# EXAMINATION: GASTRIC DISORDERS
### Based on: A Concise Textbook of Surgery
**Topics Covered:** Gastritis | Peptic Ulcer | Pyloric Stenosis | Hematemesis | Gastric Carcinoma

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## SECTION A — SHORT ANSWER QUESTIONS (2 marks each)

**Instructions:** Answer each question in 3–5 lines.

1. Define peptic ulcer. Name the two main sites where peptic ulcer most commonly occurs.

2. What is "hunger pain"? In which condition is it characteristic, and how is it relieved?

3. Name four causes of haematemesis.

4. What is Ramstedt's operation? State its result.

5. What is meant by "kissing ulcers"? At what site are they found?

6. Name two cells found in gastric glands and state the secretion of each.

7. What is the significance of *Helicobacter pylori* in peptic ulcer disease?

8. Define haematemesis and differentiate it from haematochezia.

9. Name the four lymphatic sets of the stomach and the nodes they drain into.

10. What is meant by "pyloric stenosis" as a complication of peptic ulcer disease?

11. State two indications for gastrojejunostomy.

12. What is the Virchow node (Troisier's sign) and in what condition is it clinically significant?

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## SECTION B — STRUCTURED QUESTIONS (5 marks each)

**Instructions:** Answer each question in a structured and concise manner.

### 1. Gastritis

**(a)** Classify gastritis. *(2 marks)*

**(b)** Describe the features of alkaline reflux gastritis as a post-gastrectomy complication. *(3 marks)*

> **Answer Guide:**
> - Classification: Acute gastritis (erosive, haemorrhagic, related to NSAIDs/alcohol/stress) and Chronic gastritis (Type A - autoimmune, fundal; Type B - antral, H. pylori-associated; Type C - chemical/reflux).
> - Alkaline reflux gastritis: Occurs in a small number of patients following partial gastrectomy. The patient complains of severe, continuous burning epigastric pain aggravated by meals. It is due to reflux of bile and alkaline duodenal contents into the stomach. Bile acids disrupt the mucosal barrier, causing mucosal damage. Treatment involves promotility agents; surgery (Roux-en-Y diversion) is required in severe cases.

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### 2. Peptic Ulcer — Differences

Compare the clinical features of **chronic gastric ulcer** and **chronic duodenal ulcer** under the following headings: age, sex, constitution, pain characteristics. *(5 marks)*

> **Answer Guide (from textbook, p. 725):**
>
> | Feature | Chronic Gastric Ulcer | Chronic Duodenal Ulcer |
> |---|---|---|
> | Age | Middle-aged | Young adult to mid-adult (25–40 years) |
> | Sex | More common in males | Males dominate, though less exclusively |
> | Constitution | Thin and anaemic with J-shaped hypotonic stomach | Healthy male, steer-horn stomach, high in position |
> | Pain — timing | Aggravated by food; occurs shortly after eating | Appears ~3 hours after food (hunger pain); relieved by food |
> | Pain — site | Midepigastrium or slightly to its left | Transpyloric plane, slightly to the right |
> | Pain — nature | Boring or pricking; radiates to back if penetrating | More severe and spasmodic |
> | Periodicity | Less marked; attacks last weeks, intervals 2–6 months | Well-marked periodicity; spring and autumn |

---

### 3. Haematemesis

**(a)** What are the common causes of haematemesis? *(2 marks)*

**(b)** Describe the initial management of a patient presenting with massive haematemesis. *(3 marks)*

> **Answer Guide:**
> **(a)** Common causes:
> 1. Oesophageal varices (portal hypertension)
> 2. Peptic ulcer (gastric or duodenal) — most common cause of upper GI bleeding
> 3. Mallory–Weiss tear (mucosal tear at oesophagogastric junction)
> 4. Acute erosive gastritis / stress ulcers
> 5. Gastric carcinoma
> 6. Leiomyoma/leiomyosarcoma of stomach
>
> **(b)** Management:
> - **Resuscitation**: Establish IV access, begin IV blood transfusion; cross-match blood.
> - **Nil by mouth**: Nothing orally. Insert nasogastric tube for aspiration and to monitor bleeding.
> - **Identify source**: Emergency oesophagogastroduodenoscopy (OGD) is gold standard.
> - **Iced saline gastric lavage** may be performed to slow bleeding.
> - **Specific measures** depend on cause: endoscopic banding/sclerotherapy for varices; adrenaline injection / haemostatic clips for peptic ulcer bleeding.
> - **Surgery** is indicated when bleeding is continuous or profuse despite conservative treatment.

---

### 4. Pyloric Stenosis — Infantile Hypertrophic Pyloric Stenosis (IHPS)

**(a)** Describe the clinical presentation of IHPS. *(2 marks)*

**(b)** Describe the metabolic disturbance and its correction before surgery. *(1 mark)*

**(c)** Briefly describe Ramstedt's operation (pyloromyotomy). *(2 marks)*

> **Answer Guide (from textbook, pp. 711–712):**
> **(a)** Presentation:
> - Affects infants (2–6 weeks of age), males > females (5:1).
> - **Projectile vomiting** — forceful, non-bilious vomiting immediately after or during feeding. Vomit is milk-coloured and may contain old blood (coffee-ground).
> - Infant is hungry and cries after vomiting.
> - **Visible gastric peristalsis** from left to right across the epigastrium.
> - **Palpable pyloric tumour ("olive")**: a firm, ovoid mass felt in the right hypochondrium especially during a test feed.
> - Progressive dehydration, constipation, and weight loss.
>
> **(b)** Metabolic disturbance:
> - **Hypochloraemic, hypokalaemic metabolic alkalosis** due to loss of HCl and K+ in vomit.
> - **Correction**: Half-normal saline with 30 mEq KCl/litre IV until dehydration and electrolytes are corrected. Surgery must be delayed until metabolic correction is complete (this is not a surgical emergency).
>
> **(c)** Ramstedt's operation (Pyloromyotomy):
> - Grid-iron incision in upper right quadrant.
> - The hypertrophic pylorus is delivered out of the wound.
> - An incision is made on the superior (least vascular) surface of the pylorus, through serosa and hypertrophied muscle.
> - Muscle fibres are split by blunt dissection using artery forceps (Koop's modification uses scalpel handle) until the mucosa bulges freely — mucosal integrity is preserved.
> - Air is insufflated into the stomach to check for mucosal perforation.
> - Result: Virtually 100% cure with almost no mortality or recurrence.

---

### 5. Gastric Carcinoma

**(a)** Enumerate the predisposing/aetiological factors for gastric carcinoma. *(2 marks)*

**(b)** Describe the clinical features and staging investigations. *(3 marks)*

> **Answer Guide (from textbook, pp. 755–764):**
>
> **(a)** Predisposing factors:
> - Chronic atrophic gastritis with achlorhydria and intestinal metaplasia
> - *Helicobacter pylori* infection (classified as Group 1 carcinogen by WHO)
> - Pernicious anaemia
> - Adenomatous gastric polyps
> - Previous partial gastrectomy (stump carcinoma)
> - Dietary factors: high salt, smoked/pickled foods, nitrosamines; low fruit/vegetable intake
> - Blood group A (higher incidence)
> - Genetic predisposition / family history
> - Male sex, advancing age; higher incidence in Japan
>
> **(b)** Clinical features:
> - **Early**: Often asymptomatic. Non-specific dyspepsia, anorexia, early satiety, mild epigastric discomfort.
> - **Late / advanced**:
>   - Progressive weight loss and cachexia
>   - Persistent epigastric pain (boring, radiating to back if posterior penetration)
>   - Haematemesis or melaena
>   - Vomiting (pyloric obstruction if antral involvement)
>   - Dysphagia (cardio-oesophageal junction involvement)
>   - Left supraclavicular lymphadenopathy (Virchow's node / Troisier's sign)
>   - Sister Mary Joseph's nodule (periumbilical metastasis)
>   - Ascites (peritoneal spread)
>   - Palpable epigastric mass (late sign)
>
> **Investigations:**
> - Upper GI endoscopy with biopsy — gold standard for diagnosis
> - Double-contrast barium meal: "leather bottle" appearance (linitis plastica) or filling defect
> - CT scan of chest/abdomen/pelvis — staging (TNM)
> - Endoscopic ultrasound (EUS) — T-staging, nodal status
> - Laparoscopic staging — detect peritoneal disease before curative resection

---

## SECTION C — LONG ESSAY QUESTIONS (10 marks each)

**Instructions:** Write a comprehensive essay. Use headings and subheadings.

---

### Essay 1: Peptic Ulcer Disease

**Discuss peptic ulcer disease under the following headings:**
1. Definition and sites (1 mark)
2. Aetiopathogenesis — role of H. pylori, acid, and mucosal defence (2 marks)
3. Complications (2 marks)
4. Investigations (2 marks)
5. Surgical management (3 marks)

> **Answer Guide:**
>
> **1. Definition and Sites**
> A peptic ulcer is a breach in the mucosa of the alimentary tract exposed to acid-peptic activity. Sites: gastric (lesser curvature, antrum), duodenal (first part, anterior/posterior wall), oesophageal (cardiac end), Meckel's diverticulum, anastomotic (marginal) ulcer.
>
> **2. Aetiopathogenesis**
> Peptic ulcer results from imbalance between aggressive factors (acid, pepsin, H. pylori, NSAIDs, bile reflux) and defensive factors (mucus-bicarbonate barrier, mucosal blood flow, prostaglandins, tight junctions).
> - *H. pylori*: A gram-negative spiral organism colonising the antrum. It causes antral gastritis, reduces somatostatin secretion, and raises gastrin levels, thereby increasing acid output. It is found in 90–95% of duodenal ulcers and 70–80% of gastric ulcers.
> - NSAIDs inhibit COX-1, reducing prostaglandin synthesis, weakening mucosal defence.
> - Excess acid (e.g. Zollinger–Ellison syndrome) overwhelms mucosal protection.
>
> **3. Complications**
> - **Haemorrhage**: Most common complication. Posterior wall duodenal ulcer erodes the gastroduodenal artery. Presents as haematemesis and/or melaena. Cullen's triad for diagnosing bleeding.
> - **Perforation**: Most common in anterior wall of the first part of the duodenum. Presents with sudden severe epigastric pain, board-like rigidity, and obliteration of liver dullness (pneumoperitoneum). Radiograph shows gas under the diaphragm.
> - **Pyloric stenosis (cicatricial stenosis)**: Repeated healing and fibrosis of duodenal ulcer causes narrowing. Features: projectile vomiting of undigested food (without bile), visible gastric peristalsis, succussion splash, hypochloraemic alkalosis.
> - **Malignant change**: Rare in duodenal ulcer; occasionally in chronic gastric ulcer.
> - **Penetration**: Posterior gastric ulcer penetrates pancreas causing intractable back pain.
> - **Haematemesis** from erosion of large vessel.
>
> **4. Investigations**
> - Upper GI endoscopy: First line; allows direct visualisation, biopsy (to exclude malignancy for gastric ulcers), and H. pylori testing.
> - Barium meal: Niche sign for ulcer crater; deformity of duodenal cap ("clover-leaf" deformity).
> - *H. pylori* testing: Rapid urease test (CLO test) on biopsy, urea breath test (13C-UBT), stool antigen test, serology.
> - Gastric acid studies (BAO/MAO): Useful in suspected Zollinger–Ellison syndrome.
> - Serum gastrin levels: For Z–E syndrome.
> - Blood tests: FBC (anaemia), LFTs, serum amylase (penetration).
>
> **5. Surgical Management**
> Indications for surgery: failure of medical treatment, haemorrhage not controlled by endoscopy, perforation, pyloric stenosis, suspected malignancy.
>
> **(a) Vagotomy** (reduces acid secretion by denervating parietal cells):
> - Truncal vagotomy: Both vagi divided above hepatic and coeliac branches; requires drainage procedure (pyloroplasty or gastrojejunostomy) due to impaired gastric emptying.
> - Selective vagotomy: Preserves hepatic and coeliac branches; still requires drainage.
> - Proximal gastric vagotomy (Highly Selective Vagotomy / HSV): Divides only the parietal cell mass branches, preserving nerves of Latarjet that supply antrum and pylorus. Does NOT require drainage procedure. Lowest complication rate. Operation of choice for duodenal ulcer.
>
> **(b) Gastrectomy**:
> - Billroth I (partial gastrectomy with gastroduodenostomy): Preferred for gastric ulcer.
> - Billroth II (Polya gastrectomy with gastrojejunostomy): Duodenal stump closure + gastrojejunostomy. Used for duodenal ulcer when anatomy difficult.
>
> **(c) For Perforation**: Graham's patch repair (omental patch closure) + peritoneal lavage; or definitive ulcer surgery (if stable patient).
>
> **(d) For Pyloric Stenosis**: Vagotomy + gastrojejunostomy; or vagotomy + pyloroplasty.

---

### Essay 2: Gastric Carcinoma

**Write a comprehensive essay on carcinoma of the stomach covering:**
1. Incidence and epidemiology (1 mark)
2. Aetiology / predisposing factors (2 marks)
3. Pathology — macroscopic and microscopic types (2 marks)
4. Clinical features and diagnosis (2 marks)
5. Surgical and other treatment (3 marks)

> **Answer Guide (from textbook, pp. 755–764):**
>
> **1. Incidence and Epidemiology**
> - Gastric carcinoma is the second most common cause of cancer death worldwide.
> - Much higher incidence in Japan, China, Eastern Europe, and South America.
> - Incidence declining in Western countries (possibly related to reduced H. pylori prevalence, dietary changes, refrigeration).
> - Male to female ratio: approximately 2:1.
> - Peak incidence: 5th–7th decade.
>
> **2. Aetiology / Predisposing Factors**
> - *H. pylori* infection (Group 1 carcinogen; causes chronic atrophic gastritis → intestinal metaplasia → dysplasia → carcinoma).
> - Chronic atrophic gastritis with intestinal metaplasia and achlorhydria.
> - Pernicious anaemia (3× increased risk).
> - Adenomatous polyps of stomach (true neoplasm, potentially malignant).
> - Previous partial gastrectomy (stump carcinoma, 15–20 years post-surgery, at gastrojejunal anastomosis).
> - Diet high in salt, nitrates, smoked/pickled/cured foods; low in vitamins C and E.
> - Genetic: Blood group A, hereditary diffuse gastric cancer (CDH1 mutation), family history.
> - Socioeconomic: Lower socioeconomic status, poor living conditions.
>
> **3. Pathology**
> *Macroscopic types (Borrmann classification):*
> - Type I: Polypoid/fungating — projects into the lumen.
> - Type II: Ulcerating with elevated edges (malignant ulcer).
> - Type III: Ulcerating and infiltrating.
> - Type IV: Diffusely infiltrating — "linitis plastica" or leather-bottle stomach (thickened, rigid stomach wall).
>
> *Microscopic:*
> - Lauren classification: **Intestinal type** (gland-forming, associated with environmental factors, better prognosis) and **Diffuse type** (signet ring cells infiltrating stroma, associated with H. pylori, young females, worse prognosis).
> - Most are adenocarcinomas.
>
> **4. Clinical Features and Diagnosis**
> *Features:* (See Section B, Question 5(b) above)
>
> *Differential diagnosis of malignant vs benign gastric ulcer:*
> - Benign ulcer: Regular punched-out edges, overhanging margins, surrounding mucosal folds reach edge.
> - Malignant ulcer: Irregular, rolled, shouldered edges; mucosal folds interrupted before reaching edge; surrounding rigidity; nodularity.
>
> *Diagnosis:*
> - Endoscopy + biopsy (multiple biopsies from edges): Gold standard.
> - Barium meal: Filling defect, leather-bottle stomach, malignant ulcer niche.
> - CT scan: Staging — extent of tumour, lymph node involvement, liver/peritoneal metastases.
> - EUS: T-staging and N-staging.
> - Staging laparoscopy before curative surgery.
>
> **5. Treatment**
> *Surgery (only curative option):*
> - **Radical subtotal gastrectomy**: For distal (antral/pyloric) tumours. Removal of distal 3/4 of stomach with regional lymph nodes (D1 or D2 dissection), greater and lesser omentum. Reconstruction by Billroth I or Polya.
> - **Total gastrectomy**: For proximal tumours (body/fundus/cardia). Oesophagojejunostomy (Roux-en-Y) reconstruction. Splenectomy and distal pancreatectomy may be added.
> - **D2 lymphadenectomy**: Recommended in Japan and increasingly worldwide — improves staging accuracy and may improve survival.
> - **Palliative surgery**: Gastrojejunostomy for pyloric obstruction; feeding jejunostomy; total gastrectomy for bleeding/perforation.
>
> *Radiotherapy:*
> - Limited role due to radiosensitive surrounding tissues.
> - Useful for painful bone metastasis.
>
> *Chemotherapy:*
> - More effective than radiotherapy.
> - Best results with cis-platinum + 5-fluorouracil + epirubicin (ECF regimen) by continuous infusion.
> - Perioperative chemotherapy (FLOT regimen) now standard in many centres.
> - Japan: Mitomycin C (intraperitoneal route via lymphatics).
>
> *Prognosis:*
> - 5-year survival: ~25–50% in Western countries; 50–70% in Japan (due to early gastric cancer detection programmes).
> - Early gastric cancer (confined to mucosa/submucosa) has 90%+ 5-year survival.

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## SECTION D — APPLIED/CLINICAL VIVA QUESTIONS

**Instructions:** These are short oral-type vignettes for self-testing.

---

**Q1.** A 5-week-old male infant presents with projectile, non-bilious vomiting after every feed. He appears hungry but loses weight. On examination there is visible peristalsis across the epigastrium and a firm olive-sized mass is palpable in the right hypochondrium.
- What is the diagnosis?
- What metabolic abnormality do you expect?
- What is the definitive treatment?

> **Diagnosis**: Infantile hypertrophic pyloric stenosis (IHPS).
> **Metabolic abnormality**: Hypochloraemic, hypokalaemic metabolic alkalosis (loss of HCl and K+ in vomit; urine shows paradoxical aciduria).
> **Treatment**: Correct dehydration and electrolyte imbalance first with IV 0.45% NaCl + 30 mEq KCl/L, then perform Ramstedt's pyloromyotomy — virtually 100% curative.

---

**Q2.** A 55-year-old man presents with progressive dyspepsia, 8 kg weight loss over 3 months, early satiety, and a palpable left supraclavicular lymph node.
- What is the most likely diagnosis?
- Name the sign eponymously.
- What single investigation would you request first?

> **Diagnosis**: Carcinoma of the stomach with nodal metastasis.
> **Eponymous sign**: Virchow's node / Troisier's sign (Virchow's node = enlarged left supraclavicular node due to metastasis via the thoracic duct).
> **Investigation**: Upper GI endoscopy with multiple biopsies.

---

**Q3.** A 40-year-old male known peptic ulcer patient presents with sudden, severe epigastric pain that rapidly spreads to the whole abdomen. His abdomen is board-like rigid and there is obliteration of liver dullness on percussion.
- What complication has occurred?
- What does the X-ray likely show?
- Outline your management.

> **Complication**: Perforation of peptic ulcer (most commonly anterior wall of 1st part of duodenum).
> **X-ray finding**: Erect chest X-ray shows gas (air) under the right diaphragm (pneumoperitoneum).
> **Management**:
> - Resuscitate: IV fluids, nasogastric aspiration, urinary catheter, analgesia.
> - IV antibiotics.
> - Emergency surgery: Laparotomy — Graham's omental patch closure of the perforation + peritoneal lavage. If stable, add definitive procedure (HSV or truncal vagotomy).
> - Post-op H. pylori eradication therapy.

---

**Q4.** A patient undergoes Polya (Billroth II) gastrectomy. 6 months later he develops severe, continuous burning epigastric pain aggravated by meals with bilious vomiting. Endoscopy shows bile in the stomach and mucosal erythema.
- What is this complication?
- What is the mechanism?
- How is it managed?

> **Complication**: Alkaline (bile) reflux gastritis.
> **Mechanism**: Bile and alkaline duodenal contents reflux into the gastric remnant through the gastrojejunal stoma; bile acids disrupt the gastric mucosal barrier causing chemical gastritis.
> **Management**: Medical (metoclopramide, cholestyramine, antacids). Surgical if refractory: Roux-en-Y conversion to divert bile away from the gastric remnant.

---

**Q5.** In haematemesis, what does the term "coffee-ground vomiting" indicate, and what is its significance?

> Coffee-ground vomiting is the vomiting of dark brown, grainy material resembling coffee grounds. It indicates that blood has been in contact with gastric acid, which converts haemoglobin to haematin (brown). This suggests the bleeding rate is slow or that bleeding has stopped (vs. fresh red haematemesis = active brisk bleeding). It still requires urgent investigation and management.

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## SECTION E — MULTIPLE CHOICE QUESTIONS (1 mark each)

**Circle the single best answer.**

**1.** The most common cause of upper GI haemorrhage (haematemesis) is:
- A. Oesophageal varices
- B. Mallory–Weiss tear
- C. **Peptic ulcer** ✓
- D. Gastric carcinoma

**2.** Which artery, when eroded by a posterior duodenal ulcer, causes a major haemorrhage?
- A. Left gastric artery
- B. **Gastroduodenal artery** ✓
- C. Superior mesenteric artery
- D. Right gastroepiploic artery

**3.** Ramstedt's pyloromyotomy is the treatment for:
- A. Pyloric stenosis from duodenal ulcer
- B. **Infantile hypertrophic pyloric stenosis** ✓
- C. Gastric outlet obstruction from carcinoma
- D. Adult pyloric stenosis

**4.** Which of the following gastric cells secretes hydrochloric acid?
- A. Chief (zymogenic) cells
- B. G cells
- C. Neck cells
- D. **Parietal (oxyntic) cells** ✓

**5.** The "leather-bottle stomach" (linitis plastica) in gastric carcinoma corresponds to Borrmann type:
- A. I
- B. II
- C. III
- D. **IV** ✓

**6.** Pyloric stenosis as a complication of peptic ulcer causes which metabolic disturbance?
- A. Hyperkalaemic metabolic acidosis
- B. **Hypochloraemic, hypokalaemic metabolic alkalosis** ✓
- C. Hypernatraemic dehydration
- D. Respiratory alkalosis

**7.** Which operation is considered the operation of choice for uncomplicated duodenal ulcer due to the lowest complication rate?
- A. Truncal vagotomy + gastrojejunostomy
- B. Billroth I gastrectomy
- C. **Proximal gastric (highly selective) vagotomy** ✓
- D. Polya gastrectomy

**8.** An enlarged, hard, left supraclavicular lymph node in a patient with gastric carcinoma is called:
- A. Sister Mary Joseph's nodule
- B. Blumer's shelf
- C. Krukenberg tumour
- D. **Virchow's (Troisier's) node** ✓

**9.** Which of the following is the gold standard investigation for diagnosing gastric carcinoma?
- A. CT scan of abdomen
- B. Barium meal
- C. **Upper GI endoscopy with biopsy** ✓
- D. PET scan

**10.** Acute haemorrhagic gastritis (stress ulcers) is most commonly associated with:
- A. *H. pylori* infection
- B. Blood group A
- C. **Severe burns, head injury, or critical illness (Curling's and Cushing's ulcers)** ✓
- D. Pernicious anaemia

**11.** In the surgical treatment of a perforated peptic ulcer, the standard procedure performed at laparotomy is:
- A. Subtotal gastrectomy
- B. Highly selective vagotomy
- C. Billroth II reconstruction
- D. **Graham's omental patch repair** ✓

**12.** The conversion of pepsinogen to active pepsin requires a gastric pH of:
- A. < 5.0
- B. < 4.0
- C. < 3.5
- D. **< 2.5** ✓

**13.** Gastric carcinoma has the highest incidence in which country?
- A. USA
- B. UK
- C. **Japan** ✓
- D. Australia

**14.** Which complication is more common with posterior duodenal ulcers compared to anterior ulcers?
- A. Perforation
- B. **Haemorrhage** ✓
- C. Malignant transformation
- D. Pyloric stenosis

**15.** The best chemotherapy combination yielding the most encouraging results in gastric carcinoma includes:
- A. Methotrexate + vincristine
- B. Adriamycin + bleomycin
- C. **Cis-platinum + 5-fluorouracil + epirubicin** ✓
- D. Cyclophosphamide + prednisolone

---

## ANSWER KEY — MCQ

| Q | Answer | Q | Answer |
|---|---|---|---|
| 1 | C | 9 | C |
| 2 | B | 10 | C |
| 3 | B | 11 | D |
| 4 | D | 12 | D |
| 5 | D | 13 | C |
| 6 | B | 14 | B |
| 7 | C | 15 | C |
| 8 | D | | |

---

## MARKING SCHEME SUMMARY

| Section | Questions | Marks |
|---|---|---|
| A — Short Answer | 12 × 2 marks | 24 |
| B — Structured | 5 × 5 marks | 25 |
| C — Long Essay | 2 × 10 marks | 20 |
| D — Applied/Viva | 5 (self-assessment) | — |
| E — MCQ | 15 × 1 mark | 15 |
| **Total** | | **84** |

---

*All content derived from: A Concise Textbook of Surgery (relevant pages: 706–767, esp. 719–764).*

# EXAM-ORIENTED NOTES: GASTRIC DISORDERS
### Source: A Concise Textbook of Surgery

**Topics:** Gastritis | Peptic Ulcer | Pyloric Stenosis | Haematemesis | Gastric Carcinoma

---

> **HOW TO USE THESE NOTES**
> Each topic follows the standard surgical exam pattern:
> Definition → Aetiology → Pathology → Clinical Features → Investigations → Treatment → Complications
> Key facts, high-yield comparisons, and exam buzzwords are **bolded** throughout.

---

# PART 1 — GASTRITIS

## Definition
Gastritis is inflammation of the gastric mucosa. It may be acute or chronic.

---

## Classification

### A. Acute Gastritis
- **Erosive / haemorrhagic gastritis**
- Causes:
  - NSAIDs and aspirin (inhibit COX-1 → reduce prostaglandins → break mucosal barrier)
  - Alcohol
  - Corticosteroids
  - Stress: severe burns (**Curling's ulcer**), head injury (**Cushing's ulcer**), major surgery, sepsis, trauma
  - Helicobacter pylori acute infection
  - Bile reflux

### B. Chronic Gastritis
| Type | Features |
|---|---|
| **Type A (Autoimmune)** | Involves fundus/body; antibodies to parietal cells and intrinsic factor; associated with pernicious anaemia; achlorhydria; risk of gastric cancer |
| **Type B (Bacterial / H. pylori)** | Involves antrum; most common type; caused by H. pylori; associated with peptic ulcer and gastric cancer |
| **Type C (Chemical)** | Due to bile reflux or NSAIDs; antral predominance; also called reflux or reactive gastritis |

### C. Alkaline Reflux Gastritis (Post-gastrectomy)
- Occurs after partial gastrectomy (more common after Polya/Billroth II)
- Bile and alkaline duodenal contents reflux through the stoma → damage mucosal barrier
- **Symptoms**: Severe, continuous burning epigastric pain **aggravated by meals**; bilious vomiting; **pain not relieved by vomiting**
- **Diagnosis**: Endoscopy — bile in stomach, mucosal erythema, histological gastritis
- **Treatment**: Medical (prokinetics, cholestyramine, antacids); surgical — **Roux-en-Y diversion** if refractory

---

## Helicobacter pylori — High-Yield Facts
- Gram-negative, spiral, microaerophilic organism
- Colonises the **antrum** predominantly
- Produces **urease** → breaks down urea → ammonia → mucosal damage
- Associated with: chronic type B gastritis, peptic ulcer (90–95% DU, 70–80% GU), gastric adenocarcinoma, MALT lymphoma
- **Tests**: CLO test (rapid urease on biopsy), urea breath test (13C-UBT), stool antigen test, serology
- **Eradication**: Triple therapy — PPI + clarithromycin + amoxicillin (or metronidazole) × 7–14 days

---

## Pathological Changes in Chronic Gastritis
- Normal gastric mucosa → chronic inflammation → **atrophic gastritis** → **intestinal metaplasia** → **dysplasia** → **carcinoma**
- This sequence (Correa's cascade) is the basis for gastric cancer risk in chronic type B gastritis

---

# PART 2 — PEPTIC ULCER

## Definition
A peptic ulcer is a **breach in the mucosa** of the alimentary tract that is exposed to acid-peptic activity, extending at least through the muscularis mucosae.

---

## Sites
1. **Gastric** — lesser curvature, antrum (most common)
2. **Duodenal** — 1st part of duodenum (most common site overall)
3. Cardiac end of oesophagus
4. Meckel's diverticulum (ectopic gastric mucosa)
5. **Anastomotic (marginal) ulcer** — any bowel segment surgically anastomosed to gastric fundus

---

## Types
- **Acute peptic ulcer**: Shallow, involve only mucosa and submucosa; multiple; associated with stress, drugs, burns
- **Chronic peptic ulcer**: Penetrate the muscle coat; usually solitary; undergo healing and fibrosis repeatedly

---

## Aetiopathogenesis — Aggressive vs Defensive Factors

```
AGGRESSIVE                      DEFENSIVE
Acid (HCl)                      Mucus-bicarbonate barrier
Pepsin                          Mucosal blood flow
H. pylori                       Prostaglandins (PGE2, PGI2)
NSAIDs                          Tight epithelial junctions
Bile reflux                     Rapid epithelial cell turnover
Smoking                         Alkaline tide
Zollinger-Ellison syndrome
```

**Gastric ulcer** → predominantly **mucosal defence failure**
**Duodenal ulcer** → predominantly **acid hypersecretion**

---

## Gastric Cells — Exam Essential

| Cell | Location | Secretion |
|---|---|---|
| **Parietal (oxyntic) cells** | Body/fundus | HCl + **Intrinsic factor** |
| **Chief (zymogenic) cells** | Body/fundus | **Pepsinogen** (→ pepsin at pH <2.5) |
| **G cells** | Antrum/pylorus | **Gastrin** |
| Surface epithelial cells | Mucosa | Mucus (alkaline, sodium-rich) |
| Neck cells | Gastric pit entrance | Buffer acid |
| Endocrine cells | Gastric glands | Gastrin, serotonin |

> **Note**: Antral and pyloric glands contain **no parietal or chief cells**. G-cells are found in this region.

---

## Phases of Gastric Acid Secretion

| Phase | Stimulus | Mediator |
|---|---|---|
| **Cephalic** | Sight, smell, taste of food | Vagus nerve → ACh → parietal cells |
| **Gastric** | Food in stomach, distension | Gastrin (from G cells) |
| **Intestinal** | Chyme enters duodenum | Gastrin from duodenum (minor) |

---

## Clinical Features

### Comparing Chronic Gastric and Duodenal Ulcer

| Feature | **Chronic Gastric Ulcer** | **Chronic Duodenal Ulcer** |
|---|---|---|
| **Age** | Middle-aged | Young adult, 25–40 years |
| **Sex** | Males >> females | Males > females (less exclusively) |
| **Constitution** | Thin, anaemic; **J-shaped hypotonic stomach** | Healthy male; **steer-horn stomach**, high in position |
| **Periodicity** | Less marked | **Well marked**; attacks in spring and autumn |
| **Pain — timing** | **Shortly after food** (aggravated by eating) | **Hunger pain** — ~3 hours after food, when stomach empty |
| **Pain — relief** | Not well relieved by food | **Relieved by food** or antacids |
| **Pain — site** | Midepigastrium or slightly **left** | **Transpyloric plane**, slightly right |
| **Pain — nature** | Boring or pricking; radiates to back if penetrating | More severe and spasmodic |
| **Vomiting** | Common, food-laden | Less common |
| **Night pain** | Rare | **Common** (hunger pain at night) |
| **Haemorrhage** | Less common | More common (posterior wall) |
| **Malignant change** | **Possible** (~2–10%) | **Almost never** |

---

## Pathology of Chronic Peptic Ulcer
- Usually **solitary** (multiple in 10–15% of duodenal ulcers)
- **Gastric ulcer**: Most common at lesser curvature at angulus. Punched-out appearance with overhanging margins. Granulating base with mucopurulent debris.
- **Duodenal ulcer**: Most common at superior surface or anterior wall of 1st part. Multiple ulcers on anterior + posterior walls = **"kissing ulcers"** → scarring → pyloric stenosis.
- **Anterior DU** → perforation
- **Posterior DU** → haemorrhage (erodes gastroduodenal artery)

---

## Investigations

1. **Upper GI Endoscopy (OGD)**: Gold standard. Allows direct visualisation, biopsy for H. pylori (CLO test), and to exclude malignancy in gastric ulcers.
2. **Barium meal**: **"Niche sign"** = ulcer crater filling with barium. **"Clover-leaf" deformity** of duodenal cap in chronic DU. Filling defect in malignancy. **"Leather-bottle"** in linitis plastica.
3. **H. pylori tests**: CLO test (biopsy), 13C-urea breath test, stool antigen, serology.
4. **Pentagastrin (acid secretion) test**: BAO and MAO measured. DU: BAO 4–9 mmol/hr; MAO 30–50+ mmol/hr.
5. **Serum gastrin**: For **Zollinger–Ellison syndrome**.
6. **Blood tests**: FBC (anaemia), group and crossmatch if bleeding.

---

## Treatment

### Medical
- **H. pylori eradication** (triple therapy) — heals the majority of peptic ulcers
- **Proton pump inhibitors (PPIs)**: Most effective acid suppression
- **H2-receptor antagonists**: Ranitidine, cimetidine
- **Antacids**: Symptomatic relief
- **Sucralfate**: Mucosal protectant
- **Avoid**: NSAIDs, smoking, alcohol

### Surgical — Indications
1. Failure of medical treatment (non-healing after 12 weeks)
2. Haemorrhage not controlled endoscopically
3. Perforation
4. Pyloric stenosis (cicatricial)
5. Suspected malignancy (gastric ulcer)

---

## Surgical Operations

### Vagotomy
**Purpose**: Reduce vagal stimulation of parietal cells → reduce acid secretion

| Type | Description | Drainage Required? |
|---|---|---|
| **Truncal vagotomy** | Both vagal trunks divided (5–7 cm excised); ALL gastric branches + hepatic + coeliac divided | **Yes** (pyloroplasty or GJ) |
| **Selective vagotomy** | Only gastric branches divided; hepatic + coeliac spared | **Yes** |
| **Proximal gastric / Highly Selective (HSV)** | Only parietal cell branches divided; **nerves of Latarjet preserved** (antrum/pylorus innervated) | **No** — operation of choice |

> **Nerves of Latarjet** run along the lesser curvature 2–5 cm from it and supply the antrum and pylorus. Preserving them in HSV maintains normal gastric emptying.

### Gastrectomy
| Operation | Procedure | Indication |
|---|---|---|
| **Billroth I** | Distal 2/3 stomach excised → **gastroduodenostomy** (end-to-end) | **Gastric ulcer** (operation of choice) |
| **Polya (Billroth II)** | Distal 2/3 excised, duodenal stump closed → **gastrojejunostomy** | Duodenal ulcer, technically difficult DU |
| **Gastrojejunostomy (GJ)** | Stomach joined to jejunum without gastric excision | Pyloric stenosis, palliation in carcinoma |

### Acid Secretion Guide to Operation Selection (Pentagastrin test)
- MAO **30–40 mmol/hr**: Vagotomy + drainage (pyloroplasty/GJ)
- MAO **40–50 mmol/hr**: Vagotomy + antrectomy
- MAO **>50 mmol/hr**: Partial gastrectomy or vagotomy + antrectomy

---

## Complications of Peptic Ulcer — The Big Five

### 1. Haemorrhage *(most common complication)*
- **Posterior DU** erodes **gastroduodenal artery** → haematemesis + melaena
- See Part 4 (Haematemesis) for full management

### 2. Perforation *(most dramatic complication)*
- **Anterior DU** or lesser curvature GU perforates into peritoneum
- **Features**: Sudden, severe **"knife-like"** epigastric pain; patient lies still; **board-like rigidity**; **obliteration of liver dullness** (gas displaces liver)
- **X-ray**: **Gas under right hemidiaphragm** (erect CXR) — present in 70% of cases
- **Management**:
  1. Resuscitate: IV fluids, NG tube, catheter
  2. Antibiotics IV
  3. Emergency laparotomy:
     - **Graham's omental patch repair** (3 interrupted sutures + omental plug) + peritoneal lavage ± drain
     - Definitive operation if stable + experienced surgeon: Billroth I (gastric ulcer), vagotomy + pyloroplasty (DU)
  4. Post-op H. pylori eradication

### 3. Pyloric Stenosis *(see Part 3)*

### 4. Malignant Change
- **Gastric ulcer** only — DU virtually never becomes malignant
- Ulcers near **greater curvature** and **below angulus** are most prone
- **Pyloric segment ulcers**: 20% are primarily malignant
- **Large indolent posterior wall ulcers**: 10% malignant change
- Loss of periodicity + vomiting that does not relieve pain → suspect malignancy

### 5. Penetration
- Posterior ulcer penetrates **pancreas** → **intractable back pain** aggravated by lying down
- Pain changes character: loses periodicity; constant boring back pain
- Serum amylase may be mildly elevated

---

## Complications of Gastric Operations (Post-gastrectomy Syndromes)

### Early (within 1 year)
| Complication | Features | Treatment |
|---|---|---|
| Paralytic ileus | Post-op | NG suction + IV fluids |
| Haemorrhage from suture line | Fresh blood in NG tube | Adrenaline lavage; re-exploration |
| Duodenal stump blow-out | Leakage from Billroth II stump; peritonitis; 10–15% mortality | Immediate drain + surgery |
| **Dumping syndrome** (early) | 15–30 min after meal: sweating, palpitations, dizziness, diarrhoea; hypertonic food in jejunum → fluid shift | Small frequent meals; lie flat after eating |
| **Dumping** (late) | 2–3 hrs after meal: hypoglycaemia symptoms (rapid glucose absorption → insulin surge → rebound hypoglycaemia) | Small frequent meals; avoid concentrated sugars |
| Intestinal herniation | Herniation through defect in mesentery (6–20th post-op day) | Surgery |

### Late (after 1 year)
| Complication | Notes |
|---|---|
| **Alkaline reflux gastritis** | Bile reflux → severe burning pain aggravated by food; Roux-en-Y for refractory cases |
| **Iron deficiency anaemia** | 40% if duodenum by-passed; supplement iron routinely |
| **Megaloblastic anaemia** | Reduced intrinsic factor → B12 deficiency; 5–10 years post-op; give IM cyanocobalamin 100 mcg weekly |
| **Steatorrhoea** | Poor mixing of pancreatic enzymes after GJ or Polya |
| **Calcium deficiency** | 40% after duodenal bypass; give calcium supplements; associated bone disease |
| **Weight loss** | Reduced absorption; more common after total/Polya gastrectomy than Billroth I |
| **Bolus obstruction** | Food bolus at narrowest part of small bowel; advise thorough mastication |
| **Diarrhoea post-vagotomy** | 5–20% after truncal vagotomy; insert reversed jejunal segment (Henley loop) for severe cases |

---

# PART 3 — PYLORIC STENOSIS

## Two Distinct Conditions — Do Not Confuse!

| Feature | **Infantile Hypertrophic Pyloric Stenosis (IHPS)** | **Adult Pyloric Stenosis (Cicatricial)** |
|---|---|---|
| Cause | Hypertrophy of pyloric muscle | Fibrosis from chronic duodenal/juxtapyloric ulcer |
| Age | 2–6 weeks of age | Adults with long history of peptic ulcer |
| Sex | **Male : Female = 5:1** | More common in women |
| Vomiting | **Projectile, non-bilious** (pyloric obstruction above ampulla of Vater) | **Copious, foul, projectile**; contains food from days before; **no bile** |
| Onset | Acute/subacute | Slow and insidious |
| Metabolic | Hypochloraemic, hypokalaemic **metabolic alkalosis** | Same — hypochloraemic, hypokalaemic metabolic alkalosis |
| Treatment | **Ramstedt's pyloromyotomy** | Vagotomy + gastrojejunostomy OR vagotomy + pyloroplasty |

---

## IHPS — Detailed Notes

### Clinical Features
- Male infants, 2–6 weeks (range 1–12 weeks)
- **Projectile, non-bilious vomiting** immediately after or during feeding
- Vomit = **milk-coloured** or may contain **old blood ("coffee-ground")** from Mallory–Weiss-type tears
- Infant is **hungry immediately after vomiting**
- **Visible gastric peristalsis** — waves moving from left to right (left hypochondrium → right hypochondrium)
- **"Olive"** — firm, smooth, ovoid mass in **right hypochondrium**, best felt during **test feed**
- Progressive dehydration, constipation, weight loss, jaundice (occasionally)

### Metabolic Disturbance
- Loss of HCl (H+ and Cl-) + K+ in vomit
- Result: **Hypochloraemic, hypokalaemic metabolic alkalosis**
- Kidneys compensate by conserving H+ → excrete K+ → **paradoxical aciduria**
- **Correction**: IV **half-normal saline (0.45% NaCl) + 30 mEq KCl per litre** until dehydration and electrolytes normalised
- **This is NOT a surgical emergency** — always correct metabolic state before operation

### Investigations
- **Ultrasound** (investigation of choice): Pyloric muscle thickness >4 mm, pyloric canal length >16 mm
- Barium meal: "String sign" (thin line of barium through narrow canal), "shoulder sign", "beak sign"
- Blood: Metabolic alkalosis, hypochloraemia, hypokalaemia

### Treatment — Ramstedt's Pyloromyotomy
- Stomach washed with saline; NG aspiration 1 hour before operation
- **Incision**: Grid-iron incision, upper right quadrant
- Hypertrophic pylorus delivered out of wound
- **Incision on superior surface** (least vascular) of pylorus through serosa and hypertrophied muscle
- After half the muscle is incised, **blunt splitting** with artery forceps (Koop's: scalpel handle) until **mucosa bulges freely**
- Air insufflated into stomach to check for mucosal perforation
- If mucosa perforated → close with 3–4 interrupted chromic catgut sutures + omental cover
- **Result**: **~100% cure; virtually no mortality; no recurrence**

### Post-operative Care
- Small feeds (≤5 ml) after a few hours; volume gradually increased
- Normal feeding by 3–4 days
- **Medical alternative** (subacute cases >2 months age): Eumydrin (atropine methylnitrate) 1:1000, 1–2 ml before each feed

---

## Adult (Cicatricial) Pyloric Stenosis

### Cause
- **Chronic cicatrisation** of chronic duodenal ulcer or juxtapyloric ulcer
- Scar contracts → gradual narrowing → months of intermittent obstruction → sudden complete obstruction
- **Not an ulcer at the pylorus itself** — usually from the 1st part of duodenum

### Clinical Features
1. **Pain**: Loses periodicity; sensation of fullness towards evening
2. **Vomiting**: Classical symptom — **copious, projectile, foul**; contains **undigested food** from current and previous days; **no bile** (pyloric obstruction above bile entry); usually in the evening
3. **Visible gastric peristalsis** left to right
4. **Succussion splash**: Audible splash on shaking the patient (retained food/fluid in stomach)
5. **Weight loss** and dehydration
6. Loss of appetite

### Signs
- **Gastric peristalsis** visible
- **Succussion splash** on shaking the abdomen (5+ hours after last meal)
- Epigastric fullness/distension
- **Metabolic alkalosis** (as in IHPS)

### Investigations
1. **Barium meal**: **"Dilated stomach with food residue"**; delayed gastric emptying; "reversed 3 sign" from bulb deformity
2. **Endoscopy**: Confirms obstruction site, dilated stomach, allows biopsy of any lesion
3. **Blood**: Hypochloraemic, hypokalaemic, metabolic alkalosis; urea often elevated (dehydration + protein catabolism)
4. Serum electrolytes, FBC, renal function

### Treatment
- **Correct metabolic state first**: IV saline + KCl; NG tube to decompress and wash stomach
- **Surgical options**:
  - **Vagotomy + gastrojejunostomy** (most successful for pyloric stenosis)
  - Vagotomy + pyloroplasty
  - Partial gastrectomy if malignancy suspected

---

# PART 4 — HAEMATEMESIS

## Definition
**Haematemesis** = vomiting of blood (bright red or altered "coffee-ground") originating from the upper GI tract (above the ligament of Treitz).

## Differentiating Haematemesis from Haemoptysis

| Feature | **Haematemesis** | **Haemoptysis** |
|---|---|---|
| Origin | GI tract | Respiratory tract |
| Colour | Dark red, brown, "coffee-ground" | Bright red, frothy |
| Mixed with | Food particles | Sputum, froth |
| pH | **Acid** (gastric) | **Alkaline** |
| Preceded by | Nausea | Cough |
| Followed by | Melaena | No change in stools |

---

## Coffee-Ground Vomiting
- Blood has been in contact with gastric acid → HCl converts haemoglobin to **haematin** (brown)
- Indicates **slow or stopped bleeding**
- Fresh bright red haematemesis = **active brisk bleeding**

---

## Causes of Haematemesis — Classified

### Common
1. **Peptic ulcer** (gastric or duodenal) — **most common cause overall**
2. **Oesophageal varices** — most dangerous; highest mortality
3. **Mallory–Weiss tear** — mucosal tear at oesophagogastric junction following forceful vomiting
4. **Acute erosive/haemorrhagic gastritis** — stress, NSAIDs, alcohol

### Less Common
5. **Gastric carcinoma**
6. **Oesophagitis** (reflux)
7. **Leiomyoma/Leiomyosarcoma** of stomach — massive haematemesis is the **only** symptom of leiomyosarcoma
8. **Dieulafoy's lesion** (submucosal artery erosion)

### Rare
9. Aortoduodenal fistula
10. Haemobilia (bleeding from biliary tree)
11. Blood dyscrasias

---

## Assessment of Severity
- Signs of **hypovolaemic shock**: tachycardia, hypotension, cold extremities, reduced urine output
- Pulse >100 or SBP <100 mmHg = significant bleed
- Postural drop in BP >20 mmHg = significant volume loss
- **Rockall score** — for risk stratification (age, shock, comorbidities, endoscopy findings)

---

## Initial Management (ABCDE + Resuscitation)

1. **Airway**: Protect airway if massive bleed or altered consciousness; consider intubation
2. **Large-bore IV access** × 2 (antecubital fossa); send: FBC, U&E, LFTs, coagulation, group + crossmatch
3. **Fluid resuscitation**: IV crystalloid (0.9% NaCl) until blood available; **blood transfusion** (crossmatched or O-negative emergency)
4. **NG tube**: Aspiration to confirm blood; decompression; **iced saline gastric lavage** may slow bleeding
5. **Nil by mouth**
6. **Urinary catheter**: Urine output ≥0.5 ml/kg/hr is target
7. **Central venous pressure (CVP)** monitoring for volume status
8. **IV PPIs**: High-dose omeprazole (80 mg bolus then 8 mg/hr infusion) for peptic ulcer bleeding

---

## Investigations
1. **Upper GI endoscopy (OGD)**: **Gold standard** — performed as soon as patient stabilised (within 24 hrs); identifies source, allows therapeutic intervention
2. **FBC**: Anaemia (may be normal early in acute bleed)
3. **Coagulation**: Especially if on anticoagulants or liver disease
4. **Barium meal**: NOT in acute setting; diagnostic for chronic conditions
5. **Coeliac angiography**: Useful when bleeding is very profuse and endoscopy cannot detect source
6. **Ultrasound liver**: For portal hypertension, liver disease (varices)

---

## Endoscopic Treatment
| Cause | Endoscopic Treatment |
|---|---|
| Peptic ulcer bleeding | Adrenaline (1:10,000) injection + haemostatic clips or heat probe |
| Oesophageal varices | **Banding** (preferred) or sclerotherapy |
| Mallory–Weiss tear | Usually self-limiting; adrenaline injection if needed |

---

## Indications for Surgery in Upper GI Haemorrhage
1. Rebleeding after admission to hospital
2. Age **>45 years**
3. Requires **≥5 units blood** to restore red cell volume and CVP
4. Conservative treatment failing
5. Possibility of associated perforation
6. History of previous bleeding within a few months

### Surgical Options
- **Peptic ulcer (DU)**: Underrunning of bleeding vessel via transverse pyloroduodenal incision + vagotomy + pyloroplasty
- **Peptic ulcer (GU)**: Gastrotomy + underrunning bleeding vessel + four-quadrant biopsy + vagotomy; Billroth I if wide involvement
- **Varices**: Emergency porto-systemic shunt, oesophageal transection, or TIPSS
- **Mallory–Weiss tear**: Long proximal gastrotomy → oversewing mucosal tear; recurrence almost nil

---

## Melaena
- **Black, tarry, offensive stools** from altered blood
- Indicates ≥50–100 ml blood loss in upper GI tract
- Can persist for days after bleeding stops (blood in bowel)

---

# PART 5 — GASTRIC CARCINOMA

## Epidemiology
- **2nd most common cancer death** worldwide
- Very high incidence in **Japan**, China, Eastern Europe, South America
- Incidence **declining** in Western countries (improved diet, refrigeration, reduced H. pylori)
- **Male : Female** = approximately 2:1 to 3:1
- Peak incidence: **5th–7th decade** (average age ~59)
- **Blood group A** — higher incidence

---

## Aetiology

### Causative Factors
1. **H. pylori infection** — Group 1 carcinogen (WHO); causes Type B gastritis → atrophic gastritis → intestinal metaplasia → cancer; associated with **distal (body + antrum) cancer** more than proximal
2. **Dietary**: High salt, smoked/pickled/cured food, nitrosamines, N-nitroso compounds; **low fruit/vegetable intake**
3. **Age/Sex**: Males, 50–70 years

### Predisposing Conditions
1. **Chronic atrophic gastritis with intestinal metaplasia**: Normal glands absent; achlorhydria; 10% develop cancer over 20 years (vs 0.6% normal stomach)
2. **Pernicious anaemia**: 10% develop malignancy; achlorhydria is the link
3. **Chronic gastric ulcer**: Ulcers near **greater curvature** or **pyloric segment** (20% malignant); large indolent posterior wall ulcers (10%); lesser curvature ulcers rarely undergo malignant change
4. **Gastric polyps**: Adenomatous polyps are premalignant; hyperplastic polyps — 30% coexist with invasive carcinoma; polyps >2 cm have higher malignant risk
5. **Previous partial gastrectomy**: **Stump carcinoma** — risk rises 15–20 years post-surgery; occurs at the gastrojejunal anastomosis
6. **Heredity**: First-degree relatives have 2× risk; blood group A; hereditary diffuse gastric cancer (CDH1 mutation)

---

## Pathology

### Macroscopic Classification (Borrmann)
| Type | Description |
|---|---|
| **I — Polypoid** | Projecting mass into lumen; best prognosis |
| **II — Ulcerating with elevated edges** | Malignant ulcer; raised, shouldered margin |
| **III — Ulcerating + infiltrating** | Ulcer with infiltrating edges |
| **IV — Diffusely infiltrating** | **Linitis plastica / "leather-bottle stomach"**; no discrete ulcer; all layers infiltrated; worst prognosis |

### Microscopic (Lauren Classification — Exam Favourite)
| Type | Features | Association |
|---|---|---|
| **Intestinal type** | Gland-forming; resembles colonic adenocarcinoma; well-differentiated | Environmental factors, H. pylori, atrophic gastritis; **better prognosis** |
| **Diffuse type** | **Signet-ring cells** infiltrating stroma without gland formation; poorly differentiated | Young patients, women; blood group A; genetic (E-cadherin); linitis plastica; **worse prognosis** |

> **Note**: Nearly all gastric carcinomas are **adenocarcinomas**.

### Spread
- **Direct**: To oesophagus (proximal), duodenum (distal), pancreas, transverse colon
- **Lymphatic**: Along gastric lymph nodes; **Virchow's node** (left supraclavicular); Troisier's sign
- **Blood-borne**: Liver (most common); lung; bone; brain
- **Transcoelomic (peritoneal)**: **Krukenberg tumour** (ovarian metastasis from signet-ring cells); **Blumer's shelf** (pelvic peritoneal metastasis felt on rectal exam); **Sister Mary Joseph's nodule** (periumbilical metastasis); ascites

---

## Clinical Features — Six Groups (Textbook Classification)

| Group | Presentation | Notes |
|---|---|---|
| **I — Early/dyspeptic** | Non-specific dyspepsia, loss of appetite, nausea, loss of weight | **Early gastric cancer** — often asymptomatic at this stage; Japan mass screening catches this |
| **II — Insidious onset** | Greater curvature or body tumour; epigastric discomfort, anorexia, nausea, weight loss; **haematemesis/melaena or occult blood loss → anaemia** | Microcytic anaemia common |
| **III — Pain** | Continuous epigastric pain or discomfort; **no periodicity**; not relieved by food; substernal pain with cardiac involvement; **coffee-ground vomiting**; weight loss always present | Most common presenting symptom (~95% at time of diagnosis) |
| **IV — Obstructive** | Pyloric carcinoma → **projectile vomiting, fullness, belching**; cardiac carcinoma → **dysphagia** | No bile in vomit (pyloric) |
| **V — Lump** | Incidental epigastric mass in 1/4 of cases; vague dyspepsia | Palpable mass is a late sign |
| **VI — Metastases** | Ascites, jaundice, pleural effusion, Virchow's node, Krukenberg tumour, back pain (vertebral metastasis) | Primary may remain silent until metastatic presentation |

---

## Physical Examination Findings

| Sign | Meaning |
|---|---|
| **Epigastric mass** | Primary tumour (late sign); firm, non-tender, movable if not adherent |
| **Hepatomegaly** (irregular, hard) | Liver metastasis |
| **Virchow's node** (Troisier's sign) | Enlarged **left supraclavicular** lymph node; metastasis via thoracic duct |
| **Sister Mary Joseph's nodule** | **Periumbilical** nodule; peritoneal metastasis |
| **Krukenberg tumour** | Ovarian metastasis (bilateral); palpable on pelvic exam |
| **Blumer's shelf** | Pelvic peritoneal deposits felt as hard shelf on **rectal/vaginal exam** |
| **Trousseau's sign** | Phlebothrombosis of leg veins (hypercoagulability of malignancy) |
| **Ascites** | Peritoneal metastasis or portal hypertension from liver deposits |

---

## Investigations

### Bloods
- **FBC**: Low Hb, low RBC, **high ESR** (present in ~80% of patients)
- **Stool**: Occult blood (faecal occult blood test positive)
- LFTs: Abnormal if liver involved

### Imaging
1. **Upper GI endoscopy + biopsy** — **Gold standard** for diagnosis; multiple biopsies (minimum 6–8) from edge and base of lesion
2. **Barium meal** (double contrast): **Filling defect** (polypoid); malignant ulcer niche with **"shouldered" or "rolled" edges** and interrupted mucosal folds; **"leather-bottle stomach"** (linitis plastica); persistent peristalsis failure
3. **CT scan** (chest/abdomen/pelvis): Staging — T-stage (wall invasion), N-stage (nodes), M-stage (metastases); gold standard for staging
4. **Endoscopic ultrasound (EUS)**: T-stage and N-stage accuracy; best for local wall invasion
5. **Staging laparoscopy**: Before curative resection — detects peritoneal disease and small liver metastases not seen on CT

### Distinguishing Benign vs Malignant Gastric Ulcer (Barium / Endoscopy)

| Feature | **Benign** | **Malignant** |
|---|---|---|
| Margins | Regular, punched-out | Irregular, rolled, shouldered |
| Mucosal folds | Radiate to edge, regular | Interrupted/amputated before reaching edge |
| Base | Smooth, clean | Nodular, irregular |
| Surrounding mucosa | Normal | Rigid, thickened |
| Ulcer projection | Projects **beyond** stomach wall | Within stomach wall |

---

## Staging (TNM — Brief)
- T1: Mucosa/submucosa (**early gastric cancer**)
- T2: Muscularis propria
- T3: Subserosa
- T4: Serosa/adjacent structures
- N0–3: Lymph node involvement
- M0/M1: No/distant metastasis

**Early gastric cancer** = confined to mucosa/submucosa (T1); 5-year survival **>90%**

---

## Treatment

### Surgery — Only Curative Option

| Operation | Indication | Reconstruction |
|---|---|---|
| **Radical subtotal gastrectomy** | Distal (antral/pyloric) tumours | Billroth I or Polya (Billroth II) |
| **Total gastrectomy** | Proximal (body/fundus/cardia), diffuse | Roux-en-Y oesophagojejunostomy |
| **D1 dissection** | Perigastric nodes only | Standard minimum |
| **D2 dissection** | D1 + coeliac axis nodes | Recommended; Japan standard |
| **Palliative gastrojejunostomy** | Pyloric obstruction, unresectable | Anterior GJ |
| **Feeding jejunostomy** | Cardial obstruction, unresectable | Palliation |

**What is resected at total gastrectomy?**: Whole stomach + greater and lesser omentum + regional lymph nodes ± spleen ± distal pancreas

### Perioperative/Post-operative Details
- Short-term complications: Anastomotic leak (check with water-soluble contrast swallow at day 5–7), duodenal stump leakage
- Long-term: Small meals required; virtually no functional difference between total and subtotal gastrectomy; **Vitamin B12 deficiency** post-total gastrectomy (replace routinely); dumping; diarrhoea (less common after gastric cancer surgery than peptic ulcer surgery)

### Prognosis (5-Year Survival)
- **Western countries**: 25–50%
- **Japan**: 50–70% (due to early detection programmes and mass screening)
- **Early gastric cancer**: >90%

### Radiotherapy
- **Limited role** — surrounding radiosensitive tissues restrict dose
- **Palliative use**: Painful bone metastasis

### Chemotherapy
- More effective than radiotherapy
- **Best combination**: **Cis-platinum + 5-fluorouracil + epirubicin (ECF)** by continuous infusion
- **Japan**: Mitomycin C-impregnated charcoal, intraperitoneal route (peritoneal lymphatics absorb it)
- **Perioperative chemotherapy** (e.g., FLOT, ECF regimen) → improves resectability and survival

---

# QUICK REFERENCE TABLES

## High-Yield Eponymous Signs in Gastric Pathology

| Eponym | Sign | Condition |
|---|---|---|
| **Virchow's node / Troisier's sign** | Enlarged left supraclavicular node | Gastric carcinoma (lymphatic spread via thoracic duct) |
| **Sister Mary Joseph's nodule** | Periumbilical nodule | Gastric/other GI carcinoma (peritoneal metastasis) |
| **Krukenberg tumour** | Bilateral ovarian metastasis | Gastric carcinoma (signet ring cells) |
| **Blumer's shelf** | Hard pelvic shelf on PR exam | Gastric carcinoma (peritoneal deposits) |
| **Trousseau's sign** | Phlebothrombosis of superficial leg veins | Visceral malignancy (gastric carcinoma) |
| **Ramstedt's operation** | Pyloromyotomy | Infantile hypertrophic pyloric stenosis |
| **Curling's ulcer** | Acute gastric/duodenal ulcer | Severe burns |
| **Cushing's ulcer** | Acute gastric/duodenal ulcer | Head injury / raised ICP |
| **Graham's patch** | Omental patch closure of perforation | Perforated peptic ulcer |
| **Mallory–Weiss tear** | Mucosal tear at OGJ from vomiting | Haematemesis after retching |

---

## Gastric Acid Secretion — Key Numbers

| Parameter | Normal | Duodenal Ulcer |
|---|---|---|
| BAO (Basal Acid Output) | 0–5 mmol/hr | **4–9 mmol/hr** |
| MAO (Maximal Acid Output) | 15–25 mmol/hr | **30–50+ mmol/hr** |
| Pepsin activation pH | — | **< 2.5** |
| Intrinsic factor produced by | — | Parietal cells |

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## Pyloric Stenosis Metabolic Abnormality — Memory Aid

```
IHPS / Adult Pyloric Stenosis:
Loss of HCl (H+ + Cl-)  →  Hypochloraemia + Alkalosis
Loss of K+ in vomit      →  Hypokalaemia
Kidney conserves H+      →  Excretes K+ in urine
Result: PARADOXICAL ACIDURIA (acid urine in the setting of metabolic alkalosis)
```

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## Surgical Operations Quick Reference

| Operation | What is done | Key indication |
|---|---|---|
| **Ramstedt's pyloromyotomy** | Split pyloric muscle, preserve mucosa | IHPS |
| **Graham's patch** | Omental plug closure + 3 sutures | Perforated peptic ulcer |
| **Highly selective vagotomy (HSV)** | Divide only parietal cell branches; preserve nerves of Latarjet | Duodenal ulcer (elective surgery of choice) |
| **Truncal vagotomy + pyloroplasty** | Both vagi divided + pylorus widened | DU with pyloric obstruction |
| **Billroth I (partial gastrectomy)** | Distal 2/3 removed + gastroduodenostomy | Gastric ulcer (elective surgery of choice) |
| **Polya (Billroth II)** | Distal 2/3 removed + duodenal stump closed + gastrojejunostomy | DU (difficult anatomy), recurrent ulcer |
| **Gastrojejunostomy** | Stomach anastomosed to jejunum without resection | Pyloric stenosis, palliative gastric Ca |
| **Total gastrectomy** | Entire stomach removed + Roux-en-Y | Proximal / diffuse gastric carcinoma |
| **Subtotal gastrectomy** | Distal 3/4–4/5 removed | Distal gastric carcinoma |

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## Differentiation of Common Causes of Haematemesis

| Feature | Peptic Ulcer | Oesophageal Varices | Mallory–Weiss |
|---|---|---|---|
| History | Dyspepsia, NSAIDs | Alcohol, liver disease | Retching/vomiting |
| Blood type | May be coffee-ground or red | **Bright red, copious** | Bright red, after retching |
| Shock | Variable | **Severe, rapid** | Usually mild |
| Mortality | ~10% | **30–40%** per episode | Usually self-limiting |
| Endoscopy Rx | Adrenaline + clips | **Banding** | Adrenaline |
| Surgery | Underrunning + vagotomy | Porto-systemic shunt | Oversew mucosal tear |

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## Most Common / Most Important — At a Glance

| "Most..." | Answer |
|---|---|
| Most common site of peptic ulcer | **1st part of duodenum** |
| Most common complication of peptic ulcer | **Haemorrhage** |
| Most dramatic complication of peptic ulcer | **Perforation** |
| Most common cause of haematemesis | **Peptic ulcer** |
| Most dangerous cause of haematemesis | **Oesophageal varices** |
| Vessel eroded in posterior DU bleed | **Gastroduodenal artery** |
| Most common site of perforation | **Anterior wall, 1st part duodenum** |
| Operation of choice for DU (elective) | **Highly selective vagotomy (HSV)** |
| Operation of choice for GU (elective) | **Billroth I partial gastrectomy** |
| Operation of choice for IHPS | **Ramstedt's pyloromyotomy** |
| Treatment of pyloric stenosis (adult) | **Vagotomy + gastrojejunostomy** |
| Most common predisposing factor for gastric Ca | **H. pylori / Chronic atrophic gastritis** |
| Country with highest gastric Ca incidence | **Japan** |
| Most common microscopic type of gastric Ca | **Adenocarcinoma** |
| Best curative treatment for gastric Ca | **Radical surgery (gastrectomy + D2 node dissection)** |
| Best chemotherapy regime for gastric Ca | **Cis-platinum + 5-FU + epirubicin (ECF)** |
| 5-year survival of early gastric Ca | **>90%** |
| Cell producing intrinsic factor | **Parietal (oxyntic) cell** |
| Pepsin activation pH | **< 2.5** |

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*Source: A Concise Textbook of Surgery, Chapter 44 — The Stomach and Duodenum (pages 706–767)*