Infringements of peripheral circulation
What can cause an arterial hyperemia:
1. Occlusion of arterioles
2. Action of the raised atmospheric pressure
3. Influence on vessels of biologically active materials, such as epinephrine, Vasopressinum
4. Influence on vessels of biologically active materials, such as Histaminum, Bradikinin, excitation of vasodilator nerves
5. Occlusion of veins
Note the attributes of an arterial hyperemia:
1. Pail skin
2. Coldness
3. Warming, reddening
4. Decrease of volume of tissue
5. Blue skin
Name mechanisms of an arterial hyperemia:
1. Excitation of vasoconstrictor nerves or centers
2. Drop of tone of vasoconstrictor nerves or centers, excitation of vasodilator nerves
3. Rising tone of muscles of arteria
4. Change of tone of muscles of arteria
5. Downdrop of tone of vasodilator nerves
What mechanism of post-ischemic hyperemia:
1. Vasodilatation by blood acting under the large pressure
2. Change of tone of vessels in connection with decrease or absence of blood flow, vasohyvesselonic influence on wall of vessels of biochemical and physical-chemical changes arising in region of ischemia
3. Reflex rising of tone of vessels in ischemic field
4. Reflex rising of tone of venules
5. Vaso-constrictive action of epinephrine
Name possible consequences of an arterial hyperemia:
1. Atrophy of specific elements of tissue
2. Bleeding, damage of wall of vessels
3. Clottage
4. Stasis
5. Growth of connective tissue
Name the causes of venous hyperemia:
1. Compression of arterias
2. Compression of veins, occlusion of veins
3. Spastic stricture of arterias
4. Occlusion of arterias
5. Disclosing of collaterals
At what type of collaterals the white infarct educes:
1. Rather poor collaterals
2. A collateral, where there are a lot of anastomosises
3. Absolutely sufficient collaterals
4. Absolutely poor collaterals, collateral where there are not enough of anastomosises
5. Development of collaterals have no any value
Name possible consequences of venous hyperemia:
1. Atrophy of specific elements of tissue, growth of connective tissue
2. Bleeding
3. Ischemia
4. Stasis
5. Rising of metabolism
Name mechanisms of originating of true stasis:
1. Vasculomotor dilating of arterioles and capillaries
2. Mechanical interrupting for outflow of blood
3. Intensifying of inflow of blood
4. Rising of permeability of capillaries and pachyemia, change of physical-chemical properties of colloids, aggregation and adhesion of erythrocytes
|
|
|
5. Ischemia
Name the causes of ischemia:
1. Compression of arteria, arteriospasm, occlusion of arteria
2. Compression of veins
3. Occlusion of veins
4. Compression of a vein
5. Breakage of an arteria
As the lumen of vessel in the field of venous hyperemia is changed:
1. The arterias are narrowed
2. The capillaries are narrowed
3. The lumen of an arteria does not change
4. The veins are dilated
5. The veins are narrowed
What are pre-stasis change of blood flow:
1. Acceleration of blood flow
2. Retardationof blood flow
3. Pendulum- like locomotion of blood, jerking locomotion
4. Stopping of blood flow
5. Arrest of blood flow
What possible outcomes of stasis:
1. Intensifying function of tissue
2. Intensifying inflow of blood
3. Intensifying venous blood flow
4. Necrosis, infarct
5. Embolism
How changes hemo- and lympho-dynamic in ischemia:
1. The volumetric rate of blood flow is enlarged
2. The lymphopoiesis is enlarged
3. The arterial pressure is enlarged
4. The volumetric rate of blood flow and lymphopoiesis decreases
5. The inflow of blood is enlarged
How can gas embolism arise:
1. Work of diver in depth
2. During the rise of diver, at sharp decrease of atmospheric pressure
3. In operating time in caisson
4. At sharp rising of atmospheric pressure
5. At height
What wound of vessels can result in air embolism:
1. Femoral arteria
2. Carotid artery
3. Upper caval vein, bulbar vein
4. Femoral vein
5. Aortic arch
Which from the named factors promote formation of thrombus:
1. Acceleration of blood flow
2. Retardation of blood flow, damage of wall of vessel
3. Augmentation in blood of Heparinum
4. Decrease of amount of thrombocytes
5. Augmentation of amount of erythrocytes
What possible consequences of clottage of arterias:
1. Hyperemia
2. Occlusion of arterias, infarct
3. Venous hyperemia
4. Arterial hyperemia
5. Growth of connectiv tissue
|
|
|
What possible consequences of clottage of vein:
1. Embolism, venous hyperemia
2. Arterial hyperemia
3. Ischemia
4. Infarct
5. Re-perfusion syndrome
What changes in composition of blood interfere with formation of clottage:
1. Decrease of quantity of Heparinum
2. Augmentation of quantity of Heparinum, augmentation of rate of blood flow
3. Augmentation of amount of thrombocytes
4. Augmentation of amount blood cells
5. Pendulum -like locomotion of blood
At what forms of local circulatory disturbances the volumetric rate of blood flow is enlarged:
1. Arterial hyperemia
2. Venous hyperemia
3. Ischemia
4. Clottage
5. Embolism
What forms of local circulatory disturbances produce fast rising of temperature of tissue:
1. Ischemia
2. Venous hyperemia
3. Arterial hyperemia
4. Stasis
5. Infarct
List the the humoral factors capable to cause vasomotor spasm:
1. Histaminum
2. Serotonin
3. Epinephrine
4. Bradykinin
5. Kalidin
The vasomotor spasm is:
1. Intensifying of blood flow
2. veno-dilation
3. Dilating of arteria
4. Long constriction of arterias of pathological character
5. Augmentation of blood inflow in organ
To thrombogenesis promotes:
1. Decrease of viscosity of blood
2. Intensifying of blood flow
3. Decrease of amount of thrombocytes
4. Retardation of blood flow, damage of intima of vessels
5. Decrease of viscosity of blood
Complication of ischemia is:
1. Arterial hyperemia
2. Venous stasis in organ
3. Regeneration of blood flow
4. Infarct
5. Embolism
Edema of tissues usually educes at:
1. Venous stasis
2. Arterial hyperemia
3. Ischemia
4. Advanced enough collateral circulation
5. Bleeding
The ischemia of organs and tissues is dangerous because:
1. Infringement of feeding, decrease of delivery О2
2. Intensifying of oxidative processes
3. Augmentation of blood in vessels
4. High intravascular pressure
5. Bleeding
The infarct usually is a complication of:
1. Arterial hyperemia
2. Venous stasis
3. Clottage of veins
4. Collateral circulation
|
|
|
5. Embolism of arterias, ischemia
To venous hyperemia leads:
1. Spastic stricture of arterioles
2. Clottage, compression of veins
3. Intensifying function of an organ
4. Dilating arterioles
5. Compression of arterias
At long venous hyperemia color of an organ:
1. Red
2. Pail
3. Cyanotic
4. Usual
5. Mixed
The cyanotic color of tissue at long venous hyperemia is explained:
1. Plenty of restored hemoglobin
2. Presence of oxyhemoglobin
3. Decrease of blood in vessels
4. Drop of blood pressure
5. Rising of blood pressure
At fractures of large tubular bones there is an embolism:
1. Parasitogenic
2. Air
3.. Thromboembolism
4. Fatty tissue
5. Gas
What is "sledge syndrome":
1. Formation of thrombocyte-leukocyte aggregate on wall of the microvessels
2. Pachyemia due to loss of fluids
3. Coagulation of blood proteins
4. Agglutination of blood cells in lumen of vessels
5. Decrease of viscosity of blood
In what organs and tissues there are functionally absolutely poor collateralies:
1. Lien
2. Kidneys
3. Lungs
4. Cardiac muscle
5. Liver
Specify the basic kind of infringements of metabolism determining pathogenic value of ischemia:
1. Intensifying of disintegration of proteins
2. Intensifying of glycolysis, accumulation of hydrogen ions
3. Intensifying of disintegration of lipids
4. Decrease of accumulation of hydrogen ions
5. Rising synthesis of protein
Specify the basic pathogenetic factors of thrombogenesis
1. Erythrocytopenia
2. Thrombocytopenia
3. Acceleration of blood flow
4. Retardation of blood flow, rising of viscosity of blood
5. Leukopenia
Specify the possible causes of air embolism:
1. Wound of large veins
2. Wound of small arterias
3. Fast transferring from the increased atmospheric pressure to normal
4. At work in the large depth
5. At caisson works
Specify what microcirculatory change are characteristic for an arterial hyperemia:
1. Narrowing of arterioles
2. Narrowing of pre-capillary sphincters
3. Decrease of transudation and lymph flow
|
|
|
4. Dilating arterioles and capillaries, augmentation of transudation and lymph flow
5. Narrowing of post-capillary sphincters
Specify what microcirculatory change are characteristic for venous hyperemia:
1. Narrowing of arterioles
2. Augmentation of gradient of blood pressure along the capillaries
3. Dilating of veins, high quantity of functioning capillaries and their dilating
4. Decrease of quantity of functioning capillaries
5. Augmentation of number of plazmatic capillaries
What possible consequences of clottage of arterias:
1. Embolism
2. Ischemia, infarct
3. Venous hyperemia
4. Arterial hyperemia
5. Ischemia, arterial hyperemia
That is the cause of an arterial hyperemia:
1. Action of heat, action on an organism of beams of the solar spectrum
2. Action of increased atmospheric pressure
3. . Influence on vessels of epinephrine, Vasopressinum
4. Occlusion of arterioles
5. Occlusion of veins
Name possible consequences of an arterial hyperemia:
1. Atrophy of specific elements of a tissue
2. Bleeding
3. Clottage
4. Stasis
5. Growth of connective tissue
Name possible consequences of venous hyperemia:
1. Bleeding
2. Ischemia
3. Rising of metabolism
4. Stasis
5. Growth of connective tissue, atrophy of specific elements of a tissue
What you perceive as embolism:
1. Intravital coagulation of blood in vessels
2. Circulation in blood of blood cells
3. Circulation in blood of particles not meeting in norm
4. Exit of blood out of vessels
5. Coagulation of blood which vented in tissue
What is anemia:
1. Decrease of inflow of blood to organs
2. Stopping of blood flow
3. Efflux of blood from vessels
4. Intensifying of outflow of blood
5. Rising of vascular permeability
Kind of hyperemia educing in divers and caisson workers:
1. Inflammatory
2. Angioneurotic
3. Vacant
4. Hyperemia after anemia
5. Collateral
The axons – reflexes participate in development:
1. Physiological hyperemia, functional hyperemia
2. Stasis
3. Ischemia
4. Myocardial infarction
5. venous hyperemia
Outcomes of pathological arterial hyperemia can be:
1. Development of collateral circulation
2. Growth of connective tissue
3. Breakage of vessels, bleeding
4. Decrease of outflow of blood
5. Atrophy of organ
The compressional ischemia can be produced:
1. Compression of arteria by surrounding liquid
2. Thrombus
3. Embolus
4. Vasomotor spasm
5. Breakage of desmosoms
Note attributes of arterial hyperemia:
1. Paleness
2. Coldness
3. Pain
4. Reduction of volume of tissue
5. Redness
The angiospasm is:
1. Intensifying of blood circulation
2. Phlebodilution
3. Dilating of artery
4. Long constriction of arteries of pathological character
5. Augmentation of blood filling of an organ
How is the lumen of vessels changed at the focus of venous hyperemia
1. Arteries constricted
2. capillaries constricted
3. lumen of arteries does not change
4. venous dilation
5. venous constriction
At what forms of local disorders of blood circulation is volumetric velocity of blood increased:
1. arterial hyperemia
2. venous hyperemia
3. ischemia
4. thrombosis
5. embolism
Unfavorable outcome of ischemia is:
1. arterial hyperemia
2. venous stasis in organ
3. restoration of blood circulation
4. infarction
5. embolism
What are the mechanisms of postischemic hyperemia:
1. Vasodilatation by blood acting under large pressure
2. Change of tone of vessels due to decrease or absence of blood circulation
3. Vasoconstriction
4. Reflex downdrop of tonus of vessels in ischemic zone
5. Reflex rising of tone of vessels
What are the pre-stasis changes of blood circulation:
1. Acceleration of blood circulation
2. Retardation of blood circulation
3. pendulum-like movement of blood
4. jerky locomotion
5. Stopping of blood circulation
To venous hyperemia lead:
1. Spastic stricture of arterioles
2. Clottage of veins
3. Intensifying of function of an organ
4. Dilation of arterioles
5. Dilation of veins
Name the possible consequences of arterial hyperemia:
1. Atrophy of specific elements of tissue
2. Bleeding
3. Clottage
4. Stasis
5. Growth of connecting tissue
Name the reasons of venous hyperemia:
1. Compression of arteries
2. compression of veins
3. Dilation of veins
4. A spasm of arteries
5. Clottage of arteries
What probable outcomes of a stasis:
1. Amplification of function of tissue
2. Amplification of inflow of blood
3. Amplification of venous blood flow
4. Necrosis
5. Clottage of arteries
What from the named factors promote formation of blood clot:
1. Acceleration of bloodflow
2. Necrosis
3. Increase in blood of Heparinum
4. Reduction of amount of thrombocytes
5. Damage of wall of vessel
The hypostasis of tissue usually develops at:
1. Venous stagnation
2. Arterial of hyperemia
3. An ischemia
4. Advanced enough of collateral blood circulation
5. A bleeding
In what organs and tissues are available functionally absolutely insufficient collaterals:
1. Spleen
2. Kidneys
3. Lungs
4. Miocardium
5. liver
Inflammation
Specify internal cardinal components of inflammation:
1. Erythema, sweeling, alteration
2. Distress of microcirculation, proliferation
3. Pain
4. Infringement of function of organ
5. Retardation of metabolism
Specify external attributes of inflammation:
1. Infringement of function, erythema, swelling
2. Alteration
3. Exudation
4. Proliferation
5. Emigration of leukocytes
To chemical factors producing inflammation relate:
1. High temperature
2. Sodium chloridum
3. Hydrochloric acid, battle poisoning materials of dermatovesical action
4. CO gas
5. Methemoglobin producers
To the endogenous causes producing inflammation relate:
1. Thrombs, deposits of salts, hypersensibility of child skin to physiological excretes
2. Chronic hemorrhage
3. Circulatory insufficiency
4.Fever
5. Rising of blood sedimentation rate
Specify why inflammation is named a typical pathological process:
1. Various causes
2. Diversification of place of localization
3. Biological significance for an organism
4. Complexity of the causal-sequence relations in its development
5.The basic features proceeds equally independent on cause and localization
To local attributes of inflammation does not relate:
1. Swelling
2. Local rising of temperature
3. Fervescence, leukocytosis
4. Pain
5. Infringement of function
To general reaction of an organism in inflammation relate:
1. Swelling
2. Rise of body temperature
3. Local hyperemia
4. Rising of metabolism in the focus of inflammation
5. Decrease of blood sedimentation rate
To hyperergic inflammation relate:
1. Inflammation of immediate allergic response type, inflammation of delayed type allergic response
2.Fibrinous pericarditis
3. Caseous regional lymphadenitis
4. Pulmonary tuberculosis
5. Leprosy
The primary alteration is a result of influences on tissue:
1. Physical, chemical, biological factors
2. Liberated from cells lysosomal factors
3. Flogogen factors
4. Active metabolites
5. Oncogenic factors
The secondary alteration grows out of influences on tissue:
1. High temperature
2. Liberated from cells lysosomal enzymes, accumulation in tissues of lactic acid and tricarboxylic acids
3. Low temperature
4. Appearance in vessels of thrombs
5. Ionizing radiation
Primary alteration at inflammation:
1. Depends on force and duration of flogogenic factor, for its originating the influence of flogogenic factor is necessary
2. For its development no need for presence of flogogen
3. Answer-back reaction to thrombs formed in vessels
4. It is a reaction to damage already caused by harmful agent
5. Arises at action of acids, alkalis
The start of inflammation causes by damage of:
1. Device Gouldzhy
2. Nucleus
3. Cytoplasmic membrane, lysosomes
4. Ribosomes
5. Microsomas
The drop of respiratory coefficient in zone of primary alteration is linked to:
1. Damage of lysosomes
2. Damage of mitochondrions, intensifying of glycolysis
3.Rising of permeability of cytoplasmic membrane and exit of K-ions
4. Development of venous hyperemia
5. Development of arterial hyperemia
Specify the causes of rising of oncotic and osmotic pressure in the locus of inflammation:
1. Appearance of biologically active materials
2. Remission of ions of vesselassium in destruction of cells, Albumin exit in connection with rising of vascular permeability, active hydrolysis of protein
3. Amplified glycolysis of polysaccharides
4. Increased synthesis of protein
5. Appearance of keton bodies
Infringement of acid-base balance in locus of inflammation expresses as:
1. Gas alkalosis
2. Gas acidosis
3. Non- gas alkalosis
4. Non- gas, metabolic acidosis
5. Excretory acidosis
The primary vasospasm in the locus of inflammation as a result of:
1. Excitation of parasympathetic ganglions
2. Release of hydrocortisone by adrenals
3. Release of epinephrine from presynaptic fibers
4. Release of Histaminum from mast cells
5. Formation in the locus of inflammation of Vasopressinum
To development of arterial plethora in inflammation lead:
1. Infringement of outflow of blood
2. Reflex vasodilatation, paralysis of muscular layer under influence of mediators formed in the locus of inflammation
3. Pachyemia
4. Compression of vein
5. Emigration of leukocytes
Specify the causes of turning of arterial hyperemia into venous in the locus of inflammation:
1. Rising of vascular permeability and exit of fluid part of blood, regional standing of leukocytes, venous microclottage
2. Proliferation of cells in the locus of inflammation
3. Decrease of viscosity of blood
4. Hypoproteinemia
5. Thrombocytopenia
Exhibitions of acute inflammation are:
1. Rising temperature in field
2. Dropping temperature in field
3. Drop of turgor
4. Edema
5. Dropping temperature
To classical local attributes of inflammation relate:
1. Paleness of skin
2. Anesthesia
3. Acceleration of BSR
4. Pain, erythema, infringement of function
5. Increase of body temperature
External attributes of venous hyperemia at inflammation are all, EXCEPT FOR:
1. Rising turgor, rising of temperature, field of inflammation is of scarlet color
2. Tumor owing to edema
3. Field of inflammation of purple-dark blue color
4. Drop of a turgor
5. Paleness of field
The exit of leukocytes out of vessels refers to as:
1. Cytopempis
2. Exudation
3. Emigration
4. Diapedesis
5. Chemotaxis
The exit of erythrocytes from vessels in inflammation refers to as:
1. Emigration
2. Diapedesis
3. Exudation
4. Cytopempis
5. chemotaxis
Mediators relating to biogenic amines are:
1. Histaminum, serotonin
2. Bradykinin
3. Neuropeptids
4. Kallidin
5. Prostaglandin
To pre-descending to cellular mediators of inflammation relate:
1. Active metabolites of Oxygen
2. Lymphokines
3. Vasoactive amines (Histaminum, Serotonin)
4. Monokin
5. Metabolites of arachidonic acid
To extravascular factors of exudation at inflammation relate:
1. Rising tone of veins
2. Hyperosmia, hyperoncia in the locus of inflammation
3. Regional standing of leukocytes
4. Formation of bradykinin
5. Pachyemia
To the intravascular factors of exudation in inflammation relate:
1. Rising hydrostatic pressure in capillaries, dropping of colloid osmotic pressure of blood
2. Rising of tissue pressure
3. Rising of colloid osmotic pressure in tissues
4. Rising of coagulability of blood
5. Dropping of tissue pressure
The basic causes of exudation in the locus of inflammation are:
1. Rising hydrostatic pressure in microvessels, intensifying of disintegration of tissues and accumulation in them of osmotically active materials
2. Rising of oncotic pressure inside vessels
3. Decrease of oncotic pressure in tissues
4. Dropping of permeability of microvessels
5. Rising of tissue pressure
The causes of rising permeability in vessels at inflammation:
1. Extension of vessels in venous plethora
2. Development at inflammation of arterial hyperemia
3. Enzymes released at damage of lysosomes, appearance in the locus of mediators of inflammation
4. Rising tone of veins
5. Rising tone of arterias
How emigration refers to as:
1. Escaping of erythrocytes out of vessels.
2. Directed locomotion of leukocytes to the locus of inflammation
3. Exit of leukocytes from blood in the locus of inflammation
4. Exit of fluid part of blood in the locus of inflammation
5. Exit of small proteins from vessels
First of all into the locus of inflammation go:
1. Monocytes
2. Lymphocytes
3. Neutrophils
4. Erythrocytes
5. Plasmocytes
Emigrations of leukocytes includes:
1. Regional standing of leukocytes, exit of leukocytes through vascular wall
2. Exit of erythrocytes
3. Phagocytosis
4. Absorption of foreign particles
5. Digestion of bacteria
To mediators of inflammation of cellular nature (pre-descending) relate:
1. Lektin
2. Neuropeptids, Serotonin
3. Leukotrien
4. Thromboxan
5. Complement
The factor triggering contact system of blood at inflammation is:
1. C - reactive protein
2. Factor Chageman’s
3. High- molecular kininogen
4. Fibrinogen
5. Factor С-5 of complement
Proliferation in the locus of inflammation is provided:
1. Mononuclear phagocytes, hystiocytes
2. Neutrophils
3. Lymphocytes
4. Basophils
5. Eosinophils
Secondary alteration at inflammation invoke:
1. Carcinogens
2. Flogogens
3. Hormons
4. Products of primary alteration
5. Neuromediators
To newly formed cellular mediators at inflammation relate:
1. Histaminum
2. Thromboxan, factor activating macrophages
3. Serotonin
4. Bradykinin
5. Kalidin
Vascular changes at inflammation for the first time has described:
1. Virchov
2. Kongame
3. Mechnikov
4. Shade
5. Menkin
A biological role of leukocytes in the locus of inflammation for the first time has specified:
1. Shade
2. Virchov
3. Mechnikov
4. Kongame
5. Menkin
The founder of the physical-chemical theory of inflammation is:
1. Shade
2. Mechnikov
3. Virchov
4. Kongame
5. Menkin
To humoral mediators of inflammation relate:
1. Eikozanoids
2. Derivants of complement, kinins
3. Prostaglandin
4. Biogenic amins: Histaminum, Serotonin
5. Lysosomal enzymes
In basis of protective role of phagocytosis at inflammation lays:
1. Digestion of an object with participation and without participation of Oxygen
2. Destruction of phagocytes, macrophages
3. The remission of antigenic determinants resulting in interrelation of cellular and humoral immunity
4. Localization of process of inflammation
5. Formation of exudate
For arterial hyperemia at inflammation are characteristic:
1. Acceleration of blood flow, reddening of the inflamed field
2. Rising inflow of blood, retardation of blood flow
3. Dropping outflow of blood, swelling
4. Augmentation of time of blood flow
5. Decrease of lymphopoiesis
Main effects of kinin system at inflammation are:
1. Dilation of capillary and post-capillary venules
2. Spastic stricture of arterias
3. Depressing of chemotaxis
4. Oppression of thromboxan production
5. Activation of proliferation
Infringement of activity of enzymes in tricarbonic acid cycle at inflammation result in accumulation:
1. Uric acid
2. Alpha – ketoglutar piruvic acid
3. Homogentisinic acid
4. Oleinic acid
5. Linoleic acid
For arterial hyperemia at inflammation is characteristic:
1. Augmentation of blood flow rate and number of functioning capillaries
2. Rising of intra-capillary pressure
3. Drop of rate of blood flow
4. Decrease of volumetric rate of blood flow
5. Decrease of peripheral speed of blood flow
Specify the causes of turning of arterial hyperemia at inflammation into venous:
1. Dilating of pre-capillary sphincters
2. Regional standing of leukocytes, venous clottage
3. Paralysis of muscular layer of arterioles
4. Occlusion of arterias
5. High peripheral speed of blood flow
To mediators of inflammation - derivant of arachidonic acid relate:
1. Prostaglandins, leukotriens
2. Interleikins
3. Lymphokines
4. Cationic proteins
5. Histaminum, Serotonin
The pain at inflammation is linked with:
1. Infringement of circulation
2. Rising metabolism
3. Irritation of responsive nerves by edematous c fluid and hydrions, appearance in the locus of inflammation of Histaminum, Bradykinin
4. Rising of permeability of vascular wall
5. Raised hydrolysis of protein
The shift of рН into acidic side in the locus of inflammation is connected with:
1. Activation of oxidative phosphorylation
2. Non-use of organic acids in tricarbonic acid cycle, activation of glycolytic enzymes
3. Activation of hydrolases
4. Cytolysis of cells
5. Rising of metabolism
The rising of temperature in the locus of inflammation is inked with:
1. Exudation
2. Emigration of leukocytes in the locus of inflammation
3. Rising of metabolism in the locus of inflammation, development of arterial hyperemia
4. Development of venous hyperemia
5. Acidosis
The rising exudation in the locus of inflammation is caused:
1. Drop of colloid osmotic pressure in tissues of the locus of inflammation
2. Rising permeability of capillaries, rising of colloid osmotic pressure in tissues
3. Dropping hydrostatic pressure in capillaries
4. Rising hydrostatic pressure in tissues
5. Rising of lymphopoiesis
Specify a sequence of exit of cells in the locus of inflammation:
1. Lymphocytes – monocytes-basophils
2. Monocytes - lymphocytes-neutrophils
3. Lymphocytes - monocytes-neutrophils-basophils
4. Neutrophils - lymphocytes-monocytes
5. Basophils - moncytes-lymphocytes-neutrophils
Protective role of exudation as a component of inflammation:
1. Maintenance of destruction of foreign agent by system of complement, encircling of the locus of inflammation through compression of circulatory and lymphatic microvessels
2. Intensifying of system of fibroblasts
3. Mechanical irritation of the nervous terminals as a result of pressure boost in the locus of inflammation
4. Delay of flogogens and products of cytolysis in the locus of inflammation
5. Phagocytosis
Name the basic cellular effectors of proliferation:
1. Activated mononuclear phagocytes secreting cytokin, fibroblasts
2. Thrombocytes
3. Neutrophils
4. Erythrocytes ensuring feeding by Oxygen
5. Cell-bound immune complexes
The rising of hydrostatic pressure in microvessels of the locus of inflammation is caused:
1. Rising vascular permeability
2. Spastic stricture and clottage of venules, lymph-vessels
3. Augmentation of number of functioning capillaries
4. Filling of interstitial spaces with exudates
5. Action of lymphokines
The rising permeability of wall of microvessels in the locus of inflammation is connected with:
1. Local growth of flogogens
2. Rising metabolism in the locus of inflammation
3. Action of Histaminum, Serotonin, Bradykinin, action of lymphokines
4. Pachyemia
5. Raised lymphopoiesis
The following physical -chemical changes are characteristic for a field of acute inflammation:
1. Hyperoncia, hyperosmia, acidosis
2. Hyperosmia, hypooncia
3. Hypoosmia, alkalosis
4. Acidosis, hypooncia
5. Rising concentration of ions of vesselassium in cells
Mediators of n inflammation invoking augmentation of vascular permeability at inflammation are:
1. Heparinum, Histaminum
2. Histaminum, Bradykinin
3. Interferon, Serotonin
4. Serotonin, Heparinum
5. Slowly reacting substances of allergy
Mediators of inflammation formed from phospholipids of cellular membranes are:
1. Prostaglandins, Leukotriens, factor of activation of thrombocytes
2. Histaminum
3. Bradykinin
4. Bradykinin, Kalidin
5. Complement
To signs characterizing the reaction of acute phase of inflammation relate:
1. Fever, augmentation of BSR, neutrophilic leukocytosis
2. Cramp
3. Edema
4. Rising appetite
5. Sleepiness
The chemical factors producing an inflammation are :
1. High temperature
2. Sodium chloride
3. Hydrochloric acid
4. CO gas
5. Low temperature
First of all into the focus of inflammation get:
1. Monocytes
2. lymphocytes
3. Neutrophils
4. erythrocytes
5. Plasmocytes
To humoral mediator of inflammation relate:
1. Eucozanoides
2. Serotonin
3. Cynins
4. Biogenic amine: hystaminum
5. Lysosomal enzymes
Classic local sign of inflammation:
1. paleness of skin
2. loss of tactility
3. increase of BSR
4. pain
5. local hypertonia
Exit of leukocytes out of vessels at inflammation calls:
1. cytopempis
2. exudation
3. emmigration
4. diapedesis
5. chemotaxis
A biological role of leukocytes in the focus of inflammation for the first time has specified:
1. Shade
2. Virchov
3. Mechnicov
4. Congeim
5. Menkin
Main effects of the kinin system at inflammation are:
1. Dilation of capillary and postcapillary venules
2. Activation of phagocytosis
3. Depression of chemotaxis
4. Oppression of thromboxan production
5. Activation of proliferation
The pain at inflammation is linked to:
1. Infringement of blood circulation
2. Rising of metabolism
3. Irritation of susceptible nerves by edematous fluid and hydrogen ions
4. Appearance in the inflammatory focus an edema
5. Rising permeability of vascular wall
The begining of inflammation is damage of :
1. Apparatus
2. GoldgyNucleus
3. Mitochondrium
4. Ribosomes
5. Lysosomes
To the precursors of cellular mediators of inflammation relate:
1. Active metabolites of Oxygen
2. Lymphokines
3. Vasoactive amines (Histamin, Serotonin)
4. Monokin
5. Metabolites of arachidonic acid (Eycosanoids)
To the cellular mediators of inflammation relate:
1. Cytokins
2. Kinins
3. Thromboxans- the factors of Complement
4. Serotonin
5. Neuropeptids
Biochemical changes in the focus of inflammation were detailed by :
1. Mechnicov
2. Congeim
3. Shade
4. Virchov
5. Menkin
To again formed cellular mediators at an inflammation relate:
1. Histaminum
2. Tromboxan
3. Serotonin
4. Bradycynin
5. Kynins
To humoral mediators inflammations relate:
1. Eucozanoides
2. Serotonin
3. Kynins
4. Biogenic amines
5. Lysosomal enzymes
For venous hyperemia at an inflammation are characteristic:
1. Delay of bloodflow
2. Acceleration of bloodflow
3. Rise of temperature in a site
4. Increase of temperature
5. Reddening of a site of an inflammation
Specify what explains an antiinflammatory effect of glucocorticoids:
1. Increase of permeability of vessels
2. Development of a hypostasis
3. Increase of permeability of basal membranes
4. Duplication of cells
5. Stabilization of lysosomal membranes
Point why an inflammation is a typical path. process:
1. different causes
2. different focuses of localization
3. biologic significance
4. complexity of casual-consequence relation in its developing
5. mainly develops equally independently from causes and focuses of localization
Macrophages are:
1. neutrophils
2. basophils
3. eosinophils
4. Lymphocytes
5. monocytes
Vascular changes at inflammation were depicted first by:
1. Virchov
2. Kongame
3. Mechnikov
4. Shadie
5. Menkin
Founder of physics-chemical theory of inflammation is:
1. Shadie
2. Mechnikov
3. Virchov
4. Kongame
5. Menkin
Дата добавления: 2018-02-18; просмотров: 480; Мы поможем в написании вашей работы! |
Мы поможем в написании ваших работ!