NON-Opioid Analgesics (Exam #2) Flashcards
(31 cards)
What is the rate limiting step of PG synthesis, and what are the two possible pathways following this step (what is made in each)?
RLS is Arachidonic Acid
- Lipoxygenase = leukotrienes
- Cyclooxygenase = PGs
Prostacyclin:
- Produced by COX-1 or COX-2?
- Vasoconstriction or Vasodilation?
- Inhibit platelet aggregation or promote platelet aggregation?
PROSTACYCLIN (PGI2)
- COX-2
- Vasodilation
- Inhibits platelet aggregation
Thromboxane:
- Produced by COX-1 or COX-2?
- Vasoconstriction or Vasodilation?
- Inhibit platelet aggregation or promote platelet aggregation?
THROMBOXANE (TXA2)
- COX-1
- Vasoconstriction
- Promote platelet aggregation
What is one additional benefit and one additional risk associated with COX-1 (NOT seen with COX 2)?
- Benefit: protects against GI irritation
- Risk: promotes inflammation
What is the MOA of ASA?
IRREVERSIBLE inhibitor of COX-1 AND COX-2
What is the metabolism of ASA (2)?
- Low dose = first order kinetics
- High dose = zero order kinetics
What are the four uses/properties of ASA? Which are also seen with NSAIDs (3) and Acetaminophen (2)?
ALL 3: analgesic, antipyretic
- ASA: also anti-inflammatory, anti-platelet
- NSAIDs: also anti-inflammatory
What AE is seen with ASA at low doses? High doses?
- Low dose = respiratory ALKAlosis
- High dose = metabolic and respiratory ACIDosis
Use of ASA with which condition should be avoided, and why (think excretion)?
GOUT
- ASA is an acid so it competes with uric acid for excretion → uric acid buildup = Gout
What respiratory AE is seen with ASA? What other two systems are affected?
- Respiratory = “aspirin asthma”
- GI UPSET (COX-1 protects GI and it is inhibited)
- Renal failure (inhibit PGs causes vasoconstriction)
What condition can be induced with the use of ASA in children (hence it is CI)? What is the DOC instead?
Reye’s Syndrome
- DOC is Acetaminophen
How do Non-Acetylated Salicylates differ from ASA (think MOA)?
Non-Acetylated Salicylates = reversible inhibition of COX
What are the two possible MOAs of NSAIDs?
- Specific reversible inhibitors of COX-2
- NON-specific reversible inhibitors of COX-1 AND COX-2
What is the MOA of Celecoxib (Celebrex)?
Selective reversible inhibitor of COX-2
What AE is decreased with Celecoxib (Celebrex)? What AE are you at increased risk for, and why?
ONLY COX-2 is inhibited and COX-1 is not…
- LESS GI issues (COX-1 protection of GI is intact)
- Increased risk for CV diseases (COX-1 causes vasoconstriction and platelet aggregation - balance of COX-1 and COX-2 is off so COX-1 dominates)
Of the NSAID drugs that are NON-specific reversible inhibitors of COX-1 AND COX-2, which is preferred and which two are least preferred?
- PREFERRED = Ibuprofen
- Worst (most potent): Indomethacin, Phenylbutazone
Which NSAID reduces PMN migration, is very potent and has a high incidence of AEs?
Indomethacin
- One of last options, used for patent ductus arteriosus
Which NSAID decreases arachidonic acid availability? What other drug is it often combined with, and why?
Diclofenac
- Combined with Misoprostol to decrease GI AEs
Which NSAID is used as an analgesic post-operatively?
Ketorolac (Toradol)
Which NSAID is often stopped after 5 days of use, and why?
Ketorolac (Toradol)
- Frequent GI AEs after 5 days of use
What is the DOC of NSAIDs, and why?
Ibuprofen
- Lowest incidence of AEs
How does Naproxen (Naprosyn) differ from other NSAIDs
Half life is 13 hours = can be taken ONCE daily
Why is Acetaminophen often preferred to ASA (2)?
- Better tolerated
- Lacks undesirable AEs
What is the most serious AE associated with Acetaminophen?
Fatal hepatic necrosis
