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Pharmacology > Anaesthetics > Flashcards

Anaesthetics Flashcards

1
Q

What are some inhalation and IV anaesthetics?

A 
Inhalational:
Nitrous oxide N2O
Isoflurane
Desflurane
Sevoflurane

Intravenous
Propofol
Ketamine

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2
Q

What are effects of general anaesthesia?

A
  • Sedation to the point of unconsciousness
  • Amnesia
  • Muscle relaxant
  • Reflex suppression
  • Immobilisation
  • Anxiolysis
  • Analgesa

No one drug can produce all these effects, so we use anaesthetics + adjuvants.

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3
Q

What are the different types of anaesthesia?

A

General anaesthesia
Regional
Local
Dissociative

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4
Q

Describe general anaesthesia

A

General anaesthesia affects the whole body – you use IV and inhalational anaesthetics, plus adjuvants, which reversibly inhibit sensory, motor and sympathetic nerve transmission – produces unconsciousness and absence of sensation

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5
Q

Describe regional anaesthesia

A

Regional anaesthesia involves rendering a region of the body insensate by inducing a blockade of transmission between it and the spinal cord. Examples include spinal and epidural anaesthesia. The patient remains conscious but may also be given adjuvants

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6
Q

describe local anaesthesia

A

Local anaesthesia is a more defined peripheral nerve block – you inject a local anaestheric. Used for tooth extraction, or procedures on the hand, fingers, foot or big toe, or internally in the urethra.

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7
Q

Describe dissociative anaesthesia

A

inhibits transmission of nerve impulses between higher and lower brain centres with drugs like ketamine – used in children and the elderly for short procedures. Can cause post-operative hallucinations in people outside these groups.

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8
Q

What area is responsible for immobilisation? Unconsciousness? Amnesia?

A

Immobilisation - spinal cord
Unconsciousness (inhaled agents) thalamus
Amnesia (inhaled agents) hippocampus

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9
Q

What is potency? how can it be predicted?

A

Concentration of a drug needed to attain 50% of its therapeutic effect
It is predicted by lipid solubility - ability to enter cell membranes

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10
Q

How are fluranes administered?

A

• Inhalational anaesthetics are vaporised
o Modern inhalational fluranes are volatile liquids at rooms temperature
• Then the agent is mixed with oxygen, air, and often nitrous oxide, which is supplied to the respiratory system via a mask

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11
Q

What is the minimal alveolar concentration?

A

Minimal Alveolar Concentration (MAC) is defined as the percentage of inhaled anaesthetic that abolishes the response to surgical incision in 50% of patients.

The lower the MAC, the more potent the anaesthetic. The MAC is also a unit of delivery – there is very little variation in MAC between individuals, and so surgical depth can be achieved with 1.2-1.5 MAC. This is why they need to be precisely controlled!

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12
Q

What are the MAC of fluranes?

A

1-6% by volume

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13
Q

Describe what absorption of anaesthetic is dependent on.

A

Absorption of the anaesthetic is determined by the blood:gas coefficient of the anaesthetic – the agent will easily pass down its concentration gradient from the alveoli into the bloodstream – the degree of absorption is determined by the blood-gas coefficient – it is the volume of gas (in liters) which can dissolve in one liter of blood. For example for isoflurane its 1.4 – the higher the coefficient the more easily it will enter the blood. The concentration in the alveoli directly determines the concentration reached in the CNS.

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14
Q

Describe what distribution of anaesthetic is dependent on

A

Distribution is dependent on blood supply to the organs and tissues, and the capacity of that tissue to take up the anaesthetic. 75% of the blood supply goes to the brain, liver and kidneys, 18% to muscle and 5% to fat.
The tissue:blood coefficient determines how the tissues take up anaesthetic from the blood. For example for isoflurane the tissue:blood coefficient is 1.6, so for the same volume of brain to blood the brain will take up 1.6 times as much anaesthetic. But the muscle:blood coefficient is much higher 0 so the muscle takes up proportionately more than the brain. The fat:blood coefficient is even greater – 45 – which provides a reservoir of anaesthetic which redistributes during recovery.

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15
Q

Describe metabolism of fluranes

A

Fluranes also undergo plasma protein binding – but this is weak and dissociates rapidly.
Fluranes are not significantly metabolised – there is a little transformation by hepatic enzymes.

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16
Q

Describe elimination of anaesthetic fluranes

A

Elimination: the anaesthetic is withdrawn ensuring adequate oxygenation. The blood concentration of anaesthetic drops and the anaesthetic moves out of the cell membranes and into the venous blood. It is then returned to the alveoli and excreted unchanged by the lungs. The well perfused tissues (brain, liver and kidney) are the first to surrender their anaesthetic, followed by muscle then finally fat. Full recovery can take hours to days (since muscle and fat have high capacity for anaesthetic and lower perfusion – and the anaesthetic they release into the blood can be redistributed back to the CNS – and affect conscious function)

17
Q

Describe the administration and distribution of propofol

A

IV bolus leads to rapid distribution to the CNS as it is well perfused, less distribution to muscle and fat. They are heavily bound to proteins in plasma therefore affected by competitive binding.
It then rapidly redistributes (after about 5 minutes) into muscle and fat. You may then continue to dose by bolus or infusion as an adjunct to lower the MAC of flurane. It can be used alone for short surgical procedures

18
Q

Describe the metabolism and elimination of propofol

A

Metabolism + elimination: undergoes hepatic and extrahepatic conjugation, so it has a half-life of 2 hours – doesn’t contribute to prolonged post-procedural hangover.

19
Q

What ion channels do anaesthetics work on?

A

GABA activated chloride channels (Inhibitory Ligand gated ion channel) - propofol

Glycine activated chloride channels (inhibitory LGIC)

Neural Nicotinic Acetylcholine Receptors (excitatory LGIC)

NMDA receptors (excitatory LGIC)

20
Q

Describe the MOA of anaesthetics binding to GABA activated chloride channels

A

Propofol
Once anaesthetics have bound they increase sensitivity to GABA, increase chloride currents, and so hyperpolarise the neurone and decrease excitability

Increases potency of inhibitory ligand + increase efficacy (binding a channel = more chlorine flows)
This is positive allosteric modulation

21
Q

Describe the MOA of anaesthetics binding to Glycine activated chloride channels

A

Structurally related to the GABAA ligand gated ion channel. Anaesthetics bind and increase sensitivity to glycine, increase chloride currents, hyperpolarises the neurone and decreases excitability. They act in the spinal cord to reduce the response to noxious stimuli

Increases potency of inhibitory ligand + increase efficacy (binding a channel = more chlorine flows)
This is positive allosteric modulation

22
Q

Describe the MOA of anaesthetics binding to neural nicotinic acetylcholine receptors

A

Anaesthetics inhibit subtypes of the nicotinic acetylcholine receptor, which reduces excitatory sodium currents. This contributes to analgesia and amnesia.

Unchanged potency, decreased efficacy – non-competitive allosteric antagonism

23
Q

Describe the MOA of anaesthetics binding to NMDA receptors

A

Nitrous Oxide and Ketamine – reduce the calcium current, reducing synaptic transmission

Unchanged potency, decreased efficacy – non-competitive allosteric antagonism

24
Q

What are used for anxiolytics and amnesia as an adjuvant to fluorine? MOA?

A

• Benzodiazepines are used for anxiolysis and amnesia. An example is Midazolam. They agonise GABAA receptors. They are given IV an hour before surgery. They carry only a low risk of cardiovascular and respiratory depression and can be used as sedatives for short procedures.

25
Q

What is nitrous oxide used for?

A

• Nitrous oxide is used for analgesia and to reduce the MAC of the inhalational agent by acting on NMDA receptors. It also helps to minimise recovery time as it is rapidly eliminated

26
Q

What are opioids used for?

A

morphine and fentanyl (100X more potent) – they are used for analgesia – fentanyl is more potent and more immediate so is better for fine control

27
Q

What other adjuncts can be used?

A

• Neuromuscular blocking agents – abolish muscle reflexes that occur with invasive procedures. Fluranes also potentiate neuromuscular relaxation.
o Competitive nicotinic acetycholine receptor antagonists – tubocurarine or pancuronium
o Nicotinic acetycholine receptor depolarising agonists – succinylcholine

28
Q

What will giving fluranes with adjuvants do to the MAC?

A

Giving fluranes with Nitrous Oxide or the opiate fentanyl can significantly reduce the MAC of the flurane (isoflurane, desflurane, sevoflurane) – this is used to therapeutic benefit so you have to give less flurane.

29
Q

What are ADRs of fluranes?

A

o Cardiovascular and respiratory depression due to reduced neuronal activity in the medulla
o Arrthymia and hypotension due to reduced vascular resistance (direct effect of anaesthetic on vascular smooth muscle)
o Increased intracranial pressure dye to decreased vascular resistance
o Bronchodilation (not an ADR)
o Isoflurane and desflurane can irritate the airway causing coughing and laryngospasm
o Malignant hyperthermia (which is muscle tetany due to flurane induces sarcoplasmic calcium release)

30
Q

What are ADRs of N2O

A

o Expansion of airway cavities (sinuses and middle ear, or where there is bowel obstruction) – Dangerous with intracranial air, pneumothorax or vascular air emboli. Occurs because is enters the alveoli much faster than nitrogen
o Diffusion hypoxia as it leaves the system so rapidly it can lower the alveolar partial pressure of oxygen – should increase inspired partial pressure of oxygen for a period following withdrawal

31
Q

What are ADRs of propofol?

A

CVS and respiratory depression

32
Q

what are ADRs of benzodiazepines and opioids?

A

REspiratory deprssion

33
Q

What should you monitor during anaesthesia?

A 
Respiratory rate
Cardiac rate and rhythm - ECG
BP
SaO2
Temperature - malignant hyperthermia
34
Q

What are the stages of anaesthesia?

A

Induction (usually propofol)
Maintenance (maintaining anaesthetic depth)
Recovery - withdrawal of agents and monitoring physiology

35
Q

What are the stages of anaesthetic depth?

A
  • Analgesia – spinothalamic tract
  • Excitement – get delirium and aggressive behaviour (not seen with propofol as so rapid)
  • Surgical anaesthesia – profound CNS depression, full relaxation of skeletal muscle – need to facilitate breathing and may affect cardiac function. Attained at MAC 1.2-1.5
  • Stage 4 = severe medullary depression leading to respiratory and cardiac arrest and then death – if you go outside of the therapeutic window.

Pharmacology (24 decks)

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