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CLINICAL PATHOLOGY > Upper GI Diseases > Flashcards

Upper GI Diseases Flashcards

1
Q

What are the names of the 2 oesophageal sphincters?

A

1) Upper end - cricopharyngeal

2) Lower end - gastro-oesophageal junction

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2
Q

What epithelium lines the oesophagus?

A

Mostly stratified squamous

BUT
distal 1.5-2cm are situated below the diaphragm
lined by glandular (columnar) mucosa

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3
Q

How far from the incisors is the squamo-columnar junction usually located?

A

40cm

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4
Q

Normal oesophageal histology involved what 3 layers?

A

1) Mucosa - made up of epithelium and underlying lamina propria
2) Submucosa
3) Muscularis propria

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5
Q

Which histological layer of the oesophagus contains the major blood vessels and lymphatics?

A

The submucosa

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6
Q

What is oesophagitis?

A

Inflammation of the oesophagus

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7
Q

What are the 2 classifications of oesophagitis?

A

Acute or chronic

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8
Q

What are the 2 main causes of oesophagitis?

A

1) Infections

2) Chemical (ingestion of corrosive substances, or reflux of gastric contents)

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9
Q

What 4 infectious agents can cause oesophagitis?

A

1) Bacteria
2) Viral - HSV1
3) Viral - CMV
4) Fungal - candida

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10
Q

What is the most common cause of oesophagitis?

A

Reflux oesophagitis

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11
Q

What is reflux oesophagitis?

A

Oesophagitis caused by reflux:

of gastric acid (gastro-oesophageal reflux)

bile (duodeno-gastric reflux)

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12
Q

What is the leading clinical symptom of reflux oesophagitis?

A

Heart burn

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13
Q

What are the 4 main risk factors for reflux oesophagitis?

A

1) Defective lower oesophageal sphincter
2) Hiatus hernia
3) Increased intrabdominal pressure (obesity)
4) Increased gastric fluid volume due to gastric outflow stenosis (Eg. antral tumour)

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14
Q

What is the most common complication of a para-oesophageal hernia?

A

Strangulation (compromised blood supply to that part of the stomach - can get ischaemia and necrosis of stomach)

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15
Q

What 4 changes are seen histologically in the squamous epithelium/lamina propria in reflux oesophagitis?

A

1) Basal cell hyperplasia (rather than being 1/2 layers thick normally, this is due to increased proliferation and cell turnover)
2) Elongation of papillae (lamina propria papillae normally project 1/3 way into epithelium, project further)
3) Increased cell desquamation (squamous epithelium is normally 8-15 layers thick, much thinner)
4) Inflammatory cell infiltration into lamina propria (neutrophils, eosinophils, lymphocytes)

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16
Q

What are the 5 main complications of reflux disease?

A

1) Ulceration - erosion of the epithelium and then underlying layers
2) Haemorrhage - ulceration gets to submucosa and hits vessels
3) Perforation
4) Benign stricturing - if get some healing by fibrosis can then get stricturing leading to segmental narrowing and dysphagia
5) Barrett’s oesophagus

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17
Q

What is the cause of Barrett’s oesophagus?

A

Long standing reflux

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18
Q

What are the 3 risk factors for Barrett’s oesophagus?

A

Same as for reflux disease

1) Male
2) Caucasian
3) Obese

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19
Q

How does Barrett’s oesophagus appear macroscopically?

A

Proximal extension of the squamo-columnar junction

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20
Q

Histologically what is Barrett’s oesophagus?

A

METAPLASIA:

Squamous epithelium replaced by glandular (columnar) mucosa

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21
Q

At what level is the squamo-columnar junction of the oesophagus normally seen?

A

Level of the diaphragm

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22
Q

What 3 types of columnar mucosa can be seen in Barrett’s oesophagus but which is most typical and almost diagnostic of Barrett’s oesophagus?

A

1) Gastric cardia type
2) Gastric body type
3) Intestinal type = most typical of Barrett’s oesophagus

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23
Q

What cells are found in the intestinal mucosa and not in the gastric mucosa which are highly suggestive of Barrett’s if seen in the oesophagus?

A

Goblet cells

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24
Q

Is Barrett’s oesophagus a malignant condition?

A

No but it is considered a premalignant condition with an increased risk of developing adenocarcinoma

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25
Q

What screening procedure is required in patients with Barrett’s oesophagus?

A

Regular endoscopic surveillance

Early detection of neoplasm

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26
Q

What are the 4 steps in the progression from Barrett’s oesophagus to adenocarcinoma, and the main histological features of each?

A

1) Barrett’s oesophagus - intestinal type epithelium, see goblet cells, normal nuclei basally located
2) Low grade dysplasia - More complex architecture, less basally located nuclei more atypical
3) High grade dysplasia - Distorted architecture and atypical nuclei
4) Adenocarcinoma - All features of dysplasia and cells breaking through basement membrane to invade other structures

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27
Q

How common is oesophageal cancer compared to other cancers?

A

8th most common in the world

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28
Q

What are the histological types of oesophageal cancer?

A

1) Squamous cell carcinoma - originating from the normal oesophageal epithelium
2) Adenocarcinoma - following on from Barrett’s, originating from glandular epithelium

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29
Q

In the UK is squamous or adenocarcinoma more common, how does this compare to other countries?

A

Adenocarcinoma more common (could be due to obesity - risk factor for Barrett’s)
Other countries squamous is more common

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30
Q

Whats the main cause of adenocarcinoma and what are the other 2 possible risk factors?

A

1) Barrett’s oesophagus
Other risk factors with a link:
Tobacco, obesity

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31
Q

What is the normal site of an adenocarcinoma?

A

Lower oesophagus

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32
Q

How would the macroscopic appearance of a polypoidal, ulcerated adenocarcinoma differ?

A

Polypoidal - sticks out into the lumen of the oesophagus, could lead to problems with swallowing
Ulcerated - appears as an ulcer

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33
Q

What are the 6 possible macroscopic structures of an adenocarcinoma?

A

1) Plaque-like
2) Nodular
3) Fungating
4) Ulcerated
5) Depressed
6) Infiltrating

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34
Q

What are the 7 risk factors for squamous carcinoma of the oesophagus?

A

1) Tobacco
2) Alcohol
3) Nutrition (potential sources of nitrosamines)
4) Thermal injury (hot beverages)
5) HPV
6) Male
7) Ethnicity (black)

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35
Q

What is the normal site of a squamous carcinoma of the oesophagus?

A

Middle and lower third

>15% in upper third of oesophagus

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36
Q

In the TMN staging of oesophageal carcinoma what does the pT stand for and what are the 4 stages?

A

pT = depth of invasion of primary tumour
pT1: invades lamina propria, muscularis mucosae or submucosa
pT2: tumour invades muscularis propria
pT3: tumour invades adventitia
pT4: tumour invades adjacent structures

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37
Q

What does the N stand for in the TMN staging of oesophageal carcinoma and what are the 4 stages?

A 
N = regional lymph nodes
pN0 = 0 nodes
pN1 = regional lymph node metastasis in 1 or 2 nodes
pN2 = in 3-6 nodes
pN3 = in 7+ nodes
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38
Q

What does the M stand for in TMN staging of oesophageal cancer and what are the 2 stages?

A 
M0 = no distant metastasis
M1 = distant metastasis
39
Q

What are the 4 anatomical regions of the stomach?

A

Cardia (around oesophageal junction)

Fundus (above oesophageal opening)

Body

Antrum

40
Q

What are the 3 histological regions of the stomach with different functions?

A

1) Cardia
2) Body
3) Antrum

41
Q

The stomach is normally a balance between aggressive (acid) and defensive forces, what are those 5 defensive forces?

A

1) Surface mucous
2) Bicarbonate secretion
3) Mucosal blood flow
4) Regenerative capacity
5) Prostaglandins

42
Q

What 7 things can lead to increased acidic forces in the stomach?

A

1) excessive alcohol
2) Drugs
3) heavy smoking
4) corrosive
5) radiation
6) chemotherapy
7) Infection

43
Q

What 5 things can impair the defences of the stomach against acid?

A

1) Ischeamia
2) Shock
3) Delayed emptying
4) Duodenal reflux
5) Impaired regulation of pepsin secretion

44
Q

What are the 3 main aetiologies for chronic gastritis?

A

ABC:

1) Autoimmune
2) Bacterial infection (H.pylori)
3) Chemical injury (NSAIDs, Bile reflux)

45
Q

What is the main pathogenic mechanism behind autoimmune chronic gastritis?

A

Anti-parietal cell and anti-intrinsic factor antibodies and sensitised T cells

46
Q

What would be the 2 main histological findings with autoimmune chronic gastritis?

A

1) Glandular atrophy in body mucosa

2) Intestinal metaplasia

47
Q

What are the main histological findings in chronic gastritis due to bacterial infection?

A

1) Multifocal atrophy: antrum > body

2) Intestinal metaplasia

48
Q

What is the main pathogenic mechanism behind bile reflux causing chronic gastritis?

A

Degranulation of mast cells

49
Q

What is the main pathogenic mechanism behind NSAID’s causing chronic gastritis?

A

Disruption of the mucus layer

50
Q

What would be the main histological findings in chronic gastritis due to a) oedema b) bile reflux?

A

a) NSAIDs - oedema

b) Bile reflux - vasodilation

51
Q

What kind of bacteria is H pylori?

A

Gram negative spiral shaped bacterium - lives on the epithelial surface protected by the overlying mucus barrier

52
Q

How does H pylori cause disease?

A

Damages the epithelium leading to chronic inflammation of the mucosa

53
Q

H pylori is more commonly found in what part of the stomach?

A

More common in the antrum than body

54
Q

What does H.pylori infection do to the stomach? 3

A

1) Glandular atrophy
2) Replacement fibrosis
3) Intestinal metaplasia

55
Q

H.pylori infected individuals can present with what 2 kinds of ulcer, which is more common?

A

1) Gastric ulcer

2) Duodenal ulcer - more common

56
Q

H.pylori infection can lead to what 2 cancers?

A

1) Gastric cancer

2) MALT lymphoma (mucosa associated lymphoid tissue)

57
Q

What is peptic ulcer disease?

A

Localised defect in the digestive tract.

Typically the stomach or duodenum, extending at least into submucosa.

58
Q

What are the 3 major sights of peptic ulcer disease?

A

1) First part of the duodenum
2) Junction of antral and body mucosa
3) Distal oesophagus

59
Q

What are the 5 main aetiological factors contributing to peptic ulcer disease?

A

1) Hyperacidity
2) H.pylori infection
3) Duodeno-gastric reflux
4) Drugs NSAID’s
5) Smoking

60
Q

What are the 3 histological features of an acute gastric ulcer?

A

1) Full thickness coagulative necrosis of mucosa (or deeper layers)
2) Covered with ulcer slough (necrotic debris + fibrin + neutrophils)
3) Granulation tissue at ulcer floor

61
Q

What are the 4 histological features of a chronic gastric ulcer?

A

1) Clear-cut edges overhanging the base
2) Extensive granulation and scar tissue at ulcer floor
3) Scarring often throughout the entire gastric wall with breaching of the muscularis propria
4) Bleeding

62
Q

What are the 4 main complications of peptic ulcers?

A

1) Haemorrhage (acute and/or chronic - anaemia)
2) Perforation - peritonitis
3) Penetration into adjacent organ (liver, pancreas)
4) Stricturing - hour glass deformity

63
Q

What is the difference in incidence between gastric ulcer and duodenal ulcer?

A

Duodenal ulcer 3x more common than gastric ulcer

64
Q

What is the difference in age distribution between gastric and duodenal ulcer?

A

Gastric ulcers increase with age

Duodenal ulcer increase up to 35 years

65
Q

How do acid levels differ in a gastric ulcer compared to a duodenal ulcer?

A

Gastric ulcer - normal or low acid levels

Duodenal ulcer - elevated or normal acid levels

66
Q

What percentage of gastric ulcer and duodenal ulcers are caused by H.pylori gastritis?

A

70% of gastric ulcers

95-100% duodenal ulcers (predominantly antrum)

67
Q

Gastric ulcers and duodenal ulcers are each more common in which blood groups?

A

Gastric - A

Duodenal - O

68
Q

Gastric cancer is most frequently what type of cancer and can be what 3 other types less frequently?

A

Most frequently - adenocarcinoma

Less frequently - endocrine tumours, MALT lymphomas, Stromal tumours (can be low grade benign or high grade malignant)

69
Q

What are the 4 main risk factors for gastric cancer?

A

1) Diet (smoked/cured meat or fish, pickled veg)
2) H pylori infection
3) Bile reflux
4) Hypochlorydia (allows bacterial growth)

70
Q

Gastric adenocarcinoma of the gastro-oesophageal junction is associated with what risk factor and which group?

A

Associated with white males
Association with GO reflux
NO association with H.pyloir/diet

71
Q

Gastric adenocarcinoma of the gastric body/antrum is associated with what risk factors?

A

Associated with H pylori, diet

NO association with GO reflux

72
Q

What are the 2 main histological types of gastric adenocarcinoma and what are their main features?

A

1) Diffuse type (signet ring cell carcinoma) - poorly differentiated, scattered growth, cadherin loss/mutation
2) Intestinal type (tubular adenocarcinoma) - Well or moderately differentiated, may undergo metaplasia and adenoma steps

73
Q

What histological type of gastric adenocarcinoma is hereditary gastric adenocarcinoma?

A

Diffuse type - hereditary diffuse type gastric cancer

74
Q

Hereditary diffuse type gastric carcinoma involves a germline mutation in which gene?

A

E-cadherin mutation

75
Q

In TMN staging of gastric adenocarcinoma what are the different T stages?

A

1) pT1: intramucosal or submucosal invasion
2) pT2: into muscularis propria
3) pT3: through muscularis propria into subserosa
4) pT4: through serosa (peritoneum) or into adjacent organs

76
Q

In TMN staging what is the N and M stages?

A 
N = lymph node involvement (same as oesophageal carcinoma)
M = distant metastasis (0 or 1 if metastasis)
77
Q

What is the estimated prevelance of ceoliac disease?

A

0.5-1%

78
Q

What is the pathogenesis of coeliac disease?

A
  • Gliadin (alcohol soluble component of gluten) induces epithelial cells to express IL-15/interleukine 15
  • IL-15 produced by the epithelium activates and induces proliferation of CD8+ Intraepithelial lymphocytes (IELs)
  • CD8+ cells are toxic and kill enterocytes
  • CD8+ IELs do not recognise gliadin directly
  • Gliadin induced IL15 secretion by epithelium is the mechanism
79
Q

Ceoliac disease commonly affects adults of what age?

A

30 - 60 years

80
Q

What are the 4 typical symptoms of symptomatic coeliac patients?

A

1) Anaemia
2) Chronic diarrhoea
3) Bloating
4) Chronic fatigue

81
Q

Why is diagnosis of coeliac disease difficult?

A

1) Can have atypical presentations/ non specific symptoms
2) Can have silent disease - positive serology, villous atrophy but no symptoms
3) Can have latent disease - positive serology but no villous atrophy

82
Q

What 2 other diseases is coeliac disease associated with?

A

1) Dermatitis herpetiformis - 10% of patients

2) Lymphocytic gastritis and lymphocytic colitis

83
Q

What 2 cancers is coeliac disease associated with?

A

1) Enteropathy- associated T-cell lymphoma

2) Small intestinal adenocarcinoma

84
Q

What is the gold standard diagnostic tool for coeliac disease?

A

Tissue biopsy (before and after having a gluten free diet)

85
Q

Which non invasive serological tests are used prior to biopsy in the diagnosis of coeliac disease?

A

1) IgA Ab to tissue transglutaminase (TGG)
2) IgA or IgG Ab to deamidated gliadin
3) Anti-endomysial Abs - highly specific but less sensitive

86
Q

What is the treatment for coeliac disease?

A

Gluten free diet - symptomatic treatment for most patient but also reduces the chances of long term complications

87
Q

What 4 long term complications of coeliac disease are reduced by taking a gluten free diet?

A

1) Anaemia
2) Female infertility
3) Osteoporosis
4) Cancer

88
Q

Helicobacter pylori is associated with…

A

Gastritis
Peptic Ulcer Disease
Gastric cancer

89
Q

NSAIDs commonly cause

A

gastric ulcers

90
Q

Gastric ulcers may harbour…

A

Adenocarcinoma

91
Q

How common is stomach cancer in the UK?

A

17th most common in the UK

92
Q

Coeliac disease is associated with which histopathological features?

A

Villous atrophy
Crypt elongation
Increased intraepithelial lymphocytes

93
Q

Common presentation of coeliac disease

A

Diarrhoea
Bloating
Malabsorption

CLINICAL PATHOLOGY (56 decks)

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