AMC MCQ (CAT) gastroenterology questions

In a young patient with typical reflux symptoms and no alarm features, Therapeutic Guidelines recommend an empirical trial of a proton pump inhibitor as the initial diagnostic and therapeutic step, without the need for endoscopy. Symptom response supports the diagnosis of GORD and avoids unnecessary invasive investigation. Endoscopy is reserved for patients with alarm features or those who fail to respond to an adequate PPI trial. pH monitoring and manometry are used for atypical or refractory cases, not first-line. H. pylori testing is more relevant to suspected peptic ulcer disease than typical reflux without ulcer features.

• A. pH monitoring is reserved for atypical symptoms or when diagnosis remains unclear after empirical treatment fails.
• C. Barium swallow has low sensitivity for GORD and is not recommended as an initial investigation.
• D. Endoscopy is not first-line in a young patient with typical reflux symptoms and no alarm features.
• E. H. pylori testing is indicated for suspected peptic ulcer disease, not uncomplicated reflux symptoms.

Dysphagia, weight loss and anaemia in a patient over 55 years are alarm features that mandate prompt endoscopic evaluation to exclude oesophageal or gastric malignancy. Therapeutic Guidelines and RACGP recommend bypassing empirical PPI therapy in this setting, as symptomatic treatment may mask or delay diagnosis of a serious underlying cause. Endoscopy allows direct visualisation, biopsy and histological diagnosis. Barium swallow is less sensitive and does not allow tissue sampling, making it inappropriate when malignancy is suspected.

• A. Prokinetics do not address the need for urgent investigation of alarm symptoms.
• C. Faecal occult blood testing alone is inadequate when dysphagia and weight loss suggest possible oesophageal malignancy.
• D. Empirical PPI therapy risks delaying diagnosis of malignancy when alarm features are present.
• E. Barium swallow lacks the sensitivity and biopsy capability required when malignancy is suspected.

Eosinophilic oesophagitis is a chronic immune-mediated condition strongly associated with atopy, and food bolus impaction in a young adult with a history of dysphagia and allergic disease is a classic presentation. Diagnosis requires oesophageal biopsy demonstrating a dense eosinophilic infiltrate of 15 or more eosinophils per high-power field in the setting of compatible symptoms, after exclusion of other causes of oesophageal eosinophilia such as GORD. Endoscopy may show rings, furrows or strictures, though the mucosa can appear normal. Management includes topical corticosteroids, dietary elimination and proton pump inhibitors, with endoscopic dilation reserved for fibrostenotic disease.

• A. A neutrophilic infiltrate with crypt abscesses is characteristic of inflammatory bowel disease, not eosinophilic oesophagitis.
• B. Intestinal metaplasia with goblet cells is the hallmark of Barrett's oesophagus, not eosinophilic oesophagitis.
• D. Dysplastic squamous epithelium suggests a premalignant process, not an eosinophilic inflammatory condition.
• E. Submucosal granulomas suggest Crohn disease involvement, which rarely affects the oesophagus in this manner.

The clinical picture of progressive dysphagia to solids and liquids, regurgitation and a 'bird's beak' tapering on barium swallow is classic for achalasia, caused by degeneration of inhibitory neurons in the oesophageal myenteric plexus. Manometry is the gold standard test and demonstrates absent or disordered peristalsis in the oesophageal body together with incomplete or absent relaxation of the lower oesophageal sphincter on swallowing. Diffuse simultaneous contractions with normal sphincter relaxation describe distal oesophageal spasm, a different motility disorder. A hypotensive sphincter with normal peristalsis is typical of GORD rather than achalasia, and a hypercontractile pattern suggests jackhammer oesophagus.

• A. Simultaneous high-amplitude contractions with normal sphincter relaxation describe distal oesophageal spasm, not achalasia.
• B. An isolated hypotensive sphincter with normal peristalsis is typical of GORD, not achalasia.
• C. Normal peristalsis with upper sphincter dysfunction does not fit the clinical and radiological picture described.
• D. Hypercontractile swallows with normal peristalsis describe jackhammer oesophagus.

Squamous cell carcinoma of the oesophagus arises from the native stratified squamous epithelium lining most of the oesophagus, and its major risk factors, tobacco and alcohol, act as direct mucosal carcinogens causing field change and dysplasia in this squamous lining. This contrasts with oesophageal adenocarcinoma, which typically arises from Barrett's metaplasia in the distal oesophagus as a consequence of chronic gastro-oesophageal reflux, and is more strongly associated with obesity and GORD than with smoking and alcohol. Helicobacter pylori is not an established risk factor for oesophageal squamous cell carcinoma and may even be inversely associated with reflux-related adenocarcinoma.

• A. Obesity and hiatus hernia relate to the pathogenesis of reflux-associated adenocarcinoma, not squamous cell carcinoma.
• B. H. pylori is not an established mechanism for squamous cell carcinoma and is more relevant to gastric pathology.
• C. Barrett's metaplasia is the precursor lesion for adenocarcinoma, not squamous cell carcinoma.
• E. Columnar metaplasia from reflux is the mechanism underlying adenocarcinoma, not squamous cell carcinoma.

Plummer-Vinson syndrome (also called Paterson-Brown-Kelly syndrome) is defined by the triad of dysphagia due to an upper oesophageal web, iron deficiency anaemia, and glossitis, and occurs predominantly in middle-aged women with chronic iron deficiency, often from menorrhagia or poor dietary intake. The anaemia, atrophic glossitis, koilonychia and angular stomatitis together with a proximal oesophageal web on imaging are characteristic. Treatment involves iron repletion, which can improve dysphagia and may allow the web to resolve, along with endoscopic dilation if needed. The condition carries an increased risk of postcricoid and oesophageal squamous cell carcinoma, warranting surveillance.

• A. Eosinophilic oesophagitis is linked to atopy and food bolus obstruction, not iron deficiency and glossitis.
• B. Zenker diverticulum causes dysphagia with regurgitation and halitosis but is not linked to iron deficiency or glossitis.
• D. Schatzki ring occurs at the gastro-oesophageal junction and is not associated with anaemia or glossitis.
• E. While Plummer-Vinson syndrome increases cancer risk, the presentation here with anaemia, glossitis and a thin web fits the syndrome itself rather than an established carcinoma.

The combination of forceful vomiting followed by severe chest pain, tachycardia, hypotension, fever and subcutaneous emphysema (Mackler triad plus crepitus) is highly suggestive of Boerhaave syndrome, a spontaneous transmural oesophageal rupture usually at the left posterolateral distal oesophagus. CT chest with water-soluble contrast swallow is the investigation of choice, as it rapidly confirms the site and extent of perforation, identifies mediastinal contamination, and guides urgent surgical management. Barium is avoided as it is more irritant to the mediastinum if extravasation occurs. Plain chest X-ray may show pneumomediastinum or pleural effusion but lacks the sensitivity and anatomical detail of CT. Endoscopy risks worsening the perforation and is not the first investigation of choice in this acute unstable setting.

• A. Plain chest X-ray alone lacks sufficient sensitivity and detail to confirm perforation site and extent.
• B. Endoscopy risks extending the perforation and worsening mediastinal contamination in the acute setting.
• C. Barium is avoided in suspected perforation due to its irritant effect on the mediastinum if it extravasates.
• E. Echocardiography does not assess the oesophagus and is not the investigation for suspected perforation.

Proton pump inhibitors suppress H. pylori activity and can cause false-negative results on urea breath testing, stool antigen testing, and biopsy-based urease or histology testing. Current guidelines recommend ceasing PPI therapy for at least 2 weeks before performing a urea breath test or stool antigen test to avoid false negatives. Serology detects antibodies rather than active infection, is not affected by PPI use, but cannot distinguish current from past infection and is not recommended as a sole diagnostic test. Where possible, non-invasive testing (urea breath test or stool antigen) after an adequate PPI washout is preferred over endoscopic biopsy in a patient without alarm features.

• A. Serology remains unreliable for confirming current infection even after stopping the PPI.
• B. Endoscopy is invasive and unnecessary in this patient without alarm features, and PPI use would still reduce biopsy test sensitivity.
• C. PPI use suppresses the organism and gives a false-negative urea breath test if not ceased beforehand.
• E. Serology cannot distinguish current from previous infection, so it is not the preferred confirmatory test regardless of PPI use.

First-line empirical H. pylori eradication per Therapeutic Guidelines is standard triple therapy: a PPI (such as esomeprazole), amoxicillin and clarithromycin, given twice daily for 7 days. This combination achieves high eradication rates in populations with low clarithromycin resistance and is the recommended first-line regimen in Australia. Bismuth-based quadruple therapy is reserved for second-line treatment after failed triple therapy or in areas of known high clarithromycin resistance. Dual therapy regimens are inadequate due to unacceptably low eradication rates.

• A. Dual therapy without a second antibiotic has unacceptably low eradication rates.
• B. Quadruple bismuth-based therapy is reserved as second-line treatment after first-line failure.
• C. Dual therapy with only one antibiotic is inadequate for eradication.
• D. This combination omits amoxicillin and is not the standard first-line regimen.

In patients at high risk of NSAID-induced peptic ulcer disease, including those with a prior ulcer history or concurrent aspirin use, co-prescription of a proton pump inhibitor for the duration of NSAID therapy is recommended to reduce ulcer risk. PPIs are more effective than H2-receptor antagonists at standard doses for this indication. Low-dose aspirin should generally be continued if there is a clear cardiovascular indication, with gastroprotection added rather than ceasing a necessary secondary prevention medication. Sucralfate has not been shown to reliably reduce NSAID-associated ulcer risk and is not recommended for this purpose.

• A. Switching analgesic without a trial of gastroprotection does not address the risk from continued NSAID or aspirin use.
• B. Aspirin should generally be continued for cardiovascular protection, with gastroprotection added rather than stopping a necessary medication.
• D. Sucralfate is not an effective or recommended agent for NSAID-ulcer prophylaxis.
• E. H2-receptor antagonists at standard doses are less effective than PPIs for NSAID ulcer prophylaxis in high-risk patients.

An erect chest X-ray is the most appropriate rapid initial imaging test in suspected perforated peptic ulcer, as it can demonstrate free air under the diaphragm (pneumoperitoneum) in a high proportion of cases and is quick, inexpensive and widely available. If the chest X-ray is non-diagnostic but clinical suspicion remains high, CT abdomen with contrast is the next step, as it is more sensitive for detecting smaller amounts of free air and fluid. Barium studies are contraindicated in suspected perforation due to risk of peritoneal contamination. Ultrasound and MRI are not first-line for detecting pneumoperitoneum in this acute setting.

• B. Barium studies are contraindicated in suspected perforation due to the risk of peritoneal contamination.
• C. Ultrasound is not reliable for detecting pneumoperitoneum and is not the standard initial test.
• D. Supine abdominal X-ray is less sensitive than an erect chest X-ray for detecting free intraperitoneal air.
• E. MRI is not practical or standard for this acute, unstable presentation.

Recurrent, refractory, or atypically distributed peptic ulcers (extending beyond the duodenal bulb) combined with secretory diarrhoea should raise suspicion for Zollinger-Ellison syndrome, caused by a gastrin-secreting neuroendocrine tumour (gastrinoma). A fasting serum gastrin level is the key initial screening test; a markedly elevated level in the presence of gastric acid hypersecretion is diagnostic, and secretin stimulation testing can be used for confirmation if levels are equivocal. PPI therapy can falsely elevate gastrin levels, so interpretation requires correlation with the clinical picture or temporary cessation where feasible. The other tests do not evaluate gastrin-driven acid hypersecretion and would not explain this clinical picture.

• A. Amylase and lipase assess pancreatitis and do not explain recurrent refractory ulceration with diarrhoea.
• B. pH monitoring assesses gastro-oesophageal reflux and does not evaluate for a gastrin-secreting tumour.
• C. Faecal calprotectin screens for intestinal inflammation such as inflammatory bowel disease, not gastrin-driven ulcer disease.
• D. VIP is elevated in VIPoma, which causes profuse watery diarrhoea but not recurrent peptic ulceration.

The Glasgow-Blatchford score stratifies patients with suspected upper gastrointestinal bleeding by risk of needing intervention or death. A score of 0 to 1 identifies patients at very low risk, who can be safely managed as outpatients with early gastroscopy arranged, avoiding unnecessary hospital admission. This patient has normal vital signs, a normal haemoglobin, and a normal urea, consistent with a low-risk presentation. Higher scores (generally 7 or above in practice, though any score above 0 to 1 warrants consideration of admission) indicate a need for admission, closer monitoring, and more urgent endoscopy.

• A. Admission without any endoscopic follow-up fails to establish the source of bleeding.
• C. CT angiography is reserved for cases of severe, ongoing bleeding not controlled or localised by endoscopy, not for a low-risk, stable patient.
• D. Transfusion is not indicated with a normal haemoglobin of 148 g/L.
• E. A score of 0 indicates very low risk, so urgent inpatient admission and intravenous PPI infusion is unnecessary over-treatment.

In massive upper gastrointestinal haemorrhage with haemodynamic instability, the immediate priority is resuscitation: securing two large-bore intravenous cannulae and commencing fluid resuscitation to restore circulating volume and organ perfusion, followed by transfusion of blood products as indicated. Airway protection should also be considered given the risk of aspiration and reduced consciousness from hypoperfusion. Endoscopy, vasoactive drugs such as terlipressin, and balloon tamponade are important subsequent or adjunctive measures once the patient is adequately resuscitated and stabilised, but they do not substitute for initial resuscitation. CT angiography is not a first-line step and delays definitive care in an acutely unstable patient.

• B. CT angiography delays essential resuscitation and is not the immediate priority in an unstable, actively bleeding patient.
• C. Endoscopy must follow adequate resuscitation and stabilisation; proceeding without intravenous access first is unsafe.
• D. Balloon tamponade is a temporising measure reserved for uncontrolled variceal bleeding after resuscitation and usually after failed endoscopic therapy.
• E. Terlipressin is an important adjunct in variceal bleeding but does not replace the need for fluid and blood product resuscitation.

This patient has a non-variceal upper GI bleed with haemodynamic stability and a Glasgow-Blatchford-type risk profile suggesting urgent but not emergency endoscopy. Current guidelines recommend endoscopy within 24 hours of presentation for most patients with acute upper GI bleeding, after adequate resuscitation. Earlier endoscopy (within 6 hours) is reserved for haemodynamically unstable patients with signs of ongoing bleeding such as haematemesis of fresh blood or shock unresponsive to initial fluids. Endoscopy should never precede adequate resuscitation, as haemodynamic stabilisation reduces procedural risk and improves visualisation.

• A. Delaying beyond 24 hours increases the risk of missing a treatable bleeding lesion and worsens outcomes.
• B. Endoscopy is indicated regardless of symptom recurrence to identify and treat the bleeding source.
• C. Resuscitation must precede endoscopy to ensure the patient can safely tolerate the procedure.
• D. Six-hour endoscopy is reserved for unstable patients with ongoing bleeding or shock, not this stable patient.

In suspected variceal upper GI bleeding, a splanchnic vasoconstrictor such as terlipressin should be started as soon as the diagnosis is suspected, before endoscopic confirmation, to reduce portal pressure and bleeding severity. Prophylactic antibiotics, typically intravenous ceftriaxone, are given concurrently to all patients with suspected variceal bleeding, as they reduce the risk of bacterial infection, rebleeding, and mortality in cirrhotic patients. Waiting for endoscopic confirmation before starting either treatment delays care and worsens outcomes. Terlipressin acts on vasopressin receptors in splanchnic vascular smooth muscle, causing vasoconstriction and reduced portal blood flow.

• A. Antibiotics should be started empirically at presentation, not delayed until endoscopic confirmation of varices.
• C. Tranexamic acid is not recommended in variceal bleeding and metronidazole does not provide appropriate prophylactic cover.
• D. Octreotide is an alternative vasoactive agent in some settings, but oral amoxicillin is inadequate antibiotic prophylaxis and inappropriate in an unstable patient who may not tolerate oral intake.
• E. Adrenaline is not used for portal pressure reduction and vancomycin is not first-line prophylaxis in this setting.

Severe retching followed by severe chest pain, subcutaneous emphysema (neck crepitus), and mediastinal air on imaging indicates full-thickness oesophageal rupture, classically following forceful vomiting. This is a surgical emergency requiring urgent CT imaging and surgical consultation, in contrast to a Mallory-Weiss tear, which is a mucosal tear producing painless or mildly uncomfortable haematemesis without systemic sepsis features or mediastinal air. The combination of chest pain, subcutaneous emphysema, and pleural effusion after vomiting is highly specific for this diagnosis. Early recognition is critical because delayed treatment markedly increases mortality from mediastinitis.

• A. A Mallory-Weiss tear causes mucosal bleeding from retching but does not cause mediastinal air, subcutaneous emphysema, or severe systemic illness.
• B. Aspiration pneumonitis would present with respiratory symptoms and infiltrates on imaging, not mediastinal air or neck crepitus.
• D. Spontaneous pneumothorax does not explain the mediastinal air, neck crepitus, or the clear association with forceful vomiting.
• E. Peptic ulcer perforation causes acute abdominal pain and peritonism rather than chest pain with neck crepitus and mediastinal air after vomiting.

Skip lesions with intervening normal mucosa, terminal ileal involvement, transmural inflammation, non-caseating granulomas, and perianal fistulising disease are classic features of Crohn disease. Ulcerative colitis, in contrast, produces continuous mucosal inflammation beginning in the rectum and extending proximally, with inflammation confined to the mucosa and submucosa, and it does not cause perianal fistulas or granulomas. The combination of ileal involvement, skip lesions, and granulomatous transmural inflammation on histology is diagnostic of Crohn disease rather than other inflammatory or infectious causes of colitis.

• A. Ischaemic colitis occurs in older patients with vascular risk factors and presents acutely, not as a chronic relapsing illness with fistulising disease.
• B. Ulcerative colitis causes continuous mucosal inflammation from the rectum proximally, without skip lesions, granulomas, or perianal fistulas.
• C. Infectious colitis is typically acute and self-limiting and does not produce granulomas or fistulising perianal disease.
• E. Intestinal tuberculosis typically shows caseating granulomas and is usually associated with systemic features of tuberculosis, which are absent here.

Faecal calprotectin is a sensitive marker of intestinal mucosal inflammation and is recommended to distinguish inflammatory bowel disease from irritable bowel syndrome in patients with lower gastrointestinal symptoms without alarm features. A low faecal calprotectin has a high negative predictive value for IBD, allowing many patients to avoid unnecessary colonoscopy, while an elevated level warrants further investigation including colonoscopy. Serum inflammatory markers such as CRP are less sensitive for mucosal inflammation and can be normal in IBD, particularly early or mild disease. This test is recommended as a first-line triage investigation before colonoscopy in appropriate primary care patients.

• A. Faecal occult blood testing is used for colorectal cancer screening and lacks sensitivity for inflammatory mucosal disease.
• C. Abdominal ultrasound is not a sensitive or specific first-line tool for detecting bowel mucosal inflammation.
• D. Anti-tissue transglutaminase antibody is used to screen for coeliac disease, not to differentiate IBD from IBS.
• E. Serum CRP can be normal even in active inflammatory bowel disease and is less sensitive than faecal calprotectin for mucosal inflammation.

This patient meets Truelove and Witts criteria for acute severe ulcerative colitis, with eight or more bowel motions daily plus systemic features including fever, tachycardia, and anaemia. First-line treatment is intravenous corticosteroids, such as hydrocortisone, which act faster than oral steroids and are appropriate in this unwell inpatient who may have impaired oral absorption. If there is inadequate response within 72 hours, escalation to infliximab or ciclosporin (rescue therapy) is considered. Oral therapies and immunomodulators such as azathioprine have no role in inducing remission in acute severe flares and are reserved for maintenance therapy.

• A. Oral mesalazine is used for mild to moderate disease and maintenance therapy, not for inducing remission in acute severe colitis.
• B. Infliximab is reserved as rescue therapy if there is inadequate response to intravenous corticosteroids after 72 hours, not first-line.
• C. Oral prednisolone has slower onset and less reliable absorption than intravenous corticosteroids in acute severe disease.
• E. Azathioprine is a maintenance immunomodulator with delayed onset of action and has no role in acute severe flares.

TPMT metabolises thiopurines; low or absent activity leads to accumulation of 6-thioguanine nucleotides and a markedly increased risk of severe, potentially fatal myelosuppression. Testing TPMT activity or genotype before starting azathioprine identifies patients who need a reduced dose or an alternative agent. Full blood count monitoring is still required regularly after starting therapy regardless of TPMT status, as it does not eliminate risk entirely. This is standard practice recommended in Therapeutic Guidelines before thiopurine initiation.

• B. Vitamin B12 and folate are not affected by thiopurines and are not part of pre-treatment screening.
• C. Thiopurines are not associated with dyslipidaemia; this is not relevant pre-treatment testing.
• D. Hepatitis C is not a specific contraindication or pre-thiopurine screening requirement.
• E. Pancreatitis is a recognised idiosyncratic reaction to azathioprine but amylase/lipase are not routinely checked before starting; they are checked if symptoms develop.

Anti-TNF therapy can reactivate latent tuberculosis and hepatitis B, sometimes with fulminant hepatitis, so screening for both is mandatory before starting treatment. Screening for latent TB includes an interferon-gamma release assay or tuberculin skin test plus chest X-ray, while hepatitis B surface antigen and core antibody identify active or past infection requiring antiviral prophylaxis. This patient's country of birth raises her pre-test probability of latent TB and chronic hepatitis B, making screening even more important. Therapeutic Guidelines recommend this screening for all patients before starting biologic therapy for IBD, regardless of symptoms.

• A. Tuberculosis screening is required before anti-TNF therapy because of the reactivation risk with these agents.
• B. Chest X-ray alone without an interferon-gamma release assay or tuberculin test is insufficient to exclude latent TB, and hepatitis B screening is also required.
• C. Hepatitis B screening is also mandatory before anti-TNF therapy; omitting it risks fulminant reactivation.
• D. HIV and varicella screening are not the specific mandatory pre-biologic screens for anti-TNF reactivation risk; TB and hepatitis B are the key concerns.

Primary sclerosing cholangitis is a chronic cholestatic liver disease strongly associated with ulcerative colitis, affecting up to 5% of UC patients, and classically produces a cholestatic liver profile with a beaded, multifocal stricturing pattern of the bile ducts on cholangiography. It can occur independently of bowel disease activity and increases the risk of cholangiocarcinoma and colorectal cancer, warranting earlier and more frequent colonoscopic surveillance. Diagnosis is usually made non-invasively with MRCP showing the characteristic biliary tree appearance. Autoimmune hepatitis and primary biliary cholangitis typically show a hepatitic or antimitochondrial-antibody-associated pattern rather than this cholangiographic appearance.

• A. Primary biliary cholangitis is associated with antimitochondrial antibodies and affects middle-aged women predominantly, not linked to UC, and does not cause this large duct beading.
• B. Autoimmune hepatitis typically causes a hepatitic (ALT-predominant) pattern with positive autoantibodies, not this cholangiographic beading.
• C. Choledocholithiasis typically causes a focal stricture or filling defect with biliary colic, not multifocal intrahepatic and extrahepatic beading.
• D. Drug-induced cholestasis would not produce the structural beaded appearance of the bile ducts on imaging.

Extensive ulcerative colitis carries an increased risk of colorectal cancer that rises with disease duration, prompting guideline recommendations to begin surveillance colonoscopy 8-10 years after symptom onset. Chromoendoscopy with targeted biopsies improves detection of dysplasia compared with random biopsies and is now the preferred surveillance technique. Surveillance intervals are then individualised, typically every 1-3 years, based on risk factors such as extent of disease, concurrent primary sclerosing cholangitis, family history and prior dysplasia. Symptom status does not reliably predict dysplasia or cancer risk in long-standing colitis, so surveillance must proceed regardless of symptoms.

• A. CT colonography cannot reliably detect flat dysplasia and does not allow biopsy; it is not the recommended surveillance tool in IBD.
• C. Standard population faecal occult blood screening is not sufficiently sensitive for dysplasia surveillance in longstanding colitis and is not the recommended modality.
• D. Waiting for symptoms misses the window for detecting pre-malignant dysplasia, which is usually asymptomatic.
• E. Dysplasia and cancer can develop silently in long-standing UC, so absence of symptoms does not avoid the need for surveillance.

This presentation meets Rome IV criteria for irritable bowel syndrome: recurrent abdominal pain at least one day per week for the preceding three months, associated with two or more of a relationship to defecation, change in stool frequency, or change in stool form, with symptom onset at least six months prior. The absence of alarm features, together with normal inflammatory markers, blood count and coeliac serology, supports a functional diagnosis without need for further invasive testing. Faecal calprotectin being normal makes significant mucosal inflammation from IBD unlikely. IBS is a positive clinical diagnosis based on symptom pattern once red flags and mimics are excluded by simple first-line tests.

• A. Lactose intolerance typically causes symptoms related temporally to dairy intake rather than this chronic pattern meeting Rome IV criteria, and would not be the single best diagnosis here.
• B. Microscopic colitis typically causes chronic watery diarrhoea without the pain-predominant, defecation-related pattern described, and usually occurs in older patients.
• C. Normal faecal calprotectin and the absence of alarm features make inflammatory bowel disease unlikely.
• E. Normal coeliac serology makes coeliac disease unlikely as the explanation for her symptoms.

Unintentional weight loss, rectal bleeding, altered bowel habit, and iron deficiency anaemia in a patient over 50 years are red flag features that mandate colonoscopy to exclude colorectal cancer or other significant structural pathology. These features fall outside the pattern expected for a functional disorder and cannot be safely managed with empirical dietary or symptomatic treatment alone. Even in the absence of a family history, age and alarm symptoms alone are sufficient indications for urgent investigation under Australian guidelines. Delaying definitive investigation in the presence of these features risks missing a treatable early-stage malignancy.

• A. Calprotectin may support a diagnosis of inflammation but does not exclude malignancy and is not a substitute for colonoscopy when red flags are present.
• B. Dietary modification is appropriate for functional symptoms, but red flag features here mean organic pathology must first be excluded.
• C. Watchful waiting risks delayed diagnosis of a significant underlying condition such as colorectal cancer.
• D. Symptomatic treatment without investigation is inappropriate when alarm features suggest possible malignancy.

When lifestyle measures such as adequate fluid, fibre, and mobility fail to relieve chronic constipation, an osmotic laxative such as macrogol is recommended first-line, as it draws water into the bowel lumen to soften stool and is well tolerated in older people. Bulk-forming agents require adequate fluid intake to be effective and can worsen symptoms or cause obstruction in patients with poor fluid intake or reduced mobility, making them less suitable here. Stimulant laxatives are typically reserved as an add-on if osmotic laxatives alone are insufficient. Colonoscopy is not indicated in the absence of red flag features and would not address the functional problem.

• A. There are no red flag features here to justify urgent colonoscopy.
• B. Stimulant laxatives are generally used as add-on therapy when osmotic laxatives alone do not achieve adequate response, not as the initial agent.
• C. Bulk-forming laxatives require good fluid intake to work safely and are relatively contraindicated in patients with reduced fluid intake and mobility, risking faecal impaction.
• E. Regular enemas are not appropriate first-line therapy and are reserved for refractory cases or faecal impaction.

Opioid-induced constipation results from mu-opioid receptor activity in the enteric nervous system, reducing peristalsis and secretions, and typically does not respond adequately to osmotic agents alone. Therapeutic Guidelines recommend adding a stimulant laxative such as senna to increase colonic motility, and if constipation remains refractory, a peripherally acting mu-opioid receptor antagonist such as naloxegol or methylnaltrexone can be used because it targets peripheral opioid receptors without reversing central analgesia. Bulk-forming laxatives are generally avoided in opioid-induced constipation because reduced gut motility increases the risk of obstruction. Ceasing an effective analgesic is not appropriate when the goal is to manage the constipation while maintaining pain control.

• B. Fibre alone is often ineffective and may worsen bloating or discomfort in opioid-induced constipation with reduced colonic motility.
• C. There is no indication of obstruction on examination, so imaging is not required before a trial of appropriate laxative therapy.
• D. Stopping effective analgesia is not appropriate; the constipation should be managed pharmacologically while continuing pain control.
• E. Bulk-forming laxatives are relatively contraindicated in opioid-induced constipation due to the risk of worsening obstruction with reduced gut motility.

Anti-tissue transglutaminase (anti-tTG) IgA is the recommended first-line serological test for coeliac disease because of its high sensitivity and specificity, but it must always be interpreted alongside total serum IgA, since IgA deficiency (which occurs more often in coeliac disease) causes a false-negative anti-tTG IgA result. Testing must be performed while the patient continues a gluten-containing diet, as gluten withdrawal can normalise antibody levels and compromise diagnostic accuracy. If IgA deficiency is found, IgG-based tTG or deamidated gliadin peptide testing is used instead. Positive serology is followed by referral for endoscopic duodenal biopsy to confirm the diagnosis.

• A. Anti-gliadin IgG antibody has poor sensitivity and specificity and is not recommended for routine coeliac screening.
• B. Total serum IgE is unrelated to coeliac disease and reflects atopic or parasitic conditions.
• C. HLA-DQ2/DQ8 genotyping has high sensitivity but poor specificity and is mainly used to exclude coeliac disease, not as a first-line diagnostic test.
• D. Anti-endomysial antibody testing is typically IgA-based and used as a supplementary test, not first-line, and is more operator-dependent (immunofluorescence).

Despite strongly positive serology, Australian and international guidelines recommend confirming coeliac disease with duodenal biopsy (showing villous atrophy, crypt hyperplasia and intraepithelial lymphocytosis) before committing a patient to a lifelong gluten-free diet. Biopsy should be performed while the patient is still eating gluten, as dietary withdrawal before confirmation causes histological changes to regress and can prevent accurate diagnosis. Starting a gluten-free diet first risks a false-negative biopsy if confirmation is later required. Even markedly elevated serology titres do not replace histological confirmation in adults.

• A. Starting a gluten-free diet before biopsy risks mucosal healing, making subsequent histological confirmation unreliable.
• B. Repeating serology does not provide the histological confirmation required before diagnosis.
• C. Proceeding straight to dietary therapy without biopsy risks misdiagnosis and unnecessary lifelong dietary restriction.
• D. HLA-DQ2/DQ8 testing has a high negative predictive value but cannot confirm the diagnosis since the alleles are common in the general population.

Lactose intolerance results from lactase enzyme deficiency and causes symptoms specifically after ingestion of lactose-containing dairy products, with no reaction to gluten-containing foods that do not contain lactose. Coeliac disease is an immune-mediated reaction to gluten and would be expected to cause symptoms with wheat, rye and barley regardless of dairy intake. Bloating and loose stools are non-specific and occur in both conditions, so they do not discriminate between them. A hydrogen breath test can confirm lactose intolerance if the diagnosis remains uncertain after dietary correlation.

• A. Bloating and loose stools are non-specific symptoms seen in both lactose intolerance and coeliac disease.
• B. A normal full blood count does not exclude coeliac disease, particularly in milder or earlier presentations.
• D. Negative serology makes coeliac disease less likely but is not the distinguishing clinical feature described in this history.
• E. Absence of weight loss can occur in either condition, especially early or mild coeliac disease.

Confirmed chronic hepatitis C infection, defined by positive antibody and detectable RNA, is an indication for direct-acting antiviral (DAA) therapy, which achieves cure rates greater than 95%. In Australia, DAAs are listed on the Pharmaceutical Benefits Scheme and can be prescribed by general practitioners without specialist referral in most uncompromised cases, reflecting a deliberate policy to widen access and support elimination of hepatitis C. Active or past injecting drug use is not a contraindication to treatment, and current guidelines explicitly recommend treating regardless of ongoing drug use to reduce transmission and disease burden. Interferon-based regimens are obsolete given the superior efficacy and tolerability of DAAs.

• A. Uncomplicated chronic hepatitis C without cirrhosis can be managed by general practitioners or non-specialist prescribers under the PBS without mandatory hepatologist referral.
• B. RNA PCR positivity on a single occasion together with antibody positivity is sufficient to establish chronic infection; treatment should not be delayed for repeat testing.
• C. Current guidelines recommend treating hepatitis C regardless of ongoing substance use, as abstinence is not a prerequisite for DAA therapy.
• D. Interferon-based therapy has been superseded by DAAs due to superior efficacy, shorter duration and fewer side effects.

A Maddrey discriminant function score of 32 or greater identifies severe alcoholic hepatitis, which carries a high short-term mortality risk and is an indication for corticosteroid therapy (typically prednisolone) according to Therapeutic Guidelines, provided active infection and gastrointestinal bleeding have been excluded. Corticosteroids reduce the hepatic inflammatory response and have been shown to improve short-term survival in this severe subgroup, though their benefit on longer-term mortality is less certain. Close monitoring for sepsis is essential, as corticosteroids increase infection risk, and the Lille model is used at day 7 to assess treatment response and guide whether to continue therapy. Nutritional support and strict abstinence counselling remain essential adjuncts regardless of steroid use.

• A. Transplantation assessment is considered in selected refractory severe cases unresponsive to medical therapy, not as the initial step for a first presentation with no evidence of decompensated failure.
• B. Supportive care alone is insufficient for severe alcoholic hepatitis (discriminant function greater than 32), where corticosteroids have demonstrated a short-term survival benefit.
• D. Ursodeoxycholic acid is used in cholestatic liver diseases such as primary biliary cholangitis, not alcoholic hepatitis.
• E. N-acetylcysteine is used for paracetamol-induced liver injury, not alcoholic hepatitis.

The FIB-4 index combines age, AST, ALT and platelet count to stratify the risk of advanced liver fibrosis in patients with non-alcoholic fatty liver disease. A FIB-4 score above 2.67 in patients aged over 35 indicates a high probability of advanced fibrosis and warrants referral to a hepatologist or gastroenterologist for further assessment, which may include transient elastography or liver biopsy. Scores below approximately 1.3 (or 2.0 in those over 65) indicate low risk and can generally be managed in primary care with lifestyle modification and metabolic risk factor control. Intermediate scores require further non-invasive testing such as elastography to clarify fibrosis risk.

• A. A FIB-4 score of 0.9 falls in the low-risk range, indicating advanced fibrosis is unlikely and specialist referral is not required.
• B. A FIB-4 score of 1.1 is within the low-risk range and does not meet the threshold for referral.
• D. A FIB-4 score of 0.6 is well within the low-risk range and suggests advanced fibrosis is unlikely.
• E. A FIB-4 score of 1.3 is at the upper limit of the low-risk range and does not indicate high probability of advanced fibrosis.

In a patient with raised transferrin saturation (>45%) and raised ferritin suggestive of iron overload, HFE genotyping for the C282Y and H63D mutations is the recommended next step to confirm hereditary haemochromatosis before considering biopsy. Homozygosity for C282Y confirms the diagnosis in the great majority of cases, avoiding an invasive liver biopsy. Biopsy is reserved for cases with atypical genetics, markedly elevated ferritin to assess fibrosis, or when another liver disease is suspected. Early diagnosis allows venesection therapy to prevent cirrhosis, diabetes progression, and cardiomyopathy.

• A. Caeruloplasmin is used to investigate Wilson disease, not iron overload.
• B. Urinary copper excretion is a test for Wilson disease, not relevant to this iron overload picture.
• D. Ultrasound may show hepatomegaly or fibrosis but does not establish the underlying diagnosis.
• E. Biopsy is invasive and reserved for cases where genetic testing is negative or equivocal, or to stage fibrosis once diagnosis is confirmed.

The combination of neuropsychiatric symptoms, liver disease, and Kayser-Fleischer rings in a young patient is classic for Wilson disease, a disorder of copper metabolism caused by mutations in the ATP7B gene. Initial testing involves low serum caeruloplasmin (often but not always reduced) and elevated 24-hour urinary copper excretion, supported by slit-lamp examination for Kayser-Fleischer rings. Confirmation may require liver biopsy with quantitative copper content or ATP7B genetic testing in equivocal cases. Early diagnosis is essential because untreated Wilson disease progresses to irreversible neurological damage and liver failure, whereas copper chelation therapy can reverse or halt progression.

• A. Ferritin and transferrin saturation assess iron overload, relevant to haemochromatosis, not Wilson disease.
• B. Alpha-1 antitrypsin phenotype is tested for a different genetic cause of liver disease, not copper overload.
• C. ANA and anti-smooth muscle antibody are used in the diagnosis of autoimmune hepatitis.
• E. Antimitochondrial antibody is used in the diagnosis of primary biliary cholangitis.

This woman has markedly elevated transaminases, hypergammaglobulinaemia, and a personal history of another autoimmune disease, a picture consistent with autoimmune hepatitis. Type 1 autoimmune hepatitis, the most common form in adults, is characterised by positive antinuclear antibody and/or anti-smooth muscle antibody together with elevated IgG. Liver biopsy typically shows interface hepatitis with a lymphoplasmacytic infiltrate, confirming the diagnosis. Treatment with corticosteroids with or without azathioprine induces remission in most patients and should be guided by histology and serology together.

• A. Low caeruloplasmin suggests Wilson disease, which typically presents at a younger age with neuropsychiatric features.
• B. Antimitochondrial antibody is characteristic of primary biliary cholangitis, not autoimmune hepatitis.
• D. Elevated ferritin and transferrin saturation suggest haemochromatosis, which does not fit this clinical and serological picture.
• E. Viral hepatitis serology is already stated as negative, making this an inconsistent and irrelevant finding.

A cholestatic liver enzyme pattern with pruritus and fatigue in a middle-aged woman, in the absence of biliary obstruction on imaging, is characteristic of primary biliary cholangitis. Antimitochondrial antibody is positive in over 90% of cases and is highly specific for this diagnosis. Diagnosis is established when at least two of three criteria are met: cholestatic liver enzymes, positive antimitochondrial antibody, and compatible histology on liver biopsy, though biopsy is often unnecessary when serology is positive. First-line treatment is ursodeoxycholic acid, which slows disease progression.

• A. Anti-smooth muscle antibody is associated with autoimmune hepatitis, which typically presents with a hepatitic rather than cholestatic pattern.
• B. Hepatitis B surface antigen would indicate active viral hepatitis, which does not typically cause isolated cholestasis with pruritus of this nature.
• C. HFE mutation testing is used for haemochromatosis, which does not explain this cholestatic itch picture.
• D. Caeruloplasmin is used to investigate Wilson disease, which typically presents at a younger age.

The clinical picture of fever, right upper quadrant pain and a positive Murphy sign (inspiratory arrest on palpation) is consistent with acute cholecystitis, and ultrasound is the first-line investigation given its high sensitivity and specificity, low cost and lack of radiation. Characteristic findings include gallbladder wall thickening greater than 3 mm, pericholecystic fluid, gallstones and a sonographic Murphy sign, which together support the diagnosis. Ultrasound also allows rapid bedside assessment and guides early surgical referral for cholecystectomy. CT and oral cholecystography are not first-line for suspected cholecystitis in current practice.

• A. Plain X-ray rarely shows gallstones, as most are not calcified, and is not diagnostic of cholecystitis.
• B. This finding indicates bowel obstruction, not biliary pathology.
• D. A markedly elevated lipase suggests pancreatitis rather than cholecystitis, though mild elevation can occur with biliary disease.
• E. Oral cholecystography is an outdated test, superseded by ultrasound and not used in acute assessment.

This patient has Charcot's triad of fever, jaundice and right upper quadrant pain, together with hypotension and confusion, indicating Reynolds' pentad and severe (grade III) acute cholangitis, a biliary emergency caused by obstruction (commonly choledocholithiasis) with superimposed infection. Management requires immediate intravenous fluid resuscitation, broad-spectrum antibiotics covering gram-negative enteric organisms and anaerobes, and urgent biliary decompression, usually by endoscopic retrograde cholangiopancreatography, once the patient is haemodynamically stabilised. Delay in decompression in severe cholangitis is associated with significant mortality. Cholecystectomy is not the priority in cholangitis and is usually deferred until after resolution of sepsis and duct clearance.

• B. This presentation represents sepsis with shock and altered mental status; observation alone risks death and is not appropriate.
• C. Ursodeoxycholic acid dissolves cholesterol gallstones over months and has no role in acute cholangitis.
• D. Cholecystectomy addresses gallbladder disease, not the infected obstructed common bile duct causing sepsis, which is the immediate threat here.
• E. Outpatient imaging is inappropriate given the patient's sepsis and haemodynamic instability, which require urgent inpatient intervention.

The diagnosis of acute pancreatitis requires two of three criteria: characteristic epigastric pain radiating to the back, serum lipase or amylase greater than three times the upper limit of normal, and characteristic imaging findings. This patient has classic pain and a lipase level more than twenty times normal, satisfying diagnostic criteria regardless of the inconclusive ultrasound. Chronic heavy alcohol use is one of the two most common causes of acute pancreatitis in Australia, alongside gallstones. Identifying the cause guides subsequent management, including alcohol cessation counselling in this case.

• A. Gastritis does not cause lipase elevations of this magnitude or back radiation of pain.
• C. The ultrasound shows a normal gallbladder without stones or wall thickening, making cholecystitis unlikely.
• D. Mesenteric ischaemia classically causes pain disproportionate to examination findings with a markedly raised lactate, not a markedly elevated lipase.
• E. Perforated ulcer typically causes a markedly rigid, peritonitic abdomen and free air on erect chest X-ray, not an isolated marked lipase rise.

Current evidence and guidelines support early oral feeding in mild acute pancreatitis as soon as the patient can tolerate it, rather than enforcing prolonged fasting, as this reduces length of hospital stay and does not increase complication rates. Initial management also includes adequate intravenous fluid resuscitation to maintain organ perfusion and appropriate analgesia, typically with opioids. Routine nasogastric suction and prolonged fasting are outdated practices not supported by current evidence in uncomplicated mild pancreatitis. Nutritional support such as parenteral nutrition is reserved for patients unable to tolerate oral or enteral feeding, such as those with severe disease or prolonged ileus.

• A. Waiting for normalisation of lipase delays feeding unnecessarily; clinical tolerance, not a specific lipase value, guides refeeding.
• C. A high-fat diet is not appropriate during acute pancreatitis; feeding typically starts with a low-fat, soft diet as tolerated.
• D. Parenteral nutrition is not first-line in mild pancreatitis when oral or enteral feeding is feasible and carries higher infection risk.
• E. Prolonged fasting for 7 days is not evidence-based for mild pancreatitis and increases complications such as gut mucosal atrophy.

Chronic pancreatitis causes progressive exocrine insufficiency, leading to steatorrhoea and weight loss due to malabsorption of fat, as reflected by the low faecal elastase in this patient. Pancreatic enzyme replacement therapy should be taken with the first mouthful of food at each meal and snack, since enzymes must mix with food in the stomach and duodenum to aid digestion. Capsules contain enteric-coated microspheres designed to survive gastric acid and release enzymes in the alkaline small bowel, so they should be swallowed whole, not crushed or chewed. Taking enzymes before or after meals, or only intermittently, reduces their effectiveness in controlling malabsorption.

• A. Enzymes should be taken with every meal and snack to control malabsorption continuously, not only during symptomatic flares.
• B. Enzymes taken well before food will not be present in the stomach when food arrives, reducing their digestive effect.
• D. Crushing destroys the enteric coating designed to protect enzymes from gastric acid, reducing efficacy.
• E. Once-daily dosing at bedtime does not coincide with meals and would not effectively aid digestion of food eaten throughout the day.

The National Bowel Cancer Screening Program (NBCSP) invites all Australians to complete a free immunochemical faecal occult blood test (iFOBT) every two years from age 45 to 74 years, with people aged 45-49 able to opt in and request a kit. This is a population-based screening strategy for average-risk, asymptomatic individuals and does not require colonoscopy or sigmoidoscopy as the primary screening modality. People with a positive test or significant family history require further individualised assessment. Screening at this interval and age range balances detection benefit against the harms and cost of over-testing.

• A. Flexible sigmoidoscopy is not the screening modality used in the NBCSP.
• B. Annual testing from age 40 is more frequent and starts earlier than the NBCSP recommendation.
• C. This excludes the eligible 45-59 year age group within the actual program range.
• D. Colonoscopy is not the primary screening test in the population program; it is used after a positive FOBT or for high-risk individuals.

A positive iFOBT, regardless of symptoms or examination findings, warrants referral for colonoscopy because it is the most sensitive and specific investigation for detecting colorectal neoplasia and allows biopsy or polypectomy at the same time. Repeating the FOBT is not appropriate as a single positive result already meets the threshold for further investigation and a negative repeat would not exclude pathology. CT colonography is reserved for patients in whom colonoscopy is incomplete or contraindicated. Reassurance without further work-up risks missing a colorectal cancer or advanced adenoma.

• A. CEA is not used as a diagnostic or screening test for colorectal cancer.
• B. Continuing routine screening ignores the positive result and delays diagnosis.
• C. A positive result mandates diagnostic work-up, not repeat screening, which risks a false-negative delay.
• E. CT colonography is a second-line option when colonoscopy cannot be performed or completed, not the first step.

Mild, uncomplicated acute diverticulitis in a haemodynamically stable patient who can tolerate oral intake can be managed in the community with oral antibiotics such as amoxicillin-clavulanate, covering gram-negative and anaerobic bowel flora, along with simple analgesia and a temporary low-fibre or fluid diet during the acute phase, as per Therapeutic Guidelines. Hospital admission with intravenous antibiotics is reserved for complicated disease, significant comorbidities, inability to tolerate oral intake, or systemic sepsis. Colonoscopy should be deferred for six to eight weeks after the acute episode to avoid perforation risk and to exclude underlying malignancy once inflammation has settled.

• B. Surgery is not indicated for a first uncomplicated episode without complications such as abscess or perforation.
• C. Selected mild cases without significant symptoms may sometimes avoid antibiotics, but this patient has fever and elevated inflammatory markers warranting antibiotic treatment.
• D. Colonoscopy during the acute phase carries a perforation risk and should be deferred until the inflammation resolves.
• E. Intravenous antibiotics and admission are reserved for complicated or severe disease, not mild uncomplicated cases.

This patient has signs of complicated diverticulitis, including a palpable mass, high fever, tachycardia, hypotension and markedly elevated inflammatory markers, raising concern for a diverticular abscess, perforation or obstruction. Contrast-enhanced CT of the abdomen and pelvis is the investigation of choice to confirm the diagnosis, characterise any abscess or free perforation, and guide management, including possible percutaneous drainage or surgical intervention. Oral antibiotics alone are inadequate given the severity of illness and signs suggesting a surgical complication requiring hospital admission and imaging first.

• A. Dietary advice alone does not address a likely abscess or perforation requiring urgent imaging and inpatient care.
• B. Discharge is inappropriate given hypotension, a palpable mass and markedly elevated inflammatory markers suggesting a complication.
• C. Oral antibiotics without admission and imaging are inadequate for a patient with signs of complicated disease and systemic sepsis.
• E. Colonoscopy is contraindicated in acute complicated diverticulitis due to perforation risk and is not the next investigative step.

This patient has a classic clinical presentation of acute appendicitis, with migratory pain, localised right iliac fossa tenderness, guarding, and supportive signs such as a positive Rovsing's sign, together with a raised white cell count and CRP. In a young patient with a typical history and examination, clinical diagnosis is sufficient and she should be referred for urgent surgical assessment rather than delayed by further imaging, since imaging is primarily reserved for atypical presentations or diagnostic uncertainty, such as in women where gynaecological pathology needs to be excluded or in older patients. Prompt surgical referral reduces the risk of perforation.

• A. CT is reserved for atypical presentations or diagnostic uncertainty, not needed when the clinical picture is classic.
• B. Pelvic ultrasound is useful when gynaecological pathology is suspected, but this presentation is classic for appendicitis and a negative beta-hCG lowers ectopic pregnancy likelihood.
• C. Antibiotics alone in the community are inappropriate; this is a surgical emergency requiring prompt assessment.
• E. Discharge is inappropriate given the classic signs of appendicitis and risk of perforation with delay.

Although haemorrhoids are visible, this patient has red-flag features, including age over 50 years, unintentional weight loss, a change in bowel habit and unexplained anaemia, which should never be attributed to haemorrhoids without excluding colorectal cancer first. Colonoscopy is required to directly visualise the entire colon and rectum and obtain biopsies of any suspicious lesion. Assuming haemorrhoids are the sole cause of bleeding in the presence of these alarm features risks missing a significant proportion of colorectal cancers that coexist with benign anorectal disease.

• A. Treating the haemorrhoids without first excluding malignancy fails to address the alarm symptoms present.
• C. FOBT is a population screening tool and is not appropriate once a patient already has symptomatic bleeding and red-flag features; direct colonoscopy is needed.
• D. Attributing bleeding to haemorrhoids alone ignores red-flag symptoms of weight loss, anaemia and altered bowel habit.
• E. Treating haemorrhoids does not address the need to exclude a more serious underlying cause given alarm features.

In a returned traveller with diarrhoea, the priority is oral rehydration to correct dehydration, together with stool microscopy, culture and sensitivity and examination for ova, cysts and parasites to identify the causative organism, since bacterial, parasitic and viral causes all differ in management and empirical antibiotics are not routinely recommended for mild to moderate watery diarrhoea without dysentery or systemic sepsis. This structured approach avoids unnecessary antibiotic use, which can contribute to resistance and does not benefit most self-limiting travellers' diarrhoea. Antibiotics are reserved for moderate to severe disease, dysentery or confirmed specific pathogens.

• A. Hospital admission with intravenous antibiotics is not warranted for a mildly dehydrated, haemodynamically stable patient tolerating oral fluids.
• C. Loperamide without investigation risks missing a treatable or notifiable infection and ignores the need for rehydration assessment.
• D. Empirical antibiotics without testing are not first-line for mild to moderate watery diarrhoea in a stable patient.
• E. Empirical metronidazole targets specific parasitic infections and should not be started before stool results guide the diagnosis.