Pathophysiology

One of these symptoms is jaundice, which is characterized by yellowish skin and eyes because of an inability of the liver to remove bilirubin from the blood. Patient with cirrhosis also suffering from itching, due to deposited bile's products in the skin. This patient also suffers from accumulation of fluid in legs that is called edema. As a result of the blockage of blood flow via the liver, fluid accumulation in abdomen which is worsen by the decrease in protein production. Other symptoms include fatigue, weakness, loss of appetite, weight loss and nausea. As the disease progress, complications may develop ,such as varices that happens with cirrhosis patient when the blood flow through the liver slows, so the blood from intestine go back to the vessels of the stomach and esophagus, these vessels are not meant to carry this much of blood so they dilate (varices), with increasing

Cyanosis refers to a bluish skin color rather than a yellow skin color. It is the result of decreased tissue oxygenation.

Hepatitis B is the most common liver infection in the world and is caused by the hepatitis b virus. The hepatitis b virus enters the body and travels to the liver via the bloodstream. In the liver the virus attacks the healthy liver cells and then multiplies. The cells create copies of them selves and the multiplying of the virus cells then triggers a response from the bodies’ immune system. Most people at this stage of the virus are unaware the have the virus as there are no symptoms that can be seen or felt. Hepatitis B can lead to cirrhosis (scaring of the liver), liver cancer or liver failure if not treated quickly enough. Some signs and symptoms of hepatitis include abdominal pain, dark urine, fever, joint pain, loss

Gilberts syndrome could be one of the diagnoses for patient L as it is caused by the incapability of the hepatocytes to take up bilirubin from the blood. This causes the level of unconjugated bilirubin level to accumulate whilst the conjugated bilirubin level remains within range. As a result, the total bilirubin level is increased. Another diagnosis was Crigler-Najjar Type I syndrome, which takes place when unconjugated bilirubin is retained by the body whilst conjugation is impaired. This causes an increase in the total bilirubin level, as shown by its parameter reading value

Although excess bilirubin can have extreme consequences, it is not always so dire. Gilbert’s syndrome, also known as constitutional hepatic dysfunction or familial nonhemolytic jaundice is the result of an inherited gene mutation. It is a harmless liver condition in which bilirubin is not properly processed. It is not always noticeable until a blood test shows elevated bilirubin levels, and only occasionally do people show symptoms of jaundice (

Pathological hyperbilirubinemia refers to jaundice that arises from factors that alter the usual process involved in bilirubin metabolism in the liver. It is significant in the first 24hrs of life, especially if there is Rh incompatibility.

It is a largest internal organ and largest gland in human body. It weighs about 3-4 lbs. Its two major cell types are Kupffer cells and hepatocytes. The major function of liver is to produce, store and excretion of bile. It also helps in digestion and removes poisonous substances from body. Signs and symptoms of liver disease include but not limited to Jaundice (yellowish skin), abdominal and lower legs swelling, dark urine, loss of appetite and vomiting. Hepatitis viruses are one of the major causes of liver infection. Most common liver tests are serum bilirubin, serum albumin, International normalized ratio (INR), alanine transaminase and 5`- nucleotidase test. Several liver biopsies are also performed to obtain tissue samples. The three basic types of liver biopsies are percutaneous, transjugular and laparoscopic. These procedures are performed with the help of medical imaging modalities. The focus of the remaining paper will be on most common percutaneous liver biopsy. (Lynn, 2016,

Gilbert’s syndrome is an autosomal recessive disorder characterized intermittent jaundice. It is due to mutations in the promoter region of the gene coding the enzyme UDP-glucuronyl transferase. As a result Hepatic bilirubin UGT activity is consistently decreased to approximately 30% of normal in individuals with Gilbert syndrome. People with Gilbert’s Syndrome experience deepening of jaundice with vigorous exercise, dehydration, febrile illnesses, stress, alcohol consumption and fasting. Prognosis is excellent. Two provocative tests, energy deprivation (fasting test) and nicotinic acid administration, have been used to diagnose the condition. Within 48 hours of the start of a fast, there is usually a 2- to 3-fold rise in the

Well, my name Hepatitis means “liver” so I naturally attack the liver. I create a liver infection causing fever, fatigue, loss of appetite, nausea, vomiting, abdominal pain, dark urine, grey-colored stool, joint pain, and jaundice. Although, I can cause liver infection I don’t cause chromic liver

A six year male child presented with chief complaints of yellow discoloration of eyes and associated history of passing high coloured urine for three months. It was associated with nausea, diffuse abdominal pain and decreased appetite. There was no history of irritability, change in behaviour or altered sleep pattern and no bleeding from any site. He had not received blood transfusion any time in the past. There was no similar illness any of the family members. The child was admitted to a private institution for a two week period, but as there was no improvement, he was referred to our institute. At admission, he was afebrile and vitals were stable. General physical examination revealed mild pallor and severe jaundice. Gastrointestinal systemic examination revealed moderate hepatomegaly along with an enlarged left lobe of liver. There were no other clinical features suggestive of chronic liver disease. Investigations revealed a total serum bilirubin of 15.6mg/dl with conjugated fraction of 13.40mg/dl.

Another disease explained is G6PD deficiency is a hereditary enzyme disease. Also known as favism, signs of G6PD deficiency are yellowing of the skin, dark urine, fatigue, rapid breathing, and a weak, fast pulse. G6PD - an acronym for glucose-6-phosphate dehydrogenase - is found to be in every cell, and is a necessary component in red blood cells for protection. The function of the G6PD is to prevent free radicals, an atom with unpaired electrons, from killing red blood cells by eliminating them. Thus, to have G6PD deficiency means that red blood cells are vulnerable to free radicals, and the patient is prone to hemolytic anemia: when red blood cells die off too quickly, and the body is unable to produce them fast enough to replace them. If

The color blue symbolizes a lot of things. One thing that it symbolizes is trust. If you asked any of my family or friends they will tell you that I am trustworthy. People can trust me with secrets. People can talk to me about things and not have to worry about me telling anyone.

Cyanosis is a bluish discoloration of the skin resulting from a lack of circulation or inadequate oxygenation of the blood. Red blood cells carry oxygen throughout the body, and mostly all the red blood cells in arteries are provided with a fully supply of oxygen, making them appear with a red hue. Cells who lack oxygen have a blue or purple tint, so when there is an insufficient amount of fresh oxygen in the bloodstream or blood cells are being too slow to reoxygenate quick enough, people with cyanosis's skin appear bluish. It is connected with the circulatory, respiratory, and immune systems.

This keeps up for a few days and you begin to feel a loss of appetite as well as nausea. A low grade fever between 100 °f - 102 °f is present. A pain and discomfort in the abdomen above the liver is also common, due to enlargement of the liver. After a few days of torture, a person’s urine becomes darker than usual and then jaundice, (a yellowish discoloration of the skin) appears. Jaundice and the dark urine indicate that liver is not functioning properly in removing a reddish-yellow pigment called bilirubin from the blood.

According to Murray and Mckinney (2014) a major function of the liver is the conjugation of bil-irubin. Jaundice is the result of hyperbilirubinemia, which is excessive bilirubin in the blood. Pre-term babies have an 80% chance of this happening to them, and term babies have a 60% chance since newborn livers might not be able to break down the bilirubin. After birth, fewer erythro-cytes are needed and bilirubin is the source of hemolysis of erythrocytes. The red blood cells (RBC) release their components in the blood, but bilirubin is unusable in the blood. It is toxic to the body and needs to be excreted. Bilirubin is first released in unconjugated form also called indirect bilirubin, which is soluble in fat but not in water. Since this