Metaplasia of lower oesophagus due to oesophagitis - Histology: Spectrum - oesophageal (stratified squamous) -> gastric (simple columnar) -> intestinal (simple columnar + goblet cells) - Metaplasia can lead to dysplasia (50x risk of oesophageal adenocarcinoma) - treating at GORD stage reduces risk

Upper GI Flashcards by Beth T

Layers of GI tract

Mucosa (glandular epithelium, lamnia propria sheet, muscular mucosa thin muscle layer)
Submucosa
Muscularis externa (thick muscle layer - inner circular, outer longitudinal)
Serosa / adventitia

Variation observed in epithelium of different GI tract regions

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Key features of oesophagus

3 layers of non-keratinised stratified squamous epithelium (protects against food)
2 types of mucus producing glands - sub-mucosal glands in submucosa and cardiac glands in lamnia propria
Muscularis externa - upper 1/3 striated, middle 1/3 mixed, lower 1/3 smooth
Outer layer - thoracic oesophagus adventita / abdominal oesophagus (+ rest of GI tract) serosa

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Difference in thoracic oesophagus vs. abdominal oesophagus

Adventitia = loose CT (thoracic oesophagus) 'T for titia'
Serosa = mesothelium (abdominal oesophagus)

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GOJ

Stratified squamous -> simple columnar

Pale -> pink

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Key features of stomach

Simple columnar
Two main regions = body/fundus (top)
Gastric glands - products depend on location - ALL have foveolar cells (mucus) at top, NE cells (gastrin, histamine, serotonic, CCK, somatostatin) at base, glands in fundus/body have parietal (gastric acid, IF) + chief cells (pepsinogen, lipase)
Muscularis externa has 3 layers instead of 2 (oblique / circular / longitudinal) for churning / functional pyloric sphincter / bolus movement respectively

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4 types of cells in gastric glands

Foveolar cells (mucus)
NE cells (gastrin, histamine, serotonic, CCK, somatostatin)
Parietal (gastric acid, IF)
Chief cells (pepsinogen, lipase)

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Produce gastric acid, IF

Parietal cells

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Produce pepsinogen, lipase

Chief cells

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Key features of small intestine

Simple columnar with goblet cells (mucus)
Crypts + villi (crypts contain replicating stem cells to replace epithelial cells, immune Paneth cells, goblet cells - crypts in colon don’t have Paneth)

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Normal villous: crypt ratio

> 2:1

Decreased in coeliac disease

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Brunner’s glands

Duodenum
(alkaline secretions)
‘Duo running secretions’

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Plicae circularis

Jejenum

out-foldings of mucosa and sub-mucosa decorating the villi

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Peyer’s patches

Ileum

organised lymphoid tissue aggregations

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Acute oesophagitis

Oesophagus inflammation
Most commonly due to reflux
- Histology: surface epithelium eroded, necrotic slough replaced by granulation tissue. Chronic inflammation leads to fibrosis. Baal cell hyperplasia. Vascular papillae extend into upper epithelium
- Barrett’s oesophagus in 10%; haemorrhage, perforation, stricture

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Barrett’s oesophagus

Metaplasia of lower oesophagus due to oesophagitis

Histology: Spectrum - oesophageal (stratified squamous) -> gastric (simple columnar) -> intestinal (simple columnar + goblet cells)
Metaplasia can lead to dysplasia (50x risk of oesophageal adenocarcinoma) - treating at GORD stage reduces risk

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What is the difference between UK and USA Barrett’s classification?

In UK we call it Barett’s if there is metaplasia to stomach (simple columnar) or SI (simple columnar + goblet cells). In the USA only SI

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Alcohol / tobacco use
Mid oesophagus
IC bridges + keratin
Commonest worldwide

Squamous cell oesophageal carcinoma

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Barrett’s oesophagus
Lower oesophagus
Glands + mucin production
Commonest in UK

Oesophageal adenocarcinoma

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Two types of oesophageal carcinoma

Squamous cell carcinoma

Adenocarcinoma

Process of adenocarcinoma development

Metaplasia -> Dysplasia -> Adenocarcinoma

Dysplasia = features of malignancy without BM Invasion

p53 mutation

Oesophageal carcinoma

What is the venous drainage of the oesophagus

Upper 2/3 oesophageal veins into SVC

Lower 1/3 superficial veins in submucosa into portal vein

Oesophageal varices

Veins in lower oesophagus dilate + rupture due to portal hypertension (usually cirrhosis)

Gastritis

Acute or chronic inflammation of stomach
May be acute insult (aspirin, NSAIDs, alcohol, corrosive, H pylori) or chronic (NSAIDs, bile reflux after surgery, PA, IBD (Crohn’s), H pylori
H PYLORI MOST COMMON
- Histology: Lymphocytes +/- neutrophils; MALT induction indicates intestinal metaplasia
- Complications: Ulceration / erosion (perforation), gastric cancer (carcinoma via intestinal metaplasia (like Barrett’s) or MALToma)

Curved flagellate Gram negative rod Binds mucosa, injects toxoid into intercellular junctions CAG positive

H pylori

Where does H pylori mainly affect?

Antrum ('H pylori bug - ant')

Effects of H pylori

Direct - stimulates inflammation itself | Indirect - stimulates G cells to produce gastrin -> gastric acid production = further inflammation

Discontinuous mucosa down to lamina propria only (partial thickness)

Erosion

Discontinuous mucosa beyond lamnia propria (full thickness - can perforate)

Ulcer

Pain at meal times

Gastric ulcer

Pain a few hours after meals

Duodenal ulcer

Gastric carcinoma

95% adenocarcinomas (remaining 5% squamous cell, MALToma/lymphoma (B cell ass. w/ chronic inflammation, can also be by H pylori) Lauren classification splits into intestinal (well differentiated - gastritis > intestinal metaplasia > dysplasia pathway - good prognosis) + diffuse (poorly differentiated - signet ring cells - bad prognosis) H pylori key risk factor for intestinal type. Poor diet, smoking, high incidence Japanese men

Lauren classification

Classification of gastric adenocarcinoma - Intestinal (well differentiated - gastritis > intestinal metaplasia > dysplasia pathway - H pylori - good prognosis) Diffuse (poorly differentiated - signet ring cells - bad prognosis)

Leather boot stomach

Gastric carcinoma

Signet ring cells

Diffuse gastric carcinoma | Cells distended by lots of mucus production

Diagnostic test coeliac

IgA TTG antibodies

3 histological features of coeliac disease

1. Increased intraepithelial CD8+ lymphocytes 2. Crypt hyperplasia 3. Villous atrophy

Coeliac patient stops eating gluten | Inflammatory changes with normal crypt + villi architecture

Lymphocytic duodenitis - inflammatory

What can cause a similar picture to coeliac disease?

Other malabsorptive diseases, e.g. Tropical Sprue

Cancer originating from B cells in MALT of stomach / duodenum

MALToma

Gastric vs. duodenal MALToma

Gastric caused by H pylori | Duodenal caused by coeliac disease

Describe the nomenclature of epithelial tumours

A malignant epithelial tumour is a carcinoma. If the cell involved is glandular epithelium (glands, mucin production) it is an adenocarcinoma. If the cell involved is squamous epithelium (IC bridges, keratinisation, squamous pearls) it is a squamous cell carcinoma

What is the allergen in coeliac disease?

Gliadin in gluten | AI production of tissue tranglutaminase + endomysial antibodies (TTG more specific)

Duodenitis

Inflammation and/or ulceration of duodenal mucosa due to excess gastric acid Chronic H pylori most common cause - other pathogens can also cause (Giardia, Whipple's) - Histology: Gastric metaplasia, ulceration / erosion (perforation)

Cut-off between upper and lower GI

Duodenum upper / jejenum lower