Term
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Definition
Orally bioavailable but requires acidic medium for absorption.
-Half life is 10
-Adverse effects:
D, N, V, abdominal pain, HA, peripheral neuropathy, rash, elevated hepatic enzymes.
Effects CYP enzymes |
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Term
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Definition
Used in combination with ritonavir in resistance patients.
-adv effects: Because it contains a sulfonamide, used cautiously in patients with allergy to sulfonamides.
Effects CYP enzymes. |
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Term
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Definition
-Another sulfonamide containing PI
-Fosamprenavir is the phosphorylated prodrug of amprenavir that is rapidly hydrolyzed by enzymes in the intestinal epithelium.
-Most often administered in combination with low-dose ritonavir |
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Term
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Definition
Requires an acidic environment for optimal absorption thus must be taken on an empty stomach.
Maximum absorption after oral administration is 65% |
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Term
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Definition
High oral bioavailability that increases with food.
Serum half life = 4-5h.
Metabolized by CYP system.
Excretion in the feces. |
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Term
| Ritonavir (Abbott) adv effects |
|
Definition
Dose related adverse effects include: GI disturbances, paresthesias (i.e., pins and needles), elevated hepatic enzymes, elevated lipids, N,V,D etc. Drug-drug interactions.
May be carcinogenic!
Used in low doses with other PI’s because of its high affinity for the CYP system and it is well tolerated! |
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Term
| Entry Inhibitors: Enfuvirtide |
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Definition
| Binds to GP41 subunit, preventing required conformational changes required for fusion. |
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Term
| Entry Inhibitors: Maraviroc |
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Definition
-Binds specifically and selectively to the cellular CCR5 co-receptor in HIV strains using the CCR5 trophic pathway exclusively (no heteroreceptors).
-Useful in adults that have CCR5 trophic HIV-1 infections resistant to other agents.
-Excellent penetration into cervicovaginal fluids (4x higher than serum). |
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Term
| Entry Inhibitors: Maraviroc resistance |
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Definition
| Resistance is associated with mutations in the GP120 V3 loop (a critical binding domain). |
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Term
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Definition
| Inhibiting integrase from performing its essential functions therefore blocks stable integration of HIV-1 DNA into the host genome and prohibits the establishment of viral latency within the host cell, preventing high-level HIV-1 replication and infection of new cells by competent virus. |
|
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Term
| Integrase Inhibitors: Raltegravir |
|
Definition
Its β-hydroxy-ketone structural motif possesses metal-chelating functions, and it is postulated these functional groups interact with divalent metals within the active site of HIV-1 integrase inhibiting stand transfer, the third and final step in provirus integration.
-Because of this unique mechanism, cross resistance with other antiviral agents does not occur so it is used in patients infected with resistant virus |
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Term
| Raltegravir drug interactions |
|
Definition
| No interaction with CYP450 system |
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Term
|
Definition
| Resistance can occur via a point mutation in codons 148 or 155 (reducing viral replication capacity and thus sensitivity to inhibitors |
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Term
|
Definition
Are host glycoprotein cytokines
-Interferon a triggers inhibition of viral entry, processing, maturation and release programs.
Interferon a also increases the expression of major histocompatability complexes, enhances the phagocytic activity of macrophages and augments proliferation and survival of cytotoxic T cells. |
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Term
|
Definition
Routes of administration differ upon subtype.
Half lives also differ upon sub-type.
Metabolism is by proteolytic cleavage.
Often used as a pegylated derivative resulting in longer half lives and slower metabolism |
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Term
| Interferons (a) adv effects |
|
Definition
Adverse effects include flu-like symptoms (which are typically transient) and elevated liver enzymes.
- |
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Term
| Interferons (a) contraindication |
|
Definition
| Contraindicated in patients with hepatic decompensation, autoimmune diseases and /or a history of cardiac arrhythmia |
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Term
| Adefovir Dipivoxil (a NRTI) moa |
|
Definition
-Phosphorylated by cellular kinases to the active diphosphate metabolite and acts by inhibiting HBV DNA polymerase resulting in chain termination after incorporation into viral DNA.
-It is also active against a wide range of RNA and DNA viruses including HIV and Herpes |
|
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Term
| Adefovir Dipivoxil (a NRTI) activity |
|
Definition
-Antihepatitis B agent
-It is also active against a wide range of RNA and DNA viruses including HIV and Herpes |
|
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Term
| Adefovir Dipivoxil (a NRTI) pk |
|
Definition
| It is orally bioavailable and unaffected my meals. |
|
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Term
| Adefovir Dipivoxil (a NRTI)adv effects |
|
Definition
Well tolerated but long term therapy leads to resistance.
Adverse effects include nephrotoxicity, H, N, V, asthenia and abdominal pain. |
|
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Term
|
Definition
-antihep B agent
An orally administered guanosine nucleoside analog |
|
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Term
|
Definition
Competitively inhibits HBV DNA
Base priming
Reverse transcriptase of the negative strand and
Synthesis of the positive strand.
-anti-hep B agent |
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Term
|
Definition
Does not cure HBV and may not prevent complications of chronic hepatitis B such as cirrhosis of the liver or liver cancer.
Does not prevent the spread of HBV to other people.
-antihep B agent |
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Term
|
Definition
Higher barrier to resistance than lamivudine.
anti-hep B agent |
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Term
| Amantadine (and its a-methyl derivative, rimantadine), are tricyclic amines. |
|
Definition
block the M2 proton ion channel within the viral membrane of the virus particle and inhibit uncoating of the viral RNA within the infected host cells, preventing replications.
-anti-influenza agent |
|
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Term
| Amantadine (and its a-methyl derivative, rimantadine) PK |
|
Definition
Amantadine is well absorbed and 70% protein bound. Plasma half life is 12 – 18 h and varies with creatinine clearance.
Rimantadine is 40% protein bound and has a half life of 24 – 36 h.
-anti influenza |
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Term
|
Definition
Resistance is a single, stable point mutation gene producing the M2 protein.
anti influenza |
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Term
| Amantadine (and its a-methyl derivative, rimantadine), Adv effects |
|
Definition
| Side effects are GI and CNS, with potentially serious neurotoxicity leading to death especially in elderly. |
|
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Term
Oseltamivir (Tamiflu) and Zanamivir
MOA |
|
Definition
Analogs of sialic acid, these compounds interfere with the release of progeny influenza virus A and B from infected to new host cells in the respiratory tract.
-They compete reversibly at the active site of neuraminidase at low nanomolar concentrations, Neuraminidase is responsible for the release of newly produced virions as well as respiratory tract mucins. |
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Term
Oseltamivir (Tamiflu) and Zanamivir
resistance |
|
Definition
Rates of resistance among the H1N1 viruses have risen abruptly, reaching 98% in tested strains in the USA from 2008 and 2009 but!!!
…no strains were resistant to Zanamivir and all Influenza B strains were susceptible to both oseltamivir and Zanamivir. |
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Term
|
Definition
|
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Term
|
Definition
| delivered directly into the respiratory tract IV inhalation. |
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