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Leila's Yr 5 Pathology > Histopathology 9 - Upper GI disease > Flashcards

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
Q

SCC oesophagus associations

A

Smoking and alcohol

26
Q

Histology of Oesophagus SCC

A

Keratin producing cells + intercellular bridges

27
Q

Histology of oesophagus ACA

A

Mucin, glandular epithelium

28
Q

2 main causes of acute gastritis

A

Chemical (NSAIDs, aspirin, alcohol) or bacterial (H.pylori)

29
Q

The ABCDs of chronic gastritis

A 
A = Autoimmune (pernicious anaemia)
B = Bacterial (H.pylori)
C= Chemical
D = IBD
30
Q

Which part of the stomach do anti-parietal cell antibodies effect?

A

The body

31
Q

Which part of the stomach do the bacterial and chemical causes of chronic gastritis affect?

A

THe antrum

32
Q

Lymphoid follicles in the stomahc, what is the cause?

A

H.pylori infection causing MALT (associated with increased risk of lymphoma)

33
Q

What are atrophic and non-atrophic H.pylori infection associated with, respectively?

A

Atrophic –> adenocarcinoma

Non-atrophic –> MALToma

34
Q

3 main consequences of H.pylori associated gastritis

A

CLO –> IM –> Dysplasia
Adenocarcinoma (8x increased risk)
Lymphoma/MALToma

35
Q

Which strain of H.pylori is most worrying?

A

Cag-A positive H.pylori: has a needle like appendage which injects toxins into intracellular junctions

36
Q

Other causes of gastritis, commonly seen in immunocompromised people?

A

CMV, strongyloides

37
Q

What are the two main pathways that lead to GI cancer?

A

Metaplasia-dysplasia pathway which is seen in upper GI cancers
Adenoma-carcinoma pathway (has polyps etc, lower GI)

38
Q

Technical definitino of gastric ulcer

A

Depth of the tissue loss goes beyond the mucosa (into the submucosa)

39
Q

What feature determines the difference between chronic and acute gastric ulcers?

A

There is fibrosis in chronic ulcers

40
Q

What should be done to ALL gastric ulcers?

A

They shuold be biopsied to eXCLUDE MALIGNANCY

41
Q

Complications of ulcers

A

Perforation (peritonitis), bleeidng (anaemia, shock)

42
Q

Characteristic feature of gastric intestinal metaplasia

A

Presence of goblet cells in the stomach mucosa

43
Q

Which type of gastric carcinoma is most common?

A

Adenocarcinoma

44
Q

Some other types of gastric cancer

A

SCC, MALToma, GIST, NETs (Zollinger Ellison syndrome)

45
Q

How can gastric adenocarcinomas be divided?

A

Intestinal and diffuse

46
Q

Name one type of diffuse gastric adenocarcinoma

A

Signet ring tumour (Can metastasise to ovaries = Krukenbger tumour)

47
Q

What type of tumour is a gastric MALToma?

A

B cell NHL

48
Q

Cancer associated with chronic immune stimulation by H. Pylori

A

Gastric MALToma (B CELL1!!)

49
Q

Cancer associated with Coeliac disease

A

Duodenal MALToma AKA EATL (T CELL LYMPHOMA!!!)

50
Q

How can H.pylori affect the duodenum?

A

Increased acid in the antrum spills in to the dudoenum –> chronic inflammatin –> gastric metaplasia

51
Q

What is the only cause of duodenal ulcers?

A

H.pylori

52
Q

Why do we not biopsy duodenal ulcers?

A

They are ALWAYS benign

53
Q

Common parasite in children which causes duodenitis?

A

Cryptosporidium

54
Q

Histopahtological features of malabsorption/Coeliac

A

Villous atrophy, crypt hyperplasia and INCREASED intraepithelial lymphocytes (>20 per 100 epithelial cells)

55
Q

Lymphocytic duodenitis vs coeliac

A

You get increased intraepithelial lymphocytes/inflammatory changes WITHOUT any architectural changes. Usually have coeliacs or are going to develop it.

56
Q

What does the diagnosis of coeliacs require?

A

Both serology (anti-endomysial and anti-TTGs) and a biopsy on gluten rich diet

57
Q

What is another cause of malabsorption with a similar histology to coeliacs?

A

Tropical sprue

Leila's Yr 5 Pathology (100 decks)

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