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MRCP PART 1 · GASTROENTEROLOGY AND HEPATOLOGY

Gastroenterology and hepatology questions
for MRCP Part 1.

Clinora has 383 gastroenterology and hepatology single best answer questions covering 366 topics. Every question explains all five options, separates the key clue from what it means and what to do next, and links to its source. Try the 5 sample questions below, then practise more for free.

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FREE SAMPLE QUESTIONS

Try 5 gastroenterology and hepatology questions

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Question 1Gallstone/cholestatic diseaseMedium

A 50-year-old woman has right upper quadrant pain, fever and jaundice. Liver function tests show a cholestatic pattern with raised bilirubin, alkaline phosphatase and gamma-glutamyl transferase. Ultrasound shows a dilated common bile duct with gallstones. What is the most likely diagnosis and immediate management priority?

  1. AAscending cholangitis; urgent antibiotics and biliary decompression (for example, ERCP)
  2. BSimple biliary colic; discharge with analgesia only
  3. CAcute pancreatitis; no antibiotics required
  4. DHepatitis A; supportive care only, no imaging needed
  5. EGallbladder cancer; palliative care referral only
Show answer and explanation

Answer: A Ascending cholangitis; urgent antibiotics and biliary decompression (for example, ERCP)

Fever, jaundice and right upper quadrant pain is Charcot's triad, and with a cholestatic picture and a dilated common bile duct containing stones it points to acute (ascending) cholangitis. Obstruction lets bile stagnate and become infected under pressure, so bacteria and endotoxin enter the blood quickly. Management is resuscitation, blood cultures and prompt broad-spectrum antibiotics covering Gram-negative organisms and anaerobes, then biliary drainage. The Tokyo Guidelines grade severity: severe cholangitis (organ dysfunction) needs urgent drainage once resuscitated, and moderate cholangitis needs early drainage. ERCP with stone extraction or stenting is the usual first choice, with percutaneous drainage if ERCP fails or is not possible. If confusion and hypotension are added (Reynolds' pentad), the patient is septic and drainage is even more urgent. Cholecystectomy is planned later to prevent recurrence.

Key clue
Charcot's triad with biliary duct dilation and stones
What it means
Ascending cholangitis
What to do
Start urgent antibiotics, resuscitate, and arrange urgent biliary decompression (ERCP or percutaneous drainage)

Why the other options are less appropriate

  • B Biliary colic is pain alone, with no fever, jaundice or duct dilatation. This patient is septic and obstructed.
  • C Gallstone pancreatitis causes epigastric pain radiating to the back with a raised amylase or lipase. Fever, jaundice and a dilated stone-filled duct here mean cholangitis, which needs antibiotics.
  • D Hepatitis A causes a hepatitic picture with very high transaminases, not an obstructive pattern with a dilated duct full of stones.
  • E Malignancy can cause obstructive jaundice, but this acute febrile illness with ductal stones is cholangitis. Moving straight to palliation would deny treatment that can save her life.

Source: Tokyo Guidelines 2018: diagnostic criteria and severity grading of acute cholangitis

Question 2Acute liver failureHard

A 28-year-old woman develops jaundice, coagulopathy (INR 3.5) and altered mental state four days after taking a large paracetamol overdose. What is the most appropriate immediate priority?

  1. ANo specific liver-directed treatment is needed
  2. BDischarge with outpatient follow-up once symptoms settle
  3. CDelay N-acetylcysteine because it is too late to be of benefit
  4. DManage entirely as an outpatient with oral fluids only
  5. EUrgent discussion with a specialist liver unit for consideration of transfer, alongside N-acetylcysteine and supportive care
Show answer and explanation

Answer: E Urgent discussion with a specialist liver unit for consideration of transfer, alongside N-acetylcysteine and supportive care

Jaundice, coagulopathy and encephalopathy days after a paracetamol overdose mean acute liver failure. It can progress within hours to cerebral oedema, multi-organ failure and death, and liver transplantation can save life. The priority is to discuss her early with a specialist liver unit, which may arrange transfer and transplant assessment, while she is managed in a high-dependency setting. Continue or start acetylcysteine: it still helps after liver damage has begun, even when given late. Support her with careful fluids, glucose monitoring (hypoglycaemia is common), and watching for infection, kidney injury and worsening encephalopathy. The modified King's College criteria help to identify who needs transplantation. They include arterial pH below 7.3 after fluid resuscitation, or the combination of INR above 6.5, creatinine above 300 µmol/L and grade 3–4 encephalopathy, and a rising lactate. Do not correct the INR with clotting products unless she is bleeding, because the INR is used to track prognosis.

Key clue
Jaundice, coagulopathy and encephalopathy after paracetamol overdose
What it means
Acute liver failure due to paracetamol toxicity
What to do
Continue N-acetylcysteine, contact a specialist liver unit urgently, and assess against transplant listing criteria (for example, King's College Criteria)

Why the other options are less appropriate

  • A Acute liver failure needs active specialist management, including possible transplantation. It is never managed by observation alone.
  • B Encephalopathy and an INR of 3.5 mean she could deteriorate quickly. She needs inpatient specialist care, not discharge.
  • C Acetylcysteine still helps in established paracetamol liver injury, even when started late, so it should be continued or started.
  • D Outpatient care is unsafe for anyone with acute liver failure and encephalopathy.

Source: TOXBASE / UK National Poisons Information Service: Management of paracetamol poisoning

Question 3Endoscopy timingMedium

A patient has ongoing haematemesis, systolic blood pressure 78 mmHg and cool peripheries. Intravenous access, blood sampling and resuscitation are underway. When should upper gastrointestinal endoscopy occur?

  1. ABefore resuscitation because haemostasis always takes priority
  2. BImmediately after adequate resuscitation
  3. CWithin twelve hours regardless of response to resuscitation
  4. DWithin twenty-four hours despite persistent shock
  5. EAfter seventy-two hours if haemoglobin remains stable
Show answer and explanation

Answer: B Immediately after adequate resuscitation

Ongoing haematemesis with a systolic blood pressure of 78 mmHg and cool peripheries indicates severe upper GI bleeding with haemorrhagic shock. Endoscopy finds the source and stops the bleeding, but sedating and scoping a patient in shock is dangerous. NICE CG141 therefore advises immediate endoscopy after resuscitation for unstable patients with severe acute upper GI bleeding, and endoscopy within 24 hours of admission for everyone else. Resuscitation includes two large-bore cannulas, crossmatch, blood transfusion guided by the clinical picture (often as a major haemorrhage protocol), and airway protection if the patient is vomiting large volumes or has a reduced conscious level. Platelets are given if the patient is actively bleeding and the count is below 50 × 10^9/L. If varices are suspected, give terlipressin and prophylactic antibiotics at presentation. Proton pump inhibitors should not be given before endoscopy. For non-variceal bleeding, adrenaline should not be used alone; combine it with a mechanical method (clips), thermal coagulation, or fibrin or thrombin.

Key clue
A patient has ongoing haematemesis, systolic blood pressure 78 mmHg and cool peripheries. Intravenous access, blood sampling and resuscitation are underway. When should upper gastrointestinal endoscopy occur
What it means
Severe unstable upper gastrointestinal bleeding requires immediate endoscopy after resuscitation; stabilisation must precede the procedure.
What to do
Immediately after adequate resuscitation

Why the other options are less appropriate

  • A Endoscopy before resuscitation risks cardiac arrest and aspiration. The circulation and airway must be stabilised first.
  • C A twelve-hour target is not based on NICE guidance and would leave an unstable patient bleeding.
  • D Endoscopy within twenty-four hours is for stable patients. Ongoing bleeding with shock needs it immediately after resuscitation.
  • E A stable haemoglobin is unreliable early on and does not justify a delay while the patient is in shock with haematemesis.

Source: NICE CG141: Acute upper gastrointestinal bleeding in over 16s — recommendations

Question 4Helicobacter pyloriEasy

A patient taking omeprazole requires a carbon-13 urea breath test for Helicobacter pylori. How long should the PPI be stopped before testing?

  1. ATwo weeks
  2. BTwenty-four hours
  3. CThree days
  4. DSix weeks
  5. ENo washout is needed
Show answer and explanation

Answer: A Two weeks

The carbon-13 urea breath test detects urease made by live Helicobacter pylori. PPIs reduce the number of organisms and their urease activity, and can push them higher into the stomach, so testing during PPI treatment can give a false negative. NICE CG184 advises testing for H. pylori with a carbon-13 urea breath test, a stool antigen test or a validated laboratory serology test, and leaving a 2-week washout after a PPI. Antibiotics also suppress the organism, so leave at least 4 weeks after them. If symptoms are troublesome during the washout, an antacid or alginate can be used. Serology stays positive after eradication, so it cannot confirm a cure. NICE advises against routine retesting after eradication. If a retest is done, use a breath test, not serology. People with a gastric ulcer and H. pylori should have repeat endoscopy 6 to 8 weeks after starting treatment, with retesting at that point. First-line eradication is a PPI with amoxicillin and either clarithromycin or metronidazole. Choose the regimen based on previous antibiotic exposure and penicillin allergy.

Key clue
A patient taking omeprazole requires a carbon-13 urea breath test for Helicobacter pylori. How long should the PPI be stopped before testing
What it means
PPIs can suppress H pylori and cause false-negative testing, so NICE specifies a two-week washout before breath or stool antigen testing.
What to do
Two weeks

Why the other options are less appropriate

  • B PPIs suppress H. pylori and urease for much longer than 24 hours, so this washout risks a false negative.
  • C Three days is too short for the organism's urease activity to recover. NICE specifies 2 weeks.
  • D Six weeks is longer than needed and leaves the patient without symptom control for no gain in accuracy.
  • E Testing during PPI treatment reduces the sensitivity of breath and stool tests, so a washout is needed.

Source: NICE CG184: Gastro-oesophageal reflux disease and dyspepsia in adults — recommendations

Question 5Acute severe ulcerative colitisHard

A patient is admitted with acute severe ulcerative colitis and is reviewed jointly by gastroenterology and colorectal surgery. Previous systemic corticosteroids caused severe steroid psychosis, making intravenous corticosteroids contraindicated. Infection has been assessed. Which initial disease-directed strategy should be considered?

  1. ADischarge with oral mesalazine and review after four weeks
  2. BStart azathioprine alone because it acts within hours
  3. CGive loperamide while awaiting spontaneous improvement
  4. DConsider intravenous ciclosporin or surgery after individualised multidisciplinary discussion
  5. EPerform full colonoscopy with bowel preparation before beginning treatment
Show answer and explanation

Answer: D Consider intravenous ciclosporin or surgery after individualised multidisciplinary discussion

The key detail is that IV corticosteroids, the standard first-line treatment for acute severe ulcerative colitis, are contraindicated by previous steroid psychosis. NICE NG130 advises that when IV corticosteroids are contraindicated or declined, IV ciclosporin or surgery should be considered in line with the person's preferences, with the decision made jointly by a gastroenterologist and a colorectal surgeon. Acute severe colitis is defined by the Truelove and Witts criteria: 6 or more bloody stools a day plus at least one sign of systemic toxicity, such as pulse above 90, temperature above 37.8°C, haemoglobin below 105 g/L or ESR above 30 mm/h. Ciclosporin is given IV, typically 2 mg/kg/day, with monitoring of drug levels, blood pressure, renal function and magnesium; low magnesium or cholesterol increases the risk of seizures. Infliximab is the alternative rescue drug if ciclosporin is unsuitable. Supportive care includes stool culture and C. difficile testing, LMWH prophylaxis against VTE, fluid and electrolyte replacement.

Key clue
A patient is admitted with acute severe ulcerative colitis and is reviewed jointly by gastroenterology and colorectal surgery. Previous systemic corticosteroids caused severe steroid psychosis, making intravenous corticosteroids contraindicated. Infection has been assessed. Which initial disease-directed strategy should be considered
What it means
When intravenous corticosteroids are contraindicated in acute severe ulcerative colitis, NICE advises considering intravenous ciclosporin or surgery, incorporating risks and patient preferences.
What to do
Consider intravenous ciclosporin or surgery after individualised multidisciplinary discussion

Why the other options are less appropriate

  • A Acute severe colitis is a medical emergency needing inpatient IV treatment. Oral mesalazine and review in four weeks would be dangerously slow.
  • B Azathioprine takes about 3 months to work, so it has no role as rescue therapy in acute severe colitis.
  • C Antimotility drugs can precipitate toxic megacolon in severe colitis and do nothing for the inflammation.
  • E Bowel preparation and full colonoscopy risk perforation in severe colitis. An unprepared flexible sigmoidoscopy is enough to confirm active disease.

Source: NICE NG130: Ulcerative colitis — management recommendations

That is 5 of 383. Carry on with gastroenterology and hepatology in the practice bank, with progress tracking, flashcards and timed sessions.

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Topics covered

Show all 366 gastroenterology and hepatology topics
  • A potentially removable biliary stent
  • A small improving diverticular abscess
  • Abetalipoproteinaemia
  • Abnormal liver tests
  • Achalasia
  • Acute cholangitis
  • Acute cholecystitis
  • Acute colonic pseudo-obstruction
  • Acute diverticulitis
  • Acute liver failure
  • Acute lower GI bleeding
  • Acute mesenteric ischaemia
  • Acute mesenteric ischaemia despite normal lactate
  • Acute pancreatitis
  • Acute pancreatitis diagnosis
  • Acute pancreatitis fluids
  • Acute portal vein thrombosis
  • Acute pouchitis
  • Acute severe UC
  • Acute severe ulcerative colitis
  • Adrenaline alone is insufficient
  • Adult coeliac disease
  • Alcohol advice when pancreatitis has another cause
  • Alcohol history and anchoring in recurrent pancreatitis
  • Alcohol-related decompensated cirrhosis
  • Alcohol-related hepatitis
  • Alpha-1 antitrypsin deficiency
  • An asymptomatic pseudocyst with vascular compression
  • Analgesic risk in diverticular disease
  • Antibiotic stewardship in acute pancreatitis
  • Antibiotics in cirrhotic upper-GI bleeding
  • Antibiotics in immunosuppressed uncomplicated diverticulitis
  • Apparent inflammatory bowel disease flare
  • Applying the NICE enhanced liver fibrosis threshold
  • Ascending cholangitis
  • Ascites is not an automatic antibiotic indication
  • Ascitic fluid analysis
  • Aspirin after haemostasis
  • Aspirin proposed solely for Barrett chemoprevention
  • Asymptomatic common bile duct stones versus gallbladder-only stones
  • Autoimmune enteropathy
  • Autoimmune hepatitis
  • Autoimmune hepatitis induction therapy
  • Autoimmune hepatitis steroid selection
  • Autoimmune hepatitis treatment
  • Autoimmune pancreatitis
  • Autoimmune pancreatitis type 1
  • Balancing surveillance benefit against severe comorbidity
  • Barrett biopsies reported as indefinite for dysplasia
  • Barrett oesophagus
  • Barrett's oesophagus
  • Beta-catenin-activated hepatocellular adenoma
  • Bile acid diarrhoea
  • Bile-acid diarrhoea
  • Biliary decompression when pancreatic cancer is unresectable
  • Biochemical confirmation of an acute porphyria attack
  • Blue rubber bleb naevus syndrome
  • Breastfeeding after appropriate neonatal HBV immunisation
  • Budd–Chiari syndrome
  • Budesonide for limited Crohn's disease
  • Caecal volvulus
  • Cameron lesions
  • Cap polyposis
  • Cardiac ascites
  • Caroli disease
  • Carvedilol in advanced decompensation
  • Caustic ingestion
  • Choledocholithiasis
  • Choosing durable bypass for malignant duodenal obstruction
  • Choosing post-pyloric feeding after failed gastric feeding
  • Chronic hepatitis B
  • Chronic hepatitis B initial assessment
  • Chronic pancreatitis
  • Cirrhosis
  • Cirrhosis pharmacotherapy safety
  • Coeliac disease
  • Coeliac disease follow-up
  • Coeliac disease sampling
  • Coeliac disease serology
  • Coeliac plexus neurolysis for persistent pancreatic cancer pain
  • Coeliac testing in unexplained transaminitis
  • Coeliac-associated splenic dysfunction
  • Colorectal cancer
  • Common variable immunodeficiency
  • Compensated cirrhosis
  • Complementary cross-sectional cyst imaging
  • Complicated diverticulitis when contrast CT is contraindicated
  • Constipation-predominant IBS
  • Continuous versus cyclical parenteral nutrition
  • Cramping in non-inflammatory diverticular disease
  • Crohn disease
  • Crohn disease maintenance
  • Crohn maintenance after steroid response
  • Cronkhite–Canada syndrome
  • Cyst fluid beyond cytology
  • D-lactic acidosis
  • Dedicated lumen for parenteral nutrition
  • Diarrhoea-predominant IBS
  • Dietary adherence
  • Dietary restrictions after incidental diverticulosis
  • Distal ileal Crohn disease
  • Distal oesophageal spasm
  • Diverticular abscess
  • Diverticular disease
  • Diverticulitis complications
  • Dominant pancreatic duct stone when surgery is unsuitable
  • Dominant stricture in primary sclerosing cholangitis
  • Drug-induced liver injury
  • Dubin–Johnson syndrome
  • Dysphagia red flags
  • Eating during uncomplicated acute pancreatitis
  • ELF rises despite treatment
  • Endoscopic haemostasis
  • Endoscopy complications
  • Endoscopy timing
  • Enteric hyperoxaluria
  • Enteropathy-associated T-cell lymphoma
  • Eosinophilic oesophagitis
  • Equivocal liver lesion before pancreatic resection
  • Exocrine follow-up beyond diabetes screening
  • Extensive mild ulcerative colitis
  • Extensive ulcerative colitis
  • F3 fibrosis requires a cirrhosis surveillance plan
  • Faecal biomarkers
  • Faecal calprotectin
  • Faecal elastase in watery diarrhoea
  • Failed endoscopic treatment of a symptomatic pseudocyst
  • Failure to improve with a diverticular abscess
  • Familial adenomatous polyposis
  • Feeding after uncomplicated PEG placement
  • Fibrostenotic Crohn disease
  • Fitness changes first-line metastatic treatment
  • Follow-up after a low-risk ELF result in an adult
  • Fundal gastric variceal haemorrhage
  • Fundoplication requested to prevent Barrett progression
  • Gallbladder drainage when empyema fails conservative care and surgery is unsafe
  • Gallstone ileus
  • Gallstone pancreatitis
  • Gallstone pancreatitis with cholangitis
  • Gallstone/cholestatic disease
  • Gastric antral vascular ectasia
  • Gastric MALT lymphoma
  • Gastric outlet obstruction biochemistry
  • Gastro-oesophageal reflux disease
  • Gilbert syndrome
  • Gluten-free oats in established coeliac disease
  • Groove pancreatitis
  • H pylori eradication
  • H pylori testing
  • Haemobilia
  • Haemochromatosis
  • HBeAg negativity does not establish inactive hepatitis B
  • HBV genotype before initial treatment
  • HCC surveillance risk assessment without established HBV cirrhosis
  • Helicobacter pylori
  • Hepatic encephalopathy
  • Hepatic encephalopathy precipitant
  • Hepatic epithelioid haemangioendothelioma
  • Hepatic hydrothorax
  • Hepatitis B in pregnancy
  • Hepatitis B reactivation
  • Hepatitis C testing
  • Hepatitis E
  • Hepatocellular adenoma
  • Hepatocellular carcinoma surveillance
  • Hepatopulmonary syndrome
  • Hepatorenal syndrome
  • Hereditary diffuse gastric cancer
  • Hereditary haemochromatosis
  • Hereditary pancreatitis and cancer surveillance
  • High liver stiffness and detectable HBV DNA
  • High-output stoma
  • Histological staging of a suspected superficial oesophageal cancer
  • Home tube feeding is a coordinated intervention
  • Hospitalised inflammatory bowel disease
  • Hypoxic hepatitis
  • IBD colorectal surveillance
  • IgA deficiency and coeliac testing
  • Ileocaecal disease
  • Inadequate nutrition despite an adequate prescription
  • Indeterminate distal biliary stricture
  • Indeterminate pancreatic cyst
  • Induction treatment
  • Infected necrosis without an endoscopic access route
  • Infected pancreatic necrosis
  • Inflammation distorts trace-element concentrations
  • Infusion schedule in a severely ill patient
  • Inherited pancreatic cancer risk
  • Initial fibrosis assessment in newly referred hepatitis B
  • Initial symptom treatment in established refractory coeliac disease
  • Intermediate elastography in chronic hepatitis B
  • Irritable bowel syndrome dietary management
  • Ischaemic colitis
  • Lactulose in hepatic encephalopathy
  • Late dumping syndrome
  • Laxative-related loose-stool leakage
  • Life-threatening complications
  • Limited ulcerative proctitis
  • Limits of HLA positivity in initial diagnosis
  • Linaclotide after inadequate laxative trials
  • Localised pancreatic cancer
  • Long-term enteral access
  • Long-term parenteral access planning
  • Long-term surveillance in chronic pancreatitis
  • Loperamide during an acute UC flare
  • Low albumin during an acute inflammatory response
  • Low stiffness does not end assessment in a young adult with active HBV
  • Low-risk UGIB disposition
  • Lynch syndrome
  • Lynch syndrome and one affected close relative
  • Ménétrier disease
  • Mesenteric ischaemia
  • Metabolic dysfunction-associated steatotic liver disease
  • Microbiology after diverticular abscess drainage
  • Microscopic colitis
  • Mirizzi syndrome
  • Monitoring after a new fibrosis medicine
  • New ascites
  • New HIV exposure before HBV antiviral treatment
  • NG tube position cannot be inferred from auscultation
  • No varices on the first scope
  • Nodal staging after submucosal invasion is identified
  • Nodular regenerative hyperplasia
  • Non-variceal bleeding endotherapy
  • Non-variceal upper GI bleeding
  • Normal aminotransferases cannot stage MASLD fibrosis
  • Normal antibodies do not prove complete dietary exclusion
  • NSAID-associated ulcer prevention
  • Nutrition after pancreatoduodenectomy
  • Obstructive jaundice
  • Oesophageal-varix surveillance
  • Omega-3 proposed as liver treatment
  • Painful obstructive chronic pancreatitis
  • Pancreatic cancer
  • Pancreatic cyst risk stratification
  • Pancreatic exocrine insufficiency
  • Pancreatic pleural effusion
  • Pancreatic pseudocyst
  • Pancreatitis with no gallstones or alcohol explanation
  • Paracetamol overdose
  • PBC–AIH overlap
  • Peginterferon in decompensated hepatitis B
  • Peptic ulcer disease
  • Perianal Crohn disease
  • Pernicious anaemia
  • Persistent faecal incontinence after initial care
  • Persistent symptoms despite a diverticular label
  • Persistently high titres after verified gluten exclusion
  • Persisting symptoms on gluten avoidance
  • Peutz–Jeghers intussusception
  • Pharmacological treatment belongs in specialist care
  • Pharyngeal pouch
  • Pioglitazone contraindication in advanced fibrosis
  • Pneumatosis cystoides intestinalis
  • Portal biliopathy
  • Portal hypertensive gastropathy
  • Portopulmonary hypertension
  • Positive diagnosis
  • Postoperative Crohn disease monitoring
  • Postpartum monitoring after HBV antiviral prophylaxis
  • Preparation for Helicobacter pylori testing
  • Primary biliary cholangitis
  • Primary intestinal lymphangiectasia
  • Primary prevention of spontaneous bacterial peritonitis
  • Primary sclerosing cholangitis
  • Progressive dysphagia
  • Protein-losing enteropathy
  • PRSS1 surveillance modality
  • PRSS1-related hereditary pancreatitis
  • PSC and IBD surveillance
  • PSC-associated colitis
  • Psychological therapy for refractory IBS
  • Quantifying an inadequate peginterferon response in HBeAg-negative disease
  • Reactive anti-TNF therapeutic drug monitoring
  • Recognising a quiet swallowing hazard
  • Refeeding syndrome
  • Refractory ascites
  • Refractory coeliac disease
  • Refractory coeliac disease type II
  • Refractory peptic ulcer
  • Renal tubular surveillance during tenofovir disoproxil treatment
  • Requirements before diagnosing refractory coeliac disease
  • Rescue decision in acute severe ulcerative colitis
  • Resectable pancreatic cancer
  • Restoring gluten exposure before diagnostic testing
  • Restriction for six days, not severe refeeding risk
  • Retesting after a previously negative coeliac screen
  • Reviewing insulin need in pancreatogenic diabetes
  • Reviewing intravenous antibiotics after CT
  • Routine postoperative tube feeding is not automatic
  • Rumination syndrome
  • SBP prophylaxis
  • Sclerosing mesenteritis
  • Second-line neuromodulation in IBS
  • Secondary bacterial peritonitis masquerading as SBP
  • Secondary sclerosing cholangitis
  • Selecting enteral nutrition
  • Selecting first-line antiviral treatment in decompensated HBV liver disease
  • Selecting parenteral nutrition
  • Selective antibiotic use in uncomplicated diverticulitis
  • Seronegative suspicion
  • Severe acute hepatic porphyria attack
  • Severe alcohol-related hepatitis
  • Severity classification after transient organ failure in pancreatitis
  • Short anticipated parenteral course and vascular access
  • Short bowel syndrome
  • Short-segment Barrett without intestinal metaplasia
  • Short-term peripheral parenteral nutrition
  • Sigmoid volvulus
  • Sinusoidal obstruction syndrome
  • Small intestinal bacterial overgrowth
  • Small-volume peritoneal disease before pancreatic resection
  • Smoking after diagnosis of chronic pancreatitis
  • Spontaneous bacterial empyema
  • Spontaneous bacterial peritonitis
  • Spontaneous oesophageal perforation
  • Starting feed after an uncomplicated PEG insertion
  • Starting parenteral nutrition in a stable postoperative patient
  • Sterile pancreatic necrosis
  • Steroid-dependent ulcerative colitis
  • Steroid-refractory acute severe colitis
  • Steroid-refractory ulcerative colitis
  • Steroid-sparing misconception in Crohn induction
  • Stool consistency as an IBS titration target
  • Stopping hepatitis B treatment after seroconversion in cirrhosis
  • Stopping unnecessary tube feeding after recovery
  • Superior mesenteric artery syndrome
  • Supplemental parenteral support when enteral delivery remains insufficient
  • Suspected common bile duct stone
  • Suspected obstruction before a prokinetic
  • Suspected variceal bleeding
  • Suspicious oesophageal stricture
  • Symptomatic triage
  • Systematic sampling during Barrett surveillance
  • Targeted calcium and vitamin D support in coeliac disease
  • Testing after self-imposed restriction
  • Testing an asymptomatic relative
  • The score before endoscopy
  • The six-month liver surveillance interval
  • The statin is not automatically stopped
  • Thiopurine pharmacogenetic safety
  • Timing an endoscopy after resuscitation
  • Timing intervention for pancreatic necrosis
  • Toilet access in functional faecal incontinence
  • Toxic megacolon
  • Treatment after first-line FOLFIRINOX
  • Type 3c diabetes
  • Ulcerative colitis extent
  • Ulcerative colitis maintenance
  • Ulcerative proctitis
  • Uninvestigated dyspepsia
  • Unresectable pancreatic cancer nutrition
  • Upper gastrointestinal bleeding
  • Upper GI bleeding resuscitation
  • Using MELD to monitor compensated cirrhosis
  • Using the gastrocolic response
  • Variceal bleed: the early pair
  • Variceal bleeding antibiotics
  • Varices found at diagnostic endoscopy
  • Visible dysplasia in ulcerative colitis
  • Volvulus
  • Weak positive tTG
  • Weight change caused by fluid rather than nutritional recovery
  • When parenteral nutrition can end
  • Wilson disease
  • Wilsonian acute liver failure

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