Pharmacology-PA Word Scramble

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Question	Answer
1. What is the trade name for Lamivudine?	3TC
2. T/F The molecular compound of Lamivudine is?	2',3'-dideoxy-3'-thiacytidine
3. T/F The brand names for Lamivudine are Zeffix, Heptovir, Epivir, and Epivir-HBV.	True
4. What is the MOA of Lamivudine?	terminates synthesis of proviral DNA and inhibits reverse transcriptase of HIV and HBV
5. What is Lamivudine used to treat?	Used for treatment of chronic hepatitis B at a lower dose than for treatment of HIV.
6. T/F Unlike AZT, Lamivudine does not produce bone marrow suppression.	True
7. T/F Combination of zidovudine with lamivudine slows development of zidovudine resistance.	True
8. T/F Long term use of lamivudine unfortunately leads to emergence of a resistant hepatitis B virus (YMDD) mutant.	True
9. What are the drug interactions of Lamivudine?	concurrent administration with TMP/SMX increases bioavailability of lamivudine
10. What are the ADR of Lamivudine?	Pancreatitis
11. T/F Every DNA strand is consisted a nucleotides.	True
12. T/F Nucleotides are monomers that are made of a phosphate, a sugar (deoxyribose) and a heterocyclic base (Thimine, Cytosine -pyrimidines- Adenine, Guanine - purines-).	True
13. T/F The combination of a sugar and an heterocyclic base is a nucleoside. When a phosphate is added to the molecule, a nucleotide is created.	True
14. What is the trade name of Stavudine?	d4T
15. T/F The molecular compound of Stavudine is?	2'-3'-didehydro-2'-3'-dideoxythymidine
16. What is the MOA of Stavudine?	analog of thymidine that converts to triphosphate form
17. T/F When administering Stavudine, the Intracellular phosphorylation inhibited by AZT prevents co-administration.	True
18. What does Stavudine inhibit?	Inhibits reverse transcriptase and DNA polymerase
19. T/F Stavudine Penetrates the blood-brain barrier.	True
20. What is the ADR of Stavudine?	peripheral neuropathy, renal toxicity
21. What should be taken with caution with the drug Stavudine?	patients with renal impairment
22. What is the trade name for Zalcitabine?	ddC, Hivid
23. T/F The molecular compound of Zalcitabine is?	2'-3'-dideoxycytidine, ddC and is also called dideoxycytidine. True
24. What is Zalcitabine?	It is a nucleoside analog reverse transcriptase inhibitor (NARTI)
25. T/F Zalcitabine is sold under the trade name Hivid.	True
26. What is the MOA of Zalcitabine?	analog of deoxycytidine converted to triphosphate form which incorporates into viral DNA and inhibits reverse transcriptase
27. T/F In Zalcitabine, competitive inhibitor of dCTP is for the active site of viral reverse transcriptase.	True
28. What does Zalcitabine inhibit?	Inhibits viral and cellular DNA synthesis.
29. How potent is Zalcitabine?	approximately 10 times more potent than zidovudine against HIV
30. What drug decreases the absorption due to Food or antacids?	Zalcitabine
31. What is ADR of Zalcitabine?	rash, stomatitis, peripheral neuropathy, Pancreatitis
32. What does Zalcitabine cause?	causes pancreatitis, rarely fatal
33. T/F Patients who have pancreatitis or a history of pancreatitis, or are at risk for pancreatitis, either should not take zalcitabine or should take it with extreme caution.	True
34. T/F When administering Zalcitabine, what should be monitored?	Serum amylase levels
35. What is the normal range of serum amylase level?	The normal range is 23 to 85 U/L
36. T/F Patients with moderate to severe peripheral neuropathy should not take zalcitabine.	True
37. T/F Patients with renal impairment may be at increased risk of toxicity due to decreased clearance of Zalcitabine through the kidneys.	True
38. What is the tradename for Didanosine?	ddI, Videx, Videx EC
39. T/F The molecular compound of Didanosine is 2',3'-dideoxyinosine.	True
40. What is the MOA Didanosine?	incorporates into the DNA chain, causing termination of chain elongation and inhibits RT.
41. When taking Zalcitabine, what is it not recommended for?	Not recommended for initial treatment of HIV, best for AZT-resistant HIV
42. T/F Didanosine are Acid labile (available in chewable tablets or solution) all oral formulations contained or are compounded with buffering agents to increase the gastric pH.	True
43. How are the chewable tablets of Didanosine?	The chewable tablets were large, fragile, and foul-tasting
44. What does the buffering compound of Didanosine cause?	Buffering compound would cause diarrhea.
45. T/F New Videx EC (trade name for Didanosine) formulations uses smaller capsule containing coated microspheres instead of using a buffering compound.	True
46. T/F Didanosine is approved by the FDA for once-a-day dosing.	True
47. T/F Didanosine were the first generic anti-HIV drug marketed in the United States.	True
48. T/F Food substantially reduces didanosine bioavailability, when administered on an empty stomach.	True
49. What is the half-life of Didanosine in the plasma and in intracellular environment?	The half-life in plasma is only 1.5 hours, but 12 hours in the intracellular environment.
50. How is Didanosine eliminated?	Elimination is predominantly renal
51. What is the ADR for Didanosine?	pancreatitis, peripheral neuropathy
52. When administering Didanosine, what drug does it interfere?	May interfere with absorption of other drugs (ketoconazole)
53. What is the trade name for Tenofovir?	Viread
54. T/F Tenofovir is also available in a fixed-dose combination with emtricitabine in a product with the brand name Truvada for once-a-day dosing.	True
55. T/F Emtricitabine, which is marketed in combination with Tenofovir that makes Truvada, is also marketed as a single compound product called Emtriva, also by Gilead.	True
56. What can Tenofovir cause?	Acute renal failure, fanconi syndrome, proteinuria, and tubular necrosis.
57. What does Tenofovir increase?	It increases didanosine and Atazanavir concentration protease inhibitors
58. What does Protease inhibitors (PIs) target?	Protease inhibitors (PIs) target viral assembly by inhibiting the activity of the HIV-1 protease.
59. T/F HIV protease cleaves nascent polypeptides into mature proteins for final assembly of new virons.	True
60. In Protease Inhibitors, target HIV-1 protease is essential for?	Target HIV-1 protease is essential for the final step of viral replication
61. T/F HIV protease cleaves nascent proteins for final assembly of new virons.	True
62. What are the Protease Inhibitor Agents?	1-Saquinavir, 2-Ritonavir, 3-Nelfinavir, 4-Amprenavir, 5-Indinavir
63. What is the MOA of Protease Inhibitors?	Reversibly inhibit the proteinase that is essential for the final step of viral proliferation HIV Protease in the fully open conformation, about to bind a protease inhibitor
64. What is the trade name for Saquinavir?	Invirase, Fortovase
65. T/F Invirase is a poorly-absorbed hard gel capsule which quickly led to viral resistance in many of the pioneer patients.	True
66. T/F Fortovase was a soft gel capsule reformulated for improved bioavailability, which now superseded by Invirase + ritonavir.	True
67. How is Sasquinavir administered?	Oral administration with high fat meals to maximize absorption
68. T/F Oral bioavailability of Saquinavir in both formulations significantly increases when patients also receive ritonavir.	True
69. T/F Ritonavir inhibits the cytochrome P450 3A4 enzyme.	True
70. T/F When Saquinavir is administered with co-administration delavirdine (an NNRTI), the plasma levels increase.	True
71. What are the ADR of Saquinavir?	headache, fatigue, nausea, diarrhea, loose stools, abdominal discomfort, increased LFT’s
72. What is the tradename for Indinavir?	Crixivan
73. T/F Indinavir is well-absorbed orally, and is the least protein bound of all of the protease inhibitors.	True
74. T/F Indinavir requires precise dosing every 8 hours.	True
75. T/F Indinavir is being replaced by newer drugs that are more convenient and less likely to promote resistant virus, such as lopinavir or atazanavir.	True
76. T/F When administering Indinavir, acidic gastric conditions are necessary for absorption.	True
77. What are the ADR for Indinavir?	nausea, vomiting, headache, diarrhea, fatigue, nephrolithiasis, hyperlipidemia, hyperbilirubinemia, lipodystrophy
78. What is the tradename for Ritonavir?	Norvir
79. T/F Ritonavir is no longer utilized as a single PI agent due to excessive side effects.	True
80. T/F Ritonavir is now frequently used to “boost” plasma concentrations of other Protease Inhibitors, which reduced dosages and frequencies.	True
81. T/F Ritonavir’s bioavailability is unaffected by food, but is unpalatable.	True
82. T/F Ritonavir is an inhibitor of cytochrome P450 3A4 enzymes.	True
83. What are the ADR of Ritonavir?	nausea, vomiting, diarrhea, asthenia, headache, circumoral paresthesia, elevated aminotransferase and triglyceride levels, taste alteration
84. T/F One of Ritonavir's side effects is hyperglycemia.	True
85. T/F It appears that Ritonavir directly inhibits the GLUT4 insulin regulated transporter, keeping glucose from entering fat and muscle cells.	True
86. T/F Nelfinavir in combination with lamivudine and zidovudine, decreases viral load by at least 100-fold and increases CD4+ counts.	True
87. T/F Nelfinavir may be administered with food.	True
88. What is the ADR of Nelfinavir?	diarrhea, nausea, flatulence, rash
89. What is the prodrug of Fosamprenavir?	It is a Prodrug for amprenavir
90. T/F Fosamprenavir slows conversion to amprenavir, which leads to long plasma half-life & permits twice daily dosing (reduced # pills).	True
91. T/F Fosamprenavir offers no clinical advantage over other protease inhibitors.	True
92. What is the ADR of Fosamprenavir?	nausea, diarrhea, vomiting, oral and perioral paresthesia, rash
93. What are other potential users of Protease inhibitors?	Protease inhibitors can be used as anti-protozoals (against malaria and Giardia) and as anti-cancer Agents.
94. T/F NNRTIs are “Non-nukes”.	True
95. What does the Non-nucleoside reverse transcriptase inhibitors (nNRTI) inhibit?	They inhibit reverse transcriptase directly by binding to the enzyme and interfering with its function.
96. T/F Non-Nucleoside Reverse Transcriptase Inhibitors (nNRTI) are highly selective, non-competitive inhibitors of HIV-1 reverse transcriptase.	True
97. T/F Non-Nucleoside Reverse Transcriptase Inhibitors (nNRTI) has no effect on 1-nucleoside triphosphatesm or 2-human DNA polymerases.	True
98. What are the major advantages of nNRTI having no effect of the nucleoside triphosphatesm or human DNA polymerases?	Major advantages are the there is a lack of cross-resistance with nucleoside reverse transcriptase inhibitors and there is a lack of effect on the host blood cell precursors
99. What are the Non-Nucleoside Reverse Transcriptase Inhibitors (nNRTI) Agents?	1-Atevirdine, 2-Bishetero.arylpiperazine*, 2-Delavirdine, 3-Nevirapine, 4-Efavirenz
100. What is the trade name for Nevirapine?	NVP, Viramune
101. T/F Nevirapine was more effective than placebo in raising CD4 counts and reducing viral load in patients who have had previous antiretroviral therapy.	True
102. T/F Nevirapine is very lipophilic, therefore widely distributed.	True
103. What is the ADR of Nevirapine?	rash, fever, headache, elevated serum transaminases, hepatotoxicity
104. T/F When Nevirapine is administered with NRTIs, no dosage adjustment is necessary.	True
105. T/F Nevirapine increases the metabolism of protease inhibitors, which adjusts dosages.	True
106. Nevirapine increases the metabolism of what drugs?	Increases metabolism of oral contraceptives, ketoconazole, metronidazole, warfarin, quinidine, theophylline
107. T/F Delavirdine has efficacy that is lower than other NNRTIs, especially efavirenz, and has an inconvenient schedule, which is why it is omitted from initial therapy.	True
108. T/F The addition of Delavirdine to NRTIs is more effective than NRTIs alone and is considered in salvage therapy.	True
109. T/F Delavirdine is extensively plasma protein bound, and the absorption is not affected by the presence of food.	True
110. T/F The complex set of drug interactions make the place of Delavirdine in second-line and salvage therapy is unclear, that is why it’s rarely used.	True
111. T/F Like Ritonavir, Delavirdine inhibits cytochrome P450 3A4 also.	True
112. What is the ADR of Delavirdine?	rash, nausea, dizziness, Headache
113. T/F Delavirdine is an inhibitor of drug metabolism.	True
114. What drugs increases delavirdine plasma levels?	Fluoxetine and ketoconazole
115. What drugs decrease plasma levels of delavirdine?	Phenytoin, phenobarbital and carbamazepine
116. What is the trade name of Efavirenz?	Sustiva
117. T/F Efavirenz is indicated for initial therapy of HIV-1.	True
118. How is the dosing for Efavirenz?	Once a day dosing
119. T/F Department of HHS Panel on Antiretroviral Guidelines currently recommends Efavirenz in combination with lamivudine/zidovudine (Combivir) or tenofovir/emtricitabine (Truvada) in adults and adolescents.	True
120. What is lamivudine/zidovudine called?	Combivir
121. What is tenofovir/emtricitabine called?	Truvada
122. T/F the treatment of Efavirenz in combination with Combivir or Truvada, results in the increase in CD4 cell count and decreases the viral load.	True
123. T/F Efavirenz is well distributed, including CNS and with a half-life over 40 hours.	True
124. What is the ADR of Efavirenz?	dizziness, headache, loss of concentration, vivid dreams, rash
125. Efavirenz is an inducer of?	Inducer of cytochrome P-450
126. T/F Two NRTIs plus a PI can be an Initial Therapy.	True
127. T/F Two NRTIs plus a NNRTI can be an Initial Therapy.	True
T/F Two NRTIs plus a PI and NNRTI can be an Initial Therapy.	True
128. T/F Two NRTIs and two PIs can be an Initial Therapy.	True
129. T/F Three NRTIs (less potent alternative) can be an Initial Therapy.	True
130. T/F Efavirenz + zidovudine + lamivudine is one of the preferred initial regimens.	True
131. T/F Efavirenz + tenofovir + emtricitabine is one of the preferred initial regimens.	True
132. T/F Lopinavir boosted with ritonavir + zidovudine + lamivudine is one of the preferred initial regimens.	True
133. T/F Lopinavir boosted with ritonavir + tenofovir + emtricitabine. is one of the preferred initial regimens.	True
134. T/F Part of the monitoring therapy, Plasma HIV RNA is monitored for load reduction below detectable levels.	True
135. T/F CD4 cell counts are done to assess immune status of patient.	True
136. T/F Initially, monitoring performed every 4 weeks for immune status of patients.	True
137. How long does the undetectable HIV RNA need to be monitored?	Every 3 Months
138. T/F One of the results of treatment failure is when less than a 10 fold reduction of viral load is after 4-6 weeks.	True
139. T/F One of the results of treatment failure is when there is failure to reach undetectable viral load after 4-6 months of treatment.	True
140. T/F One of the results of treatment failure is when there is detection of virus after initial complete suppression of viral load (resistance).	True
141. T/F One of the results of treatment failure is when there is persistent decline of CD4 cells or clinical Deterioration.	True
142. What does Fusion Inhibitors interfere with?	Fusion Inhibitors interfere with the interactions that enable membrane fusion between the virus, or an HIV-infected cell and an uninfected cell, reducing replication (AMD-3100, FP-21399)
143. What do the Immune stimulators do?	It uses the body’s chemical messengers to stimulate an immune response (Interleukin 2, HIV-1 Immunogen, Reticulose)
144. What does the Fusion/attachment inhibitors Entry inhibitors (or fusion inhibitors) interfere with?	It interferes with binding, fusion and entry of HIV-1 to the host cell by blocking one of several targets.
145. What are the two currently available agents in the class of Fusion?	Maraviroc and enfuvirtide
146. What do Integrase Inhibitors inhibit?	They inhibit HIV integrase enzyme, which is a key step in the reproduction cycle of HIV (Zintevir)
147. What are the other Integrase Inhibitors?	Thalidomide, Hydroxyurea, Interferon
148. T/F Integrase inhibitors inhibit the enzyme integrase, which is responsible for integration of viral DNA into the DNA of the infected cell.	True
149. T/F There are several integrase inhibitors currently under clinical trial, and Raltegravir became the first to receive FDA approval in October 2007.	True
150. What is the first drug to target the CCR5 coreceptor on the surface of the cell?	Maraviroc
151. What is the first drug in the integrase inhibitor class?	Raltegravir
152. T/F Etravirine is a second-generation nonnucleoside reverse transcriptase inhibitor (NNRTI) "with clear activity against some NNRTI-resistant viruses."	True
153. T/F There are 6 things to consider when choosing the Choice of drug.	True
154. T/F One of the considerations of DOC is that there are now approx 20 approved anti-HIV drugs and more in development (see page 16 of the i-Base guide).	True
155. T/F One of the considerations of DOC is that some are more potent than others.	True
156. T/F One of the considerations of DOC is that a few cannot be used together (ex: d4T and AZT).	True
157. T/F One of the considerations of DOC is that recent studies and guidelines recommend using: 2 NRTIs + 1 NNRTI or 2 NRTIs + 1 PI-based on combination as being most effective: 1-[AZT / 3TC / efavirenz] or 2-[AZT / 3TC / lopinavir/r (Kaletra)]	True
158. T/F One of the considerations of DOC is that there are other combinations that are better for some people.	True
159. T/F One of the considerations of DOC is that every drug has different advantages and disadvantages, and newer drugs are being used as first line therapy.	True
160. T/F Regarding Inhibiting mother-child transmission, the WHO guidelines state that pregnant women should start Zidovudine (AZT) from 28 weeks or as soon as possible from that point.	True
161. T/F Regarding Inhibiting mother-child transmission, the mother should receive single-dose Nevirapine (NVP) when entering labor.	True
162. T/F Regarding Inhibiting mother-child transmission, the mother should receive AZT+3TC for one week following delivery.	True
163. T/F Regarding Inhibiting mother-child transmission, the child should be given single dose Nevirapine immediately after delivery and daily Zidovudine until one week old.	True
164. T/F Regarding Mother-child Transmission, Complementary measures include caesarian section and formula feeding.	True
165. T/F Regarding Mother-child Transmission, in some settings, the interventions have succeeded in reducing the risk of infection from 25% to about 1%.	True
166. T/F In HIV Treatment, the treatment with less than 3 drugs or missing doses (even one dose a week) will lead to resistance, and the combination will fail.	True
167. T/F In HIV Treatment, Once resistance develops it never reverses.	True
168. T/F In HIV Treatment, Resistance to one drug or drug combination is associated with increased likelihood of resistance to the next combination (cross-resistance) between most drugs in each class.	True
169. T/F During HIV replication, error-prone Reverse Transcriptase produces frequent mutations.	True
170. T/F Most of the mutations are insignificant, but some will produce resistance to specific drugs.	True
171. What is the main cause of resistance?	poor adherence

Created by: sap_213

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