Pathology of the upper GI tract Flashcards Preview

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Flashcards in Pathology of the upper GI tract Deck (56):
1

3 main conditions of oesophageal pathology

gastro-oseophageal reflux
Barrett's oseophagus
Oseophageal carcinoma.

2

what is the epithelial lining of (most of) the oesophagus

squamous epithelium

3

what are the names of the 2 oesophageal sphincters

cricopharyhgeal- upper end
Gastro-oseophageal- lower end.

4

what is the epithelial lining of the lower 1.5-2 cm of the oesophagus

glandular columnar

5

what is the length of the oesophagus

25 cm

6

where is the squamo-columnar junction located

about 40 cm from the incisor teeth.

7

what 3 histological layers can be found in the oesophagus

mucosa- stratified squamous epithelium
submucosa-blood vessels
Muscularis Propria- muscle for contraction

8

define oesophagitis

inflammation of the oesophagus

9

what causes oesophagitis

infection-bacterial, viral (HSV, CMV), fungal
chemical- ingestion of a corrosive substance, reflux of gastric contents.

10

commonest cause of oesophagitis

reflux of gastric acid or bile

11

risk factors for developing oesophagitis

defective lower oesophageal sphincter
hiatus hernia
increased intra-abdominal pressure
increased gastric fluid volume due to gastric outflow stenosis

12

define hiatus hernia

abnormal bulging of a portion of the stomach through the diaphragm

13

2 types of hiatus hernia

sliding hernia- reflux symptoms
paraoesophageal hernia- strangulation, separate part of the stomach which requiresblood supply and as it does not receive it becomes necroized.

14

what histiological chafes occur in reflux oesophgitis

basal hyperplasia, elongation of papillae, increased cell desquamatation
lamina propria- inflammatory cells infiltrate.

15

complications of reflux oesophagi tis

ulceration- wearing of epithelium
haemorrages- goes through blood vessels.
perforation- goes through oesophageal wall.
benign stricture- where fibrosis occurs for healing.
barrett's oesophagus

16

what is the main cause of barrett's oesophagus

longstanding reflux

17

what is the main histological change in barrette's oesophagus

proximal extension of the squamocolumnar junction.
squamous mucosa replaced by columnar mucosa.

18

what is the main difference between squamous and columnar epithelium

column epithelium is more glandular (mucous secreting glands)- process is known as glandular metaplasia

19

what are the 3 types of columnar mucosa in the GI

gastric cardia type
gastric body type
intestinal type= specialised barrett's mucosa.

20

what is the main histiologically difference (in terms of cells) in between intestinal and gastric epithelium

Contains goblet and paneth cells

21

what condition can barrett's oesophagus predispose toe

adenocarcioma.

22

what is the pathogenesis to get from barrette's oesophagus to adenocarcinoma

barrett's oesophagus- basal rounded nuclei, goblet cells.
low grade dysplasia- nuclei are rounded and have goblet cells.
high grade dysplasia
Adenomcarcinoma- cells break through the basement membrane

23

2 histiological subtypes of oesophageal carcinoma

squamous cell
adenocarcinoma

24

Other than barrette's oesophagus name 2 other causes of adenocarcionoma

tobacco, obesity

25

which part of the oesophagus does adenocarcinoma occur?
lower, upper or middle

lower

26

what is the macroscopic appearance of adenocarcinoma

plaque like, nodular, fun gating, ulcerated, depressed, infiltrating, polypoidal (protrudes into lumen), stricture

27

What are the main risk factors of squamous carcinoma

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

28

which part of the oesophagus is shamus cell carcinoma
lower, upper or middles

upper and middle

29

what is the pathogenesis of shamus carcinoma

preceded by squamour dysplasia- nuclei are atypical and enlarged, mitosis rise towards the surface, but the basement membrane is not yet breached.
once basement membrane breached becomes carcinoma.

30

what are the macroscopic features of squamous cell carcinoma

ulcerative, stricture, polypoidal.

31

what staging is used for oesophageal tumours

TNM staging

32

What are the 3 main conditions which affects the gastric system

chronic gastritis
peptic ulceration
gastric carcinoma.

33

4 anatomical regions of the stomach

cardia, fundus, body, antrum

34

3 histological regions of the body

cardia, body and antrum

35

what causes increased aggression upon the gastric lining e.g. increased stomach acidity

excessive alcohol, drugs, heavy smoking, corrosive, radiation, chemotherapy, infection.

36

what causes the stomach lining defences to become impaired

ischaemia, shock, delayed emptying, duodenal reflux, impaired regulation of pepsin secretion

37

what 2 types of ulcers does H pylori cause

duodenal
gastric

38

what type of bacteria is H pylori

• Gram negative spiral shaped bacterium

39

main causes of peptic ulcer

– Hyperaciditiy
– H.pylori infection
– Duodeno- gastric reflux
– Drugs- NSAID’s
– Smoking

40

which layers do peptic ulcers form in

mucosa and submucosa

41

what are the main sites where peptic ulcers forms

first part of duodenum
junction of antral and body mucosa
distal oesophagus

42

what is the histology of a acute gastric ulcer

full thickness coagulative necrosis of mucosa
covered with ulcer slough- (necrotic debris, fibrin and neutrophils.)
Granulation tissue at ulcer floor
haemorrage.

43

what is the histology of a chronic gastric ulcer

clear cut edges overhang the base
extensive granulation and scar tissue on ulcer floor
scarring often throughout the entire gastric wall with breaching of muscularis propria
bleeding

44

what are the main complications of peptic ulcers

haemorrage
perfonation-peritonitis
penetration into a organ
stricturing- hour glass deformity (stomach is in 2 separate parts due to narrow stricture between them).

45

what causes a 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

Is carcinoma of the gastro-oesophageal junction caused by H-pylori and diet

No

47

is carcinoma of the gastric body or antrum associated with H pylori and diet

Yes

48

what is used to treat H pylori

PPI's

49

what are the macroscopic subtypes of gastricadenocarcinoma

• Superficial exophytic
• Flat of depressed
• Superfical excavated
• Exophytic
• Linits plastic
• Exacvated

50

what are the main 2 histological subtypes of gastric adenocarcinoma

• Scattered growth- diffuse (spreads) type (signet ring cell carcinoma)- POORLY DIFFERENTIATED
– Common in hereditary or lintis plastica.
• Non scattered type – intestinal type (tubular adenocarcinoma), forms glands like intestinal tumour.- WELL DIFFERENTIATED.

51

what mutation results in Hereditary diffuse type gastric cancer (HDGC)

• Germline CDH1/E-cadherin mutation

52

what molecule contains most of the disease producing part of coeliacs disease

gliadin
– Induces epithelial cells to express IL-15

53

what is the pathogenesis of coeliacs

gliadin induces epithelial cells to express IL-15.
this activates proliferation of CD8 and IELs.
These are cytotoxic and kill enterocytes.

54

what are the 3 different types of clinical presentation of coeliac

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

55

what tests are used to determine coeliacs

• IgA antibodies to tissue transglutaminase (TTG)
• IgA or IgG antibodies to deamidated gliadin
• Anti-endomysial antibodies - highly specific but less sensitive
biopsy before and after gluten free diet.

56

treatment for coeliacs

– Gluten-free diet à symptomatic improvement for most patients