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BS314 Pharmacology
Lecture 1-6 drug notes
| Question | Answer |
|---|---|
| Drugs that affect neuronal transmission in parasympathetic and sympathetic pathways | cholinergic drug and adrenergic drugs |
| Difference between Sympathetic pathway and parasympathetic pathway | Postganglionic neurons: Adrenergic(sym), Cholinergic(parasym) Target tissue transmission: NE/Epi-AdrenergicR alpha or beta (sym) and ACh-CholinergicR muscarinic (parasym) |
| Drugs that can be hydrolysed by Acetylcholinesterase | acetylcholine and methacholine |
| binding affinity of ACh and MCh | ACh binds to mus and nic receptors with high affinity but MCh binds to mus receptors with high affinity and binds with low affinity to nicotinic receptors |
| Cholinergic drug that prevents ACh packaging into vesicles | Vesamicol |
| how hemicholinium affects synthesis of ACh in parasympathetic pathway? | inhibits the energy-dependent carrier system that co-transports Na+ with choline from extracellular fluid into cytoplasm of cholinergic neuron |
| what does botulinum toxin blocks? | Blocks exocytosis (vesicle containing ACh cannot fuse at nerve ending to release the neurotransmitters) |
| Non-depolarising blocking agents that block pre/post-synaptic nic ACh receptor | tubocurarine |
| Acetylcholine is hydrolyzed to ________ and ________before being recycled back into presynaptic neuron via choline carrier | acetate and choline choline is transported back via choline carrier to be recycled and packaged into vesicles |
| Drug(s) that prevent breakdown of ACh | Anticholinesterases: neostigmine,edrophonium (reversible) and organophosphates (irreversible) |
| A person have accidentally injested organophosphate(sarin gas). How would you treat them? | treat with Pralidoxime and atropine |
| Mechanism by which organophosphate acts and egs of drugs | organophosphate phosphorylates enzyme at the catalytic site and no spontaneous catalysis can occur |
| neostigmine action as a medium-duration drug compared to edrophonium as a short-acting drug | neostigmine has stronger binding cos it occupies both the catalytic and anionic sites hence takes a longer time for the carbamyl group in the catalytic site to break down. However edrophonium binds only at the anionic site of the enzyme |
| examples of organophosphate | Dyflos, echothiophate, parathion, sarin |
| What are the cholinergic agonists? | ACh, Carbachol, Bethanechol, Pilocarpine |
| examples of organophosphate | Dyflos, echothiophate, parathion, sarin |
| What are the cholinergic agonists? | ACh, Carbachol, Bethanechol, Pilocarpine |
| Drug to treat urine retention | bethanechol (stimulate bladder sm muscle contraction to release urine) can treat bladder and gastrointestinal hypotonia |
| therapeutic uses of anticholinesterases | myasthenia gravis, glaucoma, Alzheimer's and reverse non-depolarising neuromuscular block |
| What is myasthenia gravis | serious muscle weakness caused by antibodies blocking Ach receptors at the postsynaptic neuromuscular junction |
| what is glaucoma | loss of retinal ganglionic cells that is caused by increased intraocular pressure treated with echothiopate |
| what is bradycardia | slow resting heart rate (compared to normal) caused by reduced firing at SA node or by block at SA node |
| general side effects of cholinergic stimulation | sweating, salivation, flushing, decreased bld pressure, nausea, abdominal pain, diarrhea, bronchospasm |
| Treatment drugs for glaucoma and how. | Pilocarpine= stimulates circular sm contraction, increase drainage of aqueous humour and reduce intraocular pressure Carbachol= cause papillary contraction and decrease intraocular pressure beta-AR blocker = timolol |
| Atropine has opposite effects of __________ | pilocarpine |
| side effects of pilocarpine treatment for glaucoma | sweating and salivation |
| What is timolol? | beta-adrenergic blocker to treat glaucoma but not effective for immediate decrease of intraocular pressure |
| treatment drugs for myasthenia gravis | neostigmine(long duration) and edrophonium (short duration) |
| What is the action of Tubocurarine? | block presyn and postsyn nic ACh receptors |
| Drug that initiate opposite effects of tubocurarine | Suxamethonium: depolarising blocking agent that stimulates postsyn nic ACh receptor |
| which drugs belong to muscarinic agonists category? | bethanechol and pilocarpine |
| Muscarinic antagonists | atropine, scopolamine(anti-emtic drug), ipratropium(treat asthma & bronchitis), pirenzepine (treat peptic ulcer), darifenacin(treat urinary incontinence) |
| Atropine clinical uses | adjunct for anaesthesia, anticholinesterase poisoning, bradycardia,gastrointestinal hypermotility(antispasmodic) |
| inhibitor of gastric secretions by action on ganglionic cells | pirenzepine |
| Ganglionnic agonists | nicotine: initial stimulatory effects but prolonged depolarization leads to blockade (depolarising block) |
| Ganglionic blockers | agonists= nicotine (stimulate then block) antagonists= hexamethonium, trimetaphan (transmission block) |
| Nicotinic drugs at NMJ | Agonists= succinylcholine Antagonists = tubocurarine,pancuronium, atracurium, vecuronium |
| depolarising blocking agent | suxamethonium = succinylcholine Act as muscle relaxant |
| Action mechanism of depolarising blocking agents | Phase1: excitation Phase2: blockade (drug bound to receptor too long thus loss of excitability of Na+ channel) |
| Side effects of tubocurarine | may induce histamine release lower bld pressure promote ganglionic blockade |
| Drugs affecting NE synthesis | alpha-methyltyrosine carbidopa disulfiram |
| describe the NE synthesis and what are the enzymes involved | refer to notes lec2 pg8 |
| drugs affecting NE storage | reserpine = deplete NE stores by blocking NE storage vesicle MAO inhibitor= affect NE metabolism into metabolites so this drug increases NE at nerve ending methyldopa=gives rise to false NT, methylNE hence lowering level of NE transmission |
| How methylNE reduces NE release | MethylNE is specific to alpha2 receptors, which leads to negative feedback on NE release |
| Reuptake of NE | 2 ways: uptake1(presyn) and uptake2(postsyn)1 Uptake1 is most impt |
| Drugs affecting NE release | direct= guanethidine (exocytosis) indirect= amphetamine (uptake1) |
| What are sympathomimetics? | Sympathomimetics are drugs that mimic adrenergic effects (amphetamine) |
| decrease in heart electrical conduction | decrease in heart rate |
| sodium-potassium pump | 3Na+ out and 2K+ in |
| sodium-calcium pump | 3Na+ in and 1Ca2+ out |
| Name 3 beta antagonists | timolol propranolol metoprolol |
| Name alpha antagonists | tamsulosin prazosin phentolamin(reversible) phenoxybenzamine(irreversible) |
| treatment drugs for angina | metoprolol(selective) and propranolol(nonselective) |
| Common actions of alpha/beta receptor activation | alpha-R:vasoconstriction,decrease GIT motility beta1-R:increase heart rate&CO,renin release beta2-R:vasodilation in artery to skeletal muscle,contract spincter muscle,relax detrusor muscle of bladder, bronchial sm relaxation |
| Clinical uses of beta antagonists | Angina, hypertension, cardiac dysrhythmias |
| Treatment drugs for asthma | Epinephrine, Isoproterenol, Salbutamol |
| treat heart failure | dobutamine (beta1 agonist) |
| alpha agonist used for (phenylephrine or pseudoephedrine, methoxamine) | nasal decongestion (by causing vasoconstriction there will be less fluid build up hence relief nasal blockade) |
Created by:
moonstars87
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