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ESA 3 - Gastrointestinal System > Gastric Disease > Flashcards

Gastric Disease Flashcards

1
Q

Give 3 common gastric disorders

A
  1. Gastro-oesophageal reflux disease (GORD)
  2. Peptic ulcer disease (PUD)
  3. Helicobacter pylori infection
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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
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3
Q

What state is the lower oesophagus sphincter usually in?

A

Closed

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4
Q

What happens to the lower oesophageal sphincter as part of the physiology of swallowing?

A

It transiently relaxes

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5
Q

Why does the lower oesophageal sphincter transiently relax?

A

To allow the bolus to move into the stomach

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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
  1. Peristalsis
  2. Diaphragm
  3. Lower oesophageal sphincter
  4. Intra-abdominal oesophagus
  5. Mucosal valve
  6. Unumpeded gastric emptying
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7
Q

Is acid reflex ever normal?

A

Yes, some is

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8
Q

How is mild acid reflex normally dealt with?

A
  • Secondary peristaltic waves
  • Gravity
  • Salivary bicarbonate
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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

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10
Q

What are the clinical features of GORD?

A

Dyspepsia

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11
Q

What is dyspepsia?

A

Heartburn

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12
Q

What makes dyspepsia from GORD worse?

A
  • Lying down
  • Bending over
  • Drinking hot drinks
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13
Q

How is a clinical diagnosis of GORD usually made?

A

Without investigation- based on symptoms alone

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14
Q

When is there a need to investigate GORD?

A
  • When there are alarming symptoms, such as dysphagia
  • When hiatus hernia is suspected
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15
Q

What investigation is made when a hiatus hernia is suspected?

A

Endoscopy

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16
Q

What are the two areas of management for GORD?

A
  • Lifestyle
  • Medication
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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
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18
Q

What food groups are known to aggrevate GORD?

A
  • Chocolate
  • Fatty foods
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19
Q

What medications are given to manage GORD?

A
  • Simple antacids
  • Raft antacids (alginates)
  • PPIs
  • H2 antagonists
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20
Q

Give an example of a simple antacid?

A

Calcium carbonate

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21
Q

How to simple antacids treat GORD?

A

They neutralise acid

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22
Q

Give an example of a raft antacid

A

Gaviscon liquid

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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

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24
Q

Give an example of a PPI?

A

Omeprazole

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25
Q

How do PPIs treat GORD?

A

Reduce acid secretion by parietal cells

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26
Q

Give an example of a H2 antagonist?

A

Ranitidine

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27
Q

How do H2 antagonists treat GORD?

A

They block H2 receptors which reduce acid secretion

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28
Q

What are the potential complications of GORD?

A

Barrett’s oesophagus

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29
Q

What causes Barrett’s oesophagus?

A

Continual contact of gastric juices with oesophageal mucus leading to metaplasic change

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30
Q

What factors are associated with GORD?

A
  • Pregnancy
  • Obesity
  • Fat, chocolate, coffee, or alcohol ingestion
  • Cigarette smoking
  • Drugs
  • Systemic sclerosis
  • After treatment for achalasia
  • Hiatus hernia
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31
Q

What drugs are assoicated with GORD?

A
  • Antimuscarinic
  • Calcium-channel blockers
  • Nitrates
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32
Q

What is a peptic ulcer?

A

A break in superficial epithelial cells penetrating down into Muscularis mucosa of either stomach (gastric ulcer) or duodenum (duodenal ulcer)

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33
Q

Where are most duodenal ulcers found?

A

In the duodenal cap

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34
Q

Where are most gastric ulcers found?

A

In the lesser curvature of the stomach

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35
Q

What is the leading cause of peptic ulcer disease in the developed world?

A

The use of NSAIDs

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36
Q

Why does the use of NSAIDs lead to peptic ulcer disease?

A

Because the inhibit the production of prostaglandins, which prevents production of protective unstirred layer, which is an innate protection against gastric acid

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37
Q

What % of patients taking long term NSAIDs have mucosal damage?

A

50%

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38
Q

What % of patients taking long term NSAIDs have peptic ulceration?

A
  • 30% when endoscoped
  • Only 5% symptomatic
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39
Q

What % of patients on long term NSAIDs will have complications such as a GI bleed?

A

1-2%

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40
Q

What is the prevalance of duodenal ulcers?

A

Found in ~10% of adult population

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41
Q

How does the prevalance of duodenal ulcers compare to that of gastric ulcers?

A

Duodenal ulcers are 2-3 times more common

42
Q

How is the prevalance of duodenal ulcers changing?

A
  • 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
Q

What are the clinical features of peptic ulcer disease?

A
  • Recurrent, burning epigastric pain
  • Nausea
  • Vomiting
  • May be asymptomatic
  • With GUs, weight loss and anorexia
44
Q

When may pain caused by a DU be worse?

A
  • Night
  • When hungry
45
Q

When may pain from a DU be relieved?

A
  • Eating
  • Antacids
46
Q

What does persistent, severe pain suggest with peptic ulcer disease?

A

Penetrtation of ulcer into other organs

47
Q

What does back pain suggest with peptic ulcer disease?

A

Posterior ulcer

48
Q

How common are the symptoms of nausea and vomting with PUD?

A

Less common

49
Q

If PUD is asymptomatic, how may it present for the first time?

A

Hematemesis

50
Q

When will PUD present with hematemesis?

A

When the ulcer has perforated blood vessel(s)

51
Q

What investigations will be undertaken when PUD is suspected?

A
  • Investigate H pylori infection
  • In older patients (over 55) or with other alarming symptoms, perform endoscopy
52
Q

Why is an endoscopy performed in PUD patients who are older or have other alarming symptoms?

A

To exclude cancer

53
Q

How is PUD caused by a H pylori infection managed?

A

Triple therapy-

  • Proton pump inhibitor
  • Antibiotics
  • H2 antagonist
54
Q

Give an example of a proton pump inhibitor?

A

Omeprazole

55
Q

What antibiotics are given to treat PUD caused by H pylori infections?

A
  • Clarithromycin
  • Amoxicillin
56
Q

Give an example of a H2 antagonist

A

Cimetidine

57
Q

How is PUD caused by taking NSAIDs managed?

A
  • Stop or review
  • Use alternatives
    • NSAIDs with a lower risk of causing PUD
  • Use prophalatic PPI as well as NSAID
58
Q

What are the potential complications of PUD?

A
  • Haemorrhage of blood vessels which ulcer has eroded
  • Perforation of the ulcer
  • Gastric outlet obstruction
59
Q

How does haemorrhage of a blood vessel which an ulcer has eroded present?

A
  • Hematemesis
  • Melena
60
Q

Is perforation of the ulcer more common in GUs or DUs?

A

DUs

61
Q

Where do peptic ulcers usually perforate into?

A

The peritoneal cavity

62
Q

What are the potential types of gastric outlet obstruction caused by PUD?

A
  • Pre-pyloric
  • Pyloric
  • Duodenal
63
Q

How does PUD cause gastric outlet obstruction?

A

Either because of active ulcer with oedema, or due to healing of an ulcer with associated fibrosis

64
Q

How does gastric outlet obstruction normally present?

A

Vomiting without pain

65
Q

What are the characteristics of the H pylori bacterium?

A
  • Gram negative
  • Aerobic
  • Helical
66
Q

What chemical does H pylori produce?

A

Urease

67
Q

Where does H pylori reside?

A

In the stomach of infected individuals

68
Q

What does production of urease produce?

A

Ammonia

69
Q

Why is the production of ammonia important for H pylori?

A

Because it neutralises the acidic environment, which allow the bacterium to survive

70
Q

Where does H pylori colonise?

A

Gastric epithelium, in mucous layer or just beneath

71
Q

How does damage to the gastric epithelia occur?

A
  • Through enzymes released
  • Through induction of apoptosis
  • The inflammatory response to the infection
72
Q

What conducts the inflammatory response to H pylori infection?

A

Inflammatory cells and mediators

73
Q

How is a diagnosis of H pylori made?

A
  • IgG detected in serum
  • 13C-urea breath test
  • Gastric sample by endoscopy and detect by histology and culture
74
Q

What is the advantage of testing for IgG in the serum when seeking a diagnosis of H pylori?

A

It has relatively good sensitivity and specificity

75
Q

Why can a 13C-urea breath test be used to make a diagnosis of H pylori infection?

A

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
Q

What is the treatment for H pylori infection?

A

Triple therapy-

  • Proton Pump Inhibitor
  • Two antibiotics
  • H2 antagonist
77
Q

When is a H2 antagonist given to treat H pylori infection?

A

If its severe

78
Q

How effective is the standard eradication therapy for H pylori?

A

Successful in eradiating infection in 90% of patients

79
Q

What does the success of the eradication therapy for H pylori depend on?

A

Local resistance

80
Q

How long does the standard eradication therapy for H pylori take?

A

7-14 days

81
Q

What is the advantage of a 14 day eradication treatment for H pylori?

A

It is more effective

82
Q

What is the disadvantage of a 14 day eradication therapy for H pylori?

A

Side-effects of treatment may put patients off finishing the full course

83
Q

What gastric diseases can be caused by H pylori?

A
  • Gastritis
  • Peptic ulcer disease
  • Gastric cancer
84
Q

What is the usual effect of a H pylori infection?

A

Asymptomatic gastritis

85
Q

What does chronic gastritis cause?

A

Hypergastrinaemia

86
Q

Why does chronic H pylori cause hypergastrinaemia?

A

Due to gastrin release from astral G cells

87
Q

What happens in hypergastrinaemia?

A

There is increased acid production

88
Q

What are the symptoms of hypergastrinaemia?

A
  • Usually asymptomatic
  • Can lead to duodenal ulceration which will eventually produce symptoms
89
Q

What is happening to the prevalence of DU due to H pylori?

A

It is falling

90
Q

Why is the prevalance of DU due to H pylori falling?

A

Due to a decreased prevalance of H pylori infections

91
Q

What is the effect of eradication of H pylori infection in patients with DUs caused by the infection?

A
  • Relief of symptoms
  • Decreased chance of recurrence
92
Q

In what % of people with H pylori infection do DU occur?

A

15%

93
Q

How does H pylori cause DUs?

A

Precise mechanism unclear, but factors implicated through are;

  • Genetic predispositions
  • Bacterial virulence
  • Increase gastrin secretion
  • Smoking
94
Q

What are gastric ulcers caused by H pylori associated with?

A

Gastritis affecting the body as well as antrum

95
Q

What can gastritis affecting the body as well as the antrum cause?

A

Parietal cell loss leading to reduction in acid production

96
Q

How is it thought that H pylori causes GU?

A

Due to reduction in gastric mucosal resistance due to cytokine production as a result of infection

97
Q

How can acid secretion be reduced?

A

By inhibition of-

  • Histamine at H2 receptors
  • Proton Pump Inhibitors (PPIs)
98
Q

Give an example of a H2 receptor antagonist

A

Cimetidine

99
Q

What is the effect of H2 receptor antagonists?

A

Removes the amplification of Gastrin/Ach signal

100
Q

Give an example of a PPI

A

Omeprazole

101
Q

How do PPI reduce gastric acid secretion?

A

They prevent H+ ions being pumped into parietal cell canaliculi

ESA 3 - Gastrointestinal System (12 decks)

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