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62 Cards in this Set

  • Front
  • Back
what is an opiate?
drug derived from opium
what is an opioid?
drugs that bind to an opioid receptor
what are the types of opioids?
endogenous (endorphins) and exogenous (natural-morphine, synthetic-fentanyl)
where are opioid receptors found?
presynaptic and post synaptic, CNS, spinal cord (dorsal horn), and periphery
what happens when activation (agonism) of opioid receptors occurs?
decrease in excitatory neurotransmitters, hyperpolarized neurons, attenuates spontaneous discharges and evoked responses, decreased pain info transmission
what are the classifications of opioids?
full agonist, partial agonist, antagonist
what is an example of a full opioid agonist?
morphine
what is an example of a partial opioid agonist?
buprenorphine
what is an example of a opioid antagonist?
naloxone
what are the types of opioid receptors?
mu receptor (u; morphine, hydromorphone, oxymorphone), kappa receptor (k; butorphanol), delta receptor (d)
what are the general effects of opioids?
analgesia, sedation, side effects
what are the CNS effects of opioids?
analgesia and sedation (euphoria, dysphoria, excitement; species and dose dependent), CNS depression can be additive or synergistic with other CNS depressants (ie alpha-2 agonists, acepromazine)
what are the cardiovascular effects of opioids?
slows SA node firing, slows conduction through AV node, causes bradycardai and /or 2nd degree heart block
how is opioid potency determined?
in relation to morphine (expressed as a factor of morphine)
what are the respiratory effects of opioids?
respiratory depression (dose dependent, pure mu opioids > partial mu > kappa), exaggerated with other CNS depressant
what is the effect of morphine on histamine release?
IV dosing, vasodilation and hypotension, less common in domestic animals (not caused by hydromorphone, fentanyl, oxymorphone)
what are the GI effects of opioids?
nausea and vomiting, slows GI motility (can lead to colic, concern with ileus/constipation), can see non-propulsive hypermotility (ropy guts)
what are the analgesic effects of opioids?
analgesia for acute pain, less effective with tolerance, chronic pain, neuropathic pain, neoplastic pain
what is the metabolism of opioids?
metabolized extensively in the liver (exception remifentanil which is metabolized by plasma esterases), liver disease can prolong activity, some metabolites have biologic activity (morphine-6-glucuronide: M6G)
what is the pharmacokinetics of opioids?
duration of action (particular drug-butorphanol is short vs buprenorphine is long, route of administration, species) and route of administration (IV, IM, SQ, orally, trans-mucosal-buprenorphine, transdermal-fentanyl patches, epidural, spinal, topical (?), oral
what are miscellaneous effects of opioids?
thermoregulation (re-setting the thermoregulatory center; species dependent), pupil size (miosis = dogs, pigs, people, mydriasis = cats, horses)
how must opioids be managed?
as controlled drugs; 2 key lock-box, DEA approval, strict record keeping
what are the general effects of morphine?
pure mu opioid agonist, prototypical opioid, most sedating opioid, duration of action lasts ~4hrs, limited lipophilicity (lasts longer in epidural space)
what are the side effects of morphine?
bradycardia, hypoventilation, most likely to cause vomiting, histamine release is possible with IV
what are the general effects of fentanyl?
pure mu opiod agonist, doesn’t cause vomiting or dysphoria, short acting (~20 min, CRI/patch)
when is fentanyl administered CRI?
moderate to severe respiratory depression/apnea, bradycardia
what occurs when fentanyl accumulates?
cumulative effect; causes a prolonged recovery from anesthesia
what are the general effects of fentanyl patch?
temperature dependent, therapeutic serum levels (~<6hr in horse, ~12-24hr in dog, ~6-24hr in cat), clean dry skin, good contact
what are the general effects of hydromorphone?
pure mu opioid agonist, more potent than morphine (5-10x)
what are the side effects of hydromorphone?
bradycardia, hypoventilation, hyperthermia in cats (being colud during anesthesia may contribute to hyperthermia)
what are the general effects of remifentanil?
pure mu opioid agonists, potent (~50x), metabolized by plasma esterases (not the liver), duration of action is very short (~5min) so administered by CRI
what are the general effects of carfentanil/etorphine?
ultra potent pure mu opioid agonists, large wildlife immobilizations, very potent (respiratory arrest in humans via mucous membrane exposure), use only by trained individuals
what are the general effects of buprenorphine?
partial mu agonist (kappa antagonist), strong binding affinity (extended duration of action up to 8hr, difficult to reverse), cats have a positive behavior profile, transmucosal administration (dogs, cats, horses)
what are the general effects of butorphanol?
kappa opioid agonist (mu antagonist; very weak agonist), good analgesic, behaviorally favorable (cats/horses), short acting (60-90min CRI)
what are the general effects of tramadol?
oral analgesic, classified as a weak mu-opioid agonist, active metabolite, effects on serotonin and norepinephrine
what is the purpose of reversal of opioids?
remove wanted or unwanted effects of ligand, consequences of reveral include remove analgesia (endogenous or exogenous), remove sedation, remove side effects, do NOT always have to do full reversal
what are the general effects of naloxone?
non selective antagonist (all 3 opioid receptors), reverses (side effects of respiratory, sedation, etc) and analgesia associated with the agonist, duration of action is ~60-90min (risk of re-narcotizing)
what are the general effects of naltrexone?
similar to naloxone but longer acting at <8hr, injectable or PO -active orally (behavior treatment and chemical dependance in humans)
what are the general effects of butorphanol (as a reversal agent)?
reverse the mu-opioid effects (respiratory depression, sedation), provides some kappa agonist pain relief, useful when reversal is needed in a patient that is in pain
what are the basics of butorphanol?
kappa, A/Ant, ~1hr
what are the basics of buprenorphine?
mu, partial, ~8hr
what are the basics of morphine?
mu, full, ~4hr
what are the basics of hydromorphone?
mu, full, ~4hr
what are the basics of oxymorphone?
mu, full, ~4hr
what are the basics of fentanyl?
mu, full, ~20min
what is a neurolept analgesia?
opioid + sedative/tranquilizer, increases sedation and analgesia, effects of each class are potentiated (more sedation and more analgesia)
what are examples of neurolept analgesia (include affected receptor?
acepromazine + hydromorphone (mu), acepromazine + butorphanol (kappa), xylazine + butorphanol, midazolam + hydromorphone (mu), midazolam + butorphanol (kappa)
what are some anticholinergics?
glycopyrrolate, atropine, scopolomine
what are glycopyrrolate, atropine, scopolomine?
anticholinergics
what do anticholinergics do?
antagonize binding neurotransmitter acetylchonline (AcH); mostly anti-muscarinic effects with minimal nicotinic effects; muscarinic receptors in heart, salivary gland, smooth muscle of GI, GU, eye (agonisms increases VAGAL/parasympathetic activity, antagonism increasese sympathetic/SNS activity)
what to anticholinergics result in?
increased sympathetic tone; increases HR, bronchodilation, decreases salivary secretions, tracheal & bronchial secretions, tear production, volume gastric secretions, GI tone & motility
what are indications for the use of anticholinergics?
treat or prevent bradycardia (from drugs; opioids, general anesthetics, anticholinesterase agents like edrophonium/tensilon), increased vagal tone (traction/pressure on eye or viscera), increase cardiac output (CP = HR x SV)
what are the general effects of atropine?
quickest and greatest increase in HR (best for emergencies), causes rapid heart rate (increases myocardial work and O2 demands, increse incidence of ventricular arrhythmias or PVC's), crosses blood brain barrier/placenta (anxiety/anxiousness, minimal fetal effects)
what are the general effects of glycopyrrolate?
slower to effect and longer duration of action (more for routine use), less intense HR effect (fewer dysrhythmias, less demands), does not cross blodd-brain barrier/placenta (quaternary amine), more potent (2-4x) anti-sialorrheic than atropine (can make secretions viscous)
what are contraindications for anticholinergics?
tachycardia/tachyarrhythmias, concerns about myocardial O2 demand, horses (increased risk of colic?), may increase viscosity of secretions (can occlude small airways especially in pocket-pets)
why do we need oxygen?
aerobic metabolism (oxidative phosphorylation), production of energy-ATP (36/glucose), maintain normal physiologic functions (cellular gradients, conduction, proteine synthesis), without O2 = anaerobic metabolism; mall amoun of energy (2/glucose), inadequate to meet demands, lactate byproduct
when would we pre-oxygenate a patient?
if patient is likely to develop hypoxemia/hypoxia (upper airway obstruction, plural space/parenchymal disease, drug side effects via opioid/propofol inductions, anemia)
why do we pre-oxygenate a patient?
increase O2 reserve 4-5x compared to room air at ~21%, incrase margin of safety (room air = ~1.5 min until hypoxemic vs 100% O2 = ~7min until hypoxemic), use whenever concerned about apnea/respiratory depression, obstruction, pulmonary disease
when do we pre-oxygenate a patient?
immediately prior to induction (oxygen diffuses quickly in and out), do NOT force mask on patient (increasing stress increases O2 demands), keep mask in place until intubation
what are the most common side effects to opioids?
bradycardia and hypoventilation
what receptor was previously identified as an opioid receptor but is not?
sigma
CD59 is a regulatory element in:

Possible answers:
a. C3 convertase Alternative Pathway
b. C3 convertase Classic Pathway
c. C5 convertase Alternative Pathway
d. C5 convertase Classic Pathway
e. MAC
MAC