Gastroenterology

01 The GI System — Anatomy Essentials

Gastroenterology covers the entire alimentary canal from the upper esophageal sphincter to the anus, plus the accessory digestive organs (liver, gallbladder, biliary tree, and pancreas). A gastroenterologist's clinical domain spans luminal disease (reflux, ulcers, IBD, tumors, bleeding), hepatology (viral hepatitis, cirrhosis, HCC), pancreatobiliary disease (pancreatitis, stones, strictures, cancer), and a heavy procedural workload centered on endoscopy. A scribe has to understand this anatomy because the attending will routinely dictate findings like "pan-ulcerative colitis to the hepatic flexure," "LA grade C esophagitis at the GE junction," or "2 cm sessile polyp in the sigmoid" — and you are expected to chart each of those accurately.

The Upper GI Tract

The esophagus is a 25 cm muscular tube running from the pharynx, behind the trachea and heart, through the diaphragmatic hiatus, and into the stomach at the gastroesophageal (GE) junction, typically 38–40 cm from the incisors. The upper third is skeletal muscle, the middle third mixed, and the lower third smooth muscle. Two functional sphincters matter: the upper esophageal sphincter (UES), which is the cricopharyngeus muscle, and the lower esophageal sphincter (LES), a high-pressure zone at the GE junction that prevents reflux. The Z-line is the squamocolumnar junction between pale esophageal squamous mucosa and salmon-colored gastric columnar mucosa — displacement of the Z-line is how Barrett esophagus is recognized endoscopically.

The stomach is divided into the cardia (just below the GE junction), fundus (the dome above the cardia), body (the main central portion with rugal folds), antrum (the distal portion leading to the pylorus), and pylorus (the muscular outlet into the duodenum). The incisura angularis is the notch on the lesser curvature that marks the junction of body and antrum — a common site for ulcers and gastric cancer. Parietal cells (body/fundus) secrete acid and intrinsic factor; chief cells secrete pepsinogen; G cells (antrum) secrete gastrin.

The Small Intestine

The small intestine is roughly 6 meters long and divided into three segments: the duodenum (C-shaped, ~25 cm, retroperitoneal after the first portion, divided into D1 bulb, D2 descending, D3 horizontal, D4 ascending; the ampulla of Vater drains pancreatic and bile ducts into D2), the jejunum (~2.5 m, proximal, tall villi, prominent plicae circulares), and the ileum (~3.5 m, distal, Peyer patches, terminal ileum absorbs B12 and bile salts and is the classic site of Crohn disease). The ligament of Treitz (at the duodenojejunal flexure) is the anatomic boundary that divides "upper" from "lower" GI bleeding.

The Colon, Rectum & Anus

The colon runs from the ileocecal valve through the cecum (with the appendix), ascending colon, hepatic flexure, transverse colon, splenic flexure, descending colon, sigmoid colon, and into the rectum and anal canal. The ileocecal valve, appendiceal orifice, and triradiate fold are the landmarks the endoscopist uses to confirm a complete colonoscopy to the cecum. The rectosigmoid junction lies ~15 cm from the anal verge; the dentate (pectinate) line divides the rectal columnar mucosa from squamous anoderm and is the boundary between internal (above) and external (below) hemorrhoids.

Liver, Biliary Tree & Pancreas

The liver has functional segments I–VIII (Couinaud) based on portal and hepatic venous anatomy. It receives a dual blood supply: ~75% from the portal vein (draining the splanchnic circulation) and ~25% from the hepatic artery. The biliary tree begins as intrahepatic ducts that merge into the right and left hepatic ducts, join as the common hepatic duct, and after the cystic duct joins from the gallbladder, become the common bile duct (CBD), which passes posterior to the duodenum and enters the ampulla of Vater at the major duodenal papilla. The pancreas lies retroperitoneally across L1–L2 with a head (cradled by the duodenum), uncinate process, neck, body, and tail (extending to the splenic hilum). The main pancreatic duct (duct of Wirsung) joins the CBD at the ampulla.

02 Scribe Documentation Framework

GI encounters span clinic new patients, follow-ups, procedure visits, and inpatient consults (GIB, pancreatitis, decompensated cirrhosis). Each has a distinct documentation rhythm, but all use the standard SOAP structure. Your goal as a scribe is to capture the attending's reasoning in real time so the note writes itself by the end of the encounter.

03 GERD & Esophagitis Luminal

Gastroesophageal reflux disease (GERD) is the retrograde movement of gastric contents into the esophagus causing troublesome symptoms or mucosal injury. It is the single most common diagnosis in a GI clinic. The mechanism is failure of the anti-reflux barrier — a hypotensive LES, transient LES relaxations, hiatal hernia, delayed gastric emptying, or increased intra-abdominal pressure (obesity, pregnancy).

Clinical Presentation

Typical symptoms are heartburn (retrosternal burning, often postprandial and worse when supine) and regurgitation. Atypical symptoms include chronic cough, hoarseness, throat clearing, globus, asthma exacerbation, non-cardiac chest pain, and dental erosions. Dysphagia, odynophagia, weight loss, anemia, hematemesis, or melena are alarm features and mandate prompt EGD.

Diagnosis & LA Classification

In patients with typical symptoms and no alarm features, empiric PPI therapy is both diagnostic and therapeutic. Endoscopy is indicated for alarm features, refractory symptoms, or Barrett screening. When esophagitis is seen on EGD, it is graded using the Los Angeles (LA) classification.

Ambulatory pH monitoring (24-hour pH-impedance or Bravo capsule) is reserved for refractory symptoms, atypical presentations, or pre-anti-reflux surgery evaluation. High-resolution esophageal manometry is performed before fundoplication to exclude achalasia.

Management

ACG clinical guidelines on GERD (2022) are the standard reference. First-line therapy is lifestyle modification (weight loss in overweight patients, head-of-bed elevation, avoiding late meals, trigger food avoidance) plus an 8-week course of once-daily PPI taken 30–60 minutes before breakfast. Step-up to BID dosing or step-down to the lowest effective dose is common. Erosive esophagitis (LA C/D) or Barrett esophagus warrants indefinite PPI therapy. Refractory GERD may warrant anti-reflux surgery (Nissen fundoplication, LINX magnetic sphincter augmentation) or endoscopic therapies (TIF, Stretta).

04 Barrett Esophagus & Esophageal Cancer Oncology

Barrett esophagus (BE) is the replacement of normal squamous esophageal epithelium with specialized intestinal metaplasia (columnar epithelium with goblet cells) in response to chronic acid reflux. It is the only known precursor to esophageal adenocarcinoma (EAC). Risk factors include chronic GERD ≥ 5 years, male sex, white race, age > 50, central obesity, smoking, and family history of BE or EAC.

Diagnosis & Surveillance

Diagnosis requires both endoscopic salmon-colored columnar mucosa extending ≥ 1 cm above the GE junction and histologic confirmation of intestinal metaplasia with goblet cells. Extent is described using the Prague C & M criteria (C = circumferential length, M = maximal length). Dysplasia is graded as: no dysplasia, indefinite for dysplasia, low-grade dysplasia (LGD), or high-grade dysplasia (HGD).

ACG Barrett esophagus guidelines (2022) recommend surveillance EGD every 3–5 years for non-dysplastic BE, every 6–12 months for LGD (or endoscopic eradication), and endoscopic eradication therapy for HGD or intramucosal cancer using radiofrequency ablation (RFA), endoscopic mucosal resection (EMR), or endoscopic submucosal dissection (ESD).

Esophageal Cancer

Two histologies dominate: adenocarcinoma (distal esophagus/GE junction, arises from Barrett, rising incidence in the West, linked to GERD/obesity) and squamous cell carcinoma (mid-esophagus, linked to smoking, alcohol, hot beverages, achalasia, tylosis; higher incidence globally). Presentation is classic: progressive solid-food dysphagia with weight loss, often late in disease. Diagnosis is by EGD with biopsy; staging uses CT chest/abdomen, PET-CT, and endoscopic ultrasound (EUS) for T and N staging. Management depends on stage: endoscopic resection for T1a, esophagectomy for localized disease, and chemoradiation +/- surgery for locally advanced disease.

05 Eosinophilic Esophagitis & Motility Disorders Luminal

Eosinophilic Esophagitis (EoE)

EoE is a chronic immune/antigen-mediated disease characterized by symptoms of esophageal dysfunction and histologic evidence of eosinophil-predominant inflammation (≥ 15 eosinophils per high-power field on biopsy). It is increasingly common, classically in young males with atopy (asthma, allergic rhinitis, food allergies, eczema). Presentation: solid-food dysphagia, food impaction, chest pain, and heartburn unresponsive to PPI. Endoscopy shows rings ("feline esophagus" or trachealization), linear furrows, white exudates, edema, and strictures — captured in the EREFS score. Diagnosis requires multiple biopsies from proximal and distal esophagus. Treatment: PPI, swallowed topical steroids (budesonide or fluticasone), dietary elimination (6-food, 4-food, or targeted), dupilumab (IL-4Rα mAb, FDA-approved for EoE), and dilation for strictures.

Achalasia

Achalasia is a primary motility disorder characterized by failure of LES relaxation and absent esophageal peristalsis due to loss of inhibitory neurons in the myenteric plexus. Presentation: progressive dysphagia to both solids and liquids, regurgitation of undigested food, weight loss, and nocturnal cough. Barium swallow shows the classic "bird's beak" tapering at the GE junction. High-resolution manometry is the gold standard and subtypes achalasia using the Chicago Classification (Type I = classic, Type II = with panesophageal pressurization, best prognosis, Type III = spastic). Treatment options include pneumatic dilation, peroral endoscopic myotomy (POEM), surgical Heller myotomy with partial fundoplication, or botulinum toxin injection for poor surgical candidates.

Other Motility Disorders

Distal esophageal spasm, jackhammer esophagus, ineffective esophageal motility, gastroparesis (documented with gastric emptying scintigraphy — > 10% retention at 4 hours is diagnostic), and functional dysphagia round out the motility differential. Gastroparesis is classically seen in long-standing diabetes and presents with early satiety, postprandial fullness, nausea, vomiting of undigested food, and bloating.

06 Peptic Ulcer Disease, H. pylori & Gastritis Luminal

Peptic ulcer disease (PUD) encompasses gastric and duodenal ulcers — mucosal defects extending through the muscularis mucosae. The two dominant causes are Helicobacter pylori infection and NSAID use. Other causes include Zollinger-Ellison syndrome, stress ulcers (in the critically ill), corticosteroids (synergistic with NSAIDs), smoking, and alcohol.

Clinical Presentation

Classic but inconsistent patterns: duodenal ulcers produce epigastric burning that is relieved by food and recurs 2–3 hours postprandial or at night; gastric ulcers produce pain that is worsened by food. Many ulcers are silent until they bleed or perforate. Complications include GI bleeding (most common), perforation (acute severe pain, peritonitis, free air on imaging), penetration (into the pancreas, causing pancreatitis-like pain), and gastric outlet obstruction from pyloric channel scarring.

H. pylori

H. pylori is a gram-negative spiral bacterium that colonizes the gastric mucosa, causing chronic gastritis, PUD, MALT lymphoma, and gastric adenocarcinoma. Testing options include stool antigen (sensitive, specific, cheap, confirms eradication), urea breath test (similar accuracy, requires fasting and PPI hold), serology (cannot distinguish active from prior infection, rarely used now), and histology with rapid urease (CLO) test on EGD biopsies. PPI must be stopped 2 weeks before non-serology testing to avoid false negatives.

ACG H. pylori treatment guidelines (2024) now favor bismuth quadruple therapy (PPI + bismuth + tetracycline + metronidazole x 14 days) as first-line in most regions because of rising clarithromycin resistance. Clarithromycin-based triple therapy (PPI + clarithromycin + amoxicillin) is acceptable only where local resistance is < 15%. Vonoprazan-based dual or triple therapy is an FDA-approved alternative. Eradication must be confirmed with stool antigen or urea breath test ≥ 4 weeks after completing therapy and after holding PPI for 2 weeks.

Gastritis

Gastritis is histologic inflammation of the gastric mucosa. Patterns include H. pylori gastritis (most common), autoimmune atrophic gastritis (body-predominant, anti-parietal cell antibodies, pernicious anemia, increased risk of type 1 gastric NETs and cancer), reactive/chemical gastropathy (NSAIDs, bile reflux), and stress gastritis (ICU patients). Erosive gastritis differs from ulcer by depth — erosions do not penetrate the muscularis mucosae.

07 Gastric Cancer & Gastric Neoplasms Oncology

Gastric adenocarcinoma accounts for ~95% of gastric cancers. Two histologic types: intestinal type (well-differentiated, glandular, linked to H. pylori chronic atrophic gastritis, follows Correa cascade: normal → atrophic gastritis → intestinal metaplasia → dysplasia → carcinoma) and diffuse type (poorly differentiated, signet-ring cells, younger patients, linked to CDH1 mutations, includes the infiltrative linitis plastica presentation). Risk factors: H. pylori, smoking, diet high in salted/smoked foods, pernicious anemia, family history, blood type A. Symptoms are vague (dyspepsia, early satiety, weight loss) until advanced. Diagnosis is by EGD with biopsy; staging uses CT, EUS, and diagnostic laparoscopy. Other gastric neoplasms include MALT lymphoma (often H. pylori-driven, may regress with eradication), GIST (gastrointestinal stromal tumor, c-KIT/CD117 positive, treated with imatinib), and neuroendocrine tumors (NETs).

08 Functional GI: IBS, Functional Dyspepsia, Constipation Functional

Functional GI disorders are now called disorders of gut-brain interaction (DGBIs). They are defined by the Rome IV criteria and diagnosed on symptoms after exclusion of organic disease. They are real, common, and often debilitating — the "functional" label does not mean the symptoms are imagined.

Irritable Bowel Syndrome (IBS)

ACG IBS monograph (2021) is the standard citation. Rome IV criteria for IBS: recurrent abdominal pain on average ≥ 1 day/week in the last 3 months, with symptom onset ≥ 6 months earlier, associated with ≥ 2 of the following: related to defecation, associated with change in stool frequency, associated with change in stool form.

Red flags that mandate workup beyond IBS include age > 50 at onset, weight loss, nocturnal symptoms, rectal bleeding, anemia, family history of colon cancer or IBD, and short symptom duration. Basic workup includes CBC, CRP, celiac serology (tTG-IgA), and in IBS-D a fecal calprotectin to exclude IBD.

Functional Dyspepsia

Defined by bothersome postprandial fullness, early satiety, epigastric pain, or epigastric burning, for ≥ 3 months with onset ≥ 6 months earlier, in the absence of structural disease that would explain the symptoms. Subtypes: postprandial distress syndrome (PDS) and epigastric pain syndrome (EPS). Management: H. pylori test and treat, PPI trial, TCAs, prokinetics, and psychological therapies.

Chronic Constipation

Types: normal-transit (most common), slow-transit, outlet dysfunction (dyssynergic defecation), and IBS-C. Workup: history, DRE (for outlet dysfunction — paradoxical contraction, anismus), thyroid, calcium, colonoscopy if alarm features, anorectal manometry and balloon expulsion for suspected outlet dysfunction, colonic transit study (Sitzmark) for slow-transit. Treatment ladder: fiber → osmotic laxatives (PEG) → stimulant laxatives → secretagogues (linaclotide, plecanatide, lubiprostone) → prokinetics (prucalopride) → biofeedback for dyssynergia.

09 Inflammatory Bowel Disease (UC & Crohn) Inflammatory

Inflammatory bowel disease (IBD) encompasses ulcerative colitis (UC) and Crohn disease (CD). Both are chronic relapsing immune-mediated conditions with bimodal age distribution (peak 15–35, second peak 50–70), increased risk with family history, smoking (protective in UC, worsens CD), and NSAID use. ACG UC guideline (2019) and ACG Crohn disease guideline (2018) are the core management references.

Ulcerative Colitis

UC involves continuous inflammation limited to the colonic mucosa, beginning in the rectum and extending proximally in a contiguous pattern. Extent is classified by the Montreal classification: E1 proctitis, E2 left-sided (up to splenic flexure), E3 extensive (beyond splenic flexure, including pancolitis). Presentation: bloody diarrhea, urgency, tenesmus, abdominal cramping, and in severe cases fever, tachycardia, anemia, weight loss. Labs: elevated CRP, ESR, fecal calprotectin; anemia; hypoalbuminemia. Colonoscopy shows continuous, circumferential erythema, loss of vascular pattern, friability, erosions, ulcerations.

Crohn Disease

CD can involve any part of the GI tract from mouth to anus, classically the terminal ileum. Inflammation is transmural, discontinuous (skip lesions), and often includes granulomas histologically. Montreal classification for CD captures age at diagnosis (A), location (L1 ileal, L2 colonic, L3 ileocolonic, L4 upper GI, +/- perianal), and behavior (B1 non-stricturing non-penetrating, B2 stricturing, B3 penetrating/fistulizing). Presentation: abdominal pain (often RLQ), chronic diarrhea (may or may not be bloody), weight loss, fatigue, fevers, perianal disease (fistulas, abscesses, fissures), extraintestinal manifestations (peripheral arthritis, sacroiliitis, ankylosing spondylitis, erythema nodosum, pyoderma gangrenosum, uveitis, episcleritis, primary sclerosing cholangitis).

Severity Scoring

Management Overview

Therapy is now stratified by severity and disease phenotype, with an emphasis on early effective therapy and treat-to-target strategies (clinical remission, biochemical normalization, endoscopic healing). Classes used:

Surveillance colonoscopy for dysplasia begins 8 years after diagnosis of UC or Crohn colitis, with chromoendoscopy or high-definition white-light and targeted biopsies. Acute severe UC (Truelove-Witts criteria: ≥ 6 bloody stools/day plus any of HR > 90, temp > 37.8, Hb < 10.5, ESR > 30) is a medical emergency requiring hospitalization, IV corticosteroids, VTE prophylaxis, and early surgical consultation.

10 Celiac Disease & Microscopic Colitis Inflammatory

Celiac Disease

Celiac disease is an autoimmune enteropathy triggered by gluten (wheat, barley, rye) in genetically susceptible individuals (HLA-DQ2 or HLA-DQ8). It produces villous atrophy in the small intestine, malabsorption, and a wide spectrum of intestinal and extraintestinal manifestations. Classic presentation is chronic diarrhea, steatorrhea, weight loss, bloating, and iron-deficiency anemia, but many patients present atypically with only anemia, osteoporosis, transaminitis, infertility, dermatitis herpetiformis, or neurologic symptoms.

Diagnosis requires serology and confirmatory biopsy while on a gluten-containing diet. First-line serology is tTG-IgA (tissue transglutaminase IgA) with total IgA level (to exclude selective IgA deficiency, which is 10x more common in celiac patients). Confirmatory EGD with 4–6 duodenal biopsies (including bulb) shows intraepithelial lymphocytosis, crypt hyperplasia, and villous atrophy (graded by the Marsh classification, 0–3c). Treatment is a strict lifelong gluten-free diet; follow-up includes tTG trend, DEXA, and iron/B12/folate/vitamin D monitoring.

Microscopic Colitis

Microscopic colitis (collagenous and lymphocytic subtypes) presents with chronic watery non-bloody diarrhea, often in middle-aged to older women. Colonoscopy is macroscopically normal; diagnosis is made on random biopsies showing either a thickened subepithelial collagen band (collagenous) or increased intraepithelial lymphocytes (lymphocytic). Associations include NSAIDs, PPIs, SSRIs, celiac disease, and autoimmune disease. Treatment: stop offending medications and use budesonide 9 mg daily as first-line.

11 Diverticular Disease & Diverticulitis Luminal

Diverticulosis is the presence of diverticula (outpouchings of mucosa and submucosa through the muscularis propria at sites of vasa recta penetration), overwhelmingly in the sigmoid colon in Western populations. It is common (> 50% of adults over 60) and usually asymptomatic, but complications include diverticular bleeding (painless hematochezia, most common cause of lower GI bleeding in older adults) and diverticulitis.

Acute diverticulitis is inflammation/micro-perforation of a diverticulum producing LLQ pain, fever, leukocytosis, and sometimes a palpable mass. CT with IV/PO contrast is the imaging of choice and classifies severity using the Hinchey classification:

Outpatient management of uncomplicated disease is appropriate for reliable patients without high-risk features; recent guidelines support selective rather than routine antibiotic use in uncomplicated diverticulitis. Colonoscopy is recommended 6–8 weeks after resolution of a first episode if the patient has not had a recent high-quality colonoscopy, to exclude underlying malignancy.

12 Colorectal Cancer, Polyps & Screening Oncology

Colorectal cancer (CRC) is the third most common cancer and second leading cause of cancer death in the US. Most CRC arises from adenomatous polyps via the adenoma-carcinoma sequence (APC → KRAS → DCC → p53) or from sessile serrated lesions via the serrated pathway. Risk factors: age, family history (first-degree relative < 60), hereditary syndromes (Lynch, FAP, MUTYH), IBD, obesity, smoking, red/processed meat, alcohol.

Screening

USPSTF colorectal cancer screening (2021) now recommends starting screening at age 45 for average-risk adults and continuing through age 75; ages 76–85 are individualized. ACG CRC screening guidelines (2021) align with the 45 start age. Options include:

Polyps

Polyp types and significance: tubular adenoma (most common, premalignant, risk increases with size > 10 mm, villous architecture, high-grade dysplasia), tubulovillous and villous adenomas (higher malignant potential), sessile serrated lesion (SSL) (right-sided, flat, easily missed, premalignant via serrated pathway), traditional serrated adenoma, hyperplastic (usually benign, distal), and hamartomatous (juvenile, Peutz-Jeghers).

Post-polypectomy surveillance intervals follow USMSTF 2020 recommendations: 10 years for 1–2 small (< 10 mm) tubular adenomas, 7–10 years for 3–4 small adenomas, 3–5 years for 5–10 adenomas, 3 years for advanced adenomas (≥ 10 mm, high-grade dysplasia, villous), and 1 year for > 10 adenomas or piecemeal resection of a large lesion.

Hereditary CRC Syndromes

Lynch syndrome (HNPCC) — mismatch repair gene mutations (MLH1, MSH2, MSH6, PMS2, EPCAM), associated with early-onset CRC, endometrial, ovarian, urothelial, and small bowel cancer. Familial adenomatous polyposis (FAP) — APC mutation, hundreds to thousands of adenomas, 100% CRC by age 40 without colectomy. MUTYH-associated polyposis — autosomal recessive, attenuated polyposis. Peutz-Jeghers, juvenile polyposis, and Cowden are hamartomatous polyposis syndromes.

13 Hemorrhoids & Anorectal Disease Luminal

Hemorrhoids are dilated submucosal vascular cushions in the anal canal. Internal hemorrhoids arise above the dentate line, are covered by columnar/transitional epithelium, are usually painless, and present with bright red blood per rectum (BRBPR) on the tissue or coating the stool and with prolapse. They are graded:

External hemorrhoids arise below the dentate line, are covered by anoderm (squamous, innervated), and are painful when thrombosed. Other anorectal diagnoses: anal fissure (painful tear, often posterior midline, from hard stool; treatment is fiber, sitz baths, topical nifedipine or nitroglycerin, botulinum toxin, lateral internal sphincterotomy for refractory cases), perianal abscess/fistula (often requiring I&D; Crohn-related fistulas managed with biologics and seton placement), and pruritus ani.

14 GI Bleeding (UGIB & LGIB) Emergency

Upper GI bleeding (UGIB) is bleeding from a source proximal to the ligament of Treitz; lower GI bleeding (LGIB) is from distal. Presentation varies: hematemesis and coffee-ground emesis are UGIB; melena (black tarry stool from digested blood) is usually UGIB but can occur with right colon bleeding; hematochezia (bright red blood) is usually LGIB but massive UGIB can present with hematochezia and hemodynamic instability.

UGIB Causes & Management

Most common causes: peptic ulcer disease (most common), esophageal/gastric varices, Mallory-Weiss tear, erosive esophagitis/gastritis, Dieulafoy lesion, angiodysplasia, malignancy. Initial management is resuscitation first: two large-bore IVs, type and cross, restrictive transfusion (Hb target 7 g/dL in most, 8 in cardiac patients), IV PPI (pantoprazole 80 mg bolus then 8 mg/hr or intermittent BID), correct coagulopathy, IV octreotide and ceftriaxone if variceal bleeding suspected (cirrhotic patient), and EGD within 24 hours for most stable patients, sooner for hemodynamic instability.

Variceal bleeding in cirrhosis carries a mortality up to 20% per episode. Endoscopic management is band ligation for esophageal varices and cyanoacrylate glue injection for gastric varices. Rescue therapies for uncontrollable bleeding include balloon tamponade (Sengstaken-Blakemore, Minnesota tube), self-expanding esophageal stents, and transjugular intrahepatic portosystemic shunt (TIPS). Secondary prophylaxis after a variceal bleed is non-selective beta-blocker (nadolol, propranolol, or carvedilol) plus serial band ligation.

LGIB Causes & Management

Most common causes: diverticular bleeding (most common, painless, often self-limited), angiodysplasia, ischemic colitis, hemorrhoids, neoplasia, post-polypectomy bleeding, IBD, radiation proctitis. Initial workup: resuscitate, rule out UGIB (NG lavage or upper endoscopy if brisk), then colonoscopy after rapid bowel prep. CT angiography is increasingly used for brisk bleeding to localize before intervention, and interventional radiology embolization is an option for unstable patients. Tagged RBC scan can detect slow bleeding but localization is imprecise.

15 Acute & Chronic Pancreatitis Panc/Bil/Hep

Acute Pancreatitis

Acute pancreatitis diagnosis requires 2 of 3: (1) characteristic abdominal pain (epigastric, radiating to the back, constant), (2) lipase or amylase > 3x upper limit of normal, (3) characteristic findings on imaging. Most common etiologies: gallstones and alcohol (together ~80%). Other causes: hypertriglyceridemia (> 1000 mg/dL), hypercalcemia, post-ERCP, medications (azathioprine, thiazides, valproate, GLP-1 agonists rarely), autoimmune, trauma, viral (mumps, coxsackie), genetic (PRSS1, CFTR, SPINK1), and idiopathic. The mnemonic I GET SMASHED captures most etiologies.

AGA acute pancreatitis guidelines emphasize early aggressive (but not excessive) fluid resuscitation with lactated Ringer's, early enteral nutrition within 24–72 hours when tolerated, avoidance of prophylactic antibiotics in sterile necrosis, and urgent ERCP only for concurrent cholangitis or persistent biliary obstruction. Same-admission cholecystectomy is recommended for mild gallstone pancreatitis.

Other severity tools include BISAP (Bedside Index for Severity in Acute Pancreatitis, 0–5 based on BUN, altered mental status, SIRS, age, pleural effusion) and APACHE II. Complications: peripancreatic fluid collection, pseudocyst, acute necrotic collection, walled-off necrosis (WON > 4 weeks), infected necrosis (requires step-up drainage), pancreatic ascites, splenic vein thrombosis, and disconnected pancreatic duct syndrome.

Chronic Pancreatitis

Chronic pancreatitis is irreversible fibrosis of the pancreas causing chronic abdominal pain, exocrine insufficiency (steatorrhea, fat-soluble vitamin deficiency), and endocrine insufficiency (diabetes, "type 3c"). Alcohol is the most common cause in adults; other causes include smoking, genetic (PRSS1 hereditary pancreatitis, CFTR), autoimmune (IgG4-related), obstructive, and idiopathic. Imaging shows calcifications, ductal dilation with strictures and stones (chain-of-lakes). Management: alcohol cessation and smoking cessation (critical), pancreatic enzyme replacement therapy (PERT) for steatorrhea, fat-soluble vitamins, pain management (avoiding chronic opioids), celiac plexus block, ERCP for stones/strictures, and surgery (Frey, Puestow, Whipple) in selected patients.

16 Pancreatic Cancer & Biliary Disease Panc/Bil/Hep

Pancreatic Adenocarcinoma

Pancreatic ductal adenocarcinoma (PDAC) is the most lethal common cancer in the US. Risk factors: smoking, family history, hereditary syndromes (BRCA1/2, Lynch, PRSS1, Peutz-Jeghers), chronic pancreatitis, long-standing diabetes, obesity. Presentation depends on location: head tumors — painless obstructive jaundice, weight loss, steatorrhea, and pruritus (Courvoisier sign: palpable, non-tender gallbladder with painless jaundice); body/tail tumors — vague abdominal/back pain and late presentation. Diagnosis by contrast-enhanced pancreatic protocol CT and EUS with FNA biopsy. CA 19-9 is used as a tumor marker (not for screening; can be falsely elevated by cholestasis). Management: Whipple (pancreaticoduodenectomy) for resectable head tumors, distal pancreatectomy for body/tail, neoadjuvant chemotherapy (FOLFIRINOX or gemcitabine/nab-paclitaxel) for borderline resectable/locally advanced, palliative chemotherapy for metastatic.

Pancreatic Cystic Lesions

Common cystic lesions include IPMN (intraductal papillary mucinous neoplasm, main duct or branch duct, premalignant), MCN (mucinous cystic neoplasm, women, body/tail, premalignant), SCA (serous cystadenoma, benign microcystic), and pseudocysts. The Fukuoka guidelines stratify IPMN risk using "worrisome features" and "high-risk stigmata" to decide between surveillance and resection.

Gallstones & Biliary Disease

Cholelithiasis is common and usually asymptomatic. Symptomatic disease includes:

17 NAFLD/MASLD & Viral Hepatitis Panc/Bil/Hep

MASLD (formerly NAFLD)

The field renamed NAFLD to MASLD (metabolic dysfunction-associated steatotic liver disease) in 2023, with MASH replacing NASH. MASLD is defined as hepatic steatosis plus at least one cardiometabolic risk factor (overweight/obesity, T2DM, dyslipidemia, hypertension) in the absence of other causes. It is the most common liver disease in the world. Workup: rule out other causes (hepatitis serologies, iron studies, ceruloplasmin, AMA, ANA), assess fibrosis non-invasively with FIB-4, NFS, vibration-controlled transient elastography (FibroScan), or MR elastography. Biopsy is reserved for uncertain cases. Management: weight loss (≥ 7–10% of body weight improves steatosis and inflammation), GLP-1 agonists, treatment of comorbidities, and the first FDA-approved MASH drug resmetirom (Rezdiffra), a selective thyroid hormone receptor-β agonist approved in 2024.

Viral Hepatitis

Hepatitis B Serology

AASLD HBV guidance informs when to treat chronic HBV (HBeAg status, ALT, HBV DNA, fibrosis, age). AASLD/IDSA HCV guidance is the continually updated source for pan-genotypic DAA regimens; nearly all HCV is now curable (> 95% SVR) with 8–12 weeks of oral therapy.

18 Autoimmune Liver Disease (AIH, PBC, PSC) Panc/Bil/Hep

Autoimmune Hepatitis (AIH)

AIH is an immune-mediated hepatitis classically in women, presenting with fatigue, jaundice, or asymptomatic transaminitis. Labs: elevated ALT/AST (hepatocellular pattern), hypergammaglobulinemia (IgG), positive ANA, anti-smooth muscle (SMA) or anti-LKM1. Biopsy shows interface hepatitis, plasma cell infiltrate, rosetting. Treatment: prednisone +/- azathioprine; most patients require long-term maintenance.

Primary Biliary Cholangitis (PBC)

PBC (formerly "primary biliary cirrhosis") is a chronic cholestatic autoimmune disease destroying small intrahepatic bile ducts, classically in middle-aged women with fatigue and pruritus. Labs: elevated ALP and GGT (cholestatic pattern), positive AMA (anti-mitochondrial antibody) in > 95%. Treatment: ursodeoxycholic acid (UDCA, ursodiol) 13–15 mg/kg/day is first-line, with obeticholic acid or fibrates added for inadequate response.

Primary Sclerosing Cholangitis (PSC)

PSC is a chronic cholestatic disease causing multifocal strictures of intra- and extrahepatic bile ducts, classically in young men, strongly associated with IBD (especially UC). MRCP shows "beaded" ducts. No medical therapy slows progression; management is surveillance for cholangiocarcinoma (MRCP + CA 19-9 annually), ERCP for dominant strictures, and liver transplant for end-stage disease. PSC-IBD patients need annual surveillance colonoscopy from the time of PSC diagnosis due to high CRC risk.

19 Cirrhosis, Portal HTN & HCC Panc/Bil/Hep

Cirrhosis is the end-stage of chronic liver injury, characterized by fibrosis and nodular regeneration. Causes: MASLD/MASH, alcohol, chronic HCV, chronic HBV, autoimmune (AIH, PBC, PSC), hemochromatosis, Wilson disease, A1AT deficiency, cryptogenic. Clinically divided into compensated (no complications, often asymptomatic) and decompensated (variceal bleeding, ascites, hepatic encephalopathy, jaundice). AASLD practice guidance on cirrhosis is the core reference.

Child-Pugh Score

MELD Score

MELD (Model for End-Stage Liver Disease) is the objective score used for liver transplant allocation. Current MELD 3.0 (adopted by UNOS in 2023) includes bilirubin, creatinine, INR, sodium, albumin, and sex. Higher scores indicate worse prognosis; MELD ≥ 15 is typically the threshold for transplant listing. Scribes will see MELD trended at every hepatology visit.

Portal Hypertension Complications

Hepatocellular Carcinoma (HCC)

HCC arises in cirrhotic livers and in chronic HBV even without cirrhosis. AASLD HCC guidance recommends screening every 6 months with ultrasound +/- AFP in all cirrhotic patients and high-risk HBV. Diagnosis can be made noninvasively by characteristic imaging features on multiphase CT or MRI using LI-RADS. Staging uses the BCLC (Barcelona Clinic Liver Cancer) system:

20 Endoscopic & GI Procedures Procedures

Endoscopy is the defining procedural activity of gastroenterology. Scribes working in endoscopy suites will pre-populate procedure notes and chart findings, interventions, and specimens. Know each procedure cold.

Pre-Procedure Documentation

Every endoscopy note begins with indication, consent, sedation plan (moderate sedation with fentanyl/midazolam, MAC with propofol, or general anesthesia), Mallampati and ASA class, aspiration risk, and anticoagulation status. ASGE guidelines stratify procedures as low- or high-risk for bleeding to decide on holding antiplatelets and anticoagulants.

Post-Procedure & Complications

Post-procedure recovery includes monitoring vital signs, pain, and sedation recovery (Aldrete score). Findings are reviewed with the patient/family after the patient is alert. Common complications to know: perforation (abdominal pain, tachycardia, subcutaneous emphysema, free air on imaging), bleeding (post-polypectomy bleeding can be immediate or delayed up to 2 weeks), post-ERCP pancreatitis (most common ERCP complication, 3–15% depending on risk; rectal indomethacin and pancreatic duct stenting reduce risk), post-polypectomy syndrome (transmural thermal injury without frank perforation), aspiration pneumonia, and sedation-related events (hypoxia, hypotension).

21 GI Imaging, Labs & Diagnostics Special

Key Labs

Imaging Modalities

22 Medications You Must Know Meds

Acid Suppression & Motility

Antiemetics

IBD Medications

See the IBD management table in Section 09 for the complete class breakdown (5-ASA, corticosteroids, immunomodulators, anti-TNF, anti-integrin, anti-IL-12/23, anti-IL-23, JAK inhibitors, S1P modulators). Pre-biologic screening mandates: TB (IGRA or PPD), HBV (HBsAg, anti-HBc, anti-HBs), varicella, and updated vaccines.

Hepatology Medications

Pancreatic Enzymes & Other

23 Classification Systems — Consolidated Special

24 Physical Exam, Abbreviations & Sample HPIs

The GI & Hepatology Physical Exam

Specific signs to know and document when present: Murphy sign (cessation of inspiration with RUQ palpation — cholecystitis), McBurney point (1/3 from ASIS to umbilicus — appendicitis), Rovsing, Psoas, and Obturator signs (appendicitis/pelvic inflammation), Cullen sign (periumbilical ecchymosis — severe pancreatitis, hemoperitoneum), Grey Turner sign (flank ecchymosis — retroperitoneal hemorrhage, severe pancreatitis), Courvoisier sign (palpable non-tender gallbladder with jaundice — pancreatic head cancer), shifting dullness and fluid wave (ascites), Terry nails and Muehrcke lines (hypoalbuminemia), asterixis (hepatic encephalopathy, uremia), caput medusae, spider angiomas, palmar erythema, gynecomastia, testicular atrophy (chronic liver disease).

Abbreviations Master List

Anatomy

Diagnoses

Procedures & Imaging

Labs & Scores

Sample HPI Templates

25 References & Sources

Clinical Practice Guidelines

Diagram & Figure Sources