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Presented by
Ved prakash panda
M.Pharm (pharmacology)
 Introduction
 Epidemiology
 Aetiology
 Pathophysiology
 Clinical menifestation
 Diagnosis
 Treatment
 Defination :rheumatoid arthritis is a long
term autoimmune disorder that primarily
affects joints. It typically result in swollen &
painful joints. Most commonly, the wrist &
hands are involved, with the same joints
typically involved on both sides of the body.
 Epidemiology: approximately 1% of the
population world wide is affected by
rheuatoid arthritis, with females being 3
times more commonly affected then men.
 Aetiology :
1. genetic factors contributes 60% of the risk
of developing the disease. A MHC antigen
HLA- DR4 is the major genetic factor.
2. Cigaratte smoking is a strong risk factor for
developing Rheumatoid arthritis
3. Synovial injury/ infection with joints leads
to cause of rheumatoid arthritis.
 As all the above factors cause modification
of auto antigen.
 Pathologically, RA is characterised by the
infiltration of variety of inflammatory cells into
the joints.
 Synovial membrane is made up of the cell called
fibroblast or synovocytes.
 Because of modification of auto antigen, this is
recognised by antigen presenting cell, which
activates APC to initiate an immune response.
 APC migrate to lymph nodes and activates T- cell
& B- cell.
 B- cell proliferate into plasma cell and produce
antigen against your own antibody, and migrate
to joint tissue.
 Macrophage in synovium secrete cytokines
like THF-alpha, IL-1, IL-6.
 Cytokines stimulate synovial fibroblast, they
are activated, proliferate & stimulate RANKL
expression which stimulate osteoblast activity
i.e bone erosion.
 Synovial fibroblast secrete protease causing
cartilage degradation.
 The synovial membrane becomes highly
vascularised & hypertrophied, creating a
pannus formation and inflamation.
 Clinical manifestation:
 Pain, stiffness & swelling of finger, thumbs,
wrists, knee & toes.
 Morning stiffness may last for 30min to
several hours.
 Symmetric arthritis
 Extraarticular features, including
osteoporosis, subcutaneous nodules.
 Ankylosis formation( fusion of bone in the
joints).
 Diagnosis:
 Blood test, x- rays for presence of synovitis &
erosion of bones or cartilage.
 Morning stiffness for at least 6 weeks
 Swelling of 3 or more joints for at least 6
weeks.
 Presence of positive rheumatoid factors, it is
an auto antibody present in 80% of patient
with rheumatoid arthritis and term as
seropositive.
 Treatment:
 Non-pharmacological treatment:
1. Physiotherapy is found to be effective in
treating both acute as well as chronic state.
2. Heat, cold & electrotherapy
3. Exercise
4. Surgeries:
Joint replacement procedure- Arthroplasty
Bonegrafting- artrodesis
Synovial membrane is removed- synovectomy
 4 main categories of drugs employed in the
management of rheumatoid arthritis:
1. NSAIDs
2. DMARD’S
3. GLUCOCORTICOIDS
4. BIOLOGICAL THERAPIES
 NSAIDs:
 Inhibition of cyclooxygenase(COX) enzyme
 NSAIDs inhibit production of inflammatory
prostanoids.
 Drugs:
 salicylates-aspirin
 Acetates- diclofenac
 Indoles-indomethacin
 Propionates-ibuprofen
 Cox-2 selective inhibitors:
 Celecoxib
 valdecoxib
 Disease modifying anti-rheumatic
agents(DMARDs):
 All DMARDs inhibit the release or reduce the
activity of inflamatory cytokines such as TNF-
alpha, IL-1,IL-2,IL-6.
 DRUGS:
 Sulfasalazine
 Methotrexate
 Cyclosporin
 Azarhiprine
 CORTICOSTEROIDS:
 Inhibit chemotaxis & migration of leukocyes
and activity of B & T cells.
 Drugs:
 Methylprednisolone.
 Triamcinlone acetonide.
 CYTOKINES INHIBITORS:
 TNF alpha- Inhibitors-Infliximab, Etanercept
 IL-1 Antagonist-Anakinra
Rheumatoid arthritis by ved prakash panda

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Rheumatoid arthritis by ved prakash panda

  • 1. Presented by Ved prakash panda M.Pharm (pharmacology)
  • 2.  Introduction  Epidemiology  Aetiology  Pathophysiology  Clinical menifestation  Diagnosis  Treatment
  • 3.  Defination :rheumatoid arthritis is a long term autoimmune disorder that primarily affects joints. It typically result in swollen & painful joints. Most commonly, the wrist & hands are involved, with the same joints typically involved on both sides of the body.  Epidemiology: approximately 1% of the population world wide is affected by rheuatoid arthritis, with females being 3 times more commonly affected then men.
  • 4.  Aetiology : 1. genetic factors contributes 60% of the risk of developing the disease. A MHC antigen HLA- DR4 is the major genetic factor. 2. Cigaratte smoking is a strong risk factor for developing Rheumatoid arthritis 3. Synovial injury/ infection with joints leads to cause of rheumatoid arthritis.  As all the above factors cause modification of auto antigen.
  • 5.  Pathologically, RA is characterised by the infiltration of variety of inflammatory cells into the joints.  Synovial membrane is made up of the cell called fibroblast or synovocytes.  Because of modification of auto antigen, this is recognised by antigen presenting cell, which activates APC to initiate an immune response.  APC migrate to lymph nodes and activates T- cell & B- cell.  B- cell proliferate into plasma cell and produce antigen against your own antibody, and migrate to joint tissue.
  • 6.
  • 7.  Macrophage in synovium secrete cytokines like THF-alpha, IL-1, IL-6.  Cytokines stimulate synovial fibroblast, they are activated, proliferate & stimulate RANKL expression which stimulate osteoblast activity i.e bone erosion.  Synovial fibroblast secrete protease causing cartilage degradation.  The synovial membrane becomes highly vascularised & hypertrophied, creating a pannus formation and inflamation.
  • 8.  Clinical manifestation:  Pain, stiffness & swelling of finger, thumbs, wrists, knee & toes.  Morning stiffness may last for 30min to several hours.  Symmetric arthritis  Extraarticular features, including osteoporosis, subcutaneous nodules.  Ankylosis formation( fusion of bone in the joints).
  • 9.  Diagnosis:  Blood test, x- rays for presence of synovitis & erosion of bones or cartilage.  Morning stiffness for at least 6 weeks  Swelling of 3 or more joints for at least 6 weeks.  Presence of positive rheumatoid factors, it is an auto antibody present in 80% of patient with rheumatoid arthritis and term as seropositive.
  • 10.  Treatment:  Non-pharmacological treatment: 1. Physiotherapy is found to be effective in treating both acute as well as chronic state. 2. Heat, cold & electrotherapy 3. Exercise 4. Surgeries: Joint replacement procedure- Arthroplasty Bonegrafting- artrodesis Synovial membrane is removed- synovectomy
  • 11.  4 main categories of drugs employed in the management of rheumatoid arthritis: 1. NSAIDs 2. DMARD’S 3. GLUCOCORTICOIDS 4. BIOLOGICAL THERAPIES
  • 12.  NSAIDs:  Inhibition of cyclooxygenase(COX) enzyme  NSAIDs inhibit production of inflammatory prostanoids.  Drugs:  salicylates-aspirin  Acetates- diclofenac  Indoles-indomethacin  Propionates-ibuprofen  Cox-2 selective inhibitors:  Celecoxib  valdecoxib
  • 13.  Disease modifying anti-rheumatic agents(DMARDs):  All DMARDs inhibit the release or reduce the activity of inflamatory cytokines such as TNF- alpha, IL-1,IL-2,IL-6.  DRUGS:  Sulfasalazine  Methotrexate  Cyclosporin  Azarhiprine
  • 14.  CORTICOSTEROIDS:  Inhibit chemotaxis & migration of leukocyes and activity of B & T cells.  Drugs:  Methylprednisolone.  Triamcinlone acetonide.  CYTOKINES INHIBITORS:  TNF alpha- Inhibitors-Infliximab, Etanercept  IL-1 Antagonist-Anakinra