Upper GI Pathology Flashcards

1
Q

What are the layers of the gut?

A
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2
Q

What is the Z line?

A

Transitional line from squamous to columnar

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3
Q

What are the parts of a normal stomach?

A
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4
Q

What are the layers of the stomach in the body?

A
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5
Q

What are the layers of the stomach in the antrum?

A
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6
Q

What is normal duodenal epithelium?

A
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7
Q

What is this?

A

Acute oesophagitis

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8
Q

What is the presentation and complications of GORD?

A
  • Gastro-oesophageal reflux disease
  • Commonest cause of oesophagitis
  • Reflux of acidic gastric contents

Ulceration

–necrotic slough

–inflammatory exudate

–granulation tissue

•Fibrosis

Complications

  • haemorrhage
  • perforation
  • stricture
  • Barrett’s oesophagus
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9
Q

What is this?

A

BARRETT’S OESOPHAGUS

•Re-epithelialisation by metaplastic columnar epithelium usually with goblet cells
(intestinal type epithelium)

•AKA columnar lined oesophagus (CLO)

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10
Q

What is 1,2 and 3?

A
  1. Normal
  2. CLO
  3. CLO with IM
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11
Q

What changes lead to cancer?

A

Metaplastic glandular epithelium (intestinal type)

Dysplasia changes showing some of the cytological and histological features of malignancy but no invasion through the basement membrane

Adenocarcinoma invasion through the basement membrane

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12
Q

What is the most common type of oesophageal cancer?

A

Adenocarcinoma of the oesophagus (lower- associated with reflux)

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13
Q

What is this?

A
  • Associated with alcohol and smoking
  • Mid/lower oesophagus
  • Invasion into the submucosa
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14
Q

What is this?

A

SCC of oesophagus

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15
Q

What is the prognosis of an oesophageal carcinoma?

A
  • Prognosis poor
  • Diagnosis of pre-invasive stage important
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16
Q

What is the oesophageal varices?

A

caused by: cirrhosis, Budd Chiari/ PV thrombosis

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17
Q

What is gastritis?

A
  • inflammation of the gastric mucosa
  • Acute gastritis - acute insult
  • Chronic gastritis - chronic / persistent insult
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18
Q

What might cause acute gastritis?

A

Chemical

  • aspirin/NSAIDs
  • alcohol
  • corrosives

Infection

e.g. Helicobacter pylori

19
Q

What causes chronic gastritis?

A
  • H. pylori associated
  • Chemical (NSAIDs, bile reflux; antrum )
  • Autoimmune (body, auto-antibodies e.g. antiparietal)
  • Lymphocytes +/- Neutrophils

Mucosal Associated Lymphoid Tissue (MALT)induction

20
Q

What is H Pylori associated gastritis?

A

•Cause

H. pylori

•Pattern

chronic gastritis +/- activity

•Outcome

CLO-IM-Dysplasia,

Adenocarcinoma

Lymphoma (MALToma)

21
Q

How is Helicobacter a carcinogen?

A
  • Helicobacter infection is associated with an 8x increased risk of (non-cardia) gastric cancer
  • cag-A-positive H.pylori have a needle like appendage that injects toxin into intercellular junctions allowing the bacteria to attach more easily.
  • This strain is associated with more chronic inflammation.
  • Treatment of the infection with antibiotics drastically reduces the risk of cancer.
22
Q

What else causes gastritis?

A

•Infection

e.g. CMV, strongyloides

(immunosuppression)

•Inflammatory bowel disease

Crohn’s Disease

23
Q

What is this?

A

Gastric ulcers

All ulcers should be biopsied to exclude malignancy

24
Q

What are the complications of ulcers?

A

•Bleeding

Anaemia

Shock (massive haemorrhage)

•Perforation

Peritonitis

25
Q

What is intestinal metaplasia?

A
  • As in the oesophagus:
  • intestinal metaplasia in gastric mucosa in response to long term damage
  • Increased cancer risk
26
Q

What is gastric epithelial dysplasia?

A
  • Abnormal epithelial pattern of growth
  • Some of the cytological and histological features of malignancy are present, but no invasive through the basement membrane
27
Q

What are factors contributing to gastric cancer?

A
28
Q

Who gets gastric cancer?

A
  • High incidence in Japan, Chile, Italy, China, Portugal, Russia
  • More common in men (1.8:1 ♂:♀)
  • >95% of all malignant tumors in stomach are adenocarcinomas
29
Q

What type of cancers are gastric cancers?

A

95% of stomach cancers are adenocarcinoma

These are split morphologically into:

  • Intestinal – well differentiated
  • Diffuse – poorly differentiated (Linitis plastica), includes signet ring cell carcinoma
  • The remaining 5% is made up of:

–Squamous cell carcinoma

–Lymphoma (MALToma) [Haematology]

–Gastrointestinal stromal tumour (GIST) [Endocrinology]

–Neuroendocrine tumours [Endocrinology]

•Overall survival rate is 15%

30
Q

What is gastric lymphoma?

A

•Chronic inflammation

–Chronic immune stimulation

  • B cell (marginal zone) lymphocytes
  • Treatment

–If limited to the stomach and H.pylori is present: H.pylori eradication

31
Q

What is duodenitis?

A
  • Increased acid production in the stomach which spills over into duodenum
  • Chronic inflammation and gastric metaplasia with helicobacter infection
32
Q

What is a duodenal ulcer?

A

Duodenitis and DU

good correlation between endoscopy and biopsy pathology

Endoscopy “itis”:

73.5% progress to ulcer, mainly erosive duodenitis (biopsy – neutrophils)

33
Q

What other pathogens can cause a duodenal ulcer?

A
  • Immunosuppressed
  • CMV
  • Cryptosporidiosis
  • Giardia lamblia infection
  • Whipple’s disease -Tropheryma whippelii.
34
Q

What causes malabsorption in partial villous atrophy?

A
  • Histology
  • Villous atrophy
  • Crypt hyperplasia
  • Increased Intraepithelial lymphocytes

(normal range less than 20 lymphocytes /100 enterocytes)

35
Q

What does the second half of this image show?

A

Flattening in villous atrophy

36
Q

What is required for the diagnosis of coeliac disease?

A

•Diagnosis requires:

endomysial antibodies and tissue transglutaminase antibodies

Duodenal biopsies:

On gluten rich diet showing villous atrophy

Off gluten showing normal villi

There are other causes of malabsorption with similar histology e.g. tropical sprue

37
Q

What is a duodenal MALToma?

A

Patients with coeliac disease have an increased risk of GIT cancers

  • MALToma associated with Coeliac is
  • in the duodenum
  • T-cell origin
  • (Enteropathy Associated T-cell Lymphoma)
38
Q

What is this?

A

Duodenal maltoma

39
Q
A
40
Q

What are the 2 types of Barretts?

A

Without gobelt cells (gastric metaplasia)

With goblets cells (intestinal metaplasia)

41
Q

What is CLO?

A

Barrett’s oesophagus (metaplastic change in oesophagus)

42
Q

What is associated with SCC of the oesophagus?

A

Commonest in developing countries

Associated with alcohol and smoking

Mid/ lower oesophagus

43
Q

Do cancers arise from pre existing adenomas in the oesophagus and stomach?

A

No (but this is not true in colon)

44
Q

In a patient with coeliac disease on a diet containing gluten, which is the most likely histological change in the duodenum?

A

Villous atrophy, increased intra-epithelial lymphocytes