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pharm > autonomic nervous system > Flashcards

autonomic nervous system Flashcards

1
Q

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

A

autonomic pharmacology

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2
Q

what is the importance of autonomic pharmacology

A

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

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3
Q

Divisions of the ANS

A

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

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4
Q

relevance of autonomic drugs

A

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

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5
Q
  • “Fight or Flight” response
  • Uses norepinephrine (NE) as the primary neurotransmitter
  • Key effects: Increased heart rate, bronchodilation, pupil dilation, vasoconstriction
A

sympathetic nervous system (SNS)

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6
Q
  • “Rest and Digest” response
  • Uses acetylcholine (ACh) as the neurotransmitter
  • Key effects: Decreased heart rate, bronchoconstriction, increased digestion
A

parasympathetic nervous system (PNS)

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7
Q

sympathetic is what kind of agonist

A

adrenergic agonist

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7
Q

Balance between SNS and PNS:

A

Autonomic drugs manipulate this balance to treat various
conditions

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8
Q

parasympathetic is what kind of agonist

A

cholinergic agonist

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9
Q

Eye
Contraction of the radial muscle

A

dilation or mydriasis (SNS)

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9
Q

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

A

sympathetic (fight or flight)

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10
Q

Eye
Contraction of the circular muscle

A

constriction or miosis (PNS)

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11
Q

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

A

parasympathetic (rest and digest)

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12
Q

PNS pupils

A

constrict

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12
Q

Vascular smooth muscle innervated ONLY by

A

SNS

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13
Q

Regulates blood pressure and peripheral vascular resistance

Alpha-1 and beta-2 receptors found in:

A

vascular smooth muscle innervated only by SNS

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14
Q

PNS HR and contractility

A

slow

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15
Q

PNS bronchioles

A

constrict

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16
Q

PNS bladder

A

relax

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16
Q

PNS GI tract

A

motility

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17
Q

SNS pupils

A

dilate

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18
Q

SNS HR and contractility

A

increase

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19
Q

SNS bronchioles

A

dilate

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20
Q

SNS GI tract

A

slow

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21
Q

SNS bladder

A

constrict

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22
Q

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

A

acetylcholine

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23
Q

o Norepinephrine
o Epinephrine

A

catecholamines

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24
Q

how is norepinephrine/epi action terminated

A

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

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25
Q

what are the receptors of cholinoreceptors (parasympathetic)

A
  • muscarinic
  • nicotinic
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26
Q

what are the receptors of adrenoreceptors (sympathetic)

A
  • alpha 1 and 2
  • beta 1,2, and 3
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27
Q

location of muscarinic M1

A

CNS neurons, sympathetic postganglionic neurons

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28
Q

location of muscarinic M2

A

myocardium, smooth muscle, CNS neurons

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29
Q

location of muscarinic M3

A

exocrine glands, vessels, CNS neurons

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30
Q

location of muscarinic M4

A

CNS neurons

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31
Q

location of Muscarinic M5

A

vascular endothelium, CNS neurons

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32
Q

location of alpha 1

A

vascular smooth muscle

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33
Q

location of alpha 2

A

presynaptic adrenergic nerve terminals

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34
Q

location of beta 1

A

heart

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35
Q

location of beta 2

A

vascular smooth muscle and cardiac muscle

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36
Q

location of beta 3

A

lipocytes and bladder

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37
Q

o Mimic the effects of the PNS
o Bethanechol, Pilocarpine

A

cholinergic agonists = parasympathomimetics

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38
Q

o Block the effects of the PNS
o Atropine, Scopolamine

A

Cholinergic antagonists/anticholinergic drugs
= Parasympatholytics

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39
Q

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

A

Adrenergic agonists = Sympathomimetics

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40
Q

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

A

Adrenergic antagonists = Sympatholytics

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41
Q

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

A

direct acting cholinergic agents

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42
Q

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

A

indirect acting cholinergic agents

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43
Q

what is cholinergic agonists MOA

A

These drugs stimulate cholinergic receptors, mimicking parasympathetic effects

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44
Q

activation of cholinergic receptors produces what response on eye

A

constriction

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45
Q

activation of cholinergic receptors produces what response on cardiovascular

A

decreased HR and contractility

46
Q

activation of cholinergic receptors produces what response on respiratory

A

bronchoconstriciton and increased secretions

47
Q

activation of cholinergic receptors produces what response on GI

A

increased motility, relaxation of sphincters

48
Q

activation of cholinergic receptors produces what response on GU

A

bladder wall contraction, relaxation of sphincters

49
Q

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

A

increased secretions (to help digestion)

50
Q

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

A

Direct muscarinic agonists
Esters = Bethanechol

51
Q

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

A

Direct muscarinic agonists
Alkaloids = Pilocarpine, Muscarine, Nicotine

52
Q

Contraindications of using direct muscarinic agonists

A

asthma, GI obstruction, PUD, pronounced bradycardia or HOTN

53
Q
A
54
Q

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

A

o Neostigmine
o Pyridostigmine
o Donepezil
o Galantamine
o Rivastigmine

55
Q

irreversible cholinesterase inhibitors
- highly lipophilic

A

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

56
Q

Clinical uses of cholinesterase inhibitors

A

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

57
Q

Cholinesterase inhibitors
* Adverse Effects

A

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

58
Q

Cholinesterase inhibitors toxicity

A

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

59
Q

Blocking the Action of Acetylcholine
Produces What Response?
Eye

A

mydriasis

60
Q

Blocking the Action of Acetylcholine
Produces What Response?
cardiovascular

A

increased HR (high doses)

61
Q

Blocking the Action of Acetylcholine
Produces What Response?
respiratory

A

bronchodilation and decreased secretions

62
Q

Blocking the Action of Acetylcholine
Produces What Response?
GI

A

reduced motility

63
Q

Blocking the Action of Acetylcholine
Produces What Response?
GU

A

urinary retention

64
Q

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

A

decreased secretions (reduced sweating/flushing)

65
Q

Blocking the Action of Acetylcholine
Produces What Response?
CNS

A

drowsiness, hallucinations, coma

66
Q

MOA of anticholinergics

A

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

67
Q

therapeutic use of atropine

A

reversal agent, pre-op for drying agents

68
Q

therapeutic use of scopolamine

A

motion sickness, drying up secretions

69
Q

therapeutic use of dicyclomine (bentyl)

A

GI antispasmodic (IBS)

70
Q

therapeutic use of oxybutynin (ditropan XL)

A

urinary frequency, urgency and incontinence

71
Q

therapeutic use of benztropine (cogentin)

A

drug induced extra pyramidal symptoms; Parkinsonism

72
Q

therapeutic use of glycopyrrolate

A

reduction of secretions (“death rattle”), PUD

73
Q

therapeutic use of trihexyphenidyl

A

drug induced extra pyramidal symptoms; parkinsonism

74
Q

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

A

chronic obstructive pulmonary disease (COPD)

75
Q

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

A

muscarinic antagonist

76
Q

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

A

nicotinic antagonist

77
Q

Diphenhydramine (Benadryl)

A

first generation antihistamine

78
Q

amitriptyline (TCAs)

A

antidepressants

78
Q

Haloperidol (Haldol)

A

typical antipsychotics

79
Q

Anticholinergics
ADRs

A
  • 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)

80
Q

Anticholinergics Contraindications

A
  • Untreated narrow angle glaucoma
  • GI obstruction or constipation (watch the elderly!)
  • Bladder obstruction (caution any urinary retention)
  • Benign prostatic hypertrophy (BPH)
81
Q

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

A

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

82
Q

reversal agent of anticholinergic syndrome

A

Physostigmine

83
Q

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

A

neuromuscular blockers

84
Q

binds to the receptor and opens the ion channel
- Succinylcholine

A

depolarizing anticholinergic: NMB

85
Q

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

A

non-depolarizing anticholinergic: NMB

86
Q

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

A

alpha 1

87
Q

Lower blood pressure via decrease of sympathetic nervous system

A

alpha 2

88
Q

Heart = tachycardia and increased cardiac output

A

beta 1

89
Q

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

A

beta 2

90
Q

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

A

adrenergic agonists

91
Q

Phenylephrine = decongestant (used in HOTN to increase BP

A

alpha 1

92
Q

Clonidine = HTN

A

alpha 2

93
Q

Dobutamine = CHF (increase contractility

A

beta 1

94
Q

Albuterol = bronchodilation, asthma

A

beta 2

95
Q

Epinephrine and Norepinephrine = vasopressors, Epi for anaphylaxis

A

Alpha + Beta agonists

96
Q
  • 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
A

indirect acting agonists

97
Q

Adrenergic Agonists
ADRs

A
  • Hypertension
  • Tachycardia
  • Increased risk for stroke or myocardial
    infarction
  • Arrhythmias
  • Mydriasis and photophobia
98
Q

adrenergic agonists Contraindications/Precautions

A
  • Do not use within 14 days of
    MAO-I
  • CV disease
  • Increased intraocular
    pressure/glaucoma (check before
    eye exam)
  • BPH
  • Seizure disorder
  • Thyroid dysfunction
99
Q
  • 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
A

adrenergic antagonists

100
Q
  • 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
A

alpha 1 blockers

100
Q

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

A

Central Alpha-2 Agonists

101
Q

alpha 1 blocker (tamsulosin) ADR

A

ejaculation decreased, absent, or retrograde

102
Q

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
A

beta blockers

103
Q

cardioselective beta blockers

A
  • acebutolol*
  • atenolol
  • bisoprolol
  • esmolol
  • metoprolol
104
Q

nonselective beta blockers

A
  • propanolol
    -nadolol
  • penbutolol*
  • pindolol*
  • timolol
105
Q

act as antagonist for catecholamines with low level Beta response

A

ISA

106
Q

Beta Blockers
ADRs:

A
  • 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)
107
Q
  • 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)
A

Mixed Alpha and Beta blockers

108
Q

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

A

hypertension

109
Q

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

A

asthma/COPD

110
Q

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

A

heart failure

111
Q

therapeutic use of muscarinic agonists (pilocarpine)

A

glaucoma

112
Q

therapeutic use of muscarinic antagonists (scopolamine)

A

motion sickness

113
Q

how to manage tremors and rigidity from Parkinson’s disease

A

anticholinergics (benztropine)

114
Q

how to increase ACh levels in alzheimers disease

A

acetylcholinesterase inhibitors (donepezil)

115
Q

how to reduce bladder spasms in an overactive bladder

A

anticholinergics (oxybutynin)

pharm (3 decks)

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