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VETM 443 Pharmacology > Pain Pharmacology > Flashcards

Pain Pharmacology Flashcards

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
Q

List 1 partial kappa agonist

A

morphine

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26
Q

List 1 full delta agonist

A

etorphine

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27
Q

Compare opiate vs opioid

A

opiates are from poppies and opioids are synthetic opiates

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28
Q

Which parts of the pain pathway does opioids target

A

Works on multiple levels
- mainly brain and spinal cord modulation
- some effect on sensory neurons

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29
Q

List the types and functions of different opioid receptors. Where are they found (generally)?

A

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
Q

What type of receptors are opioid receptors? What are 3 main mechanisms of action?

A

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
Q

What are 5 clinical uses of opioids

A

analgesia

sedative (usually add alpha 2 agonist)

antitussive

antidiarrheal

local use - epidural or interarticular block

32
Q

How to reverse opioids

A

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
Q

List 5 ways opioids can be formulated. Provide examples for each formulation

A

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
Q

List 6 adverse effects of opioids

A

respiratory depression

constipation.ileus

pruritis

histamine release

hyperthermia

CNS excitation

35
Q

How do opioids cause respiratory depression

A

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
Q

What are 2 reasons a dog might be panting

A

nausea

resetting of thermoregulatory set point

36
Q

What opioid should you not use to premed a horse

A

morphine

causes dangerous excitation in recovery

37
Q

How do opioids impact constipation/ileus

A

CNS and PNS mechanisms

in small animals it increases colon motility causing defecation followed by constipation

watch out in horses

38
Q

When is histamine release typically seen as an adverse effect from opioid administration

A

when IV morphine is used

causes vasodilation and hypotension

39
Q

When is hyperthermia typically seen as an adverse effect from opioid administration

A

post hydromorphone

(not with buprenorphine)

mainly in cats

40
Q

In what animals is CNS excitation due to opioids more common? Why? How to mitigate?

A

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
Q

What contraindications are there for opioid use

A

head trauma
- can increase cranial pCO2 causing vasodilation

high doses of methadone cause predispose to arrhythmias

42
Q

What are the pharmacokinetic properties of opioids?

A

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
Q

How are opioids/opioid receptors regulated locally

A

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
Q

How should opioids be used in patients that have CKD or are pregnant

A

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
Q

How is opioid potency evaluated

A

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
Q

What is the mechanism of action of morphine

A

mu agonist and partial kappa agonist

47
Q

What is morphine commonly used for

A

analgesic

anesthetic pre med

sedative combo

It is safe/cheap/effective

48
Q

What are the adverse effects associated with morphine

A

histamine release - at high doses

dont use in horses = CNS effects
- can use locally in a epidural/intrathecal/intraarticular block

49
Q

What is the mechanism of action of hydromorphone

A

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
Q

What are the adverse effects associated with hydromorphone

A

emesis

but less histamine release than morphine

51
Q

What is the mechanism of action of methadone

A

mu agonist

NMDA antagonist

norepi/serotonin re-uptake inhibitor

52
Q

What are the benefits of methodone

A

no histamine release

good for chronic pain

less CNS impact

less emesis

similar potency to morphine

53
Q

How is methadone administered

A

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
Q

What is methadone used for commonly

A

cats in severe pain
- pelvic fracture
- HBC

55
Q

What is the mechanism of action of fentanyl

A

mu agonist

56
Q

What are the effects of fentanyl

A

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
Q

How is fentanyl administered

A

CRI or bolus q1-2h

or transdermal patch (slower onset)

58
Q

What is the mechanism of action of buprenorphine

A

partial mu agonist

kappa antagonist

not as strong of an effect as a full mu agonist

59
Q

How is buprenorphine administered

A

transmucosal (poor bioavailability if PO)

60
Q

How does buprenorphine’s interaction with its receptor influence reversal

A

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
Q

What is the mechanism of action of butorphanol

A

kappa agonist

mu antagonist or partial agonist

62
Q

What is butorphanol commonly used for

A

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
Q

What is the mechanism of action of tramadol

A

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
Q

How is tramadol administered

A

PO

65
Q

How should tramadol be used?

A

with other analgesics because it is not effective alone

do not use as sole analgesic in dogs (it is more effective in cats)

66
Q

What are 3 opioids you might use for mild to moderate pain

A

buprenorphine
butorphanol
tramadol

67
Q

What are 4 opioids you might use for severe pain

A

morphine - but not in cats

hydromorphone

methadone

fentanyl

68
Q

What 3 opioids can you only give in clinic? Why?

A

injectable

morphine
hydromorphone
methadone

69
Q

What 4 opioids can you use at home

A

buprenorphine (transmucosal)
fentanyl (transdermal)
butorphanol (PO)
tramadol (PO)

70
Q

What opioids can you use in cats? Which can you not use?

A

NOT morphine

YES
- buprenorphine
- butorphanol
- tramadol
- hydromorphone
- methadone
- fentanyl

71
Q
A

VETM 443 Pharmacology (11 decks)

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