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Pharmacology

1. Involves activation of second messengers C. Gastric Enzymes


such as diacylglycerol, IP3, and cAMP D. Phase II Enzymes
A. G-protein coupled receptor 10. Used to determine the range of plasma
B. Intracellular Receptor levels that is acceptable when designing a
C. Ligand-gated ion channels receptors dosing regimen
D. Tyrosine Kinase coupled Receptors A. Therapeutic Index
2. Which of the following exhibits B. Therapeutic Window
metabolism by digestive and gastric C. Quantal Dose Curve
enzymes? D. Dose-Response Curve
A. Penicillin 11. The antagonist binds to the agonist making
B. Insulin it unavailable to interact with the receptor
C. Epinephrine A. Chemical Antagonism
3. A parameter that measures ability of the B. Physiologic Antagonism
body to eliminate the drug C. Competitive Antagonism
A. Volume of Elimination D. Non-Competitive Antagonism
B. Clearance 12. These are gene active receptors
C. Volume of Distribution A. Intracellular Receptors
D. Excretion Rate B. G-protein coupled Receptors
4. One drug opposes the effect of the other C. Ligand-gated ion channels receptors
by biding at a different receptor and D. Tyrosine Kinase Coupled Receptors
counteract its effect 13. The concentration is high relative to the
A. Chemical Antagonism Km causing the rate of elimination to be
B. Physiologic Antagonism almost independent of concentration
C. Competitive Antagonism A. First Order
D. Non-Competitive Antagonism B. Steady State
5. Converts the parent drug to a more polar C. Zero Order
conjugate D. Pseudo Zero Order
A. Phase I 14. Exemplified by the interaction between
B. Phase II atropine, a muscarinic antagonist and
6. Receptors for Lipid Soluble Drugs metoprolol
A. Intracellular Receptors A. Chemical Antagonism
B. G-protein coupled receptor B. Physiologic Antagonism
C. Ligand-gated ion channels receptors C. Competitive Antagonism
D. Tyrosine Kinase Coupled Receptors D. Non-competitive Antagonism
7. Synthetic Reaction 15. Response is decreased due to prolonged
A. Phase I exposure to drug
B. Phase 2 A. Tachyphylaxis
8. Response Intensity is increased in a given B. Hyporeactive Response
dose of the drug C. Hyperreactive Response
A. Idiosyncratic Response D. Tolerance
B. Hyporeactive Response 16. Median Effective dose, median toxic dose,
C. Hyperractive Response and median lethal dose are derived from
D. Tolerance this
9. The Smooth Endoplasmic Reticulum A. Graded-Dose Response Relationship
contains high concentration of which B. Quantal-Dose Relationship
enzymes: C. Both
A. Digestive Enzymes D. Neither
B. Phase I Enzymes

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Pharmacology

17. Exemplified by the interaction between A. Chemical Antagonist


epinephrine and propranolol, a beta B. Physiologic Antagonist
blocker C. Competitive Antagonist
A. Chemical Antagonism D. Non-competitive Antagonist
B. Physiologic Antagonism 23. Non-synthetic Reaction
C. Competitive Antagonism A. Phase I
D. Non-Competitive Antagonism B. Phase 2
18. Rate of Elimination wherein clearance is 24. The largest receptor family and are also
constant called seven-transmembrane or serpentine
A. First-order receptors
B. Steady State A. Intracellular receptor
C. Zero-Order B. G-protein coupled receptors
D. Pseudo-Zero Order C. Ligand-gated ion channels receptors
19. In the presence of this antagonist, the D. Tyrosine Kinase Coupled Receptors
dose-response curve of the agonist is 25. Rate of drug administration is equal to rate
shifted to the right but the maximal of elimination
efficacy remains the same A. First Order
A. Chemical Antagonist B. Steady State
B. Physiologic Antagonist C. Zero Order
C. Competitive Antagonist D. Pseudo Zero Order
D. Non-Competitive Antagonist 26. Response intensity is diminished in a given
20. Unmasking of a polar group dose of the drug
A. Phase I A. Idiosyncratic Response
B. Phase II B. Hyporeactive Response
21. This type of agonist produces less specific C. Hyperreactive Response
effects and is less easy to control D. Tolerance
A. Chemical Antagonist 27. Exemplified by the interaction between
B. Physiologic Antagonist heparin and protamine sulfate.
C. Competitive Antagonist A. Chemical Antagonism
D. Non-Competitive Antagonist B. Physiologic Antagonism
22. In the presence of this antagonist, the C. Competitive Antagonism
potency and maximal efficacy of the D. Non-competitive Antagonism
agonist is reduced no matter how much
the dose of the agonist is increased.
A. Inverse Relation B. Direct Relation C. No Relation
28. Therapeutic Window and Drug Efficacy 35. Accumulation and Fraction Dose Lost
29. Kd and Drug Safety 36. Therapeutic Index and Drug Efficacy
30. Volume of Distribution and Half Life 37. Rate of Elimination and Concentration
31. LD50 and Drug Safety 38. KD and Drug Affinity for the Receptors
32. ED50 and Potency 39. Clearance and Half-Life
33. Therapeutic Window and Drug Safety 40. LD50 and Drug Affinity for the Receptors
34. TD50 and Clinical Efficacy 41. Therapeutic Index and Drug Safety

A. i > ii B. i < ii C. i = ii
42. Margin of Safety 43. Solubility of Weak Acid in Lipid
i. Therapeutic Index = 50 i. pH < 7
ii. Therapeutic Index = 2 ii. pH > 7

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Pharmacology

44. Margin of Safety ii. Full Agonist + noncompetitive


i. Therapeutic Window = 10 agonist
ii. Therapeutic Window = 150 47. Maximal Efficacy
45. Potency of Drug i. Partial Agonist
i. ED50 = 40 mg/kg ii. Full Agonist
ii. ED50 = 10 mg/kg
48. Dominant form of Drug at pH >
pKa
46. Maximal Efficacy
i. Protonated Form
i. Full Agonist alone
ii. Unprotonated Form

A. Phase I Reaction B. Phase II Reaction


49. Hydrolysis 57. Desulfuration
50. H2O Conjugation 58. Dechlorination
51. Hydroxylation 59. Glutathione Conjugation
52. Methylation 60. Deamination
53. Sulfation 61. Acetylation-acetyl CoA
54. Reduction 62. Dehydrogenation
55. Epoxidation 63. Glycine Conjugation
56. Oxidative Dealkylation 64. Glucuronidation

A. Additive C. Potentiation
B. Synergistic D. Antagonism
65. Ethanol + Sedative 67. Heparin + Protamine
66. Cimetidine + Anticoagulant 68. Penicillin G + Gentamicin

If there are two possible answers, write both letters.


A. Transdermal D. Topical
B. Oral E. Rectal
C. Sublingual
69. Maximize concentration at the site of action
70. Prolong duration of drug absorption
71. Provides direct access to systemic veins
72. For convenience
73. Avoid first-pass effect
74. Minimize concentration outside site of action
75. Enter vessels that drain into the inferior vena cava

A. True B. False
76. The degree of inhibition produced by a competitive antagonist depends on the concentration
of the agonist competing for binding to the receptors.
77. Inert binding sites are completely not significant.
78. When CP450 is inhibited, metabolism of drug is diminished causing an increased effect
produced.

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Pharmacology
79. A weak acid is in its lipid soluble form when it is protonated, that is at pH greater than 7
80. The cross-sectional area of the diffusion path is directly proportional to the flux of drug
molecules
81. The steady-state concentration achieved by continuous infusion or the average concentration
following intermittent dosing depends only on clearance.
82. Systemic clearance is affected by bioavailability.
83. Clearance can affect the extent of availability because it determines the extraction ratio.
84. The difference in toxicity is a predictable consequence of the different patterns of
concentration and the saturable clearance mechanism.
85. Changes in drug effects will not be delayed if the plasma concentration is changed.
86. Blood flow is not a determinant of drug delivery.
87. Low bioavailability is also due to incomplete absorption.
88. The liver, although responsible for drug metabolism, may excrete the drug into the bile.
89. For an intravenous dose, bioavailability is assumed to be equal to unity.
90. The two major sites of drug elimination are the kidneys and the urinary bladder.
91. Although individual differences exist in drug distribution and rates of drug metabolism and
elimination, the dose and frequency of administration required to achieve effective therapeutic
blood and tissue levels remain the same.
92. Sex-dependent variations in drug metabolism exists.
93. Enzyme induction, a determinant of biotransformation rate, increases the rate of synthesis of
enzymes.
94. Diet and environmental factors affect biotransformation rate such as a charcoal inhibiting the
effects of drugs.
95. Ketoconazole is an example of enzyme inhibitor that may reduce drug effects.
96. Drugs with very high volumes of distribution means that they have much higher concentrations
in extravascular tissue than in the vascular compartment, in other words, are heterogeneously
distributed.
97. Adverse reactions include intolerance and idiosyncrasy but not allergy.
98. Ketamine is an example of drug which has more potent S or (-) enantiomer.
99. The total response when a full agonist is with a partial agonist gradually decreases reaching the
value produced by the partial agonist alone.
100. Enzyme induction enhances the drug effect.

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