Gastroenterology

Gastro-oesophageal reflux disease — symptomatic reflux of acid through an incompetent lower oesophageal sphincter, causing heartburn and regurgitation. Managed with lifestyle change and a full-dose PPI. Chronic reflux can cause Barrett oesophagus (intestinal metaplasia — a pre-malignant change needing surveillance). The key skill is recognising ALARM features that mandate endoscopy.

Protrusion of the stomach through the oesophageal hiatus of the diaphragm. Sliding (commonest) — the gastro-oesophageal junction slides up, predisposing to reflux. Rolling/para-oesophageal — the fundus herniates beside the oesophagus with the junction in place, risking strangulation. Often asymptomatic; managed as GORD, with surgery for large/para-oesophageal or complicated hernias.

Ulceration of the gastric or duodenal mucosa, driven by Helicobacter pylori infection or NSAIDs (the two big causes). Epigastric pain (duodenal classically relieved by food/worse at night; gastric worse with food). Complications: bleeding (commonest), perforation, gastric outlet obstruction. Test-and-treat H. pylori; stop NSAIDs; PPI healing. Refractory/multiple ulcers → think Zollinger-Ellison.

Usually adenocarcinoma of the stomach, presenting late with dyspepsia, weight loss, early satiety and anaemia. Risk factors: H. pylori (intestinal-type via atrophic gastritis → intestinal metaplasia → dysplasia), pernicious anaemia, smoking, diet, family history (E-cadherin/CDH1 in diffuse type — linitis plastica). Diagnosed by endoscopy + biopsy; often advanced at presentation.

Cancer of the oesophagus presenting with PROGRESSIVE dysphagia (solids then liquids) and weight loss. Two main types: squamous cell carcinoma (upper/middle third — smoking, alcohol, achalasia) and adenocarcinoma (lower third — GORD/Barrett, obesity — now commonest in the UK). Diagnosed by endoscopy + biopsy; barium shows an irregular 'apple-core'/shouldered stricture. Often advanced at diagnosis.

A primary motility disorder — failure of the lower oesophageal sphincter to relax with loss of distal peristalsis, from degeneration of the myenteric (Auerbach) plexus. Causes dysphagia to BOTH solids and liquids from the outset, regurgitation and weight loss. Barium shows a dilated oesophagus tapering to a 'bird-beak'; manometry confirms. Long-standing achalasia raises squamous-cancer risk. (Chagas disease is the secondary/infective cause.)

An immune-mediated enteropathy triggered by gluten (gliadin) in genetically susceptible people (HLA-DQ2/DQ8), causing villous atrophy and malabsorption. Presents with diarrhoea, bloating, weight loss, iron/folate deficiency anaemia — or silently. Diagnosed by tTG-IgA serology (on a gluten-containing diet) + duodenal biopsy. Lifelong gluten-free diet is the only treatment; associated with dermatitis herpetiformis and hyposplenism.

Impaired absorption of nutrients, producing steatorrhoea (pale, bulky, offensive, hard-to-flush stools), weight loss and specific deficiencies. Causes group into mucosal (coeliac, Crohn, Whipple), luminal/digestive (chronic pancreatitis, bile-salt deficiency, bacterial overgrowth) and structural/post-surgical (short bowel, resection). The task is to find the cause and replace what's missing.

Inability to digest lactose from reduced intestinal lactase — primary (genetically programmed decline, common in non-European ancestry) or secondary (transient, after gastroenteritis/coeliac/Crohn damaging the brush border). Lactose ingestion causes bloating, cramps, flatulence and watery (osmotic) diarrhoea. Diagnosed clinically/with a hydrogen breath test; managed by reducing lactose.

Inadequate blood supply to the bowel. ACUTE mesenteric ischaemia (SMA embolus/thrombosis, or venous/non-occlusive) — sudden severe abdominal pain OUT OF PROPORTION to signs, an emergency with high mortality. CHRONIC mesenteric ischaemia — post-prandial pain ('gut claudication'), weight loss, food fear. ISCHAEMIC COLITIS — transient colonic ischaemia (watershed splenic flexure), bloody diarrhoea, usually self-limiting.

A common functional bowel disorder — abdominal pain related to defecation with altered bowel habit (IBS-D/C/M), bloating, and NO structural/biochemical abnormality. A positive clinical diagnosis (Rome/NICE criteria) after excluding red flags and key mimics (coeliac, IBD). Managed with diet, lifestyle and symptom-targeted drugs; reassurance is central.

A chronic relapsing inflammatory bowel disease — transmural, granulomatous inflammation that can affect ANY part of the gut (mouth to anus), classically the terminal ileum, with SKIP lesions. Causes diarrhoea (often non-bloody), abdominal pain, weight loss and perianal disease, with strictures and fistulae. Smoking WORSENS it. Managed by inducing then maintaining remission (steroids → thiopurines/methotrexate → biologics); surgery is not curative.

A chronic relapsing inflammatory bowel disease — CONTINUOUS mucosal inflammation starting at the rectum and extending proximally (proctitis → left-sided → pancolitis), limited to the colon. Bloody diarrhoea with mucus, urgency and tenesmus. Smoking PROTECTS (the opposite of Crohn). Managed with aminosalicylates first-line, escalating to steroids/biologics; acute severe colitis and toxic megacolon are emergencies; long-standing disease needs cancer surveillance.

Diverticula are acquired outpouchings of colonic mucosa (commonest in the sigmoid), driven by low fibre and raised intraluminal pressure. Diverticulosis (asymptomatic) → diverticular disease (symptomatic — pain, altered habit) → diverticulitis (inflamed/infected diverticulum: left iliac fossa pain, fever, raised inflammatory markers). Complications: perforation/abscess, fistula, obstruction, bleeding. Uncomplicated diverticulitis may need no antibiotics.

Adenocarcinoma of the colon/rectum — the third commonest cancer — arising via the adenoma-carcinoma sequence. Presentation differs by side: LEFT/rectal (change in bowel habit, PR bleeding, tenesmus, obstruction) vs RIGHT (iron-deficiency anaemia, weight loss, mass — often silent). Screened by FIT (faecal immunochemical test). Diagnosed by colonoscopy + biopsy; staged (TNM/Dukes); treated by resection ± chemo/radiotherapy. Inherited: FAP (APC) and Lynch (HNPCC).

Infrequent, difficult or incomplete defecation with hard stools. Mostly primary/functional (low fibre/fluid, inactivity, ignoring urge), but secondary causes matter: drugs (opioids, iron, anticholinergics, calcium-channel blockers), metabolic (hypothyroidism, hypercalcaemia), neurological, obstruction (cancer), and in children stool-withholding. Managed with lifestyle + a stepped laxative approach; red flags need investigation.

Infectious inflammation of the colon. Clostridioides difficile (antibiotic-associated pseudomembranous colitis — toxin-mediated, after broad-spectrum antibiotics, esp. the '4 Cs': clindamycin, cephalosporins, co-amoxiclav, ciprofloxacin/quinolones) causes watery/bloody diarrhoea, with toxic megacolon as the feared complication. Invasive bacterial colitis (Shigella, Campylobacter, EHEC, Salmonella) causes bloody diarrhoea (dysentery). Managed by stopping the offending antibiotic + targeted therapy + infection control.

Acute infective diarrhoea ± vomiting, usually viral (norovirus, rotavirus in children) and self-limiting; bacterial (Campylobacter — commonest UK bacterial cause, Salmonella, Shigella, E. coli, C. difficile) and protozoal (Giardia, Cryptosporidium, Entamoeba) in specific contexts. Management is rehydration; antibiotics are reserved for specific pathogens/severe disease; the priorities are hydration, public-health notification and recognising the dysentery/HUS/typhoid red flags.

A life-threatening complication of severe colitis — acute non-obstructive dilatation of the colon (transverse colon >6 cm) with systemic toxicity. Causes: acute severe ulcerative colitis (and Crohn), C. difficile, ischaemic/infective colitis. Risks perforation and death. Managed with aggressive medical therapy and urgent surgery (colectomy) if no improvement; antimotility agents and colonoscopy are avoided.

Inflammation of the appendix, usually from luminal obstruction (faecolith/lymphoid hyperplasia) — the commonest cause of the acute surgical abdomen. Classic migration of central/periumbilical pain to the right iliac fossa (McBurney point) with anorexia, nausea and low-grade fever. A largely clinical diagnosis; treated by appendicectomy. Perforation → peritonitis/abscess. Beware atypical presentations (children, elderly, pregnancy, retrocaecal/pelvic appendix).

Failure of aboral passage of bowel contents. MECHANICAL obstruction — small bowel (commonest: adhesions, hernias; also Crohn, tumour) or large bowel (commonest: colorectal cancer; also volvulus, diverticular stricture). Paralytic ILEUS — functional, no mechanical block (post-operative, electrolyte derangement, opioids, peritonitis). Presents with colicky pain, distension, vomiting and absolute constipation; AXR shows dilated loops. Decompress, resuscitate, and treat the cause.

A full-thickness breach of the gut wall, spilling contents into the peritoneum and causing peritonitis. Causes by site: perforated peptic ulcer (upper), perforated diverticulitis/appendicitis/cancer/ischaemia (lower), Boerhaave (oesophagus). Presents with sudden severe abdominal pain and a rigid 'board-like' abdomen. The radiological hallmark is FREE intraperitoneal gas — sub-diaphragmatic on erect CXR, or pooling to the non-dependent side on a lateral decubitus film. An emergency: resuscitate and operate.

Inflammation of the peritoneal cavity — secondary (commonest, from a perforated/inflamed/ischaemic viscus or contamination) or primary/spontaneous (SBP — infection of ascitic fluid in cirrhosis, without a perforation). Localised peritonitis gives focal guarding; generalised peritonitis gives a rigid abdomen and sepsis. Treat the cause (often surgery) for secondary; antibiotics for SBP.

Twisting of a bowel loop around its mesenteric axis, causing a closed-loop obstruction with ischaemia/perforation risk. SIGMOID volvulus — elderly, constipated, institutionalised; AXR shows a large 'coffee-bean'/inverted-U loop arising from the pelvis. CAECAL volvulus — younger, embryo-shaped loop in the upper abdomen. Neonatal MIDGUT volvulus (with malrotation) — bilious vomiting in a neonate, a surgical emergency (cross-ref child health).

Protrusion of a viscus (usually bowel/omentum) through a defect in its containing wall. Inguinal (commonest — indirect via the deep ring, direct through Hesselbach's triangle), femoral (below/lateral to the pubic tubercle — higher strangulation risk, commoner in women), umbilical, incisional, hiatus. Most are reducible; the danger is incarceration → obstruction → strangulation (ischaemia). Repair electively, or urgently if irreducible/obstructed/strangulated.

A serious neonatal GI emergency — ischaemic-inflammatory necrosis of the bowel wall, mainly in PREMATURE/low-birth-weight infants (also formula feeding, hypoxia). Presents in the first weeks with feed intolerance, bilious vomiting/aspirates, abdominal distension and bloody stools, progressing to systemic collapse. The AXR signs are key: PNEUMATOSIS INTESTINALIS (intramural gas) and portal venous gas; perforation gives free gas. (Primarily a child-health/neonatal condition — carried here for the radiograph discrimination.)

Symptomatic enlargement of the anal vascular cushions, driven by raised pressure (constipation/straining, pregnancy, low fibre). Internal haemorrhoids cause PAINLESS bright-red rectal bleeding (on the paper/coating the stool) ± prolapse; external/thrombosed ones are painful. Graded I–IV. Managed with fibre/fluids and topical agents; banding or surgery for higher grades. The rule: never attribute rectal bleeding to haemorrhoids without excluding cancer in at-risk patients.

A painful tear in the squamous lining of the anal canal, usually in the posterior midline, from hard stool/constipation. Causes severe PAIN on defecation ('passing glass') with a small amount of bright-red blood. Acute fissures heal with stool softening and topical GTN/diltiazem (which relax the sphincter); chronic ones may need botulinum toxin or sphincterotomy. Lateral/multiple fissures → look for an underlying cause (Crohn, infection, malignancy).

Infection of the anal glands (cryptoglandular theory) producing a perianal/ischiorectal ABSCESS — a painful, throbbing, fluctuant perianal swelling needing incision and drainage. A chronic epithelialised tract between the anal canal and skin = fistula-in-ano (recurrent discharge). Recurrent/complex/atypical perianal sepsis → think CROHN'S DISEASE. Antibiotics alone do not treat an abscess.

Protrusion of the rectal wall through the anus — full-thickness (true) prolapse or mucosal prolapse. Associated with chronic straining/constipation, pelvic-floor weakness and multiparity (and in children, cystic fibrosis/malnutrition). Presents with a protruding mass, mucus discharge, bleeding and faecal incontinence. Managed by treating constipation and surgical repair; reduce an incarcerated prolapse promptly.

Bleeding from the upper GI tract (proximal to the duodenojejunal flexure) — haematemesis ('coffee-ground' or fresh) and/or melaena. Commonest cause is PEPTIC ULCER; also oesophageal VARICES (cirrhosis), Mallory-Weiss tear, oesophagitis/gastritis, malignancy. Risk-stratified (Glasgow-Blatchford pre-endoscopy, Rockall post-endoscopy); resuscitate, then ENDOSCOPY within 24 h (immediately if unstable/variceal). The cause changes the drugs.

Dilated portosystemic collateral veins (oesophageal/gastric varices) that form when portal hypertension (usually cirrhosis) drives blood through collaterals. They can bleed catastrophically. Acute variceal haemorrhage is managed with resuscitation, terlipressin + prophylactic antibiotics and endoscopic band ligation; primary/secondary prevention uses non-selective beta-blockers and banding. A medical emergency with high mortality.

A mucosal (partial-thickness) tear at the gastro-oesophageal junction caused by a sudden rise in intra-abdominal/intraluminal pressure — classically forceful retching or vomiting (alcohol binge, bulimia, hyperemesis), THEN haematemesis. Usually self-limiting and managed supportively. The key contrasts are with variceal bleeding (no liver disease) and Boerhaave (full-thickness rupture — much more dangerous).

Bleeding from the colon/rectum/anus — fresh red or dark blood per rectum (haematochezia). Commonest causes: diverticular disease (painless brisk bleeding) and angiodysplasia (often elderly/aortic stenosis/renal disease); also colorectal cancer, IBD, ischaemic colitis, haemorrhoids/fissure. Most settle; resuscitate, exclude an upper GI source if brisk/unstable, then localise (CT angiography/colonoscopy). The priority is excluding cancer in at-risk patients.

Spontaneous FULL-THICKNESS rupture of the oesophagus from a sudden rise in intra-oesophageal pressure against a closed glottis — classically forceful vomiting/retching (often after alcohol). Leads to mediastinitis and sepsis. The Mackler triad: vomiting → severe chest pain → subcutaneous emphysema. A life-threatening surgical emergency, distinct from the benign mucosal Mallory-Weiss tear.

Inflammation of the liver caused by hepatotropic viruses. A and E — faeco-oral, acute, self-limiting (E is dangerous in pregnancy). B and C — blood/sexual/vertical, can become CHRONIC (cirrhosis/HCC risk); D only co-infects with B. Presents with prodromal malaise, jaundice, RUQ pain and deranged LFTs (hepatitic: high ALT/AST). Diagnosed serologically; chronic B/C are treated with antivirals. (Hepatitis B is also carded on sexual health — cross-reference.)

Chronic immune-mediated inflammation of the liver, typically in women (bimodal — young and peri/post-menopausal), associated with other autoimmune disease. Presents acutely (hepatitic) or with established chronic liver disease; raised IgG and autoantibodies (ANA, anti-smooth-muscle [type 1]; anti-LKM1 [type 2]). Responds to immunosuppression (steroids + azathioprine) — important because it's treatable.

A spectrum of liver injury from chronic excess alcohol: fatty liver (steatosis, reversible) → alcoholic hepatitis (acute inflammation, can be severe/fatal) → cirrhosis. Suggested by an AST:ALT ratio >2 and a raised GGT/MCV. Severe alcoholic hepatitis (high discriminant function/MELD) may benefit from corticosteroids. Manage alcohol withdrawal (risk of seizures/delirium tremens) and give thiamine (Wernicke prophylaxis).

Fat accumulation in the liver associated with metabolic dysfunction (obesity, type 2 diabetes, dyslipidaemia, metabolic syndrome) — formerly NAFLD. A spectrum from simple steatosis to steatohepatitis (MASH/NASH — inflammation) to fibrosis/cirrhosis. Usually asymptomatic with incidental fatty liver/mildly raised ALT. The key task is risk-stratifying fibrosis (the prognostic driver) and managing metabolic risk; now the commonest chronic liver disease.

End-stage fibrosis and nodular regeneration of the liver from chronic injury (alcohol, MASLD, viral hepatitis B/C, autoimmune, haemochromatosis/Wilson, PBC/PSC). Compensated cirrhosis may be silent; DECOMPENSATION brings the complications of portal hypertension and liver failure: ascites/SBP, variceal bleeding, hepatic encephalopathy, jaundice, coagulopathy and HCC. Managed by treating the cause, preventing/treating complications, and surveillance.

Rapid loss of liver function (coagulopathy + hepatic ENCEPHALOPATHY) developing within weeks in a patient WITHOUT pre-existing chronic liver disease. In the UK the commonest cause is PARACETAMOL overdose; also viral (B, E in pregnancy, A), drug reactions, Wilson's, Budd-Chiari, autoimmune. A medical emergency — supportive critical care, treat the cause (N-acetylcysteine for paracetamol), and consider transplant (King's College criteria).

Accumulation of fluid in the peritoneal cavity. In cirrhosis it results from portal hypertension + low albumin (high serum-ascites albumin gradient, SAAG ≥11 g/L). Managed with salt restriction, spironolactone (± furosemide) and drainage for tense ascites. SPONTANEOUS BACTERIAL PERITONITIS — infection of the ascitic fluid (neutrophils ≥250/mm³) without a surgical source — must be excluded by diagnostic tap in any decompensating cirrhotic and treated with antibiotics.

The commonest primary liver cancer, arising almost always in a background of CHRONIC LIVER DISEASE/cirrhosis (hepatitis B — even without cirrhosis, hepatitis C, alcohol, MASLD, haemochromatosis, aflatoxin). Often detected on surveillance (USS ± AFP 6-monthly) or presents with decompensation/weight loss/RUQ pain. Diagnosed on characteristic imaging (arterial enhancement + washout) ± biopsy; treated by resection/transplant/ablation/TACE or systemic therapy.

A collection of pus in the liver — PYOGENIC (commonest in the UK; from biliary disease/ascending cholangitis, portal spread from appendicitis/diverticulitis, or haematogenous; often polymicrobial incl. E. coli, Klebsiella) or AMOEBIC (Entamoeba histolytica — travel/endemic, classically a single right-lobe 'anchovy-paste' abscess). Presents with fever, RUQ pain and deranged LFTs; treated with drainage + antibiotics (pyogenic) or metronidazole (amoebic).

Stones in the gallbladder (cholesterol — the '5 Fs': fat, female, forty, fertile, family; or pigment — haemolysis). Most are asymptomatic. BILIARY COLIC = a stone transiently obstructing the cystic duct/Hartmann's pouch → episodic RUQ/epigastric pain (post-fatty-meal, no fever/inflammation). The complications form a family: cholecystitis, cholangitis, gallstone pancreatitis, obstructive jaundice, gallstone ileus. Symptomatic stones → laparoscopic cholecystectomy.

Inflammation of the gallbladder, usually from sustained cystic-duct obstruction by a stone (acalculous in the critically ill). Unlike biliary colic, there is INFLAMMATION: persistent RUQ pain, fever and a positive Murphy sign with raised inflammatory markers but NORMAL LFTs (the duct is the cystic, not the common bile duct). Treated with antibiotics, analgesia and early laparoscopic cholecystectomy (within ~1 week).

Infection of an obstructed biliary tree (usually a common-bile-duct stone, also stricture/tumour/post-ERCP) — bile stasis + bacterial infection. Charcot's TRIAD: RUQ pain + fever/rigors + jaundice; Reynolds' PENTAD adds hypotension + confusion (suppurative cholangitis — septic shock). A medical emergency: resuscitate, IV antibiotics, and urgent biliary DECOMPRESSION (ERCP).

Acute inflammation of the pancreas from premature enzyme activation/autodigestion. The two commonest causes are GALLSTONES and ETHANOL (the 'I GET SMASHED' mnemonic — also trauma, steroids, mumps, autoimmune, scorpion, hyperlipidaemia/hypercalcaemia, ERCP, drugs). Severe epigastric pain radiating to the back with vomiting and a raised amylase/lipase. Severity is scored (Glasgow/APACHE); management is supportive (aggressive fluids, analgesia, treat the cause). Complications: necrosis, pseudocyst, organ failure.

Chronic inflammation and irreversible fibrosis of the pancreas — most commonly from chronic ALCOHOL (also genetic, autoimmune, obstructive, hypertriglyceridaemia). Causes chronic epigastric pain, and progressive loss of function: EXOCRINE failure (steatorrhoea, malabsorption, weight loss — low faecal elastase) and ENDOCRINE failure (diabetes). Pancreatic CALCIFICATION on imaging is characteristic. Managed with pain control, pancreatic enzyme replacement, and diabetes treatment.

Usually ductal adenocarcinoma, most often in the HEAD of the pancreas, presenting late with PAINLESS obstructive jaundice (a palpable non-tender gallbladder — Courvoisier's law), weight loss and epigastric/back pain; or new-onset diabetes/migratory thrombophlebitis (Trousseau). Risk: smoking, chronic pancreatitis, hereditary. Poor prognosis; only a minority are resectable (Whipple's). CA19-9 is a marker.

A chronic autoimmune cholestatic liver disease - immune destruction of the small intrahepatic bile ducts leading to cholestasis, fibrosis and cirrhosis. Classically a middle-aged WOMAN with FATIGUE and ITCH (pruritus); cholestatic LFTs with a positive ANTI-MITOCHONDRIAL ANTIBODY (AMA). Treated with ursodeoxycholic acid. Associated with other autoimmune disease (Sjogren, thyroid).

A chronic cholestatic disease of progressive inflammation, fibrosis and STRICTURING of the intra- and extra-hepatic bile ducts. Classically a MAN with ULCERATIVE COLITIS; cholestatic LFTs with a characteristic BEADED (multifocal stricture) appearance on MRCP. Raised cholangiocarcinoma and colorectal cancer risk. No effective medical therapy slows it; manage strictures and complications; transplant for end-stage disease.

Malignancy of the bile-duct epithelium (intra-hepatic, perihilar/Klatskin, or distal). Presents like other malignant biliary obstruction - PAINLESS obstructive jaundice, weight loss, RUQ pain - often late and unresectable. Risk factors: primary sclerosing cholangitis, liver flukes, choledochal cysts, chronic biliary inflammation. CA19-9 raised; diagnosed on imaging/cytology; only a minority are resectable.

A classic triad: DYSPHAGIA + IRON-DEFICIENCY ANAEMIA + an upper OESOPHAGEAL WEB (post-cricoid). Typically a middle-aged woman; the web causes intermittent solid-food dysphagia. Important because it is a recognised PRE-MALIGNANT condition (post-cricoid/oesophageal squamous cell carcinoma). Treated by iron replacement and dilatation of the web.

The commonest congenital GI anomaly - a true diverticulum from a persistent vitellointestinal (omphalomesenteric) duct, often containing ectopic GASTRIC or pancreatic mucosa. The RULE OF 2s: 2% of people, 2 feet from the ileocaecal valve, 2 inches long, often presents under age 2, 2 types of ectopic mucosa. Classically PAINLESS rectal bleeding in a child (ectopic gastric mucosa ulcerates the ileum); can also cause obstruction (lead point for intussusception/volvulus) or mimic appendicitis.

A chronic immune/antigen-mediated oesophageal disease defined by symptoms of oesophageal dysfunction plus dense eosinophilic infiltration (≥15 eosinophils/high-power field) on biopsy, with other causes of oesophageal eosinophilia excluded. Typically affects young atopic men. The classic exam trap is recurrent solid-food dysphagia or a food-bolus obstruction with heartburn that does NOT respond to a PPI.

A low-grade (usually indolent) extranodal marginal-zone B-cell lymphoma arising in gastric MALT, the great majority driven by chronic Helicobacter pylori infection. The high-yield point: localised H. pylori-positive disease regresses with eradication therapy alone in most cases — so you eradicate first and confirm regression endoscopically.

Acute colonic pseudo-obstruction — gross dilatation of the colon (especially caecum and right colon) in the absence of any mechanical obstructing lesion or colitis. Typically in frail, elderly, post-operative or severely unwell patients, often with electrolyte derangement and on opioids/anticholinergics. The danger is caecal perforation, the risk of which rises sharply once the caecum exceeds ~12 cm.

Acquired degenerative vascular ectasias, most often in the caecum and right colon, that are a common cause of obscure/occult lower-GI bleeding and iron-deficiency anaemia in the elderly. Classically associated with aortic stenosis (Heyde syndrome — acquired type 2A von Willebrand disease) and with chronic kidney disease.