Pain Management Flashcards
(331 cards)
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
2
Q
what factors can the experience of pain be influenced by?
A
biological
psychological
social
3
Q
define nociception according to the IASP definition
A
the neural process of encoding noxious stimuli (physiological processes)
4
Q
what forms may the consequences of encoding of stimuli take?
A
autonomic
behavioral
5
Q
is pain sensation implied when nociception occurs?
A
not necessarily
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
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.
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
9
Q
what is the term nociceptive pain used to describe?
A
pain occurring with a normally functioning somatosensory nervous system
10
Q
define neuropathic pain according to the IASP definition
A
a lesion or disease of the somatosensory nervous system
11
Q
what is the term neuropathic pain a clinical description of?
A
a demonstrable lesion or a disease
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
13
Q
when is the term disease commonly used when discussing neuropathic pain?
A
when the underlying cause of the lesion is known
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
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
16
Q
of nociceptive and neuropathic pain, which can be harder to treat?
A
neuropathic
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
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)
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)
20
Q
define allodynia according to the IASP definition
A
pain due to a stimulus that does not normally produce pain
21
Q
give an example of allodynia
A
due to underlying injury/disease a cat now finds being stroked (a non-noxious stimulus) painful
22
Q
how long does acute pain last for?
A
a short period of time - minutes and hours to weeks
23
Q
how long does chronic pain last for?
A
longer than a few weeks
24
Q
what may happen if acute pain is not adequately treated?
A
may lead to a chronic pain state
25
what may chronic pain arise from?
chronic medical conditions such as osteoarthritis and skin disorders
26
is chronic pain generally protective or beneficial to the sufferer?
no it is usually detrimental
27
when may acute pain be productive?
can stop an animal from causing itself further damage
28
what can untreated or poorly treated pain lead to?
up-regulation of the pain processing system making the pain harder to treat and the establishment of pain states
29
what can be reduced by untreated or poorly treated chronic pain?
quality of life
30
why is recognition and quantification of pain so important?
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
31
what are the 3 key stages in the quantification of pain?
categorization of pain as absent, mild, moderate, severe
assess treatment efficacy
make judgements about quality of life
32
what does the categorization of pain as absent, mild, moderate and severe influence?
how we decide to treat the pain
33
how can treatment efficacy be assessed?
observing weather pain score reduces if a treatment is used
34
what judgements about quality of life may be made using quantification of pain?
should the animal be treated or is euthanasia a prefurrable option?
35
what is the key challenge of assessing pain in animals?
they cannot talk
36
what can be used to assess pain?
behavioural signs
| physiological signs
37
what are the physiological signs associated with pain?
increased HR, blood pressure and body temperature
altered respiration (rate and pattern)
stress hormones increasing
EEG (electroencephalogram) activity
38
what is a key issue with using physiological signs to indicate pain?
they are non-specific and may increase or decrease along with things other than pain
39
what stress hormones could be used to indicate pain?
cortisol, noradrenaline and adrenaline
40
what is the difficulty of using EEG to determine presence of pain?
is this pain or nociception
41
are behavioural signs of pain species specific?
yes
42
why may behavioural signs of pain vary between individuals within a species?
depending on temperament or their response to a stressful environment which may cause them to hide pain
43
why do prey species tend to hide signs of pain?
so they do not stand out to a predator
44
what are behavioural signs associated with pain specific to?
species
individual
condition
45
what are the shared behavioural signs associated with pain exhibited by cats and dogs?
```
hunched appearance
'pain' face
lack of grooming
inappetance
specific signs (e.g. lameness)
```
46
what are the behavioural signs associated with pain that are specific to cats?
```
absence of normal behavioural repertoire
hide away at back of cage
unwilling to relax
fear-aggression
resent human contact
```
47
what are the behavioural signs associated with pain that are specific to dogs?
positive behavioural signs rather than reduced repertoire
more likely to seek attention
submissive
more likely to vocalize
48
what are the behavioural signs associated with pain that are specific to rabbits?
```
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
```
49
when is immobility in rabbits particularly acute?
post-op or traumatic pain however they may show this behaviour in unusual environments when there is no pain at all
50
define bruxism
tooth grinding
51
what is an essential consideration when handling animals in pain?
prey animals with a strong fight or flight response which means that they can react violently to severe pain
52
what are the behavioural signs associated with pain that are specific to horses?
```
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
```
53
what are the main chronic pain indicators in all species?
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
54
what is the NRS?
numerical rating scale which requires patient to assign their pain a score from 1-10
55
what is VAS?
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
56
what is SDS?
simple descriptive scale where patients assign themselves a category relating to a description of a pain level that is matched to a number
57
what can be used to score pain in animal patients?
NRS, VAS or SDS
58
who awards the scores during pain assessment of animals?
caregiver
59
what can make pain scoring more accurate?
dynamic interaction with animal rather than just observing
60
what is an issue with using NRS, VAS or SDS in a veterinary environment?
interobserver variation which can be an issue in a practice where there is likely to be multiple caregivers
61
what is the purpose of composite pain scales?
over come some of the limitations of the VAS, NRS and SDS
62
how do composite pain scales work?
multiple items are assessed for each patient and given a score. These are them added to give an overall score
63
what must happen to composite pain scales in order for them to be useful?
must be validated which requires lots of clinical testing
64
what is often suggested by composite pain scales?
an intervention level/ score at which the patient should receive an intervention (analgesic medication)
65
what is the composite pain scale used for dogs?
SF-GCPS: glasgow composite pain scale
66
what is the SF-GCPS score out of if the dog cannot stand?
20
67
what is the SF-GCPS score out of if the dog can stand?
24
68
what is the intervention level of the SF-GCPS?
5/20 or 6/24
69
what is the drawback of the SF-GCPS?
poor differentiation between sedation and pain which is an issue immediately post-op
70
what is the composite pain scale used for cats?
CMPS
71
what is the maximum score of the CMPS?
20
72
what is the recommended intervention level of the CMPS?
5/20
73
what is essential to remember when filling in composite pain scores?
follow the order and scores on the sheet
74
are there composite pain scores for rabbits and horses?
not really at the moment
75
when may owners be helpful in filling in pain scoring?
to show pain levels over time and levels when not in the veterinary environment. Useful for post-op or chronic pain
76
what is involved in chronic pain assessment?
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
77
are there chronic pain composite pain scores available?
yes, tend to be condition and species specific used to collect data on pain and impact on life functions
78
with owner pain scoring of chronic pain what are the questions more often about?
quality of life as opposed to specific questions about pain at a single point in time
79
how does the LOAD questionnaire for OA work?
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
80
what is another way of monitoring chronic pain?
client specific outcome measures
81
what is involved with client specific outcome measures?
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)
82
what is a key benefit of client specific outcome measures?
very specific to pet (tailored)
quick to complete
easy to track changes over time
83
what are the main advantages of owner questionnaires for chronic pain?
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
84
what is the benefit of videos as add on or stand alone assessment?
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
85
why is assessment of health related quality of life useful?
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
86
what is involved in health-related quality of life assessment?
assessment of quality of life in relation to analgesia and chronic pain
87
what is preventative anaesthesia?
administration of effective analgesia before, during and after the surgery/procedure, well into the post operative recovery period
88
what is the aim of preventative analgesia?
prevention of upregulation of the nervous system in the presence of noxious stimuli (e.g. surgery) by administering effective analgesia
89
what should be seen in response to preventative analgesia?
reduction both in intensity and duration of acute pain and a reduction in persistent (chronic) pain
90
what is multi-modal analgesia?
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
91
what is a benefit of multi-modal analgesia?
leads to more effective analgesia often with lower doses of analgesic agents
92
what are the 6 main analgesic agents used in veterinary practice?
```
opioids
NSAIDs
local anaesthetics
Alpha-2 agonists
ketamine
others/misc
```
93
what is different about alpha 2 agonists and ketamine?
alpha-2 agonists are sedatives which are analgesic
ketamine is an anaesthetic that is analgesic
rather than being only analgesics
94
what schedule of drugs are full opioid agonists?
schedule 2
95
give an example of 2 full opioid agonists
methadone and fentanyl
96
what schedule of controlled drugs are partial opioid agonists?
schedule 3
97
give an example of 2 partial opioid agonists
buprenorphine and butorphanol
98
what are the requirements for schedule 2 drugs?
special prescription, storage, destruction and record keeping
99
what are the requirements for schedule 3 drugs
special prescription and some have special storage requirements (e.g. bupe must be locked away)
100
where do opioids licensed for cats, dogs and horses act within the body?
endogenous opioid receptors primarily in the brain and spinal cord
101
what are the 3 key opioid receptors?
delta, kappa and mu
102
what sorts of agonists may opioids be?
full agonists, partial agonists, mixed agonist antagonist or antagonist
103
give an example of an opioid mixed agonist-antagonist
butorphanol
104
give an example of an opioid antagonist
naloxone
105
which type of receptor agonists are associated with analgesia?
mu
106
what type of agonists provide the most effective analgesia?
full mu agonists
107
under what circumstances are opioids used?
acute pain - preventative and part of multi-modal analgesia regimens
108
define potency
mg/kg of drug required to show effect
109
define efficacy in terms of drugs
the maximum response possible from a specific drug
110
why is fentanyl so dangerous?
is highly potent and efficacious - very little required to overdose
111
how may opioids be administered?
```
IV
oral
SC
IM
buccal
```
112
what opioid must not be given IV?
pethidine
113
what drug may not be so effective when given SC to cats?
buprenorphine
114
how does buccal administration differ from oral?
buccal requires transmucosal absorption by oral mucous membranes, oral medication is absorbed in the small intestine
115
why is there poor bio-availability of orally administered opioids?
significant first pass metabolism so they are broken down very quickly and easily by the liver
116
what does poor bio-availability of opioids mean for chronic pain?
limited role in management of chronic pain
117
give an example of a short acting mu agonist
fentanyl
118
when are short acting mu agonists used?
intra-operative and short term infusion
119
give an example of a long acting full mu agonist
methadone
120
when are long acting full mu agonists used?
general use for acute and pre, peri and post operative pain
121
how long do long acting full mu agonists tend to last?
2-4hr
122
give an example of a partial mu agonist
buprenorphine
123
when are partial mu agonists often used?
general use for acute and pre, peri and postoperative pain
124
how long to partial mu agonists last for?
6hrs
125
give an example of a K agonist and mu receptor
butorphanol
126
when would a mixed K agonist and mu receptor be used?
general use for acute and pre, peri and postoperative pain
127
how long do mixed K agonist and mu receptor drugs last for?
2hrs
128
what are the key side effects of opioid use at clinical doses?
```
respiratory depression
sedation
excitation
minimal effect on inotropy
bradycardia
nausea and vomiting
antitussive
decrease GI motility
various effects on urinary system
```
129
when are respiratory depression effects most often seen when using opioids?
dose dependent and mostly during anaesthesia
130
when are sedation side effects seen during opioid use?
species and dose dependant, more sedation seen in dogs
131
when is excitation often seen as a side effect of opioid use?
at high doses particularly in pain free animals. can cause box walking in horses and excitement in cats
132
what is inotropy?
force of heart contraction
133
what causes bradycardia as a side effect when giving opioids?
vagal effect
134
how can bradycardia as a side effect of opioid use be managed?
use of an anticholinergic such as atropine
135
when does nausea and vomiting most often occur in patients receiving opioids?
seen in dogs and cats and more common in pain free animals
136
what is an antitussive effect?
reduction of cough
137
what effect may opioids have on GI motility?
decrease
138
how much of an issue is decreased gut motility in dogs and cats?
not too problematic
139
when is decreased gut motility in opioid use more of an issue?
chronic use
140
when are side effects of opioids on the urinary system of clinical significance?
not unless administered epidurally
141
what does NSAID stand for?
non steroidal anti-inflammatory drugs
142
how do most NSAIDs work?
inhibition of prostaglandin production either through inhibition of COX (cyclo-oxygenase) or LOX (lipoxygenase) enzymes
143
what are NSAID side effects directly linked to?
protective effects that prostaglandins have on the body
144
where are NSAIDs metabolised?
the liver
145
what are NSAIDs effective analgesics for?
acute and chronic pain
146
when is caution needed when giving NSAIDs?
if administering pre/peri-operatively or if a patient is dehydrated or hypotensive
147
in what regimens are NSAIDs useful?
multi-modal analgesic
148
can more than one NSAID be used in a multi-modal analgesic approach?
no - due to side effects
149
what are the 2 main NSAIDs licensed for use in dogs and cats?
meloxicam
| carprophen
150
who can most NSAIDs be administered to the patient?
injection or oral
151
what is the main NSAID used in rabbits?
meloxicam
152
what are the main NSAIDs used in horses?
meloxicam
| phenylbutazone
153
what are the main side effects of NSAID use at clinical doses?
```
GI ulceration
Renal ischaemia
Hepatopathy
blood clotting
CNS effects
```
154
when should special care be taken when giving NSAIDs?
those with history of GI ulceration
any patient with reduced drug clearance capacity
during anaesthesia of dogs and cats
155
why can NSAIDs cause renal ischemia?
during hypotension prostaglandins protect renal blood flow and so this action is blocked by NSAIDs
156
with what type of NSAIDs is clotting an issue?
the less commonly used non-COX selective NSAIDs
157
what information should be given to owners about safe use of NSAIDs in dogs and cats?
GI side effects are most common
will present as vomiting and diarrhoea
may see digested blood (coffee grounds)
general malaise
158
what should owners do if they see any side effects of NSAID use?
discontinue medication immediately and ring the practice
159
what information should be given to owners about safe use of NSAIDs in horses?
GI side effects most common: GI ulceration presenting as colic, diarrhoea, dehydration and weight loss
renal effects
malaise
160
when do side effects of NSAIDs most commonly occur in horses?
overdose
chronic administration
weight loss
161
when are renal effects of NSAIDs more of an issue in the horse?
when dehydrated
162
what information should be given about safe use of NSAIDs in rabbits?
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
when do NSAIDs side effects most commonly occur?
in chronic use
164
what is the key pharmacology of local anaesthetics?
enter nerve fibre and block voltage gated Na+ channel so blocking nerve conduction
165
which fibres are preferentially blocked by local anaesthetics?
C fibres and A-delta fibres
166
what type of blockade is achieved by blocking C and A-delta fibres during local anaesthetic?
nociceptive blockade before proprioceptive, mechanoreceptive and motor blockades
167
what type of molecules are most local anaesthetics?
weak bases (pKa = 8-9)
168
what form of the weak base can penetrate lipid membranes and enter the nerve cell?
uncharged form
169
how does ionisation (pKa) affect onset of local anaesthetic action?
higher pKa will be more ionised in plasma and so have a slower onset of action
170
what happens to local anaesthetic if the pH of the tissue decreases (e.g. inflammation)?
greater proportion of the drug is ionized and therefore less drug can penetrate the nerve membrane to bind to the sodium channel
171
where is local anaesthetic less effective?
inflamed tissue
172
what are the 2 linkages that may be found in different local anaesthetics?
ester
| amide
173
how stable are ester and amide linkages?
ester are relatively unstable
| amide are more stable
174
how rapidly are ester and amide linkages broken down?
ester - rapidly by plasma psudocholinesterase
| amide - subject to bio-transformation with conjugation in the liver
175
how long are ester and amide linkage half-lives?
ester - short local anaesthetic half life
| amide - longer plasma half life
176
how can you tell which local anaesthetic drugs have ester and amide linkages?
ester - no 'i' in name before 'caine'
| amide - 'i' in name before 'caine'
177
what is formed as a byproduct of hydrolysis of ester linkages that can provoke allergic reactions?
PABA
178
give an example of an ester linkage LA
procaine
179
give an example of an amide linkage LA
lidocaine
180
what does the toxicity/side effects of LA depend on?
the dose - safe total dose must never be exceeded
181
what are the side affects associated with LA?
CNS toxicity
| CVS toxicity
182
what effects are seen with CNS toxicity of LA?
minor behavioral changes
muscle twitching and tremors
tonic-clonic convulsions
CNS depression/ respiratory depression and death
183
what are the effects seen with CVS toxicity of LA?
hypotension
| dysrhythmias
184
does CNS or CVS toxicity occur at lower doses?
CNS
185
what is involved in treatment of CNS/CVS side effects of LA?
symptomatic treatment
186
what animals is lidocaine licensed for?
horses, dogs and cats and is used in rabbits
187
what is the onset of action of lidocaine?
rapid, 2-5 mins
188
how long acting is lidocaine?
short - 20-40 mins
189
what is an advantage of lidocaine over bupivacaine?
lower cardiotoxicity
190
when are local anaesthetics used?
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
what class of drugs does paracetamol fall under?
not an NSAID but can be considered one
192
what is the mechanism of action of paracetamol?
not fully understood
193
to what species is paracetamol very toxic?
cats
194
when is paracetamol useful in dogs?
when NSAIDs are contraindicated
195
when is paracetamol used in horses?
useful as an adjunctive analgesic in very painful cases and also where NSAIDs are contraindicated
196
what is the mode of action of tramadol?
multi-modal
| mu opioid system, noradrenergic system and serotonergic system
197
what are the actions of tramadol associated with?
some with tramadol enantiomers and some with its metabolites
198
what is tramadol used for?
acute and chronic pain conditions
| believed to have a wide therapeutic index and lower risk of abuse than opioids
199
what drug schedule does tramadol fall under?
schedule 3
200
how should tramadol be administered to dogs?
IV as oral is unlikely to be effective
201
does current evidence suggest that tramadol should be used alone?
no - should only be used as a co-analgesic
202
how effective is tramadol in cats?
some analgesic effect given IV, may have effects on chronic pain when given orally
203
can tramadol be used in horses?
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
what is the oral bio-availability of tramadol like in horses?
variable
| has a short half life
205
how does gabapentin work?
precise mechanism of action unknown; analgesic action is attributed to binding voltage gated calcium channel
206
what does binding of gabapentin to voltage gated calcium channels lead to ?
decreased release of excitatory neurotransmitters in the dorsal horn of the spinal chord - reduction in pain sensation in cases of allodynia, hyperalgesia etc
207
what may gabapentin be used for?
management of neuropathic type pain conditions
208
what is a major side effect of gabapentin?
sedation
209
why should liquid solutions containing xylitol be avoided?
due to potential for toxicity as this is a human medication and the sweetner is toxic to veterinary patients
210
how should gabapentin administration be stopped?
slowly - reduce dose over 1-2 weeks
211
what is amantadine?
oral NMDA receptor agonist
212
what is amantadine used for?
antihyperalgesic so should be used alongside an analgesic
213
how is amantadine excreted?
via kidneys so should be used cautiousl in patients with reduced renal function
214
when may amantidine be useful?
chronic pain states to reverse or obtund central sensation
215
how long any it take to see benefit of amantadine therapy?
3-4 weeks
216
why are animals premedicated prior to anaesthesia?
```
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
how can balanced anaesthesia be produced by premedicating animals prior to anaesthetic induction?
reduce dose of induction and maintenance agents
218
how does premedication reduce the side effects of anaesthetic drugs?
either by giving less or by administering something that counteracts the side effects
219
what are the 5 main classes of drugs used for premedication?
```
phenothiazines
alpha-2 agonists
benzodiazepines
butyrophenones
opioids
```
220
do phenothiazines have sedative and analgesic action?
sedative but not analgesic
221
do alpha-2 agonists have sedative and analgesic action?
yes
222
do benzodiazepines have sedative and analgesic action?
sedative but not analgesic
223
do butyrophenones have sedative and analgesic action?
sedative but not analgesic
224
do opioids have sedative and analgesic action?
some have sedative action (species dependent) all have analgesic action
225
what is the mode of action of phenothiazines?
dopamine receptor agonist in the CNS
226
what is the mode of action of alpha-2 agonists?
alpha-2 adrenergic receptor agonist in the CNS
227
what is the mode of action of benzodiazepines?
enhance the effect of gamma-aminobutyric acid (GABA) at the GABA-alpha receptor
228
what is the mode of action of butyrophenones?
dopamine receptor antagonist in the CNS, also interferes with GABA, noradrenaline and serotonin-mediated neuronal activity
229
what is the vet licenced phenothiazine in the UK?
Acepromazine (ACP)
230
what are the vet licenced alpha-2 agonist in the UK?
dexmedetomidone and medetomidine are most common
| also romifidine and xylazine
231
what are the vet licenced benzodiazepines in the UK?
diazepam and midazolam
232
what is the vet licenced butyrophenone in the UK?
Fluanisone - only available in a combination product with fentanyl (Hypnorm)
233
what are the licenced species for phenothiazines in the UK?
ACP - dog and cat
234
what are the licensed species of the vet licensed alpha-2 agonists in the UK?
all licensed in dogs and cats
235
what are the licensed species for veterinary licensed benzodiazepines in the UK?
diazepam in dogs and cats
| midazolam in horses
236
what are the licensed species for veterinary licensed butyrophenones in the UK?
rabbits
237
what is the advantage of IV premed?
rapid onset of action
| predictable effect
238
what is the advantage of IM premed?
fairly rapid onset of action
| predictable effect
239
what is the advantage of SC premed?
easier to do than IV or IM
240
what is the advantage of OTM (oral transmucosal) premed?
not useful routinely - can be helpful in special cases (e.g. feral cats)
241
what is the disadvantage of IV premed?
requires restraint and/or IV catheter placement before anaesthesia
242
what is the disadvantage of IM premed?
painful
243
what is the disadvantage of SC premed?
not all drugs are absorbed by this route
can be unpredictable
slower onset than IM
244
what is the disadvantage of OTM (oral transmucosal) premed?
not all drugs are absorbed by this route
can be unpredictable
slower onset than IM
245
what are the key clinical effects of ACP (phenothiazine)?
sedation
| anxiolytic
246
what is ACP often used in combination with in premeds?
opioids
247
what is ACP widely used for in cats and dogs?
sedation for procedures and premedication
248
what is ACP used for in rabbits?
premedication although not licenced
249
what is ACP sedation level dependent on?
dose up to plateau dose
250
how can ACP sedation be improved?
combination with opioid
| if animal is left in a quiet environment for 30-40 mins
251
how effective is SC injection of ACP for sedation?
non-irritant and efficacious, particularly in cats
252
should the same does of ACP be used for sedation and premedication?
lower doses for premed than for sedation
253
what are the physiological effects of ACP on the CVS?
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
what is the time to clinical effect from administration of ACP IV?
10-15 mins (slower than alpha-2 agonists)
255
when is the clinical effect of ACP seen after IM administration?
30-40 mins
256
where should animals be left to become sedated with ACP?
quiet area
257
how long is the duration of action of ACP?
4-6 hours
258
how is ACP metabolised?
in the liver
259
in what animals is the action of ACP prolonged?
those with liver diease
260
how good is the oral bio-availabilty of ACP?
poor
261
what are the clinical effects of alpha-2 agonists?
sedation
analgesia
muscle relaxation
262
what is the duration and level of sedation with alpha-2 agonists dependent on?
dose
263
are alpha-2 agonists potent?
yes - use body surface area rather than weight to calculate dose
264
what type of drugs are alpha-2 agonists often used with?
opioids
265
what effect can occur when alpha-2 agonists are combined with other sedatives/analgesics?
additive or synergistic effects
266
what are the key advantages of alpha-2 agonists?
significant dose reduction for anaesthetic induction and maintenance agents
reversible using antagonist (atipamazole)
267
what antagonist can be used to reverse alpha-2 agonists?
atipamazole
268
what are the physiological effects of alpha-2 agonists on the CVS?
bradycardia
reduced cardiac output
second degree AV block
initial rise in BP which will then fall to normal or hypotension
269
what are the physiological effects of alpha-2 agonists on the respiratory system?
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
what can the CVS effects of ACP be managed by?
administration of fluids
271
what are the physiological effects of alpha-2 agonists on the GI system?
can be emetic in dogs and cats
| can depress GI activity and has been reported to cause GI stasis in dogs
272
why should deep chested dog breeds avoid alpha-2 agonists?
risk of GDV
273
what are the physiological effects of alpha-2 agonists on animal behaviour?
some temporary behavior and personality changes in dogs and cats (similar to other sedatives)
274
what are the physiological effects of alpha-2 agonists on the pancreas?
reduced secretion of insulin - may see transient hyperglycaemia which is not harmful to the animal but may mess with blood work
275
what are the physiological effects of alpha-2 agonists on the renal system?
increase in urine production by a decrease in secretion of vasopressin
276
what should happen to animals receiving alpha-2 agonists by CRI?
catheterisation
277
what are the physiological effects of alpha-2 agonists on the uterus?
can affect contractility dependent on dose and concentrations of oestrogen and progesterone
278
at what life stage should alpha-2 agonists be avoided?
pregnancy - near term due to its effect on uterine contractility and risk of abortion
279
how long until full clinical effect of alpha-2 agonists after IV administration?
5 minutes
280
at what time after administration are alpha-2 agonist effects seen?
30 mins
281
what is the duration of action of alpha-2 agonists if atipamezole isnt used?
2-3 hours
282
in what animals is the duration of alpha-2 agonists prolonged?
those with liver disease
283
how are alpha-2 agonists metabolized?
in the liver
284
what are the clinical effects of benzodiazepines?
minor tranquilisers
muscle relaxation
anticonvulsant
285
what is sedation with benzodiazapines like in healthy animals?
unreliable and can cause excitement when administered alone
286
to what animals do benzodiazapines provide good sedation?
the young or sick
287
what can benzodiazapines be combined with to improve sedation?
opioid, ketamine or alpha-2 agonists
288
what are benzodiazepines often used for?
adjuncts to anaesthetic induction agents for co-induction
289
why are benzodiazepines a good choice for unhealthy patients?
they have minimal effects on CVS and respiratory system
290
what are the effects of benzodiazepines on the CVS?
minimal depression - commonly used with unwell patients or those with CVS disease
291
what are the effects of benzodiazepines on the respiratory system?
mild, dose dependant respiratory depression
292
what are the effects of benzodiazepines on the musculoskeletal system?
enhances inhibitory action of GABA (allosteric binding) which prevents muscle contraction
293
what are benzodiazepines often administered with due to their effects on the musculoskeletal system?
drugs that do not provide muscle relaxations (e.g. ketamine)
294
why must benzodiazepines be administered slowly IV?
rapidly cross blood brain barrier
295
when do benzodiazepines have good bio-availability?
when given intranasally
296
what has been reported rarely in cats following diazepam?
idiosyncratic liver failure
297
which has a shorter plasma half life out of diazepam and midazolam?
diazepam
298
how are benzodiazepines metabolised?
liver
299
what gives diazepam its prolonged effect?
metabolites of diazepam remain active after it is metabolised in the liver
300
what benzodiazepine can be given by CRI without significant accumulation?
midazolam
301
what is the benzodiazepine reversal agent?
Flumazenil - expensive!
302
what can be provided by fentanyl alone?
surgical anaesthesia for minor surgery/diagnostic techniques
303
what is the duration of sedation/immobilisation associated with fentanyl?
30-60 mins
304
what is the muscular relaxation like with fentanyl administered alone?
poor
305
what can provide good muscle relaxation and good surgical anaesthesia if administered alongside fentanyl?
midazolam/diazepam
306
what respiratory effects may be seen with fentanyl?
moderate to severe respiratory depression
307
how may depression of the respiratory system by fentanyl be reversed?
reversed or partially reversed by the administration of butorphanol/buprenorphine
308
how should ASA I and II influence anaesthesia?
standard protocols with routine monitoring
309
how should ASA III influence anaesthesia?
thorough stabilization should be performed before anaesthesia is attempted. IV catheterisation, fluid therapy and airway protection advised
310
how should ASA IV and V influence anaesthesia?
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
what is the ASA I and II protocol for dogs and cats?
ACP and opioid
| alpha-2 agonist and opioid
312
what is the ASA I and II protocol for rabbits?
ACP and opioid
alpha-2 agonist and opioid
Fentanyl (Hyponorm) alone or with benzodiazepine
313
what is the ASA III protocol for dogs?
ACP and opioid
| BDZ and opioid
314
what is the ASA III protocol for cats?
BDZ (midazolam) and ketamine
315
what is the ASA III protocol for rabbits?
BDZ and opioid
316
what is the ASA IV and V protocol for dogs, cats and rabbits?
BDZ and opioid
BDZ and ketamine
opioid alone
no premed but need higher doses of induction
317
how should the sedated/premedicated patient be cared for?
```
quiet environment
observed regularly (with all senses!)
ABC
monitor temperature, pulse, RR and MM
use pulse ox if possible
record obs
```
318
what can go wrong during sedation/premed?
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
what parameters should be monitored in the sedated/premedicated patient?
```
temperature
pulse
RR
MM
pulse ox
```
320
what is the difference between sedation and premedication?
during sedation the patient is sedated but not anaesthetised, there is no loss of consciousness
premedication is administered before anaesthetic
321
how do drug doses differ between premedication and sedation?
same drug combinations often used but doses for premedication will be lower than sedation
322
what is sedation?
patient is not fully awake but is not fully unconscious (anaesthetic)
323
what is the purpose of sedation?
allows procedures that may/would be impossible in a fully concoius patient
324
what is the difference in sedation between large and small animals?
in farm animals it is common to perform procedures including invasive surgery using (standing) sedation and LA
very unusual in small animals
325
when is sedation appropriate in small animal practice?
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
why may sedation be safer that full GA for small animals?
theoretically less extreme
327
why is sedation not necessarily safer than full GA in small animals?
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
what methods of sedation are best used in feral/dangerous cases?
IM in crush cage
| OTM can be squirted in
329
what sedation can be reversed?
alpha-2 agonists, opioids and benzodiazepines can all potentially be reversed. usually only alpha-2 agonists reversed. (atipam)
fentanyl
330
what can be used to reverse sedation with fentanyl?
opioid partial agonist/agonist antagonist/antagonist
331
define potency
mg/kg of drug required to show effect
