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NSAIDS
Lakshmi Ananth
NSAIDS 1
INTRODUCTION OF PAIN AND
NOCICEPTION Nociception is the mechanism whereby noxious peripheral stimuli
are transmitted to t...
ACUTE & CHRONIC PAIN
Acute Pain Chronic Pain
Sudden onset Persistent – usually lasting
more than six months
Temporary (dis...
PROSTANOIDS AND MOA OF NSAIDS
NSAIDS 4
Prostanoi
ds
Membrane
Phospholipids
Arachidonic
Acid
Leukotrienes Prostaglandins Pr...
CYCLOOXYGENASE ENZYME AND
ITS ISOZYMES
NSAIDS 5
COX 1 COX 2 COX 3
Responsible for the
Physiologic production of
Prostanoid...
CLASSIFICATION OF NSAIDS
Non-Selective COX Inhibitors. Selective COX Inhibitors.
Drugs with Analgesic & Marked Anti-
infla...
ASPIRIN PROFILE
NSAIDS 7
• As anti-inflammatory: Aspirin irreversibly acetylates both isoforms of
cyclooxygenase enzyme. T...
ASPIRIN PROFILE
NSAIDS 8
• Adverse effects of Aspirin
GI disturbances (Can be prevented if given with misoprostol,
enteric...
ASPIRIN PROFILE
NSAIDS 9
• Contraindications
• Peptic ulcer.
• Hemophilia.
• Aspirin hypersensitivity Children with a vira...
ACETAMINOPHEN PROFILE
NSAIDS 10
• Rapid absorption from GIT.
• Significant First pass metabolism in gut wall & liver.
• Us...
SELECTIVE COX 2 INHIBITORS
• these are 10-20 times more selective to cox-2 and is
reversible.
• Celecoxib: chemically sulp...
SELECTIVE COX 2 INHIBITORS
Pharmacologic Effects & advantages:
Analgesic, Antipyretic, Anti-inflammatory effects
No inhibi...
CLINICAL USES OF NSAIDS
NSAIDS 13
NSAIDS 14
GENERIC NAME TRADE NAME SPECIFIC USES ADVERSE REACTIONS
Celecoxib Celebrex • Rheumatoid arthritis and
osteoarthr...
NSAIDS 15
GENERIC NAME TRADE NAME SPECIFIC USES ADVERSE
REACTIONS
Naproxen Aleve,
Anaprox*
• Management of
inflammatory di...
ADVERSE REACTIONS OF NSAIDS
• Gastrointestinal tract: nausea, vomiting, diarrhea, constipation,
epigastric pain, indigesti...
CONTRAINDICATIONS & INTERACTIONS
• Contraindicated in patients with known hypersensitivity and in
third trimester of pregn...
IN BRIEF….
NSAIDS 18
Advantage
s
disadvantag
es
NSAIDS
NSAIDS 19
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Pharmacology of NSAIDs Slide 1 Pharmacology of NSAIDs Slide 2 Pharmacology of NSAIDs Slide 3 Pharmacology of NSAIDs Slide 4 Pharmacology of NSAIDs Slide 5 Pharmacology of NSAIDs Slide 6 Pharmacology of NSAIDs Slide 7 Pharmacology of NSAIDs Slide 8 Pharmacology of NSAIDs Slide 9 Pharmacology of NSAIDs Slide 10 Pharmacology of NSAIDs Slide 11 Pharmacology of NSAIDs Slide 12 Pharmacology of NSAIDs Slide 13 Pharmacology of NSAIDs Slide 14 Pharmacology of NSAIDs Slide 15 Pharmacology of NSAIDs Slide 16 Pharmacology of NSAIDs Slide 17 Pharmacology of NSAIDs Slide 18 Pharmacology of NSAIDs Slide 19
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Nonsteroidal anti inflammatory drugs (NSAIDS)
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Nonsteroidal anti-inflammatory drugs (usually abbreviated to NSAIDs /ˈɛnsɛd/ en-sed), also called nonsteroidal anti-inflammatory agents/analgesics (NSAIAs) or nonsteroidal anti-inflammatory medicines (NSAIMs), are a drug class that groups together drugs that provide analgesic (pain-killing) and antipyretic (fever-reducing) effects, and, in higher doses, anti-inflammatory effects.

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Pharmacology of NSAIDs

  1. 1. NSAIDS Lakshmi Ananth NSAIDS 1
  2. 2. INTRODUCTION OF PAIN AND NOCICEPTION Nociception is the mechanism whereby noxious peripheral stimuli are transmitted to the central nervous system.  Pain is an unpleasant sensory and emotional experience with actual or potential tissue damage.  Superficial:  Stimulation of skin & mucous membranes.  Fast response  Deep:  Arises from muscles, joints, tendons, heart ..etc.  Fast response  When tissues become injured, they release chemicals called prostaglandins and leukotrienes that make the pain receptors more sensitive and thus causing pain. NSAIDS 2
  3. 3. ACUTE & CHRONIC PAIN Acute Pain Chronic Pain Sudden onset Persistent – usually lasting more than six months Temporary (disappears once stimulus is removed) Cause unknown – may be due to neural stimulation or a decrease in endorphins Physiological responses to acute pain include increased RR, HR, BP and reduction in gastric motility. Physiological responses are less obvious especially with adaptation. Psychological responses may include depression. NSAIDS 3
  4. 4. PROSTANOIDS AND MOA OF NSAIDS NSAIDS 4 Prostanoi ds Membrane Phospholipids Arachidonic Acid Leukotrienes Prostaglandins Prostacyclins Thromboxane Phospholip ase Cyclooxygena se Corticostero ids NSAID s
  5. 5. CYCLOOXYGENASE ENZYME AND ITS ISOZYMES NSAIDS 5 COX 1 COX 2 COX 3 Responsible for the Physiologic production of Prostanoids. Expressed only in brain, kidney & bone. COX-3 more effects in CNS Regulates the normal cellular processes  Gastric cytoprotection  Vascular homeostasis  Platelet aggregation  Kidney function.  Responsible for the elevated production of Prostanoids in inflammation & disease.  Expression at sites is increased in inflammation. ?? Non selective COX inhibitors eg. Aspirine
  6. 6. CLASSIFICATION OF NSAIDS Non-Selective COX Inhibitors. Selective COX Inhibitors. Drugs with Analgesic & Marked Anti- inflammatory Celecoxib , Etoricoxib, Meloxicam, Nimesulide. Salicylic Acid Derivatives (Aspirin) Pyrazolon Derivatives (Phenylbutazone) Acetic Acid Derivatives (Diclofenac, Sulindac) Oxicams (Piroxicam, Tenoxicam) Drugs with Analgesic & Moderate Anti- inflammatory Propionic acid derivatives (Ibuprofen, Naproxen) Fenamates (Meclofenamic) Drug with Analgesic & no Anti- inflammatory Para aminophenol Derivative NSAIDS 6
  7. 7. ASPIRIN PROFILE NSAIDS 7 • As anti-inflammatory: Aspirin irreversibly acetylates both isoforms of cyclooxygenase enzyme. There by inhibits biosynthesis of PG which helps in modulation of inflammation. Aspirin inhibits inflammation in Rheumatoid Arthritis but it neither arrests the progress of disease. • As analgesic: reduces production of PGE2 (involves in sensitizing nerve ending) there by repress sensation of pain. Toothache, Dysmenorhoea, used along with opioids in post operative pain. Inhibit pain stimuli at subcortical sites -Thalamus & Hypothalamus. • As antipyretic: Aspirin lowers raised body temperature , no effect on normal temperature. • As antiplatelet: In low doses Inhibit Platelet Aggregation, as TXA2 promotes platelet aggregation. • Dosage of Aspirin:
  8. 8. ASPIRIN PROFILE NSAIDS 8 • Adverse effects of Aspirin GI disturbances (Can be prevented if given with misoprostol, enteric coated aspirin) Impaired hemostasis Allergy or Hypersensitivity reactions Hyperuricemia (Retention of uric acid at low doses) Decreased renal function Salicylism (Vomiting, tinnitus, vertigo) Respiratory depression in toxic doses (by affect on CNS) Increased risk of Reye’s Syndrome (Acetaminophen or Ibuprofen should be used)
  9. 9. ASPIRIN PROFILE NSAIDS 9 • Contraindications • Peptic ulcer. • Hemophilia. • Aspirin hypersensitivity Children with a viral illness. • Chronic liver disease. • Aspirin should be stopped one week before elective surgery. • Avoid high doses in G-6-PD deficient. • Avoid in pregnancy & lactation. There is no antidote till date
  10. 10. ACETAMINOPHEN PROFILE NSAIDS 10 • Rapid absorption from GIT. • Significant First pass metabolism in gut wall & liver. • Used for mild to moderate pain Toxicity: At therapeutic doses drug fever mild increase in hepatic enzymes At over doses(above 15g) Hepatic necrosis Renal tubular necrosis Hypoglycemic coma N-acetyl Cysteine is antidote
  11. 11. SELECTIVE COX 2 INHIBITORS • these are 10-20 times more selective to cox-2 and is reversible. • Celecoxib: chemically sulphonamide having half life of 11hrs. • Meloxicam: Related to Piroxicam. Preferentially selective COX- 2 inhibitor. • Etoricoxib: Long half life: 22 hrs, Monitoring of hepatic functions required. • Nimesulide: new compound less gastric irritation. • Valdecoxib & Rofecoxib: Withdrawn due to. higher risk of incidence of Cardiovascular thrombotic events Myocardial Infarction & stroke. NSAIDS 11
  12. 12. SELECTIVE COX 2 INHIBITORS Pharmacologic Effects & advantages: Analgesic, Antipyretic, Anti-inflammatory effects No inhibition of platelet aggregation. Does not prolong bleeding time. No inhibition of protective gastric PGs No gastric irritation. • Adverse effects: Potential for increasing thrombotic events Myocardial infarction & stroke Renal toxicities similar to non selective NSAIDs Skin rashes for Celecoxib NSAIDS 12
  13. 13. CLINICAL USES OF NSAIDS NSAIDS 13
  14. 14. NSAIDS 14 GENERIC NAME TRADE NAME SPECIFIC USES ADVERSE REACTIONS Celecoxib Celebrex • Rheumatoid arthritis and osteoarthritis. ophthalmic changes Diclofenac Sodium Voltaren* • Rheumatoid arthritis and osteoarthritis. • Ankylosing spondylitis Gastric and duodenal ulcers formation. GI bleeding. Fenoprofen Nalfon • Long term management to mild to moderate pain Visual disturbances Jaundice Peptic ulcers Ibuprofen Advil, Genpril • Mild to moderate pain. • Painful dysmenorrhea. • Rheumatoid arthritis. GI Disturbances Nausea, Dizziness GI Bleeding Indomethacin Indocin • Rheumatoid arthritis • Ankylosing spondylitis • Acute gouty arthritis Hematologic changes Nausea, Constipation Duodenal Ulcers meflofenamate meflofenamate* • mild to moderate pain. • Painful dysmenorrhea. Rash Bleeding Headache, Dizziness, Nausea, Dyspepsia
  15. 15. NSAIDS 15 GENERIC NAME TRADE NAME SPECIFIC USES ADVERSE REACTIONS Naproxen Aleve, Anaprox* • Management of inflammatory disorders. • Mild to moderate pain. • Painful dysmenorrhea. visual changes, nausea, vomiting GI bleeding. Rofecoxib Vioxx • Signs and symptoms of osteoarthritis. • Management of acute pain • Primary dysmenorrhea. Visual Disturbances Sulindac Clinoril* • Mild to moderate pain. • Rheumatoid arthritis • Ankylosing spondylitis • gouty arthritis nausea, vomiting, Diarrhoea, constipation, GI bleeding. Gastric and duodenal ulcers formation. Valdecoxib Bextra • osteoarthritis. • Rheumatoid arthritis Anemia, Headache, Dyspepsia,
  16. 16. ADVERSE REACTIONS OF NSAIDS • Gastrointestinal tract: nausea, vomiting, diarrhea, constipation, epigastric pain, indigestion, abdominal distress or discomfort, intestinal ulceration, stomatitis, jaundice, bloating, anorexia, and dry mouth • Central nervous system: dizziness. headache, drowsiness, insomnia. • Cardiovascular: decrease or increase in blood pressure, and cardiac arrhythmias • Renal: hematuria and acute renal failure In those with impaired renal function • Special senses: visual disturbances, blurred or diminished vision. • Hematologic: anemia NSAIDS 16
  17. 17. CONTRAINDICATIONS & INTERACTIONS • Contraindicated in patients with known hypersensitivity and in third trimester of pregnancy and during lactation. •If a patient is allergic to one NSAID, there is an increased risk of an allergic reaction with any other NSAID (Cross sensitivity) • Cautiously in patients with bleeding disorders, renal disease, cardiovascular disease, or hepatic impairment. • Increased risk of Ulcers in patients of age 65 and above. • Prolong bleeding time and increase the effects of anticoagulants. • May decrease the effects of diuretics or antihypertensive drugs. NSAIDS 17
  18. 18. IN BRIEF…. NSAIDS 18 Advantage s disadvantag es
  19. 19. NSAIDS NSAIDS 19
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Nonsteroidal anti-inflammatory drugs (usually abbreviated to NSAIDs /ˈɛnsɛd/ en-sed), also called nonsteroidal anti-inflammatory agents/analgesics (NSAIAs) or nonsteroidal anti-inflammatory medicines (NSAIMs), are a drug class that groups together drugs that provide analgesic (pain-killing) and antipyretic (fever-reducing) effects, and, in higher doses, anti-inflammatory effects.

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