What is Fatty tissue degeneration?

Question

What is Fatty tissue degeneration and how and how long does it become full cirrhosis and how long can someone with full blown cirrhosis live. Pls give me as much details as you can .Thanks

Answer 1

Cirrhosis is a consequence of chronic liver disease characterized by replacement of liver tissue by fibrotic scar tissue as well as regenerative nodules, leading to progressive loss of liver function. Cirrhosis is most commonly caused by alcoholism and hepatitis C, and was the 12th leading cause of death in the United States in 2000.[1] Ascites is the most common complication of cirrhosis and is associated with a poor quality of life, increased risk of infections, and a poor long term outcome. In advanced stages of cirrhosis, the condition is irreversible and the only option would be a liver transplant.

Symptoms and signs
The following signs and symptoms may occur in the presence of cirrhosis or as a result of the complications of cirrhosis. Many are nonspecific and may occur in other diseases and does not necessarily point to cirrhosis. Likewise, the absence of any does not rule out the possibility of cirrhosis.

Spider angiomata. Vascular lesions consisting of central arteriole surrounded by many smaller vessels due to an increase in estradiol.
Palmar erythema. Exaggerations of normal speckled mottling of the palm, due to altered sex hormone metabolism.
Nail changes.
Muehrcke's nails --- paired horizontal bands separated by normal color due to hypoalbuminemia
Terry's nails --- proximal two thirds of the nail plate appears white with distal one-third red, also due to hypoalbuminemia
Clubbing. Angle between the nail plate and proximal nail fold > 180 degrees
Hypertrophic osteoarthropathy. Chronic proliferative periostitis of the long bones that can cause considerable pain.
Dupuytren's contracture. Thickening and shortening of palmar fascia that leads to flexion deformities of the fingers. Thought to be due to fibroblastic proliferation and disorderly collagen deposition. It is relatively common (33% of patients).
Gynecomastia. Benign proliferation of glandular tissue of male breasts presenting with a rubbery or firm mass extending concentrically from the nipples. This is due to increased estradiol and can occur up to 66% of patients.
Hypogonadism. Manifested as impotence, infertility, loss of sexual drive, and testicular atrophy due to primary gonadal injury or suppression of hypothalamic or pituitary function.
Liver size. Can be enlarged, normal, or shrunken.
Splenomegaly. Due to congestion of the red pulp as a result of portal hypertension
Ascites. Accumulation of fluid in the peritoneal cavity giving rise to flank dullness (needs about 1500 mL to detect flank dullness).
Caput medusa. In portal hypertension, the umbilical vein may open. Blood from the portal venous system may be shunted through the periumbilical veins into the umbilical vein and ultimately to the abdominal wall veins, manifesting as caput medusa.
Cruveilhier-Baumgarten murmur. Venous hum heard in epigastric region due to collateral connections between portal system and the remnant of the umbilical vein in portal hypertension.
Fetor hepaticus. Sweet pungent smell in breath due to increased dimethylsulphide due to severe portal-systemic shunting.
Jaundice. Yellow discoloring of the skin, eye, and mucus membranes due to increased bilirubin (at least 2-3 mg/dL). Urine may also appear dark.
Asterixis. Bilateral asynchronous flapping of outstretched, dorsiflexed hands seen in patients with hepatic encephalopathy.
Other. weakness, fatigue, anorexia, weight loss

[edit] Complications
As the disease progresses, complications may develop. In some people, these may be the first signs of the disease.

Bruising and bleeding due to decreased production of coagulation factors.
Jaundice due to decreased processing of bilirubin.
Itching due to bile products deposited in the skin.
Hepatic encephalopathy - the liver does not clear ammonia and related nitrogenous substances from the blood, which affect cerebral functioning: neglect of personal appearance, unresponsiveness, forgetfulness, trouble concentrating, or changes in sleep habits.
Sensitivity to medication due to decreased metabolism of the active compounds.
Hepatocellular carcinoma is primary liver cancer, a frequent complication of cirrhosis. It has a high mortality rate.
Portal hypertension - blood normally carried from the intestines and spleen through the portal vein flows more slowly and the pressure increases; this leads to the following complications:
Ascites - fluid leaks through the vasculature into the abdominal cavity.
Esophageal varices - collateral portal blood flow through vessels in the stomach and esophagus. These blood vessels may become enlarged and are more likely to burst.
Problems in other organs. Cirrhosis can cause immune system dysfunction, leading to infection. Fluid in the abdomen (ascites) may become infected with bacteria normally present in the intestines (spontaneous bacterial peritonitis). Cirrhosis can also lead to impotence, brain dysfunction and renal failure (hepatorenal syndrome) and osteoporosis.

[edit] Causes
Cirrhosis has many possible causes; sometimes more than one cause are present in the same patient. In the Western World, chronic alcoholism and hepatitis C are the most common causes.

Alcoholic liver disease (ALD). Alcoholic cirrhosis develops in 15% of individuals who drink heavily for more than a decade. There is great variability in the amount of alcohol needed to cause cirrhosis (as little as 3-4 drinks a day in some men and 2-3 in some women). Alcohol seems to injure the liver by blocking the normal metabolism of protein, fats, and carbohydrates. Patients may also have concurrent alcohol hepatitis with fever, hepatomegaly, jaundice, and anorexia. AST and ALT are both elevated but less than 300 IU/L with a AST:ALT ratio > 2.0, a value rarely seen in other liver diseases. Liver biopsy may show hepatocyte necrosis, Mallory bodies, neutrophilic infiltration with perivenular inflammation.
Chronic hepatitis C. Infection with this virus causes inflammation of and low grade damage to the liver that over several decades can lead to cirrhosis. Can be diagnosed with serologic assays that detect hepatitis C antibody or viral RNA. The enzyme immunoassay, EIA-2, is the most commonly used screening test in the US.
Chronic hepatitis B. The hepatitis B virus is probably the most common cause of cirrhosis worldwide, especially South-East Asia, but it is less common in the United States and the Western world. Hepatitis B causes liver inflammation and injury that over several decades can lead to cirrhosis. Hepatitis D is dependent on the presence of hepatitis B, but accelerates cirrhosis in co-infection. Chronic hepatitis B can be diagnosed with detection of HBsAG > 6 months after initial infection. HBeAG and HBV DNA are determined to assess whether patient will need antiviral therapy.
Non-alcoholic steatohepatitis (NASH). In NASH, fat builds up in the liver and eventually causes scar tissue. This type of hepatitis appears to be associated with diabetes, protein malnutrition, obesity, coronary artery disease, and treatment with corticosteroid medications. This disorder is similar to that of alcohol liver disease but patient does not have an alcohol history. Biopsy is needed for diagnosis and appears similar to that in alcohol liver disease.
Primary biliary cirrhosis. May be asymptomatic or complain of fatigue, pruritus, and non-jaundice skin hyperpigmentation with hepatomegaly. There is prominent alkaline phosphatase elevation as well as elevations in cholesterol and bilirubin. Gold standard diagnosis is antimitochondrial antibodies with liver biopsy as confirmation if showing florid bile duct lesions.
Primary sclerosing cholangitis. PSC is a progressive cholestatic disorder presenting with pruritus, steatorrhea, fat soluble vitamin deficiencies, and metabolic bone disease. There is a strong association with inflammatory bowel disease (IBD), especially ulcerative colitis. Diagnosis is best with contrast cholangiography showing diffuse, multifocal strictures and focal dilation of bile ducts, leading to a beaded appearance. Non-specific serum immunoglobulins may also be elevated.
Autoimmune hepatitis. This disease is caused by the immunologic damage to the liver causing inflammation and eventually scarring and cirrhosis. Findings include elevations in serum globulins, especially gamma globulins. Therapy with prednisone +/- azathioprine is beneficial. Cirrhosis due to autoimmune hepatitis still has 10-year survival of 90%+. There's no specific tool to diagnose autoimmune but it can be beneficial to initiate a trial of corticosteroids.
Hereditary hemochromatosis. Usually presents with family history of cirrhosis, skin hyperpigmentation, diabetes mellitus, pseudogout, and/or cardiomyopathy, all due to signs of iron overload. Labs will show fasting transferrin saturation of > 60% and ferritin > 300 ng/mL. If hepatic iron > 71 umol/g, it is highly suggestive of homozygous HH and warrants genetic testing or liver biopsy. Biopsy is stained with Prussian blue and may detect fibrosis. Heterozygotes do not develop cirrhosis.
Wilson's disease. Autosomal recessive disorder characterized by low serum ceruloplasmin and increased hepatic copper content on liver biopsy. May also have Kayser-Fleischer rings in the cornea and altered mental status.
Alpha 1-antitrypsin deficiency (AAT). Autosomal recessive disorder. Patients may also have COPD. Serum AAT will be low.
Cardiac cirrhosis. Due to chronic right sided heart failure which leads to liver congestion.
Galactosemia
Glycogen storage diseases
Cystic fibrosis
Drugs or toxins, including chronic use of acetaminophen.
Certain parasitic infections (like schistosomiasis).

[edit] Diagnosis
The gold standard for diagnosis of cirrhosis is a liver biopsy, through a percutaneous, transjugular, laparoscopic, or fine-needle approach. Histologically cirrhosis can be classified as micronodular, macronodular, or mixed, but this classification has been abandoned since it is nonspecific to the etiology, it may change as the disease progresses, and serological markers are much more specific. However, a biopsy is not necessary if the clinical, laboratory, and radiologic data suggests cirrhosis.

Answer 2

Cirrhosis is a slowly progressing disease in which healthy liver tissue is replaced with scar tissue, eventually preventing the liver from functioning properly. The scar tissue blocks the flow of blood through the liver and slows the processing of nutrients, hormones, drugs, and naturally produced toxins. It also slows the production of proteins and other substances made by the liver.

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Answer 3

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RE:
What is Fatty tissue degeneration?
What is Fatty tissue degeneration and how and how long does it become full cirrhosis and how long can someone with full blown cirrhosis live. Pls give me as much details as you can .Thanks

Answer 4

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Answer 5

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