Anaesthetic Drugs Flashcards

1
Q

What is the triad of anaesthesia?

A
  • triad of what anaesthetist aim to achieve during major surgery
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2
Q

What are the 3 parts of the triad of anaesthesia used during major surgery?

1 - analgesia, amnesia and low HR
2 - amnesia, low HR and muscle relaxation
3 - analgesia, low HR and muscle relaxation
4 - muscle relaxation, analgesia and amnesia

A

4 - muscle relaxation, analgesia and amnesia

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3
Q

What are some of the roles an anaesthetist performs during the day?

A
  • pre-assessment prior to surgery
  • anaesthetise
  • monitor recovery
    post-operative visits
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4
Q

Do all drugs used in anaesthesia target the same places in the body?

A
  • no
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5
Q

What are some of the sites in the CNS where analgesic drugs target?

A
  • thalamus
  • cerebral cortex
  • reticular activating system
  • spinal cord
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6
Q

What are some of the receptors involved in analgesic drugs?

A
  • GABA and glutamate receptors
  • voltage gated ion channels
  • glycine and serotonin receptors
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7
Q

What are analgesic agents able to do excitable tissues?

A
  • suppress excitable tissues
  • important for all 3 aspects of the triad of anaesthesia
  • especially consciousness
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8
Q

Analgesic agents possess an important feature which allows them to move freely in different compartments of the body, especially crossing the blood brain barrier (BBB). What is the property that they possess that allows them to cross the BBB?

1 - steroid like structure
2 - bind with CO2 and cross BBB
3 - lipid soluble

A

3 - lipid soluble

- meaning they can cross lipid membranes

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9
Q

There are 2 general delivery methods anaesthetist use, what are they?

A

1 - inhaled

2 - intravenous

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10
Q

What are the 3 common inhaled analgesic drugs used today?

A

1 - sevoflurane
2 - isoflurane
3 - desflurane

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11
Q

What is the core intravenous analgesic drug that we need to know?

1 - propofol
2 - thiopentone
3 - etomidate
4 - ketamine

A

1 - propofol

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12
Q

What is the main action of gamma-Aminobutyric acid also known as γ-aminobutyric acid, but referred to as GABA?

A
  • opens Cl- channels, increasing negative charge in a cell

- reduces chance of an action potential

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13
Q

What is the mechanism of action of propofol that is most commonly described?

1 - inhibits GABA
2 - inhibits serotonin receptors
3 - potentiates GABA
4 - potentiates serotonin

A

3 - potentiates GABA

  • binds to GABA-A receptor
  • essentially increases the inhibition of neurotransmitters
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14
Q

Once propofol is administered intravenously does it become bound (to proteins so it remains in the bloodstream) or unbound so it can be absorbed by cells?

A
  • both
  • bound means it acts as a reserve (most of it)
  • unbound is active
  • lipid soluble so can move anywhere in the body, including crossing the blood brain barrier
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15
Q

As propofol is administered intravenously it has 100% bioavailability, which means it peaks in the blood very quickly. When it is administered it enters the venous system. To enter the circulation it must travel to which organ?

1 - heart
2 - lungs
3 - liver
4 - kidneys

A

1 - heart

  • returns to right side of the heart
  • travels to the lungs
  • back to left side of the heart
  • enters systemic circulation
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16
Q

As propofol is administered intravenously it has 100% bioavailability, which means it peaks in the blood very quickly. It is lipid soluble so it is able to cross the blood brain barrier. Generally how quickly can propofol reach the brain?

1 - around 60 seconds
2 - around 6 minutes
3 - around 60 minutes
4 - > 60 minutes

A

1 - around 60 seconds

  • lipid soluble so the unbound can enter the brain
  • once it reaches the brain they become unconscious
17
Q

Propofol is both bound and unbound in the body when administered. Why is it important that the majority of this drug remains in the bound form in the blood?

A
  • acts as a reserve for propofol

- ensures concentration gradient so it can flow down concentration into tissues. especially the brain

18
Q

Does the concentration of propofol in the blood reduce due to the metabolism of the drug or re-distribution in other tissues?

A
  • re-distribution in other tissues

- not metabolised and cleared until much later

19
Q

What is the class of inhaled drugs currently used in analgesic called?

A
  • halogenated esters
20
Q

Etherisation is the administered delivery of halogenated esters. What are the 3 common stages, which are essentially a reduction in consciousnesses, if halogenated esters are administered slowly?

A

1 - analgesia (pain relief)
2 - excitement (agitated, delirium, enthusiasm)
3 - surgical anaesthesia (no pain in surgery or recollection of whats happened)

21
Q

Inhalation anaesthetics have 3 main adverse effects, what are they?

A

1 - post-operative nausea and vomiting (PONV)
2 - irritant, makes gas induction difficult (coughing)
3 - emergence phenomena (delirium)

22
Q

What are neuromuscular blocking agents (NMBA)?

A
  • drugs that block neuromuscular transmission at the neuromuscular junction
  • paralysis of the affected skeletal muscles follows
23
Q

Neuromuscular blocking agents (NMBA) are drugs that block neuromuscular transmission at the neuromuscular junction, causing paralysis of the affected skeletal muscles. Should these be given too conscious or unconscious patients?

A
  • only unconscious patients

- very distressing to have paralysis whilst conscious

24
Q

Neuromuscular blocking agents (NMBA) are drugs that block neuromuscular transmission at the neuromuscular junction, causing paralysis of the affected skeletal muscles. These are only administered once a patient is unconscious. What are the 2 main times NMBA are administered?

A

1 - facilitate intubation

2 - facilitate surgery of ventilation

25
Q

Neuromuscular blocking agents (NMBA) are drugs that block neuromuscular transmission at the neuromuscular junction, causing paralysis of the affected skeletal muscles. These are only administered once a patient is unconscious. They can be divided into 2 categories, what are they?

A

1 - depolarising

2 - non-depolarising

26
Q

Quaternary ammonium compounds are non-depolarising Neuromuscular blocking agents (NMBA). What is the mechanism of action of these drugs?

1 - competitively bind to ACh receptors
2 - bind to ACh in synaptic cleft and inhibit binding to ACh receptors
3 - inhibit ACh release from pre-synapse
4 - increase levels of acetylcholinesterase

A

1 - competitively bind to same site as ACh

- inhibit action potential in muscles without initially causing depolarisation

27
Q

Succinylcholine is a depolarising Neuromuscular blocking agents (NMBA). What is the mechanism of action of these drugs?

1 - competitively bind to ACh receptors
2 - bind to ACh in synaptic cleft and inhibit binding to ACh receptors
3 - inhibit ACh release from pre-synapse
4 - increase levels of acetylcholinesterase

A

1 - competitively bind to ACh receptors

  • initially they cause action potential and fasciculations (muscle twitch)
  • succinylcholine is not degraded by acetylcholinesterase so channels remain open
  • receptors become desensitised and eventually re-polarise and muscle relaxes
28
Q

Neuromuscular blocking agents (NMBAs) are used routinely by anaesthetists. What are some of the main purposes they are used for?

A
  • intubation (ICU)
  • surgery (especially if muscles do not relax)
  • ventilation
  • electroconvulsive therapy (suppress before giving therapy)
  • transfer of patients
  • lethal injection
29
Q

If a patient has been identified as having cholinesterase deficiency, why can the administration of succinylcholine, a depolarising neuromuscular blocking agent be bad?

A
  • cholinesterase degrades succinylcholine (choline in the name)
  • caused prolonged paralysis
30
Q

What is Botulinum toxin?

A
  • a purified substance derived from bacteria
  • blocks nerve signals to the muscle at pre-synapse
  • stops vesicles containing ACh from being released
  • muscle is not able to contract
31
Q

What is the most poisonous substance to humans that is known?

1 - rocuronium
2 - botulinum toxin
3 - succinylcholine
4 - entacapone

A

2 - botulinum toxin

- 2 nanograms/ml can kill