3rd BAMS Coaching – FREE & ONLINE Annadravashoola-Parinamashoola (Acid peptic disease)
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Course lesson

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.

  1. Core presentations: epigastric burning/gnawing pain, meal-related dyspepsia, occult or overt GI bleed.
  2. 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 TypeSitePain TimingKey Notes
Duodenal ulcerFirst part duodenumClassically 2–3 h post-meal, relieved by food/milk4× commoner than GU, nocturnal pain
Gastric ulcerLesser curvature antrum/bodyImmediately after meal; food aggravatesWt-loss frequent, malignancy must be excluded
Stress-ulcerFundus & proximal duodenumCritically ill pts, painless bleedICU setting, burns, head-injury
NSAID-inducedAnywhereOften asymptomatic until bleedElderly, concomitant aspirin
Refractory/Z-EMultiple post-bulbar ulcersSevere diarrhoea, high fasting gastrinGastrinoma

3. Major Aetiological Factors

  1. Helicobacter pylori infection – 70–90 % DU; 40–60 % GU
  2. NSAIDs / Aspirin / steroids – prostaglandin inhibition
  3. Gastric acid hyper-secretion – Z-E syndrome, systemic mastocytosis
  4. Lifestyle: smoking, alcohol, spicy meals (risk modifiers)
  5. Severe physiological stress – burns, sepsis, head injury
  6. Others: Crohn’s, CMV/HSV (immunodeficiency), irradiation, post-Billroth surgery.

4. Etiopathogenesis (Modern Perspective)

  1. 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
  2. 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

ConditionDistinguishing Clues
Gastro-oesophageal reflux (GERD)Retro-sternal heart-burn, regurgitation, worse lying flat
Functional/Non-ulcer dyspepsiaNormal endoscopy, pain unrelated to meals
Biliary colicRUQ radiation to back, ultrasound gall-stones
Pancreatitis (chronic)Epigastric boring pain, steatorrhoea, CT changes
Gastric carcinomaPersistent vomiting, early satiety, weight loss, anaemia
Cardiac angina (microvascular)Exertional, relieved by nitrates, normal endoscopy

6. Diagnostic Work-up

  1. Bed-side – Full history, NSAID/H-pylori risk, stool colour, anaemia signs.
  2. Laboratory – CBC (microcytic anaemia), LFT, serum gastrin if refractory.
  3. Non-invasive H. pylori tests –
    • Urea breath test (UBT) – gold standard for cure confirmation 
    • Stool antigen ELISA 
    • Serology (IgG) – only for screening.
  4. Upper GI endoscopy (OGD) – FIRST-LINE if alarm features (>60 y, bleed, dysphagia, weight-loss). Allows biopsy for histology ± urease test.
  5. Imaging – Barium meal (if endoscopy not feasible), CT for complications.
  6. 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

  1. General Measures
    • Stop NSAIDs/aspirin where possible.
    • Smoking & alcohol cessation, small frequent meals.
  2. 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.
  3. 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
  4. Mucosal Protectants
    • Sucralfate 1 g QID before meals
    • Bismuth sub-citrate 120 mg QID
    • Misoprostol 200 µg QID (NSAID prophylaxis).
  5. Treatment of Complications
    • Endoscopic adrenaline/clip for bleed, IV pantoprazole infusion.
    • Surgical repair – Graham patch (perforation), Vagotomy + antrectomy (rare now).
  6. 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 EntityProbable Āyurvedic CounterpartRationale
Duodenal UlcerPariṇāma-śūla (Vāta-pittaja)Pain in mid-digestion, relief by food
Gastric Ulcer / DyspepsiaŪrdhvaga AmlapittaSour eructation, burning soon after meals
Erosive GastritisPittaja Āmā ChardiHaematemesis 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)

  1. Pittāśamana (śīta-tikta-madhura dravya)
  2. Vāta-anulomana (snigdha basti, ghṛta)
  3. Mṛdu virecana to expel Vidagdha-pitta
  4. Ropaṇa (ulcer healing) with ghṛta-kalpa, yashtimadhu, śata-dhauta ghṛta
  5. Agni-dīpana (non-tīkṣṇa) & grahaṇī-sthira karaṇa

9.5 Doṣaja Cikitsā-Sūtra

  1. “Tikta-ghṛta-snehapānaṁ pitta-parikalpita-pariṇāma-śūle”
  2. “Sūtasekharābhyaṅgaḥ mṛdu-virecana-pūrvaḥ”
  3. “Kṣīra-basti vāta-saṁsṛṣṭe vyathe”
  4. “Śīta-madhura-dravyaiḥ stambhanaṁ rakta-darśane”

9.6 Cikitsā-Yojanā (Protocol)

StageTherapyClassical Yoga (Dose)Notes
Poorva-karmaSnehapānaTikta-ghṛta 40–60 ml OD × 3–5 dMonitor for sātmyata
ŚodhanaMṛdu VirecanaAvipattikara cūrṇa 8-10 g HSEspecially in adhoga amlapitta
BastiKṣīra-bastiMilk 300 ml + Ghṛta 50 ml + Yashtimadhu 10 g × 5 alt. daysFor Vāta-associated pain
Śamana–
Sūtaśekhara Rasa 125 mg TID with honey-gheePittaja burning, nausea
Kāmdudha Rasa (Moti yukta) 250 mg BID with cool milkUlcer bleed prophylaxis
Praval-Pañcāmṛta 500 mg BIDNeutralises acid, provides Ca²⁺
Dhātrī-Lauha 500 mg BIDAnti-ulcer + iron
Yashtimadhu Ghṛta 10 ml HSMucosal repair
Saṃskṛta Nārikel Lavan 1–2 g BDDuodenal ulcer, excellent pH buffer
RasāyanaŚatāvarī-Ghṛta 10 ml HS × 1 monthPrevent 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)

  1. Alarm symptoms? ➔ Urgent endoscopy ± PPI infusion
  2. H. pylori +ve ➔ PPI-based quadruple therapy + start Āyurvedic Pittāśamana (Kāmdudha) day-4 onward
  3. No ulcer on OGD but dyspepsia ➔ treat as functional + Amlapitta regimen (Avipattikara, Shatadhauta Ghṛta)
  4. At 4 weeks reassess: 
    • If asymptomatic & GU → repeat OGD to confirm healing 
    • Begin Rasāyana (Śatāvarī-ghṛta) 1–2 months
  5. Lifestyle & pathya counselling each visit to prevent relapse.

11. Prognostic Summary

ScenarioModern OutlookĀyurvedic Yuktī
Uncomplicated DUHeals >90 % with PPI & HP eradicationŚighra-sādhyā under Pitta-śamana & pathya
GU with benign histologyGood, needs repeat scopeSādhya; ghṛta-kalpa prevents scarring
Refractory / Z-ERequires life-long PPI ± surgeryKṛcchra-sādhyā; dūṣya balāvipatti
Bleed / perforationMortality 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

  1. Malfertheiner P. et al. Management of Helicobacter pylori: Maastricht VI/Florence Consensus Report. Gut 2022.
  2. Bailey & Love’s Short Practice of Surgery, 27th Edition, 2018.
  3. Mādhava-kara. Mādhava Nidāna with Madhukośa, Ch. 51.
  4. Cakrapāṇi: Charaka Saṃhitā – Cikitsā-sthāna 15.
  5. American College of Gastroenterology. Clinical Guideline: Diagnosis & Management of PUD, 2021.
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