Pharm Mod 4

  1. OD on Acetaminophen can cause?
    serious or fatal hepatic injury
  2. Maximum safe dose of Acetaminophen.
    4 grams per day (> 12 years)
  3. Caution using Acetaminophen with what other drug?
  4. Analgesic/antipyretic dosing for ASA
  5. Anti-inflammatory dosing for ASA.
    1000mg (3-5 g/day)
  6. What happens with Salicylate overdose?
    • metabolic acidosis
    • tinnitis
  7. Why is ASA rarely used as an anti-inflammatory?
    GI side effects
  8. When should ASA never be used? Why?
    • viral syndromes in kids and teens
    • risk of Reye's Syndrome
  9. Non-acetylated salicylates do not interfere with __________
    platelet aggregation
  10. What type of salicylates are well tolerated by asthma pts?
    non-acetylated salicylate
  11. More effective analgesic than full doses of aspirin or APAP
    Traditional NSAIDs
  12. Analgesic effect equal or greater than usual doses of an opioid combined with APAP
    Traditional NSAIDs
  13. Liver toxicity is not seen with _________ like it is with _______. Why?
    • NSAIDs
    • Acetaminophen
    • They are metab & excreted in urine
  14. Why are NSAIDs not used for cardioprotection like ASA is?
    b/c NSAIDs block platelet aggregation reversibly
  15. How can NSAIDs lead to PUD by inhibiting PGs?
    • PGs protect gastric & duodenal mucosa
    • Inhibition → ↓ mucus production & gastric BF
    • Inhibition → ↑ acid production
    • →→→PUD
  16. Risk factors for GI AE of NSAIDs.
    • High doses,
    • prolonged use,
    • previous GI ulcer or bleeding,
    • excessive ETOH intake,
    • elderly,
    • corticosteroid use
  17. Other than inhibiting PGs, how do NSAIDs cause GI AE?
    • (Local irritation)
    • Lipid soluble at low pH → enter gastric mucosal cells → lose lipid solubility → become ionized & trapped in gastric mucosal cells
  18. What drugs can be used in combo with NSAIDs to prevent ulcers?
    • Prostaglandin analog misoprostil (Cytotec)
    • Diclofenac/misoprostol (Arthrotec)
    • PPIs
    • H2-receptor antagonists
  19. Why would Sucralfate (Carafate) be used in combo with NSAIDs?
    To prevent dispeptic symptoms only (not prevent ulcers)
  20. Drugs with low Risk of GI Adverse Effects
    • Ibuprofen and naproxen at low doses
    • Etodolac, Sulindac
    • Celecoxib
  21. Drugs with Moderate Risk of GI Adverse Effects
    • Ibuprofen and naproxen at mod-high doses
    • Diclofenac,
    • oxaprozin,
    • meloxicam,
    • nabumetone
  22. Drugs with High Risk of GI Adverse Effects
    • Tolmetin,
    • piroxicam,
    • aspirin,
    • indomethacin,
    • ketorolac
  23. What is the main difference b/w drugs that have a low risk of GI effects and drugs that have high risk?
    • High risk inhibit COX1 more than COX2
    • Low risk inhibit COX2 more than COX1
  24. Acetaminophen is _________ toxic at high doses, where NSAIDs have a risk for _______ effects.
    • hepatically
    • renal
  25. Risk factors for renal SE of NSAIDs.
    • Old age,
    • CHF, HTN,
    • renal insufficiency,
    • ascites, volume depletion, diuretic therapy
  26. Why do NSAIDs lead to renal AE?
    • Decreased synthesis of renal vasodilator PGs (PGE2)
    • → decreased renal blood flow &
    • → Fluid and sodium retention
  27. Major AEs of NSAIDs
    • renal failure or hypertension
    • Interstitial nephritis (rare)
  28. “Renal sparing” NSAIDs (lower risk, not devoid).
    • Sulindac, nabumetone
    • Celecoxib
  29. There is increased risk of renal AE with highly potent NSAIDS such as?
    • Ketorolac
    • Indomethacin
  30. How do NSAIDs increase levels of what drugs?
    • Warfarin (also highly protein-bound)
    • Digoxin  (also highly protein-bound)
    • Phenytoin  (also highly protein-bound)
    • Sulfonylureas  (also highly protein-bound)
    • Sulfonamides  (also highly protein-bound)
  31. NSAIDs decrease the effects of what class of drugs?
    • diuretics
    • BB
    • ACEIs
  32. Warfarin is least likely to interact with which NSAIDs?
    • diclofenac,
    • ibuprofen,
    • tolmetin,
    • naproxen
  33. NSAIDs suppress PGs, and potentially suppress effects of ______ drugs, such as _________.
    • Hypertensive
    • diuretics, β-blockers, ACEIs
  34. _________ increases levels of most NSAIDs.
  35. Avoid Probenicid with __________. Why?
    • ketorolac
    • Probenicid increases levels (ketorolac highly potent already)
  36. Do not exceed _______ of ketorolac use
    5 days
  37. Serious AE of Ketorolac.
    • Serious GI bleeding,
    • ulceration, perforation and/or
    • renal toxicity can occur (especially in the elderly)
  38. What is Celecoxib?
    Only COX2 selective NSAID available
  39. What is the lowest effective dose for Celecoxib? What is it equal to for naproxen?
    • ≤200 mg/day
    • 200 mg/day = naproxen 500 mg BID
  40. When should Celecoxib be taken?
    with food (it is PO)
  41. What does the μ (mu) 1 opioid receptor result in when agonized?
    • supraspinal analgesia
    • bradycardia
    • resp depression, sedation
    • decreased GI motility
    • pupillary constriction
  42. Which drugs are primarily agonists at mu opioid receptors?
    • Morphine
    • Heroin
    • Fentanyl
    • Codeine
  43. What is Buprenorphine (Buprenex)?
    Most commonly used partial/mixed agonist-antag for pain control
  44. Why isn't morphine as effective when given PO?
    • b/c of first-pass metabolism
    • most of it won't make it to systemic circulation
  45. Why is it important to consider renal fxn with morphine?
    • *pts w/ renal insufficiency may not be able to clear active metabolites!**
    • build-up  → Nausea, myoclonus, hallucinations
  46. How does morphine cause pruritus?
    due to an off-target effect of releasing histamine
  47. When given PO,  codeine is combined with which drugs?
    APAP, guaifenesin, promethazine
  48. How is codeine metabolized?
    10% is metab by CYP450 2D6 to morphine
  49. ______ is better for cough at lower doses than for pain relief.
  50. Hydrocodone is always combined with one of which drugs?
    • APAP,
    • ASA,
    • ibuprofen, or
    • antihistamine
  51. Hydrocodone is a _________ and a _________.
    Analgesic and antitussive
  52. Administration routes for hydrocodone.
  53. Oxycodone is available by itself or in combo with which drugs? Route of admin?
    • APAP or ASA
    • *PO only*
  54. Why are oxycodone, methadone, and hydromorphone safer in patients with renal dysfunction?
    no active metabolites
  55. What is oxycontin?
    ER form of hydrocodone
  56. Routes of admin for hydromorphone.
    • PO,
    • IM, IV, SubQ,
    • rectal,
    • epidural
  57. Routes of admin for methadone.
    PO, IV, SubQ
  58. Indication for Meperidine.
    • post-op shaking and chills
    • (short-term 24-48 hrs)
  59. Main metabolite of meperidine and effects.
    • normeperidine
    • Accumulation = CNS excitation/anxiety and convulsions
  60. Cautions for meperidine.
    • elderly,
    • renal dysfunction
    • (Long half-life (15-20 hrs))
  61. In 2010, _______ was removed from market due to serious cardiac toxicity
    Propoxyphene (PO)
  62. Route of admin for Fentanyl.
    • IV,
    • transdermal patch,
    • transmucosal lozenge,
    • buccal tablets
  63. How often is Fentanyl patch applied?
  64. Fentanyl is _______ more potent than morphine.
  65. __________ is similar to pentazocine, butorphanol, nalbuphine and has a ceiling effect.
  66. _________ is a partial opioid agonist can precipitate withdrawal symptoms if already on a full agonist.
    Buprenorphine (displaces full agonists from mu receptors)
  67. Route of admin for Buprenorphine
    SL, parenteral
  68. Sublingual tablets for treatment of opioid dependence
    • Buprenorphine alone (Subutex) or
    • combined with naloxone (Suboxone)
  69. Why is heroin 3x more potent than morphine?
    due to greater lipid solubility (crosses BBB quicker and to greater extent)
  70. ________ is 1000x more potent than morphine
    3-methylfentanyl (China White)
  71. Most common AE of opioids.
    Sedation, dizziness, nausea, vomiting, itching, sweating and constipation
  72. Most serious AE of opioids.
    Respiratory depression
  73. What to give pts who will be on opioids for extended period of time.
    • Stimulant laxative with or without a stool softener
    • Senna/Docusate
  74. ___________ Blocks reuptake of norepinephrine and serotonin
    Tramadol (PO)
  75. Effectiveness in combination with ASA or APAP comparable to codeine and propoxyphene combination
  76. Seizures possible in patients taking MAOIs, antipsychotics with this drug.
  77. Analgesia only partially reversible with naloxone.
  78. DOC for reversal of opioid overdose associated with respiratory depression, sedation, coma, hypotension, opioid-induced psychotomimetic effects
    Naloxone (Narcan)
  79. Reversal of opioid-induced anesthesia
    Naloxone (Narcan)
  80. How is Narcan administered?
    Parenterally only (not PO)
  81. Approved for treatment of alcoholism
    Naltrexone (Revia)
  82. Post-operative reversal of opioids and treatment of opioid overdose
    Nalmephene (Revex)
  83. Drugs used to treat somatic symptoms of withdrawal from opioids.
    • Clonidine
    • Benzodiazepines
    • Antiemetics
    • Antidiarrheals
    • Analgesics (non-opioid)
  84. Maintenance tx for withdrawal from opioids.
    • Methadone
    • Buprenorphine
    • Buprenorphine/naloxone SL (Suboxone)
  85. Low-dose IV/IM, Analgesic for cancer and post operative pain; Reduces n/v
  86. Used for tx of pain and also for HTN.
    Transdermal clonidine patch
  87. Analgesic tx for OA.
    • APAP
    • NSAIDs
    • COX-2 Inhibitors
  88. Inflammation tx for OA
    • NSAIDs
    • COX-2 Inhibitors
    • Intra-articular corticosteroids
  89. Why can't APAP be used to tx RA?
    It is not an anti-inflammatory
  90. Prodrug for mercaptopurine and used to tx Crohns.
    Azathioprine (PO)
  91. Primarily for mild RA; also an anti-malarial drug
    Hydroxychloroquine (PO)
  92. Effective for mild to moderate RA; also for Crohns Disease, Ulcerative Colitis
    Sulfasalazine (PO)
  93. Can turn body fluids yellow-orange.
    Sulfasalazine (PO)
  94. _________  can bind iron and decrease absorption. When should a pt
  95. If a pt is taking Sulfasalazine, what could reduce conversion to its active form?
  96. Folate antagonist
    Methotrexate (PO, IM, subQ)
  97. Main AE of methotrexate. How is it treated?
    • megaloblastic anemia
    • Folic acid replacement
Card Set
Pharm Mod 4
Exam 2