Week Three Flashcards

1
Q

What are adrenergic agonists also known as?

A) Sympatholytics
B)Sympathomimetic
C) Cholinergics
D) Antagonists

A

Correct Answer: B) Sympathomimetics

Rationale: Adrenergic agonists are commonly referred to as sympathomimetics because they mimic the effects of the sympathetic nervous system.

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2
Q

Which of the following mechanisms is the most common method by which adrenergic agonists activate adrenergic receptors?

A) Inhibition of norepinephrine inactivation
B) Direct receptor binding
C) Promotion of norepinephrine release
D) Inhibition of norepinephrine reuptake

A

Correct Answer: B) Direct receptor binding
Rationale: The most common mechanism for activating adrenergic receptors by adrenergic agonists is through direct receptor binding.

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3
Q

Which indirect mechanism is used by adrenergic agonists to enhance adrenergic receptor activation?

A) Direct receptor binding
B) Inhibition of norepinephrine reuptake
C) Inhibition of norepinephrine inactivation
D) Promotion of norepinephrine release

A

Correct Answer: D) Promotion of norepinephrine release
Rationale: One of the indirect mechanisms that adrenergic agonists use to activate adrenergic receptors is the promotion of norepinephrine release.

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4
Q

Which of the following is NOT a mechanism by which adrenergic agonists activate adrenergic receptors?

A) Promotion of norepinephrine release
B) Inhibition of norepinephrine reuptake
C) Direct receptor binding
D) Direct inhibition of adrenergic receptors

A

Correct Answer: D) Direct inhibition of adrenergic receptors
Rationale: Direct inhibition of adrenergic receptors is not a mechanism by which adrenergic agonists activate these receptors; rather, they promote activation through direct binding or indirect methods.

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5
Q

Which mechanism is associated with the inhibition of norepinephrine reuptake by adrenergic agonists?

A) Direct receptor binding
B) Indirect mechanism
C) Direct mechanism
D) Promotion of norepinephrine inactivation

A

Correct Answer: B) Indirect mechanism
Rationale: Inhibition of norepinephrine reuptake is classified as an indirect mechanism that increases the availability of norepinephrine at adrenergic receptors, enhancing their activation.

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6
Q

Which of the following are the two chemical classes of adrenergic agonists?

A) Alpha and beta agonists
B) Agonists and antagonists
C) Catecholamines and non-catecholamines
D) Sympathomimetics and sympatholytics

A

Correct Answer: C) Catecholamines and non-catecholamines
Rationale: Adrenergic agonists are classified into two chemical classes: catecholamines and non-catecholamines, based on their chemical structure and properties.

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7
Q

Which of the following factors is NOT used to differentiate between catecholamines and non-catecholamines?

A) Ability for oral administration
B) Duration of action
C) CNS activity
D) Heart rate response

A

Correct Answer: D) Heart rate response
Rationale: The differentiation between catecholamines and non-catecholamines is based on their ability for oral administration, duration of action, and CNS activity, not specifically on heart rate response.

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8
Q

Which chemical class of adrenergic agonists can be administered orally?

A) Catecholamines
B) Non-catecholamines
C) Both catecholamines and non-catecholamines
D) Neither catecholamines nor non-catecholamines

A

Correct Answer: B) Non-catecholamines
Rationale: Non-catecholamines are generally capable of being administered orally, while catecholamines are usually given by injection due to their rapid metabolism and inability to withstand the gastrointestinal tract.

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9
Q

Which of the following characteristics typically distinguishes catecholamines from non-catecholamines?

A) Longer duration of action
B) Greater CNS activity
C) Ability for oral administration
D) More potent agonistic effects

A

Correct Answer: C) Ability for oral administration
Rationale: Catecholamines are usually not suitable for oral administration due to their rapid metabolism, while non-catecholamines can often be given orally.

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10
Q

What is one major difference between catecholamines and non-catecholamines regarding their duration of action?

A) Catecholamines have a longer duration of action than non-catecholamines.
B) Non-catecholamines have a longer duration of action than catecholamines.
C) Both classes have the same duration of action.
D) Duration of action is not applicable to either class.

A

Correct Answer: B) Non-catecholamines have a longer duration of action than catecholamines.
Rationale: Non-catecholamines generally have a longer duration of action compared to catecholamines, which are rapidly metabolized and have shorter durations of effect.

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11
Q

Which of the following accurately describes the chemical structure of catecholamines?

A) Comprised of a catechol group and an amine group
B) Comprised of a catechol group and a hydroxyl group
C) Comprised of an amine group and a phenol group
D) Comprised of a carbon chain and an ether group

A

Correct Answer: A) Comprised of a catechol group and an amine group
Rationale: Catecholamines are characterized by their chemical structure, which includes a catechol group (a benzene ring with two hydroxyl groups) and an amine group.

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12
Q

Which enzymes are responsible for the inactivation of catecholamines?

A) AChE and PDE
B) MAO and COMT
C) Dipeptidase and pepsin
D) CYP450 and GST

A

Correct Answer: B) MAO and COMT
Rationale: Catecholamines are inactivated by the enzymes monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT).

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13
Q

Which statement is true regarding the administration of catecholamines?

A) They can be given orally.
B) They are given as a continuous IV infusion only.
C) They are administered via intramuscular injection.
D) They can be taken as a tablet.

A

Correct Answer: B) They are given as a continuous IV infusion only.
Rationale: Catecholamines are typically administered as continuous intravenous infusions due to their short half-life and instability when exposed to the gastrointestinal tract.

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14
Q

What is a characteristic of catecholamines regarding their ability to cross the blood-brain barrier (BBB)?

A) They can easily cross the BBB.
B) They cannot cross the BBB.
C) Their ability to cross the BBB varies by drug.
D) They only cross the BBB if administered orally.

A

Correct Answer: B) They cannot cross the BBB.
Rationale: Catecholamines do not cross the blood-brain barrier due to their chemical structure, which limits their ability to penetrate lipid membranes.

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15
Q

What should be done if a catecholamine solution oxidizes and changes color?

A) Use the solution if it’s still effective.
B) Discard the solution and do not use it.
C) Store it in a cool place to prevent further oxidation.
D) Use it only after testing its pH.

A

Correct Answer: B) Discard the solution and do not use it.

Rationale: If a catecholamine solution oxidizes and changes color, it indicates that the drug has degraded and should not be used, as it may be ineffective or potentially harmful.

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16
Q

Which of the following is NOT an example of a catecholamine?

A) Norepinephrine (NE)
B) Epinephrine (Epi)
C) Isoproterenol
D) Atropine

A

Correct Answer: D) Atropine

Rationale: Atropine is an anticholinergic medication, not a catecholamine. Examples of catecholamines include norepinephrine, epinephrine, isoproterenol, dopamine, and dobutamine.

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17
Q

Which of the following correctly describes the chemical structure of non-catecholamines?

A) They contain a catechol molecule.
B) They have a different structure with no catechol molecule.
C) They are composed only of amine groups.
D) They are identical in structure to catecholamines.

A

Correct Answer: B) They have a different structure with no catechol molecule.

Rationale: Non-catecholamines are characterized by their different structure, which does not include a catechol molecule.

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18
Q

Which of the following statements is true regarding non-catecholamines and COMT?

A) Non-catecholamines are substrates for COMT.
B) COMT can inactivate non-catecholamines.
C) COMT cannot inactivate non-catecholamines.
D) Non-catecholamines have no interaction with COMT.

A

Correct Answer: C) COMT cannot inactivate non-catecholamines.
Rationale: Non-catecholamines are not substrates for catechol-O-methyltransferase (COMT), meaning COMT cannot inactivate these drugs.

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19
Q

What is a key difference in the metabolism of non-catecholamines compared to catecholamines?

A) Non-catecholamines are metabolized faster by MAO.
B) Non-catecholamines are substrates for COMT.
C) Non-catecholamines have a slower metabolism by MAO.
D) Non-catecholamines have no metabolism by MAO.

A

Correct Answer: C) Non-catecholamines have a slower metabolism by MAO.
Rationale: Non-catecholamines are metabolized more slowly by monoamine oxidase (MAO) compared to catecholamines.

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20
Q

Which of the following characteristics is NOT associated with non-catecholamines?

A) Longer half-life
B) Oral administration possible
C) Short duration of action
D) Ability to cross the blood-brain barrier

A

Correct Answer: C) Short duration of action
Rationale: Non-catecholamines typically have a longer duration of action, unlike catecholamines, which have a brief duration.

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21
Q

Which of the following non-catecholamines can cross the blood-brain barrier (BBB)?

A) Phenylephrine
B) Albuterol
C) Norepinephrine
D) Epinephrine

A

Correct Answer: B) Albuterol

Rationale: Non-catecholamines, such as albuterol, can cross the blood-brain barrier, unlike catecholamines, which generally cannot.

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22
Q

Which of the following is an example of a non-catecholamine?

A) Dopamine
B) Phenylephrine
C) Isoproterenol
D) Epinephrine

A

Correct Answer: B) Phenylephrine
Rationale: Phenylephrine is an example of a non-catecholamine, while dopamine, isoproterenol, and epinephrine are classified as catecholamines.

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23
Q

Which of the following drugs is NOT classified as an alpha-1 agonist?

A) Norepinephrine (NE)
B) Phenylephrine
C) Ephedrine
D) Albuterol

A

Correct Answer: D) Albuterol

Rationale: Albuterol is a beta-2 agonist and does not act as an alpha-1 agonist, while norepinephrine, phenylephrine, and ephedrine are all classified as alpha-1 agonists.

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24
Q

What therapeutic response is primarily associated with alpha-1 activation?

A) Bronchodilation
B) Vasoconstriction
C) Increased heart rate
D) Decreased gastrointestinal motility

A

Correct Answer: B) Vasoconstriction
Rationale: Alpha-1 activation primarily causes vasoconstriction, particularly in the skin, viscera, and mucous membranes.

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25
Q

What is one of the clinical uses of alpha-1 agonists in managing hypotension?

A) They promote bronchial dilation.
B) They increase heart rate.
C) They induce vasoconstriction to elevate blood pressure.
D) They decrease peripheral resistance.

A

Correct Answer: C) They induce vasoconstriction to elevate blood pressure.

Rationale: Alpha-1 agonists can elevate blood pressure by inducing vasoconstriction; however, they are not typically the first line for treating hypotension.

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26
Q

Which alpha-1 agonist is commonly used to cause pupil dilation during eye exams?

A) Ephedrine
B) Norepinephrine
C) Phenylephrine
D) Pseudoephedrine

A

Correct Answer: C) Phenylephrine
Rationale: Phenylephrine is commonly used to induce pupil dilation for eye exams and surgery due to its alpha-1 agonist properties.

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27
Q

Alpha-1 agonists are rarely used for mydriasis. What is the primary therapeutic use of mydriasis?

A) Pain relief
B) Hemostasis
C) Eye exams and surgeries
D) Nasal decongestion

A

Correct Answer: C) Eye exams and surgeries

Rationale: Mydriasis (pupil dilation) is primarily used for eye exams and surgical procedures, although the use of alpha-1 agonists for this purpose is rare.

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28
Q

Which of the following is a benefit of using alpha-1 agonists as an adjunct to local anesthesia?

A) Increased metabolism of the anesthetic
B) Delay in systemic absorption
C) Enhanced analgesic effect
D) Rapid onset of anesthesia

A

Correct Answer: B) Delay in systemic absorption
Rationale: Alpha-1 agonists are used as adjuncts to local anesthesia to delay systemic absorption of the anesthetic, which prolongs its effects.

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29
Q

What is a primary adverse effect of alpha-1 agonist activation that can lead to significant complications?

A) Hypotension
B) Bradycardia
C) Hypertension
D) Respiratory depression

A

Correct Answer: C) Hypertension
Rationale: Alpha-1 agonist activation can cause widespread vasoconstriction, leading to hypertension, especially with continuous IV infusions.

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30
Q

When monitoring a patient receiving continuous IV infusions of alpha-1 agonists, which parameters are essential to assess?

A) Respiratory rate, temperature, and skin color
B) Heart rate, rhythm, blood pressure, and urine output
C) Capillary refill, muscle strength, and appetite
D) Weight, blood glucose levels, and pain scale

A

Correct Answer: B) Heart rate, rhythm, blood pressure, and urine output
Rationale: Continuous monitoring of cardiac status, including heart rate, rhythm, blood pressure, and urine output, is essential to assess for adverse effects from alpha-1 agonists.

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31
Q

What causes bradycardia in patients receiving alpha-1 agonists?

A) Increased stroke volume
B) Activation of the baroreceptor reflex due to hypertension
C) Direct cardiac effects of the medication
D) Decreased peripheral resistance

A

Correct Answer: B) Activation of the baroreceptor reflex due to hypertension
Rationale: Bradycardia can occur as a result of the baroreceptor reflex being triggered by hypertension caused by alpha-1 agonists.

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32
Q

Why is necrosis a potential adverse effect associated with IV administration of alpha-1 agonists?

A) Direct tissue toxicity from the drug
B) Leakage from blood vessels into surrounding tissue due to vasoconstriction
C) Reduced blood flow to the area of injection
D) Allergic reactions to the medication

A

Correct Answer: B) Leakage from blood vessels into surrounding tissue due to vasoconstriction
Rationale: Necrosis can occur if there is infiltration of the drug from blood vessels into the tissue due to vasoconstriction, leading to reduced blood flow and tissue damage.

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33
Q

What is considered best practice for administering alpha-1 agonists to minimize the risk of necrosis?

A) Administer via a peripheral IV line only
B) Administer through a central line (e.g., PICC line)
C) Use a larger gauge needle for injections
D) Infuse at the highest concentration possible

A

Correct Answer: B) Administer through a central line (e.g., PICC line)
Rationale: Administering alpha-1 agonists through a central line is considered best practice to reduce the risk of necrosis from infiltration.

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34
Q

What nursing responsibility is crucial when administering alpha-1 agonists via IV?

A) Monitor the patient for gastrointestinal distress
B) Assess the patency of IVs and central lines regularly
C) Administer the medication as a bolus
D) Change the IV site every 12 hours

A

Correct Answer: B) Assess the patency of IVs and central lines regularly
Rationale: It is essential for nurses to monitor the patency of IVs and central lines to prevent infiltration and ensure safe administration of alpha-1 agonists.

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35
Q

What is the primary action of alpha-2 agonists when activated?

A) Increase norepinephrine (NE) release
B) Inhibit norepinephrine (NE) release
C) Increase heart rate
D) Induce vasodilation

A

Correct Answer: B) Inhibit norepinephrine (NE) release
Rationale: Activation of alpha-2 receptors inhibits the release of norepinephrine, leading to decreased sympathetic transmission.

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36
Q

Where are alpha-2 receptors primarily located?

A) Post-synaptic neurons
B) Peripheral blood vessels
C) Pre-synaptic neurons
D) Cardiac tissues

A

Correct Answer: C) Pre-synaptic neurons
Rationale: Alpha-2 receptors are primarily located on pre-synaptic neurons, where their activation inhibits the release of norepinephrine.

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37
Q

Which of the following is a significant therapeutic effect of alpha-2 agonists?

A) Increased blood pressure
B) Pain relief
C) Enhanced sympathetic transmission
D) Increased heart rate

A

Correct Answer: B) Pain relief
Rationale: Alpha-2 agonists are known for providing pain relief and decreasing sympathetic transmission to the heart and blood vessels

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38
Q

What is a peripheral clinical significance of alpha-2 agonists?

A) Their effects are primarily peripheral.
B) They have minimal peripheral clinical significance.
C) They are only effective in peripheral tissues.
D) They induce significant vasoconstriction in peripheral vessels.

A

Correct Answer: B) They have minimal peripheral clinical significance.
Rationale: While alpha-2 agonists have some effects on peripheral tissues, their clinical significance is considered minimal compared to their central nervous system effects.

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39
Q

Which of the following is a potential adverse effect of alpha-2 agonists?

A) Hypertension
B) Increased heart rate
C) Sedation
D) Tachycardia

A

Correct Answer: C) Sedation
Rationale: Alpha-2 agonists can cause sedation due to their central nervous system effects, while they typically reduce sympathetic transmission.

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40
Q

In which scenario would alpha-2 agonists be particularly beneficial?

A) Treating acute asthma attacks
B) Managing chronic pain
C) Reducing anxiety and promoting sedation
D) Increasing cardiac output

A

Correct Answer: C) Reducing anxiety and promoting sedation
Rationale: Alpha-2 agonists can be used to reduce anxiety and promote sedation, making them beneficial in various CNS-related conditions.

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41
Q

Question 1
What is a primary therapeutic effect of beta-1 agonists when activated?

A) Decreased heart rate
B) Improved peripheral circulation
C) Increased force of contraction and cardiac output
D) Vasodilation of blood vessels

A

Correct Answer: C) Increased force of contraction and cardiac output
Rationale: Activation of beta-1 receptors in the heart increases the force of contraction and improves cardiac output, making beta-1 agonists useful in heart failure.

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42
Q

Which of the following drugs is NOT a beta-1 agonist?

A) Dobutamine
B) Isoproterenol
C) Epinephrine
D) Phenylephrine

A

Correct Answer: D) Phenylephrine
Rationale: Phenylephrine is primarily an alpha-1 agonist and does not have significant beta-1 agonist activity, while the other options do activate beta-1 receptors.

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43
Q

In the management of heart failure, what is the effect of beta-1 agonists on the heart?

A) Decrease cardiac output
B) Increase force of contraction
C) Induce bradycardia
D) Cause vasodilation

A

Correct Answer: B) Increase force of contraction
Rationale: Beta-1 agonists increase the force of contraction of the heart, which is beneficial in treating heart failure.

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44
Q

What role do beta-1 agonists play in the treatment of shock?

A) They decrease heart rate to conserve energy.
B) They improve cardiac output to enhance perfusion to vital organs.
C) They promote vasodilation to lower blood pressure.
D) They inhibit cardiac contractions to stabilize the heart.

A

Correct Answer: B) They improve cardiac output to enhance perfusion to vital organs.
Rationale: Beta-1 agonists improve cardiac output, which is critical in managing shock and ensuring adequate perfusion to vital organs.

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45
Q

How do beta-1 agonists assist in cases of cardiac arrest?

A) They slow down the heart rate.
B) They promote peripheral vasodilation.
C) They can help initiate contraction in a still heart.
D) They inhibit norepinephrine release.

A

Correct Answer: C) They can help initiate contraction in a still heart.
Rationale: In cardiac arrest, beta-1 agonists can help initiate contractions in the heart, which is essential for restoring circulation.

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46
Q

What is a common clinical use of beta-1 agonists in patients with AV block?

A) To increase heart rate
B) To improve conduction within the heart
C) To reduce myocardial oxygen demand
D) To induce vasodilation

A

Correct Answer: B) To improve conduction within the heart
Rationale: Beta-1 agonists improve conduction in the heart, which can be beneficial for patients with AV block due to poor electrical conduction.

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47
Q

What adverse effect can result from overstimulation of beta-1 receptors?

A) Bradycardia
B) Altered heart rate or heart rhythm
C) Peripheral vasodilation
D) Hypotension

A

Correct Answer: B) Altered heart rate or heart rhythm
Rationale: Overstimulation of beta-1 receptors can lead to tachycardia or abnormal heart rhythms as adverse effects.

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48
Q

Which of the following is a potential adverse effect of beta-1 agonists related to myocardial oxygen demand?

A) Bradycardia
B) Hypoglycemia
C) Angina (chest pain)
D) Peripheral edema

A

Correct Answer: C) Angina (chest pain)
Rationale: Beta-1 agonists can increase myocardial oxygen demand, which may worsen angina in susceptible patients.

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49
Q

In which patient population should beta-1 agonists be administered with caution due to the risk of angina?

A) Patients with low blood pressure
B) Patients with a history of myocardial infarction
C) Patients with a high risk for angina
D) Patients with diabetes mellitus

A

Correct Answer: C) Patients with a high risk for angina
Rationale: Caution is advised when administering beta-1 agonists to patients at high risk for angina, as these medications can increase oxygen demand on the heart.

50
Q

What is a common cardiovascular adverse effect associated with the use of beta-1 agonists?

A) Hypotension
B) Tachycardia
C) Peripheral vasoconstriction
D) Heart block

A

Correct Answer: B) Tachycardia
Rationale: Tachycardia is a common cardiovascular adverse effect due to the stimulation of beta-1 receptors in the heart.

51
Q

Which of the following findings would indicate a potential adverse effect of beta-1 agonist therapy?

A) Decreased heart rate
B) Increased blood pressure
C) Chest pain upon exertion
D) Improved cardiac output

A

Correct Answer: C) Chest pain upon exertion
Rationale: Chest pain upon exertion could indicate worsening angina, a potential adverse effect of beta-1 agonists due to increased myocardial oxygen demand.

52
Q

What should be monitored closely in patients receiving beta-1 agonists to prevent adverse effects?

A) Blood glucose levels
B) Electrocardiogram (ECG) for heart rhythm changes
C) Respiratory rate
D) Renal function tests

A

Correct Answer: B) Electrocardiogram (ECG) for heart rhythm changes
Rationale: Continuous monitoring of ECG is important to detect any altered heart rates or rhythms that may occur due to beta-1 agonist overstimulation.

53
Q

What is a primary therapeutic effect of beta-2 agonists in the treatment of asthma?

A) Decreased respiratory rate
B) Bronchodilation
C) Increased mucus production
D) Peripheral vasoconstriction

A

Correct Answer: B) Bronchodilation
Rationale: Beta-2 agonists promote bronchodilation, which helps alleviate symptoms of asthma by relaxing bronchial smooth muscle.

54
Q

Which of the following beta-2 agonists is most commonly used for asthma management?

A) Phenylephrine
B) Epinephrine
C) Albuterol
D) Isoproterenol

A

Correct Answer: C) Albuterol
Rationale: Albuterol is a beta-2 selective agonist frequently used in inhalers for asthma management due to its bronchodilatory effects.

55
Q

Why are beta-2-selective drugs preferred for treating asthma?

A) They have a longer duration of action.
B) They minimize systemic side effects.
C) They are less expensive.
D) They cause vasoconstriction.

A

Correct Answer: B) They minimize systemic side effects.
Rationale: Beta-2-selective drugs target the beta-2 receptors in the lungs more specifically, reducing the risk of systemic side effects that can occur with non-selective agonists.

56
Q

Why are beta-2 agonists primarily administered by inhalation for asthma treatment?

A) To increase systemic absorption
B) To achieve rapid local effects in the lungs
C) To minimize the risk of side effects
D) To enhance muscle contraction

A

Correct Answer: B) To achieve rapid local effects in the lungs
Rationale: Inhalation allows for direct delivery of the medication to the lungs, providing quick bronchodilation and minimizing systemic exposure.

57
Q

Which of the following adverse effects is associated with beta-2 receptor activation in the liver and skeletal muscles?

A) Hypoglycemia
B) Hyperglycemia
C) Bradycardia
D) Hypotension

A

Correct Answer: B) Hyperglycemia
Rationale: Activation of beta-2 receptors in the liver and skeletal muscles promotes glycogenolysis, which can lead to increased blood glucose levels, particularly in people with diabetes.

58
Q

Why are individuals with diabetes considered most at risk for hyperglycemia when using beta-2 agonists?

A) They have decreased liver function.
B) Their body cannot produce sufficient insulin.
C) They often use more potent beta-2 agonists.
D) They experience higher levels of tremors.

A

Correct Answer: B) Their body cannot produce sufficient insulin.
Rationale: Individuals with diabetes may have impaired insulin production or sensitivity, making it harder for them to regulate blood sugar levels in response to hyperglycemia caused by beta-2 agonists.

59
Q

What is a common adverse effect of beta-2 agonists that can result from skeletal muscle activation?

A) Nausea
B) Tremor
C) Hypotension
D) Dizziness

A

Correct Answer: B) Tremor
Rationale: Tremors are a common adverse effect caused by beta-2 receptor activation in skeletal muscles, resulting in contractions. Starting at a low dose can help minimize this effect.

60
Q

Why might tremors caused by beta-2 agonists be particularly concerning for individuals with diabetes?

A) They indicate severe dehydration.
B) They may lead to loss of coordination.
C) They can increase stress levels and contribute to hyperglycemia.
D) They are a sign of overdose.

A

Correct Answer: C) They can increase stress levels and contribute to hyperglycemia.
Rationale: Tremors may increase physiological stress, which can exacerbate hyperglycemia in individuals with diabetes, making blood glucose management more challenging.

61
Q

What is the primary effect of dopamine activation on peripheral dopamine receptors?

A) Increased heart rate
B) Dilation of renal vasculature
C) Bronchodilation
D) Peripheral vasoconstriction

A

Correct Answer: B) Dilation of renal vasculature
Rationale: Activation of peripheral dopamine receptors causes dilation of renal blood vessels, which improves renal perfusion.

62
Q

Which receptor does dopamine uniquely activate in addition to peripheral dopamine receptors?

A) Alpha-1 receptors
B) Beta-2 receptors
C) Beta-1 receptors
D) Alpha-2 receptors

A

Correct Answer: C) Beta-1 receptors
Rationale: Dopamine is the only drug that works on dopamine receptors and can also activate beta-1 receptors in the heart, impacting cardiac function positively.

63
Q

In what way does dopamine activation on beta-1 receptors positively impact the heart?

A) Increases heart rate and contractility
B) Decreases heart rate and contractility
C) Reduces myocardial oxygen demand
D) Enhances coronary artery dilation

A

Correct Answer: A) Increases heart rate and contractility
Rationale: Activation of beta-1 receptors increases heart rate and the force of contraction, contributing to improved cardiac output.

64
Q

What is a key therapeutic use of dopamine in shock management?

A) Reducing heart rate
B) Dilation of pulmonary vasculature
C) Dilation of renal blood vessels to improve perfusion
D) Increasing blood viscosity

A

Correct Answer: C) Dilation of renal blood vessels to improve perfusion
Rationale: In shock, dopamine dilates renal blood vessels, improving renal perfusion and decreasing the risk of renal failure.

65
Q

How does dopamine help decrease the risk of renal failure during shock?

A) By causing systemic vasodilation
B) By increasing urine output
C) By dilating renal blood vessels
D) By improving cardiac rhythm

A

Correct Answer: C) By dilating renal blood vessels
Rationale: Dopamine helps improve perfusion to the kidneys by dilating renal blood vessels, thereby decreasing the risk of renal failure during shock.

66
Q

What dose-dependent effect does dopamine have on the heart?

A) At low doses, it only dilates renal vessels; at high doses, it increases cardiac output.
B) It has no impact on the heart.
C) It increases blood pressure at low doses and decreases heart rate at high doses.
D) It reduces vascular resistance at low doses and causes severe hypotension at high doses.

A

Correct Answer: A) At low doses, it only dilates renal vessels; at high doses, it increases cardiac output.
Rationale: Dopamine’s effects are dose-dependent: lower doses primarily dilate renal blood vessels, while higher doses activate beta-1 receptors, increasing cardiac output.

67
Q

What receptors does epinephrine activate?

A) Alpha-1 and beta-2 receptors only
B) Alpha-1, alpha-2, beta-1, and beta-2 receptors
C) Beta-1 and dopamine receptors only
D) Alpha-1 and beta-1 receptors only

A

Correct Answer: B) Alpha-1, alpha-2, beta-1, and beta-2 receptors
Rationale: Epinephrine activates multiple adrenergic receptors, including alpha-1, alpha-2, beta-1, and beta-2, making it a versatile catecholamine.

68
Q

Which of the following is a common adverse effect associated with epinephrine use?

A) Bradycardia
B) Hypertensive crisis
C) Hypoglycemia
D) Constipation

A

Correct Answer: B) Hypertensive crisis
Rationale: A hypertensive crisis is a significant adverse effect of epinephrine due to its potent vasoconstrictive properties.

69
Q

What is one of the major pharmacological uses of epinephrine?

A) To induce bradycardia
B) To treat severe allergic reactions (anaphylaxis)
C) To lower blood pressure
D) To promote gastrointestinal motility

A

Correct Answer: B) To treat severe allergic reactions (anaphylaxis)
Rationale: Epinephrine is commonly used to treat severe allergic reactions by causing vasoconstriction, bronchodilation, and increasing heart rate.

70
Q

What is the pharmacokinetic route of administration for epinephrine?

A) Oral only
B) Subcutaneous only
C) Topical, IM, and IV
D) Inhalation only

A

Correct Answer: C) Topical, IM, and IV
Rationale: Epinephrine can be administered topically, intramuscularly (IM), or intravenously (IV), allowing for rapid therapeutic effects in emergency situations.

71
Q

Why is the half-life of epinephrine considered short?

A) It is metabolized by catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO).
B) It has a high volume of distribution.
C) It is quickly excreted by the kidneys.
D) It is poorly absorbed in the gastrointestinal tract.

A

Correct Answer: A) It is metabolized by catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO).
Rationale: Epinephrine has a short half-life due to its rapid metabolism by enzymes such as COMT and MAO, which inactivate the drug quickly.

72
Q

Which of the following adverse effects should a nurse monitor for when administering epinephrine?

A) Hypoglycemia and fatigue
B) Arrhythmia and hyperglycemia
C) Sedation and dizziness
D) Hypotension and bradycardia

A

Correct Answer: B) Arrhythmia and hyperglycemia
Rationale: Patients receiving epinephrine may experience arrhythmias due to increased cardiac stimulation and hyperglycemia from glycogenolysis induced by beta-2 receptor activation.

73
Q

What effect do MAO inhibitors have when administered with epinephrine?

A) They decrease the effect of epinephrine.
B) They enhance and intensify the effect of epinephrine.
C) They have no significant interaction with epinephrine.
D) They convert epinephrine into a non-active form.

A

Correct Answer: B) They enhance and intensify the effect of epinephrine.
Rationale: MAO inhibitors can enhance and intensify the effects of epinephrine by inhibiting the breakdown of catecholamines, leading to prolonged effects.

74
Q

How do tricyclic antidepressants affect the action of epinephrine?

A) They decrease the half-life of epinephrine.
B) They block the synthesis of catecholamines.
C) They intensify and prolong the effect of epinephrine.
D) They inhibit the binding of epinephrine to receptors.

A

Correct Answer: C) They intensify and prolong the effect of epinephrine.
Rationale: Tricyclic antidepressants block the reuptake of catecholamines into adrenergic neurons, which prolongs the action of epinephrine and other catecholamines.

75
Q

What is an important nursing consideration when administering epinephrine?

A) Monitor patients for signs of hypotension.
B) Monitor patients for toxicity and be prepared to give an alpha or beta antagonist if necessary.
C) Administer epinephrine without monitoring vital signs.
D) Educate patients about potential sedative effects.

A

Correct Answer: B) Monitor patients for toxicity and be prepared to give an alpha or beta antagonist if necessary.
Rationale: Nurses should monitor for toxicity when administering epinephrine and have antagonists available to counteract any adverse effects if needed.

76
Q

What should a nurse administer if extravasation occurs with an epinephrine infusion?

A) A beta-agonist
B) Phentolamine (an alpha antagonist)
C) A calcium channel blocker
D) A vasodilator

A

Correct Answer: B) Phentolamine (an alpha antagonist)
Rationale: If extravasation occurs, phentolamine can be administered to counteract the vasoconstrictive effects of epinephrine and restore blood flow to the affected area.

77
Q

What effect do alpha and beta-adrenergic blocking drugs (antagonists) have on epinephrine?

A) They enhance the effects of epinephrine.
B) They have no significant effect on epinephrine.
C) They oppose the effects of epinephrine and reduce its action.
D) They increase the half-life of epinephrine.

A

Correct Answer: C) They oppose the effects of epinephrine and reduce its action.
Rationale: Alpha and beta-adrenergic antagonists work by blocking the receptors that epinephrine acts upon, thereby reducing its overall effects in the body.

78
Q

Why is it important to monitor patients closely when administering epinephrine?

A) To ensure they remain sedated and comfortable.
B) To assess for any signs of respiratory distress.
C) To detect potential toxicity and manage adverse effects promptly.
D) To determine if they need additional medications for pain management.

A

Correct Answer: C) To detect potential toxicity and manage adverse effects promptly.
Rationale: Close monitoring is essential to identify any signs of toxicity or adverse effects from epinephrine administration, allowing for timely intervention.

79
Q

What is the primary mechanism of action for adrenergic antagonists?

A) They promote the release of norepinephrine.
B) They directly activate adrenergic receptors.
C) They directly block adrenergic receptors.
D) They inhibit the reuptake of norepinephrine.

A

Correct Answer: C) They directly block adrenergic receptors.
Rationale: Adrenergic antagonists work by directly blocking adrenergic receptors, preventing the action of adrenergic agonists such as epinephrine and norepinephrine.

80
Q

Which statement is true regarding the blockade produced by most adrenergic antagonists?

A) They cause irreversible blockade of adrenergic receptors.
B) They produce competitive blockade, which is reversible.
C) They have no effect on adrenergic receptors.
D) They permanently alter the receptor structure.

A

Correct Answer: B) They produce competitive blockade, which is reversible.
Rationale: Most adrenergic antagonists exert a reversible (competitive) blockade, meaning that their effects can be overcome by increasing levels of agonists.

81
Q

What distinguishes the mechanism of action of adrenergic antagonists from adrenergic agonists?

A) Adrenergic antagonists enhance sympathetic activity.
B) Adrenergic antagonists inhibit norepinephrine release.
C) Adrenergic antagonists block adrenergic receptors while agonists activate them.
D) Adrenergic antagonists promote vasodilation.

A

Correct Answer: C) Adrenergic antagonists block adrenergic receptors while agonists activate them.
Rationale: Adrenergic antagonists inhibit the effects of norepinephrine and epinephrine by blocking their respective receptors, whereas adrenergic agonists activate these receptors to produce physiological responses.

82
Q

Which of the following best describes the action of the non-reversible adrenergic antagonist?

A) It competes with adrenergic agonists for receptor binding.
B) It permanently binds to the receptor and blocks its function.
C) It enhances the effects of norepinephrine.
D) It has no significant clinical applications.

A

Correct Answer: B) It permanently binds to the receptor and blocks its function.
Rationale: Unlike reversible adrenergic antagonists, non-reversible antagonists permanently bind to the receptor, leading to a lasting blockade that cannot be overcome by increasing levels of agonists.

83
Q

What is the primary therapeutic effect of alpha adrenergic antagonists in the treatment of essential hypertension?

A) They increase heart rate.
B) They cause vasodilation by blocking alpha-1 receptors on arterioles and veins.
C) They promote fluid retention.
D) They enhance catecholamine release.

A

Correct Answer: B) They cause vasodilation by blocking alpha-1 receptors on arterioles and veins.
Rationale: Alpha adrenergic antagonists work by blocking alpha-1 receptors, leading to vasodilation, which reduces blood pressure in patients with essential hypertension.

84
Q

In which condition would the administration of an alpha adrenergic antagonist be particularly beneficial?

A) Bradycardia
B) Pheochromocytoma
C) Acute asthma attack
D) Heart failure

A

Correct Answer: B) Pheochromocytoma
Rationale: Alpha adrenergic antagonists are used to manage blood pressure in patients with pheochromocytoma by reducing the hypertensive effects of excess catecholamines.

85
Q

Which of the following effects does an alpha adrenergic antagonist have on the bladder and prostate?

A) Increases bladder capacity.
B) Decreases contraction in the prostatic capsule and bladder neck.
C) Promotes urinary retention.
D) Causes urinary incontinence.

A

Correct Answer: B) Decreases contraction in the prostatic capsule and bladder neck.
Rationale: Alpha adrenergic antagonists can help alleviate symptoms of benign prostatic hyperplasia (BPH) by decreasing contractions in the prostatic capsule and bladder neck, facilitating easier urination.

86
Q

Which of the following adverse effects is associated with alpha-1 adrenergic antagonists due to their action on veins?

A) Reflex bradycardia
B) Orthostatic hypotension
C) Hyperglycemia
D) Tachypnea

A

Correct Answer: B) Orthostatic hypotension
Rationale: Alpha-1 adrenergic antagonists can cause orthostatic hypotension by reducing muscle tone in the veins, leading to blood pooling and decreased blood return to the heart when a patient stands up, resulting in lower blood pressure.

87
Q

A patient receiving an alpha-1 adrenergic antagonist reports feeling dizzy and lightheaded when standing up. What is the appropriate nursing intervention?

A) Encourage the patient to increase fluid intake.
B) Instruct the patient to stand up quickly.
C) Monitor the patient’s heart rate regularly.
D) Educate the patient on safety measures to prevent falls.

A

Correct Answer: D) Educate the patient on safety measures to prevent falls.
Rationale: Patients experiencing orthostatic hypotension should be educated on safety measures to prevent falls, such as standing up slowly and using assistive devices if necessary.

88
Q

Reflex tachycardia may occur in patients taking alpha-1 adrenergic antagonists. What causes this phenomenon?

A) Direct stimulation of the heart
B) Increased sympathetic nervous system activity
C) Baroreceptor reflex activation
D) Decreased blood volume

A

Correct Answer: C) Baroreceptor reflex activation
Rationale: Reflex tachycardia occurs as a compensatory mechanism when blood pressure drops; the baroreceptors detect the decrease and stimulate the heart to increase the heart rate.

89
Q

Which adverse effect of alpha-1 adrenergic antagonists is caused by vasodilation of the nasal mucosa?

A) Reflex bradycardia
B) Orthostatic hypotension
C) Nasal congestion
D) Ejaculatory dysfunction

A

Correct Answer: C) Nasal congestion
Rationale: Alpha-1 adrenergic antagonists can cause nasal congestion due to vasodilation of the nasal mucosa, which may lead to increased blood flow and swelling in that area.

90
Q

Prazosin is primarily used for which of the following conditions?

A) Heart failure and shock
B) Hypertension and benign prostatic hyperplasia (BPH)
C) Asthma and chronic obstructive pulmonary disease (COPD)
D) Anxiety and depression

A

Correct Answer: B) Hypertension and benign prostatic hyperplasia (BPH)
Rationale: Prazosin is an alpha-1 adrenergic antagonist that is commonly used to treat hypertension and relieve urinary symptoms associated with benign prostatic hyperplasia (BPH).

91
Q

How can the use of alpha-1 adrenergic antagonists affect sexual function in male patients?

A) They enhance libido.
B) They inhibit ejaculation.
C) They improve erectile function.
D) They cause gynecomastia.

A

Correct Answer: B) They inhibit ejaculation.
Rationale: Alpha-1 adrenergic antagonists can inhibit ejaculation because ejaculation is mediated by alpha-1 receptors. It is important for healthcare providers to discuss this potential side effect with male patients to improve compliance with medication regimens.

92
Q

A patient is prescribed prazosin. Which nursing consideration is essential for managing potential adverse effects?

A) Instruct the patient to abruptly change positions to increase blood flow.
B) Educate the patient about the possibility of nasal congestion and reflex tachycardia.
C) Encourage the patient to take the medication at any time of day.
D) Advise the patient to take higher doses to minimize side effects.

A

Correct Answer: B) Educate the patient about the possibility of nasal congestion and reflex tachycardia.
Rationale: It is important to educate patients about potential adverse effects of prazosin, including nasal congestion and reflex tachycardia, to ensure they understand what to expect and when to seek help.

93
Q

What is the recommended nursing action to minimize postural hypotension in a patient taking prazosin?

A) Administer the medication in the morning.
B) Encourage the patient to increase fluid intake.
C) Instruct the patient to sit or lie down if feeling dizzy.
D) Advise the patient to take the medication with food.

A

Correct Answer: C) Instruct the patient to sit or lie down if feeling dizzy.
Rationale: Patients taking prazosin should be advised to sit or lie down if they experience dizziness to prevent falls related to postural hypotension.

94
Q

Which nursing consideration is specifically recommended for administering prazosin to reduce the effects of postural hypotension?

A) Administer before bed
B) Administer with a full glass of water
C) Administer with a high-fat meal
D) Administer in the morning with breakfast

A

Correct Answer: A) Administer before bed
Rationale: Administering prazosin before bedtime can help reduce the effects of postural hypotension, as the risk of dizziness upon standing is minimized during nighttime when the patient is already lying down.

95
Q

When prescribing prazosin, what is the recommended approach regarding dosing?

A) Start with the maximum dose to quickly control symptoms.
B) Begin with smaller doses and gradually increase as needed.
C) Use the same dose for all patients, regardless of symptoms.
D) Discontinue medication if the patient experiences side effects.

A

Correct Answer: B) Begin with smaller doses and gradually increase as needed.
Rationale: Starting with smaller doses of prazosin helps minimize adverse effects and allows for adjustments based on the patient’s response to the medication.

96
Q

What is the primary pharmacological effect of propranolol?

A) Selective blockade of beta-1 receptors only
B) Nonselective blockade of both beta-1 and beta-2 receptors
C) Selective stimulation of beta-1 receptors
D) Nonselective stimulation of both beta-1 and beta-2 receptors

A

Correct Answer: B) Nonselective blockade of both beta-1 and beta-2 receptors
Rationale: Propranolol is a nonselective beta-adrenergic antagonist, meaning it blocks both beta-1 and beta-2 receptors.

97
Q

Which of the following is a common use of propranolol?

A) Management of asthma
B) Treatment of hypertension and angina
C) Treatment of diabetes mellitus
D) Management of allergic reactions

A

Correct Answer: B) Treatment of hypertension and angina
Rationale: Propranolol is commonly used for cardiac conditions, including hypertension, angina, and dysrhythmias

98
Q

A patient taking propranolol experiences bradycardia. Which of the following actions should the nurse take?
A) Increase the dosage of propranolol.
B) Notify the healthcare provider and monitor the patient’s heart rate.
C) Administer a dose of epinephrine.
D) Encourage the patient to increase physical activity.

A

Correct Answer: B) Notify the healthcare provider and monitor the patient’s heart rate.
Rationale: Bradycardia is a known adverse effect of propranolol; the nurse should notify the healthcare provider and monitor the patient’s heart rate for any further changes.

99
Q

What adverse effect may result from the nonselective blockade of beta-2 receptors by propranolol?

A) Hypertension
B) Bronchoconstriction
C) Tachycardia
D) Hyperglycemia

A

Correct Answer: B) Bronchoconstriction
Rationale: Nonselective beta blockers like propranolol can cause bronchoconstriction due to the blockade of beta-2 receptors in the lungs, which is particularly concerning for patients with asthma or other respiratory conditions.

100
Q

Which statement regarding the pharmacokinetics of propranolol is correct?

A) It is water-soluble and does not cross the blood-brain barrier.
B) It is lipid-soluble and can cross the blood-brain barrier.
C) It is only effective when administered orally.
D) It has a long half-life and is administered once daily.

A

Correct Answer: B) It is lipid-soluble and can cross the blood-brain barrier.
Rationale: Propranolol is lipid-soluble, allowing it to cross the blood-brain barrier and affect central nervous system functions, which can lead to CNS-related adverse effects.

101
Q

What should the nurse educate a patient about when discontinuing propranolol?

A) It can be stopped abruptly without any consequences.
B) Gradual tapering of the medication is necessary to prevent rebound excitation.
C) There is no need to adjust the dosage over time.
D) Discontinuation will not affect heart rate.

A

Correct Answer: B) Gradual tapering of the medication is necessary to prevent rebound excitation.
Rationale: Abrupt discontinuation of propranolol can lead to rebound excitation, causing increased heart rate and blood pressure; therefore, it should be tapered gradually under medical supervision.

102
Q

A patient with a severe allergy is prescribed propranolol. What important information should the nurse provide regarding the use of epinephrine in case of an allergic reaction?

A) Epinephrine will be effective despite the propranolol.
B) Epinephrine may not be as effective due to blockade of beta receptors.
C) The patient can safely use both medications simultaneously.
D) The patient should not carry epinephrine if taking propranolol.

A

Correct Answer: B) Epinephrine may not be as effective due to blockade of beta receptors.
Rationale: Propranolol blocks beta receptors, which can reduce the effectiveness of epinephrine in treating severe allergic reactions.

103
Q

Which of the following patient conditions should the nurse be cautious about when administering propranolol?

A) Asthma
B) Hypertension
C) Osteoporosis
D) Hyperlipidemia

A

Correct Answer: A) Asthma
Rationale: Propranolol is a nonselective beta blocker and can cause bronchoconstriction, making it potentially harmful to patients with asthma.

104
Q

What effect can propranolol have on insulin-induced hypoglycemia in diabetic patients?

A) It enhances the recognition of hypoglycemia symptoms.
B) It has no effect on hypoglycemia recognition.
C) It can impede early recognition of hypoglycemia and inhibit the body’s ability to correct it.
D) It increases the insulin levels, making hypoglycemia more severe.

A

Correct Answer: C) It can impede early recognition of hypoglycemia and inhibit the body’s ability to correct it.
Rationale: Propranolol can mask the symptoms of hypoglycemia and inhibit glycogenolysis, making it harder for patients to recognize and correct low blood sugar levels.

105
Q

When considering drug interactions with propranolol, which of the following combinations could lead to excessive cardiosuppression?

A) Propranolol and insulin
B) Propranolol and calcium channel blockers
C) Propranolol and non-steroidal anti-inflammatory drugs (NSAIDs)
D) Propranolol and diuretics

A

Correct Answer: B) Propranolol and calcium channel blockers
Rationale: Calcium channel blockers can have a similar effect on heart rate and contractility as propranolol, and using them together can lead to synergistic effects and excessive cardiosuppression.

106
Q

In educating a patient with diabetes who is starting propranolol, what key point should the nurse emphasize?

A) Propranolol will improve their insulin sensitivity.
B) They will not need to monitor their blood glucose levels as often.
C) Propranolol can mask symptoms of hypoglycemia and affect blood sugar control.
D) They should increase their carbohydrate intake while on propranolol.

A

Correct Answer: C) Propranolol can mask symptoms of hypoglycemia and affect blood sugar control.
Rationale: It’s essential for patients with diabetes to be aware that propranolol may mask the symptoms of hypoglycemia, making it harder to recognize low blood sugar levels.

107
Q

What is a key characteristic of beta blockers with intrinsic sympathomimetic activity (ISA)?

A) They completely block beta receptors, preventing any activation.
B) They act as strong agonists, increasing heart rate and cardiac output.
C) They bind to beta receptors but produce a limited degree of activation.
D) They have no effect on heart rate or cardiac output.

A

Correct Answer: C) They bind to beta receptors but produce a limited degree of activation.
Rationale: Beta blockers with ISA, such as pindolol, partially activate beta receptors while preventing strong agonists from binding.

108
Q

Why might pindolol be prescribed to a patient with bradycardia?

A) It increases heart rate significantly.
B) It has no effect on heart rate.
C) It provides some activation of beta receptors, helping to manage heart rate.
D) It completely blocks beta receptors, preventing any further decrease in heart rate.

A

Correct Answer: C) It provides some activation of beta receptors, helping to manage heart rate.
Rationale: Pindolol, as a beta blocker with ISA, offers a limited degree of activation which can be beneficial in patients with bradycardia.

109
Q

Which statement accurately describes the effect of beta blockers with intrinsic sympathomimetic activity on the sympathetic nervous system (SNS)?

A) They cause significant SNS activation and increase heart rate.
B) They prevent strong agonists from binding and causing significant activation.
C) They have no impact on the sympathetic nervous system.
D) They completely inhibit all adrenergic responses.

A

Correct Answer: B) They prevent strong agonists from binding and causing significant activation.
Rationale: Beta blockers with ISA can inhibit the full activation of beta receptors by strong agonists while still providing some degree of activation themselves.

110
Q

What is the primary benefit of using a beta blocker with intrinsic sympathomimetic activity in patients with certain cardiac conditions?

A) It eliminates the risk of bradycardia.
B) It prevents hypotension by enhancing cardiac output.
C) It minimizes the effects of excessive sympathetic activation while providing some receptor activity.
D) It increases myocardial oxygen demand significantly.

A

Correct Answer: C) It minimizes the effects of excessive sympathetic activation while providing some receptor activity.
Rationale: Beta blockers with ISA can help manage conditions where some receptor activation is desired without the full effect of stronger agonists.

111
Q

Which of the following patients would most likely benefit from a beta blocker with intrinsic sympathomimetic activity?

A) A patient with uncontrolled hypertension and tachycardia.
B) A patient with bradycardia and a history of heart failure.
C) A patient experiencing frequent angina attacks.
D) A patient recovering from a myocardial infarction.

A

Correct Answer: B) A patient with bradycardia and a history of heart failure.
Rationale: A beta blocker with ISA like pindolol can provide necessary receptor activity without exacerbating bradycardia, making it suitable for patients with this condition.

112
Q

Which patient condition would likely benefit from the use of indirect-acting antiadrenergic agents?

A) A patient experiencing acute heart failure.
B) A patient with hypertension requiring long-term management.
C) A patient with bradycardia and low cardiac output.
D) A patient with chronic obstructive pulmonary disease (COPD).

A

Correct Answer: B) A patient with hypertension requiring long-term management.
Rationale: Indirect-acting antiadrenergic agents are often used to manage hypertension by reducing sympathetic nervous system activity and lowering blood pressure.

113
Q

What is a primary therapeutic goal of using indirect-acting antiadrenergic agents?

A) To increase heart rate and cardiac output.
B) To enhance peripheral vasoconstriction.
C) To reduce blood pressure by decreasing sympathetic outflow.
D) To stimulate the release of norepinephrine in the CNS.

A

Correct Answer: C) To reduce blood pressure by decreasing sympathetic outflow.
Rationale: These agents aim to lower blood pressure by inhibiting SNS activity, which leads to decreased norepinephrine levels and reduced peripheral adrenergic receptor activation.

114
Q

Which of the following best describes the action of indirect-acting antiadrenergic agents?

A) They act only on alpha receptors in the periphery.
B) They mimic the effects of adrenergic agonists.
C) They have similar effects to adrenergic antagonists (blockers).
D) They directly stimulate beta receptors in the heart.

A

Correct Answer: C) They have similar effects to adrenergic antagonists (blockers).
Rationale: Indirect-acting antiadrenergic agents function similarly to adrenergic antagonists by reducing sympathetic nervous system activity and decreasing norepinephrine’s effects on adrenergic receptors.

115
Q

What is the ultimate effect of using indirect-acting antiadrenergic agents on peripheral adrenergic receptors?

A) Increased activation of peripheral adrenergic receptors.
B) Decreased activation of peripheral adrenergic receptors.
C) No change in activation of peripheral adrenergic receptors.
D) Direct stimulation of peripheral adrenergic receptors.

A

Correct Answer: B) Decreased activation of peripheral adrenergic receptors.
Rationale: By inhibiting the firing of SNS neurons, these agents decrease the amount of norepinephrine released, leading to reduced activation of peripheral adrenergic receptors.

116
Q

Which of the following is a primary therapeutic use of clonidine?

A) Asthma
B) Hypertension
C) Diabetes
D) Parkinson’s Disease

A

Correct Answer:
B) Hypertension

Rationale:
Clonidine is a central-acting α2 agonist used primarily for the treatment of hypertension by reducing sympathetic outflow to the heart and blood vessels, which lowers blood pressure. It is not used to treat asthma, diabetes, or Parkinson’s disease.

117
Q

Clonidine works by activating α2 receptors in which part of the body?

A) Peripheral blood vessels
B) Kidneys
C) Brainstem
D) Heart muscle

A

Correct Answer:
C) Brainstem

Rationale:
Clonidine acts centrally by activating α2 receptors in the brainstem, particularly in areas involved in the autonomic regulation of the cardiovascular system, reducing sympathetic nerve signals to the heart and blood vessels. This mechanism lowers blood pressure.

118
Q

Which of the following is a common adverse effect of clonidine?

A) Hypertension
B) Dry mouth (xerostomia)
C) Increased heart rate
D) Insomnia

A

Correct Answer:
B) Dry mouth (xerostomia)

Rationale:
A very common adverse effect of clonidine is dry mouth (xerostomia), which often contributes to non-compliance in patients. The drug decreases sympathetic outflow, which can reduce salivation. Hypertension, increased heart rate, and insomnia are not common side effects; in fact, clonidine lowers blood pressure and heart rate and may cause sedation.

119
Q

Which of the following adverse effects can occur with clonidine withdrawal?

A) Hypotension
B) Rebound hypertension
C) Increased salivation
D) Hyperglycemia

A

Correct Answer:
B) Rebound hypertension

Rationale:
Abrupt withdrawal of clonidine can cause rebound hypertension due to rapid sympathetic outflow. This effect is significant because clonidine reduces blood pressure by inhibiting sympathetic nerve activity, and stopping the drug suddenly can lead to a surge in blood pressure. Gradual tapering is necessary to avoid this.

120
Q

Which patient population should avoid using clonidine based on animal studies?

A) Diabetic patients
B) Pregnant women
C) Patients with hypertension
D) Adolescents

A

Correct Answer:
B) Pregnant women

Rationale:
Clonidine has shown to be embryotoxic in animal studies, meaning it poses risks to the developing fetus. Therefore, it should be used with caution or avoided in pregnant women unless absolutely necessary.