NSG 501 – A&P
GI - Article Summary #1
January 17, 2015

Reference
Cope, G. (2013). Understanding smoking and nicotine effects on the gastrointestinal tract. Gastrointestinal Nursing, 11(1), 44-48.
Summary
Smoking remains a large problem worldwide with approximately one-quarter of the global population using tobacco products despite the worldwide campaign aimed to reduce tobacco use. Smoking and, more specifically, nicotine have many well-documented health impacts such as lung cancer and heart disease. However, the purpose of this article is to present the implications of smoking and nicotine on the gastrointestinal (GI) system. The author describes systematically how smoking and nicotine affect the stomach, small intestine, and colon as well as the causative agents that damage and protect the GI tract and their mechanisms of action.
Research Methodology The information presented by the author in this article came from a literature review. The author gleaned relevant data from nursing and medical research to offer the currently understood consequences of smoking and nicotine use on the GI system.
Application to Gastrointestinal A&P The author describes the anatomy, physiology, and pathophysiology of the GI tract as it pertains to smoking and nicotine.
What Did I Learn Within the stomach, smoking has been shown to prevent the production of bicarbonate ions by reducing prostaglandin synthesis, which controls bicarbonate secretion. Bicarbonate ions are important to the stomach mucosa because they help to form “a pH gradient, from strongly acidic on the luminal surface to neutral at the mucosa.” The absence of sufficient bicarbonate ions makes the mucus layer of the stomach susceptible to erosion, potentially leading to the development of peptic ulcers. It is important to note that peptic ulcer susceptibility can be exacerbated by the presence of heavy metals such as cadmium and arsenic in the gastric mucosa, which are absorbed from cigarette smoke. Within the small intestine, smoking is a known risk factor for the development of Crohn’s Disease (CD). Similar to the stomach, it is thought that the risk for CD is related to the compromise of the gastric mucosa caused by cigarette smoke. Additionally, there is concern that cigarette smoke is related to an alteration in immune response within the epithelial barrier of the small bowel. This alteration could be associated with the chronic inflammation present with CD, and subsequently, could be a factor in the “27-fold increased risk of adenocarcinoma of the small intestine.” In regard to treatment, it has been shown that smokers are more likely to need longer maintenance treatment, increased dose of medications, including immunosuppressants, and have a poorer response to treatment. Within the colon, smoking is a risk factor for such problems as appendicitis and collagenous colitis. On the other hand, smokers have been considered “protected” from the development of ulcerative colitis; though, the rationale behind this is not well understood. It s also believed that carcinoma of the colon, which has been linked with high alcohol intake, is exacerbated by smoking due to the “synergistic effect between tobacco and alcohol” in the formation of colorectal adenomatous polyps. Lastly, the article described the effect nicotine has on the immune system. “Animal studies show that nicotine lowers antibody production and T-cell proliferation, causing abnormal transmission of antigen-receptor-mediated signals, so that T-cells do not enter the cell cycle as expected and macrophages respond differently.”