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Which factor is NOT typically associated with the development of peptic ulcers?
What is the primary purpose of 'triple therapy' in treating peptic ulcer disease?
Which class of medication is primarily associated with reducing stomach acid production?
Which of the following medications is used to manage nausea and vomiting?
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What mechanism do histamine H2 antagonists primarily target in the treatment of gastrointestinal disorders?
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What is the most common symptom of a peptic ulcer?
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At what age range do duodenal ulcers most commonly appear?
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Which factor is NOT an inhibitory regulator of gastric acid secretion?
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What role do prostaglandins play in the stomach?
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Which of the following is an aggressive factor that can contribute to the development of peptic ulcers?
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How do parietal cells primarily increase histamine release?
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Which symptom can signal a serious complication of a peptic ulcer?
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What is the primary physiological balance affecting peptic ulcers?
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Which of the following is a non-serious symptom of a peptic ulcer?
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What type of ulcer is more common in women over the age of 60?
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What percentage of individuals over 40 are likely to have H. pylori in their stomach?
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What is a common mechanism by which H. pylori can survive stomach acid?
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What is the lifetime risk of developing an endoscopic ulcer for H. pylori positive individuals?
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Which combination is preferred for first-line therapy against H. pylori?
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What is the common duration for H. pylori treatment?
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What action should be taken if infection persists after the treatment?
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Which of the following antibiotics is least likely to display resistance in H. pylori treatment?
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What is the primary reason for using two different antibiotics in H. pylori treatment?
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What is a primary effect of chronic NSAID use on the stomach?
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Which COX enzyme is primarily responsible for mediating inflammation and pain?
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What must be considered when withdrawing NSAIDs from a patient?
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What type of medication is commonly used alongside NSAIDs to promote healing of ulcers?
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What is the effect of NSAIDs on mucosal blood flow?
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Patients with NSAID-induced GI events should be tested for which bacterium?
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Which of these is NOT a consequence of NSAID usage?
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What is a common challenge when managing patients with chronic pain who need NSAIDs discontinued?
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What is the primary reason for treatment failure in H pylori eradication?
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Which of the following side effects is commonly associated with proton pump inhibitors (PPIs)?
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How does sucralfate provide protection to ulcerated tissue?
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What is a significant side effect of misoprostol?
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Which class of drugs is the mainstay for treating gastro-oesophageal reflux disease (GERD)?
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What is a common cause of poor adherence in patients being treated for H pylori infection?
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What is one of the roles of H2 receptor antagonists in acid-related diseases?
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What is a potential side effect of calcium-containing antacids?
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What is the mechanism of action thought to be used by bismuth salts in treating ulcers?
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Which of the following is a common non-pharmacological recommendation for treating gastro-oesophageal reflux disease (GERD)?
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What should patients be cautious about when taking antacids, especially those containing magnesium?
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Which medication is considered a prodrug that needs to be activated in an acidic environment?
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What is the typical treatment success rate for H pylori eradication therapy?
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Study Notes
Peptic Ulcer Disease
- Peptic ulcers are open sores that develop on the inside lining of the stomach and the upper part of the small intestine.
- Caused by acid-induced damage to the mucosa.
- Common causes include NSAID use and Helicobacter pylori (H.pylori) infection.
- Other contributing factors include genetics, stress, spicy foods, and smoking.
- Incidence: 1 in 10 individuals develop a peptic ulcer at some point in their lives.
- Duodenal ulcers commonly appear between ages 30 and 50, more common in men than women.
- Gastric ulcers occur later in life, after the age of 60, more common in women than men.
Peptic Ulcer Symptoms
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Mild Symptoms:
- Pain in the abdomen, described as burning or gnawing, often between meals or at night.
- Feeling of fullness, bloating, or belching.
- Intolerance to fatty foods.
- Heartburn.
- Nausea.
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Serious Symptoms:
- Dark blood in stools.
- Vomiting or vomiting blood.
- Trouble breathing.
- Feeling faint.
- Unexplained weight loss.
Gastric Acid Secretion
- Parietal cells are responsible for gastric acid secretion.
- Gastric acid secretion is complex and involves several control mechanisms.
Regulation of Gastric Acid Secretion
-
Stimulatory Factors:
- Gastrin: Released from G cells, acts on parietal cells and ECL cells, increasing calcium levels and histamine release.
- Acetylcholine (ACh): Released by mucosal nerves, acts on parietal cells and ECL cells via M3 receptors, increasing calcium levels and histamine release.
- Histamine: Released from ECL cells, acts locally on H2 receptors of parietal cells, increasing cAMP and PKA activity.
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Inhibitory Factors:
- Somatostatin: Released from D cells, inhibits gastrin, histamine, and acid secretion.
- Prostaglandins (PGE2/PGI2): Inhibit acid secretion, stimulate mucus and bicarbonate secretion, increase mucosal blood flow, and promote epithelial repair.
Pathophysiology of Peptic Ulcers
- A balance exists in healthy individuals between gastric acid secretion and gastroduodenal mucosal defense.
-
Mucosal Defense Mechanisms:
- Mucosal blood flow.
- Mucus secretion.
- Mucosal bicarbonate secretion.
- Mucosal cell restitution.
- Epithelial cell renewal.
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Aggressive Factors:
- Gastric acid.
- Pepsin.
- Bile salts.
- Helicobacter pylori (H. pylori) infection
- Nonsteroidal anti-inflammatory drugs (NSAIDs)
Drug-induced Ulceration
- Nonsteroidal anti-inflammatory Drugs (NSAIDs) commonly used to relieve pain, reduce inflammation, and lower fever.
- NSAIDs inhibit COX-1 and COX-2 enzymes, leading to reduced synthesis of prostaglandins (PGs) that protect the stomach lining.
- Chronic use of NSAIDs increase gastric acid secretion, decrease mucus and bicarbonate secretion, reduce mucosal blood flow, and hinder epithelial restitution, promoting ulcers.
Treatment of NSAID-induced Ulcers
- Discontinuation of NSAID often leads to ulcer healing.
- Proton pump inhibitors (PPIs) can be used to promote healing.
- Patients with NSAID-induced ulcers should be tested for H.pylori infection and treated if present.
Summary of NSAID-induced Ulcers
- Chronic NSAID use can cause peptic ulcers due to inhibition of COX enzymes and decreased synthesis of PGs.
- Treatment typically involves withdrawal of NSAIDs and use of PPIs.
Helicobacter pylori and Peptic Ulcer Disease
- Helicobacter pylori (H.pylori) is a spiral-shaped bacteria that commonly infects the stomach lining.
- Lifetime risk of developing a peptic ulcer in H. pylori-positive individuals is 10-20%.
- H. pylori survives in stomach acid by producing urease, which neutralizes acid.
- H. pylori infection causes gastric inflammation and epithelial cell death, leading to loss of the gastric barrier and increased vulnerability to acid and pepsin, resulting in ulcers.
Treatment of H.pylori Infection
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Triple Therapy:
- Two different antibiotics are used simultaneously to minimize the development of antibiotic resistance. Commonly used antibiotics include amoxicillin, clarithromycin, metronidazole, and tetracycline.
- An acid-suppressing drug such as omeprazole, pantoprazole, or esomeprazole is prescribed to heal the stomach lining.
- Treatment duration is typically 14 days.
- Repeat breath test at least two weeks after stopping PPI treatment and four weeks after finishing antibiotics.
- If infection is eradicated, the risk of re-infection within three years is approximately 10%.
- If infection persists, consider second-line therapy.
HSE Recommendations for H.pylori Treatment
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First-Line Therapy: Clarithromycin triple therapy is preferred:
- PPI.
- Clarithromycin.
- Amoxicillin or metronidazole.
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Alternative for Penicillin-Allergic Patients:
- Metronidazole and clarithromycin.
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Previous Metronidazole treatment:
- Clarithromycin and amoxicillin.
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Previous Clarithromycin treatment:
- Amoxicillin and metronidazole.
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Penicillin-Allergic and Previous Clarithromycin Treatment:
- Quadruple Therapy: PPI, metronidazole, tetracycline, and bismuth.
Treatment Failure of H.pylori Infection
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Causes of Treatment Failure:
- Antibiotic resistance, especially to clarithromycin and metronidazole.
- Poor adherence to treatment, often due to side effects like abdominal pain, diarrhea, altered taste, headache, and vomiting.
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Second-line Therapy:
- Use different antibiotics from first-line therapy and consider bismuth.
Summary of H.pylori and Peptic Ulcer Disease
- H.pylori infection is a common cause of peptic ulcer disease.
- Treatment involves triple therapy (two antibiotics and a PPI) aimed at eliminating H.pylori.
- Treatment success depends on lack of antibiotic resistance and patient adherence.
- Second-line therapy uses different antibiotics for patients with treatment failure.
Gastro-oesophageal Reflux Disease (GORD)
- When the lower oesophageal sphincter (LOS) does not close completely, stomach acid can reflux into the oesophagus, leading to heartburn.
- GORD is chronic and frequent reflux.
- GORD causes oesophageal inflammation (oesophagitis) and ulcers, and ultimately, Barrett's oesophagus.
- Diagnosis is made through upper GI endoscopy.
- Treatment:
- Lifestyle changes: diet, eating habits, and weight management.
- Oral medications: antacids, H2 antagonists, and PPIs.
Proton Pump Inhibitors (PPIs)
- Most potent class of acid-suppressing drugs.
- Mainstay of treatment for acid suppression in peptic ulcer disease, GORD, and prevention of ulcer development.
- Irreversibly inhibit the hydrogen potassium ATPase (H+-K+ -ATPase), the pump responsible for gastric acid secretion.
- PPIs are prodrugs activated by acid and convert to sulfenamide, which covalently binds to the pump.
- Examples include omeprazole, esomeprazole, lansoprazole.
Properties of PPIs
- Orally administered, taken 30 minutes before food.
- High bioavailability (80-90%).
- Short half-life (1-2 hours), rapidly metabolized in the liver.
- Long duration of action (48-72 hours) due to irreversible inhibition.
Side Effects of PPIs
- Well tolerated, occasional side effects include headache, nausea, dizziness, and rash.
- Drug interactions:
- Alter drug absorption due to increased gastric pH: - Increased digoxin absorption. - Decreased ketoconazole absorption.
- Interactions with the cytochrome P450 system can affect the metabolism of other drugs.
H2 Receptor Antagonists
- Histamine is released from ECL cells and acts on H2 receptors of parietal cells, increasing cAMP and PKA activity.
- H2 receptor antagonists competitively block H2 receptors, reducing histamine-stimulated acid secretion.
- Examples include cimetidine, ranitidine, and famotidine.
Properties of H2 Receptor Antagonists
- Rapid oral absorption from the small intestine.
- Peak concentration occurs 1-3 hours after administration.
- Eliminated via glomerular filtration and tubular secretion.
Side Effects of H2 Receptor Antagonists
- Generally safe.
- Mild side effects include diarrhea, dizziness, and muscle pain.
-
Drug Interactions:
- Cytochrome P450 Inhibition (cimetidine), affecting the metabolism of other drugs like phenytoin, theophylline, and warfarin.
- Increased gastric pH, reducing the absorption of drugs requiring an acidic environment such as ketoconazole and aspirin.
- Rare cases of nephrotoxicity and hepatotoxicity.
- Contraindicated in patients with hepatic failure or renal insufficiency.
Cytoprotective Agents
-
Misoprostol:
- Stable analog of prostaglandin E2.
- Reduced acid secretion from parietal cells, increases mucus and bicarbonate secretion, and inhibits histamine release from ECL cells.
- Effective in NSAID-induced ulcers.
- Side effects: Diarrhea, abdominal cramps, and uterine contractions.
-
Sucralfate:
- Forms a protective coating over ulcerated tissue.
- Binds to proteins in the ulcerated mucosa, forming a viscous protective gel that protects it from acid, pepsin, and bile salts.
- Increases mucosal PG concentration, maintaining mucosal blood flow and increasing bicarbonate and mucus secretion.
- Side effects: Constipation, nausea, and hypophosphatemia.
- Can affect drug bioavailability (e.g., tetracyclines, digoxin).
Bismuth Salts
- Given orally as bismuth subsalicylate.
- Mechanism of action unclear, but it protects mucosal lesions, inhibits pepsin activity, increases mucus secretion, and is toxic to H. pylori.
- Used in quadruple therapy for H.pylori infection.
- Side effects: Nausea, vomiting, reversible blackening of the tongue and feces.
Antacids
- Relieve mild and infrequent acid-related symptoms.
- Composed of calcium, magnesium, aluminum, or sodium salts.
- Directly neutralize stomach acid, increasing pH.
- Rapidly acting, within minutes, but have a short duration of action (30 minutes on an empty stomach, 3 hours after a meal).
- Increase in pH inhibits pepsin activity.
- Should not be used for more than 14 days without consulting a doctor.
- Well-tolerated.
Side Effects of Antacids
- Magnesium salts: May cause diarrhea.
- Aluminum salts: May cause constipation.
- Combination products: Can maintain normal bowel function by balancing magnesium and aluminum salts.
- Aluminum and magnesium: Systemic absorption can cause toxicity in patients with renal insufficiency.
-
Calcium salts (e.g., calcium carbonate): Potent antacids.
- Calcium absorption can lead to hypercalcemia, kidney stones, and milk-alkali syndrome.
- All antacids: Can bind phosphate in the gut, leading to hypophosphatemia and bone demineralisation.
-
Sodium antacids (e.g., sodium bicarbonate):
- Sodium retention may cause hypertension.
- Systemic alkalosis may cause nausea, muscle spasms, tremors, confusion, difficulty breathing.
- Allergic reactions: Very rare.
-
Drug interactions:
- Decrease absorption of acidic drugs like digoxin and ketoconazole.
- Inhibits absorption of some drugs by chelation with divalent ions (e.g., tetracyclines and fluoroquinolones).
- Altered dissolution of pH-sensitive enteric coatings.
- Urinary alkalisation can affect the elimination of many drugs (e.g., salicylates).
- Important Note: Antacids should be separated from interacting drugs by at least two hours.
Raft-forming agents
- Not acid-neutralizing.
- Form a viscous solution that floats on top of gastric contents, preventing acid reflux.
- Examples include guar gum, xanthan gum, carrageenan, pectin, locust bean gum, alginates (alginic acid).
Nausea and Vomiting
- Nausea - a stomach distress characterized by distaste for food and an urge to vomit.
- Vomiting - disgorging the contents of the stomach, and sometimes the small intestine, through the mouth.
- Vomiting is a natural body defense mechanism to prevent poisoning and infection.
- Vomiting can also be a symptom of underlying illness.
Control of Vomiting
- Vomiting is a reflex controlled by the central nervous system.
- Structures responsible for controlling vomiting are found in the medulla oblongata, a primitive part of the brain that regulates basic life-sustaining functions.
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Description
This quiz explores the essential aspects of Peptic Ulcer Disease, including its causes, symptoms, and incidence rates. Learn about the differences between gastric and duodenal ulcers and the factors that contribute to their development. Test your knowledge on this common gastrointestinal condition.
