Abstract

Peptic ulcer is a common term used to generalize a gastrointestinal or stomach or duodenal ulcer. This digestive system disorder affects approximately 4.6 million people yearly in both male and female, and its mortality rate is about 1 in 10000 individuals, and the mortality rate due to an ulcer induced hemorrhage is about 5% (Stratemeier, & Vignogna, 2012). In the USA, about 10% of the population will develop the disease sometime in their life span (Stratemeier, & Vignogna, 2012).

Although peptic ulcer is rare compared to other known digestive system disorders, the disease can be life threatening if ignored and not treated.  It could lead to perforation of the digestive system and may cause significant damage to other organs or tissues of the body (Stratemeier, & Vignogna, 2012). Nevertheless, the aim of this study is to evaluate the causes of peptic ulcer and how important it is to distinguish the causes in relationship to the type of treatments administered.

Digestive System Disorder Case Study (DSDCS)

Regardless of the etiology of peptic ulcer, it simply involves the erosion or degradation of the mucous membrane lining of the digestive tract, thus causing a gradual tissue breakdown of the gastrointestinal walls (Stratemeier, & Vignogna, 2012). Before scientists discovered some of the major causes and risks of the disease, it was presumed that the disease were only caused by smoking, eating habit and stress. In the contrary, recent research discovered additional causes and risks associated with peptic ulcer onset. Peptic ulcer may be caused by other things, and the major factors include the imbalance of gastric acids and pepsin in the digestive tract, Gene effects, Aspirin and Nonsteroidal anti-inflammatory drugs (NSAIDs), and bacteria called Helicobacter Pylori (H. pylori) (Stratemeier, & Vignogna, 2012)

The imbalance of gastric acids and pepsins in the digestive tract is the inability of the digestive tract to neutralize and protect the mucous lining from harsh acidity environment of the gastrointestinal tracts (Stratemeier, & Vignogna, 2012). Naturally, the digestive system produces hydrochloric acid and pepsin to digest food in the stomach, but when acids are not buffered by the mucous lining of the stomach, intestine or duodenum; then they override the defense mechanism of the gastrointestinal tract and start eroding the mucosal wall (Stratemeier,  & Vignogna, 2012).

COX-1 gene is a constitutively expressed gene that produces prostaglandins (PG) which protects the stomach from the high acidity by inducing the secretion of mucous and mucosal blood flow, which buffers the stomach acidity. Scientists have been able to show that Aspirin and NSAIDs produce anti-thrombotic effects, which irreversibly acetylate serine in cyclooxygenase-1 (COX-1) and stops the production of thromboxane A2 (Shiotani, Sakakibara, Yamakanaka, et.al. 2009). Scientists also have shown that COX-1 has at least 9 single nucleotide polymorphisms (SNPs) and among the nine SNPs identified, 2 of the SNPs A-842G and C50T show increased sensitivity to acetylsalicylic acid (ASA) also known as Aspirin; and thus, the increase in sensitivity causes lower PG synthesis (Shiotani, Sakakibara, Yamakanaka, et.al. 2009). In fact, scientists have shown that there is a significant association between peptic ulcer among COX-1 variant population and aspirin users even at low doses, which shows that variant 1676T allele, for example, has a significant susceptibility effect for Aspirin related ulcers (Shiotani, Sakakibara, Yamakanaka, et.al. 2009).

Furthermore, Aspirin is a PG inhibitor, therefore, able to cause tropical initiation effect on epithelium cells. Moreover, due to an increased use of aspirin among older people as a palliative alternative to manage joint and muscular pain, ischemic heart, peripheral artery diseases, and stroke; the increased use of Aspirin has led to an increased prevalence of peptic ulcer among this age group (Ozdil, Cosar, Akkiz, et.al 2011). Ozdil, B et.al showed in their study that 10-25% of patients using NSAID show signs and symptoms of peptic ulcer while H. pylori ulcer related obstruction and perforation prevalence ranges from 1.3-5%. The study further showed that hemorrhage rate for patients using NSAIDs is about 61.5% and 74% for patients using ASA (Ozdil, Cosar, Akkiz, et. al 2011). Consequently, the study showed that 83.6% of patients with cardiovascular disease (CVD) and ulcer have hemorrhage, but only 20% of patients without CVD had hemorrhage. Thus, suggesting that CVD is associated with an increase in hemorrhage. On the other hand, among older patients, ulceration increases due to atrophy of gastric goblet cells. However, they concluded that age, CVD, ASA & NSAIDs have synergistic effects in reducing mucus production and regeneration potentials of the stomach lining and thus increased risk of ulceration (Ozdil, Cosar, Akkiz, et.al 2011).

Another associated factor that has an indirect relationship with peptic ulcer is the increase in the production of interleukin-1beta (IL-1β) due to enhanced inhibition of gastric acid, which triggers H. pylori to thrive in the stomach and causes significant damage to the stomach lining (Shiotani, Sakakibara, Yamakanaka, et.al. 2009). Therefore, H. pylori are also another strongly established and a significant factor that causes peptic ulcer.

According to Koskensola and Leppaniemi’s study, they showed that 10% of ulceration in their study was caused by H. pylori (Koskensola, & Leppaniemi, 2010). However, not everyone who is exposed to H. pylori will end up developing peptic ulcer, but people who are newly exposed to the bacteria will develop symptoms within few weeks of infection.  Scientists are still conducting studies to establish the relationship between those that has H. pylori with peptic ulcer and those that has the bacteria without the incidence of the disease. Nevertheless, one thing is clear and has been established. The infection pattern of H. pylori is common among lower-socioeconomic class and the elderly, which infected some people in their childhood and spans through their lifetime (Stratemeier, & Vignogna, 2012).

Regardless of what the etiology of peptic ulcer is; symptoms, signs and risk factors are usually the same, however, treatment methodology differs (Stratemeier, & Vignogna, 2012). Some of the indication of peptic ulcer is abdominal pain, urine or fecal bleeding, black-tarry sticky-looking stools, nausea, vomiting, loss of appetite, weight loss and fatigue to mention but a few (Stratemeier, & Vignogna, 2012). It is also important to know that these symptoms can occur in a variety of other diseases. Therefore, it is very important to perform upper gastrointestinal series (UGI) X-Ray, or Endoscopy (EGD) to confirm if peptic ulceration is the cause of the aforementioned symptoms (Stratemeier, & Vignogna, 2012). In addition, once peptic ulceration is confirmed, it is still very important to determine whether the disease is caused by H. pylori or other factors, or combinations of factors to be able to initiate effective treatment. Some of the ways to test for H. pylori are via Blood sample, Tissue biopsy and Breath test (which involves intake of special liquid that is readily metabolized by H. pylori and thus increases carbon dioxide exhalation) (Stratemeier, & Vignogna, 2012).

Peptic ulcer is a curable digestive system disease, and once the etiology is established, then the appropriate treatment can be initiated. “Triple therapy” or “Dual therapy”, which includes some antibiotics, may be used to treat peptic ulcer caused by H. pylori, and if the disease is not caused by bacteria, then acid inhibitor such as Omeprazole may be recommended, if the disease is due to acidification of the stomach (Stratemeier, & Vignogna, 2012). In a situation where the disease has progress to perforation stage, then surgery is required to correct and treat the injury, and a post-surgery medication will follow to treat the cause of the disease. In addition, lifestyle changes is required to help for the cure and recovery. For instance, peptic ulcer patient who is a smoker, must stop smoking, because smoking increases gastric acid and weakens the mucosal barrier of the gastrointestinal wall (Stratemeier, & Vignogna, 2012).

Researchers have done an amazing job in understanding the roots of this disease and have advanced combinations of preventative measures and treatment regime for this disease, yet, the disease mortality and prevalence is still relatively the same if not slightly higher every year (Stratemeier, & Vignogna, 2012). Although there may be many reasons associated with this slight increase in the prevalence of peptic ulcer despite all the etiological and therapeutic breakthroughs, major reasons for the increase of prevalence of this curable and preventative disease deals with lack of proactive public awareness programs relating to possible causes of the disease, and the increase of use of Aspirin and NSAIDs.

References

Digestive System Disorder (2012). Peptic Ulcer Disease. Dsdisorder.com. Retrieve from http://www.dsdisorders.com/2010/09/peptic-ulcer-disease-helicobacer-pylori.html

Koskensola, S. & Leppaniemi, A. (2010). Perforated duodenal ulcer: has anything changed?European, Journal of Trauma & Emergency Surgery, 36(2), 145-150.  Retrieve from  http://web.ebscohost.com.ezp.waldenulibrary.org/ehost/detail?vid=3&hid= 10&sid=b2a06830-496a-40be-9c04-9267c71623dc%40sessionmgr11&bdata=JnNp dGU9ZWhvc3QtbGl2ZQ%3d%3d#db=rzh&AN=2010635053.

Ozdil, B., Cosar, A., Akkiz, H., et.al (2011). Atherosclerosis and acetylsalicylic acid are  independent risk factors for hemorrhage in patients with gastric or duodenal ulcer. Anatolian Journal of Cardiology/Anadolu Kardiyoloji Dergisi, 11(1), 53-56. Retrieve from http://web.ebscohost.com.ezp.waldenulibrary.org/ehost/detail?vid=4&hid=10&     sid=b2a06830-496a-40be-9c04-9267c71623dc%40sessionmgr11&bdata=JnNpdGU9ZWhvc 3QtbGl2ZQ%3d%3d#db=rzh&AN=2010919156.

Shiotani, A., Sakakibara, T., Yamakanaka, Y., et.al. (2009). The preventive factors for aspirin-induced peptic ulcer: aspirin ulcer and corpus atrophy. Journal of Gastroenterology,44(7),717-725. Retrieve from http://web.ebscohost.com. ezp.waldenulibrary.org/ehost/detail?vid= 4&hid=10&sid=b2a06830-496a-40be-9c04-9267c71623dc%40ses sionmgr11&bdata=JnN pdGU9ZWhvc3QtbGl2ZQ%3d%3d#db=rzh&AN=2010337027.

Stratemeier, M., & Vignogna, L., (2012). Peptic Ulcers. eMedicine Health.com. Retrive from             http://www.emedicinehealth.com/peptic_ulcers/article_em.htm.