Gastroenterology Practice Questions

Q: All are complications of ulcerative colitis, except?

Fistula formation. **Explanation:** The key to answering this question lies in understanding the depth of inflammation in Inflammatory Bowel Disease (IBD). **Why Fistula formation is the correct answer:** Fistulae are abnormal communications between two epithelial-lined surfaces. They occur when inflammation is **transmural** (involving all layers of the bowel wall). **Ulcerative Colitis (UC)** is characterized by superficial inflammation limited to the **mucosa and submucosa**. Therefore, it does not typically lead to fistula or abscess formation. In contrast, fistula formation is a hallmark complication of **Crohn’s Disease**, where inflammation is transmural. **Analysis of incorrect options:** * **Hemorrhage:** Since UC involves diffuse mucosal ulceration and vascular engorgement (friability), bloody diarrhea and significant gastrointestinal hemorrhage are very common. * **Stricture:** While less common than in Crohn’s, strictures do occur in UC. However, a stricture in UC is considered **malignant until proven otherwise**, as it often signifies underlying adenocarcinoma. * **Malignant change:** Patients with long-standing UC (usually >8–10 years) have a significantly increased risk of developing **Colorectal Carcinoma**. The risk correlates with the duration and anatomical extent of the disease (pancolitis > left-sided colitis). **High-Yield Clinical Pearls for NEET-PG:** * **Toxic Megacolon:** A life-threatening complication of UC where the colon dilates (>6 cm) due to neuromuscular paralysis. * **Extraintestinal Manifestations:** Primary Sclerosing Cholangitis (PSC) is more specifically associated with UC than Crohn’s. * **Lead Pipe Appearance:** Seen on barium enema in chronic UC due to loss of haustrations. * **Surgery:** Proctocolectomy with Ileal Pouch-Anal Anastomosis (IPAA) is the gold standard curative surgery for UC.

Q: What is true about Crigler-Najjar syndrome type II?

Inherited as a recessive trait. Crigler-Najjar Syndrome (CNS) is a rare genetic disorder characterized by non-hemolytic unconjugated hyperbilirubinemia due to a deficiency of the enzyme **UDP-glucuronosyltransferase (UGT1A1)** [1]. **1. Why Option B is Correct:** Crigler-Najjar Type II (also known as **Arias Syndrome**) is inherited as an **autosomal recessive** trait (though some rare cases show dominant inheritance with variable penetrance). It involves a partial deficiency of UGT1A1, with enzyme activity typically <10% of normal [1]. **2. Analysis of Incorrect Options:** * **Option A:** CNS Type II is associated with a deficiency of **monoglucuronides** and **diglucuronides** (conjugated bilirubin), leading to a rise in unconjugated bilirubin [2]. * **Option C:** Kernicterus (bilirubin encephalopathy) is **rare** in Type II because bilirubin levels usually stay between 6–20 mg/dL. In contrast, Kernicterus is common and often fatal in **CNS Type I**, where bilirubin levels exceed 20–50 mg/dL [1]. * **Option D:** Phenobarbital is the **mainstay of treatment** for Type II. It acts as an enzyme inducer, stimulating the residual UGT1A1 activity and reducing serum bilirubin by 25% or more [2]. In Type I, Phenobarbital has no effect because enzyme activity is completely absent [1]. **High-Yield Clinical Pearls for NEET-PG:** * **CNS Type I:** Autosomal Recessive; 0% enzyme activity; No response to Phenobarbital; Treatment: Phototherapy, Plasmapheresis, Liver Transplant [1]. * **CNS Type II:** Autosomal Recessive; <10% enzyme activity; **Responds to Phenobarbital** [1]. * **Gilbert Syndrome:** Most common hereditary hyperbilirubinemia; ~30% enzyme activity; triggered by stress/fasting [1].

Q: Which of the following can be done in obstructive jaundice?

Vitamin K injections. In obstructive jaundice, the flow of bile into the duodenum is blocked (e.g., due to gallstones or malignancy). Since bile salts are essential for the emulsification and absorption of fat-soluble vitamins (**A, D, E, and K**), their absence leads to malabsorption [1]. **Explanation of the Correct Option:** * **Vitamin K Injections:** Vitamin K is a fat-soluble vitamin required for the hepatic synthesis of clotting factors **II, VII, IX, and X**. In obstructive jaundice, the lack of intestinal bile leads to Vitamin K deficiency, resulting in a prolonged Prothrombin Time (PT) and an increased risk of bleeding. Administering parenteral (injection) Vitamin K bypasses the malabsorption issue, corrects the coagulopathy, and is a standard preoperative step before any surgical intervention in these patients [1]. **Explanation of Incorrect Options:** * **Vitamin C Injections:** Vitamin C is a water-soluble vitamin. Its absorption is independent of bile salts; therefore, deficiency is not a characteristic feature of obstructive jaundice. * **Dehydration Therapy:** Patients with obstructive jaundice are actually at high risk for **hepatorenal syndrome**. They require aggressive hydration (pre-procedure) to maintain renal perfusion and prevent acute kidney injury, rather than dehydration therapy. **High-Yield Clinical Pearls for NEET-PG:** * **Kone’s Test:** If PT improves after parenteral Vitamin K, the jaundice is **obstructive** (surgical). If PT does not improve, it suggests **parenchymal liver disease** (medical), as the liver cannot utilize the vitamin [1]. * **Courvoisier’s Law:** In the presence of jaundice, a palpable gallbladder is usually not due to stones but due to malignant obstruction (e.g., Periampullary carcinoma). * **Pruritus** in obstructive jaundice is primarily due to the deposition of bile salts in the skin.

Q: Which of the following variables does NOT predict survival in a patient with primary sclerosing cholangitis?

Presence of AMA in high titre. **Explanation:** The correct answer is **C. Presence of AMA in high titre.** **Primary Sclerosing Cholangitis (PSC)** is a chronic cholestatic liver disease characterized by fibrosing inflammation of the intrahepatic and extrahepatic bile ducts [1]. Unlike Primary Biliary Cholangitis (PBC), where **Anti-Mitochondrial Antibodies (AMA)** are a hallmark diagnostic marker (found in >95% of cases), AMA is typically **absent** in PSC [2]. Therefore, its presence or titre does not correlate with the disease process or predict survival in PSC patients. **Analysis of Incorrect Options:** * **Serum Bilirubin Level:** This is one of the most potent predictors of survival. Rising bilirubin indicates progressive cholestasis and deteriorating liver function; it is a core component of the Mayo PSC Risk Score. * **Splenomegaly:** The presence of an enlarged spleen signifies the development of portal hypertension, a late-stage complication that indicates a poorer prognosis and reduced survival. * **Histologic Stage:** Liver biopsy findings (Stages I-IV) are predictive. Advanced stages (Stage III: Septal fibrosis; Stage IV: Cirrhosis) are associated with significantly shorter survival times compared to early-stage disease. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard Diagnosis:** MRCP (shows "beaded appearance" of bile ducts). * **Strongest Association:** Approximately 70-80% of PSC patients have **Ulcerative Colitis** [1]. * **Antibody Marker:** p-ANCA is often positive in PSC (60-80%), though not specific [1]. * **Malignancy Risk:** PSC patients have a high risk of **Cholangiocarcinoma** and Colorectal Cancer. * **Mayo Risk Score Variables:** Age, Bilirubin, Albumin, AST, and history of Variceal Bleeding.

Q: A 52-year-old man presents with jaundice and extrapyramidal symptoms. An ophthalmic examination reveals a characteristic finding. What is the most appropriate treatment for this condition?

Penicillamine. **Explanation:** The clinical presentation of **jaundice** (liver involvement) and **extrapyramidal symptoms** (neurological involvement), combined with a characteristic ophthalmic finding (**Kayser-Fleischer rings**), is diagnostic of **Wilson’s Disease** (Hepatolenticular degeneration). This is an autosomal recessive disorder of copper metabolism leading to toxic accumulation of copper in the liver, brain, and cornea. **Why Penicillamine is correct:** **Penicillamine** is the drug of choice for Wilson’s Disease. It is a potent **chelating agent** that binds to copper, forming a soluble complex excreted in the urine. It also induces the synthesis of metallothionein, which sequesters copper in a non-toxic form. **Analysis of Incorrect Options:** * **A. BAL (British Anti-Lewisite/Dimercaprol):** Primarily used for acute poisoning of heavy metals like **Arsenic, Mercury, and Lead**. While it can chelate copper, it is not the first-line treatment for Wilson's due to its toxicity and the requirement for IM administration. * **C. Calcium edetate (Ca-EDTA):** The preferred chelator for **Lead poisoning**. It has poor penetration into the CNS and is not effective for copper removal. * **D. Desferrioxamine:** A specific chelating agent used for **Iron toxicity** (acute poisoning or chronic overload like Thalassemia). **High-Yield Pearls for NEET-PG:** * **Kayser-Fleischer (KF) rings:** Copper deposition in the **Descemet’s membrane** of the cornea. * **Diagnosis:** Decreased serum ceruloplasmin, increased 24-hour urinary copper excretion. * **Alternative Treatment:** **Trientine** (preferred if Penicillamine is not tolerated due to side effects like nephrotoxicity or SLE-like syndrome) and **Oral Zinc** (prevents copper absorption). * **Neurological site:** The **Putamen** (Lenticular nucleus) is the most common site of brain involvement.

Q: All of the following extraintestinal manifestations of ulcerative colitis respond to colectomy except?

Primary sclerosing cholangitis. Extraintestinal manifestations (EIMs) of Ulcerative Colitis (UC) are classified based on their relationship with bowel disease activity and their response to surgical intervention (colectomy). ### **Why Primary Sclerosing Cholangitis (PSC) is the Correct Answer** **Primary Sclerosing Cholangitis (PSC)** is the most important EIM that follows an **independent course** [1]. Its progression is not related to the severity of colonic inflammation, nor is it cured by a total proctocolectomy. Even after the colon is removed, the biliary destruction in PSC can progress to cirrhosis or cholangiocarcinoma [1]. ### **Analysis of Incorrect Options** The following EIMs typically parallel the activity of the colitis and **resolve or significantly improve** following a colectomy [2]: * **Peripheral Arthralgia (Type 1):** Large joint involvement usually mirrors bowel flares; removing the diseased colon eliminates the inflammatory trigger [2]. * **Episcleritis:** This ocular manifestation is highly correlated with intestinal disease activity and resolves when the underlying colitis is treated or surgically removed. * **Pyoderma Gangrenosum:** While its relationship with bowel activity is sometimes less predictable than Erythema Nodosum, it generally responds to the removal of the diseased colon in refractory cases [2]. ### **High-Yield Clinical Pearls for NEET-PG** * **Independent Course (Does NOT respond to colectomy):** PSC and Ankylosing Spondylitis (AS) [1]. * **Dependent Course (Responds to colectomy):** Erythema nodosum, Episcleritis, and Type 1 Peripheral Arthritis [2]. * **Most common EIM of IBD:** Arthritis (Peripheral is more common than Axial). * **PSC-UC Link:** Approximately 70-80% of patients with PSC have underlying UC, but only 5% of UC patients develop PSC [1]. PSC increases the risk of colorectal cancer even after colectomy (in the ileal pouch).

Question 1

All are complications of ulcerative colitis, except?

Accepted Answer

Fistula formation

Answer

Hemorrhage

Answer

Stricture

Answer

Malignant change

Question 2

Which of the following is NOT useful for the management of severe Clostridium difficile infection?

Accepted Answer

Neomycin enema

Answer

Intravenous metronidazole

Answer

Fecal transplant

Answer

Tigecycline

Question 3

What is the treatment of choice for Zollinger Ellison syndrome (ZES)?

Accepted Answer

Proton pump inhibitors (PPIs)

Answer

Somatostatin analogues

Answer

Streptozocin

Answer

Sucralfate

Question 4

What is true about Crigler-Najjar syndrome type II?

Accepted Answer

Inherited as a recessive trait

Answer

Associated with diglucuronide deficiency

Answer

Kernicterus is commonly seen

Answer

Phenobarbital is not useful in management

Question 5

Secretory diarrhea is not seen in which of the following conditions?

Accepted Answer

Celiac disease

Answer

Magnesium injection

Answer

Cholera

Answer

Ulcerative colitis

Question 6

Which of the following can be done in obstructive jaundice?

Accepted Answer

Vitamin K injections

Answer

Vitamin C injections

Answer

Dehydration therapy

Answer

All of the above

Question 7

Which of the following variables does NOT predict survival in a patient with primary sclerosing cholangitis?

Accepted Answer

Presence of AMA in high titre

Answer

Serum bilirubin level

Answer

Splenomegaly

Answer

Histologic stage

Question 8

Which of the following is associated with nonalcoholic steatohepatitis?

Accepted Answer

Amiodarone therapy

Answer

Thin body habitus

Answer

Phenytoin sodium therapy

Answer

Right hemicolectomy

Question 9

A 52-year-old man presents with jaundice and extrapyramidal symptoms. An ophthalmic examination reveals a characteristic finding. What is the most appropriate treatment for this condition?

Accepted Answer

Penicillamine

Answer

BAL (British Anti-Lewisite)

Answer

Calcium edetate

Answer

Desferrioxamine

Question 10

All of the following extraintestinal manifestations of ulcerative colitis respond to colectomy except?

Accepted Answer

Primary sclerosing cholangitis

Answer

Pyoderma gangrenosum

Answer

Episcleritis

Answer

Peripheral arthralgia

Gastroenterology — MCQs

Gastroenterology — MCQs

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