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Pharmacology-PA

Antivirals-Lecture #1

QuestionAnswer
1. T/F Herpesviridae family of DNA virus names are derived from the Greek word herpein. True
2. What does the herpein mean? ("to creep")- referring to the latent, recurring infections
3. T/F Herpesviridae family of DNA virus exhibit latent and lytic phases in the course of infection. True
4. What is Lytic activation often accompanied by? by emergence of non-specific symptoms such as low grade fever, headache, sore throat, malaise
5. What are the clinical signs of the Herpesviridae family of DNA virus? The clinical signs are rash, swollen or tender lymph nodes
6. What are the immunological findings of the Herpesviridae family of DNA virus? Immunological findings include reduced levels of natural killer cells
7. What is HHV-1? Herpes Simplex Virus-1 (HSV-1)
8. What is the Subfamily of Herpes Simplex Virus-1? a (alpha)
9. What is the primary target cell for herpes simplex virus-1? Mucoepithial
10. What is the pathophysiology of herpes simplex virus-1? Oral and/or genital herpes (predominately orofacial)
11. What is the Site of Latency of herpes simplex virus-1? Neuron
12. What is the means of spread of herpes simplex virus-1? Close Contact
13. What is HHV-2? Herpes Simplex virus-2 (HSV-2)
14. What is the subfamily of Herpes Simplex virus-2? A (alpha)
15. What is the primary target cell for Herpes Simplex virus-2? Mucoepithelial
16. What is the pathophysiology of Herpes Simplex virus-2? Oral and/or genital herpes (predominately genital)
17. What is the site of latency of Herpes Simplex virus-2? Neuron
18. What is the means of spread for Herpes Simplex virus-2? Close contact (sexually transmitted disease)
19. What is HHV-3? Varicella Zoster virus (VZV)
20. What is the subfamily of Varicella Zoster virus? a (alpha)
21. What is the primary target cell of Varicella Zoster virus? Mucoepithelial
22. What is the pathophysiology of Varicella Zoster virus? Chickenpox and shingles
23. What is the site of latency for Varicella Zoster virus? Neuron
24. What is the means of spread for Varicella Zoster virus? Respiratory and close contact
25. What is HHV-4? Epstein-Barr virus (EBV) or lymphocryptovirus
26. What is the subfamily of Epstein-Barr virus (EBV)? Y (gamma)
27. What is the primary target cell of Epstein-Barr virus (EBV)? B cells and epithelial cells
28. What is the pathophysiology of Epstein-Barr virus (EBV)? Infectious mononucleosis, Burkitt’s lymphoma, CNS lymphoma in AIDS patients, post-transplant lympoproliferative syndrome (PTLD), nasopharyngeal carcinoma, HIV-associated hairy leukoplakia
29. What is the site of latency for Epstein-Barr virus (EBV)? B cells
30. What is the means of spread for Epstein-Barr virus (EBV)? Saliva (kissing disease)
31. What is HHV-5? Cytomegalovirus (CMV)
32. What is the subfamily of Cytomegalovirus? B (beta)
33. What is the primary target cell of Cytomegalovirus? Monocyte, lymphocyte, and epithelial cells
34. What is the pathophysiology of Cytomegalovirus? Infectious mononucleosis-like syndrome, retinitis, etc
35. What is the site of latency for Cytomegalovirus? Monocyte, lymphocyte, and ???
36. What is the means of spread for Cytomegalovirus? Close contact, transfusion, tissue transplant and congenital
37. What is the HHV-6? Roseolovirus and/or Herpes lymphotropic virus
38. What is the subfamily for Roseolovirus and/or Herpes lymphotropic virus? B –beta
39. What are the primary target cells for Roseolovirus and/or Herpes lymphotropic virus? T cells and ??
40. What is the pathophysiology of Roseolovirus and/or Herpes lymphotropic virus? Sixth disease (roseola infantum or exanthema subitum)
41. What is the site for latency for Roseolovirus and/or Herpes lymphotropic virus? T cells and ???
42. What is the means of spread for Roseolovirus and/or Herpes lymphotropic virus? Respiratory and close contact?
43. What is HHV-7? Roseolovirus
44. What is the subfamily of Roseolovirus? B (beta)
45. What are the primary target cells for Roseolovirus? T cells and ???
46. What is the pathophysiology of Roseolovirus? Sixth disease (roseola infantum or exanthema subitum)
47. What is the site of latency for Roseolovirus? T cells and ???
48. What are the means of spread for Roseolovirus? Don’t know
49. What is HHV-8? Kaposi’s sarcoma-associated herpesvirus (KSHV)
50. What kind of a virus is Kaposi’s sarcoma-associated herpesvirus? A type of rhadinovirus
51. What is the subfamily of Kaposi’s sarcoma-associated herpesvirus? Y (gamma)
52. What are the primary target cells for Kaposi’s sarcoma-associated herpesvirus? Lymphocyte and other cells
53. What is the pathophysiology of Kaposi’s sarcoma-associated herpesvirus? Kaposi’s sarcoma, primary effusion lymphoma, some types of multicentric Castleman’s disease
54. What is the site of latency for Kaposi’s sarcoma-associated herpesvirus? B cell
55. What are the means of spread of Kaposi’s sarcoma-associated herpesvirus? Close contact (sexual), saliva??
56. What are the Agents for Herpes virus Infections? Antiherpetic agents
57. What do antiherpetic agents do? Antiherpetic agents exert their effects during the acute phase of viral infections, but are without effect during the latent phase
58. What are the Antiherpetic Agents? 1-Acyclovir, 2-Cidofovir, 3-Famciclovir, 4-Foscarnet, 5-Ganciclovir, 6-Penciclovir, 7-Trifluridine, 8-Vidarabine, 9-Valacyclovir
59. What does every DNA strand consists of? Nucleotides
60. What are nucleotides? Monomers that are made of 3 components: a phosphate, a sugar (deoxyribose) and a heterocyclic base (Thimine, Cytosine -pyrimidines- Adenine, Guanine - purines-)
61. What is the combination of a sugar and a heterocyclic base? Nucleoside
62. What is created when a phosphate is added to the molecule of Nucleoside? A nucleotide is created
63. What are the nucleosides/nucleotides? The nucleosides/nucleotides adenosine (A), guanosine (G), thymidine (T) and cytidine (C)
64. What is the tradename for Acyclovir? Zovirax
65. What is the MOA of Acyclovir? guanosine analog
66. In the drug Acyclovir, what happens when the triphosphate is converted? It competes with deoxyguanosine triphosphate (dGTP) for viral DNA polymerase, which inhibits the polymerase
67. In the drug Acyclovir, what is caused by the inhibition of the polymerase? The premature viral DNA chain termination
68. What is the Resistance of Acyclovir? alteration in viral DNA polymerase, CMV
69. What viruses are included in the antiviral spectrum for Acyclovir? HSV-1, HSV-2, VZV and some Epstein-Barr virus
70. T/F Does Acyclovir reduce pain/speeds healing in VZV? True
71. What does Acyclovir prevent the outbreak of? Prevents outbreak of genital herpes
72. T/F Does Acyclovir prevent the spread of genital herpes? False, it prevents the outbreak but not the spread
73. Is Acyclovir effective against CMV? No
74. What is the ADR of Acyclovir? Local irritation (topical form), Head ache (HA), nausea-vomiting-diarrhea (NVD), transient renal dysfunction (high doses)
75. What is the tradename for Vidarabine? Ara-A
76. What is the analog of Vidarabine? Analog of adenosine with the D-ribose sugar, replaced with D-arabinose.
77. What is the MOA of Vidarabine? When converted to triphosphate form, it inhibits viral DNA synthesis
78. What is the Spectrum of activity of Vidarabine (ara-A)? HSV-1, HSV-2, VZV
79. What is Vidarabine used to treat? For treatment of immunocompromised patients with HSV keratitis, HSV encephalitis and VZV infections
80. T/F Vidarabine penetrates the CNS after IV administration. True
81. What is the Vidarabine ointment for? Ointment for herpetic/vaccinial keratitis and HS keratoconjunctivitis
82. What are the ADR for Vidarabine? CNS disturbances, fluid overload
83. In what situations should you use caution when administering Vidarabine? Caution in: impaired renal or hepatic function
84. What is the tradename for Valacyclovir? Valtrex
85. What is Valacyclovir a prodrug for? Acyclovir
86. What is the drug Valacyclovir used to treat? For the treatment of acute herpes zoster(shingles) infections and treatment of suppression of genital HSV infections
87. What are the ADR of Valacyclovir? nausea, rarely CNS disturbances
88. What is the tradename for Penciclovir? Denavir
89. What is Penciclovir a derivative of? Acyclic guanosine nucleoside
90. How is Penciclovir administered? only administered topically
91. What is the MOA of Penciclovir? It undergoes monophosphorylation by viral thymidine kinase
92. Why does Penciclovir undergo monophosphorylation by viral thymidine kinase? To convert to a triphosphate form to inhibit DNA polymerase
93. How is the intracellular half life of Penciclovir compared to Acyclovir triphosphate? The intracellular half-life is 20-30 times longer than acyclovir triphosphate
94. How is Penciclovir absorbed? Negligibly absorbed from topical application
95. How is the healing and pain shortened with the administration of Penciclovir? Shortened by one half day duration
96. What is Famciclovir an analog of? Acyclic analog of deoxyguanosine
97. What is Famciclovir a prodrug of? Penciclovir
98. What is Famciclovir approved to treat? Only approved for use against herpes zoster
99. What is the ADR for Famciclovir? headache, nausea
100. What is Ganciclovir? a nucleoside analogue
101. How does Ganciclovir differ from acyclovir? It differs from acyclovir by a single carboxyl side chain.
102. T/F Taking into consideration of the difference between Ganciclovir and Acyclovir, the drug Ganciclovir approximately has 50 times more activity against CMV than Acyclovir. True
103. Why is Ganciclovir active against CMV? Because it does not require TK for phosphorylation.
104. What is Acyclovir not well phosphorylated in CMVinfected cells? Due to the absence of the gene for thymidine kinase (TK) in CMV.
105. What does Ganciclovir triphosphate act to inhibit? The viral DNA polymerase.
106. What is Ganciclovir used to treat? It is commonly used for cytomegalic retinitis in immunocompromised patients
107. How is Ganciclovir distributed in the body? Distributed throughout the body and into CSF
108. How is Ganciclovir excreted? It is excreted in the urine and may accumulate in patients with renal failure
109. What is the ADR of Ganciclovir? Severe, dose dependent neutropenia, carcinogenic, embryotoxic, and teratogenic
110. What is the trade name for Foscarnet? Foscavir
111. T/F Foscarnet is an antiviral medication. True
112. What is Foscarnet used to treat? It is used to treat herpes viruses, including CMV, HSV-1, and HSV-2
113. What is the MOA of Foscarnet? Foscarnet mimics pyrophosphate and binds the pyrophosphate binding site on viral DNA polymerases at concentrations that do not affect human DNA polymerases, which results in the termination of the chain elongation
114. T/F Because foscarnet does not require activation by thymidine kinase, it is unaffected by loss of thymidine kinase activity in viruses which mutations that produce resistance to acyclovir or ganciclovir. True
115. What is the Resistance of Foscarnet? from mutation of polymerase Structure
116. How should Foscarnet be administered? Must be injected IV, due to poor Absorption
117. What is the ADR of Foscarnet? nephrotoxicity, anemia, nausea, fever, hypocalcemia, hypomagnesemia, hypokalemia, hypophosphatemia, seizures, arrhythmias
118. T/F When administering Foscarnet, avoid the use of other nephrotoxins. True
119. What drug should you not use concomitant use Foscarnet? Pentamidine b/c it may cause hypocalcemia.
120. What is Trifluridine used to treat? For topical treatment of HSV keratoconjunctivitis
121. What is the MOA of Trifluridine? pyrimidine analog that is incorporated into DNA disrupting viral function.
122. What analog is Cidofovir? Nucleotide analog of cytosine
123. Is the phosphorylation of Cidofovir dependent on viral enzymes? No
124. What is Cidofovir approved to treat? Approved for CMV-induced retinitis in AIDS patients
125. T/F Cidofovir has prolonged dosage intervals? True
126. What is the ADR of Cidofovir? Significant kidney toxicity, neutropenia, metabolic acidosis, ocular hypotony
127. What is the CI of Cidofovir? pre-existing renal impairment, concurrent use of nephrotoxic drugs like NSAIDS
128. T/F In HSV encephalitis adult patients, the most common early symptoms are headache and fever. True
129. What are the additional symptoms of Cidofovir? Additional symptoms include intellectual impairment, aphasia, meningeal signs, seizures, and paresthesias.
130. T/F Early treatment is crucial to a good outcome, and empirical acyclovir therapy can be initiated before a definitive diagnosis is established. True
131. Of the Impact of HIV Treatment, the absence of highly active antiretroviral therapy (HAART), median progression from HIV infection to AIDS is how many years? median progression from HIV infection to AIDS is 9-10 years
132. Of the Impact of HIV Treatment, the absence of highly active antiretroviral therapy (HAART), what is the median survival time after developing AIDS? 9.2 months
133. When on the highly active antiretroviral therapy (HAART) and if the treatment has been started when the CD4 count is 350, what is the average survival time? average survival is 32 years from the time of infection
134. How effective is the HAART regimen? HAART regimens may be effective in less than fifty percent of patients.
135. Why is the HAART regimen not that effective on everyone? This is due to medication intolerance/side effects, prior ineffective antiretroviral therapy and infection with a drug-resistant strain of HIV.
136. T/F Non-adherence and non-persistence with antiretroviral therapy is still the major cause of treatment failure. True
137. What are the Agents for HIV/AIDS? 1-Dideoxynucleoside Analogs, 2-Protease Inhibitors, 3-Non-nucleoside Reverse Transcriptase Inhibitors, 4-Integrase Inhibitors
138. What are NRTIs called? “Nukes”
139. What does nucleoside and nucleotide reverse transcriptase inhibitors (NRTI) inhibit? They inhibit reverse transcription by being incorporated into the newly synthesized viral DNA and preventing its further elongation.
140. T/F In order to be incorporated into the viral DNA, NRTIs must be activated in the cell by the addition of three phosphate groups to their deoxyribose moiety, to form NRTI triphosphates. True
141. How is the phosphorylation step of Nucleoside Analog Reverse Transcriptase Inhibitors (NARTIs,NRTIs) carried out? They are carried out by cellular kinase enzymes.
142. What are the Nucleoside Analog Reverse Transcriptase Inhibitors (NARTIs,NRTIs) Agents? 1-Zidovudine (AZT), 2-Lamivudine (3TC), 3-Stavudine (d4T), 4-Zalcitabine (ddC), 5-Didanosine (ddI), 6-Abacav
143. What are the nucleosides/nucleotides? adenosine, guanosine, thymidine and cytidine.
144. What is the MOA for Zidovudine? thymidine analog converted to nucleoside triphosphate by thymidine kinase and is incorporated into viral DNA
145. What is the Spectrum of Zidovudine? HIV
146. What is the resistance for Zidovudine? Effectiveness ↓ w/ time due to mutations in viral reverse transcriptase
147. What is the tradename for Zidovudine? AZT and/or Retrovir
148. What is the ADR for Zidovudine? bone marrow toxicity (severe anemia, leukopenia), headaches and seizures
149. T/F In the drug interactions of Zidovudine, the probenecid inhibits glucuronidation, which prolongs zidovudine activity through competition for glucuronidation enzymes. True
150. T/F Since both Zidovudine and acetaminophen are metabolized by hepatic conjugation, competition for conjugating enzymes may result in reduced elimination of either or both agents with a potential for increased toxicity. True
151. How are Zidovudine and Acetaminophen metabolized? By hepatic Conjugation
152. Of what drug does Zidovudine increased the plasma clearance? benzodiazepine.
Created by: sap_213
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