1. THE LEADING FACTOR IN DEVELOPMENT OF NEPHRITIC EDEMA IS

2. INADEQUATE (EXCESSIVE) PRODUCTION OF ANTIDIURETIC HORMONE WILL LEAD TO THE DEVELOPMENT OF

3. Respiratory acidosis is characterized by:

4. THE DEVELOPMENT OF RESPIRATORY ACIDOSIS IS DUE TO

5. THE PRODUCTION OF ALDOSTERONE IN ADRENAL GLANDS IS STIMULATED BY

6. PRIMARY CHANGES OF THE BICARBONATE BUFFER IN THE RESPIRATORY ALKALOSIS ARE DUE TO

7. FACTORS WHICH LEAD TO DEVELOPMENT OF EDEMA ARE

8. The development of respiratory acidosis may be due to:

9. HYPERKALEMIA IS TYPICAL FOR FOLLOWING DISORDER

10. THE COMPENSATORY MECHANISM OF RESPIRATORY ALKALOSIS IS

11. HYPOCHLOREMIA IS TYPICAL FOR FOLLOWING DISORDER

12. ALKALOSIS OCCURS DUE TO

13. The development of respiratory alkalosis may be due to:

14. FOR ISOOSMOLAR REDUCTION OF THE TOTAL VOLUME OF EXTRACELLULAR FLUID ARE CHARACTERISTIC THE FOLLOWING SIGNS

15. ACIDOGENESIS IN RENAL TUBULES IN INCREASED PRODUCTION OF ALDOSTERONE

16. DECREASE OF THE BLOOD HYDROSTATIC PRESSURE IS LEADING FACTOR IN THE DEVELOPMENT OF FOLLOWING TYPES OF EDEMAS

17. PRIMARY CHANGES OF THE BICARBONATE BUFFER IN THE RESPIRATORY ACIDOSIS ARE DUE TO

18. THE PROXIMAL RENAL TUBULAR ACIDOSIS, «SALT- LOSING» KIDNEY AND DIURETICS LEADS TO DEVELOPMENT OF

19. CAUSES OF RESPIRATORY ALKALOSIS ARE

20. THE CONCENTRATION OF HYDROGEN IONS IN ALKALOSIS

21. THE ONCOTIC FACTOR PLAYS A LEADING ROLE IN THE PATHOGENESIS OF FOLLOWING EDEMAS

22. HYPERCHLOREMIA IS TYPICAL FOR FOLLOWING DISORDER

23. METABOLIC ALKALOSIS DEVELOPS IN THE FOLLOWING CONDITIONS

24. THE USE OF «LOOP DIURETICS» MAY LEAD TO

25. ODEMAS AS A RESULT OF HEART FAILURE, RENAL FAILURE, LIVER CIRRHOSIS DEVELOP DUE TO

26. THE BLOOD VOLUME DURING CARDIAC EDEMA

27. THE LEADING FACTOR IN THE DEVELOPMENT OF INFLAMMATORY EDEMAS IS

28. FOLLOWING PROCESSES PARTICIPATE IN COMPENSATED RESPIRATORY ACIDOSIS

29. THE RESORPTION FROM TISSUES INTO VESSELS IS DECREASED DUE TO

30. THE MEMBRANE FACTOR PLAYS A KEY ROLE IN THE PATHOGENESIS OF FOLLOWING EDEMAS

31. MECHANISMS OF COMPENSATION IN HYPOOSMOLAR DEHYDRATION ARE

32. THE MOST EFFECTIVE MECHANISM OF COMPENSATION IN ISOOSMOLAR HYPERHYDRATION IS

33. THE REABSORPTION OF HCO 3 – IN KIDNEYS IN THE HYPOKALEMIA

34. THE CHLORIDE ION CONCENTRATION IN THE BLOOD IN RESPIRATORY ALKALOSIS

35. FOLLOWING PROCESSES PARTICIPATE IN COMPENSATED RESPIRATORY ALKALOSIS

36. THE LEADING FACTOR IN THE DEVELOPMENT OF ALLERGIC EDEMAS IS

37. METABOLIC ACIDOSIS DEVELOPS IN THE FOLLOWING CONDITIONS

38. The main factor of the development of nephrotic edema is:

39. The main factor of the development of cardiac edema is:

40. THE TRIGGERING FACTOR IN THE DEVELOPMENT OF «HUNGRY» EDEMAS IS

41. THE CONCENTRATION OF HYDROGEN IONS IN ACIDOSIS

42. MECHАNISMS OF COMPENSATION IN HYPEROSMOLAR DEHYDRATION ARE

43. CHANGES OF pH OF THE BLOOD IN THE DECOMPENSATED ACIDOSIS ARE CHARACTERISED BY

44. THE REABSORPTION OF HCO 3 – IN KIDNEYS IS STIMULATED BY

45. THE LEADING FACTOR IN THE DEVELOPMENT OF TOXIC EDEMAS IS

46. Hyper-K+emia is typical sign of the following disorder:

47. THE DEVELOPMENT OF PULMONARY EDEMA IS A RESULT OF THE FAILURE OF

48. THE CHLORIDE ION CONCENTRATION IN THE BLOOD IN RESPIRATORY ACIDOSIS

49. The main factor of the development of allergic edema is:

50. THE TRIGGERING FACTOR IN THE DEVELOPMENT OF «NEPHROTIC» EDEMAS IS

51. Metabolic acidosis is characterized by:

52. PRIMARY CHANGES OF THE BICARBONATE BUFFER IN THE METABOLIC ACIDOSIS ARE DUE TO

53. THE SEVERE DIARRHEA, INCREASED SWEATING LEAD TO DEVELOPMENT OF

54. Compensatory mechanism of isoosmolar hyperhydration is:

55. NEUROMUSCULAR EXCITABILITY IN DECOMPENSATED RESPIRATORY ALKALOSIS

56. Hypo-K+emia is typical sign of the following disorder:

57. The main mechanisms of edema development are:

58. pCO 2 IN THE BLOOD WILL DECREASE IN

59. THE DEVELOPMENT OF RESPIRATORY ALKALOSIS IS DUE TO

60. THE COMPENSATORY MECHANISM OF RESPIRATORY ACIDOSIS IS

61. THE INITIAL STAGE OF PULMONARY EDEMA LEADS TO

62. THE ALBUMIN-GLOBULIN INDEX OF PLASMA (WHEN TOTAL CONTENT OF PROTEIN IS NORMAL) FOR OCCURRENCE OF HYPOONKIA (DECREASE OF
ONCOTIC PRESSURE) MUST

63. MECHANISMS OF COMPENSATION IN ISOOSMOLAR DEHYDRATION ARE

64. Respiratory alkalosis is characterized by:

65. THE MOST TYPICAL LOCATION OF RENAL EDEMAS IS

66. pCO 2 IN THE BLOOD WILL INCREASE IN

67. CHANGES OF pН OF THE BLOOD IN DECOMPENSATED ALKALOSIS INCLUDE

68. ACIDOSIS OCCURS DUE TO

69. HYPOKALEMIA IS TYPICAL FOR FOLLOWING DISORDER

70. Metabolic alkalosis is characterized by:

71. THE INTRAVASCULAR VOLUME DURING DECREASE OF THE BLOOD COLLOID-OSMOTIC PRESSURE

72. THE TRIGGERING FACTOR IN THE DEVELOPMENT OF CONGESTIVE EDEMAS IS

73. All of the following are compensatory mechanisms of metabolic acidosis, except:

74. BLOOD LOSS LEADS TO THE DEVELOPMENT OF

75. THE LIQUID FILTRATION FROM VESSELS INTO TISSUES IS INCREASED DUE TO

76. THE COMPENSATORY MECHANISM OF RESPIRATORY ALKALOSIS IS

77. INTRODUCTION OF BICARBONATE IN RESPIRATORY ACIDOSIS IS NECESSARY

78. THE MOST EFFECTIVE MECHANISM OF COMPENSATION IN PRIMARY HYPERALDOSTERONISM IS

79. Compensatory mechanism of hyperosmolar hyperhydration is:

80. PRIMARY CHANGES OF THE BICARBONATE BUFFER IN THE METABOLIC ALKALOSIS ARE DUE TO

81. DEVELOPMENT OF OSTEOPOROSIS OCCURS IN THE FOLLOWING CASES

82. THE DECREASED SYNTHESIS OF ACIDS AND AMMONIUM IN RENAL TUBULES LEADS TO DEVELOPMENT OF

83. EDEMAS OF EXTREMITIES DEVELOP AS A RESULT OF THE FAILURE OF

84. Compensatory mechanism of hypoosmolar dehydration is:

85. HYPO-ONCOTIC EDEMAS ARE

86. DECREASE OF THE BLOOD CONCOTIC PRESSURE IS LEADING FACTOR IN THE DEVELOPMENT OF FOLLOWING TYPES OF EDEMAS

87. THE ACTIVATION OF RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM IS LEADING FACTOR IN THE DEVELOPMENT OF FOLLOWING TYPES OF EDEMAS

88. CAUSES OF METABOLIC ALKALOSIS ARE

89. HIDDEN (LATENT) TETANY OCCURS IN

90. THE MAIN FACTOR IN THE DEVELOPMENT OF CARDIAC EDEMAS IS

91. THE USE OF CARBONIC ANHYDRASE INHIBITORS MAY LEAD TO

92. HYDROSTATIC PRESSURE IS LEADING FACTOR IN THE DEVELOPMENT OF FOLOWING EDEMAS

93. THE BLOOD ONCOTIC PRESSURE DECREASES DUE TO