Medical GI exam

Serum amylase, lipase, alkaline phosphatase, and bilirubin may be elevated. • Normal amylase and lipase does not exclude the diagnosis even in an acute attack. • Excess fecal fat in stool or pancreatic insufficiency on secretin stimulation. • A secretin stimulation test, if available, has a high negative predictive value for early chronic pancreatitis). • Genetic tests for the major trypsinogen gene mutations. • Elevated IgG4 levels, antinuclear antibody, and antibodies to lactoferrin, carbonic anhydrase II, peptide AIP(1-7), and ubiquitin-protein ligase E3 component n-recognin 2 are often seen in cases of autoimmune pancreatitis.

Colonoscopy: biopsy of intestine reveals granulomas in 25%

Insidious onset of intermittent bouts of low-grade fever, diarrhea, and RLQ pain, tender mass • Radiographic or endoscopic evidence of ulceration, stricturing, or fistulas of the small intestine or colon

Mild-to-moderate disease: mesalamine orally or by rectal suppository; balsalazide or sulfasalazine orally; corticosteroids (delayed-release budesonide orally) • Moderate-to-severe disease with inadequate response to agents listed above: corticosteroid therapy (eg, prednisone orally; methylprednisolone or hydrocortisone intravenously; hydrocortisone enemas), infliximab, adalimumab, golimumab, or vedolizumab • Severe or refractory disease: corticosteroids (methylprednisolone intravenously) or cyclosporine orally, or infliximab intravenously • Toxic megacolon: add broad-spectrum antibiotics to infliximab or cyclosporine

Cramping abdominal pain and tenderness, nonbloody diarrhea, liquid bowel movements • Chronic inflammatory disease: malaise, loss of energy, intermittent diarrhea, cramping or steady RLQ or periumbilical pain, focal RLQ tenderness, mass in lower abdomen • Intestinal obstruction: postprandial bloating, cramping pains, and loud borborygmi • Intra-abdominal or retroperitoneal abscesses: fevers, chills, abdominal mass, leukocytosis • Sinus tracts and fistulas: intra-abdominal or retroperitoneal abscesses, recurrent bladder or vagina infections, cutaneous fistulas • Perianal disease: skin tags, anal fissures, perianal abscesses and fistulas • Extraintestinal manifestations: arthralgias, arthritis, iritis or uveitis, pyoderma gangrenosum, erythema nodosum, oral aphthous lesions, gallstones, nephrolithiasis

Esophagogastroduodenoscopy confirms the presence of varices. • Liver biopsy confirms cirrhosis, HCC.

Ultrasound-guided aspiration, percutaneous cholecystostomy, or an endoscopic stent may postpone or avoid need for surgery in selected patients. • Cholecystectomy is mandatory when there is evidence of gangrene or perforation.

Avoidance of strenuous physical exertion, alcohol, and hepatotoxic agents.

Adenocarcinomas grow slowly and may be asymptomatic. • Right-sided colon cancers cause iron-deficiency anemia, fatigue, and weakness from blood loss. • Left-sided colon cancers cause obstructive symptoms, colicky abdominal pain, changes in bowel habits, constipation alternating with loose stools, and stool streaked with blood. • Rectal cancers cause rectal tenesmus, urgency, and recurrent hematochezia. • Weight loss is uncommon unless disease is metastatic. • Physical examination findings are usually normal except in advanced disease in which a mass may be palpable in the abdomen. • Hepatomegaly suggests metastatic spread.

IV proton pump inhibitor (eg, esomeprazole or pantoprazole) reduces risk of rebleeding in patients with peptic ulcers with high-risk features (active bleeding, visible vessel, or adherent clot) after endoscopic treatment. • High doses of oral proton pump inhibitors are sufficient for lesions at low risk for rebleeding (esophagitis, gastritis, clean-based ulcers, and Mallory-Weiss tears). • Octreotide bolus and continuous drip for bleeding related to portal hypertension. • Terlipressin may be preferred to octreotide in countries where available (not in the United States).

Lower GI bleeding is defined as that arising below the ligament of Treitz (ie, small intestine or colon; ≤95% of cases arise in the colon). • Lower GI bleeding is less common than upper GI bleeding and tends to be more benign. • Spontaneous cessation occurs in >85%; the hospital mortality rate is <4%. • The most common causes in patients younger than age 50 years are infectious colitis, anorectal disease, and inflammatory bowel disease. • The most common causes in patients older than age 50 years are diverticulosis coli (50%), colonic angioectasias, neoplasms, ischemia, varices, and ulcers. • In 20% of cases, no source of bleeding can be identified.

Complete blood count, platelet count, prothrombin time and international normalized ratio (INR). • Serum creatinine and liver enzymes. • Blood typing and screening or cross-matching. • Hematocrit is not a reliable indicator of the severity of acute bleeding.

Signs of chronic liver disease implicate bleeding caused by portal hypertension, but a different lesion is identified in 25% of patients with cirrhosis. • Dyspepsia, NSAID use, or history of previous peptic ulcer suggests peptic ulcer disease. • Heavy alcohol ingestion or retching suggests a Mallory-Weiss tear.

Ulcerative colitis • Irritable bowel syndrome • Appendicitis • Yersinia enterocolitica enteritis • Mesenteric adenitis • Intestinal lymphoma • Segmental colitis caused by ischemic colitis, tuberculosis, amebiasis, Chlamydia • Diverticulitis with abscess • Nonsteroidal anti-inflammatory drug-induced colitis

Sigmoidoscopy establishes the diagnosis. • Colonoscopy should not be performed in patients with fulminant disease because of the risk of perforation but is recommended after improvement.

Hematochezia is usually present, although 10% of hematochezia is caused by an upper GI source. • Stable patients can be evaluated by colonoscopy. • Massive active bleeding calls for evaluation with sigmoidoscopy, upper endoscopy, angiography, or nuclear bleeding scan.

Abrupt onset of deep epigastric pain, often with radiation to the back • Nausea, vomiting, sweating, weakness, fever, abdominal tenderness, and distention • Leukocytosis, elevated serum amylase, elevated serum lipase • History of previous episodes, often related to alcohol intake

Local ablative techniques (cryosurgery, embolization) for unresectable hepatic metastases. • Following surgical resection with total mesorectal excision, adjuvant 5-FU–based therapy (generally with the FOLFOX regimen, extrapolating from its benefit in patients with similarly staged colon cancers) is recommended for a total of approximately 6 months of perioperative therapy including any neoadjuvant chemoradiation.

Nasogastric tube aspiration or upper endoscopy in massive hematochezia to exclude upper GI tract source • Anoscopy • Colonoscopy in patients in whom bleeding has ceased and in patients with moderate active bleeding (often after rapid purge with polyethylene glycol solution) • Small intestine push enteroscopy or video capsule imaging in patients with unexplained recurrent hemorrhage of obscure origin suspected as originating from the small intestine

Barium enema or CT colonography (“virtual colonoscopy”) for initial diagnosis if standard colonoscopy is not available. • Chest, abdominal, and pelvic CT scan for preoperative staging. • Pelvic magnetic resonance imaging and endorectal ultrasonography may guide operative management of rectal cancer.

Regular diet with limited caffeine and gas-producing vegetables; may require NPO (nothing by mouth) status in severe exacerbations

Often self-limited, but prompt evaluation is warranted with fever, WBC >15,000/μL, bloody diarrhea, severe abdominal pain, dehydration, organ failure, immunocompromised or frail older patients, nursing home residents, health care-associated diarrhea, antibiotic exposure, or systemic illness. • Stool cultures, ova and parasites, fecal leukocytes, complete blood count, serum electrolytes, albumin, thyroid-stimulating hormone. • If malabsorption is suspected, obtain serum folate, vitamin B12, iron, vitamin A and D levels, prothrombin time or international normalized ratio. • Stool C difficile toxin assay or PCR testing if recent history of antibiotic exposure or hospitalization. • Rectal swab cultures in sexually active patients with suspected proctitis. • Serologic testing for celiac sprue with IgA tissue transglutaminase or antiendomysial antibody. • 24-hour stool collection and fecal fat may help with chronic diarrhea to elucidate cause.

• Bloody diarrhea, cramps, abdominal pain, fecal urgency and tenesmus. • Tenderness, evidence of peritoneal inflammation, bright red blood on digital rectal examination. • Severity of symptoms depends on severity of disease. • Toxic megacolon can occur with colonic dilatation, signs of toxicity, and risk of perforation. • Extracolonic manifestations occur in 50%: oral ulcers, erythema nodosum, pyoderma gangrenosum, uveitis, spondylitis or sacroiliitis, arthritis, sclerosing cholangitis.

Plain films of the abdomen may show radiopaque gallstones in 15% of cases. • RUQ abdominal ultrasonography may show gallstones but is only 67% sensitive for acute cholecystitis. • 99mTc hepatobiliary imaging (using iminodiacetic acid compounds; HIDA scan) is useful in demonstrating obstructed cystic duct; the test is very sensitive and specific for acute cholecystitis. • CT may show complications of acute cholecystitis, such as gallbladder perforation or gangrene.

Plain abdominal radiographs may show gallstones (if calcified), a “sentinel loop,” or the “colon cutoff sign.” • Ultrasonography may identify gallstones but is otherwise often unhelpful for diagnosis. • CT can differentiate from other catastrophes and assess prognosis and complications. • Endoscopic ultrasonography is useful for occult biliary disease (eg, small stones, sludge)

ERCP is the most sensitive study for chronic pancreatitis.

Crohn disease is a transmural process. • Crohn disease may involve the small bowel only, colon alone, or both; it is most common in the terminal ileum. • It is a chronic illness with exacerbations and remissions. • One-third of patients have associated perianal disease (fistulas, fissures, abscesses). • Fewer than 5% of patients have symptomatic involvement of the upper intestinal tract.

Colonoscopy visualizes the entire colon and permits biopsy of lesions. • Staging by the TNM (tumor, node, metastasis) system determines therapy and estimates the patient’s long-term survival.

Excellent vascular access with (usually) two 18-gauge (or larger) peripheral IV lines. • Volume repletion with IV fluids. • Close monitoring of blood counts and coagulation panel with transfusion support as needed. • Therapeutic colonoscopy: high-risk lesions (eg, diverticulum with active bleeding or a visible vessel, or an angioectasia) can be treated endoscopically with saline or epinephrine injection, cautery (bipolar or heater probe), or application of metallic clips or bands. • Angiography with selective embolization achieves immediate hemostasis in >95% of patients when a bleeding lesion is identified.

The acute attack is often precipitated by a large or fatty meal. • It consists of relatively sudden, severe, steady pain that is localized to the abdominal RUQ or epigastrium and that may gradually subside over a period of 12 to 18 hours. • Vomiting occurs in about 75% of patients and affords variable relief in 50%. • RUQ abdominal tenderness, often with guarding and rebound pain, is seen. • A palpable gallbladder is present in about 15% of cases. • Jaundice is present in 25% of cases and suggests possible choledocholithiasis. • Fever is usually present.

Epigastric pain, steatorrhea, weight loss, abnormal pancreatic imaging

Complete blood cell count, platelet count, prothrombin time and international normalized ratio (INR), type and cross-match for transfusion • Serum creatinine, blood urea nitrogen

Assess volume (hemodynamic) status using blood pressure, heart rate, and postural hypotension. • Upper endoscopy should be done after the patient is hemodynamically stable to identify the source of bleeding, determine risk of rebleeding, guide triage, and render endoscopic therapy. • Consider biopsy of ulcers for H pylori at time of endoscopy.

Risk factors: chronic viral hepatitis, alcoholism, drug toxicity, autoimmune and metabolic liver disease; may have multiple synergistic risk factors. • Celiac disease appears to be associated with an increased risk of cirrhosis. • Three clinical stages: compensated, compensated with varices, and decompensated (ascites, variceal bleeding, encephalopathy, or jaundice). • Patterns include micronodular, macronodular, and mixed cirrhosis. • Micronodular cirrhosis: most common, with regenerating nodules <1 mm, typical of alcoholic liver disease (Laennec cirrhosis). • Macronodular cirrhosis: nodules are several centimeters large; may be posthepatitic or follow episodes of massive necrosis and stromal collapse.

Endoscopic retrograde cholangiopancreatography (ERCP) can be done if there is associated cholangitis.

Obtain CBC to look for anemia of chronic inflammation, blood loss, iron deficiency, or vitamin B12 malabsorption. • Leukocytosis with abscesses. • Elevated erythrocyte sedimentation rate or C-reactive protein. • Send stool for culture (routine pathogens), ova and parasites, leukocytes, fat, and Clostridium difficile toxin assay or PCR testing.

Second leading cause of death from malignancy in the United States. • Usually adenocarcinomas. • About 50% occur within reach of detection by flexible sigmoidoscopy. • Most colorectal cancers arise from malignant transformation of an adenomatous polyp (tubular, tubulovillous, or villous adenoma), serrated polyp (traditional serrated adenoma, or sessile serrated adenoma), or less commonly, hyperplastic polyp. • Up to 5% are caused by polyposis syndromes or hereditary nonpolyposis colorectal cancer. • Risk factors include older age, personal or family history, inflammatory bowel disease (ulcerative colitis and Crohn colitis), high-fat and red meat diets, and race (blacks > whites).

Ultrasonography to assess liver size and consistency, and to detect ascites, nodules, or portal hypertension

Personal or family history of adenomatous polyps or colorectal cancer are important risk factors. • Symptoms or signs depend on tumor location; proximal colon cancer causes fecal occult blood and anemia, distal colon cancer causes change in bowel habits and hematochezia. • Diagnosis established with colonoscopy.

Liver biopsy may be indicated for diagnosis, staging, and predicting response to therapy. • Serum FibroSURE testing or ultrasound elastography may be used to identify the absence of fibrosis or presence of cirrhosis in hepatitis C.

Loperamide, atropine, or tincture of opium for symptomatic diarrhea. • Broad-spectrum antibiotics if bacterial overgrowth or microperforations with exacerbations. • Early introduction of biologic therapy for patients with risk factors for aggressive disease (young age, perianal disease, stricturing disease, or need for corticosteroids). 5-Aminosalicylic acid agents such as mesalamine work for colonic but not small bowel disease; however, current treatment guidelines recommend against use of these agents. Antibiotics (metronidazole, ciprofloxacin, rifaximin). • Ileal-release preparation budesonide. • Corticosteroids (eg, prednisone) are the mainstay for treatment of severe exacerbations. Immunomodulatory drugs: mercaptopurine and azathioprine are more commonly used than methotrexate. Anti-TNF therapies: infliximab, adalimumab, and certolizumab are used to induce and maintain remission in moderate-to-severe Crohn disease as well as to treat extraintestinal manifestations (except optic neuritis). Anti-integrins: vedolizumab is indicated for moderate-to-severe Crohn disease in whom anti-TNF therapy has failed or is not tolerated.

Pancreatic rest program including NPO, bed rest, nasogastric suction. • ERCP with endoscopic sphincterotomy and stone extraction indicated for severe pancreatitis resulting from choledocholithiasis.

Serum amylase and lipase are increased, usually more than three times normal. • Leukocytosis, proteinuria, granular casts, glycosuria, hyperglycemia, and elevated bilirubin are present. • Blood urea nitrogen (BUN) and serum creatinine and alkaline phosphatase may be elevated. • Hypocalcemia correlates with the severity of disease.

Cholecystectomy (generally laparoscopic) should be performed within 24 hours of admission because of the high risk of recurrent attacks (up to 10% by 1 month and over 30% by 1 year). • Compared with delayed surgery, surgery within 24 hours is associated with a reduced risk of major bile duct injury and death. • Surgical treatment of chronic cholecystitis is the same as for acute cholecystitis.

Hemoptysis. • Peptic ulcer disease. • Esophageal or gastric varices. • Erosive gastritis (eg, NSAIDs, alcohol, stress). • Mallory-Weiss syndrome. • Portal hypertensive gastropathy. • Angioectasias (angiodysplasias), such as idiopathic arteriovenous malformation, CREST (calcinosis, Raynaud syndrome, esophageal dysmotility, sclerodactyly, and telangiectasia) syndrome, hereditary hemorrhagic telangiectasias. • Gastric cancer. • Rare causes include erosive esophagitis, duodenal varices, aortoenteric fistula, Dieulafoy lesion (aberrant gastric submucosal artery), hemobilia (from hepatic tumor, angioma, penetrating trauma, pancreatic cancer, and hemosuccus pancreaticus [pancreatic pseudoaneurysm]).

Total proctocolectomy with ileostomy required in 25% of patients • Indications for surgery include severe refractory disease, unresponsive toxic megacolon or perforation, or neoplasia Therapeutic Procedures

For mild pancreatitis with cholelithiasis, cholecystectomy or cholecystotomy. • Debridement of infected pancreatic necrosis. • Biliary sphincterotomy for recurrent acute pancreatitis attributable to sphincter of Oddi dysfunction. • Necrosectomy may improve survival in necrotizing pancreatitis.

Sigmoidoscopy or colonoscopy with mucosal biopsy

Bland diet with avoidance of high-fiber foods, fats, mild products, caffeine, and alcohol • Rehydration with oral electrolyte solutions (eg, Infalyte, Pedialyte, Gatorade) or intravenous fluids

Diet high in fiber and low in fat and lactose; vitamin B12 supplementation

Perforated peptic ulcer • Acute pancreatitis • Appendicitis • Perforated colonic carcinoma or diverticulum of hepatic flexure • Acute hepatitis or liver abscess • Pneumonia with pleurisy on right side • Myocardial infarction • Radicular pain in a T6 to T10 dermatome (eg, preeruptive zoster)

Hemoglobin, erythrocyte sedimentation rate, and serum albumin reflect disease severity. • Stools for bacterial culture, C difficile toxin assay or PCR testing, ova and parasites.

Abstinence from alcohol, vitamin and diet supplementation, vaccinations for hepatitis A and B viruses, pneumococcus, influenza. • Large-volume paracentesis (>5 L) is effective in patients with massive ascites refractory to diuretics or with consequent respiratory compromise. • Transjugular intrahepatic portosystemic shunt (TIPS) reduces ascites and portal hypertension but increases risk of hepatic encephalopathy.

Onset may be abrupt or insidious. • Malaise, myalgia, arthralgia, easy fatigability, upper respiratory symptoms, and anorexia. • Nausea and vomiting are frequent; diarrhea or constipation may occur. • Abdominal pain, mild and constant, in the RUQ. • Jaundice, hepatomegaly, splenomegaly, acholic stools. • Enlarged cervical or epitrochlear lymph nodes. • HCV infection may be asymptomatic.

Surgery is indicated in patients with ongoing bleeding that requires >6 units of blood transfusion within 24 hours or >10 total units in whom endoscopic or angiographic therapy has failed. • Limited resection of the bleeding segment of small intestine or colon, if possible, which may be guided by nuclear scan or angiography. • Total abdominal colectomy with ileorectal anastomosis if the bleeding site cannot be precisely identified.

Abdominal radiographs; barium enema is not useful and may precipitate toxic megacolon

Acute diarrhea has a duration of 4 weeks. • Traveler’s diarrhea is usually a benign, self-limited disease occurring about a week into travel.

Insert two 18-gauge or larger IV lines, fluid repletion as needed for hemodynamics. • Nasogastric tube placed for aspiration and serial monitoring of blood counts. • Packed red blood cells to maintain a hemoglobin of 7 to 9 g/dL, platelets to keep count >50,000/μL, and fresh-frozen plasma for patients with coagulopathy (INR >1.8). • Transfuse blood in patients with massive active bleeding regardless of the hematocrit. • Uremic patients with active bleeding should be given desmopressin (DDAVP). • Endoscopic therapy such as cautery, injection of a sclerosant or epinephrine, or application of a rubber band or metallic clips; endoscopy can be performed safely if the INR is <2.5. • Consider intra-arterial embolization or transvenous intrahepatic portosystemic shunts (TIPS) procedures in those for whom endoscopic therapy has failed.

ndications for surgery: intractability to therapy, intra-abdominal abscess, bleeding, obstruction

Cholecystitis usually subsides on a conservative regimen that includes IV fluids, antibiotics, and analgesics.

Acute hepatitis A, B, C Prodrome of anorexia, nausea, vomiting, malaise, aversion to smoking Fever, enlarged and tender liver, jaundice Markedly elevated aminotransferases Normal-to-low white blood cell count • Chronic hepatitis A, B, C Chronic hepatitis does not develop with hepatitis A. Chronic hepatitis B and C are continuing inflammatory reactions of the liver after >3 to 6 months, most often with persistently elevated aminotransferase levels. In chronic hepatitis B, there is persistent detection of serum hepatitis B surface antigen (HBsAg). In chronic hepatitis C, there is persistent detection of serum antibody to hepatitis C virus (HCV Ab).

Melena or hematemesis; hematochezia can occur in large, brisk upper GI tract bleeds. • Use volume (hemodynamic) status to determine the severity of blood loss; hematocrit is a poor early indicator of blood loss. • Endoscopy is diagnostic and may be therapeutic.

Steatorrhea is treated with pancreatic enzyme supplements at the start of, during, and at the end of meals, with high doses sometimes required. • H2-receptor antagonists and proton pump inhibitors may further decrease steatorrhea. • Pain may be alleviated by the use of pancreatic enzymes or octreotide subcutaneously. • Autoimmune pancreatitis is treated with prednisone.

Cholelithiasis • Diabetes mellitus • Malabsorption from other causes • Intractable duodenal ulcer • Pancreatic cancer • Irritable bowel syndrome

Correctable coexistent biliary tract disease should be treated surgically. • Surgery may drain persistent pseudocysts, treat other complications, or relieve pain. • In advanced cases, subtotal or total pancreatectomy may be considered as a last resort but has variable efficacy and is associated with a high rate of pancreatic insufficiency and diabetes mellitus.

Adjuvant chemotherapy reduces recurrence in stage II disease and increases survival in stage III disease. • FOLFOX (oxaliplatin, fluorouracil, and leucovorin) is preferred for stage III disease. • FOLFOX or FOLFIRI (addition of irinotecan to fluorouracil and leucovorin) is used in stage IV (metastatic) disease. • Ziv-aflibercept, a novel antiangiogenic agent, is FDA-approved for use in second-line therapy of stage IV colorectal cancer in combination with FOLFIRI. • Biological agents (bevacizumab, cetuximab, panitumumab, and ramucirumab) demonstrate further improvement in response rates in stage IV disease. • Regorafenib, a multitargeted kinase inhibitor, is FDA approved for patients with metastatic, refractory colorectal cancer after progression on standard regimens

Steady, severe pain, and tenderness in the abdominal RUQ or epigastrium • Nausea and vomiting; fever and leukocytosis

Resection of the primary colonic or rectal cancer with lymph node removal for staging • For unresectable rectal cancer, diverting colostomy, radiation therapy, laser fulguration, or placement of an expandable wire stent • For metastatic disease, resection of isolated liver or lung metastases

Can be asymptomatic for long periods; symptoms are usually insidious in onset but may be abrupt. • Fatigue, disturbed sleep, muscle cramps, anorexia, and weight loss are common. • Nausea and occasional vomiting. • Reduced muscle strength and exercise capacity. • Jaundice—usually not an initial sign—is mild at onset, increases in severity with progression of cirrhosis. • Abdominal pain can result from hepatic enlargement and stretching of Glisson capsule or from ascites. • Hematemesis is the presenting symptom in 15% to 25% of cases. • Fever usually reflects associated alcoholic hepatitis, spontaneous bacterial peritonitis, or intercurrent infection. • Erectile dysfunction, loss of libido, sterility, and gynecomastia in men; amenorrhea in women. • Liver may be enlarged and firm with a sharp or nodular edge; splenomegaly occurs in 35% to 50%. • Ascites, pleural effusions, peripheral edema, and ecchymoses are late findings. • Encephalopathy is characterized by day–night reversal, asterixis, tremor, dysarthria, delirium, drowsiness, and coma; encephalopathy occurs late unless precipitated by an acute hepatic insult or episode of GI bleeding or infection. • Skin findings include spider angiomas on the upper half of the body, palmar erythema, dilated superficial veins of the abdomen, and glossitis or cheilosis from vitamin deficiencies.

Acute diarrhea Infectious: viruses (Norwalk, rotavirus, adenovirus), preformed toxin (Staphylococcus aureus, Bacillus cereus, C perfringens), toxin production (enterotoxigenic Escherichia coli, Vibrio cholera), protozoa (Giardia lamblia, Cryptosporidium, Cyclospora, Isospora), invasive or inflammatory (Shigella, Salmonella, Campylobacter, Shiga toxin–producing E coli, C difficile) Noninfectious: drugs, antibiotics, inflammatory bowel disease, laxative abuse, radiation colitis • Chronic diarrhea Osmotic: lactase deficiency, medications (antacids, lactulose, sorbitol, olestra), factitious Secretory: hormonal (carcinoid, VIPoma, medullary thyroid carcinoma, adrenal insufficiency) Inflammatory conditions: inflammatory bowel disease, microscopic colitis, radiation colitis Malabsorption: celiac sprue, small bowel resection, pancreatic insufficiency, bacterial overgrowth, reduced bile salts Motility disorders: irritable bowel syndrome, postsurgical, systemic disease such as diabetes mellitus Chronic infections: giardiasis, amebiasis, strongyloidiasis

Viruses: hepatitis A, B, C, D (δ agent, always in the presence of B), E, infectious mononucleosis, cytomegalovirus, Epstein-Barr virus, herpes simplex virus, parvovirus B19, yellow fever, Middle East respiratory syndrome, Ebola virus, influenza; rarely, if ever, hepatitis G. • Other infections: leptospirosis, secondary syphilis, brucellosis, Q fever. • Alcoholic hepatitis and nonalcoholic steatohepatitis. • Drugs and toxins (predictable): acetaminophen, Amanita mushrooms, tetracycline, valproic acid. • Drugs and toxins (idiosyncratic): isoniazid, nonsteroidal anti-inflammatory drugs, statins, azole antifungals, halothane, ecstasy, kava. • Vascular: right-sided heart failure, shock liver, portal vein thrombosis, Budd-Chiari syndrome. • Metabolic: Wilson disease, hemochromatosis, acute fatty liver of pregnancy, Reye syndrome. • Autoimmune hepatitis. • α1-Antiprotease (α1-antitrypsin) deficiency. • Lymphoma or metastatic cancer. • TT virus; SEN-V virus may cause posttransfusion infection and hepatitis.

Infectious colitis: Salmonella, Shigella, Campylobacter, amebiasis, Clostridium difficile, enteroinvasive E coli • Ischemic colitis • Crohn disease • Diverticular disease • Colon cancer • Antibiotic-associated diarrhea or pseudomembranous colitis • Infectious proctitis: gonorrhea, Chlamydia, herpes, syphilis • Radiation colitis or proctitis • Cytomegalovirus colitis in immunocompromised persons

Transmission of HAV is by the fecal–oral route; incubation averages 30 days. • HBV contains an inner core protein (hepatitis B core antigen [HBcAg]) and outer surface coat (HBsAg). • HBV is usually transmitted by blood, sexual contact, or mother-to-infant (“vertical”) transmission; it has an insidious onset; coinfection with HCV is common in persons infected with HIV. • HCV is mostly transmitted by injection drug use, but body piercing, tattoos, and hemodialysis are risk factors; source of hepatitis C infection is unknown in many patients.

Diverticulosis or diverticulitis • Hemorrhoids • Adenomatous polyps • Ischemic colitis • Inflammatory bowel disease • Irritable bowel syndrome • Infectious colitis • Iron deficiency from another cause

Diverticulosis coli • Angioectasias, such as idiopathic arteriovenous malformations, CREST (calcinosis, Raynaud syndrome, esophageal dysmotility, sclerodactyly, and telangiectasia) syndrome, hereditary hemorrhagic telangiectasias • Colonic polyps • Colorectal cancer • Inflammatory bowel disease (ulcerative colitis, Crohn disease) • Hemorrhoids • Anal fissure • Ischemic colitis • Infectious colitis • Radiation colitis or proctitis • Nonsteroidal anti-inflammatory drug-induced ulcers of the small bowel or right colon

Positive fecal occult blood test results; complete blood cell count may reveal iron-deficiency anemia. • Elevated liver tests, particularly alkaline phosphatase, are suspicious for metastatic disease. • Carcinoembryonic antigen (CEA) level should normalize after complete surgical resection; persistently elevated levels suggest persistent disease.

Nuclear technetium-labeled red blood cell scan may be helpful in patients with significant active bleeding but is often nondiagnostic. • Selective mesenteric angiography is used in patients with massive bleeding or positive technetium scans.

Prescribe a low-fat diet and alcohol avoidance; treat associated complications such as diabetes. • Dilation or stenting of the duct via ERCP; sphincterotomy. • Celiac plexus nerve block may be considered

Acute cholecystitis • Acutely perforated duodenal ulcer • Acute intestinal obstruction • Leaking aortic aneurysm • Renal colic and acute mesenteric ischemia

Macrocytic anemia from suppression of erythropoiesis by alcohol, folate deficiency, hypersplenism, hemolysis, and blood loss from the GI tract. • Thrombocytopenia is secondary to marrow suppression, sepsis, folate deficiency, and splenic sequestration. • Modest elevations of serum aspartate aminotransferase (AST), bilirubin, and alkaline phosphatase; serum albumin is low and prothrombin time prolonged from decreased synthetic function.

Sometimes a history of alcohol intake or a heavy meal immediately preceding the attack or a history of milder similar episodes or biliary pain in the past • One classification of the severity of acute pancreatitis has been proposed, as follows Mild: absence of organ failure and pancreatic or peripancreatic necrosis or fluid collections or systemic complications Moderate: presence of sterile (peri) pancreatic necrosis and/or transient (<48 hours) organ failure (using the Sequential Organ Failure Assessment [SOFA] score) or local or systemic complications, or both Severe: presence of infected (peri) pancreatic necrosis or persistent (≥48 hours) organ failure • Pain Severe, epigastric abdominal pain, abrupt in onset, usually radiating to the back Pain often made worse by walking and lying flat and made better by sitting and leaning forward • Upper abdominal tenderness, most often without guarding, rigidity, or rebound • Abdominal distention and absent bowel sounds from paralytic ileus • Nausea and vomiting; weakness, sweating, and anxiety in severe attacks • Fever of 38.4°C to 39.0°C; tachycardia; hypotension (even shock); pallor; and cool, clammy skin in severe cases

Increased stool frequency or liquidity. • Physical examination may reveal abdominal tenderness or peritonitis. • When the cause is an invasive bacterial pathogen (eg, Shigella, Campylobacter, Salmonella), stools may be bloody, and fever may be present. • Osmotic diarrheas: abdominal distention, bloating, flatulence. • Secretory diarrhea: high-volume, watery diarrhea; dehydration; electrolyte imbalance. • Inflammatory conditions: abdominal pain, fever, weight loss, hematochezia. • Malabsorption syndromes: weight loss, osmotic diarrhea, steatorrhea, nutritional deficiencies.

Persistent or recurrent episodes of epigastric and LUQ pain with referral to the upper left lumbar region may occur. • Anorexia, nausea, vomiting, constipation, flatulence, and weight loss are common. • During attacks tenderness over the pancreas, mild muscle guarding, and ileus may be noted. • Attacks may last only a few hours or as long as 2 weeks; pain may eventually be almost continuous. • Steatorrhea (as indicated by bulky, foul, fatty stools) may occur late in the course.

Acutely, IV hydration and glucose can be given if needed; parenteral nutrition can be used if nausea and vomiting are pronounced or if oral intake is low for a prolonged period. • Corticosteroids produce no benefit. • In acute hepatitis B, antiviral therapy is generally unnecessary except in cases of fulminant hepatitis. • Chronic hepatitis B is treated with antiviral agents (entecavir, tenofovir, adefovir, telbivudine, lamivudine) or with peginterferon α-2a in selected patients with active viral replication. • In chronic hepatitis C, treatment once consisted of peginterferon α-2b or α-2a with or without the addition of ribavirin with incomplete response rates and significant side effects. • Now, direct-acting and host-targeting antiviral agents for chronic hepatitis C have led to high response rates often with all-oral regimens. • These newer chronic hepatitis C targeted agents include HCV protease inhibitors (boceprevir, telaprevir, simeprevir, paritaprevir, asunaprevir, grazoprevir), NS5A inhibitors (daclatasvir, ledipasvir, ombitasvir, elbasvir, GS-5816), and HCV polymerase inhibitors (sofosbuvir, dasabuvir, beclabuvir).

Ulcerative colitis is an idiopathic inflammatory condition that involves the mucosal surface of the colon, resulting in diffuse friability and erosions with bleeding. • It may involve the rectosigmoid region, left side of the colon, or the entire colon. • Most affected patients experience periods of symptomatic flare-ups and remissions.

Patients with bloody diarrhea, high fever, or systemic toxicity should not receive antidiarrheal medications. • Opioids, loperamide, bismuth, or diphenoxylate with atropine are effective for symptomatic treatment. • Octreotide subcutaneously for secretory diarrheas caused by neuroendocrine tumors. • Cholestyramine, colestipol, or colesevelam for patients with bile salt-induced diarrhea. • Empiric antibiotic treatment with fluoroquinolones, azithromycin, doxycycline, or trimethoprim-sulfamethoxazole. • Specific antimicrobial treatment for shigellosis, cholera, Salmonella, listeriosis, C difficile, giardiasis, amebiasis. • Antibiotics are not recommended in nontyphoid Salmonella, Campylobacter, Aeromonas, Yersinia, or Shiga toxin-producing E coli infection except in severe disease.

End result of injury that leads to both fibrosis and regenerating nodules. • May be reversible if the cause is removed. • Clinical features result from hepatic cell dysfunction, portosystemic shunting, and portal hypertension.

Usually occurs when a stone becomes impacted in the cystic duct and inflammation develops behind the obstruction. • Acalculous cholecystitis should be considered after major surgery or in a critically ill patient without any oral intake for a prolonged period. • May be caused by infectious agents (eg, cytomegalovirus, cryptosporidiosis, or microsporidiosis) in patients with AIDS or by vasculitis (eg, polyarteritis nodosa, Henoch-Schönlein purpura).

Brown stools mixed or streaked with blood suggest a rectosigmoid or anal source. • Maroon stools suggest a right colon or small intestine source. • Black stools (melena) suggest a source proximal to the ligament of Treitz, but dark maroon stools arising from small intestine or right colon may be misinterpreted as “melena.” • Bright red blood per rectum with upper GI bleeding is almost always in the setting of massive hemorrhage with shock. • Bloody diarrhea associated with cramping abdominal pain, urgency, or tenesmus suggests inflammatory bowel disease (especially ulcerative colitis), infectious colitis, or ischemic colitis. • Diverticular bleeding is acute, painless, and usually subsides spontaneously, although it may recur. • Angioectasias cause painless occult blood loss, melena, or hematochezia. • Neoplasms cause chronic occult blood loss or intermittent anorectal hematochezia. • Anorectal disease often produces small amounts of bright red blood on the toilet paper or blood streaking of the stool.

Acute diarrhea is most commonly caused by infectious agents, bacterial toxins, or drugs. • Recent exposures, ingestions, medical history, and travel may suggest causes of diarrhea. • Inflammatory diarrhea is distinguished from noninflammatory diarrhea by the presence of fecal blood and leukocytes. • Medications that can commonly cause diarrhea include metformin, allopurinol, orlistat, selective serotonin reuptake inhibitors, cholinesterase inhibitors, proton pump inhibitors, and nonsteroidal anti-inflammatory drugs. • Osmotic diarrheas resolve during fasting; secretory diarrheas do not. • Immunocompromised patients are susceptible to many infectious causes of diarrhea. • Traveler’s diarrhea is a risk factor for development of irritable bowel syndrome.

Chronic viral hepatitis • Alcoholism • Nonalcoholic fatty liver disease • Metabolic (eg, hemochromatosis, α1-antiprotease deficiency, Wilson disease, gluten enteropathy) • Primary biliary cirrhosis • Secondary biliary cirrhosis (chronic obstruction caused by stone, stricture, neoplasm) • Cryptogenic cirrhosis • Heart failure or constrictive pericarditis • Hereditary hemorrhagic telangiectasia

Most often caused by a passed gallstone, usually ≤5 mm in diameter, or heavy alcohol intake. • Rarely, may be the initial manifestation of a pancreatic or ampullary neoplasm. • Pathogenesis may include edema or obstruction of the ampulla of Vater, bile reflux into pancreatic ducts, and direct injury of the pancreatic acinar cells.

Plain radiographs show calcifications caused by pancreaticolithiasis in 30% of patients. • CT may show calcifications, ductal dilatation, and heterogeneity or atrophy of the gland. • MRCP (including secretin-enhanced MRCP) or endoscopic ultrasonography (EUS).

Abdominal computed tomography for suspected chronic pancreatitis, pancreatic cancer, neuroendocrine tumors

Barium upper gastrointestinal series with small bowel follow through • Computed tomography enterography or capsule (video) imaging of small intestine

The WBC count is often elevated. • Total serum bilirubin may be mildly elevated even in the absence of common bile duct obstruction; serum aminotransferase and alkaline phosphatase levels are often elevated. • Serum amylase may also be moderately elevated.

Ascites and edema: bed rest; restrict sodium and fluid intake; spironolactone (usually with furosemide) for diuresis. • Anemia: folic acid; ferrous sulfate; packed red cells for GI bleeding. • Severe hypoprothrombinemia: vitamin K or fresh-frozen plasma if there is bleeding or before surgery. • Liver transplantation is indicated in selected cases of irreversible, progressive liver disease. • Absolute contraindications to transplantation include nonhepatic malignancy, sepsis, and advanced cardiopulmonary disease.

Chronic pancreatitis occurs most often with alcoholism (45%–80% of all cases); the risk increases with the duration and amount of consumption. • Tobacco smoking is a risk factor for idiopathic chronic pancreatitis and may accelerate progression of alcoholic chronic pancreatitis. • Pancreatitis develops in about 2% of patients with hyperparathyroidism. • Tropical pancreatitis, related to malnutrition, is a common cause in Africa and Asia. • A stricture, stone, or tumor obstructing the pancreas can lead to obstructive chronic pancreatitis. • Autoimmune pancreatitis is associated with hypergammaglobulinemia. • The pathogenesis may be related to a first episode of acute pancreatitis, which initiates an inflammatory process that results in injury and then fibrosis. • Genetic factors may predispose to chronic pancreatitis in some cases (eg, CFTR gene mutations). • Between 10% and 30% of cases are idiopathic.

Upper GI bleeding leads to 250,000 hospitalizations per year in the United States. • Hematemesis is either bright red blood or brown “coffee grounds” material. • Melena develops after as little as 50 to 100 mL of blood loss. • Hematochezia requires >1000 mL of blood loss. • Upper GI bleeding is self-limited in 80% of cases; urgent medical therapy and endoscopic evaluation are required in the remainder. • Peptic ulcers account for about 40% of cases. • Variceal bleeding accounts for 10% to 20% of cases. • Mallory-Weiss tears, lacerations of the gastroesophageal junction, are responsible for 5% to 10% of cases. • Vascular anomalies, such as angioectasias, telangiectasias, and Dieulafoy lesion (an aberrant, large caliber submucosal artery in proximal stomach) account for 7% of cases. • Gastric neoplasms (1% of cases). • Erosive gastritis (<5% of cases) due to NSAIDs, alcohol, or severe medical or surgical illness (stress-related mucosal disease).

Meperidine intramuscularly as needed for pain. • Nothing by mouth and IV fluids until the patient is pain free and has bowel sounds. • Then begin clear liquids and gradually advance to a low-fat diet, as tolerated. • For mild pancreatitis, judicious early fluid resuscitation (lactated Ringer solution preferable to normal saline) may reduce the frequency of systemic inflammatory response syndrome and organ failure. • For severe pancreatitis, large volume of IV fluids to maintain intravascular volume. If shock persists after adequate volume replacement (including packed red cells), consider vasopressors. • Enteral nutrition via a nasogastric or nasojejunal tube is preferable to parenteral nutrition. • Parenteral nutrition (including lipids) should be considered in severe pancreatitis with ileus. • IV calcium gluconate for hypocalcemia with tetany. • Fresh-frozen plasma or serum albumin may be needed for coagulopathy or hypoalbuminemia. • Imipenem, ciprofloxacin and metronidazole, or cefuroxime for pancreatic necrosis or infection.

Elevated serum aspartate or alanine aminotransferase is followed by elevated bilirubin and alkaline phosphatase. • Prolongation of prothrombin time indicates synthetic dysfunction and severe disease. • Anti-HAV IgM indicates acute illness; IgG may indicate previous exposure or immunity if not associated with symptoms. • HBsAg (surface antigen) indicates chronic HBV infection in patients without acute disease. • Anti-HBs (surface antibody) alone indicates HBV immunity because the vaccine has only surface proteins and no core proteins. • Anti-HBc (core antibody) indicates HBV exposure and is diagnostic in acute hepatitis. • HBV DNA can be used for prognosis and consideration of treatment. • Antibodies to HCV are first used for diagnosis; HCV RNA assay confirms diagnosis and establishes disease activity.

Bloody diarrhea, lower abdominal cramps, fecal urgency • Anemia, low serum albumin, negative stool culture results • Sigmoidoscopy is key to diagnosi