After reading this note you will be able to describe the clinical approach to dyspepsia and peptic ulcer disease, list relevant local risk factors, interpret key investigations and outline safe initial and definitive management – remembering to verify doses and local protocols against the Kenya MoH guideline and your hospital formulary.
Definition
- Dyspepsia: persistent or recurrent pain or discomfort centered in the upper abdomen, often accompanied by early satiety, post‑prandial fullness, bloating, nausea or belching, lasting ≥ 4 weeks.
- Peptic ulcer disease (PUD): mucosal breach ≥ 5 mm in the stomach or duodenum that extends through the muscularis mucosa, confirmed endoscopically or radiologically, and associated with typical ulcer‑related symptoms.
Anatomy and physiology you need
| Structure | Relevance to dyspepsia/PUD |
|---|---|
| Esophagogastric junction (lower esophageal sphincter) | Barrier to reflux; dysfunction contributes to epigastric pain. |
| Gastric fundus & body | Parietal cell acid secretion; H. pylori colonisation often in antrum. |
| Duodenal bulb | Common site of duodenal ulcer; exposed to gastric acid and bile. |
| Mucosal protective layer (bicarbonate, mucus, prostaglandins) | Deficiency predisposes to ulcer formation. |
| Vagus nerve (parasympathetic) | Stimulates acid secretion; vagotomy reduces ulcer recurrence. |
| Submucosal blood flow | Ischaemia impairs healing, relevant in NSAID‑related ulcers. |
Causes and risk factors
| Category | Specific factors in Kenya |
|---|---|
| Infectious | Helicobacter pylori infection, HIV‑associated gastritis, intestinal TB involving the duodenum |
| Medications | NSAIDs, low‑dose aspirin, corticosteroids, antiretrovirals (e.g., protease inhibitors) |
| Lifestyle | Heavy alcohol use, smoking, khat chewing, irregular meals |
| Systemic disease | Sickle cell disease (gastric ischaemia), rheumatic fever (auto‑immune gastritis), chronic malaria (stress ulcer risk) |
| Socio‑economic | Low socioeconomic status, crowded living conditions (higher H. pylori prevalence) |
| Others | Stress (critical illness), Zollinger‑Ellison syndrome (rare) |
Pathophysiology
- H. pylori infection → bacterial urease ↑ → gastric pH ↑ → bacterial colonisation → chronic gastritis → mucosal damage → ulcer.
- NSAID/aspirin use → cyclo‑oxygenase inhibition → prostaglandin ↓ → mucus & bicarbonate ↓ + mucosal blood flow ↓ → ulcer.
- Acid hypersecretion (e.g., Zollinger‑Ellison) → gastric acid ↑ → overwhelms mucosal defenses → ulcer.
- Ischaemia (sickle cell, severe malaria) → mucosal blood flow ↓ → impaired repair → ulcer.
- Stress/critical illness → sympathetic surge → reduced mucosal perfusion + acid ↑ → stress ulcer.
Arrows illustrate the cascade: trigger → loss of protection → acid injury → ulcer formation.
Clinical features
| Aspect | Key questions / findings | Why it matters |
|---|---|---|
| Onset | “When did the discomfort start? Was it sudden or gradual?” | Acute onset may suggest complications (bleed, perforation) or infection (e.g., H. pylori‑related gastritis). |
| Location & character | Epigastric pain vs. burning vs. heaviness; radiation to back or chest. | Epigastric burning typical of acid‑related disease; back radiation raises suspicion of penetrating ulcer. |
| Timing related to meals | “Does it occur before a meal, during, or 2‑3 h after eating?” “Does eating relieve or worsen it?” | Pain that improves with food → duodenal ulcer; pain that worsens with food → gastric ulcer or gastritis. |
| Nocturnal symptoms | “Do you wake up with pain?” | Night pain suggests acid hypersecretion or refractory ulcer. |
| Associated symptoms | Nausea, vomiting (especially coffee‑ground), early satiety, bloating, belching, weight loss, dysphagia, odynophagia, hematemesis, melena, anemia‑related fatigue. | Vomiting of blood or melena points to bleeding ulcer; weight loss or dysphagia may indicate malignancy or severe gastropathy. |
| Red‑flag features | Age > 55, unexplained weight loss, persistent vomiting, anemia, GI bleeding, dysphagia, odynophagia, family history of gastric cancer, NSAID use > 3 months. | Prompt endoscopic evaluation is required; higher pre‑test probability of malignancy or complicated ulcer. |
| Medication history | NSAIDs, aspirin, steroids, antiplatelets, PPIs, H2‑blockers, herbal remedies, antiretrovirals, anti‑TB drugs. | NSAIDs and steroids impair mucosal defence → ulcer; antiretrovirals (especially protease inhibitors) increase gastric acidity. |
| Social & exposure history | Alcohol intake, smoking, coffee/tea consumption, stress, recent travel, known H. pylori infection, HIV status, TB exposure, malaria episodes, sickle‑cell crises. | Smoking, alcohol, and stress aggravate acid secretion; HIV, TB, malaria, sickle‑cell disease can cause gastritis/ulcer through mucosal ischemia or opportunistic infection. |
| Past GI history | Previous ulcer disease, endoscopic findings, H. pylori eradication, surgeries. | Recurrence risk is higher after prior ulcer; informs need for repeat testing. |
Examination findings and rationale
| Finding | Expected result | Pathophysiological explanation |
|---|---|---|
| General appearance | Pallor, cachexia, dehydration | Chronic blood loss → anemia; poor intake → weight loss; vomiting → volume depletion. |
| Vital signs | Tachycardia, hypotension (if bleeding); fever (if infection) | Hemodynamic response to acute bleed; fever may indicate perforation or secondary infection (e.g., TB peritonitis). |
| Abdominal inspection | Visible peristalsis, distension | May be present in severe gastric outlet obstruction. |
| Palpation | Epigastric tenderness, guarding, rigidity (perforation); palpable mass (advanced cancer) | Local inflammation or peritoneal irritation; mass effect from tumor or enlarged lymph nodes. |
| Auscultation | Hyperactive bowel sounds (early obstruction) or absent (perforation with ileus) | Reflects motility changes secondary to pain or inflammation. |
| Percussion | Tympanic over gas‑filled stomach (gastric outlet obstruction) | Accumulation of gastric contents due to obstructive ulcer scar. |
| Rectal exam | Melena or occult blood | Confirms upper GI bleeding when stool is black/tarry. |
| Extra‑intestinal signs | Oral thrush, lymphadenopathy (HIV), hepatosplenomegaly (TB, malaria) | Systemic infections that can predispose to mucosal ulceration. |
Differential diagnosis
| Condition | Points toward it | Distinguishing features |
|---|---|---|
| Peptic ulcer disease | Epigastric burning, meal‑related timing, NSAID/H. pylori risk | Endoscopic ulcer, positive H. pylori test, response to acid suppression |
| Functional dyspepsia | No alarm features, normal endoscopy, symptom chronicity > 3 months | Absence of structural lesion, symptom improvement with low‑dose PPI or prokinetic |
| Gastric cancer | Age > 55, weight loss, anemia, persistent vomiting, family history | Endoscopic mass, malignant histology, often refractory to acid suppression |
| Gastritis (infective) | Recent malaria, TB, HIV, sickle‑cell crisis, NSAID use, mucosal erythema on endoscopy | Histology showing inflammatory infiltrate, often resolves with eradication of infection |
| Gastro‑esophageal reflux disease | Heartburn, regurgitation, symptoms worse after lying down | Endoscopy shows esophagitis, not ulcer; response to lifestyle + PPI |
| Pancreatitis | Upper abdominal pain radiating to back, elevated amylase/lipase, alcohol use | Enzyme elevation, CT findings, pain not relieved by food |
| Gallstone disease / biliary colic | RUQ pain, post‑prandial, radiates to right shoulder | Ultrasound shows stones, liver function tests abnormal |
Investigations
| Test | What it answers | Interpretation |
|---|---|---|
| Full blood count | Anemia, infection | Low Hb → chronic bleed; leukocytosis → infection/perforation |
| Serum electrolytes & renal function | Dehydration, renal impairment | Elevated urea/creatinine suggests volume loss or bleed |
| Liver function tests | Hepatobiliary disease | Raised ALP/ bilirubin → consider biliary cause |
| Stool occult blood | Hidden GI bleed | Positive → supports ulcer or malignancy |
| Urea breath test / stool antigen | Active H. pylori infection | Positive → need eradication therapy |
| Serology for HIV / TB | Underlying immunosuppression or infection | Positive guides adjunctive therapy |
| Upper GI endoscopy | Direct visualization, biopsy, therapy | Ulcer grade, malignancy, H. pylori testing; biopsies for cancer |
| Abdominal ultrasound | Exclude gallbladder disease, assess liver, detect free fluid | Normal gallbladder supports ulcer; free fluid suggests perforation |
| CT abdomen (if perforation suspected) | Detect free air, abscess | Free intra‑peritoneal air confirms perforation |
Diagnosis and severity
- Confirmatory diagnosis
- Endoscopic evidence of a mucosal break ≥ 5 mm with clean base → peptic ulcer.
- Absence of ulcer on endoscopy with normal histology → functional dyspepsia.
- Malignant lesion on biopsy → gastric cancer.
- Severity grading (based on endoscopic findings and clinical status)
| Grade | Endoscopic appearance | Clinical correlates |
|---|---|---|
| Mild | Small (< 5 mm) superficial ulcer, no bleeding stigmata | Minimal pain, no anemia, stable vitals |
| Moderate | Ulcer 5‑10 mm, visible vessel or adherent clot, mild anemia | Intermittent melena, mild tachycardia |
| Severe / complicated | Ulcer > 10 mm, active spurting bleed, perforation, obstruction, or malignant features | Hemodynamic instability, peritonitis, massive melena, obstructive symptoms |
- Risk stratification for urgent endoscopy
- High‑risk: age > 55, anemia, overt GI bleed, weight loss, NSAID use, comorbid HIV/TB.
- Low‑risk: younger, no alarm features, stable vitals → can defer endoscopy 4‑6 weeks after empiric therapy.
The clinical approach proceeds from thorough history and focused exam, through targeted investigations, to endoscopic confirmation and grading, allowing timely initiation of acid‑suppression, eradication of H. pylori, and management of complications.
Management
Immediate stabilisation
- Assess airway, breathing, circulation; give supplemental O₂ if SpO₂ < 94 %.
- Establish IV access; give crystalloid bolus for hypotension or signs of volume depletion (e.g., orthostatic drop, tachycardia).
- Treat active upper GI bleed urgently:
– Resuscitate, transfuse packed cells to keep Hb > 8 g/dL (or > 10 g/dL in pregnancy).
– Give a proton‑pump inhibitor (PPI) bolus intravenously, then continuous infusion.
– Call endoscopy team for urgent (< 12 h) upper GI endoscopy.
Definitive treatment
| Situation | First‑line therapy | Rationale |
|---|---|---|
| Uncomplicated dyspepsia (no alarm features) | Empiric PPI trial (8 weeks) | Acid suppression heals most functional dyspepsia and small ulcers. |
| H. pylori‑positive ulcer disease | Triple therapy (PPI + clarithromycin + amoxicillin) or quadruple therapy (PPI + bismuth + metronidazole + tetracycline) for 14 days | Eradicates infection; reduces recurrence. |
| H. pylori‑negative ulcer disease | PPI alone (8 weeks) ± H2‑blocker if needed | Allows ulcer healing by suppressing acid. |
| NSAID‑induced ulcer | Stop/replace NSAID, start PPI (high‑dose) and consider misoprostol if NSAID cannot be stopped | Protects mucosa and promotes healing. |
| HIV‑associated ulcer (CMV, TB) | Treat underlying infection (antiretroviral optimisation, anti‑TB regimen, ganciclovir for CMV) + PPI | Addresses the specific pathogen driving ulceration. |
| Refractory ulcer after 8 weeks therapy | Repeat endoscopy, test for resistant H. pylori, consider second‑line eradication regimen, assess for malignancy | Ensures missed pathology is not overlooked. |
Monitoring & safety
- Re‑evaluate symptoms after 4–8 weeks of therapy; if persistent, arrange endoscopy.
- Check for PPI side‑effects (e.g., magnesium loss, C. difficile risk) in long‑term users.
- For patients on long‑term NSAIDs, add PPI prophylaxis and monitor renal function.
- In HIV/TB patients, monitor drug interactions (e.g., rifampicin reduces PPI levels).
Contra‑indications
- PPI: caution in severe hepatic impairment (dose adjustment) and known hypersensitivity.
- Clarithromycin: avoid in patients with QT prolongation or taking drugs that inhibit CYP3A4.
- Metronidazole: contraindicated in first‑trimester pregnancy and severe hepatic disease.
Complications and prognosis
- Bleeding (most common acute complication): presents as haematemesis or melena; mortality rises if not controlled promptly.
- Perforation: sudden severe epigastric pain with rigid abdomen; requires emergency surgery; prognosis depends on time to operation.
- Penetration into adjacent organs (pancreas, liver): may cause persistent pain, fistula formation.
- Gastric outlet obstruction: chronic ulcer scarring leads to pyloric stenosis; presents with vomiting of undigested food.
- Malignancy: chronic H. pylori infection increases risk of gastric adenocarcinoma and MALT lymphoma; eradication reduces long‑term risk.
Overall, with appropriate eradication of H. pylori and acid suppression, most ulcers heal within 8 weeks and recurrence is low. Untreated complications carry significant morbidity and mortality.
High‑yield exam points
- Look‑alike conditions: functional dyspepsia, gastro‑oesophageal reflux disease, gastric cancer, pancreatitis, biliary colic.
- Commonest wrong first step: ordering endoscopy in a young patient without alarm features before a therapeutic trial of PPI.
- Bedside examiner questions:
- “What alarm features would make you bypass a PPI trial and go straight to endoscopy?”
- “Explain why you would test for H. pylori before starting long‑term PPI therapy.”
- “How does HIV alter the differential diagnosis of a gastric ulcer?”
- “What is the rationale for adding a bismuth compound in quadruple therapy?”
Clinical case
Case: A 38‑year‑old male farmer presents with a 3‑week history of epigastric burning, worsened on meals, and occasional early satiety. No vomiting. He reports a 4 kg weight loss and occasional black stools. He is HIV‑positive, on antiretroviral therapy, and frequently uses ibuprofen for chronic knee pain. Examination shows mild epigastric tenderness, no guarding, and a hemoglobin of 11 g/dL.
Questions
- What is the most appropriate next investigation?
Answer: Urgent upper GI endoscopy with biopsies (to assess for ulcer, bleeding source, and rule out malignancy).
- Which management step should be initiated immediately?
Answer: Start intravenous PPI infusion and arrange blood transfusion if needed; stop ibuprofen.
- If H. pylori testing is positive, what regimen is preferred in this patient?
Answer: Bismuth‑based quadruple therapy (PPI + bismuth + metronidazole + tetracycline) because clarithromycin resistance is common and drug interactions with antiretrovirals are less problematic.
Practice questions
Question 1
A 45‑year‑old woman with dyspepsia for 2 months reports new onset vomiting of coffee‑ground material. Her vitals show BP 90/60 mmHg, pulse 112 bpm. What is the next best step?
A. Start oral PPI and arrange outpatient endoscopy
B. Give IV fluids, transfuse, and request urgent endoscopy
C. Order abdominal ultrasound
D. Begin H. pylori stool antigen test
Answer: B. Give IV fluids, transfuse, and request urgent endoscopy
Explanation: Hematemesis with hemodynamic instability mandates resuscitation and urgent endoscopic evaluation.
Question 2
A 30‑year‑old male with HIV presents with epigastric pain and a positive H. pylori urea breath test. Which eradication regimen is least appropriate?
A. PPI + clarithromycin + amoxicillin
B. PPI + metronidazole + amoxicillin
C. PPI + bismuth + metronidazole + tetracycline
D. PPI + rifabutin + amoxicillin
Answer: D. PPI + rifabutin + amoxicillin
Explanation: Rifabutin is not a standard component of H. pylori therapy and adds risk of drug interactions with antiretrovirals.
Question 3
A patient on long‑term NSAIDs develops a duodenal ulcer confirmed on endoscopy. Which adjunct is most effective in preventing recurrence?
A. H2‑blocker only
B. High‑dose PPI only
C. PPI plus misoprostol
D. Switching to acetaminophen
Answer: C. PPI plus misoprostol
Explanation: Combined acid suppression and mucosal protection gives the greatest recurrence reduction when NSAIDs cannot be stopped.
Question 4
Which of the following is NOT an alarm feature that mandates immediate endoscopy?
A. Unexplained weight loss
B. Persistent dyspepsia > 6 weeks despite therapy
C. Dysphagia to solids
D. New onset anemia
Answer: B. Persistent dyspepsia > 6 weeks despite therapy
Explanation: While concerning, it does not alone mandate urgent endoscopy without other alarm signs.
Question 5
A 60‑year‑old man with a known gastric ulcer presents with sudden severe abdominal pain, rigid abdomen, and absent bowel sounds. What is the most likely complication?
A. Perforation
B. Bleeding
C. Gastric outlet obstruction
D. Malignancy
Answer: A. Perforation
Explanation: Acute abdomen with rigidity suggests free perforation of the ulcer.
Drafted with AI assistance from standard references and reviewed for structure. Check details against your lecture notes and the Kenya MoH guideline.