Thursday, 18 December 2014

Fatty Liver Disease

 Some fat in the liver is normal. But if fat makes up more than 5%-10% of the weight of your liver, you may have alcoholic or nonalcoholic liver disease. In some cases, these diseases can lead to serious complications.

Alcoholic Liver Disease (ALD)


More than 15 million people in the U.S. abuse or overuse alcohol. Almost all of them -- 90%-100% -- develop fatty livers. 
Fatty liver can occur after drinking moderate or large amounts of alcohol. It can even occur after a short period of heavy drinking (acute alcoholic liver disease).
Genetics or heredity (what is passed down from parent to child) plays a role in alcoholic liver disease in two ways: It may influence how much alcohol you consume and your likelihood of developing alcoholism. And, it may also affect levels of liver enzymes involved in the breakdown (metabolism) of alcohol.
Other factors that may influence your chances of developing alcoholic fatty liver disease include:
·                                 Hepatitis C (which can lead to liver inflammation)
·                                 An overload of iron
·                                 Obesity
·                                 Diet

Nonalcoholic fatty liver disease (NAFLD)


Nonalcoholic fatty liver disease is now the most common cause of chronic liver disease in the U.S. Some people with excess fat in the liver simply have what's called a fatty liver. Although this is not normal, it is not serious if it doesn't lead to inflammation or damage.
Others have what's called nonalcoholic steatohepatisis (NASH). Although it is similar to alcoholic liver disease, people with this type of fatty liver disease drink little or no alcohol. NASH can lead to permanent liver damage. The liver may enlarge and, over time, liver cells may be replaced by scar tissue. This is called cirrhosis. The liver can't work right and you may develop liver failure, liver cancer, and liver-related death. NASH is one of the leading causes of cirrhosis.
Both types of NAFLD are becoming more common. Up to 20% of adults may have either fatty liver or NASH. And more than 6 million children have one of these conditions, which are most common in Asian and Hispanic children. Recent evidence indicates that NAFLD increases the risk of heart disease in children who are overweight or obese.

Causes of Nonalcoholic Fatty Liver Disease (NAFLD)


The cause of nonalcoholic fatty liver disease is not clear. Certain factors tend to increase risk, but in some cases, no risk factors show up. However, NAFLD tends to run in families. It also shows up most often in people who are middle-aged and overweight or obese. These people often have high cholesterol ortriglycerides and diabetes orprediabetes (insulin resistance), as well.
Other potential causes of fatty liver disease include:
·                                 Medications
·                                 Viral hepatitis
·                                 Autoimmune or inherited liver disease
·                                 Rapid weight loss
·                                 Malnutrition
Recent studies show that an overgrowth of bacteria in the small intestine and other changes in the intestine may be associated with nonalcoholic fatty liver disease. Some researchers now suspect this may play a role in the progression of NAFLD to NASH.

Acute Fatty Liver of Pregnancy


Though very rare, fat can build up in the liver of a mother duringpregnancy, putting both mother and fetus at serious risk. Either may develop liver failure, kidney failure, severe infection, or hemorrhage. No one fully understands its cause, but hormones may play a role.
Once a diagnosis is confirmed, the baby is delivered as quickly as possible. Although the mother may need intensive care for several days, liver function often returns to normal within a few weeks.

Symptoms of Fatty Liver Disease


Fatty liver disease is often silent, producing no symptoms, especially in the beginning. If the disease advances -- which is usually over a period of years, or even decades -- it can cause vague problems such as:
·                                 Fatigue
·                                 Weight loss or loss of appetite
·                                 Weakness
·                                 Nausea
·                                 Confusion, impaired judgment, or trouble concentrating
These symptoms may also be present:
·                                 Pain in the center or right upper part of the abdomen 
·                                 An enlarged liver
·                                 Patchy, dark skin discoloration, usually on the neck or underarm area
With alcoholic liver disease, symptoms may worsen after periods of heavy drinking. With NAFLD, the disease process can stop or reverse, or it may worsen. If cirrhosis develops, the liver loses its ability to function. This can cause signs and symptoms such as:
·                                 Fluid retention
·                                 Muscle wasting
·                                 Internal bleeding
·                                 Jaundice (yellowing of skin and eyes)
·                                 Liver failure

Diagnosis of Fatty Liver Disease


Often a fatty liver shows up during a routine checkup. Your doctor might notice that your liver is slightly enlarged or see signs of a fatty liver on a blood test. Or, your doctor may suspect a problem after taking a health history or doing a physical exam.
Blood tests. During routine blood tests, elevations in certain liver enzymes may show up. These might include alanine aminotransferase (ALT) or aspartate aminotransferase (AST).
Imaging studies. A fatty liver may also show up on imaging tests, such as an abdominal ultrasound. 
Liver biopsy. The only way to confirm a diagnosis of fatty liver disease is with a liver biopsy. This is usually done once other causes have been ruled out. After application of local anesthesia, the doctor inserts a needle through the skin to remove a tiny piece of liver. This is then examined under a microscope for signs of fat, inflammation, and damaged liver cells. If inflammation or damage is not present, the diagnosis is simply a fatty liver.

Treatment of Fatty Liver Disease


There is no specific treatment at this time for fatty liver disease. However, getting treatment for any underlying disease, such as diabetes, is essential. And you can take other steps to improve your condition.
If you have alcoholic liver disease and you are a heavy drinker, quitting drinking is the most important thing you can do. Find the support you need to be successful. With ALD, continued use of alcohol can lead to advanced disease, including alcoholic hepatitis or cirrhosis. Even for those with NAFLD, however, avoiding alcohol may help.
If you are overweight or obese, do what you can to gradually lose weight-- no more than 1 or 2 pounds a week. A recent study showed that weight loss of at least 9% over a period of months can help reverse NASH. Even less weight loss than this can help lessen buildup of fat in the liver.
Eat a balanced and healthy diet and increase your physical activity. In addition to limiting calories, avoid diets rich in refined, rapidly digested carbohydrates. This includes limiting foods such as bread, grits, rice, potatoes, corn, and concentrated sugar that is found in sports drinks and juice.
Treatment of Fatty Liver Disease continued...
Avoiding unnecessary medicationscan also help slow or reverse the disease. Clinical trials are also looking at the effectiveness of certain antioxidants and newer diabetes medications in treating fatty liver disease (because of disease's link to oxidative stress and diabetes). These include:
  • Vitamin E
  • Selenium
  • Betaine
  • Metformin
  • Rosiglitazone
  • Pioglitazone
Note that even vitamins and minerals can lead to health problems. The best way to get their benefits is through food sources that contain them.
New findings about the role of bacteria in the development of fatty liver disease may lead to still other options for treatment, such as by counteracting unbalanced diets with probiotics. These are dietary supplements containing healthy live bacteria or yeasts.
If cirrhosis becomes severe, a liver transplant may be needed. A surgeon removes the damaged liver and replaces it with a healthy one.
WebMD Medical Reference
Reviewed by William Blahd, MD on July 09, 2014
© 2014 WebMD, LLC. All rights reserved.


What Is Atherosclerosis?

Atherosclerosis -- hardening and narrowing of the arteries -- gets a lot of bad press but with good reason. This progressive process silently and slowly blocks arteries, putting blood flow at risk.
Atherosclerosis is the usual cause of heart attacks, strokes, and peripheral vascular disease -- what together are called "cardiovascular disease." Cardiovascular disease is the No. 1 killer in America, with more than 800,000 deaths in 2005.
How does atherosclerosis develop? Who gets it, and why? This deadly process is preventable and treatable. Read on, and get to know your enemy.

What Causes Atherosclerosis?

First, an Anatomy 101 review: Arteries are blood vessels that carry blood from the heart throughout the body. They're lined by a thin layer of cells called the endothelium. The endothelium works to keep the inside of arteries toned and smooth, which keeps blood flowing.
According to experts, atherosclerosis begins with damage to the endothelium caused by high blood pressure, smoking, or highcholesterol. That damage leads to the formation of plaque.
When bad cholesterol, or LDL, crosses the damaged endothelium, the cholesterol enters the wall of the artery. That causes your white blood cells to stream in to digest the LDL. Over years, the accumulating mess of cholesterol and cells becomes a plaque in the wall of the artery.
Plaque is a jumble of cholesterol, cells, and debris that creates a bump on the artery wall. As atherosclerosis progresses, that bump gets bigger. And when it gets big enough, it can create a blockage. That process goes on throughout your entire body. As a result, not only is your heart at risk but you are also at risk for stroke and other kinds of health problems.
Atherosclerosis usually causes no symptoms until middle or older age. But as narrowings become severe, they choke off blood flow and cancause pain. Blockages can also suddenly rupture, causing blood to clot inside an artery at the site of the rupture.

Atherosclerosis and Plaque Attacks

Plaques from atherosclerosis can behave in different ways.
·                                 They can stay within the artery wall. There, the plaque grows to a certain size and stops. Since this plaque doesn't block blood flow, it may never cause symptoms.
·                                 Plaque can grow in a slow, controlled way into the path of blood flow. Eventually, it causes significant blockages. Pain on exertion (in the chest or legs) is the usual symptom.
·                                 The worst-case scenario consists of plaques that suddenly rupture, allowing blood to clot inside an artery. In the brain, this causes a stroke; in the heart, a heart attack.
The plaques of atherosclerosis cause the three main kinds of cardiovascular disease:
·    Coronary artery disease: Stable plaques in the heart's arteries causeangina (chest pain on exertion). Sudden plaque rupture and clotting causes heart muscle to die. This is a heart attack, or myocardial infarction.
·         Cerebrovascular disease: Ruptured plaques in the brain's arteries causes strokes with the potential for permanent brain damage. Temporary blockages in an artery can also cause transient ischemic attacks (TIAs), which are warning signs of stroke; however, there is no brain injury.
·    Peripheral artery disease: Narrowing in the arteries of the legs caused by plaque causes poor circulation. This causes pain on walking and poor wound healing. Severe disease may lead to amputations.

Who Gets Atherosclerosis?

It might be easier to ask, who doesn'tget atherosclerosis?
Atherosclerosis starts early. In autopsies of young American soldiers killed in action in the Korean and Vietnam wars, half to three-quarters had early forms of atherosclerosis.
Even today, a large number of asymptomatic young people have evidence of atherosclerosis. A 2001 study of 262 apparently healthy people's hearts may surprise you:
·                                 52% had some atherosclerosis.
·                                 Atherosclerosis was present in 85% of those older than 50.
·                                 17% of teenagers had atherosclerosis.
No one had symptoms, and very few had severe narrowings in any arteries. This was very early disease, detectable only by special tests.
If you are 40 and generally healthy, you have about a 50% chance of developing serious atherosclerosis in your lifetime. The risk goes up as you get older. The majority of adults older than 60 have some atherosclerosis but often do not have noticeable symptoms.
There is good news. Rates of death from atherosclerosis have fallen by 25% since 30 years ago. This is thanks to both better lifestyles and improved treatments.

Atherosclerosis Prevention

Atherosclerosis is progressive, but it's also preventable. For example, nine risk factors are to blame for upwards of 90% of all heart attacks:
·                                 Smoking
·                                 High cholesterol
·                                 High blood pressure
·                                 Diabetes
·                                 Abdominal obesity ("spare tire")
·                                 Stress
·                                 Not eating fruits and vegetables
·                                 Excess alcohol intake (more than one drink for women, one or two drinks for men, per day)
·                                 Not exercising regularly
You may notice all of these have something in common: You can do something about them! Experts agree that reducing your risk factors leads to a lower risk of cardiovascular disease.
For people at moderate or higher risk -- those who’ve had a heart attack or stroke, or who suffer angina -- taking a baby aspirin a day can be important. Aspirin helps prevent clots from forming. Ask your doctor before starting daily aspirin, as it can have side effects.

Atherosclerosis Treatment

Once a blockage has developed, it's generally there to stay. Withmedication and lifestyle changes, though, plaques may slow or stop growing. They may even shrink slightly with aggressive treatment.
·     Lifestyle changes: Reducing the lifestyle risk factors that lead to atherosclerosis will slow or stop the process. That means a healthydiet, exercise, and no smoking. These lifestyle changes won't remove blockages, but they’re proven to lower the risk of heart attacks and strokes.
·      Medication: Taking drugs for high cholesterol and high blood pressure will slow and perhaps even halt the progression of atherosclerosis, as well as lower your risk of heart attacks and stroke.
Using invasive techniques, doctors can also open up blockages from atherosclerosis, or go around them:
·    Angiography and stenting:Cardiac catheterization with angiography of the coronary arteries is the most common angiography procedure performed. Using a thin tube inserted into an artery in the leg or arm, doctors can access diseased arteries. Blockages are visible on a live X-ray screen. Angioplasty (catheters with balloon tips) and stenting can often open up a blocked artery. Stenting helps to reduce symptoms, although it does not prevent future heart attacks.
·    Bypass surgery: Surgeons "harvest" a healthy blood vessel (often from the leg or chest). They use the healthy vessel to bypass a segment blocked by atherosclerosis.
These procedures involve a risk of complications. They are usually saved for people with significant symptoms or limitations caused by atherosclerosis.



Indications for measurement of cardiac enzymes

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Troponins T and I

Cardiac troponin I and T have displaced myoglobin and creatine kinase-MB as the preferred markers of myocardial injury.[2] However, uncertainties and questions remain on the value of high-sensitivity cardiac troponin assays, including their best clinical use.[3] 
Troponin is a protein released from myocytes when irreversible myocardial damage occurs. It is highly specific to cardiac tissue and accurately diagnoses myocardial infarction with a history of ischaemic pain or ECG changes reflecting ischaemia. Cardiac troponin level is dependent on infarct size, thus providing an indicator for the prognosis following an infarction.[4] 
New high-sensitivity cardiac troponin assays have been developed that can measure troponin values at much lower levels. With the use of these high-sensitivity assays, more patients with unstable angina will be classified as having non-ST-elevation myocardial infarction. These assays may therefore define a high-risk patient population and may lead to more appropriate therapy and improved outcomes in these patients.[5] 
·                 Cardiac troponins T and I are highly sensitive and specific for cardiac damage. Troponin I and T are of equal clinical value.
·                 Serum levels increase within 3-12 hours from the onset of chest pain, peak at 24-48 hours, and return to baseline over 5-14 days.[1] 
·                 Troponin levels may not be detectable for six hours after the onset of myocardial cell injury. The most sensitive early marker for myocardial infarction is myoglobin.
·                 Troponin levels should be measured at presentation and again 10-12 hours after the onset of symptoms. When there is uncertainty regarding the time of symptom onset, troponin should be measured at twelve hours after the presentation.
·                 The risk of death from an ACS is directly related to troponin level and patients with no detectable troponins have a good short-term prognosis.
·                 Elevated troponin levels can occur in patients without an ACS and are associated with adverse outcomes in many other clinical situations, including congestive heart failure, sepsis, acute pulmonary embolism and chronic kidney disease. Other cardiac causes include myocarditis and aortic dissection.
·                 Myocardial muscle creatine kinase (CK-MB) is found mainly in the heart.
·                 CK-MB levels increase within 3-12 hours of onset of chest pain, reach peak values within 24 hours, and return to baseline after 48-72 hours.
·                 Sensitivity and specificity are not as high as for troponin levels.


Myoglobin levels

·                 Myoglobin is found in cardiac and skeletal muscle.
·                 It is released more rapidly from infarcted myocardium than troponin and CK-MB and may be detected as early as two hours after an acute myocardial infarction.
·                 Myoglobin has high sensitivity but poor specificity. It may be useful for the early detection of myocardial infarction.
·                 Studies in several types of ACS have shown that elevated levels of natriuretic peptides - eg, B-type natriuretic peptide (BNP) - are independently associated with adverse outcomes - especially mortality.[6][7]
·                 Leukocytosis may be seen within several hours after an acute myocardial infarction. It peaks in 2-4 days and returns to normal levels within one week.
·                 Patients without biochemical evidence of myocardial necrosis but with elevated C-reactive protein (CRP) level are at increased risk of a subsequent ischaemic event.
·                 Erythrocyte sedimentation rate (ESR) rises above reference range values within three days and may remain elevated for weeks.
There are a number of novel biomarkers under investigation, but none has been tested and proven to alter outcome of therapeutic intervention.[4] Although some have improved prediction of outcome in acute myocardial infarction, none has been demonstrated to alter the outcome of a particular therapy or management strategy.
·                 Heart-type fatty acid binding protein and copeptin (in combination with cardiac troponin) diagnose myocardial infarction or ACS in the early hours following symptoms.
·                 Mid-regional pro-atrial natriuretic peptide, ST2, C-terminal pro-endothelin 1, mid-regional pro-adrenomedullin and copeptin all provide information in predicting death and heart failure.
·                 Growth differentiation factor-15 and high-sensitivity CRP may predict death following an ACS.


Heart Disease Health Center
Diagnosis & Tests
Exactly when do you go from having risk factors to having heart disease? These links take you to information on the tests a doctor uses to diagnose heart disease.
Diagnosis
The first step is getting a doctor's exam. Here's a description of what the doctor will do.
Tests
Whether you spell it EKG or ECG, it's an electrocardiogram. Learn the basics here.
Why get a chest X-ray? What happens? Click here for quick answers.
Does your heart respond well to exertion? That's what a stress test looks for. Here's a straightforward description, including how to prepare for a stress test.
The head-up tilt table test is used to help find the cause of fainting spells. Here's what you need to know.
There are several variations on the echocardiogram, or "echo," as doctors call it. Learn about these ultrasound-like tests of the heart -- and find out what to expect -- here.
Cardiac catheterization -- also called a coronary angiogram -- means running a catheter into your heart. It's done to help doctors see what's going on in there, and whether they need to operate. Here's where to learn about it.
Electrophysiology -- the EP test -- takes measurements of your heart rhythm -- recording the electrical activity and pathways of your heart. Start preparing for it by clicking here.
Computed tomography (CT scan) of the heart can visualize your heart’s anatomy. Calcium-score heart scan and coronary CT angiography are just a few types used to diagnose heart disease.
A myocardial biopsy is when a doctor uses a special catheter to remove a piece of your heart tissue for examination. Click here to learn why it's done.
A heart MRI is a great way for doctors to get a look -- from the outside -- at how your heart is working. Read about it here.
Pericardiocentesis -- also called a pericardial tap -- means using a needle to get a sample of the fluid in the sac surrounding the heart. Here's what you need to know.