Autonomics Flashcards

1
Q

What is the primary neurotransmitter for symphathetic preganglionic?

A

Acetylcholine

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2
Q

What is the primary neurotransmitter for sympathetic postganglionic?

A

Norepinephrine

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3
Q

What is the primary neurotransmitter for parasympathetic preganglionic?

A

Acetylcholine

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4
Q

What is the primary neurotransmitter for parasympathetic postganglionic?

A

Acetylcholine

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5
Q

What is the primary postsynaptic receptor type for sympathetic preganglionic?

A

Nicotinic-2

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6
Q

What is the primary postsynaptic receptor type for sympathetic postganglionic?

A

Adrenergic (alpha and beta)

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7
Q

What is the primary postsynaptic receptor type for parasympathetic preganglionic?

A

Nicotinic-2

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8
Q

What is the primary postsynaptic receptor type for parasympathetic postganglionic?

A

Muscarinic

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9
Q

What is the length of sympathetic preganglionic fibers?

A

Short

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10
Q

What is the length of sympathetic postganglionic fibers?

A

Long

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11
Q

What is the length of parasympathetic preganglionic fibers?

A

Long

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12
Q

What is the length of parasympathetic postganglionic fibers?

A

Short

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13
Q

What is the rate limiting factor in acetylcholine synthesis?

A

Choline availability

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14
Q

This synthetic enzyme for acetylcholine is used as a cholinergic marker

A

Choline acetyltransferase

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15
Q

Receptors in cholinergic transmission are of either of these types

A

Muscarinic or nicotinic

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16
Q

Termination of cholinergic neurotransmission occurs by ACh degradation, involving this enzyme in the synapse

A

Acetylcholinesterase

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17
Q

Termination of cholinergic neurotransmission occurs by ACh degradation, involving this enzyme in the blood and liver

A

Pseudocholinesterases

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18
Q

This is the rate limiting factor of catecholamine synthesis

A

Tyrosine hydroxylase enzyme

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19
Q

How does termination of cholinergic transmission occur?

A

By acetylcholine degradation

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20
Q

How does termination of adrenergic transmission occur?

A

Synpatic reuptake

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21
Q

Type of adrenergic receptor that increases calcium, causes contraction or secretion

A

Alpha 1

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22
Q

Type of adrenergic receptor that decreases neurotransmitter release (presynaptic effect), and causes contraction (postsynaptic effect)

A

Alpha 2

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23
Q

Type of adrenergic receptor that relaxes renal and mesenteric vascular smooth muscle

A

D1 (dopamine 1)

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24
Q

Type of adrenergic receptor that increases heart rate and force of contraction

A

Beta 1

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25
Q

Type of adrenergic receptor that relaxes smooth muscle

A

Beta 2

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26
Q

Type of adrenergic receptor that promotes relaxation of bladder

A

Beta 3

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27
Q

This is the single metabolite endpoint associated with dopamine biotransformation
Changes in this compound crudely reflect dopamine activity levels

A

HVA: homovanillic acid

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28
Q

This is sometimes used as a neuronal marker of activity and MAO, especially in the brain, is located in the nerve terminal
Changes crudely reflect brain dopamine activity

A

Dihydroxyphenylacetic acid (DOPAC)

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29
Q

Dihydroxyphenylacetic acid (DOPAC) is sometimes used as a neuronal marker of the activity of this enzyme
DOPAC changes crudely reflect brain dopamine activity

A

MAO (especially in the brain)

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30
Q

Isoform of monoamine oxidase that has nonspecific location and action

A

MAO-A

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31
Q

Monoamine oxidase isoform that has preference for dopamine; highest in CNS

A

MAO-B

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32
Q

In response to high blood pressure, the baroreceptors discharge and:
Heart rate falls due to these 2 factors

A

Vagal stimulation and loss of sympathetic tone

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33
Q

In response to high blood pressure, the baroreceptors discharge and:
Force of contraction falls due to these 2 factors

A

Vagal stimulation and loss of sympathetic tone

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34
Q

In response to high blood pressure, the baroreceptors discharge and:
Vasodilation occurs mainly by this

A

Loss of sympathetic tone
(to decrease peripheral resistance)

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35
Q

In response to high blood pressure, the baroreceptors discharge and have these 3 effects

A

Heart rate falls
Force of contraction falls
Vasodilation occurs

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36
Q

Type of cholinergic receptors that stimulates secretion of GI glands

A

M1 receptors (Gq)

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37
Q

Type of cholinergic receptors that act on the heart (atria but not ventricles)
SA node to slow heart rate and AV node to slow conduction velocity

A

M2 receptors (Gi)

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38
Q

M2 receptors act on the SA node to slow this

A

heart rate

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39
Q

M2 receptors act on the AV node to slow this

A

conduction velocity

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40
Q

M1 receptors stimulate secretion of these

A

GI glands

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41
Q

M2 receptors act on this organ

A

Heart

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42
Q

Type of cholinergic receptors that act on smooth muscle, eye, lung, GI tract, bladder, sphincters and glands

A

M3 receptor (Gq)

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43
Q

What effect do M3 receptors have on sphincter muscles of the eye?

A

Cause contraction for miosis

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44
Q

What effect do M3 receptors have on ciliary muscles in the eye?

A

Contract for accommodation for near vision

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45
Q

What effect do M3 receptors have on the GI tract?

A

Increase motility and activity

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46
Q

Form of cholinesterase that is located neuronally pre- and post-junctional

A

Acetylcholinesterase

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47
Q

Form of cholinesterase that is located in liver and plasma

A

Pseudocholinesterase

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48
Q

Do Methacholine, Bethanechol and Carbachol cross the blood brain barrier?

A

No; they are quaternary amines

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49
Q

Methacholine, Bethanechol and Carbachol are this type of amine so they do not cross the blood brain barrier

A

Quaternary amines

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50
Q

Cholinergic agonist that is used for bladder and bowel activation

A

Bethanechol

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51
Q

Do Cevimeline and Pilocarpine cross the blood brain barrier?

A

Yes; are tertiary amines
Thus produce central changes - Parkinson and seizures

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52
Q

Cevimeline and Pilocarpine are this type of amine, so they cross into the CNS

A

Tertiary amines

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53
Q

This muscarinic agonist has a black box warning for bronchial hyperreactivity

A

Methacholine

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54
Q

What reaction does tyrosine hydroxylase catalyze?

A

Tyrosine to Dopa

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55
Q

What enzyme catalyzes the conversion of tyrosine to dopa?

A

Tyrosine hydroxylase

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56
Q

What reaction does Aromatic L-amino acid decarboxylase catalyze?

A

Dopa to Dopamine

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57
Q

What enzyme catalyzes the conversion of Dopa to dopamine?

A

Aromatic L-amino acid decarboxylase

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58
Q

What reaction does Dopamine β-hydroxylase catalyze?

A

Dopamine to Norepinephrine

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59
Q

What enzymes catalyzes the conversion of dopamine to norepinephrine?

A

Dopamine β-hydroxylase

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60
Q

Degradative enzyme in adrenergic transmission that is located mainly in terminal

A

Monoamine oxidase

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61
Q

Degradative enzyme in adrenergic transmission that is located terminally, in plasma and liver

A

Catechol-O-methyltransferase

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62
Q

What enzyme in adrenergic biosynthesis is a therapeutic target?

A

Aromatic L-amino acid decarboxylase

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63
Q

What enzyme in adrenergic biosynthesis is rate limiting?

A

Tyrosine hydroxylase

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64
Q

Agonists to this cholinergic receptor can be used to treat glaucoma (both primary open-angle and closed-angle)

A

Muscarinic agonist
(causes contraction of ciliary muscle and iris sphincter)

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65
Q

Agonists to this cholinergic receptor can be used to treat dry mouth in Sjogren’s syndrome

A

Muscarinic agonist

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66
Q

Agonists to this cholinergic receptor can be used to treat urine retention, leading to urine release

A

Muscarinic agonists

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67
Q

Agonists to this cholinergic receptor can be used in diagnosis of bronchial hyperreactivity

A

Muscarinic agonists

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68
Q

Agonists to this type of receptor are contraindicated in asthma patients

A

Muscarinic agonist

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69
Q

Agonists to this cholinergic receptor are contraindicated in Parkinsonism

A

Muscarinic agonists

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70
Q

Agonists to this type of receptor are contraindicated in hyperthyroidism

A

Muscarinic agonists

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71
Q

Agonists to this type of receptor are contraindicated in seizure disorders

A

Muscarinic agonists

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72
Q

A patient with a tumor on the adrenal gland may have increased levels of this molecule that crudely reflects dopamine activity levels

A

HVA: homovanillic acid

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73
Q

Homovanillic acid is the breakdown product of this

A

Dopamine biotransformation

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74
Q

Catechol-0-methyl transferase is involved in this process

A

Adrenergic biotransformation

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75
Q

What effect does cholinergic (parasympathetic) transmission have on heart rate?

A

Decreases

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76
Q

What effect does cholinergic (parasympathetic) transmission have on heart force?

A

Decreases

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77
Q

What effect does cholinergic (parasympathetic) transmission have on bronchial tree?

A

Bronchoconstriction

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78
Q

What effect does cholinergic (parasympathetic) transmission have on circular muscle of iris?

A

Miosis

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79
Q

What effect does cholinergic (parasympathetic) transmission have on ciliary muscle of eye?

A

Accommodation

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80
Q

What effect does cholinergic (parasympathetic) transmission have on GI tract?

A

Contraction

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81
Q

What effect does adrenergic (sympathetic) transmission have on heart rate?

A

Increases (by beta 1)

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82
Q

What effect does adrenergic (sympathetic) transmission have on heart force?

A

Increases (by beta 1)

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83
Q

What effect does adrenergic (sympathetic) transmission have on arterial vessels?

A

Vasoconstriction (by alpha 1)

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84
Q

What effect does adrenergic (sympathetic) transmission have on skeletal blood vessels?

A

Vasodilation (by beta 2)

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85
Q

What effect does adrenergic (sympathetic) transmission have on venous vessels?

A

Vasoconstriction (by alpha 2)

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86
Q

What effect does adrenergic (sympathetic) transmission have on bronchial tree?

A

Bronchodilation

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87
Q

What effect does adrenergic (sympathetic) transmission have on the uterus?

A

Contraction (by alpha 1)

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88
Q

What effect does adrenergic (sympathetic) transmission have on radial muscle of iris?

A

Mydriasis (by alpha 1)

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89
Q

What effect does adrenergic (sympathetic) transmission have on the kidney?

A

Renin release increased by beta 1
Renin release decreased by alpha 1

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90
Q

What effect does adrenergic (sympathetic) transmission have on the ureter?

A

Contraction (by alpha 1)

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91
Q

What effect does adrenergic (sympathetic) transmission have on the GI tract?

A

Relaxation (by alpha 2)

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92
Q

What effect does adrenergic (sympathetic) transmission have on insulin release?

A

Decreases (by alpha 1)

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93
Q

Renin release is increased by this adrenergic receptor

A

Beta 1

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94
Q

Renin release is decreased by this adrenergic receptor

A

Alpha 1

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95
Q

Carbamates and organophosphates inhibit this enzyme

A

Cholinesterase
(thus prolong acetylcholine duration and are analogous to agonist action)

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96
Q

Ambenonium, Edrophonium, Neostigmine, Physostigmine, Pyridostigmine are examples of this type of drug

A

Carbamates
(cholinesterase inhibitors)

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97
Q

Edrophonium is this type of drug

A

Carbamate

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98
Q

Carbamate that is indicated in diagnosis of myasthenia gravis and treatment

A

Edrophonium

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99
Q

Carbamate that is indicated in reversal of neuromuscular blockage by non-depolarizing muscle relaxants

A

Edrophonium

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100
Q

Edrophonium is this type of amine

A

Quaternary

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101
Q

Carbamate that is quarternary and highly water soluble
Rapid renal elimination

A

Edrophonium

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102
Q

Edrophonium is used in diagnosis and treatment of this condition

A

Myasthenia gravis

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103
Q

Carbamate that is a tertiary amine and is readily absorbed
Penetrates the CNS (crosses blood brain barrier)

A

Physostigmine

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104
Q

Physostigmine is this type of drug

A

Carbamate

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105
Q

DUMBBELSS is an acronym describing the toxicities of this type of drug
(Diarrhea, urination, miosis, bronchoconstriction, bradycardia, excitation (muscles and CNS), lacrimation, salivation and sweating)

A

Cholinesterase inhibitors
(e.g. carbamates, organophosphates)

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106
Q

What are the toxicities of cholinesterase inhibitors?

A

DUMBBELSS
Diarrhea
Urination
Miosis
Bronchoconstriction
Bradycardia
Excitation (muscles and CNS)
Lacrimation
Salivation
Sweating

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107
Q

Delayed toxicity of organophosphates is related to this, and results in flaccid and spastic paralysis

A

Demyelination
(delayed toxicity is independent of cholinesterase inhibitory activity)

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108
Q

Delayed toxicity of this type of drug is related to demyelination and results in flaccid and spastic paralysis

A

Organophosphate

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109
Q

What is the MOA of carbamates?

A

Cholinesterase inhibitors

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110
Q

What is the MOA of organophosphates?

A

Cholinesterase inhibitors

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111
Q

The treatment of cholinesterase inhibitor overdose involves administration of this type of drug FIRST

A

Anticholinergic (e.g. atropine)

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112
Q

Atropine may be given first in overdose of this type of drug

A

Cholinesterase inhibitor
(e.g. Carbamates, organophosphates)

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113
Q

In overdose of cholinesterase inhibitors, is atropine or pralidoxime chloride (2-PAM) given first?

A

Atropine
(atropine saves the patient, 2-PAM saves the enzyme)

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114
Q

In overdose of cholinesterase inhibitor, this is always supplemental to atropine and will improve neuromuscular toxicity by restoring cholinesterase activity

A

Pralidoxime chloride (2-PAM)

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115
Q

Do quaternary amines cross the blood brain barrier?

A

No
so they remain peripheral
(examples: Methacholine, Bethanechol)

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116
Q

Cholinergic agonist that is used for bladder and bowel activation

A

Bethanechol

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117
Q

Bethanechol is a cholinergic agonist used to treat this

A

Bladder and bowel activation

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118
Q

Bethanechol is an agonist to this, and is used for bladder and bowel activation

A

Cholinergic agonist

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119
Q

Methacholine, Bethanechol and Carbachol are agonists to this

A

Cholinergic agonists

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120
Q

Are Methacholine, Bethanechol and Carbachol found centrally or peripherally?

A

Peripherally - are quaternary amines so they do not cross blood brain barrier

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121
Q

Do tertiary amines cross into the CNS?

A

Yes
(examples: Cevimeline and Pilocarpine)

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122
Q

Cevimeline and Pilocarpine are agonists to this type of receptor

A

Cholinergic agonists

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123
Q

Methacholine is this type of drug

A

Cholinergic (muscarinic) agonist

124
Q

Methacholine has this black box warning

A

Bronchial hyperreactivity

125
Q

How do you treat cholinesterase inhibitor overdose?

A

Administration of anticholinergic (atropine) THEN pralidoxime chloride (2-PAM)
Atropine saves the patient - 2-PAM saves the patient

126
Q

Cholinesterase inhibitors are indirect agonists to this

A

Cholinergic agonists

127
Q

Organophosphate that is used as insecticides as mammals inactivate the cholinesterase forms of each drug before toxic to mammalian system
Insects do not detoxify the toxic form

128
Q

Atropine, Darifenacin, Oxybutynin, Scopolamine, Solifenacin, Tolterodine are antagonists to this

A

Muscarinic receptors

129
Q

Atropine, Darifenacin, Oxybutynin, Scopolamine, Solifenacin, Tolterodine are this type of drug

A

Muscarinic antagonists

130
Q

Do muscarinic agonists or antagonists inhibit sweating?

A

Antagonists

131
Q

Do muscarinic antagonists cause mydriasis or miosis?

132
Q

Do muscarinic antagonists increase or decrease aqueous outflow resistance of the eye?

133
Q

Do muscarinic antagonists result in increased or decreased GI tract salivation and secretions?

134
Q

What effect do muscarinic antagonists have on the bladder?

A

Urinary retention

135
Q

Do muscarinic antagonists cause bronchial dilation or constriction?

A

Dilations
(and decreased secretions)

136
Q

Do muscarinic antagonists cause bradycardia at high or low doses?

A

Presynpatic and central low dose effect

137
Q

Muscarinic antagonist indicated for bradycardia

138
Q

Muscarinic antagonist indicated for cycloplegia or mydriasis

139
Q

Muscarinic antagonist indicated for aspiration prophylaxis

140
Q

Muscarinic antagonist indicated for overactive bladder and urinary incontinence

A

Darifenacin

141
Q

Muscarinic antagonist indicated for amnesia and sedation induction

A

Scopolamine

142
Q

Muscarinic antagonist indicated for motion sickness

A

Scopolamine

143
Q

Muscarinic antagonist indicated for Parkinson’s disease

A

Scopolamine

144
Q

Are muscarinic agonists or antagonists contraindicated in glaucoma?

A

Antagonists

145
Q

Type of drugs that are contraindicated in glaucoma, prostatic hyperplasia and cardiac disease

A

Muscarinic antagonists

146
Q

Infants are more likely to become hyperthermic with use of this type of drug

A

Muscarinic antagonists

147
Q

Infants are more likely to have this with use of muscarinic antagonists

A

Hyperthermia

148
Q

Blurred vision, dry mouth/skin, confusion, mydriasis, constipation, urinary retention and sedation are toxicities of this type of drug

A

Muscarinic antagonists

149
Q

Hyperthermia may occur in small individuals with use of this type of drug

A

Muscarinic antagonists

150
Q

What are some of the toxicities of Muscarinic antagonists?

A

Blurred vision
Dry mouth/skin (hyperthermia)
Confusion
Mydriasis (dilated pupils)
Constipation
Urinary retention
Sedation

151
Q

This compound stimulates and desensitizes receptors

152
Q

What effect do nicotine agonists have on heart rate?

153
Q

What effect do nicotine agonists have on BP?

154
Q

How do nicotine agonists increase heart rate and BP?

A

Stimulates adrenal release of catecholamines

155
Q

This drug is a partial agonist at some nicotinic receptor sites (a4B2) and full agonist at other (a7) sites

A

Varenicline

156
Q

Varenicline is a partial agonist at some of these sites

A

Nicotinic receptor sites (a4B2)
(is a full agonist at other sides; a7)

157
Q

What is an adverse effect of Varenicline?

A

Negative mood and behavioral changes

158
Q

Adverse neuropsychiatric events (unusual and aggressive behavior) as a result of Varenicline use may be worsened with concomitant use of this

159
Q

Adverse neuropsychiatric events (unusual and aggressive behavior) as a result of use of this drug may be worsened with concomitant use of alcohol

A

Varenicline

160
Q

OnabotulinumtoxinA inhibits this

A

Acetylcholine release

161
Q

What are the two phases of depolarizing neuromuscular blockers?

A

1: depolarization block
2: desensitization

162
Q

These inhibitors will not reverse a depolarizing blocker but may intensify blockade

A

Cholinesterase inhibitors
(do not treat paralysis with cholinesterase inhibitors)

163
Q

Succinylcholine is inactivated by this enzyme

A

Pseudocholinesterase

164
Q

Adverse effect of this includes malignant hyperthermia, especially when used with halothane (inhalation anesthetic)

A

Depolarizing muscular blockers - Succinylcholine

165
Q

Depolarizing muscular blockers (Succinylcholine) can cause malignant hyperthermia, especially when used with this

A

Halothane (inhalation anesthetic)

166
Q

Depolarizing muscular blockers (Succinylcholine) can cause this, especially when used with Halothane (inhalation anesthetic)

A

Malignant hyperthermia

167
Q

Rocuronium is this type of drug

A

Non-depolarizing neuromuscular blockers (AKA competitive nicotinic receptor inhibitors)

168
Q

At low doses, this type of drug is competitive reversible blockers of the neuromuscular junction

A

Non-depolarizing neuromuscular blockers (AKA competitive nicotinic receptor inhibitors)
E.g. Rocuronium

169
Q

These can reverse the action of Non-depolarizing neuromuscular blockers (AKA competitive nicotinic receptor inhibitors; e.g. Rocuronium)

A

Cholinesterase inhibitors

170
Q

Cholinesterase inhibitors can reverse action of this type of drug

A

Non-depolarizing neuromuscular blockers (AKA competitive nicotinic receptor inhibitors)
E.g. Rocuronium

171
Q

Can cholinesterase inhibitors reverse the action of Rocuronium?

A

Yes
(Rocuronium is a non-depolarizing neuromuscular blocker)

172
Q

Nicotine effects on heart are triggered by nicotine release of these from adrenal

A

Catecholamines

173
Q

This is a partial nicotine agonist and has some increased risk of psychiatric problems with use
Is used for tobacco cessation

A

Varenicline

174
Q

This inhibits release of acetylcholine by interfering with SNAP25

A

OnabotulinumtoxinA

175
Q

OnabotulinumtoxinA inhibit release of acetylcholine by interfering with this

176
Q

OnabotulinumtoxinA inhibit release of this by interfering with SNAP25

A

Acetylcholine

177
Q

Varenicline is a partial agonist of this and has some increased risk of psychiatric problems with use

178
Q

This causes tachyphylaxis at neuromuscular junction and results in total paralysis
Should only last minutes due to rapid inactivation by pseudocholinesterases (patient deficit in this enzyme and paralysis may last hours)

A

Succinylcholine

179
Q

What effect does succinylcholine have at the neuromuscular junction?

A

Causes tachyphylaxis
(results in total paralysis)

180
Q

Reversible neuromuscular receptor blockers allow greater dosage flexibility and can be reversed by these inhibitors

A

Cholinesterase

181
Q

What is a Alpha-1 Adrenergic action on vascular smooth muscle, pupillary radial (dilator) muscle and prostate?

A

Contraction

182
Q

What is a Alpha-1 Adrenergic action on the heart?

A

Increased force of contraction

183
Q

What is alpha-2 adrenergic effect on presynaptic nerve terminals?

A

Inhibition of neurotransmitter release

184
Q

What are two beta-1 adrenergic effects on the heart?

A

Increase heart rate at SA node
Increase force of contraction

185
Q

Beta-1 adrenergic action on heart includes increased heart rate at this

186
Q

What is beta-1 adrenergic effect on the kidney?

A

Increase renin release

187
Q

What is beta-2 adrenergic effect on skeletal muscle?

A

Stimulates glycogenolysis to promote contractility (tremor)

188
Q

What is beta-2 adrenergic effect on bronchioles and uterus?

A

Relaxation

189
Q

What is beta-3 adrenergic effect on the bladder?

A

Relaxes detrusor smooth muscle

190
Q

What is dopamine-1 effect on renal, mesenteric and coronary vasculature?

A

Vasodilation

191
Q

Norepinephrine, epinephrine, isoproterenol, dopamine, and dobutamine are agonists of this

A

Adrenergic agonists

192
Q

Norepinephrine is an agonist of these adrenergic receptors

A

Alpha-1 and -2, beta-1 and -3
(more powerful at alpha activation)

193
Q

Epinephrine is an agonist of these adrenergic receptors

A

Alphas and betas

194
Q

Dopamine is an agonist of these adrenergic receptors

A

Dopamine-1, beta-1, alpha-1

195
Q

With norepinephrine, heart rate may decrease by this reflex

A

Vagal reflex

196
Q

What effect does norepinephrine have on arteries and veins?

A

Vasoconstriction

197
Q

Tissue necrosis and sloughing in extravasation are black box warnings of this adrenergic agonist

A

Norepinephrine

198
Q

What is an adverse effect of norepinephrine?

A

Tissue necrosis and sloughing in extravasation (black box)

199
Q

Epinephrine results in vasoconstriction in most arterial beds except:

A

Vasodilation in skeletal muscle beds

200
Q

Epinephrine results in this effect on vasculature in most arterial beds (except skeletal muscle beds)

A

Vasoconstriction

201
Q

Adrenergic agonist used for emergency treatment of anaphylactic shock

A

Epinephrine

202
Q

Is atropine indicated for bradycardia or tachycardia?

A

Bradycardia

203
Q

What effect does Isoproterenol have on arteries?

A

Vasodilation

204
Q

What effect does Isoproterenol have on lungs?

A

Bronchodilation

205
Q

These are adverse effects of this adrenergic agonist:
Palpitation, headache, flushed skin
Tachycardia
Cardiac ischemia and arrhythmias

A

Isoproterenol

206
Q

Adrenergic agonist used for short-term cardiovascular support (shock - following hypovolemia correction)

207
Q

Extravasation of this adrenergic agonist can produce ischemic necrosis and sloughing (black box warning)

208
Q

Extravasation of dopamine can produce this

A

Ischemic necrosis and sloughing (black box warning)

209
Q

Does the alpha or beta effect predominate with use of dobutamine?

210
Q

Type of adrenergic agonists used as bronchodilators and smooth muscle relaxants

A

Beta-selective agents

211
Q

Type of adrenergic agonists used for asthma and uterine relaxation

A

Beta-selective agents

212
Q

Type of adrenergic agonist with adverse effects of:
Tremor
Cardiovascular effects (tachycardia)
Decreased arterial oxygen tension
Possible increased risk of death

A

Beta-selective agents

213
Q

Tachycardia is an adverse effect of beta-selective agents that is mainly due to this stimulation

214
Q

Do beta-selective agents have an adverse effect of bradycardia or tachycardia?

A

Tachycardia (mainly due to beta-1 stimulation)

215
Q

Tachycardia is an adverse effect of this type of adrenergic agonist mainly due to beta-1 stimulation

A

Beta-selective agents

216
Q

Arterial oxygen tension may fall during treatment of asthma with beta-selective agents due to vasodilation of these

A

Pulmonary beds

217
Q

Arterial oxygen tension may fall during treatment of asthma with beta-selective agents due to vasodilation or vasoconstriction of pulmonary beds?

A

Vasodilation

218
Q

Salmeterol is this type of adrenergic agonist

A

Beta-selective agent

219
Q

Salmeterol is a beta-selective agent with this black box warning

A

Possible increased risk of death and near death from asthma

220
Q

Possible increased risk of death and near death from asthma is a black box warning for this beta-selective agent

A

Salmeterol

221
Q

Adrenergic agonist that is a beta-3 selective agent

A

Mirabegron

222
Q

What effect does Mirabegron have on the bladder?

A

Relaxes the detrusor smooth muscle to increase bladder capacity

223
Q

Oxymetazoline, Phenylephrine, and Pseudoephedrine are this type of adrenergic agonist

A

Alpha-1 selective agents

224
Q

Type of adrenergic agonist used for nasal decongestant, mydriasis, maintenance of BP during surgery

A

Alpha-1 selective agents
(examples: Oxymetazoline, Phenylephrine, Pseudoephedrine)

225
Q

Oxymetazoline, Phenylephrine, and Pseudoephedrine are selective agonists of this adrenergic receptor

226
Q

Clonidine and Alpha-methyldopa are selective agents of this adrenergic receptor

227
Q

What is the MOA of Clonidine and Alpha-methyldopa?

A

Alpha-2 selective agents so Antihypertensive actions

228
Q

Alpha-2 selective agents (e.g. Clonidine, Alpha-methyldopa) have this dominant action

A

Antihypertensive

229
Q

Rebound effect may occur with abrupt discontinuation of this type of adrenergic agonist

A

Alpha-2 selective agents
(E.g. Clonidine, Alpha-methyldopa)

230
Q

This alpha-2 selective agent is a substrate for catecholamine synthesis pathway
End product of alpha-methyl norepinephrine

A

Alpha-methyl Dopa

231
Q

Alpha-methyl Dopa is an alpha-2 selective agent that is a substrate for this synthesis pathway

A

Catecholamine

232
Q

Alpha-methyl Dopa is an end product of this
(involved in catecholamine synthesis pathway)

A

Alpha-methyl norepinephrine

233
Q

Adverse effects of this type of adrenergic agonist includes low incidence of rebound hypertension, hemolytic anemia, Parkinson-like effect and hyperprolactinemia

A

Alpha-2 selective agents
(e.g. Clonidine, Alpha-methyldopa)

234
Q

Hemolytic anemia is an adverse effect of this type of adrenergic agonist

A

Alpha-2 selective agents
(e.g. Clonidine, Alpha-methyldopa)

235
Q

Parkinson-like effect and hyperprolactinemia are adverse effects of this type of adrenergic agonist

A

Alpha-2 selective agents
(e.g. Clonidine, Alpha-methyldopa)

236
Q

Alpha-methyl dopamine is partial agonist at this receptor

237
Q

Alpha-methyl dopamine is this type of agonist at dopamine receptor

238
Q

What effect do mixed action agonists have on vascular resistance and BP?

239
Q

What effect do mixed action agonists have on respirations?

240
Q

Type of adrenergic agonists with central actions including Increased respiration, increased alertness/confidence, Psychogenic effects, Appetite suppressant

A

Mixed action agonists

241
Q

Amphetamine, Methamphetamine, Methylphenidate, Ephedrine, and Tyramine are this type of adrenergic agonist

A

Mixed action agonist

242
Q

Pulmonary hypertension (especially in women) is an adverse effect of this type of adrenergic agonist

A

Mixed action agonist

243
Q

In presence of monoamine oxidase inhibitors, this mixed action agonist can result in increased pressure (systolic increase > 30 mmHg)

244
Q

In presence of this type of drug, tyramine can result in increased pressure (systolic increase > 30 mmHg)

A

Monoamine oxidase inhibitors

245
Q

In presence of monoamine oxidase inhibitors, tyramine can result in increased pressure (systolic increase > 30 mmHg), mainly through this mechanism

A

Release of catecholamine

246
Q

In presence of monoamine oxidase inhibitors, tyramine can result in increased pressure (systolic increase > 30 mmHg), mainly through the release of these

A

Catecholamines

247
Q

Adrenergic receptor that:
vasoconstricts the peripheral vascular system (increases resistance), increase heart force

248
Q

Adrenergic receptor that is a weaker vasoconstrictor, presynaptic modulator

249
Q

Adrenergic receptor that increases heart rate and force of contraction

250
Q

Adrenergic receptor that relaxes bronchial structures, relaxes skeletal muscle vessels (reduces resistance), and triggers tremor

251
Q

Adrenergic receptor that enlarges bladder

252
Q

Is norepinephrine mainly an alpha or beta response?

253
Q

Is epinephrine mainly an alpha or beta response?

254
Q

Adrenergic agonist that maintains heart rate and opens mesenteric/ renal vascular beds

255
Q

Type of adrenergic agonist that relaxes bronchioles for treatment of hyperreactive airways

A

Beta 2 selectives

256
Q

Adrenergic agonist that enlarges bladder

A

Mirabegron

257
Q

Non-selective alpha antagonists are used for acute control of this

A

Hypertension

258
Q

Phenoxygenzamine is a non-selective alpha antagonist that is a reversible or irreversible binding agent?

A

Irreversible

259
Q

Phentolamine is a non-selective alpha antagonist that is a reversible or irreversible binding agent?

A

Reversible

260
Q

Phenoxybenzamine is this type of drug

A

Non-selective alpha antagonist

261
Q

Phentolamine is this type of drug

A

Non-selective alpha antagonist

262
Q

This type of adrenergic antagonist has cardiovascular effects including vasodilation, hypotension, tachycardia and venous pooling

A

Non-selective alpha antagonist
(Phenoxybenzamine, Phentolamine)

263
Q

Non-selective alpha antagonists are used for control of this in pheochromocytoma

A

Blood pressure

264
Q

Non-selective alpha antagonists are used for blood pressure control in patients with this

A

Pheochromocytoma

265
Q

Type of adrenergic antagonist used for BP control in pheochromocytoma

A

Non-selective alpha antagonist
(Phenoxybenzamine, Phentolamine)

266
Q

Type of adrenergic antagonist used for benign prostatic hypertrophy

A

Non-selective alpha antagonists
(Phenoxybenzamine, Phentolamine)

267
Q

What is the First Doses effect?

A

Severe postural hypotension that occurs early in therapy or when dose is increased

268
Q

Antagonists to this have First Doses effect

A

Alpha
(Non-selective alpha antagonists especially)

269
Q

Hypotension, tachycardia and sexual dysfunction are adverse effect to these types of drugs

A

Non-selective alpha antagonists
(Phenoxybenzamine, Phentolamine)

270
Q

This non-selective alpha antagonist can be used in clonidine-withdrawal hypertension

A

Phentolamine

271
Q

Drug names that end in -osin are this type of drug

A

Selective alpha-1 antagonists

272
Q

Are selective alpha-1 antagonists reversible or irreversible blockers?

A

All are reversible blockers

273
Q

Selective alpha-1 antagonists have names ending in this

A

“-osin”

274
Q

Type of adrenergic antagonist that is indicated for general treatment of hypertension and benign prostatic hypertrophy

A

Selective alpha-1 antagonists

275
Q

What effect do Selective alpha-1 antagonists have on vascular resistance?

276
Q

Do non-selective alpha or selective alpha-1 antagonists have a lower incidence of postural hypotension?

A

Selective alpha-1 antagonists

277
Q

Fluid retention, tachycardia and nasal stuffiness are adverse effects to this type of adrenergic antagonist

A

Selective alpha-1 antagonists

278
Q

Drug names that end in -olol are this type of drug

A

Beta blockers

279
Q

Beta blockers have drug names that end in this

A

“-olol”

280
Q

Severe bradycardia, bronchospasm, peripheral vascular disease and withdrawal with abrupt stoppage of drug are adverse effects of this type of adrenergic antagonist

A

Non-specific beta blockers

281
Q

Do alpha antagonists cause bradycardia or tachycardia?

A

Tachycardia

282
Q

Do beta blockers cause bradycardia or tachycardia?

A

Bradycardia

283
Q

Depression, elevated LDL and triglyceride levels, and blunted responses and recovery from hypoglycemia are common toxicities to this type of adrenergic antagonists

A

Beta blockers

284
Q

A toxicity of this type of drug includes blunted responses and recovery from hypoglycemia - may increase risk of diabetes

A

Beta blockers

285
Q

As a result of use of beta blockers, loss of vasodilation from this increases alpha vasoconstriction in extremities

286
Q

With use of beta blockers, patients may have blunted responses and recovery from this

A

Hypoglycemia

287
Q

The first letter of this type of drug spells “BEAM”

A

Beta-1 antagonists
(Acebutolol, Atenolol, Bisoprolol, Esmolol, Metoprolol)

288
Q

Acebutolol, Atenolol, Bisoprolol, Esmolol, and Metoprolol are this type of drug

A

Beta-1 antagonists

289
Q

These 2 drugs are non-selective beta blockers that are also alpha-1 blockers

A

Carvedilol and Labetalol

290
Q

Carvedilol and Labetalol are non-selective beta blockers that also block this

291
Q

Beta 2 blockage increases risk for patients with these 3 conditions

A

Diabetes
Asthmatics
Peripheral artery disease

292
Q

Pindolol and Acebutolol are this type of adrenergic antagonist

A

Beta blockers with ISA (intrinsic sympathomimetic activity)

293
Q

Beta blocker with ISA (intrinsic sympathomimetic activity) that is primarily used in patients with low resting heart rate (50 beats/min)

A

Acebutolol

294
Q

Acebutolol is a beta blocker with ISA (intrinsic sympathomimetic activity) that is primarily used in patients with this

A

Low resting heart rate (50 beats/min)

295
Q

This is the enzyme that mediates the initial step of norepinephrine and epinephrine metabolism the in presynaptic cell cytoplasm

A

Monoamine oxidase

296
Q

This compound blocks neuronal uptake transporter (NET) function, thereby inhibiting termination of adrenergic neurotransmission

297
Q

Cocaine blocks neuronal uptake transporter (NET) function, thereby inhibiting termination of this type of neurotransmission

A

Adrenergic

298
Q

This drug treats glaucoma by inducing miosis to allow drainage of aqueous humor via the trabecular meshwork (Canal of Schlemm)

A

Pilocarpine

299
Q

What is the MOA of pilocarpine in treatment of glaucoma?

A

Induces miosis
(allows drainage of aqueous humor via the trabecular meshwork)

300
Q

Pilocarpine is this type drug

A

Cholinergic agonist

301
Q

This adrenergic receptor induces both chronotropic and ionotropic effects on cardiac muscle contraction

302
Q

Which 2 beta adrenergic inhibitor drugs are indicated to treat hypertension in patients with bradycardia?

A

Acebutolol and Pindolol

303
Q

Why are Acebutolol and Pindolol indicated to treat hypertension in patients with bradycardia and not other beta blockers?

A

Because they have sympathomimetic activity

304
Q

This beta-2 selective agent is not recommended for acute treatment of asthma due to slow onset of action

A

Salmeterol

305
Q

Uterine relaxant is a secondary use for this beta-2 selective agent, which arrests premature labor

A

Terbutaline

306
Q

Terbutaline is a selective adrenergic agonist for this