LHS Syllabus Drugs Flashcards
(33 cards)
Amiodarone
Class III antidysrhythmic drugs
Potassium channel block - repolarisation
Lengthen cardiac AP
Increase refractory period to stop ectopic beats and prevent re-entry
Treat tachycardia with Wolff-Parkinson-White syndrome.
Side effect: Supraventricular and ventricular tachyarrhythmias
Adrenaline
Adrenoceptor agonist
Used in cardiac arrest (B1), and to relieve bronchospasm in asthmatic attacks, anaphylactic shock (B2)
Side effects: hypertension, vasoconstriction, tachycardia
Amphetamine
Indirectly acting Sympathomimetic
Enters nerve terminal by uptake 1 and vesicles by vesicular mono amine transporter, in exchange for NA which accumulates in the cytosol
Some NA degraded by MAO
Some NA escapes in exchange for amphetamine via the NA transporter to act on post-synaptic receptors
Amphetamine reduces NA re uptake via transporter, enhancing NA action
Aspirin
Inhibit platelet aggregation, used in MCI therapy
Oldest NSAID
Weak acid, so stomach environment best for absorption but most actually in ileum due to SA from Microvilli
Inhibits prostaglandin synthesis by irreversibly inactivating cyclo-oxygenase (COX-1) and COX-2
Causes stomach bleeding because prostaglandins protect stomach cells
Atenolol
Beta-1 selective antagonist
Reduce sympathetic activity
Improves O2 supply –> reduce ischaemia cause of dysrhythmias
Lengthens AP to improve coordination
Reduce pacemaker to prevent ectopic beats
Treat angina, hypertension, dysrhythmias
Atropine
Non-selective muscarinic antagonist, competitive
Adjunct for anaesthesia (reduced secretions, bronchodilatation)
treat bradycardia because reduced parasympathetic inner action causes slight tachycardia but no change in ventricular contraction
Smooth muscle relaxation in bronchial, biliary, GI and urinary
Botulinum toxin
Inhibits vesicular release
Enzymatically cleaves docking proteins blocking their release
Treat muscle spasm, cervical dystopia, lower limb spasm associated with cerebral palsy, reduce wrinkles, treat hyperhydrosis
Digoxin
Cardiac glycoside
Cardiac slowing and reduced rate of contraction through AV node, giving more time for filling, increasing cardiac output
Increased force of contraction, due to more Na inside, less Ca extruded so more in SR
Increase vagal activity and inhibit Na/K pump, by binding to K+ site (low K+ reduces competition, increasing effect of glycoside)
As pump is electrogenic - inhibition can cause depolarisation - predisposing to disturbance of cardiac rhythm
Dobutamine
Beta-1 agonist, mimics sympathetic
Positively inotropic and chronotropic as elevates cAMP, PKA, phosphorylates Ca channels to increase probability that they will open
cAMP can increase if current, so increased number of AP in a given time
Treat cardiogenic shock
May cause dysrhythmias. Increase O2 consumption of the heart more than increase cardiac work, therefore reduced efficiency –> angina
Isoprenaline
Most potent ligand at B receptors, and he least at a receptors
Used to be used to treat asthma and heart block
Removed by tissue uptake and COMT
Risk of tachycardia and dysrhythmias
Lidocaine
Sodium channel blocker
Associates and dissociates quickly within normal heartbeat to abort premature beats and using as antidysrhythmic drug
Extend the effective refractory period to prevent re-entry as the propagation time is likely to fall below the length of the refractory period
Reduce risk of spontaneous depolarisation as excitability is reduced
Local anaesthetic - rapid onset and medium duration
Risk of dysrhythmias as reduces contractility which can reduce coronary flow leading to ischaemia
Neostigmine (physostigmine)
Anticholinesterase drugs so increase level of ACh at adrenergic synapses because it reduces its hydrolysis
Reverse the action of non-depolarising
neuromuscular-blocking drugs
Treat myasthenia gravis
Propranolol
Beta blocker (non-selective) Negatively inotropic and chronotropic Treat angina (as reduce cardiac work and increase cardiac efficiency), hypertension (because fall in cardiac output lowers blood pressure), cardiac dysrhythmias, anxiety tremor, glaucoma May cause bronchoconstriction
Salbutamol
Beta-2 agonist
Given by aerosol, can be oral or intravenous
Treat asthma by dilation of the bronchi and delay premature labour
Risk of tachycardia, dysrhythmias no peripheral vasodilation
Suxamethonium
Depolarising blocking agent of nicotinic acetylcholine receptors
More rapid onset so used for intubation
Agonists of receptor but remain bound for much longer producing prolonged depolarisation
Initially causes muscle twitching and then paralysis as Na channels become inactivated
Due to summation in slow twitch fibres it increases their force of contraction, but decreases in fast twitch because sodium channels become inactivated
Can be hydrolysed by butyrylcholinesterase but can have genetic inactive form, patient couldn’t recover
Tetrodotoxin
Voltage-gated sodium channel blocker
Inhibits action potentials by abolishing the upward stroke
Tubocurarine
Non-depolarising blocker of nicotinic acetylcholine receptor
Competitive antagonist
Increasing block causes a graded decrease in muscle contraction because more fibres are prevented from contraction
Acts on fast-twitch muscle fibres not slow, because fast-twitch have a single axon
Vecuronium
Neuromuscular blocking agent - non-depolarising , competitive antagonists
Modern alternative to tubocurarine as has a shorter action and fewer side effects
Verapamil
Calcium channel blocker
Slows conduction in the SA and AV nodes, as action potentials here have slow inward calcium current
Reduced ectopic beats in ischaemic cells, as AP here may also rely on Ca current
Class IV antidysrhythmic drug
Side effect: significant negative inotropy
Acetazolamide
Carbonic anhydrase inhibitor that acts in the PCT
Prevents the reabsoortion of bicarbonate, and hence sodium, chloride, H+, K+ and water
However not potent as effects can be modulated later in the tubule
Amiloride
Inhibits ENaC
Decreases K+ secretion, so is potassium sparing
Acts in the distal tubule
Limited efficacy as a diuretic as only a small amount of Na is reabsorbed here
Bendroflumethiazide
Inhibits the NaCl transporter in the distal tubule
They bind to the Cl binding site
Causes the loss of sodium, chloride and water
Risk of hypokalaemia as less sodium for NA/K ATPase
Furosemide
Loop diuretic that binds to the Cl binding site of NKCC transporter in the thick ascending limb
Reduces pumpin of sodium into the medullary interstitium refusing osmotic gradient
It increases NA delivery to the distal part causing loss of K and H, as affects Na/K ATPase and Na/H exchange
Insulin
Used to treat diabetes
Particularly in type 1 where receptors still exist b the pancreas can no longer produce insulin
