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Pathology and Treatment of Gallstones - Research Paper Example

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The "Pathology and Treatment of Gallstones" paper focuses on a disease of a specific organ of the body, which is the gallbladder. A common pathology of this organ is the formation of gallstones. It is therefore necessary to discuss a bit about the gallbladder and how gallstones can form inside it…
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Pathology and Treatment of Gallstones
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? GALLSTONES – BHSC 1143 (A research essay on abdomen form and function) of (affiliation) Introduction . Thefocus of this paper is on an illness or disease of a specific organ of the body, which is the gallbladder. A common pathology of this organ is the formation of gallstones. It is therefore necessary to discuss a bit about the gallbladder and how gallstones can form inside it. A related or corollary topic are the observable structural changes and altered functions once these gallstones are formed and also related to it, how one avoids this quite common ailment. The pathology and treatment of gallstones is still relatively not very well understood; gallstones can range in size from smaller than a grain of sand and can grow large to a size of a spherical marble and when these cause blockages that these become a problem (Moore, Agur, & Dalley, 2011). Many people can have gallstones and not know about it because there are no symptoms. Discussion The gallbladder is a small sac-like organ that forms a part of the digestive system and found just under the liver. Its main function is to store bile, the dark-green and bitter-tasting fluid produced by the liver. Its primary purpose is to aid in the digestion of food when bile is released into the duodenum (first section of small intestines) when chyme (semi-fluid partly-digested food from the stomach) enters the duodenum; bile is released by the hormone cholecystokinin (CKK). The CKK in turn relaxes the hepatopancreatic sphincter and stimulates contractions of the gallbladder so the bile can be pushed outwards to the duodenum. The bile is the agent that helps digestion by breaking down lipids (naturally-occurring fats, sterols, waxes, and other fat-soluble vitamins). Without the gallbladder and bile, food eaten will be useless as it is not broken down to be absorbed by the body and its nutrients flushed out as waste (Goldberg & Williams, 1991). Bile is composed mostly of water (85%) together with bile salts (10%), mucus and other pigments (3%), various fats (1%), and other inorganic salts (1%). The gallbladder is a hollow organ composed of its three main parts which are the neck, body, and fundus (the bottom of any organ or the opposite of its opening which is the neck). The gallbladder measures 3.1 inches in length x 1.6 inches in diameter and holds up to 40 to 70 milliliters of bile when fully distended in a healthy adult human being (see Figure 1 in Appendix). This small but vital organ is located in the fossa or bed of visceral portion of the liver’s right lobe (Moore, Agur, & Dalley, 2011). The gallbladder also performs the function of concentrating bile in addition to storing it; the concentration of bile can be changed due to two actions: the addition of water into the system when it is absorbed and if the gallbladder performs its function of concentrating the components of bile such as the bile salts and other solutes. These actions and other factors can result into the most common pathology of gallbladders which are gallstones. Bile is made or produced by the body primarily to hasten the digestive process by a chemical action known as emulsification (breaking down large fat globules into much smaller but now uniformly-sized particles). Gallstones are crystals formed out of insoluble salts, minerals, and cholesterol when the bile either gets too concentrated from lack of water or when the relative concentration of the three common components found in bile (salts, minerals, and cholesterol) become abnormal due to a mixture of factors such as a diet high in fats or cholesterol, and eating too much salty foods. The etiology of gallstones can be traced to these two primary factors. The part where gallstones usually get stuck is on the Hartmann’s pouch which is the mucosal fold located at the neck of the gallbladder (see Figure 2). If the stones are quite small, they can pass easily through bile ducts. Problems start when the gallstones get large enough they get stuck along the bile ducts and causes biliary reflux which happens whenever the gallbladder contracts and sends bile down to the common bile duct but the blockage from gallstones returns or backs it up the pancreatic duct, causing some pain, pancreatitis (inflammation of the pancreas) or an infected gallbladder Structural change happens in the epithelial cells lining gallbladder walls that disrupt cholesterol absorption (see Figure 3). An ultrasound of the belly area is the best test (see Figure 4). The prevalence of cholecystolithiasi is one of the financially-costly gastrointestinal disorders, with its morbidity reaching high rates in Europe and the United States of America but lower in Asia and less-developed countries of the Third World (Adler, Blum, Fuchs, & Stange, 2004). Most people with gallstones (60% to 80%) are asymptomatic their entire lives while the probability of developing symptoms of gallstones 10 years after first diagnosis is about 2% to 4% (see Figure 5). If the ultrasound is equivocal, then a hydroxyiminodiacetic acid (HIDA) scan is highly recommended to confirm any initial findings of gallstones (see Figure 6). Potential risk factors for the ailment include age, heredity (family history), obesity (diet) and an additional suspected risk which is gender as females are more prone (Barnes 2010) but only in most West European populations and other risks not yet fully documented such as that due to extreme fasting, drastic weight reduction, certain medications, and in some hemolytic disorders. Some studies indicate erythromycin will improve gallbladder function of contractility by helping promote bile flow easier and prevent gallstone formation (Fromm, 1996). The first symptom of gallstones is a complaint of localized pain and tenderness felt in the right upper quadrant (DiMarino & Benjamin, 2002) due to obstruction of the cystic duct from impaction of a gallstone and leading to cholecystitis in 95% of cases (see Figure 7). Microscopic changes that occur on the cellular level during the early phase before formation of gallstones indicate injury to the gallbladder epithelial cells (Lee & Scott, 1982) in studies done on mice and this seems to be confirmed by further studies done on humans (Corradini & Liquori, 2001) in which abnormalities in gallbladder epithelial cell function can cause cholesterol stones formation due to impaired absorption of biliary cholesterol leading to crystal precipitation. But on the other hand, functional changes caused by gallstones are mainly due to the biliary reflux it generates that in turn can cause gastroduodenal inflammation, duodenal ulcers, an impaired pancreatic bicarbonate secretion, and greatly increased pepsinogen release (Jacobs, 1996). This causes gallbladder smooth muscle dysfunction negatively affecting its motility (Barrett el al., 2006) and reduces bile outflow leading to gallstone pathogenesis, mostly from that of cholesterol. This was confirmed in a study conducted by Bobba et al. in which there was a reduced mean ejection period of bile (total duration of gallbladder emptying) in addition to reduced ejection fraction for patients with gallstones (Bobba et al., 1984). Conclusion Treatment for gallstones includes surgical (see Figure 8) and non-surgical interventions. Dissolution of stones can be done orally but this is successful only in cases of cholesterol gallstones and a functioning gallbladder; otherwise it is not recommended. Other approaches include fragmentation using high-energy sound waves called as extracorporeal shock wave lithotripsy (ESWL) and in rare cases, cholecystectomy (surgical removal of a gallbladder). The other method used to confirm gallstones is by computed tomography (CT) scan (see Figure 9). The best antidote is to drink plenty of water, avoid fatty and salty foods, eat a balanced diet, and live a healthy lifestyle that avoids risk factors such as diabetes, obesity and alcohol. References Adler, G., Blum, H. E., Fuchs, M. & Stange, E. F. (2004). Gallstones: Pathogenesis and treatment. Dordrecht, The Netherlands: Kluwer Academic Publishers. Balentine, J. R. (2011, January 24). “Gallstones.” Retrieved November 14, 2013 from http://www.emedicinehealth.com/gallstones-health/article_em.htm Barnes, D. S. (2010, August 1). “Gallbladder and biliary tract disease.” The Cleveland Clinic. Retrieved November 14, 2013 from http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/hepatology/gallbladder-biliary-tract-disease/ Barrett, K. E., Ghishan, F. K., Merchant, J. L., Said, H. M., & Wood, J. D. (2006). Physiology of the gastro-intestinal tract. San Diego, CA: Academic Press. Bobba, V. R., Krishnamurthy, G. T., Kingston, E., Turner, F. E., Brown, P. H., & Langrell, K. (1984, January 1). “Gallbladder dynamics induced by a fatty meal in normal subjects and patients with gallstones: Concise communication.” The Journal of Nuclear Medicine, 25(1), 21-4. Boundless.com (n.d.). “Digestive system disorders: Gallstones.” Retrieved November 13, 2013 from https://www.boundless.com/physiology/the-digestive-system/digestive-system-disorders-and-clinical-cases/gallstones/ Corradini, S. G. & Liquori, F. (2001, July-August). “Recent studies on the pathogenesis of cholelithiasis: The role of the gallbladder epithelium.” Recent Progress in Medicine, 92 (7-8), 471-6. Dawn, Y. (2011, December 8). “Hartmann's pouch.” [Blog entry]. Retrieved November 13, 2013 from http://yebudawn.blog.com/2011/12/08/hartmann-pouch/ DiMarino, A. J. & Benjamin, S. B. (2002). Gastrointestinal disease: An endoscopic approach. Thorofare, NJ: Slack Books Incorporated. Elmasry, M. (2010, July 31). “Gallstone ileus on CT scans.” Radiology Spirit. Retrieved November 14, 2013 from http://radiologyspirit.blogspot.com/2010/07/gallstone-ileus-on-ct-scans.html Fromm, H. (1996). Bile acids, cholestasis, gallstones: Advances in basic and clinical bile acid research. Dordrecht, The Netherlands: Kluwer Academic Publishers. Gillian, G. K. (2003, January 1). “Strategies for lowering the rate of bile duct injuries in laparoscopic cholecystectomy.” Society of Laparoendoscopic Surgeons. Retrieved November 13, 2013 from http://www.laparoscopytoday.com/2003/01/strategies_for_.html Goldberg, I. & Williams, R. (1991). Biotechnology and food ingredients. New York, NY: Springer Books. Hemmings, D. E. (2013, July 12). “What is a gallbladder scan?” Health Grades Incorporated. Retrieved November 14, 2013 from http://www.healthgrades.com/procedures/gallbladder-scan Jacobs, C. (1996). Replacement of renal function by dialysis. New York, NY: Springer Books. Lee, S. P. & Scott, A. J. (1982, July). “The evolution of morphologic changes in the gallbladder before stone formation in mice fed a cholesterol-cholic acid diet.” The American Journal of Pathology, 108 (1), 1-8. Meddean (n.d.). “What are the useful imaging modalities to investigate cholecystitis?” Loyola University of Chicago. Retrieved November 14, 2013 from http://www.meddean.luc.edu/lumen/MedEd/Radio/curriculum/Surgery/cholecystitis_list2.htm Moore, K. L., Agur, A. M. R. & Dalley, A. F. (2011). Essential clinical anatomy (4th ed.). Baltimore, MD: Lippincott Williams & Wilkins. Weston, G. (2011, October 24). “Mapping the body: Gallbladder.” The Guardian. Retrieved November 12, 2013 from http://www.theguardian.com/lifeandstyle/2011/oct/24/gallbladder-digestion-bile-gallstones Zaki, M. & Al-Refeidi, A. (2009). “Histological changes in the human gallbladder epithelium associated with gallstones.” Oman Medical Journal, 24, 269-73. Appendix Figure 1. Gallbladder shown in green color. It is located right below the liver (Weston, 2011). Figure 2. The Hartmann's Pouch is located at the junction of the gallbladder neck and the cystic duct. This is where most gallstones get stuck along the way (Dawn, 2011). Figure 3. A section of cholecystitic human gallbladder with a disrupted epithelium. This figure shows the structural changes in the gallbladder when gallstones are starting to form (Zaki & Refeidi, 2009). Figure 4. The gallstones are indicated by the arrow while the gallbladder has thickened walls. An ultrasound (US) also reveals the presence of pericholecystic fluid (Meddean, n.d). Figure 5. Gallstones shown inside the gallbladder and also in the pancreatic duct (carried away). If these become large enough, they caused blockage and pain (Balentine, 2011). Figure 6. A HIDA scan (also called as hepatobiliary iminodiacetic acid) uses radioactive substance that is injected into the vein and traces the flow of the isotope through the biliary tree. Its aim is to locate any blockage due to gallstones (Hemmings, 2013). Figure 7. Gallstones which were large enough and did not pass out of the gallbladder. This size can cause severe pain and needs surgical interventions (Boundless.com n. d.) Figure 8. Gallbladder surgical removal is the gold standard for severe cases of gallstones. It is a minimally-invasive surgery (MIS) but can lead to bile duct injury (Gillian, 2003). Figure 9. A CT scan is useful as a complement to US. It is best used when a US is difficult to do such as due to obesity or if there are abscess formations suspected (Elmasry, 2010). Read More
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