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intro to ans
pharm exam 1
| 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 |
| The ANS is a component of? | the peripheral nervous system |
| what does the ANS regulate? | involuntary physiologic processes |
| what involuntary physiologic process does the ANS regulate? | heart rate, blood pressure, pupil diameter, respiration, digestion and excretion, glandular activity, renal function, conversion of glycogen to glucose |
| the ANS is not under ____ control | direct conscious |
| some features of the ANS | high-level integration in the brain, the ability to influence processes in distant regions of the body, extensive use of negative feedback |
| two parts of the peripheral nervous system | somatic nervous system, autonomic nervous system |
| two parts of the autonomic nervous system | sympathetic nervous system, parasympathetic nervous system |
| parts of the sympathetic and parasympathetic nervous system | blood vessels, smooth muscles, glands, internal organs |
| rest and digest portion of the nervous system | parasympathetic |
| activation of the parasympathetic nervous system causes? | stimulates flow of saliva, slows heartbeat, constricts bronchi, stimulates peristalsis and secretion, stimulates release of bile, contracts bladder |
| fight or flight part of the nervous system | sympathetic |
| activation of the sympathetic nervous system causes? | dilates pupils, inhibits flow of saliva, accelerates heartbeat, dilates bronchi, inhibits peristalsis and secretion, conversion of glycogen to glucose, secretion of adrenaline and noradrenaline, inhibits bladder contraction |
| the ANS consists of neurons that give rise to _____, and other neurons that give rise to _____ | preganglionic fibers and postganglionic fibers |
| ganglion | collection of nerve cell bodies |
| what do preganglionic fibers originate from? | cells located in the brainstem or spinal cord and project to a ganglion |
| what do all preganglionic fibers use as their neurotransmitter? | ACh |
| preganglionic fibers of the sympathetic nervous system exit the CNS from what regions of the spinal cord? | thoracic, lumbar and sacral regions |
| preganglionic fibers of the parasympathetic NS exit the CNS via? | the cranial nerves, particularly nIII, nVII, nIX, and nX |
| where is the parasympathetic ganglion located? | next to an organ |
| where is the sympathetic ganglion located? | adjacent to spinal cord |
| postganglionic fibers of the sympathetic NS originate from? | ganglia |
| where of the ganglia that postganglionic fibers of the sympathetic NS orginate from 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) |
| where do postganglionic fibers project to? | the end organs |
| postganglionic fibers of the parasympathetic NS originate from? | cells located near the end organ |
| What receptors does ACh act on located on ganglionic cells? | nicotinic receptors |
| drugs that increase ACh activity increase? | sweating |
| What does the adrenal medulla release when it receives sympathetic preganglionic fibers? | epinephrine and norepinephrine |
| preganglionic fibers of both the SNS and PNS use ___ as their neurotransmitter | acetylcholine |
| most postganglionic fibers of the SNS use what as their neurotransmitter? | norepinephrine (NE) |
| What does NE act on? | adrenergic receptors located in the end organs, except SNS innervation of sweat glands |
| SNS innervation of sweat glands uses what as their neurotransmitter? | ACh |
| postganglionic fibers of the PNS use what as their neurotransmitter? | ACh |
| ACh in postganglionic fibers acts on? | muscaranic receptors located in the end organs |
| how many receptors can each neurotransmitter bind to? | multiple receptor subtypes |
| what are subtypes organized into? | families |
| how are subtypes classified? | as 'type' according to pharmacological effects and mechanism of action |
| major types of neurotransmitter receptors | ionotropic receptors, metabotropic receptors |
| ionotropic receptors | form ion channel, activation alters membrane conductance |
| metabotropic receptors | act through G proteins, can activate or inhibit second messenger systems, also can be associated with an ion channel |
| natural ligand for adrenergic receptors | norepinephrine |
| all of the adrenergic receptors are? | metabotropic receptors |
| most of the cholinergic receptors are? | metabotropic receptors, with the exception of nicotine receptors |
| all nicotine receptors are? | ionotropic |
| both adrenergic and cholinergic receptors have multiple? | receptors subtypes |
| two main groups of adrenergic receptors | a and B |
| how many subtypes of adrenergic receptors are there? | at least 9 |
| all subtypes of adrenergic receptors are? | metabotropic |
| a receptors are divided into? | a1 (Gq-coupled) and a2 (Gi-coupled) |
| subtypes of a1 | 3 subtypes- a1A, a1B, a1D |
| subtypes of a2 | 3 subtypes- a2A, a2B, a2C |
| B receptors are divided into? | B1, B2, and B3 |
| What do B receptors couple with? | Gs, but B2 and B3 also can couple with Gi |
| adrenaline (epinephrine) or norepinephrine are receptor ligands to either? | a1, a2, or B adrenergic receptors |
| effect of activation of a1 | excitatory, activates phospholipase C-> smooth muscle contraction-> increases BP |
| effect of activation of a2 | inhibitory, inhibition of NE release/ sympathetic tone; smooth muscle contraction |
| effect of activation of B | excitatory, activates adenyl-cyclase-> heart muscle contraction, smooth muscle relaxation, glycogenolysis |
| effect of activation of B1 | increased cardiac output, increased BP |
| effect of activation of B2 | smooth muscle relaxation |
| types of adrenergic receptors | alpha-1, alpha-2. beta-1, beta-2 |
| activation of alpha-1 effects | vasoconstriction, increased peripheral resistance (blood flow), increased blood pressure, mydriasis, increased closure bladder sphincters |
| activation of alpha-2 effects | inhibits norepinephrine release, inhibits acetylcholine release, inhibits insulin release |
| activation of beta-1 effects | increased heart rate, increased lipolysis, increased myocardial contractility, increased renin (increases cardiac output bc increased HR) |
| activation of beta-2 effects | vasodilation, decreases peripheral resistance, bronchodilation, increased glycogenolysis (muscle, liver), increased glucagon release, relaxes uterine smooth muscle |
| what does Alpha-1 activate? | SNS |
| Alpha-2 decreases? | sympathetic tone, puts brain to sleep because norepinephrine is inhibited |
| where is Beta-1 located? | in the heart |
| example of beta-2 medication | albuterol, opens airways by causing smooth muscles in bronchial tubes to relax |
| relative potency at alpha-1 receptor | E vs NE? |
| relative potency at alpha-2 receptor | E>NE |
| relative potency at Beta-1 receptor | E=NE |
| relative potency at Beta-2 receptor | E>>NE |
| sympathomimetic agents mimic? | activation of the SNS by increasing adrenergic receptor activity |
| direct agonists | directly interact with and activate adrenoceptors |
| examples of adrenoceptors that direct agonist interact with | NE, epi, isoproterenol (B), albuterol (B2), etc |
| direct a2 agonist | yohimbine |
| indirect agonists | dependent on ability to enhance the actions of endogenous catecholamines |
| how do indirect agonists work? | by enhancing release from nerve terminals, by blocking re-uptake/removal of the transmitter, by preventing enzymatic degredation of the neurotransmitter |
| examples of indirect agonists that enhance release from nerve terminals | reserpine, amphetamines, tyramine |
| examples of indirect agonists that block re-uptake/removal of the transmitter | cocaine, methylphenidate |
| examples of indirect agonists that prevent enzymatic degredation of the neurotransmitter | MAOIs, COMT inhibitors |
| 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, a1 antagonists |
| examples of beta blockers | propranolol, metoprolol, atenolol |
| examples of a1 agonists | prazosin (minipress) |
| examples of a2 agonists | clonidine (catapres) |
| effects of ANS | increased HR, BP, CO, blood flow to brain, heart, and skeletal muscles, increased blood glucose, sweating, and cellular metabolism; pupil dilation; increased rate and depth of respiration; reduced saliva production; reduction gut motility and urine flow |
| patient: diaphoretic, mydriasis, fever, tachycardia, tachypnea, confusion, xerostomia, hypertension | stimulant poisoning; sympathomimetic effect (in this case cocaine poisoning) |
Created by:
camrynfoster