Week 6 Upper Tract GI Flashcards Preview

Year 2 clinical pathology > Week 6 Upper Tract GI > Flashcards

Flashcards in Week 6 Upper Tract GI Deck (79)
1

What is the length of the oesophageus and what is it normally lined with?

25 cm long muscular tube mostly lined by squamous epithelium

2

Where are the spincters of the oesophagus found?

Sphincter at upper end (cricopharyngeal) and lower end (gastro-oesophageal junction)

3

What part of the oesophagus is lined by glandular mucosa?

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

4

Where is the squamo-columnar junction situated?

The squamo-columnar junction is usually located at 40 cm from the incisor teeth

5

What is Oesophagitis?

Inflammation of the oesophagus

6

What is the classifications of oesophagitis?

Acute
Chronic

7

What is the aetiology of oesophagitis?

Infectious--> not common unless you are immunocompromised
Bacterial, viral (HSV1, CMV), fungal (candida)

Chemical
Ingestion of corrosive substances
Reflux of gastric contents --> gastro reflux disease most common type

8

What is the commenst form of oesophagitis?

Reflux oesophagitis

9

What is the cause of reflux oesophagitis?

Caused by reflux of gastric acid (gastro-oesophageal reflux) and/or bile (duodeno-gastric reflux)

10

What are the risk factors of Reflux oesophagitis?

Defective lower oesophageal sphincter

Hiatus hernia  part of the stomach will herniate through the diaphragm to the thorax

Increased intra-abdominal pressure

Increased gastric fluid volume due to gastric outflow stenosis

11

What is the main clinical symptom of reflux oesophagitis and what is the possible complications?

Heart burn is the main symptom.

Ulceration
Haemorrhage
Perforation
Benign stricture (segmental narrowing)
Barrett’s oesophagus

12

Whata are the two types of hiatus hernia?

Sliding Hiatus Hernia
Paraesophageal hiatus hernia

13

What are the symptoms of sliding and paraesophageal hiatus hernia?

Sliding --> reflux symptoms

Para-oesophageal hernia --> strangulation which can lead to a lack of blood to that area and can get necrosis

14

What are the epithelial changes that takes place in reflux oesophagitis?

Squamous epithelium --> Basal cell hyperplasia, elongation of papillae, increased cell desquamation

Lamina propria -->Inflammatory cell infiltration (neutrophils, eosinophils, lymphocytes)

15

What is the cause of Barrett's oesophagus?

Longstanding reflux

16

Risk factors of Barrett's oesophagus?

Same as for reflux (male, Caucasian, overweight)

17

What is the macroscopic features of Barretts oeophagus?

Proximal extension of the squamo-columnar junction = caused by metaplasia = change from normal squamous lining to a columnar lining in the stomach --> this is trying to combat the acid content

18

What is the histological change in Barrett's oeophagus?

Squamous mucosa replaced by columnar mucosa > “glandular metaplasia

19

What are the types of columnar mucosa in Barrett's oeophagus?

Get a type of gastric epithelium that represents
Gastric cardia type
Gastric body type

Intestinal type = “specialised Barrett’s mucosa”

20

What is the importance of specialised barrett's mucosa in terms of diagnosis?

Characteristic feature of Barrett's oesophagus = Confirm diagnostic when you find this in the oesophageal tube

21

What is adenocarcinoma?

A malignant tumour formed from glandular structures in epithelial tissue

22

Barret's oesophagus increases the risk of what disease?

Barret’s oesophagus is a premalignant condition with an increased risk of developing adenocarcinoma of the oesophagus

23

How is neoplasia of the oesophagus detected?

Regular endoscopic surveillance is recommended for early detection of neoplasia

24

What is a treatment if you get adenocarcinoma of the oesophagus?

Replacement of the esophagostomy= remove it and then replace with colon

25

What is the disease progression from Barrett's oesophagus too adenocarcinoma?

Barrett's oesophagus --> low grade dysplasia --> high grade dysplasia --> adenocarcinoma

26

What are the two histological types of oesophageal carcinoma?

Squamous cell carcinoma --> originating from the normal oesophageal epithelium

Adenocarcinoma --> following on from Barrett's, originating from glandular epithelium

27

Where is incidence of adenocarcinoma highest?

Risen in industrial country due to increase in number of overweight people.
There is a ratio of 7;1 for males/female preponderance.
Hight incidence among caucasions

28

What is the aetiology of adenocarcinoma?

Barrett’s oesophagus
(tobacco, obesity)

29

Where is adenocarcinoma found and what is the macroscopic profile?
Finally how does spread and staging?

Localisation:
Lower oesophagus --> see the barest metaplasia

Macroscopy:
Plaque-like, nodular, fungating, ulcerated, depressed, infiltrating

Spread and staging:
Same as squamous cell carcinoma

30

How common is oesophageal carcinoma in the world?

It is the 8th most common cancer

31

What is more common squamous carcinoma or adenocarcinoma in the UK?

Adenocarcinoma?

32

What are the risk factors of Squamous carcinoma?

Tobacco and alcohol
Nutrition (potential sources of nitrosamines)
Thermal injury (hot beverages)
HPV
Male
Ethnicity (black)

33

What is the location of squamous carcinoma?

Middle and lower third (

34

What system is used for staging cancer and what does each part mean?

Use the TNM system
T--> depth of invasion of the primary tumour
N--> Regional lymph nodes
M --> distant metastasis

35

What are the different grades of T in the TNM system for Squamous carcinoma and adenocarcinoma staging?

pT1: tumour invades lamina propria, muscularis mucosae or submucosa
pT2: tumour invades muscularis propria thick muscle layer
pT3: tumour invades adventitia through the muscularis propria
pT4: tumour invades adjacent structures move outside the eosophageus

36

What are the different grades of N and M in the TNM system for Squamous carcinoma and adenocarcinoma staging?

pN0: no regional lymph node metastasis
pN1: regional lymph node metastasis in 1 or 2 nodes
pN2: regional lymph node metastasis in 3 to 6 nodes
pN3: regional lymph node metastasis in 7 or more nodes


M0: no distant metastasis
M1: distant metastasis

37

What are the 4 anatomcal regions of the stomach?

Cardia
Fundus
Body
Antrum

38

What are the 3 histological regions with different functions?

Cardia
Body
Antrum

39

What type of glands are found in the cardia and antrum of the stomach?

Mucous glands

40

What type of glands are found in the body of the stomach?

Body get specialist glands that produce the enzymes to digest

41

Normally how does a stomach balance beteen the aggressive acid and defences forces?

Surface mucous
Bicarbonate secretion
Mucosal blood flow Regenerative capacity Prostaglandins

42

What is a cause of increased aggression in the stomach?

Excessive alcohol-
Drugs --> NSAIDS
Heavy smoking
Corrosive
Radiation
Chemotherapy
Infection

43

What is a cause of impaired defences of the stomach?

Ischaemia --> reduction in mucosal blood flow
Shock
Delayed emptying
Duodenal reflux
Impaired regulation of pepsin secretion

44

Describe the type of bacteria H. Pylori is and its structure?

Gram negative spiral shaped bacterium
2.5-5.0 micrometres long
4 to 6 flagellae
Lives on the epithelial surface protected by the overlying mucus barrier

45

What is the actions of H.pylori?

Damages the epithelium leading to chronic inflammation of the mucosa

More common in gastric antrum than body

Results in glandular atrophy lead to replacement fibrosis over time and intestinal metaplasia

46

What are the complications of H.pylori?

Gastric ulcer = 2-5%
Duodenal ulcer = 10-15%

47

What is the 3 main aetiology category that causes chronic gastritis?

Autoimmune
Bacterial infection
Chemical injury

48

What is the pathogenic mechanism of autoimmune chronic gastritis?

Anti-parietal cell and anti-intrinsic factor antibodies
Sensitised T lymphocytes

49

What is the histological findings of autoimmune chronic gastritis?

Glandular atrophy in body mucosa intestinal metaplasia

50

What is the main histological findings of chronic gastritis caused by Bacterial infection?

1) Active chronic inflammation

2) Multifocal atrophy: Antrum> body intestinal metaplasia

51

What is the pathogenic mechanism for chronic Gastritis causd by NSAIDS and bile reflux?

NSAIDS --> disruption of the mucus layer

Bile reflux --> Degranulation of mast cells

52

Histological findings of oedema, vasolidation or paucity of inflammatory cells in chronic gastritis is due to?

Oedema --> NSAIDS
Vasolidation --> bile reflux
paucity of inflammatory cells --> Alcohol

53

What two cancers can be caused by H.pylori?

Gastric cancer
MALT lymphoma

54

What is peptic ulcer?

Localised defect extending at least into submucosa

55

What are the 3 major sites of peptic ulcers?

First part of duodenum
Junction of antral and body mucosa
Distal oesophagus (GOJ)

56

What is the 5 main aetiological factors of peptic ulcers?

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

57

What are the histological findings of acute gastric ulcers?

Full-thickness coagulative necrosis of mucosa (or deeper layers)

Covered with ulcer slough (necrotic debris + fibrin + neutrophils)

Granulation tissue at ulcer floor

58

What are the histological findings of chronic gastric ulcers?

Clear-cut edges overhanging the base

Extensive granulation and scar tissue at ulcer floor

Scarring often throughout the entire gastric wall with breaching of the muscularis propria

Bleeding

59

What are the 4 complications of peptic ulcers?

Haemorrhage (acute and/or chronic --> anaemia)

Perforation --> peritonitis --> through the full thickness of the wall

Penetration into an adjacent organ (liver, pancreas)

Stricturing --> hour-glass deformity

60

Is gastric or duodenal ulcer more common and what is the age distribution?

Duodenal ulcer is more common.

Gastric ulcer --> increase with age
Duodenal ulcer --> incrase up to 35 yrs

61

What are the acid levels in gastric and duodenal ulcers?

Gastric --> normal or low
Duoednal --> elevated or normal

62

How often does H.pylori caused Gastric and Duodenal ulcers?

Gastric --> 70% the other 30% is caused due to gastric cancer, chemicals, drugs

Duodenal -->95-100% ( predominatly in the antrum)

63

What blood groups is gastric ulcer and duodenal ulcers found in?

Gastric --> blood group A

Duodenal --> blood group O

64

What is the most common gastric cancer?

Adenocarcinoma

65

What are less frequent gastric cancers?

Endocrine tumours
MALT lymphomas
Stromal tumours (GIST)--> from stromal cells

66

How common is gastric adenocarcinoma in the world?

5th most common cacncer in the world

67

What are the causes of gastric adenocarcinoma?

Diet (smoked/cured meat or fish, pickled vegetables)

Helicobacter pylori infection

Bile reflux (e.g. post Billroth II operation)

Hypochlorhydria (allows bacterial growth)

~1% hereditary

68

What is the assoications with carcinoma of the gastroesophageal junction?

White males
- Association with GO reflux
- No association with H. pylori / diet
- Increased incidence in recent years with overweight individuals

69

What are the associations of carcinoma in the gastric body/atrum?

- Association with H. pylori
- Association with diet (salt, low fruit
& vegetables)
- No association with GO reflux
- Decreased incidence in recent years

70

What is the 2 main histological subtypes of gastric cancer and whata are there features?

Diffuse types (signet ring cell carcinoma) --> worse prognosis . Poorly differentiated. Scattered growth. Cadherin loss/mutation

Intestinal type ( tubular adenocarcinoma)
-well or moderately differentiated
May undergo intestinal metaplasia and adenoma steps

71

What type of gatric cancer is hereditary and what is teh mutation?

Hereditary diffuse type gastric cancer (HDGC)
Caused by Germline CDH1/E-cadherin mutation

72

What is the TNM staging for gastric cancer?

pT1: intramucosal or submucosal
pT2: into muscularis propria
pT3: through muscularis propria into subserosa
pT4: through serosa (peritoneum)or into adjacent organs

pN0: no lymph node metastases
pN1: 1 to 2 lymph node metastases
pN2: 3 to 6 lymph node metastases
pN3: more than 6 lymph node met.

M0: no distant metastases
M1: distant metastases present

73

What is Coeliac disease and what is its estimated prevalence?

Sensitivity to Gluten

Immune mediated enteropathy

Fairly common, estimated prevalence of 0.5% to 1%

74

What are the 2 pathogensis causes of coeliac disease?

Reaction to GLIADIN

Alcohol soluble component of gluten
Contains most of the disease-producing components
Induces epithelial cells to express IL-15

CD8+ Intraepithelial lymphocytes (IELs)

IL15 produced by the epithelium  activation / proliferation of CD8+ IELs
These are cytotoxic and kill enterocytes
CD8+ IELs do not recognise gliadin directly
Gliadin-induced IL15 secretion by epithelium is the mechanism 

75

What is the diagnosis of Coeliac disease?

Commonly affects adults between 30 and 60 years

No geneder preference

Diagnosis is often difficult
Atypical presentations / non specific symptoms
Silent disease
Positive serology / villous atrophy but no symptoms
Latent disease
Positive serology but no villous atrophy
Symptomatic patients
Anaemia, chronic diarrhoea, bloating, or chronic fatigue

76

What other diseases and cancer is coeliac disease associated with?

Disease:
Dermatitis herpetiformis - 10% of patients
Lymphocytic gastritis and lymphocytic colitis

Cancer:
Enteropathy-associated T-cell lymphoma 
Small intestinal adenocarcinoma 

77

What is the diagnosis of coeliac disease?

Non-invasive serologic tests usually performed before biopsy

The most sensitive tests--> serology test
IgA antibodies to tissue transglutaminase (TTG)
IgA or IgG antibodies to deamidated gliadin
Anti-endomysial antibodies - highly specific but less sensitive

Tissue biopsy is diagnostic (2nd biopsy after GFD) --> Gold standard

78

Treatment for Coeliac disease

Gluten-free diet --> symptomatic improvement for most patients

79

What are the long term consequences of coeliac disease if not treated?

Anaemia, female infertility, osteoporosis, and cancer