Chapter 23
The Digestive System
881
23
Tanks to these various jobs, blood leaving the liver contains
fewer nutrients and waste materials than the blood that entered it.
Te regenerative capacity of the liver is exceptional. It can
regenerate to its former size in 6–12 months even aFer surgical
removal or loss of 80% of its mass. When the liver is injured,
hepatocytes secrete
growth factors
that prompt endothelial cells
lining the sinusoids to proliferate and release other growth fac-
tors. Tese, in turn, prompt the hepatocytes to multiply and
replace dead and dying liver tissue.
Secreted bile flows through tiny canals, called
bile cana-
liculi
(kan
0
ah-lik
9
u-li; “little canals”), that run between adjacent
hepatocytes toward the bile duct branches in the portal triads
(±igure 23.25c). Although most illustrations show the cana-
liculi as discrete tubular structures (shown here in green), their
walls are actually formed by the apical membranes of adjoining
hepatocytes. Notice that blood and bile flow in opposite direc-
tions in the liver lobule. Bile entering the bile ducts eventually
leaves the liver via the common hepatic duct to travel toward
the duodenum.
Homeostatic Imbalances of the Liver
Hepatitis
(hep
0
ah-ti
9
tis), or inflammation of the liver, is most
oFen due to viral infection. So far six hepatitis-causing vi-
ruses have been identified, from A to ±. ²wo of these (HVA
and HVE) are transmitted enterically (acquired through eating
contaminated food), and the infections they cause tend to be
self-limiting. Tose transmitted via blood—most importantly
HVB and HVC—are linked to chronic hepatitis and liver cir-
rhosis (see discussion below). HVD is a mutated virus that
needs HVB to be infectious. So far, little is known about HV±.
Nonviral causes of acute hepatitis include drug toxicity and
wild mushroom poisoning.
In the United States, over 40% of hepatitis cases are due to
HVB, which is transmitted via blood transfusions, contami-
nated needles, or sexual contact. A serious problem in its own
right, hepatitis B carries with it a greater menace—an elevated
risk of liver cancer. However, childhood immunization using
vaccines produced in bacteria is sweeping the feet out from un-
der HVB, and the incidence of acute hepatitis from this strain
has fallen dramatically since its peak in 1985.
Hepatitis A, commonly called infectious hepatitis and ac-
counting for about 32% of cases, is a more benign form fre-
quently observed in day-care centers. It is transmitted via
sewage-contaminated food, raw shellfish, water, and by the
feces-mouth route, which explains why it is important for res-
taurant employees to scrub their hands aFer using the wash-
room. Te highly successful HepA vaccine helps prevent
hepatitis A infection and shedding of the virus in feces.
Hepatitis E is transmitted in a way similar to hepatitis A. It
causes waterborne epidemics, largely in developing countries,
and is a major cause of death (up to 25%) in pregnant women. It
is relatively insignificant in the United States.
Hepatitis C has emerged as the most important liver disease
in the United States because it produces persistent or chronic
liver infections (as opposed to acute infections). More than 4
million Americans are infected and over 10,000 die annually
due to sequels of HVC infection. However, the life-threatening
C form of hepatitis is now being successfully treated by com-
bination drug therapy entailing weekly injections of interferon
and ribavirin (Rebetol), an oral antiviral drug.
Cirrhosis
(sĭr-ro
9
sis; “orange colored”) is a progressive
chronic inflammation of the liver that typically results from
severe chronic hepatitis or chronic alcoholism. Te damaged
hepatocytes regenerate, but the liver’s connective (scar) tissue
regenerates faster. As a result, the liver becomes fatty and fi-
brous, depressing its activity. Te scar tissue obstructs blood
flow throughout the hepatic portal system, causing
portal
hypertension
.
Some veins of the portal system anastomose with veins that
drain into the venae cavae (
portal-caval anastomoses
). However,
these connecting veins are small and tend to burst when forced
to carry large volumes of blood. Signs of their failure include
vomiting blood, and a snakelike network of distended veins
surrounding the navel. Tis network is called
caput medusae
(kap
9
ut mĕ-du
9
se; “medusa head”) aFer a monster in Greek my-
thology whose hair was made of writhing snakes. Other compli-
cations due to portal hypertension include esophageal varices
(swollen veins in the esophagus) and ascites (accumulated fluid
in the peritoneal cavity.)
Liver transplants are the only clinically proven effective treat-
ment for patients with end-stage liver disease. Te one- and
five-year survival rate of such transplants is approximately 90%
and 75%, respectively. However, donor organs are scarce and
many patients die while waiting for a suitable organ.
Composition of Bile
Bile
is a yellow-green, alkaline solution containing bile salts,
bile pigments, cholesterol, triglycerides, phospholipids (lecithin
and others), and a variety of electrolytes. Of these,
only
bile salts
and phospholipids aid the digestive process.
Bile salts
, primarily cholic and chenodeoxycholic acids,
are cholesterol derivatives. Teir role is to
emulsify
fats—break
them down into smaller pieces and distribute them throughout
the watery intestinal contents, just as a dish detergent breaks
up a pool of fat drippings in a roasting pan. Bile salts physically
separate large fat globules entering the small intestine into mil-
lions of smaller, more accessible fatty droplets that provide large
surface areas for the fat-digesting enzymes to work on. Bile salts
also facilitate fat and cholesterol absorption (discussed later). In
addition, they help solubilize cholesterol, both that contained in
bile and that entering the small intestine in food.
Many substances secreted in bile leave the body in feces, but
bile salts are not among them. Instead, a recycling mechanism
called the
enterohepatic circulation
conserves bile salts. In this
process, bile salts are (1) reabsorbed into the blood by the ileum,
(2) returned to the liver via the hepatic portal blood, and then
(3) resecreted in newly formed bile. Tis pool of bile salts recir-
culates two or three times for a single meal.
Te chief bile pigment is
bilirubin
(bil
0
ĭ-roo
9
bin), a waste prod-
uct of the heme of hemoglobin formed during the breakdown of
worn-out erythrocytes (see Chapter 17). Te globin and iron parts
of hemoglobin are saved and recycled, but bilirubin is absorbed
from the blood by liver cells, excreted into bile, and metabolized
in the small intestine by resident bacteria. One of its breakdown
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