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Pharm Exam 3 > Viruses > Flashcards

Viruses Flashcards

1
Q

Influenza Virus

A
  • causes acute respiratory illness
  • ss RNA

Influenza A : most common, pathogenic
Hemagglutinin & Neuraminidase surface proteins

Influenza B

Influenza C

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2
Q

Amantidine

A

Prevent & treat influenza A virus

MOA: inhibit uncaring of viral RNA ; preventing replication

Crosses BBB = CNS effects = Parkinson disease (increase CNS dopaminergic response)

Monitor renal function

CDC does not recommended for influenza A d/t CNS effects & renal function

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3
Q

Rimantidine

A

Prevent & treat influenza A virus

MOA: inhibit uncaring of viral RNA ; preventing replication

Crosses BBB = less CNS effects than amantidine = Parkinson disease (increase CNS dopaminergic response)

Monitor renal function & LFTs

CDC does not recommended for influenza A d/t CNS effects & renal function

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4
Q

Oseltamivir

A

Prevention & treatment of influenza A and B viruses

MOA: inhibits neuraminidase of influenza A and B ; preventing release of vision from the host cell and prevent entry

Prodrug , ORAL agent
GOLD STANDARD

Being within TWO DAYS OF ONSET

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5
Q

Zanamivir

A

Prevention & treatment of influenza A and B viruses

MOA: inhibits neuraminidase of influenza A and B ; preventing release of vision from the host cell and prevent entry

Prodrug , ORAL INHALATION
* coadminister with bronchodilator (albuterol)

Avoid in dairy allergy
* CONTAINS MILK

Being within TWO DAYS OF ONSET

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6
Q

Herpesvirus

DNA or RNA
Monitoring what in these drugs
Nucleoside analogs

A

ds-DNA
(HSV-1/2, CMV, VZV, EBV)

Monitoring Renal function with these drugs

Nucleoside analogs ; synthetic analogs of purines or pyrimidines that inhibit viral replication

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7
Q

Trifluridine

A

Herpes Drug

OCULAR HSV

Ophthalmic solution formation only - refrigerate
Treat for 7 additional days

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8
Q

Cidofovir

A

Herpes Drug

CMV infections* ; HSV activity
HHV agent - Pyrimidine analog
Good for systemic spread, CMV meningitis

IV only** = RENALLY TOXIC = hydrate prior to therapy
May be given with probenecid to maintain plasma concentrations

*Measure I&O

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9
Q

Acyclovir

A

HSV, VZV - Herpes Virus

Only effective against actively replicating virus **
Not effective against latent virus

Oral, IV, Topical

IV formulation renally toxic === hydrate

Poor bioavailability (Valacyclovir)

Monitor renal function

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10
Q

Valacyclovir

A

HSV, VZV - Herpes Drug

Prodrug of acyclovir (better bioavailability)

Only active against replicating virus

ORAL formulation only **

Better bioavailability vs acyclovir - less frequent dosing

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11
Q

Famciclovir

A

Prevention and Treatment of HSV and VZV
- good for chicken pox

Prodrug of penciclovir - better bioavailability

MOA: Uses viral thymidine kinase for activation for activation - inhibits viral DNA polymerase - preventing viral DNA synthesis

Monitor renal function

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12
Q

Penciclovir

A

Treatment of HSV infection (H. Labialis, H. facials)

Active metabolite of famciclovir

Uses viral thymidine kinase for activation

TOPICAL formulation only
“pen” ~ writing on top of paper ~ topical

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13
Q

Ganciclovir

A

Treatment and Prevention of CMV infection only

Oral, IV, topical ophthalmic, intravitreal implantation

IV infusion in large peripheral veins or central vein
IV formulation is really toxic ==== HYDRATE

Monitor

  • CBC w/ diff == hematological effects
  • LFTs
  • Renal function
  • Serum electrolytes
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14
Q

Valganciclovir

A

Prevention and Treatment of CMV infections

Prodrug of ganciclovir

Oral tablet - take with food!

Monitor:

  • CBC w/ diff
  • Renal function

oral product, if pt has CMV in the hospital and has been treated and safe to D/C will transfer to this oral agent

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15
Q

Foscarnet

A

Prevention and treatment CMV; treatment of HSV & VZV

MOA: not a nucleoside analog (inorganic pyrophosphate analog)

  • inhibits viral specific DNA polymerases and RT at pyrophosphate binding site
  • *** does not require thymidine kinase = good for HSV deficient in kinases

IV formulation only

  • ** accumulates in bone and cartilage
  • Renal toxic == hydrate

Monitor:

  • Chem 10 : for renal function and electrolyte loss
  • CBC w/ diff - d/t bone marrow suppression
  • ECG changes - AV block, ST wave changes
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16
Q

Hep A

A

Incubation period 14 - 28 days

Does not cause chronic disease
Person to person exposure
fecal - oral route

Check HAV IgG/IgM antibodies

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17
Q

Vaqta

A

HAV vaccine

HAV only

Indication : > 12 months of age
2 dose - 2nd dose 6-18 months later

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18
Q

Havrix

A

HAV vaccine

HAV only

Indication : > 12 months of age
2 dose - 2nd dose 6-12 months later

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19
Q

Twinrix

A

HAV vaccine

HAV / HBV combo ** only one

Indication : > 18 y/o
3 dose -
2nd = @ 1 month
3rd @ 6 months

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20
Q

Results for Acute infected / highly infectious HBV

A

+ : HBsAg, HBcAg, Anti-HBc, HBeAg

  • : Anti- HBs
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21
Q

Results for chronic infection HBV

A

+ : HBsAg, HBcAg, Anti-HBc
+/- : HBeAg

  • : Anti- HBs
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22
Q

Results for resolved infection or

immune d/t natural infection

A

+ : Anti- HBs, Anti-HBc

  • : HBsAg, HBcAg, HBeAg
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23
Q

Immune due to vaccination

A

Only positive Anti-HBs

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24
Q

Hepatitis B

DNA or RNA
ROT
Monitoring with these drugs

A

ds-DNA-RT

Blood, sexual

Monitoring LFTs/ Renal
all renal dosed CrCl <50

  • Renal function
  • LFTs
  • HBV labs (viral load, serologies)
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25
Q

Peg-interferon Alfa - 2a

Inferferon Alfa 2b

A

HBV drug

MOA: activate NKC and macrophages ; inhibits viral protein production

Peg - administered SQ ; hepatic dosing
Interfron - administered IV, IM, SQ

**CNS EFFECTS

Monitor:

  • Anemias - CBC w/ diff
  • Infections - chest x-ray
  • Arrhythmias - EKG
  • LFTs
  • Hypothyroidism - thyroid function
  • PSYCH CHANGES - moods

not using these d/t arrhythmias, mood changes & secondary infections

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26
Q

Adefovir

A

HBV
- effective against Iamivudine - resistant HBV *** 184 mutation seeing used the most

Oral tablet

MOA: prodrug metabolized by cellular kinases - preventing DNA synthesis

Renal Dosed** , when CrCl < 50
- HD dosing 10mg PO every 7 days after HD

Monitor

  • Renal function
  • LFTs
  • HBV labs (viral load, serologies)

DO NOT USE WITH TENOFOVIR

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27
Q

Lamivudine

A

HBV : 100 mg PO
HIV-1 , HIV-2 : 300 mg PO

Classified as Nucleoside Reverse Transcriptase inhibitor

*** Cross coverage if no resistance mutation ; if someone has 184 mutation in HIV and then gets HBV it will also have 184 so can’t use

Oral tab = oral solution

Renal dosed ; CrCL < 50

Monitor :

  • Blood glucose
  • CBC with Diff
  • HIV VL/CD4 count
  • HBV VL
  • LFTs
  • Renal function
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28
Q

Entecavir

A

HBV

Inhibits HBV RT - suppressed DNA replication ; weak activity towards HIV RT

Oral tab does not = oral solution

    • decrease dose switching from tab to solution
    • MUST take on empty stomach for optimal absorption

Renal dosed CrCl < 50

Monitor:

  • Renal function
  • LFTs
  • T.bili
  • Bfs (especially in DM patients)
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29
Q

Telbivudine

A

HBV

Oral tab

Renal dosed when CrCl <50

ADR - LFTs

rarely used

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30
Q

HCV

DNA/RNA
ROT
Who should get tested 
When to initiate treatment
Common ADRs in drugs
A

ssRNA

objective for Hep C is to cure

ROT = contaminated devices , IV needles ; sexual contact higher prevalence in MSM

All person between 1945-1965

IVDU, HIV, MSM

For all patient with chronic HCV initiate treatment exception short life expectancy <12 month that cannot be treated with transplantation or with remediated treatment

  • Fatigue / headache/ GI
  • No renal dosing ; caution in ClCr <30
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31
Q

NS5B polymerase inhibitor

A

SOfosbuvir

nucleoside analoe incorporate into HCV RNA leading to chain termination = stops HCV replication

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32
Q

NS3/4A Protease Inhibitor

A

Inhibits the cleavage of polyproteins into nonstructural proteins essential in HCV replication

LOWER barrier to resistance (Q80K)

“Previr”

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33
Q

NS5A inhibit

A

inhibits the phosphorylation of proteins required for HCV RNA replication preventing HCV RNA replication

Associated with resistance mutation = decreases activity

‘Asvir”

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34
Q

Sofosbuvir

MOA
Metabolism
Substrate

A

MOA: NS5B RNA nucleotide polymerase inhibitor: nucleoside analoe incorporate into HCV RNA leading to chain termination = stops HCV replication

genotype 1,2,3,4

  • Prodrug
  • Pangenotypic

Metabolism - hydrolysis - NO CYP450 interactions

Substrate p-gp efflux pump & BRCP
- DDI with inducers

Pregnancy - Category B
Male mediated teratogenicity d/t ribavirin exposure

  • NOT for monotherapy
  • increased renal toxicity with Tenofovir
35
Q

Sofosbuvir / Ledipasvir

(Harvoni)

ADRs
DDI

A

Ledipasvir - NS5A inhibitor ;inhibits the phosphorylation of proteins required for HCV RNA replication preventing HCV RNA replication

Associated with resistance mutation = decreases activity

  • metabolized via oxidation - No DDI by CYP450
  • Elimination - pop efflux pumps and BCRP

ADR

  • Asthenia
  • Hyperbilirubinemia
  • Fatigue / headache/ GI
  • No renal dosing ; caution in ClCr <30
  • No hepatic dosing

DDI

  • Acid suppressants
  • Tenofovir - nephrotoxicity
  • Amiodarone - symptomatic bradycardia

Recommended for non-black, non-HIV, with HCV VL <6 mill without cirrhosis (with cirrhosis not recommended)

36
Q

Velpatasvir / Sofosbuvir

Epclusa

A

NEW GOLD STANDARD IN HCV MANAGMENT

Velpatasvir - NS5A inhibitor ;inhibits the phosphorylation of proteins required for HCV RNA replication preventing HCV RNA replication

Pangenotypic for genotypes 1 - 6
Metabolized - 3A4
Eliminated in feces

ADRs
- Anemia
- Gi, headache, fatigue 
- No hepatic dosing
- No renal dosing 
Caution in eGFR < 30

** Lots of DDIs

37
Q

Voxilaprevir / Velpatasvir / sofosbuvir

Vosei

A 
Voxilaprevi = NS3/4A protease inhibitor 
Velpatasvir = NS5A inhibitor

Pangenotype for genotype 1 - 6
Once daily w/ foot
Metabolized CYP3A4 = DDI

Significant DDI with ACID suppressants
- need to separate dose by 4 hours

Renal issues = do NOT used when eGFR < 30

ADRs

  • headache, fatigue, GI
  • Rash
  • Depression
  • Elevated lipase , CPK, t.billi

“Think 3” cyp3a4 , eGFR <30, 3 elevations

38
Q

Elbasvir / Grazoprevir

Zepatier

A

Elbasvir - NS5A inhibitor
Grazoprevir - NS3/4A protease inhibitor

metabolized - CYP3A4

ADRs

  • GI
  • Fatigue
  • Headache
  • Anemia
  • Elevated LFTs, hyperbilirubinemia
  • No renal or hepatic doing

LOTs of DDIs

39
Q

Viekira Pak

A

Inhibits all non structural proteins in one

Paritaprevir - major DDIs
Ritonavir
Ombitasvir
Dasbuvir

Must be taken with food
very complicated dosing schedule

No renal or hepatic dosing

ADR - GI , rash, LFTs

Pak is 3 pills in morning 1 in evening
XR is 1 pill 3x a day with food

40
Q

Viekira XR

A

Genotypes 1a and 1b only

must be taken with food

too Manny DDIs

Viekira Pak is not = to XR
cannot interchange them

41
Q

Simeprevir

A

NS3/4A protease inhibitor for Genotype 1 only
Q80K resistance mutation = reduction in efficacy based on SVR
- more effective in 1b

Metabolized via 3A4 - interactions
Asians&raquo_space; Caucasians and AA patients

Take with food

SULFOnamide allergy

ADRs:
- Rash, LFTs, GI, hyperbilirubinemia

“Simple but not quite effective”
Simple Genotype 1 only
Quite = Q80K
But ~ B > effect

42
Q

Daclatasvir

A

NS5A inhibitor

Indication - HCV genotype 3
MUST BE COADMINISTERED W/ SOFOSBUVIR

Metabolism CYP3A4 - DDI
Coadministered with 3A4 inhibitor = reduce 30 mg
coadministered with 3A4 inducer = increase 90 mg

Pgp efflux pump substrate and inhibit - DDI

ADRs
- Anemia, fatigue, GI effects, headache

43
Q

Glecaprevir / Pibrentasvir

Mavyret

A

Glecaprevir = NS3/4A protease inhibitor
Pibrentasvir - NS5A inhibitor

Pangenotypic for genotype 1 - 6

1 tab daily w/ food

Glec - minimal 3A4
pib - met via bilirary fecal route

No renal dosing

ADRs
- Headache, fatigue, gi, elevated t.bili

44
Q

Interferon

Intron A, Infergen, Peg-intron, Pegasys

A

MOA: Induces the innate antiviral immune response

side effects - flu like symptoms

BBW - neuropsychiatric

Weekly SQ injection

HCV

45
Q

Ribavirin

A

MOA: increase mutation frequency and inhibits HCV polymerase

Indication: use in combo with PEG-IFN therapy

Side effects - GI symptoms, neutropenia

BBW - hemolytic anemia & teratogenicity

46
Q

HCV genotypes

A

Genotype 1 - more resistant to therapy

1a
- NS3/4A mutation - Q80K polymorphism - decreases activity of simeprevir

  • NS5A mutations - 5 fold reduction in NS5A inhibits
47
Q

Recommendations prior to starting HCV therapy

A

Assess Child Turcotte Pugh Liver score (CTP)
- Avoid NS3 PI : current or prior h/o decompen liver disease or CTP > 7
Avoid paritaprevir/ritonavir : CTP score of 5 or 6 if the patient cannot be closed monitored

All pt should be assessed for HBV infection

Assess potential DDI with DAA

Check labs 12 weeks prior to starting DAA
(CBC, INR, LFTs, eGFR, HCV genotype, HCV VL, resistance testing)

48
Q

HCV management : Monitoring

A

Prior to therapy (within 12 weeks)
- CBC, INR, complete LFT panel, TSH, eGFR

On therapy

  • Check HCV VL at week 4 and 12 weeks
  • Discontinue therapy of detectable at week 6 or alter
  • check routine labs

SVR = sustained virology cure
- undetectable HCV VL at least 12 weeks after the completion of therapy

49
Q

HIV

RNA/DNA
when initiate HIV therapy
what to initiate

A

ss-RNA

therapy at any CD4 count
INSTI-based ART is preferred

50
Q

Nucleoside Reverse Transcriptase Inhibitors
(NRTIs)

MOA
Class effect

A

Competitively inhibits of HIV-1 RT

MOA:
target catalytic site on RT - stops DNA prolongation
competitive, TEMPORARY inhibition (endogenous nucleotide competes for site)

Class effect 
- Renal dosed (except Abacavir) 
- Mitochondrial toxicity 
(due to inhibitor of mitochondrial DNA polymerase, lactic acidosis, hepatic steatosis) 
- Lipoatrophy - fat wasting 
- extremities, buttock, face
51
Q

Abacavir

A

NRTI - HIV

  • Hypersensitivity reaction , occasionally fatal
  • CVD risk
  • DO NOT USE : baseline HIV VL > 100k copies
  • testing for HLA-B5701 allele before initiation to ID pt with increased risk of hypersensitivity reactions
52
Q

Didanosine

A

NRTI - HIV

Dose dependent pancreatitis*
peripheral neuropathy *
lipoatrophy

53
Q

Zidovudine

A

NRTI - HIV

*bone marrow suppression 
Myelosuppresion 
macrocytic anemia
neutropenia
high level resistance seen
54
Q

Lamivudine

A

NRTI- HIV

*well tolerated, headache

also active against HBV
rapidly selects for mutation - M184V

55
Q

Emtricitabine

A

NRTI - HIV

*Hyperpigmentation (A-A)
Active against HBV

56
Q

Stavudine

A

NRTI - HIV
* weight based pancreatitis, peripheral neuropathy

  • lactic acidosis w/ hepatic steatosis
  • lipodystrophy
57
Q

Tenofovir Disoproxil Fumarate

TDF

A

NRTI - HIV

formulated in lactose ; LACTOSE INTOLERANCE PT caution

  • nephropathy - renal failure
  • fanconi syndrome
  • osteomalacia
58
Q

Tenofovir Alafenamide

TAF

A

Prodrug of tenofovir

Safer vs TDF

no renal changes
no bone mineral changes

59
Q

NNRTIs

MOA

A

taret allosteric site on RT - conformational change - stop DNA prolongation, non-competitive

binds noncompetitivelty to alleosteric site
baseline genotypic resistance testing recommended
adherence forgiving d/t long t1/2
resistance occurs rapidly with mono therapy and results from single mutation - lowest genetic barrier to resistant

most common NNRTI resistant mutation = K103N

PERMANENT inhibition

good for noncompliant pt

60
Q

Efavirenz

A

1st generation NNRTI - HIV

Qhs dosing ; take on empty stomach

ADRs - CNS effects - somnolence, fatigue, psych changes, SI/SA - rash, LFTs

Metabolized by CYP3A4; induces and inhibits CYp3A4

Recommended for pregnancy after 1st trimester

**caution in someone with undiagnosed psy issues or suicide

61
Q

Nevirapine

A

1st generation NNRTI - HIV

Do not use in females with CD4 >250 cells
Do not use in males with CD4 >400 cells

metabolized by CYP3A4 and induced

ADR- rash , liver toxicity**

62
Q

Etravirine

A

2nd gen NNRTI - HIV

active against K103 N

ADR:
Rash , LFTs, minor CNS effects < efavirnzr

63
Q

Rilpivirine

A

2nd gen NNRTI - HIV

Active against K103N virus

must take with food ; 900 kcal

ADRs: rash, LFTs, CNS effects

Do not use : Baseline HIV VL >100K

64
Q

Protease inhibitors

MOA
Class effect
Metabolized

A

MOA: inhibit the activation of immature proteins
block the GAG - POL region within protease inhibit the cleave of proteins

Class effect:

  • Rash, LFTs,
  • increased BGs – DM
  • increases TG and LDL
  • Lipodystrophy (central adiposity)
  • increases CVD risk

All metabolized by CYP3A4
most a potent inhibitor

high genetic barrier to resistance

65
Q

Ritonavir

A

Most 3A4 potent inhibitor
PI Agent - HIV

ADR - GI

66
Q

Atazanavir

A

PI agent - HIV

ADR -
PR interval prolongation
hyperilirubinemia

GI neutral
lipid neutral

“Tasmanian devil” - trying to keep that hyper devil neutral for awhile

67
Q

Darunavir

A

PI agent - HIV

must co - admin w/ ritonavir

Sulfonamide cautious with sulfa allergy
GI
lipid neutral

68
Q

Fosamprenavir

A

PI agent - HIV

Sulfonamide - cautious with sulfa allergy

ADR = GI

69
Q

Indinavir

A

PI agent - HIV

Nephrolithiasis
hyperbilirubinemia

Hydrate

70
Q

Lopinavir

A

PI agent - HIV

ADR - GI

71
Q

Saquinavir

A

PI agent - HIV

ADR - GI

CVD risk - own independent risk

72
Q

TIpranavir

A

PI agent - HIV

Only CYP3A4 inducer
Must co-admin w/ ritonavir
sulfonamide - cautious with sulfa allergy

ADR - intracranial hemorrhage

73
Q

3 PI agents sulfonamide ADR

A

Fosamprenavir

Darunavir

Tipranavir

DTF

74
Q

2 PI agents lipid neutral

A

Atazanavir

Darunavir

Indinavir

75
Q

2 PI agents must co-admin with ritonavir

A

Darunavir

Tipranavir

DTR

76
Q

Cobicistat

A

PK booster

used as a 3A4 booster
3A4 inhibitor

FDA to boost atazanavir and darunavir only at 800 mg

not approved for darunavir 600mg

NO HIV activity

DDI = Ritonavir

ADE = renal impairment

Do not use COBI + TDF when CrCl <70

77
Q

Enfuvirtide

A

Fusion inhibitor HIV

only SQ product
inhibits QP41 and prevents fusion of HIV to CD4 cell surface

ADR injection site reaction , GI

78
Q

Maraviroc

A

Entry inhibitor HIV

inhibits HIV co receptor CCR5 - tropic HIV - 1 infection

Must rest for co receptor tropism prior to using

Dose - 300 mg q 12 h
with inhibitor 150 mg po
with inducer 600 mg po

ADRs: LFTs , rash, pyrexia, orthostasis

79
Q

Raltegravir

A

HIV integrase inhibitor

MOA: blocks the catalytic activity of HIV encoded inters preventing integration of virus DNA into host

metabolized by glucuronidation and does not interact with CYP450

eliminated by p-gp

ADR - rash, LFTs, increase CPK, pyrexia

80
Q

Elvitegravir/COBI/TDF/ Emtricitabine

A

“quad pill””

Treatment naive patients

cannot use ClCr >70 due to TDF with COBI

ADR:

  • new or worsening renal function
  • bone mineral density losses
  • GI

DDI - too many contraindications

81
Q

Elvitegravir/COBI/TAF/Emtricitabine

A

Genvoya

Safe in patients with CrCl >30

82
Q

Dolutegravir

A

if pt resistant to raltegravir or elvitegravir can still use this drug

most potent HIV drug

ADR:

  • hypersensitivity reaction
  • LFTs (esp in HBV or HCV coinfections)
  • insomnia
  • hyperglycemia (>125)
  • hypertriglyceridemia

DDI polyvalent cations
space DVG 2 hours or 6 hours after cations

83
Q

Bictegravir/TAF/emtricitabine

A

treatment naive and as SWITCH regiment

1 tab po once daily

Renal issue CrCl <30 = due to TAF

ADR: GI and headache

Pharm Exam 3 (6 decks)

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