Gastritis, peptic ulcers and celiac's disease Flashcards
How does chemical gastritis appear histologically?
Long, turtuous gastric pits
hyperplasia of lamina propria
What are the 5 possible complications of chronic peptic ulcers?
Perforation - if there aren’t organ overlying > generalised peritonitis > septicaemia
Penetration - acid into overlying organ (pancreas, liver or colon)
Stenosis - due to scar
Haemorrhage (rapid or slow) - if an artery is eroded
Neoplasm
What are some other causes of intraepithelial lymphocytosis, villi atrophy and crypt hyperplasia?
Tropical sprue
Small bowel bacterial overgrowth
Certain Immunodeficiency
What is acute gastritis characterised by?
Acute bleeding
Erosion of epithelium
Local inflammation/oedema
How are prostaglandins protective in the stomach?
Inhibit gastric acid secretion
Stimulate mucous and bicarbonate secretion
Increase mucosal blood flow
Modifiy local inflammation
What happens if gluten peptide passes through the epithelium?
It is deaminated by tissue transglutaminase (tTG) converting glutamine into negatively charged glutamate
Where do H. pylori bacteria sit during infection?
Gastric cell surface and intercellular junctions
What pattern of scarring is left post gastric ulceration?
Radial
What are the three main types of ulcers?
A - Autoimmune
B - Helicobacter pylori
C - Chemicals
How does H. pylori survive in the acid environment of the stomach?
Colonises the mucosal barrier
What can damage the mucosal barrier?
Helicobacter pylori
Alcohol
NSAIDs
Bile
Which cells are targeted in autoimmune gastritis?
Parietal
What can form in the stomach in pan gastritis that usually aren’t present?
MALT and subsequent B cell lymphomas
How does damage occur in celiac disease?
CD4+ cells releasing TNF-alpha and IL-4
CD8+ cell inducing apoptosis
What on parietal cells do antibodies in autoimmune gastritis target?
Na/K ATPase
Intrinsic factor
Gastrin receptor
T/F The lamina propria contains continual mild inflammation?
True
Where in the GIT is glucose absorbed?
Duodenum
What is the ratio of the villi length to crypt length in the duodenum?
4:1
What is the clinical presentation of celiac’s diseaese?
GI symptoms: diarrhoea, vomiting, bloating, flatulance
Anaemia vitamin deficiences
Lethargy
Failure to thrive as infant
Other immunopathologies
Osteoporesis
Malabsorption of nutrients
HCl reaching the lamina propria causes what?
Activation of mast cell to produce histamine inflammatory mediators
What is the significance of the overhang of folds over the ulcerated tissue in chronic peptide ulcers?
Carcinomas don’t have that
Chronic *H. pylori *infection and inflammation can lead to what serious sequelae?
Atrophy
Metaplasia > hyperplasia > adenocarcinoma
Lymphoma
What are valves of Kerckring another name for?
Circular folds/plica circulares
In which type of gastritis is gastric acid secretion the greatest?
Antrum-predominant
In what cause of acute gastritis is there particularly low amounts of inflammation?
NSAID caused
What is chemical gastritis caused by?
Reflux of bile and alkaline duodenal juices into the antrum of the stomach
What environmental factors contribute to the development of celiacs
Exposure to gluten (eg too much too soon)
Breast milk is protective
Infections
Why is healing in response to acute gastritis quick?
Due to rapid turn over of gastric epithelium 24-48 hours
What are the two patterns of gastritis?
Antrum-predominant
Pan gastritis
What are the peak ages of development of celiac disease?
30-50
T/F Everyone with HLA-DQ2 and DQ8 have celiac disease and everyone with the disease have them?
False, 20-30% of the population at risk don’t have disease despite having the HLA subtypes.
The latter is true
What makes a peptic ulcer different from mucosal erosion?
Peptic ulcers penetrate through the muscularis mucosae
What does IELs stand for?
Intra-epithelial lymphocytes
What are three methods of diagnosis for celiac disease?
Serology for anti tTG or
Genetic testing for HLAs
Biopsy of intestine after gluten ingestion
Which organ is most effected in celiac’s disease?
Small intestine
What is the average rate of H. pylori infection the developing world?
>80%
What colonisation factors does H. pylori have?
Adhesins
Motility
Urease
Microaerophilism
Do acute peptic ulcers leave radial scars on healing?
No, there is restoration of submucosa and mucosa
What HLA subtypes are strongly associated with the development of celiac’s disease? In which ethic groups are they most prevalence?
HLA-DQ2, -DQ8
European and Middle Eastern
Are IELs CD4 or CD8?
CD8
In what age group in chronic inflammation causing cancer most prominent?
>70+ y.o.
How does the body of the stomach look histologically in autoimmune gastritis?
Loss of secreting tubules
Greater number of goblet and neuroendrocrine cells
Chronic inflammation
Where in the GIT is vitamin B12 most absorbed?
Ileum
What is the problem is not diagnosing celiacs disease?
It increases the risk of:
MALT lymphoma (x30)
Oesophageal cancer
S. intestine adenocarcinoma
Overall mortality (x2)
What can happen to the duodenum in antrum-predominant gastritis?
It changes to become more like the stomach > H. pylori can infect it
What does Marsh type II celiac’s disease look like?
Increase IELs
Longer, branched crypts
Villi still present but fatter with immune cell infiltration
What are Cushing ulcers? What are they caused by?
Ulcers in the stomach or duodenum in response to head injury
How does autoimmune gastritis cause anaemia?
Low intrinsic factor > No B12 absorption > Anaemia
What happens to villi and crypts in advanced celiac disease?
Villis disappear
Crypts lengthen
Does H. pylori usually cause acute gastritis?
No, usually chronic, not self limiting
What contributes to pain in chronic peptic ulcers?
Hypertrophied nerves
How is gluten able to remain intact and get through the epithelium to act as an antigen?
It is high in proline (35%) and glutamine (20%) that are resistant to acids and proteases
In terms of percentage of the total, does *H. pylori *cause more duodenal ulcers or gastric ulcers?
Duodenal
What happens to microvilli in celiac’s disease?
Distort, shorten, completely lost
How is celiac histology characterised in Marsh’s system?
Three types
In chronic peptic ulcers, how far does the damage go?
Through the muscularis externa and up to the serosa
Why do crypts lengthen in celiac disease?
Zone of proliferation are lengthing to compensate for cell loss
After a head injury, what are drug patients in ICU put on?
Proton pump inhibitors
T/F Stem cell zones in crypts are where most cell replication in the small intestines occur?
False, it’s in zones of proliferation above the stem cell zones
In terms of immune cells what happens in celiac disease?
More IELs, more plasma cells in the lamina propria
What is a Curling’s ulcer? What is it in response to?
An acute peptic ulcer
Burns
Acute gastritis is usually caused by what? Examples?
Acute sources of damage
eg Alcohol
Aspirin
Toxins
Burns
Shock
Head injury
Septicaemia
Staphlyococcal poisoning
How does the antrum of the stomach look histologically in autoimmune gastritis?
Normal, it’s uneffected
What is the ratio of IELs to enterocytes in normal duodenum?
1:5
What is the second highest cause of gastric and duodenal ulcers?
NSAIDs
At what point to antibodies appear in *H. pylori *infection?
Post 4 weeks
What is the term given to acute *H. pylori *infection?
Neutrophilic gastritis
What is the problem with negatively charged glutamate?
It bind efficiency to HLA-DQ2 and 8 therefore is presented T cells
How does the small intestine respond to greater cell loss?
Increase the size of the zone of proliferation
