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pharm > pharm 3B: virals > Flashcards

pharm 3B: virals Flashcards

1
Q

brefily explain the DNA replication process**reread notes

A
  1. virion’s nuclear mateiral is surrounded by capsid. it has glycoproteion on the capsid which is needed to fuse w the host cell
  2. fuses w the host cell, uncoating process beging where the genetic viral material is released into the cytosol/nucleus of host cell
  3. viral DNA uses this to make mRNA throuhg translation+transcription
  4. cycle repeast
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2
Q

what type is papillomavirus, poxviruses, picornaviruses, falvivirus, orthomyxovirus, paramyxovirus?

A

papillomavirus - dna
poxviruses - dna
picornaviruse - rna, polio
falvivirus - rna, west nile, yellow fever zika
orthomyxovirus - flu
paramyxovirus - meseals + mumps

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3
Q

what connects to the 1 2 3 4 5’ of the pentose sugar?

A

1’ - connects pentose sugar to base via glycosidic bond
2’ has OH/H depending on dna/rna
3’ OH group to attach to phosphate of next NS
4’ dont matter
5’ has phosphoric acid for binding

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4
Q

whcih direction do you add NT to ?

A

add NT to the 3’ group

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5
Q

how does DNA polymerase work?

A
  • DNA POLYMERASE can only work if the NT is a triphosphate
    1. we have a base, it needs to be converted to monotriphosphate VIA THYMIDINE KINASE
    2. now we have a monophosphate which need to be converted to triphosphate VIA **NUCLEOSIDE MONOPHISPHATE KINASE **
    3. now we have a triphosphate that DNA polymerase can work with
    4. DNA polymerase will add the deoxy triphosphate to the growing chain fo the DNA molecuel and a PYROPHOSPHATE IS RELEASED
  • the releeasing of pyrophispahte is NEEDED for growing chain to continue
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6
Q

whats the diff between acylovir and valacyclovir?

A

aclyclovir - without cyclic structure
valacyclovir - sterofide PRO DRUG of acyclovir

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7
Q

what is the MOA for acyclovir?

A
  1. the cell infected takes up the aylcovir rx
  2. acyclovir is turned into monophosphate to get activated VIA VIRAL THYMIDINE KINASE
  3. acylcovir monophosphate gets turned into acylcovir triphosphate via **HOST NUCLEOSDIE MONOPHOSPHATE KINASE **
  4. DNA polymerase adds this to the growing chaine –> casues termination –> the new molecular has NO 3’ postion (since theres no cyclic structure) so ELONGATION STOPS
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8
Q

how deos ganciclovir work?

A
  • its difference than acylcivor and works best with CMV
    1. it does get phospholated via viral thyimidien kinsase but it doesnt get changed into triphosphate via (ns monophopshate kinease) but instead HAS ITS OWN ** VIRAL TRANSFERSE** that converts it
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9
Q

what are the indication/pharmacokineitcs/S/E of acyclvoir meds?

A

indication: HSV1 HSV2, CMV (ganciclovir)
pharmacokinetics: PO, parental formation for serious infx (such as mengintitis w HSV1
S/E: GI, HA, renal dz –> MEDICATION is excreted in kidney unmetbaolized so it can crystialize and cause crystialluria or azotemia

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10
Q

how does acyclovir become resisitant and how does HSV reoccur?

A

HSV travels up the sesnroy nerve and lies dormant in the ganglion until it comes out during stress, trauma, etc

Resistant happens when theres a mutation on the viral thymidine kinase (thats how acylcovir becomes activated)

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11
Q

what drugs do you use if you are resisitant to acylcovir or ganciclovir?

A

CTF
cidoflovir
trifluridine
foscarnet

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12
Q

what is the MOA/indication for cidofovir and trifluriidne?

A

CIDOFOVIR
- MOA: it gets activated by the HOST CELL (not the viral tymidine kinase) goes into the DNA cell and STOPS elongation
- indications: warts so papillomatosis, mossuslcom, aclyvoir/ganciclvoir resisitant

TRIFLURIDINE
- MOA: it gets activated to triphosphate trifluridine, goes into host cell and STOPS DNA elongation

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13
Q

what type of drug is foscarnet and its MOA and indication?

A
  • foscarnet is a pyrophosphate analog
  • MOA: it prevents the DNA polymerase from cleaving and releasing pyrophosphate which inhibits the growing chain
  • THIS IS THE ONLY DRUG THAT DOES NOT NEED TO BE ACTIVATED, IT CAN GET TO WORK RIGHT AWAY

-indications: CMV - BEST TO USE with ganiciclovir + foscarnet
and acylcvior resisitnat HSV

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14
Q

what is the best combo tx for CMV?

A

ganciclovir and foscarnet = GOOD

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15
Q

which viral drug crystalizes in the kidney and can casue crystaluria or azotemia?

A

acylcovir since its unmetabolized in the kidney

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16
Q

which drug binds to JAK-STAT receptor to intiaite an immune resposne agaisnt virus?

A

INFERRON-A

17
Q

what is the MOA + indication + pharmokinetics for interferon-a?

A

MOA - it binds to JAK-STAT receptor to bring in lymphocytes, NKC, macrophages to intiate an immune repsosne agaisnt virus

indication:
- warts condolyma
- hep B hep C
- kaposi sarcoma :(

pharmacokinets:
- given IM, subQ once weekly

18
Q

which viral drug works best for kaposi sarcoma?

A

interferon - a

19
Q

what are the s/e to interfeorn-a?

A
  • flu like SX
  • depression :( AMS changes
  • myelosuppresion - more of an issue w those w aids
  • neurotoxciity - seizures
  • HYPOthyroidsim
  • alopecia - hair loss :(
20
Q

what is the MOA for HIV? expalin the MANY steps girl

A
  1. HIV envelope has three proteins: gp41 which helps it to fuse with the host cell, gp120 which binds to the CD4 receptors, and CCR5 which binds to chemokine 5 receptros to use as coreceptor to enter the host cell
  2. now the HIV is inside the host cell, it undergoes reverse transcriptase to turn RNA –> DNA
  3. DNA is not that good so theres alot of mutation so its good to gain retsisitant to drugs
  4. new viral DNA enters the nucleus with VIRAL INTERGRASE which helps it to integrate into the host cell genome
  5. now we have viral DNA in the host cell genome and it will make immature proteins called POL-GAG
  6. viral DNA will bud off and proteases will cleave the immature POL-GAG protein into mature proteins –> CAN INFECT OTHER CELLS
21
Q

what are the three ways to prevent HIV form infecting other cells? think about the process

A
  1. you can inhibit the reverse transcriptase
  2. you can inhibit the integrade enzyme
  3. you can inhibit the protease enzyme
22
Q

which is the first FDA approve drug for RTI?

A

lamivudine

23
Q

what are the two types of RTI ?

A

nucleoside RTI and non nucleoside RTI

24
Q

what are the nucleoside RTI drugs and their importnace?

A
  1. zidovudine - thymidine analog lacking OH 3’ group
  2. lamivudine - 1st FDA approved, high rate of resistance after 2-3 years, used to tx HEP B
  3. emtricitabine
  4. abacavir
  5. tenofovir
  6. stavudine
25
Q

what is the MOA for nucleoside RTI such as zidovudine?

A

zudovudine gets phosphorlayted into zidovudine triphosphate –> goes into the viral DNA via reverse transcription –> **B/C theres NO 3’ OH GROUP, it stops DNA elongation **

26
Q

what are the s/e to nucleosoide RTI?

A
  1. flu sx, GI issues
  2. anemia - affected normal cells and rapidly dividng blodo cell
  3. neutropenia
  4. myopathy
27
Q

which viral drug has s/e of myopathy or neutropenai, or anemia ?

A

nucleoside RTI

28
Q

what are the non nucleoside RTI, MOA, and S/e?

A

rilpivirine, efavirenz, neviparine (REN)
MOA; bind DIRECTLY to reverse transcriptase enzyme –> prevent it from working
S/E; drug drug interaction +/- P450, rashes, arrthmias

29
Q

whats the famous s/e to efavirenz?

A

Efavirenz is a non nucleoside RTI
s/e - bad dreams, psychaitric distrubances, mood cahnges

30
Q

what are the drugs that are integrade inhibitor? MOA? S/E?

A

raltegravir
- elvitegravir, dolutegrevir, cabotegravir
- MOA: it inhibit the inegrade enzymes so preventing the viral DNA going into the host cell
- S/E: elevated liver enzymes, CNS changes

31
Q

what is the MOA, pharmacokinetics and s/E to maraviroc?

A

maraviroc is a drug that blocks the chemokine 5 receptors so people with R5 variant can benefit this
- use would use the tropism test to see if the pt will benefit frm this drug - not first in line
- CYP3A4, do theres drug drug interaction
- S/E: drug drug, orthostasis

32
Q

what is the MOA for enfuvirtide?

A

enfuvirtide prevents the fusion of GP41 to the host cell

only effective to HIV 1 and not HIV 2

33
Q

what are the two regimine for HAART? tell me the drug name and the type

A
  • ZIA **Zidovudine, lamivudine, atazanavir **– two reverse transcriptase inhibitors + proteases inhibitor
  • CR ** Cabotegravir + rilpivirine **– integrase inhibitor + non nucleotide reverse transcriptase inhibitor
34
Q

what are the many protease inhibitor drugs? it ends with -vir

A
  • Darunavir
  • Saquinavir, indinavir, ritonavir, fosamprenavir, atazanavir, tipranavir, lopinavir
35
Q

what is the MOA/pharmacokinetics for protease inhibitor drugs such as darunavir?

A

it inhibit the protease enzyme so it deosnt cleave GAG-POL proteins into mature proteins –> no mature protiens cannot infect other cells

  • CYP3A4 metabzolied
36
Q

when is ritonavir given?

A

ritonavir is a protease inhibtor
ONLY GIVEN WITH LOPINAVIR
- ritonavir is a POWERFULL INHIBITOR of CYP3A4 but when combined to lopinavir, it increases blood concentration of lopinavir so dec doses

37
Q

what is the S/e to proteases inhibitors?

A
  • GI, rash
  • cushing like syndrome - 50% on this will get this, centralize obseity, buffalo hump, moonlight face
  • drug drug interaction since its metabolzlied through CYP3A4
38
Q
A

pharm (13 decks)

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