Australia Pestle Essays

Australia Pestle Essays Australia Pestle Essay Australia Pestle Essay Australia and Fosters Well to begin with Australia, worldâ„ ¢s smallest continent ¦came into worlâ„ ¢d view in 1901 when the six colonies federated and became the Commonwealth of Australia. Political Environment Type of Government system:- The form of government used in Australia is a Constitutional Monarchy â€Å" Constitutionalâ„ ¢ because the powers and procedures of the Commonwealth Government are defined by a written constitution, and Monarchyâ„ ¢ because Australiaâ„ ¢s Head of State is Queen Elizabeth II. In Australia rule making powers are distributed between the Commonwealth, six States and two Territories: New South Wales, (NSW) Victoria, Queensland, Western Australia, South Australia, Tasmania, the Australian Capital Territory (ACT) and Northern Territory (see map â€Å" Norfolk Island Territory has also been given some local rule making powers by the national government) (Australiaâ„ ¢s government system is a liberal democratic one a political system that has free elections, a multiplicity of political parties, political decisions made through an independent legislature, and an independent judiciary, with a state monopoly on law enforcement , in short a system working in the interest of the citizens.) Control structure of Australia:- The Australian government structure is quite centralized as major areas such as taxation, defence, foreign affairs, postal and telecommunications services are managed by the federal government while rest of the matters such as police, hospitals, education and public transport are taken care of by the state and local government. Benefit of centralization Things run more smoothly and decisions take less time. There is strong power centrally located so problems are just altogether swiftly executed. Centralized government means that one body makes all the important decisions for the nation or state, and handles all responsibiliites, it is best for smaller nations that dont have much territory to control, therefore must keep everything tight and concentrated. POLITICAL PARTIES:- Three political parties dominate the center of the Australian political spectrum. 1) The Liberal Party (LP), nominally representing urban business interests, and its smaller coalition partner. 2) The Nationals, nominally representing rural interests, are the more conservative parties. 3) The Australian Labor Party nominally represents workers, trade unions, and left-of-center groups. Julia Gillard Prime Minister of Australia â€Å" Member of which party What is that partyâ„ ¢s morals and how it would impact the country Economic Environment For Australia, the terms of trade are at their highest level since the early 1950s, and national income is growing strongly as a result. In the household sector thus far, there continues to be a degree of caution in spending and borrowing, which has led to a noticeable increase in the saving rate. Asset values have generally been little changed over recent months and overall credit growth remains quite subdued, notwithstanding evidence of some greater willingness to lend. Employment growth has been very strong over the past year, though some leading indicators suggest a more moderate pace of expansion in the period ahead. After the significant decline last year, growth in wages has picked up somewhat, as had been expected. Some further increase is likely over the coming year. From 1980â„ ¢s many structural reforms were witnessed which transformed Australia from a conservative, highly protected and regulated market place to an open, internationally competitive, export-oriented economy. Since the 1980s, Australia has undertaken significant structural reform of its economy and has transformed itself from an inward-looking, highly protected, and regulated marketplace to an open, internationally competitive, export-oriented economy. Many economic reforms were undertaken resulting in economic liberalization for the country. They were:- 1) Unilaterally reducing high tariffs and other protective barriers to free trade 2) Floating the Australian Dollar The advantages of floating rates include automatic stabilisation of the exchange rate. Floating rates offer greater flexibility of trade Will have to take explanation on the concept of Floating currency 3) Deregulating the financial services sector including liberalizing access for foreign banks 4) Reforming the taxation system including introducing a broad based Goods and Services Tax (GST) and large reductions in income tax rates. Australia is a mixed economy, with major state-owned enterprises in communications, transport, banking, energy generation and health services, as well as privately owned enterprises in the same areas. In common with capitalist economies such as the UK and New Zealand, Australian governments are reducing these activities by privatizing state-operated businesses. (Australias economy is dominated by its services sector, yet its economic success is based on abundance of agricultural and mineral resources. Australias comparative advantage in the export of primary products is a reflection of the natural wealth of the Australian continent and its small domestic market. (ENVIRONMENTAL BACKGROUND POINT) Social Environment Australia has a diverse culture and lifestyle. It reflects liberal democratic traditions and values. This diverse culture is because of millions of migrants who are settled in Australia from a long time. When people migrate to new place they spread their culture and knowledge also. Australia is a unique blend of different traditions and cultures. Australiaâ„ ¢s original inhabitants were the Aboriginal and Torres Strait Islander peoples; they have been living in Australia for at least 60,000 years. The rest of the Australia has migrants or descendants of migrants who have arrived in Australia from all across the globe. In the year 1945, Australiaâ„ ¢s population was around 7 million, but today it is more than 21 million people. These migrants have enriched Australian culture; it has influenced traditional customs, lifestyle, education system, culture and arts. It has turned society in many ways creating a broader outlook. The defining feature of Australia is not only its diversity but it is the extent to which they are united despite of differences in culture. Australian laws allow everyone to express their culture and customs. Over the years the rate at which the GDP of Australia has improved, GPI i.e. Genuine Progress Indicator reflected a minimal growth. So what is the catch in this point This indicates that higher economic growth and social growth didnâ„ ¢t go hand in hand. Its high economic growth did not have much impact on the welfare and quality of life of Australians. An overview if Australia definitely gives a nice view with higher standard of living and longer life expectancies however this is true for certain groups in Australian society. While searching for the details I was looking for some positive notes but came across this data which changes the mindset and gives a totally different view of Social envt of Australia. There are still certain groups in Australian society under the burden of unemployment, poverty, homelessness and inadequate housing, education and health. Socio-demographic change is an important factor underpinning many of the trends and issues analysed in the following pages. Australiaâ„ ¢s population is ageing, increasingly mobile, more and more reliant on overseas migration for population growth as fertility rates decline, and organised in increasingly diverse ways with a fall in overall household size and growth in diverse family and household formations. Immigration Australia has one of the highest immigration rates of all developed countries, and has sustained high immigration for most of the past 60 years Traditionally, Australia has relied on immigration to sustain economic growth For most industries, population growth means market growth, and some industries, particularly the residential construction industry, have a very strong interest in high immigration levels. Even the government finds immigration attractive it helps keep the population young, thus maintaining a high proportion of tax-paying working Australians and a comparatively lower number of older Australians drawing pensions and health care benefits. AGEING POPULATION An aging population can have a significant impact on society in Australia. In one of the sources it was mentioned that by the year 2027, there will be a marked increase in the number of Australians over sixty four years of age. Another cause of Australiaâ„ ¢s aging population is improved life expectancies. The first positive economic effect on the Australian economy will be economic growth and expansion. As older generations tendency to save more in the form of investments in financial sector will act as an injection into the economy causing the economy to expand. The second positive economic effect on the Australian economy will be increased government spending which will lead to economic growth It is important to take into account the negative effects that an aging population could give rise to. Which is nothing but an indication of rise in unemployment a negative sign for any economy. Australias population, like that of most developed countries, is ageing as a result of sustained low fertility and increasing life expectancy. This is resulting in proportionally fewer children (under 15 years of age) in the population. Over the next several decades, population ageing is projected to have significant implications for Australia, including for health, labour force participation, housing and demand for skilled labour. Technological Environment Research and development Australiaâ„ ¢s strong business performance in recent years has been underpinned by a record of innovation and a longstanding commitment to research and development (RD), aimed at increasing productivity, building new markets and boosting international competitiveness. The Australian Government supports RD through direct funding as well as providing significant tax concessions to encourage private sector investment. RD priority areas include information and communications technology (ICT), biotechnology, manufacturing, mining and the food industry. Technology greatly impacts on farming in Australia. Scientific and technical advances have helped to make Australian farmers some of the worlds leaders in efficiency and productivity. As previously said, Australiaâ„ ¢s economy is dominated by the Service sector. And this is visible through the Information and communications technology The telecommunications sector in Australia has undergone a significant transformation in the past decade ¦ The Internet and e-commerce have boosted the international competitiveness of Australian businesses. Many Australian firms are now using internet technology to expand into new foreign markets. Important research is also being conducted by the Australian Government-funded Commonwealth Scientific and Industrial Research Organisation (CSIRO) ICT Centre. This research focuses on innovation that creates a competitive advantage for Australia and leads to globally adopted solutions. Australia is today well connected, both domestically and internationally, with a modern fibre-optic backbone, satellite coverage and an extensive mobile network. Over the past two decades, Australia has failed to build significant positions in the technological revolution that has transformed the global economy. In high-tech industries such as software and electronics Australia has been left behind, and in emerging sectors such as biotechnology, it threatens to be. There is no intrinsic reason for Australias poor innovation performance. Australia is not less entrepreneurial than other developed countries or less scientifically creative. We have the human and financial resources. The challenge is to ensure policy settings provide the right incentives to encourage and develop frontier technologies such as biotechnology and nanotechnology, as well as ensuring the diffusion and upgrading of new technologies within established industries. The CEDA report contains analysis of Australias recent innovation performance by a group of leading innovation experts. Key findings include: Australia has failed to develop financial and organisational vehicles capable of managing the inherently risky nature of investment in technological innovation, which is characterized by far greater levels of risk than routine production. In no successful economy is innovation risk managed by markets alone. Nations that have established sets of institutions to achieve risk-sharing have succeeded in innovating in complex and uncertain fields such as software, electronics and the life sciences. Those that havent developed such national systems of innovation have failed to build those industries. In almost no country other than Australia does the stock market attempt to finance innovation in its early phases. If Australia wishes to participate in technology creation (as opposed to simply consuming technology) appropriate risk management vehicles need to be developed. Policy attention has tended to focus on science-based industries with high levels of direct RD and strong links to universities (such as computing, electronics, pharmaceuticals and biotechnology). While these high-tech industries are very important and can potentially act as transforming platforms, they are also very small (accounting for only 3 per cent of GDP in most OECD economies). The role of low and medium technology industries tends to be neglected. This is a serious failing. These industries (such as food processing, timber products, textiles, wine, mechanical engineering and services such as transport and health) are intensive users of RD and scientific knowledge. Economic growth is based not just on the creation of new sectors but on the internal transformation of sectors that already exist-that is, on continuous technological upgrading. Potential growth trajectories may rest as much on sectors such as engineering, food, wine and vehicles as on radically new sectors such as ICT or biotechnology. Australia has a conservative innovation system that is only slowly generating new paths of technological accumulation. The majority of innovation is incremental, involving improvements in products, processes and methods and is based on knowledge sourced from overseas. Despite a decade of strong economic growth, many standard indicators of innovation have been failing. While Australia has high levels of technological specialization in mining and agriculture and patenting in biotechnology and pharmaceuticals has grown rapidly over the past decade, we have one of the lowest levels of change in technological specialization among OECD countries. Australia has not seen the emergence of any major new sector such as telecommunications in Finland and Sweden, oil in Norway, semiconductors in Korea and Taiwan and motor vehicles in Germany. The report argues that an effective national innovation system plays a central role in enhancing competitive capability. If current weaknesses in Australias innovation track record are not addressed, our future economic development will be seriously impeded. Legal close regulation of key economic sectors, he Australian economy will have to increasingly address environmental and Aboriginal issues. Environmental damage caused by mining and agriculture, especially, have come under frequent media attack. Current issues include soil erosion caused by overgrazing, urbanization, and poor farming practices; increases in soil salinity largely due to farming practices; depletion of fresh water supplies, again largely due to farming and urbanization; and coastal damage, especially around the Great Barrier Reef on the Queensland coast, caused by shipping and extensive tourism. Mining impacts on the environment, such as the release of toxic substances, tend to be more localized. Mining and agricultural enterprises are becoming more responsive to environmental issues, but there is still room for improvement. Envt emergence of a green economy in Australia Energy industries have emerged as the greatest emitter of green houses gases in Australia. LEGAL/REGULTORY FACTORS Australia, the member of OECD escaped the Global financial crisis. OECD mentioned that Australiaâ„ ¢s strong regulatory frameworks and sound policies have helped Australia weather the global crisis better than the other OECD countries. The monetary and fiscal policy played a key role in supporting the Australian economy MONETARY policy The Reserve Bank of Australia is responsible for formulating and implementing monetary policy. Since the early 1990s, inflation targeting has been the main objective of Australias monetary policy framework as controlling inflation preserves the value of money. The current inflation rate is 2.80% and the RBA has set policy to achieve an inflation rate of 2-3 per cent on average. The inflation target is achieved through periodic adjustments to the Central Bank interest rate target i.e. the interbank rate (cash rate) at which the banks lend to each other overnight for cash flow purposes. To control inflation, the interest rate plays a significant role ¦.if interest rate is high, the aggregate demand tends to lower thus stabilizing the prices. In 2010, there was constant rise in the interest rate and the now the current interest rate has been maintained at 4.75% The rate of inflation tends to increase when the overall demand for goods and services exceeds the economys capacity to sustainably supply goods and services. Hence To help avoid the country falling in recession, the Australian central bank cut interest rates to a 45-year low of 3.25% in February. FISCAL POLICY Fiscal policy uses two actions:-Taxation and Government spending to steer the economy. Taxation

Understanding a Mystery in Different Types of Writing

Understanding a Mystery in Different Types of Writing A mystery purveys the element of shock and awe. We explore hidden paths or explore the unknown until we discover the truth. A mystery is usually presented in the form of a novel or a short story, but it could also be a non-fiction book that explores uncertain or illusory facts. Murders in the Rue Morgue Edgar Allan Poe (1809-1849) is usually recognized as the father of the modern mystery. Murder and suspense are evident in fiction before Poe, but it was with Poes works that we see the emphasis on using clues to get to the facts. Poes Murders in the Rue Morgue (1841) and The Purloined Letter are among his famous detective stories. Benito Cereno Herman Melville first serially published Benito Cereno in 1855, and then republished it with five other works in The Piazza Tales the next year. The mystery in Melvilles tale starts with the appearance of a ship in sad repair. Captain Delano boards the ship to offer assistanceonly to find mysterious circumstances, which he cant explain. He fears for his life: am I to be murdered here at the ends of the earth, on board a haunted pirate ship by a horrible Spaniard?Too nonsensical to think of! For his tale, Melville borrowed heavily from an account of the Tryal, where slaves overpowered their Spanish masters and tried to force the captain to return them to Africa. The Woman in White With The Woman in White (1860), Wilkie Collins adds the element of sensationalism to the mystery. The discovery by Collins of a young and very beautiful young woman dressed in flowing white robes that shone in the moonlight inspired this story. In the novel, Walter Hartright encounters a woman in white. The novel involves crime, poison, and kidnapping. A famous quote from the book is: This is a story of what a womans patience can endure, and what a mans resolution can achieve. Sherlock Holmes Sir Arthur Conan Doyle (1859-1930) wrote his first story at the age of six, and published his first Sherlock Holmes novel, A Study in Scarlet, in 1887. Here, we learn how Sherlock Holmes lives, and what has brought him together with Dr. Watson. In his development of the Sherlock Holmes, Doyle was influenced by Melvilles Benito Cereno and by Edgar Allan Poe. The novels and short stories about Sherlock Holmes became enormously popular, and the stories were collected into five books. Through these stories, Doyles depiction of Sherlock Holmes is amazingly consistent: the brilliant detective encounters a mystery, which he must solve. By 1920, Doyle was the most highly paid writer in the world. The successes of these early mysteries helped to make mysteries a popular genre for writers. Other great works include G.K. Chestertons The Innocence of Father Brown (1911), Dashiell Hammetts The Maltese Falcon (1930), and   Agatha Christies Murder on the Orient Express (1934). To learn more about the classic mysteries, read a few of the mysteries of Doyle, Poe, Collins, Chesterton, Christie, Hammett, and the like. Youll learn about the drama, the intrigue, along with the sensational crimes, kidnappings, passions, curiosities, mistaken identities, and puzzles. Its all there on the written page. All of the mysteries are designed to baffle until you discover the hidden truth. And, you may come to understand what really happened!

EU Law Case Studies Study Example | Topics and Well Written Essays - 2000 words

EU Law Studies - Case Study Example Astrid, Klaus's wife, had every right to apply for a job as an estate agent. The fact that Astrid was discriminated against because she did not pass a Spanish language test in Spain-although she had completed and passed a similar test in Germany-is illegal because member EU states must treat other EU member citizens equally.4 The fact that Klaus did not receive the same company pension entitlement as Spanish nationals who also worked as his company is a blatant form of discrimination against Klaus as a German national living in Spain, again because EU members are supposed to receive the same social benefits of domestic members.5 Another social benefit6 Klaus should have received based on the fact that he is an EU members was his five extra holidays, just as his Spanish national counterparts.7 Similarly, in Astrid's case, she was discriminated against by not being able to receive the same social advantage8 of receiving free banking as her Spanish national counterparts who worked at the bank as well. Sophie was discriminated against on the basis of nationality9 due to the fact that, at college, only students in her course who had lived in Spain for at least ten years could claim a special financial payment to cover the enrollment fee. This is because Sophie had only been in Spain for a few months. Still, however, this was a discriminatory practice. Additionally, since Heinrich wanted to apply for a student maintenance grant but was told that it was only available to Spanish nationals, this is another form of discrimination based on nationality.10 Klaus and Heinrich, respectively-had prior convictions in Germany for handling stolen motor vehicles and dealing illegal drugs-can argue that they were trying to start a new life in Spain but were discriminated against in their pursuits of operating legally in the country of Spain. Klaus could not receive social security benefits or the same company pension as the other workers at his job who were Spanish nationals. Heinrich needed a grant to go to school. Based on these exclusion from receiving the proper compensation and remuneration, which is a legal right of EU member citizens,11 it could be argued in court that Klaus reverted to an illegal venture in order to make ends meet. Similarly, the same argument could be made of Astrid-that she was forced into a bank job by virtue of discrimination12 as a German national and was forced to resort to illegal methods to help ensure her family's well-being in Spain. Freedom of establishment13 in another member EU country is a right guaranteed to individuals who are EU citizens. In court, it could be argued that Klaus and Astrid were denied this basic right.14 Regarding Heinrich, it could be argued in court that-because he was not allowed to get a grant based on discrimination due to him being a German national15 while residing in Spain-Heinrich turned to dealing illegal drugs as an activity to pay for his schooling, which would not have been an issue had he not been discriminated against.16 With regard to Sophie, the political group which she had joined was under surveillance by authorities in Spain, however she was not committing an illegal act

Explanation Graphic Essay Example | Topics and Well Written Essays - 500 words

Explanation Graphic - Essay Example he current method of registering students, the new system will be able to register students in the appropriate class and provide access on the start date of the course. This will be much easier than the current process, as a sales person register a student, and the IT person has to configure a lab machine for the students use. The registration will save administrative work, and provide a lower production cost while providing better quality. The system will provide a friendlier login process for the students. With the new system, integration will occur through the student portal, making it easier for the student to connect to a virtual lab machine, without having to use additional logon information throughout the duration of the course (Rijlaarsdam et al 9). Students will also find it easier to register for future courses and also see and previous courses they have attended. The lab machine will be automatically available on the start date of the course, and can undergo automatic extension for an additional 30 days access with a simple click of a button. Students now can convert into other classes efficiently, unlike the current method. The communication plan helps in setting up standards for communication. The project leader would need to establish the standards within which the communication will occur. The stakeholders would also need to be aware of the course of the communication with the indication of how and when it will take place. The communication plan enables the project leader to set the scope for all the communications that are relevant to the project. The communication plan is also significant for scheduling various projects, within a period, thereby making the stakeholders to be aware of the progress. According to Schriver’s model, the graphic is efficient in proper management of time since it offers the option of a search engine (Rijlaarsdam et al 9). Time saving is important in any project management especially when there is need to achieve a

Mark Twain, His Life and Inspiration to Write Research Paper

Mark Twain, His Life and Inspiration to Write - Research Paper Example His younger schooling life was troublesome as he was plagued by illness during the first seven years of his life. His behaviour was almost eccentric, and he had a tendency to wander away from home and as a boy he read adventure stories of pirates and knights in the heroic fiction and poetry of such authors as Sir Walter Scott, Lord Byron and James Fennimore Cooper. He thought of these writers as exemplary and he would not have become the highly original writer that in time he became. He was always a reader though he usually chose to present himself as far from being bookish. When his schooling came to close, he took a part time job that would later become his career. He served as a delivery boy and an office boy, became a printer’s apprentice for the hometown newspaper, the Hannibal Courier as he was following in the footstep of his brother Orion, nearly six years his elder, who has the same career in 1839. Two decades later, he wrote, â€Å"Education continued in the offices of the Hannibal ‘Courier’ & the ‘Journal,’ as an apprentice printer†. He served in all capabilities, including staff work as the Courier’s makeshift library introduced him to humorous publications such as The Spirit of the Times. He later found his concerns with victimisation and humiliation particularly congenial to his talents and attributes. For a short time, he adopted from the south frontier stories on the use of slang and elaborate misspellings. Like many of other writers associated with his school, he adopted a pen name. The successful publication of his work in the East made him turn his attention to local publication and was able to publish several items, some as a consequence of a... The successful publication of his work in the East made him turn his attention to local publication and was able to publish several items, some as a consequence of a disagreement with the editor of the Hannibal Tri-Weekly Messenger, whom he tried to embarrass. In May 1853, young Mark was awarded â€Å"our Assistant’s Column† and the column criticised newspapers that borrowed without credit. In mid-august, having been unable to find work in New York he took up a job as a typesetter and developed a literary technique he was to make good use of throughout his career. In the spring of 1854, he was obliged to leave the east because of what he latter termed as financial stress and then took his printing skills back to the Mississippi valley, sitting upright in the smoking car for two to three days and nights, as his interest in humour and in writing arose directly from his pleasure in books and in printer’s libraries and later his own substantial collection, he was an insatiable writer.

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.

Pearl S. Buck - A Modern Day Hero Essay -- essays research papers

Pearl S. Buck - A Modern Day Hero Introduction A friend of mine gave me a copy of The Good Earth as a birthday gift. Until then, I had never heard of the literary masterpiece or the author, Pearl S. Buck. The story captivated me. I found myself engrossed in the story of the poor farmer Wang Lung whose love for his land allowed him to overcome many odds including famine, flood and a revolution. Through hard work and dedication, Wang Lung became one of the wealthiest landowners in the Anweih province of China. Sadly, Wang Lung’s two sons did not share his passion for â€Å"the good earth† and cared only for their bequest. Wang Lung was still on his death bed when the two sons decided that as soon as their father died, they would sell the land and split their inheritance (Buck, P.S., 1931). The Good Earth instantly became one of my favorite books and Pearl S. Buck, one of my favorite authors. Peter Conn wrote the introduction of the book in the form of a short biography of the author. I usually do not read the introductions until after I read the story because I never want other people’s review to influence my own opinion of the book. So, I saved the introductory pages for last. It wasn’t until I read of Pearl S. Buck’s memoirs that I began to truly admire her, not only for her writing but for her humanitarian and altruistic contributions. Who is Pearl S. Buck? Pearl Sydenstricker was born in Hillsboro, West Virginia in 1892. Her missionary parents, Absalom and Carrie Sydenstricker brought her to China when she was three months old. By the time she was four, she spoke and wrote Chinese as well as English (Conn, NDA). She was at first educated by her mother and tutored by a Chinese Confucian Scholar (Author’s Calendar, 2002). While her parents carried out their Christian mission all over the Chinkiang province of China, Pearl was left under the care of her â€Å"amah† or governess. It was her amah that fascinated her with Chinese folklores and mythical tales of ancient magic, fairies and dragons (Conn, NDA). Growing up, Pearl spent hours wandering the streets of Chinkiang observing how the people lived. She became familiar with their rituals, practices, and traditions. Her first hand experience with the Chinese culture led her to write many novels, including her most critically acclaimed book, The Good Earth. Her intimate knowledge of the Chinese culture was evident in ... ...ca Online: http://www.search.eb.com/eb/article?tocId=9017878 Buck, Pearl S. (1931), The Good Earth, NY: The John Day Company Conn, Peter (NDA), Pearl S. Buck (Introduction: The Good Earth), NY: Simon & Schuster, Inc. Doyle, Paul. A (2000), American National Biography Online: Buck, Pearl S., Retrieved on April 20, 2005 from the World Wide Web: http://www.anb.org/articles/16/16-00214.html Frenz, Horz (1969). The Nobel Lectures, 1901-1967, Amsterdam: Elservier Publishing Company Merriam-Webster Online (NDA). Retrieved from http://www.merriam-webster.com on March 9, 2005 PSBI Website (NDA), Pearl S. Buck International Online, Retrieved on April 11, 2005 from the World Wide Web: http://www.pearl-s-buck.org/psbi/ Mythology Themes (2000), Sparknotes Online: Themes in Mythology, Retrieved on April 20, 2005 from the World Wide Web: http://www.sparknotes.com/lit/mythology/themes.html Spencer, Stephen (2002), The Journal of American Popular Culture, Vol. 1, Issue 1: The Discourse of Whiteness: Chinese-American History, Pearl S. Buck and The Good Earth, Retrieved on April 11, 2005 from the World Wide Web: http://www.americanpopularculture.com/journal/articles/spring_2002/spencer.htm