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Submitted to-: 
Pranaywal Sir 
Submitted by-: 
Priya Katiyar 
M.Pharm 
IInd sem
What is rheumatic arthritis? 
When immune system of body mistakenly attacks on lining tissue (synovium) of 
joint, joint become inflammed results over prodution of joint fluid (synovial 
fluid)and cause permanent joint distruction 
auto immune disease 
 progressive/chronic disease 
 affect in symmetrical pattern 
 affect people of all age 
 cause permanent distruction of joint 
 affect both male and female
Etiology 
RA is caused by combination of genetic and environmental factor that trigger an 
abnormal immune response 
Possible cause - 
Genetic factor- Certain genes that play a role in the immune system are 
associated with RA development 
Environmental factor- certain infectious agents, such as some viruses 
or bacteria may increase suseptibility to RA 
Other factor- some hormonal factor may promote RA development in 
combination with genetic factors and environmental exposure
Sign and symptoms 
 Symmetrical joint pain 
 Swelling of joint 
 Joint stiffness 
 Low grade fever 
 Fatigue 
 Malaise 
 redness on joint 
 Warmth joiny 
 Loss of fuction
Treatment 
The goal of treatment of RA - 
Relieve pain and inflammation 
Prevent joint destruction 
Preserve and improve a patient functional activity 
Maintain patient normal life 
Types of treatment- 
There are two types of treatment 
1)Non pharmacological 
2)Pharmacological
Non- pharmacological treatment 
weight loose 
Occupational therapy 
Regular exercise 
physiotherapy 
healthy diet
Pharmacological Treatment 
Traditionally treatment for RA was introduce in a stepwise ‘pyramidal’ manner- 
First line drug - such as analgesic and NSAIDS are used 
Second line drug - such as Sulfasalazine 
Third line drug- such as Azathioprine 
Note- 
First line drugs are used to relieve pain and second or third line drugs are used 
when symptoms are adequately not controlled.
NSAID act by direct inhibition of COX-1 and COX-2 by blocking COX 
enzyme site. Cyclo-oxygenase converts the fatty acid arachidonic into 
prostaglandin which cause inflammation. 
Ex- Aspirin ( dose – 4 to 6 gm/day) 
Ibuprofen ( dose – 400 to 600 mg/day) 
Side Effect- 
GIT complication like ulcer. 
GI toxicity. 
Intolerence like Dyspepsia. 
NSAID 
(Non-steroidal anti-inflammatory drug)
Preventive therapies for side effect of NSAID 
Misoprostol - which is a synthetic prostaglandin effective in prevention of 
NSAID induced ulcer by enhancing mucus secretion 
Omeprazole - It is also effective in the prevention of NSAID induced GI 
complication .It is more effective than misoprostol in maintaining remission 
Ranitidine – H 2 receptor antagonist used in the prevention of NSAID 
induced GI toxicity
DMARD 
(Disease modifying anti-rheumatic drug) 
 Have a major role in managing rheumatic arthritis 
 Have very different mechanism of action and chemical structure 
 Has been shown to slow progression of disease 
 Choice of these drugs depend upon the balance between adverse effect and 
efficacy 
 Slow onset of action 
 Response to treatment usually expected within 4- 6 month 
Ex- Methotrexate , Sulfasalazine , Cyclosporin , Azathioprine , Leflunomide etc.
SULFASALAZINE 
Most commonly prescribed DMARD due to its favourable risk- benefit ratio 
Has high continuation rate. 
Low rate of serious adverse effect. 
Has been shown to disease progression slow. 
Dose- initially 500mg once daily 
increasing in weekly steps of 500 mg to 1gm twice daily. 
Side effect- Nausea , rashes, marrow suppression, reversible male infertility. 
To reduce side effect of nausea the dose is usually titrated from 500 mg to 1gm 
twice daily .
METHOTREXATE 
Used in first line drug therapy 
Most effective DMARD 
Has a high 5 year continuation rate. 
And a low incidence of adverse effect at low weekly dose. 
Rapid onset of action of 4-6 weeks. 
Easy to administer as a single weekly dose 
High response rate of 40-50 %. 
Dose- 5-25 mg once weekly. 
Side effect - hepatic fibrosis, liver toxicity, stomatitis. 
To reduce nausea and stomatitis,folic acid is added to methotrexate therapy.
Steroid 
Mainly corticosteroid is used 
Suppress cytokines and produce a rapid improvement in sign and symptoms of 
disease. 
Potent anti inflammatory effect, inc mobility and reduce deformity of joint. 
Ex- Prednisolone, methyl prednisolone acetate. 
Oral prednisolone is used to provide temporary relief until a DMARDS become 
effective. 
Dose- 40 mg for large joint at interval of 1-5 weeks. 
( dose depend upon joint size) 
Side effect- prophylaxis and osteoporosis. 
To reduce side effect- calcium supplement is used with this therapy..
LEFLUNOMIDE-New 
oral DMARD for RA treatment, isoxazole derivative 
Has both anti inflammatory and immuno modulatory properties 
Act by inhibiting the synthesis of DNA and RNA in immuno response cell 
particularly T-cell 
Also inhibit the production of cytokines 
Rapid on set of action 
Side effect- GIT disturbance, alopecia ,hypertension 
Dose- 100 mg given once a week ( up to 3 weeks) 
To reduce side effect- avoide alcohal, not use in pregnant lady, reduce salt 
absorption
TNF-alfa inhibitor 
It is also a inflammatory mediator that contributes to the pathogenesis of 
synovitis and joint destruction substance produced by our body. 
These inhibitor can help reduce pain ,stiffness and tender or swollen joint 
Ex- Etanercept 
is a recombinant human soluble TNF receptor 
mechanism of action is competitive inhibition of TNF , binding to cell 
surface receptor and prevent TNF mediate cellular response 
given subcutaneously 
Dose – 4-6 mg/kg( every week) 
Side effect- injection site reaction , rhinitis
Arthritis ppt priya

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Arthritis ppt priya

  • 1. Submitted to-: Pranaywal Sir Submitted by-: Priya Katiyar M.Pharm IInd sem
  • 2. What is rheumatic arthritis? When immune system of body mistakenly attacks on lining tissue (synovium) of joint, joint become inflammed results over prodution of joint fluid (synovial fluid)and cause permanent joint distruction auto immune disease  progressive/chronic disease  affect in symmetrical pattern  affect people of all age  cause permanent distruction of joint  affect both male and female
  • 3. Etiology RA is caused by combination of genetic and environmental factor that trigger an abnormal immune response Possible cause - Genetic factor- Certain genes that play a role in the immune system are associated with RA development Environmental factor- certain infectious agents, such as some viruses or bacteria may increase suseptibility to RA Other factor- some hormonal factor may promote RA development in combination with genetic factors and environmental exposure
  • 4. Sign and symptoms  Symmetrical joint pain  Swelling of joint  Joint stiffness  Low grade fever  Fatigue  Malaise  redness on joint  Warmth joiny  Loss of fuction
  • 5. Treatment The goal of treatment of RA - Relieve pain and inflammation Prevent joint destruction Preserve and improve a patient functional activity Maintain patient normal life Types of treatment- There are two types of treatment 1)Non pharmacological 2)Pharmacological
  • 6. Non- pharmacological treatment weight loose Occupational therapy Regular exercise physiotherapy healthy diet
  • 7. Pharmacological Treatment Traditionally treatment for RA was introduce in a stepwise ‘pyramidal’ manner- First line drug - such as analgesic and NSAIDS are used Second line drug - such as Sulfasalazine Third line drug- such as Azathioprine Note- First line drugs are used to relieve pain and second or third line drugs are used when symptoms are adequately not controlled.
  • 8. NSAID act by direct inhibition of COX-1 and COX-2 by blocking COX enzyme site. Cyclo-oxygenase converts the fatty acid arachidonic into prostaglandin which cause inflammation. Ex- Aspirin ( dose – 4 to 6 gm/day) Ibuprofen ( dose – 400 to 600 mg/day) Side Effect- GIT complication like ulcer. GI toxicity. Intolerence like Dyspepsia. NSAID (Non-steroidal anti-inflammatory drug)
  • 9. Preventive therapies for side effect of NSAID Misoprostol - which is a synthetic prostaglandin effective in prevention of NSAID induced ulcer by enhancing mucus secretion Omeprazole - It is also effective in the prevention of NSAID induced GI complication .It is more effective than misoprostol in maintaining remission Ranitidine – H 2 receptor antagonist used in the prevention of NSAID induced GI toxicity
  • 10. DMARD (Disease modifying anti-rheumatic drug)  Have a major role in managing rheumatic arthritis  Have very different mechanism of action and chemical structure  Has been shown to slow progression of disease  Choice of these drugs depend upon the balance between adverse effect and efficacy  Slow onset of action  Response to treatment usually expected within 4- 6 month Ex- Methotrexate , Sulfasalazine , Cyclosporin , Azathioprine , Leflunomide etc.
  • 11. SULFASALAZINE Most commonly prescribed DMARD due to its favourable risk- benefit ratio Has high continuation rate. Low rate of serious adverse effect. Has been shown to disease progression slow. Dose- initially 500mg once daily increasing in weekly steps of 500 mg to 1gm twice daily. Side effect- Nausea , rashes, marrow suppression, reversible male infertility. To reduce side effect of nausea the dose is usually titrated from 500 mg to 1gm twice daily .
  • 12. METHOTREXATE Used in first line drug therapy Most effective DMARD Has a high 5 year continuation rate. And a low incidence of adverse effect at low weekly dose. Rapid onset of action of 4-6 weeks. Easy to administer as a single weekly dose High response rate of 40-50 %. Dose- 5-25 mg once weekly. Side effect - hepatic fibrosis, liver toxicity, stomatitis. To reduce nausea and stomatitis,folic acid is added to methotrexate therapy.
  • 13. Steroid Mainly corticosteroid is used Suppress cytokines and produce a rapid improvement in sign and symptoms of disease. Potent anti inflammatory effect, inc mobility and reduce deformity of joint. Ex- Prednisolone, methyl prednisolone acetate. Oral prednisolone is used to provide temporary relief until a DMARDS become effective. Dose- 40 mg for large joint at interval of 1-5 weeks. ( dose depend upon joint size) Side effect- prophylaxis and osteoporosis. To reduce side effect- calcium supplement is used with this therapy..
  • 14. LEFLUNOMIDE-New oral DMARD for RA treatment, isoxazole derivative Has both anti inflammatory and immuno modulatory properties Act by inhibiting the synthesis of DNA and RNA in immuno response cell particularly T-cell Also inhibit the production of cytokines Rapid on set of action Side effect- GIT disturbance, alopecia ,hypertension Dose- 100 mg given once a week ( up to 3 weeks) To reduce side effect- avoide alcohal, not use in pregnant lady, reduce salt absorption
  • 15. TNF-alfa inhibitor It is also a inflammatory mediator that contributes to the pathogenesis of synovitis and joint destruction substance produced by our body. These inhibitor can help reduce pain ,stiffness and tender or swollen joint Ex- Etanercept is a recombinant human soluble TNF receptor mechanism of action is competitive inhibition of TNF , binding to cell surface receptor and prevent TNF mediate cellular response given subcutaneously Dose – 4-6 mg/kg( every week) Side effect- injection site reaction , rhinitis