You are on page 1of 12

LIVER AND GALLBLADDER WORKSHEET

1. Define the following term rel!te" to li#er !n" g!ll$l!""er "ie!e%
A&ite: accumulation of fluid in the space between the lining of the abdomen and the abdominal organs, also
knows as the peritoneal cavity
V!ri&e: abnormally dilated vessel with a tortuous course – usually occur in the venous system, but may also
occur in arterial or lymphatic vessels – blood flow through the portal vein slows due to cirrhosis (portal
hypertension), blood from the intestines/spleens backs up into blood vessels in the stomach and esophagus –
these blood vessels may become enlarged and are at risk to burst
'!(n"i&e: yellowish pigmentation of the skin and other mucous membranes caused by hyperbilirubinemia
(increased levels of bilirubin in the blood) – often seen in liver disease. Can occur in newborns and is treated
with ! light in the clinical setting, or in mild cases with sun e"posure.
)ort!l h*+ertenion: #lood from the intestines and spleen is carried to the liver through the portal vein.
Cirrhosis slows this flow of blood, which increases the pressure inside of it. $ortal hypertension is defined as
elevation of the venous pressure gradient.
E"em!% abnormal accumulation of fluid in the interstitium (locations beneath the skin or in one or more cavities
of the body) – clinically shown as swelling
,!tt* li#er: or fatty liver disease (%&') is a reversible condition where large vacuoles of triglyceride fat
accumulate in liver cells via the process of steatosis (abnormal retention of lipids within the cells). (t is seen
with e"cessive alcohol consumption and in the obese. $rogressive inflammation of the liver (hepatitis) called
steatohepatitis may also occur.
He+!ti& &om!: end stage of hepatic encephalopathy
He+!ti& en&e+h!lo+!th*: the occurrence of confusion, altered consciousness and/or coma as a result of liver
failure. (n advanced stages it is called hepatic coma, and may lead to death. (t is caused by an accumulation
in the bloodstream of to"ic substances that are normally removed by the liver. (t can be reversible with
treatment. )epatic damage to the brain cells occurs due to inability of the liver to metaboli*e ammonia to urea
Ateri-i: a tremor of the hand when e"tended – inability to actively maintain a position – this can be a sign of
hepatic encephalopathy
.holelithi!i: crystalline concretion formed within the gallbladder by accretion of bile components – formed in
gallbladder, but may pass into other parts of biliary tract (cystic duct, common bile duct, pancreatic duct) – may
lead to acute cholecystitis
.hole&*titi: inflammation of the gallbladder occurring most commonly due to obstruction of the cystic duct
with gallstones. +his blockage causes accumulation of bile in the gallbladder and increased pressure within
the gallbladder. ,welling/inflammation can reduce normal blood flow, which can lead to cell death due to
insufficient o"ygen.
L!enne&/ &irrhoi: named after %rench physician who invented the stethoscope – disease of the liver in
which the normal lobular architecture is lost, with fibrosis and later nodular regeneration – can be associated
with inflammatory polyarthritis (affecting shoulders, elbows, and knees)
.hole&*te&tom*: surgical removal of the gallbladder – common treatment for symptomatic gallstones
Bili!r* "*0inei!: altered tonus of the sphincter of -ddi (usually increased pressure), disturbance in the
coordination of contraction of the biliary ducts and/or reduction in the speed of emptying of the biliary tree
.hole"o&holithi!i: presence of gallstones in the common bile duct – causes .aundice and liver cell damage,
and re/uires treatment by cholecystectomy
1. I"entif* the following "i!gnoti& tet in li#er "ie!e%
A Li#er )!nel or )epatic %unction panel usually includes: 0&+, 0,+, bilirubin, 0&$
+his table from &ab +ests -nline
1
shows &iver $anel results that may be seen in certain combinations in those
with liver disease.
T*+e of li#er &on"ition or
"ie!e
Bilir($in ALT !n" AST AL) Al$(min )T
A&(te li#er "!m!ge 2"(e3
for e-!m+le3 to infe&tion3
to-in or "r(g3 et&.4
2ormal or increased
usually after 0&+ and
0,+ are already
increased
sually greatly
increased3 0&+ is usually
higher than 0,+
2ormal4
moderately
increased
2ormal sually normal
.hroni& form of
#!rio( li#er "ior"er
2ormal or increased 5ildly or moderately
increased
2ormal 4slightly
increased
2ormal 2ormal
Al&oholi& He+!titi 2ormal or increased 0,+ is moderately
increased, usually at
least twice the level of
0&+
2ormal or
moderately
increased
2ormal 2ormal
.irrhoi 5ay be increased but
this usually occurs
later in the disease
0,+ is usually higher
than 0&+ but levels
usually lower than in
alcoholic disease
2ormal or
increased
2ormal or
decreased
sually prolonged
Bile "(&t o$tr(&tion3
&holet!i
2ormal or increased3
increased in complete
obstruction
2ormal to moderately
increased
(ncreased3 often
greater than 6
times what is
normal
sually
normal4 if
chronic,
levels may
decrease
sually normal
.!n&er th!t h!
met!t!i5e" to li#er
sually normal 2ormal or slightly
increased
sually greatly
increased
2ormal 2ormal
.!n&er origin!ting in the
li#er 2he+!to&ell(l!r
&!r&inom!3 H..4
5ay be increased,
especially if the
disease has
progressed
0,+ higher than 0&+ but
levels lower than that
seen in alcoholic
disease
2ormal or
increased
2ormal or
decreased
sually prolonged
A(toimm(ne 2ormal or increased 5oderately increased3
0&+ usually higher than
0,+
2ormal or slightly
increased
sually
decreased
2ormal
Ser(m $ilir($in: bilirubin is orange/yellow pigment, a waste product produced by the normal breakdown of
heme (substance in hemoglobin in 7#C) –increased serum bilirubin levels 8 can appear .aundiced – adults
may need to fast (nothing but water) several hours before the test 4 increased serum bilirubin can be due to
liver disease (cirrhosis), gallstones, tumors, or scaring of the bile ducts
o Direct (conjugated) bilirun: 0-0.3mg/dL
o Total bilirubin: 0.3-1.9mg/dL
AL): 0lkaline $hosphatase – en*yme found on the edges of cells that .oin to form bile ducts where it helps
digest fat in the diet – levels can increase due to blocked bile ducts or liver disease (often from a gallstone)
o Normal range: 44-14 !"/L
AST 2SGOT4: 0spartate 0minotransferase or ,erum 9lutamic4-"aloacetic +ransaminase – used to detect liver
damage, usually ordered with 0&+ – when the liver is damaged or in.ured, it releases 0,+ into the blood – this
test is most useful in detecting liver damage due to hepatitis, drugs to"ic to the liver, cirrhosis, and alcoholism
induced liver damage – 0,+ is not specific for the liver, so levels could be increased due to conditions affecting
other parts of the body
o Normal range: 10-34 !"/L
ALT 2SG)T4: 0lanine 0minotransferase is an en*yme found mostly in liver or kidney cells – when liver is
damaged it releases 0&+ into the blood, usually before other symptoms arise, like .aundice – a good test to
catch liver disease/damage early on 4 test is most useful in detecting liver damage due to hepatitis and
drugs that are to"ic to the liver – 0&+ is not specific to the liver, increases could be due to conditions affected
other parts of the body
o Normal range: 10-40 !"/L
)rothrom$in time: measures how long it takes for a clot to form in a sample of blood – increased $+ can be
due to bile duct obstruction, liver disease,
o Normal range: 11-13.# $econd$
Ammoni! 2NH64: measures the amount of ammonia in the blood – ammonia is produced by intestinal bacteria
and by proteolysis, it is a waste product normally transported by the liver where it is converted into urea and
glutamine – the urea is carried to the kidneys and e"creted as urine – if this urea cycle does not complete the
breakdown of ammonia, ammonia can build up in the blood and pass through the blood/brain barrier  hepatic
encephalopathy can result (mental and neurological changes that can lead to confusion, disorientation,
sleepiness, etc). – can be caused by liver damage/disease, renal failure, decreased blood flow to the liver, urea
cycle disorders
o Normal range: 1#-4# mcg/dL
6. Wh!t "o e!&h of the following me"i&!tion "o for the m!n!gement of li#er "ie!e
1
7
L!&t(loe: synthetic sugar used to treat constipation/reduce the amount of ammonia in the blood of patients
with liver disease – works by pooling ammonia from the blood into the colon where it is removed from the body
4 this drug increases the absorption of Ca and 5g, so do 2-+ take Ca or 5g supplements or antacids
4 decreases serum ammonia, increases glucose in diabetics
4 monitor electrolytes in geriatric or debilitated4 long term use
Neom*&in% oral antibiotic used to control the growth of ammonia4producing bacteria in the intestine
.*&lo+orine: immunosuppressant:s used to prevent transplant re.ection (liver, kidney, or heart transplants) –
has lots of drug interactions so the patient should tell doctor and pharmacist all medication they are on
(supplements included) – avoid grapefruit/grapefruit .uice and may have to limit potassium in the diet
!itamin ; may increase absorption of drug. 0void ,<=. Caution with red wine. Caution with diabetes4
increased glucose
)ro+!nolol: beta blocker, rela"es blood vessels and slows heart rate to improve blood flow 4 can affect 0&$
levels in the blood – often given to reduce blood pressure (which is usually elevated due to prednisone)
4 'ecrease sodium, decreased calcium maybe recommended.
4 0void natural licorice
4 0lcohol may decrease drug effect
4 Caution with diabetes. 5ay mask symptoms of/ or prolong hyperglycemia, may reduce insulin release
in response to hyperglycemia.
IV !l$(min: protein used for end4stage liver disease patients with cirrhosis to improve circulatory and renal
functions
)re"nione: corticosteroid that is used to treat autoimmune hepatitis – also helps to prevent re.ection after a
transplant – can cause bones to thin and may sometimes cause severe in.ury to bone – suppresses the
immune system and will make patients more susceptible to infection – can cause hypertension
Nutrition Implications of Steroids:
- 5ay cause stomach irritation if taken without food.
- 'ecrease sodium, increase calcium, vitamin ', protein. 5ay need increased vitamins 0, C.
(ncrease potassium, phosphorus. ,upplementation may be necessary.
- Calcium, vitamin ' supplementation recommended with &+ use.
- Chromium deficiency may increase risk for steroid induced diabetes
- ,teroids may also cause a dramatic increase in appetite. (ncrease in weight.
- &ong term use of >1 g for ? mo4 osteoporosis, necrosis, fractures, muscle wasting, @ABC
.holet*r!mine: used with diet changes (restricting of cholesterol and fat) to reduce the amount of cholesterol
and certain fatty substances in the blood.
- %at soluble vitamins in water miscible form and folate suppl. recommended with &+ use.
S+ironol!&tone: opposes a hormone that makes patients with cirrhosis retain fluid (ascites)
- 0void e"cessive D intake, D suppl., salt subs. 'ecrease sodium and decreased calcium may be
recommended.
)rogr!f: (+acrolimus) lowers your body:s immune system, used with liver transplant patients
- 0void D sup, or salt subs. 0void grapefruit/related citrus. 0void ,<=.
8. Briefl* "e&ri$e the f(n&tion !n" +!rt of the li#er. Define the m!9or etiologie of he+!titi3 !l&oholi&
li#er "ie!e !n" &irrhoi.
• ,(n&tion: the liver is involved with many bodily processes including:
o )omeostasis
 9lucose – protein – fat and cholesterol – hormones – vitamins (esp. 0, ', ;, D)
o ,ynthesis
 #lood clotting factors 4 #ile acids 4 Cholesterol – +riglycerides – !&')s – )'&s
 0lbumin, globulin, fibrinogen, prothrombin, transferrin
o Conversions
 Carotene converted to vitamin 0 4 %olate converted to E4+)%0 4 !itamin ' activated via A
nd

hydro"ylation
 9alactose and fructose to glucose – glycogen to glucose
 $roteins to glucose – o"idi*es fatty acids for energy and ketones
o ,torage
 !itamin/5inerals (fat soluble vitamins, *inc, iron, copper, magnesium, vitamin #1A)
 Cholesterol – glycogen storage
o ;"cretion / %ilter
 Cholesterol/phospholipids 4 #ilirubin – drugs – heavy metals, poisons, pesticides
 0mino acids, sugars, fats – (g0 – nitrogen waste (ammonia)
o 'efense
 ;"cretion of (g0 (defense against bacteria gut) 4 5acrophages consume bacteria that cross
the gut barrier
• )!rt of the li#er:
Li#er% receives nutrients from the 9( tract and processes them for distribution throughout the body
Li#er e+!r!te" $* Lo$e – each made up of millions of hepatic cells – lobes are the functional units of
the liver
 7ight lobe: larger portion of the liver
 &eft lobe: smaller and more flattened than the right lobe
 %alciform ligament: separates the right and left lobe

Bile !n" $ili!r* flow
#iliary tree/tract: anatomical term for the path by which bile is secreted by the liver and transported to the ,(
(duodenum)
(ncludes gallbladder (stores/secretes bile) and bile ducts (which conduct bile from the liver to
gallbladder/intestines)
o #ile is created in the liver and collected in the bile canaliculi  merge to form bile ducts
 Intr!he+!ti& "(&t% within the liver (hepatic ducts, common hepatic duct)
 E-tr!he+!ti& "(&t: outside the liver (cystic duct 8 gallbladder)
o $0+)=0F: #ile canaliculi  drain into the left and right hepatic ducts  common hepatic duct 
.oins cystic duct from the gallbladder  to form the common bile duct drains directly into the 
duodenum via common bile duct OR temporarily stored in the gallbladder via cystic duct
o Common bile duct and pancreatic duct enter the second part of the duodenum together at the
ampulla of !ater

Bloo" flow
o )epatic artery: on top of the liver, supplies GAEC of the liver:s blood supply 4 carries o"ygen rich
blood from the aorta
o )epatic vein: returns blood from the liver to the heart
o $ortal vein: underneath the liver, supplies GHEC of the liver:s blood supply 4 carries venous blood
containing digested nutrients from the entire 9( tract, spleen, and pancreas
o 9( tract veins: transport absorbed nutrients to the portal vein
• G!ll$l!""er: underneath the right lobe
• He+!titi: inflammation of the liver, usually caused by viruses like hepatitis 0, #, and C – can have non4
infectious causes too like heavy drinking, drugs, allergic reactions or obesity
o 5alaise, muscle and .oint aches, fever, dark urine, yellowing of eyes and skin (.aundice) abdominal
discomfort
• Al&oholi& Li#er Die!e: term that characteri*es manifestations of alcohol overconsumption including: fatty
liver alcoholic hepatitis, and chronic hepatitis with hepatic fibrosis or cirrhosis – chronic alcohol
consumption produces secretion of pro4inflammatory cytokines, o"idative stress, lipid pero"idation, and
acetaldehyde to"icity
• .irrhoi: long4term damage to the liver from any cause can lead to permanent scarring (cirrhosis) – the liver
then becomes unable to function well – once the cells have scarred they are unable to ever work properly
again
:. De&ri$e the effe&t of &hroni& !l&oholim on the met!$olim of .HO3 f!t3 +rotein3 #it!min !n"
miner!l. How &!n li#er "!m!ge !ffe&t the met!$olim of &!r$oh*"r!te3 f!t3 +rotein3 nitrogen !n"
#it!min7
.HRONI. AL.OHOLIS;
0lcohol is absorbed in the small intestines and in the stomach to a lesser degree. (t must be broken down
(mostly in the liver) by alcohol dehydrogenases (0')) Imade with *inc. 0lcohol absorption and metabolism
re/uires less time and lower doses of alcohol to cause liver damage in females vs. males.
0lcoholics can e"perience primary and secondary malnutrition. $rimary malnutrition is when the person
consumes ma.ority of their calories per day from alcohol (ethanol, Hkcal/g). ,econdary malnutrition can set
in due to inade/uate digestion and absorption (due to intestinal villi damage caused by alcohol) of nutrients
related to heavy ethanol consumption. %or e"ample, alcohol consumption can limit the amino acid uptake
and protein synthesis in the liver.
%o$$ible %&' $tatement (or c)ronic alco)oli$m:
3
 &*ce$$i+e alco)ol inta,e -.#-30g/d related to dail/ con$um0tion abo+e t)i$ le+el$ a$
e+idenced b/ alco)ol-induced li+er injur/1 ele+ated L2T$ and a$cite$.
;et!$olim I(e with &hroni& !l&ohol (e:
 C)-
•  glucose absorption
•  hypoglycemia
 %at
•  mobili*ation of fatty acids,  hepatic synthesis of fatty acids,  triglyceride
production,  triglycerides trapped in the liver (steastosis)
•  absorption of lipids (due to reduced bile secretions and pancreatic en*ymes to
digest fat)
•  o"idation of fatty acids
 $roteins
•  absorption of 00 in small intestine
 !itamins/minerals
•  absorption of thiamin, folic acid, vitamin #1A, *inc (which is needed for 0')
production)
•  absorption of fat4soluble vitamins (especially vitamin 0)
•  iron accumulation (adds o"idative stress to an already stressed liver)
LIVER DA;AGE
St!ge of !l&ohol rel!te" li#er "ie!e +rogreion:
- )epatic steatosis4fatty liver infiltration
- 0lcoholic hepatitis
- Cirrhosis
- 2ecrosis (cells are dead, cannot be regenerated)
%o$$ible %&' $tatement (or t)i$ condition
3
 !nade3uate oral (ood and be+erage inta,e reacted to anore*ia a$ e+ident b/ inta,e onl/
about #04 and 5eig)t lo$$ o( 66 lb in t)e 0a$t 3 mont)$ (#4 "78).
;et!$olim I(e with li#er "!m!ge
 C)-
•  glucose sensitivity (glucose intolerance sets in)
•  glucagon (may lead to early satiety and hypophagia)
•  gluconeogenesis
 %at
•  absorption of lipids and serum lipid levels
•  mobili*ation of fatty acids
 $roteins
•  plasma aromatic amino acid (000) concentrations (see Juestion 1B)
•  risk of muscle wasting, weight loss and malnutrition
 !itamins/minerals
•  absorption of thiamin, folic acid, vitamin #1A, *inc (which is needed for 0')
production)
•  absorption of fat4soluble vitamins
A""ition!l &!(e of m!ln(trition in +!tient with li#er "!m!ge
 0nore"ia, ascites, altered mental status (encephalopathy), delayed gastric emptying, early satiety,
inade/uate diet, 7" causing 9( distress, nausea
 0ccelerated 9( transit, accelerated proteolysis, anemia from impaired 9(/liver function, bacterial overgrowth,
biliary flow changes, choline depletion and betaine, decreased hepatic production/storage of nutrients,
diuresis, paracentesis,

Norm!l .HO met!$olim
<. Wh* i !n !l&oholi& gi#en thi!min intr!#eno(l* (+on !"miion to !n emergen&* room7
!itamin #1 (thiamin) is a water4soluble vitamin that is associated with the metabolism of lipids and glucose
along with the production of glucose4derived neurotransmitters. #ecause of this, thiamin deficiency can lead to
neurological and cardiovascular problems. +hiamin deficiency is a spectrum disorder ranging from #eriberi to
=ernicke:s encephalopathy, to Dorsakoff:s psychosis. ;arly symptoms of thiamin deficiency include: weakness,
emotional disturbances, and fatigue. ,evere thiamin deficiency can progress into =ernicke:s encephalopathy
(=;). Classical signs of =; include: ocular motility disorders, ata"ia, mental changes, confusion, drowsiness,
pre4coma and coma. =ernicke:s encephalopathy, if left untreated, can progress into Dorsakoff:s psychosis
(amnesia, disorientation, short term memory loss, long4term institutionali*ation).
6

(t has been well documented that alcoholism and low levels of thiamin go hand in hand. 0lcoholism is the most
fre/uent cause of thiamin deficiency in the =estern world. ;thanol directly interferes with the guts ability to
absorb thiamin. 'aily thiamin re/uirements are G1.Emg and deficiency can occur within A4K weeks. -ral
absorption of thiamin, at best, is 6.Emg, but if alcohol was consumed recently oral absorption ma"es out at
GB.Lmg. +herefore, parenteral thiamin is advised for those at risk or diagnosed with =;. (! infusion is
necessary to achieve the high blood thiamine levels necessary for rapid diffusion and transport across the
blood brain barrier. -ral thiamine would not increase the blood levels sufficiently or /uickly enough in patients
diagnosed or with suspected =;. ,tudies show that an infusion (over a KB minute period) tends to reduce
possible side effects including: flushing, anaphyla"is, and bronchospasms. 'oses upon arrival to an ;7 range
from AEB4EBBmg once to three times a day for at least K4E days, or until clinical improvement is recogni*ed.
E

=. Aeing the +!tient with li#er "ie!e &!n $e ! &h!llenge (ing the t*+i&!l n(trition +!r!meter of
weight !n" !l$(min. Wh* i thi7 Wh!t wo(l" $e the $et w!* to !e ! +!tient with li#er "ie!e7
0lbumin is a protein produced by the liver and can be measured through a blood test (testing the serum
albumin levels). =hen levels are decreased it can be a sign of chronic liver disease. 0 known conse/uence of
low albumin levels is edema (water retention). =ater retention can mask possible weight loss (seen in liver
patients). ;ven if a patient:s weight on the scale does not change3 the patient could be still be e"periencing
loss of weight in the form of lean body mass.
$re4albumin is an alternative lab value that will detect acute changes in protein status and is a more accurate
snapshot of the patients: nutritional status. +he pre4albumin lab test assists physicians and 7':s in diagnosing
protein4calorie malnutrition. &ow concentrations of pre4albumin illustrate liver disease, protein4caloric
deficiencies, serious infection, chronic illness, or inflammation. )owever, concentrations of pre4albumin, as well
as albumin, can be low due to low levels of synthesis and not poor nutritional status.
0nthropometric measurements can be effective if the reliability of the tester is good. 0nthropometric
measurements that may be useful include the triceps4skinfold and mid4arm circumference tests. +he
,ub.ective 9lobal 0ssessment (,90) combines multiple elements of nutritional assessment to classify severe
malnutrition and is a validated measurement tool.
?

(t is important to point out that prednisone, a common corticosteroid used in liver disease treatment, can
increase pre4albumin concentrations.
>. De&ri$e the form!tion !n" f(n&tion of $ile.
#ile is a water4like substance containing electrolytes, bile acids, cholesterol, phospholipids, and bilirubin.
)umans produce G 6BB4LBBml of bile per day. +his mi"ture moves through the biliary tract into the gut (small
intestine) where it aids in digestion and absorption of fats/fat4soluble vitamins and assists in eliminating waste
products from the body through feces.
#ile formation begins in liver cells where cholic acid and chenodeo*ycholic acid, (the two main types of bile
acid), are synthesi*ed. %rom the liver, these two bile acids are secreted into the lumen of the small intestine.
)ere, the primary bile acids are dehydro"ylated to form the secondary bile acids deo"ycholic and lithocholic
acids. (n a process known as enterohepatic circulation, all four of these bile acids can be absorbed into the
blood stream, returned to the liver, and re4secreted. -ther substances, called bile salts, can be made from the
primary bile acids. Con.ugated bile acids produce bile salts, which have a very low p) and will not be absorbed
into the blood for hepatic circulation. +he ratio of bile acids to bile salts is important for the formation of
micelles.
7idding the body of e"cess cholesterol, eliminating catabolites form the liver, formation of micelles to
encompass lipids and fat4soluble vitamins through the intestine wall and transported via the lacteal system, as
well as assisting in the decrease of bacteria flora in the small intestine are all actions produced by bile.

?. Wh!t enter!l form(l! !re &ommer&i!ll* !#!il!$le for the +!tient with li#er "ie!e7 Wh!t i (ni@(e
!$o(t thee form(l!7
$atients with liver disease have uni/ue nutritional needs that have to be considered when choosing an enteral
formula. +he 7' will want to make sure of the proper #C00 and 000 ratio (see /uestion 1B), standard amounts
of vitamins and minerals, with increased amounts of polyunsatured fatty acids (like medium change
triglycerides), and ade/uate amounts of protein. %at emulsion should be used cautiously in patients with severe
liver disease because of their decreased ability to clear infused fat, which could lead to fat overload syndrome.
+his syndrome results from an increased fat deposition in the liver.
-verfeeding with glucose can result in hyperglycemia and fatty liver. 0dditional folic acid may be added to the
standard package. (ron is not included in the standard package for patients with liver failure or biliary
obstruction. 5ineral considerations include limiting patients to *inc, because copper and manganese are
eliminated from the body by biliary e"cretion.
H

0long with specific nutritional considerations, the 7' should also keep in mind that caloric needs are greatly
increased G1.E" normal with hepatic distress. =ith all of these considerations in mind, a commercial product
like )epatic40id (( by )ormel )ealthlabs is recommended. +his nutrition support product has 1.Akcals/m&,
EH.KC C)-, AH.HC %at, 1EC $ro, increased levels of leucine, isoleucine, and valine. -mega4K
supplementation within the enteral formula will also help protect the patients: liver. $atients: whose bilirubin
number declines after 1 week of therapy are seen as progressing well and indicates a positive response to
treatment.
1A. E-+l!in the role of B.AA 2$r!n&he" &h!in !mino !&i"4 #. AAA 2!rom!ti& !mino !&i"4 in li#er "ie!e.
$lasma concentrations of 000s (methionine, glutamine, aspargine, and histidine) are elevated in patients with
liver cirrhosis due to rapid muscle proteolysis and a decrease in protein synthesis. #C00 (leucine, isoleucine,
and valine) counteract 000 buildup, but are not elevated in cirrhosis patients. +hus, and imbalance occurs.
=hen there is an imbalance of #C00 and 000, ammonia levels in the brain can be affected, causing hepatic
encephalopathy. ,upplementation with #C00s may reduce uptake of tryptophan in the brain, improving
encephalopathy. 7esearch shows that supplementation of #C00s over a long period of time may be related to
a decrease in hepatic failure and improved nutrition status among cirrhosis patients.
L

LIVER AND GALLBLADDER MODULE
O$9e&ti#e ,atisfactory 2ot
Completion 0pplicable
Review
1.+he student will discuss with the rotation coordinator the functions of the
liver and the difficulties in the nutritional assessment of patients with
liver disease.

A.+he student will discuss with the rotation coordinator the role of nutrition
for liver and gallbladder disease (including hepatitis, alcoholic liver
disease, fatty liver and cirrhosis). (nclude in the discussion, but not
limited to, all the following that are applicable:
a. etiology and treatment
b. pathophysiology
c. metabolic/nutritional alterations
d. current medical treatments/trends
K.+he student will discuss with the rotation coordinator the ways that
alcoholism can cause malnutrition.
6. 'iscuss the dietitian:s role as part of the health care team
Assess
E. sing height/weight/labs and other pertinent information the student will
assess the appropriateness of:
a. the 5':s order
b. diet
c. energy/protein/nutrient re/uirements
?. +he student will obtain diet histories.
MNNNNNNN (9oal of K or more)
H. +he student will complete nutrition care plans.
MNNNNNN (9oal of K or more)
Educate
L.+he student will utili*e the diet history and care plan as well as any
other pertinent educational material to instruct patients and/or family
member on his/her specific dietary regimen.
M NNNNNN (9oal of K or more)
Document
O. sing the format appropriate for the site, the student will document all
pertinent information in the medical record.
MNNNNNNNN(9oal of K or more)
6/11
Referen&e%
1. &iver $anel. &ab +ests -nline. =eb site. http://labtestsonline.org/understanding/analytes/liver4
panel/tab/test/. pdated <une 6, AB16. 0ccessed <une KB, AB16.
A. $ronsky P5, Crowe <$. 2ood and 9edication !nteraction$. 1H ed. #irchrunville, $0: %ood45edication
(nteractions $ublishing Co3 AB1A.
K. 02'. (nternational 'ietetics and 2utritional +erminology ((dnt) 7eference 5anual, ,tandard &anguage for
the 2utrition Care $rocess. 0C0';5F -% 2+7(+(-2 Q '(;+;+(C,3 AB1A.
6. 0gabio 7. +hiamine 0dministration in 0lcohol4'ependent $atients. :lco)ol ; :lco)oli$m. ABBE36B(A):1EE4
1E?.
E. %essler +0. +hiamine 'eficiency4 7's 0re Dey $layers in $revention and +reatment. Toda/<$ Dietitian.
AB1B31A(1B):HL.
?. )enkel 0,, #uchman 0&. 2utritional ,upport in Chronic &iver 'isease. Nat =lin %rac >a$troenterol
?e0atol. ABB?3 K(6):ABA4ABO.
H. 2utrition Care 5anual. 0cademy of 2utrition and 'ietetics. =eb site.
http://www.nutritioncaremanual.org/topic.cfmR
ncmNcategoryNid81QncmNtocNid8O66OQncmNheading82utrition
CareQncmNcontentNid8HOOEBM(mplementationofthe2utrition(ntervention$arenteral2utrition. 0ccessed <uly
1, AB16.
L. Dawaguchi +, (*umi 2. #ranched Chain 0mino 0cids as $harmalogical 2utrients in Chronic &iver 'isease.
)epatology. AB113E6(K): 1B?K41BHB. http://onlinelibrary.wiley.com/doi/1B.1BBA/hep.A661A/pdf. 0ccessed
<uly 1, AB16.