pathology of the stomach Flashcards

1
Q

symptoms of gastritis

A

abdominal pain - ill defined, variable in severity
nausea
vomiting
occasionally erosive gastritis can lead too bleeding - haematemesis or malaena

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2
Q

gastritis characterised by site or aetiology

A

antrum
bondy/fundus
pangastritis

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3
Q

causes of gastritis

A

increased acid
infection disrupting protective barriers
chemical irritants

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4
Q

specific causes of gastritis

A

drugs
alcohol
bacterial infections
bile reflux

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5
Q

aggressive factors in gastritis

A

drug effect, bile, ischaemia, infection, acute stress (shock), chronic stress, allergy, toxic effects and direct trauma

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6
Q

3 types of microscopic morphology of gastritis

A

acute, chronic or active chronic

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7
Q

acute gastritis

A

neutrophils present

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8
Q

chronic gastritis

A

plasma cells present

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9
Q

active chronic gastritis

A

both acute and chronic inflammatory cells present

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10
Q

reactive/chemical gastritis

A

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

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11
Q

H. pylori gastritis is usually located

A

tends to be in the antrum, although may extend to involve the entire stomach

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12
Q

what does H pylori do

A

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

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13
Q

macroscopic appearance of gastritis

A

erythema, mild oedema, sometimes erosions or frank ulceration

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14
Q

atrophic gastritis

A

chronic inflammation of the gastric mucosa causing a losss of the gastric glands

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15
Q

2 main causes of atrophic gastritis

A

H pylori and autoimmune gastritis

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16
Q

autoimmune gastritis

A

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

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17
Q

atrophic gastritis is associated with

A

intestinal metaplasia and prominence of pyloric type glands, with hyper plastic foveae and reduction in mucosal folds

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18
Q

atrophic gastritis increases risk of

A

neuroendocrine tumours of the stomach as well as gastric carcinoma

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19
Q

why does pernicious anaemia result from autoimmune atrophic gastritis

A

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

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20
Q

location of h pylori associated atrophic gastritis

A

antrum

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21
Q

location of autoimmune atrophic gastritis

A

body

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22
Q

inflammatory infiltrate of H pylori atrophic gastritis

A

neutrophils, sub epithelial plasma cells

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23
Q

inflammatory infiltrate of autoimmune gastritis

A

lymphocytes and macrophages

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24
Q

serology of H pylori atrophic gastritis

A

antibodies to h pylori

25
Q

serology of anutimmine atrophic gastritis

A

antibodies to parietal cells

26
Q

sequelae of h pylori atrophic gastritis

A

peptic ulcer, adenocarcinoma, MALToma

27
Q

sequelae of autoimmune atrophic gastritis

A

atrophy, pernicious anaemia, adenocarcinoma, carcinoid tumour

28
Q

peptic ulcer disease

A

mucosal ulceration affecting the stomach (gastric ulcer) or duodenum (duodenal ulcer)

29
Q

peptic ulcer most commonly caused by

A

H pylori
astral gastritis and ulceration is associated with increased gastric acid secretion and decreased duodenal bicarbonate secretion

30
Q

caused of PUD

A

same causes as gastritis but additionally may be malignant ulcers associated with carcinoma

31
Q

presentation of peptic ulcer disease

A

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)

32
Q

morphology of PUD

A

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

33
Q

chronic complications of peptic ulcer

A

dysplasia

carcinoma

34
Q

H pylori associated peptic ulcer can cause

A

mucosal inflammation and inflammatory polyp
mucosal atrophy and intestinal metaplasia
lymphoid hyperplasia and MALT lymphoma

35
Q

3 main complications of peptic ulcer disease

A

bleeding
perforation
obstruction

36
Q

bleeding as a complication of PUD

A

most frequent complication
may be life threatening
may be the first indication of an ulcer

37
Q

perforation as a complication of PUD

A

two third of ulcer related deaths

rarely a first indication

38
Q

obstruction as a complication of PUD

A

mostly in chronic ulcers
secondary to oedema and scarring
causes incapacitating, crampy abdominal pain
can rarely cause total obstruction and intractable vomiting

39
Q

benign gastric tumours

A

polyps - cystic funds gland polyp, hyperplastic polyp

gastric adenoma

40
Q

malignant gastric tumours

A

carcinoma
MALT lymphoma
gastrointestinal stromal tumour

41
Q

hyperplastic polyps

A

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

42
Q

fundic gland polyp

A

occur in the fundus, cystic dilation of oxyntic glands
usually asymptomatic, increased incidence with proton pump inhibitors
only rarely become dysplastic

43
Q

adenoma

A

morphology similar too colonic adenomas

neoplastic polyp with low or high grade dysplasia

44
Q

gastric carcinoma

A

usually adenocarcinoma

incidence varies with geography - more frequent in Japan

45
Q

gastric cancer is associated with

A

tobacco
low socio economic - untreated helicobacter can happen in these context
salted/smoked foods

46
Q

clinical presentation of gastric cancer

A

metastasis often present at diagnosis, including regional nodes and with spread to supraclavicular sentinel lymph nodes

47
Q

survival of gastric cancer

A

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

48
Q

2 main categories of gastric cancer

A

intestinal type adenocarcinoma

diffuse/poorly cohesive adenocarcinoma

49
Q

intestinal type adenocarcinoma

A

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

50
Q

diffuse adenocarcinoma

A

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

51
Q

characteristic of cells of diffuse adenocarcinoma

A

signet ring morphology

52
Q

loss of cadherin expression in diffuse adenocarcinoma

A

leads to poorly cohesive cells that infiltrate the stomach wall and undermine the. mucosa

53
Q

MALT lymphoma

A

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

54
Q

gastrointestinal stromal tumour

A

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

55
Q

gastrointestinal stromal tumour arises from which cells

A

interstitial cells of Cajal

56
Q

predictors of behaviour of GI stromal tumours

A

location
tumour size
mitotic count

57
Q

treatment of GI stromal tumour

A

complete surgical resection

58
Q

molecular characteristics of GI stromal tumour

A

usually gain of function mutation in the RTK KIT