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Pharmacology > GYN/Final: anti-virals > Flashcards

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
Q

HSV-1 and CMV

-when do the drugs have greatest effect

A

drugs for tx have greatest effects during ACUTE phase of infections

26
Q

which herpetiform can lay dormant in body for life

A

CMV (HVV-5)** and HSV-1

27
Q

when can CMV be fatal

list the s/s

A 
immunocomp 
Congenital CMV 
***colitis 
***retinitis 
***esophagitis 
***encephalitis
28
Q

list the drugs we use to tx Herpes viruses

A
  • Acyclovir
  • Cidofovir
  • Foscarnet
  • ganciclovir
29
Q

Acyclovir

*inds

A

INDS—“grandfather of antiherpetic tx agents”

  • ***TOC in HSV encephalitis
  • MC use is gential herpes
30
Q

Cidofovir
-inds

  • SE
  • how to get rid of one of the SE?
A

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
Q

how to decr incidence rate of nephrotoxicty with IV Cidofovir ?

A

PO probenecid—uricosurics–lowers uric acid in body
+
IV NSS

32
Q

Foscarnet
-inds

-se

A

INDS

  • CMV retinitis in immunocomp
  • Acyclovir resistant HSV

SE

  • nephrotoxicity
  • anemia
  • nausea
  • fever
  • *****HYPOmag and *HYPOcalcemia—-can lead to arrhythmias
33
Q

Ganciclovir

  • INDS
  • SE
A

INDS—-analog of acyclovir

INDS

  • **greater efficacy against CMV
  • CMV retinitis
  • prophylaxis in transplant PTs

SE

  • Dose dep neutropenia
  • carcinogenic
  • teratogenic
34
Q

which is better for kidneys— acyclovir or ganciclovir

A

Ganciclovir

35
Q

HIV

  • list the drugs used to tx (6)
  • comination of drugs are called?
A

ANTI-RETROVIRALS:

NRTIs

NON NRTIs

Protease inhibitors (PIs)

Entry inhibitors

Integrade inhibitors

Boosters

36
Q

Nucleoside reverse transcriptase inhibitors

  • list them (3)
  • MOA
  • routes
  • SE
  • resistance?
A
  1. Lamivudine—PO
  2. Tenofovir—PO
  3. Zidovudine—PO, IV (only one)

Resistance

37
Q

what drug class was the first agents available to tx HIV

A

Nucleotide reverse transcriptase inhibs

38
Q

Non NRTIs

-MOA

A

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
Q

Protease Inhibitors

  • drug names
  • name the MC one and why its MC
  • SE
A

MC ONE: Atazanavir bc it has least SE profile
*Lopinavir/Ritonavir

-avir

SE

  • hypertriglyceridemia
  • parasthesias
  • hyperglycemia
40
Q

which drug class lowered mortality rates in HIV patients

A

Protease Inhibitors

41
Q

which drug class lowered mortality rates in HIV patients

A

Protease Inhibitors

42
Q

List the protease inhibitors

A

MC=Atazanavir

Lopinavir/Ritonavir

43
Q

list the drugs that cannot be administered with Protease Inhibitors (10)
-ex of each category

A
  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
Q

Entry Inhibitors

-MOA

A

MOA

  • work on entry of HIV into the host cell
  • block conformational change that is necessary for HIV cell to enter host cell
45
Q

Enfuviride

  • drug class
  • route
  • se
A
  • entry inhibitors
  • SQ only
  • not given to tx in Naive patients (pt who never had this tx b4)
46
Q

Maraviroc

  • drug class
  • route
  • se
A
  • entry inhibitors
  • PO
  • hepatoxicity
47
Q

Integrase Inhibitors (INSTIs)

  • MOA
  • drugs
  • SE
  • reistance?
A

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
Q

Pharmacokinetic Enhancers

-aka?

A

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

Pharmacology (28 decks)

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