Upper GI infections Flashcards by Emily Southall

what is the Z line in the normal oesophagus

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

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histology of eosophagus

Start stratified squyaemous epi
Muscularis mucosi
Oesophageal gland
Muscularis extra

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macro structure of the stomach

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histology of the body of the stomach

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histology of the antral stomach

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histology of normal duodenum

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macro and micro pathology of acyte oesophagitis

Red swell pain loss of func heat

All acute inflam processes - neutrophils - lobular nuceli

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summarise reflux oesophagitis/GORD

commonest cause of oesophagitis
reflux of acidic gastric contents

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complications of reflux oesophagitis

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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summarise barratt’s oesophagus

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

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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summarise adenoca of oesophagus

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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Summarise squamous cell carcinoma of the oesophagus

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

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summarise px of oesophageal carcinoma

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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cause of oesophageal varices and pathology

commonest - cirrhosis

high mortality when bleed

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summarise gastritis

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

causes of acute gastritis

chemical
* aspirin, NSAIDs,
* alcohol
* corrosives

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

causes of chronic gastritis and where does each cause effect

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

summarise H pylori associated gastritis

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.

summarise H pylori as a carcinogen

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

other causes of gastritis

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

IBD - Crohn’s disease - common in children

why worry about gastritis

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

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

ix if have gastric ulcer

all biopsied to exclude malignancy

difference between an erosion and ulcer

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

complications of ulcer

bleeding -> anaemia and shock perforation - peritonitis

summarise intestinal metaplasia

intestinal metaplasia in gastric mucosa in response to long term damage increased cancer risk

summarise gastric epithelial dysplasia

abnormal epithelial pattern of growth some histological and cytological features of malignancy - preinvasive stage of cacer, rasied nucleus, more mitosis no invasion through membrane

epidemiology of gastric cancers

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%

classification of gastric adenocarcinoma

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)

summarise Gastrointestinal stromal tumour (GIST)

spindel cell tumour like sarcoma vary from very benogn to very malignant

px of gastric neuroendocrine tumours

poor

summarise gastric MALToma/lymphoma

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

pathophysiology of duodenal ulcer

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

biopsy of duodenal ulcer - white cells

neutrophils

other pathogens that cause duodenal ulcers

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

histology of malabsorption due to partial villous atropy

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 *

Summarise coeliac disease

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

causes of villous atrophy other than coeliac

Tropical sprue Drugs can cause it

summarise duodenal MALToma/lymphoma

coeliac -> increased risk of GIT ca in duodenum T cell origin - enteropathy associated T cell lymphoma

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Upper GI infections Flashcards

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