Pharmacology Questionnaire

August 2, 2018 | Author: Wynlor Abarca | Category: Receptor Antagonist, Agonist, Receptor (Biochemistry), Pharmaceutics, Biochemistry
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Pharmacology

1. Involves activation of second messengers such as diacylglycerol, IP 3, and cAMP A. G-protein coupled receptor B. Intracellular Receptor C. Ligand-gated ion channels receptors D. Tyrosine Kinase coupled Receptors 2. Which of the following exhibits metabolism by digestive and gastric enzymes? A. Penicillin B. Insulin C. Epinephrine 3. A parameter that measures ability of the body to eliminate the drug A. Volume of Elimination B. Clearance C. Volume of Distribution D. Excretion Rate 4. One drug opposes the effect of the other by biding at a different receptor and counteract its effect A. Chemical Antagonism B. Physiologic Antagonism C. Competitive Antagonism D. Non-Competitive Antagonism 5. Converts the parent drug to a more polar conjugate A. Phase I B. Phase II 6. Receptors for Lipid Soluble Drugs A. Intracellular Receptors B. G-protein coupled receptor C. Ligand-gated ion channels receptors D. Tyrosine Kinase Coupled Receptors 7. Synthetic Reaction A. Phase I B. Phase 2 8. Response Intensity is increased in a given dose of the drug A. Idiosyncratic Response B. Hyporeactive Response C. Hyperractive Response D. Tolerance 9. The Smooth Endoplasmic Reticulum contains high concentration of which enzymes: A. Digestive Enzymes B. Phase I Enzymes

10.

11.

12.

13.

14.

15.

16.

C. Gastric Enzymes D. Phase II Enzymes Used to determine the range of o f plasma levels that is acceptable when designing a dosing regimen A. Therapeutic Index B. Therapeutic Window C. Quantal Dose Curve D. Dose-Response Curve The antagonist binds to the agonist making it unavailable to interact with the receptor A. Chemical Antagonism B. Physiologic Antagonism C. Competitive Antagonism D. Non-Competitive Antagonism These are gene active receptors A. Intracellular Receptors B. G-protein coupled Receptors C. Ligand-gated ion channels receptors D. Tyrosine Kinase Coupled Receptors The concentration is high relative to the Km causing the rate of elimination to be almost independent of concentration A. First Order B. Steady State C. Zero Order D. Pseudo Zero Order Exemplified by the interaction between atropine, a muscarinic antagonist and metoprolol A. Chemical Antagonism B. Physiologic Antagonism C. Competitive Antagonism D. Non-competitive Antagonism Response is decreased due to prolonged exposure to drug A. Tachyphylaxis B. Hyporeactive Response C. Hyperreactive Response D. Tolerance Median Effective dose, median toxic dose, and median lethal dose are derived from this A. Graded-Dose Response Relationship B. Quantal-Dose Relationship C. Both D. Neither

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Pharmacology

A. Chemical Antagonist 17. Exemplified by the interaction between 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 D. Tyrosine Kinase Coupled Receptors 19. In the presence of this antagonist, the 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 dose of the drug 20. Unmasking of a polar group A. Phase I A. Idiosyncratic Response B. Phase II B. Hyporeactive Response C. Hyperreactive Response 21. This type of agonist produces less specific 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 C. Competitive Antagonism 22. In the presence of this antagonist, the 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 42. Margin of Safety i. Therapeutic Index = 50 ii. Therapeutic Index = 2

B. i < ii

C. i = ii 43. Solubility of Weak Acid in Lipid i. pH < 7 ii. pH > 7

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Pharmacology

44. Margin of Safety i. Therapeutic Window = 10 ii. Therapeutic Window = 150 45. Potency of Drug i. ED50 = 40 mg/kg ii. ED50 = 10 mg/kg

ii.

47. Maximal Efficacy i. Partial Agonist ii. Full Agonist 48. Dominant form of Drug at pH > pKa i. Protonated Form ii. Unprotonated Form

46. Maximal Efficacy i. Full Agonist alone

A. Phase I Reaction 49. 50. 51. 52. 53. 54. 55. 56.

Hydrolysis H2O Conjugation Hydroxylation Methylation Sulfation Reduction Epoxidation Oxidative Dealkylation

A. Additive B. Synergistic

Full Agonist + noncompetitive agonist

B. Phase II Reaction 57. 58. 59. 60. 61. 62. 63. 64.

Desulfuration Dechlorination Glutathione Conjugation Deamination Acetylation-acetyl CoA Dehydrogenation Glycine Conjugation Glucuronidation

C. Potentiation D. Antagonism

65. Ethanol + Sedative 66. Cimetidine + Anticoagulant

67. Heparin + Protamine 68. Penicillin G + Gentamicin

If there are two possible answers, write both letters. A. Transdermal B. Oral C. Sublingual 69. 70. 71. 72. 73. 74. 75. A. True

D. Topical E. Rectal

Maximize concentration at the site of act ion Prolong duration of drug absorption Provides direct access to systemic veins For convenience Avoid first-pass effect Minimize concentration outside site of action Enter vessels that drain into the inferior vena c ava B. False

76. The degree of inhibition produced by a competitive antagonist depends on the concentration of the agonist competing for binding to the receptor s. 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 i s 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 c learance. 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.

Changes in drug effects will not be delayed if the plasma concentration is changed. Blood flow is not a determinant of drug delivery. Low bioavailability is also due to incomplete absorption. The liver, although responsible for drug metabolism, may excrete the drug into the bile. For an intravenous dose, bioavailability is assumed to be equal to unity. The two major sites of drug elimination are the kidneys and the urinary bladder. Although individual differences exist in drug distribution and rates of drug met abolism 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 r ate of synthesis of enzymes. 85. 86. 87. 88. 89. 90. 91.

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 e ffects. 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 wo rds, 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 re aching the value produced by the partial agonist alone. 100.

Enzyme induction enhances the drug effect.

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