Pharmacology Flashcards
(30 cards)
What causes flaccid paralysis of the NMJ?
Results from prolonged stimulation in the presence of anti-cholinesterases.
What is a Mini end plate potential (m.e.p.p.) caused by?
When acetylcholine granules fuse with the post-synaptic membrane, without an impulse down the axon, and cause a small depolarisation.
What does maintaining muscle contraction require?
A series of asynchronous muscle fibre twitches.
What two drugs block the sodium channels in the NMJ?
Local anaesthetics
Tetrodotoxin
What are the effects of botulinum toxin on the NMJ?
inhibits the release of Ach.
What steps are involved in recovery of the NMJ?
Recovery of the nerve
Degradation of Ach
Repolarisation of the endplate
Muscle fibre relaxation
Does each muscle contract with an all-or-nothing response or is it each muscle fibre?
Each muscle fibre, whole muscle contraction is the summation of all the individual muscle fibres contracting.
What type of drug is vecronium and how does it block transmission at a NMJ?
Competitive antagonist of Ach.
Competes with Ach for binding at Type II nicotinic receptors at the NMJ.
What is the mode of action of Neostigmine and how is this related to Vecronium?
Inhibition of AchE, causing the rise in Ach at the junction
Can be used to reverse the action of vecronium.
What is the difference in using vecronium in patients with myasthenia gravis?
There is an enhanced effect, so the transmission block is enhanced.
This is because there are less nicotinic receptors.
What is the mode of action of suxamethonium?
It is chemically related to Acetylcholine so it will stimulate the nicotinic receptors but not be broken down by AChE, this causes flaccid paralysis, the end plate membrane will remain depolarised.
What eventually breaks down suxamethonium?
Plasma cholinesterases
Effect of myasthenia gravis on the action of suxamethonium?
Depolarising block is reduced, as there are fewer sites of action.
Differences in neostigmine and suxamethonium?
Vecronium: Competitive blocker, Reversed by neostigmine, Block enhanced in myasthenia gravis.
Suxamethonium: Depolarising blocker, Unchanged by neostigmine, Block reduced in myasthenia gravis.
Three anticholinesterases and their clinical uses ?
Edrophonium: Short acting and used in the diagnosis of myasthenia gravis.
Neostigmine: Used to reverse competitive block and to treat myasthenia gravis, will not diffuse across blood-brain barrier.
Physostigmine: Will cross blood-brain barrier, used to treat glaucoma.
What type of drug in an organophosphate?
Irreversible AChE inhibitor.
Treatment of organophosphate poisoning?
Pralidoxime - cleaves Organophosphate-AchE complex.
Artificial respiration (respiratory muscles are paralysed).
Atropine to reverse the overactivity of the parasympathetic nervous system.
What limits the duration of action of thiopentone?
The fact it is distributed into muscle (later into fat)
Usually is a distinct distribution phase seen in oral administration of a drug? Why? What is seen?
Usually there is no distinct distribution phase as absorption is slow from the small intestine and so distribution is essentially complete as soon as absorption is.
A slow rise to peak concentration is soon (usually about an hour after administration)
How is levodopa transported into the brain? what implications does this have?
Through the large neutral amino acid transporter
This means if a amino-acid rich meal (e.g. lots of protein), or amino acids is given less levodopa will make it into the brain
Why do salicylates slowly enter the brain?
They are water-soluble
Tolerance to what effects of morphine develop slowly/not at all?
Respiratory depression
Constipatory
What drug is used in acute opiate overdose?
Naloxone
What type of pain is tacked more effectively by opiates?
Dull chronic pain
