Anti-Ulcer Drugs Flashcards

1
Q

What are the two types of peptic ulcer?

A

Gastric ulcer

Duodenal ulcer

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2
Q

Describe how gastric ulcers and duodenal ulcers can be distinguished based on their symptoms.

A

Gastric ulcer – pain at meal times when gastric acid is secreted

Duodenal ulcer – pain relieved by a meal as the pyloric acid closes –pain -3 hours after a meal

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3
Q

Which type of peptic ulcer is more common?

A

Duodenal (4:1)

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4
Q

What are the protective factors that protect the stomach lining from damage?

A

Mucous lining the stomach

Bicarbonate produced by cells in the stomach

Prostaglandins facilitate a good blood flow in the stomach, increase mucous and bicarbonate production and inhibit acid secretion

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5
Q

Which cells produce stomach acid?

A

Parietal cells

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6
Q

Which cells produce pepsinogens?

A

Gastric chief cells

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7
Q

State some factors that could contribute to the pathogenesis of ulcers.

A

Increase in acid production

Decrease in bicarbonate production

Decreased thickness of mucosal layer

Increase in pepsin

Decreased mucosal blood flow

Increase in H. pylori

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8
Q

What is the aim of antibiotics treatment with regards to ulcers?

A

90% eradication of H. pylori within 7-14 days

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9
Q

What treatments can be put together to form the best practice ‘Triple Therapy’?

A

Antibiotics

Drugs that reduce gastric acid secretion

Drugs that promote healing

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10
Q

Where are parietal cells found in the stomach?

A

Fundus

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11
Q

Which cells in the stomach produce histamine?

A

H cells

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12
Q

Explain how the parasympathetic nervous system affects gastric acid production.

A

The parasympathetic nervous, via the vagus nerve, stimulates histamine production by H cells

Histamine then stimulates an increase in acid production by parietal cells

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13
Q

Which cells in the stomach produce gastrin and where are these cells found?

A

G cells

Located in the antrum

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14
Q

What triggers gastrin release from G cells?

A

The breakdown of food in the stomach and the liberation of amino acids stimulate gastrin release

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15
Q

What are the effects of gastrin?

A

They trigger the release of histamine from H cells

They also directly trigger acid production by the parietal cells

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16
Q

What do D cells release?

A

Somatostatin

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17
Q

What are the effects of somatostatin (in stomach)?

A

It is inhibitory – it decreases the release of histamine and gastrin

18
Q

What type of ion transporter is the proton pump found in parietal cells?

A

H+/K+ ATPase

19
Q

Which cells produce bicarbonate?

A

Superficial epithelial cells

20
Q

Give an example of a proton pump inhibitor.

A

Omeprazole

21
Q

What is the mechanism of action of PPIs?

A

Irreversible inhibitors of H+/K+ ATPase

22
Q

What are the effects of PPIs?

A

Inhibits basal and stimulated gastric acid secretion from the parietal cells by >90%

23
Q

What features of PPIs limits its action on other proton pumps around the body?

A

Inactive at neutral pH

It is a WEAK BASE so it accumulates in the cannaliculi of the parietal cells – this concentrates its actions in the cannaliculi

24
Q

What are some uses of PPIs?

A

Peptic ulcers

GORD - gastro oesophageal reflux disease

Prophylaxis of ulcers in the intensive care setting, and among high-risk patients being prescribed aspirin, NSAIDs, anti-platelets and anticoagulants

25
Q

Describe the pharmacokinetics of omeprazole (PPI).

A

Orally active

Enteric-coated slow release formulation

26
Q

What are the unwanted effects of omeprazole (PPI)?

A

Rare with short-term use

Long-term and high-dose use is associated with enteric infections, community acquired pneumonia, hip fracture

27
Q

Give two examples of histamine receptor antagonists (H2- anti ulcer ones).

A

Cimetidine

Ranitidine

28
Q

What are the effects of histamine receptor antagonists?

H2- anti ulcer ones

A

Inhibits gastric acid secretion from the parietal cells by about 60%

29
Q

Describe the pharmacokinetics of histamine receptor antagonists. (H2- anti ulcer ones).

A

Orally active

Ranitidine is longer acting than cimetidine

30
Q

What are the unwanted effects of histamine receptor antagonists? (H2- anti ulcer ones).

A

Rare – dizziness, headache

Ranitidine has fewer side effects

31
Q

Give three examples of cytoprotective drugs.

A

Sucralfate
Bismuth Chelate
Misoprostol

32
Q

What is sucralfate composed of?

cytoprotective drug

A

It is a polymer containing aluminium hydroxide and sucrose octa-sulfate

33
Q

Describe the mechanism of action of sucralfate.

cytoprotective drug

A

It acquires a strong negative charge when in an acidic environment

It binds to positively charged groups in large molecules (proteins, glycoproteins) resulting in gel-like complexes

The gel-like complexes coat and protect the ulcer, limit H+ diffusion and pepsin degradation of mucus

It also increases prostaglandin synthesis and reduces H. pylori

34
Q

What are the unwanted effects of sucralfate?

cytoprotective drug

A

Most of the orally administered sucralfate remains in the GI tract and this may cause constipation or reduced absorption of other drugs

35
Q

How does bismuth chelate work? (cytoprotective drug)

A

Same as sucralfate

36
Q

What is misoprostol? (cytoprotective drug)

A

It is a prostaglandin analogue (PGE1)

37
Q

What are the unwanted effects of misoprostol? (cytoprotective drug)

A
Diarrhoea  
Abdominal cramps 
Uterine contractions (not to be given during pregnancy)
38
Q

Give three examples of antacids and their speed of onset.

A
Sodium bicarbonate (FAST) 
Aluminium hydroxide (slow) 
Magnesium trisilicate (slow)
39
Q

What is the drug of choice for gastroesophageal reflux disease?

A

Proton pump inhibitors e.g. omeprazole

40
Q

What other type of drug could be given with PPIs to reduce the risk of reflux?

A

Drugs that increase gastric motility and gastric emptying e.g. dopamine receptor antagonists

41
Q

Why is it important to treat GORD?

A

Chronic GORD can progress to pre-malignant mucosal cells that can potentially lead to oesophageal adenocarcinoma- Barrett’s oesophagus