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VETM 443 Pharmacology > Pain Pharmacology > Flashcards

Pain Pharmacology Flashcards

(72 cards)

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1
Q

Define pain

A

It is a subjective sensory and emotional experience that is negative

Biologic, psychologic, and social factors contribute to it

There may or may not be associated tissue damage

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2
Q

Define nociception

A

It is the neural process that detects noxious stimuli that surpass the threshold of sensory neurons

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3
Q

Define nociceptor

A

It is a high threshold sensory neuron that transmits in response to noxious stimuli

They can be very specific to the type of stimuli
- ex. visceral tissue senses nociception from pressure but not sharp cuts

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4
Q

Define nociceptive neuron

A

CNS or PNS neuron that is part of the somatosensory system that encodes noxious stimuli

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5
Q

What are 3 main mechanisms used to control pain

A

anti-nociception
- remove neural response to painful stimuli

analgesia
- remove the pain in response to stimuli that is normally painful

general anesthesia
- drug induced unconsciousness through reversible depression of the CNS

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6
Q

Compare pain threshold and pain tolerance level

A

threshold
- minimum intensity that causes pain

tolerance
- maximum intensity that the subject is willing to accept in a given situation

measurement of pain is subjective

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7
Q

What are 4 classifications of pain

A

duration: acute vs chronic

pathogenesis
- nociceptive
- inflammatory
- neuropathic

location: msk vs visceral

severity (mild/mod/severe)

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8
Q

What are 2 types of nociceptive fibres? What type of response do they cause? How?

A

A fibres
- in skin, SC, fascia, bone
- sharp/well localized pain
- use glutamate NT

C fibres
- in muscle/viscera
- diffuse/dull pain
- use substance P NT (which binds to NK1 receptors)

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9
Q

What is the stimuli causing nociceptive pain

A

tissue damage

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10
Q

What is the stimuli causing inflammatory pain

A

inflammation

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11
Q

What is the stimuli causing neuropathic pain

A

damaged/dz neurons

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12
Q

What are 2 consequences of inflammatory pain

A

hyperalgesia
- increases sensitivity to nociception

allodynia
- non-painful stimuli becomes painful

due to an increase in inflammatory mediators resulting in activation of nociceptive receptors

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13
Q

What are 3 indications of neuropathic pain

A

migraine

headshaking in horses

some OA

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14
Q

Can you use NSAID for neuropathic pain

A

no - non responsive

but can use opioid, antidepressant, antiseizure, or systemic lidocaine

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15
Q

How do nociceptors contribute to inflammation

A

when stimulated they increase inflammatory mediator production through
- vasodilation
- plasma extravasation
- mast cell activation
- neutrophil activation

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16
Q

What is the pain pathways and at which step do different analgesics work?

A
  1. nociceptor
  2. first order neuron
    - local anesthetics
  3. second order neuron (spinal cord)
    - opioids and alpha 2 agonists
  4. third order neuron (brain)
    - antidepressants and opioids

The brain modulated the pain response by sending out pro and anti pain signals

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17
Q

What is wind up

A

It is when more pain signalling will sensitize the body to more pain

through increase production and response from second order neurons

It cannot be prevented by general anesthesia because it does not prevent against nociception

pre-emptive analgesia can reduce this effect

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18
Q

Explain the mechanism of wind up

A

nociceptors go to the CNS via the dorsal horn of the spinal cord in either..

spinocervicothalamic tract
- second order synapse in C1/C2 to thalamus
- transits touch and superficial pain

spinoreticular tract
- goes to diencephalon and reticular formation
- deep/visceral pain
- regulated consciousness (noxious stimuli cause increase in heart and resp rate)

Wind up changes the dorsal horn of the spinal cord
- activation of N-methyl D aspartate (NMDA) receptors
- upregulate post synaptic receptors

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19
Q

How is pain inhibited by the CNS naturally?

A

Descending inhibitory pathways result in reduced neurotransmitter release from primary afferents and reduced excitability of secondary neurons
- ex. periaqueductal grey matter

mechanisms
- endogenous opioid agonists like endorphins/ekephalins/dynorphins
- increase peripheral opioid receptors (triggered by inflammation)
- migration of opioid producing leukocytes (in response to selectin at injury site)

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20
Q

Which neurotransmitters are part of pain inhibition and what receptors do they use

A

serotonin
- 5HT1 = antinociceptive
- 5HT2 and 3 = pronociceptive

dopamine
- D1 = pronociceptive
- D2 and 3 = antinociceptive

GABA

Opioid

Cannabanoid

Norepi
- alpha 2 receptor = antinocicpective

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21
Q

What are 4 places that analgesics can act on to reduce pain

A

peripheral nociceptors

stop transmission to spinal cord

stop transmission to brain

increase descending inhibitory pathways

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22
Q

Provide 5 examples of full mu agonists

A

morphine
hydromorphone
fentanyl
methadone
etorphine

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23
Q

List 3 partial mu agonists

A

buprenorphine

tramadol

+/-butorphanol

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24
Q

List 2 full kappa agonists

A

etorphine

butrophanol

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25
List 1 partial kappa agonist
morphine
26
List 1 full delta agonist
etorphine
27
Compare opiate vs opioid
opiates are from poppies and opioids are synthetic opiates
28
Which parts of the pain pathway does opioids target
Works on multiple levels - mainly brain and spinal cord modulation - some effect on sensory neurons
29
List the types and functions of different opioid receptors. Where are they found (generally)?
mu - analgesia, sedation, euphoria = strong - increase vagal tone (resp depression/bradycardia/ileus) - increase locomotion in horse kappa - analgesia, sedation, dysphoria = mild - diuretic delta - analgestion = mild subtypes of each receptor can result in species differences expressed in CNS, PNS, GI - also immune cells and other tissues
30
What type of receptors are opioid receptors? What are 3 main mechanisms of action?
All G protein coupled receptors inhibit adenyl cyclase resulting in lowered cAMP - cause reduced Ca influx Inhibit presynaptic Ca channel = no neurotransmitter release increase K outflow in post synaptic neuron = excess hyperpolarization
31
What are 5 clinical uses of opioids
analgesia sedative (usually add alpha 2 agonist) antitussive antidiarrheal local use - epidural or interarticular block
32
How to reverse opioids
competitive opioid receptor antagonist - short effect naloxone - antagonize all receptors, especially mu - GABA antagonist - small doses q2-3min IV, IM, SC natrexone - antagonize all receptors longer than naloxone - reverse with carfentanil
33
List 5 ways opioids can be formulated. Provide examples for each formulation
injectable - morphine, hydromorphone, fentanyl, methadone, etorphine, butorphanol, buprenorphine tab - morphine sustained release tabs (varies absorption) - butorphanol (antitussive) - tramadol - hydrocodone transdermal - fentanyl transmucosal - buprenorphine liquid - hydrocodone
34
List 6 adverse effects of opioids
respiratory depression constipation.ileus pruritis histamine release hyperthermia CNS excitation
35
How do opioids cause respiratory depression
It is CNS mediated due to an increase in pCO2 It usually is not a problem in healthy animals - is a problem if resp dz or if neonate at high doses it can cause apnea
36
What are 2 reasons a dog might be panting
nausea resetting of thermoregulatory set point
36
What opioid should you not use to premed a horse
morphine causes dangerous excitation in recovery
37
How do opioids impact constipation/ileus
CNS and PNS mechanisms in small animals it increases colon motility causing defecation followed by constipation watch out in horses
38
When is histamine release typically seen as an adverse effect from opioid administration
when IV morphine is used causes vasodilation and hypotension
39
When is hyperthermia typically seen as an adverse effect from opioid administration
post hydromorphone (not with buprenorphine) mainly in cats
40
In what animals is CNS excitation due to opioids more common? Why? How to mitigate?
horses and cats usually after high doses cats more sensitive to morphine vs dogs horses excitable if given buprenorphine due to distribution of opioid receptors in the brain To mitigate, usually give another sedative - xylazine and butorphanol
41
What contraindications are there for opioid use
head trauma - can increase cranial pCO2 causing vasodilation high doses of methadone cause predispose to arrhythmias
42
What are the pharmacokinetic properties of opioids?
They are lipid soluble and can affect CNS good PO/IM/IV/SC absorption - some have varies PO ability short half life - for severe pain use as CRI - 2-4h duration of action metabolized by glucuronidation and excreted in the urine - renal/hepatic disease can affect
43
How are opioids/opioid receptors regulated locally
opioid receptor expression is increased in response to inflammatory cytokines - mainly mu > kappa > delta prevent Ca influx into neuron = prevent neurotransmitter release intra-articular morphine = potent analgesia/anti-inflam and few adverse
44
How should opioids be used in patients that have CKD or are pregnant
CKD - not a lot of research - in humans, buprenorphine is safer than morphine pregnant - opioids safer than NSAID - neonates more susceptible t respiratory depression - commonly used in SA, in LA used with sedation
45
How is opioid potency evaluated
all based off of morphine (standard) higher potency results in a higher risk of adverse effects - risk of apnea is higher if given fentanyl vs buprenorphine
46
What is the mechanism of action of morphine
mu agonist and partial kappa agonist
47
What is morphine commonly used for
analgesic anesthetic pre med sedative combo It is safe/cheap/effective
48
What are the adverse effects associated with morphine
histamine release - at high doses dont use in horses = CNS effects - can use locally in a epidural/intrathecal/intraarticular block
49
What is the mechanism of action of hydromorphone
It is a mu agonist (derivative of morphine) It has a short (30-90min) half life in small animals - will increase as dose increases
50
What are the adverse effects associated with hydromorphone
emesis but less histamine release than morphine
51
What is the mechanism of action of methadone
mu agonist NMDA antagonist norepi/serotonin re-uptake inhibitor
52
What are the benefits of methodone
no histamine release good for chronic pain less CNS impact less emesis similar potency to morphine
53
How is methadone administered
IM/SC/IV or CRI can be q4h if needed half life is 2-4h if given IV and its longer if given SC or IM but poor PO bioavailability
54
What is methadone used for commonly
cats in severe pain - pelvic fracture - HBC
55
What is the mechanism of action of fentanyl
mu agonist
56
What are the effects of fentanyl
it is over 100x more lipophilic and 100x more potent than morphine - fast and strong CNS effect It has a wide safety margin in dogs but high doses can cause apnea it increases motor activity in horses Less adverse effects - especially in cats
57
How is fentanyl administered
CRI or bolus q1-2h or transdermal patch (slower onset)
58
What is the mechanism of action of buprenorphine
partial mu agonist kappa antagonist not as strong of an effect as a full mu agonist
59
How is buprenorphine administered
transmucosal (poor bioavailability if PO)
60
How does buprenorphine's interaction with its receptor influence reversal
It has a high affinity for the mu receptor = high potency but low efficacy It can displace other opioids - may cause withdrawl response in addicts - may cause longer but less strong anti-nociceptive impacts - may require multiple doses of reversal
61
What is the mechanism of action of butorphanol
kappa agonist mu antagonist or partial agonist
62
What is butorphanol commonly used for
sedation (good at lower doses) - sedation > analgesia effects antiemetic antitussive may be used to partially reverse mu agonists (not in cats) can use with sedatives for LA - standing castrations - camelid sedation - good in horses
63
What is the mechanism of action of tramadol
the metabolite is a mu agonist muscarinic antagonist targets serotonin reuptake inhibitor (5HT) and norepi reuptake inhibitor (alpha 2) multimodal pain control - mild/moderate effects But relies on metabolism into active metabolite - there is significant individual variation and so effects can be varied
64
How is tramadol administered
PO
65
How should tramadol be used?
with other analgesics because it is not effective alone do not use as sole analgesic in dogs (it is more effective in cats)
66
What are 3 opioids you might use for mild to moderate pain
buprenorphine butorphanol tramadol
67
What are 4 opioids you might use for severe pain
morphine - but not in cats hydromorphone methadone fentanyl
68
What 3 opioids can you only give in clinic? Why?
injectable morphine hydromorphone methadone
69
What 4 opioids can you use at home
buprenorphine (transmucosal) fentanyl (transdermal) butorphanol (PO) tramadol (PO)
70
What opioids can you use in cats? Which can you not use?
NOT morphine YES - buprenorphine - butorphanol - tramadol - hydromorphone - methadone - fentanyl
71

VETM 443 Pharmacology (23 decks)

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