Gout, 274.9
Osteoarthritis, 715.9
Rheumatoid arthritis, 714.0
I. Definition
A. Osteoarthritis (OA) is a progressive joint disorder that is characterized by slow destruction of the normal collagen architecture, which is followed by attempts of chondrocytes to produce replacement articular cartilage of joint surfaces.
B. OA is now classified as inflammatory because inflammatory changes occur as the result of synovial response to reactive new bone formation.
C. OA is classified as primary or secondary.
II. Etiology/incidence/predisposing factors
A. Thought to be “wear and tear” syndrome; 16 million affected in the U.S.
B. Increased age: People older than age 60 have a 60% chance of developing OA.
C. Sex: Both sexes are affected equally between the ages of 45 and 55.
1. After age 55, women are more likely to be affected.
2. Black women have twice the incidence of white women.
3. Men more often have OA in the hips; women have OA more often in the hands and fingers.
D. Genetics
1. Evidence suggests that OA may be genetically inherited as an autosomal recessive trait.
2. Genetic/congenital conditions such as congenital hip dysplasia; increased incidence of Heberden’s nodules in OA in distal interphalangeal (DIP) joint caused by a single gene that has not yet been identified
E. Metabolic abnormalities such as Paget’s disease
F. Height and weight alterations such as abnormal height or increased weight-to-height ratio (i.e., obesity)
H. Prior trauma, especially sprains, dislocations, and fractures that extend into the joint
I. Chemicals such as organic or heavy metals that stimulate cartilage-injuring enzyme activity
J. Neurologic disorders such as diabetic neuropathy, Charcot’s, and neuropathic joints
K. Hematologic/endocrine disorders such as hemochromatosis and acromegaly
III. Subjective findings
A. Pain in one or more joints, usually in weight-bearing joints such as hips and knees, but also in central and peripheral joints such as fingers, hands, and wrists
B. Stiffness of affected joints after prolonged sitting that quickly dissipates upon arising
C. “Grating” sensation during any range of motion (ROM); usually worsens as day progresses
D. Feeling of instability, locking, or buckling of the knees, especially when climbing or descending stairs
IV. Physical findings
A. Bony induration or enlargement of affected joints; some effusions with warmth and redness
B. Heberden’s nodules—enlargements on DIP joints
C. Bouchard’s nodules—enlargements on proximal interphalangeal (PIP) joints
D. Angular deformities of affected joints (valgus and varus), especially the knees
E. Limited ROM with palpable/audible crepitus
F. Pain on palpation of the joint line
V. Laboratory/diagnostic findings
A. Plain x-rays show narrowing of joint space with cyst formations.
B. Anteroposterior and lateral knee films should be taken bilaterally and standing to detect and measure degrees of varus and valgus deformity if they exist.
C. Synovial fluid analysis reveals clear, yellow fluid with normal WBC count (less than 1000/mm3) and glucose levels that approximate patient’s serum glucose.
D. No laboratory test is specific for OA; complete blood count and biochemical panel should be drawn to detect any hematologic or renal impairment when treatment with NSAIDs is considered.
E. Bone scan, MRI, and CT should be considered if there is a question about infection, malignancy, or spur formations, or if compression of soft tissue structures is suspected.
VI. Management
A. Goals
1. Relieve symptoms.
2. Maintain or improve function.
4. Avoid drug toxicity.
B. Multidisciplinary team approach is best.
C. Weight reduction, if applicable
D. Rest and joint protection: may require occupational therapy consultation
E. Heat and cold therapy; physical therapy evaluation
F. Aspirin (ASA) 650 mg PO 4 times a day as initial therapy
G. Acetaminophen 650 mg PO 3 times a day if ASA allergic
H. Intra-articular joint injection: Hyaluronic acid, a disaccharide that is the major component of the proteoglycan aggregates needed for functioning of cartilage, is injected weekly for 3 weeks into the affected joint and can provide pain relief with increased ROM, although recent meta-analytic studies have found the benefits to be minimal.
1. Sodium hyaluronate (Hyalgan)
2. Hylan G-F (Synvisc)
I. NSAIDs
1. Act by inhibiting the enzyme cyclooxygenase (COX), which is required for the synthesis of prostaglandins and thromboxanes
a. Two isoforms have been identified: COX-1 and COX-2.
b. COX-1 is believed to be tissue-wide and is thought to protect the gastric mucosa.
c. COX-2 is induced mainly at the inflammation site.
2. Older NSAIDs act by blocking both COX isoforms, leading to possible gastric ulceration. COX-2 drugs are selective, thus providing greater gastric protection.
a. Celecoxib (Celebrex), 100-200 mg PO daily
i. Members of the FDA panel that has been reviewing COX-2 drugs unanimously agree that these drugs do cause heart problems in many patients. However, panel members also found that these drugs provide some benefit; therefore, they advised that there is no need to recall Celebrex at this time. Some drugs such as rofecoxib and valdecoxib have been removed from the U.S. market. The panel has recommended that Celebrex should carry the strictest form of warning, highlighted in a black box, on the label.
b. Concurrent use of zafirlukast, fluconazole, and fluvastatin may increase serum concentration of celecoxib.
J. Glucosamine: over-the-counter preparation sold as a nutritional supplement in the U.S. Recent studies showed no effect of glycosylated hemoglobin (HgA1c) in type 2 diabetes.
K. Surgical options: Refer to orthopedist for definitive surgical treatment.
1. Total joint replacement
2. Arthrotomy/arthroscopy for joint debridement
3. Osteotomy
4. Autogenous cartilage implantation and osteochondral grafting
I. Definition
A. Rheumatoid arthritis (RA) is a chronic, systemic autoimmune disease of unknown origin that causes inflammation of connective tissue.
B. Synovium of joints is primarily affected first; then, the disorder spreads to articular cartilage, tendons, ligaments, and other soft tissues, including renal, cardiovascular, hematopoietic, and pulmonary structures. Systemic involvement may occur because of the disease or as a result of treatment.
II. Etiology/incidence/predisposing factors
A. Approximately 6 million people in the U.S. are affected; 75% are women, and the female-to-male ratio is 3:1. Two thirds of those affected have moderate to severe disease.
B. Cause is unknown; probably multifactorial, with genetic, environmental, hormonal, and reproductive components
C. Exposure to Epstein-Barr virus, bacteria, and mycoplasma
D. Autoimmune response in genetically predisposed individuals with defects in HLA-DR4, HLA-DQ, and HLA-DP areas of histocompatibility complex
E. Decreased reproductive hormones after birth exacerbate disease.
F. The proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) is thought to play a dominant role in the pathogenesis of RA.
G. The annual cost of treating patients with rheumatoid arthritis and other rheumatologic diseases is approximately $250 million.
III. Subjective findings
A. Symmetric joint and muscle pain that is usually worse in the morning and improves as the day progresses
B. Weakness, fatigue
C. Anorexia
D. Weight loss
E. Generalized malaise
IV. Physical examination findings
A. Articular
1. Swelling of joints with typical “boggy” feel on palpation. Most frequently seen in metacarpophalangeal (MCP) joints, wrists, and PIP joints
2. Warmth and redness of skin over affected joints
3. Multiple, symmetric joint involvement
4. Deformity of joints, especially PIP, DIP, and MCP of hands
5. Multiple nodules on volar aspect of forearms
6. Osteopenia of fingers occurs early in disease process.
B. Extra-articular
1. Pleural effusions
2. Scleritis and episcleritis: inflammation of the sclerae and surrounding ophthalmologic structures
3. Arteritis
4. Pericarditis, conduction defects, myocarditis
6. Pulmonary nodules and fibrosis may be caused by disease or drugs used to treat disease.
V. Laboratory/diagnostic studies
A. Granulocytopenia (Felty’s syndrome): neutrophil count less than 500/microliter
B. Anemia (hypochromic, microcytic)
1. Low hemoglobin count (normal, 14 to 18 g/dl in males and 12 to 16 g/dl in females)
2. Low serum ferritin and low or normal total iron-binding capacity
C. May have positive rheumatoid factor, although nonspecific
D. Antinuclear antibody may be elevated.
E. Erythrocyte sedimentation rate is usually elevated.
F. Radiographs reveal joint swelling, then progressive cortical thinning, osteopenia, and joint space narrowing.
G. Radiographs of cervical spine are needed to detect cervical spine instability due to atlantoaxial (C1-C2) subluxation.
H. Synovial fluid: yellow, turbid fluid with friable mucin clot; elevated WBC up to 100,000/mm3; normal glucose
I. RA is a clinical diagnosis, not a laboratory or radiologic diagnosis.
J. See Table 54-1 for diagnostic studies commonly used in rheumatic diseases.
| Test and Purpose | Normal Value | Significance |
|---|---|---|
| Antinuclear Antibody (ANA) | ||
ANAs are gamma globulins that react to specific antigens ANA titer indicates the presence of antibodies that are produced in response to the nuclear part of the white blood cell If antibodies are present, further tests determine the type of ANA circulating in the blood | Titer <1:32 | A small number of healthy adults have a positive ANA test ANA levels may increase with age, even in those without immune disease Positive titers (1:10-1: 30) are associated with SLE, SS, dermatomyositis, and Sjögren’s syndrome The higher the titer, the greater the degree of inflammation A negative test for ANA is strong evidence against the diagnosis of SLE |
| C4 Complement | ||
Method to determine serum hemolytic complement activity Complement is a protein that binds antigen-antibody complexes for purposes of lysis Activation of the entire complement system leads to an inflammatory response that destroys/damages cells When the number of antigen-antibody complexes increases markedly, complement is used for lysis, thus decreasing its availability | Men: 12-72 mg/dL Women: 13-75 mg/dL | Increased in active inflammatory disease and in autoimmune disorders (rheumatoid spondylitis, JRA) May be decreased in RA and SLE |
| C-Reactive Protein (CRP) | ||
| Indicates presence of abnormal plasma protein (glycoprotein) that appears as a nonspecific response to a variety of inflammatory stimuli | Trace to 6 mg/mL | CRP is a nonspecific antigen-antibody reaction test to help determine the extent/severity of a disease process Elevated measurements indicate active inflammation, both infectious and noninfectious Elevated in RA, bacterial and viral infections, disseminated lupus erythematosus In RA, the test becomes negative with successful therapy, indicating that the inflammatory reaction has disappeared, although the ESR may continue to be elevated |
| Erythrocyte Sedimentation Rate (ESR) | ||
| Measures the rate at which red blood cells settle out of unclotted blood in 1 hr | Wintrobe Men: 0-7 mm/hr Women: 0-25 mm/hr Men: 0-20 mm/hr Women: 0-30 mm/hr | Increased rate seen in inflammation and necrotic processes Increase often seen in any inflammatory connective tissue disease An increase often indicates increased inflammation, resulting in clustering of red blood cells, which makes them heavier than normal; the higher the sedimentation rate, the greater the inflammatory activity Particularly useful as a guide to the management of the patient with RA Decreased in salicylate toxicity Falsely elevated with excessive, exercise anxiety, pain, or dehydration |
| HLA-B27 Antigen | ||
Measures the presence of HLA-B27, which is used for tissue typing/tissue recognition Five series have been designated for HLA: A, B, C, D, DR, each with 10-20 distinct antigens Measures the values of immunoglobulins, serum antibodies produced by the plasma cells of the B lymphocytes Five classes:
IgA—protects mucous membranes from viruses and bacteria IgM—first responder to appear after antigens enter body; produces antibody against rheumatoid factor
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