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pharm 3 > viruses > Flashcards

viruses Flashcards

1
Q

viruses

A

obligate intracellular parisites

adsorption, uncoating, multiplication, assembly, release

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2
Q

immunization

A

most effective option
Active: vaccination
Passive- injection of immune globulin often blocks viral penetration, lasts a few weeks

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3
Q

palivizumab

A

humanized monoclonal Ab to prevent sever RSV in high risk pediatric patients

MOA: binds to fusion protein of RSV to prevent fusion to host cells

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4
Q

amantadine and rimantadine

A

Amantadine and rimantadine

Use: prophylaxis against influenza A but not influenza B

primary use: prophylaxis of influenza A
therapeutic use: for influenza A, reduces fever in 50% of pts and illness duration by 1-2 days if given within first 2 days of illness, for the last several years flu strains have been amantadine-resistant

MOA: blocks viral uncoating by interfering with influenza A M2 protein (an ion channel)

admin oral and well distributed

metabolism: rimatidine- liver metabolism, amantidine, renal (avoid in renal diseasE)
toxicity: amantadine: CNS - slurred speech anxiety

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5
Q

oseltamivir

A

MOA: prodrug, competitive inhibitor of influenza neuraminidases, interferes with viral release and viral penetration

Uses: treatment of uncomplicated influenza A and B, given within 48 hours of symptom onset, influenza prophylaxis, admin- oral

SE: nausea/vomiting/diarrhea, bronchitis, cough

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6
Q

trifluridine

A

MOA: interferes w/DNA synthesis, thymidine analog

Use: ophthalmic- herpes simplex types 1 and 2 (conjunctivis)

SE: burning stinging, hypersensitivity

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7
Q

acyclovir

A

MOA: phosphorylated form is produced 40-100x faster in infected cells by herpes thymidine kinase, inhibits herpes DNA polymerase 10-30x more than host cell DNA polymerase, acts as a competitive inhibitor of dGTP and as a DNA chain terminator

Use: intravenous drug of choice for serious systemic herpes simplex virus (HSV), disseminated neonatal HSV, severe initial genital herpes

Oral: primary genital herpes, primary herpetic gingivostomatosis

Topical: some effect when applied early to primary genital herpes

Rash, itch, headache and fatigue

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8
Q

famcyclovir

A

MOA: Similar to acyclovir, prodrug converted to peniciclovir phosphorylated, inhibits viral DNA polymerase

Use: acute herpes zoster (shingles) 3 days duration, treatment and suppression of recurrent genital herpes

Admin/excretion: prodrug absorbed better than acyclovir,

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9
Q

Peniciclovir

A

MOA: very similar to acyclovir
Use: recurrent herpes of the lips and face
adminL topical

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10
Q

Ganciclovir

A

MOA: same as acyclovir, but monophosphorylation is catalyzed by CMV protein kinase

Use: CMV retinitis in aids pts, CMV prophylaxis for transplant ptss

Toxicity: bone marrow suppression, leukopenia, thrombocytopenia, anemia

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11
Q

Foscarnet

A

MOA: inhibits CMV DNA polymerase by binding to its pyrophosphate-binding site

Does not require conversion to triphosphate form to be active

Use: AIDS pts with CMV retinits, approved for acyclovir-resistant herpes simplex

SE: renal damage, electrolyte imbalances, seizures

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12
Q

Lamivudine

A

MOA: nucleoside analog converted by cell enzymes to the triphosphate form, that competitively inhibits the reverse transcriptase domain of the HBV polymerase, causes DNA chain termination

Use: approved for hepatitis B

Toxicity: nausea, diarrhea, rash and vomiting

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13
Q

tenofovir

A

MOA: monophospate prodrug, phosphorylated by cell enzymes to triphosphate form that completitively inhibits the reverse trascriptase domaine if the HBV polymerase, causes DNA chain terminateion

Use: approved for hepatitis B

Toxicity GI upset, rash, headache

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14
Q

interferon a general information

A

most cells produce IFN a and B in response to viral infections

They are potent cytokines that have multiple antiviral effects both directly and indirectly. stimulate cytotoxic lymphocytes and natural killer cells, activate proteins that block viral mRNA transcription. Block viral mRNA protein translation in many ways (decrease mRNA cap methylation, activate oligoadenylate synthase, activates protein kinase P1, activates phosphodiesterase). Inhibits glycosyltransferase , blocks viral release

Therapeutic use relies on large scale production of recombinant human interferon

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15
Q

approved antiviral uses for recombinant alpha-interferons

A

Condyloma acuminata (venereal warts, papilloma virus)

Hepatitis B and C (used in combination with other drugs)

Pegylation decreases clearance

SE: flulike syndrome, leukopenia, bone marrow suppression, neurotoxicity, myalgia

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16
Q

Ribavirin

A

MOA: interferes with viral mRNA synthesis, inhibits inosine 5-P dehydrogenase and thus GTP synthesis (mono form), Tri form inhibits GTP-dependent capping of viral mRNA

Use: aerosol use in infants and young children with documented severe lower respiratory syncytial virus (RSV), hepatitis C in combo with PEG-interferon a and other drugs

SE: Aerosol use (drug may precipitate in and clog respiratory equipment), pulmonary function deterioration, rash

IV or oral use: hemolytic anemia, bone marrow suppression

17
Q

Simeprevir

A

MOA: reversibly inhibits hepatitis C NS3/NS4A protease and blocks cleavage of the polyprotein and formation of infectious virus

Use: hepatitis C genotype 1 in combo with other drugs

Toxicity: Rash, nausea itching, inhibitor CYP3A

18
Q

sofosbuvir

A

MOA: nucleoside analog prodrug, converted to triphosphate form that inhibits HCV NS5B RNA polymerase, causes chain termination

Use: all hepatitis C genotypes, given with other genotype-specific drugs

Toxicity: avoid potent inducers of p-glycoprotein (Pgp)

19
Q

ledipasvir

A

MOA: inhibits HCV NS5A phosphoprotein

use: hep C genotypes 1 4 5 6 in combo with sofosbuvir

SE: avoid potent inducers of P-glycoprotein (Pgp)

20
Q

HCV (hep c virus) drug regimen

A

use 2 or more drugs with different mechanisms, avoid IFNa when possible, genotype-appropriate therapy, look at side effects

21
Q

Zidovudine AZT

A

MOA: nucleoside analog, AZT triphosphate competitively inhibits reverse transcriptase (RT) also acts as DNA chain terminator

Use: nucleoside RT inhibitor for treatment of HIV in adults and children

Toxicity: bone marrow suppression, neutropenia, anemia, drugs that inhibit glucuronyl transferase increase hematologic toxicity of AZT and should be avoided, myopathy

22
Q

tenofovir

A

MOA: adenosine monophosphate prodrug –> tiphosphate form that competitively inhibits RT, causes DNA chain termination

Use: combination therapy for HIV-infected patients

23
Q

lamivudine

A

MOA: nucleoside analog to triphosphate form that cometitively inhibits reverse transcriptase, causes DNa chain termination

Use: synergistic with AZT, its difficult for HIV to become resistant to both drugs

24
Q

emtricitabine

A

MOA: analog of lamivudine, samee MOA as lamivudine

Use: combo therapy for HIV

25
Q

Abacavir

A

MOA: nucleoside analog triphosphate form inhibits RT and causes DNA chain termination

Use: combo therapy for HIV

Toxicity: hypersensitivity reactions (HLAB 5701 antigen) potentially fatal

26
Q

SEs of all NRTI

A

lactic acidosis, hepatic steatosis

27
Q

efavirenz

A

MOA: NNRTI does not require phosphorylation for activity

Use: as part of multidrug therapy for HIV

SE: rash CNS/psychiatric symptoms, nightmares

28
Q

aspartic protease

A

lopinavir, ritonavir

Use: incombination with inhibitors of RT, significantly decreases viral blood load, ritonavir used to boost levels of other PIs

MOA: prevents viral protease from cleaving Gag-pol polypeptide into separate functional proteins, competitive inhibitor, results in non-infectious viral particles

SE: diabetes, alterations in lipid metabolism, fat redistribution, alters metabolism of many drugs (CYP3A inhibitor)

lopinavir- diarrhea
ritonavir- avoid other drugs metabolized by CYP3A, its also used to boost levels of other protease inhibitors

29
Q

fusion inhibitors

A

Enfuvirtide

Use: effective against HIV 1 only, for treatment-experienced HIV patients with detectable viral replication despite ongoing therapy

MOA: inhibits the fusion of viral (HIV-1) and cellular (CD4+) membranes, binds to gp41 subunit of HIV glycoprotein, blocking membrane fusion

SE: local injection site reactions, diarrhea, nausea, fatigue

30
Q

Maraviroc

A

Use: treatment of CCR5-tropic HIV1, works of strains resistant to other drugs

MOA: chemokine co-receptor (CCR5) antagonist blocks entry of HIV into cells

SE: heptotoxicity, cardiovascular events (ischemia, MI)

31
Q

Raltegravir

A

Use: treatment of HIV 1, works on virus that is resistant to other drugs

MOA: inhibits HIV 1 integrase, preventing integration of HIV1 DNA into the genome

SE: skin and hypersensitivityd reactions, myopathy

32
Q

HIV therapy

A

Use 3 or more drugs per pt (2 or more drug classes)

keep replication at zero to prevent resistance)

Start therapy asap

pharm 3 (11 decks)

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