Ch.19b: Opioids (Vickroy) Flashcards
4 opioids
butorphanol
morphine
fentanyl
naloxone
Is naloxone CD?
NO. Nearly all other opioids are!!
morphine class
opioid agonist
butorphanol class
partial (mixed) opioid agonist. Stimulates some receptor subtypes, but antagonizes others of the same family
fentanyl class
potent synthetic opioid agonist
naloxone class
opioid antagonist
main therapeutic uses of opioid drugs
- analgesic
- neuroleptanalgesic
- immobilization/restraint
pain
unpleasant sensory and emotional experience assoc. with actual or potential tissue damage. Requires a functional CNS
physio signs of pain
- CV activation
- inc. stress response
- hyperglycemia
- red. GI activity
- red. immune fx
how is pain classified?
duration, anatomical location, site of origin
i.e. acute, chronic, cutaneous, somatic, visceral
nociception**
ability to perceive and sense pain. Opiates produce “anti-nociception”
analgesia
absence of pain in response to stimuli that are normally painful w/o loss of consciousness
hyperalgesia
extreme responsiveness to stimuli that’s usually only mod. painful
allodynia
pain caused by a stim. that woudn’t normally provoke pain
analgesic
drug that block the formation, release or actions of substances that stimulate sensory n. endings (transuction) (i.e. NSAIDs, glucocorticoids)
pain transmission pathway
transduction –> transmission (in sensory afferents)–> modulation –> perception
3 major classes of opioid receptors**
mu, kappa, delta
most opioid receptors are stimulation by ____ and blocked by ____**
morphine (agonist), naloxone (antagonist)
most common cause of death from opioids in humans***
ventilatory depression
opioid receptors are highly species dependent
:)
where are highest densities of opioid receptors?
brain, spinal cord, GI tract
major effects of opioid receptor stimulation
- analgesia
- resp. depression
- nausea
- GI stasis
- CV depression
“gut-brain” peptides
diverse group of peptides that are most prevalent in CNS and GI tissues. 1ary endogenous substances that activate opioid receptors. Include enkephalins, endorphins, dynorphins, and endomorphins
roles of endogenous opioid peptides
- response to painful stimuli, etc.
- acupuncture
- laser therapy
analgesia is most effective against what type of pain?
dull, constant pain.
where do opioids modulate pain?
spinal cord (dec. substance P release) brain
opioids in cats often mixed with ___. Why??
ketamine. Cats can become aggressive, hyperresponsive to opioids
opioids in horses often mixed with:
xylazine
hallmark of opioids***
marked species differences!
are opioids additive with other CNS depressants?
yes
how can ventilatory depression from opioids be reversed?
naloxone
how is nausea stimulated from opioids?
-stim. of brainstem chemoreceptor trigger zone (CTZ)
CNS actions of opioids
- analgesia
- sedation
- ventilatory depression
- nausea/emesis
- cough suppression
- pupillary constriction
- mood alterations
- tolerance and physical dependence
- neuroendocrine effects (i.e. increased ADH release)
GI actions of opioids
-GI stasis
CV actions of opioids
(unwanted side effects)
- CV depression
- can be reversed by anti-cholinergic agents
side effects of opiods*
- depend on agent, dose/route of admin, and species
- depressed ventilation
- sedation/excitation
- constipation
- parasymp. actions
- CV depression
- M. rigidity
signs of opioid toxicity
- depressed ventilation
- pinpoint pupils
- coma
contraindications for opioid use**
- large animal, felines
- pregnancy
- shock/CV dysfunction
- closed head injury
- pulmonary dysfx
opioid drug interactions**
- oral admin.
- ALL CNS depressants**
- breathing pure O2
- cholinergic drugs or AChe
chars. of morphine**
- prototype opioid agonist
- opium-derived alkaloid
- class 2**
- act on all opiate receptors
- slowly crosses BBB
- relatively high first pass metabolism with fairly slow GI absorption**
how is morphine metabolized?**
via glucuronide conjugation
chars. of naloxone**
- prototype opioid antagonist
- relatively short half-life, so must keep giving***
- reversal agent for opioid intoxication
Most opioids are DEA class ___
II
butorphanol is DEA class__
IV
DEA class I drug def.
Schedule I drugs, substances, or chemicals are defined as drugs with no currently accepted medical use and a high potential for abuse. Schedule I drugs are the most dangerous drugs of all the drug schedules with potentially severe psychological or physical dependence.
DEA class II drug def.
drugs with a high potential for abuse, less abuse potential than Schedule I drugs, with use potentially leading to severe psychological or physical dependence. These drugs are also considered dangerous.
DEA class III drug def.
drugs with a moderate to low potential for physical and psychological dependence. Schedule III drugs abuse potential is less than Schedule I and Schedule II drugs but more than Schedule IV.
DEA class IV drug def.
drugs with a low potential for abuse and low risk of dependence.
DEA class V drug def.
drugs with lower potential for abuse than Schedule IV and consist of preparations containing limited quantities of certain narcotics. Schedule V drugs are generally used for antidiarrheal, antitussive, and analgesic purposes.
fentanyl has more/less CV impact than morphine
less. However, it is 100x more potent than morphine for most indications!
buprenorphine DEA class __
III
neuroleptanalgesia
drug-induced condition in which the animal is unresponsive to sensory stimuli and shows no response to pain but is NOT completely unconscious.
- produced by combo of neuroleptic agent (DA antagonist, which prevents m. rigidity) with opioid analgesic
- produces additive CNS depression
T/F: it is more common for sedative/opioid combinations to be used in hospital setting than neuroleptic/opioid combos**
T
