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CVNT > pain > Flashcards

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

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2
Q

nociception vs pain

A

nociception is the neural process of encoding noxious stimuli (physiology)
pain is how the patient interprets nociception

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3
Q

nociceptive pain definition

A

pain that arises from actual or threatened damage to non-neural tissue due to activation of nociceptors

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4
Q

neuropathic pain definition

A

pain caused by a lesion or disease of the somatosensory nervous system

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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)

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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)

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7
Q

importance of recognition and quantification of pain

A
  • allows us to categorise severity of pain
  • assess treatment efficacy
  • judge quallity of life
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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)
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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
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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
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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)

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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

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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
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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)
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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
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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
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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
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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
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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
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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
Q

tramadol and dogs

A
  • oral unlikely to be effective
  • parental tramadol evidence is unclear- limited efficacy
  • use as co-analgesic if anything
26
Q

tramadol in cats

A

limited evidence, some effects when given orally or parentally

27
Q

tramadol in horses

A
  • 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
Q

tramadol in rabbits

A
  • minimal data
  • pharmacokinetic evidence would suggest rabbits need a much higher dose to be effective
29
Q

gabapentin

A
  • 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
Q

gabapentin side effects

A
  • sedation
  • avoid liquid solutions containing xylitol due to toxicity potential
  • reduce dose over 1-2 weeks before stopping
31
Q

amantadine

A
  • 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
Q

examples of practical application of LA

A
  • infraorbital block for dental surgery
  • cornual nerve block- calves
  • topical admin to desensitise feline larynx for intubation
33
Q

2 main classes of drugs commonly used to produce local anaesthesia

A
  • amides (i in name before the ‘caine’)
  • esters (no i in name before the ‘caine’)
34
Q

commonly used local anaesthetics and licensing

A

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
Q

pharmacochemical factors affecting onset and duration of action

A
  • lipid solubility (lipid membrane)
  • binding strength
  • speed of removal (tissue perfusion)
  • metabolism of LA (ester vs amide)
36
Q

preventing toxicity

A
  • 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
Q

CNS toxicity and management

A
  • behaviour changes, muscle twitching, convulsions
    symptomatic treatment:
  • BDZs (benzodiasepines) to control seizures
  • O2 supplementation
  • intubation and controlled ventilation if needed
38
Q

CVS toxicity and management

A

hypotension
dysrhythmias
symptomatic treatment:
- manage bradycardia with anticholinergic
- fluid therapy
- intralipid IV may be useful to mop up LA

39
Q

shock definition

A

an imbalance between oxygen delivery to the tissues and oxygen consumption by the tissues

40
Q

4 main types of shock

A
  • hypovolaemic
  • cardiogenic
  • obstructive
  • distributive
41
Q

physiological response to hypovolaemic shock

A
  • 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
Q

clinical signs of hypovolaemic shock in dogs

A

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
Q

clinical signs of hypovolaemic shock in equines

A

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
Q

feline response to hypovolaemia

A
  • less predictable than other animals
  • bradycardia
  • hypothermia
45
Q

treatment of hypovolaemic shock

A
  1. rapid admin of fluids to restore intravascular vol and tissue perfusion
  2. treat underlying cause
  3. potential blood transfusion
46
Q

fluid therapy plan for canine hypovolaemic patient

A
  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
Q

fluid therapy plan for feline hypovolaemic patient

A
  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
Q

determining efficacy of treatment

A
  • 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
Q

purpose of hypertonic fluids

A
  • 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

CVNT (7 decks)

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