RHEUMATOID ARTHRITIS
BY: DR. AYOOLA T.S
 INTRODUCTION/DEFINITION
 EPIDEMIOLOGY
 PATHOPHYSIOLOGY
 ETIOLOGY
OUTLINE
 PRESENTATION
 DIAGNOSIS/DIFFERENTIALS
 TREATMENT
 COMPLICATIONS
 CONCLUSION
 Arthritis is a broad term that simply means joint
inflammation.
 It includes swelling, pain, and stiffness of any of the joints.
INTRODUCTION
/DEFINITION
 Rheumatoid arthritis is one of the seropositive forms of
arthritis and is a chronic, systemic inflammatory disease and
is usually characterised by symmetric, deforming
polyarthritis that affects the hands and feet.
 Can affect any joint lined by a synovial membrane but less
commonly affects large joints.
 RA is theorized to develop when a genetically
susceptible individual experiences an external trigger
e.g. trauma, infection, that triggers an autoimmune
reaction.
 They have a 2-3 fold increased risk of developing
cardiovascular disease.
 Incidence: Worldwide, annual incidence rate of RA is
approx. 3 cases per 10,000 population.
 Prevalence: Roughly 1%. Increases in smokers.
EPIDEMIOLOGY
 Age: Affectation peaks between the ages of 35 and 50
years.
 Sex distribution: Women more commonly affected than
men (3:1)
 Ethnic groups: Affects all populations, however, much
more prevalent in the Native American group and less
prevalent in black persons from the Caribbean region.
 First-degree relatives of individuals with RA are at a 2-3
fold higher risk for the disease.
 Concordance rate in monozygotic twins is approx. 1520%.
 Associated with HLA -DR4 and HLA-DR1 which serves
as a pointer to disease severity.
 Pathogenesis not fully understood.
 An external trigger that sets off an autoimmune
PATHOPHYSIOLOGY
reaction, leading to synovial hypertrophy and chronic
joint inflammation along with the potential for extraarticular manifestations, is theorised to occur in
genetically susceptible individuals.
 The onset of clinically apparent RA is preceded by
periods of pre-rheumatoid arthritis(pre-RA).
 Phases in the development and progression of pre-RA
to RA include:
• Phase I – Interaction of genetic and environmental risk
factors.
• Phase II – Production of RA autoantibodies such as
Rheumatoid factor (RF) and anti-cyclic citrullinated
peptide (anti-CCP).
• Phase III – Development of arthralgia or joint stiffness
without any clinical evidence of arthritis.
• Phase IV – Development of arthritis in one or more joints
(if intermittent, it is termed palindromic rheumatism).
• Phase V – Established RA.
Synovial cell
hyperplasia
and
endothelial
cell activation
Uncontrollable
inflammation
Destruction of
bones,
cartilages,
ligaments,
tendons, blood
vessels.
Genetic
Environmental
ETIOLOGY
Infectious
Hormonal
Immunologic
 Typical presentation involves symmetrical swollen,
painful and stiff small joints of the hands and feet,
usually worse in the morning.
 Affectation of the large joints (less common)
PRESENTATION
 Less common presentations include:
• Sudden-onset widespread arthritis
• Recurring mono/polyarthritis of various joints
(palindromic)
• Persistent monoarthritis (knee, shoulder, hip)
• Polymyalgic onset – vague limb girdle aches.
• Recurrent soft tissue problems e.g. frozen shoulder,
carpal tunnel syndrome, de Quervain’s tenosynovitis.
 Signs
 Can be classified into early and late
 Early signs are signs of inflammation with no joint
damage e.g. swollen joint, painful joints but joint
architecture is preserved.
 Late signs - They include:
• Ulnar deviation
• Subluxation of the wrist and fingers
• Boutonierre (buttonhole) deformity
• Swan neck deformity
• Z deformity
• Hand extensor tendon rupture
• Atlanto-axial subluxation (rare, causing cord
compression syndrome)
Boutonierre’s
deformity
Ulnar deviation
Swan neck
deformity
Z deformity
 EXTRA-ARTICULAR MANIFESTATION
 Affects about 40% of patients. They include:
I. Nodules: Found in the olecranon process, proximal ulna, back
of the heel, occiput, ischial tuberosity are common sites.
II. Lungs: Pleural disease, Interstitial fibrosis, Bronchiolitis
obliterans, Organising pneumonia
III. CVS: IHD, Pericarditis, Pericardial effusion
IV. Ocular: Episcleritis, Scleritis, Scleromalacia,
Keratoconjuctivitis sicca
V. Others: Osteoporosis, Carpal tunnel syndrome, peripheral
neuropathy, Felty syndrome (RA, Splenomegaly,
Neutropaenia)
 Investigative workup for patients suspected to have RA
include:
Laboratory studies
• Serology
 Rheumatoid factor assay: +ve in 60-80% of patients, non-specific for
RA. Predicts radiographic progression of bone erosions.
 Anticyclic citrullinated peptide (anti-CCP) antibody: Highly
DIAGNOSIS
specific (>98%) with sensitivity of about 80%. Used to predict
disease progression.
 Anti-mutated citrullinated vimectin (anti-MCV) antibody:
Comparable sensitivity with anti-CCP antibody but lower
specificity
 Antinuclear antibody (ANA) assay: Present in about 40% of patients.
• Haematology
 FBC: Anaemia of chronic disease, thrombocytosis
 Elevated ESR
 Elevated CRP
Radiographic studies
• Xray: Juxta-articular osteopaenia, soft tissue
sweeling, reduced joint space.
• MRI: Used primary in patients with abnormalities of
the cervical spine.More accurate assessment and
early detection of lesions.
• Ultrasonography: Recognition of effusion and cysts,
visualization of tendon sheaths, changes and
degree of vascularization of synovial membrane,
and erosions.
 According to the 2010 ACR/EULAR diagnostic criteria:
 Rheumatic fever
 SLE
 Degenerative joint disease
DIFFERENTIALS
 Gouty arthritis
 Pyogenic arthritis
 Polymyalgia rheumatica
 Lung and gastric carcinomas, causing hypertrophic
pulmonary osteoarthropathy
 Treatment options include:
TREATMENT
i.
Pharmacologic therapy
ii. Non-pharmacologic therapy
 PHARMACOLOGIC THERAPY
 Aimed at retarding disease progression and inducing
disease remission
 Pharmacological agents used include:
• NSAIDS e.g. Celecoxib, Diclofenac, Naproxen, Piroxicam
• Corticosteroids
• Disease Modifying Anti-Rheumatoid Drugs (DMARDs)
 DMARDs
 Divided into:
a. Non-biologics e.g. Methotrexate, Hydroxychloroquine,
Sulfasalazine, Leflunomide, Azathioprine, Cyclosporin
b. Biologics
a. TNF-∝ inhibitors: Etanercept, Infliximab, Adalimumab
b. 𝛽-cell depleters: Rituximab
c. IL-1 and IL-6 inhibitors: Tocilizumab, Anakinra
d. T-cell stimulation inhibitors: Abatacept
 DMARDs are first-line agents but they are commenced
after 3 months of NSAID use with no improvement.
 For early RA <6 months, administer DMARD
monotherapy in atients with low-high disease activity.
 If disease activity remains moderate/high despite
monotherapy, use combination DMARDs or a biologic
agent.
 For established RA, combination DMARDs < anti-TNF
biologic < non-TNF biologic < Tofacitinib
 NON-PHARMACOLOGICAL THERAPY
 Exercise
 Diet
 Counselling
 Heat and cold therapy
 Physiotherapy
 Occupational therapy
 Surgery
 Anaemia
 Infections
 GI problems
 Osteoporosis
COMPLICATIONS
 Pulmonary fibrosis
 Ischaemic heart disease
 Sjogren syndrome
 Felty syndrome
 Lymphomas and other cancers.
 Rheumatoid arthritis is a chronic, systemic inflammatory disease
and is usually characterised by symmetric, deforming polyarthritis
that affects the hands and feet.
 Specific cause is unknown but it is theorised to be brought on by
an interplay among genetic, environmental, immunologic,
hormonal and infectious factors.
 There are articular and extra-articular manifestations of the
CONCLUSION
disease.
 Treatment options include pharmacologic and non-pharmacologic
approaches.
 DMARDs are the mainstay of treatment.
 Prognosis depends largely on disease progression and effective
management.