1) Interpretation of biochemistry results and initial diagnosis
The BUN, AST, amylase and glucose are raised above the normal ranges. It reveals a derangement within the billiary system or the pancreas. TGs and Albumin are within the normal rages wile calcium and paO2 are low. The WCC is slightly above the normal ranges and these points to an inflammatory process taking place within the body. The serum urea level is raised above the normal ranges. Therefore, the is a breakdown in the system that facilitates urea breakdown and excretion. The most significant determinants are that AST and amylase levels. The results points out the diagnosis of a biliary system.
The initial diagnosis of this patient is most likely to be acute cholecystitis. This is due to the high levels of AST and amylase. Ardengh et al., 2010, p.27-31, notes that liver enzymes AST and ALT are usually elevated when common bile duct is blocked or there is inflammation of gall bladder. They further argue that in pancreatitis, the difference between cholecystitis and pancreatitis is the measure of ALT. In pancreatitis, ALT rises threefold.
2) Clinical tools for diagnosis and understanding if the severity of the condition.
The 60 year old patient is admitted with increasingly severe epigastric pain, and guarding upon examination. The patient also reports nausea and vomiting with signs of jaundice. The presence of the epigastric pain, guarding behavior points out to a billiary system disorder but the guarding aspect is mainly associated with gall bladder inflammation. The consumption of junk food and large amounts of alcohol supports the fact that the condition is a biliary disorder. Mathur et al., 2012,p.39-41 notes that major risk factors for acute cholecystitis are old age of 60 and above, male sex, the presence of a cardiovascular disease or presence of diabetes. There are also results implicating use of food containing high cholesterol levels with the occurrence of cholecystitis
The patient is in the tachycardic state with lowered partial oxygen tension. The patient is also developing jaundice. The haemoglobin breakdown system has been altered. The hemodynamic state has been altered. The patient is moving towards acidosis.
3) Etiology of presenting jaundice and the underlying cause of the patients condition.
Jaundice is a common condition commonly associated with liver disease, red blood cell disorders and gall bladders disease. It occurs due to the elevated levels of bilirubin. Elevation of bilirubin in the body leads to its deposition in the tissues like the skin and sclera. Cholecystis is caused by an infection or accumulation of gallstones. The gallbladder usually stores bilirubin as a portion of the bile from the liver to be utilized in digestion when it is emptied into the ileum. Inflammation of the gall bladder or a gallstone blocks he bile duct preventing adaequate empting of the bile. A blocked bile duct thus allows bilirubin to move in retrograde fashion into the liver and back into the bloodstream (Vitek and Carey, 2012, p.122-129).
The decreased level of the PaCO2,and raised serum urea and BUN is a manifestation in the respiratory and excretory problem. The fact that there are low oxygen levels with high urea signifies a derangement in the blood haemoglobination. The presence of high biliribun level and decreased hemoglobin breakdown lead to low oxygen levels. The presenting symptoms will be tachycardia and tachypnoea. The elevated levels of AST serves to support that there is a blockage of the bile duct The cause of the underlying condition is most likely to be a gallstone(Venneman, and van Erpecum, 2010, p.171-183). Vennem and van Erpecum,2010, observe that there is always an associated rise of amylase due to the blockage of the extra hepatic duct by gallstones. The argument supports the biochemistry data.
4) Treatment of the condition
The treatment can be supportive or definitive. The approach depends on the severity and presence of complications. Uncomplicated cases of cholecystitis can be managed as outpatient depending on the cause. Cholecystitis caused by infections will involve the administration of antibiotics to manage the infection. Complicated case requires surgical approach. A percutaneous trans-hepatic cholecystectomy is appropriate for drainage. Definitive therapy involves cholecystectomy, either open or laparoscopic, and placement of a drainage device (Festi et al., 2010, p.719-7240).
The non-surgical management of the condition also involves use of low fat diet
5) Prognosis of the patient
The prognosis of the patient is favorable in majority of the cases. The patient on the case is most likely to be unfavorable. The patient on case is on a risk of developing perforation of the gallbladder and developing secondary pancreatitis and the resultant poor blood sugar control. There is also a likelihood of the patient developing a secondary infection and recurrent gallstones. It is because patient engages in a high risk behaviors. The biochemical profile is highly deranged and is expected to show greater variations from the normal if treatment is not initiated on time.
Ardengh, J.C., Malheiros, C.A., Rahal, F., Pereira, V. and Ganc, A.J., 2010. Microlithiasis of the gallbladder: role of endoscopic ultrasonography in patients with idiopathic acute pancreatitis. Revista da Associacao Medica Brasileira, 56(1), pp.27-31.
Festi, D., Reggiani, M.L.B., Attili, A.F., Loria, P., Pazzi, P., Scaioli, E., Capodicasa, S., Romano, F., Roda, E. and Colecchia, A., 2010. Natural history of gallstone disease: Expectant management or active treatment? Results from a populationbased cohort study. Journal of gastroenterology and hepatology, 25(4), pp.719-724.
Mathur, S.K., Duhan, A., Singh, S., Aggarwal, M., Aggarwal, G., Sen, R. and Garg, S., 2012. Correlation of gallstone characteristics with mucosal changes in gall bladder. Tropical Gastroenterology, 33(1), pp.39-44.
Vitek, L. and Carey, M.C., 2012. New pathophysiological concepts underlying pathogenesis of pigment gallstones. Clinics and research in hepatology and gastroenterology, 36(2), pp.122-129.
Venneman, N.G. and van Erpecum, K.J., 2010. Pathogenesis of gallstones.Gastroenterology clinics of North America, 39(2), pp.171-183.
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