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Kelsey ConradKNH 411 Professor MatuszakSeptember 24, 2013Case Study 12: Cirrhosis of the LiverUnderstanding the Disease and PathophysiologyThe liver is an extremely complex organ that has a particularly important role in nutrient metabolism. Identify three functions of the liver related to each of the following:Carbohydrate metabolismGlucogenesis, Gluconeogenesis, Oxidation via TCA Cycle (p. 440)Protein metabolismSynthesis of Serum Proteins, Synthesis of Prothrombin, Globin of Hemoglobin (p. 440)Lipid metabolismLipogenesis, Lipolysis, Ketogenesis (p. 440)Vitamin and mineral metabolismFormation of acetyl CoA from pantothenic acid, Formation of 5-methyltetrahydrofolic acid (THFA), Methylation of niacinamide, Formation of coenzyme B12 (p. 440)Nemls, M., Sucher, K. P., Lacey, K., & Roth, S. L. (2011). Diseases of the Liver, Gallbladder, and Exocrine Pancreas. In Y. Cossio (Ed.), Nutrition Therapy & Pathophysiology (pp. 437-470). Belmont, CA: Wadsworth. The CT scan and liver biopsy confirm the diagnosis of cirrhosis. Explain this diagnosis. The diagnosis also includes a MELD score. What is this, and how does her score relate to the severity of liver failure?The diagnosis of cirrhosis “represents the end of the pathophysiology spectrum for a wide variety of chronic liver diseases in which healthy tissue is replaced by scar tissue, blocking the flow of blood through the organ and resulting in the loss of liver function” (p. 456-7). A MELD score is a clinical tool used to determine prognosis in patients with cirrhosis. MELD represents the prognostic model for end-stage liver disease and is based on three blood tests: international normalized ratio (INR), bilirubin, and creatinine (p 457). It estimates an individuals 90-day mortality rate. With a MELD score of 23, this patient’s 90-day mortality rate is .35, giving her a 35% change of death in the next 3 months (Mayo Clinic, 2013). Mayo Clinic (2013). MELD Score and 90-Day Mortality Rate for Alcoholic Hepatitis. Retrieved from , M., Sucher, K. P., Lacey, K., & Roth, S. L. (2011). Diseases of the Liver, Gallbladder, and Exocrine Pancreas. In Y. Cossio (Ed.), Nutrition Therapy & Pathophysiology (pp. 437-470). Belmont, CA: Wadsworth. The most common cause of cirrhosis is alcohol ingestion. What are other potential causes of cirrhosis? What is the cause of this patient’s cirrhosis?Other potential causes of cirrhosis are hepatitis C, cryptogenic causes, hepatitis B, which may be coincident with hepatitis D, autoimmune hepatitis, cystic fibrosis, Wilson’s disease, type IV glycogen storage disease, and many more (p. 458). The cause of this patient’s cirrhosis is hepatitis C. Nemls, M., Sucher, K. P., Lacey, K., & Roth, S. L. (2011). Diseases of the Liver, Gallbladder, and Exocrine Pancreas. In Y. Cossio (Ed.), Nutrition Therapy & Pathophysiology (pp. 437-470). Belmont, CA: Wadsworth. Explain the systemic physiological changes that occur as a result of cirrhosis.The systemic physiological changes that that occur as a result of cirrhosis are portal hypertension, hepatic encephalopathy, ascites, hepatorenal syndrome, and esophageal varices (p. 457-8). The altered liver function that occurs due to cirrhosis can affect the heart and circulatory system, the brain, the lungs, the immune system, and the kidneys (Fowler, 2009). Fowler, C. (2009). Critical nursing challenge: patients with end-stage liver disease. Retrieved from Nemls, M., Sucher, K. P., Lacey, K., & Roth, S. L. (2011). Diseases of the Liver, Gallbladder, and Exocrine Pancreas. In Y. Cossio (Ed.), Nutrition Therapy & Pathophysiology (pp. 437-470). Belmont, CA: Wadsworth. List the most common signs and symptoms of cirrhosis, and relate each of these to the physiological changes discussed in question #4.The most common sign of cirrhosis is an enlarged liver that results from the accumulation of fat and necrosis of the liver cells (p. 457). Symptoms associated with hepatic encephalopathy include impaired speech, movement, and mental function (Longstreth, G. F., 2011). Symptoms of portal hypertension include gastrointestinal bleeding, ascites, confusion, forgetfulness, esophageal varices, and reduced levels of platelets, blood cells that help form blood clots, or white blood cells (WebMD, 2013). Hepatorenal syndrome is known to cause abdominal swelling, confusion, dark-colored urine, nausea, vomiting, and jaundice (Hepatorenal syndrome, 2012). Other symptoms include fatigue, weakness, poor appetite, malaise, light stools, steatorrhea, itching, and bloating (p. 457). Malnutrition, including vitamin and mineral deficiencies, are common and can lead to depressed hematocrit and hemoglobin values and decreased vitamin K absorption resulting in coagulopathy (p. 457). Hepatorenal syndrome. (2012). U.S. National Library of Medicine. Retrieved from , G. F. (2011). Hepatic encephalopathy. MedlinePlus. Retrieved from Nemls, M., Sucher, K. P., Lacey, K., & Roth, S. L. (2011). Diseases of the Liver, Gallbladder, and Exocrine Pancreas. In Y. Cossio (Ed.), Nutrition Therapy & Pathophysiology (pp. 437-470). Belmont, CA: Wadsworth. WebMD. (2013). What is portal hypertension? Digestive Disorders Health Center. Retrieved from reading this patient’s history and physical, identify her signs and symptoms consistent with her diagnosis.The signs and symptoms that are consistent with her diagnosis are fatigue, weakness, weight loss, bruising, jaundice, abdominal distension, light stools, cloudy amber-colored urine, and lack of appetite. Hypoglycemia is a symptom cirrhotic patients may experience. What is the physiological basis for this? How might this affect Ms. Wilcox’s nutritional status?The physiological basis for hypoglycemia in cirrhotic patients is that the liver is key to glucose homeostasis. Because cirrhosis alters the liver’s function, its ability to maintain normal glucose homeostasis is also altered. This disruption affects hepatic glucose output, which could lead to hypoglycemia (Akry, R. A., 1989). This could severely compromise Ms. Wilcox’s nutritional status, which is evidenced by her laboratory results. Akry, R. A. (1989). Hypoglycemia associated with liver disease and ethanol [Abstract]. Endocrinol Metabolic Clinic North America, 18(1), 75-90. What are the current medical treatments for cirrhosis? The current medical treatments for cirrhosis include abstention from alcohol, treatment of the complications resulting from the cirrhosis listed in questions 4 and 5, and nutrition therapy (p. 458). Nemls, M., Sucher, K. P., Lacey, K., & Roth, S. L. (2011). Diseases of the Liver, Gallbladder, and Exocrine Pancreas. In Y. Cossio (Ed.), Nutrition Therapy & Pathophysiology (pp. 437-470). Belmont, CA: Wadsworth. What is hepatic encephalopathy? Identify the stages of encephalopathy, and outline the major theories regarding the etiology of this condition.Hepatic encephalopathy is a syndrome characterized by central nervous system dysfunction in association with liver function (p. 438). This syndrome is broken down into stages as follows (p. 446):Stage 0 – No abnormality detectedStage 1 – Trivial lack of awareness, euphoria or anxiety, shortened attention span, impairment in performance of additionStage 2 – Lethargy or apathy, minimal disorientation for time or place, subtle personality changes, inappropriate behavior, impaired performance on subtractionStage 3 – Somnolence to semi-stupor but responsive to verbal stimuli, confusion, gross disorientationStage 4 – ComaThree hypotheses surround the etiology of this condition. The ammonia hypothesis considers the fact that liver disease interferes with the metabolism of ammonia by the liver. The metabolism of ammonia is then performed in the skeletal muscle, where it is used in the conversion of glutamate to glutamine. Muscle wasting in these patients reduced the patient’s ability to metabolize this ammonia, which therefore accumulates in arterial blood. This leads to elevated levels in the brain and, because the brain lacks significant activity of urea cycle enzymes and cannot synthesize urea, the ammonia is detoxified via the conversion of glutamate to glutamine. This depletion of glutamate and accumulation of glutamine is thought to contribute to this condition (p. 445-446). The synergistic neurotoxin hypothesis states that a series of neurotoxins that accumulate in liver failure are responsible for this condition (p. 447). The false neurotransmitter hypothesis suggests that false neurotransmitters that are produced as a result of elevated phenylalanine levels may displace catecholamines from their receptors and lead to this condition (p. 447). This occurs due to the livers inability to metabolize these products that are toxic to the brain. Despite these hypotheses, the pathogenesis of hepatic encephalopathy is unknown (p. 445). Nemls, M., Sucher, K. P., Lacey, K., & Roth, S. L. (2011). Diseases of the Liver, Gallbladder, and Exocrine Pancreas. In Y. Cossio (Ed.), Nutrition Therapy & Pathophysiology (pp. 437-470). Belmont, CA: Wadsworth. Protein-energy malnutrition is commonly associated with cirrhosis. What are potential causes of malnutrition in cirrhosis? Explain each cause.One potential cause of malnutrition in cirrhosis is the patients inability to consume adequate amounts of food due to early satiety caused by the effect of ascites on the stomach’s capacity to expand. Impaired nutrient absorption and digestion can also occur due to portal hypertension, decreased pancreatic enzyme production and/or secretion, and villus atrophy. Vasodilation and expanded blood volume also increases energy expenditure, which can lead to energy malnutrition. In the later stages of liver failure, hypoglycemia frequently occurs as a result of hyperinsulinemia. Hyperglycemia, however, may also be evident because 40%-50% of all patients with end-stage liver disease suffer from insulin-resistant diabetes mellitus. All of these are contributing factors to protein-energy malnutrition in these patients (p. 459). Nemls, M., Sucher, K. P., Lacey, K., & Roth, S. L. (2011). Diseases of the Liver, Gallbladder, and Exocrine Pancreas. In Y. Cossio (Ed.), Nutrition Therapy & Pathophysiology (pp. 437-470). Belmont, CA: Wadsworth. Understanding the Nutrition Therapy11. Outline the nutrition therapy for stable cirrhosis and the rational for each modification.Calorie recommendations for these patients are 35 to 40 kcal/kg per day with a protein intake of up to 1.6 g/kg per day to combat the protein-energy malnutrition associated with this condition. Vegetable and dairy protein sources are recommended for patients with mild encephalopathy because they are lower in aromatic amino acids. 30% of total calories or less should come from fat to minimize steatorrhea. Carbohydrates should be consumed throughout the day in order to minimize hypoglycemia and hyperglycemia. Sodium should be restricted to manage ascites. Enteral and parenteral support should be considered to provide adequate nutrition to patients who are not getting adequate nutrition orally through meals and supplements or are comatose. A mechanically soft diet may be recommended to patients with esophageal varices to reduce the risk of bleeding (p. 459). Nemls, M., Sucher, K. P., Lacey, K., & Roth, S. L. (2011). Diseases of the Liver, Gallbladder, and Exocrine Pancreas. In Y. Cossio (Ed.), Nutrition Therapy & Pathophysiology (pp. 437-470). Belmont, CA: Wadsworth. Nutrition Assessment12. Measurements used to assess nutritional status may be affected by the disease process and not necessarily be reflective of nutritional status. Are there any components of nutrition assessment that would be affected by cirrhosis? Explain.Many components of nutrition assessment, including anthropometric and biochemical assessment methods, are affected by cirrhosis. Due to edema and ascites, for example, dry weight may not be obtainable. Edema and ascites can also result in inaccurate electrical impedance analysis results. Additionally, hepatic dysfunction can result in abnormal liver protein lab values, making it impossible to use these values to determine visceral protein status. Due to these complications, alternative nutritional status methods are being recommended and implemented, including the Subjective Global Assessment (SGA), the measurement of mid-arm muscle circumference (MAMC) or mid-arm circumference (MAC), and triceps skin fold thickness (TST) (p. 459).Nemls, M., Sucher, K. P., Lacey, K., & Roth, S. L. (2011). Diseases of the Liver, Gallbladder, and Exocrine Pancreas. In Y. Cossio (Ed.), Nutrition Therapy & Pathophysiology (pp. 437-470). Belmont, CA: Wadsworth. 13. Dr. Horowitz notes that Ms. Wilcox has lost 10 lbs since her last exam. Assess and interpret Ms. Wilcox’s weight.Ms. Wilcox’s current weight is 125 pounds (56.8 kg), and at a 5’8” (1.7 m), her BMI is about 19.0 kg/m2. Although this BMI classifies Ms. Wilcox as normal, she is very close to entering the underweight category.BMI = 56.8 kg ÷ 1.7 m2BMI = 19.03 kg/m2 Additionally, Ms. Wilcox has lost 10 pounds since her last office visit, which was 6 months ago. This significant decrease in weight suggests that Ms. Wilcox is experiencing anorexia, malnutrition, and/or an increased metabolic rate due to her hepatitis C and cirrhosis. Furthermore, Ms. Wilcox has stated that she has not had an appetite the past couple of weeks. Also, using the Hamwi Method, Ms. Wilcox’s ideal body weight is roughly 140 pounds; thus, the current weight of Ms. Wilcox is substantially lower than what it should be. (p. 456)Women: 100 pounds for the first five feet of height; add 5 pounds for every inch over 5 feet:5’8” = 100 + 40 = 140 pounds14. Calculate the patient’s energy and protein needs. Provide the rationale for the standards you used for these calculations.It is recommended for cirrhosis patients to consume 35-40 kcal/kg per day and up to 1.6 g/kg of protein per day depending on the degree of malnutrition and other medical complications. Therefore, according to these recommendations, Ms. Wilcox’s energy and protein needs are as follows:Energy Requirements: 35 kcal/kg × 56.8 kg = 1,988 40 kcal/kg × 56.8 kg = 2,272Ms. Wilcox’s energy requirements are about 2,000 – 2,300 kcal per dayProtein Requirements: 1.6 g × 56.8 kg = 90.88 gMs. Wilcox’s protein needs are about 90 – 91 grams of protein per day. I used 1.6 g/kg as the standard because Ms. Wilcox is experiencing malnutrition as evidenced by her weight loss and her lack of appetite. (p. 459)15. Evaluate the patient’s usual nutrition intake using nutrient analysis.According to Ms. Wilcox’s usual dietary intake she has been drinking water, juice and diet coke only, and has not eaten the past two days. She states that she has not had an appetite for the past couple of weeks. Ms. Wilcox stated that she drinks calcium-fortified orange juice for breakfast most mornings. Her lunch consists of soup and crackers with a diet coke, and dinner is usually at home or carry out. She stated that if she does do carry out for dinner it is usually Chinese or Italian. From this dietary recall, her diet is lacking in protein and many important vitamins and minerals. Also, the foods she is consuming are high in sugar and salt. 16. Her appetite and intake have been significantly reduced for the past several days. Describe factors that may have contributed to this change in her ability to eat. Patients with cirrhosis, like Ms. Wilcox, experience impaired nutrient digestion and absorption due to portal hypertension, decreased pancreatic enzyme production and/or secretion, and villus atrophy. Cirrhosis increases energy expenditure because of vasodilation and expanded blood volume. This can explain why Ms. Wilcox has lost weight, as well as why she is feeling fatigued and weak. Although, Ms. Wilcox does not have ascites, ascites commonly contribute to inadequate intake of food due to early satiety caused by the effect of ascites on the stomach’s ability to expand. Esophageal varices can result in swallowing difficulty, which would contribute to inadequate oral and food beverage intake, as well as cause disordered eating patterns. (p. 459)17. Why was a soft, 4-g Na, high-kcalorie diet ordered? Should there be any other modifications?Ms. Wilcox’s current diet order is a soft, 4-g Na, high-kcalorie diet. A mechanically soft diet is usually recommended for patients with esophageal varices as a preventive measure to reduce risk of bleeding. This may also help with the difficulty of swallowing as a result of the esophageal varices. It is recommended that sodium is restricted to 2-g per day to manage and reduce the risk of ascites. Therefore, I would modify the 4-g Na recommendation to 2-g Na per day. A high-kcalorie diet is recommended for patients with cirrhosis for many reasons. Ms. Wilcox’s increased metabolic weight and malnutrition warrant a high-kcalorie diet. Furthermore, since Ms. Wilcox’s blood-glucose levels are a bit higher than the reference range, her carbohydrate intake should be spread out by offering multiple meals throughout the day to minimize hyperglycemia. (p. 459)18. This patient takes multiple dietary supplements. Identify the possible rationale for each, and identify any that may pose a risk for someone with cirrhosis.Patients with cirrhosis experience impaired nutrient digestion and absorption due to portal hypertension, decreased pancreatic enzyme production and/or secretion, and villus atrophy. Supplementation is sometimes recommended to ensure adequate nutrient intake. Ms. Wilcox takes in 400 mg of Vitamin E, 600 mg of calcium, and 400 IU of vitamin D. Vitamins’ E and D are fat-soluble vitamins which are beneficial for Ms. Wilcox because her liver is compromised and unable to produce sufficient bile salts required for nutrient absorption. Vitamin E is also an antioxidant. Some evidence states that antioxidants might help in treating primary biliary cirrhosis, a condition in which the bile ducts of the liver are slowly destroyed. Calcium can be supplemented to increase bone density and bone mass and to reduce the risk of fractures and osteoporosis. The multivitamin/mineral she takes daily should only be taken by doctor approval. Ms. Wilcox also takes in 200 mg of milk thistle twice daily. Some evidence shows that a substance in milk thistle (silymarin) can protect the liver from damages caused by toxins, viruses, alcohols, and certain drugs. . Examine the patient’s chemistry values. Which labs support the diagnosis of cirrhosis? Explain their connection to the diagnosis.Ms. Wilcox’s albumin, Ammonia, Alkaline phosphatase, ALT, AST, Lactate Dehydrogenase, Bilirubin, and Urobilinogen levels all support the diagnosis of cirrhosis. The decreased albumin level of 2.1 suggests hepatic disease, which also suggests the functional status of parenchymal cells. Although the ammonia level of 33 is technically within the reference of 9-33, it is still increased which increases in patients with cirrhosis, liver failure, and with portacaval shunting of the blood. Ms. Wilcox’s alkaline phosphatase is 275, which is way above the reference range of 30-120. Increased activity occurs in hepatic disease and malignancy and in chronic obstruction of the biliary duct. Ms. Wilcox’s ALT level of 62 suggests hepatocellular injury and her AST level of 230 also suggests hepatic disease. Her elevated lactate dehydrogenase level of 658 is indicative of hepatitis. Finally, the increase in bilirubin and urobilinogen in her urine is indicative of biliary obstruction. (p. 443)20. Examine the patient’s hematology values. Which are abnormal, and why? Does she have any physical symptoms consistent with your findings?Ms. Wilcox’s hematology values indicate that her RBC (red blood cell) count is abnormal. Her RBC count is 4.1 L, when 4.2-5.4 L is the normal range for a female. This is common in patients with cirrhosis, and reveals that the patient is in oxidative stress. Her hemoglobin and hematocrit levels are also decreased which can be a result of vitamin and mineral deficiencies associated with cirrhosis of the liver. Also, Ms. Wilcox’s elevated PT (prothrombin time) suggests that the liver is not producing the blood clotting factors a healthy liver would. PT is tested in order to measure how quickly the blood clots. This is also evident in the bruising Ms. Wilcox is experiencing. (p. 457)21. What signs and/or symptoms would you monitor to determine further liver decompensation?I would closely monitor her anorexia since she has been experiencing a lack of appetite and is losing weight very quickly. I would want to make sure that the anorexia does not worsen because this would also indicate an insufficient and inadequate nutrient and energy intake. Thus, her body would be too weak to handle the cirrhosis diagnosis and won’t be able to properly treat the disease. (p. 459)22. Dr. Horowitz prescribes two medications to assist with the patient’s symptoms. What is the rationale for these medications, and what are pertinent nutritional implications of each? Dr. Horowitz prescribed Spironolactone 25 mg and Propranolol 40 mg. Spironolactone is a potassium-sparing diuretic that prevents your body from absorbing too much slat while keeping potassium levels from getting too low. This helps treat edema in cirrhosis patients. This medicine may cause an increased loss of sodium in the urine, and Ms. Wilcox should avoid excess K intake, salt substitutes, and natural licorice. This medication may also lead to increased thirst, diarrhea, and/or gastritis. The second medication prescribed, Propranolol, is a beta-blocker, which affects blood flow through arteries and veins and decreases blood pressure. In cirrhosis patients, this medication may be prescribed to help treat portal hypertension. If propranolol is taken with calcium, antacids, or high doses of vitamin C it may affect the absorption within the body. One should avoid natural licorice while using this medicine. (p. 449)Nutrition Diagnosis23. PES statement: NI-1.2 Inadequate energy intake related to lack of appetite as evidenced by a ten pound weight loss and patient statements.Nutrition Intervention24. 25. 26.Evaluation and Monitoring27. When you see Ms. Wilcox 1 month later, her weight is now 140 lbs. She is wearing flip-flops because she says her shoes do not fit. What condition is she most probably experiencing? How could you confirm this?Her swollen feet can be attributed to edema, or fluid retention from her liver damage. This is a common symptom of portal hypertension, and is typically accompanied with ascites of the abdomen. The doctor should physically examine her abdomen to she if there is any bulging. The weight gain of 15 pounds in four weeks can also be attributed to the ascites and fluid retention, or “water weight”. A 24-hour urine collection should be ordered to measure how much sodium she is excreting. 28. Her diet history is as follows:1. Breakfast: 1 slice toast with 2 tbsp peanut butter, 1 c skim milk Lunch: 2 oz. potato chips, grilled cheese sandwich (1 oz. American cheese with 2 slices of whole-wheat bread; grilled with 1 tbsp margarine), 1-cup skim milkDinner: 8 BBQ chicken wings, French fries 2 c, 2c lemonade2. What changes might you make to her nutrition therapy? Identify foods that should be eliminated and make suggestions for substitutions.I believe that her breakfast is appropriate, since she is consuming an adequate amount of protein, calories, and fluid, while it is still very low in sodium. I would suggest including a piece of fruit, in order to increase her vitamin intake. Her lunch is also adequate. However, I would recommend that the potato chips are baked with a sodium substitute and/or spices. I would also suggest adding a vegetable, like steamed broccoli or green beans. Finally, I believe that her meal choice during dinner is too high in fat and sodium. Instead of BBQ wings, I would recommend lean meat, like grilled chicken or fish. I would also recommend a baked potato as a substitute for the French fries. Furthermore, including a fruit and vegetable at dinnertime would be recommended. Another concern I have with her diet is her consumption of three large meals throughout the day. I would suggest having smaller, more frequent meals throughout the duration of the day, to encourage adequate energy intake. Lastly, I would recommend a multivitamin to decrease any nutrient deficiencies. Her doctor should be consulted first before she begins taking a multivitamin in case of any drug-nutrient interactions. ................
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