GYN/Final: anti-virals Flashcards

1
Q

do viruses carry out metabolic processes

A

no

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2
Q

to target viral therapy, we need to target?

A

areas infected by the host

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3
Q

list the respiratory viruses

A

Influenza A, B

RSV

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4
Q

preferred method for tx of the resp viruses

-other tx

A

vaccination *****

Other tx= Neuraminidase inhibitors—for influenza A/B

  • **Oseltamivir
  • **Zanamivir
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5
Q

Oseltamivir

  • MOA
  • Kinetics (routes, metabolism)
  • SE
A

MOA= inhibition of neuraminidase (viruses exhibit this into the host cell for replication of virons)

Kinetics

  • PO
  • Hepatic metabolism

SE

  • N/V
  • take with food
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6
Q

Zanamivir

  • MOA
  • Kinetics (route, excretion)
  • SE
A

MOA=inhibition of neuraminidase (viruses exhibit this into the host cell for replication of virons)

Kinetics

  • inhaled
  • Excreted via urine

SE

  • Irritation of respiratory tract
  • N/V
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7
Q

when do you start neuraminidase inhibitors?

A

within 48 hours of s/s

*after 48 hrs—— cannot give

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8
Q

RSV

  • what is it
  • what is MC infected
  • s/s
  • dx
  • tx
A

viral pathogen that causes severe resp tract infections in INFANTS
***infects mucosal lining of the lung–causing SYNCYTIUM

**lower resp tract most commonly infected

s/s
*onset in premies + infants–>cough, wheezing that does not subside

DX: nasal swab + clinical

Tx: Ribavirin PO or INH

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9
Q

Ribavirin

  • MOA
  • inds
  • routes
  • SE
A

MOA: inhibs replication of RNA and DNA viruses

Inds: RSV

Kinetics

  • PO
  • INH

SE:

  • dose dependent anemia….. elevated bilirubin
  • **most premies have elevated bilirubin already*
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10
Q

list the other viral infections we can treat (5)

A

Active Hep B and C
CMV
HSV 1
HIV

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11
Q

Hep B

-diagnosis for active infection

A
SEROLOGY: 
\+HBsAG 
\+IgM anti-HBc 
\+anti-HBc 
-anti-HBs
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12
Q

what must you always do before tx for Hep B or any other hepatic dz?

A

baseline creatinine

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13
Q

tx for Hep B

  • class of drugs?
  • list them
A

Nucleoside Reverse Transcript inhibitors (NRTIs)

  • Lamivudine
  • Tenofovir
  • Entecavir
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14
Q

Lamuvudine

  • inds
  • moa
  • se
A

inds=HIV***, Acute Hep B
**NOT FOR chronic Hep B bc of resistance

MOA: NRTI

SE:

  • Nausea
  • very well tolerated
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15
Q

Tenofovir

  • inds
  • moa
  • se (4)
A

MOA: NRTI

INDS

  • Acute and chronic HBV infection
  • HIV

SE

  • Depression
  • backache
  • cough
  • N/V/D
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16
Q

Entecavir

  • moa
  • inds
  • se
A

MOA: NRTI

INDS

  • **HBV infection
  • effective against Lamivudine resistant strains

SE=Nephrotoxicity

***needs renal dosing

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17
Q

Which NRTI needs renal dosing

A

Entecavir

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18
Q

Chronic Hep B treatments–list the drug class

A

Interferons: alpha, beta, gamma and pegylated

**Peginterferon alfa-2

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19
Q

Peginterferon-alfa 2

  • MOA
  • inds
  • se
A

MOA: not widely understood— believed to inhibit viral RNA translation

INDS: Chronic Hep B

SE
*Flu like s/s—>fever, chills, myalgias, GI

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20
Q

How does Hep C virus infect liver

A
  • enters hepatocyte–>cleaving proteins–>replication complex–>replicates viral genome
  • very very slow replication **

**proteins that it cleaves= NS3/ Ns4A, NS5A, NS5B— can be inhibited from forming– target of therapy

**DAAs= direct acting antivirals

21
Q

what is DAA

A

direct acting anti-virals

**prevent the proteins NS3/ NS4A,NS5A, NS5B from forming HEp C

22
Q

Hep C treatments– list the drugs

A

Ledipasvir-Sofobuvir**

Ledipasvir=NS5A-replication complex inhib
Sofobuvir=PI

*****Ribavirin and Interferon (but older txs)

23
Q

Ledipasvir-Sofobuvir

  • inds
  • drug class/MOA
A

Hep C infection

NS5A replication comple inhibitor (Ledipasvir) + protease inhibitor (sofobuvir)
–inhibit the proteins on viral cells

24
Q

Ribavirin
-inds

-SE

A

INDS

  • Chronic Hep C + other DAAs
  • Hep C, Hep B, RSV–>good with combination tx for synergism

SE:
*Elevated bilirubin

25
HSV-1 and CMV | -when do the drugs have greatest effect
drugs for tx have greatest effects during ACUTE phase of infections
26
which herpetiform can lay dormant in body for life
CMV (HVV-5)**** and HSV-1
27
when can CMV be fatal | list the s/s
``` immunocomp Congenital CMV ***colitis ***retinitis ***esophagitis ***encephalitis ```
28
list the drugs we use to tx Herpes viruses
* Acyclovir * Cidofovir * Foscarnet * ganciclovir
29
Acyclovir | *inds
INDS---"grandfather of antiherpetic tx agents" * ***TOC in HSV encephalitis * MC use is gential herpes
30
Cidofovir -inds - SE - how to get rid of one of the SE?
INDDS *CMV retinitis in pt with AIDS SE * significant renal toxicity * neutropenia * metabolic acidosis*** Probenecid + NSS IV solution will help decrease risk of developing nephrotoxicity
31
how to decr incidence rate of nephrotoxicty with IV Cidofovir ?
PO probenecid---uricosurics--lowers uric acid in body + IV NSS
32
Foscarnet -inds -se
INDS * CMV retinitis in immunocomp * Acyclovir resistant HSV SE * nephrotoxicity * anemia * nausea * fever * *************HYPOmag and *HYPOcalcemia----can lead to arrhythmias
33
Ganciclovir - INDS - SE
INDS----analog of acyclovir INDS * **greater efficacy against CMV * CMV retinitis * prophylaxis in transplant PTs SE * Dose dep neutropenia * carcinogenic * teratogenic
34
which is better for kidneys--- acyclovir or ganciclovir
Ganciclovir
35
HIV - list the drugs used to tx (6) - comination of drugs are called?
ANTI-RETROVIRALS: NRTIs NON NRTIs Protease inhibitors (PIs) Entry inhibitors Integrade inhibitors Boosters
36
Nucleoside reverse transcriptase inhibitors - list them (3) - MOA - routes - SE - resistance?
1. Lamivudine---PO 2. Tenofovir---PO 3. Zidovudine---PO, IV (only one) Resistance
37
what drug class was the first agents available to tx HIV
Nucleotide reverse transcriptase inhibs
38
Non NRTIs | -MOA
MOA-->highly selective noncompetitive inhibitors of HIV reverse trnascriptase -->bind to allosteric site next to active site-->then cause a conformational change-->results in enzyme inhibition *****not as great as NRTIs
39
Protease Inhibitors - drug names - name the MC one and why its MC - SE
MC ONE: Atazanavir bc it has least SE profile *Lopinavir/Ritonavir -avir SE * hypertriglyceridemia * parasthesias * hyperglycemia
40
which drug class lowered mortality rates in HIV patients
Protease Inhibitors
41
which drug class lowered mortality rates in HIV patients
Protease Inhibitors
42
List the protease inhibitors
MC=Atazanavir Lopinavir/Ritonavir
43
list the drugs that cannot be administered with Protease Inhibitors (10) -ex of each category
1. H2 Blockers--- bc it needs acidic envi for absoprtion 2. Antiarrhythmics-->Amiodarone 3. Ergot Derivatives 4. Antimycobacterial drugs--Rifampin 5. Benzos--Triazolam 6. Inhaled corticos---fluticasone 7. herbals--st. johns wort 8. HMG CoA Reductase Inhibitors-->Lovastatin, Simvastatin 9. Fentanyl 10. B2 agonists---Salmeterol
44
Entry Inhibitors | -MOA
MOA * work on entry of HIV into the host cell * block conformational change that is necessary for HIV cell to enter host cell
45
Enfuviride - drug class - route - se
- entry inhibitors - SQ only - not given to tx in Naive patients (pt who never had this tx b4)
46
Maraviroc - drug class - route - se
- entry inhibitors - PO - hepatoxicity
47
Integrase Inhibitors (INSTIs) - MOA - drugs - SE - reistance?
MOA * inhibits insertion of pro viral DNA into host cell-->for this to work----active site of integrase inhibitor binds to DNA and serves as a target for the INSITI * INSTI stops viral integration * Raltegravir * Elvitegravir * Dolutegravir * Bictregravir SE * well tolerated * N/D MC Resistance can occur
48
Pharmacokinetic Enhancers | -aka?
BOOSTERS MOA *two drugs are used to enhance bioavail of the drugs used in combination therapy for HIV Drugs: *Ritonavir & Cobicistat-->works as a potent inhibitor of CYP3A which allows the bioavail of a concomitant dose PI----boost PI to help prevent resistance