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pharm
intro to the ANS
| Question | Answer |
|---|---|
| mydriasis | dilation of the pupils |
| miosis | constriction of the pupils |
| tachypnea | heavy breathing |
| diaphoretic | heavy sweating |
| tachycardia | increased heart rate |
| bradycardia | slow heart rate |
| xerostomia | dry mouth |
| sialorrhea | hypersalivation |
| hypertension | high BP |
| the ANS is | a component of the peripheral nervous system |
| ANS regulates | involuntary physiologic processes |
| ANS is not | under conscious control |
| what are some of the involuntary physiologic processes ANS controls | heart rate, BP, pupil diameter, respiration, digestion and excretion, glandular activity, renal function, conversion of glycogen to glucose |
| some features of ANS include | high-level integration in the brain, the ability to influence processes in distant regions of the body, extensive use of negative feedback |
| ANS is under the | peripheral nervous system |
| PNS splits into | ANS and SNA |
| ANS splits into | sympathetic and parasympathetic |
| sympathetic and parasympathetic control | blood vessels, smooth muscles, glands, internal organs |
| the parasympathetic NS aka | rest and digest |
| the parasympathetic NS actions | stimulates flow of saliva, slows heartbeat, constricts bronchi, stimulates peristalsis, stimulates the release of bile, contracts bladder to make it easier to empty |
| the sympathetic NS aka | fight or flight |
| the sympathetic NS actions | dilates pupil, inhibits flow of saliva, accelerates heartbeat, dilates bronchi, inhibits peristalsis and secretion, conversion of glycogen to glucose so rapid access to energy, secretion of adrenaline and noradrenaline, inhibits bladder contraction |
| ANS consists of neurons that give rise to | preganglionic fibers and postganglionic fibers |
| a ganglion is | a collection of nerve cell bodies |
| preganglionic fibers originate from | cells located in the brainstem or spinal cord and project to a ganglion |
| all preganglionic fibers use | ACh as their neurotransmitter |
| preganglionic fibers of the sympathetic NS exit the CNS from | thoracic, lumbar and sacral regions of the spinal cord |
| preganglionic fibers of the parasympathetic NS exit the CNS via the | cranial nerves - CN III, CN VII, CN IX, CN X |
| postganglionic fibers of sympathetic NS originate from | ganglia located either in a chain next to the spinal cord (paravertebral) or located along the midline in front of the heart and spinal column (prevertebral) |
| postganglionic fibers of sympathetic NS project to the | end organs |
| postganglionic fibers of parasympathetic NS originate from | cells located near the end organ |
| sweat glands use ACh so | drugs that include ACh will induce sweat |
| neurotransmitters depend on | parasympathetic or sympathetic |
| most sympathetic postganglionic fibers use | NE |
| preganglionic fibers of both SNS and PNS use | ACh as neurotransmitters |
| ACh acts on | nicotinic receptors located on the ganglion cells |
| most postganglionic fibers of the SNS use | NE as their neurotransmitter |
| NE acts on | adrenergic receptors located in the end organs |
| exception for postganglionic fibers is | SNS innveration of sweat glands because they use ACh |
| postganglionic fibers of the PNS use | ACh as their neurotransmitter which acts on muscarinic receptors located in the end organs |
| neurotransmitter receptors | each neurotransmitter can bind to multiple receptor subtypes |
| subtypes are organized into families and are classified as | 'type' according to pharmacological effects and mechanism of action (MOA) |
| major types of neurotransmitters | ionotropic receptors and metabotropic receptors |
| ionotropic receptors | form ion channel, activation alters membrane conductance (membrane potential) |
| metabotropic receptors | act through G-proteins, can activate or inhibit second messenger systems, can be associated with an ion channel |
| adrenergic receptors | respond to NE, are metabotropic receptors |
| cholinergic receptors | most are metabotropic receptors |
| cholinergic receptors exception | nicotinic receptors are ionotropic |
| both adrenergic and cholinergic receptors have | receptor subtypes |
| 2 main groups of adrenergic receptors | alpha and beta, at least 9 subtypes in total, all metabotropic (working through g-proteins) |
| natural ligand for adrenergic receptors is | NE |
| alpha receptors are divided into | a1 and a2 |
| a1 subtypes | a1A, a1B, a1D |
| a2 subtypes | a2A, a2B, a2C |
| beta receptors are divided into | B1, B2, and B3 |
| a1 | excitatory, smooth muscle contraction, increases BP |
| a2 | inhibitory, inhibits release of NE/sympathetic tone, smooth muscle contraction |
| b | excitatory, heart muscle contraction, smooth muscle relaxation, glycogenolysis |
| b1 | increase of cardiac output and BP |
| b2 | smooth muscle relaxation |
| adrenergic receptors | a1, a2, b1, b2 |
| what alpha-1 is activated then... | vasoconstriction, increase of peripheral resistance, increase BP, myadriasis (pupils dilate), increase closure of bladder sphincters |
| what alpha-2 is activated then... | inhibits NE release, inhibits ACh release, inhibits insulin release |
| what beta-1 is activated then... | increase HR (and BP and cardiac output), increase lipolysis, increase myocardial contractility, increase renin release |
| what beta-2 is activated then... | vasodilation, decrease peripheral resistance, bronchodilation (smooth muscle relaxes and opens airways), increase glycogenolysis (increase available energy), increase glucagon release, relaxes uterine smooth muscle |
| beta-2 example | albuterol, dilates airways with b2 agonist and makes it easier to breathe |
| sympathomimetic agents mimic activation of SNS by | increasing adrenergic receptor activity |
| sympathomimetic agents: direct agonists | directly interact with and activate adrenoceptors - NE, epi, isoproternol, albuterol) |
| sympathomimetic agents: indirect a2 antagonists | yohimbine (helps brain to sleep) |
| sympathomimetic agents: indirect agonists are dependent on | ability to enhance the actions of endogenous catecholamines |
| sympathomimetic agents: indirect agonists work by | enhancing release of NE from nerve terminals, blocking re-uptake/removal of the transmitter, preventing enzymatic degradation of the neurotransmitter |
| sympatholytic agents reduce activation of the SNS by | reducing adrenergic receptor activity by blocking the actions of NE and Epi on adrenergic receptors |
| examples of sympatholytic agents | beta blockers (used for BP), a1 antagonists, a2 agonsists |
| cardiac effects of SNS activation | increased HR, arterial BP and cardiac output increased blood flow to brain, heart, and skeletal muscles |
| other effects of SNS activation | inc blood glucose, pupil dilation, inc sweating, inc rate of cellular metabolism and rate and depth of breathing, reduced salivation and gut mobiliy and urine flow |
| why are sympathomimetic and sympatholytic drugs so important | because they are used in so many conditions |
| what conditions are sympathomimetic and sympatholytic drugs used for | cardiogenic shock, anaphylactic shock, hypotension, CHF, bronchial asthma, nasal decongestion, narcolepsy, ADHD |
| what is HTN treated with | sympatholytics |
| HTN drug classes that act specificially via the adrenergic SNS | beta-blockers - to reduce strength of contractions alpha-1 blockers - relaxes smooth muscles of blood vessels alpha-2 receptor agonists - relaxes smooth muscles of blood vessels combined alpha and beta-blockers |
| beta-blockers used for HTN | atenolol, metoprolol, propanolol |
| alpha-1 blockers used for HTN | praxosin (minipress) |
| alpha-2 receptor agonists used for HTN | clonidine |
| combined alpha and beta-blockers used for HTN | carvedilol, labetalol, dilevlol |
| inadequate heart function: hypotension is treated with | NE, phenylephrine - causes vasoconstriction which increases BP |
| inadequate heart function: cardiogenic shock or acute heart failure is treated with | dopamine, dobutamine - for inotropic effect (ex: increasing force and speed of cardiac output) |
| inadequate heart function: cardiac arrest is treated with | isoproterenol, epinephrine - increases strength of contractions in heart and causes vasoconstriction |
| asthma is treated with | direct b-agonists to relax smooth muscles in (open) airways - EX: albuterol |
| anaphylaxis is treated with | epinephrine (epi pen!) |
| epinephrine receptors | b1 agonists - increase cardiac output (and BP) b2 agonists - relaxes constricted bronchioles a1 agonists - constricts capillaries and increases BP (and heart flow) |
| glaucoma is treated with | beta blockers but now mostly replaced by prostaglandins |
| nasal congestion is treated with | oxymetazoline, phenylephrine, pseudophedrine |
| oxymetazoline | a1 and a2 agonist in arterioles of nasal mucosa - vasoconstriction |
| phenylephrine | a1 agonist in arterioles of nasal mucosa - vasoconstriction |
| pseudophedrine | acts on both a and b receptors to cause vasoconstriction |
| cholinergic receptors are classified as | nicotinic or muscarinic based on whether they have high affinity for nicotine or muscarine |
| nicotinic receptors are | ionotropic |
| muscarinic receptors are | metabotropic |
| there are multiple subtypes of | each subclass of receptor |
| nicotinic receptors | ionotropic and pentomeric consisting of 5 subunits |
| nicotinic receptors have multiple isoforms of | a and b subunits |
| nicotinic receptors have | 4 transmembrane domains |
| nicotinic receptors primarily act as | sodium channels |
| KNOW! nicotinic receptors are | ionotropic and form a sodium channel |
| muscarinic receptors | metabotropic and have 2 suptypes |
| 2 subtypes of muscarinic receptors | M1: M1, M3 and M5 receptors - excitatory M2: M2 and M4 receptors - inhibitory |
| what are the differences of muscarinic receptors due to | g proteins |
| eye sphincter receptor and response | M3 - contraction, miosis |
| eye ciliary muscle receptor and response | m3 - contraction, accommodation for near vision |
| heart SA node receptor and response | M2 - decreases HR |
| heart AV node receptor and response | M2 - decrease conduction velocity - negative dromotropy |
| lungs bronchioles receptor and response | M3 - contraction, bronchospasm |
| lungs glands receptor and response | M3 - secretion |
| GIT stomach receptor and response | M3 - increase motility, cramps in gut |
| GIT glands receptor and response | M1 - secretion |
| GIT intestine receptor and response | M3 - contraction, diarrhea and involuntary defecation |
| bladder receptor and response | M3 - contraction, relaxation, voiding, urinary incontinence |
| sphincters receptor and response | M3 - relaxation except for lower esophageal which contracts |
| glands receptor and response | M3 - secretion, sweat/salivation/lacrimation |
| blood vessels receptor and response | M3 - dilation, no innervation or effects of indirect agonists |
| parasympathomimetic agents mimic | activation of the PNS by increasing muscarinic cholinergic receptor activity |
| parasympathomimetic direct agonists directly interact with and activate | muscarinic cholinergic receptors - ACh, methacholine, bethanechol, muscarine, pilocarpine |
| parasympathomimetic indirect agonists impact | neurotransmitter release and uptake, enhance ACh effects by inhibiting cholinesterase thereby blocking degredation (neostigmine, physostigmine, donepezil, galantamine, rivastigmine) |
| parasympatholytic agents reduce activation of PNS by | blocking the actions of ACh on muscarine receptors (atropine, scopolamine) |
| cardiac effects of PNS activation | decreases heart rate, arterial BP and cardiac output |
| effects of PNS activation | decreased blood glucose, pupil constriction, increased sweating and tearing, increased saliva production, increased gut motility and urine flow, decreased rate of cellular metabolism, bronchoconstriction |
| cholinergic mimetic drugs for GI and urinary tract | treated with bethanechol or neostigmine (inhibits breakdown of ACh) |
| cholinergic mimetic drugs for dry mouth | to stimulate salivary secretions, treated with pilocarpine and cevimeline |
| cholinergic mimetic drugs for dysfunction at the neuromuscular junction | myastehnia gravis which is associated with reduced nAChR function, treated with cholinesterase inhibitors like pyridostigmine (prevent degredation of ACh) |
| cholinergic mimetic drugs act as | antidote to overdose of tricycle antidepressants |
| cholinergic mimetic drugs for memory disorders associated with AD and PD | cholinesterase inhibitors like donepezil, galantamine, rivastigmine |
| parasympatholytic drugs also are used to | treat a variety of disorders |
| parasympatholytic drugs examples | atropine, methantheline (banthine), propantheline (pro-banthine), diphenhydramine (benadryl) |
| atropine poisoning | typically a relavtively safe drug in adults, however, poisoning can occur with extreme doses |
| atropine poisoning symptoms because physiologic affects of PNS are blocked | dry mouth, mydriasis, tachycardia, hot and flushed skin, elevated body temp, agitation, delirium for as long as 1 week |
| summary of adrenergic and cholinergic responses | adrenergic and cholinergic responses usually have opposing actions, net effector response is a balance between the two, should be able to predict pharmacology from the physiology |
| atropine | prototypical non-selective antimuscarinic agent, used to treat bradycardia, to reduce salivation and bronchial secretions before surgery, and as antidote for overdose of cholinergic drugs |
| methantheline (banthine) | dries salivary secretions |
| propantheline (pro-banthine) | reduces GI motility |
| diphenhydramine (benadryl) | blocks muscarinic cholinergic receptors and blocks H1 histamine receptors, dries nasal secretions, antiemetic effects, sedation |
Created by:
leh195