Anaesthesia: Clinical Induction and Maintenance and Pain Flashcards
What is pain?
An unpleasant sensory and emotional experience associated with, or resembling that associated with actual or potential tissue damage
What is nociception?
Relay of noxious stimulus from the periphery to the central nervous system
How does nociception translate to pain?
Integration and processing of nociceptive input by the brain allowing stimulus to be perceived as pain
What are the three types of acute pain?
Somatic
Visceral
Neuropathic
What is somatic pain?
Chemical, thermal or mechanical stimulus to skin, muscles, bones etc usually localised to injury site
‘sharp stabbing’ sensation
What is visceral pain?
Inflammation, ischemia (restriction of blood flow) or distension of viscera
Poorly localised, diffuse
‘Burning dull sensation’
Possible autonomic components- vomiting, sweating, tacyhcardia
What is neuropathic pain?
Primary lesion or dysfunction within the nervous system
May be localised or diffuse (depending on degree of nerve injury)
‘burning, tingling’ sensation may be intermittent
Can be component of chronic pain
What is the difference between acute pain and chronic pain?
Acute pain
Associated with tissue damage due to surgery, injury or disease. Rapidly alters animals behaviour (to minimise damage, optimise conditions for tissue healing), varies in severity, easy to treat
Chronic pain
Persists beyond expected time frame of tissue healing, may be associated with ongoing disease, maladaptive, often poorly responsibe to treatment
What are the three altered pain states?
Hyperalgesia
Allodynia
Spontaneous/idiopathic/functional pain
What is hyperalgesia?
Hyperalgesia is an altered pain state where exaggerated pain is felt in response to noxious stimulus
Use your brain- Hyper- algesia
What is allodynia?
An altered pain state where perception of pain sensation in response to normally non-noxious stimulus
Allo? that hurt!- unexpected
What is spontaneous/idiopathic/functional pain?
An altered pain state where pain arises in absence of detectable tissue or nerve injury
Difficuly to identify/prove in animals
Possible component of neuropathic pain- ‘phantom limb pain’
What are the two kinds of sensitisation?
Peripheral
Central
What is peripheral sensitisation?
Increased responsivness of nociceptors (reduced threshold)
‘Silent’ nociceptors activated
Occurs with tissue damage and inflammation
Altered expression of ion channels in nociceptive neurons
Causes primary hyperalgesia and allodynia at injury site
What is central sensitisation?
Increased efficiency of nociceptive signal transmission that may persist after end of nociceptive input
Changes in membrane exitability and upregulation of post-synaptic receptors (especially NMDA)
Results from intense, prolonged and/or repeated nociceptive input
Causes secondary hyperalgesia outside area of injury
May result in chronic pain
What happens if pain is not adequatley managed?
It causes unstable general anaesthesia
Poor animal welfare- 5 freedoms
Prolonged hospitalisation/delayed recovery
Development of central sensitisation- could lead to chronic pain- ongoing welfare problem for animal and owner/caregiver, behaviour issues
What are the 4 stages of nociception?
Transduction
Transmission
Modulation
Perception
What are the components of the ‘pain experience’?
Sensory- discriminative
Motivational- affective
Cognitive- evaluative
How can effective analgesia be provided?
Pre-emptive analgesia
Administration of analgesics prior to noxious stimuli maximises their effect, reduces sensitisation and enhances post operative analgesia
Once pain is established it should be treated aggresively- sensitisation to chronic/long term pain and difficult managment
How can effective analgesia be multimodal?
Formulation of an analgesic plan that targets as mant stages of the nociceptive pathway as possible
Transduction, transmission, modulation, perception
What drugs act on the nerve terminal (transduction)?
NSAIDs
Local anaesthetics
Opiates
What is the only drug to act on transmission part of pathway?
Local anaesthetics
What drugs act on the dorsal horn of the spinal cord (modulation)?
NSAIDs
Opiates
NMDA antagonists
Calium channel blockers
Tramadol
What drugs act on the brainstem/cerebrum (perception)?
NSAIDs
Opiates
NMDA antagonists
Calcium channel blockers
Tramadol
What drugs act on all of the following parts of the nociceptive pathway?:
Transduction
Modulation
Perception
NSAIDs
Opiates
What drugs act on all the following parts of the nociceptice pathway?:
Modulation
Perception
NMDA antagonists
Calcium channel blockers
Tramadol
What does choice of drugs for pain depend on?
Degree of pain present
Drug availability
Efficacy of drug
Site/mechanism
Time of onset
Duration of effect
Administration
Legal/safety
What is the acronym to remember the analgesic drugs?
NO PLAN
NSAIDs, Opioids, Paracetamol, Local anaesthetics, Alpha 2 agonists, NMDA antagonists
What is the mode of action for NSAIDs?
What are the side effects?
MOA:
COX inhibitors- reduce production of inflammatory mediators to reduce nociceptor sensitisation- after transduction, modulation and perception
Side effects:
Renal, GI, Hepatic, Coagulation- ulceration
COX-2 selective NSAIDs not necessarily ‘safer’
When are opiods often used?
Usually indicated for moderate to severe pain
Commmonly included in premed
What are the central and perihperal effects of opioids?
Central:
Opiod u receptors expressed in spinal cord dorsal horn and stimulate descending inhibitory pathways and reduce neurotransmitter release
Peripheral:
u receptor expression upregulated in inflamed tissues
1) What areas of the nociceptive pathway do opioids affect?
2) What are opioids side effects?
3) What are the names of 6 opioids?
- Affect modulation and perception- slightly transduction
- Multiple side effects- less common in animals with pre-existing pain- ileus, prutitus, nausea/vomiting, urinary retention, dysphoria
- Butorphanol, Buprenorphine, Pethidine, Morphine, Methadone, Fentanyl
BPM BPF- ?
Which opioid is only a partial u agonist and which is a u antagonist and k agonist?
Buprenorphine is a partial u agonist
Butorphanol is a u antagonist and partial k agonist
What kind of drug is tramadol?
What is it’s mode of action?
What are the side effects?
Why does it have a poor palatability?
Atypical opioid- weak u receptor
MOA:
Inhibits serotonin and noradrenaline reuptake- some alpha 2 agonists properties- M1 metabolite has greater analgesic efficacy than parent drug
Side effects: salivation, vomiting, dysphoria, sedation and seizures
Bitter taste
What is paracetamols mode of action?
What animals can it be given to and not given to?
Got you- the MOA is not fully understood
Licensed orally in dogs (combined with codeine) for up to 5 days
Toxic to cats
What are local anaesthetics mode of action?
How do different agents differ?
MOA:
Sodium channel blockers- prevention of generation of action potential and propagation of action potentials- inhibit transmission in all nerve types- true analgesics
Agents differ in terms of speed of onsed and duration of effect
Be aware of overdose with systemic absorption
1) What are alpha 2 agonists commonly used for?
2) Where does analgesia occur and how?
3) What are alpha 2 agonists synergistic with?
4) What are its side effects?
5) What do you need to be careful about when using alpha 2 agonists?
- Premed, analgesia, sedation, muscle relaxation
- Analgesia at spinal and supraspinal- descending sertonergic and noradrenergic inhibitory pathways- affects modulation
- Opioids
- CVS, GI, endocrine
- Sedation does not mean analgesia- analgesia peaks later then sedation and shorter duration
What drugs have NMDA antagonist properties?
Amantadine
Memantine
N2O
Xenon
Methadone
Pethidine
Ketamine
What are NMDA antagonists MOA and what part of the nociceptive pathway do they affect?
What are the side effects of NMDA antagonists?
MOA: may prevent/reverse central censitisation
Affect modulation and perception
Side effects- few at analgesic doses- muscle rigidity, exitation
What is the mode of action of gabapentinoids and what are some examples?
Calcium channel blockers- modulation and perception
Gabapentin, Pregabalin
What are NK-1 antagonists licensed for in cats and dogs?
How do they work as an analgesic?
Licensed as an anti-emetic in cats and dogs
Substance P binds to NK-1 receptos in PNS and CNS leads to inflammation and central sensitisation- antagonists!
What are non-pharmalogical methods of acute pain managment?
Anxiolysis/Sedation
Wound dressing and external coaptation
Appropriate environment and good nursing care- warmth, comfort, stimulation, empty bladder, clean
How can pain be recognised in animals?
Non-verbal
Behaviour indicators
Physiological markers
Response to analgesia
How is dogs acute pain assessed?
Multidimensional composite pain scales e.g
Glasgow (short form) canine pain scale:
- Validated for assesing acute pain in dogs
- Quick and easy in clinical setting
- Assess in kennel and when walked
- Assess reaction to palpation around wound/painful area
- Scores out of 20 (non-ambulatory) or 24 (ambulatory)
- Threshold for rescue analgesia >5/20, >6/20
How is cats pain assesed?
Several multidimensional pain scales described e.g
Glasgow feline pain scale
- Validated for assessing pain in cats
- Quick and easy to perform
- Assess cat in kennel, interaction with observer, palpation of wound/painful area
- Assess facial expression
- Score out of 20 >5/20 threshold for analgeisa
How is pain assessed in food producing animals?
- Cow pain scale
- Locomotion scoring- dairy cattle
- Grimace scales- dairy cattle, sheep, piglets
- UNESP-Botucatu pain scales validated for acute pain
How is pain assessed in horses?
Hard as they try to mask pain
Physiolocial parameters considered unreliable
Behaviour indicators- decreased weight baring, pawing, flank watching, rolling restlessness, reduced appetite
Assessment of facial expression now considered important
