Pharm Test 2 Antivirals

Front 1

1)Viral Life cycle steps?

Back 1

1)Recognize receptor, Attach, Penetrate, Entry, Uncoating, Replication, RNA and Protein Synthesis, Assembly and Maturation, Release

Front 2

Respiratory Viral Infections (Influenza A, B, RSV)

1)The 2 neuraminidase inhibitors
2)The 2 inhibitors of viral uncoating
3)The Synthetic Guanosine Analog

Back 2

1)Oseltamivir, Zanamivir

2)Amantadine, Rimantadine

3)Ribavirin

Front 3

Neuraminidase inhibitors:

1)What do they do?
2)Effective Against?
3)How do you use?
4)MOA

Back 3

1)Inhibit viral release

2)Both Influenza A and B


3)Can administer as prophylaxis (BEST USE) or 24 to 48 hour infection (only modest effect)

Front 4

Neuraminidase Inhibitors:

4)MOA

5)How do you take Oseltamivir (Tamiflu)? Zanamivir?

6)How are both drugs eliminated? Thus what drug can you give so that can give lower conc of these 2 drugs (d/t decreased secretion)

Back 4

4)normally, virus binds to receptor containing sialic acid (a hemagglutinin) on cell and uses to enter. To then exit cell and infect other cells, must cleave this receptor with Neuraminidase. So if inhibit neuraminidase, cell CANT RELEASE virus (thus very useful for prophylaxis, not as much for after infection, because cells already infected)(drug only prevents further infections)

5)Oseltamivir -> Orally Active (activated by liver)
Zanamavir -> Must be inhaled (not orally active)

6)Unchanged in urine. Probenecid (doubles the level of the drug in blood)

Front 5

Neuraminidase Inhibitors:

5)AE of Oseltamivir
6)AE of Zanamivir
7)How get resistance?

Back 5

5)GI Probs (lessened with food)

6)Airway irritation (dont give to Severe Asthma, COPD) (NO GI Probs)

7)Neuraminidase mutations

Front 6

Oseltamivir (Tamiflu)

Back 6

Oral Neuraminidase Inhibitor

Front 7

Zanamivir

Back 7

Inhaled Neuraminidase Inhibitor

Front 8

Ion Channel Blockers (Amantadine, Rimantadine)

1)What do they do?
2)Effective Against
3)How do you use?

Back 8

1)Act on the uncoating step

2)ONLY Influenza A
(because target onlly expressed on A)

3)Equally protective for Prophylaxis and Treatment, and dont impair the activity of the vaccine)

Front 9

Ion Channel Blockers

1)MOA
2)How are both given?
3)What are the 2 difference between Amantadine and Rimantadine?

4)Which of the 2 would you give to renal impaired?

Back 9

1)normally, M2 (H+ Channel) required for fusion of virus with cell membrane so can form an endosome-> drug blocks M2 (H+ Channel) (specific to Influenza A), so cant make endosome and thus cant uncoat

2)Oral

3)Amantadine can cross the BBB, and Rimantadine can NOT;
-Amantadine is NOT metabolized and accumulates in urine (as active) (thus renal impaired more at risk to amantadine); Rimantadine IS metabolized and eliminated by kidney (no risk to kidney)

4)Rimantadine

Front 10

Ion Channel Blockers

1)AE to Amantadine?
2)AE to Rimantadine
3)Who should you not give Amantadine too?

4)CONTRA for both Amantadine and Rimantadine?

Back 10

1)CNS (10%) (insomnia, dizzy, ataxia->hallucinate, seizures) (so be careful with patients that already have neuro problems)

2)No CNS problems because does not cross BBB

3)Patients with renal problems or psychiatry disorders

4)Pregnancy, Nursing (FDA Cat C)

Front 11

Ion Channel Blockers

1)Resistance?
2)Can use for prophylaxis?

Back 11

1)HUGE PROBLEM (50%)
Cross Resistance does occur (give to 1 and have resistance -> will also be resistance to other drug)

2)NO! use is restricted d/t resistance, only give if no other option (like swine flu)

Front 12

Amantadine

Back 12

Ion Channel Blocker

(not to be given to neuro and renal)

Front 13

Rimantadine

Back 13

Ion Channel Blocker

(safe for neuro and renal)

Front 14

Ribavirin

1)What is it?
2)Effective Againsts
3)MOA

Back 14

1)Purine/Pyrimadine analog that inhibits DNA/RNA synthesis

2)Broad Spectrum (RNA and DNA viruses -> RSV,HCV,Lassa Virus)

3)activated to ribavirin-triphosphate -> inhibits guanosine triphosphate formation -> prevents viral mRNA CAPPING (thus cant stabalize mRNA) -> inhibits RNA dependent RNA polymerase

Front 15

Ribavirin

1)AE
2)Contra

Back 15

1)DOSE DEPENDENT transient anemia (because can bind to RBC) (see inc bilirubin)

2)Pregnancy (FDA Cat X) (IN NO CIRCUMSTANCES CAN U GIVE IT) (very teratogenic) (must give pregnancy test before can give) (because can give in Aerosol form, someone that is taking it, cant live in same household as someone that is pregnant)

Front 16

1)Most common causes of chronic hepatitis, cirrhosis, and hepatocellular carcinoma are?

2)What are the interferon drugs used to treat hepatic viral infections?

3)What are the nucleotide/nucleoside analogs used to treat hepatic viral infections?

4)What do both these types of drugs do?

Back 16

1)Hepatitis B and C

2)interferon alpha, beta, gamma

3)Lamivudine, Adefovir, Entecavir, Telbivudine

4)Both prevent RNA/DNA Synthesis

Front 17

Interferons

1)MOA

2)How do you give?

3)AE

Back 17

1)use your own immune response (so not directly targeting virus genes) to induce protein expression to inhibit virus RNA and DNA synthesis (interferons are naturally part of ur immune system, and also made synthetically)

2)Must be taken IV, subcutaneously, or intalesionally (takes longer to be absorbed, because normally proteins, easily broken down)

3)Flu Like Symptoms

Front 18

Interferons

4)Effect on Theophylline
5)Effect on Zidovudine

Back 18

4)Inc accumulation (d/t impaired liver metabolism)

5)potentiate its myelosuppression

Front 19

Interferons

6)CU of Interferon Alpha

Back 19

6)HBV, HCV, Condyloma Acuminata, Hairy Cell Leukemia, Kaposi's Sarcoma

7)Multiple Sclerosis

Front 20

Nucleoside/Nucleotide Analogs

1)Are they active?

2)What's the problem with these drugs?

Back 20

1)No, Must be phosphorylated by cellular enzymes to Triphosphate (Active) form

2)When take patient off of them, can have severe worsening of hepatitis

Front 21

Lamivudine

1)MOA
2)CU

Back 21

1)competitively inhibits HBV DNA Polymerase

2)HBV, HIV

Front 22

Adefovir

1)MOA
2)CU
3)Why is this drug special?

Back 22

1)incorporated into viral DNA -> terminates DNA synthesis

2)HIV and hepatic viruses

3)Can be given only once a day (better for compliance)

Front 23

Entacavir

1)MOA

2)CU

3)What must you do before give this drug?

Back 23

1)competes with deoxyguanosine triphosphate for viral reverse transcriptase -> inhibits DNA/RNA synthesis

2)Lamivudine Resistant Strains of HBV (thus no cross resistance between the drugs of this group)
HIV

3)Assess renal function because fully excreted into kidneys in its active form

Front 24

Telbivudine

1)MOA

2)CU

3)What is this drug special?

Back 24

1)either competes w/ thymidine triphosphate, or incorporates into viral DNA -> terminates DNA chain elongation

2)NOT EFFECTIVE ON HIV
just hepatic viruses

3)Oral once a day administration

Front 25

1)What is special about the herpes virus?

2)What are the purine/Pyrimidine Analogs

3)The 2 other drugs are?

4)What do all these drugs do?

Back 25

1)Can form latent infection; Drugs made are only for actively replicating virus (can do nothing for the latent infection)

2)The 5 Ovir's and Vidarabine and Trifluridine

3)Fomivirsen and Foscarnet

4)They all effect DNA/RNA synthesis

Front 26

Acyclovir

1)CU
2)DOC
3)Used commonly in what types of infections?
4)What is big problem in this drug?

Back 26

1)HSV 1 and 2
Varicella Zoster (VZW)
EBV (HSV 4)

2)HSV Encephalitis

3)Genital herpes
Prophylaxis for immunocompromised and transplant patients
4)Resistance

Front 27

Acyclovir

5)Minimal activity against?

6)MOA

Back 27

5)CMV (does not have the necessary phosphorylation enzyme)

6)requires 3 phoshorylation steps to be activated -> is MONOphosphorylated by herpes encoded enzyme THYMIDINE KINASE (thus only effective against virus infected cells)(very selective)->host cell completes the Di and Tri phosphorylation -> competes with dGTP and incorporated into DNA ->causes chain termination and in inhibits viral DNA polymerase

Front 28

Acyclovir

6)How do you give?

7)AE

8)Resistance?

Back 28

6)IV, oral, topical (herpes can present in many ways)

7)Depends on route of admin:
topical -> local irritation
oral -> headache, GI

8)Altered or deficient thymidine kinases causes this (THERE IS CROSS RESISTANCE TO OTHER CYCLOVIRS) (IF RESISTANT TO ACYCLOVIR, likely also to rest)

Front 29

Cidofovir

1)CU
2)Difference wth Acyclovir
3)MOA

Back 29

1)CMV Induced Retinitis in HIV/AIDS

2)NOT phoshorylated by viral kinases (thus not as specific)
Requires activation by host cell kinases

3)DNA Chain terminator and DNA polymerase Inhibitor

Front 30

Cidofovir

1)How do you give?
2)What drug do you NEED to give it with?
3)AE
4)Resistance?

Back 30

1)IV, IntraVITREAL, TOpical

2)Probenecid (blocks tubular secretion, so wont lose drug out of kidney)

3)Nephrotoxicity (dec when give with Probenecid)

4)get if mutation to viral DNA Polymerase

Front 31

Ganciclovir

1)DOC for?
2)What is its oral viersion?
3)Which is more potent, Acyclovir or this?

Back 31

1)CMV Retinitis, and CMV Prophylaxis in Immunocompromised

2)Valganciclovir (but metabolized to ganciclovir in intestine and liver)

3)THIS
4)Phosphorylation by Viral and Celll Kinases -> DNA chain termination and DNA polymerase inhibitor

Front 32

Ganciclovir

1)AE
2)Contra
3)Resistance?

Back 32

1)Myelosuppression
Severe DOSE DEPENDENT neutropenia

2)Pregnancy (FDA Cat C)

3)get if dec intracellular phosphorylation or mutations in viral DNA polyermerase

Front 33

Famciclovir

1)Converted to?
2)CU
3)Penciclovir CU
4)Famciclovir CU

Back 33

1)Penciclovir (thus famciclovir is prodrug)

2)HSV 1,2
VZW

3)Topical treatment of HSV (Cold Sores) (is TOPICAL)

4)Acute Herpes Zoster
Recurrent Genital HErpes infections in Immunocompromised

Front 34

Famciclovir

5)MOA
6)How give penciclovir, how give famciclovir?
7)What penciclovir different from Acyclovir?

Back 34

5)DNA chain termination and DNA polymerase inhibitor

6)Penciclovir -> Topical
Famciclovir - > Oral

7)Penciclovir has 20-30x greater half life

Front 35

Vidarabine

1)CU
2)MOA
3)Given As
4)AE

Back 35

1)Limited to treatment of Immunocompromised Patients with Herpes and Vaccine Keratitis and HSV Keratoconjunctivitis

2)converted to Triphosphate and inhibits viral DNA synthesis

3)Opthalmic ointment
4)Eye problems: Pain, photophobia, Punctate keratitis

Front 36

Trifluridine

1)DOC
2)MOA
3)How to give

Back 36

1)HSV keratoconjunctivitis
REcurrent Epithelial Keratitis

2)incorporated into viral DNA causing fragmentation

3)Opthalmic ointment (very short half life, must be given multiple times a day)

Front 37

Fomivirsen

1)CU
2)MOA
3)How to give
4)AE

Back 37

1)Other therapies for CMV Retinitis fail

2)binds to CMV mRNA inhibiting CMV protein synthesis

3)Intravireally
4)Iritis, Vitriits, Changes in vision and inc Intraoc pressure

Front 38

Foscarnet

1)CU
2)MOA
3)How do you give?
4)AE

Back 38

1)CMV retinitis in immunocompromised patients
Acyclovir resistant HSV and CMV Retinitis
Ganciclovir Resistant CMV and VZW

2)does not require phosphorylation (activation);
Selectively inhibits virus specific DNA polymerase and Reverse transcriptase

3)IV

4)Nephrotoxicity
Hypocalcemia

Front 39

PRINT OUT SUMMARY OF ANTI VIRAL DRUG CHART AT END

Back 39

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Front 40

1)Neuroaminidase inhibitors used to treat?

2)Inhibitors of Viral Uncoating used to treat?

3)Synthetic Guanosine Analog Used to treat?

Back 40

1)Influenza A and B

2)Influenza A, Parkinsonism (amantadine

3)RSV, Hep C (with interferons)

Front 41

Treat

1)HCV, HBV, HSV8, Hairy Cell LEukemia, Codyloma Acuminatum

2)Multiple Sclerosis

3)HIB, HIV

Back 41

1)Interferon alpha

2)Interferon Beta

3)Nucleoside Analogs (Telbivudine does not work for HIV)

Front 42

Treat

1)HSV,VZW
2)CMV Retinitis

3)DOC for CMV Retinitis and CMV Prophylaxis

4)Herpes Simplex Cold Sores

Back 42

1)Acyclovir
2)Cidofovir
3)Ganciclovir
4)Penciclovir

Front 43

Treat

5)Acute VZW, and Recurrent Genital Herpes infections in Immunocompromised

6)HSV Keratitis or Keratoconjunctivities in Immunocompromised

Back 43

5)Famciclovir

6)Vidarabine or Trifluridine