Although the person may not recognise the connection, self-harm often becomes a response to profound and overwhelming emotional pain that cannot be resolved in a more functional way.The motivations for self-harm vary, as it may be used to fulfill a number of different functions. These functions include self-harm being used as a coping mechanism which provides temporary relief of intense feelings such as anxiety, depression, stress, emotional numbness and a sense of failure or self-loathing. There is also a positive statistical correlation between self-harm and emotional abuse. Self-harm may become a means of managing and controlling pain, in contrast to the pain experienced earlier in the persons life over which they had no control (e.g., through abuse).Other motives for self-harm do not fit into medicalized models of behavior and may seem incomprehensible to others, as demonstrated by this quotation:
"My motivations for self-harming were diverse, but included examining the interior of my arms for hydraulic lines. This may sound strange. "Assessment of motives in a medical setting is usually based on precursors to the incident, circumstances, and information from the patient. However, limited studies show that professional assessments tend to suggest more manipulative or punitive motives than personal assessments.A UK Office for National Statistics study reported only two motives: "to draw attention" and "because of anger". For some people, harming themselves can be a means of drawing attention to the need for help and to ask for assistance in an indirect way.
Aminoaciduria occurs when the urine contains abnormally high amounts of amino acids. In the healthy kidney, the glomeruli filter all amino acids out of the blood, and the renal tubules then reabsorb over 95% of the filtered amino acids back into the blood.In overflow aminoaciduria, abnormally high concentrations of amino acids in the blood plasma overwhelm the resorptive capacity of the renal tubules, resulting in high concentrations of amino acids in the urine. This may be caused by congenital disorders of amino acid metabolism, for example, phenylketonuria, or may be secondary to liver disease.In renal aminoaciduria, the renal tubules are unable to reabsorb the filtered amino acids back into the blood, causing high concentrations of amino acids in the urine. This may be caused by a defect in the transport proteins in the renal tubule, for example, as occurs in Hartnup disease, or may be due to damage to the kidney tubule, for example, as occurs in Fanconi syndrome. References


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