Rheumatoid Arthritis

1. RHEUMATOI
D
ARTHRITIS
A U D I H U S N A A F F A N
C h r o n i c , p r o g r e s s i v e , i n f l a m m a t o r y
j o i n t d i s e a s e

2. INTRODUCTION
 The most common cause of chronic inflammatory joint disease
 Most typical features:
a. A symmetrical polyarthritis and tenosynovitis
b. Morning stiffness
c. Elevation of the erythrocyte sedimentation rate (ESR)
d. Appearance of autoantibodies that target immunoglobins in the serum
 It is a systemic autoimmune disease and changes can be widespread in a
number of tissues of the body
 RA tend to die younger than their peers as a result of the effects of chronic
inflammation on a number of organ systems
 Chief among these is early ischemic heart disease secondary to the effects of
inflammation on the cardiovascular system.

3. EPIDEMIOLOGY
 Affects 1 – 3% of the population world wide
 With a peak prevalence between the ages of 30 and 50 years
 Women are affected 3 or 4 times more commonly than men

4. CAUSES
 Important factors in the evolution of RA are:
a. Genetic susceptibility
b. An immunological reaction; possible involving a foreign antigen,
preferentially focused on synovial tissue
c. An inflammatory reaction in joints and tendon sheaths
d. The appearance of rheumatoid factors in the blood and synovium
e. Perpetuation of the inflammatory process
f. Articular cartilage destruction

5. PATHOLOGY
 RA is a systemic disease but the
most characteristic lesions are seen
in the synovium or within
rheumatoid nodules.
 The synovium is engorged with new
blood vessels and packed full of
inflammatory cells

6. PATHOLOGY
 Before RA becomes clinically apparent the immune pathology is already
beginning.
 Raised ESR, C-reactive protein (CRP), and RF may be detectable years
before the first diagnosis.
STAGE 1 – pre-clinical

7. PATHOLOGY
 Early changes are:
a. Vascular congestion with new blood vessel formation
b. Proliferation of synoviocytes
c. Infiltration of the sub synovial layers by polymorphs, lymphocytes and
plasma cells.
 There is thickening of the capsular structures, villous formation of the
synovium and a cell-rich effusion into the joints and tendon sheath.
STAGE 2 – synovial

8. PATHOLOGY
 Persistent inflammation causes joint and tendon destruction.
 Articular cartilage is eroded.
 At the margins of the joint, bone is also eroded by granulation tissue invasion
and osteoclastic resorption.
 Similar changes occur in tendon sheaths, causing tenosynovitis.
 Partial or complete rupture of tendons.
 Swelling of the joints, tendons and bursae.
STAGE 3 - destruction

9. PATHOLOGY
 Combination of articular destruction, capsular stretching and tendon rupture
leads to progressive instability and deformity of the joints.
 The inflammatory process usually continues but the mechanical and
functional effects of joint and tendon disruption now become vital.
STAGE 4 – deformity

10. CLINICAL FEATURES
 Early feature (synovitis)
I. Most commonly affected MCPJ and PIPJ, wrist, tendon sheaths around
the joints (wrist – feet – knee – shoulder)
II. Bilateral symmetrical polysynovitis
III. Pain, fusiform swelling, stiffness, loss of mobility
IV. Constitutional symptom:
a. LOA, LOW, malaise and low grade fever
b. Tenosynovitis

11. CLINICAL FEATURES

12. CLINICAL FEATURES
 Late feature (DESTRUCTIVE)
I. Spread to other joint – wrist, ankle, knee, shoulder (in order of frequency)
II. Morning stiffness (more than 30 min) – improve with activity
III. Activity of daily living will be affected – quality of life affected

13. CLINICAL FEATURES

14. CLINICAL FEATURES
 More later (DEFORMITY)
I. Pain, deformity, instability, decreased ROM
II. Joint deformity – movement restricted and painful
 Thumb – Z-deformity
 Fingers – Swan neck deformity/ Boutonniere’s deformities, ulnar
deviation
 Wrist – radial and volar displacement
 Elbow – limited extension
 Shoulder - limited abduction
 Knees – swollen, flexion an vulgus
 Toes – clawed

15. CLINICAL FEATURES

16. CLINICAL FEATURES

17. CLINICAL FEATURES

18. DIAGNOSIS
 Mostly clinical:
I. Bilateral, symmetrical
polyarthritis
II. Involving proximal
joints of hand or feet
III. Present for at least 6
weeks
IV. Confirmed with
subcutaneous nodules
or periarticular
erosions on x-ray

19. CLASSIFICATION
E U L A R R H E U M ATO I D A R T H R I T I S C L A S S I F I C AT I O N C R I T E R I A

20. INVESTIGATION
H E M ATO LO G I C A L
1. FBC- normocytic hypochromic anaemia (due to abnormal erythropoiesis
from chronic inflammation), WBC
2. Inflammatory markers- ESR, CRP elevated (its use as indication of
disease progression monitoring, treatment response)
3. Rheumatoid factor(RF)- anti-IgG auto Ab 80% will have it
4. Anti- cyclic citrullinated peptide(CCP) Ab

21. INVESTIGATION
J O I N T A S P I R AT I O N

22. INVESTIGATION
I M A G I N G
 For disease monitoring, treatment response.
 EARLY STAGE(SYNOVITIS)
Soft tissue swelling, periarticular osteopenia
 LATER STAGE(DESTRUCTIVE)
Juxta- erosions, narrowing of joint space
 ADVANCE STAGE(DEFORMITY)
Articular destruction and joint deformity

23. INVESTIGATION
I M A G I N G

24. MANAGEMENT
 There is no cure for rheumatoid arthritis
 Aim to delay the progression of the disease, alleviate symptoms, reduce
functional limitation
 Supportive and palliative

25. MEDICATION
1. NSAIDs
 Ibuprofen, indomethacin, COX-2 inhibitors like celecoxib and
valdecoxib (reduce inflammation and relieves pain)
2. Analgesics
 Morphine and acetaminophen (reduce pain)
3. Glucocorticoids or prednisolone
 Prescribed in a small dose to slow joint damage caused by inflammation

26. SURGERY
 Improve quality of life
 Synovectomy
When one or two joints are affected more severely than others, this
procedure is used to reduce the amount of inflammatory tissue by removing
the diseased synovium or lining of the joint. It may result in less swelling
and pain and the slowing or prevention of further joint damage
 Arthroscopic Surgery
Thin tube with a light at the end inserted into the joint through a small
incision. It is connected to a closed-circuit television and we can see the
extent of the damage in the joint. Tissue samples taken, remove loose
cartilage, repair tears, smooth a rough surface or remove diseased synovial
tissue. It is most commonly performed on the knee and shoulder

27. MEDICATION
4. Disease Modifying Antirheumatic Drugs (DMARD)
 There are used with NSAIDs and/or prednisolone to slow joint
destruction caused by RA over time. Examples are methotrexate,
injectable gold, penicillamine, azathioprine, chloroquine,
hydroxychloroquine, sulfasalazine and oral gold.
5. Biologic Response Modifiers
 These drugs directly modify the immune system by inhibiting proteins
called cytokines, which contribute to inflammation. Examples of these
are abatacept, etanercept, infliximab, adalimumab, and anakinra.
6. Protein – A Immunoadsorption Therapy
 This is not a drug, but a therapy that filters the blood to remove
antibodies and immune complexes that promote inflammation

28. SURGERY
 Osteotomy
Literally meaning, “to cut bone,” this procedure is used to increase stability by
redistributing the weight on the joint. Osteotomy isn’t often used with RA
because there are other options available besides cutting the bones.
 Joint Replacement Surgery or Arthroplasty
This is the surgical reconstruction or replacement of a joint. Successfully used
to help people who otherwise might be in a wheelchair, joint replacement
surgery involves the removal of the joint, resurfacing and relining of the ends of
bones and replacing the joint with a man-made component. This procedure is
usually recommended for people over 50 or who have severe disease
progression. Typically a new joint will last between 20 and 30 years
 Arthrodesis or fusion
This procedure fuses two bones together. While it limits movement, it does
decrease pain and increase stability of the joints in the ankles, wrists, fingers,
toes and spine.

29. TREATMENT
• Onset of disease
o NSAIDs/analgesic
o Exercise
• Early ( 1st 6-12 month )
o NSAIDs, analgesic, low dose corticosteroid
o Disease modifying drug
o Physiotherapy
o Splintage
• Progressive erosive (1-5 years)
o Disease modifying drug
o Splintage
o Surgical management ( synovectomy, arthroscopic surgery ), late ( 5-20 years)
o Reconstructive surgery ( arthrodesis, osteotomy, arthroplasty)

30. COMPLICATION
 Fixed deformities
 Muscle weakness
 Infection
 Spinal cord compression
 Systemic vasculitis
 Amyloidosis- Renal failure