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| Rheumatoid Arthritis Concept Map - Click to enlarge image |
Rheumatoid Arthritis Concept Map: An Overview
You can access this map for free. But if you want it as a printable version or a folded poster, please order here.Definition
Rheumatoid Arthritis is a chronic inflammatory
autoimmune disease that involves the joints and may cause systemic
manifestations.
Etiology
It is an autoimmune disease with unknown cause and contributing factors
(genetic & environmental factors). Environmental factors like: viral
infections and cigarette smoking; trigger and maintain joint inflammation.
Epidemiology
- Prevalence; 1% worldwide
- Gender; Women : Men = 3:1 (after 50 years
old, gender difference is less marked)
- Age; peaks at 35-45 years old, although it
can occur at any age - when it occurs in childhood, it is called "Juvenile
Idiopathic Arthritis"
- Limitations of activities:
*
33% have major activities limited
*
29% cannot perform major activities
Pathophysiology
Rheumatoid arthritis pathophysiology is shown
in the map in the form of a cascade process that starts by an "Autoimmune
Reaction" and ends by "Joint Destruction."
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| Etiology and Pathophysiology of Rheumatoid Arthritis |
Clinical Presentation
Nonspecific signs & symptoms (for weeks/months): fever,malaise,arthralgias, and weakness
Specific signs and symptoms that take weeks to months to appear
Joint symptoms are characteristically
symmetric, include:
- Stiffness lasts > 60 minutes after rising
in the morning but may occur after any prolonged inactivity (called gelling).
- Erythema, warmth, swelling, and limitation of
motion.
Joints involved in rheumatoid arthritis,
include
The most common joints involved are;
-
Wrists, feet (MTP), and the index (2nd) and middle (3rd) metacarpophalangeal (MCP) joints
Other joints include;
-
Proximal interphalangeal (PIP) joints, shoulders, elbows, hips, knees, and ankles.
Any joint, except the distal interphalangeal
(DIP) joints
Irreversible Joint Deformities may occur due to disease progression
- Ulnar deviation of the fingers
- Boutonniere Deformity (hyperextension of the DIP & flexion of the PIP joint)
- Swan Neck Deformity (hyperextension of the PIP & flexion of the DIP joint)
- Hammer toe deformity
Progression
Disease progresses most rapidly during the
first 6 years, particularly the first year; 80% of patients develop some
permanent joint abnormalities within 10 years.
Extra-articular Manifestations
Most of rheumatoid arthritis extra-articular manifestations are collected in this image:
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| Rheumatoid arthritis extra-articular manifestations |
Diagnosis
(x-ray) - ACR Rheumatoid Arthritis Diagnostic Criteria (2010). In addition, a comparison between rheumatoid arthritis and osteoarthritis is included.
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| Rheumatoid Arthritis vs Osteoarthritis |
Treatment
Treatment goals for rheumatoid arthritis are
linked to medications used in managing the diseases.
Medications to Reduce Pain and Inflammation
1) Non-Steroidal Anti-inflammatory Drugs (NSAIDs)
e.g., ibuprofen, naproxen, ketoprofen,
piroxicam, and diclofenac
- adjunctive therapy
- treat symptoms and decrease inflammation but do not affect disease progression.
- dose can be decreased or discontinued with
successful Disease-modifying antirheumatic drugs (DMARDs) therapy.
- adverse effects: GI toxicity, headache,
confusion and other CNS symptoms, increased BP, worsening of hypertension,
edema, and decreased platelet function. NSAIDs increase cardiovascular risk.
Non-steroidal anti-inflammatory drug drugs mechanism of action is shown in this diagram:
Non-steroidal anti-inflammatory drug drugs mechanism of action is shown in this diagram:
 |
| Non-steroidal Anti-inflammatory Drugs - Mechanism of Action |
2) COX-2 inhibitor (only celecoxib)
See the map.3) Low-dose systemic corticosteroids (CS)
- adjunctive therapy
- decrease inflammation and other symptoms rapidly and efficiently
- slow bone erosion
- In early RA, low-dose oral prednisone (<10 mg/day) in combination with DMARDs for up to 6 months, as symptomatic effects ↓ with time
- In established RA, CS may be used as 'bridging' therapy when DMARDs are initiated, and should be withdrawn once DMARDs have controlled the disease
- May be used for severe joint or systemic manifestations of RA (eg, vasculitis, pleurisy, pericarditis)
- Relative contraindications include PUD, HTN, untreated infections, DM, and glaucoma
- The risk of latent TB should be considered before CS therapy is begun
4) Intraarticular depot corticosteroids
- Temporarily control severe monarticular or
even oligoarticular symptoms
- Triamcinolone hexacetonide may suppress
inflammation for the longest time
- Triamcinolone acetonide and
methylprednisolone acetate are also effective
- No single joint should be injected with a
corticosteroid more than 3 to 4 times a year, as too-frequent injections may
accelerate joint destruction
- Because injectable corticosteroid esters are
crystalline, local inflammation transiently increases within a few hours in
< 2% of patients receiving injections
- Although infection occurs in only <
1:40,000 patients, it must be considered if pain occurs > 24 h after
injection
Medications to Prevent Disease Progression & loss of joint function
1) Disease-modifying antirheumatic drugs (DMARDs)
Also called "nonbiologic DMARDs,"
include: methotrexate (MTX), hydroxychloroquine (HCQ), azathioprine (AZA),
sulfasalazine (SSZ), and leflunomide.
Other available but rarely used DMARDs include
minocycline, azathioprine, cyclosporine, and tacrolimus.
- Early treatment of RA (< 6 months after the onset of symptoms) with DMARDs retard disease progression more efficiently and induce more remissions.
- Until the full action of DMARDs takes effect, anti-inflammatory or analgesic medications may be required as bridging therapy to reduce pain and swelling.
- They differ from each other chemically and pharmacologically.
- Patients should be informed about the risks of DMARDs and monitored closely for evidence of toxicity.
- Combinations of DMARDs may be more effective than single drugs. Also, combining a DMARD with another drug, such as methotrexate plus a TNF-α antagonist or an IL-1 receptor antagonist or a rapidly tapered corticosteroid, may be more effective than using DMARDs alone.
A comparison between DMARDs is available in the map. The comparison is showing: mechanisms of actions, indications, doses, adverse effects, monitoring parameters, and contraindications.
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| Disease Modifying Anti-Rheumatic Drugs (DMARDs) - Table Comparison |
2) Biologic Agents
- Also called "biologic DMARDs"
- They are not given in combination with each other due to increased frequency of infections.
- Approved by the FDA to treat moderate to severe RA not responded to an one or more of the traditional DMARDs
- They may be used alone, but are often in combination with other DMARDs, to increase the efficacy and decrease AE
- Start biologic agents while patients remain on NSAID and/or corticosteroid
A comparison between biologic agents is available in the
map. The comparison is showing: mechanisms of actions, indications, doses,
onset of action, adverse effects, contraindications, and warnings/cautions.
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| Biologic DMARDs - Table Comparison |
3) Other immunomodulatory, cytotoxic, and immunosuppressive drugs
e.g.,
Azathioprine, and cyclosporin A. Rarely
cyclophosphamide and d-Penicillamine
- Efficacy is similar to DMARDs but more toxic.
- Used in case of treatment failure with DMARDs or to ↓ the need for CSs.
- Used infrequently unless there are extra-articular complications.
And here is a comparison between them:
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| Other immunomodulatory, cytotoxic, and immunosuppressive drugs - Table Comparison |
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Version: 2.0
Last updated in: 10 June 2014
Last updated in: 10 June 2014
References
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Osteoarthritis Concept Map
1-
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