USMLE Step 2 Review 20 03 Drugs of Choice GERD Meds

USMLE Step 2 Review 20 03 Drugs of Choice GERD Meds

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Let’s start our USMLE Review with Drugs of Choice from the Gold Standard USMLE Step 2 Audio Review program.

Play USMLE Audio MP3 20 03 Drugs of Choice GERD Meds Below

 

Begin 20 03 Drugs of Choice GERD Meds Transcription

What older class of drugs were the first to successfully treat Gastro-Esophageal Reflux Disease?

  • These were the histamine receptor antagonists.

The other name for them?

  • H2 Blockers or H2 receptor antagonists.

What are the 2 best known H2 blockers?

  • Ranitidine or Cimetidine.

Trade name for Ranitidine?

  • Zantac.

And trade name for Cimetidine?

  • Tagamet.

What is the newer class of drugs for GERD which are more effective than the H2 blockers?

  • Proton Pump Inhibitors.

What percentage of patients have proton pump inhibitors been shown to give both symptom relief and healing of esophagitis?

  • 80%.

What is the primary proton pump inhibitor?

  • Omeprazole.

Trade name for Omeprazole?

  • Prilosec.

And what is the newer proton pump inhibitor, introduced in ’95 after Omeprazole?

  • Lansoprazole.

And the trade name for Lansoprazole?

  • Prevacid.

What is the other class of agents that do not work directly on the stomach acid, that have been used clinically for GERD, especially in combination with the H2 blockers?

  • The prokinetic agents.

And what is the primary prokinetic agent?

  • Cisapride.

Trade name for Cisapride?

  • Propulsid.

Cisapride (trade name Propulsid) has been shown in clinical trials to cause a approximately 50-70% improvement in the healing of esophagitis when used with a particular H2 blocker.

What is the H2 blocker?

  • Cimetidine.

Trade name?

  • Tagamet.

While it would be logical to use Cisapride (trade name Propulsid) in combination with a proton pump inhibitor, such as Omeprazole (trade name Prilosec), to increase symptom release and healing of esophagitis beyond what either could achieve alone, to my knowledge, there is not yet clinical trial results on that combination.

Is it possible for the patient to progress to Barrett’s esophagus while on effective acid suppressant medication?

  • Yes it is.

Why?

  • Because most of damage to the esophagus is actually done by the bile salts from the duodenum, not the gastric acid. In fact, using acid suppressant therapy may make the situation worse.

How?

  • The gastric acid refluxing into the esophagus actually protects the esophagus from the bile salts. The bile salts have more dilaterious effect on the esophagus in a non-acid pH.

In addition, acid suppression therapy may relieve what symptom while the patient continues to progress to Barrett’s Esophagus?

  • Heartburn.

What’s the bottom-line message, then, for following these patients?

  • Even though they may appear to become symptom free on H2 blockers or proton pump inhibitors or prokinetic agents, or some combination of those 3, you still may need to scope them later to double-check and make sure that they’re esophagitis has healed.

What class of medication has been most implicated in the formation of gastric ulcers?

  • The NSAIDs.

In addition to ulcers in the stomach, NSAIDs may also cause ulcers in what other structure?

  • The duodenum.

About what percentage of patients chronically taking NSAIDs have NSAID-associated ulcers?

  • 10-15%.

Which site for an NSAID- associated ulcer is more likely to bleed?

  • A duodenal NSAID ulcer.

And what percentage of patients chronically taking NSAIDs will suffer the complication of bleeding or even perforation?

  • 1-3%.

What disease condition most commonly illicits chronic taking of NSAIDs?

  • Rheumatoid arthritis.

After an initial acute episode of gout, what 4 interventions can be tried to prevent recurrence of gout that do not involve giving a medication?

  • First, weight loss. Second, avoiding organ meats in the diet, such as sweetbreads and liver. Third, minimizing or eliminating alcohol, and fourth, discontinuing medications which may precipitate gout attacks.

In general, there are 2 processes which may precipitate a gout attack by causing hyperuricemia.

What are they?

  • Overproduction of uric acid or underexcretion of uric acid.

From what organ?

  • The kidneys.

What general class of drugs are most likely to cause overproduction of uric acid?

  • The cytotoxic chemotherapeutic drugs for the treatment of cancer.

What poison may cause underexcretion, resulting in a kind of gout called “Saturnine gout”?

  • Lead.

How can alcohol lead to underexcretion of uric acid?

  • Via causing lactic acidosis.

There are 7 drugs or drug classes most associated with causing underexcretion of uric acid and thus, liable to precipitate a gout attack. In alphabetical order, what are they?

  • Cyclosporin, the Diuretics, Ethambutol, Levadopa, Nicotinic Acid, Pyrazinamide, and Salicylates.

Keeping in mind that list, if you have a patient worried about colon cancer, who seems to be getting recurrent gout, what questions should you ask them?

  • Are they taking a baby aspirin every day.

****END OF TRANSCRIPTION****

 

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