The liver is a vital organ present in humans It has a wide range of functions, including detoxification, protein synthesis, and

production of biochemical necessary for digestion. The liver is necessary for survival; there is currently no way to compensate for the absence of liver function long term, although liver dialysis can be used short term.

Glucose Metabolism The liver plays a role in the metabolism of glucose and the regulation of blood glucose concentration. After a meal, glucose is taken up from the portal venous blood by the liver and converted into glycogen, which is stored in the hepatocytes. The glycogen is converted back to glucose (glycogenolysis) and released as needed into the blood stream to maintain normal levels of blood glucose. Additional glucose can be synthesized by the liver through a process called gluconeogenesis.

Ammonia Conversion Use of amino acids from protein for gluconeogenesis results in the formation of ammonia as a by product. The liver converts this metabolically generated ammonia into urine. Ammonia produced by bacteria in the intestines is also removed from portal blood for urea synthesis.

Protein Metabolism It synthesizes almost all of the plasma proteins (except gamma-globulin), including albumin, alpha and beta globulins, blood clotting factors, specific transport proteins and most of the plasma lipoproteins. Vitamin K is required by the liver for synthesis of prothrombin and some of the other clotting factors. Amino acids are used by the liver for protein synthesis.

Fat Metabolism Fatty acids are broken down for the production of energy and the production of ketone bodies (acetoacetic acid, beta-hydroxybutyric acid and acetone). Ketone bodies are small compounds that can enter the bloodstream and provide a source of energy for muscles and other tissues. Breakdown of fatty acids into ketone bodies occurs primarily when the availability of glucose for metabolism is limited, as in starvation or in uncontrolled diabetes. Fatty acids and their metabolic products are also used for the synthesis of cholesterol, lecithin, lipoproteins and other complex lipids.

Vitamin and Iron Storage Vitamin A, B and D and several of the Bcomplex vitamins are stored in large amounts in the liver. Certain substances, such as Iron and Copper, are also stored in the liver because the liver is rich in these substances, liver extracts have been used for therapy for a wide range of nutritional disorders.

Drug Metabolism The liver metabolizes many medications such as barbiturates, opioids, sedative agents, anesthetics and amphetamines. Generally results in inactivation of the medication, although in some cases, activation of medication may occur. One of the important pathways for medication metabolism involves conjugation (binding) of the medication with a variety of compounds, such as glucuronic acid or acetic acid, to form more soluble substances.

Bioavailability is the fraction of the administered medication that actually reaches the systemic circulation. The bioavailability of an oral medication can be decreased if the medication is metabolized to a great extent by the liver before it reaches the systemic circulation; this is known as Firstpass effect.

Bile Formation Bile is continuously formed by the hepatocytes and collected in the canaliculi and bile ducts. It is composed mainly of water and electrolytes such as sodium, potassium, calcium, chloride and bicarbonate, and it also contains significant amounts of lecithin, fatty acids, cholesterol, bilirubin and bile salts. Bile is collected and stored in the gallbladder and is emptied into the intestine when needed for digestion.

Bilirubin Excretion Bilirubin is a pigment derived from the breakdown of hemoglobin by cells of the reticuloendothelial system, including the Kupffer cells of the liver. Hepatocytes remove bilirubin from the blood and chemically modify it through conjugation of glucuronic acid which makes the bilirubin more soluble in aqueous solution. In the small intestine, bilirubin is inverted into urobilinogen, which is partially excreted in the feces and partially absorbed through the intestinal mucosa into the portal blood. The bilirubin concentration in the blood may be increased in the presence of liver disease, if the flow of bile impeded, or if there is excessive destruction of red blood cells.

The liver, the largest gland of the body, can be considered a chemical factory that manufactures, stores, alters, and excrete a large number of substances involved in metabolism. The location of the liver is essential in this function, because it receives nutrient-rich blood directly from the GI tract and then either stores or transforms these nutrients into chemicals that are used elsewhere in the body for metabolic needs. The liver is especially important in the regulation of glucose and protein metabolism.

The liver manufactures and secretes bile, which has a major role in the digestion and absorption of fats in the GI tract. The liver removes waste product from the bloodstream and secretes them into the bile. The bile produced by the liver is stored temporarily in the gallbladder until it is needed for digestion at which the gallbladder empties and bile enters the intestine.

The liver is located behind the ribs in the upper right portion of the abdominal cavity. It weighs about 1,800 grams in men and 1,400 in women and is divided into 4 lobes. A thin layer of connective tissue surrounds each lobe, extending into the lobe itself and dividing the liver mass into small, functionally units called lobules. The circulation of the blood into and out of the liver is of nature importance of liver function. Approximately 75% of the blood supply comes from the portal vein, which drains the GI tract and is rich in nutrients.

The remainder of the blood supply enters by way of the hepatic artery and is rich in oxygen. Terminal branches of these two blood vessels join to form common capillary bed, which constitute the sinusoids of the liver. The sinusoids empty into venules that occupy the center of each liver lobule and are called the central veins. The central veins join to form the hepatic vein, which constitutes the venous drainage from the liver and empties into the inferior vena cava, close to the diaphragm.

The smallest bile ducts called canaliculi, are located between the lobules of the liver. The canaliculi receives secretions from the hepatocytes and carry them to larger bile ducts, which eventually form the hepatic duct. The hepatic duct from the liver and the cystic duct from the gallbladder join to form the common bile duct, which empties to the small intestines.

Health History If the liver function test are abnormal, the patient is evaluated for liver disease. In such cases, the health history focuses on previous exposure of the patient to hepatotoxic substances or infectious agents. The patients history of alcohol and drug use, including but not limited to the use of IV/injection drugs, provides additional information about exposure to toxins and infectious agents. A thorough medication history to assess hepatic dysfunction should address all current and past prescription medications, OTC medications, herbal remedies and dietary supplements.

Men who consume 60-80g of alcohol per day (approx. four glasses of beer, wine, or mixed drinks) and women whose alcohol intake is 4060g/day are estimated to be at high risk of cirrhosis. The history also includes an evaluation of the patients past medical history to identify risk factors for the developing of liver disease.

Symptoms that may have their origin in liver disease but are not specific to hepatic dysfunction include jaundice, malice, weakness, fatigue, pruritis, abdominal pain, fever, anorexia, weight gain, edema, increasing abdominal girth, hematemesis, melena, hematochezia (passage of bloody stools), easy bruising, changes in mental acuity, personality changes, sleep disturbances, and decrease libido and secondary amenorrhea in women.

Physical Examination The nurse assesses the pt for physical signs that may occur with liver dysfunction, including the pallor often seen with chronic illness and jaundice. The skin, mucosa and sclerae are inspected for jaundice and the extremities are assessed for muscle atrophy, edema, and skin excoriation secondary to scratching. The nurse observes the skin for petichiae or ecchymotic areas (bruises), spider angiomas, and palmar erythema. The male pt is assessed for unilateral or bilateral gynecomastia and testicular atrophy due to hormonal changes.

Patients cognitive status (recall, memory, abstract thinking) and neurologic status are assessed; the nurse observes for general tremor, asterixis (liver flap), weakness and slurred speech. The nurse assesses for the presence of abdominal fluid wave, the abdomen is palpated to assess liver size and to detect any tenderness over the liver. The liver may be palpable in the right upper quadrant.

Liver Function Tests Liver Biopsy Additional Studies: Ultrasonography, Computed Tomography (CT) Scan, Magnetic Resonance Imaging (MRI), Electroencephalogram, Angiography, and Endoscopic Retrograde Cholangiopancreatography (ERCP) Protein Studies, Bile formation and secretion, Fat Metabolism, Liver Detoxification, Enzyme Production

LFT is measured in terms of serum enzyme activity (ie, serum amino transferases, alkaline phosphatase, lactic dehydrogenase) and serum concentrations of proteins (albumin and globulins), bilirubin, ammonia, clotting factors, and lipids. Serum aminotransferase (also called Transaminases) are sensitive indicators of injury to the liver cells and are useful in detecting acute liver disease such as hepatitis. Alanine aminotransferase (ALT), aspartate aminotrasferase (AST), and gamma-glutamyl transferase (GGT) are the most frequently used tests for liver damage.

It is the removal of a small amount of liver tissue usually through needle aspiration. The most common indication is to evaluate diffuse disorders of the parenchyma and to diagnose space-occupying lesions. Liver biopsy is especially useful when clinical findings and lab tests are not diagnostic. Bleeding and bile peritonitis after liver biopsy are the major complications; therefore coagulation studies are obtained, their values are noted and abnormal results are treated before liver biopsy is performed.

A liver biopsy can be performed percutaneously with ultrasound guidance or intravenously through the right internal jugular vein to right hepatic vein under fluoroscopy control.

Clinical Functions To detect abnormalities that occur with hepatic coma Ultrasonography To show size of abdominal organs and presence of masses Computed To detect hepatic neoplasm; Tomography (CT) Scan diagnose cysts, abscesses, and hematomas; and distinguish between obstructive and nonobstructive jaundice. Detects cerebral atrophy in hepatic encephalopathy. Additional Studies Electroencephalogram

Additional Studies Angiography

Clinical Functions To visualize hepatic circulation and detect presence and nature of hepatic masses.

To detect hepatic neoplasm; diagnose cysts, abscesses, and hematomas. Detects cerebral atrophy in encephalopathy. Endoscopic retrograde To visualize biliary cholangiopancreatography structures via endoscopy.

Magnetic Resonance Imaging (MRI)

Test and Purpose Bile Formation and Secretion 1. Serum bilirubin (van den Bergh reaction) Measures bilirubin in the blood; this determines the ability of the liver to take up, conjugate and excrete bilirubin. Bilirubin is the product of the breakdown of hemoglobin.

Normal

Clinical & Nursing Significance

Direct (conjugted) Soluble in water Indirect (unconjugated) Insoluble in water Total Serum Bilirubin

0-5.1 mol/L

0-14 mol/L

Abnormal in biliary and liver dse, causing jaundice clinically. Abnormal in hemolysis and in functional disorders of uptake or conjugation.

1.7-20.5 mol/L

Test and Purpose

Normal

Clinical and Nursing Significance Mahogany-colored urine; when specimen is shaken, yellow tinted foam can be observed. Confirm with Icto-test tablet or Dipstick. If phenazopyridine (Pyridium) is being taken, there may be a false-positive bilirubin result. Urine specimen is collected over 2 hours period after lunch. Place specimen in dark brown container and send it to lab immediately to prevent decomposition. If the pt is receiving antimicrobials, mark lab slip to this effect, as production of urobilinogen can be falsely reduced.

2. Urine Bilirubin None (0) Not normally found in urine, but if direct serum bilirubin is elevated, some spills into urine.

3. Urobilinogen Formed in small intestine by action of bacteria on bilirubin. Related to amount of bilirubin excreted into bile.

Urine urobilinogen up to 0.09-4.23 mol/24hr. Fecal urobilinogen 0.068-0.34 mmol/24hr

Test and purpose Protein studies 1. Albumin and globulin measurement is of greater significance than total protein measurement Albumin-produced by liver cells Globulin- produce in lymph nodes,spleen and bone marrow and kupffers cells of liver Total Serum protein

Normal

Clinical and normal significance

35-55gm/L

15-30gm/L

Albumin decrease cirrhosis and chronic Hepatitis Globulin increase cirrhosis,chronic obstructive jaundice, viral hepatitis

60-80gm/L

Test and purpose 2. Prothrombin time (PT) Prothrombin and other clotting factors are manufactured in the liver; its rate is influenced by the supply of vitamin k.

Normal 100% of control

Clinical and nursing significance Prothrombin time may be prolonged in liver disease which case it will not return to normal with vitamin k. it may also be prolonged in malabsorption of fat and fat soluble vitamins, in which case it will return to normal with vitamin k.

Fat metabolism 1. Cholesterol It is possible to measure lipid metabolism by determining serum cholesterol levels

3.90-6.50mmol/L Serum cholesterol level is esters=60% of total decreased in parenchymal liver disease. Serum level is increased in biliary obstruction

Test and Purpose Liver Detoxification

Normal

Clinical & Nursing Significance

1. Serum alkaline 20-90 U/L at 30oC phosphatase Because bile disposes this enzyme, any impairment of liver cell excretory function will cause an elevation. In cholestasis or obstruction, increased synthesis of enzyme causes very high levels in blood.

Abnormalities: The level is elevated to more than 3 times normal in obstructive jaundice, intrahepatic cholestasis, liver metastasis, or granulomas. Also elevated in osteoblastic diseases, Pagets disease, and hyperparathyroidism

Test and Purpose Enzyme Production Transaminase (SGOT) (Aspartate aminotransferase or AST) Transaminase (SGPT) (Alanine aminotransferase or ALT)

Normal

Clinical & Nursing Significance An elevation in these enzymes indicates liver cell damage. Note: Opiates may also cause a rise in SGOT and SGPT. Aspirin may cause an increase or decrease in SGOT and SGPT. Enzyme found in liver, kidney, heart, pancreas, spleen, brain. An elevation confirms hepatic involvement in the presence of an elevated alkaline phosphatase.

4.8-19 U/L

2.4-17 U/L

LDH

80-192 U/L

Gamma glutamyl transpeptidase (GGT)

0-30 U/L at 30oC

Test and Purpose

Normal

Clinical & Nursing Significance Ammonia levels rise when the liver is unable to convert it to urea. Elevated serum bile acids are seen in the presence of hepatic diseases.

Ammonia (serum)

11.1-67.0 mol/L

Bile acids radioimmunoassay (after cholecystokinin stimulation) Total Chenodeoxycholic acid Cholic acid Deoxycholic acid Lithocholic acid

35.0-14.0 mmol/L 10.0-61.4 mmol/L 6.8-81.0 mmol/L 2.0-18.0 mmol/L 0.8-2.0 mmol/L

Jaundice is a symptom of dysfunction or disease and not a disease itself. Dysfunction of several body organs or systems may be implicated when jaundice occurs. Hepatocellular Jaundice Also known as hepatic jaundice is due to an inability of diseased liver cells to clear the normal amount of bilirubin from the blood. Causes Infection-hepatitis viruses

Drug or chemical toxicity-carbon tetrarchloride, chloroform, phosphorous, arsenicals, ethanol, halothane, isoniazid, acetaminophen, mushroom poisoning Clinical Manifestations Mildly or severely ill patient Lack of appetite, nausea, loss of vigor and strength, weight loss Elevated aspartate aminotransferase (AST, transaminase or SGOT) and alanine aminotransferase (ALT, SGPT) 2 enzymes that are liberated with cellular necrosis.


 Rise in bromsulphalein or (BSP) and bilirubin. Alkaline phosphatase mildly elevated. Abnormal serum proteins in prolonged illness; prothrombin time increased. Headache and chills possible in infectious condition. Bile acid radioimmunoassay tests are replacing BSP tests.

Pathophysiology

Contributing Factors: Portal hypertension, increased in capillary pressure and obstruction of venous blood flow through the damage liver. Suspected Causative Factors: the vasodilation that occurs in the splanchnic circulation. The failure of the liver to metabolize aldosterone increases sodium and water retention by the kidney.

Sodium and water retention, increase intravascular fluid volume, increased lymphatic flow and decreased synthesis of albumin by the damage liver all contribute to the movement of the fluid from the vascular system into the peritoneal space. The process becomes self-perpetuating as loss of fluid into the peritoneal space causes further sodium and water retention by the kidney in an effort to maintain the vascular fluid volume. As a result of liver damage, large amounts of albumin rich fluid, 15L or more, may accumulate in the peritoneal cavity as ascites.

With the movement of albumin from the serum to the peritoneal cavity, the osmotic pressure of the serum decreases. These, combined with increased pressure, results in the movement of fluid into the peritoneal cavity.

Clinical Manifestations Increased abdominal girth and rapid weight gain are common presenting symptoms of ascites. The patient may be short of breath and uncomfortable from the enlarged abdomen, and striae and distended veins may be visible over the abdominal wall. Umbilical hernias also occur frequently in those patients with cirrhosis. Fluid and electrolytes imbalances are common.

Assessment and Diagnostic Evaluations The presence and extent of ascites are assessed by caution of the abdomen. When fluid has accumulated in the peritoneal cavity, the flanks bulge when the patient assumes a supine position. The presence of fluid can be confirmed either by percussing for shifting dullness or by detecting a fluid wave. A fluid wave is likely to be found only if a large amount of fluid is present.

Daily measurement and recording of abdominal girth lymphatic and body weight are essential to assess the progression of ascites and its response to treatment. Daily measurement and recording of abdominal girth lymphatic and body weight are essential to assess the progression of ascites and its response to treatment.

Nursing Management If a patient with ascites from liver dysfunction is hospitalized, nursing measures include assessment and documentation of intake and output, abdominal girth, and daily weight to assess fluid status. The nurse monitors serum ammonia and electrolyte levels to assess electrolyte balance, response to therapy, and indicators of encephalopathy.

Promoting Home and Community-based Care Teaching Patients Self-care The patient treated for ascites is likely to be discharged with some ascites still present. Before hospital discharge, the nurse teaches the patient and family about the treatment plan, including the need to avoid all alcohol intakes, adhere to a low-sodium diet, take medications as prescribed, and check with the physician before taking any new medications.

Daily measurement and recording of abdominal girth lymphatic and body weight are essential to assess the progression of ascites and its response to treatment. Continuing Care A referral for come care may be warranted, especially if the patient leaves alone or cannot provide self-care. The home visit enables the nurse to assess change in the patients condition and weight, abdominal girth, skin, and cognitive and emotional status.

The home care nurse assesses the home environment and the availability of resources needed to adhere to the treatment plan (e.g., a scale to obtain daily weights, facilities to prepare and store appropriate foods, resources to purchase needed medications). It is important to assess the patients adherence to the treatment plan and the ability to buy, prepare, and eat appropriate foods. The nurse reinforces previous teachings and emphasizes the need for regular follow-up and the importance of keeping scheduled health care appointments.

Hepatic encephalopathy, a life-threatening complication of liver disease, occurs with profound liver failure and may result from the accumulation of ammonia and other toxic metabolites in the blood. Hepatic coma represents the most advanced stage of hepatic encephalopathy. Although the exact cause is not fully understood, false or weak neurotransmitters have been suggested as a cause.

These neurotransmitters maybe generated from an intestinal source or from metabolism of protein by the liver and may precipitate encephalopathy. Many other theories exists because the causes of encephalopathy, including synergistic effects of other chemicals (e.g., serotonin) with ammonia, and the generation of endogenous benzodiazepines of opiates. Benzodiazepine-like chemicals (compounds) have been detected in the plasma and cerebrospinal fluid of patients with hepatic encephalopathy due to cirrhosis.

Portal-systemic encephalopathy, the most common type of hepatic encephalopathy, occurs primarily in patients with cirrhosis who have portal hypertension and portal systemic shunting. Pathophysiology Ammonia, which is constantly entering the blood stream, accumulates because damaged liver cells fail to detoxify and convert ammonia to urea. Ammonia enters the bloodstream as a result of its absorption from the GI tract and its liberation from the kidney and muscle cells.

The increased ammonia concentration in the blood causes brain dysfunction and damage, resulting in hepatic encephalopathy. Circumstances that increase serum ammonia levels tend to aggravate or precipitate hepatic encephalopathy. The largest source of ammonia is the enzymatic and bacterial digestion of dietary and blood proteins in the GI tract Ammonia from these sources increases as a result of GI bleeding (e.g., bleeding esophageal varices, chronic GI bleeding), high protein diet, bacterial infection, or uremia.

The ingestion of ammonium salts also increases the blood ammonia level. In the presence of alkalosis or hypokalemia, increased amounts of ammonia are absorbed from the GI tract and from the renal tubular fluid. Conversely, serum ammonia is decreased by elimination of protein from the diet and by the administration of antibiotic agents, such as neomycin sulfate, that reduce the number of intestinal bacteria capable of converting urea to ammonia.

Other factors: unrelated to increased serum ammonia levels that can cause hepatic encephalopathy in susceptible patients include excessive diuresis, dehydration, infections, surgery, fever, and some medications (sedatives, tranquilizers, analgesic, and diuretics that cause potassium loss)

Clinical Manifestations The earliest symptoms of hepatic encephalopathy include minor mental changes and motor disturbance. The patient appears slightly confused and unkempt and has alterations in mood and sleep patterns. The patient tends to sleep during the day and have restlessness and insomnia at night. As hepatic encephalopathy progresses, the patient may become difficult to awaken. Asterixis (flapping tremor of the hands) may occur.

Simple task, such as handwriting, become difficult . A handwriting or drawing sample (e.g., star figure), taken daily, may provide graphic evidence of progression or reversal of hepatic encephalopathy. Inability to reproduce a simple figure is referred to as constructional apraxia. In the early stages of hepatic encephalopathy, the deep tendon reflexes disappear and the extremities may become flaccid.

Assessment and Diagnostic Findings The electroencephalogram (EEG) shows generalized slowing, an increase in the amplitude of brain waves, and characteristic triphasic waves. Occasionally, fetor hepaticus, a sweet, slightly fecal odor to the breath that is presumed to be of intestinal origin, may be noticed. The odor has also been described as similar to that of freshly mowed grass, acetone, or old wine. Fetor hepaticus is prevalent with extensive collatral portal circulation in chronic liver disease.

In a more advanced stage, there are gross disturbances of consciousness and the patient is completely disoriented with respect to time and place. With further progression of the disorder, the patient lapses intro fank coma and may have seizures. The survival rate after a first episode of overt hepatic encephalopathy in patients with cirrhosis is approximately 40% at 1 year. Patients should be referred for liver transportation after a first episode of encephalopathy.

Medical Management Lactulose (Cephulac) is administered to reduce serum ammonia levels. It acts by several mechnisms that promote the excretion of ammonia in the stool: (1) ammonia is kept in the ionized state, resulting in a decrease in colon pH, reversing the normal passage of ammonia from the colon to the blood; (2) evacuation of the bowel takes place, which decreases the ammonia absoredb from the colon; and (3) the fecal flora are change to organisms that do not produce ammonia from urea.

Two or three soft stools per day are desirable; this indicates that lactulose is performing as intended. Possible side effects include intestinal bloating and cramps, which usually disappear within a week. To mask the sweet taste, which some patients dislike, lactulose can be diluted with fruit juice. The patient is closely monitored for hypokalemia and dehydration. Other laxatives are not prescribed during lactulose administration, because their effects disturb dosage regulation.

Lactulose may be administered by nasogastric tube or enema for patients who are comatose or for those in whom oral administration is contraindicated or impossible. Other aspects of management include IV administration of glucose to minimize protein breakdown, administration of vitamins to correct deficiencies, and correction of electrolyte imbalances (especially potassium).

Additional principles of management of hepatic encephalopathy include the following: Therapy is directed toward treating or removing the cause. Neurologic status is assessed frequently Mental status is monitored by keeping a daily record of handwriting and arithmetic performance. Fluid intake and output and body weight are recorded each day. Vital signs are measured and recorded every 4 hours.

Potential sites of infection (peritoneum, lungs) are assessed frequently, and abnormal findings are reported promptly. Serum ammonia levels is monitored daily Protein intake is moderately restricted in patients who are comatose or who have encephalopathy that is refractory to lactulose and antibiotic therapy. Reduction in the absorption of ammonia from the GI tract is accomplished by the use of gastric suction, enemas, or oral antibiotics. Electrolyte status is monitored and corrected if abnormal.

Sedatives, tranquilizers, and analgesic medications are discontinued. Benzodiazepine antagonists such as flumazenil (Romazicon) may be administered to improve encephalopathy, whether or not the patient has previously taken benzodiazepines.

Nursing Management The nurse is responsible fort maintaining a safe environment to prevent injury, bleeding, and infection. The nurse administers the prescribed treatments and monitors the patient for the numerous potential complications. The nurse also communicates with the patients family, to inform them about the patients status, and supports them by explaining the procedures and treatments that are part of the patients care.

If the patient recovers from hepatic encephalopathy and coma, rehabilitation is likely to be prolonged. Therefore, the patient and family will require assistance to understand the causes of this severe complications and to recognize that it may recur.

Hepatitis A Previous names Infectious hepatitis Epidemiology Cause

Hepatitis B Serum hepatitis

Hepatitis C Non-A, nonB hepatitis

Hepatitis D

Hepatitis E

Hepatitis A Hepatitis B Hepatitis C virus (HAV) virus (HBV) virus (HCV) Fecal-oral route; poor sanitation. Person-toperson contact. Waterborne; food borne. Parenterally by intimate contact with carriers or those with acute disease; sexual and oral-oral contact. Transfusion of blood and blood products; exposure to

Hepatitis D Hepatitis E virus virus (HDV) (HEV) Fecal-oral route; person to person contact may be possible, although risk appears low

Mode of transmission

Same as HBV. HBV surface antigen necessary contaminated for blood replication; through pattern equipment similar to or drug that of paraphernali hepatitis B a.

Hepatitis A Transmission possible with oral-anal contact during sex.

Hepatitis B Perinatal transmission from mothers to infants. An important occupational hazard for health care personnel.

Hepatitis C Transmission possible with sex with infected partner; risk increased with STD.

Hepatitis D

Hepatitis E

Incubation (days) Immunity

15-50 days Average: 30 days Homologous

28-160 days Average: 7080 days Homologous

15-160 days Average: 50 days second attack may indicate weak immunity or infection with another agent.

21-140 days Average: 35 days Homologous

15-65 days Average: 42 days Unknown

Hepatitis A Nature of Illness Signs and symptoms May occur without symptoms; flulike illness Preicteric phase: Headache, malaise , fatigue, anorexia, fever Icteric phase: Dark urine, jaundice of sclera and skin, tender liver

Hepatitis B

Hepatitis C

Hepatitis D

Hepatitis E

May occur without symptoms May develop arthralgias, rash

Similar to HBV; less severe and anicteric

Similar to HBV

Similar to HAV. Very severe in pregnant women.

Hepatitis A Outcome Usually mild with recovery. Fatality rate: <1%. No carrier state or increased risk of chronic hepatitis, cirrhosis, and hepatic cancer.

Hepatitis B May be severe. Fatality rate: 1-10%. Carrier state possible. Increased risk of chronic hepatitis, cirrhosis, and hepatic cancer

Hepatitis C Frequent occurrence of chronic carrier state and chronic liver disease. Increased risk of hepatic cancer.

Hepatitis D similar to HBV but greater likelihood of carrier state, chronic active hepatitis, and cirrhosis

Hepatitis E Similar to HAV except very severe in pregnant women.

Clinical Manifestations Many patients are anicteric (without jaundice) and symptomless. When symptoms appear, they resemble those of a mild, flulike upper respiratory tract infection, with low grade fever. Anorexia, and early symptom, is often severe. It is thought to result from release of a toxin by the damaged liver or from failure of the damaged liver cells to detoxify an abnormal product. Later, jaundice and dark urine may become apparent.

Indigestion is present in varying degrees, marked by vague epigastric distress , nausea, heartburn, and flatulence. The patient may also develop a strong aversion to the taste of cigarettes or the presence of cigarette smoke and other strong odors. These symptoms tend to clear as soon as the jaundice reaches its peak, perhaps 10 days after its initial appearance. Symptoms may be mild in children; in adults, they may be mote severe, and the course of the disease prolonged.

        

Signs and Symptoms Nausea Vomiting Diarrhea, especially in children Low-grade fever Loss of appetite Rash Tiredness, fatigue Jaundice - A yellow discoloration of the skin and the whites of the eyes Urine is dark brownish in color, like cola or strong tea. Pain in area of liver - On the right side of the abdomen, just under the rib cage

Nursing Management Management usually occurs in the home unless symptoms are severe. Therefore, the nurse assists the patient and family in coping with the temporary disability and fatigue that are common in hepatitis and instructs them to seek additional health care if the symptoms persist or worsen.

The patient and family also need specific guidelines about diet, rest, follow-up blood work, and the importance of avoiding alcohol, as well as sanitation and hygiene measures (particularly handwashing) to prevent spread of the disease to other family members. Specific teaching to patients and families about reducing the risk for contracting hepatitis A includes a good personal hygiene, stressing careful handwashing (after bowel movements and before eating) and environmental sanitation (safe food and water supply, effective sewage disposal).

Treatment There are no specific medicines to cure infection with hepatitis A. Most people require no treatment except to relieve symptoms. If you have been exposed to someone who is infected with HAV, there is a treatment that may prevent you from becoming infected. It is called immune globulin and is more likely to be effective when given within 2 weeks of exposure.

Clinical Manifestation Clinically, the disease closely resembles hepatitis A, but the incubation period us much longer (1 to 6 months) Signs and symptoms of hep B may be insidious and variable; fever and respiratory symptoms are rare; some patients have arthralgias and rashes The patient may have loss of appetite, dyspepsia, abdominal pain, generalized aching, malaise, and weakness

  

       

Risk Factors Frequent exposure to blood, blood products, or other body fluids Health care workers: hemodialysis staff, oncology, and chemotherapy nurses, personnel at risk for needle-sticks, operating room staff, respiratory therapies, surgeons, dentists Hemodialysis Male homosexual and bisexual activity IV/injection drug use Close contact with carrier of HBV Travel to or residence in area with uncertain sanitary conditions Multiple sexual partner Recent history of sexually transmitted disease Receipt of blood products (eg.clotting factor concentrate)

     

 

Signs and Symptoms Appetite loss Feeling tired (fatigue) Nausea and vomiting Itching all over the body Pain over the location of the liver (on the right side of the abdomen, under the lower rib cage) Jaundice (a condition in which the skin and the whites of the eyes turn yellow in color) Dark urine (the color of cola or tea) Pale-colored stools (grayish or clay colored)

Prevention The goal of prevention are to interrupt the chain of transmission, to protect who are at risk by active immunization through the use of hepatitis B vaccine, and to use passive immunization for unprotected people exposed to HBV.

Treatment Acute hepatitis B usually resolves on its own and does not require medical treatment. If very severe, symptoms such as vomiting or diarrhea are present, the affected person may require treatment to restore fluids and electrolytes. There are no medications that can prevent acute hepatitis B from becoming chronic. If a person has chronic hepatitis B, they should see their health care provider regularly.

Nursing Management Convalescence may be prolonged, with complete recovery sometimes requiring 3 to 4 months or longer. During this stage, gradual resumption of physical activity is encouraged after the jaundice has resolved. The nurse identifies psychosocial issues and concern, particularly the effects of separation from family and friends if the patient is hospitalized during the acute and infective stages. Even if not hospitalized, the patient will be unable to work and must avoid sexual contact.

Blood transfusion and sexual contact once accounted for most cases of hepatitis C in the United States, other parenteral means, such as sharing of contaminated needle by IV/injection drugs users and unintentional needle sticks and other injuries in health care workers, now account for a significant number of cases. Individuals who are at risk of hepatitis include IV/injection drug users, sexual active people with multiple partners, patients receiving frequent transfusions, those who require large volume of blood, and health care personnel.

      

 

Signs and Symptoms Nausea Vomiting Diarrhea Loss of appetite Fatigue Pain over the liver (on the right side of the abdomen, just under the rib cage) Jaundice - A condition in which the skin and the whites of the eyes turn yellow Dark-colored urine (may look like cola or tea) Stools become pale in color (grayish or clay colored)

Treatment Self-Care at Home  If you have symptoms, these measures will help you feel better faster.  Take it easy; get plenty of rest.  Drink plenty of fluids to prevent dehydration.  Do not drink alcohol of any kind, including beer, wine, and hard liquor.  Avoid medicines and substances that can cause harm to the liver such as acetaminophen (Tylenol) and other preparations that contain acetaminophen.  Avoid prolonged, vigorous exercise until symptoms start to improve.

Hepatitis D virus (delta agent) infection occurs in some cases of hepatitis B. Because the virus requires hepatitis B surface antigen for its replication, only individuals with hepatitis B are at risk for hepatitis D. Anti-delta antibodies in the presence of HBAg on testing confirm the diagnosis. Hepatitis D is common among IV/injection drug users, hemodialysis patients, and recipients of multiple blood transfusions. Sexual contact with those with hepatitis b is considered to be an important mode of transmission of hepatitis B and D.

            

Signs and Symptoms Fatigue Excessive tiredness Not feeling very hungry Nausea or vomiting Diarrhea A low-grade fever Muscle pain Joint pain Sore throat Mild abdominal pain (or stomach pain) Dark urine Light-colored stool.

   

 

Prevention The best way to prevent hepatitis D is to get vaccinated for hepatitis B. This is because a person cannot get hepatitis D unless he or she has hepatitis B. The hepatitis B vaccine is usually given through three injections over a period of six months. Candidates for hepatitis B vaccination can include the following groups of people . All girls and boys from 0 to 18 years old. Anyone whose sex partner has chronic hepatitis D.

 

  

Men who have sex with men Someone who has recently been diagnosed with a sexually transmitted disease (STD) People with multiple sex partners Anyone who shoots drugs Someone who lives with a person who has chronic hepatitis B or hepatitis D People whose jobs expose them to human blood.

Prevention As hepatitis D virus cannot exist without hepatitis B infection, infection can be prevented by taking measures to avoid hepatitis B infection. If a patient is hepatitis B positive, they must avoid further exposure to blood products and body fluids, for example by avoiding needle sharing and unprotected sex.

Is caused by a nonenveloped, single-strand RNA virus. It transmitted by the fecal-oral route but is hard to detect because it is inconsistently shed in the feces. Is has a self-limited course with an abrupt onset. Jaundice is almost always present, chronic forms do not develop.

           

Signs and Symptoms These symptoms(especially early ones) may be similar to the stomach flu and can include: Fatigue Excessive tiredness A lack of appetite Nausea Diarrhea A low-grade fever Muscle pain Joint pain A sore throat Dark urine Pale-colored stool Stomach pain (or abdominal pain) on the right side.

Treatment There are no specific medicines that can cure hepatitis E. Therefore, treatment of hepatitis E is focused on dealing with any symptoms or complications that may occur. This is known as supportive care. Even without specialized treatment for acute hepatitis E, most people recover completely within a few weeks. However, there are some things you can do that might help you feel better. There are also certain things that you should avoid.

Nursing Management Provide contacts (or parents/guardians) with advice about the risk of infection; counsel them to watch for signs or symptoms of hepatitis occurring within 9 weeks of exposure and seek medical attention early if symptoms develop. Advice about careful hygiene should be given, particularly about hand washing after going to the toilet. It is especially important that any food handlers monitor their own development of hepatitis symptoms after contact with the disease and seek medical attention promptly if symptoms are detected.

Proper surveillance of the community and the source of water should be emphasized to the community leaders. Teach the children as well as the adults of proper hand washing and good hygiene. Evaluate the source of water supply in the community and refer to the leaders of the community if the source of drinking water is at danger of making the transmission of Hepatits E possible. Emphasize to the leaders of the community the political will to provide hygienic sanitation to each of the houses in the community.

Alcoholic hepatitis describes liver inflammation caused by drinking alcohol. Though alcoholic hepatitis is most likely to occur in people who drink heavily over many years, the relationship between drinking and alcoholic hepatitis is complex. Not all heavy drinkers develop alcoholic hepatitis, and the disease can occur in people who drink only moderately. People who continue to drink alcohol can go on to develop more serious liver damage in the form of cirrhosis and liver failure.

Clinical Manifestations Symptoms: Mild forms of alcoholic hepatitis may not cause noticeable problems, but as the disease becomes more advanced and the liver more damaged, signs and symptoms are likely to develop. These may include: Loss of appetite Nausea and vomiting Abdominal pain and tenderness Yellowing of the skin and whites of the eyes (jaundice) Fever

Abdominal swelling due to fluid accumulation (ascites) Mental confusion Fatigue Clinical signs: fatigue, liver pain, sexual dysfunction, impotence, hepatomegaly (mild alcoholic hepatitis, hepatomegaly 36% -71%, medium 2 / 3 hepatomegaly, severe all hepatomegaly) also available for reference. These inspection items are non-specific, and therefore, in specific patients, relying on the presence or absence of the non-specific changes to distinguish mild, moderate and severe is imprecise, conditional, it should do to help determine the severity of liver biopsy degree.

Causes Alcoholic hepatitis occurs when the liver is damaged by alcohol you drink. Just how alcohol damages the liver and why it does so only in a minority of heavy drinkers isn't entirely clear. What is known is that the process of breaking down ethanol the alcohol in beer, wine and liquor produces highly toxic chemicals, such as acetaldehyde. These chemicals trigger inflammation that destroys liver cells. In time, web-like scars and small knots of tissue replace healthy liver tissue, interfering with the liver's ability to function.

This irreversible scarring, called cirrhosis, is the final stage of alcoholic liver disease. Risk increases with time, amount consumed Heavy alcohol use can lead to liver disease, and the risk increases with the length of time and amount of alcohol you drink. But because many people who drink heavily or binge drink never develop alcoholic hepatitis or cirrhosis, it's likely that factors other than alcohol play a role. These may include:

Alcohol use. Consistent heavy drinking or binge drinking is the primary risk factor for alcoholic hepatitis, though it's hard to precisely define what constitutes heavy drinking because people vary greatly in their sensitivity to alcohol. Moderate drinking is generally defined as no more than two drinks a day for men and one for women. Binge drinking is usually defined as more than four alcoholic drinks in one sitting for women, and more than five drinks in one sitting for men.

 Also a matter of debate is whether certain types of alcohol cause more harm than others. Some experts believe that wine is less damaging than hard liquor or beer, but this has yet to be proven.

Complications Increased blood pressure in the portal vein. Blood from your intestine, spleen and pancreas enters your liver through a large blood vessel called the portal vein. If scar tissue slows normal circulation through the liver, this blood backs up, leading to increased pressure within the vein (portal hypertension).

Enlarged veins (varices). When circulation through the portal vein is blocked, blood may back up into other blood vessels in the stomach and esophagus. These blood vessels are thin walled, and because they're filled with more blood than they're meant to carry, they're likely to bleed. Massive bleeding in the upper stomach or esophagus from these blood vessels is a life-threatening emergency that requires immediate medical care.

Fluid retention. Alcoholic hepatitis can cause large amounts of fluid to accumulate in your abdominal cavity (ascites). Abdominal fluid may become infected and require treatment with antibiotics. Although not life-threatening in itself, ascites is usually a sign of advanced alcoholic hepatitis or cirrhosis. Bruising and bleeding. Alcoholic hepatitis interferes with the production of proteins that help your blood to clot.

 As a result, you may bruise and bleed more easily than normal. Jaundice. This occurs when your liver isn't able to remove bilirubin the residue of old red blood cells from your blood. Eventually, bilirubin builds up and is deposited in your skin and the whites of your eyes, causing a yellow color. Hepatic encephalopathy. A liver damaged by alcoholic hepatitis has trouble removing toxins from your body normally one of the liver's key tasks.

 The buildup of toxins can damage your brain, leading to changes in your mental state, behavior and personality (hepatic encephalopathy). Signs and symptoms of hepatic encephalopathy include forgetfulness, confusion and mood changes, and in the most severe cases, coma.

Scarred liver (cirrhosis). Over time, the liver inflammation that occurs in alcoholic hepatitis can cause irreversible scarring of the liver (cirrhosis). Cirrhosis frequently leads to liver failure, which occurs when the damaged liver is no longer able to adequately function.

Tests and diagnosis Because there are numerous liver diseases and a wide range of factors that can cause them, including viral infections, drugs and environmental toxins, diagnosing alcoholic hepatitis can be challenging. Medical history and physical exam. Your doctor will ask you questions about your health history, including alcohol use, and conduct a physical exam. Blood tests. These check for high levels of certain liver-related enzymes, such as aspartate aminotransferase (AST) and alanine aminotransferase (ALT).

Ultrasound. Your doctor may use this noninvasive imaging test to view your liver and to rule out other liver problems. Liver biopsy. In this procedure, a small sample of tissue is removed from your liver and examined under a microscope. Liver biopsy usually involves inserting a long, thin needle through your skin and into your liver in order to draw out a sample of tissue.

Treatments Stop drinking alcohol If you've been diagnosed with alcoholic hepatitis, you must stop drinking alcohol. It's the only way to reverse liver damage or, in more advanced cases, to prevent the disease from becoming worse. If you continue to drink alcohol, you're likely to experience serious complications. If you are dependent on alcohol and want to stop drinking, your doctor can recommend a therapy that's tailored for your needs.

 This might include medications, counseling, Alcoholics Anonymous, an outpatient treatment program or a residential inpatient stay. Medications to reduce liver inflammation People with severe alcoholic hepatitis may consider short-term treatment with medications to control liver inflammation.

 In certain situations, your doctor may recommend corticosteroids or pentoxifylline. Liver transplant When liver function is severely impaired, a liver transplant may be the only option for some people. Although liver transplantation is often successful, the number of people awaiting transplants far exceeds the number of available organs. For that reason, liver transplantation in people with alcoholic liver disease is controversial.

 Some medical centers may be reluctant to perform liver transplants on people with alcoholic liver disease because they believe a substantial number will return to drinking after surgery, won't take the necessary anti-rejection medications, or will require more care and resources than will other patients. Most of these objections have not been borne out in practice, however, and many doctors now feel that some people with alcoholic liver disease are good candidates for transplant surgery.

 But requirements are still stringent, including abstinence from alcohol for at least six months before surgery and enrollment in a counseling program.

Nursing Intervention 1. Determine presence of condition(s), as listed above. Note whether problem is acuteviral hepatitis or acetaminophen overdoseor chroniclong-standing alcoholic hepatitis. Rationale: Influences choice of interventions. 2. Review medicationssulfonamides, phenothiazines, isoniazidfor hepatotoxic drugs or OTC drug use such as acetaminophen. Rationale: May require changes in usual medication regimen and client education about hepatic effects of OTC drugs.

3. Ascertain if client works in high-risk occupation; for example, performs tasks that involve contact with blood, blood contaminated body fluids, other body fluids, or sharps or needles. Rationale: Helps in identifying source of infectionoccupational high risk for exposure to HBV and HCV. 4. Assess for exposure to contaminated food or untreated drinking water or for evidence of poor sanitation practices by foodservice workers, if source is known. Rationale: Helps in identifying source of infectionrisk for exposure to enteric viruses, such as HAV and HEV.

5. Review results of laboratory tests, such as hepatitis viral titers, liver function, and other diagnostic studies. Rationale: Identifies cause of hepatitis, influences choice of interventions, and monitors response to therapies. 6. Assist with treatment of underlying condition. Rationale: Supports organ function and minimizes liver damage and risk of organ failure. For chronic HBV and HCV infections, in particular, the goals of therapy are to reduce liver inflammation and fibrosis and to prevent progression to cirrhosis and the associated complications.

7. Administer medications, as indicated, for example: Antivirals, such as, amantidine (Symmetrel), famciclovir (Famvir), and entecavir (Baraclude) Rationale: The particular or combination of medication used depends on the type of infection. Inhibit viral reproduction. 8. Lamivudine (Epivir), adefovirdipivoxil (Hepsera), tenofovin (Viread), and telbivudine (Tyzeka) Rationale: Help reduce viral load and treat chronic active HBV. Alternative choice for individuals unable or unwilling to use interferon; or, in the presence of impaired immune function such as coinfection with HIV.

9. BMRs, such as interferon alpha-2a (Roferon A) and interferon alpha-2b (Intron A) Rationale: Reduce viral load and treat symptoms of HCV; may lead to temporary improvement in liver function. Also used in HDV. Note: Interferons have been found to induce remission in 25% to 50% of clients with chronic HBV and in 40% of those with chronic HCV. 10. Steroid therapy, such as prednisone (Deltasone), alone or in combination with azathioprine (Imuran).

Rationale: Steroids may be contraindicated because they can increase risk of relapse or development of chronic hepatitis in clients with viral hepatitis; however, anti-inflammatory effect may be useful in chronic active hepatitis, especially idiopathic, to reduce nausea and vomiting and to enable client to retain food and fluids. A brief course may also be useful in cholestatic HAV to shorten the illness . Steroids may decrease serum aminotransferase and bilirubin levels, but they do not affect liver necrosis or regeneration. Combination therapy has fewer steroid-related side effects.

Cirrhosis is scarring of the liver. Your liver is a large organ that is located in your upper abdomen. The liver carries out several essential functions, such as detoxifying harmful substances in your body, purifying your blood and manufacturing vital nutrients. Cirrhosis occurs in response to chronic damage to your liver. With mild cirrhosis, your liver can repair itself and continue to do its job. But with more advanced cirrhosis, more and more scar tissue forms in the liver, making it impossible to function adequately. A number of diseases and conditions can cause the chronic liver damage that leads to cirrhosis.

Clinical Manifestation The severity of manifestations helps to categories the disorder as compensated or decompensated cirrhosis. Compensated cirrhosis, with its less severe, often vague symptoms, may be discovered secondarily at a routine physical examination The hall-marks of decompensated cirrhosis result from failure of the liver to synthesize proteins, clotting factors and other substances and manifestations of portal hypertension

        

Signs and Symptoms Fatigue Bleeding easily Easy bruising Fluid accumulation in your abdomen Loss of appetite Nausea Swelling in your legs Weight loss

Treatment Treatment for cirrhosis cannot reverse liver damage, but it can stop or slow progression of the disease and reduce complications. It depends on what is causing the cirrhosis and which particular complications, if any, have appeared.

Prevention

   

The best way to avoid cirrhosis is to avoid the underlying conditions that cause it. Know the risk factors for hepatitis B and hepatitis C and avoid them as much as possible. Avoid risky behaviors such as alcohol abuse, IV drug use, and unprotected sexual intercourse. Drink alcohol only in moderation, if at all. Develop healthy habits. Avoid using tobacco. Eat a healthy diet, get plenty of physical activity and rest, and maintain your weight in a healthy range.

Talk to your health care provider before taking vitamin supplements. Large doses of vitamins and minerals, especially vitamin A, iron, or copper, can actually worsen liver damage. Hepatitis B immunizations are available to health care workers and others at high risk of contacting the disease. Immunization of all American children against hepatitis B, now required, will reduce the incidence of cirrhosis in the future. No effective hepatitis C vaccination is available.

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Reporters:
Alisto, Rhona joy Ayaba. Roselyn Binay-an, Chelsie Cortes, Bethsaida Galbin, Sandra Gallejo, Grecilli Ann Lacasandile, Joville Allen Langbayan, Sheryl Magsakay, Daphne Joy