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BS - GI CLINICAL > Dyspepsia & Peptic Ulcers > Flashcards

Dyspepsia & Peptic Ulcers Flashcards

1
Q

What stimulates gastric acid secretion?

How may this occur directly and indirectly?

A

Acetylcholine and gastrin

Occurs directly by binding to receptors on parietal cells

Occurs indirectly by stimulation of histamine release from ECL cells

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2
Q

How is gastric acid secretion inhibited?

A

Through somatostatin and prostaglandin PGE2

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3
Q

How does prostaglandin PGE2 work?

A

It binds to a receptor on parietal cells to activate an inhibitory G protein

This inhibits activation of adenyl cyclase

This decreases gastric acid production

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4
Q

What are the 5 types of cells found in the crypts of gastric mucosa?

What do they secrete?

A
  1. goblet cells - mucus
  2. parietal cells - gastric acid
  3. Chief cells - pepsinogen
  4. D cells - somatostatin
  5. G cells - gastrin
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5
Q

What are ECL cells and what do they secrete?

A

enterochromaffin-like cells

They produce histamine, which promotes acid secretion

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6
Q

What does stimulation of parietal cells lead to?

A

Stimulation of parietal cells stimulates a proton pump which secretes both H+ and Cl- ions

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7
Q

How does the action of G cells affect acid secretion?

A

G cells secrete gastrin

gastrin affects the ECL cells, increasing histamine production

This causes parietal cells to produce more HCl

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8
Q

How does the nervous system influence parietal cells?

A

Enteric neurones secrete acetylcholine

This causes parietal cells to secrete more gastric acid

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9
Q

What are the 3 interventions to prevent acid secretion by parietal cells?

A
  1. anti-histamines
  2. vagotomy
  3. proton pump inhibitors (PPIs)
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10
Q

How do anti-histamines work?

A

They are H2 blockers

They prevent histamine secretion, which reduces secretion of HCl

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11
Q

What is a vagotomy?

How does this reduce gastric acid secretion?

A

It involves selectively cutting the nerves which supply the parietal cells through the vagus nerve

This reduces stimulation of the parietal cells through ACh

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12
Q

How do PPIs work to reduce gastric acid secretion?

A

They affect the ATPase that pushes the H+ and Cl- ions out of the cell

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13
Q

What is the actual mechanism which leads to gastric acid secretion by parietal cells?

A
  1. When the stimulatory hormone binds to the receptor, this activates adenylate cyclase
  2. this converts ATP to cAMP
  3. cAMP activates protein kinase A
  4. protein phosphorylation activates the H+/K+ ATPase
  5. this leads to the secretion of gastric acid
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14
Q

When does a peptic ulcer occur?

A

When there is a break in the epithelial cells of the stomach or duodenum

This penetrates to the muscularis mucosa in either the stomach or the duodenum

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15
Q

How common is duodenal and gastric ulceration?

A

It is extremely common

It affects more than 10% of the population at some time in their lives

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16
Q

What is encompassed by the term peptic ulceration?

What is the problem with identifying symptoms?

A

Peptic ulceration is a broad term that encompasses ulceration of the oesophagus, duodenum and stomach

The site of the ulcer influences the type of pain and signs associated with it

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17
Q

What are typical symptoms of peptic ulceration?

A
  1. belching, bloating, distention
  2. heartburn
  3. chest discomfort
  4. unexpected weight loss and anorexia
  5. nausea and vomiting
  6. feeling full easily
  7. dark stools
  8. epigastric pain
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18
Q

What are the 3 potential complications arising from peptic ulceration?

A
  1. haemorrhage
  2. perforation of the stomach lining
  3. gastric outlet obstruction
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19
Q

What are the 2 main causes of peptic ulceration?

A
  1. infection with Helicobacter pylori
  2. use of non-steroidal anti-inflammatory drugs
    e. g. aspirin, ibuprofen

These risk factors are independent and additive

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20
Q

What are less common causes of peptic ulceration?

A
  1. Zollinger-Ellison syndrome

2. crohn’s disease

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21
Q

What is Zollinger-Ellison syndrome?

A

A tumour arises in the islet cells of the pancreas

It secretes gastrin, which increases gastric acid secretion

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22
Q

What is H. Pylori and where is it found?

A

It is a slow-growing gram-negative bacterium which colonises the mucus layer in the stomach (and can be found in the duodenum)

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23
Q

What does H. pylori adhere to and what damage does it cause?

A

It adheres to gastric mucosal cells and causes gastritis and damage to the gastric epithelium

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24
Q

When is H. pylori infection usually acquired?

A

Childhood

But in developed countries, infection is more common in older people

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25
Q

What is H. pylori infection generally linked to?

A

Poor levels of hygiene

It is more common in lower income groups, where housing conditions are poorer

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26
Q

What enzyme is expressed by H. pylori?

Why is this significant?

A

Urease which converts urea into water and ammonia

Ammonia is alkaline so helps to neutralise the stomach acid

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27
Q

Which toxins are expressed by some strains of H. pylori?

What are these strains associated with?

A

CagA and VacA

These strains are associated with higher levels of inflammation and cause more gastric ulceration

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28
Q

How does H. pylori cause gastric ulceration?

A

It expresses the toxins CagA and VacA which inflame the stomach lining

It causes infection which damages the gastric mucosa and leads to increased gastrin and gastric acid secretion

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29
Q

In what other ways can H. pylori affect the stomach?

A

it can lead to stomach cancer

It is also associated with stomach pain, bloating and nausea

30
Q

What 4 tests can be used to diagnose H. pylori infection?

A
  1. blood antibody test
  2. urea breath test
  3. stool antigen test
  4. stomach biopsy
31
Q

How do the blood antibody, stool antigen and urea breath tests identify H. pylori?

A
  1. blood antibody test sees whether the body has made antibodies against H. pylori
  2. urea breath test can identify H. pylori in the stomach
  3. stool antigen test looks for blood and H. pylori antigens
32
Q

Which patients should undergo endoscopy?

A

Older patients who express “alarm symptoms”

e.g. higher risk of stomach cancer

33
Q

What is the basic treatment for H. pylori infection?

A

10 days - 2 weeks of antibiotics

Such as amoxicillin

34
Q

What are the antibiotics combined with for treatment of H. pylori?

A

A PPI (antacid)

These inhibit the H+ ATPase enzyme

35
Q

What lifestyle advice is given to someone with H. pylori infection?

A

Avoid stress, alcohol, spicy food and smoking

36
Q

What are NSAIDs?

What are they most commonly used for?

A

Non-steroidal anti-inflammatory drugs

They are used as minor painkillers and for the relief of inflammation

37
Q

When else may NSAIDs be used?

A
  1. chronic inflammatory conditions, such as arthritis
  2. treatment of blood clotting disorders
  3. prevention of MI and stroke
38
Q

What is the main side effect of NSAIDs?

A

Gastrointestinal bleeding

10-25% of patients on long term NSAID therapy will suffer from GI problems

39
Q

What is the mechanism behind how NSAIDs work?

A

They inhibit cyclo-oxygenase (COX) enzymes

40
Q

What is the role of cyclo-oxygenase enzymes?

A

They are responsible for the conversion of arachidonic acid into:

  1. prostaglandins
  2. thromboxane
  3. prostacyclin
41
Q

What is the role of thromboxane?

A

It is involved in platelet aggregation (blood clotting)

42
Q

What is the role of prostaglandins?

A

They are paracrine hormones which promote:

  1. inflammation
  2. vasodilation
  3. smooth muscle contraction
43
Q

What is expression of COX 1 like?

A

It is expressed constitutively (all the time) in a range of tissues

e.g. gastric mucosa, kidney, platelets and vascular endothelial cells

44
Q

What is expression of COX 2 like?

A

COX 2 expression is induced in monocytes and macrophages in response to inflammation

45
Q

Why would a COX 2 specific NSAID be preferable to ibuprofen for long-term use?

A

Ibuprofen acts on COX 1 and COX 2

A COX 2 specific NSAID will target inflammation, but will not target the gut

46
Q

What is the main problem with using aspirin as an NSAID?

A

Aspirin is more inclined to promote haemorrhage from peptic ulcers

47
Q

Why is aspirin more inclined to promote haemorrhage?

A

Blocking thromboxane production reduces the amount of blood clotting that can occur

48
Q

What are examples of H2 antagonists?

What are they used for?

A

Ranitidine (Zantac) and Famotidine (Pepcid)

They are available over-the-counter for common indigestion symptoms

49
Q

How do H2 antagonists work?

A

They bind to and block the histamine H2 receptor

This suppresses acid secretion

50
Q

What are examples of proton pump inhibitors?

A
  1. lansoprazole
  2. omeprazole
  3. pantoprazole
51
Q

How do PPIs work?

A

They directly inhibit the H+/K+ ATPase which pumps H+ ions into the stomach

52
Q

Why are dark stools a symptom of a peptic ulcer?

A

They result from bleeding from the ulcer in the upper part of the digestive system

The blood mixes with digestive fluids

53
Q

Why do patients with a gastric ulcer become breathless?

What can this lead to?

A

Ulcers can cause hidden bleeding

This leads to symptoms of anaemia, such as fatigue and abdominal pain

54
Q

What would blood tests of someone with a peptic ulcer show?

A

Low Hb levels due to anaemia

Raised urea due to blood proteins being digested to produce urea

55
Q

Why may a kidney function test be performed on someone with a peptic ulcer?

A

If someone has been on long-term NSAID therapy, the kidneys may be damaged

56
Q

What are the 4 types of dyspepsia?

A
  1. dyspepsia with alarm symptoms
  2. uncomplicated (or simple) dyspepsia
  3. un-investigated dyspepsia
  4. functional (“non-ulcer”) dyspepsia
57
Q

What defines each type of dyspepsia?

A

Uncomplicated dyspepsia is dyspepsia without the “red-flag” features

Un-investigated dyspepsia is presenting to a physician for the first time

Functional dyspepsia has no structural cause for the symptoms at upper GI endoscopy

58
Q

What are the alarm symptoms of dyspepsia?

A
  1. weight loss
  2. dysphagia or odynophagia
  3. persistent vomiting
  4. haematemesis or melaena
  5. palpable epigastric mass
  6. family history of gastric cancer
  7. dyspepsia onset over the age of 45-55 years
59
Q

What is odynophagia?

A

Painful swallowing

60
Q

What is haematemesis and melaena?

A

Haematemesis is vomiting blood

Melaena is dark, sticky stools containing partly digested blood

61
Q

What are the main causes of dyspepsia?

A
  1. gastro-oesophageal reflux disease
  2. peptic ulcers
  3. gastric cancer
62
Q

What % of people with dyspepsia have a normal endoscopy result?

A

80%

This is an example of functional dyspepsia

63
Q

What is the prevalence and prognosis of dyspepsia?

A

Prevalence is 20 - 40%

40% of people experience long-term symptoms

60% of people experience resolution of symptoms

64
Q

What is the treatment for dyspepsia with alarm symptoms?

A

Alarm symptoms warrant an urgent endoscopy

65
Q

What are the 2 options for treatment of uncomplicated (simple) dyspepsia?

A
  1. test individuals for H. pylori, with eradication therapy for those who test positive
  2. give all patients PPIs to reduce acid secretion
66
Q

Which of the 2 options for treating uncomplicated dyspepsia is preferred?

A

Method 1 is preferred when prevalence of H.pylori is greater than 10% of the population

If not, method 2 is preferred

67
Q

What actually causes peptic ulcers?

A

They are not caused by a single factor

They are caused by a breakdown in the balance between the protective and defensive mechanisms

68
Q

What are the 3 complications of peptic ulcers?

A
  1. perforation leads to gas under the diaphragm and leaking into the peritoneal cavity
  2. peptic ulcer may bleed
  3. pyloric stenosis
69
Q

What is pyloric stenosis?

A

Gastric outlet obstruction leads to the pylorus/antrum being scarred with ulcers

70
Q

What does pyloric stenosis lead to?

A

The stomach is unable to empty properly

This leads to a massively distended stomach with fluid and food debris

71
Q

What usually treats perforation and pyloric stenosis?

A

Surgery

72
Q

What usually treats bleeding?

A

Surgery or medication

Injection of adrenaline causes vasoconstriction

Heat can be applied to cause coagulation of the vessel

BS - GI CLINICAL (4 decks)

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