1. What does general pathophysiology study?a) General rules of the origin, onset, evolution and resolution of typical pathological processesb) General rules of the origin, onset, evolution and resolution of pathological processes in

organs and systemsc) General rules about pathogenesis of clinical syndromes and nosological entitiesd) General rules about structural modifications and dysfunctions at the cellular, tissue, system

and integral level in typical pathological processese) General rules about structural modifications and dysfunctions of organs and systems in

typical pathological processes

2. What does special pathophysiology study? a) General rules of the origin, onset, evolution and resolution of typical pathological processes b) General rules of the origin, onset, evolution and resolution of pathological processes in

organs and systems c) General rules about the pathogenesis of clinical syndromes and nosological entitiesd) General rules about structural modifications and dysfunctions at the cellular, tissue, system

and integral level in typical pathological processese) General rules about structural modifications and dysfunctions of organs and systems in

pathological processes

3. What does clinical pathophysiology study?a) General rules of the origin, onset, evolution and resolution of typical pathological

processesb) General rules of the origin, onset, evolution and resolution of pathological c) General rules about the pathogenesis of clinical syndromes and nosological entities d) General rules about structural modifications and dysfunctions at the cellular, tissue, system

and integral level in typical pathological processese) General rules about structural modifications and dysfunctions of organs and systems in

pathological processes

4. What is general etiology?a) The compartment of pathophysiology that studies causes and conditions of the disease’s

onset b) The compartment of pathophysiology that studies causes of the disease’s development c) The compartment of pathophysiology that studies conditions of the disease’s development d) The compartment of pathophysiology that studies causes and conditions of the disease’s

development and evolutione) The compartment of pathophysiology that studies the role of pathogenetic factors in

disease’s evolution

5. Which factors can cause the disease development?a) Action of energy on the organism b) Action of substance on the organism c) Action of information on the organism d) Action of the heterogenous biological field on the organism e) Action of hostile aura on the other person

6. What are the exogenous causes of diseases? a) Mechanical, physical, chemical and biological factors from the environment b) Resident microflora of the intestines and respiratory pathways c) Intestinal parasites and blood parasitesd) Chromosome aberration resulting from the action of ionizing radiatione) inherited genetic defects

7. What are the endogenous causes of diseases? a) Mechanical, physical, chemical and biological factors from the environmentb) Resident microflora of the intestines and respiratory pathwaysc) Intestinal parasites and blood parasitesd) Chromosome aberration resulting from the action of ionizing radiatione) Inherited genetic defects

8. What conditions are necessary for the disease onset? a) Different forms of energy b) Material factorsc) Informational factors d) Proper and heterogenous biological fielde) Interaction between proper aura and aura of another person

9. What conditions are considered favorable for the organism?a) Conditions that promote action of the cause and disease appearanceb) Conditions that impede action of the cause and retain the disease appearance c) Conditions that decrease body’s resistanced) Conditions that increase the body’s resistance e) Genetic defects

10. What conditions are considered unfavorable for the organism?a) Conditions that promote action of the cause and disease appearance b) Conditions that impede action of the cause and retain the disease appearancec) Conditions that decrease the organism’s resistance d) Conditions that increase the organism’s resistancee) Genetic defects

11. Which conditions are exogenous?a) Ecological factors b) Climate factors c) The body’s constitutiond) The body’s reactivity e) The body’s resistance

12. Which conditions are endogenous?a) Climate factorsb) Microclimate factorsc) The body’s constitutiond) The body’s reactivitye) The body’s resistance

13. What is the role of the cause in the disease appearance?a) determines the possibility of the disease appearance b) determines the specificity of the disease c) determines the moment of the disease appearanced) impedes the appearance of the diseasee) accelerates the appearance of the disease

14. What is the role of conditions in the disease appearance?a) determines the possibility of the disease appearanceb) determines the specificity of the disease c) determines the moment of the disease appearance d) impedes the appearance of the disease e) accelerates the appearance of the disease

15. What does injury represent?a) functional disturbances at any level of the organism’s organizationb) structural changes at any level of the organism’s organizationc) the combination of structural changes and functional disturbances at any level of the

organism’s organizationd) structural, biochemical and functional dyshomeostasis at any level of the organism’s

organizatione) persistent and irreparable disturbances of the structural, biochemical and functional

homeostasis

16. On what does the localization of general injuries depend?a) different sensibility of the body’s structures to the harmful factorb) the intensity of etiological factor that causes the disorderc) the affinity of pathogenic factor to the body structuresd) on blood velocity in the tissuee) the intensity of pathogenic factor action

17. What are the possible variants of relationship between general and local injuries?a) There are diseases with exclusive locally injuries

b) There are diseases with exclusive general injuries

c) There are some diseases with combination of local and general injuries

d) Any disease is an integrity of local and general injuries

e) The disease starts with local or general injuries, and later makes an integration between them

18. What do pathogenetic factors represent?a) the effects of the primary cause action

b) the chain of effects resulting from the action of conditions of disease

c) the chain of effects resulting from the primary cause action

d) the cause and conditions that provoked the disease

e) the conditions that promote the action of primary cause

19. What does the chain of cause-effect in pathogenesis represent?a) the totality of cause-effect links from the onset of the disease till the resolution of it

b) the totality of injuries encountered during disease evolution

c) the totality of body reactions encountered during disease evolution

d) the totality of injuries and body reactions encountered during disease evolution

e) the totality of injuries and body reactions linked by the cause-effect relationship encountered during disease evolution

20. What is the main link of pathogenesis? a) the cause that provoked diseaseb) the injuries caused by the action of the primary causec) the injuries that provoke directly the death of the body d) the pathogenetic factor on which depends the development of the disease and which

removal can stop the diseasee) the pathogenetic factor caused by the primary cause action, on which depends the

development of the disease and which removal can stop the disease

21. What is pathogenetic therapy?a) the therapy oriented to remove the cause of disease from the organism b) the therapy oriented to remove the primary injuriesc) the therapy oriented to attenuate the pathogenic action of the etiological factord) the therapy oriented to remove the main pathogenetic linke) active or passive immunization

25. What is the symptomatic therapy?a) the therapy oriented to remove the primary injuriesb) the therapy oriented to attenuate the pathogenic action of the etiological factorc) the therapy oriented to remove the main pathogenetic link d) the therapy oriented to remove the main clinical manifestationse) the therapy oriented to remove the disturbances that threatens the patient’s life

26. What is the specific prophylaxis of the disease?a) prophylaxis by active or passive immunizationb) prophylaxis by the consumption of vitamins and oligoelementsc) prophylaxis by „tempering” the bodyd) prophylaxis that is effective only for one disease e) prophylaxis that is effective for many diseases

27. What is the non specific prophylaxis of the disease?a) prophylaxis by active or passive immunizationb) prophylaxis by the consumption of vitamins and oligoelementsc) prophylaxis by „tempering” the bodyd) prophylaxis that is effective for only one disease

e) prophylaxis that is effective for many diseases

28. What does a physiological reaction mean? a) it is a reaction that is adequate to the specific excitation

b) it is a reaction that has a dyshomeostatic character c) it is a reaction that has a homeostatic character d) it is a reaction that is inferior to the excitant’s intensity

e) it is a reaction that exceeds the excitant’s intensity

29. What does a pathological reaction mean?a) it is a reaction that doesn’t correspond to the excitant’s specificityb) it is a reaction that quantitatively corresponds to the excitant’s intensityc) it is a reaction that has a homeostatic character

d) it is a reaction that is inferior to the excitant’s intensitye) it is a reaction that exceeds the excitant’s intensity

30. What is normoergic reaction? a) it is a reaction that adequate to the excitant’s specificity

b) it is a reaction that quantitatively corresponds to the excitant’s intensityc) it is a reaction that has a homeostatic character

d) it is a reaction that is inferior to the excitant’s intensitye) it is a reaction that exceeds the excitant’s intensity

31. What is adaptive reaction?a) it is a reaction that is oriented to the organism survival in the new life conditionsb) it is a reaction that is oriented to prevent, attenuate and eliminate the action of pathogenic

factor c) it is a reaction that is oriented to ensure the functional homeostasis in damaged structures

by the hyperfunction of other synergistic structuresd) it is a reaction that is oriented to recover the structural defect and restoration of structural

homeostasis e) it is a reaction that is oriented to change the genotype according to life conditions

26. What is compensatory reaction?

a) it is a reaction that is oriented to the organism survival in the new life conditionsb) it is a reaction that is oriented to prevent, attenuate and eliminate the action of pathogenic

factor c) it is a reaction that is oriented to ensure the functional homeostasis in damaged structures

by the hyperfunction of other synergistic structuresd) it is a reaction that is oriented to recover the structural defect and restoration of structural

homeostasis e) it is a reaction that is oriented to change the genotype according to life conditions

27. What is protective reaction?a) it is a reaction that is oriented to the organism survival in the new life conditions

b) it is a reaction that is oriented to prevent, attenuate and eliminate the action of pathogenic factor

c) it is a reaction that is oriented to ensure the functional homeostasis in damaged structures by the hyperfunction of other synergistic structures

d) it is a reaction that is oriented to recover the structural defect and restoration of structural homeostasis

e) it is a reaction that is oriented to change the genotype according to life conditions

28. What is reparative reaction?a) it is a reaction that is oriented to the organism survival in the new life conditions

b) it is a reaction that is oriented to prevent, attenuate and eliminate the action of pathogenic factor

c) it is a reaction that is oriented to ensure the functional homeostasis in damaged structures by the hyperfunction of other synergistic structures

d) it is a reaction that is oriented to recover the structural defect and restoration of structural homeostasis

e) it is a reaction that is oriented to change the genotype according to life conditions

29. What is characteristic for the latent period of the disease?

a) absence of any clinical manifestations

b) absence of specific manifestationsc) Presence of non-specific manifestations

d) Presence of both specific and non-specific manifestations

e) absence of non-specific manifestation

30. What is characteristic for the prodromal period of the disease?

a) absence of any clinical manifestations b) absence of specific manifestationsc) presence of non-specific manifestationsd) presence of both specific and non-specific manifestationse) disappearance of the disease’s manifestations

31. What is characteristic for the period of complete disease manifestation? a) absence of any clinical manifestations b) absence of specific manifestations

c) presence of non-specific manifestationsd) presence of both specific and non-specific manifestationse) disappearance of the disease’s manifestations

32. What does the pathological process include?a) the totality of injuries caused by the action of primary cause b) the totality of injuries caused by the action of primary cause and the subsequent

pathogenetic factorsc) the totality of injuries caused by the action of primary cause plus the subsequent

pathogenetic factors plus the protective, compensatory and reparative reactionsd) the totality of local injuriese) the totality of local and general injuries

33. What does the disease represent?a) the combination of injuries and homeostatic reactions of the organismb) the combination of local and general injuriesc) the combination of structural and functional processesd) the combination of pathogenetic and sanogenetic processese) the pathological process localized in one organ

34. What does “vicious circle” in pathogenesis represent?a) the totality of causes and effects that forms pathogenetic chain

b) closed „cause-effect” chain of causes and effects in which the last cause provokes similar effect like of the primary cause

c) closed „cause-effect” chain that maintains itself and progressively is amplified

d) closed „cause-effect” chain that can be removed only by medical intervention

e) the totality of pathological processes of one disease linked by the causal relations

35) What are eventual causes of the primary cell injuries?a) Hereditary defectsb) Exogenous pathogenic factorsc) Endogenous pathogenic factorsd) Intracellular dyshomeostasise) Mitochondrial injury with energy deficiency

36) What are eventual causes of the secondary cell injuries?a) Hereditary defectsb) Exogenous pathogenic factorsc) Endogenous pathogenic factorsd) Intracellular dyshomeostasise) General dyshomeostasis

37) What structures of cytoplasmic membrane are damaged and lead to disintegration of the cell?

a) Membrane glycoproteins

b) Membrane channelsc) Membrane receptorsd) Membrane pumpse) Hormonal cytoplasmic receptors

38) What intracellular dyshomeostasis results from cessation of membrane ionic pumps function?

a) Increased concentration of Ca2+ ions in hyaloplasmb) Increased concentration of K+ ions in hyaloplasmc) Increased concentration of Na+ ions in hyaloplasmd) Increased concentration of Ca2+ ions in the endoplasmic reticulume) Increased concentration of Ca2+ ions in interstitial space

39) What are the consequences of annihilation of the transmembrane Ca2+ ions gradient?a) Myocyte relaxation b) Inhibition of intracellular enzymes c) Activation of the intracellular enzymes d) Activation of several extracellular enzymese) Myocytes contraction

40) What are the consequences of activation of the non specific intracellular phospholipases?a) Breakdown of intracellular proteins and initiation of the cell autolysisb) Breakdown of nucleoproteins and initiation of apoptosisc) Breakdown of macroergic complexes and energy depletion d) Breakdown of membrane phospholipids e) Initiation of anaerobic glycolysis

41) What are the consequences of the intracellular ATP-ases activation?a) Breakdown of intracellular proteins and initiation of the cell autolysisb) Breakdown of nucleoproteins and initiation of apoptosisc) Breakdown of macroergic complexes and energy depletiond) Breakdown of AMP and ADPe) Initiation of anaerobic glycolysis

42) What are the consequences of the intracellular proteases activation?a) Breakdown of the intracellular proteic complexes and initiation of the cell autolysisb) Breakdown of nucleoproteins and initiation of cell apoptosisc) Breakdown of macroergic complexes and energy depletion in the celld) Breakdown of membrane phospholipidse) Breakdown of the intracellular proteic complexes and initiation of the cell apoptosis

43) What are the consequences of the intracellular nucleoproteases activation?a) Breakdown of intracellular proteins and initiation of the cell autolysisb) Breakdown of nucleic acids and initiation of cell apoptosis c) Breakdown of macroergic complexes and energy depletiond) Breakdown of membrane phospholipids e) Breakdown of nucleic acids and initiation of cell autolysis

44) What are the sources of cellular enzymes circulating in the blood?a) Intact exocrine glandsb) Intact endocrine glandsc) Cells with mutations d) Gastrointestinal tract e) Any damaged cell

45) What is the origin of the digestive enzymes circulating in the blood?a) Translocation from the damaged digestive glandsb) Translocation from the intact endocrine glandsc) Are produced by cells with mutations d) Are produced by intact digestive tracte) Translocation from the intact exocrine glands

46) What is the significance of the increased intracellular enzymes activity in the blood?a) Activation of the intracellular metabolic processesb) Activation of metabolic processesc) Activation of catalytic activity of enzymes that lead to cell apoptosisd) Activation of catalytic activity of enzymes that lead to cell injuriese) Activation of catalytic activity of enzymes that lead to cell dystrophy

47) What are the general causes of energy depletion that trigger cell dystrophy?

a) Chronic local hypoxia b) Deprivation of foodc) Acute hypoxiad) Activation of oxidative processes by toxinse) Activation of anabolic processes in acute stress

48) What are the general causes of energy depletion that trigger cell dystrophy?

a) disturbances of oxidative phosphorylation that lead to ATP depletion

b) disturbances of anabolic processes that lead to ATP depletion

c) disturbances of the transmembrane electrolytes transport

d) disturbances of the intracellular transport of macroergic phosphates

e) disturbances of cellular glycogenogenesis

49) What pathological processes are developed in dystrophy of desmodontal structures?

a) Progressive tissues atrophy

b) Progressive tissues hypertophy

c) Progressive tissue hyperplasia

d) It is followed by retraction of periodontium

e) It is not followed by retraction of periodontium

50) What pathological processes are developed in dystrophy of desmodontal structures? a) It is followed by retraction of periodontium

b) It is not followed by retraction of periodontium

c) It is followed by formation of periodontal pockets

d) It is not followed by formation of periodontal pockets

e) It is followed by progressive tissue hypertrophy

51) What are the organs that most often are prone to develop lipid dystrophy?

a) liver

b) lungs

c) kidneys

d) brain

e) sexual glands

52) What are the etiological factors of lipid dystrophy?

a) Alimentary hyperglycemia

b) Deficiency of lipids in the diet

c) Deficiency of proteins in the diet

d) Excess of proteins in diet

e) Alimentary hypolipidemia

53) What are the pathogenic mechanisms of lipid dystrophy?

a) inability of cell to catabolise lipid excess

b) Increased synthesis of apoproteins and lipoproteins that increases export of lipids

from cells

c) Decreased apoprotein level and inability to export lipids form cells

d) Hypoxia inhibits fatty acid oxidation and leads to acumulation of lipids

e) Hypoxia activates fatty acid oxidation and leads to acumulation of lipids

54) What is the pathogenetic factor of fatty liver?

a) Hyperlipidemia

b) Hypolipidemia

c) Starvation

d) Insulin excess

e) abundant synthesis of ketone bodies

55) What are the consequences of dystrophy?

a) Inflamation

b) Sclerosis

c) Aplasia

d) Hyperplasia

e) Hypertrophy

56) What is the programmed cell death?a) Cell death initiated by the genetic program of the animal speciesb) Cell death initiated by the cellular genetic programc) Cell death initiated by the extrinsic tanatogenic programd) Cell death initiated by the immune system programe) Cell death initiated by the endocrine system program

57) What is the biological significance of apoptosis?a. Maintenance of the quantitative homeostasis of cellular population

b. Maintenance of the qualitative homeostasis of cellular population

c. Maintenance of the individual biological entity

d. Maintenance of the species biological entity

e. Maintenance of the species death program

58) What cells are involved in apoptosis?

a) Cells with congenital defects

b) senescent old cells

c) cells infected with viruses

d) Ischemic body's cells

e) Cells with reparable injuries

59) What are positive signals of apoptosis initiation?a) Irreparable cell injuries of any originb) lack of prolactin for the mammary glandc) Glucocorticoids for lymphocytesd) testosterone for the prostate e) lack of estrogens for the endometrium

60) What are negative signals of apoptosis initiation?a) Absence of the growth factors

b) Absence of growth hormone (somatotropin)

c) absence of estrogens for the endometrium

d) absence of estrogens for the mammary gland

e) absence of prolactin for the endometrium

61) What is characteristic for the first period of apoptosis?

a) Condensation of the nucleus

b) Condensation of cytoplasm

c) Karyorrhexis

d) Condensation of the mitochondria

e) Karyolysis

62) What is characteristic for the second period of apoptosis?

a) Cell vacuolization

b) Karyorrhexis

c) Karyolysis

d) Disorganization of the intercellular structures and isolation from the adjacent cells

e) Phagocytosis of apoptotic bodies

63) What is characteristic for the final period of apoptosis?

a) Phagocytosis of apoptotic bodies

b) Karyorrhexis

c) Karyolysis

d) Disintegration of apoptotic bodies inside phagocytes

e) Degradation of biochemical components of apoptotic bodies in the liver

64) What conditions are necessary for apoptosis?

a) Accumulation of Ca2+ ions in the cytoplasm

b) Maintaining the apoptotic bodies integrity

c) Disorganization of the intercellular structures and isolation from the adjacent cells

d) Loose of apoptotic bodies integrity and easier recognition by macrophages

e) Maintenance of energogenesis

65) What are the consequences of exaggerated apoptosis?

a) Progressive reduction of the cell population

b) Inflammation of the resident organ

c) Atrophy of the organs with functional insufficiency

d) Parenchymatouse dystrophy of the resident organ

e) Hypersplenism and functional hepatomegaly

66) What are the general consequences of necrosis for the organism?

a) Cell death by necrosis initiate cell dystrophy in the affected tissue b) Cell death by necrosis has negative consequences for the affected organ onlyc) Cell death by necrosis has no negative consequences for the whole organismd) Cell death by necrosis initiates the acute phase reactione) Cell death by necrosis initiates fever

67) What are the general consequences of apoptosis for the organism?

a) Cell death by apoptosis initiates feverb) Cell death by apoptosis doesn’t provoke quantitative modifications of the cellular

populationc) Cell death by apoptosis initiates the acute phase reactiond) Cell death by apoptosis has no negative consequences for another structures of the

organisme) Cell death by apoptosis has negative consequences for the whole organism

68) What are the general consequences of the cell necrosis for the whole organism?

a) death of the whole organism

b) enzymemia

c) hyperkaliemia

d) hypernatriemia

e) hypercloremia

69) What are the pathogenetic mechanisms of necrosis due to cytoplasmic membrane damage?

a) Sodium and potasium outflow from the cell

b) Sodium outflow and potasium inflow to the cell

c) Sodium inflow and potassium outflow from the cell

d) Cell and cellular organells shrinkage

e) Cell and cellular organelles swelling

70) What are the pathogenetic mechanisms of necrosis due to mitochondrial injury?

a) decrease the oxidative phosphorrhylation processes

b) increase the oxidative phosphorrhylation processes

c) excess of ADP in mitochondria

d) decrease of ADP in mitochondria

e) increase of mitochondrial membrane potential

71) What is the pathogenetic role of free radicals in necrosis?

a) Peroxidation of membrane phospholipids

b) Peroxidation of saturated fatty acids

c) Peroxidation of carbohydrates

d) Peroxidation of cations

e) Peroxidation of nucleic acids

72) What is the pathogenetic role of calcium in necrosis?

a) Calcium is accumulated in the hyaloplasm

b) Calcium is accumulated in the endoplasmic reticulum

c) Calcium inhibits phospholipases in the hyaloplasm

d) Calcium activates phospholipases in the hyaloplasm

e) Calcium activates phospholipases in the endoplasmic reticulum

73) What is the pathogenetic role of hypoxia in necrosis?

a) Increased resting potential

b) Inhibitory depolarization

c) Dysfunction of the membrane ionic pumps

d) Dysfunction of the membrane ionic channels

e) Inhibitory hyperpolarization

74) What is the pathogenetic role of ATP depletion in necrosis?

a) Increases of AMP concentration

b) Decreases of AMP concentration

c) Activation of anaerobic glycolysis that lead to intracellular acidosis

d) Activation of aerobic glycolysis that lead to intracellular alkalosis

e) inhibition of anaerobic glycolysis that lead to intracellular acidosis

75) What are the manifestations of cell necrosis?

a) leakage of lysososmal enzymes in hyaloplasm

b) no leakage of lysosomal enzymes in hyaloplasm

c) cell swelling

d) cell shrinkage

e) fragmentation of the cytoplasm and formation of apoptotic bodies

76) What are the local consequences of necrosis?

a) inflammation

b) demarcation

c) incapsulation

d) Infiltration with platelets

e) Infiltration with erythrocytes

77) What factors can cause necrosis of the oral cavity?

a) Lead compounds

b) Ibuprofen administration

c) Ethanol administration in high concentration

d) Aspirin administration

e) Antiviral substances administration

78) What disorders can lead to ulcerative changes of oral mucosa?

a) Stomach ulcer

b) Hepatitis

c) Thyroiditis

d) Enterocolitis

e) Glomerulonephritis

79) What disorders can lead to ulcerative changes of oral mucosa?

a) Pancreatitis

b) Hepatitis

c) Thyroiditis

d) Enterocolitis

e) Glomerulonephritis

80) What are the conditions for formation of parietal thrombus?

a) exposure of subendothelial matrix

b) turbulent blood flow

c) enhanced blood velocity

d) increased platelet count

e) linear blood flow

81) What are the mechanisms of primary hemostasis?

a) thrombocytes activation

b) release of thromboplastin

c) formation of active thrombin

d) spasm of injured vessel

e) dilation of injured vessel

82) What are the mechanisms of secondary hemostasis?

a) retraction of fibrin clot

b) activation of plasminogen

c) release of thromboplastin

d) adhesion of thrombocyte to vessel wall

e) aggregation of thrombocytes

83) What is the physiological role of fibrinolytic system?

a) dissolution of fibrinogen excess during coagulation process

b) dissolution of fibrinogen excess after finish of thrombogenesis process

c) dissolution of parietal white thrombus in primary hemostasis

d) dissolution of fibrin excess after finish of thrombogenesis process

e) dissolution of thrombus surplus in primary hemostasis

84) What are the causes of hypercoagulation?

a) reduced level of thromboplastin

b) surplus of thromboplastin

c) increased plasminogen level in the blood

d) decreased plasminogen level in the blood

e) increased level of heparin

85) What are the pro-coagulant factors?

a) plasminogen

b) thromboplastin

c) prothrombin

d) antithrombin III

e) plasmin

86) In what condition can develop insufficiency of anti-coagulant system?

a) deficiency of heparin

b) deficiency of fibrinogen

c) deficiency of antithrombin III

d) excess of antithrombin III

e) deficiency of thromboplastin

87) When can develop heparin deficiency?

a) reduced protein level in the blood

b) reduced lipid level in the blood

c) high lipid level in the blood

d) high protein level in the blood

e) high glucose level in the blood

88) What pathological processes can lead to development of vascular purpura?

a) disorders of vascular intima trophicity

b) vascular hyperpermeability

c) changes of vascular tonus

d) spasm of smooth muscles of vessels

e) atheromatous change of blood vessels

89) What does represent thrombocytopathy?

a) decreased thrombocyte number

b) thrombocyte areactivity to thrombin

c) thrombocyte areactivity to ADP

d) deficit of coagulation plasmatic factors

e) excessive release of thromboxane by thrombocytes

90) What does represent the hemorrhagic syndrome of plasmatic origin?

a) hereditary or acquired deficit of plasmin

b) hereditary deficit of thrombocyte coagulation factors

c) hereditary or acquired deficit of prothrombin

d) hereditary or acquired deficit of thromboxane

e) hereditary or acquired deficit of thromboplastin

91) What are the manifestations of cellular alterations in the inflammatory focus?

a) cell injury

b) cell dystrophy

c) cell apoptosis

d) fibrosis

e) cell hyperplasia

92) What are the biological effects of prostaglandins PGD2, PGE2, PGF2a alpha?

a) vasodilatation

b) vasoconstriction

c) bronchodilation

d) bronchoconstriction

e) activation of the compliment system

93) What are the biological effects of thromboxane TxA2, TxB2?

a) stimulates platelet aggregation

b) suppress platelet aggregation

c) vessel spasm

d) bronchodilation

e) stimulates proliferation of fibroblasts

94) What are the biological effects of prostacyclin?

a) Stimulates platelet aggregation

b) Suppress platelet aggregation

c) Vasoconstriction

d) Bronchial spasm

e) increased vascular permiability

95) What are the biological effects of leukotrienes?

a) bronchospasm

b) pseudo allergic reactions

c) stimulate chemotaxis of polymorphonuclear leukocytes

d) vasodilation and increased vascular permiability

e) synergism with histamine

96) What inflammatory mediators are released from neutrophils?

a) histamine

b) reactive oxygen species

c) halogenated compounds

d) cationic proteins

e) antimicrobial antibodies

97) What is the sequence of vascular reactions in the inflammatory focus?

a) ischemia - arterial hyperemia - venous hyperemia – stasis

b) ischemia – venous hyperemia - arterial hyperemia – stasis

c) stasis - ischemia – arterial hyperemia - venous hyperemia

d) ischemia - arterial hyperemia - Stasis - venous hyperemia

e) arterial hyperemia - venous hyperemia - stasis – ischemia

98) What mediators lead to development of inflammatory arterial hyperemia?

a) tryptase

b) anaphylatoxins resulted from activation of the complement system

c) bradykinin

d) membrane attack complex resulted from activation of the complement system

e) lymphotoxin

99) What are the features of inflammatory arterial hyperemia?

a) persistent character

b) myoparalitic mechanism

c) neurotonic mechanism

d) is combined with decreased permeability of the blood vessels

e) is combined with increased peripheral vascular resistance

100) What is the pathogenesis of increased permeability of the blood vessel walls in the inflammatory focus?

a) effect of complement fraction C5-C9

b) efect of bradykinin

c) effect of tryptase

d) effect of catecholamines

e) e)effect of complement fraction C3a and C5a

101) What is the pathogenesis of inflammatory venous hyperemia?

a) effect of fraction C3a and C5a of the complement system

b) effect of bradykinin released into inflammatory focus

c) efect of histamine released into inflammatory focus

d) endothelial cell contraction

e) alteration of rheological proprieties of the blood

102) What is the biological significance of inflammatory venous hyperemia?

a) contributes to leukocyte emigration from vessel into inflammatory focus

b) contributes to exudate formation into inflammatory focus

c) contributes to spreading of primary alteration in the inflammatory focus

d) inhibits leucocyte emigration and phagocytosis in the inflammatory focus

e) limits the area of secondary alteration in the inflammatory focus

103) What are the characteristics of inflammatory stasis?

a) is associated with intravascular aggregation of blood cells

b) enhances the spreading of secondary alteration in the inflammatory focus

c) limits the spreading of primary alteration in the inflammatory focus

d) limits the spreading of secondary alteration in the inflammatory focus

e) is associated with reduced platelets aggregation

104) What are the hallmarks of serous exudate?

a) small molecular weight proteins up to 2-3%

b) high molecular weight proteins up to 2-3%

c) many polymorphonuclear leukocytes

d) lack of polymorphonuclear leucocytes

e) presence of lysosomal enzymes

105) What is the hallmark of purulent exudate?

a) small molecular weight proteins up to 2-3%

b) high molecular weight proteins up to 2-3%

c) many polymorphonuclear leukocytes

d) hig level of fibrinogen and fibrin

e) presence of lysosomal enzymes

106) What is the mechanism of leukocyte emigration in the inflammatory focus?

a) the action of chemotactic factors

b) increased permeability of the vessels

c) active filtration of leucocytes trough vascular wall

d) passive filtration of leukocytes through vascular wall

e) increased hydrostatic pressure in the capillaries

107) What is the mechanism of leukocyte emigration in the inflammatory focus?

a) increased hydrostatic pressure in the capillaries

b) active filtration of leucocytes trough vascular wall

c) leukocyte adhesion to the vascular wall

d) passive filtration of leukocytes through vascular wall

e) the action of hydrolytic enzymes on the vascular wall structures

108) What is the biological significance of leukocyte emigration in the site of inflammation?

a) enhances exudation in the inflammatory focus

b) release of antibacterial substances

c) specific local immunity

d) release of antibodies

e) enhances lymphogenesis

109) What is the sequence of leukocyte emigration into the inflammatory site?

a) granulocytes - monocytes – lymphocytes

b) polymorphonuclear - monocytes – lymphocytes

c) lymphocytes - granulocytes – monocytes

d) granulocytes - lymphocytes – monocytes

e) monocytes - granulocytes – lymphocytes

110) What does represent regeneration in the inflammatory focus?

a) restoration of specific parenchymal structures

b) restoration of nonspecific mesenchymal structures

c) restoration of non-specific parenchymal structures

d) restoration of specific mesenchymal structures

e) angiogenesis de novo

111) What are the characteristics of normoergic inflammation?

a) qualitatively and quantitatively is adequate with flogogenic factor

b) corresponds to the reactive capacity of the individual

c) corresponds to the reactive capacity of the biological species

d) correspond with the reactive capacity of the affected tissues

e) ) qualitatively and quantitatively is inadequate with flogogenic factor

112) When can develop hyperergic inflammation?

a) is the effect of powerful flogogenic factors on the tissue with reduced reactivity

b) is the effect of a normal flogogenic factor on sensitized organisms

c) is the effect of a powerful flogogenic factor on hyposensitized organisms

d) is the effect of a normal flogogenic factor on the tissue with normal reactivity

e) is the effect of a normal flogogenic factor on the tissue with reduced reactivity

113) When can develop hypoergic inflammation?

a. is the effect of attenuated flogogenic factor on tissue with increased resistance and reactivity

b. is the effect of normal flogogenic factor on immunized organism

c. is the effect of normal flogogenic factor on hyposensitized organisms

d. is the effect of powerful flogogenic factor on tissue with reduced reactivity and resistance

e. is the effect of normal flogogenic factor on parenchymal organs

114) What are general changes in inflammation?

a) increased level of acute-phase proteins in the blood

b) stress

c) reduced level of acute-phase proteins in the blood

d) leukocytopenia

e) immunodeficiency

115) What are general manifestations of inflammation?

a) enhanced synthesis of acute-phase proteins in the liver

b) reduced erythrocyte sedimentation rate

c) reduced synthesis of acute-phase proteins in the liver

d) increased erythrocytes sedimentation rate

e) pain

116) What are the effects of mediators released from neutrophils?

a) activates the regeneration of damaged structures in the inflammatory focus

b) activates the leukocytes emigration in the inflammatory focus

c) trigger ischemia in the inflammatory focus

d) vessel vasoconstriction in the inflammatory focus

e) inhibit exudation in the inflammatory focus

117) What chemotactic factors are released form basophiles?

a) chemotactic factor for basophils

b) chemotactic factor for eosinophils

c) chemotactic factor for T-lymphocytes

d) chemotactic factor for B-lymphocytes

e) chemotactic factor for monocytes

118) What is the sequence of processes in the synthesis of prostaglandins?

a) cyclooxygenase - arachidonic acid – phospholipase – prostaglandins

b) phospholipase – arachidonic acid – prostaglandins

c) cyclooxygenase – fatty acids – phospholipase – prostaglandins

d) phospholipase – fatty acids – cyclooxygenase – prostaglandins

e) phospholipase - cyclooxygenase – arachidonic acid - prostaglandins

119) What are the biological effects of IL-1?

a) enhances exudation in the inflammatory focus

b) stimulates the secretion of lymphokines

c) fibroblasts prioliferation

d) activates natural killer lymphocytes

e) anti-inflammatory effect

120) What inflammatory mediators are released from eosinophils?

a) cationic proteins

b) histamine

c) perforins

d) anaphylatoxins

e) antibodies against parasites

121) What inflammatory mediator is released from thrombocytes?

a) thromboxane

b) histamine

c) inhibitory factor of trombocytes

d) activator factor of fibroblasts

e) thromboplastin

122) What inflammatory mediators are released from lymphocytes?

a) anaphylatoxins

b) lymphotoxin

c) immunoglobulin M and G

d) inhibitory factor of mononuclear migration

e) immunoglobulin E

123) What are the biological effects of active complement fraction?

a) procoagulant effect

b) vasoconstriction

c) chemoattractant effect

d) cytolytic effect

e) anti-clotting effect

124) What are the kinin effects in the inflammatory focus?

a) vasoconstriction

b) smooth muscle contraction

c) smooth muscle relaxation

d) pain sensation

e) antibacterial effect

125) What are the mechanisms of phagocytosis?

a) is the result of opsonization of microbes with the complement fraction C3a and easier recognition by receptors on phagocytic cells

b) is the result of interaction between specific Fc receptors on phagocytic cells and microorganisms

c) is the result of opsonization of microbes with the complement fraction C3b and easier recognition by receptors on phagocytic cells

d) is the result of electrostatic interaction between the phagocyte receptors and microbe

e) e. ) is the result of opsonization of microbes with the complement fraction C5a and easier recognition by receptors on phagocytic cells

126) What is the pathogenesis of proliferation in the inflammatory focus?

a) is the effect of substances with proliferative effect released in the inflammatory focus by microbes

b) is the effect of substances with proliferative effect released in the inflammatory focus from mesenchymal structures

c) is the effect of substances with proliferative effect released in the inflammatory focus from thrombocytes

d) is the effect of substances with proliferative effect released in the inflammatory focus from parenchymal structures

e) deficiency of substances with inhibitory effects on proliferative processes in the inflammatory focus

127) What are the cellular sources of proliferation in the inflammatory focus?

a) fibrocytes

b) monocytes emigrated from the blood in the inflammatory focus

c) neutrophils emigrated from the blood in the inflammatory focus

d) fibroblasts

e) resident parenchymal cells

128) What are the cellular sources of proliferation in the inflammatory focus?

a) fibrocytes

b) monocytes which emigrated from the blood in the inflammatory focus

c) neutrophils emigrated from the blood in the inflammatory focus

d) resident mesenchymal cells

e) resident parenchymal cells

129) What is the result of proliferation in the inflammatory focus?

a) restoration of altered parenchymal structures

b) restoration of altered mesenchymal structures

c) abundance increase of parenchymal structures

d) angiogenesis de novo

e) tissue hyperplasia

130) What is an effect of IL-1?

a) stimulates the cyclooxygenase and production of prostaglandins

b) stimulates lipoxygenase and production of leukotrienes

c) expression of selectins and integrins and contribution to leucocyte chemotaxis

d) stimulate plasma cell to produce antibodies

e) anti-inflammatory action

131) What are the effects of interleukins in inflammation?

a) stimulates synthesis of acute-phase proteins

b) stimulates the secretion of glucocorticoids and corticotrophin

c) stimulates the natural killer lymphocytes

d) stimulate leucocyte emigration in the inflammatory focus

e) inhibits synthesis of acute-phase proteins

132) What is the definition of fever?

a) pathologic compensatory reaction which is manifested by increased body’s temperature

b) protective physiological reaction manifested by increased body’s temperature

c) disturbance of thermoregulatory center manifested by increased body temperature

d) pathologic process manifested by restructuring in activity of thermoregulatory center and increased body temperature

e) pathologic state caused by increased body temperature in increased environmental temperature

133) What does represents fever?

a) persistent increasing of body temperature at the action of high environmental temperature

b) persistent increasing of body temperature at the action of catabolic substances on the thermoregulatory center in the brain

c) episodic increasing of body temperature at the action of excitatory substances on the SNS

d) episodic increasing of body temperature at the action of non-infectious agents

e) persistent increasing and maintaining of high body temperature at the action of infectious agents

134) What are exogenous infectious pyrogenic factors?

a) bacterial antigens

b) bacterial endotoxin

c) hyperimmune sera

d) heterogeneous blood compounds in hemotransfusion

e) products of cell disintegration caused by bacteria

135) What are exogenous infectious pyrogenic factors?

a) hyperimmune sera

b) proteins of the blood in blood transfusion

c) microbial lipopolysaccharide

d) microbial and fungal proteins

e) allogeneic transplantation

136) What are exogenous noninfectious pyrogenic factors?

a) hyperimmune sera

b) heterogeneous blood and plasma

c) bacterial lipopolysaccharides

d) isotonic sodium chloride solution

e) fungal proteins

137) What is an exogenous noninfectious pyrogenic factor?

a) hyperimmune sera

b) viral and fungal proteins

c) bacterial lipopolysaccharides

d) hypertonic NaCl solution

e) progestagenic hormones

138) What are the primary endogenous pyrogenic factors?

a) products of cell necrosis

b) products of cell disintegration

c) interleukin IL-1

d) bacterial lipopolysaccharides

e) Tumor necrosis factor

139) What are the primary endogenous pyrogenic factors?

a) immunoglobulins

b) interleukin IL-1 and IL-2

c) products of erythrocyte hemolysis

d) progestagenic hormones

e) acute phase proteins

140) What is a primary endogenous pyrogenic factor?

a) immunoglobulins

b) interleukin IL-1 and IL-2

c) products of cell necrosis

d) prostaglandins

e) acute phase proteins

141) What are the secondary endogenous pyrogenic factors?

a) products of cell necrosis

b) prostaglandins

c) acute phase proteins

d) immunoglobulin

e) bacterial endotoxin released in the blood

142) What are the secondary endogenous pyrogenic factors?

a) interleukin IL-1 and IL-2

b) products of hemolysis

c) progestagenic hormones

d) immunoglobulin

e) TNF-alpha

143) What is a secondary endogenous pyrogenic factor?

a) products of cell necrosis

b) products of hemolysis

c) acute phase proteins

d) immunoglobulin

e) progestagenic hormones

144) What is the correct sequence of pathological processes in fever?

a) primary exogenous pyrogens – secondary endogenous pyrogens – fever

b) primary endogenous pyrogens – secondary endogenous pyrogens - fever

c) primary exogenous pyrogens – secondary endogenous pyrogens – primary endogenous pyrogens – fever

d) primary exogenous pyrogens - primary endogenous pyrogens – fever

e) primary exogenous pyrogens – secondary exogenous pyrogens – primary endogenous pyrogens – secondary endogenous pyrogens – fever

145) What is the pathogenesis of fever?

a) increased body temperature in increased environmental temperature

b) increased thermolysis

c) reduced thermolysis

d) excessive catabolic processes in the body

e) restructuration in the activity of thermoregulatory center

146) What are the mechanisms of increased thermogenesis in fever?

a) simpatho-adrenal activation and enhanced catabolic reactions

b) simpatho-adrenal inhibition and enhanced catabolic reactions

c) activation of anabolic reactions in the body

d) muscle hyperkinesia

e) reduced pulmonary ventilation

147) What are the mechanisms of increased thermogenesis in fever?

a) inhibition of catabolic reactions

b) simpatho-adrenal inhibition

c) activation of catabolic reactions

d) muscle hyperkinesia

e) activation of anabolic reactions

148) What are the mechanisms of reduced thermolysis in the initial period of fever?

a) spasm of peripheral blood vessel

b) pulmonary hypoventilation

c) tonic muscular contractions

d) excessive sweating

e) pulmonary hyperventilation

149) What are the mechanisms of reduced thermolysis in the initial period of fever?

a) peripheral vasoconstriction

b) tonic muscular contractions

c) peripheral vasodilation

d) excessive sweating

e) reduced sweating

150) What are the mechanisms of enhanced thermolysis in the final stage of fever?

a) peripheral vasodilation

b) bradypnea

c) tachypnea

d) clonic muscular contractions

e) reduced sweating

151) What does represents the process of thermoregulatory center restructuration in the first period of fever?

a) simultaneous stimulation of thermogenesis and thermolysis

b) stimulation of thermogenesis and inhibition of thermolysis

c) inhibition of thermogenesis and activation of thermolysis

d) simultaneous inhibition of thermogenesis and thermolysis

e) stimulation of thermogenesis with unchanged thermolysis

152) What are the mechanisms of activation of thermogenesis in fever?

a) excitation of the sympathetic nervous system

b) excitation of the parasympathetic nervous system

c) tonic muscular contractions

d) activation of lipolysis and glycogenolysis

e) hypersecretion of anabolic hormones

153) What are the mechanisms of activation of thermogenesis in fever?

a) tonic muscular contractions

b) excitation of the parasympathetic nervous system

c) activation of catabolic reactions

d) clonic muscular contractions

e) hypersecretion of insulin

154) What are the metabolic changes in the second stage of fever?

a) enhanced anabolic processes

b) depletion of liver glycogen

c) enhanced lipolysis and glycogenolysis

d) enhanced lipogenesis and glycogenogenesis

e) positive nitrogen balance

155) What are the metabolic changes in the second stage of fever?

a) enhanced anabolic reactions

b) enhanced catabolic reactions

c) positive nitrogen balance

d) enhanced lipogenesis and glycogenogenesis

e) negative nitrogen balance

156) What are the cardiovascular changes in the second period of fever?

a) tachycardia

b) generalized spasm of blood vessels

c) centralization of blood circulation and redistribution to vital organs (brain, lungs)

d) arterial hypertension

e) arterial hypotension caused by excessive sweatining

157) What are the cardio-vascular changes in the third period of fever?

a) tachycardia

b) generalized spasm of blood vessels

c) centralization of blood circulation and redistribution to vital organs (brain, lungs)

d) arterial hypertension caused by peripheral vasoconstriction

e) arterial hypotension

158) What is the biological significance of fever?

a) reduces the systemic manifestations of inflammation

b) stimulates phagocytosis

c) inhibits allergic reactions

d) reduces the local manifestations of inflammation

e) enhances the bacteriostatic effect of antibiotics

159) When the pyrotherapy is justified?

a) hypoergic inflammation

b) chronic inflammation

c) acute inflammation

d) inflammatory reaction with immunodeficiency

e) hyperergic inflammation

160) When the pyrotherapy is justified?

a) hyperergic inflammation

b) chronic inflammatory processes

c) specific inflammatory processes

d) inflammatory reaction with immunodeficiency

e) hypoergic inflammatory processes in exhausted patients

161) When the antipyretic therapy is justified?

a) hyperergic inflammation

b) autoimmune processes

c) allergic diseases

d) moderate fever but intolerable for patients

e) in all cases of fever, antipyretic therapy is indicated

162) What are the characteristics of complete antigen?

a) causes humoral immune responses by stimulation of antibody synthesis

b) doesn’t causes humoral immune responses but interact with previously synthesized antibodies

c) causes cellular immune reactions by stimulating the sensitization of lymphocytes

d) doesn’t cause cellular immune responses but interacts with previously sensitized lymphocytes

e) causes humoral immune response by interaction with sensitized lymphocytes

163) What are the characteristics of incomplete antigen?

a) causes humoral immune response by stimulation of antibody synthesis

b) doesn’t causes humoral immune responses but interact with previously synthesized antibodies

c) causes cellular immune responses by stimulating the sensitization of lymphocytes

d) doesn’t causes cellular immune reaction but interact with previously sensitized lymphocytes

e) causes humoral immune response by interaction with sensitized lymphocytes

164) What is the biological significance of allergic reactions?

a) represents a pure immune reaction which underlies on the basis of natural immunity

b) represents an immune reaction with elements of cell injury

c) represents an immune reaction associated with inflammation

d) represents a pure immune reaction which underlie on the basis of adaptive immunity

e) represents a pure inflammatory reaction

165) What is the feature of immediate hypersensibility?

a) underlies on the basis of humoral immune reactions

b) underlies on the basis of cellular immune reactions

c) underlies on the basis of acute inflammatory reaction

d) underlies on the basis of chronic inflammatory reaction

e) underlies on the basis of mixed immune reactions - humoral and cellular

166) What is the feature of immediate hypersensibility?

a) underlies on the basis of immunoglobulin production

b) underlies on the basis of cellular immune reactions

c) underlies on the basis of acute inflammatory reaction

d) underlies on the basis of chronic inflammatory reaction

e) underlies on the basis of production of sensitized lymphocytes

167) What is the feature of delayed hypersensibility?

a) underlies on the basis of humoral immune reactions

b) underlies on the basis of cellular immune reactions

c) underlies on the basis of acute inflammatory reaction

d) underlies on the basis of chronic inflammatory reaction

e) underlies on the basis of mixed immune reactions - humoral and cellular

168) What is the feature of delayed hypersensibility?

a) underlies on the basis of humoral immune reactions

b) underlies on the basis of production of sensitized lymphocytes

c) underlies on the basis of immunoglobulin production

d) underlies on the basis of chronic inflammatory reaction

e) underlies on the basis of mixed immune reactions - humoral and cellular

169) What substances are complete antigens?

a) nucleoproteins

b) proteins

c) lipopolysaccharides

d) simple organic substances

e) inorganic substances

170) What substances are incomplete antigens?

a) nucleoproteins

b) proteins

c) lipopolysaccharides

d) simple organic substances

e) inorganic substances

171) What does represents the endogenous antigen?

a) products of cell injury which are released in the blood

b) products of the bacterial or fungal origin which are released in the blood

c) natural components of the human body which lack the immunological tolerance

d) natural components of the human body which have immunological tolerance

e) natural components of the human body changed by action of harmful factors

172) What are the characteristics of type I allergic reactions?

a) reaction between free allergen in circulation and fixed antibodies on parenchymal cells

b) reaction between allergen fixed on the cells and free antibodies in circulation

c) reaction between allergen and antibodies both in circulation

d) reaction between allergen and sensitized lymphocytes

e) reaction between free allergen in circulation and antibodies fixed on mast cells

173) What are the characteristics of type II allergic reactions?

a) reaction between free allergen in circulation and fixed antibodies on parenchymal cells

b) reaction between allergen fixed on the cells and free antibodies in circulation

c) reaction between allergen and antibodies both in circulation

d) reaction between allergen and sensitized lymphocytes

e) reaction between free allergen in circulation and antibodies fixed on mast cells

174) What are the characteristics of type III allergic reactions?

a) reaction between free allergen in circulation and fixed antibodies on parenchymal cells

b) reaction between allergen fixed on the cells and free antibodies in circulation

c) reaction between allergen and antibodies both in circulation

d) reaction between allergen and sensitized lymphocytes

e) reaction between free allergen in circulation and antibodies fixed on mast cells

175) What are the cells involved in anaphylactic allergic reactions?

a) cytotoxic lymphocytes

b) B lymphocytes

c) macrophages

d) natural killer lymphocytes

e) plasma cells

176) What are the end-effectors in anaphylactic allergic reactions?

a) immunoglobulins E

b) immunoglobulin A

c) immunoglobulin G4

d) sensitized B lymphocytes

e) sensitized T lymphocytes

177) What mediators are produced in the mast cells via cyclooxygenase pathway?

a) histamine

b) chemotactic factors

c) platelet activating factor

d) leukotrienes

e) prostaglandins

178) What mediators are produced in the mast cells via lipoxygenase pathway?

a) histamine

b) chemotactic factors

c) platelet activating factor

d) leukotrienes

e) prostaglandins

179) How can be performed the specific hyposensitisation in anaphylactic reaction?

a) fractional administration high doses of specific allergen

b) fractional administration of low doses of specific allergen

c) administration of antibodies specific for allergen

d) fractional administration of high doses of non-specific allergen

e) transfer of sensitized lymphocytes from another sensitized person

180) How can be performed the hyposensitisation by inhibition of antibody synthesis in anaphylactic reactions?

a) administration of immunosuppressant

b) administration of antihistamines

c) administration of non-steroidal anti-inflammatory drugs

d) administration anti-leukotrienes drug

e) administration of mast cell stabilizers

181) How can be diminished the pathochemical processes in anaphylactic reactions?

a) administration of anti-leukotrienes and antihistamines

b) stabilization of mast cells

c) administration of steroid drugs

d) administration of non-steroid drugs

e) inhibition of complement activity

182) How can be diminished the pathophysiological processes in anaphylactic reactions?

a) administration of anti-leukotrienes and antihistamines

b) administration of immune suppressors

c) administration of choline blockers

d) administration of glucocorticoids

e) administration of mast cell stabilizer

183) What are the characteristics of allergic reactions type II?

a) are directed against own defective, mutant, degenerated cells

b) are directed toward own aging cells

c) directed against own healthy cells, which are presenting the antigen

d) directed against own healthy cells coated with antibodies IgE

e) directed against own healthy cells coated with antibodies IgM

184) 281. What is the antigen which can trigger type II allergic reaction?

a) iso-antigenic erythrocytes and platelet which are opsonized with IgM

b) iso-antigenic erythrocytes and leucocytes which are opsonized with IgA

c) heterogeneous immune sera which stimulates production of IgM

d) heterogeneous immune sera which lead to production of sensitized lymphocytes

e) iso-antigenic erythrocytes, leukocytes, platelet, in association with drugs

185) What is the mechanism of cytolysis in allergic reactions type II (cytotoxic, cytolytic)?

a) direct destruction of the cells by IgM and IgG

b) phagocytosis of cells opsonized with IgE and IgG4 by macrophages

c) direct destruction of the cells by complement C5-C9 fraction

d) direct destruction of the cells by complement fraction C3a and C5a

e) phagocytosis of cells opsonized with IgM by macrophages

186) What are the final effects in type II allergic reactions?

a) hemolytic anemia

b) neutropenia

c) lymphocytosis

d) thrombocytosis

e) lymphocytopenia

187) What are the characteristics of type III allergic reaction?

a) interaction between antigen and IgM and IgG in the blood

b) interaction between antigen and IgE fixed on mast cells

c) interaction between IgM and IgG with antigen fixed on somatic cells

d) involvement of T helper lymphocytes and B lymphocytes

e) involvement of T helper lymphocytes and sensitized lymphocytes

188) What are the pathogenetic factors involved in pathochemical phase of allergic reactions type III?

a) C5-C9 fraction of the complement system with vasoconstriction effect

b) neutrophil chemotaxis and release of lysosomal enzymes

c) mast cell degranulation and platelet activation

d) C3a and C5a fraction of the complement system with vasodilation

e) tissue infiltration with sensitized lymphocytes

189) What are the effects of mediators involved in the allergic reaction type III?

a) bronchoconstriction

b) injury of endothelial cells

c) alterative inflammation

d) proliferative inflammation

e) granulomatous inflammation

190) What structures are frequently involved in allergic reactions type III?

a) lymph nodes

b) skeletal muscles

c) renal glomeruli

d) gastrointestinal tract

e) bronchial mucosal layer

191) What are local manifestations in allergic reaction type III?

a) arterial hyperemia

b) proliferative inflammation

c) ischemia

d) infiltration with neutrophils leukocytes

e) infiltration with T lymphocytes

192) What disorders underlie on the basis of II allergic reactions?

a) myasthenia gravis

b) endemic goiter

c) cretinism

d) thyroid adenocarcinoma

e) thyrotoxicosis

193) What is the pathogenesis of allergic reaction type II?

a) antigen-antibody interaction on T cell membrane

b) antigen-antibody interaction on mast cell membrane

c) antigen-antibody interaction on the surface of parenchymal cells

d) interaction of parenchymal cells with sensitized T cells

e) antigen-antibody interaction on the surface of mesenchymal cells

194) What can be the antigen in type II allergic reaction?

a) specific antigens in the bloodstream

b) specific receptors on the cell membrane

c) exogenous substance in the bloodstream

d) endogenous substance in the bloodstream

e) hyperimmune sera in the blood

195) What antigens can trigger delayed hypersensibility?

a) autoantigens

b) bacteria

c) sequestered unchanged endogenous antigen

d) endogenous antigens changed by pathogenetic factors

e) endogenous antigen with immunological tolerance

196) What does represent allergic reactions type IV?

a) immediate hypersensibility

b) delayed hypersensibility

c) allergic reactions involving sensitized T lymphocytes

d) allergic reactions with the participation of B lymphocytes and plasma cells

e) allergic reactions involving activation of the complement system

197) What are the mediators of pathochemical phase of allergic reactions type IV?

a) lymphokines

b) lymphotoxin

c) histamine

d) immunoglobulin M and G

e) immunoglobulin E

198) What is the pathogenesis of physiological phase in allergic reactions type IV?

a) direct action of cytotoxic lymphocytes

b) proteolysis performed by lysosomal enzymes

c) effects of lymphotoxin

d) direct action of IgM and IgG

e) direct action of natural killer lymphocytes

199) What is the final effect of allergic reactions type IV?

a) exudative inflammation

b) fibrinous inflammation

c) proliferative inflammation

d) necrosis with scarring

e) purulent inflammation

200) What disorders underlie on the basis of delayed hypersensibility?

a) tuberculosis

b) serum sleekness

c) glomerulonephritis

d) Sjogren's syndrome

e) bronchial asthma

201) What does represent the autoimmune reactions?

a) represents reactions against endogenous biologic active substances

b) represents reactions based on humoral immune reactions

c) represents reactions against endogenous toxins

d) represents reactions based on cellular immune reactions

e) represents pseudoallergic reactions

202) What antigens can trigger autoimmune reaction?

a) own native antigens which lack the immunological tolerance

b) own native antigens changed by physical action

c) own native antigens which have immunological tolerance

d) transplant rejection in allogeneic transplantation

e) transplant rejection in heterogeneous transplantation

203. What does involve the microcirculatory system?a. Arterial-venular anastomosis, metarterioles, capillaries, venules, veinsb. Arteries, arterioles, metarterioles, capillaries, venules, veinsc. Arterioles, metarterioles, arterial-venular anastomosis, capillaries, venulesd. Arterioles, metarterioles, capillaries, venules, veins

e. Arterioles, arterial-venous anastomosis, capillaries, venules

204. What ions have vasoconstrictive effect?a) sodiumb) potassiumc) calciumd) hydrogene) magnesium

205. What ions have vasodilatory effect?

a) zincb) potassiumc) hydrogend) carbone) calcium

206. What is the correlation between the inflow and outflow of blood in arterial hyperemia?a. Inflow and outflow are reducedb. Inflow is increased and outflow is reducedc. Inflow and outflow are enhanced d. Outflow is increased and inflow is unchanged e. Inflow is increased and outflow is unchanged

207. What is characteristic for neurotonic mechanism of arterial hyperemia?a) Decreased parasympathetic influences of arterioles

b) Increased parasympathetic influences on arteries with their dilation

c) Increased parasympathetic influences on arterioles

d) Decreased sympathetic influences on arteries

e) Decreased vascular reactivity to catecholamines

208. What is characteristic for neuroparalytic mechanism of arterial hyperemia?a) Decreased parasympathetic influences on arterioles b) Decreased vascular reactivity to acetylcholinec) Decreased vascular reactivity to catecholamines d) Increased parasympathetic influences on arterioles e) Decreased sympathetic influences on arterioles

209. What mechanisms are specific for functional arterial hyperemia?a. Metabolic b. Neurotonic c. Mechanicald. Neuroparalytice. Humoral

210. What are the metabolic changes in arterial hyperemia?a. Decreased arterial - venous oxygen differenceb. Increased arterial - venous oxygen differencec. Increased oxygen pressure in venous blood d. Increased oxygen pressure in arterial bloode. Increased supply and decrease consumption of oxygen

211. What are the external changes of arterial hyperemia?

a. Diffuse general erythemab. Local erythema c. Decreased tissue turgord. Increased local temperature e. Hyperthermia of the body

212. What etiological factors are responsible for developing of vinous hyperemia?

a) Increased elasticity of the venous wallb) Decreased arterial-venous pressure difference in heart failure c) Decreased aspiration force of the thorax

d) Increased aspiration force of the thorax e) Increased arterial-venous pressure difference in heart failure

213. What are the metabolic changes in venous hyperemia?

a. Decreased aerobic metabolic process

b. Increased aerobic metabolic process

c. Increased anaerobic metabolic processes

d. local metabolic alkalosis

e. Decreased anaerobic metabolic processes

214. What are the metabolic changes in venous hyperemia?a) Enhanced glycolysis b) Increased energogenesisc) Reduced glycolysisd) Metabolic alkalosise) Metabolic acidosis

215. What are the external manifestations of venous hyperemia?a) Decreased tissular turgorb) Decreased local temperature c) Decreased body temperatured) General cyanosise) Local cyanosis

216. What are the pathogenetic mechanisms of edema in venous hyperemia?a) Increased hydrostatic pressure in the arteriolesb) increased hydrostatic pressure in the capillaries c) decreased lymphatic reflux from the organ d) decreased oncotic pressure in the capillaries e) decreased lymphogenesis and lymphodynamics

217. What are the pathogenetic mechanisms of external changes in venous hyperemia?a) Decreased local temperature due to reduction of arterial blood inflow b) Decreased local temperature due to tissular swellingc) Increased local temperature due to increased energogenesisd) Decreased local temperature due to decreased energogenesis e) Increased local temperature due to increased metabolic processes

218. What are the consequences of venous hyperemia?a) Hyperplasiab) Hypertrophyc) Organ sclerosisd) Local edemae) General edema

219. What are the general consequences of venous hyperemia?a) Decreased cardiac output b) Renal insufficiencyc) Decreased arterial blood pressure d) Decreased central output venous pressuree) Increased cardiac

220. What are the pathogenetic mechanisms of ischemia?a) Vasoconstriction, vasodilation, acute hemorrhageb) Neurogenic mechanism, obstruction, compression, redistribution of blood c) Neurogenic mechanism, obstruction, compression, storage of the bloodd) Neurogenic, endocrine, neuroparalytic, cardiogenic mechanisme) Redistribution of blood, compression, renal mechanism by vasodilation

221. What are the metabolic changes in ischemia?a) local acidosis b) local alkalosisc) Decreased aerobic metabolic processes d) Increased aerobic metabolic processese) Decreased anaerobic metabolic processes

222. What are the external manifestations of ischemia?a) Increased turgor of the skinb) Decreased turgor of the skinc) Redness of ischemic tissued) Paleness of ischemic tissuee) Swelling of the tissue

223. What is the pathogenetic mechanism of decreased volume of the ischemic organ?a. Increased volume of interstitial fluidb. Decreased volume of interstitial fluid c. Increased volume of intracellular fluid

d. Decreased volume of intracellular fluid

e. Reduced lymphogenesis and lymphodynamics

224. What types of embolisms are considered as endogenous?a. Atheromatous b. Gaseous c. With amniotic fluid d. With aire. Microbial

225. How are classified emboli by the direction of their circulation? a) Orthograde

b) Anterograde c) Retrograde d) Paradoxical e) Turbulent

226. What are the causes of air embolism?a) Trauma of aortab) Trauma of venous cranial sinusc) Trauma carotid artery d) Trauma of jugular veinse) Trauma of pulmonary artery

227. In what conditions can develop gaseous embolism? a) Decrease of dissolved gas concentration in the blood b) Sudden decrease in atmospheric pressure c) Decreased solubility of gases in the blood d) Increased solubility of gases in the bloode) Sudden increase in atmospheric pressure

228. When can develop embolism in the systemic circulation?a) Thrombophlebitis in arm venab) Thrombophlebitis of leg venac) Dilation varicesd) Myocardial aneurism e) Paradoxical embolism

229. What are the general consequences of embolism?a) pulmonary failure b) Thrombophlebitisc) Hypertension in systemic circulationd) Sudden death e) Hypotension in pulmonary circulation

230. What are the pathogenetic factors of capillary stasis?a) Intracapillary aggregation of erythrocytesb) Increased concentration of albumins in the bloodc) Increased blood viscosityd) Decreased blood viscosity e) Decreased concentration of globulins in the blood

231. What are the pathogenetic factors of capillary stasis?a) Decreased blood velocity b) Hemodilution c) Decreased concentration of plasma globulinsd) Increased concentration of plasma globulins e) Increased blood velocity

232. What are the manifestations of stasis?a) Decreased local temperature

b) Decreased body temperaturec) Reduced tissular turgord) Local cyanosis e) General cyanosis

233. What are the manifestations of stasis?a) Cyanosis due to decreased blood velocity b) Cyanosis due to increased blood velocityc) Cyanosis due to accumulation of carbhemoglobin in vessels d) Cyanosis due to decreased oxyhemoglobin in vesselse) Cyanosis due to accumulation of carboxihemoglobin in vessels

234. What are the manifestations of stasis?a) Microhemorrahages due to increased hydrostatic pressure

b) Microhemorrhages due to decreased hydrostatic pressure

c) Microhemorrhages due to increased permiability of the vessels

d) Microhemorrhages due to decreased permiability of the vessels

e) Microhemorrhages due to increased blood velocity

235. What is homeostatic regeneration? a) Recovery of used structures that were excluded from physiological activity b) Regeneration that is initiated by functional overloading of the organ c) Regeneration oriented to protection of the organ from pathogenic actiond) Regeneration initiated by functional overloading of the organ in pathological processe) Restitution of the cellular population of the organ affected by pathogenic factor

236. What is adaptive regeneration? a) Regeneration initiated by the functional overuse induced by new environmental conditions b) Recovery of used structures that were excluded from utilizationc) Regeneration initiated by functional overloading of the organ in pathological processd) Regeneration oriented to protection of the organ from pathogenic actione) Restitution of the cellular population of the organ affected by pathogenic factor

237. What is compensatory regeneration?

a) Recovery of used structures that were excluded from utilizationb) Regeneration initiated by functional overloading of the organ in pathological processc) Regeneration initiated by functional overloading of the organ in pathological process in

synergic organ d) Regeneration oriented to protection of the organ from pathogenic actione) Restitution of the cellular population of affected organ by pathogenic factor

238. What is protective regeneration?a) Recovery of used structures and those that have been excluded from utilization

b) Regeneration initiated by functional overloading induced by environmental conditions

c) Regeneration oriented to protection of the organ from pathogenic action

d) Regeneration initiated by functional overloading of the organ in pathological process

e) Restitution of the cellular population of affected organ by pathogenic factor

239. What is reparative regeneration?

a) Recovery of used structures during physiologic activity

b) Regeneration initiated by functional overloading induced by new environmental conditions

c) Regeneration initiated by functional overloading of the organ in pathological process

d) Restitution of the cellular population of affected organ by pathogenic factor

e) Regeneration oriented to protect the organ from pathogenic action

240. What is pathological regeneration?

a) Dysplasia

b) Metaplasia

c) Hyperplasia

d) Hypertrophy

e) Anaplasia

241. What does the physiological regeneration represent?a) Defect regeneration with a recovery of the initial tissue volumeb) Defect regeneration with tissue excess c) Defect regeneration with tissue deficiency d) Regeneration of the pathogen factor induced defect with a similar tissuee) Regeneration of the pathogen factor induced defect with an atypical tissue

242. What is characteristic of pathological regeneration?

a) It isn’t quantitative adequate b) It isn’t qualitative adequatec) Regeneration of defect with a recovery of the initial tissue volume

d) Regeneration of defect induced by pathogen factor with a similar tissuee) Regeneration of defect with a recovery of the initial tissue volume

243. What does the sclerosis of organ mean?a) Pathological regeneration b) Reparative physiological regenerationc) Compensatory physiological regeneration d) Protective physiological regeneration e) The last phase of the inflammation

244. Which structures from oral cavity have high regenerative potential?

f) Oral cavity epithelium

g) Chewing muscles

h) Granular periodontal tissue

i) Tooth enamel

j) Odontoblasts

245. In what conditions can develop symptomatic gingival hypertrophy?

a) Endocrine disorders

b) electrolytic disorders

c) anemia

d) Glomerulopathy

e) Liver disorders

246. What are the disorders that could lead to teeth attrition?a) Disorders of thyroid glandb) Disorders of parathyroid glandc) Disorders of adrenal glandsd) Disorders of gonadse) Disorders of liver

247. In what conditions can develop atrophy of the mouth mucosa?a) Bacterial infectionb) collagen diseasec) chronic inflammationd) acute inflammation

e) viral infection

248. What are the pathogenetic mechanisms of scleroderma in oral cavity?a) lingual edemab) macrocirculatory disordersc) tissue atrophyd) tissue hypertrophye) tissue hyperplasia

249. What are the pathogenetic mechanisms of scleroderma in oral cavity?a) microcirculatory disordersb) macrocirculatory disordersc) tissue hyperplasia d) tissue hypertrophye) inflammatory processes

250. What are the trigger factors for development of hypertrophy?a) Increased workload of the organb) Decreased workload of the organc) Hormonal hypersecretiond) Hormonal hyposecretione) Hypersecretion of vasoactive agents

251. What atrophy is considered as physiological?a) Peripheral endocrine gland atrophy in the hypophyseal tropic hormone hyposecretion b) Atrophy of hormone dependent organ in the deficiency of peripheral hormone c) Organ atrophy due to organism aging d) Organ atrophy in the hyponutrition e) Atrophy of organ in the denervation

252. What factor induces sclerosis?a) Cell lesions b) Cell mitosis cessation c) Primary hypofunction of the organ d) Growth factors lack e) Apoptosis

253. What are the pathogenetic mechanisms of sclerosis?

a) Increased synthesis of the collagen fibers by proliferation of fibroblastsb) Increased synthesis of the collagen fibers by proliferation of fibrocytesc) Increased synthesis of the collagen fibers by proliferation of macrophagesd) Activation of the collagenolytic processese) Inhibition of the collagenolytic processes

254. What is one of the consequences of sclerosis?a) Organ malignancyb) Fatty dystrophy of the organ

c) Organ deformation d) Hypertrophy of the organ e) Cell dedifferentiation

255. What is the normal concentration of Na+ ions in the blood?

a) less than 100 - mEq/L

b) 100 -125 mEq/L

c) 135 - 145 mEq/L

d) 140 -160 mEq/L

e) above 300 mEq/L

256. From what value of the concentration of Na+ ions in the blood there is considered hypernatremia?

a) above 100 mEq/L

b) above 152 mEq/L

c) above 142 mEq/L

d) above 132 mEq/L

e) above 300 mEq/L

257. From what value of the concentration of Na+ ions in the blood there is considered hyponatremia?

a) less than 100 mEq/L

b) less than 152 mEq/L

c) less than 140 mEq/L

d) less than 120 mEq/L

e) less than 300 mEq/L

258. What does represent hypernatremia?

a) blood sodium concentration above 140 mmol/L

b) blood sodium concentration above 140 mEq/L

c) blood sodium concentration above 152 mEq/L

d) sodium concentration in the interstitial fluid above 140 mEq/L

e) sodium concentration in the interstitial fluid above 152mEq/L

259. What are the main pathogenetic mechanisms of hypernatremia?

a) dehydration with excessive loss of body water

b) release of sodium ions from damaged cells

c) decreased synthesis of renin in the kidneys

d) hyperhydration with excessive gain of body water

e) increased synthesis of renin in the kidneys

260. What does mean hyponatremia?

a) decreased blood sodium concentration below 120 mEq /l

b) decreased concentration of sodium in the interstitial fluid below 135 mEq /L

c) decreased blood sodium concentration below 100 mEq /L

d) decreased blood sodium concentration below 100 mmol/L

e) decreased concentration of sodium in the interstitial fluid below 100 mEq /L

261. What are the causes of absolute hyponatremia?

a) hyperproduction of glucocorticoids

b) hyperproduction of mineralocorticoids

c) excessive renin production in the kidneys

d) insufficiency of mineralocorticoid

e) deficiency of renin production in the kidneys

262. What are the main pathogenetic mechanisms of hyponatremia?

a) excessive gain of body fluids

b) excessive loss of body fluids

c) deficiency of mineralocorticoids

d) excessive release of sodium from damaged cells

e) hypersecretion of mineralocorticoids

263. What is the normal concentration of K+ ions in the blood?

a) 5,5 - 6,5 mEq/L

b) 3,5 – 5,5 mEq/L

c) 2,5 – 3,5 mEq/L

d) less than 2,5 mEq/L

e) less than 1,5 mEq/L

264. From what value of K+ ions concentration in the blood there is considered hyperkalemia?

a) above 5,5 mEq/L

b) above 4,5 mEq/L

c) above 3,5 mEq/L

d) above 7,5 mEq/L

e) above 2,5 mEq/L

265. From what value of K+ ions concentration in the blood there is considered hypokalemia?

a) less than 5,5 mEq/L

b) less than 4,5 mEq/L

c) less than 3,5 mEq/L

d) less than 2,5 mEq/L

e) less than 7,5 mEq/L

266. What is the physiological role of potassium in the body?

a) maintains the plasmatic osmotic pressure

b) maintains the plasmatic oncotic pressure

c) ensures the active membrane potential in the excitable cells

d) ensures the resting membrane potential in the excitable cells

e) maintains the threshold potential in the excitable cells

267. What is the physiological role of potassium in the body?

a) formation of resting membrane potential of excitable cells

b) formation of active membrane potential in the excitable cells

c) the maintenance of extracellular fluid osmolarity

d) participate in protein synthesis

e) maintains sympathetic nervous system activity

268. In what disorders can be found hyperkalemia?

a) hyperhydration with gain of body fluids

b) hypersecretion of aldosteron

c) enhanced catabolism of tissue proteins

d) increased plasma renin concentration

e) decreased plasma renin concentration

269. What can be the causes of hypokalemia?

a. deficiency of renin in the blood

b. hypersecretion of glucocorticoids

c. excessive renin in the blood

d. deficiency of glucocorticoids

e. overhydration of the body

270. What are the pathogenetic mechanisms that contribute to development of hypokalemia?

a) disturbances of glomerular filtration and water retention in the body

b) excessive loss of potassium in the kidneys in hypersecretion of aldosteron

c) excessive loss of potassium in the kidneys in hyposecretion of aldosteron

d) hypersecretion of vasopressin

e) deficiency of vasopressin

271. What is the mechanism of hypokalemia in chronic liver disorders?

a) reduced consumption of K+ for protein synthesis

b) low level of aldosteron in the blood

c) high level of aldosteron in the blood

d) reduced consumption of K+ for glycogenolysis

e) enhanced catabolism of tissue proteins

272. What is the normal concentration of Ca++ ions in the blood?

a) 1,5 – 2,5 mmol/L

b) 2,1 – 2,6 mmol/L

c) 4,5 – 5,5 mmol/L

d) less than 1,0 mmol/L

e) more than 3,5 mmol/L

273. From what value of the concentration of Ca++ ions in the blood there is considered hypercalcemia?

a) above 2,6 mmol/L

b) above 3,5 mmol/L

c) above 1,6 mmol/L

d) above 2,0 mmol/L

e) above 7,0 mmol/L

274. From what value of the concentration of Ca++ ions in the blood there is considered hypocalcemia?

a) less than 5,3 mmol/L

b) less than 0,5 mmol/L

c) less than 2,1 mmol/L

d) less than 1,0 mmol/L

e) less than 7,0 mmol/L

275. What is the physiological role of Ca++ ions in the body?

a) acts as intracellular second messenger

b) maintains plasma osmotic pressure

c) provides electrical charge to plasma proteins

d) participates in protein synthesis

e) maintains resting membrane potential of excitable cell

276. What intracellular enzymes are activated by Ca++ ions?

a. superoxide dismutase

b. cytochrome oxidase

c. protease

d. phospholipases

e. catalase

277. What are the main mechanisms which maintain the calcium homeostasis?

a) redistribution of Ca++ ions between intra- and extracellular compartment of the body

b) removing of calcium salts with bile in the gastrointestinal tract

c) incorporation and mobilization from bone matrix

d) incorporation and mobilization from teeth matrix

e) reabsorption on calcium in the proximal renal tubules

278. What are the most important mechanisms regulating homeostasis of calcium ions?

a. parathyroid hormone increases mobilization of Ca++ from bone tissue

b. parathyroid hormone increases incorporation of Ca++ in the bone tissue

c. active form of vitamin D inhibits Ca++ absorption from gastrointestinal tract

d. calcitonin increases incorporation of Ca++ in the bone tissue

e. calcitonin increases mobilization of Ca++ from bone tissue

279. What are the causes of hypercalcemia?

a) hypersecretion of parathyroid hormone

b) hereditary defective of calcium-dependent receptors (for parathyroid hormone)

c) hyposecretion of calcitonin

d) deficiency of vitamin D

e) hyposecretion of parathyroid hormone

280. What are the causes of hypercalcemia?

a) hypersecretion of mineralocorticoids

b) hyposecretion of calcitonin

c) excessive vitamin D

d) deficient vitamin D

e) deficiency of mineralocorticoids

281. What are the main pathogenetic mechanisms of hypercalcemia?

a) redistribution between intra- and extracellular compartment

b) increased mobilization from teeth matrix

c) increased mobilization from bone matrix

d) reduced renal reabsorption

e) reduced renal secretion

282. What are the clinical manifestations of hypercalcemia?

a) neuronal inhibition

b) neuronal excitation

c) muscle hypertonia

d) hyperreflexia

e) muscle paralysis

283. What are the causes of hypocalcemia?

a) hypersecretion of calcitonin

b) hypersecretion of parathyroid hormone

c) hyposecretion of calcitonin

d) Hyperphosphatemia

e) hypophosphatemia

284. What are the main pathophysiological mechanisms of hypocalcemia?

a) deficient mobilization from the bone in deficiency of PTH

b) deficient mobilization from the bone in excessive PTH

c) decreased incorporation in the bone in hyposecretion of calcitonin

d) enhanced calcium secretion in the proximal renal tubes

e) enhanced calcium reabsorption in the proximal renal tubes

285. What are the causes of hyperphosphatemia?

a) mobilization from bone matrix

b) hyposecretion of PTH

c) hypersecretion of PTH

d) intracellular-extracellular shift

e) hypersecretion of calcitonin

286. What are the main manifestations of hyperphosphatemia?

a) muscle cramps

b) blood hyperosmolarity

c) hypocalcemia

d) hypercalcemia

e) muscle paralysis

287. What is the cause of hypophosphatemia?

a) hypersecretion of PTH

b) hyposecretion of PTH

c) hypersecretion of calcitonin

d) hyposecretion of calcitonin

e) metabolic alkalosis

288. What are the main manifestations of hypophosphatemia?

a) hemolytic anemia

b) osteomalacia

c) tetany

d) muscle cramps

e) enhanced neuronal excitability

289. What is normal blood glucose level?

a) 120 -140 mg/dl

b) 60 -80 mg/dl

c) 5,5 -6,0 mmol/L

d) 4,5 – 5,5 mmol/L

e) 80 – 120 mg/dl

290. What can be the causes of carbohydrates maldigestion?

a) injuries at the level of small intestine mucosal layer

b) insufficiency of salivary amylase

c) insufficiency of gastric pepsi

d) insufficiency of pancreatic amylase

e) insufficiency of pancreatic carboxypeptidase

291. What is the consequence of cellulose deficiency in the diet?

a) inhibition of microflora growth

b) enhanced gastrointestinal peristaltic movements

c) decreased secretion of digestive enzymes

d) inhibition of gastrointestinal peristaltic movements

e) enhanced secretion of digestive enzymes

292. What are the causes of carbohydrates malabsorption?

a) atrophy of mucosal layer in the small intestine

b) atrophy of mucosal layer in the large intestine

c) atrophy at the level of gastric mucosal layer

d) inflammation at the level of small intestine mucosal layer

e) inflammation at the level of large intestine mucosal layer

293. What are the carbohydrate metabolic disorders in starvation?

a. Excess of acetyl KoA

b. deficiency of oxaloacetate

c. Excessive oxaloacetate

d. Metabolic alkalosis

e. Deficiency of acetyl KoA

294. What are the carbohydrate metabolic disorders in starvation?

a) Excessive production of ketone bodies

b) deficiency of NADPH

c) Excessive oxaloacetate

d) deficient production of ketone bodies

e) excessive NADPH

295. What are the consequences of excessive carbohydrates intake?

a) hyposecretion of glucagon

b) enhanced protein synthesis

c) enhanced lipid synthesis

d) hypersecretion of glucagon

e) enhanced lipolysis

296. What factors can cause hyperglycemia?

a) reduced glycogenolysis

b) enhanced glycogenolysis

c) enhanced glycolysis

d) reduced gluconeogenesis

e) enhanced gluconeogenesis

297. What can be the causes of hypoglycemia?

a) enhanced gluconeogenesis

b) reduced gluconeogenesis

c) hypersecretion of glucocorticoids

d) hyposecretion of glucocorticoids

e) enhanced glycogenolysis

298. What are the compensatory reactions in hyperglycemia?

a) glucocorticoid hyposecretion

b) inhibition of gluconeogenesis

c) glucocorticoid hypersecretion

d) increased lipolysis

e) enhanced glycogenolysis

299. What are the compensatory reactions in hypoglycemia?

a) glucagon hypersecretion

b) glucagon hyposecretion

c) increased glycogenolysis

d) glucocorticoid hyposecretion

e) increased lipogenesis

300. What can be the potential consequences of hypoglycemia?

a) excessive deposition of fat in the adipose tissue

b) reduced production of ketone bodies

c) carbohydrate dystrophy in the liver

d) fatty dystrophy in the liver

e) excessive production of ketone bodies

301. What are the possible consequences of alimentary hyperglycemia?

a) obesity

b) carbohydrate dystrophy in the liver

c) fatty dystrophy in the liver

d) enhanced production of ketone bodies

e) glucosuria

302. What endocrine factors can contribute to development of hyperglycemia?

a) excessive insulin

b) excessive glucagon

c) deficiency of glucagon

d) deficiency of thyroid hormones

e) excessive glucocorticoids

303. What endocrine factors can contribute to development of hypoglycemia?

a) deficiency of insulin

b) excessive glucagon

c) deficiency of glucagon

d) excessive thyroid hormones

e) deficiency of glucocorticoids

304. What is the anabolic factor that reduces the blood glucose level?

a) insulin by enhancing glucose up-take in the cells

b) insulin by enhancing gluconeogenesis

c) glucocorticoids by enhancing glucose breakdown in the cells

d) thyroid hormones by enhancing glucose up-take in the cells

e) glucagon by stopping breakdown of glycogen

305. What carbohydrates can be absorbed from the gastrointestinal tract?

a) lactose

b) glucose

c) glycogen

d) maltose

e) galactose

306. What are the possible consequences of hyperglycemia in healthy persons?

a) enhanced oncotic pressure in the blood

b) enhanced lipid synthesis

c) increased osmotic pressure in the blood

d) stimulation of cortisol secretion

e) enhanced lipid breakdown

307. What are the possible consequences of hypoglycemia in healthy persons?

a) enhanced lipid synthesis

b) enhanced lipid breakdown

c) stimulation of cortisol secretion

d) stimulation of insulin secretion

e) inhibition of glucagon secretion

308. What are the factors that may cause hyperlipidemia?

a) hypersecretion of insulin

b) hypersecretion of glucocorticoids

c) hyposecretion of insulin

d) hyposecretion of glucagon

e) hyposecretion of glucocorticoids

309. Lack of what digestive enzyme leads to lipid maldigestion?

a) pancreatic amylase

b) pancreatic carboxypeptidase

c) salivary lipase

d) pancreatic lipase

e) hepatic lipase

310. What lipoproteins are synthesized by the liver?

a) chylomicrons

b) very low density lipoproteins

c) low density lipoproteins

d) high density lipoproteins

e) esterified cholesterol

311. What lipid substances are synthesized in the body?

a) triglyceride

b) urea

c) polyunsaturated fatty acids

d) Phospholipids

e) liposoluble vitamins

312. What are the metabolic consequences of excessive consumption of fat?

a) high blood level of VLDL

b) enhanced lipogenesis

c) enhanced lipolysis

d) enhanced production of ketone bodies

e) infiltration of tissues with chylomicrons

313. What are the consequences of lipid deficiency in the diet?

a) hypercoagulation state

b) hypocoagulation state

c) decreased blood level of saturated fatty acids

d) decreased blood level of polyunsaturated fatty acids

e) increased blood level of polyunsaturated fatty acids

314. What are the metabolic consequences of lipid maldigestion?

a) enhanced lipolysis

b) disturbances of steroid hormones synthesis

c) high level of chylomicrons in the blood

d) excess of liposoluble vitamins

e) deficiency of liposoluble vitamins

315. In what form the absorbed lipids are transported from the small intestine?

a) triglycerides

b) chylomicrons

c) free fatty acids

d) low density lipoproteins

e) very low density lipoproteins

316. In what form the lipids mobilized from adipose tissue are transported in the blood?

a) chylomicrons

b) very low density lipoproteins

c) low-density lipoprotein

d) free cholesterol and triglycerides

e) high density lipoproteins

317. In what form the cholesterol is transported from the peripheral tissues to the liver?

a) chylomicrons

b) very low density lipoproteins

c) high density lipoproteins

d) low density lipoproteins

e) esterified cholesterol

318. What are the possible causes of hypoproteinemia?

a. deficiency of pancreatic amylase

b. Hemodilution

c. proteinuria

d. renal failure

e. hemoconcentration

319. What are the possible consequences of hypoproteinemia?

a) energy deficiency

b) low oncotic pressure

c) high osmotic pressure

d) low osmotic pressure

e) edema

320. Lack of what digestive enzymes lead to protein maldigestion?

a) intestinal peptidases

b) pancreatic carboxypeptidase

c) pancreatic amylase

d) salivary proteases

e) salivary amylase

321. What is the possible consequence of direct absorption of protein from the digestive tract?

a) hyperproteinemia

b) food allergy

c) hypoproteinemia

d) anaphylactic shock

e) infiltration of the liver with protein

322. What are the metabolic and digestive disorders in maldigestion of proteins?

a) low osmotic pressure

b) low oncotic pressure

c) food allergy

d) gastrointestinal auto-intoxication

e) inhibition of putrefaction processes in the bowels

323. What are the consequences of amino acids malabsorption in the digestive tract?

a) deficiency of essential aminoacids

b) gastro-intestinal autointoxication

c) mobilization of protein storages

d) deficiency of non-essential aminoacids

e) mobilization of fat storages

324. What substances which represent proteins are present in the blood?

a) urea

b) prothrombin

c) very low density lipoproteins

d) bradykinin

e) histamine

325. What pathological states are associated with hypoproteinemia?

a) diarrhea

b) Hemodilution

c) hemoconcentration

d) polyuria

e) combustions with plasmorrhagia

326. What pathological states are associated with hyperproteinemia?

a) Hemodilution

b) hemorrhage

c) renal insufficiency

d) diarrhea

e) polyuria

327. What are the causes of intestinal auto-intoxications?

a) liver failure

b) protein maldigestion and malabsorbtion

c) lipid maldigestion and malabsorbtion

d) enteritis

e) carbohydrates maldigestion and malabsorbtion

328. What is the action of excitatory mediators on the postsynaptic membrane?

a) opening of sodium channels with depolarization

b) opening of sodium channels with hyperpolarization

c) opening of potassium channels with repolarization

d) opening of potassium channels with increased resting potential

e) opening of sodium channels with decreases resting potential

329. What is the action of inhibitory mediators on the postsynaptic membrane?

a) opening of chloride channels with depolarization

b) opening of chloride channels with hyperpolarization

c) opening of sodium channels with hyperpolarization

d) increases the resting potential

e) reduces the resting potential

330. What are excitatory mediators?

a) glycine

b) Acetylcholine

c) Dopamine

d) gamma-oxibutyric acid

e) serotonin

331. What are inhibitory mediators?

a) noradrenalin

b) acetylcholine

c) dopamine

d) serotonin

e) gamma-oxibutyric acid

332. Disorders of what receptors lead to sensibility disturbances?

a) proprioceptors

b) thermoreceptors

c) contact exteroreceptors

d) nociceptors

e) chemoreceptors

333. What are the manifestations of increased sympathetic vegetative tonus?

a) miosis

b) mydriasis

c) hyposalivation

d) reduced peripheral vascular resistance

e) increased peripheral vascular resistance

334. What are the manifestations of increased sympathetic vegetative tonus?

a) miosis

b) bronchodilation

c) hyposalivation

d) bronchial spasm

e) mucus hyposecretion

335. What are the manifestations of increased parasympathetic vegetative tonus?

a) hyposalivation

b) mucus hyposecretion

c) bronchospasm

d) bronchodilation

e) gastric hypersecretion

336. What are the manifestations of sympathetic nervous system paralysis?

a) Hyperglycemia

b) hypoglycemia

c) diarrhea

d) mydriasis

e) hypersalivation

337. What are the manifestations of parasympathetic nervous system paralysis?

a) Hyperglycemia

b) hypoglycemia

c) miosis

d) mydriasis

e) constipation

338. Activation of what nervous structures can trigger temporo-mandibular pain?

a) sensitive neurons of posterior medullar horns

b) sensitive neurons of cerebral cortex

c) sensitive neurons of limbic system

d) motor neurons of posterior medullar horns

e) motor neurons of the cerebral cortex

339. What are the local manifestations of glosalgia?

a) burn sensation

b) hypersalivation

c) hyposalivation

d) paresthesia

e) tongue edema

340. What are the causes of facial pain?

a) inflammatory processes in the mouth

b) trauma of dental-maxillary apparatus

c) periosteal disorders

d) injuries of salivary glands

e) injuries of perivascular tissue

341. When can develop dental hyperesthesia?

a) thin enamel layer

b) naked dentin

c) injuries at the level of sensorial neurons in the spinal chord

d) increased excitability threshold

e) injuries at the level of sensorial neurons in the cerebral cortex

342. When can develop pulp pain?

a) disorders of microcirculation

b) excessive osteoblast proliferation

c) excessive osteoclast proliferation

d) edema in tooth alveoli

e) paradontosis

343. What are the causes of primary endocrine disorders?

a) disorders of endocrine hypothalamus

b) disorders of adenohypophysis

c) disorders of neurohypophysis

d) disorders of peripheral endocrine glands

e) disorders of peripheral hormonal reception

344. What are the causes of secondary endocrine disorders?

a) disorders of endocrine hypothalamus

b) disorders of adenohypophysis

c) disorders of neurohypophysis

d) disorders of peripheral endocrine glands

e) disorders of peripheral hormonal reception

345. What are the causes of tertiary endocrine disorders?

a) disorders of endocrine hypothalamus

b) disorders of adenohypophysis

c) disorders of neurohypophysis

d) disorders of peripheral endocrine glands

e) disorders of peripheral hormonal reception

346. What type of hormone is increased in gigantism?

a) triiodothyronine

b) somatotropin

c) tetraiodthyronine

d) cortisol

e) somatoliberine

347. What type of hormones are increased in Graves-Bazedov disease?

a) Triiodothyronine

b) somatotropin

c) somatoliberine

d) tetraiodthyronine

e) cortisol

348. What hormonal disturbance is characteristic for myxedema?

a) deficiency of triiodothyronine

b) excess of triiodthyronine

c) deficiency of thyroxin

d) excess of thyroxin

e) deficiency of cortisol

349. What hormonal disturbance is characteristic for diabetes insipidus?

a) deficiency of vasopressin

b) excess of vasopressin

c) excess of thyroxin

d) deficiency of thyroxin

e) deficiency of cortisol

350. What are the organogenetic effects of somatotropin hypersecretion?

a) stimulation of osteoblast proliferation

b) inhibition of osteoblast proliferation

c) stimulation of chondroblast

d) inhibition of chondroblast proliferation

e) inhibition of striate myocytes proliferation

351. What are organogenetic effects of somatotropin hypersecretion?

a) Inhibition of chondroblast proliferation

b) stimulation of striate myocytes proliferation

c) inhibition of striate myocytes proliferation

d) stimulation of fibroblast proliferation

e) inhibition of fibroblast proliferation

352. What are the metabolic manifestations of somatotropin hypersecretion?

a) intensification of carbohydrates catabolism

b) intensification of carbohydrates anabolism

c) intensification of lipid catabolism

d) intensification of lipid anabolism

e) intensification of protein catabolism

353. What are the metabolic changes in hypersecretion of thyroid hormones?

a) increased intracellular synthesis of ATP

b) increased intracellular concentration of ADP

c) glycogenolysis

d) increased glycogenogenesis

e) increased lypogenesis

354. What are the somatic effects in hypersecretion of thyroid hormones?

a) Periorbital edema

b) Retrobulbar edema

c) Weight gain

d) hypertrophy of skeletal muscles

e) atrophy of skeletal muscles

355. What are the metabolic changes in hyposecretion of thyroid hormones?

a) Decreased protein anabolism

b) Increased protein anabolism

c) Decreased glycogenolysis

d) Increased glycogenolysis

e) Increased lipolysis

356. What hormonal disturbances induce hyperglycemia?

a) Hypersecretion of insulin

b) Hypersecretion of glucagon

c) Hypersecretion of glucocorticoids

d) Hyposecretion of glucagon

e) Hyposecretion glucocorticoids

357. What hormonal disturbances induce hypoglycemia?

a) hypersecretion of insulin

b) hyposecretion of insulin

c) hypersecretion of thyroid hormones

d) hyposecretion of thyroid hormones

e) hyposecretion of glucocorticoids

358. What hormonal disturbance induces glycogenogenesis?

a) Hypersecretion of insulin

b) hypersecretion of glucagon

c) Hyposecretion of insulin

d) hypersecretion of thyroid hormones

e) hypersecretion of glucocorticoids

359. What hormonal disturbances induce glycogenolysis?

a) Hypersecretion of insulin

b) hypersecretion of glucagon

c) hyposecretion of glucagon

d) hyposecretion of thyroid hormones

e) hypersecretion of thyroid hormones

360. Which hormones have catabolic effect?

a) insulin

b) glucagon

c) glucocorticoids

d) thyroid hormones

e) parathyroid hormone

361. Which hormones have anabolic effect?

a. Insulin

b. glucagon

c. glucocorticoids

d. thyroid hormones

e. parathyroid hormone

362. What hormonal disturbances induce tachycardia?

a) hypersecretion of catecholamines

b) hyposecretion of catecholamines

c) hypersecretion of thyroid hormones

d) hyposecretion of thyroid hormones

e) hypersecretion of somatotropin

363. What are the metabolic manifestations of glucocorticoids hypersecretion?

a) Increased gluconeogenesis

b) Decreased gluconeogenesis

c) Increased glycogenogenesis

d) Increased proteolysis

e) Increased proteosynthesis

364. What are the somatic manifestations of glucocorticoids hypersecretion?

a) Increased bones demineralization

b) Decreased bones demineralization

c) proliferation of lymphoid tissue

d) atrophy of lymphoid tissue

e) hypertrophy of muscular tissue

365. What hormonal disturbances induce hyperlipidemia?

a) Hypersecretion of insulin

b) Hyposecretion of insulin

c) Hypersecretion of glucagon

d) Hyposecretion of glucagon

e) Hyposecretion of glucocorticoids

366. What hormonal disturbances induce proteolysis?

a) Excess of insulin

b) Excess of glucocorticoids

c) Deficiency of glucocorticoids

d) Excess of thyroid hormones

e) Deficiency of thyroid hormones

367. What hormones in pharmacologic doses induce immunosuppression?

a) Excess of insulin

b) Excess of glucocorticoids

c) Excess of thyroid hormones

d) Excess of somatotropin

e) Excess of glucagon

368. What are the metabolic effects of insulin?

a) stimulates glycogenogenesis

b) stimulates glycogenolysis

c) stimulates lipogenesis

d) stimulates lipolysis

e) stimulates gluconeogenesis

369. What are metabolic effects of glucagon?

a) stimulates glycogenogenesis

b) stimulates glycogenolysis

c) stimulates lypogenesis

d) stimulates lipolysis

e) stimulates glycolysis

370. What is the pathogenesis of polyuria in insulin deficiency?

a) insulin deficiency – ADH hypersecretion- inhibition of water canalicular reabsorbtion – polyuria

b) insulin deficiency – hyperglycemia – increased glomerular filtration – polyuria

c) insulin deficiency – hyperglycemia – incomplete glucose reabsorbtion – glucosuria – polyuria

d) insulin deficiency – hyperglycemia – inhibition of aldosterone secretion – hypernatremia – polyuria

e) insulin deficiency – hyperglycemia – glucosuria – blockade of aquaporine – polyuria

371. What are parameters of normocythemic normovolemia?

a. Total blood volume 7% of body weight; erythrocyte count 7×10 12/L; hematocrit 56%

b. total blood volume 5% from body weight; erythrocyte count 3×1012/L; hematocrit 32%

c. total blood volume 7% from body weight; erythrocyte count 3×1012/L; hematocrit 32%

d. total blood volume 9% from body weight; erythrocyte count 7×.1012/L; hematocrit 56%

e. total blood volume 7% from body weight; erythrocyte count 5×1012/L; hematocrit 45%

372. Under what conditions can be found normocythemic hypovolemia?

a) 30-40 minutes after acute bleeding

b) 72 hours after acute bleeding

c) 30-40 minutes after chronic bleeding

d) In case of burn shock

e) In case of body overheating

373. What are parameters of oligocythemic hypovolemia?

a) total blood volume 5% of body weight; erythrocyte count 5×10 12/L; hematocrit 42%

b) total blood volume 7% from body weight; erythrocyte count 7×1012/L; hematocrit 56%

c) total blood volume 5% from body weight; erythrocyte count 3×1012/L; hematocrit 32%

d) total blood volume 7% from body weight; erythrocyte count 3×1012/L; hematocrit 32%

e) total blood volume 5% from body weight; erythrocyte count7×1012/L; hematocrit 56%

374. Under what conditions can be found oligocythemic hypovolemia?

a) first minutes after acute bleeding

b) 24 hours after acute bleeding

c) 30-40 minutes after acute bleeding

d) In case of erythrem

e) In case of body overheating

375. What are parameters of polycythemic hypovolemia?

a) total blood volume 5% of body weight; erythrocyte count 5×10 12/L; hematocrit 42%

b) total blood volume 7% from body weight; erythrocyte count 7×1012/L; hematocrit 56%

c) total blood volume 5% from body weight; erythrocyte count 7×1012/L; hematocrit 56%

d) total blood volume 7% from body weight; erythrocyte count 3×1012/L; hematocrit 32%

e) total blood volume 9% from body weight; erythrocyte count7×1012/L; hematocrit 56%

376. Under what conditions can be found polycythemic hypovolemia?

a) In case of body dehydration

b) In case of burns

c) In case of erythremia

d) In case of anemia

e) In case of body hyperhydration

377. What are parameters of oligocythemic hypervolemia?

a. total blood volume 9% of body weight; erythrocyte count 3× 10 12/L; hematocrit 42%

b. total blood volume 7% from body weight; erythrocyte count 7×1012/L; hematocrit 56%

c. total blood volume 5% from body weight; erythrocyte count 3×1012/L; hematocrit 32%

d. total blood volume 7% from body weight; erythrocyte count 3×1012/L; hematocrit 32%

e. total blood volume 9% from body weight; erythrocyte count 3×1012/L; hematocrit 32%

378. Under what conditions can be found oligocythemic hypervolemia?

a) massive infusion of saline solution

b) blood transfusion

c) body dehydration

d) body hyperhydration

e) diarrhea

379. What are parameters of polycythemic hypervolemia?

a) total blood volume 9% of body weight; erythrocyte count 5×10 12/L; hematocrit 42%

b) total blood volume 7% from body weight; erythrocyte count 7×.1012/L; hematocrit 56%

c) total blood volume 5% from body weight; erythrocyte count 3×1012/L; hematocrit 32%

d) total blood volume 9% from body weight; erythrocyte count 7×1012/L; hematocrit 32%

e) total blood volume 9% from body weight; erythrocyte count 7×1012/L; hematocrit 56%

380. Under what conditions can be found polycythemic hypervolemia?

a) In case of erythremia

b) In case of erythropenia

c) blood transfusion

d) In case of body dehydration

e) plasma transfusion

381. What are the signs of intracellular hemolysis?

a) Hemoglobinemia

b) Hemosiderinuria

c) Hemoglobinuria

d) Hyperbilirubinemia with free bilirubin (indirect bilirubin)

e) Hyperbilirubinemia with conjugated bilirubin (direct bilirubin)

382. What changes of hemogram are characteristic for iron deficiency anemia?

a) Macrocytosis

b) hypochromic erythrocytes

c) microcytosis

d) hyperchromic erythrocytes

e) drepanocytosis

383. Under what pathological conditions can be found neutrophilia?

a) bacterial infection

b) myocardial infarction

c) purulent otitis

d) viral infections

e) influenza

384. What does “left” nuclear shift represent?

a) increased number of agranulocytes in peripheral blood

b) increased number of granulocytes in peripheral blood

c) increased number of immature neutrophils in peripheral blood

d) increased number of mature neutrophils in peripheral blood

e) increased number of hyper-segmented neutrophils in peripheral blood

385. Under what pathological conditions can be found primary absolute lymphocytosis?

a) tuberculosis

b) septicemia

c) bronchial asthma

d) chronic lymphoid leucosis

e) Hodgkin lymphomas

386. Under what pathological conditions can be found secondary absolute lymphocytosis?

a) tuberculosis

b) infectious mononucleosis

c) bronchial asthma

d) chronic lymphoid leucosis

e) acute lymphoid leucosis

387. Under what pathological conditions can be found monocytosis?

a) in acute infection

b) granulomatous inflammation

c) in chronic infection

d) bronchial asthma

e) bacterial infection

388. What does agranulocytosis represent?

a) severe increased of lymphocytes in peripheral blood

b) severe decrease or absence of agranulocytes in peripheral blood

c) severe increased count of agranulocytes in peripheral blood

d) severe decreased or absence of granulocytes in peripheral blood

e) increased number of hyper-segmented neutrophils in peripheral blood

389. Under what pathological conditions can be found agranulocytosis?

a) aplastic anemia

b) cytostatic administration

c) parasitic diseases

d) allergic diseases

e) septicemia

390. What are the hematologic signs of absolute secondary erythrocytosis?

a) hemoglobin content more than 160 g/L

b) hemoglobin content less than 160g/l

c) erythrocyte count more than 5,5 ×1012/L

d) total blood volume less than 7% from body weight

e) total blood volume less than 5% from body weight

391. What are hematologic signs of absolute secondary erythrocytosis?

a) reticulocyte count more than 0,5%

b) reticulocyte count less than 0.5%

c) total blood volume less than 7% from body weight

d) hematocrit more than 45%

e) hematocrit less than 45%

392. What are the signs of relative erythrocytosis?

a) erythrocyte count more than 5×1012/L

b) erythrocyte count less than 5×1012/L

c) reticulocyte count more than 0,5%

d) total blood volume less than 7% from body weight

e) total blood volume more than 7% from body weight

393. What is the sign of relative erythrocytosis?

a) hemoglobin count more than 160 g/L

b) hemoglobin count less than 160 g/l

c) reticulocyte count more than 0,5%

d) reticulocyte count more than 1%

e) hyper-proliferation of erythrocyte series in bone marrow

394. What are the signs of primary absolute erythrocytosis?

a) Granulocytosis

b) erythrocyte count more than 5,5 ×1012/L

c) erythrocyte count less than 5,5 ×1012/L

d) reticulocyte count less than 0,5%

e) agranulocytosis

395. What are the signs of primary absolute erythrocytosis?

a) Low erythropoietin level

b) High erythropoietin level

c) Reticulocyte count more than 2.5%

d) Thrombocytopenia

e) Reticulocyte count less than 0,5%

396. What are signs of secondary absolute erythrocytosis?

a) Low erythropoietin level

b) High erythropoietin level

c) erythrocytes count more than 5,5 ×1012/L

d) erythrocyte count less than 5,5 ×1012/L

e) Reticulocyte count less than 1,5%

397. What processes are disturbed in hypoplastic anemia?

a) proliferation of erythroblastic series

b) differentiation of erythroblastic series

c) hemoglobin synthesis

d) erythrodieresis

e) erythrocytes maturation

398. What processes are disturbed in hemolytic anemias?

a) proliferation of erythroblast series

b) differentiation of erythroblast series

c) hemoglobin synthesis

d) erythrodieresis

e) erythrocyte maturation

399. What processes are disturbed in iron deficiency anemia?

b) proliferation of erythroblast series

c) differentiation of erythroblast series

d) hemoglobin synthesis

e) erythrodieresis

f) erythrocyte maturation

400. What processes are disturbed in B12 deficiency anemia?

a) proliferation of erythroblast series

b) differentiation of erythroblast series

c) hemoglobin synthesis

d) erythrodieresis

e) erythrocyte maturation

401. What is the sign of absolute leukocytosis?

a) increased number of young and mature leucocytes in the blood

b) increased number of young leucocytes in the blood

c) total blood count of leucocytes is 6-7×109/L

d) decreased production of leucocytes in the bone marrow

e) increased number of mature leukocytes in the blood

402. What are the causes of neutrophilia?

a) Viral infection

b) allergic diseases

c) cocci infection

d) acute infection disease

e) chronic infection disease

403. What are the causes of eosinophilia?

a) insufficiency of adrenal glands

b) insufficiency of thyroid gland

c) allergic diseases

d) bacterial infection

e) viral infection

404. What is the etiologic factor of lymphocytosis?

a) bacterial infection

b) viral infection

c) acute infection disease

d) chronic infection disease

e) allergic disease

405. What are the manifestations of agranulocytosis in the oral cavity?

a) Ulcero- necrotic tonsillitis

b) hyperemia of mouth mucosa

c) thinning of tooth enamel

d) thinning of dentine

e) ischemia of mouth mucosa

406. What are the manifestations of B12 deficiency anemia in the oral cavity?

a) Presence of painful sensation of the tongue

b) atrophy of lingual mucosa

c) hyperplasia of lingual mucosa

d) hyperplasia of lingual papilla

e) absence of painful sensation of the tong

407. What are manifestations of hemolytic anemia in the mouth?

a) hyperemia of the mouth mucosa

b) ischemia of the mouth mucosa

c) gingival micro-bleeding

d) gingival hyperplasia

e) hyperplasia of lingual papilla

408. What are manifestations of chronic bleeding in the mouth?

a) atrophy of mouth mucosa

b) hyperplasia of mouth mucosa

c) hypertrophy of mouth mucosa

d) redness of mouth mucosa

e) paleness of mouth mucosa

409. What are manifestations of iron deficiency anemia in the mouth?

a) atrophy of mouth mucosal

b) hypertrophy of mouth mucosa

c) green-grey coloration of mouth mucosa

d) yellow coloration of mouth mucosa

e) hyperplasia of mouth mucosa

410. How has been modeled spinal reflex in the frog?

a) By total anesthesia

b) By decapitation on the anterobulbar line of the brain

c) By destroying of spinal cord

d) By decapitation on the retrobulbar line of the brain

e) By the section of sciatic nerve

411. How has been demonstrated the role of different components of the spinal reflex arc in sensibility disorders?

a) By the removal of peripheral receptors

b) By the section of sciatic nerve

c) By the inhibition of the brain

d) By the destruction of spinal motoneurons

e) By the inhibition of the pyramidal system

412. How has been demonstrated the role of different components of the spinal reflex arc in sensibility disorders?

a) By the removal of peripheral receptors

b) By the retrobulbar section of the encephalon

c) By the inhibition of the brain

d) By the destruction of spinal motoneurons

e) By the inhibition of the pyramidal system

413. How has been demonstrated the role of different components of the spinal reflex arc in sensibility disorders?

a) By the removal of peripheral receptors

b) By the section of sciatic nerve

c) By the inhibition of the brain

d) By the destruction of spinal sensitive nerves

e) By the inhibition of the pyramidal system

414. How has been demonstrated the role of different components of the spinal reflex arc in sensibility disorders?

a) By the removal of peripheral receptors

b) By the destruction of spinal sensitive nerves

c) By the inhibition of the brain

d) By the stimulation of sciatic nerve

e) By the inhibition of the pyramidal system

415. How has been demonstrated the role of different components of the spinal reflex arc in sensibility disorders?

a) By the destruction of spinal sensitive nerves

b) By the section of sciatic nerve

c) By the inhibition of the brain

d) By the stimulation of sciatic nerve

e) By the inhibition of the pyramidal system

416. How has been demonstrated the role of different components of the spinal reflex arc in sensibility disorders?

a) By the stimulation of sciatic nerve

b) By the destruction of spinal sensitive nerves

c) By the inhibition of the brain

d) By the destruction of spinal motoneurons

e) By the inhibition of the pyramidal system

417. How has been demonstrated the role of different components of the spinal reflex arc in sensibility disorders?

a) By the removal of peripheral receptors

b) By the stimulation of sciatic nerve

c) By the inhibition of the brain

d) By the destruction of spinal motoneurons

e) By the inhibition of the pyramidal system

418. How has been demonstrated experimentally in the frog the role of the exteroreceptors in reflex activity?

a) absence of flexion reflex at degloved limb in contact with sulfuric acid 75%

b) absence of flexion reflex at intact limb in contact with sulfuric acid 75%

c) preserving of flexion reflex at degloved limb in contact with sulfuric acid 75%

d) preserving of flexion reflex at intact limb in contact with sulfuric acid 75%

e) delay of flexion reflex at degloved limb in contact with sulfuric acid 75%

419. How has been demonstrated experimentally in the frog the role of conduction pathway in reflex activity?

a) Absence of flexion reflex at degloved limb in contact with sulfuric acid 75%

b) Absence of flexion reflex at intact limb in contact with sulfuric acid 75%

c) Absence of flexion reflex at limb with sectioned sciatic nerve in contact with sulfuric acid 75%

d) Preserving of flexion reflex at limb with intact sciatic nerve in contact with sulfuric acid 75%

e) Preserving of flexion reflex at degloved limb in contact with sulfuric acid 75%

420. How has been demonstrated the role of spinal nervous centers in reflex activity?

a. Absence of flexion reflex at degloved limb at contact with sulfuric acid 75%

b. Absence of flexion reflex at intact limb at contact with sulfuric acid 75%

c. Absence of flexion reflex at limb with sectioned sciatic nerve at contact with sulfuric acid 75%

d. Absence of flexion reflex at frog with destroyed spinal cord at contact with sulfuric acid 75%

e. Preserving of flexion reflex at frog with intact spinal cord at contact with sulfuric acid 75%

421. How has been modeled acute adrenocortical insufficiency in rats?

a) due to ligation of suprarenal arteries

b) due to administration of drugs that block cholesterol metabolism

c) due to bilateral surgical removal of adrenal glands

d) due to unilateral surgical removal of adrenal glands

e) due to administration of cytostatics

422. To what stressful factors were subjected laboratory animals in experimental hypocorticosolism?

a) hypobaric hypoxia

b) cold water

c) starvation

d) physical effort

e) electrical shock

423. To what stressful factors were subjected laboratory animals in experimental hypocorticosolism?

a) hypobaric hypoxia

b) artificial hypervolemia

c) starvation

d) physical effort

e) electrical shock

424. To what stressful factor were subjected laboratory animals with acute experimental hypocorticosolism?

a) hypobaric hypoxia

b) artificial hypervolemia

c) starvation

d) cold water

e) electrical shock

425. What is the stress hormone?

a) Cortisol

b) Insulin

c) Epiandrosteron

d) Somatotropin

e) Thyroxin

426. What is the stress hormone?

a) Parathyroid hormone

b) Insulin

c) Catecholamines

d) Somatotropin hormone

e) Thyroxine hormone

427. What mechanisms determine the resistance to the action of stressful factors?

a) Hyperglycemia

b) Hypoglycemia

c) Heart hyperfunction

d) Heart hypofunction

e) Increased the body’s needs of O2

428. What mechanisms determine the resistance to the action of stressful factors?

a) Hyperlipidemia

b) Hypolipidemia

c) Increased the muscle tonus

d) Decreased the muscle tonus

e) Increased the body’s needs of O2

429. What mechanisms determine the resistance to the action of stressful factors?

a) Hyperglycemia

b) Hypoglycemia

c) Increased the muscle tonus

d) Decreased the muscle tonus

e) Increased the body’s needs of O2

430. What mechanisms determine the resistance to the action of stressful factors?

a) Heart hyperfunction

b) Heart hypofunction

c) Hyperlipidemia

d) Hypolipidemia

e) Increased the body’s needs of O2

431. What mechanism determines the resistance to the action of stressful factors?

a) Hyperproteinemia

b) Hypoglycemia

c) Hyperlipidemia

d) Hypolipidemia

e) Increased the body’s needs of O2

432. What mechanism determines the resistance to the action of stressful factors?

a) Hyperproteinemia

b) Hypoglycemia

c) hyperglycemia

d) Hypolipidemia

e) Increased the body’s needs of O2

433. What mechanism determines the resistance to the action of stressful factors?

a) Hyperproteinemia

b) Increased the muscle tonus

c) Hypolipidemia

d) Decreased the muscle tonus

e) Increased the body’s needs of O2

434. What mechanism determines the resistance to the action of stressful factors?

a) Hyperproteinemia

b) Heart hyperfunction

c) Heart hypofunction

d) Decreased the muscle tonus

e) Increased the body’s needs of O2

435. What mechanisms determine the resistance to the action of stressful factors?

a) Hyperproteinemia

b) Hyperlipidemia

c) Hypolipidemia

d) Hyperglycemia

e) Hypoglycemia

436. What mechanisms determine the resistance to the action of stressful factors?

a) Hyperproteinemia

b) Heart hyperfunction

c) Heart hypofunction

d) Decreased the muscle tonus

e) Increased the muscle tonus

437. What does the primary hyperthyroidism mean?

a) Primary increasing of thyroid gland function

b) Disturbance of ratio T3/T4

c) Increasing of thyroid gland function due to high secretion of thyrotropin

d) Increasing of thyroid gland function due to high secretion of thyroliberin

e) Excess of thyrotropin hormone and thyroid hormones

438. What does the primary hypothyroidism mean?

a. Disturbance of ratio T3/T4

b. Primary decreasing of thyroid gland function

c. Decreasing of thyroid gland function due to deficiency of thyrotropin

d. Decreasing of thyroid gland function due to deficiency of thyroliberin

e. Deficit of thyrotropin hormone and thyroid hormones

439. By what method has been modeled hyperthyroidism in rats?

a) by administration of methyluracil

b) by administration of caffeine

c) by administration of chloral hydrate

d) by administration of L – thyroxin

e) by administration of NaCl

440. By what method has been modeled hypothyroidism in rats?

a) by administration of methyluracil

b) by administration of caffeine

c) by administration of chloral hydrate

d) by administration of L – thyroxin

e) by administration of NaCl

441. What is mechanism of hypothyroidism at methyluracil administration?

a) Intensification of iodine absorption from the blood

b) Intensification of iodine uptake by the thyrocytes

c) Inhibition of iodine uptake by the thyrocytes

d) Destruction of the thyroglobulin in thyrocytes

e) Inhibition of thyroid hormones exocytose

442. How has been evaluated the role of thyroid hormones in pathology?

a) Expose of animals with hypo- and hyperthyroidism at hyperoxia

b) Expose of animals with hypo- and hyperthyroidism at hypobaric hypoxia

c) Expose of animals with hypo- and hyperthyroidism at normobaric hypoxia

d) Expose of animals with hypo- and hyperthyroidism at hyperbaric hypoxia

e) Expose of animals with hypo- and hyperthyroidism at hypothermia

443. Which of the experimental animal with changed thyroid function was more sensitive to the action of hypoxia?

a) The animal that had received methyl uracil

b) The animal that had received mercazolil

c) The animal that had received novocaine

d) The animal that had received L-thyroxine

e) The animal that had received NaCl

444. Which of the experimental animal with changed thyroid function was more resistant to the action of hypoxia?

a) The animal that had received methyluracil

b) The animal that had received mercazolil

c) The animal that had received novocaine

d) The animal that had received L-thyroxine

e) The animal that had received NaCl

445. What mechanisms reduce the resistance of the rat with experimental hyperthyroidism to hypoxia?

a) intensification of basal metabolic rate

b) increased O2 consumption

c) decreased basal metabolic rate

d) exhaustion of neuronal metabolic substrate

e) decreased O2 consumption

446. What mechanisms reduce the resistance of the rat with experimental hyperthyroidism to hypoxia?

a) Decreased oxido- reduction reactions

b) increased O2 consumption

c) decreased basal metabolic rate

d) exhaustion of neuronal metabolic substrate

e) decreased O2 consumption

447. What mechanisms reduce the resistance of the rat with experimental hyperthyroidism to hypoxia?

a) intensification of basal metabolic rate

b) Decrease of oxido- reduction reactions

c) decreased basal metabolic rate

d) exhaustion of neuronal metabolic substrate

e) decreased O2 consumption

448. What mechanisms reduce the resistance of the rat with experimental hyperthyroidism to hypoxia?

a) intensification of basal metabolic rate

b) increased consumption of O2

c) decreased basal metabolic rate

d) Decrease of oxido- reduction reactions

e) decreased O2 consumption

449. What mechanism reduces the resistance of the rat with experimental hyperthyroidism to hypoxia?

a) Increased rate of basal metabolic

b) Decreased rate of oxido- reduction reactions

c) Decreased rate of basal metabolic

d) Increased membrane resting potential of the neuron

e) Decreased O2 consumption

450. What mechanism reduces the resistance of the rat with experimental hyperthyroidism to hypoxia?

a) decreased rate of oxido - reduction reactions

b) increased O2 consumption

c) decreased rate of basal metabolic

d) increased membrane resting potential of the neuron

e) decreased O2 consumption

451. What mechanism reduces the resistance of the rat with experimental hyperthyroidism to hypoxia?

a) Increased membrane resting potential of the neurons

b) Decreased rate of oxido- reduction reactions

c) Decreased rate of basal metabolic

d) exhaustion of neuronal metabolic substrate

e) decreased O2 consumption

452. What pathological process demonstrates the hemogram in adult patient with following hematological parameters: Red cell blood count – 3,7 x 1012/L; Hemoglobin - 100 g/l; Reticulocyte - 5 ‰; Thrombocytes - 310000 per 1mkl of blood; ESR - 15 mm/h ; White blood cell count -6,5 x 109/L. Leucocyte formula: basophils – 1 %, eosinophils - 4%, non-segmented neutrophils – 5%, segmented neutrophils - 56%, lymphocytes – 27%, monocytes – 7%.

a) neutrophilia

b) lymphocytosis

c) anemia

d) erythrocytosis

e) leukemia

453. What pathological process demonstrates the hemogram in adult patient with following hematological parameters: Red cell blood count – 7,5 x 1012/L.; Hemoglobin - 160 g/l.; Reticulocytes – 5,0 ‰ ; Thrombocytes - 310 000 per 1mkl of blood; ESR – 15 mm/h ; White cell blood count - 6,5 x

109/L; Leucocyte formula: basophils – 1 %, eosinophils - 4%, non-segmented neutrophils – 5%, segmented neutrophils - 56%, lymphocytes – 27%, monocytes – 7%.

a) neutrophilia with left nuclear shift

b) lymphocytosis

c) anemia

d) erythrocytosis

e) leukemia

454. What pathological process demonstrates the hemogram in adult patient with following hematological parameters: Red cell blood count – 4,9 x 1012/L.; Hemoglobin - 144 g/l.; Reticulocytes - 5 ‰; Thrombocytes - 300 000 per 1mkl of blood; ESR – 15 mm/h ; White cell blood count – 14,5 x 109/L; Leucocyte formula: basophils – 1 %, eosinophils - 4%, non-segmented neutrophils – 3%, segmented neutrophils - 27%, lymphocytes – 58%, monocytes – 7%.

a) neutrophilia with left nuclear shift

b) lymphocytosis

c) neutrophilia with right nuclear shift

d) erythrocytosis

e) monocytosis

455. What pathological process demonstrates the hemogram in adult patient with following hematological parameters: Erythrocytes – 4,2× 1012 /L, Hb – 130 g/L, leucocytes – 15×10 9 /L, ESR – 20 mm/h; Leucocyte formula: eosinophils – 5%, basophils – 1%, segmented neutrophils – 60%, non-segmented neutrophils – 8%, metamyelocytes – 1%, lymphocytes – 20%, monocytes – 6%,

b) monocytosis

c) lymphocytosis

d) basophilic leukocytosis

e) neutrophilia with left nuclear shift

f) neutrophilia with right nuclear shift

456. What pathological process demonstrates the hemogram in adult patient with following hematological parameters: Red cell blood count – 2,9 x 1012/L, Hemoglobin - 80 g/l, Thrombocytes - 180 000 per 1mkl of blood Reticulocytes - 6 ‰ . Leucocytes – 90,0 ×10 9 /L. Leucocyte formula: basophils – 1%, eosinophils - 4%, myeloblast - 60%, segmented neutrophils - 15%, lymphocytes – 16%, monocytes – 4%.

a) neutrophilia with left nuclear shift

b) neutrophilia with right nuclear shift

c) erythrocytosis

d) Thrombocytosis

e) leukemia

457. What pathological process demonstrates the hemogram in adult patient with following hematological parameters: Red cell blood count – 4,9 x 1012/L; Hemoglobin - 135 g/l; Reticulocytes - 4 ‰ ; Thrombocytes - 150 000 per 1mkl of blood; White cell blood count – 8,5 ×109 /L.; Leucocyte formula: basophils – 1 %, eosinophils - 4%, non-segmented neutrophils – 3%, segmented neutrophils - 27%, lymphocytes – 38%, monocytes. – 7%.

a) erythrocytopenia

b) thrombocytopenia

c) agranulocytosis

d) neutrophilia with left nuclear shift

e) lymphocytosis

458. For what disorder there is characteristic the following changes in the hemogram?

Red cell blood count – 1,0 x 1012/L, Hemoglobin - 80 g/l, Thrombocytes - 100 000 per 1mkl of blood, Reticulocytes - 1 ‰ , ESR – 10 mm/h, white blood cell count - 2,5 ×10 9 /L. Leucocyte formula: basophils – 1%,eosinophils - 3%, metamyelocytes - 1%, non-segmented neutrophils – 10%, segmented neutrophils - 40%, lymphocytes – 40%, monocytes – 5%. In the blood smear: hyperchromic erythrocytes, megalocytes, giant neutrophils with hypersegmented nucleus.

a) iron deficiency anemia

b) aplastic anemia

c) hemolytic anemia

d) B12 – deficiency anemia

e) chronic post-bleeding anemia

459. For what disorder there is characteristic the following changes in the hemogram?

Red cell blood count - 3,0 x 1012/L, Hemoglobin - 70 g/l, Thrombocytes - 190 000 per 1mkl of blood, Reticulocytes - 10 ‰, White cell blood count – 6,8 ×109 /L. Leucocyte formula: basophils – 1%, eosinophils - 2%, metamyelocytes - 3%, non-segmented neutrophils – 7%, segmented neutrophils - 57%, lymphocytes – 25%, monocytes. – 5%. In the blood smear: anulocytosis, microcytosis, hypochromic erythrocytes.

a) hemolytic anemia

b) aplastic anemia

c) iron deficiency anemia

d) B12 deficiency anemia

e) chronic post-bleeding anemia

460. For what disorder there is characteristic the following changes in the hemogram?

Red cell blood count – 2,8 x 1012/L, Hemoglobin - 80 g/l, Thrombocytes - 200 000 per 1mkl of blood, Reticulocytes - 18 ‰. In the blood high level of unconjugated bilirubin and hemosiderin. White cell blood count – 6,8 x 1012/L. Leucocyte formula: basophils – 1%, eosinophils - 2%, metamyelocytes - 3%, non-segmented neutrophils – 7%, segmented neutrophils - 57%, lymphocytes – 25%, monocytes – 5%. In the blood smear: anysocytosis, ovalocytosis, microcytosis.

a) hemolytic anemia

b) aplastic anemia

c) iron deficiency anemia

d) B12 deficiency anemia

e) acute post-bleeding anemia

461. For what disorder there is characteristic the following changes in the hemogram?

Red cell blood count – 1,9 x 1012/L, Hemoglobin - 70 g/l, Thrombocytes - 110 000 per 1mkl of blood, Reticulocytes – 0 ‰. White cell blood count - 2,8 x 1012/L. Leucocyte formula: basophils – %, eosinophils - 1%, non-segmented neutrophils – 3%, segmented neutrophils - 57%, lymphocytes – 34%, monocytes. – 5%.In the blood smear: anysocytosis, microcytosis, hypochromic erythrocytes.

a) hemolytic anemia

b) aplastic anemia

c) iron deficiency anemia

d) B12 deficiency anemia

e) acute post-bleeding anemia

462. What pathological process demonstrates the hemogram in adult patient with following hematological parameters:

Erythrocytes – 4,4× 1012 /L, Hb – 130 g/L, leucocytes – 15×109 /L.Leucocyte formula: eosinophils – 5%, segmented neutrophils – 60%, non-segmented neutrophils – 8%, metamyelocyte– 1%, myelocytes – 2%, lymphocytes – 28%, monocytes – 6%.

a) neutrophilia with left nuclear shift

b) absolute lymphocytosis

c) relative lymphocytosis

d) neutrophilia with right nuclear shift

e) eosinophilia

463. For what disorder there is characteristic the following changes in the hemogram?

Erythrocytes – 4,2× 1012 /L, Hb – 130 g/L, leucocytes – 14×109 /L.Leucocyte formula: eosinophils – 5%, segmented neutrophils – 60%, non-segmented neutrophils – 15%, metamyelocytes – 2%, lymphocytes – 14%, monocytes – 6%.

a) viral infections

b) infections with staphylococcus and streptococcus

c) parasite invasion

d) intracellular infections

e) allergic diseases

464. For what disorder there is characteristic the following changes in the hemogram?

Erythrocytes – 4,0× 1012 /L, Hb – 130 g/L, leucocytes – 15×109 /L. Leucocyte formula: eosinophils – 8%, segmented neutrophils – 58%, non-segmented neutrophils – 5%, metamyelocytes – 0%, lymphocytes – 17%, monocytes – 12%.

a) viral infections

b) infections with staphylococcus and streptococcus

c) parasitic invasion

d) intracellular infections

e) allergic disorders

465. For what disorder there is characteristic the following changes in the hemogram?

Erythrocytes – 4,0× 1012 /L, Hb – 130 g/L, leucocytes – 15×109 /L.Leucocyte formula: eosinophils – 3%, segmented neutrophils – 22%, non-segmented neutrophils – 5%, metamyelocytes – 0%, lymphocytes – 50%, monocytes – 20%.

a) viral infections

b) infections with staphylococcus and streptococcus

c) parasitic invasion

d) intracellular infections

e) allergic diseases

466. What value of arterial pressure does represent pulmonary hypertension?

a) systolic pressure 20-25 mmHg

b) systolic pressure more than 30 mmHg

c) systolic pressure more than 60 mmHg

d) average pressure 10-17 mmHg

e) average pressure more than 20 mmHg

467. What value of arterial pressure does represent systemic hypertension?

a) systolic pressure more than120 mmHg

b) systolic pressure more than 140 mmHg

c) systolic pressure more than 150 mmHg

d) diastolic pressure more than 80 mmHg

e) diastolic pressure more than 70 mmHg

468. Which are the signs of cardiac insufficiency?

a) systolic volume less than 60 ml

b) systolic volume less than 50 ml

c) cardiac output less than 5 L/min

d) cardiac output less than 4L/min

e) blood circulation time 20-23 sec

469. What are the signs of vascular insufficiency?

a) decreased volume of circulating blood

b) decreased arterial pressure

c) decreased central venous pressure

d) increased central venous pressure

e) increased volume of circulating blood

470. What are the causes of volume overload of the heart?

a) stenosis of aortic valves

b) insufficiency of mitral valves

c) arterial hypertension

d) insufficiency of aortic valves

e) stenosis of aortic valves

471. What are the causes of resistance overload of the heart?

a) stenosis of aortic valve

b) insufficiency of mitral valves

c) hypervolemia

d) insufficiency of aortic valves

e) arterial hypertension

472. What pathogenic factors increase heart preload?

a) stenosis of aortic valves

b) insufficiency of mitral valves

c) stenosis of mitral valves

d) insufficiency of aortic valves

e) increased peripheral vascular resistance

473. What pathogenic factors increase heart afterload?

a) stenosis of aortic valves

b) insufficiency of mitral valves

c) enhanced circulatory blood volume

d) insufficiency of aortic valves

e) increased peripheral vascular resistance

474. What pathogenic factors trigger heterometric heart hyperfunction?

a) stenosis of aortic valves

b) insufficiency of mitral valves

c) enhanced circulatory blood volume

d) stenosis of mitral valves

e) increased peripheral vascular resistance

475. What pathogenic factors trigger heterometric heart hyperfunction?

a) stenosis of aortic valves

b) insufficiency of pulmonary valves

c) enhanced circulatory blood volume

d) stenosis of mitral valves

e) increased peripheral vascular resistance

476. What pathogenic factors induce homeometric heart hyperfunction?

a) stenosis of aortic valves

b) insufficiency mitral valves

c) enhanced circulatory blood volume

d) insufficiency of aortic valves

e) increased peripheral vascular resistance

477. What is the main pathogenic factor which triggers myocardial hypertrophy?

a) increased total work load performed by the heart

b) increased work load for every mass unit of the heart

c) increased arterial pressure in systemic circulation

d) increased arterial pressure in pulmonary circulation

e) increased circulatory blood volume

478. What are the cardiac mechanisms of compensation in circulatory failure?

a) increased force of heart contraction

b) increased end-diastolic volume

c) increased systolic volume

d) reduced cardiac output

e) increased end-systolic volume

479. What are the immediate extracardiac mechanisms of compensation in circulatory failure?

a) reduction of circulatory blood volume by partly blood sequestration

b) increased volume of circulating blood by mobilization of stored blood

c) even distribution of heart output to organs

d) distribution of cardiac output to vital organs

e) generalized vascular spasm to maintain arterial pressure

480. What are the late extracardiac mechanisms of compensation in circulatory failure?

a) hydro-electrolytic retention

b) pulmonary hyperventilation

c) hyposecretion of vasopressin

d) heart hypertrophy

e) hypersecretion of erythropoietin

481. What are the signs of left ventricular failure?

a) hypotension in systemic circulation

b) hypertension in systemic circulation

c) pulmonary edema

d) ascites

e) hypotension in pulmonary circulation

482. What are the signs of right ventricular failure?

a) hypertension in systemic circulation

b) hypertension in pulmonary circulation

c) pulmonary edema

d) ascites

e) liver enlargement

483. What is the cause of sinus tachycardia?

a) increased intracerebral pressure

b) intoxication with digitalics

c) hypothermia

d) hyperthermia

e) vagotonia

484. What are the causes of sinus bradycardia?

a) intoxication with β-adrenergic drugs

b) increased intracerebral pressure

c) heart sympathicotonia

d) intoxication with digitalics

e) intoxication with α-adrenergic drugs

485. What are forms of heart excitability disorders?

a. ventricular extrasystole

b. paroxysmal tachycardia

c. sinus tachycardia

d. atrio-ventricular block

e. sinus bradycardia

486. What are forms of myocardial conductibility disorders?

a) ventricular extrasystole

b) paroxysmal tachycardia

c) atrial fibrillation

d) atrio-ventricular block

e) sino-atrial block

487. What does represent hypercapnia?

a) partial pressure of CO2 in venous blood more than 46 mmHg

b) partial pressure of O2 in arterial blood less than 60 mmHg

c) partial pressure of CO2 in arterial blood more than 46 mmHg

d) partial pressure of CO2 in the cells more than 46 mmHg

e) partial pressure of CO2 in arterial blood less than 40 mmHg

488. What does represent hypoxemia?

a) partial pressure of CO2 in venous blood more than 46 mmHg

b) partial pressure of O2 in arterial blood less than 60 mmHg

c) partial pressure of CO2 in arterial blood less than 46 mmHg

d) partial pressure of O2 in venous blood less than 60 mmHg

e) reduced O2 pressure in the cells

489. What does represent pulmonary restriction?

a) reduced compliance of lung alveoli

b) reduced total compliance of thoracic cage or lungs

c) reduced elasticity of lung alveoli

d) reduced patency of superior airways

e) reduced patency of inferior airways

490. What disturbances lead to extra-parenchymatous restriction?

a) bronchial asthma

b) pneumothorax

c) pulmonary hypoperfusion

d) disorders of neuro-muscular apparatus

e) pulmonary fibrosis

491. What are the causes of pulmonary restrictive disease?

a) pulmonary fibrosis

b) pulmonary emphysema

c) obstruction of superior airways

d) pulmonary atelectasis

e) obstruction of inferior airways

492. What does represent intra-parenchymatous pulmonary restriction?

a) reduced total compliance of respiratory system by reduced compliance of the lungs

b) reduction of total compliance of respiratory system

c) reduced total compliance of respiratory system by reduced compliance of thoracic cavity

d) reduced total compliance and elasticity of thoracic cavity

e) reduced total compliance and elasticity of pleura

493. What does represent pulmonary obstruction?

a) disorders of gas diffusion thought the alveolar-capillary membrane

b) reduced lung compliance with hypoventilation

c) increased resistance of airways with hypoventilation

d) increased resistance of airways with hyperventilation

e) decreased resistance in airways with hypoventilation

494. What factors can lead to upper airways obstruction?

a) spasm of terminal bronchioles

b) spasm of tracheal muscles

c) tracheal obstruction

d) stenosis of the larynx

e) spasm of laryngeal muscles

495. What factors can lead to inferior airways obstruction?

a) hypersecretion of bronchial mucus

b) spasm of terminal bronchioles

c) spasm of tracheal muscles

d) stenosis of the larynx

e) spasm of laryngeal muscles

496. What does represent dyspnea?

a) changes of respiratory frequency and amplitude

b) changes of gas diffusion through the alveolar-capillary membrane

c) changes of pulmonary ventilation with hypercapnia

d) changes of gaseous composition of the blood

e) subjective sensation of air insufficiency

497. What does represent inspiratory dyspnea?

a) prolonged duration of inspiration and expiration

b) short inspiration with long expiration

c) increased inspiratory effort with passive expiration

d) increased inspiratory effort with forced expiration

e) reduced inspiratory effort with passive expiration

498. What does represent expiratory dyspnea?

a) prolonged duration of inspiration and expiration

b) prolonged duration of expiration

c) increased inspiratory effort with passive expiration

d) forced expiration

e) reduced inspiratory effort with passive expiration

499. Which type of hypoxia does develop in alpine disease?

a) exogenous normobaric hypoxia

b) exogenous hyperbaric hypoxia

c) exogenous hypobaric hypoxia

d) respiratory hypoxia

e) hystotoxic hypoxia

500. Which type of hypoxia does develop when there is inability of the cell to use oxygen?

a. Hystotoxic hypoxia

b. cardiogenic hypoxia

c. respiratory hypoxia

d. interstitial hypoxia

e. anemic hypoxia

501. What pathological process is associated with hemic hypoxia?

a) hemolysis

b) formation of carbhemoglobin

c) reduced circulatory blood volume

d) cardiac insufficiency

e) vascular insufficiency

502. What structure is the most sensitive to hypoxia?

a) bones

b) nervous tissue

c) connective tissue

d) cartilage

e) myocardium

503. What is the cause of respiratory hypoxia?

a) decreased pressure of oxygen in inspired air with hypoxemia

b) disorders of external respiration with hypoxemia

c) heart failure and lung hypoperfusion with hypoxemia

d) disorders of internal respiration with hypoxemia

e) pulmonary hyperventilation with hypoxemia

504. What are the compensatory reactions in long-lasting hypoxia?

a) hypersecretion of erythropoietin

b) mitochondrial hyperplasia and hypertrophy

c) hyposecretion of erythropoietin

d) hypersecretion of thyroid hormones

e) hyposecretion of thyroid hormones

505. What are the compensatory reactions in long-lasting hypoxia?

a) erythropoietin hyposecretion

b) enhanced diffusion area in the lungs

c) hypertrophy of heart muscle

d) hypersecretion of thyroid hormones

e) hyposecretion of thyroid hormones

506. What pathological processes are activated during hypoxia?

a) hypersecretion of glucocorticoids

b) activation of respiratory chain enzyme

c) decreased activity of antioxidant system

d) hyposecretion of glucocorticoids

e) reduced activity of the lysosomal enzymes

507. What pathological processes are activated during hypoxia?

a) hyposecretion of glucocorticoids

b) inactivation of respiratory chain enzyme

c) decreasing the activity of antioxidant enzymes system

d) activation of lipid peroxidation

e) intensification of the activity of the lysosomal enzymes

508. What are the changes in exogenous hypobaric hypoxia?

a) arterial hypoxemia, hypercapnia, alkalosis

b) arterial hypoxemia, hypocapnia, alkalosis

c) arterial hypoxemia, hypocapnia, acidosis

d) arterial hypoxemia, hypercapnia, acidosis

e) hypoxia, hypercapnia, alkalosis

509. What are the consequences of hypoxia?

a) alveolar hyperventilation

b) alveolar hypoventilation

c) respiratory acidosis

d) respiratory alkalosis

e) brain hemodynamic disorders

510. What are the changes in respiratory hypoxia?

a) arterial hypoxemia, hypocapnia, respiratory acidosis

b) arterial hypoxemia, hypercapnia, respiratory acidosis

c) arterial hypoxemia, hypercapnia, respiratory alkalosis

d) arterial hypoxemia, normal CO2 pressure, respiratory alkalosis

e) arterial hypoxemia, hypocapnia, respiratory alkalosis

511. What represents hypersalivation?

a) saliva secretion more than 2L/24 h

b) saliva secretion more than 1L/24 h

c) saliva secretion more than 1,5L/24h

d) saliva secretion more than 0,5 L/24h

e) saliva secretion more than 0,3L/24 h

512. What can be causes of pathologic hypersalivation?

a) in children during teeth eruption

b) ingestion of dry aliments

c) stomatitis

d) mouth tumors

e) Parkinson disease

513. What are possible consequences of sialorrhea?

a) neutralization of gastric juice

b) decreased stomachal pH

c) increased stomachal pH

d) body dehydration

e) hypervolemia

514. What are causes of pathologic hyposalivation?

a) emotional states

b) ingestion of fluid aliments

c) dehydration

d) parotiditis

e) salivatory ducts obstruction

515. Stomachal hypersecretion can be induced by:

a) caffeine

b) ethanol

c) gastrin excess

d) pepsin excess

e) vagotony

516. How evacuation function of the stomach is affected in hypersecretion with hyperacidity?

a) increases

b) decreases

c) doesn’t change

d) develops gastric chymostasis

e) develops dumping syndrome

517. How intestinal transit is affected in case of stomachal hypersecretion with hyperacidity?

a) increases

b) decreases

c) doesn’t change

d) frequent constipations

e) diarrhea

518. What represent achlorhydria?

a) lack of Cl ions in the blood

b) absence of HCl in gastric juice

c) lack of enzymes in gastric juice

d) increased blood pH

e) decreased blood pH

519. What can be causes of achlorhydria?

a) gastrin lack

b) atrophic chronic gastritis

c) gastric cancer

d) hypertrophic gastritis

e) gastric ulcer

520. What are consequences of HCl absence in gastric juice?

a) increased intestinal peristaltic movement

b) decreased intestinal peristaltic movements

c) maldigestion

d) malabsorbtion

e) constipations

521. What can be consequences of vomiting?

a) Hypochloremia

b) hyperkaliemia

c) alkalosis

d) acidosis

e) activation of renin-angiotensin-aldosterone system

522. What are the causes of exocrine insufficiency of the pancreas?

a) chronic pancreatitis

b) pancreatic tumor

c) pancreatic duct obturation

d) vagotony

e) sympathicotonia

523. Which are consequences of insufficient pancreatic secretion?

a) Maldigestion

b) Malabsorbtion

c) Malnutrition

d) ulcerogenesis

e) constipations

524. What represents steatorrhea?

a) presence of lipids in the blood

b) excessive elimination of lipids with stool

c) excessive accumulation of lipids in hepatic parenchyma

d) lipid elimination with urine

e) lack of lipids in feces

525. What can be causes of steatorrhea?

a) Acholia

b) insufficiency of pancreatic lipase

c) pepsin insufficiency

d) cholemia

e) hyperlipidemia

526. What represents acholia?

a) lack of bile in the blood

b) lack of bile in intestine

c) presence of bile in the blood

d) decoloration of feces

e) lack of bilirubin in bile

527. What can be consequences of disaccharides maldigestion?

a) Diarrhea

b) Dehydration

c) constipations

d) hyperhydration

e) hypoglycemia

528. What can be consequences of protein maldigestion?

a) Hypoproteinemia

b) decreased oncotic pressure

c) edemas

d) proteinuria

e) immunodeficiency

529. What can be consequences of lipid maldigestion?

a) hyperlipidemia

b) steatorrhea

c) blood hypocoagulation

d) diarrhea

e) constipations

530. What can be causes of intestinal autointoxication?

a) intensification of putrefaction processes in the intestine

b) excessive consumption of proteins

c) constipations

d) diarrhea

e) liver failure

531. What are manifestations of intestinal autointoxication?

a) arterial hypotension

b) arterial hypertension

c) headache

d) hypoglycemia

e) hyperglycemia

532. What pathologic processes disturb digestion in the mouth?

a) Hypersalivation

b) Hyposalivation

c) lack of salivary amylase

d) lack of lysosim

e) alkaline reaction of the saliva

533. What are digestive disturbances in case of salivary amylase lack?

a) disorders of polysaccharides digestion

b) disorders of disaccharides digestion

c) disorders of cellulose digestion

d) disorders of proteins digestion

e) disorders of lipid digestion

534. How does stomach tonus and motility change in hypochlorhydria?

a) Hypotonus

b) hypertonus

c) accelerated evacuation

d) stomachal chymostasis

e) vomiting

535. How does stomach tonus and motility change in hyperchlorhydria?

a) hypotonus

b) hypertonus

c) accelerated evacuation

d) stomachal chymostasis

e) vomiting

536. What are factors involved in stomach ulcerogenesis?

a) HCl

b) Bile

c) Helicobacter pylori

d) Salmonella

e) anaerobe flora

537. What stomach digestive changes can be found in hypochlorhydria?

a) develops maldigestion of polysaccharides

b) develops maldigestion of proteins

c) develops maldigestion of lipids

d) improvement of gastric digestion

e) develops maldigestion of cellulose

538. What stomach digestive changes can be found in hyperchlorhydria?

a) develops maldigestion of polysaccharides

b) develops maldigestion of proteins

c) develops maldigestion of lipids

d) improvement of gastric digestion

e) develops maldigestion of cellulose

539. What digestive changes are found in exocrine insufficiency of the pancreas?

a) develops maldigestion of polysaccharides

b) develops maldigestion of proteins

c) develops maldigestion of lipids

d) improvement of intestinal digestion

e) develops cellulose maldigestion

540. What are digestive changes in bile secretion insufficiency?

a) polysaccharides maldigestion

b) intestinal atonia

c) steatorrhea

d) amylorrhea

e) Creatorrhea

541. What are digestive changes in disorders of mucosa of small intestine?

a) disorders of polysaccharides breakdow

b) disorders of disaccharides breakdown

c) disorders of polypeptides breakdown

d) disorders of dipeptides breakdown

e) disorders of lipids breakdown

542. Absorbtion of what substances is affected in disorders of small intestine mucosa?

a) proteins

b) aminoacids

c) disaccharides

d) monosaccharides

e) water

543. Absorbtion of what substances is affected in disorders of large intestine?

a) proteins

b) aminoacids

c) mineral salts

d) monosaccharides

e) water

544. How does carbohydrates metabolism change in liver failure?

a) exaggerate postprandial hyperglycemia

b) fasting hypoglycemia

c) fructosemia

d) glycogen storages diminishes

e) glycogen storage increases

545. How does protein metabolism change in liver failure?

a) develops hyperglobulinemia

b) develops hypoalbuminemia

c) develops hyperaminoacidemia

d) synthesis of gamma-globulins is disturbed

e) there is increased concentration of urea in the blood

546. How does lipid metabolism change in liver failure?

a) there is intense lipolysis in the liver

b) there is steatosis of the liver

c) in the blood increase concentration of very low density lipoproteins

d) in the blood increase concentration of very high density lipoproteins

e) in the blood there increase concentration of non-esterified fatty acids

547. Which are biochemical changes in liver failure?

a) there is increased concentration of urea in the blood

b) hyperammoniemia

c) there is increased concentration of aromatic aminoacids

d) hypoalbuminemia

e) hypoprothrombinemia

548. Which are biochemical manifestations of cholemia?

a) hyperbilirubinemia with free bilirubin

b) hyperbilirubinemia with conjugated bilirubin

c) hypercholesterolemia

d) cholalemia

e) hypoprothrombinemia

549. Which are consequences of choledoc obstruction?

a) hyperbilirubinemia with free bilirubin

b) cholestasis

c) acholia

d) hyperbilirubinemia with conjugated bilirubin

e) lipid maldigestion

550. Which are manifestations of infectious hepatitis in organs of the mouth?

a) edema of the mouth mucosa

b) jaundice of the mouth mucosa

c) teleagiectasia

d) Fourdis granules

e) paleness of mouth mucosa

551. How is modelated experimental hypervolemia?

a) by administration of isotonic solution in the vascular bed

b) by administration of adrenalin in the vascular bed

c) by administration of noradrenaline in the vascular bed

d) by administration of caffeine in the vascular bed

e) by administration of hypertonic solution in the vascular bed

552. What are compensatory reactions in experimental hypervolemia?

a) blood storage

b) dilation of resistive blood vessels

c) increased diuresis

d) reduced erythrocytopoiesis

e) activation of renin-angiotensin-aldosteron system

553. What are compensatory reactions in experimental hypervolemia?

a) reduced diuresis

b) dilation of resistive blood vessels

c) enhanced glomerular filtration rate

d) enhanced erythrocytopoiesis

e) activation of renin-angiotensin-aldosteron system

554. What are compensatory reactions in experimental hypervolemia?

a) Storage of blood in deposits

b) reduced diuresis

c) enhanced capillary filtration

d) enhanced capillary reabsorption

e) enhanced aldosteron production

555. What are compensatory reactions in experimental hypervolemia?

a) Enhanced capillary filtration

b) dilation of resistive blood vessels

c) reduced glomerular filtration rate

d) hypersecretion of vasopressin

e) hypersecretion of aldosteron

556. What is a compensatory reaction in experimental hypervolemia?

a) Reduced erythrocytopoiesis

b) reabsorption of fluid from interstitium in the blood vessels

c) filtration of fluid in the interstitium

d) activation of renin-angiotensin-aldosteron system

e) hypersecretion of vasopressin

557. What is a compensatory reaction in experimental hypervolemia?

a) blood storage in deposits

b) spasm of resistive blood vessels

c) reduced glomerular filtration rate

d) hypersecretion of aldosteron

e) activation of renin-angiotensin-aldosteron system

558. What is a compensatory reaction in experimental hypervolemia?

a) reduced diuresis

b) dilation of resistive blood vessels

c) enhanced reabsorption of fluid in the vessels

d) enhanced erythrocytopoiesis

e) enhanced vasopressin production

559. What is the method of measurement of blood pressure in the rabbit during experimental hypervolemia?

a) indirect method with Riva-Roci device placed on posterior limbs

b) indirect method with Riva-Roci device placed on anterior limbs

c) direct intra-arterial method with hydrargyrum manometer

d) indirect method with Riva-Roci device placed on thorax

e) direct intra-arteriolar method with hydrargyrum manometer

560. How blood pressure (BP) and breathing rate (BR) change in painful stimulation?

a) BP increase, BR increase

b) BP decrease, BR decreases

c) BP unchanged, BR increase

d) BP increase, BR unchanged

e) BP decrease, BR unchanged

561. What are the mechanisms of increased blood pressure in painful excitation?

a) high secretion of catecholamines

b) increased number of adrenoreceptors

c) increased peripheral vascular resistence

d) activation of MAO

e) activation of kallikrein-kinin system

562. What is the mechanism of increased blood pressure in painful stimulation?

a) enhanced secretion of renin

b) increased number of painful receptors

c) decreased peripheral vascular resistence

d) activation of MAO

e) increased number of adrenoreceptors

563. What are the mechanisms of increased blood pressure in painful stimulation?

a) increased renin secretion

b) increased number of adrenoreceptors

c) increased peripheral vascular resistence

d) increased number of nociceptors

e) activation of kallikrein-kinin system

564. What is the mechanism of restoration of blood pressure following painful stimulation?

a) Activation of MAO

b) Hypersecretion of acetylcholine

c) activation of renin-angiotensin-aldosteron system

d) blood storage in deposits

e) centralization of hemocirculation

565. What is the mechanism of restoration of blood pressure in hypercatecholaminemia?

a) activation of monoamine-oxidase

b) increased level of acethylcholin

c) activation of renin-angiotensin-aldosteron system

d) blood storage

e) inhibition of monoamine-oxidase

566. What are the causes of death in rats exposed to reduced atmospheric pressure?

a) decreased pressure of oxygen in inspiratory air

b) hypobaria

c) respiratory hypoxia

d) hypoxemia

e) circulatory hypoxia

567. What is the cause of death in rats exposed to reduced atmospheric pressure?

a) Atmospheric hypoxia

b) Reduced atmospheric pressure

c) respiratory hypoxia

d) hemic hypoxia

e) circulatory hypoxia

568. What is the cause of death in rats exposed to reduced atmospheric pressure?

a) hemic hypoxia

b) reduced atmospheric pressure

c) respiratory hypoxia

d) hypoxemia

e) circulatory hypoxia

569. What manifestations develop in rats exposed to reduced atmospheric pressure?

a) dyspnea

b) hypoglycemia

c) hypothermia

d) meteorism

e) hyperthermia

570. What manifestations develop in rats exposed to reduced atmospheric pressure?

a) hypoglycemia

b) cyanosis

c) paleness

d) hyperglycemia

e) hyperthermia

571. What manifestations develop in rats exposed to reduced atmospheric pressure?

a) dyspnea

b) cyanosis

c) paleness

d) hypoglycemia

e) hyperthermia

572. What manifestations develop in rats exposed to reduced atmospheric pressure?

a) paleness

b) hypoglycemia

c) hyperglycemia

d) meteorism

e) hyperthermia

573. What manifestations develop in rats exposed to reduced atmospheric pressure?

a) hyperglycemia

b) hypertension

c) convulsions

d) hypotension

e) hyperthermia

574. What manifestations develop in rats exposed to reduced atmospheric pressure?

a) dyspnea

b) paleness

c) hypertension

d) seisures

e) hyperthermia

575. What manifestations develop in rats exposed to reduced atmospheric pressure?

a) hypertension

b) cyanosis

c) convulsions

d) hypotension

e) hyperthermia

576. What absorber for CO2 was used for model of normobaric hypoxia without hypercapnia?

a) calcium bicarbonate

b) sodium chloride

c) carbon chloride

d) sublimate

e) bicarbonate

577. What manifestations develop in the mouse in condition of normobaric hypoxia?

a) hyperemia of sclera

b) cyanosis

c) tachycardia

d) paleness

e) meteorism

578. What manifestations develop in the mouse in condition of normobaric hypoxia?

a) cyanosis

b) bradycardia

c) hyperemia of sclera

d) convulsions

e) meteorism

579. What manifestations develop in the mouse in condition of normobaric hypoxia?

a) tachycardia

b) paleness

c) hyperemia of sclera

d) seisures

e) meteorism

580. What manifestations develop in the mouse in condition of normobaric hypoxia?

a) tachycardia

b) bradycardia

c) hyperemia of sclera

d) cyanosis

e) meteorism

581. What manifestation develops in the mouse in condition of normobaric hypoxia?

a) Paleness

b) hyperemia of sclera

c) bradycardia

d) seizures

e) meteorism

582. What manifestation develops in the mouse in condition of normobaric hypoxia?

a) cyanosis

b) paleness

c) hyperthermia

d) hyperemia of sclera

e) meteorism

583. What manifestation develops in the mouse in condition of normobaric hypoxia?

a) paleness

b) cyanosis

c) bradycardia

d) hyperglycemia

e) meteorism

584. What manifestation develops in the mouse in condition of normobaric hypoxia?

a) hyperthermia

b) hyperglycemia

c) hypoglycemia

d) convulsions

e) meteorism

585. What manifestation develops in the mouse in condition of normobaric hypoxia?

a) hyperglycemia

b) hypoglycemia

c) tachycardia

d) hyperthermia

e) meteorism

586. What manifestation develops in the mouse in condition of normobaric hypoxia?

a) hyperthermia

b) hyperglycemia

c) cyanosis

d) hypoglycemia

e) meteorism

587. What metabolic disorders can be attested in the mouse exposed to normobaric hypoxia without hypercapnia?

a) metabolic acidosis

b) metabolic alcalosis

c) respiratory acidosis

d) hypercapnia

e) hypoxemia

588. What metabolic disorders can be attested in the mouse exposed to normobaric hypoxia without hypercapnia?

a) metabolic acidosis

b) metabolic alcalosis

c) respiratory acidosis

d) hypercapnia

e) respiratory alcalosis

589. What metabolic disorders can be attested in the mouse exposed to normobaric hypoxia without hypercapnia?

a) respiratory alcalosis

b) metabolic alcalosis

c) respiratory acidosis

d) hypocapnia

e) hyperoxia

590. What endogenous factors lead to different effects of hypoxia and hypobaria on rats?

a) age

b) functional state of SNC

c) functional state of endocrine system

d) hypoproteinemia

e) hyperglycemia

591. What endogenous factors lead to different effects of hypoxia and hypobaria on rats?

a) age (new-born or adult animal)

b) hydric balance in the animal

c) functional state of endocrine system

d) functional state of the immune system

e) glucose level in the blood

592. What endogenous factors lead to different effects of hypoxia and hypobaria on rats?

a) Metabolism intensity

b) functional state of SNC

c) glucose level in the blood

d) hydric metabolism in the rat

e) functional state of the immune system

593. What endogenous factors lead to different effects of hypoxia and hypobaria on rats?

a) Intensity of aerobic metabolic processes

b) functional state of the endocrine system

c) hydric metabolism in the rat

d) functional state of the immune system

e) intensity od anaerobic metabolic reactions

594. What endogenous factors lead to different effects of hypoxia and hypobaria on rats?

a) Glucose level in the blood

b) functional state of SNC

c) functional state of the immune system

d) protein level in the blood

e) age

595. What endogenous factors lead to different effect of hypoxia and hypobaria on rats?

a) age (new-born or adult animal)

b) intensity of anaerobic metabolism

c) functional state of the immune system

d) glucose level in the blood

e) intensity of aerobic metabolism

596. What endogenous factors lead to different effect of hypoxia and hypobaria on rats?

a) Intensity of glycogenolysis in the liver

b) functional state of the immune system

c) functional state of the endocrine system

d) intensity of anaerobic metabolic reactions

e) intensity of aerobic metabolic reactions

597. What endogenous factors lead to different effect of hypoxia and hypobaria on rats?

a) functional state of SNC

b) functional state of the immune system

c) intensity of glycolysis in the liver

d) intensity of anaerobic metabolic reactions

e) functional state of the endocrine system

598. What endogenous factors lead to different effects of hypoxia and hypobaria on rats?

a) Glucose level in the blood

b) functional state of SNC

c) functional state of the endocrine system

d) intensity of glycogenolysis in the liver

e) functional state of the immune system

599. What endogenous factor leads to different effects of hypoxia and hypobaria on rats?

a) Hydroelectrolytic balance in the rat

b) functional state of the immune system

c) intensity of glycogenolysis in the liver

d) intensity of anaerobic metabolic reactions

e) intensity of aerobic metabolic reactions

600. What endogenous factor leads to different effects of hypoxia and hypobaria on rats?

a) age of the experimental animal

b) functional state of the immune system

c) hydroelectrolytic balance in the rat

d) intensity of anaerobic metabolic reactions

e) intensity of glycogenolysis

601. What endogenous factor leads to different effects of hypoxia and hypobaria on rats?

a) functional state of the immune system

b) electrolytic balance in the rat

c) functional state of the endocrine system

d) intensity of glycogenolysis

e) hydric metabolism in the rat

602. What endogenous factor leads to different effects of hypoxia and hypobaria on rats?

a) electrolytic balance in the rat

b) functional state of the CNS

c) intensity of anaerobic metabolic reactions

d) genetic factors

e) functional state of the immune system

603. What animals are more sensible to action of hypobaric hypoxia?

a) adult animals

b) new-born animals

c) animals with excited CNS

d) animals with inhibited CNS

e) animals with intensified anaerobic metabolism

604. What animals are more sensible to action of hypobaric hypoxia?

a) adult animals

b) new-born animals

c) animals with hyperglycemia

d) animals with immune deficiency

e) animals with decreased anaerobic metabolism

605. What animals are more sensible to action of hypobaric hypoxia?

a) adult animals

b) new-born animals

c) animals with increased anaerobic metabolic reactions

d) animals with immune deficiency

e) animals with increased aerobic metabolic reactions

606. How reactivity and resistance to hypobaric hypoxia will change in a rat with excited CNS?

a) reactivity increases, resistance to hypoxia decreases

b) reactivity and resistence to hypoxia increase

c) reactivity and resistence to hypoxia decrease

d) reactivity decrease, resistence to hypoxia increase

e) reactivity increase, resistance to hypoxia unchanged

607. How reactivity and resistence to hypobaric hypoxia will change in a rat with inhibition of CNS?

a) reactivity increases, resistence to hypoxia decreases

b) reactivity and resistence to hypoxia increase

c) reactivity and resistence to hypoxia decrease

d) reactivity decrease, resistence to hypoxia increase

e) reactivity increase, resistence to hypoxia unchanged

608. What are microcirculatory changes on frog’s tongue in arterial hyperemia?

a) dilation of arterioles, capillaries and venules

b) increased number of functional capillaries

c) decreased linear blood velocity

d) decreased volumetric blood velocity

e) decreased number of functional capillaries

609. What are microcirculatory changes on frog’s tongue in arterial hyperemia?

a) dilation of arterioles, narrowing of venules

b) increased number of functional capillaries

c) decreased linear blood velocity

d) increased linear blood velocity

e) decreased number of functional capillaries

610. What is a microcirculatory change on frog’s tongue in arterial hyperemia?

a) dilation of arterioles, narrowing of capillaries and venules

b) decreased number of functional capillaries

c) decreased volumetric blood velocity

d) increased linear blood velocity

e) decreased number of functional capillaries

611. What is a microcirculatory change on frog’s tongue in arterial hyperemia?

a) dilation of arterioles, capillaries and venules

b) decreased number of functional capillaries

c) dilation of arterioles and capillaries with narrowing of venules

d) decreased hydrostatic pressure

e) decreased number of functional capillaries

612. What are microcirculatory changes on frog’s tongue in arterial hyperemia?

a) dilation of arterioles, narrowing of venules

b) increased number of functional capillaries

c) decreased linear blood velocity

d) increased volumetric blood velocity

e) decreased capillary network

613. What are microcirculatory changes on frog’s tongue in arterial hyperemia?

a) dilation of arterioles, capillaries and venules

b) increased number of functional capillaries

c) decreased linear blood velocity

d) dilation of arterioles, narrowing of venules

e) increased number of non-functional capillaries

614. What are microcirculatory changes on frog’s tongue in arterial hyperemia?

a) reduced linear blood velocity

b) intensification of lymphogenesis

c) reduction of lymphogenesis

d) hyperperfusion

e) spasm of capillaries and venules with arteriolar dilation

615. What are microcirculatory changes on frog’s tongue in arterial hyperemia?

a) decreased linear blood velocity

b) intensification of lymphogenesis and lymphodynamics

c) intensification of lymphogenesis and reduction of lymphodynamics

d) intensification of capillary network

e) spasm of capillaries and venules with arteriolar dilation

616. What is a microcirculatory change on frog’s tongue in arterial hyperemia?

a) decreased linear blood velocity

b) reduced lymphogenesis and lymphodynamics

c) reduced lymphogenesis with enhanced lymphodynamics

d) enhanced lymphogenesis and lymphodynamics

e) spasm of capillaries and venules with arteriolar dilation

617. What are microcirculatory changes on frog’s tongue in arterial hyperemia?

a) increased linear and volumetric blood velocity

b) intensification of lymphogenesis and lymphodynamics

c) increased linear blood velocity and reduced volumetric blood velocity

d) reduced lymphogenesis

e) spasm of capillaries and venules with arteriolar dilation

618. What are microcirculatory changes on frog’s tongue in venous hyperemia?

a) increased volumetric blood velocity

b) dilation of venules

c) increased venous outflow

d) narrowing of arterioles

e) reduced linear blood velocity

619. What is a microcirculatory change on frog’s tongue in venous hyperemia?

a) Increased linear blood velocity

b) narrowing of arteriole, capillaries and venules

c) reduction of capillary network

d) narrowing of arterioles and capillaries

e) amplification of capillary network

620. What is a microcirculatory change on frog’s tongue in venous hyperemia?

a) increased linear blood velocity and reduced volumetric blood velocity

b) dilation of venules and capillaries

c) increased arteriolar inflow and venous outflow

d) dilation of venules with narrowing of capillaries and arterioles

e) narrowing of venules and capillaries

621. By what experimental method arterial hyperemia was modelated on frog’s tongue?

a) mechanical excitation of the tongue

b) chemical excitation of the tongue

c) ligation of lingual artery

d) unilateral ligation of main veins of the tongue

e) administration of adrenaline solution

622. By what experimental method venous hyperemia was modelated on frog’s tongue?

a) mechanical excitation of the tongue

b) chemical excitation of the tongue

c) ligation of lingual artery

d) unilateral ligation of main vein of the tongue

e) bilateral ligation of lingual veins

623. By what experimental method stasis was modelated on frog’s tongue?

a) mechanical excitation of the tongue

b) chemical excitation of the tongue

c) bilateral ligation of lingual veins

d) section of main lingual vein

e) unilateral ligation of main vein of the tongue

624. By what experimental method ischemia was modelated on frog’s swimming membrane?

a) mechanical excitation of the swimming membrane

b) chemical excitation of the swimming membrane

c) ligation of veins on swimming membrane

d) section of main veins on swimming membrane

e) administration of adrenaline solution on swimming membrane

625. What are microcirculatory changes on frog’s tongue in prestasis?

a) pulsatile movements

b) pendulatory movements

c) turbulent movements

d) diminished inflow

e) centripetal movements

626. What are microcirculatory changes on frog’s tongue in prestasis?

a) accelerated movements

b) pendulatory movements

c) turbulent movements

d) diminished arterial inflow

e) centripetal movements

627. What are microcirculatory changes on frog’s tongue in prestasis?

a) accelerated movements

b) pulsatile movements

c) turbulent movements

d) diminished arterial inflow

e) centripetal movements

628. By what experimental method was modelated the development of white thrombus in mesenterial vessels in the frog?

a) by ligation of mesenterial vessels

b) by applying a crystal of NaCl on mesenterial vessel bifurcation

c) by applying a crystal of AgNO3 on mesenterial vessel bifurcation

d) by applying heparin solution on mesenterial vessels

e) by applying adrenalin solution on mesenterial vessels

629. By what experimental method was modelated the development of red thrombus in mesenterial vessels in the frog?

a) by ligation of mesenterial vessels

b) by applying a crystal of NaCl on mesenterial vessel bifurcation

c) by applying a crystal of AgNO3 on mesenterial vessel bifurcation

d) by applying heparin solution on mesenterial vessels

e) by mechanical injury of the vessel

630. What are the causes for thrombus development?

a) Endothelial injury

b) increased blood velocity

c) increased level of pro-coagulant factors

d) intensification of blood flow

e) activation of the complement system

631. What are the causes for thrombus development?

a) vessel catheterization

b) turbulent blood flow

c) release of thromboplastin

d) laminar blood flow

e) release of heparin

632. What are the causes for thrombus development?

a) Endothelial cell injury

b) reduced perfusion

c) exposure of subendothelial matrix

d) increased blood velocity

e) laminar blood flow

633. What are the causes for thrombus development?

a) Excessive release of thromboplastin

b) Deficiency of plasminogen

c) Excessive production of plasminogen

d) intensification of blood flow

e) deficiency of thromboplastin

634. What are stages of white thrombus development?

a) activation of Hageman factor

b) release of thromboplastin

c) thrombocyte aggregation

d) thrombocyte adhesion

e) release of plasminogen

635. How was modelated experimental fat embolism in the mesenterial vessels in the frog?

a) by administration of oil emulsion in the heart ventricles

b) by administration of oil emulsion orally

c) by administration of oil solution in the dorsal lymphatic sack

d) by administration of oil solution intraperitoneally

e) by administration of oil solution transcutaneously

636. How alteration was modelated on frog’s tongue?

a) by administration of adrenalin solution 0,1%

b) by bilateral ligation of lingual veins

c) by applying crystal of AgNO3 on the tongue

d) by ligation of lingual arteries

e) by unilateral ligation of lingual vein

637. What is the mechanism of primary alteration on frog’s tongue after administration of AgNO3 crystals?

a) chemical cell injury

b) development of venous hyperemia

c) development of blood stasis

d) development of arteriolar spasm

e) thrombogenesis

638. What structures are primarily affected after administration of AgNO3 crystals on frog’s tongue?

a) cell membrane

b) cell organelles

c) cell nucleus

d) mitochondria

e) blood cells

639. What substance was used to color the focus of primary alteration on frog’s tongue?

a) methylene blue

b) acetylcholine

c) HCl

d) adrenaline

e) heparin

640. What are the mechanisms of dyeing of dead cells in the focus of primary alteration?

a) alive cell actively absorb the colorant

b) the colorant passively enters in the alive cell

c) the colorant actively enters in the dead cell

d) the colorant passively enters in the dead cell

e) the colorant doesn’t enter in the alive cell

641. What are the mechanisms of secondary alteration on frog’s tongue?

a) dysregulation of subcellular units functions

b) disorders in the biochemical homeostasis of the cell

c) injury of the nervous structures

d) injury in the blood vessels

e) direct action of AgNO3 crystals

642. What is the sequence of vascular reactions in inflammatory focus on frog’s tongue?

a) arterial hyperemia→ venous hyperemia →ischemia → stasis

b) venous hyperemia → arterial hyperemia → ischemia → stasis

c) venous stasis → venous hyperemia → arterial hyperemia → ischemia

d) ischemia → arterial hyperemia → venous hyperemia → stasis

e) ischemia → venous hyperemia → arterial hyperemia → stasis

643. What factors cause arterial hyperemia in the inflammatory focus on frog’s tongue?

a) vessel breakdown and bleeding

b) release of mediators with vasoconstrictor effect

c) release of mediators with vasodilator effect

d) acidosis in inflammatory focus

e) thrombogenesis in inflammatory focus

644. What factors cause arterial hyperemia in the inflammatory focus on frog’s tongue?

a) vessel breakdown and bleeding

b) release of thromboxane

c) release of histamine

d) acidosis in inflammatory focus

e) thrombogenesis in inflammatory focus

645. What factors cause arterial hyperemia in the inflammatory focus on frog’s tongue?

a) release of endothelin in the result of endothelial injury

b) release of thromboxane

c) release of prostaglandins

d) release of histamine

e) thrombogenesis in inflammatory focus

646. What factors cause venous hyperemia in inflammatory focus on frog’s tongue?

a) thrombosis in the venules

b) leucocytes margination at the level of microvessels

c) accumulation of exudate

d) arteriolar dilation

e) dilation of venules

647. What factors cause venous hyperemia in inflammatory focus on frog’s tongue?

a) Accumulation of exudate

b) leucocytes margination at the level of microvessels

c) accumulation of transudate

d) arteriolar and capillary dilation

e) dilation of capillaries and venules

648. What factors cause venous hyperemia in inflammatory focus on frog’s tongue?

a) thrombosis in the arterioles

b) leucocytes margination at the level of microvessels

c) thrombosis in the venules

d) thrombosis in the capillaries

e) accumulation of transudate

649. What factors cause venous hyperemia in inflammatory focus on frog’s tongue?

a) thrombosis in the venules

b) narrowing of arterioles and capillaries

c) accumulation of exudate

d) accumulation of transudate

e) dilation of venules and capillaries

650. What factor causes venous hyperemia in inflammatory focus on frog’s tongue?

a) Accumulation of exudate

b) accumulation of transudate

c) narrowing of arterioles and dilation of venules

d) narrowing of venules and dilation of capillaries

e) dilation of venules and capillaries

651. What factor causes venous hyperemia in inflammatory focus on frog’s tongue?

a) accumulation of transudate

b) margination of leucocytes in microvessels

c) thrombosis in the arterioles

d) dilation of venule and capillaries

e) dilation of arteriole and constriction of venule

652. What factor causes venous hyperemia in inflammatory focus on frog’s tongue?

a) thrombosis in the arterioles and capillaries

b) narrowing of arterioles and capillaries

c) accumulation of transudate in the inflammatory focus

d) endothelial cell contraction and sphericisation

e) dilation of venules and capillaries

653. What are the pathogenetic mechanisms of inflammatory venous hyperemia?

a) endotheliocyte contraction

b) reduced vascular permeability

c) erythrocytes and thrombocytes aggregation

d) lymph vessels dilation

e) reduced blood viscosity

654. What are the pathogenetic mechanisms of inflammatory venous hyperemia?

a) endothelial sphericisation

b) enhanced lymphogenesis

c) aggregation of erythrocytes and thrombocytes

d) dilation of lymphatic vessels

e) reduced blood viscosity

655. What are the pathogenetic mechanisms of inflammatory venous hyperemia?

a) endothelial contraction

b) enhanced lymphogenesis

c) increased blood viscosity

d) dilation of lymphatic vessels

e) reduced blood viscosity

656. What are the manifestations of venous hyperemia on frog’s tongue?

a) Overfilling of arterioles with blood

b) Overfilling of capillaries with blood

c) Reduced volumetric blood velocity

d) Increased linear blood velocity

e) Reduced number of functional capillaries

657. What are manifestations of venous hyperemia on frog’s tongue?

a) reduced filling of arterioles with blood

b) reduced linear blood velocity

c) Reduced volumetric blood velocity

d) Increased linear blood velocity

e) Reduced number of functional capillaries

658. What are manifestations of venous hyperemia on frog’s tongue?

a) reduced filling of arterioles with blood

b) dilation of capillaries

c) amplification of vascular network

d) Increased linear blood velocity

e) Reduced number of functional capillaries

659. What is a manifestation of venous hyperemia on frog’s tongue?

a) increased volumetric blood velocity

b) amplification of capillary network

c) overfilling of arterioles with arterial blood

d) Increased linear blood velocity

e) Reduced number of functional capillaries

660. What microcirculatory disorders lead to development of stasis on frog’s tongue?

a) ischemia

b) venous hyperemia

c) arterial hyperemia

d) embolism

e) e thrombosis

661. What are the consequences of long-lasting stasis in the inflammatory focus?

a) Intravascular aggregation of erythrocytes

b) pendulatory blood movements

c) hypoperfusion

d) reduced capillary network

e) pulsatile blood movements

662. What are the consequences of long-lasting inflammatory stasis on frog’s tongue?

a) spreading of secondary alteration

b) localization of inflammatory focus

c) spreading of primary alteration

d) spreading of inflammatory focus

e) improved tissular hydration

663. What are the consequences of long-lasting inflammatory stasis on frog’s tongue?

a) enhanced phagocytosis

b) localization of inflammatory focus

c) spreading of primary alteration

d) spreading of inflammatory focus

e) impair phagocytosis

664. What are the consequences of long-lasting inflammatory stasis on frog’s tongue?

a) enhanced phagocytosis

b) accumulation of cellular debris

c) spreading of primary alteration

d) spreading of inflammatory focus

e) impairs phagocytosis

665. What are the consequences of long-lasting inflammatory stasis on frog’s tongue?

a) spreading of secondary alteration

b) accumulation of cellular debris

c) spreading of primary alteration

d) spreading of inflammatory focus

e) impairs phagocytosis

666. What is a consequence of long-lasting inflammatory stasis on frog’s tongue?

a) enhanced aerobic metabolic processes

b) enhanced phagocytosis

c) spreading of primary alteration

d) spreading of inflammatory focus

e) impairs phagocytosis

667. What is a consequence of long-lasting inflammatory stasis on frog’s tongue?

a) localization of inflammatory focus

b) enhanced anaerobic metabolic processes

c) spreading of primary alteration

d) spreading of inflammatory focus

e) impairs phagocytosis

668. How anaphylactic shock was triggered in the experimental rabbit?

a) by parenteral administration of horse serum

b) by parenteral administration of glucose solution

c) by parenteral administration of isotonic solution

d) by parietal administration of adrenaline solution

e) by parenteral administration of bicarbonate solution

669. What is the pathogenetic mechanism of pathologic phenomena observed in experimental anaphylactic shock?

a) Degranulation of mast cell

b) Degranulation of basophils

c) Degranulation of eosinophils

d) Activation of T lymphocytes

e) Activation of B lymphocytes

670. What is the pathogenetic mechanism of pathologic phenomena observed in experimental anaphylactic shock?

a) release of anaphylaxia mediators

b) Degranulation of plasma cells

c) Degranulation of eosinophils and basophils

d) Activation of the complement system

e) Activation of B lymphocytes

671. What are pathogenetic mechanisms of pathologic phenomena observed in experimental anaphylactic shock?

a) release of anaphylaxia mediators

b) Degranulation of plasma cells

c) Degranulation of mast cells

d) Activation of the complement system

e) Activation of B lymphocytes

672. How long is the period of sensitization of experimental animal in anaphylactic shock?

a) 5-10 minutes

b) 1-2 days

c) 7-8 days

d) 30 days

e) 24 hours

673. What are pathogenetic mechanisms of pathologic phenomena observed in experimental anaphylactic shock?

a) release of histamine

b) Degranulation of plasma cells

c) Degranulation of mast cells

d) Activation of the complement system

e) release of bradykinin

674. What are pathogenetic mechanisms of pathologic phenomena observed in experimental anaphylactic shock?

a) bronchoconstriction with respiratory failure

b) bronchial dilation with mucous hypersecretion

c) reduced vascular peripheral resistance with hypotension

d) increased vascular peripheral resistance with hypertension

e) reduced heart contractions frequency

675. What was the dose of antigen used for triggering the experimental anaphylactic shock in rabbit?

a) 1 ml

b) 10 times greater that dose for sensitization

c) Identical with dose for sensitization

d) 10 times lower that dose for sensitization

e) 0,5 ml

676. What are the manifestations of experimental anaphylactic shock in the rabbit?

a) Spasm of bronchial muscles with respiratory failure

b) Bronchial dilation

c) Mucous hypersecretion with rhinorrhea

d) Mucous hyposecretion with dry mucosa

e) Spasm of laryngeal muscles with respiratory failure

677. What are the manifestations of experimental anaphylactic shock in the rabbit?

a) reduced vascular peripheral resistance

b) increased vascular peripheral resistance

c) Mucous hypersecretion

d) Mucous hyposecretion

e) Spasm of laryngeal muscles with respiratory failure

678. What are the manifestations of experimental anaphylactic shock in the rabbit?

a) Spasm of bronchial muscles with respiratory failure

b) increased vascular peripheral resistance

c) vasodilation with hypotension

d) spasm of trachea with respiratory failure

e) Spasm of laryngeal muscles with respiratory failure

679. When the experimental anaphylactic shock will start in the rabbit?

a) At the second contact with specific allergen

b) At the second contact with every allergen in the air

c) At the first contact with specific allergen

d) At contact with specific immunoglobulins from class M

e) At contact with specific immunoglobulins from class G

680. What are respiratory changes in the rabbit in experimental anaphylactic shock?

a) Forced breathi

b) Reduced breathing frequency

c) Agonal breathing

d) Superficial breathing

e) Increased breathing amplitude

681. What are respiratory changes in the rabbit in experimental anaphylactic shock?

a) Forced breathing

b) Reduced breathing frequency

c) breathing arrest

d) Superficial breathing

e) Increased breathing amplitude

682. What are respiratory changes in the rabbit in experimental anaphylactic shock?

a) agonal breathing

b) Reduced breathing frequency

c) breathing arrest

d) inspiratory dyspnea

e) Increased breathing amplitude

683. What is a respiratory change in the rabbit in experimental anaphylactic shock?

a) agonal breathing

b) Reduced breathing frequency

c) expiratory dyspnea

d) inspiratory dyspnea

e) Increased breathing amplitude

684. What is a respiratory change in the rabbit in experimental anaphylactic shock?

a) forced breathing

b) Reduced breathing frequency

c) expiratory dyspnea

d) inspiratory dyspnea

e) Increased breathing amplitude

685. What are pathogenetic mechanisms of respiratory changes in the rabbit in experimental anaphylactic shock?

a) Spasm of smooth bronchial muscles

b) Mucosal hypersecretion and edema

c) Spasm of smooth tracheal muscles

d) Spasm of smooth laryngeal muscles

e) Cerebral hypoperfusion and disturbances in the respiratory center

686. What is a pathogenetic mechanism of respiratory changes in the rabbit in experimental anaphylactic shock?

a) Spasm of smooth bronchial muscles

b) paralysis of respiratory muscles

c) Spasm of smooth tracheal muscles

d) Spasm of smooth laryngeal muscles

e) Cerebral hypoperfusion and disturbances in the respiratory center

687. What is the pathogenetic mechanism of bronchial spasm in experimental anaphylactic shock?

a) Release of histamine from mast cells

b) Release of thromboxane from mast cells

c) Activation of compliment system

d) Release of histamine from plasma cells

e) Release of thromboxane from mast cells

688. What neurological disturbances developed in experimental anaphylactic shock in the rabbit?

a) Enhanced motor activity

b) Tonic seizures

c) Clonic seizures

d) Diminished motor activity

e) Ischemic stroke

689. What neurological disturbances developed in experimental anaphylactic shock in the rabbit?

a) Enhanced motor activity

b) hemorrhagic stroke

c) Clonic seizures

d) Diminished motor activity

e) Ischemic stroke

690. What are the causes of death of the rabbit in experimental anaphylactic shock?

a) Cerebral coma

b) Cardiac arrest

c) Asphyxia

d) Arterial collapse

e) Ischemia in the brain

691. What are the causes of death of the rabbit in experimental anaphylactic shock?

a) Cerebral coma

b) Cardiac arrest

c) respiratory arrest

d) Arterial collapse

e) Ischemia in the brain

692. What is a cause of death of the rabbit in experimental anaphylactic shock?

a) Cerebral coma

b) Cardiac arrest

c) bleeding in the brain

d) Arterial collapse

e) Ischemia in the brain