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Edit YEAR 5: Histopathology > Histo: Upper GI Disease > Flashcards

Histo: Upper GI Disease Flashcards

1
Q

What is a key histological feature of the oesophageal mucosa?

A

Presence of submucosal glands

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2
Q

what is the Z-line?

A

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

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3
Q

What does the body and fundus of the stomach have in abundance?

A

Specialised glands responsible for producing acid and enzymes

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4
Q

Which part of the stomach tends to be affected by H. pylori-associated gastritis?

A

Pylorus and antrum

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5
Q

What are the three layers of the gastric mucosa?

A
  • Columnar epithelium
  • Lamina propria
  • Muscularis mucosa
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6
Q

Where do cells proliferate in the intestinal lining?

A

In the crypt

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7
Q

What happens to cells after they proliferate in the crypt?

A

They migrate upwards to the tip of the villous and shed at the top.

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8
Q

What is the normal villous: crypt ratio?

A

2:1

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9
Q

What does the 2:1 villous to crypt ratio depend on?

A

The height of the villi and the depth of the crypts.

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10
Q

How does the proportion of crypts change if the villi are shorter?

A

The crypts take up a bigger proportion of the total length.

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11
Q

What happens to the crypts when the villi get damaged?

A

The crypts will proliferate to replace the damaged villi.

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12
Q

What does the presence of goblet cells in the stomach signify?

A

Intestinal metaplasia

NOTE: goblet cells are NOT normally seen in the stomach

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13
Q

What is the characteristic histological feature of acute oesophagitis?

A

Presence of lots of neutrophils- hallmark of acute inflammation

This is usually caused by GORD

The redness is a cardinal sign of inflammation

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14
Q

What can acute oesophagitis result in?

A
  • Ulceration
  • Fibrosis

Complications
* Haemorrhage
* Perforation
* Stricture
* Barrett’s oesophagus

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15
Q

What does ulceration of the oesophagus produce?

A

produces a necrotic slough, inflammatory exudate and granulation tissue

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16
Q

Define Barrett’s oesophagus.

A

Metaplastic process by which the normal sqaumous epithelium of the lower oesophagus is replaced by columnar epithlieum

NOTE: this is also known as columnar-lined epithelium (CLO)

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17
Q

What further degree of metaplasia is associated with an even greater risk of cancer than Barrett’s oesophagus?

A

Intestinal metaplasia - goblet cells become visible

NOTE: metaplasia is reversible

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18
Q

Describe the histological route to cancer

A

Metaplasia –> Dysplasia –> Cancer

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19
Q

Why is metaplasia not technically pre malignant? What can metaplasia lead to?

A

Metaplasia is NOT technically pre-malignant because it is REVERSIBLE

However, once you have metaplasia you can progress to dysplasia

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20
Q

Define dysplasia.

A

Changes showing some of the cytological and histological features of malignancy but with no invasion through the basement membrane.

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21
Q

What histological stage does the screening process for Barrett’s oesophagus aim to identify?

A

the screening process for Barrett’s oesophagus is aimed at identifying patients at the dysplastic stage

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22
Q

What is adenocarcinoma?

A

Adenocarcinoma is when the abnormal cells invade through the basement membrane

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23
Q

Why is adenocarcnioma difficult to remove for surgeons?

A

adenocarcinomas can spread underneath the columnar epithelium - this is a massive issue for surgeons because they don’t know exactly where to stop cutting

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24
Q

What is squamous carcinoma of the oesophagus associated with? Which area does it affect? Where is it common?

A
  • Smoking and alcohol
  • It tends to affect the middle/lower oesophagus
  • Invades into the submucosa
  • It is the most common type of oesophageal cancer in Africa
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25
Q

What are the hallmark histological features of squamous cell carcinoma of the oesophagus?

A

Cells produce keratin (normal oesophageal squamous epithelium is non-keratinised)

Intercellular bridges

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26
Q

What is this slide showing

A

Squamous cell carcinoma at bottom

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27
Q

Prognosis of oesophageal carcinoma

A

o Poor prognosis
o Diagnosis at the pre-invasive stage is important

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28
Q

How is eosinophilis oesophagitis treated?

A
  • Steroids
  • Allergen removal

NOTE: this is associated with an allergic reaction (asthma of the oesophagus). It is due to allergy to food causing muscle spasm and dysphagia.

29
Q

What is the commonest cause of oesophageal varices?

A
  1. Cirrhosis of the liver (Most common)
  2. Portal vein thrombosis
30
Q

List some causes of chronic gastritis

A
  • Autoimmune (body, auto-antibodies e.g. antiparietal)
  • Bacterial (H. pylori)
  • Chemical (NSAIDs, bile reflux)

o NOTE: this can be remembered as ‘the ABC of chronic gastritis’: Autoimmune, Bacteria, Chemical)

NOTE: the key inflammatory cells in chronic gastritis are lymphocytes

31
Q

Which inflammatory cells would you see in chronic gastritis.

A

lymphocytes = chronic inflammation

NOTE: the presence of co-existing acute processes can mean that you may also see a lot of neutrophils

32
Q

What is mucosa-associated lymphoid tissue and what is their presence indicative of?

A
  • Chronic gastritis caused by H. pylori infection induces lymphoid tissue in the stomach -It induces the development of lymphoid follicles in germinal centres
  • The presence of lymphoid follicles in a stomach biopsy, is highly suggestive of H. pylori infection (normal stomach mucosa does not contain lymphoid follicles)
  • This is important because it is associated with an increased risk of lymphoma
33
Q

Name a key virulence factor/toxin that enables H. pylori to cause chronic infection.

A

Cag-A positive H. pylori has a needle-like appendage that injects toxins into intercellular junctions allowing bacteria to attach more easily

Associated with chronic inflammation.

34
Q

Does Helicobacter pylori directly invade the epithelium in gastritis?

A

No, H. pylori binds to epithelial cells and injects toxins but does not directly invade the epithelium.

35
Q

What is the sequence of conditions that can result from H. pylori associated gastritis?

A

CLO (columnar-lined oesophagus ) → IM (intestinal metaplasia) → Dysplasia.

36
Q

What is the increased risk of adenocarcinoma due to H. pylori associated gastritis?

A

8 times increased risk.

37
Q

What type of lymphoma can be a consequence of H. pylori associated gastritis?

A

Lymphoma (MALToma).

38
Q

How does the treatment of H. pylori infection with antibiotics impact cancer risk?

A

It drastically reduces the risk of cancer.

39
Q

List some other cause of gastritis.

A

Infection
*CMV
* Strongyloides

( tend to occur in immunocompromised individuals )

IBD
* Crohn’s disease

40
Q

What are the two pathways that lead to the development of GI cancer?

A
  • Metaplasia-Dysplasia pathway (e.g. oesophageal cancer)
  • Adenoma-Carcinoma pathway (e.g. colon cancer)
41
Q

Define gastric ulcer.

A

The depth of the loss of tissue goes beyond the muscularis mucosa (into the submucosa)

NOTE: if you only get loss of surface epithelium with or without involvement of the lamina propria then it is an erosion, NOT an ulcer)

42
Q

What is the difference between acute and chronic ulceration?

A

Chronic ulcers are accompanied by scarring and fibrosis

43
Q

What must you do with all gastric ulcers?

A

They should all be biopsied to rule out malignancy.

44
Q

List some complications of gastric ulcers.

A

Bleeding (anaemia, shock-massive haemorrhage)

Perforation (peritonitis)

45
Q

What signifies the presence of intestinal metaplasia in the stomach?

A

The presence of goblet cells in the mucosa of the stomach.

46
Q

What causes intestinal metaplasia in the stomach?

A

It occurs in response to long-term damage.

47
Q

What is the association between intestinal metaplasia and cancer?

A

Increased risk of cancer.

48
Q

What characterizes gastric epithelial dysplasia?

A

An abnormal epithelial pattern of growth.

49
Q

What features are present in gastric epithelial dysplasia?

A

Some cytological and histological features of malignancy.

50
Q

Is there invasion through the basement membrane in gastric epithelial dysplasia?

A

No

51
Q

Risk factors for gastric cancer

A
52
Q

Epidemiology of gastric cancer

A
  • High incidence in Japan, Chile, Italy, China, Portugal and Russia
  • More common in MALES
53
Q

What type of cancer is gastric cancer?

A
  • 95% adenocarcinoma
  • 5% squamous cell carcinoma, lymphoma (MALToma), gastrointestinal stromal tumour (GIST), neuroendocrine tumours
54
Q

What are the two main morphological subtypes of gastric adenocarcinoma? What are their key features?

A
  • Intestinal: well-differentiated, presence of big gland containing mucin
  • Diffuse: poorly differentiated, composed of single cells with no attempt at gland formation
55
Q

Name two types of diffuse adenocarcinoma of the stomach.

A
  • Linitis plastica
  • Signet ring cell carcinoma
56
Q

What is the overall survival rate of gastric cancer?

A

15%

57
Q

What is gastric lymphoma?

A
  • Lymphoma of the gastric mucosa that is driven by chronic inflammation (H. pylori gastritis)
  • Consists of lots of B lymphocytes (marginal zone)

NOTE: if H. pylori is also present, crypts may also contain lots of neutrophils
* If you treat H. pylori, the lymphoma could be reversed

58
Q

What causes duodenitis and duodenal ulcers?

A
  • Caused by increased acid produced in the stomach that spills into the duodenum
  • It can also occur due to chronic inflammation and gastic metaplasia with H. pylori infection
59
Q

Why does the intestinal epithelium change to look more like gastric epithelium in duodenitis?

A

gastric epithelium is well designed to deal with acid

60
Q

List some other pathogens that affect the duodenum.

A
  • CMV
  • Cryptosporidium
  • Giardiasis
  • Whipple’s disease (Tropheryma whippelii)
61
Q

List some histological features of malabsorption.

A
  • Villous atrophy
  • Crypt hyperplasia
  • Increased intraepithelial lymphocytes (>20 per 100 enterocytes) - normal range is less than 20 per 100 enterocytes

NOTE: the T cell response to gliadin in Coeliac disease is responsible for the damage to villi. Crypt hyperplasia occurs in an attempt to regenerate the damaged villi

62
Q

What are the architectural and inflammatory changes In coeliac disease?

A

Architectural - loss of villi and crypt hyperplasia

inflammatory - increased intraepithelial lymphocytes

63
Q

What is lymphocytic duodenitis?

A
  • When you get the inflammatory changes (increased intraepithelial lymphocytes) without architectural changes
  • Many people with this condition either have coeliac disease or will go on to develop coeliac disease
64
Q

How is coeliac disease diagnosed?

A

Antibodies: anti-tTG, anti-endomysial

Anti antibodies of:
* Endomysial Antibodies
* Tissue Transglutaminase Antibodies

Duodenal biopsy

NOTE: duodenal biopsy will be normal in people with coeliac disease who have been following a strict gluten-free diet

Biopsy
* ON gluten rich diet showing villous atrophy
* OFF gluten rich diet showing normal villi

To see biopsy changes would need to be eating gluten for a month prior otherwise false negative

65
Q

Which other condition has very similar clinical and histological features to coeliac disease?

A

Tropical sprue
Differentiate because coeliac is to do with diet and this is to do with tropics (eg. Argentina)

66
Q

What type of lymphoma is duodenal lymphoma?

A

T cell lymphoma

NOTE: lymphomas in the stomach due to H. pylori are B cell lymphomas

67
Q

What do patients with coeliac disease have an increased risk of?

A

GIT cancers

68
Q

Where are MALTomas associated with coeliac disease found?

A

duodenum

Edit YEAR 5: Histopathology (26 decks)

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