DISEASES OF STOMACH

• Stomach develops from distal portion of foregut

• Normal volume 1200-1500mls
• Starts extends from just left to midline where it joins the esophagus to just right
midline where it joins the duodenum.
CONGENITAL:
1. Pyloric Stenosis:
 Hypertrophy and narrowing of pyloric lumen.
 Predominant in male children (infantile type).
 Adult from- rare, acquired.
 Aetiology-unknown:
familial tendency-recessive inheritance.
gastritis or tumours
 PATHOLOGY:

• Hypertrophy and hyperplasia of circular layer of muscle in pyloric sphincter.

• Some degree of fibrosis.
• Features:
- male infant 3-6 weeks old.
- projectile vomiting + visible peristalsis.
- palpable lump.
- constipation.
 INFLAMMATORY CONDITIONS.

1. Gastritis : May be acute or chronic.

2. Peptic ulcer.

ACUTE GASTRITIS:
o A transient inflammatory response.
o Involves mainly mucosa.
 AETIOPATHOGENESIS

Variety of agents:
1. Diet and personal habits:
- highly spiced foods.
- excessive alcohol intake.
- malnutrition.
- heavy smoking.
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2. infections;
- Bacteria: Helicobacter pylori.
diphtheria.
Salmonellosis.
Staph. food poisoning.
- Viral: Hepatitis, influenza.
3. Drugs: NSAIDS.
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4. Chemicals and physical agents:

- corrosives: caustic soda, lysol, phenol.
- gastric irradiation.
5. Severe stress:
- emotional factors; shock, anger, resentment.
- extensive burns, trauma.
- surgery.
 MECHANISM OF MUCOSAL INJURY.

a. Reduced blood flow: ischaemic damage.

b. Increased acid secretion due to H. pylori.
# end result- damage to epithelial barrier.
c. Decreased production of bicarbonate buffer.
 PATHOLOGY:

Gross:
 Oedematous mucosa with heamorrhagic spots.
Micro:
 Oedema, neutrophils infiltrate in lamina propria.
 Mucosal sloughing may occur.
 Usually healing occurs with epithelial cell regeneration .
 CHRONIC GASTRITIS.

 Commonest histologic change in gastric biopsies.

 Microscopic change poorly correlated to symptomatology.
 Seen in 35 % of endoscopically normal mucosal biopsies.
 More frequent with advancing age.
 PATHOGENESIS

 Some causes of acute gastritis may lead to chronic gastritis.

 Reflux of duodenal contents
 Associated disease of stomach or duodenum- PU or cancer.
 Chronic hypochromic anaemia associated with atrophic gastritis.
 Autoimmunity: parietal and Intrinsic Factor (IF) antibodies.
 EFFECT:

• Chronic gastric injury is a result of cytotoxicity to gastric mucosal epithelium.

• Outcome: Barrier broken, inciting inflammatory response.
 CLASSIFICATION:

1. Type A (Autoimmune) gastritis.

 Involves body and fundus.
 Autoantibodies against parietal cells and IF demonstrated in serum.
 End result is gastric atrophy with intestinal metaplasia.
 Some patients develop pernicious anemia .
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 End result is hypochlohydria or achlorhydria due to destruction of gastric acid

producing cells.
 Hyperplasia of gastrin-producing G cells in antrum leading to hypergastronaemia .
2. Type B gastritis (H. pylori related)
 Antral mucosal region involved.
 Hypersecretory gastritis ( excessive HCl secretion due to H. pylori infection).
 Patients may have associated duodenal or gastric ulcer.
 No association with autoimmune mechanisms
 PATHOLOGY.

Gross:
 Features not conclusive.
 Mucosa may be normal, atrophic or oedematous.
Histology based on :
i. Extent of inflammatory changes in mucosa( superficial or deep).
ii. Activity of inflammation( quiscent or active)
iii. Presence of intestinal metaplasia.
 SIMPLE CLASSIFICATION:

1. Chronic superficial gastritis.

2. Chronic atrophic gastritis.
3. Gastric atrophy.
4. Chronic hypertrophic gastritis
( Menetrier’s disease).
 1. CHRONIC SUPERFICIAL GASTRITIS

• Inflammatory cell infiltrate- plasma cells & lymphocytes.

• Inflammation is limited to superficial mucosa.
• May resolve or progress to chronic atrophic gastritis.
• H. pylori present in over 95 % of active cases( 65 % in quiscent cases).
• Risk of malignant change.
2. CHRONIC ATROPHIC GASTRITIS
• Inflammatory infiltrate in deeper mucosa.
• Atrophy of epithelial cells and gland destruction.
• Two types of metaplasia:
 Intestinal metaplasia( goblet cells, paneth cells and endocrine
cells present.
Absent or very few parietal cells.
 Pseudopyloric metaplasia
 Replacement of body glands by proliferated mucous neck cells of normal pyloric
glands.
 3. GASTRIC ATROPHY.

• Thinning of gastric mucosa with loss of glands.

• Classically no inflammation.
 4. CHRONIC HYPERTROPHIC GASTRITIS

• Uncommon.
• Enormous thickening of gastric ruggal folds.
• Site = fundic - body mucosa.
• Features dyspepsia, haematemesis & melaena.
 PEPTIC ULCERS.

• Exposure of mucosa to acid-pepsin.

• 99 % duodenum or stomach.
• May be acute or chronic.
 ACUTE PEPTIC (STRESS) ULCERS.

• Usually multiple, small, mucosal erosions.

• Commonly in stomach, rarely in duodenum.
Aetiology:
 Severe stress
 Psychological
 Physiological stress: shock, septicaemia, extensive burns ( Curling’s ulcer)
 Drugs, irritants
 PATHOGENESIS.??

Gastric acid secretion- normal or below normal.

Ischaemic hypoxic injury= more likely.
Depletion of gastric mucus barrier.
 PATHOLOGY:

Gross: multiple ulcers.

shallow, oval or circular.
Micro:margins & base show inflammatory response.
Outcome: complete healing with re-epithelialization.
 CHRONIC PEPTIC ULCERS.

 Include gastric and duodenal ulcers.

 2 distinct diseases with regard to aetiology, pathogenesis and clinical features.
 Pathological findings are similar.
 Incidence: middle age 5th -6th decade ( M> F).
 Duodenal ulcer 4 times more common than gastric.
 AETIOLOGY

• Normal protective mucosal barrier disturbed by acid-pepsin which digests mucosa

• In contrast to DU, GU patients have low to normal gastric acid secretion .
• 10-20 % of GU patients may have coexistent DU as well.
• Thus aetiology of PU not explainable on a single factor BUT may be multifactorial
 PREDISPOSING FACTORS

1. Helicobacter pylori.
 15-20 % infected patients develop DU.
 Gastric colonization does not lead to ulceration in some and remain asymptomatic.
 H. pylori is identified in histological sections, culture and serology.
2. Acid pepsin secretions.
 Essential for DU & GU development.
 PUs never occur in association with pernicious anaemia.
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3. Mucus secretion defect.

 Damage to protective mucus barrier occurs.
4. Gastritis:
 Present in all forms of PU around the lesion. “cause and effect” ???.
5. Local irritants;
 Pyloric antrum & lesser curvature exposed to irritants for a long time.
 Are common sites for G. ulcer.
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6. Dietary factors- nutritional deficiencies.

7. Psychological factors:
 Stress- anxiety, fatigue.
 Ulcer-type personality

8. Genetic factors;
 BG O tend to get PU than others.
 Genetic influence more in DU.
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9. Hormonal factors.
 Hormone secretion by certain tumours .
# Gastrin in Zollinger-Ellison syndrome .
# Endocrine secretion by parathyroid , adrenal or anterior pituitary tumours.
10. Miscellaneous causes
Alcoholic cirrhosis
Chronic renal failure
Hyperparathyroidism
 PATHOGENESIS

i. Exposure of mucosa to gastric acid and pepsin .

ii. Strong aetiological association with H. pylori infection.
 DUODENAL ULCER

• High acid-pepsin secretion very strong association.

• Such people have hypersecretion of acid during night (vagal stimulation).
• Patients have rapid gastric emptying.
• H. Pylori gastritis in 95 -100 % of cases.
 GASTRIC ULCER.

• Impaired gastric mucosal defence to acid pepsin.

• Other factors:
o Hyperacidity- atonic stomach with high gastrin secretion.
o Damaging effect of other factors (gastric acid low or normal).
o Protective gastrin mucus “barrier” vs acid-pepsin depleted.
 PATHOLOGY.

Gross:
 Gastric ulcer:
o Lesser curvature- pyloric antrum.
o Usually posterior wall.
 Duodenal ulcer
o 1st part , post pyloric.
o Anterior wall common
o Usually solitary in 80 % of cases.
o Small, round/oval, punched out.
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Microscopy:
4 histologic zones:
i. superficial exudative zone= fibrinous exudate, necrosis, PMNs.
ii. Necrotic zone- underneath.
iii. Granulation tissue zone.
iv. Zone of cicatrization( fibrosis, thrombosis & sclerotic arteries).
 COMPLICATIONS OF PU.

1. Obstruction.
2. Haemorrhage.
3. Perforation.
4. Malignant change: < 1 %.
 TUMOURS AND TUMOUR LIKE
CONDITIONS OF STOMACH.
A. TUMOUR LIKE CONDITIONS(POLYPS).
I. Hyperplastic polyps.
- commonest polyps 90 %.
- single or multiple.
- site pyloric region.
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ii. Hamartomatous polyps.

- not true tumours but developmental malformations.
- include ;
Peutz-Jegher’s syndrome;
Juvenile polyps.
Pancreatic heterotopia
Inflammatory fibroid polyp.
 BENIGN TUMOURS

Uncommon incidental findings.

i. Adenomas ( adenomatous polyps).
ii. Spindle cell (stromal) tumours.
 GASTRIC CARCINOMA

Aetiology:
1. H. pylori infection.
2. Dietary factors:
 smoked fish,
 high intake of salts,
 nitrites in preservatives,
 pickled vegetables,
 tobacco smoke,
 alcohol consumption.
 AETIOLOGY (CT)

3. Geographic factors:
 High incidence in Japan, Chile, Finland and Iceland.
 Low incidence in UK, US and Canada.
 In Tanzania higher incidence Tanga, Kilimanjaro.
“Environmental factors”
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4. Racial factors ??.

 Incidence higher in Blacks, American Indians and Chinese in Indonesia.
5. Genetic factors.
 Blood group A higher tendency.
6. Pre-malignant conditions.
 i. hypo-achlorhydria.
 ii. Adenomatous polyps.
 iii. Stump carcinoma.
 iv. Chronic gastric ulcer ( ulcer cancer).
Location
 pre-pyloric region, lesser curvature
 pylorus and antrum
Stages:
 In situ carcinoma
 Early gastric carcinoma
 Advanced gastric carcinoma
• May be:
i. Ulcerative
ii. Fungating ( polypoid)
iii. Schirrous ( linitis plastica)
iv. Clloid (mucoid ) carcinoma
v. Ulcer-cancer.
Also classified into:
 Expanding ( intestinal ) type
 Infiltrating ( diffuse) type.
 EARLY GASTRIC CARCINOMA

• Term used to describe cancer limited to mucosa and submucosa

• May be polypoid, superficial elevated, superficial flat or depressed and ulcerative
type.
• Histology- glandular carcinoma with/without regional node involvement.
 ADVANCED GASTRIC CARCINOMA

• Extension into the muscularis propria or beyond

• 5 subtypes:
i. Ulcerative carcinoma- commonest
ii. Fungating (polypoid) carcinoma
iii. Schirrous carcinoma- wall thickened .
iv.Colloid carcinoma
v. Ulcer-cancer < 1 %
 CLINICAL FEATURES

• Most patients with gastric cancer have metastases by the time they present to
hospital
• Symptoms and signs are those of advanced cancer
• Obstruction of gastric outlet in large tumours of antrum or pre-pyloric region
• Chronic bleeding (occult blood) and anaemia
• Two-thirds of patients have achlorhydria
• Carcinoembryonic antigen levels increased in blood in 1/3 of cases
Prognosis:
Even in the presence of node metastases, early gastric carcinoma has considerably
better prognosis than advanced gastric carcinoma
Spread:
a. Direct to peritoneal cavity with seeding onto the ovaries ( Krukenberg tumour)
b. Lymphatic to regional nodes, supra clavicular ( Virchow’s node)
c. Haematogenous to liver, lungs bones etc
• Other tumours of stomach:
Leiomyoma/leiomyosarcoma,
Carcinoid tumour
Lymphomas of stomach( MALT lymphomas)
MWISHO