GORD & Peptic Ulcer Disease: PPIs, H2 Blockers & H. pylori
From heartburn to bleeding ulcers — understanding acid suppression, eradication therapy, and long-term PPI stewardship for UK nurses.
Proton pump inhibitors (PPIs) are among the most commonly prescribed medications in the UK — and also among the most misunderstood. You will give omeprazole, lansoprazole, or pantoprazole on nearly every drug round. But do you know how they differ from H2 antagonists? Why Helicobacter pylori matters? And what risks come with long-term use? As a nurse, you are not just administering a tablet — you are in a position to question, review, and educate patients on one of the most over-prescribed drug classes in clinical practice.
This guide covers gastro-oesophageal reflux disease (GORD) and peptic ulcer disease from mechanism to monitoring, fully aligned with NICE guidance and BNF recommendations — including the red flags that mean “stop antacids and investigate now.”
1. National Guidance
All content aligned with: NICE Guideline CG184 — Gastro-oesophageal Reflux Disease and Dyspepsia; NICE NG23 — Suspected Peptic Ulcer Disease; and Maastricht VI/Florence Consensus on H. pylori management. Drug monitoring and duration cross-referenced with current BNF Chapter 1.1.
📎 Source: NICE CG184 — GORD & Dyspepsia
📎 Source: NICE NG23 — Suspected Peptic Ulcer
⚠️ Local endoscopy referral thresholds vary. Your trust may use different age cut-offs or red-flag criteria for urgent investigation. Always follow local pathways.
2. GORD vs Peptic Ulcer — What’s the Difference
Both involve stomach acid, but at different sites and for different reasons — and the red flags differ significantly:
| Condition | Site | Core Problem | Typical Symptoms |
|---|---|---|---|
| GORD | Oesophagus — lower sphincter | Weakened barrier lets acid reflux upwards | Retrosternal burning, worse lying down, after large meals, or caffeine/alcohol. Water brash, nocturnal cough. |
| Gastric Ulcer | Stomach lining | Mucosal break >5mm, depth to submucosa — acid pepsin digests exposed tissue | Pain worse on eating → weight loss. Epigastric, gnawing. Nausea common. |
| Duodenal Ulcer | First part of small intestine | Excess acid or reduced protective mucus | Pain relieved by eating → weight gain. Often nocturnal, rhythmic. Highly linked to H. pylori. |
Key Causes & Risk Factors
- H. pylori infection: Responsible for ~90% of duodenal ulcers and 70% of gastric ulcers. Gram-negative bacterium colonising gastric mucosa — disrupts protective mucus, triggers chronic inflammation, drives excess gastrin → excess acid. Transmitted faecal-oral; more common in crowded/low-sanitation settings.
- NSAID use: Inhibits protective prostaglandins → mucosal vulnerability. Long-term or high-dose NSAIDs carry highest risk. Including low-dose aspirin — not harmless to the gut.
- Excess acid secretion: Zollinger-Ellison syndrome (rare gastrinoma), smoking, high-fat meals, obesity, hiatal hernia, pregnancy.
- Reduced mucosal defence: Ageing, chronic illness, steroids, alcohol, psychological stress.
3. Drug Classes — How They Actually Work
There are three main tiers of acid-related medication. Knowing which tier you’re giving explains why one patient gets Gaviscon, another omeprazole, and a third both.
3.1 Antacids & Alginates — Neutralise & Float
These are physical treatments — they do not stop acid production. They work instantly but effects are short-lived:
| Type | Examples | Mechanism | Nursing Notes |
|---|---|---|---|
| Antacids | Magnesium trisilicate, calcium carbonate, aluminium hydroxide | Chemically neutralise existing stomach acid → rapid pain relief | Mg salts → diarrhoea; Al salts → constipation. Give 1–2 hours after meals. Interfere with absorption of many drugs — separate by 2 hours. |
| Alginates | Gaviscon — sodium alginate + potassium bicarbonate | Forms foam “raft” on top of stomach contents → physical barrier against reflux | Best taken after meals and at bedtime — empty stomach = raft clears too fast. Higher sodium content — caution in heart failure or hypertension. |
3.2 H2-Receptor Antagonists — The “Middle Tier”
Histamine stimulates acid secretion via H2 receptors on parietal cells. These drugs block that signal — reduce but do not eliminate acid production:
| Drug | Usual Dose | Key Points |
|---|---|---|
| Famotidine | 20–40 mg daily, usually at night | Fewer interactions than cimetidine. Renal dose adjustment needed. Not for long-term unsupervised use. |
| Cimetidine | 200–400 mg up to 4× daily | Strong CYP450 inhibitor — interacts with warfarin, digoxin, theophylline. Gynecomastia risk with long-term use. |
H2 blockers are less effective than PPIs, tolerance develops in ~2 weeks, and they don’t heal oesophagitis as reliably. NICE recommends stepping down to them as maintenance after PPI control, not as first-line for severe GORD or proven ulcer.
📎 Source: NICE CG184 — Initial & Maintenance Treatment
3.3 Proton Pump Inhibitors — The Gold Standard
These act at the final common pathway of acid secretion — the H⁺/K⁺-ATPase enzyme (“proton pump”) on the surface of the acid-producing cell. By blocking this pump directly, they reduce acid by up to 90% and heal oesophageal/duodenal ulcers in 4–8 weeks. They are the most effective acid suppressors available — and the most potent.
| Drug | Standard Dose | Nursing Administration Rule |
|---|---|---|
| Omeprazole | 20–40 mg once daily | Best taken 30–60 mins before breakfast — parietal cells most active then; food delays absorption. |
| Lansoprazole | 15–30 mg once daily | Before food. Orally disintegrating tablets available for dysphagia — place on tongue, dissolve, swallow no water needed. |
| Pantoprazole | 20–40 mg once daily | More stable at neutral pH — IV option available for NBM patients. Less CYP450 interaction than omeprazole. |
| Esomeprazole | 20–40 mg once daily | Pure isomer of omeprazole — slightly higher bioavailability, similar effect. Often brand-prescribed. |
PPIs are prodrugs — they only activate in actively secreting acid. If given after a meal, the pump is already busy and the drug passes through largely inactive. Patients taking omeprazole with or after breakfast are effectively taking half a dose. Check the timing on every admission and teach it on discharge.
4. H. pylori — Triple & Quadruple Eradication
Detecting and treating H. pylori changes patient outcomes permanently — ulcers stop recurring in ~90% of cases after successful eradication. NICE recommends non-invasive testing first in uninvestigated dyspepsia under 55 without red flags.
4.1 Testing — Urea Breath Test vs Stool Antigen
- Urea Breath Test (UBT): Patient ingests labelled urea. If H. pylori present, enzyme breaks it down → labelled CO₂ in breath. PPIs must be stopped 2 weeks before and bismuth 4 weeks before — false negatives otherwise.
- Stool Antigen Test: Detects bacterial proteins in faeces. Equivalent accuracy; fewer restrictions on acid suppression but still stop PPIs where possible.
- Serology (blood test): Detects antibodies — cannot distinguish active from past infection. NICE advises against using it as the sole test.
📎 Source: NICE CG184 — H. pylori Testing
4.2 First-Line Triple Therapy
Standard 7–14 day course — local resistance patterns determine choice:
| Component | Example | Purpose & Key Safety |
|---|---|---|
| PPI (high dose) | Omeprazole 20 mg twice daily | Suppress acid → antibiotics work (many are acid-sensitive). Twice daily during eradication, not once. |
| Antibiotic 1 | Amoxicillin 1 g twice daily | Penicillin-based — always confirm allergy first. Macrolide alternative if penicillin-allergic. |
| Antibiotic 2 | Clarithromycin 250–500 mg twice daily OR Metronidazole 400 mg three times daily | Clarithromycin resistance rising locally — check trust formulary. Metronidazole: no alcohol (disulfiram reaction). |
If first-line fails → second-line quadruple therapy adds bismuth subsalicylate and extends course. Retest after treatment — UBT or stool antigen minimum 4 weeks post-completion.
5. Long-Term PPI Use — Risks & Deprescribing
PPIs are often started in hospital and never reviewed. NICE and the MHRA both highlight that many patients remain on them longer than clinically necessary. These are the evidence-based associations you need to know:
- Bone fractures: Reduced calcium absorption + altered osteoclast activity → increased hip/spine fracture risk, especially >1 year, high dose, age >50. Ensure adequate calcium/vitamin D intake — covered in exam preparation.
- Clostridioides difficile infection: Acid suppression removes a primary gut defence → significantly higher risk. Review before starting broad-spectrum antibiotics in at-risk patients.
- Nutrient malabsorption: Iron, B12, magnesium, and folate all need acid for uptake. Check levels on long-term use — covered in clinical case studies.
- Renal injury: Interstitial nephritis — rare but idiosyncratic. Watch for rising creatinine/eGFR with no other cause — see AKI guide.
- Rebound acid hypersecretion: Sudden stop = symptoms worse for 1–2 weeks. Taper down — reduce dose or alternate days over 4–8 weeks.
📎 Source: NICE CG184 — Review & Deprescribing | MHRA — Long-term PPI Safety
Deprescribing — The Nurse’s Role
Every patient on a PPI should have a documented review date. The stepped approach:
- Confirm indication — still active GORD? Healed ulcer needing maintenance? Or just carried over from admission?
- Step down from full to half dose → alternate days → PRN alginate only
- Lifestyle reinforcement: weight loss, smaller meals, avoid trigger foods, elevate bed head, no eating within 3 hours of sleep
- Document patient understanding and follow-up plan
6. Red Flags — When to Refer Urgently
These “alarm symptoms” mandate urgent investigation (NICE 2-week wait pathway). Age >55 with new-onset dyspepsia alone qualifies:
| Red Flag | What It May Indicate | Action |
|---|---|---|
| Dysphagia — difficulty swallowing, food sticking | Oesophageal stricture, malignancy | Refer 2-week wait. Do NOT just increase PPI dose — covered in deterioration recognition. |
| Odynophagia — painful swallowing | Ulceration, candidiasis, malignancy | Investigate promptly — can’t manage safely in primary care alone. |
| Unexplained weight loss / anorexia | Gastric/oesophageal cancer; malabsorption | Urgent referral. Check BMI and nutritional status — see exam assessment skills. |
| Haematemesis / Melaena | Bleeding ulcer — upper GI haemorrhage | Assess: BP, pulse, NEWS2. IV access, cross-match, escalate urgently. Melaena = black tarry stool = significant blood loss. |
| Iron-deficiency anaemia no other cause | Occult GI bleeding | Faecal occult blood test → endoscopy. Do NOT just prescribe iron and discharge. |
| Palpable epigastric mass | Advanced malignancy | Urgent referral. |
📎 Source: NICE NG23 — Endoscopy & Suspected Cancer Referral
7. Drug Interactions You Must Know
PPIs are enzyme inhibitors — they change how other drugs are cleared. These combinations appear on every ward:
- Clopidogrel + Omeprazole/Esomeprazole: Controversial but widely cited — omeprazole may reduce clopidogrel’s antiplatelet effect via CYP2C19. Pantoprazole or lansoprazole preferred in acute coronary/stent patients per many trust formularies.
- Warfarin + any PPI: Reduced metabolism → INR rises. Monitor more frequently when starting/stopping — see anticoagulation monitoring.
- Digoxin + PPI: Acid changes affect absorption — levels may shift. Check levels and clinical response.
- Iron supplements + PPI: Oral iron needs gastric acid to convert to absorbable form → reduced efficacy. Space doses where possible.
- Methotrexate + PPI: Rare but serious — PPIs can reduce methotrexate clearance → toxicity risk. Discuss with prescriber.