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Pharmacology 2 > Exam #01d - NSAID & APAP > Flashcards

Exam #01d - NSAID & APAP Flashcards

1
Q

Name the rare syndrome of liver degeneration and encephalitis in children treated with aspirin during viral infection?

A

Reye’s syndrome

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2
Q

What is the brand name of Diclofenac?

A

Voltaren

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3
Q

What are the 4 major effects of NSAIDs?

A
  1. anti-inflammatory
  2. analgesic
  3. antipyretic
  4. antiplatelet
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4
Q

If arachidonic acid metabolism is inhibited by an NSAID inhibiting COX, what will that do to the amount of available arachidonic acid?

A

The amount of arachidonic acid will increase…meaning more will be available to be metabolized by other enzymes, like lipoxygenase, and form leukotrienes

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5
Q

Indicate which major NSAID effect this MOA refers to: decrease in the PG response to IL-1 (PG enhances activity of IL)?

A

antipyretic

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6
Q

Indicate which major NSAID effect this MOA refers to: reversible inhibition of thromboxane (platelets) synthesis? Is there an exception here?

A

antiplatelet

Yes, aspirin causes IRREVERSIBLE inhibition of thromboxane (platelets) synthesis

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7
Q

Indicate which major NSAID effect this MOA refers to: decrease in vasodilator PG, less vasodilation, less edema?

A

antiinflammatory

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8
Q

Indicate which major NSAID effect this MOA refers to: less PGs means less sensitization of nociceptive nerve endings to mediators such as bradykinin and 5-HT?

A

analgesic

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9
Q

Indicate the following ASA dose ranges you’d find to produce the following major NSAID effects:

  1. Anti-inflammatory
  2. Analgesic/Antipyretic
  3. Antiplatelet

At what dose range will GI bleed occur?

A
  1. Anti-inflammatory - 2,400-4,000 mg
  2. Analgesic/Antipyretic - 300-2,400 mg
  3. Anti-platelet -
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10
Q

What is the NSAID AE of GI ulceration due to? What medications (2) can be given with NSAIDs to prevent GI ulceration?

A

inhibition of COX1

  1. Misoprostol
  2. PPI
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11
Q

True or False - coating NSAID can help with preventing GI bleeds?

A

False

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12
Q

List the (5) symptoms of salicylism (aspirin overdose)?

A
  1. tinnitus
  2. vertigo
  3. HA
  4. fever
  5. change in mental status
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13
Q

True or False - NSAID AE’s increase with age and are greater in women?

A

True

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14
Q

What is the difference between COX-1 and COX-2 with regards to where they are present?

A

COX-1 is expressed in most tissues, whereas COX-2 is induced only in inflammatory cells

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15
Q

Which COX is constitutively (always) active and which COX is inducible?

A

COX-1 is always active

COX-2 is inducible

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16
Q

Which COX is necessary for cytoprotection in GI tract?

A

COX-1

17
Q

Name (2) selective COX-2 inhibitors?

A
  1. rofecoxib (Vioxx)

2. celecoxib (Celebrex)

18
Q

Give the brand name for the following OTC NSAIDs:

  1. Diflunisal
  2. Etodalac
  3. Fenoprofen
  4. Flurbiprofen
  5. Ibuprofen
  6. Indomethacin
  7. Ketoprofen
  8. Ketorolac
  9. Nabumentone
  10. Naproxen
  11. Oxaprozin
  12. Phenylbutazone
  13. Piroxicam
  14. Sulindac
  15. Tolmetin
A
  1. Diflunisal - Dolobid
  2. Etodalac - Lodine
  3. Fenoprofen - Nalfon
  4. Flurbiprofen - Ansaid
  5. Ibuprofen - Nuprin
  6. Indomethacin - Indocin
  7. Ketoprofen - Orudis
  8. Ketorolac - Toradol
  9. Nabumentone - Relafen
  10. Naproxen - Aleve
  11. Oxaprozin - Daypro
  12. Phenylbutazone - SAME
  13. Piroxicam - Feldene
  14. Sulindac - Clinoril
  15. Tolmetin - Tolectin
19
Q

What are the (2) major therapeutic actions of APAP?

A
  1. analgesia
  2. antipyretic

NOT clinically anti-inflammatory or antiplatelet

20
Q

What is the major route of metabolism of APAP? How is it excreted?

A

Metabolism primarily hepatic glucuronidation and sulfation (phase 2) to non-toxic metabolites and excreted in urine

21
Q

True or False - there is no GI bleeding AE associated with APAP?

A

True

22
Q

What is the major AE of concern?

A

hepatic toxicity (potentially lethal hepatic necrosis at high doses or with excess ethanol)

23
Q

List the (3) ways APAP could cause liver toxicity?

A
  1. alcohol
  2. OD
  3. not enough glutathione (detoxifies the small amount of toxic metabolite produced during APAP metabolism)
24
Q

What is the rate-limiting factor in glutathione synthesis?

A

the availability of cysteine (glutathione is synthesized from cysteine, glutamate, and glycine

25
Q

What drug is given to treat APAP OD?

A

Acetylcysteine (rapidly absorbed and hydrolyzed to cysteine to form plenty of glutathione)

Pharmacology 2 (16 decks)

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