The gastrointestinal tract is a digestive tube extending to the anus from the mouth. In its walls, various epilithic cells are protecting the microbial pathogens. They constitute a transmembrane responsible for digestive maintenance, absorption, and secretion. On the barrier, there are resident immune cells and intact mucus. However, a drug abuse can erode the surface, hence removing the protective layer. As a result, the patient is susceptible to multiple diseases. It is worth noting that gastrointestinal system’s primary function is nutritional uptake and digestion.
In a healthy individual, the colonization of gastrointestinal tract by pathogens is impossible due to the cells’ constant turnover given that they survive for less than 72 hours. Drug abuse facilitates high cell turnover rate hence increasing the vulnerability to tumor formation and mutagenic compounds. The gastrointestinal tract compromise occurs due to pathogenic micro-organismic challenges (Smith et al., 2012). Medications such as Prednisone and Synthroid have antacids. The ingredient not only neutralizes the stomach acid but also ensures the proliferation of microorganisms. In addition, the medical therapy leads to pathogen colonization by killing the microbiota bacteria. The patient’s symptoms and drug abuse history indicate a likelihood of preformed microbial toxin ingestion hence normal cell function interference.
In the United States, gastrointestinal ailments cause three thousand deaths a year (Everhart & Ruhl, 2014). Diarrhea occurs due to the contaminated food ingestion, although the pathology depends on the intoxication and the infection area in the gastrointestinal tract. Alternatively, the bacterium can attach on or infect the host cells especially when the patient has low immunity. The pathogenic attachment on the host cell results in toxin production thus cell death or damage.
The doctors should localize the pathology for effective treatment. While hepatobiliary disorders are self-limiting, medical therapy for gastrointestinal tract infection is necessary for inhibiting severe complications. Diarrhea point to a chronic intestinal infection but the doctor should conduct an endoscopic procedure for pathological visualization.
Patients with gastrointestinal and hepatobiliary disorders experience epigastric pain within three hours of food ingestion. Indigestion and vomiting are also common specifically in individuals with Hepatitis B history. In extreme cases, dysentery (bloody diarrhea with mucus) is common. A poor liver performance leads to dark urine and localized abdominal pain. To treat the primary biliary cholangitis in the liver, the doctor focuses on medication that suppresses the pathogenic process (Kumpf, 2014). In particular, the disease recurrence is avoidable by destroying the interlobular hepatic ducts. The physician should provide daily doses of 13 mg/kg of UDCA. The patient has to ingest the drug before bedtime and after meals. Furthermore, the doctor has to monitor the blood tests quarterly. In case there is normalization at the end of six months, the patient should continue UDCA intake, but the repetition of liver and gastrointestinal biopsy should occur within 20 months. The continuation of UDCA is indefinite even after an improved or stable biopsy repetitive after three years.
In the year 2014, the FDA recommended the combination of UDCA and obeticholic acid in gastrointestinal and hepatobiliary disorder treatment especially if the adult patient is unresponsive to other drug therapies due to alkaline phosphatase non-reduction (Beuers, 2015). Diarrhea can last for a few days hence does not require medication. However, the condition can be a symptom of a chronic gastrointestinal ailment thus a medical examination is necessary. Doctors should avoid antidiarrheal medications especially if a parasite or bacteria is the causative agent. I advise a prescription of antibiotics until the patient’s condition improves. Moreover, the ailing individual should avoid over-the-counter medication as a symptom reliever.
- Beuers, U. (2015). Drug Insight: Mechanisms and Sites of Action of Ursodeoxycholic Acid in Cholestasis. Nature Clinical Practice Gastroenterology & Hepatology, 3(6), 318-328.
- Everhart, J. E., & Ruhl, C. E. (2014). The Burden of Digestive Diseases in the United States Part I: Overall and Upper Gastrointestinal Diseases. Gastroenterology, 136(2), 376-386.
- Kumpf, V. J. (2014). Parenteral Nutrition-Associated Liver Disease in Adult and Pediatric Patients. Nutrition in Clinical Practice, 21(3), 279-290.
- Smith, L. H., Fromm, H., & Hofmann, A. F. (2012). Acquired Hyperoxaluria, Nephrolithiasis, and Intestinal Disease: Description of a Syndrome. New England Journal of Medicine, 286(26), 1371-1375.
