1

Stephanie Ensign

March 7, 2012

Clinical Nutrition

Liver Disease

INTRODUCTION

The liver is one the most important organs in the body. A person cannot survive without a

liver because it is vital for so many important functions in the body (1). These functions include

the metabolization of carbohydrate, protein, and fat, the storage and activation of vitamins and

minerals, the formation and excretion of bile which is then used to digest and absorb fat and fat-

soluble vitamins, the conversion of ammonia to urea, the metabolization of steroids, and the

detoxification of drugs and alcohol. However, a person doesn’t need all of their liver to survive.

In fact, only 10% to 20% of the functioning liver is needed to sustain life (1). However, it is

important that the liver is functioning properly so that it can perform all of the functions it is

supposed to. Therefore, any disease of the liver is concerning and can potentially lead to many

complications and even death.

DISEASE DESCRIPTION

Liver disease is defined as any disease that reduces the function of the liver, and it can be

classified as being either acute or chronic and inherited or acquired (1). There are many different

diseases of the liver, including acute viral hepatitis, fulminant hepatitis, chronic hepatitis, and

many others. Chronic liver disease and cirrhosis is the tenth leading cause of death in the United

States as of 1998, and the number of liver-related deaths from viral hepatitis and hepatic

malignancies have been steadily increasing (2). About one in 679 people in the United States

have either chronic liver disease or cirrhosis, and the number has been steadily climbing (3). It is

important that people understand the adverse effects of alcohol on the liver so that the rates of

liver disease can start to decline.

2

ETIOLOGY

There are many different kinds of liver disease, and they all have different causes. Some

of the general causes of liver failure include different hepatitides, cytomegalovirus, human

herpes virus-6, parvovirus B19, biliary disease (cholelithiasis), alcohol abuse, non-alcoholic fatty

liver disease, autoimmune liver diseases, tumors, and hereditary diseases such as

hemochromatosis, α-antitrypsin deficiency, and Wilson’s disease (1). Hepatitis B, D, and C can

lead to chronic hepatitis, cirrhosis, and eventually liver failure, and they are all transmitted by

blood, body-fluid contact, or vertical transmission (4). Alcohol can cause cirrhosis, which

eventually causes end stage liver disease and complete liver failure, so it is important for alcohol

to either be avoided or consumed in small amounts. The biggest risk factors for liver disease

include the consumption of large amounts of alcohol, predisposing genetics (ability to

metabolize alcohol, increased risk for alcohol abuse, etc.), gender (women), malnutrition,

declining mental health, the elderly, overweight and obesity, and poor social and economic

circumstances (5).

PATHOPHYSIOLOGY AND COURSE OF THE DISEASE

End stage liver disease damages the liver tissue and keeps it from working like it should.

If this damage is not stopped, the liver gradually loses its ability to carry out its normal functions

(1). End stage liver disease can be caused by many different diseases of the liver. Acute viral

hepatitis is widespread inflammation of the liver and is caused by Hepatitis viruses A,B,C,D, and

E. Chronic hepatitis, which is defined as at least a 6-month course of hepatitis and unresolving

hepatic inflammation, can be caused by hepatitis viruses B, C, and D especially (1). Most of the

clinical symptoms for chronic hepatitis are nonspecific and mild, although if it advances far

enough, it can lead to jaundice, muscle wasting, ascites, and hepatic encephalopathy.

3

Nonalcoholic fatty liver disease is a large spectrum of liver disease with 3 stages: simple

fatty liver (steatosis), nonalcoholic steatohepatitis (NASH), and cirrhosis (6). This disease occurs

in individuals who don’t drink alcohol and it is defined as the accumulation of fat (fatty

infiltration) in the liver cells. NASH can lead to fibrosis (scarring of the liver), and then

eventually cirrhosis, which is irreversible, advanced scarring of the liver.

Alcoholic liver disease is the most common liver disease in the US and it is caused by

acetaldehyde which damages the mitochondrial membrane structure and function (1). The three

stages of alcoholic liver disease are hepatic steatosis, alcoholic hepatitis, and cirrhosis. Hepatic

steatosis can lead to increased mobilization of fatty acids from adipose tissue, increased hepatic

synthesis of fatty acids, decreased fatty acid oxidation, increased triglyceride production, and the

trapping of triglycerides in the liver (1). However, it is reversible with the abstinence of alcohol.

If it progresses into alcoholic hepatitis, it can be resolved if alcohol is discontinued but more

often it progress to cirrhosis. Alcoholic hepatitis is characterized by hepatomegaly, a modest

elevation in transaminase levels, increased serum bilirubin concentrations, normal or depressed

serum albumin concentrations, and anemia. The third stage of alcoholic liver disease, cirrhosis, is

much like alcoholic hepatitis except that there is gastrointestinal bleeding in the patient along

with hepatic encephalopathy, portal hypertension, and ascites. Portal hypertension is an elevated

blood pressure in the portal venous system caused by obstruction of blood flow through the liver,

and ascites is the accumulation of fluid in the abdominal cavity (1).

There are many cholestatic liver diseases that result in cirrhosis and end stage liver failure.

Primary biliary cirrhosis is an autoimmune disease that is caused by the progressive destruction

of small and intermediate-size intrahepatic bile ducts. It is immune-mediated by serum

autoantibodies, elevated immunoglobulin levels, circulating immune complexes, and a depressed

4

cell-mediated immune response (1). IgM is enhanced because of the accumulation of endotoxin

and IgA is increased in alcoholic-induced cirrhosis (7). Sclerosing cholangitis is another

cholestatic liver disease and it occurs when there is fibrosing inflammation of segments of

extrahepatic bile ducts (1). Finally there is hepatic osteodystrophy which occurs from vitamin D

and calcium malabsorption and results in secondary hyperparathyroidism and osteomalacia or

rickets (1).

The last important group of liver disease is inherited disorders, which include

hemochromatosis, Wilson’s disease, and α-antitrypsin deficiency. Hemochromatosis is an

inherited disease of iron overload, where people are storing up to 20-40 grams of iron compared

to normal stores of 0.3-0.8 grams (8). It is an autosomal recessive disorder that affects the HFE

gene. There are four main pathophysiologic mechanisms: increased intestinal absorption of

dietary iron, decreased expression of iron-regulatory hormone hepcidin, altered function of HFE

protein, and iron-induced tissue injury and fibrogenesis. In this disease, hepcidin, an iron-

regulatory hormone, plays a role in iron homeostasis by increasing or decreasing iron absorption,

mobilization, and storage so that it can meet the iron requirements of erythropoiesis (8).

Wilson’s disease is also an autosomal recessive disorder, and it affects the secretion of

copper from the bile duct (9). In this disease, copper accumulates in various tissues such as the

liver, brain, cornea, and kidneys, and it results in low serum ceruloplasmin levels and the

presence of Kayser-Fleischer rings (9).

Some complications of liver disease include portal hypertension caused from nodules and

scar tissue compressing the veins in the liver, ascites, hyponatremia which is caused by a

decreased ability to excrete water from sodium restriction and anti-diuretics, glucose alterations

such as insulin resistance in peripheral tissue and decreased availability of glucose from

5

glycogen, fat malabsorption, hepatorenal syndrome which is renal failure associated with severe

liver disease with no intrinsic kidney abnormalities, osteopenia caused by depressed osteoblastic

function and osteoporosis from hemochromatosis, and hepatic encephalopathy which is

characterized by impaired mentation, neuromuscular disturbances, and altered consciousness (1).

In hepatic encephalopathy, ammonia collects in the body as a cerebral toxin, and

neurotransmitters are altered (1).

METHODS OF MEDICAL DIAGNOSIS

The main way that liver disease is diagnosed is through a liver biopsy (10). A biopsy is

safe, simple, and valuable, and it can be used to diagnose cirrhosis, hepatitis, drug reaction,

granulomas, and tumors. If a patient has unexplained hepatomegaly, persistent elevated liver

enzyme levels, suspected primary or metastatic tumor, unexplained jaundice, suspected hepatitis,

or suspected infiltrative diseases, a liver biopsy is performed. This is done by inserting a

specifically designed needle through the abdominal wall and into the liver, and then a piece of

liver tissue is removed for microscopic examination (10).

Lab assessments can also be used to diagnose liver disease. Enzyme assays are used to

measure the release of liver enzymes from the liver (1). Alanine aminotransferase, aspartate

aminotransferase, serum lactic dehydrogenase, and serum globulin are all increased with liver

cell damage. Serum albumin is low if there is a problem with the liver.

Total serum bilirubin is tested to see if there are increased amounts which could indicate

a bilirubin overproduction or a defect in hepatic uptake on conjugation (1). Bilirubin is usually

conjugated in the liver and then is bound to bile and secreted out with the feces (11). In liver

failure, bilirubin can’t find bile to bind to, and so it causes jaundice (1). Serum bile acids reflect

the efficacy of ileal resorption and hepatic extraction of bile acids from portal circulation and

6

they are increased with liver disease. Ammonium is also tested because the liver converts

ammonia to urea, with hepatic failure resulting in increased amounts of ammonia (1).

CURRENT MEDICAL THERAPIES

The goal for providing medical therapies to patients is to prevent further liver damage

and reduce complications (12). Complications are treated with a variety of different therapies.

Bleeding varices are treated with upper endoscopy banding and sclerosis, and a transjugular

intrahepatic portosystemic shunt (TIPS) (13). TIPS is a catheter that is placed through the skin of

the neck into a vein, and is then guided into a vein in the liver using an x-ray (14). The stent

connects the portal vein to one of the hepatic veins and allows for a better flow of blood, and less

pressure on veins in the stomach, esophagus, intestines, and liver. TIPS is effective in 80-90% of

portal hypertension cases, and is much safer than surgery since it requires no cutting or stitches

(14). However, complications include damage to blood vessels, fever, infection, bruising, or

bleeding, blockage in the stent, cutting of the blood vessels of the liver, heart problems, and

infection of the stent (14).

Other treatments include diuretics, fluid and salt restriction, and paracentesis, all of which

are effective when treating ascites (13). Patients whose ascites or edema did not regress after bed

rest and sodium restriction were given a diuretic as well as albumin, and it was found that this

caused patients to be more responsive, to have a decreased hospital stay and a decreased

recurrence of edema, and a lower cumulative probability of developing ascites (15). Other

diseases, such coagulopathy, are treated with blood products or vitamin K. Confusion or

encephalopathy is treated with lactulose medication and antibiotics, and infections are also

treated with antibiotics (13).

7

If liver disease progresses to end-stage liver disease and failure, a liver transplant may be

needed (12). Over 6.000 liver transplants are done a year in the US. Livers can come from either

living or non-living donors, although there is contradictory evidence about whether live donors

should donate part of their liver, since complications including death can arise (16). With living

donors, however, the liver is split into two parts, with one part removed for transplantation. It

then takes about 6 to 8 weeks for the liver to grow back to normal size in the donor and the

recipient. Prognosis is fairly good for liver transplants, with most recipients returning to their

regular lifestyle six months to a year after the transplant, and 75% of patients living five years

after the transplant occurs (12). However, liver disease can recur even in patients who have had

transplants, in which case they would need to receive another transplant (12). There is a chance,

however, that patients will reject their new liver, with liver rejection occurring in 60-70% of

patients (17). If rejection happens, the patient will develop a fever, swelling over the new liver,

flu-like feelings, clay-colored stools, dark, tea-colored urine, and jaundice (17). It’s important for

doctors to keep up with their patients’ liver function blood tests so that they can detect early

signs of rejection and treat it quickly.

APPROPRIATE TOOLS TO USE IN NUTRITION ASSESSMENT

It’s important to take into consideration anthropometric measurements as well as dietary

intake evaluation when doing a nutrition assessment (1). However, the best way to perform a

nutrition assessment is to combine anthropometric measurements and dietary intake evaluation

with the subjective global assessment (SGA) approach. The history of the patient must be looked

at, with weight change, appetite, taste changes and early satiety, dietary recall, and persistent

gastrointestinal problems all taken into account. Weight change is important to take into

consideration because fluctuations in weight resulting from ascites and edema are potentially

8

extremely important when conducting a nutritional assessment. Physical aspects such as muscle

wasting, fat stores, and ascites and edema are essential to be examined as well, along with

existing conditions such as the state of the disease, and the nutritional rating of the patient (1).

The Harris Benedict equation is an appropriate tool to use when calculating energy needs

for a liver disease patient, and a stress factor of 1.2 to 1.4 is usually appropriate, based on dry

weight. However, if the patient has ascites, infection, or malabsorption, a stress factor of 1.5 to

1.75 is more often used. Laboratory tests are another important tool in a nutrition assessment,

and nutritional deficiencies of vitamin D, folic acid, B12, thiamin, and others should be looked at

(1).

MNT

For patients with liver disease and liver failure, medical nutrition therapy is extremely

important because of all of the different metabolic functions the liver performs. Carbohydrates,

fats, and protein are all metabolized in the liver, so it is important that a patient is fed the right

diet so that nutritional inadequacies won’t be a concern. Malnutrition is a very significant

concern in patients who have liver disease, and many patients aren’t eating enough orally

because of nausea, vomiting, drugs, and anorexia (1). There is also a lot of maldigestion going on

because bile isn’t being produced like it should, and steatorrhea and drugs are interfering with

absorption as well. Many patients have early satiety, especially if ascites is a complication, and

so small frequent meals, oral supplements, and enteral feedings are often extremely beneficial (1).

Energy requirements vary among patients, but in general, patients with ascites have

increased energy needs. With end stage liver disease patients who don’t have ascites, 120%-

140% of the REE is usually the recommended amount of energy they should be getting each day.

Carbohydrates needs are difficult to determine because the liver is so involved with metabolism,

9

and so lipids and amino acids are preferred for the patient. Patients should not fast however,

because with fasting their prognosis goes down (1).

Patients are recommended to get 25%-40% of their calories from lipids. Although lipid

metabolism is increased in liver patients, the storage capability of the liver remains the same, so

fat is beneficial to give patients. 0.8 to 1 g/kg of protein should be given to patients with

uncomplicated cirrhosis without encephalopathy, with protein needs increasing with nitrogen

accumulation and stressful situations such as alcoholic hepatitis, sepsis, infection, GI bleeding,

and severe ascites (1).

Vitamins and minerals are recommended because of the liver’s role in vitamin storage.

Providing vitamins and minerals to the patient can help prevent anemia, neuropathy, confusion,

and osteopenia (1). Alcoholic liver disease often results in deficient water soluble vitamins such

as thiamin, B6, B12, folate, and niacin. Iron deficiency is also common because of gastrointestinal

bleeding. However, if the patient has hemochromatosis, hemosiderosis, or cholestatic liver

disease, iron supplementation as well as copper supplementation should not be given (1).

There has been some speculation on whether herbal supplements are useful or not for

patients with liver disease. Complementary and alternative medicine has been growing in

popularity, and although some studies have been done showing potential mechanisms of action

for these and other herbs, caution needs to be taken because of the limited number of clinical

trials done (18). Herbal supplements aren’t recommended unless they have been proven safe to

use and ingest.

For patients with hepatic encephalopathy, it has been tradition for them to be put on

protein restricted diets (1). However, it has been found that 95% of patients have inadequate

protein, and no benefits from protein restriction have been found. It is now recommended that

10

protein isn’t restricted since it causes increased protein catabolism, the release of amino acids

from the muscle, and can potentially worsen hepatic encephalopathy (19). Many doctors are also

giving their patients probiotics and synbiotics because they reduce ammonia as well as

inflammation and oxidative stress (1).

LONG TERM PROGNOSIS

Patients whose liver disease progresses to cirrhosis and end stage liver disease have a

poorer prognosis than patients who don’t develop cirrhosis. Patients with alcoholic fatty liver

disease have about a 20 year shorter life span than the general population, while patients with

non-alcoholic fatty liver only have a 10 year shorter life span than the general population (20).

Patients who receive liver transplants have a better prognosis, with 75% of them living five years

after the transplant (12).

The prognosis is good for patients with alcoholic liver disease who only progress to

hepatic steatosis. If they abstain from drinking alcohol, their liver will recover completely and

they can lead a normal life (1). However, if cirrhosis develops, their prognosis is poor, and a

liver transplant may be the only option (12).

Diseases of the liver are concerning because the liver is vital in performing many

important functions for the body. Therefore, it is extremely important for care to be taken to

prevent liver disease and cirrhosis. Often, poor prognosis is shown when patients with liver

disease don’t abstain from alcohol. It is also important that alcohol be abstained from to prevent

liver disease from occurring if at all possible (20). Although liver disease isn’t always caused by

alcohol, it has been found that alcoholic liver disease often has a poorer prognosis than liver

disease that isn’t caused by alcohol consumption, and so by consuming less alcohol, many

potential liver disease patients may have a better prognosis for life.

11

REFERENCES

(1) Hasse JM, Matarese LE. Medical nutrition therapy for liver, biliary system, and exocrine

pancreas disorders. In: Mahan LK, Escott-Stump S, ed. Krause’s Food and Nutrition

Therapy. 12th ed. Philadelphia: Elsevier; 2008:707-728.

(2) Kim WR, Brown RS, Terrault NA, El-Serag H. Burden of liver disease in the United

States: Summary of a workshop. Mayo Clinic, Rochester, MN, February 2, 2002.

(3) RD. Prevalence and incidence of chronic liver disease. Available at

http://www.rightdiagnosis.com/c/chronic_liver_disease/prevalence.htm. Accessed March

7, 2012.

(4) Lu J, Zhou Y, Lin X, Jiang Y, Tian R, Zhang Y, Wu J, Zhang F, Zhang Y, Wang Y, Bi S.

General epidemiological parameters of viral hepatitis A, B, C, and E in six regions of

China: a cross-sectional study in 2007. PLoS One. 2009;4(12):8467.

(5) International Center for Alcohol Policies. “At-risk” populations. Available at:

http://www.icap.org/PolicyTools/ICAPBlueBook/BlueBookModules/8AtriskPopulations/

tabid/169/Default.aspx. Accessed March 3, 2012.

(6) MedicineNet.com. Fatty liver: Nonalcoholic fatty liver disease (NAFLD) and

nonalcoholic steatohepatits (NASH). Available at:

http://www.medicinenet.com/fatty_liver/article.htm. Accessed March 3, 2012.

(7) Thomas HC. The immune response in hepatic cirrhosis: animal and human studies. Proc

R Soc Med. 1977;70:521-525.

(8) Bacon BR, Britton RS. Hemochromatosis. In: Feldman M, Friedman LS, Brandt LJ, ed.

Sleisenger’s and Fordtran’s Gastrointestinal and Liver Disease. 9th ed. Philadelphia:

Elsevier; 2010:1239-1247.

12

(9) Cox DW, Roberts EA. Wilson disease. In: Feldman M, Friedman LS, Brandt LJ, ed.

Sleisenger’s and Fordtran’s Gastrointestinal and Liver Disease. 9th ed. Philadelphia:

Elsevier; 2010:1249-1257.

(10) Liver biopsy. In: Pagana KD, Pagana TJ, ed. Mosby’s Manual of Diagnostic and

Laboratory Tests. 4th ed. St. Louis, MI: Mosby Elsevier; 2010:776-779.

(11) Judd AM. Lecture slides. Pathophysiology, Brigham Young University, September 20,

2011.

(12) The American Liver Foundation. Liver Transplants. Available at

http://www.liverfoundation.org/abouttheliver/info/transplant/. Accessed February 29,

2012.

(13) PubMed Health. Cirrhosis. Available at

http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001301/. Accessed March 3, 2012.

(14) PubMed Health. Transjugular intraheptaic portosystemic shunt (TIPS). Available at

http://www.ncbi.nlm.nih.gov/ pubmedhealth/PMH0004476/. Accessed March 3, 2012.

(15) Gentilini P, Casini-Raggi V, Di Fiore G, Romanelli RG, Buzzelli G, Pinzani M, La Villa

G, Laffi G. Albumin improves the response to diuretics in patients with cirrhosis and

ascites: results of a randomized, controlled trial. J Hepatol. 1999;30(4):639-645.

(16) Moonka D, Saab S, Trotter J. Living Donor Liver Transplantation. May 7, 2007.

Brochure.

(17) The University Hospital. After the Transplant. Available at

http://www.theuniversityhospital.com /livertransplant

/html/transplantprocess/afterthetransplant.htm. Accessed February 29, 2012.

13

(18) Levy C, Seef LD, Lindor KD. Use of herbal supplements for chronic liver disease. Clin

Castroenterol Hepatol. 2004;2(11):947-56.

(19) Milke GMP. Nutritional support in the treatment of chronic hepatic encephalopathy. Ann

Hepatol. 2011;10(2):45-9.

(20) Dam-Larsen S, Franzmann M, Andersen IB, Christoffersen P, Jensen LF, Sorensen TI,

Becker U, Bendtsen F. Long term prognosis of fatty liver: Risk of chronic liver disease

and death. Gut. 2004;53(5):750-755.

8/24/2012

Liver Function

Martha Ellsworth

Julie Loveland

Stephanie Ensign

Ashlee Whipple

Normal Liver Functions

Physiology

● The liver is able to regenerate itself

● Only 10% to 20% of the functioning liver is needed to sustain life

● Metabolizes carbohydrate, protein, and fat

● Stores and activates vitamins and minerals: all fat-soluble vitamins, B12, Zn, Fe, Cu, Mg

● Forms and excretes bile which is used to digest and absorb fat and fat-soluble vitamins

Physiology

• Converts ammonia to urea

• Metabolizes steroids: inactivates and excretes aldosterone, glucocorticoids, estrogen, progesterone, and testosterone

• Detoxifies drugs and alcohol

• Filter and flood chamber: removes bacteria and debris by action of Kupffer cells

Carbohydrate Metabolism

● Galactose and fructose are converted into glucose in the hepatocyte or liver cell

● The liver stores glucose as glycogen (glycogenesis) and then returns it to the blood when blood glucose levels are low (glycogenolysis)

● Gluconeogenesis from lactic acid, glycogenic amino acids, and intermediates of tricarboxylic acid

Protein Metabolism

● Transamination and oxidative deamination convert amino acids to substrates that are used in energy and glucose production, and in creating nonessential amino acids

● Forms serum proteins: albumin, α-globulin, β-globulin, transferrin, ceruloplasm, lipoproteins

Fat Metabolism

● Fatty acids are converted to acetyl-coenzyme A to produce energy

● Ketone bodies produced

● Synthesizes and hydrolyzes triglycerides, phospholipids, cholesterol, and lipoproteins

Pathophysiology of Different Liver Diseases

● Liver disease can be classified as:

– Acute or chronic

– Inherited or acquired

● Various kinds of liver diseases:

– Acute viral hepatitis

– Fulminant hepatitis

– Chronic hepatitis

– Other liver diseases

• Various kinds of liver diseases:

• Non-alcoholic steatohepatitis (NASH)

• Alcoholic hepatitis

• Cirrhosis

• Cholestatic liver diseases

• Inherited disorders

End Stage Liver Disease (ESLD)

● Liver failure

● Caused by cirrhosis

● Damages the liver tissue and keeps it from working like it should

● If the damage is not stopped, the liver gradually loses its ability to carry out its normal functions

HAV and HEV→ Acute Hepatitis •Vaccine created for prevention

HBV/HDV and HCV→ Chronic Hepatitis→ Cirrhosis→ Liver failure

Type of Hepatitis Virus Transmission

Hepatitis A (HAV) Picornaviridae hepatovirus Fecal-oral routes

Hepatitis B (HBV) Hepadnaviridae orthohepadnavirus

Blood, body-fluid contact, vertical transmission (mother to child)

Hepatitis C (HCV) Flavivuridae hepacivirus Blood, body-fluid contact, vertical transmission (usually asymptomatic)

Hepatitis D (HDV) Deltavirus Depends on HBV for survival and propagation coinfection or superinfection

Hepatitis E (HEV) Hepeviridae hepevirus Fecal-oral routes

Remission- Hepatitis C

● Severity ranging from a mild illness lasting a few weeks to a serious, lifelong illness that attacks the liver

● Often asymptomatic but if symptoms occur they happen in the first 6-7 weeks then usually go away

● Therefore, it doesn’t really go into remission, it just doesn’t show any symptoms until liver problems have already developed.

S/S of Liver disease

• Anorexia

• Fatigue

• Splenomegaly (hepatitis)

• Jaundice

• Ascites and edema

• Hepatic encephalopathy

• Portal hypertension

• Altered amino acid levels

• Vitamin/mineral deficits

• Glucose intolerance or fasting

hypoglycemia

• N/V

• Diarrhea

• Constipation

• Difficulty chewing or

swallowing

• Right upper quadrant

abdominal pain

• Dark urine

External Symptoms and Internal Symptoms of Cirrhosis

Etiology

● Different hepatitides

● Cytomegalovirus

● Human herpes virus-6

● Parvovirus B19

● Biliary disease (cholelithiasis)

● Alcohol abuse

● Non-alcoholic fatty liver disease

• Autoimmune liver diseases

• Tumor

• Hereditary diseases

• Hemochromatosis

• α-antitrypsin deficiency

• Wilson’s disease

Diagnosis - Liver Biopsy

● Safe, simple, valuable

● Used for diagnosis of:

– Cirrhosis, hepatitis, drug reaction, granuloma, tumor

● Used for patients with conditions:

– Unexplained hepatomegaly, persistently elevated liver enzyme levels, suspected primary or metastatic tumor, unexplained jaundice, suspected hepatitis, suspected infiltrative diseases

Lab Assessments

● Enzyme Assays

– Measure the release of liver enzymes

● Other Tests

– Measure liver function

Hepatic Enzymes

● Alanine aminotransferase (ALT)

– In cytosol of hepatocyte

● Found in other body tissues but highest in the liver

– ↑’d with liver cell damage

● Aspartate aminotransferase (AST)

– In cytosol and mitochondria of hepatocyte

● Also in cardiac and skeletal muscle, brain, pancreas, kidney, leukocytes

– ↑’d with liver cell damage

Hepatic Enzymes

• Serum lactic dehydrogenase

• In liver, RBCs, cardiac muscle, kidney

• ↑’s with liver disease

• Lacks sensitivity and specificity because found in most other body tissues

Serum Proteins ● Serum Albumin

• Main export protein made in liver; important in oncotic pressure

• ↓’d synthesis with liver dysfunction

● Can also be a sign of other dysfunctions

● Serum Globulin

• Synthesized in the liver

• ↑’d with chronic liver disease

• Limited diagnostic use in hepatobiliary disease

●Conjugation of Bilirubin ● Heme breaks down from hemeoglobin, myoglobin, and etc. to form

unconjugated bilirubin

● Not soluble in water

● Bound to albumin and goes to the liver

● In liver, bilirubin is conjugated

● Water soluble

● Most is bound to bile and secreted out with the feces

– Gives the stool its dark color

● Reabsorbed bile goes back to the liver

● Some is secreted back into the SI and some is excreted into the urine

– Gives urine its characteristic yellow color

Other Tests ● Total Serum Bilirubin

● If ↑’d may indicate bilirubin overproduction or a defect in hepatic uptake on conjugation

● Indirect Serum Bilirubin

● Unconjugated bilirubin

● ↑’d with excessive bilirubin production (hemolysis), immaturity of enzyme systems, inherited defects, drug effects

● Direct Serum Bilirubin

● Conjugated bilirubin

● ↑’d with depressed bilirubin excretion, hepatobiliary disease, intrahepatic or extrahepatic cholestasis, benign postoperative jaundice and sepsis, and congenital conjugated hyperbilirubinemia

●Other Tests—Cont’d ● Urine Bilirubin

● More sensitive than total serum bilirubin

● Confirms if liver disease is cause by jaundice

● Urine Urobilirubin

● Objective jaundice is expected—rarely used

● Serum Bile Acids

● Reflects efficacy of ileal resorption and hepatic extraction of bile acids from portal circulation

● ↑’d with liver disease

● Has little clinical use

● Ammonium

● Liver converts ammonia to urea

● May ↑ with hepatic failure and portal-systemic shunts

Acute Liver Failure

● Also known as fulminant hepatic failure.

● The liver rapidly loses its ability to function.

● Can develop in a matter of days.

● Complications include excessive bleeding and increasing pressure in the brain.

● S/S: jaundice, pain in the upper right of abdomen, nausea, vomiting, a general sense of not feeling well, difficulty concentrating, disorientation and confusion, and sleepiness.

Acute Viral Hepatitis

•Widespread inflammation of the liver

•Caused by hepatitis viruses A,B,C,D, and E as well as Epstein-Barr virus, cytomegalovirus, herpes simplex, yellow fever, and rubella

Chronic Hepatitis

•To be defined as chronic hepatitis, a patient must have at least a 6-month course of hepatitis or have biochemical and clinical evidence of liver disease with confirmatory biopsy findings of unresolving hepatic inflammation.

•Clinical symptoms are usually nonspecific, occur intermittently, and are mild.

Fulminant Hepatitis

•Severe liver dysfunction is accompanied by hepatic encepholopathy.

–Characterized by impaired mentation, neuromuscular disturbances, and altered consciousness.

Absence of pre-existing liver disease.

Extrahepatic complications:

●Cerebral edema

●Coagulopathy and bleeding

●Cardiovascular abnormalities

●Renal failure

●Pulmonary complications

●Acid-base disturbances

●Electrolyte imbalances

●Sepsis

●Pancreatits

Fulminant Hepatitis

Caused by:

●Viral hepatitis (75% of cases)

●Chemical toxicity

–Acetaminophen

–Drug reactions

–Poisonous mushrooms

–Industrial poisons

Other causes

–Wilson’s disease

–Fatty liver of pregnancy

–Reye’s syndrome

–Hepatic ischemia

–Hepatic vein obstruction

–Disseminated malignancies

Nonalcoholic Fatty Liver Disease (NAFLD)

•Refers to a large spectrum of liver disease.

•3 stages:

–Simple fatty liver (steatosis)

–Nonalcoholic steatohepatitis (NASH)

–Cirrhosis

•The accumulation of fat (fatty infiltration) in the liver cells (hepatocytes).

•Occurs in individuals who don’t drink alcohol.

NASH

● Intermediate stage of NAFLD.

● Defined as the accumulation of fat droplets in the hepatocytes, which are surrounded by acute and chronic inflammatory cells.

● It resembles alcoholic liver disease but isn’t caused by alcohol.

● Occurs most often in people who are overweight or obese.

•Causes:

–Drugs

–Inborn errors of metabolism

–Acquired metabolic disorders

•Type 2 diabetes

•Lipodystrophy

•Jejunal ileal bypass

•Obesity

•Malnutrition

NASH

•Treatments include weight loss and the use of insulin-sensitizing drugs.

Alcoholic Liver Disease

● Most common liver disease in the US.

● Damage to mitochondrial membrane structure and function caused by acetaldehyde.

● 3 stages:

– Hepatic steatosis

– Alcoholic hepatitis

– Cirrhosis

• Predisposing factors: • Genetic polymorphism of alcohol-metabolizing enzymes

• Gender (female)

• Simultaneous exposure to other drugs

• Infections with hepatotropic viruses

• Immunologic factors

• Poor nutrition status

Alcoholic Liver Disease

Alcohol Liver Disease

● Acetaldehyde, a toxic by product of alcohol metabolism, causes damage to mitochondrial membrane structure and function

● Develops in three stages:

● Hepatic steatosis

• ↑ in mobilization of FA from adipose tissue

• ↑ in hepatic synthesis of FA

• ↓ in FA oxidation

• ↑ in TGA production

• Trapping of TGA in liver

• Reversible with abstinence from alcohol

Alcohol Liver Disease- Cont’d

● Alcoholic Hepatitis

● Hepatomegaly

● Modest elevation in transaminase levels

● ↑ serum bilirubin concentrations

● Normal or depressed serum albumin concentrations

● Anemia

● May resolve if with discontinued use of alcohol but usually progresses to third stage

• Alcoholic Cirrhosis

• S/S may be like stage two

• GI bleeding

• Hepatic encephalopathy

• Portal Hypertension (elevated BP in portal venous system caused by obstruction of blood flow through liver)

• Ascites

Alcohol Liver Disease- Cont’d

Cholestatic Liver Diseases

● Primary biliary cirrhosis (PBC): caused by progressive destruction of small and intermediate-size intrahepatic bile ducts.

– Extrahepatic biliary tree and larger intrahepatic ducts are normal

– Slow progressing disease that eventually results in cirrhosis, portal hypertension, liver transplantation, or death

Cholestatic Liver Diseases

• Immune-mediated: serum autoantibodies, elevated immunoglobulin levels, circulating immune complexes, depressed cell-mediated immune response.

• Mild elevation of liver enzymes

• Pruritus and fatigue

• Treatment: ursodeoxycholic acid slow progression • Nutritional complications from cholestatis can occur

including osteopenia, hypercholesterolemia, fat-soluble vitamin deficiencies.

● Sclerosing cholangitis: fibrosing inflammation of segments of extrahepatic bile ducts.

• Hepatic osteodystrophy

• Vitamin D and calcium malabsorption

• Results in secondary hyperparathyroidism and osteomalacia or rickets

• Ursodeoxycholic acid may improve lab values (serum bilirubin, alkaline phosphatase, albumin)

Cholestatic Liver Diseases

Inherited Disorders

● Hemochromatosis

– Inherited disease of iron overload

– Autosomal recessive disorder: HFE gene

– 4 main pathophysiologic mechanisms:

• Increased intestinal absorption of dietary iron

• Decreased expression of iron-regulatory hormone hepcidin

• Altered function of HFE protein

• Iron-induced tissue injury and fibrogenesis

Stores 20-40 g of iron

Normal person stores 0.3-0.8 g

Inherited Disorders ● Wilson’s Disease

– Autosomal recessive disorder: impaired biliary copper excretion

– Copper accumulates in various tissues such as the liver, brain, cornea, and kidneys

– Results in low serum ceruloplasmin levels and the presence of Kayser-Fleischer rings

● α-Antitrypsin

– Glycoprotein

– Inhibits neutrophil proteinases

– Causes cholestasis or cirrhosis

Metabolic Derangement

●Malnutrition

–Common, very significant to prognosis

–Inadequate oral intake – N/V, drugs, anorexia

–Maldigestion – steatorrhea / drugs

–Altered nutrient storage

●Feeding problems

–Early satiety, especially w/ ascites

–Small frequent meals

–Oral supplements/Enteral feedings

–Stay above 0.8 g/kg protein and 30 kcal/kg if malnourished

●Energy requirements

–Varies among patients

–Patients with ascites have ↑ energy needs

–ESLD w/o ascites = 120-140% REE

–150-175% REE if ascites, infection or malabsorption present

–Equates to 25-35 kcal/kg

●Carbohydrates

–Difficult to determine needs; liver is essential in carbohydrate metabolism

–Change in insulin, glucagon, cortisol and epinephrine levels

–Lipids and animo acids preferred for energy

–Patients do not fare well in fasting

●Lipids

–Lipid metabolism ↑

–Storage capability remains the same

–25%-40% of kcal recommended from fats

●Protein

–0.8-1 g/kg protein for uncomplicated cirrhosis w/o encephalopathy

–1.2-1.3 g/kg for nitrogen accumulation

–1.5 g/kg for stress situations (alcoholic hepatitis, sepsis, infection, GI bleeding, severe ascites)

●Vitamins and Minerals

–Required because of the liver's role in vitamin storage

–Prevent anemia, neuropathy, confusion, osteopenia

–Fat-soluble vitamin deficiency

•Treated with water soluble forms

–Alcoholic liver disease deficiency – thiamine, B6, B12, folate, niacin

–GI bleeding – Iron deficiency

•Avoid supplementation w/ hemochromatosis/hemosiderosis

–Cholestatic liver disease – surplus serum copper

●Wilson's disease – ↑ Cu excretion, ↑ Cu in organs, ↓ Serum Cu

–Calcium, Magnesium, Zinc malabsorbed

•RDI level supplement

● Herbal supplements

– Milk thistle – viral hepatitis/alcoholic liver

– Reduces free radicals?

– S-adenosyl-L-methionine (SAMe)

– Methyl donator?

●Diuretic + Albumin

● In a controlled study, patients whose ascites/edema in cirrhosis did not regress after bed rest and sodium restriction were given a diuretic or diuretic + albumin

● Diuretic + albumin

● More responsive

● Decreased Hospital Stay

● Decreased recurrence of edema

● Lower cumulative probability of developing ascites

Complications of Liver Disease

● Portal hypertension

– Nodules and scar tissue compress veins in liver causing high BP

– Increased collateral blood flow, results in varices in GI tract, which can lead to bleeding

– If NPO > 5 days, treated by Parenteral Nutrition

● Ascites

– Fluid retention in the abdominal cavity caused by high pressures forcing fluid out of blood vessels in the liver

– Treated by paracentesis and/or diuretic therapy

● Na+ restriction

– 2 g/day

– Watch protein needs

• Hyponatremia

• Caused by a decreased ability to excrete water from Na+ restriction, anti-diuretics, paracentesis

• Fluid restricted to 1-1.5 L/day

• Glucose alterations

• 66% Cirrhosis patients develop this

• Insulin resistance in peripheral tissue

• Decreased availability of glucose from glycogen

• Fasting hypoglycemia – acute liver disease

• Fat malabsorption

• Decreased bile salt secretion, pancreatic enzyme deficiency.

• Stools are greasy, floating, or light or clay colored • MCT replacement for LCT • Low fat diet may resolve diarrhea

•Hepatorenal syndrome • Renal failure associated with severe liver disease

• No intrinsic kidney abnormalities

• Urine sodium level < 10 mEq/L

• Dialysis required if conservative therapies fail

● Osteopenia

• Hemochromatosis causes depressed osteoblastic function and osteoporosis

• Long term treatment of corticosteriods

• Weight maintenance

• Adequate protein

• 1500 mg calcium

• 400-800 units Vitamin D

Hepatic Encephalopathy

●AKA Portal systemic encephalopathy ●Characterized by impaired mentation, neuromuscular disturbances and altered consciousness ●Multiple causes, multiple theories of etiology

–Ammonia theory –Dietary protein –Altered neurotransmitter theory

Four stages: I. Mild confusion, agitation, irritability, sleep disturbance, decreased attention

II. Lethargy, disorientation, inappropriate behavior, drowsiness

III. Somnolent but arousable, incomprehensible speech, confused, aggressive behavior when awake

IV. Coma

Hepatic Encephalopathy

Hepatic Encephalopathy

●Ammonia theory ●Liver unable to convert ammonia to urea ●Sources of ammonia: protein metabolism, breakdown of bacteria and blood from GI bleeding ●Ammonia collects in body as a cerebral toxin –Ammonia levels in serum and cerebrospinal fluid do not correlate with severity of disease.

–Glutamine and α-ketoglutarate correlate with disease

●Treatments - Lactulose & Neomycin –Lactulose retains ammonium ion in colon by acidifying colonic contents

–Neomycin decreases ammonia production

MNT - Hepatic Encephalopathy

● Tradition – protein restriction ● But, 95% of patients have inadequate protein ● Studies vary as to the effectiveness of BCAA-

enriched formulas. ● Vegetable and Casein proteins

● Higher in BCAAs, lower in AAAs ● Fiber benefit

● Probiotics and synbiotics ● Reduces ammonia, decrease inflammation and oxidative

stress

●Hepatic Encephalopathy

●Dietary Protein? ●Dietary protein → increases ammonia levels → hepatic encephalopathy ●Not proven ●Higher protein intakes correlated with lower blood urea and creatinine levels

●Hepatic Encephalopathy

●Altered Neurotransmitter theory ●In ESLD, Branched-chain AAs ↓, Aromatic AAs↑ ●BCAAs provide 30% of energy when gluconeogenesis and ketogenesis fail. ●Serum BCAAs ↓, Serum AAAs ↑ from muscle proteolysis ●AAAs compete BCAAs for carrier-mediated transport at the Blood-brain barrier.

●MNT - Hepatic Encephalopathy

●Tradition – protein restriction ●But, 95% of patients have inadequate protein ●Studies vary as to the effectiveness of BCAA-enriched formulas. ●Vegetable and Casein proteins ●Higher in BCAAs, lower in AAAs ●Fiber benefit

●Probiotics and synbiotics ●Reduces ammonia, decrease inflammation and oxidative stress

Immune Response to Cirrhosis

•Primary biliary cirrhosis is immune-mediated

–Destruction of small and intermediate-size intrahepatic biles ducts

–Reduced hepatic phagocytosis results in increased antigenic stimulation to the spleen

–Increased immune responses to thymus independent antigens

–Endotoxin is accumulated which enhances IgM responses

–IgA is increased in alcoholic-induced cirrhosis

–Mild elevation of liver enzymes

At Risk Populations for Liver Disease

•Alcohol consumption

•Genetics (ability to metabolize alcohol, increased risk for alcohol abuse, etc.)

•Gender (women)

•General health status (malnourished)

•Mental health

•Age (elderly)

•Social and economic circumstances

Treatments

General

•Goal: prevent further liver damage and reduce complications.

•Maintain a healthy lifestyle

•Limit salt in the diet

•Avoid raw shellfish

•Stop drinking alcohol

Treatments for Complications

•Bleeding varices -- upper endoscopy with banding and sclerosis, transjugular intrahepatic portosystemic shunt (TIPS)

•Excess abdominal fluid (ascites) -- take diuretics, restrict fluid and salt, and remove fluid (paracentesis)

Treatments for Complications

•Coagulopathy -- blood products or vitamin K

•Confusion or encephalopathy -- lactulose medication and antibiotics

•Infections -- antibiotics

•End-stage liver disease and failure– liver transplant

Bleeding Esophogeal Varices

•Swollen veins in walls of the lower part of the esophagus that start to bleed

•Scarring from cirrhosis causes the veins to balloon outward

•Severe bleeding results from rupture

•Evidenced by black, tarry stools, bloody stools, vomiting blood

Treatment- Stop Bleeding

•Directly inject varices with a clotting medicine or place rubber band around bleeding veins using an endoscope

•Give vasoconstriciton medications (octreotide, vasopressin)

•Insert tube into stomach through the nose and inflate with air to create balloon tamponade

•Place patient on ventilator to protect airways and prevent blood from going into lungs if massive bleeding occurs

Complications and Prevention

•Encophalopathy

•Esophageal stricture

•Hypovolemic shock

•Infection (pneumonia, peritonitis)

•Return of bleeding

•Give propranolol or nadolol (beta blockers) to reduce risk of bleeding

•Transjugular intrahepatic portosystemic shunt (TIPS): creates new connections between blood vessels in the liver to decrease vein pressure and prevent future bleeding

TIPS

•When the liver is damaged, blood coming from the esophagus, stomach and intestines to the liver cannot flow very easily, leading to portal hypertension. This can lead to :

–Bleeding from veins in stomach, esophagus, intestines (variceal bleeding)

–Buildup of fluid in abdomen (ascites)

–Buildup of fluid in chest (hydrothorax)

–Clotting in vein carrying blood from liver to heart (Budd-Chiari syndrome)

•Creates new connections between blood vessels in the liver to decrease vein pressure and prevent future bleeding

TIPS Procedure:

-A catheter is placed through the skin of the neck into a vein

-Using x-ray, the catheter is guided into a vein in the liver

-The balloon is blown up to place the stent

-The stent connects the portal vein to one of the hepatic veins

-60-90 minute procedure

-The new pathway allows for better flowing of blood. It eases pressure on veins in the stomach, esophagus, intestines, and liver

TIPS Complications and Prognosis •Damage to blood vessels

•Fever

•Infection, bruising, or bleeding

•Reactions to medicines or the contrast dye

•Stiffness, bruising, or soreness in the neck

•Bleeding in the belly

•Blockage in the stent

•Cutting of the blood vessels of the liver

•Heart problems or abnormal heart rhythms

•Infection of the stent

-Effective in 80-90% of portal hypertension cases

-Safer than surgery; requires no cutting or stitches

Liver Transplant

•Needed when the liver fails from cirrhosis

•Over 6,000 transplants a year in the US

•Transplant surgery takes between four and twelve hours

•Patients remain in hospital up to three weeks after surgery

Transplant Eligibility

•Doctor refers the patient to a transplant center

• Transplant team evaluates the physical health, mental health, ability to pay for expenses, emotional support from family and friends and decides if the person is eligible

•If determined eligible, the name of the patient is added to the national transplant waiting list by the center, with the people in the most critical condition prioritized to be at the top of the list

Liver Availability

•The waiting list has over 16,000 names. The wait differs from person to person, depending on how critical their condition is

•Livers can come from living or non-living donors

•Most donated livers are from people who recently died with healthy livers who agreed to be organ donors, or their families decide after they pass

•The donor’s liver is split into two parts. One part is removed for the transplant. The surgeon then closes the wound with sutures or staples.

•The remaining liver begins to heal and grow new tissue.

• It takes about 6 to 8 weeks for the liver to grow back to normal size in the donor and recipient

Prognosis

•Most return to their regular lifestyle six months to a year after the transplant

•75% of patients are alive five years later

•Sometimes the disease they had before the transplant returns and they may need to receive another transplant

Transplant Rejection

•Rejection occurs in 60-70% of patients

•Signs of rejection

•Fever above 100 degrees

•Swelling or tenderness over the new liver

•Flu-like feelings

•Clay-colored stools

•Dark, tea-colored urine

•Jaundice (yellow skin or eyes - late sign)

Transplant Rejection

- Rejection can happen at any time, so it’s important to keep up with liver function blood tests to detect signs of rejection

- If caught early, it is generally very treatable

Medications

•Initially 10-15 medications one to four times a day

•By one year, two to six a day

•Immunosuppressive medications -- help prevent rejection of the new liver; taken for life

•Nntibiotics/antivirals -- first 3-6 months after surgery when immunosuppression is highest to prevent viral/bacterial infections

•Antacids -- prevent upset stomach

•Antihypertensives -- may be prescribed to lower blood pressure

•Diuretics-- may be needed to remove fluid

Medications

•Multivitamins, calcium, and vitamin D

•Insulin -- occasionally needed to treat diabetes caused by the prednisone or other immunosuppressive medications

•Cholesterol-lowering drugs -- may be started later high cholesterol occurs

•Iron --prescribed in some cases for low blood counts

•Aspirin -- may be prescribed for narrowing or blood clots in blood vessels supplying the liver

Immunosuppressant Drugs and Side Effects

•Azathioprine: side effects – macrocytic anemia, mouth sores, nausea, diarrhea, sore throat

•Antithymocyte globulin: nausea, vomiting

•Basiliximab: None

•Cyclosporine: sodium retention, hyperkalemia, hyperlipidemai, hyperglycemia, hypertension

•Daclizumab: None reported

- Glucocorticoids: sodium retention, hyperglycemia, false hunger, protein wasting

- Muromonab-CD3:nausea, vomiting, anorexia

- Mycophenolate mofetil: nausea, vomiting, anorexia

- Sirolimus: hyperglycemia, hyperlipidemia

- Tacrolimus: hyperglycemia, hyperkalemia, nausea, vomiting

- 15-Deoxysperagualin: GI symptoms

Immunosuppressant Drugs and Side Effects

Case Study

Case Study ● TW

● Age 26

● Female

● Chief complaint: can’t get enough rest, feels week, and is so tired that she can’t go to campus to teach her classes. Her skin looks yellow.

● Hx: Hepatitis C, c/o fatigue, anorexia, N/V, weakness

● Dx: probable cirrhosis secondary to chronic hepatitis C

● Tx plan: YAZ 1 tab po, allegra, CT scan of liver and biopsy, endoscopy, test stool for occult blood, daily I/O, spironolactone 25 mg qid, propranolol 40 mg bid, soft, high-kcal, high-protein diet with small frequent meals, multivitamin/mineral supplement, bed rest

●Nutritional Assessment

● Anthropometric

● Ht 5’9”

● Wt 125 lbs (UBW 136)

● BMI 18.5

● 92% UBW

● 86% IBW

● Biochemical

● Low labs for albumin, total protein, prealbumin, transferrin, HDL-C, RBC, HGB, HCT, ferritin

● High for bilirubin, ALT, AST, alkaline phosphate, CPK, LDH, VLDL, TG, MCV, PT

● Clinical

● Enlarged esophageal veins in the throat

● Bruising on lower arms and legs

● Telangiectasias on chest

● Mild distention RUQ, splenomegaly without hepatomegaly

● Fatigue, anorexia, N/V, weakness

●Nutritional Assessment

● Dietary Assessment

● Patient states that she hasn’t had an appetite for the past few weeks

● Usual dietary intake: sips of water, juice, and Diet Coke only, hasn’t eaten for the past 2 days

● Previous nutrition therapy: 3 years ago: small, frequent meals, plenty of nutrition

● Vit/min intake: 400 mg vitamin E, 600 mg calcium, 400 IU vitamin D, multivitamin/mineral daily, 200 mg milk thistle twice daily, chicory 3 g daily, 500 mg ginger at least twice daily

● Current diet order: soft, 4 gram sodium, high-kcal

●Nutritional Assessment

● Estimated calorie needs:

● Harris Benedict: 1394 kcal

● Stress factor of 1.2-1.4: 1673-1952 kcal

● Protein Needs:

● 1.2-1.3 g/kg: 68-74 g protein

●Nutritional Assessment

● Genetic

● Mother has HTN, diverticulitis, cholecystitis, carpal tunnel syndrome

● Father had diabetes mellitus, peptic ulcer disease

● Maternal grandmother: cholecystitis, bilateral breast cancer

● Maternal grandfather: leukemia

● Paternal grandfather: cirrhosis

● Paternal grandmother: amyotrophic lateral sclerosis

●PES Statement

● Inadequate oral intake related to decreased appetite as evidenced by significant weight loss

● Intervention:

● Soft, high protein, high-kcal foods

●One-day Sample Diet

● Breakfast

● 1 cup Hash browns, frozen potatoes

● 1 cup Milk, fat free (skim)

● 2 medium Pancakes, plain

● 3 tablespoon Syrup

• Dinner

• 1 cup Chili beef soup

• 1 piece Cornbread

• Lunch

• 2 regular slice Bread, 100% whole wheat

• ¾ cup canned green beans

• 3 slices Ham

• 1 tablespoon Light Mayonnaise

• ½ slice (1 oz) Cheese, Cheddar or Colby, low fat

• Snacks

• 1 cup, sauce Applesauce, unsweetened

• 1 medium Banana, raw

• 6 oz yogurt, fruit, light

References

•Bacon BR, Britton RS. Hemochromatosis. In: Feldman M, Friedman LS, Brandt LJ, ed. Sleisenger’s and Fordtran’s Gastrointestinal and Liver Disease. 9th ed. Philadelphia: Elsevier; 2010:1239-1247

•Cox DW, Roberts EA. Wilson disease. In: Feldman M, Friedman LS, Brandt LJ, ed. Sleisenger’s and Fordtran’s Gastrointestinal and Liver Disease. 9th ed. Philadelphia: Elsevier; 2010:1249-1257

•WebMD. Liver failure. Available at: http://www.webmd.com/digestive-disorders/digestive-diseases-liver-failure. Accessed March 3, 2012.

•MedicineNet.com. Liver disease (hepatic disease). Available at: http://www.medicinenet.com/liver_disease/article.htm. Accessed March 3, 2012.

•Mayo Clinic. Nonalcoholic fatty liver disease. Available at: http://www.mayoclinic.com/health/nonalcoholic-fatty-liver-disease/DS00577. Accessed March 3, 2012.

•MedicineNet.com. Fatty liver: Nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatits (NASH). Available at: http://www.medicinenet.com/fatty_liver/article.htm. Accessed March 3, 2012.

•Judd AM. Lecture slides. Pathophysiology, Brigham Young University, September 20, 2011.

•Gentilini P, Casini-Raggi V, Di Fiore G, Romanelli RG, Buzzelli G, Pinzani M, La Villa G, Laffi G. Albumin improves the response to diuretics in patients with cirrhosis and ascites: results of a randomized, controlled trial. J Hepatology. 1999;30(4):639-645.

References

•National Digestive Diseases Information Clearinghouse. Nonalcoholic steatohepatits. Available at: http://digestive.niddk.nih.gov/ddiseases/pubs/nash/. Accessed March 3, 2012.

•Gunter JA, Barton ED. Cirrhosis. Available at: http://www.emedicinehealth.com/cirrhosis/article_em.htm. Accessed March 3, 2012.

•Thomas HC. The immune response in hepatic cirrhosis: animal and human studies. Proc R Soc Med. 1977;70:521-525.

•International Center for Alcohol Policies. “At-risk” populations. Available at: http://www.icap.org/PolicyTools/ICAPBlueBook/BlueBookModules/8AtriskPopulations/tabid/169/Default.aspx. Accessed March 3, 2012.

•Tajiri K, Shimizu Y. Practical guidelines for diagnosis and early management of drug-induced liver injury. World J Gastroenterol. 2008; 14(44): 6774-6785.

•Lu J, Zhou Y, Lin X, Jiang Y, Tian R, Zhang Y, Wu J, Zhang F, Zhang Y, Wang Y, Bi S. General epidemiological parameters of viral hepatitis A, B, C, and E in six regions of China: a cross-sectional study in 2007. PLoS One. 2009; 4(12): e8467.

•Hasse JM, Matarese LE. Medical nutrition therapy for liver, biliary system, and exocrine pancreas disorders. In: Mahan LK, Escott-Stump S, ed. Krause’s Food and Nutrition Therapy. 12th ed. Philadelphia: Elsevier; 2008:707-728.

•Liver biopsy. In: Pagana KD, Pagana TJ, ed. Mosby’s Manual of Diagnostic and Laboratory Tests. 4th ed. St. Louis, MI: Mosby Elsevier; 2010:776-779.

•Hep C Connection. Common Q&A. Available at http://www.hepc-connection.org/default.asp?page=1161. Accessed March 3, 2012.

●References ● The American Liver Foundation. Liver Transplants. Available at http://www.liverfoundation.org/abouttheliver/info/transplant/.

Accessed February 29, 2012.

● The University Hospital. After the Transplant. Available at http://www.theuniversityhospital.com /livertransplant /html/transplantprocess/afterthetransplant.htm. Accessed February 29, 2012.

● PubMed Health. Cirrhosis. Available at http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001301/. Accessed March 3, 2012.

● Medline Plus. Bleeding Esophageal Varies. Available at http://www.nlm.nih.gov/medlineplus/ency/article/000268.htm. Accessed March 3, 2012.

● Garcia-Tsao G, Sanyal AJ, Grace ND, Carey W, Practice Guidelines Committee of the American Association for the Study of Liver Diseases, Practice Parameters Committee of the American College of Gastroenterology. Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis. Hepatology 2007;46(3):922-38.

● PubMed Health. Transjugular intraheptaic portosystemic shunt (TIPS). Available at http://www.ncbi.nlm.nih.gov/ pubmedhealth/PMH0004476/. Accessed March 3, 2012.

● Moonka D, Saab S, Trotter J. Living Donor Liver Transplantation. May 7, 2007. Brochure.

● United States Department of Veterans Affairs. Hepatitis C Complications/Medications. Available at http://www.hepatitis.va.gov/patient/complications/transplant-complications.asp. Accessed March 3, 2012.

Find a dietitian near you by visiting

EATRIGHT.ORG

• Eat small, frequent meals

• Take oral liquid

supplements as needed

• Consume 0.8 g/kg of

protein

• Consume 30 kcal/kg

• Restrict sodium to manage

fluid retention

• Control carbohydrate

intake for hyperglycemia

NUTRITION TIPS

Nutritional Guidelines

Managing

LIVER DISEASE

For more info visit:

www.liverfoundation.org

www.liver.org

● Breakfast

● 1 cup Hash browns, frozen

potatoes

● 1 cup Milk, fat free (skim)

● 2 medium Pancakes, plain

● 3 tablespoon Syrup

• Lunch

• 2 regular slice Bread, 100%

whole wheat

• ¾ cup canned green beans

• 3 slices Ham

• 1 tablespoon Light

Mayonnaise

• ½ slice (1 oz) Cheese, Cheddar

or Colby, low fat

• Dinner

• 1 cup Chili beef soup

• 1 piece Cornbread

• Snacks

• 1 cup, sauce Applesauce,

unsweetened

• 1 medium Banana, raw

• 6 oz yogurt, fruit, light Liver

Liver disease can be classified as:

-Acute or chronic

-Inherited or acquired

Various kinds of liver diseases:

-Acute viral hepatis

-Fulminant hepatitis

-Chronic hepatitis

-Other liver diseases

-Non-alcoholic steatohepatitis

-Alcoholic hepatitis

-Cirrhosis (scarring of tissue)

-Cholestatic liver diseases

• Inherited

● The liver is able to regenerate

itself

● Only 10% to 20% of the

functioning liver is needed to

sustain life

● Metabolizes carbohydrate,

protein, and fat

● Stores and activates vitamins

and minerals: all fat-soluble

vitamins, B12, Zn, Fe, Cu, Mg

DISORDERS OF THE

LIVER

SAMPLE ONE DAY DIET

THE AMAZING LIVER