Upper GI

Question 1

Layers of GI tract

Answer 1

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

Question 2

Key features of oesophagus

Answer 2

• 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

Question 3

Difference in thoracic oesophagus vs. abdominal oesophagus

Answer 3

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

Question 4

GOJ

Answer 4

Stratified squamous -> simple columnar

Pale -> pink

Question 5

Key features of stomach

Answer 5

• 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

Question 6

4 types of cells in gastric glands

Answer 6

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

Question 7

Produce gastric acid, IF

Answer 7

Parietal cells

Question 8

Produce pepsinogen, lipase

Answer 8

Chief cells

Question 9

Key features of small intestine

Answer 9

• 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)

Question 10

Normal villous: crypt ratio

Answer 10

> 2:1

Decreased in coeliac disease

Question 11

Brunner’s glands

Answer 11

Duodenum
(alkaline secretions)
‘Duo running secretions’

Question 12

Plicae circularis

Answer 12

Jejenum

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

Question 13

Peyer’s patches

Answer 13

Ileum

organised lymphoid tissue aggregations

Question 14

Acute oesophagitis

Answer 14

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

Question 15

Barrett’s oesophagus

Answer 15

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

Question 16

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

Answer 16

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

Question 17

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

Answer 17

Squamous cell oesophageal carcinoma

Question 18

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

Answer 18

Oesophageal adenocarcinoma

Question 19

Two types of oesophageal carcinoma

Answer 19

Squamous cell carcinoma

Adenocarcinoma

Question 20

Process of adenocarcinoma development

Answer 20

Metaplasia -> Dysplasia -> Adenocarcinoma

Dysplasia = features of malignancy without BM Invasion

Question 21

p53 mutation

Answer 21

Oesophageal carcinoma

Question 22

What is the venous drainage of the oesophagus

Answer 22

Upper 2/3 oesophageal veins into SVC

Lower 1/3 superficial veins in submucosa into portal vein

Question 23

Oesophageal varices

Answer 23

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

Question 24

Gastritis

Answer 24

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)

Question 25

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

Answer 25

H pylori

Question 26

Where does H pylori mainly affect?

Answer 26

Antrum ('H pylori bug - ant')

Question 27

Effects of H pylori

Answer 27

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

Question 28

Discontinuous mucosa down to lamina propria only (partial thickness)

Answer 28

Erosion

Question 29

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

Answer 29

Ulcer

Question 30

Pain at meal times

Answer 30

Gastric ulcer

Question 31

Pain a few hours after meals

Answer 31

Duodenal ulcer

Question 32

Gastric carcinoma

Answer 32

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

Question 33

Lauren classification

Answer 33

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

Question 34

Leather boot stomach

Answer 34

Gastric carcinoma

Question 35

Signet ring cells

Answer 35

Diffuse gastric carcinoma | Cells distended by lots of mucus production

Question 36

Diagnostic test coeliac

Answer 36

IgA TTG antibodies

Question 37

3 histological features of coeliac disease

Answer 37

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

Question 38

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

Answer 38

Lymphocytic duodenitis - inflammatory

Question 39

What can cause a similar picture to coeliac disease?

Answer 39

Other malabsorptive diseases, e.g. Tropical Sprue

Question 40

Cancer originating from B cells in MALT of stomach / duodenum

Answer 40

MALToma

Question 41

Gastric vs. duodenal MALToma

Answer 41

Gastric caused by H pylori | Duodenal caused by coeliac disease

Question 42

Describe the nomenclature of epithelial tumours

Answer 42

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

Question 43

What is the allergen in coeliac disease?

Answer 43

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

Question 44

Duodenitis

Answer 44

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)

Question 45

Cut-off between upper and lower GI

Answer 45

Duodenum upper / jejenum lower