Gastroenterology — MCQs
On this page
The Child-Pugh score is used for assessing the prognosis of which condition?
Nongastrointestinal complications of Crohn's disease include:
A 50-year-old male presented with acute onset of retrosternal chest pain radiating to the back, accompanied by dysphagia, regurgitation, and heartburn. The patient reported similar episodes of chest pain in the past. Barium swallow and esophageal manometric studies were performed, and the ECG was normal. Manometry revealed aperistalsis in greater than 30% of wet swallows with 20% of contractions being simultaneous, and amplitudes greater than 30 mm Hg in the distal three-fifths of the esophagus. Which of the following drugs can be used to relieve the symptoms in this condition?
Ekiri syndrome is seen in infection with which organism?
Which of the following statements is true regarding alcoholic liver disease?
A 69-year-old man presents with acute upper gastrointestinal hemorrhage after repeated vomiting. Fiberoptic gastroscopy reveals three linear mucosal tears at the gastroesophageal junction. What is the diagnosis?
All of the following statements about trientine use in Wilson's disease are true except?
Which of the following syndromes is characterized by an esophageal web with resulting dysphagia, atrophic changes in the mucous membranes of the mouth, and a hypochromic microcytic anemia?
What is the most important triad of symptoms in portal hypertension?
A man who had undergone total gastrectomy remains well for five years. Then he develops anaemia. What is the most likely cause of this anaemia?
Gastroenterology Indian Medical PG Practice Questions and MCQs
Question 141: The Child-Pugh score is used for assessing the prognosis of which condition?
- A. Chronic liver disease (Correct Answer)
- B. COPD
- C. Chronic renal failure
- D. Dilated cardiomyopathy
Explanation: The **Child-Pugh score** (also known as the Child-Turcotte-Pugh score) is a validated clinical tool used to assess the prognosis and severity of **Chronic Liver Disease (CLD)**, particularly cirrhosis [1]. It predicts the risk of complications and survival rates, helping clinicians determine the necessity of liver transplantation. ### Why Option A is Correct: The score evaluates liver function based on five parameters (mnemonic: **ABCDE**): 1. **A**lbumin (Serum) 2. **B**ilirubin (Total) 3. **C**oagulation (INR/Prothrombin Time) 4. **D**istension (Ascites) 5. **E**ncephalopathy [1] Patients are categorized into three classes: **Class A** (5–6 points; well-compensated), **Class B** (7–9 points; significant functional impairment), and **Class C** (10–15 points; decompensated/poor prognosis). ### Why Other Options are Incorrect: * **B. COPD:** Severity is assessed using the **GOLD criteria** or the **BODE index** (BMI, Obstruction, Dyspnea, Exercise capacity) [3]. * **C. Chronic Renal Failure:** Staged based on the **eGFR** (Glomerular Filtration Rate) and albuminuria levels (KDIGO classification) [4]. * **D. Dilated Cardiomyopathy:** Prognosis and functional status are typically assessed using the **NYHA Classification** or **ACC/AHA Staging**. ### High-Yield Clinical Pearls for NEET-PG: * **MELD Score:** While Child-Pugh is used for bedside prognosis, the **MELD score** (Model for End-Stage Liver Disease) is used for **organ allocation** in liver transplants [2]. It uses Bilirubin, Creatinine, and INR. * **Modified Child-Pugh:** In some contexts, the score is modified to include the etiology of the disease. * **Surgical Risk:** Child-Pugh Class C patients have an extremely high perioperative mortality rate (>80%) and are generally contraindicated for elective non-cardiac surgery.
Question 142: Nongastrointestinal complications of Crohn's disease include:
- A. Renal calculi
- B. Cholelithiasis
- C. Arthritis
- D. All of the above (Correct Answer)
Explanation: **Explanation:** Crohn’s disease is a systemic inflammatory disorder. While it primarily affects the gastrointestinal tract, up to 40% of patients experience **extraintestinal manifestations (EIMs)**. These complications occur due to shared genetic susceptibility, immune-mediated mechanisms, or as a direct consequence of intestinal pathophysiology (malabsorption). * **Arthritis (Option C):** This is the **most common** extraintestinal manifestation of Inflammatory Bowel Disease (IBD). It presents in two forms: **Peripheral arthritis** (often mirroring bowel activity) and **Ankylosing spondylitis/Sacroiliitis** (which follows a course independent of bowel disease). * **Renal Calculi (Option A):** Crohn’s disease specifically involving the ileum leads to fat malabsorption. Unabsorbed fatty acids bind to calcium, leaving oxalate free to be absorbed in the colon (**Enteric Hyperoxaluria**), resulting in **Calcium Oxalate stones**. Additionally, dehydration from diarrhea can lead to uric acid stones. * **Cholelithiasis (Option B):** Bile salts are normally reabsorbed in the terminal ileum. In Crohn’s (ileal disease or resection), the bile salt pool is depleted. This increases the lithogenicity of bile (higher cholesterol-to-bile salt ratio), leading to the formation of **cholesterol gallstones**. **Conclusion:** Since all three conditions are well-documented systemic complications of Crohn's disease, **Option D** is the correct answer. **High-Yield Clinical Pearls for NEET-PG:** * **Most common EIM:** Peripheral Arthritis. * **HLA Association:** HLA-B27 is strongly linked with Ankylosing Spondylitis in IBD patients. * **Skin Manifestations:** Erythema Nodosum (correlates with bowel activity) and Pyoderma Gangrenosum (does not correlate with bowel activity). * **Ocular:** Episcleritis (correlates with activity) and Uveitis (independent). * **Primary Sclerosing Cholangitis (PSC):** Much more common in Ulcerative Colitis than in Crohn’s disease.
Question 143: A 50-year-old male presented with acute onset of retrosternal chest pain radiating to the back, accompanied by dysphagia, regurgitation, and heartburn. The patient reported similar episodes of chest pain in the past. Barium swallow and esophageal manometric studies were performed, and the ECG was normal. Manometry revealed aperistalsis in greater than 30% of wet swallows with 20% of contractions being simultaneous, and amplitudes greater than 30 mm Hg in the distal three-fifths of the esophagus. Which of the following drugs can be used to relieve the symptoms in this condition?
- A. Sildenafil (Correct Answer)
- B. Botulinum toxin
- C. Octreotide
- D. Terlipressin
Explanation: The clinical presentation of retrosternal chest pain, dysphagia, and regurgitation, combined with specific manometric findings, points toward **Diffuse Esophageal Spasm (DES)**. **1. Why Sildenafil is Correct:** The manometric criteria for DES include simultaneous contractions (in >20% of wet swallows) and intermittent normal peristalsis. The underlying pathophysiology involves an imbalance between excitatory and inhibitory neurotransmission, leading to excessive smooth muscle contraction. **Sildenafil**, a Phosphodiesterase-5 (PDE-5) inhibitor, increases intracellular cGMP levels. This promotes nitric oxide-mediated smooth muscle relaxation in the esophagus, thereby reducing the amplitude of contractions and relieving both chest pain and dysphagia. **2. Why the Other Options are Incorrect:** * **Botulinum toxin:** While used for Achalasia Cardia to relax the Lower Esophageal Sphincter (LES) [1], it is not the first-line pharmacological choice for the diffuse muscular spasms seen in DES. * **Octreotide:** A somatostatin analogue used primarily in the management of variceal bleeding and acromegaly; it has no role in relaxing esophageal smooth muscle. * **Terlipressin:** A vasopressin analogue used for acute variceal hemorrhage and Hepatorenal Syndrome; it causes vasoconstriction and would not benefit esophageal motility disorders. **Clinical Pearls for NEET-PG:** * **DES Hallmark:** "Corkscrew" or "Rosary bead" appearance on Barium Swallow. * **Manometry:** The gold standard for diagnosis. Look for "Simultaneous, multi-peaked, high-amplitude contractions" [2,5]. * **Differential:** Always rule out cardiac causes (Normal ECG was a key clue here). * **First-line Medical Rx:** Nitrates and Calcium Channel Blockers (CCBs) are typically used first [2]; PDE-5 inhibitors like Sildenafil are effective alternatives.
Question 144: Ekiri syndrome is seen in infection with which organism?
- A. Salmonella
- B. E.coli
- C. Shigella (Correct Answer)
- D. Pseudomonas
Explanation: **Explanation:** **Ekiri Syndrome** (also known as Fulminant Encephalopathy) is a rare but lethal complication of **Shigellosis**, most commonly associated with *Shigella sonnei* and *Shigella flexneri*. It is characterized by a rapid onset of high-grade fever, seizures, and toxic encephalopathy, often occurring before the onset of significant diarrhea or dysentery [1]. **Why Shigella is correct:** The syndrome involves a sudden increase in cerebral pressure and brain edema. While the exact pathogenesis is debated, it is believed to be a combination of a host's hyper-immune response and the effects of Shiga toxins. It primarily affects children (ages 2–10) and is notorious for its high mortality rate despite minimal dehydration. **Why the other options are incorrect:** * **Salmonella:** Typically causes enteric fever (Typhoid) or gastroenteritis [1]. While it can cause neurological symptoms (Typhoid state/muttering delirium), it does not present as the specific Ekiri phenotype. * **E. coli:** Enterohemorrhagic E. coli (EHEC) is famously associated with **Hemolytic Uremic Syndrome (HUS)** [1] due to Shiga-like toxins, but not Ekiri syndrome. * **Pseudomonas:** This is an opportunistic pathogen causing pneumonia, UTI, or sepsis (Ecthyma gangrenosum), but it is not a primary cause of toxic dysentery syndromes. **High-Yield Clinical Pearls for NEET-PG:** * **Shigella species:** *S. dysenteriae* (Type 1) is the most severe; *S. sonnei* is the most common in developed countries. * **Infective Dose:** Shigella has a very low ID50 (only 10–100 organisms), making it highly contagious. * **Other Complications:** HUS (associated with *S. dysenteriae* Type 1), Reactive Arthritis (Reiter’s Syndrome), and rectal prolapse. * **Drug of Choice:** Ceftriaxone or Azithromycin (due to increasing Ciprofloxacin resistance).
Question 145: Which of the following statements is true regarding alcoholic liver disease?
- A. Gynaecomastia is a marker of the development of portal hypertension.
- B. An ALT:AST ratio >2 is typical of alcoholic liver disease.
- C. Concomitant HCV infection accelerates the development of cirrhosis. (Correct Answer)
- D. The Fagerstrom questionnaire is used to diagnose alcohol-related problems in a patient.
Explanation: ### Explanation **Correct Option: C. Concomitant HCV infection accelerates the development of cirrhosis.** Alcohol and Hepatitis C Virus (HCV) act synergistically to cause liver damage [1]. Patients with chronic HCV who consume alcohol have significantly higher rates of oxidative stress, viral replication, and accelerated fibrogenesis [3]. This leads to an earlier onset of cirrhosis and a higher risk of developing Hepatocellular Carcinoma (HCC) compared to patients with either condition alone. **Analysis of Incorrect Options:** * **Option A:** Gynaecomastia is a feature of **hyperestrogenism** (due to the liver's inability to metabolize estrogen and alcohol's direct effect on the testes). It is a sign of hepatic failure, not a specific marker for portal hypertension (which is characterized by splenomegaly, ascites, and varices). * **Option B:** In alcoholic liver disease, the **AST:ALT ratio is typically >2:1**. This occurs because alcohol causes a deficiency of pyridoxal-5'-phosphate (Vitamin B6), which is a cofactor for ALT synthesis, and alcohol induces the release of mitochondrial AST [1]. * **Option D:** The **Fagerstrom questionnaire** is used to assess **nicotine dependence**. For alcohol-related problems, the **CAGE questionnaire** or **AUDIT** (Alcohol Use Disorders Identification Test) are the standard screening tools [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Maddrey Discriminant Function (DF):** Used to assess the severity of alcoholic hepatitis. A score **>32** indicates severe disease and warrants corticosteroid therapy (Prednisolone). * **Histology:** Look for **Mallory-Denk bodies** (eosinophilic intracytoplasmic inclusions) and "chicken-wire" fibrosis (perivenular/pericellular fibrosis). * **First sign of recovery:** Normalization of the AST:ALT ratio and a decrease in GGT levels [2].
Question 146: A 69-year-old man presents with acute upper gastrointestinal hemorrhage after repeated vomiting. Fiberoptic gastroscopy reveals three linear mucosal tears at the gastroesophageal junction. What is the diagnosis?
- A. Reflux esophagitis with ulceration
- B. Barrett's esophagus
- C. Carcinoma of the esophagus
- D. Mallory-Weiss tear (Correct Answer)
Explanation: ### Explanation **Correct Option: D. Mallory-Weiss tear** The clinical presentation of hematemesis following repeated bouts of vomiting or retching is the classic hallmark of **Mallory-Weiss Syndrome (MWS)**. * **Pathophysiology:** MWS involves **longitudinal (linear) mucosal lacerations** at the gastroesophageal junction or the gastric cardia [1]. These tears are caused by a sudden increase in intra-abdominal pressure (e.g., vomiting, coughing, or straining), which leads to the stretching of the mucosa against a closed sphincter. * **Endoscopic Findings:** Gastroscopy typically reveals 1 to 3 linear tears, often located just below the Z-line. --- ### Why the other options are incorrect: * **A. Reflux esophagitis:** Presents with heartburn and dyspepsia. Endoscopy shows diffuse erythema, erosions, or circumferential ulcers, not isolated linear tears triggered by vomiting. * **B. Barrett's esophagus:** A chronic complication of GERD characterized by intestinal metaplasia (columnar epithelium). It appears as "salmon-pink" tongues of mucosa on endoscopy and does not cause acute bleeding post-vomiting. * **C. Carcinoma of the esophagus:** Usually presents with progressive dysphagia and weight loss. Endoscopy would reveal a friable mass, stricture, or malignant ulcer rather than superficial linear tears. --- ### NEET-PG High-Yield Pearls: * **Most common site:** Just distal to the squamocolumnar junction (gastric side of the GE junction). * **Risk Factors:** Alcoholism (most common), hyperemesis gravidarum, and bulimia. * **Management:** Most cases (80-90%) stop bleeding spontaneously [1]. For active bleeding, endoscopic therapy (epinephrine injection, clipping, or thermal coagulation) is the treatment of choice [1]. * **Distinction:** Do not confuse MWS with **Boerhaave Syndrome**, which is a *transmural* esophageal perforation (full thickness) leading to mediastinitis and surgical emergency.
Question 147: All of the following statements about trientine use in Wilson's disease are true except?
- A. It is less potent than penicillamine. (Correct Answer)
- B. It is used as an alternative to penicillamine in patients intolerant to penicillamine.
- C. It should not be administered within 2 hours of iron supplementation.
- D. It can cause iron deficiency anemia which is reversible by oral iron supplements.
Explanation: Wilson’s disease is a disorder of copper metabolism requiring lifelong chelation therapy. The primary agents used are D-Penicillamine and Trientine. **1. Why Option A is the Correct Answer (The "Except" Statement):** Contrary to historical belief, recent clinical studies and guidelines (such as AASLD) suggest that **Trientine is equally effective (equipotent)** to D-Penicillamine in achieving clinical improvement and copper excretion. While D-Penicillamine was traditionally the first-line agent, Trientine is now frequently used as a first-line therapy due to its superior side-effect profile. **2. Analysis of Incorrect Options:** * **Option B:** Trientine is the standard **second-line agent** for patients who develop hypersensitivity or severe side effects (like nephrotic syndrome or bone marrow suppression) to D-Penicillamine. * **Option C:** Trientine is a chelator that can bind to other metals. It should not be taken within **2 hours of iron intake**, as they will chelate each other in the gut, reducing the absorption and efficacy of both drugs. * **Option D:** Trientine can lead to **iron deficiency** by chelating dietary iron. This is a known side effect but is easily reversible with oral iron supplementation (provided the 2-hour dosing gap is maintained) [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Trientine (triethylene tetramine dihydrochloride) is a polyamine chelator that promotes cupriuresis (urinary copper excretion). * **Side Effects:** Unlike D-Penicillamine, Trientine does not cause sensitivity reactions or nephrotoxicity, but it can cause **sideroblastic anemia** or **gastritis** [1]. * **Neurological Worsening:** Both D-Penicillamine and Trientine can cause paradoxical neurological worsening upon initiation [2]; however, this risk is slightly lower with Trientine. * **Monitoring:** Treatment efficacy is monitored via 24-hour urinary copper excretion and clinical improvement.
Question 148: Which of the following syndromes is characterized by an esophageal web with resulting dysphagia, atrophic changes in the mucous membranes of the mouth, and a hypochromic microcytic anemia?
- A. Marfan's syndrome
- B. Plummer-Vinson syndrome (Correct Answer)
- C. Meckel's syndrome
- D. Sjögren's syndrome
Explanation: **Explanation:** The correct answer is **Plummer-Vinson syndrome (PVS)**, also known as Paterson-Brown-Kelly syndrome. This condition is classically defined by a clinical triad: 1. **Iron-deficiency anemia** (Hypochromic microcytic anemia). 2. **Esophageal webs** (Post-cricoid, causing painless dysphagia). 3. **Atrophic glossitis** (Smooth, red tongue due to mucosal atrophy). The underlying pathophysiology involves severe, chronic iron deficiency, which leads to the depletion of iron-dependent oxidative enzymes in the rapidly dividing cells of the esophageal mucosa, resulting in mucosal atrophy and web formation. **Analysis of Incorrect Options:** * **Marfan's syndrome:** A connective tissue disorder caused by mutations in the FBN1 gene (fibrillin-1). It presents with skeletal abnormalities (arachnodactyly), ectopia lentis, and aortic root dilation, not esophageal webs. * **Meckel's syndrome:** A rare, lethal ciliopathy characterized by a triad of occipital encephalocele, large polycystic kidneys, and postaxial polydactyly. * **Sjögren's syndrome:** An autoimmune destruction of exocrine glands (lacrimal and salivary). While it causes dry mouth (xerostomia) and dysphagia due to lack of saliva, it is not associated with esophageal webs or iron-deficiency anemia. **Clinical Pearls for NEET-PG:** * **Demographics:** Most common in middle-aged Caucasian women. * **Malignancy Risk:** PVS is a **premalignant condition**. Patients have an increased risk of developing **Squamous Cell Carcinoma** of the esophagus and pharynx (post-cricoid region). * **Physical Findings:** Look for **koilonychia** (spoon-shaped nails) and cheilosis. * **Treatment:** Iron supplementation often resolves the dysphagia; however, mechanical dilation may be required for persistent webs.
Question 149: What is the most important triad of symptoms in portal hypertension?
- A. Splenomegaly, Hepatomegaly, and Ascites
- B. Splenomegaly, Esophageal varices, and Ascites (Correct Answer)
- C. Hemorrhoids, splenomegaly, and generalized anasarca
- D. Esophageal varices, hemorrhoids, and generalized anasarca
Explanation: Portal hypertension (PHTN) is defined as a pathological increase in the portal venous pressure gradient (above 5 mmHg). The classic clinical triad consists of **Splenomegaly, Esophageal Varices, and Ascites**. [1] 1. **Splenomegaly:** This is often the first clinical sign. Increased pressure in the splenic vein leads to passive congestion and sequestration of blood cells within the spleen. 2. **Esophageal Varices:** These are the most clinically significant portosystemic collaterals. When portal pressure exceeds 10–12 mmHg, blood is diverted from the portal system to the systemic circulation via the left gastric vein to the esophageal venous plexus. [1][2] 3. **Ascites:** This occurs due to a combination of increased sinusoidal hydrostatic pressure and splanchnic vasodilation, often exacerbated by hypoalbuminemia in cirrhotic patients. [1] **Analysis of Incorrect Options:** * **Option A:** While hepatomegaly can occur in early cirrhosis or Budd-Chiari syndrome, the liver in chronic portal hypertension (cirrhosis) is typically **shrunken and nodular**, not enlarged. * **Options C & D:** While hemorrhoids (anorectal varices) are a feature of portosystemic shunting, they are less common and less clinically diagnostic than esophageal varices. **Generalized anasarca** suggests systemic issues like heart failure or nephrotic syndrome; in PHTN, fluid accumulation is typically localized to the peritoneal cavity (ascites) initially. [1] **High-Yield Clinical Pearls for NEET-PG:** * **Normal Portal Pressure:** 5–10 mmHg. * **Clinically Significant PHTN:** Gradient ≥10 mmHg (predicts varices). [1] * **Risk of Variceal Bleed:** Gradient ≥12 mmHg. * **Most common cause of PHTN (India/World):** Cirrhosis. [1] * **Caput Medusae:** Dilated veins around the umbilicus, another classic sign of portosystemic collateralization. [1]
Question 150: A man who had undergone total gastrectomy remains well for five years. Then he develops anaemia. What is the most likely cause of this anaemia?
- A. Protein deficiency
- B. Zinc deficiency
- C. Folic acid deficiency
- D. Vitamin B12 deficiency (Correct Answer)
Explanation: ### Explanation **1. Why Vitamin B12 Deficiency is the Correct Answer:** The stomach plays a critical role in Vitamin B12 absorption. Parietal cells in the gastric body and fundus secrete **Intrinsic Factor (IF)**. After a total gastrectomy, the source of IF is completely removed. Vitamin B12 (cobalamin) cannot be absorbed in the terminal ileum without binding to IF. The **five-year timeline** is the classic clinical clue. The human liver stores significant amounts of Vitamin B12 (approx. 2–5 mg), which is sufficient to meet the body's requirements for **3 to 5 years** [1]. Once these hepatic stores are exhausted post-gastrectomy, megaloblastic anemia develops. **2. Why the Other Options are Incorrect:** * **A. Protein Deficiency:** While gastrectomy affects protein digestion (loss of pepsin), it rarely presents as isolated anemia after five years. It usually manifests as weight loss or muscle wasting much earlier. * **B. Zinc Deficiency:** Zinc is primarily absorbed in the jejunum. While deficiency can occur in malabsorption syndromes, it typically presents with dermatitis, alopecia, and impaired wound healing, not primary anemia. * **C. Folic Acid Deficiency:** Unlike B12, body stores of folate are minimal (lasting only **3 to 4 months**). Anemia due to folate deficiency would likely manifest much sooner than five years if it were the primary cause [2]. **3. NEET-PG High-Yield Pearls:** * **Iron Deficiency Anemia (IDA):** This is actually the *most common* cause of anemia post-gastrectomy due to the loss of gastric acid (which converts ferric iron to the absorbable ferrous form). However, in exams, if a **long latent period (5 years)** is specified, **Vitamin B12 deficiency** is the preferred answer. * **Site of Absorption:** Remember the "Rule of B": **B**12 is absorbed in the **B**ottom (Terminal Ileum); **I**ron is absorbed in the **I**nlet (Duodenum). * **Prophylaxis:** Patients with total gastrectomy require lifelong parenteral (IM) Vitamin B12 supplementation.
Practice by Chapter
Esophageal Disorders
Practice Questions
Peptic Ulcer Disease
Practice Questions
Inflammatory Bowel Disease
Practice Questions
Irritable Bowel Syndrome
Practice Questions
Malabsorption Syndromes
Practice Questions
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
Practice Questions
Gastrointestinal Malignancies
Practice Questions
Want unlimited practice?
Get full access to all questions, explanations, and performance tracking.
Start For Free