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Block 6 Week 5 > Viral chemotherapy > Flashcards

Viral chemotherapy Flashcards

1
Q 
What are these:
Poliovirus
Mumps, measles
Yellow fever
Dengue fever
Rhinovirus
Influenza
HIV
A

RNA viruses

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2
Q 
What are these:
Papilloma
Zoster
Adenovirus
Epstein-Barr
Cytomegalovirus 
Herpes simplex
A

DNA viruses

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3
Q

What are the stages of viral replication?

A
  1. adsorption, penetration and uncoating
  2. synthesis of viral components
  3. assembly and release of virus
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4
Q

What is vector control?

A

controlling mosquitos or something to control dengue and yellow fever

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5
Q

What is immunological control?

A

vaccines and gamma globulin

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6
Q

How do you control viral infections by activation of host resistance?

A

utilize interferon

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7
Q

What are the four ways to control viral infections?

A

vector control
immunizaation
activation of host resistance
drugs (selective toxicity, timing)

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8
Q

What are the 2 major fundamental problems that need ot be overcome in developing antiviral drugs?

A
  • host’s biochemical machinery is used in replication of the virus. This reduces the opportunities for selective action by drugs that block protein and nucleic acid synthesis.
  • clinical signs of viral infection occur after the virus is already replicating and the immune response has been elicited.
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9
Q

There are RNA viruses made up of influenze (balnk,blank, and blank)

A

A B and C

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10
Q

(blank) can be serotyped based on antibody responses to hemaglglutinin (HA) and neuraminidase (NA) on the outside of the viral particle.

A

Influenza A

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11
Q

What are the commonly found strains of influenza?

A

H1, 2, 3

N1 and 2

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12
Q

How many known subtypes are there in influenza?

A

16 H and 9N

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13
Q

What caused the asiatic (russian) flue?

A

H2N2

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14
Q

What caused the spanish flu?

A

H1N1

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15
Q

What caused the Asian flu?

A

H2N2

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16
Q

What caused the Hong Kong flu?

A

H3N2

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17
Q

What caused the swine flu?

A

H1N1

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18
Q

Explain influenza virus replication

A
  1. virus binds to cell surface with hemagglutinin
  2. endocytosis
  3. endosome
  4. uncoating
  5. vRNA
  6. mRNA
  7. Protein synthesis
  8. structural and non structural proteins
  9. budding
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19
Q

Where does amantadine work?

A

it inhibits uncoating

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20
Q

Where does zanamivir and oseltamivir work?

A

Release

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21
Q

How does amantadine work?

A

Binds to M2 protein of influenza A2 and Inhibits uncoating and viral assembly

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22
Q

(blank) prevent spread of influenze A2 and reduces duration of influenza symptoms.

A

amantadine

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23
Q

What are the adverse reactions of amantadine?

A

dizziness, nervousness, confusion, hallucinations, hypotension
CNS: releases dopamine, dopamine agonist

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24
Q

How should you give amantadine?

A

orally (well absorbed from GI tract)

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25
Q

Amantadine is a synthetic compound that inhibits (blank) of replication. It also acts to prevent uncoating of viral RNA.

A

Stage 1

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26
Q

When shoud you give amantadine?

A

for prophylaxis and treatment of the elderly or persons with compromised immune systems during influenza epidemics

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27
Q

What does Zanamivir and Oseltamivir do?

A

they are neuraminidase inhibitors that inhibit replication of influenza A and B

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28
Q

What does early use of zanamivir and oseltamivir do?

A

reduces severity and duration of influenza symptoms

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29
Q

What are the adverse reactions to zanamivir and oseltamivir?

A

nausea, headache, vomiting, diarrhea, abdominal pain

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30
Q

What are the purine antiviral nucleosides and nucleotide analogs?

A 
acylovir
adefovir
gancyclovir
pencyclovir
ribavirin
didanosine (DDI)
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31
Q

What are the pyrmidine nucleoside and nucleotide analogs?

A 
azidothymidine
zalcitabine, ddC
stavudine d4T
trifluridine
cidofovir
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32
Q

How does the herpesvirus replicate.

A
  1. attachment
  2. uncoating
  3. viral DNA to host cell nucleus
  4. make mRNA and replicate viral DNA
  5. proteins
  6. assembly of viron and budding
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33
Q

What does acyclovir block?

A

it blocks synthesis of viral DNA in herpesvirus

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34
Q

What does acyclovir, vidarabine, foscarnet, ganciclovir do?

A

inhibit viral DNA polymerse

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35
Q

Viral thymidine kinase converts the drug to a monophosphate. Host enzymes convert it to the triphosphate (acyclo GTP) which preferentially inhibits viral DNA polymerase. This causes chain termination. What is this?

A

acyclovir (acycloguanosine)

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36
Q

What is acyclovir effective in treating?

A

most effective drug in treating herpes simplex types 1 and 2, and varicella zoster infection

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37
Q

How should you take acyclovir?

A

parenteral and oral formulations

38
Q

What are the adverse reactions of acyclovir?

A

IV admin -nephrotoxicity, phlebitis and local irritation
topical-local irritation
oral- causes headache, diarrhea, nausea, vomiting, vertigo, arthlagia.

39
Q

How does Gancylovir work?

A

activated by HCMV phosphotransferase and inhibits DNA polymerase

40
Q

What do you use Gancylovir for?

A 
herpes simplex, varicella-zoster
very active agaist HCMV
HCMV retinitis (primary use) and pneumonia
41
Q

What are the adverse reactions of ganciclovir?

A

high incidence of bone marrow suppression (neutropenia and thrombocytopenia) and CNS effects

42
Q

What drug does this:
Phosphorylated by host enzymes. Ribavirin monophosphate inhibits inosine 5’ phosphate dehydrogenase resulting in decreased synthesis of guanine nucleotides and ultimately decreased synthesis of RNA and DNA. The triphosphate inhibits RNA polymerase.

43
Q

How does Ribavirin work?

A

phosphorylatd by host enzymes to inhibitio iosine 5 phosphate dehydrogenase which results in decreased synthesis of guanine and thus decreased synthesis of RNA and DNA AND triphosphate inhibits RNA polymerase

44
Q

What is ribavirin used on?

A

Respiratory syncytial virus, influenza

Hepatitis C, Myxovirus, paromyxovirus, adenovirus, herpes virus, poxviruses,

45
Q

If you give ribavarin in an aerosolized form, what will you be treating?

46
Q

if you are giving ribavarin orally what will you be treating?

A

influenza A and B and hep C

47
Q

Explain HIV replication

A
  1. viron binding- CD4, chemokines
  2. reverse transcriptase (RNA to DNA)
  3. Integration of viral DNA
  4. Replication of viral RNA
  5. protease
  6. Assembly of virions
  7. release
48
Q

How does Zidovudine (Azidothymidine (AZT)) work?

A

AZT is phosphrylated to triphosphate. This inhibits reverse transcriptase. (somewhat selective)

49
Q

What do you use Zidovudine (AZT) for?

A

to treat AIDS.

reduces morbidity and mortality in HIV infected patiens. Increases T4 lymphocyte count

50
Q

What are the clinical effects of Zidovudine (AZT)?

A

increases CD4 count
decreased opportunistic infections
increases survival time
combination therapy is more effective than zidovudine alone (HAART-highly active antiretroviral therapy)

51
Q

What are the adverse reactions of Zidovudine (Azidothymidine, AZT)?

A
  • Bone marrow depression leading to anemia, granulocytopenia (30-40%) or thrombocytopenia
  • headache, nausea, vomiting, myalgia
  • myopathy
52
Q

What is resistance to zidovudine (AZT) caused by?

A

Resistance is a function of stage of infection and duration of treatment

53
Q

How do dideoxynucleosides work?

A

they are prodrugs that are metabolized to triphosphates that act as competitive inhibitors of reverse transcriptase that cause chain termination (nRTI).

54
Q

What are dideoxynucleosides used for?

A

treating AZT-resistant HIV

55
Q

What are the three kinds of dideoxynucleosides?

A

ZALCITABINE (DIDEOXYCYTIDINE),
DIDANOSINE (DIDEOXY¬INOSINE),
STAVUDINE (DIDEOXY¬THYMIDINE)

56
Q

What is HAART made up of?

A

AZT, protease inhibitor and nnRTI

57
Q

What are the adverse effects of nRTI?

A

Dose-limiting toxicities include peripheral neuropathy and gastro¬intestinal distress,
Extended use has identified limiting toxicities including a rare potentially fatal lactic acidosis.

58
Q

What are the four protease inhibitors?

A

NELFINAVIR, RITONAVIR, SAQUINAVIR, INDINAVIR

59
Q

How do protease inhibitors work?

A

they inhibit an aspartate protease necessary for cleaving the gag/pol pro-protein of HIV
-blocks viral maturation

60
Q

Combinations of (blank) with (blank) reduce morbidity in AIDs significantly/ Now part of the standard “highy active antiretrovral therapy “ (HAART)

A

protease inhibitors

nucleotide analogs

61
Q

What are the adverse reactions to protease inhibitors?

A

GI distress, hepatotoxicity, a Cushing’s like syndrome, metabolic syndrome

62
Q

All PI are processed by CYPs and important (blank) can occur

A

drug interaxns

63
Q

What are the three Non-nucleoside reverse transcriptase inhibitors (nnRTIs)?

A

nevirapine
delaviridine
efavirenz

64
Q

What is nevirapine?

A

a drug used in combination with nucleoside RTIs

65
Q

what is nevirapine metabolized by and why is this important?

A

Metabolized by Cytochrome P450 – potential drug interactions

66
Q

what are the adverse reactions of nevirapine?

A

Relatively well tolerated, causes rashes (16%), fever, nausea, hepatitis

67
Q

How do nnRTIs work?

A

inhibit reverse transcriptase by binding to a different site than do the nucleside RTIs. HIV strains resistant to nRTIs remain sensitive to the nnRTIs

68
Q

What are the adverse reactions to nnRTIs?

A

rashes, stevens-johnson syndrome

69
Q

What should you not use nnRTIs with?

A

RIfampin (because they are metabolize by cytochrome p450)

70
Q

(blank) inhibits DNA polymerase and reverse transcriptase.

71
Q

What do you use foscarnet for?

A

AIDS, HCMV retinitis in AIDS patient

72
Q

(blank) prevents fusion of the HIV virus with the host cell.

A

Enfuviritide (T20)

an antiretroviral fusion inhibitor

73
Q

How exactly do antiretroviral fusion inhibitors (Enfuviritide) work?

A

mimick components of HIV fusion machinery. Binds to gp120 on CD4+ cells to prevent the creation of an entry pore for the virus

74
Q

What protects healthy CD4+ cells from HIV infection?

A

antiretroviral fusion inhibitor

75
Q

What should you use antiretroviral fusion inhibitors with?

A

other antiretrovirals

76
Q

What are common adverse reactions to antiretroviral fusion inhibitors?

A

injection site reactions, peripheral neuropathy, insomnia, depression and athralgia. Hypersensitivity can occur (.1-1.1% of patients)

77
Q

(blank) is used in treatment of kaposis sarcoma, genital warts, herpes zoster in AIDS patients and hep C.

A

interferon alpha

78
Q

(blank) block several key steps in viral replication including transcription, translation, protein processing and virus maturation

A

interferon alpha

79
Q

(blank) is a fusion inhibitor that is a peptide that binds to gp41 on the viral envelope. Administered by subcutaneous injection. Can trigger hypersensitivity reactions on injection.

A

Enfuvirtide

80
Q

(blank) is an antisense oligonucleotide against mRNA coding CMV immediate early protein 2.

A

Fomivirsen

81
Q

Where do you put fomivirsen in?

Who do you treat with this?

A

into the vitreous humor to treat CMV retinitis in AIDS patients

82
Q

What are some investigational drugs and what do they do?

A

viral entry inhibitors -> CD4 blockers, chemokine receptor antagonists
Integrase inhibitors

83
Q

T or F

HAART therapy reduces HIV infection rate

84
Q

What are the three phases of AIDs?

A

acute phase
clinical latency phase
chronic infections

85
Q

What are the common opportunistic infections in AIDS patients during the actue phase?

A 
Acute retroviral syndrome
fever
rash
lymphadenopathy
pharyngitis
86
Q

What are the common opportunistic infections in AIDS patients during the clinical latency phase?

A 
Thrush
Kaposi sarcoma
TB reactivation
Herpes zoster
Herpes simpex
bacterial sinusitis
pneumonia
pneumocystic carinii
pneumonia
87
Q

What are the common opportunistic infections in AIDS patients during the chronic infection phase?

A 
Systemic fungal infections
primary TB
crytosporiadisis
cerebral tooplasmosis
progressive mutlifocal leukencepholapthy
peripheral neurpathy
cerivcal carcinoma
cytomegalovirus disease
disseminated
mycobacterium avium complex
non-hodgkins lymphoma
CNS lymphoma
AIDS dementia complex
88
Q

Where do you get a spike in CD4 counts in AIDS?

A

12 weeks between the acute phase and clinical latency phase

89
Q

What is the CD4 count in the acute phase?

A

between 1000 and 500

90
Q

What is the CD4 count in latency period?

A

b/w 800 and 200

91
Q

What is the cd4 count in the chronic period?

A

200 to none (death)

Block 6 Week 5 (10 decks)

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