Murray Brown Case Study Sample

Cirrhosis of The Liver

Contents

Pathophysiology of liver cirrhosis.

Follow-up care and interventions.

Risk factors of liver cirrhosis.

Long term complications of liver cirrhosis.

Medications for liver cirrhosis and their pharmokinetics and pharmodynamics.

References.

Pathophysiology of Liver Cirrhosis

Murray Brown has been suffering from liver cirrhosis from the past 12 years. He has been drinking and smoking heavily, however, after his diagnosis of liver ailment he has been sober. The liver cirrhosis can occur due to many reasons and this goes in three stages and these are fatty liver (deposition of fat causing its enlargement), liver fibrosis (formation of scar tissues due to liver injury) and cirrhosis (scar tissues impairs working of liver). In his case, the advance stage of liver damage has occurred due to two decades of heavy drinking.

Liver is the main organ where alcohol is metabolised apart from the gastrointestinal tract. It is metabolized through two ways and these are cytochrome P450 (CYP) 2E1 and alcohol dehydrogenase. The alcohol dehydrogenase is a hepatocyte cytosolic enzyme which transforms alcohol into acetaldehyde. This acetaldehyde is then converted to acetate by the acetaldehyde dehydrogenase. CYP 2E1 is a membrane protein which also converts alcohol to acetaldehyde. Both the alcohol and acetaldehyde dehydrogenase are involved in the reduction of NAD to NADH. Fatty liver occurs when the ratio of NAD/NADH is altered. This altered ratio leads to inhibition of gluconeogenesis and oxidation of fatty acids. CYP 2E1 is also upregulated in cases of chronic alcohol use. This generates free radicals by the NADPH oxidation to NADP. Hepatic macrophages are also activated due to chronic alcohol exposure and these produce tumor necrosis factor-alpha (TNF-alpha). This leads to oxidative stress and causes necrosis and death of liver cells. Free radicals cause inflammation and there occurs fibrosis which over time develops into liver scars (Vozzo, et al June, 2018).

The liver is not able to function properly due to the formation of scars and fibres which occurs as a repair process for the injury caused by chronic alcohol intake (O'shea, et al 2010). Due to this the normal flow of blood in liver is obstructed. Portal hypertension occurs in the liver veins which brings blood from the spleen and intestines. With the increased pressure in the hepatic portal vein fluid can accumulate in legs and in the abdomen. Murray has ascites and 4+ pitting oedema which shows that there is increased pressure in the hepatic portal vein. In liver cirrhosis, there is reduced metabolism of aldosterone and this disturbs the renin-angiotensin system. This disruption leads to reduction in the renal blood flow and hence the kidney gets the signal of retaining salt and water. Salt and water is then retained in body leading to ascites in the abdomen (Cunha, July 03, 2019). When excess water and salt accumulate in the tissues underlying skin of the legs and ankles then it is termed as pitting oedema. Ascites and oedema can also occur due to reduced production of proteins like albumin by liver (Tsochatzis, Bosch, and Burroughs, 2014).

Murray has symptoms of nausea, anorexia and abdominal discomfort which also denotes impaired liver function. Liver has important role in digestion and toxin removal in body therefore, as these functions are impaired the patient feels loss of appetite (anorexia), nausea and abdominal discomfort. Owing to this, he remain malnourished and thin as the liver is unable to process nutrients leading to weight loss.

His liver and spleen are palpable. Portal hypertension causes swelling of the spleen as white blood cells and platelets are trapped in the spleen. Hepatomegaly is caused by alcoholic liver disease and is the common physical sign of liver cirrhosis. Scarring of the liver tissue in this condition can lead to hepatomegaly.

Liver has a main function in the excretion of bilirubin. It is formed from haeme of blood and in liver it is conjugated implying that it is made water soluble and can be then easily excreted. However, when the liver is unable to function properly then the bilirubin is not excreted from blood. This excess of bilirubin is then stored in other body parts like skin and sclera of eye.

As per the lab tests, he has a high value of total bilirubin. Normal range of bilirubin is from 5.1 to 17.0 mmol/L while in this case it was 257 mmol/L. This also confirms impaired liver function. The ALT test has shown a high value of 201 U/L as the normal range lies between 10 to 40 units per liter (U/L). Alanine transaminase (ALT) is a liver enzyme which is used in the conversion of proteins into energy by hepatocytes. However, in case of liver damage, the ALT is released into the blood and this makes its levels to rise. The Aspartate transaminase (AST) is an enzyme which is responsible for the metabolism of amino acids. When liver is damaged then this enzyme increases in the bloodstream however, this test is not a specific test for ascertaining liver damage. In this case, AST test gave a value of 190u/L which is very high as the normal range is from 8 to 48 units per litre. Elevated AST in conjugation with ALT denotes a liver damage (Davis, June 22, 2020).

Further, assessment can be done for ascertaining the extent of liver damage in this case. Magnetic resonance imaging (MRI), computerized axial tomography (CAT), ultrasound or scanning the liver with a radioisotope can be done in this case. A liver biopsy will also confirm the diagnosis which is the examination of the liver tissue for scarring and other signs of liver damage. A doctor can also assess the liver using a laparoscope (an instrument which relays back pictures on screen when inserted into the abdomen).

Follow-up Care and Interventions

In this case, the liver damage has been done by alcohol abuse therefore, the community nurse can educate Murray to stop drinking alcohol for stopping liver damage. Nurse can maintain a follow-up care for him which is inclusive of routine tests. These shall be for ascertaining the functional chemistries of liver, kidney and blood count. The community nurses can provide a healthy diet with low sodium plan so that retention of fluid in the body can be checked. Care has to be taken in avoiding infections so that liver does not have work hard.

Risk Factors of Liver Cirrhosis

The presence of underlying infections like viral hepatitis, diabetes, obesity, excessive alcohol consumption are the major risk factors in liver cirrhosis (Chiang, Pritchard, and Nagy, 2011). Chronic hepatitis infection from hepatitis B and C also increases the risk of progressing liver cirrhosis. Genetics is also a risk factor as there are people who face problems in digesting alcohol. Fatty liver disease (which is non-alcoholic steatohepatitis), autoimmune liver disease (like autoimmune hepatitis, primary sclerosing cholangitis, primary biliary cirrhosis), hemochromatosis, Wilson and other rare inherited diseases of liver. However, in this case, the main risk factor is excessive alcohol consumption as the healthcare intervention will not succeed if alcohol consumption is continued.

Lifestyle modifications are thereby required in this case. The community nurse must provide education to Murray and his family regarding the ills of alcohol abuse on his liver health. The complications arising from the liver damage must be explained to him. Further, the ways in which he can reduce his dependency on alcohol must be communicated by the community nurse. However, the lifestyle changes cannot cure liver cirrhosis but it reduce the severity of the symptoms and also delay the further progression of the disease (Frazier, et al 2011). He must not drink alcohol, maintain a proper diet, must avoid raw food items like seafood so that infection of liver is avoided. Vitamin and mineral supplements can be given as with cirrhosis deficiencies can occur.

Long-term Complications of Liver Cirrhosis

With liver cirrhosis, permanent liver damage can occur if interventions like taking medications and abstaining from alcohol are not done. Long term complications also include gastrointestinal bleeding which occurs when pressure builds up in the veins causing them to burst. This may lead to blood in stool or blood in vomit. Further, the liver damage can cause hepatic encephalopathy in which the brain functions are impaired due to building up of toxins. This leads to mental confusion and can also progress into coma. Ascites can progress further causing difficulty in breathing as the pressure from the retain fluid on the diaphragm causes obstruction in lung expansion during breathing.

Medications for Liver Cirrhosis and Their Pharmokinetics and Pharmodynamics

As the liver cirrhosis is alcohol related therefore, abstaining from alcohol is highly prescribed by doctors. However, the patients face difficulty in abstaining from its consumption and therefore drugs like Naltrexone is given. For reducing the inflammation of the liver corticosteroids and pentoxifylline and other drugs may also be used in people who are suffering from alcoholic hepatitis (Leggio, and Lee, 2017).

Pharmacodynamics of Naltrexone – this is one of he competitive antagonists at the receptors for μ-opioid (Mason, et al 2002). Therefore, it blocks the receptors for opioids which helps in checking the alcohol dependency.

Pharmokinetics of Naltrexone- liver metabolizes it in 6 beta naltrexol with the help of enzyme called dihydrodiol dehydrogenase. There are other metabolites which are formed from this drug and these are then conjugated with glucuronide.

Pentoxifylline can also be prescribed to Murray. It is a methylxanthine derivative and it functions by inhibiting the phosphodiesterase and hence influences the blood rheology. It enhances the flow of blood by enhancing the flexibility of erythrocyte and leukocyte. It stops the aggregation of platelets and modulates the immunologic activity with the stimulation of the cytokine production. It has immunomodulatory properties which helps in decreasing organ damage (De, et al 2009).

Pharmacokinetics – when this drug is taken orally in aqueous solution then it is completely absorbed. It goes under a first-pass effect and soon the different metabolites occur in the blood plasma. Peak levels of the metabolites are seen within one hour of dosing (Magnusson, 2009). The main metabolites are Metabolite 5 (1-[3-carboxypropyl]-3, 7-dimethylxanthine) and Metabolite l (1-[5-hydroxyhexyl]-3,7-dimethylxanthine). After the consumption of aqueous solutions having 100 to 400 mg of this drug, the pharmacokinetics of the parent and the metabolite compound are found to be dose related and this is non-linear and not proportional. Its half-life and the area in the blood-level time curve (the AUC) increases with the increasing dose. 

The plasma half-life of this drug apparently ranges from 0.4 to 0.8 hours and for its metabolites it ranges from 1 to 1.6 hours. This drug is excreted from urine totally and the main bio-transformed product is the metabolite V. However, no parent drug is found in urine. In spite of the large variations of the plasma levels for its parent compound and the metabolites, the recovery of the metabolite V is consistent. It also shows proportionality with consumed dose. Lower than 4 percent of the administered dose is excreted through feces.

Pharmacodynamics – it is a synthetic dimethylxanthine derivative. And this is structurally related to the caffeine and theophylline. It is also used for the treatment of the sickle cell disease, diabetic neuropathy, peripheral vascular diseases and cerebrovascular insufficiency. It works by inhibiting the erythrocyte phosphodiesterase, which increases activity of erythrocyte cAMP. It also decreases the blood viscosity by reducing the concentration of plasma fibrinogen and increasing the fibrinolytic activity. It helps in lowering the portal hypertension and hence relieves the liver damage symptoms.

References for Murray Brown Case Study

Chiang, D., Pritchard, M., & Nagy, L. (2011). Obesity, diabetes mellitus, and liver fibrosis. American Journal of Physiology-Gastrointestinal and Liver Physiology, 300(5), G697-G702.

Cunha, J. P. (July 03, 2019). Cirrhosis (Liver) https://www.medicinenet.com/cirrhosis/article.htm

Davis, C. (2020). Liver Blood Tests (Normal, Low, and High Ranges & Results). Retrieved from https://www.medicinenet.com/liver_blood_tests/article.htm

De, B. K., Gangopadhyay, S., Dutta, D., Baksi, S. D., Pani, A., & Ghosh, P. (2009). Pentoxifylline versus prednisolone for severe alcoholic hepatitis: a randomized controlled trial. World journal of gastroenterology: WJG, 15(13), 1613.

Frazier, T. H., Stocker, A. M., Kershner, N. A., Marsano, L. S., & McClain, C. J. (2011). Treatment of alcoholic liver disease. Therapeutic advances in gastroenterology, 4(1), 63-81.

Leggio, L., & Lee, M. R. (2017). Treatment of alcohol use disorder in patients with alcoholic liver disease. The American journal of medicine, 130(2), 124-134.

Magnusson, M. V. (2009). Pharmacokinetics and pharmacodynamics of pentoxifylline and metabolites. Lund University, Faculty of Medicine, Doctoral Dissertation Series, 29.

Mason, B., Goodman, A., Dixon, R., Hameed, M., Hulot, T., Wesnes, K. & Boyeson, M. (2002). A pharmacokinetic and pharmacodynamic drug interaction study of acamprosate and naltrexone. Neuropsychopharmacology, 27(4), 596-606.

O'shea, R., Dasarathy, S., McCullough, A., & Practice Guideline Committee of the American Association for the Study of Liver Diseases and the Practice Parameters Committee of the American College of Gastroenterology. (2010). Alcoholic liver disease. Hepatology, 51(1), 307-328.

Tsochatzis, E., Bosch, J., & Burroughs, A. (2014). Liver cirrhosis. The Lancet, 383(9930), 1749-1761.

Vozzo, F., Welch, N., Romero-Marrero, C., & Fairbanks, K. (2018). Alcoholic Liver Disease. Retrieved from http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/hepatology/alcoholic-liver-disease/

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