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STEP > ID 19 > Flashcards

ID 19 Flashcards

1
Q

griseofulvin uses

A

1) oral treatment of superficial infections

2) inhibits growth of dermatophytes (tinea, ringworm)

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2
Q

other griseofulvin AE

A

metabolizes Warfarin

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3
Q

permethrin MOA

A

blocks sodium channels (*thus neurotoxic)

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4
Q

malathion mechanism

A

acetylcholisterase inhibitor

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5
Q

lindane mechanism

A

blocks GABA channels (*thus neurotoxic)

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6
Q

chloroquine MOA

A

blocks detoxification of heme into hemozoin –> heme accumulates and is toxic to plasmodia

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7
Q

resistance to chloroquine?

A

membrane pump that decreases intracellular concentration of drug.

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8
Q

only drug you can’t use chloroquine for?

A

p falciparum

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9
Q

p falciparum treatment options

A

1) artemether/lumefantrine

2) atovaquone/proguanil

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10
Q

life-threatening malaria treatment

A

artesunate

*quinidine in US (quinine elsewhere)

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11
Q

chloroquine AE’s

A

retinopathy

pruritus (especially in dark-skinned individuals)

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12
Q

drug like oseltamivir…

A

zanamivir

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13
Q

oseltamivir/zanamivir uses

A

treatment and prevention of both influenza A and B

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14
Q

Why do acyclovir/valacyclovir have few adverse effects in uninfected cells?

A

not phosphorylated

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15
Q

acyclovir/valacyclovir usage caveat

A

no effect on latent forms of HSV and VZV

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16
Q

difference between valacyclovir and acyclovir?

A

valacyclovir is a prodrug of acyclovir that has better oral bioavailability

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17
Q

acyclovir/valacyclovir MOA of resistance

A

mutated viral thymidine kinase

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18
Q

acyclovir/valacyclovir AE’s

A

1) Obstructive crystalline nephropathy

2) ARF

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19
Q

Ganciclovir MOA

A

5-monophosphate formed by a CMV viral kinase. Guanosine analog. Triphosphate formed by cellular kinase. Preferentially inhibits viral DNA polymerase.

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20
Q

ganciclovir prodrug

A

valganciclovir, better oral bioavailability.

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21
Q

ganciclovir MOA of resistance

A

mutated viral kinase

22
Q

Foscarnet MOA

A

Viral DNA/RNA polymerase inhibitor and HIV reverse transcriptase inhibitor.
*binds to pyrophosphate-binding site of enzyme (pyrophosphate analog)

23
Q

foscarnet vs. ganciclovir/acyclovir

A

foscarnet doesn’t require kinase activation.

24
Q

foscarnet uses

A

1) CMV retinitis in immunocompromised patients when ganciclovir fails
2) acyclovir-resistant HSV

25
Q

foscarnet AE’s

A

1) nephrotoxicity
2) electrolyte abnormalities (hypo or hypercalcemia, hypo or hyperphosphatemia, hypokalemia, hypomagnesemia)
3) seizures

26
Q

MOA of resistance with foscarnet

A

mutated DNA polymerase

27
Q

Cidofovir and phosphorylation?

A

doesn’t require phosphorylatoin

28
Q

cidofovir MOA

A

inhibits viral DNA polymerase

29
Q

cidofovir pharmacokinetics

A

long half-life

30
Q

cidofovir uses

A

1) CMV retinitis in immunocompromised patients

2) acyclovir-resistant HSV

31
Q

cidofovir AE’s

A

nephrotoxic

32
Q

how to reduce cidofovir toxicity?

A

coadminster with probenecid and IV saline

33
Q

HAART composition

A

2 NRTIs + integrase inhibitor

34
Q

NRTIs

A 
Abacavir (ABC)
Didanosine (ddl)
Emtricitabine (FTC)
Lamivudine (3TC)
Stavudine
Tenofovir (TDF)
Zidovudine (ZDV, formerly AZT)
35
Q

NRTI MOA

A

competitively inhibit nucleotide binding to reverse transcriptase and terminate DNA chain (lack a 3’ OH group)

36
Q

What is unique about Tenofovir?

A

nucleo”T”ide, unlike nucleoside, and needs to be phosphorylated.

37
Q

NRTI AE’s

A

1) bone marrow suppression (reverse with G-CSF and ego)
2) peripheral neuropathy
3) lactic acidosis (nucleosides)
4) anemia (ZDV)
5) pancreatitis (didanosine)

38
Q

thing to remember about abacavir

A

contraindicated if patient has a HLA-B5701 mutation

39
Q

NNRTIs

A

Delaviridine
Efavirenz
Nevirapine

40
Q

NNRTI mechanism

A

bind reverse transcriptase at site different from NRTIs.

*no phosphorylation required.

41
Q

NNRTI AE’s

A

1) rash
2) hepatotoxic
3) efavirenz – vivid dreams + CNS symptoms
4) delavirdine and efavirenz contraindicated in pregnancy

42
Q

protease inhibitors

A

all the -navirs

43
Q

protease inhibitor that’s a CYP-45O inhibitor…

44
Q

protease inhibitor AE’s

A

Hyperglycemia
GI intolerance (nausea, diarrhea)
lipodystrophy (Cushing-like syndrome
Nephropathy, hematuria (indinavir)

45
Q

protease inhibitor contraindicaion

A

rifampin (potent CYP/UGT inducer) that can decrease concentration.

46
Q

integrase inhibitors

A

raltegravir
elvitegravir
dolutegravir

47
Q

integrase inhibitor AE

A

increase creatine kinase

48
Q

enfuvurtide AE

A

skin reaction at injection sites

49
Q

enfuvirtide MOA

A

Binds gp41, inhibiting viral entry

50
Q

maraviroc MOA

A

binds CCR-5 on surface of T cells/monocytes inhibiting interaction with gp120

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