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PATHOLOGY > Upper GI infections > Flashcards

Upper GI infections Flashcards

1
Q

what is the Z line in the normal oesophagus

A

oesophagus open to stomach
oesophagus lined by stratified squamous, non-keratising endothelium - then sharp change to stomach - gastrooesophageal junction

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2
Q

histology of eosophagus

A

Start stratified squyaemous epi
Muscularis mucosi
Oesophageal gland
Muscularis extra

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3
Q

macro structure of the stomach

A
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4
Q

histology of the body of the stomach

A
Columnar epi - produce mucus. Will get adenoca
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5
Q

histology of the antral stomach

A
Lacks the specialised cells
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6
Q

histology of normal duodenum

A
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7
Q

macro and micro pathology of acyte oesophagitis

A

Red swell pain loss of func heat

All acute inflam processes - neutrophils - lobular nuceli

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8
Q

summarise reflux oesophagitis/GORD

A

commonest cause of oesophagitis
reflux of acidic gastric contents

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9
Q

complications of reflux oesophagitis

A

ulceration
haemorrhage
perforation
stricture
barrett’s oesophagus - metaplastic process (one type change to another epi - it is REVERSIBLE) but is first step in change to oesophageal ca

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10
Q

summarise barratt’s oesophagus

A

metaplastic process (one type change to another epi - it is REVERSIBLE) but is first step in change to oesophageal ca
also called columnar oesophagus
squamous -> columnar

2 types:
* w/o goblet cells - gastric metaplasia
* w goblet cells - intestinal type metaplasia because no goblet cells in normal stomach - biggest risk to develop ca.

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11
Q

how do upper and lower GI vary in their pathogenesis to malignancy

A

Polyp RF for carcinoma in colon -> adenoma -> carcinoma IN LOWER GI

In upper GI - NO POLYPS;; squ epi -> metaplasia -> low grade dysplasia -> high grade -> adenoca. Also the same pathway in the stomach

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12
Q

summarise adenoca of oesophagus

A

commonest oesophageal carcinoma in developed countries
associated with reflux
lower oesophagus

Adeno in oesophagus because had metaplasua to columna from squamous cells
Adenoca make glands and secrete mucin

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13
Q

Summarise squamous cell carcinoma of the oesophagus

A

commonest in developing countries
associated with alcohol and smoking
mid/lower oesophagus
Most common in mid oesophagus - then lower - then upper

Ca would expect in the oesophagus - the cells that are there

Produces keratin (pink stuff) and strong intercellular bridges between the cells
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14
Q

summarise px of oesophageal carcinoma

A

poor px
dx of pre-invasive stage is important

Immunotheray is good and prognosis is getting better but it is still bad - therefore need to diagnose early

Persistant reflux triggers referral to endoscopy

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15
Q

cause of oesophageal varices and pathology

A

commonest - cirrhosis

high mortality when bleed

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16
Q

summarise gastritis

A

inflammation of gastric mucosa
acute gastritis - acute insult
chronic gastritis - chronic/persistent insult

17
Q

causes of acute gastritis

A

chemical
* aspirin, NSAIDs,
* alcohol
* corrosives

infection
* H pylori - will cause chronic but start as acute

18
Q

causes of chronic gastritis and where does each cause effect

A

autoimmune - antiparietal ab - body of stomach
bacterial - H pylori - stomach
Chemical - NSAIDs, bile reflux - antrum

19
Q

summarise H pylori associated gastritis

A

chronic gastritis +- acute exacerbations

metaplasia -> dysplasia

outcome - CLO-IM-dysplasia, adenocarcinoma, lymphoma (MALToma)

MALToma - monoclonal proliferation, if eliminate the H pylori the lymphoma will regress.

20
Q

summarise H pylori as a carcinogen

A

associated with increased risk of non-cardia gastric cancer

cag-A-positive H.pylori have a needle like
appendage that injects toxin into intercellular
junctions allowing the bacteria to attach more
easily.
This strain is associated with more chronic
inflammation.
Treatment of the infection with antibiotics
drastically reduces the risk of cancer

21
Q

other causes of gastritis

A

infection -
* CMV (immune suppressed with transplants) ,
* strongyloides (most severe in immunosuppressed)

IBD - Crohn’s disease - common in children

22
Q

why worry about gastritis

A

chronic gastritis -> intestinal metaplasia -> dysplasia -> cancer

In stomach - h pylori main cause - put any cause of chronic inflammation can cause it

23
Q

ix if have gastric ulcer

A

all biopsied to exclude malignancy

24
Q

difference between an erosion and ulcer

A

ulcer goes through the muscularis mucosi, erosiion is much more superficial

25
Q

complications of ulcer

A

bleeding -> anaemia and shock

perforation - peritonitis

26
Q

summarise intestinal metaplasia

A

intestinal metaplasia in gastric mucosa in response to long term damage

increased cancer risk

27
Q

summarise gastric epithelial dysplasia

A

abnormal epithelial pattern of growth
some histological and cytological features of malignancy - preinvasive stage of cacer, rasied nucleus, more mitosis

no invasion through membrane

lots of big nuclei
28
Q

epidemiology of gastric cancers

A

high incidence in japan, chile, italy, china, portugal, russia
>men
mosty are adenocarcinomas - form glands and secrete mucin s
Lymphomas are another kind of malignancy in stomach

The remaining 5% is made up of:
– Squamous cell carcinoma
– Lymphoma (MALToma)
– Gastrointestinal stromal tumour (GIST)
– Neuroendocrine tumours
* Overall survival rate is 15%

29
Q

classification of gastric adenocarcinoma

A

intestinal - well differentiated

diffuse - poorly differentiated (lintis plastica), includes signet ring cell carcinoma: no architecture, lost cohesion. Signet ring cells (white circles) - still making mucin but inside the cells. Single cells scattered all over place (Linitis plastica)

30
Q

summarise Gastrointestinal stromal tumour (GIST)

A

spindel cell tumour like sarcoma

vary from very benogn to very malignant

31
Q

px of gastric neuroendocrine tumours

A

poor

32
Q

summarise gastric MALToma/lymphoma

A

Chronic inflammation – Chronic immune stimulation
B cell (marginal zone) lymphocytes

Single clone - that makes lymphomas
B lymphocytes - marginal zone lymphocytes around edge of lymphoid follicle

rx – If limited to the stomach and H.pylori is
present: H.pylori eradication
If turn into high grade - have to treat them like normal high grade lymphomas

33
Q

pathophysiology of duodenal ulcer

A

In stomach h pylori is the commonest cause of gastric ulcer
Increased gastrin secretion associated with h pylori = increased acid secretion = spill into duodenum - produces changes: increased acid = gastric metaplasia cells replaced by gastric like mucosa - and now have gastric mucosa then H pylori happy
Almost all duodenal ulcers are associated with h pylori

34
Q

biopsy of duodenal ulcer - white cells

A

neutrophils

35
Q

other pathogens that cause duodenal ulcers

A
  • Immunosuppressed
    * CMV
  • Cryptosporidiosis
    * Giardia lamblia infection - one of commonest causes of travellers diarrhoea, treatable
  • Whipple’s disease -Tropheryma
    whippelii
36
Q

histology of malabsorption due to partial villous atropy

A

Villous atrophy

Crypt hyperplasia

Increased Intraepithelial lymphocytes
(normal range less than
20 lymphocytes /100
enterocytes)

*T cells damage epi -> atrophy -> crypt hyperplasia
Lymphocytes initiate the pathological process *

37
Q

Summarise coeliac disease

A

to dx need:
endomysial ab and tissue transglutaminase Ab

duodenal biopsy - atrophy if eating gluten, if not eating then normal villi
Early stage of coeliac - no atrophy but increased lymophocytes
If just stooped taking gluten - may have atrophy and normal lymphocytes

38
Q

causes of villous atrophy other than coeliac

A

Tropical sprue
Drugs can cause it

39
Q

summarise duodenal MALToma/lymphoma

A

coeliac -> increased risk of GIT ca

in duodenum

T cell origin - enteropathy associated T cell lymphoma

High grade T cell lymphoma - enteropathy associated T cell lymphoma

PATHOLOGY (94 decks)

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