Anaesthesia: Clinical Induction and Maintenance and Pain Flashcards by Patrick Enion

What is pain?

An unpleasant sensory and emotional experience associated with, or resembling that associated with actual or potential tissue damage

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What is nociception?

Relay of noxious stimulus from the periphery to the central nervous system

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How does nociception translate to pain?

Integration and processing of nociceptive input by the brain allowing stimulus to be perceived as pain

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What are the three types of acute pain?

Somatic

Visceral

Neuropathic

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What is somatic pain?

Chemical, thermal or mechanical stimulus to skin, muscles, bones etc usually localised to injury site

‘sharp stabbing’ sensation

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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

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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

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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

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What are the three altered pain states?

Hyperalgesia

Allodynia

Spontaneous/idiopathic/functional pain

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What is hyperalgesia?

Hyperalgesia is an altered pain state where exaggerated pain is felt in response to noxious stimulus

Use your brain- Hyper- algesia

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What is allodynia?

An altered pain state where perception of pain sensation in response to normally non-noxious stimulus

Allo? that hurt!- unexpected

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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’

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What are the two kinds of sensitisation?

Peripheral

Central

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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

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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

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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

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What are the 4 stages of nociception?

Transduction

Transmission

Modulation

Perception

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What are the components of the ‘pain experience’?

Sensory- discriminative

Motivational- affective

Cognitive- evaluative

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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

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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?

1. Affect modulation and perception- slightly transduction 2. Multiple side effects- less common in animals with pre-existing pain- ileus, prutitus, nausea/vomiting, urinary retention, dysphoria 3. 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?

1. Premed, analgesia, sedation, muscle relaxation 2. Analgesia at spinal and supraspinal- descending sertonergic and noradrenergic inhibitory pathways- affects modulation 3. Opioids 4. CVS, GI, endocrine 5. 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