Please reply to the discussion post. There are two discussion post below. Please respond to each post with a minimum of ONE PARAGRAH FOR EACH POST
Please respond to at least two of your fellow students. These posts should critically engage your fellow student. Try thinking critically about the exposure that the student discussed. What research refutes that this relationship is causal? Is it disputed? Why or why not?
Nicasze Augustin
Week 4 discussion
COLLAPSE
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Shingles
Shingles is a painful rash that develops on the body due to the reactivation of the chickenpox virus in the body also known as Varicella Zoster Virus. If you have gotten chickenpox as a child and recovered from it, the virus stay dormant in the body. Then as you get older it may reactivate itself as shingles. Shingles consists of blisters that scab over in 7-10 days but takes up to a month before it completely clears up. It is transmitted through direct contact with the fluid from your rash blisters. It can spread the VZV to people who have never had chickenpox or never received the chickenpox vaccine. If they get infected, they will develop chickenpox, not shingles. They could then develop shingles later in life. Some signs and symptoms include pain on the affected area, blisters, scabs, burning sensation and fatigue.
According to the CDC, you can get shingles at any age but people who are 50 years of age and older are more prone to getting the disease. 90% of adults in the United States carry VZV and are at risk for the development of herpes zoster (Cohen KR et al., 2013). In one population based study there is a 0.3% rate of VZV reactivation in the overall population compared with 1.0% in persons older than age 80. In another study the incidence rate of VZV reactivation was 0.5% in people older than age 75. This helps confirm that people who are 50 years and older are more prone to getting this disease.
This to me would be considered a temporal relationship since we know that what causes shingles. Due to the population based studies we see that the incidence rate in people over the age of 50 are the ones who are more affected by it.
Citation Cohen KR, Salbu RL, Frank J, Israel I. Presentation and management of herpes zoster (shingles) in the geriatric population. P T. 2013;38(4):217-227.
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Sheri Groves Wills
H. pylori
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Looking at Peptic Ulcers and Gastric Cancers in Relation to infection with Helicobacter pylori (H. pylori). According to our textbook (Gordis, 2014), until the 1980s, the major cause of peptic ulcer disease were considered to be lifestyle choices such as smoking and stress factors. Peptic ulcer disease has long been attributed to the effect of gastric acid, and susceptibility to gastric acid has been linked to alcohol consumption, cigarette smoking, and the use of anti-inflammatory agents. Therapy was primarily directed at inhibiting acid secretion and protecting the mucosal surfaces from acid, and although therapies sometimes helped in healing, relapse was very common. Australian physicians by name of Drs. J. Robin Warren and Barry J. Marshall announced in 1984 that they have observed small curved bacteria that colonize the lower part of the stomach in patients with peptic ulcers and gastritis (later named Helicobacter pylori or H. pylori). Many of these patients had biopsies performed and it showed the evidence of inflammation present in the gastric mucosa close to where the bacteria were seen. Researchers have now established that H. pylori causes up to 80 % of gastric ulcers and more than 90% of duodenal ulcers. The link between H pylori infection and subsequent peptic and gastric ulcer disease has been established through antibiotic treatment study, studies of human volunteers, and epidemiological studies. According to Uemura and colleagues (2011), who prospectively studied 1,526 Japanese patients that had gastric, duodenal ulcers, 1,246 of them had H. pylori infection and 280 did not. The mean follow-up period was 7.8 years. Gastric cancers were developed in 36 (2.9%) of the infected patients, but not in the non-infected patients. Patients who carry the antibodies to H. pylori were 2-3 times at higher risk of developing stomach cancer than those who did not. Evidence is supporting the idea that therapy against H. pylori may prevent gastric cancer
References
Gordis, L. (2014). Epidemiology, 5th edition with STUDENT CONSULT online access. New York: Elsevier Health Sciences.
Uemura N., Okamoto S, Yamamoto S, et al. (2011). Helicobacter Pylori infection and the development of gastric cancer. New England Medical Journal 345:784-789.
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