Gastrointestinal Disorders

Learning Objectives

By the end of this topic, you should be able to:

• Explain the pathophysiology, diagnosis, and treatment of peptic ulcer disease (PUD), including the role of H. pylori and NSAIDs
• Differentiate Crohn's disease from ulcerative colitis by location, depth of inflammation, and complications
• Describe the compensated-to-decompensated spectrum of chronic liver disease and cirrhosis
• Distinguish upper from lower GI bleeding by presentation and outline the initial workup
• Recognize red-flag ("alarm") symptoms that mandate urgent endoscopy or referral
• Interpret common investigations (endoscopy, H. pylori testing, liver panels) in a clinical scenario

Quick Answer

Gastrointestinal disorders span the entire tube from esophagus to rectum, but four groups dominate exam questions and clinical practice: peptic ulcer disease (mucosal breaks from acid, H. pylori, or NSAIDs), inflammatory bowel disease (Crohn's disease and ulcerative colitis — chronic, immune-mediated gut inflammation), liver disease (progressing from fatty liver or hepatitis to cirrhosis and portal hypertension), and GI bleeding (upper vs. lower, a true emergency). They matter because together they account for a huge share of emergency presentations, hospital admissions, and long-term morbidity — and because each has a classic, testable pattern of history, exam findings, and investigations that distinguishes it from its look-alikes.

Peptic Ulcer Disease (PUD)

A peptic ulcer is a break in the mucosal lining that extends through the muscularis mucosae, most often in the stomach (gastric ulcer) or first part of the duodenum (duodenal ulcer). It happens when the balance between acid/pepsin (aggressive factors) and mucus, bicarbonate, and blood flow (protective factors) tips toward damage.

Two causes explain over 90% of ulcers:

• Helicobacter pylori infection — a spiral, urease-producing bacterium that colonizes the gastric antrum, triggers chronic inflammation, and weakens mucosal defenses. It is the dominant cause of duodenal ulcers.
• NSAID use — these drugs inhibit cyclooxygenase-1 (COX-1), which normally makes protective prostaglandins in the gastric mucosa. Without them, the mucosa is defenseless against acid. This is the leading cause when H. pylori is negative, especially in elderly patients on chronic NSAIDs.

Less common causes: Zollinger-Ellison syndrome (gastrin-secreting tumor causing massive acid hypersecretion), smoking (impairs healing), and severe physiological stress (Curling's ulcer in burns, Cushing's ulcer in raised intracranial pressure).

Clinical clue that examiners love: duodenal ulcer pain classically improves with food (food buffers acid) and wakes the patient at night; gastric ulcer pain classically worsens with food (food stimulates acid secretion against an already-damaged mucosa) — though this distinction is not perfectly reliable in practice.

Diagnosis: Upper endoscopy is the gold standard, especially in patients over 55 or with alarm features, because it allows direct visualization and biopsy (gastric ulcers must be biopsied to exclude malignancy — duodenal ulcers are almost never malignant, so routine biopsy isn't required). H. pylori testing includes the urea breath test, stool antigen test, or biopsy-based rapid urease test; serology only tells you about past exposure, not active infection.

Treatment: If H. pylori positive, give triple or quadruple eradication therapy (a proton pump inhibitor plus antibiotics — classically clarithromycin + amoxicillin, or bismuth quadruple therapy in areas of clarithromycin resistance). Stop NSAIDs if possible. All patients get acid suppression with a PPI to allow healing. Confirm eradication with a repeat breath or stool test at least 4 weeks after treatment.

Complications to recognize immediately: bleeding (hematemesis/melena — most common complication), perforation (sudden severe pain, rigid abdomen, free air under the diaphragm on erect chest X-ray), and gastric outlet obstruction (from scarring, causing early satiety and non-bilious vomiting).

Inflammatory Bowel Disease (IBD)

IBD refers to chronic, relapsing-remitting immune-mediated inflammation of the gut. The two forms — Crohn's disease and ulcerative colitis — are frequently compared because they share symptoms (diarrhea, abdominal pain, weight loss, fatigue) but differ sharply in pattern, and this contrast is one of the most commonly tested comparisons in medicine.

Crohn's disease can affect any part of the GI tract from mouth to anus (though it favors the terminal ileum), inflames the bowel wall transmurally (full thickness), and characteristically skips areas of normal bowel between diseased segments ("skip lesions"). Because inflammation goes all the way through the wall, Crohn's is prone to fistulas, abscesses, and strictures. Granulomas are seen on biopsy in some cases.

Ulcerative colitis is confined to the colon and rectum, always starts at the rectum and spreads proximally in continuity (no skip lesions), and involves only the mucosa and submucosa. Because the disease doesn't penetrate the full wall, fistulas are rare, but continuous mucosal inflammation causes bloody diarrhea as its hallmark symptom, and long-standing disease raises colorectal cancer risk requiring surveillance colonoscopy.

Shared management principles: 5-aminosalicylates (mesalamine) for mild disease, corticosteroids for flares, immunomodulators (azathioprine) and biologics (anti-TNF agents like infliximab) for moderate-to-severe or steroid-dependent disease. Surgery is curative in ulcerative colitis (removing the colon removes the disease) but is not curative in Crohn's disease (it can recur anywhere else in the GI tract).

Chronic Liver Disease and Cirrhosis

Chronic liver injury — from viral hepatitis (B, C), alcohol, or non-alcoholic fatty liver disease (NAFLD/NASH) — leads to progressive fibrosis. Over years, this fibrosis can organize into cirrhosis: regenerative nodules surrounded by fibrous scar tissue that distort the liver's normal architecture and blood flow.

Cirrhosis exists on a spectrum. In compensated cirrhosis the liver still manages its jobs (protein synthesis, detoxification, bile production) despite the scarring, and patients may be asymptomatic. In decompensated cirrhosis, the liver can no longer keep up, and specific complications emerge:

• Portal hypertension — scarred liver tissue increases resistance to portal blood flow, forcing blood through collateral vessels. This produces esophageal varices (which can rupture and bleed catastrophically), splenomegaly, and caput medusae.
• Ascites — a combination of portal hypertension and low albumin (reduced oncotic pressure) allows fluid to accumulate in the peritoneal cavity.
• Hepatic encephalopathy — the liver fails to clear ammonia and other gut-derived toxins, which accumulate and impair brain function, causing confusion, asterixis, and in severe cases coma.
• Coagulopathy — the liver makes most clotting factors, so synthetic failure raises INR and bleeding risk.
• Jaundice — impaired bilirubin conjugation and excretion.

Why this matters clinically: the same underlying disease (cirrhosis) produces very different presentations depending on which complication dominates, so recognizing the pattern (distended abdomen vs. confusion vs. vomiting blood) points to the underlying mechanism.

Gastrointestinal Bleeding

GI bleeding is classified by its location relative to the ligament of Treitz, the anatomical landmark marking the duodenojejunal junction.

Upper GI bleeding (proximal to the ligament of Treitz — esophagus, stomach, duodenum) presents with hematemesis (vomiting blood, either bright red or "coffee-ground" from partial digestion by acid) and/or melena (black, tarry, foul-smelling stool from digested blood — blood needs roughly 14+ hours of transit through the gut to turn black). Common causes: peptic ulcers, esophageal varices, Mallory-Weiss tears (mucosal tear from severe vomiting/retching), gastritis.

Lower GI bleeding (distal to the ligament of Treitz — jejunum, ileum, colon, rectum) classically presents with hematochezia (bright red or maroon blood per rectum). Common causes: diverticulosis (most common cause overall in older adults), hemorrhoids, colorectal cancer, angiodysplasia, and IBD.

Important exception examiners test: a brisk upper GI bleed can move through the gut too fast to be digested and can also present as hematochezia — so hemodynamic instability with bright red blood does not automatically rule out an upper source. This is exactly why the initial workup starts with resuscitation and risk stratification, not just anatomical guessing.

Initial management (the same first step regardless of source): assess and secure the airway, establish two large-bore IV lines, send blood for type and crossmatch, and begin fluid resuscitation. Only once the patient is stabilized does the workup pivot to identifying the exact source with endoscopy.

Diagnosis and Testing Across GI Disease

• Upper endoscopy (EGD): direct visualization of esophagus, stomach, duodenum; allows biopsy and therapeutic intervention (clipping, injection, banding of varices)
• Colonoscopy: visualizes the entire colon and terminal ileum; essential for diagnosing and staging IBD, detecting colorectal cancer, and localizing lower GI bleeds
• H. pylori testing: urea breath test and stool antigen test detect active infection; biopsy with rapid urease test done at time of endoscopy
• Liver function tests: AST/ALT reflect hepatocyte injury, alkaline phosphatase and GGT reflect cholestasis, albumin and INR reflect synthetic function
• Imaging: abdominal ultrasound for liver morphology and ascites; CT for complications like perforation or abscess

Key Terms

Term	Definition
Peptic ulcer	A mucosal break extending through the muscularis mucosae in the stomach or duodenum, usually from H. pylori or NSAIDs
Helicobacter pylori	A urease-producing bacterium that colonizes the gastric mucosa and is the leading infectious cause of peptic ulcers and gastric cancer
Melena	Black, tarry, foul-smelling stool caused by digested blood, typically from an upper GI source
Hematochezia	Bright red or maroon blood passed per rectum, typically from a lower GI source (but not always)
Transmural inflammation	Inflammation extending through the full thickness of the bowel wall, characteristic of Crohn's disease
Skip lesions	Patches of diseased bowel separated by normal, uninvolved segments, characteristic of Crohn's disease
Portal hypertension	Elevated pressure in the portal venous system, usually from cirrhosis, causing varices, splenomegaly, and ascites
Hepatic encephalopathy	Confusion and neurological impairment from the liver's failure to clear ammonia and other neurotoxins
Ligament of Treitz	The anatomical landmark at the duodenojejunal junction used to classify GI bleeding as upper or lower
Compensated cirrhosis	Cirrhosis in which the liver still performs its essential functions despite structural scarring

Common Mistakes

Misconception: "Bright red blood per rectum always means a lower GI source." Why it's wrong: A rapid, high-volume upper GI bleed (e.g., ruptured varix or large ulcer) can pass through the bowel too quickly to be broken down into melena, presenting instead as hematochezia. Correct understanding: Hemodynamic instability with hematochezia should still prompt consideration of an upper GI source, and initial management is resuscitation first, localization second.

Misconception: "Spicy food and stress directly cause peptic ulcers." Why it's wrong: While these can aggravate symptoms in someone who already has a mucosal defect, they are not the underlying cause. The two dominant causes are H. pylori infection and NSAID use. Correct understanding: Always screen for H. pylori and NSAID use in a patient with suspected PUD; treating the actual cause (eradication or stopping the drug) is what heals the ulcer.

Misconception: "Crohn's disease and ulcerative colitis are basically the same disease with different names." Why it's wrong: They differ in location (anywhere vs. colon/rectum only), continuity (skip lesions vs. continuous), and depth (transmural vs. mucosal), which changes their complications and whether surgery is curative. Correct understanding: Surgery cures ulcerative colitis (remove the colon, remove the disease) but does not cure Crohn's disease, which can recur anywhere in the GI tract — this single fact is tested constantly.

Comparison and Connections

Feature	Crohn's Disease	Ulcerative Colitis
Location	Anywhere, mouth to anus (favors terminal ileum)	Colon and rectum only
Distribution	Skip lesions (patchy)	Continuous, starts at rectum
Depth of inflammation	Transmural (full thickness)	Mucosa and submucosa only
Characteristic complications	Fistulas, strictures, abscesses	Bloody diarrhea, toxic megacolon
Cancer risk	Present but lower	Higher with long-standing pancolitis
Curative surgery	No — can recur elsewhere	Yes — colectomy is curative

Feature	Upper GI Bleed	Lower GI Bleed
Location	Proximal to ligament of Treitz	Distal to ligament of Treitz
Classic presentation	Hematemesis, melena	Hematochezia
Common causes	Peptic ulcer, varices, Mallory-Weiss tear	Diverticulosis, hemorrhoids, angiodysplasia, cancer
First-line investigation	Upper endoscopy	Colonoscopy (after stabilization)

Practice Questions

Recall

1. What are the two most common causes of peptic ulcer disease? Answer guidance: Helicobacter pylori infection and NSAID use — together they account for the vast majority of cases.

2. Which structure marks the boundary between an "upper" and a "lower" GI bleed? Answer guidance: The ligament of Treitz, at the duodenojejunal junction.

Understanding

3. Explain why NSAIDs predispose to peptic ulcers. Answer guidance: NSAIDs inhibit COX-1, reducing protective prostaglandin synthesis in the gastric mucosa, which normally maintains mucus and bicarbonate secretion and mucosal blood flow. Without this protection, acid damages the mucosa unopposed.

4. Why is surgery curative for ulcerative colitis but not for Crohn's disease? Answer guidance: Ulcerative colitis is confined to the colon and rectum, so removing the colon removes all diseased tissue. Crohn's disease can affect any part of the GI tract, so disease can recur in a segment that wasn't resected.

Application

5. A 60-year-old man on daily ibuprofen for knee arthritis presents with black, tarry stools and lightheadedness. What is the most likely diagnosis and what should be done first? Answer guidance: Likely an NSAID-induced peptic ulcer causing an upper GI bleed (melena suggests upper source). First priority is resuscitation — IV access, fluids, type and crossmatch — before arranging urgent upper endoscopy.

6. A 28-year-old woman has recurrent bloody diarrhea and colonoscopy shows continuous inflammation starting at the rectum and extending proximally, limited to the mucosa. What is the diagnosis, and how does this differ from what you'd expect in Crohn's disease? Answer guidance: Ulcerative colitis. Crohn's disease would show skip lesions, could involve any part of the GI tract (not just colon/rectum), and would show transmural inflammation possibly with fistulas or strictures.

Analysis

7. A cirrhotic patient develops confusion and asterixis. Explain the underlying mechanism and how it connects to the liver's normal function. Answer guidance: This is hepatic encephalopathy. The liver normally clears ammonia and other nitrogenous toxins produced by gut bacteria; when synthetic/detoxification function fails (or portosystemic shunting bypasses the liver), these toxins accumulate and impair brain function, producing confusion and the flapping tremor (asterixis).

8. Compare how you would distinguish a duodenal ulcer from a gastric ulcer using the history alone, and explain why this distinction is imperfect. Answer guidance: Classically, duodenal ulcer pain improves with food and wakes the patient at night, while gastric ulcer pain worsens with food. This distinction is imperfect because symptom overlap is common, so endoscopy with biopsy (especially for gastric ulcers, to exclude malignancy) remains the definitive diagnostic step.

FAQ

1. Is peptic ulcer disease always caused by stress? No. Stress and spicy food can worsen symptoms but do not cause ulcers on their own. The two major causes are H. pylori infection and NSAID use; rare causes include Zollinger-Ellison syndrome.

2. Can ulcerative colitis turn into Crohn's disease, or vice versa? No, they are distinct diseases, though a small subset of cases is labeled "indeterminate colitis" when features overlap and the distinction isn't clear on biopsy.

3. Why do gastric ulcers need a biopsy but duodenal ulcers usually don't? Gastric ulcers carry a real risk of being malignant, so biopsy is required to exclude gastric cancer. Duodenal ulcers are overwhelmingly benign, so routine biopsy isn't necessary.

4. Why does liver disease cause bleeding problems? The liver synthesizes most clotting factors. As synthetic function declines in cirrhosis, INR rises and bleeding risk increases — on top of the separate risk of variceal bleeding from portal hypertension.

5. How urgent is a suspected GI bleed? Very urgent. Any GI bleed with hemodynamic instability (tachycardia, hypotension) is a medical emergency requiring immediate resuscitation before diagnostic workup; even stable-appearing patients need prompt evaluation because bleeding can escalate quickly.

Quick Revision

• Peptic ulcer disease: mainly caused by H. pylori or NSAIDs; diagnose with endoscopy +/- H. pylori testing
• Duodenal ulcer pain classically improves with food; gastric ulcer pain classically worsens with food
• Gastric ulcers need biopsy to exclude malignancy; duodenal ulcers usually don't
• Crohn's disease: anywhere in GI tract, skip lesions, transmural, fistulas/strictures, surgery not curative
• Ulcerative colitis: colon/rectum only, continuous from rectum, mucosal only, bloody diarrhea, surgery curative
• Cirrhosis complications: portal hypertension (varices, splenomegaly), ascites, hepatic encephalopathy, coagulopathy, jaundice
• Ligament of Treitz divides upper GI bleed (hematemesis/melena) from lower GI bleed (hematochezia)
• A brisk upper GI bleed can still present as hematochezia — don't rule out upper source just because blood is bright red
• Diverticulosis is the most common cause of lower GI bleeding in older adults
• First step in any GI bleed: resuscitate (IV access, fluids, crossmatch) before localizing the source
• Hepatic encephalopathy results from failure to clear ammonia; presents with confusion and asterixis
• H. pylori confirmed by urea breath test or stool antigen; serology only shows past exposure

Related Topics

Prerequisites

• Basic anatomy of the GI tract (esophagus, stomach, small and large intestine)
• Normal physiology of gastric acid secretion and digestion

Related Topics

• General Surgery — surgical management of GI bleeding, perforation, and IBD complications
• Pharmacology — proton pump inhibitors, H2 blockers, and antibiotic regimens for H. pylori eradication
• Pathology — histological features of gastritis, IBD, and cirrhosis

Next Topics

• Hepatobiliary and Pancreatic Disorders
• Nutrition and Malabsorption Syndromes
• Gastrointestinal Malignancies