Hyperammonemia Case Study Essay

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Register to read the introduction… Primarily, it is created in the intestinal tract, usually from the bacterial degradation of nitrogen found in ingested food, filtered out into urea by the liver, and excreted by the kidneys. The ammonia that is breathed in is usually also immediately breathed out. Ammonia that is ingested is also immediately absorbed into the bloodstream and is excreted immediately or turned into a less harmful substance. Its most toxic effects are found at the areas of direct contact such as the mucous membranes, skin, and digestive tract. While the body does a superb job of maintaining the correct balance of ammonia essential for human life, there are instances where ammonia can build up and become toxic to the body. This elevation of ammonia levels in the bloodstream, Hyperammonemia, is usually indicative of liver or kidney insufficiency or failure or drug and alcohol abuse. Hyperammonemia could also be indicative of failure of other organ such as heart and small and large intestines (Lewis, 1030).
Hyperammonemia can have
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T.C. arrived in the emergency department with altered mental status. His medical history included extreme liver failure and he was on the waiting list for a liver transplant. He also had a history of social smoking and drinking which are huge risk factor for liver damage. Upon assessing, his serum ammonia level is 78 mg/dl, where the normal range is 15-45 mg/dl, a finding that is consistent with his diagnosis of hepatic encephalopathy. Laboratory results usually also show signs of hepatic dysfunction and electrolyte imbalances such as hyponatremia and hypokalemia. Mr. T.C. was treated with Xifacan, antibiotics to decrease the production of ammonia. Lactulose to aide in excreting the ammonia through stool production, as well as normal saline for fluid loss resulting in

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