rheumatoid arthritis modern point of view

systemic disease, bilateral symmetry

1. DR VEENU YADAV
MD KAYACHIKITSA
RHEUMATOID ARTHRITIS

2. •Long -termautoimmune disorder
•Disease of joints
•Destructive disease
•Progressive
•Symmetrical
•Peripheral polyarthritis

3. Aetiological factors
•Genetic- HLADR3 and HLADR4
•Environment
•Smoking
•Silica dust
•Gut microbiomes
•Teeth disease

4. PATHOPHYSIOLOGY
•Dysregulation of immune response
•Breakdown of self tolerance
•So there is time period gap for clinical appearance
•Three phases of progression of RA are an initiation phase (due
to non-specific inflammation), an amplification phase (due toT
cellactivation), and chronic inflammatory phase, with tissue
injury resulting from thecytokines,IL–1,TNF-alpha, andIL–6.

5. •Arginine changes to vimentine
•But due to these factors changed into citrulline
•Body recognise it as antigen and immune response start in our body

6. •Once the generalized abnormal immune response has
become established –which may take several years before
any symptoms occur –plasma cells derived from B
lymphocytes produce rheumatoid factors and ACPA of the IgG
and IgM classes in large quantities.
•Antigen presenting cells like dentritic cells activate T cells and CD4
cells , activates b cells to form antibodies like RE,Anca

9. ❑Morning stiffness(>1hr)
❑Arthritis of three or more Joint areas
❑Arthritis of hand joints
❑Symmetrical arthritis
❑Rheumatoid nodules
❑Rheumatoid factor
❑Radiological changes
❑Duration>6weeks
ARC 1988 CRITERIA FOR
RHEUMATOID ARTHRITIS

10. EULAR CRITIERIA 2010
CRITERIA POINTS
1.JOINT INVOLVEMENT 0-5
1 large joint 0
2-10 to large joints 1
1-3small joints 2
4-10small joints 3
>10joints;at least one small joint 5
2. SEROLOGY 0-3
Negative RF and negative ACPA 0
Low positive RF or low positive ACPA 2
High positive RF or high positive ACPA 3
3.ACUTE PHASE REACTANTS 0-1
Normal CRP and normal ESR 0
Abnormal CRP or abnormal ESR 1
4.DURATION OF SYMPTOMS 0-1
<6Weeks 0
>6Weeks 1

11. •Swan neck deformity-DIP flexion with PIP hyperextension
•Boutonniere deformity(button hole deformity)-proximal
interphalangeal joint (PIP) is flexed and the distal interphalangeal joint
(DIP) is hyperextended.
•Z deformity
•Ulnar deviation
•Cockup deformity
•In case of shoulder rotator cuff injury
•In elbow synovitis
JOINT INVOLVEMENT IN R.A.

13. Extra manifestations

14. INVESTIGATION
•Blood count- anaemia
•ESR and/or CRP- raised
•Serology- RF ,ACPA/Anti CCP, ANA
•X-rays- for erosions
•Aspiration of the joint- in severe cases
•Musculoskeletal ultrasound- for treatment purpose

15. FACTOR FOR POOR PROGNOSIS
•Older age
•Female sex
•Symmetrical small joints
•Morning stiffness
•>4 swollen joints
•Cigarette smoking
•C reactive protein more than 20g/dl
•Positive RF and Anti ccp

16. TREATMENT
•No curative agent exists for RA but early recognition and an
intensified treat to target (T2T) regime, with regular review.
•NSAIDs-
•Corticosteroids- in oral and parenteral form
•DMARDs
•Biological therapy
•Physical therapy
•Surgery

17. •NAÏVE Dmard
•Naïve biologics
•Seronegative arthritis

18. NSAIDs
•only pain and anti inflammatory action
•ibuprofen, andnaproxen
Corticosteroids- cause osteopenia
Methylprednisolone most commonly used

19. DMARDs
•Methotrexate- 7.5-15mg orally
takes time to work 4-6 weeks
folate antagonist so folic acid
liver hepatotoxicity
avoid in pregnant females and liver disease
•Sulfasalazine- initial dose of 500mg
used in pregnancy also
IBD cases

20. •Hydroxychloroquine- 200-400mg
irreversible retinopathy,cardiac issues
•Leflunomide- 20mg
long term use

•TNF alpha blockers- used after DMARDs
Like Adalimumab,Etanercept,Infliximab,Golimumab

21. TYPE 1 HYPERSENSITIVITY
•In type I hypersensitivity,Bcellsare stimulated
(byCD4
+
T
h2cells) to produceIgEantibodies specific to an
antigen.
•The difference between a normal infectious immune response
and a type 1 hypersensitivity response is that in type 1
hypersensitivity, the antibody isIgEinstead ofIgA,IgG,
orIgM.
•Duringsensitization, the IgEantibodies bind
toFcεRIreceptors on the surface of tissuemast cellsand
bloodbasophils.Mast cells and basophils coated by IgE
antibodies are "sensitized".

23. •Later exposure to the same allergen cross-links the bound IgE
on sensitized cells, resulting inanaphylactic degranulation,
which is the immediate and explosive release of
pharmacologically activepre-formed mediatorsfrom
storagegranulesand concurrent synthesis of inflammatory
lipid mediators fromarachidonic acid;someof these mediators
includehistamine,leukotriene(LTC4 and LTD4 and LTB4),
andprostaglandin, which act onproteins(e.g.,G-protein
coupled receptors) located on surrounding tissues.
•The principal effects of these products arevasodilation
andsmooth-musclecontraction.

24. THANK YOU