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Clinical 2 (Part B) > 17 - Rheumatoid Arthritis > Flashcards

17 - Rheumatoid Arthritis Flashcards

1
Q

Describe RA

A
  • chronic systemic autoimmune disease
  • synovial inflammation - joint swelling, stiffness, tenderness
  • leads to cartilage injury, bone erosions, and joint damage
  • long-term disability
  • affects ppl of all ages
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2
Q

more common in _____

A

women

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3
Q

What is RA associated with?

A
  • reduced QOL
  • disability
  • decreased life expectancy
  • increased risk of CV disease and CV mortality, lympoproliferative disease and depression
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4
Q

If not treated appropriately, what can happen?

A

can result in joint destruction and severe disability that can disrupt multiple aspects of a patients life (physical and social impairment)

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5
Q

Compare a healthy joint to RA joint

A

RA joint will have:

  • inflamed tendon
  • bone erosion
  • hyperplastic synovium
  • inflammatory cells
  • thinning of cartilage
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6
Q

Most patients with RA form antibodies called _____ ____

A

rheumatoid factors

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7
Q

Briefly compare OA to RA

A

OA:

  • later onset
  • bigger joints
  • wear and tear
  • morning stiffness < 1 hour
  • no systemic symptoms

RA:

  • earlier onset
  • smaller joints (hands, wrists)
  • morning stiffness > 1 hour
  • systemic symptoms common
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8
Q

Risk factors for RA

A
  • genetic predisposition
  • exposure to unknown environmental factors
  • age
  • gender (women)
  • obesity
  • smoking
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9
Q

There are two branches of the disease. Describe them.

A
  • Early RA (ERA) is defined as patients with symptoms of less than 3 months duration.
  • Established disease - patients have symptoms due to inflammation and/or joint damage.
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10
Q

___% of people have cyclic-type of progressive disease course

A

80

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11
Q

__% have mild disease

A

10

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12
Q

___% have severe/aggressive disease

A

15

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13
Q

Time to what is crucial? (2 things)

A
  • diagnosis

- initiation of DMARD therapy

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14
Q

What classifies an early diagnosis?

A

within 6 months of the onset of joint symptoms

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15
Q

Joint damage begins within ___ years of symptoms

A

2

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16
Q

Describe the criteria for diagnosing RA

A

Need more than or equal to 6 points for diagnosis of RA:

Joint involvement:

  • 1 medium to large joint (0)
  • 2-10 medium to large joints (1)
  • 1-3 small joints (2)
  • 4-10 small joints (3)
  • More than 10 joints (at least 1 of them small) (5)

Serology:

  • negative RF and negative anti-CCP (0)
  • low positive RF or low positive anti-CCP (2)
  • high positive RF or high positive anti-CCP (3)

Acute phase reactants:

  • normal CRP and normal ESR (0)
  • abnormal CRP or abnormal ESR (1)

Duration of symptoms:

  • Less than 6 weeks (0)
  • 6 weeks or more (1)
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17
Q

What is RF and anti-CCP ?

A

RF = rheumatoid factors

Anti-CCP = anti cyclic citrullinated protein

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18
Q

Symptoms of RA

A
  • joint pain and stiffness > 6 weeks, stiffness lasts more than one hour
  • may experience fatigue, weakness, low-grade fever, loss of appetite
  • muscle pain and afternoon fatigue may be present
  • joint deformity is generally seen late in the disease
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19
Q

Signs of RA

A
  • joint involvement is frequently symmetrical
  • tenderness and warmth and swelling over affect joints (usually hands and feet)
  • systemic symptoms may be present
  • rheumatoid nodules may also be present
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20
Q

Describe the lab values in diagnosis

A
  • Labs normal >30% of the time
  • RF or anti-CCP (+) patients: worse prognosis
  • RF detectable in 60-70% of patients
  • Anti-CCP detectable in 50-85% (can be detected years before diagnosis)
  • Acute phase reactants may also be elevated (not specific to rheumatic disease (CRP, erythrocyte sedimentation rate)
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21
Q

What are some other diagnostic tests?

A
  • Joint fluid aspiration may show increased WBC counts without infection, crystals.
  • Joint radiographs may show periarticular osteoporosis, joint space narrowing, or erosions.
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22
Q

What are goals of therapy?

A
  • Fully control signs and symptoms of the disease and half radiographic progression and joint damage
  • Obtain rapid clinical improvement with a goal of 50% improvement within 3 months and ideally clinical remission.
  • Remission can be defined using multiple composite disease activity measures
  • Treatment should alleviate pain, stiffness and fatigue; prevent any further joint damage and destruction; maintain physical function and work capacity; and maximize quality of life
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23
Q

Describe the DAS28 score

A
  • Number of swollen joints at 28 sites
  • Number of tender joints at 28 sites
  • Patient estimate of global status
  • ESR or CRP value
  • Score > 5.1 = high disease activity
  • Score > 3.2 to > 5.1 = moderate disease activity
  • Score 2.6 to <3.2 = low disease activity
  • Score < 2.6 = remission
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24
Q

Methotrexate:

What category ?

A

synthetic DMARD

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25
Q

Methotrexate:

Place in therapy?

A

Methotrexate is the preferred DMARD with respect to efficacy and safety and should be the first DMARD used in patients with RA unless contraindicated

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26
Q

Methotrexate:

Efficacy?

A

most effective traditional oral synthetic DMARD

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27
Q

Methotrexate:

Onset of action?

A

4-6 weeks in most patients

  • effective for all levels of disease activity
  • SQ MTX weekly is recommended for those who lose benefit over time
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28
Q

Methotrexate:

Dose ?

A

Titrated to a usual max dose of 25mg per week by rapid dose escalation

  • given weekly
  • dangerous to give once daily
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29
Q

Methotrexate:

Safety?

A

Best side effect to efficacy ratio of any other synthetic or biological DMARD

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30
Q

Methotrexate:

Common SE ?

A

stomatitis, nausea, diarrhea and possibly alopecia

*can decrease incidence of some SE by giving folic acid tab

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31
Q

Methotrexate:

What is recommended for GI intolerant patients?

A

SQ MTX weekly

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32
Q

Methotrexate:

Significant ___ consumption should be strictly avoided.

A

alcohol

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33
Q

Methotrexate:

Can it be given in pregnancy?

A

no - it is teratogenic

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34
Q

Almost all meds given in RA require ____ monitoring

A

lab

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35
Q

What needs to be monitored for methotrexate?

A

CBC, PLT, ALT, alk phos, albumin, sCr:

  • Months 1-3: check q2-4 weeks
  • Months 3-6: check q8-12 weeks
  • After 6 months: check q12weeks

Baseline screen for HBV, HCV & HIV recommended in high risk patients (ppl with multiple partners, drug abuse, HCP)

Baseline chest x-ray: baseline measure in case pulmonary infiltrates & pneumonitis develop (rare)

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36
Q

Methotrexate:

_____ dosing

A

weekly

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37
Q

Initial ____ therapy with traditional DMARD should be considered for certain patients

A

combination

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38
Q

Methotrexate:

To reduce SE, give with ___ ____

A

folic acid (either 1 mg daily or 5 mg weekly) following the MTX dose can be useful in reducing MTX side effects

IF YOU’RE RECOMMENDING MTX, NEED TO MENTION FOLIC ACID

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39
Q

Leflunomide:

Category?

A

synthetic oral DMARD

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40
Q

Leflunomide:

Who is it recommended for?

A

recommended in all guidelines as an alternative to TMX in those intolerant

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41
Q

Leflunomide:

Efficacy ?

A

considered - equally effective as MTX

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42
Q

Leflunomide:

common SE

A

diarrhea, alopecia, rash, headache, hepatotoxicity

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43
Q

Leflunomide:

can be given in pregnancy ?

A

nope - teratogenic

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44
Q

Leflunomide:

Due to long ____, elimination protocol suggested in pregnancy (male or female) or if severe toxicity occurs

A

t 1/2

45
Q

Leflunomide:

Lab monitoring?

A

CBC, PLT, ALT, alk phos, albumin, sCr

46
Q

Leflunomide:

_____ dosing

A

daily

47
Q

Leflunomide:

____ expensive than MTX

A

more

$130/month

48
Q

Leflunomide:

What dose?

A

10-20 mg PO daily

49
Q

Hydroxychloroquine (HCQ):

Category?

A

synthetic oral DMARD

50
Q

Hydroxychloroquine (HCQ):

Who is it recommended for?

A

recommended as mono therapy only for mild disease; usually used in combination

51
Q

Hydroxychloroquine (HCQ):

Efficacy?

A

least effective oral DMARD

52
Q

Hydroxychloroquine (HCQ):

Onset?

A

2-6 months

53
Q

Hydroxychloroquine (HCQ):

Safety?

A

best tolerated DMARD

54
Q

Hydroxychloroquine (HCQ):

Most common SE

A

They are infrequent:

  • rash
  • GI (cramps, diarrhea)
  • headache

Unique SE:
-blurred vision or difficulty seeing at night (reversible upon discontinuation)

  • ocular toxicity is possible
  • hemolysis possible in G6PD deficiency patients
55
Q

Hydroxychloroquine (HCQ):

Lab monitoring ?

A

CBC, PLT, ALT, alk phos, albumin, sCr

*routien lab monitoring not needed after baseline

56
Q

Hydroxychloroquine (HCQ):

What other type of exam needed at baseline then annually for high risk?

A

eye exam

high risk patients (age > 60, retinal disease, liver disease)

*patients at low risk can get eye exam every 5 years

57
Q

Hydroxychloroquine (HCQ):

What type of dosing?

A

BID or OD

58
Q

Hydroxychloroquine (HCQ):

Dose?

A

200-300mg twice daily; after 1-2 months may decrease to 200mg OD-BID

59
Q

Sulfasalazine (SSZ):

Category ?

A

synthetic oral DMARD

60
Q

Sulfasalazine (SSZ):

Place in therapy ?

A

2nd line Tx if patient has contraindication to MTX; 1st line option when used in combination

61
Q

Sulfasalazine (SSZ):

Efficacy?

A

less active anti-RA drug than MTX (avoid as mono therapy in poor prognosis disease features)

62
Q

Sulfasalazine (SSZ):

Onset?

A

2-3 months

63
Q

Sulfasalazine (SSZ):

SE ?

A

Dose-limiting GI side effects:

  • nausea
  • anorexia
  • diarrhea
  • rash also common
64
Q

Sulfasalazine (SSZ):

_____ dose slowly for GI tolerability

A

titrate

65
Q

Sulfasalazine (SSZ):

What are some rare but serious SE?

A

hepatitis, leukopenia and agranulocytosis

hemolysis possible in G6PD deficiency pts

66
Q

Sulfasalazine (SSZ):

What labs do we need to monitor ?

A

CBC, PLT, ALT, alk phos, albumin, sCr

67
Q

Sulfasalazine (SSZ):

CI in ____ allergy

A

sulfa

68
Q

Sulfasalazine (SSZ):

Dosing ?

A

BID-TID dosing need

69
Q

Sulfasalazine (SSZ):

What is the dose ?

A

500 mg twice daily, then increase to 1 g twice daily

70
Q

What are some other DMARDs?

A
  • Azathioprene
  • Cyclosporine
  • Tacrolimus
  • Gold salts
  • Minocycline
  • Penicillamine
71
Q

Tofacitinib:

Class? How does it work?

A
  • Janus kinase (JAK) inhibitor

- Decreases signalling by a number of cytokine and growth factor receptors

72
Q

Tofacitinib:

Place in therapy ?

A
  • used as mono therapy or with MTX

- role in RA therapy yet to be determined

73
Q

Tofacitinib:

Efficacy ?

A
  • Studied in patients with inadequate responses to MTX +/- other DMARDs
  • 40-60% of patients have >20% improvement of symptoms
74
Q

Tofacitinib:

Safety ?

A
  • Black box warnings for risk of serious infections (similar to biologics); not approved for use with biologics or other stronger immunosuppressant DMARDs (azathioprine, cyclosporine)
  • Abnormalities in liver enzymes and lipids reported
75
Q

Tofacitinib:

Daily dosing?

A

5mg po BID

76
Q

Tofacitinib:

Cost?

A

Very expensive and not covered.

$17,550/year

77
Q

Describe monitoring for RA

A
  • Monitoring effectiveness is a crucial aspect to RA therapy
  • Monitoring of disease activity every 1-3 months (every 6-12 months once goals are met)
  • Add or change DMARDs every 3-6 months
  • Titrating doses can occur rapidly every 1-3 months (ex. MTX)
78
Q

Goals for effectiveness?

A

Remission

  • Low disease activity may be an appropriate goal for patients with more severe, long-standing disease (or during the early/initial Tx phase)
  • Radiographs: hands and feet every 6-12 months or longer in more established disease
79
Q

What is the role of oral glucocorticoids?

A

Short-term use at initial diagnosis for symptom control or during flares

80
Q

Oral glucocorticoids:

More effective than ____

A

NSAIDs

81
Q

Oral glucocorticoids:

What types of effects?

A

DMARD-types of effects - slowing of radiographic progression

82
Q

Oral glucocorticoids:

Generally well tolerated at the usual RA dose of prednisone _____ mg OD (or equiv)

A

5-10

83
Q

Oral glucocorticoids:

____ effective dose should be used. (ex. < 10 mg daily)

A

Lowest

84
Q

Oral glucocorticoids:

Larger doses have been used for ?

A
  • initial bridging therapy

- flares

85
Q

Oral glucocorticoids:

SE

A
  • hyperglycemia
  • CNS effects (insomnia, anxiety, irritability)
  • GI irritation
  • impaired wound healing
  • HTN
  • lipids
  • infection
86
Q

Oral glucocorticoids:

Can cause what with long-term use?

A
  • HPA-axis sup
  • osteoporosis
  • osteonecrosis
  • glaucoma/cataracts
  • weight gain/fluid retention
  • increased infection risk
87
Q

Oral glucocorticoids:

Appropriate ___ _____ needed to prevent disease flares

A

down titration

88
Q

Glucocorticoids:

When is it appropriate to use intraarticular injection ?

A

can be used when 1 or a few joints are excessively swollen or tender compared with the other affected joints

89
Q

Glucocorticoids:

How often can you do intraarticular injections?

A

can be done every 3 months (not more than 2-3 ing per joint/yr)

90
Q

Glucocorticoids:

What do we need to monitor?

A
  • Hyperglycemia
  • Test BG if DM at baseline & daily; every 3-6 months in others
  • CNS effects
  • BP & lipids q3-6 months
91
Q

Biologics:

All work by 1 of 3 mechanisms:
Describe them

A
  • Interfere with cytokine function and/or growth factor receptors
  • Inhibit the “second signal” required for T cell activation
  • Deplete B cells
92
Q

List some anti-TNF agents

A
  • Infliximab (Remicade)
  • Etanercept (Enbrel)
  • Adalimumab (Humira) or Golimumab (Simponi)
  • Certolizumab pegol (Cimzia)
93
Q

Principle behind anti-TNF therapy?

A
  • TNF alpha causes joint inflammation and degeneration so we are inhibiting that here
  • given when a patient fails on DMARD
  • these meds do not require lab monitoring but carry a small increased risk of infections
  • before starting should be tested for presence of Tb
  • if they get an infection while on biologics, they should stop biologic until infection is cured
  • can’t give live vaccine while on a biologic
  • assess vaccine Hx before starting biologic (ex. may need shingles vaccine and can’t give that once you start biologic)
94
Q

List some biologics that inhibit T cell activation

A
  • Abatacept (Orencia)
  • Toclizumab (Actemra)
  • Anakinra (Kineret) & Canakinumab (Ilaris)

*should be given with methotrexate

95
Q

List a biologic that depletes B cells

A
  • Rituximab

* inhibits pro-inflammatory effects of B cells

96
Q

Role of biologic DMARDs?

A
  • 30-50% of patients have an inadequate response to DMARDs
  • All considered equal as per RCT data
  • Except anakinra: inferior response rates compared with other biologics
97
Q

Biologic DMARDs:

Onset?

A

1-4 weeks

98
Q

Biologic DMARDs:

All biologics have improved efficacy when used with ____

A

MTX

99
Q

Biologic DMARDs:

Choice of agent depends on ?

A

Patient preference:

  • Route of administration - IV vs SQ self injection
  • Frequency of administration
  • Cost
  • Clinician experience
100
Q

TNF-alpha inhibitors:

When should they be considered?

A

After 3-6 months of 2 DMARDS (1 being methotrexate) alone or in combination

101
Q

TNF-alpha inhibitors:

When are they considered as an initial option?

A

in Tx naive patients +/- MTX in high disease activity + poor prognosis

102
Q

TNF-alpha inhibitors:

Describe the efficacy of TNF-alpha inhibitors compared to oral DMARDs

A
  • quickest onset
  • largest/best symptom and joint structure outcomes
  • largest achievement of remission
103
Q

Use biologics with _____ = more effective than biologic mono therapy

*especiallly infliximab - never use as monotherapy

A

MTX

104
Q

Biologics are Part __ EDS

A

3

105
Q

Biologics should only be used in MTX naive patients if ?

A

Patient meets similar eligibility criteria of RCTs in this population:

  • high/severe disease activity
  • ESR > 20-30 mm/h
  • bone erosions by radiograph or MRI
  • positive anti-CCP or RF
  • large number of affected joints (SJC & TJC)
106
Q

Describe the safety of TNF agents

A
  • Serious infections (bacterial sepsis, reactivation of latent TB, viral or fungal opportunistic pathogens) have been reported.
  • All patients should be monitored for signs/symptoms of infection
  • Must be withheld during active systemic infection
  • Tb screening is mandatory for all biologics
  • Risks of neoplasm (esp lymphomas); ongoing controversy, still not known if risk is due to drugs or RA itself
  • Avoid use in patients with a recent history (<5 yr) of malignancy
  • Rarely, may cause worsening of existing HF/or precipitate new onset HF
  • Patients with pre-existing demyelinating disorders (ex. MS) should not receive due to worsening of disease and symptoms
107
Q

How should we taper doses or DC therapy?

A
  • Unclear
  • Significant risk for disease flares upon discontinuation of synthetic DMARD therapy (>50%)
  • Remission must first be stably/persistently achieved for several months (12 months)
  • General principles:
    • remove NSAIDs/GCs first
    • remove least active drugs next
    • typically want long-term maintenance dose of MTX indefinitely

If patient on biological:

  • Remove NSAIDs/GC first
  • Watch for maintenance of remission
  • Try expanding the interval between doses or reducing the dose of biological and eventually D/C
108
Q

Non-pharms for RA

A
  • patient education and counselling
  • rest
  • exercise
  • physical therapy
  • occupational therapy
  • nutrition and dietary therapy
  • bone protection
  • CV risk reduction
  • vaccinations
  • quit smoking
  • address high lipids or high BP

Clinical 2 (Part B) (30 decks)

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