Sedation and general anaesthesia Flashcards

1
Q

Explain the role of sedation in dentistry

A
  • Make is possible to treat anxious/ phobia patients
  • Ensure unpleasant procedures don’t cause distress to the patient
  • To avoid general anaesthesia for patients with special needs
  • Avoid onset of medical conditions that are triggered/ aggravated by stress
  • For medical conditions affecting the patient’s ability to cooperate
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2
Q

Remember the names of drugs used to sedate patients for PAINLESS dental procedures

A

First line drugs (wide margin of safety)
Benzodiapzines
• Children: Midazolam
• Adult: diazepam, triazolam, lorazepam

Second-line drugs (narrow margin of safety, specialist technique)
• Propofol
• Sevoflurane

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3
Q

Remember the names of drugs used to sedate patients for PAINFUL dental procedures

A

• Consider local anaesthetic in all cases

Minimal to moderate sedation:
• Nitrous oxide (inhalation)
• Benzodiazepines

Moderate sedation:
• Ketamine (IV or IM)

General anaesthesia:
• Propofol + fentanyl (IV, specialist technique)

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4
Q

Define minimum alveolar concentration (MAC)

A
  • The alveolar concentration of an inhaled anaesthetic at which 50% of patients will respond well i.e, no motor response to an incision
  • 99% will not respond to 1.3 MAC
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5
Q

List the disadvantages of oral sedation

A
  • Takes long for drug to take effect
  • Unreliable drug absorption
  • Inability to achieve desired drug effect (lack of titration)
  • Prolonged duration of action: 3 to 4 hours
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6
Q

Define “never events”

A
  • Death or severe harm as a result of overdose of midazolam injection
  • Death or severe harm as a result of the administration of the wrong gas, or failure to administer any gas, through a line designated for medical gas pipeline systems (MGPS) or through a line connected directly to a portable gas cylinder.
  • Death or severe harm as a result of failure to monitor or respond to oxygen saturation levels in a patient undergoing general or regional anaesthesia
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7
Q

Describe the mode of action of glutamate

A
  • Glutamate is a powerful excitatory neurotransmitter
  • It is released by nerve cells in the brain
  • Glutamate is released by the pre-synaptic neuron
  • It binds to ligand-gated ion channels in the post synaptic neuron
  • This allows Na+ ions to come in and cause depolarisation
  • When the electrical potential goes from -65mV to -40mV, voltage gated sodium channels will open. This allows even more Na+ to enter and cause -40mV to go to 40mV
  • Action potential occurs
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8
Q

Describe the mode of action of GABA

A
  • GABA is an inhibitory neurotransmitter
  • GABA molecules bind to their receptors called GABAA
  • This allows Cl- ions to enter the neuron. Since Cl- is negatively charged, it drops the electrical potential of the membrane further
  • It also means that a huge amount of glutamate molecules will be required to raise the electrical potential and generate an action potential
  • Thus, high levels of GABAergic transmission decrease action potentials
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9
Q

List the mode of administration and describe the mechanism of action of benzodiazepines: Drug names; most end with lam or pam

A

Mode of administration
• IV sedation
• Minimum to moderate anaesthesia

Mechanism of action
• Benzodiazepines act as a sedative; slowing down the body’s functions
• They work by increasing the effect of GABA
• Bind to “benzodiazepine receptors”located between alpha and gamma subunits of GABAA receptor
• After binding, it increases the frequency of the chloride ion channel opening, thereby increasing the inhibitory effect of GABA on neuronal excitability
• GABA needs to be present for benzodiazepine effects to be detectable
• Works in the limbic system, thalamus & hypothalamus

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10
Q

List the mode of administration and describe the mechanism of action of propofol

A

Mode of administration
• IV sedation
• General anaesthesia

Mechanism of action
• Propofol increases GABAergic transmission.
• Binds to beta sites on GABAA receptor
• This increases the affinity of GABAA receptor to GABA
• Also, it decreases the rate of dissociation of the GABA from the receptor = longer GABAergic effect
• In addition, it will block the pores of voltage gated sodium channels to stop Na+ from coming in = no action potential

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11
Q

Describe the mechanism of action of magnesium in blocking transmission

A
  • A NMDA receptor (glutamate receptor) opens, when 2 molecules of glutamate bind to it
  • When the channel is open it allows cations to come in, especially Na+ ions = depolarisation
  • Mg+ can block NMDA pores = no action potential
  • If the voltage changes, Mg+ will no longer block the pore and an action potential can be generated
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12
Q

List the mode of administration and describe the mechanism of action of ketamine

A

Mode of administration
• IV sedation
• Moderate anaesthesia to general anaesthesia

Mechanism of action
• Binds to inside pore of NDMA receptor and blocks it
• Na+ ions cannot pass through = no depolarisation = no action potential
• Neuronal activity decreases = sedation

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13
Q

List the mode of administration and describe the mechanism of nitrous oxide

A

Mode of administration
• Inhalation
• Minimum to moderate anaesthesia

Mechanism of action
• Binds to inside pore of NDMA receptor and blocks it
• Na+ ions cannot pass through = no depolarisation = no action potential
• Neuronal activity decreases = sedation
• K2P receptors normally allow K+ to leave the cell, allows the neuron to polarise again
• N20 bids to K2P receptors to keep it open for longer so that K+ can continue leaking and cause the electrical potential to remain negative for longer

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