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Pharmacology Sem 1 > NSAIDs > Flashcards

NSAIDs Flashcards

(55 cards)

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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?

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A

drug acidity and prostaglandin inhibition

24
Q

What are s/s of aspirin overdose?

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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
What is the dose of acetaminophen?
325-650 mg Q4-6h (total not to exceed 4,000 mg/24 hrs, 2000 for chronic alcholocis) 1000 mg Q6 Ofirmev IV
26
What are indications to give tylenol?
has analgesic and antipyretic properties
27
What is the mechanism of action of acetaminophen?
central analgesic effect through: activation of serotonergic pathways antagonism of NMDA, substance P, and nitric oxide pathways No anti-inflammatory actions
28
How is tylenol metabolized?
in the liver | leading cause of acute liver failure in US chronic usage <2g not associated with liver damage
29
Why does liver damage result with tylenol?
active metabolite N-acetyl-p-benzoquinoneimine leads to liver failure by depleting glutathione, a natural antioxidant
30
How do you treat tylenol OD?
aimed at removing acetaminophen (charcoal) and replacing glutathione (aceylcystein administration)
31
What is the structure of Gabapentin?
Gabapentin is a structural analogue of gamma-aminobutyric acid (GABA)- it acts on voltage-dependent Ca channels by inhibiting glutamate
32
What are the uses of gabapentin?
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
Describe the absorption of Gabapentin?
limited to a small part of the duodenum and can be impaired by antacids has minimal protein binding and excreted without significant metabolism
34
What is the dosing of gabapentin?
Preop 1200 mg 1-2 h. before surgery | 600 mg Q8 x 14 days
35
What are the side effects of gabapentin?
sedation, dizziness, HA, and visual disturbances
36
What is the pH of lidocaine?
slightly above that of physiologic pH, it is a weak base
37
When is IV lidocaine used?
as part of a multimodal pain management plan to supplement general anesthesia
38
What is the mechanism of action of lidocaine?
unknown; may involve sodium channels; block priming of polymorphonuclear granulocytes
39
How is lidocaine metabolized?
undergoes first pass extraction in the lungs (like propofol) and is metabolized in the liver (prolonged in pts under general anesthesia)
40
What is the dosing of lidocaine?
1.5 mg/kg bolus dose (IBW) | 1-2 mg/kg/hour infusion
41
What surgical procedures are lidocaine indicated for?
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
What is a concern with lidocaine?
accumulation is a concern but at doses given during ERAS protocols serum levels are well below toxicity monitoring at risk patients is advised
43
What is the mechanism of action of magnesium sulfate?
analgesic properties related to: regulation of Ca influx into cells, antagonism of NMDA receptors in CNS
44
What is the dosing of magnesium sulfate?
30-50 mg/kg bolus | 10 mg/kg/h infusion
45
What are side effects of magnesium sulfate?
bradycardia and hypotension prolongs muscle relaxant shows a decrease in opioid consumption and pain
46
What is the mechanism of action of capsaicin?
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
What is capsacin?
the major pungent ingredient of chili peppers and botanicals | applied topically for neuralgia and neuropathies
48
What is the dosing for ketamine?
0.5-1 mg/kg prior to surgical incision
49
What are side effects of ketamine?
psychomimetic (give them versed) | dizziness, blurred vision, n/v
50
What is the mechanism of action of ketamine?
NMDA antagonist modulates central sensitization induced by incision and tissue damage role in preventing opioid-induced hyperalgesia
51
What is the mechanism of action of dexmedtominidine?
selective alpha-2 agonist | blunts central sympathetic response via acting on the locus cereleus
52
What is the dosing for dexmedetomindine?
0.5-2 mcg/kg
53
What are side effects of dexmedetomindine?
Hypotension & bradycardia
54
Peripherally acting opioids can
reduce plasma extravasation, vasodilation, proinflammatory neuropeptides, immune mediators, and tissue destruction
55
Peripheral opioids have a role in
arthroplasty and inflammatory bowel disease

Pharmacology Sem 1 (14 decks)

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