pathology of the stomach Flashcards
symptoms of gastritis
abdominal pain - ill defined, variable in severity
nausea
vomiting
occasionally erosive gastritis can lead too bleeding - haematemesis or malaena
gastritis characterised by site or aetiology
antrum
bondy/fundus
pangastritis
causes of gastritis
increased acid
infection disrupting protective barriers
chemical irritants
specific causes of gastritis
drugs
alcohol
bacterial infections
bile reflux
aggressive factors in gastritis
drug effect, bile, ischaemia, infection, acute stress (shock), chronic stress, allergy, toxic effects and direct trauma
3 types of microscopic morphology of gastritis
acute, chronic or active chronic
acute gastritis
neutrophils present
chronic gastritis
plasma cells present
active chronic gastritis
both acute and chronic inflammatory cells present
reactive/chemical gastritis
tends to occur in the gastric body around the greater curvature
thought to be due to the gastric contents settling here with gravity, combined with reduction in prostaglandin synthesis with NSAIDS
H. pylori gastritis is usually located
tends to be in the antrum, although may extend to involve the entire stomach
what does H pylori do
produced toxins and enzymes including urease, with catalyses breakdown of urea to ammonia and CO2, neutralising the acid and protecting the bacterium, but damaging the cells
macroscopic appearance of gastritis
erythema, mild oedema, sometimes erosions or frank ulceration
atrophic gastritis
chronic inflammation of the gastric mucosa causing a losss of the gastric glands
2 main causes of atrophic gastritis
H pylori and autoimmune gastritis
autoimmune gastritis
auto antibodies being produced against the parietal cells and/or against intrinsic factor
causes loss of acid secreting cells leading to low B12 and pernicious anaemia
atrophic gastritis is associated with
intestinal metaplasia and prominence of pyloric type glands, with hyper plastic foveae and reduction in mucosal folds
atrophic gastritis increases risk of
neuroendocrine tumours of the stomach as well as gastric carcinoma
why does pernicious anaemia result from autoimmune atrophic gastritis
no IF means B12 is not absorbed by the ileum
slow onset because it tales 3 years for the B12 stores in the liver to be depleted
location of h pylori associated atrophic gastritis
antrum
location of autoimmune atrophic gastritis
body
inflammatory infiltrate of H pylori atrophic gastritis
neutrophils, sub epithelial plasma cells
inflammatory infiltrate of autoimmune gastritis
lymphocytes and macrophages
serology of H pylori atrophic gastritis
antibodies to h pylori
serology of anutimmine atrophic gastritis
antibodies to parietal cells
sequelae of h pylori atrophic gastritis
peptic ulcer, adenocarcinoma, MALToma
sequelae of autoimmune atrophic gastritis
atrophy, pernicious anaemia, adenocarcinoma, carcinoid tumour
peptic ulcer disease
mucosal ulceration affecting the stomach (gastric ulcer) or duodenum (duodenal ulcer)
peptic ulcer most commonly caused by
H pylori
astral gastritis and ulceration is associated with increased gastric acid secretion and decreased duodenal bicarbonate secretion
caused of PUD
same causes as gastritis but additionally may be malignant ulcers associated with carcinoma
presentation of peptic ulcer disease
may be similar to gastritis
or may have epigastric burning or aching pain 1-3 hours after meals and at night, usually relieved by food
can also present with
- iron deficiency anaemia
- haemorrhage
- perforation (severe pain referred to back or chest, free gas under the diaphragm)
morphology of PUD
defect in the epithelium, firkin and inflammatory cells at surface, necrotic dibris and slough, extending into and sometimes through the wall
background changes or active chronic gastritis
chronic complications of peptic ulcer
dysplasia
carcinoma
H pylori associated peptic ulcer can cause
mucosal inflammation and inflammatory polyp
mucosal atrophy and intestinal metaplasia
lymphoid hyperplasia and MALT lymphoma
3 main complications of peptic ulcer disease
bleeding
perforation
obstruction
bleeding as a complication of PUD
most frequent complication
may be life threatening
may be the first indication of an ulcer
perforation as a complication of PUD
two third of ulcer related deaths
rarely a first indication
obstruction as a complication of PUD
mostly in chronic ulcers
secondary to oedema and scarring
causes incapacitating, crampy abdominal pain
can rarely cause total obstruction and intractable vomiting
benign gastric tumours
polyps - cystic funds gland polyp, hyperplastic polyp
gastric adenoma
malignant gastric tumours
carcinoma
MALT lymphoma
gastrointestinal stromal tumour
hyperplastic polyps
most common type of gastric polyp
not neoplastic
occur in chronic inflammation leading to mucosal prolapse and hyperplasia
can become ulcerated and bleed
can also become dysplastic especially when large
fundic gland polyp
occur in the fundus, cystic dilation of oxyntic glands
usually asymptomatic, increased incidence with proton pump inhibitors
only rarely become dysplastic
adenoma
morphology similar too colonic adenomas
neoplastic polyp with low or high grade dysplasia
gastric carcinoma
usually adenocarcinoma
incidence varies with geography - more frequent in Japan
gastric cancer is associated with
tobacco
low socio economic - untreated helicobacter can happen in these context
salted/smoked foods
clinical presentation of gastric cancer
metastasis often present at diagnosis, including regional nodes and with spread to supraclavicular sentinel lymph nodes
survival of gastric cancer
with surgical resection, the 5 year survival of early gastric cancer is 90% even if lymph node metastasis is present
5-year survival of advanced gastric cancer is less than 20%
in later cases efforts are usually focussed on chemotherapy, radiation and palliative care
2 main categories of gastric cancer
intestinal type adenocarcinoma
diffuse/poorly cohesive adenocarcinoma
intestinal type adenocarcinoma
develops from precursor lesions
mean age at presentation is 55 years, more common in males
chronic inflammation leading to increased risk of dysplasia
mutations that result in increased signalling in the Wnt pathways
diffuse adenocarcinoma
no identified precursor lesions
incidence is relatively uniform - similar prevalence in males and females
changes in CDH1 leading to silencing or loss of e-cadherin expression
leads to diffuse infiltration of the stomach wall leading to thickening of the wall
characteristic of cells of diffuse adenocarcinoma
signet ring morphology
loss of cadherin expression in diffuse adenocarcinoma
leads to poorly cohesive cells that infiltrate the stomach wall and undermine the. mucosa
MALT lymphoma
the spectrum of haematolymphoid tumours is largely the same throughout the GIT, however the frequencies differ in the various anatomical sites if the digestive system and some types are largely site specific
gastrointestinal stromal tumour
most common mesenchymal tumour of the abdomen
uncommon
slow growing usually diagnosed at 60 years of age
can occur anywhere in the GIt
arise from the interstitial cells of Cajal
gastrointestinal stromal tumour arises from which cells
interstitial cells of Cajal
predictors of behaviour of GI stromal tumours
location
tumour size
mitotic count
treatment of GI stromal tumour
complete surgical resection
molecular characteristics of GI stromal tumour
usually gain of function mutation in the RTK KIT
