Patients with Hepatic Cirrhosis Nursing Process

Patients with Hepatic Cirrhosis Nursing Process

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Patients with Hepatic Cirrhosis Nursing Process

Patients with Hepatic Cirrhosis Nursing Process

This paper contains about a little knowledge about the Nursing Process Patient oneheath.blogspot.com Hepatic Cirrhosis, Hepatic Cirrhosis Patients Nursing Process must be done correctly. The following paper on the Nursing Process Patients with Hepatic Cirrhosis by oneheath.blogspot.com

Patients with Hepatic Cirrhosis Nursing Process

The liver is one organ that is very important role in regulating the body's metabolism, which is in the process of anabolism or synthesis of materials essential to human life such as protein synthesis and the formation of glucose, while in the process of catabolism by doing detoxification ingredients such as ammonia, various types of hormones and drugs. In addition, the liver also acts as a storage shed where materials such as glycogen and some vitamins and maintain splanchnic blood flow normal. Therefore there is damage to liver cells parenkhim severe acute or chronic, these functions will have the disorder or chaos, so that abnormalities can arise such as hepatic encephalopathy (Akil., 1998).


A. DEFINITION KOMA hepatic (hepatic encephalopathy)

Describe the stages of hepatic coma hepatic encephalopathy further.

Here are some definitions according to some figures, including:

· Hepatic encephalopathy is a neuropsychiatric syndrome, has a broad clinical spectrum, may arise due to severe liver disease, either acute or chronic disorder characterized by behavioral, neurologic symptoms, astriksis, various degrees of disturbance of consciousness to coma, and abnormal electro ensefalografi ( Blei., 1999).

· Hepatic Enselafalopati (EH) is a neuropsychiatric syndrome that occurs in liver disease. The definition menyiratkn that the clinical spectrum (EH) is very broad, because it also termauk patients with fulminant hepatitis and cirrhosis in patients with stage Subclinical Hepatic Encephalopathy (EHS) (Budihusodo., 2001).

· Hepatic encephalopathy is a complex of a central nervous system disorders encountered who develop liver failure. The disorder is characterized by memory impairment and personality changes (Corwin., 2001).

· Hepatic encephalopathy (portal system encephalopathy, hepatic coma) is a disorder in which brain function decline due to toxic substances in the blood, which normally removed by the liver (Stein 2001).

· Hepatic encephalopathy is a neuropsychiatric syndrome in patients with severe liver disease. This syndrome is characterized by mental confusion, muscle tremors and flapping tremor called asterixis (Price et al., 1995).

B. CLASSIFICATION

EH classification is widely adopted:

1) According to the occurrence

a. EH Acute type:

Arise suddenly with a short disease course, falls very quickly deteriorate into a coma, often less than 24 hours. These types include fulminant viral hepatitis, hepatitis due to drugs and toxins, Reye syndrome or can be in liver cirrhosis.

b. EH Chronic type:

Occurred in a period of time, for months to years. A classic example is that EH occurs in cirrhotic liver with extensive portal collateral system, with signs of mental disorders, emotional or nueurologik disorder that gradually more and more weight.

2) According to the etiology factor

a. EH Primary / Endogen

Occur without the presence of trigger factors, is the final stage of damage to liver cells that diffuse liver cell necrosis is widespread. In fulminant hepatitis damage liver cells and diffuse rapidly, so that impaired consciousness, restlessness, disorientation arises, screaming, and then quickly fell in a coma, while in the liver caused siridis fibrosi widespread liver cells and usually have no collateral system, ascites. Here disruption caused by toxic substances that can not be metabolized by the liver. Through the portal system / collateral affects the central nervous system.

b. EH Secondary / Exogenous

Is due to the trigger factors in pederita who already have heart abnormalities. These factors include:

1. Disorders of fluid balance, electrolyte and blood pH:

         o Dehydration / hypovolemia

        o Parasintesis abdominal

        o excessive diuresis

2. Gastrointestinal bleeding

3. Major surgery

4. Severe infections

5. Excessive protein intake

6. Constipation long protracted

7. Drug - drug narcotic / hypnotic

8. Shortcuts portal systemic, either naturally or surgically

9. Azotemia


C. Etiology

Ingredients that are absorbed into the bloodstream from the intestines, will pass through the liver, where the poison-poison dumped on hepatic encephalopathy, which occurs is:

a. These toxins are not removed because liver function is impaired.

b. Has formed a relationship between the portal and general circulation system (as a result of liver disease), so the toxins through the liver tadak.

c. Bypass surgery to correct portal hypertension (portal shunt system) will also cause some of the toxins do not cross hati.apapun cause, the result is the arrival of toxins in the brain and affect brain function.

What materials are toxic to the brain, definitely not diketahui.tetapi high levels of protein breakdown products in blood, such as ammonia, apparently memegag an important role.

In patients with chronic liver disease, encephalopathy is usually triggered by:

a. Acute infection.

b. The use of alcohol.

c. Eating too much protein, which will increase levels of protein breakdown in the blood.

d. Bleeding in the digestive tract, eg in esophageal varices, also bias the results lead to the accumulation of protein breakdown, which is langsungbisa about the brain.

e. Certain medications, especially sleeping pills, sedatives and diuretics (azotemia, hypovolemia).

f. Obstipasi increase production, absopsi nitrogen ammonia and other toxins.

C. Pathogenesis

There are currently no patagonesis accepted to explain the occurrence of EH. Several hypotheses are most often used as a reference treatment of EH is (1) Hypothesis ammonia, (2) Hypothesis neurotoksi synergistic, (3) false neurotransmitter hypothesis, (4) Hypothesis GABA / benzodiazepine (Budihusodo., 2002).

While the factors that are likely to be involved in the occurrence of EH are:

1. Effect of endogenous neurotoxins that are not sufficiently didetoksifisikasikan by cirrhotic liver.

2. Abnormal astroglia function disturbances accompanied by a secondary function of neurons.

3. Abnormalities permeablitas blood-brain barrier.

4. Changes in intracerebral neurotransmitters and their receptors.

In the simplest sense, the EH can be explained as a form of intosikiasi brain caused by intestinal contents is not in metabolism by the liver. This situation can occur when there is liver cell damage by necrosis, or the presence of shunt (pataologis or due to surgery) that allows the portal blood reaches the systemic circulation in large numbers without passing through the liver (Price et al., 1995).

Metabolite responsible for the onset of the EH is not known with certainty. The basic mechanism is apparently due to intosikasi brain by solving the metabolism of proteins by bacteria in the gut. The results of this metabolism could bypass the liver because of the disease on liver cells or because the shunt (Price et al., 1995).

EH on chronic liver disease is usually precipitated by circumstances such as gastrointestinal bleeding, excessive protein intake, diuretics, paracentesis, hypokalemia, acute infection, surgery, azotemia and administration of morphine, sedatives, or drugs that contain ammonia (Abou-assi. , 2001).

Up to now not yet fully understood pathogenesis of EH, but the knowledge gained by a study of patients and from animal experiments, have revealed several important issues regarding pathogenesis. EH is not caused by one single factor but by several factors that also play together (Blei., 1999).

Most studies show that the E there is a relationship of porto systemic circulation directly without going through the liver, and the presence of liver damage and severe physiological disturbances. Both these conditions cause tosik materials originating from the gut is not metabolized in the liver, and subsequently buried in the brain (blood brain barrier) in patients with EH which facilitates the entry of materials tosik into the central nervous system.

When patients have undergone liver cirrhosis portal hypertension, opens the possibility for the occurrence of portosistemik shortcuts, which can result in the entry of neurotoxins derived from the gastrointestinal tract (mercaptans, ammonia, manganese, etc.) into the systemic circulation. Shortcuts portosistemik may also occur due to surgical anastomosis portokaval or TIPS (transjugular intrahepatic portosystemic stent shunt) is done to resolve portal hypertension. Neurotoxin that can penetrate the blood brain barrier will accumulate in the brain and cause disturbances in brain metabolism. Barrier permeability of the blood - brain is experiencing changes in patients with decompensated liver cirrhosis, so it is more easily penetrated by metabolites such as neurotoxins (Budihusodo., 2001).

There are five processes that occur in the brain which is considered as a mechanism of EH / hepatic coma, namely:

1. Increased permeability of brain barrier (BBB).

2. Impaired balance of neurotransmitters

3. Changes (energy) metabolism of the brain.

4. Impaired membrane function of neurons.

5. Improved "endogenous benzodiazepines"

Suspected cerebral toxins act through one or more than this mechanism.

Pathogenesis of the above is a uniform concept, but the commas on the PSE and FHF there are some differences. For example on the PSE, cerebral toxins accumulate slowly, if accompanied trigger the occurrence of coma. In contrast to the EH / FHF-induced coma, because the process is so acute, the factors that contribute to the entry of toxic material into the brain of a sudden, the disappearance of protective materials, and integration of cellular changes permeablitas blood vessels of the brain and cerebral edema.

Some of the suspected toxic materials play a role:

1. Ammonia

Ammonia is the most widely investigated materials. This substance is derived from the decomposition of nitrogen by bacteria in the gut, in addition to that produced by the kidneys, peripheral muscle tissue, brain and stomach.

In theory ammonia interfere with brain physiology through.

Penaruh directly to the membranes of neurons
Affect the metabolism of the brain through a cycle of increased synthesis of glutamine and ketoglutarate, both these materials affect the Kreb cycle, causing the loss of ATP molecules required for cell oxidation.
Other researchers found that high levels of ammonia are not keeping pace with the severity of abnormal EEG recordings. Reported that the role of ammonia in the EH does not stand alone. But together other substances such as mercaptans and short chain fatty acids. Anticipated increase in ammonia levels in EH only a nonspecific indicator of brain metabolism is disturbed (A. Blake, 2003).


2. Neurotoxic amino acids (tryptophan, methionine, and mercaptans)

Triptopan serotonin and their metabolites are toxic to the CNS. Methionine in the intestinal bacteria into mercaptan metaolisme by which toxic to the CNS. In addition, mercaptans and free fatty acids will work synergistically interfere with detoxification of ammonia in the brain, and together causing coma ammonia (A. Blake, 2003).


3. Impaired balance of amino acids

Aromatic Amino Acids (AAA) is increased in EH because of the failure of deamination in the liver and decreased Asan Branch Chain Amino (AARC) due to protein catabolism in muscle and kidney that occurs hyperinsulinemia in chronic liver disease (A. Blake, 2003). AAA is competing with AARC to pass through the brain barrier, the permeability changes at the EH. Including the AAA is methionine, phenylalanine, tyrosine, while the included AARC is valine, leucine, and isoleucine (A. Blake, 2003)


4. Short chain fatty acids

In EH contained increased levels of short chain fatty acids such as butyric acid, valerate, octanoate, and kaproat, suspected as one cause of EH cerebral toxin. These materials work by suppressing the brain reticular system, saving ammonia detoxification (Gitlin., 1996).


5. Neurotramsmitter false

Neurot rasmitter fake that has been known is gamma aminobutyric acid (GABA), oktapamin, histamine, feniletanolamin, and serotonin. False neurotransmitter an inhibitor of the true kompepetif neurotrasmitter (dopamine and norephinephrine) at the synapse in the nerve endings, whose levels are decreased in patients with PSE and FHF (Gitlin., 1996).

Research indicates that GABA works synergistically with benzodiasepine form a complex, occupying a chloride ionophore receptors in the brain, called GABA receptor / BZ. Binding of these receptors will cause hiperpolarisasi brain cells, in addition also suppress the function of cortical and subcortical, a series of events that lead to impaired consciousness and motor coordination. This hypothesis opens the way for further research for the purposes of (Gitlin., 1996).


6. Glucagon

Increased AAA on EH / hepatic coma had close ties with high levels of glucagon. Elevation of glucagon contributed to the increased nitrogen load. Because this hormone release from the protein aromatic amino acids stimulate the liver to gluconeogenesis. Glucagon levels rise due to hypersecretion or hypometabolism in liver disease, especially when there is collateral circulation (A. Blake, 2003).


7. Changes in the blood brain barrier

The blood vessels of the brain under normal circumstances is not permeable to various substances. There is a strong relationship between brain capillary endothelial, this is a barrier that regulates a variety of substances spending and hold several essential substances such as neurotrasmitter original. In particular hepatic coma FHF found capillary damage, broken relationships endothelial, cerebral edema, so the material is usually removed from the brain will fit easily in large numbers are like phenylalanine, so that other woods amino acid levels increased in the brain (Gitlin., 1996).


Patients with Hepatic Cirrhosis Nursing Process

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