide?

A

inhibits pyrimidine synthesis–> decrease in lymphocyte proliferation and modulation of inflammation

21
Q

Toxicities of Leflunomide?

A

GI, hair loss, liver, bone marrow toxicity

22
Q

Contraindications fo Leflunomide?

A

liver disease

teratogenic

23
Q

What is the MOA of Hydroxychloroquine

A

dampen antigen–antibody reactions at sites of inflammation

24
Q

Toxicities of Hydroxychloroquine?

A

Lacks myelosuppressive -
Hepatic and renal toxicities
GI-N/V/D—take with food
Ocular-Visual changes including a decrease in night or peripheral vision

25
Q

What is the MOA of non-biologic Sulfasalazine

A

slide 45

26
Q

What are ADE of Sulfasalazine that may want you to decease the drug dose

A

Elevated hepatic enzymes
May turn skin to a yellow-orange color—no clinical consequence
Absorption can be decreased when antibiotics destroy colonic bacteria
Binds iron supplements—decrease sulfazalazine absorption
Can potentiate warfarin’s effects-displace from protein binding

27
Q

What is Minocycline a derivative of?

What is it’s MOA?

A

Tetracylcine

inhibit metalloproteinases active in damaging articular cartilage

28
Q

What is the MOA of Tofacitinib

A

inhibition of JAK- a tyrosine kinase–modulation and suppression of the immune system through cytokine signal reduction

29
Q

When is Tofacitinib used?

A

moderate to severe RA who have failed or intolerance to methotrexate

30
Q

What are ADE of Tofacitinib?

A

serious infections
lymphomas, and other malignancies
tested and treated for latent tuberculosis
elevated plasma liver enzymes and lipids
live vaccinations should not be given during treatment

31
Q

Definition of Biologic agents that treat RA?

A

Genetically engineered protein molecules block the pro-inflammatory cytokines

32
Q

What are the TNF-alpha drugs?

A 
Infliximab, 
entanercept, 
adalimumab, 
golimumab, 
certolizumab
33
Q

IL-1 drug?

IL-6 drug?

A

IL-1: anakinra

IL-6: tocilizumab

34
Q

MOA of TNF-alpha drugs?

Contraindications?

ADE?

A

Block the proinflammatory cytokins TNF-α

Contraindications
CHF

ADEs
MS-like illness or exacerbate MS
Increased risk of lymphoproliferative cancer

35
Q

MOA of IL-1 Anakinra?

A

binds to CD80/CD86 receptors on antigen-presenting cells

inhibits interactions between the antigen-presenting cells and T cells

prevents T-cell activation to promote the inflammatory process

36
Q

What should not be given when taking Anakinra?

A

Live vaccines should not be given to patients during treatment with Anakinra therapy

37
Q

MOA of IL-6 Tocilizumab?

A

Attaches to IL-6 receptors preventing the cytokine from interacting with the IL-6 receptors

38
Q

ADE of Tocilizumab?

A 
Increased infection risk
Elevated plasma lipids
Elevated liver enzymes
Risk of Gastrointestinal perforation
Inducer of CYP450 3A4 (warfarin)
39
Q

What should be avoided when taking Tocilizumab?

A

Tested and treated for latent tuberculosis

Live vaccinations should not be given during treatment

40
Q

What should be avoided when taking Tocilizumab?

A

Tested and treated for latent tuberculosis

Live vaccinations should not be given during treatment

41
Q

What is the MOA of biologic DMARD Riuximab?

What should be avoided when taking this?

A

Binds to B cells
nearly complete depletion of peripheral B cells

No live vaccines while in treatment

42
Q

What is the MOA of biologic DMARD Abatacept?

A

Binds to CD80/86 on T cells to prevent the costimulation needed to fully activate T cells

43
Q

What are ADE of Abatacept?

A

HA, nasopharyngitis, dizziness, cough, back pain, HTN, dyspepsia, UTI, rash, extremity pain

44
Q

What should be avoided with Abatacept?

A

No live vaccines during treatment or for 3 months after completion of therapy

Pharmacology (12 decks)

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