Pharm II (NSAIDS)

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Pharm II (NSAIDS)
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2011-01-25 18:52:35
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Pharm II NSAIDS
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Pharm II (NSAIDS)
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  1. What do you treat Sharp pain wih?
    What do you treat Dull pain with?
    • NSAIDs
    • Opioids
  2. What are some Roles of Prostaglandins?
    • -Inhibit Gastric acid secretion and increase the secretion of protective mucus.
    • - Involved in labor induction/ maintenance
    • -Maintain BF to the kidney
    • -TXA2 causes Vasoconstriction
    • -PGI2 causes Vasodilation and antiplatlet action.
  3. What is the Mech for the prodiction of Prostaglandins, TXA2 and Leukotrienes?
    • Phospholipase A2 takes phospholipids and turns them into Arachidonic acid.
    • This is then Brokendown By two things.
    • COX (1&2)--- Giving rise to Prostaglandins and TXA2

    And Lipoxygenases ---- Giving rise to Leukotrienes.
  4. Info on the two COX enzymes.
    COX-1: it is Constitutive. Involved in Homeostatic functions (GI,Renal, Platlets..)

    COX-2: is Induced by IL1 and TNF. Involved in Inflamation.
  5. NSAIDS
    • -Are slightly acidic
    • -Inhibit the COX enzymes
    • -Have Antipyretic, analgesic and anti-inflammatory actions.
  6. Name the Traditional NSAIDS
    • -Salicylic acids (Aspirin)
    • -Propionic acid (Ibuprofen, Ketoprofen, Naproxen)
    • -Acetic acid (Indomethacin)
    • -Oxicams (Piroxicam, Meloxicam)

    -Others: Ketorolac, Diclofenac
  7. Aspirin

    What is an adverse effect? What can treat this?
    IRREVERSIBLY acetylates and inactivates COX. (the rest are reversible)

    Aspirin is Anti-inflammatory, analgesic and anti-pyretic.

    • -It inhibits the synthesis of Mucus in the stomach and increases the production of Acid--> ulcers
    • -Treat the ulcers with Misoprostol (PGE-1 analogue)
  8. What is the effect of low dose of Aspirin?

    What is the effect of high dose of Aspirin?
    Irreversibly inhibits COX-1 --> decreasing TXA2 production in platlets.

    Irrecersibly inhibits COX-2 --> no PGI2 production in Endothelial cells.
  9. What should Aspirin not be used in? Why?
    Gout, because it decreases uric acid secretion at low doses makeing the gout worse. Also, at high doses it increase the excretion of urate--> urate stones.
  10. What is a consiquence of long term NSAIDS use?
    • -Nephrotoxiciy
    • -Aspirin at high doses causes uncoupling of the ETC. increasing O2 demand on the cell and decreasing ATP production--> leading to hyperventilation and respiratory alkylosis.
    • -Can also cause respiratory paralysis--> to acidosis.
  11. What is Reys syndrome?
    It is associated with fatal hepatitus during the viral infection in children. DO NOT use Aspirin for FEVERs in children.
  12. Aspirins adverse effects


    What can you use to treat Aspirin overdose?
    • N/V
    • Hyperventilation
    • Tinnitus (ringing ears)
    • Hallucinations (High doses)
    • restlessness
    • Cunvulsions
    • Acidosis


    -Treat with Sodium Bicarbinate
  13. What are the kinetics of aspirin?
    • They follow the Zero order kinetics
    • If you double the dose= 10X the concentration in the blood
  14. What are the Propionic acid derivatives?
    What are they used for?
    Ibuprofen and Naproxen

    • -Used in the treatment of RA and Osteoarthritis
    • -Ibuprofen is also as effective as Indomethacin in closing the patent ductus arteriosis
  15. What are the Oxicam derivatives?

    What are they used for?
    Piroxicam and Meloxicam

    - They are sed to treat RA, Osteparthritis and ankylosing spondylitis.

    (note: they block COX 2 more than Cox 1)
  16. What are the Acetic acid derivatives?
    What are they used for?
    Indomethacin

    - Used in the treatment of Gout and ankylosing spondylitis. And also to close the PDA.
  17. Name a COX2 selective inhibitor

    What is it used for?
    Celecoxib

    RA and Osteoarthritis

    -They have a lower risk of ulcers and have no effect on platlets.
  18. What is Acetaminophen?
    It is an analgesic and antipyretic (tylenol)

    The drug is a weak anti inflammatoy action because it is destroyed by peroxidases in the inflamed tissue

    It inhibits COX in the CNS (not the periphery)
  19. What are the Two pathways of Acetaminophen metabolism?
    Major: Undergos Glucuronide/Sulfate conjugation in the liver and excreted in the urine

    Minor: produces NABI reactive intermediate the conjugates with glutathione and gets excreted in the urine.
  20. What are some Toxicities of Acetaminophen?

    What do you used to treat this?
    It can deplete the Glutathione stores --> leading to Hepatotoxicity and necrosis.

    • -RTN may also occur
    • -Treat with Acetylcysteine

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