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D&D Unit 4 > Anti-viral Agents (complete) > Flashcards

Anti-viral Agents (complete) Flashcards

1
Q

What are the different classifications of anti-viral agents for flu?

A

1) Inhibition of viral neuraminidase

2) Inhibition of uncoating

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2
Q

What are the different classifications of anti-viral agents for herpes?

A

1) Inhibition of viral genome replication (viral DNA polymerase)
2) Inhibitors of viral penetration

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3
Q

What are the different classifications of anti-viral agents for RSV?

A

Only one type

1) Purine nucleoside analogy

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4
Q

What are the different classifications of anti-viral agents for cytomegalovirus?

A

1) Inhibition of viral DNA polymerase
2) Ganciclovir/Valganciclovir
3) Foscarnet

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5
Q

What are the two anti-virals for flu that are neuraminidase inhibitors?

A

1) Oseltamivir

2) Zanamivir

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6
Q

Describe the mechanism of action for neuraminidase inhibitors of flu

A
  • Works against influenza A and B
  • If NA activity is blocked virions clump at cell surface => decrease viral infectivity
  • NA inhibition impairs viral penetration through mucin secretions => decreased infection of other respiratory epithelial cells
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7
Q

Describe flu’s resistance to NA inhibitors

A
  • It’s rare

- If it does happen, through mutations in neuraminidase or hemagluttinin

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8
Q

How is oseltamivir absorbed?

A

PO

  • a prodrug
  • 80% bioavailability
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9
Q

How is zanamivir absorbed?

A

Via inhalation

Goal: to deliver to respiratory tract

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10
Q

How is oseltamivir eliminated?

A
  • kidneys (glomer filtration-tubular secretion)

- Dosage must be changed if pt has renal probs

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11
Q

How is zanamivir eliminated?

A
  • 10-20% of inhaled dose is absorbed

- Remainder excreted via urine

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12
Q

Describe the clinical use of oseltamivir

A 
Who:
Children (>1yo) and adults)
When: 
Start w/in 48hrs of symptoms
Purpose:
decreases severity and duration of flu

Can be given prophylactically => 70-90% effective in prevention

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13
Q

Describe the clinical use of zanamivir

A 
Who:
Those >7yo
When:
Start w/in 2 days of symptoms
Purpose:
Shorten duration -- decrease lower respiratory tract complications
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14
Q

What are the adverse rxns associated with oseltamivir?

A
  • Nausea and vomiting
  • Abdominal pain

Decreased if taken w/food

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15
Q

What are the adverse rxns associated with zanamivir?

A

Cough, brochospasm

CAN BE SEVERE

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16
Q

What are the two anti-virals for flu that inhibit uncoating?

A

1) Amantadine

2) Rimantadine

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17
Q

Describe the mechanism of action for uncoating inhibitors for flu

A
  • Blocks virally-encoded H+ ion channel —AKA: M2 protein

- Prevents the pH change necessary for uncoating!

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18
Q

Describe flu’s resistance to uncoating inhibitors

A
  • Mutations in transmembrane domains of M2 proton channel

- Can no longer block that channel

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19
Q

How are amantadine/rimantadine absorbed?

A

effective PO

ACCUMULATES in LUNGS

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20
Q

How is amantadine excreted?

A

Unchanged in urine

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21
Q

How is rimantadine excreted? Discuss the limits of its distribution

A
  • Hepatic elimination

- Increased protein-bind limits distribution to CNS

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22
Q

Describe the clinical uses of amantadine and rimantadine. Why is use currently limited?

A
  • Used for prophylaxis and tx of influenza A

- Limited use: b/c of RESISTANCE

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23
Q

What are the adverse rxns associated with amantadine?

A
  • Insomnia
  • Concentration difficulty
  • Lightheadedness/dizziness
  • Headache
  • GI upset
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24
Q

What are the adverse rxns associated with rimantadine?

A

Better than amantadine but similar effects

CNS probs not as bad b/c of decreased CNS penetration

  • Insomnia
  • Concentration difficulty
  • Lightheadedness/dizziness
  • Headache
  • GI upset
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25
Q

Describe the mechanism of action of acyclovir and its analogs

A
  • Diffuse into cell => triphosphorylated by intracellular kinases
  • The Acyclo triphosphate inhibits viral DNA polymerase (more sensitive than human DNA poly)
  • A DNA chain terminator w/ irreversible binding btwn DNA poly and terminated chain
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26
Q

Describe the selectively toxic effects of acyclovir in herpes tx

A
  • 1st phosphorylation step by herpes-encoded thymidine kinase
  • Only occurs in infected cells
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27
Q

Describe viral resistance to acyclovir and its analogs

A

MOST COMMON:
- Reudction/loss of expression of viral thymidine kinase

Also:

  • altered TK substrate specificity
  • altered affinity of viral DNA poly activity

Resistance happens mainly in immunosuppressed pts receiving extended acyclovir tx regimens

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28
Q

How is acyclovir absorbed?

A

poor PO

  • PO, topically, IV
29
Q

How is valacyclovir absorbed?

A
  • valyl ester prodrug of acyclovir

- 80-90% bioavailability

30
Q

How is penciclovir absorbed?

A
  • Topical ONLY

- poor PO

31
Q

How is famciclovir absorbed?

A
  • Diacetyl ester of penciclovir

- 70% bioavailability

32
Q

Describe the distribution of acyclovir and its analogs

A

Cross cell membrane => phosphorylated => ‘trapped’ intracellularly

33
Q

How are acyclovir and penciclovir eliminated?

A
  • Kidneys

- t1/2s significantly prolong w/ kidney probs or in neonates

34
Q

Describe the clinical use of acyclovir in primary infections of HSV 1&2

A
  • Beneficial if given in first 48-72hrs
  • Oral acyclovir => 3-5doses/day for 7-10 days
  • Oral famiciclovir (tid) or valacyclovir (bid) for 7-10 days
  • Topical acyclovir/penciclovir requires frequent administration
35
Q

Describe the clinical use of acyclovir in recurrent infections of HSV 1&2

A
  • Treatment considerations: severity, recurrence fq, cost, pt preference, partner uninfected or not (may require chronic tx)
  • Ranges from no tx to epsidodic tx to chronic suppressive tx based on the above
36
Q

Describe the clinical use of acyclovir in treatment of primary infection of varicella zoster (aka chicken pox)

A
  • No tx for kids <12yo
  • Acyclovir (qid for 5d) for adults – uncomplicated
  • Acyclovir IV (tid for 7d) if immunosuppressed or severe complications
37
Q

Describe the clinical use of acyclovir in treatment of recurrent infection of varicella zoster (aka shingles)

A
  • More beneficial if started in first 72 hrs
  • Oral acyc (3-5 doses/day) => 7d
  • IV for immunosuppressed
38
Q

Describe the adverse rxns associated with acyclovir and its analogs

A
  • Tolerated well PO: only headache, n/v
  • IV route or valacyclovir: CNS effects (confusion, hallucinations, seizures)
  • Renal tox w/ IV — decreases w/ hydration
  • Preg cat B
39
Q

Describe the mechanism of action of docosanol

A
  • Long chain saturated alcohol => inhibits replication of lipid-enveloped viruses
  • Prevents fusion btwn cellular and viral envelope membranes => blocks viral entry into cell!!
40
Q

Describe the clinical uses of docosanol

A
  • Available over-the-counter (ABREVA)
  • Topical tx: 5xday
  • Must begin w/in 12 hrs of symptoms
41
Q

Describe the adverse rxns associated with docosanol

A

Well-tolerated

42
Q

Describe the mechanism of action of ganciclovir and valganciclovir

A
  • phosphorylated to Gan-MP by viral kinase (UL97) => then active Gan-TP by host kinases
  • Gan-TP incorporated into replicating viral DNA => slows and ceases DNA elongation
43
Q

Describe how cytomegalovirus develops resistance to ganciclovir and valganciclovir

A
  • Mutations in activating kinase (UL97)

- Mutations in viral DNA poly target (UL54)

44
Q

How is ganciclovir absorbed?

A
  • poor PO, still given PO

- given IV or intraocularly

45
Q

How is valganciclovir absorbed?

A
  • Valyl ester prodrug of ganciclovir
  • Has 60% bioavailability

PO

46
Q

How is foscarnet absorbed?

A

IV only

  • poor oral bioavailability and GI intolerance
47
Q

How is cidofovir absorbed?

A

IV only

  • nucleotide analog
48
Q

How is ganciclovir eliminated?

A

Kidney

  • Filtration and secretion
49
Q

How is foscarnet eliminated?

A

Kidney

50
Q

How is cidofovir eliminated?

A
  • Tubular secretion

An active metabolite w/ long intracellular t1/2

Can be admin’d w/ probenecid to block secretion and decrease nephrotoxicity

51
Q

Describe the clinical use of ganciclovir in treatment of cytomegalovirus

A
  • Induction/maintenance tx of CMV retinitis in immunocompromised pts
  • Used to prevent CMV in transplant pts

Given IV or ocular implant

52
Q

Describe the clinical use of valganciclovir in treatment of cytomegalovirus

A
  • Treats CMV retinitis

PO => bid for 21d, then once/d

53
Q

Describe the clinical use of foscarnet in treatment of cytomegalovirus

A
  • Treats CMV retinitis in pts w/ AIDS

IV => q8-12h for 14-21d, then once/d

54
Q

Describe the clinical use of cidofovir in treatment of cytomegalovirus

A

CMV retinitis if no response to ganciclovir or foscarnet

IV => once/wk x 2, then q2weeks

55
Q

Describe the adverse rxns associated w/ ganciclovir and valganciclovir

A
  • Myelosuppression (esp. IV route)

- Also nausea, diarrheam fever, rash, insomnia, headache

56
Q

Describe the adverse rxns associated w/ foscarnet

A

RENAL IMPAIRMENT!! => hypocalcemia

CNS abnormalities (HA, tremor, seizures, hallucinations)

57
Q

Describe the adverse rxns associated w/ cidofovir

A

Proximal tubular nephrotoxicity (dose dependent)

Neutropenia, uveitis

58
Q

Describe the mechanism of action of ribavirin

A
  • purine nucleoside analog
  • inhibits DNA & RNA viruses
  • MOA not completely understood
  • Converted to ribavirin-TP by cellular kinases => interferes w/ GTP & NA synthesis
  • Inhibits GTP-dependent 5’ capping of viral mRNA
  • May increase mutagenesis rates => viral suicide
59
Q

Describe how RSV develops resistance to ribavirin

A

No resistance observed to date

60
Q

How is ribavirin absorbed?

A

PO

  • Bioavailability (45-64%) goes up w/ fatty meals
61
Q

How is ribavirin eliminated?

A

Hepatic metabolism => renal excretion of unchanged drug

62
Q

Describe the half-life variation of ribavirin

A

Varies w/ route of admin

  • Inhalation (children): 6-11 hrs
  • Oral for hep C (adults): initial plasma t1/2 = 43hrs — steady state >150 hrs
63
Q

Describe the clinical uses of ribavirin in treatment of RSV

A
  • RSV brochiolitis and pneumonia in hospitalized kids => inhalation
  • RSV infection (w/IVIG) in BM transplant and other immunocompromised pts
  • Also used in hep C => PO
64
Q

Describe the adverse rxns associated w/ ribavirin when administered via inhalation

A
  • Well-tolerated — can cause conjunctival/bronchial irritation
  • Acute deterioration of resp function in pts w/ brochospastic lung disease
  • high incidence of headache/conjunctivits in HC workers

Preg category X!!!

65
Q

Describe the adverse rxns associated w/ ribavirin when administered via PO

A
  • oral-systemic => used for Hep C
  • Hemolytic anemia!!
  • When given w/ interferon (another Hep C drug) => more cough, pruritus, rash
66
Q

What is palivizumab?

A

Humanized monoclonal AB to RSV F glycoprotein

67
Q

When is palivizumab used?

A

RSV immunoprophylaxis in infants w/ congenital heart disease

68
Q

How is palivizumab administered?

A
  • Given IM monthly
  • Max of 5 doses

Before beginning of RSV season (usually Nov)

69
Q

What are some issues associated w/ palivizumab?

A

Expensive — benefits vary among risk groups

  • Generally well-tolerated w/ rare severe hypersensitivity rxn (<1 per 100K)

D&D Unit 4 (18 decks)

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