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Exam 4 Therapeutics > Kays Antifungal Agents Lecture 1 > Flashcards

Kays Antifungal Agents Lecture 1 Flashcards

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1
Q

What are the common Candida species

A

C. albicans, C. glabrata, C. parapsilosis, C. tropicalis, C. krusei, C. guilliermondii, C.
lusitaniae, C. auris (multidrug-resistant)

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2
Q

Invasive candidiasis refers to

A

to severe forms of the disease (not oropharyngeal or

esophageal candidiasis or uncomplicated candiduria

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3
Q

Risk factors for invasive candidiasis:

A

prolonged stay in ICU; central venous catheters;
prolonged therapy with broad spectrum antibacterial agents; receipt of parenteral
nutrition; recent surgery (especially abdominal); hemodialysis; diabetes mellitus

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4
Q

Aspergillus species is what type of species

A

mold that is ubiquitous in the environment

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5
Q

Aspergilluses causes infections primarily in

A

immunocompromised hosts (neutropenia) and it is difficult to treat

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6
Q

Cryptococcus neoformans is an

A

Encapsulated yeast that primarily affects the CNS and respiratory tract

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7
Q

Cryptococcus neoformans is most common in patients with

A

HIV, who have received organ

transplants, or high-dose corticosteroid

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8
Q

Zygomycetes pathogen types are

A

Rhizopus, Absidia, Mucor

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9
Q

Zygomycetes infections are common in what areas of the body

A

pulmonary system; paranasal sinuses with extension to the brain

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10
Q

Primary risk factors for Zygomycetes are:

A

diabetes mellitus
immunosuppression (with profound neutropenia)
penetrating injuries from natural disasters (tornadoes, hurricanes, volcanic eruptions) or combat

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11
Q

Histoplasma capsulatum is most common in what area of the united States

A

Midwestern states along Ohio and Mississippi river
valleys; exposure to bat guano (cave exploration) or other large birds; demolition or
construction

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12
Q

Blastomyces species is most common in whats area of the united states

A

Southeastern and Midwestern states along Ohio and

Mississippi river valleys and Great Lakes region

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13
Q

Coccidioides immitis/posadasii is most common in what area of the United States

A

cluster in southwestern United States (southern

Arizona, southern California, southwest New Mexico, west Texas)

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14
Q

Ampotericin B MOA

A

Increases membrane permeability of fungal cells by binding to ergosterol and causes leakiness and loss of membrane potential

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15
Q

Amphotericin B Resistance MOA & Pharmacodynamic monitoring parameter

A
  • decreased ergosterol biosynthesis, synthesis of alternative sterols.
    Monitoring Parameters is Peak to MIC ratio
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16
Q

Amphotericin B Spectrum of activity

A
  1. Candida species (not C. lusitaniae)
  2. Cryptococcus neoformans
  3. Blastomyces dermatitidis
  4. Histoplasma capsulatum
  5. Coccidioides immitis
  6. Aspergillus species (reduced activity against A. terreus)
  7. Mucor species (and other zygomycetes)
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17
Q

Deoxycholate distribution ) used with amphotericine

A

Poor penetration into CSF, even if meninges are inflamed (»3% of serum)
Highly protein bound (> 90%) – mainly to b-lipoproteins
not appreciably metabolized

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18
Q

Deoxycholate elimination

A

Tri-exponential elimination. 1/2 life 24-48 hours and terminal elimination in 15 days. Renal and Hepatic impairment do not affect clearance

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19
Q

Lipid associated formulations of amphotericin B an kidney concentrations

A

80-90% reduction of concentrations in the kidneys

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20
Q

Clinical Uses of Deoxycholate

A
  1. Disseminated candidiasis
  2. Cryptococcosis
  3. Aspergillosis
  4. Histoplasmosis
  5. Blastomycosis
  6. Coccidioidomycosis
  7. Mucormycosis
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21
Q

Deoxycholate Dosing and Administration

A

0.1mg/kg or 1kg over 20 to 30 minutes (do not premedicate.
Infused over 4-6 hours (rapid infusions associated with more adverse reactions.
Intrathecal/ intraventricular administration: 0.1mg then increase to a maximum o f0.5 every 48-72 Hours

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22
Q

L-AmB dosing

A

1.5-6mg/kg daily infused over 2 hours

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23
Q

ABLC Dosing

A

5mg/kg dosing daily, infused at 2.5mg/kg/hour

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24
Q

Dosing Weight for Amphotericin B

A

Use Ideal or adjusted despite lipophilicity

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25
Q

Deoxycholate infusion related Adverse reactions

A
  • Infusion related (pretreat with NSAID, antihistamine etc)

- Thrombophlebitis: slow infusion and rotate sites, consider adding heparin

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26
Q

Deoxycholate Non-infusion related adverse reactions

A
  • Dose dependent nephrotoxicity (increases in serum creatinine and BUN) can consider sodium repletion in depleted patients. use saline both before and after AMB
  • Hypokalemia, Hypomagnesemia, Bicarb wasting, anemia
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27
Q

Intrathecal Deoxycholate administration adverse effects

A

nerve pain, head ache, vomiting, paraplegia, seizures,

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28
Q

Lipid associated formulations of amphotericin B an there adverse effects

A

Less nephrotoxicity & infusion-related toxicities with lipid-associated formulations except for ABCD.
- manage L-AMB infusion reactions with diphenhydramine

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29
Q

Interactions for Amphotericin B

A
  • Nephrotoxic agents
  • Digoxin and skeletal muscle relaxants, may potentiate hypokalemia
  • Flucytosine - increase therapeutic effect and increase potential toxicity
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30
Q

FLUCYTOSINE Mechanism of Action

A
  1. 5-FC enters fungal cell –> deaminated to 5-FU –> 5-FU gets incorporated into fungal
    RNA –> interference with protein synthesis
  2. 5-FC enters fungal cell –> metabolized to 5-fluorodeoxyuridine monophosphate –>
    inhibits thymidylate synthetase –> interferes with DNA synthesis
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31
Q

FLUCYTOSINE Spectrum of activity

A
  1. Cryptococcus neoformans

2. Candida species

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32
Q

FLUCYTOSINE PK

A
  • Absorption – well absorbed orally (> 90%
  • Distribution
    a. Penetrates into CSF ( »75% of serum)
    b. Negligible protein binding (2 to 4%)
  • Metabolism/Excretion
    a. Small amount converted to 5-FU
    b. 85 to 95% excreted unchanged in urine
    c. Normal half-life – 3 to 5 hours; anephric half-life – 85 hours
    d. Removed by HD & PD
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33
Q

Flucytosine clinical use

A

primarily in combination with amphotericin B for cryptococcal meningitis

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34
Q

Flucytosine Adverse reactions

A
  1. Gastrointestinal (6%) – nausea, vomiting, diarrhea, abdominal pain, enterocolitis
  2. Hematologic – Bone marrow suppression (more common with serum concentrations > 100 μg/ml)
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35
Q

Flucytosine Dosing

A

Normal Renal Function – 100 to 150 mg/kg/DAY PO in 4 divided doses (25 to 37.5 mg/kg/DOSE Q6H) – available in 250 mg and 500 mg capsules.
Renal Dosing
see chart start at 25-37.5 when greater than 40 q 6 hours

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36
Q

Dosing body weight for Flucytosine

A

ideal body weightfor non-severe

adjusted body weight if severe

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37
Q

Flucytosine Monitoring

A

a. Baseline: CBC, platelets, Scr, BUN

b. Reduce dose in patients with bone marrow or GI toxicity

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38
Q

Ketoconazole MOA

A
  1. inhibits synthesis of ergosterol via inhibition of the fungal cytochrome P-450 dependent
    enzyme lanosterol 14-α-demethylase
  2. Blocks formation of ergosterol → damage to fungal cell membrane –> disruption of
    structural integrity –> leakage of cytoplasm –> inhibition of growth (fungistatic)
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39
Q

Ketoconazole Spectrum of Activity

A
  1. Candida albicans
  2. Cryptococcus neoformans
  3. Histoplasma capsulatum
  4. Dermatophytes (tinea
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40
Q

Ketoconazole PK

A

Absorption
a. Well absorbed orally (F=75%); peak concentration 1 to 2 hours after oral dosing
b. Absorption is inversely related to gastric pH
Distribution
a. Widely distributed throughout body (CSF penetration is negligible)
b. Protein binding 95 to 99%
Metabolism/Elimination
a. Extensively metabolized in the liver
b. Major excretory route is enterohepatic – 85 to 90% excreted in bile & feces
c. Biphasic elimination – half-life 2 hours (during the first 8-12 hours); 9 hours
thereafter
d. Dosage adjustment not needed in renal failure; not removed by HD or PD

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41
Q

Ketoconazole Clinical Uses

A
  • not used orally for first line therapy due to toxicity
  • chronic mucocutaneous candidiasis
  • histoplasmosis in immunocompetent hosts
42
Q

Ketoconazole Adverse Reactions

A
  1. Gastrointestinal (20-30%) – N/V/D; anorexia; abdominal pain
  2. Hepatotoxicity
  3. Endocrine - dose dependent inhibition of adrenal steroid and test synthesis, menstrual irregularties
43
Q

Ketoconazole Drug interactions

A

CYP3A4 inhibitor
Prolonged PT in anticoagulants
Rifampin decreases ketoconazole conc
Cyclosporinw, tacrolimus, sirolimus increased concentrations
Phenytoin decreased clearance and increased conc

44
Q

Itraconazole MOA

A
  1. Inhibits synthesis of ergosterol via inhibition of the fungal cytochrome P-450 dependent
    enzyme lanosterol 14-α-demethylase
  2. Blocks formation of ergosterol → damage to fungal cell membrane –> disruption of
    structural integrity –> leakage of cytoplasm –> inhibition of growth (fungistatic)
45
Q

Itraconazole spectrum of activity

A
  1. Aspergillus spp.
  2. Histoplasma capsulatum
  3. Blastomyces dermatitidis
  4. Candida species
  5. Coccidioides immitis
  6. Cryptococcus neoformans
  7. Sporothrix schenckii
46
Q

Itraconazole PK

A

Absorption
- after oral administration is dependent on GI acidity. oral solution better absorbed than capsules (not acid dependent. SUB-itraconazole is very bioavvailable and not acid dependent
Distribution
- widely distributed throughout body tissues poor CNS
Metabolism/Elimination
- CYP3A4 predominantly. long half-life 30-40 hours. clearance decreases with higher doses, no adjustment for renal dysfunction

47
Q

Itraconazole Clinical Uses/Dosing

A
  1. Histoplasmosis (first choice) – 200 mg PO TID x 3 days, then 200 mg PO BID
  2. Aspergillosis (not first-line) – 200 mg PO BID
  3. Blastomycosis – 200 mg PO TID x 3 days, then 200 mg PO BID
  4. Life-threatening infections – administer oral loading dose of 200 mg three times daily
    for first 3 days of therapy, then 200 mg PO daily or BID
  5. Onychomycosis of toenails – 200 mg PO daily for 12 consecutive weeks
  6. Onychomycosis of fingernails – 200 mg PO BID for 1 week; repeat 3 weeks later
48
Q

Itraconazole drug monitoring

A

Serum trough conc 0.5-1 microgram/ml associated with efficacy

49
Q

Itraconazole Adverse Reactions

A

Hepatotoxicity, CHF, QTC, amd Pregnant and nursing mothers

50
Q

Itraconazole Drug interactions

A

metabolized by CYP3A4

  • increased drug concentrations if administered with itraconazoledigozxin, quinidine, benzidiazapines, HMG-CoA reductase inhibtors
  • decreased plasma concentrations with carbamazepine, phenytoin, phenobarbital, rifampin, fiabutin, nevirapine
  • increased Itraconazole conc. clarithromycin, ininavir, and ritonavir
51
Q

Fluconazole MOA

A
  1. Inhibits synthesis of ergosterol via inhibition of the fungal cytochrome P-450 dependent
    enzyme lanosterol 14-α-demethylase
  2. Blocks formation of ergosterol → damage to fungal cell membrane ® disruption of
    structural integrity ® leakage of cytoplasm ® inhibition of growth (fungistatic)
52
Q

Fluconazole Spectrum of activity

A
  1. Candida species (less active vs. C. glabrata [up to 30% resistance]; not active vs. C. krusei)
  2. C. albicans resistance reported (2.1-5.7%)
  3. Cryptococcus neoformans
  4. Histoplasma capsulatum
  5. Blastomyces dermatitidis
  6. Coccidioides immitis
53
Q

Fluconazole PK

A 
Absorption
- good orally
Distribution
- 60% serum in uninflammed meninges 
Metabolism/Excretion
- unchanged in urine, long half life (30 hours)
- reduction required in renal insufficncy
- removed by dialysis
54
Q

Fluconazole Clinical Uses and Dosing

A
  • Noninvasive candidiasis
    a. Oropharyngeal – 200 mg on day 1, then 100-200 mg daily for 2 weeks
    b. Esophageal – 400 mg on day 1, then 200-400 mg daily for 14-21 days
    c. Vaginal – 150 mg x 1 dose
  • Invasive candidiasis (e.g., candidemia) – if C. albicans: 800 mg (12 mg/kg) loading
    dose, then 400 mg (6 mg/kg) daily; if C. glabrata: 800 mg daily (loading dose?)
    -Prophylaxis in patients undergoing bone marrow transplantation – 400 mg daily
  • Cryptococcal Meningitis - inferior alternative to amphotericin B w/ or w/o flucytosine for induction therapy
55
Q

What Body weight should be used for Fluconazole Dosing

A

TBW

56
Q

Fluconazole Adverse Reactions

A

QT prolongation, torsades de point

57
Q

Flucconazole Drug Interactions

A

Potent inhibitory of CTP2C9

Moderate inhibitor of CYP3A4

58
Q

Voricaonazole MOA

A
  1. Inhibits synthesis of ergosterol via inhibition of the fungal cytochrome P-450 dependent
    enzyme lanosterol 14-α-demethylase
  2. Blocks formation of ergosterol → damage to fungal cell membrane ® disruption of
    structural integrity ® leakage of cytoplasm ® inhibition of growth (fungistatic)
59
Q

Voriconazole SOA

A
  1. Aspergillus species (including amphotericin and itraconazole-resistant strains
  2. Scedosporium apiospermum
  3. Candida species (C. albicans, C. tropicalis, C. glabrata, C. parapsilosis. C. krusei)
  4. C. glabrata resistance (0.1-18.4%)
  5. Histoplasma capsulatum
  6. Blastomyces dermatitidis
  7. Cryptococcus neoformans
  8. Fusarium species
60
Q

Voriconazole PK

A

Absorption
- orally available, tablets taken 1 hour before or after meals
Distribution
- Extensive tissue binding
Metabolism
- Significantly metabolized by cytochrome P450 isoenzymes (2C19, 2C9, 3A4)
- Metabolism is saturable – pharmacokinetics are non-linear
Elimination
- half life 6 hours
- no dosage adjustment for oral dosing
- do not use IV Voriconazole if CRCL <50 (see dosing chart in notes)

61
Q

Voriconazole Adverse Events

A
  • Visual Disturbances
  • Elevated Liver function tests
  • QTc prolongation
  • skin reactions
  • CNS
62
Q

Voriconazole TDM

A

trough concentrations goals 1-1.5micro/ml

63
Q

Voriconazole Drug Interaction (CYP3A4, CYP2C9, CYP2C19)

A
  • Rifampin, rifabutin, carbamazepine will decrease voriconazole levels
  • increased exposure to voriconazole with (sirolimus, terfenadine, astermizole, contraindicated)
64
Q

Posaconazole MOA

A

blocks synthesis of ergosterol – same as other triazole agents

65
Q

Posaconazole SOA

A
  1. Candida species (less active against C. glabrata)
  2. Aspergillus species
  3. Cryptococcus neoformans
  4. Histoplasma capsulatum
  5. Mucor species
  6. Coccidioides species
66
Q

Posaconazole PK

A
  • Oral suspension: decreased absorption with PPI use
  • DR tablets: absorption not affected
  • Suspension absorption better with food
  • protein bound and primarily excreted with feces
  • avoid when Cr. Cl is < 50
67
Q

Posaconazole Clinical Use

A 
- Prophylaxis of invasive Aspergillus and
Candida infections in immunocompromised
patients (HSCT; hematologic malignancies
with prolonged neutropenia)
- Oropharyngeal candidiasis
- Oropharyngeal candidiasis refractory to
fluconazole and/or itraconazole
-
68
Q

Posaconazole TDM

A
  • trough concentrations < 0.7 associated with fungal breakthrough for prophylaxis
  • trough concentrations > 1 assosciated with treatment response for invasive aspergillus
69
Q

Posaconazole Drug Interaction (strong CYP3A4 inhibitor)

A

Cyclosporine, Tacrolimus, Sirolimus, Midazolam

70
Q

Posaconazole Adverse Events

A

N/V, Elevated Liver enzymes, QTC prolongation

71
Q

Isavuconazole MOA

A

Isavuconazonium sulfate is the prodrug of isavuconazole – metabolized by esterases in
blood
2. Inhibits synthesis of ergosterol (key component of fungal cell membrane) by inhibiting lanosterol 14-alpha-demethylase (responsible for conversion of lanosterol to ergosterol)
–> depletion of ergosterol weakens cell membrane structure and function

72
Q

Isavuconazole SOA

A
  1. Aspergillus species (A. flavus, A, fumigatus, A. niger)
  2. Mucor
  3. Rhizopus
73
Q

Isavuconazole PK

A

Linear PK up to 600mg ,

good oral bioavailability High VD. no dosage adjustment for renal impairment or ESRD.

74
Q

Isavuconazole Clinical Uses

A
  1. Invasive aspergillosis in patients ≥ 18 years of age

2. Invasive mucormycosis in patients ≥ 18 years of age

75
Q

Isavuconazole Adverse Events

A

N/V , infusion related reactions, Hypokalemia, Hypersensitivity, does not cause QTc prolongation

76
Q

Isavuconazole Drug Interactions (CYP3A4 substrate)

A
  • agent increases concetrations of cyclosporine, tacrolimus, sirolimus, midazolam
77
Q

Isavuconazole Contraindications

A

ketoconazole, ritonavir, rifampin, carbamazepine, st johns wart, do not use in patients with familial short QTc syndrome

78
Q

Caspofungin MOA

A

Glucan synthesis inhibitor leading to noncompetitive inhibition 1,3-β-D-glucan, an
integral polysaccharide component of fungal cell wall ® fungicidal

79
Q

Caspofungin SOA

A
  1. Aspergillus species
  2. Candida species, including azole-resistant strains (C. glabrata resistance up to 12%;
    may have activity vs. C. auris)
  3. Less active vs. C. parapsilosis
  4. Limited activity against Histoplasma capsulatum, Cryptococcus neoformans,
    Fusarium, and Mucor
80
Q

Caspofungin PK

A

IV only, polyphasic half-life, 9-11 hours, then 40 to 50, no dosage adjustment in renal or mild hepatic issues.

81
Q

Caspofungin Indications

A
  • Candidemia
  • Esophageal candidiasis
  • Empiric therapy of presumed fungal infections in febrile neutropenia
  • Invasive aspergillosis in patients who are refractory to or intolerant to other therapies
82
Q

Caspofungin Drug Interactions

A
  • Does not induce or inhibit CYP450 system, poor substrate
  • decreases tacrolimus AUC
  • Cyclosporine increases caspofungin
83
Q

Caspofungin Adverse Drug reactions

A
  • Histamine mediated symptoms
  • Fever
  • Phlebitis at infusion sites
84
Q

Micafungin MOA

A

Glucan synthesis inhibitor leading to noncompetitive inhibition 1,3-β-D-glucan, an
integral polysaccharide component of fungal cell wall ® fungicidal

85
Q

Micafungin SOA

A
  1. Aspergillus species
  2. Candida species, including azole-resistant strains (C. glabrata resistance up to 12%;
    may have activity vs. C. auris)
  3. Less active vs. C. parapsilosis
  4. Limited activity against Histoplasma capsulatum, Cryptococcus neoformans,
    Fusarium, and Mucor
86
Q

Micafungin PK

A

IV, half-life 14-17 hours, metabolized by liver and not needing renal adjustment

87
Q

Micafungin Clinical Uses

A
  • Oropharyngeal and esophageal candidaiasis
  • Candidemia
  • Aspergillosis
  • Prophylaxis of Candida infections
  • Dosing in obesity (dosing as body weight +42. up to 200 mg round to 25 mg
88
Q

Micafungin Drug Interactions

A
  • not metabolized via CYP450 pathways
89
Q

Micafungin Adverse Events

A

Byperbilirubinemia, Eosinophelia, rash pruritic

90
Q

ANIDULAFUNGIN MOA

A

Glucan synthesis inhibitor leading to noncompetitive inhibition 1,3-β-D-glucan, an
integral polysaccharide component of fungal cell wall ® fungicidal

91
Q

ANIDULAFUNGIN SOA

A
  1. Aspergillus species
  2. Candida species, including azole-resistant strains (C. glabrata resistance up to 12%;
    may have activity vs. C. auris)
  3. Less active vs. C. parapsilosis
  4. Limited activity against Histoplasma capsulatum, Cryptococcus neoformans,
    Fusarium, and Mucor
92
Q

ANIDULAFUNGIN PK

A

IV, long half-life 26.5 hours, no renal or hepatic metabolism

93
Q

ANIDULAFUNGIN Clinical Uses

A
  • Candidemia and other Candida infections
  • Esophageal candidiasis
  • Higher relapse rate than fluconazole
94
Q

ANIDULAFUNGIN Drug Interaction

A

virtually none

95
Q

Andidulafungin Adverse Events

A

Histamine mediated symptoms Hypokalemia

96
Q

IBREXAFUNGERP MOA

A
  • Similar to the echinocandins (structurally different)

- Limited cross resistance with echinocandins due to only partial overlap of binding sites

97
Q

IBREXAFUNGERP SOA

A
  1. Candida species, including azole- and echinocandin-resistant C. albicans and C.
    glabrata harboring FKS mutations, C. parapsilosis, C. auris
  2. Aspergillus species – similar activity to echinocandins; fungistatic
  3. Pneumocystis jiroveci
  4. Not active Mucor, Fusarium, Cryptococcus, or endemic fungi
98
Q

IBREXAFUNGERP PK

A
  • available orally, dependent on gastric acid, better absorbed with food.
  • large VD
  • Deep tissue penetration except for CNS
99
Q

Ibrexafungerp Clinica Uses

A
  • Vulvovaginal candidiasis (VVC) in adult and post-menarchal pediatric females
  • Verify pregnancy status prior to initiating treatment
100
Q

Ibrexafungerp Adverse Reactions

A

Does not cause QT prolongation, do not use in pregancy

101
Q

Ibrexafungerp Drug Interactions

A

metabolized by and a weak CYP3A4 inhibitor

Exam 4 Therapeutics (5 decks)

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