Living organisms constitute a machine-like automated system which controls the various chemical processes that enhance its functioning. Its anatomy comprises of different organs, with each single organ designated a unique life-enhancing role in all living organisms. The overall functioning of the living organism is determined by the condition of the organs that control its life processes, and a serious defect on one organ will result in a significant dysfunctional state of the whole system. In human beings, a defection or infection of a crucial organ can lead to the disruption of chemical balances in the body, which in turn could cause serious deteriorations in health, and eventually death. The liver particularly, is an important organ in the functioning of the human body, since it controls and regulates various life enhancing processes such as metabolism, excretion, respiration and osmoregulation. As such, an infection to the liver portends serious health consequences to the whole body. A common liver infection is inflammation, which destroys its cells and leads to liver failure. If the condition is not reversed earlier, it develops to a near-chronic condition, which in medical terms is referred to as hepatic encephalopathy. By referring to the case study of Mrs. Mary Green, the paper discusses the condition of liver failure in the human body, and its development to hepatic encephalopathy. Specifically, it details the pathophysiological characteristics that define liver dysfunction, typical signs and symptoms, its pharmacology, contextual analysis of Mrs. Green’s condition, and the effect of body mass index (BMI) on the pathophysiology of the condition.( Czaja, A. 2007)
It is also known as Portosystemtic encephalophathy. It is characterized by altered level of consciousness, coma and confusion that results from liver failure. It is called hepatic coma when in its advance stage and may lead to death.
It results from the accumulation of toxic substances in the blood stream that needs to be removed by the liver. Diagnosing hepatic encephalopathy requires an impaired liver fuction and blood tests for ammonia levels. Attacks of the disease are often precipitated by recurrent problems such as infections and constipation. Suppression in the production of toxic substance in the small intestines can reverse Hepatic encephalopathy. This is mainly done with the non –absorbable antibiotics or with laxative lactulose. Moreover, treatment of the underlying conditions can improve symptoms. In specific settings of acute liver failure, the onset of encephalopathy is likely to require kidney transplant. (Gines, P. 2005).
It is difficult to detect the mildest form of hepatic encephalopathy. However it can be demonstrated through neuropsychological testing. The main symptoms are mild confusion, forgetfulness and irritability. Severe symptoms of encephalopathy are characterized by inverted sleep-wake pattern, tremor, marked irritability, coordination difficulties and trouble writing. In more severe forms, it can lead to a worsened level of consciousness- from lethargy to samnolance and eventually to a coma. Jerking movements of the limbs can be observed in the initial stages but tend to disappear as somnolence worsens. At this stage, there is amnesia and disorientation, and in some circumstances uninhibited behavior may occur. Seizure and coma represents the advanced stage of the disease and often leads to death. (Shaffer, E. A. June 2009).
Patients with severe encephalopathy stay at risky of obstruction of their airway as a result of reduced protective reflexes like the gag reflex. This can cause respiratory arrest. The patients should be nursed in an appropriate area such as the intensive care unit with the intubations of the airway. In cases of low consciousness, there is a high risk of aspiration pneumonia. In this circumstance, a nasogastric tube is inserted to allow safe administration of medicine and nutrients. Treatment of hepatic encephalophy heavily depends on the underlying causes (types A, B or C). If it develops an acute liver failure then, a liver transplant will be necessary from a specialist centre. (McLaughlin, R. N. Sep 22, 2006)
QZ 1 Liver Failure
As a major organ of the body, the liver plays a key role in the metabolism of substances and their excretion, synthesis of proteins, regulation of nutrients such as cholesterol, glucose and amino acids. The liver’s major cells are called hepatocytes, and they are responsible for the physiological functioning of the liver (Bullock, 2007). Damage to these cells or an inhibition of their functioning is the major cause of liver failure.
By definition, liver failure is a condition characterized by the inability of the liver to function normally, especially in controlling metabolic and synthetic body processes. There are two types of liver failure:
Acute liver failure is the development of hepatic encephalopathy, which is characterized by psychological and mental interruptions, such as confusion and getting into a coma, physiological disorders such as decreased rate of protein metabolism. A rapid deterioration in the functioning of liver causes coagulopathy (poor blood clotting) and the alteration of mental functioning. Acute liver failure is mainly caused by the effect of drug toxins on the liver, a process called hepatoxicity.
Chronic liver failure results from cirrhosis, which is usually caused by damage to the liver due to heavy drinking, metabolic disorders such as excess copper or iron in the body and hepatitis B or C. Additionally, the condition is hereditary and can be inherited through genetic transfer.
Pathophysiology of Liver Failure
Acute liver failure often results in cerebral edema, which in turn causes morbidity in patients or death. It affects the normal functioning of the brain, a condition known as intra-cranial hypertension (ICH). Impaired cellular functioning of the brain due to poor osmoregulation causes fluid imbalances in the brain cells, leading to an increased brain volume, and eventually a condition known as cytotoxic edema (Heidelbaugh, 2006). Similarly, cerebral edema can result can develop due to an accumulation of glutamine in the brain. Glutamine concentration in the brain’s astrocyte cells causes swelling and brain edema. Chemical imbalances in the brain due to liver failure increase the secretion of the enzyme glutamine synthetase, which detoxifies ammonia to glutamine through the process of amidation. In alcoholic patients, liver injuries induced by “viral and therapeutic drugs can be synergistic with alcohol toxicity and lead to chronic liver failure” (Schiff, et al, 2007, 875).
Another pathophysiological phenomenon of liver failure is an upsurge of intracranial blood level and blood circulation in the cerebrum due to poor cerebral auto-regulation. Liver failure leads to poor excretion of toxic substances from the brain, especially nitric acid which widens the brain’s blood vessels through vasodilation, resulting in high rate of blood flow. This condition interferes with brain functioning, which causes perceptional failure, resulting in consciousness alteration, in which the patient fails to recognize his environment accurately. At this stage, the condition of liver failure is hepatic, which is attributed to the condition of Mrs. Green after she failed to distinguish between a cup and a plate, or a chair from a table.
QZ 2 Signs and Symptoms of Liver Failure
Swelling in the abdomen and legs
The liver plays an important role in regulating body fluids through the process of osmoregulation. Infections that damage more than 75 percent of he liver’s cells causes a serious impairment in its functioning. As a result, body fluids, called ascites, seep out of the blood stream due to the liver’s failure to produce vital blood proteins. Low levels of fluids in the blood stream causes high salt concentration in the blood stream, which in turn causes the movement of fluids into the body tissues through the process of diffusion. The seepage of fluids into body tissues especially in the abdomen and legs is responsible for the development of edema. It is characterized by a protruding belly, swellings in the legs, arms and in some cases on the face.
In cases of chronic liver failure, fibrosis, which is a scarring of the liver as a result of damage to liver cells, develops. Cirrhosis develops when the fibrosis becomes advanced. A complication of cirrhosis in turn causes ascites- excessive body fluids that accumulate in the lower abdomen, also known as the peritoneal cavity. It causes a bulging of the abdomen, which often appears as a protrusion of the belly. The development of ascites is attributed to two factors. First, there is an increase in pressure in the vein carrying blood from the intestines, spleen and stomach to the liver, which causes portal hypertension. Secondly, low levels of blood albumin, a condition known as hypoalbuminemia, leads to imbalances of blood volume. In cirrhosis, the blood volume is greatly reduced as the liver cannot not sufficiently produce albumin. The combination of high portal hypertension and hypoalbuminemia causes fluid seepage into the tissues, the dilation of verices (veins in the esophagus) and the enlargement of the spleen, leading to general edema. Generally, these conditions develop due to the increase of pressure in the veins and the accumulation of fluid in blood vessels in the abdomen. Moreover, hypoalbuminemia can make the kidney to retain body fluids and salt, and cause peripheral edema, which is the swelling of the legs.
Bleeding and poor blood clotting
The liver is responsible for the production of essential blood clotting substances, such as fibrins and prothrombin, which are involved in coagulation. Liver failure prevents the production of these substances due to damage of involved cells. This is especially the case in cirrhosis related liver failure and in alcoholic patients. The deficiency of blood proteins in the body causes gum bleeding during brushing and frequent hemorrhage in bruises and the thrombosis, which hinders clotting. Due to advanced cirrhosis, the inflammation of the liver’s cellular cells causes serious internal hemorrhage (Jutabha, 2005). Hemorrhage into the abdomen is responsible for pain in the lower abdomen, and is often life threatening.
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