Disturbance of lipids metabolism
Process of lipolysis is inhibited by:
1. insulin
2. adrenalin
3. somatotropic hormone
4. glucagon
5. thyroxin
In regulation of cholesterin synthesis by mechanism of opposite connection significant role relate to:
1. apoproteins
2. pancreatic lipase
3. bile acids
4. ketonic bodies
5. peroxide compounds
Process of fats emulsification in intestine disorder at:
1. deficiency of fatty acids in intestine
2. deficiency of bile pigments in blood
3. excess of lipase of pancreas
4. deficiency of lipase of pancreas
5. deficiency of bile acids
The most rich in cholesterin amount are lipoproteids of:
1. very high density
2. very low density
3. low density
4. high density
5. chylomicrons
Retentional hyperlipoproteidemia result from:
1. deficiency of lipase in intestine
2. deficiency of bile acids
3. increased lipids mobilization from depots
4. deficiency of lipase in blood plasma
5. excessive consumption of fats with food.
Transport hyperlipoproteidemia result from:
1. deficiency of lipase in intestine
2. deficiency of bile acids
3. increased mobilization of lipids from depot
4. deficiency of lipase in blood plasma
5. excessive consumption of fats with food
Obesity of the first degree is characterized by increment of a body mass above standard (due):
1. 10 %
2. 50 %
3. 100%
4. 30%
5. 5 %
Obesity of the second degree is characterized by increment of a body mass above standard (due):
1. 10 %
2. 50 %
3. 100%
4. 30%
5. 5 %
Obesity of the third degree is characterized by increment of a body mass above standard (due):
1. 10 %
2. 50 %
3. 100%
4. 30%
5. 5 %
Hypertrophic obesity is characterized by:
1. increase of adipocytes number
2. decrease of adipocytes number
3. increase of size of adipocytes
4. increase of size and number of adipocytes
5. decrease of size of adipocytes
The most atherogenic activity is characteristic for:
1. cholesterin LPHD
2. cholesterin LPVHD
3. cholesterin LPLD
4. cholesterin LPVLD
5. chylomicrons
Pre- lipid stage of development of an atherosclerotic patch is characterized by:
1. ulceration of patch
2. decrease of lipolytic activity of vascular wall
3. formation of detritus
4. formation of fatty strips and spots in intima layer
5. petrifaction (calcification) of patch
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Term atherocalcinosis is called:
1. ulceration of patch
2. decrease of lipolytic activity of vascular wall
3. formation of detritus
4. formation of fatty strips and spots in intima layer
5. petrifaction (calcification) of patch
Stage of atheromatosis is characterized by:
1. ulceration of patch
2. decrease of lipolytic activity of vascular wall
3. formation of detritus
4. formation of fatty strips and spots in intima layer
5. petrifaction (calcification) of patch
Stage of lipidosis is characterized by:
1. ulceration of patch
2. decrease of lipolytic activity of vascular wall
3. formation of detritus
4. formation of fatty strips and spots in intima layer
5. petrifaction (calcification) of patch
Consequence of hyperproteinemia is:
1. increase of tubular filtration in kidneys
2. aminoaciduria
3. increase of oncotic pressure in interstitium
4. decrease of tubular filtration in kidneys
5. edemas
Consequence of hypoproteinemia is:
1. increase of viscosity of blood plasma
2. edemas
3. increase of oncotic pressure of plasma
4. increase of oncotic pressure in interstitium
5. decrease of tubular filtration in kidneys
Main way of ammonia inactivation in organism is terminated by formation of:
1. creatinine
2. indican
3. urea
4. uric acid
5. creatine
Detoxication of ammonia in organism is realized by means of:
1. desalinization of aminoacids
2. synthesis of urea
3. synthesis of glycogen
4. synthesis of carbohydrates
5. synthesis of biogenic amines
Origin of albinism is linked to disturbance of metabolism of:
1. thyrosine
2. phenilalanin
3. histidine
4. methionine
5. glutamine
Change of plasma composition of proteins at acute infectious inflammatory process in lungs is manifested in:
1. increase of albumin-globulin coefficient
2. positive protein-nitrogen balance
3. increase of albumin concentration
4. appearance of C-reactive protein
5. decrease of erythrocytes sedimentation rate
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Anabolism of proteins in organism increase at:
1. stress
2. insulindepending diabetes mellitus
3. fever
4. acromegaly (excess of STH)
5. at infections and intoxications
Catabolism of proteins in organism increase at:
1. state after starvation
2. insulindepending diabeter mellitus
3. state after blood loss
4. acromegaly (excess of STH)
5. tumor of reticular zone of adrenal cortex
Going out transaminase into blood is diagnostic criterium at:
1. thyrotoxicosis
2. necrosis of separate organs (myocardium, kidneys, liver)
3. renal diabetes insipidus
4. gigantism
5. obesity
Disorder of formation and excretion of uric acid is discovered at:
1. daltonism
2. padagra
3. chronic gastritis
4. hyperthyrosis
5. hypothyrosis
Main role in synthesis of blood plasma proteins play:
1. liver
2. kidneys
3. spleen
4. gastrointestinal tract
5. parathyroid gland
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Hypoxia
Name compensatory-adaptive reaction at hypoxia:
1. Decrease of dissociation of oxyhemoglobin
2. Acceleration of respiration, intensifying of erythrogenesis, augmentation of lung ventilation
3. Retardation of circulation
4. Augmentation of dissociation of oxyhemoglobin
5. Redistribution of blood in veins, tachycardia
What factors can cause formation of methemoglobin in an organism:
1. Poisoning with oxide of Carbonum
2. Phosphoorganic materials
3. Sodium nitrats
4. Glycosides
5. Heavy metals
How the contents of Oxygen in blood changes at circulatory hypoxia:
1. In arterias remains normal, in veins is depressed
2. In arterias is reduced, in veins remains normal
3. In veins increases
4. In veins remains normal
5. In arterias is reduced, in veins is reduced
What causes can lead to development of hemic hypoxia:
1. Infringement of diffusion of Oxygen through alveolar membrane
2. Materials invoking formation of methemoglobin, anemia
3. Infringement of circulation
4. Over-dosage by barbiturates
5. Fall of tone of vessels
The listed factors result in development of circulatory hypoxia:
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1. Hemolysis of erythrocytes
2. Hypervolemia
3. Decrease of alveolar ventilation
4. Heart failure
5. Disadvantage of Ferrum in an organism
To infringements of intrinsic tissue respiration lead:
1. Disadvantage of Oxygen in inhaled air
2. Infringement of transferring of Oxygen from blood into tissue, lesion of tissue enzymes
3. Dropping рО2 in respiratory routes
4. Infringement of diffusion of О2 through alveolar membrane
5. Hemolysis of erythrocytes
What from the herein provided states can reduce affinity of hemoglobin to Oxygen and rising of dissociation of oxyhemoglobin:
1. Alkalosis gaseous
2. Drop of temperature of body
3. Metabolic alkalosis
4. Gas alkalosis, high body temperature
5. Gaseous acidosis, high body temperature
Name mechanisms of development of respiratory compensatory-adaptive reactions:
1. Activation of synthesis of nucleic acids and proteins, which lies at the basis of hypertrophy of myocardium
2. Acceleration of feedback of Oxygen by erythrocytes
3. Augmentation of lung ventilation, ventilation of additional alveoli
4. Augmentation of in blood of glucocorticoids which activate enzymes of respiratory chain and improve stability of cellular membranes
5. Tachycardia
Name mechanisms of development of long-term compensatory-adaptive reactions at hypoxia:
1. Augmentation of minute volume of heart - tachycardia
2. The activation of synthesis of nucleic acids and proteins which lies at the basis of hypertrophy of myocardium, hypertrophy of respiratory muscles
3. Augmentation of mass of circulating blood for account of entering of erythrocytes from depositions
4. Augmentation of lung ventilation
5. Augmentation of dissociation of oxyhemoglobin, rising activity of enzymatic systems
What changes in blood are characteristic for tissue hypoxia:
1. Reduction of pO2 in arterial blood
2. Decrease of oxygen capacity of blood
3. Raised contents of Oxygen in venous blood, dropping of arteriovenous difference on Oxygen
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4. Raised contents of Oxygen in arterial blood,
5. Dropped contents of Oxygen in venous blood, high arteriovenous difference on Oxygen
Name the causes invoking tissue type of hypoxia:
1. Inhalation of CO- gas
2. Collapse
3. Heart failure
4. Avitaminosis, poisoning with cyanides
5. Lesion of respiratory muscles
What factors result in development of mixed type of hypoxia:
1. Presence of exudate in pleural cavity
2. Aspiration of CO- gas
3. Traumatic shock, poisoning with Sodium nitrats
4. Avitaminosis
5. Anemia, methemoglobin- formers
Name reversible infringements at hypoxia:
1. Fatty degeneration in fibers of sceletal muscles, in myocardium
2. Degenerative changes in brain cortex
3. Necrobiosis of tissues
4. Focal hemorrhages in internal organs
5. Hypertrophy of myocardium, hypertrophy of respiratory muscles
Name irreversible infringements at hypoxia:
1. Fatty degeneration in myocardium
2. Edema of renal glomeruli
3. Degenerative changes in brain cortex, focal hemorrhages in internal organs
4. Fatty degeneration in fibers of sceletal muscles
5. Necrobiosis of tissues
Tissue hypoxia can arise owing to:
1. Disadvantage of СО2
2. Disadvantage of proteins
3. Rising functional activity of respiratory enzymes
4. Decrease of coupling of oxidation and phosphorilation, poisoning with cyanides
5. Aspiration of CO gas
For respiratory hypoxia is characteristic:
1. Dropping of oxygenous capacity of blood
2. Hypoxemia, hypercapnia
3. Rising arterio-venous difference on Oxygen
4. Hypocapnia
5. High contents of Oxygen in venous blood
For circulatory hypoxia is characteristic:
1. Dropping oxygenous capacity of blood
2. Rising of pO2 in veins
3. High arterio-venous difference on O2
4. Dropping a partial strain of Oxygenium in an arterial blood
5. Augmentation of amount of erythrocytes
What factors can cause formation of methemoglobin in an organism:
1. Poisoning with oxide of Carbonum
2. Phosphoorganic materials
3. Sodium nitrats
4. Glycosides
5. Heavy metals
How the contents of Oxygen in blood changes at circulatory hypoxia:
1. In arterias remains normal, in veins is depressed
2. In arterias is reduced, in veins remains normal
3. In veins increases
4. In veins remains normal
5. In arterias is reduced, in veins is reduced
What causes can lead to development of hemic hypoxia:
1. Infringement of diffusion of Oxygen through alveolar membrane
2. Materials invoking formation of methemoglobin, anemia
3. Infringement of circulation
4. Over-dosage by barbiturates
5. Fall of tone of vessels
The listed factors result in development of circulatory hypoxia:
1. Hemolysis of erythrocytes
2. Hypervolemia
3. Decrease of alveolar ventilation
4. Heart failure
5. Disadvantage of Ferrum in an organism
To infringements of intrinsic tissue respiration lead:
1. Disadvantage of Oxygen in inhaled air
2. Infringement of transferring of Oxygen from blood into tissue, lesion of tissue enzymes
3. Dropping рО2 in respiratory routes
4. Infringement of diffusion of О2 through alveolar membrane
5. Hemolysis of erythrocytes
What from the herein provided states can reduce affinity of hemoglobin to Oxygen and rising of dissociation of oxyhemoglobin:
1. Alkalosis gaseous
2. Drop of temperature of body
3. Metabolic alkalosis
4. Gas alkalosis, high body temperature
5. Gaseous acidosis, high body temperature
Name mechanisms of development of respiratory compensatory-adaptive reactions:
1. Activation of synthesis of nucleic acids and proteins, which lies at the basis of hypertrophy of myocardium
2. Acceleration of feedback of Oxygen by erythrocytes
3. Augmentation of lung ventilation, ventilation of additional alveoli
4. Augmentation of in blood of glucocorticoids which activate enzymes of respiratory chain and improve stability of cellular membranes
5. Tachycardia
Name mechanisms of development of long-term compensatory-adaptive reactions at hypoxia:
1. Augmentation of minute volume of heart - tachycardia
2. The activation of synthesis of nucleic acids and proteins which lies at the basis of hypertrophy of myocardium, hypertrophy of respiratory muscles
3. Augmentation of mass of circulating blood for account of entering of erythrocytes from depositions
4. Augmentation of lung ventilation
5. Augmentation of dissociation of oxyhemoglobin, rising activity of enzymatic systems
What changes in blood are characteristic for tissue hypoxia:
1. Reduction of pO2 in arterial blood
2. Decrease of oxygen capacity of blood
3. Raised contents of Oxygen in venous blood, dropping of arteriovenous difference on Oxygen
4. Raised contents of Oxygen in arterial blood,
5. Dropped contents of Oxygen in venous blood, high arteriovenous difference on Oxygen
Name the causes invoking tissue type of hypoxia:
1. Inhalation of CO- gas
2. Collapse
3. Heart failure
4. Avitaminosis, poisoning with cyanides
5. Lesion of respiratory muscles
What factors result in development of mixed type of hypoxia:
1. Presence of exudate in pleural cavity
2. Aspiration of CO- gas
3. Traumatic shock, poisoning with Sodium nitrats
4. Avitaminosis
5. Anemia, methemoglobin- formers
Name reversible infringements at hypoxia:
1. Fatty degeneration in fibers of sceletal muscles, in myocardium
2. Degenerative changes in brain cortex
3. Necrobiosis of tissues
4. Focal hemorrhages in internal organs
5. Hypertrophy of myocardium, hypertrophy of respiratory muscles
Name irreversible infringements at hypoxia:
1. Fatty degeneration in myocardium
2. Edema of renal glomeruli
3. Degenerative changes in brain cortex, focal hemorrhages in internal organs
4. Fatty degeneration in fibers of sceletal muscles
5. Necrobiosis of tissues
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