tbl 2 stomach pathology Flashcards
Gastritis – a form of inflammatory mucosal injury
- Seen on endoscopy usually as __________ – can be confirmed by biopsy
- Histologically, we can classify gastritis based on the type of inflammatory cells
Acute (active): ________ seen
Chronic Chronic inflammatory cells seen
Acute on chronic (chronic active) Both neutrophils and chronic inflammatory cells seen
Gastropathy: Mucosal injury with ______________ but
inflammatory cells are few or absent
erythema and redness; Neutrophils; regenerative epithelial changes
Aetiology of gastritis
- Normally – 1st line of defence against damaging forces is mucous secreted by ________ cells that are impermeable to acid and pepsin
o _______ supports the production of mucus and bicarbonate
o Mucosal blood flow helps remove acid that has infiltrated the mucosa and ________ helps to remove H+ ions from cells
- In injury – balance is disrupted, leading to mucosal damage
o There is a decreased or absent mucous layer with damaged epithelium and chronic inflammatory cells at the __________
o If insult persists, injuries can persist to ulcers
foveolar; Prostaglandin; epithelial ion pumps; lamina propria
Classification of gastritis
- Acute gastritis: Often temporary due to injurious insult
- Chronic gastritis: Typically H. Pylori with a small subset of autoimmune conditions
- ___________ – bile reflux or drug-related e.g. NSAIDs
- Hypertrophic gastritis (rare)
- Special types: Lymphocytic, eosinophilic and granulomatous gastritis
- Erosions – focal loss of _______ leading to a superficial mucosal defect
- Ulcers – mucosal defect extending into _______ or deeper
o All ulcers begin as erosions but not all erosions progress to ulcers
Chemical gastritis; epithelium; submucosa
Acute gastritis
- Due to sudden abrupt mucosal injury
- Ranges from mild inflammation to multiple
erosions and deeper ulcers affecting all parts of stomach
- Chemical injury – NSAID, alcohol
- Stress related (ischaemic injury) – shock (stress ulcers), severe burns (______ ulcers), raised intracranial pressure (________)
- Based on severity –
acute, acute erosive, acute erosive haemorrhagic gastritis - Symptoms – asymptomatic to dyspepsia/
_________ pain/ hematemesis - Healing occurs after removal of the injurious agent
Curling’s; Cushing ulcers; epigastric
Chronic gastritis
- Due to H.pylori or autoimmune conditions (a smaller subset)
- Location – antral, corpus, _____ gastritis
- Histology – chronic inflammatory cells, glandular atrophy and _____ metaplasia, fibrosis
- Infiltrates include lymphocytes and plasma cells
- Atrophy – loss of glands (specialised glands in the body and mucosal glands in the ______) with eventual replacement by metaplasia, commonly intestinal metaplasia
- Pattern of involvement can be diffuse or patchy or multifocal
pan; intestinal; antrum
Chronic H. Pylori gastritis
- Chronic active gastritis with chronic inflammatory infiltrate in the superficial mucosa consisting mainly of plasma cells and lymphocytes
o In addition, active inflammation can be seen with ____________ in lamina propria. - Lymphoid follicles may be present
- Curved H. Pylori organisms clustered in the surface mucus overlying ____________ and within gastric pits
- Antrum is always affected – may progress to __________ at a later stage
o Atrophy with intestinal metaplasia, multifocal in chronic inflammation - H. Pylori gastritis can progress to –
o Pangastritis, leading to eventual _______ and carcinoma
o Antral-predominant gastritis, leading to ___________ due to hyperacidity
intraepithelial neutrophils; surface foveolar cells; pangastritis; dysplasia; duodenal ulcers
Helicobacter Pylori – adapted to colonise in the harsh acidic environment of the stomach
- Present on the surface of foveolar cells, residing on the thin layer of mucous
- ________ on the outer layer, flagella for motility in mucus
- Produces urease that produce ammonia, increases pH, increases ____________ (damages the DNA) – urease is implicated in the development of neoplasias
- Adhesins – adhere to foveolar cells
- Toxins and CagA – cytotoxic associated gene A that damages cells leading to gastritis
Lipopolysaccharides; nitrosated compounds
Chronic autoimmune gastritis
- Diffuse damage of oxyntic mucosa of the body and fundus due to chronic inflammatory infiltrate in the lamina propria especially in the deeper parts of the mucosa
- Leading to diffuse atrophy, intestinal metaplasia mainly affecting the ___________ (antrum is not affected)
- Hyperplasia of __________- cells
Atrophy – multifocal and diffuse
- Normal body fundus – surface foveolar epithelium and __________ secretory glands
- Body atrophy and intestinal metaplasia – expanded lamina propria and chronic inflammatory cells, less specialised gastric glands, surviving glandular tissue shows intestinal metaplasia
o Chronic atrophic gastritis of body mucosa with intestinal metaplasia
- Both H. Pylori infection and autoimmune gastritis can lead to atrophy
body and fundus; neuroendocrine; tightly packed
Comparison of H. Pylori and autoimmune gastritis
- H.pylori is located at the _____ while autoimmune is located at the ____________
- Acid in the H.pylori is increased to slightly decreased while acid is decreased in autoimmune
- Inflammatory cells in H.pylori are ____, ____ while those in autoimmune are ____, _____
- H. pylori vs antibodies vs ______ cells antibodies
- atrophy in H.pylori is ____ while that in autoimmune is ____
- sequelae: ulcer, Intestinal Metaplasia, adenocarcinoma, MALT, MALToma for H.pylori and atrophi, vitamin B12 deficiency, pernicious anaemia, IM, adenocarcinoma, endocrine cell hyperplasia, carcinoid in autoimmune.
antrum, body & fundus;
neutrophils and plasma cells; lymphocytes & macrophages;
parietal cells
multifocal; diffused
Hypertrophic gastropathy
- Giant gastric rugal folds on endoscopy, with no inflammation
- Hyperplasia of
o Foveolar cells – Menetrier’s disease (present with _____________), risk of adenocarcinoma
o Specialised gland layer – Zollinger Ellison syndrome – multiple intractable peptic ulcers, hyperacidity, gastrinomas, MEN
§ Gastrinomas – gastrin-secreting gastrinomas at the ______________
Protein losing enteropathy;
pancreas and the small intestine
Special types of chronic gastritis
- Lymphocytic gastritis (intraepithelial lymphocytes) – associations with _______
o Similar patterns can be seen in some cases of H. Pylori infection
- Granulomatous gastritis – idiopathic or systemic, isolated granulomas of the stomach
o Infectious causes such as ______ needs to be excluded
- Eosinophilic gastritis (eosinophilic infiltrate) – allergic, food intolerances; part of eosinophilic enteritis
celiac disease; Crohn’s
Cases of long standing gastritis
Chronic gastritis with intestinal metaplasia: Tall, pale columnar mucous containing foveolar cells replaced by columnar cells with _________ cytoplasm (enterocyte-like) with interspersed ______. Lamina propria shows chronic inflammatory infiltrate.
High grade dysplasia
- Complex, crowded
glands lined by __________ nuclei and loss of ______. Both cytological and architectural changes are seen
Low grade dysplasia
- Atypical glands,
cells with hyperchromatic
basal nuclei
eosinophilic; goblet cells
hyperchromatic; polarity
Complications of chronic gastritis
- Peptic ulcer disease – especially with H. pylori or _______
- Intestinal metaplasia
- Dysplasia – low / high grade
- Adenocarcinoma
- Induced mucosa associated lymphoid tissue (MALT) (with H. pylori) later turning malignant which is ________
hyperacidity; lymphomas
Peptic ulcer disease
- Stomach or first part of duodenum or distal oesophagus – mucosa exposed to potentially injurious effects of acid and _______
- Causes – hyperacidity (important for development of
duodenal ulcers), H. pylori (PUD can also develop in
cases with low acid levels), infection, drugs (NSAID) or
smoking, reflux (_________ appears to be an important factor for gastric ulcerations)
- Peptic ulcers – clean and sharply punched out with radiating ___________, usually solitary (if multiple, may be indicative of ZES)
o ________ ulcers are more common than gastric ulcers (4:1) – H. Pylori accounts for >90%in duodenal and 70% in gastric ulcers
o Microscopy – ulceration with underlying granulation tissue and fibrosis, thick walled blood vessels with ____________ (erosion of these vessels may lead to haemorrhages)
- Mucosal defect extending into the submucosa with necrotic debris at the base,
underlying an acute infection
o Granulation tissue merging into fibrosis lying below
- Complications of PUD –
o Bleeding – 20%, commonest complication (25% of deaths)
o Penetrate full thickness
§ Can erode into pancreas or liver
§ Perforation of free wall of stomach – 5% (30% of deaths)
o Obstruction – rare 2%, in chronic ulcers with fibrosis, pylorus
§ Especially in the duodenum and pylorus – healing by fibrosis leads to
strictures resulting in gastric outlet syndrome
pepsin; bile reflux; rugal folds
Duodenal; endarteritis obliterans
Peptic ulcer disease
- Stomach or first part of duodenum or distal oesophagus – mucosa exposed to potentially injurious effects of acid and _______
- Causes – hyperacidity (important for development of
duodenal ulcers), H. pylori (PUD can also develop in
cases with low acid levels), infection, drugs (NSAID) or
smoking, reflux (_________ appears to be an important factor for gastric ulcerations)
- Peptic ulcers – clean and sharply punched out with radiating ___________, usually solitary (if multiple, may be indicative of ZES)
o ________ ulcers are more common than gastric ulcers (4:1) – H. Pylori accounts for >90%in duodenal and 70% in gastric ulcers
o Microscopy – ulceration with underlying granulation tissue and fibrosis, thick walled blood vessels with ____________ (erosion of these vessels may lead to haemorrhages)
- Mucosal defect extending into the submucosa with necrotic debris at the base, underlying an acute infection
o Granulation tissue merging into fibrosis lying below
- Complications of PUD –
o Bleeding – 20%, commonest complication (25% of deaths)
o Penetrate full thickness
§ Can erode into pancreas or liver
§ Perforation of free wall of stomach – 5% (30% of deaths)
o Obstruction – rare 2%, in chronic ulcers with fibrosis, pylorus
§ Especially in the duodenum and pylorus – healing by fibrosis leads to strictures resulting in ________________
pepsin; bile reflux; rugal folds
Duodenal; endarteritis obliterans
gastric outlet syndrome
