Page 180 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Portal Hypertension
Venous blood from stomach, intestines, from abdominal organs via vascular channels
spleen, pancreas, and gallbladder passes via that bypass the liver. These portal bypass cir-
the portal vein to the liver where, in the sinu- cuits (→ A3) use collateral vessels that are
soids after mixture with oxygen-rich blood of normally thin-walled but are now greatly di-
the hepatic artery, it comes into close contact lated (formation of varices; “haemorrhoids”
with the hepatocytes (→ A1). About 15% of of the rectal venous plexus; caput medusae
cardiac output flows through the liver, yet at the paraumbilical veins). The enlarged
its resistance to flow is so low that the nor- esophageal veins are particularly in danger
mal portal vein pressure is only 4–8 mmHg. of rupturing. This fact, especially together
If the cross-sectional area of the liver’s with thrombocytopenia (see above) and a de-
Liver vascular bed is restricted, portal vein pres- ficiency in clotting factors (reduced synthesis
in a damaged liver), can lead to massive
sure rises and portal hypertension develops.
Stomach, Intestines, the following vascular areas, although strict tension (glucagon, VIP, substance P, prostacy-
Its causes can be an increased resistance in
bleeding that can be acutely life-threatening.
The vasodilators liberated in portal hyper-
separation into three forms of intrahepatic
clins, NO, etc.) also lead to a fall in systemic
obstructions is not always present or possi-
blood pressure. This will cause a compensa-
ble:
thrombosis
vein
tory rise in cardiac output, resulting in hyper-
! Prehepatic:
portal
! Posthepatic: right heart failure, constric-
collateral (bypass) circuits.
tive pericarditis, etc. (→ A2 and p. 228);
Liver function is usually unimpaired in
6 (→ A2); perfusion of the abdominal organs and the
! Intrahepatic (→ A1): prehepatic and presinusoidal obstruction,
– presinusoidal: chronic hepatitis, primary because blood supply is assured through a
biliary cirrhosis, granuloma in schistoso- compensatory increase in flow from the he-
miasis, tuberculosis, leukemia, etc. patic artery. Still, in sinusoidal, postsinusoi-
– sinusoidal: acute hepatitis, damage from dal, and posthepatic obstruction liver dam-
alcohol (fatty liver, cirrhosis), toxins, amy- age is usually the cause and then in part also
loidosis, etc. the result of the obstruction. As a conse-
- postsinusoidal: venous occlusive disease quence, drainage of protein-rich hepatic
of the venules and small veins; Budd– lymph is impaired and the increased portal
Chiari syndrome (obstruction of the large pressure, sometimes in synergy with a re-
hepatic veins). duction in the plasma’s osmotic pressure
Enlargement of the hepatocytes (fat deposi- due to liver damage (hypoalbuminemia),
tion, cell swelling, hyperplasia) and in- pushes a protein-rich fluid into the abdomi-
creased production of extracellular matrix nal cavity, i.e., ascites develops. This causes
(→ p.172) both contribute to sinusoidal ob- secondary hyperaldosteronism (→ p.174) that
struction. As the extracellular matrix also results in an increase in extracellular vol-
impairs the exchange of substances and gas- ume.
es between sinusoids and hepatocytes, cell As blood from the intestine bypasses the
swelling is further increased. Amyloid deposi- liver, toxic substances (NH 3 , biogenic amines,
tions can have a similar obstructive effect. Fi- short-chain fatty acids, etc.) that are normal-
nally, in acute hepatitis and acute liver ne- ly extracted from portal blood by the liver
crosis the sinusoidal space can also be ob- cells reach the central nervous system,
structed by cell debris. among other organs, so that portalsystemic
Consequences of portal hypertension. (“hepatic”) encephalopathy develops (→
Wherever the site of obstruction, an in- p.174).
creased portal vein pressure will lead to dis-
orders in the preceding organs (malabsorp-
170 tion, splenomegaly with anemia and throm-
bocytopenia) as well as to blood flowing
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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