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Clinical Pathology > Pathology of the upper GI tract > Flashcards

Pathology of the upper GI tract Flashcards

1
Q

3 main conditions of oesophageal pathology

A

gastro-oseophageal reflux
Barrett’s oseophagus
Oseophageal carcinoma.

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2
Q

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

A

squamous epithelium

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3
Q

what are the names of the 2 oesophageal sphincters

A

cricopharyhgeal- upper end

Gastro-oseophageal- lower end.

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4
Q

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

A

glandular columnar

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5
Q

what is the length of the oesophagus

A

25 cm

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6
Q

where is the squamo-columnar junction located

A

about 40 cm from the incisor teeth.

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7
Q

what 3 histological layers can be found in the oesophagus

A

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

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8
Q

define oesophagitis

A

inflammation of the oesophagus

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9
Q

what causes oesophagitis

A

infection-bacterial, viral (HSV, CMV), fungal

chemical- ingestion of a corrosive substance, reflux of gastric contents.

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10
Q

commonest cause of oesophagitis

A

reflux of gastric acid or bile

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11
Q

risk factors for developing oesophagitis

A

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

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12
Q

define hiatus hernia

A

abnormal bulging of a portion of the stomach through the diaphragm

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13
Q

2 types of hiatus hernia

A

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

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14
Q

what histiological chafes occur in reflux oesophgitis

A

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

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15
Q

complications of reflux oesophagi tis

A

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

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16
Q

what is the main cause of barrett’s oesophagus

A

longstanding reflux

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17
Q

what is the main histological change in barrette’s oesophagus

A

proximal extension of the squamocolumnar junction.

squamous mucosa replaced by columnar mucosa.

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18
Q

what is the main difference between squamous and columnar epithelium

A

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

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19
Q

what are the 3 types of columnar mucosa in the GI

A

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

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20
Q

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

A

Contains goblet and paneth cells

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21
Q

what condition can barrett’s oesophagus predispose toe

A

adenocarcioma.

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22
Q

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

A

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

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23
Q

2 histiological subtypes of oesophageal carcinoma

A

squamous cell

adenocarcinoma

24
Q

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

A

tobacco, obesity

25
Q

which part of the oesophagus does adenocarcinoma occur?

lower, upper or middle

A

lower

26
Q

what is the macroscopic appearance of adenocarcinoma

A

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

27
Q

What are the main risk factors of squamous carcinoma

A 
–	Tobacco and alcohol
–	Nutrition (potential sources of nitrosamines)
–	Thermal injury (hot beverages)
–	HPV
–	Male
–	Ethnicity (black)
•
28
Q

which part of the oesophagus is shamus cell carcinoma

lower, upper or middles

A

upper and middle

29
Q

what is the pathogenesis of shamus carcinoma

A

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
Q

what are the macroscopic features of squamous cell carcinoma

A

ulcerative, stricture, polypoidal.

31
Q

what staging is used for oesophageal tumours

A

TNM staging

32
Q

What are the 3 main conditions which affects the gastric system

A

chronic gastritis
peptic ulceration
gastric carcinoma.

33
Q

4 anatomical regions of the stomach

A

cardia, fundus, body, antrum

34
Q

3 histological regions of the body

A

cardia, body and antrum

35
Q

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

A

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

36
Q

what causes the stomach lining defences to become impaired

A

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

37
Q

what 2 types of ulcers does H pylori cause

A

duodenal

gastric

38
Q

what type of bacteria is H pylori

A

• Gram negative spiral shaped bacterium

39
Q

main causes of peptic ulcer

A 
–	Hyperaciditiy
–	H.pylori infection
–	Duodeno- gastric reflux
–	Drugs- NSAID’s
–	Smoking
40
Q

which layers do peptic ulcers form in

A

mucosa and submucosa

41
Q

what are the main sites where peptic ulcers forms

A

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

42
Q

what is the histology of a acute gastric ulcer

A

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

43
Q

what is the histology of a chronic gastric ulcer

A

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
Q

what are the main complications of peptic ulcers

A

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

45
Q

what causes a gastric adenocarcinoma

A

– 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
Q

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

A

No

47
Q

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

A

Yes

48
Q

what is used to treat H pylori

A

PPI’s

49
Q

what are the macroscopic subtypes of gastricadenocarcinoma

A
  • Superficial exophytic
  • Flat of depressed
  • Superfical excavated
  • Exophytic
  • Linits plastic
  • Exacvated
50
Q

what are the main 2 histological subtypes of gastric adenocarcinoma

A

• 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
Q

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

A

• Germline CDH1/E-cadherin mutation

52
Q

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

A

gliadin

– Induces epithelial cells to express IL-15

53
Q

what is the pathogenesis of coeliacs

A

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

54
Q

what are the 3 different types of clinical presentation of coeliac

A

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
Q

what tests are used to determine coeliacs

A

• 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
Q

treatment for coeliacs

A

– Gluten-free diet à symptomatic improvement for most patients

Clinical Pathology (45 decks)

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