pain Flashcards
1
Q
pain definition
A
an unpleasant sensory and emotional experience associated with or resembling that associated with, actual or potential tissue damage
2
Q
nociception vs pain
A
nociception is the neural process of encoding noxious stimuli (physiology)
pain is how the patient interprets nociception
3
Q
nociceptive pain definition
A
pain that arises from actual or threatened damage to non-neural tissue due to activation of nociceptors
4
Q
neuropathic pain definition
A
pain caused by a lesion or disease of the somatosensory nervous system
5
Q
hyperalgesia definition and example
A
increased pain from a stimulus that normally provokes pain (palpation causes pain when a threshold is reached however with hyperalgesia, the threshold is reduced)
6
Q
allodynia definition and example
A
pain due to a stimulus that does not normally provoke pain (patient that wont let you stroke them)
7
Q
importance of recognition and quantification of pain
A
- allows us to categorise severity of pain
- assess treatment efficacy
- judge quallity of life
8
Q
physiological signs associated with pain
A
- increased TPR
- altered respiration (could be due to stress)
- stress hormones (cortisol, noradrenaline)
- EEG (pain or nociception)
- loss of body condition (chronic)
9
Q
behavioural signs associated with pain in cats + dogs, cats, dogs, horses, rabbits
A
- species specific and varies within a species
cats + dogs- hunched, grimace, inappetence
cats- fear aggression, hide, resent contact
dogs- positive behaviour, submissive, vocal
rabbits- immobility, depression, bruxism, squint
horses- low head, agitation, looking at pain area
10
Q
snapshot of scoring and quantifying pain- 4 ways
A
- numerical rating scale
- visual analogue scale
- simple descriptive scale
- dyamic interactive visual analogue scale
11
Q
scoring and quantifying pain over time
A
dogs- short form of glasgow composite pain scale
cats- composite measurer pain scale
load questionnaire
client specific outcome measures (CSOM)
12
Q
importance of preventative analgesia
A
prevents upregulation of the nervous system in the face of noxious stimuli
- admin of analgesia before, during or after surgery
13
Q
principles of multimodal analgesia
A
- no 1 analgesia that is effective for all noxious stimuli
- uses different classes of analgesic agents
- more effective leading to lower doses of a single drug
- cant use 2 NSAID in 1 regimen
14
Q
legal requirements around keeping and prescribing of opioids
A
- full opioids are schedule 2 (record keeping, specialprescription, storagem destruction)
- partial opioid agonists are schedule 3 (special prescription and some have storage requirements)
15
Q
key pharmacology of licensed opioids in cats, dogs and horses
A
- act at the endogenous opioid receptors primarily in brain and spinal cord
- delta, kappa, mu receptor agonists
- mu receptors associated with analgesia
- used for acute rather than chronic pain
16
Q
side effects of opioid use at clinical doses
A
- respiratory depression (usually seen when used during anaesthesia)
- sedation
- excitation
- minimal effect on inotropy (heart contraction)
- nausea and vomiting
- decrease GI motility
17
Q
key pharmacology of NSAIDs
A
- prostaglandins are inflammatory mediators
- most NSAIDs inhibit prostaglandin production through inhibition of cyclo-oxygenase or lipoxygenase
- metabolized in the liver
18
Q
side effects of NSAIDs at clinical doses
A
- GI ulceration
- renal ischaemia- during hypotension, PGs protect renal blood flow
- hepatopathy- rare, mostly in dogs
- blood clotting
- CNS- dullness and lethargy reported in cats
19
Q
owner information about safe use of NSAIDs in dogs and cats
A
- GI side effects are most common
- present as vomiting and/or diarrhoea
- may see digested blood which looks like coffee grounds in vomit
- discontinue medication immediately
20
Q
owner information about safe use of NSAIDs in horses
A
- GI side effects are most common
- most commonly occur with overdose, chronic admin and in susceptable populations
- renal effects
21
Q
owner information about safe use of NSAIDs in rabbits
A
- no NSAIDs are licensed for use in rabbits
- GI effects are most common
- most commonly occurs with chronic admin
22
Q
key pharmacology of local anaesthetic agents
A
- enter the neve fibre and block the voltage-operated Na+ channel blocking nerve conduction
- said the have a ‘membrane stabilising effect’
- C fibres and Adelta fibres are preferentially blocked
- therefore will get nociceptive block before proprioceptive, mechanoreceptive and motor blockade
- weak bases
- only the uncharged form can penetrate lipid membranes and enter the nerve cell
- higher Pka= more ionised, slower onset of action
- less effective in inflamed tissue due to lower ph and therefore more ionised LA agent
23
Q
key pharmacology of paracetamol
A
- not an NSAID but can be thought of as one
- mechansim of action isnt fully understood
- massively toxic to cats
dogs- helpful when NSAIDs are contradicted
horses- useful as adjunctive analgesic in very painful cases
24
Q
key pharmacology of tramadol
A
- schedule 3 drug
- perceived wide theraputic index and lower risk of abuse than opioids
- questioned efficacy
25
tramadol and dogs
- oral unlikely to be effective
- parental tramadol evidence is unclear- limited efficacy
- use as co-analgesic if anything
26
tramadol in cats
limited evidence, some effects when given orally or parentally
27
tramadol in horses
- oral bioavailabilty is variable
- short half life
- extended use of opioids in horses can lead to GI motility, consider if planning to use for chronic pain
- only use for laminitis patients that dont respond to other analgesics
28
tramadol in rabbits
- minimal data
- pharmacokinetic evidence would suggest rabbits need a much higher dose to be effective
29
gabapentin
- structural analogue of GABA
- binds to voltage gated calcium channels, reducing excitatory neurotransmitters being released
- may have role in neuropathic pain management
- used as adjunct to other analgesics
30
gabapentin side effects
- sedation
- avoid liquid solutions containing xylitol due to toxicity potential
- reduce dose over 1-2 weeks before stopping
31
amantadine
- oral NMDA receptor antagonist
- used in humans as antiviral and anti-parkinsonian
- antihyperanalgesic agent not analgesic
- pharmacokinetic data suggets short action
- excreted via kidneys
- may take 3-4 weeks to see clinical benefit
- used in horses as antiviral against influenza
32
examples of practical application of LA
- infraorbital block for dental surgery
- cornual nerve block- calves
- topical admin to desensitise feline larynx for intubation
33
2 main classes of drugs commonly used to produce local anaesthesia
- amides (i in name before the 'caine')
- esters (no i in name before the 'caine')
34
commonly used local anaesthetics and licensing
procaine- dogs, cats, horses
lidocaine- dogs, cats, horses (used in rabbits)
bupivicaine- unlicensed (used in dogs, cats, rabbits)
mepivacaine- horses
ropivacaine- unlicensed (used in small animals)
ELMA- unlicensed
proparacaine and tetracaine- unlicensed
35
pharmacochemical factors affecting onset and duration of action
- lipid solubility (lipid membrane)
- binding strength
- speed of removal (tissue perfusion)
- metabolism of LA (ester vs amide)
36
preventing toxicity
- addition of vasoconstrictors- (adrenaline) reduces speed of absorption reducing toxicity risk
- LA which bind to plasma proteins easier have longer duration of action, lower toxicity (drug must be unbound and unionised to be active)
37
CNS toxicity and management
- behaviour changes, muscle twitching, convulsions
symptomatic treatment:
- BDZs (benzodiasepines) to control seizures
- O2 supplementation
- intubation and controlled ventilation if needed
38
CVS toxicity and management
hypotension
dysrhythmias
symptomatic treatment:
- manage bradycardia with anticholinergic
- fluid therapy
- intralipid IV may be useful to mop up LA
39
shock definition
an imbalance between oxygen delivery to the tissues and oxygen consumption by the tissues
40
4 main types of shock
- hypovolaemic
- cardiogenic
- obstructive
- distributive
41
physiological response to hypovolaemic shock
- neurohormonal response to decreased circulating vol to preserve CO
- catecholamine release -> ^HR, vasoconstriction
- activation of renin-angiotensin-aldosterone system
- increases Na+ and H2O retention
- spleen may contract to release more RBCs
42
clinical signs of hypovolaemic shock in dogs
HR: >120
MM: pink-> pinker-> pale pink-> white
CRT: <2 -> <1 -> 2 -> >2
Pulse: normal -> bounding -> weak
Systolic BP: >90 until severe shock then <90
Mentation: obtunded at moderate to severe shocl
Lactated conc: 0.5-2.5 -> 3-5 -> 5-8 -> >8
43
clinical signs of hypovolaemic shock in equines
HR: >40
MM: pink -> pinker -> pale
CRT: 1.5 -> <1 -> >2
pulse: palpable -> bounding -> weak
mentation: depressed at severe shock
lactate conc: 0.5-2.5 -> 3-5 -> >8
44
feline response to hypovolaemia
- less predictable than other animals
- bradycardia
- hypothermia
45
treatment of hypovolaemic shock
1. rapid admin of fluids to restore intravascular vol and tissue perfusion
2. treat underlying cause
3. potential blood transfusion
46
fluid therapy plan for canine hypovolaemic patient
1. admin 10-20ml/kg crystalloid bolus over 15-20 mins
2. reassess
3. admin further bolus if required
4. max 45-60ml/kg with minimal improvement
5. if ongoing blood loss with PCV <20%, admin blood products
47
fluid therapy plan for feline hypovolaemic patient
1. admin 5-10ml/kg crystalloid bolus over 15-20 mins
2. reassess
3. admin further bolus if required
4. max 30-35ml/kg with minimal improvement
5. if ongoing blood loss with PCV <20%, admin blood products
48
determining efficacy of treatment
- repeat major body system assessment every 15-30mins during stabilisation
- HR, CRT, MM, temp, pulse quality
- interpret BP with caution
- lactate will decrease with effective treatment
- urine output goal= 0.5ml/kg/hr
- ECG to monitor arrhthmias
49
purpose of hypertonic fluids
- moves water from extravascular to intravascular compartment
- lowers initial volume required for vol resus
- can reduce cerebral oedema
- 4ml/kg is administered once
- needs to be followed by isotonic crystalloids
