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MD3002 > gastrooesophageal ulcers > Flashcards

gastrooesophageal ulcers Flashcards

1
Q

what can cause acute oesophagitis

A

infection in immunocompromised patients: herpes simplex, candida, cytomegalovirus
corrosives

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2
Q

what can cause chronic oesophagitis

A
  • Tuberculosis
  • Bullous pemphigoid and Epidermolysis bullosa
  • Crohn’s disease

reflux oesophagitis

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3
Q

what can cause gastro-oesophageal reflux disease

A 
alchohol and tobacco 
obesity
caffeine 
hiatus hernia
motility disorder
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4
Q

what are the features of reflux oesophagitis

A 
Squamous epithelium damaged
– Eosinophils epithelial infiltration
– Basal cell hyperplasia
– Chronic inflammation
increased desquamation
ulceration, fibrosis, stricture, obstruction
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5
Q

what is barret’s oesophagus

A

lower oesophagus becomes lined with columnar epithelium

– Intestinal METAPLASIA
– ?Role of gastric/biliary reflux
– ?Role of Helicobacter pylori
• Premalignant - risk of adenocarcinoma of
distal oesophagus 100x general population

metaplasia due to chronic acid reflux

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6
Q

what is acute gastritis

A

inflammation of the stomach lining

due to chemical injury (NSAIDs or alcohol) or H. pylori

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7
Q

what can cause chronic gastritis

A

H. pylori
autoimmune
chemical

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8
Q

what do H. pylori look like

A

Gram negative spiral-shaped or curved bacilli

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9
Q

how is H. pylori treated

A

double antibiotics and proton pump inhibitors

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10
Q

what are the histological features of H.pylori infection

A

neutrophil infiltration
lymphoid aggregates with plasma cells infiltrate lamina propria

atrophy, fibrosis, metaplasia, gastric ulcer and gastric cancer

increased gastric acid secretion
duodenal ulcers

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11
Q

what are the two distribution patterns

A

involvement of antrum and body

or just antrum

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12
Q

how can H. pylori gastritis be detected

A

faecal bacteria, urea breath test, biopsy, urease test

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13
Q

what is reflux gastritis

A

regurgitation of bile and alkaline duodenal secretion
loss of epithelial cells with compensatory hyperplasia of foveolae
defective pylorus and motility disorders

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14
Q

what is Autoimmune Chronic Gastritis

A

Autoimmune reaction to gastric parietal cells
– Loss of acid secretion (hypochlorhydria / achlorhydria)
– Loss of intrinsic factor
• Vitamin B12 deficiency
• Macrocytic anaemia (Pernicious anaemia)
• Associated with marked gastric atrophy and intestinal
metaplasia
• Increased risk of gastric cancer
• Serum antibodies to gastric parietal cells and intrinsic
factor

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15
Q

what can cause peptic ulceration

A 
hyperacidity 
– H pylori gastritis
– Duodenal reflux
– NSAIDs
– Smoking
– Genetic factors
– Zollinger-Ellison syndrome

leads to a breach in the mucosal lining of the alimentary tract as a result of acid and pepsin attack

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16
Q

what are the complication of peptic ulcers

A 
– Haemorrhage
– Penetration of adjacent organs e.g. pancreas
– Perforation
– Anaemia
– Obstruction
– Malignancy
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17
Q

what is duodenal ulcer almost always caused by

A

helicobacter gastritis

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18
Q

what can lead to acute peptic ulceration

A

acute gastritis
stress response e.g. after severe burns
a result of extreme hyperacidity

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19
Q

where do chronic peptic ulcers tend to occur

A

at mucosal junctions

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20
Q

what leads to chronic peptic ulcers

A

hyperacidity

mucosal defence defects

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21
Q

what are the normal mucosal defences

A

mucus bicarbonate barrier

surface epithelium

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22
Q

what damages the mucus bicarbonate barrier

A

biliary reflux where bile refluxes into the stomach

23
Q

what damages the surface epithelium

A

NSAIDS

H. pylori

24
Q

what are the effects of gastric injury

A

necrotic debris
inflammation
granulation tissue
fibrosis

25
Q

what causes duodenal ulcers

A 
• Increased acid production
– More important than for gastric ulcer
– Can be induced by H pylori
• Reduced mucosal resistance
– Gastric metaplasia occurs in response to
hyperacidity
– Then colonised by H pylori
26
Q

what is the histologica appearance of gastric ulcers

A

• Usually small, sharply demarcated (punched out), defined structure, granulation tissue,

27
Q

what are the complications of duodenal ulcers

A

• ‘Bleed, burst or block’
• Penetration of adjacent organs e.g. pancreas
• Malignant change: rare in gastric ulcer and ‘never’ in
duodenal ulcer

28
Q

what immune cells are involved in reflux oesophagitis

A

eosinophils

29
Q

what type of epithelia is found in barret’s oesophagus

A

columnar

30
Q

is H. pylori gram neg or pos

A

negative bacilli

31
Q

how is H. pylori spread

A

oral- oral, faecal-oral or environment

32
Q

what are the features of antrum only H.pylori infection

A

increased gastric acid secretion

duodenal ulcer

33
Q

what are the features of antrum and body H. pylori

A

Atrophy, fibrosis, intestinal metaplasia

• Associated with gastric ulcer and gastric cancer

34
Q

what is the histological appearance of chemical gastritis

A

loss of epithelia with crypt hypertrophy

35
Q

what disease involves an autoimmune reaction to gastric parietal cells

A

autoimmune chronic gastritis

36
Q

what are the two features of autoimmune chronic gastritis

A

loss of acid secretion

loss of intrinsic factor

37
Q

what are the features of pernicious anaemia

A

macrocytic anaemia

B12 is needed in order to make RBCs

38
Q

what is the histological appearance of chronic autoimmune gastritis

A

gastric atrophy and intestinal
metaplasia

increased risk of stomach cancer

antiparietal and intrinsic factor antibodies

39
Q

what blood group is more likely to get a gastric ulcer

A

A

40
Q

what blood group is more likely to get a duodenal ulcer

A

O

41
Q

what social group is most likely to get a duodenal ulcer

A

even distribution

42
Q

what social group is most likely to get a stomach ulcer

A

5

43
Q

which are more common out of stomach and duodenal ulcers

A

duodenal ulcers are 3 times more common

44
Q

what acid levels predispose to a stomach ulcer

A

normal or low

45
Q

what acid levels predispose to a duodenal ulcer

A

normal or high

46
Q

how often is H. pylori found in gastric ulcers

A

about 70%

in duodenal ulcers almost always

47
Q

What is Curling’s ulcer

A

complication of severe burns due to ischaemia and necrosis

48
Q

what can cause acute gastric ulcers

A

acute gastritis
burns
hyperacidity e.g. gastrin secreting tumour

49
Q

what pathology destroys the mucus bicarbonate barrier

A

biliary reflux

50
Q

what are the histological features of ulcers

A

fibrosis
inflammation
granulation tissue
necrosis

51
Q

how common is cancer after having an ulcer

A

rare - stomach

‘never’- duodenum

52
Q

what could cause pernicious anaemia

A

autoimmune gastritis
due to anti parietal cell and anti intrinsic factor antibodies

glandular atrophy and intestinal metaplasia

53
Q

what is the histology of an H.pylori infection

A 
cytotoxins
immune response
atrophy 
intestinal metaplasia 
peptic ulceration
54
Q

what is biliary reflux

A

bile goes into your stomach

MD3002 (56 decks)

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