Pain Flashcards
how do local anesthetics work along the axon of a neuron
they block Na+ channels in the axonal membrane
why are local anesthetics considered local?
are considered nonselective and the small/ unmyelinated neurons are easier to block
administed at their site of action!
what is an ester
a class within local anesthetics this class has higher allergic run rates this class metabolites more rapidly
what is an amide?
a class of local athletics
has less allergic rxns
metabolized by hepatic enzymes
why might a local aesthetic have CV effects?
because it is a Na+ channel blocker when there is high systemic concentrations
what is a unique adverse effect of benzocaine
methemoglobinemia
Name three types of esters
cocaine and procaine (chloroprocaine)
benzocaine
what is unique about cocaine
this drug blocks the NE reuptake and can be both a CNS / CV stimulant
why is unique about chloroprocaine
this is a type of ester that is not effective topically and has a short DOA
what is a type of amide
lidocaine
What are the signs and symptoms of local anesthetic toxicity?
- CNS stimulation = seizures or depression
- CV effects = remember the NA+ channel blocker = bradycardia and vasodilation
- allergic reactions
- methemoglobin (benzocaine )
How do inhalation anesthetics reach their site of action? Where is their therapeutic site of action?
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
what is MAC
Minimum alveolar concentration
what does it mean to have a low MAC
means that it is a very potent drug
what does it mean to have a high MAC
means not a potent drug
what is anthesisia
LOC
what is. analgesia
pain relief
What are the 5 types of IV anesthetics
- Barbituates
- Benodiazepines
- Propofol
- Etomidate
- Ketamine
how do barbiturates work
Increase GABA transmission
Quick onset (10-20seconds)
Highly lipid soluble
an adverse effect here is CV and respiratory depression
how do benzodiazepines work
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
what is the MOA of all IV anesthetics, except one (name the one)
Increase GABA transmission in most except ketamine and this relates to NMDA
when might you use etomidate over a different IV anesthetic
those who have CV depression
what is the one type of IV anesthetic that has a different MOA and what is the MOA
ketamine = Increase NMDA transmission
what IV anesthetic leads to Anterograde amnesia and Anixiolysis with A/E
Benzodiazepines
what drug would you not want to use due to profound respiratory depression and hypotension
propofol
what is mu and kappa agonism related to
thinking about analgesics and pain control
what are the effects of MU agonism
analgesic resp depression sedation euphoria physical dependence decreased GI motility
what are the effects of KAPPA agonism
analgesic
sedation
decreased GI motility
what is a opiod agonist MOA
agonize mu and kappa receptors
what is an example of a pure opiod agonist
morphine
fentanyl
oxycodone
what is the MOA of a agonist - antagonist opiod
most with antagonize mu while agonizing kappa
which agonist-antagonist opiod partially agonizes mu
buprenophrine
not on drug list
why might you use an agonist - antagonist opioid over a pure agonist opioid
less respiratory depression
less ephors
and lower abuse potential !!
what class of drugs is used to reverse most of the effects of opioids
opioid antagonist aka naloxone
what is the MOA opioid antagonist
antagonizes mu and kappa receptors
what effect of opioid agonist on the head
analgesic and euphoria
what is the effect on the respiratory system with opioid agonists
respiratory depression
what is tolerance?
prolonged use = need to increase dose
what physical dependance ?
ago through withdrawal
tapering withdrawal
abstinence syndrome
nursing assessment before and after opioid administration
need to check HR, breathing LOC, BP to make
how is methadone different from other opioids
prolongation of QTc torsades, EKG prior to administration. Avoid admin if QT >500msec, accumulation can occur
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
how is meperidine
Toxic metabolite is produced with metabolism (can build-up with prolonged use)
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)
what opioid antagonist blocks euphoric effects
naltrexone
what opioid antagonist blocks MU inhibition
methylnaltrexone
what opioid antagonist reverses effects
naloxone
How is tramadol different than other opioids?
It’s a weak mu agonist, it is a NON-OPIOID
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.
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
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
what is abortive drug therapy for headaches
aspirins, triptans (first line of attack), serotonin 1Fs, ergots (second line), CHRPs
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
Why do we avoid ergot alkaloids & triptans together?
avoid w/in 24hrs to avoid excessive vasospasm!!
cocaine
local anesthetic
ester
blocks NE reuptake
chloroprocaine
local anestehtic
ester
can not give topically and has a short DOA
benzocaine
local anestehtic
ester
metheglobinema
nitrous oxide
general anesthetic
inhalation anesthetic
lungs–> to blood –> CNS
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
Mizlazolam
benzodiazepine
diazepam
benzodiazepines
LORAZEPAM
benzodiazepines
nalbuphine
opiod
agonist - antagonist
butorphanol
opioid
agonist - antagonist
serotonin receptor agonists
- triptans
1st line of attack when thinking about abortive migraine therapy
sumatriptan
serotonin receptor agonist
migraine abortive relief
serotonin IF receptor agonist
-ditans
abortive migrane relief
lasmiditin
serotonin IF receptor agonist
abortive migraine relief
ergot alkaloids
second line of attack for migraine abortive relief
ergotaime
abortive migraine relief related to ergot alkaloids
do not mix with the triptans
