Read The Following Case Study And Answer All The Questions ✓ Solved

Read The Following Case Study And Answer All Of The Questions That Fol

Read The Following Case Study And Answer All Of The Questions That Fol

Read the following case study and answer all of the questions that follow: TS is 67 years old with a long history of knee osteoarthritis for which he self-medicates regularly with over-the-counter (OTC) naproxen. He is in the clinic today complaining of a swallowing difficulty that has progressively worsened over the past several months. He has otherwise been healthy and has not seen a doctor in many years. TS denies significant past medical history. A review of systems is negative except for arthritic symptoms and swallowing difficulty.

He denies noticing blood in his stool and vomiting blood. He denies history of gastroesophageal reflux disease (GERD) and ulcer. He does not drink alcohol, although he drank heavily many years ago. He does not smoke. TS describes the dysphagia this way: “Food gets stuck in my throat, and I can’t get it down.” The feeling occurs only after he has ingested solid food; liquids are not a problem. There is burning chest pain associated with meals. He is scheduled for an upper gastrointestinal endoscopy. What is the likely cause of his dysphagia? What advice should TS be given regarding his OTC medication at this time? What are the usual signs and symptoms of GERD? How will it be managed? Use scholarly sources for the answers/findings and citations.

Sample Paper For Above instruction

Esophageal dysphagia in elderly patients is often caused by structural abnormalities such as strictures, which may result from chronic gastroesophageal reflux disease (GERD), which leads to inflammation and scarring of the esophageal lining. In TS’s case, his symptoms of dysphagia, especially difficulty swallowing solids and the presence of burning chest pain after meals, suggest that GERD could be the underlying cause. GERD is characterized by the backflow of stomach acid into the esophagus, leading to mucosal injury, inflammation, and sometimes strictures that impede the passage of solid foods (Vakil et al., 2006).

Considering TS’s regular use of OTC naproxen, it is essential to advise him about the potential gastrointestinal side effects, particularly the risk of mucosal irritation, ulceration, and bleeding. Non-steroidal anti-inflammatory drugs (NSAIDs) like naproxen inhibit prostaglandin synthesis, which impairs mucosal defense mechanisms, thereby increasing the risk of erosions and ulcers in the gastrointestinal (GI) tract (Rainsford, 2009). Therefore, TS should be counseled to limit NSAID use, consider taking it with food or using gastroprotective agents such as proton pump inhibitors (PPIs), and report any symptoms of GI bleeding or worsening dysphagia.

The usual signs and symptoms of GERD include heartburn (a burning sensation in the chest), regurgitation of acid or food, chest pain, and sometimes dysphagia or a sore throat. Chronic GERD may lead to complications such as esophageal strictures, Barrett’s esophagus, or esophageal adenocarcinoma (Kahrilas et al., 2013).

Management of GERD typically involves lifestyle modifications and pharmacotherapy. Lifestyle changes include weight loss, elevating the head of the bed, smoking cessation, and dietary adjustments such as avoiding spicy foods, caffeine, and fatty meals. Pharmacologically, proton pump inhibitors (PPIs) are considered first-line therapy, as they effectively reduce gastric acid secretion, healing esophageal mucosa and alleviating symptoms (Moayyedi et al., 2019). In some cases, antisecretory agents like H2-receptor antagonists may be used, and surgical interventions such as fundoplication are options for refractory cases.

References

  • Kahrilas, P. J., Wei, J., & Pandolfino, J. E. (2013). Esophageal reflux and its complications. The New England Journal of Medicine, 368(11), 1079–1086.
  • Moayyedi, P., Lacy, B. E., Andrews, C. N., et al. (2019). ACG and CAG Clinical Guidelines: Management of gastroesophageal reflux disease. The American Journal of Gastroenterology, 114(1), 38–58.
  • Rainsford, K. D. (2009). Prostaglandins and NSAID-induced gastrointestinal damage. Inflammopharmacology, 17(5), 273–322.
  • Vakil, N., van Zanten, S. V., Kahrilas, P., et al. (2006). The Montreal definition and classification of gastroesophageal reflux disease: A global evidence-based consensus. The American Journal of Gastroenterology, 101(8), 1900–1920.

Causes of Type 2 Diabetes

Type 2 diabetes mellitus (T2DM) primarily results from a combination of genetic predispositions and environmental factors that lead to insulin resistance and beta-cell dysfunction. Obesity, especially central adiposity, is a significant risk factor that contributes to insulin resistance (Defronzo, 2009). Other causes include sedentary lifestyle, poor dietary habits, genetic susceptibility, and certain hormones and cytokines that interfere with insulin signaling pathways. Chronic inflammation associated with obesity further exacerbates insulin resistance (Hotamisligil, 2006).

Relationship Between Insulin Resistance and Hyperinsulinemia

Insulin resistance is a condition whereby tissues such as muscle, fat, and liver do not respond adequately to insulin, impairing glucose uptake and utilization (Shulman, 2000). To compensate for this resistance and maintain normal blood glucose levels, pancreatic beta cells increase insulin secretion, a state called hyperinsulinemia. Although initially adaptive, sustained hyperinsulinemia can lead to beta-cell exhaustion, worsening hyperglycemia over time (Bergman et al., 2001). Thus, insulin resistance and hyperinsulinemia are closely linked, with hyperinsulinemia serving as a compensatory mechanism to preserve euglycemia.

Endocrine Disrupters and Their Functions

Endocrine disrupters are chemicals that interfere with hormonal systems, disrupting hormonal synthesis, secretion, transport, binding, action, or elimination. These substances can mimic or block hormones, leading to adverse developmental, reproductive, neurological, and immune effects (Gore et al., 2015). Examples include Bisphenol A (BPA), phthalates, and polychlorinated biphenyls (PCBs). In the context of metabolic health, endocrine disrupters may influence insulin sensitivity and secretion, contributing to metabolic disorders such as obesity and T2DM (Heindel et al., 2017).

Effect of Glucose Concentration on Insulin Secretion

Glucose is the primary physiological stimulant for insulin secretion. When blood glucose levels rise after meals, glucose enters pancreatic beta cells via glucose transporter 2 (GLUT2). Increased intracellular glucose metabolism elevates ATP levels, leading to the closing of ATP-sensitive potassium channels. This results in cell depolarization, opening voltage-gated calcium channels, and the influx of calcium ions, which trigger insulin granule exocytosis (Ashcroft & Rorsman, 2012). Therefore, higher glucose concentrations promote increased insulin secretion to facilitate glucose uptake and maintain homeostasis.

Discussion of Article Findings in Relation to Endocrine Disrupters and Insulin Secretion

The study by Soriano et al. (2012) provides important insights into how endocrine disrupters like Bisphenol A (BPA) can influence pancreatic islet function. The research demonstrated that low doses of BPA rapidly enhanced insulin secretion in mouse and human islets via an estrogen receptor beta (ERβ)-dependent pathway. This supports the hypothesis that endocrine disrupters can modulate insulin secretion by interacting with specific hormone receptors in beta cells. The authors found that BPA’s insulinotropic effect occurs rapidly, suggesting a non-genomic mechanism mediated through ERβ activation, which subsequently influences intracellular signaling pathways responsible for insulin exocytosis (Soriano et al., 2012). These findings strengthen the link between endocrine disrupters and altered pancreatic function, implying that exposure to such chemicals might contribute to early or exaggerated insulin responses, potentially playing a role in the development of insulin resistance and T2DM. The data refute the notion that endocrine disrupters have no impact on insulin secretion, instead indicating that these compounds can significantly influence pancreatic endocrine activity at low doses.

References

  • Ashcroft, F. M., & Rorsman, P. (2012). Diabetes mellitus and the pancreatic beta cell: The last ten years. Cell, 148(6), 1160–1171.
  • Bergman, R. N., Ader, M., Hueckstaedt, R. E., et al. (2001). Testing the insulin resistance hypothesis: The homeostatic model assessment (HOMA). Diabetes, 50(3), 79–84.
  • Defronzo, R. A. (2009). Banting lecture: From the triumvirate to the ominous octet: A new paradigm for the treatment of type 2 diabetes mellitus. Diabetes, 58(4), 773–795.
  • Gore, A. C., Chappell, P. E., Fenton, S. E., et al. (2015). EDC-2: The endocrine disrupting chemicals review. Journal of Endocrinology, 226(3), R1–R172.
  • Heindel, J. J., Blumberg, B., Couleau, S., et al. (2017). Role of endocrine-disrupting chemicals in reproductive disorders and cancers. Reproductive Toxicology, 68, 30–44.
  • Hotamisligil, G. S. (2006). Inflammation and metabolic disorders. Nature, 444(7121), 860–867.
  • Shulman, G. I. (2000). Cellular mechanisms of insulin resistance. The Journal of Clinical Investigation, 106(2), 171–176.
  • Soriano, S., Alonso-Magdalena, P., García-Arevalo, M., Novials, A., & Muhammed, S. J. (2012). Rapid insulinotropic action of low doses of Bisphenol-A on mouse and human islets of langerhans: Role of estrogen receptor b. PLoS ONE, 7(2), e31109. doi:10.1371/journal.pone.0031109
  • Vakil, N., van Zanten, S. V., Kahrilas, P., et al. (2006). The Montreal definition and classification of gastroesophageal reflux disease: A global evidence-based consensus. The American Journal of Gastroenterology, 101(8), 1900–1920.
  • Rainsford, K. D. (2009). Prostaglandins and NSAID-induced gastrointestinal damage. Inflammopharmacology, 17(5), 273–322.

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