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GT BSN/CNL PHARM > Drugs for Pain > Flashcards

Drugs for Pain Flashcards

1
Q

Mechanism of action of local anesthetics

A

Block Na+ channels on the AXON = inability to conduct an action potential

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2
Q

What are the two classes of local anesthetics?

A

esters & amides

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3
Q

Which class of local anesthetics have a higher allergic reaction rate?

A

esters

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4
Q

How are the two classes of local anesthetics metabolized?

A

esters = plasma esterases
amides = hepatic enzymes

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5
Q

s/s of local anesthetic toxicity

A

CNS = seizures progressing to coma and death
CV = bradycardia, heart block, decreased contractility, cardiac arrest, vasodilation

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6
Q

adverse effects of local anesthetics

A

local anesthetic systemic toxicity (LAST)
allergic reactions
methemoglobinemia (only benzocaine)

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7
Q

List some ester local anesthetics

A

procaine
chloroprocaine
cocaine
tetracaine

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8
Q

List some amide local anesthetics

A

lidocaine
bupivicaine
ropivicaine
mepivicaine

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9
Q

What is the general mechanism of action of many of the general anesthetics

A

chloride influx (via GABA inhibition) & hyperpolarization of neuronal membranes
= depression of CNS activity

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10
Q

Life threatening adverse effect of inhalation anesthetics?

A

malignant hyperthermia

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11
Q

Common side effects of most of the inhaled anesthetics

A

hypotension
respiratory depression
post-operative nausea & vomiting

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12
Q

mechanism of action of propofol

A

promote GABA release
(hyperpolarization of membranes of the CNS, decrease neuronal transmission)

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13
Q

adverse effects of propofol

A

respiratory dpression
hypotension
can have bradycardia or reflex tachycardia
injection site pain

propofol infusion syndrome w/ long term infusion

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14
Q

Positive outcomes of COX inhibition

A

decreased inflammation
decreased pain
decreased fever

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15
Q

The production of which substances is inhibited with COX inhibition?

A

prostaglandins
prostacyclin
thromboxane A2

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16
Q

Major adverse effects of COX inhibition

A

increased gastric acid secretion = ulcer development

decreased vasodilation of renal artery = decreased renal blood flow

decreased platelet aggregation = bleeding risk **can be positive effect or adverse effect

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17
Q

Effects of COX1 inhibition

A

gastric erosion & ulceration
bleeding
renal impairment

BUT also decreased platelet aggregation (which can prevent MI/CVA, which is good)

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18
Q

Effects of COX2 inhibition

A

decreased inflammation
decreased pain
decreased fever

BUT also decreased vasodilation, which can promote MI/CV (which is bad)

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19
Q

What is another term for the first generation COX inhibitors

A

nonselective COX inhibitors

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20
Q

List some first generation COX inhibitors

A

aspirin
ibuprofen
naproxen
ketorolac
indomethacin

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21
Q

Who are first generation COX inhibitors contraindicated in?

A

peds (aspirin)
pregnancy
renal disease
PUD or GI bleeding
bleeding disorders

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22
Q

How is aspirin different than the other first generation COX inhibitors?

A

binding is irreversible (higher platelet inhibition)

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23
Q

How are the second generation COX inhibitors different from the first generation?

A

only inhibit COX2

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24
Q

What is the major risk that is present ONLY for second generation COX inhibitors?

A

CV events
- no suppression of platelet aggregation
- inhibition of vasodilation

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25
Q

Name a second generation COX inhibitor

A

celecoxib

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26
Q

mechanism of action of acetaminophen

A

COX inhibition only in the CNS (not peripherally)

27
Q

How are the effects of COX inhibitors and acetaminophen different?

A

acetaminophen = no anti-inflammatory, no decreased platelet aggregation, no GI issues, no decrease in renal blood flow

28
Q

site of metabolism of acetaminophen

A

liver

29
Q

how does toxicity occur in high dose acetaminophen?

A

too much of the toxic metabolite builds up without enough glutathione to convert it.

This toxic metabolite can lead to liver damage

30
Q

Treatment of acetaminophen toxicity

A

acetylcysteine (antidote to acetaminophen that can convert the toxic metabolite to inactive form)

31
Q

what is the max dose of acetaminophen

A

4g in 24hrs
*this max dose may be lower in those w/ preexisting liver disease or EtOH use

32
Q

What are the 3 opioid receptors?

A

mu
kappa
delta

33
Q

What are the effects of mu agonism

A

analgesia
respiratory depression
sedation
euphoria
physical dependence
decreased GI motility

34
Q

what are the effects of kappa agonism

A

analgesia
sedation
decreased GI motility

35
Q

What do pure opioid agonists do?

A

agonize mu and kappa

36
Q

What do opioid agonist-antagonists do?

A

either agonize or antagonize mu and do the opposite at kappa

37
Q

How do the effects of opioid agonists/antagonists compared with the pure agonists?

A

ceiling effect to analgesia
less respiratory depression
less euphoria
lower abuse potential

*can precipitate withdrawal in those w/ physical dependence

38
Q

What do the opioid antagonists do?

A

antagonize mu & kappa

39
Q

What are the effects of the opioid antagonists

A

(NO analgesia)

reverse most effects of opioids
(can precipitate withdrawal symptoms in those w/ physical dependence)

40
Q

Which two effects of opioids do patients NOT develop a tolerance to?

A

miosis
decreased GI motility

41
Q

respiratory effects of opioids

A

depression (decreased RR)
cough suppression

42
Q

hemodynamic effects of opioids

A

can slow HR d/t decreased SNS

orthostatic hypotension

43
Q

GI/GU effects of opioids

A

constipation
urinary retention

44
Q

CNS effect of opioids

A

euphoria or dysphoria
sedation
tolerance/physical dependence

45
Q

pupillary effects of opioids

A

miosis (constriction)

46
Q

what is tolerance

A

larger doses are required to produce same response

47
Q

what is physical dependence

A

state in which abstinence syndrome will develop if the drug is abruptly stopped

48
Q

how to avoid withdrawal symptoms of opioids

A

taper down doses over time

49
Q

s/s of opioid withdrawal

A

mild = yawning/rhinorrhea/sweating
severe = sneezing/weakness/N/V/diarrhea/abdominal cramps/muscle pain/spasms

50
Q

List a few pure opioid agonists

A

fentanyl
morphine
meperidine
methadone
hydromorphone
sufentanil
remifentanil

51
Q

How is meperidine different than the other pure opioid agonists

A

toxic metabolite build up occurs with prolonged use

interacts with MAO inhibitors = excitation/seizures

52
Q

How is methadone different from the other pure opioid agonists

A

very long 1/2 life
- can treat addiction
- can also lead to drug accumulation

also prolongs the QTc

53
Q

What is the active metabolite of codeine

A

morphine

54
Q

Why do some people not have analgesic effects from codeine

A

genetic variation in the CYP450 enzyme that metabolizes it

55
Q

list some opioid agonist-antagonists

A

nalbuphine
butorphanol
buprenorphine

56
Q

List some opioid antagonists

A

naloxone
methylnatrexone
naltrexone

57
Q

What is naloxone used for

A

opioid OD reversal

58
Q

Duration of action of naloxone

A

1hr

59
Q

what is methylnatrexone used for

A

opioid-induced constipation that hasn’t responded to other interventions

60
Q

what is naltrexone used for

A

to block the euphoric effects of opioids (so for opioid/alcohol abuse)

61
Q

How does tramadol work

A

weak mu agonism
antagonism of NE & serotonin reuptake

62
Q

adverse effects of tramadol

A

sedation
dizziness/HA
constipation
seizures
suicidal ideation

63
Q

When increasing opioid dosing when treating cancer pain, what is a major concern?

A

constipation

GT BSN/CNL PHARM (26 decks)

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