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Clinical Pharmacology > Antifungals, antimycobacterials, antivirals > Flashcards

Antifungals, antimycobacterials, antivirals Flashcards

1
Q

What’s a genus of bacteria that includes many species of pathogens?

A

mycobacterium

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2
Q

What are the targets of antimycobacterials?

A

enzymes that mycobacteria use to build their cell walls

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3
Q

How are mycobacteria different than typical bacteria?

A

easier to control but harder to treat because they replicate slower.
CAN exist in a dormant state which makes them resistant to nearly all abx

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4
Q

What’s the standard treatment in active mycobacterial disease?

A
  • Rifampin
  • Isoniazid
  • Pyrazinamide
  • Ethambutol

Note: takes weeks to get susceptibility results

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5
Q

How does isoniazid work?

A
  • bactericidal
  • inhibits mycolic acid synthesis!
  • effective against active AND dormant TB
  • acts as a weak MAO-I (careful with SSRI/SNRI)
  • alters pyridoxine metabolism (give B6 to all patients)
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6
Q

What are the two most important drugs for TB?

A
  1. isoniazid
  2. rifampin
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7
Q

What is isoniazid active against?

A

M. tuberculosis and M. kansasii

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8
Q

How is isoniazid clinically utilized?

A

mycobacterial infections

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9
Q

When is isoniazid your DOC?

A

latent TB, active TB

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10
Q

What are ADRs of isoniazid?

A

hepatotoxicity, peripheral neuropathy (use pyridoxine), hemolysis in G6PD deficiency

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11
Q

What are examples of rifamycins?

A
  • rifampin
  • rifabutin
  • rifapentine
  • rifaximin
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12
Q

What’s the MOA of rifamycins?

A
  • bactericidal
  • Inhibits DNA-dependent RNA polymerase
  • very good oral bioavailability
  • resistance emerges when drug is used alone
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13
Q

What should you always screen for drug ineractions?

A

rifamycins – extremely potent CYP450 inducers!!
also, reduced effectiveness of oral contraceptives

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14
Q

What are rifamycins GOOD for?

A

mycobacteria

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15
Q

What are rifampins moderate for?

A

staph, acinetobacter, enterobacterciae

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16
Q

What are rifamycins utilized for?

A

mycobacterial infections – usually in combo w/ deep seeded “typical” bacterial infections (MRSA) or if prosthetic material

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17
Q

When is rifamycin your DOC?

A

TB = tuberculosis, MAC = mycobacterium avium complex

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18
Q

What are ADRs of rifamycins?

A

orange-red colored secretions (urine, tears)

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19
Q

Do rifamycins have DIs?

A

many due to enzyme induction

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20
Q

What’s the MOA of pyrazinamide?

A
  • bacteriostaticuncertain but requires bioactivation via hydrolytic enzymes to form pyrazoic acid
  • shortens duration 9m - 6m

NOT pyridoxine
AVOID IN PREGNANCY

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21
Q

When are pyrazinamides clinically active?

A

M. tuberculosis

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22
Q

When are pyrazinamide clinically utilized and is your DOC?

A

active TB

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23
Q

What are the ADRs of pyrazinamide?

A

polyarthralgia (40%), hyperuricemia, mylagia, maculopapular rash, porphyria, photosensitivity

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24
Q

What’s the MOA of ethambutol?

A
  • bacteriostatic
  • inhibits formation of arabinoglycan, component of mycobacterial cell wall
  • only 1st 2 months of tuberculosis therapy
  • **NOT recommended in children <5yo **
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25
Q

When is ethambutol clinically active and utilized?

A
  • M. tuberculosis, M. avium-intracellulare, M. kansaii
  • active TB and MAC infections
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26
Q

What are ADRs of ethambutol?

A
  • dose-dependent visual disturbances
  • headache
  • confusion
  • hyperuricemia
  • peripheral neuritis
  • difficulty deferentiating from red and green
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27
Q

What are the increase of systemic fungal ifnections a consequence of?

A

medical advancement

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28
Q

What are types of moulds?

A

aspergillus (a. fumigatus, mucor spp, rhizopus spp)
dermatophytes

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29
Q

What are types of yeasts?

A

candida (C.albicans)
cryptococcus (C.neoformans, C. gattii)
Malassezia (M. furfur)

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30
Q

What are dimorphic fungi?

A

histoplasma capsulatum
coccidioides immitis
sporothirix schenkii
blastomyces

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31
Q

Imidazoles: COMET-K

A

Clotrimazole
Oxiconazole
Miconazole
Econazole
Tioconazole
Ketoconazole

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32
Q

Triazoles: FIT VIP

A

Fluconazole
Itraconazole
Teraconazole
Voriconazole
Isavuconazole
Posaconazole

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33
Q

Allyamines: TAN

A

Terbinafine
Amorolfin
Naftifine

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34
Q

Echinocandins: MAC

A

Micafungin
Anidulafungin
Caspafungin

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35
Q

What are examples of polyenes?

A

amphotericin B, nystatin

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36
Q

What is the MOA of polyenes?

A
  • fungicidal/fungistatic (dependent)
  • binds to ergosterol in fungal cell membranes, forming leaky pores
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37
Q

What’s used to decrease polyene side effects?

A

lipid formulations and different dosing dependent

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38
Q

What are ADRs of polyenes?

A

nephrotoxicity, infusion reactions (chills, fever, muscle spasms, hypotension), electrolyte abnormalities (hypokalemia)

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39
Q

When do polyenes have good coverage?

A

candida and aspergillus, cryptococcus neoformans, dimorphic fungi, molds

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40
Q

When do polyenes have moderate coverage?

A

zygomycetes

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41
Q

When are polyenes clinically utilized?

A

unknown fungal infections, use for candidiasis and aspergillosis (less often with newer/safer agents)

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42
Q

When are polyenes your DOC?

A

cryptococcal meningitis and serious dimorphic fungi and mold infections

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43
Q

What are DIs with polyenes?

A

nephrotoxic drugs (additive)

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44
Q

What are examples of azoles?

A

fluconazole, itraconazole, voriconazole, ketoconazole

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45
Q

What’s the MOA of azoles?

A
  • fungicidal and fungistatic (dependent)
  • inhibits fungal P450 dependent enzymes blocking ergosterol synthesis
  • mainstays of antifungal therapy
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46
Q

What’s the ADRs of azoles?

A

hepatotoxicity, Qtc prolongation, rash, upset stomach

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47
Q

What DIs do azoles have?

A

many – inhibits CYP450

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48
Q

Which is the only azole with significant utility in candiduria?

A

fluconazole

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49
Q

What’s fluconazole have good and moderate clinical activity?

A

good = candida albicans, candida tropicalis, candida parapsilosis, candida lusitaniae, cryptococcus neoformans, coccidiodes immitis

moderate = candida glabrata

50
Q

When is fluconazole utilized clinically?

A

candidiasis, cryptococcal meningitis, cocciodal meningitis
orally or IV

51
Q

When is fluconazole your DOC?

A

many susceptible fungal infections, invasive and non invasive candidiasis (NOT candida krusei)

52
Q

Why are only oral formulations availble of itraconazole?

A

caps<bioavailability than solution
* caps need to be taken with meal
* solution taken on empty stomach
* absorption drops with agents that lower gastric acidity

53
Q

When is itraconazole good and moderate clinically?

A

good = candida albicans, c. parapsilosis, c. tropicalis, c. lusitaniae, cryp. neoformans, aspergillus, dimorphic

moderate = candida glabrata and candida krusei

54
Q

When is itraconazole clinically utilized?

A
  • dermatomycosis
  • histoplasmosis
  • blastomycosis
  • coccidiomycosis
  • sporotrichosis
55
Q

When is itraconazole your DOC?

A

histoplasmosis and blastomycosis

56
Q

What is recommended with voriconazole?

A

administer 1 hour before or after a meal – 90% oral bioavalability this way.
also, monitor drug levels because of varaible nonlinear elimination

57
Q

When does voriconazole have good and moderate activity?

A

good = candida albicans, candida lusitaniae, c. parapsilosis, c. tropicalis, c. krusei, cryptococcus neoformans, aspergillus

moderate = candida glabrata, candida albicans that are flu-resistant, fusarium

58
Q

When is voriconazole clinically utilized/ yoru DOC?

A

invasive aspergillus, other molds

59
Q

What’s important to remember about posaconazole?

A

Take PO forms with food or soda, and also suspension and tab that have different dosing

60
Q

When does posaconazole have good or moderate activity?

A

good = candida albicans, candida lusitaniae, c. parapsilosis, c. tropicalis, c. krusei, aspergillus, zygomycetes, other moulds, dimorphic fungi

moderate = fusarium, c. glabrata

61
Q

When is posaconazole clinically utilized?

A

fungal infection prophylaxis, zyomycosis, resistent oropharyngeal candidiasis, fungal infections

62
Q

When is posaconazole your DOC?

A

prophylaxis for invasive aspergillosis and candidiasis

63
Q

What are examples of echinocandins?

A

caspofungin, micafungin, anidulafungin

all IV only

64
Q

What’s the MOA of echinocandins?

A

fungalstatic and fungicidal depending
inhibit glucan syntase, decreasing fungal cell wall synthesis

65
Q

What are the ADRs of echinocandins?

A

excellent safety profile – GI distress, flushing from histamine, rare hepatotoxicity

66
Q

What are DIs of echinocandins?

A

cyclosporine increase (Caspofungin) and increase sirolimus (micafungin)

67
Q

When do echinocandins have good or moderate activity?

A

Good = candida albicans, c. glabrata, c. lusitaniae, c. parapsilosis, c. tropicalis, c. krusei, aspergillus

moderate = candida parapsilosis, dimorphic fungi

68
Q

When are echinocandins clinically utilized?

A

invasive candidiasis, esophageal candidiasis, empiric therapy for fungal infections

69
Q

When are echinocandins your DOC?

A

invasive candidiasis

70
Q

What can viruses cause on the host cell?

A

death, transformation (papillomaviruses), latent infection

71
Q

Why do antiviral agents have limitations?

A

limited effectiveness at the point of symptoms

72
Q

What are antivirals for herpes?

A

acyclovir (IV/PO/topical), valacyclovir (PO), famciclovir (PO)
val and fam are prodrugs!

73
Q

What are MOAs for antivirals for herpes?

A

activated by viral thymidine kinase to forms that inhibit viral DNA polymerase

74
Q

What are ADrs for antivirals of herpes?

A

nephrotoxicity (must hydrate and renally dose) , CNS effects
Consider oral forms causing GI issues

75
Q

How are herpes antivirals good and moderately active for?

A

good = HSV-1 and HSV -2
moderate = varicella zoster

76
Q

When are antiviral for herpes your DOC?

A

severe or difficult to treat HSV infections, severe HSV outbreaks among HIV patients (acyclovir), HSV-2 infections/prevention, VZV

77
Q

How do you dose acyclovir?

A

based on ideal body weight

78
Q

What are examples of neuraminidase inhibitors?

A

oseltamivir (PO) and zanamivir (inhaled)

79
Q

What is the MOA of neuraminidase inhibitors?

A

prevents viral neuraminidase enzymes from releasing new virions from the host cell, preventing replication
most effective starting EARLY

80
Q

When should neuraminidase inhibitors be started?

A

within 2 days of symptom onset, decreases ~1 day

81
Q

What influenzas are neuraminidase inhibitors good for?

A

A and B

82
Q

When are neuraminidase inhibitors your DOC?

A

Influenza prophylaxis and influenza infection w/ symptoms <2 days

83
Q

What are ADRs of neuraminidase inhibitors?

A

oseltamivir: GI symptoms, HA and fatigue can also occur when drug is given for a longer period

zanamivir: pulmonary adverse effects, avoid w/ asthma

84
Q

How does HIV infect the body?

A

infects lymphocytes and macrophages and results in progressive decline of CD4 T-cells – leads to opportunistic infections

85
Q

How is HIV transmitted?

A

sexually, perinatally, breastfeeding, IV drugs

86
Q

What are the 3 phases of HIV disease?

A
  1. Acute seroconversion – fever, flu-like illness, lymphadenopathy, rash, several weeks
  2. asymptomatic HIV – few or no signs/symptoms but CD4 T cell count declines…may last a few years to a decade
  3. AIDS – immune system damaged enough for significant opportunistic infections, <200 CD4 T cell count
87
Q

What was the first antiretroviral drug for HIV?

A

zidovudine (AZT) in 1987

88
Q

What is ART or HAART?

A
  • current treatment regimen with 3-4 drugs
  • suppress viral replication and restore number of CD4 cells
  • ART recommended for all HIV infected indviduals
  • significantly decreases morbidity and mortality
89
Q

What should you always do with HIV treatment?

A
  • combo therapy = reduces likelihood of drug resistance, slows disease progression
  • individualized treatment
  • always check for DIs
90
Q

What are some NRTIs (nucleotide reverse transcriptase inhibitors)?

A

abacavir, emtricitabine, lamivudine, tenofovir, zidovudine

91
Q

What’s the MOA of NRTIs?

A

inhibit HIV reverse transcriptase after phosphorylation by cell enzymes

92
Q

What are ADRs of NRTIs?

A
  • peripheral neuropathy
  • GI effects
  • bone marrow suppression
  • hypersensitivity (abacavir)
  • lactic acidosis, hepatic steatosis, pancreatitis
  • nephrotoxicity
93
Q

What is generally the backbone of most ART regimens?

A

2 NRTIs – renally dosed

94
Q

What else can NRTIs be used for?

A

Hep B virus (tenofovir, emtricitabine, lamivudine)

95
Q

What are examples of NNRTIs (non-nucleotide)?

A

efavirenz, nevirapine, etravirine, rilpiverine

96
Q

What’s the MOA of NNRTIs?

A

inhibit same enzyme as NRTIs but different mechanism

97
Q

What are ADRs of NNRTIs?

A
  • Cns problems - EFV
  • rashes
  • hepatotoxicity - NVP
  • hypersensitivity w/ flu like sxs, fever, juandice, ab pain
  • lipohypertrophy “buffalo hump”
  • hyperlipidemia - EFV and NVP
  • EFV + pregnancy category D
98
Q

Why is it essential to stick to your HIV regimen?

A

easily can develop resistance

99
Q

What are some protease inhibitors?

A

atazanavir, ritonavir (boosting), ritonavir (full dose), lopinavir

100
Q

What’s the MOA of protease inhibitors?

A

Inhibit viral protein processing by binding to site of protease activity on HIV

101
Q

What are ADRs of protease inhibitors?

A
  • cardiovascular (MIs and strokes)
  • severe GI: take w/ food
  • hepatotoxicity
  • liphypertrophy
  • nephrotoxicity
102
Q

What are DIs with protease inhibitors?

A

MANY - strong CYP450 inhibitors

103
Q

Protease inhibitors are ____ resilient to development of resistance

A

more

104
Q

Protease inhibitors did what with highly active antiretroviral therapy

A

began the era – major impact on prolonging life span

105
Q

True or false: only ATV of protease inhibitors is used w/o booster

A

true

106
Q

What are examples of integrase inhibitors?

A

raltegravir, elvtegravir, dolutegravir

107
Q

What’s the MOA of integrase inhibitors?

A

block integration of proviral gene into human DNA
newest class of ART and regarded as 1st line therapy

108
Q

What are ADRs/ DIs of integrase inhibitors?

A

pretty well tolerated – increases creatine kinase, LFT, GI…minimal DIs

109
Q

What’s a CCR5 inhibitor?

A

maraviroc

110
Q

Whats the MOA of CCR5 inhibitors?

A

inhibits CCR5 receptors on cell membrane preventing entry of HIV into cell

111
Q

What are ADRs of CCR5 inhibitors?

A

hepatotoxicity – black box warning
muscle and joint pain
diarrhea

112
Q

What are DIs of CCR5 inhibitors?

A

metabolized by CYP450 – dosage adjustments are required

113
Q

True or false: you do not need genetic testing to start Maraviroc

A

false

114
Q

What do you need to test for Maraviroc?

A

HIV tropism w/ trofile test

115
Q

What must you be to use maraviroc?

A

CCR5-positive

do not use with dual/mixed or CXCR-4 tropic HIV-1

116
Q

What is paxlovid?

A

Drug for COVID-19 that’s combo but in separate tablets (Nirmatreivir and ritonavir)

reduces symptoms by 2-3 days

117
Q

What’s the MOA of nirmatreivir and ritonavir (paxlovid)?

A

protease inhibitor binding to enzyme preventing replication

118
Q

Are there any DIs with paxlovid?

A

Yes - a lot.

119
Q

What is remdesivir?

A
  • inpatient or outpatient IV
  • for covid or ebola
  • RNA polymerase inhibitor
  • may interact w/ hydroxychloroquine
  • can cause elevated liver enzymes, PT increase, renal impairments
120
Q

What is malnupiravir?

A
  • oral COVID med
  • within 5 days of symptoms
  • acts as ribonucleoside analog for viral RNA polymerase increasing mutations
  • diarrhea, nausea, dizziness
121
Q

Can antiviral medications treat viral hepatitis?

A

yes – NRTIs, NPIs, interferons, nucleoside analogues

122
Q

What’s a serious potential side effect of isoniazid?

A

peripheral neuropathy from lack of B6

Clinical Pharmacology (14 decks)

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