USE OF
CORTICOSTEROIDS AND NSAIDS IN RA
MONA YADAV
GROUP 3
CORTICOSTEROIDS
• Corticosteroids are also called steroids.
These drugs can help reduce inflammation
in RA. They may also help reduce the pain
and damage caused by inflammation.
CORTICOSTEROIDS
• glucocorticoids :-
• A) hormones :- hydrocortisone ( cortisol)
• B) synthetic :-
• Prednisolone
• Prednisone
• Methylprednisolone
• Dexamethasone
• Betamethasone
• Triamcinolone
CORTICOSTEROIDS
• 1 ) Prednisone :- is an immunosuppressant for the treatment of
autoimmune disorders; it may decrease inflammation by reversing
increased capillary permeability and suppressing
polymorphonuclear leukocyte activity. Prednisone stabilizes
lysosomal membranes and suppresses lymphocytes and antibody
production.
• dose :- Immediate-release: ≤10 mg/day PO added (DMARDs)
• Delayed-release: 5 mg/day PO initially, maintenance: lowest
dosage that maintains clinical response; may be taken at bedtime
to decrease morning stiffness with rheumatoid arthritis
CORTICOSTEROIDS
• 2) Methylprednisolone :- decreases inflammation by suppressing
the migration of polymorphonuclear leukocytes (PMNs) and
reversing increased capillary permeability.
• dose :- 40 mg/day PO divided q6-24hr.
• 3) SIDE EFFECT OF CORTICOSTEROIDS:-
• Hyperglycemia - due to increased gluconeogenesis
• Steroid-induced osteoporosis: reduced bone density
• Adrenal insufficiency (if used for long time and stopped suddenly)
NON- STEROIDAL ANTI- INFLAMMATORY DRUGS
NSAIDs are the most commonly used RA drugs.
• NSAIDs interfere with prostaglandin synthesis through
inhibition of the enzyme cyclooxygenase (COX), thus
reducing swelling and pain.
• TYPES :-
• a) acetic acid derivatives
• b) Carboxylic acid derivatives
• c) Proprionic acid derivatives
NSAIDS
• drugs :- Ibuprofen
• Naproxen
• Diclofenac
• Ketoprofen
• Celecoxib
• Aspirin
• 1 ) Ibuprofen is indicated for patients with mild to moderate
pain. It inhibits inflammatory reactions and pain by decreasing
prostaglandin synthesis.
• dose - 400mg po q6-8hr , not exceed 3000 mg/day
NSAIDS
• 2) Naproxen :- This agent inhibits inflammatory reactions and
pain by decreasing the activity of cyclooxygenase, which is
responsible for prostaglandin synthesis.
• dose - 500-1000 mg/day PO divided q12hr; may increase to
1500 mg/day if tolerated well for limited time.
• 3) Diclofenac :- is one of a series of phenylacetic acids that
have demonstrated anti-inflammatory and analgesic
properties. It is inhibit COX, which is essential in the
biosynthesis of prostaglandins.
• Diclofenac can cause hepatotoxicity; therefore, liver enzymes
NSAIDS
• dose :- Diclofenac sodium: 50 mg PO q8hr or 75 mg PO
q12hr.
• 4) Celecoxib is approved for the relief of signs and symptoms
of RA. It primarily inhibits COX-2, which is considered an
inducible isoenzyme (induced during pain and inflammatory
stimuli). Inhibition of COX-1 may contribute to NSAID
gastrointestinal (GI) toxicity. Administer the lowest possible
dose for each patient. Use of celecoxib has been associated
with an increased risk of cardiovascular toxicity.
• dose - 100-200 mg PO q12hr
NSAIDS
• side effect of nsaids: -
• Stomach problems like bleeding, ulcer and stomach upset
• High blood pressure
• Fluid retention (causing swelling, such as around the
lower legs, feet, ankles and hands)
• Rashes.
 NSAID's presentation

NSAID's presentation

  • 1.
    USE OF CORTICOSTEROIDS ANDNSAIDS IN RA MONA YADAV GROUP 3
  • 2.
    CORTICOSTEROIDS • Corticosteroids arealso called steroids. These drugs can help reduce inflammation in RA. They may also help reduce the pain and damage caused by inflammation.
  • 3.
    CORTICOSTEROIDS • glucocorticoids :- •A) hormones :- hydrocortisone ( cortisol) • B) synthetic :- • Prednisolone • Prednisone • Methylprednisolone • Dexamethasone • Betamethasone • Triamcinolone
  • 4.
    CORTICOSTEROIDS • 1 )Prednisone :- is an immunosuppressant for the treatment of autoimmune disorders; it may decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear leukocyte activity. Prednisone stabilizes lysosomal membranes and suppresses lymphocytes and antibody production. • dose :- Immediate-release: ≤10 mg/day PO added (DMARDs) • Delayed-release: 5 mg/day PO initially, maintenance: lowest dosage that maintains clinical response; may be taken at bedtime to decrease morning stiffness with rheumatoid arthritis
  • 5.
    CORTICOSTEROIDS • 2) Methylprednisolone:- decreases inflammation by suppressing the migration of polymorphonuclear leukocytes (PMNs) and reversing increased capillary permeability. • dose :- 40 mg/day PO divided q6-24hr. • 3) SIDE EFFECT OF CORTICOSTEROIDS:- • Hyperglycemia - due to increased gluconeogenesis • Steroid-induced osteoporosis: reduced bone density • Adrenal insufficiency (if used for long time and stopped suddenly)
  • 6.
    NON- STEROIDAL ANTI-INFLAMMATORY DRUGS NSAIDs are the most commonly used RA drugs. • NSAIDs interfere with prostaglandin synthesis through inhibition of the enzyme cyclooxygenase (COX), thus reducing swelling and pain. • TYPES :- • a) acetic acid derivatives • b) Carboxylic acid derivatives • c) Proprionic acid derivatives
  • 7.
    NSAIDS • drugs :-Ibuprofen • Naproxen • Diclofenac • Ketoprofen • Celecoxib • Aspirin • 1 ) Ibuprofen is indicated for patients with mild to moderate pain. It inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis. • dose - 400mg po q6-8hr , not exceed 3000 mg/day
  • 8.
    NSAIDS • 2) Naproxen:- This agent inhibits inflammatory reactions and pain by decreasing the activity of cyclooxygenase, which is responsible for prostaglandin synthesis. • dose - 500-1000 mg/day PO divided q12hr; may increase to 1500 mg/day if tolerated well for limited time. • 3) Diclofenac :- is one of a series of phenylacetic acids that have demonstrated anti-inflammatory and analgesic properties. It is inhibit COX, which is essential in the biosynthesis of prostaglandins. • Diclofenac can cause hepatotoxicity; therefore, liver enzymes
  • 9.
    NSAIDS • dose :-Diclofenac sodium: 50 mg PO q8hr or 75 mg PO q12hr. • 4) Celecoxib is approved for the relief of signs and symptoms of RA. It primarily inhibits COX-2, which is considered an inducible isoenzyme (induced during pain and inflammatory stimuli). Inhibition of COX-1 may contribute to NSAID gastrointestinal (GI) toxicity. Administer the lowest possible dose for each patient. Use of celecoxib has been associated with an increased risk of cardiovascular toxicity. • dose - 100-200 mg PO q12hr
  • 10.
    NSAIDS • side effectof nsaids: - • Stomach problems like bleeding, ulcer and stomach upset • High blood pressure • Fluid retention (causing swelling, such as around the lower legs, feet, ankles and hands) • Rashes.