Typical disorders of the liver 1. Secondary liver failure develops in a

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Typical disorders of the liver
1. Secondary liver failure develops in
a) the action of carbon tetrachloride
+ b) circulatory failure
c) phosphoric intoxication
d) viral hepatitis
e) Chronic alcohol intoxication
2. Primary liver failure develops in
a) Heart Failure
b) Shockt
c) Renal insufficiency
+ d) viral infection of the liver
e) diabetes mellitus
3. Manifestations of liver failure include:
+ a) Increasing the concentration of ammonia in the blood
+ b) Hypoproteinemia
c) decrease in the activity of ALT and AST in the blood
+ d) Bleeding
e) Dehydration
4. Violation of protein metabolism in hepatic failure are characterized by:
a) hyperproteinemia; + b) hypoproteinemia; + c) hyperasotemia;
+ d) hypoprotrombinemia; + e) hyperaminoacidemia.
5. Accumulation of ammonia in hepatic failure especially toxic to
a) the abdominal cavity; b) skin; c) muscles; d) bone; + e) of the central nervous system.
6. Disorders of carbohydrate metabolism in liver failure is characterized by
+ a) inhibition of gluconeogenesis; b) inhibition of the synthesis of ketone bodies; c) increased
glycogen synthesis; d) increased conversion of galactose and fructose to glucose.
7. Disorders of lipid metabolism in hepatic failure are characterized by
+ a) a decrease in the formation of phospholipids; b) a decrease in the formation of ketone
bodies; c) increased oxidation of fatty acids; d) an increase in the synthesis of high-density
lipoprotein; e) increasing release of triglycerides from the liver to the intestine.
8. Hypocoagulation in hepatic failure is caused by:
+ a) malabsorption of vitamin K; + b) violation of the synthesis of fibrinogen;
+ c) violation of the synthesis of prothrombin; d) impaired synthesis of antithrombin III;
e) violation of the synthesis of protein C and S.
9. Pathogenesis of hepatic coma significant dose:
+ a) Lack of neutralizing function of the liver
+ b) Metabolic acidosis
+ c) Lack ureaformation liver function
d) Increase in blood direct bilirubin
e) Hyperglycemia
10. Jaundice - is
a) sickness; b) symptom; + c) syndrome; d) pathological reaction; e) pathological state.
11. Causes hemolytic jaundice include:
+ a) Action hemolitic poisons
+ b) Rhesus conflict between maternal and fetal body
+ c) incompatible blood transfusion
d) hemorrhagic anemia
e) gallbladder dyskinesia
12. Main link of the pathogenesis of hemolytic jaundice
a) dehydration; b) heart failure; c) insulin deficiency; d) violation of the outflow of bile;
+ e) enhanced hemolysis.
13. Hemolytic jaundice is characterized by
+ a) increase in free bilirubin in the blood; b) increase of conjugated bilirubin in the blood;
c) discoloration of feces; d) violation of digestion in the intestine; e) excretion of free bilirubin in
the urine.
14. For hemolytic jaundice characterized by an increase in blood
+ a) indirect bilirubin
b) direct bilirubin
c) urobilin
d) stercobilin
e) bile acids
15. General pathogenesis obstructive jaundice is
a) Damage to hepatocytes
b) sialolithiasis
c) Urolithiasis
d) Reinforced hemolysis
+ e) Disturbance of the outflow of bile
16. Show causes of obstructive jaundice
+ a) Obturation hepatic and common bile duct
b) hemolysis
17. Is observed in obstructive jaundice:
+ a) Hypotension
+ b) bilirubinuria
+ c) Acholia
+ d) Itching
e) Tachycardia
18. Obstructive jaundice is characterized by an increase in blood
a) biliverdin
b) sterkobilinogen
c) urobilinogen
+ d) direct bilirubin
e) indirect bilirubin
19. Obstructive jaundice is characterized by:
+ a) hyperbilirubinemia; b) the increased activity of ALT and AST; + c) cholemia;
+ d) bilirubinuria; e) light urine.
20. Specify the changes in blood and urine when obstructive jaundice
+ a) cholemia, appearance of direct bilirubin in the blood, absence of urobilin in the urine;
b) increase in indirect bilirubin in the blood, urobilin in the urine.
21. Syndrome of cholemia is caused by the pathogenic action of
a) cholesterol; b) direct bilirubin; c) indirect bilirubin; d) fatty acids; + e) bile acids.
22. Cholemia is characterized by:
+ a) bradycardia; b) tachycardia.
23. Cholemia is characterized by:
+ a) lowering blood pressure; + b) appearance of skin itching; + c) bradycardia; d) tachycardia;
e) hypertension.
24. The presence of bile salts in the blood causes
a) increase in blood pressure; + b) bradycardia; c) tachycardia; d) increase in body temperature;
e) shortness of breath.
25. Acholia - is the lack of bile
a) in the blood; b) in the urine; + c) in the intestine; d) in the cerebrospinal fluid; e) in lymph.
26. For acholia is typical
a) activation of the emulsification of fat in the intestine; b) hypervitaminosis of fat-soluble
vitamins; c) increased cleavage and absorption of the fat; + d) steatorrhea; e) the dark color of
feces.
27. Steatorrhea when obstructive jaundice is associated with
+ a) malabsorption of fats in the intestine; b) activation of pancreatic lipase; c) hereditary
fermentopathy; d) activation of lipolysis; e) the development of primary malabsorption.
28. Bleeding during prolonged obstructive jaundice is caused by
a) violation of the synthesis of heparin; + b) violation of the synthesis of prothrombin due to
lower absorption of vitamin K; c) violation of the synthesis of inhibitors of fibrinolysis;
d) violation of the synthesis of antithrombin; e) violation of the synthesis of kallikrein.
29. Parenchymal jaundice is characterized by:
+ a) urobilinogenemia; b) decrease in the activity of AST and ALT in the blood; + c) cholemia;
d) hyperglycemia; + e) hypocholia.
30. Hyperbilirubinemia, which accompanied by increased levels of both free and
conjugated bilirubin in the blood is observed at
a) cholecystitis; b) sickle cell anemia; + c) Botkin's disease; d) cholangitis; e) insulinoma.
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