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Nonsteroidal anti inflammatory drugs (nsai ds) /certified fixed orthodontic courses by Indian dental academy


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The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and offering a wide range of dental certified courses in different formats.

Indian dental academy provides dental crown & Bridge,rotary endodontics,fixed orthodontics,
Dental implants courses.for details pls visit ,or call

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  • 1. Nonsteroidal Anti(inflammatory Drugs (NSAIDs INDIAN DENTAL ACADEMY Leader in continuing dental education
  • 2. Synthesis of Prostaglandins Cell membrane phospholipids #cortisol PLA Arachidonic acid #NSAIDs Cyclo-oxygenase #zileuton Lipoxygenase (Cox-1 & Cox-2) Endoperoxide HPETEs Thromboxane A2, PGs & PGI2 leukotrienes #zaferlucast lipoxins
  • 3. Classification of NSAIDs Salicylates: aspirin, Na salicylates & diflunisal. Propionic acid derivatives: ibuprofen, ketoprofen, naproxen. Aryl acetic acid derivatives: diclofenac, ketorolac Indole derivatives: indomethacin, sulindac
  • 4. Alkanones: Nabumetone. Oxicams: piroxicam, tenoxicam. Anthranilic acid derivatives (fenamates): mefenamic acid and flufenamic acid. Pyrazolone derivatives: phenylbutazone, oxyphenbutazone, azapropazone (apazone) & dipyrone (novalgine). Aniline derivatives (analgesic only): phenacetin & paracetamol.
  • 5. Salicylates Acetyl salicylic acid (aspirin). Sodium salicylates. Diflunisal (dolobid, difluorophenyl salicylate). Acetyl salicylic acid (aspirin). Kinetics: Well absorbed from the stomach, but better from the upper small intestine (large surface area). Distributed allover the body, 50-80% bound to plasma protein (albumin). Metabolized to acetic acid and salicylates (active metabolite). Salicylates is conjugated with glucuronic acid and glycine. Excreted by the kidney. Alkalinization of the urine increases the rate of salicylates excretion.
  • 6. Low dose of aspirin 0.6 g is eliminated by 1st order kinetics and its t 1/2 is 3-5 h. while high dose (more than 4 g/day) is eliminated by zero-order kinetics and its t 1/2 may increase up to 15 h. Mechanism of action: Aspirin irreversibly inhibits cyclooxygenase enzyme, so blocks synthesis of prostaglandins and thromboxane A2.
  • 7. Pharmacological effects of aspirin: Anti-infammatory effects: Inhibits prostaglandin synthesis. Blocks action of kinins which are mediated through prostaglandin synthesis. Inhibits granulocyte adherence to damaged vasculature. Stabilizes lysosomes. Inhibits migration of PMN leukocytes & macrophages into the site of inflammation.
  • 8. Analgesic effects: Centrally: it inhibits prostaglandin synthesis, so increasing pain threshold in the thalamus. Peripherally: inhibits prostaglandin synthesis, so inhibiting inflammation and diminishes activation of peripheral pain sensors. Aspirin alleviates mild to moderate pain of muscular and dental origin, postpartum states, arthritis & bursitis.
  • 9. Antipyretic effect: It inhibits prostaglandin synthesis in the CNS Resetting of temperature control in the hypothalamus. VD of the superficial BV, so increasing heat dissipation & sweating. NB: aspirin lowers elevated temperature while normal body temperature is only slightly affected.
  • 10. Platelet effect: Aspirin in small dose (75-100 mg /day) irreversibly inhibits thromboxane A2 synthesis in the platelets without affecting prostacyclin synthesis in the vascular endothelium. Aspirin must be stopped one week prior to surgery if potential bleeding complications are a concern. Aspirin has longer duration as antiplatelet than ticlopidine, dipyridamole and phenylbutazone.
  • 11. Uses: Antipyretic (0.5-2 g / day). Analgesic for mild to moderate superficial pain (headache, arthritis, toothache, myalgia) 0.5-2 g/day. Acute rheumatic fever (6-12 g/ day). Rheumatoid arthritis (6-8 g / day). Prophylaxis in thromboembolic diseases e.g. transient ischemic attack, unstable angina, & MI (75-100 mg / day). Other uses under investigation e.g. aspirin may reduce cataract formation and the incidence of cancer colon.
  • 12. A/E: GIT upset: nausea, vomiting, gastritis, ulceration & bleeding (prevented by misoprostol). Hypersensitivity: bronchial asthma, angioedema & rashes. Idiosyncracy: aspirin causes hemolytic anemia in patient with G-6-PD deficiency. Hypoprothrombinemia and bleeding tendency as aspirin competes with vitamin K, so decreasing prothrombin synthesis. Salicylism: aspirin in large doses for long time therapy causes headache, tinnitus, hearing difficulty, blurring of vision, GIT upset, irritability & hyperventilation (these symptoms disappear on stopping aspirin).
  • 13. At low toxic dose: aspirin produces respiratory alkalosis followed by acidosis Teratogenicity Nephropathy. Reye's syndrome : aspirin in children with viral infection may cause liver injury and encephalopathy.
  • 14. Acute aspirin poisoning: Restlessness, tremors, convulsion, vomiting, dehydration, hypotension, hyperventilation, hyperreflexia, hyperpyrexia & coma. Treatment: Activated charcoal 50g p.o to adsorb salicylates and prevents its absorption. Alkalinization of urine (to enhance excretion) by i.v Na HCO3 which also corrects acidosis. Anticonvulsant e.g. i.v diazepam. Cold fomentation and ice bags. Correct dehydration by i.v fluids (5% dextrose). Correct acid / base balance (alkalosis or mixed alkalosis/acidosis need no specific treatment). Correct hypoprothrombinemia by i.v vitamin K. Hemodialysis may be needed.
  • 15. Contraindications: Peptic ulcer, esophageal varices, bronchial asthma, idiosyncrasy, allergy, viral infection in children, bleeding tendency and small dose in gout (competes with uric acid excretion).
  • 16. Interactions: Alcohol increases aspirin-induced GIT bleeding. Aspirin displaces oral anticoagulants and oral hypoglycemics from their plasma protein binding sites, so increasing their activities and may lead to toxicity. Aspirin inhibits the uricosuric effects of sulphinpyrazone and probenecid. Barbiturates increase the analgesic effect of aspirin. NB: Diflunisal (difluorophenyl salicylate): it has analgesic and anti-inflammatory effects like aspirin, but has no antipyretic action.
  • 17. Locally acting salicylates Salicylic acid: keratolytic, antiseptic & fungistatic. Methyl salicylate (wintergreen oil): used as counterirritant for muscle and joint pain. Sulfasalazine : it is a combination of sulfapyridine and 5-aminosalicylic acid (5-ASA). Sulfasalazine liberates 5-ASA in the colon where it blocks the synthesis of leukotriene B4 locally and used in ulcerative colitis.
  • 18. Nonsteroidal anti-inflammatory drugs )(NSAIDs Drug Phenylbutazone Common Uses A/E Acute gout Gastritis Ibuprofen Dysmenorrhea Nephropathy Naproxen Salt &water Antirheumatic Ketoprofen Osteoarthritis retention Hypertension Indomethacin Rheumatoid Bronchospasm Sulindac arthritis Bleeding Mefenamic acid Diclofenac Piroxicam Meloxicam Contraindic ations Peptic ulcer Pregnancy Renal & liver failure
  • 19. Non-acidic NSAIDs Selective COX-2 inhibitors. are not concentrated in the gastric mucosa. and are less likely to produce peptic ulcers Examples: Nabumetone: it is a pro-drug, changed in the body to its active metabolite. It is relatively selective COX-2 inhibitor. Meloxicam, rofecoxib & celecoxib are selective COX-2 inhibitors. Rofecoxib and celecoxib may cause cardiac toxicity (myocarditis).
  • 20. ).Acetaminophen (paracetamol It is only analgesic and antipyretic, it has no anti-inflammatory effect as it acts centrally only. It doesn’t cause gastritis. It doesn’t cause bronchial asthma.
  • 21. Kinetics: Well absorbed orally and rectally, Conjugated with glucuronic acid and sulforic acid Excreted in urine.
  • 22. Dynamics: inhibits PG synthesis in the CNS only. Uses: analgesic, antipyretic especially in children and those who cannot tolerate aspirin e.g. patients with bronchial asthma, peptic ulcer or gout. A/E: Rashes, blood dyscrasias
  • 23. Toxicity of paracetamol Large toxic dose causes liver cell necrosis. Treated by: N-acetylcysteine and methioneine which supply the S-H group necessary to detoxify the toxic metabolites.
  • 24. Thank you For more details please visit