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Histopathology > Upper GI > Flashcards

Upper GI Flashcards

1
Q

Layers of GI tract

A

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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2
Q

Key features of oesophagus

A
  • 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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3
Q

Difference in thoracic oesophagus vs. abdominal oesophagus

A 
Adventitia = loose CT (thoracic oesophagus) 'T for titia'
Serosa = mesothelium (abdominal oesophagus)
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4
Q

GOJ

A

Stratified squamous -> simple columnar

Pale -> pink

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5
Q

Key features of stomach

A
  • 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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6
Q

4 types of cells in gastric glands

A 
Foveolar cells (mucus)
NE cells (gastrin, histamine, serotonic, CCK, somatostatin)
Parietal (gastric acid, IF)
Chief cells (pepsinogen, lipase)
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7
Q

Produce gastric acid, IF

A

Parietal cells

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8
Q

Produce pepsinogen, lipase

A

Chief cells

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9
Q

Key features of small intestine

A
  • 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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10
Q

Normal villous: crypt ratio

A

> 2:1

Decreased in coeliac disease

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11
Q

Brunner’s glands

A

Duodenum
(alkaline secretions)
‘Duo running secretions’

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12
Q

Plicae circularis

A

Jejenum

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

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13
Q

Peyer’s patches

A

Ileum

organised lymphoid tissue aggregations

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14
Q

Acute oesophagitis

A

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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15
Q

Barrett’s oesophagus

A

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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16
Q

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

A

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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17
Q

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

A

Squamous cell oesophageal carcinoma

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18
Q

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

A

Oesophageal adenocarcinoma

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19
Q

Two types of oesophageal carcinoma

A

Squamous cell carcinoma

Adenocarcinoma

20
Q

Process of adenocarcinoma development

A

Metaplasia -> Dysplasia -> Adenocarcinoma

Dysplasia = features of malignancy without BM Invasion

21
Q

p53 mutation

A

Oesophageal carcinoma

22
Q

What is the venous drainage of the oesophagus

A

Upper 2/3 oesophageal veins into SVC

Lower 1/3 superficial veins in submucosa into portal vein

23
Q

Oesophageal varices

A

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

24
Q

Gastritis

A

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)

25
Q

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

A

H pylori

26
Q

Where does H pylori mainly affect?

A

Antrum (‘H pylori bug - ant’)

27
Q

Effects of H pylori

A

Direct - stimulates inflammation itself

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

28
Q

Discontinuous mucosa down to lamina propria only (partial thickness)

A

Erosion

29
Q

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

A

Ulcer

30
Q

Pain at meal times

A

Gastric ulcer

31
Q

Pain a few hours after meals

A

Duodenal ulcer

32
Q

Gastric carcinoma

A

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

33
Q

Lauren classification

A

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

34
Q

Leather boot stomach

A

Gastric carcinoma

35
Q

Signet ring cells

A

Diffuse gastric carcinoma

Cells distended by lots of mucus production

36
Q

Diagnostic test coeliac

A

IgA TTG antibodies

37
Q

3 histological features of coeliac disease

A
  1. Increased intraepithelial CD8+ lymphocytes
  2. Crypt hyperplasia
  3. Villous atrophy
38
Q

Coeliac patient stops eating gluten

Inflammatory changes with normal crypt + villi architecture

A

Lymphocytic duodenitis - inflammatory

39
Q

What can cause a similar picture to coeliac disease?

A

Other malabsorptive diseases, e.g. Tropical Sprue

40
Q

Cancer originating from B cells in MALT of stomach / duodenum

A

MALToma

41
Q

Gastric vs. duodenal MALToma

A

Gastric caused by H pylori

Duodenal caused by coeliac disease

42
Q

Describe the nomenclature of epithelial tumours

A

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

43
Q

What is the allergen in coeliac disease?

A

Gliadin in gluten

AI production of tissue tranglutaminase + endomysial antibodies (TTG more specific)

44
Q

Duodenitis

A

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)

45
Q

Cut-off between upper and lower GI

A

Duodenum upper / jejenum lower

Histopathology (19 decks)

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