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Pharmocolgy > Antivirals > Flashcards

Antivirals Flashcards

1
Q

Name features of Influenza A?

A

Main seasonal outbreak
Multiple host species
Antigenic drift and shift

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2
Q

what are common complications of Influenza ?

A

Bronchitis, pneumonia
– Sinusitis
– Exacerbation of underlying disease

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3
Q

what are features of Influenza B?

A

Only in humans

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4
Q

what are the structures of Influenza A ?

A 
RNA 
Protein envelope 
Lipid envelope 
M2 and M1 
Proteins on outside :
Neuraminidase and Hemaggltuinin
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5
Q

what can Hemagglutinin do?

A

recognise human respiratory cells to stick to surface - salic acid , URT

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6
Q

what does the M2 ion channel do ?

A

once the virus enters the host cell this cannel allows H+ ion to enter to break uo the virus particle to replicate it self

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7
Q

how do Amantadine and Rimantadine work ? what do they work on ?
what else do they work on ?

A

Antivirals that work in Influnza A
Block M2 ion channels = inhibit viral uncoating
Parkinson’s

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8
Q

what are side effects of amantidine ?

A

CNS and renal

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9
Q

how was resistance developed for Amantadine ?

A

single point mutation in M2 gene which is transmissible

the shape of channel changes so drug does not bind into the channel

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10
Q

what does Neuraminidase do ?

A

Breaks the Sialic acid and Heamagglutinin bond and allows a budding virus particle to break off

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11
Q

what is the pharmokinetics of Zanamavir ?

A

Low bioavail - dry aersol needed
Acid degrades it
long half life
renally excreted

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12
Q

what is an advantage of Oesltamivir ?

A

Pro-drug with high bio avail so in tablet form

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13
Q

how does Oesltamivir and Zanamavir work?

A

competitively inhibits the NA enzymes so virus aggregation occurs and stays in the cell

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14
Q

what is a goal when starting Zanamavir and oesltamivir ? what can it lead to ?

A

start treatment early when symptoms start

severity and duration decreases , reduction in mortality

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15
Q

what is a major use of Osetltamvir ?

A

seasonal prophylaxis

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16
Q

what side effects of Zanamavir ?

A

vomiting
abdo pain
epistaxis
low side effect profile

17
Q

what is the proper name for Bird flu ?

A

H5N1 infection

18
Q

how do we reduce resistance globally ?

A

survelliance -
WHO system
NA inhibitor Susceptibility network

19
Q

how do virus’ develop resistance to NA inhibitors ?

A

Change in shape of enzyme

20
Q

what strain develop resistance in Oseltamivir ?

A

H1N1 (human strain) - not triggered by over use of antivirals

21
Q

why is Oseltamivir now still in use ?

A

circulating H1N1 human is replaced by swine H1N1 which is susceptible to it

22
Q

what are primary care guidlines in flu outbreaks?

A

Healthy people: no Rx unless pt felt to be at risk
– At risk (inc preg): oseltamivir asap (no need for confirmation)
– Severely immunosuppressed: oseltamivir or inhaled zanamivir
(esp if H1N1)

23
Q

what are secondary care guildlines in flu ?

A

if suspected give Oseltamivir asap

if H1N1 is high try Zanamivir

24
Q

what is EBV associated with?

A

non-malignant and malignant

lymphomas

25
Q

what is general structure of HSV and VZV ?

A

large double-stranded DNA genome

covered by a capsid and lipid bilayer envelope.

26
Q

how do HSV enter cells ?

A

via MHC class molecules

27
Q

how does shingles present ?

what kind of patients will you see it in ?

A

reactivation of the virus (Herpes zoster) which lies dormant in a dorsal root
ganglion after primary chickenpox infection.
elderly and immunocompromised

28
Q

What is the main treatment principle of Shingles?

A

start antivirals within 72 hours

29
Q

what is the main clincinal differences of HSV 1 and 2 ?

A 
1= genital or oral ulceration
2 = Just genital
30
Q

what is treatment of HSV?

A

Oral aciclovir or valaciclovir are administered for 7-10 days to treat the multiple
painful genital herpes lesions

31
Q

What is common complication of HSV?

A

recurrent lesions to occur from reactivation of latent

virus in the dorsal root ganglia. Symptoms are usually less severe than the primary episode.

32
Q

How does Acyclovir and Valaciclovir work ?

A

nucleoside inhibitors of viral DNA replication

33
Q

how does Aciclovir work ? why is it good for humans

A

guanosine analogue active against many DNA viruses by inhibiting synthesis of viral DNA. Initial activity
relies on phosphorylation by a viral protein (thymidine kinase) limiting their initial human cell toxicity

34
Q

how does resistance to Aciclovir develop?

A

change in thymidine kinase- prevalent in immunocompromised

35
Q

what are side effects of Aciclovir ?

what D-D interaction ocurs?

A

N+V
Photo sensitivity

antibiotics could = Nephrotoxicity

36
Q

what is PK of aciclovir ?

A

It is well distributed and most is eliminated by the kidneys with a half-life of around 3 hours

Pharmocolgy (22 decks)

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