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Peptic Ulcers: Pathophysiology and Treatment Essay

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Updated: Apr 8th, 2022

Introduction

Ulcers generally occur along the entire gastrointestinal tract beginning from the lining of the mouth to the end of the rectal region (Chan, 2005). Peptic ulcers can be described as the lesions that affect the esophagus, duodenum and the stomach. Peptic ulcers develop mostly due to gastric acid action and subsequent Helicobacter pylori infection.

Some peptic ulcers develop following a prolonged use of anti-inflammatory drugs. Several therapeutic interventions have been established to control peptic ulcers. This paper seeks to carry out the following: offer a brief discussion of the relevant pathophysiology of peptic ulcers; discuss the pharmacological management of the condition, including the mechanism of action of particular drug classes; and critically examine other relevant findings from various journal articles.

The pathophysiology of peptic ulcers

As stated in the introductory part, peptic ulcers are ulcers that generally affect the gastric, esophagus and duodenal parts of the gastrointestinal tract. As the name suggests, hydrochloric acid and pepsin are involved in the development of peptic ulcers (Tang, Lui, Cheng, Lee, & Cheng, 2009).

In certain circumstances the gastric (hydrochloric) acid is often produced excessively resulting into a damaged mucosal membrane. Normally, the mucosal membranes function to protect the stomach and other internal organs from bacterial inversion and other forms of danger. The broken membrane therefore facilitates the penetration of Helicobacter pylori that proceeds to establish internal infections. The infection results into ulceration and inflammation of the infected area.

Peptic ulcers may also develop following a prolonged use of anti-inflammatory painkillers such as aspirin and NSAIDs. The prolonged use of anti-inflammatory painkillers inhibits the synthesis of gastric prostaglandin. Gastric prostaglandins are present in the gastric mucosa and gastric juice in elevated concentrations (Tang, Lui, Cheng, Lee, & Cheng, 2009).

The prostaglandin inhibits the secretion of gastric acid, stimulates the secretion of mucus and bicarbonate, and protects the mucosa from being damaged by a variety of agents (Tan H. J., 2010). When the synthesis of prostaglandin is inhibited, all these protection is lost. This usually occurs in patients with conditions such as arthritis, which require a prolonged use of anti-inflammatory painkillers. Peptic is ulcers are identified depending on the gastrointestinal region that is affected.

If the peptic ulcer is formed in the stomach it will be referred to as a gastric ulcer; that which has formed at the duodenal level is referred to as a duodenal ulcer; and a peptic ulcer that develops in the esophagus is called esophageal ulcer (Tan & Goh, 2008). In some rare cases, peptic ulcers develop due to stomach cancer.

At times, peptic ulcers can develop into severe perforate or bleeding ulcers that are considered to be dangerous. A perforated ulcer is clinically identified by the presence of a severe mucosal tear that results into sharp pain and sourness in the abdomen. A bleeding ulcer is diagnosed by the presence of internal hemorrhage (Chan, 2005). Research indicates that the two complicated forms of peptic ulcers are more likely to cause death and therefore require urgent medical intervention.

Each year, peptic ulcers affect millions of people around the world. Initially, the disease was more prevalent in males but this has changed as current statics show an increased prevalence in females. Research evidence attributes the change to increased number of female smokers. Smoking is a major risk factor in the development of peptic ulcers.

Major symptoms of peptic ulcers are inflammation, nausea and pain. Additionally, bleeding ulcers may cause fever, vomiting of blood, presence of blood in the stool, fatigue (Cheng & Sheu, 2011). Bleeding peptic ulcers may cause anemia and necessitate blood transfusion.

Pharmacological management of peptic ulcers

There are various classes of drugs that are used in pharmacological management of peptic ulcers. The drugs are often used to correct various mechanisms that may include: treating the symptoms; healing or preventing ulceration; eradicating Helicobacter pylori; and reducing gastric acid secretion (Chan, 2005). The pharmacological interventions seek to correct the imbalances between conflicting aggressive and defensive mechanisms. The drugs for treatment and prevention of ulcers are classified as follows:

Reduction of gastric acid secretion

H2 antihistamines

H2 Blockers such as ranitidine and Famotidine are used in peptic ulcer patients to inhibit the secretion of gastric acid (Tang, Lui, Cheng, Lee, & Cheng, 2009). Mast cells release histamine following the presence of antigens or in response to an injury. Histamine stimulates H-1 and H-2 receptors. The activation of H-2 receptors elevates the secretion of gastric acid. H-2 antihistamines act by blocking the activation of the H-2 receptors and thereby reducing the secretion of gastric acid. The anti-histamines have been largely replaced by the proton pump inhibitors which are found to be more effective.

Proton pump inhibitors

Proton pump inhibitors (PPIs) such as Omeprazole and Pantoprazole are prescribed for peptic ulcers that cause bleeding in the upper gastrointestinal region (Cheng & Sheu, 2011). The proton pump inhibitors are administered intravenously and act by inhibiting a proton pump ( H+, K+-ATPase) that is bound on the membranes of parietal cells. H+, K+-ATPase secretes the intragastric Hydrochloric acid that is responsible for stomach acidity (Cheng & Sheu, 2011).

Anticholinergic

Anticholinergics such as Pirenzepine are also used to inhibit gastric acid secretion in patients with peptic ulcers. The anticholinergics act by binding to the muscarinic acetylcholine receptors (Tan & Goh, 2008). Those that are used to inhibit gastric acid secretion act by antagonizing the action of acetylcholine and in turn inhibiting all reflexes that are vagally mediated, and that include the secretion of gastric acid (Tan & Goh, 2008).

Prostaglandin analogues

Prostaglandins regulate various mechanisms that include bicarbonate and basal acid secretion. The prolonged use of NSAIDs usually results in the suppression prostaglandin synthesis and therefore causes gastric ulceration (Lanas & Ferrandez, 2006). Prostaglandin E1 analogues such as Misoprostol and Rioprostil are administered to treat and prevent NSAID induced peptic ulcers by enhancing the mucosal defense and inhibiting gastric acid secretion (Lanas & Ferrandez, 2006).

Antacids

Antacids act by neutralizing gastric acid and therefore speeding up the healing of peptic ulcerations (Tan & Goh, 2008).

Mucosa Protective

Mucosa protective agents (MPAs) such as Sucralfate and Colloidal bismuth subcitrate are used to protect the mucosa from further acid attack in patients suffering from peptic ulcers (Chan, 2005). The MPAs react with the gastric acid to produce anions that can bind to positively charged proteins in a damaged tissue to form a barrier that prevents further acid attack (Tang, Lui, Cheng, Lee, & Cheng, 2009).

Anti H-pylori drugs

H. pylorus is eradicated using antibiotics such as Amoxicillin. Various antibiotics used in the treatment of peptic ulcers exert their action through competitive binding. Vaccines are often used to prevent or help in the cure of peptic ulcers. Vaccines against H. pylori are made using various H. pylori antigens (Chan, 2005).

Anti emetics

Anti emetics or emetics are not usually indicated for patients suffering from peptic ulcers. They may however prescribed in certain circumstances, for instance, patients with bleeding peptic ulcers experience nausea as one of the symptoms and thus require anti emetics.

Other relevant findings regarding peptic ulcers

In certain circumstances, patients suffering from peptic ulcers are required to undergo surgery. Usually, it’s rare for surgery to be indicated in patients with peptic ulcers, however, in cases where endoscopic management has failed or there are other conditions such as malignancies then surgery becomes an option. Individualized plans and early surgery increases the chance survival.

The use of some anti-inflammatory drugs has been known to result into the establishment or aggravation of already established peptic ulcers. Patients are often advised to minimize or to stop the use of drugs such as NSAIDs, salicylates, caffeine, reserpine, glucocorticoids and aminophylline drugs, when they are undergoing treatment for peptic ulcers (Lanas & Ferrandez, 2006). There is a current debate regarding the role of corticosteroids in the formation of peptic ulcers.

Normally corticosteroids are co administered with NSAIDs. NSAIDs are known to cause peptic ulcers and result into an increased probability of bleeding. Some studies have demonstrated a slight increase in bleeding when corticosteroids are administered alone. The risk is doubled when they are co-administered with NSAIDs.

Normally, Proton pump inhibitors (PPIs) are prescribed along with clopidogrel to reduce the risk of bleeding ulcers in patients who have undergone acute stent implant (Cheng & Sheu, 2011). Some studies show that there are increased instances of cardiovascular events and mortality that can be attributed to this combination. Other studies are refuting this claim creating a vacuum that needs to be filled by further research.

Several studies have also shown that peptic ulcer cases that are caused by H.pylori are decreasing steadily due successful eradication treatments. Studies conducted in Japan have shown a constant decline, from 72.7% in 1974, to 54% in 1984 and 39% in 1994 (Tan & Goh, 2008). Similar trends have been observed in other areas.

Conclusion

This paper sought to carry out the following: offer a brief discussion of the relevant pathophysiology of peptic ulcers; discuss the pharmacological management of the condition, including the mechanism of action of particular drug classes; and critically examine other relevant findings from various journal articles. It has been established that peptic ulcers affect the stomach, duodenum and esophageal areas of the gastrointestinal tract (Chan, 2005).

Peptic ulcers commonly occur due to gastric acid destruction of the intestinal mucosa followed by penetration of H. pylori that causes an infection (Tang, Lui, Cheng, Lee, & Cheng, 2009). Other causes of peptic ulcers include certain classes of drugs, particularly NSAIDs, and cancer to a lesser extent. Complications usually result into bleeding or perforated peptic ulcers that are both dangerous.

The pharmacological intervention for the treatment of peptic ulcers is broad and often targets specific symptoms, causal agent or other accompanying conditions. The eradication of H. pylori and control of gastric acid are the most important aspects of the pharmacological management. Additional drugs are required in case of bleeding peptic ulcers.

References

Chan, F. K. (2005). Should we eradicate Helicobacter pylori infection in patients receiving nonsteroidal anti-inflammatory drugs or low-dose aspirin? Chinese Journal of Digestive Diseases, 6: 1-5.

Cheng, H., & Sheu, B. (2011). Intravenous proton pump inhibitors for peptic ulcer bleeding: Clinical benefits and limits. World J Gastrointest Endosc, 3 (3): 49-56.

Lanas, A., & Ferrandez, A. (2006). NSAID-induced gastrointestinal damage: Current clinical management and recommendations for prevention. Chinese Journal of Digestive Diseases, 7: 123-133.

Tan, H. J. (2010). Controversy of proton pump inhibitor and clopidogrel interaction: A review. Journal of Digestive Diseases, 11: 334-342.

Tan, H., & Goh, K. L. (2008). Changing epidemiology of Helicobacter pylori in Asia. Journal of Digestive Diseases, 9: 186-189.

Tang, J. H., Lui, N. J., Cheng, H. T., Lee, C. S., & Cheng, Y. Y. (2009). Endoscopic Diagnosis of Helicobacter pylori Infection by Rapid Urease Test in Bleeding Peptic Ulcers. J Clin Gastroenterol, 43:133–139.

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