Peptic Ulcers and Treatment Overview

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Questions and Answers

Which of the following is most frequently associated with the development of peptic ulcers?

Genetic predisposition to high stomach acid levels

Excessive consumption of fatty foods

Infection with *Helicobacter pylori* (correct)

Prolonged periods of strenuous exercise

In the urea breath test, what enzyme produced by H. pylori is responsible for breaking down urea?

Lipase

Pepsin

Urease (correct)

Amylase

A patient reports experiencing abdominal pain that improves after eating. This symptom is most suggestive of which type of ulcer?

Appendiceal ulcer

Duodenal ulcer (correct)

Esophageal ulcer

Gastric ulcer

What is the primary mechanism of action of proton pump inhibitors (PPIs)?

Inhibiting the H+/K+ ATPase pump Signup and view all the answers

Why are proton pump inhibitors (PPIs) formulated with enteric-coated granules?

To prevent their activation in the stomach Signup and view all the answers

Which of the following is NOT a recognized indication for the use of proton pump inhibitors (PPIs)?

Constipation Signup and view all the answers

How do PPIs become 'trapped' inside parietal cells?

They become protonated in the acidic environment and lose lipophilicity Signup and view all the answers

A patient with a peptic ulcer is experiencing pain that worsens immediately after eating, and a slight amount of hematemesis. This is most indicative of a:

Gastric ulcer with moderate bleeding Signup and view all the answers

Which of the following is a common side effect of long-term use of proton pump inhibitors (PPIs)?

Decreased calcium absorption Signup and view all the answers

What is the primary mechanism of action of Histamine 2 receptor antagonists?

Blocking H2 receptors to decrease gastric acid secretion Signup and view all the answers

Which antacid compound is known to potentially cause constipation?

Aluminum hydroxide Signup and view all the answers

Why are non-systemic antacids preferred over systemic antacids for symptomatic treatment of GERD?

They are less likely to cause metabolic alkalosis. Signup and view all the answers

What is the function of sucralfate as a mucosal protectant?

Creates a thick gel-like protective layer on the mucosa. Signup and view all the answers

Which of the following is a common side effect of bismuth compounds?

Black discoloration of the teeth and tongue Signup and view all the answers

What effect does Misoprostol have on the gastric mucosa?

Decreases acid secretion and increases mucosal blood flow Signup and view all the answers

What is the primary use for M1-selective muscarinic antagonists such as pirenzepine and telenzepine in the treatment of ulcers?

Treatment of ulcers that don’t respond to PPI or H2 blocker therapy Signup and view all the answers

A patient with renal failure is prescribed an antacid, what is the main risk to be aware of?

Hypermagnesaemia Signup and view all the answers

What constitutes the triple therapy for H.pylori-positive peptic ulcers?

A proton pump inhibitor, clarithromycin, and amoxicillin or metronidazole Signup and view all the answers

Study Notes

Peptic Ulcers

Peptic ulcers are breaks in the stomach or duodenum lining, penetrating the mucosa and potentially the submucosa.
Duodenal ulcers are often linked to excess stomach acid, while gastric ulcers are more associated with decreased protective factors.
Common causes include alcohol consumption, NSAID use, stress, and most significantly, Helicobacter pylori.

Helicobacter pylori

H. pylori is responsible for the majority of peptic ulcers.
Diagnosed by a urea breath test, where a patient ingests radioactive urea.
H. pylori possesses urease, breaking urea into ammonia and bicarbonate. Some bicarbonate is exhaled as CO2, allowing quantifiable measurement via the detected radioactive CO2.

Symptoms

Pain is a primary symptom.
Duodenal ulcers cause pain upon fasting, relieved by eating.
Gastric ulcers cause pain worsening with eating.
Bleeding can also occur.

Treatment: Medications

Proton Pump Inhibitors (PPIs)

Inhibit acid production by blocking the H+/K+ ATPase (proton pump).
Examples: Omeprazole, Esomeprazole, Pantoprazole, Lansoprazole
Indications: GERD, peptic ulcer, Zollinger-Ellison syndrome, acid reflux.
Mechanism: Irreversibly bind to H+/K+ ATPase; lipophilic at neutral pH, becoming protonated and trapped inside parietal cells when in the acidic environment of the parietal cell.
Dosage: Oral enteric-coated granules to prevent stomach acid destruction.
Side effects: Gastrointestinal issues, increased C. difficile infection risk, decreased iron & B12 absorption, long-term: decreased calcium absorption, osteoporosis.

Histamine 2 Receptor Antagonists (H2RAs)

Block histamine 2 receptors, which stimulate acid secretion.
Examples: Cimetidine, Ranitidine, Famotidine
Indications: GERD, peptic ulcer, stress ulcer prophylaxis
Mechanism: Decrease acid and pepsin secretion, promote ulcer healing.
Pharmacokinetics: Primarily eliminated through the kidneys
Side effects: Cimetidine: erectile dysfunction, gynecomastia; general: few

Muscarinic Antagonists

Block neuronal regulation of acid production.
Examples: Pirenzepine, telenzepine
Indications: Ulcers unresponsive to PPIs or H2RAs
Side effects: Parasympatholytic effects (bronchodilation, decreased secretions)

Antacids

Neutralize stomach acid through base interactions
Types: Systemic (absorbed, causing metabolic alkalosis) and non-systemic (not absorbed).
Examples: Sodium bicarbonate, Magnesium hydroxide, Aluminum hydroxide
Indications: Symptomatic relief for GERD, heartburn (non-systemic favoured).
Mechanism: Salts of bases neutralize stomach acid
Side effects: Potential for metabolic alkalosis(systemic), discomfort, and flatulence (due to CO2 formation). Interactions possible with other drugs.
Counterindications: Renal failure patients (hyperaluminaemia, hypermagnesaemia) should avoid. Milk-alkali syndrome risks with excessive use

Mucosal Protectants

Enhance endogenous mechanisms or provide a physical barrier.
Sucralfate: Forms a protective layer on the mucosa, needs acidic pH to work. Primarily for prophylaxis.
Bismuth compounds: Bactericide against H. pylori, protective layer, rarely used due to potential discoloration and encephalopathy
Misoprostol: Prostaglandin E1 analogue, increases mucosal protection, Decreases secretion but increases mucous secretion, blood flow. Primarily for use in long-term NSAID users to prevent NSAID related ulcers. Common side effects: Diarrhea and nausea.
Carbenoxolon: Increases gastric mucus, decreases acid secretion. Not frequently used due to potential mineralocorticoid-like side effects.

Antibacterial Treatment

Triple therapy (for H. pylori): 7 days of a PPI, clarithromycin, and either amoxicillin or metronidazole
Quadruple therapy (for H. pylori): Triple therapy plus bismuth

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Description

Explore the causes, symptoms, and treatment options for peptic ulcers in this comprehensive quiz. Learn about the role of Helicobacter pylori and the effectiveness of Proton Pump Inhibitors in managing these conditions. Test your knowledge and deepen your understanding of ulcer pathophysiology.