Pharm Workshop Ans Phrmcolgy W Exp

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Pharm Workshop Ans Phrmcolgy W Exp - Quiz

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Questions and Answers
  • 1. 

    Which of the following autonomic receptors is most prevalent in vascular endothelium?

    • A.

      Nn

    • B.

      Nm

    • C.

      Alpha-1

    • D.

      Alpha-2

    • E.

      Beta-1

    • F.

      Beta-2

    • G.

      M2

    • H.

      M3

    Correct Answer
    H. M3
    Explanation
    Cells of vascular endothelium have non innervated M3 receptors. Activation of these receptors
    triggers the release of nitric oxide which diffuses to adjacent smooth muscle cells and causes
    them to relax.

    Rate this question:

  • 2. 

    Which of the following autonomic receptors is most prevalent in cell body of neurons of otic ganglion?

    • A.

      Nn

    • B.

      Nm

    • C.

      Alpha-1

    • D.

      Alpha-2

    • E.

      Beta-1

    • F.

      Beta-2

    • G.

      M2

    • H.

      M3

    Correct Answer
    A. Nn
    Explanation
    The otic ganglion is a parasympathetic ganglion. The receptors located on the cell body of
    neurons of all autonomic ganglia are primarily Nn receptors.

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  • 3. 

    Which of the following effects of epinephrine is mainly mediated by the activation of alpha-2 receptors?

    • A.

      Increased AV conduction

    • B.

      Stimulation of insulin secretion

    • C.

      Stimulation of renin secretion

    • D.

      Bronchodilation

    • E.

      Decreased production of aqueous humor

    • F.

      Increased lipolysis

    • G.

      Contraction of bladder sphincter

    Correct Answer
    E. Decreased production of aqueous humor
    Explanation
    Activation of alpha-2 receptors decreases the production, whereas activation of beta receptors
    (mainly beta-2) increases the production.
    A, B, C, D, F, G) These effect of epinephrine are not mediated by the activation of alpha-2
    receptors

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  • 4. 

    Which of the following statements best explains why an IV injection of norepinephrine usually causes very little effects on cardiac output in normal subjects?

    • A.

      The norepinephrine-induced vasoconstriction decreases the end diastolic volume

    • B.

      The increased total peripheral resistance tends to reduce preload

    • C.

      The reflex bradycardia balances the direct increased stroke volume

    • D.

      The decreased end systolic volume balances the increase in cardiac contractility

    • E.

      The increased total peripheral resistance causes a decreased firing of baroreceptors

    Correct Answer
    C. The reflex bradycardia balances the direct increased stroke volume
    Explanation
    An IV injection of norepinephrine would cause an increase in stroke volume and heart rate, both
    due to the activation of beta-1 receptors. The consequent increase in both systolic and diastolic
    pressure elicits a reflex effect which overcomes the direct chronotropic activity so leading to a
    net decrease in heart rate. Since CO = SV x HR, even if the stroke volume is increased, cardiac
    output is not substantially affected.
    A) The norepinephrine-induced vasoconstriction tends to decrease the end diastolic volume,
    but this has little consequence on the stroke volume which is still increased, due to the increase
    in cardiac contractility.
    B) (see explanation A)
    D) The end systolic volume has nothing to do with cardiac contractility.
    E) Actually an increased total peripheral resistance would cause an increased firing of
    baroreceptors (they are stretch receptors).

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  • 5. 

    A 53-year-old man was brought to the emergency room because of a crushing substernal pain of one hour duration. Vital signs on admission were: BP 88/50, pulse 115 bpm, cardiac output 2.3 L/min. A diagnosis of cardiogenic shock was made and a therapy was started which included an IV infusion of a drug. Which of the following molecular actions most likely mediated the therapeutic effectiveness of the drug in this patient?

    • A.

      Activation of phospholipase A2

    • B.

      Increased synthesis of IP3 and DAG

    • C.

      Increased synthesis of cAMP

    • D.

      Increased synthesis of cGMP

    • E.

      Opening of ligand gated Na+ channels

    • F.

      Opening of ligand-gated K+ channels

    Correct Answer
    C. Increased synthesis of cAMP
    Explanation
    The therapy of cardiogenic shock requires a rapid acting inotropic drug to increase myocardial
    contractility and cardiac output. Dobutamine and dopamine are the two drugs most frequently
    used. In both cases the therapeutic efficacy is mediated mainly by the direct (dobutamine) or
    indirect (dopamine) activation of beta-1 receptors which in turn increases the synthesis of
    cAMP.

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  • 6. 

    A 52-year-old man was admitted to the coronary care unit with a diagnosis of myocardial infarction. Two hours later he developed a ventricular fibrillation and was defibrillated immediately but without success. A  cardiopulmonary resuscitation (CPR) was started, two additional shocks were given at a higher energy, but the patient remained unresponsive. At this time a bolus of epinephrine was given IV, while continuing the CPR. The beneficial effect of the drug in this setting seems mainly related to which of the following actions?

    • A.

      Alpha-1 receptor mediated vasoconstriction

    • B.

      Beta-2 receptor mediated vasodilation

    • C.

      Beta-2 receptor mediated increase in cardiac contractility

    • D.

      Beta-1 receptor mediated increase in renin secretion

    • E.

      Beta-2 receptor mediated bronchodilation

    Correct Answer
    A. Alpha-1 receptor mediated vasoconstriction
    Explanation
    The most appropriate management of cardiac arrest induced by ventricular fibrillation is a 200-
    joule defibrillation. Additional shocks at higher energy should be given in case of initial failure. If
    ventricular fibrillation persists, the American Heart Association indicates that epinephrine should
    be administered. Most likely epinephrine increases brain and heart flow during cardiopulmonary
    resuscitation by two main mechanisms:
    1) It prevents arterial collapse at the thoracic inlet. Collapse results from high extravascular
    intrathoracic pressure coupled with low intravascular pressure and loss of arteriolar tone. By
    constricting arterial vessels and by increasing venous return, epinephrine increases the aortic
    diastolic pressure during closed chest compression.
    2) Preferentially reduces blood flow to the renal and splanchnic beds, so facilitating the
    distribution of the limited cardiac output to the cerebral and coronary circulation during the
    external cardiac massage. In fact cerebral blood vessels are relatively insensitive to the
    vasoconstricting effect of alpha-agonists and perfusion pressure of the brain is increased.
    It seems therefore that the main beneficial effects of epinephrine in cardiac arrest are related to
    its alpha-1 receptor activation.
    It is worth to note that, unlike what happens in the normal person, epinephrine increases TPR in
    persons with cardiac arrest. In fact in this condition there is a complete loss of arteriolar tone
    and therefore the beta-2 mediated vasodilation cannot occur, whereas the alpha-1 mediated
    vasoconstriction can be still operative.
    Additional beneficial effects that are instead related mainly to beta-1 receptor activation are:
    3) To change a fine ventricular fibrillation into a coarse one which is more susceptible to
    electrical defibrillation.
    4) To stimulate spontaneous ventricular contraction in case of asystole.
    Since the benefits of epinephrine are mainly due to alpha-1 mediated vasoconstriction,
    norepinephrine could also be used. In fact a large prehospital trial failed to identify any
    difference in survival following treatment with norepinephrine or standard doses of epinephrine.
    Other vasoconstricting agents have also been evaluated. Vasopressin has recently been tested,
    with promising results.
    The fact that epinephrine is still the agent of choice in cardiac arrest is likely related to the long
    experience achieved with this drug, as well as to the additional benefits listed above. For
    example epinephrine activates bot beta-1 and beta-2 receptors and therefore it is likely more
    effective than norepinephrine in stimulating spontaneous contraction of the heart during
    asystole.
    B) The beta-2 receptor mediated vasodilation would be counterproductive, but does not occur in
    cardiac arrest (see explanation above).
    C) This action of the drug could add an additional benefit (see explanation above), but it is
    mainly related to beta-1 receptor activation (the increase in cardiac contractility due to beta-2
    receptor activation is minor). In any case the main mechanism is MOST LIKELY the alpha-1
    receptor mediated vasoconstriction.
    D, E) The beneficial effects of epinephrine induced increase in renin secretion and of
    epinephrine induced bronchodilation are, at the most, only marginal.

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  • 7. 

    A 54-year-old patient suffering from postural hypotension was admitted to the hospital for evaluation. A tyramine infusion was not able to rise the blood pressure, while a very small dose of norepinephrine caused a transient and big elevation of blood pressure. These results would suggest a degeneration of which of the following structures?

    • A.

      Medulla oblongata

    • B.

      Preganglionic sympathetic neurons

    • C.

      Postganglionic parasympathetic neurons

    • D.

      Preganglionic parasympathetic neurons

    • E.

      Postganglionic sympathetic neurons

    Correct Answer
    E. Postganglionic sympathetic neurons
    Explanation
    Tyramine is a normal byproduct of tyrosine metabolism in the body and is also found in high
    concentration in fermented food. It is normally inactive if ingested because of a very large firstpass
    effect (metabolism by hepatic MAO). If administered parenterally it has an indirect
    sympathomimetic action due to the release of stored catecholamines. This is the basis of the
    tyramine test, sometimes used clinically for the diagnosis of some ANS diseases.
    In the present case the patient is most likely affected by pure autonomic failure, a rare
    degenerative disorder of the ANS presenting in middle to late life. In this disease there is a
    degeneration of postganglionic sympathetic neurons which can explain the postural
    hypotension. An IV injection of tyramine normally causes an elevation of blood pressure due to
    the release of stored catecholamines. In the present case however the elevation did not occur
    because catecholamines had been lost from the nerve endings. On the contrary an IV injection
    of norepinephrine caused a big elevation, since norepinephrine directly activates adrenergic
    receptors. Moreover these receptors were up-regulated, due to a decrease availability of the
    neurotransmitter (denervation supersensitivity).
    B) A lesion of the preganglionic sympathetic nerve would have caused orthostatic hypotension,
    but tyramine would have caused hypertension, since the postganglionic adrenergic neurons
    were intact.
    C, D) In case of a lesion of either pre or postganglionic parasympathetic nerves tyramine would
    have been effective.
    E) Lesions of the sympathetic pathways in the medulla oblongata would have caused symptoms
    similar to those due to lesions of the preganglionic sympathetic nerves. In this case too tyramine
    would have been effective.

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  • 8. 

    The following diagram represents a noradrenergic terminal. Which of the following sites in the diagram represents the site of action of metyrosine?

    • A.

      A

    • B.

      B

    • C.

      C

    • D.

      D

    • E.

      E

    • F.

      F

    • G.

      G

    • H.

      H

    Correct Answer
    B. B
    Explanation
    Metyrosine inhibits the enzyme tyrosine hydroxylase, which catalyzes the hydroxylation of
    tyrosine to DOPA. This is the rate-limiting step in norepinephrine biosynthesis and the inhibition
    of the enzyme can cause up to a 70% decrease of norepinephrine content in adrenergic
    terminals, so leading to antiadrenergic effects.

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  • 9. 

    Which of the following actions most likely contribute to the tachycardia that may occur after the administration of prazosin?

    • A.

      Decreased firing rates of carotid baroreceptors

    • B.

      Increased cardiac contractility

    • C.

      Release of norepinephrine from cardiac adrenergic terminals

    • D.

      Increased venous return to the heart

    • E.

      Blockade of muscarinic receptors in the heart

    Correct Answer
    A. Decreased firing rates of carotid baroreceptors
    Explanation
    Prazosin is a alpha-1 selective adrenergic blocker. The blockade of alpha-1 receptors causes
    peripheral vasodilation which in turn decreases the blood pressure. A reduction in blood
    pressure decreases the firing rate of carotid baroreceptors, which are stretch receptors. Since
    the baroreceptor discharge excites the vagal outflow to the heart, a decrease firing rate will have
    the opposite effect, that is it will increase the sympathetic outflow.
    B) Cardiac contractility has nothing to do with cardiac rate.
    C) Prazosin has no actions on presynaptic alpha-2 receptors.
    D) By causing peripheral vasodilation prazosin actually decreases venous return to the heart.
    E) Prazosin has no action on muscarinic receptors of the heart.

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  • 10. 

    Which of the following effects can be elicited by both nonselective and selective beta blockers?

    • A.

      Increased intestinal peristalsis

    • B.

      Mydriasis

    • C.

      Increased duration of the diastole

    • D.

      Bronchoconstriction

    • E.

      Decreased glycogenolysis

    • F.

      Cycloplegia

    Correct Answer
    C. Increased duration of the diastole
    Explanation
    Selective beta blockers blocks mainly beta-1 receptors. Therefore the effect common to both
    selective and nonselective agents must be mediated by beta-1 receptor blockade. The
    decreased heart rate is due to blockade of beta-1 receptors and leads to an increased duration
    of diastole.
    A, D, E) These effects are mainly due to blockade of beta-2 receptors.
    B) This effect is mediated by alpha-1 receptor activation or M3 receptor blockade.
    F) This effect is mediated by M3 receptor blockade.

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  • 11. 

    An IV injection of drug X was given to a laboratory animal before and after the administration of atropine and the heart rate was recorded. The results are depicted below: Which of the following drugs was most likely drug X?

    • A.

      Epinephrine

    • B.

      Norepinephrine

    • C.

      Prazosin

    • D.

      Albuterol

    • E.

      Isoproterenol

    • F.

      Dobutamine

    Correct Answer
    B. Norepinephrine
    Explanation
    The drug causes a decrease in heart rate that is reversed by a pretreatment with atropine. This
    suggest that the bradycardia is caused by a reflex vagal discharge. Norepinephrine is the only
    listed drug that causes a vagal reflex bradycardia but can also causes direct tachycardia.

    Rate this question:

  • 12. 

    An IV injection of epinephrine was given to a laboratory animal before and after the administration of a new drug X. The change in heart rate and bronchiolar resistance were recorded. The results are depicted in the following figure: Which of the following drugs does the new agent most closely resemble?

    • A.

      Albuterol

    • B.

      Timolol

    • C.

      Metoprolol

    • D.

      Atropine

    • E.

      Propranolol

    • F.

      Prazosin

    Correct Answer
    C. Metoprolol
    Explanation
    The new drug completely antagonizes the epinephrine-induced increase in heart rate (which is
    mediated by beta-1 receptor activation) but does not antagonize the epinephrine-induced
    bronchodilation (which is mediated by beta-2 receptor activation). Therefore the drug must be a
    selective beta blocker like metoprolol.
    B, E) These drugs are nonselective beta blockers and so they would antagonize both effects of
    epinephrine.
    A, D, F) These drugs cannot antagonize (in fact they might enhance) the epinephrine-induced
    increase in heart rate.

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  • 13. 

    A 55-year-old alcoholic man with liver cirrhosis was admitted to the intensive care unit with a two week history of intermittent melena. Esophagoscopy revealed three chains of large varices in the lower esophagus with signs of recent bleeding. An appropriate treatment was performed which included a drug aimed at reducing portal pressure. Which of the following drugs was most likely administered ?

    • A.

      Albuterol

    • B.

      Propranolol

    • C.

      Methyldopa

    • D.

      Clonidine

    • E.

      Prazosin

    • F.

      Epinephrine

    Correct Answer
    B. Propranolol
    Explanation
    The creation of arteriovenous anastomoses, which occurs in cirrhosis, allows the perfusion
    pressure of the hepatic artery being partly transmitted into the portal vein. Therefore
    arteriovenous anastomoses are a main cause of portal hypertension in cirrhosis. Since the
    esophageal veins are tributaries of the portal vein, the portal hypertension cause the
    esophageal veins to dilate and become varicose. By blocking beta-2 receptors (particularly
    abundant in liver vascular bed) liver arterial vessels are constricted and the pressure
    transmitted into the portal vein decreases.
    A, F) Activation of beta-2 receptors by albuterol would worsen the varices by increasing the
    portal pressure.
    C, D, E) These drugs can reduce the systemic blood pressure but they have unpredictable
    effects on the perfusion pressure of liver arterial vessels.

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  • 14. 

    A new autonomic drug that does not enter the brain was given IV to healthy volunteers. The cardiovascular effects are tabulated below The effects of the new drug are most similar to those of which of the following agents?

    • A.

      Dobutamine

    • B.

      Epinephrine

    • C.

      Isoproterenol

    • D.

      Norepinephrine

    • E.

      Phenylephrine

    Correct Answer
    D. Norepinephrine
    Explanation
    The investigational drug causes a parallel increase in both systolic and diastolic pressure and a
    concomitant decrease in heart rate. This pattern suggests that the decrease in heart rate is due
    to a reflex vagal discharge. Drugs that cause this effect must be vasoconstricting agents (like
    norepinephrine and phenylephrine) devoid of vasodilating activity. In this case however stroke
    volume is substantially increased (stroke volume = cardiac output/heart rate; from 78.6 mL to
    100 mL). Phenylephrine would increase the stroke volume only slightly (if venous constriction
    causes an increase in venous return) or not at all, since it has no beta-adrenergic activity.
    Moreover the ejection fraction is increased, which confirms that the drug does increase cardiac
    contractility. (the ejection fraction is the ratio of the stroke volume to the end diastolic volume.
    Remember that the only way to increase the ejection fraction is to increase cardiac contractility).
    A, B, C) Epinephrine, dobutamine and isoproterenol would increases, not decrease, the cardiac
    output of the heart.
    E) (see explanation above)

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  • 15. 

    A new synthetic drug X is to be studied for its cardiovascular effects. The drug is given IV to three animals while the heart rate and blood pressure are recorded. The first animals has received no pretreatment, the second has received an effective dose of prazosin before drug X, and the third has received an effective dose of propranolol 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 drug X most closely resemble?

    • A.

      Norepinephrine

    • B.

      Epinephrine

    • C.

      Isoproterenol

    • D.

      Phenylephrine

    • E.

      Albuterol

    Correct Answer
    B. Epinephrine
    Explanation
    The drug causes no variation in the mean blood pressure and an increase in heart rate. This
    suggests that the increased in heart rate is a direct effect, since reflex variation in heart rate can
    occur only when there is a variation in mean blood pressure. Moreover in this case:
    A) Norepinephrine would have caused an increase in mean blood pressure, so causing reflex
    bradycardia. This reflex effect usually overcomes the direct effect of the drug on the heart rate,
    so the final effect would have been a decrease, not an increase, in heart rate.
    C) Phenylephrine would have caused an increase in mean blood pressure, so causing reflex
    bradycardia.
    D, E) Isoproterenol and albuterol would have caused a decrease in mean blood pressure, due to
    the beta-2 receptor mediated vasodilation.
    The fact that the drug under study is similar to epinephrine can also be predicted from the
    results of the pretreatments. Epinephrine causes negligible changes in mean blood pressure
    due to the opposite effects of alpha-1 and beta-2 receptor activation. Prazosin blocks alpha-1
    receptors so unmasking the beta-2 mediated vasodilation. Propranolol blocks beta-1 and beta-2
    receptors so counteracting the effect on heart rate and unmasking the alpha-1 mediated
    vasoconstriction.

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  • 16. 

    A 25-year-old man complained to his physician of insomnia and night-mares. He also felt pain with ambulation at both calves. The man, recently diagnosed with benign essential tremor, started two week ago a drug treatment that was able to improve the tremor. A drug with which of the following mechanisms of action was the patient most likely taking?

    • A.

      Blockade of Na+ channels in motor nerves

    • B.

      Activation of alpha-2 receptors in the spinal cord

    • C.

      Blockade of Nm receptors in motor end plate

    • D.

      Activation of GABA receptors in the brain stem

    • E.

      Blockade of beta receptors in striated muscle

    Correct Answer
    E. Blockade of beta receptors in striated muscle
    Explanation
    16) Answer: E
    Beta-blockers are effectively used in case of benign essential tremor. The mechanism of this
    therapeutic effect is still not clear but it seems related to the involvement of beta-2 receptors in
    the pathogenesis of tremor. In fact beta-2 receptor activation accelerates the sequestration of
    cytosolic Ca++ in striated muscle and enhances the discharge of muscle spindles. The
    symptoms reported by the patient are typical adverse effects of beta blockers. These drug can
    cause insomnia and nightmares in about 10% of cases, and can cause calf pain by blocking
    beta-2 receptor mediated vasodilation in skeletal muscle vessels.
    A) This would be the mechanism of action of local anesthetics. These drugs are not used for
    essential tremor and do not cause the adverse effects reported by the patient.
    B) Drugs with this mechanism of action (clonidine, tizanidine) are used to treat spasticity, but
    not essential tremor.
    C) This would be the mechanism of action of neuromuscular blocking drugs. These drugs are
    not used for essential tremor and do not cause the adverse effects reported by the patient
    D) This would be the mechanism of action of baclofen a drug used to treat spasticity, but not
    essential tremor.

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  • 17. 

    A 57-year-old man suffering from open-angle glaucoma has been receiving a topical drug that decreases the production of aqueous humor. Which of the labeled structures of the eye, in the diagram below, is the most likely site of action of that drug?

    • A.

      A

    • B.

      B

    • C.

      C

    • D.

      D

    • E.

      E

    Correct Answer
    D. D
    Explanation
    Glaucoma is characterized by an increased intraocular pressure, which in turn is due to an
    excessive amount of aqueous humor in the anterior chamber of the eye. Therefore the
    pharmacological therapy of this disease is aimed to decrease this amount, either by lowering
    aqueous humor production or by increasing aqueous humor outflow.
    All drugs that decreases the production of aqueous humor act on the ciliary epithelium, which is
    the tissue that actually produces the humor (site D in the figure).
    Activation of alpha-2 receptors in that tissue decrease the production, whereas activation of
    beta-2 receptors increases the production. Therefore in order to decrease the production, a
    drug must either activate alpha-2 receptors (like apraclonidine) or block beta-2 receptors (like
    timolol).
    A) The site A is the ciliary muscle. Drugs that contract this muscle promote the outflow of the
    aqueous humor but have no effect on the production.
    B) The site B is the iris. Drugs acting on iris muscles have no effect on aqueous humor
    production.
    C) The site C represents the trabecular meshwork and the Schlemm’s canal. These structures
    can influence the outflow, not the production, of aqueous humor.
    E) The lens is not involved in the regulation of aqueous humor production.

    Rate this question:

  • 18. 

    The following picture represents different parts of the heart. For the myocytes present in the part indicated by the arrow, which of the following would be the prevalent autonomic postreceptor mechanism?

    • A.

      Opening of ligand-gated Na+ channels

    • B.

      Increased synthesis of IP3 and DAG

    • C.

      Opening of ligand-gated K+ channels

    • D.

      Activation of phospholipase A2

    • E.

      Increased synthesis of cAMP

    Correct Answer
    C. Opening of ligand-gated K+ channels
    Explanation
    The main nerve innervating the sinoatrial node is the vagus nerve and the main autonomic
    receptors located on the myocytes of the SA node are M2 receptors. Activation of these
    receptors triggers the opening of ligand-gated K+ channels, which in turn causes an outward K+
    current. In the resting cells, outward K+ current always cause hyperpolarization of cell
    membrane.
    A) This postreceptor mechanism is mediated by the activation of nicotinic receptors
    B) This postreceptor mechanism is mediated by the activation of M1, M3 or alpha-1 receptors.
    D) This postreceptor mechanism is mediated by the activation of M1, M3 or alpha-1 receptors.
    E) This postreceptor mechanism is mediated mainly by the activation of beta receptors.

    Rate this question:

  • 19. 

    A 67-year-old patient presented for routine ophthalmic examination. Tonometry measured an intraocular pressure of 28 mm Hg in both eyes (normal 10-20). The patient has been suffering from complete AV block for two years. The ophthalmologist prescribed a treatment with drugs to be given locally by eye drops. Which of the following drugs was most likely included in the treatment?

    • A.

      Timolol

    • B.

      Prazosin

    • C.

      Isoproterenol

    • D.

      Pilocarpine

    • E.

      Albuterol

    • F.

      Homatropine

    Correct Answer
    D. Pilocarpine
    Explanation
    The patient is most likely suffering from open angle glaucoma. Pilocarpine historically was the
    initial treatment of choice, but today is used only as an alternative therapy when other drugs are
    contraindicated, as in the present case (see below)
    A) Beta-blockers are first-line therapy for glaucoma but are contraindicated in this case because
    of the AV block. In fact systemic effects can occur even after a topical administration, especially
    in the elderly secondary to inadvertent overdose due to poor administration technique. In
    patients with complete AV block the heart rate is maintained by a rhythm which is driven by a
    ventricular pacemaker and is about 50 bpm. By blocking beta receptors in the ventricle a beta
    blocker can reduce this barely sufficient heart rate, so causing heart failure. Pilocarpine is not
    dangerous since in a patient with a complete AV block the AV conduction is, by definition,
    already completely blocked and the parasympathetic control of the ventricle is negligible, due to
    lack of innervation.
    B, C, E) These drugs are not used for the therapy of glaucoma.

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  • 20. 

    A 82-year-old man resident of a nursing facility complained of frequent urinary urges which often resulted in urine leakage. A drug from which of the following classes would be appropriate to manage the patient’s incontinence?

    • A.

      Antimuscarinics

    • B.

      Cholinergics

    • C.

      Beta-2 agonists

    • D.

      Ganglionic stimulants

    • E.

      Alpha-1 antagonists

    • F.

      Beta-blockers

    Correct Answer
    A. Antimuscarinics
    Explanation
    The incontinence of the patient is most likely an urge incontinence, due to an overreactive
    bladder. This is the most common form of incontinence affecting the elderly. Since the major
    physiological stimulus for muscle contraction is the acetylcholine induced activation of M3
    receptors on bladder smooth muscle, antimuscarinics can depress involuntary bladder
    contraction from any etiology. Tolterodine, a selective antagonist on M3 receptors, is the drug
    most frequently used for urge incontinence.
    B, C, D, E) (see explanation above)

    Rate this question:

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