Block 9 Pharm Cholinergic W Exp Prt 1
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Questions and Answers
- 1.
Inhibition of cholinesterases by this drug is very short (2-10 minutes)
- A.
Acetylcholine
- B.
Bethanechol
- C.
Carbachol
- D.
Donepezil
- E.
Edrophonium
- F.
Muscarine
- G.
Neostigmine
- H.
Parathion
- I.
Pilocarpine
- J.
Pralidoxime
- K.
Physostigmine
Correct Answer
E. EdrophoniumExplanation
Edrophonium is a drug that inhibits cholinesterases. Cholinesterases are enzymes that break down acetylcholine, a neurotransmitter involved in muscle contraction and other physiological processes. The short duration of inhibition of cholinesterases by edrophonium (2-10 minutes) suggests that its effects are temporary and quickly reversible. This can be useful in certain medical situations, such as diagnosing myasthenia gravis, a neuromuscular disorder. By blocking the breakdown of acetylcholine, edrophonium can temporarily improve muscle strength in individuals with myasthenia gravis.Rate this question:
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- 2.
This drug can inhibit cholinesterases in the periphery but not in the CNS
- A.
Acetylcholine
- B.
Bethanechol
- C.
Carbachol
- D.
Donepezil
- E.
Edrophonium
- F.
Muscarine
- G.
Neostigmine
- H.
Parathion
- I.
Pilocarpine
- J.
Pralidoxime
- K.
Physostigmine
Correct Answer
G. NeostigmineExplanation
Neostigmine is the correct answer because it is a drug that inhibits cholinesterases in the periphery but not in the central nervous system (CNS). Cholinesterases are enzymes that break down acetylcholine, and by inhibiting them, neostigmine increases the levels of acetylcholine in the periphery. This can be beneficial in certain medical conditions where increased cholinergic activity is desired, such as in the treatment of myasthenia gravis or for reversing the effects of neuromuscular blocking agents. However, neostigmine does not readily cross the blood-brain barrier, so it has limited effects on cholinesterases in the CNS.Rate this question:
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- 3.
This drug can be absorbed effectively through the intact skin
- A.
Acetylcholine
- B.
Bethanechol
- C.
Carbachol
- D.
Donepezil
- E.
Edrophonium
- F.
Muscarine
- G.
Neostigmine
- H.
Parathion
- I.
Pilocarpine
- J.
Pralidoxime
- K.
Physostigmine
Correct Answer
H. ParathionExplanation
Parathion is a highly toxic organophosphate insecticide that can be absorbed effectively through the intact skin. Organophosphates are known to inhibit the enzyme acetylcholinesterase, which leads to an accumulation of acetylcholine in the body. This can result in overstimulation of the cholinergic system, leading to symptoms such as muscle twitching, sweating, and respiratory distress. Due to its high toxicity and ability to be absorbed through the skin, parathion is considered a dangerous chemical and requires proper handling and protective measures to prevent exposure.Rate this question:
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- 4.
This drug is able to regenerate cholinesterases blocked by organophosphates
- A.
Acetylcholine
- B.
Bethanechol
- C.
Carbachol
- D.
Donepezil
- E.
Edrophonium
- F.
Muscarine
- G.
Neostigmine
- H.
Parathion
- I.
Pilocarpine
- J.
Pralidoxime
- K.
Physostigmine
Correct Answer
J. PralidoximeExplanation
Pralidoxime is the correct answer because it is a drug that can regenerate cholinesterases that have been blocked by organophosphates. Organophosphates are a class of chemicals that are commonly used as insecticides and nerve agents. They work by inhibiting the activity of cholinesterases, which are enzymes that break down acetylcholine in the body. Pralidoxime works by reactivating these cholinesterases, allowing them to resume their normal function and break down acetylcholine. This helps to counteract the effects of organophosphate poisoning.Rate this question:
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- 5.
This drug can inhibit cholinesterases and activate directly Mm receptors
- A.
Acetylcholine
- B.
Bethanechol
- C.
Carbachol
- D.
Donepezil
- E.
Edrophonium
- F.
Muscarine
- G.
Neostigmine
- H.
Parathion
- I.
Pilocarpine
- J.
Pralidoxime
- K.
Physostigmine
Correct Answer
G. NeostigmineExplanation
Neostigmine is the correct answer because it is a drug that can inhibit cholinesterases and activate directly Mm receptors. Cholinesterases are enzymes that break down acetylcholine, and by inhibiting them, neostigmine increases the levels of acetylcholine in the body. Additionally, neostigmine can directly activate Mm receptors, which are a type of acetylcholine receptor. Therefore, neostigmine can enhance the effects of acetylcholine in the body, making it the correct answer.Rate this question:
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- 6.
Which of the following statements correctly pairs the effect of acetylcholine with the activation of the appropriate cholinergic receptor?
- A.
Contraction of the ciliary muscle - M1
- B.
Decreased A-V conduction - Nm
- C.
Peripheral vasodilation - Nn
- D.
Bronchoconstriction - M1
- E.
Increased firing from ganglionic neurons - Nn
Correct Answer
E. Increased firing from ganglionic neurons - NnExplanation
Answer: E
Activation of Nn receptors on the cell membrane of ganglionic neurons causes a stimulation of the
neuron and therefore an increased firing from that neuron.
A, C, D) The receptors that mediate this effect are mainly M3
B) The receptors that mediate this effect are mainly M2Rate this question:
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- 7.
Which of the following statements correctly pairs the acetylcholine effect with the postreceptor mechanism that mediates the effect?
- A.
Decreased rhythmicity of SA node - opening of ligand-gated Na+ channels
- B.
Increased intestinal peristalsis - release of NO
- C.
Decreased force of myocardial contraction -increased cAMP
- D.
Bronchoconstriction - increased IP3 and DAG
- E.
Miosis - decrease in IP3 and DAG
Correct Answer
D. Bronchoconstriction - increased IP3 and DAGExplanation
Answer: D
Bronchoconstriction is due to activation of M3 receptors. M3 receptors are mainly excitatory and
their activation increases the synthesis of IP3 and DAG. IP3 diffuses into cytoplasm ad releases
stored Ca++ which triggers smooth muscle contraction.
A) Decreased rhythmicity of SA node is due to the activation of M2 receptors. The postreceptor
mechanism triggered by this activation is the opening of ligand-gated K+ , not Na+, channels.
B) Increased intestinal peristalsis is due to activation of M3 receptors. M3 receptor activation in
endothelial cells, not in intestinal smooth muscle cells, releases NO.
C) All cholinergic actions in the heart muscle are mediated by the activation of M2 receptors. The
postreceptor mechanism triggered by this activation is the opening of ligand-gated K+
E) Miosis is due to contraction of the sphincter muscle of iris. The receptors involved are M3 and
the postreceptor mechanism is an increase, not a decrease ,of IP3 and DAG.Rate this question:
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- 8.
Which of the following cholinergic drugs given IV can cause signs of cholinergic activation in the CNS?
- A.
Acetylcholine
- B.
Carbachol
- C.
Bethanechol
- D.
Neostigmine
- E.
Physostigmine
Correct Answer
E. PhysostigmineExplanation
Answer: E
Physostigmine is an anticholinesterase agent that can cross easily the blood brain barrier, and so
can cause signs of cholinergic activation in the CNS.
A, B, C, D) All these cholinergic drugs are mainly water soluble and their crossing of blood brain
barrier is negligible.Rate this question:
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- 9.
Which of the following is the most likely effect of muscarinic agonists upon the gastrointestinal system?
- A.
Decreased pepsinogen secretion
- B.
Increased tone of pylorus sphincter
- C.
Relaxation of the external anal sphincter
- D.
Contraction of the lower esophageal sphincter
- E.
Decreased intestinal peristalsis
Correct Answer
D. Contraction of the lower esophageal sphincterExplanation
Answer: D
Activation of M3 receptors by muscarinic agonists contracts the lower esophageal sphincter. This
sphincter normally remains tonically constricted, so preventing the reflux of stomach content into
the esophagus, but can be relaxed by several causes including antimuscarinic drugs
A) Activation of M3 receptors in the peptic cells of the stomach actually increases pepsinogen
secretion.
B) The tone of all sphincters (except the lower esophageal sphincter) of gastrointestinal tract is
decreased, not increased, by parasympathetic activation.
C) The external anal sphincter is composed of a striated voluntary muscle and therefore not
sensitive to parasympathetic activation.
E) Activation of M3 receptors by muscarinic agonists actually increases intestinal peristalsis.Rate this question:
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- 10.
Which of the following effects of neostigmine is due only to the indirect activation of nicotinic receptors?
- A.
Miosis
- B.
Cyclospasm
- C.
Increased epinephrine release from adrenal glands
- D.
Increased secretion of sweat glands
- E.
Bronchoconstriction
- F.
Bradycardia
Correct Answer
C. Increased epinephrine release from adrenal glandsExplanation
Answer: C
Neostigmine inhibits cholinesterase enzymes so increasing the availability of acetylcholine in the
synaptic cleft. This causes both muscarinic and nicotinic effects. Acetylcholine induced activation
of Mn receptors in the adrenal medulla causes increased release of epinephrine.
A, B, D, E, F) All these effects are caused by the neostigmine-induced indirect activation of both
muscarinic and Nn receptors.Rate this question:
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- 11.
The following table shows the effects of some autonomic drugs on the eye when they are administered locally in the conjunctival sac. Examine the table and identify which one of the drugs A, B, C, D, E, is most likely to be physostigmine. (+ = increased ; - = decreased ; 0 = negligible effect)
- A.
A
- B.
B
- C.
C
- D.
D
- E.
E
Correct Answer
B. BExplanation
Answer: B
Physostigmine is a reversible cholinesterase inhibitor which increases the amount ov acetylcholine
in the synaptic cleft. Acetylcholine-induced activation of M3 receptors causes contraction of the
sphincter muscle of iris ( so decreasing pupillary diameter) and contraction of the ciliary muscle
(so increasing lens curvature and). Ocular pressure is decreased because the contraction of the
ciliary muscle opens the pores of the trabecular meshwork, so facilitating the outflow of the
aqueous humor into the Schlemm’s canal
A) These effects would be caused by an alpha-2 agonist, like apraclonidine.
C) These effects would be caused by a beta-blocker like timolol.
D) These effects would be caused by epinephrine.
E) These effects would be caused by an antimuscarinic drug, like scopolamine.Rate this question:
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- 12.
Which of the following is a potential adverse effect of muscarinic agonists?
- A.
Urinary retention
- B.
Xerostomia
- C.
Cough
- D.
Constipation
- E.
Difficulty in near vision
Correct Answer
C. CoughExplanation
Answer: C
Muscarinic agonists cause bronchoconstriction and mucus secretion by activating M3 receptors in
the bronchial tree. Both effects are powerful stimuli for cough which often occurs after
administration of a muscarinic agonist.
A, B, D, E) Actually muscarinic agonists tend to cause effects opposite to those listed.Rate this question:
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- 13.
Physostigmine can most effectively counteract which of the following drug-induced effects?
- A.
Atropine-induced hallucinations
- B.
Epinephrine-induced increase in blood pressure
- C.
Prazosin-induced decrease in blood pressure
- D.
Neostigmine-induced fasciculations
- E.
Nicotine-induced tachycardia
Correct Answer
A. Atropine-induced hallucinationsExplanation
Answer: A
Physostigmine increases the availability of acetylcholine in the synaptic cleft of cholinergic
terminals. Atropine and acetylcholine compete each other for the occupancy of muscarinic
receptors and physostigmine can also counteract the central symptoms of atropine overdose,
since it can enter the brain.
B) Physostigmine can decrease the blood pressure (even if this effect is not pronounced) by
inducing vasodilation and decrease of cardiac output, whereas epinephrine increases the blood
pressure by opposite effect. The two drugs can antagonize each other but they act on different
receptors and therefore the antagonism is functional (also called physiological) , not
pharmacological. A pharmacological antagonism is more effective than a physiological antagonism
in most cases.
C, D, E) All these effect are actually enhanced, not antagonized, by physostigmine.Rate this question:
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- 14.
In the figure below, curve C depicts the log dose-response curve for carbachol on contraction of nonvascular smooth muscle. Which of the curves best depicts the log dose-response curve for acetylcholine in the presence of a fixed and large dose of bethanechol?
- A.
Curve A
- B.
Curve B
- C.
Curve C
- D.
Curve D
- E.
Curve E
Correct Answer
A. Curve AExplanation
Answer: A
Carbachol and bethanechol are two full agonists at M3 receptors. When a large dose of
bethanechol is give it will have an effect even at zero carbachol concentration. Then the increasing
doses if carbachol will increase that effect up to a maximum. In other words, when a constant dose
of a full agonist is given with increasing doses of another full agonist, the log-dose effect curve of
the second agonist are shifted to the left.
B, C, D, E) (see explanation above)Rate this question:
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- 15.
A 65-year-old male suffering from open angle glaucoma has been receiving timolol over the last three months but the control of intraocular pressure has proven inadequate. The ophthalmologist decides to add a second drug and prescribed carbachol. Which of the following pairs of receptors most likely mediates the therapeutic efficacy of the drug in this patient?
- A.
Nm and M2
- B.
Nn and M3
- C.
M3 and beta-2
- D.
Nm and beta-2
- E.
Nn and M2
- F.
Nm and M3
Correct Answer
B. Nn and M3Explanation
Answer: B
Carbachol has both muscarinic and nicotinic activity. By activating Nn receptors on the
parasympathetic ciliary ganglion as well as the M3 receptors on ciliary muscle the drug causes the
contraction of the muscle, which leads to the opening of trabecular meshwork, so increasing the
outflow of the aqueous humor.
A, C, D, E, F) (see explanation above)Rate this question:
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.JPG "In the figure below, curve C depicts the log dose-response curve for carbachol on
contraction of nonvascular smooth muscle. Which of the curves best depicts the log
dose-response curve for acetylcholine in the presence of a fixed and large dose of
bethanechol?")
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Mar 21, 2023Quiz Edited by
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Jun 03, 2012Quiz Created by
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