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Flashcards in GI Pathology Deck (89):
1

How long should a normal oesophagus be?

25 cm long muscular tube mostly lined by squamous epithelium

2

What are the two oesophageal sphincters?

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

3

What is distinct about the distal 1.5-2cm of the oesophagus?

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

4

Where is the squamo-columnar junction?

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

5

What are the causes of oesophageal inflammation?

Infectious
Bacterial, viral (HSV1, CMV), fungal (candida)
Chemical
Ingestion of corrosive substances
Reflux of gastric contents

6

What is the reflux of bile called?

duodeno-gastric reflux

7

What are the risk factors for reflux oesophagitis?

Defective lower oesophageal sphincter
Hiatus hernia
Increased intra-abdominal pressure
Increased gastric fluid volume due to gastric outflow stenosis

8

What is a hiatus hernia?

Abnormal bulging of a portion of the stomach through the diaphragm

9

Histologically, what would be seen in reflux oesophagitis?

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

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

10

What can be the complications from reflux oesophagitis?

Ulceration

Haemorrhage

Perforation

Benign stricture (segmental narrowing)

Barrett’s oesophagus

11

What is Barrett's oesophagus?

Cause:
Longstanding reflux

Risk factors:
Same as for reflux (male, Caucasian, overweight)

Macroscopy:
Proximal extension of the squamo-columnar junction

Histology:
Squamous mucosa replaced by columnar mucosa > “glandular metaplasia”

12

What are the types of columnar mucosa?

Gastric cardia type

Gastric body type

Intestinal type = “specialised Barrett’s mucosa”

13

Why is Barrett's oesophagus concerning?

Premalignant condition with an increased risk of developing adenocarcinoma

Regular endoscopic surveillance is recommended for early detection of neoplasia

14

How common is oesophageal carcinoma?

8th most common cancer in the world

15

What are the 2 histological types of oesophageal carcinoma?

Squamous cell carcinoma

Adenocarcinoma

16

Which gender is oesophageal adenocarcinoma more common in?

Male 7:1

17

What is the aetiology for oesophageal adenocarcinoma?

Barrett’s oesophagus
(tobacco, obesity)

18

Where are oesophageal adenocarcinomas usually found?

lower oesophagus

19

What does an oesophageal adenocarcinoma look like?

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

20

What are the risk factors for squamous carcinoma?

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

21

Where are squamous carcinomas most common?

Iran, China, South Africa, Southern Brazil

22

How are oesophageal cancers staged?

TNM system

23

How is the depth of invasion of the primary tumour scored?

pT1: tumour invades lamina propria, muscularis mucosae or
submucosa
pT2: tumour invades muscularis propria
pT3: tumour invades adventitia
pT4: tumour invades adjacent structures

24

How are the regional lymph node involvements scored?

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

25

What are the 4 anatomical regions of the stomach?

Cardia
Fundus
Body
Antrum

26

What features normally protect the stomach from gastritis>?

- Balance of aggressive
(acid) and defensive
forces
- Surface mucous
- Bicarbonate secretion
- Mucosal blood flow
- Regenerative capacity
- Prostaglandins

27

What factors can cause increased aggression of gastritis?

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

28

What factors can impair defences against gastritis?

- Ischaemia
- Shock
- Delayed emptying
- Duodenal reflux
- Impaired regulation of
pepsin secretion

29

What are the pathogenic mechanisms of autoimmune gastritis?

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

30

What are the pathogenic mechanisms of bacterial gastritis? (H.Pylori)

Cytotoxins
Liberation of chemokines
Mucolytic enzymes
?Ammonia production by bacterial urease
Tissue damage by immune response

31

What is the pathogenic mechanisms of NSAID gastritis?

Disruption of the mucus layer

32

What is the pathogenic mechanisms of bile reflux gastritis?

Degranulation of mast cells

33

What is Helicobacter Pylori?

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

34

Where in the stomach is H.pylori most common?

the antrum

35

What does h.pylori result in?

glandular atrophy, replacement fibrosis and intestinal metaplasia

36

What can be the complications of h.pylori infection?

Gastric ulcer
gastric cancer
MALT lymphoma
pre-pyloric gastric ulcer
duodenal ulcer

(however 85% patients have no complications)

37

What is peptic ulcer disease?

Localised defect extending at least into submucosa

38

What are the major sites of peptic ulcer disease?

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

39

What are the main etiological factors of peptic ulcer disease?

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

40

What is the histology of an acute gastric ulcer?

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

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

Granulation tissue at ulcer floor

41

What is the histology of a chronic gastric ulcer?

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

42

What are the complications possible with peptic ulcers?

Haemorrhage (acute and/or chronic anaemia)
Perforation peritonitis
Penetration into an adjacent organ (liver, pancreas)
Stricturing  hour-glass deformity

43

What are the main causes of gastric cancer?

Most frequently:
Adenocarcinoma

Less frequently:
Endocrine tumours
MALT lymphomas
Stromal tumours (GIST)

44

What is the incidence of gastric adenocarcinoma?

5th most common cancer in the World
(951,594 new cases/year)
Wide geographical variation (high rates in Eastern Asia, Andean regions of South America, Eastern Europe)
Steady decline over the past decades

45

What is the aetiology 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

46

What are the features of carcinoma of GOJ?

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

47

What are the risk features of carcinoma of gastric body/antrum?

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

48

What are the 2 main histological subtypes of gastric adenocarcinoma?

Scattered growth
- Diffuse type
- (signet ring cell ca)

Non-scattered growth
Intestinal type
(tubular adenocarcinoma)

49

What is coeliac disease?

Also known as Coeliac sprue or gluten sensitive enteropathy

Immune mediated enteropathy

50

How common is coeliac disease?

Fairly common, estimated prevalence of 0.5% to 1%

51

What is GLIADIN?

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

52

What are 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 

53

Why is diagnosis of coeliac disease 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

54

What are the clinical features and associations of coeliac disease?

No gender preference

Other disease associations
Dermatitis herpetiformis - 10% of patients
Lymphocytic gastritis and lymphocytic colitis

Coeliac disease and cancer
Enteropathy-associated T-cell lymphoma 
Small intestinal adenocarcinoma 
BEWARE!!!! Symptoms despite GFD

55

How is coeliac disease diagnosed?

Non-invasive serologic tests usually performed before biopsy
The most sensitive tests
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)

56

How is coeliac disease treated?

Gluten-free diet symptomatic improvement for most patients
Reduces risk of long-term complications including anaemia, female infertility, osteoporosis, and cancer

57

What are the types of IDIOPATHIC INFLAMMATORY BOWEL DISEASE?

ULCERATIVE COLITIS
CROHN’S DISEASE
INDETERMINATE COLITIS ( 10 – 15 % )

58

What is the epidemiology of IBD?

UC 5 – 15 cases per 100,000 p.a.
CD 5 – 10 cases per 100,000 p.a.

Incidence highest in Scandinavia, UK, Northern Europe, USA
Lower in Japan, Southern Europe, Africa

Peak age incidence 20 – 40 years of age

CD more common in females 1.3 : 1

UC equally common in males and females

Incidence of UC is increased in urban areas

59

What are other risk factors for IBD?

Cigarette smoking UC 0.5 x
CD 2 x
Oral Contraceptive UC 1.4 x
CD 1.6 x
Others eg. Childhood infections
MMR
domestic hygeine
appendicectomy

60

What is the clinical presentation of ulcerative colitis?

Diarrhoea ( > 66 % ) with urgency/tenesmus

Constipation (2 %)

Rectal bleeding (> 90%)

Abdominal pain (30 – 60 %)

Anorexia

Weight loss (15 – 40 %)

anaemia

61

What are the complications of ulcerative colitis?

Toxic megacolon and perforation
Haemorrhage
Stricture ( rare )
Carcinoma

62

What are the clinical features of Chrohn's disease?

Chronic relapsing disease
Affects all levels of GIT from mouth to anus
Diarrhoea ( may be bloody )
Colicky abdominal pain
Palpable abdominal mass
Weight loss / failure to thrive
Anorexia
Fever
Oral ulcers
Peri – anal disease
anaemia

63

What is the distribution of Crohn's disease throughout the GI tract?

Ileocolic 30 – 55 %
Small bowel 25 – 35 %
Colonic 15 – 25 %
Peri-anal / ano-rectal 2 – 3 %
Gastro – duodenal 1 – 2 %

64

What complications can arise from Crohn's disease?

Toxic megacolon
Perforation
Fistula
Stricture (common)
Haemorrhage
Carcinoma
Short bowel syndrome (repeated resection)

65

What are some hepatic manifestations of IBD?

Fatty change
Granulomas
PSC
Bile duct carcinoma

66

What are some skeletal manifestations of IBD?

Polyarthritis
Sacro-ileitis
Ankylosing spondylitis

67

What are some muco-cutaneous manifestations of IBD?

Oral apthoid ulcers
Pyoderma gangrenosum
Erythema nodosum
Ocular
Iritis/uveitis
Episcleritis
retinitis

68

What are some haematological manifestations of IBD?

Anaemia
Leucocytosis
Thrombocytosis
Thrombo-embolic disease

69

What are some renal and systemic manifestations of IBD?

kidney and bladder stones

amyloid and vasculitis

70

Risk factors for colo-rectal cancer in ulcerative colitis?

Early age of onset
Duration of disease > 8-10 years
Total or extensive colitis
PSC
Family History of CRC
? Severity of inflammation ( pseudopolyps )
Presence of dysplasia

71

What are colorectal polyps?

A “mucosal protrusion”
Solitary or multiple ( polyposis )
Pedunculated , sessile or “flat”
Small or large
Due to mucosal or submucosal pathology or a lesion deeper in the bowel wall

72

What are the types of colorectal polyps?

Neoplastic , hamartomatous , inflammatory or reactive
Benign or Malignant
Epithelial or Mesenchymal

73

What are the features of a hyperplastic polyp?

Common
1 – 5 mm in size
often multiple
located in rectum and sigmoid colon
small distal HPs have NO malignant potential

NB some large right sided “hyperplastic polyps” ( sessile serrated lesions ) may give rise to microsatellite unstable carcinoma ( 10 – 15 % all colorectal cancer )

74

What are the features of a juvenile polyp?

often spherical and pedunculated
10 – 30 mm
commonest type of polyp in children
typically occur in rectum & distal colon
sporadic polyps have no malignant potential

NB juvenile polyposis associated with increased risk of colorectal and gastric cancer

75

What is PEUTZ-JEGHERS SYNDROME?

Autosomal dominant condition ( mutation in STK11 gene on chromosome 19 )

Prevalence : 1 in 50,000 – 1 in 120,000 births

Present clinically in teens or 20s with abdominal pain ( intussusception ), gastro-intestinal bleeding & anaemia

Multiple gastro-intestinal tract polyps ( predominantly small bowel )

Muco-cutaneous pigmentation
( 1 – 5mm macules peri-oral , lips , buccal mucosa , fingers and toes )

76

What is the distribution of polyps in Peutz-Jeghers Syndrome?

Small bowel 96 %
Colon 27 %
Rectum 24 %
Stomach 24 %

NB polyps also described in gallbladder, urinary bladder and nasopharynx

77

What are some examples of benign neoplastic polyps?

Adenoma
Lipoma
Leiomyoma
Haemangioma
Neurofibroma

78

What are some examples of malignant neoplastic polyps?

Carcinoma
Carcinoid
Leiomyosarcoma
GIST
Lymphoma
Metastatic tumour

79

What are the features of colorectal adenomas?

Benign epithelial tumours
Commonly polypoid but may be “flat”
Precursor of colorectal cancer (at least 80%)
Present 25% - 35% population > 50 years
Multiple in 20 – 30 % patients
Evenly distributed around colon BUT larger in recto-sigmoid and caecum

80

A small % of adenomas progress to adenocarcinoma over an average of 10 – 15 years. What are some specific risk factors for this?

“flat” adenomas
Size ( most malignant polyps > 10 mm )
Villous & Tubulo-Villous
Severe ( high grade ) dysplasia
HNPCC associated adenomas

81

What are the statistics of colorectal cancer in the UK?

2nd or 3rd commonest cancer (mortality) after bronchus, breast and prostate

Lifetime risk 1 in 18 to 1 in 20

Estimated prevalence in UK 77,000

Incidence in UK 35,300

Mortality in UK 16,220

82

What are the risk factors for colorectal cancer?

Diet
- Dietary fibre, fat, red meat, folate, calcium

Obesity / Physical Activity

Alcohol

NSAIDs

HRT and oral contraceptives

Schistosomiasis

Pelvic radiation

Ulcerative colitis and Crohns disease

83

What is FAP?

inherited gene that increases susceptibility to colorectal cancer

84

What is HNPCC?

inherited gene that increases susceptibility to colorectal cancer

1 – 2 % all colorectal cancer
Autosomal dominant
50 - 70 % lifetime risk of large bowel cancer
Increased risk of endometrial, ovarian, gastric, small bowel, urinary tract and biliary tract cancer
Due to mutations in DNA mismatch repair genes

85

What is the most common type of colorectal cancer?

Adenocarcinoma (>95%)

86

What are the ways colorectal cancer can spread?

Direct invasion of adjacent tissues

Lymphatic metastasis (lymph nodes)

Haematogenous metastasis (liver & lung)

Transcoelomic ( peritoneal ) metastasis

Iatrogenic spread eg. needle track recurrence or port site recurrence

87

How are colorectal cancers staged?

Dukes stage
TNM stage

May be clinical ( imaging ) or pathological
Describes extent of local and distant tumour spread

88

What are Duke's stages?

Stage A : adenocarcinoma confined to the bowel wall with no lymph node metastasis

Stage B : adenocarcinoma invading through the bowel wall with no lymph node metastasis

Stage C : adenocarcinoma with regional lymph node metastasis regardless of depth of invasion

Stage D : distant metastasis present

89

What are the frequency and 5yr survival rates of the different Duke's stages?

A, 10 – 20 %, > 90 %

B, 30 – 40 %, 60 – 80 %

C, 40 – 50 %, 40 – 50 %

D, 15 – 25 %,