VI. Pathophysiology

inches

Predisposing Factors Male

35 years oldRace: Asian

Nationality: FilipinoFamily History of Alcohol

Drinkers

Hepatocyte Damage

Liver Inflammation Pain, Fever,

Anorexia, Increased

WBC, Fatigue,

N/V

Alteration in Blood and Lymph Flow

Liver Necrosis

Decreased ADH and aldosterone detoxification so

INCREASED LEVELS

Decreased Adrogen and

estrogen detoxification so

INCREASED LEVELS

Decreased metabolism of

protein and carbohydrates

Decreased Fat metabolism

Decreased Bilirubin

metabolism and or biliary

tree damage or obstruction

(+)Bipedal Edema Spider angiomas

Decreased Plasma Proteins

Ascites ( Abdominal Girth:41 inches

(+)Bipedal Edema

HypoglycemiaMalnutrition

Conjugated and unconjugated

hyperbilirubinemia

Decresed Bile in Gatrointestinal tract

and Increased Urobilinogen

Precipitating FactorsAlcohol Ingestion

Exposure to toxins (lives in an old bakery)

Presence TattooNot Immunized with Hepa

VaccineEx-factory and Construction

workerLives in a congested

environment

Jaundice(icteric sclera) Dark Urine

Clay-colored stools

Liver Failure

Liver fibrosis and scarring

Portal Hypertension

AscitesSpleenomegaly

Bleeding

AnemiaThrombocytopenia

Leukopenia

Delayed Wound Healing

Infection

Inability to metabolism

ammonia to urea

Hepatic Encephalopathy

(+) Asterixis

Alteration in sleep

Respiratory Acidosis

Confusion to hepatic coma

Precipitating Factors

>Constipated for 2 weeks

Increase Serum Ammonia level

And toxins

Accumulation of Toxic substances in

the intestine

Toxins are absorbed into the portal venous flow

Toxins then circulate at

elevated concentrations in

the systemic blood

Reach the brain through the blood-brain barrier

Impair cerebral function leading to altered higher functions and consciousness

The specific cause of hepatic encephalopathy is unknown, but it is characterized by elevations of ammonia levels in the blood and cerebrospinal fluid (CSF). Ammonia is produced in the gastrointestinal tract when protein is broken down by bacteria, by the liver, and in lesser amounts, by gastric juices and peripheral tissue metabolism. The kidneys are another source of ammonia in the presence of hypokalemia. More recently implicated as a cause of encephalopathy are false neurotransmitters, elevated mercaptans (organic chemical that contain sulfhyldryl radical formed when the oxygen of an alcohol molecule is replaced by sulfur), phenol, and short-chain fatty acids.

Normally the liver converts ammonia into glutamine, which is stored in the liver and is later converted to urea and excreted through the kidneys. Blood ammonia level rise when the liver cells are unable to perform this conversion. Failure of the liver to perform this function may be due to liver cell damage and necrosis. It may also result from the shunting of blood from the portal venous system into the systemic, venous circulation (bypassing the liver). In either case, as blood ammonia level rise, many unusual compounds begin to form.

Some of these compounds (e.g. octapamine) apparently act as false neurotransmitters in the CNS. Ammonia also is a CNS toxin,

affecting glial and nerve cells; it leads to altered CNS metabolism and function.

Any process that increases protein in the intestine, such as increased dietary protein or gastrointestinal bleeding, causes elevated blood ammonia levels and possible manifestations of hepatic encephalopathy in clients with hepatocellular failure of have undergone portosystemic shunt surgery.

(Black and Hawks, Medical-Surgical Nursing: Clinical Management for Positive Outcomes 8th Edition, Vol. 1, Page 1166)

Ammonia

Entering the blood stream

Converting ammonia to urea

Muscle cellsAbsorption GI tract Liberation from kidney

S/Sx: Edema, bleeding

Increased ammonia concentration in the blood

Brain dysfunction

S/Sx:

Motor disturbances, mental changes

Damage

HEPATIC ENCEPHALOPATHY

>Incoherent

>Disoriented

>Slurred speech

>Paresis

VII. Ecologic Model

A. Hypothesis The host factors of the client have a significant effect to the client’s predisposition to hepatic encephalopathy secondary to liver cirrhosis rather than environmental factors. Specifically the age, being a male and Asian, alcohol ingestion, history of smoking, family history of alcohol drinkers, eating habits, elimination pattern, lifestyle habits and stress.

B. Predisposing Factors

1. HostAge:

35 years oldSex:

Male- The difference in incidence between the sexes is more pronounced, with male-to-female ratios as high as 8:1

Race: Asian- Most commonly found among Asian persons, due to childhood infections with hepatitis B.

Nationality: Filipino- The client belongs into a third world country where in incidence of high rates of infectious hepatitis occur.

Behavior:

Alcohol Ingestion- The client ingest 1-2 bottles of alcoholic drinks once a week for about 15 years. The primary risk for alcohol cirrhosis is alcohol ingestion, especially in the absence of proper nutrition. (Black and Hawks,

Medical-Surgical Nursing: Clinical Management for Positive Outcomes 8th Edition, Vol. 1, Page 1147)

History of smoking- The client consumes half pack of cigarettes per day for about 15 years; he has stopped just 1 year ago. The ingredients in the cigarettes affect everything from the internal functioning of the organs to the efficiency of the body’s immune system. (http:quitsmoking.about.com/od/tobaccostatistics/a/cigarettesmoke.htm)

Eating Habits- The seldom eat vegetables before, he loves to eat adobo and sinigang na baboy. He prefers meat viands than vegetables. He frequently eats street foods like “isaw”.

Elimination Pattern- Whenever he feels the urge to defecate or urinate he seldom attend to it immediately because of the proximity of their comfort room, he is having a difficulty ambulating, because he feels weak. He has been constipated for 2 weeks prior admission.

Customs: Lifestyle Habits

- Presence of tattoos-The tattoos was applied at home with Chinese ink.- Lack of Hepa Vaccinations

Heredity: Family history of alcohol drinkers-any client with a family history of alcoholism should avoid alcohol because of the increase risk. (Black and Hawks, Medical-Surgical Nursing: Clinical Management for Positive Outcomes 8th Edition, Vol. 1, Page 1147)

2. AgentChemical: Alcohol

3. Environment:

Physical: Exposure to toxins at their house (old bakery), and at the construction and factory place where he had worked. Lives in a congested environmentBiologic: Response to alcohol exposureSocio-economic: Lives in a congested environment, availability of alcohol

C. Ecologic Model

In many respects, alcohol can be considered the causal agent in alcohol psychiatric disorders because it must be present for alcoholism to occur. However, the fact that most drinkers do not become alcoholics indicates that it is a necessary, but not sufficient cause. Suitable conditions of the host and environment must also be present for disease to develop, and the concept that a number of factors influence the occurrence of disease is referred to as multiple causation or multi-factorial causation. In the past, particularly in the context of the epidemiology of infectious disease, a triangle has been used to illustrate relations between three factors that contribute to the occurrence of disease, the agent or proximal cause of the disease, the host, and the environment. Increasingly, with the study of chronic and mental disorders having a complex, multifactorial etiology, many epidemiologists have come to prefer models in which the agent is considered part of the total environment. The wheel model –de-emphasizes the role of the agent and stresses the multiplicity of interactions between the host and the environment.

The wheel model depicts the human host with his genetic makeup at its core; the surrounding environment is divided into three sectors: biologic, social, and physical.

HOST

Family History of

Alcoholism

Biological Environment Social Environment

Physical Environment

35 y/o

Asian

Ex-factory and construction worker

Alcohol Ingestion

Eating Habits

Elimination Pattern

Male

No hepa

vaccine

tattoos

Response to alcohol exposure

Availabilty of Alcohol

Lives in a congested environment

Exposure to toxins at their house (old bakery), and work place

Lives in a congested environment

D. Analysis

Cirrhosis is defined histologically as a diffuse hepatic process characterized by fibrosis and the conversion of normal liver architecture into structurally abnormal nodules. The progression of liver injury to cirrhosis may occur over weeks to years. Indeed, patients with hepatitis C may have chronic hepatitis for as long as 40 years before progressing to cirrhosis. There are many causes of cirrhosis; they include chemicals (such as alcohol, fat, and certain medications), viruses, toxic metals (such as iron and copper that accumulate in the liver as a result of genetic diseases), and autoimmune liver disease in which the body's immune system attacks the liver.

The prevalence of liver disease is influenced by many factors, including genetic factors (e.g., predilection to alcohol abuse, sex) and environmental factors (e.g., availability of alcohol, social acceptability of alcohol use, concomitant hepatotoxic insults), and it is therefore difficult to define. In general, however, the risk of liver disease increases with the quantity and duration of alcohol intake. Although necessary, excessive alcohol use is not sufficient to promote alcoholic liver disease. Only one in five heavy drinkers develops alcoholic hepatitis, and one in four develops cirrhosis.

Hepatic encephalopathy, a challenging complication of advanced liver disease, occurs in approximately 30–45% of patients with cirrhosis and 10–50% of patients with transjugular intrahepatic portosystemic shunt, while minimal hepatic encephalopathy affects approximately 20–60% of patients with liver disease. (Poordad,F. 2006) Hepatic encephalopathy is caused by disorders that affect the liver. These include disorders that reduce liver function (such as cirrhosis or hepatitis) and conditions in which blood circulation does not enter the liver. The exact cause of hepatic encephalopathy is unknown. Hepatic encephalopathy may be triggered by: dehydration, eating too much protein, electrolyte abnormalities (especially a decrease in potassium) from vomiting, or from treatments such as paracentesis or taking diuretics ("water pills"), bleeding from the intestines, stomach, or esophagus, infections, kidney problems, low oxygen levels in the body, Shunt placement or complications (See: Transjugular intrahepatic portosystemic shunt ), surgery, use of medications that suppress the central nervous system (such as barbiturates or benzodiazepine tranquilizers).Hepatic encephalopathy may occur as an acute, potentially reversible disorder. Or it may occur as a chronic, progressive disorder that is associated with chronic liver disease. ( http://www.nlm.nih.gov/medlineplus/ency/article/000302.htm)

E. Conclusion and Recommendations

I therefore conclude that the host factors have a significant effect to the client’s predisposition to hepatic encephalopathy secondary to liver cirrhosis. Since the client has already a liver cirrhosis and experienced hepatic

encephalopathy, prevention for further complications is the only one that can be provided and supported for the client. However liver damage was not yet that clinically assessed in terms of laboratory diagnosis for its extensibility or severity to be able to make necessary interventions for treatment and rehabilitation. Factors such as alcohol ingestion, application of tattoo not aseptically, lack of hepa vaccination, presence of liver cirrhosis, eating habits-increase in protein intake, elimination pattern-not attending urge to defecate are the factors that readily predisposes client to hepatic encephalopathy.

Since host factors consist of modifiable and non modifiable factors which synergized by the client’s environment to predispose into a complication of liver disease, modifiable factors must then be addressed immediately, client must have lifestyle modifications like abstinence from alcohol consumption and cigarette smoking.

We as nurses must continue facilitating patient to take less sodium and Protein intake, give medication as prescribe, Encourage patient to have a clean and safe environment for faster recovery. Rationale: Clean and safe environment promotes comfort and relaxation for faster recovery of the patient. Encourage the patient to be calm and maintain a comfort position. Educate the patient and family the importance of proper medication administration and timing. Encourage the client to inhale and exhale exercise. Rationale: To improve air gas exchange in the body. Encourage the patient to have a low cholesterol, low sodium and low carbohydrate diet Rationale:For the blood volume not to increase resulting to hypertension. Encourage the patient to continue praying and seek guidance from God Rationale:Strong faith to God helps the patient spiritually to alleviate the condition with God's will.