2. • HEPATIC FAILURE is the
pathological state when one
(several) or all liver functions get
lower than the level which is
necessary to provide the
homeostasis of the organism in
accordance with their necessity.
3. • Classification of hepatic failure:
• absolute hepatic failure develops as a
consequence of the direct damage of the liver and
become apparent under the ordinary condition;
• relative hepatic failure develops as a
consequence of the increase loading on the liver;
• Partial;
• Total;
• Acute;
• Chronic;
4. • Depending on the pathogenesis:
• 1. hepatocellular failure develops
under the direct damage of the liver.
• Reasons: physical, biological
(viruses of viral hepatitis, pathogen of
tuberculosis, syphilis, fungi, lamblia,
amoeba, helminth (echinococcus,
ascarid); chemical (alcohol, medicines —
sulphanilamides, tetracycline,
cytostatics, some antibiotics; carbon
tetrachloride, arsenic, insecticides)
Mechanism: 1- direct cytototoxic
action; 2- autoantibodies
production to the changed
hepatocytes;
5. 2. cholestatic failure develops as a
result of the disturbance of bile
forming and bile excretion;
• Cholestasis — the disturbance
of the bile outflow.
• Reasons inflammation or
dyskinesia in bile-excreting tract,
• parasites in the gallbladder,
• tumors of the head of pancreas;
• Mechanism: 1- mechanical action of the
bile on the hepatocytes which leads to
their damage; 2- toxic action of the
bile on the mitochondrion which leads
to the ATP deficit and dystrophy of
hepatocytes;
6. 3. vascular failure develops as a result
of the disturbance of blood circulation
in the liver.
• Reasons for the vascular failure
are: portal hypertension and
ischemia of the liver.
• The main mechanism of the liver
damage is hypoxia.
7. • Signs of hepatic failure
• I. A disturbance of carbohydrate
metabolism - decrease of abilities of
hepatocytes to convert glucose into
glycogen and split glycogen to
glucose. After meal hyperglycemia
develops and on an empty stomach —
hypoglycemia.
• II. A disturbance of lipid
metabolism and atherosclerosis
development.
8. • II. A disturbance of protein
metabolism:
• reduction of synthesis of albumins
of hepatocytes, that leads to
hypoonkia and ascites;
• decrease of biosynthesis of
protocoagulants (prothrombin,
fibrinogene), that causes bleeding.
9. • III. A disorder of vitamin metabolism
consists in:
• reduction of internal absorption of fat-
dissolved vitamins A, D, E, K;
• decrease of ability of hepatocytes to
convert provitamins into active vitamins
(e. g. carotene into vitamin A);
• disturbance of process of formation of
cofactors from vitamins
• hypovitaminosis.
10. • IV. reduction of intensity of
desamination of aminoacids leads to
decrease of urea in blood.
• V. A disturbance of antitoxic ("barrier")
function of the liver is characterized by
accumulation of internal poisons — phenol,
indol, skatol which have cerebrotoxic
action. The outcome of progressive hepatic
insufficiency is hepatic coma.
11. • HEPATIC COMA
• Hepatic coma is a syndrome,
caused by a toxical damage of the
CNS with profound disorders of its
functions (loss of consciousness,
absence of reflexes, cramps, a
disturbance of blood circulation,
and respiration).
• They are two variants of hepatic
coma:
• 1. shunt
• 2. hepatic-cellular.
12.
13. • The cerebrotoxic substances are:
• ammonia,
• the products of the oxidation in
intestine (e.g., cadaverin, putrescine,
phenol, indole, skatole;
• derivative substances from lactic acid
and pyruvic acid;
• Low-molecular fat acids.
14. Hepatocellular Coma
• Hepatocellular coma appears in massive necrosis
of the hepatic parenchyma, when it’s homeostatic
and barrier functions are decreased.
• The main links of pathogenesis of the Hepatic
Coma are:
• disturbance of the synaptic transmission in the
CNS due to cerebrotoxic substances
accumulation;
• disturbance of the energy metabolism which leads
to ATP deficit due to ammonia accumulation and
Krebs cycle [tricarbonic acid cycle] disturbance;
• disturbance of the cells membrane functions due
to the direct cerebrotoxic substances action;
• Metabolic acidosis development due to lactic acid
and pyruvic acid accumulation;
15. • JAUNDICES
• Jaundice is a syndrome, which appears
due to increase of bilirubin content in
blood and is characterized by yellow
coloring of the skin, mucous membranes,
sclerae.
20. Hemolytic Jaundices -
The cause of is
excessive
destruction of
erythrocytes! Feces
hypercholic because
of the ↑ ofthe
conjugatedbilirubin!
(dark brown or black
) (yellow urine - ↑
urobiline)!! Blood - ↑
unconjugatedbilirubin!
21. • Mechanical Jaundice
• Reasons:
• the stones, inflammatory, tumors of
the bile-excreting tracts,
• parasites in the gallbladder,
• tumors of the head of pancreas;
22. • Cholemia is a complex of disturbances,
which are conditioned by appearance of
bile components in blood and mainly of
bile acids.
• Yellow coloring of the skin, scleras is
provoked by increase of the level of
conjugated bilirubin in the blood.
! Feces acholic because
of the absents of the bile
inthe intestine!
Brown urine -
unconjugated bilirubin!
! Blood - ↑ conjugated
bilirubin!
23. • Hepatic Jaundice (parenchymatous
• Parenchymatous jaundice appears as a
result of:
• a direct damage of the hepatic tissue by
agents viruses, bacteria and their toxins,
malaria plasmodium and others;
• organic and inorganic poisons, e.g.,
tetrachloride hydrocarbon, high doses of
alcohol; hepatotropic antibodies and
sensitized lymphocytes; tumors and
others).
24. • The manifestations of disturbances of
hepatic functions depend on the degree of
damage and mass of impaired hepatocytes.
• high level of hepatic transaminases in
blood (ALT, AST), which easily penetrate
through the damaged cellular membrane.
» ! Feces hypocholic because of the
derease ofthebile andconjugated
bilirubininthe intestine!
» Brown urine - unconjugated bilirubin!
» ! Blood - ↑ conjugated and
unconjugated bilirubin!
