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Systemic Pharm I > Antivirals Pt. 1 > Flashcards

Antivirals Pt. 1 Flashcards

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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
What are the two inhibitors of viral uncoating?
amantadine and rimantadine
26
What are inhibitors of viral uncoating active against?
influenza A, treatment and prevention
27
What is the MOA of inhibitors of viral uncoating?
block viral membrane matrix protein M2 preventing fusion of the viral membrane with the cell membrane
28
What is the absorption of viral uncoating inhibitors?
well absorbed orally
29
Which inhibitor of viral uncoating readily penetrates the CNS and may accumulate to toxic levels in patients with renal failure?
amantadine
30
Which inhibitor of viral uncoating is extensively metabolized by the liver?
rimantadine
31
What are the adverse effects of inhibitors of viral uncoating?
GI problems, caution in pregnancy, CNS side effects with amantadine (insomnia dizziness and ataxia aka movement disorder
32
Why are inhibitors of viral uncoating infrequently used?
resistance develops rapidly and there is cross resistance between the two
33
What are the hepatic viral infection types?
ABCDE
34
Which hepatitis forms are most common cause of chronic hepatitis, cirrhosis, and hepatocellular carcinoma
Hep B and C (C worse)
35
T/F Hep B and C and blood borne
true
36
What do treatment of hepatic viral infections aim to do?
interfere with essential viral enzyme function or replication
37
What do enzyme 5A inhibitors do?
interfere with enzyme responsible for viral RNA replication and virion assembly
38
What do protease inhibitors do?
prevent viral maturation by interfering with hepatitis protease enzyme responsible for formation of essential enzymes and proteins
39
What do nucleotide/nucleoside inhibitors do?
inhibit reverse transcriptase/RNA polymerase and insert them into RNA chain resulting in termination of replication
40
Which two nucleotide/side inhibitors treat hepatitis AND HIV?
lamivudine and tenofovir
41
What does interferon alpha do?
synthesized by recombinant DNA technology for multiple uses
42
What is the MOA interferon alpha?
incompletely understood, thought to induce host cell enzymes to inhibit viral RNA translation and degradation of viral RNA
43
How is interferon alpha?
not active orally, subcutaneous delivery or IV/intralesion
44
What are the adverse effects of interferon alpha?
flu like symptoms (fever chills etc), fatigue and mental depression, symptoms improve with subsequent administration, interferon RETINOPATHY
45
What does interferon retinopathy consist of?
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
How often do you have to monitor patients on interferon alpha for retinopathy?
every 6 months or sooner if retinopathy is present
47
What is harvoni?
combination of sofosbuvir and ledipasvir (5A) don't need that memorized lol, very expensive with 95% cure rate for hepatic infections
48
What is ritonavir?
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
What are examples of infections from herpes?
cold sores, viral encephalitis, genital infections, corneal infections
50
T/F herpesvirus drugs are administered during the latent phase
false, there is no effect during the latent phase
51
When are herpes drugs effective?
during the acute phase of the infection or prophylactically
52
What is acyclovir used for?
treatment of HSV encephalitis and genital herpes
53
What is given prophylactically to seropositive (exposed) patients?
acyclovir
54
What is the MOA of acyclovir?
guanosine analog, inhibits DNA polymerase and is incorporated into viral DNA once activated by thymidine kinase (viral enzyme)
55
T/F if a patient doesn't have an active herpes infection, acyclovir will pass through the body without side effects
true, exception: patients with kidney problems
56
How is acyclovir administered?
oral, IV or topical
57
What are the pharmacokinetics of acyclovir?
passes into CSF, accumulates in patients with renal failure
58
What is notable about valacyclovir?
ester of acyclovir with greater oral availability
59
What are adverse effects of acyclovir?
local irritation, headaches and GI disturbances, renal dysfunction at high doses
60
What is resistant to acyclovir?
cytomegalovirus because it lacks specific viral thymidine kinase
61
T/F famciclovir and valacyclovir are clinically equivalent to acyclovir
true but actually have longer half life requiring smaller dose
62
Which herpes virus drug is safest in pregnancy?
famciclovir
63
What is cidofovir approved for?
treatment of CMV induced retinitis in AIDs patients
64
What is the MOA of cidofovir?
inhibits viral DNA synthesis as a nucleotide analog of cytosine
65
What is the administration of cidofovir?
IV, intravitreal, and topical
66
What is a contraindication for cidofovir?
renal impairment and nephrotoxic drugs (INCLUDING NSAIDs) produces significant toxicity to the kidney
67
What is CMV retinitis?
inflammation of nerve fiber layer that occurs during HIV
68
T/F ganciclovir must be activated by viral enzyme
true (like acyclovir)
69
How is ganciclovir administered?
IV only, penetrates CSF, 20x greater activity agains CMV
70
What is the MOA of ganciclovir?
inhibits viral DNA polymerase and can be incorporated into viral DNA
71
What is the ester of ganciclovir that has a high oral bioavailability?
valgancyclovir
72
What are the adverse effects of ganciclovir?
dose-dependent neutropenia, carcinogenic and embryotoxic
73
What is the ocular preparation of ganciclovir?
zirgan, only targets virally infected cells and is much less toxic than trifluridine
74
What is the MOA of trifluridine?
fluorinated pyrimidine nucleoside analog that inhibits DNA synthesis
75
What is too toxic for systemic use and why?
trifluridine, able to incorporate into cellular DNA of host
76
How is trifluridine administered?
topical applications in the eye, drug of choice for HSV keratoconjunctivitis and epithelial keratitis
77
What is a main issue with trifluridine administration?
short half life (12 mins) requires frequent dosing and causes lots of irritation
78
What is herpes zoster?
shingles, recurrent varicella zoster virus which is contagious to those who have NOT had chicken pox
79
What are signs and symptoms of herpes zoster?
headache, malaise, fever, chills, neuralgic pain, unilateral vesicular eruption and hot, hyperesthesia and edema on half of the face
80
What does herpes zoster ophthalmicus present as?
keratitis, corneal edema, anterior uveitis -- need to dilate looking for vitritis and retinitis
81
What can reactivate herpetic keratitis?
fever, hormonal change, UV radiation, trauma, trigeminal injury -- risk of recurrence increases as years pass
82
What are signs and symptoms of herpetic keratitis?
mild discomfort, watering eyes, blurred vision, corneal ulceration (dendritic pattern), and stomal edema, KPs, descemet scars in disciform disease
83
What is the treatment for herpetic keratitis?
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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