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Week 10 -GI > Upper Gi pathology > Flashcards

Upper Gi pathology Flashcards

1
Q

Where is the most common spread of head and neck cancers?

A

Lymph nodes in the neck, usually on the same side

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2
Q

What is a classical presentation of mouth cancer?

A

An ulcer which persists without a definite, identifiable cause (should heal within 2-3 weeks)

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3
Q

What are the main risk factors of oral cancer?

A
  • Smoking
  • Alcohol
  • HPV can be a factor in some cases (mainly tonsil, oropharynx)
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4
Q

What are the histological layers of the oesophagus?

A
  • Mucosa
  • Muscularis mucosae
  • Submucosa
  • Muscularis propria
  • Adventitia
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5
Q

What is the mucosa in the oesophagus lined by?

A

Non-keratinising stratified squamous epithelium

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6
Q

What is the pathogenesis of reflux oesophagitis?

A
  • Acid, bile and digestive enzymes injure the squamous epithelium lining of the oesophagus
  • Increased numbers of inflammatory cells and basal hyperplasia
  • Reflux of gastroduodenal secretions
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7
Q

Name a fungal infection of the oesophagus

A

Candida albicans

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8
Q

What infection of the oesophagus can occur in immunocompromised patients?

A

Herpes simplex virus

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9
Q

What conditions result in inflammation of the oesophagus?

A
  • Peptic oesophagitis/GERD: reflux of acid/bile
  • Caustics: NaOH, caustic soda
  • Pills: iron, bisphosphonates, tetracyclines
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10
Q

What is the appearance of candida oesophagitis?

A

White spots

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11
Q

What confirms a candida albicans infection of the oesophagus?

A
  • PAS stain

* Spores and hyphae seen

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12
Q

What are the symptoms of eosinophilic oesophagitis?

A

Dysphagia/food sticking

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13
Q

What is eosinophilic oesophagitis?

A

Eosinophils infiltrate the epithelium, it has an allergic aetiology

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14
Q

What is eosinophilic oesophagitis responsive to?

A

Steroids (fluticasone)

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15
Q

What is the endoscopic appearance of eosinophilic oesophagitis?

A

Ring like trachealization

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16
Q

What is the histological appearance of eosinophilic oesophagitis?

A

Large numbers of brightly staining eosinophils infiltrating the oesophageal squamous epithelium

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17
Q

Name two oesophageal cancers

A
  • Squamous carcinoma

* Adenocarcinoma

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18
Q

What is squamous carcinoma of the oesophagus associated with?

A

Smoking and drinking

19
Q

What is adenocarcinoma of the oesophagus associated with?

A

GERD (gastro-oesophageal reflux) and obesity

20
Q

What is Barrett’s oesophagus?

A
  • Metaplastic response to mucosal injury
  • Squamous cells become glandular (usually intestinal with goblet cells)
  • Associated with benign strictures but also with adenocarcinoma
21
Q

Describe the risk of progression to cancer of Barrett’s oesophagus

A
  • If no dysplasia or aneuploidy the risk is low

* Definite low or high grade dysplasia have a higher risk but the progression to cancer is still low

22
Q

What is the Seattle biopsy protocol?

A
  • Four biopsies every 2cm every 2 years

* Checking for progression to cancer in patients with Barretts oesophagus

23
Q

Describe the spectrum of dysplasia

A
  • Inflammation, reactive changes
  • Indefinite for dysplasia - when you cannot be certain
  • Mild, moderate (low grade) dysplasia
  • Severe (high grade) dysplasia
  • Invasive adenocarcinoma
24
Q

Describe low grade dysplasia

A
  • Cells polarised

* nuclei stratified

25
Q

Describe high grade dysplasia

A
  • Polarity lost
  • Nuclei rounder
  • Vesicular
  • Prominent nuclei
  • Abnormal mitoses
  • Necrosis
26
Q

What are the causes of acute gastritis in the stomach?

A
  • Alcohol
  • NSAIDs
  • Severe trauma (burns, surgery)
27
Q

What are the causes of chronic gastritis?

A
  • Autoimmune
  • Bacterial (H pylori)
  • Chemical
28
Q

Explain how autoimmune atrophic gastritis causes anaemia

A
  • Parietal cells that release intrinsic factor are targeted by anti-parietal cell antibodies in the blood
  • Intrinsic factor binds to vitamin B12 in the duodenum once hepatocorrin has been digested
  • B12 is needed for haumatopoeisis, lack of B12 results in pernicious anaemia
  • Eventual complete loss of parietal cells, pyloric and intestinal metaplasia
29
Q

What are the complications of autoimmune gastritis?

A
  • Achlorhydria results in bacterial overgrowth
  • Hypergastrinaemia (more gastrin) leads to endocrine cell hyperplasia/carcinoids
  • Persistent inflammation may lead to epithelial dysplasia and eventually cancer
30
Q

What is Zollinger-Ellison syndrome?

A

Hypersecretion of gastrin by an endocrine tumour in the pancreas or the duodenum resulting in increased gastric acid output and severe peptic ulceration

31
Q

Discuss helicobacter pylori gastritis

A
  • Potentially lifelong
  • H. pylori colonies the gastric mucosa leading to active chronic inflammation
  • IL- 8 from epithelial cells attracts neutrophils
  • There are two patterns
32
Q

What are the two patterns of helicobacter pylori gastritis?

A
  • Antral-predominant gastritis - hypergastrinaemia and duodenal ulceration
  • Pan-gastritis- hypochlorhydria, multifocal atrophic gastritis, cancer, intestinal metaplasia
33
Q

What are the causes of a chemical gastritis?

A
  • Bile reflux
  • NSAIDs
  • Ethanol
  • Oral iron
34
Q

What is the characteristic morphology of chemical gastritis?

A
  • Few inflammatory cells
  • Surface congestion oedema
  • Elongation of gastric pits
  • Tortuosity
  • Reactive hyperplasia/atypia
  • Ulceration
35
Q

What is gastric cancer associated with?

A
  • Helicobacter pylori

* Autoimmune

36
Q

What are the features of gastric cancer?

A
  • Background atrophic mucosa
  • Chronic inflammation
  • Intestinal metaplasia
  • Dysplasia
37
Q

What is the Lauren classification of gastric cancer?

A
  • Intestinal

* Diffuse

38
Q

What is the most common cause of proximal gastric cancer?

A

Acid reflux at the OG junction

39
Q

What is the most common cause of distal gastric cancer

A

Mainly helicobacter pylori infection or autoimmune

40
Q

Describe the histology of diffuse gastric cancer

A
  • Signet ring cells: individual malignant cells with mucin vacuoles
  • Linitis plastica (adenocarcinoma of the stomach): may invade extensively i.e. to muscles without being endoscopically obvious
  • weaker link with gastritis
41
Q

Where are the most likely points of metastasis from gastric cancer?

A
  • Ovaries - krukenberg tumour
  • Supraclavicular lymph node (Virchow’s)
  • Sister Joseph’s nodule (umbilical metastasis)
42
Q

What is the associated mutation in familial gastric cancer?

A

CDH1 - E-cadherin

43
Q

Describe the risk of familial gastric cancer

A
  • Penetrance is 70-80% (lifelong)
  • Small intramucosal foci or diffuse gastric cancer may be numerous
  • Prophylactic gastrectomy
  • Increased risk of lobular carcinoma of the breast

Week 10 -GI (8 decks)

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