B1 Flashcards
Atropine
An antimuscarinic agent
MoA: Atropine binds to and inhibits the muscarinic acetylcholine receptor.
Use: It prevents/abolishes bradycardia or asystole produced by injection of choline esters, anticholinesterase agents or other parasympathomimetic drugs, and cardiac arrest produced by stimulation of the vagus. Atropine may also lessen the degree of partial heart block when vagal activity is an etiologic factor.
Betamethasone
Betamethasone is a glucocorticoid receptor agonist
MoA: Binding of betamethasone to the glucocorticoid receptor, forms a complex, which moves to the nucleus, binds DNA causing alteration in gene transcription. This alter gene transcription causes the production of lipocortins, which inhibits phospholipase A2, and therefore reduces the biosynthesis of prostaglandins and leukotrienes.
Use: Anti-inflammatory, immunosuppressive and anti-mitogenic effects of steroids.
Digoxin
A cardiac glycoside
MoA: Inhibition of the Na-K-ATPase membrane pump, resulting in an increase in intracellular sodium. This causes in turn the sodium calcium exchanger (NCX) to extrude the sodium and pump in more calcium. High calcium is thought to promote activation of contractile proteins (e.g. actin, myosin).
Digoxin also acts on the electrical activity of the heart, increasing the slope of phase 4 depolarization, shortening the action potential duration, and decreasing the maximal diastolic potential.
Use: Treatment of congestive heart failure, and supraventricular arrhythmias. Still used in AF, but now very much third line treatment option. Rarely used in heart failure as much better drugs available
Edrophonium
Rapid-onset, short-acting cholinesterase inhibitor
MoA: Prolongs the action acetylcholine, via inhibiting acetylcholinesterase at sites of cholinergic transmission.
Edrophonium increases the amount of acetylcholine at the nerve endings, therefore allowing the remaining receptors to function more efficiently.
Use: Cardiac arrhythmias + diagnosis of myasthenia gravis (MG) – Tensilon test; otherwise pyridostigmine used for MG
Simulation of nicotinic acetylcholine receptors cause what?
Muscle contraction
Ketoconazole
Broad spectrum anti-fungal agent.
MoA: Inhibition of 14-α demethylase, a cytochrome P-450 enzyme which converts lanosterol to ergosterol.
This inhibition of ergosterol causes increased fungal cellular permeability.
Morphine
Opiate
MoA: Binds to mu-opioid receptors. GABA inhibitory interneurons – morphine inhibits the activity of these and therefore limits the descending pain inhibition pathway. Therefore, without the inhibitory signals, pain modulation can proceed downstream
Naloxone
Opiate antagonist
MoA: Antagonise all 3 opioid receptors (Mu, Kappa, and Gamma), although it has the strongest binding to the Mu receptor.
Use: prevents or reverses the effects of opioids (resp depression, sedation, hypotension)
Tamoxifen
Selective oestrogen receptor modulator (SERM)
MoA: Binding of to the oestrogen receptor (ER), leading to a conformational change in the receptor and therefore altering the expression of oestrogen dependent genes.
Suxamethonium
A depolarising skeletal muscle relaxant.
Class: ACh analogue
MoA: Mimic acetylcholine at the neuromuscular junction. Suxamethonium is hydrolysed much slower than ACh, causing prolonged depolarisation and therefore desensitisation, and muscle relaxation. Unlike the non-depolarising neuromuscular blocking drugs.
Note: Suxamethonium cannot be reversed and recovery is spontaneous. Suxamethonium is given after a general anaesthetic as muscle relaxation can be preceded by painful muscle fasciculations.
Neostigmine
Anticholinesterase
Use: Used together with atropine to end the effects of neuromuscular blocking medication of the non-depolarising type.
Tubocurarine
Neuromuscular blocker
MoA: Tubocurarine binds stereo-selectively to nicotinic-cholinergic receptors at the autonomic ganglia, the adrenal medulla, neuromuscular junctions, and in the brain.
Use: Has 2 main effects, stimulation and reward. The stimulatory effect occurs mainly in the cortex via the locus ceruleus whilst the reward effect is exerted in the limbic system. At low doses the stimulant effects predominate while at high doses the reward effects predominate.
Note: Tubocurarine has been superceded by Suxamethonium as the clinically used depolarising neuromuscular blocker
Pyridostigmine
A cholinesterase inhibitor
MoA: Reversible inhibition of acetylcholinesterase in the synaptic cleft by competing with acetylcholine for attachment to acetylcholinesterase. This inhibition leads to a reduction in the hydrolysis of acetylcholine, prolonging its effects.
Note: Pyridostigmine is a quaternary amine therefore it is poorly absorbed in the gut and doesn’t cross the blood-brain barrier.
