Cirrhosis: A Case Study

Glucagon acts on liver cells to promote breakdown of glycogen into glucose and formation of glucose from lactic acid and certain amino acids.

In the presented case scenario, we have Mr. Gil Martin who is a 55-year-old Hispanic male. He comes in to the clinic today with complaints of weakness, fatigue, and loss of appetite. A student nurse will be precepting your assessment of Mr. Martin and when collecting subjective and objective data it is important to pay close detail to all findings. Ultimately this patient was diagnosis with cirrhosis, which is an abnormal liver condition that leads to irreversible scarring of the liver (National Institute of Health [NIH], 2017), so during assessment we should pay attention to details leading to this diagnosis.

Cirrhosis is a consequence of chronic liver disease characterized by replacement of normal, healthy liver tissue by fibrotic scar tissue, blocking the flow of blood through the organ and preventing it from working as it should, as well as regenerative nodules leading to progressive loss of liver function. The liver, the largest organ in the body, is vital in keeping the body functioning properly. It removes or neutralizes poisons from the blood, produces immune agents to control infection, and removes germs and bacteria from the blood. It

Liver produces bile, which helps to decompose lipid molecules, during digestion. It also produces certain proteins and cholesterol that are needed in the blood plasma, and that carry fats around the body. The liver stores iron, so if the liver is negatively impacted, it can lead to iron deficiency (Stanford Children’s Health 2015). Furthermore, it is vital is removing toxin from the body, so if the liver can’t function properly, the toxins will be left in the body, causing further damage. It also regulates blood clotting, so without the liver, the body won’t be able to stop bleeding in an injury, and blood may clot in arteries, which will lead to heart attack (Stanford Children’s Health

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).

We sold everything we did not need in California, bought this 1972 trailer, had it remodeled and then moved to Saddle Butte in Oct 2015. We moved here knowing we could afford it and would not have any financial problems. Most of all, would never be late on rent or bills. Unfortunately, the worst possible thing happened, Dana was diagnosed with End Stage Liver Disease.

The progression from fibrosis to cirrhosis, the end-point of CLDs, is distinguished by a prolonged inflammatory and fibrogenic process that leads to an abnormal angioarchitecture distinctive for cirrhosis. Several mechanisms are responsible for the angiogenic switch during the pathogenesis of CLDs. First, CLDs are characterised by chronic inflammation. Increased intrahepatic vascular resistance is primarily caused by anatomical changes, such as fibrotic scar tissue compressing portal and central venules. In addition, the formation of fibrotic septa, as well as sinusoidal capillarisation, can result in an increased resistance to blood flow and oxygen delivery. This results in hypoxia and the transcription of hypoxia-sensitive pro-angiogenic

infections. When the liver is inflamed or damaged, its function can be affected. Acute Hepatitis C

Define the stage of the disease is very important for diagnosis, treatment, and follow-up . There are many ways for assessing the degree of liver fibrosis. Liver biopsy was the gold standard for assessing liver fibrosis, but now it is of limited value because it is so invasive, its high cost, poor acceptance, risk of complications, and intra/inter-observer variability (Poynard et al.,2007). During the different stages of fibrosis , there are excessive amounts of extracellular matrix of various biomarkers changed and new biomarkers appeared in the serum (Jarcuska et al.,2010 and Baranova et al. 2011).

Humans simply can not live without the liver; it is even in the name “Liver”. The liver is composed of four lobes and is located in the right side of the body. As the heaviest organ, the liver performs a plethora of functions simultaneously. It acts as a refinery by filtering and purifying blood. Moreover, the liver stores carbohydrates by converting it to simple sugars. The liver also takes a major part in digestion by producing bile. Bile is an essential component in processing fats. Bile is originally made in the liver but is stored in the gallbladder. Furthermore, the liver also takes part in the body’s immunity and the production of important blood proteins. Blood is transported to the liver via two vessels: the hepatic artery (blood from the heart), and the hepatic portal vein (blood from the guts). Blood leaves the kidney through the hepatic vein that leads to the heart. For such an important organ, it is no surprise that having a defective

Sign and Symptoms can be Jaundice yellowing of the skin which can occur from high levels of bilirubin in the liver (normal bilirubin levels are 0.1 to 1 mg/DL, Fatigue, Bleeding more easily, Bruising easily, Itchy skin, Fluid accumulation in your abdomen (ascites) may result from the liver being unable to produce albumin to attract water in the blood vessels, swelling in your legs, weight loss, Spider Like blood vessels of your skin, and Portal Hypertension can be caused by the blockage of blood flow through the liver and that causes the blood pressure to rise in the portal vein.

The liver is an organ that converts food into energy, absorbs vitamins from a person's diet, removes toxins from the blood, and makes important proteins. Alcoholic liver disease happens when the liver becomes damaged due to alcohol consumption and stops working properly.

Fatty liver disease is, lipid or fat buildup in liver cells contributing to the liver a yellow hue. The cellular injury starts dysfunctional metabolic processes which can consequence in lipid collection in liver cells (McCance, 2014). The causative metabolic processes might be: increased dispersion of fatty acids in the liver, ineffective transformation of fatty acids to triglycerides instead of phospholipids, failure to carry lipoproteins out of the cell, free radicals destruct the endoplasmic reticulum, increased synthesis of fatty acids to triglyceride, decreased synthesis of apoproteins, and un-effective binding of lipids to apoproteins and

It is important to rule out common causes of liver injury, such as alcohol, drug use, and viral hepatitis as well as other co-existing etiologies for chronic liver disease including alpha-1 antitrypsin deficiency, hemochromatosis, autoimmune liver disease (types 1 and 2), chronic viral hepatitis, and Wilson’s disease

Acute liver failure is a syndrome characterized by development of altered mental status and coagulopathy in a patient within 8 weeks of onset of liver injury [1]. A large number of inflammatory markers have been implicated in causing the liver injury; and the massive hepatic insult that occur is believed mainly due to this tissue inflammation rather than the disease process per se. It is caused by a group of hepatotropic viruses (A, B, C, D and E. Acute liver failure is the most fatal complication of acute infection of the liver by hepatotropic viruses (Hepatitis A to E). In India, the most common viruses involved in Acute liver failure are hepatitis E followed by hepatitis B [2]. Interleukin (IL)-10 is an important immunoregulatory