Page 184 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Liver Failure (see also p.170ff.)
Causes of acute liver failure (→ A) are poison- esophageal varices. The deficiency in active
ing and inflammation, for example, fulminant clotting factors, thrombocytopenia, and vari-
cholangitis or viral hepatitis (especially in ces are likely to cause severe bleeding. Final-
hepatitis B and E). The causes of chronic liver ly, portal hypertension can cause an exuda-
failure that is accompanied by fibrosis (cir- tive enteropathy. This will increase the as-
rhosis) of the liver (→ p.172) are (→ A): cites due to loss of albumin from the plasma,
– inflammation, for example, chronic per- while at the same time favoring bacteria in
sistent viral hepatitis; the large intestine being “fed” with proteins
– alcohol abuse, the most common cause; that have passed into the intestinal lumen,
– in susceptible patients, side effects of and thus increasing the liberation of ammo-
Liver – Cardiovascular causes of impairment of ve- nium, which is toxic to the brain.
drugs, for example, folic acid antagonists,
phenylbutazone;
! The hyperammonemia, which is partly re-
Stomach, Intestines, – a number of inherited diseases (→ chap. 8), memory gaps, tremor, and ultimately liver
sponsible for the encephalopathy (apathy,
nous return, for example, in right heart
coma) is increased because
failure (→ p.170)
– gastrointestinal bleeding also contributes
to an increased supply of proteins to the
for example, glycogen storage diseases,
colon;
Wilson’s disease, galactosemia, hemo-
chromatosis, α 1 -antitrypsin deficiency;
+
NH 4 )
able to convert ammonium (NH 3
to urea;
(→ p.168) for prolonged periods, for ex-
6 – intrahepatic or posthepatic cholestasis – the failing liver is no longer sufficiently
ample, in cystic fibrosis (→ p.162), a stone – the above-mentioned hypokalemia causes
in the common bile duct (→ p.164ff.), or an intracellular acidosis which activates
tumors. ammonium formation in the cells of the
The most serious consequences of liver fail- proximal tubules and at the same time
ure are: causes a systemic alkalosis. A respiratory
! Protein synthesis in the liver is reduced. component is added to the latter if the pa-
This can lead to hypoalbuminemia that may tient hyperventilates due to the encepha-
result in ascites, i.e., an accumulation of ex- lopathy.
tracellular fluid in the abdominal cavity, and Further substances that are toxic to the brain
other forms of edema (→ p. 234). Plasma vol- bypass the liver in portal hypertension and
ume is reduced as a result, secondary hyper- are therefore not extracted by it as would
aldosteronism develops causing hypokalemia, normally be the case. Those substances,
which in turn encourages alkalosis (→ A, such as amines, phenols, and short-chain fatty
left). In addition, the reduced ability of the acids, are also involved in the encephalopa-
liver to synthesize causes a fall in the plasma thy. Lastly, the brain produces “false trans-
concentration of clotting factors. mitters” (e.g., serotonin) from the aromatic
! Cholestasis occurs (→ p.168), producing amino acids, of which there are increased
not only liver damage but also aggravating amounts in plasma when liver failure occurs.
any bleeding tendency, because the lack of These transmitters probably play a part in
bile salts decreases micellar formation and the development of the encephalopathy.
with it the absorption of vitamin K from the Kidney function is impaired, giving rise to
intestine, so that γ-carboxylation of the vita- the hepatorenal syndrome (→ p.118).
min K-dependent clotting factors prothrom-
bin (II), VII, IX, and X is reduced.
! Portal hypertension develops (→ p.170)
and may make the ascites worse because of
lymphatic flow impairment. It may cause
174 thrombocytopenia resulting from spleno-
megaly, and may lead to the development of
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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