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Systemic Pharm I > Antivirals Pt. 1 > Flashcards

Antivirals Pt. 1 Flashcards

1
Q

Influenza drugs

A

oseltamivir, zanamivir, amantadine, rimantadine

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2
Q

Main drug classes for Hep B/C

A

interferon alpha, 5A inhibitors, protease inhibitors, nucleotide/nucleoside inhibitors

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3
Q

5A inhibitors

A

daclatasvir, elbasvir, ledipasvir, ombitasvir

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4
Q

Protease inhibitors

A

grazoprevir, paritaprevir, simeprevir

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5
Q

Nucleotide/nucleoside inhibitors

A

adefovir, entecavir, lamivudine, sofosbuvir, tenofovir

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6
Q

Herpesvirus drugs

A

acyclovir, famciclovir, valacyclovir, trifluridine, ganciclovir, cidofovir

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7
Q

What are characteristics of viruses?

A

obligate intracellular parasites, no cell wall, no cell membrane, do not carry out metabolic processes

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8
Q

T/F antivirals are selective enough to prevent injury to the host

A

false, not selective enough

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9
Q

What is the structure of a virus?

A

protein layer surrounds and protects the genetic material– viral genome, nucleocapsid, viral tegument, envelope, envelope protein

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10
Q

What are DNA viruses?

A

herpes (simplex, zoster, cytomegalovirus) have DNA as nucleic material and need DNA polymerase

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11
Q

What are RNA viruses?

A

influenza and hepatitis, has RNA as nucleic material and need RNA polymerase

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12
Q

What are retroviruses?

A

HIV, has RNA as nucleic material and need reverse transcriptase to incorporate DNA into host DNA

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13
Q

When do viral symptoms appear?

A

late in the disease, viral particles have already replicated so drugs blocking viral replication may have limited effectiveness

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14
Q

T/F many antivirals are used as prophylactic agents

A

true

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15
Q

What are the six steps in the virus life cycle?

A

attachment, penetration, uncoating, biosynthesis, assembly, release

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16
Q

What treatments are available for respiratory viruses and what is prefered?

A

treatments available for influenza A and B but immunization against influenza is preferred

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17
Q

When are antiviral agents used?

A

when patient is allergic to vaccine, outbreak is due to a variant of the virus, outbreaks among unvaccinated people in closed settings

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18
Q

What enzymes do viruses causes influenza contain?

A

neuraminidase

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19
Q

Which two drugs selectively inhibit neuraminidase which is essential to the virus life cycle?

A

oseltamivir and zanamivir , stops replication and prevents new virions

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20
Q

What can you give to someone for influenza even if they’ve had the vaccine and why?

A

neuraminidase inhibitors because they do not interfere with the immune response to the influenza vaccine

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21
Q

When do you have to administer a neuraminidase inhibitor for it to be effective?

A

24-48 hours after onset of infection

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22
Q

What are the pharmacokinetics of oseltamivir?

A

orally active, prodrug (needs liver metabolism)

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23
Q

How is zanamivir administered?

A

intranasally not orally

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24
Q

What are adverse effects of neuraminidase inhibitors?

A

GI disturbances for oseltamivir (take with food) and bronchospasm with zanamivir (contraindicated for asthma and COPD)

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25
Q

What are the two inhibitors of viral uncoating?

A

amantadine and rimantadine

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26
Q

What are inhibitors of viral uncoating active against?

A

influenza A, treatment and prevention

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27
Q

What is the MOA of inhibitors of viral uncoating?

A

block viral membrane matrix protein M2 preventing fusion of the viral membrane with the cell membrane

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28
Q

What is the absorption of viral uncoating inhibitors?

A

well absorbed orally

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29
Q

Which inhibitor of viral uncoating readily penetrates the CNS and may accumulate to toxic levels in patients with renal failure?

A

amantadine

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30
Q

Which inhibitor of viral uncoating is extensively metabolized by the liver?

A

rimantadine

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31
Q

What are the adverse effects of inhibitors of viral uncoating?

A

GI problems, caution in pregnancy, CNS side effects with amantadine (insomnia dizziness and ataxia aka movement disorder

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32
Q

Why are inhibitors of viral uncoating infrequently used?

A

resistance develops rapidly and there is cross resistance between the two

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33
Q

What are the hepatic viral infection types?

A

ABCDE

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34
Q

Which hepatitis forms are most common cause of chronic hepatitis, cirrhosis, and hepatocellular carcinoma

A

Hep B and C (C worse)

35
Q

T/F Hep B and C and blood borne

A

true

36
Q

What do treatment of hepatic viral infections aim to do?

A

interfere with essential viral enzyme function or replication

37
Q

What do enzyme 5A inhibitors do?

A

interfere with enzyme responsible for viral RNA replication and virion assembly

38
Q

What do protease inhibitors do?

A

prevent viral maturation by interfering with hepatitis protease enzyme responsible for formation of essential enzymes and proteins

39
Q

What do nucleotide/nucleoside inhibitors do?

A

inhibit reverse transcriptase/RNA polymerase and insert them into RNA chain resulting in termination of replication

40
Q

Which two nucleotide/side inhibitors treat hepatitis AND HIV?

A

lamivudine and tenofovir

41
Q

What does interferon alpha do?

A

synthesized by recombinant DNA technology for multiple uses

42
Q

What is the MOA interferon alpha?

A

incompletely understood, thought to induce host cell enzymes to inhibit viral RNA translation and degradation of viral RNA

43
Q

How is interferon alpha?

A

not active orally, subcutaneous delivery or IV/intralesion

44
Q

What are the adverse effects of interferon alpha?

A

flu like symptoms (fever chills etc), fatigue and mental depression, symptoms improve with subsequent administration, interferon RETINOPATHY

45
Q

What does interferon retinopathy consist of?

A

cotton wool spots and retinal hemorrhages in the posterior pole, occurs 3-5 months after starting treatment or as early as 2 weeks – improves with cessation

46
Q

How often do you have to monitor patients on interferon alpha for retinopathy?

A

every 6 months or sooner if retinopathy is present

47
Q

What is harvoni?

A

combination of sofosbuvir and ledipasvir (5A) don’t need that memorized lol, very expensive with 95% cure rate for hepatic infections

48
Q

What is ritonavir?

A

can be given as a pharmacological booster, CYP450 inhibitor that increases the plasma concentration of other drugs, not active against hepatitis but is active against HIV

49
Q

What are examples of infections from herpes?

A

cold sores, viral encephalitis, genital infections, corneal infections

50
Q

T/F herpesvirus drugs are administered during the latent phase

A

false, there is no effect during the latent phase

51
Q

When are herpes drugs effective?

A

during the acute phase of the infection or prophylactically

52
Q

What is acyclovir used for?

A

treatment of HSV encephalitis and genital herpes

53
Q

What is given prophylactically to seropositive (exposed) patients?

A

acyclovir

54
Q

What is the MOA of acyclovir?

A

guanosine analog, inhibits DNA polymerase and is incorporated into viral DNA once activated by thymidine kinase (viral enzyme)

55
Q

T/F if a patient doesn’t have an active herpes infection, acyclovir will pass through the body without side effects

A

true, exception: patients with kidney problems

56
Q

How is acyclovir administered?

A

oral, IV or topical

57
Q

What are the pharmacokinetics of acyclovir?

A

passes into CSF, accumulates in patients with renal failure

58
Q

What is notable about valacyclovir?

A

ester of acyclovir with greater oral availability

59
Q

What are adverse effects of acyclovir?

A

local irritation, headaches and GI disturbances, renal dysfunction at high doses

60
Q

What is resistant to acyclovir?

A

cytomegalovirus because it lacks specific viral thymidine kinase

61
Q

T/F famciclovir and valacyclovir are clinically equivalent to acyclovir

A

true but actually have longer half life requiring smaller dose

62
Q

Which herpes virus drug is safest in pregnancy?

A

famciclovir

63
Q

What is cidofovir approved for?

A

treatment of CMV induced retinitis in AIDs patients

64
Q

What is the MOA of cidofovir?

A

inhibits viral DNA synthesis as a nucleotide analog of cytosine

65
Q

What is the administration of cidofovir?

A

IV, intravitreal, and topical

66
Q

What is a contraindication for cidofovir?

A

renal impairment and nephrotoxic drugs (INCLUDING NSAIDs) produces significant toxicity to the kidney

67
Q

What is CMV retinitis?

A

inflammation of nerve fiber layer that occurs during HIV

68
Q

T/F ganciclovir must be activated by viral enzyme

A

true (like acyclovir)

69
Q

How is ganciclovir administered?

A

IV only, penetrates CSF, 20x greater activity agains CMV

70
Q

What is the MOA of ganciclovir?

A

inhibits viral DNA polymerase and can be incorporated into viral DNA

71
Q

What is the ester of ganciclovir that has a high oral bioavailability?

A

valgancyclovir

72
Q

What are the adverse effects of ganciclovir?

A

dose-dependent neutropenia, carcinogenic and embryotoxic

73
Q

What is the ocular preparation of ganciclovir?

A

zirgan, only targets virally infected cells and is much less toxic than trifluridine

74
Q

What is the MOA of trifluridine?

A

fluorinated pyrimidine nucleoside analog that inhibits DNA synthesis

75
Q

What is too toxic for systemic use and why?

A

trifluridine, able to incorporate into cellular DNA of host

76
Q

How is trifluridine administered?

A

topical applications in the eye, drug of choice for HSV keratoconjunctivitis and epithelial keratitis

77
Q

What is a main issue with trifluridine administration?

A

short half life (12 mins) requires frequent dosing and causes lots of irritation

78
Q

What is herpes zoster?

A

shingles, recurrent varicella zoster virus which is contagious to those who have NOT had chicken pox

79
Q

What are signs and symptoms of herpes zoster?

A

headache, malaise, fever, chills, neuralgic pain, unilateral vesicular eruption and hot, hyperesthesia and edema on half of the face

80
Q

What does herpes zoster ophthalmicus present as?

A

keratitis, corneal edema, anterior uveitis – need to dilate looking for vitritis and retinitis

81
Q

What can reactivate herpetic keratitis?

A

fever, hormonal change, UV radiation, trauma, trigeminal injury – risk of recurrence increases as years pass

82
Q

What are signs and symptoms of herpetic keratitis?

A

mild discomfort, watering eyes, blurred vision, corneal ulceration (dendritic pattern), and stomal edema, KPs, descemet scars in disciform disease

83
Q

What is the treatment for herpetic keratitis?

A

oral acyclovir will be shed in tears and is effective or topical trifluridine will work 9x/day

Systemic Pharm I (13 decks)

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