Gastric disease Flashcards
(43 cards)
1
Q
What is dyspepsia?
A
- A complex of upper GI symptoms which are typically present for 4+ weeks
- Includes upper abdominal discomfort, heartburn, acid reflux, nausea and/or vomiting
2
Q
What are the symptoms of gastro-oesophageal reflux disease?
A
- Heartburn
- Acidic taste (potential dental erosion)
- Cough and sore throat
- Can be asymptomatic
3
Q
What are the risk factors for GORD?
A
- Anything that causes increased intra-abdominal pressure
- Obesity
- Pregnancy
- Lower oesophageal sphincter dysfunction
- Hiatus hernia
- Delayed gastric emptying
4
Q
What is a hiatus hernia?
A
- Lower oesophageal sphincter herniates through diaphragm and ends up in thorax
- Lose crura muscles acting as a sling
- Not everyone with a hiatus hernia suffers from reflux
5
Q
Outline the mechanism of the lower oesophageal sphincter
A
- Muscular elements include intrinsic smooth muscles and diaphragm
- Normally contracted - only relax when food passes into stomach
- Right crus of diaphragm forms circular loop to close oesophagus off when pressure in stomach increases
- Oesophagus enters stomach at an acute angle
6
Q
What are the complications of GORD?
A
- Oesophagitis
- Ulceration
- Haemorrhage
- Strictures (can cause dysphagia)
- Metaplastic changes
7
Q
What is Barrett’s oesophagus?
A
- Reversible metaplastic change
- Stratified squamous epithelia of oesophagus changes to columnar epithelium of stomach
- Increased risk of dysplasia and adenocarcinoma
- Need regular endoscopies to check for further changes
8
Q
What lifestyle management is given to someone with GORD?
A
- Weight loss
- Avoid trigger foods
- Eat smaller meals
- Don’t eat then sleep
- Decrease alcohol and coffee consumption
- Stop smoking
9
Q
Which drugs might be prescribed for someone with GORD?
A
- Proton pump inhibitors for symptom relief and healing of inflammation
- H2 receptor antagonists
10
Q
What is the last resort treatment of GORD?
A
- Surgery - fundoplication
11
Q
What is gastritis?
A
- Inflammation of the stomach mucosa
- Inflammatory cells such as neutrophils invade lamina propria
12
Q
What are the symptoms of gastritis?
A
- Pain
- Nausea
- Vomiting
- Haemorrhage
13
Q
What are the causes of acute gastritis?
A
- NSAIDs
- High alcohol consumption
- Chemotherapy
- Bile reflux
14
Q
What are the causes of chronic gastritis?
A
- Infection with H pylori
- Autoimmune
15
Q
What pathological changes occur with acute gastritis?
A
- Epithelial damage
- Some epithelial hyperplasia
- Vasodilation - gives ‘angry looking’ appearance
- Neutrophil response
16
Q
What pathological changes occur with acute gastritis?
A
- Lymphocyte response in lamina propria
- Glandular atrophy of gastric glands
- Fibrotic changes
- Metaplastic changes
17
Q
Why does autoimmune chronic gastritis lead to anaemia?
A
- Antibodies to parietal cells
- Atrophy of parietal cells
- Decreased acid production and decreased intrinsic factor production
- Decreased absorption of vitamin B12 in ileum
- Leads to megaloblastic anaemia because vitamin B can’t be made in the body - it has to be absorbed
18
Q
Why does death of parietal cells lead to gastritis?
A
- Body of stomach atrophies
19
Q
What are the symptoms of chronic gastritis caused by an autoimmune condition?
A
- Anaemia
- Neurological symptoms
- Anorexia (loss of appetite)
- Glossitis
20
Q
Describe the properties of an H-pylori bacterium
A
- Helix shape
- Gram negative
- Microaerophilic (needs only a little O2 - stomach has prefect level)
21
Q
How does H pylori infect people?
A
- Faeco-oral
-Oral-oral - Navigates + adheres to mucosa/epithelial lining of stomach
22
Q
What are some of the key features of H. pylori?
A
- Flagellae
- Chemotaxis allows bacterium to find areas of lower acidity in stomach
- Adhesins allow bacteria to fix to gastric epithelia and resist peristalsis
23
Q
How does H. pylori produce ammonia?
A
- H. pylori contain urease enzyme that converts urea + water to CO2 + ammonia
- Ammonia de-acidifies local environment so bacteria can survive
- Ammonia toxic to epithelial cells
- Cells get damaged
24
Q
Why does H. pylori cause gastritis?
A
- Produces ammonia
- Produces mucinase - damages mucus layer
- Produces protease and lipase that breakdown structure of stomach
- Cytotoxin associated gene A
- Produces a protein that is inserted into stomach epithelium
- Generates a huge inflammatory response by stimulating interleukin B
25
How does H pylori cause damage in the stomach antrum?
- Antrum is where G cells are located
- Causes over-activity of G cells
- Increases gastrin production
- Increases number of parietal cells
- Increases acid production
- Chyme leaving stomach is more acidic
- Duodenum damaged
- Epithelium of duodenum changes to gastric epithelium
- Can lead to colonisation of duodenum
- Ulceration of duodenum
26
How does H pylori cause damage in the stomach body and/or fundus?
- Atrophy of parietal cells
- Precursor to dysplastic changes
- Increases risks of stomach cancer
27
What happens if H.pylori colonises the stomach antrum and body?
- Asymptomatic infection
28
How do we diagnose H. pylori?
- Urea breath test
- Patients ingest urea enriched with C13
- If H. pylori present, this urea is broken down into CO2 and ammonia
- C13 isotope is present in exhaled CO2
- Also stool antigen test and endoscopy with biopsy
29
How is H. pylori eradicated?
- Proton pump inhibitor
- And 2 antibiotics (e.g. clarithromycin and metronidazole)
- Side effects include diarrhoea and nausea
- Check after 7 days using urea breath test
- Treat for up to 14 days
30
What is peptic ulcer disease?
- Defect in the gastric or duodenal mucosa that extends through the muscularis mucosa
31
What are the common sites of peptic ulcer disease?
- Lesser curve and antrum of stomach
- Most commonly found in duodenum
32
Compare gastric and duodenal ulcers
gastric: duodenal
- Incidence = 1:3
- Age = increased: up to 35 years
- Social class = low: irrelevant
- Blood group = A:O
- Acid levels = normal/low: normal/high
- H. pylori = ~70%: 95-100%
33
Why is there increased incidence of duodenal ulcers with elevated acid levels?
- Overwhelms ability of small intestine to neutralise chyme
34
What are the defences of the stomach?
- Mucus layer
- Bicarbonate secretion
- Mucosal blood flow
- Prostaglandins
- Epithelial renewal
35
What are risk factors for peptic ulcer disease?
- H. pylori
- NSAIDs (decrease prostaglandin synthesis)
- Smoking (contributes to relapse)
- Massive physiological stress
36
What is the difference between acute and chronic ulcers?
- Acute ulcers develop as part of acute gastritis
- Chronic ulcers occur at mucosal junctions
37
Outline the morphology of peptic ulcer disease
- Most are <2cm
- Necrotic tissue found at base or ulcer
- Muscularis externa is replaced by scar tissue
- Ulceration can perforate wall of gut and cause peritonitis
- Scar tissue can narrow stomach lumen if ulceration is repeated
- Can lead to pyloric stenosis which causes extensive vomiting
38
What happens if an ulcer erodes into a blood vessel?
- Can erode into gastroduodenal artery
- Stomach fills up with blood
- Massive haematemesis
39
What is a sign of a relatively slow upper GI bleed?
- Malaena
- Haem component of blood is oxidised as it passes through GI tract
40
What are the symptoms of peptic ulcer disease?
- Epigastric pain leading to back pain following meals
- Pain at night (duodenal ulcers)
- Haematemesis/Malaena
- Early satiety
- Weight loss
41
How is peptic ulcer disease managed if it's due to H. pylori?
- Proton pump inhibitors
- 2x antibiotics
- Eradicate H. pylori to promote ulcer healing
42
How is peptic ulcer disease managed if it's not caused by H. pylori?
- Stop exacerbating medications
43
How do we treat active bleeding caused by peptic ulcer disease?
- Adrenaline injections
- Cautery
- Possible clip application
