pharmacology of Rheumatoid arthritis

Rheumatoid arthritis (RA) is an autoimmune disease that can cause joint pain and damage throughout your body. The joint damage that RA causes usually happens on both sides of the body. So, if a joint is affected in one of your arms or legs, the same joint in the other arm or leg will probably be affected, too.

1. RHEUMATOIDARTHRITIS
PRESENTED BY-
MOHD ASAD FAROOQI
FACULTY OF MAHARSHI COLLEGE OF PHARMACY .
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3. What Is Rheumatiod Arthritis?
RA, is a form of inflammatory arthritis and an autoimmunedisease
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 –
meaningitcan\occurthroughputbody.

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4. Sign&symptoms
joints may feel warm to the touch and decreased range of motion, as wellas
inflammation,
swelling and pain in the areas around the affectedjoints.
Stiffness
Malaises(feeling ill)
Muscleaches
Loss of appetite, which can lead to weightloss
pain
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6. Nonbiologics
Immunosupressants –methotrexate
Sulfasalazine
Chloroquine
Leflunomide
Biologics
TNF inhibitors –infliximab, adalimumab
IL-1 antagonist –Anakinra
Others –prednisolone, gold salts
Drugs used in Rheumatoidarthritis.
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7. Drugs used in Rheumatoidarthritis.
NSAIDs: (Nonsteroidalanti-inflammatorydrugs)
NSAIDs include such drugs as ibuprofen, ketoprofen ,and naproxensodium,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
prostaglandin H2 (PGH2) in thebody.
➢The prostaglandins that are formed from PGH2 are important mediators ofsensations
such as pain and processes such as fever andinflammation.
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8. Disease-Modifying Antirheumaticdrugs(DMARDs)
hydroxycholorquine,sulfasalazine,leflunomide.
Methotrexatealso
M/A
The mode of action of Sulfasalazine or 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-ASAmoiety.
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9. Corticosteroids–
prednisone, prednisolone andmethyprednisolone,
M/A:
Prednisone is a glucocorticoid receptor agonist. It is first metabolized in the liver to
its active form, prednisolone. Prednisolone crosses cell membranes and binds with
high affinity to specific cytoplasmicreceptors.
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 scartissue.
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11. Metabolic disorder –recurrent episodes of acute and
chronic arthritis
Abnormal amounts of urates in thebody
Deposition of monosodium urate crystalsin joints and
cartilages
Hyperuricemia
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12. Acutegout:
Sudden onsetfollowingrapidfluctuationsin plasma uric
acidlevel
Metatarsophalangeal joint of the greattoe
Tarsal joints, ankles, andknees
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13. 1.NSAIDs
2.Colchicine
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14. 1.NSAIDs
Indomethacin, piroxicam, diclofenac, etoricoxib
High and repeateddoses
Inhibit
urate crystalphagocytosis
Chemotactic migration of leukocytes
into the inflammed joints
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15. 2.Colchicine:
MOA: depolymerization of microtubules in granulocytes
granulocyte migration and phagocytosis Inhibits the
release of glycoprotein
reduces inflammation and jointdestruction
Antimitoticdrug
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16. Relieves acute attacks ofgout
Used for the prophylaxis of recurrent episodes of
goutyarthritis
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17. A. Uricosuric drugs: probenecid,sulfinpyrazone
B.Uricacidsynthesis inhibitors :allopurinol
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18. Allopurinol
Xanthine
oxidase
Xanthine
oxidase
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19. ThankyouTHANK YOU
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