gastrooesophageal ulcers Flashcards

(54 cards)

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
what causes duodenal ulcers
``` • 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
what is the histologica appearance of gastric ulcers
• Usually small, sharply demarcated (punched out), defined structure, granulation tissue,
27
what are the complications of duodenal ulcers
• ‘Bleed, burst or block’ • Penetration of adjacent organs e.g. pancreas • Malignant change: rare in gastric ulcer and ‘never’ in duodenal ulcer
28
what immune cells are involved in reflux oesophagitis
eosinophils
29
what type of epithelia is found in barret's oesophagus
columnar
30
is H. pylori gram neg or pos
negative bacilli
31
how is H. pylori spread
oral- oral, faecal-oral or environment
32
what are the features of antrum only H.pylori infection
increased gastric acid secretion | duodenal ulcer
33
what are the features of antrum and body H. pylori
Atrophy, fibrosis, intestinal metaplasia | • Associated with gastric ulcer and gastric cancer
34
what is the histological appearance of chemical gastritis
loss of epithelia with crypt hypertrophy
35
what disease involves an autoimmune reaction to gastric parietal cells
autoimmune chronic gastritis
36
what are the two features of autoimmune chronic gastritis
loss of acid secretion | loss of intrinsic factor
37
what are the features of pernicious anaemia
macrocytic anaemia | B12 is needed in order to make RBCs
38
what is the histological appearance of chronic autoimmune gastritis
gastric atrophy and intestinal metaplasia increased risk of stomach cancer antiparietal and intrinsic factor antibodies
39
what blood group is more likely to get a gastric ulcer
A
40
what blood group is more likely to get a duodenal ulcer
O
41
what social group is most likely to get a duodenal ulcer
even distribution
42
what social group is most likely to get a stomach ulcer
5
43
which are more common out of stomach and duodenal ulcers
duodenal ulcers are 3 times more common
44
what acid levels predispose to a stomach ulcer
normal or low
45
what acid levels predispose to a duodenal ulcer
normal or high
46
how often is H. pylori found in gastric ulcers
about 70% in duodenal ulcers almost always
47
What is Curling's ulcer
complication of severe burns due to ischaemia and necrosis
48
what can cause acute gastric ulcers
acute gastritis burns hyperacidity e.g. gastrin secreting tumour
49
what pathology destroys the mucus bicarbonate barrier
biliary reflux
50
what are the histological features of ulcers
fibrosis inflammation granulation tissue necrosis
51
how common is cancer after having an ulcer
rare - stomach | 'never'- duodenum
52
what could cause pernicious anaemia
autoimmune gastritis due to anti parietal cell and anti intrinsic factor antibodies glandular atrophy and intestinal metaplasia
53
what is the histology of an H.pylori infection
``` cytotoxins immune response atrophy intestinal metaplasia peptic ulceration ```
54
what is biliary reflux
bile goes into your stomach