Week Four Flashcards

1
Q

What are the three important processes of kidney function?

A) Filtration, diffusion, osmosis
B) Filtration, reabsorption, active tubular secretion
C) Filtration, absorption, active secretion
D) Secretion, absorption, excretion

A

Correct Answer:
B) Filtration, reabsorption, active tubular secretion

Rationale:
Kidney function relies on three main processes: filtration (where substances are filtered out of the blood), reabsorption (where important molecules like water and electrolytes are reabsorbed), and active tubular secretion (where waste products are secreted into the nephron for excretion).

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2
Q

Where does reabsorption occur in the nephron?
(Select all that apply)

A) Proximal convoluted tubule (PCT)
B) Loop of Henle
C) Early distal convoluted tubule (DCT)
D) Late distal convoluted tubule (DCT)

A

Correct Answer:
A) Proximal convoluted tubule (PCT)
B) Loop of Henle
C) Early distal convoluted tubule (DCT)
D) Late distal convoluted tubule (DCT)
Rationale:
Reabsorption occurs in multiple parts of the nephron, including the PCT, Loop of Henle, and both the early and late DCT, which are key areas where substances such as water, electrolytes, and nutrients are reabsorbed back into the bloodstream.

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3
Q

How do most diuretics work in the nephron?

A) They increase water absorption
B) They block sodium and chloride reabsorption
C) They enhance glucose excretion
D) They stimulate the release of antidiuretic hormone (ADH)

A

Correct Answer:
B) They block sodium and chloride reabsorption

Rationale:
Most diuretics work by blocking the reabsorption of sodium (Na) and chloride (Cl) in the nephron, preventing water from being reabsorbed into the bloodstream, which increases urine output.

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4
Q

What is the relationship between sodium reabsorption and urine volume?

A) The more sodium reabsorption is blocked, the less water is in the urine
B) The amount of water in the urine is proportional to the amount of sodium reabsorption that is blocked
C) Blocking sodium reabsorption decreases urine volume
D) There is no connection between sodium reabsorption and urine volume

A

Correct Answer:
B) The amount of water in the urine is proportional to the amount of sodium reabsorption that is blocked

Rationale:
The volume of water in the urine is directly proportional to how much sodium reabsorption is blocked. The more sodium reabsorption is blocked, the more water remains in the urine, leading to increased urine output.

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5
Q

Which part of the nephron would impact urine volume the most when blocked by a diuretic?

A) Proximal convoluted tubule (PCT)
B) Loop of Henle
C) Early distal convoluted tubule (DCT)
D) Collecting duct

A

Correct Answer:
B) Loop of Henle

Rationale:
Blocking sodium and chloride reabsorption in the Loop of Henle will have the greatest impact on urine volume, as a significant amount of sodium and water is reabsorbed here. A medication acting on this part of the nephron would cause the most diuretic effect, leading to a larger volume of urine.

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6
Q

How much filtrate do the kidneys create per day, and how is it managed by the body?

A) 125mL/day, most of it is excreted
B) 180L/day, most of it is reabsorbed
C) 50L/day, none of it is reabsorbed
D) 200L/day, some of it is reabsorbed

A

Correct Answer:
B) 180L/day, most of it is reabsorbed

Rationale:
The kidneys produce 125mL of filtrate per hour, which equals 180 liters per day. Most of this filtrate is reabsorbed back into the body, leaving only a small portion to be excreted as urine.

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7
Q

What could be the potential negative effects of diuretics that block sodium reabsorption?

A) Increased blood volume
B) Electrolyte imbalances and dehydration
C) Hypertension and water retention
D) Reduced urine output

A

Correct Answer:
B) Electrolyte imbalances and dehydration

Rationale:
Blocking sodium reabsorption causes more water to be excreted, which can lead to electrolyte imbalances (like low sodium or potassium) and dehydration due to increased urine output.

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8
Q

What strategies can be used to minimize the negative effects of diuretics?

A) Give long-acting diuretics
B) Time administration to allow drug-free periods
C) Increase the dose of diuretics
D) Avoid using diuretics altogether

A

Correct Answer:
B) Time administration to allow drug-free periods

Rationale:
To reduce the risk of dehydration and electrolyte imbalances, diuretics can be given as short-acting medications or administered in a way that allows the kidneys to have drug-free periods, helping the body maintain better balance between fluid and electrolyte levels.

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9
Q

What is the primary mechanism of action of loop diuretics such as Lasix and Furosemide?

A) They act on the proximal convoluted tubule
B) They act in the descending limb of the loop of Henle
C) They prevent the reabsorption of Na in the ascending limb of the loop of Henle
D) They increase the reabsorption of water in the distal convoluted tubule

A

Correct Answer:
C) They prevent the reabsorption of Na in the ascending limb of the loop of Henle

Rationale:
Loop diuretics like Lasix and Furosemide act specifically in the ascending limb of the loop of Henle, where they inhibit sodium reabsorption, leading to increased urine output.

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10
Q

What is the expected onset of diuresis when loop diuretics are administered orally versus intravenously?

A) Oral: diuresis in 5 minutes; IV: diuresis in 60 minutes
B) Oral: diuresis in 60 minutes; IV: diuresis in 5 minutes
C) Both routes cause diuresis in 30 minutes
D) Oral: diuresis in 2 hours; IV: diuresis in 1 hour

A

Correct Answer:
B) Oral: diuresis in 60 minutes; IV: diuresis in 5 minutes

Rationale:
Loop diuretics taken orally typically lead to diuresis within 60 minutes, while IV administration results in diuresis within 5 minutes, making IV use suitable for critical needs.

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11
Q

What is the duration of action for loop diuretics when given orally and intravenously?

A) Oral: 5 hours; IV: 60 minutes
B) Oral: 8 hours; IV: 2 hours
C) Both routes last for 8 hours
D) Oral: 2 hours; IV: 4 hours

A

Correct Answer:
B) Oral: 8 hours; IV: 2 hours

Rationale:
The effects of loop diuretics last approximately 8 hours when taken orally and 2 hours when given IV, reflecting their pharmacokinetic profiles.

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12
Q

What are the routes of administration for loop diuretics like Lasix and Furosemide?

A) Oral and topical
B) Oral, IV, and IM
C) Only oral
D) IV and subcutaneous

A

Correct Answer:
B) Oral, IV, and IM

Rationale:
Loop diuretics can be administered through various routes, including oral, intravenous (IV), and intramuscular (IM), providing flexibility in treatment based on the clinical scenario.

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13
Q

What are the primary uses of loop diuretics like Lasix and Furosemide?

A) To promote weight gain
B) For rapid/large fluid excretion when needed
C) To increase sodium reabsorption
D) For treating infections

A

Correct Answer:
B) For rapid/large fluid excretion when needed

Rationale:
Loop diuretics, such as Lasix and Furosemide, are primarily used when rapid or large fluid excretion is required, making them effective in various clinical situations.

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14
Q

In which situation can loop diuretics be beneficial even when kidney function is compromised?

A) Only when GFR is normal
B) When the glomerular filtration rate (GFR) is low
C) They should not be used with low GFR
D) Only in cases of chronic kidney disease

A

Correct Answer:
B) When the glomerular filtration rate (GFR) is low

Rationale:
Loop diuretics can be effective even when the GFR is low, which allows for diuresis and management of fluid overload in patients with kidney injuries.

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15
Q

What are some common adverse effects associated with the use of Lasix and Furosemide?

A) Hypernatremia and hyperchloremia
B) Hyponatremia, hypochloremia, and dehydration
C) Weight gain and hypertension
D) Increased appetite and insomnia

A

Correct Answer:
B) Hyponatremia, hypochloremia, and dehydration

Rationale:
The use of loop diuretics can lead to hyponatremia, hypochloremia, and dehydration, which are important adverse effects to monitor during treatment.

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16
Q

How can the use of loop diuretics like Lasix and Furosemide impact blood pressure?

A) They can cause hypertension
B) They can lead to hypotension
C) They have no effect on blood pressure
D) They increase heart rate but do not affect blood pressure

A

Correct Answer:
B) They can lead to hypotension

Rationale:
Loop diuretics can cause hypotension due to significant fluid loss, which is a critical adverse effect to consider when managing patients on these medications.

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17
Q

What is a common electrolyte imbalance that may occur with the use of Lasix and Furosemide?

A) Hyperkalemia
B) Hyponatremia
C) Hypercalcemia
D) Hypophosphatemia

A

Correct Answer:
B) Hyponatremia

Rationale:
The use of Lasix and Furosemide can lead to hyponatremia due to a lack of sodium reabsorption in the kidneys, which necessitates monitoring for signs and symptoms of dehydration.

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18
Q

What symptoms should be monitored to assess for dehydration in patients taking Lasix or Furosemide?

A) Weight gain and swelling
B) Dizziness, lightheadedness, and syncope
C) Increased thirst and dry skin
D) Hyperactivity and insomnia

A

Correct Answer:
B) Dizziness, lightheadedness, and syncope

Rationale:
Patients on Lasix and Furosemide should be monitored for dizziness, lightheadedness, and syncope, which are signs of hypotension and potential dehydration due to volume loss.

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19
Q

What dietary recommendations should be made to a patient taking Lasix to manage potassium levels?

A) Increase sodium intake
B) Eat potassium-rich foods or consider taking a potassium supplement
C) Limit fluid intake
D) Decrease protein consumption

A

Correct Answer:
B) Eat potassium-rich foods or consider taking a potassium supplement

Rationale:
Since Lasix and Furosemide can cause hypokalemia, it’s important to promote the consumption of potassium-rich foods or consider a potassium supplement to maintain levels within the normal range (3.5-5 mmol/L).

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20
Q

What is a potential auditory side effect of Lasix and Furosemide?

A) Hearing loss that is always permanent
B) Ototoxicity that may be transient with Lasix
C) Enhanced hearing
D) Ringing in the ears that is always reversible

A

Correct Answer:
B) Ototoxicity that may be transient with Lasix

Rationale:
Ototoxicity is a potential adverse effect of Lasix, which may be transient; however, it can be permanent with other loop diuretics, necessitating monitoring of auditory function in patients receiving these medications.

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21
Q

What are the signs and symptoms of hypotension that a patient taking Lasix should be educated to monitor for?

A) Increased appetite and weight gain
B) Dizziness, lightheadedness, and syncope
C) Elevated heart rate and sweating
D) Nausea and vomiting

A

Correct Answer:
B) Dizziness, lightheadedness, and syncope

Rationale:
Patients on Lasix should be educated to monitor for signs of hypotension, such as dizziness, lightheadedness, and syncope, due to volume loss from diuresis, which can lead to decreased blood pressure.

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22
Q

How should a nurse manage a patient experiencing dehydration due to the use of Lasix?

A) Increase the patient’s sodium intake immediately
B) Administer IV fluids as needed and monitor electrolyte levels
C) Encourage the patient to take more diuretics
D) Advise the patient to drink caffeinated beverages

A

Correct Answer:
B) Administer IV fluids as needed and monitor electrolyte levels

Rationale:
In cases of dehydration caused by Lasix, the nurse should administer IV fluids as needed and continuously monitor electrolyte levels to prevent complications such as hyponatremia and hypokalemia.

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23
Q

What is the primary concern when a patient on Lasix is also taking Digoxin?

A) Risk of hyperkalemia
B) Increased risk of toxicity when the patient is hypokalemic
C) Decreased effectiveness of Lasix
D) Increased diuretic effect

A

Correct Answer:
B) Increased risk of toxicity when the patient is hypokalemic

Rationale:
When a patient is on Lasix, there is a high risk of Digoxin toxicity if the patient becomes hypokalemic, as low potassium levels can increase the risk of adverse effects from Digoxin.

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24
Q

What should a nurse be cautious about when a patient on Lasix is prescribed another ototoxic drug?

A) The risk of electrolyte imbalance
B) Increased risk of hearing loss
C) Enhanced diuretic effect
D) Reduced effectiveness of both drugs

A

Correct Answer:
B) Increased risk of hearing loss

Rationale:
Administering Lasix with other ototoxic drugs can lead to an increased risk of hearing loss, so careful monitoring of hearing function is essential.

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25
Q

How might the administration of potassium-sparing diuretics affect a patient taking Lasix?

A) They can increase the potassium-wasting effect of Lasix.
B) They can enhance the diuretic effect of Lasix.
C) They can counteract the potassium-wasting effect of Lasix.
D) They have no effect on the action of Lasix.

A

Correct Answer:
C) They can counteract the potassium-wasting effect of Lasix.

Rationale:
Potassium-sparing diuretics can help counteract the potassium-wasting effect of Lasix, making it safer for patients who are at risk of hypokalemia.

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26
Q

Which patient statement indicates a need for further education about drug interactions with Lasix?

A) “I need to be careful if I’m taking Digoxin.”
B) “I can take any pain reliever without any concern.”
C) “I should let my doctor know if I start taking other diuretics.”
D) “I understand I might need to monitor my potassium levels.”

A

Correct Answer:
B) “I can take any pain reliever without any concern.”

Rationale:
This statement shows a lack of understanding about potential drug interactions with Lasix; some pain relievers may interact with diuretics or affect kidney function, so patients need to consult with their healthcare provider before taking them.

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27
Q

How does the diuretic effect of thiazide diuretics compare to loop diuretics?
A) Thiazide diuretics have a stronger effect than loop diuretics.
B) Thiazide diuretics have a similar effect to loop diuretics.
C) Thiazide diuretics have a less potent effect than loop diuretics.
D) Thiazide diuretics do not have a diuretic effect.

A

Correct Answer: C) Thiazide diuretics have a less potent effect than loop diuretics.
Rationale: The effect of thiazide diuretics is less than that of loop diuretics.

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28
Q

Why are thiazide diuretics not used in patients with kidney disease?
A) They can cause hyperkalemia.
B) They have no effect on urine flow.
C) They are ineffective if kidney function is impaired.
D) They cause excessive sodium retention.

A

Correct Answer: C) They are ineffective if kidney function is impaired.
Rationale: The diuretic effect of thiazide diuretics is dependent on kidney function and urine flow, making them unsuitable for patients with kidney disease.

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29
Q

What is a common outcome when using thiazide diuretics?
A) Increased potassium retention
B) Decreased excretion of sodium
C) Increased renal excretion of water
D) Increased reabsorption of chloride

A

Correct Answer: C) Increased renal excretion of water
Rationale: Thiazide diuretics increase the excretion of sodium and chloride, which leads to increased renal excretion of water.

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30
Q

Which of the following is a reason to avoid thiazide diuretics in certain patients?
A) Their effect is enhanced by kidney disease.
B) They can cause significant diuresis in all patients.
C) Their effectiveness is dependent on adequate kidney function.
D) They promote the reabsorption of sodium and water.

A

Correct Answer: C) Their effectiveness is dependent on adequate kidney function.
Rationale: Thiazide diuretics are not effective if kidney function is compromised.

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31
Q

What is the primary mechanism of action of Hydrochlorothiazide?
A) Increases water reabsorption in the loop of Henle
B) Blocks sodium and chloride reabsorption in the early segment of the distal convoluted tubule (DCT)
C) Inhibits potassium reabsorption in the nephron
D) Increases potassium secretion in the collecting duct

A

Correct Answer: B) Blocks sodium and chloride reabsorption in the early segment of the distal convoluted tubule (DCT)
Rationale: Hydrochlorothiazide works by blocking sodium and chloride reabsorption in the early segment of the DCT.

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32
Q

What percentage of sodium and chloride reabsorption occurs in the early segment of the DCT where Hydrochlorothiazide acts?
A) 20%
B) 50%
C) 10%
D) 30%

A

Correct Answer: C) 10%
Rationale: Hydrochlorothiazide blocks the reabsorption of only 10% of sodium and chloride that occurs in the early segment of the DCT.

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33
Q

When does diuresis begin after oral administration of Hydrochlorothiazide?
A) 1 hour
B) 2 hours
C) 4 hours
D) 6 hours

A

Correct Answer: B) 2 hours
Rationale: Diuresis begins about 2 hours after oral administration of Hydrochlorothiazide.

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34
Q

What is the peak effect time for Hydrochlorothiazide after administration?
A) 1 hour
B) 2 hours
C) 4 hours
D) 12 hours

A

Correct Answer: C) 4 hours
Rationale: The peak effect of Hydrochlorothiazide occurs at approximately 4 hours after administration.

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35
Q

What is a significant characteristic of Hydrochlorothiazide’s pharmacokinetics?
A) It undergoes extensive hepatic metabolism.
B) It has a long duration of action.
C) It is excreted unchanged in urine.
D) It requires renal metabolism for efficacy.

A

Correct Answer: C) It is excreted unchanged in urine.
Rationale: Hydrochlorothiazide is excreted unchanged in the urine, and there is no metabolism involved.

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36
Q

Which of the following adverse effects is associated with Hydrochlorothiazide?
A) Ototoxicity
B) Hypokalemia
C) Hyponatremia
D) Both B and C

A

Correct Answer: D) Both B and C
Rationale: Adverse effects of Hydrochlorothiazide include hypokalemia and hyponatremia, similar to loop diuretics; however, Hydrochlorothiazide does not cause ototoxicity.

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37
Q

What is the primary benefit of potassium-sparing diuretics?
A) Increased sodium reabsorption
B) Moderate diuresis and potassium retention
C) Significant fluid retention
D) Inhibition of aldosterone production

A

Correct Answer: B) Moderate diuresis and potassium retention
Rationale: Potassium-sparing diuretics are useful for moderate diuresis while retaining potassium in the kidneys.

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38
Q

Why are potassium-sparing diuretics often used in conjunction with loop or thiazide diuretics?
A) To enhance potassium excretion
B) To prevent dehydration
C) To counteract potassium-wasting effects of other diuretics
D) To increase sodium reabsorption

A

Correct Answer: C) To counteract potassium-wasting effects of other diuretics
Rationale: Potassium-sparing diuretics are used with loop or thiazide diuretics to prevent the loss of potassium, which these other diuretics can cause.

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39
Q

Which of the following types of potassium-sparing diuretics acts as an aldosterone antagonist?
A) Spironolactone
B) Hydrochlorothiazide
C) Furosemide
D) Bumetanide

A

Correct Answer: A) Spironolactone
Rationale: Spironolactone is an example of a potassium-sparing diuretic that acts as an aldosterone antagonist.

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40
Q

What are the two types of potassium-sparing diuretics?
A) Thiazide and loop
B) Aldosterone antagonist and non-aldosterone antagonist
C) Osmotic and carbonic anhydrase inhibitors
D) Proximal and distal diuretics

A

Correct Answer: B) Aldosterone antagonist and non-aldosterone antagonist
Rationale: Potassium-sparing diuretics can be classified into two types: aldosterone antagonists and non-aldosterone antagonists.

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41
Q

What is a key characteristic of potassium-sparing diuretics compared to loop or thiazide diuretics?
A) They are less effective for fluid retention.
B) They cause significant potassium loss.
C) They are primarily used for severe diuresis.
D) They do not affect potassium levels

A

Correct Answer: A) They are less effective for fluid retention.
Rationale: Potassium-sparing diuretics are useful for moderate diuresis and primarily focus on retaining potassium, making them less effective for severe fluid retention compared to loop or thiazide diuretics.

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42
Q

What is the primary mechanism of action of Spironolactone?
A) Increases sodium reabsorption in the proximal tubule
B) Blocks aldosterone in the distal nephron (DCT and collecting duct)
C) Inhibits potassium secretion in the loop of Henle
D) Enhances reabsorption of water in the collecting duct

A

Correct Answer: B) Blocks aldosterone in the distal nephron (DCT and collecting duct)
Rationale: Spironolactone works by blocking aldosterone, which reduces sodium reabsorption and promotes potassium retention in the distal nephron.

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43
Q

Why is the amount of urine output small when using Spironolactone?
A) It is a strong diuretic.
B) It only works in the proximal convoluted tubule.
C) Its mechanism is primarily focused on potassium retention.
D) It has a rapid onset of action.

A

Correct Answer: C) Its mechanism is primarily focused on potassium retention.
Rationale: Spironolactone promotes mild diuresis by blocking aldosterone, but its primary role is to retain potassium, leading to a smaller volume of urine output compared to stronger diuretics.

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44
Q

What is the onset time for Spironolactone?
A) Immediate (within 1 hour)
B) Moderate (4-6 hours)
C) Slow (up to 48 hours)
D) Rapid (within 12 hours)

A

Correct Answer: C) Slow (up to 48 hours)
Rationale: The onset of action for Spironolactone is slow, taking up to 48 hours to achieve its full effect.

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45
Q

In which conditions is Spironolactone commonly used?
A) Severe dehydration and hypotension
B) Hypertension and heart failure
C) Acute renal failure
D) Urinary tract infections

A

Correct Answer: B) Hypertension and heart failure
Rationale: Spironolactone is primarily used to manage hypertension and heart failure, particularly to counteract the potassium-wasting effects of other diuretics.

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46
Q

What is a significant adverse effect of Spironolactone that needs monitoring?
A) Hyponatremia
B) Hyperkalemia
C) Hypocalcemia
D) Dehydration

A

Correct Answer: B) Hyperkalemia
Rationale: Hyperkalemia is a significant adverse effect of Spironolactone, necessitating monitoring of potassium levels, particularly if they exceed 5 mmol/L.

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47
Q

What endocrine effects may be associated with Spironolactone due to its steroid derivative nature?
A) Weight loss and increased energy
B) Gynecomastia, menstrual irregularities, impotence, hirsutism, deepening of voice
C) Increased libido and fertility
D) Decreased appetite and nausea

A

Correct Answer: B) Gynecomastia, menstrual irregularities, impotence, hirsutism, deepening of voice
Rationale: As a steroid derivative, Spironolactone can have various endocrine effects, including gynecomastia and other hormone-related changes.

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48
Q

What drug interactions should be considered with Spironolactone?
A) Drugs that decrease blood pressure
B) Other drugs (or foods) that increase potassium levels
C) Antibiotics
D) Anticoagulants

A

Correct Answer: B) Other drugs (or foods) that increase potassium levels
Rationale: Spironolactone can interact with other medications or foods that raise potassium levels, increasing the risk of hyperkalemia.

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49
Q

What is the primary mechanism of action of Triamterene?

A) Inhibits aldosterone in the distal nephron
B) Directly disrupts ion transport (Na/K) in the distal nephron
C) Blocks sodium reabsorption in the loop of Henle
D) Increases water reabsorption in the collecting duct

A

Correct Answer: B) Directly disrupts ion transport (Na/K) in the distal nephron
Rationale: Triamterene acts by directly disrupting the sodium-potassium ion transport in the distal nephron, leading to its diuretic effects.

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50
Q

What is a characteristic of the diuretic effect of Triamterene?

A) Strong and rapid diuresis
B) Minimal diuresis
C) Prolonged diuretic effect
D) Immediate urine output

A

Correct Answer: B) Minimal diuresis
Rationale: Triamterene is associated with minimal diuresis compared to other diuretics, as it primarily disrupts ion transport rather than significantly promoting urine output.

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51
Q

What is the pharmacokinetic feature of Triamterene?

A) Slow onset of action
B) Quick onset of action
C) Extended duration of effect
D) Metabolized by the liver

A

Correct Answer: B) Quick onset of action
Rationale: Triamterene has a quick onset of action due to its direct inhibition of the transport pump in the distal nephron.

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52
Q

Which of the following conditions can Triamterene be used to treat?

A) Heart failure
B) Hypertension
C) Severe dehydration
D) Acute renal failure

A

Correct Answer: B) Hypertension
Rationale: Triamterene is used for managing hypertension, similar to spironolactone, but does not improve heart failure.

53
Q

What is a significant adverse effect associated with Triamterene?

A) Hypokalemia
B) Hyperkalemia
C) Hyponatremia
D) Hypocalcemia

A

Correct Answer: B) Hyperkalemia
Rationale: Triamterene can cause hyperkalemia, which is an important adverse effect to monitor in patients taking this medication.

54
Q

Which of the following is NOT an adverse effect of Triamterene?

A) Nausea and vomiting
B) Leg cramps
C) Ototoxicity
D) Blood disorders

A

Correct Answer: C) Ototoxicity
Rationale: Ototoxicity is not a reported adverse effect of Triamterene. Common side effects include nausea, vomiting, leg cramps, dizziness, and potential blood disorders.

55
Q

In what patient population should Triamterene be used with caution due to its potassium-sparing properties?

A) Patients with chronic kidney disease
B) Patients with dehydration
C) Patients on a sodium-restricted diet
D) Patients with liver failure

A

Correct Answer: A) Patients with chronic kidney disease
Rationale: Patients with chronic kidney disease should be monitored closely when using Triamterene due to the risk of hyperkalemia, as their kidneys may not effectively excrete potassium.

56
Q

What is the primary function of renin in the Renin-Angiotensin-Aldosterone System (RAAS)?
A) Converts angiotensin I to angiotensin II
B) Converts angiotensinogen into angiotensin I
C) Stimulates aldosterone secretion from the adrenal glands
D) Increases blood volume directly

A

Correct Answer: B) Converts angiotensinogen into angiotensin I
Rationale: Renin is an enzyme produced by juxtaglomerular cells that converts angiotensinogen, a protein produced by the liver, into angiotensin I, the first step in the RAAS pathway.

57
Q

Which of the following conditions triggers the release of renin?

A) Increased blood pressure
B) Increased plasma sodium concentration
C) Hypotension
D) Increased renal perfusion pressure

A

Correct Answer: C) Hypotension
Rationale: Renin is released in response to conditions such as hypotension, decreased blood volume, low plasma sodium concentration, and decreased renal perfusion pressure.

58
Q

What effect does increasing blood pressure have on renin release?

A) It increases renin release.
B) It has no effect on renin release.
C) It suppresses renin release.
D) It only affects aldosterone levels.

A

Correct Answer: C) It suppresses renin release.
Rationale: Increasing blood pressure, adequate blood volume, and sufficient plasma sodium content suppress the release of renin from the juxtaglomerular cells.

59
Q

What is the role of angiotensin II in the body?

A) It decreases blood volume.
B) It stimulates the production of renin.
C) It promotes aldosterone secretion, increasing sodium and water retention.
D) It has no physiological effects.

A

Correct Answer: C) It promotes aldosterone secretion, increasing sodium and water retention.
Rationale: Angiotensin II is a potent vasoconstrictor that stimulates the adrenal cortex to release aldosterone, which increases sodium and water reabsorption, ultimately raising blood pressure and blood volume.

60
Q

Which of the following factors can lead to the suppression of renin release?

A) Decreased renal perfusion pressure
B) Adequate blood volume
C) Low plasma sodium content
D) Hypotension

A

Correct Answer: B) Adequate blood volume
Rationale: Adequate blood volume, along with increased blood pressure and sufficient plasma sodium content, suppresses renin release, maintaining homeostasis in the body.

61
Q

Where is renin produced in the body?

A) Adrenal glands
B) Liver
C) Juxtaglomerular cells of the kidneys
D) Pancreas

A

Correct Answer: C) Juxtaglomerular cells of the kidneys
Rationale: Renin is produced by the juxtaglomerular cells located in the kidneys, specifically in response to various stimuli related to blood pressure and blood volume.

62
Q

What is the primary precursor for the formation of angiotensin I?

A) Angiotensin II
B) Aldosterone
C) Angiotensinogen
D) Renin

A

Correct Answer: C) Angiotensinogen
Rationale: Angiotensinogen is the precursor protein that renin converts into angiotensin I, which is then further converted into angiotensin II.

63
Q

Which type of angiotensin is considered the most clinically relevant?

A) Angiotensin I
B) Angiotensin II
C) Angiotensin III
D) Angiotensinogen

A

Correct Answer: B) Angiotensin II
Rationale: Angiotensin II is the most clinically relevant form of angiotensin due to its significant physiological effects, including vasoconstriction and stimulation of aldosterone release.

64
Q

What is one of the primary actions of angiotensin II in the body?

A) Vasodilation of blood vessels
B) Stimulation of aldosterone release from the adrenal cortex
C) Decrease in heart rate
D) Increased renal perfusion

A

Correct Answer: B) Stimulation of aldosterone release from the adrenal cortex
Rationale: Angiotensin II is known for its role in promoting the secretion of aldosterone, which increases sodium and water reabsorption, thereby raising blood pressure.

65
Q

How does angiotensin II contribute to vasoconstriction?

A) By inhibiting norepinephrine and epinephrine release
B) By causing relaxation of smooth muscle
C) By promoting the contraction of smooth muscle and releasing norepinephrine and epinephrine
D) By directly dilating blood vessels

A

Correct Answer: C) By promoting the contraction of smooth muscle and releasing norepinephrine and epinephrine
Rationale: Angiotensin II promotes vasoconstriction through the contraction of smooth muscle and stimulates the release of norepinephrine and epinephrine, which further enhances blood pressure.

66
Q

Which of the following alterations can angiotensin II cause in the cardiovascular system?

A) Decreased cardiac output
B) Cardiac and vascular structural changes, including heart failure and atherosclerosis
C) Increased oxygen supply to the heart
D) Dilation of coronary arteries

A

Correct Answer: B) Cardiac and vascular structural changes, including heart failure and atherosclerosis
Rationale: Angiotensin II can lead to structural alterations in the heart and blood vessels, contributing to conditions like heart failure and atherosclerosis.

67
Q

What are the primary physiological roles of the Renin-Angiotensin-Aldosterone System (RAAS)?

A) To lower blood pressure and decrease blood volume
B) To regulate blood pressure and fluid balance
C) To increase blood flow to the kidneys only
D) To stimulate insulin secretion from the pancreas

A

Correct Answer: B) To regulate blood pressure and fluid balance
Rationale: The RAAS plays a crucial role in maintaining blood pressure and fluid balance through mechanisms like vasoconstriction and aldosterone secretion.

68
Q

Which of the following is a pathological cardiovascular effect associated with the RAA system?

A) Decreased heart rate
B) Cardiac remodeling and fibrosis
C) Improved baroreceptor reflex sensitivity
D) Increased nitric oxide production

A

Correct Answer: B) Cardiac remodeling and fibrosis
Rationale: One of the pathological effects of the RAA system is cardiac remodeling and fibrosis, which can lead to various cardiovascular complications.

69
Q

Which mechanism does the RAA system utilize to retain sodium in the kidneys?

A) Increasing renal blood flow
B) Inhibiting diuretic hormones
C) Acting on the distal nephron
D) Enhancing filtration in the glomerulus

A

Correct Answer: C) Acting on the distal nephron
Rationale: The RAA system specifically acts on the distal nephron to promote sodium retention, which helps regulate blood volume and pressure.

70
Q

What triggers the activation of the Renin-Angiotensin-Aldosterone System (RAAS)?

A) Increased blood pressure
B) Hemorrhage
C) High sodium levels
D) Increased renal perfusion

A

Correct Answer: B) Hemorrhage
Rationale: Conditions that lower blood pressure, such as hemorrhage, dehydration, and low sodium levels, activate the RAAS to help restore blood pressure.

71
Q

Which of the following statements is true regarding the effects of Angiotensin II?

A) It promotes vasodilation and reduces peripheral resistance.
B) It causes rapid vasoconstriction, increasing peripheral resistance.
C) It decreases sodium retention in the kidneys.
D) It increases glomerular filtration rate (GFR).

A

Correct Answer: B) It causes rapid vasoconstriction, increasing peripheral resistance.
Rationale: Angiotensin II acts quickly to induce vasoconstriction, which increases peripheral resistance and helps raise blood pressure.

72
Q

How does vasoconstriction affect glomerular filtration rate (GFR)?

A) It increases GFR by enhancing blood flow to the kidneys.
B) It decreases GFR by reducing blood flow to the kidneys.
C) It has no impact on GFR.
D) It increases GFR by increasing renal perfusion.

A

Correct Answer: B) It decreases GFR by reducing blood flow to the kidneys.
Rationale: Vasoconstriction reduces blood flow to the kidneys, which subsequently decreases GFR.

73
Q

What role does aldosterone play in the RAAS?

A) It decreases sodium and water retention in the kidneys.
B) It promotes retention of sodium and water in the renal tubules.
C) It inhibits renin release from juxtaglomerular cells.
D) It causes vasodilation in peripheral blood vessels.

A

Correct Answer: B) It promotes retention of sodium and water in the renal tubules.
Rationale: Aldosterone acts on the renal tubules to promote the reabsorption of sodium and water, which helps increase blood volume and blood pressure.

74
Q

Which of the following statements accurately describes the relationship between blood pressure and the RAAS?

A) Elevated blood pressure activates the RAAS.
B) The RAAS is inhibited when blood pressure is high.
C) The RAAS has no effect on blood pressure regulation.
D) The RAAS is only activated by high sodium levels.

A

Correct Answer: B) The RAAS is inhibited when blood pressure is high.
Rationale: Conditions that raise blood pressure lead to the suppression of the RAAS, while low blood pressure stimulates it.

75
Q

What is the primary mechanism through which RAAS raises blood pressure?

A) Decreasing cardiac output
B) Inhibiting vasoconstriction
C) Increasing peripheral resistance and blood volume
D) Enhancing renal blood flow

A

Correct Answer: C) Increasing peripheral resistance and blood volume
Rationale: RAAS raises blood pressure primarily by inducing vasoconstriction (increasing peripheral resistance) and promoting sodium and water retention (increasing blood volume).

76
Q

What physiological response occurs in the RAAS when there is a low sodium concentration in the plasma?

A) Increased renin release
B) Decreased aldosterone secretion
C) Inhibition of vasoconstriction
D) Decreased peripheral resistance

A

Correct Answer: A) Increased renin release
Rationale: A low sodium concentration in the plasma triggers an increase in renin release, activating the RAAS to help restore sodium and blood pressure levels.

77
Q

What is the primary therapeutic use of Angiotensin Converting Enzyme Inhibitors (ACEIs)?

A) Manage asthma
B) Treat hypertension and heart failure
C) Promote weight loss
D) Increase blood glucose levels

A

Correct Answer: B) Treat hypertension and heart failure
Rationale: ACEIs are primarily used to treat hypertension, heart failure, diabetic nephropathy, myocardial infarction (MI), and to prevent adverse cardiac events.

78
Q

How do ACE inhibitors reduce blood pressure?

A) By increasing the production of angiotensin I
B) By dilating blood vessels and reducing blood volume
C) By increasing sodium reabsorption
D) By promoting the retention of potassium

A

Correct Answer: B) By dilating blood vessels and reducing blood volume
Rationale: ACE inhibitors reduce levels of angiotensin I, leading to the dilation of blood vessels and a reduction in blood volume, which lowers blood pressure.

79
Q

Here are multiple-choice questions based solely on the information provided about Angiotensin Converting Enzyme Inhibitors (ACEIs):

Multiple Choice Questions on ACE Inhibitors
What is the primary therapeutic use of Angiotensin Converting Enzyme Inhibitors (ACEIs)?

A) Manage asthma
B) Treat hypertension and heart failure
C) Promote weight loss
D) Increase blood glucose levels
Correct Answer: B) Treat hypertension and heart failure
Rationale: ACEIs are primarily used to treat hypertension, heart failure, diabetic nephropathy, myocardial infarction (MI), and to prevent adverse cardiac events.

How do ACE inhibitors reduce blood pressure?

A) By increasing the production of angiotensin I
B) By dilating blood vessels and reducing blood volume
C) By increasing sodium reabsorption
D) By promoting the retention of potassium
Correct Answer: B) By dilating blood vessels and reducing blood volume
Rationale: ACE inhibitors reduce levels of angiotensin I, leading to the dilation of blood vessels and a reduction in blood volume, which lowers blood pressure.

What effect do ACE inhibitors have on bradykinin levels?

A) They decrease bradykinin levels.
B) They have no effect on bradykinin levels.
C) They increase bradykinin levels.
D) They convert bradykinin into angiotensin II.

A

Correct Answer: C) They increase bradykinin levels.
Rationale: ACE inhibitors inhibit the enzyme that breaks down bradykinin (kinase II), leading to increased levels of bradykinin, which promotes vasodilation.

80
Q

What is a potential adverse effect of increased bradykinin levels due to ACE inhibitors?

A) Hypertension
B) Cough and angioedema
C) Hyperkalemia
D) Hypoglycemia

A

Correct Answer: B) Cough and angioedema
Rationale: Increased bradykinin can cause side effects such as a persistent cough and angioedema.

81
Q

Which of the following conditions are ACE inhibitors indicated for?

A) Osteoporosis and arthritis
B) Hypertension and diabetic nephropathy
C) Skin infections and allergies
D) Chronic obstructive pulmonary disease (COPD)

A

Correct Answer: B) Hypertension and diabetic nephropathy
Rationale: ACE inhibitors are used to treat conditions such as hypertension, heart failure, diabetic nephropathy, and to prevent adverse cardiac events.

82
Q

What happens when angiotensin I levels are reduced by ACE inhibitors?

A) Blood volume increases
B) Blood vessels constrict
C) Blood pressure decreases
D) Heart rate increases

A

Correct Answer: C) Blood pressure decreases
Rationale: Reducing angiotensin I levels leads to decreased vasoconstriction, promoting lower blood pressure.

83
Q

In addition to treating hypertension, what is another significant benefit of ACE inhibitors in heart failure?

A) They cause weight gain.
B) They promote sodium retention.
C) They prevent pathological changes in the heart and blood vessels.
D) They decrease heart rate.

A

Correct Answer: C) They prevent pathological changes in the heart and blood vessels.
Rationale: ACE inhibitors help prevent adverse remodeling and other pathological changes in the heart and blood vessels associated with heart failure.

84
Q

What is a unique feature of most ACE inhibitors regarding their administration route?

A) They are all given intravenously.
B) They are administered orally, with one exception.
C) They are only available as transdermal patches.
D) They are only available in injectable form.

A

Correct Answer: B) They are administered orally, with one exception.
Rationale: Most ACE inhibitors are given orally, with only one available in intravenous form., Fosinopril.

85
Q

How do most ACE inhibitors need to be taken in relation to food?

A) Only on an empty stomach
B) Only with food
C) They can be taken with or without food
D) Must be taken with a high-fat meal

A

Correct Answer: C) They can be taken with or without food
Rationale: ACE inhibitors can generally be taken with or without food, which provides flexibility in administration

86
Q

What is the significance of long half-lives in most ACE inhibitors?

A) They require frequent dosing throughout the day.
B) They are administered once daily.
C) They cannot be given to patients with hypertension.
D) They need to be taken at specific times with food.

A

Correct Answer: B) They are administered once daily.
Rationale: The long half-lives of most ACE inhibitors mean they only need to be taken once per day, making them more convenient for patients

87
Q

Which ACE inhibitor has a shorter half-life, requiring more frequent dosing?

A) Lisinopril
B) Captopril
C) Enalapril
D) Ramipril

A

Correct Answer: B) Captopril
Rationale: Captopril has a shorter half-life compared to other ACE inhibitors, so it requires more frequent dosing.

88
Q

What is the concern when administering ACE inhibitors to patients with kidney disease?

A) The drug will be metabolized too quickly.
B) There is a risk of reduced drug efficacy.
C) The drug may accumulate, causing toxicity.
D) Kidney disease patients cannot take ACE inhibitors at all

A

Correct Answer: C) The drug may accumulate, causing toxicity.
Rationale: Since ACE inhibitors are excreted by the kidneys, impaired kidney function can lead to drug accumulation and potential toxicity.

89
Q

What distinguishes fosinopril from other ACE inhibitors in patients with kidney disease?

A) It is metabolized by the liver instead of the kidneys.
B) It does not affect blood pressure.
C) It has a longer half-life in kidney disease patients.
D) It must be administered intravenously

A

Correct Answer: A) It is metabolized by the liver instead of the kidneys.
Rationale: Fosinopril is unique among ACE inhibitors because it is not exclusively excreted by the kidneys, making it a safer option for patients with kidney disease.

90
Q

Most ACE inhibitors are prodrugs. What does this mean for their activation?

A) They are already in their active form when administered.
B) They need to be activated by the liver.
C) They are converted to their active form after administration in the body.
D) They are activated by the kidneys.

A

Correct Answer: C) They are converted to their active form after administration in the body.
Rationale: Most ACE inhibitors are prodrugs, meaning they must be converted into their active form within the body to exert their therapeutic effect.

91
Q

Why are ACE inhibitors beneficial for patients with asthma compared to other antihypertensives?

A) They act as bronchodilators.
B) They do not interfere with B2-antagonists.
C) They reduce respiratory rate.
D) They block histamine receptors

A

Correct Answer: B) They do not interfere with B2-antagonists.
Rationale: ACE inhibitors are suitable for patients with asthma because they do not interfere with B2-antagonists, unlike other antihypertensives.

92
Q

Which of the following is a benefit of ACE inhibitors over thiazide diuretics for treating hypertension?

A) They do not affect potassium, urea, or glucose levels.
B) They increase potassium levels.
C) They cause greater fluid retention.
D) They increase glucose levels.

A

Correct Answer: A) They do not affect potassium, urea, or glucose levels.
Rationale: Unlike thiazide diuretics, ACE inhibitors do not interfere with potassium, urea, or glucose, making them a better choice for some patients.

93
Q

What is the impact of ACE inhibitors on diabetic and non-diabetic nephropathy?

A) They prevent nephropathy by increasing angiotensin II.
B) They slow the progression of nephropathy by decreasing angiotensin II levels.
C) They increase blood sugar, worsening nephropathy.
D) They directly repair damaged kidney tissues

A

Correct Answer: B) They slow the progression of nephropathy by decreasing angiotensin II levels.
Rationale: ACE inhibitors slow and delay the onset of nephropathy by reducing angiotensin II, which lowers glomerular filtration pressure.

94
Q

How do ACE inhibitors reduce mortality after a myocardial infarction (MI)?

A) They increase blood pressure.
B) They improve glucose metabolism.
C) They reduce the risk of heart failure by decreasing arterial tone and improving blood flow.
D) They increase heart rate.

A

Correct Answer: C) They reduce the risk of heart failure by decreasing arterial tone and improving blood flow.
Rationale: ACE inhibitors reduce mortality after MI by decreasing arterial tone, improving blood flow, and reducing the likelihood of heart failure development

95
Q

Which of the following is a key benefit of ACE inhibitors in treating heart failure?

A) They cause arterial constriction, increasing blood pressure.
B) They cause venous dilation, reducing pulmonary congestion and peripheral edema.
C) They reduce renal blood flow to decrease sodium and water excretion.
D) They increase glucose levels, providing energy to heart muscle.

A

Correct Answer: B) They cause venous dilation, reducing pulmonary congestion and peripheral edema.
Rationale: ACE inhibitors promote venous dilation, which helps reduce pulmonary congestion and peripheral edema in heart failure patients.

96
Q

What effect do ACE inhibitors have on cardiac output (CO) in heart failure patients?

A) They decrease CO by increasing afterload.
B) They improve CO by decreasing afterload.
C) They have no effect on CO.
D) They reduce CO by increasing blood pressure

A

Correct Answer: B) They improve CO by decreasing afterload.
Rationale: ACE inhibitors improve cardiac output by reducing afterload, which lowers the resistance the heart must pump against.

97
Q

How do ACE inhibitors improve renal blood flow in heart failure patients?

A) By promoting sodium and water retention.
B) By reducing blood pressure and increasing sodium and water excretion.
C) By constricting renal blood vessels.
D) By increasing angiotensin II levels.

A

Correct Answer: B) By reducing blood pressure and increasing sodium and water excretion.
Rationale: ACE inhibitors improve renal blood flow by decreasing blood pressure and promoting the excretion of sodium and water.

98
Q

What is the primary cause of first-dose hypotension when taking ACE inhibitors?

A) Rapid decrease in bradykinin levels.
B) Abrupt reduction of angiotensin II levels leading to widespread vasodilation.
C) Increase in blood glucose levels.
D) Sudden increase in sodium retention

A

Correct Answer: B) Abrupt reduction of angiotensin II levels leading to widespread vasodilation.
Rationale: The rapid reduction in angiotensin II levels with the first dose of an ACE inhibitor leads to vasodilation and a significant drop in blood pressure, causing first-dose hypotension.

99
Q

Which of the following patients is most at risk for first-dose hypotension with ACE inhibitors?

A) A well-hydrated patient with no history of hypotension.
B) A patient who has been taking diuretics and is volume depleted.
C) A patient on a high-sodium diet.
D) A patient with stable hypertension on no other medications.

A

Correct Answer: B) A patient who has been taking diuretics and is volume depleted.
Rationale: Patients taking diuretics or those who are volume-depleted are at higher risk for first-dose hypotension due to lower blood volume and the abrupt decrease in angiotensin II.

100
Q

Why might hyperkalemia develop in patients taking ACE inhibitors?

A) ACE inhibitors increase potassium excretion.
B) ACE inhibitors cause sodium retention.
C) ACE inhibitors block aldosterone, which leads to potassium retention.
D) ACE inhibitors increase renal excretion of potassium.

A

Correct Answer: C) ACE inhibitors block aldosterone, which leads to potassium retention.
Rationale: By inhibiting aldosterone, ACE inhibitors cause the kidneys to retain potassium, potentially leading to hyperkalemia.

101
Q

Which group of patients is at greater risk of developing a persistent cough when taking ACE inhibitors?

A) Elderly males of European descent.
B) Young males of African descent.
C) Elderly females of Asian descent.
D) Middle-aged females of African descent.

A

Correct Answer: C) Elderly females of Asian descent.
Rationale: The persistent cough associated with ACE inhibitors is more common in older patients, particularly females and those of Asian descent, due to the accumulation of bradykinin

102
Q

How long does it typically take for a cough to be eliminated after discontinuing ACE inhibitors?

A) 1 day.
B) 3 days.
C) 10 days.
D) 2 week

A

Correct Answer: C) 10 days.
Rationale: The cough caused by ACE inhibitors typically decreases within 3 days of discontinuation and is fully eliminated within 10 days.

103
Q

In which patients would you be most concerned about the risk of hyperkalemia when using ACE inhibitors?

A) Patients taking potassium supplements or potassium-sparing diuretics.
B) Patients with low potassium levels.
C) Patients on a low-sodium diet.
D) Patients with stable kidney function and no electrolyte imbalances.

A

Correct Answer: A) Patients taking potassium supplements or potassium-sparing diuretics.
Rationale: Since ACE inhibitors can cause potassium retention, the risk of hyperkalemia increases in patients already taking potassium supplements or potassium-sparing diuretics.

104
Q

Why can ACE inhibitors lead to renal failure in patients with renal artery stenosis?

A) ACE inhibitors increase blood pressure, causing kidney damage.
B) ACE inhibitors decrease angiotensin II, reducing glomerular filtration rate (GFR).
C) ACE inhibitors cause fluid overload in patients with renal artery stenosis.
D) ACE inhibitors block potassium excretion, leading to hyperkalemia and kidney damage.

A

Correct Answer: B) ACE inhibitors decrease angiotensin II, reducing glomerular filtration rate (GFR).
Rationale: In patients with renal artery stenosis, angiotensin II is crucial for maintaining GFR. ACE inhibitors reduce angiotensin II levels, causing a significant drop in GFR, which can lead to renal failure.

105
Q

Which adverse effect of ACE inhibitors requires immediate emergency treatment due to its potentially life-threatening nature?

A) Cough.
B) Hyperkalemia.
C) Angioedema.
D) Neutropenia.

A

Correct Answer: C) Angioedema.
Rationale: Angioedema can cause severe swelling of the tongue, lips, and throat, leading to airway obstruction and requiring emergency treatment, similar to anaphylaxis.

106
Q

What is the most appropriate action if a patient develops angioedema while taking an ACE inhibitor?

A) Continue the medication and monitor closely.
B) Administer potassium supplements.
C) Stop the medication immediately and treat as anaphylaxis.
D) Increase the dose of the ACE inhibitor to reverse the angioedema.

A

Correct Answer: C) Stop the medication immediately and treat as anaphylaxis.
Rationale: Angioedema is a serious adverse effect that can be life-threatening. Treatment should involve stopping the medication and treating it as an anaphylactic reaction.

107
Q

Which of the following adverse effects is more common with the ACE inhibitor captopril?

A) Hyperkalemia.
B) Neutropenia.
C) Angioedema.
D) Cough

A

Correct Answer: B) Neutropenia.
Rationale: Neutropenia is a rare but serious adverse effect associated with captopril, and it is more common in patients with renal impairment.

108
Q

Which patients are at higher risk of neutropenia while taking ACE inhibitors like captopril?

A) Patients with renal impairment.
B) Patients with asthma.
C) Patients with high potassium levels.
D) Patients with liver disease.

A

Correct Answer: A) Patients with renal impairment.
Rationale: Neutropenia is more common in patients with renal impairment, especially when using ACE inhibitors like captopril, and can be reversible if detected early.

109
Q

Why must ACE inhibitors be avoided during pregnancy?

A) They can cause fetal hypoglycemia.
B) They can cause fetal hyperkalemia.
C) They can cause fetal injury and malformations.
D) They increase fetal blood pressure.

A

Correct Answer: C) They can cause fetal injury and malformations.
Rationale: ACE inhibitors can cause serious fetal harm, including injury and developmental malformations, and should be avoided during pregnancy.

110
Q

Why should ACE inhibitors be used cautiously with diuretics?

A) Diuretics increase the risk of lithium toxicity.
B) Diuretics decrease the effectiveness of ACE inhibitors.
C) Diuretics increase the risk of first-dose hypotension.
D) Diuretics cause hyperkalemia when combined with ACE inhibitors

A

Correct Answer: C) Diuretics increase the risk of first-dose hypotension.
Rationale: Diuretics can lead to volume depletion, which increases the risk of severe hypotension, particularly when initiating ACE inhibitors.

111
Q

Which of the following drugs, when used with ACE inhibitors, can lead to hyperkalemia?

A) Antihypertensive agents.
B) NSAIDs.
C) Medications that increase potassium.
D) Lithium.

A

Correct Answer: C) Medications that increase potassium.
Rationale: ACE inhibitors inhibit aldosterone, leading to potassium retention. When used with potassium supplements or potassium-sparing diuretics, this can lead to hyperkalemia, which can be life-threatening.

112
Q

What effect can ACE inhibitors have on lithium levels?

A) They decrease lithium absorption.
B) They cause lithium excretion in the urine.
C) They increase the risk of lithium accumulation and toxicity.
D) They have no effect on lithium

A

Correct Answer: C) They increase the risk of lithium accumulation and toxicity.
Rationale: ACE inhibitors reduce renal clearance of lithium, leading to its accumulation and potentially toxic levels.

113
Q

How do NSAIDs interact with ACE inhibitors?

A) They enhance the effect of ACE inhibitors.
B) They reduce the effectiveness of ACE inhibitors.
C) They cause potassium loss.
D) They increase the risk of first-dose hypotension

A

Correct Answer: B) They reduce the effectiveness of ACE inhibitors.
Rationale: NSAIDs can inhibit the vasodilatory effects of ACE inhibitors by blocking prostaglandins, which reduces their efficacy, particularly in lowering blood pressure.

114
Q

Which of the following antihypertensive agents would be a concern when combined with an ACE inhibitor?

A) A beta-blocker.
B) A calcium channel blocker.
C) A potassium-sparing diuretic.
D) A thiazide diuretic.

A

Correct Answer: C) A potassium-sparing diuretic.
Rationale: Potassium-sparing diuretics can increase the risk of hyperkalemia when used with ACE inhibitors, as both promote potassium retention.

115
Q

A patient with hypertension is prescribed an angiotensin II receptor blocker (ARB). Which of the following is a key difference between ARBs and ACE inhibitors that the nurse should explain to the patient?

A. ARBs increase the release of bradykinin, leading to a cough.
B. ARBs do not block angiotensin II, unlike ACE inhibitors.
C. ARBs block angiotensin II at its receptors, causing less cough than ACE inhibitors.
D. ARBs prevent sodium and water retention but do not dilate blood vessels.

A

Answer: C. ARBs block angiotensin II at its receptors, causing less cough than ACE inhibitors.

Rationale: ARBs block angiotensin II at its receptors in blood vessels, the heart, and adrenals. Unlike ACE inhibitors, ARBs do not inhibit kinase II, meaning there is no increase in bradykinin, which is associated with the cough seen in ACE inhibitors. This is why ARBs are often used when patients cannot tolerate the cough caused by ACE inhibitors.

116
Q

A patient is prescribed an ARB for heart failure. Which effect of the medication should the nurse anticipate?

A. Increased sodium retention and increased fluid volume.
B. Dilation of arteries and veins to reduce blood pressure.
C. Increased aldosterone release and water retention.
D. Constriction of blood vessels to improve cardiac output.

A

Answer: B. Dilation of arteries and veins to reduce blood pressure.

Rationale: ARBs block angiotensin II at its receptors, leading to the dilation of arteries and veins. This helps reduce blood pressure and decreases the workload on the heart, which is beneficial for patients with heart failure.

117
Q

The nurse is reviewing a patient’s medications and notes that the patient is taking an ARB. The nurse recognizes that ARBs help manage heart failure by preventing which of the following?

A. Sodium retention and vasoconstriction.
B. Increased heart rate and stroke volume.
C. Cardiac remodeling and aldosterone release.
D. Renin release and fluid retention.

A

Answer: C. Cardiac remodeling and aldosterone release.

Rationale: ARBs prevent pathologic changes in the heart (cardiac remodeling) and reduce the release of aldosterone, leading to decreased sodium and water retention. This is crucial in managing heart failure, where these changes could worsen the condition.

118
Q

A patient is started on an ARB. The nurse understands that ARBs promote the excretion of sodium and water by:

A. Increasing bradykinin levels in the body.
B. Blocking aldosterone release from the adrenal glands.
C. Inhibiting sodium reabsorption in the proximal tubule.
D. Increasing renin production in the kidneys.

A

Answer: B. Blocking aldosterone release from the adrenal glands.

Rationale: ARBs block angiotensin II at its receptors in the adrenal glands, leading to a decrease in aldosterone secretion. This reduction in aldosterone promotes the excretion of sodium and water, helping to manage fluid balance and lower blood pressure.

119
Q

A nurse is explaining the effects of an ARB to a patient. Which statement made by the patient indicates a correct understanding of the medication?

A. “This medication will block the effects of angiotensin II to lower my blood pressure.”
B. “This drug works by increasing my heart rate to improve blood flow.”
C. “I will likely develop a cough because of the increased bradykinin.”
D. “This medication will increase the amount of sodium I retain.”

A

Answer: A. “This medication will block the effects of angiotensin II to lower my blood pressure.”

Rationale: ARBs block the effects of angiotensin II at its receptors, which leads to vasodilation and reduced blood pressure. Unlike ACE inhibitors, ARBs do not increase bradykinin, so cough is not a common side effect.

120
Q

A patient with heart failure cannot tolerate an ACE inhibitor. Which of the following medications is most appropriate to improve their symptoms and ejection fraction?

A. Furosemide
B. Valsartan
C. Losartan
D. Spironolactone

A

Answer: B. Valsartan

Rationale: Valsartan, an ARB, is indicated for heart failure and helps reduce symptoms and improve ejection fraction, especially for patients who cannot tolerate ACE inhibitors.

121
Q

An ARB can delay the development and progression of which of the following conditions in patients with diabetes?

A. Retinopathy
B. Neuropathy
C. Hyperglycemia
D. Nephropathy

A

Answer: D. Nephropathy

Rationale: ARBs can delay the development and progression of nephropathy, particularly in patients with diabetes.

122
Q

Which ARB is indicated for stroke prevention in patients over 55 who cannot take an ACE inhibitor?

A. Losartan
B. Valsartan
C. Captopril
D. Enalapril

A

Answer: A. Losartan

Rationale: Losartan is indicated for stroke prevention in patients over 55 who are unable to take ACE inhibitors.

123
Q

A patient with type 1 diabetes is prescribed an ARB to slow the development of retinopathy. The nurse knows that this treatment is most effective in which group of patients?

A. Patients with severe retinopathy
B. Patients with no existing retinopathy
C. Patients with uncontrolled blood pressure
D. Patients who are over 65 years old

A

Answer: B. Patients with no existing retinopathy

Rationale: ARBs can slow the development of retinopathy in patients with type 1 diabetes who do not already have retinopathy.

124
Q

For patients recovering from a myocardial infarction (MI), which ARB is specifically indicated to reduce mortality risk?

A. Losartan
B. Valsartan
C. Candesartan
D. Irbesartan

A

Answer: B. Valsartan

Rationale: Valsartan is indicated for reducing mortality and improving outcomes in patients recovering from a myocardial infarction (MI).

125
Q

A patient on an angiotensin II receptor blocker (ARB) reports swelling of the tongue and lips. What is the nurse’s priority action?

A. Administer an antihistamine
B. Continue the medication and monitor closely
C. Discontinue the ARB and notify the healthcare provider
D. Reduce the dosage of the ARB

A

Answer: C. Discontinue the ARB and notify the healthcare provider

Rationale: Angioedema, although less common than with ACE inhibitors, can occur with ARBs. If it develops, the ARB should be stopped immediately, and the patient should not take the drug again.

126
Q

A patient with a history of bilateral renal artery stenosis is prescribed an ARB. What is the nurse’s primary concern?

A. Hypertensive crisis
B. Risk of fetal harm
C. Potential for renal failure
D. Development of angioedema

A

Answer: C. Potential for renal failure

Rationale: ARBs can lead to renal failure in patients with renal artery stenosis because the reduction in angiotensin II can decrease glomerular filtration rate (GFR), worsening kidney function.

127
Q

Which of the following patients should not take an angiotensin II receptor blocker (ARB)?

A. A 60-year-old male with heart failure
B. A 45-year-old female who is 8 weeks pregnant
C. A 55-year-old male with hypertension
D. A 50-year-old female with diabetic nephropathy

A

Answer: B. A 45-year-old female who is 8 weeks pregnant

Rationale: ARBs can cause fetal harm and should be stopped immediately if pregnancy is detected.

128
Q

A patient with hypertension is prescribed an ARB and is taking another antihypertensive medication. The nurse knows that which adjustment may be necessary?

A. Increase the dosage of both medications
B. Discontinue the other antihypertensive
C. Reduce the dosage of the antihypertensive medications
D. Switch to an ACE inhibitor

A

Answer: C. Reduce the dosage of the antihypertensive medications

Rationale: ARBs can have additive effects when taken with other antihypertensive medications, so a dose reduction may be necessary to prevent excessive lowering of blood pressure.

129
Q

A nurse is reviewing the medication list of a patient taking an ARB. Which of the following conditions would warrant caution due to potential adverse effects of the ARB?

A. Hyperthyroidism
B. A history of angioedema
C. Uncontrolled diabetes
D. Hypokalemia

A

Answer: B. A history of angioedema

Rationale: While angioedema is less common with ARBs than ACE inhibitors, it can still occur. Patients with a history of angioedema related to ARBs should not take the drug again.