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Digestive System Diseases Dataset – Gastrointestinal Disorders Database
Digestive System Diseases Dataset
The Digestive System Diseases Dataset is a structured medical database containing a comprehensive list of conditions affecting the digestive system, including the stomach, intestines, liver, pancreas, and related organs.
Digestive diseases such as acid reflux, irritable bowel syndrome (IBS), and liver disorders are common health issues worldwide. This dataset provides organised information to support medical research, healthcare analytics, and application development.
Each record includes key clinical details such as disease descriptions, affected digestive organs, common symptoms, severity levels, and treatment approaches.
The dataset has been cleaned and structured for easy integration into spreadsheets, databases, and data analysis tools.
It is ideal for healthcare developers, researchers, educators, and data scientists working with gastrointestinal health data.
Dataset Contents
The dataset includes fields such as:
- Disease / Condition Name
- Description
- Affected Organ/System (Stomach, Intestines, Liver, Pancreas, etc.)
- Common Symptoms
- Severity Level
- Disease Category
- Risk Factors
- Treatment / Management
Example Conditions Included
- Gastroesophageal Reflux Disease (GERD)
- Irritable Bowel Syndrome (IBS)
- Crohn’s Disease
- Ulcerative Colitis
- Peptic Ulcer Disease
- Hepatitis
- Gallstones
- Pancreatitis
- Celiac Disease
- Liver Cirrhosis
...and many more digestive system conditions.
Data Preview
12 columns
25 rows shown
| No. | Disease Name | Category | Primary Cause / Etiology | Prevalence | Age of Onset | Key Symptoms | Affected Organ(s) | Diagnostic Method | Treatment Approach | Prognosis | ICD-10 Code | |
|---|---|---|---|---|---|---|---|---|---|---|---|---|
| 1 | ▸ Esophageal Diseases | |||||||||||
| 2 | 1 | Achalasia | Esophageal Diseases | Loss of inhibitory neurons (nitric oxide and VIP-producing) in the myenteric plexus; autoimmune-mediated ganglion cell degeneration; possible viral trigger (HSV-1); results in impaired LES relaxation and absent esophageal peristalsis; Chagas disease (secondary achalasia in South America) | Annual incidence 1-3 per 100,000; prevalence ~10 per 100,000; equal male/female ratio; no racial predominance; Chagas-related achalasia affects ~6 million in endemic areas | Bimodal distribution: 20-40 years and >60 years; mean age at diagnosis 50 years; can occur at any age including children; Chagas-related onset earlier | Progressive dysphagia to solids AND liquids (distinguishing from mechanical obstruction); regurgitation of undigested food; chest pain; weight loss; nocturnal cough/aspiration; heartburn (paradoxical from fermentation); difficulty belching | Esophageal body; lower esophageal sphincter; myenteric (Auerbach's) plexus | High-resolution manometry (HRM) gold standard — Chicago classification v4.0 (Types I, II, III); timed barium swallow (bird-beak sign, dilated esophagus); upper endoscopy to exclude pseudoachalasia (malignancy); functional lumen imaging probe (FLIP); CT/EUS if malignancy suspected | Pneumatic dilation (30-35mm balloon, 80-90% initial response); Heller myotomy (laparoscopic with Dor fundoplication, >90% success); peroral endoscopic myotomy (POEM, >90% success, higher GERD rates); botulinum toxin injection (temporary, 60-70% response for 6-12 months); pharmacologic (nifedipine, nitrates — limited efficacy); Type II best response to all treatments | Good with treatment; Type II achalasia best prognosis (96% response to treatment); Type I intermediate; Type III more difficult to treat; long-term risk of esophageal squamous cell carcinoma (3-8% over 25 years); POEM and Heller myotomy durable >10 years | K22.0 |
| 3 | 2 | Barrett's Esophagus | Esophageal Diseases | Chronic GERD causing intestinal metaplasia of squamous esophageal epithelium; replacement by specialized columnar epithelium with goblet cells; risk factors include chronic GERD >5 years, male sex, Caucasian race, obesity, smoking, family history | Prevalence 1.6-6.8% of patients undergoing EGD; ~1.5-2% of general population; ~3.3 million adults in US; male-to-female ratio 2:1; higher in Caucasians | Mean age at diagnosis 55 years; rare before age 20; predominantly males >50 years; risk increases with duration of GERD symptoms | Often asymptomatic; symptoms are those of underlying GERD (heartburn, regurgitation); dysphagia if stricture develops; may have reduced GERD symptoms due to reduced acid sensitivity of metaplastic epithelium | Distal esophagus; gastroesophageal junction; columnar-lined esophagus | Upper endoscopy with systematic 4-quadrant biopsies every 1-2cm (Seattle protocol); histological confirmation of intestinal metaplasia with goblet cells; Prague C&M criteria for extent classification; chromoendoscopy; confocal laser endomicroscopy | Aggressive PPI therapy (high-dose); surveillance endoscopy every 3-5 years (non-dysplastic); radiofrequency ablation (RFA) for dysplasia; endoscopic mucosal resection (EMR) for visible lesions; cryotherapy; photodynamic therapy; esophagectomy for high-grade dysplasia refractory to endoscopic treatment | Non-dysplastic: annual progression to cancer 0.3-0.5%; low-grade dysplasia: 0.5-1.7%/year; high-grade dysplasia: 5-10%/year cancer risk; RFA eliminates dysplasia in >90%; excellent prognosis with surveillance and early intervention | K22.7 |
| 4 | 3 | Eosinophilic Esophagitis (EoE) | Esophageal Diseases | Chronic immune/antigen-mediated esophageal disease; food allergens (milk, wheat, egg, soy, nuts, seafood) most common triggers; aeroallergens may contribute; Th2-mediated immune response; IL-13 and IL-5 driven eosinophilic infiltration; genetic predisposition (TSLP, calpain-14 polymorphisms); associated with atopic diseases | Prevalence 34-56 per 100,000 in adults; increasing incidence; ~1 in 2,000; most common cause of food impaction and dysphagia in young adults; male-to-female ratio 3:1; predominantly Caucasian; seasonal variation | Bimodal: children (mean 8 years) and adults (mean 30-40 years); predominantly males; strong association with atopic history (asthma, eczema, allergic rhinitis in 50-80%) | Adults: dysphagia to solids (70%), food impaction (33-50%), chest pain, heartburn not responding to PPIs; Children: feeding difficulties, vomiting, abdominal pain, failure to thrive; food avoidance behaviors; symptoms often present for years before diagnosis | Esophageal epithelium; entire length of esophagus; proximal > distal in children; distal > proximal in adults | Upper endoscopy with >=6 biopsies from proximal and distal esophagus; histology: >=15 eosinophils per high-power field; endoscopic features (rings, furrows, white exudates, strictures, crepe paper mucosa); EREFS scoring system; allergy testing (skin prick, patch testing); exclude other causes of esophageal eosinophilia | PPI therapy (omeprazole 20-40mg BID, ~50% respond); topical swallowed corticosteroids (fluticasone 880mcg-1760mcg/day or budesonide oral viscous suspension 1-2mg BID); elimination diets (6-food, 4-food, 2-food, or targeted); dupilumab (first FDA-approved biologic for EoE, 300mg weekly); endoscopic dilation for strictures; maintenance therapy required to prevent recurrence | Chronic relapsing condition; not associated with mortality; risk of esophageal stricture and narrowing increases with untreated disease duration; no progression to malignancy; excellent quality of life with treatment; dupilumab achieves histologic remission in 60% | K20.0 |
| 5 | 4 | Esophageal Adenocarcinoma | Esophageal Diseases | Arises from Barrett's esophagus metaplasia-dysplasia-carcinoma sequence; chronic GERD; obesity (visceral); tobacco use; male sex; Caucasian ethnicity; dietary factors (low fruit/vegetable intake) | Incidence rising 6-fold since 1970s in Western countries; ~8 per 100,000 in US males; accounts for ~60% of esophageal cancers in developed nations; ~600,000 new esophageal cancer cases globally (GBD 2019) | Peak incidence 60-70 years; male-to-female ratio 7:1; increasing incidence in younger males; rare before age 40 | Progressive dysphagia (solids then liquids); unintentional weight loss; odynophagia; chest or back pain; iron deficiency anemia; hoarseness if recurrent laryngeal nerve involvement; hematemesis; early satiety | Distal esophagus; gastroesophageal junction; may extend to gastric cardia | Upper endoscopy with biopsy (diagnostic); endoscopic ultrasound (EUS) for T-staging; CT chest/abdomen/pelvis for staging; PET-CT for metastatic evaluation; staging laparoscopy; biomarkers (HER2, PD-L1 expression) | Early stage: endoscopic mucosal resection or submucosal dissection (T1a); esophagectomy (Ivor Lewis or McKeown); neoadjuvant chemoradiation (CROSS regimen: carboplatin/paclitaxel + 41.4 Gy) then surgery; perioperative chemotherapy (FLOT); definitive chemoradiation for unresectable; palliative stenting; immunotherapy (nivolumab adjuvant for residual disease); trastuzumab if HER2+ | Poor overall; 5-year survival 20% all stages; 47% for localized; 25% regional; 5% distant metastases; neoadjuvant therapy improves survival by 10-15%; early detection in Barrett's surveillance improves outcomes significantly | C15.5 |
| 6 | 5 | Esophageal Diverticulum (Zenker's) | Esophageal Diseases | Pulsion diverticulum through Killian's dehiscence (weakness between thyropharyngeal and cricopharyngeal muscles of inferior pharyngeal constrictor); cricopharyngeal muscle dysfunction with elevated UES pressure; false diverticulum (mucosa and submucosa only); associated with aging and reduced muscle compliance | Prevalence 0.01-0.11% of general population; most common esophageal diverticulum; incidence 2 per 100,000/year; predominant in Northern Europe; rare in Asia and Africa | Almost exclusively >60 years; peak incidence 70-80 years; male predominance (male-to-female ratio 3:1); extremely rare before age 40 | Progressive dysphagia; regurgitation of undigested food (hours after eating); halitosis; gurgling noise during swallowing; neck swelling (left side); aspiration pneumonia; weight loss; voice changes; feeling of lump in throat | Killian's dehiscence (pharyngoesophageal junction); posterior hypopharynx; between thyropharyngeal and cricopharyngeal muscles | Barium swallow (study of choice — shows posterior outpouching at pharyngoesophageal junction); direct laryngoscopy; upper endoscopy (perform cautiously due to perforation risk); CT neck; manometry (usually not needed) | Observation for small asymptomatic diverticula (<1cm); endoscopic diverticulotomy (flexible or rigid, first-line for most patients); Dohlman procedure (rigid endoscopic stapling); cricopharyngeal myotomy; open surgical diverticulectomy or diverticulopexy with myotomy for large diverticula (>5cm); per-oral endoscopic myotomy for Zenker's (Z-POEM) | Good with treatment; endoscopic treatment success >90%; recurrence rate 5-15%; operative mortality <1%; untreated may lead to aspiration pneumonia and malnutrition; normal lifespan with treatment | K22.5 |
| 7 | 6 | Esophageal Motility Disorders (Diffuse Esophageal Spasm) | Esophageal Diseases | Premature contractions of distal esophageal smooth muscle; distal latency <4.5 seconds on HRM; nitric oxide pathway impairment; may exist on spectrum with achalasia; triggers include stress, hot/cold foods, acid reflux; hypersensitive esophageal mucosa | Rare; <5% of patients referred for esophageal manometry; prevalence ~1 per 100,000; less common than achalasia; often overdiagnosed on barium swallow | 50-70 years; equal male/female ratio; associated with anxiety and psychiatric comorbidities; may occur at any adult age | Intermittent chest pain (can mimic cardiac pain); dysphagia to solids and liquids (intermittent); pain may be triggered by eating or stress; heartburn; regurgitation; symptom-free intervals common | Distal two-thirds of esophageal body (smooth muscle); LES function usually preserved (distinguishes from achalasia) | High-resolution manometry (Chicago classification v4.0: >=20% premature contractions with DL <4.5s); barium swallow ('corkscrew' esophagus, rosary bead pattern — present in minority); upper endoscopy to exclude structural causes; cardiac workup to rule out coronary artery disease first | Reassurance and lifestyle modifications; smooth muscle relaxants (calcium channel blockers — diltiazem 60-90mg TID; nitrates); PPI if concurrent GERD; peppermint oil; tricyclic antidepressants (imipramine 25-50mg) or SSRIs for pain modulation; botulinum toxin injection; POEM for refractory cases; rarely surgical myotomy | Good; benign condition; does not progress to cancer; symptoms wax and wane; may evolve to achalasia in rare cases; quality of life may be impaired but lifespan normal; 30-50% improve with medical therapy | K22.4 |
| 8 | 7 | Esophageal Perforation (Boerhaave Syndrome) | Esophageal Diseases | Spontaneous transmural rupture of esophagus from sudden increase in intraesophageal pressure against a closed glottis; forceful vomiting (most common); iatrogenic (endoscopy, dilation — 60% of all perforations); foreign body; trauma; tumors; most perforations at left posterolateral distal esophagus | Spontaneous (Boerhaave) accounts for 15% of esophageal perforations; overall incidence 3 per 1,000,000/year; iatrogenic perforation rate 0.01-0.4% of endoscopies; mortality 10-40% depending on delay in treatment | Mean age 50-70 years; male predominance (male-to-female ratio 5:1); associated with heavy alcohol consumption and overeating; iatrogenic at any age | Mackler's triad (vomiting, lower thoracic pain, subcutaneous emphysema) present in ~50%; severe retrosternal or epigastric pain after vomiting; dysphagia; odynophagia; tachycardia; fever; subcutaneous crepitus; Hamman's sign (mediastinal crunch); pleural effusion; septic shock if delayed | Left posterolateral distal esophagus (90% spontaneous); any location for iatrogenic; mediastinum; pleural space | CT chest/abdomen with water-soluble oral contrast (sensitivity >90%); chest X-ray (pneumomediastinum, pleural effusion, subcutaneous emphysema); water-soluble contrast esophagogram (Gastrografin then thin barium); upper endoscopy (may confirm and potentially treat); blood cultures; inflammatory markers | Surgical emergency; NPO, broad-spectrum IV antibiotics, IV PPI; primary repair within 24 hours (best outcomes); surgical repair with intercostal muscle or pleural flap buttress; endoscopic management for contained perforations (endoscopic stenting, endoscopic vacuum therapy, clips); chest tube drainage; esophageal diversion for late presentations; conservative (Cameron criteria) for contained perforations: NPO, antibiotics, drainage | Variable; mortality 10-15% with early repair (<24h); 30-50% if delayed >24 hours; sepsis and multiorgan failure main causes of death; iatrogenic perforations have better prognosis (caught early); endoscopic management success 80-90% for select cases | K22.3 |
| 9 | 8 | Esophageal Squamous Cell Carcinoma | Esophageal Diseases | Alcohol and tobacco use (synergistic >30-fold risk); hot beverage consumption; nitrosamine exposure; nutritional deficiencies (zinc, selenium); achalasia; caustic injury; HPV infection (some regions); tylosis (genetic); Plummer-Vinson syndrome | Most common esophageal cancer type globally; ~400,000 new cases/year worldwide; highest incidence in 'Asian esophageal cancer belt' (Iran to central China); incidence 20-100 per 100,000 in high-risk areas; declining in Western nations | Peak incidence 60-70 years; male-to-female ratio 3-4:1; earlier onset in high-incidence regions; associated with lower socioeconomic status | Progressive dysphagia; weight loss; odynophagia; retrosternal chest pain; cough from tracheoesophageal fistula; hoarseness; aspiration pneumonia; cervical lymphadenopathy; hematemesis | Mid and upper esophagus (most common); may affect any segment; regional lymph nodes; submucosal spread | Upper endoscopy with biopsy and Lugol's iodine chromoendoscopy (unstained areas suspicious); EUS for local staging; CT chest/abdomen/pelvis; PET-CT; barium swallow; bronchoscopy if proximal tumor; p40/p63 immunohistochemistry | Endoscopic resection for superficial (T1a); neoadjuvant chemoradiation (CROSS regimen) then esophagectomy; definitive chemoradiation (cisplatin/5-FU + 50.4 Gy) for cervical or unresectable; palliative chemotherapy; immunotherapy (pembrolizumab + chemo for advanced); esophageal stenting for dysphagia palliation | Poor overall; 5-year survival 15-25% all stages; localized 45%; regional 25%; distant 5%; response to neoadjuvant therapy is key prognostic factor; pCR in 30-40% with chemoradiation | C15.4 |
| 10 | 9 | Esophageal Stricture (Peptic) | Esophageal Diseases | Chronic GERD-induced inflammation leading to fibrosis and luminal narrowing; peptic strictures account for 70-80% of benign esophageal strictures; other causes: caustic ingestion, radiation, pill esophagitis, anastomotic, eosinophilic esophagitis | Prevalence declining due to effective PPI therapy; occurs in 7-23% of untreated GERD patients; more common in elderly; decreasing incidence since 1990s with widespread PPI use | Typically >60 years; more common in males; risk increases with GERD duration and severity; associated with Barrett's esophagus | Progressive dysphagia to solids (when lumen <13mm); food impaction; weight loss; heartburn may decrease as stricture prevents reflux; odynophagia; chest pain; symptoms develop gradually over months to years | Distal esophagus; gastroesophageal junction; short segment (<2cm) in peptic strictures | Upper endoscopy with biopsy (to exclude malignancy); barium swallow (smooth, tapered narrowing); endoscopic ultrasound if malignancy suspected; manometry to assess motility | Endoscopic bougie or balloon dilation (Savary-Gilliard or TTS balloon); aggressive PPI therapy (BID dosing); repeat dilations as needed (typically 1-3 sessions); intralesional corticosteroid injection for refractory strictures; temporary self-expanding stent for recalcitrant cases; surgery for refractory strictures (rare) | Good with dilation and PPI therapy; 80-90% achieve adequate lumen with dilation; 30-40% require repeat dilations; long-term PPI prevents recurrence; refractory strictures (<10%) may need repeated interventions; normal lifespan | K22.2 |
| 11 | 10 | Esophageal Varices | Esophageal Diseases | Portal hypertension (hepatic venous pressure gradient >10 mmHg) causing portosystemic collateral formation; liver cirrhosis (most common cause); schistosomiasis; portal vein thrombosis; Budd-Chiari syndrome; progression from small to large varices over 1-2 years | Present in 50% of cirrhotic patients at diagnosis; 5-15% per year develop new varices; variceal hemorrhage in 25-40% of cirrhotics with varices; mortality per bleeding episode 15-20%; ~300,000 deaths annually worldwide | Age correlates with underlying liver disease; typically 40-65 years for alcohol-related cirrhosis; earlier for viral hepatitis in endemic regions; any age for non-cirrhotic portal hypertension | Often asymptomatic until hemorrhage; acute variceal bleeding: hematemesis (massive), melena, hematochezia, hypovolemic shock, tachycardia, hypotension, syncope; signs of chronic liver disease (ascites, jaundice, spider angiomata) | Submucosal veins of distal esophagus; gastroesophageal junction; gastric fundus (GOV1, GOV2, IGV1); portal venous system | Upper endoscopy (screening in all cirrhotics at diagnosis); grade by size (small <5mm, large >5mm); red wale marks indicate high rupture risk; transient elastography (FibroScan >20 kPa + platelets <150,000 suggests clinically significant portal hypertension); hepatic venous pressure gradient (HVPG) measurement; CT/MRI for portal vein assessment | Primary prophylaxis: non-selective beta-blockers (carvedilol 6.25-12.5mg daily preferred, or propranolol/nadolol) or endoscopic variceal ligation (EVL); acute bleeding: volume resuscitation, IV octreotide 50mcg bolus then 50mcg/hr, IV antibiotics (ceftriaxone 1g), emergency endoscopic band ligation, balloon tamponade (Sengstaken-Blakemore) as bridge; TIPS for refractory bleeding; secondary prophylaxis: EVL + beta-blocker combination | Poor without treatment; 6-week mortality after first bleed 15-20%; 1-year rebleeding rate 60% without prophylaxis; reduced to 20-30% with EVL + beta-blocker; early TIPS improves survival in high-risk patients (Child-Pugh C or B with active bleeding); liver transplant is definitive treatment for underlying cirrhosis | I85.00 |
| 12 | 11 | Gastroesophageal Reflux Disease (GERD) | Esophageal Diseases | Transient lower esophageal sphincter relaxation; impaired esophageal clearance; hiatal hernia; obesity; delayed gastric emptying; reduced LES pressure; dietary triggers (caffeine, alcohol, fatty foods) | Global prevalence 8-33% of adults; ~20% in Western populations (GBD 2019); ~264 million affected worldwide; increasing prevalence in Asia | Any age; peak onset 30-50 years; common in pregnancy; increasing prevalence with age and obesity | Heartburn (pyrosis) at least twice weekly; acid regurgitation; dysphagia; chest pain; chronic cough; laryngitis; dental erosion; globus sensation; water brash; worsened by lying down or bending | Esophagus; lower esophageal sphincter; gastric cardia | Clinical diagnosis based on symptom frequency; PPI trial (sensitivity 78%); upper endoscopy (EGD) for alarm symptoms; 24-hour pH monitoring (gold standard); impedance-pH testing; esophageal manometry; barium swallow | Lifestyle modifications (weight loss, head-of-bed elevation, dietary changes); PPI therapy first-line (omeprazole 20mg, esomeprazole 40mg daily); H2 receptor antagonists (famotidine 20mg BID); antacids PRN; baclofen for refractory cases; fundoplication (Nissen/Toupet) for PPI-refractory; LINX magnetic sphincter augmentation; transoral incisionless fundoplication (TIF) | Good with treatment; chronic relapsing condition; 80-90% symptom relief with PPIs; 5-10% develop Barrett's esophagus; rare progression to adenocarcinoma (<0.5%/year in Barrett's); lifestyle modification improves long-term outcomes | K21.0 |
| 13 | 12 | Hiatal Hernia | Esophageal Diseases | Protrusion of stomach through esophageal hiatus of diaphragm; Type I (sliding, 95%): GEJ migrates above diaphragm; Type II (paraesophageal): gastric fundus herniates alongside esophagus; Type III (mixed); Type IV (large with other organs); weakening of phrenoesophageal ligament; obesity; age-related degeneration; increased abdominal pressure; genetic factors | Very common; present in 10-60% of adults depending on age and population; prevalence increases with age; found incidentally in 50% of patients >50 years undergoing EGD; most are Type I (sliding) | Increases with age; rare before 40; >60% of patients >60 years; female predominance for paraesophageal type; associated with obesity, pregnancy, chronic cough/straining | Type I: usually asymptomatic or causes GERD symptoms (heartburn, regurgitation); large hernias: dysphagia, postprandial fullness, early satiety, chest pain; paraesophageal: intermittent volvulus, strangulation (acute pain, vomiting); Cameron lesions causing occult GI bleeding and iron deficiency anemia | Esophageal hiatus; gastroesophageal junction; gastric fundus; diaphragm | Often incidental finding; upper endoscopy (retroflexed view shows hernia size); barium swallow (best for assessing type and size); CT chest/abdomen; high-resolution manometry (LES location relative to diaphragm); pH testing for GERD evaluation | Type I: lifestyle modifications and PPI for symptomatic GERD; anti-reflux surgery (Nissen fundoplication) for refractory GERD; Type II-IV: surgical repair recommended due to risk of incarceration/strangulation (laparoscopic or robotic repair with mesh); emergency surgery for acute volvulus or strangulation; watchful waiting for asymptomatic elderly with paraesophageal hernia (controversial) | Good for Type I; excellent quality of life with PPI or surgical repair; paraesophageal hernias carry risk of acute complications (volvulus, strangulation, perforation) — 1-2% annual risk; elective repair mortality <1%; emergency repair mortality 5-17%; normal lifespan with appropriate management | K44.9 |
| 14 | 13 | Infectious Esophagitis (Candida) | Esophageal Diseases | Candida albicans (90%) infection of esophageal mucosa; immunosuppression (HIV/AIDS with CD4 <200, organ transplant, chemotherapy, prolonged corticosteroids); other risk factors: diabetes mellitus, PPI use, antibiotics, esophageal stasis (achalasia); less common: Candida glabrata, C. krusei | Most common infectious esophagitis; 10-15% of HIV/AIDS patients (declining with ART); 1-5% of transplant recipients; rare in immunocompetent; accounts for 88% of infectious esophagitis cases | Any age; depends on underlying immunosuppression; HIV patients typically 20-50 years; transplant and chemotherapy patients at any age | Odynophagia (most common); dysphagia; retrosternal chest pain; concurrent oropharyngeal thrush in 50-75%; nausea; may be asymptomatic in mild cases; weight loss if severe/chronic | Esophageal mucosa; entire esophageal length may be involved; mid and distal esophagus most common | Upper endoscopy with biopsy and brushings (white raised plaques adherent to mucosa, 'cottage cheese' appearance); histology/cytology (pseudohyphae and yeast forms on PAS or GMS stain); empiric fluconazole trial in HIV with typical symptoms (therapeutic test); culture for species identification and susceptibility if refractory | Fluconazole 200-400mg daily for 14-21 days (first-line, >80% response); itraconazole solution 200mg daily (second-line); voriconazole 200mg BID for azole-resistant species; IV micafungin 150mg daily or anidulafungin 100mg daily for refractory cases; amphotericin B for multi-resistant; treat underlying immunosuppression; ART initiation for HIV | Excellent with appropriate antifungal therapy; >90% response to fluconazole; relapse common if immunosuppression persists; prophylaxis considered for recurrent episodes; prognosis depends on underlying condition; normal esophageal function restored after treatment | B37.81 |
| 15 | 14 | Mallory-Weiss Tear | Esophageal Diseases | Longitudinal mucosal laceration at gastroesophageal junction from forceful vomiting or retching; associated with alcoholism (40-75%), severe retching, violent coughing, straining, hiccups, seizures; hiatal hernia present in 40-100% of cases; increased gastric pressure against a closed LES | Accounts for 5-10% of upper GI bleeding episodes; declining incidence with reduced alcohol abuse and effective antiemetics; predominantly in alcoholic patients; incidence ~5 per 100,000 | Mean age 40-60 years; male predominance (male-to-female ratio 2-4:1); associated with alcohol use disorder; may occur in any vomiting patient including pregnant women with hyperemesis | Hematemesis (bright red blood) after forceful vomiting; may have melena; epigastric pain; usually preceded by a history of vomiting or retching; hemodynamic instability if severe hemorrhage; most bleeding is self-limited | Gastroesophageal junction; gastric cardia; mucosal tear extending into submucosa but not through muscularis (distinguishes from Boerhaave syndrome) | Upper endoscopy (diagnostic and therapeutic) — reveals longitudinal mucosal tear; most tears are single and on the lesser curvature of the gastric cardia; Forrest classification for active bleeding; CBC and coagulation studies; type and screen if significant bleeding | Supportive care (90% stop bleeding spontaneously); antiemetics (ondansetron); PPI therapy (IV pantoprazole 80mg bolus then 8mg/hr if active bleeding); endoscopic therapy for active bleeding (hemoclipping, thermal coagulation, injection therapy, band ligation); angiographic embolization for refractory bleeding; surgery very rarely needed (<5%) | Excellent; self-limiting in 80-90%; rebleeding rate 5-8%; mortality <3% with modern management; full recovery expected; recurrence uncommon unless underlying cause (alcohol abuse) persists | K22.6 |
| 16 | 15 | Pill Esophagitis | Esophageal Diseases | Direct mucosal injury from prolonged contact with oral medications; most common culprits: doxycycline, tetracycline, NSAIDs (aspirin, ibuprofen), bisphosphonates (alendronate), potassium chloride, iron supplements, quinidine; risk factors: taking pills without water, lying down immediately after swallowing, esophageal dysmotility | Relatively common; exact prevalence unknown; accounts for ~1-4% of esophagitis cases; over 1,000 reported cases in literature; likely underreported; increasing with polypharmacy in elderly | Any age; more common in elderly (reduced esophageal motility, polypharmacy); young adults (doxycycline for acne); females more often affected | Sudden-onset odynophagia; retrosternal chest pain; dysphagia; pain worse with swallowing; symptoms typically develop within hours to days of offending medication; may mimic cardiac chest pain | Mid-esophagus most common (aortic arch compression); distal esophagus (bisphosphonates); any location of anatomic narrowing | Clinical history and temporal relationship with medication; upper endoscopy (discrete ulcers, 'kissing ulcers', focal inflammation at level of aortic arch or LES); biopsy to exclude other causes; pill fragments may be visible; barium swallow less sensitive | Discontinue or substitute offending medication; adequate water intake (>240ml) with medications; remain upright 30 minutes after pills; sucralfate suspension for mucosal protection; PPI therapy; lidocaine viscous for pain relief; most heal within 1-3 weeks after stopping offender | Excellent; self-limiting once medication is discontinued; full healing in 1-6 weeks; rarely causes stricture if chronic; prevention through proper medication administration is key; normal lifespan | K22.1 |
| 17 | 16 | Plummer-Vinson Syndrome | Esophageal Diseases | Iron deficiency anemia leading to mucosal atrophy and web formation in postcricoid esophagus; exact pathogenesis unclear; iron deficiency impairs iron-dependent oxidative enzymes causing mucosal degeneration; autoimmune predisposition; nutritional deficiencies; associated with celiac disease and thyroid disease | Extremely rare; mostly reported from Scandinavia; declining incidence due to improved nutrition and iron supplementation; prevalence largely unknown; most cases in premenopausal women | Predominantly females 40-70 years; female-to-male ratio 4-8:1; premenopausal women with chronic iron deficiency; rare in children | Dysphagia to solids (intermittent, painless); glossitis; angular cheilitis; koilonychia (spoon nails); fatigue; pallor; brittle nails; splenomegaly; weakness; weight loss in advanced cases | Postcricoid esophagus; cervical esophagus (esophageal web); tongue; oral mucosa | Upper endoscopy revealing thin esophageal web(s) in postcricoid region; barium swallow (shelf-like filling defect); CBC showing microcytic hypochromic anemia; iron studies (low ferritin, low serum iron, high TIBC); investigate for celiac disease; thyroid function | Iron supplementation (oral ferrous sulfate 325mg TID or IV iron if malabsorption); endoscopic web dilation or disruption; treatment of underlying cause of iron deficiency; nutritional support; vitamin supplementation; surveillance for postcricoid carcinoma | Good with iron replacement and dilation; webs may resolve with iron therapy alone; increased risk of postcricoid squamous cell carcinoma (up to 10%); requires long-term surveillance; normal lifespan with treatment and monitoring | D50.1 |
| 18 | ▸ Gastric & Duodenal Diseases | |||||||||||
| 19 | 17 | Acute Gastritis | Gastric & Duodenal Diseases | Acute inflammation of gastric mucosa; NSAIDs (most common cause — inhibit prostaglandin synthesis); alcohol; physiological stress (burns — Curling's ulcer; head injury — Cushing's ulcer; sepsis; ICU patients); H. pylori acute infection; caustic ingestion; cocaine; radiation; bile reflux; ischemia | Very common; NSAIDs cause gastric injury in 30-50% of chronic users; stress ulcers/gastritis in 75-100% of ICU patients; acute H. pylori infection rarely recognized; prevalence of NSAID gastropathy increasing with aging population | Any age; NSAID-related increases with age; stress gastritis in critically ill patients of any age; alcohol-related in adults 20-60 years | Epigastric pain or burning; nausea; vomiting; anorexia; hematemesis or melena (erosive gastritis); abdominal tenderness; dyspepsia; may be asymptomatic; severe cases may present with upper GI hemorrhage and hemodynamic instability | Gastric mucosa; may be diffuse or localized; fundus (stress-related); antrum (NSAID, H. pylori); entire stomach (alcohol, caustic) | Clinical history (NSAID use, alcohol, ICU setting); upper endoscopy (mucosal erythema, erosions, petechiae, hemorrhage); biopsy (acute neutrophilic infiltration); H. pylori testing; CBC (anemia if bleeding); basic metabolic panel; lipase (exclude pancreatitis) | Remove offending agent (stop NSAIDs, alcohol); PPI therapy (IV pantoprazole for severe/bleeding, then oral PPI 4-8 weeks); H2 receptor antagonist; sucralfate; stress ulcer prophylaxis in ICU (IV PPI or H2 blocker); endoscopic hemostasis for active bleeding; H. pylori eradication if positive; antiemetics for nausea/vomiting; IV fluids and blood transfusion if needed | Excellent; self-limiting once cause removed; healing within days to weeks; stress gastritis mortality related to underlying critical illness not gastritis itself; NSAID gastropathy preventable with co-prescription of PPI; full recovery expected with appropriate treatment | K29.0 |
| 20 | 18 | Autoimmune Gastritis (Pernicious Anemia) | Gastric & Duodenal Diseases | Autoimmune destruction of gastric parietal cells by anti-parietal cell antibodies; antibodies against intrinsic factor; leads to achlorhydria, hypergastrinemia, and vitamin B12 malabsorption; associated with other autoimmune conditions (thyroiditis, type 1 diabetes, vitiligo, Addison's disease); genetic predisposition (HLA-DRB1) | Prevalence 2-8% in general population; up to 25% in elderly; higher in Northern Europeans; 10-30% of first-degree relatives affected; often underdiagnosed; accounts for 20-25% of chronic gastritis cases | Peak diagnosis 50-70 years; may develop subclinically decades earlier; female predominance (female-to-male 3:1); more common in blood type A; associated autoimmune diseases in 30-50% | Often asymptomatic for years; fatigue and weakness (B12 deficiency); macrocytic anemia; glossitis (beefy red tongue); peripheral neuropathy (paresthesias, ataxia); cognitive impairment; depression; subacute combined degeneration of spinal cord; dyspepsia; early satiety | Gastric body and fundus (oxyntic mucosa — parietal cells); antrum relatively spared; stomach wall atrophy; enterochromaffin-like (ECL) cell hyperplasia | Anti-parietal cell antibodies (sensitivity 90%, specificity 50%); anti-intrinsic factor antibodies (sensitivity 50%, specificity >95%); vitamin B12 level (low); methylmalonic acid and homocysteine (elevated); serum gastrin (markedly elevated >500 pg/mL); pepsinogen I (low), pepsinogen I/II ratio (low); upper endoscopy with biopsies from body and antrum; Schilling test (historical); chromogranin A elevated | Lifelong vitamin B12 replacement (IM cyanocobalamin 1000mcg weekly x4 then monthly; or high-dose oral B12 1000-2000mcg daily if absorption adequate); iron supplementation if concurrent iron deficiency; endoscopic surveillance for gastric neuroendocrine tumors (Type 1 carcinoids) every 3-5 years; endoscopic resection of carcinoids >1cm; monitor for gastric adenocarcinoma (2-3x increased risk); treat associated autoimmune conditions | Good with B12 replacement; neurological damage may be partially irreversible if diagnosed late; Type 1 carcinoids usually benign and manageable endoscopically; 2-3x increased risk of gastric adenocarcinoma requires surveillance; normal lifespan with treatment; quality of life good with adequate replacement | D51.0 |
| 21 | 19 | Duodenal Ulcer (NSAID-Induced) | Gastric & Duodenal Diseases | NSAID inhibition of cyclooxygenase-1 (COX-1) reducing prostaglandin synthesis; impaired mucosal defense (reduced mucus, bicarbonate, and blood flow); topical mucosal injury from acidic NSAID formulations; risk factors: age >60, prior PUD, concomitant corticosteroids, anticoagulants, H. pylori co-infection, high-dose or multiple NSAIDs | NSAID users: 15-30% develop peptic ulcers (gastric > duodenal); ~1-4% per year develop complicated ulcers (bleeding, perforation); >100,000 hospitalizations/year in US for NSAID-related GI complications; 16,500 deaths/year in US attributed to NSAID GI toxicity | Risk increases with age; most common in elderly (>60 years); female-to-male ratio 1.5:1; higher in patients on chronic NSAID therapy; rheumatoid arthritis patients at particular risk | May be asymptomatic until complications (silent ulcers in 50-60% of NSAID users); epigastric pain; dyspepsia; nausea; GI bleeding (hematemesis, melena) as presenting symptom in many; perforation; iron deficiency anemia from chronic occult blood loss | Duodenum (bulb); gastric antrum and body (gastric ulcers more common with NSAIDs than duodenal); multiple ulcers common | Upper endoscopy with biopsy (exclude malignancy for gastric ulcers); H. pylori testing; CBC; iron studies; fecal occult blood testing; medication history review is essential | Discontinue NSAID if possible (switch to acetaminophen or topical NSAID); PPI therapy (omeprazole 20mg or equivalent daily for 4-8 weeks); if NSAID must continue: add PPI prophylaxis or switch to COX-2 selective inhibitor (celecoxib) with PPI; H. pylori eradication if co-infected; misoprostol 200mcg QID (less tolerated due to diarrhea); endoscopic hemostasis for bleeding; surgery for perforation or refractory bleeding | Good with NSAID discontinuation and PPI; healing rate >85% at 8 weeks; if NSAID continued with PPI: 80% healing; recurrence high without ongoing prophylaxis if NSAIDs resumed; bleeding ulcer mortality 5-10%; primary prevention with PPI in high-risk NSAID users reduces ulcer risk by 80% | K26.9 |
| 22 | 20 | Functional Dyspepsia | Gastric & Duodenal Diseases | Rome IV criteria: bothersome postprandial fullness, early satiety, epigastric pain/burning without organic cause; two subtypes: postprandial distress syndrome (PDS) and epigastric pain syndrome (EPS); pathophysiology: impaired gastric accommodation, visceral hypersensitivity, delayed gastric emptying (25-35%), duodenal eosinophilia, altered microbiome, psychosocial factors | Very common; prevalence 10-20% of general population; one of most common GI complaints; ~5-7% uninvestigated dyspepsia worldwide; female-to-male ratio 1.5:1; overlaps with IBS in 30-50% | 20-50 years; peak in young to middle-aged adults; may occur at any age; more common in females; associated with anxiety and depression | Postprandial fullness (most common); early satiation; epigastric pain or burning; nausea; bloating; belching; symptoms present >=3 days/week for >=6 months; no alarm features (weight loss, anemia, dysphagia); symptom overlap with GERD and IBS common | Stomach (fundus — impaired accommodation; antrum — delayed emptying); duodenum (eosinophilic infiltration, increased permeability); brain-gut axis | Diagnosis of exclusion (Rome IV criteria); upper endoscopy (normal or H. pylori gastritis — test and treat strategy for age <60 without alarm features); H. pylori testing; CBC; basic metabolic panel; consider gastric emptying study; consider celiac serology; exclude GERD, medications, and biliary disease | H. pylori test and treat; PPI trial 4-8 weeks (NNT 10 for EPS); prokinetics (metoclopramide, domperidone, itopride — for PDS, NNT 7); tricyclic antidepressants low-dose (amitriptyline 10-25mg nightly, NNT 6); mirtazapine 15mg for weight loss/nausea; buspirone 10mg TID for impaired accommodation; psychological therapies (CBT, hypnotherapy); acotiamide (approved in Japan for PDS); dietary modifications (low-fat, small meals) | Chronic relapsing condition; not associated with increased mortality; ~50% have persistent symptoms at 5 years; quality of life significantly impaired; spontaneous resolution in 30-40% over time; normal lifespan; responds to multimodal treatment approach | K30 |
| 23 | 21 | Gastric Cancer (Adenocarcinoma) | Gastric & Duodenal Diseases | H. pylori chronic infection (strongest risk factor, OR 5.9); intestinal type: atrophic gastritis → intestinal metaplasia → dysplasia → carcinoma (Correa cascade); diffuse type: CDH1 germline mutation (hereditary diffuse gastric cancer); dietary factors (salt, nitrosamines, smoked foods); smoking; EBV (10%); pernicious anemia; previous gastric surgery; family history; low socioeconomic status | 5th most common cancer globally; ~1.1 million new cases/year (GLOBOCAN 2020); 4th leading cause of cancer death (~769,000 deaths/year); highest incidence in East Asia (Japan, Korea, China), South America; declining globally but still major in developing nations; intestinal type more common in high-risk areas | Peak incidence 60-80 years; rare before 40 except hereditary diffuse (CDH1 carriers); male-to-female ratio 2:1; decreasing incidence in younger generations in most countries | Often asymptomatic in early stages (reason for poor prognosis in West); dyspepsia; epigastric pain; unintentional weight loss; anorexia; nausea/vomiting; dysphagia (proximal tumors); early satiety; GI bleeding; iron deficiency anemia; Virchow's node (left supraclavicular); Sister Mary Joseph nodule; Blumer shelf (rectal exam); Krukenberg tumor (ovarian metastasis); ascites | Gastric body and antrum (most common); cardia/GEJ (increasing in West); lesser curvature; linitis plastica (diffuse type infiltrating entire stomach); regional lymph nodes; peritoneum; liver; lungs | Upper endoscopy with multiple biopsies (minimum 7 biopsies from suspicious lesion); staging CT chest/abdomen/pelvis; EUS for T and N staging; PET-CT for metastatic workup; staging laparoscopy with peritoneal washings (cytology) for >=T3; HER2 testing; MSI/PD-L1 status; serum tumor markers (CEA, CA 19-9, CA 72-4); screening endoscopy in high-risk countries (Japan, Korea) | Early gastric cancer: endoscopic submucosal dissection (ESD) for selected T1a lesions; surgery: subtotal or total gastrectomy with D2 lymphadenectomy; perioperative chemotherapy: FLOT regimen (5-FU, leucovorin, oxaliplatin, docetaxel) standard in West; adjuvant chemoradiation (MacDonald protocol) or chemotherapy (S-1 in Asia); palliative chemotherapy: fluoropyrimidine + platinum + trastuzumab (if HER2+); immunotherapy: nivolumab + chemo first-line for PD-L1 CPS>=5; pembrolizumab for MSI-H tumors | Poor overall; 5-year survival 32% in US (all stages); 70-90% for early gastric cancer; 30-40% for localized; 5-10% for distant metastases; Japan/Korea: 60-70% 5-year survival due to screening; linitis plastica worst prognosis; MSI-H tumors respond well to immunotherapy; HER2+ responds to targeted therapy | C16.9 |
| 24 | 22 | Gastric Gastrointestinal Stromal Tumor (GIST) | Gastric & Duodenal Diseases | Mesenchymal tumor arising from interstitial cells of Cajal or precursor cells; activating mutations in KIT proto-oncogene (80%) or PDGFRA (5-10%); wild-type GIST (10%); stomach is most common location (60%); malignant potential based on size, mitotic rate, and location | Annual incidence 10-15 per million; ~5,000 new cases/year in US; most common mesenchymal GI tumor; ~20% of small bowel tumors; prevalence higher due to incidental small GISTs; micro-GISTs found in 20-35% of autopsies | Median age 60-65 years; rare before 40; equal male/female ratio; pediatric GIST distinct entity (SDH-deficient); no racial predominance | Often asymptomatic (incidental finding on imaging/endoscopy); GI bleeding (most common presenting symptom — submucosal ulceration); abdominal pain; early satiety; palpable mass; weight loss; fatigue from chronic bleeding; may present with acute hemorrhage or perforation | Stomach (60%); small intestine (30%); colon/rectum (5%); esophagus (<2%); mesentery/omentum (rare); arises from muscularis propria layer | CT abdomen with contrast (well-defined enhancing mass); EUS (submucosal hypoechoic mass arising from muscularis propria, EUS-FNA for tissue); PET-CT (FDG-avid, used for monitoring imatinib response); immunohistochemistry: CD117/KIT positive (95%), DOG1 positive (98%); mutation analysis (KIT exon 11 most common); biopsy via EUS-FNA, not standard endoscopic biopsy (submucosal tumor) | Surgery: complete surgical resection with clear margins (no lymphadenectomy needed); laparoscopic for <=5cm; imatinib 400mg daily neoadjuvant for large/borderline resectable; adjuvant imatinib 3 years for high-risk (>5cm, >5 mitoses/50 HPF); advanced/metastatic: imatinib 400mg daily (800mg for exon 9 mutants); second-line: sunitinib 50mg daily; third-line: regorafenib; fourth-line: ripretinib; avapritinib for PDGFRA D842V mutant | Variable based on risk stratification; very low/low risk: >95% 5-year survival; intermediate risk: 75-85%; high risk: 45-55%; localized resectable: 5-year survival 65%; imatinib transformed metastatic GIST median survival from 12 months to >5 years; KIT exon 11 mutation best imatinib response | C49.A4 |
| 25 | 23 | Gastric Outlet Obstruction | Gastric & Duodenal Diseases | Mechanical or functional blockage of gastric emptying; benign causes: peptic ulcer disease with edema/fibrosis (most common historically), pyloric stenosis, Crohn's disease, caustic ingestion; malignant causes (now most common in West): pancreatic head cancer, distal gastric cancer, ampullary carcinoma, lymphoma; extrinsic compression | Relatively uncommon; 1-5% of peptic ulcer disease complications; malignant causes now account for 50-80% of GOO in developed countries; incidence of benign GOO declining with PPI and H. pylori treatment | Benign: 30-60 years (peptic ulcer); Malignant: 60-80 years; any age for Crohn's or caustic stricture; infantile pyloric stenosis: 2-8 weeks of life (separate entity) | Progressive nausea and vomiting (often non-bilious, large volume, may contain food from hours/days prior); early satiety; postprandial fullness; epigastric pain; weight loss; dehydration; succussion splash on examination; hypochloremic hypokalemic metabolic alkalosis (classic from vomiting HCl) | Pylorus; duodenal bulb; distal stomach; periampullary region; gastric body (if diffuse tumor — linitis plastica) | CT abdomen with contrast (identify cause and level of obstruction); upper endoscopy (diagnostic and allows biopsy for malignancy); barium study (delayed gastric emptying, dilated stomach); metabolic panel (hypokalemia, hypochloremia, metabolic alkalosis); nasogastric tube decompression | Initial: NGT decompression, IV fluids, electrolyte correction; benign (PUD): IV PPI, H. pylori eradication, endoscopic balloon dilation (12-15mm, repeat sessions); malignant: endoscopic stenting (SEMS — self-expanding metallic stent) for palliation; surgical gastrojejunostomy; pyloplasty or pyloroplasty for benign refractory; highly selective vagotomy with drainage for PUD-related | Variable; benign GOO from PUD: good with PPI and dilation (80-90% respond); malignant GOO: poor prognosis reflecting advanced cancer (median survival 3-6 months); endoscopic stenting provides effective palliation; surgical bypass for better longer-term palliation if life expectancy >2 months | K31.1 |
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