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GIS > GIS17 Pathology Of Peptic Ulcers, Gastritis And Gastric Cancer > Flashcards

GIS17 Pathology Of Peptic Ulcers, Gastritis And Gastric Cancer Flashcards

1
Q

Functions of stomach

A
  1. Mixing reservoir for food
  2. Digestion of proteins
  3. HCl + pepsin: 2 main products of gastric mucosa
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2
Q

Peptic ulcer

A

Ulcers developing along Upper GI tract
- due to peptic / gastric juice action

2 types:

  • Acute
  • Chronic

Sites of occurrence (descending order of frequency):

  1. ***Duodenum (1st part, immediate post-pyloric region)
  2. ***Stomach (non-acid secreting pyloric gland mucosa: pyloric antrum, lesser curvature)
  3. ***Esophagus (reflux esophagitis)
  4. Gastroenterostomy stoma (jejunal side) (surgical connection between stomach and jejunum to bypass duodenum)
  5. Jejunum (where pathological secretin of gastrin / hypersecretion of gastric acid)
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3
Q

Risk factors / Etiology

A
  1. H. pylori infection
    - effective treatment available, seldom need gastric resection / see complications
  2. Environmental factors:
    - drugs (high-dose corticosteroid, aspirin, NSAID)
    - smoking
    - stress
  3. Hypercalcaemia (e.g. hyperparathyroidism)
    - ***stimulates gastrin production and therefore acid secretion
  4. Hormonal factor
    - male preponderance, rare in pregnant women
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4
Q

H. pylori

A
  • gram -ve
  • spiral-shaped
  • flagella
  • interface between mucus and gastric epithelial surface
  • produces Urease, Phospholipase, Catalase, Mucinase etc. —> weakens mucosa
  • ***Silver stain: Warthin-starry stain
  • class 1 carcinogen

Diseases:

  1. Gastric ulcer: chronic gastritis —> damage to gastric mucosa —> ***impaired mucosal resistance —> GU
  2. Duodenal ulcer: **high acidity —> **gastric metaplasia in duodenum —> HP infect the metaplastic epithelium in duodenum —> active chronic duodenitis —> impaired mucosal resistance —> DU
  3. ***Gastric carcinoma
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5
Q

***Acute peptic ulcer vs Chronic peptic ulcer

A 
Acute:
Macroscopic
- ***mucosa only
- erosion: less than full thickness of mucosa: healing without scarring
- ***shallow, small and multiple sites
- ***no granulation tissue
- ***no scarring
- related to stress e.g. severe burn, brain damage, aspirin
- may lead to severe gastric haemorrhage
- anywhere in stomach, rare in duodenum

Microscopic
- similar to chronic but without granulation tissue and fibrosis

Chronic:
Macroscopic
- deeper than mucosa
- **disruption of mucosa, submucosa, muscle layer
—> necrotic cellular debris + fibrinous exudate
—> **granulation tissue
—> fibrous scar tissue (loss of rugae folds)
- **deep and single
- round / oval, solitary
- sharp margins (punched-out edge)
- **oedematous surrounding mucosa
- ***fibrotic base extending to serosa with / without fibrous adhesion to adjacent organs

Microscopic
- ulcer floor:
—> uppermost: layer of **polymorphs and necrotic debris
—> middle: **granulation tissue (fibroblasts and capillaries)
—> lower: ***fibrous scarring zone disrupting muscular coat

Healing in Acute / Chronic ulcer:
healing by proliferation of epithelium from ulcer edge —> thin layer over ulcer floor —> fibrosis if chronic —> stellate scar

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6
Q

Erosion vs Ulceration

A

Erosion (i.e. Acute):
Loss of less than full thickness of mucosa: healing without scarring

Ulceration (i.e. Chronic):
Loss of full thickness of the mucosa, with varying degree of penetration into underlying coats —> healing with scarring more common in chronic ulcers

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7
Q

Pathogenesis for GU and DU

A

GU: weakening of mucosal defence
DU: increase acid

Overall: virulent factors + hypergastrinemia + hyperacidity

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8
Q

Complications of peptic ulcer

A
  1. Haemorrhage
    - small blood vessels, veins, artery (emergency)
    —> **Hematemesis: vomiting of **coffee ground material / fresh blood
    —> **Bleeding into intestine: **occult blood in stool, ***Melena (tarry stool芝麻糊), foul smelling
  2. ***Perforation
    - Duodenal ulcer > gastric ulcer
    - Anterior ulcer > posterior ulcer
    - Male > female
    - Chronic > acute
    - Peritonitis (initially chemical then bacterial)
    - Acute PU can also perforate
  3. Penetration into adjacent organs
    - pancreas (painful as lots of plexus in head of pancreas)
    - production of of gastro-colic fistula
  4. ***Fibrosis and stenosis —> obstruction
    - pyloric stenosis (vomiting immediately afternoon food)
    - hour-glass appearance
  5. Carcinoma (rare, <1%)
    - duodenal ulcer ***never undergo malignant changes
    - only for gastric lesions
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9
Q

Gastritis

A

Inflammation of gastric mucosa

  1. Acute
    - ***acute inflammatory cells (neutrophil)
    - transient
    - abdominal pain, can give rise to bleeding
    - NSAID, alcohol, smoking, stress
  2. Chronic
    - **chronic inflammatory cells (lymphocytes, plasma cells)
    —> **    Superficial: present in superficial mucosa
    —> **Diffuse: whole depth of mucosa
    —> **    Atrophic: shortening of glands
    - etiology: H. pylori, autoimmune
    - “active” chronic gastritis: polymorphs also present in addition to chronic inflammatory cells: density of neutrophil infiltrate referred to as activity and graded accordingly
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10
Q

Gastritis etiology

A
  1. ***H. pylori (>80%, mostly in antrum)
  2. Idiopathic (10-15%)
  3. Drugs (NSAIDs) / gastric irritants
  4. Auto-immune (5%, mostly in fundus —> severe mucosal atrophy: usual end result —> progressive reduction in acid secretion, pepsin, intrinsic factor —> achlorhydria / pernicious anaemia, increased risk of gastric carcinoma)
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11
Q

Stomach tumours

A
  1. Benign (<10%)
    - Adenoma
    - Leiomyoma
  2. Malignant (95%)
    - ***Adenocarcinoma ( / Lymphoma / Leiosarcoma)
    —> arise from gastric mucosa (Duodenal ulcer rarely malignancy)
    —> majority: prepyloric region
    - incidence decreasing worldwide
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12
Q

Etiology of gastric cancer

A
  1. ***H. pylori (class 1 carcinogen)
  2. Smoking
  3. Dietary / environmental factors
    - nitrosamines (from nitrites, nitrates e.g. smoked and salted fish), pickled vegetables
  4. Premalignant conditions and lesions
    - **gastric adenoma, chronic type A autoimmune gastritis, **pernicious anaemia, dysplasia
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13
Q

Macroscopic morphology of stomach carcinoma

A
  1. ***Ulcerative (凹)
  2. Polypoid / **Fungating (凸起)
    —> new vessel formation cannot keep up with lesion growth
    —> ischaemic —> necrotic —> ulcerative —> heaped up / **    everted edges
  3. Diffuse scirrhous (very firm, a carcinoma that is hard to touch)
    —> ***Linitis plastica (leather-bottle stomach)
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14
Q

Clinical features of gastric carcinoma

A
  1. > 50 years old
  2. non-specific symptoms:
    - dyspepsia
    - epigastric pain
    - vomiting
    - weight loss
    - obstructive symptoms
    - epigastric mass
    - enlarged left supraclavicular (Virchow’s lymph nodes)
    - hematemesis / perforation
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15
Q

Adenocarcinoma histological features

A
  1. Irregular, packed glands
  2. High N/C ratio
  3. Lots of mitosis
  4. Dark nuclei
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16
Q

Microscopic classification of gastric adenocarcinoma

A

Lauren’s classification:

  1. **Intestinal type (formation of **glandular structure from tumour cells)
  2. **Diffuse type (tumours cells in sheets with **minimal gland formation; with diffuse infiltrative pattern. ***Signet-ring cells (cell with large vacuole) with mucin distending cells and compressing the nucleus may be present, single / in small clusters)

WHO:

  1. Papillary / tubular
  2. Poorly cohesive / signet-ring cell phenotype (poorly differentiated: not good)
17
Q

Spread of stomach carcinoma

A
  1. Direct spread to adjacent organs (liver, duodenum / through wall: liver, pancreas, greater / less omentum, transverse colon, diaphragm, common bile duct)
  2. Regional lymph nodes (Most common, via lymphatics)
    —> around stomach
    —> advanced stage / distant: left supraclavicular lymph nodes (enlarged neck)
  3. Haematogenous spread to liver (via portal vein)
  4. Transcelomic spread through peritoneum to ovaries
    —> peritoneal tumour seedling
    —> ovaries: Krukenberg tumours (bilateral) (malignancy in the ovary that metastasized from a primary site, classically GI tract) —> commonest histological type: signet ring cell carcinoma
18
Q

Early gastric cancer

A

Gastric carcinoma ***confined to mucosa +/- submucosa
—> regardless of lymph node metastasis

***Excellent prognosis ~ 95% 5 year survival rate after surgical resection

5 morphological types:

  • Type 0-1 protruded type
  • Type 0-2a superficial and elevated type
  • Type 0-2b flat type
  • Type 0-2c superficial and depressed type
  • Type 0-3 excavated type
19
Q

***Peptic ulcer vs Ulcerated carcinoma of stomach (Malignant ulcer)

A
  1. Size:
    PU: smaller
    MU: larger
  2. Number:
    PU: single / multiple
    MU: single
  3. Margin:
    PU: **edematous, not raised
    MU: **    irregular / everted edge
  4. Edge:
    PU: sharp
    MU: sharp / irregular
  5. Floor:
    PU: **clean
    MU: **    dirty / necrotic
  6. Base:
    PU: **ulcer slough and granulation tissue with complete destruction of muscular layer —> **fibrous scar tissue
    MU: ***carcinoma cells intermixed with muscular layer

Diagnosis:
- ALWAYS make a histological examination (Fiberoptic endoscopic examination + Biopsy) to differentiate between gastric ulcer / gastric carcinoma

20
Q

Malignant lymphoma

A

Stomach is the most common site of primary lymphoma, almost all are B-cell origin

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