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PHARM3 > Antifungal-Table 1 > Flashcards

Antifungal-Table 1 Flashcards

1
Q

What are fungi?

A

Eukaryotic organisms that live as saprophytes or parasites

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2
Q

What are the fungal infections?

A

Mycoses
Superficial- skin, hair, nails, mucous membranes
Systemic- deep tissues and organs

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3
Q

What is the 4th common cause of septicemia?

A

Fungal infections in the immunosuppressed

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4
Q

What are the 3 groups of fungi that cause disease?

A

Mold, true yeast, yeast-like fungi

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5
Q

What results in fungal pathology?

A
  • Mycotoxin production
  • Allergenicity/inflammatory reactions
  • Tissue invasion
  • Opportunistic fungal infections
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6
Q

What should you base your selection of antifungal therapy off of?

A

Extent and type of infection

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7
Q

Which infections get topical? Systemic?

A

Topical: superficial and cutaneous
Systemic: follicular, nail, widespread (>20%)

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8
Q

What is the “drying effect” and how are the formulas ranked?

A

If it’s wet dry it, if it’s dry wet it

Gel>lotion/solution>cream>ointment

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9
Q

When are gels/lotions used? Creams? Ointment?

A
  • moist hary or intertriginous areas
  • scaling and non-oozing lesion
  • hyperkeratotic areas
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10
Q

How are powders used?

A

Adjuncts

Can use as an antifungal powder If absorbent

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11
Q

What are the polyene abx?

A

Amphotericin B and Nystatin

Flucytosine, Griseofulvin

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12
Q

What is the MOA of nystatin and ampho B?

A

Bind to ergosterol in the fungal cell membrane and forms a pore- makes them cidal
This leads to fatal damage- only in fungal cells

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13
Q

How does resistance develop against nystatin?

A

active transport mechanism

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14
Q

Why is resistance infrequent with AmphoB?

A

Decreased ergosterols in membrane

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15
Q

What is the ROA for ampho and nystatin?

A

Ampho B- IV

Nystatin- topical, vaginal troche, suspension for oral mucosa

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16
Q

What should you prep with when doing an ampho b IV?

A

Liposomal prep- less renal and infusion toxicity

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17
Q

When is ampho B indicated?

A

Broad spectrum indicated in potentially fatal systemic infections

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18
Q

What are potentially fatal systemic infections?

A

Candida albicans, Histoplasma capsulatum, Crytococcus neoformans, Coccidoices immites, Blastomyces dermatitides, aspergillis

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19
Q

When is nystatin indicated?

A

To suppress candidiasis on the skin and mucous membranes- oral and vaginally

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20
Q

What are ADRs of ampho B?

A

Hypotension, anemia (suppresses RBC production), nephrotoxicity, thrombophlebitis (add heparin), fever/chills (premedicate; abort with demerol), allergic reactions

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21
Q

What are the ADRs of nystatin?

A

N/V/D

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22
Q

What is the MOA of flucytosine?

A

Inhibits synthesis of fungal pyrimidines

Static

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23
Q

What is the ROA of flucytosine?

A

PO

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24
Q

When is flucytosine indicated?

A

In combo with AMphoB to tx systemic candidiasis and Cryptococcus meningitis

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25
Q

What are the ADRs of flucytosine ?

A

N/V/D, rare hepatotoxicity, thrombocytopenia, neutropenia, bone marrow suppression

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26
Q

What is the MOA of Griseofulvin?

A

Static
Binds to fungal microtubules disrupting mitotic spindles
Selectively concentrated in keratin

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27
Q

What is the duration of therapy for Griseofulvin?

A

Depends on the rate of replacement of healthy skin or nails- anywhere from 6-12 mo

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28
Q

When is Griseofulvin indicated?

A

DOC in kids for widespread dermatophyte or intractable dermatophyte infection of nails

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29
Q

What are the ADRs of Griseofulvin?

A

Fever, HA, mental confusion, rashes, GI disturbance

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30
Q

What are the drug interactions of Griseofulvin?

A

P450 inducer- barbiturates, OCP- need to use other bc method, warfain
High fat meals increase absorption and there are potential intoxicating effects with alcohol

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31
Q

What are the Azoles Imidazoles?

A 
Ketoconazole, 
Clotrimazole (Lotrimin, Mycelex)
Miconazole (Monistat, Desenex)
Terconazole (Terazol)
Butoconazole (Femstat 3)
32
Q

What is the MOA of ketoconazole?

A

Predominantly fungistatic but can be cidal dose dependent

Inhibits C14 P450 enzyme – blocks demethyl of lanosterol to ergosterol which disrupts the membrane

33
Q

What is ketoconazole active against?

A
  • Histoplasma, blastomyces, candida, coccidioides

* NOT aspergillus

34
Q

How does ketoconazole affect the human host?

A

Inhibits human steroid synthesis leading to decreased testosterone and cortisol production

35
Q

How is ketoconazole administered?

A

PO- needs gastric acid for dissolution

Only systemic IV option?

36
Q

Does ketoconazole enter the CSF?

A

No

37
Q

What are the ADRs of ketoconazole?

A
  • N/V, anorexia
  • Endocrine effects: gynecomastia, impotence, irreg menses
  • Teratogenic
38
Q

What are the drug interactions of Ketoconazole?

A

P450 inhibitor

39
Q

What leads to resistnace with keto?

A
  • Mutation in C-14 alpha-demethylase gene leading to decreased azole binding
  • Ability to pump azole out of cell
40
Q

How are the other Azoles Imidazoles administered?

A

TOPICAL ONLY- severe toxicity if IV

41
Q

What are the indications for the other Azoles Imidazoles?

A

Contact dermatitis, vulvar irritation, and edema

42
Q

What is topical miconazole a potent inhibitor of?

A

Warfarin metabolism

43
Q

What are the Azole triazoles?

A

Fluconazole, itraconazole, voriconazole, posaconazole,

44
Q

What is the MOA of fluconazole?

A

Same of keto

45
Q

How is fluc different from keto?

A

Lacks endocrine side effects and can penetrate the CSF

46
Q

What is fluconazole the DOC for?

A

Cryptococcus neoformans, candidemia and coccidioidomycosis; effective against all forms of mucocutaneous candidiasis

47
Q

When is fluconazole used prophylactically?

A

In immunocompromised pts

48
Q

What is the ROA of flucon?

A

PO or IV

49
Q

What are the ADRs of flucon?

A

N/V, rash

50
Q

What is fluco an inhibitor of?

A

Moderate inhibitor of CYP3A4 (cyclosporin, lovastatin)

strong inhibitor of CYP2C9 (phenytoin, warfarin)

51
Q

Should flucon be used in preggos?

A

NO it is teratogenic unless in cream form

52
Q

Is itraconazole static or cidal?

A

Statis- lacks endocrine side effects

53
Q

When is itraconazole the DOC?

A

for tx of blastomycosis, aspergillis, sporotrichosis, paracoccidioidomycosis, histoplasmosis

54
Q

What is the ROA for itraconazole?

A

PO- needs acid for dissolution

55
Q

What are the ADRs of itraconazole?

A

N/V, rash, hyPOKalemia, HTN edema, HA

AVOID IN PREGGO

56
Q

What are the drug interactions pf itra

A

Strong inhibitor and substrate of CYP3A4

57
Q

When is itraconazole CI?

A

with lovastatin, simvastatin, midazolam, triazolam. May decrease oral contraceptives effectiveness and increase digoxin levels.

58
Q

What is the ROA of Voriconazole?

A

PO or IV

59
Q

When is Voriconazole used?

A

Reserved for severe infection due to csf and tissue penetration
Invasive aspergillosis and serious infections caused by Scedosporium apiospermum and fusarium species

60
Q

What are the ADRs of Voriconazole ?

A

similar to other azoles; transient visual disturbance occurring shortly after dose

61
Q

What are the drug interactions of Voriconazole?

A

Inhibitor of CYP2C18, 2C9, 3A4. Contraindicated in patients taking rifampin, phenobarbital, carbamazepine. Dose adjustments may be required with statins, benzodiazepines, warfarin.

62
Q

what are the specific requirements for taking posconazole?

A

Oral suspension and needs to be taken with a high fat meal for adequate absorption

63
Q

When is posconazole more effective?

A

treating a number of fungal infections in immunosuppressed patients (myelogenous leukemia, stem cell transplantation, refractory esophageal candidiasis).

64
Q

What are the Allylamines?

A

Terbinafine

65
Q

What is the MOA of Terbinafine?

A

CIDAL

  • Prevents ergosterol synthesis by inhibiting the enzyme squalene oxidase
  • Decreased synthesis of ergosterol
  • Squalene accumulation leading to membrane disruption and cell death
66
Q

What is the PK of Terbinafine?

A

Lipophilic-so penetrates superficial tissues and fingernails

½ life 200-400 hours

67
Q

What is the ROA of Terbinafine?

A

PO

68
Q

What is the duration of tx for Terbinafine?

A

About 3 months

69
Q

When is Terbinafin indicated?

A

Active against dermatophytes and Candida albicans

70
Q

What are the ADRs of Terbenafine?

A
  • HA, N/D, rash, taste and visual disturbances
  • Rare but serious adverse effects:
    - Cholestatic jaundice, blood dyscrasias, Steven-Johnson syndrome
71
Q

What labs need to be done if you put a pt on Terbenafine?

A

Baseline LFT’s and CBC

•Repeat every 4-6 weeks during therapy

72
Q

What are tx options for onychomycosis?

A

1) terbinafine 1st line agent (not candida)

2) itraconazole alternative 1st line therapy,(preferred for candida infections)

73
Q

What are the echinocandins?

A

Caspofungin, Micafungin, Anidulafungin

74
Q

When is Caspofungin used?

A

2nd line therapy for those who have failed amphoB or itraconazole – super expensive so limited to aspergillus and candida species

75
Q

When is micafungin used?

A

Esophageal candidiasis

76
Q

When is micafungin used as prophylaxis?

A

invasive Candida infections in patients undergoing hematopietic stem cell transplantation

77
Q

What are the ADRs of the echinocandins?

A

Fever, rash, nausea, phlebitis, flushing rxn

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