Gastric Disease Flashcards Preview

ESA 3 - Gastrointestinal System > Gastric Disease > Flashcards

Flashcards in Gastric Disease Deck (101):
1

Give 3 common gastric disorders

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

2

What are the anti-reflux mechanisms to prevent reflux of gastric acid into the lower oesophagus? 

  • 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

What state is the lower oesophagus sphincter usually in? 

Closed

4

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

It transiently relaxes 

5

Why does the lower oesophageal sphincter transiently relax? 

To allow the bolus to move into the stomach 

6

Label this diagram, indicating the main antireflux mechanisms on the right

  • 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

7

Is acid reflex ever normal? 

Yes, some is 

8

How is mild acid reflex normally dealt with? 

  • Secondary peristaltic waves
  • Gravity 
  • Salivary bicarbonate 

9

When do clinical features of GORD occur? 

When antireflux mechanisms fail and there is prolonged contact of gastric juices with the lower oesophageal muscosa

10

What are the clinical features of GORD?

Dyspepsia

11

What is dyspepsia? 

Heartburn

12

What makes dyspepsia from GORD worse? 

  • Lying down 
  • Bending over
  • Drinking hot drinks

13

How is a clinical diagnosis of GORD usually made? 

Without investigation- based on symptoms alone

14

When is there a need to investigate GORD? 

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

15

What investigation is made when a hiatus hernia is suspected? 

Endoscopy 

16

What are the two areas of management for GORD?

  • Lifestyle
  • Medication

17

What lifestyle changes can be made to manage GORD?

  • Loose weight 
  • Stop smoking
  • Reduce alcohol consumption 
  • Reduce consumption of food groups known to aggrevate 

18

What food groups are known to aggrevate GORD?

  • Chocolate 
  • Fatty foods

19

What medications are given to manage GORD?

  • Simple antacids
  • Raft antacids (alginates)
  • PPIs
  • H2 antagonists

20

Give an example of a simple antacid? 

Calcium carbonate 

21

How to simple antacids treat GORD?

They neutralise acid 

22

Give an example of a raft antacid

Gaviscon liquid

23

How to raft antacids treat GORD?

They are taken after eating and create a protective raft that sits on top of the stomach contents to prevent reflux

24

Give an example of a PPI?

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 Hions being pumped into parietal cell canaliculi