Pathophysiology Module 3 Mcqs Pathophysiology Module 3 Mcqs 1. THE USE OF CARBONIC ANHYDRASE INHIBITORS MAY LEAD TO metabolic acidosis metabolic alkalosis respiratory acidosis respiratory alkalosis 2. The main factor of the development of cardiac edema is: increased hydrostatic pressure , decreased minute blood volume hypoproteinemia increased vascular permeability 3. FOR ISOOSMOLAR REDUCTION OF THE TOTAL VOLUME OF EXTRACELLULAR FLUID ARE CHARACTERISTIC THE FOLLOWING SIGNS decrease of arterial and venous pressure tachycardia tendency to orthostatic collapse increase of blood viscosity humidity of mucous membranes decrease of body temperature reduction of deep tendon reflexes stupor and coma 4. THE MOST EFFECTIVE MECHANISM OF COMPENSATION IN PRIMARY HYPERALDOSTERONISM IS increase of secretion of antidiuretic hormone activation of renin-angiotensin-aldosterone system thirst increase of glomerular filtration rate natriuretic effect of kidneys («escape phenomenon») 5. THE BLOOD VOLUME DURING CARDIAC EDEMA it increases it decreases it does not change 6. THE LIQUID FILTRATION FROM VESSELS INTO TISSUES IS INCREASED DUE TO increase of colloid-osmotic pressure in blood vessels increase of colloid-osmotic pressure in tissues increase of hydrostatic pressure in blood vessels increase of vascular permeability increase of the lymph flow 7. Hypo-K+emia is typical sign of the following disorder: acidosis alkalosis 8. HIDDEN (LATENT) TETANY OCCURS IN respiratory alkalosis metabolic acidosis metabolic alkalosis the correct answer – only 1 the correct answer – 1 and 3 9. THE REABSORPTION OF HCO 3 – IN KIDNEYS IS STIMULATED BY hypercapnia hypocapnia 10. PRIMARY CHANGES OF THE BICARBONATE BUFFER IN THE METABOLIC ALKALOSIS ARE DUE TO increase of pCO 2 decrease of pCO 2 decrease of [HCO3] increase of [HCO3] 11. THE CONCENTRATION OF HYDROGEN IONS IN ACIDOSIS it increases it decreases it does not change 12. Respiratory acidosis is characterized by: increase of pCO2 decrease of pCO2 13. Metabolic alkalosis is characterized by: decrease of [HCO3] increase of [HCO3] 14. THE USE OF «LOOP DIURETICS» MAY LEAD TO metabolic acidosis metabolic alkalosis respiratory acidosis respiratory alkalosis 15. The main factor of the development of allergic edema is: increased hydrostatic pressure hypoproteinemia increased vascular permeability 16. THE TRIGGERING FACTOR IN THE DEVELOPMENT OF CONGESTIVE EDEMAS IS increase of hydrostatic pressure hypoproteinemia increase of vascular permeability secondary hyperaldosteronism decrease in minute volume of the blood 17. INADEQUATE (EXCESSIVE) PRODUCTION OF ANTIDIURETIC HORMONE WILL LEAD TO THE DEVELOPMENT OF hypotonic hyponatremia with extracellular dehydration hypotonic hyponatremia with extracellular hyperhydration hypotonic hyponatremia with normal extracellular fluid volume 18. FOLLOWING PROCESSES PARTICIPATE IN COMPENSATED RESPIRATORY ALKALOSIS hyperkalemia binding proteins with cations and release of hydrogen ions release Н+ in the blood from cells in the exchange for potassium ions decrease of release the hydrocarbonate in the urine increase of excretion of hydrocarbonate in the urine flow of Н+ into blood from bone in exchange for Na + and Ca ++ 19. INTRODUCTION OF BICARBONATE IN RESPIRATORY ACIDOSIS IS NECESSARY Yes No 20. MECHANISMS OF COMPENSATION IN ISOOSMOLAR DEHYDRATION ARE increase of secretion of antidiuretic hormone activation of renin-angiotensin-aldosterone system decrease of glomerular filtration rate thirst increase of glomerular filtration rat 21. Compensatory mechanism of hyperosmolar hyperhydration is: decrease of the glomerular filtration rate activation of the renin-angiotensin-aldosterone system thirst natriuretic effect of kidneys 22. THE LEADING FACTOR IN DEVELOPMENT OF NEPHRITIC EDEMA IS secondary hyperaldosteronism decrease of osmotic pressure in the blood increase of hydrostatic pressure in the vascular system increase of vascular permeability decrease of oncotic pressure 23. The main mechanisms of edema development are: increased hydrostatic pressure decreased oncotic pressure increased oncotic pressure increased vascular permeability decreased hydrostatic pressure decreased vascular permeability impaired lymphatic drainage 24. METABOLIC ACIDOSIS DEVELOPS IN THE FOLLOWING CONDITIONS diabetes mellitus diuretics – carbonic anhydrase inhibitors hypercortisolism methanol poisoning renal failure 25. pCO 2 IN THE BLOOD WILL INCREASE IN respiratory alkalosis metabolic alkalosis respiratory acidosis metabolic acidosis 26. HYPOCHLOREMIA IS TYPICAL FOR FOLLOWING DISORDER metabolic acidosis metabolic alkalosis respiratory acidosis respiratory alkalosis 27. NEUROMUSCULAR EXCITABILITY IN DECOMPENSATED RESPIRATORY ALKALOSIS it increases it decreases it does not change 28. EDEMAS OF EXTREMITIES DEVELOP AS A RESULT OF THE FAILURE OF left ventricle right ventricle 29. THE SEVERE DIARRHEA, INCREASED SWEATING LEAD TO DEVELOPMENT OF hypo osmolar dehydration hyperosmolar dehydration iso osmolar dehydration 30. THE PROXIMAL RENAL TUBULAR ACIDOSIS, «SALT- LOSING» KIDNEY AND DIURETICS LEADS TO DEVELOPMENT OF hypo osmolar dehydration hyperosmolar dehydration iso osmolar dehydration 31. THE DEVELOPMENT OF PULMONARY EDEMA IS A RESULT OF THE FAILURE OF left ventricle right ventricle 32. THE LEADING FACTOR IN THE DEVELOPMENT OF ALLERGIC EDEMAS IS increase of hydrostatic pressure hypoproteinaemia increase of vascular permeability increase of the blood osmotic pressure 33. HYPO-ONCOTIC EDEMAS ARE heart oedema toxic oedema allergic oedema nephritic oedema nephrotic oedema oedema in starvation (hunger) 34. THE COMPENSATORY MECHANISM OF RESPIRATORY ALKALOSIS IS hypoventilation hyperventilation increase of the urinary excretion of ammonium chloride increase of the urinary excretion of hydrocarbonate flow into the cells of hydrogen ions in exchange for potassium ion 35. ACIDOSIS OCCURS DUE TO increase of HCO 3 – in the blood decrease of HCO 3 – in the blood increase of pCO 2 in the blood decrease of pCO 2 in the blood 36. FACTORS WHICH LEAD TO DEVELOPMENT OF EDEMA ARE increase of oncotic pressure decrease of oncotic pressure increase of venous pressure increase of blood osmotic pressure 37. Compensatory mechanism of isoosmolar hyperhydration is: increased ADH secretion increased GFR activation of RAAS thirst 38. THE BLOOD ONCOTIC PRESSURE DECREASES DUE TO heart failure nephritic syndrome starvation liver cirrhosis allergy 39. CAUSES OF RESPIRATORY ALKALOSIS ARE hypokalemia Kussmaul breathing hypoventilation overdose of sodium bicarbonate mechanical ventilation multiple fractures of ribs overdose of trisamine fast running 40. MECHАNISMS OF COMPENSATION IN HYPEROSMOLAR DEHYDRATION ARE thirst activation of renin-angiotensin-aldosterone system decrease of glomerular filtration rate increase of secretion of antidiuretic hormone 41. THE ALBUMIN-GLOBULIN INDEX OF PLASMA (WHEN TOTAL CONTENT OF PROTEIN IS NORMAL) FOR OCCURRENCE OF HYPOONKIA (DECREASE OF ONCOTIC PRESSURE) MUST decrease increase 42. CAUSES OF METABOLIC ALKALOSIS ARE hypokalemia Kussmaul breathing hypoventilation overdose of sodium bicarbonate mechanical ventilation multiple fractures of ribs overdose of trisamine fast running 43. THE CHLORIDE ION CONCENTRATION IN THE BLOOD IN RESPIRATORY ACIDOSIS it increases it decreases it does not change 44. MECHANISMS OF COMPENSATION IN HYPOOSMOLAR DEHYDRATION ARE thirst increase of secretion of antidiuretic hormone activation of renin-angiotensin-aldosterone system decrease of glomerular filtration rate 45. THE COMPENSATORY MECHANISM OF RESPIRATORY ACIDOSIS IS hypoventilation hyperventilation decrease of the urinary excretion of hydrocarbonate increase of the urinary excretion of hydrocarbonate decrease of the urinary excretion of ammonium chloride use the protein buffer system for binding of hydrogen ions 46. THE MOST TYPICAL LOCATION OF RENAL EDEMAS IS lower extremities face ascites 47. THE LEADING FACTOR IN THE DEVELOPMENT OF INFLAMMATORY EDEMAS IS increase of hydrostatic pressure in the vascular system hypoproteinaemia increase of vascular permeability increase of the blood osmotic pressure increase of oncotic pressure in tissues increase of osmotic pressure in tissues 48. HYPERCHLOREMIA IS TYPICAL FOR FOLLOWING DISORDER metabolic acidosis metabolic alkalosis respiratory acidosis respiratory alkalosis 49. ODEMAS AS A RESULT OF HEART FAILURE, RENAL FAILURE, LIVER CIRRHOSIS DEVELOP DUE TO iso osmolar hyperhydration hypo osmolar hyperhydration hyperosmolar hyperhydration 50. ALKALOSIS OCCURS DUE TO increase of HCO 3 – in the blood decrease of HCO 3 – in the blood increase of pCO 2 in the blood decrease of pCO 2 in the blood 51. THE INTRAVASCULAR VOLUME DURING DECREASE OF THE BLOOD COLLOID-OSMOTIC PRESSURE it increases it decreases it does not change 52. The development of respiratory alkalosis may be due to: hypoventilation hyperventilation 53. BLOOD LOSS LEADS TO THE DEVELOPMENT OF hypo osmolar dehydration hyperosmolar dehydration iso osmolar dehydration 54. THE DECREASED SYNTHESIS OF ACIDS AND AMMONIUM IN RENAL TUBULES LEADS TO DEVELOPMENT OF respiratory acidosis metabolic acidosis respiratory alkalosis metabolic alkalosis 55. PRIMARY CHANGES OF THE BICARBONATE BUFFER IN THE RESPIRATORY ALKALOSIS ARE DUE TO increase of pCO 2 decrease of pCO 2 increase of [HCO3] decrease of [HCO3] 56. The main factor of the development of nephrotic edema is: increased hydrostatic pressure decreased oncotic pressure increased vascular permeability 57. THE INITIAL STAGE OF PULMONARY EDEMA LEADS TO metabolic acidosis metabolic alkalosis respiratory acidosis respiratory alkalosis 58. pCO 2 IN THE BLOOD WILL DECREASE IN respiratory acidosis respiratory alkalosis metabolic acidosis metabolic alkalosis 59. Compensatory mechanism of hypoosmolar dehydration is: decreased secretion of antidiuretic hormone activation of the renin-angiotensin-aldosterone system reduced water consumption 60. All of the following are compensatory mechanisms of metabolic acidosis, except: activation of acido- and ammoniagenesis in kidneys ncreased reabsorption of hydrocarbonate in renal tubules hyperkalemia hypokalemia 61. CHANGES OF pН OF THE BLOOD IN DECOMPENSATED ALKALOSIS INCLUDE decrease of pH increase of pH normal pH 62. THE CHLORIDE ION CONCENTRATION IN THE BLOOD IN RESPIRATORY ALKALOSIS it increases it decreases it does not change 63. METABOLIC ALKALOSIS DEVELOPS IN THE FOLLOWING CONDITIONS diabetes mellitus the diuretics – carbonic anhydrase inhibitors hypercortisolism methanol poisoning renal failure 64. THE DEVELOPMENT OF RESPIRATORY ACIDOSIS IS DUE TO hypoventilation hyperventilation fibrillation 65. THE MAIN FACTOR IN THE DEVELOPMENT OF CARDIAC EDEMAS IS increase of hydrostatic pressure hypoproteinaemia increase of vascular permeability secondary hyperaldosteronism decrease in minute volume of the blood 66. THE RESORPTION FROM TISSUES INTO VESSELS IS DECREASED DUE TO increase of hydrostatic pressure in blood vessels increase of colloid-osmotic pressure in tissues decrease of colloid-osmotic pressure in blood vessels lymph stasis increase of vascular permeability) 67. HYDROSTATIC PRESSURE IS LEADING FACTOR IN THE DEVELOPMENT OF FOLOWING EDEMAS nephritic hungry congestive cardiac 68. CHANGES OF pH OF THE BLOOD IN THE DECOMPENSATED ACIDOSIS ARE CHARACTERISED BY decrease of pH increase of pH normal рН 69. THE LEADING FACTOR IN THE DEVELOPMENT OF TOXIC EDEMAS IS increase of hydrostatic pressure hypoproteinaemia increase of vascular permeability increase of the blood osmotic pressure 70. THE COMPENSATORY MECHANISM OF RESPIRATORY ALKALOSIS IS hypoventilation hyperventilation increase of the urinary excretion of ammonium chloride increase of the urinary excretion of hydrocarbonate 71. ACIDOGENESIS IN RENAL TUBULES IN INCREASED PRODUCTION OF ALDOSTERONE it increases it decreases it does not change 72. THE REABSORPTION OF HCO 3 – IN KIDNEYS IN THE HYPOKALEMIA it increases it decreases it does not change 73. THE MEMBRANE FACTOR PLAYS A KEY ROLE IN THE PATHOGENESIS OF FOLLOWING EDEMAS cardiac allergic toxic nephritic 74. THE PRODUCTION OF ALDOSTERONE IN ADRENAL GLANDS IS STIMULATED BY hypernatremia is a increase of sodium in the blood hyponatremia is a decrease of sodium in the blood hypervolemia the increase of oncotic pressure the decrease of renal blood flow hypokalaemia is a decrease of potassium in the blood) hyperkalaemia is an increase of potassium in the blood) 75. THE CONCENTRATION OF HYDROGEN IONS IN ALKALOSIS it increases it decreases it does not change 76. THE TRIGGERING FACTOR IN THE DEVELOPMENT OF «HUNGRY» EDEMAS IS increase of hydrostatic pressure hypoproteinaemia increase of vascular permeability increase of the blood osmotic pressure 77. The development of respiratory acidosis may be due to: hypoventilation hyperventilation 78. DECREASE OF THE BLOOD CONCOTIC PRESSURE IS LEADING FACTOR IN THE DEVELOPMENT OF FOLLOWING TYPES OF EDEMAS nephrotic hungry inflammatory when liver cirrhosis 79. FOLLOWING PROCESSES PARTICIPATE IN COMPENSATED RESPIRATORY ACIDOSIS activation of acido- and ammoniagenesis in kidneys increased reabsorption of hydrocarbonate in renal tubules decreased reabsorption of hydrocarbonate in renal tubules binding of excess of H + with deoxygenated hemoglobin hypokalaemia release of Na+ and K+ from proteins and their binding with H + ion 80. HYPOKALEMIA IS TYPICAL FOR FOLLOWING DISORDER acidosis alkalosis 81. THE MOST EFFECTIVE MECHANISM OF COMPENSATION IN ISOOSMOLAR HYPERHYDRATION IS increase of secretion of antidiuretic hormone increase of glomerular filtration rate activation of renin-angiotensin-aldosterone system thirst 82. Respiratory alkalosis is characterized by: increase of pCO2 decrease of pCO2 83. DEVELOPMENT OF OSTEOPOROSIS OCCURS IN THE FOLLOWING CASES acute metabolic acidosis chronic metabolic acidosis metabolic alkalosis chronic respiratory acidosis chronic respiratory alkalosis 84. PRIMARY CHANGES OF THE BICARBONATE BUFFER IN THE RESPIRATORY ACIDOSIS ARE DUE TO increase of pCO2 decrease of pCO2 decrease of [HCO3] increase of [HCO3] 85. Hyper-K+emia is typical sign of the following disorder: acidosis alkalosis 86. THE ACTIVATION OF RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM IS LEADING FACTOR IN THE DEVELOPMENT OF FOLLOWING TYPES OF EDEMAS inflammatory nephritic cardiac congestive hungry 87. THE TRIGGERING FACTOR IN THE DEVELOPMENT OF «NEPHROTIC» EDEMAS IS increase of hydrostatic pressure hypoproteinaemia increase of vascular permeability increase of the blood osmotic pressure 88. PRIMARY CHANGES OF THE BICARBONATE BUFFER IN THE METABOLIC ACIDOSIS ARE DUE TO decrease of pCO 2 increase of pCO 2 decrease of [HCO3] increase of [HCO3] 89. Metabolic acidosis is characterized by: decrease of [HCO3] increase of [HCO3] 90. THE DEVELOPMENT OF RESPIRATORY ALKALOSIS IS DUE TO hypoventilation hyperventilation fibrillation 91. THE ONCOTIC FACTOR PLAYS A LEADING ROLE IN THE PATHOGENESIS OF FOLLOWING EDEMAS allergic hungry toxic nephritic 92. HYPERKALEMIA IS TYPICAL FOR FOLLOWING DISORDER acidosis alkalosis 93. DECREASE OF THE BLOOD HYDROSTATIC PRESSURE IS LEADING FACTOR IN THE DEVELOPMENT OF FOLLOWING TYPES OF EDEMAS inflammatory congestive toxic cardiac Loading …Is fire hot or cold?
