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Posted On : 03 Sep 2018

respected madam, sir, i recently read about severe acute malnutrition and the pathophysiology{incomplete} in the aug 2010 indian pediatrics by m. golden. i want to know the complete pathophysiology of kwashiorker and marasmus, sam.
regards
sachin d

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egypt lover

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6 years ago

Answer 1

In marasmus, energy intake is insufficient for the body`s requirements, and the body draws on its own stores. Liver glycogen is exhausted within a few hours, and skeletal muscle protein is then used via gluconeogenesis to maintain adequate plasma glucose. At the same time, triglycerides in fat depots are broken down into free fatty acids, which provide some energy for most tissues, but not for the nervous system. When near starvation is prolonged, fatty acids are incompletely oxidized to ketone bodies, which can be used by the brain and other organs for energy. Thus, in the severe energy deficiency of marasmus, adaptation is facilitated by high cortisol and Growth Hormone levels and depression of Insulin and thyroid hormone secretion. Because Amino Acids are mobilized from muscle to provide the liver with substrate for protein synthesis, plasma protein levels decrease less in marasmus than in kwashiorkor.

In kwashiorkor, relatively increased carbohydrate intake with decreased protein intake leads to decreased visceral protein synthesis. The resulting hypoalbuminemia causes dependent edema, and impaired -lipoprotein synthesis causes fatty liver. Insulin secretion is initially stimulated but is reduced later in the disease. Fat mobilization and amino acid release from muscle are reduced, so that less amino acid substrate is available to the liver.

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