Rheumatoid arthritis is an autoimmune disease that causes inflammation, swelling, and pain in the joints. It affects approximately 1% of the world's population and 0.92% of the adult population in India. There are two main types - seropositive RA, where the body produces immune reactions to normal tissue, and seronegative RA, where tests for rheumatoid factor and anti-CCP antibodies are negative. Risk factors include age 40-60, family history, smoking, obesity, and female sex. Diagnosis involves evaluating symptoms, x-rays of affected joints, and blood tests for rheumatoid factor and anti-CCP antibodies. Treatment includes non-pharmacological therapies as well as drugs like

1. Dr. V.S.SWATHI
ASSISTANT PROFESSOR
Rheumatoid Arthritis

2. Definition
Rheumatoid arthritis is a long term, progressive
and disabling auto immune disease, causes
inflammation, swelling, and pain in and around
the joints and other body organs

3. Epidemiology
 In the world, Rheumatoid Arthritis is 1% and
annual incidence is 3 cases per 10,000
population
 In India, it affects about 0.92% of adult
population

4. Types
Seropositive RA
 Here there is positive results for Rheumatoid factor(R) and anti
cyclic citrullinated peptide(ACCP)
 Body produces immune reactions to normal tissue
 Chances of developing RA is four times greater if parents are
having RA
 80% of people who are having RA are with RF positive
Seronegative RA
 Here there is negative results for Rheumatoid factor(RF) and anti
cyclic citrullinated peptide(ACCP)
 RA is confirmed by other tests
Juvenile Idiopathic RA
 It is common in children younger than age 17
 Symptoms may be temporary and lasts for lifetime
 In severe conditions, it interferes with child growth and
development

5. Risk factors
 Age in between 40-60
 Family history of RA
 Environmental pollution
 Women
 Obesity
 Smoking

6. Etiology
 Abnormal expression of Human Leukocyte
Antigen gene-HLA DR4 and HLA DRB1 gene

7. Pathogenesis

8. Clinical Presentation
Early stages of disease
 Pain
 Stiffness (mostly in morning lasts for 30
minutes to several hours)
 Swelling
In metacarpophalangeal joints of fingers
In proximal interphalangeal joints of fingers
In interphalangeal joints of thumb
In metatarsophalangeal joints
In joints of wrist

9. Late stages of disease
 Boutonniere deformity of thumb
 Ulnar deviation of metacarpophalangeal joints
 Swan-neck deformity of fingers
Other manifestations
 Myalgia
 Fatigue
 Low grade fever
 Weight loss
 Depression

11. Complications
 Amyloidosis
 Carpal tunnel syndrome
 Episcleritis
 Felty’ s Syndrome
 Lymphadenopathy
 Nodules
 Osteoporosis
 Pericarditis
 Pleural and Pericardial effusion
 Scleritis
 Vasculitis
 Sjogren’ s Syndrome
 Cardiovascular Stroke
 Cervical myelopathy

12. Diagnosis
American Rheumatism Association (ARA) criteria for the
diagnosis of Rheumatoid Arthritis
 Morning stiffness in and around the joints for at least 6
weeks, lasting at least 1 hour before maximal improvement
 Swelling of 3/ more joints for at least 6 weeks
 Swelling of the wrist, metacarpophalangeal/ proximal
interphalangeal joints for at least 6 weeks
 Symmetric joint swelling for at least 6 weeks
 Hand X-ray changes typical of Rheumatoid arthritis that
must include erosions/ unequivocal bony decalcification
around the joints
 Rheumatoid subcutaneous nodules
 Positive rheumatoid factor
Interpretation: Presence of at least 4 of these indicators
diagnosis of Rheumatoid Arthritis

14. Disease Activity Score (DAS 28) using 28 joints
 Number of swollen joints out of a total 28 specified
joints
 Number of tender joints out of a total 28 specified
joints
 Erythrocyte sedimentation rate
 Patient’s interpretation of wellbeing with 0 being at
their best and 100 their worst
Interpretation:
 High disease activity: >5.1
 Moderate disease activity: 3.2-5.1
 Low disease activity: 2.6-3.2
 Remission: <2.6

15.  Anti cyclic citrullinated peptide antibody
(ACCP)
 Rheumatoid factor
 Antinuclear antibodies (ANA)
 Alkaline phosphatise
 Platelet count
 Serum albumin
 Neutrophils

16. Non Pharmacological
Treatment
 Patient education and counselling on risk
factors
 Stopping of alcohol and smoking
 Rest
 Occupational therapy
 Trancutaneous electric nerve stimulator
(TENS)
 Hydrotherapy
 Surgical interventions like Synovectomy and
Arthoplasty

18. TreatmentAlgorithm

19. Drugs used in treatment of Rheumatoid
Arthritis
Drug Category Mode of Action Dose Adverse effects
Aspirin NSAID Inhibit prostaglandin
synthesis
2.6-5.2g/day-PO  Angioedema
 Bronchospasm
 CNS alteration
 GI disturbances
 Renal damage
Diclofenac NSAID Inhibit prostaglandin
synthesis
150-200mg-PO  Abdominal
distension
 Dyspepsia
 Fluid retention
 Pruritis
 Nephrotoxicity
Prednisone Corticosteroids Inhibit inflammatory
reactions
Less than
10mg/day-PO
 Hypertension
 Decreased wound
healing
 Hirsutism
 Weight gain
 Glaucoma

20. Methyl Prednisolone Corticosteroids Inhibit
inflammatory
reactions
2-60mg/day-PO  Acne
 Decreased wound
healing
 Diabetes
 Edema
 Osteoporosis
Methotrexate DMARDs Inhibit cellular
proliferation
7.5-15mg/ week-
PO/IM
 Hyperurecemia
 Ulcerative
stomatitis
 Glossitis
 Leukopenia
 Thrombocytopenia
Hydroxychloroquine DMARDs Impair
complement
dependent antigen
and antibody
reactions
200-300mg- BD- PO  Irritability
 Aplastic anaemia
 Leukopenia
 Thrombocytopenia
 Alopecia
Sulfasalazine DMARDs Inhibit leukotriene
synthesis and
lipoxygenase
500mg-BD-PO  Anorexia
 Gastric distress
 Nausea
 Vomiting
 Headache

21. Leflunamide DMARDs Inhibit
proliferation of
cells
100mg/day for 3
days-PO then 10-
20mg/day
 Diarrhoea
 Respiratory infections
 Alopecia
 Hypertension
 Rash
Etanercept Biological
agents
Inactivates
Tissue necrotic
factor
50mg-weekly-SC  Infections
 Injection site
reactions
 Diarrhoea
 Rash
 Pruritis
Infliximab Biological
agents
Inhibits the
effective binding
of Tissue
necrotic factor
alpha with its
receptors
3m/kg-IV at 0,2,6
weeks then 8 week
 Development of Anti
nuclear antibodies
 Infection
 Infusion related
reactions
 Bronchitis
 Dyspepsia

22. Resources
 ncbi.nlm.nih.gov/pmc/articles/PMC5215647/
 https://www.ncbi.nlm.nih.gov/pmc/articles/PM
C3516026/
 https://www.ncbi.nlm.nih.gov/pmc/articles/PM
C5206883/
 https://www.ncbi.nlm.nih.gov/pmc/articles/PM
C4860498/
 https://www.ncbi.nlm.nih.gov/pmc/articles/PM
C5051257/