Annadravashoola-Parinamashoola (Acid peptic disease)
Acid-Peptic Disease (APD)
(Encompassing gastric & duodenal ulcer, erosive gastritis)
This write-up integrates contemporary gastro-enterology with Āyurvedic wisdom (primarily Amlapitta / Pariṇāma–śūla concepts). Standard modern sources: Bailey & Love (27th ed.), Sleisenger & Fordtran (11th ed.), ACG & Maastricht-VI guidelines. Classical Āyurvedic texts: Mādhava Nidāna-51, Caraka Saṃhitā Cikitsā-15, Aṣṭāṅga Hṛdaya Cikitsā-8.
1. Disease Description
Acid-Peptic Disease refers to mucosal injury of the oesophagus, stomach or duodenum caused by the caustic action of gastric acid, pepsin and (occasionally) bile.
- Core presentations: epigastric burning/gnawing pain, meal-related dyspepsia, occult or overt GI bleed.
- Pathological spectrum:
- Gastric ulcer (GU)
- Duodenal ulcer (DU)
- Erosive / hemorrhagic gastritis
- Gastroduodenitis (bulbar & pyloric channel)
- Stress-related mucosal disease (SRMD)
- Zollinger–Ellison hyper-secretory disease (rare)
2. Types & Salient Features
| Broad Type | Site | Pain Timing | Key Notes |
|---|---|---|---|
| Duodenal ulcer | First part duodenum | Classically 2–3 h post-meal, relieved by food/milk | 4× commoner than GU, nocturnal pain |
| Gastric ulcer | Lesser curvature antrum/body | Immediately after meal; food aggravates | Wt-loss frequent, malignancy must be excluded |
| Stress-ulcer | Fundus & proximal duodenum | Critically ill pts, painless bleed | ICU setting, burns, head-injury |
| NSAID-induced | Anywhere | Often asymptomatic until bleed | Elderly, concomitant aspirin |
| Refractory/Z-E | Multiple post-bulbar ulcers | Severe diarrhoea, high fasting gastrin | Gastrinoma |
3. Major Aetiological Factors
- Helicobacter pylori infection – 70–90 % DU; 40–60 % GU
- NSAIDs / Aspirin / steroids – prostaglandin inhibition
- Gastric acid hyper-secretion – Z-E syndrome, systemic mastocytosis
- Lifestyle: smoking, alcohol, spicy meals (risk modifiers)
- Severe physiological stress – burns, sepsis, head injury
- Others: Crohn’s, CMV/HSV (immunodeficiency), irradiation, post-Billroth surgery.
4. Etiopathogenesis (Modern Perspective)
- Aggressive factors
- Acid (HCl) – parietal cell hyperactivity
- Pepsin – proteolytic mucosal injury
- H. pylori – produces urease → ammonium hydroxide → ↑ acid, ↓ somatostatin, cytokine-mediated injury
- NSAIDs – ↓ COX-1-mediated protective PGE₂ → ↓ mucus, bicarbonate, mucosal blood flow
- Defensive factors
- Mucus-bicarbonate layer & surfactant phospholipids
- Adequate mucosal perfusion & prostaglandins
- Epithelial renewal & tight-junctions
Disease occurs when aggressors overwhelm defenders → epithelial break → ulcer crater → bleed / perforation.
5. Differential Diagnosis of Chronic Epigastric Pain
| Condition | Distinguishing Clues |
|---|---|
| Gastro-oesophageal reflux (GERD) | Retro-sternal heart-burn, regurgitation, worse lying flat |
| Functional/Non-ulcer dyspepsia | Normal endoscopy, pain unrelated to meals |
| Biliary colic | RUQ radiation to back, ultrasound gall-stones |
| Pancreatitis (chronic) | Epigastric boring pain, steatorrhoea, CT changes |
| Gastric carcinoma | Persistent vomiting, early satiety, weight loss, anaemia |
| Cardiac angina (microvascular) | Exertional, relieved by nitrates, normal endoscopy |
6. Diagnostic Work-up
- Bed-side – Full history, NSAID/H-pylori risk, stool colour, anaemia signs.
- Laboratory – CBC (microcytic anaemia), LFT, serum gastrin if refractory.
- Non-invasive H. pylori tests –
- Urea breath test (UBT) – gold standard for cure confirmation
- Stool antigen ELISA
- Serology (IgG) – only for screening.
- Upper GI endoscopy (OGD) – FIRST-LINE if alarm features (>60 y, bleed, dysphagia, weight-loss). Allows biopsy for histology ± urease test.
- Imaging – Barium meal (if endoscopy not feasible), CT for complications.
- Complication screening – Fecal occult blood, rapid haemoglobin drop, erect X-ray (perforation).
7. Prognosis
- Uncomplicated APD heals in 4–8 weeks with PPI + H. pylori eradication – very good outcome.
- Recurrence <10 % after successful eradication.
- Risks: GI bleed (15 %), perforation (2–5 %), gastric outlet obstruction (2 %).
- GU may harbour malignancy → biopsy essential.
8. Modern Medical Management
- General Measures
- Stop NSAIDs/aspirin where possible.
- Smoking & alcohol cessation, small frequent meals.
- Acid Suppression
- a. Proton-pump inhibitors (PPI) – Omeprazole 20 mg OD / Pantoprazole 40 mg OD × 4–8 wks (↑ dose if large ulcer).
- b. H₂-receptor blockers – Ranitidine 150 mg BD (if PPI contraindicated).
- c. Antacids – Al(OH)₃ + Mg(OH)₂ PRN.
- H. pylori Eradication (Maastricht-VI)
- Concomitant therapy × 14 days: – PPI std dose BD + Clarithromycin 500 mg BD + Amoxicillin 1 g BD + Metronidazole 500 mg BD
- Mucosal Protectants
- Sucralfate 1 g QID before meals
- Bismuth sub-citrate 120 mg QID
- Misoprostol 200 µg QID (NSAID prophylaxis).
- Treatment of Complications
- Endoscopic adrenaline/clip for bleed, IV pantoprazole infusion.
- Surgical repair – Graham patch (perforation), Vagotomy + antrectomy (rare now).
- Maintenance
- Low-dose PPI in high-risk NSAID users.
- Repeat endoscopy for GU after 8 wks to ensure healing & exclude carcinoma.
9. Āyurvedic Perspective & Management
9.1 Rogābhinava (Correlation)
| Modern Entity | Probable Āyurvedic Counterpart | Rationale |
|---|---|---|
| Duodenal Ulcer | Pariṇāma-śūla (Vāta-pittaja) | Pain in mid-digestion, relief by food |
| Gastric Ulcer / Dyspepsia | Ūrdhvaga Amlapitta | Sour eructation, burning soon after meals |
| Erosive Gastritis | Pittaja Āmā Chardi | Haematemesis possible |
Correlation aids principle selection and not a strict one-to-one mapping.
9.2 Nidāna (Causative Factors)
- Ati-uṣṇa, ati-amlalavaṇa, viruddhāhāra
- Adhyāśana, irregular meal timing, night vigil
- Alcohol, smoking, anger, stress → Pitta + Vāta prakopa.
9.3 Saṃprāpti (Pathogenesis)
Nidāna → Tikṣṇa Pācaka-pitta ↑ + Samāna-vāyu vitiation → Vidagdha-pitta corrodes gastric duodenal mucosa → Vāta spasm → Pariṇāma-śūla / Amlapitta symptoms. Chronic corrosion leads to ulcer crater (vrana) + bleeding (raktapitta upadrava).
9.4 Saṃprāpti-Vighaṭana (Therapeutic Break-Up)
- Pittāśamana (śīta-tikta-madhura dravya)
- Vāta-anulomana (snigdha basti, ghṛta)
- Mṛdu virecana to expel Vidagdha-pitta
- Ropaṇa (ulcer healing) with ghṛta-kalpa, yashtimadhu, śata-dhauta ghṛta
- Agni-dīpana (non-tīkṣṇa) & grahaṇī-sthira karaṇa
9.5 Doṣaja Cikitsā-Sūtra
- “Tikta-ghṛta-snehapānaṁ pitta-parikalpita-pariṇāma-śūle”
- “Sūtasekharābhyaṅgaḥ mṛdu-virecana-pūrvaḥ”
- “Kṣīra-basti vāta-saṁsṛṣṭe vyathe”
- “Śīta-madhura-dravyaiḥ stambhanaṁ rakta-darśane”
9.6 Cikitsā-Yojanā (Protocol)
| Stage | Therapy | Classical Yoga (Dose) | Notes |
|---|---|---|---|
| Poorva-karma | Snehapāna | Tikta-ghṛta 40–60 ml OD × 3–5 d | Monitor for sātmyata |
| Śodhana | Mṛdu Virecana | Avipattikara cūrṇa 8-10 g HS | Especially in adhoga amlapitta |
| Basti | Kṣīra-basti | Milk 300 ml + Ghṛta 50 ml + Yashtimadhu 10 g × 5 alt. days | For Vāta-associated pain |
| Śamana | – | ||
| Sūtaśekhara Rasa 125 mg TID with honey-ghee | Pittaja burning, nausea | ||
| Kāmdudha Rasa (Moti yukta) 250 mg BID with cool milk | Ulcer bleed prophylaxis | ||
| Praval-Pañcāmṛta 500 mg BID | Neutralises acid, provides Ca²⁺ | ||
| Dhātrī-Lauha 500 mg BID | Anti-ulcer + iron | ||
| Yashtimadhu Ghṛta 10 ml HS | Mucosal repair | ||
| Saṃskṛta Nārikel Lavan 1–2 g BD | Duodenal ulcer, excellent pH buffer | ||
| Rasāyana | Śatāvarī-Ghṛta 10 ml HS × 1 month | Prevent recurrence, nourish duodenal lining |
9.7 Pathya-Apathya
PATHYA (Wholesome)
- Warm cow-milk with ½ tsp ghee before sleep
- Old shāli rice, barley, bottle-gourd, pumpkin, cucumber
- Pomegranate, ripe banana, sweet grapes
- Coriander-fennel infusion, coconut water
- Small, regular meals; sit erect 30 min post-meal; early dinner
- Yoga: Vajrāsana after meals, Sheetali & Bhrāmarī prāṇāyāma
APATHYA (To Avoid)
- Pickles, tomato ketchup, vinegar, chillies, deep-fried snacks
- Sour curd at night, cola or energy drinks, smoking, alcohol
- Long fasting, late-night study, emotional outbursts
- Analgesic abuse (NSAIDs) without gastro-protection
10. Integrated Algorithm (Clinic Quick Sheet)
- Alarm symptoms? ➔ Urgent endoscopy ± PPI infusion
- H. pylori +ve ➔ PPI-based quadruple therapy + start Āyurvedic Pittāśamana (Kāmdudha) day-4 onward
- No ulcer on OGD but dyspepsia ➔ treat as functional + Amlapitta regimen (Avipattikara, Shatadhauta Ghṛta)
- At 4 weeks reassess:
- If asymptomatic & GU → repeat OGD to confirm healing
- Begin Rasāyana (Śatāvarī-ghṛta) 1–2 months
- Lifestyle & pathya counselling each visit to prevent relapse.
11. Prognostic Summary
| Scenario | Modern Outlook | Āyurvedic Yuktī |
|---|---|---|
| Uncomplicated DU | Heals >90 % with PPI & HP eradication | Śighra-sādhyā under Pitta-śamana & pathya |
| GU with benign histology | Good, needs repeat scope | Sādhya; ghṛta-kalpa prevents scarring |
| Refractory / Z-E | Requires life-long PPI ± surgery | Kṛcchra-sādhyā; dūṣya balāvipatti |
| Bleed / perforation | Mortality 5–10 % | Agantu-vyapad; post-op rasāyana vital |
Key Classical Quote
“Pāke tu pariṇāme ca śūlaṃ yad upajāyate, Dugdha-sevane śamayati tam Pariṇāma-śūla.” – A.H. Cikitsā-10/38
Selected References
- Malfertheiner P. et al. Management of Helicobacter pylori: Maastricht VI/Florence Consensus Report. Gut 2022.
- Bailey & Love’s Short Practice of Surgery, 27th Edition, 2018.
- Mādhava-kara. Mādhava Nidāna with Madhukośa, Ch. 51.
- Cakrapāṇi: Charaka Saṃhitā – Cikitsā-sthāna 15.
- American College of Gastroenterology. Clinical Guideline: Diagnosis & Management of PUD, 2021.