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Applied Clinical Veterinary Nursing > Analgesia > Flashcards

Analgesia Flashcards

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1
Q

why are opioids less commonly used for chronic pain management?

A

due to poor oral bioavailability

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2
Q

which class of analgesia is not often used for chronic pain management?

A

opioids

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3
Q

why are opioids a good choice as a perioperative drug?

A

They give good sedation and analgesia

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4
Q

What effect can opioids have at high doses?

A

excitation

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5
Q

what effect do opioids have on the heart?

A

bradycardia

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6
Q

what effect do opioids have on respiratory drive?

A

cause respiratory depression

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7
Q

what effects do opioids have on the GI system?

A

nausea and vomiting (premed), decreased GI motility

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8
Q

what effects do opioids have on the urinary system?

A

various urinary effects - bladder less sensitive to urge to urinate

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9
Q

which class of analgesic can have antitussive effects?

A

opioids

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10
Q

what effect do opioids have on inotropy?

A

minimal effect

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11
Q

what effects do opioids have on the eyes?

A

effects on the pupil - miosis in dogs (and most mammals), mydriasis in cats

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12
Q

what are the pharmacological effects of opioids in mammals?

A

analgesia
sedation
excitation
bradycardia
respiratory depression
nausea and vomiting, decreased GI motility
various urinary effects
antitussive
effects on pupil (miosis/mydriasis)

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13
Q

what type of system is the opioid system?

A

endogenous

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14
Q

what are the 3 families of naturally occurring opioid peptides (neurotransmitters)?

A

beta-endorphin
leucine and methionine - enkephalins
dynorphins

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15
Q

where are the opioid receptors mainly found?

A

in the brain and spinal cord

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16
Q

what are the 4 types of opioid receptor?

A

mu
kappa
delta
NOP (nociceptin opioid peptide) receptor

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17
Q

what are the subtypes of the delta opioid receptor?

A

delta 1 and 2

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18
Q

where are the delta opioid receptors found?

A

brain
peripheral sensory neurones

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19
Q

what is the function of the delta opioid receptors?

A

analgesia
antidepressant effects
convulsant effects
physical dependence
may modulate mu opioid receptor-mediated respiratory depression

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20
Q

what are the subtypes of the kappa opioid receptor?

A

k1, k2, k3

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21
Q

where are the kappa opioid receptors located?

A

brain
spinal cord
peripheral sensory neurones

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22
Q

what is the function of the kappa opioid receptors?

A

analgesia and sedation
anticonvulsant effects
depression
neuroprotection
dissociative/hallucinogenic effects
dysphoria
diuresis
miosis
stress

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23
Q

what are the subtypes of the mu opioid receptor?

A

mu 1, mu2, mu3

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24
Q

where are the mu opioid receptors located?

A

brain
spinal cord
peripheral sensory neurones
intestinal tract

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25
Q

what are the functions of the mu1 opioid receptors?

A

analgesia
physical dependence

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26
Q

what are the functions of the mu2 opioid receptors?

A

respiratory depression
miosis
euphoria
reduced GI motility
physical dependence

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27
Q

what are the functions of the mu3 opioid receptors?

A

possible vasodilation

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28
Q

where do opioid drugs act?

A

at the opioid receptors

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29
Q

what common opioid drugs are full agonists?

A

methadone and fentanyl

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30
Q

what common opioid is a partial agonist?

A

buprenophine

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31
Q

what common opioid is a mixed agonist-antagonist?

A

butorphanol

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32
Q

what is the antagonist for opioids?

A

naloxone

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33
Q

which opioids are associated with analgesia?

A

mu agonists

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34
Q

which opioids provide the most effective analgesia?

A

full mu agonists

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35
Q

why are full agonists effective analgesic agents?

A

they bind to and activate a receptor with the maximum response that an agonist can elicit at that receptor

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36
Q

why are partial agonists less effective than full agonists?

A

they bind to and activate a receptor but only have partial efficacy, even if they bind to all receptors

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37
Q

what is potency?

A

the amount of drug required to see a given effect

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38
Q

what is efficacy?

A

the relative ability of a drug-receptor complex to produce a maximum functional response

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39
Q

which is more potent out of methadone and buprenorphine?

A

buprenorphine

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40
Q

which is has better efficacy, methadone or buprenoprhine?

A

methadone

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41
Q

by which routes can opioids be administered?

A

IV
orally
subcut
IM
oral transmucosal (buccal)

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42
Q

why is pethidine not administered IV?

A

can induce allergic reactions

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43
Q

what route of opioid administration is less efficacious in cats?

A

subcut buprenorphine

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44
Q

why do opioids have poor oral bioavailability?

A

very significant first pass metabolism

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45
Q

what are the advantages of administering opioids IV?

A

rapid onset of action
reliable uptake
painless - drug volume unimportant

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46
Q

what are the disadvantages of administering opioids IV?

A

need IV access

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47
Q

what is the advantage of administering opioids IM?

A

reliable uptake

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48
Q

what is the disadvantage of administering opioids IM?

A

painful, particularly if administering large volumes

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49
Q

what is the advantage of administering opioids SC?

A

easy to perform

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50
Q

what is the disadvantage of administering opioids SC?

A

unreliable uptake

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51
Q

what is the advantage of administering opioids OTM?

A

easy to perform

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52
Q

what is the disadvantage of administering opioids OTM?

A

only certain opioids (cats and buprenorphine)

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53
Q

what is the advantage of administering opioids transdermally?

A

good for chronic use

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54
Q

what is the disadvantage of administering opioids transdermally?

A

no licensed products

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55
Q

what is the advantage of administering opioids epidural/spinal?

A

very effective analgesia for the right cases (mostly intraoperative)

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56
Q

what is the disadvantage of administering opioids eipdural/spinal?

A

no licensed opioids for this
technically difficult

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57
Q

what does the onset of action of a drug depend on?

A

route of administration

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58
Q

what is the peak effect of a drug?

A

the time it takes for a drug to reach the maximum concentration after administration of a drug that needs to be absorbed

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59
Q

which opioids are ultra-short-acting?

A

fentanyl (mins)
unlicensed - alfentanil, sufentanil, remifentanil

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60
Q

which opioids are short-acting (2hrs)

A

butorphanol
pethidine

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61
Q

which opioids are medium-acting (2-4hrs)

A

methadone and morphine

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62
Q

which opioids are longer-acting (6hrs)

A

buprenorphine

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63
Q

what has the main effect on duration of action of an opioid?

A

dose given

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64
Q

what are the 4 most common misconceptions surrounding opioid administration to animals?

A

opioids cause mania in cats

opioids cannot be re-dosed within their expected ‘duration of action’

respiratory depression can occur

opioids cannot be combined with other classes of analgesic drug

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65
Q

why is ‘opioids cause mania in cats’ a misconception?

A

only occurs at really high doses and generally in pain-free cats e.g. overdosing at pre-med

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66
Q

why is ‘opioids always cause respiratory depression’ a misconception?

A

it is a significant issue in humans but with vet patients it is mostly an issue with patients who are anaesthetised where there is airway control and we can ventilate if necessary

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67
Q

which other drug cannot be given with opioids?

A

tramadol (and other opioids)

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68
Q

which opioid is a partial mu agonist?

A

buprenorphine

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69
Q

which opioid is a kappa agonist?

A

butorphanol

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70
Q

what do side effects of opioids mostly relate to?

A

potency - those with greatest analgesic efficacy have the greatest likelihood of side effects

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71
Q

when are side effects of opioids less likely to be seen?

A

when the animal is in pain

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72
Q

how do opioids cause bradycardia and how can this be treated?

A

vagally mediated
can be treated with anticholinergics (atropine, glycopyrrolate)

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73
Q

what can occur with low IV doses of anticholinergics to treat bradycardia?

A

might promote a worsening of the bradycardia

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74
Q

what can occur with high IV doses of anticholinergics to treat bradycardia?

A

tachycardia

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75
Q

how should you manage accumulation of opioids in the body?

A

decrease frequency of dosing

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76
Q

why can management of gut stasis with opioid use be tricky?

A

pain causes reduced gut motility but so do opioids

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77
Q

list the common opioid drugs in order of analgesic efficacy (least to most)

A

butorphanol
buprenorphine
pethidine
methadone and morphine
fentanyl

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78
Q

when might morphine be a better choice clinically than methadone?

A

if a CRI is needed

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79
Q

what are the effects of fentanyl?

A

dose-dependent respiratory depression
bradycardia

useful for CRI as very short-acting

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80
Q

what are the advantages of methadone compared to some other opioids?

A

equi-or more efficacious analgesia and reduced nausea/vomiting compared to morphine

minimal CVS and respiratory side effects

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81
Q

why is pethidine rarely used in practice?

A

short acting - limits post-operative use
large volume - painful IM
histamine release if given IV
methadone is just better lol

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82
Q

why is buprenorphine painful on injection and not palatable to cats?

A

multi-dose preparation has preservative

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83
Q

which schedule 3 opioid should be kept in a locked cupboard?

A

buprenorphine

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84
Q

does butorphanol have good analgesic efficacy?

A

no - if any it is short lived, likely to require higher doses than given clinically

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85
Q

does butorphanol give good sedation?

A

yes

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86
Q

why is butorphanol attractive to practitioners?

A

not subject to controlled drugs regulations

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87
Q

what must be considered when using naloxone?

A

analgesic effect of opioid will also be reversed - need to provide alternative

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88
Q

what is the advantage of using intra-operative local analgesia?

A

spares inhalational agent in CVS unstable patients

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89
Q

what dosing interval should be used for methadone if being administered repeatedly over several days?

A

12-18 hours to prevent accumulation

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90
Q

which opioids are used for CRI?

A

morphine, fentanyl if morphine inadequate

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91
Q

how do local anaesthetics work (broadly)?

A

by preventing an action potential in the nerve, preventing nerve conduction

92
Q

what causes an action potential?

A

voltage-dependent opening of Na+ and K+ channels in the cell membrane

93
Q

what does the Na/K pump do?

A

pump ions against their concentration gradient to maintain an electrical gradient

94
Q

how is the membrane depolarised?

A

rate of Na+ entry exceeds K+ exit

95
Q

how is the action potential generated

A

depolarisation sets off a Na+ positive feedback whereby more voltage=gated Na+ channels open and the membrane becomes more depolarised - if a threshold is reached, an AP is generated

96
Q

how does the membrane repolarise?

A

when Na+ channels become inactivated and a special set of K+ channels open and K+ leaves the axon

97
Q

where are voltage operated Na+ channels present?

A

in all excitable tissues

98
Q

what do local anaesthetics do to the sodium channels?

A

block them, therefore blocking nerve conduction

99
Q

what effect are local anaesthetics said to have?

A

membrane stabilising effect

100
Q

what are the main types of nerves in the body?

A

motor, sensory and autonomic

101
Q

what are the different types of sensory nerves?

A

proprioceptors, mechanoreceptors and nociceptors

102
Q

what are the types of autonomic nerves?

A

preganglionic B
postganglionic C

103
Q

why are larger diameter axons more resistant to LA block?

A

they are more heavily myelinated

104
Q

which axons are more resistant to LA block?

A

larger diameter axons - more heavily myelinated

105
Q

which axons are more susceptible to LA block?

A

c fibres (unmyelinated)
Aδ fibres (thinly myelinated)

106
Q

why is there a nociceptive block before proprioceptive/mechanoreceptive/motor blockade?

A

C fibres and Aδ (nociceptive) fibres are preferentially blocked

107
Q

which types of linkage can a LA have in structure?

A

ester or amide

108
Q

what is the basic structure of a LA drug?

A

an aromatic group (lipophilic) with a basic side chain/tertiary amine (hydrophilic)
with an ester OR amide linkage

109
Q

why is the side chain important in LAs?

A

only the uncharged form can penetrate lipid membranes and enter the nerve cell

110
Q

what is the pKa of LAs?

A

weak bases (pKa 8-9)

111
Q

how does the pKa affect onset of action of LAs?

A

the higher the pKa, the slower the onset of action

112
Q

why are LAs less effective in inflamed tissue?

A

a greater proportion of the drug will be ionised and therefore less drug can penetrate the nerve membrane to bind to the sodium channel

113
Q

list lidocaine, bupivicaine, procaine and ropivacaine in order of toxicity (least to most)

A

procaine
lidocaine
bupivacaine
ropivacaine

114
Q

what is the relationship between LA toxicity and potency?

A

toxicity increases as potency increases

115
Q

what affects the duration of action of LAs?

A

ease of penetration and amount of drug reaching sodium channels (lipid solubility)

strength of binding to the sodium channels

speed of removal (dependent on tissue perfusion)

metabolism of LA (ester vs amide)

116
Q

what is the easy way to remember ester vs amide?

A

ester - no i in the name before the -caine
amide - i in the name before the -caine

117
Q

how stable are ester linkages?

A

relatively unstable

118
Q

how are ester linkages broken down?

A

rapidly broken down by pseudocholinesterase - hydrolysis of the ester link

119
Q

which LA linkage is more stable?

A

amide linkage

120
Q

how are LAs with amide linkage metabolised?

A

subject to biotransformation with conjugation in the liver

121
Q

do ester or amide linkages have a longer half life?

A

amide linkages

122
Q

what is formed as a product of ester hydrolysis?

A

PABA

123
Q

what can production of PABA result in?

A

allergic reactions

124
Q

how is PABA formed?

A

as a product of ester hydrolysis

125
Q

does the CSF contain esterases?

A

no

126
Q

what breaks down the amide link?

A

cytochrome P450 enzymes

127
Q

what can affect breakdown of amides?

A

hepatic disease can prolong or inhibit metabolism

128
Q

which drugs can increase breakdown of amides?

A

barbiturates - induce enzymes

129
Q

which drugs can inhibit breakdown of amides?

A

drugs which inhibit P450 enzymes e.g. midazolam

130
Q

why are local anaesthetics often made into a salt solution?

A

they are poorly water soluble

131
Q

why can LAs sometimes sting on injection?

A

often are made into a hydrochloride salt solution which lowers the pH

132
Q

which formulations can lidocaine come in?

A

sterile solutions for parenteral use
aerosols for nasal/airway use
topical patches

133
Q

what is baricity?

A

the weight of one substance compared with the weight of an equal volume of another substance

134
Q

why do LAs for epidural have high baricity?

A

to avoid spread high into the epidural space

135
Q

what is added to epidural LAs to make them heavier?

A

glucose

136
Q

what is the baricity comparator substance for spinal anaesthesia?

A

cerebrospinal fluid

137
Q

why is adrenaline commonly added to LAs?

A

vasoconstrictor - reduces speed of systemic absorption and therefor prolongs duration of action

138
Q

how does adrenaline prolong effects of LAs?

A

reduces the speed of systemic absorption

139
Q

what are the benefits of adding adrenaline to LAs?

A

prolongs duration of action

reduced risk of toxicity

reduces bleeding at the injection site

140
Q

what state must a drug be in to be systemically active?

A

unbound and unionised

141
Q

what is the relationship between plasma protein binding, concentration and pH?

A

percentage binding decreases as concentration rises or pH falls

142
Q

what is the significance of plasma protein binding with LAs and patients with liver failure?

A

reduced plasma proteins in patients with liver failure

143
Q

which species is lidocaine licensed for?

A

dogs, cats, horses

144
Q

what is the onset of action of lidocaine?

A

2-5 minutes

145
Q

what is the duration of action of lidocaine?

A

20-40 minutes

146
Q

which has a lower cardiotoxicity, lidocaine or bupivacaine?

A

lidocaine

147
Q

which species is bupivacaine licensed for?

A

none - has to be used under cascade, owner needs to provide consent to use it

148
Q

what is the duration of action of bupivacaine?

A

6 hours

149
Q

which has a longer onset of action, lidocaine or bupivacaine?

A

bupivacaine

150
Q

what is contained in EMLA?

A

mixture of lidocaine and prilocaine in a cream

151
Q

how can maximum absorption of EMLA be achieved?

A

cover with an occlusive dressing

152
Q

how long does it take to see the full effects of EMLA?

A

30-45 mins

153
Q

what is EMLA commonly used for?

A

IV catheterisation

154
Q

is EMLA licensed in veterinary species?

A

no

155
Q

what are the main types of toxicity caused by local anaesthetics?

A

neurotoxicity
CVS toxicity

156
Q
A
157
Q

can local anaesthetics be re-dosed?

A

no

158
Q

why should local anaesthetics always be drawn up into the smallest possible syringe?

A

essential to give accurate dose, especially in smaller patients

159
Q

what type of toxicity is seen at lower concentrations of local anaesthetic?

A

CNS toxicity

160
Q

what is seen in CNS toxicity with regards to local anaesthetic use?

A

generalised CNS depression that is proportional to the (unbound) drug -
minor behavioural changes
muscle twitching and tremors
tonic-clonic convulsions
CNS depression/respiratory depression and death

161
Q

how can we treat CNS toxicity due to LAs?

A

symptomatic treatment - BDZs to control seizures, O2 suppplementation, intubation and controlled ventilation if required

162
Q

what CVS signs are seen with LA toxicity?

A

hypotensions and dysrhythmias

163
Q

how does LA toxicity cause hypotension?

A

depression of myocardial contractility
direct relaxation of vascular smooth muscle
loss of vasomotor sympathetic tone

164
Q

which common LA typically causes dysrhythmias?

A

bupivacaine

165
Q

how are dysrhythmias caused by LA toxicity?

A

lipophilicity means rapid entry to sodium channels during systole
drug remains bound to the sodium channel during diastole
presents as re-entrant arrhythmias

166
Q

how can CVS toxicity as a result of LA use be treated?

A

symptomatically

anticholinergic for bradycardias
fluid therapy with inotropic support if needed
consider intralipid IV (‘mop up’ thr LA)

167
Q

how can LA toxicity be prevented?

A

don’t exceed ‘safe’ max dose

if greater volume needed, dilute with saline

use appropriately sized syringes for accuracy

use appropriate size needles to minimise tissue trauma

aspirate before injection to confirm not in blood vessel

168
Q

which LA blocks can RVNs carry out?

A

any that don’t enter a body cavity

169
Q

which LA blocks can RVNs not carry out?

A

epidural/pleural catheter

170
Q

what is epidural anaesthesia?

A

injection of anaesthetic drug into the epidural space

171
Q

what is spinal anaesthesia?

A

injection of an anaesthetic drug into the sac of CSF surrounding the spinal cord and nerves

172
Q

in which animals is epidural anaesthesia more difficult to perform?

A

in obese and pregnant patients

any other patients where anatomical landmarks are affected

173
Q

how can epidural injection be made easier to perform accurately?

A

use of U/S or x-ray

174
Q

what are some of the contraindications for epidural injection?

A

skin infection at puncture site
sepsis
coagulation impairments

175
Q

can anaesthetics used for epidurals have preservatives in?

A

no - must be sterile and preservative-free

176
Q

what else might be added to an epidural injection?

A

opioids
medetomidine
ketamine

177
Q

what are the possible side effects of an epidural block?

A

hypotension
hypothermia
urinary retention
infections
slowed hair regrowth

178
Q

what is the difference between local and regional anaesthesia?

A

size of affected area
local - small discrete area e.g. infiltration
regional - blocks a larger area

there is cross-over

179
Q

what are some examples of loco-regional anaesthesia?

A

blocks - ophthalmic, dental, limb nerve blocks

intravenous regional anaesthesia

intra-articular

wound soaker catheters

180
Q

which topical LAs are licensed?

A

only the laryngeal spray for feline intubation

181
Q

where can infiltration be carried out?

A

anywhere on the body provided there is enough tissue to infiltrate

182
Q

is infiltration local or regional anaesthesia?

A

local

183
Q

give some examples of infiltration

A

testicular for castration
ovarian ligament
around a skin tumour to be excised
incisional line block
ring block of distal limb/tail
intraperitoneal

184
Q

how is infiltration usually carried out?

A

injected in a V shape or reverse pyramid into the area of interest

185
Q

can RVNs perform infiltration blocks?

A

not any that require entry into a body cavity (but could act as the VS’s hands under direction)

186
Q

what are the pros of initiating NSAID therapy for chronic pain (e.g. OA) in dogs?

A

quick onset of action - non-pharmacological methods take long time

extensive evidence base to support analgesic efficacy, effective doses and re-dosing interval

licensed in dogs and cats for short and long-term treatment

187
Q

why is it important to manage chronic pain in patients?

A

chronic pain is maladaptive and of no benefit to the animal

the feeling of pain comprises the sensory discriminative aspect being processed by the brain and then interpreted with both physical and emotional components

pain is a significant welfare issue

188
Q

what is nociceptive pain?

A

pain originating from tissues which are not part of the nervous system

189
Q

what is neuropathic pain?

A

pain originating from tissues in the nervous system

190
Q

what is released when nerves are damaged?

A

cholecystokinin

191
Q

what does cholecystokinin do?

A

antagonises opioid-mediated analgesia

192
Q

why are opioids less effective in patients with neuropathic pain?

A

cholecystokinin is released by nerve damage, which antagonises opioid mediated analgesia

193
Q

which type of analgesics are less effective against neuropathic pain?

A

opioids

194
Q

how do most NSAIDS work?

A

by inhibiting prostaglandin production from arachidonic acid by inhibiting the COX enzyme

195
Q

where do most NSAIDs work?

A

in the periphery

196
Q

where can NSAIDs work in the CNS?

A

in the dorsal horn by inhibiting COX (precise mechanism of action unknown)

197
Q

what do the adverse effects associated with NSAID administration relate to?

A

the protective functions that prostaglandins have in the body

bow easily the NSAID can leave the circulation and cross into the tissues

198
Q

what are the 2 types of prostaglandins?

A

consititutive - ‘housekeeping’

inducible - those induced by inflammation

199
Q

what leads to the side effects of NSAIDs?

A

blocking of the protective functions provided by the constitutive prostaglandins

200
Q

which COX isoenzyme produces which type of prostaglandin?

A

COX-1 isoenzyme - constitutive

COX-2 isoenzyme - inducible

201
Q

why are the newer NSAIDs advantageous in terms of patient safety?

A

they are more COX-2 specific and have less effect on the constitutive (protective) prostaglandins

202
Q

what do all the veterinary NSAIDs with a peri-operative license have in common?

A

they all show COX-2 selectivity

203
Q

how can renal side effects of NSAIDs be reduced?

A

prescribing those with a degree of COX-2 selectivity

204
Q

what GI functions do prostaglandins have?

A

maintenance of mucosal blood flow

bicarbonate and mucous secretion

epithelialisation

205
Q

what GI side effects can NSAID use lead to?

A

GI ulceration and bleeding

206
Q

what do prostaglandins regulate in the renal system?

A

GFR

renin release

sodium excretion

207
Q

why should we be wary of giving NSAIDs under anaesthesia?

A

blockade of the vasodilatory PGs may cause a decreased GFR at times of low circulating blood volume (e.g. hypotension, hypovolaemia) - can induce kidney failure

208
Q

what renal side effects can NSAIDs lead to?

A

water retention and oedema

hypertension

may impair GFR in patients with renal disease of hypotension

may cause renal ischaemia in patients with hypotension

209
Q

what are the hepatic side effects of NSAID use?

A

NSAID therapy will usually induce liver enzymes in normal dogs - link to hepatopathy?

210
Q

what are the CNS side effects of NSAID use?

A

may see idiosyncratic dullness and lethargy in cats

211
Q

what is important to consider in terms of haemostasis and NSAIDs?

A

older NSAIDs that are unspecific for COX can affect clotting

212
Q

do newer NSAIDs affect blood clotting?

A

they will prolong markers of blood clotting if given for long courses (30-90 days) but these are not linked to clinical signs of bleeding

213
Q

how can we reduce the risk of side effects with chronic NSAID use?

A

do not exceed licensed dose

do not give 2 NSAIDs concurrently

do not give with corticosteroids

do not give to hypotensive/dehydrated patients

warn owners about risks of NSAIDs

214
Q

when is GI ulceration more likely with NSAID use?

A

if the animal has pre-existing GI ulceration, liver disease and/or is geriatric

215
Q

why do we not commonly combine NSAIDs with gastroprotectants?

A

there is limited evidence to support combining with gastroprotectants/antacids/H2 antagonists

216
Q

why should we not administer NSAIDs to patients with hypotension?

A

prostaglandins are essential in maintaining renal blood flow and GFR during hypotension

217
Q

what signs should we tell owners to look for when administering NSAIDs?

A

vomiting/diarrhoea

signs of blood in the faeces

dullness

anorexia

218
Q

which parameters should be monitored in animals on NSAID therapy (gold standard)?

A

clinical examination and history
haematology and biochemistry
urinalysis
blood pressure

219
Q

when should patients be re-checked after starting NSAID therapy?

A

re-check regarding side effects 1-2 weeks after starting treatment (side effects most likely to occur in first 2 weeks)

220
Q

how often should high-risk patients on NSAIDs be monitored?

A

NSAIDs should be avoided in high-risk patients

221
Q

how often should medium-risk patients on NSAIDs be monitored?

A

rechecked monthly +/- blood work/blood pressure/urinalysis

222
Q

which patients are medium-risk for side effects due to NSAID use?

A

those with concurrent disease in a target organ)

223
Q

how often should low-risk patients on NSAIDs be monitored?

A

should be re-checked every 3-6 months

224
Q

what are some other treatment options if NSAIDs are not efficacious alone/poorly tolerated?

A

NSAID cycling - swap drugs (only one licensed in cats at present)

introduction of analgesic adjunctive therapies e.g. gabapentin

non-pharmacological therapies e.g. diet, weight management, physiotherapy, acupuncture

225
Q
A

Applied Clinical Veterinary Nursing (31 decks)

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