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Pathophys/Pharm > Antiviral Drugs > Flashcards

Antiviral Drugs Flashcards

1
Q

What patient populations are of the highest risk of fatality due to viral infections?

A

Immune compromised and age (neonate and elderly)

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2
Q

What do viruses require for replication?

A

A living host cell

*they are obligate intracellular parasites

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3
Q

T/F viruses are highly antigenic due to envelope and capsid proteins

A

True

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4
Q

What part of viruses do antiviral drugs target?

A

Nucleic acids, enzymes and capsid proteins

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5
Q

What is the cycle of an active viral infection?

A
  1. Virus attaches to host cell (usually a specific cell)
  2. Viral genetic material enters that cell
  3. Viral DNA or RNA takes control of the cell
  4. Uses hosts cell to synthesize viral proteins and nucleic acids
  5. New viruses are assembled in cytoplasm of cell
  6. Viruses released by lysis of host cell or by budding from host cell membrane
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6
Q

What parts of the active virus cycle can antiviral drugs target?

A
  • Attachment and entry
  • RNA/DNA synthesis
  • DNA incorporation
  • Protein synthesis
  • Release
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7
Q

What is the structure of herpesviridae viruses?

A

Double stranded DNA virus

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8
Q

Is there a vaccine for herpesviridae viruses?

A

No, only antiviral medications

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9
Q

Where do herpesviridae viruses stay dormant?

A

Lymphatic or sensory nervous system

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10
Q

What is the difference between a canker sore and a cold sore?

A
  • Canker sores are NON-infectious, NON-contagious, singular lesions on the inner mucosa. TX is pain control
  • Cold sores are infectious, highly contagious, dormant, multiple lesions on the inner and out mucosa. TX is antiviral drugs and pain control
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11
Q

What causes a cold sore?

A

HSV (herpes simplex virus)

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12
Q

What causes a canker sore?

A

Triggers (citrus, stress, etc)

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13
Q

What is a specific treatment for a cold sore and what is its MOA?

A

Docosanol (abreva)
-Blocks viral attachment - inhibits viral entry into the host cell by interfering with fusion of the envelope with the cell membrane

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14
Q

What are three HSV antiviral drugs?

A
  1. Acyclovir (and valcyclovir)
  2. Famciclorvir
  3. Penciclovir
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15
Q

What is the MOA of acyclovir?

A
  • False guanosine metabolite
  • Inhibits viral DNA synthesis (false base)
  • It binds to DNA to form an irreversible complex with Viral DNA Polymerase
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16
Q

What forms does acyclovir come in?

A

PO, IV and topical

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17
Q

What type of drug is acyclovir?

A

Prodrug (must be metabolized to its active state)

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18
Q

What are some uses of acyclovir?

A

Genital herpes, herpes encephalitis, varicella, zoster

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19
Q

What is the bioavailability of acyclovir?

A

<30% oral bioavailability

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20
Q

How can we increase the bioavailability of acyclovir?

A

Valcyclovir - prodrug that gets converted to acyclovir

  • the valine increases the oral bioavailability
  • PO only
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21
Q

What is the MOA of famciclovir?

A
  • DNA Synthesis inhibitor (false guanosine metabolite)
  • Blocks DNA synthesis by being a competitive inhibitor of viral DNA polymerase
  • PO only
22
Q

What is penciclovir used for?

A

*Topical ONLY - used for small outbreaks typically around the mouth (NOT for genitals)

23
Q

What are the vaccines for varicella and herpes zoster?

A

Varicella - child get this vaccine

Herpes Zoster - adults get this vaccine after 50 y/o

24
Q

What is the active chicken pox vaccine?

A

Varivax

-Live, attenuated virus (can get sick from this)

25
Q

Who should not get the live, attenuated varicella vaccine?

A
  • Immune suppressed

- Pregnant

26
Q

What is the active shingles vaccine?

A

Shingrix

  • Enveloped glycoprotein E
  • Recombinant
27
Q

Can you get sick from the shingles vaccine?

A

NO, because it only has the viral protein

28
Q

What is the passive shingles vaccine?

A

Vzig

  • Antibody
  • Highly concentrated IgG
29
Q

Who should get the passive shingles vaccine?

A

Immune compromised

30
Q

What are the 8 common respiratory viruses

A
  • Adenovirus (only DNA one) - common cold
  • Influenza A - influenza
  • Influenza B - influenza
  • RSV - bronchiolitis
  • Coronavirus - common cold
  • Rhinovirus - common cold
  • Metapneumovirus - common cold
  • Para influenza - croup
31
Q

What are the key proteins that differentiate influenza A vs B and the subtypes of A and B?

A

Hemagglutinin (H) and Neuraminidase (N)

*These proteins are ON the virus

32
Q

What is the N protein responsible for?

A

RELEASE

33
Q

What is the H protein responsible for?

A

ATTACH

34
Q

If there is an antigenic drift, what will happen?

A

This is a NEW pathogen, so we have NO immunity = PANDEMIC

35
Q

What is a quadrivalent vaccine?

A

This means it has 4 strains

-Flu vaccines are quadrivalent - 2 A strains, 2 B strains

36
Q

What route is the live attenuated flu vaccine given? Who should this not be given to?

A

IN (nasal mist)

  • The virus is capable of replication, but very limited ability to cause disease
  • NEVER for immune suppressed
37
Q

What route is the inactivated flu vaccine given?

A

IM

  • Components of a dead pathogen, cannot replicate or induce disease
  • Immune suppressed people SHOULD get this
38
Q

What is a good drug target for influenza?

A

Neuraminidase inhibition - prevents mature virions from being released

39
Q

What are 3 neuraminidase inhibitor drugs for influenza?

A
  1. Oseltamivir (PO) - good against swine flu
  2. Zanavivir (inhaled)
  3. Peramivir (IV)
40
Q

What are the benefits of neuraminidase inhibitor drugs?

A
  • Shorten the duration of symptoms by 2 days
  • *Decreased incidence of secondary pneumonia
  • Predictive reduction in mortality risk
41
Q

What will hopefully be the COVID-19 drug?

A

Molnupiravir

42
Q

What is a brief overview of the HIV lifecycle?

A
  1. HIV cell fuses to the a CD4 receptor on the host cell
  2. Viral RNA is released into host cell
  3. Reverse transcriptase makes viral RNA into viral DNA
  4. Integrase places viral DNA into host DNA
  5. Viral DNA copied to viral RNA and made into protein
  6. Protease chops viral protein into subunits
  7. Re-assembled into new viral particles
  8. Released from cells
43
Q

How does HIV cause a host to become immune compromised?

A

As the new virus is created and released from the host cell, the CD4 host cells dir and their numbers fall leading to immune suppression

44
Q

What are the three steps anti-HIV drugs can inhibt?

A
  • Reverse transcription (RNA–>DNA)
  • Integrase (viral DNA into nucleus)
  • Protease (cleaves protein into viral peptides)
45
Q

What is the MOA of a reverse transcriptase antiretroviral?

A
  • Nucleotide/nucleoside reverse transcriptase inhibitors (NRTI)
  • false metabolite binds and inhibits the copying of viral RNA to DNA
  • Non-nucleoside reverse transcriptase inhibitors (NNRTI)
  • bind to enzyme in an allosteric fashion
  • doesn’t look like a base but can still inhibit the enzyme
46
Q

What are the other two main antiretroviral agents?

A
  • Protease inhibitors

- Integrase inhibitors

47
Q

What is the quickest way to lower viral load, minimize resistance, and assure complicance?

A

Combination therapies (2 or more drugs in 1 pill)

48
Q

When should someone take PEP?

A

If they have been exposed to HIV

  • Minimizes their chance of getting HIV
  • Ex: after a needle stick
49
Q

What is the highest risk for HIV transmission?

A

Blood to blood

50
Q

How long will someone normally take PEP for?

A

Sometimes a person may be on it for up to 3 months, but eventually they will discontinue the medication

51
Q

When should someone take PrEP?

A
  • This is a daily medication that can reduce the risk HIV
  • It inhibits HIV from replicating
  • More effective at preventing HIV from sexual exposure than a from IV drug exposure
52
Q

Which HIV drug is more potent? What does this mean?

A

Tenofovir TAF is more potent than Tenofovir TDF which means you need a lower dose of TAF to get the same effects.
**They have the same efficacy (both work)

Pathophys/Pharm (9 decks)

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