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PHAR 255 > Rheumatoid Arthritis > Flashcards

Rheumatoid Arthritis Flashcards

1
Q

What is rheumatoid arthritis?

A

An autoimmune condition leading to inappropriate immune system activity causing synovial and connective tissue inflammation (antibodies against self develop)

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2
Q

What is the progression in joint damage for patients with rheumatoid arthritis?

A

Chronic inflammation –> Growth of tissue (pannus) –> Loss of bone and cartilage (the body cannot replace bone and cartilage fast enough, so net loss)

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3
Q

What can trigger rheumatoid arthritis?

A

Triggered by genetics and by “stochastic” event (smoking is a common trigger, but triggers can be hard to definitively point out as a causative effect)

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4
Q

What are the consequences of inflammation in rheumatoid arthritis?

A

Can happen within 1 year of onset of RA

  • Loss of cartilage
  • Formation of scar tissue
  • Ligament laxity (they stretch out and no longer able to properly support joint)
  • Tendon contractures (they shorten and become tight)
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5
Q

How many people are affected by rheumatoid arthritis?

A

Affects 1 to 2% of the adult population (more common in women 3:1)

Can occur at any age (most common age for diagnosis is between 30 and 50)

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6
Q

What is the clinical presentation of rheumatoid arthritis?

A

Symmetrical joint pain and stiffness (lasts longer than 6 weeks)

Muscle pain (early morning stiffness, resolves within 1 hour of waking)

Fatigue, low-grade fever, appetite decrease)

Joint tenderness with warmth and swelling over affected joints

Most commonly a rapid onset starting in peripheral joints

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7
Q

What joints are most likely to be affected by rheumatoid arthritis?

A

Wrists, nads, elbows, shoulders, knees, and ankles

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8
Q

Review slide 9 for differences between rheumatoid arthritis and osteoarthritis

A
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9
Q

Review slide 12 for the visual representation of the presentation of symptoms in the hands in each of the three stages of rheumatoid arthritis

A
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10
Q

What non-joint tissues are affected in rheumatoid arthritis?

A
  • Blood vessels
  • Lungs
  • Eyes
  • Heart
  • Muscle
  • Bone
  • Skin
  • Hematological abnormalities
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11
Q

What is the impact of rheumatoid arthritis on blood vessels?

A

The autoimmune conditions starts impacting the vasculature (occurs with severe, and long-standing RA)

Can affect any blood vessel (especially those that supply/drain the skin and kidneys)

Treated with aggressive treatment of RA

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12
Q

What is the impact of rheumatoid arthritis on the lungs?

A

Pleuritis, pleural effusion, fibrosis, pulmonary nodules

Drugs used to treat RA may also affect lung function (occasional X-ray is used to monitor condition and therapy)

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13
Q

What is the impact of rheumatoid arthritis in the eyes?

A

Episcleritis, scleritis, uvetis and iritis (can cause blindness, severity depends on layer affected)

Painful, visual acuity loss

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14
Q

What is the impact of rheumatoid arthritis on the heart?

A

Pericarditis, myocarditis

Increase risk of CAD, HF, and AF

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15
Q

What is the impact of rheumatoid arthritis on the muscles?

A

Generalized weakness and pain
From synovial inflammation, myositis, vasculitis
Steroid-induced

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16
Q

What is the impact of rheumatoid arthritis on the bones?

A

Osteopenia is common

Local bone loss around affected joints

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17
Q

What is the impact of rheumatoid arthritis on the skin?

A

Rheumatoid nodules

Ulcers
Steroid-induced changes

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18
Q

How is rheumatoid arthritis diagnosed?

A

Joint involvement

Lab test findings (rheumatoid factor, elevated ESR and CRP, anti-CCP)

Duration of symptoms

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19
Q

What are the goals of treatment for rheumatoid arthritis?

A

Prevent and control joint damage

Prevent loss of function

Maintain QoL

Decrease pain

Acheive remission or low disease activity (PtGA score below 2)

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20
Q

What are the general principles of management of rheumatoid arthritis?

A
  1. Early recognition and diagnosis
  2. Early use of DMARDs (within 3 months of diagnosis)
  3. Tight control (treat until remission)
  4. Responsible NSAIDs and glucocorticoid use
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21
Q

What are some non-pharmacological therapies for rheumatoid arthritis?

A
  • Patient education (goals of therapy, drug safety)
  • Rest is important, but balance with activity (need to prevent muscle atrophy)
  • Reduce joint stress with RA friendly tools (knee braces)
  • Diet/weight loss
  • Surgery (fairly complex, associated with complications)
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22
Q

What are the maintenance therapies for rheumatoid arthritis?

A
  1. Traditional DMARDs (still used commonly)
  2. Biologic DMARDs
  3. Synthetic DMARDs (rarely used)
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23
Q

What are the flare therapies for rheumatoid arthritis?

A
  1. Corticosteroids
  2. NSAIDs/Analgesics
  3. Combinations
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24
Q

What are some characteristics of traditional DMARDs?

A
  • Slow onset of action
  • Controls symptoms
  • May delay or stop progression of disease
  • Requires regular monitoring (especially Methotrexate)
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25
Q

What are some examples of traditional DMARDs?

A

Methotrexate
Sulfasalazine
Hydroxychloroquine
Leflunomide

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26
Q

What is the mechanism of action for Methotrexate?

A

Anti-folate (less DNA synthesis, repair, cellular replication and immune response)

Targets root cause (increases immunosuppression)

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27
Q

What is the mechanism of action for Sulfasalazine?

A

Prodrug (metabolized into 5-ASA and sulfapyridine)

Modulates mediators of inflammatory response (may inhibit TNF)

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28
Q

What is the mechanism of action for Hydroxychloroquine?

A

Inhibits neutrophils and chemotaxis (impairs complement system)

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29
Q

What is the mechanism of action for Leflunomide?

A

Inhibits pyrimidine synthesis, leading to anti-inflammatory effects

Modulates many signalling pathways

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30
Q

What is the onset of effect of traditional DMARDs?

A

Usually 1-3 months, with hydroxychloroquine taking longer (2-6 months)

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31
Q

What is the methotrexate dosing regimen for rheumatoid arthritis?

A

Methotrexate 7.5 to 25mg PO weekly

Titrate to target dose (2.5 to 5mg/week increase to at least 15-25mg)

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32
Q

What is the renal dosing for methotrexate?

A

For eGFR between 10-50mL/min, reduce doses by 50%

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33
Q

Review slide 28 for dosing of traditional DMARDs

A
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34
Q

What are some commonly experienced side effects associated with Methotrexate?

A

Nausea
Fatigue
Stomatitis
Photosensitivity
Hair loss
Skin itch/burning/rash

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35
Q

What are some strategies to manage side effects associated with methotrexate use?

A

A PPI can be given 3 days around methotrexate doses to limit some GI effects

Folic acid can be given to help with methotrexate side effects (1 to 5mg/week)

Methotrexate doses can be split to help with side effects (reduced Gi and muscle fatigue)

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36
Q

What is a serious side effect associated with Hydroxychloroquine?

A

Ocular toxicity (usually after 1000g lifetime dose has been administered, usually achieved after 5 years of regular use)

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37
Q

What is a serious side effect associated with Methotrexate use?

A

Pulmonary toxicity (get lung function test to determine baseline)

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38
Q

What are the contraindications associated with hydroxychloroquine?

A

Pre-existing retinopathy

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39
Q

What are some contraindications for sulfasalazine use?

A

Hypersensitivity to salicylates or sulfonamides
Asthma attacks precipitated ASA or NSAIDs
Severe renal/hepatic impairment
Existing gastric or duodenal ulcer

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40
Q

What are some contraindications associated with Methotrexate?

A
  • Severe hepatic function
  • Severe hepatic impairment
  • Current hematologic abnormalities
  • Pregnancy/breastfeeding (Category X drug)
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41
Q

What are some contraindications associated with leflunomide?

A

Moderate-severe renal/hepatic impairment

Current hematological abnormalities or serious infection

Pregnancy/breastfeeding

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42
Q

What are some drug interactions associated with Methotrexate?

A

NSAIDs (decreased clearance of methotrexate, increased toxicity potential. Only a concern at high doses 500-2000mg weekly)

TMX (methotrexate significantly increases risk of pancytopenia)

PPIs (only in methotrexate dose is above 500mg/week

Loop diuretics (likely only an issue with high methotrexate doses)

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43
Q

How is the efficacy of traditional DMARDs monitored?

A
  • Disease (ESR, CRP) every 1 to 3 months initially
  • Radiographs of affected joint every 6-12 months
  • Patient assessment (Health Assessment Questionnaire, focus on functional status)
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44
Q

How is the safety of traditional DMARDs monitored?

A

Hydroxychloroquine (ophthalmic exam to measure ocular toxicity)

Sulfasalazine (CBC and LFTs, creatinine)

Methotrexate (CBCs and LFTs, creatinine & Chest X-rays)

Leflunomide (CBCs and LFTs, creatinine)

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45
Q

Rank traditional DMARDs by potency from highest to lowest

A

Methotrexate=Leflunomide>Sulfasalazine>Hydrochloroquine

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46
Q

What is the role of hydroxychloroquine in rheumatoid arthritis treatment?

A
  • Useful for early, mild RA
  • Best tolerated of the DMARDs
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47
Q

What is the role of sulfasalazine in rheumatoid arthritis treatment?

A
  • Use if other options not tolerated
  • Combined with other DMARDs (monotherapy rare)
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48
Q

What is the role of methotrexate in rheumatoid arthritis treatment?

A
  • Highly effective in moderate-severe disease
  • Standard therapy (should be used in all RA patients)
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49
Q

What is the role of leflunomide in rheumatoid arthritis treatment?

A
  • Replacement for methotrexate if not tolerated
  • May be added in low doses to methotrexate
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50
Q

What are the targets for biologic DMARDs?

A

Central to the RA inflammatory process, monocytes, macrophages, and fibroblasts within the synovium, which produce cytokines

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51
Q

What are the main classes of biologic DMARDs?

A
  1. TNF-alpha inhibitors
  2. IL-1 and IL-6 inhibitors
  3. T-Cell Co-stimulation inhibitors
  4. B-cell depletors
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52
Q

What are some common side effects associated with biologic DMARDs?

A

Nausea
Headache
Diarrhea
Malaise (most common after administration, usually 1 to 2 days after and resolves on its own)

53
Q

How are injection site reactions with biologic DMARDs prevented?

A

Pre-treatment with acetaminophen+antihistamine+steroid

54
Q

What are some common concerns for biologic DMARD use?

A
  1. Elevate infection risk
  2. Neutropenia
  3. Malignant disease
  4. Antibody development
55
Q

Why does infection risk increase with biologic DMARD therapy?

A

Increased infection rate (due to immunosuppression MOA of biologic DMARDs)

Common infections: sinusitis, pharyngitis, candidiasis, pneumonia, UTIs
Serious infections: TB, mycobacterial, PCP, CMV, zoster, HepB/C

56
Q

How is infection risk mitigated when using biologic DMARDs?

A
  • Screen for TB, Hep B/C, HIV prior to therapy
  • Up to date on vaccinations
  • Educate patient on signs of infection
  • Never use two biologics in combination (increased efficacy, but significant infection risk not worth benefit)
57
Q

What are the characteristics of neutropenia when starting a biologic DMARD?

A

20% will experience a decrease (important to get baseline prior to initiation of therapy)

Increases severity of infections

Not a reason to d/c therapy

58
Q

What does the elevated risk for malignant disease in patients on biologic DMARDs look like?

A

RA patients have higher cancer risk, confounding data

  • Avoid biologics in patients with malignancies
  • Preferentially avoid if patient has a history with skin cancer
  • Use rituximab in those with previous lymphoma
59
Q

What does antibody development look like in patients on biologic DMARDs?

A

Usually occurs within 2-6 months of starting therapy (can no longer use biologics from the same class)

Does not occur with IL-6 inhibitors

60
Q

What biologic DMARD is used if the patient has developed antibodies for multiple classes of biologic DMARDs?

A

IL-6 inhibitors because they do not cause the formation of antibodies against them

61
Q

What are some types of TNF-alpha inhibitors (know these)?

A
  • Adalimumab
  • Certolizumab
  • Etanercept
  • Golimumab
  • Infliximab
62
Q

What is the onset of effect for TNF-alpha inhibitors?

A

within weeks

63
Q

What are some special instructions for Infliximab/Golimumab?

A

They are only indicated in combination with methotrexate (reduces chances of biologic antibody formation)

64
Q

Review slide 52 for details about different types of TNF-alpha inhibitors

A
65
Q

Can TNF-alpha inhibitors be renally adjusted?

A

No, do not use TNF-alpha inhibitors in patients with renal dysfunction

66
Q

What is the most significant parameter that patients use to pick a preferred TNF-alpha inhibitor?

A

Usually route of administration (in general, subcutaneous formulations are preferred by patients)

67
Q

What TNF-alpha inhibitors can be used in pregnant patients?

A
  1. Adalimumab
  2. Infliximab
68
Q

What are some contraindications for the use of THF-alpha inhibitors?

A
  • Active severe infection
  • Moderate to severe HF (use a different type of biologic)
69
Q

What are some drug interactions associated with TNF-alpha inhibitors?

A
  • Live vaccines
  • Additive immunosuppresion
70
Q

What are some adverse effects associated with TNT-alpha inhibitors?

A

LFT elevations
HF
Cutaneous
Autoimmune disease
Seizure risk

71
Q

What are some characteristics of liver enzyme elevations in response to TNF-alpha inhibitor therapy?

A
  • Liver enzyme elevations uncommon
  • Concern if ALT are more than 5x beyond upper normal limit
  • Requires perioidic monitoring
72
Q

What are some characteristics of HF in response to TNF-alpha inhibitor therapy?

A

May cause or worsen existing HF (utilize low doses)

Evidence is not conclusive

73
Q

What are some characteristics of cutaneous symptoms in response to TNF-alpha inhibitor therapy?

A
  • Cellulitis
  • Autoimmune skin diseases
  • Skin malignancy
74
Q

What are some characteristics of auto-immune diseases in response to TNF-alpha inhibitors?

A

Increased risk of developing autoimmune disease with administration of TNF-alpha inhibitors

ex. Lupus, Vasculitis, Sarcoidosis, Psoriasis

75
Q

What are some characteristics of seizure risk associated with TNF-a inhibitors?

A

Avoid in patients with seizure disorder (will exacerbate their seizures)

76
Q

What are some common variables that are monitored in TNF-alpha inhibitor therapy?

A
  • TB, HIV, Hep B/C screening
  • CBCs
  • LFTs
  • Signs of infection
  • Ensure vaccinated
77
Q

What are some considerations that go into selecting a TNF-alpha inhibitor?

A
  • Frequency of dosing and route
  • Cost (consider those with a biosimilar)
  • Rheumatologist preference
  • If loss of effect experiened o ver time (check for antibodues, and consider switching or adding methadone
78
Q

What are the IL1 or IL6 and what is their mechanism of action?

A

IL-1 and Il-6 inhibitors (interleukin) antagonize these receptors and reduce in cytockine activation (less inflammation)

ex. Tocilizumab and Sarilumab (both IL-6 inhibitors)

79
Q

What is the onset of effect for IL1 or IL6 inhibitors?

A

Weeks, but reach peak effect at 5 to 6 months

80
Q

Do IL inhibitors have many contraindications?

A

No in general, but Tocilizumab is contraindicated in patients with active infections

81
Q

What is the efficacy of IL-1 inhibitor (Anakinra) in rheumatoid arthritis treatment?

A

Less effective than other biologics (used less often)

82
Q

What is the efficacy of IL-6 inhibitors (Tocilizumab/Sarilumab) in rheumatoid arthritis treatment?

A

40% acheive ACR50 (comparable to TNF-alpha inhibitors)

83
Q

How often is Ankinra (IL-1 inhibitor) dosed?

A

SC once daily

84
Q

How often is Tocilizumab/Sarilumab (IL-6 inhibitors) dosed?

A

Tocilizumab (IV every 4 weeks)

Sarilumab (SC every 2 weeks)

85
Q

What is an advantage of IL-6 inhibitors over most biologic DMARDs?

A

They are the only biologics that have good renal dysfunction dosing data (no need to adjust dose in patients with CrCl values abover 30mL/min)

86
Q

What are some adverse effects associated with IL-6 inhibitors?

A

GI perforation (rare)

Dyslipidemia (consider caution in patients that already are struggling to maintain good cholesterol management)

Antibody development not linked to decreased effect (unlike other biologics)

HTN

87
Q

What are are some drug interactions associated with interleukin inhibitors?

A

Increased CYP activity due to interleukin supression

Additive immunosuppression

Tocilizumab (simvastatin increased 4-10x, switch to a different statin)

88
Q

How are patients on IL-6 inhibitors monitored for safety?

A
  • Baseline CBC, LFTs, creatinine (then repeat in 4-8 weeks after starting, then every 3 to 6 months)
  • Lipid panel
  • BP
  • Latent/active TB, HepB/C screening
89
Q

What are some characteristics of T-cell Co-stimulation inhibitors in rheumatoid arthritis?

A

They inhibit T-cell activation (immunosupression)

Used if inadequate response to other DMARDs or TNF inhibitors

90
Q

What is the efficacy of T-cell co-stimulation inhibitors in treating rheumatoid arthritis?

A

41% acheived ACR50 (clinical response), on par compared to other DMARDs

91
Q

What are some adverse effects associated with T-cell co-stimulation inhibitor?

A

COPD exacerbations (contraindication, other options exist)

HTN and increased blood glucose (can be managed with monitoring or drug therapy)

92
Q

What is the impact of T-cell co-stimulation inhibitors on liver function?

A

None, unlike other DMARDs

Good for patients with hepatic dysfunction

93
Q

What are some monitoring parameters for T-cell co-stimulation inhibitors?

A
  • Signs and symptoms of infection
  • TB and hepatitis screening
  • CBCs, creatinine
  • Blood pressure
  • Blood glucose
94
Q

What are some characteristics associated with B-cell depletors in rheumatoid arthritis treatment?

A

They are a last-line option (used when other options have failed)

Directly prevent the formation of antibodies

ex. Rituximab

95
Q

Are B-cell depletors ever used as monotherapy for rheumatoid arthritis?

A

No, they are always in combination with methotrexate and following failure on a TNF inhibitor

96
Q

What are some dosing instructions associated with B-cell depletors?

A

2 dose course (1g IV infusion given two weeks apart)

Pretreat with steroid, acetaminophen, and diphenhydramine

Re-treat when needed (every 6 months)

97
Q

What are some adverse effects associated with B-cell depletors?

A

Infusion reactions tend to be more rapid (mild and brief)

Serious infection rate is non-existent initially, then increases on repeat courses

Mucocutaneous reactions (SJS, and TENS)

Antibody formation likely leads to increased infusion reactions and decreased efficacy

98
Q

What are some monitoring parameters for B-cell depletors?

A

Baseline CBC, LFTs, creatinine

TB, Hepatitis B/C screening

99
Q

Review slide 77 for a good summary of general concerns with all biologics

A
100
Q

What is an example of a T-cell inhibitor?

A

Abatacept

101
Q

Review slide 78 for what biologic to avoid when choosing an agent for rheumatoid arthritis in patients with comorbidities

A
102
Q

What is the place of biologics in therapy?

A

They are considered once traditional DMARDs have been tried and are not sufficient to see clinical response.

It is expected that most patients will start on methotrexate, but a biologic is added eventually

103
Q

What are Janus Kinase inhibitors?

A

They are a group of enzymes responsibles for enabling interleukin signalling

Indicated in combination with methotrexate

Last line options

ex. Tofacitinib, Baricitinib, Upadacitinib

104
Q

What are some adverse effects associated with Janus Kinase inhibitors?

A

Similar to TNF inhibitors and other biologics, including the following:
- HTN
- Infections/cytopenia
- LFTs/hepatoxicity
- Bradycardia
- GI perforation

No concern about antibody development

105
Q

What are some monitoring tips for Janus Kinase inhibitors?

A
  • Latent TB testing
  • Lipid profile
  • CBCs every 3-6 months
  • LFTs

Limited evidence for use in pregnancy/lactation

106
Q

What is the role of corticosteroids in rheumatoid arthritis?

A

It is used for flare management (most patients have been on multiple courses of steroid therapy)

Likely has DMARD properties and decreases early progression of RA

107
Q

What is the efficacy of corticosteroids in rheumatoid arthritis?

A

Subjective symptomatic improvement (more than the other drugs thet have used, increased risk of corticosteroid overuse)

Reduces joint tenderness more than placebo and NSAIDs

Reduces pain more than NSAIDs

108
Q

What is the most common treatment modality used in flare management?

A

Short-term use (doses of 10-15mg prednisone equivalent/day for 1 to 2 months per course)

109
Q

What is the purpose of chronic corticosteroid use in rheumatoid arthritis treatment?

A

Some severely affected patients may require long-term steroid dosing (benefits outweigh risk)

5-10mg prednisone equivalent per day indefinitely (osteoporosis and GI bleed risk)

110
Q

What is the purpose of pulse corticosteroid therapy in the treatment of rheumatoid arthritis?

A

Rare, more specialist territory

Safety issues (CV collapse, hypokalemia, MI, severe infection)

Considered a last resort option in RA

111
Q

What are some characteristics of intra-articular corticosteroid injections?

A

An option for patients who have oral corticosteroid overuse (needs to be administered by a MD

Effects are dramatic but temporary

Same joint should not be done more than once per 3 months

Considered palliative

112
Q

What are some issues with intra-articular corticosteroid injections for rheumatoid arthritis?

A

Tendon rupture

Acute synovitis

Localized skin hypopigmentation

Septic arthritis

113
Q

What are some guideline reccomendations associated with corticosteroid use in rheumatoid arthritis?

A

Consider for flares or as bridging (symptom relief as DMARD takes a few months to acheive full onset of action)

Aim for a max dose of 10mg prednisone/day

Never use as monotherapy (increase DMARD dose before corticosteroid dose)

FInd minimum dose/duration

114
Q

What are some reccomendations about NSAIDs in rheumatoid arthritis?

A

Provide a high NSAID dose at initial diagnosis

Use for at least 2 weeks for maximum benefit

Cautiously combined with other treatments

Considering providing GI protection

Should not be used chronically

115
Q

Should multiple biologics be used concurrently in rheumatoid arthritis treatment?

A

No, recommend against multiple biologics

116
Q

Should biologic or targeted sythetic DMARDs be tapered in patients who are in sustained remission or low disease activity (longer than 6 months)?

A

Stepwise reduction in the dose of DMARDs without d/c is recommended

For patients that do not have rapid access to care or gaining access to medication is challenging, tapering down is not recommended

117
Q

What should patients who are unsucessful in a TNF inhibitor trial for rheumatoid arthritis?

A

Try a different TNF inihibitor

Non-TNF biologic

JAK inhibitor (not reccomeded if patient has higher risk of CV morbidity)

118
Q

What is the intital therapy approach for low disease activity rheumatoid arthritis?

A

Try lowest potency traditional DMARDs first (monotherapy preferred)
(HCQ>SSZ>MTX>LEF)

119
Q

What are some initial first-line therapy approach for patients with moderate to high disease activity?

A

Methotrexate stronhly recommended over other traditional DMARDs

Methotrexate monotherapy recommended over multi-traditonal DMARD therapy

Methotrexate monotherapy recommended over combo with biologics

120
Q

What is the next step after methotrexate monotherapy fails to acheive goal of therapy?

A

Preferentially add a biologic DMARD instead of SSZ/HCQ

121
Q

What is the next step for when a biologic in rheumatoid arthritis therapy fails?

A

Switch to a biologic of a different class, rather than the same class

122
Q

When should rheumatoid arthritis therapy be escalated?

A

Failure to achieve remission or acceptable disease activity after 3 to 6 months at optimal doses

123
Q

What are some precautions for patients on methotrexate thinking about conceiving?

A

Males and females should stop methotrexate for at least 3 months prior to conception

124
Q

What DMARDs can be used safely during pregnancy?

A

All biologic agents, except b-cell depletors (rituximab) have favourable safety profiles

125
Q

What are some safe rheumatoid arthritis therapies for lactating mother?

A

NSAID use (ibuprofen) is acceptable

Low dose prednisone (less than 20mg/day)

HCQ and SSZ are safe (only traditional DMARDs that are safe, avoid methotrexate and leflunomide)

TNF inhibitors and IL-6 inhibitors are safe

126
Q

What are some characteristics of juvenile rheumatoid arthritis?

A

Defined as persistent arthritis in more than one joint for at least 6 weeks

Most common rheumatic condition in kids

Review slide 111

127
Q

What are the goals of treatment for juvenile rheumatoid arthritis?

A

Decrease chronic joint pain

Suppress inflammatory process

Maintain normal growth and development

128
Q

What are some treatment options for juvenile rheumatoid arthritis?

A

Physical Therapy

Ophthalmologic surveillance

NSAIDs

Corticosteroids

DMARDs/biologics (Tocilizumab preferred)

129
Q

Review slides 116 to 118 for a summary of rheumatoid arthritis agents

A

PHAR 255 (15 decks)

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