Pharm Anti Cholinergic W Exp Part 2

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Pharm Anti Cholinergic W Exp Part 2 - Quiz

Questions and Answers
  • 1. 

    A 71-year-old man with atrial fibrillation had diarrheal stools after eating at a restaurant during a vacation in Mexico. The man took an over-the-counter preparation, bought at a local pharmacy, in order to relieve the diarrhea. Few hours later he developed palpitations, dyspnea and an urgent need to urinate. Which of the following drugs could have facilitated the appearance of these symptoms in the patient?

    • A.

      Phenylephrine

    • B.

      Epinephrine

    • C.

      Atropine

    • D.

      Albuterol

    • E.

      Propranolol

    Correct Answer
    C. Atropine
    Explanation
    Answer: C
    Atrial fibrillation results from cardiac impulses that go mad within the atrial muscle mass,
    stimulating first one portion of the atrial muscle, then another portion, then another and
    eventually feeding back onto itself to re-excite the same atrial muscle over and over. When this
    occurs many small portions of the atrial muscle will be contracting at the same time while other
    portions will be relaxing. Except for the connection through the AV bundle, the atrial muscle
    mass is separated from the ventricular muscle mass by fibrous tissue. Therefore impulses from
    the atria can get into the ventricles only through the AV bundle.
    When the atria are fibrillating, impulses arrive from the atrial muscle to the AV node rapidly but
    also irregularly. Because the AV node will not pass a second impulse for about 0.35 seconds
    after a previous one, at least 0.35 seconds must elapse between one ventricular contraction to
    the next. An additional but variable interval of 0 to 0.6 seconds occurs before one of the
    fibrillatory impulses can get into the AV node. Thus the interval between successive ventricular
    contraction varies from a minimum of about 0.35 seconds to a maximum of about 0.95 seconds,
    causing an irregular heartbeat between 65 to 170 bpm.
    Atrial fibrillation tends to occur paroxysmally before becoming constant. Palpitations, pallor,
    weakness and nausea usually occur during the attack . Sometimes there is also a need to
    urinate, which is the consequence of an increased urine formation by the kidney, due to the
    secretion of the atrial natriuretic peptide.
    Antimuscarinic drugs are present in many over-the-counter antidiarrheal preparations, sold in
    several countries. These drugs increase the AV conduction so allowing more impulses to pass
    into ventricles. Therefore they can trigger a paroxysmal attack, like in the present case.
    A, B, D) These drugs can increase AV conduction but they are not used as antidiarrheal agents.
    E) Beta blockers actually decrease AV conduction.

    Rate this question:

  • 2. 

    A 62-year-old man has been recently diagnosed with benign prostatic hyperplasia and has been scheduled for surgery. Which of the following drugs would be absolutely contraindicated in this patient?

    • A.

      Prazosin

    • B.

      Propranolol

    • C.

      Labetalol

    • D.

      Clonidine

    • E.

      Atropine

    Correct Answer
    E. Atropine
    Explanation
    Answer: E
    Antimuscarinic drugs relax the detrusor muscle, so voiding of the bladder becomes more difficult.
    This can be especially dangerous in patients with prostatic hyperplasia who have already
    difficulty in micturition, due to prostate-induced narrowing of the urethra. In these patients
    antimuscarinic drugs can precipitate an acute urinary retention.
    A) Alpha-1 antagonists like prazosin are actually indicated in prostatic hyperplasia since they
    relax the internal sphincter of the bladder.
    B, C) Beta blockers tend to contract the smooth muscle since they block the beta-2 receptor
    mediated relaxation. However these drugs have little influence on nonvascular smooth muscles
    that are mainly under parasympathetic control.
    D) Clonidine is an alpha-2 receptor agonist. Alpha-2 receptors are mainly presynaptic receptors,
    which modulate the release of different neurotransmitters (mainly norepinephrine). This
    modulation is usually too weak to affect significantly the contractility of nonvascular smooth
    muscle.

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  • 3. 

    A 58-year-old woman is admitted to the hospital with shallow breathing, wheezing, profuse rhinorrhea, lacrimation, ocular pain and diminished vision. She refers that symptoms started when she was in her garden spraying flowers with an insecticide containing carbaryl (a reversible cholinesterase inhibitor). Which of the following drugs would be the appropriate to treat the patient’s disorder?

    • A.

      Pralidoxime

    • B.

      Albuterol

    • C.

      Epinephrine

    • D.

      Glycopyrrolate

    • E.

      Atropine

    Correct Answer
    E. Atropine
    Explanation
    Answer: E
    Atropine is always used to treat poisoning by a cholinesterase inhibitors, since it is able to
    counteract both the central and peripheral symptoms of acetylcholine excess.
    A) Pralidoxime rapidly regenerates the phosphorylated acetylcholinesterase and therefore is
    useful for the treatment of poisoning due to organophosphates (irreversible cholinesterase
    inhibitors). The drug instead is contraindicated when poisoning is due to reversible
    cholinesterase inhibitors, like in the present case. In fact the drug is not able to regenerate the
    acetylcholinesterase blocked by carbamates and has itself a weak anticholinesterase activity.
    B, C) Sympathomimetic drug are useless in case of poisoning by cholinesterase inhibitors.
    D) Glycopyrrolate is a quaternary ammonium antimuscarinic drug. Therefore it would not be able
    to counteract the central effects of acetylcholine excess because it crosses poorly the blood
    brain barrier.

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  • 4. 

    A 56-year-old male with chronic obstructive pulmonary disease started a therapy with ipratropium bromide through a metered dose inhaler. Which of the following statements best explains why ipratropium is the only antimuscarinic drug used to treat bronchospastic disorders?

    • A.

      It is more potent than other antimuscarinic drugs

    • B.

      Its oral bioavailability is higher than that of other antimuscarinic drugs

    • C.

      It has an excellent absorption, when given by inhalatory route

    • D.

      It does not decrease bronchial secretions and mucociliary clearance

    • E.

      Central effects are negligible since it does not cross the blood brain barrier

    Correct Answer
    D. It does not decrease bronchial secretions and mucociliary clearance
    Explanation
    Answer: D
    In the past, antimuscarinic drugs were used to treat bronchospastic disorder. However it has
    been realized that most antimuscarinic drugs reduce the volume of bronchial secretion, which
    becomes thick. This viscid material is difficult to remove from the respiratory tree and can
    dangerously obstruct airflow. Moreover antimuscarinic drugs decrease mucociliary clearance, an
    important function for the cleaning of the bronchial tree. Therefore today these drugs (except
    Ipratropium) are actually contraindicated in respiratory disorder. Ipratropium has, for unknown
    reasons, negligible effects on bronchial secretions and mucociliary clearance. Thus, its
    anticholinergic properties can be safely exploited in the treatment of bronchospastic disease.
    A) Potency (i.e. the inverse of the dose needed to get a predetermined effect) is almost never
    the a reason for the choice of a specific drug.
    B) ipratropium is given only by inhalatory route, so oral bioavailability is not an issue. Moreover
    oral bioavailability is very low since the drug is a quaternary ammonium compound.
    C) By definition, absorption refers to the passage of the drug into the general circulation. When
    given by inhalatory route, absorption of ipratropium is negligible.
    E) Central effects of ipratropium are negligible (the drug is poorly absorbed), but this is not the
    reason why ipratropium is the preferred antimuscarinic drug to treat bronchospastic disorders.

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  • 5. 

    A 35-year-old woman has been recently diagnosed with gastroesophageal reflux disease. Which of the following drug classes would be contraindicated in this patient?

    • A.

      Beta-1 antagonists

    • B.

      Beta-1 agonists

    • C.

      M3-antagonists

    • D.

      M3-agonists

    • E.

      Alpha-2 agonists

    Correct Answer
    C. M3-antagonists
    Explanation
    Answer: C
    Gastroesophageal reflux disease is one of the most prevalent gastrointestinal disorders.
    Population based studies show that it affects up to 15% of individuals. The disease is due to
    incompetence of the lower esophageal sphincter. This sphincter receives mainly
    parasympathetic innervation and remains tonically constricted. When this constriction is
    insufficient the gastric content can go back into the esophagus. The esophageal mucosa is not
    capable of resisting the digestive action of gastric secretion and erosion occurs. This explains
    the heartburn, which is the most prominent symptom of the disease.
    All drugs that relax smooth muscle are contraindicated in gastrointestinal reflux disease.
    Antimuscarinic drugs can be especially dangerous, since the sphincter is rich of M3 cholinergic
    receptors.
    A, B) Contraction of the smooth muscle is not mediated by beta-1 receptors.
    D) M3-agonist increase the contraction of lower esophageal sphincter. Therefore these drugs
    would be indicated, not contraindicated, in gastroesophageal reflux disease.
    E) Alpha-2 agonists have negligible effects on nonvascular smooth muscle

    Rate this question:

  • 6. 

    A 45-year-old man collapsed at work and was found to be unresponsive. When the paramedics arrived he had ventricular fibrillation and was cardioverted successfully. He was admitted to the coronary unit but shortly thereafter he developed asystole. Cardiopulmonary resuscitation was started and escalating doses of epinephrine were given without success. Another drug was tried. Which of the following drugs was most likely administered?

    • A.

      Neostigmine

    • B.

      Norepinephrine

    • C.

      Dopamine

    • D.

      Atropine

    • E.

      Ipratropium

    Correct Answer
    D. Atropine
    Explanation
    Answer: D
    Asystole is the complete ECG absence of electrical activity. Its development usually indicates a
    prolonged cardiac arrest and carries a very grave prognosis.
    In the treatment of asystole epinephrine is the initial agent of choice to hopefully generate a
    rhythm. Since enhanced parasympathetic tone, possibly also due to chest compression, may
    play a role in inhibiting supraventricular and ventricular pacemakers, anticholinergic drugs may
    be beneficial, and atropine is usually tried when epinephrine fails.
    A) Neostigmine increases cholinergic activity and is therefore absolutely contraindicated in this
    setting.
    B, C) When epinephrine does not work, the choice of other sympathomimetic drugs is
    irrational.
    E) Ipratropium is an anticholinergic agent but is only used by inhalatory route in bronchospastic
    disorders.

    Rate this question:

  • 7. 

    Which of the following drugs can most likely prevent the fast EPSP in an autonomic ganglion cell?

    • A.

      Atropine

    • B.

      Neostigmine

    • C.

      Atropine

    • D.

      Pilocarpine

    • E.

      Dopamine

    • F.

      Ipratropium

    Correct Answer
    F. Ipratropium
    Explanation
    Answer: F
    Ipratropium is an antimuscarinic drug that also has significant Nn receptor blocking activity.
    Since the activation of Nn receptor in autonomic ganglia mediates the fast EPSP production,
    blockade of these receptors can prevent the EPSP.
    B) Neostigmine is a cholinesterase inhibitor and therefore it increases acetylcholine availability
    at all cholinergic synapses. As a consequence the fast EPSP would be enhanced, not,
    prevented.
    A, C, D, E) These drugs have negligible blocking activity on Nn receptors and therefore have no
    effect on fast EPSP.

    Rate this question:

  • 8. 

    which of the following is the most likely central effect of a moderate dose of nicotine?

    • A.

      Depression of the reticular formation

    • B.

      Stimulation of respiratory center

    • C.

      Depression of vomiting center

    • D.

      Inhibition of ADH secretion

    • E.

      Depression of vasomotor centers

    Correct Answer
    B. Stimulation of respiratory center
    Explanation
    Answer: B
    The excitation of respiration is a prominent action of nicotine. The drug stimulates the respiratory
    center both directly, acting on the medulla, and reflexly by excitation of chemoreceptors of the
    carotid and aortic bodies. With toxic doses the stimulation is followed by depression due to both
    central paralysis and peripheral blockade of muscle of respiration.
    A, C, D, E) Moderate doses of nicotine actually stimulates the reticular formation, the vomiting
    center, the vasomotor centers, and the secretion of ADH from the post hypophysis.

    Rate this question:

  • 9. 

    Which of the following statement best explains the nicotine-induced ganglionic blockade that usually occurs after an initial stimulating action?

    • A.

      Long-lasting activation of nicotinic receptors

    • B.

      Long lasting blockade of M2 receptors

    • C.

      Long lasting blockade of M1 receptors

    • D.

      Prevention of acetylcholine release from presynaptic terminals

    • E.

      Prevention of catecholamine release from small intensely fluorescent cells

    Correct Answer
    A. Long-lasting activation of nicotinic receptors
    Explanation
    Answer: A
    Prolonged activation of nicotinic receptors causes a persistent depolarization of postjunctional
    cell membrane that prevent the return to the resting state . Since it is the change in the resting
    potential that triggers the action potential, the depolarized membrane is resistant to further
    depolarization and neuronal transmission is blocked (‘depolarization blockade’).
    B, C) Blockade of ganglionic M2 and M1 receptors would prevent the production of IPSP and
    early slow EPSP. These potentials are not involved in the production of the action potential .
    D, E) Nicotine does not prevent acetylcholine release or catecholamine release

    Rate this question:

  • 10. 

    Pretreatment with a ganglionic blocker will most effectively prevent which of the following drug-induced effects?

    • A.

      Neostigmine-induced increase in intestinal peristalsis

    • B.

      Nicotine-induced contraction of skeletal muscle

    • C.

      Norepinephrine-induced bradycardia

    • D.

      Epinephrine-induced tachycardia

    • E.

      Propranolol-induced hypotension

    Correct Answer
    C. Norepinephrine-induced bradycardia
    Explanation
    Answer: C
    Norepinephrine increases the mean blood pressure. This increase causes a stimulation of aortic
    baroreceptors which activates the baroreceptor reflex. The increased vagal discharge
    overcomes the direct effect of norepinephrine on the heart rate (an increase due to the activation
    of beta-1 receptors), so the final effects is a decrease in heart rate. Ganglionic blockers impair
    the baroreceptor reflex and therefore bradycardia is abolished.
    A) Neostigmine is a cholinesterase inhibitor that increases the availability of acetylcholine at
    every cholinergic synapse. Acetylcholine activates M3 receptors in the gut and Nn receptors in
    the autonomic ganglia. Both actions contribute to the increase in intestinal peristalsis. A
    ganglionic blocker can prevent the activation of Nn receptors but has no effect on the activation
    of M3 receptors. Therefore peristalsis will be decreased, but not completely abolished.
    B) Nicotine-induced contraction of skeletal muscle is due to activation of Nm receptors.
    Ganglionic blocker have negligible activity on these receptors.
    D) Epinephrine induced tachycardia is due to the activation of cardiac beta-1 and beta-2
    receptors. A ganglionic blocker cannot block these receptors.
    E). Ganglionic blockers actually cause hypotension by blocking the sympathetic discharge to the
    vessels. Therefore the propranolol-induced hypotension is in fact enhanced, not prevented.

    Rate this question:

  • 11. 

    A 3-year-old boy is rushed to the emergency department by his mother after she discovered he had put on his skin 4 medication patches found in his father drawer. The boy presents with vomiting, diarrhea, profuse salivation, cold sweat, rapid and irregular pulse, tachypnea and mental confusion. Soon after admission the boy experiences a tonic-clonic seizure. Poisoning of this patient is most likely due to which of the following drugs?

    • A.

      Clonidine

    • B.

      Scopolamine

    • C.

      Nicotine

    • D.

      Bethanechol

    • E.

      Neostigmine

    Correct Answer
    C. Nicotine
    Explanation
    Answer: C
    The history of the patient together with his signs and symptoms are consistent with the diagnosis
    of nicotine poisoning. Nicotine is sold in transdermal patches for use as an aid in the treatment
    of nicotine withdrawal following cessation of smoking. The drug causes a rapid activation of both
    the sympathetic and parasympathetic nervous system, as well as a stimulation of different areas
    of the brain. Signs of this patient due to parasympathetic activation are vomiting, loss of urine
    and feces, and profuse salivation. Sings of sympathetic activation are cold sweat (sweat glands
    are stimulated and skin vessels are constricted), and rapid and irregular pulse (activation of Nn
    receptors releases epinephrine from adrenal medulla). Central stimulation accounts for the
    mental confusion and the to tonic clonic seizure.
    A) Clonidine is sold in transdermal patches for the therapy of hypertension, but it does not cause
    most of the symptoms exhibited by the patient.
    B) Scopolamine is sold in transdermal patches for the prevention of motion sickness. The drug is
    a muscarinic antagonist and therefore the symptoms of overdose would be the opposite of those
    exhibited by the patient
    C) Bethanechol is a muscarinic agonist. Symptoms of overdose would be limited to
    parasympathetic activation.
    E) Neostigmine is a. cholinesterase inhibitors. Many symptoms of poisoning by cholinesterase
    inhibitors are similar to those of nicotine overdose (both drugs can activate, directly or indirectly,
    nicotinic receptors). In cholinesterase inhibitor overdose however the cardiovascular effects are
    usually bradycardia and vasodilation, due to the peripheral actions of accumulated
    acetylcholine. Moreover, since the skin vessels are dilated, the sweat would not be “cold”. In
    addition, in the case of neostigmine central effects would be negligible since the drug crosses
    poorly the blood brain barrier

    Rate this question:

  • 12. 

    A new synthetic drug is to be studied for its cardiovascular effects. The drug is given IV to three laboratory animals while the blood pressure is recorded. The first animals has received no pretreatment, the second has received an effective dose of mecamylamine before drug X, and the third has received an effective dose of atropine before drug X. The NET CHANGES (+ or -) in heart rate and mean blood pressure induced by drug X (not by the pretreatment) are shown in the following table. Which of the following agents does the new drug most closely resemble?

    • A.

      Epinephrine

    • B.

      Acetylcholine

    • C.

      Propranolol

    • D.

      Nicotine

    • E.

      Histamine

    Correct Answer
    B. Acetylcholine
    Explanation
    Answer: B
    Blood pressure (BP) is equal to cardiac output (CO) by total peripheral resistance (TPR).
    Therefore, in order to decrease the mean BP a drug must decrease either CO or TPR or both.
    Among the listed drugs, acetylcholine and propranolol ( mainly by decreasing CO) and histamine
    ( mainly by decreasing TPR) would cause a fall in mean blood pressure. The fall is not blocked
    by a pretreatment with a ganglion blocker, suggesting that the depressor effect must be evoked
    at a site distal to the ganglia. The fall is instead blocked by atropine and therefore a direct acting
    muscarinic stimulant like acetylcholine must be the drug under study. The drop in BP is actually
    greater in the present of ganglion blockade. Likely the acetylcholine-induced vasodilation has
    elicited a reflex sympathetic discharge that has blunted the full depressor action of the drug in
    the untreated animal.
    A, D) Epinephrine and nicotine usually increase, not decrease, the mean blood pressure.
    C) Propranolol-induced decrease of blood pressure would not be antagonized by atropine. In
    fact, by blocking the parasympathetic action in the heart atropine can cause a sympatheticallymediated
    increase in cardiac rate (and therefore in cardiac output) but this cannot occur when
    the animal is treated with propranolol.
    E) Histamine-induced decrease of blood pressure would not be antagonized by atropine. In fact
    the decrease is due to peripheral vasodilation and atropine has very little effect on vessels.

    Rate this question:

  • 13. 

    A new synthetic drug is to be studied for its cardiovascular effects. The drug is given IV to four laboratory animals while the heart rate is recorded. The first animals has received no pretreatment, the second has received an effective dose of mecamylamine before drug X, the third has received an effective dose of atropine before drug X and the fourth has received effective dose of prazosin before drug X . The NET CHANGES (+ or -) in heart rate induced by drug X (not by the pretreatment) are shown in the following table. Which of the following agents does the new drug most closely resemble?

    • A.

      An anticholinesterase agent

    • B.

      A M2 receptor agonist

    • C.

      An alpha-1 antagonist

    • D.

      An alpha-2 agonist

    • E.

      A beta-1 agonist

    Correct Answer
    E. A beta-1 agonist
    Explanation
    Answer: E
    The drug causes an increase in heart rate that is not influenced by any of the blockers.
    Therefore the drug must activate directly beta-1 receptors in the heart.
    A, B) Drugs that activate indirectly (anticholinesterase drugs) or directly (M2 receptor agonists)
    muscarinic receptors on the heart would tend to cause a decrease, not an increase, in heart rate.
    C) A drug that activates alpha-1 receptors causes vasodilation and therefore a decrease in
    blood pressure. This decrease in turn can cause reflex tachycardia. However this tachycardia
    would have been prevented by a pretreatment with a ganglionic blocker, which blocks the
    neuronal transmission in the efferent portion of the reflex arch.
    D) A drug that activate alpha-2 receptors causes a decreased release of norepinephrine from
    cardiac adrenergic terminals, therefore causing a decrease, not an increase, in heart rate.

    Rate this question:

  • 14. 

    A new synthetic drug is to be studied for its cardiovascular effects. The drug is given IV to three laboratory animals while the blood pressure is recorded. The first animals has received no pretreatment, the second has received an effective dose of mecamylamine before drug X, and the third has received an effective dose of atropine before drug X. The NET CHANGES (+ or -) in mean blood pressure induced by drug X (not by the pretreatment) are shown in the following table. Which of the following agents does the new drug most closely resemble?

    • A.

      Acetylcholine

    • B.

      Nicotine

    • C.

      Epinephrine

    • D.

      Angiotensin II

    • E.

      Neostigmine

    Correct Answer
    B. Nicotine
    Explanation
    Answer: B
    The drug causes an increase in mean blood pressure when given alone. This suggests that it
    must be similar to nicotine, angiotensin II or epinephrine. The increase is blocked by a ganglion
    blocker and is instead increased by atropine. This indicated that the increase is due to
    ganglionic sympathetic stimulation which is more evident when the vagal activity to the heart is
    blocked by atropine.
    A, E) Acetylcholine and neostigmine usually cause a decrease of mean blood pressure.
    C) Epinephrine-induced increase of mean blood pressure is due to beta-receptor activation on
    the heart and alpha-receptor activation on he vessels. Therefore it would not be prevented by
    ganglionic blockade.
    D) Angiotensin II- induced increase of mean blood pressure is due to activation of angiotensin
    receptors in the vessel. Therefore it would not be prevented by ganglionic blockade.

    Rate this question:

  • 15. 

    A new synthetic drug is to be studied for its cardiovascular effects. The drug is given IV to four laboratory animals while the heart rate and blood pressure is recorded. The first animals has received no pretreatment, the second has received an effective dose of prazosin before drug X, third has received an effective dose of propranolol before drug X and the fourth has received an effective dose of atropine before drug X. The net CHANGES (+ or -) in heart rate and mean blood pressure induced by drug X (not by the pretreatment) are shown in the following table. Which of the following agents does the new drug most closely resemble?

    • A.

      Norepinephrine

    • B.

      Epinephrine

    • C.

      Isoproterenol

    • D.

      Phenylephrine

    • E.

      Acetylcholine

    Correct Answer
    D. Phenylephrine
    Explanation
    Answer: D
    The drug causes an increase in diastolic blood pressure and a decrease in heart rate. This
    suggests that the increased blood pressure has caused a reflex bradycardia. Among the listed
    drugs only norepinephrine and phenylephrine can cause these effects, due in both cases to
    alpha-1 receptor activation. In fact both effects are prevented by a pretreatment with prazosin
    and unaffected by pretreatment with propranolol or atropine.
    A) Norepinephrine-induced decrease in heart rate is due to reflex bradycardia which overcomes
    the direct tachycardic effect due to beta-receptor activation. A pretreatment with atropine would
    antagonize the reflex bradycardia (which is vagal-mediated) so unmasking the direct tachycardic
    effect. By the same token a pretreatment with propranolol would antagonize the direct
    tachycardic, effect so enhancing the reflex bradycardia. This does not occur with phenylephrine
    which is a pure alpha agonist with no direct effects on the heart.
    B) Epinephrine usually does not cause an increase in diastolic blood pressure since the alpha-1
    mediated vasoconstriction is counterbalanced by the beta-2 mediated vasodilation.
    C, E) Isoproterenol and acetylcholine decrease, not increase, the diastolic blood pressure.

    Rate this question:

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