Gastro-Oesophgeal Inflammation and Peptic Ulceration Flashcards
(59 cards)
1
Q
Who is acute oesophagitis common in?
A
infection in immunocompromised patients
Corrosiveness (suicide attempt)
2
Q
What pathogens are responsible for acute oesophagitis?
A
- Herpes simplex viruses
- Candida
- Cytomegalovirus (CMV)
3
Q
Examples of specific chronic oesophagitis?
A
- Tuberculosis
- Bullous pemphigoid and Epidermolysis bullosa
- Crohn’s disease
4
Q
What is the most common nonspecific chronic oesophagitis?
A
reflux oesophagitis
5
Q
A
Oesophgeal inflammation
A. Multiple Herpetic Ulcers
B. Multinucleate squamous cells – Herpes virus inclusions
C. Cytomegalovirus Nuclear and cytoplasmic inclusion
6
Q
What is reflux oesophagitis?
A
- regurgitation of gastric contents
- squamous epithelium damaged
7
Q
What causes regurgitation of gastric contents?
A
- Gastro-oesophageal reflux disease (GORD)
- ‘Incompetent’ GO junction
8
Q
What can cause an ‘incompetent GO’ junction?
A
- Alcohol and tobacco
- Obesity
- Drugs e.g. caffeine!
- Hiatushernia
- Motility disorders
9
Q
What occurs when squamous epithelium is damaged?
A
- Eosinophils epithelial infiltration
- Basal cell hyperplasia
- Chronic inflammation
10
Q
A
11
Q
A
A. Scattered intraepithelial eosinophils
B. Eosinophilic esophagitis with basal zone hyperplasia
12
Q
What can severe reflux lead to?
A
ulceration
13
Q
What is stricture?
A
abdnormal narrowing of canal or duct in the body
14
Q
Describe Barrett’s Oesophagus
A
- Longstanding reflux
- Lower oesophagus becomes lined by columnar epithelium
- Intestinal metaplasia
- gastric/biliary reflux
- Helicobacter pylori (increases HCl production)
15
Q
Who is likely to get barrett’s oesophagus?
A
age 40-60
more common in men than women
16
Q
What does barrett’s oesophagus increase the risk of?
A
Premalignant - risk of adenocarcinoma of distal oesophagus 100x general population
17
Q
A
Barrett’s Oesophagus
18
Q
What is acute gastritis caused by?
A
- Chemical injury
- drugs (NSAIDs)
- alcohol (high %)
- corrosives
- Helicobacter pylori associated
- usually transient phase
- often become chronic
19
Q
What is H pylori? And how does it spread? How does it cause gastritis?
A
- Gram negative spiral-shaped or curved bacilli
- Oral-oral, faecal-oral, environmental spread
- Occupies protected niche beneath mucus where pH approx. neutral
- Does not colonise intestinal type epithelium
- Found in 90% of active chronic gastritis
20
Q
What is H pylori a causative factor for?
A
- gastritis and duodenal ulcers
- risk factor for gastric cancer (adenocarcinoma)
- Strong link with MALT (mucosa assoicated lymphoid tissue) lymphoma
21
Q
What are the associated symptoms of H pylori?
A
- Dyspepsia
- Atrophic gastritis
- Iron deficiency anaemia
- Idiopathic Thrombocytopenic Purpura
22
Q
What is produced by H pyrloi to raise the gastric pH and allow it to colonise?
A
urease
can produce bad breath
23
Q
Pethogenesis of H pylori
A
24
Q
What symptoms are assoicated with H pylori when it causes an acute infection?
A
nausea, dyspepsia, malaise and halitosis
25
How long does acute infection with H pylori tend to last?
2 weeks
26
What are the characterisitcs of the gastric mucosa with acute infection with H pylori?
Gastric mucosa is inflamed with neutrophils and inflammatory cells with marked persistent lymphocyte penetration
27
What does the outcome of H pyrlori as a chronic infection depend on?
* Pattern of inflammation
* Host response
* Bacterial virulence
* Environmental factors
* Patient age
28
* A. Helicobacter pylori silver stain
* B. Intraepithelial and lamina propria neutrophils infiltration
* C. Lymphoid aggregates, with plasma cells infiltrate in lamina propria
29
What are the 2 distribution patterns of H pyrloi associated with gastritis?
* Diffuse involvement of antrum and body
* Atrophy, fibrosis, intestinal metaplasia
* Associated with gastric ulcer and gastric cancer
* Antral but not body involvement
* Gastric acid secretion increased
* Associated with duodenal ulcer
30
What is chemical (reflux) gastritis caused by?
regurgitation of bile and alkaline duodenal secretion
31
What occurs in chemical (reflux) gastritis?
Loss of epithelial cells with compensatory hyperplasia of gastric foveolae
32
What is chemical (reflux) gastritis associated with?
* Defective pylorus
* Motility disorders
33
What occurs in autoimmune chronic gastritis?
* Autoimmune reaction to gastric parietal cells
* Loss of acid secretion (hypochlorhydria / achlorhydria)
* Loss of intrinsic factor
* Vitamin B12 deficiency
* Macrocytic anaemia (Pernicious anaemia)
34
What is autoimmune chronic gastritis assoicated with?
marked gastric atrophy and intestinal metaplasia
35
What does autoimmune chronic gastritis increase the risk of?
gastric cancer
36
What is the mechanism, histology and clinical implications of autoimmune chronic gastritis?
* Anti-parietal cell and intrinsic factor antibodies
* Glandular atrophy in gastric body, Intestinal metaplasia
* Pernicious anaemia
37
What is the mechanism, histology and clinical implications of bacterial infection chronic gastritis?
* Cytotoxins
* Immune response
* Active chronic inflammation
* Atrophy
* Intestinal metaplasia
* Peptic ulceration
* Gastric cancer
38
What is the mechanism, histology and clinical implications of chemical injury chronic gastritis?
* Direct injury
* disruption of mucus layer
* Foveolar hyperplasia
* few inflammatory cells
* gastri erosion
* gastric ulcer
39
What is peptic ulceration?
Breach in mucosal lining of alimentary tract as a result of acid and pepsin attack
40
What are the major sites of peptic ulceration (most to least common)
1. First part of duodenum
2. Junction of antral and body mucosa in stomach
3. Distal oesophagus
4. Gastro-enterostomy stoma (rare)
41
What are the aetiological factors of peptic ulceration
* Hyperacidity
* H pylori gastritis
* Duodenal reflux
* NSAIDs
* Smoking
* Genetic factors
* Zollinger-Ellison syndrome
42
What are the complications associated with peptic ulceration?
* Haemorrhage
* Penetration of adjacent organs e.g. pancreas
* Perforation
* Anaemia
* Obstruction
* Malignancy
43
Gastric Vs Duodenal Ulcer
- relative incidence
Gastric = 1
Duodenal = 3 (more common)
44
Gastric Vs Duodenal Ulcer
- Risk associated with age
Gastric = increases with age
Duodenal = increased up to 35 years
45
Gastric Vs Duodenal Ulcer
- Social Class
Gastric = higher in class V
Duodenal = evenly distributed
46
Gastric Vs Duodenal Ulcer
- Blood group
Gastric = A is more likely
Duodenal = O is more likely
47
Gastric Vs Duodenal Ulcer
- Acid levels
gastric = normal or low
duodenal = high or normal
48
Gastric Vs Duodenal Ulcer
- Helicobacter gastritis
Gastric = about 70%
Duodenal = 95-100%
49
What is an acute peptic ulcer related to?
* Related to acute gastritis
* Full thickness loss of epithelium, rather than just erosion
* Related to a stress response
* e.g. Curling’s ulcer following severe burns
* A result of extreme hyperacidity
* e.g. Gastrin-secreting tumours
50
Where do chronic peptic ulcers tend to occur?
at mucosal junctions e.g. antrum-body
51
What is the pathogenesis of a chronic peptic ulcer?
* Hyperacidity - not whole story
* Mucosal defence defects
52
What is the normal pH of gastric juice?
1-2
53
What are the normal mucosal defences?
* Mucus-bicarbonate barrier
* Surface epithelium - less important
54
What can be dissolved by biliary reflux?
mucus-bicarbonate barrier
55
What can damage the surgace epithelium in chronic gastric ulcers?
* Damaged by NSAIDs
* Injured by H pylori
56
Mechanism of gastric injury and protection
57
What is chronic duodenal ulcer caused by?
* • 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
58
What is the pathology of a chronic duodenal ulcer?
* Usually small (\<20 mm)
* Sharply ‘Punched out’ with defined edges
* Defined structure
* Granulation tissue at base
* Underlying inflammation and fibrosis
* Loss of muscularis propria
59
What are the complications assoicated with chronic duodenal ulcer?
* ‘Bleed, burst or block’
* Penetration of adjacent organs e.g. pancreas
* Malignant change: rare in gastric ulcer and ‘never’ in duodenal ulcer
