The “tanorexics” Essay Example for Free

The â€Å"tanorexics† Essay They’re desperate for a   sun fix. They spend hours incarcerated in hi-tech coffins. Cayte Williams meets the â€Å"tanorexics† Youre lying in a big plastic cocoon. Weird blue light beats down at you through hi-tech glass and there’s a strange humming noise. Youre naked and sweating profusely. Have you been abducted by aliens for experimental tests? No, youre lying on a sunbed and if youre doing it more than once a week then you could be seriously addicted. The Imperial Cancer Research Fund (ICRF) recently released a fact sheet outlining the dangerous effects of indoor tanning. â€Å"There is extreme concern for ‘tanorexics’,† says Christine Suggars, a spokesperson for the ICRF. â€Å"Especially people who have a dangerous desire for a permanent tan and use sunbeds more than once a week.† So who are these walking raisins, and why do they need a regular sunbed fix? Often tanorexics prefer to buy a sunbed rather than visit a suntanning salon. And let’s face it, anyone who’s prepared to fork out  £1,600 on the initial machinery must have one hell of a habit. â€Å"I bought a sunbed 10 years ago,† recalls Jane Horwood, a 37-year- old interior designer. â€Å"I used it once a week at first, but this gradually became once a night. I used to go on it religiously after work and hated it when I couldnt go underneath.† It’s like smoking. Even though I knew I shouldn’t be under there, I couldnt stop myself,† she confesses. â€Å"I wanted to look healthy and was really upset that when I got pregnant my doctor told me I couldn’t go on the sunbed. It’s an obsession with self image and self esteem, like anorexia. If you’re browner, you think you’re going to have a nicer lifestyle, be more attractive. If I hadn’t got pregnant I would never have stopped.† Over use of sunbeds can lead to all kinds of nasty side-effects. â€Å"Apart from premature skin ageing, people who use sunbeds for more than 20 sessions of 30 minutes per year run the risk of developing skin fragility,† says Doctor Julia Newton Bishop, consultant dermatologist at St James’ University Hospital in Leeds. â€Å"The skin becomes very thin with a transparent texture and it bruises and blisters easily. Normally I would only expect to see this problem in the elderly but I have seen some young patients suffering from  this who over-use tanning equipment.† â€Å"An average 30 minutes on a sunbed gives you the same dose of UVA rays as a day at the beach,† says Christine Suggars. â€Å"UVB rays have been linked to skin cancer for many years, but it’s only now that the concern is growing over the effects of UVA rays. UVB rays affect the top layer of the skin, the epidermis, and also the melanocyte cells, to produce brown pigment,† she explains. â€Å"UVA rays penetrate the skin more deeply, damaging the elastin (which keeps the skin supple) and collagen (which maintains the skin’s thickness) in the skin’s middle layer, causing sagging skin and wrinkles.† This is not good news for the suntanning industry The Tanning Shop opened its first branch in the UK in 1992 and now has over 150 branches around the country. The company advocates â€Å"controlled tanning† and specialised programmes can cost up to  £399 a year. â€Å"People arent happy just to pop into a booth anymore,† explains marketing co-ordinator Rachel O’Donnell. â€Å"They want us to tell them what to do.† Customers are warned about the dangers of over-tanning and are given a ‘consultation’ before their first sunbed session. â€Å"They can only ever have a session every second day and fair-skinned people are allowed six minutes a session which might go on to 10 minutes eventually. Customers are more fussy about what they get,† says O’Donnell. The Tanning Shops’ black vertical tanning booths look unnervingly like upright coffins, but tanorexics will not be put off. â€Å"I go two to three times a week,† says 27-year-old accountant, Victoria Williams. It makes me feel healthier, just like when you come back from holiday.† Victoria started using sunbeds to clear up a skin complaint, but now she’s hooked. â€Å"I did worry about addiction,† she says, â€Å"so I didnt go on the sunbed for a month, but I started to get miserable when I got pasty. I wanted that heat and warmth on my body.† Is she worried about the latest sunbed scare? â€Å"You have BSE, listeria, salmonella,† she says defiantly â€Å"I think there is some scare every week and it’s over-hyped. I would only stop using sunbeds if they were banned.† A favourite haunt of the shameless tanorexic is Electric Beach in London’s Covent Garden. Here models and media people pop in for a top-up on a regular basis. On Saturday, the last celebs seen crossing its portats were Luke and Matt Goss, formerly of Bros. Who says tanning isn’t trendy? â€Å"We are looking to cater for those people who  live a London life,† says managing director Philip Hodgeson. â€Å"People go in and they come out tanned. We use bulbs as opposed to tubes with a potassium filter, which filters out 99.9 per cent of the UVB rays.† While women openly admit to tanning addiction, men are much more secretive. Last year Paddy Ashdown suffered great embarrassment when a beautician let slip that he’d checked in for a session on a sunbed. It seemed his rugged outdoor tan was of the indoor variety and the Lib Dem office put the habit down to his doctor’s advice for soothing a minor skin complaint. John Stevens (not his real name), a 28 year old lawyer, identifies with Paddy’s blushes over his ruddy complexion. â€Å"When youre tanned you look healthy, fit and well travelled,† he says, â€Å"and in business it’s good, because it makes you look wealthier, like you can afford regular holidays. But there’s this unspoken idea that a ‘real man’ should get his tan doing something rugged and adventurous. I would never want my mates to know that I use a sunbed.† And, of course, there’s Essex Man with his perennial tandoori tan. â€Å"There’s one who co mes in every night,† says Shauney Taylor of Tanning Trends in Barking. â€Å"He’s in his 30s, he’s working out, and wants the tan to go with it. You know what men are like,† she muses. â€Å"They want to be Peter Andre.†

Eutrophication Essay -- Geology

What is eutrophication? Eutrophication is, in the simplest terms, too much of a good thing. It occurs when too many nutrients are deposited into a body of water, throwing off the established balance of production and consumption of organic matter. Eutrophication can take place in ponds, lakes, rivers, and oceans. At first, the overload of nutrients in the body of water encourages plant growth. However, soon this excess of organic material uses up most of the available oxygen in the water, taking it away from the other plants and animals. These other organisms can no longer survive with such depleted oxygen levels and die off, creating what is referred to sometimes as a "dead zone", devoid of life. Below is a table of the different trophic states, or levels of organic matter in relation to available oxygen, that a body of water traverses on its way to becoming a "dead zone". TROPHIC STATES Oligotrophic Clear waters with little organic matter or sediment and minimum biological activity. Mesotrophic Waters with more nutrients, and therefore, more biological productivity. Eutrophic Waters extremely rich in nutrients, with high biological productivity. Some species may be choked out. Hypereutrophic Murky, highly productive waters, closest to the wetland status. Many clearwater species cannot survive. Dystrophic Low in nutrients, highly colored with dissolved humic organic material. (Not necessarily a part of the natural trophic progression.) back to top What causes eutrophication? Eutrophication of bodies of water is a naturally occurring phenomenon. However, the process has been aggravated by the human population. Such man-made eutrophication is caused by excessive discharge of nutrien... ...less * and being a responsible boater by pumping out wastes. back to top Resources 1. Environmental Agency, http://www.environment-agency.gov.uk/ s-enviro/viewpoints/4health/3eutroph/4-3.html 2. Eutrophication, http://www.btnep.org/pages/eutrophication1.html 3. Fish Kills do to Harmful Algal Blooms, http://www.redtide.whoi.edu/ hab/foodweb/fishkills.html 4. Harmful Algal Bloom Photo Gallery, http://habserv1.whoi.edu/hab/ rtphotos/rtphotos.html 5. Impact of Phosphorus on Aquatic Life: Eutrophication, http://www. agnr.umd.edu/users/agron/nutrient/Factshee/Phosphorus/Eutrop.html 6. Marine Research on Eutrophication, http://www.mare.su.se/english/ index.html 7. Midatlantic Integrated Assessment, http://www.epa.gov/emfjulte/ tpmcmaia/html/eutroph.html 8. United Nations Environment Programme, http://www.grida.no Eutrophication Essay -- Geology What is eutrophication? Eutrophication is, in the simplest terms, too much of a good thing. It occurs when too many nutrients are deposited into a body of water, throwing off the established balance of production and consumption of organic matter. Eutrophication can take place in ponds, lakes, rivers, and oceans. At first, the overload of nutrients in the body of water encourages plant growth. However, soon this excess of organic material uses up most of the available oxygen in the water, taking it away from the other plants and animals. These other organisms can no longer survive with such depleted oxygen levels and die off, creating what is referred to sometimes as a "dead zone", devoid of life. Below is a table of the different trophic states, or levels of organic matter in relation to available oxygen, that a body of water traverses on its way to becoming a "dead zone". TROPHIC STATES Oligotrophic Clear waters with little organic matter or sediment and minimum biological activity. Mesotrophic Waters with more nutrients, and therefore, more biological productivity. Eutrophic Waters extremely rich in nutrients, with high biological productivity. Some species may be choked out. Hypereutrophic Murky, highly productive waters, closest to the wetland status. Many clearwater species cannot survive. Dystrophic Low in nutrients, highly colored with dissolved humic organic material. (Not necessarily a part of the natural trophic progression.) back to top What causes eutrophication? Eutrophication of bodies of water is a naturally occurring phenomenon. However, the process has been aggravated by the human population. Such man-made eutrophication is caused by excessive discharge of nutrien... ...less * and being a responsible boater by pumping out wastes. back to top Resources 1. Environmental Agency, http://www.environment-agency.gov.uk/ s-enviro/viewpoints/4health/3eutroph/4-3.html 2. Eutrophication, http://www.btnep.org/pages/eutrophication1.html 3. Fish Kills do to Harmful Algal Blooms, http://www.redtide.whoi.edu/ hab/foodweb/fishkills.html 4. Harmful Algal Bloom Photo Gallery, http://habserv1.whoi.edu/hab/ rtphotos/rtphotos.html 5. Impact of Phosphorus on Aquatic Life: Eutrophication, http://www. agnr.umd.edu/users/agron/nutrient/Factshee/Phosphorus/Eutrop.html 6. Marine Research on Eutrophication, http://www.mare.su.se/english/ index.html 7. Midatlantic Integrated Assessment, http://www.epa.gov/emfjulte/ tpmcmaia/html/eutroph.html 8. United Nations Environment Programme, http://www.grida.no

Renal Compensation Acid Base Balance Health And Social Care Essay

IntroductionAcid-base balance in the human organic structure refers to the ordinance of the free H ions present in the organic structure fluids [ 1 ] . This balance is important to the continuance of life as it influences many different systems and mechanisms in the organic structure. The mean pH of the blood when all the homeostatic controls are working efficaciously is 7.4. The pH of normal arterial blood is really 7.45 whereas the pH of normal venous blood is 7.35. This difference can be accounted for by the fact that when CO2 is picked up by tissue capillaries, this leads to the coevals of H2CO3. This in bend generates H+ doing the blood more acidic [ 1 ] . It is partially due to the actions of the kidneys which helps maintain the blood within theses rigorous bounds. All reactions affecting enzymes will necessitate that the pH of organic structure fluids remains within a narrow scope. The function of the kidneys in keeping this homeostasis is of import, but is seen as the â€Å" 3rd defense mechanism † , the first being the usage of chemical buffers in the organic structure and the 2nd being changes made in take a breathing which changes the pCO2 ( partial force per unit area of C dioxide ) and hence the concentration of H ions in organic structure fluids [ 2 ] . In this study, I will depict the changes that the kidneys make in seeking to modulate this balance, how the anatomy of the kidney maps to drive these mechanisms and the response of the kidneys when the organic structure experiences acidosis of alkalosis. Besides as portion of my study, I will discourse the effects that a high protein, low saccharide diet has on the acid-base balance of the organic structure, how this is later corrected utilizing nephritic homeostatic mechanisms, the possible nephritic pathology that can happen as a consequence, and the consequence this will hold on nephritic compensation of acid-base balance thenceforth.Important anatomy of the kidneyThe kidneys are the variety meats which are chiefly responsible for the production of urine, before it passes through the ureters to the urinary vesica in the pelvic girdle [ 3 ] . The kidneys are located within the right and left wing and situated retroperitoneally to the spinal column, between the spinal degrees of T12 to T13 [ 4 ] . The kidneys are about 11-14cm lengthwise and the kidney situated on the left side is found to be more inferior. The kidney consists of uriniferous tubule fractional monetary units, of which there are around 1million present [ 4 ] . But it is the internal constructions of the kidney which are of most involvement in relation to the care of acid-base balance ; peculiarly the function of the proximal tubule, type A and B intercalated cannular cells found in the distal and connecting tubules, and the peritubular capillaries. Figure 1 below is a diagram which depicts the cross-section of a kidney and the functional anatomy. [ 5 ] Blood is supplied to the kidneys through the nephritic arterias, which branch straight from the abdominal aorta. Branching occurs once more one time within the kidney. One group of these sub-branches are the interlobular arterias. These run through the nephritic cerebral mantle and subdivision once more to organize the sensory nerve glomerular arteriolas which supplies oxygenated blood to the glomerular capillary bed and besides, the motor nerve glomerular atrerioles. Within the nephritic cerebral mantle, some of these motorial glomerular arteriolas form the web of peritubular capillaries [ 4 ] . These capillaries can either have secreted ions from the intercalated cells, or they can pump ions into the nephritic cannular lms, from where they will be transferred into the urine [ 4 ] .Figure 2 below shows a simplified diagram of the uriniferous tubule, nevertheless efficaciously describes the chemical exchanges which take topographic point. [ 6 ] Intercalated cells Intercalated cannular cells are found in the epithelial tissue of the collection and distal tubules, along with chief cells. The cells found in these tubules, along with all other nephritic tubules are cubelike epithelial ( one exclusion is the lms of the thin limb of the cringle of henle where the cells are level ) . But it is entirely the intercalated cells involved in keeping acid-base balance. The intercalated cells can nevertheless be classified farther, into Type A and Type B. We are able to make this due the fact that these cells have different transporter proteins [ 7 ] . Type A intercalated cells – These cells are more active than type B and act in order to forestall a province of acidosis. This is done by 1 ) secernment of free H+ 2 ) resorption of HCO-3 3 ) Resorption of K+ [ 1 ] . Hydrogen ions are secreted from these cells via an H+/ATPase transporter, a proton pump, which actively secretes them. The Reabsorbtion of K+ ions occurs along side this procedure. It should besides be noted that the presence of aldosterone, which elevates the activity of the H+ -ATPase pump, increases the rate of H+ secernment. [ 4 ] Type B intercalated cells – These cells act in order to forestall a province alkalosis. This is done by Secretion of HCO-3 2 ) resorption of free H+ 3 ) secernment K+ . [ 1 ] Alternatively of the proton pump, these cells contain an H+-ATPase pump. This complex actively transports H+ ions back into the peritubular capillary from the nephritic cannular lms. But the most of import map of these cells is the secernment of HCO3- ions from the peritubular capillary into the nephritic cannular lms for elimination. This occurs in the apical membrane of the cell, where the HCO3- ions are exchanged across the membrane. The transporter through which HCO3- ions are exchanged is non the same as the pump that is utilised in type A intercalated cells. These cells work in sync in order to keep the right balance. Proximal tubule The cells found in this tubule are besides cubelike epithelial cells, nevertheless, these cells differ from the cells found in the nephritic tubules as they have a brush boundary line of microvilli [ 4 ] . This provides a larger entire surface country for the transportation of substances across the cell membranes. Many chondriosomes are besides seen in these cells histologically, in order to supply energy for procedures affecting active conveyance [ 7 ] . Physiologically, the proximal tubule has two chief functions. First, to resorb from the glomerulus any hydrogen carbonate ions which have been filtered. The proximal tubule is the chief site of bicarbonate resorption, with 85-90 % of the filtered hydrogen carbonate being reabsorbed here. Second, it is the primary site of ammonia production. The huge bulk of this production is done within the proximal tubule [ 8 ] . Both of these mechanisms will be discussed in more item in the undermentioned chapters.Nephritic mechanisms of acid-base balanceThe excess nephritic homeostatic mechanisms of acid-base ordinance consist of ; the pneumonic ordinance of pCO2 and buffer systems found in the blood and intracellularly. Interaction does take topographic point between these mechanisms and the action that the kidneys take in keeping acid-base balance [ 9 ] . There are three factors which are regulated by the kidneys refering acid-base balance: H+ elimination HCO-3 elimination NH3 secernment It should be noted that these factors are interrelated and there is no isolation when it comes to keeping their degrees in the plasma [ 1 ] . The purpose of the kidneys is to keep the physiological acid-base ratio of 1:20. This being the ratio between CO2 ( which becomes H2CO3 when dissolved in the plasma ) and HCO-3. Although the three factors mentioned above are physically changed, it is the concentration of HCO-3 which is ever altered during each mechanism, doing it the common denominator that influences plasma acid-base balance [ 10 ] . In a instance of acidosis or nearing acidosis, the buffers can merely make so much to battle the alteration in pH. The anatomy of the kidney involved in releasing H+ ‘s into the piss, in order to be ejected from the organic structure are the proximal, distal and roll uping tubules [ 1 ] . The anatomy of which is described above. These H ions are derived from CO2 found in one of three topographic points ; the plasma, the cannular fluid or fro m the intercalated tubular cells where it is synthesised due to metabolic procedures [ 1 ] . Bicarbonate ions are besides synthesised in the cannular cells from CO2 and H2O, and this reaction is catalysed by the enzyme carbonaceous anhydrase. But the kidney has two functions with respect to bicarbonate ions ; it is involved in the resorption of filtered hydrogen carbonate ions and the elimination of hydrogen carbonate that has been synthesised from its constituents.The site of this resorption within the kidney is found chiefly in the proximal tubule, but there is grounds of this taking topographic point at the distal and convoluting tubule and thick go uping limb of the henle [ 11 ] . At the nephritic atoms, Bicarbonate ions are easy filtered. But in order to forestall organic structure fluids from going greatly acidic, most of these ions must be reabsorbed [ 12 ] . This is the destiny of the huge bulk of these ions, with merely around 0.1 % being lost in the urine [ 9 ] . However as mentioned, the creative activity of new hydrogen carbonate ions occurs within the cannular c ells of the kidney. This procedure takes topographic point each clip there is 1 ) secernment of ammonium and 2 ) the elimination of acid. From the cannular cells, the hydrogen carbonate ions are absorbed into the peritubular lms. [ 13 ] Ammonium secernment is a utile manner in which the kidney can egest more H ions, as it does non affect the demand for organic buffers. The ammonium that is utilized is derived from the dislocation of protein. However as ammonium is toxic even at comparatively low degrees, in the liver, the ammonium ion is bound to a hydrogen carbonate ion in the signifier of either Urea or Glutamine. Once the glutamine is passed onto the proximal tubules in the kidney, the ammonium ion is released, ready for usage [ 9 ] . The demand for this ammonium is due to the fact that the kidneys can non overload the piss with H ions because the urine pH can non be decreased lower so 4.5. The ammonia Acts of the Apostless as a secondary buffer in this sense, along with a phosphate buffer, which is besides present in the cannular fluid [ 1 ] . The purpose of these mechanisms is to forestall the oncoming of acidosis or alkalosis. Acidosis and alkalosis can be classified, depending on which factor have been changed and the cause of this alteration. If the first alteration was in pCO2, either an addition or a lessening, the status will be known as either respiratory acidosis or alkalosis. Whereas if it is a alteration in hydrogen carbonate or H concentration, this will either be metabolic acidosis or alkalosis [ 14 ] The physiological effects of the pH of organic structure fluids rolling outwith the rigorous physiological bounds can hold body-wide systemic effects. For illustration ; fluctuations in the concentration of H ions can change the irritability of certain nerve cells. It besides can hold effects on enzyme activity and K+ degrees in the organic structure fluids [ 1 ] .Nephritic compensation of the systemic effects on acid-base balance, caused by a high protein, low saccharide diet.This diet has come into the public oculus as a manner of cut downing one ‘s organic structure weight, whilst still being able to bask nutrients that would usually be seen as inappropriate if one was on a diet. The construct behind the thought is the remotion of simple saccharides from the diet, and replacing them with high animate being protein nutrient ( e.g sausage and bacon ) [ 15 ] . It has been noted that the immediate alteration to this diet consequences in immediate weight loss. There is an lift in the rate of micturition, doing more Na to be lost, upsetting the balance of Na being taken in and Na being excreted. But the weight that is lost is due to H2O loss, non fat loss. The physiological response of aldosterone production brings the sodium/water balance back to normal [ 16 ] . In the longer term, the degree of saccharide consumed is reduced to the point where, if there was a farther decrease in the ingestion of saccharides, a province of ketonemia would follow. In a survey carried out by Reddy et Al. suggests that a decrease in carbohydrate consumption along with a high protein diet will ensue in â€Å" uncomplete oxidization of fat and attendant ketoanion production † [ 17 ] . The premiss behind this method of weight loss is that by cut downing the degree of saccharide available to the organic structure, fat will be oxidised in the liver to supply energy. In this state of affairs, it is the ketone organic structures produced by this oxidization of fatty acids that become the chief energy beginning [ 18 ] .Protein and carbohydrate metamorphosisAfter protein has been metabolised by the liver, Urea is later produced. The optimal status for urea elimination is when there are low degrees of ADH in the plasma, forestalling most of the resorption of urea by the collection tubules [ 9 ] . Dietary proteins which are ingested are broken down in the tummy by endo- and exopeptidases. The component amino acids are separated from one another by the dislocation of the peptide bonds. The amino acids are so taken up by enterocytes in the little bowel and transported to the blood stream [ 4 ] . The metamorphosis of sulphur-containing amino acids leads to the formation and construct up of ions which have an consequence on acid-base balance ( Cl, P, SO4 ) [ 20 ] . The ground that sulphur incorporating amino acids lead to an increased acid burden is that the oxidization of sulfur to sulphate green goodss protons. Therefore, an addition in protein intake consequences in an addition in the acid burden in the kidneys, due to the oxidization in the liver of aminic acids incorporating sulfur. The organic structure ab initio responds with an addition in the net acid elimination, a lessening in the degree of bicarbonate ions excreted and an addition in GFR ( Glomerular filtration rate ) which later leads to an addition in ammonium elimination. The GFR is thought to increase due to a primary addition in nephritic capillary permeableness [ 19 ] . This is a reaction to an addition in the degrees of N, due to amino acerb dislocation. However this mechanism is non plenty and as a consequence, blood urea N degrees addition. As the GFR additions, more energy is required by the kidney in order to go on to work efficaciously. In the kidney, the energy beginning is the amino acerb glutamine. The rate of its metamorphosis is increased, ensuing in an addition in the degree of ammonium hydroxide ( NH3 ) produced. As the acerb burden of the kidney and therefore figure of proton has increased, ammonium hydroxide, which has the ability to accept protons is released by cannular cells. The a mmonia ions are oxidised to ammonium and extra protons are hence excreted in the piss in the signifier of ammonium. Increased degrees of acid and NH4+ are found in the piss, whereas the degree of bicarbonate ions beads expectedly. However, it should be noted that, as in response to any cause of increased nephritic acid burden, the cardinal stimulation for amminogenesis is the lessening in urinary pH. In some instances, the extent of ammonium elimination can do a ample urinary pH addition [ 20 ] . When saccharides are ingested as portion of the diet, the saccharides are usually found as polyoses. Starch and animal starch are normally obtained chiefly from works beginnings and meat severally. One of the other saccharides found in dietetic consumption, although less common, are the disaccharides. These larger units are broken down during digestion into their constituents. This is chiefly glucose. As a simple sugar, this can be easy absorbed by the enterocytes in the little bowel [ 1 ] . The lessening in dietetic saccharides is instituted in order to do protein the primary beginning of energy, leting fatty acerb oxidization and ketone organic structure formation.Nephritic pathology as a consequence of a high protein, low saccharide dietAs has been discussed, an addition in the degree of dietetic protein ingested increases the acerb burden in the kidneys. This addition can take to different abnormalcies and pathologies happening within the kidneys. Ketosis is associated with a hig h-protein, low-carbohydrate diet when there is drastic lowering of the saccharide consumption. As mentioned antecedently, ketone organic structures are produced upon oxidization of fatty acids. These build up in the blood watercourse. As the saccharide handiness has decreased, the organic structure becomes more and more dependent on fat shops as an energy supply, constructing up the degrees of ketone organic structures. This is seen as a plus point of the diet, as an increased figure of ketone organic structures leads to a loss of appetency. Ketosis has several complications which affect different systems in the organic structure. Some of which are desiccation, irregularity and a inclination to organize kidney rocks. More inauspicious affects include lipemia, faulty neutrophil map, ocular neuropathy and osteoporosis. The mechanisms of which will be discussed in more item [ 21 ] . It has been suggested by Frassetto et Al. that due to a normal western diet, people are predisposed to a long-run, but low class acidosis. This is seen to be amplified in older people, where there is frequently a deterioration of kidney map and the kidney is unable to cover with an increased acid burden. This can frequently take to instances of metabolic acidosis. The underlying mechanism of this induced status is the increasing inefficiency of acerb elimination by the kidneys, and a lessening in the resorption of filtered hydrogen carbonate [ 22 ] . In the survey conducted by Frassetto et Al. analyzing the production of endogenous carbonaceous acids and the degrees of K and protein ions the diet, it was found that there was a strong nexus between carnal protein uptake and nephritic net acid elimination. This was non nevertheless found with vegetable protein. This reinforces the fact it is the consumption of sulphur-containing amino acids which has a greater affect on nephritic acid burden. The figure of sulfur incorporating aminic acids in veggie is much more varied [ 22 ] . There are some surveies which suggest that a high-protein diet can be connected with chronic kidney disease, due to the strain placed upon the kidney by such as diet. The cause of which is cited as the kidney being overworked when covering with some of the by merchandises of protein metamorphosis, for illustration the addition in Urea elimination, and holding to get by with an increased GFR [ 23 ] . Chronic kidney disease can be defined as a state of affairs â€Å" when the maps of the kidneys have been so reduced by a chronic disease procedure † [ 24 ] . This may be seen as a consequence of the cumulative effects of a high-protein diet. However it should be noted that there is difference among different surveies as to the badness of such a disease and which symptoms would be present, if it were to happen. In chronic nephritic failure, the status can be exacerbated by a continued high-protein diet as this can take to increased keeping of certain ions, such as K or phosphate, which are released upon digestion of protein rich nutrients. If the patient besides has a instance of acidosis, this would decline a province of hyperkalaemia. The K found within cells is replaced with H ions, let go ofing more potassium ions into the organic structure fluids [ 24 ] . This is an illustration of how chronic kidney disease can come on due to increased kidney emphasis, brought about by an increased acid burden associated with a high protein diet. Many surveies have now found a nexus between high-protein consumption and osteoporosis. The thought is centred on the fact that a high degree of protein in the diet leads to hypercalciuria, or high degrees of Ca in the piss. One of the beginnings of this Ca is from the soaking up of dietetic Ca in the bowel. However, this addition is non big plenty to propose that this is the ground for hypercalcinuria. It is believed that the beginning of this Ca is bone and hence as a consequence, there is a lessening in skeletal mass. One of the theories to explicate this provinces that, due to the increased acid burden that consequences, nephritic handling of this burden through amminogenesis is non plenty. Calcium arising from the skeleton is released to be utilised as a buffer, before being excreted in the urine [ 21 ] . In the survey carried out by Frassetto et Al. in 2000 which looked at the hip break incidence ( HFI ) rate per 100,000 in adult females aged over 50 from states where per capit a nutrient ingestion information was available, found that â€Å" HFI in adult females over 50 is straight correlated with carnal protein ingestion † [ 22 ] . It should be noted nevertheless that there are surveies which suggest that a low-protein diet leads to a loss of bone-density. A survey done by Hannan et Al. found that â€Å" lower degrees of protein intake were associated with significantly higher rates of bone loss at the hip and spinal column † [ 25 ] . Specific nephritic pathology can be associated with this diet. One illustration is the oncoming of renal lithiasis or the presence of kidney rocks [ 26 ] . As already mentioned, one of the side-effects of a high-protein diet is hypercalicuria. This is a hazard factor for renal lithiasis. Animal protein consumption is linked with other factors which besides increase the hazard. These include ; a lessening in the soaking up of base from the GI piece of land, taking to a lessening of citrate elimination in the piss. As with many jobs associated with a high-protein diet, low saccharide consumption merely worsens the state of affairs. A lower consumption of fruit and veggies reduces dietetic beginnings of base.DecisionThe kidneys and nephritic system are responsible for a broad assortment of maps impacting multiple systems around the organic structure. In relation to acid-base balance, although the kidneys act in concurrence with other mechanisms to keep acid-base homeostasis, they must b e working usually in order withstand even infinitesimal alterations in organic structure fluid pH, caused by pathology or diet. Although the actions of the kidney in acid-base ordinance can be categorised depending on the how the concentration of three chief ions are changed, in order for the mechanisms affecting these to be fulfilled, many different but specific chemical reactions affecting many different countries of nephritic anatomy and biochemical substrates have to take topographic point. Physiological ordinance of acid-base balance can be greatly altered by an addition in dietetic protein intake, the effects of which are merely exacerbated by reduced saccharide consumption. Although the negative effects of such a diet were clear in all the diaries and text editions I have referenced, there is still elucidation needed as to the specific mechanisms of secondary pathology obtained after nephritic handling of this increased acid burden has diminished.

Pursuing a Career as a Physician - 644 Words

On the eve of my fifth birthday, my mother was rushed to the hospital for an emergency C-section. On this night, my sister was born two and a half months premature with a gastrointestinal blockage that sent her straight to the operating room and kept her in the Neonatal Intensive Care Unit for over three months. Unfortunately, I only had the opportunity to visit my sister a handful of times; my parents adamantly claimed the hospital was no place for kids. The fact that the hospital was off-limits to me peaked my curiosity about what transpired behind the closed doors. I yearned to understand the roles the doctors and nurses played in helping my sister come home. I also longed to see my parents smile and converse in their usual, carefree manner. These months were extremely difficult, as I struggled to grasp the rich complexity of the situation. At a tender age, I was exposed to the frailty of life and the stresses of illness on a family. Moreover, I developed a reverence for the physi cians who enabled my sister to come home and live a normal, healthy life. At the age of ten, there was another medical emergency within my family. My uncle flew to Miami from Jamaica to undergo a delicate cardiac procedure. Her spent the following two months recovering at my home. I did not understand the science underlying his condition, but I recall him being in severe pain. I wanted to help in any way I could, so I tended to his needs before and after school; I prepared his meals andShow MoreRelatedPursuing A Career As A Physician701 Words   |  3 PagesMy decision to pursue a career as a physician was not a blinding revelation, being the daughter of two immigrant parents the thought of becoming a physician seemed distant. In high school I pursued to obtain what for me was then the highest education I perceived I would be able to achieve which was going to college and obtaining a bachelor’s degree. As the quote by Ralph Ellison highlights, â€Å"When I discover who I am, I’ll be free†. This quote resonates with the start of my sec ond year in collegeRead MoreBecoming A Doctor Is Not An Easy Process For Majority Of The Population1351 Words   |  6 Pagesprocess for majority of the population; for others it’s natural. The career I find interesting and may pursue is a Pediatrics doctor. Pediatricians are doctors who specialize in children, ranging from new born babies to eighteen years old. Individuals interested in this field will need a sense of mentality and dedication to work hard. Becoming a doctor is not an easy process; it takes time, motivation, and interest for this type of career. Once an individual is half way through the schooling process ofRead MorePersonal Statement : Family Medicine920 Words   |  4 PagesFamily Physician At first, the career that I currently want to pursue used to surprise me, because I have been rebelling in taking interest in any medical career throughout my middle school and high school years due to my parents’ constant recommendations of the pediatrician occupation. However, during the summer after my high school graduation and when I first entered college, I have been intrigued by family medicine. The Jung-Typology test further strengthened my interest in family medicine byRead MoreWhat Qualities, Skills, Talents, And Experiences Of A Good Health Care Practitioner?1418 Words   |  6 PagesA. Career Choices 1. Describe the qualities, skills, talents, and experiences of a good health care practitioner. How do you exhibit them? A physician must be well rounded in a variety of fields to provide effective care. 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Shadowing the physician gave me a good sense of what his dailyRead MoreSelecting A Career Is Like Choosing A Character When Playing A Game1668 Words   |  7 PagesChoosing a career is like choosing a character when playing a game. A person has to stick with that character throughout the whole game unless that person restarts the plot. As humans, we have to work in order to survive in most cases. When choosing a career, it is what we’re usually stuck with until retirement, unless we go back to school or some other opportunity is given. As a freshman in college, I still have the chance to switch my major befo re I make any regrets. I took a self-assessment testRead MoreApplication For The Medical Assistant Position At Your Medical Practice974 Words   |  4 PagesThis email is in support of my application for the Medical Assistant position at your medical practice in Northwest Atlanta. I am excited to find this opportunity because it closely aligns with my interests and future aspirations of becoming a Physician Assistant. What is being offered is an opportunity that will allow me to hone and polish my interpersonal, communication, and technical skills, but to also develop new skill sets that some health professionals lack. I have a Bachelor’s of Arts inRead MorePhysician Assistant ( Pa )841 Words   |  4 Pageswould live; however, that day I learned that every patient is different. As a Physician Assistant (PA) I want to consider the entire combination of factors that make each person unique, analyzing all aspects of their life – physically and emotionally. Ultimatel y, this experience motivated me to channel all of my energy towards pursuing a career as a PA. The person who first sparked my interest in pursuing a career in medicine was my Mom. She used to tell me a story and say â€Å"you are one of myRead MoreI m Planning On Pursuing A Course1405 Words   |  6 Pagesplanning on pursuing a combined MD/Ph.D. program, which combines both medicine and research to train the next generation of physician-scientists. The path to becoming a physician-scientist is daunting and long, which could take up to 15 years. Aside from having both medical and research training, successfully physician-scientist should also be a problem solver, a critical thinker, resilient, a hard worker and good writer. Writing skills are very important in this field because physician-scientistsRead MoreThe Ethics Of The Patient774 Words   |  4 Pagesthe family in terminally ill cases. I had the opportunity to explore laboratory research in hematology while I was pursuing a research project on drug resistance in multiple myeloma at King’s College, London. There, in the department of hematological medicine, I met accomplished clinicians and researchers who inspired me to strive for my dream of the clinician/scientist model of career. In addition to the critical analysis essential for scientific research, long hours in the laboratory taught me patience