Antivirals Flashcards

1
Q

Aim of antivirals

A

To treat infections or diseases caused by viruses

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2
Q

How antivirals generally work

A

Target steps in viral replication

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3
Q

Effectiveness of antivirals

A

Only a small #of viruses respond

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4
Q

Virus definition

A

Sub-microscopic infections agent that cannotgrow o reproduce outside a host cell

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5
Q

Virus structure

A

RNA or DNA, capsid, lipid envelope

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6
Q

Viral replication steps

A

Entry, uncoating, transcription, DNA replication, protein synthesis, assembly, release

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7
Q

Types of infection

A

Acute, chronic, latent, progressive, cancer

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8
Q

Main routes of transmission of sars-cov-2

A

Respiratory droplets and aerosols

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9
Q

Types of COVID-19 treatment

A

Antivirals, anti-inflammatories, antibodies

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10
Q

Remdesivir mechanism

A

Product metabolized to nucleoside monophosphate and triple phosphorylated, then incorporated into RNA and this RNA is terminated

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11
Q

Paxlovid

A

Ritonavir-boosted nirmatrelvir

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12
Q

Ritonavir mechanism

A

Protease inhibitor that increases nirmatrelvir levels

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13
Q

Nirmatrelvir mechanism

A

Inhibits Mpro, a viral protease in all coronaviruses that affect humans

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14
Q

Remdesivir adverse effects

A

Infusion site reactions, hypotension, nausea, vomiting, chest tightness, respiratory failure, altered liver enzymes, back pain, ECG abnormalities, renal impairment

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15
Q

Paxlovid adverse effects

A

Change in taste, muscle aches, swollen joints, headache, blurred vision, changes in heart rate

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16
Q

Remdesivir resistance

A

Mutations in the rna-dependent RNA polymerase so the ATP analogue isn’t incorporated

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17
Q

Nirmatrelvir resistance

A

Mutations in Mpro binding site

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18
Q

Influenza genetic material

A

RNA

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19
Q

Herpes genetic material

A

DNA

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20
Q

Antivirals for influenza

A

Oseltamivir and amantadine

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21
Q

Osaltamivir mechanism

A

Sialic acid analogue that binds and inhibits neuraminidase so the virus cannot bud off

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22
Q

Pharmacokinetics of oseltamivir

A

Pro/dung metabolized to active in liver and gi

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23
Q

Adverse effects of oseltamivir

A

Nausea and gi discomfort

24
Q

Clinical uses of oseltamiviv

A

Prevention and treatment of a and B, including H1N1

25
Q

Resistance to oseltamivir

A

Mutations in neuraminidase

26
Q

Amantadine mechanism

A

Inhibits proton ion channel M2 necessary for uncaring of virus and protein synthesis

27
Q

Pharmacokinetics of amantadine

A

Distributes throughout all tissues and is excreted unchanged by kidney

28
Q

Adverse effects of amantadine

A

Gi disturbances, CNS disturbances, renal damage in patients with renal insufficiency

29
Q

Clinical uses of amantadine

A

Treatment of early infection by a, but not H1N1

30
Q

Resistance to amantadine

A

Mutation in M2

31
Q

Herpes types

A

1: cold sores, 2: genital herpes

32
Q

Acyclovir mechanism

A

Guanosine analogue that gets activated by viral thymidine kinase and then phosphorylated twice more by our cells, then incorporated into DNA and terminates the chain

33
Q

Pharmacokinetics of acyclovir

A

Oral, iv, or topical that distribute throughout body

34
Q

Adverse effects of acyclovir

A

Nausea, vomiting, diarrhea, headache, renal damage in dehydrated patients

35
Q

Clinical uses of acyclovir

A

Treatment of active herpes

36
Q

Resistance to acyclovir

A

Altered or deficient thymidine kinase

37
Q

HIV positive

A

Infected with virus, generally symptom free, clinical latency of 2-10 years without treatment

38
Q

AIDS

A

Opportunistic infections

39
Q

HIV coreceptors

A

CCR5 or CXCR4

40
Q

Categories of HIV antivirals

A

NRTIs, NNRTIs, INIs, PIs, viral fusion inhibitors

41
Q

Azidothymidine mechanism

A

Thymidine analogue activated by mammalian kinases and incorporated into DNA → termination

42
Q

Pharmacokinetics of azidothymidine

A

Well absorbed and distributed, glucuronidation

43
Q

Adverse effects of azidothymidine

A

Anemia, leukopenia, headaches, seizures, drug interactions due to glucuronidation

44
Q

Resistance to azidothymidine

A

Rt mutation, decreased kinase activation

45
Q

Nevirapine mechanism

A

Binds to non-catalytic site of rt

46
Q

Pharmacokinetics of nevirapine

A

Well absorbed and distributed, oxidized by CYP 3A4 and 2B6 and then undergoes glucuronidation

47
Q

Adverse effects of nevirapine

A

Rash, hepatotoxicity, drug interactions because it increases 3a4, so it increases metabolism of itself, oral contraceptives, azoles, methadone, PIs

48
Q

Resistance to nevirapine

A

Rt mutation

49
Q

Raltegravir mechanism

A

Inhibits viral integrate

50
Q

Resistance to raltegravir

A

Viral integrase mutation

51
Q

Ritonavir HIV mechanism

A

Inhibits HIV aspartyl protease and inhibits CYP3A4 to enhance other drugs

52
Q

Pharmacokinetics of ritonavir

A

Good bioavailability, metabolized by 3a4

53
Q

Adverse effects of ritonavir

A

Gi disturbances, insomnia, hyperglycemia, metabolic abnormalities

54
Q

Maraviroc mechanism

A

CCR5 receptor antagonist to prevent viral entry

55
Q

Adverse effects of maraviroc

A

Muscle/joint pain, cold symptoms, dizziness, gi disturbances, liver damage and allergic reactions