Week Three Flashcards
What are adrenergic agonists also known as?
A) Sympatholytics
B)Sympathomimetic
C) Cholinergics
D) Antagonists
Correct Answer: B) Sympathomimetics
Rationale: Adrenergic agonists are commonly referred to as sympathomimetics because they mimic the effects of the sympathetic nervous system.
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
Correct Answer: B) Direct receptor binding
Rationale: The most common mechanism for activating adrenergic receptors by adrenergic agonists is through direct receptor binding.
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
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.
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
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.
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
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.
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
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.
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
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.
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
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.
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
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.
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.
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.
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
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.
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
Correct Answer: B) MAO and COMT
Rationale: Catecholamines are inactivated by the enzymes monoamine oxidase (MAO) and catechol-O-methyltransferase (COMT).
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.
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.
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.
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.
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.
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.
Which of the following is NOT an example of a catecholamine?
A) Norepinephrine (NE)
B) Epinephrine (Epi)
C) Isoproterenol
D) Atropine
Correct Answer: D) Atropine
Rationale: Atropine is an anticholinergic medication, not a catecholamine. Examples of catecholamines include norepinephrine, epinephrine, isoproterenol, dopamine, and dobutamine.
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.
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.
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.
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.
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.
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.
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
Correct Answer: C) Short duration of action
Rationale: Non-catecholamines typically have a longer duration of action, unlike catecholamines, which have a brief duration.
Which of the following non-catecholamines can cross the blood-brain barrier (BBB)?
A) Phenylephrine
B) Albuterol
C) Norepinephrine
D) Epinephrine
Correct Answer: B) Albuterol
Rationale: Non-catecholamines, such as albuterol, can cross the blood-brain barrier, unlike catecholamines, which generally cannot.
Which of the following is an example of a non-catecholamine?
A) Dopamine
B) Phenylephrine
C) Isoproterenol
D) Epinephrine
Correct Answer: B) Phenylephrine
Rationale: Phenylephrine is an example of a non-catecholamine, while dopamine, isoproterenol, and epinephrine are classified as catecholamines.
Which of the following drugs is NOT classified as an alpha-1 agonist?
A) Norepinephrine (NE)
B) Phenylephrine
C) Ephedrine
D) Albuterol
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.
What therapeutic response is primarily associated with alpha-1 activation?
A) Bronchodilation
B) Vasoconstriction
C) Increased heart rate
D) Decreased gastrointestinal motility
Correct Answer: B) Vasoconstriction
Rationale: Alpha-1 activation primarily causes vasoconstriction, particularly in the skin, viscera, and mucous membranes.
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.
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.
Which alpha-1 agonist is commonly used to cause pupil dilation during eye exams?
A) Ephedrine
B) Norepinephrine
C) Phenylephrine
D) Pseudoephedrine
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.
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
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.
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
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.
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
Correct Answer: C) Hypertension
Rationale: Alpha-1 agonist activation can cause widespread vasoconstriction, leading to hypertension, especially with continuous IV infusions.
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
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.
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
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.
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
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.
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
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.
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
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.
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
Correct Answer: B) Inhibit norepinephrine (NE) release
Rationale: Activation of alpha-2 receptors inhibits the release of norepinephrine, leading to decreased sympathetic transmission.
Where are alpha-2 receptors primarily located?
A) Post-synaptic neurons
B) Peripheral blood vessels
C) Pre-synaptic neurons
D) Cardiac tissues
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.
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
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
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.
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.
Which of the following is a potential adverse effect of alpha-2 agonists?
A) Hypertension
B) Increased heart rate
C) Sedation
D) Tachycardia
Correct Answer: C) Sedation
Rationale: Alpha-2 agonists can cause sedation due to their central nervous system effects, while they typically reduce sympathetic transmission.
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
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.
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
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.
Which of the following drugs is NOT a beta-1 agonist?
A) Dobutamine
B) Isoproterenol
C) Epinephrine
D) Phenylephrine
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.
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
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.
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.
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.
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.
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.
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
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.
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
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.
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
Correct Answer: C) Angina (chest pain)
Rationale: Beta-1 agonists can increase myocardial oxygen demand, which may worsen angina in susceptible patients.