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Histopathology > Histopathology 10 - Upper GI disease > Flashcards

Histopathology 10 - Upper GI disease Flashcards

1
Q

What is the “Z line” in the GI tract?

A

Normal appearance of squamo-columnar junction of the oesophagus

upper 2/3: squamous

lower 1/3: columnar

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2
Q

Where is the cardia portion of the stomach?

A

Junction between oesophagus and stomach

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3
Q

In a normal duodenum, what is the villous:crypt ratio?

A

>2:1

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4
Q

Where are goblet cells usually found?

A

Intestine

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5
Q

What is the most common cause of acute oesophagitis?

A

GORD

Less common- swallowing toxic substances

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6
Q

If reflux oesophagitis causes a perforation of the oesophagus, what will be the result?

A

Mediastinitis

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7
Q

What are the most common complications to remember of most GI pathologies?

A

Ulceration
Haemorrhage
Perforation
Stricture

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8
Q

How is Barrett’s oesophagus different from metaplasia?

A

Reversible

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9
Q

What is gastric metaplasia?

A

Metaplastic change in oesophagus without goblet cells

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10
Q

What is intestinal type metaplasia? and risk of this?

A

Replacement of squamous epithelium with metaplastic columnar epithelium WITH goblet cells present

note: No goblet cells naturally found in stomach

Associated with increased risk of cancer

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11
Q

What is the most common sequence of pathological progression to cancer in the upper GIT?

A

Metaplasia (reversible) –> dysplasia (hyperchromatic cells) –> Cancer (invasion of basement membrane

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12
Q

What is the most common type of oesophageal carcinoma in developed coutries?

A

Adenocarcinoma: form glands and secrete mucus

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13
Q

Where does adenocarcinoma of the oesophagus usually develop?

A

Lower oesophagus- reflux has its maximum effect here

as it’s associtaed with barret’s oesophagus

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14
Q

Which type of oesophageal cancer is most strongly associated with GORD?

A

Adenocarcinoma

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15
Q

What is the most common type of oesophageal cancer in developing coutries?

A

Squamous cell carcinoma

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16
Q

Which type of oesophageal cancer is most associated with smoking and alcohol?

A

Squamous cell carcinoma

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17
Q

Where in the oesophagus does squamous cell carcinoma tend to present?

A

Mid/lower oesophagus

middle 1/3 (50%). Upper 1/3 – 20%, Lower 1/3 – 30% oesophageal

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18
Q

Why is prognosis for oesophageal cancer particularly poor?

A

Most patients are not suitable for resection surgery

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19
Q

What other condition are oesophageal varices particularly associated with? **other than cirrhosis

what is the pathophysiology of this

A

Portal vein stenosis/thrombosis

Pathophysiology

  • Blockage of flow of blood into the liver
  • Has to find other ways of doing this
  • Opens up at sites of porto-venous anastomoses for site of entry of blood
    • Such as lower oesophagus and stomach
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20
Q

What are the morphological categories of gastric cancer?

A

Intestinal
Diffuse

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21
Q

What is a gastrointestinal stromal tumour? (GIST)

A

Tumour of the interstitial cells of Cajal in the stomach - a SARCOMA

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22
Q

What is the cause of gastric MALToma?

A

Chronic inflammation, usually due to H pylori

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23
Q

What are gastric MALTomas composed of?

A

B cells

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24
Q

What is gastric epithelial dysplasia and what may be seen on a cellular level

A

Abnormal epithelial pattern of growth

  • Big nuclei
  • Raised nucleocytoplasmic ratio- most important feature
  • Increased mitoses
  • Abnormal mitoses
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25
Q

What is the first-line treatment of gastric MALToma?

A

H pylori treatment

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26
Q

Which type of gastrointestinal tract ulcers are always benign?

A

Duodenal

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27
Q

What is cryptosporidiosis?

A

Protozoal GIT infection seen in immunosuppressed patients

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28
Q

Where does giardia lamblia infection cause pathology?

A

Villi of GIT

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29
Q

What is the route of transmission of giardia?

A

Faeco/oral route

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30
Q

How are the villi damaged in coeliac disease?

A

Cytotoxic T cells

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31
Q

In what condition are increased numbers of intraepithelial lymphocytes in the GIT seen?

A

Coeliac

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32
Q

What are the 3 main histological features of coeliac?

A

Crypt hyperplasia
Villous atrophy
Increased numbers of intraepithelial lymphocytes

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33
Q

Which two antibodies are required for diagnosis of coeliac disease?

A 
Endomysial 
Tissue transglutaminase (TTG)
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34
Q

Where is EATL associated with coeliac likely to be located?

A

Duodenum

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35
Q

What is the type of MALToma as a result of coeliac disease called? and what are the microscopic features

A

Enteropathy associated T cell lymphoma:

lymphocytes are very big, with big nuclei and prominent nucleoli and lots of mitotic figures

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36
Q

WHat’s the most common cause of acute oeosphagitis?

Complications?

A

Most common cause: acid reflux (GORD)

Complications:

  • Ulceration:
    • Which produces
      • necrotic slough,
      • inflammatory exudate
      • and granulation tissue
  • Fibrosis
  • Haemorrhage
  • Perforation
  • Stricture
  • BARRETT’s OESOPHAGUS - long term complication of reflux oesophagitis
37
Q

Barret’s oesophagus: definition

What are the two types of barret’s oesophagus?

A

Defition: metaplasia of squamous to columnar of oesohpageal epithelium (usually with goblet cells) , usually at lower end of the oesophagus which is most susceptibel to acid reflux

(also calleld columnar lined oesophagus)

Two types:

Gastric metaplasia: without goblet cells

Intestinal metaplasia: with goblet cells. (gastric metaplasia–> intestinal metaplasia). *much higher risk of dysplasia into cancer*

38
Q

Which cancer can barret’s oeosphagus progress to and by which pathway?

A

Adenocarcinoma of the oeosphagus

Via flat metaplasia–>dysplasia pathway

39
Q

what are the two types of oesophageal carcinoma and risk factors?

A

1. Adenocarcinoma

  • more common in developed countries
  • RF: barret’s oeosphagus

Other risk factors incl: smoking, obesity, prior radiation therapy Adenocarcinoma
Most common in Caucasians, M>>F

2. Squaous cell carcinoma

  • more common in developing countries
  • RF: alcohol and smoking

Other RF: achalasia of cardia, Plummer-Vinson syndrome, nutritional deficiencies, nitrosamines, HPV (in high prevalence areas)

6x more common in Afro-Carribeans, M>F

40
Q

Histology of squamous cell carcinoma of the oesophagus (x2)

A

Normally the oeosphageal squamous epithelium is non-keratinised

Cancer cells are keratinised

You also see inter-cellular bridges

41
Q

How do H pylori inject toxin into the mucosa?

A

Via cag-A needle appendage

42
Q

Risk factors for oesophageal varices

A

Cirrhosis

Portal vein thrombosis

43
Q

What are the 3 layers of the stomach wall?

A 
Gastric mucosa (columnar)
Lamina propria (containing glands) 
Muscularis mucosae

nb: difference between mucosa and mucosae

44
Q

Difference in histology of gastric body vs gastric antrum

A

Body: specialised glands in lamina propria

Antrum: non-specialised glands in lamina propria

**body is SPECIAL

45
Q

What are the 3 main causes of acute gastritis?

A

chemical:

Aspirin/NSAIDs
Alcohol- especially in combination with aspirin

infection
H pylori

46
Q

What are the 3 major causes of chronic gastritis?

A

ABC
Autoimmune (antiparietal cell Ig) >> affects body of stomach
Bacterial (H pylori, affects antrum)
Chemical (NSAIDs, bile reflux from duodenum into stomach, affects antrum)

key cells are lymphocytes as this is chronic inflammation

But presence of co-existing acute processes can mean you may also get a lot of neutrophils.

47
Q

Which types of gastric neoplasm does H pylor associated chronic gastritis predispose to?

A

1) B cell Lymphoma (MALToma)

It induces lymphoid tissue in the stomach- particularly lymphoid follicles in germinal centres.

CLO >>> IM >>>Dysplasia >>> MALToma (Mucosal associated lymphoid tissue)

2) gastric adenocarcinoma

chronic gastritis–>gastric adenocarcinoma

48
Q

Which strain of H pylori is associated with more aggressive chronic gastritis?

A

cag-A positive

strain is associated with more chronic inflammation and increases the risk of cancer

49
Q

What will be the result of a perforated gastric ulcer?

A

Peritonitis

50
Q

Which part of the stomach does H Pylori affecr?

A

Antrum but can also affect pylorus

51
Q

How do you treat gastric MALToma?

A

Treat H pylori infection with 2 antibiotics and a PPI

52
Q

What pathology can H pylori cause in the oesophagus?

A

Barret’s oesophagus –> oesophageal adenocarcinoma

53
Q

What are the cells associated with chronic gastritis? And what would make you suspect B cell lymphoma?

A

Lymphocytes as this is a chronic process

eg you would see proliferation of lymphoid follicles

If you see neutrophils- can be sign of gastric MALToma

(acute process within a chronic process)

54
Q

Definition of ulcer- how is it different to an erosion?

Complications of ulcers

A

Ulcer: when inflammation invades the muscularis mucosae into the submuocsal layer: Through the full thickness of the mucosa and into the submucosa

Erosion: loss of superficial tissue - does not invade into the submucosae

Complications: bleeding(iron deificnecy anaemia) , perforation (peritonitis), malignancy

55
Q

Why might you biopsy a gastric ulcer and indicate what might be seen/not seen

A

ALL gastric ulcers should be biopsied to exclude malignancy

Ulcers with smooth non-rolled edges are unlikely to be cancer

56
Q

What is intestinal metaplasia of the stomach and what is its significance?

A

When you see goblet cells in the intestine

Higher risk of developing into cancer

57
Q

What are the two cancer pathways in the upper GI tract?

A
  1. Flat pathway: metaplasia-dysplasia pathway : oesophageal and gastric cancer (upper GI)
  2. polyp pathway: adenoma-carcinoma pathway: colon cancer (lower GI)
58
Q

What is the key cytological feature of gastric epithelial dysplasia?

A

High nuclear cytoplasmic ratio

59
Q

What is the difference between gastic dysplasia and gastric Ca?

A

Invasion of basement membrane

60
Q

What type of carcinoma is the most common type of gastric cancer?

A

Adenocarcinoma- 95%

Other 5%:

  • squamous cell carcinoma
  • gastric maltoma
  • gastrointestinal stromal tumour
  • neuroendocrine tumours: GIT is one of the richest sites of neuroendocrine cells
61
Q

Where is gastric cancer most common?

A

Japan, by far

62
Q

What are the two types of gastric adenocarcinoma?

A

1. intestinal: intestinal metaplasia. well-differentiated glands: Form big glands and secrete mucus

​2. diffuse: undifferentiated. more aggressive = poor prognosis

  • linitis plastica
  • signet ring cell carcinoma
63
Q

What is linitis plastica?

A

Type of diffuse gastric adenocarcinoma

spreads to stomach wall muscles and makes it thicker and more rigid → leather bottle stomach

→ trouble digesting food

64
Q

What is signet ring cell carcinoma and how do they spread

A

Type of diffuse gastric adenocarcinoma

Signel ring cell: single cells with holes in them - no attempt of gland formation

65
Q

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

A

>2:1

66
Q

Effect of H pylori on duodenum

A

Chornic inflammation of the antrum of the stomach

Acid production

Spills over into the duodenum *i.e. H pylori doesn’t infect the duodenum itself*

This then causes GASTRIC METAPLASIA- adaptation to deal with increased acid production (As gastric epithelium is more well suited to deal with stomach acid)

67
Q

Which other pathogens infect the duodenum?

A
  1. cryptosporidium - protozoa
  2. CMV
  3. giardia lamblia - very common parasite which exists in immunocompetent people
  4. whipple’s disease: Infective disease via Tropheryma whippelii >>>>Infection of macrophages which involves the duodenum >>>malabsorption
68
Q

Which HLA molecules are associtaed with Coeliac disease?

A

HLA-DQ2 and HLA-DQ8

I 8 2 much

69
Q

Pathophysiogy of coeliac disease

A
  1. T cell response
    - gliadin in gluten is deamidated by TTG enzyme
    - deamidated gliadin is presented by APC to cytotoxic T cells which then activate intra-epithelial lymphocytes leading to duodenal epithelial damage
  2. antibody response
    - gliadin presented by APC–> T cells
    - T cells –> B cells
    - B cells produce high affinity isotype switched antibodies following germinal centre reaction
70
Q

Gold standard for serological testing of coeliac disease

A

IgA anti-TTG antibodies

IgA is more sensitive than IgG

*but not as useful in IgA deficient individuals*

*can also use anti endomysial antibodies*

71
Q

Gold standard for diagnosis of coeliac disease

A

Distal duodenal biopsy

*must be distal because brunner’s glands in proximal duodenum distort the arhcitecture*

Findings:

  • villous atrophy: smaller + flatter
  • crypt hyperplasia: proliferating to regeneratre the damaged Villi

–> decrease in villous:crypt ratio

-high intraepithelial lymphocytes

NB: must be on gluten rich diet at the time of the biopsy

72
Q

marker of intestinal metaplasia

A

goblet cells in the stomach, they should normally have no goblet cells in the stomach

73
Q

Complications of coeliac disease

A

Nutritional deficiencies

  • iron
  • vitamin B12
  • folate
  • vitamin D and vitamin K

MALToma

  • enteropathy associated T cell lymphoma (=/= B cell lymphoma)
74
Q

Conditions similar to coeliac disease

A
  1. lymphocytic duodenitis
    - similar to coeliac- increased intraepithelial lymphocytes
    - but no change in villous: crypt architecture
  2. tropical sprue
    - similar histology but different cause - in tropical regions
75
Q

Spread of squamous cell carcinoma of the oesophagus

A

Rapid growth and early spread (to LNs, liver and directly to proximal structures) –> palliative care

76
Q

Complications of chronic gastritis

A

1) gastric ulcer
2) cancer (metaplasia–>dysplasia)

77
Q

Gastric vs duodenal ulcer

A

Gastric: worse with food, responds to PPIs. can be malignant. more common in elderly.

Duodenal: better with food. not malignant. more common in young adults.

duodenal is more common than gastric

78
Q

Description of H pylori gastric ulcer

A

Punched out lesion with rolled margins.

79
Q

what will happen if there is atrophy and inflammation of the body of the stomach

A

inflammation and atrophy of the body will produce hypochlorhydria and blocks Interferon production

  • Intrinsic factor secretion also occurs from body of stomach
80
Q
  • marker for intestinal type epithelium
A

glandular epithelium with goblet cell

81
Q

what does lymphoid follicles in the stomach indicate

A

past or current has H. pylori infection

Normally you do NOT see lymphoid follicles in the normal stomach

marginal zone lymphocytes (which are around the follicles) proliferatre to cause MAlToma

82
Q

what are oesophageal varices

A

dilated varicose veins in the submucosa

83
Q

other causes of gastritis:

A

Infection

  • Stronglyoides – immunosuppressed patients
  • Candida is the most common in the oesophagus
  • Occurs especially in the immunosuppressed (H. pylori oesophagitis is very common)
  • CMV is the commonest opportunistic viral infection

Inflammatory bowel disease

  • Crohn’s disease
    • (lips to anus)
    • See granulomas and focal inflammation
84
Q

difference between acure ulcer vs chronic ulcer

A

chronic ulcer- scarring + fibrosis = irreversible + lymphocyte predominant

acute ulcers- reversible + neutrophil predominant

85
Q

epidemiology of gastric cancer

A
  • High incidence in Japan, Chile, Italy, China, Portugal, Russia
  • More common in men than women (1.8 M: 1 F)
86
Q

most common cause of gastric and duodenal ulcerations:

A

H. pylori

87
Q

Palpable lymph node in supraclavicular fossa

A

troissier’s sign

88
Q

The stomach mucosa is normally lined with which cell type?

A

simple columnar

89
Q

What type of epithelium is oesophagus made of?

A

stratified squamous epithelium with glands in submucosa

Histopathology (18 decks)

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