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RHEUMATOID ARTHRITIS
Dr Krishna Bhatt, ARIP
• A systemic inflammatory disease.
• Primarily affecting the synovial lining of joints as well
as other connective tissue.
• Joints are characteristically involved with early
inflammatory changes in the synovial membrane,
peripheral portions of the articular cartilage, and
subchondral spaces.
• Granulation tissue (pannus) forms, covers, and
erodes the articular cartilage, bone, and ligaments in
the joint capsule.
• Adhesions may form, restricting joint mobility.
• With progression of the disease, cancellous bone
becomes exposed.
• Fibrosis, ankylosis, or subluxation may eventually
cause deformity and disability
• Inflammatory changes also occur in tendon sheaths
(tenosynovitis).
• The tendons may rupture.
ACR Criterias for classification of RA
1. Morning stiffness – lasting at least 1 hr
2. Arthritis of 3 or more joint areas simultaneously.
3. Arthritis of hand joints – at least 1 area swollen in wrist,
MCP or PIP
4. Symmetric arthritis – simultaneous involvement of same
joint areas on both sides
5. Rheumatoid nodules- over bony prominences
6. Serum rheumatoid factor- abnormal amount of RF
7. Radiographic changes- erosions, bony decalcification
 Out of this if 4 or more of these factors are present than the
person is diagnosed with RA.
Signs & symptoms
• Morning stiffness
difficulty in movts when awaking
Joint involvement :
Bilateral & symmetric pattern
Present with signs of inflammation
Etiology
• Patients with RA produce antibodies to their own
immunoglobulin's.
• RF( Rheumatic Factor) is found in approx 70%
patients
• RF are the antibodies specific to IgG.
• Some modification of IgG causes stimulation of
production of RF.
• RA occurs in the absence of RF in some patients.
• Recent studies states that HLA are found on the cell
surface of most human cells & are capable of
generating immune response.
• 4 types- HLA-A, HLA-B, HLA-C, HLA-D
• RA is associated with increased HLA- DRW4 & HLA-
DR1 antigens.
Pathology
• Edematous appearance of synovium with hair like
projections into joint cavity.
• synovial proliferation of granulation tissue known as
Pannus.
• If RA continues, the granulation tissue results in
adhesions, fibrosis or bony ankylosis of joint.
• Chronic inflammation weakens the joint capsule &
supporting lig.
Onset & course
• Onset – generalized joint pain, stiffness lasting
weeks to months.
• Some have intermittent course, characterized
by partial to complete remissions.
• Progressive RA – unremitting destructive
process
Cervical spine
• Atlantoaxial jt.& midcervical
- instability,subluxation
• Lower cervical
-radiating pain
-nerve and cord compression
Temporomandibular joint
• Inability to open mouth
• Normal side to side gliding
Shoulder
• GH,AC&SC jts
• Pain ,loss of ROM, degeneration
• Capsule ligaments get distended
• Instability as jt.surfaces are eroded
• Tendinitis ,bursitis
Elbow
• Capsule,ligament distension
• Instability
• Flexion contracture due to persistent muscle spasm
Wrist
• Chronic inflammation of proximal carpals lead to volar-
subluxation.
• Chronic inflammation
• Destruction of the extensor Carpi ulnaris, radial collateral lig &
fibro cartilage on ulna.
• Proximal carpals slide down towards ulna
• Radial deviation of distal carpals
• So phalanges try to compensate for loss of Ulnar
deviation at wrist that causes Ulnar drift.
Hand deformities
• MCP jts : Swelling around MCP jts
• PIP jts:
• Swan neck deformity : PIP hyperextension
DIP flexion
• Occurs by 2 ways :
Swan neck deformity
• 1) synovitis of PIP
• Volar capsule is stretched
• Lateral bands move dorsally
•
• Tension in FDP
• DIP flex
• Rupture of FDS causes hyperextension of PIP.
• 2) rupture of EDC at insertion on DIP results in DIP
flex & PIP hyperextension
Boutonniere deformity
• Boutonniere deformity : PIP flex
• DIP extension
• Chronic synovitis
• Insertion of EDC at middle phalange lengthens
• Lateral bands slide volarly cause PIP flex
• Osteophytes at the PIP jts present called Bouchard’s
nodes.
• Osteophytes at DIP jts called Herbeden’s nodes.
• Mallet finger : flex of DIP
• Rupture of EDC ,unopposed pull of FDP that causes
flexion of DIP
Z Deformity
• Thumb :
• Synovial swelling
• Dorsal hood mech., joint capsule, collateral lig,
tendon of EPB & EPL are affected.
Hip
• Less common
• Groin pain
• Trochanteric bursitis
Knee
• Common due to large amount of synovium
• Distension of jt. Capsule
• Destruction of jt. Surface
• Flexion contracture
Ankle and Feet
• Hallux valgus and bunion
• Stretching of spring ligament Flattening of
medial longitudinal arch
Hammer toe
• Flexion of PIP& hyperextension of DIP
Claw toes
• Flexion of the PIP & DIP jts.
• Synovitis weakens transverse arch
metatarsals spread
splayed forefoot
• Atrophy in intrinsic muscles of hand & quadriceps in
long standing disease.
• Inflammation of tendon sheath results in
tenosynovitis that direct damage to tendon & causes
tendon rupture.
Extra articular manifestations
• Rheumatoid nodules most common extra
articular manifestation.
• Most commonly found at olecranon bursa,
achilles tendon.
• They are asymptomatic
• Vascular – rheumatoid arteritis is life
threatening.
• Neurological – mild peripheral neuropathy
nerve compression or
entrapement
CVS – pericarditis
Occular – scleritis
Investigations
• Increased ESR or CRP
• Presence of RF neither confirms nor rule out
diagnosis of RA.
• 25 % patients of RA don’t have positive RF
(seronegative RA).
• Positive RF is seen in other diseases also such as
leprosy, TB.
• Positive RF with clinical criterias can confirm the
diagnosis.
• RBC decreased
• WBC normal
• Synovial fluid analysis- in inflammed joints cloudy,
less viscous
• Presence of crystals can confirm gout or psuedo
gout.
Radiography
• Uneven, reduced or absent spacing between joint
surfaces bcoz of loss of cartilage.
• Erosion of joint surfaces
Prognosis
• RA could not cause death but such conditions as
systemic vasculitis & atlantoaxial subluxation could
be fatal.
• Patients of milder form & long term inflammation
results in joint destruction & functional loss.
• Patients with late onset have better functional
outcome than early onset.
Medical management
• Adequate drug therapy in early stages results in less
joint damage & functional loss.
• 2 major drugs are used- NSAIDS
• DMARDS
• NSAIDS- non steroidal anti inflammatory drugs
• Basic element in long term treatment
• Both analgesic & anti-inflammatory actions
• Corticosteroids- Most powerful anti-inflammatory
drugs.
• DMARDS- disease modifying anti-rheumatic drugs
• Change the course of RA for at least 1 year
i.e improved function, reduced inflammation &
slowing or prevention of structural changes.
• Slow acting
• Required 3 wks to 3 mnths to become active.
• BRM- biologic response modifying agent
• In treatment of systemic, inflammatory rheumatic
disease.
Surgical management
• Soft tissue surgeries :
synovectomy, soft tissue release, tendon
transfers.
• Bone & joint surgeries :
osteotomy, prosthetic arthroplasty, arthrodesis
PT management
• Goals :
• Decrease pain
• Increase or maintain ROM of all joints
• Increase or maintain muscle strength
• Increase endurance for functional activities
• Promote independence in all ADLs
• Improve efficiency & safety in gait pattern
• Education on management of recurrence
Acute stage of Rheumatoid Arthritis
• Pain relief :
• Physical agents- hot or cold
• Superficial heat- localized analgesia
• increase local circulation
• Delivered by- moist heat packs, lamps,
paraffin wax, hydrotherapy.
• Deep heating modalities are contraindicated
in acute stage of inflammation bcoz it may
stimulate collagenese activity within joint,
further causes destruction.
• Local cold application produces local analgesia
& increase superficial circulation following
initial vasoconstriction.
• Cold application is particularly useful for
swollen joints.
• TENS
• Hand & wrist orthoses- immobilze specific
joints & reduce pain & swelling by providing
rest & support.
• Orthoses may be used to reduce pain through
biomechanical support or correction.
Joint protection
• Because periods of active disease may last several
months to more than a year, education in the overall
treatment plan, safe activity, and joint protection
begins as soon as possible.
• It is imperative to involve the patient in the
management so he or she learns how to conserve
energy and avoid stresses during activities and when
exercising.
• Monitor activities and stop when discomfort or
fatigue begins to develop.
• Use frequent but short episodes of exercise (three to
five sessions per day) rather than one long session.
• Alternate activities to avoid fatigue.
• Decrease level of activities or omit provoking
activities if joint pain develops and persists for more
than 1 hour after activity.
• Avoid deforming positions.
• Avoid prolonged static positioning - change positions
during the day every 20 to 30 minutes.
• Avoid vigorous stretching techniques.
Energy conservation
• It is important that the patient learns to reduce
fatigue and, when tired, rests to minimize undue
stress to all the body systems.
• Because inflamed joints are easily damaged and rest
is encouraged to protect the joints, the patient is
taught how to rest the joints in nondeforming
positions.
Joint mobility
• The patient is encouraged to do active exercises
through as much (ROM) as possible (not stretching).
• If active exercises are not tolerated owing to pain
and swelling, passive ROM is used.
• Once symptoms of pain and signs of swelling are
controlled with medication, exercises can progress.
• Therapeutic exercises cannot positively alter the
pathological process of RA but if administered
carefully, they can help prevent or correct the
deforming forces that occur, especially during the
early stages of the disease, and therefore help
maintain function.
• Secondary effects of steroidal medications may
include osteoporosis and ligamentous laxity, so
exercises should not cause excessive stress to bones
or joints.
• Stretching techniques should not be performed
across swollen joints.
• Forcing motion on the distended capsule
overstretches it, leading to subsequent hypermobility
(or subluxation) when the swelling reduced.
Sub acute and Chronic Stages of RA
• Appropriate precautions must be taken because the
pathological changes from the disease process make
the parts more susceptible to damage.
• To improve function, exercise should be aimed at
improving flexibility, muscle performance, and
cardiopulmonary endurance.
• The joint capsule, ligaments, and tendons may be
structurally weakened by the rheumatic process, so
the stretching techniques used to counter any
contractures or adhesions must be carefully applied.
• Initially isometric exercises can be started.
• It should be less than maximal voluntary contraction.
• 5-10 reps. with 5sec hold
• Gradually dynamic strengthening started which
should be preformed in pain free range.
• Resistance can be applied by weights or elastic bands
or other equipments.
• Gradual progression of resistance & repetitions.
• 8-10 reps can be given.
• Exercises such as swimming and bicycling, performed
within the tolerance of the individual with RA,
improve aerobic capacity and physical activity.
• Group activities such as water aerobics also provide.
• Functional training :
• Activities of daily living (ADL) may need to be
modified in order to protect the joints.
• If necessary, splints and assistive devices should be
used to provide protection.
• Modifications include long handled devices or
devices with easier grasp.
• Rearrangement at home or work place.
• Raising chairs or bed reduce effort to stand up.
• Railings placed around bed, bath or stairs.
For mallet finger For boutonniere’s deformity
Bunion aid splint for
hallux valgus For swan neck deformity
OA RA
• Usually after age of 40
• Usually develops slowly over
many years in response to
mechanical stress
• Cartilage degradation, altered
joint architecture, osteophyte
formation
• Affects a few joints (usually
asymmetrical)
• Typically —Hips, knees,
DIP, PIP, 1st CMC of hands,
• Cervical and lumbar spine
• Usually begins between age 15
and 50
• May develop suddenly, within
weeks or months
• Inflammatory synovitis and
irreversible structural damage to
cartilage and bone
• Usually affects many joints,
usually bilateral;
• Typically —MCP and PIP of hands,
wrists, elbows, shoulders
• Cervical spine
• MTP, talonavicular and ankle
OA RA
• Morning stiffness (usually less
than 30 min), increased joint pain
with weight-bearing and
strenuous activity; crepitus and
loss of ROM
• Redness, warmth, swelling, and
prolonged morning stiffness;
increased joint pain with activity
• General feeling of fatigue, weight
loss and fever.
• May develop rheumatoid
nodules, may have ocular,
respiratory, hematological, and
cardiac symptoms
CASE Scenario:
•
• 37-year-old woman gradually developed painful wrists over 3 months;
she consulted her doctor only when the pain and early morning
stiffness stopped her from gardening
• On examination, both wrists and the metacarpophalangeal joints of both
hands were swollen and tender but not deformed. There were no nodules or
vasculitic lesions. On investigation, she was found to have a raised C-
reactive protein (CRP) level (27mg/l) (NR <10) but a normal haemoglobin
and white-cell count. A latex test for rheumatoid factor was negative and
antinuclear antibodies were not detected.
• The clinical diagnosis was early rheumatoid arthritis and she was treated
with ibuprofen. Despite some initial symptomatic improvement, the pain,
stiffness and swelling of the hands persisted and 1 month later both knees
became similarly affected. She was referred to a rheumatologist.
• Six months after initial presentation, she
developed two subcutaneous nodules on the left
elbow; these were small, painless, firm and immobile
but not tender. A test for rheumatoid factor was now
positive (titre 1/64). X-rays of the hands showed bony
erosions in the metacarpal heads. She still had a
raised CRP (43mg/l) but normal serum complement
(C3 and C4) levels and, had she had a
biopsy, pannus would have been demonstrable
histologically.
The patient is a 34-year-old Caucasian woman who initially presented
to her primary care physician with a chief complaint of pain and
swelling in multiple joints that made it difficult to carry out her duties as
executive assistant to the vice president of a trucking company. She has
been experiencing increased morning stiffness and difficulty with
simple tasks such as tying shoelaces, buttoning clothes, and typing. The
patient's primary care physician discussed the possibility of rheumatoid
arthritis (RA) and prescribed 1 month of treatment with a nonsteroidal
anti-inflammatory drug (NSAID). This treatment did not reduce the
severity of the patient's symptoms and her primary care provider
referred her to a rheumatologist.

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Rheumatoid arthitis

  • 2. • A systemic inflammatory disease. • Primarily affecting the synovial lining of joints as well as other connective tissue. • Joints are characteristically involved with early inflammatory changes in the synovial membrane, peripheral portions of the articular cartilage, and subchondral spaces.
  • 3. • Granulation tissue (pannus) forms, covers, and erodes the articular cartilage, bone, and ligaments in the joint capsule. • Adhesions may form, restricting joint mobility. • With progression of the disease, cancellous bone becomes exposed. • Fibrosis, ankylosis, or subluxation may eventually cause deformity and disability
  • 4. • Inflammatory changes also occur in tendon sheaths (tenosynovitis). • The tendons may rupture.
  • 5. ACR Criterias for classification of RA 1. Morning stiffness – lasting at least 1 hr 2. Arthritis of 3 or more joint areas simultaneously. 3. Arthritis of hand joints – at least 1 area swollen in wrist, MCP or PIP 4. Symmetric arthritis – simultaneous involvement of same joint areas on both sides 5. Rheumatoid nodules- over bony prominences 6. Serum rheumatoid factor- abnormal amount of RF 7. Radiographic changes- erosions, bony decalcification  Out of this if 4 or more of these factors are present than the person is diagnosed with RA.
  • 6. Signs & symptoms • Morning stiffness difficulty in movts when awaking Joint involvement : Bilateral & symmetric pattern Present with signs of inflammation
  • 7. Etiology • Patients with RA produce antibodies to their own immunoglobulin's. • RF( Rheumatic Factor) is found in approx 70% patients • RF are the antibodies specific to IgG. • Some modification of IgG causes stimulation of production of RF. • RA occurs in the absence of RF in some patients.
  • 8. • Recent studies states that HLA are found on the cell surface of most human cells & are capable of generating immune response. • 4 types- HLA-A, HLA-B, HLA-C, HLA-D • RA is associated with increased HLA- DRW4 & HLA- DR1 antigens.
  • 9. Pathology • Edematous appearance of synovium with hair like projections into joint cavity. • synovial proliferation of granulation tissue known as Pannus. • If RA continues, the granulation tissue results in adhesions, fibrosis or bony ankylosis of joint. • Chronic inflammation weakens the joint capsule & supporting lig.
  • 10.
  • 11.
  • 12.
  • 13. Onset & course • Onset – generalized joint pain, stiffness lasting weeks to months. • Some have intermittent course, characterized by partial to complete remissions. • Progressive RA – unremitting destructive process
  • 14. Cervical spine • Atlantoaxial jt.& midcervical - instability,subluxation • Lower cervical -radiating pain -nerve and cord compression
  • 15. Temporomandibular joint • Inability to open mouth • Normal side to side gliding
  • 16. Shoulder • GH,AC&SC jts • Pain ,loss of ROM, degeneration • Capsule ligaments get distended • Instability as jt.surfaces are eroded • Tendinitis ,bursitis
  • 17. Elbow • Capsule,ligament distension • Instability • Flexion contracture due to persistent muscle spasm
  • 18. Wrist • Chronic inflammation of proximal carpals lead to volar- subluxation. • Chronic inflammation • Destruction of the extensor Carpi ulnaris, radial collateral lig & fibro cartilage on ulna. • Proximal carpals slide down towards ulna
  • 19. • Radial deviation of distal carpals • So phalanges try to compensate for loss of Ulnar deviation at wrist that causes Ulnar drift.
  • 20. Hand deformities • MCP jts : Swelling around MCP jts • PIP jts: • Swan neck deformity : PIP hyperextension DIP flexion • Occurs by 2 ways :
  • 21. Swan neck deformity • 1) synovitis of PIP • Volar capsule is stretched • Lateral bands move dorsally • • Tension in FDP • DIP flex
  • 22. • Rupture of FDS causes hyperextension of PIP. • 2) rupture of EDC at insertion on DIP results in DIP flex & PIP hyperextension
  • 23. Boutonniere deformity • Boutonniere deformity : PIP flex • DIP extension • Chronic synovitis • Insertion of EDC at middle phalange lengthens • Lateral bands slide volarly cause PIP flex
  • 24.
  • 25. • Osteophytes at the PIP jts present called Bouchard’s nodes. • Osteophytes at DIP jts called Herbeden’s nodes. • Mallet finger : flex of DIP • Rupture of EDC ,unopposed pull of FDP that causes flexion of DIP
  • 26. Z Deformity • Thumb : • Synovial swelling • Dorsal hood mech., joint capsule, collateral lig, tendon of EPB & EPL are affected.
  • 27. Hip • Less common • Groin pain • Trochanteric bursitis
  • 28. Knee • Common due to large amount of synovium • Distension of jt. Capsule • Destruction of jt. Surface • Flexion contracture
  • 29. Ankle and Feet • Hallux valgus and bunion • Stretching of spring ligament Flattening of medial longitudinal arch
  • 30. Hammer toe • Flexion of PIP& hyperextension of DIP
  • 31. Claw toes • Flexion of the PIP & DIP jts.
  • 32. • Synovitis weakens transverse arch metatarsals spread splayed forefoot
  • 33. • Atrophy in intrinsic muscles of hand & quadriceps in long standing disease. • Inflammation of tendon sheath results in tenosynovitis that direct damage to tendon & causes tendon rupture.
  • 34. Extra articular manifestations • Rheumatoid nodules most common extra articular manifestation. • Most commonly found at olecranon bursa, achilles tendon. • They are asymptomatic
  • 35. • Vascular – rheumatoid arteritis is life threatening. • Neurological – mild peripheral neuropathy nerve compression or entrapement CVS – pericarditis Occular – scleritis
  • 36. Investigations • Increased ESR or CRP • Presence of RF neither confirms nor rule out diagnosis of RA. • 25 % patients of RA don’t have positive RF (seronegative RA). • Positive RF is seen in other diseases also such as leprosy, TB.
  • 37. • Positive RF with clinical criterias can confirm the diagnosis. • RBC decreased • WBC normal • Synovial fluid analysis- in inflammed joints cloudy, less viscous • Presence of crystals can confirm gout or psuedo gout.
  • 38. Radiography • Uneven, reduced or absent spacing between joint surfaces bcoz of loss of cartilage. • Erosion of joint surfaces
  • 39. Prognosis • RA could not cause death but such conditions as systemic vasculitis & atlantoaxial subluxation could be fatal. • Patients of milder form & long term inflammation results in joint destruction & functional loss. • Patients with late onset have better functional outcome than early onset.
  • 40. Medical management • Adequate drug therapy in early stages results in less joint damage & functional loss. • 2 major drugs are used- NSAIDS • DMARDS
  • 41. • NSAIDS- non steroidal anti inflammatory drugs • Basic element in long term treatment • Both analgesic & anti-inflammatory actions • Corticosteroids- Most powerful anti-inflammatory drugs.
  • 42. • DMARDS- disease modifying anti-rheumatic drugs • Change the course of RA for at least 1 year i.e improved function, reduced inflammation & slowing or prevention of structural changes. • Slow acting • Required 3 wks to 3 mnths to become active.
  • 43. • BRM- biologic response modifying agent • In treatment of systemic, inflammatory rheumatic disease.
  • 44. Surgical management • Soft tissue surgeries : synovectomy, soft tissue release, tendon transfers. • Bone & joint surgeries : osteotomy, prosthetic arthroplasty, arthrodesis
  • 45. PT management • Goals : • Decrease pain • Increase or maintain ROM of all joints • Increase or maintain muscle strength • Increase endurance for functional activities • Promote independence in all ADLs • Improve efficiency & safety in gait pattern • Education on management of recurrence
  • 46. Acute stage of Rheumatoid Arthritis • Pain relief : • Physical agents- hot or cold • Superficial heat- localized analgesia • increase local circulation • Delivered by- moist heat packs, lamps, paraffin wax, hydrotherapy.
  • 47. • Deep heating modalities are contraindicated in acute stage of inflammation bcoz it may stimulate collagenese activity within joint, further causes destruction. • Local cold application produces local analgesia & increase superficial circulation following initial vasoconstriction.
  • 48. • Cold application is particularly useful for swollen joints. • TENS • Hand & wrist orthoses- immobilze specific joints & reduce pain & swelling by providing rest & support. • Orthoses may be used to reduce pain through biomechanical support or correction.
  • 49. Joint protection • Because periods of active disease may last several months to more than a year, education in the overall treatment plan, safe activity, and joint protection begins as soon as possible. • It is imperative to involve the patient in the management so he or she learns how to conserve energy and avoid stresses during activities and when exercising.
  • 50. • Monitor activities and stop when discomfort or fatigue begins to develop. • Use frequent but short episodes of exercise (three to five sessions per day) rather than one long session. • Alternate activities to avoid fatigue. • Decrease level of activities or omit provoking activities if joint pain develops and persists for more than 1 hour after activity.
  • 51. • Avoid deforming positions. • Avoid prolonged static positioning - change positions during the day every 20 to 30 minutes. • Avoid vigorous stretching techniques.
  • 52. Energy conservation • It is important that the patient learns to reduce fatigue and, when tired, rests to minimize undue stress to all the body systems. • Because inflamed joints are easily damaged and rest is encouraged to protect the joints, the patient is taught how to rest the joints in nondeforming positions.
  • 53. Joint mobility • The patient is encouraged to do active exercises through as much (ROM) as possible (not stretching). • If active exercises are not tolerated owing to pain and swelling, passive ROM is used. • Once symptoms of pain and signs of swelling are controlled with medication, exercises can progress.
  • 54. • Therapeutic exercises cannot positively alter the pathological process of RA but if administered carefully, they can help prevent or correct the deforming forces that occur, especially during the early stages of the disease, and therefore help maintain function.
  • 55. • Secondary effects of steroidal medications may include osteoporosis and ligamentous laxity, so exercises should not cause excessive stress to bones or joints. • Stretching techniques should not be performed across swollen joints. • Forcing motion on the distended capsule overstretches it, leading to subsequent hypermobility (or subluxation) when the swelling reduced.
  • 56. Sub acute and Chronic Stages of RA • Appropriate precautions must be taken because the pathological changes from the disease process make the parts more susceptible to damage. • To improve function, exercise should be aimed at improving flexibility, muscle performance, and cardiopulmonary endurance.
  • 57. • The joint capsule, ligaments, and tendons may be structurally weakened by the rheumatic process, so the stretching techniques used to counter any contractures or adhesions must be carefully applied.
  • 58. • Initially isometric exercises can be started. • It should be less than maximal voluntary contraction. • 5-10 reps. with 5sec hold • Gradually dynamic strengthening started which should be preformed in pain free range. • Resistance can be applied by weights or elastic bands or other equipments.
  • 59. • Gradual progression of resistance & repetitions. • 8-10 reps can be given. • Exercises such as swimming and bicycling, performed within the tolerance of the individual with RA, improve aerobic capacity and physical activity. • Group activities such as water aerobics also provide.
  • 60. • Functional training : • Activities of daily living (ADL) may need to be modified in order to protect the joints. • If necessary, splints and assistive devices should be used to provide protection.
  • 61. • Modifications include long handled devices or devices with easier grasp. • Rearrangement at home or work place. • Raising chairs or bed reduce effort to stand up. • Railings placed around bed, bath or stairs.
  • 62.
  • 63.
  • 64. For mallet finger For boutonniere’s deformity
  • 65. Bunion aid splint for hallux valgus For swan neck deformity
  • 66.
  • 67. OA RA • Usually after age of 40 • Usually develops slowly over many years in response to mechanical stress • Cartilage degradation, altered joint architecture, osteophyte formation • Affects a few joints (usually asymmetrical) • Typically —Hips, knees, DIP, PIP, 1st CMC of hands, • Cervical and lumbar spine • Usually begins between age 15 and 50 • May develop suddenly, within weeks or months • Inflammatory synovitis and irreversible structural damage to cartilage and bone • Usually affects many joints, usually bilateral; • Typically —MCP and PIP of hands, wrists, elbows, shoulders • Cervical spine • MTP, talonavicular and ankle
  • 68. OA RA • Morning stiffness (usually less than 30 min), increased joint pain with weight-bearing and strenuous activity; crepitus and loss of ROM • Redness, warmth, swelling, and prolonged morning stiffness; increased joint pain with activity • General feeling of fatigue, weight loss and fever. • May develop rheumatoid nodules, may have ocular, respiratory, hematological, and cardiac symptoms
  • 69. CASE Scenario: • • 37-year-old woman gradually developed painful wrists over 3 months; she consulted her doctor only when the pain and early morning stiffness stopped her from gardening • On examination, both wrists and the metacarpophalangeal joints of both hands were swollen and tender but not deformed. There were no nodules or vasculitic lesions. On investigation, she was found to have a raised C- reactive protein (CRP) level (27mg/l) (NR <10) but a normal haemoglobin and white-cell count. A latex test for rheumatoid factor was negative and antinuclear antibodies were not detected. • The clinical diagnosis was early rheumatoid arthritis and she was treated with ibuprofen. Despite some initial symptomatic improvement, the pain, stiffness and swelling of the hands persisted and 1 month later both knees became similarly affected. She was referred to a rheumatologist.
  • 70. • Six months after initial presentation, she developed two subcutaneous nodules on the left elbow; these were small, painless, firm and immobile but not tender. A test for rheumatoid factor was now positive (titre 1/64). X-rays of the hands showed bony erosions in the metacarpal heads. She still had a raised CRP (43mg/l) but normal serum complement (C3 and C4) levels and, had she had a biopsy, pannus would have been demonstrable histologically.
  • 71.
  • 72. The patient is a 34-year-old Caucasian woman who initially presented to her primary care physician with a chief complaint of pain and swelling in multiple joints that made it difficult to carry out her duties as executive assistant to the vice president of a trucking company. She has been experiencing increased morning stiffness and difficulty with simple tasks such as tying shoelaces, buttoning clothes, and typing. The patient's primary care physician discussed the possibility of rheumatoid arthritis (RA) and prescribed 1 month of treatment with a nonsteroidal anti-inflammatory drug (NSAID). This treatment did not reduce the severity of the patient's symptoms and her primary care provider referred her to a rheumatologist.