autonomic nervous system Flashcards by Jasmin Maisuria

the study of drugs that influence the
autonomic nervous system (ANS), which controls involuntary physiological functions
like heart rate, digestion, and respiratory rate

autonomic pharmacology

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what is the importance of autonomic pharmacology

Drugs targeting the ANS are crucial for managing cardiovascular,
respiratory, gastrointestinal, and other systemic disorder

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Divisions of the ANS

sympathetic nervous system (SNS)
parasympathetic nervous system (PNS)

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relevance of autonomic drugs

essential for treating conditions like hypertension, asthma, and heart failure

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“Fight or Flight” response
Uses norepinephrine (NE) as the primary neurotransmitter
Key effects: Increased heart rate, bronchodilation, pupil dilation, vasoconstriction

sympathetic nervous system (SNS)

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“Rest and Digest” response
Uses acetylcholine (ACh) as the neurotransmitter
Key effects: Decreased heart rate, bronchoconstriction, increased digestion

parasympathetic nervous system (PNS)

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sympathetic is what kind of agonist

adrenergic agonist

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Balance between SNS and PNS:

Autonomic drugs manipulate this balance to treat various
conditions

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parasympathetic is what kind of agonist

cholinergic agonist

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Eye
Contraction of the radial muscle

dilation or mydriasis (SNS)

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o Catabolic
o Pre-ganglionic fibers are thoracolumbar
o Long post-ganglionic fibers

sympathetic (fight or flight)

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Eye
Contraction of the circular muscle

constriction or miosis (PNS)

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o Anabolic
o Pre-ganglionic fibers are craniosacral
o Short post-ganglionic fibers

parasympathetic (rest and digest)

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PNS pupils

constrict

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Vascular smooth muscle innervated ONLY by

SNS

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Regulates blood pressure and peripheral vascular resistance

Alpha-1 and beta-2 receptors found in:

vascular smooth muscle innervated only by SNS

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PNS HR and contractility

slow

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PNS bronchioles

constrict

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PNS bladder

relax

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PNS GI tract

motility

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SNS pupils

dilate

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SNS HR and contractility

increase

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SNS bronchioles

dilate

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SNS GI tract

slow

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SNS bladder

constrict

o Synthesized from Acetyl CoA and choline o Broken down by acetylcholinesterase

acetylcholine

o Norepinephrine o Epinephrine

catecholamines

how is norepinephrine/epi action terminated

 Reuptake into the neuron from which it is released  Inactivated by catechol-o- methyltransferase (COMT)  Inactivated by monoamine oxidase (MAO-I)

what are the receptors of cholinoreceptors (parasympathetic)

- muscarinic - nicotinic

what are the receptors of adrenoreceptors (sympathetic)

- alpha 1 and 2 - beta 1,2, and 3

location of muscarinic M1

CNS neurons, sympathetic postganglionic neurons

location of muscarinic M2

myocardium, smooth muscle, CNS neurons

location of muscarinic M3

exocrine glands, vessels, CNS neurons

location of muscarinic M4

CNS neurons

location of Muscarinic M5

vascular endothelium, CNS neurons

location of alpha 1

vascular smooth muscle

location of alpha 2

presynaptic adrenergic nerve terminals

location of beta 1

heart

location of beta 2

vascular smooth muscle and cardiac muscle

location of beta 3

lipocytes and bladder

o Mimic the effects of the PNS o Bethanechol, Pilocarpine

cholinergic agonists = parasympathomimetics

o Block the effects of the PNS o Atropine, Scopolamine

Cholinergic antagonists/anticholinergic drugs = Parasympatholytics

o Mimic the effects of the SNS o Epinephrine, Norepinephrine, Albuterol

Adrenergic agonists = Sympathomimetics

o Block the effects of the SNS o Beta-blockers, alpha-blockers

Adrenergic antagonists = Sympatholytics

o Direct action on the receptor for Acetylcholine o Can be at a muscarinic or nicotinic receptor

direct acting cholinergic agents

o Block the metabolism of Acetylcholine by cholinesterases o Increase the concentration of Acetylcholine at all cholinergic synapse

indirect acting cholinergic agents

what is cholinergic agonists MOA

These drugs stimulate cholinergic receptors, mimicking parasympathetic effects

activation of cholinergic receptors produces what response on eye

constriction

activation of cholinergic receptors produces what response on cardiovascular

decreased HR and contractility

activation of cholinergic receptors produces what response on respiratory

bronchoconstriciton and increased secretions

activation of cholinergic receptors produces what response on GI

increased motility, relaxation of sphincters

activation of cholinergic receptors produces what response on GU

bladder wall contraction, relaxation of sphincters

activation of cholinergic receptors produces what response on glands (sweat, salivary, lacrimal, etc.)

increased secretions (to help digestion)

Non-obstructive post-op ileus, urinary retention (increased bladder contraction)

Direct muscarinic agonists Esters = Bethanechol

o Acute angle-closure glaucoma o Pilocarpine = stimulates salivation, used in xerostomia (dry mouth) o Nicotine = stimulates nicotinic receptors in PNS and SNS, increases HR + BP

Direct muscarinic agonists Alkaloids = Pilocarpine, Muscarine, Nicotine

Contraindications of using direct muscarinic agonists

asthma, GI obstruction, PUD, pronounced bradycardia or HOTN

Reversible cholinesterase inhibitors - compete with Ach for a site on the AchE enzyme

o Neostigmine o Pyridostigmine o Donepezil o Galantamine o Rivastigmine

irreversible cholinesterase inhibitors - highly lipophilic

o Malthion o Parathion o Sarin o Insecticides/nerve gas o Phosphorylate AchE and inactivate

Clinical uses of cholinesterase inhibitors

Myasthenia Gravis Alzheimer’s Disease Open angle glaucoma Reversal of neuromuscular blockade after surgery

Cholinesterase inhibitors * Adverse Effects

Adverse Effects = SLUDGEM + bronchorrhea and bradycardia o Salivation/sweating o Lacrimation o Urination o Diarrhea o GI upset/gastroenteritis o Emesis o Miosis

Cholinesterase inhibitors toxicity

Toxicity is all of the above = organophosphate/pesticide exposure, nerve agents o Can lead to AMS, coma, seizures o Tx = Atropine and Pralidoxime, Benzos for seizures

Blocking the Action of Acetylcholine Produces What Response? Eye

mydriasis

Blocking the Action of Acetylcholine Produces What Response? cardiovascular

increased HR (high doses)

Blocking the Action of Acetylcholine Produces What Response? respiratory

bronchodilation and decreased secretions

Blocking the Action of Acetylcholine Produces What Response? GI

reduced motility

Blocking the Action of Acetylcholine Produces What Response? GU

urinary retention

Blocking the Action of Acetylcholine Produces What Response? glands (sweat, salivary, lacrimal, etc)

decreased secretions (reduced sweating/flushing)

Blocking the Action of Acetylcholine Produces What Response? CNS

drowsiness, hallucinations, coma

MOA of anticholinergics

block cholinergic receptors, reducing parasympathetic effects antagonize the effects of acetylcholine - act on the ion channel - compete for the binding of acetylcholine to the muscarinic receptor - block or inhibit acetylcholine

therapeutic use of atropine

reversal agent, pre-op for drying agents

therapeutic use of scopolamine

motion sickness, drying up secretions

therapeutic use of dicyclomine (bentyl)

GI antispasmodic (IBS)

therapeutic use of oxybutynin (ditropan XL)

urinary frequency, urgency and incontinence

therapeutic use of benztropine (cogentin)

drug induced extra pyramidal symptoms; Parkinsonism

therapeutic use of glycopyrrolate

reduction of secretions ("death rattle"), PUD

therapeutic use of trihexyphenidyl

drug induced extra pyramidal symptoms; parkinsonism

therapeutic use of tiotropium (Spiriva)/ ipratropium (nasal)

chronic obstructive pulmonary disease (COPD)

Atropine (increases HR, used in bradycardia), scopolamine (reduces motion sickness, used for N/V)

muscarinic antagonist

Curare (used as muscle relaxant in surgeries by blocking nicotinic receptors at neuromuscular junctions

nicotinic antagonist

Diphenhydramine (Benadryl)

first generation antihistamine

amitriptyline (TCAs)

antidepressants

Haloperidol (Haldol)

typical antipsychotics

Anticholinergics ADRs

* ANTI-SLUDGE (opposite of Salivation/sweating, Lacrimation, Urination, Defecation, GI upset, Emesis, + CNS effects) ABCDs * Agitation * Blurred vision * Constipation/confusion * Dry mouth * Stasis of urine (urinary retention)

Anticholinergics Contraindications

* Untreated narrow angle glaucoma * GI obstruction or constipation (watch the elderly!) * Bladder obstruction (caution any urinary retention) * Benign prostatic hypertrophy (BPH)

Can see in over-exposure to any anticholinergic, even Atropine poisoning

anticholinergic syndrome * "Mad as a hatter" = psychosis/delirium * "Red as a beet" = hot, flushed skin * "Dry as a bone" = dry mucous membranes, absence of secretions, constipation, and urinary retention * "Blind as a bat" = pupil dilation/mydriasis, inability to focus on near distances * "Hot as a hare/furnace" = hyperthermia/fever

reversal agent of anticholinergic syndrome

Physostigmine

Bind to all nicotinic receptors o At the neuromuscular junction o At the autonomic ganglia o Lead to skeletal muscle relaxation

neuromuscular blockers

binds to the receptor and opens the ion channel - Succinylcholine

depolarizing anticholinergic: NMB

binds to the receptor, but does NOT open the ion channel - rocuronium

non-depolarizing anticholinergic: NMB

Vascular smooth muscle = Vasoconstriction (HOTN), GI and urinary sphincter contraction

alpha 1

Lower blood pressure via decrease of sympathetic nervous system

alpha 2

Heart = tachycardia and increased cardiac output

beta 1

Respiratory = bronchodilation (asthma); Vascular smooth muscle = vasodilation, relaxation of bladder muscle and decreased GI motility

beta 2

MOA: These drugs stimulate adrenergic receptors (alpha, beta) to mimic sympathetic effects - mimic the effects of epi and norepinephrine - fight or flight

adrenergic agonists

Phenylephrine = decongestant (used in HOTN to increase BP

alpha 1

Clonidine = HTN

alpha 2

Dobutamine = CHF (increase contractility

beta 1

Albuterol = bronchodilation, asthma

beta 2

Epinephrine and Norepinephrine = vasopressors, Epi for anaphylaxis

Alpha + Beta agonists

* Act by releasing previously stored norepinephrine into the synapse * Amphetamines and their derivatives * Used clinically to treat ADHD and narcolepsy * Because they enter the CNS and act as a stimulant, they are drugs of abuse and classified as a CII medication * Pseudoephedrine is also related by acting directly on receptors as well as releasing stored norepinephrine

indirect acting agonists

Adrenergic Agonists ADRs

* Hypertension * Tachycardia * Increased risk for stroke or myocardial infarction * Arrhythmias * Mydriasis and photophobia

adrenergic agonists Contraindications/Precautions

* Do not use within 14 days of MAO-I * CV disease * Increased intraocular pressure/glaucoma (check before eye exam) * BPH * Seizure disorder * Thyroid dysfunction

* Block the effects of the SNS * Decrease sympathetic outflow from the brain * Suppress release of norepinephrine * Block postsynaptic adrenergic receptors * Divided into alpha blockers and beta blockers

adrenergic antagonists

* MOA: Alpha-1 receptor blockade that will produce vasodilation * More effective at blocking the actions of the SNS when it is “firing” * Greater vasodilation when a person is in a standing position * This is known as postural hypotension OR first dose syncope** * With systemic vasodilation the patient can also get an increase in heart rate, also known as reflex tachycardia * Most clinically useful medications are the “-azosins” * Prazosin (vasodilation, for HTN and BPH), Doxazosin, Terazosin * Used to treat hypertension and BPH * Some medications in the class have further selectivity for the alpha-1A receptor found in the genitourinary tract = smooth muscle relaxation * Tamsulosin = Flomax (kidney steone), also used to treat BPH

alpha 1 blockers

Clonidine, Methyldopa, Guanfacine, Tizanidine These alpha-2 receptors are presynaptic adrenergic receptors that create a negative feedback loop MOA: inhibit sympathetic output from the brain and the release of norepi from nerve terminals

Central Alpha-2 Agonists

alpha 1 blocker (tamsulosin) ADR

ejaculation decreased, absent, or retrograde

MOA: - Blockade of beta-1 receptors in the heart reduces the effects of sympathetic outflow and decreases heart rate - Blockade of beta-2 receptors in vascular smooth muscle and respiratory smooth muscle causes constriction * Clinical uses: * Cardiac Arrhythmias—atrial fibrillation * Hypertension * Angina * Heart Failure * Hyperthyroidism * Migraines

beta blockers

cardioselective beta blockers

- acebutolol* - atenolol - bisoprolol - esmolol - metoprolol

nonselective beta blockers

- propanolol -nadolol - penbutolol* - pindolol* - timolol

act as antagonist for catecholamines with low level Beta response

ISA

Beta Blockers ADRs:

* Decreased blood pressure * Decreased heart rate * Reduced cardiac output * Reduced exercise tolerance/fatigue * Bronchoconstriction (nonselective) * Block the effects of hypoglycemia o Normally patient has a release of epinephrine that causes tachycardia and tremors o BB are blocking beta receptors that epi binds to, preventing the full physiologic response * Heart block * Erectile dysfunction * Depression (nonselective)

* Block both beta-1 and beta-2 receptor subtypes and weak alpha-1 antagonists * Labetalol * Carvedilol * Clinical Uses: * Many the same as beta blockers * Primarily used for hypertension and heart failure (Labetalol preferred in pregnancy)

Mixed Alpha and Beta blockers

therapeutic Use of alpha-blockers (prazosin), beta-blockers (atenolol), and alpha-2 agonists (clonidine)

hypertension

therapeutic Use of beta-2 agonists (albuterol), anticholinergics (ipratropium)

asthma/COPD

therapeutic Use of beta-blockers (carvedilol), ACE inhibitors

heart failure

therapeutic use of muscarinic agonists (pilocarpine)

glaucoma

therapeutic use of muscarinic antagonists (scopolamine)

motion sickness

how to manage tremors and rigidity from Parkinson's disease

anticholinergics (benztropine)

how to increase ACh levels in alzheimers disease

acetylcholinesterase inhibitors (donepezil)

how to reduce bladder spasms in an overactive bladder

anticholinergics (oxybutynin)

autonomic nervous system Flashcards

(121 cards)