Anaesthetic Drugs Flashcards
What is the mechanism of action of lidocaine?
Binds to and blocks the cytoplasmic side of Na+ channels, preventing the influx of sodium (thereby preventing action potentials along neuronal cells).
What is the mechanism of action of suxamethonium?
This is a depolarising neuromuscular blocker. It is essentially two molecules of ACh bound together, which causes depolarisation of the NMJ, but it remains bound to the nicotinic receptor, preventing further depolarisation.
What is the mechanism of action of rocuronium?
This is a non-depolarising neuromuscular blocker. Upon binding to the nicotinic receptors of the NMJ, it acts as a competitive antagonist (i.e., it prevents depolarisation of the motor end-plate)
What is the mechanism of action of neostigmine?
Neostigmine is an anticholinesterase, i.e., it binds to and inhibits the action of cholinesterase. This means that less ACh is broken down, which allows it to accumulate to levels where it will displace drugs bound to the nicotinic receptors (e.g., vecuronium or rocuronium)
What is the mechanism of action of sevoflurane?
This is poorly understood but is most likely to involve the following:
- Increased sensitivity (i.e., activation) of GABA-A receptors (more likely to allow an influx of Cl-)
- Excitation of inhibitory glycine receptors
- Inhibition of excitatory nicotinic receptors
What is the mechanism of action of fentanyl?
Fentanyl (like morphine) is a mu-opioid agonist. These receptors are present on both pre- and post-synaptic neurons.
- Pre-synaptically, mu-opioid agonism causes activation of a G-protein which causes inhibition of calcium channels (thereby preventing the pre-synaptic release of neurotransmitters)
- Post-synaptically, mu-opioid agonism causes the openin of K+ channels, which hyperpolarises the post-synaptic cell
What is the mechanism of action of morphine?
Fentanyl (like morphine) is a mu-opioid agonist. These receptors are present on both pre- and post-synaptic neurons.
- Pre-synaptically, mu-opioid agonism causes activation of a G-protein which causes inhibition of calcium channels (thereby preventing the pre-synaptic release of neurotransmitters)
- Post-synaptically, mu-opioid agonism causes the openin of K+ channels, which hyperpolarises the post-synaptic cell
What is the mechanism of action of glycopyrulate?
This is a competitive antagonist of muscarinic ACh receptors. It is used to counter the cholinergic actions of neostigmine primarily in the heart (i.e., it prevents Vagal stimulation of the heart by exhibiting competitive antagonism at myocardial muscarinic receptors)
What is the mechanism of action of midazolam?
Midazolam is a benzodiazepine, which means that it binds to the benzodiazepine receptor (near the GABA-A receptor), which increases the frequency of opening of Cl- channels (thereby increasing the inhibitory activity in the CNS).
What is the mechanism of action of ketamine?
Ketamine is a dissociative anaesthetic that has many, many actions throughout the CNS. Its main function though is that it acts as a potent NMDA receptor antagonist.
What is the mechanism of action of metaraminol?
Metaraminol is a mixed sympathomimetic agonist (i.e., a vasoconstrictor) that acts predominantly at alpha-1 adrenergic receptors. It is used to counter the hypotension that many anaesthetic agents can cause.
What is the mechanism of action of co-amoxiclav?
This is just a combination of amoxicillin and clavulanic acid
Amoxicillin is a B-lactam antibiotic
Clavulanic acid is a B-lactamase inhibitor
Why are glycopyrolate and neostigmine often given together?
Because neostigmine causes an increase in ACh at all cholinergic receptor sites, which can cause increased Vagal stimulation at the heart (causing bradycardia). Glycopyrolate prevents these negative muscarinically-mediated effects.
What is the main reason for RSI being used instead of a normal anaesthetic induction and intubation?
RSI is used when the patient is at a high risk of pulmonary aspiration or impending airway compromise. Because RSI is a faster process, there is less time between induction of anaesthesia and intubation.
How does the sequence of RSI differ from a normal intubation?
Normally, after a patient has been paralysed, they will be ventilated with a bag-mask. However, in a patient at risk of aspiration or vomiting the bag-mask ventilation can cause gastric inflation and increase the risk of vomiting. Therefore, in RSI, as soon as the muscle relaxant is given, intubation will be attempted.
