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RHEUMATOID ARTHRITIS
PRESENTED BY-
MOHD ASAD FAROOQI
FACULTY OF MAHARSHI COLLEGE OF PHARMACY .
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What Is Rheumatiod Arthritis ?
 RA, is a form of inflammatory arthritis and an autoimmune disease
 The immune system – is designed to protect our health by attacking foreign cells
such as viruses and bacteria – instead attacks the body’s own tissues, specifically
the synovium, a thin membrane that lines the joints. As a result of the attack, fluid
builds up in the joints, causing pain in the joints and inflamation that’s systemic –
meaning it can occur throughput body.

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Sign & symptoms
 joints may feel warm to the touch and decreased range of motion, as well as
inflammation,
 swelling and pain in the areas around the affected joints.
 Stiffness
 Malaises(feeling ill)
 Muscle aches
 Loss of appetite, which can lead to weight loss
 pain
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Non biologics
Immunosupressants– methotrexate
Sulfasalazine
Chloroquine
Leflunomide
Biologics
TNF inhibitors – infliximab, adalimumab
IL-1 antagonist – Anakinra
Others – prednisolone, gold salts
Drugs used in Rheumatoid arthritis.
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Drugs used in Rheumatoid arthritis.
 NSAIDs:(Nonsteroidal anti-inflammatorydrugs)
 NSAIDs include such drugs as ibuprofen, ketoprofen ,and naproxen sodium,celecoxib.
➢ The primary mechanism of action is inhibition of an enzyme called cyclooxygenase
(COX). COX is an enzyme that is required in the conversion of arachidonic acid to
prostaglandinH2 (PGH2) in the body.
➢ The prostaglandins that are formed from PGH2 are important mediators of sensations
such as pain and processes such as fever and inflammation.
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Disease-Modifying Antirheumatic drugs(DMARDs)
 hydroxycholorquine,sulfasalazine,leflunomide.
 Methotrexate also
 M/A
 The mode of action of Sulfasalazineor 5-aminosalicylic acid (5-
ASA) and sulfapyridine
 In ulcerative colitis, clinical studies utilizing rectal administration of
Sulfasalazine,SP and 5-ASA have indicated that the major therapeutic
action may reside in the 5- ASA moiety.
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 Corticosteroids–
 prednisone, prednisolone and methyprednisolone,
 M/A:
 Prednisoneis a glucocorticoid receptor agonist. It is first metabolized in the liver to
its active form, prednisolone. Prednisolonecrosses cell membranes and binds with
high affinity to specific cytoplasmic receptors.
 the result includes inhibition of leukocyte infiltration at the site of inflammation,
interference in the function of mediators of inflammatory response, suppression of
humoral immune responses, and reduction in edema or scar tissue.
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 Metabolic disorder – recurrent episodes of acute and
chronic arthritis
 Abnormal amounts of urates in the body
 Deposition of monosodium urate crystals in joints and
cartilages
 Hyperuricemia
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Acute gout:
 Sudden onset following rapid fluctuations in plasma uric
acid level
 Metatarsophalangeal joint of the great toe
 Tarsal joints, ankles, and knees
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1. NSAIDs
2. Colchicine
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1. NSAIDs
 Indomethacin, piroxicam, diclofenac, etoricoxib
 High and repeated doses
 Inhibit
urate crystal phagocytosis
Chemotactic migration of leukocytes
into the inflammed joints
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2. Colchicine:
MOA: depolymerization of microtubules in granulocytes
granulocyte migration and phagocytosis Inhibits the
release of glycoprotein 
reduces inflammation and joint destruction
Antimitotic drug
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 Relieves acute attacks of gout
 Used for the prophylaxis of recurrent episodes of
gouty arthritis
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A. Uricosuric drugs: probenecid, sulfinpyrazone
B. Uric acid synthesis inhibitors : allopurinol
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Allopurinol
Xanthine
oxidase
Xanthine
oxidase
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ThankyouTHANK YOU
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pharmacology of Rheumatoid arthritis

  • 1. RHEUMATOID ARTHRITIS PRESENTED BY- MOHD ASAD FAROOQI FACULTY OF MAHARSHI COLLEGE OF PHARMACY . 28/10/20 20 1
  • 3. What Is Rheumatiod Arthritis ?  RA, is a form of inflammatory arthritis and an autoimmune disease  The immune system – is designed to protect our health by attacking foreign cells such as viruses and bacteria – instead attacks the body’s own tissues, specifically the synovium, a thin membrane that lines the joints. As a result of the attack, fluid builds up in the joints, causing pain in the joints and inflamation that’s systemic – meaning it can occur throughput body.  28/10/20 20 3
  • 4. Sign & symptoms  joints may feel warm to the touch and decreased range of motion, as well as inflammation,  swelling and pain in the areas around the affected joints.  Stiffness  Malaises(feeling ill)  Muscle aches  Loss of appetite, which can lead to weight loss  pain 28/10/20 20 4
  • 6. Non biologics Immunosupressants– methotrexate Sulfasalazine Chloroquine Leflunomide Biologics TNF inhibitors – infliximab, adalimumab IL-1 antagonist – Anakinra Others – prednisolone, gold salts Drugs used in Rheumatoid arthritis. 28/10/20 20 6
  • 7. Drugs used in Rheumatoid arthritis.  NSAIDs:(Nonsteroidal anti-inflammatorydrugs)  NSAIDs include such drugs as ibuprofen, ketoprofen ,and naproxen sodium,celecoxib. ➢ The primary mechanism of action is inhibition of an enzyme called cyclooxygenase (COX). COX is an enzyme that is required in the conversion of arachidonic acid to prostaglandinH2 (PGH2) in the body. ➢ The prostaglandins that are formed from PGH2 are important mediators of sensations such as pain and processes such as fever and inflammation. 28/10/20 20 7
  • 8. Disease-Modifying Antirheumatic drugs(DMARDs)  hydroxycholorquine,sulfasalazine,leflunomide.  Methotrexate also  M/A  The mode of action of Sulfasalazineor 5-aminosalicylic acid (5- ASA) and sulfapyridine  In ulcerative colitis, clinical studies utilizing rectal administration of Sulfasalazine,SP and 5-ASA have indicated that the major therapeutic action may reside in the 5- ASA moiety. 28/10/20 20 8
  • 9.  Corticosteroids–  prednisone, prednisolone and methyprednisolone,  M/A:  Prednisoneis a glucocorticoid receptor agonist. It is first metabolized in the liver to its active form, prednisolone. Prednisolonecrosses cell membranes and binds with high affinity to specific cytoplasmic receptors.  the result includes inhibition of leukocyte infiltration at the site of inflammation, interference in the function of mediators of inflammatory response, suppression of humoral immune responses, and reduction in edema or scar tissue. 28/10/20 20 9
  • 11.  Metabolic disorder – recurrent episodes of acute and chronic arthritis  Abnormal amounts of urates in the body  Deposition of monosodium urate crystals in joints and cartilages  Hyperuricemia 28/10/20 20 11
  • 12. Acute gout:  Sudden onset following rapid fluctuations in plasma uric acid level  Metatarsophalangeal joint of the great toe  Tarsal joints, ankles, and knees 28/10/20 20 12
  • 14. 1. NSAIDs  Indomethacin, piroxicam, diclofenac, etoricoxib  High and repeated doses  Inhibit urate crystal phagocytosis Chemotactic migration of leukocytes into the inflammed joints 28/10/20 20 14
  • 15. 2. Colchicine: MOA: depolymerization of microtubules in granulocytes granulocyte migration and phagocytosis Inhibits the release of glycoprotein  reduces inflammation and joint destruction Antimitotic drug 28/10/20 20 15
  • 16.  Relieves acute attacks of gout  Used for the prophylaxis of recurrent episodes of gouty arthritis 28/10/20 20 16
  • 17. A. Uricosuric drugs: probenecid, sulfinpyrazone B. Uric acid synthesis inhibitors : allopurinol 28/10/20 20 17