This document discusses drugs that act to stop pain and inflammation by targeting autacoids, the major ones being histamines and prostaglandins. It outlines that antihistamines block histamine receptors, while NSAIDs inhibit prostaglandin synthesis by binding to cyclooxygenase. Alpha2-adrenergic agonists also provide pain relief by a central nervous system mechanism of action.

1. Drugs acting to stop pain and
inflammation

2. Drugs acting to stop pain and
inflammation
Pain, inflammation and fever is mainly
triggered by Autacoids
The major autacoids involved in pain, fever
and inflammation are
histamines and
prostaglandins

3. Autacoids
 The word autacoids comes from the
Greek "Autos" (self) and "Acos"
(relief, i.e. drug).
 Autacoids are biological factors
which act like local hormones, have a
brief duration, act near the site of
synthesis, and are not blood borne

4. Introduction
 Agents that may induce release of
autacoids include
- Chemical irritants
- UV light
- Trauma
- bacterial toxins
- immune irritants

5. Major classes of autacoids
Class Example
Histamine
Biogenic Amines
Serotonin (5 HT)
Prostaglandins (Eicosanoids) , leukotrienes,
Phospholipids
Thromboxanes, Platelet activating factors
Derived
(PAF)
Angiotensin and Kinins (Bradykinin and
Polypeptides
Kallikidin)

6. Stopping pain, fever and
inflammation
There are two main groups of pain killers
-Autacoids antagonists
-CNS acting nerve blockers (alpha 2 adrenergic
drugs)
Antihistamines
Autacoids antagonists
Prostaglandin
Synthesis inhibitors

7. Antihistamines (Antagonists)
 Antihistamines act by blocking
histamine receptors
 There are four Histamine receptors
designated as H1 H2, H3, and H4, each
with different function
 Only H1 is involved with pain
 All Histamines antagonists are
competitive blockers of histamine
receptors

8. Histamine Receptors blockers
Type Examples Main functions
H1 receptor Diphenhydramine To treat
Mepyramine maleate
blockers Promethazine
allergic
hydrochloride reactions
Pheniramine maleate
Antazoline
H2 receptor Cimetidine To reduce
Burimamide
blockers Metiamide
Gastric acid
Ranitidine release
H3 receptor Burimamide To treat
Impromidine neurodegenerative
blockers Theoperamide conditions
H4 blockers Thioperamide UI

9. Non-Steroidal Antiinflammatory
Drugs (NSAIDs)
 These are basically prostaglandin
(PG) synthesis inhibitors
 Remember that prostaglandin is an
autacoid that will engineer pain
stimuli

10. How is prodtaglandin synthesized

11. How is prodtaglandin synthesized

12. Common PG synthesis inhibitors
 Aspirin
 Acetaminophen
 Phenylbutazone
 Dipyrone

13. Morden NSAIDs
 Naproxen
 Flunixin meglumine (banamine)
 Meclofenamic acid
 Ibuprofein and indomethacin
 Orgotein
 Dimethyl sulphoxide (DMSO)
 Polysulfated glycosaminoglycans
(Adequan)

14. Mechanisms of Action of NSAIDs
 Binding (reversibly and irreversibly) to
cyclo-oxygenase (PG synthase)
- Aspirin – Irreversibly
- Acetaminophen – reversibly
- Phenylbutazone – Irreversibly
- Dipyron- Irreversibly
- Naproxein – Irreversibly
- Flunixin – Irreversibly
- Meclofenamic acid - Irreversibly

15. Mechanisms of Action of NSAIDs
 Other mechanisms
Orgotein – Breaks down superoxide
free radicals to peroxides
DMSO – It also trap free radicals like
superoxides
Adequan – Inhibits the loss of
cartilaginous mucopolysaccharides

16. Alpha2-Adrenergic Agonists
 Xylazine
 Detomidine