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Case 17-Cirrhosis of the Liver with Resulting Hepatic Encephalopathy

Understanding the Disease and Pathophysiology1. The liver is an extremely complex organ that has a particularly important role in nutrient
metabolism. Identify three functions of the liver for each of the following: (2-points- state
specific names of metabolic pathways for each macronutrient and specific vitamins
metabolized/formed by the liver)
1. Carbohydrate metabolism: Glycogenesis, gluconeogenesis and glycolysis
2. Protein metabolism: Synthesis of serum proteins, synthesis of prothrombin and
degradation of some proteins to peptides and amino acids
3. Lipid metabolism: lipogenesis, esterification of fatty acids and
uptake/formation/breakdown of phosphotides
4. Vitamin metabolism: formation of acetyl CoA from pantothenic acid,
dephosphorylation of thiamin and hydroxylation of vitamin D to 25-OH D 3
2. (1-point one short paragraph) The CT scan and liver biopsy confirm the diagnosis of
cirrhosis. What is cirrhosis?
Cirrhosis represents the end of the pathophysiology spectrum of many chronic liver
diseases in which healthy tissue is replaced by scar tissue which blocks the flow of blood
through the organ and resulting in the loss of liver function. Major complications can occur
from cirrhosis such as, encephalopathy and ascites. The liver becomes enlarged because
of fat accumulation and necrosis of the liver cells.
3. (2-points) The most common cause of cirrhosis is alcohol ingestion. What are some
additional causes of cirrhosis? (All hepatitis types are considered as only one answer)
1. Chronic HCV
2. Cryptogenic causes
3. Cystic fibrosis
4. Drug-induced liver disease
4. (1-point-one short paragraph) What is hepatic encephalopathy? (make sure to include the
4 grades)
Hepatic encephalopathy is a syndrome characterized by central nervous dysfunction in
association with liver failure. Important factors are the degree of liver failure, diversion of
the portal blood through the venous systemic circulation, bleeding from varies and
exogenous factors like sepsis. To determine the severity, grades are used. There are
several scales used but one widely used criteria is the Adapted-West Haven Criteria:
Stage Adapted West Haven Criteria
Alert and attentive without signs or symptoms of encephalopathy
Alert and attentive, but with at least one of the following signs: dysarthria, ataxia,
flapping tremor or obvious decrease in the speed of mental processing
Awake but inattentive: disoriented, somnolent, easy to distract, unable to
perform easy mental tests. Speech easy to understand
Marked somnolence or psychomotor agitation. Speech is difficult to understand
Coma patient does not speak and does not follow simple commands
5. [(3-points) The pathogenesis of hepatic encephalopathy is unknown. Name and explain
the 3 current major theories regarding the etiology for the impairment of
neurotransmission in hepatic encephalopathy. Include at least 3 sentences per theory for
each explanation.

Hepatic encephalopathy is a syndrome that comes from a central nervous system dysfunction
in connection with liver failure. According to the article, the pathophysiology of hepatic
encephalopathy, there are three major theories regarding the etiology for the impairment of
neurotransmitters however the pathogenesis of hepatic encephalopathy is still unknown. The
three theories are as followed:
1st theory: The Ammonia Hypothesis: This theory is the most popular because of the role
of ammonia in the body. The liver plays an important part of synthesizing urea from ammonia
and then it is synthesized back into glutamine. Ammonia itself arises from the intestinal mucosa
through the action of glutaminase on the amino acid glutamine, by the breakdown of luminal
protein, from the activity of bacteria found in the gut and from the deamination of glutamine in
the kidneys. The theory hypothesizes that due to liver failure, the ability of the liver to
synthesize and detoxify ammonia can lead to hyperammonaemia. Too much ammonia in the
blood can be toxic and can cause an imbalance of the central nervous system. This will cause
enzyme deficiencies and conditions that are very similar to encephalopathy.
2nd theory: The Synergistic Transmission: The GABA/ Benzodiazepine synergistic
transmission theory indicates the GABA is the primary neuroinhibitory transmitter. GABA and
benzodiazepine increase levels in the central nervous system and each shares the receptor in
the brain called the GABA/benzodiazepine complex. In hepatic encephalopathy, the
accumulation of benzodiazepine acts as synergist and has an effect on GABA and causes
3rd theory: The False Neurotransmitter: This theory involves the branched chain amino
acids (BCAA) and the aromatic amino acids (AAA). The impairment of the neurotransmission in
hepatic encephalopathy in this theory occurs when liver failure is present. The BCAA levels
decrease while the AAA levels do the opposite and increase during transport to the brain. The
AAA is false neurotransmitter and is metabolized in what seems to be a neurotransmitter but is
Works Cited:
1. Faint V. The pathophysiology of hepatic encephalopathy. Nursing in Critical Care.
[Required for full credit - One Review article from a Medical Journal that pertains to this
question and has the theories explained. (SEE CALCULATION ASSIGNMENT AND CASE STUDY
GUIDELINES FOR NTR444 in Blackboard for details.)]
Suggested Key search words in PUBMED:
Ammonia Branched-chain amino acids False neurotransmitters GABA/benzodiazipines
Hepatic encephalopathy Precipitating factors
Understanding the Nutrition Therapy
6. (3-points) Outline the nutrition therapy for the following stages of cirrhosis with the
rationale for each:



High complex

No protein
1.0-1.2 g/day

for Ca+,
Zinc,Mg as




2g - Sodium
only if


w/ascites and

small meals
and snacks
High complex

40 kcal/d
caloric needs
due to
affecting poor
PO intake


due to


may be
. Can be
deficient in
may be
. Can be
deficient in


1.8g - Sodium
only if


1.8g - Sodium
restriction due
present and or

Nutrition Assessment

(1-point) For any disease, measurements used to assess nutritional status may be
affected by the disease process and not necessarily be reflective of nutritional status.
What are the components of nutrition assessment that would be affected by cirrhosis?
Because of edema and ascites, dry weight may not be obtainable and electrical
impedance analysis will not be accurate. Many liver labs to determine visceral protein
status will be abnormal due to hepatic dysfunction.

8. (1-point) Dr. Horowitz notes Ms. Wilcox has lost 10 lbs since her last exam. Assess and
interpret Ms. Wilcoxs weight.
Ms. Wilcox has poor intake due to lack of appetite. When ascites and edema happens,
weight loss is common because of early satiety and taste changes occur. These patients
suffer from persistent GI problems and malabsorption of nutrients and vitamins. Nausea
and vomiting, early satiety, anorexia, maldigestion, altered metabolism and restricted
diets all lead to malnutrition. Her appetite is limited, and has been for a while she stated
not having had an appetite for the past couple of weeks. Unfortunately anorexia and poor
appetite is a complication commonly associated with cirrhosis.
9. ( 1-points) Her appetite and intake have been significantly reduced for the past several
days. List t 3 factors that may have contributed to this change in her ability to eat.
1. Ascites
2. Esophageal varices
3. Overall fatigue, weakness, nausea, poor appetite and malaise
10.( 1-points) Examine the patients chemistry values. Which labs support the diagnosis of
cirrhosis? Explain their connection to the diagnosis.
Albumin (2.1

Due to damaged liver, causing a decrease in liver function, synthesis of
albumin is impaired.

Bilirubin (3.7
MCV (102 um3)

Due to liver cellular damage, the liver cells are unable to adequate clear
bilirubin by conversion to its soluble form.
Mean corpuscular volume is representative of large RBC. The high MCV
count is due to malabsorption and/or low intake of B12, leading to
megaloblastic macrocytic anemia.

Nutrition Intervention
11.( 2-points) List at least 4 suggestions you might make to assist with compliance for the
fluid restriction.

Avoid salty foods; stick to the sodium-restricted diet

Moisten mouth with lemon wedges, chewing gum or hard candy
Add lemon juice to ice cubes; helps reduce feelings of thirst
Rinse mouth with water, dont swallow

12.( 2-points) Over the next 6 months, Terris cirrhosis worsens. She is evaluated and found
to be a good candidate for a liver transplant. She is placed on a transplant list and, 20
weeks later, receives a transplant. After the liver transplant, what diet and nutritional
recommendations will the patient need before discharge? For the long term?


Immediate Post-transplant (First 2

120-130% of BEE or measure REE;
increase for weight gain
1.3-2 g/kg/day
30% of kcal or up to 50% with severe
50-70% of kcal


2-4 g/day
1.2-1.7 L
800-1200 mg/day


Supplement to RDA levels; encourage

intake of foods high in Mg and PO4;
supplement or restrict K based on
serum potassium levels


Long-Term Post-transplant
Maintenance 120-130% BEE
depending on activity level
1 g/kg/day
<30% of total kcal or <10% with
severe hyperglycemia
50-70% of kcal; restrict simple
3-4 g/day
1.2 L
1000-1500 mg/day (consider need
for estrogen or Vit D supplements)
Supplement to RDA levels;
encourage intake of foods high in
Mg and PO4; supplement or restrict
K based on serum potassium levels

Write your Nutrition Care Form from the standpoint of an initial nutrition consult upon admission
to the hospital with probable cirrhosis secondary to chronic hepatitis C. (10 points)

Nutrition Care Form

Age: __26___ Gender: ____F____ Height: __59______ Weight: ____125#___
Medical Diagnosis: _Cirrhosis secondary to Hep C_

Consult: _MD Consult with NTR education

Weight History: _loss of 10# over 6 mo___ Ideal Weight: __86__% Ideal Weight: __145+/- 14#___

Activity Level: Sedentary_ Medications: _YAZ 1 tab daily, Allegra 60 mg PO qd, Spironolactone 25
mg qid, Propranolol 40 mg __
Past History: __Hepatitis C dx 3 years ago, seasonal allergies treated with antihistamines__
Lab Values (Date):_ (4/9/2013) Protein 5.4 g/dL, Glucose 115 mg/dL, Bilirubin 3.7 mg/dL, TG 256
mg/dL, RBC 4.1 x 106/mm3, Hgb 10.9 g/dL 9, Ferritin 18 mg/mL
Current Diet Order: __Soft, 4 g Na, High Kcal_ Education Needs: Liver Diet
Energy Needs: _1988-2272 kcal Protein Needs: 91 g/kg Fluid Needs: ___1.5L___
Energy Intake: __N/A_____ Protein Intake: _N/A___ Fluid Intake: N/A
Problem:_Inadequate Energy Intake (NI-1.4), Inadequte protein-energy intake (NI5.3),
Malnutrition (NI-5.2)
Related To: decreased appetite/anorexia and weakness/fatigue, cirrhosis of liver
As Evidence by: 10# weight loss, diet recall___________________
NUTRITION INTERVENTION: _ Modify distribution, type, or amount of food and nutrients within
meals or at specified times (ND-1.2), Multivitamin/Mineral (ND-3.2.1), Recommended
Modifications (E-1.5)_____
Goal: _High Kcal, high biological Value Protein diet to prevent further weight loss, or protein
catabolism. Modify meal pattern to soft mechanical and small, frequent meals that include
complex carbohydrates to limit risk of hypoglycemia. Include a daily multivitamin due to
malnourished state and impaired absorption as related to cirrhosis. Limit fluid to 1.5 L/d and Na
to 2 g/d to decrease risk of ascites. Try to meet 75% of nutritional needs.
NUTRITION MONITORING: _Total Energy Intake (FH-, Meal/Snack Pattern (FH-,
Total Protein (FH-, Sodium (FH-, Weight (AD-1.1.2)__
Goal: Monitor for increase in risk of edema/ascites. Monitor anorexia and poor appetite, intake,
and risk of Protein Energy Malnutrition. Monitor Na intake, Total Protein, glucose, bilirubin, TG,
RBC and Ferritin. If glucose levels do not decrease, recommend medical consult and evaluation.
Depending on TG levels, discuss further nutrition education to decrease TG levels.
RD Signature: __Christina Taalla, RD _ Date: 4/9/2013_