Cirrhosis is a chronic liver disease marked by the widespread destruction of liver cells and their replacement by fibrous cells. This disease alters the liver’s structure and its blood vessels. The fibrous cells interfere with blood and lymph flow and ultimately cause liver failure.

Cirrhosis is twice as common in men as in women and is especially prevalent among malnourished, chronic alcoholics over age 50. The death rate is high: Many persons die within 5 years of its start. A person with the first signs of cirrhosis will benefit from diet and life­style changes.
What causes it?

*

There are many types of cirrhosis, linked to various causes:
*

Portal, nutritional, or alcoholic cirrhosis, called Laennec’s cirrhosis, is the most common type. It affects 30% to 50% of people with the disorder, and 90% of them have a history of alcoholism. Liver damage results from malnutrition, a lack of dietary protein, and heavy drinking for a long period.
*

Biliary cirrhosis (15% to 20% of cases) is caused by bile duct diseases that suppress bile flow.
*

Postnecrotic cirrhosis (10% to 30% of cases) is caused by various types of hepatitis.
*

Pigment cirrhosis (5% to 10% of cases) may be caused by disorders such as abnormal iron metabolism.
*

In about 10% of people with cirrhosis, there is no known cause.

What are the symptoms of Cirrhosis of The Liver ?

The symptoms are similar for all types, regardless of the cause. At first, symptoms are vague, but the person with cirrhosis usually has stomach troubles, including loss of appetite, indigestion, nausea, vomiting, constipation or diarrhea, and a dull ache in the abdomen. Additional symptoms develop as the liver deteriorates:

*

fluid in the lungs, reduced chest expansion, and light-headedness
*

lethargy, mental changes, slurred speech, a flapping tremor, neuritis, paranoia, hallucinations, and coma
*

nosebleeds, easy bruising, bleeding gums, and anemia
*

testicular atrophy and chest-hair loss in men and menstrual irregularities in women
*

severe itching, extreme dryness, patches on the skin and, possibly, jaundice
*

fluid accumulation in the stomach, swollen legs, and other symptoms of full-fledged cirrhosis
*

musty breath odor, loss of muscle from disuse, a fever, stomach pain that worsens when the person sits up or leans forward, bleeding from the throat, and an enlarged liver or spleen.

How is it diagnosed?

The doctor will perform a liver biopsy (obtain a tissue specimen for study) to confirm cirrhosis and may order X-ray scans to check the gallbladder and bile duct for gallstones. To learn more about the extent of the cirrhosis and its complications, the doctor may order lab tests of blood, feces, and utine.
How is it treated?

Treatment aims to remove or alleviate the cause of cirrhosis, prevent further liver damage, and prevent or treat complications. Salt and fluids are usually restricted. The person may benefit from a high-calorie and moderate- to high-protein diet (unless he or she also has hepatic encephalopathy, a condition that requires less protein).

*

If the person’s condition continues to deteriorate, he or she may need tube feedings or vitamin supplements. Recovery depends on a regimen of rest, moderate exercise, and avoidance of infections and whatever substances caused the disorder.
*

Drugs must be given cautiously, because the diseased liver can’t detoxifY harmful substances efficiently. If possible, the doctor will avoid prescribing sedatives but may prescribe an antiemetic for nausea, a vasoconstrictor to stop disease-related bleeding in the throat and, possibly, diuretics to reduce swelling.
*

The doctor may recommend surgery to repair disease-related bleeding in the throat and to remove portions of damaged organs such as the spleen. Finally, prevention and control of cirrhosis depends on the person avoiding alcohol.

Gonorrhea

Guillain Barre Syndrome

Hantavirus Pulmonary Syndrome

Herpangina

Herpes Zoster

Hookworm Disease

Inclusion Conjunctivitis

Influenza

Labyrinthitis

Lassa Fever

Leprosy

Listeriosis

Liver Abscess

Lung Abscess

Lyme Disease

Malaria

Mastoiditis

Meningitis

Meningococcal Infections

Microsporidiosis

Molluscum Contagiosum

Mononucleosis

MRSA Infection

Mucormycosis

Mumps

Myelitis

Myocarditis

Myringitis

Nonviral Hepatitis

Pancreatitis

Rabies

Reiters Syndrome

Rocky Mountain Spotted Fever

Scabies

Scarlet Fever

Schistosomiasis

Staphylococcal Scalded Skin Syndrome

Strongyloidiasis

Taeniasis

Toxic Shock Syndrome

Tuberculosis

Viral Hepatitis

Galactosemia is the name for any disorder that interferes with the body’s ability to metabolize galactose, the sugar found in milk. This disorder produces symptoms ranging from cataracts and liver damage to mental retardation. It occurs in two forms: classic galactosemia and galactokinase-deficiency galactosemia.

Although a galactose-free diet relieves most symptoms, galactosemia-induced mental impairment is irreversible, and the person may have some vision loss. Caught early, the condition can be stopped by changing from milk-based to meat- or soy-based formulas.

What causes Galactosemia?

Both forms of galactosemia are inherited as recessive traits and occur in about 1 in 60,000 births in North America. However, up to 1.25% of the population has the gene that may lead to classic galactosemia. The second form, galactokinase-denciency galactosemia, is rarer. In both forms, inability to normally metabolize the sugar causes galactose accumulation and damage. The mechanism of this defect is still unknown.

What are its symptoms?

Children who inherit the classic galactosemia gene show symptoms at birth or a few days after they start nursing. The symptoms are a failure to thrive, vomiting, and diarrhea. Other effects include yellow skin and eyes, protein in the urine, and cataracts.

If the child continues to drink milk or eat galactose-containing foods, he or she may develop mental retardation, malnourishment, and progressive liver failure and may eventually die. Although treatment may prevent mental impairment, the condition can produce a short attention span, cataracts, difficulty with spatial and mathematical relationships, and apathetic, withdrawn behavior.

How is it diagnosed?

The doctor will order blood tests and urine tests to check for evidence of both types of galactosemia, but the measurements must be precise. Some infants who consume large amounts of milk have elevated blood galactose levels but don’t have the condition. Also, new­borns excrete galactose in their urine for about a week after birth; premature infants, even longer. Other tests include biopsy of liver tissue samples and enzyme tests. Amniocentesis, the sampling of the amniotic fluid that’s done before the infant is born, is recommended when parents are known to have the gene.

How is it treated?

If galactose and lactose are eliminated from the infant’s diet, most of the symptoms disappear. The infant gains weight and the cataracts shrink. If a child has the disorder, the doctor will advise replacing cow’s milk formula or breast milk with a meat-based or soy-based formula. As the child grows, a balanced, galactose-free diet must be maintained.

A pregnant woman who carries the gene should also follow a galactose-restricted diet. Such a diet supports normal growth and development and may delay symptoms in the infant. If the parents of a child with galactosemia want to have another child, the doctor will recommend genetic counseling. In some states, screening of all new­borns for galactosemia is required by law.

There are various reasons why some people cannot absorb B 12 . Your body normally absorbs B 12 from the lower small intestine. But before this can occur the vitamin must combine in the stomach with a special substance known as intrinsic factor, which is secreted by the stomach lining. In some people, for reasons that are not fully understood, the stomach lining stops secreting enough intrinsic factor. Without it, sufficient quantities of vitamin B 12 cannot be absorbed. This is the most common type of B 12 deficiency, and it is called pernicious anemia.

If you have had some forms of digestivetract surgery, your body’s ability to absorb B 12 may be reduced, sometimes to the point where it cannot absorb any of the vitamin.

Folic acid deficiency is usually due to inadequate amounts of the vitamin in the diet. Folic acid is generally supplied by green vegetables. Your body cannot build large reserves of this vitamin, so any deficiency shows up within a few weeks as a form of anemia called folic acid deficiency. If you have celiac disease you are also susceptible to folic acid deficiency because you cannot absorb sufficient amounts of folic acid, even if it is plentiful in your diet. Finally, there are some people who have an increased requirement for folic acid, and they need more of the vitamin than an ordinary diet provides.

Both types of anemia produce the symptoms associated with anemia in general, but B I2 deficiency anemia is more serious, because B 12 is vital to the maintenance of the nervous system as well as to the production of red blood cells. Deficiency of B I2 therefore damages the brain and spinal cord, which causes additional symptoms.

What are the Symptoms?

The main symptoms of B 12 and folic acid deficiency anemia are those of other anemias. They include paleness, fatigue, shortness of breath, and palpitations, or heart fluttering, particularly if you exert yourself. In both disorders, your mouth and tongue may be sore, and your skin may become yellow in color. If the spinal cord is affected by B 12 deficiency, you may not be able to walk or keep your balance properly, and you may feel continuous tingling in your hands and feet. You may also suffer some memory loss, confusion and depression.

Pernicious anemia, the most common type of B 12 deficiency, is equally common in men and women, and rare before the age of 40. If you have a close relative who has pernicious anemia, you have a greater than average risk of contracting it. Folic acid deficiency is somewhat more common than B 12 deficiency. It often occurs in elderly people, who may live on a poor diet. It also occurs in pregnant women, who need extra supplies of the vitamin for the developing baby. It is particularly common in cases of severe alcoholism, because alcoholics often do not eat properly.

What are the Risks?

If you have B I2 or folic acid deficiency anemia, and if it is treated promptly, you will probably recover completely. If you do not obtain prompt treatment for B 12 deficiency anemia you risk permanent damage to your spinal cord and, to a lesser extent, irreversible intellectual impairment.

What should be done?

If you have symptoms of anemia, see your physician. If your movement, balance or memory are also affected, make the appointment without delay. Be sure to tell the physician if you have a close relative who has pernicious anemia. Tests on a blood sample can usually establish whether or not you have either of these vitamin deficiencies. But if you have one of them, the underlying cause usually can be determined only by examining the results of further tests.

What is the Treatment?

Once your ability to absorb vitamin B 12 through the digestive tract has been lost, it can never be regained. Treatment of pernicious anemia and other types of B 12 deficiency consists of a life-long series of vitamin B 12 injections. You may eventually be able to give them to yourself. It is important that you do not miss an injection; if you do, your symptoms will return. Problems with walking and balancing may take several months to improve. If these symptoms existed for a long time before treatment began, they may never disappear completely.

Folic acid deficiency that is caused by an inadequate diet can be cleared up completely. At first, your physician Ayres acid tablets. After that, you will probably be told how to make sure that your diet contains adequate amounts of the vitamin. If the deficiency is caused by a failure to absorb normal quantities of folic acid, or by an increased requirement for it, extra folic acid may be prescribed in tablet form for an indefinite period.

Hemolytis is a disorder in which your red blood cells are destroyed prematurely. When this occurs, your body attempts to compensate by producing new red cells at a faster rate. If destruction exceeds production, the resulting disorder is called hemolytic anemia.

Hemolytic anemia may be hereditary, in which case it is present at birth or soon after­wards, or you may acquire it later in life. In the hereditary hemolytic anemias, hemolysis occurs because a specific component of your red blood cells is abnormal. Certain drugs can damage red cells and so produce hemolysis and hemolytic anemia. This occurs if you have inherited a specific type of abnormality that triggers anemia when you take a certain type of drug or develop special infections. Then your red blood cells become less able to protect themselves against the chemical reactions caused by the drug or the infection, and they are destroyed.

One type of acquired hemolytic anemia occurs when your body produces antibodies, or substances that normally protect you from infections, that attack the body’s own red blood cells. Hemolysis may also occur when your body produces antibodies against recently transfused red blood cells. Finally, red cells may also be destroyed after they are damaged by artificial heart valves, abnormal blood vessel walls, or toxins.

The disease is rarely fatal in any of its forms, though some forms of hemolytic anemia are difficult to treat.

What are the symptoms?

The main symptoms of hemolytic anemia are paleness, fatigue, breathlessness, and palpitations, or heart fluttering, especially with exertion. In addition, your skin may become yellow, and your urine may contain blood pigment and so be darker than normal. If your red blood cells continue to be destroyed prematurely for many years, gallstones often result.

What should be done?

If you have the symptoms described, see your physician. You will probably be questioned about your symptoms, and the physician will probably arrange for a blood test.

What is the treatment?

The principal treatment for one type of hemolytic anemia, hereditary spherocytosis, is a splenectomy, an operation to remove the spleen. Most red blood cells are destroyed by the spleen as they wear out. Removing the spleen can considerably improve hemolytic anemia, but does not cure it.

Hemolytic anemia that is caused by drugs is treated by discontinuing the drugs. If the disease is caused by antibodies, your physician may prescribe various drugs.