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WEEK 6:
Autonomic Pharmacology:
| Question | Answer |
|---|---|
| aChE | acetylcholinesterase |
| IHD | ischaemic heart disease |
| BO | botanical origin |
| cAMP | cyclic adenosine monophosphate |
| GIT | gastrointestinal tract |
| mAChR | muscarinic acetylcholine receptor (metabotropic) |
| nAChR | nicotinic acetylcholine receptor (ionotropic) |
| PKA | protein kinase A |
| adrenergic receptors | receptors on cell surface responding to adrenaline/epinephrine and noradrenaline/norepinephrine |
| alpha-1 receptor function (5) | vasoconstriction, increase peripheral resistance (blood flow), mydriasis (pupil dilation), increase closure of bladder sphincters |
| alpha-2 receptor function (3) | inhibits norepinephrine release, inhibits Ach release, inhibits insulin release |
| beta-1 receptor function (4) | increase heart rate, increase myocardial contractility, increase lipolysis, increase renin |
| beta-2 receptor function (6) | vasodilation, decrease peripheral resistance, bronchodilation, increase glycogenolysis (in muscle + liver), increase glucagon release, relaxes uterine smooth muscle |
| neurotransmitter which works best in alpha 1 | NE>E |
| neurotransmitter which works best in alpha 2 | E>N |
| neurotransmitter which works best in beta 1 | E=NE |
| neurotransmitter which works best in beta 2 | E>>NE |
| B1 'cardiac' signaling mechanisms | increased cAMP -> increased PKA -> increased phosphorylation of Ca2+ channels + activate them -> increase Ca2+ influx -> cardiac contraction |
| B2 'smooth muscle' signaling mechanisms | increase cAMP -> increase PKA -> increase phosphorylation of contractile proteins -> smooth muscle relaxation |
| A1 'smooth muscle' signaling mechanisms | increase Ca2+ -> smooth muscle contraction |
| A2 'smooth muscle' signaling mechanisms | decreases cAMP -> decreases PKA -> decreases phosphorylation of contractile proteins -> smooth muscle contraction |
| agonists | drugs that activate adrenoceptors |
| antagonists | drugs that block adrenoceptors |
| drugs affecting sympathetic activity | drugs activating adrenoceptors (agonists), drugs blocking adrenoreceptors (antagonists), indirectly acting sympatholytics, indirectly acting sympathomimetics |
| example of agonists/ sympathomimetics | adrenaline + salbutamol |
| example of antagonists/ sympatholytics | propranolol |
| indirectly acting sympatholytics | drugs that inhibit noradrenaline synthesis |
| indirectly acting sympathomimetics | drugs that interfere with NA storage, promote NA release, reduce NA reuptake (eg cocaine) |
| how do adrenoceptor antagonists help treat ischaemic heart disease (IHD) and hypertension | reduce cardiac load during heart beat by reducing heart rate + output (decreases heart sympathetic tone which is mediated by B1 adrenoceptors) |
| hypertension | increased peripheral vascular resistance |
| example of indirectly acting sympathomimetics that reduce NA reuptake | cocaine |
| propranolol | non selective B blocker (bind to both B1+B2 receptors) + administered orally |
| asthma | constriction of bronchioles, reduces air flow to lungs |
| asthma symptoms | wheezing, breathlessness, coughing, in severe attack can faint |
| what triggers asthma | allergens, pollen, pet dander, dust mites |
| what can be used to treat asthma | sympathomimetics (adrenoceptor agonists) eg salbutamol |
| contraindication | situation where drug should not be used because it is harmful to patient |
| why should you not prescribe propranolol to an asthmatic who has IHD | propranolol is a B2 antagonist -> block B2 receptor -> bronchoconstriction -> bronchospasm |
| how do you treat an asthmatic who has IHD | use atenolol (antagonist which is cardiac selective at B1) |
| directly acting sympathomimetics (agonists) example | adrenaline (intravenous adrenaline - epipen) |
| anaphylactic shock | hypersensitive immune response |
| what beta and alpha receptors does an epipen (intravenous adrenaline) act on | B2 (bronchodilation), B1 (increases heart rate, cardiac output thus increasing blood pressure), A2 ( peripheral vasoconstriction -> increase blood pressure) |
| indirectly acting sympathomimetic drugs example | amitriptyline, amphetamine, cocaine |
| indirectly acting sympathomimetic drugs pathway | (1- tyrosine is synthesised into NA which is stored into vesicles using VMAT) (2- AP causes NA to leave + bind to either B or A receptor) (3- NA reuptake or broken down by MAO into metabolites) |
| atropine | parasympatholytic + anti-muscarinic (competitively blocks PNS muscarinic receptors and some CNS) |
| (heart) SA node effect + muscarinic receptor when stimulated | M2 receptors decrease heart rate |
| (heart) atrial muscle effect + muscarinic receptor when stimulated | M2 receptors decrease force in heart |
| (bronchi) smooth muscle muscarinic receptor + effect when stimulated | M3 constrict bronchi smooth muscle |
| symptoms showing affected parasympathetic nervous system/ atropine poisoning | mydriasis (dilated pupils), blurred vision, tachycardia, hot but not sweaty, dry mouth, urinary urgency + no retention, excitable, disorientated, like they have eaten berries |
| mydriasis meaning | dilated pupils |
| mAChR signaling mechanisms | M3, M2, M1 |
| explain the parasympathetic control of bladder function | stretch receptor -> sensory fibre in pelvic nerve -> interneuron (spinal cord) -> projection fibres in thalamus -> cerebral cortex -> parasympathetic preganglionic motor fibre in pelvic nerve -> postganglionic neuron in intramural ganglion -> stimulate SM |
| example of conditions causing incontinence | multiple sclerosis, diabetic neuropathy |
| example of M2/M3 mAChR antagonist | oxybutynin |
| what is used instead of atropine | tropicamide |
| opthalmic use of pilocarpine | glaucoma muscarinic agonist (parasympathomimetic) which promotes miosis (constriction of circular muscle -> opens up drainage channel -> increase aqueous humour drainage -> decrease intraocular pressure) |
| glaucoma | build up of intraocular pressure compresses optic nerve + excess aqueous humour leading to tunnel vision + blindness in 2% of population over 40 |
| therapeutic uses of hyoscine/ scopolamine | muscarinic antagonist/ non selective parasympatholytic with a higher lipophilicity than atropine so readily cross BBB -> CNS depressant -> inhibits smooth muscle motility |
| how do indirectly acting parasympathomimetics (anticholinesterases) work | competitive inhibitors which inhibit AChE (cannot break down ACh) leading to elevated ACh at synapse |
| what is ACh hydrolysed into | acetate + choline |
| anti-ChE | anticholinesterases |
| physostigmine | increase miosis in glaucoma treatment, used instead of pilocarpine, stimulate bladder in urinary retention after surgery, treatment of atropine poisoning |
| neostigmine | polar, less lipophilic, acts peripherally, more effective and NMJ, treat myasthenia gravis |
| anticholinesterases (irreversible) | non competitive inhibitors which covalently modify AChE |
| examples of irreversible anticholinesterases | organophosphorous compounds |
| how do organophosphorus compounds work | phosphorylates AChE (stable + irreversible bond that cannot be hydrolysed) with some being highly lipid soluble used in insecticides = Ach not broken down so synapse stimulated more |
| examples of short term effects of sub-lethal organophospho anticholinesterase poisoning | muscarinic + nicotinic effects and CNS symptoms |
| muscarinic short term effects of organophospho antichonlinesterase poisoning | miosis (circular muscle constrict to reduce light influx to prevent further stimulation), salivation, sweating, bradycardia |
| nicotinic short term effects of organophospho anticholinesterase poisoning | fasciculation (Skm twitching) and prolonged exposure leads to paralysis (depolarising neuromuscular block) |
| long term effects of organophosphate poisoning | demyelination of peripheral nerves ->gradual weakening + sensory loss |
| examples of treatment of anticholinesterase poisoning | anti-muscarinic (parasympatholytic) eg atropine or dephosphorylate AChE with treatment with oximes eg pralidoxime |
| general treatment of anti-AChE poisoning | used when overdose of physostigmine so use anti-muscarinic drugs eg atropine -> decreases availability of ACh receptors |
| general treatment of atropine poisoning | AchE inhibitor eg physostigmine -> increases availability of Ach |
| therapeutic use of alpha-adrenoceptor antagonists examples | hypertension |
| mACH | muscarinic acetylcholine |
| MAO | monoamine oxidase |
| MLCK | myosin light chain kinase |
| NAT | norepinephrine (noradrenaline) transporter |
| TCA | tricyclic antidepressant |
| VMAT | vesicular monoamine oxidase |
| 5-HT | 5-hydroxytryptamine |
| ADHD | attention deficit hyperactivity disorder |
| BPH | benign prostate hypertrophy |
| hypertrophy meaning | cells increase in size so the tissue/organ increases in size too |
| Cal | calmodulin |
| GDP | guanosine diphosphate |
| the nervous system splits into what | CNS + PNS |
| the PNS splits into | efferent (motor) and afferent (sensory) |
| efferent (motor) splits into | somatic (voluntary) and autonomic (involuntary) |
| autonomic (involuntary) splits up into | sympathetic, enteric, parasympathetic |
| what can adrenoceptor agonists treat | ischaemic heart disease and hypertension |
| ischaemic heart disease (IHD) | type of CHD, caused by atherosclerosis of coronary blood vessels leading to angina + increased risk of heart attack |
| how does propranolol work | non-selective B blocker administered orally, inhibits SNS action on heart to slow down heart rate + decrease output + cardiac load |
| how do sympathomimetics (adrenoceptor agonists) like salbutamol treat asthma | taken via inhalation + B2 stimulation opens air passages (bronchodilators) by relaxing smooth muscle of bronchioles |
| how do symptoms of anaphylactic shock occur | degranulation of mast cells lead to histamine release |
| symptoms of anaphylactic shock | bronchospasm (histamine constricts airways), peripheral vasodilation (leads to hypotension + fainting/unconsciousness) |
| what does peripheral vasodilation in anaphylactic shock lead to | hypotension -> fainting + unconsciousness |
| what does bronchospasm in anaphylactic shock lead to | constriction of airways (due to histamine) -> death by airway obstruction |
| explain what happens when noradrenaline binds to either a B or A receptor | B= tachycardia, A= vasoconstriction (both leading to severe hypertension) |
| how does amitriptyline affect noradrenaline synapses | release stored NA from vesicles in synapse |
| how does amphetamine affect noradrenaline synapses | block reuptake of NA |
| how does cocaine affect noradrenaline synapses | block NA reuptake |
| sympathomimetics | enhance SNS |
| sympatholytics | block/reduce SNS |
| difference between adrenoceptors and muscarinic receptors | adrenoceptors activated by noradrenaline/adrenaline but muscarinic receptors activated by ACh |
| (bronchi) gland effect + muscarinic receptor when stimulated | M3 receptors cause secretion of bronchi glands |
| (GI) smooth muscle muscarinic receptor + effect when stimulated | M3 receptors cause increased motility + contraction in GI smooth muscle |
| (GI) glands muscarinic receptor + effect when stimulated | M3 receptors cause secretion in GI tract |
| bladder muscarinic receptor + effect when stimulated | M3 receptors cause contraction of glands |
| (eye) pupil - circular muscle muscarinic receptor + effect when stimulated | M3 cause constriction of pupil (circular muscle) |
| (eye) ciliary muscle muscarinic receptor + effect when stimulated | M3 cause contraction of ciliary muscle |
| salivary glands muscarinic receptor + effect when stimulated | M3 receptors cause secretion of sweat |
| lacrimal glands (tear) muscarinic receptor + effect when stimulated | M3 receptors cause secretion of tears |
| where are M2 receptors mainly found | heart used to inhibit cardiac activity |
| where are M3 receptors mainly found | smooth muscle + glands used for contraction and secretion |
| explain M3 'glandular' signalling mechanisms | increase Ca2+ leading to exocrine section + smooth muscle contraction |
| explain M2 'cardiac' signalling mechanisms | decrease cAMP -> decrease PKA -> decrease phosphorylation of Ca2+ channels + decrease Ca2+ entry and increase K+ entry -> hyperpolarisation (more negative Vm) -> harder reach threshold for AP -> brachycardia (decreased heart rate) |
| bradycardia | decreased rate of cardiac muscle contraction |
| explain M1 'neural' signalling mechanism | 'various actions' |
| incontinence meaning | unintentional urination |
| how many people are affected by incontinence in Britain | 6 million people |
| how can you treat incontinence | M3/M2 mAChR antagonist, non selective, can inhibit reflex arc in bladder, side effects same as atropine |
| miosis | contraction of iris circular muscle |
| mydriasis | dilation of iris circular muscle |
| how does M3 agonist pilocarpine work | contracts iris circular muscle leading to miosis (constriction of iris circular muscle) |
| how does M3 antagonist atropine work | relaxes iris circular muscle leading to mydriasis (dilation of iris circular muscle) |
| lipophilicity meaning | ability to dissolve in fats |
| what is scopolamine/ hyoscine used for | prevent travel/motion sickness + alleviate bowl colic (intestinal smooth wall spasms leading to pain) + alleviate dysmenorrhea (period pain) |
| examples of reversible Anti-ChE | physostigmine + neostigmine |
| example of insecticide | dyflos |
| CNS short term symptoms of organophospho anticholinesterase poisoning | anxiety, restlessness, dizziness |
| describe aging and AChE-P (phophorylated AChE) | pralidoxime can dephosphorylate AChEP but only before AChE-P has aged (made stable bond with Pi) |
| examples of A1 adrenoceptor antagonist drugs which help treat hypertension | doxazosin (in renal patients) and prazosin |
| how do A1 adrenoceptor antagonists eg doxazosin treat hypertension | block A1 adrenoceptors -> prevent noradrenaline from binding -> vasodilation -> lower peripheral resistance -> lower blood pressure BUT postural hypotension is a side effect which reduces with long term use |
| range of hypertension normally | 140/90mm/Hg |
| range for hypertension in 80+ yr olds | 150/90mmHg |
| side effect of A1 adrenoceptor antagonists for treating hypertension | postural hypotension leading to dizziness and possible fainting when standing up but reduces with long term use |
Created by:
kablooey
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