Gastroenterology — MCQs
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A 45-year-old patient presents with massive hematemesis. The patient is alert and hemodynamically stable. What is the next immediate step in management?
Hepatic encephalopathy may be precipitated by all of the following except?
A 40-year-old male patient, a known smoker, presents with fever, fatigue, and complete aversion to cigarette smoking. On examination, he has icterus with an enlarged, tender liver. LFT shows Total bilirubin 17.5 mg%, Direct bilirubin 5.5 mg%, SGOT 700 IU, and SGPT 900 IU. What investigations will you perform to rule out acute viral hepatitis?
Which of the following statements is true regarding ulcerative colitis?
Amylase is raised in all conditions below except?
Which immunoglobulin level is specifically elevated in autoimmune pancreatitis?
Cholestatic jaundice is associated with all of the following, except:
When carcinoma of the stomach develops secondarily to pernicious anemia, in which region is it usually situated?
A patient presents with chronic small bowel diarrhea. A duodenal biopsy shows villous atrophy, and serological tests reveal positive anti-endomysial antibodies and IgA tissue transglutaminase (TTG) antibodies. What is the treatment of choice?
The gold standard for the diagnosis of Wilson disease is:
Gastroenterology Indian Medical PG Practice Questions and MCQs
Question 791: A 45-year-old patient presents with massive hematemesis. The patient is alert and hemodynamically stable. What is the next immediate step in management?
- A. Initiate blood transfusion
- B. Start intravenous fluids
- C. Perform urgent upper gastrointestinal endoscopy
- D. Position the patient in recovery position and protect the airway (Correct Answer)
Explanation: ### Explanation **Correct Option: D. Position the patient in recovery position and protect the airway** In any patient presenting with acute massive hematemesis, the management follows the **ABC (Airway, Breathing, Circulation)** protocol [2]. Even if the patient is currently hemodynamically stable, massive hematemesis carries a high risk of **aspiration pneumonia** and sudden airway obstruction due to the volume of blood [1]. Protecting the airway and placing the patient in the recovery position (to prevent aspiration) is the immediate priority before proceeding to fluid resuscitation or diagnostic interventions [2]. **Analysis of Incorrect Options:** * **A & B (Blood Transfusion and IV Fluids):** These address the 'C' (Circulation) of the ABC protocol. While fluid resuscitation is vital in GI bleeds, the question asks for the *next immediate step* [1]. Airway protection must always precede circulatory management. Furthermore, since this patient is currently hemodynamically stable, aggressive transfusion is not the most urgent requirement. * **C (Urgent Upper GI Endoscopy):** Endoscopy is the investigation of choice and is therapeutic, but it should only be performed *after* the patient is stabilized (hemodynamically and airway-wise) [1]. Performing endoscopy on an unprotected airway during active vomiting increases the risk of aspiration. **Clinical Pearls for NEET-PG:** * **Priority in GI Bleed:** Always stabilize first (ABC), then diagnose (Endoscopy) [2]. * **Endoscopy Timing:** In upper GI bleeds, endoscopy should ideally be performed within **24 hours** of admission (urgent) once the patient is stable [1]. * **Transfusion Trigger:** In stable patients without significant cardiac history, a restrictive transfusion strategy (maintaining Hb > 7 g/dL) is preferred over a liberal one. * **Prophylaxis:** In suspected variceal bleeds, start **IV Terlipressin/Octreotide** and **prophylactic antibiotics** (Ceftriaxone) as early as possible.
Question 792: Hepatic encephalopathy may be precipitated by all of the following except?
- A. Anemia
- B. Barbiturates
- C. Hyperkalemia (Correct Answer)
- D. Hypothyroidism
Explanation: **Explanation:** Hepatic Encephalopathy (HE) is a reversible neuropsychiatric syndrome caused by liver failure or portosystemic shunting, leading to the accumulation of neurotoxins (primarily ammonia) [1]. It is typically triggered by specific precipitating factors that either increase ammonia production or decrease its clearance. **Why Hyperkalemia is the Correct Answer:** **Hypokalemia**, not hyperkalemia, precipitates HE. Low serum potassium levels induce intracellular acidosis. To compensate, the kidneys exchange intracellular $H^+$ for extracellular $K^+$. This increases renal ammonia production (ammoniogenesis) and promotes the conversion of ammonium ($NH_4^+$) to ammonia ($NH_3$), which easily crosses the blood-brain barrier, worsening encephalopathy. **Analysis of Other Options:** * **Anemia:** Acute blood loss (especially GI bleeding) is a major trigger. Blood in the gut provides a massive protein load, which is broken down by bacteria into ammonia. * **Barbiturates:** Sedatives, hypnotics, and narcotics have a prolonged half-life in liver failure. They directly depress the CNS and can mask or worsen the symptoms of HE. * **Hypothyroidism:** While less common, hypothyroidism can precipitate HE by slowing gut motility (leading to constipation and increased ammonia absorption) and reducing the metabolic clearance of toxins. **NEET-PG High-Yield Pearls:** * **Most common trigger:** Infection (e.g., SBP), GI bleed, or Diuretic overuse. * **Metabolic Triggers:** Hypokalemia, Alkalosis, Dehydration, and Azotemia. * **Treatment Gold Standard:** Lactulose (converts $NH_3$ to non-absorbable $NH_4^+$) and Rifaximin (reduces ammonia-producing gut flora). * **Asterixis (Flapping tremors):** A classic sign, but not pathognomonic (also seen in uremia and $CO_2$ narcosis).
Question 793: A 40-year-old male patient, a known smoker, presents with fever, fatigue, and complete aversion to cigarette smoking. On examination, he has icterus with an enlarged, tender liver. LFT shows Total bilirubin 17.5 mg%, Direct bilirubin 5.5 mg%, SGOT 700 IU, and SGPT 900 IU. What investigations will you perform to rule out acute viral hepatitis?
- A. Hepatitis B surface antigen (HBsAg), IgM antibody to Hepatitis B core antigen (IgM anti-HBc), Hepatitis C antibody (Anti-HCV), Hepatitis E antibody (Anti-HEV)
- B. Hepatitis A antibody (Anti-HAV), Hepatitis B surface antigen (HBsAg), IgM antibody to Hepatitis B core antigen (IgM anti-HBc), Hepatitis C antibody (Anti-HCV) (Correct Answer)
- C. Hepatitis B antigen (HBAg), IgM antibody to Hepatitis B core antigen (IgM anti-HBc), Hepatitis D antibody (Anti-HDV), Hepatitis C antibody (Anti-HCV), Hepatitis E antibody (Anti-HEV)
- D. Hepatitis A antibody (Anti-HAV), IgM antibody to Hepatitis B core antigen (IgM anti-HBc), Hepatitis C antibody (Anti-HCV), Hepatitis E antibody (Anti-HEV)
Explanation: ### Explanation **Clinical Analysis:** The patient presents with a classic prodrome of **acute viral hepatitis**, characterized by fever, fatigue, and a pathognomonic sign: **aversion to smoking**. The biochemical profile shows significant hyperbilirubinemia and marked elevation of transaminases (SGOT/SGPT > 500 IU), which indicates acute hepatocellular injury [1]. **1. Why Option B is Correct:** To diagnose acute viral hepatitis, we must screen for the most common causative agents (A, B, and C) [1]. * **Anti-HAV (IgM):** Essential to rule out Hepatitis A, a common cause of acute jaundice [1]. IgM type anti-HAV is diagnostic of an acute infection as it is present at the onset of clinical illness [3]. * **HBsAg & IgM anti-HBc:** Both are required for Hepatitis B. HBsAg is the primary screening marker, but **IgM anti-HBc** is crucial to differentiate an acute infection from a chronic flare or to detect infection during the "window period." * **Anti-HCV:** Used to screen for Hepatitis C [1]. **2. Analysis of Incorrect Options:** * **Option A:** Omits Hepatitis A (Anti-HAV), which is a leading cause of acute viral hepatitis [1]. * **Option C:** Uses "HBAg" (non-standard terminology) and includes Hepatitis D (Anti-HDV). HDV is only tested if the patient is already HBsAg positive (co-infection or super-infection); it is not part of the initial routine screening panel. * **Option D:** Omits **HBsAg**. While IgM anti-HBc is specific for acute infection, HBsAg is the standard first-line screening marker for HBV. **3. NEET-PG High-Yield Pearls:** * **Aversion to smoking:** Highly specific clinical clue for Hepatitis A or acute viral hepatitis in smokers. * **Transaminase Levels:** In viral hepatitis, **ALT (SGPT) is usually higher than AST (SGOT)**. If AST > ALT (2:1 ratio), suspect Alcoholic Liver Disease. * **Window Period:** The period where HBsAg and Anti-HBs are both negative. Only **IgM anti-HBc** will be positive during this time. * **Hepatitis E:** While it causes acute hepatitis, it is typically included in screening if there is a known water-borne outbreak or in pregnant patients (due to high mortality) [2]. However, the standard "Acute Hepatitis Panel" traditionally focuses on A, B, and C.
Question 794: Which of the following statements is true regarding ulcerative colitis?
- A. It is a premalignant condition. (Correct Answer)
- B. Cobblestone mucosa is a characteristic feature.
- C. Pseudopolyps are seen exclusively in ulcerative colitis.
- D. It rarely affects the rectum.
Explanation: ### Explanation **1. Why Option A is Correct:** Ulcerative Colitis (UC) is considered a **premalignant condition**. Chronic inflammation leads to a "dysplasia-carcinoma sequence." The risk of developing **Colorectal Carcinoma (CRC)** increases significantly with the duration of the disease (usually after 8–10 years) and the extent of involvement (pancolitis carries a higher risk than proctitis) [1]. Regular surveillance colonoscopy with biopsies is mandatory for these patients. **2. Why Other Options are Incorrect:** * **Option B:** **Cobblestone appearance** is a hallmark of **Crohn’s Disease**, caused by deep longitudinal and transverse ulcers separated by areas of edematous but intact mucosa. In UC, the mucosa is typically granular and friable. * **Option C:** While **pseudopolyps** (inflammatory polyps formed by regenerating islands of mucosa) are very common in UC, they are **not exclusive** to it; they can also be seen in Crohn’s disease or any severe inflammatory insult to the colon [1]. * **Option D:** UC is characterized by **rectal involvement in >95% of cases**. It starts in the rectum (proctitis) and spreads proximally in a **continuous, symmetrical fashion** without "skip lesions" [1]. **3. High-Yield Clinical Pearls for NEET-PG:** * **Depth of Involvement:** UC involves only the **mucosa and submucosa** (Crohn’s is transmural) [1]. * **Lead Pipe Appearance:** Loss of haustrations on barium enema due to chronic scarring. * **Smoking Paradox:** Smoking is **protective** in UC (it may worsen Crohn’s). * **Extra-intestinal Manifestation:** **Primary Sclerosing Cholangitis (PSC)** is more strongly associated with UC than Crohn’s. * **Microscopy:** Presence of **Crypt abscesses** (neutrophils in crypt lumens) [1].
Question 795: Amylase is raised in all conditions below except?
- A. Parotitis
- B. Pancreatic pseudocyst
- C. Serous cystadenoma of pancreas (Correct Answer)
- D. None of the above
Explanation: **Explanation:** Serum amylase is a key biomarker in gastroenterology, primarily produced by the **pancreatic acinar cells** and the **salivary glands** [3]. Elevated levels occur when there is inflammation, ductal obstruction, or leakage from these tissues into the systemic circulation. **1. Why Serous Cystadenoma is the correct answer:** Serous cystadenoma is a **benign, slow-growing neoplastic lesion** of the pancreas. Unlike inflammatory conditions (pancreatitis) or complications like pseudocysts, these tumors do not typically cause significant destruction of acinar tissue or obstruction of the main pancreatic duct [1]. Therefore, they are generally **not associated with an increase in serum amylase levels**. **2. Analysis of Incorrect Options:** * **Parotitis (Option A):** The salivary glands produce the S-isoenzyme of amylase [3]. Inflammation of the parotid gland (e.g., Mumps) leads to the release of this enzyme into the blood, causing hyperamylasemia [2]. * **Pancreatic Pseudocyst (Option B):** A pseudocyst is a collection of pancreatic fluid rich in digestive enzymes. Persistent elevation of serum amylase following an episode of acute pancreatitis is a classic clinical sign suggesting the formation of a pseudocyst [2]. **3. NEET-PG High-Yield Pearls:** * **Macroamylasemia:** A condition where amylase binds to Immunoglobulins (IgA/IgG), becoming too large to be filtered by the kidney. Result: **High serum amylase but low urinary amylase.** * **Other causes of high amylase:** Ectopic pregnancy, intestinal perforation, and diabetic ketoacidosis (DKA). * **Lipase vs. Amylase:** Lipase is more specific for the pancreas and remains elevated longer than amylase (up to 7–14 days). * **Serous Cystadenoma:** Characteristically shows a **"sunburst" calcification** or central stellate scar on imaging [1].
Question 796: Which immunoglobulin level is specifically elevated in autoimmune pancreatitis?
- A. IgM
- B. IgE
- C. IgG4 (Correct Answer)
- D. IgG2
Explanation: **Explanation:** **Autoimmune Pancreatitis (AIP)** is a distinct form of chronic pancreatitis characterized by a fibroinflammatory process. It is the pancreatic manifestation of **IgG4-related disease (IgG4-RD)**. **Why IgG4 is the correct answer:** Type 1 AIP (the most common form globally) is characterized by high serum levels of **IgG4** and dense infiltration of IgG4-positive plasma cells in the pancreatic tissue. Histologically, this presents as Lymphoplasmacytic Sclerosing Pancreatitis (LPSP). A serum IgG4 level >135 mg/dL is a key diagnostic marker and is part of the HISORt criteria used to diagnose the condition. **Analysis of Incorrect Options:** * **IgM:** Typically elevated in primary biliary cholangitis (PBC) or acute infections. It is not a marker for AIP. * **IgE:** Associated with Type 1 hypersensitivity reactions (allergies) and parasitic infections. While some AIP patients have peripheral eosinophilia, IgE is not the specific diagnostic marker. * **IgG2:** While IgG2 is the most abundant subclass in response to bacterial capsular polysaccharides, it has no specific association with autoimmune pancreatitis. **High-Yield Clinical Pearls for NEET-PG:** * **Classic Presentation:** Painless obstructive jaundice in an elderly male, often mimicking pancreatic cancer ("sausage-shaped" pancreas on CT). * **Treatment:** AIP is highly **steroid-responsive**, which helps differentiate it from pancreatic malignancy. * **Extrapancreatic manifestations:** Look for associated Sclerosing Cholangitis, Salivary gland involvement (Küttner's tumor), or Retroperitoneal fibrosis. * **Type 2 AIP:** Unlike Type 1, Type 2 is **not** associated with elevated IgG4 and is often linked to Inflammatory Bowel Disease (UC).
Question 797: Cholestatic jaundice is associated with all of the following, except:
- A. Predominantly conjugated hyperbilirubinemia
- B. Minimal biochemical changes of parenchymal liver damage
- C. A moderate to marked increase in serum alkaline phosphatase
- D. A moderate to marked increase in SGOT (Correct Answer)
Explanation: **Explanation:** The core concept in differentiating hepatobiliary diseases is distinguishing between **hepatocellular damage** and **cholestasis** (impaired bile flow). **Why Option D is the correct answer:** In cholestatic jaundice, the primary pathology is the obstruction of bile flow (either intrahepatic or extrahepatic). While there may be minor secondary damage to hepatocytes, the levels of **SGOT (AST) and SGPT (ALT)**—which are markers of parenchymal liver cell necrosis—typically show only a **mild elevation** (usually <3 times the upper limit of normal) [1]. A moderate to marked increase in SGOT is characteristic of acute hepatitis or toxic liver injury, not cholestasis. **Analysis of incorrect options:** * **Option A:** In cholestasis, bilirubin is conjugated by the liver but cannot be excreted into the duodenum. This leads to its regurgitation into the bloodstream, resulting in **predominantly conjugated hyperbilirubinemia** (Direct bilirubin >50% of total) [3]. * **Option B:** Cholestasis is defined by the failure of bile secretion rather than the death of liver cells. Therefore, markers of **parenchymal damage** (transaminases) remain relatively low compared to the dramatic rise in obstructive markers [2]. * **Option C:** **Alkaline Phosphatase (ALP)** is synthesized by the biliary canalicular membranes. Obstruction triggers increased synthesis and release of ALP into the serum, making a moderate to marked increase (often >3x normal) a hallmark of cholestasis [2]. **NEET-PG High-Yield Pearls:** * **R-Value:** Used to differentiate liver injury. $R = (\text{ALT/ULN}) \div (\text{ALP/ULN})$. $R > 5$ suggests hepatocellular injury; $R < 2$ suggests cholestatic injury. * **Other Cholestatic Markers:** Gamma-glutamyl transferase (GGT) and 5'-nucleotidase are also elevated [2]. GGT is useful to confirm that an elevated ALP is of hepatic origin (not bone). * **Clinical Triad of Cholestasis:** Jaundice, Pruritus (due to bile salt deposition), and Pale/Clay-colored stools [4].
Question 798: When carcinoma of the stomach develops secondarily to pernicious anemia, in which region is it usually situated?
- A. Prepyloric region
- B. Pylorus
- C. Body
- D. Fundus (Correct Answer)
Explanation: The correct answer is **Fundus (Option D)**. **Pathophysiology:** Pernicious anemia is an autoimmune condition characterized by the presence of antibodies against gastric parietal cells and intrinsic factor [1]. This leads to **Type A Gastritis (Autoimmune Metaplastic Atrophic Gastritis)**. Since parietal cells are predominantly located in the **fundus and the body** of the stomach, these areas undergo significant mucosal atrophy and intestinal metaplasia [1]. This chronic inflammatory environment predisposes the tissue to adenocarcinoma. While both the body and fundus are affected, the fundus is the classic site cited for malignancies secondary to pernicious anemia in medical literature and competitive exams. **Analysis of Incorrect Options:** * **A & B (Prepyloric region and Pylorus):** These areas constitute the gastric antrum. Carcinomas associated with *H. pylori* infection (Type B Gastritis) typically occur here. In pernicious anemia, the antrum is usually spared because it lacks parietal cells [1]. * **C (Body):** While the body is affected by atrophic gastritis in pernicious anemia, the fundus is considered the more characteristic site for the development of these specific secondary carcinomas in the context of this disease. **NEET-PG High-Yield Pearls:** * **Type A Gastritis:** **A**utoimmune, **A**nemia (Pernicious), **A**chlorhydria, and involves the **A**ndrum-sparing (Fundus/Body) [1]. * **Type B Gastritis:** **B**acterial (*H. pylori*), involves the **B**ad part (Antrum). * **Risk:** Patients with pernicious anemia have a 3-fold increased risk of gastric adenocarcinoma and are also at risk for **Gastric Carcinoid tumors** (due to hypergastrinemia stimulating ECL cells). * **Marker:** Anti-parietal cell antibodies are sensitive; Anti-intrinsic factor antibodies are specific.
Question 799: A patient presents with chronic small bowel diarrhea. A duodenal biopsy shows villous atrophy, and serological tests reveal positive anti-endomysial antibodies and IgA tissue transglutaminase (TTG) antibodies. What is the treatment of choice?
- A. Gluten-free diet (Correct Answer)
- B. Antibiotics
- C. Loperamide
- D. 5-aminosalicylic acid (5-ASA)
Explanation: ### Explanation **Correct Answer: A. Gluten-free diet** The clinical presentation and diagnostic findings are classic for **Celiac Disease** (Gluten-sensitive enteropathy). The combination of chronic small bowel diarrhea, **villous atrophy** on biopsy (Marsh classification), and highly specific serology (**Anti-TTG IgA** and **Anti-endomysial antibodies**) confirms the diagnosis [1]. The underlying pathophysiology involves an immune-mediated inflammatory response to **gliadin** (a component of gluten found in wheat, barley, and rye) [1]. The definitive and lifelong treatment of choice is a strict **Gluten-free diet (GFD)** [1]. This leads to symptomatic improvement, normalization of serology, and histological recovery of the intestinal mucosa. **Why other options are incorrect:** * **B. Antibiotics:** These are used for Tropical Sprue or Small Intestinal Bacterial Overgrowth (SIBO). While Tropical Sprue also causes villous atrophy, it would not present with positive anti-TTG antibodies. * **C. Loperamide:** This is an anti-motility agent used for symptomatic relief of non-specific diarrhea [2]. It does not address the underlying autoimmune destruction in Celiac disease. * **D. 5-aminosalicylic acid (5-ASA):** This is the mainstay of treatment for Inflammatory Bowel Disease (IBD), such as Ulcerative Colitis, which typically presents with large bowel symptoms (bloody diarrhea) and different histological markers. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard Diagnosis:** D2 (Duodenal) biopsy showing villous atrophy, crypt hyperplasia, and increased intraepithelial lymphocytes [1]. * **Best Screening Test:** IgA Tissue Transglutaminase (tTG) antibody. * **Most Specific Test:** Anti-Endomysial Antibody (EMA). * **Genetic Association:** Strongly linked with **HLA-DQ2** (95%) and **HLA-DQ8** [1]. * **Associated Conditions:** Dermatitis herpetiformis (pathognomonic skin rash), Type 1 Diabetes, and IgA deficiency. * **Malignancy Risk:** Untreated Celiac disease increases the risk of **Enteropathy-associated T-cell lymphoma (EATL)**.
Question 800: The gold standard for the diagnosis of Wilson disease is:
- A. Liver biopsy with quantitative copper assay (Correct Answer)
- B. Serum ceruloplasmin along with free copper estimation
- C. 24 hour urine copper quantification
- D. Liver biopsy and copper staining
Explanation: **Explanation:** Wilson disease is an autosomal recessive disorder caused by mutations in the *ATP7B* gene, leading to impaired biliary copper excretion and systemic copper accumulation [1]. **Why Option A is Correct:** The **Gold Standard** for diagnosis is a **liver biopsy with quantitative copper assay**. A hepatic copper concentration **>250 μg/g dry weight** is diagnostic. While other tests are used for screening, the direct measurement of copper content in the liver tissue remains the most definitive evidence of the disease's pathophysiology. **Why Other Options are Incorrect:** * **Option B:** Serum ceruloplasmin is typically low (<20 mg/dL), but it is an acute-phase reactant and can be normal in 10-15% of patients. Free copper estimation is helpful but lacks the specificity of a biopsy. * **Option C:** 24-hour urinary copper (>100 μg/day) is an excellent screening tool and part of the diagnostic scoring system (Leipzig criteria), but it is not the "gold standard." * **Option D:** Copper staining (e.g., Rhodanine or Orcein) is often unreliable because copper deposition in the liver is **patchy**, especially in early stages [1]. A quantitative assay is far more accurate than visual staining. **High-Yield Clinical Pearls for NEET-PG:** * **Initial Screening Test:** Serum Ceruloplasmin (usually decreased). * **Most Sensitive Screening Test:** 24-hour urinary copper. * **Ocular Finding:** Kayser-Fleischer (KF) rings (copper deposition in Descemet’s membrane), best seen on slit-lamp exam. * **Hematology:** Coombs-negative hemolytic anemia is a classic presentation [1]. * **Treatment:** First-line is **Chelation therapy** (D-Penicillamine or Trientine). Oral Zinc is used for maintenance or asymptomatic patients.
Practice by Chapter
Esophageal Disorders
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Peptic Ulcer Disease
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Inflammatory Bowel Disease
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Irritable Bowel Syndrome
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Malabsorption Syndromes
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Pancreatitis (Acute and Chronic)
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Gastrointestinal Bleeding
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Liver Diseases and Cirrhosis
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Viral Hepatitis
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Biliary Tract Disorders
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Gastrointestinal Motility Disorders
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Gastrointestinal Malignancies
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