USMLE Step 2 Quiz: Upper Gastrointestinal Disorders

What this quiz covers

This quiz focuses on Upper Gastrointestinal Disorders, giving you a quick way to practice the rules, question types, and explanations that matter most for USMLE Step 2.

How to use this quiz

Try each quiz question before looking at the correct answer. Use the explanations to review missed ideas, then come back to similar questions until the pattern feels familiar.

Question 1

1. Achalasia
2. Esophageal stricture
3. Oropharyngeal dysphagia (correct answer)
4. Diffuse esophageal spasm

Explanation: This patient's presentation, characterized by difficulty initiating a swallow (transfer dysphagia), coughing, choking, and nasal regurgitation, is classic for oropharyngeal dysphagia. The underlying cause is most likely neuromuscular dysfunction related to his recent stroke. The hoarse voice and facial weakness further support a neurologic etiology affecting the muscles of the pharynx and upper esophagus. The most appropriate next step would be a video-fluoroscopic swallowing study.

• A) Achalasia: This is a motility disorder of the esophagus causing dysphagia to both solids and liquids, but it typically presents with the sensation of food getting stuck in the chest (esophageal dysphagia), not difficulty initiating the swallow.
• B) Esophageal stricture: This is a form of mechanical obstruction that typically causes dysphagia primarily to solids, which progresses to liquids. The sensation is of food getting stuck substernally, not difficulty with the initial swallow.
• D) Diffuse esophageal spasm: This motility disorder presents with intermittent, non-progressive dysphagia to solids and liquids, often accompanied by chest pain. It does not cause difficulty initiating a swallow.

Question 2

1. Initiate a trial of a proton pump inhibitor
2. Perform upper endoscopy (correct answer)
3. Order a barium esophagram
4. Perform esophageal manometry

Explanation: This patient presents with several alarm features for esophageal malignancy: progressive dysphagia (solids more than liquids), significant unintentional weight loss, and age >50. Additionally, his smoking and alcohol history are significant risk factors for squamous cell carcinoma of the esophagus. The presence of these alarm features warrants prompt investigation to rule out malignancy. Upper endoscopy (EGD) with biopsy is the diagnostic test of choice in this setting as it allows for direct visualization and tissue sampling.

• A) Initiate a trial of a proton pump inhibitor: While GERD can cause strictures, the alarm features in this patient make a simple PPI trial inappropriate and potentially dangerous due to the delay in diagnosing a possible cancer.
• C) Order a barium esophagram: A barium swallow can identify a stricture or mass, but it cannot differentiate between benign and malignant causes and does not allow for biopsy. Endoscopy would still be required for a definitive diagnosis.
• D) Perform esophageal manometry: Manometry is used to evaluate esophageal motility disorders like achalasia or diffuse esophageal spasm. This patient's progressive dysphagia to solids suggests a mechanical obstruction, not a motility disorder.

Question 3

1. Plummer-Vinson syndrome (correct answer)
2. Zenker diverticulum
3. Systemic sclerosis
4. Eosinophilic esophagitis

Explanation: This patient presents with the classic triad of Plummer-Vinson syndrome: dysphagia, iron-deficiency anemia, and an esophageal web. The dysphagia is typically intermittent and localized to the upper esophagus. Koilonychia (spoon-shaped nails) is a physical finding associated with chronic iron deficiency. The barium swallow finding of a thin membrane confirms the presence of an esophageal web.

• B) Zenker diverticulum: This is an outpouching of the pharyngeal mucosa that causes oropharyngeal dysphagia, halitosis, and regurgitation of undigested food. It does not cause iron-deficiency anemia.
• C) Systemic sclerosis: This can cause esophageal dysmotility and severe GERD, but it typically affects the lower two-thirds of the esophagus and does not form upper esophageal webs.
• D) Eosinophilic esophagitis: This condition is associated with dysphagia and food impaction, often in patients with atopic histories. It is characterized by eosinophilic infiltration of the esophageal mucosa, not webs, and is not typically associated with iron-deficiency anemia.

Question 4

1. Upper endoscopy
2. 24-hour esophageal pH monitoring
3. Lifestyle modifications and a trial of a proton pump inhibitor (correct answer)
4. Barium esophagram

Explanation: This patient presents with classic symptoms of uncomplicated gastroesophageal reflux disease (GERD): postprandial and nocturnal heartburn, and regurgitation. He is under 50 years old and has no alarm features (e.g., dysphagia, weight loss, anemia, hematemesis). Therefore, the most appropriate initial management is an empiric trial of a proton pump inhibitor (PPI) along with counseling on lifestyle modifications, such as weight loss, dietary changes, and elevating the head of the bed.

• A) Upper endoscopy: Endoscopy is not indicated as a first step for typical GERD symptoms in the absence of alarm features.
• B) 24-hour esophageal pH monitoring: This is the gold standard for diagnosing GERD but is reserved for patients with atypical symptoms or those who fail to respond to an empiric trial of PPIs.
• D) Barium esophagram: This test has low sensitivity for GERD and is primarily used to evaluate for structural abnormalities like strictures or hiatal hernias when dysphagia is present.

Question 5

1. Increase omeprazole to 40 mg twice daily
2. Add an H2 receptor antagonist at bedtime
3. Perform upper endoscopy (correct answer)
4. Refer for anti-reflux surgery

Explanation: This patient has symptoms of GERD that are refractory to an adequate trial of once-daily proton pump inhibitor (PPI) therapy. Failure to respond to standard-dose PPI therapy is an indication for further investigation to confirm the diagnosis, evaluate for complications of GERD (e.g., esophagitis, stricture), and rule out alternative diagnoses (e.g., eosinophilic esophagitis, achalasia). Therefore, upper endoscopy is the most appropriate next step.

• A) Increase omeprazole to 40 mg twice daily: While optimizing PPI therapy is a management option, it is generally done after an underlying cause for refractory symptoms has been investigated. An endoscopy is needed to rule out complications or an alternative diagnosis before simply increasing the dose.
• B) Add an H2 receptor antagonist at bedtime: This can be a strategy for nocturnal acid breakthrough but is less effective than optimizing PPI therapy and does not address the need for a diagnostic evaluation in refractory GERD.
• D) Refer for anti-reflux surgery: Surgery is considered for patients with confirmed GERD who are intolerant to or do not wish to take long-term PPIs, or who have complications like a large hiatal hernia. It is not appropriate before a definitive diagnosis is confirmed and other causes are excluded.

Question 6

1. Continue current management as symptoms are controlled
2. Perform upper endoscopy for Barrett's esophagus screening (correct answer)
3. Start daily therapy with a proton pump inhibitor
4. Order a 24-hour esophageal pH monitoring study

Explanation: This patient has multiple risk factors for Barrett's esophagus, a metaplastic complication of chronic GERD that predisposes to esophageal adenocarcinoma. Major risk factors include a GERD duration of >5 years, age >50, male sex, obesity, and a history of smoking. Guidelines recommend a one-time screening upper endoscopy for patients with multiple risk factors, even if their symptoms are currently controlled. This is done to detect Barrett's esophagus and any associated dysplasia.

• A) Continue current management as symptoms are controlled: While his symptoms are controlled, this approach ignores the risk of underlying malignancy, for which he has multiple risk factors.
• C) Start daily therapy with a proton pump inhibitor: While PPIs are effective for symptom control, starting them now would not address the need to screen for Barrett's esophagus, which may have already developed.
• D) Order a 24-hour esophageal pH monitoring study: This test is used to confirm a diagnosis of GERD in patients with atypical symptoms or who are refractory to treatment. It is not a screening tool for Barrett's esophagus.

Question 7

1. Discontinue naproxen (correct answer)
2. Start sucralfate therapy
3. Repeat endoscopy in 2 weeks
4. Test for serum gastrin level

Explanation: The patient has an H. pylori-negative gastric ulcer, and her daily use of naproxen, a non-steroidal anti-inflammatory drug (NSAID), is the most likely cause. NSAIDs inhibit prostaglandin synthesis, which compromises the protective gastric mucosal barrier. The most critical step in managing an NSAID-induced ulcer is to discontinue the offending agent, if clinically feasible. Healing is significantly delayed if the NSAID is continued, even with aggressive acid suppression therapy.

• B) Start sucralfate therapy: Sucralfate can provide a protective coating over the ulcer but is considered an adjunctive therapy. The primary intervention is removing the cause (NSAID) and suppressing acid (PPI).
• C) Repeat endoscopy in 2 weeks: A repeat endoscopy is necessary to ensure healing of a gastric ulcer (to rule out malignancy), but it is typically performed in 8-12 weeks, not 2 weeks. The immediate priority is stopping the NSAID.
• D) Test for serum gastrin level: This is done to screen for Zollinger-Ellison syndrome, which is a rare cause of PUD. It would be considered if the ulcer is refractory to treatment or if there are multiple ulcers, but NSAID-induced ulcer is far more likely in this patient.

Question 8

1. H. pylori serology (IgG)
2. Urea breath test (correct answer)
3. Repeat upper endoscopy with biopsy
4. Fecal calprotectin

Explanation: The urea breath test and the stool antigen test are the preferred non-invasive methods for confirming H. pylori eradication. These tests detect active infection. They should be performed at least 4 weeks after completion of antibiotic therapy and after proton pump inhibitors have been held for 1-2 weeks. Since the patient is asymptomatic and off medications, the urea breath test is an excellent choice.

• A) H. pylori serology (IgG): Serology tests for IgG antibodies against H. pylori. These antibodies can remain elevated for months to years even after successful eradication and therefore cannot be used to confirm cure.
• C) Repeat upper endoscopy with biopsy: This is an invasive method and is not necessary for confirming eradication in an asymptomatic patient with an uncomplicated ulcer. It is reserved for patients with complicated ulcers (e.g., bleeding, gastric ulcer) to ensure healing and rule out malignancy.
• D) Fecal calprotectin: This is a marker for intestinal inflammation, primarily used in the diagnosis and monitoring of inflammatory bowel disease, not for H. pylori testing.

Question 9

1. Refer for surgical resection of the ulcer
2. Measure serum gastrin level (correct answer)
3. Switch to a different proton pump inhibitor
4. Add sucralfate and continue PPI therapy

Explanation: A non-healing (refractory) gastric ulcer despite adequate high-dose PPI therapy and confirmed absence of H. pylori and NSAID use should raise suspicion for other etiologies. Zollinger-Ellison syndrome (ZES), a condition caused by a gastrin-secreting tumor (gastrinoma), leads to profound gastric acid hypersecretion and refractory peptic ulcers. Therefore, measuring a fasting serum gastrin level is the most appropriate next step to screen for ZES.

• A) Refer for surgical resection of the ulcer: While surgery may ultimately be needed for a non-healing ulcer, it is crucial to first exclude underlying causes like ZES that would not be cured by local resection.
• C) Switch to a different proton pump inhibitor: While there is some variation in metabolism, it is unlikely that switching to another PPI would lead to healing of a truly refractory ulcer. Investigating the cause is more important.
• D) Add sucralfate and continue PPI therapy: Adding sucralfate is unlikely to be effective for an ulcer that has failed to heal with 12 weeks of maximal acid suppression. The focus should be on diagnosing the cause of the refractory nature of the ulcer.

Question 10

1. Administer intravenous octreotide
2. Perform urgent upper endoscopy
3. Administer intravenous pantoprazole
4. Initiate aggressive fluid resuscitation (correct answer)

Explanation: This patient is presenting with acute upper gastrointestinal bleeding and signs of hemorrhagic shock (hypotension, tachycardia, pallor, diaphoresis). The immediate priority in managing any hemodynamically unstable patient is resuscitation. This involves securing the airway, breathing, and circulation (ABCs). In this case, establishing IV access and initiating aggressive fluid resuscitation with crystalloids (e.g., normal saline or lactated Ringer's solution) is the most critical first step to restore intravascular volume and improve tissue perfusion. Blood products should be administered if the patient does not respond to initial fluid resuscitation or has a very low hemoglobin.

• A) Administer intravenous octreotide: Octreotide is used specifically for suspected variceal bleeding. While this is a possibility, resuscitation takes precedence, and the etiology is not yet known.
• B) Perform urgent upper endoscopy: Endoscopy is crucial for diagnosis and treatment but should only be performed after the patient is hemodynamically stabilized through resuscitation.
• C) Administer intravenous pantoprazole: A PPI should be given, but it is not the most immediate life-saving intervention. Hemodynamic stabilization is the priority.

Question 11

1. Esophageal varices (correct answer)
2. Mallory-Weiss tear
3. Dieulafoy's lesion
4. Peptic ulcer disease

Explanation: In a patient with known cirrhosis and signs of portal hypertension (ascites), esophageal varices are the most common and most feared cause of massive upper gastrointestinal bleeding. Portal hypertension leads to the formation of portosystemic collaterals, including fragile, dilated submucosal veins in the distal esophagus and proximal stomach that are prone to rupture and life-threatening hemorrhage. While PUD is the most common cause of UGIB in the general population, varices are the most likely cause in this specific clinical context.

• B) Mallory-Weiss tear: This is a mucosal tear at the gastroesophageal junction caused by forceful retching or vomiting. It is a possible cause but less likely to cause such profound hemodynamic instability compared to a variceal bleed in a cirrhotic patient.
• C) Dieulafoy's lesion: This is a rare cause of UGIB resulting from a large, tortuous arteriole in the stomach wall that erodes through the mucosa. It can cause massive bleeding but is much less common than varices in a patient with cirrhosis.
• D) Peptic ulcer disease: While patients with cirrhosis can develop PUD, bleeding esophageal varices are a more specific and likely complication of their underlying liver disease.

Question 12

1. Discharge home on an oral proton pump inhibitor
2. Initiate a continuous infusion of intravenous octreotide
3. Start an intravenous infusion of a high-dose proton pump inhibitor (correct answer)
4. Arrange for transarterial embolization within 24 hours

Explanation: This patient had an ulcer with a high-risk stigmata of rebleeding (active arterial spurting). After successful endoscopic therapy for such high-risk ulcers, patients should be treated with a continuous intravenous infusion of a high-dose proton pump inhibitor (e.g., pantoprazole 80 mg bolus followed by 8 mg/hr infusion) for 72 hours. This intensive acid suppression promotes clot stability and has been shown to significantly reduce the rates of rebleeding, need for surgery, and mortality.

• A) Discharge home on an oral proton pump inhibitor: Discharging the patient is inappropriate given the high risk of rebleeding. He requires inpatient monitoring and IV therapy.
• B) Initiate a continuous infusion of intravenous octreotide: Octreotide is a somatostatin analog used to reduce splanchnic blood flow in the management of variceal hemorrhage, not non-variceal bleeding like PUD.
• D) Arrange for transarterial embolization within 24 hours: Transarterial embolization is a second-line therapy reserved for patients who have recurrent bleeding despite endoscopic treatment or in whom endoscopic therapy fails.

Question 13

1. Urgent upper endoscopy
2. Water-soluble contrast esophagram (correct answer)
3. Barium esophagram
4. Esophageal manometry

Explanation: This patient's presentation is classic for Boerhaave syndrome, a full-thickness, spontaneous perforation of the esophagus. The history of forceful vomiting followed by severe chest pain, along with physical exam findings of subcutaneous emphysema (crepitus or Hamman's crunch) and radiologic evidence of pneumomediastinum, strongly suggests this diagnosis. The diagnostic test of choice is a contrast esophagram. A water-soluble contrast agent (e.g., Gastrografin) should be used first, as it is less inflammatory to the mediastinum than barium if a leak is present. Barium may be used if the water-soluble study is negative but suspicion remains high.

• A) Urgent upper endoscopy: Endoscopy is relatively contraindicated in cases of suspected esophageal perforation because insufflation of air can extend the perforation and worsen mediastinal contamination.
• C) Barium esophagram: Barium is a more sensitive contrast agent for detecting small perforations, but it can cause severe mediastinitis if it leaks. Therefore, water-soluble contrast is always the initial choice.
• D) Esophageal manometry: This test measures esophageal pressures and is used to diagnose motility disorders. It has no role in the diagnosis of esophageal perforation.

Question 14

1. Initiate empiric triple therapy for H. pylori
2. Measure a fasting serum gastrin level (correct answer)
3. Perform a secretin stimulation test
4. Obtain a surgical consultation for vagotomy

Explanation: The patient's clinical picture of multiple, recurrent peptic ulcers (especially in atypical locations like the jejunum) that are refractory to standard therapy, combined with chronic diarrhea, is highly suggestive of Zollinger-Ellison syndrome (ZES). ZES is caused by a gastrin-secreting neuroendocrine tumor (gastrinoma), leading to massive gastric acid hypersecretion. The most appropriate initial diagnostic test is a fasting serum gastrin level. A level >1000 pg/mL in the presence of gastric pH <4 is diagnostic. The patient should be off PPIs for at least one week before the test for an accurate result.

• A) Initiate empiric triple therapy for H. pylori: The patient has already tested negative for H. pylori, making this an inappropriate step.
• C) Perform a secretin stimulation test: This is a confirmatory test for ZES used when the fasting gastrin level is elevated but non-diagnostic (e.g., 110-1000 pg/mL). It is not the initial screening test.
• D) Obtain a surgical consultation for vagotomy: Vagotomy is a procedure to reduce acid secretion but is rarely performed now due to effective medical therapies. It would not be considered before a definitive diagnosis of the underlying cause is made.

Question 15

1. Gastric ulcer
2. Duodenal ulcer (correct answer)
3. Gastroesophageal reflux disease
4. Chronic pancreatitis

Explanation: The clinical presentation is classic for a duodenal ulcer. Key features include epigastric pain that improves with food intake and worsens 2-3 hours postprandially (when the gastric acid load enters the duodenum without a food buffer). Nocturnal pain is also a common feature, as circadian acid secretion is highest at night. In contrast, pain from a gastric ulcer typically worsens with eating.

• A) Gastric ulcer: The pain of a gastric ulcer is classically exacerbated by eating, as food stimulates acid secretion that irritates the ulcerated gastric mucosa.
• C) Gastroesophageal reflux disease: GERD typically causes a burning retrosternal pain (heartburn) that is worse with lying down or after certain foods, not pain that is relieved by eating.
• D) Chronic pancreatitis: This usually causes persistent epigastric pain that radiates to the back and is often associated with malabsorption (steatorrhea, weight loss) and a history of recurrent acute pancreatitis or alcohol abuse.

Question 16

1. Test for H. pylori and treat if positive
2. Prescribe a trial of a standard-dose proton pump inhibitor
3. Perform upper endoscopy (correct answer)
4. Order an abdominal ultrasound

Explanation: This patient presents with new-onset dyspepsia and has two significant alarm features: age over 60 and unintentional weight loss. The presence of alarm features in a patient with dyspepsia warrants prompt upper endoscopy to rule out an upper gastrointestinal malignancy, such as gastric or esophageal cancer. A 'test-and-treat' strategy for H. pylori or an empiric PPI trial is inappropriate in this setting as it could delay a critical diagnosis.

• A) Test for H. pylori and treat if positive: This strategy is reserved for patients under the age of 60 with uncomplicated dyspepsia and no alarm features.
• B) Prescribe a trial of a standard-dose proton pump inhibitor: An empiric PPI trial is not appropriate in the presence of alarm features.
• D) Order an abdominal ultrasound: Ultrasound is useful for evaluating the liver, gallbladder, and biliary tree but is not the primary modality for investigating dyspepsia, especially when an intraluminal pathology like malignancy is suspected.

Question 17

1. Endoscopic band ligation
2. Initiate high-dose intravenous proton pump inhibitor
3. Admit for observation and supportive care (correct answer)
4. Refer for emergent surgical repair

Explanation: This patient's history of forceful vomiting followed by hematemesis, along with the endoscopic finding of a linear tear at the GE junction, is diagnostic of a Mallory-Weiss tear. The vast majority (>80-90%) of these tears stop bleeding spontaneously and do not require endoscopic or surgical intervention. Since the patient is hemodynamically stable and the tear is not actively bleeding on endoscopy, the most appropriate management is admission for observation and supportive care (e.g., antiemetics, acid suppression if needed). Most patients can be discharged within 24-48 hours.

• A) Endoscopic band ligation: This is a treatment for bleeding esophageal varices, not Mallory-Weiss tears.
• B) Initiate high-dose intravenous proton pump inhibitor: While a PPI may be given, it is not the primary intervention. The key is that active intervention is not needed for a non-bleeding tear. Supportive care is the cornerstone of management.
• D) Refer for emergent surgical repair: Surgery is reserved for rare cases of massive, uncontrolled bleeding from a Mallory-Weiss tear that has failed endoscopic therapy.

Question 18

1. Schatzki ring
2. Eosinophilic esophagitis
3. Achalasia (correct answer)
4. Scleroderma esophagus

Explanation: This patient's presentation of progressive dysphagia to both solids and liquids, regurgitation of undigested food, and weight loss is classic for achalasia. Achalasia is a primary esophageal motility disorder characterized by impaired relaxation of the lower esophageal sphincter (LES) and loss of peristalsis in the distal esophagus. The barium esophagram finding of a dilated esophagus with a 'bird's beak' appearance at the gastroesophageal junction is pathognomonic.

• A) Schatzki ring: This is a type of esophageal stricture that causes intermittent, non-progressive dysphagia to solids only, not liquids.
• B) Eosinophilic esophagitis: This condition can cause dysphagia to solids, often with food impaction, but dysphagia to liquids is less common. It typically affects younger men with a history of atopy.
• D) Scleroderma esophagus: This condition involves smooth muscle atrophy and fibrosis, leading to an incompetent LES and absent peristalsis. While it causes dysphagia, it is more characteristically associated with severe, refractory GERD symptoms, which this patient denies.

Question 19

1. Chronic bronchitis
2. Angiotensin-converting enzyme inhibitor side effect
3. Gastroesophageal reflux disease (correct answer)
4. Post-nasal drip syndrome

Explanation: Chronic cough, laryngitis, and globus sensation are well-recognized extraesophageal manifestations of gastroesophageal reflux disease (GERD). This is often termed 'silent reflux' or laryngopharyngeal reflux (LPR) because classic symptoms like heartburn may be absent. Given that other common causes of chronic cough (post-nasal drip, asthma) have been empirically treated without success, GERD becomes a leading diagnosis. The bitter taste in his mouth further supports reflux as the etiology. The next step would be an empiric trial of high-dose PPI therapy.

• A) Chronic bronchitis: This is defined by a productive cough for at least 3 months in 2 consecutive years and is strongly associated with smoking. This patient has a non-productive cough.
• B) Angiotensin-converting enzyme inhibitor side effect: This is a common cause of dry cough, but the patient is not described as taking an ACE inhibitor.
• D) Post-nasal drip syndrome: This typically presents with a sensation of mucus dripping down the back of the throat and frequent throat clearing. The patient has already been treated for this without improvement.

Question 20

1. Colonoscopy
2. Upper endoscopy with small bowel biopsy
3. Serum tissue transglutaminase IgA antibody testing (correct answer)
4. Hydrogen breath test

Explanation: This patient's presentation of chronic GI symptoms (bloating, diarrhea) with unexplained iron deficiency anemia and family history of autoimmune disease is highly suggestive of celiac disease. Celiac disease causes small intestinal villous atrophy leading to malabsorption of iron and other nutrients. The most appropriate initial diagnostic step is serologic testing with IgA anti-tissue transglutaminase (tTG) antibodies, which has high sensitivity and specificity for celiac disease. If positive, the diagnosis is confirmed with upper endoscopy and duodenal biopsies showing villous atrophy.

• A) Colonoscopy: Evaluates the colon for sources of bleeding but would not detect small bowel pathology causing malabsorption and iron deficiency.
• B) Upper endoscopy with small bowel biopsy: This is the confirmatory test for celiac disease, but serologic screening should be performed first due to its non-invasive nature and high diagnostic accuracy.
• D) Hydrogen breath test: Used to diagnose SIBO or carbohydrate malabsorption but would not explain the iron deficiency anemia seen with celiac disease.