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Pharmacokinetics & Pharmacodynamics Cholinergic & Anticholinergic Adrenergic & Antiadrenergic Diuretic & Antidiuretics Antihypertensive
100
C. Highly hydrophilic drugs have poor oral bioavailability, because they are poorly absorbed due to their inability to cross the lipid-rich cell membranes. Highly lipophilic (hydrophobic) drugs also have poor oral bioavailability, because they are poorly absorbed due their insolubility in aqueous stomach fluids and therefore cannot gain access to the surface of cells. Therefore, drugs that are largely hydrophobic, yet have aqueous solubility have greater oral bioavailability because they are readily absorbed.
Which of the following types of drugs will have maximum oral bioavailability?
A. Drugs with high first-pass metabolism.
B. Highly hydrophilic drugs.
C. Largely hydrophobic, yet soluble in aqueous solutions.
D. Chemically unstable drugs.
E. Drugs that are P-glycoprotein substrates.
100
A. A muscarinic agonist binds to and activates muscarinic receptors in the heart, endothelial cells (blood vessels), the gut, and iris sphincter (eye) and urinary bladder wall muscles, in addition to several other tissues. Activation of muscarinic receptors by an agonist causes a reduction in heart rate, constriction of circular muscles in the iris sphincter leading to constriction of the pupil (miosis), increased GI motility (hence, diarrhea, not constipation), and contraction of bladder muscles leading to an increase (not decrease) in urination frequency. In the endothelial cells of blood vessels, muscarinic activation produces release of nitric oxide that causes vasorelaxation and a reduction (not increase) in blood pressure.
Which of the following is a systemic effect of a muscarinic agonist?
A. Reduced heart rate (bradycardia).
B. Increased blood pressure.
C. Mydriasis (dilation of the pupil).
D. Reduced urinary frequency.
E. Constipation.
100
A. Stimulation of α1 receptors, mostly found in the blood vessels, causes vasoconstriction and increase in blood pressure. Stimulation of α2 receptors on the sympathetic presynaptic terminal reduces the release of norepinephrine. β2 receptors are not found in the heart, so activation of β2 receptors does not affect heart rate. Stimulation of β2 receptors found in the bronchial tissues causes bronchodilation, not bronchoconstriction.
Which of the following is correct regarding responses mediated by adrenergic receptors?
A. Stimulation of α1 receptors increases blood pressure.
B. Stimulation of α1 receptors reduces blood pressure.
C. Stimulation of sympathetic presynaptic α2 receptors increases norepinephrine release.
D. Stimulation of β2 receptors increases heart rate (tachycardia).
E. Stimulation of β2 receptors causes bronchoconstriction.
100
C. This is a potentially fatal situation. It is important to administer a diuretic that will reduce fluid accumulation in the lungs and, thus, improve oxygenation and heart function. The loop diuretics are most effective in removing large fluid volumes from the body and are the treatment of choice in this situation. In this situation, furosemide should be administered intravenously. The other choices are inappropriate.
An elderly patient with a history of heart disease is brought to the emergency room with difficulty breathing. Examination reveals that she has pulmonary edema. Which treatment is indicated?
A. Acetazolamide.
B. Chlorthalidone.
C. Furosemide.
D. Hydrochlorothiazide.
E. Spironolactone.
100
A. The cough is most likely an adverse effect of the ACE inhibitor enalapril. Losartan is an ARB that has the same beneficial effects as an ACE inhibitor but is less likely to produce a cough. Nifedipine, prazosin, and propranolol do not cause this side effect.
Old man was just started on therapy for hypertension and developed a persistent, dry cough. Which is most likely responsible for this side effect?
A. Enalapril.
B. Losartan.
C. Nifedipine.
D. Prazosin.
E. Propranolol
200
D. Lipid-soluble drugs readily cross the blood–brain barrier because they can dissolve easily in the membrane of endothelial cells. Ionized or polar drugs generally fail to cross the blood–brain barrier because they are unable to pass through the endothelial cells, which do not have slit junctions.
Which of the following is true about the blood–brain barrier?
A. Endothelial cells of the blood–brain barrier have slit junctions.
B. Ionized or polar drugs can cross the blood–brain barrier easily.
C. Drugs cannot cross the blood–brain barrier through specific transporters.
D. Lipid-soluble drugs readily cross the blood–brain barrier.
E. The capillary structure of the blood–brain barrier is similar to that of the liver and spleen.
200
B. Muscarinic agonists (for example, ACh, 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 circular smooth muscles in the iris sphincter and cause dilation of the pupil (mydriasis).
If an ophthalmologist wants to dilate the pupils for an eye examination, which of the following drugs/classes of drugs could be theoretically useful?
A. Muscarinic receptor activator (agonist).
B. Muscarinic receptor inhibitor (antagonist).
C. Acetylcholine.
D. Pilocarpine.
E. Neostigmine.
200
B. α2 Agonists activate α2 receptors located in the presynaptic terminal of sympathetic neurons and cause a reduction in the release of norepinephrine from sympathetic nerve terminals. This leads to a reduction in blood pressure. α2 Agonists such as clonidine and methyldopa are therefore used as antihypertensive agents
A hypertensive patient was accidentally given an α2 agonist instead of an α1 blocker. Which of the following is correct in this situation?
A. α2 Agonists can increase the release of norepinephrine from sympathetic nerve terminals.
B. α2 Agonists can reduce blood pressure in this patient.
C. α2 Agonists can increase blood pressure in this patient.
D. α2 Agonists will not affect blood pressure in this patient.
E. Blame your self
F. Blame your Pharm teacher and tutors
200
C. Acetazolamide is used prophylactically for several days before an ascent above 10,000 feet. This treatment prevents the cerebral and pulmonary problems associated with the syndrome as well as other difficulties, such as nausea.
A group of college students is planning a mountain climbing trip to the Andes. Which would be appropriate for them to take to prevent mountain sickness?
A. A thiazide diuretic such as hydrochlorothiazide.
B. An anticholinergic such as atropine.
C. A carbonic anhydrase inhibitor such as acetazolamide.
D. A loop diuretic such as furosemide.
E. A β-blocker such as metoprolol.
200
D. Prazosin produces first-dose hypotension, presumably by blocking α1 receptors. This effect is minimized by initially giving the drug in small, divided doses. The other agents do not have this adverse effect.
Which may cause reflex tachycardia and/or postural hypotension on initial administration?
A. Atenolol.
B. Hydrochlorothiazide.
C. Metoprolol.
D. Prazosin.
E. Verapamil.
300
D. A drug will reach steady state in about four to five half-lives. Thus, for this drug with a half-life of 10 hours, the approximate time to reach steady state will be 40 hours.
A drug with a half-life of 10 hours is administered by continuous intravenous infusion. Which of the following best approximates the time for the drug to reach steady state?
A. 10 hours.
B. 20 hours.
C. 33 hours.
D. 40 hours.
E. 60 hours.
300
C. Since there is already a deficiency in brain cholinergic function in Alzheimer’s disease, inhibiting cholinergic receptors or inhibiting the release of ACh will worsen the condition. Activating the acetylcholinesterase enzyme will increase the degradation of ACh, which will again worsen the condition. However, inhibiting the acetylcholinesterase enzyme will help to increase the levels of ACh in the brain and thereby help to relieve the symptoms of Alzheimer’s disease.
In Alzheimer’s disease, there is a deficiency of cholinergic neuronal function in the brain. Theoretically, which of the following strategies will be useful in treating the symptoms of Alzheimer’s 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.
E. I forget
300
D. α1 Receptors are located on the postsynaptic membrane in the effector organs such as blood vessels. α2 Receptors are mainly found on the presynaptic sympathetic nerve terminals, where they inhibit the release of norepinephrine when activated. β1 Receptors are found in the heart, in addition to some other tissues, and cause increase in heart rate and contractility when activated. β2 receptors are found in the lungs, in addition to some other tissues, and cause relaxation of bronchial smooth muscles when activated. β3 Receptors are found in adipose tissue and are involved in lipolysis.
All of the following are correct regarding adrenergic receptors, except:
A. α1 Receptors are primarily located on the postsynaptic membrane in the effector organs.
B. α2 Receptors are primarily located on the presynaptic sympathetic nerve terminals.
C. β1 Receptors are found mainly in the heart.
D. β2 Receptors are found mainly in adipose tissue.
E. Let me watch sketchy and get back to you
300
C. Spironolactone antagonizes aldosterone, which in turn prevents salt/water retention, cardiac hypertrophy, and hypokalemia. Spironolactone has endocrine effects on hormones but not on glucose.
How is spironolactone beneficial in HF?
A. Promotes potassium secretion.
B. Agonizes aldosterone.
C. Prevents cardiac hypertrophy.
D. Decreases blood glucose.
E. Euphoria during urination
300
C. The side effect profile of β-blockers, such as metoprolol, is characterized by interference with sexual performance and decreased exercise tolerance. None of the other drugs is likely to produce this combination of side effects.
A 48-year-old hypertensive patient has been successfully treated with a thiazide diuretic for the last 5 years. Over the last 3 months, his diastolic pressure has steadily increased, and he was started on an additional antihypertensive agent. He complains of several instances of being unable to achieve an erection and not being able to complete three sets of tennis as he once did. Which is the likely second antihypertensive medication?
A. Captopril.
B. Losartan.
C. Metoprolol.
D. Minoxidil.
E. Nifedipine.
400
Correct answer = A. As a general rule, weak acid drugs such as phenobarbital can be eliminated faster by alkalization of the urine. Bicarbonate alkalizes urine and keeps phenobarbital ionized, thus decreasing its reabsorption
Alkalization of urine by giving bicarbonate is used to treat patients presenting with phenobarbital (weak acid) overdose. Which of the following best describes the rationale for alkalization of urine in this setting?
A. To reduce tubular reabsorption of phenobarbital.
B. To decrease ionization of phenobarbital.
C. To increase glomerular filtration of phenobarbital.
D. To decrease proximal tubular secretion.
E. To increase tubular reabsorption of phenobarbital.
400
C. Muscarinic agonists such as ACh, pilocarpine, and bethanechol contract the circular muscles of iris sphincter and cause constriction of the pupil (miosis), whereas muscarinic antagonists such as atropine and tropicamide prevent the contraction of the circular muscles of the iris and cause dilation of the pupil (mydriasis). α-Adrenergic antagonists such as phentolamine relax the radial muscles of the iris and cause miosis.
During an ophthalmic surgical procedure, the surgeon wanted to constrict the pupil of the patient using a miotic drug. However, he accidentally used another drug that caused dilation of the pupil (mydriasis) instead. Most likely, which of the following drugs did he use?
A. Acetylcholine.
B. Pilocarpine.
C. Tropicamide.
D. Phentolamine.
E. Bethanechol.
400
E. Norepinephrine activates both α1 and β1 receptors and causes an increase in heart rate and blood pressure. A drug that prevents the increase in blood pressure caused by norepinephrine should be similar to carvedilol that antagonizes both α1 and β1 receptors. Prazosin is an α1 antagonist, clonidine is an α2 agonist, and propranolol and metoprolol are β antagonists, and these drugs cannot completely prevent the cardiovascular effects of norepinephrine.
A new antihypertensive drug was tested in an animal model of hypertension. The drug when given alone reduces blood pressure in the animal. Norepinephrine when given in the presence of this drug did not cause any significant change in blood pressure or heart rate in the animal. The new drug is similar to which of the following drugs in terms of its pharmacological mechanism of action?
A. Prazosin.
B. Clonidine.
C. Propranolol.
D. Metoprolol.
E. Carvedilol.
400
C. Hypokalemia is a common adverse effect of the thiazides and causes fatigue and lethargy in the patient. Supplementation with potassium chloride or foods high in K+ corrects the problem. Alternatively, a potassiumsparing diuretic, such as spironolactone, may be added. Calcium, uric acid, and glucose are usually elevated by thiazide diuretics. Sodium loss would not weaken the patient.
A 75-year-old woman with hypertension is being treated with a thiazide. Her blood pressure responds well and reads at 120/76 mm Hg. After several months on the medication, she complains of being tired and weak. An analysis of the blood indicates low values for which of the following?
A. Calcium.
B. Glucose.
C. Potassium.
D. Sodium.
E. Uric acid.
400
D. Increasing the dose of lisinopril or adding a second medication from a different class (such as a calcium channel blocker or diuretic) would be appropriate steps to control the blood pressure. Adding an ARB as the second medication is not recommended. ARBs have a similar mechanism of action to ACE inhibitors, and combination therapy may increase the risk of adverse effects.
A 60-year-old white female has not reached her blood pressure goal after 1 month of treatment with a low dose of lisinopril. All of the following would be appropriate next steps in the treatment of her hypertension except:
A. Increase dose of lisinopril.
B. Add a diuretic medication.
C. Add on a calcium channel blocker medication.
D. Add on an ARB medication.
E. Ask Google
500
A. For IV infusion, Loading dose = (Vd) × (desired steady-state plasma concentration). The Vd in this case corrected to the patient’s weight is 70 L. Thus, Loading dose = 70 L × 2.5 mg/L = 175 mg.
A 55-year-old male patient (70 kg) is going to be treated with an experimental drug, Drug X, for an irregular heart rhythm. If the Vd is 1 L/kg and the desired steadystate plasma concentration is 2.5 mg/L, which of the following is the most appropriate intravenous loading dose for Drug X?
A. 175 mg.
B. 70 mg.
C. 28 mg.
D. 10 mg.
E. 1 mg.
500
C. Sarin is an organophosphate cholinesterase inhibitor. It causes an increase in ACh levels in tissues that leads to cholinergic crisis by the activation of muscarinic as well as nicotinic receptors. Most of the symptoms of cholinergic crisis are mediated by muscarinic receptors and, therefore, the muscarinic antagonist atropine is used as an antidote for sarin poisoning. Cholinergic agonists such as pilocarpine, carbachol, physostigmine (indirect agonists), and nicotine will worsen the symptoms of sarin poisoning.
Sarin is a nerve gas that is an organophosphate cholinesterase inhibitor. Which of the following could be used as an antidote to sarin poisoning?
A. Pilocarpine.
B. Carbachol.
C. Atropine.
D. Physostigmine.
E. Nicotine.
500
A. If β-blocker therapy is stopped abruptly, that could cause angina and rebound hypertension. This could be due to the up-regulation of β receptors in the body. β-Blockers do not cause direct vasorelaxation. Therefore, they do not decrease peripheral resistance and are less likely to cause orthostatic hypotension. Propranolol is a nonselective β-blocker (not cardioselective). Cardioselective β-blockers antagonize only β1 receptors and do not worsen asthma as they do not antagonize β2 receptors.
Which of the following is correct regarding β-blockers?
A. Treatment with β-blockers should not be stopped abruptly.
B. Propranolol is a cardioselective β-blocker.
C. β-Blockers may cause orthostatic hypotension.
D. Cardioselective β-blockers worsen asthma.
E. β-Blockers decrease peripheral resistance by causing vasorelaxation.
500
Hydrochlorothiazide is effective in increasing calcium reabsorption, thus decreasing the amount of calcium excreted, and decreasing the formation of kidney stones that contain calcium phosphate or calcium oxalate. However, hydrochlorothiazide can also inhibit the excretion of uric acid and cause its accumulation, leading to an attack of gout in some individuals. Furosemide increases the excretion of calcium, whereas the K+-sparing osmotic diuretics, spironolactone and triamterene, and urea do not have an effect.
A 55-year-old male with kidney stones has been placed on a diuretic to decrease calcium excretion. However, after a few weeks, he develops an attack of gout. Which diuretic was he taking?
A. Furosemide.
B. Spironolactone.
C. Triamterene.
D. Urea.
E. Non of the above
500
C. Hydralazine is an appropriate choice for a hypertensive pregnant patient. ACE inhibitors, ARBs, and the direct renin inhibitor, aliskiren, are all contraindicated in pregnancy due to their potential for fetal harm.
Did you choose Fenoldopam? Why you are right! This is the Dopamine agonist that could also be used!
Which is an appropriate choice for hypertension treatment during pregnancy?
A. Aliskiren.
B. Fosinopril.
C. Hydralazine.
D. Valsartan.
E. Fenoldopam




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