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Pharmacology Exam 3 > Pain Pathways and Opioids > Flashcards

Pain Pathways and Opioids Flashcards

1
Q

pain

A
  • an unpleasant sensory and emotional experience associated with actual or potential tissue damage
  • subjective, unique to each individual (genetic)
  • physical and emotional components
  • requires a functional CNS
  • involves multiple brain areas (no single pain center)
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2
Q

pain pathway

A

nociceptors

  1. transduction (sensory afferents)
  2. transmission
  3. modulation (spinal cord)
  4. projection (spinothalamic tracts)
  5. perception

brain

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3
Q

classification of pain

A
  • categorized according to duration as well as anatomical location or site of origin
  • acute vs. chronic
  • neuropathic, visceral, somatic
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4
Q

acute pain

A
  • short-term pain often with an easily identificable cause
  • acute pain is the body’s warning of tissue damage or disease
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5
Q

chronic pain

A
  • pain that persists longer than the normal course of time associated with a particular type of injury
  • may be constant or intermittent but it has often outlived any useful purpose, does not help the body to prevent injury
  • often more difficult to treat than acute pain
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6
Q

nociception

A
  • ability to perceive or sense pain
  • opiates produce “anti-nociception”
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7
Q

analgesia

A
  • loss of sensitivity to pain without loss of consciousness
    • opiates: ‘narcotic analgesics’
    • other drugs classified as non-narcotic analgesics (NSAIDs)
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8
Q

hyperalgesia

A
  • increased response to painful stimuli
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9
Q

allodynia

A
  • pain caused by a stimulus that would not normally provoke pain
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10
Q

signs of pain

A
  • behavioral signs
  • physiological changes
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11
Q

behavioral signs of pain

A
  • can be very species dependent
  • vocalization
  • protective postures
  • mood changes (aggression)
  • self-mutilation
  • loss of appetite
  • shallow/rapid breathing
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12
Q

physiological changes with pain

A
  • species dependent
  • general CV activation (increased sympathetic activity)
  • increased stress response (activation of HPA axi)
  • hyperglycemia (increased glycogenolysis and increased lipolysis)
  • reduced GI activity (ileus)
  • reduced immune function (diminished wound healing)
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13
Q

therapeutic uses of opiod drugs

A
  • analgesic
  • anti-tussive
  • adjunct to general anesthesia
  • emetic
  • neuroleptanalgesic
  • immobilization/restraint

= CNS!

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14
Q

problems with treating pain

A
  • difficult to assess pain in animals
  • specific behavior for each species
  • training personal and use validated scales
  • time and efficiency
  • subjective assessment
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15
Q

multidimensional pain scales

A
  • accounts for:
    • pain intensity
    • sensory and affective qualities of pain
    • incorporate sensitive and specific components (behavior, grimace scale)
  • Glasglow Composite (GCMPS)
  • SF-GCMPS
  • University of Melbourne Pain Scale (UMPS)
  • categories: physiologic parameters and behavioral responses
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16
Q

approaches to alleviate pain

A
  • prevention
  • acupuncture (may activate endogenous pathways for pain suppression)
  • analgesics
17
Q

types of analgesics

A
  • drugs that block formation, release or actions of substances that stimulate sensory nerve endings -transduction (NSAIDs)
  • drugs that block impulse transmission in sensory nerves (local anesthetics)
  • drugs that block or modulate tranmission in spinal/supraspinal pathways or alter the central perception of pain (opioids)
18
Q

sites of analgesic drug action

A
  • peripheral-nociceptors (NSAIDs)
  • nerve block-sensory afferents (locals)
  • epidural injection-spinal cord (opioids)
  • CNS action-brain (alpha-2’s)
19
Q

opioid

A
  • all drugs, natural and synthetic, that have morphine-like properties
  • opioid agonists and antagonists
20
Q

opiate

A
  • morphine-like drugs that are exratcted or derived from the opium poppy
  • morphine and codeine
21
Q

drug classifications and control

A
  • nearly all opioids are controlled
  • class I, II, III, IV and V
    • I- no approved medical uses with very high abuse potential in humans
  • must have DEA license to purchase or presribe
  • must keep records of purchase and use
  • must store durgs in locked area with limited access
22
Q

opioid receptors

A
  • mu (µ) = OP3 (MOP-µ)
  • kappa (k) = OP2 (KOP-k)
  • delta (∂) = OP1 (DOP-∂)
  • most are stimulated by morphine (agonist) and blocked by naloxone (antagonist)
  • marked species variation with respect to tissue localization and responses to drugs
23
Q

pharmacological actions of opioids

A
  • diverse and drug-specific actions with marked species-dependent effects
  • in general, opioids depress CNS, GI and CV systems
24
Q

CNS actions of opioids

A
  • analgesia
  • sedation
  • ventilatory depression
  • nausea & emesis
  • cough suppression (anti-tussive)
  • pupillary effect
25
Q

analgesic action of opioids

A
  • selective reduction and/or alteration of pain sensation w/o loss of consciousness
  • spinal cord-modulation
    • decrease substance P release from sensory afferents
    • decrease post-synaptic actions of substance P
  • supraspinal level-perception
    • decrease affective response to pain
    • decrease fear/anxiety associated with pain
26
Q

sedative action of opioids

A
  • variable degree based on species, age and demeanor
  • additive depression with other CNS depressants
    • reduces overall anesthetic requirement in most animals
27
Q

ventilatory depressive actions of opioids

A
  • depress PCO2 sensitivity of brainstem respiratory center neurons
    • reversible with naloxone
28
Q

nausea and emesis actions of opioids

A
  • caused by stimulation of brainstem CTZ
  • apomorphine is extremely effective
  • reduced by phenothiazines and other dopamine antagonists
  • anti-emetic after first dose-effect of vomiting center
29
Q

pupillary effect of opioids

A
  • species differences
  • dogs, rabbits, humans -> miosis
  • cats, horses, sheep, primates -> mydriasis
  • birds -> no change
30
Q

GI actions of opioids

A
  • opioids inhibit most GI activity
    • constipation and GI stasis
  • GI effects involve local as well as CNS actions
    • decrease peristalsis and secretions
    • increase segmental contractions
31
Q

CV actions of opioids

A
  • decrease HR and BP if there is an increase in histamine release
  • reversed by anti-cholinergic agents
32
Q

codeine

A
  • morphine derivative
  • µ-agonist
  • 1/10th potency of morphine as analgesic
  • indications: orally active antitussive and mild analgesic
  • long term admin may produce constipation
  • metabolized in liver, and excreted in urine
33
Q

morphine

A
  • µ-agonist
  • natural alkaloid from opium poppy seed
  • moderate lipid solubility with intermediate ability to penetrate BBB (ideal for epidural)
  • relative high ‘first-pass’ metabolism
  • metabolized via glucuronic conjugation (cats)
  • active metabolites
  • excreted by kidneys
34
Q

fentanyl

A
  • µ-agonist
  • potent synthetic opioid agonist
  • good analgesic in dogs, cats and horses
  • less CV impact than morphine (less histamine release)
  • fairly short half life (rapid liver metabolism)
    • CRI
35
Q

buprenorphine

A
  • partial µ-agonist
    • ​binds strongly to µ-receptor and requires higher doses of naloxone to reverse
  • mild to moderate analgesic
    • give SC, IM or IV
  • sublingual (only in cats!)
  • very slow onset of analgesic effect (over 30 min) but long duration of action (6-12 hours)
36
Q

butorphanol

A
  • opioid k-agonist/µ-antagonist
  • less side effects than µ-agonists, but causes less analgesia
  • mild analgesic in dogs, cats
    • less CV and respiratory depression
    • effective anti-tussive in dogs and cats
  • good analgesic in horses and ruminants
  • can be used to reverse µ-agonist side effects
37
Q

meperidine

A
  • µ-agonist
  • mild analgesia
  • most commonly used as pre-anesthetic
  • good sedative in young and geriatric patients
  • less excitatory effects in cats and horses
  • similar structure to atropine
    • only opioid to cause increase in HR
38
Q

naloxone

A
  • potent synthetic opioid-antagonist
  • relatively short half-life compared to most opioids
    • smaller doses, but frequent
  • reversal agent or treatment of opioid intoxication
39
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 a neuroleptic agent such as phenothiazines and alpha-2 agonists

Pharmacology Exam 3 (9 decks)

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