HepaticPancreaticBiliary_2012
August 3, 2012
LIVER DISEASE PACKET
Name: Birgit Humpert
PLEASE ANSWER ALL QUESTIONS IN YOUR OWN WORDS.
A.) MEDICAL TERMINOLOGY
1. Break the following words up into their prefix, root and suffix and then provide the meaning
of the word. Not all words will have all three parts.
MEDICAL TERM
PREFIX &
MEANING
ROOT & MEANING
SUFFIX &
MEANING
Hepat - liver
ic – pertaining to
Cholestasis
chol/e - bile
stasis - stopping
Cholecystitis
cholecysto/o gallbladder
lith/o - stone
itis inflammation
iasis - condition
Hepatomegaly
hepat/o - liver
Hepatitis
hepat/o - liver
megalyenlargement
itis inflammation
Ex: Hepatic
Cholelithiasis
-
chol/e - bile
MEANING OF
MEDICAL TERM
Pertaining to the
Liver
bile flow is
stopped
inflammation of
the gallbladder
stones in the
gallbladder
enlarged liver
inflammation of
the liver
B.) LIVER DISEASES AND CONDITIONS:
PLEASE ANSWER ALL SECTIONS USING YOUR OWN WORDS.
For each of the following you are given the definition and etiology. You should provide the
pathophysiology of disease process and progression; disease impact on nutrition status; and
dietary recommendations when needed:
a. Definition
b. Etiology
c. Describe the physical changes specific to the disease process and progression (pathogenesis).
d. Explain how the disease impacts the patient’s nutritional status (in some cases there will be
no impact.)
e. Is a modified diet recommended for this condition? If so what is the diet prescription?
1.
Jaundice
a. Definition: the green-yellow staining of tissues by bilirubin, one of the most characteristic signs
of liver disease.
b. Etiology: Jaundice may result from dysfunction anywhere along the following pathophysiologic
mechanism of bilirubin metabolism:
1) Damaged or aged red cells lyse, releasing the oxygen-carrying hemoglobin molecule;
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2) Hemoglobin molecules are taken up by the reticuloendothelial system which separates heme
from globin;
3) Heme oxygenase opens the heme ring to release the central iron atom, yielding biliverdin,
which is converted to bilirubin;
4) Bilirubin is released into the plasma and transported to the liver, tightly bound to the plasma
protein albumin;
5) Free unconjugated bilirubin is lipid soluble and can be displaced from albumin by fatty acids
and some organic anions (sulfonamides, salicylates);
6) Liver cells extract unconjugated bilirubin from the plasma with special transport proteins;
7) In the cytosol, bililrubin is quickly bound (conjugated) to water-soluble derivatives of
glucuronic acid by the action of the enzyme uridine disphosphate glucuronosyltransferase
(UDPGT) located in the endoplasmic reticulum. This process yields water-soluble bilirubin
which is then actively excreted into microscopic bile ducts;
8) Bilirubin is then transported through the biliary system as a component of bile to the small
intestine where it cannot be absorbed, so it passes to the colon where bacterial enzymes break
it down to urobilinogen;
9) A small fraction of urobilinogen is absorbed from the colon and re-excreted by the kidneys
and the liver.
Classically divided into pre-hepatic, hepatic, and post-hepatic or cholestatic, but there is overlap:
Pre-hepatic – most common causes are hemolysis and ineffective erythropoiesis. The resorption
of hematomas in patients with mild liver disease is a common cause of mild jaundice due to
unconjugated hyperbilirubinemia.
Hepatic – Dysfunction of each of the hepatic steps in bilirubin metabolism (see bilirubin
metabolilsm above) may result in jaundice; genetic disorders of UDPGT synthesis; most liver
diseases such as viral hepatitis, alcoholic liver disease, and autoimmune hepatitis, result in
jaundice because dysfunction within the lever cell results in elevated levels of conjugated
bilirubin.
Post-hepatic – rare congenital disorders called Dubin-Johnson and Rotor syndromes; many drugs
such as the phenothiazines and sex hormones; in susceptible women, the sex hormone levels of
normal pregnancy can cause benign cholestasis of pregnancy; mechanical obstruction to the bile
ducts from obstructing tumors, strictures, or gallstones is the most common cause of cholestatic
jaundice.
c. Pathogenesis:
Jaundice is a symptome of an underlying disease. An increase in bilirubin in the blood leads to a
yellow color of the skin and also the whites of the eyes. The skin may be itching. Excess bilirubin
is also excretes into the urin, leading to a dark color. The stool is light colored. Other symptoms
depend on the underlying disease.
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Jaundice can also occur in newborns. It can have different causes, some of them related to
nutrition. In some breastfeeding infants it develops in the first week. Dehydration and low calorie
intake can increase enterohepatic circulation. It can also occur after the first week caused by an
increased concentration of beta-glucuronidase in breast milk which increases deconjugation and
reabsorption.
d. Nutrition risks r/t disease process: Depends on the underlying disease process.
e. MNT: Depends on the underlying disease process. See MNT for hepatitis, cirrhosis, and
pancreatitis.
Jaundice in infants that is either physiological or has it's cause in breastfeeding can be reduced by
frequent feeding with either formula or breast milk. This leads to increased motility in the GI tract
and more frequent stools so that enterohepatic circulation of bilirubin is decreased.
References:
Nelms, M., Sucher, K.P., Lacey, K., Roth, S.L. (2011). Nutrition Therapy &
Pathophysiology (2nd ed.). Belmont, CA: Wadsworth
Escott-Stump, S. (2011). Nutrition and Diagnostic Related Care (7th ed.). Lippincott
Williams & Wilkins
Neonatal hyperbilirubinemia. (2009).The Merck Manual Home Health Handbook
for Health Care Professionals. Available at
http://www.merckmanuals.com/professional/pediatrics/metabolic_electrolyte_and_toxic_disorders
_in_neonates/neonatal_hyperbilirubinemia.html
Jaundice (2009). The Merck Manual Home Health Handbook
for Health Care Professionals. Available at
http://www.merckmanuals.com/professional/hepatic_and_biliary_disorders/approach_to_the_
patient_with_liver_disease/jaundice.html?qt=jaundice&alt=sh
2.
Cirrhosis
a. Definition: Chronic degenerative, irreversible disease of the liver in which the lobes are covered
with fibrous tissues, the parachyma degenerates, and the lobules are infiltrated with fat.
b. Etiology:
1) Most commonly the result of chronic alcohol abuse and sometimes nutritional deprivation,
severe acute hepatitis, chronic hepatitis, toxic hepatitis, and metal storage diseases;
2) Biliary cirrhosis – initiated by damage to the bile ducts, which may be due to macroscopic or
microscopic biliary obstruction;
3) Examples of large-duct obstruction include:
a. gallstone disease;
b. primary sclerosing cholangitis;
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c. chronic biliary fluke infestation (endemic in Asia, acquired by eating raw fish that carry
larval cyste forms; in all sheep- and cattle-producing areas of the world, humans are
infected as accidental hosts; it is also acquired by eating fecally contaminated watercress
and other aquatic plants that harbor the immature cysts).
4) Primary sclerosing cholangitis – autoimmune condition generally seen in patients with
ulcerative colitis (80% of PCS patients have coexistent ulcerative colitis; whereas 3-5% of
ulcerative colitis patients develop PCS).
c. Pathophysiology:
Scar tissue is formed throughout the liver that inhibits the normal functions of the liver, It can
block blood flow to the portal vein and can block the flow of bile. Cirrhosis can lead to serious
complications like encephalopathy and portal hypertension. Portal hypertension can lead to ascitis
and bleeding in the GI tract from varices. Reduced production of bile in the liver can lead to
steatorrhea and malabsorption. Patients with cirrhosis can develop hepatorenal syndrome with
renal failure.
There are no symptoms when the disease first develops. With disease progression patients will
experience anorexia, fatigue, nausea, malaise, and weight loss. If bile flow is blocked jaundice
with itching of the skin, dark urine and light-colored stool can be present. It comes to steatorrhea.
The tips of fingers become enlarged (clubbing). The patient might have abdominal pain and
bloating.
d. Nutrition risks r/t disease process: In general patients with cirrhosis have an increased energy
expenditure, but often patients are unable to consume enough due to the disease process. This
imbalance leads to malnutrition, muscle wasting, and weight loss.
Anorexia, fatigue, nausea, bloating, feeling of weakness and malaise can lead to decreased food
intake and weigh loss. Ascitis can decrease stomach capacity which can lead to early satiety.
Contributing to early satiety are imbalances in blood glucose with glucose intolerance, insulin
resistance and high glucagon levels. Many patients with cirrhosis have diabetes. Steatorrhea can
lead to fat malabsorption and malabsorption of fat-soluble vitamins. If alcohol consumption is the
underlying reason this can further impair nutritional status because alcohol can replace other
nutrients in the diet and it can interfere with the metabolism of macro- and micronutrients.
Because glycogen stores in the liver tend to be depleted earlier the body uses fat more readily.
e. MNT: Depends on underlying cause, complication, and progression of the disease.
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Patients should not consume alcohol.
The diet should be high in energy (35 -40 kcal/kg) with a high intake of protein (1 - 1.6 g/kg).
Vegetable protein, dairy and in some cases supplementation of BCAA to prevent or treat
encephalopathy. 50 % energy should come from carbohydrates to spare fat and protein, less than
30 % of energy from fat, if signs of steatorrhea and fat-malabsoption. Small, frequent meals can
help improve intake, with carbohydrates spread out over the day especially for patients with
diabetes.
If ascitis sodium is restricted to 2000 mg and fluid to 1 - 2 l per day.
With varices soft food is recommended that does not irritate the esophagus, and additional fiber
and prune juice can help to avoid constipation and straining.
Micronutrients are supplemented according to individual needs. This can be based on nutritional
assessment and biochemical information. Vitamins that are often supplemented in alcoholics are
vitamin B1, B2, B6, B12, folic acid, vitamin C, vitamin E, magnesium, selenium, and zink.
Vitamin A, D and iron are supplemented if there is a clear deficiency, they can harm the liver in
large amounts. If they are not supplemented individually a multiple water-soluble vitamin with
twice the Recommened Dietary Allowance is given.
References:
Nelms, M., Sucher, K.P., Lacey, K., Roth, S.L. (2011). Nutrition Therapy &
Pathophysiology (2nd ed.). Belmont, CA: Wadsworth
Escott-Stump, S. (2011). Nutrition and Diagnostic Related Care (7th ed.). Lippincott
Williams & Wilkins
3.
Ascites
a. Definition: Pathological fluid in the peritoneal cavity; occurs in patients with advanced liver
disease complicated by portal hypertension and hypoalbuminemia.
b. Etiology:
1)
2)
3)
4)
Low serum proteins and sodium retention contribute in cases of liver failure;
Portal hypertension;
May result from fluid loss from cells because of osmolar or nutrient imbalances;
Other causes include malignancy, infection, pancreatitis, hypopthyroidism, vasculitis,
nephrosis, cardiac failure, constrictive pericarditis.
c. Pathophysiology:
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Portal hypertension, low osmotic pressure due to the inability of the liver to make adequate
amounts of protein, and an increase in sodium retention lead to accumulation of fluid in the
peritoneal cavity. Symptoms depend on the amount of fluid that accumulates. If large amount of
fluid are present the abdomen becomes distended and weight and abdominal circumference
increase.
d. Nutrition risks r/t disease process: The fluid can put pressure on the stomach and decrease the
capacity of the stomach to extend. Patients might only be able to tolerate small meals.
e. MNT: To manage ascites sodium restriction to 2000 mg and fluid restriction to 1 -2 l per day are
usually recommended. Other recommendations depend on the underlying disease and the
treatment. If paracentesis is used to remove fluid the patient also loses a lot of protein. Protein
requirements can be as high as 1.5 g/kg, energy needs can increase to 1.5 times the normal need.
Due to fluid accumulation weight can not be used to assess nutritional status
References:
Nelms, M., Sucher, K.P., Lacey, K., Roth, S.L. (2011). Nutrition Therapy &
Pathophysiology (2nd ed.). Belmont, CA: Wadsworth
Escott-Stump, S. (2011). Nutrition and Diagnostic Related Care (7th ed.). Lippincott
Williams & Wilkins
4.
Fatty Liver
a. Definition: An accumulation of triglycerides in the liver.
b. Etiology:
1) Caused by more fat being delivered to the hepatocyte than it can normally metabolize or by a
defect in fat metabolism within the cell;
2) Obesity, diabetes, excessive alcohol consumption, protein malnutrition; TPN; IV
administration of drugs such as tetracycline and corticosteroids, and exposure to toxic
substances such a carbon tetrachloride and yellow phosphorus.
c. Pathophysiology:
When the body metabolizes alcohol fatty acid oxidation and lipoprotein production decrease and
less fat is removed from the liver. There is also more fat coming into the liver because of
hyperlipidemia due to peripheral lipolysis and triglyceride synthesis. Lipid peroxidative damage to
cell membrans results in inflammation and later fibrosis. Fatty liver does not produce a lot of
symptoms at first. Patients might feel tired and sick, and have pain. The liver becomes enlarged.
With advanced fatty liver the patient can develop jaundice. Fatty liver can lead to alcoholic
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hepatitis, cirrhosis, and portal hypertension.
d. Nutrition risks r/t disease process: As long as no symptoms occur there are no immediate
consequences for the nutritional status from fatty liver itself. Nutritional status is more determined
by underlying causes like alcoholism, obesity, diabetes, cystic fibrosis et al.
e. MNT: Depends on the underlying cause. If fatty liver is caused by alcohol and alcohol is not
consumed anymore than fatty liver is reversible.
References:
Nelms, M., Sucher, K.P., Lacey, K., Roth, S.L. (2011). Nutrition Therapy &
Pathophysiology (2nd ed.). Belmont, CA: Wadsworth
Fatty liver (2009), The Merck Manual Home Health Handbook
for Health Care Professionals. Available at
http://www.merckmanuals.com/professional/hepatic_and_biliary_disorders/approach_to_the_
patient_with_liver_disease/fatty_liver.html?qt=fatty%20liver&alt=sh
5.
Clotting Issues (Vitamin K)
a. Definition: Prolonged clotting time caused by a vitamin K deficiency.
b. Etiology:
1) Decreased absorption of plant form due to a lack of the fat-digesting enzymes r/t decreased
pancreatic enzyme output;
2) Also occurs because alcohol-damaged intestinal bacteria are less able to synthesize the vitamin
that is usually produced in the large intestine.
c. Pathophysiology:
Multible factors put patients with liver disease and especially those with alcohol abuse at a greater
risk for vitamin K deficiency.
- Due to damage to the liver it comes to fat-malabsorption and also to malabsorption of fat-soluble
vitamin K.
- Alcohol can damage the intestinal mucosa leading to a decreased production of vitamin K by
intestinal bacteria.
- The liver as a primary storage site is compromised.
In the coagulation cascade seven clotting factors are vitamin K-dependent. With insufficient
intake and intestinal production, blood coagulation is compromised and it comes to bleeding.
Patients bruise easily, have nose bleeds, GI bleeding and hematuria.
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d. Nutrition risks r/t disease process: Alcohol abuse and liver damage lead to vitamin K deficiency.
Bleeding of the intestinal tract can make anorexia and malnutrition worse.
e. MNT: Vitamin K is given by mouth or subcutaneous.
References:
Vitamin K (2007) The Merck Manual for Health Care Professionals. Available at
http://www.merckmanuals.com/professional/nutritional_disorders/vitamin_deficiency_
dependency_and_toxicity/vitamin_k.html?qt=vitamin%20k&alt=sh
6.
Portal Hypertension
a. Definition: increased venous pressure in the portal circulation.
b. Etiology:
1) Caused by compression or occlusion in the portal or hepatic vascular system;
2) Sluggish blood flow through the liver results in increased pressure in the portal circulation;
3) Venous drainage of much of the GI tract is congested.
c. Pathophysiology:
Portal hypertension is often a complication of cirrhosis. The blood pressure in the portal vein is
higher than in the hepatic vein due to decreased blood flow in the liver. Normally pressure in the
portal vein is 4 to 5 mm Hg higher than in the hepatic veins. Is the difference (portal venous
gradient) higher than 5 mm Hg, this is called portal hypertension. Portal hypertension leads to
serious complications. Signs and symptoms of portal hypertension result from these
complications.
- increased pressure leads to dilation of blood vessels in the esophagus. This engorged vessels can
rupture and bleed.
- increased pressure can lead to the development of rectal varices that can also bleed
- ascites is the accumulation of fluid in the peritoneal cavity. This leads to a distended abdomen,
weight gain, abdominal pressure and possible dyspnea.
- it also comes to portal hypertensive gastropathy with changes in the stomach mucosa that can
also lead to bleeding
- because toxic substances reach the liver more slowly or not at all and are redirected into the
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normal circulation portal hypertension also contributes to encephalopathy. This leads to changes
in mental status in the patient.
d. Nutrition risks r/t disease process: The complications of portal hypertension can lead to nutritional
consequences. There is usually an increased energy and protein need due to the underlying
cirrhosis. Varices and bleeding in the gastrointestinal tract as well as the underlying liver disease
can lead to anorexia and weight loss. Ascitis can decrease stomach capacity which can lead to
early satiety.
e. MNT: If ascitis sodium is restricted to 2000 mg and fluid to 1 - 2 l per day.
With varices soft food is recommended that does not irritate the esophagus, and additional fiber
and prune juice can help to avoid constipation and straining.
References:
Nelms, M., Sucher, K.P., Lacey, K., Roth, S.L. (2011). Nutrition Therapy & Pathophysiology (2nd
ed.). Belmont, CA: Wadsworth
Portal Hypertension (2009), The Merck Manual Home Health Handbook
for Health Care Professionals. Available at
http://www.merckmanuals.com/professional/hepatic_and_biliary_disorders/approach_to_the_
patient_with_liver_disease/portal_hypertension.html
7.
Hepatic Encephalopathy
a. Definition: Neuropsychiatric syndrome characterized by symptoms ranging from mild confusion
and lethargy with altered personality to stupor and coma. Some patients exhibit dementia and
psychotic symptoms.
b. Etiology:
1) Associated with fulminant hepatic failure or severe chronic liver disease, conditions in which
liver function is severely depressed and blood is shunted around the liver;
2) The exact cause is unclear; altered or false neurotransmitters, toxic short-chain fatty acids, and
altered plasma ratios of aromatic amino acids (AAA) to branched-chain amino acids (BCAA)
remain under investigation.
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c. Pathophysiology:
Different theories exist for the development of encelopathy.
- It could either be caused by increased ammonia levels which are toxic to the brain. Ammonia is
usually detoxified in the liver and converted to urea or used for the production of glutamine. With
decreased hepatic function less ammonia can be detoxified. Ammonia is also used to convert
glutamate to glutamine in the muscle and the liver. A decreased ability of the liver to detoxify
combined with muscle wasting that results in decreased use of ammonia plus portal hypertension
result in increased levels of ammonia in the blood and the brain. But not all patients with
encephalopathy have increased ammonia levels.
- According to the synergistic neurotoxin/GABA hypothesis neurotoxins like mercaptans,
ammonia, tyramine, ooctopamine, and gamma-aminobutyric acid (GABA) are produced in the
intestines and and cross the blood-brain barrier. When GABA binds to its receptor this leads to an
increase in chloride ions in neurons, making the neuron less likely to generate an action potential.
An increased level of GABA and other substances could be involved in encephalopathy. The
GABA receptor can also bind with neurosteroids. An increased production of neurosteroids could
also play a role.
- Another theory is the falso neurotransmitter hypothesis. According to this theory an imbalance
of branched-chain amino acids (BCAA) and aromatic amino acids (AAA) is causing hepatic
encephalopathy. An increased level of ammonia leads to an increased glucagon stimulation.
Increased glucagon decreases blood glucose levels. With decreased blood glucose levels more
insulin is produced leading to an uptake of BCAA into the muscles. More AAA remain in the
blood and cross the blood-brain barrier. They are precursors for neurotansmitters and if there are
more than usual in the brain the neurotransmitter balance is altered. For example there is more
serotonine from tryptophan, false neurotransmitters like octopamin from tyrosine and a decrease
in DOPA production that can also lead to more false neurotransmitter.
Hepatic encephalopathy leads to changes in mental status, personality and neuromuscular
function. It is progressing from less severe changes like shortened attention span, euphoria,
anxiety, apathy, lethargy, personality changes, lack of awareness to more severe changes like
severe disorientation, stupor, and coma. Typical for neuromuscular changes is asterixis, small
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flapping movements of the fingers.
d. Nutrition risks r/t disease process: On top of the nutritional consequences of the underlying liver
disease, encephalopathy can lead to poor nutritional intake, poor food choices and inability to
prepare and consume food because of the changed mental status of the patient.
e. MNT: In general the diet for cirrhosis is high in calories and protein because these patients are in a
state of metabolic stress. Because the exact pathophysiology is not determined the nutrition
recommendations for patients with encephalopathy vary.
In severe encephalopathy a protein restriction was sometimes prescribed but this is usually not
done anymore because it can effect the overall nutritional status. In acute encephalopathy the
American College of Gastroenterology recommends NPO for one to two days. A short-term
protein restriction is usually followed by a gradual increase up to the recommended level.
Tolerance for higher amounts of protein in the diet is achieved by giving lactulose and antibiotics.
Lactulose can lead to nausea, vomiting, and diarrhea and can make adequate food intake difficult.
A higher intake of BCAA can be achieved by giving a vegetable based diet with dairy. BCAA
can be supplemented and there are also special enteral formulas with BCAA, but they are
expensive and use is still debated.
References: Nelms, M., Sucher, K.P., Lacey, K., Roth, S.L. (2011). Nutrition Therapy &
Pathophysiology (2nd ed.). Belmont, CA: Wadsworth
Escott-Stump, S. (2011). Nutrition and Diagnostic Related Care (7th ed.). Lippincott
Williams & Wilkins
Blei, T.B., Co´rdoba, J. and The Practice Parameters Committee of the American College of
Gastroenterology (2001). Practice Guidelines Hepatic Encephalopathy. American Journal of
Gastroenterology Vol. 96, No. 7, 2001, available from
http://webdev.med.upenn.edu/contribute/gastro/documents/ACGguidelinesforHE.pdf
8.
Wernicke’s Encephalopathy
a. Definition: Inflammatory, hemorrhagic, degenerative condition of the brain.
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b. Etiology: Thiamine deficiency, usually associated with chronic alcoholism.
c. Pathophysiology:
Decreased intake and absorption of thiamine as well as decreased conversion into its active form
may all contribute to the deficiency. The patient experiences confusion, abnormal eye movements
(nystagmus), loss of muscle coordination and unusual gait (ataxia).
d. Nutrition risks r/t disease process: Alcoholism can lead to thiamine deficiency.
e. MNT: Thiamine administration either by mouth or intravenous. To prevent Wernicke's
encephalopathy it is recommended that alcoholics take a multivitamin of water-soluble vitamins at
twice the RDA.
References: Nelms, M., Sucher, K.P., Lacey, K., Roth, S.L. (2011). Nutrition Therapy &
Pathophysiology (2nd ed.). Belmont, CA: Wadsworth
9.
Viral forms of Hepatitis
Note that acute and chronic hepatitis differ.
Acute: Acute viral hepatitis is inflammation of the liver parenchyma.
Chronic: Encompasses a group of diseases characterized by inflammation of the liver that
lasts 6 months or longer.
I am giving you the definition and etiology, please give me the pathophysiology.
Hepatitis A – Vaccine IS available
a. Definition: Liver inflammation caused by the hepatitis A virus. Acute.
b. Etiology: The virus may be spread through fecally contaminated food or water.
c. Pathophysiology: Hepatitis A can sometimes presents without symptoms and can go
unrecognized. Other times it presents with typical symptoms for hepatitis. This means after an
incubation period the patient feels ill with anorexia, fever, malaise, nausea, vomiting and pain in
the liver region. After that jaundice develops with dark urine, hepatomegaly, and splenomegaly.
Most patients feel better after the first week and recovers fully within 8 weeks. Sometimes
Hepatitis A can last up to 6 month but it does not lead to chronic hepatitis and patients don't
become carriers of the virus. Liver failure is rare.
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Hepatitis B – Vaccine IS available
a. Definition: Inflammatory liver disease caused by the Hepatitis B virus.
b. Etiology:
1) Hepatitis B virus, usually transmitted through blood and other bodily fluids by sexual contact
with an infected person, or by the use of contaminated needles and instruments.
2) Increasingly common as a sexually transmitted disease
3) Other risk factors include working in a healthcare setting, transfusion and dialysis,
acupuncture, tattooing, extended overseas travel, and residence in an institution.
c. Pathophysiology: Hepatitis B is more serious than hepatitis A and can be fatal. Disease
progression can be mild or severe. 30 % of patients develop no symptoms. As with hepatitis A
there is an incubation period after which the patient usually feels ill with anorexia, fever, malaise,
nausea, vomiting and pain in the liver region. After that the jaundice develops with dark urine,
hepatomegaly, and splenomegaly. Patients also sometimes have itchy red hives and joint pain. 5 7 % of cases progress into chronic hepatitis, this number is higher for children. 15 - 20 % develop
cirrhosis and liver cancer.
Hepatitis C – There is NO vaccine for HCV
a. Definition: Inflammatory liver disease caused by Hepatitis C virus.
b. Etiology:
1) Hepatitis C virus is most commonly transmitted by bood transfusion or percutaneous
inoculation, less commonly by sexual intercourse
c. Pathophysiology: The progression of hepatitis C can sometimes be unpredictable. Patients often
don't have symptoms until liver damage occurs. It can also present with typical symptoms like
anorexia, fever, malaise, nausea, vomiting, pain in the liver region, jaundice, dark urine,
hepatomegaly, and splenomegaly. Live function might not return to normal for month or years. If
hepatitis lasts longer than 6 month it is called chronic. The damage to the liver that leads to
chronic hepatitis is probably caused by the immune reaction to the virus. Chronic hepatitis can be
asymptomatic or can have some of the same symptoms as acute hepatitis, like malaise, anorexia,
fatigue. 75 - 85 % of hepatitis C cases become chronic. 60 - 70 % develop liver disease and 5 - 20
% cirrhosis. Hepatitis C is the main cause for liver transplantation.
Hepatitis D
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a. Definition: Form of hepatitis that occurs only in patients co-infected with hepatitis
B virus.
b. Etiology:
1) Hepatitus D virus relies on HBV replication and cannot replicate independently;
2) Transmitted through blood, sexually and through needle sharing.
c. Pathogenesis: If hepatitis D occurs together with hepatitis B the disease is usually more severe.
Hepatitis E
a. Definition: Self-limited type of hepatitis acquired by ingestion of fecally contaminated water or
food.
b. Etiology: Self-limited type of hepatitis acquired by ingestion of fecally contaminated
water or food.
c. Pathophysiology: Hepatitis E can have severe symptoms. Additional to the typical symptoms of
anorexia, fever, malaise, nausea, vomiting, pain, and jaundice the patient feels very ill and can
have joint pain.
The nutrition status and intervention is determined and implemented on an individual patient
basis, however, they are similar for all forms of hepatitis. Please describe the most common
impacts of the disease on the patient’s nutritional status, and describe the common dietary
prescriptions used:
Nutritional Status: Because the patients are anorexic while at the same time fighting an
infection which leads to increased energy needs, weight loss and malnutrition can
occure. The severity is determined by nutritional status before the infection and
progression and length of the disease.
Common Dietary Practices: For acute hepatitis there is usually no special diet. The patient
needs rest, adequate fluids, and nutrition to help the liver heal. Alcohol should be
avoided. Adequate intake of calories is important to prevent or treat weight loss. 30 - 35
kcal/kg and up to 1 - 1.2 g protein per kg are recommended. 50 - 55 % of energy should
come from carbohydrates and fat intake depends on tolerance. Small, frequent meals
are usually better tolerated. A multivitamin with B vitamines, vitamin C, vitamin K, and
zink is recommended.
For chronic hepatitis the recommendations are the same: no alcohol, an adequate
intake of energy and nutrients to promote healing of the liver and prevent or treat weight
loss. For chronic hepatitis there are several medications which could lead to food-drug
interactions.
For both acute and chronic hepatitis it is important to look at all other medications, and
herbal supplements and determine if they have an effect on the liver.
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References:
Nelms, M., Sucher, K.P., Lacey, K., Roth, S.L. (2011). Nutrition Therapy &
Pathophysiology (2nd ed.). Belmont, CA: Wadsworth
Escott-Stump, S. (2011). Nutrition and Diagnostic Related Care (7th ed.). Lippincott
Williams & Wilkins
Hepatitis (2007).The Merck Manual for Patients and Caregivers. Available at
http://www.merckmanuals.com/home/liver_and_gallbladder_disorders/hepatitis/
overview_of_hepatitis.html?qt=hepatitis&alt=sh
13. Alcoholic Hepatitis - Note: Serum AST (SGOT) marked higher than ALT (SGPT) strongly suggests a
toxic etiology, rather than acute viral hepatitis)
a. Definition: active inflammation of the centrilobular region of the liver.
b. Etiology: Excess alcohol consumption, often occurs in chronic alcoholics who gon on a “bender”
and binge on quantities much greater than their usual intake.
c. Pathophysiology: Alcoholic hepatitis occurs in 10 - 35 % of all alcoholics. It is often a
combination of inflammatory processes, fatty liver, and liver necrosis. Typical symptoms are
fatigue, fever, jaundice, pain, and hepatomegaly. Patients are more susceptible to infections like
pneumonia and peritonitis. Antibiotics and corticosteroids are medications that are frequently
used. The disease can progress to ascites, encephalopathy, varices, and liver failure.
d. Nutrition risks r/t disease process: Because the patients are anorexic while at the same time
fighting an infection which leads to increased energy needs, weight loss and malnutrition can
occure. Malnutrition and weight loss can be more severe than in nonalcoholic hepatitis because
chronic alcoholism can contribute. Alcoholic often have a poor diet because some of their calories
from food is replaced by alcohol, changes in in the gastrointestinal mucosa and enzyme secretion
decrease absorption and alcohol interferes with and metabolism of many nutrients. Socioeconomic
factors and psychological factors can also contribute to the problem of malnutrition.
e. MNT: Abstinence from alcohol and treatment of weight loss and malnutrition are most important.
Adequate energy and protein intake, fat intake restricted if there are signs of fat-malabsorption,
and supplementation of vitamins (especially B vitamines )and minerals. With alcohol abstinence
and good nutrition that helps the liver to heal patients can recover from alcoholic hepatitis. Enteral
feeding is sometimes needed for severe cases of alcoholic hepatitis.
References: Alcoholic Liver Disease (2009). The Merck Manual for Health Care Professionals.
Available at http://www.merckmanuals.com/professional/hepatic_and_biliary_disorders/
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alcoholic_liver_disease/alcoholic_liver_disease.html?qt=alcoholic%20liver%20disease&alt=sh
14. Pancreatitis – Distinguish between acute and chronic when applicable
a. Definition:
Acute: Inflammatory process that occurs suddenly.
Chronic: Defined histologically as the presence of chronic inflammatory lesions in the
pancreas, and in practice is persistence of symptoms secondary to pancreatic dysfunction
over weeks and months; results in permanent impairment of the anatomy of the pancreas.
b. Etiology:
Acute: Gallstones; biliary tract disease; excessive alcohol intake; ESRD; pancreatic
cancer.
Chronic: Most often associated with alcohol consumption, although a small percentage of
cases are idiopathic, hereditary, or associated with hyperparathyroidism (hypercalcemia),
or trauma. How alcohol causes chronic pancreatitis is not known.
c. Pathophysiology:
Acute: Obstruction either from gallstones or from protein particles leads to activation of
pancreatic enzymes inside the pancreas and their release. They damage the tissue and cause
an immune response with cytokines that leads to inflammation, edema, and sometimes
necrosis. The inflammation can be mild or severe. With gallstones the onset is usually fast,
with alcohol abuse more slowly. In mild cases the patient experiences steady abdominal pain
(can be severe and is worse after eating), nausea, vomiting, diarrhea, and steatorrhea. The
disease can also have a severe progression with necrosis and hemorrhaging of the pancreas
that leads to a systemic immune response with shock, sepsis, renal failure, respiratory or
multiorgan failure.
Chronic: The obstruction can become chronic and lead to fibrosis, edema, and necrosis.
After several years the pancreas loses his exocrine and endocrine function. 20 - 30 % of
patients develop diabetes, some also pancreatic cancer. The patient has episodes of severe
pain. These episodes become less frequent when the disease is progressed further and more
enzyme-producing cells are destroyed. Other symptoms are nausea, vomiting, diarrhea,
steatorrhea, cratorrhea (undigested muscle fiber in feces), glucose intolerance, malabsoption,
weight loss.
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d. Nutrition risks r/t disease process:
Acute: Due to the severe pain and the loss of pancreas function the patient is at risk for
malnutrition and unintentional weight loss. Nutritional status also depends on the underlying
disease, for example alcoholism.
Chronic: Due to the episodes of pain and the malabsorption the patient is at risk for
malnutrition and unintentional weight loss. Nutritional status depends on the level of
exocrine and endocrine function that remains, and the underlying disease.
e. MNT:
Acute: The patient is treated with IV fluids. Fasting to give the pancreas rest used to be the
standard dietary recommendation. Today early feeding, oral or enteral, is preferred to avoid
malnutrition and the translocation of bacteria. If oral feedings are tolerated a diet with small
frequent feedings and supplementation of pancreatic enzymes is prescribed. Alcohol,
caffeine, smoking and other irritants should be avoided. MCT fats can be given. Enteral
feeding is started if oral feedings are not tolerated or the patient is malnourished. Enteral is
preferred over parenteral because it helps to maintain a healthy gut and can reduce the
systemic inflammatory response. The gastric route should be tried first. If there is
obstruction than the feeding should go into the jejunum. The enteral formula should be
nearly fat free or include MCT oils. Omega-3 fatty acids are helpful because they have a
positive influence on the inflammatory process. Adequate amounts of vitamin C, B vitamins,
folic acid, fat-soluble vitamins in water-miscible form should be supplemented.
Chronic: A low-fat diet with < 25 g fat per day and MCT fats is recommended. The diet
should have enough energy to avoid or treat weight loss. Supplementation of pancreatic
enzymes can help with pain and steatorrhea. Alcohol, caffeine, smoking and other irritants
should be avoided. Fat-soluble vitamins should be supplemented in water-soluble form, as
well as water-soluble vitamins. Antioxidants are important because they can reduce
oxidative stress and pain. Vitamin B12 absoption can be decreased, and this vitamin should
be monitors and supplemented as needed. A diet low in fiber with small, frequent meals is
better tolerated. All patients need to be monitors for hyperglycemia and signs of diabetes.
References: Nelms, M., Sucher, K.P., Lacey, K., Roth, S.L. (2011). Nutrition Therapy &
Pathophysiology (2nd ed.). Belmont, CA: Wadsworth
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Escott-Stump, S. (2011). Nutrition and Diagnostic Related Care (7th ed.). Lippincott
Williams & Wilkins
Acute Pancreatitis and Chronic Pancreatitis (2007).The Merck Manual for Health Care
Professionals. Available at
http://www.merckmanuals.com/professional/gastrointestinal_disorders/pancreatitis/
overview_of_pancreatitis.html
C.) NUTRITION PRESCRIPTIONS
For each of the following:
a. Describe the diet – include details such as you would when explaining it to a patient
b. Explain the physiological response to the diet as it relates to diabetes
1. High Protein
Description The diet has a high percentage of protein. The RDA is 0.8
g/kg. Diets high in protein can go up to about 2 g/kg.
Foods high in protein are usually animal products like
meat, poultry, fish, eggs and dairy. Plant food has in
general less protein, plant foods high in protein are
legumes, soy products and nuts.
Response
A diet high in protein is usually given when the body is in
a catabolic situation and nitrogen balance can become
negative, for example with infections, injury, and different
diseases. A high protein diet is given to promote healing
and regeneration.
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2. Low Protein
Description The diet contains less than 0.8 g/kg. Usually no less than
0.6 g/kg is recommended. Most of the intake in this diet
comes from food with a high carbohydrate and fat (if
tolerated) content, like starches, grains, vegetables, fruits,
fats.
Response
A low protein diet is prescribed to slow down the
progression of kidney disease. A low protein diet is also
prescribed for some patients with liver disease. Dietary
protein can raise ammonia levels and those can lead to
hepatic encephalitis. But a low protein diet is no longer
standard treatment, only in cases of protein intolerance. A
low protein intake can also slow down liver regeneration
and have a negative impact on nutritional status.
3. No alcohol
Description
Response
The diet should contain no alcoholic beverages like beer,
wine or other liquor. Special attention needs to be paid to
alcohol in medications, mouthwashes, or flavoring
extracts.
The liver and pancreas can heal and regenerate.
4. High calorie
Description The diet has a high energy content either by increasing oral
intake or through supplements or enteral/parenteral nutrition
support. A higher energy intake can be achieved by adding
energy-rich foods, like fats to the diet and increasing other
macronutrients as tolerated.
Response
Patients need a higher energy intake when they are in a
state of metabolic stress, from infection, injury, or
diseases. Goal of a higher energy intake is to promote
healing and avoid malnutrition.
5. Low Calorie
Description The diet has a low energy content. Foods with a high energy
content like fats, oil, high-fat meats and dairy products and so
on are reduced.
Response
A low calorie diet is usually prescribed to achieve a
negative energy balance and promote weight loss.
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6. For each of the following diseases and conditions, list the nutrient recommendations in
the chart. Not all conditions will have recommendations for each nutrient.
Alcoholic Liver Disease
Calories/kg 30 - 35 kcal/kg
Protein/kg
about 1.5 g/kg, but can go higher
Fat
low
Fluid
-
Sodium
Cirrhosis
Calories/kg
35 -40 kcal/kg
Protein/kg
1 - 1.6 g/kg
Fat
25 - 30 % with steatorrhea
Fluid
1 - 2 l if ascitis needs to be managed
Sodium
2 g to manage ascitis
Ascites – due to cirrhosis
Calories/kg
35 -40 kcal/kg
Protein/kg
1 - 1.6 g/kg
Fat
25 - 30 % with steatorrhea
Fluid
1 - 2 l, not always fluid restriction
Sodium
2 g to manage ascitis
Portal Hypertension
Calories/kg
35 - 40 kcal/kg
Protein/kg
1 - 1.6 g/kg unless protein restriction (today out of favor), than 0.6 - 0.75 g /kg to
manage ammonia levels in encephalopathy
Fat
-
Fluid
can be restricted to 1 - 2 l to manage ascitis, usually not
Sodium
2 g/day to manage ascitis
Hepatic Encephalopathy
Calories/kg
35 - 40 kcal/kg
Protein/kg
1 - 1.6 g/kg unless protein restriction (today out of favor), than 0.6 - 0.75 g /kg to
manage ammonia levels, protein from vegetables and dairy to increase BCAAs,
supplements possible
Fat
-
Fluid
-
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Sodium
August 3, 2012
-
References for this section:
Nelms, M., Sucher, K.P., Lacey, K., Roth, S.L. (2011). Nutrition Therapy &
Pathophysiology (2nd ed.). Belmont, CA: Wadsworth
Escott-Stump, S. (2011). Nutrition and Diagnostic Related Care (7th ed.). Lippincott
Williams & Wilkins
Davidson, T. Low-Protein Diet. Diet.com. Available from
http://www.diet.com/g/lowprotein-diet
Blei, T.B., Co´rdoba, J. and The Practice Parameters Committee of the American College
of Gastroenterology (2001). Practice Guidelines Hepatic Encephalopathy. American Journal
of Gastroenterology Vol. 96, No. 7, 2001. Available from
http://webdev.med.upenn.edu/contribute/gastro/documents/ACGguidelinesforHE.pdf
7. List the BCAA’s and AAA’s.
BCAAs: leucine, isoleucine, valine
AAAs: phenylalanine, tyrosine, tryptophan
8. Describe the differences in the chemical structures of branched chain and aromatic
amino acids (BCAA, AAA).
The aromatic amino acids have aromatic side chains, phenylalanine has a phenyl ring,
tyrosine's ring has a hydroxyl group, and tryptophan has two fused rings. The branched chain
amino acids have an aliphatic side chain with a branch, one carbon is bound to more than two
other carbons.
9. Discuss the metabolism of BCAA and AAA and the resulting impact on encephalopathy
in liver disease.
According to the false neurotransmitter theory an imbalance of branched-chain amino acids
(BCAA) and aromatic amino acids (AAA) is causing hepatic encephalopathy. An increased
level of ammonia leads to an increased glucagon stimulation. Increased glucagon decreases
blood glucose levels. With decreased blood glucose levels more insulin is produced leading
to an uptake of BCAA into the muscles. More AAA remain in the blood and cross the bloodbrain barrier. They are precursors for neurotansmitters and if there are more than usual in the
brain the neurotransmitter balance is altered. For example there is more serotonine from
tryptophan, false neurotransmitters like octopamin from tyrosine and a decrease in DOPA
production that can also lead to more false neurotransmitters.
10. Discuss the controversy and current research regarding protein restriction with hepatic
encephalopathy. Are BCAA the recommended protein source?
As a byproduct of protein metabolism ammonia is produced. It is released from the cells and
reaches the liver where it normally is converted in the urea cycle. With liver disease the
amount of ammonia that can be cleared is decreased. A big source of ammonia is also the gut
and it is widely accepted that this is a major contributing factor for encephalopathy.
Ammonia levels can be high in people with cirrhosis and portal hypertension. Ammonia is
toxic and when it reaches the brain it can lead to hepatic encephalopathy. Protein restriction
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used to be a standard therapy to treat hepatic encephalopathy. But a long-term protein
reduction can also lead to protein-energy malnutrition and decrease healing and regeneration
of the liver. Today only a short-term protein restriction is recommended and than a gradual
increase in protein consumption up to 1 - 1.5 g/kg to promote healing of the liver. Protein is
increased slowly while at the same time ammonia levels are monitors. Tolerance can vary
among patients. This increased protein intake is usually combined with lactulose and
neomycin. Both lactulose and neomycin reduce the amount of ammonia from the intestines.
Lactulose feeds bacteria in the colon which in turn take up ammonia and produce an acidic
environment. Ammonia can not reenter the blood stream and blood levels decrease.
Neomycin reduces the number of bacteria in the gut that produce ammonia. Protein
restriction is no longer recommended because malnutrition is a major risk factor for death in
patients with cirrhosis. Protein restriction also leads to increased protein breakdown in the
body which in turn can contribute to increase ammonia levels. There is still no sufficient
supporting evidence for the use of branched-chain ammino acids. They are available in
formulas and can be tried for patients who's encephalopathy can not be controlled. But
because of their cost and the lack of evidence they are not recommended as a standard
treatment.
11. Discuss vegetable versus meat protein for treatment of cirrhosis.
Vegetable protein has a higher amount of branched-chain amino acids while meat is higher in
aromatic amino acids. To increase the blood levels of branched-chain amino acids and treat
the imbalance a diet rich in vegetables and dairy products is recommended. Vegetable protein
also has higher calorie to nitrogen ratio that is preferred for these patients. They also provide
fiber which can benefit the colon bacteria.
References for this section:
Nelms, M., Sucher, K.P., Lacey, K., Roth, S.L. (2011). Nutrition Therapy &
Pathophysiology (2nd ed.). Belmont, CA: Wadsworth
Blei, T.B., Co´rdoba, J. and The Practice Parameters Committee of the American College of
Gastroenterology (2001). Practice Guidelines Hepatic Encephalopathy. American Journal of
Gastroenterology Vol. 96, No. 7, 2001, available from
http://webdev.med.upenn.edu/contribute/gastro/documents/ACGguidelinesforHE.pdf
Miles, B. (2003). Amino Acid Degradation. Available from
http://www.tamu.edu/faculty/bmiles/lectures/amcat.pdf
Caruana, P., Shah, N. (2011) Hepatic Encephalopathy. Are NH4 Levels and Protein
Restriction Obsolete? Nutrition Issues in Gastroenterology, Series #95. Available from
http://www.medicine.virginia.edu/clinical/departments/medicine/divisions/digestivehealth/nutrition-support-team/nutrition-articles/Caruana%20Article.pdf
Berg JM, Tymoczko JL, Stryer L. Biochemistry. 5th edition. New York: W H Freeman; 2002.
Section 3.1, Proteins Are Built from a Repertoire of 20 Amino Acids. Available from:
http://www.ncbi.nlm.nih.gov/books/NBK22379/
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D.) NUTRITION RELATED TOPICS
1. Summarize the role of the liver in the following functions:
Function related to:
Production of bile
Digestion
Metabolism of glycogen
Metabolism of triglcerides and
lipoproteins
Metabolism of protein
Protein synthesis
Detoxification
Visceral protein related to
osmotic balance and edema
Storage of vitamins
Storage of minerals
Role of the liver
Continuous production of bile that is then secreted into
the bile duct and stored by the gallbladder.
Bile is critical for the digestion of lipids because it is an
emulsifying agent. It allows water-soluble lipase to
break triglycerides and other lipids.
The liver turns unused glucose into glycogen
(glycogenesis) and stores it. It also breaks down stored
glycogen (glycogenolysis) when glucose is needed.
The liver either reuses cholesterol that comes in or it
produces cholesterol itself. Triglycerides can also come
from diet or are produced in the liver. The liver than
sends those out in form of lipoproteins to supply body
cells with building material.
The liver produces several proteins, like serum proteins,
prothrombin, globin and others. It also breaks down
some proteins and forms urea out of breakdown
products of proteins.
The liver produces serum proteins (like albumin),
prothrombin, globin, carrier proteins , hormones
The liver is the main detoxification organ, for example
for alcohol, drugs, and toxic substances produced in the
body (like ammonia). Often these substances transfomed
into more water-soluble forms so they can be excreted.
Visceral protein, protein that is nonskeletal protein, is
mainly produced in the liver, for example albumin,
transferrin, prealbumin. These proteins provide fluid
balance by attracting water into the capillaries. Is protein
intake low and serum protein levels decrease, water
escapes into tissues and causes edema.
The liver stores mainly vitamin A, carotenoids, vitamin
K, vitamin D, folate.
The liver stores iron and copper.
Folic acid
Cholecalciferol generated in the skin and from dietary
sources reaches the liver and is converted to calcidiol
which then goes to the kidneys.
The liver stores folate.
Carotene
Carotenes are stored mainly by the liver.
Vitamin D activation
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Metabolism of steroids
Clotting factors
August 3, 2012
The liver is the main organ where steroids are
deactivated and broken down.
The liver produces six blood clotting factors: I
(fibrinogen), II (prothrombin), IV, V, VI, and VII.
References:
Nelms, M., Sucher, K.P., Lacey, K., Roth, S.L. (2011). Nutrition Therapy &
Pathophysiology (2nd ed.). Belmont, CA: Wadsworth
Insel, P. (2011) Nutrition (4th ed.) Sudbury MA: Jones and Bartlett
Steimer, T. (2008). Steroid Hormone Metabolism. Geneva Foundation for Medical Education
and Reseach. Available from
http://www.gfmer.ch/Books/Reproductive_health/Steroid_hormone_metabolism.html
Blood Clotting Factors (2005). SinoMed. Available from
http://www.sinomedresearch.org/hcv/tcm/Clotting.htm
Folic Acid. (2002) Micronutrient Information Center. Linus Pauling Institute. Available from
http://lpi.oregonstate.edu/infocenter/vitamins/fa/
2.
Explain how alcohol is metabolized.
Alcohol is absorbed in the mouth, esophagus, stomach and small intestines. The
small intestines absorb most of the alcohol. Some is oxidated, but most is
absorbed unchanged. The primary site of metabolism is the liver, but the intestines
also have enzymes that can metabolize ethanol. In the liver alcohol metabolism
has precedence over other macronutrients. Small amounts of alcohol are
metabolized through the alcohol dehydrogenase system in the liver and the
gastrointestinal tract. The enzyme alcohol dehydrogenase converts alcohol to
acetaldehyde. Acetaldehyde dehydrogenase then converts acetaldehyde to acetyl
CoA.
To metabolize larger amounts of alcohol that are too much for this system the
microsomal ethanol-oxidizing system comes into play. This system can increase in
capacity and speed if needed, it is responsible for general detoxification. Through
different enzymes alcohol is converted to acetaldehyde. Acetaldehyd is than further
metabolized to acetyl CoA.
A third pathway uses catalase but can only metabolize a small amount of alcohol.
All three pathways generate acetyl CoA. This is than used to make fatty acids. Fat
accumulation in the liver can be seen after heavy drinking and chronic alcohol
consumption can lead to fatty liver.
Acetaldehyde is more toxic than ethanol and can cause significant damage in the
liver, brain, pancreas, and gastrointestinal tract. It is also carcinogen.
3.
Women absorb and metabolize alcohol differently from me, making them more
vulnerable than men to alcohol-related organ damage. Describe how alcohol is
metabolized differently than in men.
Women are usually smaller then men and have a smaller liver with less capacity for
metabolizing alcohol. Due to their smaller statue and a different body composition
with a higher percentage of fat they also have less body water and therefor less
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capacity to dilute alcohol in the body. Alcohol-metabolizing enzymes, especially
those in the intestines are less (up to 40 %) active than in men. This makes alcohol
metabolism slower and blood alcohol remains higher for a longer period of time.
Chronic alcohol intake leads to liver disease in women faster than in men, they are
also more likely to get alcoholic hepatitis and mortality rate from cirrhosis is higher
for women than for men.
4.
Explain why malnutrition is common in chronic alcoholics with liver disease. Discuss
the ways in which alcohol contributes to malnutrition related to digestion and
absorption, and altered metabolism.
Alcohol can cause malnutrition in different ways:
- Alcoholics often replace meals with alcohol and have a disordered eating behavior. This
leads to a lower intake of energy and nutrients. Poverty, homelessness, and other living
circumstances can make this problem worse.
- Psychological factors like anxiety, depression, and isolation can contribute to anorexia.
- Alcohol damages the mucosa of the gastrointestinal tract and leads to inflammation,
diarrhea, esophagitis, esophageal stricture with dysphagia, gastritis, and other
complications. This leads to anorexia, aversion against food, and malabsorption.
- Damage to the pancreas can lead to a decreased secretion of enzymes and bile. This can
lead to steatorrhea, fat malabsoprtion and malabsorption of fat-soluble vitamines.
- Alcoholic hepatitis, cirrhosis, portal hypertension, and ascitis can also cause symptoms
(bloating, nausea, fatigue, pain, steatorrhea) that decrease appetite and lead to malnutrition.
- Alcoholic hepatitis can lead to increased risk of infection and antibiotica therapy. This can
contribute to a decreased intake of food. Antibiotics can further damage the health of the
gastrointestinal tract.
- Alteration of the mental state of the patient with encephalopathy can interfere with food
intake.
- There is an increased need for certain vitamines because alcohol or acetaldehyde interfere
with their absorption, metabolism or their activation. Excretion of some vitamins is
increased.
- Vitamin deficiency can further impair nutritional status. Thiamine deficiency can lead to
Wernicke-Korsakoff syndrome. Vitamin A deficiency can damage to gastrointestinal
mucosa and increases susceptibility to infections. Folate decifiency can make damage to the
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liver worse.
References for this section:
Insel, P. (2011) Nutrition (4th ed.) Sudbury MA: Jones and Bartlett
Alcohol metabolism: An Update. National Institute on Alcohol Abuse and Alcoholism.
Available at http://pubs.niaaa.nih.gov/publications/AA72/AA72.htm
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