Pharmacologie Doung Dararith 2017 DCEM3B
Pharmacology Quiz: Diuretics and Antihypertensives
Test your knowledge on pharmacology with our specialized quiz focusing on diuretics and antihypertensives. Dive into various mechanisms of action, side effects, and clinical applications of these important classes of drugs.
Key Features:
- Multiple choice questions
- Covers essential pharmacological concepts
- Perfect for students and professionals in medical fields
1. What is the mechanism of action of Furosemide?
Block Na channel ligand dependent
Block co-transport Na+ – K+ – 2Cl-
Block co-transport Na+ – Cl
D. Block epithelial Na+ channel
2. What is the mechanism of action of Thiazide?
A. block Na channel voltage dependent
B. Block co-transport Na+ – K+ – 2Cl-
C. Block co-transport Na+ – Cl-
D. Block epithelial Na+ channel
3. What is the mechanism of action of Triamterene?
A. block Na channel voltage dependent
B. Block co-transport Na+ – K+ – 2Cl-
C. Block co-transport Na+ – Cl-
D. Block epithelial Na+ channel
4. What is the mechanism of action of spironolactone?
A. Compete with aldosterone on its receptor
B. Inhibit enzyme carbonic anhydrase
C. Use its physicochemical property
D. Block transport of Na+
5. What is the mechanism of action of acetazolamide?
A. Compete with aldosterone on its receptor
B. Inhibit enzyme carbonic anhydrase
C. Use its physicochemical property
D. Inhibit converting enzyme
6. What are the side effects of thiazide?
A. hyperkalemia + acidosis
B. hyperkalemia + hypocalcemia
C. hypokaliemia + hypercalcemia
D. hypokalemia + hypocalcemia
7. What are the side effects of furosemide?
A. hyperkalemia + acidosis
B. hyperkalemia + hypocalcemia
C. hypokalemia + hypercalcemia
D. hypokalemia + hypocalcemia
8. Which diuretic drugs gives rise to ototoxicity while using?
A. acetazolamide
B. Furosemide
C. Thiazide
D. Triamterene
9. Which drug you select to treat a patient with hypertension associated with osteoporosis?
A. acetazolamide
B. Furosemide
C. Thiazide
D. Triamterene
10. Which drug you select to treat a patient with congestive heart failure?
A. acetazolamide
B. Furosemide
C. Thiazide
D. Triamterene
11. What are the side effects of spironolactone?
A. hyperkalemia + cough
B. hyperkalemia + gynecomastia
C. hypokalemia + ototoxicity
D. hypokalemia + hypoglycemia
12. Which diuretic used to treat glaucoma?
A. acetazolamide
B. Furosemide
C. Thiazide
D. Triamterene
13. Which diuretic used to treat polycystic ovarian?
A. acetazolamide
B. Furosemide
C. spironolactone
D. Thiazide
E. Triamterene
14. What are the effects of thiazide in reduction blood pressure?
Reduced blood volume
Reduced peripheral resistance
Reduced heart rate
Reduced cardiac contraction
Reduced blood volume and reduced peripheral resistance
Reduced heart rate and reduced cardiac contraction
Reduced peripheral resistance, reduced heart rate and reduced cardiac contraction
Reduced blood volume, reduced peripheral resistance, reduced heart rate and reduced cardiac contraction
15. What are the side effects of thiazide?
A. hyperglycemia + hypokalemia + hyperuricemia
B. hypoglycemia + hyperkalemia + gynecomastia
C. hypoglycemia + hypokalemia + hyperuricemia
D. hyperglycemia + hyperkalemia + gynecomastia
16. What are the effects of β blocker in reduction blood pressure?
Reduced blood volume
Reduced peripheral resistance
Reduced heart rate
Reduced cardiac contraction
Reduced blood volume and reduced peripheral resistance
Reduced heart rate and reduced cardiac contraction
Reduced peripheral resistance, reduced heart rate and reduced cardiac contraction
Reduced blood volume, reduced peripheral resistance, reduced heart rate and reduced cardiac contraction
17. What are the side effects of non-selective β blocker?
A. asthma + AV block + claudication
B. cough + hyperkalemia + angioedema
C. Hemolytic anemia + lupus + depression
D. tachycardia + orthostatic hypotension + edema
18. What are the effects of α1 blocker in reduction blood pressure?
A. Prevent sympathetic vasoconstriction
B. Reduced heart rate
C. Reduced blood volume
D. Reduced cardiac contraction
19. What are the side effects of α1 blocker?
A. asthma + AV block + claudication
B. cough + hyperkalemia + angioedema
C. Hemolytic anemia + lupus + depression
D. tachycardia + orthostatic hypotension + edema
20. What are the effects of α2 agonist (clonidine) in reduction blood pressure?
Reduced blood volume
Reduced peripheral resistance
Reduced heart rate
Reduced cardiac contraction
Reduced blood volume and reduced peripheral resistance
Reduced heart rate and reduced cardiac contraction
Reduced peripheral resistance, reduced heart rate and reduced cardiac contraction
Reduced blood volume, reduced peripheral resistance, reduced heart rate and reduced cardiac contraction
21. What are the adverse effects of α2 agonist (clonidine)?
A. asthma + AV block + claudication
B. cough + hyperkalemia + angioedema
C. Dry mouth, postural hypotension, sedation
D. Hemolytic anemia + lupus + depression
22. What are the effects of α2 agonist (α-methyldopa) in reduction blood pressure?
Reduced blood volume
Reduced peripheral resistance
Reduced heart rate
Reduced cardiac contraction
Reduced blood volume and reduced peripheral resistance
Reduced heart rate and reduced cardiac contraction
Reduced peripheral resistance, reduced heart rate and reduced cardiac contraction
Reduced blood volume, reduced peripheral resistance, reduced heart rate and reduced cardiac contraction
23. What are the adverse effects of α2 agonist (α-methyldopa)?
A. asthma + AV block + claudication
B. cough + hyperkalemia + angioedema
C. Dry mouth, hemolytic anemia, postural hypotension,
D. asthma + lupus + hemolytic anemia
24. What is the mechanism of action of hydralazine used in hypertension?
A. activating D1 receptor
B. block Ca2+ channel
C. opening K+ channel
D. release NO
25. What is the mechanism of action of fenoldopam used in hypertension?
A. activating D1 receptor
B. block Ca2+ channel
C. opening K+ channel
D. release NO
26. What is the mechanism of action of minoxidil used in hypertension?
A. activating D1 receptor
B. block Ca2+ channel
C. opening K+ channel
D. release NO
27. What is the mechanism of action of diazoxide used in hypertension?
A. activating D1 receptor
B. block Ca2+ channel
C. opening K+ channel
D. release NO
28. What is the mechanism of action of nitroprusside used in hypertension?
A. activating D1 receptor
B. block Ca2+ channel
C. opening K+ channel
D. release NO
29. What is the mechanism of action of verapamil used in hypertension?
A. activating D1 receptor
B. block Ca2+ channel
C. opening K+ channel
D. release NO
30. What is the mechanism of action of nifedipine used in hypertension?
A. activating D1 receptor
B. block Ca2+ channel
C. opening K+ channel
D. release NO
31. What is the mechanism of action of labetalol used in hypertension?
A. β blocker
B. α blocker
C. D blocker
D. (α + β) blocker
32. What are the side effects of hydralazine?
A. hypotension + cyanide toxicity
B. lupus + neuropathy
C. tachyphylaxis, palpitations
D. constipation + bradycardia
E. edema + tachycardia
33. What are the side effects of nitroprusside?
A. hypotension + cyanide toxicity
B. lupus + neuropathy
C. tachyphylaxis, palpitations
D. constipation + bradycardia
E. edema + tachycardia
34. What are the side effects of verapamil?
A. hypotension + cyanide toxicity
B. lupus + neuropathy
C. tachyphylaxis, palpitations
D. constipation + bradycardia
E. edema + tachycardia
35. What are the side effects of minoxidil?
A. hypotension + cyanide toxicity
B. lupus + neuropathy
C. tachyphylaxis, palpitations
D. constipation + bradycardia
E. edema + tachycardia
36. What are the side effects of nifedipine?
A. hypotension + cyanide toxicity
B. lupus + neuropathy
C. tachyphylaxis, palpitations
D. constipation + bradycardia
E. edema + tachycardia
37. What is the effect of ACEi in reduction blood pressure?
Reduced blood volume
Reduced peripheral resistance
Reduced heart rate
Reduced cardiac contraction
Reduced blood volume and reduced peripheral resistance
Reduced heart rate and reduced cardiac contraction
Reduced peripheral resistance, reduced heart rate and reduced cardiac contraction
Reduced blood volume, reduced peripheral resistance, reduced heart rate and reduced cardiac contraction
38. What is the effect of ARB in reduction blood pressure?
Reduced blood volume
Reduced peripheral resistance
Reduced heart rate
Reduced cardiac contraction
Reduced blood volume and reduced peripheral resistance
Reduced heart rate and reduced cardiac contraction
Reduced peripheral resistance, reduced heart rate and reduced cardiac contraction
Reduced blood volume, reduced peripheral resistance, reduced heart rate and reduced cardiac contraction
39. What are the side effects of ACEi?
A. asthma + AV block + claudication
B. cough + hyperkalemia + angioedema
C. Dry mouth, postural hypotension, sedation
D. Hemolytic anemia + lupus + depression
40. What are the side effects of ARB?
A. asthma
B. cough
C. hypokalemia
D. hyperkalemia
41. What is the effect of furosemide used in heart failure?
A. Reduce afterload
B. Reduce preload
C. Reduce heart rate
D. Increase contraction
E. Prevent remodeling
42. What is the effect of β used in heart failure?
A. Reduce afterload + preload
B. Reduce heart rate + prevent remodeling
C. Increase contraction + reduce heart rate
D. Reduce afterload + preload + prevent remodeling
43. What is the effect of ACEi used in heart failure?
A. Reduce afterload + preload
B. Reduce heart rate + prevent remodeling
C. Increase contraction + reduce heart rate
D. Reduce afterload + preload + prevent remodeling
44. What is the effect of digoxin used in heart failure?
A. Reduce afterload + preload
B. Reduce heart rate + prevent remodeling
C. Increase contraction + reduce heart rate
D. Reduce afterload + preload + prevent remodeling
45. What combine drugs used in heart failure to reduce mortality?
A. ACEi + β blocker
B. ACEi + diuretics
C. β blocker + diuretics
D. digoxin + diuretics
E. nitrate + diuretics
46. Which ionic disorder increase digoxin intoxication?
Hypercalcemia
Hypocalcemia
Hyperkalemia
Hypokalemia
Hypercalcemia and hypokalemia
Hypocalcemia and hyperkalemia
47. What is the mechanism of action of digoxin?
A. activate β1 receptor
B. block Na+- K+ pump
C. increase Ca++ pump
D. increase Ca++ channel
48. Which amine is best used to treat acute left heart failure?
A. dobutamine
B. dopamine
C. epinephrine
D. norepinephrine
49. Which amine whose effects change with increased doses and acts on D1 β1 α1 receptors?
A. dobutamine
B. dopamine
C. epinephrine
D. norepinephrine
50. What is the side effect of digoxin concerning rhythm disorder?
A. Increased automaticity
B. reentry
C. Early after depolarization
D. Delayed after depolarization
51. What is the side effect of ACEi concerning hemodynamic in treating heart failure?
A. Decreased blood pressure
B. Increased blood pressure
C. No change in blood pressure
All answer
52. What is the MOA of fibrinolytic drugs
A. Direct clot dissolution
B. Anti caproic acid
C. anti-fibrin formation
D. Plasmin formation
53. What fibrinolytic drugs are specific to fibrin in thrombus?
Alteplase
Duteplase
Streptokinase
Urokinase
Alteplase and duteplase
Streptokinase and urokinase
54. What fibrinolytic drugs are non-specific?
Alteplase
Duteplase
Streptokinase
Urokinase
Alteplase and duteplase
Streptokinase and urokinase
55. What fibrinolytic drug does not need endogenous plasminogen?
Alteplase
Duteplase
Streptokinase
Antistreplase
56. Fibrinolytic drug becomes effective in how many minutes after administration?
30min
60min
90min
120min
57. Fibrinolytic drug must be administered within how many hours of MI?
3h
6h
12h
24h
58. What is the MOA of aspirin?
A. Cox Inhibitor
B. Lox Inhibitor
C. PLA Inhibitor
D. PDE Inhibitor
59. What is the MOA of clopidogrel?
A. Anti ADP R
B. anti GPiib/iiia
C. PDE I
D. Cox I
60. What is the MOA of abciximab?
A. Anti ADP R
B. anti GPiib/iiia
C. PDE I
D. Cox I
61. What is the MOA of dipyridamol?
A. Anti ADP R
B. anti GPiib/iiia
C. PDE I
D. Cox I
62. What antiplatelet gives rise to orthostatic HT as side effect?
Aspirin
Clopidogrel
Abciximab
Dipyridamol
63. What antiplatelet gives rise to bronchospasm as side effect?
Aspirin
Clopidogrel
Abciximab
Dipyridamol
64. Interaction of clopidogrel with what drug → its effect ↑ result in bleeding?
Erythromycine
Ketoconazol
Omeprazol
Rifampicine
65. Interaction of Aspirin with what drug → its effect ↑ result in bleeding?
Cidofovir
Ketorolac
Omeprazol
Probenecid
66. What is the MOA of Warfarin?
A. anti-cyclooxygenase
B. anti-oxydase
C. Anti phosphodiesterase
D. Anti reductase
67. What is the MOA of LWH?
A. anti-factor II
B. anti-factor VI
C. anti-factor VII
D. anti-factor X
68. What is the MOA of Unfractionated Heparin?
D. anti-factor X
A. anti-factor II
B. anti-factor VI
C. anti-factor VII
69. Use of warfarin in what disease?
A. Deep venous thrombosis
B. Peripheral arteritis
C. ST+
D. stroke
70. Use of warfarin in what disease?
A. ST+
B. stroke
C. Peripheral arteritis
D. Atrial fibrillation
71. Interaction of warfarin with what drugs →↑free form of warfarin = bleeding
Sulfonamide
Rifampicin
Omeprazol
Ketoconazol
72. Interaction of warfarin with what drugs →↑metabolism of warfarin = its effects ↓
Sulfonamide
Rifampicin
Omeprazol
Ketoconazol
73. What is the side effect of heparin?
Thrombocytopenia
Megaloblastic anemia
Leukemia
Teratogenic
74. MOA of Nitroglycerine?
A. activating β2 receptor → cAMP↑
B. inhibiting PDE → cAMP↑
C. releasing NO → cGMP↑
D. opening K+ channel → inactivate Ca2+ channel
75. Effect of Nitroglycerine in angina?
A. ↓preload + afterload ↓ + ↑O2 supply
B. ↓ contraction + ↓ heart rate + ↑O2 supply
C. ↓preload + afterload ↓ + ↓ heart rate
D. ↓ contraction + afterload ↓+ ↑O2 supply
76. Which drug should be avoid to combine with nitroglycerine?
ACEi
CCB
Dipyridamole
Sildenafil
77. Effect of β blocker in angina?
A. ↓preload + afterload ↓ + ↑O2 supply
B. ↓ contraction + ↓ heart rate + ↓ afterload
C. ↓preload + afterload ↓ + ↓ heart rate
D. ↓ contraction + afterload ↓+ ↑O2 supply
78. Which drug you choose to use when β blocker is overdosing?
Insulin
Glucagon
Dopamine
Ephedrine
79. Effect of CCB in angina?
A. ↓preload + afterload ↓ + ↑O2 supply
B. ↓ contraction + ↓ heart rate + ↓ afterload
C. afterload ↓ + ↓ heart rate + ↓ contraction + ↑O2 supply
D. ↓ contraction + afterload ↓+ ↑O2 supply
80. What are the side effects of verapamil?
A. AV block + constipation + flush
B. AV block + asthma + bradycardia
C. Constipation + Nausea + QT long
D. Flush + Hypotension + Tachycardia
81. What is the mechanism of action of Ranolazine?
A. Block fast inward Na+ current in phase 0 of AP?
B. Block late inward Na+ current in phase 2 of AP?
C. Block inward Ca2+ current in phase 2 of AP?
D. Block outward K+ current in phase 3 of AP?
82. Effect of Ranolazine in angina?
A. ↑ supply oxygen + ↓ oxygen demand during diastole
B. ↑ supply oxygen + ↓ oxygen demand during systole
C. ↓ preload + ↓ afterload
D. ↓ heart rate + ↓ cardiac contraction
83. What are the side effects of Ranolazine?
A. AV block + constipation + flush
B. AV block + asthma + bradycardia
C. Constipation + Nausea + QT long
D. Flush + Hypotension + Tachycardia
84. What is the mechanism of action of Ivabradine?
A. Inhibition of fast sodium channels
B. Inhibition of funny channels
C. Inhibition of late sodium channels
D. Inhibition of potassium channels
85. Concerning interaction which antibiotic should be avoid to be associated with ivabradine?
Cephalosporin
Cycosporine
Erythromycin
Gentamycin
86. What is the mechanism of β blocker as antiarrhythmic?
A. activate PDE → cAMP↓
B. block β1 receptor → cAMP↓
C. block Na-K ATPase pump
D. block L-voltage calcium channel
87. What is the effect of β blocker useful as antiarrhythmic in ischemic condition?
A. Reduced pace maker automaticity
B. increased ERP
C. Decreased conduction of impulse
D. Decreased calcium overload
88. What is the effect of β blocker useful to stop arrhythmia due to delayed after depolarization?
A. Reduced pace maker automaticity
B. increased ERP
C. Decreased conduction of impulse
D. Decreased calcium overload
89. What is the effect of β blocker used in supraventricular tachyarrhythmia?
A. Reduced pace maker automaticity
B. increased ERP
C. decreased AV conduction
D. Decreased calcium overload
90. What is the mechanism of action of antiarrhythmic Class III?
A. Block phase 0 → conduction↓
B. Block phase 1 → notch ↑
C. Block phase 2 → QT↓
D. Block phase 3 → QT↑
91. What are the main effect of class III as antiarrhythmic?
A. Reduced pace maker automaticity
B. increased Effective Refractory Period (ERP )
C. decreased AV conduction
D. Decreased calcium overload
92. Explain how class III used to treat reentry tachycardia?
A. Decreased calcium overload block after depolarization
B. Effective Refractory Period > conduction time in abnormal circuit
C. make QT short block after depolarization
D. Reduced pace maker current → slow rate of spontaneous depolarization
93. Why class III have no effect in MI tissues?
A. IKr expression↓ + hyperkalemia
B. IKr expression ↑ + hypokalemia
C. Hyperpolarization in resting membrane potential
D. Partial depolarization in resting membrane potential
94. What condition favor action of class Ib in MI?
A. IKr expression↓ + hyperkalemia
B. IKr expression ↑ + hypokalemia
C. Hyperpolarization in resting membrane potential
D. Partial depolarization in resting membrane potential
95. What are the side effects of amiodarone?
A. constipation + flush + bradycardia
B. Cardiac depression + pulmonary fibrosis + renal fibrosis
c. dysthyroidism + photodematitis + corneal microdeposits
D. Diarrhea + nausea + vomiting
96. Use of amiodarone?
A. Chronic reentry tachycardia both in atrial and ventricular
B. Tachycardia by increased automaticity
C. Tachycardia by early after depolarization
D. Tachycardia by delayed after depolarization
97. What is the mechanism of action of class IV as antiarrhythmic?
A. block L-calcium voltage channel in SA and AV node
B. block L-calcium voltage channel in phase 2 of AP
C. Block late sodium channel in phase 2 of AP
D. Block fast voltage sodium channel in phase 0 of AP
98. Use of Verapamil as antiarrhythmic?
A. Atrial fibrillation with heart failure
B. AVN reentry tachycardia
C. Torsade de pointe by prolonged QT
D. Ventricular tachycardia in myocardial infarction
99. Use of digoxin as antiarrhythmic?
A. Atrial fibrillation with heart failure
B. AVN reentry tachycardia
C. Torsade de pointe by prolonged QT
D. Ventricular tachycardia in myocardial infarction
100. Use of adenosine as antiarrhythmic?
A. Atrial fibrillation with heart failure
B. AVN reentry tachycardia
C. Torsade de pointe by prolonged QT
D. Ventricular tachycardia in myocardial infarction
101. Concerning ECG what are the effects of class Ia antiarrhythmic?
A. QRS wide + prolong QT
B. QRS normal + short QT
C. QRS very large + QT normal
D. QRS normal + QT normal
102. Concerning ECG what are the effects of class Ib antiarrhythmic?
A. QRS wide + prolong QT
B. QRS normal + short QT
C. QRS very large + QT normal
D. QRS normal + QT normal
103. Concerning ECG what are the effects of class Ic antiarrhythmic?
A. QRS wide + prolong QT
B. QRS normal + short QT
C. QRS very large + QT normal
D. QRS normal + QT normal
104. What channels class Ia antiarrhythmic blocks?
A. Na+ voltage channel + delayed K+ channel
B. Na+ voltage channel + late Na+ channel
C. Na+ channel only
D. K+ channel only
105. What channels class Ib antiarrhythmic blocks?
A. Na+ voltage channel + delayed K+ channel
B. Na+ voltage channel + late Na+ channel
C. Na+ channel only
D. K+ channel only
106. What channels class Ic antiarrhythmic blocks?
A. Na+ voltage channel + delayed K+ channel
B. Na+ voltage channel + late Na+ channel
C. Na+ channel only
D. K+ channel only
107. Ib bind to Na channel in what state?
Open > close inactive
Open > close active
Close inactive > open
Close active > open
108. Ia bind to Na channel in what state?
Open > close inactive
Open > close active
Close inactive > open
Close active > open
109. Ic bind to Na channel in what state?
Open > close inactive
Open > close active
Close inactive > open
Close active > open
110. What is the dynamic of class Ib in binding Na+ channel?
Very fast < 0,1 second
Fast < 1 second
Slow in seconds
Very slow > 10 seconds
111. What is the dynamic of class Ic in binding Na+ channel?
Very fast < 0,1 second
Fast < 1 second
Slow in seconds
Very slow > 10 seconds
112. What is the dynamic of class Ia in binding Na+ channel?
Very fast < 0,1 second
Fast < 1 second
Slow in seconds
Very slow > 10 seconds
113. What is the effect of class I used in blocking reentry?
A. Decreased calcium overload block after depolarization
B. Effective Refractory Period > conduction time in abnormal circuit
C. make QT short block after depolarization
D. Reduced pace maker current → slow rate of spontaneous depolarization
114. Use of class Ib?
A. AVN reentry tachycardia
B. Atrial reentry tachycardia
C. Ventricular reentry by ischemia
D. Atrial and Ventricular tachycardia
115. Use of class Ic?
A. AVN reentry tachycardia
B. Atrial reentry tachycardia
C. Ventricular reentry by ischemia
D. Atrial and Ventricular tachycardia
116. Use of class Ia?
A. AVN reentry tachycardia
B. Atrial reentry tachycardia
C. Ventricular reentry by ischemia
D. Atrial and Ventricular tachycardia
117. What is the side effect of class Ia as pro-arrhythmia agent?
A. Delayed after-depolarization
B. Early- after-depolarization
C. Reentry
D. Increased automaticity
118. What is the side effect of class I as pro-arrhythmia agent in ischemic tissue?
A. Delayed after-depolarization
B. Early- after-depolarization
C. Reentry
D. Increased automaticity
119. Why class Ib is not used in Atrial reentry tachycardia?
A. Long duration of action potential
B. Poor expression of Na+ voltage channels
C. Short duration of AP
D. Susceptible to ischemia
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