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YR5 Histopathology > Upper Gastrointestinal Disease > Flashcards

Upper Gastrointestinal Disease Flashcards

1
Q

What are the different parts of the stomach?

A

Cardia

Fundus

Body

Pyloric antrum

Pylorus

Duodenum

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2
Q

What are normal features of a histology slide for the body of a stomach from top to bottom?

A

Lined by gastric mucosa columnar epithelium (foveolar, mucin secreting)

Specialised glands in lamina propria

Muscularis mucosa

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3
Q

What are normal features of a histology slide of the antrum of a stomach from top to bottom?

A

Lined by gastric mucosa columnar epithelium (fovelolar, mucin secreting)

Non-specialised glands in lamina propria (gastric pits)

Mucularis mucosa

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4
Q

What are normal features of a histology slide of the duodenum?

A

Glandular epithelium with goblet cells: Intestinal type epithelium.

Villous architecture- villous:crypt ratio >2:1

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5
Q

What is this?

A

Acute oesophagitis

Inflamed: red, swollen

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6
Q

What is this?

A

Acute oesophagitis

Neutrophils in epithelium

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7
Q

What is reflux oesophagitis?

A

Gastro-oesophageal reflux disease

Commonest cause of oesophagitis

Reflux of acidic gastric contents

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8
Q

What are complications associated with reflux oesophagitis?

A

Ulceration

Haemorrhage

Perforation

Stricture

Barrett’s oesophagus: Reversible.

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9
Q

What is Barrett’s oesophagus?

A

Replacement of squamous epithelium by metaplastic columnar epithelium

AKA columnar lined oesophagus (CLO).

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10
Q

What is this?

A

Barrett’s oesophagus

Islands of columnar epithelium- look like gastric epithelium

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11
Q

What is this?

A

Normal

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12
Q

What is this?

A

Barrett’s oesophagus

Simple columnar epithelium

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13
Q

What is this?

A

Barrett’s oesophagus

with goblet cells: intestinal metaplasia

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14
Q

What is the sequelae of disease progression to neoplasia?

A

“Flat pathway”

Squamous

Metaplastic glandular epithelium- Intestinal type

Dysplasia: Changes showing some cytological + histological features of malignancy but no invasion through BM

Adenocarcinoma: Invasion through BM

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15
Q

Give 4 features of squamous cell carcinoma of the oesophagus?

A

A/W: alcohol + smoking.

Mid/ lower oesophagus.

Commonest oesophageal cancer in developing countries

Invasion into the submucosa.

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16
Q

What is this?

A

Squamous cell carcinoma of the oesophagus

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17
Q

What is this?

A

Squamous cell carcinoma of the oesophagus

Produces keratin (pink)

Strong intracellular bridges

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18
Q

What is the prognosis of oesophageal carcinoma?

A

Prognosis poor

Dx of pre-invasive stage important

Early dx is important

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19
Q

What is gastritis?

A

Inflammation of the gastric mucosa

Acute: Acute insult

Chronic: Chronic/ persistent insult

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20
Q

What is this?

A

Gastritis

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21
Q

What are causes of acute gastritis?

A

Chemical:

  • Aspirin/ NSAIDs
  • Alcohol
  • Corrosives

Infection: Helicobacter pylori

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22
Q

What is this?

A

Acute gastritis

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23
Q

What are causes of chronic gastritis?

A

AI (antiparietal antibodies: to parietal cells in Body)

B: H. pylori: Antrum

Chemical (NSAIDs, bile reflux; antrum)

(ABC: AI, Bacterial, Chemical)

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24
Q

What is Helicobacter associated gastritis?

A

Caused by H. pylori.

Pattern: Chronic gastritis +/- activity spikes

Outcome:

  • CLO-IM-Dysplasia,
  • Adenocarcinoma
  • Lymphoma (MALToma)
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25
What is this?
Helicobacter associated gastritis
26
How is Helicobacter associated with cancer?
Helicobacter infection A/w 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 bacteria to attach more easily. This strain is A/w more chronic inflammation. Tx with abx drastically reduces risk of cancer.
27
What are other causes of gastritis?
Infection e.g. CMV, strongyloides (immunosuppression) **Inflammatory bowel disease:** Crohn’s Disease
28
Why worry about gastritis?
1. Chronic gastritis 2. Intestinal metaplasia 3. Dysplasia 4. Cancer “Flat pathway”
29
What is this?
Gastric ulcer
30
Why should all ulcers be biopsied?
To exclude malignancy.
31
What are complications associated with ulcers?
**Bleeding:** * Anaemia * Shock (massive haemorrhage) **Perforation:** * Peritonitis
32
What is intestinal metaplasia?
Intestinal metaplasia (goblet cells) in gastric mucosa in response to long term damage (As in oesophagus) Increased cancer risk.
33
What is this?
Intestinal metaplasia
34
What is gastric epithelial dysplasia?
Abnormal epithelial pattern of growth. Some cytological + histological features of malignancy are present, but no invasion through BM.
35
What is this?
Gastric epithelial dysplasia High nuclear: cytoplasmic ratio Lots of mitosis Abnormal mitosis
36
What is the epidemiology of gastric cancer?
High incidence in Japan, Chile, Italy, China, Portugal, Russia. M \> F \>95% of all malignant tumors in stomach are adenocarcinomas.
37
What is this?
Gastric cancer
38
What is this?
Gastric cancer
39
What is gastric cancer and how can it be split?
95% of stomach cancers are adenocarcinoma. Split morphologically into: * **Intestinal:** Well differentiated. * **Diffuse:** Poorly differentiated (Linitis plastica), inc. signet ring cell carcinoma
40
What is this? Give 3 features of this.
Intestinal gastric cancer Well differentiated Form glands Secrete mucin
41
What is this? Give 5 features of this
Diffuse gastric cancer Poorly differentiated No architecture Single cells, lost cohesion Don't form glands White dots= signet ring cells- make mucin which stays in cell
42
What are less common types of gastric cancer?
Remaining 5% is made up of: * Squamous cell carcinoma (col to squa) * Lymphoma (MALToma) * Gastrointestinal stromal tumour (GIST) * Neuroendocrine tumours
43
What is the overall survival of gastric cancer?
15%
44
What is Gastric MALToma/Lymphoma and the treatment?
**Chronic inflammation causes** chronic immune stimulation Development of single clone that proliferates: B cell (marginal zone) lymphocytes. **Tx:** If limited to stomach + H.pylori is present= H.pylori eradication.
45
What is this?
Gastric MALToma/Lymphoma
46
What is this?
Gastric MALToma/Lymphoma
47
What are the associations between duodenitis, duodenal ulcers and H. Pylori?
H pylori A/w increased acid secretion driven by increased gastrin secretion Increased acid in stomach spills over into duodenum. Chronic inflammation + gastric metaplasia Normal goblet cell containing small intestine replaced by gastric mucosa H pylori grow wherever there is gastric mucosa H pylori duodenitis + ulcer
48
What is this?
Duodenal ulcer
49
Which pathogens are responsible for duodenal ulcers?
**Immunosuppressed:** CMV, Cryptosporidiosis **Giardia lamblia infection** **Whipple’s disease** -Tropheryma whippelii.
50
What is seen on a histology slide for malabsorption?
Partial villous atrophy Crypt hyperplasia Increased Intraepithelial lymphocytes: Normal: \< 20 lymphocytes /100 enterocytes
51
Describe the histology of the gastro-oesophageal junction
Stratified squamous (same as oesophageal folds superiorly) Z line: abrupt non linear change Columnar (same as gastric rugae inferiorly)
52
What is secreted in the body of the stomach?
Acid Intrinsic Factor
53
What type of malignancy occurs in the body of the stomach?
Adenocarcinoma (Columnar mucus secreting epithelium)
54
What are the 2 types of Barrett's Oesophagus?
Without goblet cells: gastric metaplasia With goblet cells: intestinal type metaplasia, greater risk of progression to cancer
55
What is the most important risk factor for carcinoma in the colon?
Polyps
56
Give 3 features of adenocarcinoma of the oesophagus
Commonest oesophageal carcinoma in Developed countries A/w reflux Lower oesophagus (where most reflux affects)
57
What 2 features are common to all adenocarcinomas?
Make glands Secrete mucin
58
What is shown here?
1. Barrett's oesophagus 2. Adenocarcinoma
59
What is the commonest cause of oesophageal varices?
Cirrhosis Blood can't get through liver, diverts through vessels via systemic circulation Gives rise to varices, haemorrhoids, around umbilicus
60
What is this?
Gastric ulcer
61
Name 2 defects in lining of stomach wall
Ulcer: through muscular mucosa into submucosa Erosion: more superficial
62
Describe the villi in a normal duodenum
Villi twice as high as crypts Crypts: stem cell, cell proliferation, cells migrate up If something wrong with villi: villi shorten, crypts become thicker, cells proliferate more rapidly to try to regenerate villi
63
Describe the correlation between duodenitis and duodenal ulcers
Good correlation between endoscopy + biopsy pathology If “itis” on endoscopy: 74% progress to ulcer
64
What is seen here?
LHS: normal villi RHS: flattening of villi (partial villous atrophy)
65
Which antibodies are required for diagnosis of coeliac disease?
Endomysial Tissue transglutimase
66
What will be seen on duodenal biopsy in coeliac disease?
Gluten rich diet: villous atrophy GF: Normal villi
67
Give a cause of malabsorption that shows similar histology to coeliac
Tropical sprue
68
In coeliac disease which cancer is there higher risk of?
Duodenal MALToma/ lymphoma T cell origin (Enteropathy associated T cell lymphoma)
69
True or false: most oesophageal and gastric cancers arise from pre-existing adenomas
False Most arise from the flat pathway
70
In a patient with coeliac disease on a diet containing gluten, the most likely histological change in the duodenum is…
Villous atrophy (can have normal architecture with increased intra-epithelial lymphocytes in v early stages)
71
Which of the following is not a cause of chronic gastritis? Auto-immunity Infection Drugs Metabolic disease
Metabolic disease is NOT

YR5 Histopathology (27 decks)

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