77. Hepatic failure hepatic-vascular form.

Hepatic-vascular insufficiency – is developed as a result of irculation primary disorders in liver. Hypoxy is major mechanism of hepatocytes injury.

2 the most often reasons:

1. portal hypertension;

2. liver ishemia.

Experimental models:

1. porto-caval amastomoses (Ekk’s and Ekk-Pavlov’s fistule);

2. portal vein ligating;

3. hepatic veins ligating;

4. hepatic artery ligating.

78. Liver excretory function disorders. Jaundices. Liver functions

1. Central organism organ = 2/3 of all metabolism.

2. Homeostatic – liquids biochemical indexes constant level supporting.

3. Metabolic – central organ in all metabolism types.

4. Excretory – hydrophobic substances releasing with bile through alimentary tract.

5. Desintoxicational.

6. Key organ in pigment metabolism.

7. Blood depot: blood accumulation in sinuses prevents hypotension.

8. Haemopoietic function in course of embryogenesis.

Proteinic exchange

1. Protein-synthetic: 100% of albumines (13-18 g in day), 80% of of globulines (alpha, beta), gamma – in Kupher's cells; prothrombine; fibrinogen and other haemopoietic factors; acute-phase inflammatory proteins (adaptational function).

2. Aminoacids decomposition (transamination, desamination).

3. Choline and crreatine biosynthesis.

4. Ammonium ending desintoxication.

Carbohydrates metabolism

1. Glycostatic: glycogenogenesis, glyconeogenesis, glycogenolysis.

2. Glucuronic acid synthesis from glucose which is used in desintoxication.

3. Glucose oxidation in pentose-phosphate cycle (role: NADPH formation which is used in liver for cholesterol, fatty acids, ketonic bodies synthesis, NADPH is co-ensyme in microsomal oxidation for desintoxication; phosphopentoses i.e. rhibose is used for nucleotides synthesis and co-ensymes formation i. e. FAD, NAD, KoA).

4. Only in liver - hexoses (galactose, fructose, mannose) transformation in glucose.

Lipid metabolism

1. 80% of cholesterol is synthesized in liver.

2. Cholesterol oxidation in biliary acids and their excretion through alimentary tract.

3. Highest fatty acids (oleinic, linoic, linoleinic) synthesis.

4. Triacylglycerols biosynthesis.

5. Complicated lipids biosynthesis.

6. Ketonic bodies biosynthesis.

7. Lipids transport forms biosynthesis (very low-densed lipoproteins and high-densed lipoproteins formation).

Pigment metabolism

1. Indirect bilirubin desintoxication in direct one (by means of conjugation with UDP-glucuronate).

2. Urobilinogen retention in liver with its consequent oxidation to dipirroles and releasing with urine.

3. Bilirubin-releasing function with bile – is disturbed at liver insufficiency because of ATP amount decreasing.

Jaundices differentiated diagnosis

Index

Norm

Changing in blood

Changings in feaces

Changings in urine

Haemolytic (prehepatic) jaundice

General bilirubin	8,5-20,5 mcmol/l	increased
Indirect (non-conjugated) bilirubin	1,7-17,0 mcmol/l	Increased
Direct (conjugated) bilirubin	1,0-5,0 mcmol/l	normal
Stercobilin	40,0-280,0 mg/day (in faeces)		Increased - black faeces	Increased - black urine

Hepatic (parenchymal) jaundice

General bilirubin	8,5-20,5 mcmol/l	increased
Indirect (non-conjugated) bilirubin	1,7-17,0 mcmol/l	Increased
Direct (conjugated) bilirubin	1,0-5,0 mcmol/l	increased	grey faeces	increased
Urobilin (it is not found in urine under normalconditions)				Increased

Mechanic (obturatonal) jaundice

General bilirubin	8,5-20,5 mcmol/l	increased
Indirect (non-conjugated) bilirubin	1,7-17,0 mcmol/l
Direct (conjugated) bilirubin	1,0-5,0 mcmol/l	normal
Stercobilin	40,0-280,0 mg/day (in faeces)		is absent (acholic or colourless faeces)