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Duke Pharmacology- Hannah > NSAIDs > Flashcards

NSAIDs Flashcards

1
Q

What is the MOA of NSAIDs?

A

cyclooxygenase (COX) inhibitors
prevent binding of arachidonic acid to cox enzyme
inhibits the biosynthesis of prostaglandins (pain
causing)

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2
Q

What are some common effects of NSAIDs?

A

common analgesic, anti-inflammatory, and antipyretic effects

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3
Q

Which drugs most likely work on 1st order neuron?

A

NSAIDs

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4
Q

How do NSAIDs affect COX inhibitors?

A

they are either non-selective or Cox-2 selective (viox)

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5
Q

Cox 1 isoenzymes are involved in physiologic functions

A

maintenance of renal function
mucosal protection of the GI tract (more prone to developing ulcers)
production of thromboxane A2 (released by platelets to attract other platelets)

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6
Q

Cox 2 isoenzymes are

A

expression induced by inflammatory mediators

role in: mediation of pain, inflammation, & fever

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7
Q

Cox 2 isoenzymes are things we

A

want to block

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8
Q

What is a drug we can give that is Cox 2 selective?

A

celebrix but this comes with its own cardiac issues

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9
Q

non-selective nsaids are rarely used in the periop setting b/c of

A

GI toxicity and platelet dysfunction

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10
Q

What is a consideration of NSAIDs with bone healing?

A

bone healing is delayed with NSAIDs but safe in the setting of primary bone healing

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11
Q

What is the dose of toradol (ketorolac) and what is a consideration to not giving it?

A

15 mg IV or IM Q6h

do not give in patients with reduced renal function

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12
Q

What are some considerations with Celebrex?

A

have less GI toxicity since it is a Cox 2 selective inhibitor but does have cardiovascular risks

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13
Q

What is the dosing of celebrex and when might we give it?

A

part of ERAS surgery
400 mg PO preop
200 mg BID x 5 days postop

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14
Q

NSAIDs are acids or bases?

A

weak acids (like propofol and barbiturates)

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15
Q

What kind of distribution to NSAIDs have?

A

low Vd (.1-.3 L/kg)

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16
Q

Additional important pharmacokinetics of NSAIDs?

A

plasma half-life is variable
increased protein binding
GI absorption occurs rapidly

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17
Q

How are NSAIDs metabolized and excreted?

A

liver metabolizes most NSAIDs

eliminated primarily by renal and biliary excretion

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18
Q

How do NSAIDs affect platelet function?

A

primarily through Cox-1

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19
Q

What are risk factors for increased GI complications?

A

elderly, hx of previous ulcer, H. pylori infection, concomitant use of aspirin, anticoagulants, or corticosteroids

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20
Q

Aspirin is a derivative of

A

salicylic acid

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21
Q

How is aspirin metabolizied?

A

plasma esterases, erythrocytes, and liver

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22
Q

What is aspirin used for?

A

general analgesic & “irreversible” platelet inhibitor

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23
Q

What is aspirin toxicity related to?

A

drug acidity and prostaglandin inhibition

24
Q

What are s/s of aspirin overdose?

A

N/V, abdominal pain, hearing impairment, CNS depression, higher doses can result in metabolic acidosis, renal failure, CNS changes (agitation, confusion, coma), and hyperventilation with respiratory alkalosis
Urine alkalinization increases salicylate elimination

25
Q

What is the dose of acetaminophen?

A

325-650 mg Q4-6h (total not to exceed 4,000 mg/24 hrs, 2000 for chronic alcholocis)
1000 mg Q6 Ofirmev IV

26
Q

What are indications to give tylenol?

A

has analgesic and antipyretic properties

27
Q

What is the mechanism of action of acetaminophen?

A

central analgesic effect through: activation of serotonergic pathways
antagonism of NMDA, substance P, and nitric oxide pathways
No anti-inflammatory actions

28
Q

How is tylenol metabolized?

A

in the liver

leading cause of acute liver failure in US chronic usage <2g not associated with liver damage

29
Q

Why does liver damage result with tylenol?

A

active metabolite N-acetyl-p-benzoquinoneimine leads to liver failure by depleting glutathione, a natural antioxidant

30
Q

How do you treat tylenol OD?

A

aimed at removing acetaminophen (charcoal) and replacing glutathione (aceylcystein administration)

31
Q

What is the structure of Gabapentin?

A

Gabapentin is a structural analogue of gamma-aminobutyric acid (GABA)- it acts on voltage-dependent Ca channels by inhibiting glutamate

32
Q

What are the uses of gabapentin?

A

approved as an anticonvulsant medication
demonstrated efficacy in neuropathic pain
used in ERAS protocols- effective in reducing immediate postop pain and opioid consumption
can cause acute resp. depression in PACU

33
Q

Describe the absorption of Gabapentin?

A

limited to a small part of the duodenum and can be impaired by antacids
has minimal protein binding and excreted without significant metabolism

34
Q

What is the dosing of gabapentin?

A

Preop 1200 mg 1-2 h. before surgery

600 mg Q8 x 14 days

35
Q

What are the side effects of gabapentin?

A

sedation, dizziness, HA, and visual disturbances

36
Q

What is the pH of lidocaine?

A

slightly above that of physiologic pH, it is a weak base

37
Q

When is IV lidocaine used?

A

as part of a multimodal pain management plan to supplement general anesthesia

38
Q

What is the mechanism of action of lidocaine?

A

unknown; may involve sodium channels; block priming of polymorphonuclear granulocytes

39
Q

How is lidocaine metabolized?

A

undergoes first pass extraction in the lungs (like propofol) and is metabolized in the liver (prolonged in pts under general anesthesia)

40
Q

What is the dosing of lidocaine?

A

1.5 mg/kg bolus dose (IBW)

1-2 mg/kg/hour infusion

41
Q

What surgical procedures are lidocaine indicated for?

A

reduces pain and speeds up return of bowel function in laparoscopic cases
decreases pain, improves functional outcomes in prostatectomy, thoracic, and major spine cases

42
Q

What is a concern with lidocaine?

A

accumulation is a concern but at doses given during ERAS protocols serum levels are well below toxicity
monitoring at risk patients is advised

43
Q

What is the mechanism of action of magnesium sulfate?

A

analgesic properties related to: regulation of Ca influx into cells, antagonism of NMDA receptors in CNS

44
Q

What is the dosing of magnesium sulfate?

A

30-50 mg/kg bolus

10 mg/kg/h infusion

45
Q

What are side effects of magnesium sulfate?

A

bradycardia and hypotension
prolongs muscle relaxant
shows a decrease in opioid consumption and pain

46
Q

What is the mechanism of action of capsaicin?

A

transient receptor potential vanilloid (TRPV1) channel agonist
activation releases high-intensity impulses and release substance P (overload and release substance P so there’s nothing else to release)

47
Q

What is capsacin?

A

the major pungent ingredient of chili peppers and botanicals

applied topically for neuralgia and neuropathies

48
Q

What is the dosing for ketamine?

A

0.5-1 mg/kg prior to surgical incision

49
Q

What are side effects of ketamine?

A

psychomimetic (give them versed)

dizziness, blurred vision, n/v

50
Q

What is the mechanism of action of ketamine?

A

NMDA antagonist modulates central sensitization
induced by incision and tissue damage
role in preventing opioid-induced hyperalgesia

51
Q

What is the mechanism of action of dexmedtominidine?

A

selective alpha-2 agonist

blunts central sympathetic response via acting on the locus cereleus

52
Q

What is the dosing for dexmedetomindine?

A

0.5-2 mcg/kg

53
Q

What are side effects of dexmedetomindine?

A

Hypotension & bradycardia

54
Q

Peripherally acting opioids can

A

reduce plasma extravasation, vasodilation, proinflammatory neuropeptides, immune mediators, and tissue destruction

55
Q

Peripheral opioids have a role in

A

arthroplasty and inflammatory bowel disease

Duke Pharmacology- Hannah (14 decks)

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