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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
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

Clinical Pathology (45 decks)

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