Analgesia Flashcards

1
Q

What complications can arise from pain that effects mobility, occurs after abdominal or thoracic surgery and pain leading to a sympathetic response?

A

Reduced mobility leaves risk to DVT, post op complications
After abdo/thoracic surgery - decreased cough reflex leads to hypoxia, bacterial infections and lung collapse
Increased SNS leads to tachycardia and hypotension which is not ideal in heart failure

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2
Q

What is the basic pain pathway?

A

Pain picked up by nociceptors
Transduction as an electrical signal
Transmitted along nerve fibres
Into dorsal horn of the spinal cord
Spinothalamic tracts carry impulses to the thalamus
Transmitted to somatosensory cortex in post central gyrus

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3
Q

What is the difference in the fibres that carry sharp and dull pain?

A

Sharp pain by myelinated A-delta fibres

Dull pain by unmyelinated C fibres

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4
Q

Which area of the brain is pain percieved?

A

In the post central gyrus - somatosensory cortex

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5
Q

What is Gate theory and how does it explain why rubbing an effected area or having a TENS machine will reduce pain?

A

Gate theory is that pain transmitters open a gate for onward transmission but A-beta fibres that carry vibration and pressure actually act with an intermediate inhibitory neurone that prevents pain being transmitted

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6
Q

With acute pain what aspects need patient monitoring?

A
HR
BP
Level of sedation
Nausea and vomiting
Leg weakness
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7
Q

Brief overview of WHO pain ladder?

A

Start with simple - paracetamol, NSAIDs
Advance to simple opioids - codeine, tramadol
Stronger opioids - morphine

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8
Q

What is multimodal analgesia?

A

Use of drugs with different modes of action to create a synergistic effect on the pain

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9
Q

What 2 classes of drugs can be given preoperatively to reduce pain post operatively?

A

Anti convulsants like gabapentin and pregabalin

A-2 aginsts like clonidine

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10
Q

In acute pain situations what do you need to ensure is done?

A

Prescribe analgesia for the next 48-72 hours

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11
Q

6 side effects of opioid administration?

A
Sedation
Respiratory depression
Nausea
Vomiting
Constipation
itch
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12
Q

3 main SE of NSAID administration?

A

Renal impairment
Bleeding
GI complications - bleeding, ulceration, perforation

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13
Q

What is patient controlled analgesia?

A

An opioid is usually administered via a given set and IV cannula controlled by an electronic pump and patient has a handset
delivers bolus
Lock out period

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14
Q

What 2 drugs are usually given in epidural analgesia?

A

levobuprivacaine

fentanyl

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15
Q

Clinical manifestations of the sensory, motor and sympathetic block that occurs in an epidural?

A

Sensory - no hot/cold sensation, urinary retention, pain relief
Motor - reduced motor power, urinary retention
sympathetic block - hypotension

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16
Q

What are some benefits of using epidural analgesia over any other form of analgesia?

A
Great pain relief
Less VTE
Less constipation
Reduced blood and transfusion rates
Reduced stress response
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17
Q

What are some potential side effects of epidurals?

A
Ineffective or incorrect insertion leaving to inadequate pain relief
Infection 
Hypotension - associated complications
Post dural puncture headache
Neuro damage
Need for urinary catheter
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18
Q

What kind of motor black involvement are ward based epidurals meant to have a limit of?

A

Should not be a sense block

Patient should be able to raise their heels off the ground

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19
Q

What symptoms would be suggestive of epidural haematoma and what is management?

A

Onset of severe weakness and back pain

Urgent MRI, immediate referral to on-call anaesthetist

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20
Q

what happens if epidural anaesthesia reaches above the level of T4? Management?

A

Level T1-T4 controls the heart through cardio-accelerator fibres
block extending here causes profound hypotension
Stop infusion, ABCDE
Contact on-call anaesthetist

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21
Q

Who manages the epidural daily reviews, changes to analgesia, adjustments of epidural catheter position, commencement/recommencement of anticoagulants?

A

Acute pain team

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22
Q

What 2 blood monitoring is required for an epidural and what do they indicate? management if derangement is present?

A

Coagulation screen
Falling platelets
Indicative of coagulopathy or sepsis
Need urgent referral to anaesthesia

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23
Q

What is the benefit of using a wound infiltration catheter and how does it work?

A

Local anaesthetic is infiltrated into the wound via a pump at the end of the surgery to give continuous infusion

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24
Q

What kind of analgesia technique is used for a midline laparotomy when epidural is contraindicated? What nerve roots supply the anterior abdominal wall?

A

Rectus sheath catheter

Ventral rami of the thoracolumbar spinal nerves T7-L1

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25
Q

What are peripheral nerve blocks with catheter used for?

A

Post operative analgesia for upper or lower limb procedures

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26
Q

What is the definition of a local anaesthetic drug?

A

Drugs that depending on their concentration and where they are applied, cause a reversible blockade of peripheral and central neural transmission along autonomic, sensory and motor fibres

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27
Q

what is the physiology of local anaesthetic administration?

A

Causes blockade of the voltage gated sodium channels
Prevents action potentials
Prevent transmission across neurones to the cerebral cortex

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28
Q

What are 3 positive systemic effects of administratin local anaesthetic?

A

Prevents post operative hyperalgesia
Prevents inflammation
Prevents hypercoaguability

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29
Q

What is the difference in voltage inside to outside the cell during resting and depolarisation?

A
Resting = -70mV
Depolarisation = +20
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30
Q

How does a stimulated nerve produce an action potential?

A

Becomes permeable which causes the sodium ions to pass out into the cell
Sodium is positively charged

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31
Q

How does repolarisation of a nerve occur?

A

Potassium channels open and allow potassium to move out of the cell
Resting potential restored

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32
Q

How is the original distribution of ions restored via the cell membrane?

A

Na/K pump

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33
Q

How is a nerve impulse propagated?

A

Local current flows between the depolarised segment and the next segment

34
Q

How do anaesthetic molecules cause anaesthesia?

A

Enter as unionised molecules
Lipid soluble can pass through cell membranes
Become ionised in acidic conditions within cells
Ionised bind to Na’K transport ATP binding site
Prevent ATP from becoming ADP
Cell become impermeable to Na
No action potentials

35
Q

Which fibres are effected first and last by local anaesthetic? Why are they effected first and last?

A

First = nociceptive and sympathetic
Last = motor
Due to there being myelination present or not

36
Q

What is local anaesthetic? What indications are there for use of local anaesthetic?

A

SC injection

Reduce the need for GA
Reduce post op pain
Analgesia for trauma
Allow difficult procedures like bronchoscopy or awake fibreoptic intubation

37
Q

Examples of local infiltration anaesthetic administration?

A

Local infiltration analgesia in ortho

Wound soaking catheters

38
Q

Contraindication to using local infiltration of anaesthetic? why is it a contraindication?

A

infected tissues as low pH stops from working

39
Q

What is topical anaesthetic used for?

A

mainly to anaesthetise upper airways for awake laryngoscopy and intubation

40
Q

What is the proper name for regional anaesthesia? How is it usually performed

A

Peripheral nerve block
Involves injection around a singular nerve to prevent passing of signals
Can use USS guidance, anatomical landmarks, nerve stimulator to find nerve

41
Q

What can a central neuraxial block be?

A

Epidural or spinal injections

42
Q

where is a spinal injection performed and what do you inject into?

A

Below the level of the cauda equina

into the intrathecal space which is filled with CSF

43
Q

Where is an epidural injected into?

A

Extradural space of the lumbar or thoracic region

44
Q

Why is risk of LAST greater in epidural than spinal?

A

Because much more anaesthetic is required for an epidural than a spinal

45
Q

2 contraindications to an epidural?

A

septic - epidural abscess risk

Anticoagulated - risk of haematoma

46
Q

What are the 3 components of a molecule of local anaesthetic?

A

lipophillic aromatic group
hydrophillic amide group
intermediary chain connecting

47
Q

How are local anaesthetics categorised?

A

According to their intermediatory chain

48
Q

What are esters metabolized by? 3 examples

A

Plasma cholinesterases

Procaine
Cocaine
Amethocaine

49
Q

What are amides metabolised by? 5 examples

A

Liver

Lignocaine
Prilocaine
Bupivacaine
Ropivacaine
Dibucaine
50
Q

What aspects of anaesthetic molecular structure determines its effectiveness? What does the value represent?

A

pKa value

Represents the pH at which 50% of the molecules are ionised and 50% of the molecules are unionised

51
Q

4 most common local anaesthetics used?

A

Lidocaine
Bupivacaine
Levobupivacaine
Ropivacaine

52
Q

Which 2 local anaesthetics are most commonly used in theatre?

A

Levobupivacaine

Bupivacaine

53
Q

Which local anaesthetic has the shortest time to act and shortest time to wear off?

A

Lidocaine

54
Q

What is the difference between buprivacaine and levobuprivacaine?

A

Levobupivacaine is less cardiotoxic

55
Q

What is EMLA?

A

Topical anaesthesia for skin

Mix if prilocaine and lidocaine

56
Q

What is the mix that makes up topical eye drops?

A

Amethocaine and oxybuprocaine

57
Q

Why is cocaine used in ENT procedures?

A

Reduces blood loss

Vasoconstriction

58
Q

What anaesthesia is used in spinals of day cases?

A

Prilocaine

59
Q

During a peripheral nerve block, what adjunct is usually used alongside lidocaine? What benefit does this have for lidocaine?

A

Adrenaline

Causes vasoconstriction so less systemic absorption of lidocaine and therefore can administer more

60
Q

Safe max dose of lidocaine?

A

3mg/kg up to 200mg

61
Q

Safe max dose of lidocaine with adrenaline?

A

7mg/kg up to 500mg

62
Q

Safe dose and max dose of bupivacaine/levobupicavaine?

A

2mg/kg up to 150mg or 400mg in 24 hours

63
Q

Safe dose and max dose of ropivacaine?

A

3mg/kg up to 200mg

64
Q

Important points to remember about anaesthetic administration?

A
Make sure not allergic
no contraindications
informed consent
aspirate before administering
attach monitoring and IV access
Fractionate doses over 5mls and aspirate between fractions
65
Q

What is LAST? what 2 body systems are mainly effected?

A

local anaesthetic systemic toxicity

mainly effects CNS and CVS

66
Q

What is the principle determinant of the systemic effects of LAST?

A

Free fraction of local anaesthetic

67
Q

3 main types of LAST reactions?

A

instant LAST - unintentional large load directly intra-arterially or IV, cardiovascular collapse and seizures pretty quickly
Instant LAST - caused by unintentional IA injection during neck blocks, even small amounts, seizures but usually short lived and no major CV effects
Slow LAST - can occur up to 30 minutes after administration, overdosing, increased systemic absorption, decreased metabolism, decreased plasma binding (main determinant)

68
Q

What are the presenting symptoms of local anaesthetic systemic toxicity? how do they go on to develop?

A

Initially CNS symptoms - seizures, metallic taste, auditory changes, respiratory arrest, agitated, coma
CVS symptoms follow - bradycardia, decreased conduction and performance, hypotension, circulatory collapse

69
Q

What cardiotoxic effects does lidocaine have and how does it differ to the effect that bupicavaine, levobupivacaine and ropivacaine have?

A

Lidocaine blocks Na channels and effects contractility
Levobupivacaine, bupivacaine and ropivacaine have effects on conduction causing arrhythmias and also negatively inotropic

70
Q

5 groups of people that are at increased risk of LAST?

A
Pregnant
Neonates
Congestive heart failure
Hypoalbuminaemia
Severe liver or renal impairment
71
Q

Management of someone with LAST?

A

ABCDE
Call for help
Give intralipid bolus of 1.5ml/kg over 1 minute then start an infusion
Lipid emulsion therapy

72
Q

How does an intralipid bolus act to treat LAST?

A

shuttling of local anaesthetics away from heart and brain
cardiotonic effects
Post-conditioning cardioprotective effects

73
Q

identification of LAST involves looking for what signs?

A
Decreased consciousness
Alterned mental state - agitated
With or without convulsions
LOC
Bradycardia, decreased conduction, arrythmias, ventricular tachycardia, asystole
74
Q

Immediate management of LAST?

A

A - secure airways, may need nasopharyngeal
B - oxygen, hyperventilation may help metabolic acidosis
C - IV access, consider drawing bloods, consider CV status throughout
D - treat any seizures

75
Q

Treating CV collapse caused by LAST?

A

CPR
Cardiopulmonary bypass if possible
Manage arrythmias

76
Q

What is bolus volume of 20% lipid emulsion and what is IV rate?

A

Bolus = 1.5ml/kg over 1 minute

IV infusion = 15ml/kg/hour (can be doubled if CV unstable)

77
Q

What is the maximum number of lipid bolus that can be given and across what time interval?

A

3 bolus can be given with 5 minute intervals

78
Q

What are the situations in which there is a preference between use of adrenaline or noradrenaline?

A

Adrenaline is better for cardiac stimulation and increasing metabolism
Noradrenaline is better for constriction of BV

79
Q

What are alpha 1/2, beta 1/2/3 receptors predominantly located?

A
Alpha 1 = vascular 
Alpha 2 = presynaptic
Beta 1 = heart
Beta 2 = SM
Beta 3 = fat
80
Q

What needs to be excluded as a cause of lipidaemia in follow up of LAST?

A

pancreatitis - take amylase levels and lipase assays for 2 weeks