Rheumatoid arthritis is an autoimmune disease that causes chronic inflammation of the joints. It can affect multiple organs in the body. Risk factors include sex, age, family history, smoking, and obesity. Genetic factors contribute to pathogenesis. Symptoms include joint pain, stiffness, and swelling. Diagnosis is based on clinical and lab criteria. Treatments include medications like NSAIDs, DMARDs, steroids, and biologics as well as physical therapy and exercise to preserve joint function and prevent deformity. Surgery may be needed in cases of severe joint damage.

1. Welcome to My Presentation
• Muhammad Zahirul Haque
Roll-10
Batch-19th (Final year Physiotherapy Student)
National Institute Of Traumatology
Orthopedics and Rehabilitations(NITOR)

2. Presentation on
Rheumatoid Arthritis

3. Contents
• Definition
• Risk Factor
• Pathophysiology
• Cause
• Symptoms
• Diagnostic criteria
• Investigation
• Treatment
• Surgery
• Deformity
• Physical therapy

4. Definition:
• Rheumatoid arthritis (RA) is an autoimmune
disease that causes chronic inflammation of the
joints. Autoimmune diseases are illnesses that
occur when the body's tissues are mistakenly
attacked by their own immune system. The
immune system contains a complex organization
of cells and antibodies designed normally to "seek
and destroy" invaders of the body, particularly
infections. Patients with autoimmune diseases
have antibodies and immune cells in their blood
that target their own body tissues, where they can
be associated with inflammation.

5. • While inflammation of the tissue around the
joints and inflammatory arthritis are
characteristic features of rheumatoid arthritis,
the disease can also cause inflammation and
injury in other organs in the body. Because it
can affect multiple other organs of the body,
rheumatoid arthritis is referred to as a
systemic illness and is sometimes called
rheumatoid disease. Rheumatoid arthritis is a
classic rheumatic disease ( Rfe:William N
Sheil Jr)

6. Factors that may increase your risk of
rheumatoid arthritis include:
Your sex. Women are more likely than men to
develop rheumatoid arthritis.
Age. Rheumatoid arthritis can occur at any age,
but it most commonly begins between the ages
of 40 and 60.
Family history. If a member of your family has
rheumatoid arthritis, you may have an increased
risk of the disease.
Risk Factors:

7. Smoking. Cigarette smoking increases your risk
of developing rheumatoid arthritis, particularly if
you have a genetic predisposition for developing
the disease. Smoking also appears to be associated
with greater disease severity.
Environmental exposures. Although uncertain
and poorly understood, some exposures such as
asbestos or silica may increase the risk for
developing rheumatoid arthritis. Emergency
workers exposed to dust from the collapse of the
World Trade Center are at higher risk of
autoimmune diseases such as rheumatoid arthritis.

8. Obesity. People who are overweight or obese
appear to be at somewhat higher risk of
developing rheumatoid arthritis, especially in
women diagnosed with the disease when they
were 55 or younger.

9. Pathophysiology

14. Researchers have shown that people with a specific
genetic marker called the HLA shared epitope have a
fivefold greater chance of developing rheumatoid
arthritis than do people without the marker. The HLA
genetic site controls immune responses. Other genes
connected to RA include: STAT4, a gene that plays
important roles in the regulation and activation of the
immune system; TRAF1 and C5, two genes relevant to
chronic inflammation; and PTPN22, a gene associated
with both the development and progression of
rheumatoid arthritis. Yet not all people with these genes
develop RA and not all people with the condition have
these genes.(Arthritis Foundation)
Cause:

15. Symptoms: Articular Feature
• Joint pain, tenderness, swelling or stiffness for
six weeks or longer
• Morning stiffness for 60 minutes or longer
• More than one joint is affected
• Small joints (wrists, MTP, certain joints of the
hands and feet) are affected
• The same joints on both sides of the body are
affected.(Symmetrical)
• Rest pain
• Movement restricted
• Relapse and remitting
• Atlanto-axial joint

16. Symptoms: Extra-articular
manifestation
Systemic:
Fever
Fatigue
Weight loss
Susceptibility to infection
Musculoskeletal
Muscle wasting
Bursitis
Tenosynovitis
Osteoporosis

17. Hematological
Anemia
Eosinophilia
Thrombocytosis
Lymphatic
Felty’s syndrome
Splenomegaly
Nodules
Sinuses
Fistulae

18. Ocular
Episcleritis
Scleritis
Scleromalacia
Keratocunjuntivitis sicca
Vasculitis
Digital arteritis
Ulcer
Pyoderma gangrenosum
Mononeuritis multiplex
Visceral arteritis

19. Cardiac
Pericarditis
Myocarditis
Endocarditis
Conduction defects
Coronary vasculitis
Granulomatous aortitis
Pulmonary
Nodules
Pleural effusions
Fibrosing alveolitis
Bronchiolitis
Caplan’s syndrome

20. Neurological
Cervical cord compression
Compression neuropathies
Peripheral neuropathy
Mononeuritis multiplex
Amyloidosis
(Ref:Davidson’s and Arthritis
Foundation)

21. Criterion Score
Joint affected
1 Large Joint 0
2-10 Large Joints 1
1-3 Small joints 2
4-10 Small joints 5
Criteria for diagnosis of rheumatoid arthritis

22. Criterion Score
Serology
Negative RF and ACPA 0
Low Positive RF and ACPA 2
High Positive RF and ACPA 3

23. Criterion Score
Duration of Symptoms
< 6 weeks 0
>6 weeks 1
Criterion Score
Acute Phase reactants
Normal CRP and ESR 0
Abnormal CRP and ESR 1

24. Patients with a score >6 are consider to have
RA.
*European League Against
Rheumatism/American College Of
Rheumatology 2010 criteria.
(ACPA=anti-citrullinated peptide antibodies,
CRP=C-reactive protein, ESR=erythrocyte
sedimentation rate, RF= rheumatoid factor)

25. Investigation of RA
• CBC-TC,DC,Hb,ESR,CRP
• Acute phase reactants
• Rheumatic factor
• Anti-CCP antibodies

26. Acute phase reactants
• Positive acute phase reactants(↑)
Mild elevations
ceruloplasmin
Complement C3 &C4
Moderate elevations
Haptoglobulin
Fibrinogen
∝1-acid glycoprotein
∝1-proteinase inhibitor

27. Acute phase reactants
Marked Elevations
C-reactive protein
Serum amyloid A protein
Negative acute phase reactants(↓)
Albumin
Transferrin

28. Anti- CCP
• IgG-against synovial membrane peptides
damage via inflammation
• Sensitivity (65%)&specificity(95%)
• Both diagnostic and prognostic value
• Predictive and erosive disease
Disease severity
Radiologic progression
Poor functional outcomes

29. Rheumatoid Factor
• Antibody that recognize Fc portion of IgG
• Can be IgG, IgM, IgA
• 85% of the patients RA over the first two years
become RF(positive)
• A negative RF may be repeated 4-6 monthly for
the first two year or disease, since some patient
may take 18-24 month to become seropositive.
• Prognostic value : Patients with high titers of RF,
in general tend to have poor prognosis, more
extra-articular manifestation.

30. Other laboratory investigation
• Elevated APRs(ESR,CRP)
• Thrombocytosis
• Leukocytosis
• ANA:30-40%(anti-nuclear antibody)
• Inflammatory synovial fluid
• Hypoalbuminemia

31. Radiological Features
• Peri-articular osteopenia
• Uniform symmetric joint space narrowing
• Marginal subchondral erosions
• Joint subluxations
• Joint destructions
• Collapse
USG=detect the early soft tissue lesion.
MRI=Has grater sensitivity to detect Synovitis and
marrow changes.
• (Dr. Ankur Nandan varshany)

33. Goals of management
• Focused on reliving pain
• Preventing damage and disability
• Patient education about the disease
• Physical therapy
• Treatment should be early and should be
individualized

34. Treatment Modalities for RA
• NSAIDs
• Steroid
• DMARDs
• Immunosuppressive therapy
• Biological therapy
• Surgery

35. Nonsteroidal anti inflammatory
drugs(NSAIDs)
• Aspirin
• Indomethacin
• Ibupropfen
• Naproxen
• Piroxicam
• Nabumetone
• Diclofenac
*All NSAIDS should taken after meal to prevent
stomach upset.

36. COX-2 Inhibitor are
• Celecoxib
• Rofecoxiba
• Valdecoxib

37. Corticosteroids : Corticosteroid medications,
including prednisone, prednisolone and
methyprednisolone, are potent and quick-acting
anti-inflammatory medications. They may be
used in RA to get potentially damaging
inflammation under control, while waiting for
NSAIDs and DMARDs (below) to take effect.
Because of the risk of side effects with these
drugs, doctors prefer to use them for as short a
time as possible and in doses as low as possible.

38. Disease-Modifying
Antirheumatic Drugs(DMARDs)
• Methotrexate
• Sulfasalazine
• Hydroxycholoroquine
• Leflunomide
• D-penicillamine
• Gold
• Cislosporine

39. Biological Drugs
• Anti-TNF-∝
– Etanercept
– Infliximab
– Adalimumab
– Certolizumab
– Glimumab
• Anti-B-cell therapy
– Rituximab
• Inhibitory of T-cell activator
– Abatacept
• Anti-IL6
– Tocilizumab
• Anti IL-1
– Anakinra

40. Surgery : Name of surgery
• Arthroplasty
• Arthroscopy
• Nerve release and decompression
• Synovectomy
• Hand and wrist surgery
Surgery for RA, may never be needed, but it can be an
important option for people with permanent damage that
limits daily function, mobility and independence. Joint
replacement surgery can relieve pain and restore function in
joints badly damaged by RA. The procedure involves
replacing damaged parts of a joint with metal and plastic
parts. Hip and knee replacements are most common.
However, ankles, shoulders, wrists, elbows, and other joints
may be considered for replacement.

41. Deformity
Deformity in the Hand
• Swan neck deformity(Hyper extension of PIP joints
with flexion of DIP joints)
• Z-deformity of the thumb
• Boutonniere or ‘Button hole deformity’(Flexion
contractures of the PIP joints and hyperextension of
the DIP jionts)
• Ulnar deviation of the fingers at the MCP joints
• Dorsal subluxation of ulna at the radio-ulnar joints
• Swelling of PIP joints –Fusiform or spindle shaped
swelling in early stage
• Mallet Finger

42. Deformity in the Foot
• Eversion of foot
• Dorsal subluxation of the metatarsaophalangeal
(MTP)joints results in ‘cock-up’ toe deformities
• Plantar subluxation of the metatarsal heads
• Hallux valgus
• Widening of the forefoot
• Lateral deviation of the toes
• Flat foot
Popliteal(Baker’s) cysts

52. Assessment/Evaluation
• Assessment of posture
• Testing muscle strength and power
• Measuring joint movement
• Gait analysis
• Functional test: such as balance, walking,
dressing toileting(etc.)

53. Treatment goals
• To protect joint environment from further
damages
• Provide pain relief
• Prevent deformity
• Prevent disability
• Increase functional capacity
• Improve flexibility and strength
• Encourage regular exercise
• Improve general fitness

54. Management
• Cold therapy for acute phases
Dosage 10-20min/1-2times a day
• Heat therapy for chronic phases
Dosage 20-30min/1-2 times a day

56. Exercise for acute phase
• Performed at least once a day
• Gentle assisted through normal range (Joint
mobilization)
• Isometric ‘static muscle contraction’ helps to
maintain muscle tone without increasing
inflammation

58. Exercise for chronic phase
• Can progress the above exercise to include use
light resistance.
• Postural/core stability exercise.
• Swimming/walking/cycling to maintain
cardiovascular fitness.
• Gentle stretches for areas that become tight,
such as knee and calves.

60. Regular exercise
• Maintain muscle strength is important for joint
stability and preventing injury.
• Muscle can become weak following reduced
activity.
• Pain signal from your nerves and swelling can
both inhibit muscles.
• Muscle can affected by prolonged positions &
immobilization and tightness can limit daily
activities.

62. Joint protection
• Try to avoid prolonged positions.
• Balance activity with rest periods rest should
come before you get fatigued or sore.
• Look at your work and home desk set up.
• During the acute phase activities such as stair
climbing can put stress through your knees
ankles and hip try to keep the number of trips
up and down minimum.

65. Alternative therapies
• THI CHI
• MUCIAL THERAPY
• YOGA THERAPY
• RELAXATION TECHNIQUE
• PILATES
(Ref: Senthilkumar Thiayagaran)