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*Pharm Exam 2 > NSAIDs > Flashcards

NSAIDs Flashcards

1
Q

All NSAIDs, with the exception of ______, act as competitive COX enzyme inhibitors.

A

Aspirin

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2
Q

Describe the unique MOA of Aspirin.

A

It acts as an irreversible non-competitive COX enzyme inhibitor.

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3
Q

What are the 2 distinct cyclooxygenase enzymes and what is their shared function?

A

COX-1 and COX-2; both catalyze the rate-limiting conversion of membrane-derived arachidonic acid into prostaglandins and thromboxane

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4
Q

Which of the COX enzymes is constitutively expressed in most tissues?

A

COX-1

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5
Q

What are the distinct physiological roles of COX-1 and COX-2?

A

COX-1 is responsible for constant low level PG production (for housekeeping functions), while COX-2 is responsible for acute high level PG production (causing pain, inflammation, and fever).

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6
Q

What is the clinical efficacy vs. adverse effects of NSAIDs due to?

A
  • clinical efficacy: COX-2 inhibition

- adverse effects: COX-1 inhibition

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7
Q

True or false: Prostaglandins generate pain responses themselves.

A

False- prostaglandins increase responses to painful stimuli but do NOT generate pain responses themselves.

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8
Q

COX-1 activity is involved in regulating which tissues/organ systems?

A
  • GI tract
  • cardiovascular system
  • kidney
  • female reproduction
  • ductus arteriosus
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9
Q

What is the function of prostaglandins in the GI tract?

A

PGs are cytoprotective for the stomach and limit damage to stomach lining caused by gastric acid and digestive enzymes.

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10
Q

What role do prostaglandins play in female reproduction?

A

PGE2/PGF2α production stimulates uterine contraction and plays a role in birth (thus, NSAID use may delay labor)

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11
Q

When would it be beneficial to administer NSAID therapy to a newborn?

A

When the ductus arteriosus does not close spontaneously (NSAID therapy can promote closure of a patent ductus by inhibiting synthesis of fetal PGs responsible for keeping ductus open)

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12
Q

How can NSAID use during pregnancy affect the fetus?

A

It may prematurely close the ductus arteriosus and adversely affect fetal circulation. This is because prostaglandins are responsible for keeping the ductus open during fetal life.

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13
Q

What are the 3 main types of NSAIDs?

A

1) Aspirin and salicylates
2) Traditional non-selective NSAIDs
3) Coxibs (selective COX-2 inhibitors)

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14
Q

What is a unique indication for low dose Aspirin?

A
  • prophylactic prevention of cardiovascular events (like MI and stroke)
  • treatment for acute occlusive stroke
  • secondary prevention of CVD after a prior MI, stroke, or TIA
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15
Q

What is the recommended dose of aspirin for anti-platelet activity?

A

81 mg/day

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16
Q

Platelets express ONLY [COX enzyme] and produce principally _________. How do endothelial cells differ?

A

COX-1; TXA2 (thromboxane)
*Endothelial cells express COX-1 and COX-2 but lack TXA2 synthase; the primarily produce PGI2, which is a vasodilator and inhibits platelet aggregation

17
Q

What does thromboxane do?

A

It is a vasoconstrictor that promotes platelet aggregation and activation.

18
Q

The balance between which compounds regulates systemic BP and thrombogenesis?

A

TXA2 (thromboxane) and PGI2 (prostacyclin)

19
Q

When are prostaglandins especially important in the kidney?

A

in disease states (like HF and renal disease) to counteract the presence of vasoconstrictors (since PGs promote vasodilation in the kidney)

20
Q

Which of the salicylates is an ineffective anti-pyretic and why?

A

diflusinal, as it does not cross the BBB

21
Q

Why are the salicylates less potent COX inhibitors than aspirin?

A

They are non-acetylated and therefore unable to irreversibly inhibit COX-1.

22
Q

All salicylates are ______% protein-bound, giving them a high potential for _________.

A

50-90%; drug interactions

23
Q

What are examples of drugs that the salicylates interact with?

A

warfarin and sulfonylureas

24
Q

When is salicylate use more preferable to aspirin?

A

in patients w/ increased risk of GI complications (ie, gastric ulcers) and patients w/ increased risk of bleeding (hemophiliacs)

25
Q

What are the symptoms of salicylate intoxication?

A

hyperventilation, metabolic acidosis, hypoglycemia, confusion, tremors, seizures, cerebral edema, delirium, hyperthermia, respiratory depression, coma, death

26
Q

What treatment is available for salicylate toxicity/overdose?

A

alkalinization of the urine w/ sodium bicarb

27
Q

All traditional NSAIDs exhibit which 3 main effects?

A
  • anti-inflammatory
  • anti-pyretic
  • analgesic
28
Q

Which NSAIDs are used in the treatment of gout?

A

traditional NSAIDs (tNSAIDs), but not aspirin/salicylates

29
Q

What is ibuprofen ideal for treatment of, and why?

A

fever and acute pain due to its rapid onset of action (15-30 mins)

30
Q

What is naproxen ideal for, and why?

A

anti-pyretic use due to its rapid onset of action (60 mins)

31
Q

What is the serum half life of naproxen?

A

14 hours (this allows for twice daily dosing)

32
Q

What is the serum half life of oxaprozin?

A

50-60 hours (this allows for once daily dosing)

33
Q

Which NSAID is used to promote closure of patent ductus arteriosus?

A

indomethacin

34
Q

What is ketorolac mainly used for?

A

an IV analgesic for post-surgical pain; can also be used as a replacement for opioid analgesics like morphine

35
Q

What are the 2 main Aspirin-specific adverse effects?

A
  • Reye’s Syndrome**

- Increased risk of gout

36
Q

What is the most common adverse effect of all NSAIDs (except celecoxib)

A

NSAID-induced GI toxicity!

37
Q

What re the 2 main causes of NSAID-induced GI toxicity?

A
  • direct damage to gastric epithelial cells caused by ion-trapping of aspirin/NSAIDs
  • inhibition of COX-1 in stomach blocks gastric protective effect of prostaglandins
38
Q

The effects of NSAID-induced GI toxicity can be ameliorated by co-administration of:

A
  • Misprostol

- Omeprazole

*Pharm Exam 2 (4 decks)

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