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pharmacology > antiviral > Flashcards

antiviral Flashcards

1
Q

Activity of acyclovir
HSV 1 AND HSV 2 DIFFERENCE

VARICELLA ZOSTER VIRUS(CHICKEN POX)

A

is an acyclic guanosine derivative with clinical activity against HSV-1, HSV-2, and VZV, but it is approximately 10 times more potent against HSV-1 and HSV-2 than
against VZV

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2
Q

MOA

A

Acyclovir requires three phosphorylation steps for activation. It
is converted first to the monophosphate derivative by the virusspecified thymidine kinase and then to the di- and triphosphate
compounds by host cell enzymes . Because it
requires the viral kinase for initial phosphorylation, acyclovir is
selectively activated—and the active metabolite accumulates—
only in infected cells. Acyclovir triphosphate inhibits viral DNA
synthesis by two mechanisms: competition with deoxyGTP for
the viral DNA polymerase, resulting in binding to the DNA template as an irreversible complex; and chain termination following
incorporation into the viral DNA

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3
Q

bioavailability

A

bioavailability is low(15-20%)
TOPICAL, IV AND ORAL,HOWEVER, oral are effective.
Half life-2.5-3 hrs
cross CBF 20-50%
RENAL EXCRETIO>80%

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4
Q

Episodes of treatment of acylovir

A

Oral acyclovir has multiple uses. In first episodes of genital
herpes, oral acyclovir shortens the duration of symptoms by
approximately 2 days, the time to lesion healing by 4 days, and the
duration of viral shedding by 7 days

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5
Q

long term treatment for recurrent herpes virus

A

reacurrent herpes virsus, then long term treatment is required, and it decreases the
frequency of symptomatic recurrences and of asymptomatic viral
shedding, thus decreasing the rate of sexual transmissio

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6
Q

higher dose in VZV?

Formulation is organ transplantation

A

VZV is less susceptible to acyclovir than HSV, higher doses are required

prophylactically to patients undergoing organ transplantation,
oral or intravenous acyclovir prevents reactivation of HSV and
VZV infection.

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7
Q

how resistance is developed

A

Resistance to acyclovir can develop in HSV or VZV through
alteration in either the viral thymidine kinase or the DNA polymerase, and clinically resistant infections have been reported in
immunocompromised hosts

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8
Q

ADRS(ACYCYLOVIR)

A

Nausea
headache
Reversible renal toxicity
decreased testosterone level
neurologic effects (eg, tremors,
delirium, seizures).
interstitial nephritis
, crystalline nephropathy

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9
Q

ALTERNATIVE IF SOMEONE IS ACYCLOVIR RESISTANT

DRUGS HAVING SAME MAO

A

Agents such
as foscarnet, cidofovir, and trifluridine do not require activation by
viral thymidine kinase and thus have preserved activity against the
most prevalent acyclovir-resistant strains

valacyclovir, famciclovir, and ganciclovir(CROSS RESISTANT)

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10
Q

DOSE OF ACYCOLOVIR

A

400 MG 3X A DAY {7 -10DAYS}
800 MG/2X A DAY (VARICELLA) FOR 5 DAYS

ZOSTER 800 MG 5XA DAY/7-10DAYS

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11
Q

very important regarding antiviral

A

Antiviral drugs share the common
property of being virustatic; they are active only against replicating
viruses and do not affect latent virus.

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12
Q

indinavir direction for use

FLUID MANAGEMENT

COMBINATION

A

Indinavir requires an acidic environment for optimum solubility
and therefore must be consumed on an empty stomach or with a
small, low-fat, low-protein meal for maximal absorption (60–65%).
Consumption of at least 48 ounces of water daily is important to
maintain adequate hydration.

Combination with ritonavir (boosting) allows for twice-daily
rather than thrice-daily

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13
Q

kinetics indinavir

A

indinavir is an inhibitor of CYP3A4
The serum half-life is 1.5–2 hours, protein binding is approximately 60%, and the drug has a high level of cerebrospinal fluid
penetration (up to 76% of serum levels). Excretion is primarily
fecal.

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14
Q

ADRS INDINAVIR

A

The most common adverse effects of indinavir are indirect
hyperbilirubinemia and nephrolithiasis due to urinary crystallization of the drug
Thrombocytopenia, elevations of
serum aminotransferase levels, nausea, diarrhea, insomnia, dry
throat, dry skin, and indirect hyperbilirubinemia have also been
reported. Insulin resistance may be more common with indinavir

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15
Q

contraindication for ribavirin

A

Contraindications to ribavirin therapy include anemia,
end-stage renal failure, ischemic vascular disease, and pregnancy

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16
Q

high dose of ribavirin

A

Higher doses of ribavirin (ie, 1000–1200 mg/d, according to
weight, rather than 800 mg/d)

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17
Q

kinetics ribavIrin

A

The absolute oral bioavailability of ribavirin is 45–64%,
increases with high-fat meals, and decreases with co-administration of antacids. Plasma protein binding is negligible, volume of
distribution is large, and cerebrospinal fluid levels are about 70%
of those in plasma. Ribavirin elimination is primarily through the
urine; therefore, clearance is decreased in patients with creatinine
clearances less than 30 mL/min

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18
Q

MAO OF RIBAVIRIN

A

ribavirin is a guanosine analog that is phosphorylated intracellularly by host cell enzymes.

Ribavirin triphosphate inhibits the replication of a
wide range of DNA and RNA viruses, including influenza A and
B, parainfluenza, respiratory syncytial virus, paramyxoviruses,
HCV, and HIV-1.

19
Q

ADRS OF RIBAVIRIN

A

A dose-dependent hemolytic anemia occurs in
10–20% of patients.
ELEVATED LEVEL OF BILIRUBIN(JAUNDICE)
Other potential adverse effects are depression, fatigue, irritability, rash, cough, insomnia, nausea, and pruritus

20
Q

kinetics of ziduvedine

A

Zidovudine (azidothymidine; AZT) is a deoxythymidine analog
well absorbed (63%)
distributed to most body tissues cerebrospinal fluid, levels are
60–65%
Although the serum half-life averages
1 hour, the intracellular half-life of the phosphorylated compound
is 3–4 hours, allowing twice-daily dosing. Zidovudine is eliminated primarily by renal excretion .

21
Q

therapeutics of ziduvedine

A

treatment of HIV-associated dementia and thrombocytopenia.
zidovudine remains one of the first-line
agents for use in pregnant women

22
Q

ADRS OF ZIDUVEDINE

A

myelosuppression, resulting in macrocytic anemia (1–4%) or neutropenia
(2–8%).
Gastrointestinal intolerance, headaches
insomnia
Lipoatropy
Less common toxicities include thrombocytopenia, hyperpigmentation of the nails, and myotrophy

23
Q

CONCOMITANT ADMINISTRATION OF ZIDOVUDINE

HOW HEMATOLOGICAL TOXICITY IS INCREASED

A

Increased serum levels of zidovudine may occur with concomitant administration of probenecid, phenytoin, methadone, fluconazole, atovaquone, valproic acid, and lamivudine, either through
inhibition of first-pass metabolism or through decreased clearance.
Zidovudine may decrease phenytoin levels.
Hematologic
toxicity may be increased co-administration of other
myelosuppressive drugs such as ganciclovir, ribavirin, and cytotoxic agents.
Combination regimens containing zidovudine and
stavudine should be avoided due to in vitro antagonism.

24
Q

INTERFERON USE

A

Interferons are host cytokines that exert complex antiviral, immunomodulatory, and antiproliferative actions and
some have proven useful in both HBV and HCV.

25
Q

MAO
ADMINISTER
EXCRETION

A

induction of intracellular signals

SUBCUATANEOUS/IV/INTRAMUSCULAR
half-life is 2–5 hours
Renal elimination accounts
for about 30% of clearance, and clearance is approximately halved
in subjects with impaired renal function

26
Q

ADRS OF INTERFERONS

A

a flu-like syndrome
(ie, headache, fevers, chills, myalgias, and malaise)
THROMBOCYTOPENIA ALONG WITH ZYDUVEDINE
GI UPSET/HYPERACITDITY
Transient hepatic enzyme
elevations may occur in the first 8–12 weeks of therapy
neurotoxicities (mood disorders, depression, somnolence, confusion, seizures), myelosuppression, profound fatigue, weight loss, rash, cough, myalgia, alopecia, tinnitus,
reversible hearing loss, retinopathy, pneumonitis, and possibly
cardiotoxicity.

27
Q

CI of interferon

A

hepatic
decompensation, autoimmune disease, and history of cardiac
arrhythmia
psychiatric disease, epilepsy, thyroid disease, ischemic cardiac disease, severe
renal insufficiency, and cytopenia.

CI IN PREGNANCY AND PRIMATES
Drug drug interaction with theophylline ,didanosine
and methadone levels,
zidovudine may exacerbate cytopenias.

28
Q

Mechanism of action Amantadine

A

Amantadine (1-aminoadamantane hydrochloride) and its
α-methyl derivative, rimantadine, are tricyclic amines of the adamantane family that block the M2 proton ion channel of the virus
particle and inhibit uncoating of the viral RNA within infected
host cells, thus preventing its replication

29
Q

Effectiveness

A

They are active against
influenza A only. Rimantadine is four to ten times more active
than amantadine in vitro

29
Q

Effectiveness

A

They are active against
influenza A only. Rimantadine is four to ten times more active
than amantadine in vitro

30
Q

kinetics of amantadine and ramantadine

A

Amantadine is well absorbed and 67%
protein-bound.
half-life is 12–18 hours.

Rimantadine is about 40% protein-bound
half-life of 24–36 hours. cerebrospinal fluid
levels are 52–96% of those in the serum.
Amantadine is excreted unchanged in the urine, whereas rimantadine undergoes extensive metabolism by hydroxylation, conjugation, and glucuronidation before urinary excretion

31
Q

Dose of the amantadine

A

, both amantadine and rimantadine,
at 100 mg twice daily or 200 mg once daily,

32
Q

ADRS of amantadine and ramantadine

A

The most common adverse effects are gastrointestinal (nausea,
anorexia) and central nervous system (nervousness, difficulty in
concentrating, insomnia, light-headedness). More serious side
effects (eg, marked behavioral changes, delirium, hallucinations,
agitation, and seizures) may be due to alteration of dopamine
neurotransmission (

33
Q

Why amantadine has severe dopaminergic effects?

A

Bcz amantadine crosses the BBB more extensivley than Ramantadine

34
Q

Amantadine and ramantadine toxicity

A

concomitant antihistamines, anticholinergic drugs, hydrochlorothiazide, and trimethoprim-sulfamethoxazol

teratogenic

35
Q

where oseltamivir and zanamivir produce effect?

A

The neuraminidase inhibitors oseltamivir and zanamivir, analogs
of sialic acid, interfere with release of progeny influenza virus from
infected host cells, thus halting the spread of infection within the
respiratory tract.

36
Q

MAO OF Oseltamivir and zanamavir

A

These agents competitively and reversibly interact with the active enzyme site to inhibit viral neuraminidase
activity at low nanomolar concentrations. Inhibition of viral neuraminidase results in clumping of newly released influenza virions
to each other and to the membrane of the infected cell.

37
Q

Effectiveness of oseltamavir

A

activity against both influenza A and influenza B viruses.

38
Q

How the disease is stopped and course therapy?

A

influenza virus
peaks at 24–72 hours after the onset of illness.
Initiation of a
5-day course of therapy within 48 hours after the onset of illness
decreases the duration of symptoms, viral shedding and transmission, and the rate of complications such as pneumonia, asthma. Once-daily prophylaxis is 70–90%
effective in preventing disease after exposure.

39
Q

oseltamivir kinetics

A

orall, prodrug activated by hepatics esterases
75mg twice daily for 5 daysa
75mg once daily for prevention
Half life 6-10 hours
oral bioavailability 80% protein binding
Excretion by kidney

40
Q

Oseltamivir ADRS

A

Nausea, vomiting, fatigeu , diarrrhea

41
Q

Kinetics of zamatavir

Dose

ADRS

Not recommended for

A

administered by inhalation
ten to twenty percent reaches the active site
(10 mg twice daily for 5 days for
treatment and 10 mg once daily for prevention.

cough, bronchospasm (occasionally severe), reversible decrease in pulmonary function, and transient nasal and
throat discomfort. Zanamivir administration is not recommended
for patients with underlying airway disease

42
Q

Resistance

A

H1N1, H3N2, susceptible

resistant to H7N9 virus,

pharmacology (10 decks)

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