GI Bleed, Peptic Ulcer Disease & Gastritis

The stomach holds acid strong enough to digest tissue, and its own wall survives only because defense keeps pace with attack. The protective side of the ledger is mucus, bicarbonate, prostaglandins, and mucosal blood flow; the destructive side is gastric acid and pepsin. Peptic ulcer disease results from an imbalance between these protective and destructive factors: when defense weakens, the mucosal surface becomes vulnerable to the acid it normally shrugs off, and the break can extend into the muscularis propria.

Gastritis is the inflammatory sibling of the same story — inflammation of the gastric mucosa, classified by acuity (acute vs chronic), histology, or etiology. Acute stress and reactive gastritis follow insults that strip defenses fast: uremia, ischemia, shock, corrosive agents, medications, radiation, trauma, severe burns, sepsis, alkaline-bile reflux, and alcohol. The primary cause of chronic gastritis is H. pylori infection.

Two culprits cause the overwhelming majority of peptic ulcers, and each dismantles defense by a different mechanism. H. pylori, a gram-negative spiral bacterium, survives gastric acid by making urease, which hydrolyzes urea into ammonia and buffers a protective layer around the organism; its flagella then burrow it down to the epithelium. There, virulence factors CagA and VacA drive inflammation, colonization impairs bicarbonate secretion and promotes acidity and gastric metaplasia, and the resulting chronic mucosal inflammation steadily weakens the wall’s defenses.

NSAIDs attack the defense chemically. Prostaglandins normally protect the gastric mucosa; NSAIDs inhibit COX-1 and block prostaglandin synthesis, decreasing gastric mucus and bicarbonate production and reducing mucosal blood flow. Classically H. pylori accounts for about 90% of duodenal ulcers and 70–90% of gastric ulcers, with NSAIDs the second most common cause overall — though for gastric ulcers specifically, newer framing has NSAID use surpassing H. pylori as the leading cause, with gastric ulcers found in 10–30% of NSAID users.

Two teaching corrections follow from the mechanisms. First: stress and spicy foods do not cause ulcers — they can make them worse, but the causes are the bacterium and the drugs. Second: chronic H. pylori gastritis may remain asymptomatic while it progresses toward severe complications like gastric cancer — symptoms correlate poorly with pathology, which is why testing and treating the infection matters even when nothing hurts.

Where the ulcer sits changes when it hurts, and the pattern is a classic exam hook. Gastric-ulcer pain begins 15–30 minutes after a meal and worsens with eating — sharp or burning, often with mild nausea and early satiety — so patients eat less and lose weight. Duodenal-ulcer pain appears 2–3 hours after a meal, is relieved by food, and nocturnal pain is common; because eating soothes it, these patients may gain weight. The generic picture is burning epigastric pain that starts between meals or during the night, briefly stops with food or antacids, lasts minutes to hours, and comes and goes over days to weeks.

Duodenal ulcers are about four times more common than gastric ulcers, more common in men, and over 95% of them sit in the first portion of the duodenum, roughly 90% within 3 cm of the pylorus. Lifetime PUD risk runs 5–10% — and recurrence exceeds 60% in most series, which is why eradicating the cause matters more than soothing the symptom.

One more variant worth knowing: autoimmune gastritis, a T-cell-mediated destruction of the acid-producing mucosa with autoantibodies against parietal cells and intrinsic factor. It causes severe atrophic gastritis and is often discovered only when the patient presents with pernicious (B12-deficiency) or iron-deficiency anemia — no intrinsic factor, no B12 absorption.

PUD is the leading cause of upper GI bleeding (32–36% of cases, ahead of esophagitis, gastritis, duodenitis, varices, and Mallory-Weiss tears). What the blood looks like when it appears tells you where it came from and how fast it is moving. Bright-red hematemesis means active upper bleeding now. Coffee-ground emesis — vomitus with dark specks of old blood — means an older or slower bleed, altered by gastric acid. Melena, the black, sticky, tarry stool with its distinctive odor, is an upper-source signature: gastric acid converts blood to acid hematin in transit, which is exactly why upper-GI blood turns black. Hematochezia, bright-red blood per rectum, usually means a lower source — but a brisk, large-volume upper bleed can outrun the acid conversion and appear bright red below, and hematemesis occurring together with hematochezia points upper.

Bleeding can also be occult — so small that only a lab test finds it. The fecal occult blood test detects hidden blood invisible to the eye; a positive result means bleeding somewhere in the digestive tract and earns follow-up testing, most commonly colonoscopy.

The volume story is the dangerous one, because the body hides it. Early hypovolemia keeps blood pressure near-normal; tachycardia is typically the first abnormal vital sign of hemorrhagic shock, and the upright blood pressure falls before the supine one does. Only around 30% blood loss does pressure drop in any position, with mental-status changes and declining urine output; beyond 40%, hypotension comes with a narrow pulse pressure and urine output that is minimal or absent. A GI-bleed patient with a normal lying blood pressure has proven nothing — sit them up, trend the pulse, and watch the urine.