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Anaesthetics Flashcards

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1
Q

What are the two branches of spinal nerve?

A

Motor and sensory

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2
Q

What root do ventral nerves pass through?

A

Ventral Root

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3
Q

What root do sensory neurons pass through?

A

Dorsal Root

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4
Q

Summarise the function, diameter and myelination of Type a alpha neurons

A

Function: Proprioception, motor

Diameter (microM): 12-20

Myelination: Heavy

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5
Q

Summarise the function, diameter and myelination of Type a beta neurons

A

Function: Touch, pressure

Diameter (microM): 5-12

Myelination: Heavy

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6
Q

Summarise the function, diameter and myelination of Type a gamma neurons

A

Function: muscle spindles

Diameter (microM): 3-6

Myelination: Heavy

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7
Q

Summarise the function, diameter and myelination of Type a delta neurons

A

Function: pain, temperature

Diameter (microM): 2-5

Myelination: Heavy

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8
Q

Summarise the function, diameter and myelination of Type b neurons

A

Function: preganglionic ANS

Diameter (microM): <3

Myelination: Light

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9
Q

Summarise the function, diameter and myelination of Type c sensory neurons

A

Function: pain

Diameter (microM): 0.3-1.2

Myelination: None

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10
Q

Summarise the function, diameter and myelination of Type c sympathetic neurons

A

Function: postganglionic

Diameter (microM): 0.2-1.3

Myelination: none

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11
Q

Why do dorsal root ganglion neurons differ from general neurone structure?

A

Their cell bodies in the dorsal root ganglia have a single axon that splits (bifurcates) with one branch going to the periphery and the other into the spinal cord

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12
Q

What are nociceptors?

A

Pain-sensing neurons

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13
Q

What does the peripheral axon terminal of nociceptors look like?

A

Nerve terminals have bare endings that possesses receptors to noxious stimuli

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14
Q

What are 2 mediators for nociceptors?

A
  • H+
  • ATP

(Are released by damaged tissue)

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15
Q

Outline the basis for how local anaesthetics work (3 steps)

A

Local anaesthetics act by blocking sodium channels

Therefore

Local anaesthetics block action potentials

Therefore

Local anaesthetics block nociception

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16
Q

What is the structure of a sodium alpha subunit?

A
  • Has 24 membrane spanning domains
  • Clustered into groups of 4
  • Tetrameric channel
  • Voltage sensor in the 4th transmembrane domain
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17
Q

What are the three states in which a channel can exist in?

A
  • Resting
  • Open
  • Inactivated
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18
Q

What is the basic structure of local anaesthetics?

A
  • Have an aromatic group
  • Amine group
  • Either: ester or amide group linking the two
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19
Q

How can you identify if a drug has an amide linkage?

A

The prefix (part in front of the ‘caine’) will contain an ‘I’

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20
Q

Where are amide linked local anaesthetics broken down?

A

Liver

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21
Q

Where are ester linked local anaesthetics broken down?

A

Plasma esterases

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22
Q

Do ester drugs or amide drugs have a longer duration of action?

A

Amide act longer than ester linked

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23
Q

Which group on local anaesthetics can become protonated?

A

Amine group

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24
Q

What does protonated mean for local anaesthetics?

A
  • The amine group can become positive
  • The charged and uncharged forms are in equilibrium
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25
Q

What is protonation dependent upon?

A
  • The concentration of protons
  • pH
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26
Q

What form of a local anaesthetic is lipid soluble?

A

The unproponated form- therefore able to cross cell membranes

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27
Q

What does the lipid soluble nature of unproponated local anaesthetics mean for a cell?

A

The equilibrium between charged and uncharged forms exist on both sides of the membrane as the charged form is unable to cross the membrane

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28
Q

What does a lower pH mean for the action of local anaesthetics on sodium channels?

A

Block sodium channels less well

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29
Q

What chemical was used to observe the nature of pH’s action on sodium channels via local anaesthetics?

A

QX314 (tertiary amine (four groups on its nitrogen) and so has a permanent positive charge)

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30
Q

What were the results on the sodium channels when QX314 was applied to the outside of cells?

A

It does not block socium channels

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31
Q

What were the results on the sodium channels when QX314 was injected to the inside of cells?

A

Able to block sodium channels

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32
Q

What do the experiments using QX314 tell us about local anaesthetic action?

A
  • They block sodium channels from the inside
  • It is the charged form that acts on the channel
  • The uncharged form is necessary to allow local anaesthetics to pass through the membrane
  • Once inside the cell, local anaesthetic becomes protonated again and it is the charged form that blockes the channel
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33
Q

What state does the sodium channel need to be in for a stonger blockage?

A
  • Open

or

  • Inactivated
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34
Q

What is use dependence?

A

Channels that are more active (and thus either open or becoming inactivated) are blocked more strongly than resting channels

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35
Q

At what point in transmission do local anaesthetics act?

A

When an action potential reaches the spinal cord and synapses with other neurons to signal up to the brain

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36
Q

How might topical anaesthesia be applied?

A

Cream, drops, spray on the skin or mucosal tissue such as the nose, throat or eye

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37
Q

How is infiltration anaesthesia applied?

A

Injected into the tissue around the area that needs to be numbed and ususally only effects the more distal parts of the nerve (terminal branches)

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38
Q

Why can’t you inject infiltration anaesthesia or nerve block into the bloodstream?

A

They can have serious systemic effects

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39
Q

How can you increase the duration of infiltration anaesthesia and nerve block?

A

Add a vasoconstrictor such as adrenaline

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40
Q

How is nerve block applied?

A

Is injected around the spinal nerve trunk so everything distal will be numbed

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41
Q

How is the nerve block injected?

A

Through the use of imaging techniques such as ultrasound

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42
Q

How is intravenous regional anaesthesia applied?

A
  • A pressure cuff is used to cut off the blood supply to a limb
  • It is then injected intravenously
  • Wait 20 mins (allow the anaesthesia to develop and reduce concentration of local anaesthetic in blood vessels)
  • Deflate the cuff
  • Begin surgery
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43
Q

How is spinal anaesthesia applied?

A
  • Inject into subarachnoid space above the spinal cord
  • pain is lost from all regions supplied by nerves that emerge from the spinal cord below the level of injection
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44
Q

Where can the spinal anaesthesia be injected?

A

Bottom part of the spinal column as this is where the subarachnoid space is large anough to avoid damage to the spinal cord when placing the needle

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45
Q

Why is spinal anaesthesia not good for childbirth?

A

Produces motor block

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46
Q

How is epidural anaesthesia applied?

A
  • Injected into the epidural space just below the vertebral column
  • Performed via a catheter, which can be left in place to facilitate further doses being administered
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47
Q

Why is more epidural anaesthesia needed compared to spinal anaesthesia?

A

Because the epidural space is larger in volume than the subarachnoid space so onset it slower

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48
Q

What is intravenous lidocaine used for?

A

Post-operative pain management strategy in people who do not have cardiovascular problems or epilepsy

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49
Q

What is differential blockade?

A

When sympathetic nervous system function is lost first, followed by pain sensation with touch and motor function only being lost at higher doses

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50
Q

What are the three factors affecting the sensitivity of a nerve fibre to block by local anaesthetic?

A
  1. Degree of myelination
  2. Fibre diameter
  3. Position within the nerve
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51
Q

How does the degree of myelination affect the sensitivity of a nerve fibre to local anaesthetic?

A
  • Myelinated neurones transmit action potentials via saltatory conduction and have their sodium channels concentrated at the nodes of ranvier
  • Saltatory conduction only takes the blockage of a few nodes to completely prevent action potential transmission
  • Therefore, the higher the degree of myelination, the more sensitive to local anaesthetic
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52
Q

How does the fibre diameter affect the sensitivity of a nerve fibre to local anaesthetic?

A

Thin fibres are more sensitive to local anaesthesia than thicker ones- surface area to volume ratio

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53
Q

How does the position within the nerve affect the sensitivity of a nerve fibre to local anaesthetic?

A

Fibres that are closer to the surface of the nerve will be affected more strongly than those towards the centre

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54
Q

What happens to brain activity at low, medium and high doses of local anaesthetics?

A

Low: neuronal activity is depressed

Medium: activity of inhibitory neurons is suppressed more than excitatory ones so convulsions can occur

High: profound depression of the CNS leading to a coma and death

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55
Q

What are two effects of local anaesthetics on the heart?

A
  • Reduce the heart rate (arrhythmias)
  • Vasodilators
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56
Q

How do ester linked drugs sometimes cause allergic reactions?

A
  • Can be metabolised to para-aminobenzoic acid to produce allergies
  • Allergies to the preservatives used in formulating the drug for injection
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57
Q

What does anaesthesia mean?

A
  • Literally ‘without sensation’
  • The reversible loss of awareness of pain
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58
Q

What are three categories of anaesthetics?

A

Local

Regional

General

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59
Q

Where is the first place to use general anaesthetics?

A

Mesopotamia (4000 years ago)

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60
Q

Who first cultivated the opium poppy?

A

Sumerians and Babylonians

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61
Q

Who is said to have discovered inhaled general anaesthetics?

A

Humphrey Davy (nitrous oxide in 1800)

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62
Q

What was the first inhaled general anaesthetic?

A

Diethyl ether discovered by Ramon Llull (1275) but noted by Paracelsus (1525)

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63
Q

What three general anaesthetic where used in the 1800s?

A

Nitrous oxide, ether and chloroform

64
Q

What is a serious issue with ether?

A

Is highly flammable

65
Q

What is a serious issue with chloroform?

A

Can cause cardiac dysrhythmias

66
Q

Who synthesised Halothane?

A

CW Suckling of ICI in Widnes

67
Q

What anaesthetic is on the WHO list of essential medicines?

A

Halothane

68
Q

Where is halothane metabolised and what problems does this cause?

A
  • 20% in the liver
  • Therefore can cause liver damage
  • Metabolite is trifluroacetic acid which causes hepatitis
69
Q

Who established the 4 stage framework for anaesthesia?

A

Arthur Guedel

70
Q

What is Stage 1 of anaesthesia?

A

The patient is conscious but drowsy. They have a reduced response to pain

71
Q

What is Stage 2 of anaesthesia?

A
  • The patient may become delirious and hypersensitive to stimulatoin.
  • They may have an increased gag reflex making intubation difficult
  • Concerns in this phase include choking, breath holding, movement and vomiting
  • It is important to limit the amount of time the patient is in this stage
72
Q

What is Stage 3 of anaesthesia?

A
  • This is the desired state for surgery
  • There are 4 sub-stages or ‘planes’ within stage 3
  • As you move through the planes, there is a progressive shallowing of breathing and loss of muscle tone and reflexes
  • Plane 3 is said to be the ideal state for surgery, because there is relaxation of the abdominal and thoracic muscles
  • Plane 4 results in apnea due to diaphragm paralysis
73
Q

What is Stage 4 of anaesthesia?

A

In this stage there is medullary paralysis, cessation of respiration and loss of vasomotor control. Without rapid intervention, the patient will die

74
Q

What is balanced anaesthesia?

A

General anaesthesia normally makes use of a range of drugs that each contribute to making the patient’s and the surgeon’s time in the operating theatre as trouble free as possible

75
Q

What is Midazolam (benzodiazepine) used for?

A

Pre-operative sedative/anxiolytic

76
Q

What is Propofol (IV general anaesthetic) used for?

A

Induction of anaesthesia

77
Q

What is isoflurane/nitrous oxide mixture (inhaled general anaesthetics) used for?

A

Maintenance of anaesthesia

78
Q

What is suzamethonium (short acting neuromuscular blocking agent) used for?

A

Relax tracheal muscles to facilitate intubation

79
Q

What is Atracurium (neuromuscular blocking agent) used for?

A

Relax abdominal muslces to facilitate surgical access

80
Q

What is Fentanyl used for?

A

Post-operative analgesia

81
Q

What is Neostigmine (ACh esterase inhibitor) used for?

A

Reverse atracurium block

82
Q

What is glycopyrrolate (muscarinic antagonist) used for?

A

To reduce bronchial tract secretions; prevent muscarinic effects of AChE block

83
Q

What did Overton and Meyer report?

A

That the potency of a general anaesthetic is directly proportional to its lipophilicity

84
Q

What does fluidization suggest?

A

That the membrane becomes less ‘stiff’ as an anaesthetic accumulates in it

85
Q

What does volume expansion suggest?

A

The thickness of the membrane alters as anaesthetic accumulates

86
Q

What are two lipid theories of anaesthetics?

A
  • Fluidization
  • Volume expansion
87
Q

What are 4 problems with lipid theories?

A
  • The potency of alkyl alochols increases up to around 13 carbons in length, but this is the cut-off point. This suggests binding to a pocket of a defined size within the protein
  • Stereoisomers of anaesthetics have identical effects on membranes, but can differ in their anaesthetic potency
  • Temperature changes fluidize membrane but do not produce effects similar to general anaesthetics
  • Not all lipophilic molecules are general anaesthetics
88
Q

What is the current theory of how general anaesthetics work?

A

Protein theories

89
Q

What do protein theories suggest?

A

That anaesthetics alter the way the protein moves between different conformational states

90
Q

How do protein theories explain the lipophilic nature of general anaesthetics?

A
  • The binding sites on target proteins are located in their membrane regions
  • Thus, the drug would have to dissolve in the bilayer to be ableto access its target site
  • The Mayer-Overton correlatioon can be explained by the fact that anaesthetics have to cross the blood-brain barrier in order to exert their actions, and this depends on lipophilicity
91
Q

According to protein theories what are the target proteins for general anaesthetics?

A
  • Potentiating GABAA receptors and strychnine-sensitive glycine receptors
  • Extrasynaptic GABAA receptors may be particularly important targets of general anaesthetics
  • Potentiating two-pore-domain potassium channels
  • Inhibiting NMDA type or ionotropic glutamate receptors
92
Q

Two pore-domain potassium channels are apart of what family?

A

Family of channels including ‘leak channels’

93
Q

What is the structure of the two pore-domain potassium channels?

A
  • 2 pore forming domains and 4 transmembrane domains
  • They assemble as dimers with the two pores forming domains from each subunit. This forms the lining of the channel
  • As potassium moves out of the cell it causes depolarisation and inhibition
94
Q

What are 4 advantages of inhalational anaesthetics?

A
  • It is relatively easy to maintain certain levels of anaesthesia
  • There will be rapid equilibrium between inhaled gas and the patients tissues
  • Most general anaesthetics undergo only limited metabolism in the patients body, and they will leave by the same same route as they entered
  • This can give rapid emergence anaesthesia
95
Q

What are the disadvantages of inhalational anaesthetics?

A
  • Longer induction and marked stage 2
  • Equipment factors and psychological distress (mask over face)
  • Require complex, bulky, expensive equipment
  • Metabolism, toxicity (patient and staff) and environmental damage (200x the greenhouse effect of CO2)
96
Q

How is inhaled anaesthetic potency expressed?

A

As its minimum alveolar concentration (MAC)- This is the minimum concentration of the anaesthetic at 1atm pressure that is needed to prevent movement of 50% of subjects in response to incision

97
Q

What does the blood-gas parition coefficient determine?

A

The induction and recovery speed

98
Q

What is the blood-gas partition coefficient?

A

A measure of how well the drug dissolves into the blood compared with gas

99
Q

Which is better: a drug with high blood-gas partition coefficient, or low?

A

Low- will give a more rapid induction and recovery

100
Q

What is the oil-gas partition coefficient?

A

This is a measurement of anaesthetics lipid solubility and is the idea that high lipid solubility confers to high potency

101
Q

How can the oil-gas partition coefficient imact general anaesthetic pharmacokinetics?

A
  • If the anaesthetic is highly sosluble in fat, lots of anaesthetic will parition into fatty tissue
  • Because fat has a poor blood supply, the anaesthetic will take a long time to leave the tissue
  • Our patient will have a slowly resolving ‘hangover’ as the anaesthetic gradually leaks back into their blood and leaves the body via the lungs
  • This will be worse the fatter the patient and the more fat-soluble the drug
102
Q

What are the two most common anaesthetics in the UK?

A
  • Nitrous oxide
  • Isoflurane
103
Q

Which drug is no longer listed with the BNF?

A

Halothane

104
Q

What are the 4 haloethers?

A
  • Halothane
  • Isoflurane
  • Sevoflurane
  • Desflurane
105
Q

What are the three main targets for the haloethers?

A
  • Potential GABBA receptors leading to increased inhibitory transmission
  • Inihbit NMDA receptors leading to decreases in exitatory transmission
  • Potential two-pore domain potassium channels leading to increased neuronal inhibition
106
Q

Outline Isoflurane

A
  • Low toxicity- is not significantly metabolised
  • Is cheap- 2x the cost of halothane
  • Powerful coronary vasodilatory properties which may worsed ischaemia in parts of the heart that are supplied by the blood vessels with atherosclerosis (coronary steel)
  • Neurodegeneration concerns in neonatal animal models
  • Hypotension though negative inotropic means (decrease force of contraction) and can also decrease peripheral vascular resistance
  • Widely used
107
Q

Outline Sevoflurane

A
  • Has very rapid induction and recovery due to its low blood: gas coefficient
  • Neurodegeneration is likely to be caused but less than isoflurane
  • Expensive- 5X the cost of halothane
  • Low toxicity, there is some metabolism but it is not significant
108
Q

Outline Desflurane

A
  • Toxicity, it can produce significant irritation of the respiratory tract which can lead to coughing. Also high levels of sympathetic activity
  • Expensive, similar cost to sevoflurane
  • Optically active as has a chiral carbon but is used as a racaemic mixture
  • Low blood gas partition coefficient- less soluble than sevoflurane (suitable for obese patients). But has rather low potency
  • Evironmental impact is severe with 3700X the greenhouse gas potential of carbon dioxide
109
Q

How does nitrous oxide act?

A
  • Not fully understood
  • Moderately potent blocker of NMDA receptors
  • Some potentiating actions of GABAA receptors
  • Has low potency
110
Q

Why can you not use nitrous oxide as an anaesthetic alone?

A
  • Such low potency
  • Even a 80% mixture with O2 does not produce a loss of consiousness
111
Q

What is the usual composition that nitrous oxide is used at?

A
  • 50/50 with oxygen
  • Known as Entonox
112
Q

What happens when a patient stops receiving nitrous oxide?

A

The anaesthetic can transfer very rapidly from the blood to the lungs, reducing the partial pressure of oxygen in the lungs

113
Q

Why can nitrous oxide be a problem for scuba divers?

A
  • Scuba divers can have tiny bibbles of nitrogen in their blood which does not normally cause a problem
  • Nitrous oxide can transfer from the liquid phase of the blood into these bubbles and expand them to cause a gas emboli
114
Q

What class of drug is nitrous oxide?

A

Class C as of November 2023

115
Q

What vitamin is nitrous oxide implemented in?

A

B12

116
Q

What is the greenhouse gas potential of nitrous oxide?

A

300x the effect of CO2

117
Q

What is Xenon?

A

A noble gas

118
Q

Why has Xenon got low levels of toxicity?

A

Has low reactivity and is not metabolised in the body and has low greenhouse gas potential

119
Q

How does Xenon act in the body?

A

Via antagonism ofnthe glycine site on the NMDA receptors

120
Q

What 5 advantages does Intravenous Anaesthesia have over inhalational methods?

A
  • Rapid Induction
  • Limited stage 2
  • Simple apparatus
  • Relatively pleasant induction
  • No atmosphere pollution
121
Q

What are 4 disadvantages of intravenous anaesthesia compared to inhalational methods?

A
  • Once its in, its in: the level of anaesthesia can be difficult to control
  • Recovery can be slow due to redistribution metabolism
  • Anaesthesia has a finite duration (infusion can get around)
  • Vein damage can occur
122
Q

How is intravenous anaesthesia usually used?

A
  • For induction in a balanced anaesthetic protocol
  • Because there is a small stage 2- once reached stage 3- inhalational can be used to maintain anaesthesia during surgery
  • Can be used for the whole procedure in short surgeries
123
Q

What family of anaesthetics is sodium thiopental part of?

A

Barbiturate plus hypnotic/anaesthetic agents

124
Q

Why is the induction of sodium thiopental good?

A

It is very lipid soluble and so crosses the blood-brain barrier very quickly which makes induction dependent on blood flow (rapid)

125
Q

What does sodium thiopental’s oil: blood partition coefficient look like?

A

Is high

Means the hangover effect occurs

126
Q

How does sodium thiopental act in the synapse?

A
  • Positive allosteric modulation of GABAA receptors
  • Can also directly activate at high doses (dangerous)
  • Also might act as inhibitors of AMPA
127
Q

What is propofol’s trade name?

A

Divipram

128
Q

How does propofol act?

A
  • Allosterically potentiates GABAA receptors
  • At higher doses may be able to directly activate the receptor
129
Q

How is propofol administered?

A

Via emulsion (“milk of amnesia”)

130
Q

What is propofol’s recovery profile?

A
  • Is metabolised very quickly so has rapid recovery
  • Has little to no hangover effect
  • Lower rates of post-operative nausea
131
Q

What is the most common side effect of propofol and how can this be combatted?

A
  • Pain when it is injected
  • Managed using analgesic agents
132
Q

What is a scary side effect for propofol?

A

Can cause hypotension and decrease respiraoty drive

133
Q

What drug is Etomidate very similar to?

A

Propofol

134
Q

What are three side effects of Etomidate?

A
  • Post operative nausea and vomiting
  • Pain at injection site
  • Supress the production of steroids by the adrenal cortex
135
Q

How does ketamine act?

A

non-competative antagonist at NMDA receptors

136
Q

What are other drugs within the same class as ketamine?

A

PCP (angel dust) and MK801

137
Q

At low doses what does ketamine do?

A
  • Rapidly acting anti-depressant
  • Produce human models of schizophrenia
138
Q

At medium doses, what does ketamine do?

A

Produces analgesia

139
Q

At moderate doses what does ketamine do?

A

Produces a ‘dissociative state’- partly conscious but will experience a loss of perception, amnesia, sedation and immobility

140
Q

At high doses what does ketamine do?

A

Loss of consciousness

141
Q

What is a main advantage of ketamine?

A

Has little effect on respiration and blood pressure (may even increase blood pressure)

Useful in emergency situations where the patient’s injury may not be fully known

142
Q

What is ketamine sometimes used as an adjunt medication for?

A
  • Opioids
  • it acts synergistically with opioids to potentiate their action
  • This allows a lower dose of opioid to be used
143
Q

What are the main side effects of ketamine?

A
  • Can induce bizarre behaviour such as hallucinations
  • NMDA antagonism can produce neurodegeneration and bladder damage whe abused
144
Q

What type of anaesthetic causes malignant hyperthermia?

A
  • Haloether inhalational agents
  • Depolarizing neuromuscular blocking agent- suxamethonium
145
Q

What is malignant hyperthermia characterised by?

A
  • Muscle rigidity
  • Increased body temperature
  • Rhabdomyolysis
  • Kidney failure
146
Q

What type of mutation do people at high risk of malignant hyperthermia experience?

A
  • Mutation in an L type calcium channel subunit
  • Mutation in the ryanodine receptor
147
Q

What action occurs to induce malignant hyperthermia?

A

Calcium floods out of the sarcoplasmic reticulum triggering systained muscle contraction and generating a large amount of heat

148
Q

What is untreated malignant hyperthermia mortality rate?

A

80%

149
Q

What is the muscle relaxant for malignant hyperthermia called?

A

Dantrolene

150
Q

What is the mortality rate for patients who are treated with a muscle relaxant?

A

5%

151
Q

How does Dantrolene work?

A

Blocks the ryanodine receptor, preventing the release of calcium from the SR

152
Q

What is neurolept anaesthesia?

A

Involves the use of an antipsychotic and an opioid

153
Q

What are neurolept anaesthesia most commonly used for?

A

To sedate large animals

154
Q

What is Large animal Immobilon a mixture of?

A

Acepromazine and Etorphine

155
Q

What is etorphine?

A

An opioid 2000X more potent than morphine

156
Q

What is the antidote for etorphine called?

A

Revivion

Drugs and the Brain (9 decks)

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