Exam #01d - NSAID & APAP Flashcards
Name the rare syndrome of liver degeneration and encephalitis in children treated with aspirin during viral infection?
Reye’s syndrome
What is the brand name of Diclofenac?
Voltaren
What are the 4 major effects of NSAIDs?
- anti-inflammatory
- analgesic
- antipyretic
- antiplatelet
If arachidonic acid metabolism is inhibited by an NSAID inhibiting COX, what will that do to the amount of available arachidonic acid?
The amount of arachidonic acid will increase…meaning more will be available to be metabolized by other enzymes, like lipoxygenase, and form leukotrienes
Indicate which major NSAID effect this MOA refers to: decrease in the PG response to IL-1 (PG enhances activity of IL)?
antipyretic
Indicate which major NSAID effect this MOA refers to: reversible inhibition of thromboxane (platelets) synthesis? Is there an exception here?
antiplatelet
Yes, aspirin causes IRREVERSIBLE inhibition of thromboxane (platelets) synthesis
Indicate which major NSAID effect this MOA refers to: decrease in vasodilator PG, less vasodilation, less edema?
antiinflammatory
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?
analgesic
Indicate the following ASA dose ranges you’d find to produce the following major NSAID effects:
- Anti-inflammatory
- Analgesic/Antipyretic
- Antiplatelet
At what dose range will GI bleed occur?
- Anti-inflammatory - 2,400-4,000 mg
- Analgesic/Antipyretic - 300-2,400 mg
- Anti-platelet -
What is the NSAID AE of GI ulceration due to? What medications (2) can be given with NSAIDs to prevent GI ulceration?
inhibition of COX1
- Misoprostol
- PPI
True or False - coating NSAID can help with preventing GI bleeds?
False
List the (5) symptoms of salicylism (aspirin overdose)?
- tinnitus
- vertigo
- HA
- fever
- change in mental status
True or False - NSAID AE’s increase with age and are greater in women?
True
What is the difference between COX-1 and COX-2 with regards to where they are present?
COX-1 is expressed in most tissues, whereas COX-2 is induced only in inflammatory cells
Which COX is constitutively (always) active and which COX is inducible?
COX-1 is always active
COX-2 is inducible
Which COX is necessary for cytoprotection in GI tract?
COX-1
Name (2) selective COX-2 inhibitors?
- rofecoxib (Vioxx)
2. celecoxib (Celebrex)
Give the brand name for the following OTC NSAIDs:
- Diflunisal
- Etodalac
- Fenoprofen
- Flurbiprofen
- Ibuprofen
- Indomethacin
- Ketoprofen
- Ketorolac
- Nabumentone
- Naproxen
- Oxaprozin
- Phenylbutazone
- Piroxicam
- Sulindac
- Tolmetin
- Diflunisal - Dolobid
- Etodalac - Lodine
- Fenoprofen - Nalfon
- Flurbiprofen - Ansaid
- Ibuprofen - Nuprin
- Indomethacin - Indocin
- Ketoprofen - Orudis
- Ketorolac - Toradol
- Nabumentone - Relafen
- Naproxen - Aleve
- Oxaprozin - Daypro
- Phenylbutazone - SAME
- Piroxicam - Feldene
- Sulindac - Clinoril
- Tolmetin - Tolectin
What are the (2) major therapeutic actions of APAP?
- analgesia
- antipyretic
NOT clinically anti-inflammatory or antiplatelet
What is the major route of metabolism of APAP? How is it excreted?
Metabolism primarily hepatic glucuronidation and sulfation (phase 2) to non-toxic metabolites and excreted in urine
True or False - there is no GI bleeding AE associated with APAP?
True
What is the major AE of concern?
hepatic toxicity (potentially lethal hepatic necrosis at high doses or with excess ethanol)
List the (3) ways APAP could cause liver toxicity?
- alcohol
- OD
- not enough glutathione (detoxifies the small amount of toxic metabolite produced during APAP metabolism)
What is the rate-limiting factor in glutathione synthesis?
the availability of cysteine (glutathione is synthesized from cysteine, glutamate, and glycine
What drug is given to treat APAP OD?
Acetylcysteine (rapidly absorbed and hydrolyzed to cysteine to form plenty of glutathione)
