Related Experiment Video
Updated: Jun 25, 2025
07:10
Measurement of the Hepatic Venous Pressure Gradient and Transjugular Liver Biopsy
Published on: June 18, 2020
20.4K
Widespread use of proton pump inhibitors or potassium-competitive acid blocker has changed the status of
Shun Sasaki1, Kazuhiro Ota2, Makoto Sanomura3
1Second Department of Internal Medicine, Osaka Medical and Pharmaceutical University, 2-7 Daigaku-machi, Takatsuki, Osaka, 569-8686, Japan.
BMC Gastroenterology
|May 21, 2024
Summary
Proton pump inhibitors (PPIs) effectively control acid-related gastrointestinal bleeding in patients after percutaneous coronary intervention (PCI). Non-acid-related bleeding risks include older age, lower weight, and warfarin use.
Area of Science:
- Gastroenterology
- Cardiology
- Pharmacology
Background:
- Proton pump inhibitors (PPIs) and potassium-competitive acid blockers (PCABs) are used for peptic ulcer prevention.
- Their effectiveness in preventing other gastrointestinal bleeding (GIB) is not well-established.
Purpose of the Study:
- To assess the incidence of GIB in the era of widespread PPI use.
- To identify risk factors for GIB in patients undergoing percutaneous coronary intervention (PCI).
Main Methods:
- Retrospective study of 515 patients undergoing PCI between 2018-2019.
- Patients were divided into two groups: those with GIB within 2 years of PCI (Group A) and those without (Group B).
Main Results:
- GIB occurred in 4.1% of patients (21/515).
- Significant differences between groups included older age, lower weight, and higher rates of concomitant warfarin use in Group A.
- Most patients (95.9%) were on PPIs or PCABs, with no significant difference between groups.
Conclusions:
- PPIs appear effective in controlling acid-related upper GIB in post-PCI patients.
- Older age, lower weight, and warfarin use are identified as risk factors for non-acid-related bleeding.
Related Concept Videos
01:13Acid Suppressive Drugs for Peptic Ulcer Disease: Proton Pump Inhibitors
376
Peptic ulcers, often induced by H. pylori infections or NSAID usage, arise from disruptions in the delicate balance of gastric acid production. Peptic ulcers stem from heightened gastric acid levels due to H. pylori infections or NSAID use. The protective mucus layer diminishes in the presence of these factors, allowing gastric acid to erode the stomach lining and form ulcers.
Gastric acid, a potent cocktail of hydrogen and chloride ions, is produced in specialized parietal cells within the...
Gastric acid, a potent cocktail of hydrogen and chloride ions, is produced in specialized parietal cells within the...
376
01:28Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists
425
Histamine H2 receptors, which are intricately located on the basolateral membrane of parietal cells, play a crucial role in modulating gastric acid secretion. When released from enterochromaffin-like cells, histamine engages H2 receptors, initiating the cyclic AMP (cAMP) pathway. In this pathway, adenylyl cyclase converts ATP into cAMP, elevating intracellular cAMP levels. The activation of protein kinase A follows, stimulating the proton pump. This stimulation prompts the secretion of hydrogen...
425
01:26Peptic Ulcer Disease IV: Management
88
Medical treatment strategies for peptic ulcers encompass various methods. The primary goal of treatment is to diminish gastric acidity and strengthen mucosal defense mechanisms.
The therapeutic approach involves ensuring adequate rest, implementing drug therapy, promoting smoking cessation, making dietary modifications, and emphasizing long-term follow-up care.
Pharmacological management
The prevailing therapy for peptic ulcers involves a combination of managing the patient's current...
The therapeutic approach involves ensuring adequate rest, implementing drug therapy, promoting smoking cessation, making dietary modifications, and emphasizing long-term follow-up care.
Pharmacological management
The prevailing therapy for peptic ulcers involves a combination of managing the patient's current...
88
01:20Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents
408
The gastric mucosa produces prostaglandins E2 (PGE2) and prostacyclin (PGI2), crucial in maintaining gastric health. They exert cytoprotective effects, including increasing bicarbonate secretion, releasing protective mucin, reducing gastric acid output, and preventing harmful vasoconstriction. These effects are mediated through various receptors, such as EP1, EP2, EP3, and EP4.
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...
408
01:31Acid Suppressive Drugs for Peptic Ulcer Disease: Antacids
348
In the complex environment of the gastric lumen, excessive acid secretion can lead to the formation or worsening of ulcers within the delicate mucosal layer. Antacids, such as sodium bicarbonate and calcium carbonate, provide relief by neutralizing this acid, transforming it into harmless salt and water. This neutralization process raises the gastric pH from a highly acidic level of 1 to a more basic 3-4, reducing the acidity within the stomach.
However, this neutralization reaction between...
However, this neutralization reaction between...
348
01:20Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors
521
Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
521