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 is a simple way of testing for the presence of helicobacter in a subject?

A

Give a urate mixture that contains a distinctive isotope of carbon
H. pylori has urease enzymes that can break down the urate mixture and liberate the carbon isotope
This carbon isotope is then incorporated into carbon dioxide and is breathed out – this can then be detected to confirm high levels of H. pylori

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10
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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11
Q

Where are parietal cells found in the stomach?

A

Fundus

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12
Q

Which cells in the stomach produce histamine?

A

H cells

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13
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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14
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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15
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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16
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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17
Q

What do D cells release?

A

Somatostatin

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18
Q

What are the effects of somatostatin?

A

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

19
Q

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

A

H+/K+ ATPase

20
Q

Which cells produce bicarbonate?

A

Superficial epithelial cells

21
Q

Give an example of a proton pump inhibitor.

A

Omeprazole

22
Q

What is the mechanism of action of PPIs?

A

Irreversible inhibitors of H+/K+ ATPase

23
Q

What are the effects of PPIs?

A

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

24
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

25
Q

What are some uses of PPIs?

A

Peptic ulcers
GERD

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

26
Q

Describe the pharmacokinetics of omeprazole.

A

Orally active

Enteric-coated slow release formulation

27
Q

What are the unwanted effects of omeprazole?

A

Rare with short-term use

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

28
Q

Give two examples of histamine receptor antagonists.

A

Cimetidine

Ranitidine

29
Q

What are the effects of histamine receptor antagonists?

A

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

30
Q

Describe the pharmacokinetics of histamine receptor antagonists.

A

Orally active

Ranitidine is longer acting than cimetidine

31
Q

What are the unwanted effects of histamine receptor antagonists?

A

Rare – dizziness, headache

Ranitidine has fewer side effects

32
Q

Give three examples of cytoprotective drugs.

A

Sucralfate
Bismuth Chelate
Misoprostol

33
Q

What is sucralfate composed of?

A

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

34
Q

What are the unwanted effects of sucralfate?

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?

A

Same as sucralfate

36
Q

What is misoprostol?

A

It is a prostaglandin analogue (PGE1)

37
Q

What are the uses of misoprostol?

A

May be co-prescribed with oral NSAIDs when used chronically

38
Q

What are the unwanted effects of misoprostol?

A
Diarrhoea 
Abdominal cramps 
Uterine contractions (not to be given during pregnancy)
39
Q

Give three examples of antacids and their speed of onset.

A
Sodium bicarbonate (FAST) 
Aluminium hydroxide (slow) 
Magnesium trisilicate (slow)
40
Q

What is the drug of choice for gastroesophageal reflux disease?

A

Proton pump inhibitors e.g. omeprazole

41
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

42
Q

Why is it important to treat GERD?

A

Chronic GERD can progress to pre-malignant mucosal cells that can potentially lead to oesophageal adenocarcinoma

43
Q

Describe the mechanism of action of sucralfate.

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