Histopathology 9 - Upper GI disease Flashcards

1
Q

Layers of the stomach and oesophagues

A

Mucosa, submucosa and muscularis propria

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2
Q

What is the Z-line of the oesophagus?

A

The point at which the epithelium transitions from being squamous to columnar

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3
Q

Which three layers is the mucosa composed of?

A

Epithelium –> lamina propria –> muscularis mucosa

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4
Q

What is an important feature of the oesophagus?

A

The presence of submucosal glands

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5
Q

Name the three MAIN histopathological areas of the stomach

A

Fundus, body and antrum

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6
Q

Main function of body and fundus

A

They contain the most specialised glands for secreting acid and enzymes

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7
Q

Where do you commonly find H.pylori associated gastritis?

A

Antrum and pyloric canal

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8
Q

What is the normal villous:crypt ratio in the duodenum?

A

> 2:1

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9
Q

Where do the cells of the duodenum proliferate?

A

In the crypts

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10
Q

What happens when the villi get damaged?

A

The crypts will proliferate and replace the damaged villi

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11
Q

Where is it abnormal to find goblet cells and what does this suggest?

A

Goblet cells should NOT be found in the stomach, if they are then it is suggestive of intestinal metaplasia

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12
Q

Most common cause of acute oesophagitis

A

GORD

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13
Q

Histology of acute oesophagitis

A

NEUTROPHILS

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14
Q

2 main outcomes of acute oesophagitis

A

Ulceration or fibrosis, barrett’s oesophagus

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15
Q

Difference between an ulcer and erosion

A

An ulcer extends beyond the muscularis mucosa (into submucosa) but an erosion is before the muscularis mucosa

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16
Q

What is Barrett’s oesophagus?

A

Metaplastic process with Replacement of the squamous epithelium of the lower oesophagus with columnar epithelium

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17
Q

What is CLO

A

Columnar-lined oesophagus (Seenin Barrett’s)

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18
Q

What are the two main types of CLO/Barrett’s

A

CLO without IM = gastric metaplasia

CLO with intestinal metaplasia (presence of goblet cells)

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19
Q

Which type of CLO/Barrett’s has a higher cancer risk?

A

CLO with IM

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20
Q

Difference between metaplasia and dysplasia

A

Metaplasia is reversible and therefore not pre-malignant like dysplasia, dysplasia shows some of the cytological and histological features of malignancy with no invasion through BM

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21
Q

Difference between dysplasia and adenocarcinoma

A

Adenocarcinoma INVADES through the basement membrane

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22
Q

What is the commonest type of oesophageal cancer in developed countries?

A

Adenocarcinoma of the oesophagus (lower 1/3 of oesophagus)

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23
Q

Main cause of adenocarcinoma of oesophagus?

A

GORD/Barrett’s

24
Q

Most common type of oesophageal carcinoma in Africa?

A

Squamous cell carcinoma (upper 2/3)

25
SCC oesophagus associations
Smoking and alcohol
26
Histology of Oesophagus SCC
Keratin producing cells + intercellular bridges
27
Histology of oesophagus ACA
Mucin, glandular epithelium
28
2 main causes of acute gastritis
Chemical (NSAIDs, aspirin, alcohol) or bacterial (H.pylori)
29
The ABCDs of chronic gastritis
``` A = Autoimmune (pernicious anaemia) B = Bacterial (H.pylori) C= Chemical D = IBD ```
30
Which part of the stomach do anti-parietal cell antibodies effect?
The body
31
Which part of the stomach do the bacterial and chemical causes of chronic gastritis affect?
THe antrum
32
Lymphoid follicles in the stomahc, what is the cause?
H.pylori infection causing MALT (associated with increased risk of lymphoma)
33
What are atrophic and non-atrophic H.pylori infection associated with, respectively?
Atrophic --> adenocarcinoma | Non-atrophic --> MALToma
34
3 main consequences of H.pylori associated gastritis
CLO --> IM --> Dysplasia Adenocarcinoma (8x increased risk) Lymphoma/MALToma
35
Which strain of H.pylori is most worrying?
Cag-A positive H.pylori: has a needle like appendage which injects toxins into intracellular junctions
36
Other causes of gastritis, commonly seen in immunocompromised people?
CMV, strongyloides
37
What are the two main pathways that lead to GI cancer?
Metaplasia-dysplasia pathway which is seen in upper GI cancers Adenoma-carcinoma pathway (has polyps etc, lower GI)
38
Technical definitino of gastric ulcer
Depth of the tissue loss goes beyond the mucosa (into the submucosa)
39
What feature determines the difference between chronic and acute gastric ulcers?
There is fibrosis in chronic ulcers
40
What should be done to ALL gastric ulcers?
They shuold be biopsied to eXCLUDE MALIGNANCY
41
Complications of ulcers
Perforation (peritonitis), bleeidng (anaemia, shock)
42
Characteristic feature of gastric intestinal metaplasia
Presence of goblet cells in the stomach mucosa
43
Which type of gastric carcinoma is most common?
Adenocarcinoma
44
Some other types of gastric cancer
SCC, MALToma, GIST, NETs (Zollinger Ellison syndrome)
45
How can gastric adenocarcinomas be divided?
Intestinal and diffuse
46
Name one type of diffuse gastric adenocarcinoma
Signet ring tumour (Can metastasise to ovaries = Krukenbger tumour)
47
What type of tumour is a gastric MALToma?
B cell NHL
48
Cancer associated with chronic immune stimulation by H. Pylori
Gastric MALToma (B CELL1!!)
49
Cancer associated with Coeliac disease
Duodenal MALToma AKA EATL (T CELL LYMPHOMA!!!)
50
How can H.pylori affect the duodenum?
Increased acid in the antrum spills in to the dudoenum --> chronic inflammatin --> gastric metaplasia
51
What is the only cause of duodenal ulcers?
H.pylori
52
Why do we not biopsy duodenal ulcers?
They are ALWAYS benign
53
Common parasite in children which causes duodenitis?
Cryptosporidium
54
Histopahtological features of malabsorption/Coeliac
Villous atrophy, crypt hyperplasia and INCREASED intraepithelial lymphocytes (>20 per 100 epithelial cells)
55
Lymphocytic duodenitis vs coeliac
You get increased intraepithelial lymphocytes/inflammatory changes WITHOUT any architectural changes. Usually have coeliacs or are going to develop it.
56
What does the diagnosis of coeliacs require?
Both serology (anti-endomysial and anti-TTGs) and a biopsy on gluten rich diet
57
What is another cause of malabsorption with a similar histology to coeliacs?
Tropical sprue