ANS Flashcards
divisions of nervous system
-Central Nervous System (CNS):
-Includes brain and spinal cord
-integrates all body activities
-Peripheral Nervous System:
-Somatic Nervous System
-Autonomic Nervous System (ANS):
-Parasympathetic nervous system
(PNS)
-Sympathetic nervous system (SNS)
somatic nervous system
-Activates skeletal muscle contraction
-Consists of motor neurons/sensory
neurons
-Sensory (afferent) – go TO CNS
-Motor (efferent) - go FROM CNS to
skeletal muscle
-Adjusts to external environment
-VOLUNTARY
ANS
-Further subdivided into PNS and SNS
-Regulates activity of smooth muscle,
exocrine glands, cardiac tissue and
certain metabolic activities
-Sensory neurons go from smooth
muscle & cardiac muscle TO CNS
-Motor neurons go to glands, smooth & cardiac muscle FROM CNS
-Adjust to internal environment
-INVOLUNTARY
enteric nervous system
-Aka 3rd division of ANS
-Network of autonomic nerves in
gut wall
-Receives innervation from SNS &
PNS and regulates gi motility and
secretion
-Responds to Neurotransmitters –
peptides and nitric oxide
neurotransmission of ANS
-Preganglionic neuron – cell body in CNS, axon extends out of CNS
-Postganglionic neuron – innervate an
effector outside the CNS
-Ganglion – Small mass of nerve tissue containing the cell bodies of neurons
-Synapse – space b/w pre & post neurons or space b/w post neuron & effector where Neurotransmitter (NT) is released
-SNS – primary NT is Norepinephrine (NE) – may also be referred to as noradrenaline (NA)
-PNS- primary NT is ACh
neurotransmitters of the ANS
-Acetylcholine (ACH)– Primary NT of PNS. Released at ALL autonomic ganglia (PNS & SNS), at PNS neuroeffector junction (nej), somatic neuromuscular junction (nmj), and some SNS nej
-Norepinephrine/Noradrenaline (NE/NA) – Primary NT of SNS. Released at most SNS nej
-Epinephrine (Epi) – released from adrenal medulla in response to activation of SNS
-Dopamine (DA)- important NT in CNS, and released at several peripheral SNS fibers
other neurotransmitters
-Found in ANS nerves but they are nonadrenergic noncholinergic neurons (NANC)
-Primarily found in enteric nervous system of GI tract, genitourinary tract, airways and some blood vessels
-Includes peptides, ATP, GABA, substance P, nitric oxide, serotonin
-viagra- #1 drug that affects nitric oxide
ANS: general effects of PNS
-Responses are specific
-Rest & digest
-Miosis
-increase gi motility/salivation
-increase urination/defaction
-decrease HR
-Bronchoconstriction
-Erection
ANS: general effects SNS
-Responses are diffuse
-Fight or flight
-Mydriasis
-decrease gi motility/salivation
-decrease urination/defaction
-increase heart rate
-Bronchodilation
-Ejaculation
alpha 1 adrenergic receptor
-pupils mydriasis
-arteries/veins- constriction
-salivary secretion- inhibits
-liver- glycogenolysis
-just alpha -> pancreas secretion- inhibits
beta 1 adrenergic receptor
-HR- increase
-just beta -> gastric secretion- inhibit
-just beta -> salivary secretion - inhibits
beta 2 adrenergic receptor
-arteries/veins- dilation
-smooth muscle- decrease motility
-liver- gluconeogenesis
cholinergic (PNS) receptor effects
-PNS
-muscarinic
-pupil miosis
-HR decrease
-arteries/vein- dilation
-smooth muscles- increase motility
-gastric secretion- stimulate
-pancreas secretion- stimulate
-salivary secretion- stimulate
-liver- glycogenesis
-SLUDGE
cholinergic receptors (just know there are diff ones)
-muscarinic 1
-muscarinic 2
-muscarinic 3
-nicotinic N
-nicotinic M
adrenergic receptors (just know they exist)
-alpha 1
-alpha 2
-beta 1
-beta 2
-beta 3
dopamine receptors (just know they exist)
-D1
-D2
-D3
-D4
cholinergic receptors (ACh): muscarinic
-Located at PNS nej, some SNS nej (sweat glands), CNS, and autonomic ganglia
-Activated by ACh and muscarine
-Found in body in greater numbers than nicotinic receptors
-SLUDGE- salivation, lacrimation, urination, defecation, GI motility, erection
-Mediate smooth muscle contraction (except sphincter contraction)
-Stimulates gland secretion
-Decrease HR and conduction
-Bronchoconstriction
-Peripheral vasodilation
-Miosis
cholinergic receptors (ACh): nicotinic
-activated by ACh and nicotine
-Located on autonomic ganglia and when activated will excite neurotransmission
-Located at somatic neuromuscular junction and when activated will mediate muscle contraction
-Nicotinic have some opposing effects of muscarinic (tachycardia, HTN)
adrenergic receptors (NE and epi): alpha 1
-constricts vascular smooth muscle
-constricts blood vessels
-Increase basal metabolic rate
-Located at SNS nej effector (primarily smooth muscle)
adrenergic receptors (NE and epi): alpha 2
-Inhibition of NE release from nerve endings at pre synaptic post ganglionic neuron (negative feedback)
-Also located on some postsynaptic tissue & blood platelets
adrenergic receptors (NE and epi): beta 1
-HEART muscle
-Mediates cardiac stimulation (increase HR & contractility)
-Located on SNS effector (cardiac muscle, vascular smooth muscle, renal cells - increase renin release)
-Increased lipolysis
adrenergic receptors (NE and epi): beta 2
-Mediates smooth muscle relaxation
-located on SNS effector (bronchioles in lung, uterine smooth muscle and vascular smooth muscle)
-In liver and muscle – mediate glycogenolysis
non specific beta blocker
-works on beta 1 and 2
-ex. propanolol
-contraindicated in pts with asthma
drugs affecting autonomic transmission
-Can exert effects at any step in neurotransmission process depending on classification of drug
-PNS & SNS agonist- Direct or Indirect acting
-PNS & SNS antagonist- Direct or Indirect acting
direct/indirect agonist and antagonists
-Direct agonists - Activate postsynaptic receptors
-Indirect agonists:
-Stimulate release of NT
-Inhibit reuptake of NT
-Inhibit metabolism of NT
-Direct antagonists- Block postsynaptic receptors
-Indirect antagonists:
-Inhibit synthesis of NT
-Prevent vesicular storage of NT
-Inhibit release of NT
cholinergic agonists
-Direct agonists – bind and activate cholinergic receptors:
-Choline esters
-Plant alkaloids
-Indirect agonists – increase synaptic concentrations of ACH:
-Cholinesterase inhibitors
direct cholinergic agonists (choline esters)
-ACH and Carbachol – activate both nicotinic and muscarinic. ACH has limited clinical indications
-Lack of specificity for muscarinic subtypes, therefore have a wide range of effects on many organ systems
-Bethanechol** and methacholine**– activates only muscarinic
-Methacholine not commercially available
-> main ones used are bethanechol and carbachol
direct cholinergic agonists: bethanechol (urecholine)
-acts at muscarinic only
-Stimulates bladder w/o significant effects on HR or BP
-TX of urinary retention post-op & post partum
direct cholinergic agonists (choline esters): carbachol (isoptocarbachol, miostat)
-For chronic open-angle glaucoma
-Produce miosis during ophthalmic surgery
-not really used anymore
direct cholinergic agonists (plant alkaloids)
-1. muscarine – no current medical use
-2. nicotine – smoking cessation
-3. Pilocarpine (Isoptocarpine, Ocusert, Salagen)
-Higher affinity for muscarinic receptor
-Treats glaucoma: stimulate contraction of ciliary muscle fibers -> increase aqueous humor outflow -> decrease IOP
-4. Cevimeline (Exovac)- To treat dry mouth associated with Sjogren’s syndrome
indirect agonist: cholinesterase inhibitors
-MOA- Inhibit breakdown of ACH at all cholinergic synapses -> increase ACH concentration
-Reversible vs Irreversible
cholinesterase inhibitors: reversible agents
-tx for pts with issues with ACh
-can be muscle relaxor, prior to intubation, OD
-Donepezil (Aricept)– Tx of Alzheimer’s Disease
-Edrophonium (Enlon) - very short DOA. Used in Dx of Myasthenia gravis
-Neostigmine (Prostigmin) - Tx of Myasthenia gravis, antidote for skeletal muscle relaxants
-Physostigmine (Eserine) - Tx for Overdoses of drugs with anticholinergic effects (like atropine, TCAs)
-Pyridostigmine (Mestinon) – Tx of Myasthenia gravis
cholinesterase inhibitors: irreversible agents
-organophosphates
-Ecothiophate (Phospholine) – Tx of chronic refractory glaucoma. DOA of up to one week
-Pesticides (palathion and malathion)- parasites
-Soman (chemical warfare agent)
organophosphate poisoning
-SLUGE
-Augmented cholinergic neurotransmission at central and peripheral synapses
-Produces all effects of muscarinic activation -> SLUDGE, spasm, bronchoconstriction, decrease HR & CO, etc
-Cholinergic activation in CNS – seizures, respiratory depression, coma
-Excessive activation of nicotinic receptors- Neuromuscular blockade & muscle paralysis
-Treatment:
-Symptomatic - maintain VS
-Decontamination
-Antidotes – Use Atropine to counteract ACH and pralidoxime (2-PAM) to regenerate cholinesterase
cholinergic antagonists
-1. muscarinic receptor antagonists:
-plant alkaloids- atropine, scopalamine
-semi synthetic - several
-2. nicotinic receptor antagonists:
-ganglionic blockers
-neuromuscular blockers- “curium”
-depolarizing neuromuscular blocker- succinylcholine
-anesthesia
muscarinic receptor antagonists
-belladonna alkaloids- atropine, scopolamine, hyoscyamine (antispasmodic used for IBD)
-synthetic/semi synthetic- ipratropium, tolterodine, oxybutynin, propantheline, dicyclomine, benztropine, etc
-Both types inhibit effects of PNS stimulation:
-Smooth muscle relaxation, increase HR & cardiac conduction and inhibit exocrine gland secretion
muscarinic receptor antagonist: ocular effects
-Relax iris sphincter -> mydriasis
-Inhibits lacrimal gland –> dry eyes
-Therapeutic uses – mydriatic to facilitate eye exams (atropine, tropicamide, scopolamine)
-belladonna (pupil dilation) alkaloids- people used to look pretty
muscarinic receptor antagonist: cardiac effects
-increase HR and AV conduction
-Therapeutic Uses: Sinus bradycardia & AV block (atropine)
muscarinic receptor antagonist: respiratory effects
-increase Bronchodilation
-Therapeutic Uses: COPD, emphysema, bronchitis:
-ipratropium (Atrovent)- mainly COPD
-tiotropium (Spiriva)
muscarinic receptor antagonist: GI and urinary tract effects
-Relax gi muscle, reduce intestinal motility, inhibit gastric acid secretion and urinary retention
-Therapeutic Uses:
-TX of intestinal spasms/pain – Hysosamine, Donnatal, Dicyclomine
-TX of dysuria & urinary incontinence – oxybutynin, tolterodine, darifenacin, solifenacin
muscarinic receptor antagonist: CNS effects
-TX of motion sickness by blocking cholinergic transmission from vestibular apparatus to vomiting center (Scopolamine patch)
-TX of Parkinson’s Disease – reduce tremor (benztropine & trihexyphenidyl)
-CNS side effects include: sedation*, confusion, altered mental status
nicotinic receptor antagonists
-1. ganglionic blockers
-limited use due to adverse effects
-trimethaphan- used rarely for hypertensive emergency
-2. neuromuscular blocking agents
-nondepolarizing
-depolarizing
nicotinic receptor antagonists: nondepolarizing neuromuscular blocking agent
-aka curariforms
-Atracurium, pancuronium, vecuronium, rocuronium
-Competitive antagonist of ACH at nicotinic muscle receptors
-Causes muscle relaxation and paralysis
-Effects reversed by cholinesterase inhibitors*
-Used for surgery, intubation, ventilators
-sedation -> paralysis but conscious
atropine poisoning
-dry as a bone
-red as a beat
-mad as a hatter
nicotinic receptor antagonists: depolarizing neuromuscular blocking agent
-Succinylcholine
-Causes “persistent” depolarization
-Used for surgery, RSI kits
-Effects not reversed by cholinesterase inhibitors therefore no antidote** if an overdose, short duration of action
-good for rapid emergency situation
adrenergic agonists
-1. Direct Acting Agonists:
-Catecholamines (epi, NE, isoproterenol, dopamine and dobutamine)
-Non-catecholamines (albuterol, clonidine, phenylephrine)
-2. Indirect Agonists:
-Amphetamine, cocaine, tyramine
-3.Mixed direct/indirect agonists:
-pseudoephedrine
nasal decongestant
-dont need to know
-afrin - great vasoconstrictor- used for nasal surgery
-sudafed is good for decongestant -> not phenylephrine
direct adrenergic agonists: catecholamines
-Rapidly metabolized by monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT) enzymes in gut, liver and other tissues – must give parenterally
-Effects depend on affinity and specificity for type of Adrenergic receptor
direct adrenergic agonists: catecholamines: epinephrine and norepinephrine
-Epinephrine – can bind to ALL the adrenergic receptors:
-Vasoconstriction & increase BP (alpha1)
-Cardiac stimulation (beta1)
-Bronchodilation & skeletal muscle vasodilation (beta2)
-Used in anaphylactic shock and cardiac arrest
-Norepinephrine:
-Vasoconstriction & increase BP (alpha1)
-Cardiac stimulation (beta1)
-Used in hypotension and shock
-no lung involvement
direct adrenergic agonists: catecholamines: isoproterenol, dopamine, dobutamine
-Isoproterenol (Isoprel)
-Cardiac stimulation (beta1) & Bronchodilation (beta2)
-Used to TX asthma, AV block and bradycardia
-Dopamine - precursor to epi, NE
-Renal vasodilation (D1)- at a low dose -> at a long term dose it will cause kidney constriction
-Cardiac stimulation (beta1)
-increase BP (alpha1)
-Used to TX cardiogenc shock, septic shock, heart failure and adjunct to fluid administration in hypovolemic shock
-Dobutamine
-Highest affinity for beta1 receptor
-Less activity at alpha1 receptor
-Used to Tx cardiogenic shock, cardiac arrest and heart failure
-no affect on kidney -> better for a longer term dose
direct adrenergic agonists: non-catecholamines
-Phenylephrine (Neosynephrine)
-Vasoconstriction, increase BP and mydriasis (alpha1)
-Used as nasal decongestant, ocular decongestant and maintenance of BP during surgery
-given IV or topical
-Albuterol (Proventil)
-Bronchodilation (beta2)
-Used in asthma
-has alpha1 affect -> increase HR -> doesnt last though
-Clonidine (Catapres)
-Inhibits NE release from nerve terminal of postganglionic neuron (feedback inhibition: alpha2)
-Used to treat chronic hypertension
-Can have effects in CNS (sedation) - not a good drug bc of this
-Terbutaline (Brethine)
-Bronchodilation and uterine relaxation (beta2)
-Used to TX asthma and premature labor (tocolytic)
-great for children
-case reports for learning disability for premature labor use -> not proven
indirect adrenergic agonists: amphetamine
-Increase the release of NE & dopamine (DA) from SNS neurons
-Vasoconstriction, cardiac stimulation and increase BP
-Penetrates CNS - CNS stimulation (increases mood and alertness (but decreases appetite)
indirect adrenergic agonists: cocaine
-Local anesthetic
-Simulates SNS by blocking reuptake of NE & DA in the PNS & SNS – similar effects as amphetamine
indirect adrenergic agonists: tyramine
-Normal by-product of tyrosine metabolism in body
-Found in high concentrations in fermented foods such as certain cheeses, beers, red wine, certain cured meats (salami & pepperoni)
-Indirect sympathomimetic b/c it causes the release of stored catecholamines.
-Normally metabolized bymonoamine oxidase (MAO). So if taking an MAO inhibitor must avoid tyramine-containing foods
mixed acting adrenergic agents
-Cause vasoconstriction by binding to alpha1
-Increase release of NE from SNS neurons
-Nasal decongestants – Pseudoephedrine (sedofed) -> cant take it long term
adrenergic antagonists
-alpha adrenergic receptor antagonists:
-Nonselective -blockers
-Selective 1-blockers (“azosin”)
-beta adrenergic receptor antagonists (“olol”):
-Nonselective blockers
-Selective 1 blockers
-Mixed and adrenergic receptor antagonists
nonselective alpha-blockers
-Block alpha1 and alpha2 receptors
-Phenoxybenzamine (Dibenzyline)
-Noncompetitive, irreversible*
-TX hypertensive episodes associated w/ pheochromocytoma (tumor in adrenal medulla that secretes Catecholamines)
-Phentolamine (Regitine)
-Competitive, reversible*
-DX and TX hypertensive episodes from pheochromocytoma
-Tx necrosis and ischemia from extravasations of epinephrine
selective alpha1-blockers (“azosin”)
-relax vascular smooth muscle and smooth muscle in bladder and prostate.
-Produce vasodilation and decrease BP
-Used to treat hypertension and urinary retention due to benign prostatic hyperplasia (BPH)
-Agents include:
-Doxazosin (Cardura), Prazosin (Minipress), Terazosin (Hytrinon)
-Tamsulosin (Flomax) Alfuzosin (Uroxatral)– only for BPH not for HTN
-not really our go to drug for HTN
-can cause phantom ejaculation
nonselective beta-blockers
-Block beta1 receptors in heart and beta2 in smooth muscle, liver and other tissues
-beta1 blockade - decrease BP , decrease cardiac output, decrease renin release and decrease aqueous humor secretion
-beta 2 blockade – bronchoconstriction, decrease glycogenolysis (dont give to pts with diabetes), mask signs of hypoglycemia
-TX HTN, angina, arrhythmias, MI, migraine, glaucoma
-Agents include: Propranolol (Inderal), Nadolol (Corgard), Timolol (Timoptic)
selective beta1-blockers
-Selective for beta1 receptors (primarily in cardiac tissue)
-Produce less bronchoconstriction and other beta2 receptor mediated effects
-Aka cardioselective beta-blockers
-TX HTN, angina, MI
-Agents include: Atenolol (Tenormin), Metoprolol (Lopressor)
mixed alpha and beta receptor antagonists
-Block both alpha and beta receptors
-Carvedilol (Coreg) – Tx HTN and CHF
-Labetalol (Trandate) – Tx HTN -> this can be used IV in emergency
-not reaching their goals with just beta blocker
