Rheumatoid Arthritis

1. Rheumatoid Arthritis

2. Introduction & Definition
• Rheumatoid arthritis is a complex condition that is characterised by
chronic inflammation in the synovial membrane of affected joints, often
with systemic manifestations.
• chronic inflammation of the synovial membrane of affected joints
ultimately leads to loss of daily function due to chronic pain and fatigue.
• The majority of patients also have deterioration of cartilage and bone
in the affected joints, which may eventually lead to permanent disability.

3. • The most common cause of chronic inflammatory joint
disease
• Most typical features:
a.
b.
c.
d.
A symmetrical polyarthritis and tenosynovitis
Morning stiffness
Elevation of the erythrocyte sedimentation rate (ESR)
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.

4. Epidemiology
• Affects 1 – 3% of the population world wide
• No statistics available for Uganda
• With a peak prevalence between the ages of 30 and 50 years
• Women are affected 3 or 4 times more commonly than men
• Rheumatoid arthritis is associated with increased morbidity
and mortality.

5. Ep’d cont’d
• The prevalence increases with age, and sex differences diminish in the
older age group.
• RA is seen throughout the world and affects all races.
• However, the incidence and severity seem to be less in rural sub-Saharan
Africa and in Caribbean blacks.
• The onset is most frequent during the fourth and fifth decades of life,
with 80% of all patients developing the disease between the ages of 35
and 50

6. causes
• A genetic predisposition.
• For example, severe RA is found at approximately four times the
expected rate in first degree relatives of individuals with disease
associated with the presence of the autoantibody, rheumatoid factor;
approximately 10% of patients with RA will have an affected first-
degree relative.
• Moreover, monozygotic twins are at least four times more likely to be
concordant for RA than dizygotic twins, who have a similar risk of
developing RA as non twin siblings.
• Others think its interplay of both genetic and environmental factors

7. 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

8. PATHOLOGY
STAGE 1 – pre-clinical
 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.

9. PATHOLOGY
STAGE 2 – synovial
 Early changes are:
a.
b.
c.
Vascular congestion with new blood vessel formation
Proliferation of synoviocytes
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.

10. PATHOLOGY
STAGE 3 - destruction
 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.

11. PATHOLOGY
STAGE 4 – deformity
 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.

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

13. CLINICAL FEATURES

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

15. CLINICAL FEATURES

16. CLINICAL FEATURES
 More later (DEFORMITY)
I.
II.
Pain, deformity, instability, decreased ROM
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

18. CLINICAL FEATURES

19. CLINICAL FEATURES

20. EXTRA ARTICULAR FEATURES
• Rheumatoid nodules
• Sjögren’s syndrome is seen in 10% to 15% of patients with RA.
Sjögren’s syndrome can occur by itself or in conjunction with other
arthritic disorders such as RA and systemic lupus erythematosus
(SLE).
• Affected patients have diminished lacrimal and salivary gland secretion,
leading to a dry mouth; burning, itchy eyes with decreased tearing; and
photosensitivity
• Felty syndrome occurs most commonly in patients with severe,
nodule-forming RA. It is characterized by splenomegaly and
leukopenia.

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

23. DIAGNOSIS
• Heamatological
• Rheumatoid Factor; Positive in 80% of adults
• ESR and C-reactive protein (CRP) are general indicators of active
inflammation.
• An increase in antinuclear antibody (ANA) titers is also seen in some
RA patients.
• Testing for the anti-citrullinated protein antibody (ACPA) is another
important diagnostic test for RA.
• Levels of ACPA are more specific than those of RF for RA and in some
cases may allow for an earlier and more accurate diagnosis
• FBC, WBC, HB
• Synovial fluid analysis

24. IMAGING

25. CLASSIFICATION

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

27. 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

28. 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

29. MEDICATION
4. Disease Modifying Antirheumatic Drugs (DMARD)
 There are used with NSAIDs and/or prednisolone to slow joint
destruction
injectable
caused
gold,
by RA over time. Examples are methotrexate,
chloroquine,
penicillamine, azathioprine,
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 – AImmunoadsorption Therapy
 This is not a drug, but a therapy that filters the blood to remove
antibodies and immune complexes that promote inflammation

30. MEDICATION
4. Disease Modifying Antirheumatic Drugs (DMARD)
 There are used with NSAIDs and/or prednisolone to slow joint
destruction
injectable
caused
gold,
by RA over time. Examples are methotrexate,
chloroquine,
penicillamine, azathioprine,
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 – AImmunoadsorption Therapy
 This is not a drug, but a therapy that filters the blood to remove
antibodies and immune complexes that promote inflammation

31. 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)

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

33. Nursing Diagnosis
• Impaired Physical mobility related to pain, stiffness and deformity of joints
• Chronic pain related to inflammation, misuse of joints, innefective pain
measures or comfort.
• Disturbed body image related to disease process, deformities, long term
treatment, stiffness and inability to do usual activities
• Nsg mgt
• Analgesia/Antinflammatory drugs
• Rest
• Joint protection from stress, reduce on weight bearing activities on affected joint
• Pyschosocial support
• Heat & cold therapy
• Passive/active exercises