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Pharm Exam 3 > Pain > Flashcards

Pain Flashcards

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1
Q

how do local anesthetics work along the axon of a neuron

A

they block Na+ channels in the axonal membrane

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2
Q

why are local anesthetics considered local?

A

are considered nonselective and the small/ unmyelinated neurons are easier to block

administed at their site of action!

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3
Q

what is an ester

A 
a class within local anesthetics 
this class has higher allergic run rates 
this class metabolites more rapidly
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4
Q

what is an amide?

A

a class of local athletics
has less allergic rxns
metabolized by hepatic enzymes

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5
Q

why might a local aesthetic have CV effects?

A

because it is a Na+ channel blocker when there is high systemic concentrations

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6
Q

what is a unique adverse effect of benzocaine

A

methemoglobinemia

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7
Q

Name three types of esters

A

cocaine and procaine (chloroprocaine)

benzocaine

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8
Q

what is unique about cocaine

A

this drug blocks the NE reuptake and can be both a CNS / CV stimulant

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9
Q

why is unique about chloroprocaine

A

this is a type of ester that is not effective topically and has a short DOA

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10
Q

what is a type of amide

A

lidocaine

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11
Q

What are the signs and symptoms of local anesthetic toxicity?

A
  1. CNS stimulation = seizures or depression
  2. CV effects = remember the NA+ channel blocker = bradycardia and vasodilation
  3. allergic reactions
  4. methemoglobin (benzocaine )
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12
Q

How do inhalation anesthetics reach their site of action? Where is their therapeutic site of action?

A

Lung uptake and goes into alveoli which than blood takes up drug when it is flowing through the lungs. distribution occurs in the lungs as well

goal is to get to CNS

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13
Q

what is MAC

A

Minimum alveolar concentration

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14
Q

what does it mean to have a low MAC

A

means that it is a very potent drug

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15
Q

what does it mean to have a high MAC

A

means not a potent drug

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16
Q

what is anthesisia

A

LOC

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17
Q

what is. analgesia

A

pain relief

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18
Q

What are the 5 types of IV anesthetics

A
  1. Barbituates
  2. Benodiazepines
  3. Propofol
  4. Etomidate
  5. Ketamine
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19
Q

how do barbiturates work

A

Increase GABA transmission
Quick onset (10-20seconds)
Highly lipid soluble

an adverse effect here is CV and respiratory depression

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20
Q

how do benzodiazepines work

A

Increase GABA transmission
Used for low doses for sedation and in very high doses for anesthesia

less CV and respiratory depression seen BUT synergistic when used with other opioids
Anterograde amnesia
Anixiolysis

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21
Q

what is the MOA of all IV anesthetics, except one (name the one)

A

Increase GABA transmission in most except ketamine and this relates to NMDA

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22
Q

when might you use etomidate over a different IV anesthetic

A

those who have CV depression

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23
Q

what is the one type of IV anesthetic that has a different MOA and what is the MOA

A

ketamine = Increase NMDA transmission

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24
Q

what IV anesthetic leads to Anterograde amnesia and Anixiolysis with A/E

A

Benzodiazepines

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25
what drug would you not want to use due to profound respiratory depression and hypotension
propofol
26
what is mu and kappa agonism related to
thinking about analgesics and pain control
27
what are the effects of MU agonism
``` analgesic resp depression sedation euphoria physical dependence decreased GI motility ```
28
what are the effects of KAPPA agonism
analgesic sedation decreased GI motility
29
what is a opiod agonist MOA
agonize mu and kappa receptors
30
what is an example of a pure opiod agonist
morphine fentanyl oxycodone
31
what is the MOA of a agonist - antagonist opiod
most with antagonize mu while agonizing kappa
32
which agonist-antagonist opiod partially agonizes mu
buprenophrine | not on drug list
33
why might you use an agonist - antagonist opioid over a pure agonist opioid
less respiratory depression less ephors and lower abuse potential !!
34
what class of drugs is used to reverse most of the effects of opioids
opioid antagonist aka naloxone
35
what is the MOA opioid antagonist
antagonizes mu and kappa receptors
36
what effect of opioid agonist on the head
analgesic and euphoria
37
what is the effect on the respiratory system with opioid agonists
respiratory depression
38
what is tolerance?
prolonged use = need to increase dose
39
what physical dependance ?
ago through withdrawal tapering withdrawal abstinence syndrome
40
nursing assessment before and after opioid administration
need to check HR, breathing LOC, BP to make
41
how is methadone different from other opioids
prolongation of QTc torsades, EKG prior to administration. Avoid admin if QT >500msec, accumulation can occur
42
how does codeine different from other opioids
Same effects/AE as morphine, but lower analgesia, resp depression, lower abuse, Very effective as a cough suppressant! 10% of the dose is converted to morphine in liver via CYP2D6. Some people lack this gene = cannot gain analgesic effects, Some people are “ultrarapid metabolizers” – have multiple copies of this gene
43
how is meperidine
Toxic metabolite is produced with metabolism (can build-up with prolonged use)
44
Opioid antagonists are used for three different things. What are they? What is an example of a drug that does each?
``` Reverses effects (seen with the drug naloxone) Mu inhibition (seen with the drug methylnaltrexone) Block euphoric effects (seen with the drug naltrexone) ```
45
what opioid antagonist blocks euphoric effects
naltrexone
46
what opioid antagonist blocks MU inhibition
methylnaltrexone
47
what opioid antagonist reverses effects
naloxone
48
How is tramadol different than other opioids?
It’s a weak mu agonist, it is a NON-OPIOID
49
How does a PCA work?
Patient is hooked up to a line- the button can be pushed every so often depending on the settings. There is normally pain medication in the PCA. Anytime the PT needs to use it they can. The issue is sometimes they fall asleep and forget and then have pain when they wake up. Only the Pt can press the button.
50
How do goals of cancer pain treatment vary from other types of pain treatment?
Goal is to maximize relief with few adverse effects, manage pain, maximize quality of life the patient has left
51
How does pain management pharmacology change in older adults & young infants?
Kids: avoid nsaids, immature BBB -> limit opioid dosing, Adults: pain is undertreated, heightened drug sensitivity, Inc. adverse effects risk
52
what is abortive drug therapy for headaches
aspirins, triptans (first line of attack), serotonin 1Fs, ergots (second line), CHRPs
53
what are preventative drug therapy for headache
beta blockers, antiepileptic drugs, TCA, CGRP receptor antibodies, estrogens, triptans , Botox -> we use when PT has many attacks over 3+ months
54
Why do we avoid ergot alkaloids & triptans together?
avoid w/in 24hrs to avoid excessive vasospasm!!
55
cocaine
local anesthetic ester blocks NE reuptake
56
chloroprocaine
local anestehtic ester can not give topically and has a short DOA
57
benzocaine
local anestehtic ester metheglobinema
58
nitrous oxide
general anesthetic inhalation anesthetic lungs--> to blood --> CNS
59
benzodiazepines
general anesthetic iv anesthetic increases GABA transmission pros of this drug include having less respiratory/Cv depression interesting about this drug is the retrograde amnesia and anixiolysis
60
Mizlazolam
benzodiazepine
61
diazepam
benzodiazepines
62
LORAZEPAM
benzodiazepines
63
nalbuphine
opiod | agonist - antagonist
64
butorphanol
opioid | agonist - antagonist
65
serotonin receptor agonists | - triptans
1st line of attack when thinking about abortive migraine therapy
66
sumatriptan
serotonin receptor agonist | migraine abortive relief
67
serotonin IF receptor agonist | -ditans
abortive migrane relief
68
lasmiditin
serotonin IF receptor agonist | abortive migraine relief
69
ergot alkaloids
second line of attack for migraine abortive relief
70
ergotaime
abortive migraine relief related to ergot alkaloids do not mix with the triptans

Pharm Exam 3 (5 decks)

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