Gastroenterology — MCQs

Which of the following statements regarding Inflammatory Bowel Disease are true and which are false? 1. Mucosal granularity is the earliest finding seen in ulcerative colitis. 2. Coomb sign is seen in UC. 3. Lead pipe colon is seen in UC. 4. Fibrosis and strictures are more common in UC. 5. Apthous ulcers are the earliest finding seen in CD.

Q190Medium

Intrahepatic perisinusoidal portal hypertension is classically caused by?

Gastroenterology Indian Medical PG Practice Questions and MCQs

Question 181: A 40-year-old patient complains of chronic abdominal pain and diarrhea, passing 22-25 stools per day, along with weight loss. On examination, the patient has mild fever and right lower quadrant tenderness. Which of the following is the most likely diagnosis?

A. Ulcerative colitis
B. Crohn disease (Correct Answer)
C. Infective enteritis
D. Mesenteric ischemia

Explanation: **Explanation:** The clinical presentation of chronic diarrhea, significant weight loss, and localized **right lower quadrant (RLQ) tenderness** in a middle-aged patient is classic for **Crohn’s Disease**. [1] **Why Crohn’s Disease is correct:** Crohn’s disease is a chronic inflammatory bowel disease (IBD) that can affect any part of the GIT but most commonly involves the **terminal ileum** and the cecum. [1] Inflammation in the terminal ileum manifests as RLQ pain (mimicking appendicitis) and malabsorption, leading to weight loss. [1] The high frequency of stools (22-25/day) and low-grade fever indicate active transmural inflammation. **Why other options are incorrect:** * **Ulcerative Colitis:** Typically presents with bloody diarrhea and tenesmus. It primarily involves the rectum and colon [2]; therefore, pain is usually localized to the **left lower quadrant**, not the right. * **Infective Enteritis:** While it causes fever and diarrhea, it is usually **acute** in onset. The "chronic" nature and significant weight loss in this vignette point toward a chronic inflammatory process rather than a self-limiting infection. * **Mesenteric Ischemia:** Acute mesenteric ischemia presents with "pain out of proportion to physical findings" and is usually seen in older patients with cardiovascular risk factors. Chronic mesenteric ischemia presents as postprandial angina, not typically with high-frequency diarrhea and fever. **High-Yield Clinical Pearls for NEET-PG:** * **Skip Lesions:** Characteristic endoscopic finding in Crohn’s (UC is continuous). * **Transmural Inflammation:** Leads to complications like fistulas, strictures, and perianal disease. * **Cobblestone Appearance:** Seen on endoscopy due to deep longitudinal ulcers. * **String Sign of Kantor:** Classic radiological finding on barium swallow due to terminal ileal narrowing. * **ASCA vs. p-ANCA:** Crohn’s is often **ASCA positive**, while UC is **p-ANCA positive**.

Question 182: Blind loop syndrome is characterized by:

A. Diarrhea
B. Deficiency of fat-soluble vitamins
C. Diagnosis by culture obtained through an intestinal tube
D. All of the above (Correct Answer)

Explanation: **Explanation:** **Blind Loop Syndrome (BLS)**, also known as **Small Intestinal Bacterial Overgrowth (SIBO)**, occurs when anatomical abnormalities (like strictures, diverticula, or surgical "blind" loops) cause stasis of intestinal contents, leading to excessive bacterial proliferation [1]. 1. **Why Option A is correct:** Bacteria (especially anaerobes) deconjugate bile salts. Deconjugated bile salts are poorly absorbed and irritate the colonic mucosa, leading to **secretory diarrhea**. Additionally, unabsorbed fats reach the colon, causing **steatorrhea** [1]. 2. **Why Option B is correct:** Bile salt deconjugation prevents the formation of micelles, which are essential for fat absorption. This leads to malabsorption of fats and **deficiency of fat-soluble vitamins (A, D, E, and K)** [1]. 3. **Why Option C is correct:** The **Gold Standard** for diagnosing SIBO/Blind Loop Syndrome is the **quantitative culture of jejunal aspirate** (obtained via an intestinal tube/endoscopy), showing a bacterial count of **>10⁵ CFU/mL** (though some guidelines now use >10³ CFU/mL) [1]. **Clinical Pearls for NEET-PG:** * **Vitamin B12 vs. Folate:** Bacteria consume Vitamin B12 (leading to **Megaloblastic anemia**), but they synthesize **Folate**. Therefore, a classic lab finding is **Low B12 and High Folate** [1]. * **Non-invasive Tests:** The **14C-Xylose breath test** is the most sensitive/specific breath test, though the **Glucose/Lactulose Hydrogen breath test** is more commonly used in practice. * **Treatment:** The mainstay of treatment is oral antibiotics (e.g., **Rifaximin**, Metronidazole, or Tetracycline) and surgical correction of the anatomical defect [1].

Question 183: Occasional severe constipation is seen in ulcerative colitis patients with which of the following conditions?

A. Backwash ileitis
B. Pancolitis
C. Proctitis (Correct Answer)
D. Left sided colitis

Explanation: In **Ulcerative Colitis (UC)**, the hallmark symptom is typically bloody diarrhea. However, when the inflammation is limited to the rectum (**Proctitis**), a paradoxical clinical presentation occurs [1]. In these patients, the inflamed rectum becomes hypersensitive and non-compliant, leading to urgency and tenesmus. Simultaneously, the proximal, non-inflamed colon undergoes a compensatory slowing of transit, leading to **proximal constipation**. This is a high-yield clinical paradox often tested in postgraduate exams. **Analysis of Options:** * **Proctitis (Correct):** Inflammation is confined to the distal 12 cm [1]. The "proximal stasis" of stool in the healthy colon above the inflamed rectum results in constipation rather than diarrhea. * **Backwash Ileitis:** This refers to inflammation of the terminal ileum in patients with pancolitis. It is associated with more severe disease and typically presents with significant diarrhea and malabsorption, not constipation. * **Pancolitis:** Inflammation involves the entire colon up to the cecum [1]. This leads to a total loss of water absorption and significant colonic motility, resulting in severe, frequent bloody diarrhea. * **Left-sided Colitis:** Inflammation extends up to the splenic flexure. While less severe than pancolitis, the extent of mucosal involvement is usually sufficient to cause loose stools and frequent evacuations. **NEET-PG Clinical Pearls:** * **Paradoxical Constipation:** Always suspect distal proctitis if a UC patient complains of constipation. * **Treatment Note:** In proctitis, topical therapy (suppositories or foams) is the first-line treatment. * **Lead Pipe Appearance:** A classic radiologic sign of chronic UC due to loss of haustrations (most common in extensive colitis). * **Smoking Paradox:** Unlike Crohn’s disease (where smoking worsens the condition), smoking is often protective in UC, and disease may flare upon smoking cessation.

Question 184: Which hepatitis virus is notorious for causing chronic hepatitis evolving to cirrhosis?

A. HCV (Correct Answer)
B. HBV
C. HEV
D. HAV

Explanation: **Explanation:** The correct answer is **HCV (Hepatitis C Virus)**. The hallmark of HCV infection is its high propensity for chronicity. Unlike other hepatitis viruses, approximately **75%–85%** of individuals infected with HCV fail to clear the virus and develop chronic infection. Over a period of 20 years, about 20% of these chronic cases progress to **cirrhosis**, which significantly increases the risk of Hepatocellular Carcinoma (HCC). **Analysis of Options:** * **HBV (Hepatitis B Virus):** While HBV is a major cause of chronic hepatitis and cirrhosis worldwide, the rate of chronicity in adults is relatively low (only **5%–10%**). It is more notorious for causing cirrhosis in neonatal transmissions (90% chronicity). * **HEV (Hepatitis E Virus):** This is typically an acute, self-limiting infection spread via the fecal-oral route. It does not cause chronic hepatitis in immunocompetent individuals, though it is notorious for high mortality in **pregnant women**. * **HAV (Hepatitis A Virus):** HAV causes only acute hepatitis and **never** progresses to a chronic state or cirrhosis. **High-Yield NEET-PG Pearls:** * **Most common indication for liver transplant:** HCV-induced cirrhosis [1]. * **HCV Screening:** Anti-HCV antibody is the screening test; **HCV-RNA** (PCR) is the gold standard for confirming active infection [1]. * **Extrahepatic manifestations of HCV:** Mixed cryoglobulinemia, Membranoproliferative glomerulonephritis (MPGN), and Porphyria cutanea tarda. * **Rule of 80s for HCV:** 80% become chronic, 80% are asymptomatic, and (historically) 80% were genotype 1 [1].

Question 185: Plummer-Vinson syndrome is characterized by:

A. Iron-deficiency anemia (Correct Answer)
B. Aplastic anemia
C. Vitamin deficiency
D. Increased hemoglobin

Explanation: **Explanation:** **Plummer-Vinson Syndrome (PVS)**, also known as Paterson-Brown-Kelly syndrome, is a rare clinical entity classically defined by a triad of symptoms. The correct answer is **Iron-deficiency anemia (IDA)**, which is the primary hematological hallmark of this condition [1]. 1. **Why Option A is correct:** The underlying pathophysiology of PVS involves chronic, severe iron deficiency. This deficiency leads to the formation of **esophageal webs** (thin, mucosal folds in the upper esophagus) and **atrophic glossitis**. The iron deficiency is thought to cause mucosal degeneration because iron is a vital cofactor for many oxidative enzymes in the rapidly dividing cells of the esophageal mucosa [1]. 2. **Why other options are incorrect:** * **Option B (Aplastic anemia):** This involves bone marrow failure and pancytopenia, which is unrelated to the mucosal changes or iron metabolism seen in PVS. * **Option C (Vitamin deficiency):** While some vitamin deficiencies (like B12) can cause glossitis, they do not lead to the formation of esophageal webs characteristic of PVS. * **Option D (Increased hemoglobin):** PVS is associated with microcytic hypochromic anemia [2]; therefore, hemoglobin levels are significantly decreased, not increased. **Clinical Pearls for NEET-PG:** * **The Classic Triad:** 1. Iron-deficiency anemia, 2. Dysphagia (painless, for solids), 3. Esophageal webs. * **Physical Findings:** Look for **Koilonychia** (spoon-shaped nails), cheilosis, and a "beefy red" tongue (atrophic glossitis). * **Demographics:** Most commonly affects middle-aged post-menopausal women [2]. * **Malignancy Risk:** PVS is a **premalignancy condition**. It significantly increases the risk of **Squamous Cell Carcinoma** of the esophagus and pharynx. * **Diagnosis:** Best visualized using a **Barium Swallow** (lateral view) or upper GI endoscopy.

Question 186: Spider naevi can occur in which of the following conditions?

A. Rheumatoid arthritis
B. Cirrhosis of the liver
C. Pregnancy
D. All of the above (Correct Answer)

Explanation: **Explanation:** Spider naevi (also known as spider angiomas) are vascular lesions characterized by a central arteriole with radiating capillary "legs." The primary underlying mechanism for their formation is **hyperestrogenism** (elevated estrogen levels), which leads to the dilation of cutaneous arterioles. * **Cirrhosis of the Liver:** This is the most common association. In chronic liver disease, the liver's ability to metabolize and clear circulating estrogens (and androstenedione, which peripheral tissues convert to estrogen) is impaired. This leads to systemic vasodilation and the characteristic spider naevi, typically found in the distribution of the superior vena cava (face, neck, and upper chest). * **Pregnancy:** High levels of circulating estrogen during pregnancy frequently cause spider naevi. These are physiological in this context and usually disappear postpartum. * **Rheumatoid Arthritis (RA):** Though less common than in liver disease, spider naevi can occur in RA. The mechanism is thought to be related to the underlying inflammatory state and potential alterations in steroid hormone metabolism. **Clinical Pearls for NEET-PG:** 1. **The "Blanch" Test:** Pressing on the central body of a spider naevus causes the entire lesion to blanch (disappear); it refills from the center outward upon release. 2. **Distribution:** They are almost always found above the nipple line (superior vena cava distribution). 3. **Thyrotoxicosis:** This is another high-yield condition associated with spider naevi due to increased sex hormone-binding globulin (SHBG) levels. 4. **Diagnostic Significance:** While one or two may be found in healthy individuals, the presence of multiple spider naevi is highly suggestive of underlying pathology, most notably liver cirrhosis.

Question 187: A patient is admitted to the hospital with complaints of nausea, vomiting, diarrhoea, and severe abdominal pain. Which of the following would immediately alert the nurse that the patient has bleeding from the GI tract?

A. Complete blood count.
B. Guaiac test. (Correct Answer)
C. Vital signs.
D. Abdominal girth.

Explanation: **Explanation:** The **Guaiac test** (Fecal Occult Blood Test) is the most direct and immediate method to confirm the presence of blood in the gastrointestinal (GI) tract when it is not visible to the naked eye. It utilizes a chemical reaction (peroxidation of guaiac by hemoglobin) to detect heme. In a patient presenting with non-specific GI symptoms like nausea, vomiting, and pain, a positive guaiac test provides immediate objective evidence of mucosal injury or active bleeding. **Analysis of Incorrect Options:** * **A. Complete Blood Count (CBC):** While a CBC measures hemoglobin and hematocrit, it is not an immediate indicator of acute bleeding. In the early stages of a GI bleed, the hematocrit may remain normal because the patient loses whole blood (plasma and RBCs proportionately). It takes several hours for compensatory fluid shifts to occur and reflect a drop in hemoglobin. * **C. Vital Signs:** Tachycardia and hypotension are signs of **hemodynamic instability** or shock [2]. While they can occur due to massive GI bleeding, they are non-specific and can also be caused by dehydration (from vomiting/diarrhea) or sepsis. They do not confirm the *source* of the problem as GI bleeding. * **D. Abdominal Girth:** This is used to monitor ascites or bowel distension (e.g., in intestinal obstruction or perforation), but it is not a sensitive or specific indicator of GI bleeding. **NEET-PG High-Yield Pearls:** * **Melena** (black tarry stools) typically indicates an Upper GI bleed (above the Ligament of Treitz), requiring at least 50–100 ml of blood loss [2]. * **Hematochezia** (bright red blood per rectum) usually signifies a Lower GI bleed but can occur in massive Upper GI bleeds with rapid transit [1]. * **False Positives in Guaiac Test:** Can be caused by the ingestion of red meat, peroxidase-rich vegetables (broccoli, radish), or certain drugs (NSAIDs). * **BUN/Creatinine Ratio:** A ratio **>30:1** is highly suggestive of an Upper GI bleed due to the breakdown of blood proteins in the gut and subsequent absorption of urea.

Question 188: The hepatocellular pattern of drug-induced liver injury (DILI) is defined by which of the following criteria?

A. Aspartate aminotransferase (AST) greater than 3 times the upper limit of normal
B. Alanine aminotransferase (ALT)/Alkaline phosphatase (ALP) ratio more than 5 (Correct Answer)
C. Alanine aminotransferase (ALT) and Alkaline phosphatase (ALP) more than 3 times the upper limit of normal
D. Alanine aminotransferase (ALT)/Alkaline phosphatase (ALP) ratio between 2-5

Explanation: ### Explanation Drug-Induced Liver Injury (DILI) is categorized into three patterns—**Hepatocellular, Cholestatic, or Mixed**—based on the **R-value**. The R-value is the ratio of the patient's ALT to the upper limit of normal (ULN), divided by the patient's ALP to its ULN. [1] **Formula:** $R = \frac{(ALT \div ALT_{ULN})}{(ALP \div ALP_{ULN})}$ #### 1. Why Option B is Correct The **Hepatocellular pattern** is defined by an **R-value > 5**. This indicates that the magnitude of hepatocyte necrosis (reflected by ALT elevation) significantly outweighs the evidence of cholestasis (reflected by ALP elevation) [1]. Common drugs causing this pattern include Paracetamol, Isoniazid, and Rifampicin [3]. #### 2. Analysis of Incorrect Options * **Option A:** While AST/ALT > 3x ULN is a common threshold for identifying liver injury, it does not define the *pattern* of injury. * **Option C:** Simultaneous elevation of both enzymes does not categorize the injury; the relative ratio (R-value) is the diagnostic standard [1]. * **Option D:** An R-value between **2 and 5** defines a **Mixed pattern** of liver injury. If the R-value is **< 2**, it is defined as a **Cholestatic pattern** (e.g., injury from Amoxicillin-Clavulanate) [2]. #### 3. Clinical Pearls for NEET-PG * **Hy’s Law:** A patient with DILI who has hepatocellular injury (ALT > 3x ULN) AND jaundice (Total Bilirubin > 2x ULN) without other causes has a 10-50% mortality rate. * **Most common cause of DILI (Global):** Amoxicillin-Clavulanate (typically cholestatic/mixed) [2]. * **Most common cause of Acute Liver Failure (DILI):** Acetaminophen (Paracetamol) [3]. * **R-value Calculation:** Always use the first set of abnormal labs available during the acute presentation to calculate the R-value.

Question 189: Which of the following statements regarding Inflammatory Bowel Disease are true and which are false? 1. Mucosal granularity is the earliest finding seen in ulcerative colitis. 2. Coomb sign is seen in UC. 3. Lead pipe colon is seen in UC. 4. Fibrosis and strictures are more common in UC. 5. Apthous ulcers are the earliest finding seen in CD.

A. 1. True, 2. False, 3. True, 4. False, 5. True (Correct Answer)
B. 1. True, 2. False, 3. False, 4. True, 5. False
C. 1. False, 2. True, 3. True, 4. False, 5. True
D. 1. True, 2. False, 3. False, 4. False, 5. False

Explanation: This question tests the ability to differentiate between the clinical and radiological features of **Ulcerative Colitis (UC)** and **Crohn’s Disease (CD)**, a high-yield topic for NEET-PG [1]. ### **Analysis of Statements:** 1. **Mucosal Granularity (True):** In UC, the inflammation is limited to the mucosa and submucosa [1]. The earliest endoscopic sign is the loss of the normal vascular pattern and the appearance of a fine, sandpaper-like **granularity**. 2. **Comb Sign (False):** The "Comb Sign" refers to the engorgement of the vasa recta (mesenteric vessels), which is a characteristic radiological finding of **Crohn’s Disease**, not UC. It indicates active, transmural inflammation. 3. **Lead Pipe Colon (True):** Chronic UC leads to the loss of haustral folds, shortening of the colon, and mucosal thickening [1], resulting in a smooth, featureless appearance on barium enema known as the **"Lead Pipe"** appearance. 4. **Fibrosis and Strictures (False):** These are hallmarks of **Crohn’s Disease** because the inflammation is **transmural** (full-thickness) [1]. UC is superficial; therefore, significant fibrosis and strictures are rare (if a stricture is found in UC, one must rule out malignancy). 5. **Aphthous Ulcers (True):** Small, superficial "punched-out" ulcers (aphthous ulcers) are the **earliest endoscopic sign** of Crohn’s Disease, often appearing against a background of normal-looking mucosa (skip lesions). ### **High-Yield Clinical Pearls for NEET-PG:** * **UC:** Always involves the rectum (proctitis); continuous lesions; "Backwash ileitis" can occur; increased risk of Primary Sclerosing Cholangitis (PSC) [1]. * **CD:** Rectal sparing; transmural inflammation; "Cobblestone" appearance; "String sign of Kantor" (terminal ileum stricture); non-caseating granulomas are pathognomonic [1]. * **Serology:** p-ANCA is associated with UC; ASCA is associated with CD.

Question 190: Intrahepatic perisinusoidal portal hypertension is classically caused by?

A. Alcoholic hepatitis
B. Schistosomiasis (Correct Answer)
C. Budd-Chiari syndrome
D. All of the above

Explanation: **Explanation:** Portal hypertension is classified based on the anatomical site of resistance to blood flow relative to the hepatic sinusoids: **Pre-hepatic, Intra-hepatic (Presinusoidal, Sinusoidal, Postsinusoidal), and Post-hepatic.** **Why Schistosomiasis is correct:** Schistosomiasis (specifically *S. mansoni* and *S. japonicum*) is the classic cause of **Intrahepatic Presinusoidal** portal hypertension [1]. The parasite eggs lodge in the small terminal venules of the portal vein within the liver, triggering a granulomatous reaction and "pipestem" fibrosis. Because the obstruction occurs before the blood reaches the sinusoids, the wedged hepatic venous pressure (WHVP) remains normal despite elevated portal pressure [1]. **Analysis of Incorrect Options:** * **Alcoholic Hepatitis:** This is the prototype for **Intrahepatic Sinusoidal** portal hypertension. Alcohol-induced damage and subsequent cirrhosis lead to architectural distortion and collagen deposition within the Space of Disse (sinusoids). * **Budd-Chiari Syndrome:** This is a **Post-hepatic** (or Intrahepatic Postsinusoidal) cause. It results from the obstruction of hepatic venous outflow (at the level of large hepatic veins or the IVC) [3], leading to severe congestion and hepatomegaly. **High-Yield NEET-PG Pearls:** 1. **Non-Cirrhotic Portal Fibrosis (NCPF):** Another common cause of intrahepatic presinusoidal hypertension in India. 2. **WHVP vs. FHVP:** In presinusoidal causes (like Schistosomiasis), the Wedged Hepatic Venous Pressure (WHVP) is normal. In sinusoidal causes (like Cirrhosis), the WHVP is elevated [4]. 3. **Extrahepatic Pre-hepatic:** Portal vein thrombosis is the most common cause in this category [2]. 4. **Clinical Sign:** Schistosomiasis typically presents with significant splenomegaly and variceal bleeding but preserved liver function (normal albumin/INR) until late stages [1].

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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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