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Clinical Biochemistry and Haematology - Book Report/Review Example

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The research paper “Clinical Biochemistry and Haematology” seeks to evaluate differential diagnosis, which is methodical diagnostic systems that are used to spot the existence of an entity in cases where there are various alternatives are possible…
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Clinical Biochemistry and Haematology
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Clinical Biochemistry and Haematology What is the differential diagnosis? Differential diagnosis is methodical diagnostic systems that is used to spot the existence of an entity in cases where there are various alternatives are possible. Becker et al (2005) explain that it is the process is sometimes referred to as differential diagnostic procedure. The term may also be used in reference to any of the incorporated candidate alternatives; referred to as the candidate condition. One of the most important aspects of the differential diagnosis is that it is an essential process of elimination or at least of getting relevant information and details that reduces the “possibilities” of patient conditions to insignificant levels (Ferri, 2011). In real time though, the presumed patient might either have a health problem or not with the possibilities being nil or 100 percent. As asserted by Adler et al. (2008) and Gaw (2008) that the resultant probability fractions of each presentation or conditions are presumed to be the same thus in the case of Mr. Johnson it will be: Mr. Johnson’s conditions can be summed up with the differential diagnosis probability below: The significance of the full blood count and biochemistry results Mobile Reference (2007) explains that the reason for a blood count is to check the level of Haemoglobin in the body. This test performed is referred to as a full blood count and once the test for Haemoglobin falls below a certain level of count then it can be presumed that the patient has anaemia. The normal unit for checking the Haemoglobin level is g/dl. Therefore the main reason for having a full blood count will be to check the level of Haemoglobin in a patient. The full blood count can also be used to check various diseases in a patient. This is because many of the diseases in patients can be determined by the formation of the blood and how the blood count will show some abnormalities (Howard and Hamilton, 2007). The full blood count test is done using a small sample of blood that has been anti-coagulated. The test itself is the most appropriate worldwide for an examination of blood further supported by the fact that it gives an overview of the patients’ condition. A full blood count is helpful especially in diagnosing the conditions in which the numbers of blood cells are abnormally low or abnormally high or in some cases the cells themselves might be abnormal. Beckett (2010) asserts that, with a full blood count in a laboratory test it will be measure different status and features of the blood and some of the blood status that is measured through the full blood count includes: The amount of Haemoglobin in the patient’s blood: Haemoglobin is basically an iron-containing compound that can be found on the red blood cells and it is tasked with transporting the oxygen within the body. By measuring the amount of Haemoglobin the patient will be diagnosed whether he or she suffers from Anaemia. Anaemia is caused by a Haemoglobin deficiency (Azoulay et al 2010). Through the measurement, the test might also detect abnormally high concentration of Haemoglobin in a patient. This is most common especially with patients suffering from chronic lung disease especially as a result of trying to adapt to high altitude or in other cases it can be the abnormal increase in the production of the red blood cell by the bone marrow referred to as polycythaemia vera. In a normal person the normal Haemoglobin ought to be 130- 170 g/L for the adult males while for the adult female the normal Haemoglobin level should be 120-150 g/L. The full blood count also measures the level of the Red cell also referred to as Red Cell Count (RCC): This is an estimation of the amount in terms of number of the red blood cells per every litre of blood in the body of a patient. In cases where there are abnormally low numbers of red blood cell this will be an indication of anaemia resulted by loss of blood, failure in the bone marrow, malnutrition in cases like iron deficiency, being over-hydrated or whenever there is a mechanical damage on the red blood cells. The normal red cell count for adult males is supposed to be 4.5-5.5 x 1012/L, and 3.8-4.8 x 1012/L for adult females. The full blood count in this case will show us the status of Mr. Johnson and this has been quite important in the sense the full blood count has enabled the result to show the patient’s health condition in relation to the number of the blood cells whether they are abnormally high or abnormally low and in our case the blood count shows the acute level of Haemoglobin on Mr. Johnsons blood count. In the case of Haemoglobin count; the normal level ought to be between 130- 170 g/L which in this case it is lower than expected as Mr. Johnson had a 5.4 g/dL. From the laboratory tests the results show that the RCC of the patient is also on a low as the normal ought to be 4.5 to 5.5 × 1012 but according to the laboratory results the level presented is a paltry 2.04×1012/L. The results can have many assumptions presented by the low amount of the Red Blood Cells. One factor that will be a possible reason is the patient suffering from anaemia. What is the origin of the abnormalities seen on the blood film? One of the abnormalities found on the blood film includes Spherocytosis which has many origins including the patient might have had a hereditary Spherocytosis. In some cases the main reason might have been immune haemolytic anaemia or if the patient suffered from Zieve’s syndrome or even if he had Microangiopathic haemolytic anaemia this would have led to the patient having Spherocytosis. In the case of polychromasia it can be deduced that incase the patient had any situation related with reticulocytosis then this would have led to the abnormalities for example if the patient had an injury that led to bleeding then this would have been the result. In another scenario if the patient had a haemolysis cases or when the patient had developed a response to haematinic factor replacement then the effect would have resulted to polychromasia (Blann, 2007) The underlying pathology of John’s condition and the likely causes for them based on his history Form the look at the history of John’s health condition and the amount of Haemoglobin in the blood together with other aspects it can be presumed that John suffers from sickle cell disease and this is evidenced by the amount of the Haemoglobin level in his blood and also from other symptoms like jaundiced sclera and ankle oedema. It is safe to say that the resultant effect of the sickled cell sticking to the walls of the blood vessels in John’s body resulted to a blocked flow of blood which created the pains he was experiencing and also in some cases there can be organ damage if not checked well in time. The minimal oxygen delivery in the blood vessels that led to John having shorter breath can be greatly attributed to this fact that the Haemoglobin S was present in his blood hence it made the red blood cells to acquire a sickle shape making it difficult for the red blood cells to flow in the blood vessels and the result is the shortened breath due to lack of enough oxygen. Case Study 2 The differential diagnosis for Claire The differential diagnosis for Claire can be summed up as being =1.61172161 The differential diagnosis for Claire will be 1.61172161 To carry out the correct test; a clinical D-Dimer test procedure will be most appropriate to confirm the health problem that Claire might seem to be having. D-Dimer Testing: the rationale for the testing and the molecular detail of the D-Dimer in the blood. Fischbach et al. (2009, pp 36) describes D-Dimer as a product degraded from a compound fibrin. The fibrin itself is composed of different splinters made up of proteins in the blood. This happens mostly whenever there is a blood clot in the veins. Fibrinolysis is the compound that facilitates the degradation of the blood clot. Normal routine blood tests done to establish a thrombosis is mostly resolved by a D-dimer. The main purpose of the D-dimer is to perform the test to patients that are suspected of having thrombotic disorders. The rationale is that the diagnosis, if negative will rule out the presence of thrombosis while if the result is positive it will indicate the presence of thrombosis but this will not eliminate other causes. The main purpose of the d-dimer test is to exclude the thrombo embolic disease in the scenarios where their probability is quite low. Furthermore the d-dimer test can be used in the diagnosis of disseminated intravascular coagulation which is a blood disorder. The D-dimers in the human blood plasma are not present and they will only be present once the coagulation system has been activated a case in point when there is the presence of thrombosis or disseminated intravascular coagulation. The D-dimer analysis depends primarily on the binding of a monoclonal antibody in relation to a particular epitope on the D-dimer fragment. Coagulation is the formation of a blood clot referred to as thrombus. The coagulation occurs when the protein of the coagulation cascade are activated. This can happen when there is a contact with a damaged blood vessel or in other cases through activation of factor VII by tissue activating factors. In both cases it will lead to development of thrombin which will serve as a scaffold for the clotting of the blood. How the new information will be followed up According to Beek et al (2009), thrombosis implies that there is blood clot formation within the main veins resulting to serious complications that are potentially dangerous. With this in mind diagnosis for a thrombosis will have to be conducted immediately. The doctor will conduct this diagnosis in order to confirm whether there is a blood clot on Claire or not. Further tests to confirm the diagnosis In the scenario that a blood clot is discovered during the diagnosis and a thrombosis has been discovered, the medication and management of the thrombosis will be administered without delay to reduce the chances of the blood clot budding creating further life threatening risks (Colman, 2006). In case of a deep vein thrombosis then the treatment will include anticoagulant medicines like heparin and warfarin. In the case of Heparin then the medication will be done intravenously through a vein or as an injection and thus this will act very fast. In the case of Warfarin then it will medicated through the mouth and hence it will take several days to be quite effective. Both of the medication will be taken nearly at the same time thereafter Heparin will be discontinued after warfarin has started being effective. If the physician’s opinion is that the clot will be dissolved immediately then the solution will be getting a thrombolytic therapy whereby the physician will inject medication in to the clot by use of a needle or a tube called catheter (Idée & Corot, 2009). Understanding Claire’s previous pregnancy problems Claire’s pregnancy increased the risk of thrombosis to three-fold. The main reason on this was the increased risks especially on hypercoagulability which had evolved to protect the women against the bleeding challenges they experience with miscarriage and also in childbirth. The hypercoagulability was present in the pregnancy from as early as the first trimester thereby increasing the risk of thrombosis and in essence miscarriage (James 2009, Blackburn 2007). Further from the Claire’s family history it is likely that the thrombosis was an inherited and acquired thrombophilia that is evidenced from Claire’s cousins having miscarriage during the pregnancy and also on Clair’s case. Chances of Claire taking a long haul Flight Patients with thrombosis are at a high risk of aggravating the thrombosis during flights especially long haul flights that lasts above three hours (MacDougall et al, 2006). Most practitioners will not recommend a long haul flights for patients with thrombosis. In the case of Claire long haul flights will be a cause of great concern since she has symptoms that imply she might be having deep vein thrombosis or even pulmonary embolism therefore some factors that will have to be put into consideration includes the duration of flight and in this case it is a long haul flight thus another situation need to be put into the picture and that is the prothrombotic situation that is created by the venous stasis in the lower limbs (Samama, 2005). The stasis is mostly attributed by the prolonged immobilization, obstruction of the venous return by compression of the lower limb veins and as part of a general reduction in blood flow especially as a result of the in-flight dehydration (World Health Organization 2007). This means that Claire has to avoid the cramped up position and conditions like in the economy class and furthermore in long haul flights she should facilitate the movement of blood circulation by making movement in the flight as much as possible. (Chee & Watson, 886) The best way is for Claire to check the medication and consult a physician on whether she is capable of taking long flights or if splitting the flights into short stop-over will be most appropriate. Claire’s chances of having a successful pregnancy There are possibilities of Claire having a successful pregnancy and this means that once she is pregnant, she has to consult her obstetrician. A diagnosis of thrombosis will have to be done on her. This is so, in order for the doctors to see the blood clot and the extent of the clot. Furthermore with the doctor at hand, the doctor will be able to check Claire’s family history to see whether any of the family members have a history of thrombosis. If confirmed of a blood clot in the vein, the medication will be administered to ensure a safe pregnancy. The most appropriate medication will be the one that helps thins the blood to reduce the blood clot in the vein. References ADLER, S. N., ADLER-KLEIN, D., GASBARRA, D. B., & ADLER, S. N. (2008). A pocket manual of differential diagnosis. Philadelphia, Lippincott Williams & Wilkins. AZOULAY, É., MOKART, D., LAMBERT, J., LEMIALE, V., RABBAT, A., KOUATCHET, A., & SCHLEMMER, B. (2010). Diagnostic Strategy for Hematology and Oncology Patients with Acute Respiratory Failure Randomized Controlled Trial. American journal of respiratory and critical care medicine, 182(8), 1038-1046. BECK, E. R., FRANCIS, J. L., & SOUHAMI, R. L. (2005). Differential diagnosis. New York, Arco Medical. BECKETT, G. J. (2010). Lecture notes. Clinical biochemistry. Chichester, UK, Wiley-Blackwell. http://search.ebscohost.com/login.aspx?direct=true&scope=site&db=nlebk&db=nlabk&AN=439944. BEEK, E. J. R. V., BÜLLER, H. R., & OUDKERK, M. (2009). Deep vein thrombosis and pulmonary embolism. Chichester, UK, J. Wiley-Blackwell. http://site.ebrary.com/id/10346067. BLACKBURN, S. T. (2007). Maternal, fetal, & neonatal physiology: a clinical perspective. St. Louis, Mo, Saunders Elsevier. BLANN, A. D. (2007). Routine blood results explained. Keswick, Cumbria, M&K Pub. CHEE, Y.L., WATSON, H.G. (2005). Air Travel and Thrombosis. Br J Haemotol. 130(5):671-680. COLMAN, R. W. (2006). Hemostasis and thrombosis: basic principles and clinical practice. Philadelphia [u.a.], Lippincott Williams & Wilkins. FERRI, F. F. (2011). Ferri's differential diagnosis a practical guide to the differential diagnosis of symptoms, signs, and clinical disorders. Philadelphia, Pa, Elsevier/Mosby. http://site.ebrary.com/id/10513460. FISCHBACH, F. T., & DUNNING, M. B. (2009). A manual of laboratory and diagnostic tests. Philadelphia, Wolters Kluwer Health/Lippincott Williams & Wilkins. GAW, A. (2008). Clinical biochemistry: an illustrated colour text. Edinburgh, Churchill Livingstone. HOWARD, M. R., & HAMILTON, P. J. (2007). Haematology. Edinburgh, Churchill Livingstone. IDÉE, J. M., & COROT, C. (2009). Thrombotic risk associated with the use of iodinated contrast media in interventional cardiology: pathophysiology and clinical aspects. Fundamental & clinical pharmacology, 13(6), 613-623. JAMES AH.(2009) Arterioscler Thromb Vasc Biol. 29(3):326-31. James AH.(2009)Hematology American Soc Hematol Educ Program :277-85. MacDOUGALL, D. A., FELIU, A. L., BOCCUZZI, S. J., & LIN, J. (2006). Economic burden of deep-vein thrombosis, pulmonary embolism, and post-thrombotic syndrome. American journal of health-system pharmacy, 63(20 Supplement 6), S5-S15.Bottom of Form MOBILEREFERENCE. (2007). Biochemistry Quick Study Guide. Boston, MobileReference.com. http://public.eblib.com/EBLPublic/PublicView.do?ptiID=318510. SAMAMA M. (2005) An epidemiologic study of risk factors for deep vein thrombosis in medical outpatients. Archives of Internal Medicine. 160: 3415-3420 WORLD HEALTH ORGANIZATION. (2007). WHO research into global hazards of travel (Wright) project: final report of phase 1. [Geneva], World Health Organization. Read More
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