NSAIDs are a group of drugs that reduce pain, fever, and inflammation by inhibiting the COX enzymes that produce prostaglandins. COX enzymes exist in two forms, COX-1 and COX-2. NSAIDs work by blocking both forms of COX, though some are more selective for COX-2. This inhibition of COX reduces prostaglandin production and subsequent pain/fever/inflammation. However, it can also reduce platelet count and increase risk of stomach ulcers. NSAIDs are classified into several categories based on their chemical structure and mechanisms of action. The structure of individual NSAIDs influences their biological activity and side effect profiles.
presentation is based on mainly the chemistry of aspirin,A little bit introduction about nsaid is also here.The uses,doses and side effects are also in these presentation.
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presentation is based on mainly the chemistry of aspirin,A little bit introduction about nsaid is also here.The uses,doses and side effects are also in these presentation.
Corticosteroids are a class of steroid hormones that are produced in the adrenal cortex of vertebrates, as well as the synthetic analogues of these hormones
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Nsaids slideshare
1. NSAIDS – Non Steroidal Anti-
Inflammatory Drugs
Presented by : Mayuri Sompura
Class : Organic Chemistry
Department of Chemistry
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2. What are NSAIDS ?What are non steroidal anti
inflammatory drugs ?
3. NSAIDS is a group of drugs
which include
• Drug curing fever.Antipyretics
• Drugs curing pain.Analgesics
• Drugs curing
inflammation.
Anti-
inflammatory
4. How does NSAIDS work ?
It basically inhibits COX
(Cyclooxygenase) enzyme.
COX enzymes produce
PROSTAGLADINS.
Prostagladins are the active lipid
compounds (eicosanoids).
COX are of two types:
COX
cox-1 cox-2
5. What happens
when COX is
inhibited ?
Pain, fever,
inflammation is
reduced.
Reduced
potential of
blood clotting
Lower count of
platelets.
Can cause
Stomach
ulcers.
Why ?
6. How is COX metabolized or activated ?How is COX activated ?
Injury / infection / trauma
Attacks cell membrane
Cell membrane contains phospholipids
Activation of phospholipids
Formation of arachidonic acid
Metabolized by
Cycloxygena
-se pathway
Lipoxygena
se pathway
12. WHY SAR ?
Enables determination of the chemical groups
responsible for evoking the target biological effect
in the organism.
To develop drug with the increased activity.
For fewer unwanted side effects.
Changes in pharmacological properties by
performing minor changes in drug molecule.
14. Replacement of carboxyl group with other
acid functionalities decrease activity. Also,
amide analogues are inactive.
Acylation of indole nitrogen with aliphatic
carboxylic acids or aryl alkyl carboxylic
acids results in the decrease of activity.
N- benzyl derivatives substituted in the p-
position with F, Cl, CF3, and S-CH3 groups
are most active.
15. The 5th position of the indole when
substituted with OCH3, F, N(CH3), CH3,
COCH3 groups are more active than
substituted indole analogue.
Alkyl groups especially methyl groups at 2-
position are much more active than aryl
substituted analogue.
The substitution of a methyl group at the
alpha position of the acetic acid side chain
leads to equiactive analogues.
17. DISCUSSION :-
When NSAIDS interacts with the other
drugs such as diuretics and warfarin it gives
the following results.
I. Diuretics – it reduces the action of
diuretics by reducing blood
flow to kidneys.
II. Warfarin – increase bleeding by
decreasing activity of blood
platelets and thus form blood
clots.
18. Conclusion :-
on the basis of our above study we can
conclude that:-
• NSAIDS can benefit in treating
hypertension as it increase blood pressure.
•Aspirin –
only nsaid that inhibits clotting of
blood.
Useful in heartattacks and strokes.
hence we can find many more such life saving
uses by the deeper study of these drugs.