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Anesthesia Pharm: Summer > NSAIDs > Flashcards

NSAIDs Flashcards

1
Q

What catalyzes the synthesis of prostaglandins from arachidonic acid?

A

Cyclooxygenase (COX)

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2
Q

Where is COX-1 located? (3)

A

Gastric mucosa
Platelets
Renal parenchyma

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3
Q

What is COX-1 responsible for? (3)

A

GI mucosal integrity
Platelet aggregation
Renal function

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4
Q

What are 3 attributes of COX-2?

A

Pain-inducing enzyme

Mediates inflammation, pain, fever, and carcinogenesis

Released in response to injury, illness, diet

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5
Q

What is the mechanism of action of NSAIDs?

What is important to understand regarding NSAIDs activity? (2)

A

Inhibition of Cyclooxygenase

NSAIDs block both COX enzymes without specificity

CEILING EFFECT–Exceeding the recommended dose only increases the risk of toxicity

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6
Q

Describe the pharmokinetics of NSAIDs: (4)

A

Well absorbed in GI

Not a lot of 1st pass metabolism (makes PO similar to IV dose)

Highly protein bound

Elimination: ASP lost within hour, but duration for 24 hours.

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7
Q

What are the advantages of NSAIDs? (10)

A

Decrease activation of peripheral nociceptors
Absence of dependence or addiction
Synergistic with opioids
Preemptive analgesia
NO depression of ventilation
Less N/V
Long duration of action
Less variability
No pupil changes
Absence of cognitive effects

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8
Q

What are the disadvantages of NSAIDs? (7)

A

Gastric ulceration
Renal dysfunction
Hepatocellular injury
Asthma exacerbation
Allergic reactions
Bone healing
Drug Interactions

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9
Q

Why are NSAIDs contraindicated for asthma pts?

A

When prostaglandins are blocked, can bronchoconstrict enhancing effects of asthma.

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10
Q

What are GI related adverse effects? (5)

A

Dyspepsia, N/V, pain, peptic ulcer, GI hemorrhage

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11
Q

What NSAIDs are nonspecific? (5)

A

inhibit both COX-1 and -2

Ibuprofen (Motrin)
Naproxen (Aleve)
Aspirin (Acetylsalicylic Acid)
Acetaminophen (Tylenol)
Ketorolac (Toradol)

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12
Q

When do you discontinue NSAIDs prior to surgery?

A

7-10 days

Note: Platelet life is 7-10 days.

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13
Q

What are attributes of ASA (acetylsalicylic acid)? (2)

A

Irreversible acetylation of COX enzyme

Rapid GI absorption

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14
Q

What condition is ASA a first line DOC?

A

Fever

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15
Q

How low of a dose can is anti-platelet function observed?

A

40mg

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16
Q

What are the clinical uses of ASA?

A

Analgesic

Antipyretic

Antiplatelet function

17
Q

What are the side effects of ASA?

A

GI upset

Prolonged bleeding time

Prolonged Prothrombin Time (PT)

Aspirin Induced Asthma

18
Q

What are other concerns of ASA? (5)

A

CNS Toxicity

SAFE for renal pts

Allergic rxn is rare

Prolonged labor, increased hemorrhage

REYE’S SYNDROME–potentially fatal disease affecting the brain as well as other organs

19
Q

What may we want to give instead of ASA/ASP during pollen season?

A

Tylenol

20
Q

What is a safe alternative to aspirin for pediatric patients and those with peptic ulcers?

A

Acetominophen

21
Q

What is the maximum dose of IV acetominophen?

A

1000mg q 6 hrs

max 4g q 24 hrs

22
Q

What type of pain is acetaminophen good for? (2)

A

Mgmt of mild to moderate pain

Mgmt of severe pain with opioids

23
Q

What is a major adverse side effect of acetaminophen?

A

Hepatic Toxicity

24
Q

How does acetaminophen contrast to ASA?

A

No gastric irritation
No platelet aggregation effects

25
Q

What organs does acetaminophen affect?

A

kidney

liver

26
Q

What are the characteristics of Toradol? (3)

A

Potent analgesic

  • Minimal* antiinflammatory
  • *Causes renal toxicity!**
27
Q

What are the adults/peds dosages for Toradol?

A

Adult
30mg IM/IV q 6 hrs up to 72 hours

Peds
0.5mg/kg IM/IV q 6 hrs

28
Q

What NSAID is known to help close PDA (patent ductus arteriosus)?

A

Indomethacin

29
Q

What NSAIDs are Propionic Acid Derivatives ?

A

ALL of them

30
Q

What NSAIDs treat gout? (3)

A

Phenylbutazone

Colchicine

Allopurinol

31
Q

What are characteristics of COX-2 inhibitors? (3)

A

COX–2 production is selectively inhibited

Decreased pain and inflammation

Decreased side effect profile

32
Q

What are the COX-2 inhibitors?

A

Celecoxib (Celebrex)—potent anti-inflammatory

Valecoxib (Bextra)

Parecoxib (not in the US)

Rofecoxib (Vioxx)

33
Q

Why are many COX-2 inhibitors no longer used?

A

post thrombotic events

34
Q

When does COX-2 production increase?

A

increases with saturated fat and some unsaturated fat intake

35
Q

What are disease states with increased COX-2? (5)

A

Alzheimer’s Disease
Cancer
Kidney Disease
Osteoporosis
Rheumatic & Osteoarthritis

36
Q

What COX-2 inhibitor has been pulled off market?

A

Rofecoxib (Vioxx)

Anesthesia Pharm: Summer (5 decks)

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