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pharm
intro to the Autonomic Nervous System
| 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 blood pressure |
| ANS is a component of the | Peripheral Nervous System (PNS) |
| ANS regulates what processes? | involuntary |
| involuntary processes regulated by the ANS | HR, BP, pupil diameter, RR, digestion, excretion, glandular activity, renal function, glucose to glycogen conversion |
| PNS nickname | rest and digest |
| SNS nickname | fight or flight want to use energy where its needed most |
| PNS and SNS are _________ | opposites |
| ganglion | collection of nerve cell bodies |
| ANS consists of what kind of fibers | preganglionic postganglionic |
| preganglionic fibers | originate from cells located in the brainstem or spincal cord and project to a ganglion. all fibers use acetylcholine (ACh) as their NT |
| preganglion of the SNS | exit the CNS from throacic, lumber, and sacral regions of SC |
| preganglion of the PNS | exit the CNS via the cranial nerves, III, VII, IX, X |
| postganglionic fibers of the SNS | origionate from ganglion either in a chain next to the spinal cord (paravertebral) or along the midline infront of the heart and spinal cord (prevertebral) these fibers project to the end organs. |
| postganglionic fibers of the PNS | origionate from cells located near the end organ |
| sweat glands use ACh so | drugs that include ACh will induce sweat |
| neurotransmitters depend on | SNS or PNS |
| most SNS use | NE |
| preganglionic fibers of both SNS and PNS use | ACh neurotransmitters |
| ACh acts on | nicotinic receptors located on the ganglion cells |
| most postganglionic fibers of the SNS use | NE as the neurotransmitter |
| NE acts on | adrenergic receptors in the end organs |
| SNS sweat glands | is the exception 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 recptors | 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) |
| types of neurotransmitters | ionotropic receptors and metabotropic receptors |
| ionotropic receptors | form ion channel, activation alters membrane conductance (membrane potential) |
| metabotropic | act through G-proteins, can activate or inhibit second messenger systems, can be associated with an ion channel |
| all adrenergic receptors are | metabotropic receptors |
| most cholinergic receptors are metabotropic with the exception of | nicotinic receptors |
| all nicotinic receptors are | ionotropic |
| both adrenergic and cholinergic receptors have | multiple receptor types |
| the natural ligand for adrenergic receptors is | NE |
| 2 main types of adrenergic receptors | alpha and beta. 9 total. all of them are metabotropic |
| alpha receptors are divided into | alpha1 (Gq couples) and alpha2 (Gi couples) each have 3 subtypes |
| beta receptors are divided into | B1, B2, 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 cardiac output |
| b2 | smooth muscle relaxation |
| adrenergic receptors | a1, a2, b1, b2 adrenaline (or epinephrine) or NE are receptor ligands to either of these three adrenergic receptors |
| when alpha 1 is activated then | vasoconstriction, increase of peripheral resistance, increase BP, myadriasis (pupils dilate), increase closure of bladder sphincters |
| when alpha 2 is activated | inhibits NE release, inhibits ACh release, inhibits insulin release E>NE |
| when beta 1 is activated | increase HR (and BP and cardiac output), increase lipolysis, increase myocardial contractility, increase renin release E=NE |
| when beta 2 is activated | vasodilation, decrease peripheral resistance, bronchodilation (smooth muscle relaxes and opens airways), increase glycogenolysis (increase available energy), increase glucagon release, relaxes uterine smooth muscle E>>NE |
| example of beta 2 | 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 |
| 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 |
| effects of SNS activation on heart | increased HR, arterial BP and cardiac output increased blood flow to brain, heart, and skeletal muscles |
| other effects of SNS activation | increase glucose, pupil dilation, inc sweating, inc rate of cellular metabolism and rate and depth of breathing, reduced salivation and gut mobiliy and urine flow |
| what are sympathomimetic and sympatholytic drugs used for important because theyre used in so many things | cardiogenic shock, anaphylactic shock, hypotension, CHF, bronchial asthma, nasal decongestion, narcolepsy, ADHD |
| beta-blockers used for HTN | atenolol, metoprolol, propanolol used to reduce strength of contractions |
| alpha-1 blockers used for HTN | praxosin (minipress) relaxes smooth muscles of blood vessels |
| alpha-2 receptor agonists used for HTN | clonidine relaxes smoooth muscles of blood vessels |
| combined alpha and beta-blockers used for HTN | carvedilol, labetalol, dilevalol |
| inadequate heart function: hypotension is treated with | NE, phenylephrine - causes vasoconstriction which increases BP |
| inadequate heart function- cardiogenic shock or acute HF | dopamine, dobutamine - for inotropic effect, increasing force and speed of CO |
| inadequate heart function- cardiac arrest | isoproterenol, epinephrine - increases strength of contractions and causes vasodilation |
| astha is treated with | direct B2 agoinists - to relax smooth muscles in airways ex: albuterol, inhaled corticosteriods |
| anaphylaxsis is treated with | epinephrine |
| epinephrine | b1 agonists- increases cardiac output b2 agonists- relaxes constricted bronchioles a1 agonists- constricts capillaries and increases BP |
| glaucoma treated w | beta blockers, betaxolol - lowers pressure by reducing aqueous humor production (mostly replaced by prostaglandins) |
| nasal congestion 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 | nicotinic or muscarinic based on whether they have high affinity for nicotine or muscarine |
| nicotinic are | ionotropic and form a SODIUM channel |
| muscarinic are | metabotropic |
| 2 subtypes of muscarinic receptors | M1: M1, M3 and M5 receptors - excitatory M2: M2 and M4 receptors - inhibitory |
| eye sphincter receptor response | M3 contraction - miosis |
| eye cilliary muscle | M3 contraction -accommodation for near vision |
| heart SA node | M2 decreases heart rate |
| heart AV node | M2 decreases conduction velocity |
| lungs bronchioles | M3 contraction - bronchospasm |
| lungs glands | M3 secretion |
| GI tract stomach | M3 increased motility cramps |
| GI tract glands | M1 secretion |
| GI tract intestine | M3 contraction - diarrhea, involuntary bowel movement |
| bladder | M3 contraction- relaxation, voiding, urinary incontinence |
| sphincters | M3 secretion - sweat, salivation, and lacrimation |
| blood vessels | 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) |
| effects of PNS activation on the heart | decreases heart rate, arterial BP and cardiac output |
| other 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 | anti-muscarinic |
| parasympatholytic drugs examples | atropine, methantheline (banthine), propantheline (pro-banthine), diphenhydramine (benadryl) |
| atropine | prototypical non-selective antimuscarinic agent used to treat bradycardia, reduce saliva and bronchial secretions |
| methantheline (banthine) | dries salivary secretions |
| propantheline (pro-banthine) | reduces GI motility |
| diphenhydramine (benadryl) | also blocks H1 histamine receptors dried nasal receptors antiemetic effects sedation |
| atropine poisoning | typically a relavtively safe drug in adults, however, poisoning can occur with extreme doses |
| atropine poisoning symptoms | dry mouth, mydriasis, tachycardia, hot and flushed skin, elevated body temp, agitation, delirium for as long as 1 week "dry as a bone, blind as a bat, red as a beet, mad as a hatter" |
| adrenergic vs 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 |
Created by:
ago24