Rheumatoid arthritis diagnosis

3. There is no singular test for diagnosing rheumatoid
arthritis.
Instead, rheumatoid arthritis is diagnosed based
on :history & physical examination & investigations
RA is progressive, not benign.
Structural damage/disability occurs
within first 2 to 3 years of disease.
Slower progression of disease linked
to early treatment
The Importance of Early DiagnosisThe Importance of Early Diagnosis

4. 1.6 weeks of morning stiffness > 1 hr .
2.6 weeks of swelling of three or more joints .
3.6 weeks of swelling of wrist, MCP, PIP.
4.Symmetrical joint swelling.
5.X-ray changes that must include erosions or
unequivocal bony decalcification.
6.Rheumatoid nodules.
7.Positive serum rheumatoid factor.

7. Can do usual
activity ,discomfort
or limited mobility
of 1-3 joints.

8. •Are made after a full medical and family history
and physical and diagnostic testing.
•Medical testing may include a wide variety of tests
like:-
• ESR
•CRP
•RF
•ANA (Anti nuclear antibodies)
•Joint x-rays
•MRI (Magnetic resonance imaging) & US (ultra sound)
Inflammatory
markers

9. Anti cyclic citrullinated peptide (CCP):
has been found to be more specific than
rheumatoid factor in rheumatoid arthritis
And high titer anti-CCP may predict aggressive
erosive disease
Antinuclear antibody: positive in systemic
lupus erythematosus (SLE) and related
conditions; also in up to 30% of rheumatoid
arthritis patients and weakly positive in up to
10% of the normal population.
CONTD….

10. •C-Reactive protein
–Correlates with disease activity and radiologic
progression
–One of the most responsive acute phase reactants
–Can be elevated in many non-RA related
diseases
•Erythrocyte sedimentation rate
–Influenced by non-acute phase response factors
–Can be elevated in many non-RA related
diseases

11. Is an autoantibody that is present in the blood
of most people with RA (75-80%)
 Directed against host immunoglobulin

(is positive in no more than 5 percent of patients
without rheumatoid arthritis).
Repeat 6-12 months following disease onset if
negative

12. Liver function tests… mild elevation of alkaline
phosphatase and .Low serum albumin .
CBC…normochromic normocytic or Microcytic anemia .
Hemoglobin slightly decreased; hemoglobin averages
around 10 g/dL .Platelets & WBCs Usually increased.
Urinalysis … Microscopic hematuria or proteinuria
may be present, indicat connective tissue diseases.
Joint fluid … to rule out other diseases; 5,000 to
25,000 WBC with polymorphonuclear leukocytes .
cultures are negative, there are no crystals, and fluid
glucose level typically is low.

13. X-ray change
•Loss of joint space
•Soft tissue swelling
•Bony decalcification
•Erosions
•Peri-articular osteoporosis
X-Ray of both hands and wrists and feet for
suspected RA.
MRI it is more sensitive to detect RA change.

15. •Social factors
–Low socioeconomic status
–Less education
–Psychosocial stress
–female sex
•Physical factors
–Extra-articular manifestations
–Elevated CRP and ESR
–High titers of RF
–early Erosions on x-ray
–Duration of disease

16. •Goals of Treatment
•Relieve pain
•Reduce inflammation
•Slow down or stop joint damage
•Maintaining the ability to function in daily
activities, improving the quality of life.
• Current Treatment
•Non - pharmacological
•pharmacological
•Surgery
•Routine monitoring and ongoing care.

17. •Physiotherapy is a vital part of treating RA may be
useful in decreasing the symptoms of RA.
•program of exercise strengthens joints & minimize
deformity and increase the range of movement and
functions.
•Natural treatments include using massage with
herbs, magneto therapy etc..
•Occupational therapy can give advice to do every
day activities with less pain or advice on how to use
splints, skills training.
•Weight loss & Smoking cessation

18. •Analgesics
used only for pain relief

E.g.:- Oral
Paracetamol
Topical
Capsaicin
Diclofenac

19. •NSAID’s
•used as an adjunct along with DMARD’s to reduce the
inflammation and pain
•Effective reduction in swelling.
•Improves mobility, flexibility, range of motion
•Ineffective in Erosive disease
NSAID’S act by inhibiting COX-1 &2 & thus reduces
inflamation

- GI toxicity – ulcer -Nephrotoxicity
- Hepatotoxicity -Bleeding
-Aseptic meningitis

21. •DMARD,s (disease modifying anti-rheumatic
drugs)
• used to slow down the progression of disease.
E.g. Methotrexate once weekly Oral or IM
& Sulfasalazine
Advantages of DMARDs
•Slow disease progression
•Improve functional disability
•Decrease pain
•Interfere with inflammatory processes
•Retard development of joint erosions

24. Alkylating agent .
-Alopecia -Nausea
-Infertility -Infection
-BM suppression (pancytopenia)
-Renal: hemorrhagic cystitis, bladder
malignancy

25. •Combination DMARD regimen
-Does not increase toxicity levels
-long-term outcome more favorable
-Superior efficacy to single-DMARD regimen
•Possible combinations
–Methotrexate/sulfasalazine/hydroxychloroquine
–Cyclosporine/methotrexate
–Leflunomide/methotrexate

26. Biologic DMARD’s
genetically engineered medications that reduce
inflammation and structural damage to the joints.

Include:
TNFα antagonists:
Adalimumab, Etanercept , Infliximab
Interleukin-1 antagonist
Anakinra
Suppress T-Cell activation
Abatacept
Anti B-Cell monoclonal antibody
Rituximab

27. Anti-inflammatory block TNF-α (proinflammatory
cytokine) Improves Clinical Signs & Symptoms

-Etanercept- 50mg SC weekly
-Infliximab - 3mg/kg IV
-Adalimumab - 40mg SC
-Infection -Reactivated TB
-Pancytopenia -Autoantibody/SLE-like
-Exacerbate CHF -Malignancy- lymphoma

28. Active Hepatitis B Infection
Multiple sclerosis, optic neuritis
Active serious infections
Chronic or recurrent infections
Current neoplasia
History of TB or positive PPD (untreated)
Congestive heart failure (Class III or IV)

29. Early appropriately aggressive intervention
in patients with inflammatory arthritis:
critical to best possible outcome.
The combination of a biologic plus MTX is
frequently more effective than either agent
alone.

30. •Early and aggressive disease control
–Rheumatologist Referral
•Early/Undiagnosed: NSAIDs, short course
Corticosteroids
•Late/Uncontrolled: DMARD therapy
–depends on the presence or absence of joint
damage, functional limitation, presence of
predictive factors for poorer prognosis

31. Diagnosis
•Establish early diagnosis of RA
•Document baseline disease activity and
damage
•Estimate prognosis of patient
Initiate therapy
•Patient education
•Physical/occupational therapy
•Consider NSAID and/or local or low-dose steroids
•Start disease-modifying agent within 3 months
Subjective criteria
Physical exam
Laboratory tests
Radiography
Periodically assess disease
activity

32. Periodically assess disease
activity
Inadequate response
(ongoing disease activity)
Adequate response with
disease activity
Methotrexate response
Methotrexate Other
monotherapy
Suboptimal methotrexate response
Combination
therapy
Biologics
Change or add disease-modifying drugs