Rheumatoid arthritis


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Rheumatoid arthritis

  1. 1. Definition: -an autoimmune disease in which the joint lining and occasionally other tissues become inflamed as a result of overactivity of the body’s immune system. RA is a chronic, systemic, inflammatory disorder that primarily involves the joints.
  2. 2. Epidemiology:  10 cases per 1000 people, or ~ 2.1 million adults in the United States  Affects women two top four times more often than men at all ages  There is general increase in prevalence for both sexes with increasing age  There is lower prevalence of RA in native Japanese and Chinese compared to whites
  3. 3. Etiology:  like many other chronic diseases, the etiology of RA is unknown  Current research is based on a complex, but as yet incomplete, appreciation of the functions of the immune system  Based on the fact that individuals with RA produce antibodies to their own immunoglobulins, there is some reason to believe that RA is an autoimmune disorder. It is not clear, however, whether this antibody production is a primary event or results as a response to a specific antigen from an external stimulus  A specific etiological agent for RA has not been identified
  4. 4. Etiology:  Rheumatoid factors (RF) have received considerable attention in the search for a causative agent in RA because they are found in the sera of approximately 70% of all patients with RA  Recent studies have also sought to establish a genetic predisposition to the development of RA. Human leukocyte antigens (HLAs)are found on the cell surface of most human cells and are capable of generating an immune response when genetically incompatible tissues are grafted to each other for example, during organ transplants.
  5. 5. Pathophysiology:  Long-standing RA is characterized by the grossly edematous appearance of the synovium with slender villous or hair-like projections into the joint cavity  There are distinctive vascular changes, including venous distention, capillary obstruction, neutrophilic infiltration of the arterial walls, and areas of thrombosis and hemorrhage
  6. 6.  Pannus – synovial proliferation of vascular granulation tissue, dissolves collagen as it extends over the joint cartilage. Granulation tissue will eventually result in adhesions, fibrosis or bony ankylosis of the joint
  7. 7. Pathophysiology:  Chronic inflammation can also weaken the joint capsule and its supporting ligamentous structures, altering structure and function  Tendon rupture and fraying tendon sheaths may produce imbalance muscle pull resulting in deformities seen in advanced RA
  8. 8. Pathophysiology:  Key features of a synovial joint that differentiates it from other types of joints are the features that make it susceptible to persistent inflammation  High molecular weight substances such as macroglobulins and fibrinogens can pass through the synovial capillaries during periods of inflammation and are not easily cleared. Because the cartilage is avascular, antigen-antibody complexes may be sequestered within the joint cavity and may facilitate a process of phagocytosis and further development of pannus.
  9. 9. Pathophysiology:  In established synovitis, polymorphonuclear (PMN) leukocytes are chemotactically drawn into the joint cavity and contribute to the inflammatory destruction of the synovium. It is known that the lysosomal enzymes, which are released from these leukocytes, can directly injure synovial tissues
  10. 10. Clinical Manifestations: The 1987 Revised Criteria for the Classification of Rheumatoid Arthritis 1. Morning stiffness -Lasts at least an hour before maximal improvement 2. Arthritis of three or more joint areas -at least three joint areas simultaneously have had soft tissue swelling or fluid (not bony overgrowth alone) 3. Arthritis of hand joints -at least one area is swollen (wrist, MCP, or PIP joints) 4. Symmetric arthritis -simultaneous involvement of the same joint areas on both sides of the body
  11. 11. 5. Rheumatoid nodules -subcutaneous nodules over bony prominences or extensor surfaces 6. Serum rheumatoid factor -abnormal amount 7. Radiographic changes -include erosions or unequivocal bony decalcification localized in or most marked adjacent to the involved joint The joint signs and symptoms described in criteria 1-4 must have lasted for at least 6 weeks.
  12. 12. Signs and symptoms:  Systemic manifestations -morning stiffness, anorexia, weight loss, fatigue  Joint involvement -marked bilateral and symmetrical patterns -arthralgia, crepitus  Cervical spine -50% takes place at the atlanto-axial joint -ankylosing spondylitis  Temporomandibular joints -results in an inability to open the mouth fully with normal side-to-side gliding -normal approximation of the upper and lower teeth may also be altered
  13. 13.  Shoulder -involvement of GH, SC, and AC joints; scapulothoracic articulation -degeneration, pain, LOM -capsule and ligaments become distended with chronic inflammation  Elbows -capsular and ligamentous distention, and joint surface erosion may lead to elbow instability -Flexion contractures may result from persistent spasm secondary to pain
  14. 14.  Wrists -development of flexion contractures which ultimately diminishes the ability to execute power grasp -volar subluxation resulting from chronic inflammation of the proximal carpals -Stenosing tenosynovitis (deQuervain’s disease) may also occur
  15. 15.  Hand joints MCP joint: -soft-tissue swelling; volar subluxation; ulnar drift PIP joint: -swelling(sausage-like finger) -Swan-neck deformity -Boutonniere deformity -Bouchard’s nodes DIP joint: -Heberden’s nodes -mallet finger
  16. 16.  Thumb: -Type I deformity – MCP flex; IP hypext; without CMC involvement - Type II deformity – CMC is subluxed; IP hypext - Type III deformity – CMC subluxed; MCP hypext; more commonly found in RA  Mutilans Deformity (Open-Glass Hand): -grossly unstable thumb and severely deformed phalanges -transverse folds of the skin resemble a folded telescope
  17. 17.  Hip -less commonly involved in RA -severe inflammatory destruction of the femoral head and the acetabulum may push the acetabulum into the pelvic cavity (protrusio acetabuli)  Knees -distention of the joint capsule and attenuation of ligaments -painful knees may be held in slightly flexed positions, ultimately resulting to flexion contractures
  18. 18.  Ankles and feet -hindfoot pronation -flattening of the medial longitudinal arch -calcaneal exostoses -splayfoot -metatarsalgia -hallux valgus and bunion -hammer toes -cock-up or claw toes
  19. 19.  Muscle involvement -muscle weakness – may be due to either reflex inhibition secondary to pain or atrophy  Tendons -tenosynovitis – may eventually lead to a tendon rupture -lag phenomenon – refers to a substantial difference between passive and active ROM
  20. 20.  No single test is definitive in diagnosing RA.  Typical laboratory findings in active disease include:  – Rheumatoid factor (see further detail below)  – Elevated acute phase reactants: ESR and C- reactive protein (CRP)  – CBC: thrombocytosis, hypochromic microcytic anemia, eosinophilia  – Synovial fluid analysis (see below)  – Antibodies to cyclic citrullinated peptides (CCP): specific for RA and correlated with aggressive disease
  21. 21. Synovial Fluid in RA  • Low viscosity  • WBC: 1,000–75,000/mm3  • > 70% PMNs  • Transparent—cloudy  • Hypergammaglobulinemia  • Hypocomplementemia Rheumatoid Factor (RF) in RA  • 85% of the patients with RA are RF (+).  • The other 15% of patients with RA are RF (–) A ACR criteria are fulfilled with other positive findings (see above).  • Associated with increased severity of disease with increased systemic manifestations.  • Serial titers are of no value.  • RF (+) can be seen in other diseases: rheumatic (SLE, scleroderma, Sjogren’s), viral, parasitic, bacterial, neoplasms, hyperglobulinemic.
  22. 22.  Increased ESR and CRP  • Acute phase reactants  • Markers for inflammation  • Nonspecific and not used in diagnosis  • Indicate inflammation/inflammatory disorder: nonspecific for RA.
  23. 23. Impairments and Complications:  Neurological Manifestations -mild neuropathies which result from nerve compression, such as carpal tunnel or tarsal tunnel syndromes  Cardiopulmonary Complications -pericarditis (seen in 4% of the patients) -pleuritis  Ocular manifestations -dry eyes, associated with Sjogren’s syndrome
  24. 24. Impairments and Complications:  Deconditioning -compounded by inadequate levels of regular physical activity -Marked degree of cachexia and elevated resting energy expenditure -it appears that immune e system activity and inflammation creates increased metabolism  Rheumatoid nodules -usually asymptomatic, although they can be tender and may cause skin breakdown or become infected  Vascular complications -foot and wrist drop may occur as a result of vasculitis of the vasa arteriosum to the nerve supply of the radial or superficial peroneal nerves
  25. 25. Classification of Progression of Rheumatoid Arthritis Stage I, Early 1. No destructive changes on radiographic examination 2. Radiographic evidence of osteoporosis may be present Stage II, Moderate 1. Radiographic evidence of osteoporosis, with or without slight subchondral bone destruction; slight cartilage destruction may be present 2. No joint deformities, although limitation of joint mobility may be present 3. Adjacent muscle atrophy 4. Extra-articular soft tissue lesions, such as nodules and tenosynovitis may be present
  26. 26. Stage III, Severe 1. Radiographic evidence of cartilage and bone destruction, in addition to osteoporosis 2. Joint deformity, such as subluxation, ulnar deviation, or hyperextension, without fibrous or bony ankylosis 3. Extensive muscle atrophy 4. Extra-articular soft tissue lesions, such as nodules and tenosynovitis may be present Stage IV, Terminal 1. Fibrous or bony ankylosis 2. Criteria of Stage III
  27. 27. Medical Management: Treatment Options for Rheumatoid Arthritis  Medication  DMARDs (disease-modifying antirheumatic drugs)  BRMs (Biologic response modifier)  Corticosteroids  NSAIDs  Surgery  Synovectomy  Arthrodesis  Tendon reconstruction
  28. 28. PT Management: Exercise, Equipment, and Education Treatment Options in Rheumatoid Arthritis  Passive treatments  Cold/heat  Compression and elevation  Massage  TENS  Acupuncture  Orthosis
  29. 29.  Exercises  LE strengthening  Walking  Whole-body physical activity  Jogging in water  Combined LE strengthening, flexibility, and mobility  Aerobic exercises  LE range of motion, mobility, or flexibility  Manual therapy with exercises
  30. 30.  Equipment  Adaptive for ADL  Assistive for ambulation  Appropriate footwear or insoles  Education  Self-management  Weight loss (if obese)  Activity management or joint protection  Social support  Stress management/relaxation
  31. 31. ACR Revised Criteria for Classification of Functional Status in Rheumatoid Arthritis Class I  Completely able to perform usual ADLs (self- care, vocational, and avocational) Class II  Able to perform usual self-care and vocational activities, but limited in avocational activities Class III  Able to perform usual self-care activities, but limited in vocational and avocational activities Class IV  Limited in ability to perform usual self-care, vocational, and avocational activities
  32. 32. SOURCES:  O’Sullivan, S., Schmitz, T. (2007). Physical Rehabilitation (5th ed., pp. 1075- 1083).Philadelphia, PA: F.A. Davis Company.  Braddom, R. (2011). Physical Medicine and Rehabilitation (4th ed., pp. 1419). Singapore: Saunders Elsevier