Pathology of the GI Tract Flashcards

1
Q

What epithelium lines the oesophagus?

A

Squamous

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2
Q

What epithelium lines the oesophagus below the diaphragm?

A

Glandular (columnar) epithelium

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3
Q

What are the two oesophageal sphincters?

A

1) Cricopharyngeal

2) Gastro-oesophageal

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4
Q

Define: Oesophagitis

A

Acute/Chronic inflammation of the oesophagus

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5
Q

What type of Oesophagitis is the most common?

A

Reflux

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6
Q

What are the causes of Oesophagitis?

A

> Gastro-oesophageal reflux

> Duodeno-gastric (bile) reflux

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7
Q

What are the risk factors for Oesophagitis?

A

> Incr intra-abdominal pressure
Weak lower spincter
Hiatus hernia (stomach into thoracic cavity)
Gastric outflow stenosis –> increase fluid

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8
Q

What is the characteristic symptom of Reflux Oesophagitis?

A

Heartburn

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9
Q

What are the complications of Reflux Oesophagitis?

A
> Ulceration
> Haemorrhage
> Peforation
> Barrett's Oesophagus
> Benign stricture
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10
Q

What is a hiatus hernia?

A

When a part of the stomach abnormally protrudes through the diaphragm

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11
Q

What symptoms does a sliding hiatus hernia give?

A

Reflux symptoms

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12
Q

What symptoms does a para-oesophageal hernia give?

A

Strangulation

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13
Q

What occurs to the squamous epithelium in Reflux Oesophagitis?

A

> De-squamed

> Basal cell hyperplasia

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14
Q

What occurs to the lamine propria in Reflux Oesophagitis?

A

Infiltrated by inflammatory cells.

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15
Q

What is Barrett’s Oesophagus?

A

It is a premalignant condition assc with adenocarcinoma development.

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16
Q

What is the cause of Barrett’s Oesophagus?

A

Chronic Reflux

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17
Q

What are the risk factor’s for Barrett’s Oesophagus?

A

Male, Caucasian and overweight

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18
Q

What is macroscopically seen in Barrett’s Oesophagus?

A

An extension of the squamo-columnar junction

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19
Q

What is the histologically characteristic mark of Barrett’s Oesophagus?

A

Glandular metaplasia - Squamous to Columnar.

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20
Q

What is the process from Barrett’s Oesophagus to Adenocarcinoma?

A

Barrett’s Oesophagus –> Low grade dysplasia –> High grade dysplasia –> Adenocarcinoma

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21
Q

What two types of Oesophageal carcinoma are there?

A

> Squamous cell carcinoma

> Adenocarcinoma

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22
Q

Who is Adenocarcinoma higher in M or F? And by what ratio?

A

Males 7:1

23
Q

In the oesophagus where are said carcinomas localised:

1) Squamous cell carcinoma
2) Adenocarcinoma

A

1) Upper and middle third

2) Lower

24
Q

What are the risk factors for Squamous Carcinoma?

A

> Tobacco and alcohol
Nutrition (nitrosamines)
HPV
Hot thermal injury

25
Q

What precedes Squamous Carcinoma?

A

Sqaumous dysplasia

26
Q

What are each of the components of TNM tumour staging?

A
pT = Primary tumour invasion depth
N = Regional lymph node 
M = Distant metastatis
27
Q

What level does pT1 invade to?

A

Muscularis Mucosae or Submucosa

28
Q

What level does pT2 invade to?

A

Muscularis Propria

29
Q

What level does pT3 invade to?

A

Adventitia

30
Q

To where does pT4 invade to?

A

Adjacent tissues

31
Q

How many lymph nodes are invaded in pN2,3 and 4?

A

1) 1- 2
2) 3-6
3) 7+

32
Q

What is the ABC of chronic gastritis aetiology?

A

Autoimmune, Bacterial, Chemical Injury

33
Q

Explain the pathological mechanisms and histiological findings of Autoimmune chronic gastritis?

A

Pathological Mechanism:
> Anti-parietal
> Anti-intrinsic factor antibodies
> Sensitised T cells

Histiological Findings:
> Atrophied Gastric body
> Intestinal Metaplasia

34
Q

Explain the pathological mechanisms and histological findings of Bacteria caused Chronic Gastritis?

A
Pathological Mechanisms: 
> Release cytokines
> Liberate chemokines
> Release mucolytic enzymes
> Bacterial urease --> ammonia production 
> Immune response does tissue damage.

Histological findings:
> Active chronic inflammation
> Intestinal metaplasia
> Multifocal atrophy

35
Q

Explain the pathological mechanisms and histological findings of chemical injury caused Chronic Gastritis?

A

Pathological mechanism:
Direct injury

Histological findings:
Foveolar hyperplasia

36
Q

What type of bacterium is H.Pylori?

A

Gram negative spiral shaped

37
Q

Where is H.Pylori mostly found?

A

Antrum > body

38
Q

How does H.Pylori cause chronic inflammation?

A

Damaged epithelium lining.

39
Q

What is a peptic ulcer?

A

A submucosal localised lesion

40
Q

What are the major sites of a peptic ulcer?

A

> First part of the duodenum
Body-antrum mucosal junction
Gastro-oesophageal junction

41
Q

What are the main causes of a peptic ulcer?

A
> Smoking
> Drugs
> Duodeno-gastric reflux
> Hyperacidity
> H.Pylori infection
42
Q

What are the complications of a peptic ulcer?

A

> Perforation perionitis
Haemorrhage
Penetration into adjacent organs
Stricture into hourglass shape

43
Q

What is the most frequent type of gastric cancer?

A

Adenocarcinoma

44
Q

What is the incidence of gastric adenocarcinoma?

A

5th most common cancer but declining

45
Q

What causes gastric adenocarcinoma?

A

> H.Pylori
Diet (smoked meats, pickled veg)
Bile refluex
Hypochlorhydria - 1% hereditary

46
Q

What mutation can cause hereditary diffuse type gastric cancer?

A

Germline CDH1/E-cadherin mutation

47
Q

What is Coeliac disease?

A

= Gluten sensitive enteropathy (small intestine disease)

48
Q

What is the incidence of Coeliac disease?

A

0.5-1% general population

49
Q

What is Gliadin, how does it work?

A

It is the part of gluten that can induce disease.

Induces epithelial cells to produce inter-leukin 15.

50
Q

What is the pathogenesis mechanism of Coeliac Disease?

A

Gliadin stimulates epithelial cells –> release IL5.

IL5 activates CD8 and IEL –> They kill enterocytes

51
Q

What diseases are associated with Coeliac?

A

> Dermatitis Herpatiformis - 10% of pt’s

> Lymphocytic colitis/gastritis

52
Q

What cancers are assc with Coeliac?

A

> Enteropathy-associated T cell lymphoma.

> Small intestine adenocarcinoma

53
Q

What tests are done for Coeliac disease?

A

> IgA against Tissue transglutaminase (TTG)
IgA/IgG against deaminated Gliadin
Anti-endomysial antibodies - v specific but less sensitive