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USMLE Step 2 (Fach) / Gastroenterology (Lektion)

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• Colorectal cancer Third leading cause of cancer-related deaths in the US overall. Predisposing factors:- Colorectal adenomas- Family history- Hereditary syndromes: Familial adenomatous polyposis, hereditary nonpolyposis colorectal cancer (HNPCC)- Inflammatory bowel disease (IBD): ulcerative colitis and Crohn's disease- Endocarditis and bacteremia due to Streptococcus gallolyticus - Diet and lifestyle: Smoking, alcohol consumption, obesity, processed meat; high-fat, low-fiber diets- Older age Protective factors: Physical activity, diet rich in fiber, long-term use of aspirin and NSAIDs Clinical features:- Constitutional symptoms: weight loss, fever, night sweats, fatigue- Right-sided carcinomas (10%): cecum and ascending colon→ Iron deficiency anemia→ Melena→ Diarrhea- Left-sided carcinomas: transverse and descending colon→ Changes in bowel habits (size, consistency, frequency)→ Blood-streaked stools→ Colicky abdominal pain due to obstruction- Rectum (50%) and sigmoid (30%):→ Hematochezia→ ↓ Stool caliber (pencil-shaped stool)→ Rectal pain→ Tenesmus→ Flatulence with involuntary stool loss Diagnostics:- Digital rectal examination: Up to 10% of cancers are palpable- Complete colonoscopy: gold standard- If colonoscopy is incomplete → perform double-contrast barium enema- Staging: CT of abdomen, pelvis, and chest- Carcinoembryonic antigen (CEA) – useful for establishing baseline, monitoring treatment efficacy, and recurrence surveillance. Treatment:- Surgical management: Colectomy, regional lymph node dissection (for pathologic staging), resection of resectable metastases in liver and/or lung- Chemotherapy: → FOLFOX: FOLinic acid (leucovorin) + 5-Fluorouracil (5-FU) + OXaliplatin→ FOLFIRI: FOLinic acid (leucovorin) + 5-Fluorouracil (5-FU) + IRInotecan→ XELOX: capecitabine (XELoda ®) + OXaliplatin- Biologicals: Anti-VEGF antibodies (e.g., bevacizumab) or EGFR antibody (e.g., cetuximab)
• Angiodysplasia Tortuous, dilated veins in submucosa of the colon (usually proximal) wall.- Associated with advanced age (> 60 years), end-stage renal disease, von Willebrand disease, and aortic stenosis Clinical features:- Lower GI bleed- Bleeding is usually low grade, but 15% of patients may have massive hemorrhage if veins rupture. Diagnostics:- Colonoscopy (preferred over angiography) Treatment:- In about 90% of patients, bleeding stops spontaneously- Colonoscopic coagulation- If bleeding persists, a right hemicolectomy should be considered
• Acute mesenteric ischemia Epidemiology:- Mainly occurs in adults > 60 years- Young people with A-fib, vasculitis, or hypercoagulable states can also be affected Etiology:- Acute arterial embolism (∼ 50% of cases): generally resulting from atrial fibrillation, myocardial infarction, valvular heart disease, or endocarditis- Arterial thrombosis (∼ 25% of cases): due to preexisting visceral atherosclerosis, arteritis, aortic aneurysm, or dissection- Nonocclusive mesenteric ischemia (NOMI; ∼ 20% of cases)→ Typically seen in critically ill people with low cardiac output→ Hypotension, vasopressive drugs, digitalis, ergotamines, cocaine- Venous thrombosis (< 10% of cases): Predisposing factors include infection, malignancies, estrogen therapy, and hypercoagulability disorders. Clinical features:- Periumbilical pain that is disproportionate to physical findings- Nausea and vomiting- Diarrhea (bloody in later stages)- Gangrenous bowel: rectal bleeding and signs of sepsis (e.g., tachycardia, hypotension) Diagnostics:- Lab tests: ↑ Lactate, ↑ LDH, ↑ creatine kinase, leukocytosis, metabolic acidosis- CT angiography (confirmatory test) Therapy:- If signs of advanced ischemia (e.g., peritonitis, sepsis) or hemodynamically unstable patient → emergency laparotomy - Hemodynamically stable patients without signs of advanced ischemia → endovascular approach→ Balloon angioplasty and stenting→ Catheter-based pharmacologic (thrombolytics) and/or mechanical thrombectomy- Supportive: IV fluids, nasogastric tube, analgesics and broad-spectrum antibiotics- Infusion of a vasodilator (e.g., papaverine) during arteriography to relieve occlusion and vasospasm- Heparin anticoagulation in cases of venous thrombosis
• Chronic mesenteric ischemia Epidemiology:- Generally occurs in adults > 60 years Clinical features:- So-called 'abdominal/intestinal angina'→ Recurrent, dull, postprandial epigastric pain usually within the first hour after eating→ Can lead to a fear of eating → weight loss and malabsorption- Bloating, nausea, occasional diarrhea- Abdominal bruit caused by stenosis of mesenteric vessels Diagnostics:- Clinical suspicion → CT scan of the abdomen (identifies atherosclerotic vascular disease and rules out other abdominal disorders)- CT angiography or MR angiography: High-grade stenoses of at least two major vessels must be established for diagnosis- Duplex sonography of the mesenteric vessels: best screening modality in an office setting Treatment:- Nutritional support (frequent, small meals; low-fiber diet)- Long-term anticoagulation for patients not healthy enough for vascular repair- Revascularization procedures to prevent bowel infarction in patients with abdominal pain and weight loss: → Angioplasty and stenting→ Mesenteric artery bypass surgery
• Ogilvie's syndrome (Acute megacolon) Acute dilation of the colon in the absence of a mechanical obstruction, characteristically seen in severely ill or postoperative patients. Etiology:- Recent major surgery or trauma- Serious medical illnesses (e.g., sepsis, malignancy)- Drugs (e.g., anticholinergic drugs, opioid analgesics, antipsychotics, calcium channel blockers) Clinical features:- Gradual abdominal distention- Abdominal pain; constipation/diarrhea- Tympanitic abdominal percussion; decreased frequency of bowel sounds- Signs of colonic ischemia or impending perforation: Fever, tachycardia, and peritoneal signs (guarding, rigidity, rebound tenderness) Diagnostics:- Abdominal x-ray: dilation of the cecum and right colon (occasionally up to the rectum) with/without multiple air-fluid levels; haustrae are preserved- Contrast enhanced CT scan (oral and IV contrast) Treatment:- Conservative: IV fluids and bowel rest (NPO), bowel decompression- Pharmacologic management: Neostigmine- Surgical decompression with cecostomy or colostomy is a last resort
• Volvulus Twisting of a loop of bowel on its mesentery. Epidemiology:- Volvulus: 3rd most common cause (∼ 10-15%) of intestinal obstruction in the United States→ Sigmoid volvulus (most common, 80%)→ Cecal volvulus (15%)- Intestinal malrotation and midgut volvulus: neonates and infants Risk factors:- Chronic constipation, laxative abuse, antimotility drugs- Megacolon (Hirschsprung's disease, Chagas disease)- Intestinal bands/adhesions Clinical features:- Acute onset of colicky abdominal pain- Obstipation, abdominal distention- Anorexia, nausea, vomiting Diagnostics:- Abdominal x-ray (erect and supine) → Sigmoid volvulus: coffee bean sign (bent inner tube sign) → Cecal volvulus: kidney bean sign Treatment:- Initial resuscitation: IV fluids; acid-base and electrolyte imbalance correction; nil per oral; placement of a nasogastric tube- Sigmoid volvulus: Nonoperative reduction (decompression via sigmoidoscopy) is successful in >70% of cases. The recurrence rate is high, so elective sigmoid colonresection is recommended.- Cecal volvulus: Emergent surgery is indicated.
• Cirrhosis Etiology:- Long-standing alcohol abuse (one of the two most common causes of chronic liver disease in the USA)- Viral hepatitis B, C, and D - Autoimmune: Primary biliary cirrhosis, primary sclerosing cholangitis, autoimmune hepatitis- Metabolic disorders: Non-alcoholic steatohepatitis (NASH), hemochromatosis, Wilson's disease, alpha‑1 antitrypsin deficiency- Hepatic vein congestion or vascular anomalies: Budd-Chiari syndrome, cardiac cirrhosis (congestive hepatopathy)- Medications (e.g., acetaminophen, amiodarone or chemotherapy drugs such as methotrexate)- Ingesting aflatoxin created by Aspergillus Classification: Child-Pugh score- Based on bilirubin, albumin, and prothrombin time, ascites, and encephalopathy Clinical features:- Nonspecific symptoms: Fatigue, malaise, weight loss, uaundice, pruritus, asterixis, fetor hepaticus- Abdominal symptoms: Hepatomegaly (possibly causing RUQ pain), splenomegaly, ascites- Skin changes: Generally dry and atrophic, spider angiomata, caput medusae, palmar erythema- Hormone disorders: Gynecomastia, hypogonadism Diagnostics:- Lab tests: ↑ AST, ALT, ↑ bilirubin, ↑ GGT, ↑ AP, ↑ GLDH, ↑ Ammonia, ↑ Prothrombin time (↑ INR), ↓ total protein (↓ albumin), ↓ cholinesterase, thrombocytopenia- Abdominal ultrasound: Nodular liver surface, atrophy of right lobe, hypertrophy of caudate lobe- CT scan- Biopsy: Gold standard but not required- HCC screening: Abdominal ultrasound for patients with cirrhosis every 6 months and periodic monitoring of alpha-fetoprotein (AFP)- Endoscopy screening: To exclude varices, determine risk of variceal hemorrhage, prevention Treatment:- Routine vaccinations (influenza, pneumococcal disease, hepatitis A/B, tetanus)- Diet- Non‑selective beta blockers (e.g., propranolol) to lower portal pressure and prevent variceal bleeding- Spironolactone and furosemide to manage ascites- Bleeding prevention with vitamin K substitution or cryoprecipitate- Paracentesis of ascites to decompress abdomen - TIPS (transjugular intrahepatic portosystemic shunt) to lower portal pressure
• Esophageal variceal hemorrhage Esophageal variceal hemorrhage refers to the bleeding of dilated sub-mucosal veins (varices) of the distal esophagus and is a dangerous consequence of portal hypertension. It is the most common form of upper gastrointestinal bleeding in patients presenting with cirrhosis. Clinical features:- Signs of circulatory insufficiency- Hematemesis, melena, and/or hematochezia Treatment:- Resuscitation and stabilization- Octreotide for 3-5 days- Vitamin K for patients with coagulation disorders- IV antibiotic prophylaxis (e.g., ciprofloxacin or trimethoprim-sulfamethoxazole)- Endoscopic management→ Erythromycin (a strong prokinetic agent) may be administered before gastroscopy→ Endoscopic band ligation→ Alternative: injection sclerotherapy→ Balloon tamponade Primary prophylaxis:- Nadolol or propanolol- Endoscopic esophageal variceal ligation: only indicated for patients with a high risk of bleeding
• Spontaneous bacterial peritonitis Bacterial infection of ascitic fluid in the absence of other intra-abdominal causes Etiology:- Patients with progressed liver cirrhosis or patients receiving peritoneal dialysis. - Bacterial species: E. coli most common in ascites. Klebsiella spp. and streptococci are frequently involved in nosocomial cases of SBP. Pathophysiology: Migration of bacteria through the intestinal wall and colonization of mesenteric lymph nodes (bacterial translocation) Clinical features:- Often asymptomatic- Temperature ≥ 37.8 °C- Abdominal pain, tense abdominal wall- Altered menatal status- Hypotension, hypothermia, paralytic ileus with severe infection Diagnosis:- Gold standard: diagnostic paracentesis BEFORE application of antibiotics- > 250 polymorphonuclear leukocytes/μL ascites: SBP per definition- Ascitic fluid: Protein < 1 g/dL, SAAG ≥ 1.1 g/dL- If pathogens are identified = Secondary SBP Treatment:- First-line: 3rd generation cephalosporin IV broad spectrum therapy- Follow-up after 48 h via repeated paracentesis- Fluoroquinolones for SBP prophylaxis
• Wilson's disease Wilson disease (hepatolenticular degeneration) is an autosomal recessive metabolic disorder in which impaired copper excretion causes copper to accumulate in the body. Age of onset: 5-35 years  Pathophysiology: Autosomal recessive mutations in the ATP7B gene (Wilson gene) on chromosome 13, which encodes for a membrane-bound, copper-transporting ATPase → defective ATP7B protein- Inadequate incorporation of copper into apoceruloplasmin → ↓ serum ceruloplasmin- Reduced biliary copper excretion- Results in ↑ free serum copper  Clinical features:- Liver: Acute/chrnoic hepatitis, cirrhosis, hepatosplenomegaly, portal hypertension, abdominal pain, jaundice, ascites, hepatic encephalopathy- Neurological symptoms: extrapyramidal motor disturbances, but no sensory changes→ Dysarthria, parkinsonism, tremor (usually asymmetric, affecting the hands)→ Behavioral changes (e.g., depression, irritability, psychosis) → Cognitive impairment Diagnostics:- Lab tests: ↑ Transaminases, Coombs-negative hemolytic anemia, thrombocytopenia, ↓ serum ceruloplasmin (normal value > 20 mg/dL), ↑ free serum copper, but ↓ total serum copper- Slit lamp examination: Kayser-Fleischer rings- ↑ Urine copper excretion (over 24 hours)- Liver biopsy: Hepatic copper concentration (> 250 μg/g dry weight) Treatment:- Penicillamine: side effects in ∼ 30% of cases (e.g., sensitivity reactions)- Alternatives: trientine or zinc salts- Maintenance therapy: zinc salts or low dose chelating agents- Liver transplantation in cases of fulminant liver failure
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• Hemochromatosis Primary hemochromatosis:- Homozygous or heterozygous for the HFE gene defect (chromosome 6)- Most commonly affects C282Y and H63- Defective binding of transferrin to its receptor → liver stops producing the acute phase reactant hepcidin → unregulated ferroportin causes ↑ iron reabsorption in duodenal enterocytes- Inheritance: autosomal recessive with incomplete penetrance Secondary hemochromatosis:- Transfusion-related (e.g., for correcting chronic anemia)- Thalassemia- Sickle-cell anemia- Sideroblastic anemia Clinical features:- Onset of symptoms: typically between the 3rd and 5th decade of life- Abdominal pain, hepatomegaly → liver cirrhosis (+ hepatocellular carcinoma)- Fatigue, lethargy- Hyperpigmented, bronze skin - Signs of diabetes mellitus (polydipsia, polyuria)- Arthralgia, chondrocalcinosis- Erectile dysfunction, testicular atrophy, loss of libido, amenorrhea- Cardiomyopathy (restrictive or dilated) → congestive heart failure and/or cardiac conduction abnormalities (e.g., sick sinus syndrome)- Increased susceptibility to Listeria, Vibrio vulnificus & Yersinia enterocolitica Diagnostis:- Lab tests: ↑ Serum iron, ↑ ferritin in serum > 200 μg/L, ↑ transferrin saturation (> 45%), ↑ AST, ALT- Genetic tests- Liver biopsy Treatment:- Therapeutic phlebotomy (first-line treatment)- Deferoxamine
• Hepatic adenoma - Most often seen in young women (15 to 40 years of age) Etiology:- Oral contraceptive use- Anabolic steroid use Clinical features:- Usually asymptomatic- Large tumors → upper abdominal pain, fullness, and nausea Diagnostics:- Best initial test: ultrasound- Contrast-enhanced CT: Centripetal enhancement- Hepatic angiography Treatment: - Asymptomatic & < 5 cm – Discontinue oral contraceptives- Symptomatic of > 5 cm – Surgical resection Complications: Increased risk of rupture, bleeding, or malignant transformation
• Cavernous hemangioma Most common type of benign liver tumor. Etiology:- Estrogen therapy associated with increased growth in size Clinical findings- Usually asymptomatic- Large tumors → upper abdominal pain, fullness, and nausea Diagnostics:- Ultrasound - CT scan with IV contrast: Centripetal enhancement (ie, enhancement moving from periphery to center)- Biopsy contraindicated because of risk of rupture and hemorrhage Treatment- Conservative treatment is often sufficient- Surgical treatment if symptomatic and/or complications arise
• Focal nodular hyperplasia Benign liver tumor without malignant potential. - Occurs in women of reproductive age. - There is no association with oral contraceptives. Clinical features:- Usually asymptomatic- Hepatomegaly may be present Diagnostics:- Associated with anomalous arteries- Homogenous, homoechoic- Arterial flow & central scar on imaging Treatment not necessary in most cases.
• Hepatocellular carcinoma Epidemiology:- Highest incidence in Southeast Asia and Africa- Peak incidence in the US: 70-75 years Etiology:- Liver cirrhosis (80% of cases)- Risk factors independent of cirrhosis→ Chronic hepatitis B or C virus infection→ Nonalcoholic steatohepatitis (NASH)→ Hemochromatosis, Wilson's disease, alpha-1 antitrypsin deficiency→ Schistosomiasis→ Glycogen storage disease→ Chronic ingestion of food contaminated with aflatoxin Clinical features:- Weight loss, cachexia- Hepatomegaly and right upper quadrant tenderness- Ascites and jaundice Diagnostics:- ↑ AFP- Paraneoplastic syndromes: erythrocytosis, hypoglycemia, hypercalcemia- Ultrasound: first test - Abdominal CT (confirmatory test): triple-phase Treatment:- Surgical resection- Liver transplantation- If unresectable: transcatheter arterial chemoembolization (TACE), radiofrequency ablation
• Budd-Chiari syndrome Etiology:- Secondary to conditions associated with hypercoagulability (most common)→ Polycythemia vera (most important cause) → Paraneoplastic thrombocytosis→ Pregnancy→ Clotting disorders (e.g., factor V Leiden thrombophilia, antiphospholipid syndrome)→ Side effect of medication (e.g., hormonal contraception)→ Chronic inflammatory diseases- Secondary to invasion or compression of the hepatic veins (less common)→ Hepatocellular carcinoma, renal carcinoma→ Chronic infections and hepatic lesions (e.g., amebiasis, aspergillosis, syphilis, tuberculosis) Clinical features:- Abdominal pain- Tender hepatomegaly- Ascites and abdominal distention- Jaundice- Signs of increased perfusion of portocaval anastomoses Diagnostics:- Ascites fluid analysis: WBC count < 500 /μL, serum ascites albumin gradient > 1.1- Imaging (confirmatory test): Doppler ultrasound, CT, MRI with contrast Treatment:- Anticoagulation (to prevent propagation of the thrombus): Usually unsatisfactory- Localized thrombolysis- Balloon angioplasty and stenting- TIPS (transjugular intrahepatic portosystemic shunt) if complications of portal hypertension occur
• Liver function tests - Aminotransferases - ALT is more sensitive and specific than AST for liver damage.- ALT and AST usually have a similar increase. The exception is in alcoholic hepatitis, in which the AST–ALT ratio may be >2:1. - If ALT and AST levels are mildly elevated (low hundreds), think of chronic viral hepatitis or acute alcoholic hepatitis. - If ALT and AST levels are moderately elevated (high hundreds to thousands), think of acute viral hepatitis. - If ALT and AST levels are severely elevated (>10,000), extensive hepatic necrosis has occurred. Typical cases are:a. Ischemia, shock liver (prolonged hypotension or circulatory collapse)b. Acetaminophen toxicityc. Severe viral hepatitis The following can cause an elevation in ALT or AST levels in asymptomatic patients:a. Autoimmune hepatitisb. Hepatitis Bc. Hepatitis Cd. Drugs or toxins e. Ethanold. Fatty liver (triglyceridemia)g. Tumorsh. Hemodynamic disorders (e.g., CHF)i. Iron (hemochromatosis), copper (Wilson disease), or AAT deficiency
• Liver function tests - Alkaline phosphatase Not specific to liver—also found in bone, gut, and placenta. - ALK-P is elevated when there is obstruction to bile flow (e.g., cholestasis) in any part of the biliary tree. Normal levels make cholestasis unlikely. - If levels are very high (10-fold increase), think of extrahepatic biliary tract obstruction or intrahepatic cholestasis (e.g., PBC or drug-induced cirrhosis). - If levels are elevated, measure the gamma-glutamyl-transferase (GGT) level to make sure the elevation is hepatic in origin (rather than bone or intestinal). If the GGT level is also elevated, this strongly suggests a hepatic origin. If the GGT level is normal but ALK-P is elevated, consider pregnancy or bone disease.
• Cholelithiasis Epidemiology:- Sex: F > M (2-3:1)- Prevalence: approx. 10-20% of the adult population in the United States- Peak incidence: > 40 years Risk factors:- Obesity- Female sex, especially among those receiving estrogen therapy - Multiparity or pregnancy- Age (> 40 years of age)- European, Native American, or Hispanic ancestry - Family history- Black pigment stones (calcium bilirubinate): 10% of all stones: ↑ Hemolysis - Brown pigment stones (mixed): 10% of all stones: caused by bacteria, biliary parasites such as Clonorchis sinensis/Opsithorcus species, and stasis Clinical features:- Only 25% of patients with gallstones have symptoms!- Biliary colic (colicky RUQ pain): Especially postprandial; < 6 hours; may radiate to the epigastrium, right shoulder, and back (referred pain)- Nausea, vomiting, feelings of satiety- Bloating, dyspepsia Diagnostics:- Best initial test: ultrasonography- Endoscopic ultrasound (EUS) of the bile ducts to exclude choledocholithiasis Treatment:- Conservative: Decreased fat intake, spasmolytics (e.g., dicyclomine), NSAIDs- Endoscopic retrograde cholangiopancreatography (ERCP) with papillotomy- Medical litholysis with ursodesoxycholic acid- Extracorporeal shock wave lithotripsy (ESWL)- Elective laparoscopic cholecystectomy (after ERCP): Only symptomatic patients
• Cholecystitis Etiology:- Due to obstructing cholelithiasis: 90% of cases, with secondary bacterial infection (E. coli, Klebsiella, Enterobacter) Clinical features:- RUQ pain→ More severe and prolonged (> 6 hours) than in cholelithiasis→ Worse after meals→ Radiation to the right scapula→ Guarding→ Positive Murphy's sign describes sudden inspiratory arrest during RUQ palpation. - Fever, malaise- Nausea and vomiting Diagnostics:- Ultrasonography→ Enlargement of the gallbladder→ Wall thickening > 4 mm (postprandial > 5 mm)→ Gallbladder wall edema (double wall sign)→ Possible free fluid surrounding the gallbladder→ Presence of concrement or gallstones- 99mTc-hepatic iminodiacetic acid (HIDA) scan (cholescintigraphy)→ Abnormal if gallbladder not visualized within 30-60 minutes: suggests cystic duct obstruction due to edema or obstructing stone Treatment:- Conservative: IV antibiotic therapy, analgesia (e.g., meperidine), fluid and electrolyte correction, antiemetics- Early cholecystectomy (first 24-48 hours)- In patients with high-risk surgical complications and empyema of the gallbladder: percutaneous cholecystostomy
• Acalculous cholecystitis Acute cholecystitis without stones obstructing the cystic duct (up to 10% of patients with acute cholecystitis), usually seen in critically ill patients. It usually presents with secondary infection. Etiology: - Conditions that result in biliary stasis and a "stressed gallbladder" with reduced perfusion- Severe trauma or recent surgery- Prolonged fasting or TPN- Critical illness (eg, sepsis, ICU) Clinical features: Same as for acute cholecystitis - Fever, leukocytosis, ↑ LFT, RUQ tenderness Diagnostics:- Ultrasound demonstrates thickening of the gallbladder wall without presence of gallstones- HIDA or CT scan if needed- Blood cultures Treatment:- Initial treatment: antibiotics- Cholecystostomy is often preferred because it is less invasive, especially considering most patients are critically ill.- If patient does not improve after cholecystostomy, a cholecystectomy is required.
• Choledocholithiasis Etiology:- Cystic fibrosis- Prolonged total parenteral nutrition - History of cholelithiasis, though patients remain at risk of choledocholithiasis postcholecystectomy Clinical features:- Colicky RUQ/epigastric pain (more severe and prolonged than in cholelithiasis)- Nausea, vomiting- Extrahepatic cholestasis: Obstructive jaundice, pale stool, dark urine, pruritus- If complicated, may present with pancreatitis and acute cholangitis Diagnostics:- Lab tests: ↑ ALP, ↑ GGT, ↑ total and ↑ direct bilirubin, ↑ AST, ALT; Possibly pancreatic inflammation: ↑ lipase, ↑ amylase- Transabdominal ultrasonography (detects only 50% of cases): Dilated common bile duct with possible intrahepatic biliary dilatation- Confirmatory test:If high risk of choledocholithiasis → ERCP If intermediate risk → MRCP or EUSIf low risk → treatment if evidence of cholelithiasis (no further imaging) Treatment:- ERCP with papillotomy (both diagnostic and therapeutic)- Elective cholecystectomy: recommended within 72 hours of ERCP
• Cholangitis Etiology:- Obstruction of biliary tracts (e.g., caused by biliary lithiasis, stenosis, or malignancy), with secondary bacterial infection- May follow cholecystitis- Ascending infection most commonly from the duodenum after manipulation of bile tract (e.g., papillotomy, stent placement, post-ERCP) due to disruption of normal barrier mechanisms Clinical features:- Charcot cholangitis triad:1. Abdominal pain (most commonly RUQ)2. High fever3. Jaundice (less common)- Reynolds pentad: Charcot cholangitis triad + hypotension and mental status changes- Possible septic shock Diagnostics:- Lab tests: Leukocytosis, ↑ CRP; signs of cholestasis (↑ bilirubin, ↑ ALP), often ↑ AST/ALT- Ultrasound (first imaging procedure): shows biliary dilation and/or evidence of an etiology (e.g., cholelithiasis)- CT scan- If there is high suspicion for acute cholangitis (e.g., Charcot triad present) → proceed directly to diagnostic and therapeutic ERCP Treatment:- Initial treatment: broad-spectrum antibiotics and supportive therapy- Biliary drainage and decompression→ ERCP is the treatment of choice, possibly in combination with: Sphincterotomy (for cholangitis due to cholelithiasis or choledocholithiasis) or stent placement (acute suppurative cholangitis)→ Percutaneous transhepatic cholangiography (PTC) if ERCP is unsuccessful or unavailable- Interval cholecystectomy if gallstones are present
• Primary sclerosing cholangitis Primary sclerosing cholangitis (PSC) is a progressive chronic inflammation of both the intrahepatic and extrahepatic bile ducts.  Epidemiology:- Sex: M > F (2:1)- Age: The median age at diagnosis is ∼ 40. Associations:- Chronic inflammatory bowel diseases (IBD)→ ∼ 90% of PSC patients have IBD→ However, only ∼ 5% of patients with UC and < 5% of patients with Crohn's disease develop PSC.- HLA-B8 and HLA-DR3- Other autoimmune conditions (e.g., hypergammaglobulinemia IgM) Clinical features:- Signs of cholestasis: Jaundice/scleral icterus, pruritus, fatigue- Acute cholangitis: fever, chills, right upper quadrant pain- Later stages: signs of cirrhosis (hepatomegaly, portal hypertension, liver failure) Diagnostics:- Lab tests: Perinuclear anti-neutrophil cytoplasmic antibodies (pANCA) are present in up to 80% of cases; ↑ ALP, GGT, conjugated bilirubin; Potentially, ↑ transaminases (however, usually < 300 U/L)- Magnetic resonance cholangiopancreatography (MRCP)- Following diagnosis → colonoscopy (to assess for UC)- Liver biopsy: If small-bile duct PSC is suspected. "Onion-skin" finding. Treatment:- Ursodeoxycholic acid and immunosuppressives (e.g., tacrolimus)- Treatment of pruritus (e.g., cholestyramine, rifampicin, naltrexone)- Liver transplantation is the only curative option Complications: Cholangiocarcinoma
• Primary biliary cirrhosis Epidemiology:- Sex: F > M (∼ 9:1)- Age range: 30-65 years- Most common cause of vanishing bile duct syndrome Clinical features:- Fatigue (usually the first symptom)- Marked generalized pruritus- Hepatomegaly, dull lower margin, RUQ discomfort, portal hypertension- Jaundice- Maldigestion (may involve manifestations of deficiency of fat-soluble vitamins, e.g., osteoporosis)- Xanthomas and xanthelasma- Common associations: sicca syndrome, autoimmune thyroid disease, CREST syndrome, rheumatoid arthritis Diagnostics:- Lab tests: ↑ Cholestasis parameters (ALP, γ-GT, conjugated bilirubin); transaminases (AST/ALT) are within normal limits or slightly elevated; ↑ antimitochondrial antibodies (AMA) (> 95%); ↑ ANA (up to 70%); ↑ IgM- Liver biopsy: Necessary for staging- Abdominal ultrasound or CT scan to rule out biliary obstruction Treatment:- First-line medical therapy: ursodeoxycholic acid (aka ursodiol, or UDCA)- Treatment of cholestatic pruritus- Liver transplantation necessary if liver cirrhosis is advanced
• Cholangiocarcinoma Risk factors:- Primary sclerosing cholangitis (most common risk factor)- Liver fluke infection (e.g., Clonorchis sinensis, Opisthorchis viverrini)- Choledocholithiasis- Chronic viral hepatitis (e.g., hepatitis B, hepatitis C)- Liver cirrhosis- Environmental toxin exposure (e.g., asbestos)- Congenital biliary tract abnormalities (e.g., choledochal cysts, congenital hepatic fibrosis) Clinical features:- Extrahepatic cholangiocarcinoma:→ Signs of cholestasis: jaundice, pale stools, dark urine, pruritus→ Abdominal pain and weight loss is usually a sign of late (unresectable) disease.→ Courvoisier sign- Intrahepatic cholangiocarcinoma→ Usually asymptomatic in early stages→ Nonspecific symptoms (e.g., weight loss, nausea, fever, weakness, fatigue)→ Dull abdominal pain (RUQ or epigastric) Diagnostics:- Tumor markers: ↑ AFP, ↑ CA 19-9 and ↑ CEA- Ultrasound: initial testing- MRI/MRCP (magnetic resonance cholangiopancreatography) or MDCT (multidetector computed tomography)- Endoscopic retrograde cholangiography (ERCP) Treatment:- Surgical- Palliative (90% of cases): Drainage stent, transarterial chemoembolization (TACE)
• Choledochal cysts Cystic dilatations of biliary tree involving either the extrahepatic or intrahepatic ducts, or both. - More common in women (4:1) Clinical features: epigastric pain, jaundice, fever, and RUQ mass Complications: cholangiocarcinoma (most feared complication – risk is about 20% over 20 years), hepatic abscess, recurrent cholangitis/pancreatitis, rupture, biliary obstruction, cirrhosis, and portal HTN Diagnostics:- Ultrasound is the best noninvasive test- ERCP is definitive for diagnosis Treatment: Complete resection of the cyst with a biliary-enteric anastomosis
• Bile duct stricture Etiology:- Iatrogenic injury (e.g., prior biliary surgery such as cholecystectomy, liver transplantation)- Recurring choledocholithiasis- Chronic pancreatitis- PSC Clinical features: those of obstructive jaundice Complications can be life-threatening: secondary biliary cirrhosis, liver abscess, and ascending cholangitis. Treatment:- Endoscopic stenting (preferred)- Surgical bypass if obstruction is complete or if endoscopic therapy fails
• Appendicitis - Lifetime risk: ∼ 8%- Peak incidence: 10-19 years of age Etiology: Obstruction of appendiceal lumen by- Lymphoid tissue hyperplasia- Fecalith- Less common: foreign bodies, worm infestations, intestinal infections, tumors (e.g., carcinoid tumor), hemolytic diseases Clinical features:- Progressive fever, anorexia, nausea, vomiting, diarrhea, and/or constipation- Initially, dull migratory periumbilical pain (due to visceral peritoneum irritation) - After 4-24 hours, sharp RLQ pain (due to parietal peritoneum irritation by a distended and inflamed appendix) with rebound tenderness- McBurney point tenderness- Rovsing's sign- Psoas sign- Obturator sign Diagnostics:- Inflammatory markers: ↑ CRP, mild leukocytosis (11,000-15,000 cells/μL) with left shift- Abdominal ultrasound: non-compressible and enlarged appendix (> 6-8 mm)→ Target sign → Wall thickening→ Edema surrounding the appendix→ Appendix not compressible→ In perforation → intra-abdominal free fluid- Abdominal CT scan Treatment:- Bowel rest (keep patient NPO), IV fluid therapy, and observation- Analgesia- Antibiotics with anaerobic and gram negative cover (e.g., cefazolin and metronidazole) - Appendectomy
• Acute pancreatitis Etiology:- Biliary pancreatitis (e.g., gallstones, constriction of the ampulla of Vater) ∼ 40% of cases- Alcohol-induced (∼ 30% of cases)- Idiopathic (∼ 15%–25% of cases)- Hypertriglyceridemia, hypercalcemia- Post-ERCP- Toxic drugs (e.g., steroids, azathioprine, sulfonamides, furosemide, estrogen, protease inhibitors, NRTIs)- Viral infections (e.g., coxsackievirus B, mumps)- Trauma- Autoimmune and rheumatological disorders (e.g., Sjögren's syndrome)- Pancreas divisum- Hereditary (e.g., mutation of the trypsinogen gene, cystic fibrosis) Clinical features:- Constant, severe epigastric pain → Classically radiating towards the back→ Worse after meals and when supine→ Improves on leaning forwards- Nausea, vomiting- Signs of shock: tachycardia, hypotension, oliguria/anuria- Possibly jaundice in patients with biliary pancreatitis- Abdominal tenderness, distention, guarding- Ileus with reduced bowel sounds and tympany on percussion- Ascites- Skin changes: Cullen's sign (perumbillical), Grey Turner's sign (flank), Fox's sign (ecchymosis over the inguinal ligament) Diagnostics:- Lipase ≥ 3 x the upper reference range, amylase (nonspecific)→ The enzyme levels are not directly proportional to severity or prognosis!- Tests to assess severity: Hematocrit (Hct), WBC count, blood urea nitrogen, ↑ CRP and procalcitonin levels, ↑ ALT- Tests to determine etiology: AP, bilirubin levels (evidence of gallstone pancreatitis), serum calcium levels, serum triglyceride levels- Ultrasound (most useful initial test)- CT scan: only when diagnosis is in doubt- MRCP and ERCP: when suspected biliary or pancreatic duct obstructions- X-ray: → Sentinel loop sign = dilatation of a loop of small intestine in the upper abdomen→ Colon cut off sign = gaseous distention of the ascending and transverse colon that abruptly terminates at the splenic flexure Treatment:- Fluid resuscitation: aggressive hydration with crystalloids - Analgesia: fentanyl or hydromorphone- Bowel rest (NPO) and IV fluids are recommended until the pain subsides- Begin enteral feeding as soon as the pain subsides- Fenofibrates: in hyperlipidemia-induced acute pancreatitis- Biliary pancreatitis: Urgent ERCP and sphincterotomy (within 24 hours) Prognosis: Ranson criteria are used to determine prognosis and mortality rates.
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• Pancreatitis - Complications 1. Pancreatic necrosis (may be sterile or infected)- Sterile pancreatic necrosis – infection may develop, but half of all cases resolve spontaneously. These patients should be monitored closely in an ICU. Prophylactic antibiotics are controversial but if necrosis involves more than 30% of pancreas, antibiotics should be strongly considered.- Infected pancreatic necrosis – has high mortality rate (results in multiple organ failure in 50% of cases); surgical débridement and antibiotics indicated.- The only way to distinguish sterile from infected necrosis is via CT-guided per-cutaneous aspiration with Gram stain/culture of the aspirate. 2. Pancreatic pseudocyst- Encapsulated fluid collection that appears 2 to 3 weeks after an acute attack – unlike a true cyst, it lacks an epithelial lining- Complications of untreated pseudocysts include rupture, infection, gastric outlet obstruction, fistula, hemorrhage into cyst, and pancreatic ascites. It may impinge on adjacent abdominal organs (e.g., duodenum, stomach, transverse colon) if large enough; or if located in the head of the pancreas, it may cause compression of the CBD.- Diagnosis: CT scan is the study of choice.- Treatment• Cysts < 5 cm: observation• Cysts > 5 cm: drain either percutaneously or surgically 3. Hemorrhagic pancreatitis- Characterized by Cullen sign, Grey Turner sign, and Fox sign- CT scan with IV contrast is the study of choice 4. Adult respiratory distress syndrome – a life-threatening complication with high mortality rate 5. Pancreatic ascites/pleural effusion – the most common cause is inflammation of peritoneal surfaces- Do not tap or drain 6. Ascending cholangitis – due to gallstone in ampulla of Vater, leading to infection of biliary tract 7. Pancreatic abscess (rare) – develops over 4 to 6 weeks and is less life-threatening than infected pancreatic necrosis
• Chronic pancreatitis Etiology:- Alcohol abuse (60-70% of cases, esp. men)- Pancreatic ductal obstruction (< 10%): strictures (e.g., due to trauma, stones)- Tobacco use- Idiopathic pancreatitis (20-30%)- Hereditary pancreatitis (∼1%): autosomal dominant inheritance (PRSS1 gene mutation), age of onset < 20 years- Autoimmune pancreatitis- Severe hypertriglyceridemia (levels > 1000 mg/dl)- Primary hyperparathyroidism (hypercalcemia)- Cystic fibrosis: ∼ 2% of cystic fibrosis patients develop chronic pancreatitis- Tropical pancreatitis: most common cause in the Tropics (esp. Southern India); young age at onset Clinical features:- Epigastric abdominal pain (main symptom)→ Pain radiates to the back, is relieved on bending forwards and exacerbated after eating→ Pain is initially episodic and becomes persistent as the disease progresses- Often associated with nausea and vomiting- Pancreatic insufficiency (after 90% of the pancreatic parenchyma is destroyed) → Steatorrhea (exocrine hormone deficiency)→ Malabsorption and weight loss→ Pancreatic diabetes (endocrine hormone deficiency) Diagnostics:- Abdominal CT (plain and contrast-enhanced): best initial imaging modality to screen for chronic pancreatitis- MRCP: indicated when CT findings are equivocal but clinical suspicion of CP is high- Abdominal x-ray- Ultrasound- Lipase and amylase not always elevated- Fecal elastase-1 activity (confirms that steatorrhea is due to pancreatic lipase insufficiency)→ Elastase-1 level < 200 μg/g → pancreatic exocrine insufficiency- 72-hour quantitative fecal fat estimation: Fecal fat > 7 g per day is diagnostic of steatorrhea- Genetics: in patients with family history, young patients → PRSS-1, CFTR gene Treatment:- Analgesics: NSAIDs, opioids for severe pain (e.g., long-acting fentanyl/morphine), low dose tricyclic antidepressants (e.g., amitriptyline)- Abstinence from alcohol and nicotine- Small, regular meals (rich in carbohydrates, low in fat)- Pancreatic enzyme replacement- Parenteral administration of fat-soluble vitamins (A, D, E, K) if necessary- Endocrine insufficiency: Insulin administration- Pancreaticojejunostomy: if cancer is suspected or in those with intractable pain Complications: - Pancreatic pseudocysts- Splenic vein thrombosis- Pancreatic ascites
• Pancreatic cancer Epidemiology:- Sex: M > F- Age of onset: 60-80 years- More common in African Americans Risk factors:- Smoking- Chronic pancreatitis- High alcohol consumption- Type 2 diabetes- Obesity- Exposure to chemicals used in the dry cleaning and metal working industries Inherited genetic syndromes (10% of pancreatic cancers): Familial pancreatic carcinoma, familial pancreatitis (mutations in the PRSS1 gene), Peutz-Jeghers syndrome, BRCA1 and BRCA2 mutations, HNPCC Clinical features:- Often no early signs present!- Belt-shaped epigastric pain which may radiate to the back- Jaundice- Courvoisier sign = enlarged gallbladder and painless jaundice- Pale stools, dark urine, and pruritus- Weight loss, nausea, weakness, poor appetite- Diarrhea (possibly steatorrhea secondary to exocrine pancreatic insufficiency)- Superficial thrombophlebitis (in 10% of cases, aka Trousseau syndrome or Thrombophlebitis migrans)- Thrombosis (e.g., phlebothrombosis, splenic vein thrombosis)- Impaired glucose tolerance (rarely) Diagnostics:- Tumor markers: CA 19-9 and CEA- First test: usually either contrast-enhanced abdominal CT or ultrasound → Double-duct sign- ERCP/MRCP: to rule out choledocholithiasis Pancreatic exocrine tumors (95%):- Mostly ductal adenocarcinoma- Less common: acinar adenocarcinoma Pancreatic endocrine tumors (neuroendocrine tumors/NET, < 5% of tumors):- Insulinomas (result in hypoglycemia)- Gastrinomas- Vasoactive intestinal peptide-producing tumors (VIPomas), pancreatic polypeptide-secreting endocrine tumors of the pancreas, glucagonomas, somatostatinomas Treatment:- Pancreatic head carcinoma: pancreaticoduodenectomy ("Whipple procedure")- Pancreatic body and tail carcinoma: Resection of the left side of the pancreas with splenectomy- Neoadjuvant or adjuvant chemoradiotherapy
• Gastrointestinal bleeding Upper gastrointestinal bleeding (70-80%): The source is located proximal to the ligament of Treitz. Lower gastrointestinal bleeding (20-30%): The source is located distal to the ligament of Treitz (usually in the colon). Etiology:Upper gastrointestinal bleeding:- Gastric or duodenal ulcers (∼ 30% of cases)- Erosive gastritis or duodenitis- Esophageal variceal hemorrhage- Dieulafoy lesion- Esophageal or gastric carcinoma- Mallory-Weiss syndromeLower gastrointestinal bleeding:- Diverticulosis (∼ 30% of cases)- Inflammatory bowel disease (IBD), ulcerative colitis, Crohn disease- Infectious diarrhea- Hemorrhoids- Ischemia (e.g., ischemic colitis, mesenteric ischemia)- Angiodysplasia- Colorectal and anal cancer- Colon polyps Clinical features:- Anemia due to chronic blood loss - Acute hemorrhage: signs of hypovolemic shock (tachycardia, hypotension, reduced viligance)- UGIB: Melena (black, tarry stool), hematemesis, hematochezia (indicates brisk bleeding)- LGIB: Hematochezia, helena, colonic bleeding (maroon, jelly-like traces of blood in stools), rectal bleeding (streaks of fresh blood on stools) Diagnostics:- Occult bleeding or hemodynamically stable hematochezia → colonoscopy → if negative, perform esophagogastroduodenoscopy (EGD)- Melena (more common with a UGI source of bleeding) → EGD → if negative, perform colonoscopy- Hemodynamically unstable hematochezia→ Consider nasogastric tube aspiration to differentiate upper from lower GI bleeding→ In the case of massive, life-threatening bleeding: angiography- If EGD and colonoscopy fail to locate the bleeding → evaluate small bowel bleeding or consider angiography for vascular etiologies (e.g., angiodysplasia)- Small bowel bleeding: Push enteroscopy, video capsule endoscopy, radionuclide scan Treatment:- General support: oxygen supplementation, IV substitution of fluids (no oral intake of food or fluids)- IV proton pump inhibitors- Prepare for blood transfusion (typing and cross-matching)- Emergency EGD: in the event of significant bleeding- Angiography: vasoconstriction via vasopressin- Surgery (laparotomy): if bleeding cannot be contained
• Esophageal cancer Risk factors:Adenocarcinoma- Gastroesophageal reflux: Barrett's esophagus- Obesity- Smoking- Achalasia- Localization: mostly in the lower ⅓ of the esophagusSquamous cell carcinoma (SCC)- Alcohol consumption- Smoking- Diet low in fruits and vegetables- Drinking hot beverages- Diverticula (e.g., Zenker's diverticulum)- Achalasia- Nitrosamines exposure (e.g., cured meat, fish, bacon)- Radiotherapy- Plummer-Vinson syndrome- Esophageal candidiasis- Localization: mostly in the upper ⅔ of the esophagus Clinical features:- Dysphagia- Weight loss- Retrosternal chest or back pain- Anemia- Less common: Hematemesis, melena, hoarseness Diagnostics:- Esophagogastroduodenoscopy (best initial and confirmatory test)- Barium swallow in case of severe stricture, suspected fistula- Staging: Transesophageal endoscopic ultrasound, chest and abdominal CT and/or PET Treatment:- Endoscopic submucosal resection for removal of superficial, epithelial lesions - Subtotal or total esophagectomy with gastric pull-through procedure or colonic interposition- Neoadjuvant chemoradiation- Palliative: Chemoradiation, stent placement
• Achalasia Etiology:- Primary achalasia (most common): cause is unknown- Secondary achalasia (pseudoachalasia): The presentation and manometric findings of a mechanical cause of obstruction (e.g., a malignancy) that mimics achalasia.→ E.g. Stomach cancer, esophageal cancer, Chagas disease, amyloidosis Clinical features:- Dysphagia to solids and liquids- Regurgitation- Retrosternal pain and cramps- Weight loss Diagnostics:- Barium esophagram: bird's beak- Upper endoscopy: to rule out pseudoachalasia- Manometry: Confirmatory test, irrespective of the initial image findings Treatment:- Low-surgical risk: Pneumatic dilation; Heller myotomy- High surgical risk: Botulinum toxin injection in the LES Complications:- Pulmonary complications (e.g., pneumonia, abscess, asthma) caused by aspiration- Megaesophagus- Increased risk of esophageal cancer
• Diffuse esophageal spasms Clinical features:- Dysphagia- Retrosternal chest pain: Squeezing type, occurs with eating- Regurgitation Diagnostics:1. Rule out MI with ECG and troponins2. Manometry→ Simultaneous multi-peak contractions→ High pressure contractions→ Intermittent normal peristalsis3. Esophagram: Corkscrew esophagus (pseudodiverticulosis) Treatment:- Avoid trigger foods- Medical: CCB, nitrates, anticholinergics- Endoscopic: Bougie dilation (severe dysphagia), botox injections- Surgery: long esophagomyotomy (for severe symptoms)
• Esophageal hiatal hernias Etiology:- Lax diaphragmatic esophageal hiatus: Advanced age, smoking, obesity, genetic predisposition (rare)- Prolonged periods of increased intra-abdominal pressure: Pregnancy, ascites, chronic cough, constipation Type I: Sliding hiatal hernia- Most common type (95% of cases)- The GEJ and the gastric cardia slide up into the posterior mediastinum.- The gastric fundus remains below the diaphragm.Type II: Paraesophageal hiatal hernia- Part of the gastric fundus herniates into the thorax.- The GEJ remains in its anatomical position below the diaphragm.- Upside-down stomach (extreme type): A rare type of paraesophageal hernia in which the entire stomach herniates into the thoracic cavity and rotates on its organoaxial axis. It is associated with a high mortality and morbidity rate due to strangulation of the stomach. Clinical features:- Type I: symptoms of GERD- Type II: Epigastric/substernal pain, early satiety, retching, symptoms of GERD- Saint's triad: A combination of cholelithiasis, diverticulosis, and hiatal hernia may occur in ∼ 1.5% of patients. Diagnostics:- Barium swallow: most sensitive test- Endoscopy: used to diagnose hiatal hernia and evaluate for possible complications Treatment:- Conservative management: Lifestyle modifications; PPIs or H2R-antagonists if symptoms of GERD occur- Surgery: laparoscopic/open fundoplication + hiatoplasty- Type II hernias can become strangulated and should be repaired surgically. Complications:- Sliding hiatal hernias (type I): GERD (most common), reflux esophagitis (with risk of Barrett esophagus/cancer), aspiration- Paraesophageal hernias (type II): potentially life-threatening; include obstruction, hemorrhage, incarceration, and strangulation.
• Mallory-Weiss syndrome Longitudinal mucous membrane tears (limited to the mucosa and submucosa) at the gastroesophageal junction. Precipitating factors:- Severe vomiting- Blunt abdominal trauma- Strained defecationPredisposing conditions:- Alcoholism- Bulimia nervosa- Hiatal hernia (higher pressure gradient)- Gastroesophageal reflux disease (GERD) Clinical features:- Epigastric or back pain- Hematemesis- Possible shock with massive hemorrhage Diagnostics: Esophagogastroduodenoscopy Differential diagnosis:1. Boerhaave syndrome2. Esophagitits3. Esophageal ulcers Treatment:- Control of precipitating factors (e.g., omeprazole for GERD), inpatient monitoring- Most cases (90%) stop bleeding spontaneously- If actively bleeding patient: esophagogastroduodenoscopy→ Therapeutic injection of an adrenaline solution or a fibrin sealant→ Electrocoagulation→ Endoscopic band ligation- Second-line treatment: angiography (embolization, vasopressin infusion)
• Plummer-Vinson syndrome Triad of:1. Upper esophageal webs 2. Dysphagia3. Iron deficiency anemiaOther: Koilonychia (spoon-shaped fingernails), atrophic oral mucosa 10% of patients develop SCC of the oral cavity, hypopharynx, or esophagus Treatment: esophageal dilatation; correct nutritional deficiency.
• Schatzki ring A circumferential ring in the lower esophagus that is always accompanied by a sliding hiatal hernia. Etiology:- Ingestion of alkali, acids, bleach, or detergents (e.g., in suicide attempts). Clinical features:- Usually asymptomatic- Episodic (months in between) dysphagia with odynophagia- Only large diameter foods get stuck ("Steakhouse dysphagia") Diagnostics:- Barium swallow: Narrowed lumen- EGD: Definitive diagnosis Treatment:- If symptomatic (but no reflux), consider esophageal dilatation- If the patient has reflux, consider antireflux surgery- Esophagectomy if full-thickness necrosis has occurred- Steroids and antibioticsComplications: stricture formation and risk of esophageal cancer.
• Esophageal diverticula Localization:- Upper esophageal diverticulum→ Pharyngoesophageal diverticulum→ Most common type: Zenker's diverticulum at Killian's triangle- Middle esophageal diverticulum: diverticulum at the tracheal bifurcation- Lower esophageal diverticulum: epiphrenic diverticulum Clinical features:- Dysphagia (most common)- Regurgitation of undigested food- Aspiration- Coughing after food intake- Retrosternal pressure sensation and pain- Halitosis - Weight loss - Neck mass Diagnostics:- Barium swallow (best confirmatory test) with dynamic continuous fluoroscopy - Endoscopy: to rule out malignancy Treatment:- Zenker's diverticulum: cricopharyngeal myotomy- Epiphrenic diverticula: esophagomyotomy
• Peptic ulcer disease Etiology:- H. pylori→ Duodenal ulcers: up to 90% are due to H. pylori infection→ Gastric ulcers: up to 80% are due to H. pylori infection- Chronic gastritis of other etiology - Long-term use of NSAIDs, glucocorticoids- Smoking, alcohol consumption- Age > 65 years- Stress - Zollinger-Ellison syndrome (gastrinoma) Clinical features:- Dyspepsia: postprandial heaviness, early satiety, and gnawing, aching or burning epigastric pain- Pain relief with antacids- Potential signs of internal bleeding (anemia, hematemesis, melena)- ∼ 70% of patients with PUD are asymptomatic- Gastric ulcer: Pain increases shortly after eating → weight loss- Duodenal ulcer: Pain on an empty stomach that is relieved with food intake → weight gain Diagnostics:- ≤ 60 years of age without alarm features: Urea breath test for H. pylori- > 60 years of age or presence of ≥ 1 alarm features: EGD with biopsies and rapid urease testing for H. pylori Treatment:- H. pylori positive → amoxicillin + clarithromycin + PPI and supportive treatment → continue PPIs for 4-8 weeks → follow-up- H. pylori negative → PPI and supportive treatment for 4-8 weeks → follow-up- Surgical treatment: If refractory, cancer is suspected, complications occur Complications:- Perforation- Bleeding- Subhepatic abscess- Gastric outlet obstruction
• Gastroesophageal reflux disease Risk factors/associations:- Lifestyle habits such as smoking, caffeine and alcohol consumption- Stress - Obesity - Pregnancy- Diaphragm dysfunction- Angle of His enlargement (> 60°) - Iatrogenic (e.g., after gastrectomy)- Gastrointestinal malformations and tumors: gastric outlet obstruction, gastric cardiac carcinoma- Scleroderma - Sliding hiatal hernia: ≥ 90% of patients with severe GERD Clinical features:- Retrosternal burning pain (heartburn) that worsens while lying down (e.g., at night) and after eating- Pressure sensation in the chest- Belching, regurgitation- Dysphagia- Chronic non-productive cough and nocturnal cough - Halitosis Diagnostics:- If GERD is clinically suspected and there are no indications for endoscopy → empiric therapy – lifestyle modifications and short trial with PPIs should be initiated- No response → Esophagogastroduodenoscopy (EGD) + Biopsy- Esophageal pH monitoring: Before surgical treatment- Esophageal manometry Differential diagnosis:- Pill-induced esophagitis- Infectious esophagitis- Caustic esophagitits- Eosinophilic esophagitis Treatment:- Lifestyle modifications: → Dietary: Small portions; avoid eating (< 3 hours) before bedtime; Avoid foods with high fat content → Physical: Normalize body weight; elevate the head of the bed for patients with nighttime symptoms→ Avoid toxins: nicotine, alcohol, coffee, and certain drugs (e.g., calcium channel blockers, diazepam)- Treatment of choice: Standard-dose of PPI for at least 8 weeks (once daily therapy)→ No response: further diagnostic evaluation→ Partial response: increase the dose (to twice daily therapy) or switch to a different PPI→ Good response: discontinue PPI after 8 weeks- Surgical: Fundoplication Complications:- Reflux esophagitis- Esophageal stricture- Barrett esophagus- Schatzki's ring- Aspiration
• Acute gastritis Etiology:- NSAIDs/aspirin- H. pylori infection- Alcohol, smoking, caffeine- Extreme physiologic stress (e.g., shock, sepsis, burns) Clinical features:- Hematemesis (coffee-ground appearance or bright red in color), possibly melena- Epigastric pain is possible - Nausea, vomiting- Abdominal paresthesia and dyspepsia Treatment:- Empiric therapy with acid suppresion: PPIs, antacids, sucralfate, or H2-receptor blockers- If there is no positive response after 4 to 8 weeks of treatment → Esophagogastroduodenoscopy and ultrasound (to rule out gallstones), and test for H. pylori infection → Helicobacter pylori eradication therapy
• Chronic gastritis Etiology:- H. pylori infection (> 80% of cases)- Autoimmune gastritis Clinical features:- Mostly asymptomatic- Epigastric pain- Dyspepsia- Nausea and vomiting Diagnostics:- Esophagogastroduodenoscopy and biopsy- Helicobacter pylori diagnostics Treatment:- H. pylori eradication with triple therapy Complications:- Peptic ulcer disease- Gastric carcinoma- Mucosa-associated lymphoid tissue lymphoma
• Gastric cancer Epidemiology:- Peak incidence: 70 years- High incidence in South Korea and Japan Etiology:- Atrophic gastritis- H. pylori infection: ↑ risk of intestinal gastric cancer but not with diffuse gastric cancer- Gastric ulcers- Partial gastrectomy- Adenomatous gastric polyps- Menetrière disease- Diet rich in nitrates and/or salts (e.g., dried, preserved food) - Alcohol and nicotine use- Low socioeconomic status- Hereditary factors (positive family history, hereditary non‑polyposis colorectal cancer)- Blood type A Clinical features:- General signs: Weight loss, chronic iron deficiency anemia (paleness, fatigue, headaches)- Abdominal pain- Early satiety- Nausea or vomiting- Dysphagia- Acute gastric bleeding (hematemesis or melena)- Late-stage: Gastric outlet obstruction, Virchow's node, Sister Mary Joseph's node, acanthosis nigricans Diagnostics:- Upper endoscopy with biopsy (best initial test)- Lab tests: Iron deficiency anemia, serologic tests- Staging: Abdominal ultrasound, endosonography, CT-scan Lauren classification: Intestinal type (~ 50%), diffuse type (~ 40%), mixed type (~ 10%) Treatment: Depending on staging and type of tumor- Endoscopic resection- Surgery (Roux-en-Y gastric bypass)- Perioperative chemotherapy, sometimes radiotherapy- Trastuzumab is indicated for HER2+ gastric adenocarcinomas
• Gastric MALToma - Peak incidence: 7th and 8th decades Etiology:- Association with H. pylori Clinical features:- Present similarly to peptic ulcer disease and gastritis- Abdominal pain- Melena, hematemesis, potentially anemia- Fatigue, weight loss Diagnostics:- Blood analysis: anemia- Histopathology and immunohistochemistry: markers of B-cell lymphoma (e.g., CD20)- Imaging: CT, MRI for tumor staging- Upper gastrointestinal (UGI) endoscopy with biopsy Treatment:- First-line: H. pylori eradication therapy→ Should be performed even if patient tests negative→ Eradication of H. pylori is curative in up to 90% of low-malignant gastric MALTomas- If H. pylori eradication therapy fails → radiotherapy or chemotherapy- Surgery: gastric resection only necessary if complications (e.g., perforation, bleeding, obstruction) occur.
• Small bowel obstruction Etiology:- Adhesions (e.g., postoperative, prior abdominal surgery)- Incarcerated hernia- Malignant tumors or metastases- Strictures (e.g., Crohn's disease, congenital, radiation enteritis)- Foreign body- Superior mesenteric artery syndrome = SMA passes in close proximity anterior to the third segment of the duodenum- Additional causes in children: Congenital intestinal atresia, pyloric stenosis, intussusception Clinical features:- Proximal: Nausea and vomiting (worse with food intake, may be bilious) with early discontinuation of PO intake, late-onset obstipation- Distal: late-onset vomiting, possible fecal vomiting- Constipation or obstipation with abdominal distention (tympanic abdomen)- Abdominal pain/discomfort: vague or periumbilical cramping, colicky pain (corresponding to peristalsis)- Mechanical bowel obstruction: increased high-pitched, tinkling bowel sounds- Closed loop obstruction: lumen occluded at two points; can lead to ischemia requiring emergency surgery Diagnostics:- Abdominal x-ray (initial test): dilated loops of small bowel, air-fluid levels proximal to the obstruction, and minimal gas in colon- CT abdomen with IV and oral contrast- Barium or gastrografin enema- Lab tests: Leukocytosis, blood gas analysis, ↑ serum lactate, electrolyte imbalance (e.g., hypokalemia, hypochloremia) Treatment:- Conservative – appropriate if partial obstruction, complete obstruction with no signs of ischemia/necrosis (leukocytosis, metabolic acidosis, persistent pain) or clinical deterioration (fever, tachycardia)→ Nasogastric tube for intestinal decompression→ Fluid resuscitation, electrolyte correction→ Bowel rest (NPO)→ Antibiotics: If perforation is suspected- Surgery – if complete obstruction with the above signs of ischemia/necrosis or clinical deterioration, persistent partial obstruction (>3-5 days), suspected intestinal strangulation
• Paralytic ileus Etiology:- Intra-abdominal surgery or trauma (e.g., laparotomy, retroperitoneal hemorrhage)- Medication (e.g., anticholinergics, opioids, antidepressants)- Electrolyte disturbances (e.g., hypokalemia)- Neurosurgical procedures (e.g., spinal surgery)- Vascular (e.g., mesenteric infarct)- Inflammation of intra-abdominal organs (e.g., appendicitis, cholecystitis) and peritonitis- Endocrine (e.g., diabetes mellitus, hypothyroidism, porphyria, uremia) Diagnostics:- Abdominal x-ray: Uniform distribution of gas in the small bowel, colon, and rectum (in contrast to small bowel or colonic obstruction)- Abdominal ultrasound: absent peristalsis- Lab tests: ↑ inflammatory markers Treatment:- IV fluids- NPO- Correction of electrolyte imbalances (especially hypokalemia)- Nasogastric suction- Placement of a long tube if ileus persists postoperatively

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