This document discusses analgesics and anti-inflammatory agents. It begins by defining pain and inflammation, then discusses how analgesics work by selectively relieving pain without altering consciousness. It classifies different types of analgesics and anti-inflammatory agents like salicylates, propionic acid derivatives, aryl-acetic acid derivatives, and preferential/selective COX-2 inhibitors. For each drug class, it provides examples of drugs, discusses mechanisms of action, pharmacokinetics, uses, and adverse drug reactions. The document concludes by summarizing the mechanism of action of NSAIDs in inhibiting cyclooxygenase and thereby decreasing prostaglandin formation and pain/inflammation.

1. ANALGESICS & ANTI-INFLAMATORY AGENTS
By
Dr.S.KAMESHWARAN.,M.Pharm.,Ph.D.,
Associate Professor, Excel College of Pharmacy
Komarapalayam, Tamilnadu

2. ANALGESICS AND ANTIINFLAMATORY
AGENTS
They are also known as
Nonnarcotic, Nonopioid
Analgesics.
PAIN:
Also known as ALGESIA
”IT IS AN ILL DEFINEED, UNPLEASANT
SENSATION, USUALLY EVOKED BY AN
EXTERNAL OR INTERNAL NOXIOUS
STIMULANT”

3. ANALGESICS:
“A DRUG THAT SELECTIVELY RELIEVES PAIN
BY ACTING IN THE CNS/ON PERIPHERAL
PAIN MECHANISMS WITH OUT
SIGNIFICANTLY ALTERING
CONSCIOUSNESS”
INFLAMMATION:
“INFLAMMATION IS THE BODY’S EFFORT TO
INACTIVATE TO DESTROY INVADING
ORGANISM, REMOVE IRRITANTS AND SET
THE STAGE FOR TISSUE REPAIR”

4. CLASSIFICATION:
NONSELECTIVE COX INHIBITORS:
SALICYLATES
ASPIRIN
PROPIONIC ACID DERIVATIVES:
IBUPROFEN,
KETOPROFEN,
FLUBIPROFEN.
ANTHRANILIC ACID DERIVATIVES:
MEPHENANTIC ACID
ARYL-ACETIC ACID DERIVATIVES:
DICLOFENAC,
ACECLOFENAC

5. OXICAM DERIVATIVES:
PIROXICAM,
TENOXICAM,
PYRROLO-PYRROLE DERIVATIVES:
KETOROLAC
INDOLE DERIVATIVES:
INDOMETHACIN
PYRAZOLONE DERIVATIVES:
PHENYL BUTAZONE
OXYPHENBUTAZONE

6. PREFERENTIAL COX-2 INHIBITORS:
NIMESULIDE
MELOXICAM
SELECTIVE COX-2 INHIBITORS:
CELECOXIB
ETORICOXIB
PARECOXIB

7. ANALGESICS, ANTIPYRETICS WITH POOR
ANTI INFLAMMATORY ACTION
PARA AMINO PHENYL DERIVATIVES:
PARACETAMOL
PYRAZOLONE DERIVATIVES:
METAMIZOL
BENZOXAZOCINE DERIVATIVES:
NEFOPAM

8. SALICYLATES
Eg: ASPIRIN
It is acetyl salicylic acid.
Aspirin is rapidly converted in the body to
salicylic acid and which is responsible for
most of the actions.
It is the one of the oldest analgesic- anti-
inflammatory drug and is still widely used

9. Aspirin is a weak organic acid.
Salicylates are Reversible Inhibitors of COX.
It is reversibly acetylates [inactivates]
cyclooxygenase enzyme (COX)
Aspirin is converted in to the body as salicylic
acid by rapid deacetylation
Salicyclic acid has Antipyretic, Anti
inflammatory and analgesic effects.
Antipyretic and analgesic effects are due to
the BLOCKADE OF PG SYNTHESIS, at the
thermoregulatory centre in the Hypothalamus
and at Peripheral sites.

10. ANTIINFLA MMATORY ACTIONS
Aspirin inhibits COX ACTIVITY,
It diminish the formation of PROSTAGLANDINS,
Block inflammation in arthritis.
ANALGESIC ACTION
PGE2 -Sensitize nerve ending to the action of
Bradykinin ,Histamine and other chemical
mediators released locally by the inflammatory
process,
By decreasing PGE 2 synthesis aspirin repress the
sensation of pain.

11. ANTI PYRETIC ACTION:
FEVER
Occurs WHEN THE SET – POINT OF THE ANTERIOR
HYPOTHALAMIC THERMOREGULATORY CENTER
IS ELEVATED DUE TO THE SYNTHESIS OF PGE2.
SALICYLATES – Lowers body temperature by
impending PGE2 synthesis & release and it
resists the thermostat toward normal.

12. PHARMACOKINETICS:
Absorbed from stomach and intestine
Rapidly deacetylated in the gut wall, liver,
plasma and other tissues to release the
salicylic acid
Salicylic acid is the major circulating and
active forms
It is 80% bound to plasma proteins
Slowly enters brain & crosses placenta
Metabolized by GA conjugation
Excreted by glomerular filtration & tubular
secretions

13. ADR:
Nausea
Vomiting
Epigastric distress
Blood in stools
Peptic ulcer
Hypersensitivity
Dizziness
Vertigo
Reversible impairment of gearing and vision

14. USES:
• As analgesic
• As antipyretic
• In acute rheumatic fever
• Rheumatoid arthritis
• Osteoarthritis

15. PROPIONIC ACID DERIVATIVES:
IBUPROFEN,
 It is the first member of this class of drug
 Introduced as a better tolerated alternative
to aspirin
 All drugs have similar pharmacodynamic
properties
 Duration of action differs action differs for
each drug
 All drugs inhibit PG synthesis
 Naproxen is the most potent drug in this class
of drug

16. PHARMACOKINETICS
All are well absorbed orally
Highly bound to plasma proteins
All drugs enters brain
Largely metabolized in liver
Excreted in urine and bile
ADR:
Ii is better tolerated than aspirin
Gastric discomfort
Nausea
Vomiting
Gastric erosion
Head ache

17. ARYL ACETIC ACID DERIVATIVE:
DICLOFENAC SODIUM:
Similar in efficacy to naproxen
Most extensively used NSAIDs
Affords quick relief of pain and wound edema
It inhibits PG synthesis & somewhat COX-2
selective
Reduce the inflammation
Exerting extended therapeutic action in joints
Well absorbed orally
99% protein bound
Metabolized and excreted both in urine and bile
The plasma t1/2 is 2 hours
It has good tissue penetrability

18. ADR
Epigastric pain
Nausea
Head ache
Dizziness
Rashes
Gastric ulceration
USES:
In rheumatoid and osteoarthritis
Ankylosing spondylitis
Toothache
Dysmenorrhoea
Post operative inflammatory conditions

19. PREFERENTIAL COX-2 INHIBITORS
This newer NSAID is a relatively weak inhibitor of PG
synthesis
Anti-inflammatory action may be exerted by other
mechanisms as well
Eg:
Reduced generation of superoxide by neutrophils
Inhibition of PAF synthesis
Free radical scavenging
Initially it was used for short lasting painful inflammatory
conditions
Completely absorbed orally
99% plasma protein bound
Extensively metabolized
Excreted mainly in urine

20. SELECTIVE COX-2 INHIBITORS
These drugs inhibiting the COX-2 enzyme without
affecting COX-1 function
Currently 3 selective COX-2 inhibitors are available in
India
CELECOXIB, ETORICOXIB, PARECOXIB
Rofecoxib And Valdocoxib have been withdrawn
from for increasing cardoivascular risk
Selective COX-2 inhibitors should be used only in
patients at high risk of peptic ulcer, perforation or
bleeds.
It should be avoided in patients with history of
Ischaemic heart disease/ hypertension/ cardiac
failure/ cerebrovascular disease.

21. CELECOXIB
It exerts antiinflammatory, analgesic and
antipyretic actions with low ulcerogenic potential
In rheumatoid arthritis it is effective as diclofenac
with out affecting COX-1 activity in GI mucosa
Tolerability of celecoxib is better than traditional
NSAID’s
Slowly absorbed on oral dose
97% plasma protein bound
Metabolized in liver by CYP2C9 enzyme
It is approved for use in osteo and rheumatoid
arthritis in the dose of 100-200 mg.BD

22. PARA-AMINO PHENOL DERIVATIVES
PARACETAMOL:
Also known as Acetaminophen
It is the de ethylated active metabolite of phenacetin
Commonly used in the year of 1950s
It act by raising the pain threshold
It is a weak antiinflammatory component
It is a good and promptly acting antipyretic
It poorly inhibits the PG synthesis in peripheral tissues
It has no effect on CVS
Gastric irritation is insignificant
In case of overdose produce mucosal erosion and
bleeding
Antagonis for paracetamol poisoning:
N- ACETYLCYSTEINE

23. PHARMACOKINETICS
Well absorbed orally
Uniformly distributed in the body
Metabolized in liver by glucaronic acid
conjugation and sulfate conjugation
Excreted rapidly through urine
ADR:
Safe and well tolerated drug
Nausea and rashes occures occasionally
Leukopenia is rare
Hepatotoxicity

24. NSAID’S MECHANISM OF ACTION:
They are the competitive & reversible inhibitors of
COX
WOUND
↓
MEMBRANE PHOSPHOLIPID
↓liberates
ARACHIDONIC ACID
↓ COX – NSADI’S
NO PROSTAGLANDINE FROMATION
↓
NO PAIN & INFLAMMATION

25. THANK U ALL