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 several effects on the different body systems but especially on the digestive system. Patients with elevated ammonia levels might present with nausea and vomiting, loss of appetite, back, flank, or abdominal pain, weakness and fatigue, et cetera. Hyperammonemia can also cause great damage when it travels through the blood stream into the nervous system. Such as in the case study, a patient with liver damage is at a great risk for hepatic encephalopathy, which is the failure of the brain to function correctly due to toxic buildup caused by liver insufficiency. Ammonia exists in the blood in both its toxic, gaseous and nontoxic, ionic state. Because it cannot cross the blood-brain barrier in its ionized state, the more toxic, gaseous form enters the blood-brain barrier by means of diffusion (Goldbecker, 2010). Once in the brain, ammonia affects neurons and astrocytes adversely by impairing their function and eventually killing them. Neurons lack the capacity to fight against high ammonia levels so they are most affected. Astrocytes, however, are home to glutamine synthetase, an enzyme which combines the amino acid glutamate with ammonia to form glutamine which can then be used by the kidneys and intestines for energy production (). Adversely, excessive accumulation of glutamine can cause ammonia-induced astrocytic impairments that may result in cerebral edema, which can be a cause of hepatic encephalopathy associated death. Increasing ammonia levels also increase the permeability of the blood-brain barrier which creates a continuous cycle. Although the astrocytes work hard to eliminate the ammonia, they are unable to get rid of all of it, especially with the increased permeability. Ammonia also short-circuits the transport of potassium into glial cells resulting in an accumulation of potassium around nerve cells which causes a decrease in defense against the toxicity. The main function of neurons is signal transmission between the central nervous system and peripheral nervous system. Therefore, the patient diagnosed with hepatic encephalopathy may present with confusion, irritability, lack of focus, delirium, and headache (Lewis, 2014). In this case study, 68 year old Mr. …show more content…
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 confusion. An electroencephalography test is usually administered for patients presenting with altered mental status and cirrhosis in order to rule out seizure activity. An EEG is not, however, used to diagnose hepatic encephalopathy. After diagnosis, the treatment plan involves treating the underlying cause (liver cirrhosis), rather than the symptoms. References Goldbecker, A., Buchert, R., Berding, G., Bokemeyer, M., Lichtinghagen, R., Wilke, F., . . . Weissenborn, K. (2010). Blood–brain barrier permeability for ammonia in patients with different grades of liver fibrosis
Hyperammonemia can have several effects on the different body systems but especially on the digestive system. Patients with elevated ammonia levels might present with nausea and vomiting, loss of appetite, back, flank, or abdominal pain, weakness and fatigue, et cetera. Hyperammonemia can also cause great damage when it travels through the blood stream into the nervous system. Such as in the case study, a patient with liver damage is at a great risk for hepatic encephalopathy, which is the failure of the brain to function correctly due to toxic buildup caused by liver insufficiency. Ammonia exists in the blood in both its toxic, gaseous and nontoxic, ionic state. Because it cannot cross the blood-brain barrier in its ionized state, the more toxic, gaseous form enters the blood-brain barrier by means of diffusion (Goldbecker, 2010). Once in the brain, ammonia affects neurons and astrocytes adversely by impairing their function and eventually killing them. Neurons lack the capacity to fight against high ammonia levels so they are most affected. Astrocytes, however, are home to glutamine synthetase, an enzyme which combines the amino acid glutamate with ammonia to form glutamine which can then be used by the kidneys and intestines for energy production (). Adversely, excessive accumulation of glutamine can cause ammonia-induced astrocytic impairments that may result in cerebral edema, which can be a cause of hepatic encephalopathy associated death. Increasing ammonia levels also increase the permeability of the blood-brain barrier which creates a continuous cycle. Although the astrocytes work hard to eliminate the ammonia, they are unable to get rid of all of it, especially with the increased permeability. Ammonia also short-circuits the transport of potassium into glial cells resulting in an accumulation of potassium around nerve cells which causes a decrease in defense against the toxicity. The main function of neurons is signal transmission between the central nervous system and peripheral nervous system. Therefore, the patient diagnosed with hepatic encephalopathy may present with confusion, irritability, lack of focus, delirium, and headache (Lewis, 2014). In this case study, 68 year old Mr. …show more content…
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 confusion. An electroencephalography test is usually administered for patients presenting with altered mental status and cirrhosis in order to rule out seizure activity. An EEG is not, however, used to diagnose hepatic encephalopathy. After diagnosis, the treatment plan involves treating the underlying cause (liver cirrhosis), rather than the symptoms. References Goldbecker, A., Buchert, R., Berding, G., Bokemeyer, M., Lichtinghagen, R., Wilke, F., . . . Weissenborn, K. (2010). Blood–brain barrier permeability for ammonia in patients with different grades of liver fibrosis