Arthritis ppt priya

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) ofjoint, joint become inflammed results over prodution of joint fluid (synovialfluid)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