Hepatic Fibrosis Case Study

Table 2 shows some of the chemical mediators involved in Mr X’s inflammatory process, causing it to become more severe and uncontrolled, resulting in a further decline in his clinical presentation.

The MD Anderson Liver Tumor biospecimen resource has been invaluable for a large number of studies or clinical development. The sixth and subsequent editions of the American Joint Committee on Cancer (AJCC) staging of hepatocellular cancer, which was developed by an international consortium led by Jean-Nicolas Vauthey, MD, Professor of Surgery at MD Anderson and co-leader on project 2 of the SPORE, was based upon pathologic review of resected specimens in the Liver Tumor Bank (Vauthey JN J Clin Oncol 2002 20:1527-36). In addition, investigators at MD Anderson examined tissues in the Liver Tumor Bank to elucidate the prognostic significance of the ribonucleoprotein Human Antigen R (HuR) showing that patients with high HuR tumor expression had

Although Fibrocystic Disease is common, women don’t know about it until they actually get it. The physicians are not calling this a disease, but rather a condition now.

Cirrhosis is the 11th leading cause of death by disease in the United States. Almost one half of these are alcohol related. About 25,000 people die from cirrhosis each year.

With limited number or organs available to those in need of a new one, there must be a way in which people are granted their spot on the recipient list. Many factors in organ allocation must be considered as organs are a scarce resource. Such factors must include, life style, age, prognosis, other comorbidities and most importantly the cause for the transplant. To explore these ideas, I will focus on the Zambrano article introduced in class. In this article, the author explores the argument of responsibility in respect to people with Alcohol Related End of Stage Liver Disease (ARESLD). The argument of responsibility states that “alcoholics who have ARESLD should be given lower priority for (scarce) medical resources when they are competing

Punnen .I. Joseph spoke only to a select few on his last couple of days on Earth. He didn’t often have much to say to people, because his actions always spoke louder than his words. Compassionate, intelligent, and at times stern, is how I remember my grandfather. Sadly, he passed away to the disease known to the world today as Pulmonary Fibrosis at the age of seventy-nine. Though he was in excruciating pain, my grandfather called from India to talk to my brother and I during his final days. I knew that he was ill but could not fathom the idea that I could lose him. I recall hearing the news from my dad, and the painful days that followed. Nevertheless,

Treatment for pulmonary hypertension may include medications such as vasodilators, endothelin receptor antagonists, calcium channel blockers, anticoagulants, diuretics, and oxygen (Pulmonary Hypertension, 2015). Surgeries may include atrial septostomy or transplantation of heart of lungs (Pulmonary Hypertension, 2015).

Symptoms may range from minor signs of impairment of brain function to clear neurological and / or psychiatric signs up to deep coma. Asterixis has a good orientation value for the diagnosis, although it is not specific to the hepatic origin of encephalopathy. There is usually a hepatic fetor. Convulsive seizures are possible. Encephalopathy may also occur in chronic form, manifested by a permanent psychomotor slowing or evoking a psychiatric

Martinez, F. J., Andrade, J. A., Anstrom, K. J., King Jr, T. E., Raghu, G., & King, T. J., Randomized trial of acetylcysteine in idiopathic pulmonary fibrosis (2014).

As we know that pulmonary fibrosis is a restrictive disease. People who are suffered from pulmonary fibrosis lives a difficult life as they have trouble taking air in to the lungs. The major symptom related to this disease is dyspnea. In common terms, pulmonary fibrosis is considered as scarring in the lungs. The scar in the lungs makes it difficult for oxygen to get into the blood. It also makes difficult for the patient to feel short of breath especially during exercise or walking. I support the idea of pulmonary rehabilitation to improve quality of life and strengthen muscles. It was a great review to know about different oxygen cylinders. I have never changed the regulator of H cylinder, but I would definitely want to learn about it. I

Pulmonary fibrosis is a subset of interstitial lung disease (ILD), a general category that includes various lung conditions. These disorders affect the absorption of oxygen into the lungs and impede normal breathing. Pulmonary fibrosis, like other interstitial lung diseases, affect the interstitium, the lace-like network of tissues that provides support to the lungs’ tiny air sacs, or alveoli. Tiny blood vessels travel through the interstitium, allowing gas exchange between the blood and lungs. Normally, the interstitium is too delicate to be seen in a chest x-ray or CT scan, but interstitial lung diseases like pulmonary fibrosis cause the interstitium to thicken due to scarring, extra fluid or inflammation. If you suspect you or someone you

Prognosis - Generally prognosis for pneumonia is good if the patient is not immune-compromised, old, or very young. Unfortunately, this baby was very young and the issue may not have been recognized by his parents as being life threatening until far too late in the process to provide appropriate

1) What are the Hepatic Ducts and what do they do? The Hepaticduct that carries bile from the liver into the common bile ductwhich conveys it to the duodenum (the upper part of the small intestine).(Webmd)

In this connection, the role of the macrophage has already been highlighted. An additional factor limiting the regression of established fibrosis is the previously mentioned increased survival of activated myofibroblasts. Increased expression of anti-apoptotic pathways is a hallmark of chronic myofibroblast activation and, for example, expression of the anti-apoptotic protein B-cell lymphoma gene-2 (Bcl-2) is markedly evident in myofibroblast-like cells that are present in areas of fibrosis in liver tissue obtained from patients with HCV-related cirrhosis. It is, therefore, plausible that long-term fibrogenesis is characterized, in addition to the biochemical evolution of scar tissue and the lack of appropriate degradation machinery, by the immovability of a critical mass of profibrogenic cells (Iredale,

One of the early reports of their role in an animal model of NASH was the observation that adoptive transfer of EVs isolated from the serum of high fat diet-fed mice into chow diet-fed mice results in immature myeloid cells activation and homing to the liver, which was associated with increased levels of hepatic proinflammatory markers and serum aminotransferases.32 Subsequent reports demonstrated a significant increase in the release of EVs from hepatocytes upon treatment with lipids such as palmitate and its active metabolite lysophosphatidylcholine (LPC),27 28 33 toxic lipid-induced EV release by hepatocytes was observed across different species.28 EVs derived from hepatocyte under lipotoxic stress are heterogeneous regarding their biogenesis, selected cargo, release, and intended target cells. For example, LPC-induced EV release is mediated by the stress kinase mixed lineage kinase 3 (MLK3).33 Furthermore, MLK3 regulates the chemotactic cargo of the EVs. Genetic or pharmacological inhibition of MLK3 results in a reduced abundance of the potent C-X-C motif chemokine ligand 10 (CXCL10) in vesicles derived from LPC-treated hepatocytes.33 Likewise, MLK3-/- mice fed a NASH-inducing diet34 have reduced CXCL10 levels in their plasma EVs. This, in turn, is