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.

The Rural Non-Farm Economy

The Rural Non-farm Economy The nonfat economy includes all economic activities other than production of primary agricultural commodities. Nonfat, thus, includes mining, manufacturing, utilities, construction, commerce, transport and a full gamut of financial, personal and government services. Corresponding – the transformation of raw agricultural products by milling, packaging, bulking or transporting – forms a key component of the rural nonfat economy.A broad definition of rural regions as encompassing both dispersed rural settlements as well as the functionally linked rural towns where any corresponding and ancillary nonfat service and commercial activities congregate to service surrounding agricultural settlements. Size: Policy interest in the rural nonfat economy arises in large part because of its increasing importance as a source of income and employment across the developing world. Evidence from a wide array of rural household surveys suggests that nonfat income accounts for about 35 percent of rural income in Africa and roughly 50 percent in Asia and Latin America.Standing roughly 20 percent higher than rural nonfat employment shares, hose income shares confirm the economic importance of part-time and seasonal nonfat activities. Rural residents across the developing world earn a large share of their income?35-50 percent?from nonfat activities. Agricultural households count on nonfat earnings to diversify risk, moderate seasonal income swings, and finance agricultural input purchases, whereas landless and near-landless households everywhere depend heavily on nonfat income for their survival.Over time, the rural nonfat economy has grown rapidly, contributing significantly to both employment and rural income growth. Income data, which include earnings from seasonal and part-time activity, offer a more complete picture of the scale of the ERNE. Rural nonfat employment holds special importance for women. Women account for about one-quarter of t he total full time ERNE workforce in most parts of the developing world. Given their frequently heavy household obligations and more limited mobility, women also participate in part-time ERNE activity, particularly in household-based manufacturing and service activities.Composition: The rural nonfat economy includes a highly heterogeneous collection of trading, crisscrossing, manufacturing, commercial and service activities. Even within the same country, strong differences emerge regionally, as a result of differing natural resource endowments, labor supply, location, infrastructural investments and culture. The scale of individual rural nonfat businesses varies enormously, from part-time self-employment in household-based cottage industries to large-scale corresponding and warehousing facilities operated by large multinational firms.Often highly seasonal, rural nonfat activity fluctuates with the availability of agricultural raw materials and in rhythm with household labor and fina ncial flows twine farm and nonfat activities Remittances account for a large share of rural income in some locations. In the mining economies of Southern Africa, remittances may account for as much as half of all rural household income. They likewise form an important part of household income diversification and risk reduction strategies.In of nonfat earnings, while remittances and transfers typically account for to 20% of non-agricultural rural income and 5% to 10% of total rural income. Equity Implications: The extreme heterogeneity of rural nonfat activity results in widely varying productivity and profitability. Returns vary substantially, normally as a function of differing physical and human capital requirements. Women dominate many of the low-return cottage industries, while the poor dominate other low-return activities, such as small-scale trading and unskilled wage labor used in construction, powering, and many personal services.Wage labor, in both agriculture and nonfat bu siness, also accrues primarily to the poor. The low capital requirements and small scale of many rural nonfat businesses, poor households dominate large segments of the rural nonfat economy. For this reason, many policy makers view the rural inform economy (ERNE) as a potentially important contributor to poverty reduction. Pull Scenario: Where new agricultural technologies and modern farm inputs become available, they lead to agricultural surpluses in some commodities and increased opportunities for trade.In these settings, a growing agriculture stimulates growth of the ERNE through a number of key linkages. Rising labor productivity on the farm increases per capita food supplies and releases farm family workers to undertake nonfat activities. For this reason, green revolution India has seen agricultural labor all from 75% to 65% of rural labor force in the first 25 years following the release of green revolution rice and wheat varieties. Equally important, increases in farm incomes , together with high rural savings rates, make capital available for investment in nonfat activities.These savings rates have reached up to 25-35% in many areas of green revolution Asia Farm households, as their incomes grow, increase their expenditure share on non-food items, thereby accelerating demand for nonfat goods and services. To meet this growing demand, rural households increasingly versify into production of rural nonfat goods and services. The composition of rural nonfat activity changes perceptibly over time in these buoyant agricultural settings. Increases in real wages raise the opportunity cost of labor, thereby making low-return nonfat activities uneconomic.This leads to the demise of many low- return craft and household manufacturing activities and to the growth of higher- return nonfat activities such as mechanical milling, transport, commerce, personal, health and educational services. Growing agricultural incomes attract labor into more productive, higher return rural nonfat services. Push Scenario: In regions without a dynamic economic base, patterns of growth in the rural nonfat economy unfold very differently. Sluggish income growth in agriculture leads to anemic consumer demand, limited corresponding and agricultural input requirements and stagnant wages.Taken together, these tendencies stymie both entrepreneurial and wage-earning opportunities in the rural nonfat economy. Without technological advance in agriculture, labor productivity and per capita farm production fall. In such settings, growing landlines pushes labor force increments into nonfat activity by default. Falling agricultural labor productivity, low opportunity cost of labor and declining household purchasing power induce diversification into low-return, labor- intensive nonfat activities such as basket making, gathering, pottery, weaving, embroidery and mat making.Specialized nonfat enterprises and households opportunities in agriculture and a shortage of both rural sav ings and invertible capital. Arbitration and Migration: Although the prosperity of rural regions and their rural nonfat economies typically depends on agricultural performance during the early stages of economic growth, this link gradually weakens over time as agriculture's share in national economies declines.Rapid arbitration and globalization have opened up new market opportunities for rural nonfat producers of treatable goods and services and for rural workers to migrate and remit. Where conditions permit, these opportunities can stimulate regional economic growth, in some instances benefiting backward regions with poor agricultural potential and in others enhancing opportunities in already rapidly growing rural economies.Rising arbitration and national economic growth, together with improved transport and communication networks, provide important economic linkages between urban and rural areas, opening up new opportunities for rural households Evidence from India, for example, suggests that rapid rural nonfat growth is occurring along transport corridors linked to major urban centers, largely independent of their agricultural base Similarly, in Southeast Asia and in China high population density and low transport costs have led to rapid growth in urban-to-rural subcontracting for labor- intensive manufactures destined for international export markets.The importance of migration and remittance income proves highly context-specific, varying both locations and over time. Empirical evidence suggests that migrant remittances may serve to increase rural investment, finance schooling, house construction and agricultural inputs in some locations. Less beneficial are the impacts on migrant worker health and on family social cohesion. Liberalizing and Globalization: Beginning in the sass, widespread economic liberalizing has opened up the rural nonfat economy as never before – to new opportunities and to new threats.Liberalizing, by reducing direct governmen t involvement in production and marketing, has opened up new market opportunities for the private sector, articulacy in agricultural processing, input supply and trade. Relaxed controls on foreign exchange and investment have unleashed a flood of foreign direct investment into Latin America, Asia and Africa. As a result, large exporters, agribusiness firms and supermarket chains increasingly penetrate rural economies of the developing world, altering the scale and structure of rural supply chains as they do.This rapidly changing environment opens up opportunities for some rural suppliers to access new markets. But liberalizing and globalization expose other rural genuineness to new threats, as quantity requirements and quality standards impose new ways of doing business that risk excluding intellectualized rural enterprises on which the rural poor often rely. Available evidence suggests that rapid concentration has triggered the bankruptcy of thousands of small firms in recent decad es.Although many of these bankruptcies affected urban traders, emerging evidence suggests that small rural traders and the wholesale markets they serve likewise risk being displaced by larger, specialized wholesalers. Some categories of rural nonfat activity have thrived in the past because of protection from outside intention by high transport costs, restrictive production policies subsidized inputs and credit, and preferential access to key markets Globalization and market transition may prove brutally abrupt for many traditional small-scale manufacturing activities whose products cannot compete with higher quality, mass-produced goods.For this reason, the initial stages of depreciation can lead to significant Job losses in the ERNE, even though many of these may later be recovered as new types of rural nonfat activity sprout up, as in India during the sass. Since poor households and male-dominated activities predominate among the low-investment, low-productivity rural nonfat acti vities, they tend to face the most difficult adjustment during this transition. Agriculture has historically played an important role in expanding the economic base of rural regions in the developing world.In regions where agriculture has grown robustly, the ERNE has also typically enjoyed rapid growth. Regions with poor agricultural potential have seen more limited prospects for rural nonfat growth, except in places where the availability of other important rural treatable such as mining, logging, and entree ¶t trade offer an alternative economic platform for sustaining regional growth. In recent years, globalization, arbitration and improved infrastructure have opened up new opportunities in many rural areas, thereby reducing their dependence on agriculture.These developments seemingly offer new prospects for stimulating rural economic growth and, perhaps, new pathways out of poverty. Policymakers hold high hopes that rural nonfat growth can offer a pathway out of poverty for a large segment of the rural poor. Given the enormous diversity observed across rural regions and within the rural nonfat economy itself, opportunities, constraints, and appropriate policies will clearly differ across settings. Although general guidelines cannot substitute for detailed understanding of a specific rural nonfat setting, several broad policy guidelines do emerge from this review.Available evidence suggests the rural nonfat economy can significantly expand economic opportunities for the rural poor if two conditions hold. First, the rural nonfat economy must itself be growing robustly. Both rural nonfat employment and income per worker must be growing if nonfat growth is to contribute effectively to poverty reduction. Typically, this growth in the rural nonfat economy requires investments in the productive capacity and productivity of activities related to rural treatable, such as agriculture, tourism, or natural resource-based activities, in order to ensure their competit iveness in external markets.Alternatively, where low-cost rural labor and low transportation costs coincide, rural households can sometimes compete in urban or export markets through commuting, short-term migration, or urban-to-rural subcontracting arrangements. From a policy perspective, accelerating output and productivity Roth in the rural economic base will require investing in agricultural technology, rural education, communications, transportation, and electrification.Together with a favorable policy environment, these investments encourage rural nonfat business development as well as short-term commuting and migration strategies, both of which serve to increase rural nonfat incomes and investment. But a growing rural nonfat economy does not guarantee access by the poor. Wealthy households, well- endowed with financial, human, and political capital, often prove better equipped to sake advantage of growth in the high-productivity segments of the rural nonfat economy, both as en trepreneurs and as wage employees.Meanwhile, poor backwaters of the rural nonfat economy. Migration opportunities likewise remain bifurcated, with highly educated households more apt to land lucrative positions in towns. Thus, policymakers cannot assume that an expanding rural nonfat economy will translate automatically into pro-poor growth. This bifurcation leads to the second requirement for pro-poor rural nonfat growth: access by the poor to growing nonfat market niches.For nonfat earnings to offer a pathway out of poverty, rural households and policymakers may need to invest in rural education and health in order to improve the human capital stock of the poor. At the same time, policymakers will need to remove economic and social barriers that limit poor people's entry into lucrative nonfat professions. Fluid labor markets, with good transportation and communication systems connecting rural households to regional and urban labor markets, will provide a key bridge linking the rur al poor to growing opportunities in the nonfat economy.

A Village Singer

â€Å"A village singer† portrays the internal conflict, the bitterness and responses of Candace when she was dismissed from the choir that served for forty years. The story partially points out the social norm that set down for women. In this community, women are not considered equal and have the same feelings as men which represent through Reverend Pollard and Williams Emmons. Williams Emmons is three years older than Candace, but he still holds his choir leader position. If they complain that her voice has worsened, Williams's voice logically must have the same situation as her. However, Emmons is not dismissed and remain his choirmaster position. The minister just like Candace also serves at the church for forty years. He hesitates of his speech and could not keep the freshness for his sermons. He still can stay in the church and continue his duties since nobody asks him to leave his position and gives him a photograph album. Candace indicates that all of them have the same position in the church and change according to age, but the congregation chooses to dismiss her as she is a woman. Candace's bitterness, pain, and conflict become more intense due to the betrayal of people around her. A betrayal of Emmons who had sung duets and had walked Candace home after rehearsals in Saturday night when he said â€Å"a most outrageous proceeding† for Candace action. He critics her voice with Alma and supports the dismissal. Even Candace's nephew, Wilson Ford, threats to throw her organ out of the window if she continues to disturb Alma's solo. He does not express any sympathy or even gently discuss her grief. She also feels hurt and betrayed by members of the choir since they celebrate a surprise party for her and leave a photograph album with the letter informing her dismissal from the choir. However, the way that Candace responses and against to conflict is full of anger, foolishness, disregard, and arrogance. She says that the member of the church pretends to be a Christian; however, she also goes against what the church teaches. She uses photograph album as a footstool, disturbs Alma's solo, refuses to pray â€Å"‘I don't see any use prayin' about it,' said she. ‘I don't think the Lord's got much to do with it, anyhow'† and challenge other people to stop her † I'd like to see anybody stop me.† Besides that, the story carries the message of kindness and forgiveness. At the end of the story, Candace forgives to all people who have wronged her and also ask for the forgiveness from those people. She apologizes to the minister, reconciles with Alma, and forgive Wilson.

Biotechnology And Its Applications Research Notes

Biotechnology and its Applications – Research Notes Topic: Bioremediation Description The world of today is fuelled by fossil fuels. Petroleum products like oil are used for generating electricity, generating light and heat, manufacturing, and vehicle fuels, among numerous other uses. Much of these fuels are extracted from below the Earth’s surface using machinery and technology, some of which may be decades old – but as technology has proven itself to be unreliable at times, accidents such as oil spills are inevitable. Oil spills have devastating detrimental effects, both towards humans and other animals, as well as the environment. For example, drinking water may be polluted and marine life killed, consequently lowering the quality of life in affected areas. As the quality of the environment is inextricably linked to the quality of life on Earth, it is essential to properly clean up incidents such as oil spills to protect the quality of the environment and therefore the quality of life. Bioremediation involves the use of microorganisms as a waste management system to neutralize or remove contaminants from polluted sites, such as the areas around oil spills. This method of treatment uses microbes that occur naturally, including some forms of prokaryotes, like bacteria, to break down hazardous substances – which may have detrimental health effects – into non-toxic or less toxic material. 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Although the United States Food and Drug Administration has established that the foodRead MoreThe Policy Of Genetically Modified Crops1401 Words   |  6 Pagesthe policy of genetically modified crops in India, regarding the approach towards the development of economy, the technological impact on the nation and also the relationships between farming and business communities. The supporting parties of Biotechnology in agriculture argue that the genetically modified crops could be the solution to most of the existing problems in the country’s agriculture; opposing parties argue that it could have negative impact on the environment and livelihood of farmersRead MoreFactors Affecting Consumers Intention Of Genetically Modified Foods3157 Words   |  13 PagesShahub Sayareh SOC 102 – RA #2 June 30, 2015 Topic: Factors Affecting Consumers’ Intention of Genetically Modified Foods 1.0 Introduction Biotechnology has become an important field in the global market. All the global players are striving towards dominating the field in order to boost their economy. Food biotechnology is one of the dimensions of biotechnological industry that deals in improvement of the food production technology and product differentiation in the food industry which would alsoRead MoreBioethical Issues on Genetically Modified Organisms (Gmos) in Malaysia: Biting Into the Legal Protection Under the Biosafety Act 20074399 Words   |  18 Pages2011 2nd International Conference on Biotechnology and Food Science IPCBEE vol.7 (2011)  © (2011) IACSIT Press, Singapore Bioethical Issues on Genetically Modified Organisms (GMOs) In Malaysia: Biting Into the Legal Protection under the Biosafety Act 2007 Assoc Prof. Dr. Zaiton Hamin Siti Hafsyah Idris Faculty of Law, Universiti Teknologi MARA (UiTM), 40450, Shah Alam, Selangor, Malaysia. Email: zaiton303@salam.uitm.edu.my, yasmin_yazid99@yahoo.com Abstract— Of late, a growing number of ongoingRead MoreCase Study: Health Care Industry (Eli Lilly and Company)1735 Words   |  7 Pagestwo grandsons, Eli Lilly and Josiah K. Lilly Jr., each served as president of the company. It was his grandson who led the company into the industrialized era by stressing upon the need of biomedical research and installing modern equipments to make the research successful. His interest in research paid off and since its inception the company has grown to be one of the largest and most influential pharmaceutical companies in the world, offering key pharmaceutical products in almost every key therapeutic