Brief Description Of the Complaint Selected

Helicobacter pylori (H. pylori) infection arises when the H. pylori bacilli contaminate any area of the gastrointestinal tract. H. pylori infection is the common frequent etiology of both duodenal and gastric ulcerations. H. pylori is a gram-negative, spiral-shaped organism with sheathed flagella detected in at least 90% of patients with duodenal ulcers (Cash et al., 2021).

Additionally, this pathogen has further been detected in about 40% to 70% of individuals with gastric ulcers (Cash et al., 2021). Approximately 15% is the predicted lifetime danger for acquiring PUD in H. pylori-infected individuals (Wang et al., 2015). At the same time, gastric cancer remains the third preeminent originator of cancer-related death globally, plus H. pylori infection implies accountability for 74.7% of total noncardia gastric cancer occurrences (Wang et al., 2015). However, H. pylori infection is likewise observed in individuals with asymptomatic gastritis and dyspepsia without ulceration; yet, eradicating the organism does not seem to make a difference in symptoms in patients with these conditions.

Evidence explicates that H. pylori disease might be present in a significant, exceeding number of individuals worldwide. However, the vast majority are not cognizant of this ailment due to the lack of self-evident signs or symptoms of active disease. The annual incidence of peptic ulcers is estimated to range from 0.1% to 1.8% (Cash et al., 2021). The ulcer incidence in

1. pylori-infected individuals is about 1% per year (Cash et al., 2021). There are two fundamental pathophysiological causes of ulcer formation: decreased mucosal protection and increased acid production (Berkowitz, 2020). As mentioned previously, infection with H-pylori is one of the most common causes of ulcer. Particularly, H. pylori lead to ulcer formation by both mechanisms: the bacterium damages the mucosal lining and creates an inflammatory process that leads to increased acid secretion.

Furthermore, the infection with H. pylori remains transmitted via the oral-fecal and oral- oral route, and rates of infection approach 100% in developing nations with impure water supplies (Berkowitz, 2020). In developed nations with pure water supplies, at least 75% of the population older than 50 years have been infected at some time (Berkowitz, 2020). Eradication of the organism dramatically alters the risk of relapse. Thus, social determinants such as living in an overcrowded household, living without a reliable supply of clean water, residing in a developing country, residing with one diagnosed with Helicobacter pylori infection in the past; all predispose higher risk factors for acquiring the disease (Diaconu et al., 2017). However, there are numerous antimicrobial combinations and evidence-based management considerations that are effective in treating H-pylori infections.

Necessary Review Of Systems

Infection by H. pylori proceeds to signify the most prevalent and persistent bacterial infection worldwide; consequently, obtaining an accurate, detailed, necessary review of the systems is imperative. Current evidence shows that H. pylori infection not only jeopardizes the balance within the gastrointestinal tract but also affects other systems such as cardiac, hematological, neurological, and metabolic syndromes.

Diaconu et al. (2017) denote that the role of H. pylori in developing idiopathic thrombocytopenic purpura, vitamin B12 deficiency, and iron deficiency anemia is thoroughly recognized. Furthermore, current evidence reveals that children diagnosed with type 1 diabetes signify a risk of acquiring H. pylori infection, even more so in incidents with a more prolonged duration of diabetes (Bazmamoun et al., 2016). Another study analysis to take into consideration

converges on the link between Helicobacter pylori infection and preeclampsia. This clinical study data shows abnormal uterine arteries Doppler velocimetry, proposing an impact of H. pylori infection in undermining placental development and resulting in a more eminent risk for acquiring preeclampsia (Di Simone et al., 2017). Additionally, evidence explicates matter further that H. pylori infection is correlated with metabolic syndrome disorders. According to Upala et al., infection with Helicobacter pylori is profoundly correlated with higher triglyceride, body mass index, homeostatic model assessment of insulin resistance (HOMA-IR), systolic blood pressure, and lower HDL (2016).

Thus, H. pylori infection mainly occurs in the gastrointestinal tract; however, relevant evidence-based research promptly urges the association of H. pylori with diverse conditions outside the gastrointestinal tract. Admittedly, this bacterium generates a low-grade inflammatory phase, induces molecular mimicry mechanisms, plus interferes with the absorbance of nutrients and drugs, probably influencing the incident or the progression of numerous conditions (Roubaud Baudron et al., 2013). Therefore, screening of H. pylori infection is helpful by assessing multiple systems holistically and disregarding the solely focus on merely the gastrointestinal system. The research evidence appraisal presented above unfolds the innovative perspective of assessing multiple body systems correlated with H. pylori infections.

What Would Be Seen On Physical Examination For This Complaint?

The clinical hallmarks of Helicobacter pylori infection are not always evident though they differ from asymptomatic gastritis to gastrointestinal malignancy. The response to H. pylori is variable. Not all individuals affected with H. Pylori proceed on to develop ulcers. On the one hand, H. pylori leads to intestinal metaplasia in the stomach resulting in chronic atrophic gastritis and, in some cases, stomach cancer (Diaconu et al., 2017). On the other hand, H. pylori alters gastric secretion and produces tissue damage, leading to Peptic Ulcer Disease (PUD) (Diaconu et al., 2017). In short, the response to H. pylori and its clinical manifestations are influenced by numerous factors, including genetics, the location and type of PUD, environment, and diet.

When it comes to the topic of specific clinical manifestations of H. pylori, multiple research considerations denote no notable variations in the appearance, including recurrence of manifestations, such as nausea, vomiting, pain, heartburn, or diarrhea, in patients who are affected with H pylori and those who remain free of this bacterium (Santacroce & Bhutani, 2021). No conclusive data exhibits a definite correlation among the manifestations of H pylori– related gastritis, abdominal pain, or dyspeptic symptoms from other diseases (Santacroce & Bhutani, 2021).

However, explicit health conditions where H. pylori infection remains the primary contributing factor can exhibit particular clinical manifestations. For instance, in duodenal ulcers, the most prevalent etiology is the presence of an ongoing H. pylori infection. Thus, presenting signs and symptoms for this specific condition involves epigastric burning, gnawing pain about

2-3 hours after meals, relief with foods and antacids, tender at the epigastrium, and left upper quadrant of the abdomen, and slightly hyperactive bowel sounds (Fitzgerald, 2017).

Additionally, non-erosive gastritis, chronic type B (antral) gastritis are primarily induced by an

1. pylori infection. Nausea, burning, and pain limited to the upper abdomen without reflux symptoms are the standard presenting signs and symptoms (Fitzgerald, 2017). Primary-care clinicians often encounter individuals with dyspepsia, which can emerge from a diversity of events. However, evidence shows that between 20% and 60% of individuals with functional dyspepsia hold evidence of Helicobacter pylori gastritis (Diaconu et al., 2017).

Differential Diagnoses Related to H. Pylori With Rationale Supporting It

Acute Gastritis:

• This condition incorporates a broad spectrum of events that aggravate inflammatory alterations in the gastric Many distinctive disorders contribute to similar overall clinical manifestations; nevertheless, they diverge in their exclusive histologic features. Besides, this disorder can be subdivided into erosive and non-erosive (regularly evoked by Helicobacter pylori) (El-Nakeep, 2020).

Peptic Ulcer Disease:

• PUD is circumscribed ulceration of the GI mucosa befalling in areas endangered to acid and pepsin. The clients’ antecedent ulcer records tend to prognosticate expected behavior and pathological probability of future Although the definite mechanisms of ulcer development continue inadequately understood, the process seems to include the interaction of acid production, pepsin secretion, H. pylori bacterial infection, and mucosal defense mechanisms (Cash et al., 2021).

Gastric Mucosa-Associated Lymphoid Tissue (MALT) Lymphoma:

• Research data is revealing the pathogenetic cascade of gastric lymphoma. It has been illustrated that H. pylori-related gastritis is the leading agent of MALT on the gastric mucosa. Certainly, the expansion of MALT in gastric mucosa may be deemed a pathological indication of H. pylori infection (Zullo et al., 2014). Conversely, every infected individual is at significant implied risk of exhibiting gastric MALT lymphoma, notably during a prolong infection (Zullo et al., 2014).

A Comparison and Contrast of Two Clinical Guidelines For H. Pylori

Clinical Guidelines are designed to render clinicians with updated evidence-based recommendations on the treatment of any disorder. For the purpose of this assignment, the two clinical guidelines for the treatment of H. Pylori incorporate recommendations from the American College of Gastroenterology and the American Family Physicians.

One implication of both guidelines is that all patients with active peptic ulcer disease (PUD), a history of PUD,(MALT) lymphoma or a history of endoscopic resection of early gastric cancer (EGC) should be tested for H. pylori infection (American College of Gastroenterology, 2017; American Family Physicians, 2015). Continuously, non-endoscopic testing for H. pylori infection is a plan for those individuals below 60 years of age displaying signs of dyspepsia without any other alarm features (American College of Gastroenterology, 2017; American Family Physicians, 2015). Both guidelines also claim that whenever H. pylori is recognized and treated, retesting to determine complete eradication of the infection must be implemented. This complete eradication confirmation should be arranged by utilizing a urea breath test, fecal antigen test, or biopsy-based testing at least four weeks following the end of antibiotic treatment plus following a withhold of 1 to 2 weeks of the usage of PPIs (American College of Gastroenterology, 2017; American Family Physicians, 2015).

Although much of the evidence examined was equivalent between the two guidelines, some inconsistencies were remarked. On the one hand, the American College of Gastroenterology suggests that all patient patients with unexplained iron deficiency (ID) anemia, despite an appropriate evaluation, should be tested for H. pylori infection (2017). On the other hand, the American Academy of Physicians advises testing for H. Pylori in patients diagnosed with ID only if dyspepsia is present (2015). Continuously, the quadruple bismuth therapy consisting of a PPI, bismuth, tetracycline, and a nitroimidazole for 10–14 days is a recommended first-line treatment option (American College of Gastroenterology, 2017). Although the American Academy of Physicians agrees that other regimens may be used, they insist that the non–bismuth-based quadruple therapy has the highest success rate in eradicating H. pylori (2015). Furthermore, the American Academy of Physicians insists that quadruple bismuth therapy is not considered first-line therapy; however, it may be used as first-line therapy in areas of high resistance or when the cost is an imperative consideration (2015).

Evidence-Based Diagnostic Plan

Stool antigen testing is the most well-known cost-effective method of diagnosing H. pylori, particularly when coupled with a clinical presentation consistent with other disorders based on multiple relevant research appraisals. Additionally, endoscopy with biopsy is the most accurate test, and the rapid urease test is the diagnostic test of choice for H. Pylori, according to recent evidence-based literature. For instance, in a relevant Cochrane report analysis, data from 99 comparisons were adopted to examine the diagnostic accuracy of these non-invasive tests to detect any infection concerning H. Pylori bacterium (Fischbach, & Malfertheiner, 2018). The study results endorse that the breath tests are, in fact, more diagnostically accurate than the serology tests but a similar accuracy with the stool antigen detection test (Fischbach, & Malfertheiner, 2018).

Acknowledgedly, the organism produces urease, which breakdowns urea into ammonia and CO2; this allows the organism to control pH in its local environment in the stomach by neutralizing H+ ions in gastric acid (Fitzgerald, 2017). As a result, urea breath testing is a valuable diagnostic method when attempting to establish the presence of H. pylori infection, though it is usually more expensive than the stool antigen test. Important data information recalls that current PPI use could result in a false negative with fecal and urea breath testing. Ideally, the patient should not take PPI for two weeks before these tests (American College of Gastroenterology, 2017).

Serological testing for H. pylori is similarly available, except for the flaw that titers can take years to fade even following satisfactory treatment. However, 50% of serologically tested individuals hold undetectable titers 12 to 18 months following therapy (Fitzgerald, 2021).

Endoscopy with biopsy tests in adults older than 50 years of age who manifest with new-onset PUD signs and symptoms should be adopted to determine the presence of H. Pylori, gastric ulcers or cancers (American College of Gastroenterology, 2017).

Evidence Based Management plan

Pharmacological Regimen

The Empirical pharmacological treatment for H. Pylori is the eradication of the H. Pylori bacteria in infected individuals. The current pharmacological approach follows a combination of antimicrobial and antisecretory agents. Additionally, although the mechanism of action is not well-defined, phytomedicines and probiotics are being adopted to enhance the eradication of H. pylori (Yang et al., 2014). Guidelines for the management of H. pylori infection are still unfolding and, depending on the geographic areas, the recommendation for first-line therapy, second third, and subsequent are supported differently. According to current evidence-based guidelines, the standard triple therapy constituted of a PPI, and two antibiotics (clarithromycin and amoxicillin/metronidazole) are generally adopted as the first-line regimen for treating H. Pylori infection. Therefore, the standard triple therapy for H. Pylori will incorporate clarithromycin (Biaxin) 500mg BID plus amoxicillin 1g BID or metronidazole (Flagyl) 500mg BID if allergic to amoxicillin for 14 days plus a PPI for 4 to 8 weeks.

In addition, bismuth-containing quadruple therapy (BQT) is approved as a first-line optional therapy for eradicating H. pylori in areas with high or low clarithromycin resistance because of its high efficiency and safety, and tolerance (Hu et al., 2020). This quadruple therapy consists of 12 days of treatment of bismuth subsalicylate tablet 525mg four times daily plus metronidazole 250mg four times daily plus tetracycline cap 500mg four times daily and a PPI or ranitidine 150mg twice daily. Subsequent therapies and failure therapies regimens for H. Pylori are available for clinical use, but it varies upon prognostics and eradication success outcomes.

Patient Education

Education regarding adequate pharmacological treatment to avoid antimicrobial resistance or complications is fundamental to be given to the individual affected by H. Pylori. Educate the client about ingesting the prescription as ordered. Do not stop the medication even if signs and symptoms have improved. Specific education in regards to medications should also be considered. For instance, advise the patient that metronidazole or clarithromycin may induce a metallic taste in the mouth.

Also, education in regards to the use of probiotics and vitamins must be delivered.

According to evidence-based research, probiotics as an adjunct to triple therapy can also improve the effectiveness of triple therapy and lessen the incidence of therapy-related diarrhea, which could preserve and restore the intestinal microbiota in adults and children undergoing therapy for

1. Pylori (Hu et al., 2020). Furthermore, an RCT study evaluated the impact of H. pylori therapy and vitamin supplementation (C&E) on the incidence and mortality of gastric cancer. This study found that vitamin C and E are recorded to produce an inhibitory effect on H. pylori intensity and neutrophilic activity, which benefit the eradication of H. pylori (Li et al., 2019)

Additionally, education regarding lifestyle modifications, avoid alcohol and cigarette smoking as it may interact with current medication taking or worse symptoms of the H. Pylori infection. Avoid caffeine, spicy food, chocolate, peppermint as it may increase acid production (Cash et al., 2021). Also, decrease salt consumption, as evidence shows that high dietary salt exacerbates H. pylori-induced inflammation (Haley & Gaddy, 2016).

Lastly, education concerning when to notify the primary care provider about worsening symptoms is also fundamental.

Follow-Up

A therapeutic trial of lifestyle changes combined with the appropriate pharmacological treatment should provide relief. There must be follow-up visits after the entire course of the therapy is completed. Repeating the breath test to confirm the eradication of H. Pylori is empirical. If the initial therapy was unsuccessful, alternative therapies should be considered. The central determinants of successful H. pylori eradication are the selection of regimen, the patient’s adherence to a multi-drug regimen with various side effects, and the sensitivity of the H.

pylori strain to the combination of antibiotics administered (Chey et al., 2017). In short, to determine the eradication of an H. Pylori infection, the clinician must order a urea breath test, fecal antigen test, or biopsy-based testing at least four weeks after the completion of antibiotic therapy and after 1–2 weeks of withholding the use of PPI (Chey et al., 2017).

Referrals

There is a need for consultation with both surgeon and gastroenterologist and admit the client to a hospital when symptoms of hemorrhage, penetration, perforation, or gastric outlet obstruction are present. In addition, clients with recurrences or refractory disease need a referral to a physician to evaluate H. Pylori by endoscopy or breath test.

Case Study

M.M is a 64-year-old Hispanic female who arrives in the clinic with a four-week history of intermittent, burning/gnawing epigastric pain moderately in intensity. The patient denied having signs and symptoms of melena, hematochezia, or hematemesis. Her medical history was notable for peptic ulcer disease. M.M reports traveling from a rural town in Colombia to Camden city about two months ago. M.M resides with her all-extended family. M.M recalls her husband having the same sign and symptoms. She also admitted to past use of an over-the-counter analgesic consisting of acetaminophen, aspirin, and caffeine. On examination, bowel sounds were present in all four quadrants. However, mild tenderness was noted over the epigastrium. Conclusion

Nurse Practitioners are essential clinicians in multiple healthcare settings in aiding the H. Pylori diagnosis and treatment based on current evidence-based research. This paper presented the management of H. Pylori based on current guidelines to treat and eradicate the infection successfully. In short, this paper presented the available interventions, along with the regimen goals for the treatment of H. Pylori, focusing on alleviating pain, discomfort, promote healing, limit complications, and preventing recurrences while minimizing the cost and side effects of treatment.

References

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Discuss the drug therapy used in the treatment of H. pylori to alleviate symptoms, promote healing, prevent complications, and prevent recurrence.

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