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Pharm 2 - Exam 4 > Lecture 6 - AntiViral > Flashcards

Lecture 6 - AntiViral Flashcards

1
Q

Nucleoside vs nucleotide?

A

Nucleoside = sugar + base

Nucleotide = sugar + base + phosphate

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2
Q

All antivirals are ____ - no action against latent virus

A

virustatic

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3
Q

What is the MOA of anti-herpes drugs?

A

inhibit viral DNA polymerase

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4
Q

Acyclovir

A

topical, PO, IV

Indications: 
effective against HSV >> VZV
shortens duration of HSV if given early 
IV First line: 
herpes simplex encephalitis 
neonatal HSV 
severe HSV
VZV infection 
ADME: 
acyclic guanasine derivative 
metabolically activated by 3 phosphorylations (the first one done by viral thymidine kinase) 
acyclovir triphosphate = active form 
renal clearance

SE:
N/D/HA

Toxicities:
renal toxic, neurotoxic

Resistance:
viral thymidine kinase mutation
can be treated with agents not requiring viral phosphorylation like Foscarnet

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5
Q

What are the indications for acyclovir?

A

topical, PO, IV

Indications: 
effective against HSV >> VZV
shortens duration of HSV if given early 
IV First line: 
herpes simplex encephalitis 
neonatal HSV 
severe HSV
VZV infection
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6
Q

What is the ADME of acyclovir?

A 
ADME: 
acyclic guanasine derivative 
metabolically activated by 3 phosphorylations (the first one done by viral thymidine kinase) 
acyclovir triphosphate = active form 
renal clearance
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7
Q

What are the SE and toxicities of acyclovir?

A

SE:
N/D/HA

Toxicities:
renal toxic, neurotoxic

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8
Q

What resistance is present with acyclovir?

A

Resistance:
viral thymidine kinase mutation
can be treated with agents not requiring viral phosphorylation like Foscarnet

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9
Q

What is the MOA of acyclovir?

A

inhibit viral DNA polymerase

needs to be activated by 3 phosphorylations fist - the first one being done by the virus thymidine kinase

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10
Q

CMV meds

A

anti-cytomegalovirus drugs:
ganciclovir
foscarnet

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11
Q

When are CMV infections common?

A

HIV and organ transplant pts

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12
Q

Ganciclovir

A

Indications:
CMV infections
treatment/prophylaxis for CMV post-transplantation

MOA:
inhibit viral DNA polymerase, but first it must be activated by 3 polymerizations, the first one done by CMV kinase

ADME:
acyclic guanosine analog (same as acyclovir)
requires 3 phosphorylations (similar to acyclovir)
first phosphorylation done by CMV kinase

SE: toxicity: myelosuppression (major)

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13
Q

What are the indications for ganciclovir?

A

Indications:
CMV infections
treatment/prophylaxis for CMV post-transplantation

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14
Q

What is the MOA of ganciclovir?

A

MOA:

inhibit viral DNA polymerase, but first it must be activated by 3 polymerizations, the first one done by CMV kinase

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15
Q

What are the SE/toxicities for ganciclovir?

A

SE: toxicity: myelosuppression (major)

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16
Q

What is the ADME for ganciclovir?

A

ADME:
acyclic guanosine analog (same as acyclovir)
requires 3 phosphorylations (similar to acyclovir)
first phosphorylation done by CMV kinase

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17
Q

Foscarnet

A

IV only

Indications:
CMV
useful in strains resistant to acyclovir

MOA:
inhibits viral DNA polymerase, RNA polymerase, HIV RT
- no activation required
useful in strains resistant to acyclovir

SE/toxicity:
renal toxicity
hyperphosatemia, hypokalemia/calcemia/magnesemia

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18
Q

What are the indications for foscarnet?

A

IV only

Indications:
CMV
useful in strains resistant to acyclovir

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19
Q

What is the MOA for foscarnet?

A

MOA:
inhibits viral DNA polymerase, RNA polymerase, HIV RT
- no activation required
useful in strains resistant to acyclovir

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20
Q

What are the SE and toxicities seen with foscarnet?

A

SE/toxicity:
renal toxicity
hyperphosatemia, hypokalemia/calcemia/magnesemia

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21
Q

Which influenza causes mass infection?

A

only influenza A

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22
Q

When must anti-influenza medications be given in order to effective?

A

quickly after onset of sxs (~48hours)

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23
Q

What agents are available for anti-influenza?

A

amantidine
oseltamivir (tamiflu)
zanamivir (relenza)

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24
Q

Oseltamivir

A

(tamiflu, oral)
same for zanamivir (relenza, inhalation)

Indications:
influenza A, quickly given within 48 hours of symptom onset (activity against influenza B too)
Zanamivir is useful against oseltamivir - resistant strains

MOA:
neuraminidase inhibitors

25
What are the indications for oseltamivir?
(tamiflu, oral) same for zanamivir (relenza, inhalation) Indications: influenza A, quickly given within 48 hours of symptom onset (activity against influenza B too) Zanamivir is useful against oseltamivir - resistant strains
26
What are the indications for Zanamivir?
Zanamivir is useful against oseltamivir - resistant strains influenza A, quickly given within 48 hours of symptom onset (activity against influenza B too)
27
What is the MOA of oseltamivir and zanamivir?
neuraminidase inhibitors
28
Why is there so much resistance seen with HIV drugs?
retroviral replication is ERROR PRONE which means a lot of mutations which means more resistance
29
NRTIs
nucleoSIde reverse transcriptase inhibitors Abacavir Lamivudine/Emtricitabine (not on drug list: Zidovudine/AZT)
30
What is the MOA of NRTIs?
resembles nucleoside competitive inhibitor of RT --incorporates into DNA
31
What resistance is seen with NRTIs?
mutations in viral RT
32
What toxicities are seen with NRTIs?
lactic acidosis with hepatic steatosis | D/t NRTI mediated inhibition of mitochondrial function --build up of triglycerides --> hepatic steatosis
33
Abacavir
NRTI ADME: guanosine analog administered in combo with lamivudine (or emtricitabine) MOA: nucleoside analog (guanosine) competitive inhibitor of RT --incorporates into DNA unique toxicities: myocardial infarction (caution in CV disease) hypersensitivity reactions associated with HLAb5701 (Can be fatal) Resistance: slow. requires 2-3 RT mutations
34
What is the MOA of abacavir?
NRTI ADME: guanosine analog administered in combo with lamivudine (or emtricitabine) MOA: nucleoside analog (guanosine) competitive inhibitor of RT --incorporates into DNA
35
What toxicities are seen with abacavir?
Unique toxicities: myocardial infarction (caution in CV disease) hypersensitivity reactions associated with HLAb5701 (Can be fatal) in addition to the overall class toxicity of lactic acidosis with hepatic steatosis
36
What resistance is seen with abacavir?
Resistance: | slow. requires 2-3 RT mutations
37
Lamivudine
NRTI Emtricitabine is a fluorinated form of lamivudine --making it have a longer half life (once daily dosing) ``` MOA: nucleoside analog (cystine) competitive inhibitor of RT --incorporates into DNA ``` Indications: HIV combo (administered with tenofovir called truvada) HBV (inhibits HBV RT)
38
What are the indications for lamivudine/emtrictabine?
Indications: HIV combo (administered with tenofovir called truvada) HBV (inhibits HBV RT)
39
What is the difference between lamivudine and emtricitabine?
Emtricitabine is a fluorinated form of lamivudine --making it have a longer half life (once daily dosing)
40
What is the MOA of lamivudine/emtricitabine?
``` MOA: nucleoside analog (cystine) competitive inhibitor of RT --incorporates into DNA ```
41
NtRTIs
nucleoTide reverse transcriptase inhibitors tenofovir
42
Tenofovir
NtRTI ADME: acyclic nucleoTide analog of adenosine given as a pro-drug: disoproxil fumarate (DF) or alafenamide (AF) MOA: competitive inhibitor of HIV RT = chain termination after incorporation into DNA Indication: first line RTI therapy when combined with emtricitabine Toxicities: renal accumulation: tubular necrosis, renal failure, Fanconi's syndrome (less with AF)
43
What is the MOA of tenofovir?
NtRTI ADME: acyclic nucleoTide analog of adenosine given as a pro-drug: disoproxil fumarate (DF) or alafenamide (AF) MOA: competitive inhibitor of HIV RT = chain termination after incorporation into DNA
44
What is the indication for tenofovir?
Indication: | first line RTI therapy when combined with emtricitabine
45
What toxicities are seen with tenofovir?
Toxicities: | renal accumulation: tubular necrosis, renal failure, Fanconi's syndrome (less with AF)
46
NNRTIs
non-nucleoside reverse transcriptase inhibitors efavirenz
47
Efavirenz
NNRTI MOA: binds directly to HIV1 reverse transcriptase and inhibit RNA and DNA dependent DNA polymerase activity no phosphorylation needed since it's not a nucleoside binding site of NNRTIs is distinct from that of NRTIs (allosteric) Drug-drug interactions: Extensive metabolism/induction via CYP3A4 pathway Resistance: can occur rapidly with single mutation in RT Toxicity: nightmares/psychiatric disturbances (at start of therapy, then resolve)
48
What is the MOA of efavirenz?
NNRTI MOA: binds directly to HIV1 reverse transcriptase and inhibit RNA and DNA dependent DNA polymerase activity no phosphorylation needed since it's not a nucleoside binding site of NNRTIs is distinct from that of NRTIs (allosteric)
49
What drug drug interaction are present with efavirenz?
Drug-drug interactions: | Extensive metabolism/induction via CYP3A4 pathway
50
What toxicities are present with efavirenz?
Toxicity: nightmares/psychiatric disturbances (at start of therapy, then resolve)
51
What resistance is present with efavirenz?
Resistance: can occur rapidly with single mutation in RT
52
HIV protease inhibitors
Ritonavir Darunavir Atazanvir ADME: Pepitdomimetics MOA: Inhibits proteolytic cleavage of Gag and Gag-pol in HIV 1 and 2 Drug-drug interactions: Metabolized by, inhibitors of CYP3A4 Toxicities as a class: Redistribution and accumulation of body fat (lipodystrophy) Increase triglycerides/LDL
53
Ritonavir
HIV Protease Inhibitor Inhibitor of CYP3A4 — used with other PIs to increase their serum levels Less frequent dosing (BOOSTER) Taken with food Toxicities: Increase triglycerides/LDL Elevated serum aminotransferase levels
54
Atazanavir
HIV protease inhibitor ``` Toxicities: Hyperbilirubinemia Rash Kidney stones Cholelithiasis ``` Only available as a fixed dose combo with ritonavir since ritonavir inhibits CYP3A4 and increases blood levels
55
Maraviroc
CCR5 receptor antagonist/Entry inhibitor Not first line therapy Binds selectively to CCR5 - one of the two co-receptors necessary for entrance of HIV into CD4+ cells
56
Enfuvirtide
Fusion inhibitors Binds to gp41 subunit of the viral envelope glycoprotein, preventing the conformational changes required for the fusion of the viral and cellular membranes NOT for HIV2 SubQ injection (peptide—long change) Only for treatment experienced HIV pts with ongoing HIV replication
57
Dolutegravir
Integrase strand transfer inhibitors (INSTIs) Inhibits viral DNA strang integration in host genome Toxicities: Hypersensitivity Elevated liver enzymes with HCV/HBV co-infection
58
What is the latest recommendation for PEP?
Pre/pst exposure prophylaxis Raltegravir/dolutegravir + TDF/emtricitabine for PEP TDF/emtricitabine for pre-exposure

Pharm 2 - Exam 4 (9 decks)

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