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NSAIDs as antibacterial agents
Outline
Introduction
Mechanism of Action
NSAIDs as antibacterial agents
Adverse effects of NSAIDs
Contraindication to NSAIDs
Conclusion
Synthesis of Naproxen
Nonsteroidal anti-inflammatory drugs (NSAIDs) are a drugs for
use as
Introduction
• Antipyretic • Anti-inflammatory • Analgesic agents
Mechanism of action
 The main mechanism of action of NSAIDs is the inhibition of the enzyme cyclooxygenase
(COX). Cyclooxygenase is required to convert arachidonic acid into thromboxane's,
prostaglandins, and prostacyclin’s.
 Thromboxane play a role in platelets adhesion, prostaglandins cause vasodilation, increase
the temperature set-point in the hypothalamus, and play a role in anti-nociception.
 There are two cyclooxygenase isoenzymes, COX-1 and COX-2. COX-1 gets expressed in
the body, and it plays a role in maintaining gastrointestinal mucosa lining, kidney function,
and platelet aggregation. COX-2 is not expressed in the body, and instead it inducible
expresses during an inflammatory response.
 Most of the NSAIDs are nonselective and inhibit both COX-1 and COX-2. However, COX-
2 selective NSAIDs (ex. celecoxib) only target COX-2 and therefore have a different side
effect profile.
 Importantly, because COX-1 is the prime mediator for ensuring gastric mucosal integrity
and COX-2 is mainly involved in inflammation, COX-2 selective NSAIDs should provide
anti-inflammatory relief without compromising the gastric mucosa
Mechanism of action
NSAIDs
COX-1/COX-2
Inhibit
Thromboxane Prostaglandins prostacyclin
Convert
Arachidonic acid
Synthesis of Naproxen
2-methoxynaphthalene 2-acetyl-6methoxynaphalene
Naphthyl acetic acid
NSAIDs as antibacterial agents
 Aspirin
 Etodolac
 Ibruphen
 Ketoprofen
 Mefenamic acid
 Naproxen
 Diclofenac
 Solindac
 Flurbiprofen
Selective
 Rofecoxib
 Valdecoxib
 Celecoxib
Non-Selective
Tooth Pain IB,APAP
Treponema denticolla
Tanneralla forsythia
Porphyromonas gingivalis
TB carprofen
Mycobaterium tuberculosis
Ibruphen,
indomethacin
Helicobactor pylori
Contact lenses/corneal
epithelial cells
pseudomonas aeruginosa
Ibruphen
Urinary tract infections
Escherichia coli
IB and amoxicillin
Entrococcus faecalis
Aspirin
Escherichia coli, Candida
albicans, Pseudomonas cepacia
Staphylococcus aureus
Adverse effects of NSAIDs
Gastric lining Functions Cardiovascular functions
Hematologic functions
Liver functions
Renal functions
Contraindications to NSAIDs
Trimester of pregnancy
Urticaria
Asthma
Coronary artery bypass graft surgery
Conclusion
 NSAIDs used largely for the treatment of pain, inflammation
and fever.
 Adverse effects occur at a much higher rate in patients with
specific diseases, it is crucial for physicians, nurses, and
pharmacists to pay close attention to a patient's history and to
educate the patient accordingly on risks and dosing.
 The patient should not use NSAIDs as an OTC agent.
 We should take NSAIDs with the doctor’s prescription.
Thanks for your Attention!

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animated presentation on NSIDs.pptx

  • 2. Outline Introduction Mechanism of Action NSAIDs as antibacterial agents Adverse effects of NSAIDs Contraindication to NSAIDs Conclusion Synthesis of Naproxen
  • 3. Nonsteroidal anti-inflammatory drugs (NSAIDs) are a drugs for use as Introduction • Antipyretic • Anti-inflammatory • Analgesic agents
  • 4. Mechanism of action  The main mechanism of action of NSAIDs is the inhibition of the enzyme cyclooxygenase (COX). Cyclooxygenase is required to convert arachidonic acid into thromboxane's, prostaglandins, and prostacyclin’s.  Thromboxane play a role in platelets adhesion, prostaglandins cause vasodilation, increase the temperature set-point in the hypothalamus, and play a role in anti-nociception.  There are two cyclooxygenase isoenzymes, COX-1 and COX-2. COX-1 gets expressed in the body, and it plays a role in maintaining gastrointestinal mucosa lining, kidney function, and platelet aggregation. COX-2 is not expressed in the body, and instead it inducible expresses during an inflammatory response.  Most of the NSAIDs are nonselective and inhibit both COX-1 and COX-2. However, COX- 2 selective NSAIDs (ex. celecoxib) only target COX-2 and therefore have a different side effect profile.  Importantly, because COX-1 is the prime mediator for ensuring gastric mucosal integrity and COX-2 is mainly involved in inflammation, COX-2 selective NSAIDs should provide anti-inflammatory relief without compromising the gastric mucosa
  • 5. Mechanism of action NSAIDs COX-1/COX-2 Inhibit Thromboxane Prostaglandins prostacyclin Convert Arachidonic acid
  • 6. Synthesis of Naproxen 2-methoxynaphthalene 2-acetyl-6methoxynaphalene Naphthyl acetic acid
  • 7. NSAIDs as antibacterial agents  Aspirin  Etodolac  Ibruphen  Ketoprofen  Mefenamic acid  Naproxen  Diclofenac  Solindac  Flurbiprofen Selective  Rofecoxib  Valdecoxib  Celecoxib Non-Selective Tooth Pain IB,APAP Treponema denticolla Tanneralla forsythia Porphyromonas gingivalis TB carprofen Mycobaterium tuberculosis Ibruphen, indomethacin Helicobactor pylori Contact lenses/corneal epithelial cells pseudomonas aeruginosa Ibruphen Urinary tract infections Escherichia coli IB and amoxicillin Entrococcus faecalis Aspirin Escherichia coli, Candida albicans, Pseudomonas cepacia Staphylococcus aureus
  • 8. Adverse effects of NSAIDs Gastric lining Functions Cardiovascular functions Hematologic functions Liver functions Renal functions
  • 9. Contraindications to NSAIDs Trimester of pregnancy Urticaria Asthma Coronary artery bypass graft surgery
  • 10. Conclusion  NSAIDs used largely for the treatment of pain, inflammation and fever.  Adverse effects occur at a much higher rate in patients with specific diseases, it is crucial for physicians, nurses, and pharmacists to pay close attention to a patient's history and to educate the patient accordingly on risks and dosing.  The patient should not use NSAIDs as an OTC agent.  We should take NSAIDs with the doctor’s prescription.
  • 11. Thanks for your Attention!