Gastric Disease Flashcards
1
Q
Give 3 common gastric disorders
A
- Gastro-oesophageal reflux disease (GORD)
- Peptic ulcer disease (PUD)
- Helicobacter pylori infection
2
Q
What are the anti-reflux mechanisms to prevent reflux of gastric acid into the lower oesophagus?
A
- Lower oesophagus sphincter
- Oesophagus enters stomach in abdominal cavity
- Pressure in abdominal cavity is higher than that of thoracic
- Right crus of diaphragm acts as slight around the lower oesophagus
3
Q
What state is the lower oesophagus sphincter usually in?
A
Closed
4
Q
What happens to the lower oesophageal sphincter as part of the physiology of swallowing?
A
It transiently relaxes
5
Q
Why does the lower oesophageal sphincter transiently relax?
A
To allow the bolus to move into the stomach
6
Q
Label this diagram, indicating the main antireflux mechanisms on the right
A
- A - Fundus
- B - Cardia
- C - Body
- D - Antrum
- E - Pylorus
- F - Duodenum
- Peristalsis
- Diaphragm
- Lower oesophageal sphincter
- Intra-abdominal oesophagus
- Mucosal valve
- Unumpeded gastric emptying
7
Q
Is acid reflex ever normal?
A
Yes, some is
8
Q
How is mild acid reflex normally dealt with?
A
- Secondary peristaltic waves
- Gravity
- Salivary bicarbonate
9
Q
When do clinical features of GORD occur?
A
When antireflux mechanisms fail and there is prolonged contact of gastric juices with the lower oesophageal muscosa
10
Q
What are the clinical features of GORD?
A
Dyspepsia
11
Q
What is dyspepsia?
A
Heartburn
12
Q
What makes dyspepsia from GORD worse?
A
- Lying down
- Bending over
- Drinking hot drinks
13
Q
How is a clinical diagnosis of GORD usually made?
A
Without investigation- based on symptoms alone
14
Q
When is there a need to investigate GORD?
A
- When there are alarming symptoms, such as dysphagia
- When hiatus hernia is suspected
15
Q
What investigation is made when a hiatus hernia is suspected?
A
Endoscopy
16
Q
What are the two areas of management for GORD?
A
- Lifestyle
- Medication
17
Q
What lifestyle changes can be made to manage GORD?
A
- Loose weight
- Stop smoking
- Reduce alcohol consumption
- Reduce consumption of food groups known to aggrevate
18
Q
What food groups are known to aggrevate GORD?
A
- Chocolate
- Fatty foods
19
Q
What medications are given to manage GORD?
A
- Simple antacids
- Raft antacids (alginates)
- PPIs
- H2 antagonists
20
Q
Give an example of a simple antacid?
A
Calcium carbonate
21
Q
How to simple antacids treat GORD?
A
They neutralise acid
22
Q
Give an example of a raft antacid
A
Gaviscon liquid
23
Q
How to raft antacids treat GORD?
A
They are taken after eating and create a protective raft that sits on top of the stomach contents to prevent reflux
24
Q
Give an example of a PPI?
A
Omeprazole
25
How do PPIs treat GORD?
Reduce acid secretion by parietal cells
26
Give an example of a H2 antagonist?
Ranitidine
27
How do H2 antagonists treat GORD?
They block H2 receptors which reduce acid secretion
28
What are the potential complications of GORD?
Barrett's oesophagus
29
What causes Barrett's oesophagus?
Continual contact of gastric juices with oesophageal mucus leading to metaplasic change
30
What factors are associated with GORD?
* Pregnancy
* Obesity
* Fat, chocolate, coffee, or alcohol ingestion
* Cigarette smoking
* Drugs
* Systemic sclerosis
* After treatment for achalasia
* Hiatus hernia
31
What drugs are assoicated with GORD?
* Antimuscarinic
* Calcium-channel blockers
* Nitrates
32
What is a peptic ulcer?
A break in superficial epithelial cells penetrating down into Muscularis mucosa of either stomach *(gastric ulcer)* or duodenum *(duodenal ulcer)*
33
Where are most duodenal ulcers found?
In the duodenal cap
34
Where are most gastric ulcers found?
In the lesser curvature of the stomach
35
What is the leading cause of peptic ulcer disease in the developed world?
The use of NSAIDs
36
Why does the use of NSAIDs lead to peptic ulcer disease?
Because the inhibit the production of prostaglandins, which prevents production of protective unstirred layer, *which is an innate protection against gastric acid*
37
What % of patients taking long term NSAIDs have mucosal damage?
50%
38
What % of patients taking long term NSAIDs have peptic ulceration?
* 30% when endoscoped
* Only 5% symptomatic
39
What % of patients on long term NSAIDs will have complications *such as a GI bleed?*
1-2%
40
What is the prevalance of duodenal ulcers?
Found in ~10% of adult population
41
How does the prevalance of duodenal ulcers compare to that of gastric ulcers?
Duodenal ulcers are 2-3 times more common
42
How is the prevalance of duodenal ulcers changing?
* Falling for younger people
* Especially pen
* Increasing in older people
* Especially women
* In developed countries;
* Increased prevalence of NSAID-associated DUs
* Decreasing prevalance of H pylori associated ulceration
43
What are the clinical features of peptic ulcer disease?
* Recurrent, burning epigastric pain
* Nausea
* Vomiting
* May be asymptomatic
* *With GUs,* weight loss and anorexia
44
When may pain caused by a DU be worse?
* Night
* When hungry
45
When may pain from a DU be relieved?
* Eating
* Antacids
46
What does persistent, severe pain suggest with peptic ulcer disease?
Penetrtation of ulcer into other organs
47
What does back pain suggest with peptic ulcer disease?
Posterior ulcer
48
How common are the symptoms of nausea and vomting with PUD?
Less common
49
If PUD is asymptomatic, how may it present for the first time?
Hematemesis
50
When will PUD present with hematemesis?
When the ulcer has perforated blood vessel(s)
51
What investigations will be undertaken when PUD is suspected?
* Investigate *H pylori* infection
* In older patients *(over 55)* or with other alarming symptoms, perform endoscopy
52
Why is an endoscopy performed in PUD patients who are older or have other alarming symptoms?
To exclude cancer
53
How is PUD caused by a *H pylori* infection managed?
Triple therapy-
* Proton pump inhibitor
* Antibiotics
* H2 antagonist
54
Give an example of a proton pump inhibitor?
Omeprazole
55
What antibiotics are given to treat PUD caused by *H pylori* infections?
* Clarithromycin
* Amoxicillin
56
Give an example of a H2 antagonist
Cimetidine
57
How is PUD caused by taking NSAIDs managed?
* Stop or review
* Use alternatives
* NSAIDs with a lower risk of causing PUD
* Use prophalatic PPI as well as NSAID
58
What are the potential complications of PUD?
* Haemorrhage of blood vessels which ulcer has eroded
* Perforation of the ulcer
* Gastric outlet obstruction
59
How does haemorrhage of a blood vessel which an ulcer has eroded present?
* Hematemesis
* Melena
60
Is perforation of the ulcer more common in GUs or DUs?
DUs
61
Where do peptic ulcers usually perforate into?
The peritoneal cavity
62
What are the potential types of gastric outlet obstruction caused by PUD?
* Pre-pyloric
* Pyloric
* Duodenal
63
How does PUD cause gastric outlet obstruction?
Either because of active ulcer with oedema, or due to healing of an ulcer with associated fibrosis
64
How does gastric outlet obstruction normally present?
Vomiting without pain
65
What are the characteristics of the *H pylori* bacterium?
* Gram negative
* Aerobic
* Helical
66
What chemical does *H pylori* produce?
Urease
67
Where does *H pylori* reside?
In the stomach of infected individuals
68
What does production of urease produce?
Ammonia
69
Why is the production of ammonia important for *H pylori*?
Because it neutralises the acidic environment, which allow the bacterium to survive
70
Where does *H pylori* colonise?
Gastric epithelium, in mucous layer or just beneath
71
How does damage to the gastric epithelia occur?
* Through enzymes released
* Through induction of apoptosis
* The inflammatory response to the infection
72
What conducts the inflammatory response to *H pylori* infection?
Inflammatory cells and mediators
73
How is a diagnosis of *H pylori* made?
* IgG detected in serum
* 13C-urea breath test
* Gastric sample by endoscopy and detect by histology and culture
74
What is the advantage of testing for IgG in the serum when seeking a diagnosis of *H pylori*?
It has relatively good sensitivity and specificity
75
Why can a 13C-urea breath test be used to make a diagnosis of *H pylori* infection?
13C-urea ingested, and if *H pylori* present the urease produced will break down 13C-urea to NH3 and CO2. CO2 *(where the carbon is in 13C)* will be exhaled on breath and detected
76
What is the treatment for *H pylori* infection?
Triple therapy-
* Proton Pump Inhibitor
* Two antibiotics
* H2 antagonist
77
When is a H2 antagonist given to treat *H pylori* infection?
If its severe
78
How effective is the standard eradication therapy for *H pylori*?
Successful in eradiating infection in 90% of patients
79
What does the success of the eradication therapy for *H pylori* depend on?
Local resistance
80
How long does the standard eradication therapy for *H pylori* take?
7-14 days
81
What is the advantage of a 14 day eradication treatment for *H pylori*?
It is more effective
82
What is the disadvantage of a 14 day eradication therapy for *H pylori*?
Side-effects of treatment may put patients off finishing the full course
83
What gastric diseases can be caused by *H pylori*?
* Gastritis
* Peptic ulcer disease
* Gastric cancer
84
What is the usual effect of a *H pylori* infection?
Asymptomatic gastritis
85
What does chronic gastritis cause?
Hypergastrinaemia
86
Why does chronic *H pylori* cause hypergastrinaemia?
Due to gastrin release from astral G cells
87
What happens in hypergastrinaemia?
There is increased acid production
88
What are the symptoms of hypergastrinaemia?
* Usually asymptomatic
* Can lead to duodenal ulceration *which will eventually produce symptoms*
89
What is happening to the prevalence of DU due to *H pylori*?
It is falling
90
Why is the prevalance of DU due to *H pylori* falling?
Due to a decreased prevalance of *H pylori* infections
91
What is the effect of eradication of *H pylori* infection in patients with DUs caused by the infection?
* Relief of symptoms
* Decreased chance of recurrence
92
In what % of people with *H pylori* infection do DU occur?
15%
93
How does *H pylori* cause DUs?
Precise mechanism unclear, but factors implicated through are;
* Genetic predispositions
* Bacterial virulence
* Increase gastrin secretion
* Smoking
94
What are gastric ulcers caused by *H pylori* associated with?
Gastritis affecting the body as well as antrum
95
What can gastritis affecting the body as well as the antrum cause?
Parietal cell loss leading to reduction in acid production
96
How is it thought that *H pylori* causes GU?
Due to reduction in gastric mucosal resistance due to cytokine production as a result of infection
97
How can acid secretion be reduced?
By inhibition of-
* Histamine at H2 receptors
* Proton Pump Inhibitors (PPIs)
98
Give an example of a H2 receptor antagonist
Cimetidine
99
What is the effect of H2 receptor antagonists?
Removes the amplification of Gastrin/Ach signal
100
Give an example of a PPI
Omeprazole
101
How do PPI reduce gastric acid secretion?
They prevent H+ ions being pumped into parietal cell canaliculi
