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Haematology > Sweatman antiretroviral therapy > Flashcards

Sweatman antiretroviral therapy Flashcards

1
Q

Primary means by which we treat HIV

A

> antimetabolite inhibitors of viral RT and
inibitors of viral aspartate protease
*3 or more drugs before symptoms appear=best outcome

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2
Q

Name the NRTI’s

A 
ABACAVIR
LAMIVUDINE (3-TC) TENOFOVIR DISOPROXIL 
ZIDOVUDINE (AZT) EMTRICITABINE 
didanosine (ddI)
stavudine (D4T)
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3
Q

NRTI’s MOA

A

prodrugs that must be converted by HOST kinases to trinucleotides in the body–>competitively inhibit dNTP bind site and cause chain termination
*lack 3’ hydroxyl group–next attachment is therefore impossible

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4
Q

resistance to NRTI’s occurs thru

A

mutations in the pol gene

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5
Q

guanisine analog NRTI

A

abacavir

*slow resistance

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6
Q

NRTI contraindicated in pregnancy and young pt.’s, renal.heaptic dysfunction

A

Emtricitabine

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7
Q

common side effect of emtricitibine

A

asthenia, gi distress, hyperpigmentation of the palms

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8
Q

lamivudine excretion

A

excusively kidney

*adjust dose if kidney problems

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9
Q

lamivudine NRTI is also useful against

A

HBV

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10
Q

Nucleotide that acts as a NRTI

A

tenofovir

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11
Q

tenofovir aslo useful against..

A

HBV

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12
Q

oral F of tenofovir

A

25-40%

  • half life is 60 hrs
  • renal elimination
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13
Q

tenofovir contraindicated if…

A

concurrent acyclovir. ganciclovir tx.

fanconi’s anemia

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14
Q

lamivudine aka

A

3-tc

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15
Q

zidovudine (zdv) formerly known as

A

azt

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16
Q

prototype NRTI

A

zidovudine

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17
Q

Distribution of ZDV

A

most tissues including CNS

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18
Q

elimination of ZDV

A

hepatic metabolism to glucuronides and renal excretion

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19
Q

DOsage reduction of ZDV indicated if

A

uremic pt.’s and those with cirrhosis

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20
Q

primary toxicity of ZDV

A

bone marrow supression–> leading to anemia and neutropenia possibly requiring transfusions

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21
Q

drugs that increase the concentration of ZDV

A

azoles, and protease inhibitors

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22
Q

drugs that decrease concentration of ZDV

A

rifampin increases clearance

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23
Q

NRTI’s taken with other antiretroviral agents may cause

A

lactic acid acidemia and sever hepatomegaly with steatosis

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24
Q

Name the NNRTI’s

A

Efavirenz

Nevirapine

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25
Q

used to prevent vertical transmission of HIV during childbirth

A

nevirapine an NNRTI

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26
Q

NNRTI MOA

A

bind to a site on RT that is NOT the active site–> p66 of RT causing a conformational change (inhibit it)

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27
Q

Do NNRTI’s need to be converted

A

no–> they are administered in the active form (unlike NRTI’s) do not reauire phosphrylation to comepete with Nucleotides

28
Q

resistance to NNRTI’s

A

mutations in the POL gene (occurs rapidly if used as monotherapy)

29
Q

Efavirenz bioavailability can be increased via

A

take with fatty foods

30
Q

Efavirenze metabolism

A

hepatic cyp450’s–> many drug-drug interxns

31
Q

toxicity of Efavirenze

A

CNS dysfuntion, Skin rash, hyperlipidemia

32
Q

should efavrienze NNRTI be taken dureing pregnancy

A

NO–> especially in first trimester

33
Q

Nevirapine bioavailability

A

good, penetrates most tissues including CNS

34
Q

metabolism of nevirapine

A

hepatic CYP3a4

35
Q

toxicity of nevirapine

A

rash (15-20%)

Stevens-Johnson syndrome–> toxic epidermal skin necrolysis

36
Q

nevirapine blood levels increased by

A

cimetidine and macrolide ab’s

37
Q

plasma blood levels of nevirapine decreased by

A

rifampin (cyp 3a4 inducer)

38
Q

name the aspartate protease inhibitors

A 
ATAZANAVIR
 RITONAVIR 
amprenavir 
indinavir 
lopinavir 
nelfinavir 
saquinavir
39
Q

How do protease inhibitors work

A

disallows HIV1 aspartate protease inhibitor from cleaving precursor polyproteins to form the final structural proteins of the mature virion core–> mature virions cannot be made and inhibitos viral load

40
Q

assembly of mature vririons relies on

A

HIV-1 specific aspartate protease inhibitor encoded by POL gene–>

41
Q

resistance to protease inh=

A

mutations in the POL gene

42
Q

all PI’s are substrates for

A

cyp3a4

43
Q

PI with the most profound inhibitory effect on cyp3a4

A

ritonavir

44
Q

oral absorption of azatanovir requires

A

acidic environment–> should avoid antacids by 12 hrs

45
Q

elimniation of atazanavir

A

biliary

46
Q

distribution of atazanavir

A

CSF and seminal fluid

47
Q

High doses of atazanavir-

A

prolonged QT–> proarrhythmogenic

48
Q

cyps inhibited by atazanavir

A

cyp3a4 and cyp2d6

49
Q

elimination of ritonavir

A

hepatic–> dosage reduction if liver fialure

50
Q

drugs that reduce conc. of ritonavir

A

anticonvulsants and rifampin

51
Q

drugs that increase con. of ritonavir

A

azoles, cimetidine, erythromycin

52
Q

ritonavir is a substrate for which cyp

A

CYP3a4

53
Q

rationale for combo use to 2 PI’s

A

subtherapeutic ritonavir will be metabolized by CYP3a4 and will inhibit it..therfore the other PI will have greater availability and a greater effect

54
Q

CCR5 inibitor

A

maraviroc

55
Q

name the fusion inhibitors

A

maraviroc

enfuvirtide

56
Q

target of maraviroc

A

CCR5

*HUMAN PROTEIN TARGET–BIG DEAL!

57
Q

CCR5 MAINLY ON

A

MACROPHAGES AND ALSO A LITTLE ON T CELLS

CXCR4 ONLY ON T CELLS–> THIS MUTATION ACCOUNTS FOR RAPID LOSS OF CD4 T CELL IN AIDS

58
Q

MARAVIROC ELEIMINATION

A

CYP3A4–> DOSAGE ADJUSTMENT IF OTHER DRUGS TARGETING THIS SUCH AS PI’S
DISTRIBUTION IS GOOD

59
Q

SIDE EFFECT OF MARAVIROC

A

INCREASE HEPATIC TRANSAMINASES–>LIVER DAMAGE

60
Q

ENFUVIRTIDE MOA

A

binds gp41 and her2 subunit and disallows fusion stalk from undergoing needed conformational changes forming–> HIV cannot get into the cell

61
Q

resistance to Enfuvirtide=

A

env gene

62
Q

indication for enfuvirtide

A

in pt’s with persistent HIV1 repliation in site of ongoing therapy

63
Q

metabolism of anfuvirtide

A

hydrolysis and NOT metabolized by CYP’s

64
Q

HIV1 integrase inhibitor

A

raltegravir

65
Q

will work on HIV1 and HIV2

A

raltegravir

66
Q

used to treat HIV naive pt.’s

A

raltegravir–>usually in combo regimens

67
Q

metabolism of raltegravir

A

glucuronidation and not CYP metabolism

Haematology (7 decks)

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