38.3 Gastroenterology and Hepatology: GERD and Peptic Ulcer Disease, Upper and Lower GI Bleeding, Diarrhea and GI Infections, Acute Pancreatitis and Biliary Disease, Viral Hepatitis, Cirrhosis and Portal Hypertension, Liver and GI Cancers

Why this area matters

The Philippines has a high burden of chronic hepatitis B, which drives cirrhosis and hepatocellular carcinoma, one of the leading causes of cancer death in Filipino men. Infectious diarrhea, typhoid and amebiasis remain common, and peptic ulcer bleeding is a frequent admission. Board questions focus on resuscitation, serology interpretation, and when to scope, refer or operate.

GERD and dyspepsia

• GERD:
  • heartburn and regurgitation, worse after meals and lying down;
  • extraesophageal symptoms: chronic cough, hoarseness, asthma, dental erosions;
  • a PPI trial for 8 weeks both diagnoses and treats typical symptoms;
  • lifestyle: weight loss, raising the head of the bed, avoiding late meals and trigger foods, stopping smoking.
• Alarm features needing endoscopy:
  • dysphagia or odynophagia;
  • weight loss, persistent vomiting;
  • GI bleeding or iron deficiency anemia;
  • a mass, or onset at an older age (ACG suggests endoscopy for dyspepsia from age 60).
• Complications of GERD:
  • erosive esophagitis and peptic stricture;
  • Barrett esophagus (intestinal metaplasia), which increases the risk of adenocarcinoma and needs surveillance endoscopy.
• Dyspepsia without alarm features: test and treat for H. pylori (urea breath test or stool antigen), or a PPI trial.
• Functional dyspepsia is diagnosed after a normal evaluation.

Gastrointestinal Hemorrhage: Triage, Resuscitation & Interventions

Gastrointestinal bleeding is anatomically demarcated by the ligament of Treitz (suspensory muscle of the duodenum) into Upper Gastrointestinal Bleeding (UGIB) and Lower Gastrointestinal Bleeding (LGIB).

Upper Gastrointestinal Bleeding (UGIB)

• Clinical Manifestations: Hematemesis (bright red blood or "coffee-ground" emesis), melena (black, tarry, foul-smelling stools resulting from bacterial degradation of hemoglobin over $\ge 14\text{ hours}$ in the gut; requires as little as $50-100\text{ mL}$ of blood), and occasionally brisk hematochezia (seen in massive, life-threatening UGIB with $> 1,000\text{ mL}$ blood loss and hemodynamic instability).
• Common Etiologies: Peptic ulcer disease ($50\%$), gastroesophageal varices ($15-20\%$), Mallory-Weiss mucosal lacerations ($5-10\%$, often post-retching), gastroduodenal erosions, Dieulafoy lesions (aberrant submucosal caliber-persistent arteriole), and gastrointestinal malignancies.
• Risk Stratification Scores:
  • Glasgow-Blatchford Score (GBS): Pre-endoscopic risk stratification based on BUN, hemoglobin, systolic blood pressure, pulse, presentation with melena or syncope, and hepatic/cardiac comorbidities. A score of $0$ indicates very low risk, eligible for safe outpatient evaluation.
  • Rockall Score: Incorporates age, shock, comorbidities, endoscopic findings, and stigmata of recent hemorrhage (active spurting, visible vessel, adherent clot) to predict mortality and rebleeding risk.
• Emergency Resuscitation & Pharmacotherapy Protocol:
  1. Airway & Hemodynamic Access: Endotracheal intubation for massive hematemesis, encephalopathy, or severe agitation. Establish two large-bore ($16\text{- or }18\text{-gauge}$) peripheral IV lines; initiate crystalloid resuscitation.
  2. Restrictive Transfusion Strategy: Transfuse Packed Red Blood Cells (PRBCs) at a hemoglobin threshold of $< 7.0\text{ g/dL}$, targeting a post-transfusion hemoglobin of $7.0\text{ to }8.0\text{ g/dL}$. Restrictive transfusion significantly improves survival and reduces rebleeding compared to liberal transfusion ($< 9.0\text{ g/dL}$), as excessive volume expansion exacerbates portal venous pressure and clot disruption. (A higher threshold of $\ge 8.0\text{ g/dL}$ is reserved for acute coronary syndrome).
  3. High-Dose Intravenous PPI: Administer intravenous Pantoprazole or Esomeprazole ($80\text{ mg}$ IV bolus, followed by $8\text{ mg/hour}$ continuous infusion or $40\text{ mg}$ IV BID). Raising intragastric $\text{pH} > 6.0$ stabilizes fibrin clot formation and suppresses pepsin-mediated clot lysis.
  4. Vasoactive Infusion for Suspected Varices: Initiate Octreotide ($50\text{ }\mu\text{g}$ IV bolus, followed by continuous infusion of $50\text{ }\mu\text{g/hour}$) or Terlipressin immediately upon presentation in patients with known or suspected cirrhosis. Octreotide induces selective splanchnic vasoconstriction, reducing portal inflow and variceal pressure.
  5. Short-Course Antibiotic Prophylaxis: In cirrhotic patients presenting with UGIB, administer intravenous Ceftriaxone ($1\text{ g/day}$ for up to 7 days). Prophylactic antibiotics dramatically reduce bacterial infections, spontaneous bacterial peritonitis, early rebleeding, and in-hospital mortality.
  6. Endoscopic Timing & Therapy: Diagnostic and therapeutic esophagogastroduodenoscopy (EGD) should be performed within 24 hours of presentation (within 12 hours for suspected acute variceal hemorrhage following hemodynamic stabilization). Therapeutic modalities include Endoscopic Band Ligation (EBL) for esophageal varices, and dual endoscopic therapy (hemoclips, thermal contact coagulation, or sclerotherapy combined with epinephrine injection) for high-risk bleeding ulcers.

Lower Gastrointestinal Bleeding (LGIB)

• Etiology: Arises distal to the ligament of Treitz. Diverticulosis is the most common cause ($30-50\%$, presenting as sudden, painless, large-volume hematochezia), followed by angiodysplasia (vascular ectasia in right colon), ischemic colitis (crampy abdominal pain followed by bloody diarrhea in watershed zones: splenic flexure and rectosigmoid), colorectal polyps/carcinoma, internal hemorrhoids, and inflammatory bowel disease.
• Diagnostic Approach: In hemodynamically unstable patients with massive hematochezia, an upper GI source must be excluded first via nasogastric lavage or urgent upper endoscopy. Once stabilized, colonoscopy is the primary diagnostic and therapeutic modality. Active ongoing bleeding can be localized with CT Angiography (detects bleeding rates $\ge 0.3-0.5\text{ mL/min}$) or Technetium-99m labeled red blood cell scintigraphy (detects rates $\ge 0.1\text{ mL/min}$).

---

Acid-Peptic Disease & Helicobacter pylori

Gastric versus Duodenal Ulcer Disease

Helicobacter pylori Eradication Protocols

Helicobacter pylori is a microaerophilic, spiral, flagellated gram-negative rod producing abundant urease, inducing chronic active gastritis and predisposing to peptic ulceration, gastric adenocarcinoma, and MALT lymphoma.

• First-Line Regimen in High-Resistance Regions: Bismuth Quadruple Therapy (14 Days) Where clarithromycin resistance exceeds $15\%$ or is unknown, bismuth quadruple therapy is the preferred empiric first-line regimen (Maastricht VI; ACG 2024). Philippine resistance data are limited and inconsistent between studies, so local susceptibility should guide therapy:
  1. Proton Pump Inhibitor (PPI): Omeprazole $20\text{ mg}$ BID, Esomeprazole $40\text{ mg}$ BID, or Lansoprazole $30\text{ mg}$ BID.
  2. Bismuth Subsalicylate / Subcitrate: $300\text{ to }524\text{ mg}$ four times daily (acts as a topical mucosal protectant and antibacterial).
  3. Metronidazole: $500\text{ mg}$ three to four times daily.
  4. Tetracycline: $500\text{ mg}$ four times daily.
• Alternative (Clarithromycin Triple Therapy - 14 Days): PPI BID + Clarithromycin $500\text{ mg}$ BID + Amoxicillin $1,000\text{ mg}$ BID. Used only when local clarithromycin resistance is documented below $15\%$ or the strain is known to be susceptible, and in patients without prior macrolide exposure.
• Confirmation of Eradication: Must be performed $\ge 4\text{ weeks}$ after completion of antibiotic therapy and $\ge 2\text{ weeks}$ after stopping PPIs. Non-invasive tests include the Urea Breath Test ($^{13}\text{C}$ or $^{14}\text{C}$) and the Monoclonal Stool Antigen Test. Serum antibody serology remains positive for months to years and cannot be used to prove eradication.

More on bleeding and ulcers:

• Variceal bleeding:
  • endoscopic band ligation within 12 hours;
  • balloon tamponade (Sengstaken-Blakemore) as a temporary bridge;
  • TIPS for refractory bleeding;
  • secondary prevention: a nonselective beta-blocker (propranolol or carvedilol) plus repeated band ligation;
  • primary prevention of large varices: a nonselective beta-blocker or band ligation.
• Ulcer complications:
  • perforation: sudden severe pain, a board-like abdomen and free air under the diaphragm, needing surgery;
  • gastric outlet obstruction: vomiting of undigested food, a succussion splash and hypochloremic hypokalemic metabolic alkalosis.
• NSAID ulcers: stop the NSAID; if it must continue, use a PPI or a COX-2 selective drug.
• Zollinger-Ellison syndrome (gastrinoma): multiple or distal ulcers with diarrhea, linked to MEN 1.

Diarrhea and GI infections

• Acute diarrhea:
  • most cases are viral or toxin-mediated and self-limited;
  • assess dehydration and replace losses with oral rehydration solution;
  • bloody diarrhea with fever (dysentery) suggests Shigella, Campylobacter, enteroinvasive E. coli or amebiasis;
  • rice-water stools with severe dehydration suggest cholera, treated with rapid rehydration and a single dose of doxycycline (or azithromycin);
  • antibiotics are for dysentery, severe illness, cholera and immunocompromised patients;
  • avoid antimotility drugs in bloody diarrhea.
• Typhoid fever: stepwise fever, relative bradycardia, rose spots and hepatosplenomegaly. Diagnosed by blood culture (bone marrow culture is the most sensitive). Treated with azithromycin, ceftriaxone, or a fluoroquinolone only where isolates are susceptible (fluoroquinolone resistance is widespread in South Asia). Complications are intestinal perforation (third week) and bleeding.
• Amebic liver abscess: fever and right upper quadrant pain in men, with an anchovy-paste abscess. Treated with metronidazole followed by a luminal agent (paromomycin or diloxanide).
• Chronic diarrhea (more than 4 weeks):
  • inflammatory bowel disease: ulcerative colitis (continuous from the rectum, bloody diarrhea) and Crohn disease (skip lesions, transmural, fistulas, perianal disease); always exclude intestinal TB in the Philippines before starting steroids or biologics;
  • irritable bowel syndrome (abdominal pain linked to defecation without alarm features, by the Rome IV criteria);
  • malabsorption, parasites (Giardia, Strongyloides, Capillaria in some provinces) and HIV-related infections;
  • microscopic colitis and colon cancer in older patients.
• C. difficile after antibiotics: treated with oral vancomycin or fidaxomicin.

Pancreatitis and biliary disease

• Acute pancreatitis:
  • causes: gallstones and alcohol most commonly, then hypertriglyceridemia (more than 1,000 mg/dL), hypercalcemia, drugs, post-ERCP and trauma;
  • diagnosis needs 2 of 3: typical epigastric pain radiating to the back, lipase or amylase more than 3 times the upper limit of normal, and characteristic imaging;
  • CT is not needed early unless the diagnosis is uncertain or the patient deteriorates after 72 hours;
  • severity (revised Atlanta): mild (no organ failure), moderately severe (transient organ failure under 48 hours or local complications), severe (persistent organ failure over 48 hours);
  • treatment: moderate goal-directed fluids with lactated Ringer solution (aggressive fluids cause overload), analgesia, and early oral feeding as tolerated, or enteral rather than parenteral nutrition;
  • no prophylactic antibiotics; treat proven infected necrosis, delaying drainage or necrosectomy for about 4 weeks when possible;
  • ERCP within 24 hours for gallstone pancreatitis with cholangitis;
  • cholecystectomy during the same admission for mild gallstone pancreatitis.
• Chronic pancreatitis: pain, steatorrhea and diabetes, with calcifications; usually alcohol. Treated with enzymes, analgesia and abstinence.
• Acute cholangitis:
  • Charcot triad: fever, jaundice and right upper quadrant pain; Reynolds pentad adds shock and confusion;
  • treated with IV antibiotics and biliary drainage (ERCP), urgently in severe cases;
  • surgical aspects of gallstones and cholecystitis are covered in the surgery chapter.

Viral Hepatitis & Acute Liver Failure

Serologic Decoding of Hepatitis B Virus (HBV)

Highlights of Other Viral Hepatitides

• Hepatitis A (HAV): Fecal-oral transmission; RNA picornavirus. Anti-HAV IgM confirms acute infection. Does not cause chronic hepatitis or carrier state.
• Hepatitis C (HCV): Bloodborne/parenteral; single-stranded RNA flavivirus. High chronicity rate ($75-85\%$). Screening is performed with Anti-HCV; active infection requires confirmation with quantitative HCV RNA PCR. Direct-acting antiviral (DAA) pan-genotypic regimens (Sofosbuvir/Velpatasvir or Glecaprevir/Pibrentasvir) for 8 to 12 weeks achieve sustained virologic response (cure) in $> 95\%$ of patients.
• Hepatitis D (HDV): Defective single-stranded circular RNA virus requiring HBsAg coat for assembly. Co-infection (simultaneous acute HBV and HDV) presents like severe acute HBV; Superinfection (acute HDV in a chronic HBsAg carrier) precipitates acute hepatic decompensation or rapid cirrhosis.
• Hepatitis E (HEV): Fecal-oral, waterborne. High fatality rate ($15\% - 25\%$) in pregnant women due to fulminant hepatic necrosis.

Acute Liver Failure (ALF / Fulminant Hepatic Failure)

Defined by the triad of:

1. Severe acute liver injury (elevated serum transaminases, jaundice).
2. Hepatic coagulopathy: International Normalized Ratio (INR) $\ge 1.5$.
3. Any degree of hepatic encephalopathy developing within 26 weeks of initial symptoms in a patient without preexisting cirrhosis.

Etiologies & Specific Antidotes: Acetaminophen toxicity is the most common cause in Western nations (treated with intravenous N-Acetylcysteine); viral hepatitis is common in developing regions; Amanita phalloides mushroom poisoning (penicillin G and silibinin); Wilson disease (penicillamine, plasma exchange); ischemic hepatitis ("shock liver"). Emergency transfer to a liver transplant center is mandatory.

---

Cirrhosis & Complications of Portal Hypertension

Cirrhosis is the irreversible end-stage of chronic hepatic injury, defined by diffuse parenchymal bridging fibrosis and regenerative architectural nodule formation.

Ascites & Serum-Ascites Albumin Gradient (SAAG)

Diagnostic abdominal paracentesis must be performed in all patients with new-onset ascites or hospital admission for cirrhotic decompensation. $\text{SAAG} = \text{Serum Albumin Concentration} - \text{Ascitic Fluid Albumin Concentration}$

• Medical Management of Cirrhotic Ascites:
  • Dietary sodium restriction ($< 2,000\text{ mg/day}$ or $88\text{ mmol/day}$). Fluid restriction is unnecessary unless serum sodium falls below $125\text{ mEq/L}$.
  • Dual Diuretic Therapy: Administer oral Spironolactone and Furosemide in a fixed 100:40 mg single daily morning ratio (e.g., $100\text{ mg}$ spironolactone with $40\text{ mg}$ furosemide, uptitrated together every 3-5 days to maximum $400\text{ mg} : 160\text{ mg}$). This ratio maintains normokalemia by balancing spironolactone-induced potassium retention with furosemide-induced kaliuresis.
  • Large-Volume Paracentesis (LVP): Indicated for tense, refractory ascites. When $> 5\text{ liters}$ of ascites is removed, intravenous Albumin ($6\text{ to }8\text{ g}$ per liter of ascites removed) must be infused to prevent Post-Paracentesis Circulatory Dysfunction (PICD), rapid ascites re-accumulation, renal failure, and death.

Spontaneous Bacterial Peritonitis (SBP)

Spontaneous infection of preexisting ascitic fluid without an identifiable surgically treatable intra-abdominal focus, caused by bacterial translocation (Escherichia coli, Klebsiella pneumoniae, Streptococcus pneumoniae).

• Diagnostic Hallmark: Ascitic fluid Absolute Polymorphonuclear Neutrophil (PMN) Count $\ge 250\text{ cells/}\mu\text{L}$ (calculated as total leukocyte count $\times \%\text{ neutrophils}$). A positive culture is not required to initiate therapy.
• Therapy: Intravenous third-generation cephalosporin (Ceftriaxone $2\text{ g}$ IV daily or Cefotaxime $2\text{ g}$ IV q8h) for 5 days.
• Renal Protection Protocol: Intravenous Albumin ($1.5\text{ g/kg}$ within 6 hours of diagnosis, followed by $1.0\text{ g/kg}$ on Day 3) significantly decreases the incidence of hepatorenal syndrome and reduces mortality from $29\%$ to $10\%$.
• Secondary Prophylaxis: Indicated after a single episode of SBP (daily oral Ciprofloxacin $500\text{ mg}$ or Trimethoprim-sulfamethoxazole $1$ double-strength tablet daily) indefinitely or until liver transplantation.

Hepatic Encephalopathy (HE)

Neuropsychiatric abnormalities caused by portosystemic shunting and impaired hepatic metabolic clearance of gut-derived neurotoxins, predominantly ammonia ($\text{NH}_3$).

• Clinical Signs & West Haven Stages: Early sleep reversal, mood alterations, progressed to lethargy, disorientation, asterixis ("liver flap", bilateral flapping tremor of dorsiflexed wrists), somnolence, and coma.
• Precipitating Factors: Gastrointestinal bleeding (massive nitrogen load), infection/SBP, hypokalemic metabolic alkalosis (enhances conversion of $\text{NH}_4^+$ to permeable $\text{NH}_3$), constipation, excessive dietary protein, sedative medications, and over-diuresis/dehydration.
• Treatment:
  1. Identify and correct the precipitating event.
  2. Lactulose (First-Line): Oral synthetic disaccharide degraded by colonic flora into lactic and acetic acids, lowering colonic $\text{pH}$. Acidification converts lipophilic diffusible ammonia ($\text{NH}_3$) into charged, non-absorbable ammonium ions ($\text{NH}_4^+$), trapping it in stool ("ammonia trapping"). It also acts as an osmotic cathartic. Titrated to achieve 2 to 3 soft, semi-formed bowel movements per day.
  3. Rifaximin (Second-Line / Add-on): Oral non-absorbable rifamycin antibiotic ($550\text{ mg}$ BID) that eradicates urease-producing gut bacteria, suppressing ammonia synthesis. Added to lactulose for recurrent or refractory encephalopathy.

Hepatorenal Syndrome (HRS)

Extreme functional renal vasoconstriction mediated by intense splanchnic arterial vasodilation in advanced portal hypertension.

• Diagnostic Criteria (HRS-AKI): Cirrhosis with ascites; serum creatinine increase $\ge 0.3\text{ mg/dL}$ in 48 hours or $\ge 50\%$; absence of shock; no response after $\ge 48\text{ hours}$ of diuretic withdrawal and volume expansion with IV albumin ($1\text{ g/kg/day}$, maximum $100\text{ g/day}$); absence of proteinuria ($< 500\text{ mg/day}$) or hematuria ($< 50\text{ RBCs/hpf}$); and normal renal ultrasonography.
• Management: Combination of vasoconstrictor therapy (intravenous Terlipressin, or continuous infusion of Norepinephrine, or Octreotide + Midodrine) PLUS intravenous Albumin ($20-40\text{ g/day}$). Definitive curative therapy is orthotopic liver transplantation.

---

Prognostic Scoring Systems in Cirrhosis

Child-Turcotte-Pugh (CTP) Classification

Evaluates functional hepatic synthetic reserve and perioperative mortality using five parameters (scoring 1 to 3 points each):

• Class A (5 - 6 Points): Well-compensated cirrhosis; $100\%$ 1-year survival; perioperative mortality $< 10\%$.
• Class B (7 - 9 Points): Significant functional compromise; $80\%$ 1-year survival; perioperative mortality ~30%.
• Class C (10 - 15 Points): Decompensated end-stage cirrhosis; $45\%$ 1-year survival; perioperative mortality $> 75-80\%$ (relative contraindication to elective non-transplant surgery).

Model for End-Stage Liver Disease (MELD-Na)

A continuous objective mathematical score incorporating Bilirubin, INR, Serum Creatinine, and Serum Sodium. Used to prioritize patients for deceased-donor liver transplantation (the United States moved to MELD 3.0, which adds sex and albumin, in 2023) and predicts 90-day mortality.

More on liver disease:

• Chronic hepatitis B treatment:
  • indicated for active hepatitis (raised ALT with high HBV DNA), cirrhosis with any detectable DNA, and some special groups;
  • tenofovir or entecavir long-term, which suppress the virus and reduce cirrhosis and HCC;
  • prevention by hepatitis B birth dose vaccination within 24 hours of birth, and HBIG for babies of HBsAg-positive mothers; antivirals in late pregnancy for mothers with high viral loads.
• Other chronic liver diseases:
  • alcohol-associated hepatitis: AST higher than ALT (ratio about 2:1), fever and jaundice; a Maddrey discriminant function of 32 or more suggests steroid treatment;
  • metabolic dysfunction-associated steatotic liver disease (MASLD), formerly NAFLD: linked to obesity and diabetes, and now a leading cause of cirrhosis;
  • Wilson disease (low ceruloplasmin, Kayser-Fleischer rings), hemochromatosis, autoimmune hepatitis, and primary biliary cholangitis (anti-mitochondrial antibodies).
• Hepatocellular carcinoma:
  • risk factors: hepatitis B (even without cirrhosis), hepatitis C, alcohol, MASLD and aflatoxin;
  • surveillance with ultrasound every 6 months, with or without AFP, in cirrhosis and high-risk HBV carriers;
  • diagnosed by arterial enhancement with washout on multiphase CT or MRI (often no biopsy needed);
  • treated by resection, ablation, transplantation (Milan criteria), TACE or systemic therapy depending on stage and liver function.
• Other GI cancers:
  • gastric cancer: H. pylori, smoked and salted foods; dyspepsia with weight loss, early satiety, a Virchow node or Sister Mary Joseph nodule;
  • esophageal cancer: squamous (smoking, alcohol, hot drinks) or adenocarcinoma (Barrett); progressive dysphagia to solids then liquids;
  • colorectal cancer: screening from age 45 to 50 with FIT or colonoscopy.