DISCUSSION
CLASSIFICATION OF HEPATOCELLULAR CARCINOMA
Hepatocellular carcinoma (HCC) is a primary malignancy of the liver. HCC is now the third foremost cause of cancer deaths. It is a destructive tumour that most commonly occurs in a background of chronic liver disease and cirrhosis. The occurrence of HCC is most frequent in Asia and Africa. This can be attributed to the high prevalence of hepatitis B and hepatitis C which strongly influences the development of chronic liver disease and the ensuing development of HCC. It is unfortunately identified very late in the disease progression, and thus has a median survival following diagnosis that ranges from 6 to 20 months1.
The presentation of HCC has changed significantly over recent years especially in developed countries. In the past, HCC generally presented at an advanced stage with right upper quadrant pain, weight loss, and signs of decompensated liver disease. It is currently more regularly identified at an earlier stage as a result of routine screening of patients with known cirrhosis. This screening usually comes in the form of imaging studies and serum alpha-fetoprotein measurements2.
In terms of management, certain patients may profit from liver resections. Numerous patients given the advanced stage of their cancer at diagnosis or their grade of liver disease could be cured by liver transplantation. Worldwide, only a minute percentage of all patients have access to transplantation. However, organ shortage is still the fundamental problem. In these patients, local ablative therapies, including radiofrequency ablation, chemoembolization, and potentially novel chemotherapeutic agents, may extend life and provide palliation.
Currently available therapeutic options for HCC are ...
... middle of paper ...
...method of management is correct and in keeping with suggested evidence based medicine. A potential future step in managing Mr. Burombo is to add doxorubicin. The benefit of this combination was studied in a phase II trial whereby all patients had received doxorubicin and they were randomly prescribed either sorafenib or a placebo. The combination therapy showed an improvement in median time to progression, overall survival, and progression-free survival when compared to monotherapy. However, important variables to consider is the fact that the population group of the study included patients who were diagnosed with advanced HCC and that had a Child Pugh stage A. Currently the combination of sorafenib and doxorubicin is not yet available for clinical use12. Further studies are also required to assess the efficacy of this combination against sorafinib alone.
HPI: MR is a 70 y.o. male patient who presents to ER with constant, dull and RUQ abdominal pain onset yesterday that irradiate to the back of right shoulder. Client also c/o nauseas, vomiting and black stool x2 this morning. He reports that currently resides in an ALF; they called the ambulance after his second episodes of black stool. Pt reports he drank Pepto-Bismol yesterday evening without relief. Pt states that he never experienced similar symptoms in the past. Denies any CP, emesis, hematochezia or any other associated symptoms at this time. Client was found with past history gallbladder problems years ago.
Liver percusses to 8 cm at midclavicular line, one fingerbreadth below right costal margin: This indicates that the patient does not have signs or symptoms of liver disease or ascites.
•The forty five year old patient is diagnosed with the progressive cirrhosis inflaming the liver along with the parenchymal cells. The plain symptoms is manifested primarily because of the augmentation of edema internally in the lower abdomen.
Kanwal, F., Hoang, T., Kramer, J. R., Asch, S. M., Goetz, M. B., Zeringue, A., Richardson, P., & El-Serag, H. B. (2011). Increasing prevalence of HCC and cirrhosis in patients with chronic hepatitis C virus infection. Gastroenterology, 140(4), 1182-1188. doi: 10.1053/j.gastro.2010.12.032.
The sonographic appearance varies depending on of the Hepatitis is acute or chronic. In acute hepatitis you will see a normal texture or portal veins will be more prominent. The liver appears hypoechoic. Attenuation might be present in acute Hepatitis. Gallbladder walls are thickened and hepatosplenomegaly. In chronic Hepatitis the parenchyma will appear coarsed with decreased brightness of the portal triad. Attentuaion is not as great in chronic Hepatitis. Fibrosis may occur with soft shadowing. The size of the liver is decreased and appears hyperechoic.
The signs and symptoms of blood borne pathogens vary based on the type of disease it is and the ability of a person’s immune system to fight it off. In most cases hepatitis B does not need to be treated and the body can fight it off on its own. However a long-term infection can develop in some people that can cause liver damage. There is a vaccination available to prevent acquiring the disease. The signs and symptoms for hepatitis C are usually mild. It can take two weeks to six months after contact before signs begin to show, or there may not be any symptoms at all. Hepatitis C typically becomes is a long-term infection and after many years will cause liver ...
Cirrhosis is a deterioration of the liver resulting from heavy scarring, causing the liver to not be able to function properly. If cirrhosis becomes severe, a liver transplant may be the only solution (“Beyond Hangovers: Understanding Alcohol's Impact on Your Health” 14). It is difficult to calculate when a person will develop cirrhosis, because an alcoholic could never develop the disease, but someone who drinks socially could. It is also unknown why cirrhosis is more prevalent in women (Freeman).... ...
Alternative splicing facilitates the development of HCC either by generating oncogenic variants or by inactivating the tumor suppressors. For example, an alternative POLDIP3 transcript promotes hepatocellular carcinoma progression (18). POLDIP3 is a target of ribosomal protein S6 kinase 1, and regulates DNA replication and mRNA translation. The alternative POLDIP3 transcript (POLDIP3-β), which lacks exon 3 and 29 amino acids, was found to be significantly up-regulated in clinical hepatocellular carcinoma (HCC) tissues compared to paired adjacent noncancerous hepatic tissues. This POLDIP3-β isoform has been shown to increase HCC cell proliferation, inhibit HCC cell apoptosis, enhance HCC cell migration, and promote xenograft growth. Another example is the cell fate determinant protein, Numb, which is aberrantly spliced in HCC and promotes proliferation and invasion (19).
The Phase I trial will be discussed here as it pertains to the topic at hand. The typical treatment for cervical cancer if surgery is not a viable option – like if the cancer has spread, then called locally advanced cervical cancer – is chemotherapy and radiation treatment at the same time. This phase I clinical trial is simply looking to add ipilimumab to this regimen, but once the chemo/radiation has been completed (LACC article). Chemo and radiation destroy tumor cells, which causes tumor-associated antigens to be released. Once released, these antigens are exogenous (outside the cell) and will be presented to helper T cells to initiate an immune response.
Now imagine if it were you, that needed a liver, heart, or other organ transplant. You want to live to see so much more in life, but you did not get on the list in time and there is a shortage in organ donors. You must say good bye to life, your loved ones and every thing else. This is not a good thing to imagine, yet people die everyday with this feeling.
This case study is about Abdul Chidiac, a 51 year old male, married with 4 children. He had a medical history of hypertension, hypercholesterolaemia and cirrhosis with two admissions in the last six months. He is a smoker and drinks beer, 5-6 bottles per day. As Carithers & McClain (2010) explained the patient’s medical history is another indicator of the risk for cirrhosis; the progression to cirrhosis is adaptable and may take time over weeks or many years. Cirrhosis is a liver disease characterized by permanent scarring of the liver that interferes with its normal functions including alcoholism. Most people who drink large amounts of alcohol cause harm to the liver in some way (Heidelbaugh & Bruderly, 2006). The cause of cirrhosis is not yet known, but the connection between cirrhosis and excessive alcohol ingestion is established (Jenkins & Johnson, 2010). Common causes of cirrhosis include: alcohol abuse, hepatitis B infection, hepatitis C infection and non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (Schuppan & Afdhal, 2008).
It involves the whole liver rather than a small part even though on occasion the fibrosis may be more severe in one or other lobe. Fibrosis results partially from collapse of the new fibre formation and is usually regarded as a consequence of liver-cell necrosis. The nodules of a cirrhotic liver are the surviving parenchyma. But they are strutually altered. They vary greatly in size and appearance. Within them, there may be little organized structure which is similar to normal lobule and acini. In biliary cirrhosis and haemochromatosis, the parenchyma remains normal for a long period and fibrosis is the dominant pathological process. But true cirrhosis occurs only when lobular architecture becomes altered.
This was his second episode since 10 days ago where he develop the same pain at his right flank. He suddenly experienced severe pain 8 hours before admission when the pain shifts to his right lower quadrant of his abdomen. The onset is at 6.30 am before worsening at 10 p.m to 2 p.m. He described the pain as continuous sharp pain and gradually increased in severity. There is no radiation of the pain. The pain was exaggerated on movement and touch. There were no relieving factor and he scale the severity as 7/10. He experienced fever for 1 day prior to admission. It was a mild grade continuous fever. He does not experienced chills and rigor. The patient does not experience any nausea or vomiting, no dysphagia, no pain during micturition and no alteration in bowel habit. He experienced loss of appetite but not notice any weight loss.
The purpose of this paper is to analyze, diagnose, and to determine a proper treatment plan to work toward the beneficial prognosis for the individual indicated within the case study.
The research fellowship focuses on all aspects of preventive medicine with special focus on evidence-based medicine. Throughout the course of my training, I have conducted several systematic reviews and meta-analysis that supported important clinical practice guidelines for several scientific societies. As a methodologist, I have had a great opportunity to support the American Association for the Study of Liver Disease (AASLD) in producing their current guideline in the management of chronic Hepatitis B virus and currently we are working on similar guidelines for the management of hepatocellular carcinoma. I have honored to be the leading methodologist in both