British Involvement in Arabic Peninsula Dissertation

British Involvement in Arabic Peninsula - Dissertation Example However, the interest into the Arabic Peninsula is motivated by the beautiful landscape of the place. The terrain and climate of the Peninsula had successfully kept away any adventurers for years. The British contact into the area was just on the individual level and not on governmental level at all (ROGERS, 2006). These individuals were mainly explorers who were visiting the place, and many other places around the world, for adventure. It is through the activity of these explorers that the world came to know about the Arabic peninsula. Some of the outstanding explorers were Charles Doughty and Richard Burton who get the credit for opening up this place to the western world. The peninsula’s location in the Arabic region was the spark to the British interest. For a long time, traffic from between the Orient and Europe used to pass through a corridor which bordered the Sahara on the south-west, and the mountains of turkey and Persia on the north-eastern region. It is along this corridor that the Arabic peninsula stretches. The corridor was, therefore, completely not penetrable. Explorers and people on adventure had to pass around the region by either going through Syria towards the Euphrates and then down to the Gulf, or across the Red Sea through Egypt. Even though Vasco da Gama had discovered the Cape route in the 15th century, the all-sea route was still preferred by many who sought to go around Africa. In the beginning of Britain’s interests in the Middle East, the main objective was commercially motivated. It was in the 17th century that the British government started to show interest in the Arabic Peninsula. During this time, the East India Company opened new offices in locations around the region such as the Red Sea, Basra and the Persian Gulf coast. The company main objective was to seek for new markets in the Middle East region. Although the intention of the British was purely economic at first, it started to take a political perspective towards the end of the 18th century (BALFOUR-PAUL, 1994). During this time, the British had already consolidated the Indian empire and, therefore, cared less about the local trade ventures. Consequently, they turned their interests to the strategic location of the Gulf because it was a major route into India. Because of this, the British administration turned all the offices in the region outside India from trade centers into political and diplomatic hubs. These centers were now used for purposes preservation and protection of the British’s interests in the region. The British notably coined some clever treaties that enabled them to preserve and protect their presence in the region. In these treaties, the British offered to protect the local Arabian rulers from their rivals in return of the Britons dominance in the region. The British, therefore, achieved the command of the Indian Ocean gateways. In this way, they were able to deny any other international powers the ports of the sea. When the British learnt of a Napoleonic entry into Egypt, they sought an agreement with the Sultan of Muscat so that they can prevent the French from expanding their territories towards the Arabic Gulf region. In other measures to protect their interests in the Arabic Peninsula region, the British signed numerous treaties with the surrounding kingdoms. These treaties were aimed at reducing piracy in the Gulf region and to safe guard trade. British have been consistent in fighting off other colonies that posed a threat to the Britons’ supremacy in the Gulf region. Among these are the Egyptians, French and Russians who have posed threat to the Ottoman Empire. The British are much concerned with the interference of the Russians, who have showed increased

The role of the IMF in helping poor and debt-troubled countries Research Paper

The role of the IMF in helping poor and debt-troubled countries - Research Paper Example The IMF is tasked with the role of assisting nations suffice their budgets or invest in areas that positively influence the social welfare or the economy of a country. Most of the support activities that IMF undertakes are backed by global policies. An example is the IMF helps less developed nation to improve health care, education and security which is in line with the United Nations Millennium Development goals. Another reason why the IMF helps poor nation is to stabilize nations in economic and social terms. A debt ridden country has a high probability of social disorder, thus more economic failures (Ghosh, Zalduendo, Thomas, Ramakrishnan, Kim &Joshi 2008). Globalization has ensured that all nations are interlinked economically, thus, failure of an economy to meet its obligations can impact on the global economy, which might lead to a crisis. Despite the fact that the IMF is tasked to issue loans to member countries, there are several conditions that must be met as part of eligibility criteria. First, a country is supposed to design a program that is supposed to address the problem that has made it resort to the IMF for assistance (IMF Factsheet). Before the IMF considers a loan, country must identify the causes of the deficit and the strategies that are in place to mitigate the situation. In deficits situations, the IMF holds that countries should engage in activities that try to resolve the deficit since it affects other economies of the world. Second, the International Monetary Fund should be allowed to assess the programs that are under its support. This is meant to ensure that funds are channeled to the intended functions. Moreover, the process also ensures that the intended benefits are realized. The assessment programs are mostly conducted in less developed nations due to inefficiencies, misappropriation and also embezzlement of funds by few individuals. The institution employs structural benchmarks that are meant to protect IMF interests in the

Sodium, Potassium and Urea Measurement

Sodium, Potassium and Urea Measurement Introduction Electrolytes are solutions that conduct electricity. Any molecule that becomes an ion when mixed with water is an electrolyte. Salts such as sodium, potassium, calcium and chloride are examples of electrolytes. When these molecules dissolve in water, they release ions with an electric charge, positive or negative, that attracts or repels other ions during a chemical reaction. In living cells, most chemical reaction occur in an aqueous environment since approximately 75% of the mass of the living cell is water. Normally 70kg man, represent with 42 litres of total body water that contribute for about 60% of the total body weight. (Marshall, 2000). 66% of this water is in the intracellular fluid (ICF) and 33% in the extracellular fluid (ECF). The principle univalent cations in the ECF and ICF are sodium (Na+) and potassium (K+) respectively. Sodium (Na+) Sodium is the major cation of the extracellular fluid (ECF). It represents almost one-half the osmatic strength of plasma. It plays an important role in maintaining the normal distribution of water and osmatic pressure in the ECF compartment. Sodium levels in the body are regulated ultimately by the kidneys (it excrete excess sodium). The main source of sodium is sodium chloride (NaCl- table salt) which is used in cooking. The daily requirement of the body is about 1 2 mmol/day. Sodium is filtered freely by the glomeruli. About 70 80 % of the filtered sodium load is reabsorbed actively in the proximal tubules (with chloride and water passively) and anther 20 25 % is reabsorbed in the loop of Henle (along with chloride and more water). Normal ECF sodium concentration is 135 145 mmol/L while that of the intracellular fluid (ICF) is only 4-10 mmol/L. sodium is lost via urine, sweat or stool. (Marshall, 2000). Hypernatraemia Hypernatraemia (high sodium levels in the blood) may occurs due to increase sodium intake, decrease excretion, dehydration (water loss) or failure to replace normal water losses. It can also occurs because of excessive mineral corticoid (such as Aldosterone) production acting on renal reabsorption. The clinical features of hypernatraemia are non-specific or masked by underlying conditions. Nausea, vomiting, fever and confusion may occur. A history of long standing polyuria, polydipsia, and theist indicates diabetes insipidus. Hypernatraemia is caused by many diseases such as renal failure, Cushings syndrome or Conns syndrome. Conns syndrome is a disease of the adrenal glands involving excess production of a hormone, called aldosterone. Another name for the condition is primary hyperaldosteronism. Hyponatraemia Hyponatraemia (low sodium levels in the blood) is caused by impaired renal reabsorption of sodium. This occurs in Addisons disease of the adrenal gland due to loss of aldosterone producing zona glomerulosa cortical cells. Sodium decreases in severe sweating in a hot climate or during physical exertion such as marathon running. Falsely low serum sodium concentration may be found in hyperlipidaemic states where the sodium concentration in the aqueous phase of the serum is actually normal, but the lipid contributes to the total volume of serum measured. The symptoms are non-specific and include headache, confusion and restlessness. Hyponatraemia is seen in Addisons disease and/or excessive diuretic therapy. (Kumar Clark, 2002) Potassium (K+) It is the major intracellular cation. It is average concentration in tissue cells is 150mmol/L and in RBCs is 105 mmol/L. The body requirement for K+ is satisfied by a dietary intake. K+ is absorbed by the gastrointestinal tract and distributed rapidly, with a small amount taken up by cells and most excreted by the kidneys. Potassium which filtered by the glomeruli is reabsorbed almost completely in the proximal tubules (PT) and then secreted in the distal tubules (DT) in exchange for sodium under the influence of aldosterone. Factors that regulate distal tubular secretion of potassium include intake of sodium and potassium, water flow rate in distal tubules, plasma level of mineralocorticoids, and acid-base balance. Renal tubular acidosis, as well as metabolic and respiratory acidosis and alkalosis also affect renal regulation of potassium excretion. (Kumar Clark, 2002). Hyperkalaemia Hyperkalaemia is high K+ levels in the blood. Potassium is in high concentration within cells than in extracellular fluids. This means that relatively small changes in plasma concentration can underestimate possibly larger changes in intracellular concentrations. In addition, extensive tissue necrosis can liberate large amounts of potassium into the plasma causing the concentration to reach dangerously high levels. The commonest cause of hyperkalaemia is kidney failure causing decreased urinary potassium excretion. Severe hyperkalaemia (> 6.5 mmol/l) is a serious medical emergency needs treatment as fast as possible because of the risk of developing cardiac arrest. Moderate hyperkalaemia is relatively asymptomatic emphasising the importance of regular biochemical monitoring to avoid sudden fatal complications Hypokalaemia Hypokalaemia (low potassium levels in the blood) has many causes; the most common are diuretic treatment (particularly thiazides), hyperaldosteronism and renal disease. Hypokalaemia is often associated with a metabolic alkalosis due to hydrogen ion shift into the intracellular compartment. Clinically, it presents with paralysis, muscular weakness and cardiac dysrhythmais. (Kumar Clark, 2002) Aldosterone Aldosterone is a steroidal hormone secreted by the adrenal cortex. It is the hormone that regulates the bodys electrolyte balance. This hormone synthesized exclusively in the zona glomerulosa region of the adrenal cortex. This zona contains 18-hydroxysteroid dehydrogenase enzyme which a requisite enzyme for the formation of Aldosterone. Aldosterone acts directly on the kidney tubules to decrease the secretion rate of sodium ion (with accompanying retention of water), and to increase the excretion rate of potassium ion. The secretion of aldosterone is regulated by two mechanisms. First, the concentration of sodium ions secreted may be a factor since increased rates of aldosterone secretion are found when dietary sodium is severely limited. Second, reduced blood flow to the kidney stimulates certain kidney cells to secrete the proteolytic enzyme renin, which converts the inactive angiotensinogen globulin in the blood into angiotensin 1. Another enzyme then converts angiotensin I into a ngiotensin II, its active form. This peptide, in turn, stimulates the secretion of aldosterone by the adrenal cortex. Pathologically elevated aldosterone secretion with concomitant excessive retention of salt and water often results in edema. (Kumar Clark, 2002) Urea is a by-product of protein metabolism that is formed in the liver is formed by the enzymatic deamination of amino acids (urea cycle). The immediate precursor of urea is arginine, which is hydrolyzed to give urea and Ornithine. The urea is excreted by the kidneys and Ornithine in the liver combine with ammonia, formed by the catabolism of amino acids, to regenerate arginine and thereby continue the process of urea formation. The blood urea nitrogen (BUN) test measures the level of urea nitrogen in a sample of the patients blood. In healthy people, most urea nitrogen is filtered out by the kidneys and leaves the body in the urine, because urea contains ammonia, which is toxic to the body. If the patients kidneys are not functioning properly or if the body is using large amounts of protein, the BUN level will rise. If the patient has severe liver disease, the BUN will drop. High levels of BUN may indicate kidney disease or failure; blockage of the urinary tract by a kidney stone or tumour; a heart attack or congestive heart failure; dehydration; fever; shock; or bleeding in the digestive tract. High BUN levels can sometimes occur during late pregnancy or result from eating large amounts of protein-rich foods. A BUN level higher than 100 mg/dl, points to severe kidney damage. (Kumar Clark, 2002) Materials and method Please refer to medical biochemistry practical book (BMS2). Result The equation obtained from the graph used to calculate the Urea concentration of patients is: Y = 0.0238 X Where Y = absorbance X = urea concentration Patient 1 = 0.231/0.0238 = 9.7 mmol/L Patient 2 = 0.149/0.0238 = 6.3 mmol/L Patient 3 = 0.188/0.0238 = 7.89 x 10 = 78.9 mmol/L Patient 4 = 0.376/0.0238 = 7.5 mmol/L Discussion The concentration of sodium and potassium for the four patients was measured by using the flame photometer. For the estimation of urea concentration, a standard calibration curve using different standard concentrations been plotted which used to determine the test samples concentrations. In this practical, the abnormal conditions are varying for each of the patients. Addisons disease is a disorder of the adrenal cortex in which the adrenal glands are under active, resulting in a deficiency of adrenal hormones. Addisons disease can start at any age and affects males and females equally. The adrenal glands are affected by an autoimmune reaction in which the bodys immune system attacks and destroys the adrenal cortex. The glands may also be destroyed by cancer, an infection such as tuberculosis, or another identifiable disease. In infants and children, Addisons disease may be due to a genetic abnormality of the adrenal glands. The majority of the clinical features of adrenal failure are due to lack of glucocorticoid and mineralcorticoid. In Addisons disease cortisol levels are reduced which lead, through feedback, to increase corticotrophin-releasing hormone (CRH) and adrenocorticotrophic hormone (ACTH) production. When the adrenal glands become under active, they tend to produce inadequate amounts of all adrenal hormones. Thus, Addisons disease aff ects the balance of water, sodium, and potassium in the body, as well as the bodys ability to control blood pressure and react to stress. In addition, loss of androgens, such as dehydroepiandrosterone (DHEA), may cause a loss of the body hair in women. A deficiency of aldosterone in particular causes the body to excrete large amount of sodium and potassium, leading to low levels of sodium and high levels of potassium in the blood. The kidneys are not able to concentrate urine, so when a person with Addisons disease drinks too much water or loses too much sodium, the level of sodium in the blood falls. Inability to concentrate urine ultimately causes the person to urinate excessively and become dehydrated. Severe dehydration and low sodium level reduce blood volume and can culminate in shock. Dehydration also causes a high blood urea level. In Addisons disease, the pituitary gland produces more corticotrophin in an attempt to stimulate the adrenal glands. Corticotrophin also stimulat es melanin production, so dark pigmentation of the skin and the lining of the mouth often develop. People with Addisons disease are not able to produce additional corticosteroids when they are stressed. Therefore, they are susceptible to serious symptoms and complications when confronted with illness, extreme fatigue, severe injury, surgery, or possibly severe psychological stress. Secondary adrenal insufficiency is a term given to a disorder that resembles Addisons disease. In this disorder, the adrenal glands are under active because the pituitary gland is not stimulating them, not because the adrenal glands have been destroyed. Blood tests may show low sodium level and high potassium level and usually indicate that the kidneys are not working well. The cortisol level may be low and corticotrophin level may be high. However, the diagnosis is usually confirmed by measuring cortisol level after they have been stimulated with corticotrophin. If cortisol level is low, further tests are needed to determine if problem is Addisons or secondary adrenal insufficiency. Patient-1 has very low sodium 116 mmol/L (135-145 mmol/L), high potassium 6.2 mmol/L (3.6-5.0 mmol/L) and high urea 9.7 mmol/L (3.3-7.5 mmol/L). These abnormal results mostly fit Addisons disease. Sodium been lost in urine in exchange with potassium which causes depletion of Na+ in the blood and increase K+ as both cortisol and aldesterone hormones are absent. Urea level is elevated as a secondary to dehydration and could be due to renal perfusion. ACTH measurement can be used to confirm the diagnosis. Conns syndrome is known as primary aldostronism, is due to the hyper secretion of aldesterone, usually by adenoma of the adrenal cortex or loss often nodular hyperplasia. It characterised by sodium retention and potassium depletion, because plasma renin feed back mechanism is depressed. Under normal conditions aldesterone is regulated by the renin angiotensim mechanism. The principle physiological function of aldesterone is to conserve Na+ . It dose this mainly by facilitating the reabsorption of Na+ and excretion of K+ and H+ in the distal renal tubule. Aldesterone also plays a major role in regulating water and electrolytes balance and blood pressure. The renin-angiotension aldesterone system is the most important controlling mechanism, but ACTH, Na+ and K+ also affect aldesterone secretion. The release of the enzyme renin is stimulated by fall in circulating blood volume or renal perfusion pressure and loss of Na+. The enzyme stimulate the osmoreceptors in the hypothalamus which c auses the release of antidiuretic hormone (ADH) from posterior pituitary gland. ADH targets the kidneys to increase the water reabsorption and causes arterioles to constrict. Renin also acts on its substrate and splits off the inactive decapeptide angiotensim I. Then angiotenism-converting enzyme (ACE), present in lung and plasma, converts angiotensim I to the active angiotensim II which stimulates the release of aldesterone by the adrenal cortex. Aldosterone increases the retention of sodium, chloride ions and water by the kidneys. The laboratory findings include low serum potassium which is a consequence of increased renal potassium excretion, normal or slightly increased sodium in plasma due to increased reabsorption from the renal tubules. Also the renin level will be low and do not rise in response to sodium depletion as they would be in normal persons. In addition, prolonged potassium depletion and hypertension are signs of renal damage. The clinical significance of Coons disease represented with hypertension, muscular weakness and anther neurological manifestation due to loss of K+ which play role in muscles and neurons contraction. Polyuria and thirst secondary to poor renal concentration. Any patient represent hypertension with low potassium concentration should be suspected to have Coons disease. Any patient under diuretic treatment should be monitored overnight as this manifest low potassium. Patient-2 has normal urea level 6.3 mmol/L (3.3-7.5 mmol/L), sodium result is 144 mmol/L, just below the upper limit (135-145 mmol/L) and very low potassium which supports the diagnosis of Coons syndrome. The high aldosterone level in the blood acts on the kidneys to increase the loss of mineral potassium in the urine and facilitate the reabsorption of Na+. Renal failure is the inability of the kidneys to adequately filter metabolic waste products from the blood. Chronic kidney failure is a gradual decline in kidney function which may be explained in terms of a full solute load fall in on a reduced number of functionally normal nephrons. The glomerular filtration rate (GFR) is invariably reduced, associated with retention of urea, creatinine, urate and other organic substances. The kidneys are less able to control the amount and distribution of body water (fluid balance) and the levels of electrolytes (sodium, potassium, calcium, phosphate) in the blood and blood pressure often rise. The kidneys lose their ability to produce sufficient amounts of a hormone (erythropoietin) that stimulates the formation of new red blood cells, resulting in a low red blood cell count (anemia). In children, kidney failure affects the growth of bones. In both children and adults, kidney failure can lead to weaker, abnormal bones. The increased solute load per nephrons impairs the kidneys ability to reduce concentrated urine. As the GFR falls to lower levels retention of Na+ occurs but there is no consistent pattern alteration in plasma Na+ in these cases and in many the results remain normal. Potassium clearance may be increased and raised plasma K+ is uncommon in spite of the tendency for K+ to come out of cells due to the metabolic acidosis that is usually present. However, patients with renal failure are unable to excrete large loads of K+. The level of urea and creatinine will also rise as a result of decreased excretion by the kidneys. Patient-3 has a normal sodium levels 137 mmol/L with a high potassium .8.7 mmol/L and very high urea (78.9 mmol/l) levels which indicates abnormal kidney function. The patient is most probably suffering from chronic renal failure. The numbers of healthy functioning normal nephrons are reduced therefore; there will be a reduction in the execration of urea which will accumulates in the blood. Because of the low GRF, potassium blood levels are increased. The patient must undergo renal dialysis. Diabetic ketoacidosis (DKA) is a common acute complication of insulin-dependent, or type 1 diabetes mellitus (IDDM) due to insulin deficiency which is accompanied by raised plasma concentration of diabetogenic hormones (Adrenaline, Cortisol, Growth hormone and Glucagon ).Before the discovery of insulin in the 1920s, patients rarely survived diabetic ketoacidosis. This complication is still potentially lethal, with an average mortality rate between 5 and 10%. Although the risk of diabetic ketoacidosis is greatest for patients with IDDM, the condition may also occur in patients with non- insulin-dependent diabetes (NIDDM) under stressful conditions, such as during a myocardial infarction. Common symptoms are thirst due to dehydration, polyuria, nausea and weakness that have progressed over several days, which result in coma over the course of several hours. Because of the variable symptoms, diabetic ketoacidosis should be considered in any ill diabetic patient, particularly if the patient presents with nausea and vomiting. Common clinical findings include tachycardia, tachypnea, dehydration, altered mental status and a fruity breath odour, indicating the presence of ketones. Plasma glucose is normally maintained between 4.5 and 8.0mmol/1. Without insulin, most cells cannot use the sugar that is in the blood. Cells still need energy to survive, and they switch to a back-up mechanism to obtain energy. Fat cells begin to break down, producing compounds called ketones. Ketones provide some energy to cells but also make the blood too acidic (ketoacidosis). Since plasma glucose diabetic ketoacidosis exceed the renal threshold; glucose is always present in the urine of patients (glycosuria) with ketoacidosis, the pH of the blood is important in determining the severity of the condition. Blood normally has a pH of 7.35-7.45, maintained by the buffering systems, the most important of which is the bicarbonate buffer system. When acids accumulate in the blood, they dissociate with an increase in hydrogen ion concentration. Bicarbonate can usually neutralise hydrogen ions by incorporating them into water. DKA is associated with electrolyte imbalances; sodium and potassium levels in particular are affected. Serum sodium levels may be low, high or normal. When evaluating the serum sodium level, it is helpful to remember that hyperglycemia causes a shift of free water into the extracellular space, diluting the measured sodium concentration which results in lost of sodium via lie urine as a result of osmotic diuresis. In addition, vomiting, a common feature of ketoacidosis is associated with a loss of sodium from the gastrointestinal tract. This might not always be reflected in the blood results because it is a measure of concentration and, as has already been illustrated, dehydration will be present. Normal plasma sodium levels are maintained between 135 and 145mmol/l, however, despite the actual deficit, patients with DKA might display wide-ranging plasma sodium levels depending on the relative losses of water and sodium. Total body potassium is always depleted in ketoacidosis as potassium is also lost in urine and vomit. The plasma concentration of potassium, however, remains relatively high due to the passage of potassium out of the cells and into the extracellular fluid. One of the mechanisms that normally control the passage of potassium into and out of cells is the sodium/potassium pump. This pump requires intracellular glucose, which is not available in ketoacidosis, consequently, the pump cannot function and potassium leaks out of the cell and into the plasma. Furthermore, potassium is freely exchangeable with hydrogen across the cell membrane. If the hydrogen concentration is high as in DKA, hydrogen will move into the cell in exchange for potassium. So, despite an overall potassium deficit, plasma levels are usually raised in ketoacidosis, at the expense of the body cells. The kidneys can malfunction, resulting in kidney failure that may require dialysis or kidney transplantation. Doctors usu ally check the urine of people with diabetes for abnormally high levels of protein (albumin), which is an early sign of kidney damage. At the earliest sign of kidney complications, the person is often given angiotensin-converting enzyme (ACE) inhibitors, drugs that slow the progression of kidney disease by decreasing blood flow to the kidneys which prevent the kidneys from excreting normal amounts of potassium leads to mild hyperkalaemia. The result obtained for patient-4 corresponding with the clinical findings found in diabetic ketoacidosis. The sodium is reduced (130 mmol/L) and the potassium reading is relatively high (5.8 mmol/L) when compared with the normal reference range. There is a marked increase in urea (15.6 mmol/L) because as mentioned earlier the kidneys can malfunction, resulting in kidney failure that will concentrate fluid in the extracellular compartment. Conclusion Patient 1 is suffering from Addisons disease Patient 2 is suffering from Coons syndrome Patient 3 is suffering from chronic renal failure Patient 4 is suffering from diabetic ketoacidos Questions Calculate the osmolarity (mmol/L) for each patient. Why would patients3s (the diabetic) osmolarity be underestimate? Osmolarity is a property of particles of solute per liter of solution. If a substance can dissociate in solution, it may contribute more than one equivalent to the osmolarity of the solution. The expected osmolarity of plasma can be calculated according to the following formula. Calculated osmolarity (mOsm/kg) = 2*[Na +] + 2*[K+] + (glucose) + (urea) Patient 1 = 2 x 116 + 2 x 6.2 + [glucose] + 9.7 Patient 2 = 2 x 144 + 2 x 2.8 + [glucose] + 6.3 Patient 3 = 2 x 137 + 2 x 8.7 + [glucose] + 78.9 Patient 4 = 2 x 130 + 2 x 5.8 + [glucose] + 15.7 The final result is not obtained as the glucose values are not given, so the calculation can not be done without glucose values. The patient 3 (the diabetic) osmolarity is underestimated because of insulin deficiency, the cells uptake of glucose, which causes hyperglycaemia. What is the abnormality in the clinical condition Diabetes Insipidus, and how does it affect water electrolyte balance? Many different hormones help to control metabolic activities within the body. One of these is called anti-diuretic hormone (ADH) and its function is to help control the balance of water in the body. It does this by regulating the production of urine. ADH is produced by the hypothalamus and then stored in the pituitary gland until it is needed. Diabetes Insipidus usually results from the decreased production of antidiuretic hormone. Alternatively, the disorder may be caused by failure of the pituitary gland to release Antidiuretic hormone into the bloodstream. Other causes of diabetes Insipidus include damage done during surgery on the hypothalamus or pituitary gland; a brain injury, particularly a fracture of the base of the skull; a tumor; sarcoidosis or tuberculosis; an aneurysm (a bulge in the wall of an artery) or blockage in the arteries leading to the brain; some forms of encephalitis or meningitis; and the rare disease Langerhans cell granulomatosis (histiocytosis X). Another type of diabetes Insipidus, nephrogenic diabetes Insipidus, may be caused by abnormalities in the kidneys. Diabetes Insipidus suspected in people who produce large amounts of urine. They first test the urine for sugar to rule out diabetes mellitus. Blood tests show abnormal levels of many electrolytes, including a high level of sodium. The best test is a water deprivation test, in which urine production, blood electrolyte (sodium) levels, and weight are measured regularly for a period of about 12 hours, during which the person is not allowed to drink. A doctor monitors the persons condition throughout the course of the test. At the end of the 12 hours, or sooner if the persons blood pressure falls or heart rate increases or if he loses more than 5% of his body weight, the doctor stops the test and injects Antidiuretic hormone. The diagnosis of central diabetes Insipidus is confirmed if, in response to Antidiuretic hormone, the persons excessive urination stops, the urine becomes mor e concentrated, the blood pressure rises, and the heart beats more normally. The diagnosis of nephrogenic diabetes Insipidus is made if, after the injection, the excessive urination continues, the urine remains dilute, and blood pressure and heart rate do not change. How do diuretics work? And what are the three main groups of diuretics? Diuretics work in the kidneys to increase the elimination of water and electrolytes, thereby causing more urine to form. Because the amount of fluid in the body is lowered, blood pressure goes down, too. Different chemical types work in different areas of the nephrons; so many different classes of diuretics are used. Three of the most common classes of diuretics are: Thiazide and Thiazide-Like Diuretics Drugs containing the chemical Thiazide and similar chemicals like indapamide and metolazone are suggested as the first drugs to try for most people with high blood pressure. They affect the distal convoluted tubule, where large amounts of sodium and water are absorbed back into the body. By blocking the re-absorption process, these drugs force more sodium and more water into the urine to be removed from the body. Thiazides may also relax the muscles in blood vessel walls, making blood flow more easily. Loop Diuretics More powerful than the Thiazide are classes of diuretics that work in the area of the Loop of Henle. These loop diuretics mainly interfere with the bodys re-absorption of chloride, but they also keep sodium from re-entering the blood. Unfortunately, loop diuretics are also more likely to promote the elimination of calcium, magnesium and especially potassium. Shortages of any of these essential electrolytes can cause serious problems such as irregular heartbeats. Potassium-Sparing Diuretics The third common group of diuretics consists of drugs that are much weaker than the Thiazides or the loop diuretics but potassium-sparing diuretics do not reduce potassium levels nearly as much as other kinds of diuretics do. They inhibit aldosterone and/or block sodium reabsorption and inhibit potassium excretion in the distal tubule. Sodium, Potassium and Urea Measurement Sodium, Potassium and Urea Measurement Introduction Electrolytes are solutions that conduct electricity. Any molecule that becomes an ion when mixed with water is an electrolyte. Salts such as sodium, potassium, calcium and chloride are examples of electrolytes. When these molecules dissolve in water, they release ions with an electric charge, positive or negative, that attracts or repels other ions during a chemical reaction. In living cells, most chemical reaction occur in an aqueous environment since approximately 75% of the mass of the living cell is water. Normally 70kg man, represent with 42 litres of total body water that contribute for about 60% of the total body weight. (Marshall, 2000). 66% of this water is in the intracellular fluid (ICF) and 33% in the extracellular fluid (ECF). The principle univalent cations in the ECF and ICF are sodium (Na+) and potassium (K+) respectively. Sodium (Na+) Sodium is the major cation of the extracellular fluid (ECF). It represents almost one-half the osmatic strength of plasma. It plays an important role in maintaining the normal distribution of water and osmatic pressure in the ECF compartment. Sodium levels in the body are regulated ultimately by the kidneys (it excrete excess sodium). The main source of sodium is sodium chloride (NaCl- table salt) which is used in cooking. The daily requirement of the body is about 1 2 mmol/day. Sodium is filtered freely by the glomeruli. About 70 80 % of the filtered sodium load is reabsorbed actively in the proximal tubules (with chloride and water passively) and anther 20 25 % is reabsorbed in the loop of Henle (along with chloride and more water). Normal ECF sodium concentration is 135 145 mmol/L while that of the intracellular fluid (ICF) is only 4-10 mmol/L. sodium is lost via urine, sweat or stool. (Marshall, 2000). Hypernatraemia Hypernatraemia (high sodium levels in the blood) may occurs due to increase sodium intake, decrease excretion, dehydration (water loss) or failure to replace normal water losses. It can also occurs because of excessive mineral corticoid (such as Aldosterone) production acting on renal reabsorption. The clinical features of hypernatraemia are non-specific or masked by underlying conditions. Nausea, vomiting, fever and confusion may occur. A history of long standing polyuria, polydipsia, and theist indicates diabetes insipidus. Hypernatraemia is caused by many diseases such as renal failure, Cushings syndrome or Conns syndrome. Conns syndrome is a disease of the adrenal glands involving excess production of a hormone, called aldosterone. Another name for the condition is primary hyperaldosteronism. Hyponatraemia Hyponatraemia (low sodium levels in the blood) is caused by impaired renal reabsorption of sodium. This occurs in Addisons disease of the adrenal gland due to loss of aldosterone producing zona glomerulosa cortical cells. Sodium decreases in severe sweating in a hot climate or during physical exertion such as marathon running. Falsely low serum sodium concentration may be found in hyperlipidaemic states where the sodium concentration in the aqueous phase of the serum is actually normal, but the lipid contributes to the total volume of serum measured. The symptoms are non-specific and include headache, confusion and restlessness. Hyponatraemia is seen in Addisons disease and/or excessive diuretic therapy. (Kumar Clark, 2002) Potassium (K+) It is the major intracellular cation. It is average concentration in tissue cells is 150mmol/L and in RBCs is 105 mmol/L. The body requirement for K+ is satisfied by a dietary intake. K+ is absorbed by the gastrointestinal tract and distributed rapidly, with a small amount taken up by cells and most excreted by the kidneys. Potassium which filtered by the glomeruli is reabsorbed almost completely in the proximal tubules (PT) and then secreted in the distal tubules (DT) in exchange for sodium under the influence of aldosterone. Factors that regulate distal tubular secretion of potassium include intake of sodium and potassium, water flow rate in distal tubules, plasma level of mineralocorticoids, and acid-base balance. Renal tubular acidosis, as well as metabolic and respiratory acidosis and alkalosis also affect renal regulation of potassium excretion. (Kumar Clark, 2002). Hyperkalaemia Hyperkalaemia is high K+ levels in the blood. Potassium is in high concentration within cells than in extracellular fluids. This means that relatively small changes in plasma concentration can underestimate possibly larger changes in intracellular concentrations. In addition, extensive tissue necrosis can liberate large amounts of potassium into the plasma causing the concentration to reach dangerously high levels. The commonest cause of hyperkalaemia is kidney failure causing decreased urinary potassium excretion. Severe hyperkalaemia (> 6.5 mmol/l) is a serious medical emergency needs treatment as fast as possible because of the risk of developing cardiac arrest. Moderate hyperkalaemia is relatively asymptomatic emphasising the importance of regular biochemical monitoring to avoid sudden fatal complications Hypokalaemia Hypokalaemia (low potassium levels in the blood) has many causes; the most common are diuretic treatment (particularly thiazides), hyperaldosteronism and renal disease. Hypokalaemia is often associated with a metabolic alkalosis due to hydrogen ion shift into the intracellular compartment. Clinically, it presents with paralysis, muscular weakness and cardiac dysrhythmais. (Kumar Clark, 2002) Aldosterone Aldosterone is a steroidal hormone secreted by the adrenal cortex. It is the hormone that regulates the bodys electrolyte balance. This hormone synthesized exclusively in the zona glomerulosa region of the adrenal cortex. This zona contains 18-hydroxysteroid dehydrogenase enzyme which a requisite enzyme for the formation of Aldosterone. Aldosterone acts directly on the kidney tubules to decrease the secretion rate of sodium ion (with accompanying retention of water), and to increase the excretion rate of potassium ion. The secretion of aldosterone is regulated by two mechanisms. First, the concentration of sodium ions secreted may be a factor since increased rates of aldosterone secretion are found when dietary sodium is severely limited. Second, reduced blood flow to the kidney stimulates certain kidney cells to secrete the proteolytic enzyme renin, which converts the inactive angiotensinogen globulin in the blood into angiotensin 1. Another enzyme then converts angiotensin I into a ngiotensin II, its active form. This peptide, in turn, stimulates the secretion of aldosterone by the adrenal cortex. Pathologically elevated aldosterone secretion with concomitant excessive retention of salt and water often results in edema. (Kumar Clark, 2002) Urea is a by-product of protein metabolism that is formed in the liver is formed by the enzymatic deamination of amino acids (urea cycle). The immediate precursor of urea is arginine, which is hydrolyzed to give urea and Ornithine. The urea is excreted by the kidneys and Ornithine in the liver combine with ammonia, formed by the catabolism of amino acids, to regenerate arginine and thereby continue the process of urea formation. The blood urea nitrogen (BUN) test measures the level of urea nitrogen in a sample of the patients blood. In healthy people, most urea nitrogen is filtered out by the kidneys and leaves the body in the urine, because urea contains ammonia, which is toxic to the body. If the patients kidneys are not functioning properly or if the body is using large amounts of protein, the BUN level will rise. If the patient has severe liver disease, the BUN will drop. High levels of BUN may indicate kidney disease or failure; blockage of the urinary tract by a kidney stone or tumour; a heart attack or congestive heart failure; dehydration; fever; shock; or bleeding in the digestive tract. High BUN levels can sometimes occur during late pregnancy or result from eating large amounts of protein-rich foods. A BUN level higher than 100 mg/dl, points to severe kidney damage. (Kumar Clark, 2002) Materials and method Please refer to medical biochemistry practical book (BMS2). Result The equation obtained from the graph used to calculate the Urea concentration of patients is: Y = 0.0238 X Where Y = absorbance X = urea concentration Patient 1 = 0.231/0.0238 = 9.7 mmol/L Patient 2 = 0.149/0.0238 = 6.3 mmol/L Patient 3 = 0.188/0.0238 = 7.89 x 10 = 78.9 mmol/L Patient 4 = 0.376/0.0238 = 7.5 mmol/L Discussion The concentration of sodium and potassium for the four patients was measured by using the flame photometer. For the estimation of urea concentration, a standard calibration curve using different standard concentrations been plotted which used to determine the test samples concentrations. In this practical, the abnormal conditions are varying for each of the patients. Addisons disease is a disorder of the adrenal cortex in which the adrenal glands are under active, resulting in a deficiency of adrenal hormones. Addisons disease can start at any age and affects males and females equally. The adrenal glands are affected by an autoimmune reaction in which the bodys immune system attacks and destroys the adrenal cortex. The glands may also be destroyed by cancer, an infection such as tuberculosis, or another identifiable disease. In infants and children, Addisons disease may be due to a genetic abnormality of the adrenal glands. The majority of the clinical features of adrenal failure are due to lack of glucocorticoid and mineralcorticoid. In Addisons disease cortisol levels are reduced which lead, through feedback, to increase corticotrophin-releasing hormone (CRH) and adrenocorticotrophic hormone (ACTH) production. When the adrenal glands become under active, they tend to produce inadequate amounts of all adrenal hormones. Thus, Addisons disease aff ects the balance of water, sodium, and potassium in the body, as well as the bodys ability to control blood pressure and react to stress. In addition, loss of androgens, such as dehydroepiandrosterone (DHEA), may cause a loss of the body hair in women. A deficiency of aldosterone in particular causes the body to excrete large amount of sodium and potassium, leading to low levels of sodium and high levels of potassium in the blood. The kidneys are not able to concentrate urine, so when a person with Addisons disease drinks too much water or loses too much sodium, the level of sodium in the blood falls. Inability to concentrate urine ultimately causes the person to urinate excessively and become dehydrated. Severe dehydration and low sodium level reduce blood volume and can culminate in shock. Dehydration also causes a high blood urea level. In Addisons disease, the pituitary gland produces more corticotrophin in an attempt to stimulate the adrenal glands. Corticotrophin also stimulat es melanin production, so dark pigmentation of the skin and the lining of the mouth often develop. People with Addisons disease are not able to produce additional corticosteroids when they are stressed. Therefore, they are susceptible to serious symptoms and complications when confronted with illness, extreme fatigue, severe injury, surgery, or possibly severe psychological stress. Secondary adrenal insufficiency is a term given to a disorder that resembles Addisons disease. In this disorder, the adrenal glands are under active because the pituitary gland is not stimulating them, not because the adrenal glands have been destroyed. Blood tests may show low sodium level and high potassium level and usually indicate that the kidneys are not working well. The cortisol level may be low and corticotrophin level may be high. However, the diagnosis is usually confirmed by measuring cortisol level after they have been stimulated with corticotrophin. If cortisol level is low, further tests are needed to determine if problem is Addisons or secondary adrenal insufficiency. Patient-1 has very low sodium 116 mmol/L (135-145 mmol/L), high potassium 6.2 mmol/L (3.6-5.0 mmol/L) and high urea 9.7 mmol/L (3.3-7.5 mmol/L). These abnormal results mostly fit Addisons disease. Sodium been lost in urine in exchange with potassium which causes depletion of Na+ in the blood and increase K+ as both cortisol and aldesterone hormones are absent. Urea level is elevated as a secondary to dehydration and could be due to renal perfusion. ACTH measurement can be used to confirm the diagnosis. Conns syndrome is known as primary aldostronism, is due to the hyper secretion of aldesterone, usually by adenoma of the adrenal cortex or loss often nodular hyperplasia. It characterised by sodium retention and potassium depletion, because plasma renin feed back mechanism is depressed. Under normal conditions aldesterone is regulated by the renin angiotensim mechanism. The principle physiological function of aldesterone is to conserve Na+ . It dose this mainly by facilitating the reabsorption of Na+ and excretion of K+ and H+ in the distal renal tubule. Aldesterone also plays a major role in regulating water and electrolytes balance and blood pressure. The renin-angiotension aldesterone system is the most important controlling mechanism, but ACTH, Na+ and K+ also affect aldesterone secretion. The release of the enzyme renin is stimulated by fall in circulating blood volume or renal perfusion pressure and loss of Na+. The enzyme stimulate the osmoreceptors in the hypothalamus which c auses the release of antidiuretic hormone (ADH) from posterior pituitary gland. ADH targets the kidneys to increase the water reabsorption and causes arterioles to constrict. Renin also acts on its substrate and splits off the inactive decapeptide angiotensim I. Then angiotenism-converting enzyme (ACE), present in lung and plasma, converts angiotensim I to the active angiotensim II which stimulates the release of aldesterone by the adrenal cortex. Aldosterone increases the retention of sodium, chloride ions and water by the kidneys. The laboratory findings include low serum potassium which is a consequence of increased renal potassium excretion, normal or slightly increased sodium in plasma due to increased reabsorption from the renal tubules. Also the renin level will be low and do not rise in response to sodium depletion as they would be in normal persons. In addition, prolonged potassium depletion and hypertension are signs of renal damage. The clinical significance of Coons disease represented with hypertension, muscular weakness and anther neurological manifestation due to loss of K+ which play role in muscles and neurons contraction. Polyuria and thirst secondary to poor renal concentration. Any patient represent hypertension with low potassium concentration should be suspected to have Coons disease. Any patient under diuretic treatment should be monitored overnight as this manifest low potassium. Patient-2 has normal urea level 6.3 mmol/L (3.3-7.5 mmol/L), sodium result is 144 mmol/L, just below the upper limit (135-145 mmol/L) and very low potassium which supports the diagnosis of Coons syndrome. The high aldosterone level in the blood acts on the kidneys to increase the loss of mineral potassium in the urine and facilitate the reabsorption of Na+. Renal failure is the inability of the kidneys to adequately filter metabolic waste products from the blood. Chronic kidney failure is a gradual decline in kidney function which may be explained in terms of a full solute load fall in on a reduced number of functionally normal nephrons. The glomerular filtration rate (GFR) is invariably reduced, associated with retention of urea, creatinine, urate and other organic substances. The kidneys are less able to control the amount and distribution of body water (fluid balance) and the levels of electrolytes (sodium, potassium, calcium, phosphate) in the blood and blood pressure often rise. The kidneys lose their ability to produce sufficient amounts of a hormone (erythropoietin) that stimulates the formation of new red blood cells, resulting in a low red blood cell count (anemia). In children, kidney failure affects the growth of bones. In both children and adults, kidney failure can lead to weaker, abnormal bones. The increased solute load per nephrons impairs the kidneys ability to reduce concentrated urine. As the GFR falls to lower levels retention of Na+ occurs but there is no consistent pattern alteration in plasma Na+ in these cases and in many the results remain normal. Potassium clearance may be increased and raised plasma K+ is uncommon in spite of the tendency for K+ to come out of cells due to the metabolic acidosis that is usually present. However, patients with renal failure are unable to excrete large loads of K+. The level of urea and creatinine will also rise as a result of decreased excretion by the kidneys. Patient-3 has a normal sodium levels 137 mmol/L with a high potassium .8.7 mmol/L and very high urea (78.9 mmol/l) levels which indicates abnormal kidney function. The patient is most probably suffering from chronic renal failure. The numbers of healthy functioning normal nephrons are reduced therefore; there will be a reduction in the execration of urea which will accumulates in the blood. Because of the low GRF, potassium blood levels are increased. The patient must undergo renal dialysis. Diabetic ketoacidosis (DKA) is a common acute complication of insulin-dependent, or type 1 diabetes mellitus (IDDM) due to insulin deficiency which is accompanied by raised plasma concentration of diabetogenic hormones (Adrenaline, Cortisol, Growth hormone and Glucagon ).Before the discovery of insulin in the 1920s, patients rarely survived diabetic ketoacidosis. This complication is still potentially lethal, with an average mortality rate between 5 and 10%. Although the risk of diabetic ketoacidosis is greatest for patients with IDDM, the condition may also occur in patients with non- insulin-dependent diabetes (NIDDM) under stressful conditions, such as during a myocardial infarction. Common symptoms are thirst due to dehydration, polyuria, nausea and weakness that have progressed over several days, which result in coma over the course of several hours. Because of the variable symptoms, diabetic ketoacidosis should be considered in any ill diabetic patient, particularly if the patient presents with nausea and vomiting. Common clinical findings include tachycardia, tachypnea, dehydration, altered mental status and a fruity breath odour, indicating the presence of ketones. Plasma glucose is normally maintained between 4.5 and 8.0mmol/1. Without insulin, most cells cannot use the sugar that is in the blood. Cells still need energy to survive, and they switch to a back-up mechanism to obtain energy. Fat cells begin to break down, producing compounds called ketones. Ketones provide some energy to cells but also make the blood too acidic (ketoacidosis). Since plasma glucose diabetic ketoacidosis exceed the renal threshold; glucose is always present in the urine of patients (glycosuria) with ketoacidosis, the pH of the blood is important in determining the severity of the condition. Blood normally has a pH of 7.35-7.45, maintained by the buffering systems, the most important of which is the bicarbonate buffer system. When acids accumulate in the blood, they dissociate with an increase in hydrogen ion concentration. Bicarbonate can usually neutralise hydrogen ions by incorporating them into water. DKA is associated with electrolyte imbalances; sodium and potassium levels in particular are affected. Serum sodium levels may be low, high or normal. When evaluating the serum sodium level, it is helpful to remember that hyperglycemia causes a shift of free water into the extracellular space, diluting the measured sodium concentration which results in lost of sodium via lie urine as a result of osmotic diuresis. In addition, vomiting, a common feature of ketoacidosis is associated with a loss of sodium from the gastrointestinal tract. This might not always be reflected in the blood results because it is a measure of concentration and, as has already been illustrated, dehydration will be present. Normal plasma sodium levels are maintained between 135 and 145mmol/l, however, despite the actual deficit, patients with DKA might display wide-ranging plasma sodium levels depending on the relative losses of water and sodium. Total body potassium is always depleted in ketoacidosis as potassium is also lost in urine and vomit. The plasma concentration of potassium, however, remains relatively high due to the passage of potassium out of the cells and into the extracellular fluid. One of the mechanisms that normally control the passage of potassium into and out of cells is the sodium/potassium pump. This pump requires intracellular glucose, which is not available in ketoacidosis, consequently, the pump cannot function and potassium leaks out of the cell and into the plasma. Furthermore, potassium is freely exchangeable with hydrogen across the cell membrane. If the hydrogen concentration is high as in DKA, hydrogen will move into the cell in exchange for potassium. So, despite an overall potassium deficit, plasma levels are usually raised in ketoacidosis, at the expense of the body cells. The kidneys can malfunction, resulting in kidney failure that may require dialysis or kidney transplantation. Doctors usu ally check the urine of people with diabetes for abnormally high levels of protein (albumin), which is an early sign of kidney damage. At the earliest sign of kidney complications, the person is often given angiotensin-converting enzyme (ACE) inhibitors, drugs that slow the progression of kidney disease by decreasing blood flow to the kidneys which prevent the kidneys from excreting normal amounts of potassium leads to mild hyperkalaemia. The result obtained for patient-4 corresponding with the clinical findings found in diabetic ketoacidosis. The sodium is reduced (130 mmol/L) and the potassium reading is relatively high (5.8 mmol/L) when compared with the normal reference range. There is a marked increase in urea (15.6 mmol/L) because as mentioned earlier the kidneys can malfunction, resulting in kidney failure that will concentrate fluid in the extracellular compartment. Conclusion Patient 1 is suffering from Addisons disease Patient 2 is suffering from Coons syndrome Patient 3 is suffering from chronic renal failure Patient 4 is suffering from diabetic ketoacidos Questions Calculate the osmolarity (mmol/L) for each patient. Why would patients3s (the diabetic) osmolarity be underestimate? Osmolarity is a property of particles of solute per liter of solution. If a substance can dissociate in solution, it may contribute more than one equivalent to the osmolarity of the solution. The expected osmolarity of plasma can be calculated according to the following formula. Calculated osmolarity (mOsm/kg) = 2*[Na +] + 2*[K+] + (glucose) + (urea) Patient 1 = 2 x 116 + 2 x 6.2 + [glucose] + 9.7 Patient 2 = 2 x 144 + 2 x 2.8 + [glucose] + 6.3 Patient 3 = 2 x 137 + 2 x 8.7 + [glucose] + 78.9 Patient 4 = 2 x 130 + 2 x 5.8 + [glucose] + 15.7 The final result is not obtained as the glucose values are not given, so the calculation can not be done without glucose values. The patient 3 (the diabetic) osmolarity is underestimated because of insulin deficiency, the cells uptake of glucose, which causes hyperglycaemia. What is the abnormality in the clinical condition Diabetes Insipidus, and how does it affect water electrolyte balance? Many different hormones help to control metabolic activities within the body. One of these is called anti-diuretic hormone (ADH) and its function is to help control the balance of water in the body. It does this by regulating the production of urine. ADH is produced by the hypothalamus and then stored in the pituitary gland until it is needed. Diabetes Insipidus usually results from the decreased production of antidiuretic hormone. Alternatively, the disorder may be caused by failure of the pituitary gland to release Antidiuretic hormone into the bloodstream. Other causes of diabetes Insipidus include damage done during surgery on the hypothalamus or pituitary gland; a brain injury, particularly a fracture of the base of the skull; a tumor; sarcoidosis or tuberculosis; an aneurysm (a bulge in the wall of an artery) or blockage in the arteries leading to the brain; some forms of encephalitis or meningitis; and the rare disease Langerhans cell granulomatosis (histiocytosis X). Another type of diabetes Insipidus, nephrogenic diabetes Insipidus, may be caused by abnormalities in the kidneys. Diabetes Insipidus suspected in people who produce large amounts of urine. They first test the urine for sugar to rule out diabetes mellitus. Blood tests show abnormal levels of many electrolytes, including a high level of sodium. The best test is a water deprivation test, in which urine production, blood electrolyte (sodium) levels, and weight are measured regularly for a period of about 12 hours, during which the person is not allowed to drink. A doctor monitors the persons condition throughout the course of the test. At the end of the 12 hours, or sooner if the persons blood pressure falls or heart rate increases or if he loses more than 5% of his body weight, the doctor stops the test and injects Antidiuretic hormone. The diagnosis of central diabetes Insipidus is confirmed if, in response to Antidiuretic hormone, the persons excessive urination stops, the urine becomes mor e concentrated, the blood pressure rises, and the heart beats more normally. The diagnosis of nephrogenic diabetes Insipidus is made if, after the injection, the excessive urination continues, the urine remains dilute, and blood pressure and heart rate do not change. How do diuretics work? And what are the three main groups of diuretics? Diuretics work in the kidneys to increase the elimination of water and electrolytes, thereby causing more urine to form. Because the amount of fluid in the body is lowered, blood pressure goes down, too. Different chemical types work in different areas of the nephrons; so many different classes of diuretics are used. Three of the most common classes of diuretics are: Thiazide and Thiazide-Like Diuretics Drugs containing the chemical Thiazide and similar chemicals like indapamide and metolazone are suggested as the first drugs to try for most people with high blood pressure. They affect the distal convoluted tubule, where large amounts of sodium and water are absorbed back into the body. By blocking the re-absorption process, these drugs force more sodium and more water into the urine to be removed from the body. Thiazides may also relax the muscles in blood vessel walls, making blood flow more easily. Loop Diuretics More powerful than the Thiazide are classes of diuretics that work in the area of the Loop of Henle. These loop diuretics mainly interfere with the bodys re-absorption of chloride, but they also keep sodium from re-entering the blood. Unfortunately, loop diuretics are also more likely to promote the elimination of calcium, magnesium and especially potassium. Shortages of any of these essential electrolytes can cause serious problems such as irregular heartbeats. Potassium-Sparing Diuretics The third common group of diuretics consists of drugs that are much weaker than the Thiazides or the loop diuretics but potassium-sparing diuretics do not reduce potassium levels nearly as much as other kinds of diuretics do. They inhibit aldosterone and/or block sodium reabsorption and inhibit potassium excretion in the distal tubule.

A College Writing Course in the 21st Century :: Writing Writers Education School Essays

A College Writing Course in the 21st Century Throughout the 21 century the basis of a college writing course was to make people become the best writers they can possibly be according to the colleges standards. The whole idea and purpose was to make everyone use the same techniques and formats in order to answer and write essays. Although this was a very good idea but the minority of the writers weren't as fortunate because they had their own way of expressing their thoughts which was very sufficient but it never met the colleges' standards therefore they weren't able to become what they wanted to because of their different format and use of the English language. The basis of college is pretty much to prepare us for the future and make us aware of the upcoming challenges which we are going to be faced with everyday of our lives as we go on into the world on our own. But what I actually began to realize as the years went on is that schools these days are focusing and narrowing every individual to use only a certain format in orde r to write and read even though there are many individuals out there that are very talented in the English language its just that they were never given a chance to show their writing skills but instead they were always taught to do it one way and not their own. In Amy Tan's reading I noticed an interesting experience which she had mentioned from her past which pointed out an interesting argument "I started writing nonfiction as a freelancer the week after I was told by my former boss that writing was my worst skill and I should hone my talents toward account management" (Tan 4). There it seems even though Tan loved writing it wasn't her best skill therefore the instructor directed her toward another field which she could succeed although she loved to write. From that point I could see that many college courses today try and point you toward what your good at but not what you like therefore it has to be you that makes that first step forward because if you really believe in yourself then do what ever it takes to meet your goal just like Tan accomplished. Whenever your judged by a professor in school its only an opinion coming from their own point, its how they see your skills through their own eyes and not how they see your skills through y our own eyes.

Finance Internship Report

Internship / Project Title: Revenue Operations Specialist Internship / Project Progress: I worked in a Saas-based company as a revenue operation specialist. My main responsibilities were to work closely with the CFO with weekly cash flow analysis and to apply cash, book journal entries and created A/R aging reports in Net Suite and GP. Also, I completed monthly GL account reconciliations and revenue waterfalls and prepared SOX filing, such as sales order and journal entry samples.Furthermore, I worked closely with account executives in managing over 350 customers, generating invoices and processing payments in Quickbooks and Xero. When my company transferred system, I migrated over 5 GB of system data using Pivot Table and Vlookup and created novel collection metrics and invoice billing charts on daily basis. Besides, I helped AP team to verified over 100 weekly expense reports for employee expense reimbursements and assisted with accounting logs and billing/revenue close process.I a lso supported in preparation of financial statements and management reporting and managed billing schedules for revenue recognition This position helps me understand how a finance department runs in the daily work. Also, I built many skills relevant to accounting in the software industry, such as revenue recognition, account receivables and VSOE. I summarized what I learnt and contributed for my company below.Revenue and Budgeting: Assisted financial team to reached $29 million quarterly revenue target in ahead of one month; Managed P&L, aged receivables, income statement, bank reconciliation reports and journal entry for monthly revenue reconciliation; Handled revenue waterfall month end closures in an accurate and timely manner, finishing a week before official due date and exceeding manager expectation. Maintained the budgeting model by the development and improvement of budgeting process to decrease 10% cost on delivery rates and advertisement occupancy.Account Management: Engag ed professionally with sales personnel to manage over 350 customer master files in QuickBooks and 300 customers in Xeros and to implement leads generations in Salesforce. com CRM; Built and developed customer relationships to enhance performance in the bank and generated 10% in portfolio revenue. Data Management: Posted daily cash applications and journal entries in various accounts in Net Suite, kept track of over checking and money market accounts simultaneously and maintained onsistently 100% accuracy; Reconstructed over 5 GB of system data using vlookup and combination formulas in Excel, handled software compatibility issues, input and output parsing, saved company over 30 hours in automating the manual migration of data. Overall, what I learn from class in ITU is well applied to my job. For instance, in Financial Accounting class, we learnt the knowledge about three important financial statements, which I used and reviewed in my job.

Kindness and security Essay

At the end of scene IX, a woman comes outside selling flowers for the dead. This brings back her memories of Belle Reve, but she talks of them out loud as if she is reliving them at that moment. This shows that these memories still haunt her. At the beginning of scene X, Blanche has been drinking for hours after Mitch left. She has been packing and drinking, and is now in the soiled dress. She is still trying to forget what has happened by drinking. She is also talking to herself about a fun time, either in the past or in her head. She is trying to escape the present and go into the past by using alcohol. â€Å"Tremblingly she lifts up the hand mirror for a closer inspection. She catches her breath and slams the mirror face down with such violence that the glass cracks†. This shows that she forgets that it is now the present and she is angry that she is no longer who she was and does not look like who she was. Later in scene X, she tells Stanley about what happened with Mitch, but then she says that he returned with roses to say sorry, and then she told him to go. This is what she would have liked to happen, and maybe she doesn’t realise that it isn’t reality. Earlier in the play she had said; â€Å"I don’t want realism†¦ I want magic. † She also says that she had got a telegram from Shep Huntleigh inviting her on a cruise. Once Stanley tells her this is not true, she sees a ‘grotesque and menacing form’ in the shadow on the wall. This shows that she is not able to cope with the harsh reality, so she makes it up and believes it. In scene X, Blanche is raped by Stanley. After he tells her that he knows about her past, Blanche starts to see strange reflections on the wall and hear weird noises. This shows that her past is directly linked to her seeing things, and also with her fear of her past and Stanley’s dominance over her. It also shows that she cannot cope with her past. In scene XI, it shows Blanche cross fully into madness. She believes that the Doctor coming for her is Shep Huntleigh. When the matron turns up to take her, she lashes out and becomes violent, which she would never have done before as she would have wanted to be seen in a good light. Lastly, when the doctor shows her some kindness, she follows him quietly, as all she wants is kindness and security, even if it is from a stranger.

The Origin of Our Solar System

The Origin of Our Solar System One of the most-asked questions of astronomers is: how did our Sun and planets get here? Its a good question and one that researchers are answering as they explore the solar system. There has been no shortage of theories about the birth of the planets over the years. This is not surprising considering that for centuries the Earth was believed to be the center of the entire universe, not to mention our solar system. Naturally, this led to a misevaluation of our origins. Some early theories suggested that the planets were spat out of the Sun and solidified. Others, less scientific, suggested that some deity simply created the solar system out of nothing in just a few days.  The truth, however, is far more exciting and is still a story being filled out with observational data.   As our understanding of our place in the galaxy has grown, we have re-evaluated the question of our beginnings. But in order to identify the true origin of the solar system, we must first identify the conditions that such a theory would have to meet. Properties of Our Solar System Any convincing theory of the origins of our solar system should be able to adequately explain the various properties therein. The primary conditions that must be explained include: The placement of the Sun at the center of the solar system.The procession of the planets around the Sun in a counterclockwise direction (as viewed from above the north pole of Earth).The placement of the small rocky worlds (the terrestrial planets) nearest to the Sun, with the large gas giants (the Jovian planets) further out.The fact that all the planets appear to have formed around the same time as the Sun.The chemical composition of the Sun and planets.The existence of comets and asteroids. Identifying a Theory The only theory to date that meets all of the requirements stated above is known as the solar nebula theory. This suggests that the solar system arrived at its current form after collapsing from a molecular gas cloud some 4.568 billion years ago. In essence, a large molecular gas cloud, several light-years in diameter, was disturbed by a nearby event: either a supernova explosion or a passing star creating a gravitational disturbance. This event caused regions of the cloud to begin clumping together, with the center part of the nebula, being the densest, collapsing into a singular object. Containing more than 99.9% of the mass, this object began its journey to star-hood by first becoming a protostar. Specifically, it is believed that it belonged to a class of stars known as T Tauri stars. These pre-stars are characterized by surrounding gas clouds containing pre-planetary matter with most of the mass contained in the star itself. The rest of the matter out in the surrounding disk supplied the fundamental building blocks for the planets, asteroids, and comets that would eventually form. About 50 million years after the initial shock wave instigated the collapse, the core of the central star became hot enough to ignite nuclear fusion. The fusion supplied enough heat and pressure that it balanced out the mass and gravity of the outer layers. At that point, the infant star was in  hydrostatic equilibrium, and the object was officially a star, our Sun. In the region surrounding the newborn star, small, hot globs of material collided together to form larger and larger worldlets called planetesimals. Eventually, they became large enough and had enough self-gravity to assume spherical shapes.   As they grew larger and larger, these planetesimals formed planets. The inner worlds remained rocky as the strong solar wind from the new star swept much of the nebular gas out to colder regions, where it was captured by the emerging Jovian planets. Today, some remnants of those planetesimals remain, some as Trojan asteroids that orbit along the same path of a planet or moon. Eventually, this accretion of matter through collisions slowed down. The newly formed collection of planets assumed stable orbits, and some of them migrated out toward the outer solar system.   Does the Solar Nebula Theory Apply to Other Systems? Planetary scientists have spent years developing a theory that matched the observational data for our solar system. The balance of temperature and mass in the inner solar system explains the arrangement of worlds that we see. The action of planet formation also affects how planets settle into their final orbits, and how worlds are built and then modified by ongoing collisions and bombardment. However, as we observe other solar systems, we find that their structures vary wildly. The presence of large gas giants near their central star doesnt agree with the solar nebula theory. It probably means that there are some more dynamical actions scientists havent accounted for in the theory.   Some think that the structure of our solar system is the one that is unique, containing a much more rigid structure than others. Ultimately this means that perhaps the evolution of solar systems is not as strictly defined as we once believed.

When Do SAT Subject Test Scores Come Out

When Do SAT Subject Test Scores Come Out SAT / ACT Prep Online Guides and Tips After you take the SAT Subject Tests, you probably want to find out your results right away. You'll have to be a little patient, though, as you might need to wait between two and six weeks to get your SAT Subject Test scores. We've compiled the exact score delivery dates below. We also offer tips on how to track down your scores and what to do after you get them. Read on to find out just when you'll get your SAT Subject Test scores. SAT Subject Test Score Release Dates 2019-2020 After some delays in score delivery in recent years, the College Board now promises online score delivery within three weeks for most SAT and SAT Subject Test dates. Additionally, any colleges you designate as score recipients should get your SAT scores within 10 days after you get your own score report. As you can see, delivery dates (to both students and their selected schools) can range from two weeks to more than five weeks (for June score deliveries). In the chart below, you'll find windows for score release dates for the rest of the 2018-2019 Subject Test dates: Test Date Online and Paper Score Delivery Date Scores Sent to Colleges By May 4, 2019 May 17, 2019 May 27, 2019 June 1, 2019 July 10, 2019 July 20, 2019 Source: The College Board And here are our estimated dates for the 2019-2020 Subject Test dates: Test Date Online and Paper Score Delivery Date Scores Sent to Colleges By Aug 24, 2019 Sept 6, 2019 Sept 16, 2019 Oct 5, 2019 Oct 18, 2019 Oct 28, 2019 Nov 2, 2019 Nov 15, 2019 Nov 25, 2019 Dec 7, 2019 Dec 20, 2019 Dec 30, 2019 May 2, 2020 May 15, 2020 May 25, 2020 June 6, 2020 July 15, 2020 July 25, 2020 Source: The College Board The College Board delivers paper score reports at the same time SAT Subject Test scores become available online; however, they're not explicit about when exactly colleges will get SAT Subject Test scores, only promising that colleges should get them within 10 days after students get their own score reports. At least you know exactly when you can get your scores online, though. Read on for a step-by-step explanation of how to access your SAT Subject Test scores on the dates above. Disappointed with your scores? Want to improve your SAT score by 160 points? We've written a guide about the top 5 strategies you must be using to have a shot at improving your score. Download it for free now: Raise Your SAT Score by 160 Points(Free Download) How to Get Your SAT Subject Test Scores Internet score delivery for SAT Subject Tests should take place around 8 am Eastern Time (5 am Pacific Time). According to students, the scores sometimes appear a few hours earlier. To get your scores, log on to your College Board account and go to "My Test Scores." Once there, you'll see your scores from any and all SAT Subject Tests you've taken. You'll need your username and password to be able to log in and view your scores. If you don't remember one or both of these, go through the steps to recover this info with the email associated with your account. If you need to recover your username and/or password, try to do so before score release day. It wouldn't be any fun to go through this rigmarole as your scores wait in your account, just out of reach! According to the dates above, your paper score report should be delivered to you around the same time they come out online. You can also get your Subject Test scores over the phone by calling 866-756-7346 (domestic) or 212-713-7789 (international). This service costs $15 per call, so you'll need to have a credit card on hand. Now that you know when to expect your SAT Subject Test scores and how to access them, is there anything else to keep in mind about the Subject Tests? How to Schedule Your SAT Subject Tests Since you now know when you'll get your SAT Subject Test scores, you should design your testing schedule with these dates in mind, especially when it comes to college application deadlines. At present, the College Board does not commit to having scores to colleges by specific dates, only stating when they'll start to deliver them. Therefore, I suggest giving yourself at least a week of leeway between your score release date and your application deadline. It's possible that colleges will be more lenient because of past score release delays, but I wouldn't risk it or risk getting stressed out about it. You want to leave enough time for colleges to get your scores. You might also leave extra time to retake a Subject Test or two if you end up being disappointed with your scores. Remember that all the SAT Subject Tests are multiple choice and your answer sheets are scored by a machine. Make sure to keep them neat and not make any stray marks or doodles, as the machine won't be able to tell the difference between a real answer and a stray mark. As long as you schedule your SAT Subject Tests with enough time for colleges to receive your score reports, you'll be all set- you just have to wait out the weeks until you get your scores! What to Do After You Get Your SAT Subject Test Scores You've gotten your SAT Subject Test scores. Now what? Do you focus on SAT/ACT prep? Apply to college? Or just totally forget about your scores? Here's a step-by-step guide on what to do after you see your SAT Subject Test scores. Step 1: Determine How Good Your Scores Are First, it's important to check that your Subject Test scores are up to par (or even better than) the average Subject Test scores at the schools you're applying to. This lets you see whether you're on track to being a competitive applicant or whether you need to work a little harder on presenting yourself as an ideal candidate to schools. To find the average SAT Subject Test score for a college, search for "[School Name] SAT Subject Test scores" or "[School Name] average SAT Subject Test scores" on Google. Look for links to the school's official website and click the one that's most relevant. A good score will be one that's equal to or higher than the school's average. Unfortunately, not all schools list average SAT Subject Scores. If you're having trouble finding your school's average or recommended SAT Subject Test scores, try comparing your scores with official Subject Test averages and percentiles. This will tell you how many test takers you scored higher than on a Subject Test. Step 2: Decide Whether to Submit Your Scores to Schools Now that you have an idea of how well you did on your Subject Tests, it's time to decide whether you want to submit your scores to schools. (Note that if you elected to use the College Board's four free score reports when you registered for the tests, your scores will be automatically sent to the schools you chose before you can know what your scores actually are.) If a school requires Subject Test scores and you're only going to take the tests once, go ahead and submit your scores, even if they weren't as high as you hoped they'd be. You don't really have much of a choice here since not submitting them means your application will be disqualified! On the other hand, if Subject Test scores are completely optional, only submit your scores if they're higher than the averages at the school. If you got a low score, it's better to not submit it since all it'll do is bring down the quality of your application. (By contrast, if you submit no scores, this won't have any effect on your application.) If your school strongly recommends SAT Subject Test scores, it's best to send them in. That said, if you scored poorly on a test, you can choose to not send in that score and instead opt to retake the test at a later point (if you can do so before your college applications are due, that is). Check out our guide for a list of all SAT Subject Test dates. Step 3: Start Working On Your College Applications If you decided to submit your Subject Test scores to your schools, congrats! Now, it's time to start buckling down on your college applications. You'll want to present yourself in the best possible light, so make sure to write a great personal statement, submit strong letters of recommendation, and get involved in extracurricular activities you're interested in. If you decided to retake a Subject Test, you'll want to balance your time wisely by studying for the test and getting a jumpstart on your college applications. I suggest making a study schedule so you can pace yourself and space out the things you'll need to prepare for your college applications. What's Next? Have you chosen the dates you'll take your SAT Subject Tests on? Check out our article for the best dates to take the tests, and get tips on how to balance them with the general SAT or ACT. Are you also taking the SAT? Make sure you know all the steps to getting and sending your SAT scores, and figure out how high of an SAT score you should aim for. If you're taking the ACT, learn how to get and send your ACT scores and what ACT score you should aim for. Want to get a perfect SAT or ACT score? Read our guides to learn how you can score a perfect 1600 on the SAT or a full 36 on the ACT. Need a little extra help prepping for your Subject Tests? We have the industry's leading SAT Subject Test prep programs (for all non-language Subject Tests). Built by Harvard grads and SAT Subject Test full or 99th %ile scorers, the program learns your strengths and weaknesses through advanced statistics, then customizes your prep program to you so that you get the most effective prep possible. Learn more about our Subject Test products below:

Case study of demonstrating learning in practice

Case study of demonstrating learning in practice The purpose of this assignment is to provide evidence that will demonstrate my learning in practice. It will contain four reflective accounts that will display my ability to meet the learning outcomes of this module. Amulya (no date) describes reflection as a process of exploring your own actions and experiences, and further states that the purpose of reflection is to develop learning. Johns (2004), expands on this and describes different layers of reflection, for example reflection in action. This type of reflection occurs at the time of experience, pausing to make sense of the situation and proceeding to a desired conclusion. I will be reflecting on experiences, which is defined by Johns (2004 p 50) as â€Å"learning through experiences†, thus changing perceptions of myself, practice and gaining new insights. Benner (2001) supports learning from experience and states that through experiences it enables the nurse to move from, competent to proficient, further stating that th e proficient nurse will be able to hone in on the most important problems. These learning outcomes will be addressed in turn, discussing what I have learned and highlighting areas for future development. Further evidence can be viewed in Section 2, Appendix’s 1 to four and Section 3; these documents are my learning contracts from the placement I completed. Learning outcome 1 is to recognise and explain the inter-related nature of aetiology, pathophysiology and clinical features of named conditions that cause health care problems. The appropriate evidence based management required and the anticipated outcomes. Campbell (2006) states an understanding of physiology and pathophysiology is deemed necessary in the understanding of treatment and the management of patients, thus improving patient care. Dunning (2003) supports this view and says the nurses understanding of pathophysiology and classification of the disease process such as diabetes improves the care they provide. This i s a reflective account, of an episode of care, which I was involved in. My patient had been admitted for ketoacidosis. Diabetes UK (no date) describes ketoacidosis as acidity of the blood caused by excessive amounts of ketones. Johnson (2004) expands on this and states it occurs from the lack of glucose entering the cell which is used as energy. As a result the body then uses its own store of fat as an alternative for energy and this use of energy produces an acid known as ketones. Dunning (2003) describes clinical features as hyperglycaemia, which is a result of decreased use of glucose by the cells and the increased glucose produced by the liver; dehydration and electrolyte loss resulting from polyuria and lastly acidosis is due to the breakdown of fatty acids and production of ketones. They go on to say that symptoms include, increased thirst, this is the bodies attempt to flush out the ketones; fatigue, abdominal pain, kussmauls breathing and tachycardia. As the ketones rise the person may also start to vomit, however vomiting reduces the urine output thus reducing the flushing out of ketones. As a result a coma will develop and this if left untreated can be fatal. Diabetes National Service Framework: Standard (2002) states treatment for ketoasidosis , consists of the administration of insulin, potassium and fluids. Brunner & Suddarths (2004) says fluids are given intravenously to manage dehydration, insulin would be given as a 5 unit bolus every hour, however the amount of insulin to be administered is calculated by the amount of glucose detected in the blood. This is what is referred to as an insulin sliding scale, the set amounts are shown on the insulin recording documentation. Potassium is also given to manage the electrolyte loss.

Planning Document Research Paper Example | Topics and Well Written Essays - 1500 words

Planning Document - Research Paper Example The plans established during project planning stage will aid the manager to save time, resources, quality, challenges, transformations and other issues. Additionally, it helps the manager to manage team, members of staff and outside stakeholders to ensure project timely project deliverance and within schedule. Introduction Experts agree that project-planning stage is mainly the most problematic stage for human resource managers because they need to produce skilled staff, adequate resources and tools required to complete the project. They may also require organizing and communicating the plan, project scope, procurement activities and work breakdown structures for the success of the program. This paper explains my project charter for benefit and compensation package revamping, communication plan, the scope of the project and the work breakdown structure for my compensation and benefit package as a new appointed human resource manager in charge of small teams. Discussion Project Charte r for Project Benefit and Compensation Package Revamping As a new human resource head appointee and now responsible for a small team management, I have a critical role ahead. The next project based on this new task is to revamp the benefit and employee compensation package that workers are receiving at the organization. Workforce benefits and compensation are intensively crucial and significant aspects in the process of new hire approval and workforce retention. Similarly, it is my responsibility to revamp, build and provide a valuable benefit and compensation products, that motivate and retain the most crucial and experienced workforce while making them accepted, proud and approved by the company members. The primary goal and purpose of workforce compensation is to offer effective and equal benefits to workforce at a level, which align their expertise, capabilities and contributions to the organization. Compensation is the role of human resource management, which handles all forms of rewards that people receive for their better performance – such as nonfinancial and economic benefits. My financial benefits plan will entail direct rewards like salary, time off pays, wages, any form of bonus and increases on merit basis as well as other plans for profit sharing. Indirect rewards like workforce benefits, (Armstrong & Cummins, 2011). Additionally, nonfinancial benefits involve anything in workstation, which promotes workforce’s self-esteem and self-respect sense by others. Therefore, as a new human resource manager, I will design packages for compensation and benefits for the entire workforce and perspective new recruits. I will design and implement the team’s expectations to prevent miscommunication concerning employees’ requirements. The project charter will include a policy concerning the number of work hours, overtime, time compensation and time off payments (such as Holidays, emergency leaves and personal holidays). In addition, t he least or base grades of salary will be based on position or title of the job, job description, job qualification and educational qualification will be established to determined workforce salary. A compensation plan is what motivates long-term workforce that is rewarded without evaluating their jobs or establishing an entitlement sense. Therefore, as a new human resource leader, I will have to provide this material to higher management and right stakeholders for the project approval. The aim is to indicate where the dollars that workforce spends on after taxation by

Motivation Essay Example | Topics and Well Written Essays - 500 words - 9

Motivation - Essay Example Like other doctorate students, I joined the Walden University to pursue a doctorate in Business Administration-Healthcare Management. After my undergraduate studies, I thought that I had obtained all the knowledge that I needed to survive in the real world. However, I later realized that a single degree was not sufficient for me to handle the emerging and dynamic challenges of life. I realized that there were many concepts that were unfamiliar to me, and my desire for continued physical and intellectual stimulation was still hot in my mind. Further, there was a strong need to push myself beyond the limits by breaking through the challenges of doctorate education, and strengthen my coping capacities because education can become frustrating at times. According to Mujtaba et al. (2006), the comprehensive dissertation process and the complex exams are the climax of doctorate degrees. They consume a substantial amount of a student’s time and resources before successful completion. Doctorate studies increase the job potential of an individual  by orienting a student to research of high education, and business language and vocabularies (Mujtaba et al., 2006). Business administration course is a comprehensive field, which has many vocabularies and conceptual language that only experts can understand. Healthcare management is another complex field that requires people who are highly trained and competent professionals to run the activities in this field. My chief motivation for pursuing a doctorate in this field was the increasing demand for effective management of healthcare resources. This will ensure that citizens of this nation receive high quality health services, which will facilitate a decrease in the number of deaths caused by poor management. During the course of my study, I expect to gain sufficient insights into administrative concept like strategic planning, strategic production, distribution and

Political science. Palestine and Orientalism Essay

Political science. Palestine and Orientalism - Essay Example In his study Said blended political polemic and literary excursion. He writes: "The Orient is not only adjacent to Europe; it is also the place of Europe's greatest and richest and oldest colonies, the source of its civilizations and languages, its cultural contestant, and one of its deepest and most recurring images of the Other" (Said, 1979, pp.1-2) Said claims that Orientalism is an academic area which causes interest in a variety of academic institutions, because all teachers, sooner or later begin to research Orient and apply their knowledge in the areas of their competence. Said holds that since the end of eighteenth century the scholarly and academic meanings of Orientalism have been quite 'politically correct' and the related efforts have been restricted. Furthermore, Said believes that Orientalism reflects Western style of domination and is close-knit with Western mind, usually related to perceiving Orient as a 'younger brother' or 'poorer kin'. Said holds that the antagonistic political relationship between the Sast and the West lies in the earliest development the struggle between Islam and Christianity. According to Said, Orientalism, which presents Christian world as 'higher', is used as a demonstration of European power and is seen as a comparative theory, in which two eternal rivals - the East and the West - make an 'argument' with predicted conclusion which is to sum up that European beliefs and culture are more humanistic and more suitable and more appropriate for harmonious development of an individual. Similarly to other '-isms', Orientalism has been ill-treated from the ancient times up to the present. From the other angle of view, Orientalism is a natural movement, whose toughness is quite sufficient in its universal authenticity. This movement is a product of synergy, which takes place among different studies, accumulated by different followers, who are interested in one of the richest world cultures, and Oriental culture. Moreover, Said's study has itself caused a number of responses, either positive or negative.Lewis attempted to criticize Said's approach -in particular, in his article ' The question of Orientalism', which defended Middle Eastern studies, and in particular, Palestinian studies. On the other hand, Lewis was a newcomer to the United States, and his refutation - a forceful defense of the European and Palestinian traditions (which sometimes converts into an attack) - did not canceled Said's complaints about the problems and complications of American Middle Eastern studies. Lewis, for instance, writes that, in fact, Europe hasn't yet experienced (or probably, hasn't noticed) such considerable influence of Orientalism on its tradition. Lewis's main notes were following: 1) Firstly, it would be wrong to claim that Oriental studies are limited to the study of Muslim culture, while in fact Biblical research is an essential and substantial element or Orientalism. Palestine as the country of diverse religions supports both religious doctrines, so it needs more profound inquiry than Said has done. 2) Secondly, there is no doubt that an identifiable part of Western studies was stimulated by either political or religious propaganda "and appeared throughout the ages with distorted images of Islam, the East and its cultures; however, this movement cannot be termed "Orientalism", rather it is "False Orientalism" (Lewis, 1982,

Film research paper Example | Topics and Well Written Essays - 250 words

Film - Research Paper Example â€Å"Last Indie Standing: The Special Case of Lions Gate in the New Millennium.† Both Schamus and Perren define vertical integration with respect to independent cinema and in support of the thesis that the primary purpose of vertical integration is not to gain greater artistic control, but to ensure continued growth of revenues, although Schamus adapts a pessimistic tone by showing that vertical integration is an impossible feat for indie films by explaining the processes, money, and people involved in producing, marketing, and distributing independent films, while Perren uses a more positive tone in discussing the vertical integration success of Lions Gate by adapting to changing and numerous content demands and characteristics of niche markets. The economics of film business affects independent cinema, according to both Schamus and Perren, which affect their definitions of vertical integration. Schamus defines vertical integration in the context of independent cinema, which is still embedded in the mainstream film industry, where money-making goals remain supreme. On the one hand, indie films are supposed to be no-budget and focus on artistic, sometimes even social and political goals. On the other hand, Schamus keeps it real by underscoring that indie films are also subjected to the â€Å"poetics of late capitalism† (91). He integrates the definition of vertical integration by explaining the details of the capitalist system that drives the film industry. Like Schamus, Perren also explores the meaning of vertical integration for independent studios through their rise in the film industry. She examines how indie film studios survived the twenty-first century, when many other studios have become bankrupt or have been acquired by other larger or equally large competitors by mentioning several examples of studio success and failures. The impact of her examples is to show that not all indie studios benefit from vertical integration, and some were even financially

Innovation at apple Coursework Example | Topics and Well Written Essays - 2000 words - 1

Innovation at apple - Coursework Example We chose a different path. Our belief was that if we kept putting great products in front of customers, they would continue to open their wallets† Steve Jobs 1. Introduction: Several companies today are caught up in a relentless pursuit of innovation and intentional development of novel ideas, products and services in a bid to capture the imagination of their target consumers. The role of innovation in organizational development and its contribution in organizational success have been amply substantiated in literature, over the years. Organizational ambidexterity has emerged as one of the most influential concepts in recent times whereby highly creative and innovation driven organizations have proven their might in the market by not only sustaining their competitive advantage over their rival firms, but by leading the industry as well. Apple Inc. is one such example which has managed to successfully evade the competition by constant innovation and research and capturing a relat ively larger market share through sheer creativity. The above quote aptly mirrors the collective sentiment at Apple Inc. This essay aims to discuss, analyze, and examine the case of Apple Inc., through various theoretical perspectives and models in a bid to explain the role and influence of technological innovation in organizational development. 2. ... eir initial phase strive to survive in the market by designing their policies in accordance with the present market environment and adapt to their surrounding environment (Hart and Christensen, 2002). This theory helps in assessing and evaluating the various aspects of firm behaviour with regard to technological change and the resultant scope of the firm to survive in a new market (Loasby, 1976; Casson, 2005). Apple was founded by Steve Jobs and Ronald Wayne on April 1, 1976 which was mainly focused on designing a personal computer that was popularly known and sold as Apple I. After the incorporation of Apple as a company in the year 1977 the company grew and shifted its strategy to innovation and creativity as the key drivers to sustain the market competition. This strategy helped Apple Inc in introducing highly innovative products in the market based on latest state-of-the-art technologies that helped them differentiate their products from that of their rivals. (Innovation at Apple , p. 1). The theories of entrepreneurship developed over the years indicate judgemental decision making as a key aspect of entrepreneurial behaviour (Shane, 2003). This theory entails that entrepreneurs at times may differ greatly in terms of their strategies by displaying attitudes that exhibit a high degree of optimism which in turn is based on the critical information available at their disposal as well as their conviction to deliver positive outcomes (Casson, 2005). Steve Jobs inspired the culture of innovation at Apple Inc. and created a highly favourable working environment whereby employees were constantly encouraged to come up with innovative and creative ideas. The key focus of the management was to hire people who displayed high level of motivation and commitment towards the