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Principles of anaesthesia > Pain pathophysiology, recognition, and management > Flashcards

Pain pathophysiology, recognition, and management 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

Definition of nociception

A

Neural processes of encoding and processing noxious stimuli

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3
Q

Pain physiology

A

Nociceptors (specialised nerve endings)

High activation threshold

Skin, muscles, joints, viscera, meninges

Noxious mechanical, thermal, electrical, chemical stimuli -> nociceptor activation -> action potential -> dorsal horn spinal cord

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4
Q

Types of fibres involved in pain transmission

A

As(sigma) fibres

C fibres

AB(beta) fibres

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5
Q

As(sigma) fibres

A

Medium diameter, lightly myelinated, rapid conduction

Well localised, sharp pain

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6
Q

C fibres

A

Small diameter, unmyelinated, slow conduction

Poorly localised, slow, dull pain, burning sensation

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7
Q

AB(beta) fibres

A

Large diameter, thick myelination, very rapid conduction

Non-noxious stimuli, touch, pressure, proprioception, noxious stimuli (neuropathic pain)

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8
Q

Modulation

A

Spinal cord recieves and processes somatosensory info

Synapsis with 2nd order neurons

Release of excitatory or inhibitory neurotransmitters to activate 2nd order neuron

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9
Q

Excitatory neurotransmitters

A

Glutamate
Substance P
Nerve growth factor

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10
Q

Inhibitory neurotransmitters

A

Gamma-amino-butyric acid (GABA)
Enkephalin
Glycine
Serotonin
Dopamine
Opioids

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11
Q

Projection

A

2nd order neurons from dorsal horn of spinal cord project info to:

Thalamus -> somatosensory cortex, frontal motor cortex

Lymbic system -> emotions

Reticular formation + hypothalamus, pons -> autonomic responses, sympathetic nervous system activation, catecholamines

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12
Q

Pain modulation

A

Either inhibitory or facilitatory

Peripheral nociceptors
Spinal cord
Supraspinal structures

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13
Q

Descending inhibitory pathways

A

Inhibition of interneurons (stimulated by 1st order neurons)

Secretion of inhibitory neurotransmitters (opioids, noradrenaline, GABA, serotonin, dopamine

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14
Q

Acute pain

A

Results of traumatic, surgical, or infectious events

Begins abruptly

Resolves in days/weeks

Self limiting

Serves a biological purpose

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15
Q

Chronic pain

A

Persists beyond normal time of healing/pain caused by conditions where healing has not occurred

> 1-3mo in duration

A disease, no biological purpose, usually involves changes in CNS

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16
Q

Somatic pain

A

Superficial - pain associated with skin

Deep - associatedd with muscles, joints, tendons, bones

Well localised, aching, sharp, intense

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17
Q

Visceral pain

A

Pain associated with visceral organs

Stretching capsule, distension, contration, ischaemia, inflammation

Dull, diffused, poorly defined

Often associated with feelings of nauseau, vomiting, change in autonomic system

Referred pain

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18
Q

Inflammatory pain

A

Associated with tissue injury, immune cells activation

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19
Q

Cancer pain

A

It has characteristics of both inflammatory and neuropathic pain

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20
Q

Neuropathic pain

A

Caused by injury of the nervous sytem (peripheral nerves, spinal cord, or CNS)

Increased activation of peripheral nociceptors

Increased CNS neurons excitability

Peripheral or central sensitisation

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21
Q

Peripheral sensitisation

A

Activation, sensitisation, change of nociceptors caused by tissue injury/inflammation

Reduction in activation threshold, increase in responsiveness of nociceptors, amplified response with recruitment of other nociceptive fibres

22
Q

Central sensitisation

A

Increase efficiency in pain signal transmission, even after nociceptors have stopped signalling

Change in membrane excitability, decreased inhibition, increase secretion of excitatory neurotransmitters, increase responsiveness

23
Q

Allodynia

A

Pain sensation in response to an innocuous stimulus

24
Q

Hyperalgesia

A

Exaggerated pain sensation in response to a normally painful stimulus

25
Q

Wind up

A

Spontaneous activity and temporal summation of sub-threshold stimuli -> increased response

26
Q

Consequences of pain

A

Sympathetic nervous system activation (tachycardia, arrhythmias, increased respiratory rate, increased blood pressure)

Stress response

Immunodepression

Delayed wound healing

Inflammation

Deterioration of QOL

Decrease appetitie/anorexia

27
Q

Challenges of pain assessment

A

Absence of verbal communication

Aggressive/stoic patients

Individual normal behaviour

Behaviour during hospitalisation vs with owner

Species variations

Subjectivity

Fear/anxiety

Sedation

Emergency delirium

Dysphoria/euphoria

Nausea/vomiting

Distended bladder

28
Q

Physiological parameters used to measure pain

A

Heart rate
Arterial BP
Resp rate
Plassma cortisol, catecholamine levels, endorphines

29
Q

How often should you do pain assessments?

A

During recovery phase: ideally q15min then hourly for first few hours, then q4

Before next analgesic medications is due

In between dosages

If additional analgesia has been administered - reassess after 15mins

30
Q

Facial pain signs

A

Orbiatal tightening
Ear position
Nose bulge
Cheeks
(Whiskers)

31
Q

Pain assessment in rodents

A

Difficult

Teeth grinding, changes in posture, locomotion, or gait

Decreased activity levels and behaviour display

Food and water consumption and weight changes

Faecal output

Knowing animals normal behaviours/owners involvement

32
Q

Pain assessment in reptiles

A

Difficult

Facial signs? Vocalisation?

Owner, history, subtle changes

Consider temperature

Anorexia, weight loss

Immobility, abnormal posture/locomotion

Dull colouration

Aggression

33
Q

Pain assessment in birds

A

Difficult

Change in behaviour/appearance
- drooping
- fluffed up
- eyes closed
- poor appearance/feather quality/hunched
- lameness, decreased weight-bearing, one legged standing
- difficulty perching/climbing/falling
- inappetance

34
Q

Pre-emptive analgesia

A

To prevent central sensitisation
To limit subsequent pain experience
Reason to administer analgesic drugs in premed

35
Q

Options for analgesia

A

Opioids
Alpha2 agonists
NSAIDs
Local anaesthetics
Ketamine
Gabapentin
Amantadine

36
Q

Opioids

A

Reduce pre-synaptic neurotransmitter release

Hyperpolarise post-synaptic membrane

Activates descending inhibitory pathways

Inhibits ascending nociceptive input

Located in midbrain, spinal cord, periphery etc.

Most effective analgesic: used to treat mild to severe pain

Distribution of opioid receptors and response to treatment is species dependent

37
Q

Side effects of opioids

A

Cardiovascular
- decrease HR

Respiratory depression

GI effects

38
Q

Alpha 2 agonists

A

Sedation and analgesia
- decreased sympathetic discharge (decreased noradrenaline)
- modulation nociceptive transmission
- inhibit neurotransmitter release from nociceptive neurons
- alteration in transmission ascending nociceptive signals
- descending inhibitory pathways

Synergistic with opioids, ketamine and local anaesthetics

Reversible (atipam)

39
Q

Side effects of alpha 2 agonists

A

Vasocontriction

Bradycardia

Hypotension

Vomiting

Hyperglycaemia

In ruminants: bronchoconstriction, increase in pulmonary vascular resistences, oedema

40
Q

NSAIDs

A

Ant-inflammatory, analgesic, antipyretic action

Effective on acute and chronic pain

Standard perioperative use for inflammatory pain and acute pain unless contraindicated

Wide availability, long duration of action, low cost, easy to administer

41
Q

Examples of NSAIDs

A

Meloxicam
Carprofen
Robenacoxib
Phenylbutazone
Flunixin Meglumine

Grapiprant (galliprat) - not fully understood but used for osteoarthritis in dogs

42
Q

Side effects of NSAIDs

A

Vomiting
Diarrhoea
Renal injury
Hepatic injury

43
Q

Paracetamol

A

Acetaminophen

Poor anti-inflammatory properties

Exact MoA unknown
- prostaglandin inhibition
- COX-3 inhibition
- Serotinergic pathway activation
- Endocannabinoids enhancement

DO NOT USE IN CATS

44
Q

Ketamine

A

NMDA receptor antagonist

Anaesthetic
Analgesic
Anti-inflammatory
Local anaesthetic properties
Interaction with opioid receptors

Good for acute and chronic pain

Bolus or CRI

Peri- and post-operatively

45
Q

Side effects of ketamine

A

Dysphoria

Muscle rigidity

SNS stimulation + negative inotropic effect - increase in HR and BP, care if they have heart conditions

Apneustic breathing

46
Q

Local anaesthetics

A

Na+ channel blockers

Block transmission of nociceptive inputs to the spinal cord

Gold standard

Decrease other analgesic drug needs

Low cost, but needs practice

Narrow therapeutic index, work below toxic doses to avoid side effects on CNS and CV system

Lidocaine and bupivacaine are most used

47
Q

Lidocaine vs bupivacaine

A

Lidocaine: fast onset, shorter duration

Bupivacaine: slower onset, longer duration

48
Q

Lidocaine

A

Can be administered IV in dogs

Bolus/CRI

Cats high toxicity level so not commonly used

Antiarrythmic (class 1B)

Anti-inflammatory (sepsis)

Visceral, somatic analgesia

Inhibitory descending pathways

49
Q

Side effects of lidocaine

A

Nausea
Vomiting
CNS depression
Seizures
CV depression
Arrhythmias

50
Q

Monoclonal antibodies anti-nerve growth factor

A

Frunevetmab - solensia (cats), bedinvetmab - librela (dogs)

Feline/canine monoclonal Ab (mAb) targets nerve growth factor (NGF) which inhibits NGF mediated cell signalling to reduce pain

Monthly SC injection - easy but high cost

Only licenced for pain associated with osteoarthritis

51
Q

Cannabidiol oil (CBD oil)

A

Found in cannabis and hemp

Does not contain THC

Interacts with endocannabinoid receptors

Not allowed to promote or advertise in UK

Different formulations

Reduces acute/chronic pain, anxiety, inflammation

More research needed

52
Q

Gabapentin

A

Anticonvulsant drug

Used to treat chronic neuropathic pain

Blockage of calcium channels - decreased calcium influx - decreased release of excitatory neurotransmitters

Use in associated with NSAIDs, opioids

Sedation (helpful with stressed

Principles of anaesthesia (9 decks)

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