Exam 3- Renal Flashcards

1
Q

Question 1: What percentage of total body water (TBW) is typically water content?
A. 30%
B. 50%
C. 60%
D. 70%

A

Answer: C. 60%
Rationale: The slide indicates that approximately 60% of total body water is water, and this can vary with gender, age, and body fat percentage.

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2
Q

Which hormone primarily regulates osmolar homeostasis by causing the kidneys to reabsorb water?
A. Atrial Natriuretic Peptide (ANP)
B. Renin
C. Antidiuretic Hormone (ADH)
D. Aldosterone

A

Answer: C. Antidiuretic Hormone (ADH)
Rationale: According to the slide, the pituitary release of Vasopressin, also known as Antidiuretic Hormone, is stimulated by osmolality-sensors in the anterior hypothalamus to regulate osmolar homeostasis by increasing water reabsorption in the kidneys.

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3
Q

Question 3: What is the role of Atrial Natriuretic Peptide (ANP) in fluid/volume homeostasis? (Select all that apply)
A. Promotes sodium and water reabsorption
B. Reduces blood volume and blood pressure
C. Dilates blood vessels
D. Increases sympathetic nervous system activity

A

Answers: B. Reduces blood volume and blood pressure, C. Dilates blood vessels
Rationale: Atrial Natriuretic Peptide works by promoting sodium and water excretion in the kidneys, which reduces blood volume and blood pressure. It also dilates blood vessels and inhibits renin and aldosterone secretion, leading to lowered vascular resistance and increased urine production. It does not increase sympathetic nervous system activity; it decreases it.

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4
Q

What triggers the Renin-Angiotensinogen-Aldosterone System (RAAS) to cause sodium and water reabsorption?
A. Increased volume sensed by the juxtaglomerular apparatus
B. Decreased volume sensed by the juxtaglomerular apparatus
C. Increased osmolarity sensed by the osmolality-sensors
D. Decreased osmolarity sensed by the osmolality-sensors

A

Answer: B. Decreased volume sensed by the juxtaglomerular apparatus
Rationale: The slide specifies that the juxtaglomerular apparatus senses changes in volume, and a decrease in volume at the juxtaglomerular apparatus triggers the Renin-Angiotensinogen-Aldosterone System, which results in sodium and water reabsorption to maintain volume homeostasis.

The correct answer is “B. Decreased volume sensed by the juxtaglomerular apparatus,” which aligns with the mechanisms described across the sources. Reduced renal perfusion pressure, which can be interpreted as a decreased volume status, and a lower sodium chloride concentration at the macula densa both stimulate renin release, ultimately triggering the RAAS​​​​. This system plays a crucial role in the regulation of blood volume and systemic blood pressure by adjusting kidney function.

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5
Q

What is considered the normal range for serum sodium concentration?
A. 125-135 mEq/L
B. 135-145 mEq/L
C. 145-155 mEq/L
D. 155-165 mEq/L

A

Answer: B. 135-145 mEq/L
Rationale: The slide indicates that the normal serum sodium concentration range is between 135-145 mEq/L.

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6
Q

At which serum sodium concentration levels should elective surgery be corrected prior to proceeding?
A. ≤125 or ≥145 mEq/L
B. ≤125 or ≥155 mEq/L
C. ≤130 or ≥150 mEq/L
D. ≤135 or ≥145 mEq/L

A

Answer: B. ≤125 or ≥155 mEq/L
Rationale: The slide specifies that serum sodium concentrations of ≤125 mEq/L or ≥155 mEq/L are the cutoff ranges at which correction should be sought prior to an elective surgical case due to concerns about acute changes.

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7
Q

Which of the following conditions is associated with euvolemic hyponatremia? (Select all that apply)
A. Diuretic excess
B. Hypothyroidism
C. Nephrotic syndrome
D. Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)

A

Answers: B. Hypothyroidism, D. Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)
Rationale: The slide presents euvolemic hyponatremia as being related to conditions where there is normal volume status but an imbalance in solute and water, citing endocrine-related issues such as hypothyroidism and SIADH as underlying causes. SIADH is specifically characterized by excessive retention of water with dilutional hyponatremia.

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8
Q

In the context of hyponatremia, what does an elevated endogenous vasopressin level indicate?
A. Decreased water reabsorption
B. Over-resuscitation with fluids
C. Excessive sodium loss
D. Reduced catecholamine release

A

Answer: B. Over-resuscitation with fluids
Rationale: The slide mentions that one cause of hyponatremia can be over fluid-resuscitation, which is related to an increased endogenous vasopressin level leading to increased water reabsorption. Elevated vasopressin levels enhance the reabsorption of water in the kidneys, which can dilute sodium in the body, causing hyponatremia.

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9
Q

which clinical findings are indicative of hypovolemic hyponatremia?
A. Decreased skin turgor and orthostatic hypotension
B. Peripheral edema and rales
C. Muscle cramps and lethargy
D. Nausea and headache

A

Answer: A. Decreased skin turgor and orthostatic hypotension
Rationale: The slide’s algorithm suggests that clinical signs of hypovolemic hyponatremia include physical examination findings such as decreased skin turgor, dry mucous membranes, orthostatic hypotension, tachycardia, and oliguria.

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10
Q

In the setting of euvolemic hyponatremia, what laboratory findings would you expect with regard to urine sodium concentration?
A. Urine sodium (U_Na) > 20 mEq/L
B. Urine sodium (U_Na) < 20 mEq/L
C. Urine sodium (U_Na) variable
D. Urine sodium (U_Na) not relevant

A

Answer: A. Urine sodium (U_Na) > 20 mEq/L
Rationale: The diagnostic algorithm points out that in cases of euvolemic hyponatremia, such as with Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH), the urine sodium concentration is typically greater than 20 mEq/L, reflecting the kidney’s excretion of sodium while retaining water.

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11
Q

When evaluating a patient with hypervolemic hyponatremia, which of the following would NOT be an expected underlying cause according to the diagnostic algorithm?
A. Acute renal failure
B. Diuretic excess
C. Nephrotic syndrome
D. Cardiac failure

A

Answer: B. Diuretic excess
Rationale: The flowchart indicates that hypervolemic hyponatremia is commonly associated with conditions that cause fluid overload, such as acute renal failure, chronic renal failure, nephrotic syndrome, cardiac failure, and cirrhosis. Diuretic excess is typically associated with hypovolemic hyponatremia, as it leads to sodium and water loss.

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12
Q

Which of the following symptoms are commonly associated with mild hyponatremia (serum sodium 130-135 mEq/L)- select all?
A. Headache
B. Seizures
C. Muscle cramps
D. Respiratory arrest

A

Answer: A. Headache and C. Muscle cramps
Rationale: The slide indicates that mild hyponatremia with serum sodium levels ranging from 130 to 135 mEq/L can present with symptoms such as headache, nausea, vomiting, fatigue, confusion, muscle cramps, and depressed reflexes. Seizures and respiratory arrest are not typically associated with mild hyponatremia but with more severe cases.

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13
Q

At what serum sodium level do the most severe consequences of hyponatremia, such as seizures, coma, and death, generally occur?
A. 120-130 mEq/L
B. Less than 120 mEq/L
C. 130-135 mEq/L
D. More than 135 mEq/L

A

Answer: B. Less than 120 mEq/L
Rationale: According to the slide, the most severe neurological consequences of hyponatremia, including seizures, coma, and death, typically occur when serum sodium levels drop below 120 mEq/L.

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14
Q

Which symptom is shared between the clinical presentations of mild and moderate hyponatremia- select all?
A. Headache
B. Muscle cramps
C. Lethargy
D. Confusion

A

Answer: A. Headache and D. Confusion and C. Lethargy/malaise
Rationale: Both mild (serum sodium 130-135 mEq/L) and moderate (serum sodium 120-130 mEq/L) hyponatremia can present with headache and confusion. These symptoms appear to worsen as the severity of the hyponatremia increases.

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15
Q

What is the maximum recommended rate of sodium correction in the treatment of hyponatremia to prevent osmotic demyelination syndrome?
A. 0.5 mEq/L/hr
B. 1.0 mEq/L/hr
C. 1.5 mEq/L/hr
D. 2.0 mEq/L/hr

A

Answer: C. 1.5 mEq/L/hr
Rationale: The slide states that sodium correction should not exceed 1.5 mEq/L/hr when treating hyponatremia to avoid rapid increases which can lead to osmotic demyelination syndrome, a condition that can cause permanent neurological damage.

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16
Q

In the event of hyponatremic seizures, what is the initial treatment approach?
A. Administration of hypertonic saline at 3-5 ml/kg over 20 minutes
B. Rapid infusion of normal saline
C. Administration of electrolyte drinks
D. Continuous infusion of diuretics

A

Answer: A. Administration of hypertonic saline at 3-5 ml/kg over 20 minutes
Rationale: The slide outlines that hyponatremic seizures are a medical emergency and should be treated with 3-5 ml/kg of 3% hypertonic saline over 20 minutes to quickly raise serum sodium levels and control the seizures. It is important to treat cautiously to avoid complications associated with rapid sodium correction.

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17
Q

During the treatment of hyponatremia, how often should sodium levels be checked?
A. Every 2 hours
B. Every 4 hours
C. Every 6 hours
D. Once daily

A

Answer: B. Every 4 hours
Rationale: The instruction on the slide to “Check Na+ level q 4 hr while replacing” suggests that serum sodium levels should be monitored every 4 hours during the replacement therapy to safely manage the correction rate and avoid complications from too rapid an increase in sodium concentration.

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18
Q

Which patient population is at a higher risk for developing hypernatremia due to poor oral intake?
A. Adolescents and young adults
B. Middle-aged adults
C. Very young and very old individuals
D. Individuals with enhanced physical activity

A

Answer: C. Very young and very old individuals
Rationale: The slide indicates that very young and very old individuals, especially those with altered mental status, are at higher risk for hypernatremia due to poor oral intake, which may lead to dehydration and increased serum sodium concentration.

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19
Q

What is a potential endocrine cause of hypernatremia?
A. Hyperthyroidism
B. Hypothyroidism
C. Addison’s disease
D. Diabetes insipidus

A

Answer: D. Diabetes insipidus
Rationale: Diabetes insipidus is listed as a common cause of hypernatremia. This condition is characterized by the loss of dilute urine due to the body’s inability to concentrate urine, which can lead to an increased concentration of sodium in the blood.

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20
Q

Which iatrogenic action can lead to hypernatremia, select all?
A. Administration of Bicarb
B. Use of nonsteroidal anti-inflammatory drugs (NSAIDs)
C. Overcorrection of hyponatremia
D. Use of antibiotic medications

A

Answer: C. Overcorrection of hyponatremia & A. Excessive sodium bicarb (treating acidosis)

Rationale: The slide identifies overcorrection of hyponatremia as a common cause of hypernatremia. This can occur when the sodium levels in a hyponatremic patient are increased too rapidly, leading to an abnormally high sodium concentration in the blood.

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21
Q

What are the clinical findings associated with hypovolemic hypernatremia?
A. Peripheral edema and ascites
B. Decreased skin turgor and orthostatic hypotension
C. Central diabetes insipidus and gestational diabetes insipidus
D. Hyperaldosteronism and Cushing’s syndrome

A

Answer: B. Decreased skin turgor and orthostatic hypotension
Rationale: The slide lists clinical findings associated with hypovolemic hypernatremia, such as decreased skin turgor, flat neck veins, dry mucous membranes, orthostatic hypotension, tachycardia, and oliguria. These symptoms suggest a deficit in total body water with a relative excess of sodium.

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22
Q

Which conditions can cause euvolemic hypernatremia according to the diagnostic algorithm?
A. Inadequate sodium intake and intravenous sodium bicarbonate administration
B. Renal salt and water loss and gastrointestinal losses
C. Central diabetes insipidus and insensible losses
D. Saltwater drowning and hypertonic saline enemas

A

Answer: C. Central diabetes insipidus and insensible losses
Rationale: Euvolemic hypernatremia occurs when there is a loss of water without a significant change in sodium level, which is illustrated in the slide by conditions such as central diabetes insipidus and insensible losses through the respiratory tract or skin.

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23
Q

For a patient presenting with hypervolemic hypernatremia, which of the following is a likely cause?
A. Excessive administration of diuretics
B. Profound glycosuria
C. Excessive sodium intake through intravenous therapy
D. Sweating and diarrhea

A

Answer: C. Excessive sodium intake through intravenous therapy
Rationale: Hypervolemic hypernatremia is described on the slide as being associated with conditions that cause an increase in sodium, such as excessive sodium intake through intravenous therapy, hyperaldosteronism, and Cushing’s syndrome.

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24
Q

What is the recommended rate of sodium reduction in the treatment of hypernatremia to prevent neurological complications?
A. 0.5 mEq/L/hr and no more than 10 mEq/L per day
B. 1 mEq/L/hr and no more than 12 mEq/L per day
C. 1.5 mEq/L/hr and no more than 15 mEq/L per day
D. 2 mEq/L/hr and no more than 20 mEq/L per day

A

Answer: A. 0.5 mEq/L/hr and no more than 10 mEq/L per day
Rationale: The slide specifies that the sodium reduction rate should not exceed 0.5 mEq/L/hr, and the total daily decrease should not surpass 10 mEq/L to avoid complications such as cerebral edema, seizures, and neurologic damage.

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25
Q

Which treatment is appropriate for a patient with euvolemic hypernatremia?
A. Administration of normal saline
B. Administration of diuretics
C. Water replacement orally or with D5W (5% dextrose in water)
D. Restriction of fluid intake

A

Answer: C. Water replacement orally or with D5W (5% dextrose in water)
Rationale: The slide indicates that the treatment for euvolemic hypernatremia is water replacement, which can be done orally or with intravenous fluids such as 5% dextrose in water (D5W). This approach helps to correct the water deficit without significantly affecting the sodium level.

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26
Q

What are the severe symptoms of hypernatremia that may indicate a medical emergency?
A. Orthostasis and restlessness
B. Tremor and muscle twitching
C. Seizures and death
D. Spasticity and lethargy

A

Answer: C. Seizures and death
Rationale: The slide lists seizures and death among the severe symptoms of hypernatremia, highlighting the urgency of medical intervention when these symptoms are present due to the risk of severe neurological outcomes.

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27
Q

What is the normal serum potassium range that is considered safe for proceeding with surgery?
A. 2.5-4.0 mmol/L
B. 3.0-4.5 mmol/L
C. 3.5-5.0 mmol/L
D. 4.0-5.5 mmol/L

A

Answer: C. 3.5-5.0 mmol/L
Rationale: The slide indicates that the normal potassium level is between 3.5-5.0 mmol/L. This range is typically considered safe for surgery as it reflects a normal balance of potassium, which is a critical electrolyte for cellular function, especially in heart muscle cells

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28
Q

What role does aldosterone play in potassium regulation?
A. It decreases potassium secretion and sodium reabsorption.
B. It increases potassium secretion and decreases sodium reabsorption.
C. It decreases both potassium secretion and sodium reabsorption.
D. It increases potassium secretion and increases sodium reabsorption.

A

Answer: D. It increases potassium secretion and increases sodium reabsorption.
Rationale: According to the slide, aldosterone causes the distal nephron to secrete potassium and reabsorb sodium. This hormonal regulation helps maintain potassium balance in the body and is part of the renin-angiotensin-aldosterone system.

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29
Q

In patients with renal failure, how is potassium excretion affected?
A. Potassium excretion increases, leading to hypokalemia.
B. Potassium excretion is unaffected.
C. Potassium excretion declines, shifting more burden to the gastrointestinal system.
D. Potassium excretion increases through the respiratory system.

A

Answer: C. Potassium excretion declines, shifting more burden to the gastrointestinal system.
Rationale: The slide explains that in renal failure, potassium excretion declines because the kidneys are less able to excrete potassium. To compensate, the body shifts more potassium excretion to the gastrointestinal system. This adjustment is important because potassium accumulation can have serious cardiac effects.

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30
Q

When evaluating a patient for surgery, a CRNA notes the patient’s medication includes a drug that affects aldosterone. How would this impact potassium regulation in the body?
A. Decrease potassium excretion, risking hyperkalemia
B. Increase potassium excretion, potentially leading to hypokalemia
C. Have no effect on potassium levels
D. Increase potassium retention, risking hyperkalemia

A

Answer: B. Increase potassium excretion, potentially leading to hypokalemia
Rationale: Aldosterone promotes potassium excretion and sodium retention. A medication affecting aldosterone could therefore increase potassium excretion, and a CRNA would need to be vigilant for signs of hypokalemia, which could have significant perioperative implications.

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31
Q

Select all that apply. Which conditions are known causes of hypokalemia due to increased renal potassium loss?
A. Use of thiazide diuretics
B. High-dose glucocorticoids therapy
C. Hyperaldosteronism
D. High dietary intake of potassium

A

Answer: A, B, C
Rationale: Thiazide diuretics, loop diuretics, high-dose glucocorticoids, and hyperaldosteronism are mentioned on the slide as causes of hypokalemia due to increased renal potassium loss. High dietary intake of potassium is not listed as a cause of renal potassium loss.

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32
Q

What medical treatment is associated with hypokalemia due to the consumption of natural products?
A. Licorice
B. Cranberry juice
C. Echinacea
D. St. John’s Wort

A

Answer: A. Licorice
Rationale: The slide specifically mentions that excessive licorice consumption can lead to hypokalemia, likely due to the presence of glycyrrhizin, which can mimic aldosterone and cause increased potassium excretion.

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33
Q

What treatment options are recommended for patients with hypokalemia- select all?
A. Intravenous potassium supplementation
B. Oral potassium supplementation
C. Potassium-sparing diuretics
D. Dietary potassium intake

A

Answer: B. Oral potassium supplementation, C. Potassium-sparing diuretics, D. Dietary potassium intake
Rationale: Oral potassium chloride is often the treatment of choice, especially for patients who are not critically low in potassium and can safely ingest and absorb oral medications. In patients with low-normal or mild hypokalemia, increasing dietary potassium is also appropriate, especially for those with hypertension or heart disease. Potassium-sparing diuretics can be used to address ongoing diuretic-induced potassium loss or in certain cases of hyperaldosteronism. In severe cases, intravenous potassium may be necessary, especially when there are significant ECG changes, symptoms of severe hypokalemia, or if the patient cannot tolerate oral potassium (Cleveland Clinic​​, AAFP​​, GGC Medicines​​).

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34
Q

What ECG change is commonly associated with hypokalemia?
A. ST-segment elevation
B. P-wave enlargement
C. U wave
D. QRS widening

A

Answer: C. U wave
Rationale: The presence of U waves on an ECG is a sign that may be observed in hypokalemia, which indicates a potassium imbalance affecting cardiac electrical activity.

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35
Q

For a patient with hypokalemia, which route of potassium administration is generally preferred when both options are feasible?
A. Intravenous (IV)
B. Oral (PO)
C. Subcutaneous
D. Intramuscular

A

Answer: B. Oral (PO)
Rationale: Oral administration is usually preferred for potassium replacement as it works effectively and is associated with fewer risks compared to intravenous administration. However, if a patient’s condition is severe or they cannot tolerate oral administration, IV potassium may be necessary.

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36
Q

What is the maximum rate of intravenous potassium replacement usually recommended to avoid complications such as arrhythmias?
A. 5-10 mmol/L/hr
B. 10-20 mmol/L/hr
C. 20-40 mmol/L/hr
D. 40-60 mmol/L/hr

A

Answer: B. 10-20 mmol/L/hr
Rationale: The slide suggests that when intravenous potassium replacement is necessary, it’s generally done at a controlled rate of 10-20 mEq/L/hr to avoid rapid changes that could lead to complications.

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37
Q

Select all that apply. Which factors can cause a shift of potassium into cells, leading to hypokalemia?
A. Beta-agonists
B. Insulin
C. Bicarbonate
D. Diuretics

A

Answer: A, B, C
Rationale: Beta-agonists, insulin, and bicarbonate are known to drive potassium into cells, which can reduce the amount of potassium in the extracellular fluid and potentially exacerbate hypokalemia. Diuretics typically cause hypokalemia by increasing renal excretion of potassium, not by shifting it into cells.
Hyperventilation can as well.

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38
Q

What ECG changes are indicative of severe hyperkalemia?
A. Peaked T waves
B. P wave disappearance
C. Sine wave pattern
D. All of the above

A

Answer: D. All of the above
Rationale: Severe hyperkalemia can be indicated on an ECG by a progression of changes starting with peaked T waves, followed by the disappearance of P waves, prolongation of the QRS complex, and potentially leading to a sine wave pattern, which is a pre-terminal rhythm, indicating an urgent need for medical intervention.

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39
Q

Which medications or conditions should be carefully managed or monitored due to their potential to increase serum potassium levels? (Select all that apply)
A. Drugs that inhibit the renin-angiotensin-aldosterone system (RAAS)
B. Depolarizing neuromuscular blockers like succinylcholine
C. Drugs that promote potassium excretion
D. Hypoaldosteronism

A

Answer: A, B, D
Rationale: Drugs that inhibit RAAS or potassium excretion can lead to increased serum potassium levels. Succinylcholine is known to increase serum potassium acutely, especially in certain patient populations. Hypoaldosteronism can also result in increased potassium levels due to decreased excretion.

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40
Q

What populations are at a higher risk of developing hyperkalemia with the use of succinylcholine?
A. Patients with chronic kidney disease (CKD)
B. Diabetic patients
C. Women
D. A and B only

A

Answer: D. A and B only
Rationale: Patients with conditions that affect potassium homeostasis, such as those with chronic kidney disease, are at higher risk of hyperkalemia with the use of succinylcholine. Diabetic patients can also be at increased risk due to potential baseline kidney damage and altered insulin levels, which affect cellular potassium shifts.

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41
Q

What is the initial treatment for hyperkalemia to stabilize the cell membrane?
A. Dialysis
B. Administration of Calcium
C. Administration of Insulin with Glucose
D. Hyperventilation to increase pH

A

Answer: B. Administration of Calcium
Rationale: Calcium is often used as the first line of treatment for hyperkalemia to stabilize the cardiac cell membrane, especially when ECG changes are present or if the patient is symptomatic.

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42
Q

What treatment can be used to shift potassium into cells, thus temporarily lowering serum potassium levels?
A. Bicarbonate
B. Insulin with Glucose
C. Loop Diuretics
D. Both A and B

A

Answer: D. Both A and B
Rationale: Both bicarbonate and insulin with glucose can cause a shift of potassium into cells (works in 10-20 min). Insulin facilitates the uptake of glucose into cells, which also drives potassium inside, and bicarbonate can correct acidosis, which can help shift potassium into cells as well.

also Hyperventilation - > quick drastic change.
Hyperventilation (↑pH by 0.1 →↓K+ by 0.4-1.5 mmol/L)

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43
Q

Why should succinylcholine be avoided in the treatment of patients with hyperkalemia?
A. It can cause hypertension.
B. It may further increase serum potassium levels.
C. It reduces the effectiveness of insulin and glucose.
D. It leads to hyperventilation.

A

Answer: B. It may further increase serum potassium levels.
Rationale: Succinylcholine, a depolarizing neuromuscular blocking agent, can cause an acute rise in serum potassium levels, which can be dangerous in the setting of hyperkalemia.

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44
Q

What is the normal range for ionized calcium in the blood?
A. 0.8-1.0 mmol/L
B. 1.2-1.38 mmol/L
C. 1.5-1.8 mmol/L
D. 2.0-2.5 mmol/L

A

Answer: B. 1.2-1.38 mmol/L
Rationale: The slide states that the normal range for ionized calcium (iCa++) is 1.2-1.38 mmol/L. Ionized calcium is the physiologically active form of calcium in the blood.

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45
Q

How does blood pH affect ionized calcium levels?
A. An increase in pH leads to increased binding of calcium to albumin, decreasing ionized calcium.
B. A decrease in pH leads to increased binding of calcium to albumin, decreasing ionized calcium.
C. An increase in pH leads to decreased binding of calcium to albumin, increasing ionized calcium.
D. A decrease in pH leads to decreased binding of calcium to albumin, increasing ionized calcium.

A

Answer: A
Rationale: Alkalosis, or an increase in blood pH, causes more calcium to bind to albumin, which reduces the level of ionized (free) calcium in the blood. Conversely, acidosis, or a decrease in blood pH, causes less calcium to bind to albumin, which increases the level of ionized calcium.

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46
Q

Which hormone decreases blood calcium levels by inhibiting bone resorption and renal reabsorption of calcium?
A. Parathyroid hormone (PTH)
B. Vitamin D
C. Calcitonin
D. Growth hormone

A

Answer: C. Calcitonin
Rationale: Calcitonin lowers blood calcium levels primarily by inhibiting osteoclasts, the cells that break down bone and release calcium into the bloodstream, and by reducing renal reabsorption of calcium

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47
Q

what is a common complication after thyroid or parathyroid surgery that can lead to hypocalcemia?
A. Hyperparathyroid hormone secretion
B. Decreased parathyroid hormone secretion
C. Increased calcitonin secretion
D. Hypercalcemia

A

Answer: B. Decreased parathyroid hormone secretion
Rationale: Decreased secretion of parathyroid hormone (PTH) is a known complication post-thyroid or parathyroid surgery and can result in hypocalcemia, as PTH is crucial for the regulation of blood calcium levels.

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47
Q

What are the primary actions of parathyroid hormone (PTH) in calcium regulation? (Select all that apply)
A. Increases gastrointestinal absorption of calcium
B. Increases renal excretion of calcium
C. Increases bone resorption
D. Increases renal reabsorption of calcium

A

Answer: A, C, D
Rationale: PTH raises blood calcium levels by increasing calcium absorption in the gastrointestinal tract, promoting calcium reabsorption in the kidneys, and stimulating the release of calcium from bones

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48
Q

Why is magnesium important in the context of calcium balance in the body?
A. It directly increases calcium absorption in the gut.
B. It is required for the production of parathyroid hormone.
C. It binds calcium and increases blood calcium levels.
D. It inhibits the action of vitamin D.

A

Answer: B. It is required for the production of parathyroid hormone.
Rationale: Magnesium is essential for the proper function of the parathyroid glands and for the production of PTH, which in turn is crucial for maintaining calcium balance.

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49
Q

After how many units of packed red blood cells (PRBCs) transfusion should ionized calcium (iCa++) be checked due to the risk of hypocalcemia?
A. After 1-2 units
B. After 2-3 units
C. After 3-4 units
D. After 4+ units

A

Answer: D. After 4+ units
Rationale: Citrate, which is used as a preservative in blood products, binds calcium and can lead to hypocalcemia, especially after transfusion of multiple units of blood. It is advisable to check ionized calcium levels after 4 or more units of PRBCs have been transfused to prevent and treat potential hypocalcemia.

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50
Q

What serum calcium level is generally indicative of hyperparathyroidism?
A. >9 mg/dL
B. >11 mg/dL
C. >13 mg/dL
D. >15 mg/dL

A

Answer: B. >11 mg/dL
Rationale: The slide indicates that a serum calcium level greater than 11 mg/dL is typically associated with hyperparathyroidism, a condition where the parathyroid glands secrete too much parathyroid hormone, leading to elevated levels of calcium in the blood.

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51
Q

Which condition is characterized by excessively high calcium levels due to malignancy?
A. Hyperparathyroidism
B. Hypoparathyroidism
C. Serum Ca++ > 13
D. Vitamin D deficiency

A

Answer: C. Cancer-associated hypercalcemia
Rationale: The slide points out that a serum calcium level greater than 13 mg/dL is often seen in cancer, suggesting cancer-associated hypercalcemia, which occurs when cancer leads to the breakdown of bone tissue or the production of parathyroid hormone-related protein.

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52
Q

Which of the following is a less common cause of hypercalcemia? (Select all that apply)
A. Vitamin D intoxication
B. Milk-alkali syndrome
C. Granulomatous diseases like sarcoidosis
D. Hypoaldosteronism

A

Answer: A, B, C
Rationale: The slide lists vitamin D intoxication, milk-alkali syndrome (excessive gastrointestinal calcium absorption), and granulomatous diseases such as sarcoidosis as less common causes of hypercalcemia. Hypoaldosteronism is not mentioned as a cause of hypercalcemia on this slide.

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53
Q

Which symptom is commonly associated with hypocalcemia?
A. Hypertension
B. Paresthesias
C. Confusion
D. Seizures

A

Answer: D. seizures

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53
Q

What electrocardiogram (ECG) change is indicative of hypocalcemia?
A. Short QT interval
B. Prolonged QT interval
C. Short PR interval
D. Elevated ST segment

A

Answer: B. Prolonged QT interval
Rationale: A prolonged QT interval can occur in hypocalcemia, reflecting changes in cardiac muscle excitability.

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54
Q

What life-threatening complication should be carefully monitored for after parathyroidectomy?
A. Hypercalcemia
B. Laryngospasm
C. Myocardial depression
D. Hypertension

A

Answer: B. Laryngospasm
Rationale: Post-parathyroidectomy hypocalcemia can induce laryngospasm, a critical complication requiring immediate attention and management.

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55
Q

What cardiac dysrhythmia is commonly associated with hypomagnesemia?
A. Atrial fibrillation
B. Bradycardia
C. Polymorphic ventricular tachycardia, specifically Torsades de Pointes
D. Sinus tachycardia

A

Answer: C. Polymorphic ventricular tachycardia, specifically Torsades de Pointes
Rationale: Hypomagnesemia can lead to several types of ventricular dysrhythmias, among which Torsades de Pointes is particularly associated with low magnesium levels.

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56
Q

What is a primary cause of hypomagnesemia?
A. Excessive dietary intake of magnesium
B. Renal wasting
C. Hyperparathyroidism
D. Use of calcium channel blockers

A

Answer: B. Renal wasting
Rationale: Renal wasting, a condition where the kidneys excrete too much magnesium, is a common cause of hypomagnesemia.

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57
Q

What is the recommended initial treatment for seizures associated with hypomagnesemia?
A. Oral magnesium oxide supplements
B. 2 grams of magnesium sulfate intravenously
C. Intravenous calcium gluconate
D. Intramuscular magnesium injection

A

Answer: B. 2 grams of magnesium sulfate intravenously
Rationale: For acute treatment of seizures caused by hypomagnesemia, intravenous administration of magnesium sulfate is often recommended. Same treatment for torsades

58
Q

What level of serum magnesium is associated with severe symptoms such as paralysis, apnea, and cardiac arrest?
A. >4 mEq/L
B. >6 mEq/L
C. >8 mEq/L
D. >10 mEq/L

A

Answer: D. >10 mEq/L
Rationale: Serum magnesium levels exceeding 10 mEq/L can lead to life-threatening symptoms like paralysis, apnea, heart blocks, and cardiac arrest.

59
Q

Which of the following is a treatment option for hypermagnesemia?
A. Administration of IV magnesium
B. Diuresis
C. IV Calcium
D. B and C are correct

A

Answer: D. B and C are correct
Rationale: Diuresis can be used to promote the excretion of excess magnesium, and intravenous calcium is given to counteract the effects of magnesium on the heart and other muscles. stabilize membrane

60
Q

Hypermagnesemia is most commonly due to what cause ?
A. Insufficient dietary intake
B. Genetic disorders
C. Over treatment, particularly in conditions like pre-eclampsia/eclampsia
D. High potassium intake

A

Answer: C. Over treatment, particularly in conditions like pre-eclampsia/eclampsia
Rationale: Hypermagnesemia is typically a result of over treatment, such as when using magnesium sulfate to manage pre-eclampsia or eclampsia, and not due to dietary intake. Also in pheos.

61
Q

Where are the kidneys located in relation to the vertebral column?
A. Between T10-T12
B. Between T12-L2
C. Between T12-L4
D. Between L1-L5

A

Answer: C. Between T12-L4

62
Q

How is the position of the right kidney typically described relative to the left kidney?
A. The right kidney is higher due to the position of the liver.
B. The right kidney is at the same level as the left kidney.
C. The right kidney is slightly caudal (lower) compared to the left kidney.
D. The right kidney is significantly caudal to the left kidney to accommodate the spleen.

A

Answer: C. The right kidney is slightly caudal (lower) compared to the left kidney

63
Q

What is the significance of the kidneys being located in the retroperitoneal space?
A. They are more susceptible to injury.
B. They are more protected by the rib cage.
C. They have less mobility compared to other abdominal organs.
D. They are positioned for better gravity-assisted filtration.

A

They are more protected by the rib cage.
Rationale: Retroperitoneal organs like the kidneys have only their anterior surfaces covered by peritoneum, which places them more posterior in the abdomen and partly protected by the lower rib cage.

64
Q

What is the initial structure in the nephron where blood filtration begins?
A. Distal Convoluted Tubule (DCT)
B. Loop of Henle
C. Glomerulus
D. Collecting duct

A

Answer: C. Glomerulus

65
Q

Approximately how many nephrons does each kidney contain?
A. 100,000
B. 500,000
C. 1 million
D. 2 million

A

Answer: C. 1 million

66
Q

The tubular system of the nephron includes which of the following structures? (Select all that apply)
A. Bowman capsule
B. Proximal Tubule (PCT)
C. Distal Tubule (DCT)
D. Ascending Limb of Loop of Henle
E. Collecting duct

A

Answer: A, B, C, D, E
Rationale: The tubular system comprises all mentioned structures, which sequentially participate in the filtration and modification of urine.

67
Q

What percentage of cardiac output do the kidneys receive?
A. 10%
B. 20%
C. 30%
D. 40%

A

Answer: B. 20%

68
Q

Which part of the kidney receives the majority of renal blood flow?
A. Medulla
B. Cortex
C. Renal pelvis
D. Ureters

A

Answer: B. Cortex

69
Q

What renal structure is particularly vulnerable to damage due to hypotension?
A. Glomerulus
B. Distal Convoluted Tubule
C. Loop of Henle
D. Collecting duct

A

Answer: C. Loop of Henle

70
Q

Which mechanism is involved in the body’s response to volume and blood pressure regulation that can influence kidney function?
A. Renin-angiotensin-aldosterone system (RAAS)
B. Antidiuretic hormone (ADH) release
C. Parasympathetic nervous system activation
D. Sympathetic nervous system inhibition

A

Answer: A. Renin-angiotensin-aldosterone system (RAAS)

71
Q

What laboratory test is considered the most reliable measure of glomerular filtration rate (GFR)?
A. Serum creatinine
B. Blood urea nitrogen (BUN)
C. Creatinine clearance
D. Urine specific gravity

A

Answer: C. Creatinine clearance

72
Q

How does dehydration typically affect glomerular filtration rate (GFR) values?
A. Increases GFR
B. Decreases GFR
C. Does not affect GFR
D. Causes variable changes in GFR

A

Answer: B. Decreases GFR

73
Q

What can a doubling of serum creatinine indicate about glomerular filtration rate (GFR)?
A. No change in GFR
B. An increase in GFR by 50%
C. A drop in GFR by 50%
D. GFR remains within normal range

A

Answer: C. A drop in GFR by 50%

74
Q

What does a high BUN:Creatinine ratio typically indicate?
A. Overhydration
B. Adequate hydration status
C. Dehydration
D. Glomerular injury

A

Answer: C. Dehydration

75
Q

A patient presents with proteinuria levels significantly above 150 mg/dL (around 750). What could this suggest?
A. Adequate glomerular function
B. Glomerular injury or urinary tract infection (UTI)
C. Overhydration
D. Effective concentration of urine

A

Answer: B. Glomerular injury or urinary tract infection (UTI)

76
Q

What does specific gravity measure in the context of renal function?
A. The kidney’s ability to excrete large molecules
B. The kidney’s ability to concentrate urine
C. The presence of glucose in the urine
D. The hydration status of the body

A

Answer: B. The kidney’s ability to concentrate urine

77
Q

What clinical sign is considered a late indicator of volume depletion?
A. Increase in urine output (UOP)
B. Decrease in blood pressure
C. Decrease in urine output (UOP)
D. Increase in heart rate

A

Answer: C. Decrease in urine output (UOP)
Rationale: A drop in urine output is a late sign of volume loss and indicates that the kidneys are conserving water due to decreased blood volume. Normal UOP is around 0.5-1 ml/kg/hr.

78
Q

In the context of volume status assessment, what does a negative base excess (BE) in blood tests typically indicate?
A. Metabolic alkalosis
B. Metabolic acidosis
C. Respiratory alkalosis
D. Respiratory acidosis

A

Answer: B. Metabolic acidosis
Rationale: A negative base excess suggests a deficit of base in the blood, which can indicate metabolic acidosis, often associated with conditions such as dehydration or renal failure.

79
Q

Which lab value is likely to increase in response to volume depletion and metabolic acidosis?
A. Hemoglobin
B. Lactate
C. Sodium
D. Calcium

A

Answer: B. Lactate
Rationale: An increase in lactate can occur with metabolic acidosis, often seen in states of volume depletion where tissue perfusion is compromised.

Normal Values for Context:

Urine output (UOP): Euvolemic status is typically maintained with a UOP of around 30 ml/hr or 0.5-1 ml/kg/hr.
Base excess (BE): A normal BE is zero, indicating a balanced amount of base in the blood.
Lactate: Normal blood lactate levels are 0.5-2.2 mmol/L, and levels above this range may indicate lactic acidosis, often associated with poor tissue perfusion.

80
Q

What is the purpose of using ultrasound to assess the inferior vena cava (IVC) in volume status monitoring?
A. To measure blood flow to the kidneys
B. To determine the ejection fraction of the heart
C. To evaluate the degree of IVC collapse during respiration as an indicator of volume status
D. To visualize the structure of the heart valves

A

Answer: C. To evaluate the degree of IVC collapse during respiration as an indicator of volume status
Rationale: Ultrasound assessment of the IVC involves measuring the degree of collapse during respiration. A compressed IVC, particularly with greater than 50% collapse, can indicate volume depletion.

81
Q

What hemodynamic measurement is a powerful stimulus for renal vasoconstriction when elevated?
A. Central venous pressure (CVP)
B. Renal arterial pressure (RAP)
C. Left atrial pressure (LAP)
D. Pulmonary capillary wedge pressure (PCWP)

A

Answer: D. Pulmonary capillary wedge pressure (PCWP)
Rationale: An elevated PCWP, which reflects left ventricular end-diastolic pressure, can be a powerful stimulus for renal vasoconstriction.

82
Q

For the stroke volume variation (SVV) to be a valid indicator of volume status, what conditions must be assumed? (Select all that apply)
A. The patient is in sinus rhythm.
B. The patient is undergoing mechanical ventilation.
C. The patient is hypotensive.
D. The patient is in atrial fibrillation.

A

Answer: A. The patient is in sinus rhythm, B. The patient is undergoing mechanical ventilation
Rationale: SVV is a dynamic measure of volume status that assumes the patient is in sinus rhythm and is undergoing controlled mechanical ventilation, as it compares inspiratory vs expiratory pressures.

83
Q

What does a greater than 50% collapse of the inferior vena cava (IVC) on ultrasound typically indicate?
A. Overhydration
B. Euvolemia
C. Volume deficit
D. Right heart failure

A

Answer: C. Volume deficit
Rationale: A significant collapse of the IVC greater than 50% during inspiration as assessed by ultrasound is suggestive of a fluid deficit

84
Q

Azotemia is characterized by the buildup of what substances in the blood?
A. Potassium and sodium
B. Nitrogenous products such as urea and creatinine
C. Hemoglobin and myoglobin
D. Calcium and phosphate

A

Answer: B. Nitrogenous products such as urea and creatinine
Rationale: Azotemia, which is the buildup of nitrogenous waste products like urea and creatinine in the blood, is a hallmark of acute kidney injury (AKI).

85
Q

n cases of Acute Kidney Injury (AKI) with multi-system organ failure (MSOF) requiring dialysis, what is the associated mortality rate?
A. Less than 10%
B. Around 30%
C. Greater than 50%
D. About 75%

A

Answer: C. Greater than 50%
Rationale: AKI with MSOF that necessitates dialysis treatment carries a very high mortality rate, exceeding 50%.

For optimal patient management and prognosis, early detection and intervention are crucial. Continuous Venovenous Hemodiafiltration (CVVHD) is a treatment option that provides renal support during AKI.

86
Q

Which condition is not typically a risk factor for acute kidney injury (AKI)?
A. Chronic Heart Failure (CHF)
B. Hypertension
C. Peripheral Vascular Disease (PVD)
D. Diabetes

A

Answer: B. Hypertension
Rationale: While hypertension can lead to chronic kidney disease, it is not listed on the slide as a risk factor for AKI. The slide specifically mentions CHF, PVD, diabetes, and other conditions as risk factors for AKI.

87
Q

What does the presence of sepsis indicate in the context of AKI risk?
A. Direct injury to the kidney cells
B. Risk due to associated hypotension
C. A bacterial infection within the kidney
D. Urinary tract obstruction

A

Answer: B. Risk due to associated hypotension
Rationale: Sepsis can lead to systemic hypotension, which in turn can cause reduced renal perfusion and acute kidney injury.

88
Q

What is a common procedural risk factor for AKI?
A. Biopsy
B. Endoscopy
C. Major operative procedures
D. Blood transfusion

A

Answer: C. Major operative procedures
Rationale: Major surgical interventions are risk factors for AKI, potentially due to changes in hemodynamics, exposure to nephrotoxic agents, or direct renal insult.

89
Q

According to the AKI Diagnostic Criteria, what increase in serum creatinine (SCr) is considered diagnostic for AKI within 48 hours?
A. Increase by 0.1 mg/dL
B. Increase by 0.2 mg/dL
C. Increase by 0.3 mg/dL
D. Increase by 0.5 mg/dL

A

Answer: C. Increase by 0.3 mg/dL. (normal is around 0.7-1.3)

90
Q

An acute decrease in creatinine clearance by what percentage is diagnostic for AKI?
A. 25%
B. 50%
C. 75%
D. 100%

A

Answer: B. 50%

91
Q

Which of the following is not necessarily observed in all cases of AKI?
A. Asymptomatic presentation
B. Increased SCr by 50% within 7 days
C. Abrupt oliguria
D. Hypotension (HoTN)

A

Answer: C. Abrupt oliguria
Rationale: While abrupt oliguria is a common symptom of AKI, it is not always present in every case.

92
Q

Which condition is a direct cause of nephron injury leading to renal azotemia?
A. Hemorrhage
B. Acute glomerulonephritis
C. Nephrolithiasis
D. Trauma

A

Answer: B. Acute glomerulonephritis

93
Q

What is the typical cause of postrenal azotemia?
A. Renal perfusion deficit
B. Nephron injury
C. Outflow obstruction
D. Muscle injury

A

Answer: C. Outflow obstruction
Rationale: Postrenal azotemia is usually due to an obstruction in the urinary flow, which can be due to conditions like nephrolithiasis or benign prostatic hyperplasia (BPH).

94
Q

Myoglobinuria can lead to which type of kidney injury?
A. Prerenal azotemia
B. Renal azotemia
C. Postrenal azotemia
D. None of the above

A

Answer: B. Renal azotemia
Rationale: Myoglobinuria, usually resulting from significant muscle injury, can cause renal azotemia as myoglobin is toxic to the kidneys and can lead to acute tubular necrosis if not managed promptly.

95
Q

What is the BUN:Creatinine ratio typically observed in pre-renal azotemia?
A. Greater than 10:1
B. Greater than 15:1
C. Greater than 20:1
D. Less than 20:1

A

Answer: C. Greater than 20:1
Rationale: A BUN:Creatinine ratio greater than 20:1 is indicative of pre-renal azotemia, suggesting that the cause of kidney impairment is due to a factor outside of the kidneys, such as reduced renal blood flow (RBF), which leads to increased reabsorption of BUN.

96
Q

In pre-renal azotemia, what is the primary treatment goal?
A. To reduce the production of BUN and creatinine
B. To restore renal blood flow (RBF)
C. To increase urine output at any cost
D. To correct underlying hormonal imbalances

A

Answer: B. To restore renal blood flow (RBF)
Rationale: The main objective in treating pre-renal azotemia is to restore adequate renal blood flow. This can be achieved through fluid resuscitation, and if necessary, the use of osmotic diuretics like mannitol, and cautious use of loop diuretics after ensuring adequate intravascular volume. Pressors are typically not the first line of treatment due to their potential to further decrease renal perfusion unless necessary to maintain mean arterial pressure (MAP).

97
Q

What can untreated pre-renal azotemia lead to if not promptly and properly addressed?
A. Renal azotemia
B. Hypernatremia
C. Overhydration
D. Pulmonary edema

A

Answer: A. Renal azotemia
Rationale: If pre-renal azotemia, which is often reversible with appropriate treatment, is not corrected, it can lead to intrinsic renal damage or acute tubular necrosis, resulting in a more severe form of kidney injury known as renal azotemia.

98
Q

In renal azotemia, what is the BUN:Creatinine ratio often observed?
A. Less than 15:1
B. Exactly 20:1
C. Greater than 20:1
D. Greater than 30:1

A

Answer: A. Less than 15:1
Rationale: In renal azotemia, due to intrinsic renal disease and decreased reabsorption in the proximal tubule, the BUN:Creatinine ratio is often less than 15:1, differentiating it from pre-renal azotemia where the ratio is typically greater than 20:1 due to increased reabsorption.

99
Q

A decrease in which of the following is a late sign of renal azotemia?
A. Blood pressure
B. GFR
C. Urine output
D. Serum potassium levels

A

Answer: B. GFR
Rationale: A decreased glomerular filtration rate (GFR) is a late sign of renal azotemia and indicates worsening renal function intrinsic to the kidneys.

100
Q

What laboratory finding is characteristic of renal azotemia?
A. Increased blood urea nitrogen (BUN)
B. Decreased serum creatinine
C. Increased creatinine filtration
D. Increased blood creatinine

A

Answer: D. Increased blood creatinine
Rationale: In renal azotemia, decreased creatinine filtration due to intrinsic renal disease leads to increased blood creatinine levels

101
Q

What is the primary cause of post-renal azotemia?
A. Decreased renal perfusion
B. Glomerular damage
C. Outflow obstruction
D. Infection

A

Answer: C. Outflow obstruction
Rationale: Post-renal azotemia is caused by obstruction of the outflow of urine, which leads to increased nephron tubular hydrostatic pressure.

102
Q

In the management of post-renal azotemia, what is the primary treatment approach?
A. Antibiotic therapy
B. Aggressive fluid resuscitation
C. Removing the source of obstruction
D. Administering diuretics

A

Answer: C. Removing the source of obstruction
Rationale: The treatment for post-renal azotemia focuses on removing the obstruction if possible to restore normal urine flow and prevent permanent damage to the tubular epithelium. Easiest to treat

103
Q

How does the duration of the obstruction affect the reversibility of post-renal azotemia?
A. Reversibility is directly proportional to the duration of the obstruction.
B. Reversibility is inversely related to the duration of the obstruction.
C. Duration of obstruction has no impact on reversibility.
D. Only obstructions lasting less than 24 hours are reversible.

A

Answer: B. Reversibility is inversely related to the duration of the obstruction
Rationale: The longer the duration of the urinary obstruction, the less likely the renal function is to fully recover, making early detection and relief of the obstruction crucial. Increase nephron hydrostatic pressures leads to tubular damage.

104
Q

What does a fractional excretion of sodium (FeNa) of less than 1% suggest in the context of acute kidney injury (AKI)?
A. Pre-renal AKI
B. Intrinsic renal AKI
C. Postrenal AKI
D. No AKI present

A

Answer: A. Pre-renal AKI
Rationale: A low FeNa (<1%) generally indicates pre-renal AKI, where sodium reabsorption is increased as the body attempts to conserve water and maintain blood volume.

105
Q

In AKI, what is indicated by a fractional excretion of urea (FeUrea) typically less than 35%?
A. Pre-renal AKI
B. Intrinsic renal AKI
C. Postrenal AKI
D. Nephrotic syndrome

A

Answer: A. Pre-renal AKI
Rationale: Similar to FeNa, a low FeUrea suggests pre-renal AKI, reflecting the body’s conservation of urea along with sodium to retain water and improve volume status.

106
Q

In the evaluation of AKI, what would a urine sodium concentration greater than 20 mEq/L most likely indicate?
A. Pre-renal AKI
B. Intrinsic renal AKI
C. Postrenal AKI
D. Excessive dietary sodium intake

A

Answer: B. Intrinsic renal AKI
Rationale: A urine sodium concentration greater than 20 mEq/L is indicative of intrinsic renal AKI, where the kidneys’ ability to reabsorb sodium is impaired due to tubular damage. Would be normal in post renal. and low in pre-renal

107
Q

Which neurological condition can improve with dialysis in patients with acute kidney injury (AKI)?
A. Stroke
B. Seizures
C. Myopathies
D. Uremic Encephalopathy

A

Answer: D. Uremic Encephalopathy
Rationale: Uremic encephalopathy is a result of the build-up of toxins due to kidney failure, which can often be improved with dialysis by removing these waste products from the bloodstream.

108
Q

What is a common cause of neurological complications in AKI?
A. Direct injury to neural tissue
B. Electrolyte imbalances only
C. Protein and amino acids buildup in the blood
D. Traumatic injury to the spinal cord

A

Answer: C. Protein and amino acids buildup in the blood
Rationale: In AKI, the kidneys’ failure to filter blood effectively leads to the accumulation of protein and amino acids, among other substances, which can contribute to various neurological disorders.

109
Q

What is the sequence of cardiovascular complications that can occur due to acute kidney injury (AKI), starting from the most common?
A. Hypertension → Left ventricular hypertrophy → Congestive heart failure → Arrhythmias → Pulmonary edema → Uremic cardiomyopathy
B. Uremic cardiomyopathy → Arrhythmias → Pulmonary edema → Congestive heart failure → Left ventricular hypertrophy → Hypertension
C. Congestive heart failure → Pulmonary edema → Hypertension → Uremic cardiomyopathy → Left ventricular hypertrophy → Arrhythmias
D. Arrhythmias → Uremic cardiomyopathy → Pulmonary edema → Hypertension → Left ventricular hypertrophy → Congestive heart failure

A

Answer: A. Hypertension → Left ventricular hypertrophy → Congestive heart failure → Arrhythmias → Pulmonary edema → Uremic cardiomyopathy
Rationale: Hypertension is often the initial cardiovascular complication in AKI, leading to left ventricular hypertrophy due to the increased workload on the heart. Over time, this can progress to congestive heart failure. If unaddressed, further complications like arrhythmias can develop, along with pulmonary edema and, ultimately, uremic cardiomyopathy due to the accumulation of uremic toxins affecting the heart muscles.

110
Q

What is uremic cardiomyopathy and its association with AKI?
A. A condition characterized by excessive heart rate due to AKI
B. A type of heart muscle disease that is unrelated to AKI
C. A heart muscle disease that can result from long-standing AKI
D. An inflammation of the heart’s outer layer due to AKI

A

Answer: C. A heart muscle disease that can result from long-standing AKI
Rationale: Uremic cardiomyopathy is a form of heart muscle disease specifically associated with the chronic retention of uremic toxins that can occur in the setting of long-standing AKI. It affects the heart’s structure and function, leading to impaired cardiac performance.

111
Q

In the context of AKI, why can arrhythmias occur as a complication?
A. Due to direct infection of the heart
B. Because of the physical strain from fluid overload
C. As a result of electrolyte imbalances secondary to AKI
D. From the administration of nephrotoxic drugs only

A

Answer: C. As a result of electrolyte imbalances secondary to AKI
Rationale: Arrhythmias can occur in AKI due to electrolyte imbalances that affect the electrical conductivity of the heart muscle. Electrolytes like potassium, calcium, and magnesium are often deranged in AKI and play a crucial role in cardiac electrical activity.

112
Q

How does anemia arise as a complication in acute kidney injury (AKI)?
A. Increased erythropoietin (EPO) production
B. Decreased platelet count
C. Increased red cell survival
D. Decreased erythropoietin production and red cell survival

A

Answer: D. Decreased erythropoietin production and red cell survival
Rationale: In AKI, the kidneys’ ability to produce erythropoietin—a hormone necessary for red blood cell production—is impaired. This decrease in erythropoietin production, along with reduced red cell survival, contributes to the development of anemia.

113
Q

What role does desmopressin (DDAVP) play in managing hematological complications of AKI?
A. It decreases von Willebrand Factor (vWF) and Factor VIII to reduce coagulation.
B. It is used prophylactically to increase vWF and Factor VIII to improve coagulation.
C. It functions as an anticoagulant to prevent blood clots.
D. It suppresses erythropoietin production to manage polycythemia.

A

Answer: B. It is used prophylactically to increase vWF and Factor VIII to improve coagulation.
Rationale: Desmopressin (DDAVP) is administered prophylactically in patients with AKI to increase levels of vWF and Factor VIII, which are important for proper coagulation. This can help manage the platelet dysfunction and bleeding risk associated with uremia in AKI.

114
Q

Which test is valuable for assessing platelet dysfunction in AKI?
A. Complete Blood Count (CBC)
B. Erythropoietin level test
C. Platelet function assay or Thromboelastography (TEG)
D. Coombs test

A

Answer: C. Platelet function assay or Thromboelastography (TEG)
Rationale: Platelet dysfunction is a common hematological complication of AKI. Platelet function assays and Thromboelastography (TEG) are valuable diagnostic tools to evaluate the efficiency of platelets and the overall coagulation process in patients with AKI. These tests can guide appropriate interventions to manage the increased risk of bleeding.

115
Q

Which metabolic complication of acute kidney injury (AKI) can lead to dysrhythmias and is directly associated with the renal function?
A. Hypokalemia
B. Hyponatremia
C. Hyperkalemia
D. Hypercalcemia

A

Answer: C. Hyperkalemia
Rationale: Hyperkalemia is a common metabolic complication in AKI due to the kidneys’ reduced ability to excrete potassium. Elevated potassium levels can lead to dangerous cardiac arrhythmias and are therefore a critical concern in the management of AKI.

116
Q

What is a common consequence of proteinuria seen in patients with AKI?
A. Hyperlipidemia
B. Hyperalbuminemia
C. Hypoalbuminemia
D. Hyperglycemia

A

Answer: C. Hypoalbuminemia
Rationale: Hypoalbuminemia in AKI is often due to the loss of protein through the glomeruli, a condition known as proteinuria, where the damaged kidneys allow albumin to escape into the urine.

117
Q

In the context of AKI, how does the parathyroid gland respond to calcium imbalance?
A. Decreased parathyroid hormone (PTH) secretion
B. Parathyroid in overdrive to increase calcium reabsorption
C. Parathyroid gland atrophy
D. Increased calcitonin production

A

Answer: B. Parathyroid in overdrive to increase calcium reabsorption
Rationale: Hyperparathyroidism can occur as a compensatory response in AKI when the damaged kidneys are unable to reabsorb calcium adequately, prompting the parathyroid glands to secrete more PTH to stimulate calcium reabsorption.

118
Q

What type of intravenous solution is preferred in patients with acute kidney injury (AKI) to manage volume status and why?
A. Hypertonic saline
B. Normal saline
C. Lactated Ringer’s
D. Dextrose 5% in water

A

Answer: B. Normal saline
Rationale: Normal saline (NS) is preferred for volume resuscitation in AKI because it does not contain potassium, which is important given that hyperkalemia is a concern in AKI patients.

119
Q

During anesthesia for a patient with AKI, what is the preferred approach for maintaining renal blood flow (RBF) using vasopressors?
A. Preferentially use alpha-agonists
B. Avoid vasopressors altogether
C. Use vasopressin due to its action on the efferent arteriole
D. Use any vasopressor available

A

Answer: C. Use vasopressin due to its action on the efferent arteriole
Rationale: Vasopressin is preferred because it preferentially constricts the efferent arteriole, which can help maintain glomerular filtration rate (GFR) and renal blood flow in AKI patients.

120
Q

What is the role of prophylactic sodium bicarbonate in the management of patients with AKI?
A. To provide sedation
B. To increase urine output
C. To decrease the formation of free radicals and prevent acute tubular necrosis (ATN)
D. To treat hyperkalemia

A

Answer: C. To decrease the formation of free radicals and prevent acute tubular necrosis (ATN)
Rationale: Prophylactic sodium bicarbonate is used in AKI to alkalinize the urine, which can help decrease the formation of free radicals and prevent the progression of ATN into established renal failure.

121
Q

What is a critical consideration regarding hemodynamic monitoring in patients with acute kidney injury (AKI) undergoing anesthesia?
A. Perform only non-invasive blood pressure monitoring.
B. Have a low threshold for invasive hemodynamic monitoring.
C. Invasive hemodynamic monitoring is not recommended.
D. Rely solely on clinical signs for hemodynamic assessment.

A

Answer: B. Have a low threshold for invasive hemodynamic monitoring.

122
Q

For a patient with AKI scheduled for surgery, which of the following preoperative measures is often recommended to facilitate anesthesia management?
A. Routine prophylactic antibiotics
B. Avoiding any preoperative testing
C. Preoperative dialysis, if applicable
D. Ensuring the patient has fasted for 24 hours

A

Answer: C. Preoperative dialysis, if applicable
Rationale: Preoperative dialysis may be recommended for patients with AKI to manage electrolyte imbalances, particularly hyperkalemia, and fluid overload, thus optimizing the patient for anesthesia and surgery.

123
Q

When considering drug dosing for a patient with AKI undergoing anesthesia, which practice is recommended?
A. Standard dosing as per body weight
B. Higher doses to ensure efficacy
C. Tailored drug dosing based on renal function
D. The lowest possible dose regardless of renal function

A

Answer: C. Tailored drug dosing based on renal function
Rationale: Anesthesia drug dosing should be tailored for patients with AKI due to the potential for altered drug metabolism and excretion, which could lead to prolonged drug effects or toxicity. Avoid drugs w/ active metabolites like Demerol and Morphine

123
Q

What are the most common causes of chronic kidney disease (CKD)?
A. Medications and acute infections
B. Genetic disorders and medication overdose
C. Diabetes and hypertension
D. Unknown factors and acute kidney injury

A

Answer: C. Diabetes and hypertension
Rationale: CKD is often a result of long-standing diseases that affect kidney function. Diabetes and hypertension are the leading causes of CKD, as depicted in the pie chart. They can cause damage to the small blood vessels in the kidneys, leading to decreased kidney function over time.

124
Q

Which types of surgeries are patients with CKD commonly presented for?
A. Cosmetic surgeries
B. Elective non-invasive procedures
C. Surgery for dialysis access and amputations due to diabetic complications
D. Emergency surgeries unrelated to their CKD

A

Answer: C. Surgery for dialysis access and amputations due to diabetic complications
Rationale: Patients with CKD often undergo surgeries related to their underlying disease process, including procedures to create dialysis access points like arteriovenous fistulas or grafts, as well as toe or foot debridements and amputations, especially if they have complications from diabetes like non-healing wounds.

125
Q

Which stage of Chronic Kidney Disease (CKD) is characterized by kidney damage with a glomerular filtration rate (GFR) that is normal or increased?
A. Stage 1
B. Stage 2
C. Stage 3
D. Stage 4

A

Answer: A. Stage 1
Rationale: Stage 1 CKD is identified by a GFR greater than 90 mL/min/1.73m² along with other signs of kidney damage. This can include abnormalities found in blood or urine tests or imaging studies. Despite a normal or high GFR, the presence of kidney damage classifies the condition as CKD.

126
Q

At which stage of CKD does kidney failure occur, necessitating renal replacement therapy or transplantation?
A. Stage 3
B. Stage 4
C. Stage 5
D. Stage 2

A

Answer: C. Stage 5
Rationale: Stage 5 CKD, also known as end-stage renal disease (ESRD), is characterized by a GFR of less than 15 mL/min/1.73m². At this stage, kidneys can no longer sustain life, and dialysis or kidney transplantation is required.

127
Q

Question 64: What is the expected trend in GFR as a person ages, starting from age 20?
A. Increases by 10 per decade
B. No change with age
C. Decreases by 10 per decade
D. Decreases by 5 per decade

A

Answer: C. Decreases by 10 per decade
Rationale: The GFR typically decreases by about 10 mL/min/1.73m² per decade of life, starting from age 20. This is a normal part of aging and not necessarily indicative of disease, but it’s important to monitor GFR trends over time to detect any abnormal decline that could signal CKD.

128
Q

What is the first-line pharmacological treatment for hypertension associated with Chronic Kidney Disease (CKD)?
A. Beta-blockers
B. Calcium Channel Blockers
C. Thiazide Diuretics
D. Alpha-blockers

A

Answer: C. Thiazide Diuretics
Rationale: For patients with Chronic Kidney Disease (CKD), controlling blood pressure is crucial to slow the progression of renal damage. Thiazide diuretics are often used as first-line agents for hypertension in CKD because they help reduce blood pressure by promoting sodium and water excretion, decreasing blood volume, and lowering systemic resistance.

129
Q

Follow-up Question: Why might patients with CKD and systemic hypertension also require ACE inhibitors (ACE-I) or angiotensin receptor blockers (ARBs)?
A. To increase blood volume
B. To stimulate the renin-angiotensin-aldosterone system
C. To protect renal function by reducing intraglomerular pressure
D. To increase retention of sodium and water

A

Answer: C. To protect renal function by reducing intraglomerular pressure
Rationale: ACE inhibitors and ARBs are beneficial in CKD patients not only for their antihypertensive effects but also for their ability to decrease intraglomerular pressure. This pressure reduction is achieved by dilating the efferent arterioles of the glomeruli, which can help to preserve kidney function over time.

130
Q

Question: When managing a patient with chronic kidney disease (CKD) undergoing surgery, why might the perioperative continuation of ACE inhibitors or ARBs be considered on a case-by-case basis?

A. To prevent hypotension
B. To reduce the risk of intraoperative hypertension
C. To manage chronic hypertension effectively during surgery
D. To avoid the risk of profound intraoperative hypotension

A

Answer: D. To avoid the risk of profound intraoperative hypotension
Rationale: Angiotensin-converting enzyme inhibitors (ACE-Is) and angiotensin receptor blockers (ARBs) are commonly used in the management of CKD due to their beneficial effects on blood pressure and glomerular pressure. However, their use may be reconsidered on the day of surgery due to the risk of profound hypotension after induction of anesthesia. The decision to continue or withhold these medications is often made on a case-by-case basis, considering the patient’s overall cardiovascular stability and the potential need for vasopressors such as vasopressin, norepinephrine, or epinephrine to manage blood pressure intraoperatively. This tailored approach seeks to balance the benefits of ACE-Is/ARBs in protecting renal function against the risks associated with anesthesia and surgical stress.

131
Q

Which populations are at an increased risk for a ‘silent’ myocardial infarction (MI), and what might be a contributing factor in patients with chronic kidney disease (CKD)?

Select all that apply:

A. Women
B. Diabetics
C. Patients with dyslipidemia
D. Patients with peripheral and autonomic neuropathy
E. Patients with hypertension

A

Answer: A. Women, B. Diabetics, D. Patients with peripheral and autonomic neuropathy

Rationale: Patients with chronic kidney disease (CKD) are predisposed to a range of cardiovascular complications, including dyslipidemia, which is characterized by high levels of triglycerides and LDL cholesterol. Additionally, CKD can lead to peripheral and autonomic neuropathy, which may blunt sensations, including the pain associated with myocardial ischemia. This can result in ‘silent’ MIs, where the classic symptoms of a heart attack are not present or are significantly muted. This risk is particularly heightened in women and diabetics, who are statistically more prone to experiencing silent MIs. Monitoring for cardiovascular events in these populations is crucial, especially in the presence of CKD-related neuropathies, which can obscure typical clinical presentations.

132
Q

In patients with chronic kidney disease (CKD), which treatment is used to manage anemia, and what is the target hemoglobin level?

A. Iron supplements, targeting Hgb of 12-16 g/dL
B. Blood transfusion, targeting Hgb of 13-17 g/dL
C. Exogenous erythropoietin, targeting Hgb of 10 g/dL
D. Platelet transfusion, targeting platelet count of 150,000/µL

A

Answer: C. Exogenous erythropoietin, targeting Hgb of 10 g/dL

Rationale: Anemia is a common hematologic effect of CKD, often due to a decrease in the production of erythropoietin by the kidneys. Treatment with exogenous erythropoietin can stimulate red blood cell production. The target hemoglobin (Hgb) level in this treatment is generally around 10 g/dL to improve symptoms and quality of life without reaching levels that could increase the risk of vascular events or require transfusion, which carries its own set of risks, such as acidosis and hyperkalemia. It’s important to balance the risks and benefits of transfusion in CKD patients, as excessive hemoglobin can lead to hyperviscosity and sluggish circulation.

133
Q

Which form of dialysis is generally considered more efficient and is commonly used in clinical settings?

A. Peritoneal dialysis (PD)
B. Hemodialysis (HD)
C. Continuous renal replacement therapy (CRRT)
D. Nocturnal home dialysis (NHD)

A

Answer: B. Hemodialysis (HD)

Rationale: Hemodialysis (HD) is often considered more efficient than peritoneal dialysis (PD) due to its ability to more quickly remove waste products, excess fluid, and electrolytes from the blood. HD is commonly used in both acute and chronic kidney failure cases and can be done in a hospital, dialysis center, or at home with proper equipment and training. However, HD is associated with more dramatic fluid and electrolyte shifts, which may not be suitable for all patients, such as those with poor cardiac function who cannot tolerate these shifts. In such cases, PD might be a better option as it is gentler and allows for slower fluid removal.

134
Q

hat is a common side effect of hemodialysis that patients should be monitored for during treatment?

A. Hypertension
B. Hypotension
C. Hyperkalemia
D. Hyponatremia

A

Answer: B. Hypotension

Rationale: Hypotension, or low blood pressure, is the most common side effect during hemodialysis. It can occur due to the rapid removal of fluids from the blood, affecting vascular volume and cardiac output.

135
Q

What is the leading cause of death in patients undergoing dialysis?

A. Malnutrition
B. Hypokalemia
C. Infection
D. Hyperphosphatemia

A

Answer: C. Infection

Rationale: Patients on dialysis often have impaired immune systems, making infection the leading cause of death. Dialysis access points can be potential sites for infection.

136
Q

For patients with end-stage renal disease (ESRD) undergoing surgery, when should body weight measurements be taken to assess fluid status?

A. 1 week before surgery
B. Immediately after dialysis
C. Within 24 hours of surgery
D. 2 days post-surgery

A

Answer: C. Within 24 hours of surgery

Rationale: Monitoring the body weight changes pre and post dialysis within 24 hours of surgery is crucial for assessing fluid status and minimizing the risk of perioperative fluid-related complications in ESRD patients.

137
Q

What medication can be administered pre-operatively to a patient with ESRD to reduce the risk of uremic bleeding?

A. Heparin
B. Aspirin
C. Warfarin
D. Desmopressin

A

Answer: D. Desmopressin

Rationale: Desmopressin (DDAVP) can be given pre-operatively to enhance the release of von Willebrand factor and factor VIII, thereby improving platelet function and reducing the risk of bleeding associated with uremia. It has a peak action of 2-4 hours and lasts 6-8 hours but can develop tachyphylaxis; thus, it should be used judiciously.

138
Q

Which neuromuscular blocking agent (NMB) is considered best for patients with chronic kidney disease (CKD)?

A. Succinylcholine
B. Rocuronium
C. Cisatracurium
D. Vecuronium

A

Answer: C. Cisatracurium

Rationale: Cisatracurium is often favored in patients with CKD because it undergoes Hofmann elimination, a non-enzymatic process that occurs at physiological pH and temperature, making it independent of renal or hepatic elimination pathways. This feature makes it a safer option for patients with renal impairment.

139
Q

Which analgesic should be avoided in patients with CKD due to its active metabolites?

A. Fentanyl
B. Acetaminophen
C. Morphine
D. Ibuprofen

A

Answer: C. Morphine

Rationale: Morphine has active metabolites that can accumulate in patients with renal impairment, potentially leading to prolonged or exaggerated effects. Therefore, it’s advisable to avoid morphine in patients with CKD and consider alternative analgesics with fewer renal elimination concerns.

140
Q

What is the recommended maximum potassium level (K+) for a patient undergoing elective surgery?
A. > 5.5 mEq/L
B. < 5.5 mEq/L
C. > 4.5 mEq/L
D. ≤ 4.0 mEq/L

A

B. < 5.5 mEq/L

141
Q

When should dialysis patients be dialyzed in preparation for elective surgery?
A. 48 hours before surgery
B. Within 24 hours preceding surgery
C. A week before surgery
D. Immediately before surgery

A

B. Within 24 hours preceding surgery

142
Q

Which of the following is a crucial prophylactic measure in diabetic patients undergoing surgery?
A. Antibiotic prophylaxis
B. Aspiration prophylaxis
C. Anticoagulant prophylaxis
D. Analgesic prophylaxis

A

B. Aspiration prophylaxis

143
Q

The activation of which receptors results in afferent arteriole constriction and decreased renal blood flow (RBF)?
A. Beta-1 receptors (β1-Rs)
B. Alpha-1 receptors (α1-Rs)
C. Beta-2 receptors (β2-Rs)
D. Alpha-2 receptors (α2-Rs)

A

B. Alpha-1 receptors (α1-Rs)

144
Q

Which physiological response can lead to a decrease in renal blood flow (RBF) and glomerular filtration rate (GFR) during surgery?
A. Increased parasympathetic nervous system outflow
B. Decreased sympathetic nervous system outflow
C. Increased sympathetic nervous system outflow
D. Decreased histamine release

A

C. Increased sympathetic nervous system outflow. Anesthesia and surgery can activate the sympathetic nervous system, leading to vasoconstriction and reduced RBF and GFR.