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Question 1781Question →

Match each esophageal motility disorder with its characteristic finding on high-resolution esophageal manometry.

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Items

Achalasia
Diffuse esophageal spasm
Systemic sclerosis (scleroderma)
Hypercontractile (Jackhammer) esophagus

Matches

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Answer

Achalasia matches with absent distal peristalsis and incomplete LES relaxation. Diffuse esophageal spasm matches with premature, simultaneous contractions and normal LES relaxation. Systemic sclerosis matches with absent peristalsis and decreased LES resting pressure. Hypercontractile esophagus matches with extremely high-amplitude peristaltic contractions and normal LES relaxation.
Each matching pair accurately reflects the underlying pathophysiology of the respective esophageal motility disorder as demonstrated on high-resolution manometry. The LES resting pressure and relaxation, along with the presence, amplitude, and coordination of distal peristalsis, provide the diagnostic hallmarks for each condition.

Step-by-Step Solution

1
Evaluate the LES function for each disorder.
Identify that Achalasia has incomplete LES relaxation, Systemic Sclerosis has decreased LES resting tone, while Diffuse Esophageal Spasm and Hypercontractile Esophagus typically have normal LES relaxation.
LES pressure is the primary differentiator between achalasia, scleroderma, and other motility disorders.
2
Evaluate the peristalsis patterns for the remaining conditions.
Diffuse esophageal spasm features uncoordinated, simultaneous contractions. Hypercontractile esophagus features high-amplitude but coordinated (peristaltic) contractions.
Contraction coordination and amplitude separate the hypercontractile states.

Key Concept

Esophageal motility disorders have distinct manometric signatures based on their effect on the lower esophageal sphincter and distal smooth muscle.
Question 1782Question →

A medical student is reviewing characteristic jugular venous pressure (JVP) waveform abnormalities during a cardiology rotation. Match each specific JVP finding with its most likely underlying cardiovascular pathology.

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Items

Absent Y descent with a prominent X descent
Prominent, sharp Y descent (Friedreich's sign)
Intermittent, irregular cannon A waves
Large, bounding V waves that merge with C waves

Matches

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Answer

Absent Y descent matches with Cardiac tamponade; Prominent, sharp Y descent matches with Constrictive pericarditis; Intermittent cannon A waves match with Complete AV block; Large V waves match with Severe tricuspid regurgitation.
The JVP waveform directly reflects right atrial hemodynamics. Cardiac tamponade abolishes the Y descent due to restricted early diastolic filling. Constrictive pericarditis causes a rapid Y descent due to rapid early diastolic filling that suddenly halts against a rigid pericardium. Complete AV block causes AV dissociation, leading to intermittent cannon A waves when the atrium happens to contract against a closed tricuspid valve. Tricuspid regurgitation causes massive retrograde volume into the atrium during systole, creating large merged C-V waves.

Step-by-Step Solution

1
Analyze the physiology of the normal JVP waveform to establish a baseline.
The A wave represents atrial contraction, the X descent is atrial relaxation, the V wave is venous filling during ventricular systole, and the Y descent is passive atrial emptying into the right ventricle.
Understanding normal hemodynamics is required to deduce how structural or electrical pathologies alter the waveform.
2
Evaluate the 'absent Y descent' finding.
It correlates with cardiac tamponade because pericardial fluid compression prevents early passive diastolic filling of the right ventricle.
Tamponade physiology restricts the heart throughout the entire cardiac cycle, severely limiting passive emptying (Y descent).
3
Evaluate the 'prominent Y descent' finding.
It correlates with constrictive pericarditis because the thickened pericardium allows for extremely rapid early diastolic filling before abruptly stopping it.
Constriction physiology differs from tamponade in that early diastolic filling is unhindered until the pericardial volume limit is suddenly reached.
4
Evaluate 'intermittent cannon A waves'.
It correlates with complete AV block due to atrioventricular dissociation.
When the atria depolarize and contract independently of the ventricles, they will occasionally contract while the tricuspid valve is closed (during ventricular systole), sending a large pressure wave backward into the jugular veins.
5
Evaluate 'large, bounding V waves'.
It correlates with tricuspid regurgitation.
Systolic backflow of blood from the right ventricle into the right atrium causes massive volume overload during the phase when the V wave normally forms, obliterating the normal X descent.

Key Concept

Jugular venous pressure (JVP) waveform abnormalities in cardiovascular pathology.
Estimated Time:1m 30s
Question 1783Question →

A 4th-year medical student is reviewing the endocrine laboratory profiles of four distinct patients being evaluated for suspected adrenal pathology. Match each patient's serum laboratory and dynamic testing profile to the most likely underlying etiology.

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Items

Low 8:00 AM serum cortisol, high ACTH, hyponatremia, and hyperkalemia
Low 8:00 AM serum cortisol, low ACTH, normal serum sodium and potassium
High 8:00 AM serum cortisol, high ACTH, cortisol suppresses >50%>50\% with high-dose dexamethasone
High 8:00 AM serum cortisol, high ACTH, cortisol does NOT suppress with high-dose dexamethasone

Matches

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Answer

Primary adrenal insufficiency features low cortisol, high ACTH, and electrolyte abnormalities; secondary adrenal insufficiency features low cortisol and ACTH with normal electrolytes; pituitary adenomas feature high cortisol/ACTH that suppress with high-dose dexamethasone; and ectopic ACTH secretion features high cortisol/ACTH that do not suppress.
Each laboratory profile distinctly maps to the underlying pathophysiology of the HPA axis, specifically regarding feedback loops and mineralocorticoid preservation.

Step-by-Step Solution

1
Analyze the patients with low 8:00 AM cortisol to identify the cause of adrenal insufficiency.
Differentiate based on ACTH and electrolyte levels.
High ACTH and abnormal electrolytes indicate primary adrenal failure. Low ACTH and normal electrolytes indicate secondary failure.
2
Analyze the patients with high 8:00 AM cortisol and high ACTH to identify the cause of ACTH-dependent Cushing syndrome.
Differentiate using the high-dose dexamethasone suppression test.
Pituitary sources retain partial feedback sensitivity and suppress; ectopic sources are completely autonomous and do not suppress.

Key Concept

Diagnosis and differentiation of adrenal insufficiency and Cushing syndrome using ACTH levels, electrolyte panels, and dexamethasone suppression testing.
Question 1784Question →

Match each physical examination finding describing a characteristic cardiac murmur to the most likely underlying cardiovascular condition or pathology.

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Items

A mid-systolic click followed by a late systolic murmur; the click occurs earlier in systole upon abrupt standing.
A holosystolic murmur at the left lower sternal border that prominently increases in intensity during inspiration.
An early diastolic decrescendo murmur that is auscultated best along the right sternal border.
A harsh, crescendo-decrescendo systolic murmur at the left lower sternal border that increases in intensity during the Valsalva maneuver.
A mid-diastolic rumbling murmur with a presystolic accentuation, immediately following a high-pitched early diastolic sound at the apex.

Matches

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Answer

L1 matches with Mitral valve prolapse; L2 matches with Tricuspid regurgitation; L3 matches with Aortic root dilation; L4 matches with Hypertrophic cardiomyopathy; L5 matches with Mitral stenosis.
Each physical examination finding uniquely describes the hemodynamics and acoustic properties of specific structural heart diseases, which can be distinguished using proper auscultation locations and dynamic bedside maneuvers.

Step-by-Step Solution

1
Analyze the murmur and dynamic maneuver in the first finding.
A click moving earlier in systole with standing indicates a smaller LV volume causing earlier prolapse.
Standing decreases preload. This is a classic feature of Mitral valve prolapse.
2
Evaluate the effect of inspiration on the second finding.
Inspiration increases right-sided murmurs (Carvallo's sign).
A holosystolic murmur at the left lower sternal border that increases with inspiration points to Tricuspid regurgitation.
3
Locate the maximal intensity point for the third finding.
An early diastolic murmur best heard at the right sternal border suggests aortic root pathology.
Valvular aortic regurgitation is best heard at the left sternal border, whereas aortic root dilation murmurs project to the right sternal border.
4
Determine the hemodynamic change during Valsalva for the fourth finding.
Valsalva decreases preload, worsening the murmur.
This behavior is characteristic of Hypertrophic cardiomyopathy, where reduced LV volume worsens the outflow tract obstruction.
5
Identify the components of the fifth finding.
An opening snap followed by a mid-diastolic rumble with presystolic accentuation.
These classic auscultatory findings are the hallmark of Mitral stenosis.

Key Concept

Differentiation of structural heart diseases and valvular pathologies through careful auscultation and dynamic maneuvers.
Estimated Time:2m 0s
Question 1785Question →

Match each of the following clinical trauma presentations with the single most appropriate next step in management.

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Items

A 34-year-old male with blunt abdominal trauma, a blood pressure of 70/40 mm Hg, and free fluid in the hepatorenal recess on focused assessment with sonography for trauma (FAST).
A 22-year-old male with blunt chest trauma, a blood pressure of 80/50 mm Hg, distended neck veins, and absent breath sounds over the right hemithorax.
A 45-year-old female with an anterior-posterior compression injury of the pelvis, a blood pressure of 75/45 mm Hg, and a completely negative FAST examination.
A 29-year-old female with a high-speed motor vehicle collision, a blood pressure of 115/75 mm Hg, a seat belt sign across the abdomen, and diffuse abdominal tenderness.

Matches

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Answer

The correct matching pairs are: Unstable patient with positive FAST to immediate exploratory laparotomy; Tension pneumothorax presentation to immediate tube thoracostomy; Unstable pelvic fracture with negative FAST to pelvic binder application; Hemodynamically stable patient with abdominal trauma to contrast-enhanced computed tomography (CT).
Correct management directly follows ATLS guidelines based on the triad of hemodynamic status, mechanism of injury, and initial bedside diagnostic findings (such as FAST or physical exam). Unstable patients with intra-abdominal fluid require laparotomy, those with tension pneumothorax require chest decompression, those with retroperitoneal pelvic bleeding require mechanical stabilization, and strictly stable patients are safe to undergo CT scanning.

Step-by-Step Solution

1
Evaluate the hemodynamic status of each patient based on blood pressure.
Three patients are in shock (hypotensive and unstable), and one patient is normotensive (stable).
Hemodynamic stability dictates whether a patient can safely travel to the CT scanner or if they require immediate bedside or operative intervention.
2
Analyze the source of shock in the three hemodynamically unstable patients.
A positive FAST indicates intraperitoneal bleeding. Absent breath sounds with distended neck veins indicate a tension pneumothorax. A pelvic fracture with a negative FAST indicates retroperitoneal bleeding.
Identifying the distinct physiological mechanism of hemorrhagic or obstructive shock determines the specific definitive life-saving intervention required.
3
Match the clinical diagnoses with the definitive Advanced Trauma Life Support (ATLS) management steps.
Intraperitoneal hemorrhage is managed with laparotomy; tension pneumothorax is managed with a chest tube; retroperitoneal pelvic hemorrhage is managed with a binder; stable trauma is investigated with CT imaging.
Following standard trauma resuscitation algorithms ensures rapid, appropriate care and avoids fatal delays.

Key Concept

Hemodynamic stability and mechanism of injury dictate the advanced trauma life support pathway, differentiating between the need for immediate surgical intervention, bedside stabilization, or advanced diagnostic imaging.
Question 1786Question →

A resident is evaluating four patients who all present with significant hypokalemia and metabolic alkalosis. Pair each patient's specific clinical and laboratory profile with the most likely underlying etiology.

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Items

A 24-year-old woman with a BMI of 18 kg/m², normal blood pressure, and a spot urine chloride concentration of 12 mEq/L.
A 28-year-old healthcare worker with normal blood pressure, an extensive medication history, and a spot urine chloride concentration of 55 mEq/L.
A 42-year-old man with blood pressures consistently >160/100 mm Hg, elevated plasma aldosterone, and undetectable plasma renin activity.
A 65-year-old man with severe hypertension, an abdominal bruit, elevated plasma aldosterone, and elevated plasma renin activity.

Matches

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Answer

The normal-blood-pressure patient with low urine chloride matches surreptitious vomiting; the normal-blood-pressure patient with high urine chloride matches diuretic abuse; the hypertensive patient with low renin matches primary hyperaldosteronism; and the hypertensive patient with high renin matches renovascular hypertension.
Evaluating hypokalemic metabolic alkalosis requires a structured approach. First, assess blood pressure. If normal, use urine chloride to distinguish GI losses (low Cl) from renal losses (high Cl). If hypertensive, use the aldosterone-to-renin ratio to differentiate primary (low renin) from secondary (high renin) hyperaldosteronism.

Step-by-Step Solution

1
Categorize the patients based on their blood pressure status.
The two younger female patients are normotensive, whereas the two older male patients are hypertensive.
Blood pressure distinguishes normotensive volume-depleted states from hypertensive mineralocorticoid excess states.
2
Differentiate the two normotensive patients using spot urine chloride concentrations.
The patient with a low urine chloride (< 20 mEq/L) is experiencing gastrointestinal losses (vomiting), while the patient with a high urine chloride (> 20 mEq/L) is experiencing renal losses (diuretic abuse).
The kidney's ability to conserve chloride indicates whether the primary defect is extrarenal (allowing appropriate renal compensation) or intrarenal (tubular blockade).
3
Differentiate the two hypertensive patients using the aldosterone and renin profiles.
The patient with low renin has primary adrenal disease, while the patient with high renin has secondary hyperaldosteronism from reduced renal blood flow.
Unregulated adrenal secretion directly suppresses renin via negative feedback, whereas impaired renal perfusion actively stimulates renin release.

Key Concept

Algorithm for evaluating hypokalemic metabolic alkalosis using blood pressure, urine chloride, and renin-aldosterone levels.
Question 1787Question →

Match each patient presentation and history of infective endocarditis to the most likely causative organism.

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Items

A 65-year-old man who recently underwent a cystoscopy for benign prostatic hyperplasia.
A 72-year-old man who recently underwent a colonoscopy revealing a suspicious colonic mass.
A 28-year-old man with a history of intravenous drug use presenting with a tricuspid valve vegetation.
A 45-year-old woman with a history of mitral valve prolapse who recently had a dental extraction.
A 55-year-old man who had a prosthetic aortic valve placed 3 weeks ago.

Matches

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Answer

1 matches to Enterococcus faecalis (GU manipulation), 2 matches to Streptococcus gallolyticus (colon cancer), 3 matches to Staphylococcus aureus (IV drug use), 4 matches to Viridans streptococci (dental work), and 5 matches to Staphylococcus epidermidis (recent prosthetic valve).
The correct matches reflect the established epidemiological associations between specific patient risk factors and the organisms most likely to cause infective endocarditis in those clinical scenarios.

Step-by-Step Solution

1
Analyze each patient's clinical history for specific risk factors.
Identified risk factors: genitourinary procedure, colonic mass, intravenous drug use, dental procedure, and early prosthetic valve.
Different pathogens have specific portals of entry and affinities for different host conditions.
2
Map the identified risk factor to the normal flora or common pathogen associated with that site.
GU tract correlates with enterococci; colon correlates with S. gallolyticus; skin/IV trauma correlates with S. aureus; oral cavity correlates with viridans streptococci; implanted hardware correlates with S. epidermidis.
Establishing the portal of entry allows for accurate prediction of the causative microbe.

Key Concept

Microbial associations and risk factors for infective endocarditis.
Estimated Time:1m 30s
Question 1788Question →

Match each hepatobiliary disorder with its most characteristic histopathologic finding on liver biopsy.

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Items

Primary biliary cholangitis
Primary sclerosing cholangitis
Autoimmune hepatitis
Alpha-1 antitrypsin deficiency
Non-alcoholic steatohepatitis

Matches

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Answer

Primary biliary cholangitis matches with florid duct lesions. Primary sclerosing cholangitis matches with 'onion skin' periductal fibrosis. Autoimmune hepatitis matches with prominent lymphoplasmacytic infiltrate causing interface hepatitis. Alpha-1 antitrypsin deficiency matches with PAS-positive, diastase-resistant globular inclusions. Non-alcoholic steatohepatitis matches with macrovesicular steatosis and Mallory-Denk bodies.
Each hepatobiliary condition possesses distinctly unique histopathological hallmarks essential for definitive diagnosis when clinical and serological findings are equivocal. Recognizing these specific liver biopsy patterns allows for appropriate diagnosis and guides distinct therapeutic management strategies for each chronic liver disease.

Step-by-Step Solution

1
Evaluate the histologic finding of 'onion skin' periductal fibrosis.
This is paired with Primary sclerosing cholangitis.
This finding represents the progressive fibro-obliteration of bile ducts characteristic of primary sclerosing cholangitis.
2
Evaluate the histologic finding of florid duct lesions and granulomas.
This is paired with Primary biliary cholangitis.
Primary biliary cholangitis specifically targets small, interlobular intrahepatic bile ducts with granulomatous inflammation.
3
Evaluate the histologic finding of interface hepatitis with plasma cells.
This is paired with Autoimmune hepatitis.
A lymphoplasmacytic infiltrate spilling into the lobules is the histopathologic hallmark of autoimmune hepatitis.
4
Evaluate the histologic finding of PAS-positive, diastase-resistant inclusions.
This is paired with Alpha-1 antitrypsin deficiency.
These inclusions represent unsecreted, misfolded alpha-1 antitrypsin protein trapped in the endoplasmic reticulum of hepatocytes.
5
Evaluate the histologic finding of steatosis with ballooning and Mallory-Denk bodies.
This is paired with Non-alcoholic steatohepatitis.
These distinct findings define steatohepatitis, distinguishing it from simple hepatic steatosis.

Key Concept

Histopathologic diagnosis of chronic hepatobiliary diseases
Question 1789Question →

Match each clinical vignette describing a patient with an endocrine or renal-related blood pressure/electrolyte abnormality to their expected pathophysiologic laboratory profile.

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Items

A 45-year-old man with treatment-resistant hypertension, muscle cramps, and spontaneous hypokalemia.
A 26-year-old woman with severe hypertension, hypokalemia, and a right-sided abdominal systolic-diastolic bruit.
A 50-year-old man with hypertension, hypokalemia, and a history of consuming large amounts of natural black licorice extract daily.
A 32-year-old woman with chronic fatigue, weight loss, salt craving, hyperpigmentation, and hyperkalemia.

Matches

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Answer

The correct matches depend on analyzing the renin-angiotensin-aldosterone axis feedback loop: autonomous adrenal aldosterone suppresses renin; renal ischemia stimulates renin which raises aldosterone; mineralocorticoid-receptor activation by exogenous substances suppresses both; and adrenal destruction eliminates aldosterone, causing a massive compensatory rise in renin.
Each clinical presentation uniquely disrupts the RAAS axis. By establishing the primary site of disease (adrenal vs. renal vs. exogenous) and following the feedback loops (volume status affecting renin), the corresponding lab profiles can be accurately mapped.

Step-by-Step Solution

1
Analyze each patient vignette to determine the primary source of the pathology.
Identify if the problem is in the adrenal gland (Conn syndrome, Addison disease), the renal artery (fibromuscular dysplasia), or exogenous/mimicker (licorice ingestion).
Knowing the etiology allows you to predict where the hormonal axis is initially disrupted.
2
Determine the impact of the primary pathology on circulating volume and blood pressure.
Conn syndrome, fibromuscular dysplasia, and licorice ingestion cause volume expansion (hypertension). Addison disease causes volume depletion (hypotension).
Plasma renin activity is tightly controlled by renal perfusion and circulating volume.
3
Apply negative and positive feedback principles to the Renin-Angiotensin-Aldosterone System (RAAS).
Volume expansion suppresses renin (except in fibromuscular dysplasia, where ischemia artificially acts as the primary driver of renin). Aldosterone is high if it is the primary tumor product or stimulated by renin, but low if destroyed (Addison's) or suppressed by a mimicker (licorice).
This logical sequence perfectly predicts the hormonal laboratory profile for each diagnosis.

Key Concept

Pathophysiologic regulation and feedback of the Renin-Angiotensin-Aldosterone System in Endocrine Hypertension and Adrenal Insufficiency
Question 1790Question →

Hepatitis B virus (HBV) serologic testing is crucial for determining a patient's exact infectious status and immunity. Different combinations of surface and core antigens, along with their respective antibodies, reflect specific phases of the disease. Match each HBV serologic profile below to its most accurate clinical interpretation.

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Items

HBsAg (+), Anti-HBc IgM (+), Anti-HBs (-)
HBsAg (+), Anti-HBc IgG (+), Anti-HBs (-)
HBsAg (-), Anti-HBc IgG (+), Anti-HBs (+)
HBsAg (-), Anti-HBc (-), Anti-HBs (+)
HBsAg (-), Anti-HBc IgM (+), Anti-HBs (-)

Matches

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Answer

Each serologic profile uniquely corresponds to a specific phase of Hepatitis B infection or immunity based on the presence of viral surface antigens (HBsAg) and host antibodies (Anti-HBc IgM/IgG, Anti-HBs).
Accurate interpretation of Hepatitis B serologies requires analyzing three main components. HBsAg represents the actively circulating virus. Anti-HBs represents neutralizing immunity. Anti-HBc represents systemic exposure to the actual virus, where IgM signifies acute, recent exposure and IgG signifies chronic or historical exposure.

Step-by-Step Solution

1
Evaluate HBsAg status to determine active infection.
Positive HBsAg indicates active (acute or chronic) viral replication. Negative HBsAg indicates immunity, susceptibility, or the window period.
HBsAg is the surface protein of the virus, and its continued presence confirms the virus has not been cleared.
2
Evaluate Anti-HBc (Core Antibody) status.
IgM indicates an acute infection or window period. IgG indicates a chronic infection or a resolved past infection. A completely negative core antibody implies no previous natural exposure.
Core antibodies only develop from natural exposure to the whole viral particle, not from the recombinant surface antigen used in vaccines.
3
Evaluate Anti-HBs (Surface Antibody) status.
Positive Anti-HBs indicates definitive immunity. Negative indicates active infection, susceptibility, or the window period.
Anti-HBs are neutralizing host antibodies that confer long-term protection against the virus.

Key Concept

Interpretation of Hepatitis B Serologic Markers
Estimated Time:1m 30s
Question 1791Question →

Match the following clinical scenarios with their most likely characteristic finding on microscopic urinalysis.

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Items

A 72-year-old man with acute kidney injury following prolonged hypotension from cardiogenic shock.
A 28-year-old man with hemoptysis and rapidly declining renal function due to anti-glomerular basement membrane disease.
A 45-year-old woman with new-onset generalized edema, hypoalbuminemia, and 5 grams of proteinuria per day.
A 55-year-old man with acute kidney injury, fever, and a maculopapular rash 10 days after starting cephalexin.
A 65-year-old woman with long-standing, poorly controlled hypertension and diabetes mellitus now presenting with an estimated GFR of 12 mL/min.

Matches

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Answer

The correct matches are: Cardiogenic shock (ATN) with muddy brown granular casts; Anti-GBM disease (nephritic syndrome) with red blood cell casts; Nephrotic syndrome with fatty casts; Antibiotic-induced AIN with white blood cell casts; and Advanced CKD with broad waxy casts.
The correct matches accurately pair the specific mechanism of renal injury with its corresponding cast formation in the tubules. Ischemic acute tubular necrosis produces muddy brown granular casts from sloughed necrotic cells. Glomerulonephritis allows RBCs to leak into the filtrate, forming RBC casts. Nephrotic syndrome results in significant lipiduria, visualized as oval fat bodies and fatty casts. Acute interstitial nephritis causes tubular inflammation with WBC casts. Finally, chronic kidney disease involves dilated tubules with sluggish flow, leading to broad waxy casts.

Step-by-Step Solution

1
Identify the underlying pathophysiological process for each clinical scenario.
Ischemic injury (ATN), glomerular inflammation (Nephritic), podocyte/membrane damage (Nephrotic), interstitial allergic inflammation (AIN), and chronic tubular hypertrophy (CKD).
Different etiologies of kidney disease affect distinct structures within the nephron, producing specific urinary findings.
2
Correlate the pathophysiological process with its hallmark urinary sediment finding.
Ischemia yields necrotic debris (muddy brown), glomerular bleeding yields RBC casts, severe proteinuria yields lipiduria (fatty casts), interstitial inflammation yields WBC casts, and chronic stasis yields broad waxy casts.
Matching the mechanism of injury to the cast composition confirms the diagnosis.

Key Concept

Urinary sediment patterns and corresponding etiologies
Question 1792Question →

Match each patient's clinical vignette and laboratory profile to the most accurate underlying pathophysiologic mechanism describing their calcium and bone metabolism disorder.

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Items

A 58-year-old woman with recurrent nephrolithiasis and constipation. Labs show calcium 11.4 mg/dL, phosphorus 2.3 mg/dL, and intact PTH 105 pg/mL.
A 45-year-old woman with perioral tingling and carpopedal spasm 48 hours after a total thyroidectomy. Labs show calcium 7.4 mg/dL, phosphorus 5.6 mg/dL, and intact PTH 8 pg/mL.
A 70-year-old housebound man with bone pain and proximal muscle weakness. Labs show calcium 8.2 mg/dL, phosphorus 2.1 mg/dL, and intact PTH 145 pg/mL.
A 62-year-old man with fatigue, pruritus, and an eGFR of 12 mL/min/1.73 m 2^2. Labs show calcium 7.8 mg/dL, phosphorus 7.1 mg/dL, and intact PTH 410 pg/mL.

Matches

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Answer

The correct matches are: the nephrolithiasis patient to autonomous proliferation (Primary Hyperparathyroidism), the post-thyroidectomy patient to iatrogenic removal (Hypoparathyroidism), the housebound patient to cholecalciferol deficiency (Vitamin D deficiency), and the patient with a low eGFR to loss of functioning nephrons (CKD-MBD).
Calcium and phosphate homeostasis is strictly regulated by PTH and Vitamin D. Correctly matching these scenarios requires analyzing the direction of calcium and phosphorus derangements alongside the PTH response (compensatory vs. autonomous).

Step-by-Step Solution

1
Analyze the serum calcium and phosphorus levels for each patient.
Identified hypercalcemia vs. hypocalcemia and associated high vs. low phosphorus levels.
Calcium and phosphorus generally move in opposite directions under the influence of PTH, providing the first clue to the disorder.
2
Evaluate the intact parathyroid hormone (PTH) response.
Determined if the PTH level is appropriate (compensatory) or inappropriate (autonomous or deficient) for the serum calcium level.
The PTH level distinguishes primary parathyroid disorders from secondary responses to other metabolic derangements.
3
Correlate the laboratory profile with the patient's clinical history.
Matched the specific lab profile to the corresponding pathophysiologic mechanism.
Clinical context (e.g., prior surgery, chronic kidney disease, housebound status) confirms the mechanism driving the lab abnormalities.

Key Concept

Evaluation of calcium and phosphate disorders using intact parathyroid hormone (PTH) levels and clinical context.
Estimated Time:1m 30s
Question 1793Question →

Correlate each of the described clinical scenarios with its characteristic pattern of thyroid function testing.

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Items

Tender, enlarged thyroid gland with fever and palpitations following a viral upper respiratory infection
Prolonged intensive care unit admission for severe sepsis and multiorgan failure
Weight loss and tachycardia with an atrophic, nonpalpable thyroid gland in a healthcare worker
New-onset isolated hypercholesterolemia discovered during a routine examination of an otherwise asymptomatic patient

Matches

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Answer

1 matches with the inflammatory high T4/low uptake profile; 2 matches with the high reverse T3 profile; 3 matches with the low thyroglobulin profile; 4 matches with the isolated high TSH profile.
The correct matches require distinguishing the pathophysiologic mechanisms of varying thyroid states. Subacute thyroiditis presents with a painful goiter, high T4, low TSH, high ESR, and low radioiodine uptake due to glandular destruction. Euthyroid sick syndrome is an adaptive response to severe illness, showing low T3 and high reverse T3 due to altered peripheral conversion. Factitious thyrotoxicosis shows high T4 and low TSH, but uniquely low thyroglobulin because exogenous hormone suppresses endogenous gland function. Subclinical hypothyroidism features isolated TSH elevation with normal T4, often discovered via hyperlipidemia.

Step-by-Step Solution

1
Analyze the clinical scenario of the post-viral painful thyroid.
Identified as subacute granulomatous (de Quervain) thyroiditis.
The inflammation causes release of preformed hormones and decreased iodine uptake, with elevated inflammatory markers.
2
Evaluate the critically ill patient in the intensive care unit.
Identified as euthyroid sick syndrome.
Severe illness alters peripheral deiodination, reducing T3 and increasing reverse T3 without primary thyroid pathology.
3
Assess the healthcare worker with thyrotoxicosis and a nonpalpable gland.
Identified as factitious thyrotoxicosis (exogenous thyroid hormone intake).
Exogenous hormone suppresses TSH and thyroglobulin production, while the gland atrophies.
4
Examine the asymptomatic patient with new hyperlipidemia.
Identified as subclinical hypothyroidism.
Mild thyroid dysfunction often first presents with elevated TSH, normal T4, and altered lipid metabolism.

Key Concept

Differentiation of thyroid disorders based on integrated laboratory profiles, including TSH, free T4, T3, reverse T3, thyroglobulin, and radioiodine uptake.
Question 1794Question →

Match each of the following dynamic auscultation findings with the most likely underlying structural or valvular pathology.

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Items

A harsh crescendo-decrescendo systolic murmur at the left lower sternal border that becomes louder with the Valsalva maneuver
A mid-systolic click followed by a late systolic murmur at the apex that occurs later in systole with rapid squatting
A harsh crescendo-decrescendo systolic murmur at the right second intercostal space that decreases in intensity with the Valsalva maneuver
A holosystolic murmur at the apex that radiates to the axilla and increases in intensity with sustained handgrip

Matches

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Answer

The dynamic auscultation findings accurately map to hypertrophic cardiomyopathy (louder with Valsalva), mitral valve prolapse (later with squatting), aortic stenosis (softer with Valsalva), and mitral regurgitation (louder with handgrip).
Each maneuver predictably alters cardiac hemodynamics (preload and afterload), which changes the intensity or timing of murmurs depending on their underlying anatomical mechanism.

Step-by-Step Solution

1
Evaluate the murmur that becomes louder with the Valsalva maneuver.
The Valsalva maneuver decreases preload. A murmur that intensifies with decreased left ventricular volume is characteristic of hypertrophic cardiomyopathy.
Decreased left ventricular volume exacerbates the dynamic outflow tract obstruction.
2
Evaluate the murmur with a click that occurs later with squatting.
Squatting increases both preload and afterload, enlarging left ventricular volume. This delays leaflet prolapse in mitral valve prolapse.
A larger left ventricular volume keeps the mitral leaflets tense for a longer period before they prolapse into the left atrium.
3
Evaluate the crescendo-decrescendo murmur that decreases with the Valsalva maneuver.
Decreased preload results in a lower stroke volume across the aortic valve, which softens the murmur of aortic stenosis.
Most forward-flow murmurs decrease in intensity when preload is reduced.
4
Evaluate the holosystolic murmur that increases with sustained handgrip.
Handgrip increases afterload, which raises the backward pressure gradient. This amplifies retrograde flow and murmur intensity in mitral regurgitation.
Higher systemic vascular resistance forces more blood back through the incompetent mitral valve.

Key Concept

Hemodynamic effects of dynamic auscultation maneuvers on structural heart murmurs
Estimated Time:1m 30s
Question 1795Question →

Match each clinical presentation of a hereditary gastrointestinal polyposis or cancer syndrome with its corresponding underlying genetic mutation.

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Items

A 32-year-old man with childhood intussusception, buccal mucocutaneous hyperpigmentation, and multiple hamartomatous intestinal polyps.
A 45-year-old woman with early-onset right-sided colon cancer, a family history of endometrial cancer, and 3 adenomatous colonic polyps.
A 25-year-old woman with macrocephaly, facial trichilemmomas, a history of breast cancer, and widespread hamartomatous gastrointestinal polyps.
A 38-year-old man with >100 adenomatous colon polyps, mandibular osteomas, and congenital hypertrophy of the retinal pigment epithelium.
A 30-year-old man with >100 adenomatous colon polyps and an autosomal recessive pattern of inheritance (unaffected parents, affected sibling).

Matches

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Answer

The correct matches pair Peutz-Jeghers syndrome with STK11, Lynch syndrome with MMR genes, Cowden syndrome with PTEN, FAP/Gardner syndrome with APC, and MUTYH-associated polyposis with MUTYH.
Gastrointestinal polyposis and hereditary cancer syndromes each have distinct phenotypic manifestations tied to specific genetic mutations. Peutz-Jeghers syndrome presents with hamartomas and mucocutaneous hyperpigmentation (STK11). Lynch syndrome presents with right-sided colon cancer and endometrial cancer, with few or no polyps, due to defective DNA mismatch repair. Cowden syndrome presents with hamartomas, macrocephaly, and trichilemmomas (PTEN). Familial adenomatous polyposis (and its Gardner variant) presents with >100 adenomatous polyps, osteomas, and CHRPE due to APC gene mutations. MUTYH-associated polyposis clinically resembles FAP but follows an autosomal recessive inheritance pattern.

Step-by-Step Solution

1
Analyze the clinical presentation of the patient with buccal hyperpigmentation and hamartomas.
Identified as Peutz-Jeghers syndrome.
Mucocutaneous hyperpigmentation and hamartomatous polyps are the classic diagnostic criteria for Peutz-Jeghers.
2
Analyze the patient with right-sided CRC, endometrial cancer, and few polyps.
Identified as Lynch syndrome (HNPCC).
Early-onset right-sided colon cancer and a strong family history of endometrial cancer without diffuse polyposis are characteristic of Lynch syndrome.
3
Analyze the presentation of the patient with macrocephaly, trichilemmomas, and breast cancer.
Identified as Cowden syndrome.
The triad of macrocephaly, characteristic mucocutaneous lesions (trichilemmomas), and hamartomatous polyps points definitively to Cowden syndrome.
4
Analyze the patient with >100 adenomas, osteomas, and CHRPE.
Identified as Gardner syndrome, a variant of Familial Adenomatous Polyposis (FAP).
Profuse adenomatous polyposis combined with extraintestinal manifestations like osteomas is pathognomonic for FAP.
5
Analyze the patient with >100 adenomas and an autosomal recessive family history.
Identified as MUTYH-associated polyposis (MAP).
MAP clinically mimics FAP but is distinguished by its autosomal recessive inheritance and MUTYH gene involvement.
6
Correlate each identified syndrome with its underlying genetic mutation.
Matched Peutz-Jeghers with STK11, Lynch with MMR, Cowden with PTEN, FAP with APC, and MAP with MUTYH.
These are the established genetic etiologies for each respective hereditary syndrome.

Key Concept

Clinical and genetic correlation of hereditary gastrointestinal polyposis and cancer syndromes.
Question 1796Question →

A group of patients recently started various new antidiabetic therapies and subsequently developed medication-induced complications. Based on the distinct pharmacological profiles of these agents, match each antidiabetic medication to the clinical scenario that best describes its most characteristic adverse effect.

Click a left item, then click its matching right item

Items

Canagliflozin
Pioglitazone
Liraglutide
Glipizide
Metformin

Matches

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Answer

Canagliflozin maps to perineal pruritus (candidiasis). Pioglitazone maps to dyspnea/edema (heart failure exacerbation). Liraglutide maps to epigastric pain/elevated lipase (pancreatitis). Glipizide maps to hypoglycemia. Metformin maps to lower extremity numbness/macrocytic anemia (B12 deficiency).
Each antidiabetic medication has a distinct side effect profile based on its mechanism of action. SGLT2 inhibitors (canagliflozin) increase urinary glucose, leading to genitourinary fungal infections. Thiazolidinediones (pioglitazone) promote fluid retention by acting on the collecting tubule, worsening heart failure. GLP-1 agonists (liraglutide) stimulate the pancreas but carry a known risk of pancreatitis. Sulfonylureas (glipizide) directly stimulate beta-cell insulin release independent of serum glucose, precipitating hypoglycemia. Metformin impairs intestinal absorption of vitamin B12, leading to megaloblastic anemia and subacute combined degeneration if left uncorrected.

Step-by-Step Solution

1
Identify the pharmacologic class of each listed antidiabetic medication.
Canagliflozin is an SGLT2 inhibitor, Pioglitazone is a TZD, Liraglutide is a GLP-1 agonist, Glipizide is a Sulfonylurea, and Metformin is a Biguanide.
Medication class dictates the mechanism of action and the specific adverse effect profile.
2
Analyze each clinical vignette for the classic presentation of a drug adverse effect.
The vignettes describe candidiasis, heart failure exacerbation, acute pancreatitis, severe hypoglycemia, and vitamin B12 deficiency, respectively.
Recognizing the toxicity signature allows accurate matching to the offending agent.
3
Map the drug classes to their respective clinical toxicities.
SGLT2 inhibitors cause yeast infections; TZDs cause fluid retention; GLP-1 agonists cause pancreatitis; Sulfonylureas cause hypoglycemia; Metformin causes B12 deficiency.
Establishing the final diagnostic pairs based on standard internal medicine pharmacological knowledge.

Key Concept

Adverse effect profiles of distinct antidiabetic medication classes.
Question 1797Question →

Match each clinical presentation following a recent acute myocardial infarction with the most likely specific structural or inflammatory complication.

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Items

Sudden-onset profound hypotension, jugular venous distention, and pulseless electrical activity 6 days after an anterior myocardial infarction
New-onset harsh holosystolic murmur at the left lower sternal border with a palpable thrill and signs of biventricular failure 4 days after an anteroapical myocardial infarction
Sudden-onset severe pulmonary edema and a new soft, blowing holosystolic murmur at the apex 3 days after an inferior myocardial infarction
Pleuritic chest pain, low-grade fever, and a pericardial friction rub 4 weeks after an extensive anterior myocardial infarction

Matches

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Answer

The correct pairings match each specific post-myocardial infarction clinical presentation to its underlying complication based on the typical timeframe (days vs. weeks) and physical examination findings (murmur characteristics or signs of tamponade).
Each post-myocardial infarction complication can be distinguished by recognizing its classic timeframe and physical findings. Ventricular free wall rupture causes rapid tamponade and PEA at 5-14 days. Papillary muscle rupture (often after inferior MI) causes acute mitral regurgitation (apical murmur) and pulmonary edema at 3-5 days. Septal rupture causes a harsh parasternal murmur with a thrill at 3-5 days. Dressler syndrome causes pericarditis weeks to months later.

Step-by-Step Solution

1
Analyze the first presentation (hypotension, PEA, and JVD at day 6).
Identified as sudden cardiac tamponade due to ventricular free wall rupture.
PEA and rapid shock occurring roughly a week after an anterior MI are classic hallmarks of free wall rupture leading to hemopericardium.
2
Analyze the second presentation (harsh left lower sternal border murmur with thrill at day 4).
Identified as interventricular septal rupture.
A harsh holosystolic murmur with a thrill at the lower sternal border indicates a ventricular septal defect created by necrotic tissue.
3
Analyze the third presentation (soft apical murmur and severe pulmonary edema at day 3 after inferior MI).
Identified as papillary muscle rupture.
Inferior MIs frequently compromise the blood supply to the posteromedial papillary muscle, leading to acute severe mitral regurgitation and sudden flash pulmonary edema.
4
Analyze the fourth presentation (pleuritic pain, fever, and rub at week 4).
Identified as Dressler syndrome.
The delayed timeline (weeks to months) and features of pericarditis indicate an immune-mediated post-cardiac injury syndrome.

Key Concept

Complications of acute myocardial infarction manifest with distinct timelines, hemodynamic profiles, and physical examination findings.
Estimated Time:1m 30s
Question 1798Question →

Match each clinical exposure scenario with the most appropriate guideline-directed post-exposure prophylaxis (PEP) or preventative management.

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Items

A 24-year-old healthcare worker sustains a deep, hollow-bore needlestick injury after drawing blood from a patient with untreated HIV.
A 19-year-old college student shares a small dormitory room with a peer recently hospitalized for Neisseria meningitidis meningitis.
A 35-year-old camper awakens in a cabin to find a bat flying around the room, though no bite or scratch marks are found.
A 28-year-old pregnant woman in her second trimester has a toddler at home who was just diagnosed with Bordetella pertussis infection.

Matches

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Answer

The correct pairings successfully match HIV occupational exposure with a 28-day three-drug antiretroviral regimen, meningococcal exposure with a single dose of ciprofloxacin or ceftriaxone, occult bat exposure with rabies immune globulin and vaccine series, and pertussis exposure during pregnancy with a 5-day course of azithromycin.
The correct matches pair each specific infectious exposure with its evidence-based post-exposure prophylaxis. High-risk HIV exposure requires a 28-day three-drug antiretroviral regimen. Meningococcal exposure for close contacts necessitates rapid eradication of nasopharyngeal carriage with agents like ciprofloxacin or ceftriaxone. Occult bat exposures demand immediate rabies PEP (immune globulin and vaccination) due to the fatal nature of the disease and potential for undetectable bites. Finally, pertussis contacts, including pregnant women, require macrolide prophylaxis to prevent transmission to vulnerable individuals.

Step-by-Step Solution

1
Analyze the occupational HIV exposure scenario.
Identified the need for full three-drug antiretroviral post-exposure prophylaxis.
Due to the high-risk nature of the deep, hollow-bore injury involving an untreated HIV source, maximum prevention with a regimen such as tenofovir-emtricitabine and dolutegravir is required.
2
Evaluate the meningococcal exposure scenario.
Determined that sharing a dormitory qualifies as a close contact exposure requiring clearance of nasopharyngeal colonization.
Close contacts of patients with Neisseria meningitidis are at high risk for secondary cases and require immediate chemoprophylaxis via ceftriaxone, ciprofloxacin, or rifampin.
3
Assess the bat exposure scenario.
Recognized that sleeping in the same room as a bat is an absolute indication for rabies prophylaxis.
Rabies immune globulin and the vaccine series must be administered since bat bites can be entirely imperceptible and rabies is universally fatal without prophylaxis.
4
Review the pertussis exposure in a pregnant patient.
Identified that the pregnant woman is a household contact of a toddler with pertussis and requires a macrolide.
Azithromycin is the drug of choice for pertussis post-exposure prophylaxis and is well-established as safe during pregnancy.

Key Concept

Identifying appropriate post-exposure prophylaxis (PEP) regimens based on specific infectious exposures
Question 1799Question →

Match each clinical presentation with its corresponding classic arterial blood gas and basic metabolic panel profile.

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Items

A 28-year-old healthy pregnant woman at 32 weeks gestation presents for a routine prenatal check-up.
A 50-year-old man presents with profound weakness and severe, intractable vomiting over the past 4 days due to gastric outlet obstruction.
A 35-year-old man with progressive ascending muscle weakness over the past week is brought to the emergency department exhibiting shallow breathing and poor diaphragmatic excursion.
A 20-year-old man with type 1 diabetes mellitus presents with diffuse abdominal pain, polyuria, and deep, rapid Kussmaul respirations.

Matches

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Answer

Pregnancy matches with chronic respiratory alkalosis; vomiting matches with saline-responsive metabolic alkalosis; neuromuscular respiratory failure matches with acute respiratory acidosis; and diabetic ketoacidosis matches with high anion gap metabolic acidosis.
Each clinical vignette presents a classic etiology for one of the four primary acid-base disorders. Accurate diagnosis requires matching the clinical mechanism (hyperventilation, acid loss, hypoventilation, or acid overproduction) to its expected mathematical footprint on the blood gas panel.

Step-by-Step Solution

1
Analyze the pregnant patient's expected physiology
Identify chronic respiratory alkalosis
Progesterone directly stimulates the medullary respiratory center. The resulting hyperventilation lowers pCO2pCO_2, and the kidneys compensate over days by decreasing HCO3−HCO_3^- reabsorption.
2
Evaluate the patient with intractable vomiting
Identify metabolic alkalosis with volume contraction
Loss of gastric H+H^+ raises serum pH. Concurrent loss of volume and Cl−Cl^- leads to a saline-responsive state where the kidneys avidly retain Na+Na^+ at the expense of K+K^+ and H+H^+, yielding a urine Cl−Cl^- below 10 mEq/L.
3
Assess the patient with ascending weakness and shallow breathing
Identify acute respiratory acidosis
Neuromuscular weakness impairs ventilation, causing an acute buildup of CO2CO_2. The HCO3−HCO_3^- is only slightly elevated because renal metabolic compensation has not had time to occur.
4
Examine the patient with type 1 diabetes and rapid breathing
Identify high anion gap metabolic acidosis with respiratory compensation
Insulin deficiency leads to ketogenesis. The unmeasured ketones increase the anion gap and consume HCO3−HCO_3^-. The rapid, deep Kussmaul respirations represent respiratory compensation (lowering pCO2pCO_2).

Key Concept

Acid-Base Disorders and Compensatory Mechanisms
Question 1800Question →

During cardiovascular physiology rounds, a medical student is asked to interpret the central venous pressure waveforms of various patients. Match each specific jugular venous pulsation (JVP) waveform abnormality with the underlying cardiac pathology that most commonly produces it.

Click a left item, then click its matching right item

Items

Prominent 'x' descent with an absent or blunted 'y' descent
Rapid and steep 'x' and 'y' descents forming a 'W' pattern
Intermittent, irregular giant 'a' waves
Prominent, rapidly ascending 'v' waves that obliterate the 'x' descent
Prominent, consistent 'a' waves occurring with every cardiac cycle

Matches

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Answer

Cardiac tamponade maps to absent 'y' descent. Constrictive pericarditis maps to steep 'x' and 'y' descents. Complete AV block maps to intermittent giant 'a' waves. Tricuspid regurgitation maps to prominent 'v' waves obliterating the 'x' descent. Pulmonary hypertension maps to regular prominent 'a' waves.
Each specific waveform abnormality directly correlates to the mechanical and hemodynamic changes in the right atrium and ventricle. Cardiac tamponade abolishes the early diastolic 'y' descent. Constriction accentuates both 'x' and 'y' descents. AV dissociation produces intermittent cannon 'a' waves. Tricuspid regurgitation yields large 'v' waves erasing the 'x' descent. Right ventricular non-compliance from pulmonary hypertension causes regular, amplified 'a' waves.

Step-by-Step Solution

1
Analyze the normal physiological components of the jugular venous pulse (JVP) waveform.
Identified that the 'a' wave represents right atrial contraction, the 'x' descent represents atrial relaxation, the 'v' wave represents passive venous filling, and the 'y' descent represents early diastolic ventricular filling.
Establishing baseline hemodynamics is necessary before interpreting pathologic deviations.
2
Evaluate patterns of restricted right heart filling.
Determined that tamponade blunts the 'y' descent due to continuous external compression, whereas constrictive pericarditis allows rapid early filling, creating a steep 'y' descent.
Distinguishing the specific diastolic filling impairments is critical for differentiating pericardial diseases.
3
Assess variations in the atrial contraction ('a') wave.
Deducted that regular prominent 'a' waves suggest constant resistance to atrial emptying (e.g., pulmonary hypertension), while intermittent giant 'a' waves indicate occasional AV dissociation (e.g., complete AV block).
The frequency and regularity of amplified 'a' waves distinguish structural heart disease from electrical conduction abnormalities.
4
Correlate systolic venous waves with valvular competence.
Concluded that severe tricuspid regurgitation replaces the normal systolic 'x' descent with a giant 'v' wave due to massive retrograde flow.
Regurgitant volume dramatically alters the right atrial pressure curve during ventricular systole.

Key Concept

Jugular venous pulse (JVP) waveform interpretation and hemodynamic profiles of right-sided heart pathologies.
Estimated Time:1m 30s
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