Peptic Ulcer Disease: When Acid Bites Back

A small sore with big ambitions

The stomach, that muscular bag of acid and appetite, is built for abuse. It churns, digests, and disinfects, bathing itself daily in a cauldron of hydrochloric acid strong enough to dissolve a nail.

Yet, occasionally, its defences falter. The mucosal barrier thins, the acid seeps in, and an ulcer forms.
That, my friends, is Peptic Ulcer Disease, the great leveller of mankind, afflicting kings and commoners alike, from Alexander the Great to the man with a takeaway addiction.

The anatomy of an ulcer

peptic ulcer is simply a break in the mucosal lining of the stomach or duodenum that penetrates the muscularis mucosae, forming a crater. Depending on where that crater sits, it earns one of two names:

  • Gastric ulcer: usually on the lesser curvature of the stomach.
  • Duodenal ulcer: typically in the first part of the duodenum.

Together, they make up a disease of imbalance: the equilibrium between the stomach’s aggressive forces (acid and pepsin) and defensive mechanisms (mucus, bicarbonate, mucosal blood flow) collapses. The result: digestion of one’s own gut wall.

Two main culprits: bugs and drugs

Forget stress and spicy food, those are supporting actors. The real villains of the piece are Helicobacter pylori and NSAIDs.

1. Helicobacter pylori: the microbe that rewrote textbooks

Once upon a time, ulcers were blamed on anxiety and bad temper. Then in 1982, two Australian doctors, Barry Marshall and Robin Warren, discovered H. pylori, a spiral-shaped bacterium that burrows into the gastric mucosa, neutralises acid with urease, and triggers inflammation.

By the 1990s, it was clear: H. pylori causes most duodenal and many gastric ulcers. The Nobel Committee eventually caught up in 2005.

2. NSAIDs: the chemical saboteurs

Non-steroidal anti-inflammatory drugs (aspirin, ibuprofen, naproxen) inhibit prostaglandin synthesis. Prostaglandins normally protect the mucosa by enhancing mucus and bicarbonate secretion and maintaining blood flow. Remove them, and acid gains the upper hand.
Add steroids, smoking, or alcohol, and the damage multiplies.

Pathophysiology: the acid wars

The stomach’s lining is a battlefield of offence and defence:

Offense (Aggressors)Defence (Protectors)
Hydrochloric acidMucus-bicarbonate layer
PepsinMucosal blood flow
H. pyloriCell regeneration
NSAIDsProstaglandins

When acid and pepsin overwhelm these protective systems, the mucosa erodes, and an ulcer forms. In H. pylori infection, chronic gastritis leads to increased acid production in duodenal ulcers, or mucosal atrophy and reduced acid in gastric ulcers. Either way, balance is lost.

The pain that knows the clock

Peptic ulcer pain has a personality, it follows a schedule.

  • Duodenal ulcer: pain comes hours after eating, often waking patients at night; relieved by food or antacids.
  • Gastric ulcer: pain occurs soon after eating, sometimes worsened by meals.

Patients describe it as a dull, burning, or gnawing ache in the epigastrium, occasionally radiating to the back. Nausea, bloating, and early satiety are common. In some, the first sign is dramatic: vomiting blood (haematemesis) or passing black, tarry stools (melaena).

Diagnosis: beyond the barium meal

The days of barium studies and “niche” shadows on X-rays are gone. Today’s diagnosis is direct and elegant.

  • Endoscopy (OGD): the gold standard. It visualises the ulcer, allows biopsy (to exclude malignancy), and tests for H. pylori.
  • H. pylori detection:
    • Urea breath test: highly accurate, non-invasive.
    • Stool antigen test: equally effective.
    • Biopsy urease test (CLO test): rapid, done during endoscopy.
    • Serology: less useful now (can’t distinguish past from current infection).

Always biopsy a gastric ulcer, cancer can masquerade as one. Duodenal ulcers, in contrast, are almost always benign.

Management: heal the mucosa, tame the acid, kill the bug

The principles are simple but sacred: eradicate the cause, suppress the acid, protect the lining.

1. Eradicate H. pylori

The standard triple therapy:

  • Proton pump inhibitor (PPI) +
  • Clarithromycin +
  • Amoxicillin (or Metronidazole if penicillin-allergic)

Duration: 14 days. Test for cure at least 4 weeks after completion, with a urea breath or stool antigen test.

2. Stop NSAIDs and other offenders

If possible, discontinue NSAIDs. If they’re essential (e.g., for arthritis), co-prescribe a PPI or switch to a selective COX-2 inhibitor.

3. Suppress acid

PPIs (omeprazole, lansoprazole, pantoprazole) are the cornerstone. They promote healing faster and more completely than H2 blockers (like ranitidine, now largely obsolete).

4. Protect the mucosa

Add sucralfate or misoprostol if needed.
Misoprostol restores prostaglandin protection but is contraindicated in pregnancy (it induces uterine contractions).

Complications: when ulcers misbehave

Most ulcers heal quietly. Some, however, declare war on their host.

ComplicationDescription / Clinical Clue
BleedingMost common. Haematemesis or melaena; check for anaemia.
PerforationSudden severe pain, rigid abdomen, air under diaphragm. Surgical emergency.
Gastric outlet obstructionFrom chronic scarring; causes vomiting, distension, and dehydration.
Malignant transformationRare, but always exclude in gastric ulcers.

Life after the ulcer

Once healed, prevention becomes the mission.
Eradicate H. pylori, avoid NSAIDs, and manage stress and diet wisely. Contrary to myth, coffee and chilli are not primary causes, but moderation is always sensible.

Smoking cessation improves healing, and alcohol reduction helps the mucosa recover.

The legacy of an old disease

For centuries, peptic ulcers were blamed on nerves and character. “Ulcer personality,” they called it, driven, anxious, perfectionist.
Then came H. pylori, proving the world wrong and reminding medicine that even small discoveries can topple big dogmas.

Today, we can cure most ulcers with tablets and time. What remains are the complications of neglect, bleeding ulcers in the elderly on aspirin, perforations in those who mistake pain for indigestion, and the rare malignancy masquerading as a benign sore.

Clinical pearls

  • Epigastric pain relieved by food → duodenal ulcer.
  • Epigastric pain worsened by food → gastric ulcer.
  • Never trust a gastric ulcer until it’s biopsied twice.
  • If a patient on NSAIDs presents with anaemia or black stools, assume the worst until proven otherwise.

A final thought

The stomach is an organ of strength and discipline, it keeps the peace between acid and tissue every single day.
Peptic ulcer disease is what happens when that peace treaty collapses.

So, respect your stomach.
Feed it sensibly, protect it from needless drugs, and never underestimate a dull ache in the epigastrium.

Because when acid bites back, it bites deep.

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