Gastroenterology — MCQs
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A 41-year-old male patient presented with recurrent episodes of bloody diarrhea for 5 years. Despite regular treatment with adequate doses of sulfasalazine, he has had several exacerbations of his disease and required several weeks of steroids for the control of flares. What should be the next line of treatment for him?
Which of the following is NOT a precipitating factor of hepatic encephalopathy in a patient with chronic liver disease?
Hereditary pancreatitis is characterized by all except:
Oral ulceration resembling aphthae are encountered in which of the following conditions?
A 40-year-old male presents with hematemesis. On examination, his BP was 90/60 mmHg and heart rate was 120/min. Splenomegaly was also present. What is the most probable cause of his bleeding?
A 56-year-old man presents with jaundice and mild fatigue over the past 2 months. He is not on any medications and has no significant past medical history. Physical examination reveals scleral icterus. Laboratory findings include: SGOT: 0.58 microkat/L, SGPT: 0.58 microkat/L, Total bilirubin: 91.7 micromol/L, Direct bilirubin: 85.5 micromol/L, and Alkaline phosphatase: 12 microkat/L. What is the next appropriate diagnostic step?
A 40-year-old woman presents with a 2-month history of burning epigastric pain that usually occurs between meals. The pain can be relieved with antacids or food. The patient also reports a recent history of tarry stools. She denies taking aspirin or NSAIDs. Laboratory studies show a microcytic, hypochromic anemia (serum hemoglobin = 8.5 g/dL). Gastroscopy reveals a bleeding mucosal defect in the antrum measuring 1.5 cm in diameter. An endoscopic biopsy shows that the lesion lacks mucosal lining cells and is composed of amorphous, cellular debris and numerous neutrophils. Which of the following is the most important factor in the pathogenesis of this patient's disease?
What is the drug of choice in the treatment of tropical sprue?
A patient with chronic liver disease presents with ascites and has no history of bleeding varices. The patient develops hematemesis and melena. What is the next step in management?
A false positive D-xylose test is seen in which of the following conditions?
Gastroenterology Indian Medical PG Practice Questions and MCQs
Question 541: A 41-year-old male patient presented with recurrent episodes of bloody diarrhea for 5 years. Despite regular treatment with adequate doses of sulfasalazine, he has had several exacerbations of his disease and required several weeks of steroids for the control of flares. What should be the next line of treatment for him?
- A. Methotrexate
- B. Azathioprine (Correct Answer)
- C. Cyclosporine
- D. Cyclophosphamide
Explanation: ### Explanation The patient presents with chronic, relapsing **Ulcerative Colitis (UC)** that is **steroid-dependent**. He has failed maintenance therapy with 5-ASA (Sulfasalazine) and requires repeated courses of corticosteroids to control flares. [1] **1. Why Azathioprine is Correct:** In inflammatory bowel disease (IBD), when a patient cannot taper off steroids without a relapse or requires frequent steroid pulses, they are classified as "steroid-dependent." The standard next step in management is the introduction of **Thiopurines (Azathioprine or 6-Mercaptopurine)**. These are "steroid-sparing agents" used for the maintenance of remission in UC. [1] They take 3–6 months to reach peak efficacy, making them unsuitable for acute flares but ideal for long-term control in this scenario. **2. Why Other Options are Incorrect:** * **A. Methotrexate:** While used as a second-line immunomodulator in **Crohn’s Disease**, its efficacy in Ulcerative Colitis is not well-established and is generally not the first-choice steroid-sparing agent for UC. * **C. Cyclosporine:** This is a potent immunosuppressant used for **acute severe ulcerative colitis** (refractory to IV steroids) as "rescue therapy" to avoid emergency colectomy. It is not used for routine maintenance in a stable but steroid-dependent patient. * **D. Cyclophosphamide:** This drug has no established role in the standard management of Ulcerative Colitis due to its significant toxicity profile. **Clinical Pearls for NEET-PG:** * **Step-up Therapy:** 5-ASA → Steroids (for induction) → Thiopurines (for maintenance) → Biologics (Infliximab/Adalimumab) → Surgery. [1] * **Monitoring:** Before starting Azathioprine, check **TPMT (Thiopurine Methyltransferase)** activity to predict the risk of severe bone marrow suppression. * **Side Effects:** Monitor for pancreatitis, leucopenia, and increased risk of non-melanoma skin cancer/lymphoma.
Question 542: Which of the following is NOT a precipitating factor of hepatic encephalopathy in a patient with chronic liver disease?
- A. TIPS (Transjugular Intrahepatic Portosystemic Shunt)
- B. High dietary protein load
- C. Hyperkalemia (Correct Answer)
- D. Infection
Explanation: Hepatic Encephalopathy (HE) is a reversible neuropsychiatric syndrome caused by the accumulation of neurotoxins (primarily ammonia) in the brain due to liver failure or portosystemic shunting [1]. **Why Hyperkalemia is the Correct Answer:** **Hypokalemia**, not hyperkalemia, is a classic precipitant of HE. When potassium levels are low, the body attempts to conserve $K^+$ in the renal tubules by exchanging it for $H^+$ ions. This intracellular acidosis in renal cells stimulates the enzyme glutaminase, leading to increased **renal ammoniagenesis** (production of $NH_3$). Furthermore, hypokalemia-induced alkalosis shifts the equilibrium from ammonium ($NH_4^+$) to ammonia ($NH_3$), which easily crosses the blood-brain barrier. **Analysis of Incorrect Options:** * **TIPS:** This procedure creates a low-resistance tract between the portal and systemic circulation [1]. By bypassing the liver's detoxification process, neurotoxins reach the systemic circulation directly, making HE a common post-procedural complication. * **High Dietary Protein:** Protein breakdown by colonic bacteria produces ammonia [1]. A sudden large protein load (or GI bleed, which is essentially a protein load) increases ammonia production beyond the liver's capacity to clear it. * **Infection:** Sepsis and spontaneous bacterial peritonitis (SBP) increase tissue catabolism and impair renal function, both of which elevate blood ammonia levels and increase the permeability of the blood-brain barrier. **High-Yield Clinical Pearls for NEET-PG:** * **Most common precipitant:** Azotemia (often due to over-diuresis) and Infections. * **Electrolyte disturbances:** Hypokalemia, Hyponatremia, and Metabolic Alkalosis all precipitate HE. * **Drug of choice:** **Lactulose** (converts $NH_3$ to non-absorbable $NH_4^+$ and acts as an osmotic laxative). * **Second-line/Add-on:** **Rifaximin** (non-absorbable antibiotic that reduces ammonia-producing gut flora).
Question 543: Hereditary pancreatitis is characterized by all except:
- A. Equal prevalence in males and females
- B. Autosomal recessive inheritance (Correct Answer)
- C. Mutation of trypsinogen gene on long arm of chromosome 7
- D. Penetrance is generally accepted to be approximately 80%
Explanation: Hereditary pancreatitis is a rare genetic disorder characterized by recurrent episodes of acute pancreatitis starting in childhood, often progressing to chronic pancreatitis. **1. Why Option B is the correct answer (The Exception):** Hereditary pancreatitis follows an **Autosomal Dominant** inheritance pattern, not autosomal recessive. It is primarily caused by mutations in the **PRSS1 gene**, which encodes for cationic trypsinogen. Because it is dominant, a single copy of the mutated gene from one parent is sufficient to cause the disease. **2. Analysis of other options:** * **Option A:** Unlike alcoholic pancreatitis, which shows a male predominance, hereditary pancreatitis affects **males and females equally**. * **Option C:** The PRSS1 gene is located on the **long arm of chromosome 7 (7q35)**. The most common mutation is **R122H**, which prevents the deactivation of trypsin, leading to premature intrapancreatic enzyme activation and autodigestion. * **Option D:** The disease exhibits incomplete penetrance, generally accepted to be approximately **80%** [1]. This means 20% of individuals carrying the mutation may never develop clinical symptoms. **Clinical Pearls for NEET-PG:** * **Triad of Risk:** Patients have a significantly increased risk (up to 40-50 fold) of developing **Pancreatic Adenocarcinoma**, especially if they smoke. * **Early Onset:** Symptoms typically begin before age 20 (often before age 10). * **Other Genes:** While PRSS1 is the most common, mutations in **SPINK1** (Serine protease inhibitor Kazal-type 1) and **CFTR** are also associated with idiopathic/hereditary chronic pancreatitis [2]. * **Management:** Focuses on pain control, pancreatic enzyme replacement therapy (PERT), and screening for diabetes and malignancy.
Question 544: Oral ulceration resembling aphthae are encountered in which of the following conditions?
- A. Gluten enteropathy (Correct Answer)
- B. Chronic smokers
- C. Excess of B-complex vitamins
- D. Anti-malarial medication
Explanation: **Explanation:** **1. Why Gluten Enteropathy is Correct:** Gluten enteropathy (Celiac Disease) is a common systemic cause of recurrent aphthous-like ulcers. These oral lesions often precede gastrointestinal symptoms. The underlying mechanism is two-fold: first, the **malabsorption** of essential nutrients (specifically Iron, Vitamin B12, and Folate) due to villous atrophy in the small intestine; and second, an **immunological cross-reactivity** where the oral mucosa becomes a target of the inflammatory process. In many patients, a gluten-free diet leads to the complete resolution of these ulcers. **2. Why the Other Options are Incorrect:** * **Chronic Smokers:** Interestingly, smoking is considered "protective" against aphthous ulcers. Nicotine stimulates the production of adrenal steroids and increases keratinization of the oral mucosa, making it less susceptible to ulceration. Ulcers often flare up *after* smoking cessation. * **Excess of B-complex vitamins:** It is the **deficiency** (specifically B1, B2, B6, and B12), not the excess, that causes oral manifestations like glossitis, cheilosis, and aphthous ulcers. * **Anti-malarial medication:** While some drugs (like NSAIDs or Nicorandil) cause oral ulcers, anti-malarials (e.g., Hydroxychloroquine) are actually sometimes used off-label to *treat* severe recurrent aphthous stomatitis due to their immunomodulatory effects. **Clinical Pearls for NEET-PG:** * **RAS (Recurrent Aphthous Stomatitis)** is also strongly associated with **Behçet’s Disease** (pustular/genital sores) and **IBD** (Crohn’s > UC). * **Dermatitis Herpetiformis** is the pathognomonic skin manifestation of Celiac disease. * **Screening Gold Standard:** IgA Anti-tissue Transglutaminase (tTG) antibodies.
Question 545: A 40-year-old male presents with hematemesis. On examination, his BP was 90/60 mmHg and heart rate was 120/min. Splenomegaly was also present. What is the most probable cause of his bleeding?
- A. Portal hypertension (Correct Answer)
- B. Gastric ulcer
- C. Duodenal ulcer
- D. Drug-induced GI injury
Explanation: ### Explanation The clinical presentation of **hematemesis** associated with **splenomegaly** and signs of **hemodynamic instability** (hypotension and tachycardia) strongly points toward **Portal Hypertension**, most commonly due to liver cirrhosis or non-cirrhotic portal fibrosis [1]. **1. Why Portal Hypertension is correct:** In portal hypertension, the increased pressure in the portal venous system leads to the development of portosystemic collaterals [2]. The most clinically significant collaterals are **esophageal and gastric varices**, which are prone to rupture, causing massive, life-threatening hematemesis [2]. The presence of **splenomegaly** is a hallmark sign of portal hypertension, resulting from chronic passive congestion of the spleen (congestive splenomegaly) [1]. **2. Why the other options are incorrect:** * **Gastric and Duodenal Ulcers (Options B & C):** While Peptic Ulcer Disease (PUD) is the most common cause of upper GI bleeding overall, it does **not** cause splenomegaly [1]. The presence of an enlarged spleen specifically shifts the differential toward portal venous pathology. * **Drug-induced GI injury (Option D):** NSAIDs or steroids can cause erosive gastritis or ulcers leading to hematemesis, but like PUD, they do not account for the finding of splenomegaly [1]. **Clinical Pearls for NEET-PG:** * **Most common cause of Portal HTN in India:** Liver Cirrhosis (Alcoholic/Viral). * **Most common cause of massive hematemesis in children with splenomegaly:** Extrahepatic Portal Venous Obstruction (EHPVO). * **Management Priority:** In a patient with BP 90/60 and HR 120, the immediate priority is **hemodynamic stabilization** (IV fluids/blood) before diagnostic endoscopy [1]. * **Drug of choice for active variceal bleed:** Terlipressin or Octreotide. * **Definitive treatment for acute variceal bleed:** Endoscopic Variceal Ligation (EVL).
Question 546: A 56-year-old man presents with jaundice and mild fatigue over the past 2 months. He is not on any medications and has no significant past medical history. Physical examination reveals scleral icterus. Laboratory findings include: SGOT: 0.58 microkat/L, SGPT: 0.58 microkat/L, Total bilirubin: 91.7 micromol/L, Direct bilirubin: 85.5 micromol/L, and Alkaline phosphatase: 12 microkat/L. What is the next appropriate diagnostic step?
- A. Ultrasound (Correct Answer)
- B. Liver biopsy
- C. Review of peripheral blood smear
- D. Endoscopic retrograde cholangiopancreatography (ERCP)
Explanation: ### Explanation The patient presents with **obstructive jaundice**, characterized by a significant elevation in direct bilirubin (85.5 µmol/L out of 91.7 µmol/L) and a markedly elevated Alkaline Phosphatase (ALP) [4]. In contrast, the transaminases (SGOT/SGPT) are relatively normal, pointing toward a cholestatic pattern rather than hepatocellular injury [1]. **1. Why Ultrasound is the Correct Step:** In any patient with biochemical evidence of cholestasis, the first priority is to differentiate between **intrahepatic cholestasis** and **extrahepatic biliary obstruction**. * **Ultrasound (USG) Abdomen** is the initial investigation of choice because it is non-invasive, cost-effective, and highly sensitive in detecting **biliary ductal dilatation** (e.g., dilated common bile duct or intrahepatic biliary radicles) [2]. It also helps identify the cause, such as gallstones or pancreatic masses. **2. Why Other Options are Incorrect:** * **Liver Biopsy:** This is generally reserved for intrahepatic causes (e.g., PBC, PSC) after extrahepatic obstruction has been ruled out by imaging. Performing a biopsy in the presence of biliary obstruction carries a risk of bile peritonitis [3]. * **Review of Peripheral Blood Smear:** This is useful for diagnosing hemolytic anemia (pre-hepatic jaundice), which would present with elevated **indirect** bilirubin [4]. * **ERCP:** While ERCP is both diagnostic and therapeutic, it is invasive and carries risks like pancreatitis. It is performed only after non-invasive imaging (USG or MRCP) confirms an obstruction that requires intervention (e.g., stone extraction or stenting). **Clinical Pearls for NEET-PG:** * **Direct Hyperbilirubinemia + High ALP** = Cholestatic Pattern. * **Initial Investigation:** Ultrasound Abdomen. * **Gold Standard for CBD Stones:** ERCP (but MRCP is the diagnostic non-invasive gold standard). * **Courvoisier’s Law:** In a patient with painless jaundice and a palpable gallbladder, the cause is unlikely to be gallstones and more likely to be a malignancy (e.g., periampullary carcinoma).
Question 547: A 40-year-old woman presents with a 2-month history of burning epigastric pain that usually occurs between meals. The pain can be relieved with antacids or food. The patient also reports a recent history of tarry stools. She denies taking aspirin or NSAIDs. Laboratory studies show a microcytic, hypochromic anemia (serum hemoglobin = 8.5 g/dL). Gastroscopy reveals a bleeding mucosal defect in the antrum measuring 1.5 cm in diameter. An endoscopic biopsy shows that the lesion lacks mucosal lining cells and is composed of amorphous, cellular debris and numerous neutrophils. Which of the following is the most important factor in the pathogenesis of this patient's disease?
- A. Achlorhydria
- B. Acute ischemia
- C. Autoimmunity
- D. Helicobacter pylori infection (Correct Answer)
Explanation: The clinical presentation of epigastric pain relieved by food/antacids, combined with melena (tarry stools) and microcytic anemia, is classic for **Peptic Ulcer Disease (PUD)**. The gastroscopy finding of a 1.5 cm mucosal defect in the antrum confirms a gastric ulcer. **1. Why H. pylori is correct:** *Helicobacter pylori* is the most important etiological factor for PUD worldwide, accounting for approximately 70% of gastric ulcers and over 90% of duodenal ulcers. In the absence of NSAID use (as specified in the prompt), *H. pylori* is the most likely cause [1]. It induces chronic inflammation by secreting urease and cytotoxins (CagA, VacA), which break down the protective mucosal barrier, allowing gastric acid to cause autodigestion and ulceration [1]. **2. Why other options are incorrect:** * **Achlorhydria:** This is the absence of gastric acid. PUD requires the presence of acid ("No acid, no ulcer"). Achlorhydria is associated with Pernicious Anemia and Gastric Adenocarcinoma, not PUD. * **Acute Ischemia:** This typically causes "stress ulcers" (e.g., Curling’s or Cushing’s ulcers) in patients with severe trauma, burns, or shock [1]. It presents acutely rather than over a 2-month period. * **Autoimmunity:** Autoimmune gastritis involves antibodies against parietal cells/intrinsic factor [1]. It leads to mucosal atrophy and Vitamin B12 deficiency (Megaloblastic anemia), not localized peptic ulceration. **High-Yield NEET-PG Pearls:** * **Most common site for H. pylori:** Gastric Antrum [1]. * **Gold standard for diagnosis:** Endoscopic biopsy followed by Rapid Urease Test (RUT) or Histopathology (Warthin-Starry stain). * **Non-invasive test of choice:** Urea Breath Test (used for confirming eradication). * **Complications:** Bleeding (most common), Perforation (most common in anterior ulcers), and Gastric Outlet Obstruction.
Question 548: What is the drug of choice in the treatment of tropical sprue?
- A. Tetracycline (Correct Answer)
- B. Prednisolone
- C. Gliadin
- D. Cyclosporine
Explanation: Explanation: **Tropical Sprue** is a chronic diarrheal syndrome characterized by malabsorption and megaloblastic anemia, occurring primarily in residents of or visitors to tropical regions [2]. While the exact etiology is unknown, it is widely believed to be caused by a persistent **bacterial overgrowth** in the small intestine, often following an episode of acute infectious diarrhea. 1. **Why Tetracycline is correct:** Since the underlying cause is bacterial colonization, long-term antibiotic therapy is the mainstay of treatment. **Tetracycline** (250 mg four times daily) for 3 to 6 months is the **drug of choice**. It effectively reduces the bacterial load, allowing the intestinal mucosa to heal and improving nutrient absorption. It is often combined with **Folic acid** (5 mg/day) to treat the associated megaloblastic anemia and promote mucosal repair. 2. **Why other options are incorrect:** * **Prednisolone:** This is a corticosteroid used for Celiac disease (refractory cases) or Inflammatory Bowel Disease (IBD), but it has no role in treating the infectious/bacterial nature of Tropical Sprue. * **Gliadin:** This is a component of gluten. Avoiding gliadin (Gluten-free diet) is the treatment for **Celiac Sprue**, not Tropical Sprue [1]. * **Cyclosporine:** This is an immunosuppressant used in severe, refractory Celiac disease or transplant medicine; it is not indicated for Tropical Sprue. **High-Yield Clinical Pearls for NEET-PG:** * **Biopsy findings:** Similar to Celiac disease (villous atrophy, crypt hyperplasia), but in Tropical Sprue, changes are seen throughout the small intestine (including the **ileum**), whereas Celiac is more prominent in the proximal duodenum. * **Deficiencies:** Unlike Celiac disease, Tropical Sprue frequently involves the distal ileum, leading to **Vitamin B12 deficiency** in addition to Folate deficiency. * **Key differentiator:** Tropical Sprue responds to antibiotics; Celiac disease responds to a gluten-free diet.
Question 549: A patient with chronic liver disease presents with ascites and has no history of bleeding varices. The patient develops hematemesis and melena. What is the next step in management?
- A. Injectable vitamin K
- B. Injectable Tranexamic acid
- C. Fresh frozen plasma transfusion (Correct Answer)
- D. Platelet transfusion
Explanation: **Explanation:** In a patient with chronic liver disease (CLD), the liver's synthetic function is compromised, leading to a deficiency of multiple clotting factors (II, VII, IX, X, protein C, and S). When such a patient presents with an acute upper GI bleed (hematemesis and melena), immediate correction of the underlying coagulopathy is vital to achieve hemostasis [1]. **Why Fresh Frozen Plasma (FFP) is the Correct Choice:** FFP contains all coagulation factors and proteins present in the plasma. In the setting of acute bleeding in CLD, FFP is the preferred initial treatment to rapidly replace the deficient clotting factors and correct the prolonged Prothrombin Time (PT/INR). It provides a comprehensive replacement that single-agent therapies cannot offer. **Analysis of Incorrect Options:** * **Injectable Vitamin K:** While Vitamin K is necessary for the synthesis of factors II, VII, IX, and X, it requires a functional liver to produce these factors. In advanced CLD, the liver cannot utilize Vitamin K effectively. Furthermore, it takes 6–24 hours to show an effect, making it unsuitable for acute, life-threatening hemorrhage. * **Injectable Tranexamic Acid:** This is an antifibrinolytic. While used in trauma or postpartum hemorrhage, it is not the primary treatment for coagulopathy caused by factor deficiency in liver disease and does not address the root cause of the bleeding. * **Platelet Transfusion:** This is only indicated if the patient has significant thrombocytopenia (usually <50,000/µL) alongside active bleeding [1]. It does not correct the global clotting factor deficiency. **Clinical Pearls for NEET-PG:** * **Target INR:** In acute variceal or non-variceal bleeding in CLD, the goal is to maintain hemodynamic stability; however, over-transfusion of FFP should be avoided as it can increase portal pressure. * **Child-Pugh Score:** Remember that PT/INR is a key component of the Child-Pugh and MELD scores, reflecting the severity of liver dysfunction. * **Terlipressin/Octreotide:** In clinical practice, these are started simultaneously to reduce portal pressure while coagulation is being corrected [2].
Question 550: A false positive D-xylose test is seen in which of the following conditions?
- A. Blind loop syndrome (Correct Answer)
- B. Ascites
- C. Renal failure
- D. Antibiotic therapy
Explanation: The **D-xylose test** is used to differentiate between malabsorption caused by intestinal mucosal disease (e.g., Celiac disease) and malabsorption due to pancreatic insufficiency. D-xylose is a pentose sugar that is absorbed in the proximal small intestine via passive diffusion and does not require pancreatic enzymes. **1. Why Blind Loop Syndrome is the Correct Answer:** In **Blind Loop Syndrome** (Small Intestinal Bacterial Overgrowth - SIBO), there is an overgrowth of bacteria in the small bowel [1]. These bacteria metabolize and consume the D-xylose before the intestinal mucosa can absorb it. This results in low urinary excretion of D-xylose, mimicking a mucosal disease pattern [2]. Therefore, it is considered a **false positive** result because the intestinal mucosa itself is actually intact. **2. Analysis of Incorrect Options:** * **Ascites:** This can lead to a **false positive** result. D-xylose is distributed into the ascitic fluid, delaying its excretion in the urine. * **Renal Failure:** This causes a **false positive** result. Since D-xylose is excreted by the kidneys, impaired renal function leads to low urinary levels despite normal intestinal absorption. * **Antibiotic Therapy:** This would actually lead to a **false negative** (or normalization) of the test in a patient with SIBO, as the antibiotics kill the bacteria that were consuming the sugar. **High-Yield Clinical Pearls for NEET-PG:** * **Normal Test:** >4g excreted in urine over 5 hours (after a 25g oral dose). * **Low D-xylose (Positive):** Celiac disease, Tropical sprue, Whipple’s disease, SIBO, and Giardiasis. * **Normal D-xylose in Malabsorption:** Pancreatic insufficiency (e.g., Chronic pancreatitis) because enzyme secretion is not required for D-xylose absorption. * **False Positives (Low urine levels despite normal mucosa):** SIBO, Renal failure, Ascites, and Elderly age (decreased GFR).
Practice by Chapter
Esophageal Disorders
Practice Questions
Peptic Ulcer Disease
Practice Questions
Inflammatory Bowel Disease
Practice Questions
Irritable Bowel Syndrome
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Malabsorption Syndromes
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Pancreatitis (Acute and Chronic)
Practice Questions
Gastrointestinal Bleeding
Practice Questions
Liver Diseases and Cirrhosis
Practice Questions
Viral Hepatitis
Practice Questions
Biliary Tract Disorders
Practice Questions
Gastrointestinal Motility Disorders
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Gastrointestinal Malignancies
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