Upper GI — Disease Index & Clinical Criteria

Written by Betra Youhanna, a medical student and not a doctor — check every detail against your own teaching.

Disease Index · 94 entries across 20 categories · deck-derived, finals-triage

Criteria & Scores · 52 scoring systems, classifications

C/P — Clinical Presentation

Inves — Investigations

Mng — Management

Special — Pathognomonic / disease-unique

Reflux disease & complications

4 entries

Gastro-oesophageal reflux disease (GORD/GERD)

C/P

Typical symptoms – heartburn, regurgitation; with reflux oesophagitis (erosive) or without (non-erosive reflux disease, NERD)
Atypical symptoms – noncardiac chest pain, hoarseness, chronic cough, asthma, pulmonary fibrosis, hiccups, dental erosion
Very common – prevalence 18–27% North America, 9–25% Europe, 2–8% East Asia, 9–33% Middle East, 11% Australia, 23% South America
Reflux of gastric/duodenal contents into lower oesophagus; squamous epithelium prone to acid injury; may be erosive or non-erosive
Aetiology – ↑ intra-abdominal pressure (obesity, pregnancy, low-residue diet, chronic cough); GO laxity (alcohol, hiatus hernia, smoking)
Pain may be mistaken for MI (and MI misdiagnosed as reflux)

Inves

Diagnostic tools – symptom analysis, PPI therapeutic trial, GI endoscopy, ambulatory pH monitoring (preferably MII)
Algorithm – reflux symptoms → PPI trial; persistent → endoscopy; normal endoscopy → pH monitoring + manometry
Severity of symptoms is NOT related to histology; endoscopy normal in 50–60% of symptomatic patients → biopsy if clinically suggestive
When to scope – PPI trial failure; alarm features; known grade C/D (every 2 months); >50y with Barrett's/adenocarcinoma risk factors; chronic patient with unusual disappearance of heartburn off treatment
Ambulatory pH monitoring (incl. Bravo capsule) = gold standard – assesses acid exposure + symptom-event association; not required for diagnosis
MII (impedance) – acid vs non-acid content, flow direction/proximal extent, composition (liquid/gas/mixed), total reflux events, symptom association

Mng

Step-up – lifestyle changes, antacids, H2RA (ranitidine 150 mg ×2), then switch to PPI if symptoms persist
Step-down – start PPI 20 or 40 mg, step down to lowest controlling dose (10 or 20 mg); step-down superior (71% vs 42% step-up)
Maintenance – all GORD + ~2/3 NERD need long-term Rx at lowest effective dose; continuous therapy beats on-demand for symptom control/QoL/endoscopic remission
PCABs – compete with K+ at H+/K+ ATPase (reversible); acid-stable, longer-lasting, fewer drug interactions vs PPI
Baclofen (GABA agonist) 40 mg – reduces postprandial TLESR, reflux episodes, and acid exposure time
Prokinetics (domperidone, itopride) – no concrete evidence of effectiveness
Lifestyle has little influence on pathogenesis, only weak evidence for symptom aggravation; weight matters only if BMI >30

Special

Complications – oesophageal erosion/ulcer, strictures, Barrett's oesophagus, oesophageal adenocarcinoma
Long-term Rx exceptions (no trial-off): LA grade C & D, and Barrett's oesophagus
Aggravating drugs – LES impairment (β-agonists, theophylline, anticholinergics, TCAs, progesterone, α-antagonists, diazepam, CCBs); mucosal damage (ASA/NSAIDs, tetracycline, quinidine, bisphosphonates)
H. pylori eradication does NOT increase development of oesophagitis/GORD symptoms

physiology · background · low-yield

Physiology

Transient reflux is normal (esp. after meals) and usually asymptomatic; GORD occurs when the threshold is exceeded and reparative capacity of mucosa is impaired; bile reflux (worst type) may also contribute

Mechanism

Reflux–airway link – direct contact/micro-aspiration of refluxate, and vasovagal reflex via oesophageal chemoreceptor vagal afferent loop → reflex bronchospasm/cough

Other

Post-prandial AF and atrial tachyarrhythmias described with hiatus hernia + GORD (direct & vagal mechanisms)

Epidemiology/Risk

HRM cutoff LES–CD separation 1.85 cm identifies hiatal hernia (Sens 92%, Spec 95%), exceeding endoscopy/radiography (both 73%)

Barrett's oesophagus (BO/BE)

C/P

Benign condition – glandular/columnar metaplasia of the distal oesophageal mucosa; considered a protective response to chronic acid injury (lower 1/3)
Definition – change in oesophageal epithelium of any length, recognised at endoscopy, confirmed intestinal metaplasia on biopsy of tubular oesophagus, excludes intestinal metaplasia of the cardia
Affects 10% of GORD patients and 40% of peptic strictures
Patients may be asymptomatic; prevalence increases with duration of reflux symptoms

Inves

Diagnosis is endoscopic and based on microscopic findings
Microscopy – squamous epithelium replaced by glandular (gastric/cardiac or intestinal type); intestinal type shows goblet cells
Enhancement imaging – chromoendoscopy, narrow-band imaging (NBI), endomicroscopy; IPCL patterns grade neoplastic risk under magnification/NBI
Surveillance – endoscopic follow-up + repeated biopsy to identify dysplasia/early malignancy

Mng

Endoscopic surveillance with repeat biopsy targeting dysplastic change/early malignancy
Long-term PPI therapy (Barrett's is a maintenance-therapy exception – no trial-off)

Special

30–40 fold increased risk of oesophageal adenocarcinoma (deck also cites 40–125 fold vs general population)
50% of patients with high-grade dysplasia already have malignancy
Imaging limitation – 'changes' seen in up to 40% of asymptomatic subjects; requires expertise, small area, time-consuming, poor inter/intra-observer agreement

physiology · background · low-yield

Background

Metaplasia at the gastro-oesophageal junction (GOJ); definition specifically excludes intestinal metaplasia of the cardia

Oesophagitis (reflux, infective, eosinophilic, pill/chemical)

C/P

Definition – inflammatory condition caused by damage to the oesophageal mucosa
Oesophageal symptoms – heartburn, regurgitation ± dysphagia; extra-oesophageal – persistent cough, asthma, bronchitis, laryngitis, precordial pain
Most common cause = GORD
Other causes – infection, chemicals, alcohol, radiation therapy
Infective – fungal (Candida), viral (HSV, CMV)
Chemical injury (alkali/acid), physical injury (radiation, NG tubes), hyperacidity, alcohol abuse

Inves

Endoscopy – may be grossly visible but 50–60% of symptomatic reflux patients have normal mucosa endoscopically → biopsy required even if endoscopy normal
Multiple biopsies indicated; microscopy far clearer than gross appearance
Acute microscopy – intraepithelial neutrophils/eosinophils/T-lymphocytes, basal cell hyperplasia, elongated rete ridges, epithelial erosion/ulceration, granulation tissue, reactive atypia
Chronic microscopy – intraepithelial eosinophils & lymphocytes, ++ basal hyperplasia, ++ elongation of papillae, congestion, oedema

Mng

Treat the underlying GORD to treat the oesophagitis

Special

Eosinophilic oesophagitis – named as a cause of persistent symptoms and food-bolus impaction (suspected at endoscopy alongside LA grade B/C/D and long-segment Barrett's)
Pill/drug mucosal damage – ASA/NSAIDs, tetracycline, quinidine, bisphosphonates
Reactive changes to continuous acid injury → columnar metaplasia (protective, lower 1/3) → Barrett's oesophagus
Up to 1/3 of chronic GORD patients have normal endoscopy; hyperemia may be the only finding in very mild disease

Hiatus hernia (sliding & rolling)

C/P

Definition – partial or total herniation of the stomach or GOJ through the diaphragmatic hiatus
Epidemiology – 25% of adults, age 50s, 10% asymptomatic
Aetiology – ↑ intra-abdominal pressure (obesity, pregnancy, low-residue diet, trauma); diaphragmatic laxity (previous surgery, connective tissue disorders)
Sliding (axial) – 95%; involves both stomach and GOJ
Rolling (para-oesophageal) – 5%; only the stomach herniates (usually greater curvature; whole stomach may herniate)

Inves

HRM – LES–CD separation 1.85 cm is the optimal cutoff for hiatal hernia (Sens 92%, Spec 95%), exceeding endoscopy/radiography (both 73%)

Mng

Managed along anti-reflux principles (deck gives no dedicated surgical protocol for hiatus hernia itself)

Special

Complications result from reflux oesophagitis
Associated with GORD and post-prandial AF/atrial tachyarrhythmias
A risk factor for oesophageal adenocarcinoma and an underlying cause of food-bolus impaction

physiology · background · low-yield

Epidemiology/Risk

Listed as a risk factor for oesophageal adenocarcinoma in the carcinoma lecture

Motility & functional disorders

2 entries

Achalasia (achalasia cardia)

C/P

Oesophageal 'tightness' impairing propulsion/digestion; easily confused with GORD
Caused by damaged nerves (per deck)
Causes dysphagia; an underlying disorder in food-bolus impaction; listed among functional causes of gastric-outlet-type obstruction (pylorospasm or achalasia)

Inves

Manometry – shows low oesophageal contractility (diagnostic)

Special

Achalasia cardia is a risk factor for oesophageal squamous cell carcinoma

physiology · background · low-yield

Background

Functional oesophageal disorders (globus, functional heartburn)

C/P

Symptoms arising from the GI tract not attributable to anatomic or biochemical defects
Oesophageal functional disorders named in the lectures – globus, functional heartburn, reflux hypersensitivity

physiology · background · low-yield

Background

Listed only in the Functional GI Disorders classification [068]; no detail/management taught

Oesophageal trauma & emergencies

4 entries

Oesophageal perforation (incl. Boerhaave syndrome)

C/P

Most serious perforation of the alimentary tract; near-uniformly fatal without optimal management; mortality 15–25%
Aetiology – iatrogenic most common (oesophagoscopy ± dilation/biopsy/stent, TEE, EUS); barogenic ~20% (Boerhaave – spontaneous, sudden pressure ↑ e.g. vomiting, classically the drunk patient); traumatic (blunt/penetrating, surgery); ingestion (caustic/foreign body); neoplastic; infectious
Most common site – thoracic oesophagus (>80%); occurs at areas of normal anatomic narrowing (proximal to cricopharyngeus, distal oesophagus)
Main symptom – pain (near-uniform); suspect with atypical neck/chest discomfort after instrumentation; Boerhaave = excruciating burning chest/upper-abdo pain (mimics MI or aortic dissection)
Also dysphagia, odynophagia, dysphonia
Signs (nonspecific/late) – subcutaneous crepitus (rare, very late), tachycardia (inflammatory), hypotension (late – suggests delay from event)

Inves

Essential info – cause, exact location, duration from event, underlying oesophageal disease, comorbidities
Labs – reflect hypovolaemia + inflammatory response (leukocytosis, ↑CRP)
Plain chest films – nonspecific (pleural effusion, subcutaneous emphysema, pneumomediastinum, hydropneumothorax); not uncommonly normal
Contrast swallow = gold standard – Gastrografin (light, water-soluble, sit upright to avoid aspiration) vs textbook barium (lower false-negatives but spill irritates mediastinum)
CT (with contrast/Gastrografin) complements contrast swallow
Endoscopy – does not add significant risk; useful for location/associated pathology; false-negatives not infrequent

Mng

Standard care – broad-spectrum antibiotics (gram +ve/−ve/anaerobes) + antifungal (esp. recent PPI use → fungal colonisation); physiologic support, analgesia
Principles – control leak, drain infection, eradicate sepsis, maintain GI continuity
Timing – <24 h: primary buttressed repair/anastomosis; >24 h: diversion (spit fistula + staple stomach off); resect if underlying pathology
Approach by level – cervical → left neck; mid/upper thoracic → right thoracotomy; distal/lower thoracic → left thoracotomy or transhiatal
Operative options — indication for each:
• Primary buttressed repair — most common; for <24 h; buttress with intercostal muscle flap or pleural rotational flap (pleural integrity often inadequate)
• Closure over a T-tube — for the physiologically unstable patient (technically straightforward)
• Diversion & exclusion — for >24 h; 4 steps: cervical spit fistula + gastrostomy tube + staple off distal oesophagus + wide mediastinal drainage
• Resection ± reconstruction — if underlying oesophageal pathology (selected cases)
• Endoscopic stent — perforation recognised at endoscopy, or a contained perforation → limits mediastinal contamination; fully-covered self-expanding removable metal/plastic stent ± endoscopic clipping
• EVT (endoscopic vacuum therapy) — small extraluminal collection adjacent to the defect; polyurethane sponge on a naso-oesophageal tube + continuous 125 mmHg suction, controls the collection at the same time (obviates separate drainage); usable throughout the oesophagus incl. cervical + GOJ
Non-operative (contained, minimal symptoms, no distal pathology) – stent, NG decompression, antibiotics, nutrition, ICU
Endoscopic – oesophageal stent if recognised at endoscopy; EVT (negative pressure ~125 mmHg via nasoesophageal sponge)

Special

Overall mortality ~20%; Boerhaave (spontaneous) ~36%; instrumental ~18%; cervical lowest, thoracic highest; delay >24h markedly ↑ mortality
Leaked enteric contents cause a chemical burn + bacterial/fungal contamination; negative intrathoracic pressure and rib movement exacerbate spill
Contrast evaluation of the repair ~1 week post-op

physiology · background · low-yield

Background

Spillage cascade top-to-bottom: oesophagus (aerobes/anaerobes/acid, fungal if on antacids) → gastric acid → small-bowel aerobes → large-bowel aerobes+anaerobes

Mallory-Weiss tear (gastro-oesophageal laceration syndrome)

C/P

Also known as gastro-oesophageal laceration syndrome
Longitudinal tears in the mucosa at the GOJ → upper GI bleed
Usually caused by severe alcoholism, retching, coughing, or vomiting; also severe morning sickness in pregnancy
Mean age >60

Inves

Endoscopy identifies the mucosal tear at the gastro-oesophageal junction

Mng

Most tears heal spontaneously within 24–48 h
Ongoing bleeding – oesophageal clips or sclerotic agent via endoscopy
Surgical intervention rarely needed

Special

A common oesophageal cause of upper GI bleeding (vs variceal bleed, oesophagitis, malignancy)

Corrosive / caustic oesophageal injury

C/P

Types – strong acids and alkalis, oxidants (bleach)
Alkalis are worse → perforation + liquefactive necrosis (e.g. sodium hydroxide / cleaning products); acids → strictures + coagulative necrosis
Forms – solids (max damage mouth/pharynx), liquids (oesophagus + stomach burns), vapour aspiration (ammonia, formaldehyde → airway burns)
Context – accidental (mainly children, small quantities; alkalis more often swallowed as acids cause immediate pain) vs deliberate (adults/teens, suicide attempt, larger quantities)
C/P – child or suicidal adult; odynophagia/drooling; severe: stridor, facial burn, vomiting, haematemesis, shock

Inves

Labs – CBC, CRP, blood gases, serum electrolytes, β-hCG (young women), LFTs, renal function
Plain radiographs (neck/chest/abdo) – free air bubbles = perforation
CT with contrast = gold standard; endoscopy if CT unavailable/contraindicated (drawback: cannot accurately predict transmural necrosis)
CT grades – A homogenous enhancement; B-I wall oedema + mediastinal stranding; B-II external enhancement + internal necrotic mucosa; C absent post-contrast enhancement

Mng

First aid/resuscitation – airway management, haemodynamic support
Drugs – antibiotics, steroids, PPI, analgesics
Nutrition by grade – A oral; B TPN/tube (NGT/NJT); C jejunostomy
Definitive by grade – A first aid only; B endoscopy after 3 weeks ± dilatation → fail → stent → fail → surgery; B-II surgery; C surgery
Surgery indications – perforation, stricture with failed dilatation (to 14 mm ×5 successive sessions at 3-day intervals), severe bleeding

Special

Systemic effects – hypocalcaemia (phosphoric/hydrofluoric acid), hyponatraemia (strong acid/alkali), hypokalaemia, acidosis
Oesophagus preferentially/most severely affected at the striated–smooth muscle interface (slower clearance)
Bleeding/perforation may be immediate or delayed up to 7 days; late cancer 1–4% within 10–40 years

physiology · background · low-yield

Epidemiology/Risk

History of caustic ingestion is a risk factor for oesophageal squamous cell carcinoma

Ingested foreign body

C/P

Types – coins, batteries, toys, magnets
Typical patients – children, psychotics, prisoners
Presentation – odynophagia, drooling
80–90% pass spontaneously

Inves

Plain radiographs (neck/chest/abdo) – presence, location, size, shape, number, signs of perforation; ~45% false-negative (food bolus, thin metal, wood, plastic, glass, fish/chicken bones)
CT (± contrast) – 90–100% positive
Endoscopy (diagnostic + therapeutic) – indicated for sharp/pointed objects, batteries, magnets, impaction, persistent symptoms despite negative radiograph

Mng

Endoscopic retrieval – balloon catheter, baskets, snares, grasping forceps (Raptor, rat-tooth, Roth net, basket, 3–4 prong)
Surgery indications – irretrievable FB; complications (perforation → mediastinitis/empyema/fistula, severe bleeding)
Procedures – oesophagotomy + extraction + primary closure (limited contamination, viable edges); rescue oesophagectomy (perforation + extensive contamination/devitalised edges)

Special

Impaction suggests an underlying disorder in 25%: stricture, hiatus hernia, oesophageal web/Schatzki ring, eosinophilic oesophagitis, achalasia, tumours

Webs, rings & strictures

2 entries

Plummer-Vinson syndrome

C/P

Upper oesophageal web
Associated with upper oesophageal dysmotility, atrophic oesophageal mucosa, and iron-deficiency anaemia (the cause)

Inves

Oesophageal web demonstrated on the webs figure (endoscopy/contrast)

Special

Risk factor for oesophageal squamous cell carcinoma
An underlying disorder in food-bolus impaction

Oesophageal webs, rings & strictures (Schatzki ring)

C/P

Schatzki ring – lower oesophageal web at the squamocolumnar junction (SCJ), associated with GERD; found in up to 15% of GERD patients
Symptoms occur only if diameter <13 mm
Strictures – long-term consequence of chronic GORD/reflux oesophagitis and of caustic injury (40% of peptic strictures harbour Barrett's)

Inves

Endoscopy (web/ring/stricture); contrast/barium swallow

Mng

Peptic stricture – managed within reflux control; caustic stricture – endoscopic dilatation ± stent → surgery if failed (to 14 mm ×5 sessions)

Special

Underlying cause of foreign-body/food-bolus impaction
Contrast pair: Schatzki = lower web, GERD-associated; Plummer-Vinson = upper web, iron-deficiency

Oesophageal tumours

1 entries

Oesophageal carcinoma (SCC & adenocarcinoma)

C/P

Recent, progressive dysphagia – commonest presenting feature (two-thirds of the lumen must be occluded before dysphagia appears)
Often advanced and inoperable at presentation – only palliative treatment possible
No odynophagia – odynophagia points to inflammatory lesions (reflux, candida) instead
Regurgitation (not reflux) – increases with size of the proximally dilated oesophagus
Anorexia, severe weight loss, cachexia; substernal or abdominal pain
Back pain – paraoesophageal/coeliac nodal spread
Bronchopneumonia (from regurgitation/aspiration); melaena
Hoarseness – recurrent laryngeal nerve involvement; hiccough – phrenic nerve involvement
Features of broncho-oesophageal fistula in upper-third tumours
Palpable left supraclavicular lymph nodes; ascites (peritoneal/liver deposits)
Epidemiology: 6th commonest cancer worldwide, <1% of all cancers, 7% of GI malignancies; peaks 6th–7th decade; M:F 3.5:1
SCC – commonest worldwide; usually middle third (upper:middle:lower = 15:50:35)
Adenocarcinoma – commonest in US/West; usually lower third (65%); incidence risen dramatically over last 20 yrs

Inves

Barium swallow – shouldering sign + irregular filling defect
Oesophagoscopy + biopsy – almost always diagnostic; shows lesion, extent, type (ulcerative/proliferative)
EUS – assesses T stage (depth) and regional nodes; detects nodes <5 mm that CT misses
CECT chest + abdomen – local extension, nodal status, vascular infiltration, mediastinal fat, tracheobronchial tree
PET-CT – distant metastases, staging, and response to therapy
Bronchoscopy (upper-third invasion), laryngoscopy (vocal cord palsy), CXR (aspiration pneumonia)
Laparoscopy – only reliable method to detect peritoneal seedlings; prevents unnecessary laparotomy
U/S abdomen (liver + abdominal nodes); endoscopic iodine staining – normal mucosa stains brown, carcinoma stays pale
EMR – diagnostic biopsy tool, therapeutic in early/premalignant (T1a) lesions; ESD removes up to muscularis propria
Staging pathway: endoscopy in every patient with dysphagia → CECT + PET for distant mets → if none, EUS for T stage + regional nodes

Mng

Only 20% present early/curable; two intents – curative vs palliative
Curative surgery = radical oesophagectomy for early growth with no nodal spread; proximal margin 10 cm above, distal margin 5 cm below tumour; proximal stomach removed in lower-third tumours
Node-positive → multimodal approach (curative resection + radiotherapy + chemotherapy)
Neoadjuvant chemotherapy ± radiotherapy (pre-op) may improve survival
Aggressive chemoradiation as definitive/curative therapy – esp. upper-third growths and patients unfit for surgery
Post-cricoid / upper-third SCC → mainly radiotherapy; pharyngolaryngectomy with gastric or colonic transposition (free jejunal transfer alternative)
Upper-third operable → McKeown 3-phase oesophagectomy (laparotomy → right thoracotomy 5th space → left neck; anastomosis in neck)
Middle-third → Ivor Lewis (Lewis-Tanner 2-phase) oesophagectomy – laparotomy + right thoracotomy; oesophagogastric anastomosis in the thorax
Lower-third (SCC & adeno) → left thoracoabdominal partial oesophagogastrectomy; or Orringer transhiatal blind total oesophagectomy with left-neck anastomosis
Oesophageal substitute: stomach preferred > colon (fewer postprandial problems) > jejunum (last option)
Minimally invasive: thoracoscopic-laparoscopic oesophagectomy + lymphadenectomy; radical oesophagectomy with 3-field clearance
Palliation (unfit / blood or adjacent-organ / peritoneal-liver spread) – relieve pain & dysphagia, prevent aspiration & bleeding
Palliative options: external + intraluminal RT (brachytherapy), chemotherapy
Self-expanding metal stents (SEMS) – ideal method of palliation, minimal perforation
Intubation tube (guidewire under C-arm) – perforation risk 10%
Nd:YAG laser – cores a channel through tumour (85% palliation success); bipolar diathermy; photodynamic therapy

Special

Lacks a serosa (like rectum) → early local invasion; spreads mainly by lymphatics (70%)
SCC risk factors: alcohol + tobacco, male, HPV 16/18, Plummer-Vinson syndrome, achalasia cardia, tylosis (RHBDF2), Fanconi anaemia (FANCD1/BRCA2), caustic ingestion, nitrosamines, vit A & C deficiency, mycotoxins; p53 / loss of 3p & 9q / cyclin D1 & EGFR mutations
Adenocarcinoma risk factors: Barrett's oesophagus, GERD, hiatal hernia, Zollinger-Ellison, obesity, smoking, male
Direct spread: recurrent laryngeal nerve (hoarseness), aorta (fatal haemorrhage), trachea/bronchus → broncho-/tracheo-/aorto-oesophageal fistulas
Complications of oesophagectomy: 5–10% mortality, chylothorax (thoracic duct), anastomotic leak (thoracic leak most dangerous), hoarseness (RLN palsy), stricture (40%), GERD, conduit necrosis, colonic dysmotility
Poor prognosis; nodal involvement carries bad prognosis; 5-yr survival only 10%
Indications favouring palliation: nodes >5 involved, poorly differentiated grade, length >8 cm, abnormal oesophageal axis on barium, Horner's syndrome, weight loss >20%, metastatic disease

physiology · background · low-yield

Epidemiology/Risk

SCC commonest type worldwide (China, South Africa, Asian countries); adenocarcinoma commoner in the US; ~17,000 US cases/yr and 480,000 worldwide; African-American:White male incidence 5:1

Background

Pathological classification: preinvasive neoplasia (intraepithelial neoplasia; glandular dysplasia / adenocarcinoma in situ in Barrett's mucosa) vs invasive (SCC, adenocarcinoma, adenoid cystic, mucoepidermoid, adenosquamous, small cell, carcinoid, malignant melanoma, sarcomas)
Anatomy: 25 cm muscular tube, cricopharyngeus (cricoid) to GE junction, spans C7–T10, 4 constrictions; submucosal lymphatics extend long distances (traditional resection margins ≥5 cm proximal and distal)

Oesophageal traumatic emergencies

1 entries

Corrosive (caustic) oesophageal injury

C/P

Child (accidental, small quantity) or suicidal adult/teenager (deliberate, greater quantity)
Alkalis are worse – liquefactive necrosis, deeper penetration, perforation; swallowed accidentally more often (acids cause immediate pain)
Acids – coagulative necrosis, limited penetration, strictures
Odynophagia, drooling; severe cases: stridor, facial burn, vomiting, haematemesis, shock
Forms: solids → maximum damage to mouth/pharynx; liquids → oesophagus & stomach burns; vapour aspiration (ammonia, formaldehyde) → airway burns
Common agents: strong acids and alkalies, oxidants (e.g. bleach), cleaning products (sodium hydroxide)

Inves

Labs: CBC, CRP, blood gases, serum electrolytes, β-hCG (young women), LFTs, renal function
Plain radiographs (neck/chest/abdomen): free air bubbles = perforation
CT with contrast = gold standard; graded A–C by enhancement
Endoscopy when CT unavailable/contraindicated (renal, radiation, contrast allergy) or interpretation uncertain; major drawback – cannot accurately predict transmural necrosis
Systemic effects: hypocalcaemia (phosphoric/hydrofluoric acids), hyponatraemia (strong acids/alkalis), hypokalaemia, acidosis

Mng

First aid / resuscitation: airway management + haemodynamic support
Drugs: antibiotics, steroids, PPI, analgesics
Nutrition by grade: A → oral; B → TPN / tube (NGT/NJT); C → jejunostomy
Definitive by grade: A → first aid only; B → endoscopic assessment after 3 weeks ± dilatation → fail: stent → fail: surgery; B-II → surgery (high stricture + perforation risk); C → surgery (very high perforation risk)
Surgery indications: perforation; stricture with failed dilatation (to 14 mm for 5 successive sessions at 3-day intervals); severe bleeding

Special

Preferentially and most severely affected at the striated–smooth muscle interface (slower clearance there)
Phases of lye injury: acute necrotic (1–4 days) → ulceration-granulation (from 3–5 days, lasts 10–12 days – oesophagus weakest) → cicatrization/scarring (from 3rd week – contraction and stricture)
Bleeding and perforation may be immediate or delayed up to 7 days
Late cancer (1–4%) may develop within 10–40 years
CT grade predicts stricture risk: B-I → 20%, B-II → 80%; Grade C → perforation

Gastritis

4 entries

Acute gastritis (acute erosive gastritis)

C/P

Acute inflammation of the gastric mucosa characterised by a neutrophil infiltrate
Dyspepsia, nausea and vomiting, epigastric pain; loss of appetite, indigestion
Melaena; heartburn listed among symptoms ([056]) — but heartburn is NOT a typical/usual symptom of gastritis ([082])
Causes: alcohol, smoking, aspirin & NSAIDs, chemotherapy, H. pylori / HSV / CMV, stress

Inves

Endoscopy/gross: multiple erosive, haemorrhagic foci in gastric mucosa; congestion and erythema
Microscopy: infiltration of mucosa by neutrophils with congestion and oedema (features of acute inflammation)

Mng

Treat the cause (e.g. H. pylori)
PPI, P-CABs, antibiotics; symptomatic treatment; treat complications

Special

Progression: ↓mucosal protection / direct epithelial damage → acid diffusion → neutrophil infiltrate, oedema, congestion → erosions & haemorrhage (→ haematemesis & melaena) → ischaemia, necrosis, ulceration, perforation, shock
Repair → chronic gastritis

physiology · background · low-yield

Mechanism

Mild & transient in most; severe end of spectrum = ischaemia, ulceration, perforation, shock & death

Chronic gastritis

C/P

Sustained inflammatory response to gastric mucosal damage — chronic inflammation (plasma cells) ± acute component
May lead to intestinal metaplasia and glandular atrophy
Symptoms absent or mild (without complications); episodic pain, nausea ± vomiting

Inves

Histologic classification: updated Sydney system (2001) — aetiology, topography, morphology

Mng

Treat the cause

Special

Complications: pernicious anaemia/malabsorption; erosions & bleeding; peptic ulcer disease
Increased risk of tumours: adenocarcinoma, carcinoid (autoimmune), MALT lymphoma (H. pylori)

physiology · background · low-yield

Background

Gastritis vs gastropathy: "-itis" includes inflammatory cells; "-opathy" = pathology with minimal inflammatory cells (chemical/physical, e.g. PHG, NSAID)

H. pylori gastritis (bacterial / type B, antral)

C/P

90% of chronic gastritis affecting the antrum is caused by H. pylori
Mucosa (esp. antrum) erythematous and mamillated; accentuation of the areae gastricae pattern
Duodenitis: erythema and erosions; varioliform (raised erosions) gastritis may occur
Association: low socio-economic status, poverty

Inves

Stool Ag (very common, very specific); urea breath test (enzymatic action); serum Ab
Endoscopic tests: rapid urease test, histopathology
Microscopy: H. pylori within mucus over epithelial cells; neutrophils in lamina propria/intraepithelial/gastric-pit abscesses; plasma cells, lymphocytes, macrophages → lymphoid follicles
Warthin–Starry silver stain

Mng

Eradication therapy (see PUD eradication regimens); treat the cause

Special

Virulence factors: flagella (motility in mucus), urease (ammonia from urea → ↑pH, protects from acid), adhesins (adhere to foveolar cells), toxins (ulcer/cancer)
H. pylori gastritis → ↑acid secretion → peptic ulcer (stomach or duodenum)
Damaging effect supervenes → pangastritis → multifocal atrophic gastritis (↓acid, intestinal metaplasia) → gastric adenocarcinoma risk; lymphoid follicles → MALT lymphoma

physiology · background · low-yield

Microbiology

H. pylori adapts to the niche in gastric mucus; progression driven by interaction between host immunity and the bacterium

Autoimmune gastritis (type A, pernicious anaemia)

C/P

~10% of cases of chronic gastritis
Characteristically spares the antrum; affects the body alone (body/fundus)
Associations: autoimmune disease, thyroiditis, DM

Inves

Antibodies to parietal cells and intrinsic factor in serum and gastric secretions
Reduced serum pepsinogen I
Antral endocrine cell hyperplasia
Vitamin B12 deficiency
Achlorhydria (defective gastric acid secretion)

Mng

B12 replacement / treat pernicious anaemia (deck: symptomatic + treat complications)

Special

Pathogenesis: anti-parietal cell Ab → loss of parietal cells → deficient acid → gastrin release → hypergastrinaemia → antral G-cell hyperplasia
Deficient intrinsic factor → ↓B12 absorption → megaloblastic (pernicious) anaemia
Chief cell loss → ↓pepsinogen I
Neuroendocrine hyperplasia → carcinoid risk

Peptic ulcer disease

4 entries

Peptic ulcer disease (PUD)

C/P

Definition: chronic mucosal defects (+ submucosa) from acid and pepsin attack; lifetime risk 5–10%
Sites: 1st part duodenum; stomach (lesser curvature & pyloric antrum); lower oesophagus (reflux); Meckel's diverticulum (ectopic gastric mucosa); distal duodenum & jejunum in ZES; gastrojejunostomy stomal ulcer
98% in 1st part duodenum (75%) or stomach (25%)
Symptoms (relapsing/remitting): epigastric pain, nausea/vomiting, haematemesis ± melaena, weight loss, anaemia
Pain described as "gnawing", "aching" or "burning"
Aetiology: acute/chronic gastritis, H. pylori, NSAIDs, smoking, alcohol, stress, bile reflux, Zollinger–Ellison

Inves

Signs & symptoms, history, laboratory, endoscopy, biopsy
H. pylori: stool Ag, urea breath test, serum Ab, rapid urease test, histopathology
No point biopsying a duodenal ulcer (most benign); gastric ulcers can turn malignant

Mng

Medical: PPIs, H2R antagonists, antacids, H. pylori treatment
Endoscopic treatment; surgical treatment
Eradication regimens: bismuth quadruple therapy = current first-line; clarithromycin-/levofloxacin-based largely dropped (resistance); salvage; high-dose dual therapy (HDDT)
Test-and-treat H. pylori (ACG 2017): active PUD, past PUD, MALT lymphoma, post-resection early gastric cancer, dyspepsia <55 without alarm features, long-term low-dose aspirin, chronic NSAIDs, unexplained IDA, ITP

Special

Pathogenesis = imbalance between mucosal protection and acid/pepsin: hyperacidity (H. pylori, ZES, chronic stress) + ↓mucosal defence (mucus-bicarbonate barrier; epithelial barrier — NSAIDs, corticosteroids, H. pylori, smoking)
In gastric PUD, breakdown of mucosal defence > excess acid; in duodenal PUD, H. pylori gastritis with high acid production is the main cause
Gross: 90% single, well demarcated, <4 cm, round/oval, clean base "punched out", surrounding chronic gastritis
Complications: bleeding 15–20% (25% of ulcer deaths), perforation 5% (66% of ulcer deaths), obstruction 2%, fibrosis/stricture/hourglass stomach, anaemia, ↑malignancy risk

physiology · background · low-yield

Physiology

Histological zones of a peptic ulcer: surface fibrinous debris → acute inflammation → granulation tissue → fibrosis/fibrous scar

Gastric ulcer (GU)

C/P

Can be malignant or benign
Common in late middle age; incidence ↑ with age; M:F 2:1; blood group A
Pain provoked by food intake, localized epigastric (main hallmark); nausea and vomiting
Less related to H. pylori than DU — about 80%
NSAIDs: 3–4× increased risk of gastric ulcer
10–20% have a concomitant duodenal ulcer
Most common site: lesser curvature at junction of fundus and antrum
Causes: H. pylori, delayed gastric emptying, defective mucosal barrier, bile reflux (pyloric dysfunction → back-diffusion → HCl), NSAIDs

Inves

Endoscopy + biopsy, radiography (barium meal)
Biopsy essential — gastric ulcers can turn malignant

Mng

As PUD: PPI/H2RA/antacids + H. pylori eradication; endoscopic/surgical if complicated

Special

Benign ulcer: smooth regular rounded edge, flat smooth base, radiating folds
Malignant ulcer: irregular overhanging margins, ulcerated mass protruding into lumen, nodular/irregular folds
Recurrence 40–60% within 2 years of healing

Duodenal ulcer (DU)

C/P

Almost always benign; usually small (≤0.5 cm), penetrating to muscle (erosion = superficial, does not reach muscle)
Duodenal sites 4× as common as gastric; peak 30–50 yrs; M:F 4:1; blood group O; smoking twice as common; ↑serum pepsinogen; 3× in 1st-degree relatives
H. pylori up to 95%
Pain relieved by food intake; upper abdomen radiating to back; on empty stomach; "burning"
Vomiting in 25%
Causes: H. pylori, gastric-acid hypersecretion, ↑parietal cells, ↑parietal cell sensitivity to gastrin, reduced gastrin inhibition, increased gastric emptying, reduced neutralizing capacity

Inves

Endoscopy, radiography (barium meal); no point in biopsy (benign)

Mng

As PUD: PPI/H2RA/antacids + H. pylori eradication

Special

Recurrence very common — 95%; 50% within 6–8 months after healing
Key discriminator: GU pain provoked by food; DU pain relieved by food

Zollinger-Ellison syndrome (gastrinoma)

C/P

Gastrin-secreting tumour (gastrinoma) → ZES: massive peptic ulcers, steatorrhoea & diarrhoea
Chronic epigastric pain, reflux, unexplained diarrhoea, upper GI bleeding (melaena), ulcers
PUD features in ZES: multiple, refractory to therapy, giant, recurrent ulcers; ulcers with unexplained diarrhoea (indicates hypersecretion); DU not related to H. pylori or NSAIDs
Ulcers in distal duodenum & jejunum / upper GIT at unusual sites (acid hypersecretion)
Associated with MEN-1 (with insulinoma, VIPoma, pituitary adenoma, parathyroid hyperplasia)

Inves

Fasting hypergastrinaemia — patient must be off H2 blockers/PPIs
Gut hormone panel: fast overnight, stop PPIs 2 weeks, H2 antagonists 72 h; sample on ice
Chromogranin A (general NET marker)

Mng

PPIs (high dose), H2 blockers, surgical care

Special

Acid-hypersecretion cause of PUD via hypergastrinaemia
Diarrhoea alongside ulcers is a key clue to hypersecretion

physiology · background · low-yield

Background

One of the GI neuroendocrine tumours (NETs); gastrinoma mediator = gastrin, effect = Zollinger–Ellison syndrome

Complicated peptic ulcer disease

3 entries

Bleeding peptic ulcer (haemorrhage)

C/P

Most common complication of PUD; occurs in ~20%
Results from penetration of ulcer into blood vessels: small vein → haematemesis/melaena; artery → profuse haematemesis
Weakness and dizziness common
Haematemesis: dark coffee-ground (acid haematin); melaena: altered blood in stools; progressive shock
Self-limited in 75%; 25% bleed/re-bleed in hospital

Inves

EGD / gastroscopy = most important assessment tool (diagnostic AND therapeutic)
Exclude false haematemesis (examine nose & pharynx); exclude portal hypertension / bleeding varices (commonest cause of haematemesis)
Bleeding severity: microscopic; mild (granulation tissue); moderate (small vessel erosion); severe (large extra-gastric vessel e.g. gastroduodenal artery — usually fatal)

Mng

First: resuscitate — IV crystalloids + blood transfusion (fresh blood = best single item); monitor pulse/BP/haematocrit; IV H2 blockers or omeprazole; antacids; correct bleeding tendency
Second: endoscopic haemostasis — injection (adrenaline/alcohol), heater/thermal probe, laser coagulation, diathermy, clipping
Indications for endoscopic haemostasis: actively bleeding ulcer; stigmata of recent bleeding (visible vessel, fresh clot)
Angiographic embolization if endoscopy fails or surgery contraindicated
Treat with PPI + evaluate/eradicate H. pylori
Surgery if all fail — indicated in massive bleeding, failed endoscopy, recurrent haemorrhage, or neoplasm: cessation of bleeding + acid-reduction procedure

Special

Non-refractory ulcer → anterior gastrotomy, ulcer oversewing + biopsy (procedure of choice)
Truncal vagotomy only for ulcers refractory to PPI + H. pylori eradication
Distal gastrectomy for stable patients with refractory large antral ulcers
Higher-risk group: shock at presentation, 4–6 units blood, repeated hospitalization, ulcer >2 cm, age >60, concurrent perforation/obstruction, no endoscopy/blood available

physiology · background · low-yield

Background

Peptic ulcer remains the most common cause of upper GI bleeding; H. pylori and NSAID use are the most frequent inciting factors in bleeding gastric ulcers

Perforated peptic ulcer

C/P

2nd most common complication; more frequent in duodenal ulcer
Presentation = acute abdomen: history of PUD, sudden severe abdominal pain, shock/sepsis (neurogenic/vagal or septic shock)
Abdominal exam: tenderness, guarding, board-like rigidity, rebound tenderness
Now most common in elderly, esp. women; majority due to NSAID use
Clinical stages: [A] shock (sudden severe pain, vomiting once, neurogenic shock, board-like rigidity); [B] lucid interval (pain diminishes, walks in; obliteration of liver dullness, shifting dullness); [C] septic peritonitis (distension, dead silent abdomen, absolute constipation, hypovolaemic shock, dies in days)

Inves

Erect X-ray abdomen: free air under diaphragm (~80%), esp. right side
Labs: electrolytes, leukocytosis, ABGs → lactate; amylase often raised (but 3× → pancreatitis)
CT abdomen
Generally do NOT endoscope (air insufflation worsens perforation)

Mng

Urgent operation (open or laparoscopic)
Preop: Ryle's tube + continuous aspiration, IV fluids (guided by electrolytes/pH), IV antibiotics, IV H2 blockers/PPIs, attention to respiration, blood transfusion in late toxaemic cases
At operation (simplest): closure of perforation with covering omental patch + thorough peritoneal toilet + drainage; biopsy if gastric ulcer
Postop: treated medically for ulcer disease
Subacute perforation (small, rapidly sealed) can be treated conservatively

Special

Natural history: chemical peritonitis (acid) → lucid interval → bacterial peritonitis (undigested food)
DU perforation less serious (longer lucid interval): contents more sterile, less irritant, smaller; flow along right paracolic gutter → localize in right iliac fossa; only 1st part duodenum is intraperitoneal
GU perforates directly into general peritoneal cavity → generalized peritonitis
DDx: perforated appendicitis, acute cholecystitis, acute pancreatitis, intestinal obstruction; at onset differentiate from MI

Gastric outlet obstruction (obstructing peptic ulcer / pyloric stenosis)

C/P

Complication of healing ulcers (fibrous contractures): pyloric stenosis, hourglass stomach, teapot/handbag stomach
Occurs in ~2% of PUD
Long history of ulcer dyspepsia; loss of initial periodic ulcer pain → epigastric fullness; progressive constipation
Vomiting: projectile, not bile-stained, contains food of previous meals/days, foul odour (fermentation), characteristically in the evening
Signs: underweight; epigastric fullness (contour of enlarged stomach); succussion splash; visible peristalsis left→right

Inves

Hb/Hct, serum electrolytes
Endoscopy: pyloric ring inactive, won't pass endoscope tip; detect tumour + biopsy
Barium meal: dilated stomach reaching the pelvis (soup-dish appearance), delayed gastric emptying, irregular filling defect if carcinoma

Mng

Not an emergency — needs proper preop prep: suck & wash stomach (NG tube), correct fluid/electrolyte/acid-base, high-protein fluid diet + IV alimentation, parenteral vitamins, packed cells for anaemia, chest physio + antibiotics
Some cases (muscle spasm + inflammation around active DU) respond to medical treatment
Surgery: standard = truncal vagotomy + gastrojejunostomy; gastrojejunostomy alone (elderly/unfit); endoscopic balloon dilatation (transient, ultimately fails); partial gastrectomy + gastrojejunostomy

Special

Complications of repeated vomiting: metabolic alkalosis ± tetany; hyponatraemia & hypokalaemia; dehydration, weight loss, avitaminosis; antral stasis releases gastrin → other ulcers; respiratory tract infection from inhalation of vomitus
Tetany mechanism: alkalosis → ↓H⁺ → frees albumin → binds calcium
Pathology: pylorus cicatrized/stenosed; stomach hypertrophied then dilated; mucosa hypertrophic → atrophic gastritis + true hypoacidity (stagnation/fermentation)
DDx: traumatic (foreign body, corrosive, post-pyloroplasty); inflammatory (cicatrized DU/prepyloric GU, TB, Crohn's, syphilis); neoplastic (cancer pylorus, sarcoma, leiomyoma); pressure (LN, bands, pancreatic head tumour); functional (pylorospasm, achalasia)

physiology · background · low-yield

Other

Post-gastrectomy complications: anastomotic bleeding (first 24 h & days 4–7), duodenal stump leak (Billroth II — bile-stained drainage), gastric retention, dumping syndrome (early 30 min: vertigo/tachycardia/syncope/sweating; late 90 min–3 h), iron-deficiency anaemia, fat malabsorption

Gastric epithelial tumours

2 entries

Gastric adenocarcinoma (gastric carcinoma)

C/P

Most patients present at advanced stage — early disease is often asymptomatic
Epigastric pain, bloating, early satiety, postprandial fullness, nausea & vomiting, dysphagia, dyspepsia, anorexia
Weight loss (e.g. 10 kg in 4 weeks)
Upper GI bleeding — haematemesis, melena, iron-deficiency anaemia
General signs (advanced): anaemia, cachexia
Abdominal signs: epigastric mass, hepatomegaly, malignant ascites
Metastatic signs: jaundice (liver met/obstructive), Blumer's shelf (rectal shelf), Virchow's node (left supraclavicular), Sister Mary Joseph nodule (umbilical), Krukenberg tumour (ovarian met)
Predisposing risk: pernicious anaemia & atrophic gastritis (achlorhydria), previous gastric resection, chronic peptic ulcer (~1%), smoking, alcohol
Environmental: H. pylori (6–9× risk), low socio-economic status, Japanese nationality, diet (smoked/salted food, nitrates, low fruit & veg)
Genetic: blood group A, HNPCC, family history (8–10%)
Incidence highest in Japan (70/100,000/yr) > Europe > UK > USA (10); decreasing worldwide; falls in Japanese immigrants to USA (environmental factor)

Inves

UGI endoscopy (EGD) — diagnostic study of choice / gold standard; accuracy 98% if up to 7 biopsies taken; shows ulcers (25%), polypoid mass (25%), superficial spreading (10%) or infiltrative linitis plastica (hard to detect)
Double-contrast barium UGI X-ray — accuracy 90%; misses early superficial lesions; signs: filling defect, string sign (pylorus), linitis plastica (fixed narrow proximal stomach); cannot definitively distinguish benign ulcer from ulcerating adenocarcinoma
Endoscopic ultrasound (EUS) — assesses depth of invasion (T stage) through mucosa/submucosa/muscularis propria/serosa
CT, MRI, US — wall thickness, metastases (peritoneum, liver, LNs); laparoscopy detects peritoneal metastases
Bloods: FBC (IDA), LFT, RFT, amylase & lipase, stool occult blood
Tumour markers CA72-4, CEA, CA19-9 — not specific

Mng

Surgery is the main curative option
Pre-op: careful staging to avoid futile radical surgery; optimise nutrition (parenteral/enteral), correct fluid/electrolytes & anaemia, prophylactic antibiotics, ABO/crossmatch, stop smoking, DVT prophylaxis
Total (radical) gastrectomy — for midbody & proximal disease; remove stomach + distal oesophagus + proximal duodenum + omenta + LNs; reconstruct oesophagojejunostomy with Roux-en-Y
Subtotal gastrectomy — for antral (distal 1/3) disease; reconstruct gastrojejunostomy (Billroth II)
Palliative surgery — relieve obstruction/bleeding/perforation (resection or gastrojejunal bypass) for advanced inoperable symptomatic disease
Early T1–T2 N0 M0 — endoscopic resection (EMR: submucosal cushion + snare; ESD/ESR: submucosal knife dissection for larger/deeper lesions) or interventional radiology
Chemotherapy (Marsden regimen): epirubicin + cisplatin + 5-FU (3 wks × 6 cycles), response ~40%; used to downsize tumour for resectability
Post-op radiotherapy may reduce recurrence; prevention = fruit & veg, stop alcohol; early diagnosis remains the key challenge

Special

Virchow's node (left supraclavicular) = Troisier's sign
Krukenberg tumour — transperitoneal spread to ovaries (a GIT tumour that spreads to ovary)
Linitis plastica — diffuse infiltrative adenocarcinoma giving a shrunken 'leather-bottle' stomach
Signet-ring cell type — diffuse carcinoma; isolated cells with loss of E-cadherin
Spread: direct (pancreas, colon, liver), lymphatic (submucosal/subserosal channels), transperitoneal (ascites), blood-borne (liver first, then lung & bone)
2 key prognostic factors: depth of invasion & lymph node involvement
Bormann types III & IV are incurable
Complications: GI bleeding, pyloric/gastric-outlet obstruction, hypochlorhydria + intrinsic factor deficiency → anaemia, malignant ascites/pleural effusion, intrahepatic jaundice from hepatomegaly

physiology · background · low-yield

Mechanism

Intestinal-type pathway: H. pylori or autoimmune gastritis → atrophic gastritis → intestinal metaplasia → dysplasia → carcinoma

Background

Differential: benign gastric ulcer (cancer pain not relieved by antacids, not periodic, not relieved by eating/vomiting), other gastric neoplasms, gastritis, gastric polyp, Crohn's disease
Microscopic types also include mucoid carcinoma, anaplastic carcinoma, and large-cell/small-cell neuroendocrine carcinoma
'The more distal, the less invasive' — distal tumours may allow subtotal gastrectomy; more proximal disease requires total gastrectomy

Hereditary Diffuse Gastric Cancer (HDGC, CDH1)

C/P

Germline CDH1 mutation — encodes the cell-adhesion protein E-cadherin, essential for epithelial glandular structure
Presents as diffuse gastric cancer / linitis plastica; younger patients, M=F, whole-stomach involvement
Female carriers have a 60% lifetime risk of lobular breast carcinoma

Inves

IGCLC criteria trigger CDH1 testing (see Criteria)
Endoscopic surveillance for diffuse gastric cancer is inadequate
Precursor lesion: tubular / signet-ring neck dysplasia

Mng

Carriers advised prophylactic gastrectomy to remove DGC risk
Manage the associated lobular breast cancer risk in female carriers

Special

CDH1/E-cadherin loss → dis-cohesive signet-ring cells with no glandular structure
Surrounding mucosa is non-atrophic and non-metaplastic (unlike intestinal type)

Mesenchymal tumours

1 entries

Gastrointestinal Stromal Tumour (GIST)

C/P

Most common mesenchymal tumour of the GI tract; the most common type of sarcoma
Arises from / shares phenotype with interstitial cells of Cajal in the myenteric plexus of the muscularis propria
Stomach = most common site (60%), then ileum & jejunum (30%)
M:F ≈ 1:1, no sex predilection; mean age at diagnosis 60–65 yrs
Most common presentation: GI bleeding or abdominal pain; often incidental
Micro/mini/subclinical GIST: minute 1–10 mm growths of ICC / GIST-like cells

Inves

CT — solid, heterogeneous mass
Endoscopy — subepithelial lesion (smooth bulge, normal overlying mucosa)
EUS — hypoechoic solid mass
Definitive diagnosis only by histology + immunohistochemistry
Gross: solitary, well-circumscribed, fleshy submucosal/intramural mass; mean 6 cm (range 0.4–40 cm)
Micro: 3 morphologic types — spindle (70%), epithelioid (20%), mixed (10%)
IHC: DOG1 = most specific marker; c-KIT (CD117) = most useful marker (targeted therapy)

Mng

Most GISTs → surgical resection (small: wedge resection; large: gastrectomy)
Imatinib mesylate (Gleevec) — tyrosine kinase inhibitor of KIT & PDGFRα; used as bridging treatment
Complete surgical resection improves local recurrence rate & overall survival; incomplete resection → higher recurrence risk

Special

Molecular: c-KIT mutation 75–80%, PDGFRA mutation 5% (test PDGFRA if c-KIT negative)
ICC express c-KIT, sit in muscularis propria, act as pacemaker cells for gut peristalsis
May differentiate towards smooth muscle, neural, mixed, or neither cell type
Prognosis depends on tumour size, mitotic rate, and site of origin (gastric less aggressive than small-intestinal)
Intraoperative tumour rupture → poorer prognosis
New mutations allow resistance to imatinib

physiology · background · low-yield

Background

Previously labelled leiomyoma / leiomyosarcoma (<1% of gastric tumours)

Lymphoma

1 entries

Gastric MALT lymphoma (MALToma)

C/P

Primary lymphomas ≈ 5% of all gastric malignancies
MALToma = the most common type of primary gastric lymphoma (other = diffuse large B-cell lymphoma)
Stomach = most common site for extranodal lymphoma (20%); most are MALTomas
80% arise on a background of H. pylori-associated gastritis (acquired MALT)
Presentation similar to carcinoma; may have peripheral adenopathy, abdominal mass, splenomegaly

Inves

Composed of morphologically heterogeneous small B-cells; no specific immunophenotype; CD20 positive
Infiltrate is in the marginal zone of reactive B-cell follicles, extending into the interfollicular region
Lymphoepithelial lesions — neoplastic cells infiltrate glandular epithelium (key diagnostic intraepithelial lesion)
May show plasmacytoid differentiation and follicular colonisation
Diagnosis: EGD, contrast X-ray, CT-guided biopsy
Adjacent mucosa: epithelial erosion (61%), intestinal metaplasia (59%), H. pylori (57%), lymphoid follicles (39%), atrophy (37%)

Mng

H. pylori eradication antibiotics — long-term favourable outcome; ~50% treated with antibiotics achieve excellent remission
Radiotherapy
Surgery for gastric lymphoma: total/subtotal gastrectomy with splenectomy; adjunct radiotherapy (improves 5-yr survival) / chemotherapy (prevents recurrence)
t(11;18)(q21;21) tumours are unlikely to respond to H. pylori eradication alone; trisomy 3 also non-responsive

Special

Extranodal marginal-zone B-cell neoplasm of 'acquired lymphoid tissue'
Usually indolent; when it spreads it involves other mucosal sites; 5-yr survival 94%
May have positive H. pylori serology even if histology-negative — such patients may still respond to eradication
Antigen-driven T cells support B-cell growth initially

physiology · background · low-yield

Epidemiology/Risk

MALToma accounts for ~8% of GI malignancies

Neuroendocrine tumours

7 entries

Neuroendocrine tumours (NETs)

C/P

Heterogeneous group derived from neuro-endocrine cells — GI tract (commonest), lung, adrenals (phaeochromocytoma), thyroid (medullary carcinoma)
Most occur sporadically
Genetic-syndrome association: MEN-1, VHL (von Hippel-Lindau), tuberous sclerosis, neurofibromatosis type 1
Functioning (symptomatic): synthesise peptides causing specific syndromes
Silent (non-functioning): present with tumour-bulk symptoms — obstruction, jaundice, bleeding, abdominal mass; often incidental
General presentation: diarrhoea & GI symptoms or syndrome-specific features

Inves

Chromogranin A — general marker (positive = NET somewhere) plus specific hormones (gastrin, pro-insulin, glucagon)
Biochemical tests + specific hormone assays
Imaging: ultrasound, CT, MRI, PET
Radio-labelled somatostatin analogue (octreotide) scan
Endoscopy & biopsy
May be benign or malignant

Mng

Multidisciplinary approach; depends on presence of metastases
Surgical resection — optimal management of the primary lesion
Debulking (including liver metastases) facilitates systemic treatment
Somatostatin analogues (octreotide, lanreotide) — control hormonal symptoms and have a tumour-modulating effect
Chemotherapy agents

Special

Gut hormone panel precautions: hormones very unstable — patient fasts overnight, stop PPIs 2 weeks & H2 antagonists 72 h, sample sent immediately on ice, separated within 30 min, transported on dry ice

physiology · background · low-yield

Mechanism

Autoimmune (atrophic) gastritis predisposes to gastric carcinoid — hypergastrinaemia drives neuroendocrine (G/ECL-cell) hyperplasia; deck lists carcinoid, adenocarcinoma and MALT lymphoma as tumours of chronic gastritis

Gastrinoma (Zollinger-Ellison syndrome)

C/P

Mediator: gastrin → Zollinger-Ellison syndrome
Massive peptic ulceration, steatorrhoea & diarrhoea
Case: chronic epigastric pain, reflux, unexplained diarrhoea, upper GI bleed (melena), ulcers
PUD features in ZES: multiple, refractory to therapy, giant, recurrent; duodenal ulcer NOT related to H. pylori or NSAIDs; ulcers with unexplained diarrhoea indicate hypersecretion

Inves

Fasting hypergastrinaemia — patient must be OFF H2 blockers/PPIs

Mng

High-dose PPIs, H2 blockers, surgical care

Special

Diarrhoea plus multiple/refractory ulcers is the discriminator
Associated with MEN-1 (pancreatic tumours)

Carcinoid tumour / carcinoid syndrome

C/P

Mediator: serotonin (metabolised to 5-HIAA), kinins
Cutaneous flushing; diarrhoea / recurrent abdominal pain
Wheezing / asthma-like syndrome (bronchial constriction)
Cardiac: right-sided valvular heart lesions (fibrosis)
Case: severe flushing, palpitations, ventricular failure, pulmonary murmur, liver metastases

Inves

24-hour urine 5-HIAA in an acidified bottle
Octreotide scan confirms carcinoid

Mng

Somatostatin analogues (octreotide) per NET management principles

Special

Right-sided valvular fibrosis is the classic discriminating feature

Insulinoma

C/P

Mediator: insulin → recurrent hypoglycaemia
Episodic hunger, confusion, fainting; worse with fasting/exercise, relieved markedly by food
Weight gain; anxiety, nausea, vomiting and lightheadedness during episodes
Case: 30-year-old lady, 2-month history

Inves

Whipple's triad: hypoglycaemia symptoms + low blood glucose at the time of symptoms + resolution on glucose administration
Supervised prolonged fast with symptom monitoring
Measure blood glucose, insulin and C-peptide to confirm hypoglycaemia

Mng

NET management principles — resection/debulking (deck gives no insulinoma-specific drug)

Special

Whipple's triad is the named diagnostic criterion

Glucagonoma

C/P

Mediator: glucagon
Skin rash — migratory necrotising (necrolytic) erythema: erythematous polycyclic migratory lesions with scaling advancing borders and central resolution, healing in ~2 weeks as new lesions appear elsewhere
Diabetes; weight loss, anorexia, weakness, glossitis, angular stomatitis
Case: 65-year-old lady, steroid-unresponsive eczema-like rash, long-standing T2DM, recurrent DVT

Inves

Serum glucagon markedly elevated (case 2340 pg/mL; normal 55–177); insulin low
US: hypoechoic tumour in distal pancreas; CT: hypervascular tumour in tail
Skin biopsy in the advanced phase

Mng

NET management principles

Special

The 4D syndrome: Diabetes, Dermatitis (migratory necrotising erythema), DVT, Depression
Do not confuse with non-specific dermatitis

VIPoma (Verner-Morrison syndrome)

C/P

Mediator: VIP (vasoactive intestinal peptide) → Verner-Morrison syndrome
WDHA: Watery Diarrhoea (profuse despite fasting — dominant symptom), Hypokalaemia, Achlorhydria; plus flushing
Muscle cramps → weakness/paresis (from hypokalaemia); weight loss; normal abdomen
Volume depletion, dehydration, exhaustion
Case: 45-year-old man, 1-year watery diarrhoea despite fasting, 5–6 motions/day

Inves

Markedly elevated plasma VIP by radioimmunoassay (case 119.4 pmol/L; normal 0–30)
Labs: severe hypokalaemia (K+ 2.4 mEq/L), acidosis (pH 7.32); stool analysis/culture negative
US: pancreatic head tumour + hepatic metastasis

Mng

NET management principles (correct K+/fluid; treat tumour)

Special

Watery secretory diarrhoea persisting despite fasting is the discriminator

Somatostatinoma

C/P

Mediator: somatostatin (broad inhibitory action)
Inhibitory pentad: diabetes mellitus (inhibits insulin), cholelithiasis/gallstones (inhibits CCK/gallbladder), weight loss, steatorrhoea & diarrhoea (inhibits pancreatic enzymes), hypochlorhydria/achlorhydria (inhibits gastrin)
Mediator table also: non-ketotic diabetes mellitus, steatorrhoea, gallstones

Inves

Fasting serum somatostatin level

Mng

NET management principles

Special

Pentad reflects somatostatin's inhibition of insulin, CCK, pancreatic enzymes and gastrin

Upper GI Bleeding

8 entries

Upper GI Bleeding (UGIB)

C/P

Potentially life-threatening abdominal emergency
Bleeding from a source proximal to the ligament of Treitz (demarcation line between upper and lower GI tract)
Source may be oesophagus, stomach or duodenum
Haematemesis (vomiting blood) and melena (tarry black stool)
Hematochezia (fresh blood in stool) — usually LGIB but can occur in brisk UGIB
Also: syncope, dyspepsia, heartburn, abdominal pain, dysphagia, weight loss, jaundice
Signs of chronic liver disease — spider angiomata, gynaecomastia, splenomegaly, ascites, pedal oedema, asterixis
Cirrhotic patient starting haematemesis → likely variceal bleeding
Most common causes: PUD (incl. aspirin/NSAIDs), H. pylori, variceal haemorrhage, Mallory-Weiss tears, gastric/duodenal erosions, neoplasms
Additional causes: oesophagitis, vascular ectasias, Dieulafoy lesions
Anticoagulants (e.g. warfarin, DOACs) and thrombolytics — drug precipitants/aggravators of UGIB (elicit on history + consider reversal); separate from aspirin/NSAID-induced PUD

Inves

CBC with platelet count, renal + liver function tests and coagulation profile
Type and screen or type and crossmatch — crossmatch 2–6 units based on rate of active bleeding
Assess for haemodynamic instability / poor perfusion early to triage massive bleeds to ICU
Shock signs: tachycardia >100 bpm, SBP <90 mmHg, cool extremities, syncope, ongoing brisk haematemesis, maroon/bright-red stools (need rapid transfusion)
Orthostatic vitals (supine + upright) — significant postural change = acute loss of ≥20% blood volume
Absent dorsalis pedis pulse = red flag for perfusion
Nasogastric lavage: red blood not clearing = active bleeding; improves endoscopic visualisation; NOT contraindicated in suspected varices
Endoscopy (OGD) for diagnosis and therapy

Mng

Resuscitation (ABCDE) first + assessment (history, physical, bloods), then treat/control the cause — always the priority
Transfusion threshold: Hb 8.5 if ischaemic heart disease; 7.5 if otherwise well
Non-variceal — endoscopic: mechanical clipping, thermal sealing, injection (sclerosant), Hemospray (local adrenaline not used alone)
Non-variceal — pharmacological: PPI (e.g. omeprazole); treat cause — H. pylori eradication, stop NSAIDs
Non-variceal — refractory: interventional radiology trans-catheter arterial embolisation (TAE); surgery (e.g. gastrectomy)
Variceal: Terlipressin (vasopressin analogue → venoconstriction) + prophylactic antibiotics (prevent SBP)
Variceal — endoscopic: band ligation (1st line); sclerotherapy if band ligation fails; TIPS

Special

Forrest classification — estimates rebleeding risk in peptic ulcer bleeding
Ligament of Treitz = anatomical dividing line for upper vs lower GI bleed
Bleeding varices carry the highest morbidity and mortality of all causes of GI bleeding
Endoscopic adrenaline is never used alone
Band ligation is 1st line for variceal bleeding; sclerotherapy reserved for band failure

physiology · background · low-yield

Mechanism

Hemospray mechanism: (1) contact with active luminal bleed, (2) water absorption by the powder, (3) formation of a mechanical barrier over the bleeding point

Background

TIPS creates a shunt connecting the portal vein (high pressure) directly to the hepatic vein (low pressure), bypassing the cirrhotic liver to reduce portal hypertension

Oesophageal Varices (Variceal Bleeding)

C/P

Dilated sub-mucosal veins
A consequence of portal hypertension — blood diverted from the portal system into lower-pressure areas
Collateral circulation develops in lower oesophagus, abdominal wall, stomach and rectum → varicosities
Strong tendency to bleed
Commonly due to cirrhosis
Uphill varices develop in the distal one-third of the oesophagus (flow redirected through the left gastric vein)

Inves

Endoscopy — varices bearing a "cherry spot" (ruptured capillaries) indicate high risk of bleeding

Mng

Terlipressin (vasopressin analogue → venoconstriction)
Prophylactic antibiotics (prevent spontaneous bacterial peritonitis)
Band ligation — 1st-line treatment
Sclerotherapy if band ligation fails (e.g. N-butyl-2-cyanoacrylate "superglue" injected into gastric varices)
TIPS (transjugular intrahepatic porto-systemic shunt)

Special

Bleeding varices = highest morbidity and mortality of all GI bleeds
"Cherry spot" on endoscopy signals imminent bleeding risk
Uphill varices in the distal oesophageal third

Mallory-Weiss Syndrome (Gastro-oesophageal Laceration Syndrome)

C/P

Longitudinal tears in the mucosa of the gastro-oesophageal junction (GOJ)
Bleeding from mucosal tears at the GOJ
Usually caused by severe alcoholism, retching, coughing or vomiting
May be associated with severe morning sickness in pregnancy
Mean age >60

Mng

Most tears heal spontaneously within 24–48 h
Ongoing bleeding: oesophageal clips or sclerosant via endoscopy
Surgical intervention rarely needed

Special

Also known as gastro-oesophageal laceration syndrome
Longitudinal mucosal tears at the GOJ (partial-thickness, not full-wall rupture)

Dieulafoy Lesion

C/P

An aberrantly large artery in the submucosa of the stomach or duodenum that bleeds
The arteriole breaches the mucosa causing a bleed rather than an ulcer
A rare lesion, often missed at endoscopy — multiple endoscopies may be required to diagnose

Inves

Endoscopy: arterial (spurting) bleeding, often just distal to the GOJ; bleeding point is a small defect without ulceration

Special

Bleeds without an ulcer — a small mucosal defect overlying a large submucosal artery
Frequently missed; may need repeated endoscopy to identify

Aorto-enteric Fistula (AEF)

C/P

Can occur after AAA (abdominal aortic aneurysm) repair
Often a smaller "herald bleed" followed by a catastrophic bleed
Strongly consider in patients with an abdominal aortic aneurysm or aortic graft

Mng

A high index of suspicion is required — surgery can be lifesaving

Special

"Herald bleed" characteristically precedes catastrophic haemorrhage

Oesophagitis (bleeding source)

C/P

Inflammation of the oesophagus
Most common cause: GORD
Other causes: chemical injury (alkaline/acid), physical injury (radiation therapy, NG tubes), hyperacidity, alcohol abuse
Infective — fungal: Candidiasis; viral: Herpes Simplex, CMV

Gastritis (bleeding source)

C/P

Inflammation of the stomach
Causes: H. pylori, NSAIDs, Crohn's disease, autoimmune disease (e.g. pernicious anaemia)

Duodenitis (bleeding source)

C/P

Inflammation of the duodenum
Causes: H. pylori, NSAIDs, Crohn's disease

Functional GI Disorders

3 entries

Functional GI Disorders (overview)

C/P

Symptoms arising in the mid/lower GI tract not attributable to anatomic or biochemical defects
Symptoms: abdominal pain, early satiety, nausea, bloating, distention, various symptoms of disordered defecation
The 3 most common functional bowel disorders: IBS, constipation, functional dyspepsia

Special

Oesophageal: globus, functional heartburn, reflux hypersensitivity
Gastroduodenal: functional dyspepsia, nausea & vomiting disorders, belching disorders
Bowel: IBS, functional constipation, functional diarrhoea, functional abdominal bloating/distension
Centrally mediated GI pain: CAPS, narcotic bowel syndrome / opioid-induced GI hyperalgesia
Gallbladder & Sphincter of Oddi: biliary pain, functional pancreatic SO disorder
Anorectal: faecal incontinence, functional anorectal pain, functional defecation disorders

Irritable Bowel Syndrome (IBS)

C/P

GI syndrome — chronic abdominal pain and altered bowel habits in the absence of any organic cause
The most commonly diagnosed GI condition
Pain typically crampy, variable intensity with periodic exacerbations; location and character vary widely
Emotional stress and eating exacerbate pain; defecation often relieves it
Altered bowel habit: diarrhoea (IBS-D) or constipation (IBS-C)

Inves

Alarm/atypical symptoms (not compatible with IBS): rectal bleeding, nocturnal or progressive abdominal pain, weight loss, lab abnormalities (anaemia, raised inflammatory markers, electrolyte disturbances)
Any alarm symptom → further imaging and/or colonoscopy
No alarm symptoms + no family history of IBD/CRC → limited testing; many require no testing at all
Diarrhoea-predominant: stool cultures + giardiasis testing (not routine), coeliac screening, faecal calprotectin/lactoferrin + CRP, 24-h stool collection if malabsorption suspected, colonoscopy/flexible sigmoidoscopy + biopsy if alarm features
Constipation-predominant: colonoscopy/flexible sigmoidoscopy if alarm features

Mng

Patient education — most important; establish a therapeutic doctor–patient relationship (non-judgmental, realistic expectations, consistent limits, involve patient); explain the chronic and benign nature
Dietary: FODMAP restriction, gluten avoidance, lactose avoidance, food-allergy testing, dietary fibre; encourage physical activity
IBS-C (after failed soluble fibre e.g. psyllium/ispaghula): osmotic laxatives (PEG), lubiprostone (chloride channel activator), linaclotide (guanylate cyclase agonist), tegaserod/prucalopride (5-HT4 agonists)
IBS-D: loperamide, eluxadoline (mu/delta opioid agonist/antagonist), bile-acid sequestrants (cholestyramine, cholestipol), alosetron (5-HT3 antagonist — ischaemic colitis side effect)
Pain/bloating: antispasmodics (clidinium/chlordiazepoxide, hyoscyamine, mebeverine), antidepressants (TCA amitriptyline; SSRI fluoxetine/duloxetine), rifaximin + probiotics, peppermint oil
Refractory: behavioural therapy, faecal microbiota transplantation

Special

Rome IV criteria — recurrent abdominal pain ≥1 day/week for 3 months (onset ≥6 months prior) + ≥2 of: related to defecation, change in stool frequency, change in stool form
Subtyped by Bristol stool consistency: IBS-C, IBS-D, mixed, unsubtyped
Alosetron carries a risk of ischaemic colitis

Functional Dyspepsia

C/P

ACG definition: predominant epigastric pain lasting at least 1 month
May be associated with any other upper GI symptom — epigastric fullness, nausea, vomiting, heartburn — provided epigastric pain is the primary concern

Foodborne & Waterborne Infections

20 entries

Foodborne & waterborne infection — clinical approach

C/P

Food-borne infection – illness from food/water contaminated with bacteria and/or toxins, or parasites, viruses, chemicals
Outbreak = similar (often GI) illness in ≥2 people + evidence of food as the source
Commonest cause overall = viruses; in children Rotavirus, in adults Norovirus & Campylobacter
Risk: impaired immunity (extremes of age, chronic disease, pregnancy, immunocompromised), improper handling/preparation/storage, cross-contamination
May present with nausea, vomiting, fever, abdominal pain, diarrhoea — or be non-GI: botulism (paralysis), ciguatera/scombroid (headache, tingling), amnesic shellfish poisoning (amnesia), Hep A/E (hepatitis), Listeria (meningitis/abortion)

Inves

History triad: presenting symptoms, exposure to a particular food, and time interval (incubation) between exposure and onset
Stool stains: Gram stain & Loeffler methylene blue for WBCs (invasive vs non-invasive)
Stool O&P (ova & parasites); stool culture mandatory for enteric pathogens (Salmonella, Shigella, Campylobacter) if WBC/blood +ve, fever, or symptoms >3–4 days
Blood culture if notably febrile; CBC, electrolytes, BUN/creatinine (inflammation & dehydration)
C. difficile assay if recent/current antibiotics; abdominal X-ray if bloating/severe pain/obstruction/perforation
Sigmoidoscopy/colonoscopy + biopsy if stool non-diagnostic (esp. immunocompromised, bloody diarrhoea); EGD + duodenal aspirate/biopsy in immunocompromised

Mng

Cornerstone = fluids; ORS (water, salts, sugar) for mild/moderate, IV fluids for severe
Antibiotics generally not needed; reserve for fever + bloody diarrhoea
Prevention: hand washing, clean water, waste disposal, fly control, Rotavirus vaccine in children, continued breastfeeding in babies

Special

Fever suggests invasive disease; blood/mucus in stool = mucosal invasion
Profuse rice-water stool → cholera; abdominal cramps → electrolyte loss (severe cholera)
Reactive arthritis after Salmonella, Shigella, Campylobacter, Yersinia
Proctitis syndrome (shigellosis): frequent painful BMs with blood/pus/mucus, prominent tenesmus
Bloating → suspect giardiasis; Yersinia enterocolitis may mimic appendicitis

physiology · background · low-yield

Mechanism

Non-inflammatory diarrhoea: enterotoxins impair small-bowel secretion without invasion → large-volume watery stool, no blood/pus, dehydration; toxin preformed or made in gut. Inflammatory diarrhoea: cytotoxins invade/destroy mucosa (colon/distal small bowel) → bloody mucoid stool with leukocytes, febrile/toxic, less dehydration; faecal leukocytes/lactoferrin +ve

Background

Timing (this lecture): acute <2 weeks, persistent 2–4 weeks, chronic >4 weeks

Microbiology

Localized viral GIT infection (e.g. Rotavirus) = fecal-oral, disease at same site (GIT), short incubation, IgA; systemic (e.g. Hepatitis A, Poliovirus) = disease distant from portal of entry, longer incubation, IgG+IgA

Staphylococcus aureus food poisoning

C/P

Vomiting-predominant: nausea, vomiting, abdominal cramps within 1–6 h; fever/diarrhoea in a minority
Caused by ingestion of preformed heat-stable enterotoxin → rapid onset
Source: foods prepared by a food handler (dairy, produce, meats, eggs, salads) left at room temperature

Inves

Usually clinical; vomitus/food can be tested for enterotoxin

Special

Member of the "vomiting = major symptom" triad (S. aureus, B. cereus, Norovirus); preformed toxin ingested → quick onset 1–6 h

Bacillus cereus food poisoning

C/P

Emetic form: rapid (1–6 h) nausea & profuse vomiting; separate diarrhoeal form with watery diarrhoea & cramps
Preformed heat-stable emetic enterotoxin in starchy foods (rice) — classically improperly cooked fried rice
Gram-positive aerobic bacterium

Inves

Usually clinical; disease is self-limited

Special

Preformed toxin ingested → quick onset (1–6 h), vomiting predominant

Clostridium perfringens

C/P

Brief illness with watery diarrhoea, cramps & fever
Spores germinate in meats, poultry, or gravy; associated with undercooked/unrefrigerated food
Toxin produced in the host gut (not preformed) → delayed onset (>1 day)

Norovirus & Rotavirus gastroenteritis

C/P

Norovirus: very common cause of acute gastroenteritis — nausea, vomiting, watery diarrhoea
Large outbreaks (e.g. cruise ships); readily spread from food, vomitus, aerosol, person-to-person
Lasts 48–72 h with rapid recovery, but no long-lasting immunity
Rotavirus/enterovirus mainly in children (Rotavirus = commonest foodborne cause in children)

Mng

Rotavirus vaccine recommended for prevention in children

Special

Norovirus is a "vomiting = major symptom" triad member

Enterotoxigenic E. coli (ETEC) — traveller's diarrhoea

C/P

Common cause of traveller's diarrhoea; watery
Transmission via fecal contamination of food/water from an infected person
Enterotoxin made in the intestine (delayed onset)

Cryptosporidium

C/P

Persistent/chronic watery diarrhoea in immunocompromised patients
Endemic in cattle; acquired from contaminated water, fresh produce, unpasteurized milk, or person-to-person
Incubation ~1 week (up to 28 days); causes large outbreaks

Inves

Acid-fast staining of stool, immunofluorescence, or enzyme immunoassay

Special

Can cause chronic diarrhoea (also in TB, HIV, Giardia)

Cyclospora cayetanensis

C/P

Transmission via fecally-contaminated water; classically linked to fresh basil

Inves

Direct acid-fast microscopy of stool

Mng

Readily treatable with trimethoprim-sulfamethoxazole

Salmonella (typhoidal & non-typhoidal)

C/P

Non-typhoidal: watery diarrhoea, fever, abdominal pain & vomiting; from undercooked poultry & eggs (S. enteritidis); animal-gut source; incubation 1–3 days
Typhoidal (S. typhi/paratyphi): colonize humans, fecally-contaminated food/water → systemic enteric fever with little/no diarrhoea
Sign: rose spot macules on upper abdomen + hepatosplenomegaly (S. typhi)

Inves

Routine stool cultures

Mng

Antibiotics needed only for severe disease or immunocompromised patients

Special

Reactive arthritis association; epithelial-invasion mechanism

Campylobacter

C/P

Abdominal pain, bloody diarrhoea; highest incidence in children & young adults
From raw/undercooked meats; common cause of inflammatory diarrhoea in adults in developed countries

Special

Reactive arthritis association; epithelial-invasion mechanism

Shiga toxin E. coli (STEC / EHEC, O157:H7)

C/P

Starts watery → becomes bloody; O157:H7 commonest serotype
Source: ground beef, unpasteurized juice, raw fruit/veg; incubation ~1 day–1 week
Most common cause of bloody diarrhoea in the absence of fever

Inves

Shiga toxin-based assays (advantage over conventional sorbitol-MacConkey test)

Mng

Antibiotics may increase the risk of HUS — caution

Special

Complication: haemolytic uraemic syndrome (HUS)

Shigella

C/P

Bloody diarrhoea with fever & often bacteraemia; from contaminated food/water, especially travel
Colonizes humans/primates; fecal contamination or from a food handler; salads (potato, tuna, shrimp), raw veg, milk, poultry, water
Proctitis syndrome: frequent painful BMs with blood/pus/mucus, prominent tenesmus

Inves

Isolated routinely in clinical labs

Special

Reactive arthritis association

Vibrio species & Cholera

C/P

V. parahaemolyticus: vomiting, diarrhoea, abdominal pain after raw/undercooked shellfish (within preceding 48 h)
V. vulnificus: invasive, life-threatening in immunocompromised / chronic liver disease; skin infections → bacteraemia & systemic disease
V. vulnificus / V. alginolyticus may present with cellulitis & otitis media
Cholera: profuse rice-water stool (enterotoxin made in gut)

Inves

Vibrio needs a specific request to the lab (not routinely cultured); V. vulnificus needs special media; incubation 1–7 days

Botulism (Clostridium botulinum)

C/P

Life-threatening; visual disturbance and/or descending paralysis
From foods where C. botulinum spores germinated & produced toxin — home-canned foods, fermented fish, herb-infused oils, foods held warm

Inves

Test stool & serum for toxin (reference labs)

Special

A non-GI foodborne illness (neurologic)

Ciguatera poisoning

C/P

GI (2–6 h): nausea, vomiting, diarrhoea, abdominal pain
Neuro: paraesthesia, weakness, reversal of hot/cold sensation; cardiovascular abnormalities can follow
Source: large reef fish (grouper, red snapper, barracuda) — fish consume dinoflagellates producing heat-stable ciguatoxin

Scombroid poisoning

C/P

Onset within minutes to hours of consumption
Flushing, burning sensation, urticaria, dizziness, paraesthesia
Mechanism: build-up of biogenic amines (histamine) in fish (or cheese) — blue fish, tuna, mackerel, marlin

Listeriosis (Listeria monocytogenes)

C/P

Rare but deadly (~20% mortality); risk = immunocompromised, elderly, pregnant
Source: deli meat, raw hot dogs, unpasteurized soft cheese
May cause meningitis or spontaneous abortion; long incubation (up to 6 weeks)

Inves

Culture from blood or CSF; stool cultures unhelpful (5–10% of population are carriers)

Special

Systemic-illness pattern via bacterial epithelial invasion

Hepatitis A (foodborne)

C/P

Transmission via raw shellfish, fresh produce, or an infected food handler
Presentation: acute hepatitis up to acute liver failure — no chronicity
Incubation 15–50 days

Inves

Serology

Brucellosis

C/P

From unpasteurized dairy or undercooked meat from infected animals
Species: B. melitensis, B. abortus, B. suis, B. canis
Fever with weight loss, malaise, night sweats, arthralgias

Inves

Brucella IgM serology (part of the BINDS diarrhoea workup — with Widal)

Intestinal tapeworms

C/P

Cause diarrhoea and other symptoms
Taenia saginata (undercooked beef), Taenia solium (undercooked pork), Diphyllobothrium latum (undercooked fish)

GI Infection Pathology

13 entries

Pseudomembranous colitis (C. difficile)

C/P

Severe form of acute non-suppurative inflammation where normal mucosa is replaced by a false membrane (pseudomembrane) of necrotic tissue & fibrin
Symptoms: severe diarrhoea, fever, vomiting, cramp-like abdominal pain
Usually a few days after broad-spectrum antibiotics

Inves

Detection of clostridial toxins in stool
Endoscopy: typical raised yellow plaques on the mucosa

Special

Virulent bacteria (C. difficile, a normal gut commensal) secrete exotoxins → mucosal necrosis + submucosal inflammation → false membrane
Precipitated by broad-spectrum antibiotics (clindamycin, lincomycin); may also arise from bowel ischaemia
Endoscopy/gross: light tan/yellow pseudomembranes over hyperaemic/erythematous colon
Micro: "mushroom" lesion / volcanic eruption — necrotic debris, acute inflammatory cells, fibrin & mucus (not a real membrane)

Intestinal spirochetosis

C/P

Colonization of colon/appendix by non-pathogenic filamentous non-treponemal spirochetes — Brachyspira aalborgi & B. pilosicoli
Fecal-oral; B. pilosicoli is zoonotic; assoc. anal intercourse (30% male homosexuals), HIV, low socioeconomic conditions; seen in 3–10% of normal people
Generally non-invasive; may cause persistent diarrhoea

Inves

H&E: spirochetes embed in luminal border of colonocytes → blue haematoxyphilic line / fuzzy blue fringe
Best seen with silver (Warthin-Starry) = black; PAS = magenta; also Giemsa, Alcian-blue

Special

Diarrhoea likely from blunting/destruction of microvilli (loss of absorptive surface) rather than invasion

Yersinia enterocolitis

C/P

Y. enterocolitica (less commonly Y. pseudotuberculosis); gram-negative rods, aerobic & motile
Zoonotic; from contaminated food, undercooked pork, unpasteurized milk, water; commonest in childhood
Clinical: diarrhoea (mild self-limited → typhoid-like), bowel rupture, peritonitis, pharyngitis, pericarditis

Special

Invades ileal mucosa, multiplies in Peyer's patches & regional LNs (also right colon/appendix)
Ulcers over lymphoid nodules, necrotizing microgranulomas, mesenteric lymphadenitis (suppurative granuloma with central neutrophils = stellate abscess)
May mimic appendicitis; assoc. erythema nodosum & exudative pharyngitis

Intestinal (colonic) tuberculosis

C/P

Chronic infectious granulomatous disease — Mycobacterium tuberculosis
Primary: swallowing human/bovine bacilli (dust/infected milk) → primary complex (terminal ileum Peyer's patches → tuberculous lymphangitis → mesenteric lymphadenitis / tabes mesenterica, cold abscess)
Secondary: swallowing infected sputum (pulmonary TB); mainly small intestine & ileocaecal area
Clinical: pain, diarrhoea, weight loss, fever, 50% palpable mass; may cause obstruction & stricture

Special

TB granuloma (tubercle): central caseation necrosis, epithelioid cells (activated macrophages), lymphocytes, Langhans giant cells (nuclei in horse-shoe periphery)
Gross: transverse ulcers (perpendicular to long axis) with yellow caseous floor
Micro: caseating/non-caseating granulomas, ulceration, desmoplasia, mesenteric LN granulomas
vs Crohn's: Crohn's commoner in West, no acid-fast bacilli, no caseation, no coalescing granulomas (TB = caseating; Crohn's = non-caseating)

Whipple disease (intestinal lipodystrophy)

C/P

Rare systemic infection by Tropheryma whippelii (gram-positive intracellular actinomycete)
Affects whites, age 30–49, 90% male
Malabsorption with diarrhoea, weight loss, abdominal pain; systemic: polyarthritis, CNS complaints, lymphadenopathy, hyperpigmentation
Fatal without antibiotics

Inves

Hallmark: distended macrophages in lamina propria containing PAS+ (diastase-resistant) granules (magenta)
EM shows rod-shaped bacilli

Special

Dilated lymphatics / fat vacuoles with no other inflammatory-cell response

H. pylori gastritis (pathology)

C/P

H. pylori found within mucous overlying epithelial cells (chronic active gastritis)

Inves

Stains: Warthin-Starry silver = black; Giemsa = small curved/spiral rod in surface mucus

Special

Neutrophils in lamina propria, intraepithelial & in gastric pits (pit abscesses); plasma cells, lymphocytes, lymphoid follicles
Complications: MALToma lymphoma; intestinal metaplasia (goblet cells/villi in stomach) → adenocarcinoma risk

Giardiasis

C/P

Commonest gut protozoan; feco-oral; mainly duodenal (also gastric antrum/ileal)
Watery diarrhoea and malabsorption; bloating
Attaches to mucosa but does not invade, no toxins → blocks nutrient absorption / damages microvilli → villous blunting

Inves

Organism: teardrop/pear shape with paired nuclei (owl-eye) and central longitudinal axostyle; size ~enterocyte nucleus
Histology: mucosa usually intact ± villous blunting, increased inflammatory cells

Mng

(Diarrhoea lecture) empiric metronidazole for giardiasis

Special

A recognised cause of chronic diarrhoea

Amoebic enterocolitis (amoebiasis)

C/P

Ingestion of Entamoeba histolytica cysts; excyst in small intestine (alkalinity) → 4 amoebae → division
Amoebae release cytotoxic enzymes and burrow into colon wall → flask-shaped ulcer (halted by muscularis propria, spreads laterally in submucosa)
Discrete ulcers with normal intervening mucosa, classically caecum/ascending colon; mild to very bloody diarrhoea

Inves

Micro: amoebae at edges & floor of ulcers, surrounded by clear zones (tissue lysis), small nucleus, vacuolated cytoplasm
Erythrophagocytosis (ingested RBCs) = indicates tissue invasion

Special

Complication: amoebic liver abscess (via blood supply) — chocolate "anchovy sauce" debris

Schistosomiasis (bilharziasis)

C/P

Chronic granulomatous disease caused by a blood fluke
S. mansoni (gut/stool; S America/Africa/ME), S. japonicum (gut; SE Asia), S. haematobium (bladder/urine; Africa/ME)
Intermediate host freshwater snails (release cercariae); infective cercaria penetrates skin → migrates via circulation to liver (matures) → mesenteric venules
Diagnostic stage = ova/eggs in stool or urine

Inves

Egg spines: S. mansoni lateral spine; S. haematobium terminal spine
Colon micro: ova in loose submucosa, surrounded by granulomas (macrophages/epithelioid, eosinophils, giant cells engulfing ova); healed = fibrous granuloma with calcified (blue) eggs

Special

Bilharzial polyps = commonest intestinal lesion (repeatedly trapped ova → mucosal hyperplasia → polyp)
Complications: recurrent haemorrhage → anaemia; obstruction (uncommon, via fibrous stenosis); spread to liver/lungs

Strongyloidiasis (Strongyloides stercoralis)

C/P

Filariform larvae in fecally-contaminated ground penetrate skin → systemic circulation → lungs (inflammation) → climb tracheobronchial tree → swallowed → adults mature in intestine
Eggs hatch in intestine, release rhabditiform larvae that are excreted
Diarrhoea, weight loss, abdominal pain, malabsorption
Severe/fatal infection in immunocompromised (worms disseminate to other organs)

Inves

Micro: tissue eosinophilia + neutrophilic infiltration (may abscess); adult worms/larvae within crypts; ± granuloma

Enterobius vermicularis (pinworm)

C/P

Usually found in the appendix of children 7–11 y as an incidental finding; may occasionally be associated with appendicitis
Worms reside in caecum (1.3 cm); a mass of worms may cause obstruction
Eggs deposited at night on perianal skin → pruritus ani

Inves

Cross-section of female shows lateral alae, intestinal & intrauterine eggs

HSV colitis & hepatitis

C/P

HSV1 (oral-labial) / HSV2 (genital); primary infection mild/asymptomatic in immunocompetent, latency in sensory ganglia; disease in immunocompromised
Colitis: watery/bloody diarrhoea, fever, abdominal pain, nausea, fatigue, weight loss; gross = painful discrete ulcers/vesicles/pustules in distal rectum or perianal skin
Hepatitis: rare, non-zonal haemorrhagic necrosis, usually fatal; immunocompromised & neonates (a TORCH infection)

Inves

Serum HSV IgG/IgM; HSV DNA PCR in colonic biopsy more reliable; IHC for HSV-2
Hepatitis labs: marked ↑ AST, ALT, bilirubin, ALP, GGT; HSV DNA PCR

Special

Colitis micro: cryptitis, crypt abscess, multinucleated giant cells, eosinophilic inclusions in epithelial cells
Hepatitis micro: geographic necrosis without inflammation; Cowdry type A (eosinophilic) / type B (basophilic) inclusions, ground-glass nuclei; HSV immunostain confirms

GI candidiasis

C/P

Candida albicans normal flora overgrows with diabetes, neutropenia, AIDS, immunosuppression, xerostomia, antibiotics
Usually mucosal lesions (rarely perforation); oesophagus = most common GI site
Types: pseudomembranous (gray-white membranes that easily wipe off), erythematous (painful erosions)

Inves

Gold standard = culture; micro = PAS-positive hyphae within keratin layer, neutrophilic background, lamina propria infiltrate

Mng

Antifungals = treatment of choice

Symptom Approach

2 entries

Constipation

C/P

Diagnosis = ≥2 of: <3 motions/week, incomplete evacuation, straining >25% of defecation time, manual/digital evacuation
Primary types: normal-transit, slow-transit, pelvic floor dysfunction
Normal-transit: defect in fluid/fibre intake → defecates within normal CTT but lumpy hard stool; common in winter/prolonged fasting, on diuretics
Slow-transit: well-formed (not hard) stool but frequency beyond 72 h; common with IBS; ↓ frequency of HAPCs
Pelvic floor dysfunction: difficulty defecating despite the desire (failure of RAIR-mediated coordination)

Inves

Investigate after 2 months of failed treatment
Labs: CBC (anaemia), faecal occult blood (chronically constipated middle-aged/elderly → obstructing neoplasm), thyroid profile, calcium, potassium, HbA1c
Imaging: plain AXR (acute — faecal loading), CT/MRI abdomen with contrast, MRI pelvic floor / defecography if pelvic floor dysfunction suspected
Physiologic: anorectal manometry (ARM) and colon transit time (CTT / Sitz markers); colonoscopy

Mng

Conservative: education, exercise, fluids, fibre, citrus fruits, cereals
Amiprostone (lubiprostone) — Cl⁻ channel activator — for normal-transit + laxatives
Prucalopride — 5-HT4 agonist (induces peristalsis) — for slow-transit + laxatives
Biofeedback & pelvic floor physiotherapy (train anal sphincters to relax)
Surgery for malignancy, volvulus
Laxative classes: bulk-forming (Normacol, Agiolax), osmotic (lactulose, Mg citrate, PEG 3350), stimulant (senna, Na picosulfate), intestinal secretagogue (lubiprostone), 5-HT4 agonist (prucalopride)

Special

Alarm symptoms → colonoscopy: haematochezia, unintentional weight loss, FHx colorectal cancer, unexplained anaemia, age >50 y
Colon transit time normally 20–72 h
Secondary causes: structural (neoplasm, volvulus, ischaemia, intussusception, stricture; rectocele, inflammation, prolapse, fissure); metabolic/systemic (hypokalaemia, hypercalcaemia, hypothyroid, DM, scleroderma); drugs (opiates, antidepressants, iron, Ca-antacids, CCBs, diuretics); neurological (MS, Parkinsonism, Hirschsprung's)

physiology · background · low-yield

Physiology

Colon motility driven by serotonin (5-HT): bolus distends wall → enterochromaffin cells release 5-HT → enteric reflex → ACh contracts behind bolus, nitric oxide relaxes in front. Two movements: non-propulsive contractions (absorb/mix) and high-amplitude propagated contractions (HAPC) — morning, accentuated by eating/drinking, inhibited during sleep to avoid incontinence

Exam technique

History clues that flag a systemic secondary cause: cold intolerance → hypothyroidism, polyuria → diabetes, rigidity → Parkinsonism

Clinical approach to diarrhoea

C/P

Diarrhoea = ≥3 loose/watery stools/day, or an increase over the individual's normal
Acute <14 days, persistent 14–30 days, chronic >30 days
Acute mostly self-limiting ± fever, malaise, vomiting; causes = infection (viral Rota, bacterial E. coli, protozoal Giardia), traveller's, drugs (antibiotics, laxatives, chemo, radiotherapy), diverticulitis, stress
Chronic mechanisms: osmotic, malabsorption, inflammatory, motility, secretory

Inves

Acute: test only in BINDS (Bloody, Immunosuppressed, Nosocomial, Dehydration, Severe >10 days) → stool analysis/culture, C. difficile toxin, Widal & Brucella IgM
Chronic: detailed history first to separate malabsorptive/small-bowel from inflammatory/large-bowel
Chronic labs: CBC, CRP, ESR, HIV Ab, TB Quantiferon gold, thyroid profile, HbA1c, Giardia stool antigen, anti-endomysial Ab, faecal calprotectin, faecal fat, stool osmolarity
Imaging/scope: CT/MRI with contrast, enterography (suspected IBD), colonoscopy; upper endoscopy for malabsorption

Mng

Acute: rehydration is the key step; antibiotics/antiprotozoals NOT routine except in BINDS; loperamide to stop diarrhoea
Chronic: treat the cause; dairy-free diet 3 weeks (lactase deficiency); gluten-free 6 weeks (coeliac); loperamide 2 mg; empiric metronidazole for giardiasis

Special

Alarm features → endoscopy: onset >50 y, rectal bleeding/melena, weight loss, FHx IBD/CRC, iron-deficiency anaemia
Osmotic improves with fasting, stool osmotic gap >50 mOsm/L; secretory = large watery stool, normal osmotic gap
Malabsorption = weight loss with good appetite, high faecal fat
Chronic infections: TB, HIV, Cryptosporidium, Giardia; post-surgical adhesions/strictures → SIBO (small intestinal bacterial overgrowth)

physiology · background · low-yield

Mechanism

Chronic diarrhoea types: osmotic = non-absorbable substance (lactose); malabsorption = villous absorption defect (coeliac, Whipple, chronic pancreatitis); secretory = ↑ electrolyte secretion via hormones activating Cl channels (VIP, ZES/gastrinoma, carcinoid); inflammatory = villous defect + pus/mucus (UC, Crohn's, TB, radiation enteritis); motility = colonic hypercontractility (IBS, DM, thyrotoxicosis)

Exam technique

History associations pointing to a specific cause: bronchial asthma → carcinoid, peptic ulcer → ZES, neuropathy → DM, IV drug use / multiple sexual partners → HIV, milk/wheat sensitivity → coeliac or lactose intolerance

Nutrition

3 entries

Malnutrition (undernutrition)

C/P

State from lack of intake or uptake of nutrition → ↓ fat-free mass & body cell mass, diminished physical/mental function, impaired clinical outcome
Results from starvation, disease, or advanced ageing (e.g. >80 y), alone or combined
Acute disease/injury-related: ICU/trauma, burns, closed head injury, major surgery — pronounced stress metabolism
Chronic DRM with inflammation (cachexia): end-stage organ disease — cancer, COPD, IBD, CHF, CKD (CRP >5 mg/L, seldom >40)
DRM without inflammation: dysphagia, neuro disease (stroke, Parkinson's, ALS, dementia), anorexia nervosa/depression, malabsorption/short bowel, anorexia of ageing
Non-DRM: hunger-related (famine, disasters), socioeconomic/psychologic (poverty, self-neglect, hunger strike)

Inves

Screen within first 24–48 h then at regular intervals; ESPEN: NRS-2002 or MUST; older persons MNA/MNA-SF
Assessment tools: Subjective Global Assessment (SGA), Mini Nutritional Assessment (MNA) — done for those screened at-risk
Assess weight, height, BMI, body composition, biochemical indices + medical/social/psychological & nutrition history

Mng

Multidisciplinary nutritional care plan (patient-centred); energy/fluid by indirect calorimetry or validated equations
Protein 0.8 g/kg/day (healthy) up to 1.5 g/kg/day or higher (depletion/disease)
Route: oral, enteral tube, or parenteral; plan includes goals, duration, monitoring, discharge planning
Monitor: anthropometry (weight, FFM, FM), biochemistry, function (hand-grip strength)

Special

Diagnostic criteria: ≥2 of — low energy intake, weight loss, loss of muscle mass, loss of subcutaneous fat, fluid accumulation, reduced hand-grip strength
Sarcopenia: progressive generalised loss of skeletal muscle mass, strength & function; screen from age 65 (gait speed → handgrip/muscle mass); primary (ageing) vs secondary (disease/activity/nutrition-related)
Protein malnutrition figure: wasting (emaciated child) vs Kwashiorkor (distended abdomen / oedema)

Micronutrient deficiencies

C/P

Deficit of ≥1 micronutrient vs requirements; can be dramatic or subtle (e.g. after bariatric surgery)
Vitamin A: night blindness, xerophthalmia, ↓ immunity
Vitamin B12 (vegan/vegetarian): megaloblastic anaemia (large oval RBCs, hypersegmented neutrophils), depression/dementia
Folic acid: megaloblastic anaemia
Iron: hypochromic microcytic anaemia, koilonychia (spoon nails)
Calcium / Vitamin D: tetany (Trousseau/carpopedal spasm), osteoporosis/osteomalacia

Inves

Laboratory-assessed concentrations for long-standing deficiency or monitoring; on long-term supplementation → labs every 6 months

Mng

Vitamin A: all adults 3000 mcg (10,000 IU); severe disease 60,000 mcg (200,000 IU) — reduces child mortality 35–70%
Iron: ferrous sulfate 325 mg (65 mg elemental) tid, or lower 15–20 mg elemental/day (fewer side effects); take with vitamin C, avoid tea/coffee
Reserve parenteral iron for malabsorption or worsening anaemia despite oral (expensive, greater morbidity)

Special

Micronutrient excess (individual supplements) → specific symptoms; monitor every 6 months on long-term supplementation

Refeeding syndrome

C/P

Severe disruption in electrolyte/fluid balance precipitated when feeding is begun too aggressively in malnourished subjects
High-risk patients: chronic alcoholism, severe chronic undernutrition, anorexia nervosa, depleted patients with acute illness
Symptoms: peripheral oedema, congestive heart failure, cardiac arrhythmia, respiratory failure, delirium/encephalopathy, severe organ dysfunction
Timing: usually within first 4 days of starting nutrition therapy

Inves

Diagnostic criteria: hypophosphataemia, hypomagnesaemia, hypokalaemia; fluid imbalance; disturbed glucose homeostasis; hyperlactataemia (suggesting vitamin B1/thiamine deficiency)

Special

Key mechanism: hypophosphataemia drives many complications, ± hypokalaemia, hypomagnesaemia, hypocalcaemia
High risk (≥1): BMI <16, weight loss >15% in 3–6 mo, little/no intake >10 days, low K/PO₄/Mg before feeding
Moderate risk (≥2): BMI <18.5, weight loss >10% in 3–6 mo, little/no intake >5 days, alcohol misuse or drugs (insulin, antacids, diuretics)

Candida Oesophagitis

C/P

C. albicans (normal flora) overgrows with: diabetes, neutropenia, AIDS, immunosuppression, xerostomia, antibiotics
Oesophagus is the most common GIT site
Usually mucosal lesions; rarely perforations
Two types: pseudomembranous (superficial gray-white membranes that easily wipe off) and erythematous (painful erosions)

Inves

Gold standard for diagnosis = culture
Micro: PAS-positive hyphae within keratin layer, neutrophilic background, prominent inflammatory infiltrate in lamina propria

Mng

Antifungals (treatment of choice)

Special

Risk increased with recent PPI use (fungal colonisation of stomach)

Small Bowel & Malabsorption

8 entries

Malabsorption — Approach & Workup

C/P

Impaired absorption of nutrients — defect of digestion AND/OR absorption; generalized (all classes; commoner) vs specific/single-nutrient (e.g. lactase deficiency)
Symptom → deficiency: steatorrhoea (fat/fat-soluble vitamins) · weight loss (fat/carb/protein) · anaemia (Fe/B12/folate) · easy bruising (vit K) · oedema (albumin) · bone pain/tetany (Ca/vit D) · night blindness (vit A) · glossitis/angular stomatitis (Fe/B vits) · peripheral neuropathy (B12) · pellagra (niacin)
3 workup questions: is there malabsorption? · digestion vs absorption defect? · nutritional effects?
3 phases food can break at: luminal (pancreatic — hydrolysis/micelle) · mucosal (brush-border/absorption — coeliac) · post-absorptive · + abnormal transit (hyper: hyperthyroid/bypass; hypo: scleroderma/hypothyroid)
Small-intestinal causes differential: coeliac · tropical sprue · bacterial overgrowth · intestinal resection · Whipple's · radiation enteropathy · Giardia
Other causes (drug/endocrine/tumour): colestyramine & neomycin (→ steatorrhoea) · orlistat (lipase inhibitor → diarrhoea/steatorrhoea) · thyrotoxicosis (hypermotility) · Zollinger–Ellison · intestinal lymphangiectasia · small-bowel lymphoma · parasites (Giardia, Cryptosporidium; HIV-prone)

Inves

First-line bloods: CBC · B12/folate/iron · bone profile · albumin · prothrombin time
Faecal fat — normal 2–7 g/24h (~21 g/72h), min 3-day collection; gives NO indication of cause
14C-triolein breath test — rapid (2–8 h) fat-malabsorption; unreliable if abnormal CO₂ production; not in children/pregnancy/COAD
D-xylose test — jejunal absorptive capacity (absorbed + excreted unchanged in urine); falsely low with low GFR, delayed gastric emptying, oedema
14C-glycocholate breath test — bacterial overgrowth (bacteria deconjugate bile salt → 14C CO₂)
Faecal elastase — first-line for pancreatic exocrine insufficiency; >200 μg/g excludes; no cross-react with Creon
Cause-routing: coeliac → anti-tTG IgA + total IgA · SIBO/lactose → breath test · pancreatic → faecal elastase · IBD vs IBS → faecal calprotectin · hyperthyroid → TFTs
Niche: sweat electrolytes (CF) · brush-border biopsy (disaccharidase/lactase deficiency) · Schilling test (B12; obsolete)

Mng

Treat the cause + replace the specific deficient nutrients (nutrient-directed)

Special

Steatorrhoea = clinical hallmark of fat malabsorption
Only the terminal ileum absorbs bile salts + B12 (site-specific vulnerability)

Coeliac Disease

C/P

Chronic diarrhoea ± weight loss, floating/steatorrhoeic stools, postprandial bloating/flatulence
Microcytic iron-deficiency anaemia; unexplained raised aminotransferases
Oral aphthous ulcers, enamel defects
Extra-intestinal: growth failure, metabolic bone disease / premature osteoporosis, peripheral neuropathy, thyroid disease
Dermatitis herpetiformis — itchy vesicles on extensor surfaces (elbows/knees)
Associations: Down's, Turner's, Type 1 DM

Inves

IgA anti-tissue transglutaminase (tTG) — preferred single test; + endomysial IgA
Total IgA if high pre-test probability + possible IgA deficiency
Patient must be ON gluten (≥1 meal/day for ≥6 weeks) before serology
Duodenal biopsy — mucosa only; villous atrophy, crypt hyperplasia, ↑ lamina propria plasma cells/lymphocytes; pursue even if serology negative when suspicion high
HLA-DQ2/DQ8 not routine; D-xylose & small-bowel follow-through not recommended
Endoscopy: scalloped duodenal folds

Mng

Strict lifelong gluten-free diet (no wheat, barley, rye); refer to CD-knowledgeable dietitian
Test/treat micronutrient deficiencies: iron, folate, vit D, B12
Monitor adherence via history + serology

Special

Gliadin (alcohol-soluble gluten fraction) intolerance; tissue transglutaminase modifies gliadin → HLA-DQ2 presentation → CD4⁺ Th1 (IL-1, IFN-γ, TNF-α) villous damage
Dermatitis herpetiformis = pathognomonic cutaneous manifestation
Normal villous-to-crypt ratio 4–5:1 (biopsy reference)

Small Intestinal Bacterial Overgrowth (SIBO)

C/P

Abdominal distension + diarrhoea + malabsorption
Predisposed by dysmotility (diabetic autonomic neuropathy, scleroderma, amyloidosis), upper-GI surgery / gastrojejunal anastomosis / antral resection, gastrocolic & jejuno-colic fistulae, achlorhydria / vagotomy, IBS, cirrhosis, short bowel, immunodeficiency (AIDS), ESRD, pancreatic insufficiency

Inves

Glucose / 14C-glycocholate hydrogen breath test
Duodenal aspirate — overgrowth + antibiotic sensitivity
Normal duodenal biopsy + negative tTG excludes coeliac

Mng

Treat the underlying disease / anatomic defect that potentiated overgrowth (primary)
Antibiotics
Surgical correction for strictures / fistulae

Special

Normal anti-overgrowth defences: gastric acid + bile · pancreatic/biliary enzymes · mucosal integrity + mucin · secretory Ig + macrophages · Lactobacillus low pH · ileocaecal valve (blocks colonic reflux)

Lactose Intolerance

C/P

Bloating, flatulence, cramps, rumbling, diarrhoea after dairy

Inves

Hydrogen breath test after oral lactose challenge (20–50 g); baseline then every 30 min
Brush-border biopsy shows lactase deficiency

Mng

Avoid dairy and/or lactase enzyme supplement

Special

Neutral lactase splits lactose → glucose + galactose (absorbed via SGLT-1); undigested lactose fermented by colonic bacteria → gas + acids

Bile Salt Malabsorption

C/P

Chronic watery diarrhoea + steatorrhoea, typically after terminal-ileum resection

Inves

Clinical (terminal-ileum resection history)

Mng

Special

Terminal ileum = site of specific bile-salt reabsorption; bile acids reaching colon drive secretory diarrhoea + loss of micelle formation → steatorrhoea

Pancreatic Exocrine Insufficiency (malabsorption angle)

C/P

Steatorrhoea + weight loss; chronic (alcoholic) pancreatitis — recurrent epigastric pain radiating to back

Inves

Faecal elastase — first-line non-invasive; >200 μg/g excludes; no cross-react with Creon
CT abdomen: pancreatic calcifications (chronic calcific pancreatitis)
Invasive stimulation test (Lundh meal, or CCK / Secretin / CCK + Secretin = gold standard) — direct sampling; picks up mild; rarely used

Mng

Pancreatic enzyme replacement (Creon)

Special

Luminal-phase malabsorption (failed hydrolysis + micelle formation) — x-ref Pancreatic Disorders (Hepatobiliary tab)

Radiation Enteritis / Proctitis

C/P

Acute proctitis: diarrhoea + tenesmus ± blood after pelvic RT
Chronic (≥3 months): abdominal pain from obstruction; diarrhoea

Inves

Clinical + endoscopy

Mng

Acute proctitis: topical (local) steroids; argon plasma coagulation for persistent bleeding / mucosal telangiectasia
Chronic: surgery ONLY for obstruction or perforation (medical management often fails)

Special

>40 Gy damages intestine; ileum + rectum most affected (pelvic RT)
Chronic tissue triad: muscle-fibre atrophy · ischaemic ulceration · fibrotic strictures
Dual malabsorption: SIBO in dilated segments + mucosal damage

Short Bowel Syndrome / Intestinal Failure

C/P

Failure to maintain protein-energy / fluid / electrolyte / micronutrient balance → IV supplementation required
Follows resection for Crohn's, mesenteric occlusion, radiation enteritis, trauma, volvulus, NEC, tumour
Ileal resection worse tolerated than jejunal (ileum less able to adapt; low GLP-2)

Inves

Clinical + nutritional; classify by type I/II/III (see Criteria)

Mng

Antisecretory: H2RA, PPI (oral/IV), octreotide (SC/IV), clonidine (oral/patch)
Antimotility: loperamide, atropine, codeine, tincture of opium
Teduglutide (GLP-2 analogue) — promotes intestinal adaptation
Intestinal transplant indications: impending/overt liver failure · thrombosis of ≥2 central veins · frequent line sepsis · severe recurrent dehydration despite HPN · congenital mucosal disorders / ultra-short bowel · narcotic dependency / can't function / unwilling to accept long-term HPN

Special

Only ileum absorbs bile salts + B12 → ileal resection uniquely damaging
Post-ileal resection: bile-salt diarrhoea · steatorrhoea + gallstones · oxalate renal stones · B12 deficiency
Oxalate stones: unabsorbed fatty acids bind luminal calcium → free oxalate absorbed by colon → urinary oxalate stones
Jejunal resection → gastric hypersecretion + high gastrin

Los Angeles (LA) classification of reflux oesophagitis

Reference

Grade	Mucosal break
A	≥1 mucosal break ≤5 mm, not extending between the tops of two mucosal folds
B	≥1 mucosal break >5 mm, not extending between the tops of two mucosal folds
C	Mucosal break continuous between the tops of ≥2 folds, involving <75% of circumference
D	Mucosal break involving ≥75% of the oesophageal circumference

Grade B is the most prevalent grade of oesophagitis.

CT grades of corrosive oesophageal injury

Reference

Grade	CT findings	Outcome
A	Homogenous wall enhancement	Complete resolution
B-I	Wall oedema, mediastinal fat stranding	Stricture in 20%
B-II	External wall enhancement; internal non-enhanced necrotic thick mucosa	Stricture in 80%
C	Absence of post-contrast wall enhancement	Perforation

Phases of lye (caustic) injury

Reference

Acute necrotic (1–4 days) – coagulation of intracellular proteins → cell necrosis; intense surrounding inflammatory reaction
Ulceration & granulation (from 3–5 days) – superficial necrotic tissue sloughs, granulation fills the defect; lasts 10–12 days — oesophagus is at its weakest
Cicatrization & scarring (from 3rd week) – connective tissue contracts → narrowing; adhesions form pockets and bands; efforts must reduce stricture formation

Sliding vs rolling hiatus hernia

Reference

Type	%	Features
Sliding (axial)	95%	Both stomach and GOJ herniate
Rolling (para-oesophageal)	5%	Only the stomach (usually greater curvature); whole stomach may herniate

Oesophageal perforation — mortality by type

Reference

Overall mortality ~20%
Spontaneous (Boerhaave) ~36%
Instrumental ~18%
Primary emergency repair ~12%
Cervical perforations – lowest mortality; thoracic – highest
Treatment delay >24 h significantly increases mortality

AJCC TNM classification – oesophageal carcinoma

Reference

Category	Definition
Tis	High-grade dysplasia
T1	Invades muscularis mucosa (T1a) or submucosa (T1b)
T2	Invades into but not beyond muscularis propria
T3	Invades adventitia
T4a	Invades adjacent resectable structures (diaphragm, pericardium)
T4b	Invades unresectable structures
N0 / N1 / N2 / N3	0 / 1–2 / 3–6 / ≥7 regional lymph nodes
M0 / M1	No / present distant metastasis

Stage groupings – oesophageal squamous cell carcinoma

Reference

Stage	T	N	M	G	Location
0	Tis (HGD)	N0	M0	1	Any
IA	T1	N0	M0	1	Any
IB	T1 / T2–3	N0	M0	2–3 / 1	Any / Lower
IIA	T2–3	N0	M0	1	Upper, middle
IIB	T2–3 / T1–2	N0 / N1	M0	2–3 / Any	Upper,middle / Any
IIIA	T1–2 / T3 / T4a	N2 / N1 / N0	M0	Any	Any
IIIB	T3	N2	M0	Any	Any
IIIC	T4a / T4b / Any	N1–2 / Any / N3	M0	Any	Any
IV	Any	Any	M1	Any	Any

SCC vs adenocarcinoma – oesophageal carcinoma

Reference

	Squamous cell carcinoma	Adenocarcinoma
Frequency	Commonest worldwide (China, S. Africa, Asia)	Commonest in US/West; rising over last 20 yrs
Site	Middle third (up:mid:low = 15:50:35)	Lower third (65%)
Key risk factors	Alcohol + tobacco, HPV 16/18, Plummer-Vinson, achalasia, tylosis, caustic ingestion, nitrosamines, vit A/C deficiency	Barrett's oesophagus, GERD, hiatal hernia, Zollinger-Ellison, obesity, smoking

physiology · background · low-yield

Epidemiology/Risk

Further SCC risk factors – Fanconi anaemia (FANCD1/BRCA2), mycotoxins, and molecular changes: p53 mutation, loss of 3p & 9q alleles, Cyclin D1 & EGFR mutations

Anatomical regions of the oesophagus (distance from incisor)

Reference

Cervical – cricoid cartilage to thoracic inlet (15–18 cm)
Upper thoracic – thoracic inlet to tracheal bifurcation (18–24 cm)
Midthoracic – tracheal bifurcation to just above GE junction (24–32 cm)
Lower thoracic – to GE junction (32–40 cm)

C10

CT grading of corrosive oesophageal injury (Grades A–C)

Reference

Grade	CT findings	Outcome
A	Homogenous enhancement	Complete resolution
B-I	Wall oedema, mediastinal fat stranding	Stricture in 20%
B-II	External wall enhancement; internal non-enhanced necrotic thick mucosa	Stricture in 80%
C	Absence of post-contrast wall enhancement	Perforation

C11

Grade-based definitive management of corrosive injury

Reference

Grade	Nutrition	Definitive treatment
A	Oral	First aid only – no risk
B	TPN / tube (NGT/NJT)	Endoscopic assessment after 3 wks ± dilatation → fail: stent → fail: surgery
B-II	TPN / tube	Surgery (high stricture + perforation risk)
C	Jejunostomy	Surgery (very high perforation risk)

C12

Phases of caustic (lye) injury

Reference

Acute necrotic phase (1–4 days) – coagulation of intracellular proteins → cell necrosis with intense surrounding inflammation
Ulceration & granulation phase (from 3–5 days, lasts 10–12 days) – necrotic tissue sloughs; oesophagus is weakest here
Cicatrization & scarring phase (from 3rd week) – connective tissue contracts → narrowing/stricture, adhesions, pockets and bands

C13

Oesophageal perforation – surgical approach by site

Reference

Cervical → left neck incision
Upper / mid-thoracic → right thoracotomy
Lower thoracic / distal → left thoracotomy (7th ICS) or transhiatal approach
Timing: <24 h → primary anastomosis; >24 h → diversion (spit fistula + staple stomach)

C14

Updated Sydney system (2001) — classification of gastritis

Reference

Part endoscopic (pathology) + part histopathology; addresses aetiology, topography, morphology
Aetiology — Infectious: H. pylori, Treponema pallidum, mycobacteria, CMV, herpes virus, Candida, Histoplasma capsulatum, Giardia lamblia, Cryptosporidium
Aetiology — Non-infectious: autoimmune, NSAIDs (FANS), alcohol, bile reflux, chemotherapy, radiation, gluten allergy, foreign bodies, Crohn's disease, systemic diseases
Topography: where the gastritis is located
Morphology (grading): 1) acute inflammation 2) chronic inflammation 3) atrophic gastritis 4) intestinal metaplasia 5) H. pylori density

C15

H. pylori vs autoimmune gastritis

Reference

Feature	H. pylori–associated	Autoimmune
Location	Antrum	Body
Inflammatory infiltrate	Neutrophils, subepithelial plasma cells	Lymphocytes, macrophages
Acid production	Increased – slightly decreased	Decreased
Gastrin	Normal – decreased	Increased
Serology	Antibodies to H. pylori	Antibodies to parietal cells (H⁺/K⁺-ATPase, intrinsic factor)
Other lesions	Hyperplastic, inflammatory polyps	Neuroendocrine hyperplasia
Associations	Low socio-economic status, poverty	Autoimmune disease, thyroiditis, DM

C16

Gastric vs duodenal ulcer

Reference

Feature	Gastric ulcer	Duodenal ulcer
Share of PUD	25%	75% (4× as common)
Age	Late middle age, ↑ with age	Peak 30–50 yrs
M:F	2:1	4:1
Blood group	A	O
H. pylori	~80%	Up to 95%
Pain vs food	Provoked by food	Relieved by food
Malignancy / biopsy	Can be malignant → biopsy	Almost always benign → no biopsy
Recurrence	40–60% within 2 yrs	95% (50% within 6–8 months)

C17

Benign vs malignant gastric ulcer (endoscopic)

Reference

Benign: smooth, regular, rounded edge; flat smooth base; surrounding mucosa shows radiating folds
Malignant: irregular overhanging margins; ulcerated mass often protrudes into lumen; surrounding folds nodular and irregular

C18

H. pylori eradication regimens (titles)

Reference

Clarithromycin-based (stopped — resistance): triple, concomitant, hybrid, sequential
Levofloxacin-based (stopped — resistance): triple, quadruple (LOAD), sequential
Bismuth quadruple therapy — first line of current therapy
Salvage therapy
High-dose dual therapy (HDDT)

C19

Who to test & treat for H. pylori (ACG 2017)

Reference

Active peptic ulcer disease; history of PUD
MALT lymphoma
History of endoscopic resection of early gastric cancer
Uninvestigated dyspepsia in patients <55 yrs without alarm features
Long-term low-dose aspirin use; patients initiating chronic NSAIDs
Unexplained iron-deficiency anaemia despite appropriate evaluation
Adults with ITP

C20

Bleeding severity in peptic ulcer

Reference

Microscopic: part of the disease process
Mild: from granulation tissue in ulcer floor
Moderate: erosion of a small vessel in ulcer floor
Severe: penetration of a large extra-gastric vessel (e.g. gastroduodenal artery) — usually fatal

C21

Stages of perforated peptic ulcer

Reference

Pathology stages — [A] perforation (yielding of ulcer base → gastric contents into peritoneum); [B] chemical peritonitis (serous alkaline fluid neutralizes acid; duration depends on perforation size, stomach contents, patient resistance); [C] septic peritonitis (body resistance fails → microorganisms invade → pus)
Clinical stages — [A] shock (sudden severe upper-abdo pain, vomiting once, neurogenic shock, board-like rigidity); [B] lucid interval (relieved from shock, pain diminishes, walks in; obliteration of liver dullness, shifting dullness); [C] septic peritonitis (vomiting, distension, dead silent abdomen, absolute constipation, hypovolaemic shock)

C22

Bormann classification — gross picture (Types I–IV)

Reference

Type I – Polypoid: well-circumscribed polypoid tumour (exophytic, circumscribed mass)
Type II – Fungating: fungating tumour with marked central infiltration (bulky, exophytic with central invasion)
Type III – Ulcerated: ulcerated tumour with infiltrative margins
Type IV – Infiltrating: diffusely infiltrating tumour with loss of rugae = linitis plastica ('leather-bottle' stomach)

Types III & IV are incurable.

C23

Lauren classification — Intestinal vs Diffuse gastric carcinoma

Reference

Feature	Intestinal	Diffuse
Age / gender	Older, M>F	Younger, M=F
Risk factor	H. pylori, high-salt diet, smoking	CDH1 gene mutation
Gastric site	Antrum	Whole stomach
Gross picture	Exophytic, bulky	Ulcerative & linitis plastica
Pathogenesis	H. pylori/autoimmune gastritis → atrophic gastritis → intestinal metaplasia → dysplasia → carcinoma	Germline CDH1 mutation → loss of E-cadherin
Precursor lesion	Adenoma / dysplasia	Tubular neck dysplasia
Microscopy	Glandular / tubular structures	Individual tumour cells (signet-ring)
Surrounding mucosa	Atrophic gastritis & intestinal metaplasia	Non-atrophic, non-metaplastic

C24

Microscopic types of gastric carcinoma

Reference

Adenocarcinoma — Intestinal type (forms glands); Diffuse/dis-cohesive type (isolated cells, loss of E-cadherin) → signet-ring or non-signet-ring (NOS)
Mucoid carcinoma
Anaplastic carcinoma
Neuroendocrine carcinoma — large-cell or small-cell

C25

Depth classification — Early vs Advanced gastric cancer

Reference

Early gastric cancer: limited to mucosa & submucosa, ± LN (T1, any N); curable, 5-yr survival ~90%
Advanced gastric cancer: involves the muscularis; has 4 Bormann types; types III & IV incurable

C26

TNM staging of gastric cancer

Reference

Category	Definition
Tis	Carcinoma in situ (intraepithelial, no lamina propria invasion)
T1	Invades lamina propria or submucosa
T2	Invades muscularis propria or subserosa
T3	Penetrates serosa (visceral peritoneum) without invading adjacent structures
T4	Invades adjacent structures
N1	Perigastric (along lesser & greater curvatures)
N2	Along the left gastric artery
N3	Along common hepatic, splenic & coeliac arteries
M0 / M1	No / distant metastasis (liver, lung, bone, peritoneum)

C27

Lymph-node stations, tiers & D-level dissection

Reference

Lymphatic zones: Zone 1 – left & right gastric nodes; Zone 2 – gastroepiploic, suprapyloric, subpyloric; Zone 3 – splenic, short gastric, suprapancreatic.

N1 (stations 1–6, perigastric): right/left cardiac, lesser & greater curvature, suprapyloric, subpyloric
N2 (stations 7–11, main arterial trunks): left gastric, common hepatic, coeliac axis, splenic hilum, splenic artery
N3 (stations 12–16, para-aortic/distant): hepatoduodenal ligament, retroduodenal, root of mesentery, middle colic, para-aortic

D1: perigastric nodes (N1) — 'conservative'
D2: D1 + N2 (left gastric, hepatic, coeliac, splenic) — 'extended' (standard curative intent)
D3: D2 + N3 (hepatoduodenal, retropancreatic, mesenteric root)

C28

Stage vs 5-year survival (Table 18.6)

Reference

Stage	5-yr survival
T1 N0 M0	95+%
T1 N1 M0	70–80%
T2 N1 M0	45–50%
T3 N2 M0	15–25%
M1	0–10%

2 key prognostic factors: depth of invasion & lymph node involvement.

C29

IGCLC criteria for CDH1 testing (HDGC)

Reference

International Gastric Cancer Linkage Consortium criteria — test if either:

Two or more documented cases of diffuse gastric cancer in first-/second-degree relatives, at least one diagnosed before age 50; OR
Three or more first-/second-degree relatives with diffuse gastric cancer at any age

C30

MEN syndromes association

Reference

Feature	MEN-1	MEN-2A	MEN-2B	FMTC
Pancreatic tumours	Insulinoma, gastrinoma, VIPoma	–	–	–
Pituitary adenoma	Yes	–	–	–
Parathyroid hyperplasia	Yes	Yes	–	–
Medullary thyroid carcinoma	–	Yes (100%)	Yes (100%)	Yes
Phaeochromocytoma	–	Yes (50%)	Yes (50%)	–
Marfanoid habitus	–	–	80%	–
Multiple mucosal neuromata	–	–	>95%	–

C31

Common NETs — mediators & syndromes

Reference

Tumour	Mediator / marker	Effects / syndrome
Gastrinoma	Gastrin	Zollinger-Ellison: massive peptic ulcer, steatorrhoea & diarrhoea
Insulinoma	Insulin	Recurrent hypoglycaemia
VIPoma	VIP	Verner-Morrison: watery diarrhoea, hypokalaemia, achlorhydria, flushing
Glucagonoma	Glucagon	Migratory necrotising erythema, diabetes
Somatostatinoma	Somatostatin	Non-ketotic diabetes, steatorrhoea, gallstones
Carcinoid	Serotonin, kinins	Flushing, wheezing, right-sided cardiac valvular disease
All NETs	Chromogranins	Marker of NET presence

C32

Whipple's triad (insulinoma)

Reference

Symptoms of hypoglycaemia
Low blood glucose measured at the time of symptoms
Symptoms resolve on correction of hypoglycaemia (glucose administration)

C33

Glucagonoma — the 4D syndrome

Reference

Diabetes
Dermatitis (migratory necrotising erythema)
DVT
Depression

C34

VIPoma — WDHA triad

Reference

Watery Diarrhoea (profuse despite fasting; dominant symptom)
Hypokalaemia (→ muscle cramps/paresis)
Achlorhydria

C35

Somatostatinoma — inhibitory pentad

Reference

Diabetes mellitus (inhibits insulin)
Cholelithiasis / gallstones (inhibits CCK/gallbladder contraction)
Weight loss
Steatorrhoea & diarrhoea (inhibits pancreatic enzymes)
Hypochlorhydria / achlorhydria (inhibits gastrin)

C36

Forrest Classification (peptic ulcer bleeding)

Reference

Used for peptic ulcer bleeding to estimate rebleeding risk.

Stage	Endoscopic finding	Rebleeding risk
Ia	Jet arterial bleeding	90%
Ib	Oozing	50%
IIa	Visible vessel (non-bleeding)	25–30%
IIb	Adherent clot	10–20%
IIc	Black spot in ulcer crater	7–10%
III	Clean base ulcer	3–5%

C37

Causes of UGI Bleeding (by site)

Reference

Oesophageal	Gastric	Duodenal
Mallory-Weiss syndrome	PUD	PUD
Variceal bleeding	Varices	Ectopic varices
Oesophagitis	Malignancy	Duodenitis
Malignancy	Gastritis	Malignancy
Vascular (AEF)	Vascular (Dieulafoy, angioectasia)	Vascular (angioectasia)

C38

Rome IV Criteria for IBS

Reference

Criteria fulfilled for the past 3 months, with symptom onset at least 6 months before diagnosis
Recurrent abdominal pain on average at least 1 day/week in the last 3 months, associated with at least 2 of:
- Related to defecation
- Associated with a change in frequency of stool
- Associated with a change in form (appearance) of stool
IBS-D subtype: >25% Bristol stool types 6 or 7 and <25% Bristol types 1 or 2

C39

IBS Subtypes (Bristol stool consistency)

Reference

IBS-C (constipation): hard/lumpy stools ≥25% and loose/watery <25% of bowel movements
IBS-D (diarrhoea): loose/watery stools ≥25% and hard/lumpy <25% of bowel movements
Mixed IBS: hard/lumpy stools ≥25% and loose/watery ≥25%
Unsubtyped IBS: insufficient abnormality of stool consistency to meet the above subtypes

C40

Classification of Functional GI Disorders (Rome IV, by region)

Reference

Oesophageal: globus, functional heartburn, reflux hypersensitivity
Gastroduodenal: functional dyspepsia, nausea and vomiting disorders, belching disorders
Bowel: IBS, functional constipation, functional diarrhoea, functional abdominal bloating/distension
Centrally mediated GI pain: centrally mediated abdominal pain syndrome (CAPS), narcotic bowel syndrome / opioid-induced GI hyperalgesia
Gallbladder & Sphincter of Oddi: biliary pain, functional pancreatic SO disorder
Anorectal: faecal incontinence, functional anorectal pain, functional defecation disorders

C41

Constipation — diagnostic criteria

Reference

Presence of at least 2 of:

Infrequent stool <3 motions/week
Incomplete evacuation
Straining in >25% of the defecation time
Manual manipulation or digital evacuation

C42

Bristol Stool Chart

Reference

Type	Description	Interpretation
1	Separate hard lumps	Severe constipation
2	Lumpy, sausage-like	Mild constipation
3	Sausage with surface cracks	Normal
4	Smooth soft sausage/snake	Normal
5	Soft blobs, clear-cut edges	Lacking fibre
6	Mushy, ragged edges	Mild diarrhoea
7	Liquid, no solid pieces	Severe diarrhoea

C43

Types of chronic diarrhoea

Reference

Type	Aetiology	Characteristics
Osmotic	Lactose intolerance; drugs (lactulose)	Improves with fasting; stool osmotic gap >50 mOsm/L
Malabsorption	Coeliac, Whipple; chronic pancreatitis	Weight loss with good appetite; high faecal fat
Secretory	Hormones activating Cl channels — VIP, ZES (gastrinoma), carcinoid	Large watery stool; normal osmotic gap
Inflammatory	Ulcerative colitis, Crohn's, TB, radiation enteritis	Fever; bloody stool & mucus; tenesmus
Motility	IBS, DM, thyrotoxicosis	—

C44

Acute diarrhoea — when to investigate (BINDS)

Reference

Testing not indicated except:

Bloody diarrhoea
Immunosuppressed (old age, DM, pregnancy, immunosuppressive drugs)
Nosocomial infection (e.g. C. difficile)
Dehydration (low BP, tachycardia, or AKI)
Severe diarrhoea (>10 days)

Tests: stool analysis & culture, C. difficile toxin, Widal & Brucella IgM.

C45

Malabsorptive (small bowel) vs inflammatory (large bowel) diarrhoea

Reference

Feature	Malabsorptive / small bowel	Inflammatory / large bowel
Amount	Large	Small
Steatorrhoea	Yes (difficult to flush)	No
Blood	No	Bloody
Tenesmus	No	Yes (due to mucus)
Pain location	Periumbilical	Lower quadrant

C46

Foodborne diarrhoea — non-inflammatory vs inflammatory

Reference

	Non-inflammatory	Inflammatory
Mechanism	Enterotoxins impair small-bowel secretion, no invasion	Cytotoxins invade & destroy mucosa
Site	Small intestine	Colon / distal small bowel
Stool	Large-volume watery, no blood/pus	Bloody, mucoid, leukocytes present
Systemic	Dehydration may result	Febrile/toxic, less dehydration
Marker	—	Faecal leukocytes / lactoferrin +ve

C47

Major pathologic mechanisms of foodborne illness

Reference

Mechanism	Organisms	Characteristics
Enterotoxin ingested (preformed)	S. aureus, B. cereus	Quick onset (1–6 h); vomiting predominant
Enterotoxin made in intestine	C. perfringens, ETEC/STEC, V. cholerae	Delayed onset (>1 day); watery/bloody diarrhoea
Bacterial epithelial invasion	Campylobacter jejuni, non-typhoidal Salmonella, Listeria	Variable onset; watery/bloody diarrhoea, fever, systemic illness (Listeria)

C48

Malnutrition — diagnostic criteria

Reference

≥ 2 criteria for potential diagnosis:

Low energy intake
Weight loss
Loss of muscle mass
Loss of subcutaneous fat
Fluid accumulation
Reduced hand-grip strength

C49

Nutritional Risk Screening (NRS-2002)

Reference

Initial screen (any 'Yes' → proceed to final): BMI <20.5? · Weight loss in last 3 months? · Reduced dietary intake in last week? · Severely ill (e.g. intensive therapy)? If all 'No' → re-screen weekly.

Final screen — impaired nutritional status:

Score 1 (mild): weight loss >5% in 3 mo, or intake 50–75% of requirement in preceding week
Score 2 (moderate): weight loss >5% in 2 mo, or BMI 18.5–20.5 + impaired condition, or intake 25–60%
Score 3 (severe): weight loss >5% in 1 mo (>15% in 3 mo), or BMI <18.5 + impaired condition, or intake 0–25%

+ disease-severity score; if age ≥70: add 1. Total ≥3 = at-risk (start care plan); <3 = weekly re-screen.

physiology · background · low-yield

Background

Disease-severity score examples – Score 1: hip fracture, chronic patients (cirrhosis, COPD), chronic haemodialysis, diabetes, oncology; Score 2: major abdominal surgery, stroke, severe pneumonia, haematologic malignancy; Score 3: head injury, bone-marrow transplant, ICU (APACHE >10)

C50

Refeeding syndrome — risk stratification

Reference

High risk (1 or more):

BMI <16 kg/m²
Unintentional weight loss >15% in 3–6 months
Little or no intake >10 days
Low potassium, phosphate or magnesium before feeding

Moderate risk (2 or more):

BMI <18.5 kg/m²
Unintentional weight loss >10% in 3–6 months
Little or no intake >5 days
History of alcohol misuse or drugs (insulin, antacids, diuretics)

C51

Intestinal Failure — Type I / II / III

Reference

Type I — acute, short-term, usually self-limiting
Type II — prolonged acute; metabolically unstable; MDT + IV supplementation over weeks–months
Type III (Chronic IF) — metabolically stable; IV supplementation over months–years; may be reversible or irreversible

C52

Malabsorption — Test Reference Values

Reference

Faecal fat: normal 2–7 g/24h (~21 g/72h)
Faecal elastase: >200 μg/g excludes pancreatic exocrine insufficiency
Villous-to-crypt ratio: normal 4–5:1