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Glucose Tolerance Test: Results and Analysis - Lab Report Example

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The author of the "Glucose Tolerance Test: Results and Analysis" paper examines two methods of administering Glucose Tolerance Test that practiced in a given diabetic case, namely, (a) Urine Analysis with the use of a dipstick test; and (b) Trinder’s Method…
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Glucose Tolerance Test: Results and Analysis
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I.Glucose Tolerance Test Results & Analysis Introduction There are two types of diabetes both of which are ified by the World Health Organization (WHO 2012) as chronic disease. Type 1 is the classification given to diabetes whenever a person’s pancreas fails to produce adequate insulin to regulate the glucose level in the blood. Type 2 diabetes is acquired by adults, usually due to overweight maintenance and a very inactive physical lifestyle pattern like sitting in the office the whole day and just going home to sleep. The body produces adequate insulin but does not utilize it effectively to regulate blood sugar level. Glucose Tolerance Test is meant to screen Type 2 Diabetes (Mayo Clinic Staff 2013). If not identified and controlled early enough, it can “damage the heart, blood vessels, eyes, kidneys, and nerves” (WHO 2012, par.11). Glucose is supposed to provide energy for the cells of the body. It normally comes from the carbohydrates consumed during meals, examples of which would be potatoes (delicious French Fries), rice, bread, pizza, spaghetti or instant noodles. Vegetables, fruits, milk, refined sugars, coffee, softdrinks, and many of the processed food consumed frequently actually contain carbohydrates that the body will convert into glucose. By performing Glucose Tolerance Test, the professional health care specialist can be guided by the results in order to prevent progression of the disease. If found positive with Type 2 Diabetes Mellitus(T2DM), the proper treatment should be done before complications take place. Two methods of administering Glucose Tolerance Test were practiced in a given diabetic case, namely, (a) Urine Analysis with the use of a dipstick test; and (b) Trinder’s Method. The results were as follows: Table 1 – Findings of Urine Samples Analyzed Using A] Dipstick Tests & B] Absorbances Patients / Status A.Glucose Pad Color After 60 seconds indicated B.Absorbances # 1 patient – after fasting = negative 0.025 # 1 patient – after 2 hours of glucose source food intake = negative 0.056 # 2 patient – after fasting = negative 0.054 # 2 patient – after 2 hours of glucose source food intake = negative 0.102 # 3 patient – after fasting = negative 0.103 # 3 patient – after 2 hours of glucose source food intake = positive 0.163 (dark yellow color) Patient # 3 is suspected of having “Glucosoria” or the presence of glucose in the urine. To confirm the findings from the Dipstick Test, Trinder’s Methods were utilized. Details of those methods are in a separate manual and made part of the case instructions. If by using the Trinder’s Methods, the glucose concentration found in the urine exceeds the normal threshold = 11 mmol / L, there will be evidence of Glucosoria, one of the features of Diabetes Mellitus. It means the body was not able to convert glucose into energy using the available insulin or there is insufficient insulin produced by the Pancreas (Sherwood 2002). While fasting, few parts of the body (brain, blood-RBC, kidney medulla, platelets, and leukocytes) depend on glucose for its energy supply. If the brain runs out of glucose supply, it can experience dehydration and eventual comatose. In contrast, if the brain experiences a very high glucose concentration (exceeding 600 mg / dL ), it will also experience comatose. Other parts burn or oxidize the available fatty acids of the body along with ketone. It is the Liver, together with glycogen from muscles, which maintains glucose levels in the fluid parts of the system within the body (Plasma.). A normal Liver can synthesize glucose out of amino acids in the body through a process known as glucogenesis. It is capable of storing glucose into glucogen (polymerized glucose with the help of enzymes) whenever the body has excess glucose for energy requirements, so that when the body lacks glucose, another set of enzymes can convert the stored glucogen into glucose through a process known as glucogenolysis. If the storage capacity of the Liver for glucogen has been filled, the remaining glucose will be converted by adipose cells into fat. Normal values found in fasting serum (containing plasma)has 80 – 120 mg/dL glucose concentration. Below 60 mg / dL glucose concentration in the plasma indicates hypoglycaemia. The corresponding symptoms would include palpitation of the heart, weakness, feeling faint, dizzy, anxious, experiencing tremors, hunger, or cold sweat, confusion, poor motor coordination of body parts. Loss of consciousness takes place when the plasma concentration falls below 40mg / dL for adults and 25 to 30 mg / dL for infants. Convulsions can take place. Table 2 – Glucose Level Standards for the Blood/Plasma (Source: AACC. Lab Test Online: Glucose. American Association of Clinical Chemistry, 2013. Viewed January 21, 2013 @ http://labtestsonline.org/understanding/analytes/glucose/tab/test ) The Trinder’s methods involve the following sample laboratory instrumentation, namely, (a) the Photometer set to have a wavelength of 540 nm, autoanalyzer, or semi-autoanalyzer; (b) Curvette or light path – 1 cm, (c) water @ 37oC, (d) Lab supplies : Pipettes, Test Tubes, Racks, Dispenser Tips. Calculations include blood sample x 100 Standard Concentration = mg / dL glucose per sample = Standard . The conversion factor is 1 mg / dL x 0.0555 = mmol / L. Linearity specifications can be up to 600 mg / dL of plasma with a measurement range of 25 – 600 mg / dL. 2 mL of blood is collected after fasting for at least 9 hours. It should be processed for glucose analysis within 3 hours from collection time (Ramakrishnan, S. p.4-5). The patient is given 75 gms. Of sugar rich food or drinks. Every ½ hour, blood and urine samples are taken after taking source of glucose. After 2 hours from intake, there should be no sugar in the urine. The blood sample should return to normal level (See normal standard range.). Table 3 – Laboratory Materials Standards Utilized H2O (ml) Standard Glucose (ml) Glucose Concentration (mmol/L) 1.0 0 0 0.9 0.1 5 0.8 0.2 10 0.7 0.3 15 0.6 0.4 20 0.5 0.5 25 Table 4 – Findings of Blood Samples Using Trinder’s Method Patient Samples (Fasting) Absorbance @520 nm Patient Samples (2 hrs. after fasting & after glucose load) Absorbance @ 520 nm Blood Glucose Concentration (Fasting) Blood Glucose Concentration (after fasting) Patient # 1 – 0.025 mmol / L # 1 - 0.056 mmol # 1 X=0.025 Y=0.0141 absorbance X/Y = 0.025 mmol / 0.0141 = 1.773 # 1 X=0.056 Y=0.0141 absorbance X/Y = 0.056 mmol/0.0141 = 3.9716 Patient # 2 – 0.054 mmol / L # 2 – 0.102 mmol (same formula) 3.830 mmol / L (same formula) 7.234 mmol / L Patient # 3 – 0.103 mmol / L # 3 - 0.164 mmol 7.305 mmol / L 11.56 mmol / L The basis of computing the glucose concentration was based on the standard absorbance linear equation of a normal reading. See Chart below. The value = 0.014 came from the linear formula Y = mX where Y is the Absorbence data while X is the Glucose Concentration data. And the slope m= 0.014. After computing for the Lab Test Data, it appeared that only Patient # 3 was actually diabetic even during fasting and was above the normal glucose concentration in the blood after glucose load. II. Kidney Test The standards for the Kidney Test are as follows: H20 (ml) Standard (ml) Creatinine Concentration (in uM / L) 1 0 0 0.9 0.1 100 0.8 0.2 200 0.7 0.3 300 0.6 0.4 400 0.5 0.5 500 0.4 0.6 600 0.3 0.7 700 0.2 0.8 800 0.1 0.9 900 0 1 1000 Table 5 – Water Content Used to Determine Concentration Creatinine Standards (uM/ L) Absorbance 0 0 200 0.216 400 0.402 600 0.592 800 0.793 1000 1.012 Table 5 – Relative Absorbance to Standard Solution The kidneys should be able to clear creatinine within a minute. It has “glomerular filters” to eliminate waste products from the internal system of the body while keeping blood and protein within the bloodstream. When the “glomerular filters” get damaged, protein and red blood cells RBC leak out in the urine. Tests are done to determine how much protein in milligrams per gram of creatinine is released in urine. Another way is by testing the blood for blood urea nitrogen (BUN) and creatinine. Urea is a waste product from the use of protein when it breaksdown. Creatinine, on the other hand is a waste product of muscle activities. Both may not be excreted normally and may accumulate in the blood. An increase in BUN and creatinine within the blood would be an indication of a deteriorated kidney function. The normal range for creatinine should be 0.7 to 1.2 mg / dL or 62-106 uML creatrinine concentration. It also depends on the muscle mass of the patient. Very muscular 1.5 mg / dL or 132 uM / L) Small or elderly 0.5 mg / dL or 44 uM / L Results of urine analysis and blood test from the three (3) patients were as follows: Samples from Patients Absorbence Creatine Concentration (uM / L) P1 Urine 0.728 0.728 / 0.001 =728; 728x21=15288 P1 Plasma 0.088 0.088 x 0.001= 88 P2 Urine 0.327 0.327 / 0.001=327 ; 327x21=6867 P2 Plasma 0.575 0.575 x 0.001 = 575 In Patient # 1, the amount of creatinine cleared was (15288 x 1000) / (88 x 1440) mls per minute based on the formula (U x V) / (P x T). The result for P1 was therefore 120.64.mls./min. In Patient # 2, using the same formula, (6867 x 3000) / (575 x 1440) ml. per min. = 24.88 mls./min. Comparing the results of computations with the different stages of kidney disease (shown in Table 6 below, the conclusion is that Patient # 1 has a normal renal function. But Patient # 2 is in Stage 3 of kidney deterioration which is considered severe. Stage of Kidney Deterioration Description GFR mL / min / 1.73m2 1 Normal. 60 to 120 2 Moderate decline of kidney 30 to 59 3 Severe kidney function deterioration 16 - 29 4 Indicates kidney failure 15 or less Glomenrular Filtration Rate (GFR) is the blood test to measure the volume of blood filtered per minute. (NKDEP 2012) Figure 1 – Guide to the Determination of Kidney Condition (Source: National Kidney Disease Education Program (NKDEP). Explaining Your Kidney Test Results. NKDEP National Institute of Health, Dept. of Health, Maryland, USA. August 10, 2012. Viewed January 21, 2013 @ http://nkdep.nih.gov/resources/explaining-kidney-test-results.shtml) III. Liver Test It is said that the largest human organ is the liver. It absorbs and processes amino acids from the intestines and converts amino acids into protein. It detoxifies the system and excretes waste products, which is why some continuous dosages of medication can result in an accumulation of toxins in the liver if the liver is no longer able to function normally enough to excrete those toxins. It is supposed to be capable of “regeneration” according to Lee, M. (2009, p. 236). The modern way of deciding which Liver Test should be performed depends on the initial findings about a patient. By interviewing patients, an information to serve as clue as to which Liver Test to perform can be discovered. For example, if the patient has been an alcoholic for some time, a blood test to determine the extent of cirrhosis would be part of the Liver Function Test (LFT) that would have to be performed. But it can also require the use of Ultrasound and/or CT scan. Ideal Values in Liver Test Liver Test Type Normal Range Values Alkaline Phosphate (mmol / L) 30 to 901 U / L Bilirubin ( umd / L ) Up to 20 umd / L Standard Results H2O ml Phenol Standard m / L Phenol Concentration mmol/L 1.0 0 0 0.9 0.1 0.2 0.8 0.2 0.4 0.7 0.3 0.6 0.6 0.4 0.8 0.5 0.5 1.0 Test of Protein, Albumin, and Aspartite Transaminae in the Liver Given Data Normal Values for Liver Function Test Patient # 1 Patient # 2 Total Protein ( g / L ) 60 – 80 g / dl 70 g / L 68 g / L Albumin ( g / L ) 35 to 50 g / dL 38 g / L 40 g / L Aspartate Amino-Tranferase 10 to 50 IU /L* 45 u / L 450 u / L (indicates Liver injury) Total Serum Bilirubin Up to 20 mmol / L or 1 mg / dL (MayoClinic 2013) 1 mg = 1/0.0555 mmol = 18.01 mmol / L 388.98 umol / L or 0.39 mmol 35.58 mmol / L Urine Bilirubin negative Alkaline Phosphatase or ALP 30 – 90 ImU / ml 37.8 36.06 Alanine Aminotransferase 5 – 35 IU / L Patient # 2 must be the person with acute hepatitis due to the 450 u / L result of the Liver Function Test of Aspartate Aminotransferase which should be only within the range of 10 to 50 IU / L. “High levels of AST may be caused by liver damage from conditions such as hepatitis and cirrhosis.” (WebMD 2013 p.2) It should be noted that the normal standard may vary. For example, Lee, Mary (2009, p.217) says that the normal range differs between males and females. Males Aspartate Aminotransferase normal = 0 to 37 IU / L which is equal to 0.617 nmol sec / L Females Aspartate Aminotransferase (AST) Normal = 0 to 31 IU / L or 0 – 517 nmol sec/ L The AST enzyme synthesizes amino acids while it is distributed in the human organs like th pancreas, kidneys, heart, RBC, skeletal muscles, and the liver. Alkaline Phosphate Test Phenol Standard Absorbance @ 520 nm Wavelength 0 0 0.2 0.176 0.4 0.372 0.6 0.553 0.8 0.763 1.0 0.964 P1 - blank 0.567 P1 0 P2 - blank 0 P2 0.541 Calculations for the Alkaline Phosphate Test P1 ( 0.567 x 1000 / 15 ) / Y = 37.8 Note: This is within the normal range P2 ( 0.541 x 1000 / 15 ) / Y = 36.06 Note: This is within the normal range. Liver Bilirubin Test Absorbence Standard 0.413 Standard blank 0.000 P1 0.459 P1 blank 0.000 P2 0.042 P2 blank 0.000 Calculations for the Bilirubin Test P1 P1 absorbance / Std. serum absorbance x Absorbence Std.= .0.459 / 0.413 x .350 = .38898 umol / L or 0.39 mmol / L P2 0.42 / 0.413 x .350 = 35.59 mmol / L Conclusion of Liver Test Indications of the ALT results, Alkaline Phosphatase, and Bilirubin tests, Patient # 2 is suffering from a Liver Disease, while Patient # 1 appeared to have normal findings. Practical Medical Biochemistry Based on a Lab Report: A Case Study A 30-year old female had felt weakness in her ability to go up and down the stairs for the past few weeks. She finally reported the problem to a General Practitioner who then took a blood sample for the laboratory to assess. There was no other symptom except a disclosure from the patient about having hypertension before and weak muscles. Discussion Based on the results of laboratory tests, it appeared that the patient had very low level of Potassium in her blood and should be confined for emergency treatment with i.v.Potassium, monitored for safe recovery, and made to recover with the required normal supply of Potassium needed by a female adult at her age. This is actually an emergency case because the infusion via intravenous method (the fastest way to replenish the blood) can result in heart troubles. The logical steps should be as follows: Step 1. Emergency Replenishment of Potassium via I.V. Administration A very low level of Potassium 2.1 mmol / L versus the normal 3.5 to 5.5 mmol / L is enough indication to justify confinement of the patient in a hospital for the slow administration of injectable Potassium and monitoring of recovery. The rationale behind is about a possible encounter with heart problems during the intravenous replenishment. Her very low level of Potassium shows the need for an emergency room, says Dr. Cunja, J.P. (2013, p.7). After favourable signs of recovery which can be checked by another blood sample test, the patient should be diagnosed further. Step 2. Proceed to Further Diagnosis While Confined in a Hospital. The proper diagnosis of the 30-year old female should start with an interview to discover other symptoms aside from feeling muscular weakness while climbing up and down the stairs. So far, the best clue is a very low Potassium level. This should not yet be concluded to mean that she has Conn’s Syndrome. It may just be a failure in the maintenance of balanced diet or the effect of a medicine against hypertension (diuretic). But further diagnosis may lead to such a finding because Conn’s Syndrome was reported to commonly take place in females from the age of 30s to 60s (Meeking, D., 2011 p.64). Causes may be also due to a family history of hypertension (Mayo clinic Staff 2013), or the intake of Thiazides (diuretic) to control hypertension (Marshall, W.J. and Bangert, S.K. 2008, p.803), or failure to maintain a regular balanced diet wherein Potassium intake has been insufficient for quite some time. Bit it can also be due to a tumor on the adrenal glands. While the given case can be diagnosed as a possible symptom caused by “tumor”, it would be too hasty or lacking in prudence to say so without first considering natural ways of overcoming Potassium deficiency. The mere thought of “tumor” forewarns about cancer. And surgical removal would be a depressing suggestion to any patient. Although Ahmed, N., et.al. (2007, p.187) mentions that Conn’s Syndrome is often caused by a tumor, Mayo Clinic Staff (2013) says it is “in rare cases, primary aldosteronism may be caused by cancerous (malignant) growths in the outer layer (cortex) of the adrenal gland”. Mayo Clinic equates Conn’s Syndrome to primary aldosteronism. More common causes of Conn’s Syndrome were identified to be (1) an over activity of adrenal glands – both of them; (2) benign growth also known as aldosteronoma on the adrenal gland or adrenal adenoma. Taking multiple medications against hypertension increases the probability of having Conn’s Syndrome, since according to the Mayo Clinic Staff – 2 (2013), high BP plus multiple medication against hypertension serve as a main symptom “of primary aldosteronism”. As a matter of fact, low Potassium (K) discovery after a blood sample test of the patient (Potassium (K) = 2.1 mmol / L versus normal adult (K) = 3.5 to 5.5 mmol / L) is classified by the Mayo Clinic as a complication of primary aldosteronism. Together with hypertension, it creates heart problems and kidney problems. Thus, it can end up in one of the following: (1) heart attack or heart failure, (2) hypertrophy or enlargement of the heart’s left ventricle, (3) stroke, (4) kidney disorders or failure to function properly. As a result of low Potassium level in the body, the reported feeling of weakness while walking up and down the stairs for the past few weeks became the apparent symptom. Step 3. Recommend Verification of Possible Effects to Check for Existing Complications Has the heart been weakened by any of the possible complications mentioned earlier? The immediate way is by checking on the heartbeat rate. But the more thorough diagnosis of the heart would be with the use of the ECG and Chest X-Ray to discover any sign of enlargement of the left ventricle. A Brain Scan should also be recommended to trace any sign of stroke since this is one other complication following a suspected primary aldosteronism and is very possible for someone with hypertension while having low level Potassium. A justification for undergoing these major tests would be the need to determine if her initial symptom which was experienced for past weeks had already reached a point of complication. There would be no other way of knowing if it did, while medical findings have proven such a trend for diseases not treated immediately. While preparing for these major check ups, the Kidney Function can be assessed via laboratory test of the urine. A “rapid urine test” after doctor consultation can identify the following: Substance Purpose Standard Reference PH value To determine the acidity 5 to 7 is normal. Protein Negative (only a trace) Sugar To determine the glucose level negative Nitrite negative Ketone negative Bilirubin To determine the presence of haemoglobin breakdown negative Urobilinogen To determine the breakdown of Bilirubin negative Red Blood Cells To identify erythrocytes Negative; normal value = 0-2/HPF White Blood Cells To identify leukocytes Negative; normal value = 0-2/HPF The pH level value < 5 indicates acidic urine which can mean a high risk of developing Kidney stones, whereas a pH level value > 7 can mean bacterial UTI. The presence of Leukocytes and Nitrite also in the urine will validate the existence of bacterial infection. Kidney inflammation can be revealed by the presence of high protein in the urine. Sugar and Ketone in urine are evidence of probable Diabetes Mellitus. A follow up Urinalysis to examine the Creatinine can measure the rate of kidney filtration. Urinalysis will expose cholesterol crystals, if any, which can be assessed to be high or low. A Liver function urine test can lead to discovery of a Liver disease by giving methacetin or caffeine to a patient via “intravenous infusion of a stable isotope-labeled caffeine while consuming oral caffeine” (Stolzke, T. 2013). Patients with cirrhosis of the liver will not decrease the clearance of caffeine whereas normal urine will show a decreased clearance on spot urine test after the challenge. Since the case says there is no other symptom aside from low Potassium in the blood, the test should first prove whether there is high or low aldosterone. Of course, the hypothesis is that there is a high level of aldosterone. A low aldosterone will include Addison’s Disease as a possibility. So far, the laboratory test proves only very low Potassium, which therefore gives priority to the hypothesis that Conn’s Syndrome is more likely if indeed there is a complication. In Addison’s Disease, the anticipated level of Potassium is high. There was no report of excessive urination which can happen in someone with Conn’s Syndrome, and which is oftentimes the symptom of Diabetes Insipidus. This question should be specifically asked during the interview. Has she been frequently urinating? If yes, then the diagnosis should include tests to identify the root causes of excessive release of urine, e.g. tests to find out if she is diabetic as well. Urine analysis of volume, color, and odor can divulge some hints about the patient’s condition. For example, (1) Little urine released and characterized with very dark color will say there must be lack of fluids or kidney failure. (2) UTI is characterized by “cloudy or flaky urine”.. In the given case, soonafter the provision of Potassium i.v. and through proper diet, a urine test will be valuable to determine if the body is able to retain Potassium or excreting too much Potassium via the urine. Two instances can be tested. First is whenever the patient takes the usual diuretics or Thiazides, and while adequate Potassium is consumed. If Potassium is excreted in urine(as per urine test), the hypothesis will suspect the negative effect of the patient’s diuretics. The 2nd instance should be after withdrawing the medication against hypertension. Without Thiazides, and assuming the patient consumes adequate Potassium, will substantial Potassium be excreted in the urine? If not, then the cause of the low Potassium level is identified. If after eliminating Thiazides, Potassium is still excreted substantially in the urine, then another cause will be suspected. There may be a tumor or the failure of the adrenal glands to function properly may be due to inherited weakness in early adulthood. Frequently, the intake of diuretics such as thiazides for a patient to control hypertension was discovered to be the cause of hypokalaemia. And the recommended remedy is to stop taking diuretics. Instead, a patient should be given Potassium along with 100 mmol / day Sodium (Na). (Marshall W.J. and Bangert, S.K. 2008, p.803) Meeking, D. (2011, p.64) described Conn’s Syndrome as excessive aldosteronism which retains Sodium while “Potassium and Hydrogen ions” are lost to frequent urination. In Conn’s Syndrome, diagnosis involves discovery of low Potassium (K), slightly increased or normal Sodium (Na), The underlying is often “a tumor which should be removed surgically”(Ahmed, N., et.al. 2007, p.187). Another possible source was identified to be “hyperplasia of both adrenals” (Chew, S.L., et. al. 2006, p. 26). Given the case fact that the 30-year old female had hypertension, an interview of the patient should include asking whatever medication she takes to treat her hypertension. Another important inquiry would be about what she usually eats and drinks daily, and what she actually consumed over the most recent days. The fact that her blood contained low Potassium (K) could be due to lack of natural sources of Potassium (K), e.g. White Beans which contains 561 mg Potssium per 100 g., or Dark Green Spinach which contains 535 mg. pf Potassium per 100 g., Other rich sources are baked potatoes, baked squash, Yogart, Salmon Fish, Avocado, Mushrooms, and Bananas. (Medical University of Vienna 2012) (Soource: Mayo Clinic. Adrenal Glands. MayoClinic.com, August 2012. Viewed January 17, 2013 @ http://www.mayoclinic.com/health/medical/IM03191 ) Meeking, D. (2010, p.64) recommends testing for Conn’s Syndrome by “serum potassium, urinary potassium excretion, and serum aldosterone : rennin ratio”. In the serum Potassium test, a low K or 70% or less of the normal standard indicates the presence of Conn’s Disease. In the urinary Potassium test greater than 30 mmol within 24 hours confirms Conn’s Disease. Prior to conducting the test in one morning while standing up, antihypertension drugs have to be withdrawn. Plasma aldosterone should be measured in one morning along with rennin and cortisol after the patient is made to lie down at night, and after the patient remains in an upright position for about 4 hours. Hypokalemia or having very low Potassium level increases the risk of having Type 2 Diabetes Mellitus (Chatterjee, R., et. al.. 2011, 665-672). Therefore, while the patient is in the hospital, aside from conducting a Liver Function Test and Renal Test, a Glucose Tolerance Test should also be done to determine if the patient has become diabetic or not as a result of Hypokalemia. The additional findings resulting from the series of recommended tests can eliminate or proceed to further verifications if the patient is exposed or not to the risks of having other diseases like Addison’s Disease and/or Diabetes Insipidus. With the limited information to begin with, the indications do not give a hint of any of these two other diseases. For Addison’s Disease for example, the usual symptom include: nausea, weight loss, getting tiered easily, discoloured parts of the skin, dizziness or fainting spell, low blood pressure, weak feeling. Of these, only the feeling of being weak matches with the patient’s symptom. For Diabetes Insipidus, the usual major symptom should be frequent urination and large volume of urination. These were not reported in the initial case facts. There is also a possibility that the 30-year old female does not yet have Conn’s Syndrome because one of the usual symptoms of this disease is also excessive urination resulting in the rapid loss of Potassium. Further interviews and investigation while the patient is hospitalized and resuscitated with Potassium, the actual disease or just poor health maintenance will be established. In summary, although it will make the GP very thorough to perform all the possible tests to identify the root cause of the problem, the patient will have to give the go signal for each of the tests that would have to be performed. If cost of medication will not be a problem, and the patient might be amenable to the idea, why not? But in the practical world, justifications have to be given. There has to be a good reason for suggesting a test. And the doctor should start with those critical or necessary diagnostic tests. In this case, so much will depend on what will be the other findings while the patient is confined and trying to recover from the loss of Potassium in her blood. Given no other findings after further interview, she can be informed about the possible complications as a result of not reporting the sickness for past weeks. It would be important to conduct a series of tests on those parts which medical science has proven to show complications following substantial loss of Potassium in the blood. Since that means verifying the condition of the heart, especially the left ventricle, the brain (for any indication of stroke), and the kidneys which failed to hold Potassium and excreted substantial Potassium instead thereby causing an imbalance, those tests related to heart, brain, and kidneys should take priority over other tests. Further Blood Sample Tests, Urinalysis, ECG, Brain Scan, Renal Function Test, and Glucose Tolerance Test should be given priority. The Liver Function Test depends on findings in the Urinalysis. If an toxins or bacteria or a viral infection is identified in the urine, there is a possibility of a soft Liver of the human body to be damaged as well. There being no fact to support a good reason why, its test should have a lower priority. The main diagnosis should focus more on finding out why very low Potassium was found in the blood sample. The questions to be answered would have to be: (1) Will the system of this patient become normal if her diuretic is withdrawn? This can be proven by just the Urine Test and Blood Sample Test after withdrawal of the diuretic. (2) If yes, what should be the alternative remedy for the patient to prevent hypertension and be able to maintain adequate Potassium as well? If no, given the right supply of Potassium, might there be a tumor or infection of the adenal glands causing them to malfunction by overproducing aldosterone? Is it a cancerous tumor or benign? (3)Is there any evidence of complications following the weeks of maintaining very low Potassium level in the body? What are the findings in the ECG test? What are the findings in the Brain Scan test? What are the findings in the additional Blood Sample Tests, Urine Test? Renal Function Test? Works Cited Ahmed, Nessar; Dawson, Maureen; Smith, Chris; Wood, Ed. Biology Disease. UK: Taylor & Francis Group, 2007. Print Association for Clinical Biochemistry. Adrenal Insufficiency and Addison’s Disease. Lab Test Online-UK. October 25, 2011. Viewed January 14, 2013 @ http://www.labtestsonline.org.uk/understanding/conditions/addisons-disease/ Chew, Sherri L.; Leslie, David; and Leslie,R.D.G. Clinical Endiocrinology and Diabetes: An Illustrated Color Tex, 2nd Edition. China: Elsevier Health Sciences, 2006 Chatterjee, Ranee; Yeh, Hsin-Cheh; Edelman, David; Brancati, Frederick. Potassium and Risk of Type 2 Diabetes. Expert Review of Endocrinology and Metabolism. 2011, Vol. 6 Issue 5. pp. 665-672. Viewed January 17, 2013 @ http://www.medscape.com/viewarticle/750236_3 Daniels, Rick RN, COL, PhD. Manual of Laboratory and Diagnostic Tests, 2nd Edition. USA: Delmar Cengage Learning, 2009. Print Lee, Mary. Basic Skills in Interpreting Laboratory Data, 4th Edition. ASHP, February 2009. Marshall, William J. and Bangert, Stepehn K. Clinical and Biochemistry 2e: Metabolic and Clinical Aspects. USA: Elsevier Health Sciences, 2008. Print Mayo Clinic Staff. Primary Aldosteronism: Causes. MayoClinic.com, 2013. Web. Viewed January 17, 2013 @ http://www.mayoclinic.com/health/primary-aldosteronism/DS00563/DSECTION=causes Mayo Clinic Staff – 2. Symptoms of Primary Aldosteronism. MayoClinic.com, 2013. Web. Viewed January 17, 2013 @ http://www.mayoclinic.com/health/primary-aldosteronism/DS00563/DSECTION=symptoms Mayo Clinic Staff - 3. Glucose Tolerance Test. MayoClinic.com, 2013. Viewed January 20, 2013 @ http://www.mayoclinic.com/health/glucose-tolerance-test/MY00145 Meeking, Darryl. Understanding Diabetes and Endocrinology: A Problem Oriented Approach. UK: Manson Publishing, February 2011. Print. NHS England. Addison’s Disease Diagnosis. National Health Services, Gov.UK 2013. Viewed January 14, 2013 @ http://www.academia-research.com/writer/orders/vieworder/orderid/783601 NKDEP. Explaining Your Kidney Test Results. National Kidney Disease Education Program, Maryland, USA, August 10. 2012. Viewed January 21, 2013 @ http://nkdep.nih.gov/resources/explaining-kidney-test-results.shtml Ramakrishnan, Sankara and Sulochana, K.N.Manual of Medical Laboratory Techniques. India: JP Brothers Medical Publishers Ltd., March 31, 2012 Sherwood. L..Human Physiology: From Cells to Systems. London: West Publishing Co. 2002 Stolzke, Tito. Liver Function Urine Tests. SANANET. Viewed January 17, 2013 @ http://www.liver-products.com/liver-diagnostic/liver-function-urine-tests.html Top 10 Foods Highest in Potassium. Healthaliciousness.com, 2012. Web. Viewed January 15, 2013 @ http://www.healthaliciousness.com/articles/food-sources-of-potassium.php WebMD. Aspartate Aminotransferase. WebMD.com 2013. Viewed January 21, 2013 @ http://www.webmd.com/digestive-disorders/aspartate-aminotransferase-ast?page=2 WHO. Diabetes. World Health Organization, 2012. Viewed January 20, 2013 @ http://www.who.int/mediacentre/factsheets/fs312/en/index.html Read More
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“Glucose Tolerance Test: Results and Analysis Lab Report”. https://studentshare.org/health-sciences-medicine/1792281-medical-biochemistry-practical.
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