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1. Choose the best answer and short explanation
1. A patient with chronic-stable angina is on prophylactic beta-
blocker therapy, with sublingual nitroglycerin used PRN (as
needed) for managing acute angina. One day he experiences
particularly severe angina and takes the usually recommended
dose of sublingual nitroglycerin (NTG). His discomfort is not
reduced at all. Seeking relief, he repeats the usual recommended
dose of NTG dose 6 times over a period of about 10 minutes,
and now has taken far too much of the nitrovasodilator.
An electrocardiogram taken by the paramedics, who were called
for the patient’s emergency, shows changes consistent with
myocardial ischemia. The patient incurs a massive infarction,
goes into cardiac arrest, and cannot be resuscitated.
Which of the following is the most likely cause of or
contributing factor to the patient’s ultimately fatal response to
the excessive dosage of NTG? Assume the patient was taking no
other drugs except the NTG and a beta-blocker.
A. Cyanide, or toxic metabolite of NTG, accumulated.
B. NTG directly induced coronary vasoconstriction.
C. NTG lowered arterial (coronary perfusion) pressure
excessively
D. Beta-blocker counteracted the effects of NTG and
increased the risk of ischemia
2. Dopamine, epinephrine (or norepinephrine) and histamine are
important neurotransmitter agonists. When these ligands
interact with their cellular receptors, how do they mainly elicit
their responses?
A. Activate adenylyl cyclase directly, leading to increased
intracellular cAMP levels
B. Activate phospholipase C
C. Induce or inhibit synthesis of ligand specific intracellular
proteins
D. Open or close ligand gated ion channels
E. Regulate intracellular second messengers through G-protein-
coupled receptors
3. A 65-year old man with heart failure is unable to climb a
flight of stairs without experiencing dyspnea. After several
years of therapy with carvedilol, captopril and furosemide, the
therapeutic plan probably needs to change now. You empiri cally
add digoxin to improve cardiac muscle contractility. Within 4
week he has a marked improvement in his symptoms. Which of
the following best describes the main cellular action of digoxin
that accounts for its ability to improve his cardiovascular
function?
A. Activates beta1-adrenergic receptors
B. Facilitates GTP binding to specific proteins
C. Increases mitochondrial calcium (Ca++) release
D. Inhibits sarcolemmal Na/K-ATP-ase
4. A patient has frequent episodes of paroxysmal
supraventricular tachycardia (PSVT). Which of the following
drugs would be most suitable for outpatient prophylaxis of these
events?
A. Adenosine
B. Lidocaine
C. Nifedipine
D. Verapamil
5. A patient with chronic-stable angina begins taking
metoprolol, and once blood levels reach the therapeutic range
the frequency and severity of angina attacks and the need for
sublingual nitroglycerin were reduced. Which of the following
states the direct pharmacologic action by which the beta-blocker
produced the desired effects?
A. Decreased myocardial oxygen demand
B. Dilated coronary vasculature
C. Directly inhibited angiotensin II synthesis
D. Reduced total peripheral resistance
6. A patient with newly diagnosed essential hypertension starts
treatment with a commonly used antihypertensive drug at a dose
that is considered to be therapeutic for the vast majority of
patients. Soon after starting therapy the patient experiences
crushing chest discomfort. ECG changes show myocardial
ischemia. Studies in the cardiac catheterization lab show
episodes of coronary vasospasm, and it is likely the
antihypertensive drug provoke the vasospasm. Which
antihypertensive drug most likely caused the ischemia and the
angina?
A. Atenolol
B. Diltiazem
C. Hydrochlorothiazide
D. Lozartan
7. A 28-year-old woman is receiving drug therapy for essential
hypertension. She subsequently becomes pregnant. You realize
that the drug she’s been taking for her blood pressure can have
serious, if not fatal, effects on the fetus. As a result, you stop
the current antihypertensive drug and substitute it with another
drug that is deemed to be equally effective in terms of her blood
pressure, and safer for the fetus. Which of the following drugs
was she most likely taking before she became pregnant?
A. Alpha-Methyldopa
B. Captopril
C. Furosemide
D. Labetalol
E. Verapamil
8. The use of propranolol as an antiarrhythmic agent is
contraindicated in patients with:
A. COPD
B. Asthma
C. Severe heart failure
D. A and C
E. All of the above
9. A patient has frequent episodes of paroxysmal atrial
fibrillation. He has received a medication for prophylaxis of
these events. Which of the following is the most suitable for
long term use?
A. Nifedipine
B. Adenosine
C. Amiodarone
D. Heparin
E. Lidocaine
10. A 52-year-old woman with essential hypertension,
hypercholesterolemia, and chronic-stable angina, develops
severe constipation. Which of the following drugs is the most
likely cause?
A. Atorvastatin
B. Captopril
C. Labetalol
D. Nitroglycerin
E. Verapamil
Alpha adrenergic antagonists compete with endogenous
catecholamines for binding at alpha- 1 and alpha -2 receptors.
Because norepinephrine and epinephrine cannot bind to a
receptor that is occupied by an antagonist, the actions of
catecholamines are inhibited.
Adrenergic receptor blockers are used to treat hypertension.
What side effects can be expected?
_________________________________________
_________________________________________
Nonspecific beta blockers (block both beta- 1 and beta -2
receptors) have been used as first-step antihypertensive agents.
Because these agents block beta-2 as well as beta -1 receptors,
bronchospasm may occur. Newer agents are beta-2 specific and
are not contraindicated in asthmatic patients.
Give some examples and your explanations for the benefits and
risks associated with these medications.
_______________________________________________
2. Solve this case and answer case-related questions:
Case. A patient (76 years old female) with compromised cardiac
function was hospitalized due to significant volume overload
and generalized edema.
Chest X-ray confirmed pulmonary edema, ejection fraction was
estimated - 20%.
Patients’ heart rate and blood pressure have been monitored.
Despite intravenous use of diuretics she still feels significant
shortness of breath, her blood pressure is now 90/60 mm Hg.
Blood tests confirmed that renal function is worsening. Blood
creatinine – 2.0 mg/L, Na – 132 mEq/L; K – 3.9 mEq/L.
Intravenous therapy with Dobutamine was initiated.
Questions:
What group of cardiovascular drugs does dobutamine belong to?
What is mechanism of action?
What effect this drug has on cardiac and vascular adrenergic
receptors?
After intensive treatment at the hospital for more than a week,
this patient was released home and will be followed by primary
care physician. Along other medication lisinopril was
prescribed.
Questions:
What group of cardiovascular drugs does lisinopril belong to?
What is mechanism of action?
What effect this drug has on patient’s neurohumoral responses?
What potential side effects can be related to long term lisinopril
use?
Two months later this patient was readmitted for an episode for
cardiac arrhythmia. She was diagnosed with atrial fibrillation.
Amiodarone was initiated for her arrhythmia treatment.
Questions:
What group of cardiovascular drugs does Amiodarone belong
to?
What is the mechanism of action?
What effect this drug has on patient’s heart rate?
What potential side effects can be related to long term
Amiodarone use?
4.
1. A 51-year-old man asks his physician for a prescription for
sildenafil to improve his sexual performance. Because of risks
from a serious drug interaction, this drug should not be
prescribed and the patient should be urged not to try to obtain it
from other sources, if he is also taking which of the following
drugs?
A. Angiotensin-converting enzyme inhibitor
B. Beta-adrenergic blocker
C. Nitrovasodilator (eg. Nitroglycerin)
D. Thiazide or loop diuretic
2. A patient with heart failure, hypertension and hyperlipidemia
is taking furosemide, captopril, atenolol, and simvastatin.
During a scheduled physical examination, about a month after
starting all the drugs, the patient reports a severe, hacking and
relentless cough.
Which of the following is the most likely cause of the cough?
A. An expected effect of the captopril
B. An allergic reaction to the statin
C. Dyspnea due to captopril’s bronchoconstrictor action
D. Hyperkalemia caused by an interaction between furosemide
and captopril
E. Excessive doses of furosemide, which lead to hypovolemia
3. Flecainide and propafenone are in Vaughan-Williams
(antiarrhythmic) Class IC. What is the clinically relevant “take
home” message about this class of drugs?
A. Are only given for arrhythmias during acute myocardial
infarction (MI)
B. Are particularly suited for patients with low ejection fraction
or cardiac output
C. Are preferred drugs for relatively non-severe ventricular
arrhythmias
D. Have a significant pro-arrhythmic effect (induction of lethal
arrhythmias)
E. Cause pulmonary fibrosis and a hypo-thyroid syndrome when
given long term.
7

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1. Choose the best answer and short explanation1. A patient wi

  • 1. 1. Choose the best answer and short explanation 1. A patient with chronic-stable angina is on prophylactic beta- blocker therapy, with sublingual nitroglycerin used PRN (as needed) for managing acute angina. One day he experiences particularly severe angina and takes the usually recommended dose of sublingual nitroglycerin (NTG). His discomfort is not reduced at all. Seeking relief, he repeats the usual recommended dose of NTG dose 6 times over a period of about 10 minutes, and now has taken far too much of the nitrovasodilator. An electrocardiogram taken by the paramedics, who were called for the patient’s emergency, shows changes consistent with myocardial ischemia. The patient incurs a massive infarction, goes into cardiac arrest, and cannot be resuscitated. Which of the following is the most likely cause of or contributing factor to the patient’s ultimately fatal response to the excessive dosage of NTG? Assume the patient was taking no other drugs except the NTG and a beta-blocker. A. Cyanide, or toxic metabolite of NTG, accumulated. B. NTG directly induced coronary vasoconstriction. C. NTG lowered arterial (coronary perfusion) pressure excessively D. Beta-blocker counteracted the effects of NTG and increased the risk of ischemia 2. Dopamine, epinephrine (or norepinephrine) and histamine are important neurotransmitter agonists. When these ligands interact with their cellular receptors, how do they mainly elicit
  • 2. their responses? A. Activate adenylyl cyclase directly, leading to increased intracellular cAMP levels B. Activate phospholipase C C. Induce or inhibit synthesis of ligand specific intracellular proteins D. Open or close ligand gated ion channels E. Regulate intracellular second messengers through G-protein- coupled receptors 3. A 65-year old man with heart failure is unable to climb a flight of stairs without experiencing dyspnea. After several years of therapy with carvedilol, captopril and furosemide, the therapeutic plan probably needs to change now. You empiri cally add digoxin to improve cardiac muscle contractility. Within 4 week he has a marked improvement in his symptoms. Which of the following best describes the main cellular action of digoxin that accounts for its ability to improve his cardiovascular function? A. Activates beta1-adrenergic receptors B. Facilitates GTP binding to specific proteins C. Increases mitochondrial calcium (Ca++) release D. Inhibits sarcolemmal Na/K-ATP-ase 4. A patient has frequent episodes of paroxysmal supraventricular tachycardia (PSVT). Which of the following drugs would be most suitable for outpatient prophylaxis of these events?
  • 3. A. Adenosine B. Lidocaine C. Nifedipine D. Verapamil 5. A patient with chronic-stable angina begins taking metoprolol, and once blood levels reach the therapeutic range the frequency and severity of angina attacks and the need for sublingual nitroglycerin were reduced. Which of the following states the direct pharmacologic action by which the beta-blocker produced the desired effects? A. Decreased myocardial oxygen demand B. Dilated coronary vasculature C. Directly inhibited angiotensin II synthesis D. Reduced total peripheral resistance 6. A patient with newly diagnosed essential hypertension starts treatment with a commonly used antihypertensive drug at a dose that is considered to be therapeutic for the vast majority of patients. Soon after starting therapy the patient experiences crushing chest discomfort. ECG changes show myocardial ischemia. Studies in the cardiac catheterization lab show episodes of coronary vasospasm, and it is likely the antihypertensive drug provoke the vasospasm. Which antihypertensive drug most likely caused the ischemia and the angina? A. Atenolol B. Diltiazem
  • 4. C. Hydrochlorothiazide D. Lozartan 7. A 28-year-old woman is receiving drug therapy for essential hypertension. She subsequently becomes pregnant. You realize that the drug she’s been taking for her blood pressure can have serious, if not fatal, effects on the fetus. As a result, you stop the current antihypertensive drug and substitute it with another drug that is deemed to be equally effective in terms of her blood pressure, and safer for the fetus. Which of the following drugs was she most likely taking before she became pregnant? A. Alpha-Methyldopa B. Captopril C. Furosemide D. Labetalol E. Verapamil 8. The use of propranolol as an antiarrhythmic agent is contraindicated in patients with: A. COPD B. Asthma C. Severe heart failure D. A and C E. All of the above 9. A patient has frequent episodes of paroxysmal atrial fibrillation. He has received a medication for prophylaxis of these events. Which of the following is the most suitable for
  • 5. long term use? A. Nifedipine B. Adenosine C. Amiodarone D. Heparin E. Lidocaine 10. A 52-year-old woman with essential hypertension, hypercholesterolemia, and chronic-stable angina, develops severe constipation. Which of the following drugs is the most likely cause? A. Atorvastatin B. Captopril C. Labetalol D. Nitroglycerin E. Verapamil Alpha adrenergic antagonists compete with endogenous catecholamines for binding at alpha- 1 and alpha -2 receptors. Because norepinephrine and epinephrine cannot bind to a receptor that is occupied by an antagonist, the actions of catecholamines are inhibited. Adrenergic receptor blockers are used to treat hypertension. What side effects can be expected? _________________________________________
  • 6. _________________________________________ Nonspecific beta blockers (block both beta- 1 and beta -2 receptors) have been used as first-step antihypertensive agents. Because these agents block beta-2 as well as beta -1 receptors, bronchospasm may occur. Newer agents are beta-2 specific and are not contraindicated in asthmatic patients. Give some examples and your explanations for the benefits and risks associated with these medications. _______________________________________________ 2. Solve this case and answer case-related questions: Case. A patient (76 years old female) with compromised cardiac function was hospitalized due to significant volume overload and generalized edema. Chest X-ray confirmed pulmonary edema, ejection fraction was estimated - 20%. Patients’ heart rate and blood pressure have been monitored. Despite intravenous use of diuretics she still feels significant shortness of breath, her blood pressure is now 90/60 mm Hg. Blood tests confirmed that renal function is worsening. Blood creatinine – 2.0 mg/L, Na – 132 mEq/L; K – 3.9 mEq/L. Intravenous therapy with Dobutamine was initiated. Questions: What group of cardiovascular drugs does dobutamine belong to? What is mechanism of action?
  • 7. What effect this drug has on cardiac and vascular adrenergic receptors? After intensive treatment at the hospital for more than a week, this patient was released home and will be followed by primary care physician. Along other medication lisinopril was prescribed. Questions: What group of cardiovascular drugs does lisinopril belong to? What is mechanism of action? What effect this drug has on patient’s neurohumoral responses? What potential side effects can be related to long term lisinopril use? Two months later this patient was readmitted for an episode for cardiac arrhythmia. She was diagnosed with atrial fibrillation. Amiodarone was initiated for her arrhythmia treatment. Questions: What group of cardiovascular drugs does Amiodarone belong to? What is the mechanism of action? What effect this drug has on patient’s heart rate? What potential side effects can be related to long term Amiodarone use?
  • 8. 4. 1. A 51-year-old man asks his physician for a prescription for sildenafil to improve his sexual performance. Because of risks from a serious drug interaction, this drug should not be prescribed and the patient should be urged not to try to obtain it from other sources, if he is also taking which of the following drugs? A. Angiotensin-converting enzyme inhibitor B. Beta-adrenergic blocker C. Nitrovasodilator (eg. Nitroglycerin) D. Thiazide or loop diuretic 2. A patient with heart failure, hypertension and hyperlipidemia is taking furosemide, captopril, atenolol, and simvastatin. During a scheduled physical examination, about a month after starting all the drugs, the patient reports a severe, hacking and relentless cough. Which of the following is the most likely cause of the cough? A. An expected effect of the captopril B. An allergic reaction to the statin C. Dyspnea due to captopril’s bronchoconstrictor action D. Hyperkalemia caused by an interaction between furosemide and captopril E. Excessive doses of furosemide, which lead to hypovolemia 3. Flecainide and propafenone are in Vaughan-Williams
  • 9. (antiarrhythmic) Class IC. What is the clinically relevant “take home” message about this class of drugs? A. Are only given for arrhythmias during acute myocardial infarction (MI) B. Are particularly suited for patients with low ejection fraction or cardiac output C. Are preferred drugs for relatively non-severe ventricular arrhythmias D. Have a significant pro-arrhythmic effect (induction of lethal arrhythmias) E. Cause pulmonary fibrosis and a hypo-thyroid syndrome when given long term. 7