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)
2
Q
pain pathway
A
nociceptors
- transduction (sensory afferents)
- transmission
- modulation (spinal cord)
- projection (spinothalamic tracts)
- perception
brain
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
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
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
6
Q
nociception
A
- ability to perceive or sense pain
- opiates produce “anti-nociception”
7
Q
analgesia
A
- loss of sensitivity to pain without loss of consciousness
- opiates: ‘narcotic analgesics’
- other drugs classified as non-narcotic analgesics (NSAIDs)
8
Q
hyperalgesia
A
- increased response to painful stimuli
9
Q
allodynia
A
- pain caused by a stimulus that would not normally provoke pain
10
Q
signs of pain
A
- behavioral signs
- physiological changes
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
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)
13
Q
therapeutic uses of opiod drugs
A
- analgesic
- anti-tussive
- adjunct to general anesthesia
- emetic
- neuroleptanalgesic
- immobilization/restraint
= CNS!
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
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
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
