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Then answer the following questions: In the case study by Lunn et al (1998) the child is described as having "mild pitting oedema" and a moderately enlarged liver. Using appropriate literature briefly discuss the role of mechanisms that have been proposed to explain the development of these symptoms in subjects with kwashiorkor.
Kwashiorkor is a form of malnutrition that occurs when the diet is carbohydrate based, without the appropriate intake of protein, it has primarily identified in the developing world where the primary diet is easily accessible grains (Pelletier et al, 1995' Akiyam et al, 2008). The result is that although the calorie intake may be sufficient in the case of the British child, the body is starved of the necessary protein to have the body's growth and digestive system to function properly (Detsky et al, 1994). Therefore the necessary fat stores can reduce to just 5% and the remaining stores in the liver, which gives the impression of a "fatty" or slightly enlarged liver (Shah 2007). The impact of the protein malnutrition also causes the organ to enlarge and the pancreas, the result is that the fluid levels are increased and secreted throughout the system, because in part it is similar to the poisoning of the liver, which causes changes in the liver cells (Shah 2007). Also the endrocrine system is changed and the change in the lymphs, thyroids and liver affects the body secretions causing changes in the body including swelling of the legs and ankles (oedema) (Lunn 1998). The cause of oedema can be marked by albumin concentration of less than 30g/l that results in oedema from decreased oncoitic pressure (Shah 2007). This is due to the body's inability to process a purely carbohydrate diet, because the proteins that are necessary to build muscle mass and provide energy to the body are missing. (Lunn 1998) Whilst a carbohydrate only diet affects the glucose levels, because the carbohydrate metabolism has caused a reliance on the sugars in the body; however there is a level of intolerance to the glucose in carbohydrates that explains the poisoning effects that result in the malnutrition, fatty liver and the close down of the digestive system (Detsky et al, 1994). (Words 318)
How relevant are these mechanisms in the aetiology of the case of kwashiorkor described by Lunn et al (1998)?
There is a significant link to the patient in Lunn et al (1998), because although the patient is in Britain, the diet of choice was carbohydrate based. This means that there are a lot of parallels to the cases of kwashiorkor in the developing world. There are some significant differences, which include the supplementing of vitamins and the provision of pure glucose. The result is the same, because the essential protein/carbohydrate balance is missing. However, as Lunn et al (1998) identify the case is less severe and rapid stabilisation occurs when the patient gets a balanced diet, which will be in part to the parent's provision of essential vitamins and minerals that would be missing in the cases in the developing world.
What type of PEM is the patient in the case study by Hoffer (2001) suffering from?
From the BMI reduction and the reversibility of the condition in four weeks the case would be a moderate type of PEM, i.e. the body adapts to the changes to compensate, which means that it is possible to revert to pre-PEM state with a balanced diet. (45 words)
Explain, using appropriate literature, why this type of PEM is known as adaptive PEM. In your answer to this question do not rely solely on the information provided by Hoffer et al (2001) about adaptation. The biochemical basis for this adaptation must form part of your discussion.
If the body is malnourished it will automatically try to compensate to continue its survival; hence the term adaptive PEM (Lazzerini & Rofani, 2008). Therefore the body continues to function in a manner that can survive on a lower calorie intake (Emery, 2005). As Hoffer et al (2001) indicate the body will reduce its protein store and reduce its metabolic rate in order to achieve a zero protein and energy balance. If the balance is achieved then the body can continue to survive in this adaptive state (Lazzerini & Rofani, 2008). Therefore, the patient's weight is important to identify the type of PEM. The adaptive PEM can be identified with reduced muscle mass, serum prealbumin, reduced but constant body weight and normal serum albumin. It is the connection between the serum albumin that is the most significant indicator in adaptive PEM (Hoffer et al, 2001). The reason for the albumin to remain the same is indicative that the organs and the body have managed to function in the lower nutritional state; hence no oedema (Morley, 1999). However, the prealbumin is directly related to protein intake and as protein intake decreases so does the prealbumin (Morley, 1999). Therefore, in adaptive PEM there is normal albumin and reduced prealbumin (Hoffer et al, 2001). The key biomedical function is that the metabolism has altered its state so that additional stress and pressures are not placed on the main organs and survival is switched on (Lazzerini & Rofani, 2008). How the body does this is that the body minimises the protein metabolising mechanisms and diverts the energy to the mechanisms of the vital organs, which includes the amino acids being diverted to the vital organs (Morley, 1999). These amino acids are recycled by the liver for creation of the needed key proteins, albumin is maintained; gamma globulins increased to battle the increased probability of infections and the prealbumins are decreased as not needed to metabolise protein (Morley, 1999). This survival mode when switched on and maintained means that if nutrition, especially the increased intake of protein, are increased to normal levels the body re-adapts to the normal body functions far easier (Lazzerini & Rofani, 2008). However, if there is additional metabolic stress, micronutrient deficiency and/or the starvation is too severe then the adaptation fails and if not quickly reversed (if possible) then death is inevitable (Hoffer et al, 2001). (395 Words)
In the introduction to the case study by Lunn et al (1998) it states that: "The central role of dietary protein inadequacy particularly in the presence of an adequate intake of energy has been confirmed" (in the development of kwashiorkor). Using appropriate literature discuss the validity of this statement. In discussing the validity of this statement you must also address the conclusion made by Lunn et al (1998): "... and the term 'kwashiorkor' limited to the metabbolic disorder resulting primarily from dietary protein insufficiency in the presence of a relative adequacy of energy."
The term kwashiorkor was developed in 1933 and relates to malnutrition and the over focus on the intake of carbohydrates (Lunn 1998). It has been further highlighted by the misunderstanding in breastfeeding in the developing world, where the foods after weaning have been poor in protein (Lunn et al, 2008). A lot of research has been collated in the developing world where the changed patterns in breastfeeding by Western norms caused children to have higher instances of malnutrition, because the mother eating the limited protein is able to produce protein for the milk which the child consumes (Pelletier et al, 1995). However, the weaning diet is carbohydrate rich, which causes starvation and malnutrition because the necessary proteins are missing to help the body grow and function. Hence the instances of kwashiorkor are more apparent in the developed world where grains are easily accessible; however proteins are too expensive to produce (Pelletier et al, 2005). Therefore the lack of protein is the key indicator of kwashiorkor, because the differences between the longer breastfed baby's chances to the early weaner is a key indicator of the role in protein in the diet this has lead to the breastmilk is best slogan by the WHO, which is reflected in case of the British child where the baby is a early weaner on primarily carbohydrates (Lunn et al, 1998). In the terms of Lunn (1998) original study and the understanding of kwashiorkor is due to limited protein resulting in a lack of energy, which results in starvation or adaptation. Therefore it is important to retain this term in relation to protein based deficiencies; otherwise the term will be used incorrectly and the diagnosis may not help the patient. It is important that there is a link between maramus and kwashiorkor, because they are different stages of protein malnutrition; however maramus is the case where the body has adapted to the protein malnutrition and referred to sometimes as kwashiorkor-maramus. Yet there is validity in the argument of Lunn et al (1998) to ensure that the treatments and biomedical traits are identifiable. (Words 355)
The case study by Hoffer (2001) briefly discusses the impact of some malignancies on body weight and the role of cytokines and acute phase proteins. Using appropriate literature critically discuss the role of cytokines and acute phase proteins in contributing to the PEM you have identified in your answer to the first part of question 2. Include in your answer how such a factor, malignancy, can contribute to failed adaptation to PEM. In addition, your discussion must also address the role of other factors that may contribute to PEM associated with malignancy.
The cytokines are the biomedical functions that cause the increase and decrease in albumin, as Morley (1999) indicates the transport proteins such as prealbumin are a primary indicator of whether the patient is responding to treatment. It increases, because the cytokines are increased and decreased accordingly. Protein is essential to cytokine production and without this necessary protein they decrease, which causes the intake of food to be reduced (Hoffer et al, 1998). Therefore, therapeutic diets are the greatest cause of malnutrition because the person causes a chemical depression because the food is not appealing, which results in the body causing a decreased food intake (Morley, 1999). In the developing world, this malnutrition is enforced by the situation, a carbohydrate heavy diet and the body purposely going into starvation mode (Pelletier et al, 2005). The cytokine reduction is creating the body synthesis to adapt to the lack of nutrition or desire for the food, creating survival mode. In the case of Hoffer et al's (2001) patient has mirrored this process because of the timing, pain and inability to access the food, which has resulted in the cytokines producing the survival mode which is indicated in the prealbumin reduction, but the albumin stabilisation. However, as Hoffer et al (2001) and Morley (1999) indicate the measurement of the whether a cytokine reduction is difficult to measure, both in the albumin levels and prealbumin levels. Hence the importance of cytokine production is that it plays an important role in the feeling of satiation, which is a primary reason that there can be an increased malnutrition and PEM in elderly patients because the process goes haywire and the patients are unable to adjust their food intake (Roberts et al, 1994). This may also be reflective in the depressed patient syndrome, because their body is unable to regulate its intake, which relates into an inability to eat (Morley, 1999). This can go to the other extreme as well (Morley, 1999). Hence it is very important that the cytokine process and its indicators, such as albumin and prealbumin are better understood in order to identify the clinical and biomedical differences between the adaptive and maladaptive states of PEM (Hoffer et al, 1998). (Words 365)
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