Jennifer Axford

Nutrition 409
Joan Rupp
Case Study #12

1. The 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 metabolism
o

The liver stores glucose as glycogen through a process called glycogenesis, and when
circulating blood glucose becomes low it is released from the liver into the bloodstream in a
process called glycogenolysis. Gluconeogenesis, the creation of glucose from non-carbohydrate
sources occurs in the liver.

Protein metabolism
o

Two important metabolic pathways that convert amino acids into substrate form needed in
energy production and synthesis of nonessential amino acids, called transamination and
oxidative deamination occur in the liver. Blood clotting factors such as fibrinogen are produced
in the liver, as well as serum proteins such as albumin.

Lipid metabolism
o

Fatty acids are converted by the liver into acetyl-coenzyme A to produce large amounts of
energy. The liver synthesizes lipids such as triglycerides and phospholipids, as well as
preforming lipolysis.

Vitamin and mineral metabolism

o

The liver stores fat soluble vitamins, the water soluble vitamin B12, as well as minerals zinc,
iron, copper and magnesium. The liver produces the transport proteins that transport vitamin A,
iron, zinc and copper into the blood stream. Many vitamins are converted to their active forms in
the liver, such a carotene into vitamin A.

3. The most common cause of cirrhosis is alcohol ingestion. What are the other potential causes of
cirrhosis? What is the cause of this patients cirrhosis?

There are many liver diseases can cause cirrhosis if left untreated. Some of these include chronic
hepatitis; nonalcoholic fatty liver disease, cholestatic liver diseases and some inherited disorders such
as hemochromatosis and Wilsons disease; and other liver diseases such as liver tumors and systemic
diseases. The patients cause of cirrhosis is chronic Hepatitis C. HCV is considered chronic if the
course of the virus lasts longer than six months. HCV is spread by blood and bodily fluids, and unlike
hepatitis A and B, there is no vaccine to prevent or cure Hepatitis C.

4. Explain the systemic physiological changes that occur as a result of cirrhosis.

Several systemic physiological changes can occur as a result of cirrhosis that include malnutrition, fat
malabsorption, glucose intolerance, portal hypertension and varices, hepatic encephalopathy, ascites
and hepatorenal syndrome.

Because the liver is responsible for the metabolism of carbohydrates, lipids, protein and
vitamins/minerals many complications in metabolism can occur, putting those with cirrhosis at high risk
for malnutrition. Decreased bile production can result in reduced fat absorption and glucose intolerance
due to insulin resistance and increased insulin production can occur in patients with cirrhosis.

Portal hypertension can cause varices (enlarged, swollen veins) that occur in the gastrointestinal that
can occur in the esophagus as well. Esophageal varices develop when normal blood flow to the liver is
obstructed by scar tissue in the liver or a clot. Seeking a way around the blockages, blood flows into
smaller blood vessels that are not able to carry large volumes of blood. The vessels may leak blood or
even rupture, causing life-threatening bleeding.

Hepatic encephalopathy is a syndrome of impaired mental status and abnormal neuromuscular function
that results from major liver failure. This is due to the liver being unable to remove harmful toxins from
the blood. Stage IV encephalopathy can cause coma and death.

Accumulation of fluid, called ascites, can occur when serum proteins and electrolytes within the
peritoneal cavity caused by increased pressure from portal hypertension, decreased production of
albumin, lymphatic obstruction and renal retention of sodium and fluids. The strain on the kidneys
caused by liver disease can lead to hepatorenal syndrome.

5. List the most common signs and symptoms of cirrhosis, and relate each of these to the physiological
changes discussed in question #4.

There are numerous clinical manifestations of cirrhosis due to the number of functions the liver is
responsible for, which include over 500 different tasks. The most common signs and symptoms of
cirrhosis include: fatigue, weakness, anorexia, enlarged liver, ascites, varices, jaundice and dark
colored urine. Fatigue, weakness and anorexia are complications related to malnutrition and other
metabolic disturbances caused by cirrhosis. Portal hypertension can cause GI bleeding, ascites,
confusion, memory loss and esophageal varices. Hepatic encephalopathy causes mental and
neuromuscular impairment. Hepatorenal syndrome causes abdominal edema, confusion, dark-colored
urine, nausea, vomiting, jaundice and fatigue.

6. After reading this patients history and physical, identify her signs and symptoms consistent with her
diagnosis.

The patient reports feeling weak and fatigued, is experiencing anorexia, jaundice, bruising without injury
and has unintentional weight loss of ten pounds within the last six months. Her physical examination
revealed enlarged esophageal veins, telangiectasias on her chest, mild distention of the right upper
quadrant of the abdomen, and hepatomegaly. The patient also has a family history of cirrhosis.

8. What are the current medical treatments for cirrhosis?

Although cirrhosis is non-reversible, treating the symptoms of cirrhosis can prevent further deterioration
of liver function. The most important treatment is ceasing consumption of alcohol and other drugs.
Proper nutrition and supplementation is recommended to prevent any nutritional inadequacies. Other
medical nutrition therapies that can aide cirrhosis patients are consuming soft diets to avoid rupturing
varices in the esophagus, and treatment of fluid and electrolyte imbalances. Dialysis therapy and bed
rest to aid dieresis may be recommended. Medications must be closely monitored for

pharmacodynamic interactions and hepatotoxicity. In the most severe cases, liver transplantation
should be considered.

9. What is hepatic encephalopathy? Identify the stages of encephalopathy, and outline the major
theories regarding the etiology of this condition.

Hepatic encephalopathy is the buildup of toxins such as ammonia in the brain due to altered liver
function, therefore protein must be limited in patients with altered liver function. Hepatic
Encephalopathy can lead to neuromuscular disturbances, intellectual impairment and altered
consciousness and in extreme cases, permanent heart failure, coma, and death.
o Stage 1 is characterized by symptoms of mild confusion, agitation, sleep disturbance and

attention problems.
Stage 2 by lethargy, disorientation, drowsiness and uninhibited behaviors.

Stage 3 progresses into aggressive behavior, confusion and incomprehensible speech.

Stage 4 results in coma and/or death.

11. Outline the nutrition therapy for stable cirrhosis and the rationale for each modification.

Stable cirrhosis patients require a carefully planned diet to prevent the progression of liver damage. A
low sodium diet of less than 2,000 mg/day is recommended to treat ascites associated with cirrhosis.
Fluid intake should be restricted to 1-1.5 L/day if edema and ascites is severe. PN nutrition may be
required for those with acute bleeding episodes caused by varices in the GI tract due to portal
hypertension. Carbohydrate needs are difficult to assess in cirrhosis patients and should be tailored to
individual cases. Recommended protein needs in those with stable cirrhosis is 0.8 g/kg/day, as nitrogen
losses are only associated with more aggressive forms of cirrhosis. Vitamins and minerals should be
supplemented in all cirrhosis patients due to impaired nutrient absorption. No alcohol should be
consumed.

13. Dr. Horowitz notes that Ms. Wilcox has lost 10 lbs. since her last exam. Assess and interpret Ms.
Wilcoxs weight.

Ms. Wilcoxs current weight is 125 pounds (56.8 kg) and she is 59 (1.7 m) tall. Her BMI is 18.5 kg/m2,
putting her in the underweight category. Ms. Wilcox is at 93% of her UBW of 135 lbs, and 86% of her
IBW of 145 lbs, making her at risk for mild malnutrition.

14. Calculate the patients energy and protein needs. Provide the rationale for the standards you used
for these calculations.

Energy Needs: 2,565 kcal/day

o

45 kcal/kg was used to determine energy needs, based on her underweight status with an
activity factor of 1.5

Protein Needs: 45 g/day

o

0.8 g/kg/day protein is recommended for patients with stable cirrhosis of the liver.

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.

Her reduced appetite is directly related to the symptoms she has been exhibiting: anorexia, N/V
malnutrition and fatigue; caused by her cirrhosis. Nausea and vomiting are common for individuals with
cirrhosis, affecting calorie intake and the desire to eat. Fatigue can also impede a persons ability to
prepare food while reducing their overall appetite.

19. Examine the patients chemistry values. Which labs support the diagnosis of cirrhosis? Explain their
connection to the diagnosis.

The patients BUN is high (21 mg/dL). Liver disease may result in impairment of the organ's ability to
convert ammonia to urea, as well as impair the kidneys ability to filter out urea, causing BUN to
increase.

Glucose is slightly elevated to 11 mg/dL. Insulin resistance is common in cirrhosis patients and can lead
to impaired blood glucose.

High bilirubin 3.7 mg/dL. A diseased liver is unable to properly process bilirubin, a byproduct of RBC
production, due to inadequate bile production, and blood levels of the substance become elevated. A
high level of bilirubin is also indicative of biliary obstruction and red blood cell hemolysis.

Low protein, albumin and pre-albumin: 5.4 g/dL, 2.1 g/dL, 12 mg/dL indicate malnutrition and/or a
protein deficiency. The liver is important in amino acid synthesis and metabolism, in addition to
symptoms of liver disease cause decreased appetite and difficulties eating.

Liver enzymes alkaline phosphatase, ALT, and AST were elevated: 275 U/L, 62 U/L, 230 U/L. Increased
alkaline phosphatase activity occurs in hepatic disease and in chronic obstruction of the biliary duct.
ALT is the most sensitive test to detect hepatocellular injury. AST is also a marker of liver function and
increased levels are in line with the diagnosis of cirrhosis.

CPK levels elevated to 138 U/L. Conditions that affect the brain, heart, or skeletal muscle cause cellular
destruction that increase CPK activity, resulting in increased lab values.

Slightly low HDL cholesterol levels (50 mg/dL) and increases triglycerides (256 mg/dL) signify an
increased risk of developing heart disease, and is likely due to the portal hypertension from cirrhosis.

20. Examine the patients hematology values. Which are abnormal, and why? Does she have any
physical symptoms consistent with your findings?

Coagulation factors PT, INR and PTT were shown to be higher than normal (18.5 sec, 2.2, 41 sec),
showing that the liver was not producing the blood clotting factors a healthy liver would. This may be
causing her symptoms of easy bruising.

Low RBC count (4.1 L) is common in cirrhosis patients, and is indicative of oxidative stress.

Low hemoglobin (10.9 g/dL) and low hematocrit (35.9%), is common in patients with cirrhosis, chronic
disease, fluid retention, splenomegaly, anemia, or nutritional deficit. This may be causing her symptoms
of weakness and fatigue.

26. Using the information from her usual dietary intake, what suggestions might you make to assist with
compliance with the fluid and sodium restrictions?

The patient has been consuming a nutritionally inadequate diet based on her nutrition information.
Her usual intake consist of primarily liquids, and the solid foods include soup and take-out which are
notoriously high in sodium. To comply with her new diet regimen, Ms. Wilcox may benefit from a soft
food diet low in sodium and cease her consumption of soda and juice.

27. When you see Ms. Wilcox one month later, her weight is now 140 lbs. She is wearing sandals
because she says her shoes do not fit. What condition is she most probably experiencing? How could you
confirm this?

Mrs. Wilcox is demonstrating edema in her extremities (feet). Edema is a common symptom of
portal hypertension and is often accompanied by abdominal ascites. Her weight gain of 15 lbs in
four weeks also indicates edema or possible ascites. A press test on the ankle could determine the
level of edema the patient is experiencing.