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By- kajal sansoya
 Definition
 Etiology
 Pathophysiology
 Clinical presentation
 Sign and symptoms
 Classification and progression
 RA at different joints
 Investigation
 Complication
 Management
it is an autoimmune disorder in which
the joint lining and other tissues
become inflamed as a result of over
activity of body immune system.
RA is chronic, systemic, inflammatory
disorder that primarily involves the
joints.
• 10 cases per 1000 people or 2.1 million
adults in the united states
• Affects women two times more than
males at all ages.
• There is general increase in prevalence
for both gender with increasing age.
• Like many other chronic disease the etiology of
RA is unknown.
• A specific etiological agent for RA has not been
identified.
• 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 whether this antibody
production is a primary event or result as a
response to a specific antigen from an external
stimulus.
• RHEMUATOID FACTOR-
RF have received considerable attention
in search for a causative agent in RA
because they are found in the serum of
approximately 70% of all patients with
RA.
• Chronic RA is characterized by the
grossly edematous appearance of the
synovium with 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
• Pannus - synovial proliferation of
vascular granulation tissue, dissolves
collagen as it extends over the joint
cartilage. Granulation tissue will
eventually result in adhesion, fibrosis or
bony ankylosis of the joint.
• Chronic inflammation can also weaken
the joint capsule and it supporting
ligamentous structures, altering
structures and function.
• Tendon rupture and damaged tendon
sheath may produce imbalance muscle
pull resulting in deformities seen in
advanced RA.
1. Morning stiffness
2. Arthritis of three or more joint areas-
at least three joint areas
simultaneously have had soft tissues
swelling or fluid.
3. Arthritis of hand joints ( wrist, MCP,
PIP).
4. Symmetric arthritis
5. Rheumatoid nodules
6. Serum rheumatoid
factor
7. Radiographic changes-
include erosion or
unequivocal bony
decalcification
localized in or most
marked adjacent to
the involved joint.
• No destructive changes on radiographic
examination
• Radiographic evidence of osteoporosis
may be present.
• Radiographic evidence of osteoporosis with
or without slight subchondral bone
destruction , slight cartilage destruction
may be present.
• No joint deformities ,but limitation of ROM
may be present.
• Adjacent muscle atrophy
• Extra – articular soft tissue lesions such as
nodules and tenosynovitis may be present
• Radiographic evidence of cartilage and bone
destruction in addition to osteoporosis.
• Joint deformity such as subluxation, ulnar
deviation or hyperextention , without
fibrous or bony ankylosis
• Extensive muscle atrophy
• Extra- articular soft tissue lesion such as
nodules and tenosynovitis may present
• Fibrous or bony ankylosis
• Criteria of stage 3
• 50 % takes place at
the atlanto-axial
joint.
• Ankylosing
spondylitis
• Involvement of
GH, SC, AC joint
and ST also
• Degeneration ,
pain, low ROM.
• Capsule and
ligaments become
distended with
chronic
inflamation
• Capsular and
ligamentous
distention, and joint
surface erosion may
lead to elbow
instability.
• Flexion contracture
may result from
persistent spasm
secondary to pain.
• Development of flexion contractures
which ultimately diminishes the ability
to execute power grasp.
• Volar subluxation results from chronic
inflammation of the proximal carpals
• Stenosing tenosynoitis may also occur
• 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
• Type 1 deformity- MCP flex, IP
hyperextension without CMC
involvement .
• Type II deformity- CMC is subluxed , IP
hyperextension.
• Type III deformity- CMC subluxed , MCP
hyperextension commonly found in RA.
• Less
commonly
involved in RA
• Severe
inflammatory
destruction of
the femoral
head and the
acetabulum
into the pelvic
cavity .
• Distention of the
joint capsule and
attenuation of
ligaments.
• Painful knees may
be held in slightly
flexed positions,
ultimately
resulting to
flexion
contractures.
• Hindfoot pronation
• Flattening of the ML arch
• Calcaneal exostoses
• Splayfoot
• Metatarsalgia
• Hallux valgus and bunion
• Hammer toes
• Claw toes
• ESR and CRP
• Ultrasound or MRI
• RH factor
• X- rays
• Functional assessment
• CBC
• Urea, creatinine , liver function test
• RHEUNATOID FACTOR – 85% of the
patient with RA are RF positive
• RF (+) can be seen in other diseases such
as rheumatic , viral, bacterial, parasitic,
neoplasm .
• Medications – DMARD’s , BRM’s ,
corticosteroids, NSAIDs.
• Synovectomy
• Arthrodesis
• Tendon reconstruction
• GOALS-
• relief of pain
• Prevention of deformities
• Correction of deformity
• Restoration & maintance of joint motion
• Improve muscle strength & endurance
• Gait training
• Education on management of re-occurance
Acute phase 3-4 weeks
Correct bed posture & supported positioing
of involved joints.
• Provide supported positioing of involved
joints& correct bed posture
• Use firm mattress & back support to correct
posture
• Limb is placed in position of minimal
discomfort.
 Additional support to limbs- provide by splints and
sandbags. Special attention is needed for the knee &
elbow joint as they develop flexion contracture.
 Improve vital capacity
 Improve ROM & Muscle strength-isometrics, slow&
relax isometrics
 Functional mobility
 Postural guidance
 TENS, pulsed ultrasound
 Hydrotherapy
Chronic phase
• Thermotherapy
• Active and functional therapeutic program
• Stretching exercises
• Active and passive resisted exercises
• Gait training
Equipment
Adaptive for ADL
Assistive for ambulation
Appropriate footware or insoles
Education
Self management
Weight loss
Activity management or joint protection
Social support
Stress management / relaxation
rheumatoid arthritis.
rheumatoid arthritis.

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rheumatoid arthritis.

  • 2.  Definition  Etiology  Pathophysiology  Clinical presentation  Sign and symptoms  Classification and progression  RA at different joints  Investigation  Complication  Management
  • 3. it is an autoimmune disorder in which the joint lining and other tissues become inflamed as a result of over activity of body immune system. RA is chronic, systemic, inflammatory disorder that primarily involves the joints.
  • 4.
  • 5. • 10 cases per 1000 people or 2.1 million adults in the united states • Affects women two times more than males at all ages. • There is general increase in prevalence for both gender with increasing age.
  • 6. • Like many other chronic disease the etiology of RA is unknown. • A specific etiological agent for RA has not been identified. • 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 whether this antibody production is a primary event or result as a response to a specific antigen from an external stimulus.
  • 7. • RHEMUATOID FACTOR- RF have received considerable attention in search for a causative agent in RA because they are found in the serum of approximately 70% of all patients with RA.
  • 8. • Chronic RA is characterized by the grossly edematous appearance of the synovium with 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
  • 9. • Pannus - synovial proliferation of vascular granulation tissue, dissolves collagen as it extends over the joint cartilage. Granulation tissue will eventually result in adhesion, fibrosis or bony ankylosis of the joint.
  • 10. • Chronic inflammation can also weaken the joint capsule and it supporting ligamentous structures, altering structures and function. • Tendon rupture and damaged tendon sheath may produce imbalance muscle pull resulting in deformities seen in advanced RA.
  • 11.
  • 12.
  • 13. 1. Morning stiffness 2. Arthritis of three or more joint areas- at least three joint areas simultaneously have had soft tissues swelling or fluid. 3. Arthritis of hand joints ( wrist, MCP, PIP). 4. Symmetric arthritis 5. Rheumatoid nodules
  • 14. 6. Serum rheumatoid factor 7. Radiographic changes- include erosion or unequivocal bony decalcification localized in or most marked adjacent to the involved joint.
  • 15.
  • 16.
  • 17. • No destructive changes on radiographic examination • Radiographic evidence of osteoporosis may be present.
  • 18. • Radiographic evidence of osteoporosis with or without slight subchondral bone destruction , slight cartilage destruction may be present. • No joint deformities ,but limitation of ROM may be present. • Adjacent muscle atrophy • Extra – articular soft tissue lesions such as nodules and tenosynovitis may be present
  • 19. • Radiographic evidence of cartilage and bone destruction in addition to osteoporosis. • Joint deformity such as subluxation, ulnar deviation or hyperextention , without fibrous or bony ankylosis • Extensive muscle atrophy • Extra- articular soft tissue lesion such as nodules and tenosynovitis may present
  • 20. • Fibrous or bony ankylosis • Criteria of stage 3
  • 21. • 50 % takes place at the atlanto-axial joint. • Ankylosing spondylitis
  • 22. • Involvement of GH, SC, AC joint and ST also • Degeneration , pain, low ROM. • Capsule and ligaments become distended with chronic inflamation
  • 23. • Capsular and ligamentous distention, and joint surface erosion may lead to elbow instability. • Flexion contracture may result from persistent spasm secondary to pain.
  • 24. • Development of flexion contractures which ultimately diminishes the ability to execute power grasp. • Volar subluxation results from chronic inflammation of the proximal carpals • Stenosing tenosynoitis may also occur
  • 25.
  • 26. • 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
  • 27.
  • 28.
  • 29. • Type 1 deformity- MCP flex, IP hyperextension without CMC involvement . • Type II deformity- CMC is subluxed , IP hyperextension. • Type III deformity- CMC subluxed , MCP hyperextension commonly found in RA.
  • 30. • Less commonly involved in RA • Severe inflammatory destruction of the femoral head and the acetabulum into the pelvic cavity .
  • 31. • Distention of the joint capsule and attenuation of ligaments. • Painful knees may be held in slightly flexed positions, ultimately resulting to flexion contractures.
  • 32. • Hindfoot pronation • Flattening of the ML arch • Calcaneal exostoses • Splayfoot • Metatarsalgia • Hallux valgus and bunion • Hammer toes • Claw toes
  • 33.
  • 34. • ESR and CRP • Ultrasound or MRI • RH factor • X- rays • Functional assessment • CBC • Urea, creatinine , liver function test
  • 35. • RHEUNATOID FACTOR – 85% of the patient with RA are RF positive • RF (+) can be seen in other diseases such as rheumatic , viral, bacterial, parasitic, neoplasm .
  • 36.
  • 37. • Medications – DMARD’s , BRM’s , corticosteroids, NSAIDs. • Synovectomy • Arthrodesis • Tendon reconstruction
  • 38. • GOALS- • relief of pain • Prevention of deformities • Correction of deformity • Restoration & maintance of joint motion • Improve muscle strength & endurance • Gait training • Education on management of re-occurance
  • 39. Acute phase 3-4 weeks Correct bed posture & supported positioing of involved joints. • Provide supported positioing of involved joints& correct bed posture • Use firm mattress & back support to correct posture • Limb is placed in position of minimal discomfort.
  • 40.  Additional support to limbs- provide by splints and sandbags. Special attention is needed for the knee & elbow joint as they develop flexion contracture.  Improve vital capacity  Improve ROM & Muscle strength-isometrics, slow& relax isometrics  Functional mobility  Postural guidance  TENS, pulsed ultrasound  Hydrotherapy
  • 41. Chronic phase • Thermotherapy • Active and functional therapeutic program • Stretching exercises • Active and passive resisted exercises • Gait training
  • 42. Equipment Adaptive for ADL Assistive for ambulation Appropriate footware or insoles
  • 43. Education Self management Weight loss Activity management or joint protection Social support Stress management / relaxation