Investigations to Carry Out a Diagnosis - Assignment Example

Mr. Robinson was redirected to the Emergency unit with a cycle of medical conditions. He had vomited massive amount of blood. There was therefore an agent need for a though testing to clearly establish what his condition actually was. The series of lab tests he went through are as tabulated in the below. Lab Test Lab results References Specimen A(serum) 1. Sodium value: 139mmol/L 2. Potassium: 4.5mmol/L 3. Creatinine: 97mmol/L 4. Urea: 15mmol/L 1. Sodium value: 135-145mmol/L 2. Potassium: 135-145mmol/L 3. Creatinine: 70-150mmol/L 4. Urea: 2.5-6.7mmol/L Specimen B Hb: 8g/dL HCT: 28 Total WBC: 10.0 x 10^9L Platelet 266 x 10^9/L Hb: 12.6-16.1 g/dL HCT: 38-47.7% Total WBC: 4-11 x 10^9/L Platelet:15-400 x 10^9/L Liver function test Alanine transaminase:(ALT) AST: ALT: 9-52 IU/L Serology Test Hypetension positive for Peptic Ulcer Disease Questions Why were tests done on the patient? What would be the correct diagnosis for the condition he was suffering and on what basis? Explain the clinical signs and symptoms with reference to the above pathophysiology Briefly provide any other investigations you would likely carry out to affirm your diagnosis. 1. Question 1) These tests were conducted so as to clearly examine the condition of the patient. Given the signs and symptoms portrayed by the patient, the physician would be in a position to provide a likely diagnosis as well as any additional information concerning the patient. The specimen B test on full blood count was performed in order to establish what condition the patient was suffering from and create a methodology that could be useful for diagnosis. The platelet cell count of the patient was within the normal range while that of WBC cells is high. The cells count of both Hb and HCT is relatively low (Karp, 2008) Blood specimen A was tested in order to establish blood pressure. The patient is likely to be suffering from low blood pressure given that he has heightened levels in volume of the blood. Hylemic shock is likely to be caused by a large amount of blood in the vomit. In mild or pronounced results hypovolemia is likely to lead to tachycardia. Loss in blood volume of up to 50 percent is likely to result in supine hypotension (Saltzman, 2013). This is because it amounts to inadequate tissue perfusion and reduced intravascular volume. When circulating in low volumes it is likely lead to a reduction venous return to cardiac output and the heart. What results will be low volumes to the tissues which will only allow tissues limited supply both nutrients and oxygen. In the event of Hypovolemic shock, fatality could be present through strained respiratory diseases, a severe tubular necrosis or likely organ failure (Yamada, t. & Alpers, d. h.2008) In a bid to comprehend how the body aptly reacts to hypertension the tests would be useful. Normally, it responds by activation of compensatory mechanisms. The carotid and aortic receptors identify the low volume of blood and increase the sympathetic activity which causes increased heart rate and peripheral vasoconstriction. The vasoconstriction is the likely result of cold, clammy skin while tachycardia is characterized by increased heart rate. Inadequate perfusion results in low blood flow to the brain causing tissue hypoxia, thus, anxiety and confusion. The body is likely to switch to anaerobic metabolism from aerobic metabolism as a result of tissue anoxia causing lactic upsurge in lactic acid and metabolic acidosis. In response, there is an increased rate in respiration causing hyperventilation as oxygen’s partial pressure in the arteries is intensified. In order to actively maintain Hypovolemic shock recovery of fluid, sufficient distribution of oxygen, airway maintenance and establishing the location of the cause of bleeding should be done instantly. Question 2) The findings in the lab can be helpful in establishing the right identification to the severe cause of the patient’s GI hemorrhage. Severe hemorrhage can be well studied by obtaining a full blood count, Serum creatinine, serum electrolytes, and Blood urea nitrogen, coagulation studies and liver function tests. These will be significant in establishing the correct approach to the final diagnosis. Severe upper gastrointestinal bleeding could be indicated through either blood in vomit or blood in stool. In its wake, the patient has a massive upper GI blood loss through vomiting which causes hypovolemia. The severe upper GI bleeding can be associated with vital pathological states allied to specific risk factors, causes, pathophysiology and laboratory differentials. Factors such as recent medical history of the patient, lifestyle habits Age, stress and diet are essential in order to make the right diagnosis (Friedman, 2001) Considering the amount of blood in vomit is also significant alongside hemorrhage site. If the patient heaves blood that is bright red in color as a result of prior hemorrhage also known as Hematemesis, this is an indication of upper GI source close to the ligament of Treitz. The percentage of patients that are admitted for upper cutting out of 100 is 1% while 0.2 % of the patients are hospitalized as a result of lower GI hemorrhage in the US. This course is greatly influenced by blood loss, exposure to GI irritants and any co-morbid conditions (WILSON, 1990). Condition of the kidney tubules is likely to be suggested through samples of serum (sodium and potassium) electrolytes. One is able to know whether the body is ion a condition or not working normally as retention of secreted electrolytes and active re-absorption remains in renal tubular cells. If the renal tubular cells are not working normally there is a relapse of serum electrolytes while the levels of serum potassium and sodium increase and reduce respectively. The tubular necrosis is indicated by augmented (more than 1 percent) fractional sodium excretion, which is likely to indicate that the tubular cells are not able to actively reabsorb sodium (Tierney et al. 2008). In the event that the serum levels of sodium and potassium are close to normal, high rates of urea absorption and high ratio between serum creatine and serum urea, otherwise called Prerenal azotemia renal tubular function occurs. Hypoperfusion of the kidney is a more likely cause of Prerenal azotemia. As partial seepage of serum sodium is maintained at minimum, the ration of blod urea nitrogen to that of creatinine is 1:20 (Tierney et al. 2008). An increase in active re-absorption of nitrogenous products into the ileum is likely to result in significant increase in the amount of serum urea as compared to the level of serum creatinine. These nitrogenous products will accumulate in the gut and likely the difference in the levels of serum urea and serum creatinine causes Prerenal azotemia.(Mushlin & Greene 2009). From the lab analysis of the patient , specimen B indicate levels of 8g/dL in haemoglobin while haematocrit is at 28g/dL. Initially, the level of haemoglobin immediately after hemorrhage is not likely to decrease, however, after a day or more, the extra-vascular fluid influx dilutes blood into the vascular space in order to compensate for low levels of blood which will indicate low haemoglobin level. Falsely, low levels of haemoglobin are likely to be influenced by hydration. The levels of haematocrit do not necessarily indicate the hemorrhage experienced by the patient, rather, they decrease after endogenous and exogenous fluids have refilled the vascular space. Establishing whether the patient is likely to have chronic blood loss enables the physician to not only balance the low levels of haemoglobin and haematocrit but also ascertains the probability of pochromic microcytosis. In an event where there has been severe loss of blood a normocytic normochromic blood picture would be otherwise seen. The levels of prothrombin and hemorrhage time amongst other coagulation studies are significant as they help to gauge the liver function in the clinical setting of acute upper GI hemorrhage.. The liver’s failure to develop a coagulation property causes poor coagulation which is a factor that necessitates platelet aggregation and clot formation leading to excessive hemorrhage. Common in alcoholic hepatitis is a heightened number of white blood cells. During severe GI hemorrhage, the amounts of white blood cells increases reasonably but does not pass the 15, 000/ mm^3 mark, thus, leucocytosis are not likely to be associated with the hemorrhage unless there is an infection (Yamada, T & Alpers, 2008).The platelet count and total white blood cell analysis are used to suggest whether or not a patient is experiencing any liver pathology or current infection associated an event of severe GI hemorrhage. Question 3) From the analysis and clinical procedures done on the patient, the physician is now able to diagnose that the likely cause of large amount of blood in vomit is due to an infection; peptic ulcer hemorrhage which led to hypovnmolemic shock and prerenal azotemia. The risk that include alcoholism, smoking that is habitual as well as work related anxiety could probably lead to peptic ulcers. The patient has been unemployed for some time and is likely to be apprehensive over job relations and this might have plummet him into alcohol abuse and maybe smoking over a long period of time. Research has shown that constant smoking and alcohol abuse are strong gastro duodenal irritants that result in a number of pathological conditions. Weighty acetylsalicylic acid intake can be a probable cause of excessive hemorrhage or gastric ulcerations. Peptic ulceration does not necessarily occur due to moderate alcohol intake. Conversely, in excessive amounts, the danger of gastric hemorrhage can be significant especially in the event of prior lacerations. Smoking of cigarette is also likely to contribute significantly to duodenal and gastric ulceration impaired healing of the previous ulcers and subsequent recurrences of ulcers (Yamada, T & Alpers, 2008) Severe upper GI hemorrhage in alcoholics is also caused by esophageal varices as a result of cirrhosis. Within the abdomen and the gut, varices are likely to be observed in about half of patients suffering from cirrhosis. These are distended veins as a result of high pressure, and most veins are superficially located within the gut and the upper abdomen. Patients that have engorged veins might be under a severe threat of sudden tear leading to massive blood loss, which could deteriorate the diagnosis (Bode & Bode, 1997). Conversely, varices located around the gut are coupled with signs of portal hypertension as indicated by disturbed coagulation studies, not seen in the given clinical case. Additionally, it is easier to establish other causes of GI hemorrhage through samples of stress levels, gastritis test, alcohol or tissue tear.. Alcohol intake in excessive amounts could cause gastritis which is shown by emesis ,nausea, slight hematemesis and dyspepsia, (Tierney, et al., 2008). The data collected allows the physician to make a prognosis that about 60% of hemorrhage in chronic alcohol abusers is as a result of peptic ulcers. Approximately 4% of patients in a NSAID research were found to have alcoholic gastropathy which can only be associated with portal hypertension. In a subsequent study, the risk of proclaimed peptic ulcers was attributed to excessive alcohol intake couple with smoking. Alcohol intake of more than 42 drinks per week is likely to heighten a patient’s risk of hemorrhage ulcer four times as compared to one who drinks less weekly (Bak Andersen et al. 2000).Research taken on 656 females and 36 males gave a clear indication that the risk of peptic ulcers in smokers is twice as much if coffee and alcohol is also involved. Commonly, excessive alcoholism has been attributed to have unfavorable effects on the gastrointestinal system. The reason to this is that there is secretion of an augmented amount of gastric acid in the stomach. Conversely, there is no exoneration of the specific means. Injuries of gastric mucosal are as a result of alcohol and in this case it is accompanied by reduced secretions of prostaglandin, inflammation as well as the stomach mucosal barriers are affected (Mcphee, 2008). On the other hand, smoking raises the threat of ulcer as it increases the duodenal load of acid as well as damaging the duodenal and pancreatic bicarbonate secretion. Acoording to research,it is evident that social problems,post traumatic stress that is associated with work and depression enhances the chances of having peptic alcers as well as other associated problems. For this peptic alcer the gut wall’s defects are seen to extend via the muscuris mucosa to what is referred to as muscularis propria.The result of this is that there is severe wounds being formed due to the secresion of the acid together with defence barriers of the mucosa.This takes place particularly in the duodenum and the abdomen. Infections of Helicobacter pylori are likely to result in gastric ulcers, whereas, hypersecretion of acid is a likely association of duodenal ulcers. Peptic ulcers can result in hemorrhage without a prior history or earlier signs it. Normally, the abdomen or the duodenum postero –inferior wall is the one that is affected. An ulcers is known to be a big threat of extensive hemorrhage. The reason for this is that it is location close to the major vessels can easily wear down into the vessel (Bode, 1997). Ulcer is known to corrode into the vessels’ lateral walls as a result of this, there is extensive hemorrhage. Question 4) Biochemical investigations: Liver Function tests are very significant especially serum ALT and AST as they allow the physician to establish any liver pathologies that were caused by alcoholism. Prothrombin time on the other hand needs to be undertaken in order to evaluate the patient’s coagulation. Such could contribute to the ruling out of the causes related to cirrhosis as well as hepatitis cause caused by alcohol. Investigations Related to Non-Biochemical The most probable test for the upper gastrointestinal hemorrhage is referred to as ‘‘Esaphago gastro duodenoscopy’’ and not only assists to locate the hemorrhage site but also provides salutary intercessions such as heater probe coagulation and adrenaline injections (Mclatchie et al. 2007). The ulcer damage or erosion to peritoneum in the pepetic ulcer chronicle is the probable test that could be established through an x-ray procedure. There should be abdomen decubitus films in order to indicate intra-peritoneal air that is free in the seventy five percent cases, thus, it should be conducted to rule out its snag. Bibliography Bakandersen,I.Jorgensen,T.Bonnevie,O.Gronbek,M and Sorensen,T.I.A (2000).Smoking and alcohol intake as risk factors for bleeding and perforated peptic ulcers: a population-based cohort study. 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