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Pulmonology > Sweatman - Anti-Fungals > Flashcards

Sweatman - Anti-Fungals Flashcards

1
Q

What are the presentation and characteristics of Candida albicans (yeast)?

A
  • Fever, tachycardia, patchy infiltrates on chest film
  • Uncommon cause of pneumonia; hematogenous spread seen in immuncompromised patients
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2
Q

What are the presentation and characteristics of Cryptococcus neoformans (yeast)?

A
  • Cyptococcosis
    1. Often asymptomatic; may have productive cough, fever and weight loss
    2. Associated with pigeon droppings; can produce cryptococcal meningitis
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3
Q

What are the presentation and characteristics of Aspergillus (mold) aspergillosis?

A
  • Wheezing, dyspnea and cough w/allergic broncho-pulmonary aspergillosis (ABPA): fever, cough, dyspnea, pleuritic chest pain, and hemoptysis seen in invasive forms, usually in immuno-compromised patients
  • Aspergillomas (fungal balls) can form in pre- existing cavities; the invasive form spreads hematogeneously
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4
Q

What are the presentation and characteristics of Blastomyces dermatidis (dimorphic) blastomycosis?

A

  • Fever, chills, productive cough. May also present with skin or bone lesions, or genitourinary involvement
  • Causes pneumonia-like lung disease and may progress to disseminated disease
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5
Q

What are the presentation and characteristics of Histoplasma capsulatum (dimorphic) histoplasmosis?

A

  • Often asymptomatic; young or immuno-compromised may have disseminated or chronic disease with fever, fatigue and weight loss
  • Caseating granuloma formation in tissue; the disseminated form is marked by multi-system involvement with macrophage infiltrates filled with intracellular fungi
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6
Q

What are the presentation and characteristics of Coccidoides immitis (dimorphic) coccidioidomycosis?

A

  • Fever, cough, headache, chest pain; disseminated or chronic disease produces systemic symptoms
  • May have acute, disseminated or chronic course
    1. Fungal spheres containing endospores are found in granulomas
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7
Q

What is the treatment for Candida albicans (yeast)?

A

Amphotericin B IV and fluconazole

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8
Q

What is the treatment for Cryptococcus neoformans (yeast) - cryptoccosis?

A

  • CNS: Amphotericin B IV + flucytosine PO
  • Non-CNS: fluconazole PO
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9
Q

What is the treatment for Aspergillus (mold) aspergillosis?

A

Amphotericin B IV or itraconazole

  • 1st line: Voriconazole IV
    1. Step down: Voriconazole PO
  • 2nd line: Amphotericin B IV
    1. Step down: Posaconazole PO
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10
Q

What is the treatment for Blastomyces dermatitidis (dimorphic) blastomycosis?

A

Amphotericin B IV or itraconazole

  • 1st line: Fluconazole IV or Amph B IV if severe
    1. Step down: Voriconazole or Itraconazole or Fluconazole
  • 2nd line: Amph B IV
    1. Step down: Voriconazole or Fluconazole PO
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11
Q

What is the treatment for Histoplasma capsulatum (dimorphic) histoplasmosis?

A
  • Severe or immunocompromised: Amphotericin B IV followed by itraconazole PO
  • Mild-moderate: Itraconazole PO
  • Updated Rx: Voriconazole, or posaconazole, fluconazole PO
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12
Q

What is the treatment for Coccidioides immitis (dimorphic) coccidioidomycosis?

A
  • Severe or immunocompromised: Amphotericin B IV followed by itraconazole or fluconazole PO
  • Mild-moderate: Itraconazole or fluconazole PO
  • Updated Rx: Voriconazole or posaconazole PO
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13
Q

What is the primary indication for flucytosine?

A

Cryptococcal infections

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14
Q

How has treatment for Aspergillus and Blastomyces shifted gears?

A
  • There is a move to employ one of the newer azole drugs, which are effective against theses species, rather than Amphotericin B (which remains a second-line treatment option)
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15
Q

Why are most physicians using lipid formulations of Ampho B now?

A
  • To try and avoid the nephrotoxicity associated with the deoxycholate form of the drug
  • Modest improvement, at best, in toxicity profile, and very expensive
  • 3 alternatives: AmBisome, Amphotec, and Abelcet
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16
Q

Why is azole resistance by Asperigillus on the rise?

A
  • Possibly due to increased clinical use, but also to increased agricultural use of azole-like compounds
  • Resistance seems to be associated with mutations in the promotor region of CYP51A, which encodes lanosterol-14α-sterol demethylase activity (the drug target of the azoles)
17
Q

Why is there a trend towards moving away from Itraconazole to the newer azole drugs?

A
  • Oral absorption of itraconazole is low and variable from patient to patient
  • Drug levels achieved with the newer azoles (fluconazole, voriconazole, posaconazole) are much more consistent BUT only fluconazole is able to penetrate the blood-brain barrier
18
Q

What are some potential drug interactions of the anti-fungals?

A
  • Azoles: undergo hepatic CYP metabolism and interact with concurrent drugs metabolized via CYP2C9, 2C19 & 3A4
    1. Neither Amphotericin B nor Flucytosine undergoes hepatic metabolism
  • Amphotericin B: possible interxn w/other nephro-toxic agents and drugs producing hypokelmia
  • Flucytosine: caution advised w/other hematotoxic drugs bc Flucyto can produce anemia and blood dyscrasias, including agranulocytosis
19
Q

What is the MOA of Amphotericin B?

A
  • Binds to ergosterol, the prominent sterol in fungal cell membranes -> forms pores
    1. Amphipathic: combines avidly with ergosterol along the double bond-rich side of its structure and associates with H2O molecules along the hydroxyl-rich side
  • Pore allows leakage, leading to cell death
  • Highly effective in many serious infections, but can also be very toxic
20
Q

Why (and how) does Ampho B affect the kidney?

A
  • Binds to human membrane sterols, probably accounting for the drug’s prominent renal effects
    1. 80% of pts on original formulation experience renal damage -> azotemia, hypokalemia (risk of arrhythmia), reduced GFR, and frank renal failure
21
Q

What are the common AE’s associated with Ampho B?

A
  • Immediate: infusion-related reactions
    1. Fever, chills, muscle spasms, vomiting, headache, and hypotension
    2. Test dose often used to gauge pt rxn
    3. Premedicate: antipyretics, antihistamines, meperidine, or corticosteroids
  • Delayed: renal toxicity
    1. Sometimes necessitates dialysis
    2. Na+ loading often used to reduce pre-renal toxicity (decreased renal perfusion)
    3. Anemia: 2o to renal damage (EPO)
    4. Abnormal liver function tests (LFT’s)
    5. Seizures after intrathecal drug admin
22
Q

What is the MOA of the azoles?

A
  • Prevent the conversion of lanosterol to ergosterol, interrupting cell membrane synthesis -> mediated by CYP 450 enzymes
  • Issue of specificity of drug action on fungal CYP versus mammalian is important
  • Named after the azole ring structure (all of the ones covered in this block are triazoles -> 3 nitrogens)
23
Q

Which CYP’s are affected by the azoles (table)?

A
  • All of them are capable of inhibiting CYP3A4, the major metabolic pathway for prescription meds
  • Can inhibit concurrent meds and can also experience a change in their own metabolism when they are processed through the same metabolic route

Pulmonology (18 decks)

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