Rheumatoid
arthritis (RA) is a chronic inflammatory disease of unknown etiology characterized
by symmetric polyarthritis.
Clinical
Features:
Presenting
symptoms: Early morning joint stiffness
lasting more than 1 hour that eases with physical activity.
Most
frequently involved joints: the wrists, MCP, and PIP joints (DIP is usually spared). Axial
involvement is rare, if occurs most common site is cervical vertebrae.
Flexor
tendon tenosynovitis – leading to decreased range of motion and reduced grip
strength: “Trigger” fingers.
Hyperextension
of the PIP joint with flexion of the DIP joint: “swan-neck deformity”.
Flexion of
the PIP joint with hyperextension of the DIP joint: “boutonnière deformity”
Subluxation
of the first MCP joint with hyperextension of the first interphalangeal (IP) joint:
“Z-line deformity”.
Inflammation
about the ulnar styloid and tenosynovitis of the extensor carpi ulnaris may
cause subluxation of the distal ulna, resulting in a “piano-key movement” of the ulnar styloid.
Other important
points:
Most common
pulmonary manifestation of RA: Pleuritis.
Most
frequent site of cardiac involvement in RA: Pericardium.
Most common
valvular abnormality in RA: Mitral Regurgitation.
Most common
hematologic abnormality in RA: Normochromic Normocytic anemia.
Most common
histopathologic type of Lymphoma in RA: Diffuse Large B cell Lymphoma.
Most common
cause of death: Cardiovascular disease.
Caplan’s
syndrome: RA + Pneumoconiosis that manifests as Pulmonary Nodules
Felty’s
syndrome: Neutropenia + Splenomegaly + nodular RA.
Diagnosis:
Classification
criteria for RA:
RA is
diagnosed if score is ≥ 6.
Serum IgM RF
– Positive in 75-80 % of the patient.
Serum
anti-CCP antibodies – More specificity (95%).
Plain
Radiograph: Reveals Osteopenia, symmetric joint space loss and subchondral
erosions.
MRI: Reveals
presence of Bone Marrow oedema.
Treatment:
Treatment
may be divided into:
1. NSAIDs
2. Glucocorticoids
3. Conventional DMARDs
4. Biologic DMARDs
1. NSAIDS:
NSAIDs are now considered to be adjunctive agents for management of symptoms
uncontrolled by other measures. NSAIDs exhibit both analgesic and
anti-inflammatory properties.
2. Glucocorticoids:
Can be given in several ways:
First, low to moderate doses to achieve rapid disease control before the onset
of fully effective DMARD therapy.
Second, a 1 to 2 week burst of glucocorticoids for the management of acute
disease flares, with dose and duration guided by the severity of the
exacerbation.
3. Conventional DMARDs:
Conventional DMARDs includes: Methotrexate, Hydroxychloroquine, sulfasalazine
and leflunomide.
Methotrexate is DMARD of
choice for treatment of RA. It stimulates adenosine release from
cells, producing an anti-inflammatory effect.
4. Biologic DMARDs:
IL-1 receptor antagonist: Anakinra
Anti TNF agents: Infliximab, Golimumab, Certolizumab, etanercept.
Anti CD-20: Rituximab.
Anti IL-6: Tocilizumab
Abatacept: Inhibits T cell stimulation
Tofacitinib: Inhibits JAK1 and JAK3. It is an oral agent.
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