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Pharm I > Anti-virals > Flashcards

Anti-virals Flashcards

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
Q

acute viral hepatitis ssxs?

A 
malaise
fatigue
nausea
anorexia
arthralgias
low grade fever (?)
ALT/AST over 500-1000 U/L
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26
Q

chronic viral hepatitis ssxs?

A

asx

fluctuating ALT/AST

27
Q

three phases of chronic HBV? what %age of children will go onto chronic infxn and chronic hepatits?

A

acute infxn
chronic infxn
chronic hepatitis
95% of kids!

28
Q

of the ppl who develop chronic hepatits, what %age will develop cirrhosis and what will they be at risk for developing?

A

30% will develop cirrhosis! At risk for developing hepatocellular carcinoma

29
Q

two tx options to tx chronic HBV?

A

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
Q

class/MOA of peg-interferon alfa? recommended when? dosing?

A 
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
Q

toxicities of peg-inteferon alfa? monitoring necessary? C/Is? pts to use in?

A

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
Q

goal of nucleoside or nucleotide analogs?

A

to obtain rapid and long term viral suppression

33
Q

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?

A

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
Q

class/MOA of tenofovir/viread? place in therapy? dosing?

A

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
Q

SEs of tenofovir? monitoring necessary?

A

SEs: asthenia, fatigue, lactic acidosis, acute renal failure, hypophosphatemia, osteoporosis
monitoring: ALT/AST, total bilirubin, BMP, CrCl, CBC w/diff

36
Q

class/MOA of entecavir/baraclude? place in therapy? dosing?

A

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
Q

SEs of entecavir/baraclude? monitoring? not recommended in what population?

A

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
Q

most common blood borne dz in US?

A

HCV

39
Q

4 classes that directly act on inhibiting HCV replication?

A

protease inhibitors
polymerase inhibitors (NS5B inhibitors) (nucleotide/nonnucleoside)
NS5A inhibitors
“other”

40
Q

how do we prescribe in order to tx HCV?

A

always in combination!

41
Q

how many genotypes are there of HCV?

A

6

42
Q

when is the only time you can’t use epclusa?

A

in significant renal dysfxn!

43
Q

goals of treating HIV?

A 
achieve and maintain undetectable viral load
improve immune fxn
reduce HIV-associated morbidity
prolong survival
improve quality of service
prevent transmission
44
Q

when to initiate tx w/HIV infected individuals?

A

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
Q

conditions which favor more rapid initiation of tx

A 
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
Q

4 main categories of drugs used to tx or prophylactic tx against HIV?

A 
reverse transcriptase inhibitors
protease inhibitors
fusion inhibitors
integrase inhibitors
entry inhibitors
47
Q

current tx of HIV infxn consists of what?

A

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
Q

4 NRTIs?

A

abacavir
emtricitabine
lamivudine
tenofovir

49
Q

1 protease inhibitor?

A

darunavir

50
Q

3 integrase inhibitors?

A

dolutegravir
elvitegravir
raltegravir

51
Q

2 pharmacokinetic “boosters” to increase absorption or slow break down?

A

cobicistat

ritonavir

52
Q

recommended FIRST HIV antiretroviral tx regimen?

A

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
Q

class wide issues with NRTIS?

A

renal dosing (except abacavir)
lactic acidosis and hepatic steatosis
peripheral neuropathy
lipoatrophy

54
Q

3 preferred NRTIs?

A 
lamivudine
emtricitabine
tenofovir 
all also active against HBV- even can be used in PG!
abacavir (not to be used in PG)
55
Q

MOA of protease inhibitors?

A

inhibit protease cleaving of gag and gag-pol viral proteins

56
Q

class wide SEs of protease inhibitors?

A 
GI SEs
metabolic SEs:
hyperlipidemia and hypertriglyceridemia
insulin resistance
CYP450 3A4 interactions (inhibition most common except w/tipranavir + ritonavir, which induces)
lipodystrophy
57
Q

4 preferred protease inhibitors?

A

ritonavir
atazanavir
darunavir
lopinavir/ritonavir

58
Q

MOA of integrase inhibitors?

A

inhibits strand transfer phase of HIV DNA integration into host DNA

59
Q

class wide SEs of integrase inhibitors?

A

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
Q

3 preferred integrase inhibitors?

A

raltegravir (lowest risk of interactions, preferred in PG)
dolutegravir
elvitegravir

61
Q

baseline pt assessment w/HIV (+) pt before initiating tx?

A 
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
Q

monitoring labs that should be done with HIV (+) pt?

A 
CD4 and HIV RNA
CMP
CBC w/diff
fasting lipid panel
fasting BG or HgbA1c
UA
63
Q

what vaccinations would you consider recommending to an HIV (+) pt? primary care dzs you want to counsel on?

A

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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