STEP3 Exam Questions and Answers | Exam-Dumps (Page: 7)

QUESTION: 31

A 28-year-old woman presents to your clinic complaining of feeling "on edge." Upon further questioning, you discover that she has also noticed problems with irritability, insomnia, fatigue, and restlessness. She also has a history of worrying about things that seem to not bother those around her. She states these symptoms have been present for years but have recently become worse. When you try to gather more information, she interrupts to say that she cannot stay much longer because she is afraid that she will lose her new job as a machinist.
Which of the following medications would be most appropriate in this patient?

diazepam
amitriptyline
doxepin
oxazepam
buspirone

Answer(s): E

Explanation:

This patient's symptoms are consistent with an anxiety disorder. Given her occupation, an anxiolytic medication with no sedative properties would be most preferable. Buspirone is a nonsedating anxiolytic agent that is a partial agonist at 5-HT1A receptors. Unlike benzodiazepines, such as diazepam and oxazepam (Serax), it has no hypnotic, anticonvulsant, or muscle relaxant properties. Amitriptyline and doxepin have also been used to treat anxiety, especially when associated with depression; however, these drugs are also sedating.

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QUESTION: 32

A 54-year-old male with uncontrolled type II diabetes and well-controlled hypertension presents with complaints of erectile dysfunction. The patient requests Viagra (sildenafil), as his friends have used it with success. However, he is concerned as he was told by someone that Viagra can be fatal if used with some blood pressure medications. You would advise the patient that the use of which of the following is contraindicated in patients taking sildenafil?

isosorbide mononitrate
metoprolol
verapamil
captopril
clonidine

Answer(s): A

Explanation:

Sildenafil is a phosphodiesterase inhibitor effective in the treatment of erectile dysfunction the mechanism of action of which is related to an increase in intracellular cyclic guanosine monophosphate (GMP). Nitrates increase cyclic GMP via the activation of guanylyl cyclase. When the two drugs interact, there can be a dramatic fall in blood pressure related to extreme vasodilation. The other selections can reduce blood pressure; however, since their mechanisms of action are not associated with the intracellular concentration of cyclic GMP, there is no synergistic interaction with sildenafil

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QUESTION: 33

Bupivacaine is a local anesthetic agent that is much more potent and the duration of action of which is considerably longer than procaine. Possible reasons for this difference include which of the following?

higher partition coefficient for bupivacaine than for procaine
covalent binding to the receptor site
lower protein binding of bupivacaine than procaine
decreased rate of metabolism of procaine compared to bupivacaine
bupivacaine constricts blood vessels

Answer(s): A

Explanation:

Local anesthetics exist in solution in both uncharged base and charged cationic forms. The base diffuses across the nerve sheath and membrane and then re-equilibrates within the axoplasm. It is intracellular penetration of the cation into, and attachment to a receptor at a site within the sodium channel, that leads to inhibition of sodium conductance and ultimate conduction blockade. Bupivacaine is typical of amide- linked local anesthetics with high anesthetic potency and long duration of action (class III). Procaine is typical of class I agents that are ester linked and have low anesthetic potency and short duration of action. Important features of group III compounds include: (1) high degree of lipid solubility or high partition coefficient that aid in penetration of the drug, (2) high degree of protein binding that aids in attachment of the drug once it has penetrated the cell, and (3) pKa closer to pH = 7.4 so that more of the drug is in the unionized form and is free to penetrate the membrane. Esterlinked anesthetics, such as procaine, are rapidly metabolized by pseudocholinesterases, whereas bupivacaine is slowly degraded by hepatic enzymes

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QUESTION: 34

A 68-year-old White male, with a history of hypertension, an 80 pack-year history of tobacco use and emphysema, is brought into the ER because of 4 days of progressive confusion and lethargy. His wife notes that he takes amlodipine for his hypertension. He does not use over-the-counter (OTC) medications, alcohol, or drugs. Furthermore, she indicates that he has unintentionally lost approximately 30 lbs in the last 6 months. His physical examination shows that he is afebrile with a blood pressure of 142/85, heart rate of 92 (no orthostatic changes), and a room-air O2 saturation of 91%. He is 70 kg. The patient appears cachectic. He is arousable but lethargic and unable to follow any commands. His mucous membranes are moist, heart rate regular without murmurs or a S3/S4 gallop, and extremities without any edema. His pulmonary examination shows mildly diminished breath sounds in the right lower lobe with wheezing bilaterally. The patient is unable to follow commands during neurologic examination but moves all his extremities spontaneously. Laboratory results are as follows:

Blood
Sodium: 109
Potassium: 3.8
Chloride: 103
CO2: 33
BUN: 17
Creatinine: 1.1
Glucose: 95
Urine osmolality: 600
Plasma osmolality: 229
White blood cell (WBC): 8000
Hgb: 15.8
Hematocrit (HCT): 45.3
Platelets: 410
Arterial blood gas: pH 7.36/pCO2 60/pO2 285
A chest x-ray (CXR) reveals a large right hilar mass.

What is the most likely cause of this patient's altered mental status?

sepsis syndrome with pneumonia
ischemic stroke
central pontine myelinolysis
cerebral edema
respiratory acidosis

Answer(s): D

Explanation:

The patient has hypotonic hyponatremia, which can lead to increased water shifting into the brain, resulting in cerebral edema. This patient has nothing in history or physical examination to suggest a stroke or the presence of sepsis as the etiology of his altered mental status. Central pontine myelinolysis is a potentially devastating neurologic complication that can result from the treatment of hyponatremia, not hyponatremia itself. While respiratory acidosis could potentially contribute to this patient's change in mental status, cerebral edema due to hypotonicity is the most likely etiology. The patient's laboratory studies indicate a low plasma osmolality with an inappropriately increased urine osmolality. With this degree of hypotonicity, the urine should be maximally dilute (osmolality of <100 mOsmol/kg H2O). The high urine osmolality suggests the presence of antidiuretic hormone. In psychogenic polydipsia, the urine would be maximally dilute. Choice C is unlikely since his physical examination does not suggest volume depletion; furthermore, the patient is taking a calcium channel blocker, not a diuretic, for the treatment of his hypertension. Decreased expression of renal collecting duct water channels would lead to water wasting and, thus, the development of diabetes insipidus and hypernatremia. The patient has symptomatic hypotonic hyponatremia with signs of cerebral edema.

This requires immediate attention. Choices A, C, and E are essentially hypotonic solutions which should be withheld in patients with hyponatremia. The serum sodium in this case should be increased by at least 5% for the treatment of cerebral edema. The use of 0.9% saline would require nearly 5 L of infusate to address this cerebral edema. This could lead to pulmonary edema and volume overload. The use of hypertonic saline (3% saline) is the ideal solution to use in this scenario, as the infusion of 3% saline will correct the symptoms while avoiding volume overload. As in all cases of hyponatremia management, frequent serum sodium assays are necessary in order to avoid too rapid of a correction, which could result in neurologic injury--pontine myelinolysis.

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QUESTION: 35

A 68-year-old White male, with a history of hypertension, an 80 pack-year history of tobacco use and emphysema, is brought into the ER because of 4 days of progressive confusion and lethargy. His wife notes that he takes amlodipine for his hypertension. He does not use over-the-counter (OTC) medications, alcohol, or drugs. Furthermore, she indicates that he has unintentionally lost approximately 30 lbs in the last 6 months. His physical examination shows that he is afebrile with a blood pressure of 142/85, heart rate of 92 (no orthostatic changes), and a room-air O2 saturation of 91%. He is 70 kg. The patient appears cachectic. He is arousable but lethargic and unable to follow any commands. His mucous membranes are moist, heart rate regular without murmurs or a S3/S4 gallop, and extremities without any edema. His pulmonary examination shows mildly diminished breath sounds in the right lower lobe with wheezing bilaterally. The patient is unable to follow commands during neurologic examination but moves all his extremities spontaneously. Laboratory results are as follows:

Blood
Sodium: 109
Potassium: 3.8
Chloride: 103
CO2: 33
BUN: 17
Creatinine: 1.1
Glucose: 95
Urine osmolality: 600
Plasma osmolality: 229
White blood cell (WBC): 8000
Hgb: 15.8
Hematocrit (HCT): 45.3
Platelets: 410
Arterial blood gas: pH 7.36/pCO2 60/pO2 285
A chest x-ray (CXR) reveals a large right hilar mass.
Which of the following would be the optimal choice of solution to infuse in order to adequately correct this patient's hyponatremia?

D5W with 20 meq/L KCl at 200 mL/h
0.9% saline at 125 mL/h
0.45% saline at 100 mL/h
3% saline at 35 mL/h
0.45% saline with 30 meq/L KCl at 100 mL/h

Answer(s): D

Explanation:

The patient has hypotonic hyponatremia, which can lead to increased water shifting into the brain, resulting in cerebral edema. This patient has nothing in history or physical examination to suggest a stroke or the presence of sepsis as the etiology of his altered mental status. Central pontine myelinolysis is a potentially devastating neurologic complication that can result from the treatment of hyponatremia, not hyponatremia itself. While respiratory acidosis could potentially contribute to this patient's change in mental status, cerebral edema due to hypotonicity is the most likely etiology. The patient's laboratory studies indicate a low plasma osmolality with an inappropriately increased urine osmolality. With this degree of hypotonicity, the urine should be maximally dilute (osmolality of <100 mOsmol/kg H2O). The high urine osmolality suggests the presence of antidiuretic hormone. In psychogenic polydipsia, the urine would be maximally dilute. Choice C is unlikely since his physical examination does not suggest volume depletion; furthermore, the patient is taking a calcium channel blocker, not a diuretic, for the treatment of his hypertension. Decreased expression of renal collecting duct water channels would lead to water wasting and, thus, the development of diabetes insipidus and hypernatremia. The patient has symptomatic hypotonic hyponatremia with signs of cerebral edema.

This requires immediate attention. Choices A, C, and E are essentially hypotonic solutions which should be withheld in patients with hyponatremia. The serum sodium in this case should be increased by at least 5% for the treatment of cerebral edema. The use of 0.9% saline would require nearly 5 L of infusate to address this cerebral edema. This could lead to pulmonary edema and volume overload. The use of hypertonic saline (3% saline) is the ideal solution to use in this scenario, as the infusion of 3% saline will correct the symptoms while avoiding volume overload. As in all cases of hyponatremia management, frequent serum sodium assays are necessary in order to avoid too rapid of a correction, which could result in neurologic injury--pontine myelinolysis.

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USMLE STEP3 Exam (page: 7) USMLE Step3 Updated on: 25-Dec-2025

QUESTION: 31

Explanation:

QUESTION: 32

Explanation:

QUESTION: 33

Explanation:

QUESTION: 34

Explanation:

QUESTION: 35

Explanation:

USMLE STEP3 Exam (page: 7)
USMLE Step3
Updated on: 25-Dec-2025