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Pharmacology > Ch.19b: Opioids (Vickroy) > Flashcards

Ch.19b: Opioids (Vickroy) Flashcards

1
Q

4 opioids

A

butorphanol
morphine
fentanyl
naloxone

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2
Q

Is naloxone CD?

A

NO. Nearly all other opioids are!!

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3
Q

morphine class

A

opioid agonist

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4
Q

butorphanol class

A

partial (mixed) opioid agonist. Stimulates some receptor subtypes, but antagonizes others of the same family

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5
Q

fentanyl class

A

potent synthetic opioid agonist

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6
Q

naloxone class

A

opioid antagonist

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7
Q

main therapeutic uses of opioid drugs

A
  • analgesic
  • neuroleptanalgesic
  • immobilization/restraint
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8
Q

pain

A

unpleasant sensory and emotional experience assoc. with actual or potential tissue damage. Requires a functional CNS

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9
Q

physio signs of pain

A
  • CV activation
  • inc. stress response
  • hyperglycemia
  • red. GI activity
  • red. immune fx
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10
Q

how is pain classified?

A

duration, anatomical location, site of origin

i.e. acute, chronic, cutaneous, somatic, visceral

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11
Q

nociception**

A

ability to perceive and sense pain. Opiates produce “anti-nociception”

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12
Q

analgesia

A

absence of pain in response to stimuli that are normally painful w/o loss of consciousness

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13
Q

hyperalgesia

A

extreme responsiveness to stimuli that’s usually only mod. painful

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14
Q

allodynia

A

pain caused by a stim. that woudn’t normally provoke pain

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15
Q

analgesic

A

drug that block the formation, release or actions of substances that stimulate sensory n. endings (transuction) (i.e. NSAIDs, glucocorticoids)

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16
Q

pain transmission pathway

A

transduction –> transmission (in sensory afferents)–> modulation –> perception

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17
Q

3 major classes of opioid receptors**

A

mu, kappa, delta

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18
Q

most opioid receptors are stimulation by ____ and blocked by ____**

A

morphine (agonist), naloxone (antagonist)

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19
Q

most common cause of death from opioids in humans***

A

ventilatory depression

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20
Q

opioid receptors are highly species dependent

A

:)

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21
Q

where are highest densities of opioid receptors?

A

brain, spinal cord, GI tract

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22
Q

major effects of opioid receptor stimulation

A
  • analgesia
  • resp. depression
  • nausea
  • GI stasis
  • CV depression
23
Q

“gut-brain” peptides

A

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

24
Q

roles of endogenous opioid peptides

A
  • response to painful stimuli, etc.
  • acupuncture
  • laser therapy
25
Q

analgesia is most effective against what type of pain?

A

dull, constant pain.

26
Q

where do opioids modulate pain?

A 
spinal cord (dec. substance P release)
brain
27
Q

opioids in cats often mixed with ___. Why??

A

ketamine. Cats can become aggressive, hyperresponsive to opioids

28
Q

opioids in horses often mixed with:

A

xylazine

29
Q

hallmark of opioids***

A

marked species differences!

30
Q

are opioids additive with other CNS depressants?

A

yes

31
Q

how can ventilatory depression from opioids be reversed?

A

naloxone

32
Q

how is nausea stimulated from opioids?

A

-stim. of brainstem chemoreceptor trigger zone (CTZ)

33
Q

CNS actions of opioids

A
  • analgesia
  • sedation
  • ventilatory depression
  • nausea/emesis
  • cough suppression
  • pupillary constriction
  • mood alterations
  • tolerance and physical dependence
  • neuroendocrine effects (i.e. increased ADH release)
34
Q

GI actions of opioids

A

-GI stasis

35
Q

CV actions of opioids

A

(unwanted side effects)

  • CV depression
  • can be reversed by anti-cholinergic agents
36
Q

side effects of opiods*

A
  • depend on agent, dose/route of admin, and species
  • depressed ventilation
  • sedation/excitation
  • constipation
  • parasymp. actions
  • CV depression
  • M. rigidity
37
Q

signs of opioid toxicity

A
  • depressed ventilation
  • pinpoint pupils
  • coma
38
Q

contraindications for opioid use**

A
  • large animal, felines
  • pregnancy
  • shock/CV dysfunction
  • closed head injury
  • pulmonary dysfx
39
Q

opioid drug interactions**

A
  • oral admin.
  • ALL CNS depressants**
  • breathing pure O2
  • cholinergic drugs or AChe
40
Q

chars. of morphine**

A
  • 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**
41
Q

how is morphine metabolized?**

A

via glucuronide conjugation

42
Q

chars. of naloxone**

A
  • prototype opioid antagonist
  • relatively short half-life, so must keep giving***
  • reversal agent for opioid intoxication
43
Q

Most opioids are DEA class ___

A

II

44
Q

butorphanol is DEA class__

A

IV

45
Q

DEA class I drug def.

A

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.

46
Q

DEA class II drug def.

A

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.

47
Q

DEA class III drug def.

A

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.

48
Q

DEA class IV drug def.

A

drugs with a low potential for abuse and low risk of dependence.

49
Q

DEA class V drug def.

A

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.

50
Q

fentanyl has more/less CV impact than morphine

A

less. However, it is 100x more potent than morphine for most indications!

51
Q

buprenorphine DEA class __

A

III

52
Q

neuroleptanalgesia

A

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
53
Q

T/F: it is more common for sedative/opioid combinations to be used in hospital setting than neuroleptic/opioid combos**

A

T

Pharmacology (21 decks)

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