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Spring 15 - Pharm Unit I > Rheumatoid Arthritis > Flashcards

Rheumatoid Arthritis Flashcards

1
Q

Rheumatoid Arthritis

A
  • chronic inflammatory autoimmune disorder
  • may include rheumatoid nodules, vasculitis, eye inflammation, neurologic dysfunction, cardiopulmonary dz, lymphadenopathy
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2
Q

Pathophys of RA

A
  • chronic inflammation of synovial tissue –> proliferation –> pannus (inflamed synovium) –> erosion of bone/cartilage and joint destruction
  • can develop joint damage as soon as 2 years after dz onset
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3
Q

Clinical Presentation RA

A
  • insidious onset
  • prodromal sxs: fatigue, weakness, low grade fever
  • symmetrical joint involvement, esp small joints of hands, wrists, feet
  • dz waxes and wanes
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4
Q

Joint Involvement in OA

A

-large joints, including hips, knees, neck, lower back

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5
Q

Functional Classification of RA

A

1: completely able to perform usual ADLs
2: able to perform usual self-care and work, but not recreational activities
3: able to perform self-care, but not work or recreational activities
4: limited in ability to perform any ADLs

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6
Q

Tx Goals

A
  • reduce or eliminate pain
  • protect articular structures
  • control systemic complications
  • prevent loss of joint functions
  • improve or maintain QOL
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7
Q

Non-Pharm Tx

A
  • rest
  • OT, PT
  • pt education, pt support group
  • weight reduction as needed
  • surgery
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8
Q

General Approach to Pharm Treatment

A
  • start tx early and aggressively (>1 DMARD at effective doses)
  • start DMARD therapy within 3 months of dx
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9
Q

Medication Classes Commonly Used to Tx RA

A
  • NSAIDs
  • glucocorticoids
  • nonbiologic and biologic DMARDs
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10
Q

Factors that Affect Tx Decisions

A
  • dz activity
  • dz duration (early 24 mos)
  • prognosis (poor = functional limitation, +Rh factor or anticyclic citrullinated peptide antibodies)
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11
Q

NSAIDs for RA

A
  • initial drug therapy for RA
  • decrease joint inflammation and pain
  • DO NOT prevent joint destruction or slow dz progression (should not be used alone)
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12
Q

Corticosteroids for RA

A
  • anti-inflammatory and immunosuppressive efects

- bridging therapy, continuous low dose (avoid), short term high dose bursts to control flare

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13
Q

Corticosteroids AEs

A
  • HTN, hyperglycemia, cataracts
  • skin fragility
  • fluid retention, weight gain, osteoporosis
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14
Q

Methotrexate

A
  • nonbiologic DMARD of choice

- often chosen as initial therapy

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15
Q

Methotrexate MOA

A

-inhibits dihydrofolate reductase, purines and thymidylic acid, cytokines (decrease inflammation)

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16
Q

Methotrexate AEs

A
  • stomatitis, N/D
  • possible alopecia
  • elevated LFTs, liver toxicity risk is low
  • thrombocytopenia, leukopenia
  • rare pulm and lympho toxicity
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17
Q

Methotrexate Relative CIs

A
  • liver dz
  • kidney impairment
  • significant lung dz
  • EtOH abuse
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18
Q

Methotrexate CIs

A

-do not use in pregnant or nursing women

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19
Q

Methotrexate Monitoring

A

LFT is necessary and CBC

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20
Q

Methotrexate Clinical Response

A

1-2 months

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21
Q

Methotrexate Interactions

A
  • caffeine may decrease MTX effectiveness

- PPIs, NSAIDs, ASA may decrease renal clearance of MTX

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22
Q

Leflunomide/Arava

A

-alternative option to MTX; as effective as MTX at reducing dz activity and progression

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23
Q

Leflunomide/Arava MOA

A

-inhibits pyrimidine synthesis = anti-proliferative and anti-inflammatory effects

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24
Q

Leflunomide/Arava AEs

A
  • elevated liver enzymes, esp if combined with MTX
  • hepatotoxicity
  • pancytopenia
  • agranulocytosis
  • thrombocytopenia
  • may interact w/ warfarin and increase INR
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25
Q

Leflunomide/Arava CIs

A
  • liver dz
  • viral hepatitis
  • severe immunodeficiency
  • obstructive biliary dz
  • inadequate birth control (preg cat X)
  • treatment with rifampin (increases leflunomide levels)
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26
Q

Leflunomide/Arava Monitoring

A
  • ALT, platelet, WBC, hgb/hematocrit

- baseline, monthly for 6 months then every 6-8 weeks

27
Q

Leflunomide/Arava Half-Life

A
  • undergoes enterohepatic recirculation

- half life 14-16 days

28
Q

Leflunomide/Arava Clinical Response

A

1-3 months

29
Q

Minocycline

A

-recommended for mild dz only (early dz w/ low activity)

30
Q

Minocycline MOA

A
  • unclear

- thought to have antimicrobial, anti-inflammatory, immunomodulatory and chondroprotective effects

31
Q

Minocycline AEs

A
  • photosensitivity, GI upset
  • pseudotomor cerebri (benign intracranial HTN)
  • abnormal pigmentation
  • vertigo
  • rare severe drug rxn (lupus-like)
32
Q

Minocycline CIs

A

-do not use in kids <8, pregnant or nursing women 2ary to tooth discoloration

33
Q

Minocycline Drug Interactions

A
  • antacids (antacids decrease mino activity so dose separately)
  • OCs
  • anticoagulants
34
Q

Minocycline Clinical Response

A

3-9 months

35
Q

Hydroxychloroquine/Plaquenil

A
  • often chosen as initial therapy for pts with milder or less active dz
  • does not slow dz progression
36
Q

Hydroxychloroquine/Plaquenil MOA

A

-inhibits movement of neutrophils and eosinophils

37
Q

Hydroxychloroquine/Plaquenil AEs

A
  • rash, diarrhea, abd. cramps

- increased risk of retinal toxicity > 6 gm/kg

38
Q

Hydroxychloroquine/Plaquenil Monitoring

A
  • no lab monitoring needed

- periodic ophthalmic exams for early detection of retinal toxicity

39
Q

Hydroxychloroquine/Plaquenil Clinical Response

A

2-6 months

40
Q

Sulfasalazine/Azulfidine

A

-helps slow dz progression in RA pts and may work more quickly than hydroxychloroquine

41
Q

Sulfasalazine/Azulfidine MOA

A

-pro drug cleaved by colon bacteria to metabolites thought to have anti-RA activity

42
Q

Sulfasalazine/Azulfidine AEs

A
  • nausea, abd discomfort

- mostly occur in first few months, can start with low dose

43
Q

Sulfasalazine/Azulfidine Monitoring

A
  • periodically for leukopenia

- pts may notice yellow/orange color of urine or skin

44
Q

Sulfasalazine/Azulfidine Clinical Response

A

1-3 months

45
Q

Biologic DMARDs

A
  • genetically engineered protein molecules
  • much more expensive than other DMARDs
  • all but 1 require parenteral administration
  • risk of serious infections
46
Q

MOA for Each Type of Biologic DMARD

A
  • inhibit tumor necrosis factor alpha
  • inhibit interleukin 1
  • deplete peripheral beta cells
  • inhibit full T cell activation
  • block action of interleukin 6
47
Q

Examples of TNF-alpha Inhibitors

A
  • etanercept (Enbrel)
  • adalimumab (Humira)
  • infliximab (Remicade)
48
Q

AEs of TNF-alpha Inhibitors

A
  • some may exacerbate or cause CHF (etanercept from med sheet)
  • do not use infliximab in pts with mod-severe HF and use others w/ caution in pts w/ HF
  • risk of infections and lymphomas
49
Q

Interleukin 1 Receptor Antagonist Name

A

anakinra (Kineret)

50
Q

Interleukin 1 Receptor Antagonist AEs

A

-HA, local injection site rxn, infx

51
Q

T-cell Activation Inhibitor Name

A

abatacept (Orencia)

52
Q

T-cell Activation Inhibitor AEs

A
  • HA, URTI, nasopharyngitis
  • N most common
  • acute infusion related reactions and hypersensitivity rare
  • serious infection and malignancies
53
Q

B-cell Depletion Drug Name

A

rituximab (Rituxan)

54
Q

T-cell Activation Inhibitor Name AEs

A

-HTN, hyperglycemia, cataracts, skin fragility, fluid retention, weight gain, osteoporosis

55
Q

IL-6 Blocking Drug Name

A

tocilizumba (Actemra)

56
Q

IL-6 Blocker AEs

A
  • URTI, HA, rhinitis
  • HTN, increased LDL
  • increased LFTs
57
Q

Janus kinase selective inhibitor AEs

A
  • risk of infxs and lymphomas
  • GI perfs
  • decreased lymphocytes/neutrophils/hgb
  • LFT and lipid elevations
58
Q

Combination Therapy

A

-single DMARD often inadequate for sxs control and preventing dz progression

59
Q

List 4 less frequently used DMARDs.

A
  • azathioprine
  • cyclosporine
  • D-penicillamine
  • gold
60
Q

What tx is recommended for low disease activity?

A

DMARD monotherapy

61
Q

What tx is recommended for moderate disease activity without features of poor prognosis?

A

DMARD monotherapy

62
Q

What tx is recommended for moderate disease activity WITH features of poor prognosis?

A

combination DMARD

63
Q

What tx is recommended for high dz activity without features of poor prognosis?

A
  • DMARD monotherapy OR

- HCQ and MTX

64
Q

What tx is recommended for high dz activity WITH features of poor prognosis?

A
  • anti-TNF +/- MTX OR

- combination DMARD therapy

Spring 15 - Pharm Unit I (6 decks)

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