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D&D Unit 4 > Anti-Fungal Agents > Flashcards

Anti-Fungal Agents Flashcards

1
Q

What are some factors that allow the overgrowth of fungal infections? Think opportunistic!

A

1) Alteration in oral flora
- maybe b/c of broad spectrum antibiotics

2) Immunosuppression
- via chemo
- long-term use of SAIDs
- inhaled steroids for asthma

3) Systemic disease
- AIDS, diabetes
- Adrenal suppression

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2
Q

Describe the mechanism of action for amphotericin B

A
  • a polyene => most reliable agent against most fungal pathogens
  • Binds ergosterol in fungal membrane => punches holes => cell stuff leaks out => CELL DEATH

Problem: also binds to cholesterol in mammalian cells

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3
Q

How is amphotericin B absorbed?

A
  • IV or topical

- poor PO

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4
Q

Describe the distribution of amphotericin B

A
  • Rapidly sequester in tissues (liver, spleen, lymph nodes, lungs)
  • then slowly released

Little CNS penetration

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5
Q

How is amphotericin B elminated?

A
  • Slowly via kidney
  • Major route: through biliary tract

t1/2 15 days

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6
Q

Describe the clinical use of amphotericin B

A
  • Most reliable agent against most fungi
  • DRUG OF CHOICE for all life-threatening systemic fungal infections – esp immunosuppressed pts

Often used to start therapy but the replaced by less toxic azoles

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7
Q

Describe the adverse rxns associated with amphotericin B

A
  • NEPHROTOXICITY! — in nearly all pts
  • ANEMIA (BM depression secondary to the above)
  • Fever, chills, vomiting, rigor, hypotension w/ IV use
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8
Q

Describe the mechanism of action of nystatin

A

Similar to amphotericin B

  • a polyene => most reliable agent against most fungal pathogens
  • Binds ergosterol in fungal membrane => punches holes => cell stuff leaks out => CELL DEATH
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9
Q

How is nystatin absorbed?

A
  • Topical use ONLY

Cannot be absorbed PO

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10
Q

Describe the clinical use of nystatin when treating fungal infections

A

Superficial candidal infections

skin, mucous membrane, GI tract

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11
Q

Describe the adverse rxns associated with nystatin

A

mild GI upset if swallowed

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12
Q

Describe the mechanism of action of echinocandins

A
  • Inhibits synthesis of beta(1,3)-D-glucan (this is an essential component of fungal cell walls)
  • Overall => disrupts cell wall

Higher level of selective toxicity b/c mammal’s don’t have cell walls or those enzymes

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13
Q

How is echinocandin absorbed?

A

IV infusion only

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14
Q

What are the situations in which you would want to adjust the dosage for echinocandin?

A
  • Hepatic insufficiency
  • if pt is taking an inducer of P450

No need to adjust for kidney probs

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15
Q

Describe the clinical uses of echinocandins

A
  • Invasive aspergillosis

used in pts who don’t respond to other therapies

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16
Q

Describe the adverse rxns associated with echinocandins

A
  • Histamine-mediated symptoms: rash, facial swelling

- Also fever, n/v, HA

17
Q

What are some types of triazoles?

A
  • Fluconazole

- Itraconazole

18
Q

Describe the mechanism of action of triazoles

A
  • Selective inhibition of fungal cytochrome p450
  • Prevents synthesis of ergosterol => fungistatic-cidal

Great selectivity for fungal P450 instead of mammalian

19
Q

How are triazoles absorbed?

A

PO, IV

  • Bioavailability 90-99%
20
Q

How is fluconazole eliminated?

A
  • Kidneys

May need to adjust dosage w/ renal dysfunction

21
Q

How is itraconazole eliminated?

A

Hepatic metabolism

22
Q

Describe the distribution of fluconazole

A

Can enter CNS

Therefore => used to treat meningitis

23
Q

Describe the clinical uses of fluconazole

A
  • Vaginal candidiasis (if topical tx fails)
  • Oropharyngeal/esophageal candidiasis
  • Tx/prevention of cryptococcal meningitis in pts w/ AIDS
24
Q

Describe the clinical uses of itraconazole

A
  • Dermatophytoses

- Onychomycosis

25
Q

Describe the adverse rxns associated w/ triazoles

A
  • Overall very well-tolerated
  • GI upset, HA, rash, liver enzyme probs

Can inhibition CYP450 metabolism (more so in itraconazole than fluconazole)

26
Q

What are some types of imidazoles?

A
  • Ketoconazole
  • Clotrimazole
  • Miconazole
27
Q

Describe the mechanism of action of imidazoles

A
  • Inhibits fungal p450 enzyme => decreased synthesis of ergosterol
  • Disrupts cell wall synthesis => alter membrane permeability
  • Fungistatic/fungicidal => depends on concentration
28
Q

How is ketoconazole absorbed?

A

PO, IV

Used systemically

29
Q

How are clotrimazole and miconazole absorbed?

A

Topical ONLY

poor PO

30
Q

How are imidazoles distributed?

A
  • poor CNS
  • well-distributed otherwise
  • crosses placenta
31
Q

How are imidazoles eliminated?

A
  • Hepatic metabolism (CYP450 oxidation)

- Also via breast milk

32
Q

Describe the clinical use of ketoconazole

A
  • Systemic infections like candidiasis => use is decreasing b/c of safer drugs
  • Also dermatologic indications
33
Q

Describe the clinical use of clotrimazole and miconazole

A
  • oral and vaginal candidiasis

- used as creams/troches

34
Q

Describe the adverse rxns associated with imidazoles

A
  • Anorexia, n/v

- Hepatotoxicity inhibits CYP450 drug metabolism and mammalian testosterone synthesis

D&D Unit 4 (18 decks)

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