Pharmacology: Drugs Affecting Acid Secretion Flashcards

1
Q

What are the defences that protect the gastric mucosa from acid?

A
  • Epithelial integrity
  • High cell turnover (there is a redundancy of cells in the gastric pits)
  • The mucus membrane barrier
  • Good vascular supply
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2
Q

What factors can aggravate and damage the gastric mucosa?

A
  • Acid
  • Helicobacter pylori
  • Drugs - NSAIDs, anticoags
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3
Q

How do NSAIDs cause increased risk of peptic uclers?

A

They affect the microvascular supply of the gastric mucosa - cause arterioles to contract due to lack of prostaglandins. The mucosa then becomes ischaemic and ulcers form.
The route doesnt matter (oral vs IV etc) which is a common misconception.

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4
Q

What is the role of parietal cells?

A

Epithelial cells that secrete HCl and IF.
They have a H+/K+ proton pump on the canalicular membrane.
They are stimulated by:
1. The H2 receptor (histamine)
2. The M3 receptor (Ach)
3. CCK and Gastrin

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5
Q

How do PPIs work?

Are they effective?

A

PPIs work by destroying the proton pump on the canalicular membrane.
They can only bind to active pumps therefore because not al pumps are active all the time they can take 2-3 to work.
They are v effective - it is rare to not respond to PPIs

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6
Q

How do H2 receptor antagonists work?

Are they effective?

A

The bind to and block the histamine receptor.
They have a short half life so need bd dosage.
V effective - reduce acid secretion by arounf 80%

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7
Q

Where in the GI tract does H Pylori cause ulcers?

A

75% of gastric ulcers (particularly in the antrum) are positive for H Pylori
95% of duodenal ulcers are positive for H pylori

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8
Q

What are the complications of H pylori infection?

A
  • ulcers
  • gastritis
  • stomach cancer
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9
Q

How is H pylori infection diagnosed?

A

Urea breath test - the patient swallows labelled urea. The labelled CO2 in the breath is then measured, indicates that the urea has been broken down. H Pylori is urease positive.

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10
Q

What is the treatment regime for H Pylori eradication?

A

7 day triple therapy: (all taken bd)

  1. A PPI
  2. Amoxicillin
  3. Clarithromycin or metronidazole

If allergic to penicillin use clarithromycin and metronidazole in place of amoxicillin.
Cause bad diarrhoea but must finish course.

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11
Q

What are the OTC treatment classes for peptic disorders?

A

Antacids such as rennies. Work to buffer the acid and give immediate relief.

Alginates such as gaviscon advance - adhere to the exposed mucosa to protect from acid.

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12
Q

Name some commonly prescribed H2 receptor antagonists?

A

Cimetidine (metabolised by P450 so can cause gynaecomastia)
Ranitidine
Nizatidine
Famotidine
They are considered safe- interactions and ADRs are minimal

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13
Q

Name some commonly prescribed PPIs

A
Omeprazole 
Lansopazole 
Rabeprazole 
Pantoprazole 
Esomeprazole 
Interactions are rare. Possible osteoporosis risk, increased C diff risk
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14
Q

What are the principles of treatment of GORD?

A

Symptomatic control - LOS is not working well, neutralise the acid so still got reflex but no symptoms.

Heal the oesophagitis

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15
Q

What are some lifestyle interventions for treating GORD?

A

3 evidence based interventions - raise the head of the bed, reduce chocolate intake, reduce alcohol.
Also lose weight and dont have heavy meals

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16
Q

What are the steps in the step up/down treatment pathway of GORD?

A
  1. Lifestyle
  2. Antacids / alginates
  3. H2RA
  4. PPIs
17
Q

What are the complications of GORD?

A
  • ulcers
  • oesophagitis
  • strictures
  • Barretts oesophagus
18
Q

What is Barretts oesophagus?

What are the complications?

A

Metaplasia of the lower portion of the oesophagus from stratified squamous to simple columnar.
Increased risk of adenocarcinoma.

19
Q

How is Barretts oesophagus managed?

A
  • survey with endoscopic biopsies for cancer
  • lifelong PPIs
  • ablative therapy to kill precancerous cells
  • oesophagectomy
20
Q

How are peptic ulcers treated?

A
  • Stop NSAIDs
  • Give H2RA or PPIs (6/52)
  • Eradicate H pylori