Rheumatoid arthritis (RA) is a chronic inflammatory disease that causes pain, stiffness, and swelling in the joints. It is characterized by symmetrical inflammation of multiple joints. RA affects around 1-3% of the population worldwide and is three times more common in women than men. While the cause is unknown, genetics and environmental factors are thought to play a role. Treatment involves medications like DMARDs and biologics to reduce inflammation and prevent joint damage, with the goals of relieving pain, controlling disease activity, and improving function. Poor prognostic factors include persistent active disease, early or late age of onset, high rheumatoid factor levels, and presence of rheumatoid nodules or systemic symptoms.

1. ‫الرحيم‬‫الرحمن‬ ‫هللا‬ ‫بسم‬
Rheumatoid Arthritis
(RA)

2. RA
 Is a chronic systemic inflammatory disease of
unknown etiology & is considered the
commonest inflammatory arthritis.
Characterized by:
1. Symmetrical inflammatory polyarthritis.
2. It has extra articular features
3.Progressive joint damage causing severe
disability.

3.  RA is a worldwide disease affects all racial & ethnic
groups
 Affects 1-3% of population
 Female: male is 3:1
 Females have more articular disease and males have
more systemic presentations.
 Age range is 10 – 70y. ( starts 30- 40y)
 5-10% having family history & 70% have
HLADR4.
Epidemiology

4. Genetics
 1st-degree relatives have 1.5 fold higher risk than
the general population
 Twins show heritability of 60%
 HLA-DR4 person has increased relative risk 4–5
times.

5. Etiology & Pathogenesis
 The cause is unknown & said to be an autoimmune disease
 Multifactorial ( i.e. Genetic, environment…)
 Cytokines , growth factors , tumor necrosis factors &
metalloproteases have a role .

8.  Commonly affected joints are MCPs, PIPs, wrists, MTPs & larger
joints.
 Might starts with few joints then progress& become symmetric.
 Monoarticular is not uncommon
 ( episodic)
 Thoracolumbar , sacroiliac & DIP joints are very rarely involved.
 It has systemic manifestations, extra aricular features.
Clinical Features

9. Symptoms
 Joint pain ( More in the morning & might disturb the
sleep).
 Morning stiffness. Is a prominent feature , often lasts
>= 1 hour
 General symptoms:
weight loss
fever
fatigue, malaise
depression
reduced muscle strength and cachexia
the presence of a fever of >38.3°C at any time during the clinical
course should raise suspicion of systemic vasculitis or infection.

10. Progression of the disease will lead joint
destruction resulting in:
limitation of joint motion
instability
sublaxation &
deformities
Non articular symptoms e.g. carpal tunnel
syndrome.
Signs
 Swelling, Warmth,Limitation of movements, Deformities,
Nodules

11. Hand deformities
 Radial deviation at wrist
 Ulnar deviation at MCP joints
 Swan neck deformity ( hyperextension at PIPs)
 Boutonniere deformity( flexion at PIPS) or
called Z deformity.
• Feet deformities are like those occur in hands

13. The knees
Synovial effusion
Deformities( valgus, varus &/ or flexion )
Bakers cyst in popliteal fossa which may repture.
( sudden onset of pain & swelling in calf and ankle)
diagnosed by US. & arthrogram.

14. Feature
Manifestation of
RA
Neuropathy Vasculitis
Tendon rupture Tenosynovitis
Ulcers Vasculitis
Anemia/leukopenia Felty's syndrome
Severe backache Discitis
Pulmonary
insufficiency
Pleuritis
Pneumonitis
Pleural effusion
Cardiac insufficiency Pericarditis
Carditis mitral
regurgitation
Renal dysfunction Vasculitis
Proliferative
glomerulonephritis
Gastrointestinal
symptoms
Vasculitis
Liver and spleen
abnormalities
Feltys syndrome
Sjögren's
syndrome
Headache C1-2 subluxation
Eye involvement Scleromalacia
Scleritis
Episcleritis
(nodules,
vasculitis)
SYSTEMIC MANIFESTATIONS

15. Commonly Associated Conditions
 Sjögren syndrome
 Feltys syndrome(splenomegaly, neutropenia,
nodular RA)
 Amyloidosis
 infections
 lymphomas
 Renal and cardiovascular disease

16.  American Rheumatic Association Criteria for the
diagnosis of RA (any 4 of the followings):
1. Morning stiffness for> one hour.
2. Swelling of 3 or more joints( arthritis).
3. Swelling of hand joints ( PIPs , MCPs & wrist ).
4. Symmetrical polyarthritis.
5. Subcutaneous nodules.
6. Serum rheumatoid factor.
7. Radiological changes ( erosion ).
 The duration of (1,2,3,4) for 6 weeks or more.
Diagnosis

17. Diagnostic Tests & Interpretation
Initial lab tests
 Hematocrit: Mild anemia, leucopenia (may be leucocytosis) &
thrombocytosis.
 ESR: Usually elevated
 C-reactive protein: Unspecific
 Rheumatoid factor (RF): >1:80 in 70–80% of patients with RA (most
commonly IgM Ab):
 Doesn’t correlate with disease activity but with extra articular manifistations
 Anticyclic citrullinated peptide antibodies (Anti-CCP antibodies) are
highly specific and present early( Linked to erosive RA).
 Anti-MCV assay (antibodies against mutated citrullinated Vimentin).
 Recently a serological point-of-care test (POCT) for the early detection of
RA has been developed. This assay combines the detection of rheumatoid
factor and anti-MCV for diagnosis of RA and shows a sensitivity of 72%
and specificity of 99.7%.
 Antinuclear antibody: Present in 20–30%
 Electrolytes, creatinine, liver function, urinalysis to assess comorbid states.

18. Follow-Up & Special Considerations
RF is not useful for monitoring
course of illness.
Radiographs of the hands, wrists, and
feet can be repeated to follow disease
progression.

19. Imaging
 Radiographic abnormalities are very useful in the
diagnosis and treatment.
 Periarticular osteopenia is the earliest change.
 Juxta-articular bone erosions
 Symmetrical joint space narrowing.
 CT/MRI and ultrasound are useful in cervical-spine
symptoms or detection of early joint erosions.
 Bone scan if suspected aseptic necrosis

21. Diagnostic Procedures
Synovial fluid:
No pathognomonic findings
Yellowish-white, turbid, poor viscosity
WBC increased (3,500–50,000)
Protein: ∼4.2 g/dL (42 g/L)

22. Goals:
Relieving pain
Controlling disease activity
Improving function
Preventing or correcting impairments
Treatment

23. First Line Medication
Nonbiologic DMARDs:
 DMARDs within 2 months of diagnosis if patient has ongoing
active disease despite appropriate dose of aspirin or other
NSAIDs.
 Offer proton pump inhibitors (PPIs) for chronic NSAID therapy
 Nonbiologic DMARD: Methotrexate, sulfasalazine, or
leflunomide
 low-dose corticosteroids + NSAIDs to maximize symptoms
management.

24. Biological DMARDs:
 Tumor necrosis factor (TNF) inhibitors: infliximab , adalimumab
and etanercept. Check TB prior to treatment and periodic CBC,
Risk of lymphoma, CHF.
 Anakinra : an IL-1 receptor antagonist
 Abatacept and rituximab : for active moderate to severe RA with
inadequate response to other DMARDs or failed anti-TNF agent.
 Two long-acting anti-TNF agents, Certolizumab and golimumab,

25. Older Nonbiologic DMARDs
Have been abandoned in developed countries
for the treatment of RA: Injectable gold,
D-Penicillamine, Cyclosporine, &
Azathioprine.

26. Second Line
 Intra-articular steroids: If disease is well
controlled except for a single joint or two,
after establishing that the joint is not
infected
 Hyaluronate: Hyaluronic acid , for pain
relief; exact role in RA is unclear.

27. Pregnancy Considerations
 Use effective contraception with (DMARDs)
 Modify regimen with pregnancy or breast-
feeding.
 >75% improve during pregnancy, but relapse
in 6 months.
 1st episodes may occur in pregnancy

28. Additional Treatment:
 Surgical treatment: synovectomy, tendon
reconstruction, and joint replacement.
 Encourage full activity, but avoid heavy work
or exercise during active phases.
Patient Monitoring
• Evaluate for osteoporosis,
• Cardiovascular disease due to accelerated
atherosclerosis.

29. Prognosis
Poor prognostic findings:
 Persistent moderate-to-severe disease
 Disease onset at early or advanced age
 High titre rheumatoid factor
 Rheumatoid nodules.
 Systemic manifestations
 Presence of HLADR4.