The Effects of Digestive Disorders

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Table of Contents

Introduction
The pathophysiology of inflammatory bowel disease and irritable bowel syndrome
Similarities and differences in the pathophysiology of IBD and IBS
Diagnosis and treatment of IBD and IBS
Impact of genetics on the pathophysiology and treatment of digestive disorders
Conclusion
References

Introduction

Digestion is the breakdown of food compounds into compounds suitable for the body. The digestive system is a complicated system that starts from the mouth to the anus. Gastric acid secretion controls the digestion of food compounds. The pH of the intestinal walls that control digestion is 0.8.

However, the digestive disorder is an imbalance caused by differential changes in acidity levels. Thus, digestive disorders include blood stool, heartburn, abdominal pain, weight loss, inflammatory bowel disease, GERD, irritable bowel syndrome, gallstones, constipation, chronic pancreatitis, and ventral hernia (Hanauer, 2012).

The pathophysiology of inflammatory bowel disease and irritable bowel syndrome

To understand the pathophysiology of inflammatory bowel diseases, clinicians must correlate the effects of different environmental factors. A previous study suggested that environmental factors, genetic association, microbial agents, humeral immunity, cytokines, and sensory mediator might influence the pathogenesis of IBD ((Katsanos & Tsianos, 2010)).

However, factors include an unidentified pathogenic organism, immune response phase, and an autoimmune process. The predisposing factors include genetics, abnormal immune activity, smoking, and the patient’s behavior. Clinicians believe that unidentified bacteria and dietary antigens penetrate the intestinal wall during IBD pathophysiology.

As a result, the immune response activates the immune system that triggers the inflammatory process. Thus, the activation affects the permeability of the normal intestine. Consequently, the unidentified antigen enters the immune effector cells. Finally, diet, smoking, systematic immune deregulation, 5-ASA, NSAIDs, genetic predispositions, inflammation, and extrinsic factors control the pathophysiology of inflammatory bowel disease.

Clinical examinations will assess the pathophysiology of irritable bowel syndrome. However, clinicians suggest that changes in GI motility, psychosocial factors, and visceral hyperalgesia induce the pathophysiology of irritable bowel syndrome. An essential activity occurs in the gastrointestinal tract. The enteric nervous system regulates and modulates the neurotransmitter serotonin. However, an imbalance in the GI tract alters signals transfer to the brain.

As a result, the sensory neurons are stimulated to cause pain. Clinicians suggest that the 5-HHT4 receptors influenced the breakdown of sensory communication during the pathophysiology of irritable bowel syndrome. Previous studies revealed that visceral hypersensitivity controlled the balloon dilatation in the intestinal tract.

Similarities and differences in the pathophysiology of IBD and IBS

Irritable bowel syndrome and inflammatory bowel disease share some common symptoms. The similarities of both disorders include abdominal pain, bloating, distention, persistent diarrhea, menstrual complications, urinary conditions, fibromyalgia, anxiety, and depression. Irritable bowel syndrome and inflammatory bowel disease have a common mucosal immune response system. Irritable bowel syndrome is a functional disorder while inflammatory bowel disease is a chronic condition that affects the intestine. Genetic markers have been associated with inflammatory bowel disease.

However, IBD patients experience eye irritations, fever, anemia, prolonged sexual maturation, skin irritations, weight loss, arthritis, colon cancer, osteoporosis, and liver complications (Podolsky & Xavier, 2012). Patients with irritable bowel syndrome experience alternate constipation and diarrhea.

Diagnosis and treatment of IBD and IBS

To understand the treatment options for IBD and IBS, clinicians must observe the symptoms of both disorders. Inflammatory bowel diseases cause disruptions in the small and large intestine while irritable bowel disease causes pain and cramp. As a result, the treatment option for IBS is different for inflammatory bowel disease (McPhee, & Hammer, 2012).

The treatment options for IBS include antispasmodics, antidepressants, antibiotics, dietary modifications, and psychotherapy. However, treatment options for IBD include dietary modification, alternative medicine, Ostomy surgery, medications, colitis surgery, and Crohn’s surgery. The common treatment for both disorders is dietary modification. However, clinicians can change the medication based on observable symptoms. It is difficult to combine medication for both disorders.

Impact of genetics on the pathophysiology and treatment of digestive disorders

Previous studies suggested that genes influenced the pathophysiology of both disorders. However, psychosocial and environmental factors affect IBD disorder. Thus, genetics cannot influence colon motility stimulation. Genetic factors include susceptibility and associated risk. As a result, genes influence the susceptibility of the disease (Lembo, Zaman, Jones, & Talleey, 2010). Drug administration and intervention require careful clinical examination. However, gene transfer can reduce the inflammatory process. The study of genetics and gene transfer will improve the quality of health intervention for both disorders.

Response 1

The response post suggested that early testing would improve the clinical examination. However, clinicians can use drugs to reduce abdominal pain. Dietary medication is another intervention technique. Surveys suggest that food tolerance and avoidance can improve the patient’s health status. Thus, the patient’s family history and behavior influence early detection and treatment (Centers for Disease Control and Prevention, 2011).

Response 2

The response post suggested that smoking could slow the pathophysiology of IBD and IBS. However, a previous survey revealed that environmental factors predisposed an individual to IBD. Thus, smoking habits may influence the pathophysiology of inflammatory bowel diseases. As a result, early testing will mitigate the predisposing factors of IBD. Dietary modifications and psychotherapy will improve the patient’s health status. Treatment of digestive alteration will restore body fluid, electrolyte balance and produce anti-motility cells (El-Tawil, 2010).

Conclusion

The effects of digestive disorders are substantial. Most common among them are irritable bowel syndrome and inflammatory bowel disease. The pathophysiology of inflammatory bowel disease causes inflammation, ulcer, and bowel damage. However, diagnosis depends on symptoms and conditions.

Treatment options for inflammatory bowel disease depend on the clinical observation of the patient. However, treatment for irritable bowel syndrome can reduce intestinal imbalance. The treatment options for IBS include antispasmodics, antidepressants, antibiotics, dietary modifications, and psychotherapy.

References

Centers for Disease Control and Prevention. (2011). Inflammatory bowel disease. Web.

El-Tawil, A. M. (2010). Smoking and inflammatory bowel diseases: What in smoking alters the course? International Journal of Colorectal Disease, 25(6), 671-680. Web.

Hanauer, S. (2012). Inflammatory bowel disease: Epidemiology, pathogenesis, and therapeutic opportunities. Inflamm Bowel Dis, 12(2), S3–S9). Web.

Katsanos, K. & Tsianos, E. (2010). Irritable bowel syndrome and inflammatory bowel disease Annals of Gastroenterology, 14(4), 242-243. Web.

Lembo, A., Zaman, M., Jones, M., & Talleey, N. (2010). Influence of genetics on irritable bowel syndrome, gastro-oesophageal reflux, and dyspepsia: A twin study. Alimentary Pharmacology & Therapeutics, 25(11), 1343-1350. Web.

McPhee, J., & Hammer, D. (2012). Pathophysiology of disease: An introduction to clinical medicine (Laureate custom ed.). New York, USA: McGraw-Hill Medical. Web.

Podolsky, D. & Xavier, R. (2012). Unraveling the pathogenesis of inflammatory bowel disease, J. Nature, 450(6), 454-477. Web.

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