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Anti-virals Flashcards

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1
Q

what do viruses lack? what does it have? what does it need to replicate? DNA or RNA?

A

cell wall and cell membrane
nucleic acids surrounded by protein capsid
viruses require host to replicate
can be DNA or RNA and single or double stranded

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2
Q

what few viral infxns can we tx w/drugs?

A 
few URI viruses including influenza and RSV
herpes
CMV
HIV
HBV, HCV
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3
Q

flu ssxs?

A

fever myalgia, h/a, malaise, non-productive cough, sore throat, myalgias

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4
Q

genetic material of flu? what family? what types?

A

single stranded RNA virus
orthomyxoviridae family
types A, B, C (type A subtypes determined by hemagglutinin and neuroaminidase)

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5
Q

most common type of flu? which one assoc w/sporadic outbreaks? which one rarely seen?

A

type A: regular seasonal outbreaks, all age groups affected
type B: sporadic outbreaks, less common
type C: rarely in humans, not associated w/epidemics

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6
Q

two classes of meds that can treat flu?

A

adamantanes

neuraminidase inhibitors

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7
Q

characteristics of adamantanes?

A

amantadine, rimantadine
activity against only influenza A virus
no longer recommended for tx b/c of such high rates of resistance!!
also used for tx of parkinson’s

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8
Q

characteristics of neuraminidase inhibitors?

A

oseltamivir, zanamivir
activity against influenza A and B
doesn’t allow it to bind to cell membrane so can’t replicate

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9
Q

MOA of oseltamivir and zanamivir?

A

block active site of neuraminidase
reduce amount of viral particles released from infected cells
decrease shedding of flu A and B viruses

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10
Q

treatment efficacy of neuraminidase inhibitors?

A

reduces duration of uncomplicated flu A and B illnesses
BUT greatest benefit seen when started w/in 48 hrs of illness onset
reduction in viral shedding, fever, illness
may reduce complications, death and shorten duration of hospitalization
shortens sxs by 1 or 2 days

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11
Q

when would you begin early tx (w/in 48 hrs of onset)?

A

any w/suspected or proven flu whom:
is hospitalized
has severe, complicated or progressive illness
is at higher risk for complications (less than 2, PG, chronic med conditions, residents in nursing homes, elders, those w/AI or immunocompromised)

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12
Q

which of the neuraminidase inhibitors is used more often in clinical practice?

A

oseltamivir: 75 mg PO BID x 5 d

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13
Q

is chemoprophylaxis recommended? what is chemoprophylaxis?

A

NO b/c of increased resistance

includes post-exposure prophylaxis: treat for 7 d after last known exposure

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14
Q

metabolism and excretion of oseltamivir? route of administration? ADRs? recommended when?

A

metabolism: hepatic
excretion: renal
route: oral tablet, suspension
ADRs: n/v, transient neuropsychiatric events, limited data in children
preferred in PG!
recommended for severe or complicated illnesses

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15
Q

metabolism and excretion of zanamivir? route of administration? ADRs? not recommended when?

A

metabolism: not metabolized, minimally absorbed
excretion: renal
route: orally inhaled powder
ADRs: nausea, diarrhea, h/a, cough, bronchospasm in ppl w/pulmonary dz (not recommended in them)

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16
Q

route of administration of peramivir?

A

1 time 600 mg IV infusion over 15-30 min

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17
Q

which herpes viruses do we care most about treating?

A 
HSV 1 (herpes labialis)
HSV 2 (genital herpes)
HSV 4 (varicella zoster virus: chicken pox and shingles)
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18
Q

3 main oral nucleoside analogs used to tx herpes?

A

acyclovir/zovirax
famciclovir/famvir
valacyclovir/valtrex (converted to acyclovir after oral administration, better bioavailability)

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19
Q

MOA of acyclovir? indications?

A

guanosine analog that is incorporated into the virus DNA and inhibits further viral synthesis
indications: HSV 1, HSV 2, less potent for VZV

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20
Q

when does acyclovir/zovirax work? route of administration? bioavailability? other characteristics?

A

only works against viruses that are actively replicating and ineffective against latent viruses
available PO, IV and topical ointment
low bioavailability
can cross BBB and thus tx herpes meningitis and encephalitis
resistance is increasing

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21
Q

clinical uses of acyclovir/zovirax? SEs? dose?

A

clinical uses: HSV 2, HSV 1 (modestly beneficial), varicella (need higher doses)
SEs: h/a, n/v, renal toxicity (need proper hydration), CNS effects, skin irritation
dosing: 200 mg 5x/d or 400 mg TID x 7-10 d

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22
Q

most common hepatitis viruses?

A

HAV
HBV
HEV

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23
Q

how is each hepatitis virus transmitted?

A 
HAV: feces/oral
HBV: blood/bodily fluids
HCV: blood/bodily fluids
HDV: blood/bodily fluids
HEV: feces
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24
Q

which two viral hepatitis cause chronic infxn and therefore we can treat w/anti-virals?

A

HBV, HCV

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25
acute viral hepatitis ssxs?
``` malaise fatigue nausea anorexia arthralgias low grade fever (?) ALT/AST over 500-1000 U/L ```
26
chronic viral hepatitis ssxs?
asx | fluctuating ALT/AST
27
three phases of chronic HBV? what %age of children will go onto chronic infxn and chronic hepatits?
acute infxn chronic infxn chronic hepatitis 95% of kids!
28
of the ppl who develop chronic hepatits, what %age will develop cirrhosis and what will they be at risk for developing?
30% will develop cirrhosis! At risk for developing hepatocellular carcinoma
29
two tx options to tx chronic HBV?
immunomodulatory therapy: peglyated interferon for 48 wks, goal is to maintain sustained suppression of viral replication after completing tx anti-viral agents acting on Hep B DNA polymerase: goal is to obtain rapid and long term viral suppression
30
class/MOA of peg-interferon alfa? recommended when? dosing?
``` class/MOA: cytokine that induces specific and nonspecific immune responses #1, preferred, first line treatment option! only effective tx w/HDV coinfxn, goal is to suppress viral replication with a finite duration of tx dosing: 180 mcg subQ once weekly x 48 wks ```
31
toxicities of peg-inteferon alfa? monitoring necessary? C/Is? pts to use in?
toxicities: fatigue, flu-like rxn, anemia, panctyopenia, depression, mood disturbances monitoring: CBC, TSH Q3 mos C/Is: AI dz, uncontrolled psychiatric dz, decompensated cirrhoses, uncontrolled seizures pt selection: low HBV DNA levels, high levels of ALT, lack of advanced liver dz
32
goal of nucleoside or nucleotide analogs?
to obtain rapid and long term viral suppression
33
how is duration of therapy when using nucleoside or nucleotide analogs determined? what do all require? first line antivirals for tx naive pts w/HBV?
duration of therapy is variable and influenced by HBeAg status, duration of HBV DNA suppression and presence of cirrhosis/decompensation all require dose adjustments w/ppl w/CrCl less than 50 ml/min entecavir and tenofovir= only first line
34
class/MOA of tenofovir/viread? place in therapy? dosing?
class/MOA: nucleotide analog, inhibits HB reverse transcriptase place: preferred 1st line tx, recommended for lamivudine-resistance HBV infxn dosing: 300 mg po once daily, adjust dose if renally impaired
35
SEs of tenofovir? monitoring necessary?
SEs: asthenia, fatigue, lactic acidosis, acute renal failure, hypophosphatemia, osteoporosis monitoring: ALT/AST, total bilirubin, BMP, CrCl, CBC w/diff
36
class/MOA of entecavir/baraclude? place in therapy? dosing?
class/MOA: nucleoside analog, inhibits HB polymerase place: preferred 1st line option, very low rates of resistance, not preferred w/previous hx of lamivudine resistance dosing: 0.5 mg/d, adjust if renally impaired
37
SEs of entecavir/baraclude? monitoring? not recommended in what population?
SEs: nausea, dizziness, ALT elevations, lactic acidosis, anaphylaxis monitoring: ALT/AST, renal function, HBV DNA tx and several months after completion not recommended in HIV/HBV co-infected pts not tx w/high active antiretroviral therapy dt potential for resistance
38
most common blood borne dz in US?
HCV
39
4 classes that directly act on inhibiting HCV replication?
protease inhibitors polymerase inhibitors (NS5B inhibitors) (nucleotide/nonnucleoside) NS5A inhibitors "other"
40
how do we prescribe in order to tx HCV?
always in combination!
41
how many genotypes are there of HCV?
6
42
when is the only time you can't use epclusa?
in significant renal dysfxn!
43
goals of treating HIV?
``` achieve and maintain undetectable viral load improve immune fxn reduce HIV-associated morbidity prolong survival improve quality of service prevent transmission ```
44
when to initiate tx w/HIV infected individuals?
recommended for all HIV infected individuals, regardless of CD4 T cell lymphocyte cell count, in order to reduce morbidity and mortality also includes transmission prevention
45
conditions which favor more rapid initiation of tx
``` PG AIDS-defining conditions acute opportunitistic infxn lower CD4 count (less than 200) HIV-associated nephropathy acute/early HIV infxn HBV/HIV co-infection HCV/HIV co-infection ```
46
4 main categories of drugs used to tx or prophylactic tx against HIV?
``` reverse transcriptase inhibitors protease inhibitors fusion inhibitors integrase inhibitors entry inhibitors ```
47
current tx of HIV infxn consists of what?
highly active antiretroviral therapy (HAART): 2 nucleoside reverse transcriptase inhibitors PLUS either a non-nucleoside reverse transcriptase inhibitors OR a protease inhibitor OR an integrase inhibitor
48
4 NRTIs?
abacavir emtricitabine lamivudine tenofovir
49
1 protease inhibitor?
darunavir
50
3 integrase inhibitors?
dolutegravir elvitegravir raltegravir
51
2 pharmacokinetic "boosters" to increase absorption or slow break down?
cobicistat | ritonavir
52
recommended FIRST HIV antiretroviral tx regimen?
2 NRTIs + integrase inhibitor: emtricitabin/tenofovir + raltegravir emtricitabine/tenofovir + elvitegravir/cobicistat emtricitabine/tenofovir ALAFENAMIDE + elvitegravir/cobicistat emtricitabine/tenofovir + dolutegravir lamivudine/abacavir + dolutegravir 2 NRTIs + protease inhibitor: emtricitabine/tenofovir + darunavir + ritonavir (pharmacokinetic booster)
53
class wide issues with NRTIS?
renal dosing (except abacavir) lactic acidosis and hepatic steatosis peripheral neuropathy lipoatrophy
54
3 preferred NRTIs?
``` lamivudine emtricitabine tenofovir all also active against HBV- even can be used in PG! abacavir (not to be used in PG) ```
55
MOA of protease inhibitors?
inhibit protease cleaving of gag and gag-pol viral proteins
56
class wide SEs of protease inhibitors?
``` GI SEs metabolic SEs: hyperlipidemia and hypertriglyceridemia insulin resistance CYP450 3A4 interactions (inhibition most common except w/tipranavir + ritonavir, which induces) lipodystrophy ```
57
4 preferred protease inhibitors?
ritonavir atazanavir darunavir lopinavir/ritonavir
58
MOA of integrase inhibitors?
inhibits strand transfer phase of HIV DNA integration into host DNA
59
class wide SEs of integrase inhibitors?
h/a, insomnia, CPK elevation, nausea, interactions w/divalent/polyvalent cations (antacids- Ca2+, Mg2+ containing, separate intake by at least 2 hrs), cross-resistant
60
3 preferred integrase inhibitors?
raltegravir (lowest risk of interactions, preferred in PG) dolutegravir elvitegravir
61
baseline pt assessment w/HIV (+) pt before initiating tx?
``` HIV viral load HIV genotype CD4 count, CMP, CBC, UA toxoplasmosis IgG hepatitis serologies RPR or VDRL TB screening fasting lipid panel, fasting BG or HgbA1c pap smear vaccination hx HLA-B*5701, G6PD (can't use if have these genetic variations) ```
62
monitoring labs that should be done with HIV (+) pt?
``` CD4 and HIV RNA CMP CBC w/diff fasting lipid panel fasting BG or HgbA1c UA ```
63
what vaccinations would you consider recommending to an HIV (+) pt? primary care dzs you want to counsel on?
vaccinations: pneumococcal, flu, HPV, NEVER vaccination w/live vaccines if CD4 less than 200 primary care: CVD, DM, contraception, bone density

Pharm I (18 decks)

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