Nonalcoholic Fatty Liver Disease Essay

According to the Merck Manual (2013), hyperlipidaemia is the increased synthesis of hepatic lipoproteins. Marieb (2012) explains that lipoproteins enable fat, fatty acids and cholesterol to circulate in the blood stream. They cannot do this alone due to their insolubility so they use lipoproteins as a type of transport. Nelson (2013) highlights four different varieties of lipoproteins which are chylomicrons, very low density lipoproteins (VLDL), low density lipoproteins (LDL) and high density lipoproteins (HDL).

The digestion of lipids occurs mostly in the small intestine, mainly the upper jejunum. Lipases from the pancreas are secreted into the small intestine as a part of pancreatic enzyme and breakdown lipids to fatty acids. Bile salts, created by the liver, enter the duodenum to mix with fatty acids to form micelles. The development of these micelles allows the absorption of fatty acids at intestinal villi. Pancreatic lipase, bile salts and functioning lymphatic channels help break up fat if these are working correctly then steatorrhea

The specific metabolic disorder that I picked for this discussion is Krabbe Disease or globoid cell leukodystrophy. The disease destroys the protective coating of nerve cells in the brain and throughout the body causing the nerve cells to stop responding or react unpredictably. The disease is caused by a person receiving two copies of a mutated gene that results in severely curtailed production of an enzyme called galactocerebrosidase (GALC) (Krabbe disease, n.d.). This enzyme is responsible for breaking down certain substances in a cell's recycling center. Unfortunately, in Krabbe disease, not enough GALC was produced so the cells begin accumulating fats called galactolipids which normally are responsible for maintaining the protective coating

Cirrhosis is the eighth leading cause of death in the United States and the thirteenth leading cause of death worldwide.1 Cirrhosis is the irreversible fibrosis of the liver characterized by hepatic architectural distortion secondary to fibrous tissue and the formation of regenerative nodules.2 These anatomical changes cause hepatic vascular resistance and an increase in blood flow leading to portal hypertension. Porto-systemic collaterals develop in order to overcome the increased portal pressure gradient.3 Nitric oxide, an endogenous vasodilator is also released in effort to overcome portal pressure with the expense of causing systemic vasodilation and a decrease in blood pressure. As a result, a marked activation of neurohumoral vasoactive factors occurs in an effort to maintain an effective arterial blood pressure. Hypervolemia, increased cardiac index, decreased systemic vascular resistance, and systemic hypotension are manifestations of portal hypertension.3 Chronic hepatitis B virus (HBV), hepatitis C virus (HCV), alcoholism, nonalcoholic steatohepatitis (NASH), and non-alcoholic fatty liver disease (NAFLD) are all major causes of cirrhosis.

Insulin Resistance and Type 2 Diabetes – cirrhosis causes resistance to insulin. This hormone, produced by the pancreas, enables blood glucose to be used as energy by the cells of the body. If you have insulin resistance, your muscle, fat, and liver cells do not use insulin properly. The pancreas tries to keep up with the demand for insulin by producing more. Eventually, the pancreas cannot keep up with the body's need for insulin, and Type 2 diabetes develops as excess glucose builds up in the bloodstream.

Liver failure is a serious condition that affects thousands of people every year. It can become life-threatening if it isn't treated as soon as possible, but still, many people choose to wait until their health plummets into a devastatingly dangerous condition before going to the doctor. This is usually because they didn't know what was happening to their body though. Because of this, it is important to know what symptoms to look out for and the treatment options that are available.

NAFLD is the hepatic manifestation of the metabolic syndrome (MetS). However, little is known about the natural history of NAFLD. Furthermore, the pathophysiological relationships between MetS and hepatic steatosis is not fully understood. The diagnosis of the MetS involves the presence of three of the following five risk factors: 1) hyperglycemia (fasting glucose ≥ 100 mg/dL), 2) low concentrations of high-density lipoprotein (HDL) cholesterol ( (-- removed HTML --) than 150 mg/dL), 4) increased waist circumference (102 cm for men and 89

Giving the fact that NAFLD is usually an asymptomatic disorder, it is often unrecognized in everyday clinical practice. Namely, most patients with NAFLD have no symptoms, and aminotransferase levels which are used as a marker of liver damage, are within normal values in almost half of all patients. NAFLD is strongly associated with type 2 diabetes mellitus (T2DM) and has been linked to increased cardiovascular disease (CVD) risk. It is characterized by insulin resistance and mitochondrial dysfunction6. Indeed, there is a gradual increase in the severity of insulin resistance in the range of NAFLD which may contribute to the evolution of liver damage. Also, it is associated with an increased risk of kidney disease in subjects with multiple CVD

Chylomicrons carry dietary fat from the intestine to the circulation. They deliver triglycerides to peripheral tissues. The resulting cholesterol-rich chylomicron remnant is taken up by the liver. The liver also synthesizes fatty acids from glucose in times of dietary excess, and then these are stored as triglycerides. Fatty acids that are not converted to triglycerides or used in the synthesis of other molecules are oxidized to ketone bodies in the mitochondria or in the peroxisomes. Microvesicular steatosis in hepatocytes is a sign of mitochondrial or peroxisomal disease or drug

Additionally, many chronic liver diseases can lead to cirrhosis. For example, nonalcoholic fatty liver disease (NAFLD) can lead to cirrhosis and is associated with obesity, hyperlipidemia, metabolic syndrome and type 2 diabetes mellitus. Hereditary metabolic disorders such as hemochromatosis and Wilson disease can also lead to cirrhosis (McCance & Heuther, 2014). It seems the cause of cirrhosis is multifaceted. Additionally, many diseases can lead to cirrhosis and it is understandable why the etiology of cirrhosis has not been parsed out, especially because the cause can differ from a

Cirrhosis is a serious disease of the liver where scar tissue replaces normal healthy tissue, and affects the function and structure of the liver. Liver, which is the largest organ in the body, has a vital roles which are important to keep the body functioning well. Liver makes proteins and enzymes that regulate blood clotting. It also regulates cholesterol and stores the energy. In addition, the liver removes poisons from the blood. 30% of cirrhosis's victims are diagnosed will remain alive for 5 years. Cirrhosis can be defined regarding its causes, symptoms, diagnosis, and treatment.

The liver is a crucial part of our digestive system. It is loved in the epigastric and right hypochondriac regions of the abdomen. A few of the many functions are storing glycogen and processing proteins from amino acids. Perhaps the most important function to digestion is that the liver secretes bile, a substance required to digest fats. There are many diseases that can affect this organ and the digestive system including Cirrhosis.

Non-alcoholic fatty liver disease (NAFLD) is defined as liver abnormalities ranging from simple steatosis to non-alcoholic steatohepatitis with or without developing cirrhosis, which occurs in the absence of significant alcohol intake or use of teratogenic drugs or hereditary disorders. There is a significant association between NAFLD and metabolic syndrome. Obesity, dyslipidemia and Type 2 diabetes mellitus (T2DM) are the most common metabolic risk factors associated with NAFLD. Due to increase in prevalence of metabolic syndrome, NAFLD is the most common cause of chronic liver disease in adult population. . It is estimated that 10%-29% of patients with NASH will eventually develop cirrhosis within a 10 year duration. The mortality of cirrhosis

Over production of insulin, is hard on the blood vessels. High insulin rubs away at the blood vessel damaging it. The blood vessels are thin and can easily be damaged. When the blood vessels become damaged, the body sends cholesterol to fix the damage. This leads to

Deposition of lipid within the liver represents part of an abnormal lipid partitioning pattern, most commonly associated with increased intra-abdominal fat. The typical obese child with NAFLD will usually manifest other components of the insulin resistance syndrome such as dyslipidemia, hypertension and altered glucose metabolism. As liver steatosis itself is usually asymptomatic, a high index of suspicion for its presence should be present in obese insulin resistant kid who present with dislipidemia or altered glucose metabolism or manifest anamnesttic or physical signs that suggest the presence of insulin