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LCRS Pharmacology and Therapeutics > Anti-ulcer drugs > Flashcards

Anti-ulcer drugs Flashcards

1
Q

What drugs are involved with treating ulcers/what is the triple therapy?

A

Triple therapy:
Antibiotics
Inhibitors of gastric acid secretion
Cytoprotective drugs

Antacids

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2
Q

What is a peptic ulcer?

A

An area of damage to inner lining of stomach (gastric ulcer) or upper part of duodenum (duodenal ulcer)

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3
Q

How can gastric and duodenal ulcers be distinguished?

A

Timing of symptoms
Gastric- pain at meal times when gastric acid is secreted
Duodenal- pain relieved by a meal as the pyloric sphincter closes- pain 2-3 hours after a meal

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4
Q

What is the prevalence of duodenal and gastric like in comparison to each other?

A

Duodenal:gastric 4:1

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5
Q

What are ulcers caused by?

A

Imbalance of factors that protect or damage gastrointestinal barrier

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6
Q

What is the integrity of gastrointestinal mucosal barrier important for?

A

Maintaining disease free state

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7
Q

What do protective factors do?

A

Lubricate ingested food and prevent stomach and duodenum from attack by acid and enzymes

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8
Q

What does mucous from gastric mucosa do?

A

Creates GI mucosal barrier

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9
Q

What do bicarbonate ions trapped in mucous generate?

A

pH of 6-7 at mucosal surface

Thickening of mucous

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10
Q

What do prostaglandins stimulate in GI tract?

A

Bicarbonate and mucous production and inhibits gastric acid secretion

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11
Q

What do prostaglandins facilitate?

A

A good blood supply to the stomach to allow production of a healthy amount of mucous and allow sufficient bicarbonate production

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12
Q

Which factors required for conversion of food into chyme have the potential to damage the mucosal barrier?

A

Acid secretion from parietal cells of the oxyntic glands in the gastric mucosa
Pepsinogens from the gastric chief cells which can erode the mucous layer

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13
Q

What factors can cause damage to mucosal gastrointestinal barrier?

A 
Increased acid and/or decreased bicarbonate production
Decreased thickness of mucosal layer
Increase in pepsin type I
Decreased mucosal blood flow
Infections with H pylori
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14
Q

What risk factors for ulcers are there?

A

Genetic predisposition
Stress
Diet, alcohol and smoking

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15
Q

What is the prevalence of ulcers in developed countries?

A

1 in 10

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16
Q

What are the aims of treatment for ulcers?

A

Eliminate the cause of mucosal damage

Promote ulcer healing

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17
Q

What drugs are there for stomach ulcers?

A 
Antibiotics- Eradicate H pylori
Inhibitors of gastric acid secretion- Prevent gastric acid production
Cytoprotective drugs- Promote healing
Antacids- Neutralise gastric acid
Triple therapy
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18
Q

What is the aim of the use of antibiotics in ulcer treatment?

A

Eliminate helicobacter pylori which infects a lot of people in the population

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19
Q

What is the simple way of testing for helicobacter pylori?

A

Ask the subject to swallow a urate mixture that has a unique carbon isotope in its make up.
The bacteria produces an enzyme that breaks down the urate and carbon dioxide will then be formed using the unique carbon isotope from the urate
A breath test is performed on the patient 20-30 mins after giving the urate mixture and if the carbon dioxide that they breathe out is contaminated with with the isotope then that confirms there must be a high concentration of helicobacter in the patient.

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20
Q

What is the aim of antibiotic treatment for helicobacter?

A

90% eradication within 7-14 days

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21
Q

What is currently the best practice for treating peptic ulcer disease?

A

Triple therapy:
Antibiotics
Drugs that reduce gastric acid secretion
Drugs that promote healing

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22
Q

Why are several antibiotics used in treatment?

A

A single antibiotic is not usually effective due to the development of resistance

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23
Q

What triggers acid production in the stomach?

A

Presence of food in the stomach or even smell or thought of food can trigger acid production in the stomach

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24
Q

What is found in the fundus of the stomach and what does it produce?

A

Parietal cells that are secreting HCl into the stomach- this helps digest the food

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25
What effect does parasympathetic stimulation have in GI tract?
It can act on H cells via vagus nerve to stimulate histamine production
26
What effect does histamine have in GI tract?
It stimulates parietal cells to produce more acid
27
When food is broken down, amino acids are formed, what do they stimulate?
Triggers G cells in the antrum of the stomach to secrete gastrin
28
What does gastrin do?
Triggers release of more histamine from the H cells which leads to more acid production by the parietal cells Also directly triggers acid production by parietal cells
29
In the duodenum, what is there that regulates gastric acid production?
Secretin and GIP (gastric-inhibitory peptide) that acts on the fundus of the stomach and inhibits formation of gastric acid
30
Where are D cells found?
In the lining of the stomach
31
What controls the function of D cells?
They are partly controlled by the parasympathetic nervous system and partly controlled by the local environment in the antrum
32
What effect does parasympathetic stimulation have on D cells?
Release of somatostatin
33
What can D cells in the antrum sense?
They can sense the pH in the stomach and respond by releasing somatostatin
34
What is somatostatin and what does it do?
An inhibitory molecule that will decrease the release of histamine from H cells and it will decrease the release of gastrin from G cells
35
What protein is involved in stomach acid production and what effect does this have?
It is produced by the proton pump (H+/K+ exchanger)- it allows the establishment of a high concentration of protons in the stomach lumen
36
How does histamine have an effect?
It is released from H cells and acts on H2 receptors on parietal cells and triggers activation of the proton pump via CAMP-dependent pathway
37
What triggers gastrin release?
Presence of food in the stomach and presence of amino acids
38
What are the superficial epithelial cells responsible for and how?
They provide the protective mechanisms for the stomach lining and these produce bicarbonate which interacts with the mucous to form a thick protective layer over the cells
39
What does a thick mucous layer allow the pH at the surface of the stomach be around?
7
40
What is omeprazole?
A proton pump inhibitor
41
What effect does omeprazole have?
It inhibits the basal and stimulated gastric acid secretion from parietal cells by >90% which causes a huge reduction in acid production
42
What is the mechanism of action of omeprazole?
Irreversible inhibitor of H+/K+ ATPase
43
When is omeprazole inactive and what effect does this have on its use?
It is inactive at neutral pH- limits action on other proton pumps around the body
44
Where does omeprazole accumulate and why?
As it is a weak base, it accumulates in the cannaliculi of the parietal cells where acid is produced
45
What effect does the accumulation of omeprazole at the cannaliculi have?
It concentrates its action in the cannaliculi and prolongs its duration of action (2-3 days) and minimises its effects on ion pumps elsewhere in the body
46
What are the uses of omeprazole/proton pump inhibitors?
Peptic ulcers that are resistant to H2 antagonists Component of triple therapy GERD, oesophagitis Prophylaxis of peptic ulcers in intensive care setting and among high risk patients prescribed aspirin, NSAIDs, anti-platelets and anti-coagulants
47
What are the pharmacokinetics of PPIs?
Orally active and adminstered as enteric coated slow release formulation
48
What are the side effects of omeprazole/PPIs?
Rare with short term use Long term and high dose use is associated with several potential side effects e.g. enteric infections, community acquired pneumonia and hip fracture
49
Give some examples of histamine receptor antagonists?
Cimetidine and ranitidine
50
What effect do histamine receptor antagonists have?
Inhibits gastric acid secretion from the parietal cells by about 60%- so less effective at healing ulcers than PPIs
51
What is MOA?
Competitive antagonist of H2 receptors
52
What are the pharmacokinetics of histamine receptor antagonists?
Orally administered Well absorbed Ranitidine is longer acting that cimetidine
53
What are the unwanted effects of histamine receptor antagonists?
Rare-dizziness and headache | less with ranitidine
54
What is a problem with withdrawal of histamine receptor antagonist treatment?
Relapses are likely- >90% recurrence within 1 year after initial healing This is why you need to use it as part of triple therapy
55
What do cytoprotective drugs do?
Enhance mucosal protection mechanisms and/or build a physical barrier over the ulcer
56
Give some examples of cytoprotective drugs?
Sucralfate Bismuth chelate Misoprostol
57
What is sucralfate?
Polymer containing aluminium hydroxide and sucrose octal-sulphate
58
What is the mechanism of action of sucralfate?
It acquires a strong negative charge when in acidic environment and it binds to positively charged groups in large molecules (proteins, glycoproteins) resulting in gel-like complexes which coat and protect the ulcer, limit H+ diffusion and pepsin degradation of mucous It also increases prostaglandin production in the stomach which leads to: Increase in mucous and bicarbonate production Reduced number of H pylori
59
What are the unwanted effects of sucralfate?
Most of the orally administered sucralfate remains in the GI tract which may cause constipation or reduced absorption of other drugs (antibiotics and digoxin)
60
What is the method of action of bismuth chelate like?
The same as sucralfate | It is used in triple therapy- in cases where resistance to drugs have been shown
61
What is misoprostol?
A stable prostaglandin analogue (orally active)
62
How does misoprostol have an effect?
It mimics the action of locally produced prostaglandins to maintain gasproduodenal mucosal barrier
63
How is misoprostol used?
Can be co-prescribed with oral NSAIDs when used chronically NSAIDs cause reduction in production of prostaglandins thus removing the protective effects of prostaglandins on the stomach so misoprostol causes the beneficial effects
64
What are the unwanted effects of misoprostol?
Diarrhoea Abdominal cramps Uterine contractions
65
What are antacids?
Mainly salts of Na+, Al3+ and Mg2+
66
What is the difference in onset of effects between Na+, Al3+ and Mg2+ antacids?
Sodium bicarbonate has rapid effects | Aluminium hydroxide and magnesium trisilicate have slower actions
67
What is the mechanism of action of antacids?
Neutralise acid, raises gastric pH and reduces pepsin activity
68
What are antacids primarily used for?
Non-ulcer dyspepsia
69
What are the problems with triple therapy?
Compliance- several drugs to take Antibiotic resistance Adverse response to alcohol (metronidazole interferes with alcohol metabolism)
70
What is GERD?
Gastroesophageal reflux disease- stomach and duodenal contents reflux into oesophagus causing inflammation
71
What will patients with GERD experience?
Heart burn
72
How is GERD treated?
Patients can self medicate with antacids and H2 antagonists
73
What can chronic GERD progress to?
Pre-malignant mucosal cells and potentially oesophageal adenocarcinoma
74
What is the drug of choice for chronic GERD?
Proton pump inhibitors- H2 antagonists are less effective but may be useful in patients that are resistant to PPIs. These drugs combined with drugs that increase gastric motility and emptying of stomach (dopamine receptor antagonists) further reduces the risk

LCRS Pharmacology and Therapeutics (33 decks)

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