USMLE Step 3 (Subject) / Gastroenterology (Lesson)

First Aid Step 3

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• Dysphagia – Differential Difficulty swallowing with solids alone:- Lower esophageal ring (Schatzki's ring): Characterized by intermittent symptoms or sudden obstruction with a food bolus ("steakhouse syndrome") due to a ring located at the gastroesophageal junction.- Zenker's diverticulum: Outpouching of the upper esophagus. Presents with foul-smelling breath and food regurgitation as well as with difficulty initiating swallowing.- Plummer-Vinson syndrome: Cervical esophageal web and iron-deficiency anemia. Associated with esophageal cancer.- Peptic stricture: Progressive symptoms with long-standing heartburn.- Carcinoma: Progressive symptoms in an older patient, often with weight loss.- Esophagitis: Inflammation can be 2° to a number of causes:→ Gastroesophageal reflux: Reflux of acid and stomach contents through the lower esophageal sphincter.→ Pill esophagitis: Usually caused by taking a pill with little or no fluid before lying down. Common medications include doxycycline, NSAIDs, and bisphosphonates.→ Opportunistic infections: Candida, HSV, and CMV. Usually occur in immunocompromised patients (e.g., HIV, chemotherapy).→ Eosinophilic esophagitis: Chronic inflammatory disease mediated by IL-5. Usually found in young men with a history of respiratory allergies. Thirty percent of cases have peripheral eosinophila. If difficulty is with both solids and liquids:- Achalasia: Progressive symptoms that worsen at night with no heartburn. Presents with a "bird's beak" on barium swallow.- Esophageal spasm: Intermittent symptoms with chest pain. Triggered by acid, stress, and hot and cold liquieds. Diagnosed by esophageal manometry; presents with "corkscrew esophagus" on barium swallow.- Scleroderma: Progressive symptoms with heartburn and Raynaud’s phenomenon. Patients have lower esophageal pressure and aperistalsis of the distal esophagus leading to reflux (CREST syndrome: Calcinosis cutis, Raynaud’s phenomenon, Esophageal dysmotility, Sclerodactyly, and Telangiectasia)
• Esophageal stricture Most common sequela of reflux esophagitis   Clinical features: cause solid food dysphagia Diagnostics:- Barium esophagram (best initial test): narrowing of the esophagus at the gastroesophageal junction- Endoscopy with biopsies: to rule out malignancy and eosinophilic esophagitis Treatment:- First-line treatment: dilation with bougie dilator/balloon dilator + proton pump inhibitors in patients with reflux  - In refractory cases (multiple recurrences): steroid injection prior to dilation, endoscopic electrosurgical incision- Recurrence occurs in the majority of patients; often multiple treatment attempts necessary
• Peptic ulcer disease Epidemiology:- Incidence: > 6 million cases annually in the US - Duodenal ulcers are 3 times more common than gastric ulcers.- Duodenal ulcers occur on average 10-20 years earlier than gastric ulcers. Risk factors:- 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: risk increases 5-fold- Long-term use of NSAIDs plus glucocorticoids: risk increases 10 to 15-fold! - SSRIs- Smoking, alcohol consumption- Patients with blood type O have a higher risk for duodenal ulcers  - Age > 65 years- Stress - Rare: hyperparathyroidism, Zollinger-Ellison syndrome (gastrinoma) Clinical symptoms:- 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 Diagnosis:- ≤ 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 → eradication therapy (with antibiotics and a PPI) → continue PPIs for 4-8 weeks → follow-up with fecal antigen test- H. pylori negative → medical acid suppression (with a PPI) for 4-8 weeks → follow-up with fecal antigen test
• Irritable bowel syndrome (IBS) Clinical features:- Abdominal pain→ Frequency, intensity, and localization generally vary widely from patient to patient→ Typically alleviated by defecation  - Altered bowel habits: diarrhea and/or constipation  - Other gastrointestinal symptoms→  Nausea, reflux, early satiety→ Passing of mucus, abdominal bloating- Extraintestinal symptoms→ Generalized somatic symptoms (e.g., pain or fatigue, as in fibromyalgia)→ Disturbed sexual function→ Dysmenorrhea→ Increased urinary frequency and urgency Rome IV criteria for irritable bowel syndrome: Recurrent abdominal pain on average at least 1 day per week during the previous 3 months that is associated with 2 or more of the following:- Pain related to defecation- Change in stool frequency- Change in stool form or appearance Treatment:- Dietary adjustments: Plenty of fluid, high‑fiber foods- Symptom-directed:- Diarrhea → Antidiarrheals (loperamide)  - Constipation→ Soluble fibers/bulk‑forming laxatives (psyllium)→ Osmotic laxatives (polyethylene glycol)→ Lubiprostone (chloride channel activator)  - Cramping/pain→ Antispasmodics (dicyclomine, hyoscyamine)  → Tricyclic antidepressants (e.g., amitriptyline, nortriptyline)  
• Celiac disease Epidemiology:- Bimodal distribution:→ At 8-12 months (or 2-3 months following the first exposure to gluten through diet containing wheat)→ Third to fourth decade of life- More common in individuals of northern European descent Etiology:- Genetic predisposition HLA-DQ2 (90-95%) and HLA-DQ8 (5-10%)- Consuming gliadin from grains such as wheat, rye, and barley leads to an autoimmune reaction within the small intestinal wall. Gastrointestinal symptoms:- Chronic or recurring diarrhea: steatorrhea- Flatulence, abdominal bloating, and pain- Nausea/vomiting- Lack of appetite- Constipation (rarely) Extraintestinal symptoms and associations:- Malabsorption symptoms: fatigue, weight loss, vitamin deficiency, iron deficiency anemia, osteoporosis, hypocalcemia- In children: failure to thrive, growth failure, delayed puberty- Dermatologic associations: dermatitis herpetiformis- Neuropsychiatric symptoms: peripheral neuropathies (numbness, burning and tingling of the hands and feet), headache, ataxia, depression, irritability - Gynecological associations: reduced fertility or infertility  - Endocrine associations: autoimmune thyroid disease, type 1 diabetes mellitus- Associated chromosomal syndromes: Turner syndrome, Down syndrome- Other associated conditions: autoimmune hepatitis, inflammatory bowel disease, rheumatoid arthritis, sarcoidosis, selective IgA deficiency Diagnostics:- Gold standard: IgA (anti‑)tissue transglutaminase antibody (tTG)- IgG deamidated gliadin peptide (DGP): for children under the age of 2- Anti-endomysial antibody (EMA)  - Confirmatory test: Endoscopy with small intestine biopsy Complications:- Malabsorption- Secondary lactase deficiency- Enteropathy-associated T-cell lymphoma (EATL)
• Tropical sprue A disease characterized by chronic diarrhea with subsequent malabsorption in association with a stay in the tropics or subtropics. Epidemiology: occurs in residents of the tropics and subtropics or in travelers returning from these areas (after trips lasting several weeks) Etiology: most likely caused by a bacterial infection that leads to structural damage of the intestinal mucosa   Clinical findings:- Chronic diarrhea with steatorrhea- Abdominal cramps- Progressive weight loss- Fatigue- Clinical features of malabsorption Diagnostics:- Blood tests: megaloblastic anemia, hypoalbuminemia, hypocalcemia, vitamin D deficiency- Serology for antibodies to rule out celiac disease- Stool analysis→ Fecal fat 10–40 g/d  → Rule out infection with pathogens (e.g., Giardia lamblia, Entamoeba histolytica)- Endoscopy of the small bowel and biopsy: villous atrophy, elongated crypts, presence of inflammatory cells (plasma cells, lymphocytes, eosinophils) Treatment: tetracycline in combination with folic acid for 3-6 months
• Whipple disease Definition: infection with the bacteria Tropheryma whipplei Epidemiology: very rare, mainly males 30-60 years of age Clinical features:- Intestinal manifestations: malabsorption syndrome, abdominal pain- Extraintestinal manifestations: enteropathic arthritis (60% of cases), sacroiliitis (40% of cases), fever, polyserositis, lymphadenopathy, cardiac symptoms (e.g., valve insufficiencies), and neurological conditions (myoclonia, ataxia, impairment of oculomotor function) Diagnostics:- Small intestine biopsies: detection of PAS-positive macrophages- PCR testing and immunohistochemistry staining- If neurological complaints occur → liquor diagnostics, potentially MRI Treatment:- IV ceftriaxone for 2 weeks- Maintenance treatment with oral trimethoprim-sulfamethoxazole for 1 year; Whipple disease is lethal if left untreated!
• Upper gastrointestinal bleeding Most common etiologies: Peptic ulcer disease, gastritis, varices, Dieulafoy lesion, Mallory-Weiss syndrome Clinical features:- May present with dizziness, lightheadedness, weakness, and nausea- Melena (black, tarry stool)  - Hematemesis  - Hematochezia: indicates brisk bleeding; may cause severe blood loss with hemodynamic instability- Acute hemorrhage: signs of circulatory insufficiency or hypovolemic shock→ Tachycardia→ Hypotension (dizziness, collapse, shock)  → Reduced vigilance Diagnostics:- Check hematocrit (may be normal in acute blood loss), platelet count, PT/PTT, and LFTs. ↑ BUN indicates digestion of blood.- Hematemesis or melena → EGD → if negative, perform colonoscopy- Nasogastric tube aspiration→ Can be considered if suspicion of UGIB is only low to moderate→ Bright red blood or coffee-ground material is indicative of UGI source- If EGD and colonoscopy fail to locate the bleeding → evaluate small bowel bleeding Treatment:- General support: nasal cannula oxygen supplementation, IV substitution of fluids (no oral intake of food or fluids)- Consider elective intubation in patients with altered mental or respiratory state and severe, ongoing hematemesis- IV proton pump inhibitors  - Prepare for blood transfusion (typing and cross-matching)   - Treat variceal bleeds with octreotide, PPIs, endoscopic sclerotherapy, or band ligation. If the bleed is severe, balloon tamponade is appropriate, followed by embolization, transjugular intrahepatic portosystemic shunt (TIPS), or a surgical shunt if endoscopic therapy fails.- For PUD, use PPIs, endoscopic epinephrine injection, thermal contact, and ligation with clip placement. Begin H pylori eradication measures. - Mallory-Weiss tears usually stop bleeding spontaneously.- Treat esophagitis/gastritis with PPIs. Avoid aspirin and NSAIDs.
• Lower gastrointestinal bleeding Most common etiologies: Hemorrhoids, diverticulosis, angiodysplasia, carcinoma, IBD, polyps, ischemic colitis, infectious colitis, postpolypectomy bleeding, and Meckel's diverticulum. Clinical features:- Hematochezia  - Melena  - 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 using push enteroscopy, video capsule endoscopy, radionuclide scan (RBCs labeled with technetium 99)  
• Acute pancreatitis Etiology:- Biliary pancreatitis (e.g., gallstones, constriction of the ampulla of Vater) ∼ 40% of cases  - Alcohol-induced (∼ 30% 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- General physical examination→ Signs of shock: tachycardia, hypotension, oliguria/anuria  → Possibly jaundice in patients with biliary pancreatitis- Abdominal examination→ Abdominal tenderness, distention, guarding  → Ileus with reduced bowel sounds and tympany on percussion→ Ascites- Skin changes (rare)  → Cullen's sign: periumbilical ecchymosis and discoloration (bluish-red)  → Grey Turner's sign: flank ecchymosis with discoloration  → Fox's sign: ecchymosis over the inguinal ligament Diagnostics:- Tests to confirm clinical diagnosis→ ↑ Serum pancreatic enzymes  → Lipase: if ≥ 3 x the upper reference range → highly indicative of acute pancreatitis→ Amylase (nonspecific)  The enzyme levels are not directly proportional to severity or prognosis!  - Tests to assess severity→ Hematocrit (Hct): Should be conducted at presentation as well as 12 and 24 hours after admissions↑ Hct (due to hemoconcentration) indicates third space fluid loss and inadequate fluid resuscitation↓ Hct indicates the rarer acute hemorrhagic pancreatitis→ WBC count  → Blood urea nitrogen  → ↑ CRP and procalcitonin levels  → ↑ ALT  - Tests to determine etiology→ Alkaline phosphatase, bilirubin levels (evidence of gallstone pancreatitis)→ Serum calcium levels→ Serum triglyceride levels (fasting) - Ultrasound (most useful initial test): indicated in all patients with acute pancreatitis- CT scan: not routinely indicated- MRCP and ERCP Treatment:- Fluid resuscitation: aggressive hydration with crystalloids (e.g., lactated Ringer's solution, normal saline)  - Analgesia: IV opioids (e.g., fentanyl)- Bowel rest (NPO) and IV fluids are recommended until the pain subsides  - Nasogastric tube insertion: not routinely recommended; indicated in patients with vomiting and/or significant abdominal distention-  Nutrition  → Begin enteral feeding (oral/nasogastric/nasojejunal) as soon as the pain subsides  → Total parenteral nutrition: only in patients who cannot tolerate enteral feeds (e.g., those with persistent ileus and abdominal pain)  - Analgesics: fentanyl or hydromorphone; consider pump administration (patient controlled analgesia = PCA)- Fenofibrates: in hyperlipidemia-induced acute pancreatitis- Biliary pancreatitis→ Urgent ERCP and sphincterotomy (within 24 hours): in patients with evidence of choledocholithiasis and/or cholangitis; followed by cholecystectomy→ Cholecystectomy (preferably during same admission once the patient is stabilized; or within 6 weeks): in all patients with biliary pancreatitis  
• Pancreatitis – Complications Bacterial superinfection of necrotic tissue → fever- Diagnosis: CT-guided percutaneous drainage + culture of the aspirate- Treatment: surgical debridement, antibiotics- High mortality rate; multiple organ failure in ∼ 50% of cases Pancreatic pseudocysts Pancreatic abscess- Walled-off infected necrotic tissue or pancreatic pseudocyst; typically develops > 4 weeks after an attack of acute pancreatitis- Abdominal CT: visible contrast-enhanced abscess capsule with evidence of fluid (pus)- Ultrasound: complex cystic, fluid collection with irregular walls and septations- Treatment: cannulation and drainage; necrosectomy if other measures are not effective Pleural effusion   Abdominal compartment syndrome Blood vessel erosion with bleeding   Systemic:- SIRS, sepsis, DIC- Pneumonia, respiratory failure, ARDS- Shock- Prerenal failure due to volume depletion- Hypocalcemia- Pleural effusion, pancreatic ascites- Paralytic ileus
• Pancreatitis – Indicators of severity - Age > 55- Gastrointestinal bleeding- Abnormal hematocrit within 48 hours→ Acute hemorrhagic pancreatitis: ↓ Hct→ Third space fluid loss: ↑ Hct- Hypocalcemia and/or hyperglycemia- Inflammatory markers: ↑↑ CRP, ↑ IL-6, ↑ IL-8- Evidence of shock and/or organ failure→ ↑ AST, ↑ ALT→ ↑ BUN, creatinine→ ↑ LDH→ ABG: pO2 < 60 mmHg, metabolic acidosis with a base deficit > 4 mmol/L- CT findings: pancreatic edema, peripancreatic fluid collection, and/or necrosis of > 33% of the pancreas
• 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 > 1000mg/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: Late manifestation (after 90% of the pancreatic parenchyma is destroyed)  → Steatorrhea (exocrine hormone deficiency)→ Cramping abdominal pain, bloating, diarrhea, weight loss→ May cause fat-soluble vitamin deficiencies (A, D, E, and K)→ Malabsorption and weight loss  → Pancreatic diabetes (endocrine hormone deficiency) Diagnostics:- Abdominal CT (plain and contrast-enhanced): best initial imaging modality to screen for CP→ Findings: pancreatic atrophy, pancreatic ductal dilations; pancreatic ductal calcifications on plain CT (more sensitive than x-ray); “chain of lakes” appearance  → MRCP: indicated when CT findings are equivocal but clinical suspicion of CP is high  - Ultrasound- Serum pancreatic enzyme levels: lipase (specific) and amylase (non-specific): often normal- Pancreatic function test: Fecal elastase-1 (FE-1) activity: confirms that steatorrhea is due to pancreatic lipase insufficiency.  → Elastase-1 level < 200 μg/g → pancreatic exocrine insufficiency→ Elastase-1 level < 100 μg/g → severe pancreatic exocrine insufficiency- Genetic testing Treatment:- Abstinence from alcohol and nicotine- Small, regular meals (rich in carbohydrates, low in fat), supplementation with medium-chain triglycerides (MCT)- Pancreatic enzyme replacement (with meals)  - Parenteral administration of fat-soluble vitamins (A, D, E, K) if necessary- Endocrine insufficiency: Insulin administration- Analgesics: NSAIDs, opioids for severe pain (e.g., long-acting fentanyl/morphine), low dose tricyclic antidepressants (e.g., amitriptyline)
• Pancreatic pseudocysts Encapsulated collection of pancreatic fluid which develops 4 weeks after an acute attack of pancreatitis; can occur in both acute and chronic pancreatitis   Pathophysiology: pancreatic secretions leak from damaged ducts → inflammatory reaction of surrounding tissue → encapsulation of secretions by granulation tissue Clinical features:- Often asymptomatic- Painless abdominal mass- Pressure effects→ Gastric outlet obstruction (early satiety, non-bilious vomiting, abdominal pain)→ Obstruction of the distal duodenum (bilious vomiting)→ Results in steatorrhea→ Bile duct obstruction with jaundice Diagnostics: abdominal ultrasound/CT/MRI → extrapancreatic fluid collection within well-defined wall/capsule, no solid cyst components detectable Treatment: Surgical/endoscopic cystogastrostomy/cystoduodenostomy/cystojejunostomy; ultrasound/CT-guided percutaneous drainage Complications- Infection → fever, abdominal pain, sepsis- Rupture → pancreatic ascites/pancreaticopleural fistula  - Erosion into an abdominal vessel with hemorrhage into the cyst → sudden abdominal pain, signs of hemorrhagic shock  
• Splenic vein thrombosis Can occur in 10% of patients with chronic pancreatitis Pathophysiology: inflammation of the splenic vein  → thrombus formation → left-sided portal hypertension → gastric varices   Clinical features: can present with upper GI bleeding, ascites, and splenomegaly Diagnosis: ultrasound with doppler, CT/MR angiography Treatment:- Acute: anticoagulation and/or thrombectomy- Chronic and symptomatic: splenectomy
• Acute cholecystitis Cholelithiasis (most common) or biliary sludge → inflammation of gallbladder wall Clinical features:- RUQ pain- Fever- Murphy sign Diagnostics:- Lab findings: ↑ WBC, CRP- US: gallbladder wall thickening and/or edema (double wall sign)- HIDA scan if diagnosis uncertain Treatment:- Supportive care, analgesics- IV antibiotics- Cholecystectomy (timing depends on severity)- For patients who are not candidates or surgery, consider a percutaneous biliary drain.
• Acute cholangitis Choledocholithiasis → obstruction and stasis within the biliary tract → subsequent bacterial infection Clinical features:- Charcot triad: RUQ pain, fever, jaundice- Reynold pentad: Charcot cholangitis triad PLUS hypotension and mental status changes Diagnostics:- ↑ WBC and CRP- ↑ ALP- ↑ AST, ALT- ↑ Total bilirubin- US: biliary dilation and/or evidence of obstruction (e.g., cholelithiasis)- MRCP if diagnosis uncertain Treatment:- Supportive care, analgesics- IV antibiotics- Urgent biliary decompression (e.g., ERCP)- Interval cholecystectomy if gallstones are present or concurrent cholecystitis
• Hepatitis Clinical symptoms:- In acute cases, patients may present with anorexia, nausea, vomiting, malaise, and ever but are requently asymptomatic.- Exam is often normal but may reveal an enlarged and tender liver, dark urine, and jaundice. Differential:- With a high level of transaminase elevation (> 10-20 times the upper limit of normal), consider acute viral infection as well as ischemia (“shock liver”), acute choledocholithiasis, autoimmune hepatitis, or toxins (acetaminophen).- With moderate transaminase elevation, consider the most common cause, nonalcoholic fatty liver disease. Also consider chronic viral infection, mononucleosis, CMV, 2° syphilis, drug-induced illness, alcohol, Budd-Chiari syndrome, hemochromatosis, celiac disease, IBD, right-sided heart failure, and muscle damage (eg, rhabdomyolysis).
• Cirrhosis Etiology:- Hepatotoxicity→ Long-standing alcohol abuse→ Medications (e.g., acetaminophen, amiodarone or chemotherapy drugs such as methotrexate)→ Ingesting aflatoxin created by Aspergillus- Inflammation→ (Chronic) viral hepatitis B, C, and D→ Primary biliary cirrhosis  → Primary sclerosing cholangitis→ Autoimmune hepatitis→ Parasitic infections (e.g., schistosomiasis, leishmaniasis, malaria)  - 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)Alcoholic liver disease, Hepatitis C, and NASH are the most common causes of cirrhosis in the US. Classification: Child-Pugh score Clinical features:- Fatigue, malaise, weight loss- Jaundice  - Pruritus- Asterixis  - Fetor hepaticus (sweet, pungent smell caused by an accumulation of dimethyl sulfide)- Dupuytren's contracture- Hepatomegaly (possibly causing RUQ pain)  - Splenomegaly  - Ascites- Skin changes: Generally dry and atrophic, telangiectasia, caput medusae: periumbilical dilation of subcutaneous veins, palmar erythema, white nails with ground glass opacity  - Hyperestrogenism- GynecomastiaGynecomastia can also be caused by treatment with spironolactone!- Hypogonadism (testicular atrophy)- Decreased body hair (e.g., loss of chest hair, female pattern of pubic hair distribution)- Reduced libido; erectile dysfunction; infertility Diagnostics:- Hepatocyte destruction: ↑ Liver enzymes (AST, ALT), ↑ Bilirubin,↑ Gamma‑glutamyl transpeptidase (GGT), ↑ Alkaline phosphatase, ↑ GLDH, ↑ Ammonia  - Impaired hepatic synthesis: ↑ Prothrombin time (↑ INR), ↓ Total protein (↓ albumin), ↓ Cholinesterase  - Macrocytic anemia due to vitamin deficiency (B12, folic acid)  - Microcytic anemia due to chronic blood loss- Thrombocytopenia in hypersplenism  - Serum protein electrophoresis: ↓ Albumin band, ↑ Gamma band   - Abdominal ultrasound should be performed first.- HCC screening: abdominal ultrasound for patients with cirrhosis every 6 months and periodic monitoring of alpha-fetoprotein (AFP)   Treatment:- Avoidance of hepatotoxic substances (e.g., alcohol, medication)  - Routine vaccinations (influenza, pneumococcal disease, hepatitis A/B, tetanus) - Supplemental B vitamins  - Non‑selective beta blockers (e.g., propranolol) to lower portal pressure and prevent variceal bleeding - Spironolactone and furosemide to manage ascites and edema in patients with hypoalbuminemia- In cases of coagulation factor deficiency (possibly combined with thrombocytopenia)→ Treatment with vitamin K substitution→ Cryoprecipitate transfusion
• Hepatic encephalopathy Triggers:- Deterioration of liver function- Infections (e.g., spontaneous bacterial peritonitis)- Gastrointestinal bleeding  - Constipation- Portal vein thrombosis- Hypovolemia/exsiccosis and electrolyte disturbances (hypokalemia, hyponatremia)- Renal failure- Excessive protein consumption Clinical manifestations  - Disturbances of consciousness, ranging from mild confusion to coma- Multiple neurological and psychiatric disturbances like:→ Asterixis  → Fatigue, lethargy, apathy→ Memory loss→ Impaired sleeping patterns→ Irritability→ Disoriented, socially aberrant behavior (for e.g., defecating/urinating in public, shouting at strangers, etc.)→ Slurred speech→ Muscle rigidity Diagnostics:- Elevated blood ammonia levels  - Assessment of mental status: Number connection test, psychometry‑based diagnostic method (e.g., Mini‑Mental State Examination, MMSE)   Treatment:- Avoidance of trigger substances (e.g., hepatotoxic medication, alcohol)- Lactulose: First-line treatment for HE  - Rifaximin
• Hepatorenal syndrome (HRS) Deterioration of kidney function in patients with advanced liver disease. The condition is caused by renal vasoconstriction resulting in hypoperfusion of the kidneys. Triggers: loss of volume- Drainage of ascites- Gastrointestinal bleeding- Forced diuresis- Excess use of laxatives (lactulose) Symptoms:- Oliguria up to anuria with progressive kidney failure- Clinically associated with decompensated cirrhosis- Renal water retention leads to edema and hydrops (ascites, pleural, or pericardial effusion) Diagnosis:- Serum creatinine > 1.5 mg/dL- Elevated BUN:creatinine ratio (> 20:1)- Protein excretion < 500 mg/d- Hyponatremia with relative sodium deficiency  - Low sodium excretion in urine (< 10 mmol/L)   Therapy- Improvement of liver function if possible (e.g., cessation of alcohol use)- Pharmacotherapy: combination of midodrine, octreotide, and albumin  - Placement of a transjugular intrahepatic portosystemic shunt (TIPS)  - A liver transplant is the only curative option in advanced liver disease
• Ascites Etiology:- The etiology can be determined using the serum-ascites albumin gradient (SAAG) based on Starling's law. - Calculation: SAAG = (albumin levels in serum) - (albumin levels in ascitic fluid)- High SAAG: ≥ 1.1 g/dL (obsolete term: transudate)- Low SAAG: < 1.1 g/dL (obsolete term: exudate) Clinical features:- Progressive abdominal distension  - Fluid wave test: a wave produced by tapping one side of the abdomen in a patient in supine position; this wave will be transmitted to the other side via ascitic fluid.- Shifting dullness: change of resonance from dull to tympanic when patient changes from supine to lateral decubitus position.  - Abdominal pain may be present- Abdominal wall hernias (e.g., umbilical, inguinal, or incisional hernias)  - Peripheral or generalized edema- Symptoms associated with increased abdominal distension: Early satiety, Weight gain, Dyspnea  - Signs of underlying disease:→ Enlarged liver, jaundice, spider angioma, palmar erythema: liver disease→ Elevated jugular venous pressure: heart failure→ Virchow's node and weight loss: upper abdominal malignancy Diagnostics:- Dilutional hyponatremia as a result of overhydration despite normal or increased sodium concentration- Hypoalbuminemia- Ultrasound (best initial test): Reliable detection even of smaller quantities of ascitic fluid: lower limit of detection approx. 30 mL- CT scan- Ultrasound-guided diagnostic paracentesis→ Indications: first diagnosed ascites, worsening ascites or suspected complication.  - Ascitic fluid analysis→ Appearance and color→ Cell count and differentiation  → Albumin und total protein→ LDH  → Direct detection of pathogens  → Diagnostic (cyto‑)pathology   Treatment:- Sodium restriction  - Regular weight control- Water restriction or avoiding overhydration- Diuretic therapy: Indications→ Portal hypertensive ascites: usually responsive; may be treated in the same way as ascites caused by liver cirrhosis (see treatment of cirrhosis).→ Non-portal hypertensive ascites (exudate): usually not effective; therefore it is essential to focus on treating the underlying disease!→ Spironolactone- Therapeutic large-volume paracentesis  - Transjugular intrahepatic portosystemic shunt (TIPS)
• Spontanous bacterial peritonitis Bacterial infection of ascitic fluid in the absence of other intra-abdominal causes (which would otherwise lead to secondary bacterial peritonitis) Etiology and risk factors:- Often seen in 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  - Abdominal pain, tense abdominal wall, and fever is possible.   Diagnosis:- Gold standard: diagnostic paracentesis BEFORE application of antibiotics  - > 250 polymorphonuclear leukocytes/μL ascites: SBP per definition- Determination of pathogens is rarely successful   Treatment:- First-line: 3rd generation cephalosporin IV broad spectrum therapy - Follow-up after 48 h via repeated paracentesis→ If granulocytes decrease to < 250/μL, treatment can be terminated after five additional days→ If granulocytes do not decrease by ≥ 25%: modify treatment according to resistogram Prognosis: high recurrence and mortality rate
• Ascites – Subtypes Chylous ascites:- Definition: collection of lymph in the abdominal cavity, which is characteristically triglyceride-rich and has a milky appearance- Etiology: malignancy (e.g., lymphoma), hepatic cirrhosis, or other lymph disorders (e.g., lymphatic hyperplasia) which result in increased lymph production   Bloody ascites:- Definition: ascitic fluid with RBC > 50,000 mm3- Etiology: may be spontaneous (e.g, malignant mass eroding into vessels) or iatrogenic (e.g., following paracentesis or biopsy in patients with cirrhosis)
• Acetaminophen toxicity Minimum toxic dose: 7.5 g/day in adults  Leading cause of acute hepatic failure in the US Pathophysiology: Exhaustion of hepatic metabolic pathways causes increased formation of a toxic metabolite of acetaminophen, N-acetyl-p-benzoquinoneimine (NAPQI). Glutathione initially inactivates NAPQI, but its reserves are eventually depleted, leading to NAPQI build-up. NAPQI causes irreversible oxidative hepatocyte injury → liver cell necrosis. Clinical features:- Nonspecific symptoms (nausea, vomiting, pallor lethargy) or asymptomatic in the first 24 hours after ingestion- Progressive liver impairment (RUQ pain, liver enlargement and tenderness, abnormal liver function tests) - If acute liver failure does not develop, patients typically begin to recover within 2 weeks after ingestion.- Acute kidney failure occurs in approx. 50% of patients with acute hepatic failure.   Management:- Activated charcoal administered < 4 hours after ingestion- Antidote: PO or IV N-acetylcysteine (NAC)  - Measure acetaminophen (APAP) levels 4 hours after ingestion (or immediately, if ingestion occurred > 4 hours prior to presentation)- Treatment of liver failure- Liver transplant in severe cases
• Hemochromatosis Epidemiology: The most frequent genetic disease in the white population Primary (hereditary) hemochromatosis- Homozygous or heterozygous for the HFE gene defect: Located on chromosome 6- Associated with HLA-A3 genotype- Inheritance: autosomal recessive with incomplete penetrance Secondary hemochromatosis: Caused by iron overload- Transfusion-related (e.g., for correcting chronic anemia)- Thalassemia- Sickle-cell anemia- Sideroblastic anemia→ Pathogenesis: ineffective erythropoiesis with disturbances in the uptake of iron in heme or iron metabolism disorder → iron overload→ Examples: hereditary sideroblastic anemia; anemia of chronic disease- Excessive alcohol consumption   Clinical features:- Asymptomatic in 75% of cases- The 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  - Features of cardiac hemochromatosis:→ Cardiomyopathy (restrictive or dilated)  → Cardiac arrhythmias: paroxysmal atrial fibrillation (most common), sinus node dysfunction, complete AV block, atrial and ventricular tachyarrythmias, and sudden cardiac death  → Congestive heart failure Diagnostics:- Laboratory tests: ↑ Serum iron,↑ Ferritin in serum > 200 μg/L, ↑ Transferrin saturation (> 45%), ↑ Liver enzymes (AST, ALT)- Genetic tests: Homozygote C282Y mutation of the HFE gene confirms the diagnosis.- Liver biopsy: With Prussian blue Treatment:- Dietary changes: Diet low in iron, Restriction of alcohol and vitamin C supplements, Consumption of tea  - Therapeutic phlebotomy (first-line treatment)- Drug-induced iron chelation with deferoxamine  
• Wilson's disease Age of onset: 5-35 years (mean age 12-23 years) Pathophysiology: Autosomal recessive mutations in the ATP7B gene on chromosome 13 Clinical features:- Liver: different degrees of liver disease possible, including acute liver failure, acute or chronic hepatitis, and cirrhosis→ Hepatosplenomegaly→ Portal hypertension→ Abdominal pain→ Jaundice→ Ascites→ Hepatic encephalopathy- Kayser-Fleischer rings: Copper accumulation in Descemet membrane of the cornea results in 1-2 mm wide, green-brown rings in the periphery of the iris. - Neurological symptoms: extrapyramidal motor disturbances, but no sensory changes→ Dysarthria→ Parkinsonism→ Drooling→ Tremor (usually asymmetric, affecting the hands)→ Behavioral changes (e.g., depression, irritability, psychosis) → Cognitive impairment Diagnostics:- Slit lamp examination: Kayser-Fleischer rings (best initial test)- Blood tests: ↑ Transaminases, Coombs-negative hemolytic anemia, thrombocytopenia, ↓ Serum ceruloplasmin (normal value > 20 mg/dL), ↑ Free serum copper, but ↓ total serum copper, ↑ Urine copper excretion (over 24 hours)  - Liver biopsy: if other tests are inconclusive- Screen family members for mutation if diagnosis is confirmed. Treatment:- Low-copper diet: avoid foods such as organs, shellfish, nuts, and chocolate- Regular check-ups: liver biochemical tests every 6 months if disease is stable- Initial therapy: Penicillamine, trientine or zinc salts- Maintenance therapy: zinc salts or low dose chelating agents   
• Alpha-1 antitrypsin deficiency A congenital disorder characterized by the accumulation of defective alpha-1 antitrypsin enzyme. Epidemiology: more common in individuals of European descent Etiology: mutations in SERPINA1 gene - M is the normal allele.- S mutation causes a moderate decrease in AAT production.- Z mutation causes a significant decrease in AAT production. Inheritance: autosomal codominant Clinical features:- Severe form: prolonged neonatal jaundice, hepatitis, cirrhosis, barrel chest, diminished breath sounds, wheezing, and dyspnea  - Mild form: manifests in adolescence, primarily with pulmonary disease; hepatic symptoms may also be present - Increased risk of hepatocellular carcinoma (HCC)   Diagnostics:- Serum: decreased antitrypsin protein levels- Electrophoresis: decreased alpha-1 peak - Chest x-ray: low and flat diaphragm, widened intercostal spaces, hyperinflation and increased basilar radiolucency of both lungs with rarification of peripheral pulmonary vessels  - Chest CT: panacinar emphysema (in contrast to centriacinar emphysema in smoking-related emphysema), bronchiectasis, bullae- Liver biopsy: PAS-positive, spherical inclusion bodies in periportal hepatocytes   Treatment:- Avoid active and passive exposure to cigarette smoke.- Symptomatic treatment: bronchodilators, pulmonary rehabilitation, preventive vaccination, nutritional support if necessary- Antitrypsin replacement: patients with severe AAT deficiency (e.g., ATT < 57 mg/dL) and evidence of decreased airflow
• Autoimmune hepatitis Bimodal distribution: 10-20 years and 45-70 years  AIH is commonly associated with other autoimmune conditions (e.g., type 1 diabetes mellitus, Hashimoto's thyroiditis, celiac disease). Clinical features:- Fatigue- Abdominal pain- Weight loss- Signs of acute liver failure (∼ ⅓ of patients): Jaundice, RUQ pain, Fever Diagnosis:- ↑ ALT and ↑ AST  - Autoantibodies: antinuclear antibodies (ANA) and anti-smooth muscle antibodies (ASMA)  - Hypergammaglobulinemia (↑ IgG)- Liver biopsy: Biopsy should be performed following the detection of AIH antibodies to confirm the diagnosis. Treatment:- Initial therapy: combination of prednisone and azathioprine- Maintenance therapy: azathioprine or prednisolone
• Primary biliary cholangitis Clinical features:- Fatigue (usually the first symptom)- Marked generalized pruritus- Hyperpigmentation- Hepatomegaly, dull lower margin, RUQ discomfort- Splenomegaly- Jaundice- Maldigestion (may involve manifestations of deficiency of fat-soluble vitamins, e.g., osteoporosis)- Xanthomas and xanthelasma  - Common associations include: sicca syndrome, autoimmune thyroid disease, CREST syndrome, rheumatoid arthritis   Diagnostics:- ↑ 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 Treatment:- First-line medical therapy: ursodeoxycholic acid (aka ursodiol, or UDCA)
• Primary sclerosing cholangitis Age: The median age at diagnosis is ∼ 40. Associations:- Chronic inflammatory bowel diseases (IBD): ∼ 90% of PSC patients have IBD (from these patients, 87% have ulcerative colitis (UC) and 13% have Crohn's disease)- 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- Symptoms of chronic inflammatory bowel disease, which is frequently associated with PSC, or other associated comorbidities Diagnostics:- Perinuclear anti-neutrophil cytoplasmic antibodies (pANCA) are present in up to 80% of cases  - ↑ ALP, GGT, conjugated bilirubin- Potentially, ↑ transaminases (however, they are usually < 300 U/L)- Cholangiography: Method of choice: magnetic resonance cholangiopancreatography (MRCP)- Ultrasound- Following diagnosis → colonoscopy (to assess for UC) Treatment:- Ursodeoxycholic acid and immunosuppressives (e.g., tacrolimus)- Treatment of pruritus (e.g., cholestyramine, rifampicin, naltrexone)- Supplementation of fat-soluble vitamins- In the case of bile duct stenosis: ERCP with duct dilation; potentially, stent placement  
• Drugs associated with drug-induced pancreatitis Analgesics: - Acetaminophen- NSAIDs- Mesalamine, sulfasalazine- Opiates Antibiotics:- Isoniazid- Tetracyclines- Metronidazole- Trimethoprim-sulfamethoxazole Antiepileptics: Valproic acid, Carbamazepine Antihypertensives (sulfonamides):- Thiazides, furosemide- Enalapril, losartan Antivirals: Lamivudine, Didanosine Immunosuppresants: Azothiaprine, corticosteroids Others: Asparaginase, estrogens
• Gastroparesis Etiology:- Diabetes (autonomic neuropathy)- Medications (e.g., opiates, anticholinergic drugs)- Traumatic/postsurgical (e.g., vagus nerve injury)- Neurologic (e.g., multiple sclerosis, spinal cord injury)- Idiopathic/postviral Clinical features:- Early satiety- Bloating & abdominal pain- Weight loss- Labile glucose (diabetics)- Epigastric distension & succession splash on examination Diagnostics:- Exclude obstruction with upper endoscopy- Exclude external compression (if suspected) with CT scan- Assess motility with nuclear gastric-emptying study Treatment:- Diet: Frequent small meals with low fat & only soluble fiber- Promotility drugs: Erythromycin, metoclopramide- Gastric electrical stimulation &/or jejunal feeding tubes for refractory symptoms
• Boerhaave syndrome Boerhaave syndrome is the transmural rupture of the esophagus following an episode of forceful vomiting/retching or increased intrathoracic pressure. Associations:- Excessive intake of alcohol or food in the recent past- Repeated episodes of vomiting- Childbirth- Seizures- Prolonged coughing- Weightlifting Clinical features:- Vomiting and/or retching- Severe retrosternal pain that often radiates to the back- Subcutaneous or mediastinal emphysema → crepitus in the suprasternal notch or "crunching" or "crackling" sound on chest auscultation (Hamman's sign), respectively- Dyspnea, cyanosis Diagnostics:- Initial test: Chest x-ray→ Widened mediastinum→ Pneumomediastinum, pneumothorax, pneumoperitoneum, subcutaneous emphysema→ Pleural effusion- Confirmatory test: Contrast esophagram with gastrografin (water-soluble contrast)- CT scan: indicated in unstable/uncooperative patients, pneumoperitoneum on x-ray, or if x-rays and contrast esophagram are inconclusive Treatment:- Nothing by mouth (NPO) and supply nutritional support- Broad-spectrum IV antibiotics (e.g., ampicillin)- IV proton pump inhibitor- Emergency surgical consultation
• Meckel diverticulum A Meckel diverticulum is the most common congenital anomaly of the gastrointestinal tract and is caused by an incomplete obliteration of the omphalomesenteric duct. Epidemiology:- Prevalence: most common congenital gastrointestinal tract anomaly (∼ 2% of the population)- Sex: ♂ > ♀ (2:1)- Age: < 2 years of age   Anatomy:- Meckel diverticulum is a true diverticulum.  - Located ∼ 2 feet proximal to the ileocecal valve  - Usually ≤ 2 inches in size- There may be 2 types of mucosal lining: Native ileal mucosa, Heterotopic mucosa   Clinical features:- Asymptomatic (∼ 96%)  - Symptomatic (2-4%)→ Painless lower gastrointestinal bleeding (most common presentation)  → Hematochezia  → Tarry stools→ Currant jelly stools: Indicates intussusception with bowel ischemia Diagnostics:- Meckel scintigraphy scan (Meckel scan): a noninvasive nuclear medicine imaging technique using radiolabelled technetium (99mTc), which is preferentially absorbed by the gastric mucosa and can identify ectopic gastric mucosa   Treatment:- Asymptomatic Meckel diverticulum: no treatment necessary- Symptomatic or complicated: Surgical resection  Complications:- Hemorrhage (most common)- Bowel obstruction due to: Intussusception, Volvulus, Littre's hernia (When a Meckel diverticulum is the content of an inguinal hernia, it is called a Littre's hernia.)- Bowel perforation → peritonitis or intra-abdominal abscess- Infection (Meckel diverticulitis)  
• Gastroesophageal reflux disease (GERD) Diagnostics:- Empirical therapy: If GERD is clinically suspected and there are no indications for endoscopy, empiric therapy – ranging from lifestyle modifications to a short trial with PPIs – should be initiated. A GERD diagnosis is assumed in patients who respond to this therapeutic regimen.- Upper endoscopy (esophagogastroduodenoscopy (EGD))- Esophageal pH monitoring- Esophageal manometry   Treatment:- Lifestyle modifications→ Small portions; avoid eating (< 3 hours) before bedtime→ Avoid foods with high fat content→ Normalize body weight [7]→ 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) Medical therapy- Treatment of choice: Standard-dose of PPI for at least 8 weeks (once-daily therapy) No response: further diagnostic evaluation including 24-hour esophageal pH monitoringPartial response: increase the dose (to twice daily therapy) or switch to a different PPIGood response: discontinue PPI after 8 weeks- Maintenance therapy: if symptoms recur after discontinuation of PPIs and in the case of complications→ After 8 weeks of initial treatment, reduce PPI to lowest effective dose or switch to H2RAs (only in patients without complications!) Surgical therapy- Fundoplication→ Technique: The gastric fundus is wrapped around the lower esophagus and secured with stitches to form a cuff, leading to a narrowing of the distal esophagus and the gastroesophageal junction (GEJ) and prevents reflux. → Nissen fundoplication (= complete fundoplication)
• Colonic ischemia Pathophysiology: - Usually nonocclusive, "watershed" ischemia- Underlying atherosclerotic disease- State of low blood flow (e.g., hypovolemia) Clinical features:1. Hyperactive phase  - Sudden onset of crampy abdominal pain (usually left lower quadrant)- Fecal urgency- Bloody, loose stools- > 80% of patients recover and do not progress beyond this phase2. Paralytic phase  - Pain more diffuse- Bowel sounds become absent.  - Bloating- Bloody stools cease3. Shock phase  - Acute abdomen with abdominal guarding and rebound tenderness  - Signs of septic shock Diagnosis:- Leukocytosis, lactic acidosis- CT scan: Colonic wall thickening, fat stranding, colonic distension, pneumatosis- Endoscopy: Edematous & friable mucosa Management:- IV fluids & bowel rest- Antibiotics with enteric coverage- Colonic resection if necrosis develops
• Acute mesenteric ischemia Epidemiology:- Mainly occurs in adults > 60 years- Young people with A-fib, vasculitis (e.g., polyarteritis nodosa), or hypercoagulable states can also be affected Etiology:- Arterial occlusion of superior mesenteric artery (cardiac emboli or thrombotic)- Nonocclusive ischemia due to hyperperfusion to splanchnic circulation- Superior mesenteric vein occlusion Clinical features:- Rapid onset of periumbilical pain (often severe)- Pain out of proportion to examination findings- Nausea and vomiting- Hematochezia (late complication)- Progression of small-bowel ischemia to infarction leads to grossly distended abdomen, absent bowel sounds & peritoneal signs Diagnostics:- ↑ Lactate, ↑ LDH, ↑ creatine kinase, ↑ amylase, Leukocytosis, Metabolic acidosis, Hemoconcentration - Confirmatory test: CT (preferred) or MR angiography- Mesenteric angiography if diagnosis is unclear Treatment:- 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
• Peptic ulcer perforation Second most common complication of PUDDuodenal ulcers of the anterior wall are more likely to perforate.   Clinical presentation:- Sudden onset of intense, stabbing pain, followed by diffuse abdominal pain and distention (beginning peritonitis)- Signs of peritonitis or shock- Perforation of chronic ulcers may only cause mild symptoms.- Referred pain to the shoulder   Diagnosis:- Abdominal x-ray: free intraperitoneal air (pneumoperitoneum) under the diaphragm (if upright) or between liver and lateral abdominal wall (if lateral)  - Abdominal CT with water-soluble contrast (most sensitive) if x-ray does not yield clear findings Management: urgent explorative laparotomy- In preparation, patients should receive fluid resuscitation, broad-spectrum IV antibiotics, and IV proton-pump inhibitor therapy Complications:- Subhepatic abscess - Pyogenic liver abscess
• Bacterial enteritis Pathogenesis:- Oral-fecal transmission- Exposure to farm animals or contaminated meat- Most common causes in the US include Salmonella, Shigella, Escherichia coli, Campylobacter, Yersinia Clinical features:- Fever- Crampy abdominal pain- Diarrhea containing blood or mucus Diagnosis: Stool culture (gold standard) Treatment:- Fluid repletion- Reserve antibiotics for high-risk patients→ Immunocompromised, invasive disease (e.g., sepsis)→ Escherichia coli O157:H7 must be excluded in children
• Rectal prolapse Risk factors:- Women age > 40 with history of vaginal deliveries/multiparity- Prior pelvic surgery- Chronic straining as a result of constipation and/or benign prostatic hypertrophy (BPH)- Stroke, dementia- Pelvic floor dysfunction or anatomic defects- Chronic cough (e.g. COPD)- In children: Cystic fibrosis Clinical features:- Abdominal discomfort (not significant pain)- Straining or incomplete bowel evacuation, fetal incontinence with mucus- Digital maneuvers possibly required for defecation- Erythematous mass extending through anus with concentric rings of rectum (can be intermittent) Management:- Medical→ Considered for non-full-thickness prolapse→ Adequate fiber & fluid intake, pelvic floor muscle exercises→ Possible biofeedback for fecal incontinence→ Reduction of mucosal edema, digital repositioning of the rectum, and pressure padding the perineum  - Surgical→ Preferred for full-thickness or symptomatic prolapse (e.g., fecal incontinence, constipation, sensation of mass)→ Laparoscopic rectopexy with/without sigmoidectomy
• Acute dysentery Etiology:- Bacterial infection: EHEC, Shigella, Campylobacter, Salmonella- Intestinal amebiasis (developing countries)- Inflammatory bowel disease- Ischemic colitis Evaluation:- Stool studies: Culture, Shiga toxin, fecal leukocytes- CT scan of the abdomen if suspicion for ischemic colitis- Endoscopy if suspicion for inflammatory bowel disease Management:- Rehydration (oral rehydration preferred)- Empiric antibiotics (unless EHEC is suspected)
• Intervals for follow-up colonoscopy after polypectomy Small rectal hyperplasic polyps → 10 years 1 or 2 small (< 1 cm) tubular adenomas → 5 years - 3-10 adenomas- Any adenoma > 1 cm- Adenoma with high-grade dysplasia or villous features → 3 years More than 10 adenomas → < 3 years, consider underlying familial syndrome Large (> 2 cm) sessile polyp removed by piecemeal excision → 2-6 months Polyp with adenocarcinoma (must have minimal invasion & ≥ 2 mm margin) → 2-3 months
• Small bowel obstruction Etiology:- Bowel adhesions (e.g., prior abdominal surgery, abdominal tuberculosis)- Incarcerated hernias: second most common cause of SBO Clinical features:- Colicky abdominal pain- Vomiting: Bilious vomiting is an early symptom of SBO.- Obstipation or constipation- Abdominal distention- High-pitched, tinkling bowel sounds (early)- Absent bowel sounds (late) Diagnostics:- Abdominal series: Consists of erect and supine abdominal x-rays and an erect chest x-ray.  → Indication: Best initial test in hemodynamically unstable patients or in resource-poor health centers  - CT abdomen and pelvis indications: → With IV and oral contrast: Best initial test in hemodynamically stable patients with suspected partial bowel obstruction → With IV contrast: Indicated in patients with suspected complete bowel obstruction. Conservative treatment:- Indications: Partial bowel obstruction cases or complete bowel obstruction with no signs of ischemia/necrosis  or signs of clinical deterioration- Fluid resuscitation, correction of electrolyte imbalance- Intestinal decompression: nasogastric tube insertion  - Bowel rest (NPO)- Administration of IV analgesics and antiemetics- Gradual increase of oral intake, starting with clear fluids, can be initiated once the abdominal pain and distention subside and bowel sounds return to normal.- Fecal impaction: stool evacuation (manual disimpaction, distal softening/washout with enemas or suppositories, proximal softening/washout with oral solutions such as polyethylene glycol or sodium phosphate)- Sigmoid volvulus with no signs of strangulation: rigid/flexible sigmoidoscopic detorsion Exploratory laparotomy indications:- Suspected bowel obstruction and hemodynamic instability or features of sepsis  - Complete bowel obstruction with signs of ischemia/necrosis or clinical deterioration- Persistent partial obstruction (> 3-5 days)- Closed-loop obstruction  
• Dyspepsia Clinical features:- Epigastric pain often described as "burning"- Nausea, vomiting- Epigastric fullness- Heartburn Etiology:- Functional (75%)- Malignancy (e.g., gastric, esophageal)- Peptic ulcer, NSAIDs, Helicobacter pylori infection, GERD Workup:- Age ≥ 60: Upper endoscopy- Age < 60→ Testing and treatment for H pylori→ Upper endoscopy in high-risk patients (e.g., overt GI bleeding, significant weight loss, > 1 alarm symptom) Alarm symptoms:- Progressive dysphagia- Iron deficiency anemia- Odynophagia- Palpable mass or lymphadenopathy- Persistent vomiting- Family history of GI malignancy
• Diverticular bleeding Frequency: occurs in around 5% of cases of patients with diverticulosis Caused by erosions around the edge of diverticula   Clinical findings:- Painless hematochezia- Severe or ongoing bleeding: significant drop in hemoglobin, hemodynamic instability (hypotension, tachycardia, dizziness, reduced level of consciousness)- In 70-80% of cases bleeding ceases spontaneously  Therapy:- Endoscopic hemostasis during colonoscopy (epinephrine injection, thermal coagulation, ligation)- Angiography with vessel embolization  
• Pediatric constipation Risk factors:- Initation of solid food & cow's milk- Toilet training- School entry Clinical features:- Painful/hard bowel movements- Stool withholding- Encopresis Complications:- Anal fissures- Hemorrhoids- Enursis/UTIs Treatment:- ↑ Dietary fiber & water intake- Limit cow's milk intake to < 24 oz- Laxatives± Suppositories, enema
• Hepatic encephalopathy Hepatic encephalopathy (HE) is defined as fluctuations in mental status and cognitive function in the presence of severe liver disease. Hepatic dysfunction results in inadequate elimination of metabolic products with subsequent accumulation of neurotoxic metabolites (like ammonia).   Triggers:- Deterioration of liver function- Infections (e.g., spontaneous bacterial peritonitis)- Gastrointestinal bleeding  - Constipation- Portal vein thrombosis- Hypovolemia/exsiccosis and electrolyte disturbances (hypokalemia, hyponatremia)- Renal failure- Excessive protein consumption Clinical manifestations:- Disturbances of consciousness, ranging from mild confusion to coma- Multiple neurological and psychiatric disturbances like:→ Asterixis  → Fatigue, lethargy, apathy→ Memory loss→ Impaired sleeping patterns→ Irritability→ Disoriented, socially aberrant behavior (for e.g., defecating/urinating in public, shouting at strangers, etc.)→ Slurred speech→ Muscle rigidity Diagnostics:- Elevated blood ammonia levels  - Assessment of mental status→ Number connection test: completed slower than the age-normalized standard or cannot complete→ Psychometry‑based diagnostic method (e.g., Mini‑Mental State Examination, MMSE)   Treatment:- General measures:→ Avoidance of trigger substances (e.g., hepatotoxic medication, alcohol)→ Treatment of further complications which might aggravate HE (see “Triggers” above)- Lactulose: synthetic disaccharide laxative→ First-line treatment for HE  → Improves HE by decreasing absorption of ammonia in the bowel: lactulose is converted to lactic acid by intestinal flora → acidification in the gut leads to conversion of ammonia (NH3) to ammonium (NH4+) → ammonium is excreted in the feces → decreased blood ammonia concentration- Rifaximin: Non‑absorbable antibiotic→ May be added to lactulose to prevent recurrent episodes of HE after the second episode
• Dumping syndrome Rapid gastric emptying due to either defective gastric reservoir function or pyloric emptying mechanism, or anomalous postsurgery gastric motor function. Early dumping:- Cause: rapid emptying of undiluted chyme into the small intestine caused by a dysfunctional or bypassed pyloric sphincter  - Clinical features:→ Appears within 15-30 minutes after ingestion of a meal→ Symptoms may include nausea, vomiting, diarrhea, and cramps, as well as vasomotor symptoms such as sweating, flushing, and palpitations. - Management:→ Dietary modifications: Small meals that include a combination of complex carbohydrates and foods rich in protein and fat to cover protein and energy requirements are preferable.→ 30-60 min of rest in the supine position after meals  → Often spontaneous improvement after a couple of months Late dumping: - Clinical features:→ Appears hours after ingesting a meal.→ Gastrointestinal discomfort as in early dumping, shakiness, hypoglycemia, hunger, and decreased consciousness.- Cause: postprandial hypoglycemia; dysfunctional pyloric sphincter → chyme containing glucose immediately reaches the small intestine → glucose is quickly resorbed → hyperglycemia → excessive release of insulin → hypoglycemia and release of catecholamines- Treatment:→ Dietary modifications→ Octreotide and surgery are second and third-line therapies
• Severe malnutrition Types:- Marasmus (wasting)- Kwashiokor (edematous malnutrition)- Combination of above Management:- Rewarming for hypothermia- Antibiotics for presumed systemic infection- Rehydration→ Oral rehydration solution preferred→ Intravenous fluids if in shock- Refeed cautiously Complications of management:- Heart failure- Refeeding syndrome

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