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Pharmacology Med201 > Antivirals > Flashcards

Antivirals Flashcards

1
Q

Most antivirals are ….. (Type)

A

nucleoside analog; inhibit replication of viral nucleic acid

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2
Q

Selective toxicity comes from the advantage of differences …..?

A

in affinity of viral and host cell replicative enzymes for antiviral agents (we choose the antivirals that have more affinity to viruses replicative enzymes)

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3
Q

Most antivirals chemotherapies are? (Drugs or prodrugs)?

A

Prodrugs

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4
Q

How antivirals become active?

A

antivirals prodrugs must be phosphorylated (we must add phosphate) by viral or host cell enzymes in order to become active

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5
Q

why the therapeutic index of antiviral chemotherapies is more narrower than for antibacterial medications?

A

it’s difficult to interfere with the viral protein synthesis without disturbing the host cellular pathways

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6
Q

why it’s difficult to interfere with the viral protein synthesis without disturbing the host cellular pathways?

A

because viruses use the host cell metabolic machinery for replication and as a result host toxicity of antiviral agents is higher than antibacterial agents

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7
Q

Antiviral chemotherapies are predominantly (static or cidal)?

A

Virustatic

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8
Q

Because antiviral chemotherapies are predominantly virustatic; mention 3 results

A
  1. They do not eradicate the virus and only inhibit the replication of the virus (not curative)
  2. The current antiviral agents are ineffective to eliminate latent virus
  3. They restore the immune system homeostasis to clear the viral infection (for e.g. virus cells are 1milion, our immune system kills 800,000 so antivirals restore homeostasis to fight viruses)
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9
Q

increased risk of viral resistance is associated with ??

A

long-term antiviral treatment

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10
Q

what is the most effective way to prevent viral infection?

A

vaccination

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11
Q

why vaccination is not possible all times

A

either due to
- there’s no vaccine
or that
- the available vaccine is not useful (e.g. resistance)

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12
Q

because vaccine is not possible all the time, antivirals can be used as …?

A

chemoprophylaxis agent

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13
Q

Drug that prevents attachment?

A

Enfuvirtide

Vaccines

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14
Q

Drug that prevents uncoating?

A

Amantadine

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15
Q

Drug that prevents protein synthesis by host cell ribosome?

A

IFN-alpha2a

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16
Q

Drug that prevents the synthesis of viral DNA?

A

acyclovir

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17
Q

Drug that prevents budding?

A

Zanamivir

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18
Q

Influenza viruses are? (genome & mutations)

A

RNA viruses & undergo frequent mutations

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19
Q

Antiviral agents used to treat influenza viruses include:

A

Amantadine

Oseltamivir and Zanamivir (Neuraminidase inhibitors)

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20
Q

Amantadine (Symmetrel)
(Therapeutic uses)
- today use, what type of influenza it targets, time of giving the drug and effect, other use

A
  • Very rare use today because of resistance (nearly 100%)
  • prevent & treat influenza type A virus
  • has no activity against type B (Type B should be given Neuraminidase inhibitors)
  • Should be given within 48 hours of the onset of symptoms to be effective (after 48 hours it will be ineffective)
  • decreases the duration of viral symptoms by about 2 days
  • also used to treat Parkinson’s disease (PD); It reduces tremor & dyskinesia in about 70% of patients with PD but Amantadine effectiveness fades (sometimes quickly)
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21
Q

Amantadine (Symmetrel)

MOA

A
  • not a nucleoside analog
  • It blocks influenza A M2 ion channel protein so it reduces the influx of protons (H+) => ultimately inhibits viral capsule disassembly
  • inhibits uncoating
  • Does not bind to the influenza B M2 channel because of different amino acid sequence
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22
Q

Amantadine (Symmetrel)

Pharmacokinetics

A
  • orally available & well absorbed from the GI tract

- Eliminated by the kidney (dose must be reduced in renal insufficiency)

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23
Q

How Amantadine is eliminated?

A

by the kidney (dose must be reduced in renal insufficiency)

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24
Q

Amantadine dose must be ____in renal insufficiency, becasue _____

A

reduced

it’s eliminated by the kidney

25
Q

Amantadine (Symmetrel)

Adverse effects

A
  • Common: Tremor, nervousness, confusion and dizziness
  • Peripheral edema (Ankle edema)
  • Livedo reticularis
26
Q

Neuraminidase Inhibitors drugs

A

Oseltamivir (Tamiflu)

Zanamivir (Relenza)

27
Q 
Neuraminidase Inhibitors
(Therapeutic uses); uses, types of influenza, time given, resistance
A
  • used for the prevention and treatment of influenza caused by
    influenza A and B virus within 2 days of the onset of flu symptoms
  • Oseltamivir-resistant is more common than zanamivir
28
Q

Neuraminidase Inhibitors

Pharmacokinetics of Oseltamivir)(absorption, bioavailability, activation

A
  • Well absorbed from GIT (bioavailability > 0.8)

- A prodrug & hydrolyzed by the liver enzymes to its active metabolite

29
Q

Neuraminidase Inhibitors

Pharmacokinetics of Zanamivir)(absorption, availability

A
  • Extremely poor absorption form GIT

- Available as a dry powder for oral inhalation

30
Q

Neuraminidase Inhibitors

Adverse effects

A
  • Well-tolerated (nausea/vomiting and headache)
  • Bronchospasm
  • They have less CNS adverse effects compared to amantadine
31
Q

Neuraminidase Inhibitors

MOA

A
  • not a nucleoside and interfere with replication

- Competitive inhibitor of neuraminidase enzyme

32
Q

what happens when Neuraminidase inhibitors inhibits neuraminidase enzyme?

A

they prevent the cleave of sialic acid residues

on the surface of the infected host cell and thus prevents the release of progeny virions from infected cells

33
Q

Herpes Simplex Virus (HSV)

A

Causes infection of the genitalia, mouth, skin,

meninges and brain

34
Q

Varicella-Zoster Virus (VZV)

A

Causes chickenpox in children & herpes zoster (shingles) in adults

35
Q

Cytomegalovirus (CMV)

A
  • not common but life-threatening for the
    immunocompromised patients (e.g HIV- patient)
  • It causes retinitis with extensive haemorrhage
36
Q

Antiviral chemotherapies for herpesvirus (Nucleoside Analogs)

A

Acyclovir
Valacyclovir
Ganciclovir

37
Q

Antiviral chemotherapies for herpesvirus (Non-Nucleoside Analogs)

A

Foscarnet

38
Q

Acyclovir (Zovirax)

Therapeutic uses

A
  • Routes: topical, oral and IV
  • Antiviral spectrum of acyclovir: HSV»VZV&raquo_space;»CMV (more potent to HSV)
  • not used for CMV because high dose is required = increase the risk of side effects
39
Q

Antiviral spectrum of acyclovir

A

HSV»VZV&raquo_space;»CMV

40
Q

why acyclovir is not used in cytomegalovirus?

A

because high dose is required = increase the risk of side effects

41
Q

Acyclovir (Zovirax)

Pharmacokinetics

A
  • Widely distributed in the body include CSF
  • Metabolized by liver and eliminated by the kidneys
  • Has low oral bioavailability
42
Q

since acyclovir has low oral bioavailability, what was the solution?

A

producing valacyclovir, which is an L-valyl ester prodrug with 5-fold greater oral bioavailability compare to acyclovir and it is rapidly converted to acyclovir by liver

43
Q

Acyclovir (Zovirax)

Adverse effects

A
  • Reversible renal dysfunction due to acyclovir-induced crystalline nephropathy
  • Neurotoxicity (tremor and seizure)
44
Q

Acyclovir targets which nucleotide?

A

guanine

45
Q

what’s the prodrug of acyclovir?

A

valacylovir

46
Q

Acyclovir (Zovirax)

Structure

A

Acyclovir is acyclic nuecloside produrg, it lacks a 3’-OH group on side chain.

47
Q

Acyclovir (Zovirax)

MOA

A
  1. when it enters an infected cell; it’s converted by viral thymidine kinase (TK) to acyclo-GMP
  2. host cell TK converts acyclo-GMP to acyclo- GDP and finally acyclo-GTP inside infected cell
  3. Acyclo-GTP inhibits replication of viral DNA by mechanisms:
    3a. Acyclo-GTP is incorporated into viral DNA by viral DNA polymerase & causes
    chain termination
    3.b Acyclo-GTP inhibits viral DNA polymerase
48
Q

explain acyclovir selective toxicity?

A

Affinity for viral TK is 200-fold greater than for mammalian TK

49
Q

explain resistance to acyclovir?

A

viral thymidine kinase (TK) deficiency

50
Q

Ganciclovir

Therapeutic uses)(Routes, target viruses, toxicity

A
  • Routes: oral, IV and ocular insert
  • Has activities against all herpesviruses
  • Due to its toxicity is restricted for treatment of CMV retinitis in immunocompromised patients and prevention of CMV in transplant patients
51
Q

Restrictions of Ganciclovir

A
  • Treatment of CMV retinitis in immunocompromised patients (ocular insert)
  • Prevention of CMV infection in transplant patients
52
Q

Ganciclovir

Adverse effects

A

Myelosupression (dose-dependent)

53
Q

Non-Nucleoside Analogs for Herpes

A

Foscarnet

54
Q

Foscarnet

Therapeutic uses)(virus targets, common use

A
  • Has activity against all herpesviruses and HIV

- used mostly to treat immunocompromised patients with CMV and acyclovir–resistant HSV infections

55
Q

Foscarnet

Pharmacokinetic

A
  • It is not well absorbed by GIT, thus Usually foscarnet is given IV
  • 80% eliminated unchanged by the kidneys
56
Q

Foscarnet

MOA

A
  • It is phosphorylated analog of formic acid, thus, phosphorylation by viral or host cell kinases is not required
  • It directly Inhibits herpesvirus DNA polymerase and HIV reverse transcriptase
57
Q

drug that directly Inhibits herpesvirus DNA polymerase and HIV reverse transcriptase

A

Foscarnet

58
Q

Foscarnet

Adverse effects

A

Nephrotoxicity & electrolyte disturbances

Pharmacology Med201 (1 decks)

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