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Chapter 4 Flashcards

1
Q

act on receptors stimulated
by norepinephrine or epinephrine.

a. adrenergic drug

b. cholinergic drugs

A

a. adrenergic drug

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1
Q

act on receptors activated by acetylcholine (ACh)

a. adrenergic drug

b. cholinergic drugs

A

b. cholinergic drugs

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2
Q

Choline is transported from the
extracellular fluid into the cytoplasm of the cholinergic neuron by
an energy-dependent carrier system that cotransports sodium and
can be inhibited by the drug

a. echothiophate

b.hemicholinium

A

b.hemicholinium

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3
Q

Choline has
a quaternary _____and carries a permanent positive charge
and, thus, cannot diffuse through the membran

A

Choline has
a quaternary nitrogen and carries a permanent positive charge
and, thus, cannot diffuse through the membran

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4
Q

____is the rate-limiting step in ACh synthes

A

The uptake of
choline is the rate-limiting step in ACh synthes

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5
Q

______catalyzes the reaction of choline with acetyl coenzyme
A (CoA) to form ACh (an ester) in the cytosol.

A

. Choline acetyl-
transferase catalyzes the reaction of choline with acetyl coenzyme
A (CoA) to form ACh (an ester) in the cytosol.

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6
Q

ACh is packaged and
stored into presynaptic vesicles by an active transport process.
The mature vesicle contains not only ACh but also _____and _____

A

ACh is packaged and
stored into presynaptic vesicles by an active transport process.
The mature vesicle contains not only ACh but also adenosine
triphosphate (ATP) and proteoglycan

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7
Q

at synthesis and release of acethylcholine…When an action potential propagated
by voltage-sensitive sodium channels arrives at a nerve ending,
voltage-sensitive _____ channels on the presynaptic membrane
open, causing an increase in the concentration of intracellular
____.

A

calcium

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8
Q

at synthesis and release of acethylcholine… what will happen if their is an increase in intracellular calcium

A

Elevated calcium levels promote the fusion of synaptic
vesicles with the cell membrane and the release of contents into
the synaptic space.

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9
Q

Acethylcholines release is blocked by

a. botulinum toxin

b. Spider venom

A

a. botulinum toxin

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10
Q

this causes
release of acetylcholine.

a. botulinum toxin

b. Spider venom

A

b. Spider venom

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11
Q

Acetylcholine is rapidly
hydrolyzed by ___ in the
synaptic cleft.

a.acetyl-
cholinesterase

b. Choline acetyltransferase

A

a.acetyl-
cholinesterase

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12
Q

catalyzes the synthesis of
acetylcholine from choline
and acetyi-CoA.

a.acetyl-
cholinesterase

b. Choline acetyltransferase

A

b. Choline acetyltransferase

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13
Q

Choline is taken
up by the neuron.
This transport is
inhibited by

a. hemicholinium

b. echothiophate

A

a. hemicholinium

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14
Q

what are the two families of cholinoceptors

A

muscarinic and nicotinic
receptors,

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15
Q

belong to the class of G-protein–coupled
receptors (metabotropic receptors).

a. nicotinic receptor

b. muscarinic receptor

A

b. muscarinic receptor

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16
Q

an alkaloid in certain poi-
sonous mushrooms.

A

muscarine.

muscarinic receptor also recognize muscarine

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17
Q

the muscarinic receptors show only
a weak affinity for

a. muscarine

b. acethylcholine

c. nicotine

A

c. nicotine

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18
Q

alkaloid found in tobacco and other
plants

a. muscarine

b. acethylcholine

c. nicotine

A

c. nicotine

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19
Q

These receptors are found on
the autonomic effector organs, such as the heart, smooth muscle,
brain, and exocrine glands

a. muscarinic receptor

b. nicotinic receptor

A

a. muscarinic receptor

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20
Q

what subclass of muscaribic receptor are also found on gastric parietal cells,

a. M1

b. M 2

c. M3

A

a. M1

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21
Q

what subclass of muscarinic receptors on cardiac cells and smooth muscle

a. M1

b. M 2

c. M3

A

b. M 2

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22
Q

what subclass of muscarinic receptor receptors
on the bladder, exocrine glands, and smooth muscle.

a. M1

b. M 2

c. M3

A

c. M 3

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23
Q

what muscarinic receptor subclass are activated, the receptor undergoes a conformational
change and interacts with a G-protein that activates phospholi-
pase C. This ultimately leads to production of second messen-
gers inositol-1 ,4,5-trisphosphate (IP3) and diacylglycerol (DAG).
IP3 causes an increase in intracellular Ca2+. Calcium can then
interact to stimulate or inhibit enzymes or to cause hyperpolar-
ization, secretion, or contraction. DAG activates protein kinase C,
an enzyme that phosphorylates numerous proteins within the cell.

a. M1

b. M 2

c. M3

A

a. M1 or c. M3

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24
Q

what muscarinic receptor subtype on the cardiac muscle
stimulates a G-protein that inhibits adenylyl cyclase and increases
K+ conductance. The heart responds with a decrease in rate and
force of contraction.

a. M1

b. M 2

c. M3

A

b. M2

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25
Q

when M1 or M3
receptors are activated, the receptor undergoes a conformational
change and interacts with a G-protein that activates ___. This ultimately leads to production of second messen-
gers ___ and ____.
_____ causes an increase in intracellular Ca2+. Calcium can then
interact to stimulate or inhibit enzymes or to cause hyperpolar-
ization, secretion, or contraction. ____ activates protein kinase C,
an enzyme that phosphorylates numerous proteins within the cell.

A

when M1 or M3
receptors are activated, the receptor undergoes a conformational
change and interacts with a G-protein that activates ___. This ultimately leads to production of second messen-
gers inositol-1 ,4,5-trisphosphate (IP3) and diacylglycerol (DAG).
IP3 causes an increase in intracellular Ca2+. Calcium can then
interact to stimulate or inhibit enzymes or to cause hyperpolar-
ization, secretion, or contraction. DAG activates protein kinase C,
an enzyme that phosphorylates numerous proteins within the cell.

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26
Q

For example, when M1 or M3
receptors are activated, the receptor undergoes a conformational
change and interacts with a G-protein that activates

A

phospholi-
pase C

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27
Q

activation ofphospholipase C will lead to formation of what secondary messenger?

A

inositol-1 ,4,5-trisphosphate (IP3) and diacylglycerol (DAG).

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28
Q

what secondary messenger increase intracellular calcium?

a.inositol-1 ,4,5-trisphosphate (IP3)

b. diacylglycerol (DAG).

A

a.inositol-1 ,4,5-trisphosphate (IP3)

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29
Q

can then
interact to stimulate or inhibit enzymes or to cause hyperpolar-
ization, secretion, or contraction.

a. potassium

b. calcium

A

b. calcium

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30
Q

what will diacylglycerol (DAG) activate

A

protein kinase C,

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31
Q

an enzyme that phosphorylates numerous proteins within the cell.

A

protein kinase C,

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32
Q

what will be the respondactivation of the M2 subtype on the cardiac muscle
stimulates a G-protein that inhibits adenylyl cyclase and increases
K+ conductance

A

The heart responds with a decrease in rate and
force of contraction.

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33
Q

is a nonselective muscarinic
agonist used to treat xerostomia and glaucoma.

a. pilocarpine

b. cevimeline

A

a. pilocarpine

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34
Q

also recognize nicotine
but show only a weak affinity for muscarine

a. muscarinic receptor

b. nicotinic receptor

A

b. nicotinic receptor

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35
Q

it functions as a
ligand-gated ion channel (ionotropic receptor)

a. muscarinic receptor

b. nicotinic recrptor

A

b. nicotinic recrptor

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36
Q

Binding of two ACh
molecules elicits a conformational change that allows the entry of
sodium ions, resulting in the ___ of the effector cell.

a. repolarization

b. depolarization

A

b.depolarization

notes : Nicotine
at low concentration stimulates the receptor, whereas nicotine at high
concentration blocks the receptor

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37
Q

receptors are located in
the CNS, the adrenal medulla, autonomic ganglia, and the neuro-
muscular junction (NMJ) in skeletal muscles

a. muscarinic receptor

b. nicotinic receptor

A

b. nicotinic receptor

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38
Q

the gan-
glionic receptors are selectively blocked by

a. mecamylamine,

b. atracurium.

A

a. mecamylamine

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39
Q

nicotinic NMJ (neuro-muscular junction) receptors are specifically blocked by a. mecamylamine,

b. atracurium.

A

b. atracurium.

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40
Q

Cholinergic agonists mimic the effects of ACh by binding directly to
cholinoceptors (muscarinic or nicotinic). These agents may be broadly
classified into two groups:

A

1) choline esters, which include endogenous
ACh and synthetic esters of choline, such as carbachol and bethanechol,
and 2) naturally occurring alkaloids, such as nicotine and pilocarpine

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41
Q

which include endogenous
ACh and synthetic esters of choline

a. choline esters

b. naturally occurring alkaloids

A

a. choline esters

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42
Q

carbachol

a. choline esters

b. naturally occurring alkaloids

A

a. choline esters

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43
Q

bethanechol

a. choline esters

b. naturally occurring alkaloids

A

a. choline esters

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44
Q

nicotine

a. choline esters

b. naturally occurring alkaloids

A

b. naturally occurring alkaloids

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45
Q

pilocarpine

a. choline esters

b. naturally occurring alkaloids

A

b. naturally occurring alkaloids

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46
Q

a quaternary ammonium
compound that cannot penetrate membranes.

a. acetylcholine

b.betanechol

c. carbachol

A

a. acetylcholine

note:it lacks therapeutic importance because of its
multiplicity of actions (leading to diffuse effects) and its rapid inactiva-
tion by the cholinesterases

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47
Q

ACh has both muscarinic and nicotinic
activity.

a. acetylcholine

b.betanechol

c. carbachol

A

a. acetylcholine

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48
Q

Decrease in heart rate and cardiac output

a. acetylcholine

b.betanechol

c. carbachol

A

a. acetylcholine

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49
Q

Decrease in blood pressure

a. acetylcholine

b.betanechol

c. carbachol

A

a. acetylcholine

note:Injection of ACh causes vasodila-
tion and lowering of blood pressure by an indirect mechanism of
action. ACh activates M3 receptors found on endothelial cells lining
the smooth muscles of blood vessels. This results in the production of nitric oxide from arginine. Nitric oxide then diffuses to vascular
smooth muscle cells to stimulate protein kinase G production,
leading to hyperpolarization and smooth muscle relaxation via
phosphodiesterase-3 inhibition. In the absence of administered
cholinergic agents, the vascular cholinergic receptors have no
known function, because ACh is never released into the blood in
significant quantities. Atropine blocks these muscarinic receptors
and prevents ACh from producing vasodilation.

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50
Q

ACh activates M3 receptors found on endothelial cells lining
the smooth muscles of blood vessels. This results in the production

A

nitric oxide from arginine

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51
Q

At ACh…Nitric oxide then diffuses to vascular
smooth muscle cells to stimulate

A

protein kinase G production

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52
Q

the stimulation of protein kinase G produce

A

leading to hyperpolarization and smooth muscle relaxation via
phosphodiesterase-3 inhibition.

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53
Q

what is the effect of acethylcholine in our grastrointestinal tract

A

In the gastrointestinal {GI) tract, acetylcholine
increases salivary secretion, increases gastric acid secretion,
and stimulates intestinal secretions and motility.

note:It also enhances
bronchiolar secretions and causes bronchoconstriction.

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54
Q

blocks these muscarinic receptors
and prevents ACh from producing vasodilation.

a. Atropine

b. Metacholine

A

a. Atropine

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55
Q

a direct-acting cholinergic agonist, is used to assist
in the diagnosis of asthma due to its bronchoconstricting prop-
erties.

a. Atropine

b. Metacholine

A

b. Metacholine

note:In the genitourinary tract, ACh increases the tone of the
detrusor muscle, causing urination. In the eye, ACh is involved
in stimulation of ciliary muscle contraction for near vision and in
the constriction of the pupillae sphincter muscle, causing miosis
{marked constriction of the pupil). ACh {1% solution) is instilled
into the anterior chamber of the eye to produce miosis during oph-
thalmic surgery.

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56
Q

is an unsubstituted carbamoyl ester,
structurally related to ACh.

a. acetylcholine

b.betanechol

c. carbachol

A

b.betanechol

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57
Q

It is not hydrolyzed by AChE
due to the esterification of carbamic acid, although it is inactivated
through hydrolysis by other esterases.

a. acetylcholine

b.betanechol

c. carbachol

A

b.betanechol

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58
Q

bethanechol is inactivated by

a. esterification
b. hydrolysis

A

b. hydrolysis

it is inactivated
through hydrolysis by other esterases.

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59
Q

why betanechol lacks nicotiic actions?

a. because of its carbamoyl group
b. because of is an ester
c. because of its methyl group

A

c. because of its methyl group

but does have strong muscarinic
activity.

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60
Q

where is the major action of bethanechol?

A

Its major actions are on the smooth musculature of the bladder and Gl tract.

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61
Q

How long is the diration of action of bethanechol?

A

1 hour duration of action

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62
Q

directly stimulates muscarinic receptors,
causing increased intestinal motility and tone. It also stimulates the
detrusor muscle of the bladder, whereas the trigone and sphincter
muscles are relaxed. These effects stimulate urination.

a. acetylcholine

b.betanechol

c. carbachol

A

b.betanechol

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63
Q

is used to
stimulate the atonic bladder, particularly in postpartum or postoperative, nonobstructive urinary retention.

a. acetylcholine

b.betanechol

c. carbachol

A

b.betanechol

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64
Q

may also be
used to treat neurogenic atony as well as megacolon.

a. acetylcholine

b. betanechol

c. carbachol

A

b.betanechol

65
Q

what are the side effects of bethanechol?

A

can cause generalized cholinergic stimulation {Figure 4.6), with sweating, salivation, flushing, decreased blood pressure {with reflex tachycardia), nausea,
abdominal pain, diarrhea, and bronchospasm.

66
Q

has both muscarinic and nicotinic actions.

a. acetylcholine

b. betanechol

c. carbachol

A

c. carbachol

66
Q

what should be administered to overcome severe cardiovascular or bronchoconstrictor responses caused by bethanechol?

a. carbachol

b. atropine sulfate

A

b. atropine sulfate

67
Q

it can cause miosis

a. acetylcholine

b. betanechol

c. carbachol

A

c. carbachol

68
Q

is the drug of choice for emergency lowering of intraocular
pressure of both open-angle and angle-closure glaucoma.

a. dorzolamide

b. timolol

c. Pilocarpine

A

c. Pilocarpine

69
Q

is also useful in reversing
mydriasis due to atropine.

a. dorzolamide

b. timolol

c. Pilocarpine

A

c. Pilocarpine

70
Q

Sjogren syndrome, which is characterized by dry mouth and lack
of tears, is treated with cevimeline and?

a. dorzolamide

b. timolol

c. Pilocarpine

A

c. Pilocarpine

Sjogren syndrome, which is characterized by dry mouth and lack
of tears, is treated with oral pilocarpine tablets and cevimeline, a
cholinergic drug that also has the drawback of being nonspecific.

71
Q

can cause blurred vision, night
blindness, and brow ache.

a. dorzolamide

b. timolol

c. Pilocarpine

A

c. Pilocarpine

72
Q

poisoning of this drug causes profuse sweating (diaphoresis) and salivation.

a. dorzolamide

b. timolol

c. Pilocarpine

A

c. Pilocarpine

73
Q

at doses
that can cross the blood-brain barrier, is administered to counteract the toxicity of pilocarpine.

a. dorzolamide

b. topical atropine

c. parenteral atropine

A

c. parenteral atropine

74
Q

what is/are reversible indirect acting cholinergic agonist?

A

Donepezil, Edrophonium, Galantamine, Neostigmine , Physostigmine, Pyridostigmine, Rivastigmine

75
Q

acetylcholine

a. direct acting cholinergic agonist
b. reversible indirect acting cholinergic agonist
c. irreversible indirect acting cholinergic agonist
d. reactivation of acetylcholinesterase

A

a. direct acting cholinergic agonist

76
Q

what is/are reversible indirect acting cholinergic agonist?

A

Echothiophate

77
Q

bethanichol

a. direct acting cholinergic agonist
b. reversible indirect acting cholinergic agonist
c. irreversible indirect acting cholinergic agonist
d. reactivation of acetylcholinesterase

A

a. direct acting cholinergic agonist

78
Q

carbachol

a. direct acting cholinergic agonist
b. reversible indirect acting cholinergic agonist
c. irreversible indirect acting cholinergic agonist
d. reactivation of acetylcholinesterase

A

a. direct acting cholinergic agonist

79
Q

cevimeline

a. direct acting cholinergic agonist
b. reversible indirect acting cholinergic agonist
c. irreversible indirect acting cholinergic agonist
d. reactivation of acetylcholinesterase

A

a. direct acting cholinergic agonist

80
Q

methacholine

a. direct acting cholinergic agonist
b. reversible indirect acting cholinergic agonist
c. irreversible indirect acting cholinergic agonist
d. reactivation of acetylcholinesterase

A

a. direct acting cholinergic agonist

81
Q

nicotine

a. direct acting cholinergic agonist
b. reversible indirect acting cholinergic agonist
c. irreversible indirect acting cholinergic agonist
d. reactivation of acetylcholinesterase

A

a. direct acting cholinergic agonist

82
Q

pilocarpine

a. direct acting cholinergic agonist
b. reversible indirect acting cholinergic agonist
c. irreversible indirect acting cholinergic agonist
d. reactivation of acetylcholinesterase

A

a. direct acting cholinergic agonist

83
Q

donepezil

a. direct acting cholinergic agonist
b. reversible indirect acting cholinergic agonist
c. irreversible indirect acting cholinergic agonist
d. reactivation of acetylcholinesterase

A

b. reversible indirect acting cholinergic agonist

84
Q

Edrophonium

a. direct acting cholinergic agonist
b. reversible indirect acting cholinergic agonist
c. irreversible indirect acting cholinergic agonist
d. reactivation of acetylcholinesterase

A

b. reversible indirect acting cholinergic agonist

85
Q

Galantamine

a. direct acting cholinergic agonist
b. reversible indirect acting cholinergic agonist
c. irreversible indirect acting cholinergic agonist
d. reactivation of acetylcholinesterase

A

b. reversible indirect acting cholinergic agonist

86
Q

Neostigmine

a. direct acting cholinergic agonist
b. reversible indirect acting cholinergic agonist
c. irreversible indirect acting cholinergic agonist
d. reactivation of acetylcholinesterase

A

b. reversible indirect acting cholinergic agonist

87
Q

physostigmine

a. direct acting cholinergic agonist
b. reversible indirect acting cholinergic agonist
c. irreversible indirect acting cholinergic agonist
d. reactivation of acetylcholinesterase

A

b. reversible indirect acting cholinergic agonist

88
Q

Pyridostigmine

a. direct acting cholinergic agonist
b. reversible indirect acting cholinergic agonist
c. irreversible indirect acting cholinergic agonist
d. reactivation of acetylcholinesterase

A

b. reversible indirect acting cholinergic agonist

89
Q

Rivastigmine

a. direct acting cholinergic agonist
b. reversible indirect acting cholinergic agonist
c. irreversible indirect acting cholinergic agonist
d. reactivation of acetylcholinesterase

A

b. reversible indirect acting cholinergic agonist

90
Q

Echothiophate

a. direct acting cholinergic agonist
b. reversible indirect acting cholinergic agonist
c. irreversible indirect acting cholinergic agonist
d. reactivation of acetylcholinesterase

A

c. irreversible indirect acting cholinergic agonist

91
Q

Pralidoxime

a. direct acting cholinergic agonist
b. reversible indirect acting cholinergic agonist
c. irreversible indirect acting cholinergic agonist
d. reactivation of acetylcholinesterase

A

d. reactivation of acetylcholinesterase

92
Q

is the prototype short-acting
AChE inhibitor.

a. Donepezil
b. Edrophonium
c. Galantamine
d. Neostigmine

A

b. Edrophonium

93
Q

binds reversibly to the active center of
AChE, preventing hydrolysis of ACh.

a. Donepezil
b. Edrophonium
c. Galantamine
d. Neostigmine

A

b. Edrophonium

It has a short duration of action
of 10 to 20 minutes due to rapid renal elimination.

94
Q

It is
used in the diagnosis of myasthenia gravis

a. Donepezil
b. Edrophonium
c. Galantamine
d. Neostigmine

A

b. Edrophonium

myasthenia gravis, an autoimmune disease
caused by antibodies to the nicotinic receptor at the NMJ.

Edrophonium is
a quaternary amine, and its actions are limited to the periphery.

95
Q

what kind of administration of Edrophonium that leads to a rapid increase in muscle strength in patients with
myasthenia gravis.

a. intramuscular
b. intravenous

A

b. intravenous

96
Q

Excess in Edrophine provokes a cholinergic crisis. What should be the treatment in this condition?

a. Atropine
b. Edrophonium
c. Galantamine
d. Neostigmine

A

a. Atropine

97
Q

may also be used to assess cholinesterase inhibitor therapy, for differentiating cholinergic and myasthenic crises, and for reversing the
effects of nondepolarizing neuromuscular blockers (NMBs) after surgery. Due to the availability of other agents, _________ use has
become limited.

a. Donepezil
b. Edrophonium
c. Galantamine
d. Neostigmine

A

b. Edrophonium

98
Q

is a nitrogenous carbamic acid
ester found naturally in plants and is a tertiary amine.

a. Donepezil
b. Edrophonium
c. Physostigmine
d. Neostigmine

A

c. Physostigmine

99
Q

It is a substrate
for AChE, and it forms a relatively stable carbamoylated intermediate with the enzyme, which then becomes reversibly inactivated. The
result is potentiation of cholinergic activity throughout the body.

a. Donepezil
b. Edrophonium
c. Physostigmine
d. Neostigmine

A

c. Physostigmine

100
Q

has a wide range of effects and
stimulates not only the muscarinic and nicotinic sites of the
ANS, but also the nicotinic receptors of the NMJ.

a. Donepezil
b. Edrophonium
c. Physostigmine
d. Neostigmine

A

c. Physostigmine

101
Q

Stimulation of Physostigmine with this receptor will cause contraction of Gl smooth muscles, miosis,bradycardia, and hypotension

a. Muscarinic
b. Nicotinic

A

a. Muscarinic

102
Q

Stimulation of Physostigmine with this receptor will cause skeletal muscle twitches, fasciculations, and skeletal
muscle paralysis (at higher doses)
a. Muscarinic
b. Nicotinic

A

b. Nicotinic

the duration of action of Physostigmine is 30 minutes to 2 hours.

Physostigmine can enter and stimulate the cholinergic sites
in the CNS.

103
Q

is used in the treatment of
overdoses of drugs with anticholinergic actions, such as atropine,
and to reverse the effects of NMBs.

a. Donepezil
b. Edrophonium
c. Physostigmine
d. Neostigmine

A

c. Physostigmine

104
Q

High doses of _______ may lead to convulsions. Bradycardia and a fall in cardiac output may also occur.
Inhibition of AChE at the NMJ causes the accumulation of ACh
and, ultimately through continuous depolarization, results in paralysis of skeletal muscle. However, these effects are rarely seen with
therapeutic doses.

a. Donepezil
b. Edrophonium
c. Physostigmine
d. Neostigmine

A

c. Physostigmine

105
Q

is a synthetic compound that is
also a carbamic acid ester, and it reversibly inhibits AChE in a manner similar to physostigmine.

a. Donepezil
b. Edrophonium
c. Pyridostigmine
d. Neostigmine

A

d. Neostigmine

106
Q

has a quaternary
nitrogen. Therefore, it is more polar, is absorbed poorly from the
Gl tract, and does not enter the CNS. Its effect on skeletal muscle
is greater than physostigmine, and it can stimulate contractility
before it paralyzes.

a. Donepezil
b. Edrophonium
c. Pyridostigmine
d. Neostigmine

A

d. Neostigmine

Neostigmine has an intermediate duration of
action, usually 30 minutes to 2 hours

107
Q

used to stimulate the bladder and Gl tract
and as an antidote for competitive neuromuscular-blocking agents.
It is also used to manage symptoms of myasthenia
gravis.

a. Donepezil
b. Edrophonium
c. Pyridostigmine
d. Neostigmine

A

d. Neostigmine

108
Q

what is the adverse effect of Neostigmine

A

generalized cholinergic stimulation, such as salivation, flushing,
decreased blood pressure, nausea, abdominal pain, diarrhea, and
bronchospasm.

109
Q

does not cause CNS side effects and
is not used to overcome toxicity of central-acting antimuscarinic
agents such as atropine.

a. Donepezil
b. Edrophonium
c. Pyridostigmine
d. Neostigmine

A

d. Neostigmine

110
Q

is contraindicated when
intestinal or urinary bladder obstruction is present.

a. Donepezil
b. Edrophonium
c. Pyridostigmine
d. Neostigmine

A

d. Neostigmine

111
Q

is another cholinesterase
inhibitor used in the chronic management of myasthenia gravis. Its
duration of action is intermediate (3 to 6 hours) but longer than that
of neostigmine. Adverse effects are similar to those of neostigmine.

a. Donepezil
b. Edrophonium
c. Pyridostigmine
d. Neostigmine

A

c. Pyridostigmine

112
Q

Note: Patients with Alzheimer disease have a deficiency of cholinergic neurons and therefore lower levels of ACh in the CNS. This observation
led to the development of anticholinesterases as possible remedies
for the loss of cognitive function.

A
113
Q

the first agent in this anticholinesterase category, has been replaced by others because of its hepatotoxicity.

a. Tacrine
b. Domepesil
c. Rivastigmine
d. Galantamine

A

a. Tacrine

114
Q

Despite the ability of donepezil [doe-NEP-e-zil], rivastigmine
[ri-va-STIG-meen], and galantamine [ga-LAN-ta-meen] to delay the
progression of Alzheimer disease, none can stop its progression.

What is the primary adverse effect of these drugs?

A

GI distress

115
Q

is an
organophosphate that covalently binds via its phosphate group
at the active site of AChE

a. Tacrine
b. Domepesil
c. Rivastigmine
d. Echothiophate

A

d. Echothiophate

the phosphorylated enzyme slowly
releases one of its ethyl groups. The loss of an alkyl group, which
is called aging, makes it impossible for chemical reactivators, such
as pralidoxime, to break the bond between the remaining drug and
the enzyme.

116
Q

Actions include generalized cholinergic stimulation,
paralysis of motor function (causing breathing difficulties}, and
convulsions. It also produces intense miosis and, thus,
has found therapeutic use.

a. Tacrine
b. Domepesil
c. Rivastigmine
d. Echothiophate

A

d. Echothiophate

117
Q

______ in high dosages can
reverse many of the peripheral and some of the central muscarinic
effects of echothiophate.

a. Tacrine
b. Domepesil
c. Atropien
d. Echothiophate

A

c. Atropine

118
Q

A topical ophthalmic solution of the drug is
available for the treatment of open-angle glaucoma. It is rarely used due to its side effect profile, which
includes the risk of cataracts.

a. Tacrine
b. Domepesil
c. Atropien
d. Echothiophate

A

d. Echothiophate

119
Q

a chemical reactivator which breaks the bond between the remaining Echothiopate and
the enzyme.

a. Tacrine
b. Pralidoxime
c. Atropien
d. Echothiophate

A

b. Pralidoxime

Pralidoxime is also called 2-PAM

120
Q

are
commonly used as agricultural insecticides in the United States, which
has led to numerous cases of accidental poisoning with these agents.

a. direct acting
b. indirect acting (reversible)
c. indirect acting (irreversible)
d. reactivation of acetylation of acetylcholinesterase

A

c. indirect acting (irreversible)

Irreversible AChE inhibitors (mostly organophosphate compounds}

121
Q

In
addition, they are frequently used for suicidal and homicidal purposes.

a. direct acting
b. indirect acting (reversible)
c. indirect acting (irreversible)
d. reactivation of acetylation of acetylcholinesterase

A

c. indirect acting (irreversible)

Irreversible AChE inhibitors (mostly organophosphate compounds}

122
Q

Note: Organophosphate nerve gases such as sarin are used as agents of
warfare and chemical terrorism.

A
123
Q

used to treatment of urinary retention

a. betanechol
b.carbachol
c. pilocarpine

A

a. bethanechol

124
Q

binds preferentially at muscarinic receptors

a. betanechol
b.carbachol
c. pilocarpine

A

a. bethanechol

125
Q

binds to both muscarinic and nicotinic receptors

a. betanechol
b.carbachol
c. pilocarpine

A

c, carbachol

126
Q

produces miosis during ocular surgery

a. betanechol
b.carbachol
c. pilocarpine

A

b. carbachol

127
Q

Used topically to reduce intraocular pressure in open angle or narrow angle galucoma, particulary in patients who have become tolerant to pilocarpine

a. betanechol
b.carbachol
c. pilocarpine

A

b. carbachol

128
Q

reduces intraocular pressure in open and narrow angle glaucoma

a. betanechol
b.carbachol
c. pilocarpine

A

c. pilocarpine

129
Q

bind preferentially at muscarinic receptors

a. betanechol
b.carbachol
c. pilocarpine

A

c. pilocarpine

130
Q

uncharged, tertiary amine that can penetrate the CNS

a. betanechol
b.carbachol
c. pilocarpine

A

c. pilocarpine

131
Q

increase intestinal and bladder motility

a. physostigmine
b. neostigmine
c. Edrophonium

A

a, physostigmine

132
Q

reverses CNS and cardiac effects of tricyclic antidepressants

a. physostigmine
b. neostigmine
c. Edrophonium

A

A. Physostigmine

133
Q

reverses CNS effects of Atropine

a. physostigmine
b. neostigmine
c. Edrophonium

A

A. physostigmine

134
Q

uncharged, tertiary amine that can penetrate the CNS

a. physostigmine
b. neostigmine
c. Edrophonium

A

a. physostigmine

135
Q

prevents postoperative abdominal distention and urinary retention

a. physostigmine
b. neostigmine
c. Edrophonium

A

b. neostigmine

136
Q

used in treatment of myasthenia gravis

a. physostigmine
b. neostigmine
c. Edrophonium

A

b. neostigmine

137
Q

used as an antidote for competitive neuromuscular blockers

a. physostigmine
b. neostigmine
c. Edrophonium

A

b. neostigmine

138
Q

has intermediate duration of action (0.5 ro 2 hours)

a. physostigmine
b. neostigmine
c. Edrophonium

A

b. neostigmine

139
Q

used for diagnosis of myasthenia gravis

a. physostigmine
b. neostigmine
c. Edrophonium

A

c. Edrophonium

140
Q

used as first-line treatemnts for Alzheimer disease , though confers modest benefit

a. rivastigmine , galantamine , donepezil
b. echothiphate
c. acetylcholine

A

a. rivastigmine , galantamine , donepezil

141
Q

have not been shown to reduce healthcare costs or delay institutional benefit

a. rivastigmine , galantamine , donepezil
b. echothiphate
c. acetylcholine

A

a. rivastigmine , galantamine , donepezil

142
Q

can be used with memantine ( N- methyl-D- aspartate antagonist ) in moderate to severe disease

a. rivastigmine , galantamine , donepezil
b. echothiophate
c. acetylcholine

A

a. rivastigmine , galantamine , donepezil

143
Q

used in treatment of open angle glaucoma

a. rivastigmine , galantamine , donepezil
b. echothiophate
c. acetylcholine

A

b. echothiophate

144
Q

has long duration of action (100 hours )

a. rivastigmine , galantamine , donepezil
b. echothiophate
c. acetylcholine

A

b, echothophate

145
Q

used to produce miosis in ophthalmic surgery

a. rivastigmine , galantamine , donepezil
b. echothiophate
c. acetylcholine

A

c. acetylcholine

146
Q

an reactivate inhibited AChE
(Figure 4.1 0). However, it is unable to penetrate into the CNS and
therefore is not useful in treating the CNS effects of organophosphates.

a. rivastigmine , galantamine , donepezil
b. echothiophate
c. pralidoxime

A

c. pralidoxime

note: In addition, it cannot overcome toxicity of reversible AChE inhibitors
(for example, physostigmine).

147
Q

is administered to prevent muscarinic side effects of anticholinesterase agents. Such effects include increased bronchial and salivary
secretion, bronchoconstriction, and bradycardia.

a. atropine
b. diazepam

A

a. atropine

148
Q

is also
administered to reduce the persistent convulsion caused by anticholinesterase agents

a. atropine
b. diazepam

A

a. atropine

149
Q

Botulinum toxin blocks the release of acetylcholine from
cholinergic nerve terminals. Which is a possible effect of
botulinum toxin?
A. Skeletal muscle paralysis
B. Improvement of myasthenia gravis symptoms
C. Increased salivation
D. Reduced heart rate

A

Correct answer = A. Acetylcholine released by cholinergic
neurons acts on nicotinic receptors In the skeletal muscle
cells to cause contraction. Therefore, blockade of ACh
release causes skeletal muscle paralysis. Myasthenia gra·
vis is an autoimmune disease where antibodies are produced against nicotinic receptors and inactivate nicotinic
receptors. A reduction in ACh release therefore worsens
(not improves} the symptoms of this condition. ~e~uction in
ACh release by botulinum toxin causes reduction 1n secretions Including saliva (not Increase In salivation), causing
dry mouth and an Increase (not reduction) in heart rate due
to reduced vagal activity.

150
Q

A patient develops urinary retention after an abdominal
surgery. Urinary obstruction was ruled out in this patient.
Which strategy would be helpful in promoting urination?
A. Activating nicotinic receptors
B. Inhibiting the release of acetylcholine
c. Inhibiting cholinesterase enzyme
D. Blocking muscarinic receptors

A

Correct answer = C. Activation of muscarinic receptors in
the detrusor muscle of the urinary bladder can promote
urination in patients where the tone of detrusor muscle is
low. Inhibiting cholinesterase enzyme increases the levels
of acetylcholine, and acetylcholine can Increase the tone
of the detrusor muscle. There are no nicotinic receptors
in the detrusor muscle; therefore, activation of nicotinic
receptors is not helpful. Inhibiting the release of a:etyl·
choline or blocking muscarinic receptors worsens unnary
retention.

151
Q

Which of the following drugs could theoretically improve
asthma symptoms?
A. Bethanechol
B. Pilocarpine
C. Pyridostigmine
D. Atropine

A

Correct answer = D. Muscarinic agonlsts and drugs that
increase acetylcholine levels cause constriction of bronchial
smooth muscles and could exacerbate asthma symptoms.
Bethanechol and pilocarpine are muscarinic agonists, and
pyridostlgmine is a cholinesterase inhibitor that increases
levels of acetylcholine. Atropine is a muscarinic antagonist
and therefore does not exacerbate asthma. lheoretlcally, it
should relieve symptoms of asthma (not used clinically for
this purpose).

152
Q

If an ophthalmologist wants to dilate the pupils for an eye
examination, which drug/class of drugs is theoretically
useful?
A. Muscarinic receptor activator (agonist}
B. Muscarinic receptor inhibitor (antagonist}
C. Pilocarpine
D. Neostigmine

A

Correct answer = B. Muscarinic agonists (for example, pilocarpine) contract the circular smooth muscles
in the iris sphincter and constrict the pupil (miosis).
Anticholinesterases (for example, neostigmine, physostigmine) also cause miosis by increasing the level of ACh.
Muscarinic antagonists, on the other hand, relax the Clrcular smooth muscles in the iris sphincter and cause dilation
of the pupil (mydriasis}.

153
Q

In Alzheimer disease, there is a deficiency of cholinergic neuronal function in the brain. Theoretically, which
strategy is useful in treating symptoms of Alzheimer
disease?
A. Inhibiting cholinergic receptors in the brain
B. Inhibiting the release of acetylcholine in the brain
C. Inhibiting the acetylcholinesterase enzyme in the
brain
D. Activating the acetylcholinesterase enzyme in the
brain

A

Correct answer = C. Because there is already a deficiency
in brain cholinergic function in Alzheimer disease, inhibiting cholinergic receptors or inhibiting the release of ACh
worsens the condition. Activating the acetylcholinesterase
enzyme increases the degradation of ACh, which also
worsens the condition. However, Inhibiting the acetylcholinesterase enzyme helps to Increase the levels of ACh In
the brain and thereby relieve the symptoms of Alzheimer
disease.

154
Q

An elderly female who lives in a farmhouse was brought
to the emergency room in serious condition after ingesting a liquid from an unlabeled bottle found near her bed,
apparently in a suicide attempt. She presented with
diarrhea, frequent urination, convulsions, breathing difficulties, constricted pupils (miosis), and excessive salivation. Which of the following is correct regarding this
patient?
A. She most likely consumed an organophosphate
pesticide.
B. The symptoms are consistent with sympathetic
activation.
C. Her symptoms can be treated using an anticholinesterase agent.
D. Her symptoms can be treated using a cholinergic
agonist.

A

Correct answer = A. The symptoms are consistent with that
of cholinergic crisis. Since the elderly female lives on a farm
and the symptoms are consistent with a cholinergic crisis
(usually caused by cholinesterase Inhibitors), It may be
assumed that she has consumed an organophosphate pesticide (irreversible cholinesterase inhibitor). Assuming that
the symptoms are caused by organophosphate poisoning,
administering an anticholinesterase agent or a cholinergic
agonist will worsen the condition. The symptoms are not
consistent with that of sympathetic activation, as sympathetic activation will cause symptoms opposite to that of
cholinergic crisis seen In this patient.

155
Q

A patient who received a nondepolarizing neuromuscular blocker (NMB) for skeletal muscle relaxation during
surgery is experiencing mild skeletal muscle paralysis
after the surgery. Which drug could reverse this effect of
NMBs?
A. Pilocarpine
B. Bethanechol
C. Neostigmine
D. Atropine

A

Correct answer = C. Neuromuscular blockers act by blockIng nicotinic receptors on the skeletal muscles. Increasing
the levels of ACh in the neuromuscular junctions can
1”9119rse the effects of NMBs. Therefore, neostigmine, a
cholinesterase inhibitor, could reverse the effects of NMBs.
Pilocarpine and bethanechol are preferentially muscarinic
agonists and have no effects on the nicotinic receptors.
Atropine is a muscarinic antagonist and has no effects on
nicotinic receptors.

156
Q

A 60-year-old female who had a cancerous growth in the
neck region underwent radiation therapy. Her salivary
secretion was reduced due to radiation and she suffers
from dry mouth (xerostomia). Which drug would be most
useful in treating xerostomia in this patient?
A. Acetylcholine
B. Pilocarpine
C. Echothiophate
D. Atropine

A

Correct answer= B. Salivary secretion may be enhanced by
activating muscarinic receptors in the salivary glands. This
can be achieved in theory by using a muscarinic agonist
or an anticholinesterase agent. Pilocarpine is a muscarinic
agonist administered orally for this purpose. Acetylcholine
has similar effects as that of pilocarpine; however, it cannot be used therapeutically as It Is rapidly destroyed by
cholinesterase in the body. Echothiophate Is an Irreversible
cholinesterase inhibitor, but It cannot be used therapeutically because of its toxic effects. Atropine is a muscarinic
antagonist and worsens dry mouth.

157
Q

A 40-year-old male presents to his family physician with
drooping eyelids, difficulty chewing and swallowing, and
muscle fatigue even on mild exertion. Which agent could
be used to diagnose myasthenia gravis in this patient?
A. Atropine
B. Edrophonium
C. Pralidoxime
D. Echothiophate

A

Correct answer = B. The function of nicotinic receptors in
skeletal muscles is diminished in myasthenia gravis due to
the development of antibodies to nicotinic receptors (autoImmune disease). Any drug that Increases levels of ACh
In the neuromuscular junction can improve symptoms In
myasthenia gravis. Thus, edrophonium, a reversible cholinesterase inhibitor with a short duration of action can temporarily improve skeletal muscle weakness in myasthenia
gravis, serving as a diagnostic tool. Atropine is a mu~­
rinic antagonist and has no role in skeletal muscle function.
Pralidoxime is a drug that is used to reverse the bincing
of Irreversible cholinesterase Inhibitors with cholinesterase
enzyme and helps to reactivate cholinesterase enzyme.
Hence, pralidoxlme will not be useful in improving skeletal
muscle function in myasthenia gravis.

158
Q

Atropa belladonna is a plant that contains atropine
(a muscarinic antagonist). Which of the following drugs
or classes of drugs will be most useful in treating poisoning with belladonna?
A. Malathion
B. Physostigmine
C. Muscarinic antagonists
D. Nicotinic antagonists

A

Correct answer = B. Atropine is a competitive muscarinic
receptor antagonist that causes anticholinergic effects.
Muscarinic agonists or any other drugs that increase the
levels of ACh are able to counteract effects of atropine.
Thus, anticholinesterases such as malathion and physostigmine can counteract the effects of atropine, in theory.
However, since malathion Is an Irreversible Inhibitor of acetylcholinesterase, it Is not used for systemic treatment In
patients. Muscarinic antagonists worsen the t~city of at_ropine. Nicotinic antagonists can worsen the toxiCity by a~ng
on parasympathetic ganglionic receptors and thus reduang
the release of ACh.

159
Q

is a general term for agents that bind to
cholinoceptors (muscarinic or nicotinic) and prevent the effects of acetylcholine (ACh) and other cholinergic agonists.

a. cholinergic agonist

A

kaps (16 decks)

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