hepatobiliary system. anatomy, histology, and physiology
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HEPATOBILIARY SYSTEM
ANATOMY
The liver is the second largest organ of the body, weighing 1200 to 1500 grams, or 4-5% of
body weight. It is located in the right upper abdominal quadrant, or the right hypochondriac and
epigastric regions, behind the lower ribs. The falciform ligament divides the liver anatomically
into two unequal lobes: right and left. Two additional smaller lobes, the quadrate and caudate
lobes are more visible in cross section. Physiologically though, the division is equal, following
the fossa for gall bladder and inferior vena cava. There is no evidence for difference in functions
among the four anatomical lobes.
The gall bladder is a saccular organ located
posterior to the liver that functions to store
bile. It has a mean capacity of 30-50 mL.
Mucosal folds, called the spiral valves of
Heister, maintain patency of the cystic duct
to allow passage of bile. Presence of fats in
the duodenum stimulate the gall bladder to
contract.
HISTOLOGY
The liver is histologically arranged into hexagonal lobules, which are primarily formed by
hepatocytes, the liver’s specialized epithelial cells that make up 80% of the liver parenchyma.
Each lobule is centered on a hepatic venule (central vein) and the hepatocytes are separated by
sinusoids into hepatic cords. Portal triads are located on the edges of the hexagonal lobules,
enclosed by connective tissues, and contain three important structures:
a. Hepatic artery that bring 25% of the total
blood into the liver
b. Portal veins that carries the other 75% of
portal blood from the lower digestive tract,
and
c. Bile ducts
Apical membranes of adjoining hepatocytes form the canalicular lumen; while the basolateral
membranes do not have direct contact. Rather, there is a space between the basolateral
membrane and the endothelial cells of the sinusoid, the space of Disse (perisinusoidal space).
Microvilli of hepatocytes extend towards the sinusoidal blood for vector transport. Thus,
hepatocytes act as a functional barrier between the canalicular lumen and the sinusoid to allow
transfer of solutes between bile and blood. Communication between hepatocytes is made
possible via tight and gap junctions and desmosomes. It is important to note that there is a
relatively small amount of connective tissues maintaining the structure of the liver; there is no
basement membrane.
There are four types of cells that make up the liver. Hepatocytes make up the bulk of the liver
parenchyma. Endothelial cells line the sinusoids and form fenestrations to control the entry of
plasma solutes and keep out red blood cells. Kupffer cells are the liver’s macrophages that lie
within the sinusoidal vascular space. Lastly, stellate or Ito cells contain large fat droplets in their
cytoplasm and form the storage of retinoids. They can transform into proliferative, fibrogenic,
and contractile myofibroblasts upon proper stimulation.
It has been noticed that the liver is functionally divided into zones. Periportal hepatocytes of
zone I reside close to the terminal portal venule and terminal hepatic arteriole. The high nutrition
and oxygen concentration microenvironment allows zone I cells to function for oxidative energy
metabolism with beta oxidation, amino acid metabolism, ureagenesis, gluconeogenesis,
cholesterol synthesis, and bile formation. They are thus the most resistant to circulatory demise
and nutritional deficiency and are the first to regenerate after a disease process. Zone III cells
are the most distal, or pericentral. Glycogen synthesis from glucose, glycolysis, liponeogenesis,
ketogenesis, xenobiotic metabolism, and glutamine formation are their primary functions.
Specialization of functions occurs because of adaptation to microenvironment. If the direction of
blood supply is reversed, zones will also be reversed.
Blood Supply To Liver
The liver receives blood from two sources: oxygenated arterial blood from the hepatic artery,
and portal blood draining from the lower GI via the portal vein. The two vessels drain into
hepatic sinusoids and then flow towards the central vein. Small central veins come together to
form three hepatic veins that return blood to the heart through the inferior vena cava.
Blood Supply To Bile Ducts
The right hepatic artery supplies the bile ducts by dividing into a rich capillary plexus that would
drain into the sinusoids. Hepatocytes then act for the bidirectional exchange of compounds
between bile and blood.
Biliary Flow
Bile is synthesized and secreted by hepatocytes into the canaliculi. Afterwhich, bile flows into
progressively larger ducts until bile reaches the duodenum via the greater duodenal papilla (of
Vater):
Terminal ductules (canals of Hering), surrounded by 3-6 ductal epithelial cells
perilobular ducts interlobular bile ducts surrounding portal vein septal ducts lobar
ducts 2 hepatic ducts common hepatic duct + cystic duct common bile duct +
pancreatic duct ampulla of Vater
LIVER CIRRHOSIS
Cirrhosis occurs as a result of progressive liver injury that involves inflammation and scarring of
the intrahepatic tissues. The liver presents histologically as a hard, shrunken and nodular tissue,
and many hepatocytes are replaced with connective tissues. As long as the normal architecture
of the liver is not lost, cirrhosis may still be reversed when the causative factors are withdrawn.
Chronic alcohol intake, viral infections, biliary stasis, and genetic defects can cause cirrhosis, or
it may also develop as a complication of other diseased organ systems like the heart.
Symptoms mainly arise from the decreased functional hepatocyte mass and the impairment of
normal blood circulation. The pattern of fibrosis can be centrilobular, pericellular, or periportal
and the zoning of hepatocytes are particularly important in the course of symptoms. Periportal
hepatocytes of zone I are most resistant to poor oxygenation and nutrition; while zone III
hepatocytes that function for glycolysis, liponeogenesis, ketogenesis, xenobiotic metabolism,
and glutamine formation are the first to be impaired by alcohol. As the disease progresses,
symptoms of impaired zone I functions, such as oxidative energy metabolism with beta
oxidation, amino acid metabolism, ureagenesis, gluconeogenesis, cholesterol synthesis, and
bile formation appear.
Pathogenesis
Fibrogenesis occurs when the fat-storing Ito cells are stimulated to produce connective tissues
and may be induced after an immune attack or during wound healing secondary to the release
of cytokines. The first occurs in HBV infection and schistosomiasis, while wound healing occurs
after Hepatitis A lesions. Fibrosis-inducing agents, like ethanol and iron, may also directly trigger
this response by increasing gene transcription of collagen or other connective tissues. Histologic
studies would initially yield a denser and non-cross-linked extracellular matrix. In the second
and irreversible stage, the liver would appear nodular and distorted with subendothelial collagen
cross-links and abundant myoepithelial cells. Alcoholic cirrhosis is typically micronodular with
<3mm in diameter. Characteristic Mallory bodies, which are cytokeratin residues, are seen in
hepatocytes.
Epidemiology
Chronic liver disease ranks as the 10th most common cause of deaths among adults in the
United States, 40% of which are due to liver cirrhosis. In the Philippines, as high as 80% of liver
cancers are preceded by cirrhosis, where liver cancer is the second leading cause of cancer-
related deaths in males.
Heavy drinkers and alcoholics may progress from fatty liver to alcoholic hepatitis to cirrhosis,
and it is estimated that 10 to 15 percent of alcoholics will develop cirrhosis. The severity of
alcoholic liver disease is directly related to the amount of daily alcohol intake and the duration of
alcohol abuse. Mortality rates in males are twice higher than in females due to the higher
amount of alcohol intake and because alcohol abusers are more common among males than
females. However, at any amount of alcohol, women have a higher risk of developing cirrhosis.
The underlying mechanism to this disparity is still unresolved.
Mallory BodyDense extracellular matrix
Lymphocytic infiltration
Fatty Deposits
Figure __. Normal liver
Figure __. Liver Cirrhosis. Perivenular polymorphonuclear infiltrate and ballooning degeneration of hepatocytes
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