Internal exam (gastroenterology)

GERD: Definition. Classification. Clinical manifestations. Diagnostics. Principles of treatment.

• Definition: chronic reflux of gastric contents/acid from the stomach into the esophagus due to impaired LES function → irritation and GERD symptoms.

• Classification:

  • NERD: typical GERD symptoms but no visible mucosal injury on endoscopy.

  • ERD: erosive reflux disease/esophagitis with inflammation or erosions of esophageal mucosa.

  • Barrett’s esophagus: chronic reflux → intestinal metaplasia, where normal squamous epithelium is replaced by columnar epithelium.

• Los Angeles classification:

  • Grade A: one or more mucosal breaks ≤5 mm, not extending between mucosal folds.

  • Grade B: one or more mucosal breaks >5 mm, not extending between mucosal folds.

  • Grade C: mucosal breaks extend between folds but involve <75% of esophageal circumference.

  • Grade D: mucosal breaks involve ≥75% of esophageal circumference.

• Clinical manifestations: heartburn, regurgitation, dyspepsia, epigastric/substernal pain, chest or neck pain due to shared nerve segments.

• Red flags/alarm symptoms: dysphagia, odynophagia, weight loss, persistent vomiting, anemia, GI bleeding, chronic cough/choking/respiratory symptoms.

• Diagnostics: typical heartburn/regurgitation → no investigations needed before treatment. Start empirical PPI or H2 blocker. If chest pain → exclude MI with ECG + troponin. Anamnesis, If red flags → upper GI endoscopy, esophageal pH monitoring, barium swallow (if structural abnormality suspected) . If motility/LES problem suspected → manometry.

• Treatment principles: PPI e.g. omeprazole/esomeprazole 20–40 mg/day for 4–8 weeks before meals. H2 blocker e.g. famotidine 20 mg twice daily. Lifestyle: smaller meals, stop smoking, reduce alcohol, weight loss, avoid lying down for 2–3 h after eating

G-2. Barrett's esophagus. Risk factors. Diagnostics. Principles of treatment (incl. endoscopic). Surveillance.

• Definition: chronic GERD → intestinal metaplasia of distal esophagus: normal squamous epithelium is replaced by columnar epithelium.

• Core idea: premalignant condition: metaplasia → dysplasia → adenocarcinoma.

• Risk factors: male, age >50, GERD >5 years, obesity, smoking, alcohol, European/Caucasian ethnicity, family/genetic risk.

• Diagnostics: upper endoscopy + biopsy of salmon-coloured mucosa; assess Z-line displacement ≥1 cm, metaplasia, dysplasia, visible lesions.

• Treatment: treat GERD with PPI, H2 antagonists + lifestyle changes. Visible lesion → endoscopic mucosal resection. Dysplasia, especially high-grade → radiofrequency ablation.

• Surveillance: no dysplasia → EGD every 3–5 years. Low-grade dysplasia → EGD every 6–12 months. High-grade dysplasia → endoscopic therapy + close follow-up every 3–6 months.

G-3 The main types of non-reflux esophagitis. Diagnostics. Treatment.

1. Eosinophilic esophagitis: allergic/food-triggered eosinophilic inflammation. Dx: EGD + biopsy, allergy testing/CBC. Tx: PPI, swallowed topical steroid e.g. budesonide, eliminate trigger.

2. Infectious esophagitis: Candida, HSV, CMV, less commonly bacteria/parasites. Dx: EGD + biopsy/swab/culture. Tx: fluconazole, acyclovir/ganciclovir, or antibiotics depending on cause.

3. Drug-induced esophagitis: caused by doxycycline/tetracycline, clindamycin, NSAIDs/aspirin, bisphosphonates, KCl, iron. Dx: history + EGD ± biopsy. Tx: stop causative drug + PPI.

4. Caustic/chemical esophagitis: acid/alkali/radiation injury. Dx: history + EGD. Tx: PPI + supportive therapy.

Core diagnostic idea: most types need EGD + biopsy, then add allergy tests, culture, or history depending on suspected cause

G-4 A patient with progressive dysphagia and odynophagia. Investigation algorithm.

• Start: anamnesis + physical exam.

• History: onset, duration, progression, solids vs liquids, painful swallowing, weight loss, vomiting, hematemesis, hoarseness.

• Risk factors: smoking, alcohol, age, male sex, family history.

• Physical exam: oral cavity, neck masses, lymph nodes, mucosal lesions, malnutrition signs.

• First-line: EGD + biopsy for direct visualization and histology.

• Barium swallow: if endoscopy contraindicated or to assess strictures/motility.

• Labs: CBC for anemia, CRP/infection, metabolic status; thyroid tests if relevant.

• Further tests: manometry if motility disorder suspected; CT/MRI if malignancy, compression, invasion, or staging suspected; videofluoroscopy if oropharyngeal dysphagia/aspiration suspected.

G-5 Esophageal Achalasia. Definition. Diagnostics. Differential diagnostics. Principles of treatment. Endoscopic therapy methods.

• Definition: impaired LES relaxation + loss of peristalsis in distal esophagus due to degeneration/loss of inhibitory myenteric neurons, especially NO-producing neurons.

• Symptoms/core: progressive dysphagia to solids and liquids, regurgitation, chest discomfort, weight loss.

• Gold standard dx: esophageal manometry → impaired LES relaxation + absent peristalsis.

• Other diagnostics: barium swallow → “bird-beak” narrowing; upper endoscopy → exclude cancer/pseudoachalasia.

• Differentials: pseudoachalasia, esophageal cancer, strictures, Schatzki ring, Chagas disease, scleroderma, extrinsic compression, ulcers.

• Treatment principle: no treatment restores peristalsis; treatment reduces LES pressure.

• Endoscopic/surgical options: pneumatic dilation, Heller myotomy ± fundoplication, POEM.

• If unfit for surgery: botulinum toxin injection into LES; temporary meds: nitrates or CCBs such as nifedipine.

G-6. Helicobacter pylori diagnostic methods and principles of their selection. Sensitivity and specificity. Factors affecting them

Invasive tests: used when endoscopy is indicated, e.g. alarm symptoms, older age, ulcer, malignancy suspicion.

• Rapid urease test: biopsy-based; detects urease activity by color change; sensitivity/specificity around 90–95%.

• Histology: biopsy microscopy; very sensitive/specific, useful if rapid urease negative but suspicion remains.

• Culture: confirms infection and can test antibiotic resistance.

Non-invasive tests: preferred in younger patients without alarm signs and for eradication follow-up.

• Urea breath test: labeled urea → labeled CO₂ measured in breath; high sensitivity/specificity >90%.

• Stool antigen test: detects active infection; useful for diagnosis and follow-up.

• Serology: IgG/IgA antibodies; less useful for active infection because IgG may reflect past infection.

Factors affecting diagnostic test accuracy

• Recent Antibiotic or PPI use → ↓ bacterial load → false negative results.

• Poor sample quality or inappropriate timing of testing.

• Altered gut microbiota may interfere with stool antigen results.

.G-7. Acute gastritis. Causes. Symptoms. Treatment.

• Definition: sudden inflammation of gastric mucosa.

• Causes: H. pylori, viral/fungal infection, NSAIDs/aspirin, glucocorticoids, iron, alcohol, smoking, autoimmune/Crohn/eosinophilic gastritis, severe trauma/burns, radiation, chemotherapy.

• Symptoms: epigastric/abdominal pain, nausea, vomiting, loss of appetite, postprandial fullness, bloating, dyspepsia/indigestion.

• Severe cases: hematemesis or melena.

• Treatment principle: depends on cause and pathology.

• Treatment: stop causative drugs/irritants; PPI or H2 blocker; antacids; H. pylori eradication if positive; antibiotics/antivirals/antifungals if infectious; fluids/electrolytes and supportive care if vomiting.

G-8. Functional dyspepsia. Definition (essence of the Rome IV classification). Clinical variants. Principles of treatment.

• Definition: chronic/recurrent upper abdominal discomfort without structural or biochemical disease explaining symptoms; also called non-ulcer dyspepsia.

• Rome IV essence: symptoms for ≥6 months, active during last 3 months 3x/week, with no structural disease on endoscopy.

• Rome IV symptoms: bothersome postprandial fullness, early satiation, epigastric pain, or epigastric burning.

• Clinical variants:
  EPS: epigastric pain/burning, not clearly meal-related.
  PDS: postprandial fullness and early satiety, meal-related.

Treatment:

• avoid trigger foods, small frequent meals.

• First-line meds: PPI e.g. omeprazole 20 mg/day for 8 weeks or H2 blocker e.g. famotidine.

• Second-line: low-dose TCA e.g. amitriptyline 10–25 mg at night.

• Third-line: prokinetic e.g. metoclopramide before meals.

• If refractory: psychological therapy/CBT.

G-9. Definition of chronic gastritis. Diagnostics. Clinical significance (risks). Observation. Treatment options.

Definition: long-term inflammation of gastric mucosa lasting >3 months, may lead to atrophy or intestinal metaplasia.

• Types:
  Type A: Autoimmune gastritis: autoimmune, mainly fundus/body, associated with B12 deficiency.
  Type B:Bacterial Gastritis: H. pylori, mainly antrum.
  Type C: Chemical Gastritis: chemical/reactive, due to NSAIDs, bile reflux, alcohol/irritants.

Diagnostics:

• history + physical, medication/NSAID/alcohol history, red flags.

• Labs: CBC for anemia, B12 deficiency or iron deficiency.

• H. pylori testing: urea breath test, stool antigen, rapid urease test if endoscopy done.

• Endoscopy + biopsy: especially age >60 or red flags; assesses atrophy, metaplasia, dysplasia.

Clinical significance: risk of atrophy, metaplasia, dysplasia, gastric cancer, MALT lymphoma, peptic ulcer/bleeding.

Observation: symptom monitoring, lifestyle/medication adherence, surveillance endoscopy depending on atrophy/metaplasia risk.

Treatment: remove cause: stop NSAIDs/alcohol/smoking. Type A → B12 replacement. Type B → H. pylori eradication. Against causative agent: antibiotics, antiviral, antifungal. Symptom relief → PPI/H2 blocker/antacids.

G-10. Risk factors for peptic ulcers of the stomach and duodenum. Symptoms. Diagnostics. Principles of treatment. Prevention.

• Definition: ulcerative lesion in stomach or duodenum due to acid-pepsin mucosal injury.

• Risk factors: H. pylori, NSAIDs/aspirin, glucocorticoids, alcohol, smoking, stress, chronic gastritis, Zollinger-Ellison/genetic risk.

• Symptoms: dyspepsia, epigastric burning pain, reflux/heartburn, nausea/vomiting, bloating, burping.

• Bleeding signs: anemia, hematemesis, melena.

• Gastric ulcer pattern: pain worsens after eating, usually 30–60 min after meal; may cause early satiety/weight loss.

• Duodenal ulcer pattern: pain improves with eating, returns 2–5 h after meal or at night.

• Diagnostics: history, risk factors, CBC/fecal occult blood if bleeding suspected, H. pylori testing, EGD + biopsy.

• Extra tests if needed: fasting serum gastrin for Zollinger-Ellison, PTH for hyperparathyroidism, Crohn testing if suspected.

Treatment:

• Stop NSAIDs/irritants, lifestyle - restrict alcohol, avoid smoking, etc.

• PPI/H2 blocker/antacids

• Eradicate H. pylori if positive

• Endoscopic surveillance

• Surgical treatment: Vagotomy, Partial gastrectomy (Billroth’s procedures), or total gastrectomy (Roux-en-Y)

Prevention: H. pylori screening/eradication, avoid NSAIDs/alcohol/smoking, stress management.

G-11. Indications and principles of eradication of Helicobacter pylori. Main regimens. Indication for H.pylori eradication:

• Indications: peptic ulcer disease, chronic/atrophic gastritis, gastric MALT lymphoma, persistent functional dyspepsia, first-degree relative with gastric adenocarcinoma, and anyone H. pylori-positive if no contraindications.

• Principle: give eradication regimen, then confirm eradication after treatment.

• First-line triple therapy for 14 days:
  PPI: omeprazole/esomeprazole 20–40 mg 2×/day
  Clarithromycin 500 mg 2×/day
  Amoxicillin 1000 mg 2×/day
  If penicillin allergy: replace amoxicillin with metronidazole.

After triple therapy: stop antibiotics after 14 days; continue PPI for another 14 days if needed.

• Second-line bismuth quadruple therapy for 14 days:
  Omeprazole/esomeprazole 20–40 mg 2×/day
  Bismuth subcitrate 420 mg 2×/day
  Tetracycline 375 mg 4×/day
  Metronidazole 375 mg 4×/day

Confirm eradication: urea breath test or stool antigen test ≥4 weeks after stopping antibiotics.

Important: stop PPI 2 weeks before testing to avoid false-negative result. Bismuth does not affect the result.