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Pharma 1 > Skill keeper/Checklist (CVS) > Flashcards

Skill keeper/Checklist (CVS) Flashcards

1
Q
  1. Pheochromocytoma is a tumor that originates primarily from which of the following cells?

A. Hepatic cells

B. Chromaffin cells

C. Beta cells of the pancreas

D. Osteoblasts

A

B. Chromaffin cells

Rationale: Pheochromocytoma is a rare tumor that originates from chromaffin cells, primarily found in the adrenal medulla. These cells are responsible for producing catecholamines.

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2
Q
  1. In patients with pheochromocytoma, which of the following is NOT a compensatory change observed?

A. Reduced renin levels

B. Increased aldosterone levels

C. Reduced blood volume

D. Increased hematocrit

A

B. Increased aldosterone levels

Rationale: One of the compensatory changes observed in pheochromocytoma is reduced aldosterone levels, which leads to increased excretion of salt and water by the kidneys.

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3
Q
  1. Which hormone promotes sodium and water retention in the kidneys?

A. Renin

B. Epinephrine

C. Norepinephrine

D. Aldosterone

A

D. Aldosterone

Rationale: Aldosterone is a hormone that promotes sodium and water retention in the kidneys, helping regulate blood volume and pressure.

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4
Q
  1. If a pheochromocytoma tumor predominantly releases norepinephrine, what compensatory change in heart rate might be observed?

A. Tachycardia

B. No change in heart rate

C. Bradycardia

D. Arrhythmia

A

C. Bradycardia

Rationale: If the tumor primarily releases norepinephrine, the body compensates for the resulting vasoconstriction by slowing down the heart rate, leading to compensatory bradycardia.

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5
Q
  1. In pheochromocytoma, the body’s control mechanisms for blood pressure are:

A. Reset to maintain the elevated pressure

B. Completely non-functional

C. Intact and try to maintain blood pressure constant

D. Overactive, leading to hypotension

A

C. Intact and try to maintain blood pressure constant

Rationale: Unlike essential hypertension, in pheochromocytoma, the body’s control mechanisms are intact and attempt to maintain blood pressure within a normal range.

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6
Q
  1. Which of the following catecholamines can increase heart rate and is often released by pheochromocytomas?

A. Dopamine

B. Serotonin

C. Epinephrine

D. GABA

A

C. Epinephrine

Rationale: Most pheochromocytomas release enough epinephrine to counteract bradycardia induced by norepinephrine. Epinephrine can increase the heart rate.

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7
Q
  1. Which of the following best describes a partial agonist?

A) A molecule that fully activates a receptor upon binding.
B) A molecule that binds to a receptor but does not activate it.
C) A molecule that binds to a receptor and activates it, but not to its full potential.
D) A molecule that prevents other molecules from binding to a receptor.

A

C) A molecule that binds to a receptor and activates it, but not to its full potential.

Rationale: A partial agonist is a molecule that can bind to and activate a receptor, but it does not produce the maximum possible response that a full agonist would.

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8
Q
  1. Albuterol primarily acts on which type of receptor?

A) α1-adrenergic receptors
B) β1-adrenergic receptors
C) β2-adrenergic receptors
D) Muscarinic receptors

A

C) β2-adrenergic receptors.

Rationale: Albuterol is a bronchodilator that primarily acts on β2-adrenergic receptors in the lungs to relax the bronchial muscles.

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9
Q
  1. Pindolol is a:

A) Full agonist at β receptors.
B) Antagonist at β receptors.
C) Partial agonist at β receptors.
D) Non-competitive inhibitor at β receptors.

A

C) Partial agonist at β receptors.

Rationale: Pindolol is a non-selective beta-blocker with partial agonist activity at β receptors.

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10
Q
  1. Which drug is commonly used to treat asthma due to its bronchodilating effects?

A) Pindolol
B) Albuterol
C) Propranolol
D) Atropine

A

B) Albuterol.

Rationale: Albuterol is a bronchodilator that is commonly used to treat conditions like asthma by acting on β2-adrenergic receptors in the lungs.

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11
Q
  1. What happens to the binding of pindolol to β receptors as the concentration of albuterol increases?

A) Increases
B) Decreases
C) Remains the same
D) Becomes non-competitive

A

B) Decreases.

Rationale: As the concentration of albuterol increases, it competes with pindolol for binding to the β receptors, leading to a decrease in the percentage of receptors bound by pindolol.

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12
Q
  1. Which of the following drugs can block the effects of substances like adrenaline on beta receptors but also stimulate these receptors to a certain extent?

A) Albuterol
B) Atropine
C) Pindolol
D) Epinephrine

A

C) Pindolol.

Rationale: Pindolol is a non-selective beta-blocker with partial agonist activity, meaning it can block the effects of substances like adrenaline on beta receptors and also stimulate these receptors due to its partial agonist activity.

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13
Q
  1. Which drug is primarily used to treat benign prostatic hyperplasia?

A) Metoprolol
B) Tamsulosin
C) Propranolol
D) Esmolol

A

B) Tamsulosin

Rationale: Tamsulosin is an α-blocker primarily used to treat benign prostatic hyperplasia by relaxing the smooth muscles in the prostate and bladder neck, facilitating urination.

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14
Q
  1. Which drug has a very short half-life and is rapidly metabolized by esterases in the blood?

A) Propranolol
B) Atenolol
C) Esmolol
D) Nadolol

A

C) Esmolol

Rationale: Esmolol is known for its very short half-life and is often used in acute settings like surgeries due to its rapid metabolism by blood esterases.

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15
Q
  1. Which drug class increases the outflow of aqueous humor in glaucoma patients?

A) Prostaglandin analogs
B) Beta-blockers
C) Alpha agonists
D) Rho kinase inhibitors

A

A) Prostaglandin analogs

Rationale: Prostaglandin analogs, like latanoprost, work by increasing the outflow of aqueous humor, thereby reducing intraocular pressure in glaucoma patients.

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16
Q
  1. Which drug is a selective β1-blocker primarily used for cardiac issues?

A) Labetalol
B) Pindolol
C) Metoprolol
D) Propranolol

A

C) Metoprolol

Rationale: Metoprolol is a selective β1-blocker, making it particularly useful for treating cardiac issues such as heart failure and arrhythmias.

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17
Q
  1. Which drug is used to treat hypertension, angina, and migraine prophylaxis?

A) Timolol
B) Brimonidine
C) Dorzolamide
D) Latanoprost

A

A) Timolol

Rationale: Timolol is a non-selective beta-blocker used to treat hypertension, angina, and is also used for migraine prophylaxis.

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18
Q
  1. Which drug reduces aqueous humor production by inhibiting carbonic anhydrase in the ciliary body?

A) Pilocarpine
B) Dorzolamide
C) Netarsudil
D) Tamsulosin

A

B) Dorzolamide

Rationale: Dorzolamide is a carbonic anhydrase inhibitor that acts on the ciliary body to reduce the production of aqueous humor.

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19
Q
  1. Which drug class is known to cause side effects like bronchospasm, especially in asthmatics?

A) Alpha agonists
B) Beta-blockers
C) Prostaglandin analogs
D) Rho kinase inhibitors

A

B) Beta-blockers

Rationale: Beta-blockers can cause bronchospasm, especially in asthmatic patients, due to their non-selective action on β2 receptors in the lungs.

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20
Q
  1. Which drug is known to have dual action by blocking both α and β receptors?

A) Propranolol
B) Labetalol
C) Metoprolol
D) Esmolol

A

B) Labetalol

Rationale: Labetalol is unique in its ability to block both α and β receptors, making it useful in certain hypertensive emergencies.

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21
Q
  1. Which drug is an α-blocker that primarily acts to relax the smooth muscles in the bladder neck?

A) Atenolol
B) Tamsulosin
C) Esmolol
D) Pilocarpine

A

B) Tamsulosin

Rationale: Tamsulosin is an α-blocker that targets the smooth muscles in the prostate and bladder neck, aiding in urination for those with benign prostatic hyperplasia.

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22
Q
  1. Which drug class contracts the ciliary muscle to increase the outflow of aqueous humor?

A) Prostaglandin analogs
B) Beta-blockers
C) Cholinergic agents
D) Rho kinase inhibitors

A

C) Cholinergic agents

Rationale: Cholinergic agents, like pilocarpine, work by contracting the ciliary muscle, which in turn increases the outflow of aqueous humor.

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23
Q
  1. Which drug is primarily excreted unchanged in the urine and is not significantly metabolized?

A) Propranolol
B) Atenolol
C) Esmolol
D) Nadolol

A

D) Nadolol

Rationale: Nadolol is not significantly metabolized and is primarily excreted unchanged in the urine, giving it a longer half-life compared to some other β-blockers.

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24
Q
  1. Which drug class is primarily used for its vasoconstrictive effect in the treatment of nasal congestion?

A) Alpha agonists
B) Beta-blockers
C) Prostaglandin analogs
D) Rho kinase inhibitors

A

A) Alpha agonists

Rationale: Alpha agonists, such as pseudoephedrine, cause vasoconstriction and are often used in over-the-counter medications to relieve nasal congestion.

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25
Q
  1. Which drug is a non-selective beta-blocker with intrinsic sympathomimetic activity (ISA)?

A) Labetalol
B) Pindolol
C) Metoprolol
D) Propranolol

A

B) Pindolol

Rationale: Pindolol is a non-selective beta-blocker that also has intrinsic sympathomimetic activity (ISA), allowing it to act as a partial agonist at the β receptors.

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26
Q
  1. Which drug class is known to cause side effects like dizziness, headache, and reflex tachycardia?

A) Alpha agonists
B) Alpha-blockers
C) Prostaglandin analogs
D) Rho kinase inhibitors

A

B) Alpha-blockers

Rationale: Alpha-blockers, such as tamsulosin, can cause side effects like dizziness, headache, and reflex tachycardia due to their vasodilatory effects.

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27
Q
  1. Which drug class is used to treat hypertension by reducing the production of aqueous humor?

A) Prostaglandin analogs
B) Beta-blockers
C) Alpha agonists
D) Rho kinase inhibitors

A

B) Beta-blockers

Rationale: Beta-blockers, like timolol, reduce the production of aqueous humor and are used in the treatment of hypertension and other cardiac conditions.

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28
Q
  1. Which class of drugs is primarily used to treat depression by increasing the levels of serotonin in the brain?

A) Beta-blockers
B) Alpha agonists
C) Selective serotonin reuptake inhibitors (SSRIs)
D) Rho kinase inhibitors

A

C) Selective serotonin reuptake inhibitors (SSRIs)

Rationale: SSRIs, such as fluoxetine and sertraline, work by inhibiting the reuptake of serotonin in the brain, leading to increased levels of this neurotransmitter and thereby helping in the treatment of depression.

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29
Q
  1. Which class of drugs is used to treat hypertension by blocking the renin-angiotensin-aldosterone system?

A) Beta-blockers
B) Alpha agonists
C) Angiotensin-converting enzyme (ACE) inhibitors
D) Rho kinase inhibitors

A

C) Angiotensin-converting enzyme (ACE) inhibitors

Rationale: ACE inhibitors, such as lisinopril and enalapril, work by blocking the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor. This leads to vasodilation and a reduction in blood pressure.

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30
Q
  1. Which drug is used to treat allergic reactions by blocking histamine receptors?

A) Metformin
B) Diphenhydramine
C) Esmolol
D) Pilocarpine

A

B) Diphenhydramine

Rationale: Diphenhydramine is an antihistamine that works by blocking H1 histamine receptors. This action helps to reduce the symptoms of allergic reactions such as itching, sneezing, and runny nose.

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31
Q

Question 1: What is the primary mechanism of action of hydralazine?

a) It increases heart rate.

b) It constricts blood vessels.

c) It relaxes the smooth muscles in the walls of arteries.

d) It promotes salt and water retention.

A

c) It relaxes the smooth muscles in the walls of arteries.

Rationale: Hydralazine is a vasodilator, which means its primary action is to relax the smooth muscles in the walls of arteries. This relaxation causes the arteries to widen, reducing resistance to blood flow and, consequently, lowering blood pressure.

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32
Q

Question 2: Which of the following is NOT a compensatory response to hydralazine?

a) Tachycardia

b) Activation of the renin-angiotensin-aldosterone system

c) Salt and water retention

d) Dilation of blood vessels

A

d) Dilation of blood vessels

Rationale: Hydralazine itself causes the dilation of blood vessels, which is its intended effect. The compensatory responses to hydralazine, such as tachycardia and salt and water retention, are mechanisms the body uses to counteract the drop in blood pressure caused by the drug. The dilation of blood vessels is the drug’s primary effect, not a compensatory response.

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33
Q
  1. Which drug is a direct arterial vasodilator?
    a) Metoprolol
    b) Amlodipine
    c) Losartan
    d) Hydralazine
A

d) Hydralazine
Rationale: Hydralazine works by directly relaxing the smooth muscles of the arteries, leading to vasodilation.

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34
Q
  1. Which drug class blocks the conversion of angiotensin I to angiotensin II?
    a) Beta-blockers
    b) ACE inhibitors
    c) ARBs
    d) Calcium channel blockers
A

b) ACE inhibitors
Rationale: ACE inhibitors inhibit the angiotensin-converting enzyme, preventing the conversion of angiotensin I to the more active angiotensin II.

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35
Q
  1. Which drug can cause hypertrichosis as a side effect?
    a) Prazosin
    b) Minoxidil
    c) Clonidine
    d) Reserpine
A

b) Minoxidil
Rationale: Minoxidil, when used topically, is known to promote hair growth, leading to hypertrichosis.

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36
Q
  1. Which drug acts by opening potassium channels?
    a) Hydralazine
    b) Amlodipine
    c) Minoxidil
    d) Prazosin
A

c) Minoxidil
Rationale: Minoxidil acts by opening potassium channels in smooth muscle cells, leading to relaxation and vasodilation.

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37
Q
  1. Which drug class is known to cause a persistent cough as a side effect?
    a) ARBs
    b) Beta-blockers
    c) ACE inhibitors
    d) Calcium channel blockers
A

c) ACE inhibitors
Rationale: ACE inhibitors can lead to increased levels of bradykinin, causing a persistent cough in some patients.

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38
Q
  1. Which drug acts as a central alpha-2 agonist?
    a) Prazosin
    b) Clonidine
    c) Reserpine
    d) Minoxidil
A

b) Clonidine
Rationale: Clonidine acts on the central nervous system as an alpha-2 agonist, reducing sympathetic outflow and lowering blood pressure.

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39
Q
  1. Which drug class directly blocks the action of angiotensin II at its receptor?
    a) Calcium channel blockers
    b) Beta-blockers
    c) ACE inhibitors
    d) ARBs
A

d) ARBs
Rationale: ARBs (Angiotensin II receptor blockers) block the action of angiotensin II at its receptor, preventing its vasoconstrictive effects.

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40
Q
  1. Which drug is used in hypertensive emergencies due to its rapid vasodilatory effect?
    a) Amlodipine
    b) Losartan
    c) Sodium nitroprusside
    d) Metoprolol
A

: c) Sodium nitroprusside
Rationale: Sodium nitroprusside releases nitric oxide, leading to rapid vasodilation and is used in hypertensive emergencies.

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41
Q
  1. Which drug class is known to cause edema as a side effect?
    a) Beta-blockers
    b) ACE inhibitors
    c) ARBs
    d) Calcium channel blockers
A

d) Calcium channel blockers
Rationale: Calcium channel blockers, especially the dihydropyridines, can cause peripheral edema as a side effect.

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42
Q
  1. Which drug acts by inhibiting neuronal norepinephrine release?
    a) Clonidine
    b) Reserpine
    c) Prazosin
    d) Amlodipine
A

b) Reserpine
Rationale: Reserpine inhibits the storage and release of norepinephrine in neuronal vesicles, leading to reduced sympathetic tone.

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43
Q
  1. Which drug class is primarily used to reduce heart rate?
    a) Diuretics
    b) Beta-blockers
    c) ACE inhibitors
    d) ARBs
A

b) Beta-blockers
Rationale: Beta-blockers act on beta-adrenergic receptors, reducing heart rate and myocardial contractility.

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44
Q
  1. Which drug can lead to bronchospasm, especially in asthmatic patients?
    a) Metoprolol
    b) Amlodipine
    c) Losartan
    d) Hydralazine
A

a) Metoprolol
Rationale: Non-selective beta-blockers like metoprolol can cause bronchospasm by blocking beta-2 receptors in the bronchi.

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45
Q
  1. Which drug class acts by relaxing the smooth muscles in the walls of arteries?
    a) Diuretics
    b) Beta-blockers
    c) Vasodilators
    d) ARBs
A

c) Vasodilators
Rationale: Vasodilators, like hydralazine, work by relaxing the smooth muscles in the walls of arteries, leading to vasodilation.

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46
Q
  1. Which drug is known to cause hyperkalemia as a side effect?
    a) Amlodipine
    b) Metoprolol
    c) Losartan
    d) Lisinopril
A

d) Lisinopril
Rationale: ACE inhibitors like lisinopril can lead to hyperkalemia by reducing aldosterone secretion.

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47
Q
  1. Which drug acts by blocking alpha-1 adrenergic receptors, leading to vasodilation?
    a) Clonidine
    b) Reserpine
    c) Prazosin
    d) Minoxidil
A

c) Prazosin
Rationale: Prazosin is an alpha-1 adrenergic receptor blocker, leading to vasodilation and a reduction in blood pressure.

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48
Q
  1. Which drug class can lead to electrolyte imbalances, especially when used in high doses?
    a) Diuretics
    b) Beta-blockers
    c) ACE inhibitors
    d) Calcium channel blockers
A

a) Diuretics
Rationale: Diuretics increase urine output and can lead to electrolyte imbalances, especially potassium and sodium.

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49
Q
  1. Which drug class acts by inhibiting calcium influx into vascular smooth muscle cells?
    a) Diuretics
    b) Beta-blockers
    c) Vasodilators
    d) Calcium channel blockers
A

d) Calcium channel blockers
Rationale: Calcium channel blockers inhibit calcium influx into vascular smooth muscle cells, leading to relaxation and vasodilation.

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50
Q
  1. Which drug class primarily acts by increasing urine output to reduce blood volume and blood pressure?
    a) Diuretics
    b) Beta-blockers
    c) Vasodilators
    d) Calcium channel blockers
A

a) Diuretics
Rationale: Diuretics increase urine output, leading to a reduction in blood volume and subsequently blood pressure.

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51
Q
  1. Which drug is known to act on the central nervous system to reduce sympathetic outflow?
    a) Prazosin
    b) Reserpine
    c) Clonidine
    d) Minoxidil
A

Answer: c) Clonidine
Rationale: Clonidine acts on the central nervous system as an alpha-2 agonist, reducing sympathetic outflow and lowering blood pressure.

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52
Q
  1. Which drug class is known to cause angioedema as a rare but serious side effect?
    a) ARBs
    b) Beta-blockers
    c) ACE inhibitors
    d) Calcium channel blockers
A

c) ACE inhibitors
Rationale: ACE inhibitors can lead to angioedema, a swelling of the deeper layers of the skin, often around the eyes and lips.

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53
Q
  1. Which drug class acts by blocking the effects of the sympathetic nervous system on the heart?
    a) Diuretics
    b) Beta-blockers
    c) Vasodilators
    d) ARBs
A

b) Beta-blockers
Rationale: Beta-blockers act on beta-adrenergic receptors in the heart, reducing heart rate and myocardial contractility.

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54
Q
  1. Which drug is NOT primarily used as an antihypertensive agent but can cause vasodilation by releasing nitric oxide?
    a) Amlodipine
    b) Losartan
    c) Sodium nitroprusside
    d) Metoprolol
A

c) Sodium nitroprusside
Rationale: Sodium nitroprusside releases nitric oxide, leading to rapid vasodilation. It’s used primarily in hypertensive emergencies.

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55
Q
  1. Which drug class acts by blocking the receptors for angiotensin II, preventing its vasoconstrictive effects?
    a) Calcium channel blockers
    b) Beta-blockers
    c) ACE inhibitors
    d) ARBs
A

d) ARBs
Rationale: ARBs (Angiotensin II receptor blockers) block the action of angiotensin II at its receptor, preventing its vasoconstrictive effects.

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56
Q
  1. Which drug class can lead to bronchospasm, especially in patients with respiratory conditions?
    a) Diuretics
    b) Non-selective beta-blockers
    c) ACE inhibitors
    d) Calcium channel blockers
A

b) Non-selective beta-blockers
Rationale: Non-selective beta-blockers can cause bronchospasm by blocking beta-2 receptors in the bronchi, especially in patients with conditions like asthma.

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57
Q
  1. Which drug is known to cause reflex tachycardia as a side effect?
    a) Amlodipine
    b) Lisinopril
    c) Metoprolol
    d) Losartan
A

a) Amlodipine
Rationale: Amlodipine, a calcium channel blocker, especially of the dihydropyridine class, can cause vasodilation. This drop in blood pressure can lead to a compensatory increase in heart rate, known as reflex tachycardia.

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58
Q
  1. Which class of drug does nifedipine belong to?
    a) Beta-blockers
    b) ACE inhibitors
    c) Calcium channel blockers
    d) Diuretics
A

c) Calcium channel blockers
Rationale: Nifedipine is a calcium channel blocker, specifically of the dihydropyridine class, used primarily to treat hypertension and angina.

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59
Q
  1. What is the primary therapeutic use of nifedipine?
    a) Reducing cholesterol
    b) Treating hypertension and angina
    c) Preventing blood clots
    d) Treating arrhythmias
A

b) Treating hypertension and angina
Rationale: Nifedipine is primarily used as an antihypertensive agent and for the treatment of angina.

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60
Q
  1. Which formulation of nifedipine may pose an increased risk of myocardial infarction?
    a) Slow-release
    b) Prompt-release
    c) Topical
    d) Intravenous
A

b) Prompt-release
Rationale: Studies have indicated that the prompt-release form of nifedipine might have a heightened risk of myocardial infarction due to its rapid-acting vasodilatory effects.

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61
Q
  1. What compensatory mechanism is triggered by a sudden drop in blood pressure?
    a) Decreased heart rate
    b) Reduced force of heart contractions
    c) Increased sympathetic outflow to the cardiovascular system
    d) Vasodilation
A

c) Increased sympathetic outflow to the cardiovascular system
Rationale: A sudden drop in blood pressure, such as that caused by prompt-release nifedipine, triggers an increase in sympathetic nervous system activity to the cardiovascular system to restore blood pressure.

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62
Q
  1. Which condition results from a lack of oxygen to tissues?
    a) Hyperkalemia
    b) Ischemia
    c) Edema
    d) Tachycardia
A

b) Ischemia
Rationale: Ischemia refers to the lack of oxygen supply to tissues, often due to reduced blood flow.

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63
Q
  1. What can result from severe and prolonged ischemia in the heart?
    a) Bradycardia
    b) Infarction
    c) Reflex tachycardia
    d) Hyperkalemia
A

b) Infarction
Rationale: Infarction refers to the death of tissue due to lack of oxygen. In the context of the heart, prolonged ischemia can lead to myocardial infarction or heart attack.

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64
Q
  1. Which drug formulation causes a more gradual and controlled release of the medication?
    a) Prompt-release
    b) Slow-release
    c) Topical
    d) Intramuscular
A

b) Slow-release
Rationale: Slow-release formulations are designed to release the drug gradually over time, providing a more controlled and sustained effect.

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65
Q
  1. What is the primary effect of calcium channel blockers on blood vessels?
    a) Vasoconstriction
    b) Vasodilation
    c) Blood clotting
    d) Blood thinning
A

b) Vasodilation
Rationale: Calcium channel blockers, like nifedipine, work by inhibiting calcium influx into vascular smooth muscle cells, leading to relaxation and vasodilation.

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66
Q
  1. Which side effect is NOT associated with nifedipine?
    a) Reflex tachycardia
    b) Myocardial infarction (with prompt-release)
    c) Reduced sympathetic outflow
    d) Ischemia
A

c) Reduced sympathetic outflow
Rationale: Nifedipine, especially in its prompt-release form, can cause an increase in sympathetic outflow as a compensatory mechanism to a drop in blood pressure.

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67
Q
  1. Which drug class primarily reduces heart rate and myocardial contractility?
    a) Diuretics
    b) Beta-blockers
    c) ACE inhibitors
    d) Calcium channel blockers
A

b) Beta-blockers
Rationale: Beta-blockers act on beta-adrenergic receptors in the heart, reducing heart rate and myocardial contractility.

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68
Q
  1. Which type of angina is caused by spasms of the coronary arteries?
    a) Effort Angina
    b) Vasospastic Angina
    c) Unstable Angina
    d) Chronic Angina
A

b) Vasospastic Angina
Rationale: Vasospastic angina, also known as Prinzmetal’s angina, is caused by transient spasms of the coronary arteries.

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69
Q
  1. Which drug class primarily reduces myocardial oxygen demand by decreasing heart rate?
    a) Nitrates
    b) ACE inhibitors
    c) ß Blockers
    d) Diuretics
A

c) ß Blockers
Rationale: ß Blockers act by reducing heart rate and myocardial contractility, thereby decreasing the oxygen demand of the heart.

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70
Q
  1. What is the primary therapeutic effect of nitrates in treating angina?
    a) Reduction of myocardial contractility
    b) Coronary vasodilation
    c) Decreasing heart rate
    d) Inhibition of platelet aggregation
A

b) Coronary vasodilation
Rationale: Nitrates primarily act by causing vasodilation, which includes dilation of the coronary arteries, increasing blood flow to the myocardium.

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71
Q
  1. Which condition is a precursor to myocardial infarction and requires immediate medical attention?
    a) Effort Angina
    b) Vasospastic Angina
    c) Unstable Angina
    d) Stable Angina
A

c) Unstable Angina
Rationale: Unstable angina is a condition where atherosclerotic plaques become disrupted, leading to partial occlusion of the coronary artery. It’s a precursor to myocardial infarction and is considered a medical emergency.

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72
Q
  1. Which drug combination can lead to a severe drop in blood pressure?
    a) Nitrate and ACE inhibitor
    b) Nitrate and ß Blocker
    c) Nitrate and Sildenafil
    d) ß Blocker and Diuretic
A

c) Nitrate and Sildenafil
Rationale: Both nitrates and sildenafil cause vasodilation. When combined, they can lead to a severe drop in blood pressure, which can be dangerous.

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73
Q
  1. Which therapeutic strategy aims to increase the oxygen supply to the myocardium?
    a) Reducing heart rate
    b) Decreasing myocardial contractility
    c) Coronary vasodilation
    d) Inhibiting platelet aggregation
A

c) Coronary vasodilation
Rationale: Coronary vasodilation increases blood flow to the myocardium, thereby increasing the oxygen supply.

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74
Q
  1. Which side effect is commonly associated with the use of nitrates?
    a) Bradycardia
    b) Hyperkalemia
    c) Headache
    d) Dry cough
A

c) Headache
Rationale: Nitrates, due to their vasodilatory effects, are commonly associated with causing headaches.

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75
Q
  1. Which drug class is primarily used to treat hypertension but can also provide relief from angina?
    a) Diuretics
    b) ACE inhibitors
    c) ß Blockers
    d) Anticoagulants
A

c) ß Blockers
Rationale: While ß Blockers are primarily used to treat hypertension, they are also effective in managing angina by reducing heart rate and myocardial contractility.

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76
Q
  1. Which type of angina occurs due to the inability of coronary arteries to supply sufficient oxygen during physical exertion?
    a) Effort Angina
    b) Vasospastic Angina
    c) Unstable Angina
    d) Chronic Angina
A

a) Effort Angina
Rationale: Effort angina, or stable angina, is caused by the inability of coronary arteries to supply the heart with enough oxygen during physical exertion.

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77
Q
  1. Which drug class primarily acts by inhibiting calcium influx into vascular smooth muscle cells?
    a) Nitrates
    b) Diuretics
    c) ß Blockers
    d) Calcium channel blockers
A

d) Calcium channel blockers
Rationale: Calcium channel blockers work by inhibiting calcium influx into vascular smooth muscle cells, leading to relaxation and vasodilation.

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78
Q
  1. Which condition results from the death of heart tissue due to lack of oxygen?
    a) Ischemia
    b) Infarction
    c) Angina
    d) Vasospasm
A

b) Infarction
Rationale: Infarction refers to the death of tissue due to lack of oxygen. In the context of the heart, it refers to a heart attack or myocardial infarction.

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79
Q
  1. Which drug class is NOT primarily used for the relief of anginal pain?
    a) Nitrates
    b) ß Blockers
    c) ACE inhibitors
    d) Calcium channel blockers
A

c) ACE inhibitors
Rationale: While ACE inhibitors are used in the management of cardiovascular diseases, they are not primarily used for the relief of anginal pain.

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80
Q
  1. Which therapeutic effect is common to both nitrates and calcium channel blockers?
    a) Reduction of heart rate
    b) Coronary vasodilation
    c) Decrease in myocardial contractility
    d) Diuresis
A

b) Coronary vasodilation
Rationale: Both nitrates and calcium channel blockers have the therapeutic effect of causing coronary vasodilation, increasing blood flow to the myocardium.

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81
Q
  1. Which drug class can cause edema as a side effect?
    a) Nitrates
    b) ß Blockers
    c) ACE inhibitors
    d) Calcium channel blockers
A

d) Calcium channel blockers
Rationale: Calcium channel blockers, especially the dihydropyridine class, can cause peripheral edema as a side effect.

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82
Q
  1. Which type of angina can occur at rest and is not necessarily related to coronary artery disease?
    a) Effort Angina
    b) Vasospastic Angina
    c) Unstable Angina
    d) Chronic Angina
A

b) Vasospastic Angina
Rationale: Vasospastic angina, or Prinzmetal’s angina, can occur at rest and is caused by spasms of the coronary arteries. It’s not necessarily related to coronary artery disease.

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83
Q
  1. Which drug class primarily reduces preload and afterload in the treatment of angina?
    a) Nitrates
    b) ß Blockers
    c) ACE inhibitors
    d) Diuretics
A

a) Nitrates
Rationale: Nitrates act by causing vasodilation, which reduces both preload (the volume of blood in the

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84
Q
  1. Which of the following best describes the primary cause of effort angina?
    a) Spasms of the coronary arteries
    b) Disruption of atherosclerotic plaques
    c) Inability of coronary arteries to supply sufficient oxygen during physical exertion
    d) Chronic inflammation of the coronary artery walls
A

c) Inability of coronary arteries to supply sufficient oxygen during physical exertion
Rationale: Effort angina, or stable angina, arises when the coronary arteries cannot supply the heart with adequate oxygen during physical activities, typically due to atherosclerotic plaques that restrict blood flow.

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85
Q
  1. Which combination therapy is beneficial in treating angina by reducing both preload and afterload?
    a) Nitrate and ß Blocker
    b) Nitrate and ACE inhibitor
    c) ß Blocker and Diuretic
    d) Calcium channel blocker and Diuretic
A

a) Nitrate and ß Blocker
Rationale: Nitrates primarily reduce preload through vasodilation, while ß Blockers reduce afterload by decreasing heart rate and myocardial contractility. The combination offers a comprehensive approach to managing angina.

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86
Q
  1. Which drug is contraindicated in patients with angina who are also taking nitrates?
    a) Sildenafil
    b) Lisinopril
    c) Atenolol
    d) Furosemide
A

a) Sildenafil
Rationale: Both nitrates and sildenafil cause vasodilation. When combined, they can lead to a severe drop in blood pressure, which can be dangerous.

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87
Q
  1. Which procedure aims to restore blood flow to areas of the heart with reduced blood supply due to angina?
    a) Angioplasty
    b) Pacemaker implantation
    c) Valve replacement
    d) Cardiac ablation
A

a) Angioplasty
Rationale: Angioplasty, often combined with stent placement, is a procedure used to open narrowed or blocked coronary arteries, restoring blood flow to the heart muscle.

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88
Q
  1. Which type of angina is characterized by unpredictable attacks and is considered a medical emergency due to its potential to lead to a heart attack?
    a) Effort Angina
    b) Vasospastic Angina
    c) Unstable Angina
    d) Silent Angina
A

c) Unstable Angina
Rationale: Unstable angina is unpredictable and can occur at rest or with minimal exertion. It’s considered a medical emergency because of its potential to progress to a myocardial infarction.

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89
Q
  1. Which drug class is primarily used to relax the arterial walls, leading to a decrease in systemic vascular resistance and relief from angina?
    a) Alpha-blockers
    b) Diuretics
    c) Calcium channel blockers
    d) ACE inhibitors
A

c) Calcium channel blockers
Rationale: Calcium channel blockers act by inhibiting calcium influx into vascular smooth muscle cells, leading to relaxation and vasodilation of the arterial walls.

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90
Q
  1. Which of the following is NOT a primary determinant of cardiac oxygen consumption?
    a) Heart rate
    b) Myocardial contractility
    c) Myocardial wall tension
    d) Blood glucose levels
A

d) Blood glucose levels
Rationale: While blood glucose levels can impact overall cardiovascular health, the primary determinants of cardiac oxygen consumption include heart rate, myocardial contractility, and myocardial wall tension.

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91
Q
  1. Which therapeutic strategy aims to decrease the oxygen demand of the myocardium?
    a) Increasing heart rate
    b) Coronary vasodilation
    c) Reducing myocardial contractility
    d) Promoting platelet aggregation
A

c) Reducing myocardial contractility
Rationale: Reducing myocardial contractility decreases the work of the heart, thereby reducing the oxygen demand of the myocardium.

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92
Q
  1. Which of the following best describes the mechanism of action of ß Blockers in the treatment of angina?
    a) They dilate the coronary arteries.
    b) They inhibit the renin-angiotensin-aldosterone system.
    c) They block the effects of stress hormones on the heart.
    d) They promote diuresis to reduce blood volume.
A

c) They block the effects of stress hormones on the heart.
Rationale: ß Blockers work by blocking the effects of stress hormones (like adrenaline) on the heart, leading to a reduction in heart rate and myocardial contractility.

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93
Q
  1. Which of the following conditions is characterized by the heart’s left ventricle not contracting effectively?
    a. HFpEF
    b. Myocardial infarction
    c. HFrEF
    d. Angina pectoris
A

c. HFrEF
Rationale: HFrEF, or Heart Failure with reduced Ejection Fraction, is characterized by the left ventricle’s inability to contract effectively, leading to a reduced ejection fraction.

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94
Q
  1. Loop diuretics are primarily used in the management of acute heart failure to:
    a. Increase cardiac output
    b. Reduce preload and afterload
    c. Relieve pulmonary congestion
    d. Counteract the sympathetic nervous system
A

c. Relieve pulmonary congestion
Rationale: Loop diuretics, such as furosemide, help eliminate excess fluid from the body, thus relieving symptoms like pulmonary congestion in acute heart failure.

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95
Q
  1. Which drug class is known to reduce afterload and prevent cardiac remodeling in chronic heart failure?
    a. Beta-blockers
    b. ACE inhibitors
    c. Diuretics
    d. Vasodilators
A

b. ACE inhibitors
Rationale: ACE inhibitors, like enalapril, reduce afterload and have been shown to prevent adverse cardiac remodeling in chronic heart failure.

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96
Q
  1. Digitalis drugs exert their positive inotropic effect by:
    a. Blocking beta-adrenergic receptors
    b. Inhibiting the sodium-potassium ATPase pump
    c. Activating phosphodiesterase enzymes
    d. Stimulating the sympathetic nervous system
A

b. Inhibiting the sodium-potassium ATPase pump
Rationale: Digitalis drugs, like digoxin, inhibit the sodium-potassium ATPase pump, leading to increased intracellular calcium and enhanced cardiac contractility.

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97
Q
  1. Which drug class directly counteracts the chronic activation of the sympathetic nervous system in heart failure?
    a. Diuretics
    b. ACE inhibitors
    c. Vasodilators
    d. Beta-blockers
A

d. Beta-blockers
Rationale: Beta-blockers counteract the chronic activation of the sympathetic nervous system, which can be detrimental in heart failure.

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98
Q
  1. Which of the following is a phosphodiesterase inhibitor used in heart failure to increase cardiac output?
    a. Digoxin
    b. Metoprolol
    c. Milrinone
    d. Enalapril
A

c. Milrinone
Rationale: Milrinone is a phosphodiesterase inhibitor that has a positive inotropic effect and is used in heart failure to improve cardiac output.

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99
Q
  1. A patient with heart failure who has symptoms even at rest would be classified as which NYHA class?
    a. Class I
    b. Class II
    c. Class III
    d. Class IV
A

d. Class IV
Rationale: NYHA Class IV heart failure is characterized by symptoms at rest.

100
Q
  1. Which drug is an aldosterone antagonist used in heart failure to reduce fluid overload and prevent cardiac remodeling?
    a. Furosemide
    b. Losartan
    c. Spironolactone
    d. Dobutamine
A

c. Spironolactone
Rationale: Spironolactone is an aldosterone antagonist that can help reduce fluid overload and has been shown to prevent cardiac remodeling in heart failure.

101
Q
  1. Which of the following conditions is characterized by impaired relaxation of the heart’s left ventricle?
    a. HFrEF
    b. HFpEF
    c. Myocardial infarction
    d. Angina pectoris
A

b. HFpEF
Rationale: HFpEF, or Heart Failure with preserved Ejection Fraction, is characterized by impaired relaxation of the left ventricle, leading to symptoms of heart failure despite a normal ejection fraction.

102
Q
  1. Digitalis toxicity can manifest as:
    a. Increased appetite and weight gain
    b. Bradycardia and visual disturbances
    c. Hypertension and tachycardia
    d. Shortness of breath and cough
A

b. Bradycardia and visual disturbances
Rationale: Digitalis toxicity can lead to various symptoms, including bradycardia (slow heart rate) and visual disturbances.

103
Q
  1. Which drug class can cause hyperkalemia when used in heart failure, especially when combined with other medications?
    a. Beta-blockers
    b. Diuretics
    c. ACE inhibitors
    d. Vasodilators
A

c. ACE inhibitors
Rationale: ACE inhibitors can lead to elevated potassium levels (hyperkalemia), especially when combined with other drugs like potassium-sparing diuretics.

104
Q
  1. Which of the following drugs is a beta-adrenergic agonist used in heart failure to increase cardiac output?
    a. Digoxin
    b. Dobutamine
    c. Spironolactone
    d. Enalapril
A

b. Dobutamine
Rationale: Dobutamine is a beta-adrenergic agonist that has a positive inotropic effect and is used in heart failure to improve cardiac output.

105
Q
  1. Which of the following drugs reduces the resistance the heart has to pump against, thereby improving cardiac output in heart failure?
    a. Diuretics
    b. Vasodilators
    c. Beta-blockers
    d. Digitalis
A

b. Vasodilators
Rationale: Vasodilators reduce afterload by dilating blood vessels, which reduces the resistance against which the heart must pump, thus improving cardiac output.

106
Q
  1. Which of the following is NOT a primary action of loop diuretics in heart failure?
    a. Increase cardiac output
    b. Reduce pulmonary congestion
    c. Decrease blood volume
    d. Reduce edema
A

a. Increase cardiac output
Rationale: Loop diuretics primarily work to decrease fluid overload, thus reducing symptoms like pulmonary congestion and edema in heart failure. They don’t directly increase cardiac output.

107
Q
  1. Which of the following drugs is used to counteract the adverse cardiac remodeling effects of chronic activation of the sympathetic nervous system in heart failure?
    a. Furosemide
    b. Digoxin
    c. Metoprolol
    d. Milrinone
A

c. Metoprolol
Rationale: Metoprolol is a beta-blocker that helps counteract the detrimental effects of the chronic activation of the sympathetic nervous system in heart failure, including adverse cardiac remodeling.

108
Q
  1. Which drug class is primarily used to increase the force of myocardial contraction in heart failure?
    a. Vasodilators
    b. Diuretics
    c. ACE inhibitors
    d. Positive inotropes
A

d. Positive inotropes
Rationale: Positive inotropic agents, such as digitalis and certain beta-adrenergic agonists, are used to increase the force of myocardial contraction in heart failure.

109
Q
  1. In chronic heart failure, which drug class is prescribed to reduce the risk of mortality and hospitalization?
    a. Beta-blockers
    b. Loop diuretics
    c. Digitalis glycosides
    d. Vasodilators
A

a. Beta-blockers
Rationale: Among the options, beta-blockers have been shown to significantly reduce the risk of mortality and hospitalization in patients with chronic heart failure.

110
Q
  1. Which of the following is a common side effect of ACE inhibitors?
    a. Cough
    b. Tachycardia
    c. Hypokalemia
    d. Hyperglycemia
A

a. Cough
Rationale: ACE inhibitors can cause a persistent dry cough in some patients due to the accumulation of bradykinin.

111
Q
  1. Which medication works by blocking the effects of aldosterone in heart failure?
    a. Enalapril
    b. Furosemide
    c. Spironolactone
    d. Digoxin
A

c. Spironolactone
Rationale: Spironolactone is an aldosterone antagonist that blocks the effects of aldosterone, reducing fluid overload and preventing cardiac remodeling in heart failure.

112
Q
  1. Dobutamine primarily exerts its effects by acting on which type of receptors?
    a. Alpha-1 adrenergic receptors
    b. Beta-1 adrenergic receptors
    c. Muscarinic receptors
    d. Dopaminergic receptors
A

b. Beta-1 adrenergic receptors
Rationale: Dobutamine is a beta-adrenergic agonist that primarily stimulates beta-1 adrenergic receptors, leading to increased cardiac contractility.

113
Q
  1. Which drug helps reduce symptoms in heart failure but does not significantly decrease mortality?
    a. Enalapril
    b. Metoprolol
    c. Digoxin
    d. Spironolactone
A

c. Digoxin
Rationale: While digoxin can reduce symptoms and hospitalization in heart failure, it hasn’t been shown to significantly decrease mortality.

114
Q
  1. Which drug class is used in heart failure to counteract fluid retention and edema?
    a. Beta-blockers
    b. Diuretics
    c. Positive inotropes
    d. Vasodilators
A

b. Diuretics
Rationale: Diuretics promote the elimination of excess fluid from the body, thus counteracting fluid retention and edema in heart failure.

115
Q
  1. Which drug is NOT a loop diuretic?
    a. Bumetanide
    b. Torsemide
    c. Furosemide
    d. Spironolactone
A

d. Spironolactone
Rationale: Spironolactone is an aldosterone antagonist, not a loop diuretic.

116
Q
  1. Which drug class dilates blood vessels, reducing the resistance against which the heart must pump in heart failure?
    a. Positive inotropes
    b. Beta-blockers
    c. Vasodilators
    d. Diuretics
A

c. Vasodilators
Rationale: Vasodilators cause dilation of blood vessels, reducing afterload and improving cardiac output in heart failure.

117
Q
  1. Which of the following drugs can cause hyperkalemia in heart failure patients?
    a. Furosemide
    b. Digoxin
    c. Enalapril
    d. Dobutamine
A

c. Enalapril
Rationale: ACE inhibitors, like enalapril, can lead to elevated potassium levels (hyperkalemia) in some patients.

118
Q
  1. Which of the following medications is NOT directly associated with improving cardiac contractility in heart failure?
    a. Digoxin
    b. Milrinone
    c. Dobutamine
    d. Losartan
A

d. Losartan
Rationale: Losartan is an angiotensin receptor blocker (ARB) and does not directly improve cardiac contractility. Instead, it’s used to reduce afterload and prevent cardiac remodeling.

119
Q
  1. Diuretics primarily help in heart failure by:
    a. Improving cardiac contractility
    b. Reducing afterload
    c. Enhancing vasodilation
    d. Decreasing fluid overload
A

d. Decreasing fluid overload
Rationale: Diuretics promote the removal of excess fluid from the body, primarily helping in heart failure by decreasing fluid overload.

120
Q
  1. Which of the following is a common side effect of beta-blockers?
    a. Tachycardia
    b. Dry cough
    c. Bradycardia
    d. Hyperkalemia
A

c. Bradycardia
Rationale: Beta-blockers can slow the heart rate, leading to bradycardia as a common side effect.

121
Q
  1. Which drug class has been shown to reduce both morbidity and mortality in heart failure?
    a. Loop diuretics
    b. Digitalis glycosides
    c. ACE inhibitors
    d. Vasodilators
A

c. ACE inhibitors
Rationale: ACE inhibitors have been shown to reduce both morbidity (symptoms, hospitalizations) and mortality in patients with heart failure.

122
Q
  1. In heart failure, which drug can lead to visual disturbances as a side effect?
    a. Metoprolol
    b. Furosemide
    c. Digoxin
    d. Enalapril
A

c. Digoxin
Rationale: Visual disturbances, especially yellowish vision or seeing halos around lights, can be a sign of digoxin toxicity.

123
Q

Questions 1 and 2.
A 76-year-old retired postal worker with rheumatoid arthritis and chronic heart disease presents with a cardiac arrhythmia and is being considered for treatment with procainamide. She is already receiving an ACE inhibitor, digoxin, and hydrochlorothiazide for her cardiac condition.

  1. In deciding on a treatment regimen with procainamide for this patient, which of the following statements is most correct?

(A) A probable drug interaction with digoxin suggests that digoxin blood levels should be obtained before and after starting procainamide
(B) Hyperkalemia should be avoided to reduce the likelihood of procainamide toxicity
(C) Procainamide cannot be used if the patient has asthma because it has a ß-blocking effect
(D) Procainamide cannot be used if the patient has angina because it has aß-agonist effect
(E) Procainamide is not active by the oral route

A

(B) Hyperkalemia should be avoided to reduce the likelihood of procainamide toxicity

Hyperkalemia facilitates procainamide toxicity. Procainamide is active by the oral route and has a duration of action of 2-4 h (in the prompt-release form). Procainamide has no signifi-cant documented interaction with digoxin and no significant
ß-agonist or B-blocking action. The answer is B.

124
Q

Questions 1 and 2.
A 76-year-old retired postal worker with rheumatoid arthritis and chronic heart disease presents with a cardiac arrhythmia and is being considered for treatment with procainamide. She is already receiving an ACE inhibitor, digoxin, and hydrochlorothiazide for her cardiac condition

  1. If this patient should take an overdose and manifest severe acute procainamide toxicity with markedly prolonged QRS, which of the following should be given immediately?
    (A) A calcium chelator such as EDTA
    (B) Adenosine
    (C) Nitroprusside
    (D) Potassium chloride
    (E) Sodium lactate
A

(E) Sodium lactate

The most effective therapy for procainamide (and quinidine) toxicity appears to be concentrated sodium lactate. This drug may (1) increase sodium current by increasing the sodium ion gradient and (2) reduce drug-receptor binding by alkalinizing
the tissue. The answer is E.

125
Q
  1. A 54-year-old airline pilot is admitted to the emergency department with chest pain and a rapid heart rhythm. The ECG shows an inferior myocardial infarction and ventricular tachycardia. Amiodarone is ordered. Amiodarone
    (A) Decreases PR interval in normal sinus rhythm
    (B) Increases action potential duration
    (C) Increases contractility
    (D) Often causes liver function abnormalities
    (E) Reduces resting potential
A

Amiodarone typically decreases contractility only slightly; it prolongs the PR and QRS interval, as well as the QT inter-val and action potential duration; and it has no effect on the resting potential. Its major toxicity is pulmonary fibrosis, not
liver toxicity. The answer is B.

126
Q
  1. A 36-year-old woman with a history of poorly controlled thy-rotoxicosis has recurrent episodes of tachycardia with severe shortness of breath. During elective surgery to remove her thyroid, she develops a heart rate of 200 bpm with a slightly decreased blood pressure. Which of the following drugs would be most suitable?
    (A) Amiodarone
    (B) Disopyramide
    (C) Esmolol
    (D) Quinidine
    (E) Verapamil
A

This patient is suffering from a typical perisurgical arrhyth-mia, exacerbated by her thyroid disorder. Beta blockers are the most effective agents in acute thyrotoxic arrhythmias. While ß blockers are used to decrease blood pressure in hyperten-sion, this patient’s lowered blood pressure is probably due to the arrhythmia and will normalize when the tachycardia is converted to normal sinus rhythm. Esmolol is a parenteral, rapid-acting ß blocker (see Chapter 10). The answer is C.

127
Q

A 16-year-old girl has paroxysmal attacks of rapid heart rate with palpitations and shortness of breath. These episodes occasionally terminate spontaneously but often require a visit to the emergency department of the local hospital. Her ECG during these episodes reveals an AV nodal tachycardia. Which of the following drugs would be most suitable for prophylaxis of future episodes of acute AV nodal tachycardia?
(A) Adenosine
(B) Amiodarone
(C) Flecainide
(D) Propranolol
(E) Verapamil

A

(E) Verapamil

Calcium channel blockers are effective in both treating and preventing supraventricular AV nodal tachycardias. They are orally active and have a duration of action of several hours.
Adenosine is very effective in most acute nodal tachycardias and is less toxic because of its extremely short duration of action. However, it is not useful for chronic prophylaxis because it must be given IV and has a very short duration of action. The answer is E.

128
Q

A 55-year-old man is admitted to the emergency department and is found to have an abnormal ECG. Overdose of an anti-arrhythmic drug is suspected. Which of the following drugs is correctly paired with its ECG effects?
(A) Quinidine: Increased PR and decreased QT intervals
(B) Flecainide: Increased QRS interval
(C) Verapamil: Decreased PR interval
(D) Lidocaine: Decreased QRS and PR interval
(E) Metoprolol: Increased QRS duration

A

(B) Flecainide: Increased QRS interval

All the associations listed are incorrect except flecainide (see
Table 14-1). Group 1C drugs block sodium channels but have little effect on K* and Ca* channels. The answer is B.

(A) Quinidine: Increased PR and increased QT intervals
(B) Flecainide: Increased QRS duration
(C) Verapamil: Increased PR interval
(D) Lidocaine: Minimal change in PR and QRS intervals
(E) Metoprolol: Increased PR interval

Increased QT interval (due to its effect on potassium channels, which can predispose to torsades de pointes)

Increased PR interval (due to its effect on sodium channels, leading to slowed conduction through the AV node)

129
Q

A 60-year-old woman comes to the emergency department with atypical chest pain. Her ECG reveals ventricular tachycardia with rare normal sinus beats, and ST-segment eleva-tion. Troponin C levels are markedly increased, suggesting myocardial damage. A diagnosis of myocardial infarction is made, and the woman is admitted to the cardiac intensive care unit. Her arrhythmia will probably be treated initially with
(A) Adenosine
(B) Digoxin
(C) Lidocaine
(D) Quinidine
(E) Verapamil

A

(C) Lidocaine

Lidocaine has limited applications as an antiarrhythmic drug, but emergency treatment of myocardial infarction arrhythmias is one of the most important. Procainamide or amioda-rone are used as alternative drugs in this situation. Lidocaine is also useful in digoxin-induced arrhythmias. After recovery from the acute phase of a myocardial infarction, ß blockers are used for 2 years or more to prevent sudden death arrhyth-mias. The answer is C.

130
Q
  1. Which of the following drugs slows conduction through the
    AV node and has a duration of action of 10-20 s?
    (A) Adenosine
    (B) Amiodarone
    (C) Diltiazem
    (D) Esmolol
    (E) Flecainide
    (F) Lidocaine
    (G) Mexiletine
    (H) Procainamide
    (I) Quinidine
A

(A) Adenosine

Adenosine is a very short-acting parenteral agent often used for AV nodal arrhythmias. Diltiazem also slows AV conduction and aborts AV nodal arrhythmias but has a duration of hours, not seconds. (Beta blockers also slow AV conduction but have much smaller effects on calcium channels and durations of action of hours.) The answer is A.

131
Q
  1. When working in outlying areas, this 62-year-old rancher is away from his house for 12-14 h at a time. He has an arrhythmia that requires chronic therapy. Which of the following has the longest half-life of all antiarrhythmic drugs?
    (A) Adenosine
    (B) Amiodarone
    (C) Disopyramide
    (D) Esmolol
    (E) Flecainide
    (F) Lidocaine
    (G) Mexiletine
    (H) Procainamide
    (I) Quinidine
    (J) Verapamil
A

(B) Amiodarone

Amiodarone has the longest half-life of all the antiarrhyth-mics (weeks). The answer is B.

132
Q
A

(B) Flecainide

  1. The drug effect shown in the diagram includes slowing of the upstroke of the AP but no significant change in repolarization or AP duration. This is most typical of group 1C drugs. The answer is B, flecainide.
133
Q
  1. Which of the following β-blockers is nonselective?
    a) Atenolol
    b) Metoprolol
    c) Propranolol
    d) Acebutolol
A

c) Propranolol
Rationale: Propranolol is a nonselective β-blocker, meaning it blocks both β1 and β2 receptors.

134
Q
  1. Which β-blocker is known for its very short action and is used only intravenously?
    a) Nadolol
    b) Esmolol
    c) Timolol
    d) Atenolol
A

b) Esmolol
Rationale: Esmolol is an ester and has the shortest acting duration of about 10 minutes. It is used only intravenously.

135
Q
  1. Which of the following β-blockers lacks a local anesthetic effect and is important for use in glaucoma?
    a) Acebutolol
    b) Metoprolol
    c) Timolol
    d) Esmolol
A

c) Timolol
Rationale: Timolol lacks a local anesthetic effect, making it suitable for use in glaucoma.

136
Q
  1. Which β-blocker is known for its low lipid solubility, potentially reducing CNS toxicity?
    a) Propranolol
    b) Atenolol
    c) Carvedilol
    d) Pindolol
A

b) Atenolol
Rationale: Atenolol has low lipid solubility, which may reduce its CNS toxicity.

137
Q
  1. Which of the following β-blockers offers combined β and α blockade?
    a) Esmolol
    b) Labetalol
    c) Timolol
    d) Acebutolol
A

b) Labetalol
Rationale: Labetalol offers combined β and α blockade.

138
Q
  1. Which β-blocker is a partial agonist and may be less hazardous in asthmatic patients?
    a) Nadolol
    b) Esmolol
    c) Propranolol
    d) Pindolol
A

d) Pindolol
Rationale: Pindolol is a partial agonist, which might make it less hazardous for asthmatic patients.

139
Q
  1. Which of the following is a Beta1 selective blocker?
    a) Propranolol
    b) Atenolol
    c) Timolol
    d) Carvedilol
A

b) Atenolol
Rationale: Atenolol is a Beta1 selective blocker, making it potentially less hazardous for asthmatic patients.

140
Q
  1. Which β-blocker has the longest acting duration of 14-24 hours?
    a) Esmolol
    b) Acebutolol
    c) Nadolol
    d) Atenolol
A

c) Nadolol
Rationale: Nadolol has the longest acting duration of 14-24 hours.

141
Q
  1. Which of the following β-blockers is not typically used for glaucoma?
    a) Timolol
    b) Atenolol
    c) Propranolol
    d) Metoprolol
A

b) Atenolol
Rationale: While Timolol is used for glaucoma, Atenolol is not typically used for this purpose.

142
Q
  1. Which β-blocker is known for its combined β and α blockade properties?
    a) Atenolol
    b) Esmolol
    c) Carvedilol
    d) Pindolol
A

c) Carvedilol
Rationale: Carvedilol offers combined β and α blockade.

143
Q
  1. Which of the following is not a characteristic of Esmolol?
    a) Longest acting
    b) Shortest acting
    c) Used only intravenously
    d) Partial agonist
A

a) Longest acting
Rationale: Esmolol is known for its very short action and is used only intravenously.

144
Q
  1. Which β-blocker is a partial agonist and may be less hazardous in asthmatic patients?
    a) Acebutolol
    b) Nadolol
    c) Carvedilol
    d) Metoprolol
A

a) Acebutolol
Rationale: Acebutolol is a partial agonist, which might make it less hazardous for asthmatic patients.

145
Q
  1. Which of the following β-blockers is not Beta1 selective?
    a) Atenolol
    b) Metoprolol
    c) Timolol
    d) Acebutolol
A

c) Timolol
Rationale: Timolol is a nonselective β-blocker.

146
Q
  1. Which β-blocker is not known for its low lipid solubility?
    a) Atenolol
    b) Propranolol
    c) Pindolol
    d) Esmolol
A

b) Propranolol
Rationale: Atenolol is known for its low lipid solubility, which may reduce CNS toxicity.

147
Q
  1. Which of the following β-blockers does not offer combined β and α blockade?
    a) Labetalol
    b) Carvedilol
    c) Atenolol
    d) Timolol
A

c) Atenolol
Rationale: Atenolol is a Beta1 selective blocker and does not offer combined β and α blockade.

148
Q
  1. Which β-blocker is not a partial agonist?
    a) Pindolol
    b) Acebutolol
    c) Nadolol
    d) Esmolol
A

c) Nadolol
Rationale: Nadolol is not a partial agonist.

149
Q
  1. Which of the following is not a characteristic of Nadolol?
    a) Shortest acting
    b) Longest acting
    c) Nonselective
    d) Used only intravenously
A

a) Shortest acting
Rationale: Nadolol has the longest acting duration of 14-24 hours.

150
Q
  1. Which β-blocker is not known for its combined β and α blockade properties?
    a) Carvedilol
    b) Labetalol
    c) Atenolol
    d) Pindolol
A

c) Atenolol

151
Q
  1. Which condition enhances the effects of digoxin, increasing its potential toxicity?
    a. Hyperkalemia
    b. Hypokalemia
    c. Hyponatremia
    d. Hypernatremia
A

b. Hypokalemia
Rationale: Hypokalemia facilitates the binding of digoxin to its site of action on the sodium-potassium ATPase pump, enhancing its effects and potential toxicity.

152
Q
  1. Which type of diuretic can increase the risk of a fatal digitalis arrhythmia due to induced hypokalemia?
    a. Potassium-sparing diuretics
    b. Carbonic anhydrase inhibitors
    c. Osmotic diuretics
    d. Loop diuretics
A

d. Loop diuretics
Rationale: Loop diuretics promote potassium loss, which can increase the risk of a fatal digitalis arrhythmia when used alongside digoxin.

153
Q
  1. Which diuretic can help prevent digoxin-diuretic interactions by counteracting potassium loss?
    a. Furosemide
    b. Hydrochlorothiazide
    c. Spironolactone
    d. Acetazolamide
A

c. Spironolactone
Rationale: Spironolactone is a potassium-sparing diuretic that helps retain potassium in the body, preventing digoxin-diuretic interactions.

154
Q
  1. Elevated levels of which electrolyte can lead to arrhythmias?
    a. Sodium
    b. Chloride
    c. Calcium
    d. Potassium
A

d. Potassium
Rationale: Elevated potassium levels, or hyperkalemia, can be arrhythmogenic and lead to cardiac arrhythmias.

155
Q
  1. Which of the following diuretics is least likely to be involved in digitalis toxicity?
    a. Thiazide diuretics
    b. Loop diuretics
    c. Carbonic anhydrase inhibitors
    d. Potassium-sparing diuretics
A

c. Carbonic anhydrase inhibitors
Rationale: Carbonic anhydrase inhibitors are rarely used for their systemic and diuretic effects in heart failure, making them less likely to be involved in digitalis toxicity compared to loop and thiazide diuretics.

156
Q
  1. Which drug acts by inhibiting the sodium-potassium ATPase pump in cardiac cells?
    a. Spironolactone
    b. Furosemide
    c. Digoxin
    d. Acetazolamide
A

c. Digoxin
Rationale: Digoxin exerts its effects by inhibiting the sodium-potassium ATPase pump in cardiac cells, increasing contractility.

157
Q
  1. Which diuretic can potentially lead to hyperkalemia when used in high doses or in patients with renal dysfunction?
    a. Hydrochlorothiazide
    b. Spironolactone
    c. Furosemide
    d. Mannitol
A

b. Spironolactone
Rationale: Spironolactone, a potassium-sparing diuretic, can lead to hyperkalemia, especially in high doses or in patients with compromised renal function.

158
Q
  1. Which condition is NOT a potential side effect of digoxin?
    a. Bradycardia
    b. Visual disturbances
    c. Hyperkalemia
    d. Nausea
A

c. Hyperkalemia
Rationale: While digoxin can lead to several side effects, hyperkalemia is not directly caused by digoxin. Instead, hypokalemia is a concern with digoxin use, especially when combined with potassium-wasting diuretics.

159
Q
  1. The binding of which drug to its site of action is facilitated by hypokalemia?
    a. Enalapril
    b. Losartan
    c. Digoxin
    d. Furosemide
A

c. Digoxin
Rationale: Hypokalemia facilitates the binding of digoxin to its site of action on the sodium-potassium ATPase pump, enhancing its therapeutic and toxic effects.

160
Q
  1. Which diuretic group is characterized by promoting potassium retention in the body?
    a. Thiazide diuretics
    b. Loop diuretics
    c. Osmotic diuretics
    d. Potassium-sparing diuretics
A

d. Potassium-sparing diuretics
Rationale: Potassium-sparing diuretics, as the name suggests, promote the retention of potassium in the body, countering the potassium-wasting effects of other diuretics.

161
Q
  1. Which diuretic primarily acts on the proximal convoluted tubule?
    a. Furosemide
    b. Spironolactone
    c. Acetazolamide
    d. Hydrochlorothiazide
A

c. Acetazolamide
Rationale: Acetazolamide is a carbonic anhydrase inhibitor that acts primarily on the proximal convoluted tubule.

162
Q
  1. Which drug is a sodium-glucose cotransporter 2 inhibitor?
    a. Canagliflozin
    b. Amiloride
    c. Mannitol
    d. Furosemide
A

a. Canagliflozin
Rationale: Canagliflozin is an SGLT2 inhibitor, leading to increased glucose and sodium excretion in the urine.

163
Q
  1. Which diuretic is primarily used to treat glaucoma?
    a. Mannitol
    b. Acetazolamide
    c. Furosemide
    d. Spironolactone
A

b. Acetazolamide
Rationale: Acetazolamide reduces the production of aqueous humor, making it useful for the treatment of glaucoma.

164
Q
  1. Which of the following drugs is known to cause ototoxicity?
    a. Hydrochlorothiazide
    b. Furosemide
    c. Amiloride
    d. Canagliflozin
A

b. Furosemide
Rationale: Furosemide, a loop diuretic, can cause ototoxicity, especially in high doses or when given rapidly intravenously.

165
Q
  1. Which diuretic acts by blocking aldosterone receptors?
    a. Hydrochlorothiazide
    b. Furosemide
    c. Spironolactone
    d. Mannitol
A

c. Spironolactone
Rationale: Spironolactone is an aldosterone antagonist and acts by blocking aldosterone receptors.

166
Q
  1. Which diuretic is known to promote calcium reabsorption, making it useful for patients with recurrent urinary stones?
    a. Hydrochlorothiazide
    b. Furosemide
    c. Amiloride
    d. Acetazolamide
A

a. Hydrochlorothiazide
Rationale: Thiazide diuretics, like hydrochlorothiazide, promote calcium reabsorption in the distal tubule, reducing calcium excretion in the urine.

167
Q
  1. Which drug is primarily used to treat cerebral edema?
    a. Mannitol
    b. Acetazolamide
    c. Hydrochlorothiazide
    d. Spironolactone
A

a. Mannitol
Rationale: Mannitol is an osmotic diuretic and is primarily used to treat cerebral edema by drawing water out of the brain.

168
Q
  1. Which diuretic inhibits the sodium-potassium-chloride cotransporter in the thick ascending limb of the loop of Henle?
    a. Hydrochlorothiazide
    b. Furosemide
    c. Acetazolamide
    d. Spironolactone
A

b. Furosemide
Rationale: Furosemide is a loop diuretic that inhibits the sodium-potassium-chloride cotransporter in the thick ascending limb of the loop of Henle.

169
Q
  1. Which condition is a potential side effect of spironolactone when used with ACE inhibitors?
    a. Hyponatremia
    b. Hyperkalemia
    c. Hypocalcemia
    d. Hyperglycemia
A

b. Hyperkalemia
Rationale: Spironolactone can lead to elevated potassium levels, especially when used in combination with ACE inhibitors, leading to hyperkalemia.

170
Q
  1. Which diuretic acts by inhibiting sodium-chloride cotransport in the early distal convoluted tubule?
    a. Furosemide
    b. Mannitol
    c. Acetazolamide
    d. Hydrochlorothiazide
A

d. Hydrochlorothiazide
Rationale: Hydrochlorothiazide is a thiazide diuretic that acts by inhibiting the sodium-chloride cotransport in the early distal convoluted tubule.

171
Q
  1. Which diuretic can lead to a metabolic acidosis due to its mechanism of action?
    a. Hydrochlorothiazide
    b. Furosemide
    c. Acetazolamide
    d. Mannitol
A

c. Acetazolamide
Rationale: Acetazolamide inhibits carbonic anhydrase, leading to decreased reabsorption of bicarbonate, which can result in metabolic acidosis.

172
Q
  1. The use of which drug can lead to increased excretion of glucose in the urine?
    a. Hydrochlorothiazide
    b. Mannitol
    c. Canagliflozin
    d. Spironolactone
A

c. Canagliflozin
Rationale: Canagliflozin is an SGLT2 inhibitor, leading to increased glucose excretion in the urine.

173
Q
  1. Which drug is used in the treatment of edema associated with congestive heart failure?
    a. Acetazolamide
    b. Hydrochlorothiazide
    c. Mannitol
    d. Canagliflozin
A

b. Hydrochlorothiazide
Rationale: Hydrochlorothiazide is a thiazide diuretic commonly used in the treatment of edema associated with congestive heart failure due to its ability to promote sodium and water excretion.

174
Q
  1. Which diuretic would be least effective in a patient with severe renal impairment?
    a. Furosemide
    b. Hydrochlorothiazide
    c. Mannitol
    d. Spironolactone
A

b. Hydrochlorothiazide
Rationale: Thiazide diuretics, like hydrochlorothiazide, are less effective when glomerular filtration rate (GFR) is significantly reduced, as seen in severe renal impairment.

175
Q
  1. Which diuretic is known to cause gynecomastia as a side effect?
    a. Acetazolamide
    b. Furosemide
    c. Hydrochlorothiazide
    d. Spironolactone
A

d. Spironolactone
Rationale: Spironolactone, due to its anti-androgenic effects, can lead to gynecomastia in males.

176
Q
  1. Which of the following drugs is an osmotic diuretic?
    a. Acetazolamide
    b. Mannitol
    c. Spironolactone
    d. Furosemide
A

b. Mannitol
Rationale: Mannitol is an osmotic diuretic that increases the osmolarity of the filtrate, leading to increased water excretion.

177
Q
  1. Which drug is NOT primarily excreted by the kidneys?
    a. Furosemide
    b. Hydrochlorothiazide
    c. Mannitol
    d. Canagliflozin
A

c. Mannitol
Rationale: Mannitol is filtered by the glomerulus and not reabsorbed, resulting in increased osmolarity of the filtrate and promoting diuresis. It is not metabolized and is excreted unchanged in the urine.

178
Q
  1. Which diuretic can lead to metabolic alkalosis due to its mechanism of action?
    a. Hydrochlorothiazide
    b. Furosemide
    c. Acetazolamide
    d. Spironolactone
A

b. Furosemide
Rationale: Loop diuretics, like furosemide, increase the excretion of potassium and hydrogen ions, which can lead to metabolic alkalosis.

179
Q
  1. Which drug’s mechanism involves blocking the sodium channels in the distal tubules and collecting ducts?
    a. Amiloride
    b. Furosemide
    c. Hydrochlorothiazide
    d. Mannitol
A

a. Amiloride
Rationale: Amiloride acts by blocking sodium channels in the distal tubules and collecting ducts, reducing sodium reabsorption and potassium excretion.

180
Q
  1. Which diuretic is contraindicated in patients with anuria?
    a. Acetazolamide
    b. Mannitol
    c. Spironolactone
    d. Hydrochlorothiazide
A

b. Mannitol
Rationale: Mannitol is contraindicated in patients with anuria (absence of urine production) because it may exacerbate fluid overload without producing diuresis.

181
Q
  1. Which diuretic works primarily by inhibiting carbonic anhydrase?
    a. Furosemide
    b. Spironolactone
    c. Acetazolamide
    d. Hydrochlorothiazide
A

c. Acetazolamide
Rationale: Acetazolamide works by inhibiting carbonic anhydrase, leading to decreased reabsorption of bicarbonate in the proximal tubule.

182
Q
  1. Which of the following diuretics is most likely to cause hyperuricemia?
    a. Hydrochlorothiazide
    b. Mannitol
    c. Spironolactone
    d. Acetazolamide
A

a. Hydrochlorothiazide
Rationale: Thiazide diuretics, like hydrochlorothiazide, can lead to increased uric acid levels in the blood, potentially causing hyperuricemia.

183
Q
  1. Which drug is commonly used to treat hyperaldosteronism?
    a. Mannitol
    b. Acetazolamide
    c. Hydrochlorothiazide
    d. Spironolactone
A

d. Spironolactone
Rationale: Spironolactone, being an aldosterone antagonist, is commonly used in the treatment of conditions with excessive aldosterone secretion, such as hyperaldosteronism.

184
Q
  1. Which diuretic is associated with a decreased risk of osteoporosis due to its effect on calcium reabsorption?
    a. Furosemide
    b. Acetazolamide
    c. Hydrochlorothiazide
    d. Mannitol
A

c. Hydrochlorothiazide
Rationale: Thiazide diuretics, like hydrochlorothiazide, promote calcium reabsorption in the distal tubule, leading to decreased calcium excretion in the urine. This increased calcium retention can be beneficial for bone health and might be associated with a decreased risk of osteoporosis.

185
Q
  1. Which of the following drugs is NOT a potassium-sparing diuretic?
    a. Spironolactone
    b. Amiloride
    c. Triamterene
    d. Furosemide
A

d. Furosemide
Rationale: Furosemide is a loop diuretic, not a potassium-sparing diuretic. It primarily acts on the thick ascending limb of the loop of Henle to inhibit the sodium-potassium-chloride cotransporter, leading to increased excretion of sodium, potassium, and chloride.

186
Q

Which lipoprotein is primarily responsible for transporting cholesterol from the liver to peripheral tissues?

A. HDL
B. LDL
C. VLDL
D. Chylomicrons

A

B. LDL
Rationale: LDL (Low-Density Lipoprotein) is responsible for delivering cholesterol to cells. It’s often referred to as “bad cholesterol” because high levels can lead to plaque buildup in arteries.

187
Q

Which drug class is primarily used to lower LDL cholesterol by inhibiting cholesterol synthesis in the liver?

A. Fibrates
B. Statins
C. Niacin
D. Bile acid sequestrants

A

B. Statins
Rationale: Statins inhibit HMG-CoA reductase, the enzyme responsible for cholesterol synthesis in the liver, thereby reducing LDL levels.

188
Q

Which medication can cause a flushing reaction due to prostaglandin release?

A. Ezetimibe
B. Atorvastatin
C. Niacin
D. Gemfibrozil
Answer: C. Niacin

A

C. Niacin
Rationale: Niacin can cause flushing, often alleviated by taking aspirin or NSAIDs half an hour before niacin.

189
Q

Which drug binds bile acids in the intestine, preventing their reabsorption?

A. Fibrates
B. Statins
C. Bile acid sequestrants
D. Niacin

A

C. Bile acid sequestrants
Rationale: By binding bile acids, these drugs prevent their reabsorption, leading the liver to use more cholesterol to produce bile, thereby reducing circulating LDL.

190
Q

Which of the following is NOT a primary target of hyperlipidemia therapy?

A. Lowering LDL
B. Raising HDL
C. Lowering triglycerides
D. Raising LDL

A

D. Raising LDL
Rationale: LDL is considered “bad cholesterol,” and the primary goal is to reduce its levels, not raise them.

191
Q

Elevated levels of which lipoprotein is commonly associated with coronary artery disease?

A. HDL
B. LDL
C. VLDL
D. Chylomicrons

A

B. LDL
Rationale: Elevated LDL levels contribute to atherosclerotic plaque formation, increasing the risk of coronary artery disease.

192
Q

Which medication reduces VLDL secretion and increases HDL production?

A. Niacin
B. Atorvastatin
C. Gemfibrozil
D. Ezetimibe

A

A. Niacin
Rationale: Niacin has the effect of reducing VLDL secretion from the liver and also helps in increasing HDL levels.

193
Q

Which drug class is known to activate PPAR-alpha, enhancing oxidation of fatty acids in the liver and muscle?

A. Statins
B. Bile acid sequestrants
C. Fibrates
D. Niacin

A

C. Fibrates
Rationale: Fibrates activate PPAR-alpha, leading to enhanced oxidation of fatty acids, which results in reduced triglyceride levels.

194
Q

Which of the following medications inhibits cholesterol absorption in the intestine?

A. Niacin
B. Atorvastatin
C. Gemfibrozil
D. Ezetimibe

A

D. Ezetimibe
Rationale: Ezetimibe works by blocking the absorption of cholesterol in the intestine.

195
Q

Which adverse effect is associated with the use of fibrates?

A. Flushing
B. Gallstones
C. Myopathy
D. Constipation

A

B. Gallstones
Rationale: Fibrates can increase the risk of gallstone formation due to enhanced biliary excretion of cholesterol.

196
Q

Which lipoprotein primarily scavenges cholesterol from peripheral tissues and returns it to the liver?
A. LDL
B. HDL
C. VLDL
D. Chylomicrons

A

B. HDL
Rationale: HDL (High-Density Lipoprotein) is responsible for reverse cholesterol transport, taking cholesterol from tissues back to the liver.

197
Q

Which of the following drugs can increase the risk of myopathy, especially when combined with statins?
A. Niacin
B. Fibrates
C. Bile acid sequestrants
D. Ezetimibe

A

B. Fibrates
Rationale: Both fibrates and statins have a risk of causing myopathy. The risk increases when they are taken together.

198
Q

Which drug is contraindicated in patients with liver disease due to potential hepatotoxicity?
A. Atorvastatin
B. Niacin
C. Ezetimibe
D. Gemfibrozil

A

A. Atorvastatin
Rationale: Statins, like atorvastatin, have a potential risk of hepatotoxicity and should be used cautiously in patients with liver disease.

199
Q

Which drug can cause gastrointestinal discomfort as a primary side effect?
A. Fibrates
B. Statins
C. Bile acid sequestrants
D. Niacin

A

C. Bile acid sequestrants
Rationale: Bile acid sequestrants can cause gastrointestinal issues such as constipation and bloating.

200
Q

Which of the following is a primary target of hyperlipidemia therapy in patients with high cardiovascular risk?
A. Raising HDL
B. Lowering LDL
C. Raising VLDL
D. Lowering HDL

A

B. Lowering LDL
Rationale: Lowering LDL is a primary goal in hyperlipidemia therapy, especially in patients with a high risk of cardiovascular events.

201
Q

Patients taking which drug should undergo regular liver function tests?
A. Ezetimibe
B. Atorvastatin
C. Gemfibrozil
D. Bile acid sequestrants

A

B. Atorvastatin
Rationale: Statins, like atorvastatin, can potentially cause hepatotoxicity, and regular liver function tests are recommended.

202
Q

Which medication primarily targets triglyceride reduction?
A. Fibrates
B. Statins
C. Bile acid sequestrants
D. Ezetimibe

A

A. Fibrates
Rationale: Fibrates are primarily used to lower elevated triglyceride levels.

203
Q

Which drug works by reducing VLDL secretion from the liver?
A. Niacin
B. Atorvastatin
C. Gemfibrozil
D. Ezetimibe

A

A. Niacin
Rationale: Niacin can reduce VLDL secretion from the liver, leading to decreased levels of VLDL and triglycerides in the blood.

204
Q

A patient with elevated LDL levels and normal triglycerides would most likely benefit from which drug?
A. Fibrates
B. Statins
C. Niacin
D. Bile acid sequestrants

A

B. Statins
Rationale: Statins are the first-line treatment for elevated LDL levels.

205
Q

Which medication’s primary mechanism of action is to inhibit cholesterol absorption in the intestine?
A. Atorvastatin
B. Niacin
C. Gemfibrozil
D. Ezetimibe

A

D. Ezetimibe
Rationale: Ezetimibe inhibits the absorption of cholesterol in the small intestine.

206
Q
  1. Which lipoprotein is primarily associated with the formation of atherosclerotic plaques?

A. HDL
B. VLDL
C. LDL
D. Chylomicrons

A

C. LDL
Rationale: LDL is the primary lipoprotein associated with atherosclerotic plaque formation. It can penetrate the endothelial layer of arteries, undergo oxidation, and contribute to plaque buildup.

207
Q
  1. Which dietary component should be reduced to manage hyperlipidemia?

A. Omega-3 fatty acids
B. Soluble fiber
C. Saturated fats
D. Whole grains

A

C. Saturated fats
Rationale: Reducing saturated fats is a key recommendation for dietary management of hyperlipidemia. They can raise LDL levels and contribute to heart disease.

208
Q
  1. Which drug class inhibits HMG-CoA reductase?

A. Fibrates
B. Statins
C. Bile Acid Sequestrants
D. Niacin

A

B. Statins
Rationale: Statins inhibit HMG-CoA reductase, the enzyme responsible for cholesterol synthesis, thus reducing LDL levels.

209
Q
  1. Bile Acid Sequestrants primarily lower which lipid component?

A. HDL
B. LDL
C. Triglycerides
D. VLDL

A

B. LDL
Rationale: Bile Acid Sequestrants bind bile acids in the intestine and prevent their reabsorption. This leads to a reduction in LDL levels.

210
Q
  1. What is the primary mechanism by which Fibrates exert their effect?

A. Inhibition of cholesterol synthesis
B. Activation of PPAR-alpha
C. Bile acid binding
D. Reducing VLDL secretion

A

B. Activation of PPAR-alpha
Rationale: Fibrates activate PPAR-alpha, which enhances the oxidation of fatty acids in liver and muscle, reducing triglycerides and increasing HDL.

211
Q
  1. For a patient with high LDL and low HDL, which drug combination might be beneficial?

A. Statin + Ezetimibe
B. Statin + Niacin
C. Fibrate + Bile Acid Sequestrant
D. Niacin + Ezetimibe

A

B. Statin + Niacin
Rationale: A statin would address the high LDL, and niacin can help raise HDL levels.

212
Q
  1. Chronic ethanol ingestion can have which effect on serum lipids?

A. Decrease LDL
B. Decrease VLDL
C. Increase VLDL
D. Increase HDL

A

C. Increase VLDL
Rationale: Chronic ethanol ingestion can raise serum concentrations of VLDL and triglycerides.

213
Q
  1. Which drug is associated with an increased risk of gallstone formation?

A. Statin
B. Niacin
C. Fibrate
D. Ezetimibe

A

C. Fibrate
Rationale: Fibrates can increase the risk of gallstone formation due to enhanced biliary excretion of cholesterol.

214
Q
  1. A patient with high triglycerides would benefit most from which drug?

A. Bile Acid Sequestrant
B. Ezetimibe
C. Fibrate
D. Statin

A

C. Fibrate
Rationale: Fibrates are especially effective at reducing high triglyceride levels.

215
Q
  1. Which drug is contraindicated in pregnancy due to teratogenic risks?

A. Niacin
B. Bile Acid Sequestrant
C. Statin
D. Fibrate

A

C. Statin
Rationale: Statins are contraindicated in pregnancy due to the potential risk of teratogenic effects.

216
Q
  1. Which drug class can cause hepatotoxicity as an adverse effect?

A. Statins
B. Fibrates
C. Bile Acid Sequestrants
D. Both A and B

A

D. Both A and B
Rationale: Both statins and fibrates have been associated with hepatotoxicity as a potential adverse effect.

217
Q
  1. Which drug reduces VLDL secretion and increases HDL production?

A. Ezetimibe
B. Statin
C. Niacin
D. Fibrate

A

C. Niacin
Rationale: Niacin reduces VLDL secretion and also has the effect of increasing HDL production.

218
Q
  1. Which drug binds bile acids in the intestine, preventing their reabsorption?

A. Statin
B. Fibrate
C. Bile Acid Sequestrant
D. Niacin

A

C. Bile Acid Sequestrant
Rationale: Bile Acid Sequestrants function by binding bile acids in the intestine, preventing their reabsorption and leading to a reduction in LDL levels.

219
Q
  1. Activation of which receptor enhances the oxidation of fatty acids in liver and muscle?

A. HMG-CoA Reductase
B. PPAR-alpha
C. LDL receptor
D. HDL receptor

A

B. PPAR-alpha
Rationale: Fibrates

220
Q
  1. Which of the following is a primary function of HDL?

A. Deliver cholesterol to tissues
B. Promote atherosclerotic plaque formation
C. Transport cholesterol to the liver for excretion
D. Facilitate cholesterol synthesis

A

C. Transport cholesterol to the liver for excretion
Rationale: HDL is often referred to as “good cholesterol” because it transports cholesterol from tissues back to the liver for excretion, helping to reduce atherosclerosis.

221
Q
  1. Which of the following is NOT an effect of niacin?

A. Decrease VLDL secretion
B. Increase LDL levels
C. Raise HDL levels
D. Lower triglycerides

A

B. Increase LDL levels
Rationale: Niacin is known to reduce VLDL secretion, raise HDL levels, and lower triglycerides. It does not increase LDL levels.

222
Q
  1. The mechanism of action of which drug involves inhibition of cholesterol absorption in the small intestine?

A. Gemfibrozil
B. Atorvastatin
C. Cholestyramine
D. Ezetimibe

A

D. Ezetimibe
Rationale: Ezetimibe works by inhibiting cholesterol absorption in the small intestine, leading to a reduction in LDL levels.

223
Q
  1. Which adverse effect is most commonly associated with high doses of statins?

A. Flushing
B. Myopathy
C. Gallstones
D. Constipation

A

B. Myopathy
Rationale: Statins, especially at high doses, are associated with an increased risk of myopathy, which is muscle pain or weakness.

224
Q
  1. What is the primary effect of omega-3 fatty acids on lipid profiles?

A. Increase LDL
B. Decrease HDL
C. Increase VLDL
D. Decrease triglycerides

A

D. Decrease triglycerides
Rationale: Omega-3 fatty acids, often found in fish oil, are known to decrease serum triglyceride levels.

225
Q
  1. Which drug is known to increase the risk of hyperglycemia?

A. Niacin
B. Ezetimibe
C. Statin
D. Bile Acid Sequestrant

A

A. Niacin
Rationale: Niacin can exacerbate hyperglycemia, making it a concern for patients with diabetes.

226
Q
  1. Which is the primary target lipid component for bile acid sequestrants?

A. HDL
B. VLDL
C. Triglycerides
D. LDL

A

D. LDL
Rationale: Bile acid sequestrants mainly target LDL, helping to lower its levels.

227
Q
  1. What is a potential benefit of combined drug therapy for hyperlipidemia?

A. Addressing a single lipid abnormality
B. Reducing the dose and side effects of individual drugs
C. Eliminating the need for dietary changes
D. Ensuring faster action of drugs

A

B. Reducing the dose and side effects of individual drugs
Rationale: Combining drugs can target multiple lipid abnormalities simultaneously, potentially enhancing therapeutic effects and reducing the dose (and side effects) of individual drugs.

228
Q
  1. Which drug is known to activate PPAR-alpha?

A. Statin
B. Niacin
C. Fibrate
D. Ezetimibe

A

C. Fibrate
Rationale: Fibrates activate PPAR-alpha, enhancing the oxidation of fatty acids in liver and muscle.

229
Q
  1. A patient with a primary concern of elevated triglycerides might benefit most from which drug?

A. Statin
B. Bile Acid Sequestrant
C. Ezetimibe
D. Fibrate

A

D. Fibrate
Rationale: Fibrates are particularly effective at reducing high triglyceride levels.

230
Q
  1. Which form of angina is associated with a fixed plaque that partially occludes one or more coronary arteries?

A) Vasospastic Angina

B) Angina of Effort

C) Unstable Angina

D) None of the above

A

B) Angina of Effort

Rationale: Angina of effort is caused by a fixed atherosclerotic plaque that partially obstructs coronary blood flow, especially during physical exertion.

231
Q
  1. Which angina type involves unpredictable and reversible coronary spasm?

A) Angina of Effort

B) Vasospastic Angina

C) Unstable Angina

D) All of the above

A

B) Vasospastic Angina

Rationale: Vasospastic angina is characterized by unpredictable, reversible spasms in the coronary arteries.

232
Q
  1. Which drug group is primarily used for prophylaxis of angina of effort?

A) Nitrates

B) Calcium Channel Blockers

C) β-blockers

D) Diuretics

A

C) β-blockers

Rationale: β-blockers reduce the heart’s oxygen demand by causing it to beat slower and with less force. They are primarily used for preventing angina of effort.

233
Q
  1. Which form of angina is considered a medical emergency because it might precede a myocardial infarction?

A) Angina of Effort

B) Vasospastic Angina

C) Unstable Angina

D) Both A and B

A

C) Unstable Angina

Rationale: Unstable angina can lead to myocardial infarction (heart attack) and is considered a medical emergency.

234
Q
  1. Which drug group dilates blood vessels to reduce the workload on the heart?

A) Diuretics

B) Nitrates

C) β-blockers

D) Aspirin

A

B) Nitrates

Rationale: Nitrates cause vasodilation, reducing the workload on the heart and improving blood flow to the heart muscle.

235
Q
  1. Which of the following drug groups is NOT effective for an acute attack of angina of effort?

A) Nitrates

B) Calcium Channel Blockers

C) β-blockers

D) ACE inhibitors

A

C) β-blockers

Rationale: While β-blockers are used for prophylaxis of angina of effort, they are not effective for an acute attack.

236
Q
  1. Which drug group prevents calcium from entering cells of the heart and blood vessel walls?

A) Nitrates

B) Calcium Channel Blockers

C) β-blockers

D) Diuretics

A

B) Calcium Channel Blockers

Rationale: Calcium Channel Blockers prevent calcium from entering cells, leading to relaxation and vasodilation, which helps in angina management.

237
Q
  1. Which type of angina can occur at rest and might last longer than other types?

A) Angina of Effort

B) Vasospastic Angina

C) Unstable Angina

D) None of the above

A

C) Unstable Angina

Rationale: Unstable angina can occur at rest or with minimal exertion and might last longer, making it more severe than other types.

238
Q
  1. Which drug group is beneficial for all three types of angina?

A) Diuretics

B) Nitrates

C) β-blockers

D) ACE inhibitors

A

B) Nitrates

Rationale: Nitrates are beneficial for all three types of angina as they cause vasodilation, reducing the workload on the heart.

239
Q
  1. Vasospastic angina is also known as:

A) Stable Angina

B) Variant Angina

C) Unstable Angina

D) Chronic Angina

A

B) Variant Angina

Rationale: Vasospastic angina is also referred to as Prinzmetal’s or Variant Angina.

240
Q
  1. Which form of angina is most likely to occur due to emotional stress?

A) Angina of Effort

B) Vasospastic Angina

C) Unstable Angina

D) All of the above

A

A) Angina of Effort

Rationale: Angina of effort can be triggered by both physical exertion and emotional stress.

241
Q
  1. Which of the following is NOT a direct effect of β-blockers on the heart?

A) Reducing heart rate

B) Decreasing force of heart’s contractions

C) Causing vasodilation

D) Blocking the effects of epinephrine

A

C) Causing vasodilation

Rationale: β-blockers primarily reduce heart rate and force of contractions. They do not directly cause vasodilation.

242
Q
  1. Which drug is often added to β-blockers and nitroglycerin in patients with refractory unstable angina?

A) Diuretics

B) Nitrates

C) Calcium Channel Blockers

D) ACE inhibitors

A

C) Calcium Channel Blockers

Rationale: Calcium Channel Blockers can be added to β-blockers and nitroglycerin in patients with refractory unstable angina for better management.

243
Q
  1. Which type of angina is characterized by being unpredictable and occurring mostly during the early morning hours?

A) Angina of Effort

B) Vasospastic Angina

C) Unstable Angina

D) Both A and B

A

B) Vasospastic Angina

Rationale: Vasospastic angina can occur unpredictably, often during the early morning hours.

244
Q
  1. The rupture of an atherosclerotic plaque leading to platelet aggregation is most closely associated with which type of angina?

A) Angina of Effort

B) Vasospastic Angina

C) Unstable Angina

D) None of the above

A

C) Unstable Angina

Rationale: Unstable angina often results from the rupture of an atherosclerotic plaque, leading to platelet aggregation and transient thrombus formation.

245
Q
  1. Which drug group primarily acts by blocking the effects of epinephrine on the heart?

A) Nitrates

B) Calcium Channel Blockers

C) β-blockers

D) Diuretics

A

C) β-blockers

Rationale: β-blockers work by blocking the effects of the hormone epinephrine,

246
Q
A

Pharma 1 (15 decks)

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