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Pharmacology III > NON-Opioid Analgesics (Exam #2) > Flashcards

NON-Opioid Analgesics (Exam #2) Flashcards

1
Q

What is the rate limiting step of PG synthesis, and what are the two possible pathways following this step (what is made in each)?

A

RLS is Arachidonic Acid

  • Lipoxygenase = leukotrienes
  • Cyclooxygenase = PGs
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2
Q

Prostacyclin:

  • Produced by COX-1 or COX-2?
  • Vasoconstriction or Vasodilation?
  • Inhibit platelet aggregation or promote platelet aggregation?
A

PROSTACYCLIN (PGI2)

  • COX-2
  • Vasodilation
  • Inhibits platelet aggregation
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3
Q

Thromboxane:

  • Produced by COX-1 or COX-2?
  • Vasoconstriction or Vasodilation?
  • Inhibit platelet aggregation or promote platelet aggregation?
A

THROMBOXANE (TXA2)

  • COX-1
  • Vasoconstriction
  • Promote platelet aggregation
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4
Q

What is one additional benefit and one additional risk associated with COX-1 (NOT seen with COX 2)?

A
  • Benefit: protects against GI irritation

- Risk: promotes inflammation

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5
Q

What is the MOA of ASA?

A

IRREVERSIBLE inhibitor of COX-1 AND COX-2

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6
Q

What is the metabolism of ASA (2)?

A
  • Low dose = first order kinetics

- High dose = zero order kinetics

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7
Q

What are the four uses/properties of ASA? Which are also seen with NSAIDs (3) and Acetaminophen (2)?

A

ALL 3: analgesic, antipyretic

  • ASA: also anti-inflammatory, anti-platelet
  • NSAIDs: also anti-inflammatory
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8
Q

What AE is seen with ASA at low doses? High doses?

A
  • Low dose = respiratory ALKAlosis

- High dose = metabolic and respiratory ACIDosis

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9
Q

Use of ASA with which condition should be avoided, and why (think excretion)?

A

GOUT

- ASA is an acid so it competes with uric acid for excretion → uric acid buildup = Gout

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10
Q

What respiratory AE is seen with ASA? What other two systems are affected?

A
  • Respiratory = “aspirin asthma”
  • GI UPSET (COX-1 protects GI and it is inhibited)
  • Renal failure (inhibit PGs causes vasoconstriction)
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11
Q

What condition can be induced with the use of ASA in children (hence it is CI)? What is the DOC instead?

A

Reye’s Syndrome

- DOC is Acetaminophen

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12
Q

How do Non-Acetylated Salicylates differ from ASA (think MOA)?

A

Non-Acetylated Salicylates = reversible inhibition of COX

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13
Q

What are the two possible MOAs of NSAIDs?

A
  • Specific reversible inhibitors of COX-2

- NON-specific reversible inhibitors of COX-1 AND COX-2

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14
Q

What is the MOA of Celecoxib (Celebrex)?

A

Selective reversible inhibitor of COX-2

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15
Q

What AE is decreased with Celecoxib (Celebrex)? What AE are you at increased risk for, and why?

A

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)
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16
Q

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?

A
  • PREFERRED = Ibuprofen

- Worst (most potent): Indomethacin, Phenylbutazone

17
Q

Which NSAID reduces PMN migration, is very potent and has a high incidence of AEs?

A

Indomethacin

- One of last options, used for patent ductus arteriosus

18
Q

Which NSAID decreases arachidonic acid availability? What other drug is it often combined with, and why?

A

Diclofenac

- Combined with Misoprostol to decrease GI AEs

19
Q

Which NSAID is used as an analgesic post-operatively?

A

Ketorolac (Toradol)

20
Q

Which NSAID is often stopped after 5 days of use, and why?

A

Ketorolac (Toradol)

- Frequent GI AEs after 5 days of use

21
Q

What is the DOC of NSAIDs, and why?

A

Ibuprofen

- Lowest incidence of AEs

22
Q

How does Naproxen (Naprosyn) differ from other NSAIDs

A

Half life is 13 hours = can be taken ONCE daily

23
Q

Why is Acetaminophen often preferred to ASA (2)?

A
  • Better tolerated

- Lacks undesirable AEs

24
Q

What is the most serious AE associated with Acetaminophen?

A

Fatal hepatic necrosis

25
Q

Describe the metabolism of Acetaminophen?

A

Dose dependent free radical production = eliminated by GSH (reduced glutathione)

26
Q

What are the two primary uses of Acetaminophen? How is it NOT used (2)?

A
  • Mild/moderate pain
  • Fever in children

NOT anti-inflammatory, NOT anti-platelet

27
Q

What is the antidote for Acetaminophen poisoning?

A

N-acetylcysteine

28
Q

If a patient has NO hx of PUD, what is the recommended tx?

A

ANY NSAID

29
Q

If a patient has hx of PUD but it is NOT active, what is the recommended tx (2)?

A
  • Celecoxib (Celebrex) +/- antacids

- Some NSAIDs WITH Misoprostol/PPIs

30
Q

If a patient has ACTIVE PUD, what is the recommended tx (2)?

A
  • Acetaminophen

- Opioids

31
Q

What group of medications decreases absorption of ASA?

A

Antacids (decreases AEs)

Pharmacology III (25 decks)

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