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Clinical Pathology > CP11-1 Upper GI Pathology > Flashcards

CP11-1 Upper GI Pathology Flashcards

1
Q

What are 3 main pathologies affecting the oesophagus?

A

Oesophagitis and gastro-oesophageal reflux
Barrett’s oesophagus
Oesophageal carcinoma

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2
Q

What are 3 pathologies affecting the stomach?

A

Acute and chronic gastritis
Peptic ulceration
Gastric carcinoma

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3
Q

What is an example of a pathology affecting the small bowel?

A

Coeliac disease

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4
Q

What cells make up the oesophagus?

A

Mainly stratified squamous epithelium until the distal portion around the level of the diaphragm where the cells become squamocolumnar (squamocolumnar junction) before becoming normal columnar epithelium of the stomach lining

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5
Q

What is oesophagitis?

A

Inflammation of the oesophagus. Can be acute or chronic.

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6
Q

What causes oesophagitis?

A

Usually viral e.g. HSV or CMV, or fungal like candida
Can also be chemical via ingestion of corrosive substances or due to reflux of gastric contents.

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7
Q

What is reflux oesophagitis?

A

Inflammation of the oesophagus due to reflux of gastric acid or bile.

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8
Q

What are risk factors for reflux oesophagitis?

A

Defective lower oesophageal sphincter
Hiatus hernia
Increased intra-abdominal pressure e.g. from pregnancy
Increased gastric fluid volume due to outflow stenosis.

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9
Q

What is the main symptom of reflux oesophagitis?

A

‘Heartburn’

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10
Q

How does reflux oesophagitis affect the histology of the oesophagus?

A

Basal cell hyperplasia
Elongation of papillae
Increase cell desquamation
Inflammation
Ulceration if severe

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11
Q

What are some complications of reflux oesophagitis?

A

Ulceration
Haemorrhage
perforation
Bengin stricture (segmental narrowing)
Barrett’s oesophagus

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12
Q

What is Barrett’s oesophagus?

A

Metaplastic transition of epithelium, to columnar mucosa (like in intestines with goblet cells) from stratified squamous, in the oesophagus due to longstanding gastro-oesophageal reflux

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13
Q

What are risk factors for Barrett’s oesophagus?

A

Male
Caucasian
Overweight

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14
Q

How does the oesophageal epithelium look under the microscope and histological with Barrett’s oesophagus?

A

Proximal extension of the squamocolumnar junction with the squamous mucosa replaced by columnar mucosa- glandular metaplasia

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15
Q

What does Barrett’s oesophagus increase risk of?

A

Adenocarcinoma

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16
Q

How does Barrett’s oesophagus progress to an adenocarcinoma?

A

Barrett’s oesopagus —> low grade dysplasia —> high grade dysplasia xx> adenocarcinoma

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17
Q

How are patients with Barrett’s oesophagus monitored for neoplasia?

A

Via regular endoscopic surveillance

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18
Q

What are the two main types of oesophageal carcinoma?

A

Squamous cell carcinomas
Adenocarcinomas

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19
Q

What is the epidemiology of oesophageal carcinoma?

A

8th most common cancer globally
30% of oesophageal carcinomas are squamous in the UK

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20
Q

Who is most likely to get an oesophageal adenocarcinoma? Males or females?

A

Males

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21
Q

What causes oesophageal adenocarcinomas?

A

Barrett’s oesophagus

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22
Q

What are risk factors for oesophageal SCC?

A

Tobacco and alcohol
Nutrition
Thermal injury e.g. hot drinks
HPV infection
Male
Ethnicity = black

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23
Q

What part of the oesophagus doe SCC usually develop?

A

In middle and lower third of the oesophagus (less than 15% in upper third)

24
Q

How can an oesophageal SCC look macroscopically?

A

Polypodial
With structuring
Ulceration

25
Q

What system is used to stage GI cancers?

A

TNM staging
( T = primary Tumour staging, N = lymph Node staging, M= distant Metastases)

26
Q

What is the pathogenesis of gastritis?

A

Increased acid in the stomach causes impaired defences e.g. ischaemia, shock, delayed emptying, duodenal reflux or impaired regulation of pepsin secretion.

27
Q

What can cause increased acid in the stomach disrupting the balance between aggressive and defensive forces of the stomach?

A

Excessive alcohol
Drugs
Heavy smoking
Ingestion of corrosive substances
Radiation
Chemotherapy
Infection e.g. h.pylori

28
Q

What is the cause of acute gastritis?

A

Usually chemical injury e.g through NSAIDs or alcohol
Initial response to H. Pylori infection

29
Q

What can Acute gastritis cause for the stomach?

A

Erosions
Haemorrhage

30
Q

How soon does acute gastritis heal?

A

Quickly

31
Q

What causes chronic gastritis?

A

Autoimmune problems e.g. due to anti-parietal and anti-intrinsic antibodies
Bacterial infection e.g. h. Pylori
Sustained chemical injury due to NSAIDs, bile reflux potentially alcoholism, causing direct injury

32
Q

What can h. Pylori lead to in chronic gastritis?

A

Gastric ulcers (in 2-5%)
Duodenal ulcers (in 10-15%)
Gastric cancer and MALT lymphoma

33
Q

What is h.pylori?

A
34
Q

What is peptic ulcer disease?

A

Localised defect/ ulceration of the stomach extending at least into the submucosa.

35
Q

Where are common sites of peptic ulcer disease?

A

First part of duodenum
Junction of antra, and body mucosa
Distal oesophagus

36
Q

What causes peptic ulcer disease?

A

Hyperacidity
H. Pylori infection
Duodeno-gastric reflux
Drugs (NSAIDs)
Smoking

37
Q

How do gastric ulcers and duodenal ulcer differ?

A
38
Q

What are come complications of peptic ulcers?

A
39
Q

What is the most common gastric cancer?

A

Adenocarcinomas

40
Q

What are some less common gastric cancers?

A

Endocrine tumours
Lymphomas
Stromal tumours

41
Q

What increases risk of adenocarcinoma of gastro-oesophageal junction?

A

Being a white make
Have gastrooesophafeal reflux
Incidence increasing reccentky

42
Q

What increases risk of developing an adenocarcinoma in the body/antrum of the stomach?

A

H.pylori infection
Diet high in salt and low in fruit and veg
Decreased incidence recently

43
Q

What is the epidemiology of gastric adenocarcinomas?

A

5th most common cancer globally, 17th in UK accounting for 2% of all new cancer cases
Steady decline over past decades

44
Q

What is the aetiology of gastric adenocarcinomas?

A

Diet - high in smoked/cured meat or fish and pickled by vegetables
H. Pylori infection
Bile reflux
Hydrochlorhydria
Genetics (~1% of cases)
Gastric ulcers

45
Q

What are the macroscopic subtypes of gastric adenocarcinomas?

A

Superficial exophytic
Flat or depressed
Superficial excavated
Exophytic
Linitis plastics
Excavated
Polypodial
Ulcerated

46
Q

What are the microscopic subtypes of gastric cancer?

A

Intestinal = well or moderately differentiated, may undergo intestinal metaplasia and adenoma steps

Diffuse type = poorly differentiated, scattered growth, associated with cadherin loss/mutation, can be hereditary

47
Q

What percentage of gastric adenocarcinomas are caused by a germline mutation in E-cadherin?

A

Around 1%

48
Q

What is coeliac disease?

A

An immune mediated enteropathy which is triggered by ingestion of gluten containing cereals in genetically predisposed individuals

49
Q

What is the epidemiology of coeliac disease?

A

0.5-1% of people in UK
Commonly affects adults between 30-60

50
Q

What is the pathogenesis of coeliac disease?

A

Reaction to gliadin inducing epithelial cells to express IL-15. Increased production of IL-15 causes activation and proliferation of CD8+ intraepithelial lymphocytes which are cytotoxic and kill enterocytes.

CD8+ intraepethial lymphocytes do NOT recognise gliadin directly

51
Q

How is coeliac disease diagnosed?

A

With non-invasive serologic tests performed before biopsy e.g. IgA antibodies to TTG, IgA or IgG antibodies to delaminated gliadin and anti-endomysial antibodies
Tissue biopsy is diagnostic

52
Q

How is coeliac disease treated?

A

With gluten free diet

53
Q

What are long term complication of coeliac disease if it’s not treated?

A

Anemia
Female infertility
Osteoporosis
Cancer - enteropathy associated T-cell lymphoma and small intestinal adenocarcinomas

54
Q

What are some diseases associated with coeliac disease?

A

Dermatitis herpetiformis in 10% of patients
Lymohocytic gastritis and colitis

55
Q

If a patient with coeliac disease still gets symptoms when adhering to a gluten free diet, what might they have?

A

Cancer

56
Q

How does the intestine present histologically with coeliac disease?

A

Vilous atrophy
Crypt elongation
Increased IELs
Increased lamina propria inflammation

57
Q

What are enterocytes?

A

Intestinal cells involved in absorption of nutrients

Clinical Pathology (65 decks)

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