All practice questions

8270 questions

Question 1721Question →

An asymptomatic 6565-year-old woman visits her primary care physician for an annual checkup. She mentions feeling slightly more fatigued recently, though she attributes this to a busy daily routine. Her medical history includes well-controlled essential hypertension. Her temperature is 37.0∘37.0^\circ C, blood pressure is 125/80125/80 mm Hg, and pulse is 7272/min. Physical examination reveals a normal-sized thyroid gland with no palpable nodules. A screening laboratory evaluation demonstrates the following results:

Thyroid-stimulating hormone (TSH): 7.87.8 mU/L (normal: 0.40.4-4.24.2 mU/L)
Free thyroxine (T4): 1.31.3 ng/dL (normal: 0.80.8-2.72.7 ng/dL)

Which of the following is the most likely diagnosis?

Show answer & explanation

Answer: Subclinical hypothyroidism

Answer

Subclinical hypothyroidism
The correct answer is subclinical hypothyroidism. This condition is defined biochemically as an elevated serum thyroid-stimulating hormone (TSH) level in the presence of a normal serum free thyroxine (T4) level. Patients are often asymptomatic or have mild, non-specific symptoms such as fatigue. In this vignette, the patient's elevated TSH (7.87.8 mU/L) combined with a normal free T4 (1.31.3 ng/dL) perfectly matches this definition.

Step-by-Step Solution

1
Evaluate the patient's symptoms and physical examination findings.
The patient is largely asymptomatic with a normal physical exam, pointing away from severe overt thyroid disease.
To establish the clinical context before interpreting laboratory values.
2
Interpret the thyroid function tests.
The TSH is elevated (7.87.8 mU/L), indicating decreased thyroid function, but the free T4 remains within the normal range (1.31.3 ng/dL).
To determine the specific pattern of thyroid dysfunction.
3
Synthesize clinical and laboratory findings to establish a diagnosis.
The combination of an elevated TSH and a normal free T4 level is the defining criteria for subclinical hypothyroidism.
To definitively diagnose the condition based on standard diagnostic criteria.

Key Concept

Subclinical hypothyroidism is defined biochemically by an elevated thyroid-stimulating hormone (TSH) level in the presence of a normal free thyroxine (T4) level.
Question 1722Question →

A 7272-year-old man is brought to the emergency department from a long-term care facility due to altered mental status. Facility staff report that the patient has experienced intractable vomiting and an inability to tolerate oral intake for the past 4848 hours. His past medical history includes hypertension, benign prostatic hyperplasia, and mild cognitive impairment. Upon arrival, his temperature is 38.8∘C38.8^\circ\text{C} (101.8∘F101.8^\circ\text{F}), blood pressure is 88/54 mm Hg88/54\text{ mm Hg}, pulse is 118/min118\text{/min}, and respirations are 28/min28\text{/min}. Physical examination reveals dry mucous membranes, delayed capillary refill, and diffuse abdominal rigidity with severe rebound tenderness.

Laboratory TestResult
Sodium145 mEq/L145\text{ mEq/L}
Potassium3.1 mEq/L3.1\text{ mEq/L}
Chloride90 mEq/L90\text{ mEq/L}
Bicarbonate20 mEq/L20\text{ mEq/L}
Blood urea nitrogen48 mg/dL48\text{ mg/dL}
Creatinine2.4 mg/dL2.4\text{ mg/dL}
Lactate9.5 mmol/L9.5\text{ mmol/L}
Arterial Blood Gas (Room Air)Result
pH7.437.43
PaCO2PaCO_231 mm Hg31\text{ mm Hg}
PaO2PaO_278 mm Hg78\text{ mm Hg}

Based on the laboratory data provided, which of the following combinations of primary pathophysiologic processes best explains this patient's complete acid-base status?

Show answer & explanation

Answer: Tissue hypoperfusion, loss of gastric hydrochloric acid, and primary central respiratory stimulation

Answer

The correct option is the one that identifies tissue hypoperfusion, loss of gastric hydrochloric acid, and primary central respiratory stimulation.
The correct answer accurately identifies a triple acid-base disorder by systematically applying the anion gap, the delta-delta analysis, and Winter's formula. First, the patient has a primary high anion gap metabolic acidosis (HAGMA) due to lactic acidosis from tissue hypoperfusion (Anion Gap = 3535). Second, applying the delta-delta analysis reveals an expected bicarbonate of 1 mEq/L1\text{ mEq/L}, but the actual bicarbonate is 20 mEq/L20\text{ mEq/L}. This massive discrepancy indicates a concurrent primary metabolic alkalosis, secondary to loss of gastric hydrochloric acid from severe vomiting. Finally, utilizing Winter's formula, the expected PaCO2PaCO_2 for a bicarbonate of 20 mEq/L20\text{ mEq/L} is 38±2 mm Hg38 \pm 2\text{ mm Hg}. The patient's actual PaCO2PaCO_2 is 31 mm Hg31\text{ mm Hg}, which represents an independent, primary respiratory alkalosis driven by central respiratory stimulation (SIRS/sepsis).

Step-by-Step Solution

1
Calculate the Anion Gap (AG).
AG=Na+−(Cl−+HCO3−)=145−(90+20)=35AG = Na^+ - (Cl^- + HCO_3^-) = 145 - (90 + 20) = 35.
An AG>12AG > 12 indicates the presence of a primary high anion gap metabolic acidosis (HAGMA). In this case, the highly elevated lactate (9.5 mmol/L9.5\text{ mmol/L}) due to tissue hypoperfusion is the driver.
2
Perform a Delta-Delta (Δ−Δ\Delta-\Delta) analysis to evaluate for hidden metabolic disorders.
ΔAG=35−12=23\Delta AG = 35 - 12 = 23. Expected HCO3−=24−ΔAG=24−23=1 mEq/LHCO_3^- = 24 - \Delta AG = 24 - 23 = 1\text{ mEq/L}. The actual HCO3−HCO_3^- is 20 mEq/L20\text{ mEq/L}.
Because the actual bicarbonate (20 mEq/L20\text{ mEq/L}) is drastically higher than the expected bicarbonate (1 mEq/L1\text{ mEq/L}), a concurrent primary metabolic alkalosis is present, driven by the loss of gastric hydrochloric acid from intractable vomiting.
3
Calculate the expected respiratory compensation using Winter's formula.
Expected PaCO2=(1.5×HCO3−)+8±2=(1.5×20)+8=38±2 mm HgPaCO_2 = (1.5 \times HCO_3^-) + 8 \pm 2 = (1.5 \times 20) + 8 = 38 \pm 2\text{ mm Hg} (range 36−4036-40).
The patient's actual PaCO2PaCO_2 is 31 mm Hg31\text{ mm Hg}. Because 31<3631 < 36, the patient is hyperventilating beyond physiologic compensation. This indicates a third independent disorder: a primary respiratory alkalosis, likely driven by central respiratory stimulation secondary to sepsis and an acute abdominal emergency.

Key Concept

Diagnosis of triple acid-base disorders requires a systematic three-step approach: calculating the anion gap, performing a delta-delta analysis, and applying Winter's formula.

Alternative Method

Instead of subtracting the delta gap from a normal bicarbonate level, the delta ratio (ΔAG/ΔHCO3−\Delta AG / \Delta HCO_3^-) can be utilized. A ratio >2.0> 2.0 confirms the presence of a concurrent metabolic alkalosis.
Estimated Time:2m 0s
Question 1723Question →

A 36-hour-old term male neonate is evaluated in the neonatal intensive care unit for progressive abdominal distension and two episodes of bilious emesis. He was born at 39 weeks gestation via uncomplicated vaginal delivery. Vital signs are within normal limits for age. The infant has not yet passed meconium. Physical examination reveals a markedly distended, firm abdomen without overlying erythema. Bowel sounds are hypoactive. An imperforate anus is excluded by physical examination. The clinical team proceeds with evaluating and managing the patient for the most likely underlying condition. Assume that initial non-operative therapeutic interventions prove unsuccessful in completely relieving the obstruction, necessitating surgical escalation.

Arrange the following clinical steps in the most appropriate chronological sequence for the management and subsequent care of this patient.

Drag items to arrange them in the correct order

Show answer & explanation

Answer

The correct sequence begins with immediate gastrointestinal decompression (nasogastric tube placement), followed by diagnostic plain abdominal radiographs. Next, a diagnostic and therapeutic hyperosmolar contrast enema is attempted. Since medical management fails in this scenario, surgical laparotomy is performed next. Finally, pancreatic enzyme replacement therapy is initiated postoperatively when feeds are restarted to manage the underlying cystic fibrosis.
This patient's presentation of bilious emesis, failure to pass meconium within 36 hours, and marked abdominal distension is highly suspicious for a distal neonatal bowel obstruction, specifically meconium ileus given the firm distension. The standard chronological algorithm prioritizes airway/breathing/circulation stabilization, which in cases of gastrointestinal obstruction means bowel rest and nasogastric decompression. Once decompressed, plain abdominal X-rays are the fundamental first imaging step to evaluate for obstruction patterns (e.g., absent air-fluid levels and a ground-glass/soap bubble appearance in meconium ileus) and to rule out perforation. After perforation is excluded, a water-soluble hyperosmolar contrast enema is performed to diagnose the etiology (identifying the microcolon) and to therapeutically disimpact the thick meconium. Since the clinical scenario states that initial therapeutic steps fail, an exploratory laparotomy must follow to surgically extract the meconium. Finally, because meconium ileus is inherently linked to cystic fibrosis, introducing pancreatic enzyme replacement therapy is necessary for long-term nutritional absorption once feeding begins.

Step-by-Step Solution

1
Hold enteral intake and place a nasogastric tube to continuous suction.
Decompresses the stomach and proximal bowel.
Any neonate presenting with bilious emesis and abdominal distension requires immediate stabilization to prevent aspiration of bilious fluid and to relieve progressive intestinal distension.
2
Obtain plain anteroposterior and lateral abdominal radiographs.
Reveals distended bowel loops, a 'soap bubble' (Neuhauser sign) appearance in the right lower quadrant, and rules out free intra-abdominal air.
Before any contrast studies or surgeries are attempted, plain radiography is mandatory to differentiate between proximal and distal obstruction and to ensure there is no bowel perforation.
3
Administer a hyperosmolar water-soluble contrast enema under fluoroscopic guidance.
Identifies a microcolon and attempts to flush out the inspissated meconium.
In uncomplicated meconium ileus, a Gastrografin enema serves a dual purpose. It confirms the diagnosis by showing a disused microcolon and acts therapeutically by drawing fluid into the intestinal lumen to dissolve meconium pellets.
4
Perform an exploratory laparotomy with enterotomy for meconium evacuation.
Mechanically clears the obstructing meconium from the terminal ileum.
The prompt explicitly notes that non-operative interventions fail. When a contrast enema cannot relieve the obstruction, surgical intervention is indicated to prevent bowel ischemia, necrosis, and perforation.
5
Initiate pancreatic enzyme replacement therapy upon the resumption of postoperative enteral feeds.
Allows for adequate digestion and nutrient absorption.
Virtually all patients with meconium ileus have underlying cystic fibrosis with exocrine pancreatic insufficiency. Enzyme supplementation is required as soon as enteral nutrition is reintroduced.

Key Concept

Evaluation and escalating management of meconium ileus in neonates with cystic fibrosis
Estimated Time:1m 30s
Question 1724Question →

Match each patient's clinical presentation with the most likely peripheral blood smear finding.

Click a left item, then click its matching right item

Items

A 65-year-old man with progressive fatigue, new-onset deep bone pain, hypercalcemia, and elevated serum creatinine.
A 35-year-old woman with severe fatigue, a history of heavy menses, and physical findings of koilonychia (spoon nails).
A 28-year-old asymptomatic man of Mediterranean descent found to have a mild microcytic anemia during a routine physical; iron studies are normal.
A 55-year-old woman presenting with worsening fatigue, symmetrical loss of vibratory sensation in her lower extremities, and a wide-based gait.
A 15-year-old boy presenting with scleral icterus, splenomegaly, and a family history of anemia requiring early cholecystectomy.

Matches

Show answer & explanation

Answer

The correct matches align Multiple Myeloma with Rouleaux formation, Iron Deficiency Anemia with microcytic/hypochromic cells and anisocytosis, Beta-Thalassemia Trait with target cells, Vitamin B12 Deficiency with hypersegmented neutrophils, and Hereditary Spherocytosis with spherocytes.
Each clinical vignette provides classic historical and physical findings that point directly to a specific hematologic disorder. Multiple myeloma causes excessive paraproteins that neutralize RBC charge, leading to Rouleaux formation. Iron deficiency causes a classic microcytic anemia with high RDW (anisocytosis). Beta-thalassemia trait causes microcytosis with target cells due to relative membrane excess. Vitamin B12 deficiency impairs DNA synthesis, causing megaloblastic anemia with hypersegmented neutrophils alongside neurologic deficits. Hereditary spherocytosis is a membrane defect resulting in small, spherical RBCs without central pallor.

Step-by-Step Solution

1
Analyze the first vignette describing an older man with hypercalcemia, renal failure, anemia, and bone pain.
Diagnose multiple myeloma.
This is the classic 'CRAB' criteria presentation of multiple myeloma, leading to the prediction of Rouleaux formation on the peripheral smear.
2
Analyze the second vignette describing a young woman with menorrhagia and koilonychia.
Diagnose iron deficiency anemia.
Chronic blood loss leads to iron deficiency, resulting in microcytic, hypochromic RBCs with a high degree of size variation (anisocytosis).
3
Analyze the third vignette describing an asymptomatic Mediterranean man with microcytosis but normal iron studies.
Diagnose beta-thalassemia trait.
The demographic and lab profile uniquely define thalassemia trait, which is associated with target cells and basophilic stippling rather than anisocytosis.
4
Analyze the fourth vignette describing a woman with anemia and posterior column neurologic deficits.
Diagnose vitamin B12 deficiency.
Vitamin B12 deficiency causes subacute combined degeneration of the spinal cord and a macrocytic/megaloblastic anemia with hypersegmented neutrophils.
5
Analyze the fifth vignette describing a teenager with hemolysis, splenomegaly, and a family history of early cholecystectomy.
Diagnose hereditary spherocytosis.
The clinical picture of chronic extravascular hemolysis with pigment gallstones directly corresponds to the presence of spherocytes on the blood smear.

Key Concept

Identifying hallmark peripheral blood smear findings for common hematologic disorders based on their distinct clinical presentations.
Question 1725Question →

During a routine health maintenance visit, a 4848-year-old male construction worker describes a gradual decline in his energy levels and libido over the past 1414 months. He has also developed a pervasive feeling of being cold, even during summer months, alongside chronic, dull pain in the joints of his hands. He has no significant past medical history and takes no medications.

Vital signs include a blood pressure of 112/74112/74 mmHg and a heart rate of 5858/min. Physical examination reveals a slate-gray to bronze discoloration of the skin, which is most prominent in sun-exposed areas and old scars. Palpation of the abdomen reveals a firm, non-tender liver edge 33 cm below the right costal margin. Testicular volume is reduced bilaterally. The relaxation phase of the deep tendon reflexes is noticeably delayed.

Laboratory evaluation demonstrates:

Laboratory TestResultReference Range
Fasting serum glucose162162 mg/dL<100< 100 mg/dL
Thyroid-stimulating hormone (TSH)1.41.4 μ\muU/mL0.4−4.20.4-4.2 μ\muU/mL
Free thyroxine (T4)0.50.5 ng/dL0.9−1.70.9-1.7 ng/dL
Total testosterone125125 ng/dL300−1000300-1000 ng/dL
Luteinizing hormone (LH)1.21.2 mIU/mL2−92-9 mIU/mL
Prolactin77 ng/mL2−182-18 ng/mL
Morning serum cortisol1515 μ\mug/dL5−255-25 μ\mug/dL

Based on the patient's presentation and laboratory findings, which of the following is the most appropriate next step in diagnostic evaluation?

Show answer & explanation

Answer: Measurement of serum transferrin saturation and ferritin

Answer

The most appropriate next diagnostic step is the measurement of serum transferrin saturation and ferritin to evaluate for hereditary hemochromatosis.
This patient's presentation is a classic, though advanced, manifestation of hereditary hemochromatosis. The excessive intestinal iron absorption leads to systemic iron deposition. The triad of skin hyperpigmentation, diabetes mellitus (fasting glucose ≥126\ge 126 mg/dL), and hepatomegaly is historically referred to as 'bronze diabetes.' Importantly, the anterior pituitary is highly susceptible to iron deposition. Iron preferentially accumulates in gonadotrophs and thyrotrophs, leading to central hypogonadism (low testosterone with inappropriately low/normal LH) and central hypothyroidism (low free T4 with inappropriately normal TSH). The corticotrophs and lactotrophs are relatively spared, which explains his normal cortisol and prolactin levels. The most appropriate initial screening test for hereditary hemochromatosis is the measurement of serum transferrin saturation (typically >45%>45\% in affected individuals) and serum ferritin levels, followed by confirmatory HFE gene mutation analysis.

Step-by-Step Solution

1
Analyze the thyroid and gonadal laboratory findings.
The patient has a low free T4 with an inappropriately normal TSH, and low testosterone with an inappropriately normal LH.
This specific pattern indicates secondary (central) hypothyroidism and secondary (central) hypogonadism, pointing to anterior pituitary dysfunction rather than primary glandular failure.
2
Evaluate the remaining endocrine laboratories and clinical signs.
Morning cortisol and prolactin are completely normal, ruling out Addison disease and making a large structural pituitary adenoma less likely. Fasting glucose is elevated, indicating new-onset diabetes mellitus.
Combining central endocrinopathy with new-onset diabetes, hepatomegaly, distinctive skin pigmentation, and arthropathy requires a unifying systemic diagnosis.
3
Identify the unifying underlying pathophysiology.
The clinical picture represents hereditary hemochromatosis ('bronze diabetes'), an iron overload disorder.
Excess iron systematically deposits in the liver (hepatomegaly), pancreas (diabetes), skin (hyperpigmentation), joints (arthropathy), and anterior pituitary (predominantly affecting gonadotrophs and thyrotrophs).
4
Select the best initial diagnostic test for this condition.
Measurement of serum transferrin saturation and ferritin is indicated.
These are the highly sensitive initial screening markers for systemic iron overload before proceeding to HFE gene mutation analysis or liver biopsy.

Key Concept

Hereditary hemochromatosis can present with complex multiorgan manifestations, including anterior pituitary infiltration that causes central hypogonadism and central hypothyroidism.
Question 1726Question →

A 32-year-old man comes to the clinic due to 5 days of severe, watery diarrhea. He recently returned from a trip to Southeast Asia. The patient reports having 8 to 10 loose bowel movements daily. He has been drinking plain water but has not consumed any food or electrolyte solutions. His temperature is 37.1°C (98.8°F), blood pressure is 108/64 mm Hg, and pulse is 104/min. Physical examination shows dry mucous membranes and decreased skin turgor. Laboratory studies show the following:

Laboratory TestResult
Sodium138 mEq/L
Potassium3.2 mEq/L
Chloride115 mEq/L
Bicarbonate15 mEq/L
Blood urea nitrogen28 mg/dL
Creatinine1.2 mg/dL

Based on these findings, which of the following acid-base disturbances is most likely present in this patient?

Show answer & explanation

Answer: Normal anion gap metabolic acidosis

Answer

Normal anion gap metabolic acidosis
This patient's clinical presentation of severe diarrhea has led to significant fluid and electrolyte loss. The serum chemistry shows a low bicarbonate level (15mEq/L15 mEq/L), which defines a metabolic acidosis. The next essential step in evaluating any metabolic acidosis is to calculate the serum anion gap using the formula: AG=Na+−(Cl−+HCO3−)AG = Na^+ - (Cl^- + HCO_3^-). For this patient, the calculation is 138−(115+15)=8mEq/L138 - (115 + 15) = 8 mEq/L. A normal anion gap is generally between 8 and 12 mEq/L. Therefore, this patient has a normal anion gap metabolic acidosis (NAGMA). This is physiologically consistent with his history of profuse diarrhea, which causes direct gastrointestinal loss of bicarbonate. To maintain electroneutrality, the kidneys retain chloride, resulting in the observed hyperchloremia (115mEq/L115 mEq/L).

Step-by-Step Solution

1
Identify the primary disturbance by evaluating the serum bicarbonate level.
The serum bicarbonate is low (15 mEq/L).
A low bicarbonate level in the setting of severe diarrhea strongly suggests a primary metabolic acidosis.
2
Calculate the serum anion gap to classify the metabolic acidosis.
The formula is AG=Na+−(Cl−+HCO3−)AG = Na^+ - (Cl^- + HCO_3^-). Calculation: 138−(115+15)=138−130=8mEq/L138 - (115 + 15) = 138 - 130 = 8 mEq/L.
Differentiating between high and normal anion gap metabolic acidosis is essential for identifying the underlying etiology.
3
Correlate the calculated anion gap with the patient's clinical presentation.
The anion gap of 8 mEq/L is normal. Diarrhea is a classic cause of normal anion gap metabolic acidosis.
Severe diarrhea leads to direct gastrointestinal loss of bicarbonate, which the kidneys compensate for by retaining chloride, resulting in a hyperchloremic, normal anion gap metabolic acidosis.

Key Concept

Severe diarrhea causes direct gastrointestinal loss of bicarbonate, resulting in a hyperchloremic, normal anion gap metabolic acidosis.
Estimated Time:1m 0s
Question 1727Question →

A 28-year-old woman presents to the emergency department with a 2-day history of sharp right-sided chest pain that worsens with deep inspiration. She also reports shortness of breath and generalized fatigue. She was diagnosed with systemic lupus erythematosus (SLE) three years ago and is currently prescribed hydroxychloroquine, though she admits to missing several doses recently. Her temperature is 38.1∘C38.1^\circ\text{C} (100.6∘F100.6^\circ\text{F}), blood pressure is 122/78 mm Hg122/78\text{ mm Hg}, pulse is 102/min102/\text{min}, and respirations are 22/min22/\text{min}. Physical examination reveals a pleural friction rub over the right lower lung field. Her wrists and metacarpophalangeal joints are tender and swollen bilaterally.

Laboratory studies are as follows:

ParameterValueReference Range
Leukocytes3,400/mm33,400/\text{mm}^34,500−11,000/mm34,500-11,000/\text{mm}^3
Hemoglobin10.8 g/dL10.8\text{ g/dL}12.0−15.5 g/dL12.0-15.5\text{ g/dL}
Platelets110,000/mm3110,000/\text{mm}^3150,000−400,000/mm3150,000-400,000/\text{mm}^3
TSH2.4 μU/mL2.4\text{ }\mu\text{U/mL}0.5−5.0 μU/mL0.5-5.0\text{ }\mu\text{U/mL}
Free T41.2 ng/dL1.2\text{ ng/dL}0.9−1.7 ng/dL0.9-1.7\text{ ng/dL}

Arterial blood gas analysis on room air:

ParameterValueReference Range
pH7.467.467.35−7.457.35-7.45
pCO2_232 mm Hg32\text{ mm Hg}35−45 mm Hg35-45\text{ mm Hg}
pO2_288 mm Hg88\text{ mm Hg}75−105 mm Hg75-105\text{ mm Hg}
HCO3−_3^-22 mEq/L22\text{ mEq/L}22−28 mEq/L22-28\text{ mEq/L}

Chest radiography shows a small right pleural effusion with no pulmonary infiltrates. Electrocardiography shows normal sinus rhythm.

Which of the following is the most appropriate next step in the management of this patient?

Show answer & explanation

Answer: Initiate systemic glucocorticoid therapy

Answer

The most appropriate next step is to initiate systemic glucocorticoid therapy to treat the acute systemic lupus erythematosus (SLE) flare.
The correct action is to initiate systemic glucocorticoids. This patient is presenting with a classic acute flare of systemic lupus erythematosus (SLE) triggered by medication non-adherence. The flare is characterized by serositis (evident by pleuritic chest pain, pleural friction rub, and pleural effusion), polyarthritis, and active cytopenias. Because she has a moderate-to-severe manifestation (pleuritis causing significant respiratory distress/pain), systemic glucocorticoids (e.g., prednisone) are the most appropriate first-line therapy to quickly suppress the widespread autoimmune inflammation.

Step-by-Step Solution

1
Analyze the clinical presentation.
The patient has pleuritic chest pain, a pleural friction rub, fever, and polyarthritis in the setting of known SLE and medication non-adherence.
Identifying the cluster of symptoms helps categorize the acuity and etiology of the presentation.
2
Interpret the diagnostic data.
Laboratory results show characteristic SLE cytopenias (leukopenia, anemia, thrombocytopenia) and normal thyroid function. The ABG shows respiratory alkalosis due to pain-induced tachypnea. Chest radiography reveals a sterile-appearing pleural effusion without infiltrates.
Ruling out alternative life-threatening causes such as bacterial pneumonia, hypoxemic respiratory failure, or severe metabolic derangements is crucial before attributing symptoms solely to an autoimmune flare.
3
Determine the next step in management based on the diagnosis.
The diagnosis is an acute SLE flare with serositis (pleuritis). The appropriate intervention is immunosuppression with systemic glucocorticoids.
Moderate to severe SLE flares involving major organs or serosal surfaces require prompt reduction of inflammation to prevent tissue damage.

Key Concept

Patients with systemic lupus erythematosus (SLE) commonly experience acute flares characterized by serositis (e.g., pleuritis, pericarditis), polyarthritis, and cytopenias. In the absence of infection, moderate to severe flares should be managed acutely with systemic glucocorticoids.
Question 1728Question →

Match each of the following fasting laboratory profiles, obtained during a symptomatic hypoglycemic episode, to the most likely underlying etiology. Assume normal renal and hepatic function.

Click a left item, then click its matching right item

Items

Insulinoma
Surreptitious exogenous insulin administration
Sulfonylurea or meglitinide ingestion
Non-islet cell tumor hypoglycemia (NICTH)

Matches

Show answer & explanation

Answer

The correct pairings differentiate the etiologies of hypoglycemia based on the relationship between insulin, C-peptide, and secretagogue screens. Insulinomas and sulfonylureas show high C-peptide (distinguished by the drug screen), exogenous insulin shows low C-peptide despite high insulin, and non-islet cell tumors show suppression of both.
Each etiology of hypoglycemia has a distinct biochemical signature. Endogenous hyperinsulinemia (insulinoma and sulfonylurea) elevates C-peptide, requiring a drug screen to separate the two. Exogenous insulin causes hyperinsulinemia without C-peptide elevation. Non-islet tumors suppress both.

Step-by-Step Solution

1
Analyze insulin and C-peptide levels simultaneously during the hypoglycemic episode.
Determines if the hyperinsulinemia is from an endogenous or exogenous source.
Endogenous insulin is always co-secreted in equimolar amounts with C-peptide. Exogenous insulin administration causes hyperinsulinemia but lacks C-peptide, and the resulting hypoglycemia suppresses endogenous production.
2
Evaluate the oral hypoglycemic agent screen if both insulin and C-peptide are elevated.
Differentiates an autonomous insulin-secreting tumor (insulinoma) from drug-induced endogenous secretion (sulfonylurea).
Both conditions cause endogenous hyperinsulinemia, making toxicological screening the only definitive way to distinguish them biochemically.
3
Assess for IGF-II or other extrapancreatic causes if both insulin and C-peptide are suppressed during severe hypoglycemia.
Identifies non-islet cell tumor hypoglycemia (NICTH).
Tumor-produced IGF-II activates insulin receptors directly, causing profound hypoglycemia which then appropriately suppresses the endogenous HPA and pancreatic hormone axes.

Key Concept

Differentiation of adult hypoglycemia utilizing fasting laboratory profiles of insulin, C-peptide, and toxicological screens.
Question 1729Question →

Match each clinical scenario involving professional boundaries with the most appropriate ethical action or guideline.

Click a left item, then click its matching right item

Items

A physician is asked by their brother to prescribe a new course of oral antibiotics for a suspected skin infection.
A psychiatrist considers dating a former patient whom they successfully treated for generalized anxiety disorder three years ago.
A grateful patient offers their oncologist a luxury watch valued at approximately $600 as a token of appreciation after remission.
An emergency physician is asked on a date by a patient they treated for a minor ankle sprain two months prior; the patient has established follow-up care elsewhere.

Matches

Show answer & explanation

Answer

Treating a brother requires declining due to lack of objectivity; dating a former psychiatric patient is permanently banned; accepting a $600 watch must be declined due to monetary value; and dating a former ER patient is permissible since the care was episodic and terminated.
Professional boundaries dictate specific responses to conflicts of interest and dual relationships. Treating family members is restricted to emergencies. Accepting high-value gifts is prohibited to prevent undue influence. Romantic relationships with former psychiatric patients are universally banned due to permanent vulnerability, while relationships with former patients in episodic, non-psychiatric settings (like emergency medicine) may be permissible once care is officially terminated.

Step-by-Step Solution

1
Analyze the specific type of boundary being tested in each scenario
Identified four distinct domains: treating family members, psychiatric patient relationships, high-value gifts, and non-psychiatric former patient relationships.
Different professional boundary issues are governed by specific American Medical Association (AMA) ethical guidelines.
2
Apply the relevant ethical guideline to the family member scenario
Matched the brother's antibiotic request with the rule to decline treatment outside of emergencies.
Treating family members compromises objectivity and risks poor documentation or incomplete physical exams.
3
Differentiate the rules for dating former patients based on the physician's specialty
Matched the psychiatrist with the permanent ban on dating former patients, and matched the ER physician with the allowance for dating after the relationship is terminated.
Psychiatric patients remain perpetually vulnerable due to transference, whereas episodic emergency care lacks this sustained power dynamic.
4
Apply the financial conflict of interest guideline to the gift scenario
Matched the $600 watch offer with the requirement to politely decline.
High-value gifts risk altering the clinical relationship and creating a conflict of interest, unlike small token gifts which may be accepted.

Key Concept

Professional Boundaries and Ethics in Physician-Patient Relationships
Question 1730Question →

A 42-year-old woman is brought to the emergency department by ambulance due to severe confusion, agitation, and high fever. Her husband reports she has a history of Graves' disease but stopped taking her medications three months ago. Temperature is 40.2°C (104.4°F), blood pressure is 158/68 mm Hg, and pulse is 152/min and irregularly irregular. Physical examination shows profound diaphoresis, a fine resting tremor, bilateral exophthalmos, and an enlarged, non-tender thyroid gland. An ECG confirms atrial fibrillation with rapid ventricular response. After securing the airway and initiating intravenous fluid resuscitation, the care team prepares a targeted pharmacologic regimen for her acute hypermetabolic state. Arrange the following management steps in the most appropriate chronological sequence for this patient.

Drag items to arrange them in the correct order

Show answer & explanation

Answer

The correct sequence is: 1) beta-adrenergic antagonist, 2) thionamide, 3) iodine compound, and 4) definitive therapy (thyroidectomy/ablation).
The management of thyroid storm requires a strict chronological sequence to rapidly stabilize the patient while preventing iatrogenic exacerbation of the hypermetabolic state. Beta-blockers are given first for immediate symptom control. Thionamides must be given next to halt de novo hormone synthesis. Iodine compounds are administered at least one hour after thionamides to block the release of preformed hormone. Finally, definitive therapy is delayed until the patient is completely stabilized and euthyroid.

Step-by-Step Solution

1
Identify the clinical presentation as a life-threatening thyroid storm.
The patient's fever, tachycardia, atrial fibrillation, and altered mental status in the setting of untreated Graves' disease require immediate aggressive management.
Recognizing the severity dictates a rapid, multi-modal pharmacological approach rather than stepwise outpatient management.
2
Prioritize immediate symptom control and hemodynamic stabilization.
Intravenous beta-blockers (propranolol) are administered first.
Reducing the extreme adrenergic tone is the most critical initial step to prevent cardiovascular collapse and arrhythmias.
3
Establish the correct sequence for halting thyroid hormone production and release.
A thionamide is given next, followed by an iodine compound at least one hour later.
Thionamides block new hormone synthesis. If iodine is given before the synthesis machinery is blocked, it will fuel further hormone production (Jod-Basedow phenomenon). Once blocked, iodine safely prevents the release of preformed hormone (Wolff-Chaikoff effect).
4
Determine the timing of definitive curative treatment.
Thyroidectomy or radioactive iodine ablation is delayed.
Definitive interventions can induce a massive release of thyroid hormone and are fatal if performed during an acute storm; the patient must be euthyroid first.

Key Concept

Thyroid Storm Acute Management Sequence
Question 1731Question →

A 22-day-old female neonate is evaluated in the neonatal intensive care unit for persistent cyanosis. She was born at 3939 weeks gestation via normal vaginal delivery to a 2828-year-old primigravida. The mother has a history of bipolar disorder and was maintained on her prescribed psychiatric medication throughout the pregnancy. On physical examination, the neonate appears comfortably tachypneic but cyanotic. Vital signs show a heart rate of 160160/min, respiratory rate of 6565/min, and oxygen saturation of 82%82\% on room air. Cardiac auscultation reveals a widely split S1S_1, a normal S2S_2, and a harsh holosystolic murmur heard best at the left lower sternal border. Chest radiography demonstrates massive cardiomegaly spanning nearly the entire thoracic cavity. Electrocardiography reveals right atrial enlargement and a complete right bundle branch block. Which of the following best describes the underlying cardiovascular anomaly in this patient?

Show answer & explanation

Answer: Downward displacement of the septal and posterior tricuspid valve leaflets

Answer

Downward displacement of the septal and posterior tricuspid valve leaflets
The patient's clinical presentation is classic for Ebstein anomaly, a congenital heart defect strongly associated with maternal lithium use (the primary treatment for bipolar disorder). In Ebstein anomaly, there is a downward (apical) displacement of the septal and posterior leaflets of the tricuspid valve into the right ventricle. This structural change 'atrializes' a portion of the right ventricle, leading to a massive right atrium, severe tricuspid regurgitation (creating the holosystolic murmur), and delayed conduction (right bundle branch block). The extreme right atrial dilation creates a 'wall-to-wall' appearance on chest radiography.

Step-by-Step Solution

1
Identify the key clinical findings in the neonate.
The patient has neonatal cyanosis, massive cardiomegaly on chest radiography, right atrial enlargement with a right bundle branch block on electrocardiography, and a holosystolic murmur.
Synthesizing the physical exam and diagnostic imaging helps narrow down the specific congenital heart defect.
2
Correlate the neonate's findings with the maternal history.
The mother took medication for bipolar disorder during pregnancy. The standard mood stabilizer for bipolar disorder is lithium.
Maternal teratogenic exposures strongly predispose neonates to specific cardiac anomalies.
3
Determine the structural anomaly caused by the suspected teratogen.
Prenatal lithium exposure is classically associated with Ebstein anomaly, characterized by downward displacement of the tricuspid valve leaflets.
This anomaly perfectly explains the massive cardiomegaly (due to severe right atrial enlargement) and the right-sided electrocardiographic conduction delays.

Key Concept

Ebstein anomaly is a congenital heart defect characterized by the apical displacement of the tricuspid valve, leading to severe tricuspid regurgitation and massive right atrial enlargement. It is strongly associated with maternal use of lithium during pregnancy.
Estimated Time:1m 30s
Question 1732Question →

An obstetric rapid response is called for a patient at 36 weeks36\text{ weeks} of gestation who presents to the triage unit with a 2-day2\text{-day} history of worsening jaundice, persistent nausea, and severe lethargy. She has no significant past medical history, and her prenatal course was previously unremarkable. Upon evaluation, she appears visibly confused and is difficult to arouse. Her temperature is 37.0∘C37.0^\circ\text{C} (98.6∘F98.6^\circ\text{F}), blood pressure is 132/84 mm Hg132/84\text{ mm Hg}, and heart rate is 108/min108/\text{min}. Physical examination reveals scleral icterus and right upper quadrant abdominal tenderness. The uterus is soft, and pelvic examination shows a closed cervix. A continuous fetal monitor is placed, demonstrating a baseline heart rate of 145/min145/\text{min} with moderate variability and spontaneous accelerations; there are no decelerations.

Initial laboratory studies are obtained and reveal the following:

Hemoglobin: 10.8 g/dL10.8\text{ g/dL}
Platelet count: 88,000/mm388,000/\text{mm}^3
Leukocyte count: 16,500/mm316,500/\text{mm}^3
Glucose: 42 mg/dL42\text{ mg/dL}
Aspartate aminotransferase (AST): 740 U/L740\text{ U/L}
Alanine aminotransferase (ALT): 820 U/L820\text{ U/L}
Total bilirubin: 5.6 mg/dL5.6\text{ mg/dL}
Creatinine: 1.8 mg/dL1.8\text{ mg/dL}
Prothrombin time: 22 seconds22\text{ seconds} (Reference: 11−14 seconds11-14\text{ seconds})
Activated partial thromboplastin time: 54 seconds54\text{ seconds} (Reference: 25−40 seconds25-40\text{ seconds})

Intravenous dextrose is immediately administered, and the patient becomes fully oriented. Blood products are typed and crossmatched. Which of the following is the most appropriate next step in the management of this patient?

Show answer & explanation

Answer: Induction of labor

Answer

Induction of labor
The patient's clinical picture is classic for Acute Fatty Liver of Pregnancy (AFLP), a rare but catastrophic complication typically occurring in the third trimester. It is characterized by microvesicular steatosis leading to acute liver failure. The hallmark laboratory abnormalities that distinguish AFLP from HELLP syndrome are profound hypoglycemia, elevated ammonia levels, and significant coagulopathy (prolonged PT and aPTT). The definitive treatment for AFLP is immediate delivery after initial maternal stabilization (e.g., glucose administration and ordering blood products). Because the fetal heart tracing is reassuring (Category I) and the patient has profound coagulopathy, induction of labor is the preferred route of delivery. Performing a laparotomy (cesarean delivery) on a patient with severe coagulopathy carries an unacceptably high risk of exsanguination and should be reserved only for obstetric indications or fetal distress.

Step-by-Step Solution

1
Analyze the clinical presentation and laboratory values to establish the underlying diagnosis.
The patient has 3rd-trimester jaundice, altered mental status, profound hypoglycemia (42 mg/dL42\text{ mg/dL}), and severe coagulopathy (prolonged PT and aPTT).
These specific findings distinguish Acute Fatty Liver of Pregnancy (AFLP) from severe preeclampsia and HELLP syndrome (which typically feature normal glucose and normal coagulation times).
2
Determine the definitive treatment requirement for the established diagnosis.
AFLP is rapidly fatal for both mother and fetus if the pregnancy continues; immediate delivery is required once the mother is stabilized.
The microvesicular fatty infiltration of the liver is driven by a maternal-fetal defect in fatty acid metabolism, which only resolves upon delivery of the placenta.
3
Evaluate fetal status and maternal surgical risk to select the optimal mode of delivery.
The fetal heart tracing is Category I (reassuring), and the mother has severe, life-threatening coagulopathy.
Because there is no fetal indication for operative delivery, and major abdominal surgery (cesarean) carries an extreme risk of exsanguination due to the coagulopathy, vaginal delivery via induction of labor is the preferred next best step.

Key Concept

Diagnosis and acute management of Acute Fatty Liver of Pregnancy (AFLP), prioritizing vaginal delivery due to coagulopathy.
Question 1733Question →

Paramedics bring a 3030-year-old patient at 3737 weeks of pregnancy to the trauma bay after a severe motor vehicle collision. Her obstetric history is notable for one prior uncomplicated vaginal delivery at term. She complains of unrelenting, severe lower abdominal pain and reports a small amount of dark red vaginal bleeding.

Vital signs show a blood pressure of 86/5286/52 mmHg, a heart rate of 128128/min, and a respiratory rate of 2222/min. Physical examination reveals a rigid, board-like uterus that is extremely tender to palpation. Pelvic examination demonstrates the cervix is 11 cm dilated and 50%50\% effaced.

Continuous fetal heart rate monitoring displays a baseline of 105105/min with absent beat-to-beat variability and recurrent late decelerations occurring with every spontaneous uterine contraction. Laboratory analysis reveals a hemoglobin of 9.29.2 g/dL and a normal platelet count.

Which of the following is the most appropriate next step in the management of this patient?

Show answer & explanation

Answer: Commence aggressive intravenous fluid resuscitation and transfer immediately for operative delivery

Answer

The most appropriate next step is to commence aggressive intravenous fluid resuscitation and transfer the patient immediately for operative delivery.
The patient's presentation of a rigid, tender uterus, dark vaginal bleeding, and hemorrhagic shock following blunt abdominal trauma is highly characteristic of a severe placental abruption. The shearing forces of the motor vehicle collision have caused premature separation of the placenta. This disruption in uteroplacental perfusion has led to severe fetal hypoxia, evidenced by the Category III fetal heart rate tracing (absent variability with recurrent late decelerations). In the setting of maternal hemodynamic instability and a non-reassuring fetal status, the most appropriate management is simultaneous aggressive maternal volume resuscitation (using intravenous fluids and blood products) and immediate operative delivery (cesarean delivery). Delaying intervention for imaging or attempting to prolong the pregnancy risks both maternal exsanguination and fetal demise.

Step-by-Step Solution

1
Evaluate the patient's hemodynamic status following blunt abdominal trauma.
The patient exhibits severe hypotension (86/5286/52 mmHg) and tachycardia (128128/min), indicating hemorrhagic shock.
Trauma in pregnancy requires simultaneous assessment of maternal stability and fetal well-being, with maternal stabilization being the absolute priority.
2
Identify the most likely obstetric cause for the clinical presentation.
The combination of trauma, a rigid and tender uterus, dark vaginal bleeding, and maternal shock strongly indicates a severe placental abruption.
Blunt trauma can cause shearing forces that prematurely detach the placenta from the uterine wall, leading to significant concealed or visible hemorrhage.
3
Analyze the fetal heart rate tracing to determine fetal status.
A baseline of 105105/min with absent variability and recurrent late decelerations constitutes a Category III tracing.
Placental abruption disrupts uteroplacental blood flow, resulting in severe fetal hypoxia and acidemia, manifested as a Category III tracing.
4
Determine the definitive next best step in management.
Immediate aggressive intravenous fluid and blood product resuscitation alongside emergency surgical delivery are mandated.
Maternal hemodynamic instability and a Category III fetal heart tracing require immediate operative intervention without delaying for imaging or attempting vaginal delivery.

Key Concept

Management of placental abruption with maternal hemodynamic instability and fetal distress
Question 1734Question →

A 3232-year-old female, currently in her second pregnancy (G2P1) at 3434 weeks of gestation, is evaluated in the emergency department for shortness of breath and leg swelling. She states that the breathlessness has gradually developed over the past few weeks and is most noticeable when she lies flat in bed. She denies chest pain, cough, or pain in her legs. Her medical history is unremarkable, and her pregnancy has been uncomplicated.

Vital signs show a temperature of 37.1∘C37.1^\circ\text{C} (98.8∘F98.8^\circ\text{F}), blood pressure of 112/70 mmHg112/70\text{ mmHg}, pulse of 86/min86\text{/min}, and respirations of 16/min16\text{/min}. Oxygen saturation is 99%99\% on ambient air.

Physical examination demonstrates 1+ symmetric, bilateral pitting edema extending to the ankles. The maximum circumference of the right calf is 35.0 cm35.0\text{ cm} and the left calf is 35.5 cm35.5\text{ cm}. Cardiac auscultation reveals a grade 2/6 early systolic murmur at the left sternal border. The lungs are clear to auscultation bilaterally.

Laboratory analysis reveals the following:

Hemoglobin: 10.6 g/dL10.6\text{ g/dL}
Platelet count: 145,000/mm3145,000\text{/mm}^3
D-dimer: 920 ng/mL920\text{ ng/mL} (Reference: <500 ng/mL< 500\text{ ng/mL})

Arterial blood gas analysis on ambient air:
pH: 7.447.44
PaO 2_2: 104 mmHg104\text{ mmHg}
PaCO 2_2: 29 mmHg29\text{ mmHg}
HCO 3−_3^-: 19 mEq/L19\text{ mEq/L}

Which of the following is the most appropriate next step in the management of this patient?

Show answer & explanation

Answer: Reassurance and routine obstetric follow-up

Answer

Reassurance and routine obstetric follow-up
The correct answer is reassurance and routine obstetric follow-up because this patient's clinical and laboratory findings entirely represent normal physiologic adaptations to pregnancy. Progesterone directly stimulates the medullary respiratory center, increasing minute ventilation (primarily via increased tidal volume) and resulting in a chronic, compensated respiratory alkalosis (pH slightly alkalotic, low PaCO 2_2, and a compensatory decrease in HCO 3−_3^-). The growing uterus elevates the diaphragm, which can cause a subjective feeling of breathlessness, particularly when supine. Additionally, normal pregnancy is a hypercoagulable state with physiologically increased D-dimer levels; therefore, a D-dimer test has virtually no negative predictive value in the third trimester. Her symmetric edema and grade 2/6 systolic ejection murmur are expected consequences of increased plasma volume and cardiac output. Since she lacks acute or focal signs of pathology (such as tachycardia, hypoxia, asymmetric leg swelling, or hypertension), reassurance is the most appropriate management.

Step-by-Step Solution

1
Analyze the patient's presenting symptoms and vital signs.
The patient reports a gradual onset of dyspnea and orthopnea, with symmetric leg swelling. Vital signs are strictly within normal limits, including normal oxygen saturation and heart rate.
Establishing the acuity of the presentation helps differentiate between life-threatening emergencies (e.g., pulmonary embolism) and physiologic changes of the third trimester.
2
Evaluate the physical examination findings.
Symmetric bilateral pitting edema and a 2/6 early systolic flow murmur are present. Lungs are clear, and there is no asymmetric calf swelling.
These findings are classic normal physiological adaptations driven by venous compression from the gravid uterus and increased maternal blood volume/cardiac output.
3
Interpret the laboratory and arterial blood gas (ABG) results in the context of pregnancy.
The patient has a primary respiratory alkalosis with metabolic compensation (pH 7.447.44, low PaCO 2_2, low HCO 3−_3^-). The D-dimer is elevated, and mild dilutional anemia is present.
Progesterone directly stimulates the medullary respiratory center, increasing minute ventilation and causing a chronic respiratory alkalosis. D-dimer naturally rises during normal pregnancy, rendering it useless for ruling out venous thromboembolism.
4
Synthesize the findings to determine the correct management.
Because all findings reflect normal pregnancy physiology and the patient has a Wells score of zero, no further diagnostic testing or treatment is indicated.
Empiric treatment or advanced imaging based on physiologically expected abnormal laboratory values leads to unnecessary healthcare interventions and patient anxiety.

Key Concept

Normal physiologic adaptations in the third trimester include dyspnea, symmetric lower extremity edema, systolic flow murmurs, physiologically elevated D-dimer levels, and a compensated primary respiratory alkalosis.
Question 1735Question →

A 1010-week-old male infant is brought to the pediatric emergency department by his parents due to a 33-day history of rapid breathing, poor feeding, and increased fussiness. The parents report that the infant takes twice as long to finish a bottle and frequently stops to catch his breath while sweating profusely over his forehead. He has had a mild cough but no fever. Medical history is notable for an uncomplicated full-term birth. A cardiac murmur was mentioned at his 11-month well-child visit, but the family missed the follow-up appointment. Temperature is 37.0∘C37.0^\circ\text{C} (98.6∘F98.6^\circ\text{F}), pulse is 168/min168/\text{min}, respiratory rate is 68/min68/\text{min}, and blood pressure is 85/50 mmHg85/50\text{ mmHg}. Pulse oximetry shows 94%94\% on room air. Physical examination reveals an infant in moderate respiratory distress with intercostal retractions. Lung auscultation reveals diffuse bilateral wheezes and fine crackles at the bases. Cardiovascular examination shows a hyperactive precordium, a loud S2, and a grade 3/63/6 harsh holosystolic murmur at the left lower sternal border. The liver edge is palpated 3.5 cm3.5\text{ cm} below the right costal margin. Which of the following is the most appropriate next step in the management of this patient?

Show answer & explanation

Answer: Transthoracic echocardiography

Answer

Transthoracic echocardiography is the most appropriate next step to diagnose and confirm the structural cause of the patient's acute congestive heart failure.
This infant is presenting with classic signs of acute congestive heart failure (CHF) secondary to a congenital heart defect, most likely a ventricular septal defect (VSD). Hallmarks of infant CHF include tachypnea, poor feeding, diaphoresis with exertion (such as feeding), failure to thrive, and hepatomegaly due to venous congestion. Furthermore, the grade 3/63/6 harsh holosystolic murmur at the left lower sternal border is highly specific for a VSD. Infants with large VSDs often do not present at birth because their pulmonary vascular resistance (PVR) is still physiologically elevated, restricting the left-to-right shunt. As PVR naturally falls over the first 22 to 33 months of life, the shunt increases, leading to pulmonary overcirculation and subsequent heart failure. The most appropriate next step in management is a transthoracic echocardiogram to visualize the defect, assess the direction and magnitude of the shunt, and evaluate overall cardiac function.

Step-by-Step Solution

1
Evaluate the patient's constellation of clinical signs and symptoms.
Identify the clinical syndrome as acute congestive heart failure rather than a primary respiratory illness.
The combination of tachypnea, diaphoresis during exertion (feeding), crackles, wheezing, and significant hepatomegaly strongly points to right-sided volume overload and pulmonary edema.
2
Correlate the cardiovascular exam findings with the infant's age.
Suspect a significant left-to-right cardiac shunt, most likely a ventricular septal defect (VSD).
A harsh holosystolic murmur at the left lower sternal border is characteristic of a VSD. Symptoms typically manifest at 6 to 10 weeks of life when normal physiologic pulmonary vascular resistance drops, allowing for a massive left-to-right shunt.
3
Determine the optimal next step in management.
Select transthoracic echocardiography.
Echocardiography is the gold standard, non-invasive imaging modality required to definitively define the cardiac anatomy, quantify the shunt, and guide subsequent medical and surgical interventions.

Key Concept

Clinical presentation and initial diagnostic workup of pediatric congestive heart failure secondary to a left-to-right shunt.
Question 1736Question →

A primigravid patient at 3737 weeks of gestation is currently in the labor and delivery unit. She was admitted 2424 hours ago for induction of labor due to preeclampsia with severe features. She is receiving continuous intravenous oxytocin, labetalol, and magnesium sulfate. Over the past 44 hours, her total urine output has been 45 mL45\text{ mL}. The nurse calls the physician because the patient has become increasingly somnolent and difficult to arouse. Current vital signs are temperature 37.1∘C37.1^\circ\text{C} (98.8∘F98.8^\circ\text{F}), blood pressure 135/85 mmHg135/85\text{ mmHg}, pulse 82/min82/\text{min}, and respiratory rate 8/min8/\text{min}. Oxygen saturation is 90%90\% on room air. Neurologic examination reveals absent deep tendon reflexes at the patella and biceps. The continuous fetal heart rate tracing demonstrates a baseline of 145/min145/\text{min}, minimal variability, and no decelerations. Which of the following is the most appropriate initial step in management?

Show answer & explanation

Answer: Discontinue the magnesium sulfate infusion and administer intravenous calcium gluconate

Answer

Discontinue the magnesium sulfate infusion and administer intravenous calcium gluconate
This patient has severe magnesium toxicity, characterized by absent deep tendon reflexes, somnolence, and severe respiratory depression (respiratory rate of 8/min8/\text{min}). Magnesium sulfate is exclusively excreted by the kidneys; therefore, her marked oliguria led to decreased clearance and toxic accumulation. The most appropriate initial step is to immediately discontinue the magnesium sulfate infusion and administer intravenous calcium gluconate, which antagonizes the effects of magnesium at the neuromuscular junction and reverses respiratory depression.

Step-by-Step Solution

1
Evaluate the patient's neurologic and respiratory status.
The patient is somnolent with absent deep tendon reflexes, a respiratory rate of 8/min, and hypoxia.
To rapidly identify life-threatening central nervous system and respiratory depression.
2
Correlate the clinical presentation with current medications and risk factors.
The patient is receiving magnesium sulfate and has oliguria (45 mL over 4 hours).
Magnesium is excreted exclusively by the kidneys. Oliguria leads to rapid accumulation of magnesium, causing toxicity (areflexia followed by respiratory depression).
3
Determine the most appropriate initial intervention.
Stop the magnesium infusion and administer the antidote, calcium gluconate.
Calcium competitively antagonizes magnesium at the neuromuscular junction, reversing the life-threatening respiratory depression and stabilizing the myocardium.

Key Concept

Patients with preeclampsia receiving magnesium sulfate who develop oliguria are at high risk for magnesium toxicity, which presents sequentially as loss of deep tendon reflexes, somnolence, and respiratory depression. Management requires immediate cessation of the infusion and administration of intravenous calcium gluconate.
Question 1737Question →

An 88-month-old girl is brought to a family medicine clinic in mid-December due to a persistent cough and noisy breathing. Her mother reports that the child developed a runny nose, low-grade fever, and mild nasal congestion four days ago. Yesterday, the nasal discharge became thick, and the child developed a "tight" cough. She has no prior episodes of wheezing and was born at term without complications. She has been feeding well and producing a normal number of wet diapers. Vital signs are temperature 37.8∘C37.8^\circ\text{C} (100.0∘F100.0^\circ\text{F}), heart rate 125/min125\text{/min}, respiratory rate 44/min44\text{/min}, and oxygen saturation 96%96\% on room air. Physical examination reveals a happy, interactive infant. Lung auscultation demonstrates diffuse bilateral expiratory wheezes and mild subcostal retractions. Which of the following interventions are appropriate components of the immediate management plan for this patient? (Select all that apply)

Select all that apply

Show answer & explanation

Answer: Routine nasal suctioning before feeding; Discharge home with strict return precautions

Answer

Routine nasal suctioning before feeding AND Discharge home with strict return precautions
This patient is presenting with a classic case of viral bronchiolitis, characterized by a viral prodrome (rhinorrhea, congestion) followed by lower respiratory tract signs (polyphonic wheezing, tachypnea, mild retractions) in a child under 22 years of age. Because she is maintaining adequate oxygenation (SpO2 >90%>90\%), feeding well, and appearing interactive, she meets the criteria for mild-to-moderate disease suitable for outpatient management. The standard of care for bronchiolitis is strictly supportive. Routine nasal suctioning before feeding is highly effective because infants are obligate nose breathers; clearing nasal mucus significantly reduces the work of breathing and facilitates oral intake. The patient can be safely discharged home provided the parents are given strict return precautions regarding signs of impending respiratory failure (e.g., cyanosis, severe retractions, lethargy, or poor feeding).

Step-by-Step Solution

1
Analyze the patient's symptoms and demographics.
An 8-month-old infant presenting with a viral prodrome followed by tachypnea and diffuse wheezing.
To establish the primary clinical diagnosis of acute viral bronchiolitis.
2
Assess the severity of the respiratory distress.
The infant is well-appearing, interacting normally, maintaining SpO2 at 96% on room air, and hydrating well despite mild retractions.
To determine whether inpatient admission or outpatient management is indicated.
3
Select the appropriate evidence-based interventions.
Supportive care (nasal suctioning) and discharge with return precautions are chosen, while explicitly avoiding bronchodilators, systemic steroids, and antibiotics.
To adhere to standard pediatric guidelines for uncomplicated, mild-to-moderate viral bronchiolitis.

Key Concept

The management of mild-to-moderate viral bronchiolitis is purely supportive (e.g., maintaining hydration, nasal suctioning); bronchodilators, corticosteroids, and antibiotics are physiologically ineffective and not indicated.
Estimated Time:1m 30s
Question 1738Question →

During a routine health maintenance visit, a 54-year-old G2P2 patient reports experiencing two days of light vaginal spotting the previous week. She underwent natural menopause at age 51. Her past medical history is significant for estrogen receptor-positive, node-negative breast cancer, for which she was treated with a lumpectomy and radiation therapy three years ago. Since completing her primary surgical and radiation treatment, she has been maintained on tamoxifen. Her body mass index is 26 kg/m^2. Vital signs are within normal limits. Pelvic examination demonstrates normal external genitalia, a small and mobile uterus, and no palpable adnexal masses. Speculum examination shows a small amount of dark red blood in the vaginal vault, but no active bleeding or visible cervical lesions. Which of the following is the most appropriate next step in management?

Show answer & explanation

Answer: Endometrial biopsy

Answer

Endometrial biopsy
The correct answer is endometrial biopsy. This patient presents with postmenopausal bleeding, which is abnormal and should always trigger an evaluation for endometrial cancer. Her risk is further elevated by her use of tamoxifen. Tamoxifen is a selective estrogen receptor modulator (SERM) that acts as an estrogen antagonist in breast tissue but as an estrogen agonist in the uterus. This agonistic effect promotes endometrial proliferation, increasing the risk of endometrial polyps, hyperplasia, and adenocarcinoma. The standard of care for postmenopausal bleeding is evaluation with either a transvaginal ultrasound or an endometrial biopsy. In a patient on tamoxifen, transvaginal ultrasound is often less useful because tamoxifen frequently causes subepithelial stromal hypertrophy, resulting in a falsely thickened endometrial stripe on imaging. Therefore, direct tissue sampling via endometrial biopsy is the most definitive and appropriate next step to rule out malignancy.

Step-by-Step Solution

1
Identify the primary clinical problem and demographic risk factors.
The patient is a postmenopausal woman presenting with new-onset vaginal bleeding.
Postmenopausal bleeding is the cardinal symptom of endometrial cancer and requires immediate evaluation.
2
Analyze the impact of the patient's past medical history and medication use.
The patient takes tamoxifen for breast cancer, which acts as an estrogen agonist on the endometrium.
Tamoxifen significantly increases the risk of endometrial hyperplasia and endometrial adenocarcinoma.
3
Determine the most appropriate diagnostic intervention based on the clinical presentation.
Endometrial tissue sampling is required.
Because the risk of malignancy is high, direct histologic evaluation of the endometrium via biopsy is the standard of care to definitively rule in or rule out cancer.

Key Concept

Postmenopausal bleeding in a patient taking tamoxifen requires prompt evaluation with an endometrial biopsy to rule out endometrial hyperplasia or adenocarcinoma.
Question 1739Question →

An obstetric team is attending the delivery of a macrosomic infant at 40 weeks gestation. After the fetal head emerges, it immediately retracts tightly against the mother's perineum. The anterior shoulder remains impacted behind the pubic symphysis despite routine gentle downward traction. Arrange the following management steps in the correct standard sequence of escalation to resolve this complication, from the immediate first response to the maneuver of last resort.

Drag items to arrange them in the correct order

Show answer & explanation

Answer

The correct sequence is: 1) Call for assistance and instruct the mother to stop pushing, 2) Perform the McRoberts maneuver with suprapubic pressure, 3) Execute internal rotational maneuvers, 4) Perform the Zavanelli maneuver as a last resort.
The widely established protocol for managing shoulder dystocia involves a clear stepwise progression from least invasive to most invasive. The clinician must first recognize the emergency, halt pushing, and mobilize help. The initial physical intervention is the McRoberts maneuver (often coupled with suprapubic pressure), which safely alters maternal pelvic geometry. If external maneuvers fail, the provider escalates to internal vaginal maneuvers (such as the Woods corkscrew or delivering the posterior arm) to manually alter the fetal position. Heroic measures, such as replacing the fetal head to facilitate an emergent cesarean section (Zavanelli maneuver), are strictly reserved for intractable cases where all other maneuvers have failed.

Step-by-Step Solution

1
Identify the clinical presentation as shoulder dystocia.
The retraction of the fetal head against the perineum (turtle sign) confirms the anterior shoulder is impacted behind the maternal pubic symphysis.
Immediate recognition is required to initiate a standardized management protocol and prevent hypoxic injury to the fetus.
2
Determine the initial, non-physical response.
The provider must tell the patient to stop pushing and immediately call for help.
Pushing worsens the impaction. Resolving the dystocia requires a coordinated team (e.g., an assistant to apply suprapubic pressure while the primary provider performs maneuvers).
3
Identify the first-line physical maneuvers.
McRoberts maneuver combined with suprapubic pressure should be performed first.
These external maneuvers alter the maternal pelvic geometry and are successful in relieving a large percentage of shoulder dystocias without requiring internal vaginal manipulation.
4
Identify the secondary interventions if first-line maneuvers fail.
Internal rotational maneuvers (e.g., Woods corkscrew, Rubin) or delivery of the posterior arm are the next steps.
Internal maneuvers directly alter the orientation of the fetal shoulders to bypass the bony obstruction.
5
Identify the maneuver of last resort.
The Zavanelli maneuver (replacing the fetal head into the pelvis to perform a cesarean section) is the final escalation.
Because of significant maternal and fetal morbidity, heroic measures are strictly reserved for cases refractory to all other standard maneuvers.

Key Concept

The management of shoulder dystocia follows a strict, standardized escalation protocol (e.g., HELPERR mnemonic) that begins with calling for help and using noninvasive external maneuvers, progresses to invasive internal maneuvers, and concludes with heroic measures as a last resort.
Question 1740Question →

An adolescent primigravida at 39 weeks gestation is currently in the active phase of labor following spontaneous rupture of membranes 24 hours ago. Over the last hour, she has developed a new-onset fever. She is currently receiving continuous epidural analgesia. Her temperature is 39.2°C (102.6°F), blood pressure is 112/70 mm Hg, pulse is 115/min, and respirations are 18/min. Physical examination reveals a uterus that is tender to palpation between contractions. Pelvic examination shows the cervix is 6 cm dilated and 90% effaced, with the fetal presenting part at +1 station. Uterine contractions are occurring every 5 to 6 minutes. Continuous fetal monitoring displays a baseline heart rate of 175/min with moderate variability and occasional early decelerations. Which of the following is the most appropriate next step in the management of this patient?

Show answer & explanation

Answer: Intravenous ampicillin, gentamicin, and oxytocin

Answer

The correct answer is the administration of intravenous ampicillin, gentamicin, and oxytocin.
The correct answer combines both the necessary medical treatment and the appropriate obstetric management. The patient has clinical intra-amniotic infection (fever, fetal tachycardia, uterine tenderness) occurring after prolonged rupture of membranes. Standard treatment includes broad-spectrum antibiotics (such as ampicillin and gentamicin). Additionally, because her contractions are inadequate (every 5-6 minutes in the active phase) and the fetal heart rate tracing is reassuring (Category I/II with moderate variability and early decelerations), the most appropriate obstetric step is to expedite vaginal delivery via oxytocin augmentation. Intra-amniotic infection alone is not an indication for cesarean delivery.

Step-by-Step Solution

1
Diagnose the underlying condition based on maternal vital signs and physical examination.
The maternal temperature of 39.2°C (102.6°F), accompanied by uterine tenderness and fetal tachycardia, confirms the diagnosis of intra-amniotic infection (chorioamnionitis).
Maternal fever greater than 39.0°C in labor, especially with prolonged rupture of membranes and additional infectious signs, meets the criteria for clinical intra-amniotic infection.
2
Select the appropriate pharmacologic intervention for the infection.
Intravenous broad-spectrum antibiotics, typically ampicillin and gentamicin, are required.
Prompt antibiotic administration prevents maternal morbidity (e.g., sepsis) and neonatal infectious complications.
3
Determine the appropriate obstetric management by evaluating labor progression and fetal status.
The contractions are inadequate (every 5-6 minutes) for the active phase of labor, and the fetal heart rate tracing is reassuring (moderate variability, no late/variable decelerations). Therefore, labor augmentation with oxytocin is indicated.
Intra-amniotic infection requires expeditious delivery. Because the fetus is tolerating labor well, vaginal delivery should be facilitated with oxytocin rather than proceeding to an unnecessary cesarean delivery.

Key Concept

Intra-amniotic infection (chorioamnionitis) is managed with broad-spectrum antibiotics and augmentation of labor to expedite vaginal delivery; it is not an absolute indication for cesarean delivery.
PreviousPage 87 / 414Next
All practice questions — USMLE Step 2 CK | Examkin