You’re cruising through a GI q-bank when a “hematemesis after retching” vignette pops up—and suddenly every answer choice looks plausible. Esophageal varices are a classic Step diagnosis, but the test-makers love to surround the right answer with distractors that are also real causes of upper GI bleeding. The key skill is not just knowing varices—it’s knowing why the others are wrong in that specific vignette.
Clinical Vignette (Classic Q-Bank Style)
A 54-year-old man is brought to the ED after vomiting a large amount of bright red blood. He has a history of alcohol use disorder and “fluid in his belly.” Vitals: T 37°C, HR 118, BP 92/58. Exam shows jaundice, abdominal distension with shifting dullness, and spider angiomas. Labs show thrombocytopenia and elevated INR. After initial stabilization, he undergoes upper endoscopy.
What is the most likely source of bleeding?
A. Mallory-Weiss tear
B. Esophageal varices
C. Dieulafoy lesion
D. Gastric ulcer due to H. pylori
E. Gastric adenocarcinoma
The Correct Answer: Esophageal Varices
Why it’s varices in this patient
This is portal hypertension until proven otherwise:
- Cirrhosis stigmata: spider angiomas, jaundice, ascites
- Coagulopathy: elevated INR, thrombocytopenia (hypersplenism + decreased hepatic synthesis)
- Hemodynamic instability + massive hematemesis: varices can cause brisk, life-threatening bleeding
Pathophysiology (high-yield)
Portal hypertension forces blood to reroute through portosystemic anastomoses. In the distal esophagus, the key connection is:
- Left gastric vein (portal) ↔ esophageal veins (systemic → azygos)
→ dilation of submucosal veins = esophageal varices
What endoscopy typically shows
- Dilated, tortuous submucosal veins in distal esophagus ± gastric varices
- Active bleeding may be seen as spurting/oozing from a varix
Management: What Step Expects You to Say
Initial stabilization (don’t skip this)
- ABC + 2 large-bore IVs
- Type & cross, transfuse as needed
- Restrictive transfusion strategy often targeted to Hgb ~7 g/dL in many scenarios (conceptual point: avoid overtransfusion worsening portal pressures)
Immediate variceal bleed therapy
- Octreotide (somatostatin analog) → ↓ splanchnic blood flow → ↓ portal pressure
- Endoscopic band ligation (definitive for acute control)
- Prophylactic antibiotics (e.g., ceftriaxone) in cirrhotic GI bleed
- High-yield reason: cirrhotics with GI bleed are at high risk of bacterial translocation/infection, which increases rebleeding and mortality.
If refractory/unstable despite endoscopy
- Balloon tamponade (temporary bridge)
- TIPS (transjugular intrahepatic portosystemic shunt)
- Decompresses portal system but increases risk of hepatic encephalopathy (less detoxification)
Why Every Distractor Is Tempting (and Why It’s Wrong Here)
A. Mallory-Weiss tear
What it is: Longitudinal mucosal laceration at the gastroesophageal junction due to forceful vomiting/retching.
Classic clues
- Hematemesis after repeated nonbloody vomiting/retching
- Common in alcohol use disorder, bulimia, pregnancy (hyperemesis)
Why it’s wrong here
- This vignette screams portal HTN/cirrhosis rather than “retching then blood.”
- Mallory-Weiss usually causes less massive bleeding than varices (can bleed significantly, but variceal hemorrhage is the Step archetype for shock + cirrhosis stigmata).
High-yield contrast
- Mallory-Weiss = mucosal tear
- Boerhaave = transmural rupture (more below)
C. Dieulafoy lesion
What it is: An abnormally large submucosal artery (often in the proximal stomach, near the GE junction) that erodes and bleeds massively.
Classic clues
- Sudden, massive GI bleeding in someone without classic ulcer risk factors
- Endoscopy may miss it if not actively bleeding (intermittent)
Why it’s wrong here
- No specific “Dieulafoy” clues; instead, we have a full portal HTN picture.
- Dieulafoy is a great distractor when the vignette is massive bleed without liver disease.
D. Gastric ulcer due to H. pylori
What it is: Peptic ulcer disease, classically associated with H. pylori (antral predominant) and/or NSAIDs.
Classic clues
- Epigastric pain, dyspepsia, possible melena/hematemesis
- Bleeding tends to be less abrupt than variceal hemorrhage (though it can be significant)
- Risk factors: NSAIDs, H. pylori, older age, ICU stress
Why it’s wrong here
- The question stem gives you portal hypertension clues, not ulcer clues.
- Ulcer bleeding doesn’t require cirrhosis findings like ascites/spider angiomas.
High-yield add-on
- H. pylori urease positive; linked to duodenal ulcers and gastric adenocarcinoma/MALT lymphoma, but that’s a longer chronic story—not “shock + stigmata of cirrhosis.”
E. Gastric adenocarcinoma
What it is: Malignancy associated with chronic inflammation (e.g., H. pylori, chronic atrophic gastritis, intestinal metaplasia), dietary nitrosamines, smoking, etc.
Classic clues
- Weight loss, early satiety, anorexia, anemia, Virchow node (left supraclavicular), acanthosis nigricans (paraneoplastic)
Why it’s wrong here
- Cancer can bleed, but the stem focuses on acute massive hemorrhage with portal HTN signs, not chronic constitutional symptoms or anemia.
- Massive bright red hematemesis with shock in cirrhosis is varices until proven otherwise.
Rapid-Fire Differentials: Upper GI Bleed Patterns (Step-Useful)
| Condition | Typical trigger/clue | Bleeding severity | Key distinguishing feature |
|---|---|---|---|
| Esophageal varices | Cirrhosis/portal HTN, stigmata | Massive | Treat with octreotide + banding + antibiotics |
| Mallory-Weiss tear | Retching/vomiting then hematemesis | Mild–moderate | Mucosal tear at GE junction |
| Boerhaave syndrome | Forceful vomiting + severe chest pain | Variable | Transmural rupture → mediastinitis, subcutaneous emphysema |
| Peptic ulcer disease | NSAIDs/H. pylori, epigastric pain | Moderate–severe | Visible ulcer crater; treat endoscopically + acid suppression |
| Dieulafoy lesion | Sudden bleed without ulcer history | Massive | Large-caliber artery near proximal stomach |
| Gastric cancer | Weight loss, anemia, early satiety | Chronic/occult > acute | Constitutional symptoms, alarm features |
High-Yield Pearls That Commonly Show Up in Question Explanations
Primary prophylaxis (prevention before first bleed)
- Nonselective beta-blockers (propranolol, nadolol, carvedilol) to reduce portal pressures
- Or endoscopic band ligation in select patients
Secondary prophylaxis (after a bleed)
- Nonselective beta-blocker + repeat band ligation
- Consider TIPS if recurrent despite therapy
One-liner mechanism (helps memory)
- Nonselective beta-blockers:
- blockade → ↓ cardiac output
- blockade → unopposed vasoconstriction in splanchnic circulation → ↓ portal inflow
Takeaway: How to “Win” This Question Type
When the stem hands you cirrhosis/portal hypertension (ascites, spider angiomas, coagulopathy, thrombocytopenia) plus sudden large-volume hematemesis with shock, the test is pointing straight at esophageal varices. The distractors are real entities—but they don’t match the story arc.
If you can say why each wrong answer doesn’t fit the timing, risk factors, and expected severity, you’re not just memorizing—you’re reasoning like the exam wants.