Rapid review: gastroenterology and liver

• This page is a revision shortcut through the classic gastroenterology and liver presentations: each block gives the picture in plain words, the most likely diagnosis, the first test, the first treatment, the common trap, and a pointer to the full MedGrasp topic.
• Read it after you know basic anatomy and physiology, not before: the full topics explain why each answer is right.
• Many "single best diagnosis" questions are really pattern-recognition questions, so focus on the discriminating feature in each block rather than memorising the list.
• When a number is given here, it comes from the guideline named in that block; use your local formulary and local pathway before acting on a dose.
• A red flag always wins over a favourite diagnosis.

By the end of this page you should be able to:

1. Recognise the classic presenting picture of each major gastroenterology presentation.
2. Choose the single most likely diagnosis and the best first test for each.
3. State the best first, evidence-based treatment and the most common wrong answer that an exam or a rushed clinician makes.
4. Sequence the acute abdomen using a simple flowchart.
5. Separate conjugated from unconjugated jaundice and state what each implies.
6. Distinguish IBD, coeliac disease and infection as causes of diarrhoea.
7. List the complications of cirrhosis and their first-line management.

Each section follows the same five lines, so that you can scan a whole topic in seconds. The first line is the picture as the patient or the examiner describes it. The last line is the trap: the answer that looks right, or the diagnosis you make when you stop thinking too early. Brackets such as (k) are citations to the reference list at the end of the page.

A person who says food sticks, coffee goes down the wrong way, or "I cannot get the swallow started" is describing dysphagia (pain on swallowing is odynophagia and usually means mucosal inflammation). The first fork is level: does the trouble start at the mouth and throat, with coughing, choking, nasal regurgitation or a wet voice, which is oropharyngeal (transfer) dysphagia; or is it lower down, with a hold-up sensation behind the sternum, which is oesophageal dysphagia. A useful question is "does it happen with liquids as well as solids?"; solids alone from the start suggests a mechanical block such as stricture or cancer, whereas trouble with both from the start suggests a motility disorder such as achalasia. Progression from solids to liquids is an alarm feature.

Most likely diagnosis. In older adults with gradual solids-first dysphagia and weight loss, think oesophageal malignancy until proven otherwise; in a younger patient with dysphagia to both solids and liquids and regurgitation of undigested food, think achalasia. Oropharyngeal dysphagia in the same patient is commonly neurological: stroke, Parkinson disease, motor neurone disease, myasthenia gravis, or a post-intubation or post-radiotherapy problem. Eosinophilic oesophagitis is an increasingly common cause of intermittent solid-food dysphagia in young men, often with a history of atopy.

Best first test. For oropharyngeal dysphagia, a videofluoroscopic swallow study (VFSS) with or without fibreoptic endoscopic evaluation of swallowing (FEES) is the method of choice, because it shows aspiration during the actual swallow; FEES and VFSS are regarded as gold standard assessments for silent aspiration, although they are not always available in remote settings ^[1]. For oesophageal dysphagia, upper endoscopy comes first, because it rules out mechanical obstruction or inflammatory disease; high-resolution manometry is the key test for motor disorder when endoscopy is normal, and barium swallow is a useful complementary study ^[1].

Best first treatment. Match treatment to cause: compensate for aspiration with speech and language therapy, texture-modified diet and safe-swallow precautions while the cause is sought; dilate a peptic stricture or Schatzki ring; treat eosinophilic oesophagitis with topical corticosteroid and proton pump inhibitor; manage achalasia with pneumatic dilatation or surgical myotomy. Eczema and allergy management may help eosinophilic disease, but the airway issue is the swallowing.

Commonest wrong answer. Calling the problem "globus" or anxiety, or attributing it to gastro-oesophageal reflux alone and prescribing a proton pump inhibitor without looking for cancer. Progressive solids-first dysphagia with weight loss needs urgent endoscopy with biopsies.

Full topic: Dysphagia and odynophagia (gastroenterology/dysphagia-and-odynophagia).

The patient with dyspepsia describes upper abdominal discomfort or pain, fullness after meals, early satiety, heartburn or sour regurgitation, worse after food or NSAIDs. Alarm symptoms change the answer: haematemesis, melaena, black stools, iron deficiency, weight loss, vomiting, dysphagia or new dyspepsia at an older age.

Most likely diagnosis. With alarm symptoms or NSAID use, think peptic ulcer disease (gastric or duodenal), most often due to Helicobacter pylori infection, NSAIDs or low-dose aspirin; without alarms in a young adult, think functional dyspepsia or gastro-oesophageal reflux disease. Gastric ulcers are, on average, more sinister than duodenal ones because of malignant potential.

Best first test. For uncomplicated dyspepsia in a young adult, a non-invasive Helicobacter pylori test (urea breath or stool antigen) is the appropriate first step, followed by eradication if positive. Endoscopy is the first test when alarm symptoms are present, when the patient is older, or when symptoms persist despite treatment. Proton pump inhibitors make Helicobacter tests falsely negative, so stop them for the test.

Best first treatment. Eradicate Helicobacter pylori with a guideline regimen (proton pump inhibitor plus two antibiotics) and stop the NSAID if possible; if Helicobacter-negative and NSAID-related, a proton pump inhibitor for several weeks plus acid suppression. For ulcer bleeding, resuscitate, give high-dose intravenous proton pump inhibitor and arrange urgent endoscopy with haemostasis. Continuing low-dose aspirin after a bleed should be discussed with the team once bleeding is controlled, because the cardiac benefit may outweigh risk ^[2][3]. Proton pump inhibitors reduce upper gastrointestinal bleeding risk during dual antiplatelet therapy ^[2].

Commonest wrong answer. Blaming spicy food or stress and treating indefinitely with a proton pump inhibitor without ever testing for Helicobacter pylori; or prescribing a proton pump inhibitor before the test and then treating an ulcer as "functional dyspepsia". In an acute bleed, forgetting to check the medication history (NSAIDs, aspirin, anticoagulants) and missing the source.

Full topic: Peptic ulcer disease (gastroenterology/peptic-ulcer-disease).

Acute abdomen is pain that develops over hours, often with vomiting and guarding, and it is diagnosed at the bedside and on the CT scanner before the diagnosis is certain. The classic three you must separate are appendicitis, acute cholecystitis and acute pancreatitis; the table below summarises them.

Acute appendicitis. The classically migratory pain is only present in a minority; atypical presentations are common in the young, the old and in pregnancy. The appendix can perforate, and perforated appendicitis carries a far higher mortality than uncomplicated disease (a mortality rate around 5 percent for perforated disease, against under 0.1 percent for acute non-gangrenous disease) ^[4]. Non-operative treatment with antibiotics is now an accepted option for uncomplicated disease, but recurrence and the risk of missed appendiceal pathology mean surgery remains the default for most fit patients ^[4].

Acute cholecystitis. Graded mild, moderate or severe by the Tokyo Guidelines 2018; acalculous cholecystitis occurs without stones and is especially dangerous in critically ill, burned, post-surgical and immunocompromised patients. Murphy sign (inspiratory arrest as the examining hand sits under the right costal margin during inspiration) is the classic examination finding.

Acute pancreatitis. Alcohol and gallstones account for most cases. Severity is scored (for example APACHE II or the modified Glasgow/Imrie criteria) and organ failure drives prognosis; CT severity is not required in mild disease. Do not give prophylactic antibiotics; remove the stone when indicated and address the alcohol use.

Best first test, overall. CT of the abdomen is the imaging mainstay when the diagnosis is uncertain, while directed ultrasound for right upper quadrant pain and amylase for epigastric pain are the efficient targeted first tests. Plain abdominal radiographs are rarely decisive.

Best first treatment, overall. Analgesia, intravenous fluids, antibiotics only when indicated, and then surgery or endoscopy for the underlying cause. Delaying definitive treatment while awaiting test results is the recurring error.

Commonest wrong answer. Calling a young woman with right iliac fossa pain "pelvic inflammatory disease" or "mittelschmerz" without imaging; treating urinary infection found on dipstick instead of the abdomen; or assuming all central abdominal pain is "gastroenteritis" without excluding surgical causes. Non-specific abdominal pain is common, but missed appendicitis and mesenteric ischaemia are the dangers.

Full topics: Appendicitis (gastroenterology/appendicitis); Acute cholecystitis (gastroenterology/acute-cholecystitis); Acute pancreatitis (gastroenterology/acute-pancreatitis); Peritonitis and the acute abdomen (gastroenterology/peritonitis-and-the-acute-abdomen).

Jaundice is the yellowing of skin and sclerae caused by hyperbilirubinaemia, and it usually becomes visible when bilirubin reaches about 2 to 3 mg per dL (34 to 51 micromol per L), with the sclerae the first place to see it ^[7]. The single most useful fork is pre-hepatic (unconjugated) versus hepatic/cholestatic (conjugated): dark urine and pale stools mean conjugated pigment is reaching the urine, which points to hepatocellular disease or obstruction.

Most likely diagnosis. In an adult with a short history of dark urine, pale stools, pruritus and gradual jaundice, think cholestasis from a bile duct stone or malignancy (head of pancreas, cholangiocarcinoma) until proven otherwise. In younger or sicker patients with minimal jaundice but very high transaminases, think viral or drug-induced hepatitis. In pregnancy, think obstetric cholestasis or acute fatty liver. Haemolysis and Gilbert syndrome account for most unconjugated jaundice.

Best first test. Liver blood tests (bilirubin, AST/ALT, alkaline phosphatase, GGT, albumin, INR) plus an abdominal ultrasound. The transaminase versus alkaline phosphatase pattern separates hepatocellular (marked transaminase elevation, modest alkaline phosphatase) from cholestatic disease (modest transaminases, marked alkaline phosphatase, often greater than 3 times normal) ^[7]. An unconjugated bilirubin under 3.5 mg per dL with normal transaminases and no urinary bilirubin suggests unconjugated hyperbilirubinaemia such as Gilbert or haemolysis ^[7].

Best first treatment. Treat the cause, never the colour: relieve obstruction endoscopically or surgically, stop the offending drug, treat hepatitis, and replace vitamin K when the INR is prolonged. Supportive care includes nutrition and fat-soluble vitamins in prolonged cholestasis, and ursodeoxycholic acid or rifampicin for pruritus. In obstetric cholestasis, delivery timing is a specialist decision.

Commonest wrong answer. Calling every jaundiced patient "hepatitis A" or "alcoholic liver disease without tests; confusing raised bilirubin with raised transaminases; and forgetting to check for dark urine and pale stools, which tell you whether the bilirubin is conjugated and whether the problem is in the duct.

Full topics: Abnormal liver function tests and jaundice (gastroenterology/abnormal-liver-function-tests-and-jaundice); Inherited hyperbilirubinaemias (gastroenterology/inherited-hyperbilirubinaemias).

Diarrhoea is usually defined as three or more loose or liquid stools a day ^[8]. The single most powerful split is acute (under 14 days, usually infection or a drug), persistent (14 to 30 days) and chronic (over 30 days, which raises IBD, coeliac disease, microscopic colitis and malabsorption). Blood, fever, weight loss, nocturnal symptoms and longer duration all point towards organic disease rather than irritable bowel syndrome. ^[9][14]

Most likely diagnosis. Acute watery with vomiting and sick contacts: viral gastroenteritis or food poisoning; acute bloody with fever: Shigella, Campylobacter, Salmonella or Shiga-toxin-producing E. coli (antibiotics should be avoided in the latter) ^[9]. Chronic with blood and weight loss in a young adult: inflammatory bowel disease; chronic with steatorrhoea, iron or folate deficiency, a dermatitis herpetiformis rash or first-degree relative with coeliac disease: coeliac disease. Chronic watery diarrhoea in an older adult may be microscopic colitis, often triggered by NSAIDs or proton pump inhibitors.

Best first test. In acute diarrhoea, send stool culture and PCR for pathogens when there is blood, fever or severe illness; C. difficile testing if antibiotics or healthcare exposure in the previous 8 to 12 weeks ^[9]. In chronic diarrhoea, start with faecal calprotectin to separate inflammatory from non-inflammatory disease, and with coeliac serology (tissue transglutaminase IgA plus total IgA) ^[10]. Colonoscopy with biopsies is reserved for raised calprotectin, red flags or age-appropriate colorectal cancer screening.

Best first treatment. Rehydrate with reduced osmolarity oral rehydration solution, with zinc in children ^[8][9]; antibiotics only for specific infections (Shigella, severe Campylobacter, cholera) and never for suspected Shiga-toxin-producing E. coli ^[9]. IBD is treated with mesalazine or topical therapy for mild ulcerative colitis, and with corticosteroids, immunomodulators or biologics guided by severity and extent ^[11][12]. Coeliac disease is treated with a strict lifelong gluten-free diet under a dietitian ^[10].

Commonest wrong answer. Stopping all oral intake and reaching for loperamide in a child with bloody diarrhoea (antimotility agents are avoided in children with acute diarrhoea and in anyone with suspected inflammatory diarrhoea) ^[9]; attributing chronic diarrhoea to irritable bowel syndrome without excluding IBD and coeliac; and prescribing antibiotics for uncomplicated viral gastroenteritis.

Full topics: Approach to diarrhoea (gastroenterology/approach-to-diarrhoea); Infectious diarrhoea (gastroenterology/infectious-diarrhoea); Crohn disease (gastroenterology/crohn-disease); Ulcerative colitis (gastroenterology/ulcerative-colitis); Coeliac disease (gastroenterology/coeliac-disease).

Cirrhosis is the common end point of chronic liver injury: alcohol, viral hepatitis, non-alcoholic fatty liver disease and autoimmune disease are the main causes. The decompensating events are ascites, variceal haemorrhage, hepatic encephalopathy and jaundice, and each has its own first-line treatment. Hepatocellular carcinoma surveillance (six-monthly ultrasound, with or without alpha-fetoprotein) applies once cirrhosis is established.

Most likely diagnosis (of decompensation). New large-volume ascites or a change in clinical picture in a known cirrhotic patient most often means decompensation, commonly precipitated by infection (spontaneous bacterial peritonitis), alcohol, gastrointestinal bleeding, constipation or a medication change. Variceal bleeding presents with haematemesis and melaena on a background of portal hypertension. Hepatic encephalopathy presents with confusion, flapping tremor and asterixis, often after a precipitant such as infection, bleeding, constipation or sedatives.

Best first test. Diagnostic paracentesis for any new ascites or unexplained deterioration (cell count and culture, protein, albumin, glucose); bloods including INR, renal function and electrolytes; and upper endoscopy to document varices. Ultrasound confirms nodular liver, splenomegaly and ascites.

Best first treatment. Ascites: sodium restriction, spironolactone (with or without furosemide), and therapeutic (and diagnostic) paracentesis for tense ascites with albumin replacement. Varices: non-selective beta-blocker (such as carvedilol or propranolol) for prevention, endoscopic band ligation for high-risk varices or after a bleed. Hepatic encephalopathy: lactulose and rifaximin, plus treat the precipitant. Spontaneous bacterial peritonitis: broad-spectrum antibiotics and albumin. Vitamin K does not reverse the INR in cirrhosis. NICE recommends monitoring and prevention of these complications, including detection of medium or large varices and prevention of spontaneous bacterial peritonitis and decompensation ^[13].

Commonest wrong answer. Attributing confusion to alcohol withdrawal rather than hepatic encephalopathy; diuresing without checking renal function (hepatorenal syndrome); or prescribing NSAIDs, which can precipitate renal failure and bleeding in cirrhosis. Sedatives and benzodiazepines are best avoided.

Full topics: Cirrhosis (gastroenterology/cirrhosis); Complications of cirrhosis (gastroenterology/complications-of-cirrhosis); Portal hypertension, ascites and SBP (gastroenterology/portal-hypertension-ascites-and-sbp); Hepatocellular carcinoma (gastroenterology/hepatocellular-carcinoma).

Acute GI bleeding is a life-threatening presentation until proven otherwise. Upper bleeding (haematemesis, melaena, coffee-ground vomit, anaemia with urea out of proportion to creatinine) is managed differently from lower bleeding (fresh red blood mixed with or coating stool, or dark blood with clots from the colon).

Most likely diagnosis. Upper: peptic ulcer, erosive gastroduodenitis, oesophageal or gastric varices, Mallory-Weiss tear, oesophagitis. Lower: diverticular haemorrhage, angiodysplasia, colitis (including ischaemic and IBD), colorectal cancer, haemorrhoids or an anal fissure, and Meckel diverticulum in the young. Variceal bleeding is the feared diagnosis in any patient with known or possible cirrhosis and should be assumed until endoscopy says otherwise.

Best first test. Resuscitate first. For suspected upper bleeding, upper endoscopy within 24 hours of haemodynamic stabilisation, with risk scoring (Glasgow-Blatchford or Rockall) to guide timing and transfusion ^[3]. For lower bleeding in a stable patient, colonoscopy after bowel preparation; in an unstable patient, CT angiography to localise the bleed. Upper endoscopy also rules out a bleeding lesion proximal to the ligament of Treitz before calling a bleed "lower".

Best first treatment. Resuscitate to a haemoglobin near 70 g per L in most patients, with a higher threshold if there is active coronary disease; correct clotting abnormalities (fresh frozen plasma only if there is active bleeding with a prolonged INR, vitamin K when indicated) and give high-dose intravenous proton pump inhibitor in upper bleeding followed by endoscopic therapy (clips, thermocoagulation, adrenaline injection). Adrenaline alone is insufficient; it needs thermal or mechanical haemostasis. For variceal bleeding, add vasoactive drugs (terlipressin or octreotide) and prophylactic antibiotics, and arrange urgent band ligation or balloon tamponade as a bridge ^[3]. Consider tranexamic acid only in line with local protocol. Refer early if massive or if endoscopy fails.

Commonest wrong answer. Waiting for the nasogastric aspirate to decide, which can miss a duodenal bleed; performing endoscopy in an unstabilised patient; blaming haemorrhoids for fresh bleeding without excluding a proximal source; or assuming "coffee grounds" always means slow bleeding, since variceal haemodynamically significant bleeding can look like that. Another trap is transfusing to a normal haemoglobin, which can raise portal pressure and rebleeding risk.

Full topics: Gastrointestinal bleeding (gastroenterology/gastrointestinal-bleeding); Peptic ulcer disease (gastroenterology/peptic-ulcer-disease); Portal hypertension, ascites and SBP (gastroenterology/portal-hypertension-ascites-and-sbp); Mallory-Weiss tear and oesophageal perforation (gastroenterology/mallory-weiss-tear-and-oesophageal-perforation).

Constipation is fewer than three bowel movements per week, hard stools, straining or a sense of incomplete evacuation. Acute abdominal distension with vomiting is obstruction until proven otherwise and is the emergency end of the same spectrum.

Constipation. Presenting picture: chronic difficulty passing stools, often in women and older adults, associated with low fibre, drugs (opioids, anticholinergics), hypothyroidism, depression, Parkinson disease or pelvic floor dysfunction. Most likely diagnosis: primary functional constipation, with secondary causes excluded clinically. Best first test: history and examination, including digital rectal examination and basic bloods (calcium, thyroid function, glucose); no imaging unless red flags. Best first treatment: reassurance, fluids, fibre and exercise, then a bulk or osmotic laxative: polyethylene glycol 3350 plus electrolytes is first-line for disimpaction and maintenance, with a stimulant laxative added if needed; in children, maintenance may continue for months and is not replaced by diet alone ^[14]. Commonest wrong answer: prescribing a stimulant laxative as the only long-term strategy, or relying on dietary change alone in chronic constipation; missing a rectal cancer, hypothyroidism or pelvic floor dyssynergia. Red flags: new change in bowel habit after 50 years, blood loss, anaemia, weight loss, obstruction.

Bowel obstruction. Presenting picture: colicky central abdominal pain, vomiting (early and profuse in high small bowel obstruction, late and faeculent in large bowel obstruction), abdominal distension and constipation or absolute constipation; in partial obstruction watery diarrhoea can occur. Most likely diagnosis: adhesions after previous surgery (around 60 percent of small bowel obstructions), followed by hernia, malignancy and inflammatory disease ^[15]. Best first test: CT scan is the preferred imaging test when there is any doubt, because it locates the obstruction, identifies the cause and predicts strangulation with high accuracy; plain films miss early signs of strangulation and perforation ^[15]. Best first treatment: nil by mouth, decompression with a nasogastric tube, intravenous fluids, electrolyte correction and close observation; non-operative management succeeds in most adhesive obstructions, and most authors consider up to 72 hours safe, but signs of peritonitis, strangulation or ischaemia mandate early surgery ^[15]. Low-grade obstruction may allow a water-soluble contrast challenge. Commonest wrong answer: calling vomiting with distension "gastroenteritis" and continuing oral intake; underestimating strangulation risk because the patient looks well early on; or delaying surgery once signs of ischaemia appear. Small bowel obstruction mortality is around 3 percent per episode and rises with delay ^[15].

Full topics: Constipation and faecal incontinence (gastroenterology/constipation-and-faecal-incontinence); Small bowel obstruction (gastroenterology/small-bowel-obstruction); Large bowel obstruction (gastroenterology/large-bowel-obstruction); Ileus and colonic pseudo-obstruction (gastroenterology/ileus-and-colonic-pseudo-obstruction).

• Treat the pattern, not the organ: the discriminating feature (level of dysphagia, conjugated versus unconjugated bilirubin, acute versus chronic diarrhoea, pre-hepatic pain) does most of the diagnostic work.
• A proton pump inhibitor should not be started before Helicobacter pylori testing in uncomplicated dyspepsia, because it obscures the result.
• Solids-first progressive dysphagia with weight loss is oesophageal cancer until proven otherwise.
• Early laparoscopic cholecystectomy is preferred once acute cholecystitis is diagnosed in a fit patient.
• CT is the default imaging test for the uncertain acute abdomen; directed tests are better for right upper quadrant pain and for epigastric pain.
• Jaundice is visible once bilirubin reaches 2 to 3 mg per dL; dark urine tells you the bilirubin is conjugated.
• Oral rehydration, with zinc in children, remains the first treatment of acute diarrhoea.
• Antimotility drugs are avoided in children and in suspected inflammatory or E. coli diarrhoea.
• Inflammatory bowel disease should be excluded in young adults with bloody diarrhoea or weight loss before calling it irritable bowel syndrome.
• Coeliac disease is managed with a strict lifelong gluten-free diet, not with symptom control.
• Cirrhosis care is organ-system prevention: beta-blockers or band ligation for varices, spironolactone-based diuresis for ascites, lactulose and rifaximin for encephalopathy, antibiotics and albumin for spontaneous bacterial peritonitis.
• Variceal bleeding needs vasoactive drugs, antibiotics and endoscopic control, not just blood.
• Polyethylene glycol 3350 plus electrolytes is first-line for constipation and disimpaction; diet alone is not enough when it is chronic.
• Adhesive obstruction is usually managed non-operatively, but surgery is needed when strangulation or peritonitis is present.
• Red flags (weight loss, anaemia, obstruction, bleeding) overrule any "likely benign" diagnosis.

Plain-text references to MedGrasp topics: Dysphagia and odynophagia (gastroenterology/dysphagia-and-odynophagia); Peptic ulcer disease (gastroenterology/peptic-ulcer-disease); Appendicitis (gastroenterology/appendicitis); Acute cholecystitis (gastroenterology/acute-cholecystitis); Acute pancreatitis (gastroenterology/acute-pancreatitis); Abnormal liver function tests and jaundice (gastroenterology/abnormal-liver-function-tests-and-jaundice); Approach to diarrhoea (gastroenterology/approach-to-diarrhoea); Crohn disease (gastroenterology/crohn-disease); Ulcerative colitis (gastroenterology/ulcerative-colitis); Coeliac disease (gastroenterology/coeliac-disease); Cirrhosis (gastroenterology/cirrhosis); Complications of cirrhosis (gastroenterology/complications-of-cirrhosis); Gastrointestinal bleeding (gastroenterology/gastrointestinal-bleeding); Constipation and faecal incontinence (gastroenterology/constipation-and-faecal-incontinence); Small bowel obstruction (gastroenterology/small-bowel-obstruction); Large bowel obstruction (gastroenterology/large-bowel-obstruction).