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The Biliary Systems Key Roles - Case Study Example

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The paper "The Biliary Systems Key Roles" highlights that the gallbladder concentrates, stores and releases bile generated by cells in the liver. Gallstone formation, being a female, progressing in age and comorbidities with a disease like diabetes are risk factors for developing Cholecystitis…
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Acute Cholecystitis Name Course Name and Code Instructor’s Name Dat Table of Contents Table of Contents 2 1.Introduction 3 2.Case Study 4 3.Anatomy of the biliary system 5 4.Pathology 6 4.1.Aetiology 7 4.2.Risk Factors 7 4.3.Pathogensis 8 5.Role of imaging modalities AC diagnosis 8 6.Treatment and prognosis 13 7.Summary and conclusion 14 8.References 14 1. Introduction Acute Cholecystitis (AC) is an episode of acute biliary pain accompanied by fever, Right Upper Quadrant (RUQ) tenderness, guarding, persistence of symptoms for more than 24 hours as well as leukocytosis (Odze and Goldblum 2009). About 90% of the reported cases are associated with gallstones. Ultrasonography demonstrates thickening of the gallbladder wall as well as pericholecystic fluid. The biliary system comprises of the gall bladder, bile ducts as well as associated systems which take part in the transportation and secretion of bile (Schwab 2011). The biliary system’s key roles are to drain waste products from the liver into the duodenum and control the secretion of bile that helps in food digestion (Sircar and Michael 2010). Bile consists of various elements, for instance, bile salts, cholesterol and waste products. Bile salts aid in the digestion of fats and removal of waste. Thereafter, bile is excreted from the body in the form of faeces. Cholecystitis, which is a complication of gallbladder, occurs in chronic or acute form. In Acute Cholecystitis (AC), the gallbladder is constricted while the walls are inflamed and thickened. Acute Acalculous Cholecystitis (AAC) is a severe form of Acute Cholecystitis that occurs in critically ill or injured patients after cardiac or abdominal vascular surgery, server trauma, or diabetes. ACC is an inflammation of the gallbladder without gallstones that represents 2- 15% of Acute Cholecystitis (Ganpathi et al. 2007). in which the biliary colic pains last longer AC and is commonly accompanied by a fever, high pathological findings, or Cholestasis. As the signs and symptoms of cholecystitis resemble other medical conditions, its common signs may not be well distinguished by the use of computed tomography and may therefore require accurate and high specificity diagnosis procedures (Thornell 2002). The Chronic Cholecystitis is an inflammation of the gallbladder that lasts for a long period of time and occurs due to gallstones in the gallbladder and cystic duct (Schneider and Philip 2009). It characterized by a repeated colic biliary attacks. Pathological examinations reveal that cholecystitis consist of abnormal high levels of serum enzyme viz, a large quantity of bilirubin, Aspartate transaminase, and high levels of leukocytosis (Schein 1999). This essay aims to high light the chractarrisctics of a case study has Acute Cholecystitis (AC) wit regard to the anatomy, aetiology, risk factors, pathogenesis, pathological test findings, role of imaging techniques in the diagnosis, treatment, and prognosis. 2. Case Study Annete White, a 58 year old woman was brought to an emergency room as she complained from a 12 hour severe abdominal pain that started approximately thirty minutes after a reportedly heavy fat and protein dinner meal. The pain started as a less severe abdominal ache, and then it localized to the RUQ of the abdomen. She reported abdominal discomfort and nausea, although she was not vomiting. She further stated that she had such previous pain from before, but in less severe form. The last time she had similar condition was approximately two weeks ago. Since being brought to the emergency room, the pain minimized, which was a clear indication that it had been managed effectively. Her medical history showed that she is diabetic with a mellitus type II diabetes. Her physical examination showed that she had a body temperature of 38.8 C, while her pulse rate was 189/166.The palpation of the abdomen showed tenderness in her RUQ. The examination of the pelvic, liver and the rectum did not show any signs of abnormality. The laboratory examination showed that she had a white blood cells count of 14000/ml upon her arrival to the emergency room. The composition of the serum revealed the level of alkaline phosphatase as 140 U/L, AST 40 U/L and ALT 37 U/L, total Bilirubin 1.8 mg/dL, and direct Bilirubin 0.7 mg/dL. The imaging diagnostis tools of Ultrasonology, CT Scan, and MRI on the right upper quadrant showed thickened walls of the gallbladder, stones in the gallbladder with a diameter of 4.5mm in the bile duct. 3. Anatomy of the biliary system A normal Gallbladder is a pear shaped sac, which is attached on the right lobe of the liver (Figure 1). Approximately 60% of its surface is covered with a stretch of peritoneum. However, in some cases, the surface covere may vary either more or less than 60% (Betancourt and Miskovitz 2010). In adults, the gallbladder is approximately 10 cm long, and 3-5 cm wide. The wall is approximately 1-2 cm thick, however, it’s thickness differs depending whether the gallbladder is contracted or relaxed. The gallbladder comprises of three parts namely; the fundus, which is the broad outer part, an ‘S’ shaped neck that has infundibulum, and the central body part. The neck with infundibulum connects the gall bladder with the cystic duct (Norrby 2002). The mucosa of the cystic duct forms spiral valves near the neck. The spiral valves consist of smooth muscles fibers in its lumen and play a key role in controlling the filling and drainage of the contents in the gall bladder. The GB of an adult has a capacity of 40-70 ml however, it can accommodate about 100 ml fluid (Maher and O’Connor 2011). The cystic duct is 2.5 cm long and opens into the duodenum at one end (Ellison and Zollinger, 2010). The cystic duct appears smaller compared to its anatomic length owing to the tortuous path. The gallbladder concentrates, stores and releases bile generated by cells in the liver. Additionally, gallbladder secretes mucins, which protects the epithelium tissue. Contraction of gallbladder can be caused byeating fat and protein rich-meals (Odze and Goldblum, 2009). Cholecystokinin hormone is responsible for the contraction of the gallbladder wall therefore, emptying of bile into the duodenum occurs. Figure 1: Anatomy of acute cholecystitis (From Encyclopedia Britanica 2003) 4. Pathology AC leads to sudden and severe discomfort in the upper right side of the abdomen. Many patients with gallstones have an inflamed gallbladder wall usually without infection, which may set in afterwards (Maher and O’Connor 2011). The gallbladder wall is thickened by the inner fluid. Acalculous Cholecystitis may result from critical illness, sepsis, injuries, other major surgery, and intravenous feeding or long fasts (Odze and Goldblum, 2009). This form of cholecystitis is more severe than the gallstone induced cholecystitis, and usually develops among children due to infections. 4.1. Aetiology Cholecystitis is defined as the inflammation of the gallbladder walls and the adjacent abdominal lining by the presence of gallstones in the cystic duct (Maher and O’Connor 2011). Cholecystitis can be caused by a bacterial infection in the bile duct, decline of the blood supply to the gallbladder, and a tumour of liver or pancreas (Porth 2011). Cholecystitis in pregnant women occurs as a result of a thick layer of sludge that accumulates in the gallbladder. The sludge consists of small particles whose composition is similar to those in gall stones. AC has other causes that include drug disorders, collagen diseases, microorganism infections, ischemia and allergic reactions. Acute Acalculous Cholecystitis also occurs as a result of burns, trauma and multi system failure (Jarvinen 2006). 4.2. Risk Factors There are some risk factors that considered to be major factors to cause Acute Cholecystitis (Mayo Clinic 2011); formation of gallstones in Gallbladder is highly increase the chance of developing Cholecystitis, females are at a higher risk of gallstones and developing Cholecystitis 2-3 times than males, and progressing in age (older than 60 years old), and comorbidities are another causes to form gallstones and develolpe Cholecystitis especially if the aged person has a history of diabetes, cardiovascular diseases, or cerebrovascular accident (CVA) such as Ischemic stroke or cerebral hemorrhage (Mayo Clinic 2011; Cho et al. 2010). 4.3. Pathogensis The pathogenesis of Acute Cholecystitis is mainly due to obstruction of biliary outflow by a stone (Odze and Goldblum 2009). There are other rare causes, for instance, stricture, torsion of the gallbladder, intussusception of a polyp, kinking of the cystic duct, concentrated bile. When the gallbladder distends after obstruction, the blood vessels in the gallbladder wall become contracted therefore giving rise to a patch of gangrene on the funds which ruptures and releases bile peritonitis. Stones in the gallbladder can cause obstruction as well as the accompanying acute attack (Caroline 2009). The patient is likely to develop , low-level inflammation which results in Acute Cholecystitis, where the gallbladder is calcified and fibriotic. 5. Role of imaging modalities AC diagnosis Acute Cholecystitis can be diagnosed through imaging modalities combined with a medical history and pathoclinical examinations (Odze and Goldblum 2009). Three imaginng techniques have been used to diagnose Annete (the Case study). The Ultrasound imaging (Figure 2a and Figure 2b) have showen presence of gallstones in the gallbladder. and thickening of the gallbladder walls (Figure 2a and 2b). Computed Tomography Scan (CT or CAT scan) is another diagnostic imaging technique using various x-rays, and computer technology to generate cross-sectional images for detecting diseases such as Cholecystitis (Porth 2011). Figure 3a shows a CT Scan image of the case study with Cholelithiasis and Pericholecystic inflammation. Annete also exhbited a thickening of the gallbladder walls, and an increased hepatic attenuation next to the gallbladder (Figure 3b). The patient with suspected AC was required to be diagnosed with US and CT Scan as they are the major recommended tools to confirm the disease, nevertheless, there is a struggle sometimes in detecting the gallstones particulary if it’s formed in her cystic duct or the gallbladder neck (Baroff et al. 2000). Both the US and the ST Scan are less effieicnt due to their lower sensitivity compared to Megnatic Resonance Imiging (MRI) (Adusumilli 2002). MRI imiges for Acute Uuncomplicated Cholecystitis case has the ability to show gallstones within the gallbladder neck or cystic duct, the gallbladder wall thickening, the gallbladder wall edema, the gallbladder distention, the pericholecystic fluid, and the ‘C Sign’ small amount fluid found between the liver and the right hemidiaphragm or the abdominal wall (Adusumilli 2002). Therefore, MRI is considered to be more effective and competence, and also is recommended to use it as an initial step for diagnosisng Acute Cholecystitis (Adusumilli 2002). It was requsted from Annete (the Case study) to do an MR Cholangiopancreatography (MRCP) (Tonolini et al. 2012) in order to visualize precise details of her gallbladder including biliary duct, and see if it contains small or unseen gallstones adjacent to her gallbladder. The MRCP imiges detected distended gallbladder with sludge, infundibular microlithiasis, thickened edematous walls (Figure 4a and Figure 4b), and a presnce of a clear small gallstone in the distal Common Bile Duct (Figure 4c) consistent with Acute Cholecystitis. Figure 2a. Oblique Ultrasound appearance of Acute Cholecystitis case showing gallstones (arrows) within the gallbladder; the ‘S’ indicates the marked posterior shadowing (From Baroff et al. 2000). Figure 2b. Ultrasound image of Acute Cholecysitis case; the closed arrow showing the thickened wall while the open arrows shows the gallstone in the gallbladder (From Lack 2003) Figure 3a. CT Scan image of Acute Cholecystitis case showing cholelithiasis and Pericholecystic inflammation (arrows) (From Baroff et al. 2000). Figure 3b. CT scan showing wall thickening of the gallbladder, and arrowheads showing an increased hepatic attenuation next to the gallbladder (From Baroff et al. 2000). Figure 4a and 4b. MRI showing distended gallbladder with sludge and infundibular microlithiasis, thickened edematous walls (arrowhead in a) consistent with acute cholecystitis (From Tonolini et al. 2012). Figure 4c. MRCP disclosed a small gallstone in the distal Common Bile Duct (arrowhead) that not detected by US and CT Scan (From Tonolini et al. 2012). 6. Treatment and prognosis There are number of factors that determine treatment for AC; such as general health, medical history, age of the patient, the extent of the disease, patients' preferences, tolerance to medicines and procedures (Caroline 2009). The treatment of Annete form Acute Cholecystitis started with hospitelizing her in a hospital in order to reduce the stimulation of the gallbladder. Then antibiotics course was implemented in order to fight and reduce the inflammation. This was involved with drugs composed of bile salts which plays role to dissolve the gallstone(s) . In addition, a low fat diet and pain management courses were applied. However, the patho-bioloical tests are still indicating Acute Cholecystitis, asurgical intervention had been decided to treat Annete from Acute Cholecystitis by removing the gallbladder, what so called Cholecystectomy through Laparoscopy techneque. The ultimate aims of Cholecystectomy are to relieve symptoms, stop progressions, and complications, prevent the occurance of Acute Cholecysitis disease (Maher and O’Connor 2011). Prognosis of cholecystitis patients is favourable. With some AC patients, complications might appear if other organs are involved (Porth 2011). Usually, gallstones can return in the bile duct system after the gallbladder has been removed surgically. In rare cases, some patient experience pain even after the gall bladder has been removed. It may also be due to malfunction of sphincter of Oddi, which controls the flow of bile and pancreas secretion (Merck 2011). Small stones in the bile duct, peptic ulcers a and irritable bowel syndrome can also cause pain. 7. Summary and conclusion The gallbladder concentrates, stores and releases bile generated by cells in the liver. Gallstone formatiom, being a female , progressing in age and comorbidities with other diseas like diabetes are risk factors for develolping Cholecystitis. The pathogenesis of acute cholecystitis is mainly due to obstruction of biliary outflow by a stone. Acute Cholecystitis can be diagnosed through imaging modalities combined with a medical history and clinical examination. Annete White, a 58 year old woman was complained from sudden and severe discomfort in her upper right side of the abdomen. She was diagnosed with Acute Cholecystitis based on Ultrasound, CT Scan, and MRI medical imaging techniques. Various treatment approaches were applied ended with Cholecystectomy to relieve symptoms, stop progressions, and complications, prevent the occurance of Acute Cholecystitis. 8. References Adusumilli, S., and Siegelman E. S. 2002. “MR imaging of the gallbladder”. Magn Reson Imaging Clin N Am.10:165–184. Bortoff, A., Michael Chen, David J. Ott, Neil Wolfman, and William Routh. 2000. “Gallbladder Stones: Imaging and Intervention”. RadioGraphics. 20: 751-766. Betancourt, Marian and Miskovitz, Paul. 2010. The Doctors Guide to Gastrointestinal Health: Preventing and Treating Acid. New York: John Wiley & Sons. Caroline, Nancy. 2009. Nancy Caroline Emergency Care in the Streets,Canadian Edition. Belmont: Jones & Bartlett Learning. Cho, Jai Young, Ho-Seong Han, Yoo-Seok Yoon, Keun Soo Ahn. 2010. “Risk Factors for Acute Cholecystitis and a Complicated Clinical Course in Patients With Symptomatic Cholelithiasis” Arch Surg.145(4):329-333. Ganpathi, Iyer, Ravishankark Diddapur, Huang Eugene, and Masud Karim. 2007. “Acute acalculous cholecystitis: challenging the myths”. Hepato-Pancreato Biliary Journal. 9: 131-134. DOI: 10.1080/13651820701315307 Ellison, E and Zollinger, Robert. 2010. Zollinger’s Atlas of Surgical Operations, Ninth Edition. Lack, Arthur. 2003. Core curriculum, The: Ultrasound 1st Edition. Available at www.msdlatinamerica.com Encyclopedia Britanica (2003). Pathology: Anatomy of acute cholecystitis. Available at www.britannica.com/EBchecked/topic/128149/common-bile-duct Jarvinen, Peters. 2006. Pathological analysis and history. New York: Prentice Hall Publishers Maher, Michael and O’Connor, Owen. 2011. Imaging of Cholecystitis. Cork: ARRS. MayoClinic: Cholecystitis. 2011. Risk Factors. http://www.mayoclinic.com/health/cholecystitis/DS01153/DSECTION=risk-factors (access date 06 October 2013). Merck, Alise. 2011. Cardiovascular diseases. Oxford: Oxford University Press Norrby, James. 2002. Surgical pathology and cancer. Wolters Kluwer Health/Lippincott Williams & Wilkins Porth, Carol. 2011. Essentials of Pathophysiology: Concepts of Altered Health States. New York: Lippincott Williams & Wilkins. Odze, Robert and Goldblum, John. 2009. Surgical pathology of the GI Tract, Liver, Biliary Tract and Pancrease: Expert Consult: Online and Print. Philadelphia: Elsevier Health Sciences. Tonolini, Massimo, Anna Ravelli, Chiara Villa, and Roberto Bianco. 2012. “Urgent MRI with MR cholangiopancreatography (MRCP) of acute cholecystitis and related complications: diagnostic role and spectrum of imaging findings”. Emerg. Radiol. 19:341–348. DOI 10.1007/s10140-012-1038-z Schein, Manfred. 1999. Imaging of Cholecystitis. Philadelphia: Elsevier Health Sciences. Sircar, Sabyasachi and Michael, Joel. 2010. Fundamentals of Medical Physiology. New York: Thieme. Schwab, Manfred. 2011. Encyclopedia of Cancer Volume 1. New York: Springer. Thornell, Erland. 2002. Mechanisms in the development of acute cholecystitis and biliary pain: a study on the role of prostaglandins and effects of indomethacin. Oslo [Norway]: Universitetsforlaget. Schneider Arthur and Szanto Philip. 2009. Pathology. London: Wolters Kluwer Health/Lippincott Williams & Wilkins Read More
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