MBBS viva · Gastroenterology
Gastro-oesophageal reflux disease — diagnosis, classification and management viva
A final-prof viva on the diagnostic approach to heartburn, the Los Angeles and Lyon classifications, the alarm-feature threshold for endoscopy, and stepwise management with PPI doses. Examiner expects mechanism-level reasoning and dose detail, not labels.
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NEET-PGINICETUSMLEPLAB
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Stem
The examiner presents a 50-year-old man with several months of post-prandial retrosternal burning and asks: "What is the likely diagnosis, how would you classify and investigate this condition, and what is your stepwise management?"
Interpretation
- Likely diagnosis: GORD. Retrosternal burning after meals, relieved by antacid, with regurgitation, is the cardinal clinical picture. The diagnosis is clinical in the patient without alarm features, supported by an empirical PPI trial.[1]
- Always screen for alarm features — dysphagia, weight loss, anaemia, GI bleeding, vomiting, onset over age 55, PPI non-response — which mandate urgent OGD rather than empirical therapy.
Key points
The examiner will probe each of these; be ready to defend them at viva depth:
- Definition (Montreal) — GORD develops when reflux of stomach contents causes troublesome symptoms and/or complications (mild symptoms two or more days/week, or moderate-severe one or more days/week).[1]
- Classification — two phenotypes: erosive (ERD, 30 to 40 percent) vs non-erosive (NERD, 60 to 70 percent); Los Angeles grades A to D reproduced verbatim (A under 5 mm; B over 5 mm; C bridging folds; D circumferential). LA C/D + symptoms is conclusive GORD.[1]
- Lyon Consensus 2.0 (objective diagnosis) — AET over 6 percent conclusive; under 4 percent excluded; 4 to 6 percent inconclusive; over 40 reflux episodes/day supports pathological reflux.[2]
- Pathophysiology (five mechanisms) — TLESRs (dominant, ~50 to 80 percent in NERD; targeted by baclofen), hypotensive LES (under 10 mmHg; scleroderma), hiatus hernia (over 60 percent of severe ERD), impaired clearance (poor peristalsis, low saliva), delayed gastric emptying.[2]
- Investigation hierarchy — empirical PPI trial first; OGD for alarm features; pH-impedance for refractory/uncertain cases; manometry mandatory before surgery (exclude achalasia).
- Management stepwise — lifestyle, antacid/alginate, H2RA (famotidine 20 mg bd), then PPI first-line: omeprazole 20 mg od, 30 min pre-meal, 4 to 8 weeks (8 weeks for erosive); refractory → double-dose PPI ± nocturnal H2RA ± baclofen; surgery (Nissen fundoplication) needs objective GORD + normal manometry.[1]
- Barrett oesophagus — intestinal metaplasia; ~0.5 percent/year adenocarcinoma risk; surveillance non-dysplastic at 1 year then every 2 to 3 years; high-grade dysplasia → RFA/EMR.[3]
- Long-term PPI risks — osteoporotic fracture, hypomagnesaemia, B12 deficiency, enteric infection (C. difficile, pneumonia), acute interstitial nephritis, rebound on abrupt cessation — taper, don't stop.
References
- Katz PO, et al. ACG 2022 GERD guideline. Am J Gastroenterol 2022.[1]
- Gyawali CP, et al. Lyon Consensus 2.0. Gut 2018.[2]
- Spechler SJ, Souza RF. Barrett's esophagus. N Engl J Med 2014.[3]
References3ShowHide
- [1]Katz PO, Dunbar KB, Schnoll-Sussman FH, et al. ACG Clinical Guideline for the Diagnosis and Management of Gastroesophageal Reflux Disease. Am J Gastroenterol, 2022.PMID 34807007
- [2]Gyawali CP, Kahrilas PJ, Savarino E, et al. Modern diagnosis of GERD: the Lyon Consensus. Gut, 2018.PMID 29437910
- [3]Spechler SJ, Souza RF. Barrett's esophagus. New England Journal of Medicine, 2014.PMID 25162890