Liver Cirrhosis

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LIVER CIRRHOSIS

The Liver

The liver is the largest organ (about the size of a football and

averaging about 3.5 pounds) and has more functions than any other human

organ. A person's entire blood supply passes through the liver several times

a day, and at any given time there is about a pint of blood there. The liver

produces and secretes bile (to be stored in the gallbladder until needed)

that is used to break down and digest fatty acids. It also produces

prothrombin and fibrinogen, both blood-clotting factors, and heparin, a

mucopolysaccharide sulfuric acid ester that helps keep blood from clotting

within the circulatory system.

The liver converts sugar into glycogen, which it stores until

the muscles need energy and it is secreted into the blood stream as glucose.

The liver synthesizes proteins and cholesterol and converts carbohydrates

and proteins into fats, which are stored for later use. It also produces

blood protein and hundreds of enzymes needed for digestion and other bodily

functions. As it breaks down proteins, the liver also produces urea, which

it synthesizes from carbon dioxide and ammonia. (Urea, the primary solid

component of urine, is eventually excreted by the kidneys.) The liver also

stores critical trace elements such as iron and copper, as well as vitamins

A, D, and B12.

Cirrhosis

Cirrhosis of the liver is a chronic, diffuse (widely spread

throughout the organ), degenerative liver disease in which the parenchyma

(the functional organ tissue) degenerates, the lobules are infiltrated with

fat and structurally altered, dense perilobular connective tissue forms, and

areas of regeneration often develop. The first scientist known to have

diagnosed the disease was Gianbattista Morgagni, who published 500 autopsies

in 1761. Laennec named the disease in 1826, using the Greek word for orange

color because cirrhotic livers turn a yellowish to tan color.

Cirrhosis is the seventh leading cause of death by disease in

the United States, with about 25,000 dying from it each year (down from

50,000 in 1979). About a third of the cases are compensated, meaning there

are no clinical symptoms. Such cases are usually discovered during routine

tests for other problems, or during surgery or autopsy. In most cases,

though, there is a loss of liver cell function, and an increased resistance

to blood flow through the damaged liver tissue (a condition known as portal

hypertension) leading to esophageal varices (enlarged, swollen veins at the

lower end of the esophagus). Severe cirrhosis leads to ammonia toxicity,

hepatic coma, gastrointestinal hemorrhage, and kidney failure. As liver

cells are destroyed, they are systematically replaced by scar tissue.

Symptoms

Symptoms of cirrhosis include nausea or indigestion and

vomiting, constipation or diarrhea, flatulence, anorexia, weight loss,

ascites (the accumulation of serous fluids in the peritoneal cavity),

light-colored stools, weakness or chronic dyspepsia, dull abdominal aching,

varicosities, nosebleeds, bleeding gums, other internal and external

bleeding, easy bruising, extreme dryness of skin, and spider angiomas.

Psychotic mental changes such as extreme paranoia can occur in cases of

advanced cirrhosis. Other symptoms are testicular atrophy, gynecomastia

(enlargement of the male breast), and loss of chest and armpit hair.

Complications

When blood flow in the cirrhotic liver is restricted, blood can

" back up " in the spleen, causing enlarged spleen and sequestered blood

cells. In this condition the platelet count typically falls, and abnormal

bleeding can result. In extreme cases blood can actually flow backward from

portal circulation to systemic circulation, leading to varicose veins in the

stomach (gastric varices), esophagus (esophageal varices), and rectum

(hemorrhoids). Ruptured varices bleed massively and are often fatal.

Bilirubin levels may build up in the blood, causing jaundice and bright

yellow to dark brown urine. Cirrhosis can also cause insulin resistance and

diabetes mellitus. Brain injury can result from inadequate filtering of

blood toxins. Such brain damage can have symptoms that range from poor

concentration to coma, swelling of the brain, stupor, and even death.

Cirrhosis is often associated with osteomalacia (the adult form of rickets,

a softening of the bones that often leaves them brittle) and osteoporosis (a

reduction in bone mass).

The Alcohol Factor

The most common cause of cirrhosis is believed to be alcohol

(ethanol) abuse (about 10% of American men and about 3% of American women

chronically abuse alcohol). Though it affects many organs, alcohol is

especially harmful to the central nervous system and the liver, and is a

factor in about three-fourths of the cases of cirrhosis in the United

States. Alcohol must be metabolized, and the liver performs most of that

job, suffering serious damage in the process. Not only does alcohol destroy

liver cells, it also robs them of their ability to regenerate.

Such cofactors as hepatitis C virus can increase the risk of

cirrhosis in those whose intake of alcohol is excessive. Alcohol-induced

cirrhosis is among the ten leading causes of death in the United States.

Women are at much higher risk for drinking-related cirrhosis than are men.

This may be true because less of the alcohol consumed is metabolized in the

stomach in women before being absorbed into the blood stream. Autopsies

indicate that from 10 to 15% of American alcoholics suffer from cirrhosis at

the time of death. About a third of those consuming one cup to one pint (8

to 16 ounces) of hard liquor a day (or the equivalent in other drinks) over

a 15-year period will develop cirrhosis.

In addition to cirrhosis, alcohol abuse can lead to fatty liver,

which can lead to stearohepatitis (or steatohepatitis, the older term),

scarring of the liver, and eventually to cirrhosis. Overuse of alcohol can

also lead to acute, chronic hepatitis. Complications can include liver

dysfunction, abnormal blood clotting, jaundice, and hepatic encephalopathy

(neurological dysfunction brought on by failure of the liver). Chronic

abusers of alcohol often need significant vitamin supplementation to correct

vitamin deficiencies caused as much by neglect and poor eating habits as by

damage from the alcohol. An acute thiamin (vitamin B1) deficiency is

typical.

Other Risk Factors and Causes

Cirrhosis patients are at high risk for obesity, fatal bacterial

infections, stomach ulcers, kidney problems, gallstones, and diabetes

mellitus. They are also at increased risk for liver cancer. Risk factors for

cirrhosis include nutritional deficiencies (lack of proteins, vitamins,

choline, trace elements, or methionine), hepatitis (B, C, or D) and other

bacterial and viral infections, and severe reactions to prescription or

" recreational " drugs. Vitamin B1 (thiamin) deficiency may directly cause

alcoholic cirrhosis. One study concluded that vitamin B1 deficiency is a

greater risk factor for liver cell death than heavy alcohol consumption.

Congestive heart failure and poisons (including alcohol,

phosphorus, and carbon tetrachloride) pose a serious threat to the liver and

can lead to cirrhosis. Genetic disorders, inherited metabolic diseases such

as hemochromatosis (marked by excessive iron absorption and accumulation)

and 's disease (in which the liver stores too much copper), advanced

syphilis, exposure to blood flukes, other parasitic infections (such as

schistosomiasis), and blocking of the common bile duct are all factors that

can lead to cirrhosis. Liver injury from an accident or from cystic fibrosis

can also bring on cirrhosis.

Diagnosis

Positive diagnosis of cirrhosis must be made by liver biopsy,

but X-ray, blood tests, and physical examination are all used in diagnosis,

as is observation of the symptoms mentioned earlier. CAT (computerized axial

tomography) scans, radioisotope liver scans, and ultrasound can all be used

to diagnose cirrhosis. Early diagnosis is critical in order to establish the

cause of the disease and determine the amount of damage to the liver.

Two symptoms of cirrhosis are the loss of healthy, functioning

liver cells and the scarring and distortion of the liver that eventually

take place. As fewer cells function, less albumin (a protein) is

manufactured. Lowered albumin levels permit water retention (edema) in the

legs and abdomen (ascites). Easy bruising and bleeding result, and, in some

cases, vomiting of blood. Intense skin itching can also result from

excessive bile product deposits in the skin, often accompanied by jaundice

or yellow skin.

Gallstones are more likely to form in cirrhosis patients because

there is not enough bile reaching the gallbladder. Toxins that the liver

would normally remove build up in the blood, dulling mental functions and

bringing on personality changes. Drugs the patient is taking, normally

filtered out and disposed of in urine, may remain in the bloodstream for a

much longer period and act longer than expected or even build up in body

tissue. A liver with cirrhosis is usually much larger than a healthy liver.

Precautions and Prevention

Once cirrhosis has been diagnosed, sodium and fluids should be

restricted, and all alcohol consumption must cease. Antiemetics, diuretics,

and supplemental vitamins are prescribed. Cirrhosis patients should avoid

straining at the bowel, violent sneezing and coughing, and nose blowing, and

should use stool softeners as prescribed by a qualified medical caregiver.

Untreated cirrhosis can be fatal; patients should avoid exposure to

infections and eat small but frequent meals of nutritious foods, carefully

following caregiver instructions. The liver is the only organ that can

generate healthy, new tissue in response to injury or disease. It is

therefore possible to regenerate a cirrhosis-damaged liver if extraordinary

therapies are followed and the underlying cause of the cirrhosis is

eliminated.

More than half of all liver disease could be prevented if we

acted on the knowledge we already have. Avoiding or limiting the use of

alcoholic beverages is a good place to start, because it is well documented

that alcohol destroys liver cells. Man-made chemicals also pose an extreme

threat to the liver, so take recommended precautions. Remember that all

ingested, inhaled, and absorbed toxins must be processed by the liver. When

working with hazardous chemicals use adequate ventilation; follow product

instructions; do not mix chemicals; wear protective clothing and breathing

equipment; avoid inhalation and ingestion of hazardous materials; avoid skin

contact and flush (wash) affected areas immediately; if necessary, call your

poison control center or your emergency number (such as 911). A complete

listing of toll-free poison control center numbers can be obtained online at

MediciNet.com.

Treatments

When varices result, they can be treated with a reduction of

salt intake and with diuretics, which help eliminate excess salts and fluids

from the body. Coma and encephalopathy are treated by a reduction of protein

intake, and hemorrhage from varices can be stopped by sclerotherapy

(injection of a scarring chemical into the bleeding vein). Varices can also

be compressed by the use of a special balloon that is inflated around the

enlarged vein, squeezing it as the balloon is inflated. There is a new

procedure (using radiology)-transjugular intrahepatic protosystemic shunt

(TIPS)-that shows some promise.

Interferon-alpha, a powerful antiviral, may reduce the risk of

cancer in some cirrhosis patients. In cases of total liver failure,

transplantation has been successful. >>ETC. Interesting article