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Chapter 19
Candice Quillin, BSN, CGRN
2 March 2011
1.
2.
Describe Anatomy and Physiology of normal
liver
Name three (3) diseases or diagnosis of the
liver and treatment for them.
 Hepatocytes
– secrete bile
 Sinusoid cavities are between rows of
hepatocytes
 Sinusoids are lined with Kupffer cells
 Kupffer cells remove amino acids, nutrients,
sugars, broken down RBC’s, bacteria, and
debris from blood. Detoxifies the blood.
 Secrete bile
 Bile
formation and secretion
 Metabolism of carbohydrates, proteins, fats,
and steroids
 Manufacturer of substances necessary for
coagulation and anticoagulation
 Detoxification of foreign and toxic
substances
 Vitamin and mineral storage
 Bile
is secreted into the bile canaliculi,
which branch and combine to form the right
and left hepatic ducts. The right and left
hepatic ducts merge into the common
hepatic duct. The cystic duct joins the
common hepatic duct to form the common
bile duct. The common bile duct joins the
duct of Wirsung at the ampulla of vater. Bile
then empties out into the duodenum.
Carbohydrate metabolism converts glucose,
fructose, and galactose to glycogen for storage
in the liver
 Breaks down glycogen to glucose to maintain
blood glucose levels when carbohydrate intake
decreases
 Synthesizes glucose from noncarbohydrate
nutrients to maintain blood glucose levels.
 Breaks down amino acids to produce ketoacids
and ammonia.
 Synthesizes proteins
 Hydrolyzes fats to glycerol and fatty acids.
 Metabolizes steroids, glucocorticosteroids,
estrogen, testosterone, progesterone, and
aldosterone.

 The
liver produces and synthesizes most of
the bodies clotting factors like prothrombin,
fibrinogen, Factor 5,7,9, and 10.
 Anti-coagulant
heparin and vasopressor
substances after hemorrhage.
 Mechanisms






of detoxification include:
Reduction
Hydrolysis
Conjugation
Oxidation
Excretion
Degradation
 Phagocytosis
of viruses, bacteria, dyes, and
foreign proteins also occurs in detoxification.
 Vitamins

A, B, C, D, E, and K
Minerals copper and iron.
A
liver disease that is characterized
pathologically by loss of the normal
microscopic lobular architecture, with
fibrosis and nodular regeneration.
1.
Alcoholic cirrhosis



Up to 50% of adult cases of cirrhosis are alcohol
related
Liver is enlarged and there is altered lipid
metabolism causing fatty infiltration.
Treatment includes abstinence, counseling, and
high-caloric nutrient dense diet.
2. Immune-related bile duct injury


Primary Biliary Cirrhosis (PBC) - Inflammation of the
bile ducts of the liver, which eventually blocks the
flow of bile. This obstruction damages liver cells and
leads to cirrhosis.
Primary Sclerosing Cholangitis (PSC) – A rare and
serious condition in which inflammation involves the
entire biliary tract; often related to GI or biliary
tract infection.
3. Postnecrotic cirrhosis

May be related to hepatitis, infection, metabolic
liver disease, or hepatotoxins or industrial chemicals.
 History
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
symptoms of Cirrhosis
Weight loss
Anorexia
Abdominal pain
Red spider veins under skin
Ascites
Itching especially of hands and feet at first
Bruising
Jaundice
Mental confusion
Difficulty concentrating


Abnormally increased blood pressure in the portal
venous system.
Signs and Symptoms include:
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
Melena
Hematoemesis
Jaundice
Peripheral edema
Palmar erythemia
Bleeding tendencies
Fetor hepaticus – sweet and fetid breath odor
Spleenomegaly
Varicies
Dilated abdominal veins
Spider nevi
Venous patterns on flanks
 The
goal of treatment for portal hypertension is
to divert blood flow around the liver and away
from collateral vessels.
 Treatment options include
1.
2.
3.
4.
5.
Portacaval shunt
Splenorenal shunt
Mesocaval shunt
Transjugular intrahepatic portosystemic shunt
(TIPS)
Vasoconstriction Medications: Somatostatin,
Octreotide, Nitroglycerin, Vasopressin, and
Terlipressin.
 The
effusion and accumulation of serous fluid
in the abdominal cavity
 Causes:

Portal hypertension, cancer, cardiac failure,
pancreatic causes, trauma
 Treatment:



Sodium restriction, diuretics, bed rest.
Peritoneal jugular shunt
Paracentesis.
A
syndrome characterized by functional renal
failure, oliguria, and low urinary sodium
concentration, without pathological renal
changes.
 Associated with cirrhosis and ascites or with
obstructive jaundice.
 Management is to diagnosis, remove cause, treat
factors known to cause the renal failure.
 High calorie, low protein, low sodium diet.
 Fluid challenge may help.
 Dialysis
 Liver transplant
A
condition usually occurring secondary to
advanced liver disease.
 Stage 1 – mild confusion, mood changes, sleep
disturbance, mild acterixis(rapid wrist flap)
 Stage 2 – confusion, apathy, obvious asterixis,
personality changes, disorientation, apraxia.
 Stage 3 – sever confusion, incoherence,
hyperactive deep tendon reflexes, muscular
rigidity
 Stage 4 – No reaction to stimuli, no corneal
reflex, dilated pupils, flexion or extension
posture, coma.
 Treatment
may include correcting pH and
electrolyte imbalances, restricting dietary
protein, removing excess protein from gut,
preventing constipation, and preventing GI
bleed so that protein does not get in bowel
to be absorbed.
 Treatment can include medications like
lactulose which causes osmotic diarrhea
which will promote excretion of ammonia
and proteins through GI tract.
 Antibiotics such as Metronidazole, Xifaxan or
Rifaximin may decrease the number of
bacteria that breakdown amino acids.
 Inflammation
of liver
 See chart for description of each type,
Hepatitis A,B,C,D,E,F, and G.
 Inflammation
of liver due to alcohol
consumption.
 Symptoms include: RUQ abdominal pain,
fever, vomiting, anorexia, and dark urine.
Patients do not present with jaundice.
 Signs include tender liver, spleenomegaly,
signs of chronic alcohol abuse, cirrhosis, and
mental status changes.
 Treatment includes supportive care,
counseling, abstinence from alcohol.
 Drugs
can cause hepatic injury including

Dose-related hepatotoxic reaction (Tylenol,
methotrexate, carbon tetrachloride)

Non-dose related viral-like hepatitis(Isoniazid,
Flurazepam, Methyldopa, I.V. tetracycline)

Cholestasis due to drugs like birth control pills.
 Massive
liver cell death
 Cause include poisoning, infectious disease,
ischemia, cyanotic heart, severe asphyxia,
cardiomyopathy, shock, metabolic disease.
 Sx’s – jaundice, flu like symptoms, fever,
anorexia, vomiting, abdominal pain,
confusion, coagulopathy, ascites, coma
 Rare
condition characterized by an
obstruction of the hepatic venous outflow.
 Causes include: malignancy, thrombogenic
disorders, inflammation disorders, and
hormone disorders.
 Diagnostic imaging is used to confirm.
 Treatment is based on cause and include:
anticoagulation, angioplasty, TIPS procedure
and liver transplant.
 NAFLD
is any liver condition arising without
association of alcohol exposure.
 Non-Alcoholic Steatohepatitis or NASH is
stage 3 and 4 of NAFLD and is detected by
ultrasound and diagnosed by liver biopsy. It is
fat accumulation in the liver.
 Risk factors – obesity, type 2 diabetes and
hyperlipidemia.
 Treatment for NASH can include weight loss
and exercise.
 Benign
vs. malignant
 Most benign liver tumors are hemangiomas
which rarely require any form of treatment.
 Hepatocellular carcinoma is the most
common primary malignant tumor of the
liver.
 Risk factors for HCC include: HBV carriers,
HBV cirrhosis, HCV cirrhosis, cirrhosis from
hemochromatosis, PBC, cirrhosis from autoimmune hepatitis, PSC, or repeated dietary
exposure to aflatoxin B1.
 Autosomal-recessive
disorder
 Inability to metabolize copper
 (Kayser-Fleischer ring) a pigmented ring at
the outer margin of the cornea is the most
unique sign
 Cirrhosis of the liver, liver necrosis,
dementia, brain damage and kidney failure
are among the advanced symptoms of the
disease.

Any of a group of disturbances of porphyrin metabolism,
characterized by marked increase in formation and
excretion of porphyrins or their precursors.
Acute intermittent porphyria (AIP)-autosomal dominant, most
do not develop symptoms, high intake of glucose or
carbohydrates causes disease suppression. Monitor H2O and
sodium intake during an attack
 Hereditary coproporphyria (HCP)- characterized by large
amounts of coproporphyrin III in the feces and lesser amounts
in urine. Photosensitivity. Monitor H2O and sodium intake
during an attack.
 Variegate porphyria (VP)-autosomal dominant, characterized
by large amounts of coproporphyrin in the feces and urine.
Photosensitivity.
 Porphyria cutanea tarda (PCT)-hereditary or acquired,
characterized by chronic skin lesions especially on light
exposed skin, increased hair growth, and mild liver disease
with fatty infiltration, focal necrosis.

A
disorder of iron metabolism characterized
by excess deposition of iron in the tissues
 Sx’s -bronze pigmentation of the skin,
weakness, weight loss, malaise, joint pain,
symptoms related to diabetes, loss of hair,
congestive heart failure.


Primary – Inherited – recessive gene
Secondary – Acquired during life
 Diagnosis
includes elevated serum ferritin,
elevated serum iron, hereditary
hemochromatosis DNA mutation analysis, MRI
and liver biopsy.
 Treatment includes: Therapeutic phlebotomy
and Deferoxamin which binds with iron in the
bloodstream and enhances its elimination via
urine and feces.
 Intrahepatic
biliary dysplasia (IHBD) or
Alagille syndrome is a rare autosomaldominant liver disease that incorporates a
combination of anomalies in conjunction
with chronic cholestasis.
 Biliary
atresia - Rare condition in newborn
infants in which extrahepatic duct is blocked
or absent.
 Kasai (hepatoportoenterostomy) procedure
allows for excretion of bile from the liver
into the intestine via a surgically created
duct, not a cure.
 Biliary atresia is the most common indication
for liver transplant in infants.
 Inflammation
of the liver which occurs in
early infancy. 20% due to viruses including
CMV, rubella, and hepatitis A, B, or C.
 Common
and benign congenital disorder
 Characterized by elevation in unconjugated
bilirubin
 All other liver tests are normal
 Rarely develop jaundice
 The
severity of chronic liver disease is
determined by the Model for End Stage Liver
Disease (MELD) score. Based on serum
bilirubin, INR, and creatinine.
 UNOS
A
has made modifications to the score
quick reference site to calculate MELD
scores and 90 day survival rates is
http://www.mayoclinic.org/meld/mayomode
l5.html
Liver Puzzle
 Cells
remove amino acids, nutrients, sugars,
broken down RBC’s, bacteria, and debris
from the blood.
Liver Puzzle
 Most
vascular organ of the body.
Liver puzzle
 Secreted
from the liver
Liver Puzzle
 Transmitted
food.
by the ingestion of contaminated
Liver Puzzle
 Most
common cause of Cirrhosis
Liver Puzzle
 Vascular
lesion that is a presenting sign of
chronic liver disease
Liver Puzzle
 Rare
condition characterized by an
obstruction of the hepatic venous outflow
Liver Puzzle
 Autosomal
recessive trait in which pt can not
metabolize copper
Liver Puzzle
 Disorder
of iron metabolism
Liver Puzzle
 Developmental
bile duct disorder in infants
that results in obstruction of the bile flow
through the extrahepatic duct system
Liver Puzzle
 Protein
produced by the liver converted by
thrombin into fibrin during blood coagulation
in presence of ionized calcium.
Liver Puzzle
 Study
of the liver.