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MDCM626 > Antifungals > Flashcards

Antifungals Flashcards

1
Q

Allylamines?
What do they do?

Cidal or static?

What is their problem?

A

Inhibit the conversion of squalene to squalene epoxide

Step in Sterol biosynthesis

Effectively block downstream conversion of lanosterol and ergosterol–> Malfunction

Static or cidal depends on the species

Causes build up of squalene

  1. Membrane tension, faulty membrane
  2. Build up of squalene

Problem very greasy not good systemically and first pass is an issue.

Not orally available mostly topical use

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2
Q

Name the Allylamines?

A

Naftifine

Terbinafine (topical and pill)- One example of one that can be used systemically

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3
Q

WHat are the Non-Allylamines squalene epoxidase inhibitors?

A
  • Butenafine - Broader spectrum
  • Tolnaftate - Non-prescription preparations for decades.
  • Topically used greasy
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4
Q

Conazoles

What do they do?

A

Ergosterol biosynth inhibitors

Azole group think inhbition of CYP450s

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5
Q

Antifungal coverage chart

A
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6
Q

What is the general trend with conazoles in terms of spectrum?

A

Spectrum increases as you go from:

  • Fluconazole (No molds)
  • Itraconazole
  • Voriconazole
  • Isavuconazole
  • Posaconazole (Broad and best)
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7
Q

What are the broad spectrum conazoles?

A

Vori, Isavu, Posa

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8
Q

Amphotericin spectrum?

A

Broad pretty much everything.

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9
Q

Fungin Coverage?

A
  • Good with yeast but variable efficacy with everything else
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10
Q

Difference between Human and Fungal cells

A

Sterol they have ergosterol instead of cholesterol

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11
Q

Conazole

MOA

A
  • Block synthesis at a later step than Allylamines
  • Blocking P450 resposible for oxidating Lanosterol
  • This causes leakage
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12
Q

Conazole Resistance and Main interaction with drugs and P450?

A
  • Target modification and efflux - This whole thing occurs much more slowly than bacteria
  • Interaction with Heme of P450 and Azole nitrogen lone pair.
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13
Q

Coverage of conazoles

Yeast (Candida)

Mold (Asperigillus, Fusarium, Zygomycetes)

A
  • Yeast all- Fluconazole, Itraconazole, Voriconazole, Posaconazole)
  • Asperigillus- Itra, Vori, Posa
  • Fusarium- Vori and Posa
  • Zygo- Posa
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14
Q

Conazole P450 interactions

3 points to know?

Mechanism of Human P450 interactions?

A
  • All have 3A4
  • Voriconazole has the most
  • Isavu and Posa have the fewest
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15
Q

WHat other interactions do conazoles have?

Oral bioavailability increases when?

A
  • P-glycoprotein transporters - Mostly the biggers ones
  • Increases with increase in acid (isaconazole and posaconazole)
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16
Q

Most conazoles?

Which one doesnt?

A
  • Lengthen QTc
  • But Isavuconazole shortens
17
Q

Topical and Supository Conazoles?

A
  • Clotrimazole
  • Econazole
  • Butoconazole
  • Very lipophilic not good for systemic
18
Q

Echinocandins MOA?

A

Interferes with the synthesis of the fungal cell wall

blocks 1,3-B-glucan synthase that converts UDP-glucose to B-D glucan

Ruptures the cell wall

19
Q

Echinocandins resistance?

A
  • Mutation of synthase and/or upregulation of other cell wall components.
20
Q

Echinocandins

General special properties?

administration?

Metabolism and Excretion?

A
  • The target is so unique that you dont see toxicity with these drugs
  • Peptide makes it poorly bioavailable
  • Target mutations are common –>relapse is common
  • There are no drug interactions

INJECTION

  • Slow metabolism
21
Q

What are the echinocandins

A

Caspofungin, Anidulafungin, Micafungin

They are all very similar dont need to know specifics within class

22
Q

Major coverage and uses of echinocandins (fungins)

A
  • Narrow spectrum
  • Candidal infections that are resistant to azoles
  • Apergillus infections
  • Less common
    • Esophageal candidiasis
    • Prophylactically in patients undergoing hematopoietic stem cell transplant
23
Q

Amphotericin B

Solubility?

What is it?

Preparation?

A

Polyene macrolide no bacteria effect

Amphoteric: Acidic carboxyl nd basic primary amino functional groups

Poor water solubility

Prep using emulsifying agents and liposomes

24
Q

Amphotericin B

Binding to ergosterol?

A
  • Cation
  • Greasy portions bind to each other
25
Q

Amphotericin B

Spectrum?

Cidal or static?

Toxicity?

A
  • Broad
  • Both
  • Very toxic
    • Nephrotoxic
    • Thrombophlebitis (vein clot causes inflammation)
    • Fever, shaking, chills, hypotension
26
Q

Liposomal targeting of Fungal cell wall?

Selectivity

Role of Liposomes

Toxicities of AmBisome?

A
  • Mammalian have no cell wall
  • Attracts to the fungal cell wall - targeting agent
  • This makes the drug less nephrotoxic because there is less interaction, renal toxicity can still be seen

MDCM626 (26 decks)

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