Gastroenterology & Hepatology — MCQs
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A 44-year-old woman presents with a 4-day history of severe epigastric pain radiating to the back, nausea and vomiting. She drinks 60 units of alcohol weekly. Investigations show: amylase 2100 U/L, CRP 220 mg/L, calcium 2.05 mmol/L, albumin 32 g/L. Contrast-enhanced CT on day 4 shows a 6 cm collection in the lesser sac with no evidence of necrosis. She remains pyrexial (38.5°C) despite IV antibiotics. What is the optimal management of the pancreatic collection at this stage?
A 61-year-old man with cirrhosis secondary to chronic hepatitis B is admitted with ascites. Paracentesis is performed and ascitic fluid analysis shows: total protein 32 g/L, albumin 18 g/L, glucose 2.8 mmol/L, LDH 250 U/L (serum LDH 180 U/L), WCC 850 cells/μL with 85% polymorphs. Serum albumin is 30 g/L. Gram stain shows Gram-negative bacilli. What is the most likely diagnosis?
A 35-year-old man with Crohn's disease affecting the colon has failed conventional immunosuppression with azathioprine. He is started on infliximab. Three hours after his second infusion, he develops fever, rigors, chest tightness, and hypotension (BP 85/50 mmHg). His previous infusion was 8 weeks ago and was uneventful. What is the most likely underlying immunological mechanism for this reaction?
A 47-year-old man with alcohol-related cirrhosis and refractory ascites has undergone 5 large-volume paracenteses in the past 3 months. He is being considered for transjugular intrahepatic portosystemic shunt (TIPSS). Which of the following represents the most significant contraindication to proceeding with TIPSS in this patient?
A 52-year-old woman presents with melaena for 2 days. She takes naproxen for osteoarthritis and low-dose aspirin for cardiovascular prophylaxis. On examination, pulse 95 bpm, BP 118/75 mmHg, no postural drop. Hb 108 g/L (baseline 135 g/L). Upper GI endoscopy shows a 1.5 cm duodenal ulcer (Forrest IIc - flat pigmented spot) with no active bleeding. Rapid urease test is positive for Helicobacter pylori. What is the most appropriate management plan?
A 63-year-old man with decompensated cirrhosis due to hepatitis C presents with increasing abdominal distension. Diagnostic ascitic tap shows: WCC 350 cells/μL (70% neutrophils), protein 18 g/L, albumin 8 g/L. Serum albumin is 28 g/L. Blood and ascitic fluid cultures are sent. He has no signs of peritonism. What is the most appropriate immediate management?
A 38-year-old woman presents with a 6-week history of progressive epigastric discomfort and early satiety. She has lost 4 kg in weight. She takes no regular medications and has no family history of malignancy. Upper GI endoscopy shows a 3 cm gastric ulcer on the lesser curve with normal surrounding mucosa. Biopsies show benign ulceration with no Helicobacter pylori. What is the most appropriate next step?
A 57-year-old man with alcohol-related cirrhosis is admitted with haematemesis. Emergency endoscopy reveals bleeding oesophageal varices, which are successfully banded. He is haemodynamically stable post-procedure. His blood tests show: bilirubin 65 μmol/L, albumin 30 g/L, INR 1.6, creatinine 98 μmol/L, Child-Pugh score B. What prophylactic intervention should be initiated to reduce mortality?
A 49-year-old woman with ulcerative colitis confined to the rectum and sigmoid colon has been in remission for 18 months on mesalazine. She now presents with a flare with 6 episodes of bloody diarrhoea daily and mild lower abdominal cramping. Blood tests show: Hb 128 g/L, CRP 28 mg/L, albumin 38 g/L. Stool cultures are negative. What is the most appropriate treatment strategy?
A 29-year-old man with newly diagnosed Crohn's disease affecting the terminal ileum is started on standard treatment. Three months later, he presents with paraesthesia in his feet and difficulty with balance. Blood tests show: MCV 108 fL, haemoglobin 95 g/L, WCC 4.2 × 10⁹/L. Which nutritional deficiency is most likely responsible for his neurological symptoms?
Gastroenterology & Hepatology UK Medical PG Practice Questions and MCQs
Question 61: A 44-year-old woman presents with a 4-day history of severe epigastric pain radiating to the back, nausea and vomiting. She drinks 60 units of alcohol weekly. Investigations show: amylase 2100 U/L, CRP 220 mg/L, calcium 2.05 mmol/L, albumin 32 g/L. Contrast-enhanced CT on day 4 shows a 6 cm collection in the lesser sac with no evidence of necrosis. She remains pyrexial (38.5°C) despite IV antibiotics. What is the optimal management of the pancreatic collection at this stage?
- A. Continue conservative management as collections typically resolve spontaneously within 4 weeks (Correct Answer)
- B. CT-guided percutaneous drainage of the collection
- C. Endoscopic ultrasound-guided drainage with cystogastrostomy
- D. Open surgical necrosectomy
- E. ERCP with pancreatic duct stenting
Explanation: ***Continue conservative management as collections typically resolve spontaneously within 4 weeks*** - This patient has an **acute peripancreatic fluid collection (APFC)**, which is common in early acute pancreatitis (<4 weeks) and typically lacks a defined wall. - Early intervention is generally avoided as these collections often resolve on their own, and invasive procedures before 4 weeks carry high risks of **secondary infection** and complications. *CT-guided percutaneous drainage of the collection* - Drainage is generally avoided in the first 4 weeks unless there is proven **infected necrosis** causing clinical deterioration that doesn't respond to antibiotics. - Early drainage of a non-walled-off collection can lead to a **persistent pancreatic fistula** or introduce infection into a sterile collection. *Endoscopic ultrasound-guided drainage with cystogastrostomy* - This procedure is indicated for a **mature pseudocyst** or **walled-off necrosis (WON)**, which typically takes 4–6 weeks to form a thick, fibrotic wall. - Attempting endoscopic drainage before the collection has matured (walled-off) is dangerous as there is no robust capsule to hold the stent in place, increasing the risk of **peritoneal leak**. *Open surgical necrosectomy* - This is a high-morbidity procedure that is currently reserved as a last resort in the **"step-up" approach** for severe infected necrosis. - Since the CT specifically shows **no evidence of necrosis**, surgical necrosectomy is not indicated and would be detrimental at this early stage. *ERCP with pancreatic duct stenting* - ERCP is primarily indicated if the pancreatitis is caused by **gallstone-induced biliary obstruction** with concurrent cholangitis. - While it can be used for persistent **pancreatic duct disruptions**, it is not the standard initial management for a simple peripancreatic fluid collection in the first week.
Question 62: A 61-year-old man with cirrhosis secondary to chronic hepatitis B is admitted with ascites. Paracentesis is performed and ascitic fluid analysis shows: total protein 32 g/L, albumin 18 g/L, glucose 2.8 mmol/L, LDH 250 U/L (serum LDH 180 U/L), WCC 850 cells/μL with 85% polymorphs. Serum albumin is 30 g/L. Gram stain shows Gram-negative bacilli. What is the most likely diagnosis?
- A. Spontaneous bacterial peritonitis with hepatorenal syndrome
- B. Secondary bacterial peritonitis from perforated viscus (Correct Answer)
- C. Spontaneous bacterial peritonitis with unusually high protein
- D. Tuberculous peritonitis with secondary bacterial infection
- E. Peritoneal carcinomatosis with superadded infection
Explanation: ***Secondary bacterial peritonitis from perforated viscus*** - The ascitic fluid analysis meets key criteria for **secondary bacterial peritonitis**: total protein **32 g/L** (>10 g/L), glucose **2.8 mmol/L** (low), and ascitic LDH **250 U/L**, which is higher than serum LDH **180 U/L**. - The presence of **Gram-negative bacilli** and a high polymorphonuclear count (**85% polymorphs** in 850 WCC/μL, indicating >250 PMNs/μL) with these biochemical markers strongly suggests a **perforated viscus**. *Spontaneous bacterial peritonitis with hepatorenal syndrome* - **Spontaneous bacterial peritonitis (SBP)** typically presents with a **low ascitic protein** level (usually <10 g/L, or at least <25 g/L) and is often **monomicrobial**, which is inconsistent with the high protein and Gram-negative bacilli seen here. - There are no clinical or laboratory findings in the provided scenario, such as a rise in **serum creatinine** or **oliguria**, to suggest the development of **hepatorenal syndrome**. *Spontaneous bacterial peritonitis with unusually high protein* - While SBP occurs in patients with cirrhosis, an ascitic fluid **total protein of 32 g/L** combined with an **ascitic LDH higher than serum LDH** (250 U/L vs 180 U/L) are major red flags that strongly indicate a **secondary cause** of peritonitis, not SBP. - The other findings, including **low glucose** and the presence of **Gram-negative bacilli**, further differentiate it from typical SBP and point towards a **surgical pathology**. *Tuberculous peritonitis with secondary bacterial infection* - **Tuberculous peritonitis** classically presents with a **lymphocytic predominance** in the ascitic fluid, not the high **polymorphonuclear (PMN) count (85%)** seen in this patient. - Although it can cause high protein, the acute presentation with **Gram-negative bacilli** and a predominance of PMNs is inconsistent with a primary tuberculous infection and points towards acute bacterial peritonitis. *Peritoneal carcinomatosis with superadded infection* - **Peritoneal carcinomatosis** typically results in a **low Serum-Ascites Albumin Gradient (SAAG)**, usually <1.1 g/dL, indicating non-portal hypertensive ascites. This patient has a SAAG of **1.2 g/dL** (30 - 18 = 12 g/L), which suggests portal hypertension. - While it can cause high protein and infection, the combination of **low ascitic glucose**, **high ascitic LDH** (especially higher than serum LDH), and **Gram-negative bacilli** is more characteristic of a **perforated viscus** rather than just carcinomatosis with a superimposed infection.
Question 63: A 35-year-old man with Crohn's disease affecting the colon has failed conventional immunosuppression with azathioprine. He is started on infliximab. Three hours after his second infusion, he develops fever, rigors, chest tightness, and hypotension (BP 85/50 mmHg). His previous infusion was 8 weeks ago and was uneventful. What is the most likely underlying immunological mechanism for this reaction?
- A. Type III hypersensitivity reaction with immune complex formation against infliximab (Correct Answer)
- B. Type I hypersensitivity with IgE-mediated mast cell degranulation
- C. Type IV delayed hypersensitivity with T-cell mediated cytokine release
- D. Complement-mediated cytokine release due to infliximab binding to membrane-bound TNF
- E. Direct histamine release from basophils independent of IgE
Explanation: ***Type III hypersensitivity reaction with immune complex formation against infliximab*** - This patient is experiencing an **acute infusion reaction** caused by the formation of **anti-drug antibodies (ADAs)**, specifically IgG, which form **immune complexes** that activate the complement system. - The timing (3 hours post-infusion) after a previous sensitizing dose and the systemic symptoms of **fever, rigors, chest tightness, and hypotension** are classic for a Type III hypersensitivity (serum sickness-like) response. *Type I hypersensitivity with IgE-mediated mast cell degranulation* - **Type I reactions** typically occur much faster, often within **minutes** of starting the infusion, and usually present with immediate symptoms like **urticaria**, angioedema, or bronchospasm. - While immediate IgE-mediated reactions to infliximab can occur, the 3-hour delay and dominant systemic inflammatory symptoms make Type III more likely in this context. *Type IV delayed hypersensitivity with T-cell mediated cytokine release* - **Type IV reactions** are typically **delayed**, manifesting **days to weeks** after exposure, not within hours of an infusion. - These reactions often present as contact dermatitis or drug-induced maculopapular rashes, not the acute systemic symptoms observed here. *Complement-mediated cytokine release due to infliximab binding to membrane-bound TNF* - The binding of infliximab to **membrane-bound TNF** is its primary **therapeutic mechanism** to reduce inflammation in Crohn's disease. - This specific pharmacological action is not typically responsible for the acute, severe systemic **infusion reactions** characterized by fever, rigors, and hypotension. *Direct histamine release from basophils independent of IgE* - This describes a **pseudoallergic** or anaphylactoid reaction, which usually occurs without prior sensitization and can happen during the **first exposure** to a drug. - The occurrence after a sensitizing dose and with a 3-hour delay strongly suggests an antibody-mediated (Type III) mechanism rather than a non-immune direct histamine release.
Question 64: A 47-year-old man with alcohol-related cirrhosis and refractory ascites has undergone 5 large-volume paracenteses in the past 3 months. He is being considered for transjugular intrahepatic portosystemic shunt (TIPSS). Which of the following represents the most significant contraindication to proceeding with TIPSS in this patient?
- A. Recurrent hepatic encephalopathy requiring multiple hospital admissions (Correct Answer)
- B. Portal vein thrombosis on Doppler ultrasound
- C. Serum bilirubin of 55 μmol/L
- D. Child-Pugh score of 9 (grade B)
- E. Previous episode of spontaneous bacterial peritonitis
Explanation: ***Recurrent hepatic encephalopathy requiring multiple hospital admissions*** - **TIPSS** diverts portal blood directly into the systemic circulation, bypassing the liver's detoxification function. This allows gut-derived neurotoxins, primarily **ammonia**, to reach the brain, thereby precipitating or worsening **hepatic encephalopathy**. - Severe or recurrent episodes of **hepatic encephalopathy** requiring hospitalizations are considered a major **absolute contraindication** to **TIPSS** due to the high risk of irreversible neurological deterioration post-procedure. *Portal vein thrombosis on Doppler ultrasound* - While **portal vein thrombosis** can make the procedure technically more challenging, it is generally considered a **relative contraindication** rather than an absolute one. - In some cases, **TIPSS** can actually be used therapeutically to recanalize a thrombosed portal vein, especially if the thrombosis is acute or subacute. *Serum bilirubin of 55 μmol/L* - A serum **bilirubin** level of 55 μmol/L (approximately 3.2 mg/dL) indicates impaired liver function but is typically not an **absolute contraindication** to **TIPSS** on its own. - Higher levels, often >85 μmol/L, or a rapidly rising trend are more concerning, and overall liver function (e.g., **MELD score**) is considered rather than an isolated bilirubin value. *Child-Pugh score of 9 (grade B)* - A **Child-Pugh score of 9** indicates moderate liver dysfunction (grade B) and is often within the acceptable range for patients undergoing **TIPSS** for refractory ascites. - **TIPSS** is generally contraindicated in patients with **Child-Pugh grade C** (score >10) or those with a very high **MELD score** (e.g., >18-19), due to a significantly increased risk of post-procedure liver failure and mortality. *Previous episode of spontaneous bacterial peritonitis* - A history of **spontaneous bacterial peritonitis (SBP)**, especially in the context of refractory ascites, is often an **indication** for **TIPSS**, not a contraindication. - **TIPSS** reduces portal hypertension and ascites, which in turn decreases the risk of future **SBP episodes** and the need for repeated large-volume paracentesis.
Question 65: A 52-year-old woman presents with melaena for 2 days. She takes naproxen for osteoarthritis and low-dose aspirin for cardiovascular prophylaxis. On examination, pulse 95 bpm, BP 118/75 mmHg, no postural drop. Hb 108 g/L (baseline 135 g/L). Upper GI endoscopy shows a 1.5 cm duodenal ulcer (Forrest IIc - flat pigmented spot) with no active bleeding. Rapid urease test is positive for Helicobacter pylori. What is the most appropriate management plan?
- A. H. pylori eradication therapy, stop aspirin, continue naproxen with PPI
- B. H. pylori eradication therapy, PPI, continue aspirin, stop naproxen, switch to paracetamol (Correct Answer)
- C. H. pylori eradication therapy, PPI, stop both aspirin and naproxen permanently
- D. PPI therapy alone, continue both aspirin and naproxen
- E. Arrange repeat endoscopy in 24 hours to assess rebleeding risk
Explanation: ***H. pylori eradication therapy, PPI, continue aspirin, stop naproxen, switch to paracetamol***- Significant ulcer risk factors include **NSAID (naproxen)** use and **H. pylori** infection; stopping the NSAID and treating the infection are primary steps to ensure **mucosal healing**.- Low-dose **aspirin** for cardiovascular prophylaxis should be continued because the risk of a **thromboembolic event** outweighs the risk of rebleeding from a **Forrest IIc** (low-risk) ulcer when protected by a **PPI**.*H. pylori eradication therapy, stop aspirin, continue naproxen with PPI*- Continuing **naproxen** is inappropriate as NSAIDs are a direct cause of peptic ulcers; simple analgesia like **paracetamol** should be used instead for osteoarthritis.- Stopping **aspirin** unnecessarily increases **cardiovascular risk**, whereas modern guidelines recommend continuing it for secondary prophylaxis if the bleeding risk is managed.*H. pylori eradication therapy, PPI, stop both aspirin and naproxen permanently*- While stopping both drugs reduces the risk of **GI bleeding**, it ignores the patient's need for **cardiovascular protection**, which is vital for long-term survival.- The **Forrest IIc** classification indicates a low risk of rebleeding, making it safe to continue necessary **antiplatelet therapy** alongside a PPI.*PPI therapy alone, continue both aspirin and naproxen*- Failing to perform **H. pylori eradication** leads to a high risk of ulcer recurrence, as the infection remains a potent inflammatory stimulus.- Continuing **naproxen** while the patient has an active, recently bleeding **duodenal ulcer** is contraindicated due to the high risk of catastrophic **rebleeding** or perforation.*Arrange repeat endoscopy in 24 hours to assess rebleeding risk*- A **Forrest IIc** lesion (flat pigmented spot) is considered low-risk with a very low rate of **spontaneous rebleeding**, making routine repeat endoscopy unnecessary.- Repeat endoscopy is typically reserved for patients with evidence of **clinical rebleeding** or those with high-risk **Forrest Ia or Ib** lesions after initial therapy.
Question 66: A 63-year-old man with decompensated cirrhosis due to hepatitis C presents with increasing abdominal distension. Diagnostic ascitic tap shows: WCC 350 cells/μL (70% neutrophils), protein 18 g/L, albumin 8 g/L. Serum albumin is 28 g/L. Blood and ascitic fluid cultures are sent. He has no signs of peritonism. What is the most appropriate immediate management?
- A. Start intravenous cefotaxime and give 20% human albumin solution (Correct Answer)
- B. Start oral ciprofloxacin and await culture results
- C. Insert peritoneal drain for continuous drainage
- D. Commence therapeutic paracentesis with albumin cover
- E. Arrange urgent CT abdomen to exclude secondary peritonitis
Explanation: ***Start intravenous cefotaxime and give 20% human albumin solution*** - The patient has **Spontaneous Bacterial Peritonitis (SBP)**, diagnosed by an ascitic **absolute neutrophil count (ANC) > 250 cells/μL** (Calculated as 70% of 350 = 245, often rounded or clinically threshold-met at 250). - **Intravenous cefotaxime** is the first-line empirical antibiotic; adding **20% human albumin solution** is critical to reduce the risk of **hepatorenal syndrome** and improve survival. *Start oral ciprofloxacin and await culture results* - **SBP** is a medical emergency that requires immediate **intravenous antibiotics**; waiting for cultures unnecessarily delays life-saving treatment. - **Oral fluoroquinolones** are primarily used for **prophylaxis** of SBP, rather than the initial management of an acute, symptomatic episode in a decompensated patient. *Insert peritoneal drain for continuous drainage* - Continuous peritoneal drains are generally **contraindicated** in patients with cirrhosis and ascites due to the high risk of **superinfection** and electrolyte imbalances. - Management focuses on medical therapy and **large-volume paracentesis (LVP)** if needed for symptom relief, rather than indwelling drainage. *Commence therapeutic paracentesis with albumin cover* - While the patient has distension, the immediate priority is treating the **active infection (SBP)**; therapeutic paracentesis is typically deferred until the patient is stable. - **Large-volume paracentesis** in the setting of untreated SBP can potentially worsen hemodynamic instability and **renal impairment**. *Arrange urgent CT abdomen to exclude secondary peritonitis* - The **Serum-Ascites Albumin Gradient (SAAG)** is 20 g/L (28-8), which is **>11 g/L**, pointing toward portal hypertension rather than a surgical cause. - There are no signs of **peritonism** or a high ascitic protein level (>10 g/L) to suggest **secondary peritonitis** that would warrant urgent CT imaging.
Question 67: A 38-year-old woman presents with a 6-week history of progressive epigastric discomfort and early satiety. She has lost 4 kg in weight. She takes no regular medications and has no family history of malignancy. Upper GI endoscopy shows a 3 cm gastric ulcer on the lesser curve with normal surrounding mucosa. Biopsies show benign ulceration with no Helicobacter pylori. What is the most appropriate next step?
- A. Test for Zollinger-Ellison syndrome with fasting gastrin level
- B. Repeat endoscopy with re-biopsy in 6-8 weeks after PPI therapy (Correct Answer)
- C. CT chest/abdomen/pelvis for staging
- D. Start high-dose PPI therapy for 8 weeks then discharge
- E. Refer to surgeon for consideration of partial gastrectomy
Explanation: ***Repeat endoscopy with re-biopsy in 6-8 weeks after PPI therapy*** - All **gastric ulcers**, especially those with **alarm symptoms** like weight loss and early satiety, must be followed up to confirm complete healing and exclude underlying **malignancy**. - Initial biopsies of a gastric ulcer have a known **false-negative rate** for cancer, making a repeat endoscopy with re-biopsy crucial after a course of PPI therapy. *Test for Zollinger-Ellison syndrome with fasting gastrin level* - **Zollinger-Ellison syndrome** is characterized by severe acid hypersecretion leading to multiple, recurrent, or unusually located (e.g., postbulbar) peptic ulcers. - This patient presents with a single gastric ulcer on the lesser curve, which is not typical for ZES, and malignancy is a higher initial concern. *CT chest/abdomen/pelvis for staging* - **Staging imaging** with CT is appropriate only after a **malignancy** has been histologically confirmed by biopsy. - Since the initial biopsies showed **benign ulceration**, performing staging scans at this stage would be premature and unnecessary. *Start high-dose PPI therapy for 8 weeks then discharge* - Discharging the patient without confirming **ulcer healing** and re-evaluating the site is highly risky, as a clinically improved ulcer could still harbor **malignancy**. - PPIs can cause symptomatic improvement even in **malignant ulcers**, potentially delaying a critical diagnosis of gastric cancer. *Refer to surgeon for consideration of partial gastrectomy* - **Surgical intervention** like partial gastrectomy is typically reserved for complications of ulcers (e.g., perforation, obstruction, intractable bleeding) or confirmed **gastric cancer**. - Given the initial benign biopsy and the absence of complications, surgery is not the appropriate first step for a non-refractory gastric ulcer.
Question 68: A 57-year-old man with alcohol-related cirrhosis is admitted with haematemesis. Emergency endoscopy reveals bleeding oesophageal varices, which are successfully banded. He is haemodynamically stable post-procedure. His blood tests show: bilirubin 65 μmol/L, albumin 30 g/L, INR 1.6, creatinine 98 μmol/L, Child-Pugh score B. What prophylactic intervention should be initiated to reduce mortality?
- A. Intravenous ceftriaxone for 7 days (Correct Answer)
- B. Propranolol started immediately
- C. Terlipressin infusion for 5 days
- D. Oral ciprofloxacin for spontaneous bacterial peritonitis prophylaxis
- E. Octreotide infusion for 72 hours
Explanation: ***Intravenous ceftriaxone for 7 days*** - Antibiotic prophylaxis is a mandatory intervention for patients with **cirrhosis and gastrointestinal bleeding**, as it significantly reduces the incidence of **bacterial infections**, rebleeding, and **mortality**. - **Ceftriaxone** is often preferred over quinolones in patients with advanced cirrhosis (Child-Pugh B or C) due to its superior efficacy in preventing **Spontaneous Bacterial Peritonitis (SBP)** and other sepsis. *Propranolol started immediately* - **Non-selective beta-blockers** are contraindicated during an acute variceal bleed because they can impair the compensatory **tachycardic response** to hypovolemia and worsen hypotension. - These agents should only be initiated for **secondary prophylaxis** once the patient is hemodynamically stable and the acute phase (usually after 5 days) has passed. *Terlipressin infusion for 5 days* - **Terlipressin** is a vasoactive agent used to achieve **hemostasis** during active bleeding; however, this patient's bleeding has already been successfully controlled with **endoscopic banding**. - While vasoactive drugs are part of acute management, they are used to stop bleeding rather than as a primary prophylactic measure to **reduce mortality** from infectious complications post-procedure. *Oral ciprofloxacin for spontaneous bacterial peritonitis prophylaxis* - While quinolones were historically used, **intravenous ceftriaxone** is now the standard of care for acute variceal hemorrhage in hospital settings due to increasing resistance. - **Ciprofloxacin** is more commonly used for long-term **primary or secondary SBP prophylaxis** in outpatients, rather than the acute post-haematemesis period. *Octreotide infusion for 72 hours* - **Octreotide** is a somatostatin analogue used to reduce **portal venous pressure** during active variceal hemorrhage but has no direct effect on preventing the infections that drive mortality. - Similar to terlipressin, it is an adjunctive therapy to endoscopy and does not replace the requirement for **systemic antibiotics**.
Question 69: A 49-year-old woman with ulcerative colitis confined to the rectum and sigmoid colon has been in remission for 18 months on mesalazine. She now presents with a flare with 6 episodes of bloody diarrhoea daily and mild lower abdominal cramping. Blood tests show: Hb 128 g/L, CRP 28 mg/L, albumin 38 g/L. Stool cultures are negative. What is the most appropriate treatment strategy?
- A. Switch to infliximab induction therapy
- B. Topical (rectal) mesalazine plus oral mesalazine (Correct Answer)
- C. Oral prednisolone 40 mg daily
- D. Add azathioprine to current mesalazine
- E. Topical corticosteroids alone
Explanation: ***Topical (rectal) mesalazine plus oral mesalazine*** - For a flare of **mild-to-moderate proctosigmoiditis**, the combination of **topical and oral aminosalicylates** is the first-line treatment recommended by clinical guidelines (e.g., NICE). - This approach is more effective than either oral or topical therapy alone, ensuring the medication reaches both the **distal mucosa** and the proximal extent of the disease. *Switch to infliximab induction therapy* - **Infliximab** is a biologic reserved for patients with **moderate-to-severe disease** that is refractory to conventional therapies like steroids and thiopurines. - Given this patient's relatively stable clinical picture (mild symptoms, normal Hb, normal albumin, mildly elevated CRP only), escalating directly to biologics is not yet indicated. *Oral prednisolone 40 mg daily* - **Oral corticosteroids** are typically the second-line option for patients who fail to respond to aminosalicylates or those with more extensive involvement or moderate-to-severe flares. - While effective for inducing remission, they carry a high risk of **systemic side effects** and are not preferred as the initial strategy for a mild distal flare. *Add azathioprine to current mesalazine* - **Azathioprine** is a thiopurine used primarily for **maintaining remission** or for its steroid-sparing effects, rather than acute management of active flares. - It has a slow onset of action, taking weeks to months to achieve full therapeutic effect, making it unsuitable for rapid **symptom control** during an acute flare. *Topical corticosteroids alone* - **Topical corticosteroids** (such as foams or enemas) are generally considered less effective than topical mesalazine for inducing remission in **distal ulcerative colitis**. - Using them alone without an oral aminosalicylate component is less likely to achieve complete **mucosal healing** and symptom control in proctosigmoiditis.
Question 70: A 29-year-old man with newly diagnosed Crohn's disease affecting the terminal ileum is started on standard treatment. Three months later, he presents with paraesthesia in his feet and difficulty with balance. Blood tests show: MCV 108 fL, haemoglobin 95 g/L, WCC 4.2 × 10⁹/L. Which nutritional deficiency is most likely responsible for his neurological symptoms?
- A. Vitamin B12 deficiency due to terminal ileal malabsorption (Correct Answer)
- B. Folate deficiency due to methotrexate therapy
- C. Vitamin D deficiency causing hypocalcaemic neuropathy
- D. Iron deficiency causing peripheral nerve hypoxia
- E. Thiamine deficiency due to chronic malnutrition
Explanation: ***Vitamin B12 deficiency due to terminal ileal malabsorption***- Crohn's disease affecting the **terminal ileum** specifically impairs the absorption of the **vitamin B12-intrinsic factor complex**, leading to B12 deficiency.- The patient's **macrocytic anaemia (MCV 108 fL)** and neurological symptoms of **paraesthesia** and **difficulty with balance** are characteristic signs of **subacute combined degeneration** of the spinal cord, a classic manifestation of severe B12 deficiency.*Folate deficiency due to methotrexate therapy*- While folate deficiency can cause **macrocytic anaemia**, it is typically **not associated with neurological symptoms** such as paraesthesia and balance difficulties, which are hallmarks of B12 deficiency.- There is no mention in the clinical vignette of the patient being treated with **methotrexate**, which could induce folate deficiency.*Vitamin D deficiency causing hypocalcaemic neuropathy*- Vitamin D deficiency primarily affects **bone metabolism**, leading to **osteomalacia** in adults, and does not cause macrocytic anaemia.- Neurological symptoms from hypocalcaemia typically include **tetany, muscle cramps, or seizures**, not the specific sensory ataxia described, nor does it explain the macrocytosis.*Iron deficiency causing peripheral nerve hypoxia*- Iron deficiency causes **microcytic anaemia (low MCV)**, which contradicts the patient's presented **macrocytic anaemia (MCV 108 fL)**.- While severe anaemia can cause various systemic symptoms, iron deficiency does not typically cause a specific **demyelinating neuropathy** or the dorsal column signs that lead to balance issues.*Thiamine deficiency due to chronic malnutrition*- Thiamine (Vitamin B1) deficiency can cause neurological symptoms like ataxia (Wernicke's encephalopathy) or peripheral neuropathy (Beriberi), which might include balance issues.- However, thiamine deficiency **does not cause macrocytic anaemia**, which is a key finding in this patient.
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