Zone 1 Lobular Biopsy: A Case Study

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

Mr. Wilson is a 47 year old man being evaluated for complaints of fatigue, anorexia and abdominal distention. On examination, it is noted that the skin is jaundiced and the liver enlarged. D.W. denies significant alcohol or drug use. He denies any known exposure to hepatitis and has never been vaccinated for hepatitis. He is taking no medication. Laboratory tests reveal the following and a diagnosis of acute hepatitis B is made:

Describe the clinical presentation (signs and symptoms) of viral hepatitis. List the different underlying causes of this condition.

The term fibrocystic breast disease is used to describe the benign condition that may have caused Ms. Barker's breast mass. Whether a mass is solid or cystic, a benign mass is usually three-dimensional, mobile and smooth. Borders to the mass are not irregular (Sharma, Dave, Sanadya, Sharma & Sharma, 2010). Ms. Barker has lobular hyperplasia. Furthermore, abnormal cells can increase complexity when they grow inside the lobules of the the breast but do not spread or metastasize (McCance & Huether, 2014). This condition is known as lobular carcinoma in situ (LCIS). Although LCIS is not invasive cancer, it increases the risk of getting invasive breast cancer in either breast (Types of breast cancers, 2016). Often around menses women develop fibrocystic breasts. There are often lumps noted that quickly disappear with menses, however in lobular fibrocystic breast disease lumps are found in the milk producing glands. Breast cysts are common with approximately over 1/3 of the women 35-50 having cysts (Breast lumps, 2016).

Pamela B., a 52-year-old female, presented to the emergency department complaining of abdominal distention that worsened over a two week period. She noted black, tarry stools several days after the onset of her abdominal distention, and decided to seek medical attention after experiencing three large incidences of frank hematemesis, vomiting consisting of bright red blood. She has a past medical history of cirrhosis of the liver, which is the deposition of connective tissue, collagen fibers, in the liver, resulting in the formation of nodules. These nodules can alter blood flow, and liver function (1). Additionally, she has hepatitis C, a viral infection most commonly associated with the liver, that is transmissible by blood (1). Her

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

During chronic liver disease, hepatocyte cell death results in inflammation that leads to fibrosis. In addition, the loss of functional hepatocytes results in loss of liver functions, such as the ability to metabolize bilirubin and synthesize proteins (e.g., albumin and clotting factors). Under normal conditions, blood flows from splanchnic circulation to hepatic circulation (for removal of bacteria and toxins) via the portal vein, and blood is returned to systemic circulation via the hepatic vein. Because of liver fibrosis, the distortion of hepatic architecture increases resistance to blood flow, resulting in portal hypertension. The portal collaterals relieve some of the pressure in the portal system but may contribute to cirrhosis-related complications such as varices (Liou, 2014).

Autoimmune hepatitis is a disease in which the system in the body that fights off disease (immune system) attacks the liver and causes it to become inflammed. Without treatment this condition gets worse. It can last for years and lead to scarring of the liver (cirrhosis) and liver failure.

Cirrhosis is known as a chronic disease of the liver. Cirrhosis usually develops when the scar tissue replaces normal, healthy tissue in the liver. It tends to happen whenever healthy cells are damaged over a long amount of time, usually for many years. However, the scar tissue makes the liver lumpy and hard, after a while, the organs will start to fail and the scar tissue makes it tough for the blood to get through a large vein (the portal vein) that goes into the liver. Occasionally when the blood backs up into the portal vein, it can get into the spleen (an abdominal organ involved in the production and removal of blood cells) and can really cause trouble. What causes this is other liver conditions or diseases the person may already have, which includes an (alcohol-related liver disease) by drinking too much alcohol for many years non-stop. It causes fat and inflammation in the liver. The amount of alcohol that it takes to hurt the liver is different for everyone.

MIF is constitutively expressed in low amounts by hepatocytes and has been shown to be weakly expressed within sinusoidal lining cells as well as biliary epithelial cells of the liver [1, 2]. Previous studies have described an increase in MIF levels being associated with inflammatory hepatic disorders such as cirrhosis and hepatocellular carcinoma [3], however, to date little is known about MIF and its implications in the pathogenesis of autoimmune liver disease. A recent study by Assis and colleagues evaluated changes in the levels of both circulating MIF and its soluble receptor (CD74) in sera to determine if clinical manifestations correlated with the inflammatory profile observed in autoimmune hepatitis (AIH) and primary biliary cirrhosis (PBC) [4]. Immuno-histological analysis levels of MIF and CD74 protein expression, although varied between mild and severe cases, were more abundantly expressed in liver sections in both AIH and PBC patients compared to control specimens. Serological data collected from patients in this study also confirmed that both AIH and PBC cohorts had significantly higher levels of circulating MIF compared to healthy controls. Further analysis revealed however that PBC patients had higher concentrations of the MIF soluble neutralising receptor CD74 in contrast to both AIH and control cohorts. This finding in respect to disease progression between PCB and AIH cohorts is suggested to correlate with the

Physical examination was normal except the presence of joundice. He had no history of any chronic illness, drugs or chemicals. He stated that he had a sleeve gastrectomy operation 6 months ago for obesity and he was on low caloric intake due to early satiety since sleeve gastrectomy. Preoperative laboratory studies before the gastrectomy were obtained and reevaluated. All were normal except mild indirect hyperbilirubinemia (serum total bilirubin: 1,4 mg/dl, indirect bilirubin: 1,2 mg/dl). On admission to our clinic his laboratory studies were as follows: AST: 14 U/L ALT: 16 U/L ALP: 45 U/L GGT: 28 U/L total bilirubin: 6,58 mg/dl, indirect bilirubin: 6 mg/dl, direct bilirubin: 0,58 mg/dl . Serologic tests for viral hepatitis (HBs Ag, anti HBc Ig G, anti HCV, anti HAV Ig M) were all negative. There were no clinical and laboratory sign of hemolysis; Hb: 15,2 g/dL, Hct: 44,1, Plt: 208.000 /µL and reticulocyte count was %0,5. Abdominal ultrasound showed the presence of multiple stones in the gallbladder. Common bile duct and biliary tree were found to be normal in MRCP and endosonography. Gilbert’s syndrome was diagnosed and phenobarbital 30 mg/day was initiated. Serum bilirubin concentration dropped gradually (total bilirubin: 3,5 mg/dl, indirect bilirubin: 3 mg/dl) in one week and the patient was

Hepatocellular carcinoma (HCC) is introduced as the fifth most common tumor and also the third most common cause of cancer-related deaths all around the world. Carcinogenesis of HCC is a multistep and complex process; it is known that multiple risk factors, such as chronic hepatitis B virus (HBV)or hepatitis C virus (HCV) infections, carcinogen exposure, cirrhosis and a group of single nucleotide polymorphisms, subscribe to hepatocarcinogenesis.Chronic HCV patients are susceptible to hepatic inflammation, developing liver fibrosis, cirrhosis and HCC. Such a case does not depend on virus genotype or viral load

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.

There are several ways that Cirrhosis of the liver can be diagnosed. The methods are physical examination, laboratory tests, biopsy, and several types of imaging. The laboratory tests include liver function , kidney function , and blood tests. The blood tests will check for Hepatitis viruses. A few types of imaging that could be used are MRI, CT, ultrasound, and Magnetic resonance elastography. As mentioned before most symptoms are delayed so the disease is often realized during a routine

Liver biopsy is helpful in diagnosis of many forms of liver disease such as acute and chronic hepatitis (Wilson disease, alpha-1-antitrypsin disease, glycogen storage diseases, AIH, NiemannPick disease and others), cholestatic disorders, fatty liver disease, vascular diseases, infiltrative or storage diseases, some infectious diseases, and other disorders that may be associated with characteristic histological abnormalities. It also plays a role in the diagnosis of patients with abnormal liver tests of unknown etiology (Czaja et al., 2007).