Rheumatoid Arthritis
Presented by: Layan S. Barqawi
Supervisor: Dr. Dirar Dibs
Definition
Rheumatoid arthritis (RA) is an autoimmune
disease of unknown origin that is characterized
by symmetric inflammation of joints, especially
of the hands, feet, and knees. Severity of the
disease varies widely from patient to patient and
from time to time within the same patient.
Incidence and Prevalence
• Prevalence is somewhat difficult to determine
because of lack of well-defined markers of the
disease; however, estimates range from 1% to
2% of the population. Disease onset usually
occurs between ages 35 and 50 years.
• RA is more prevalent in women than in men
by a 3 : 1 ratio.
Etiology
• The cause of RA is unknown; however, evidence seems
to implicate an interrelationship of infectious agents,
genetics, and autoimmunity. One theory suggests that a
viral agent alters the immune system in a genetically
predisposed person, leading to destruction of synovial
tissues.
• Although the disease can occur within families,
suggesting a genetic component, one specific causative
gene has not been identified. Nevertheless, many
people who develop RA have a genetic predisposition
that occurs in the form of a tissue marker called HLA-
DR4; however, not everyone with this tissue type
develops the disease.
PATHOPHYSIOLOGY
• With RA, the fundamental abnormality involves micro- vascular endothelial cell
activation and injury.2-5 Primary changes occur within the synovium, which is the
inner lining of the joint capsule (Figure 20-1). Edema of the synovium occurs,
followed by thickening and folding. This excessive tissue, composed of proliferative
and inva- sive granulation tissue, is referred to as pannus. In addi- tion, marked
infiltration of lymphocytes and plasma cells into the capsule occurs. Eventually,
granulation tissue covers the articular surfaces and destroys the cartilage and
subchondral bone through enzymatic activity (Figure 20-2). This process also
extends to the capsule and liga- ments, causing distention and rupture. New bone
or fibrous tissue then is deposited, resulting in fusion or loss of mobility.2-5
• A likely sequence of events begins with a synovitis that stimulates immunoglobulin
G (IgG) antibodies. These antibodies form antigenic aggregates in the joint space,
leading to the production of rheumatoid factor (autoantibodies). Rheumatoid
factor then complexes with IgG complement, a process that produces an inflam-
matory reaction that injures the joint space.2-5
CLINICAL PRESENTATION
Signs and Symptoms
• The usual onset of RA is gradual and subtle (Table 20-2), and the disorder is commonly preceded by
a prodromal phase of general fatigue and weakness with joint and muscle aches. Characteristically,
these symptoms come and go over varying periods. Then, painful joint swell- ing, especially of the
hands and feet, occurs in several joints and progresses to other joints in a symmetric fashion (Figure
20-3). Joint involvement persists and radually progresses to immobility, contractures, sublux- ation,
deviation, and other deformities. Characteristic features include pain in the affected joints
aggravated by movement, generalized joint stiffness after inactivity, and morning stiffness that lasts
longer than 1 hour. The joints most commonly affected are fingers, wrists, feet, ankles, knees, and
elbows. Multiple joint changes noted in the hands include a symmetric spindle-shaped swelling of
the proximal interphalangeal (PIP) joints, with dorsal swell- ing and characteristic volar subluxation
of the metacar- pophalangeal (MCP) joint (see Figure 20-3). The TMJ is reported to be involved in
up to 75% of patients.2-6 Because of the variable rate of progression and pain intensity, the median
period between onset of symptoms of RA and its diagnosis is 36 weeks.1,7
• Extraarticular manifestations include rheumatoid nodules, vasculitis, skin ulcers, Sjögren syndrome,
inter- stitial lung disease, pericarditis, cervical spine instability,
• entrapment neuropathies, and ischemic neuropathies.8 The American Rheumatism Association has
developed revised criteria for the diagnosis and classification of RA to be used in clinical trials and
epidemiologic studies (Box 20-1). These criteria have high specificity (89%) and sensitivity (91% to
94%) compared with control subjects when used to classify patients with RA. For the diagnosis of
RA to be made, four of seven criteria must be met.2-5
Laboratory Findings
• No laboratory tests are pathognomonic or diagnostic of RA,
although they are used in conjunction with clinical findings to
confirm the diagnosis. Laboratory findings most commonly seen in
RA include an increased erythrocyte sedimentation rate (ESR), the
presence of C-reactive protein (CRP), a positive result on rheuma-
toid factor assay in 85% of affected patients, and a hypochromic
microcytic anemia. In patients with Felty syndrome (RA with
splenomegaly), a marked neutropenia may be present.
• Antibodies to cyclic citrullinated proteins (CCPs) are
autoantibodies, which are important in the diagnosis of RA.9 Anti-
CCP antibodies are highly associated with RA. They occur in 70%
to 80% of patients with RA as well as in some other forms of
inflammatory arthritis. These antibodies may appear before any
signs or symp- toms of RA and therefore may prove beneficial as
early screening markers for earlier diagnosis and intervention of
RA.9
Diagnosis
• Morning stiffness
• Arthritis of three or more joint areas
• Arthritis of hand joints
• Symmetric arthritis
• Rheumatoid nodules
• Serum rheumatoid factor
• Radiographic changes
MEDICAL MANAGEMENT
• The treatment approach to RA is, by necessity, palliative
because no cure as yet exists for the disease. The ultimate
aim of management is to achieve disease remission for
the patient. Remission is elusive, however, so more
practical treatment goals are to reduce joint inflammation
and swelling, relieve pain and stiffness, and facilitate and
encourage normal function. These goals are accomplished
through a basic treatment program that consists of patient
education, rest, exercise, physical therapy, and aspirin or
other nonsteroidal antiinflammatory drugs (NSAIDs).
• Drugs for the management of RA have been tradition-
ally, but imperfectly, divided into two groups: those
used primarily for the control of joint pain and
swelling, and those intended to limit joint damage and
improve long- term outcome NSAIDs, especially aspirin,
constitute the cornerstone of treatment. Aspirin may
be prescribed in large doses on an individual basis. A
common approach is to start a patient on three 5-grain
tablets four times a day, then to adjust the dosage on
the basis of patient response. The most common sign
of aspirin toxicity is tinnitus. Should this occur, dosage
is decreased.
