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Pain Management Flashcards

1
Q

define pain according to the IASP definition

A

an unpleasant sensory and emotional experience associated with, or resembling that which is associated with, actual or potential tissue damage

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2
Q

what factors can the experience of pain be influenced by?

A

biological
psychological
social

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3
Q

define nociception according to the IASP definition

A

the neural process of encoding noxious stimuli (physiological processes)

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4
Q

what forms may the consequences of encoding of stimuli take?

A

autonomic

behavioral

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5
Q

is pain sensation implied when nociception occurs?

A

not necessarily

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6
Q

what is the key difference between nociception and pain?

A

nociception is the wiring part of the process

pain is how the patient interprets nociception

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7
Q

in two animals injected IM with the same technique are nociception and pain likely to be the same?

A

nociception is likely to be identical whereas pain, the feeling, interpretation and expression of response to nociceptive stimuli, is not.

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8
Q

define nociceptive pain according to the IASP definition

A

pain that arises from actual or threatened damage to non-neural tissues and is due to the activation of nociceptors

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9
Q

what is the term nociceptive pain used to describe?

A

pain occurring with a normally functioning somatosensory nervous system

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10
Q

define neuropathic pain according to the IASP definition

A

a lesion or disease of the somatosensory nervous system

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11
Q

what is the term neuropathic pain a clinical description of?

A

a demonstrable lesion or a disease

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12
Q

when is the term lesion used when discussing neuropathic pain?

A

when diagnostic investigations reveal an abnormality or where there was obvious trauma

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13
Q

when is the term disease commonly used when discussing neuropathic pain?

A

when the underlying cause of the lesion is known

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14
Q

what is the difference between nociceptive pain and neuropathic pain?

A

nociceptive pain arises from injury to non-neural tissue, neuropathic pain arises from damage to the somatosensory nervous system

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15
Q

why is it essential to avoid damaging neural tissue during elective surgical procedures?

A

so that neuropathic pain is is not caused alongside nociceptive

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16
Q

of nociceptive and neuropathic pain, which can be harder to treat?

A

neuropathic

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17
Q

what do the terms hyperalgesia and allodynia both describe?

A

changes in nociceptive processing that may occur in patients in an ongoing pain state

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18
Q

define hyperalgesia according to the IASP definition

A

increased pain from a stimulus that normally provokes pain (increased response at a normal threshold)

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19
Q

give an example of hyperalgesia

A

pressing on the skin can become painful if enough pressure is applied, however if the skin is bruised the pressure at which pain will be felt is much less (nociceptive threshold is lower)

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20
Q

define allodynia according to the IASP definition

A

pain due to a stimulus that does not normally produce pain

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21
Q

give an example of allodynia

A

due to underlying injury/disease a cat now finds being stroked (a non-noxious stimulus) painful

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22
Q

how long does acute pain last for?

A

a short period of time - minutes and hours to weeks

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23
Q

how long does chronic pain last for?

A

longer than a few weeks

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24
Q

what may happen if acute pain is not adequately treated?

A

may lead to a chronic pain state

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25
Q

what may chronic pain arise from?

A

chronic medical conditions such as osteoarthritis and skin disorders

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26
Q

is chronic pain generally protective or beneficial to the sufferer?

A

no it is usually detrimental

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27
Q

when may acute pain be productive?

A

can stop an animal from causing itself further damage

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28
Q

what can untreated or poorly treated pain lead to?

A

up-regulation of the pain processing system making the pain harder to treat and the establishment of pain states

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29
Q

what can be reduced by untreated or poorly treated chronic pain?

A

quality of life

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30
Q

why is recognition and quantification of pain so important?

A

if we cannot recognise pain we are unable to treat it

quantification allows categorisation of pain, assessment and judgements about quality of life to be made

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31
Q

what are the 3 key stages in the quantification of pain?

A

categorization of pain as absent, mild, moderate, severe
assess treatment efficacy
make judgements about quality of life

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32
Q

what does the categorization of pain as absent, mild, moderate and severe influence?

A

how we decide to treat the pain

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33
Q

how can treatment efficacy be assessed?

A

observing weather pain score reduces if a treatment is used

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34
Q

what judgements about quality of life may be made using quantification of pain?

A

should the animal be treated or is euthanasia a prefurrable option?

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35
Q

what is the key challenge of assessing pain in animals?

A

they cannot talk

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36
Q

what can be used to assess pain?

A

behavioural signs

physiological signs

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37
Q

what are the physiological signs associated with pain?

A

increased HR, blood pressure and body temperature
altered respiration (rate and pattern)
stress hormones increasing
EEG (electroencephalogram) activity

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38
Q

what is a key issue with using physiological signs to indicate pain?

A

they are non-specific and may increase or decrease along with things other than pain

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39
Q

what stress hormones could be used to indicate pain?

A

cortisol, noradrenaline and adrenaline

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40
Q

what is the difficulty of using EEG to determine presence of pain?

A

is this pain or nociception

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41
Q

are behavioural signs of pain species specific?

A

yes

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42
Q

why may behavioural signs of pain vary between individuals within a species?

A

depending on temperament or their response to a stressful environment which may cause them to hide pain

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43
Q

why do prey species tend to hide signs of pain?

A

so they do not stand out to a predator

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44
Q

what are behavioural signs associated with pain specific to?

A

species
individual
condition

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45
Q

what are the shared behavioural signs associated with pain exhibited by cats and dogs?

A 
hunched appearance
'pain' face
lack of grooming
inappetance
specific signs (e.g. lameness)
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46
Q

what are the behavioural signs associated with pain that are specific to cats?

A 
absence of normal behavioural repertoire
hide away at back of cage
unwilling to relax
fear-aggression
resent human contact
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47
Q

what are the behavioural signs associated with pain that are specific to dogs?

A

positive behavioural signs rather than reduced repertoire
more likely to seek attention
submissive
more likely to vocalize

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48
Q

what are the behavioural signs associated with pain that are specific to rabbits?

A 
immobility 
profound depression
eyes half closed or shut
not grooming
avoiding attention
isolating themselves from other animals
bruxism
abnormal body position such as a hunched posture and abdominal pressing
change in temperament
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49
Q

when is immobility in rabbits particularly acute?

A

post-op or traumatic pain however they may show this behaviour in unusual environments when there is no pain at all

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50
Q

define bruxism

A

tooth grinding

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51
Q

what is an essential consideration when handling animals in pain?

A

prey animals with a strong fight or flight response which means that they can react violently to severe pain

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52
Q

what are the behavioural signs associated with pain that are specific to horses?

A 
low head carriage
horse at back of stable
vocalisation (groaning or neighing)
agitation
restlessness
weight-shifting
tail swishing (with no flies present)
lameness
limb lifting
abnormal distribution of weight
'tucked up' appearance
looking at painful body part
'pain face'
bruxism
sweating
muscle fasciculations
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53
Q

what are the main chronic pain indicators in all species?

A

changes in normal behaviour described by owner (may be put down to animal getting older or slowing down)
unkempt coat if grooming is difficult
loss of body condition/ weight loss due to appetite loss and/or loss of muscle tone if exercising less
slowing down/sleeping more
could also be more restless/fidgety
reluctance to move possibly described as a loss of training (e.g. peeing in the house because they can’t get outside)
difficulty in accessing higher places

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54
Q

what is the NRS?

A

numerical rating scale which requires patient to assign their pain a score from 1-10

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55
Q

what is VAS?

A

visual analogue scale which requires patient to make a mark on a line from 1-10 to demonstrate level of pain. The position of the mark on the line is then measured to assign a number

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56
Q

what is SDS?

A

simple descriptive scale where patients assign themselves a category relating to a description of a pain level that is matched to a number

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57
Q

what can be used to score pain in animal patients?

A

NRS, VAS or SDS

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58
Q

who awards the scores during pain assessment of animals?

A

caregiver

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59
Q

what can make pain scoring more accurate?

A

dynamic interaction with animal rather than just observing

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60
Q

what is an issue with using NRS, VAS or SDS in a veterinary environment?

A

interobserver variation which can be an issue in a practice where there is likely to be multiple caregivers

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61
Q

what is the purpose of composite pain scales?

A

over come some of the limitations of the VAS, NRS and SDS

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62
Q

how do composite pain scales work?

A

multiple items are assessed for each patient and given a score. These are them added to give an overall score

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63
Q

what must happen to composite pain scales in order for them to be useful?

A

must be validated which requires lots of clinical testing

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64
Q

what is often suggested by composite pain scales?

A

an intervention level/ score at which the patient should receive an intervention (analgesic medication)

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65
Q

what is the composite pain scale used for dogs?

A

SF-GCPS: glasgow composite pain scale

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66
Q

what is the SF-GCPS score out of if the dog cannot stand?

A

20

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67
Q

what is the SF-GCPS score out of if the dog can stand?

A

24

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68
Q

what is the intervention level of the SF-GCPS?

A

5/20 or 6/24

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69
Q

what is the drawback of the SF-GCPS?

A

poor differentiation between sedation and pain which is an issue immediately post-op

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70
Q

what is the composite pain scale used for cats?

A

CMPS

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71
Q

what is the maximum score of the CMPS?

A

20

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72
Q

what is the recommended intervention level of the CMPS?

A

5/20

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73
Q

what is essential to remember when filling in composite pain scores?

A

follow the order and scores on the sheet

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74
Q

are there composite pain scores for rabbits and horses?

A

not really at the moment

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75
Q

when may owners be helpful in filling in pain scoring?

A

to show pain levels over time and levels when not in the veterinary environment. Useful for post-op or chronic pain

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76
Q

what is involved in chronic pain assessment?

A

can use VAS, NRS, SDS and CPS for a snapshot of pain at a specific time but may want to include other elements such as appetite and sleep over a period of time

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77
Q

are there chronic pain composite pain scores available?

A

yes, tend to be condition and species specific used to collect data on pain and impact on life functions

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78
Q

with owner pain scoring of chronic pain what are the questions more often about?

A

quality of life as opposed to specific questions about pain at a single point in time

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79
Q

how does the LOAD questionnaire for OA work?

A

each of the mobility questions is given a score from 0-4 (not present to most severe). The LOAD score is the sum of the questions

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80
Q

what is another way of monitoring chronic pain?

A

client specific outcome measures

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81
Q

what is involved with client specific outcome measures?

A

along with owner 4 or 5 different behaviours are identified that the animal normally performs (or used to)
changes in the frequency of these behaviours or activities are recorded over time (usually from the start of analgesic therapy)

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82
Q

what is a key benefit of client specific outcome measures?

A

very specific to pet (tailored)
quick to complete
easy to track changes over time

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83
Q

what are the main advantages of owner questionnaires for chronic pain?

A

allow owner and clinician to see impact of pain on quality of life and the impact of external factors like weather and exercise on pain and quality of life
allows ongoing monitoring and assessment of interventions

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84
Q

what is the benefit of videos as add on or stand alone assessment?

A

can be shared within the team
behaviour can be shown in the animals natural environment
week on week records can help to detect changes
visible evidence of improvement may improve owner compliance with medication
owner and vet team can see how other factors affect behaviour
any species

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85
Q

why is assessment of health related quality of life useful?

A

aids decision making about requirement for analgesia or timing of euthanasia
improved patient well-being through holistic/global care
improve continuity of treatment between clinicians or treatment centres
help to build and maintain owner and veterinary professional relationships

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86
Q

what is involved in health-related quality of life assessment?

A

assessment of quality of life in relation to analgesia and chronic pain

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87
Q

what is preventative anaesthesia?

A

administration of effective analgesia before, during and after the surgery/procedure, well into the post operative recovery period

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88
Q

what is the aim of preventative analgesia?

A

prevention of upregulation of the nervous system in the presence of noxious stimuli (e.g. surgery) by administering effective analgesia

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89
Q

what should be seen in response to preventative analgesia?

A

reduction both in intensity and duration of acute pain and a reduction in persistent (chronic) pain

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90
Q

what is multi-modal analgesia?

A

using different classes of analgesic agents/techniques to attempt to over come the fact that there is no single analgesic agent that can block all nociceptive/pain pathways

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91
Q

what is a benefit of multi-modal analgesia?

A

leads to more effective analgesia often with lower doses of analgesic agents

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92
Q

what are the 6 main analgesic agents used in veterinary practice?

A 
opioids
NSAIDs
local anaesthetics
Alpha-2 agonists
ketamine
others/misc
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93
Q

what is different about alpha 2 agonists and ketamine?

A

alpha-2 agonists are sedatives which are analgesic
ketamine is an anaesthetic that is analgesic
rather than being only analgesics

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94
Q

what schedule of drugs are full opioid agonists?

A

schedule 2

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95
Q

give an example of 2 full opioid agonists

A

methadone and fentanyl

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96
Q

what schedule of controlled drugs are partial opioid agonists?

A

schedule 3

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97
Q

give an example of 2 partial opioid agonists

A

buprenorphine and butorphanol

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98
Q

what are the requirements for schedule 2 drugs?

A

special prescription, storage, destruction and record keeping

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99
Q

what are the requirements for schedule 3 drugs

A

special prescription and some have special storage requirements (e.g. bupe must be locked away)

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100
Q

where do opioids licensed for cats, dogs and horses act within the body?

A

endogenous opioid receptors primarily in the brain and spinal cord

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101
Q

what are the 3 key opioid receptors?

A

delta, kappa and mu

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102
Q

what sorts of agonists may opioids be?

A

full agonists, partial agonists, mixed agonist antagonist or antagonist

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103
Q

give an example of an opioid mixed agonist-antagonist

A

butorphanol

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104
Q

give an example of an opioid antagonist

A

naloxone

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105
Q

which type of receptor agonists are associated with analgesia?

A

mu

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106
Q

what type of agonists provide the most effective analgesia?

A

full mu agonists

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107
Q

under what circumstances are opioids used?

A

acute pain - preventative and part of multi-modal analgesia regimens

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108
Q

define potency

A

mg/kg of drug required to show effect

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109
Q

define efficacy in terms of drugs

A

the maximum response possible from a specific drug

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110
Q

why is fentanyl so dangerous?

A

is highly potent and efficacious - very little required to overdose

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111
Q

how may opioids be administered?

A 
IV
oral
SC
IM
buccal
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112
Q

what opioid must not be given IV?

A

pethidine

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113
Q

what drug may not be so effective when given SC to cats?

A

buprenorphine

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114
Q

how does buccal administration differ from oral?

A

buccal requires transmucosal absorption by oral mucous membranes, oral medication is absorbed in the small intestine

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115
Q

why is there poor bio-availability of orally administered opioids?

A

significant first pass metabolism so they are broken down very quickly and easily by the liver

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116
Q

what does poor bio-availability of opioids mean for chronic pain?

A

limited role in management of chronic pain

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117
Q

give an example of a short acting mu agonist

A

fentanyl

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118
Q

when are short acting mu agonists used?

A

intra-operative and short term infusion

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119
Q

give an example of a long acting full mu agonist

A

methadone

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120
Q

when are long acting full mu agonists used?

A

general use for acute and pre, peri and post operative pain

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121
Q

how long do long acting full mu agonists tend to last?

A

2-4hr

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122
Q

give an example of a partial mu agonist

A

buprenorphine

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123
Q

when are partial mu agonists often used?

A

general use for acute and pre, peri and postoperative pain

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124
Q

how long to partial mu agonists last for?

A

6hrs

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125
Q

give an example of a K agonist and mu receptor

A

butorphanol

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126
Q

when would a mixed K agonist and mu receptor be used?

A

general use for acute and pre, peri and postoperative pain

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127
Q

how long do mixed K agonist and mu receptor drugs last for?

A

2hrs

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128
Q

what are the key side effects of opioid use at clinical doses?

A 
respiratory depression
sedation
excitation
minimal effect on inotropy
bradycardia
nausea and vomiting
antitussive
decrease GI motility
various effects on urinary system
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129
Q

when are respiratory depression effects most often seen when using opioids?

A

dose dependent and mostly during anaesthesia

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130
Q

when are sedation side effects seen during opioid use?

A

species and dose dependant, more sedation seen in dogs

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131
Q

when is excitation often seen as a side effect of opioid use?

A

at high doses particularly in pain free animals. can cause box walking in horses and excitement in cats

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132
Q

what is inotropy?

A

force of heart contraction

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133
Q

what causes bradycardia as a side effect when giving opioids?

A

vagal effect

134
Q

how can bradycardia as a side effect of opioid use be managed?

A

use of an anticholinergic such as atropine

135
Q

when does nausea and vomiting most often occur in patients receiving opioids?

A

seen in dogs and cats and more common in pain free animals

136
Q

what is an antitussive effect?

A

reduction of cough

137
Q

what effect may opioids have on GI motility?

A

decrease

138
Q

how much of an issue is decreased gut motility in dogs and cats?

A

not too problematic

139
Q

when is decreased gut motility in opioid use more of an issue?

A

chronic use

140
Q

when are side effects of opioids on the urinary system of clinical significance?

A

not unless administered epidurally

141
Q

what does NSAID stand for?

A

non steroidal anti-inflammatory drugs

142
Q

how do most NSAIDs work?

A

inhibition of prostaglandin production either through inhibition of COX (cyclo-oxygenase) or LOX (lipoxygenase) enzymes

143
Q

what are NSAID side effects directly linked to?

A

protective effects that prostaglandins have on the body

144
Q

where are NSAIDs metabolised?

A

the liver

145
Q

what are NSAIDs effective analgesics for?

A

acute and chronic pain

146
Q

when is caution needed when giving NSAIDs?

A

if administering pre/peri-operatively or if a patient is dehydrated or hypotensive

147
Q

in what regimens are NSAIDs useful?

A

multi-modal analgesic

148
Q

can more than one NSAID be used in a multi-modal analgesic approach?

A

no - due to side effects

149
Q

what are the 2 main NSAIDs licensed for use in dogs and cats?

A

meloxicam

carprophen

150
Q

who can most NSAIDs be administered to the patient?

A

injection or oral

151
Q

what is the main NSAID used in rabbits?

A

meloxicam

152
Q

what are the main NSAIDs used in horses?

A

meloxicam

phenylbutazone

153
Q

what are the main side effects of NSAID use at clinical doses?

A 
GI ulceration
Renal ischaemia
Hepatopathy
blood clotting
CNS effects
154
Q

when should special care be taken when giving NSAIDs?

A

those with history of GI ulceration
any patient with reduced drug clearance capacity
during anaesthesia of dogs and cats

155
Q

why can NSAIDs cause renal ischemia?

A

during hypotension prostaglandins protect renal blood flow and so this action is blocked by NSAIDs

156
Q

with what type of NSAIDs is clotting an issue?

A

the less commonly used non-COX selective NSAIDs

157
Q

what information should be given to owners about safe use of NSAIDs in dogs and cats?

A

GI side effects are most common
will present as vomiting and diarrhoea
may see digested blood (coffee grounds)
general malaise

158
Q

what should owners do if they see any side effects of NSAID use?

A

discontinue medication immediately and ring the practice

159
Q

what information should be given to owners about safe use of NSAIDs in horses?

A

GI side effects most common: GI ulceration presenting as colic, diarrhoea, dehydration and weight loss
renal effects
malaise

160
Q

when do side effects of NSAIDs most commonly occur in horses?

A

overdose
chronic administration
weight loss

161
Q

when are renal effects of NSAIDs more of an issue in the horse?

A

when dehydrated

162
Q

what information should be given about safe use of NSAIDs in rabbits?

A

aware of the fact no NSAIDs are licensed for use in rabbits
GI effects most common
if animal appears unwell (anorexia, bruxism, depression, reluctance to move) owners should discontinue medication and phone practice

163
Q

when do NSAIDs side effects most commonly occur?

A

in chronic use

164
Q

what is the key pharmacology of local anaesthetics?

A

enter nerve fibre and block voltage gated Na+ channel so blocking nerve conduction

165
Q

which fibres are preferentially blocked by local anaesthetics?

A

C fibres and A-delta fibres

166
Q

what type of blockade is achieved by blocking C and A-delta fibres during local anaesthetic?

A

nociceptive blockade before proprioceptive, mechanoreceptive and motor blockades

167
Q

what type of molecules are most local anaesthetics?

A

weak bases (pKa = 8-9)

168
Q

what form of the weak base can penetrate lipid membranes and enter the nerve cell?

A

uncharged form

169
Q

how does ionisation (pKa) affect onset of local anaesthetic action?

A

higher pKa will be more ionised in plasma and so have a slower onset of action

170
Q

what happens to local anaesthetic if the pH of the tissue decreases (e.g. inflammation)?

A

greater proportion of the drug is ionized and therefore less drug can penetrate the nerve membrane to bind to the sodium channel

171
Q

where is local anaesthetic less effective?

A

inflamed tissue

172
Q

what are the 2 linkages that may be found in different local anaesthetics?

A

ester

amide

173
Q

how stable are ester and amide linkages?

A

ester are relatively unstable

amide are more stable

174
Q

how rapidly are ester and amide linkages broken down?

A

ester - rapidly by plasma psudocholinesterase

amide - subject to bio-transformation with conjugation in the liver

175
Q

how long are ester and amide linkage half-lives?

A

ester - short local anaesthetic half life

amide - longer plasma half life

176
Q

how can you tell which local anaesthetic drugs have ester and amide linkages?

A

ester - no ‘i’ in name before ‘caine’

amide - ‘i’ in name before ‘caine’

177
Q

what is formed as a byproduct of hydrolysis of ester linkages that can provoke allergic reactions?

A

PABA

178
Q

give an example of an ester linkage LA

A

procaine

179
Q

give an example of an amide linkage LA

A

lidocaine

180
Q

what does the toxicity/side effects of LA depend on?

A

the dose - safe total dose must never be exceeded

181
Q

what are the side affects associated with LA?

A

CNS toxicity

CVS toxicity

182
Q

what effects are seen with CNS toxicity of LA?

A

minor behavioral changes
muscle twitching and tremors
tonic-clonic convulsions
CNS depression/ respiratory depression and death

183
Q

what are the effects seen with CVS toxicity of LA?

A

hypotension

dysrhythmias

184
Q

does CNS or CVS toxicity occur at lower doses?

A

CNS

185
Q

what is involved in treatment of CNS/CVS side effects of LA?

A

symptomatic treatment

186
Q

what animals is lidocaine licensed for?

A

horses, dogs and cats and is used in rabbits

187
Q

what is the onset of action of lidocaine?

A

rapid, 2-5 mins

188
Q

how long acting is lidocaine?

A

short - 20-40 mins

189
Q

what is an advantage of lidocaine over bupivacaine?

A

lower cardiotoxicity

190
Q

when are local anaesthetics used?

A

part of balanced anaesthetics regimen (e.g regional infiltration or epidural under GA)
to provide anaesthesia for standing procedures
post-operative pain relief
desensitisation for procedures (e.g. EMLA)
lameness investigation in horses

191
Q

what class of drugs does paracetamol fall under?

A

not an NSAID but can be considered one

192
Q

what is the mechanism of action of paracetamol?

A

not fully understood

193
Q

to what species is paracetamol very toxic?

A

cats

194
Q

when is paracetamol useful in dogs?

A

when NSAIDs are contraindicated

195
Q

when is paracetamol used in horses?

A

useful as an adjunctive analgesic in very painful cases and also where NSAIDs are contraindicated

196
Q

what is the mode of action of tramadol?

A

multi-modal

mu opioid system, noradrenergic system and serotonergic system

197
Q

what are the actions of tramadol associated with?

A

some with tramadol enantiomers and some with its metabolites

198
Q

what is tramadol used for?

A

acute and chronic pain conditions

believed to have a wide therapeutic index and lower risk of abuse than opioids

199
Q

what drug schedule does tramadol fall under?

A

schedule 3

200
Q

how should tramadol be administered to dogs?

A

IV as oral is unlikely to be effective

201
Q

does current evidence suggest that tramadol should be used alone?

A

no - should only be used as a co-analgesic

202
Q

how effective is tramadol in cats?

A

some analgesic effect given IV, may have effects on chronic pain when given orally

203
Q

can tramadol be used in horses?

A

only for laminitis patients that aren’t responding to other analgesics as extended use of opioids can lead to decreased gut motility and risk of impaction/colic

204
Q

what is the oral bio-availability of tramadol like in horses?

A

variable

has a short half life

205
Q

how does gabapentin work?

A

precise mechanism of action unknown; analgesic action is attributed to binding voltage gated calcium channel

206
Q

what does binding of gabapentin to voltage gated calcium channels lead to ?

A

decreased release of excitatory neurotransmitters in the dorsal horn of the spinal chord - reduction in pain sensation in cases of allodynia, hyperalgesia etc

207
Q

what may gabapentin be used for?

A

management of neuropathic type pain conditions

208
Q

what is a major side effect of gabapentin?

A

sedation

209
Q

why should liquid solutions containing xylitol be avoided?

A

due to potential for toxicity as this is a human medication and the sweetner is toxic to veterinary patients

210
Q

how should gabapentin administration be stopped?

A

slowly - reduce dose over 1-2 weeks

211
Q

what is amantadine?

A

oral NMDA receptor agonist

212
Q

what is amantadine used for?

A

antihyperalgesic so should be used alongside an analgesic

213
Q

how is amantadine excreted?

A

via kidneys so should be used cautiousl in patients with reduced renal function

214
Q

when may amantidine be useful?

A

chronic pain states to reverse or obtund central sensation

215
Q

how long any it take to see benefit of amantadine therapy?

A

3-4 weeks

216
Q

why are animals premedicated prior to anaesthesia?

A 
decreases stress and risk of injury to patients and staff
production of balanced anaesthesia
provide preventative analgesia
assists smooth recovery from anaesthesia
reduce side effects of anaesthetic drugs
217
Q

how can balanced anaesthesia be produced by premedicating animals prior to anaesthetic induction?

A

reduce dose of induction and maintenance agents

218
Q

how does premedication reduce the side effects of anaesthetic drugs?

A

either by giving less or by administering something that counteracts the side effects

219
Q

what are the 5 main classes of drugs used for premedication?

A 
phenothiazines
alpha-2 agonists
benzodiazepines
butyrophenones
opioids
220
Q

do phenothiazines have sedative and analgesic action?

A

sedative but not analgesic

221
Q

do alpha-2 agonists have sedative and analgesic action?

A

yes

222
Q

do benzodiazepines have sedative and analgesic action?

A

sedative but not analgesic

223
Q

do butyrophenones have sedative and analgesic action?

A

sedative but not analgesic

224
Q

do opioids have sedative and analgesic action?

A

some have sedative action (species dependent) all have analgesic action

225
Q

what is the mode of action of phenothiazines?

A

dopamine receptor agonist in the CNS

226
Q

what is the mode of action of alpha-2 agonists?

A

alpha-2 adrenergic receptor agonist in the CNS

227
Q

what is the mode of action of benzodiazepines?

A

enhance the effect of gamma-aminobutyric acid (GABA) at the GABA-alpha receptor

228
Q

what is the mode of action of butyrophenones?

A

dopamine receptor antagonist in the CNS, also interferes with GABA, noradrenaline and serotonin-mediated neuronal activity

229
Q

what is the vet licenced phenothiazine in the UK?

A

Acepromazine (ACP)

230
Q

what are the vet licenced alpha-2 agonist in the UK?

A

dexmedetomidone and medetomidine are most common

also romifidine and xylazine

231
Q

what are the vet licenced benzodiazepines in the UK?

A

diazepam and midazolam

232
Q

what is the vet licenced butyrophenone in the UK?

A

Fluanisone - only available in a combination product with fentanyl (Hypnorm)

233
Q

what are the licenced species for phenothiazines in the UK?

A

ACP - dog and cat

234
Q

what are the licensed species of the vet licensed alpha-2 agonists in the UK?

A

all licensed in dogs and cats

235
Q

what are the licensed species for veterinary licensed benzodiazepines in the UK?

A

diazepam in dogs and cats

midazolam in horses

236
Q

what are the licensed species for veterinary licensed butyrophenones in the UK?

A

rabbits

237
Q

what is the advantage of IV premed?

A

rapid onset of action

predictable effect

238
Q

what is the advantage of IM premed?

A

fairly rapid onset of action

predictable effect

239
Q

what is the advantage of SC premed?

A

easier to do than IV or IM

240
Q

what is the advantage of OTM (oral transmucosal) premed?

A

not useful routinely - can be helpful in special cases (e.g. feral cats)

241
Q

what is the disadvantage of IV premed?

A

requires restraint and/or IV catheter placement before anaesthesia

242
Q

what is the disadvantage of IM premed?

A

painful

243
Q

what is the disadvantage of SC premed?

A

not all drugs are absorbed by this route
can be unpredictable
slower onset than IM

244
Q

what is the disadvantage of OTM (oral transmucosal) premed?

A

not all drugs are absorbed by this route
can be unpredictable
slower onset than IM

245
Q

what are the key clinical effects of ACP (phenothiazine)?

A

sedation

anxiolytic

246
Q

what is ACP often used in combination with in premeds?

A

opioids

247
Q

what is ACP widely used for in cats and dogs?

A

sedation for procedures and premedication

248
Q

what is ACP used for in rabbits?

A

premedication although not licenced

249
Q

what is ACP sedation level dependent on?

A

dose up to plateau dose

250
Q

how can ACP sedation be improved?

A

combination with opioid

if animal is left in a quiet environment for 30-40 mins

251
Q

how effective is SC injection of ACP for sedation?

A

non-irritant and efficacious, particularly in cats

252
Q

should the same does of ACP be used for sedation and premedication?

A

lower doses for premed than for sedation

253
Q

what are the physiological effects of ACP on the CVS?

A

peripheral vasodilation
potential to decrease blood pressure particularly in animals with CVS disease or shock
vasodilation also causes fall in body temperature (issue in smaller animals)
minimal effects on respiration
anti-arrythmatic action

254
Q

what is the time to clinical effect from administration of ACP IV?

A

10-15 mins (slower than alpha-2 agonists)

255
Q

when is the clinical effect of ACP seen after IM administration?

A

30-40 mins

256
Q

where should animals be left to become sedated with ACP?

A

quiet area

257
Q

how long is the duration of action of ACP?

A

4-6 hours

258
Q

how is ACP metabolised?

A

in the liver

259
Q

in what animals is the action of ACP prolonged?

A

those with liver diease

260
Q

how good is the oral bio-availabilty of ACP?

A

poor

261
Q

what are the clinical effects of alpha-2 agonists?

A

sedation
analgesia
muscle relaxation

262
Q

what is the duration and level of sedation with alpha-2 agonists dependent on?

A

dose

263
Q

are alpha-2 agonists potent?

A

yes - use body surface area rather than weight to calculate dose

264
Q

what type of drugs are alpha-2 agonists often used with?

A

opioids

265
Q

what effect can occur when alpha-2 agonists are combined with other sedatives/analgesics?

A

additive or synergistic effects

266
Q

what are the key advantages of alpha-2 agonists?

A

significant dose reduction for anaesthetic induction and maintenance agents
reversible using antagonist (atipamazole)

267
Q

what antagonist can be used to reverse alpha-2 agonists?

A

atipamazole

268
Q

what are the physiological effects of alpha-2 agonists on the CVS?

A

bradycardia
reduced cardiac output
second degree AV block
initial rise in BP which will then fall to normal or hypotension

269
Q

what are the physiological effects of alpha-2 agonists on the respiratory system?

A

variable between species and individuals within a species
respiratory depression seen in some but not all patients - rate decrease seen but no overall effect on minute volume or blood gases

270
Q

what can the CVS effects of ACP be managed by?

A

administration of fluids

271
Q

what are the physiological effects of alpha-2 agonists on the GI system?

A

can be emetic in dogs and cats

can depress GI activity and has been reported to cause GI stasis in dogs

272
Q

why should deep chested dog breeds avoid alpha-2 agonists?

A

risk of GDV

273
Q

what are the physiological effects of alpha-2 agonists on animal behaviour?

A

some temporary behavior and personality changes in dogs and cats (similar to other sedatives)

274
Q

what are the physiological effects of alpha-2 agonists on the pancreas?

A

reduced secretion of insulin - may see transient hyperglycaemia which is not harmful to the animal but may mess with blood work

275
Q

what are the physiological effects of alpha-2 agonists on the renal system?

A

increase in urine production by a decrease in secretion of vasopressin

276
Q

what should happen to animals receiving alpha-2 agonists by CRI?

A

catheterisation

277
Q

what are the physiological effects of alpha-2 agonists on the uterus?

A

can affect contractility dependent on dose and concentrations of oestrogen and progesterone

278
Q

at what life stage should alpha-2 agonists be avoided?

A

pregnancy - near term due to its effect on uterine contractility and risk of abortion

279
Q

how long until full clinical effect of alpha-2 agonists after IV administration?

A

5 minutes

280
Q

at what time after administration are alpha-2 agonist effects seen?

A

30 mins

281
Q

what is the duration of action of alpha-2 agonists if atipamezole isnt used?

A

2-3 hours

282
Q

in what animals is the duration of alpha-2 agonists prolonged?

A

those with liver disease

283
Q

how are alpha-2 agonists metabolized?

A

in the liver

284
Q

what are the clinical effects of benzodiazepines?

A

minor tranquilisers
muscle relaxation
anticonvulsant

285
Q

what is sedation with benzodiazapines like in healthy animals?

A

unreliable and can cause excitement when administered alone

286
Q

to what animals do benzodiazapines provide good sedation?

A

the young or sick

287
Q

what can benzodiazapines be combined with to improve sedation?

A

opioid, ketamine or alpha-2 agonists

288
Q

what are benzodiazepines often used for?

A

adjuncts to anaesthetic induction agents for co-induction

289
Q

why are benzodiazepines a good choice for unhealthy patients?

A

they have minimal effects on CVS and respiratory system

290
Q

what are the effects of benzodiazepines on the CVS?

A

minimal depression - commonly used with unwell patients or those with CVS disease

291
Q

what are the effects of benzodiazepines on the respiratory system?

A

mild, dose dependant respiratory depression

292
Q

what are the effects of benzodiazepines on the musculoskeletal system?

A

enhances inhibitory action of GABA (allosteric binding) which prevents muscle contraction

293
Q

what are benzodiazepines often administered with due to their effects on the musculoskeletal system?

A

drugs that do not provide muscle relaxations (e.g. ketamine)

294
Q

why must benzodiazepines be administered slowly IV?

A

rapidly cross blood brain barrier

295
Q

when do benzodiazepines have good bio-availability?

A

when given intranasally

296
Q

what has been reported rarely in cats following diazepam?

A

idiosyncratic liver failure

297
Q

which has a shorter plasma half life out of diazepam and midazolam?

A

diazepam

298
Q

how are benzodiazepines metabolised?

A

liver

299
Q

what gives diazepam its prolonged effect?

A

metabolites of diazepam remain active after it is metabolised in the liver

300
Q

what benzodiazepine can be given by CRI without significant accumulation?

A

midazolam

301
Q

what is the benzodiazepine reversal agent?

A

Flumazenil - expensive!

302
Q

what can be provided by fentanyl alone?

A

surgical anaesthesia for minor surgery/diagnostic techniques

303
Q

what is the duration of sedation/immobilisation associated with fentanyl?

A

30-60 mins

304
Q

what is the muscular relaxation like with fentanyl administered alone?

A

poor

305
Q

what can provide good muscle relaxation and good surgical anaesthesia if administered alongside fentanyl?

A

midazolam/diazepam

306
Q

what respiratory effects may be seen with fentanyl?

A

moderate to severe respiratory depression

307
Q

how may depression of the respiratory system by fentanyl be reversed?

A

reversed or partially reversed by the administration of butorphanol/buprenorphine

308
Q

how should ASA I and II influence anaesthesia?

A

standard protocols with routine monitoring

309
Q

how should ASA III influence anaesthesia?

A

thorough stabilization should be performed before anaesthesia is attempted. IV catheterisation, fluid therapy and airway protection advised

310
Q

how should ASA IV and V influence anaesthesia?

A

as for grade III. Owners should be fully briefed as t additional anaesthetic risk. Doses for CPR should be calculated and first dose drawn up

311
Q

what is the ASA I and II protocol for dogs and cats?

A

ACP and opioid

alpha-2 agonist and opioid

312
Q

what is the ASA I and II protocol for rabbits?

A

ACP and opioid
alpha-2 agonist and opioid
Fentanyl (Hyponorm) alone or with benzodiazepine

313
Q

what is the ASA III protocol for dogs?

A

ACP and opioid

BDZ and opioid

314
Q

what is the ASA III protocol for cats?

A

BDZ (midazolam) and ketamine

315
Q

what is the ASA III protocol for rabbits?

A

BDZ and opioid

316
Q

what is the ASA IV and V protocol for dogs, cats and rabbits?

A

BDZ and opioid
BDZ and ketamine
opioid alone
no premed but need higher doses of induction

317
Q

how should the sedated/premedicated patient be cared for?

A 
quiet environment
observed regularly (with all senses!)
ABC
monitor temperature, pulse, RR and MM
use pulse ox if possible
record obs
318
Q

what can go wrong during sedation/premed?

A

excitement or excessive sedation
airway obstruction (vomit or anatomical - brachycephallic)
CVS effects up to and including arrest
patient unable to compensate for existing condition/hidden condition is exposed
something odd develops (e.g. gastric dilation)

319
Q

what parameters should be monitored in the sedated/premedicated patient?

A 
temperature
pulse
RR
MM
pulse ox
320
Q

what is the difference between sedation and premedication?

A

during sedation the patient is sedated but not anaesthetised, there is no loss of consciousness
premedication is administered before anaesthetic

321
Q

how do drug doses differ between premedication and sedation?

A

same drug combinations often used but doses for premedication will be lower than sedation

322
Q

what is sedation?

A

patient is not fully awake but is not fully unconscious (anaesthetic)

323
Q

what is the purpose of sedation?

A

allows procedures that may/would be impossible in a fully concoius patient

324
Q

what is the difference in sedation between large and small animals?

A

in farm animals it is common to perform procedures including invasive surgery using (standing) sedation and LA
very unusual in small animals

325
Q

when is sedation appropriate in small animal practice?

A

safe handling of anxious/dangerous/feral animals for procedures that would usually be performed with out sedation (e.g. blood sample)
procedures that are not painful or invasive but require the animal to be still (e.g. radiography)
minor procedures (e.g. wound redressing, de-matting)

326
Q

why may sedation be safer that full GA for small animals?

A

theoretically less extreme

327
Q

why is sedation not necessarily safer than full GA in small animals?

A

no control over airway
often no option of deepening sedation if it is inadequate for the job without progressing to full GA
staff and patient safety - will sedation do the job (e.g. radiography - will the patient jump off the table)

328
Q

what methods of sedation are best used in feral/dangerous cases?

A

IM in crush cage

OTM can be squirted in

329
Q

what sedation can be reversed?

A

alpha-2 agonists, opioids and benzodiazepines can all potentially be reversed. usually only alpha-2 agonists reversed. (atipam)
fentanyl

330
Q

what can be used to reverse sedation with fentanyl?

A

opioid partial agonist/agonist antagonist/antagonist

331
Q

define potency

A

mg/kg of drug required to show effect

X CNT 1 (4 decks)

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