Ulcers Flashcards

1
Q

Proton pump inhibitors

A

Omeprazole
Lansoprazole
Pantoprazole
Esomeprazole
Rabeprazole

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2
Q

PPIs can lead to the toxicity of which drugs? How?

A

Cyclosporine, Warfarin, Diazepam. By reducing their metabolism because it is metabolised by the same enzymes responsible for their metabolism.

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3
Q

Adverse effects of PPIs

A

GI troubles
Vit B12 deficiency
Subacute myopathy
Arthralgia
Hypergastrinemia

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4
Q

How do PPIs cause Vit. B12 deficiency?

A

The vitamins need acid for absorption. Prolonged use will impair the process.

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5
Q

What is the effect of hypergastrinemia?

A

Rebound gastric acid secretion
Gastrointestinal carcinoid tumours

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6
Q

What are the clinically administered H2 antagonists?

A

Cimetidine
Ranitidine
Famotidine
Nizatidine

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7
Q

Classes of drugs used to manage ulcers (8)

A

PPIs
H2 receptor antagonists
Muscarine receptor antagonists
Antacids

Prostaglandin analogues
Sucralfate
Colloidal bismuth compounds
Carbenoxolone

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8
Q

Examples of Muscarine receptor antagonists

A

Pirenzepine
Telenzepine

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9
Q

Some antacids stimulate PG synthesis. True or false?

A

True

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10
Q

Adverse effects of M3 receptor antagonists

A

Xerostomia
Constipation
Blurred vision
Dyspepsia
Cognitive impairment

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11
Q

Antacid examples

A
  • Sodium bicarbonate
  • Calcium carbonate
  • Aluminium hydroxide
  • Magnesium hydroxide
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12
Q

What drugs are contraindicated in the use of antacids? Why?

A

Tetracycline and iron. The antacids impair the absorption of other drugs.

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13
Q

Why is sucralfate preferred to PPIs in treatment of ulcers in critically ill patients?

A

Because increased gastric pH may be a factor in the development of nosocomial pneumonia in critically ill patients

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14
Q

Why should sucralfate be avoided in patients with renal failure

A

Because some aluminium is absorbed

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14
Q

Why should sucralfate be avoided in patients with renal failure

A

Because some aluminium is absorbed

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15
Q

Sucralfate should be taken at least 2 hours after the administration of other drugs as phenytoin and digoxin. Why?

A

It forms a viscous layer in the stomach that may inhibit the absorption of drugs

16
Q

Prostaglandins inhibit histamine-stimulated gastric acid secretion. True or false?

A

True

17
Q

Which class of anti-ulcer agents would you use as a component of quadruple therapy to heal H. pylori ulcers?

A

Bismuth subsalicylate

18
Q

Bismuth subsalicylate MOA

A
  • Coats ulcers and erosions protecting them from acid and pepsin
  • Increases prostaglandin and bicarbonate production
19
Q

Therapeutic uses of bismuth subsalicylate

A

Dyspepsia
Acute diarrhoea

20
Q

Adverse reactions of carbenoxolone

A

It has aldosterone like action and may cause:
1- Sodium retention
2- Hypokalemia
3- Oedema
4- Exacerbates hypertention

21
Q

What is the role of somatostatin in gastric acid production?

A

Increased gastric pH reduces somatostatin release. Acidification stimulates gastrin release in a negative feedback loop. It is less in H. pylori patients, leading to excess gastrin and acid release.

22
Q

At what pH is somatostatin release stimulated?

A

3

23
Q

Metabolite of PPI

A

Tetracyclic sulphenamide/sulfenic acid