Drugs
This document was uploaded by user and they confirmed that they have the permission to share it. If you are author or own the copyright of this book, please report to us by using this DMCA report form. Report DMCA
Overview
Download & View Drugs as PDF for free.
More details
- Words: 556
- Pages: 5
December 2005
Drugs – baby! At the Neuromuscular Junction: (the junction between a motor neurone and a muscle cell.) 1. An Action potential flows along the motor neurone to the presynaptic end. 2. Ca2+ flows into presynaptic terminal, causes vesicles of ACh to be released 3. ACh crosses synaptic cleft, bind to nicotinic receptors on muscle end-plate. 4. Voltage-gated Na+ channels open, and Na+ enters muscle cell, causing a depolarisation. 5. Depolarisation flows along muscle cell and causes contraction. 6. ACh is broken down to choline and acetate, which can be reused. Drug
What it does
What it is used for
Notes
Hemacholinium
Prevents choline from entering presynaptic terminal, so ACh cannot be synthesised
No therapeutic use
Vesamicol
Prevents ACh from entering vesicles
No therapeutic use
Tetrotoxin
Blocks Na+ channels in motor neurone, so stops AP
No therapeutic use
Puffer-fish Poison!
Botulinum
Prevents fusion of vesicle to membrane, so ACh is not released
No therapeutic use
Poison!
Atracurium
Non-depolarising blocker. Blocks Nicotinic receptor, no depolarisation of muscle so no contraction
Used along with general anaesthesia
Relieved by anticholinesterase.
Suxamethonium
Depolarising blocker. Blocks nicotinic receptor and causes a short depolarisation, followed by inactivation of receptor
Short duration of action, so used for quick procedures such as intubation.
Not relieved by anti-cholinesterase.
Edrophonium
Short-acting Anti-cholinesterase.
Diagnosis of Myasthenia gravis.
1
December 2005 Neostigmine
Medium-acting Anti-cholinesterase
Treatment of Myasthenia gravis.
Ecothiopate
Long-lasting Anti-cholinesterase
Treatment of glaucoma
Sarin
Long-lasting Anti-cholinesterase
No therapeutic use
Direct-acting muscle relaxant
Used to save the life of people with Malignant Hyperthermia (who can die if they are given suxamethonium)
Dantrolene
2
Nerve Gas!
December 2005 In the Parasympathetic NS:
Muscarinic Receptors, five types: M1 – Stomach M2 – Heart M3 – Smooth muscle / exocrine glands M4/M5 – Brain Effects: (think R ‘n R) • Contracts gut • Contracts Bladder • Contracts Bronchioles • Decreases HR, BP and force of heart • Increases secretions • Contracts pupils Agonists – mimic these effects (parasympathomimetics) Antagonists – block Parasympathetic NS, so sympathetic NS predominates. Parasympathetic Agonists Bethanechol
Kick starts GI tract and bladder after a long Op, used to prevent constipation.
Pilocarpine
Treatment of Glaucoma (contraction of pupil releases pressure) Parasympathetic Antagonists
Atropine
Cardiac arrest – kick starts heart.
Hyoscine
Motion sickness, “pre-op” to dry up secretions..
Tropicamide
Dilates pupil for eye examination (raises intraocular pressure so don’t give if patient has glaucoma!)
3
December 2005 In Sympathetic NS: NA / adreno Long post-ganglion
CNS
(ACh / Mus in sweat glands)
Effector organ
ACh / Nic
4 main types of Adrenergic Receptor: α 1: Activates PLC, forms IP3 and DAG. α 2: Inactivates adenylyl cyclase, decreases cAMP. β 1: Activates adenylyl cyclase, increases cAMP. β 2: Activates adenylyl cyclase, increases cAMP. (β3: in adipose tissue, involved in lipid metabolism) Effects of Sympathetic NS (think Fight or Flight): • Relaxes GI tract • Relaxes Bladder • Dilates bronchioles • Increases HR, BP, force of contraction • Less secretion • Dilates pupils • Piloerection α1 Agonist
NA / A Phenylephrine
α2 Agonist
NA / A Clonidine
α1 Antagonist α2 Antagonist
Phenyoxybenzamine Doxazosin
Nasal Decongestion
Decrease BP in people with hypertension.
β1 Agonist
NA / A
β2 Agonist
A Salbutamol
Treatment of Asthma (it dilates the bronchioles)
β1 Antagonist
Atenolol Propanolol
“Beta-blockers” after an MI, for Angina, cardiac arrhythmias, hypertension.
4
(don’t need to know β2 antagonist)
5
December 2005
Drugs – baby! At the Neuromuscular Junction: (the junction between a motor neurone and a muscle cell.) 1. An Action potential flows along the motor neurone to the presynaptic end. 2. Ca2+ flows into presynaptic terminal, causes vesicles of ACh to be released 3. ACh crosses synaptic cleft, bind to nicotinic receptors on muscle end-plate. 4. Voltage-gated Na+ channels open, and Na+ enters muscle cell, causing a depolarisation. 5. Depolarisation flows along muscle cell and causes contraction. 6. ACh is broken down to choline and acetate, which can be reused. Drug
What it does
What it is used for
Notes
Hemacholinium
Prevents choline from entering presynaptic terminal, so ACh cannot be synthesised
No therapeutic use
Vesamicol
Prevents ACh from entering vesicles
No therapeutic use
Tetrotoxin
Blocks Na+ channels in motor neurone, so stops AP
No therapeutic use
Puffer-fish Poison!
Botulinum
Prevents fusion of vesicle to membrane, so ACh is not released
No therapeutic use
Poison!
Atracurium
Non-depolarising blocker. Blocks Nicotinic receptor, no depolarisation of muscle so no contraction
Used along with general anaesthesia
Relieved by anticholinesterase.
Suxamethonium
Depolarising blocker. Blocks nicotinic receptor and causes a short depolarisation, followed by inactivation of receptor
Short duration of action, so used for quick procedures such as intubation.
Not relieved by anti-cholinesterase.
Edrophonium
Short-acting Anti-cholinesterase.
Diagnosis of Myasthenia gravis.
1
December 2005 Neostigmine
Medium-acting Anti-cholinesterase
Treatment of Myasthenia gravis.
Ecothiopate
Long-lasting Anti-cholinesterase
Treatment of glaucoma
Sarin
Long-lasting Anti-cholinesterase
No therapeutic use
Direct-acting muscle relaxant
Used to save the life of people with Malignant Hyperthermia (who can die if they are given suxamethonium)
Dantrolene
2
Nerve Gas!
December 2005 In the Parasympathetic NS:
Muscarinic Receptors, five types: M1 – Stomach M2 – Heart M3 – Smooth muscle / exocrine glands M4/M5 – Brain Effects: (think R ‘n R) • Contracts gut • Contracts Bladder • Contracts Bronchioles • Decreases HR, BP and force of heart • Increases secretions • Contracts pupils Agonists – mimic these effects (parasympathomimetics) Antagonists – block Parasympathetic NS, so sympathetic NS predominates. Parasympathetic Agonists Bethanechol
Kick starts GI tract and bladder after a long Op, used to prevent constipation.
Pilocarpine
Treatment of Glaucoma (contraction of pupil releases pressure) Parasympathetic Antagonists
Atropine
Cardiac arrest – kick starts heart.
Hyoscine
Motion sickness, “pre-op” to dry up secretions..
Tropicamide
Dilates pupil for eye examination (raises intraocular pressure so don’t give if patient has glaucoma!)
3
December 2005 In Sympathetic NS: NA / adreno Long post-ganglion
CNS
(ACh / Mus in sweat glands)
Effector organ
ACh / Nic
4 main types of Adrenergic Receptor: α 1: Activates PLC, forms IP3 and DAG. α 2: Inactivates adenylyl cyclase, decreases cAMP. β 1: Activates adenylyl cyclase, increases cAMP. β 2: Activates adenylyl cyclase, increases cAMP. (β3: in adipose tissue, involved in lipid metabolism) Effects of Sympathetic NS (think Fight or Flight): • Relaxes GI tract • Relaxes Bladder • Dilates bronchioles • Increases HR, BP, force of contraction • Less secretion • Dilates pupils • Piloerection α1 Agonist
NA / A Phenylephrine
α2 Agonist
NA / A Clonidine
α1 Antagonist α2 Antagonist
Phenyoxybenzamine Doxazosin
Nasal Decongestion
Decrease BP in people with hypertension.
β1 Agonist
NA / A
β2 Agonist
A Salbutamol
Treatment of Asthma (it dilates the bronchioles)
β1 Antagonist
Atenolol Propanolol
“Beta-blockers” after an MI, for Angina, cardiac arrhythmias, hypertension.
4
(don’t need to know β2 antagonist)
5
December 2005
