Rheumatoid Arthritis Medical treatment

RHEUMATOID ARTHRITIS

It is a chronic inflammatory systemic disease of young or middle aged adult
chatact by – destructive & proliferative changes in the synovial membrane
periarticular structure, skeletak muscle& perineural sheath.
Eventually joints are deformed and ankylosed

Etilogy –

Exact cause unknown
Theories
(1) Infection – haemolytic /nonhaemolytic streptococci have been isolated from
joint & regional lymph node
(2) Endocinal - suggested by response to adrenocortical steroid
(3) Allergies – exhibit various allergic manifestations. Eosinophilia +
(4) Metabolic
(5) Immune overactivity –
- +nt of antibody immunoglobulin – RA factor
- Infilteration of synivial tissue by immunologically competent cells eg
plasma cell , lymphocytes
- +nt of Ag-Ab complexes with leucocytesbin synivialfluid & blood
- Lowered complement level in synovial fluid
(6) Genetic factors – tendancy for aggregating in family
(7) Vascular changes – alteration of peripheral vascular bed , perhaps by
autonomic influxes
Age – young & middle age ( mean age of onset – 40 years)
Sex – Women > Men (3 :1)

Pathogenesis –

Most widely accepted theory – immunological response in synovial tissue
Exogenous antigen (Ag)
↓ entry
Defender cell (WBC – T lymphocyte) + Ag
Transform in to ↓
Plasma cell
↓
Ab + Ag → Ag-Ab complexes ← phagocytes engulf
↓
Lysosomal enzyme releases (proteases)
↓
Inflammation → destruction of tissues (synovium & cartilages)
↓
Pannus – is a granulomatous mass that grows over & destroys cartilage, tendon,
ligament
Under electron microscope,the lining consist of thee types of synovial cells
Type A – phagocytic .Take up Ag-Ab complexes & particulate matter from
synovial fluids
Type B – resembles fibroblast & are belived to synthesis protein & hyaluronic acid
which are +nt in synivial effusion
Type C – Undifferentiated . can become type A or B
In response to human immunoglobulin IgG autoantibodies are synthesized in
rheumatoid synovial tissue (RA factor - RF). It not only reacts with human IgG but
also with IgG of no.of other anomal species making it feasible to test for RF with
sheep cells coated with rabbit IgG. Patient with high titer of Rf have a poor
prognosis.
Standard test for RF determines - only IgM RF (most rapidly measured)
Elevated RF seen in
- RA
- SLE
- Scleroderma
- Polymyositis & dermatomyositis
- Sarcoidosis
- Chronic bacterial endocarditis
- TB
- Chronic hepatitis
- S’jogren syndrome
- Haemochromatosis
- Haemophilic arthritis

Medical management –

• Disease suppressing drugs
• Disease midifying drugs
• Immunosuppressant
(A) Disease suppressing drugs
1. Salicyclates –
Eg – acetylsalicyclate (Aspirin) ,Mg salicayclate, Mg choline
Antiinflammatory ,antipyretic & analgesics
Serum salicyclates level should be monitored. Non therapeutics anti-inflammatory
level are 20-30 mg/dl
Metabolized in Liver & excreted by kidney
C/I – Asthama (Bronchoconstriction)
Bleeding tendencies (platelet inhibition)
Hyperurecemia (Urate retention)
Acute renal/hepatic failure
Side effect – GIT – dyspepsia, nausea,vomiting,occult bleed
CNS – titnitus ,deafness, convulsion
Hy50-75 mg bid/tdspersensitivity reaction
2. NSAID’s –
Reversible PG synthetase inhibitor - Antiinflammatory ,antipyretic & analgesics
Side effect – GI irritation, platelet inhibition, headache,dizziness, ARF,nephritic
syndrome, GN, Steven –Johnson syn,aplastic anaemia
Indomethacine – most potent NSAID Dose – 25 mg bid/tds , Max-150 mg/day
Diclofenac Na - 50-75 mg bid/tds ,Max – 200 mg/day
Ibuprofen – 400 mg tds/qid ,Max 3200 mg/day
Phenylbutazone – 100 mg tds
(B)Disease modifying agents
1.Gold salts –
More effective than NSAID’s
Retards progession of bony erosions & cartilage loss – alter natural course of RA
Reuires close clinical & lab monitoring
Used in Juvenile RA, Psoriatic arthritis, Felty’s syndrome
Indication – patient with acute synovitis who does not respond to conservative
management with NSAID, Sylicyclates
- patient with rapidly progressive erosive arthritis
Metabolism -