1) Arachidonic acid is released from cell membranes and converted by COX enzymes into prostaglandins, which mediate pain and inflammation. 2) NSAIDs like aspirin work by inhibiting COX enzymes, reducing prostaglandin production and thus pain and inflammation, but can increase risk of ulcers. 3) COX-2 selective inhibitors like etoricoxib mainly inhibit COX-2, providing anti-inflammatory effects with fewer gastrointestinal side effects than non-selective NSAIDs.

1. ANALGESIC-
COX
INHIBITORS
PROMED PHARMACEUTICALS LTD.

3. ARACHIDONIC ACID PATHWAY
Arachidonic acid is present in cell membranes and accounts for 5 to 15% of the fatty acids in phospholipids. After
arachidonic acid is released from phospholipids by the action of phospholipase A2, the cyclooxygenase (COX) and
peroxidase activities of COX (also called prostaglandin H2 synthase) catalyze the production of PGH2, the
precursor of other prostaglandins and thromboxanes.
WHAT HAPPENS WITH CELL INJURY?
When cell membranes are injured (which are mainly phospholipid) they activate an enzyme called ‘phospholipase’.
This enzyme converts some of the phospholipids into prostaglandins. These prostaglandins mediate pain,
inflammation and fever.

4. NONSTEROIDAL ANTI-INFLAMMATORY DRUG
- NSAIDS
 Non-steroidal anti-inflammatory drugs[(NSAID) are members of a therapeutic drug
class which reduces pain, decreases inflammation, decreases fever,and prevents
blood clots. Side effects depend on the specific drug, its dose and duration of use, but
largely include an increased risk of gastrointestinal ulcers and bleeds, heart attack,
and kidney disease.
 There are two general types of NSAIDs available: non-selective, and COX-2
selective. Most NSAIDs are non-selective, and inhibit the activity of both COX-1 and
COX-2. These NSAIDs, while reducing inflammation, also inhibit platelet
aggregation and increase the risk of gastrointestinal ulcers and bleeds. COX-2
selective inhibitors have fewer gastrointestinal side effects, but promote thrombosis.
 COX-2 inhibitors are a type of nonsteroidal anti-inflammatory drug (NSAID) that
directly targets cyclooxygenase-2, COX-2, an enzyme responsible
for inflammation and pain. Targeting selectivity for COX-2 reduces the risk of peptic
ulceration

5. ETORICOXIB
 Etoricoxib is a selective COX-2 inhibitor.
 Etoricoxib is indicated for the treatment of rheumatoid arthritis, psoriatic
arthritis, osteoarthritis, ankylosing spondylitis, chronic low back pain, acute pain, and gout.
 Like any other selective COX-2 inhibitor ("coxib"), etoricoxib selectively inhibits isoform 2 of
the enzyme cyclooxygenase (COX-2). It has approximately 106-fold selectivity for COX-2
inhibition over COX-1. This reduces the generation of prostaglandins (PGs) from arachidonic
acid. Among the different functions exerted by PGs, their role in the inflammation cascade
should be highlighted.
 Selective COX-2 inhibitors show less activity on COX-1 compared to traditional non-steroidal
anti-inflammatory drugs (NSAID). This reduced activity is the cause of reduced
gastrointestinal side effects.
 The highest recommended daily dose for chronic use is 90 mg for rheumatoid arthritis and 60
mg for osteoarthritis and chronic low back pain. The recommended daily dose for acute pain
relief treatment from primary dysmenorrhea and acute gouty arthritis is 120 mg.

6. SKELETAL MUSCLE
RELAXANTS
 Skeletal muscle relaxants are drugs that act peripherally at neuromuscular
junction or centrally in the cerebrospinal axis to reduce/decrease muscle tone
 Muscle tone – muscle’s resistance to passive stretch during resting state.
 Muscle relaxant classified in two therapeutic group
I. Neuromuscular Blockers (acts Peripherally)
II. Spasmolytics (acts centrally)

7. CENTRALLY ACTING
MUSCLE RELAXANTS
 These are drugs which reduce skeletal muscle tone by a selective action on
cerebrospinal axis, without altering consciousness
 They selectively depress spinal and spura spinal polysynaptic reflex involved in
the regulation of muscle tone.
 Drugs acting are:
I. Benzodiazepines – Diazepam
II. GABA mimetics – Baclofen, Thiocolchicoside
III. Cental alpha 2 agonist – Clonidine, Tizanidine

8. SPINAL POLYSYNAPTIC
REFLEX

10. THANK YOU
WILLIS KHEDIA