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AU 15 - Pharm Final > Antifungals > Flashcards

Antifungals Flashcards

1
Q

What is the major difference between bacteria and fungi

A

Fungi differ from bacteria because they are eukaryotic (80S ribosomes as compared to 70S) - so many antibacterial agents are ineffective

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2
Q

Which are larger, fungi or bacteria?

A

Fungi are much larger and slower growing

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3
Q

What is the difference in the cell wall of fungi and bacteria?

A

Fungi have a rigid cell wall made of chitin and glucans - whereas bacteria have mucopeptide cell walls

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4
Q

What is unique about fungi cell membranes?

A

Fungi contain ergosterol instead of cholesterol

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5
Q

Where are fungal infections common? Why are they difficult to treat?

A

Poorly vascularized tissues, or skin, nails, and hair

Difficult to treat since antifungal agents are poorly soluble and not distributed or retained well

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6
Q

What sort of response do fungi cause?

A

They cause a cellular immune response - which may interfere with drug penetration

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7
Q

How do treatments differ between fungi and bacterial infections?

A 
Bacterial = use short term low toxicity therapy
Fungal = use long term high toxicity therapy
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8
Q

What are the different types of fungal infections?

A

Superficial/cutaneous
Subcutaneous
Systemic

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9
Q

Griseofulvin Mechanism

A

Mitotic Inhibitor

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10
Q

Is Griseofulvin static or cidal?

A

Static

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11
Q

Griseofulvin selectivity

A

Taken up by keratinocytes or precursor cells

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12
Q

Griseofulvin Clinical uses

A

Active against dermatophytes (hair, skin, nails)
Fungi are lost as hair and nails fall out
Used to treat ringworm

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13
Q

Griseofulvin toxicity

A

Well tolerated, but long term use can lead to headache, memory loss, skin rashes, photosensitivity rxsns, porphyria

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14
Q

Griseofulvin Resistance

A

Rare, but likely related to decreased transport into cells

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15
Q

5-Flucytosine Mechanism

A

Inhibits or alters DNA/RNA synthesis

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16
Q

5-Flucytosine static or cidal?

A

Both

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17
Q

5-Flucytosine Clinical uses

A

Effective in combo with Amphotericin B to treat cryptococcal meningitis
Use with Amphotericin B also decreases the incidence of resistance

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18
Q

5-Flucytosine Toxicities

A

Bone marrow depression, neutropenia, throbocytopenia

Careful to monitor patients who ahve renal insufficiency to avoid toxicity

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19
Q

5-Flucytosine Resistance mechanisms

A

High resistance

Due to transport alterations, cytosine deaminase alterations, and anabolic enzyme alterations

20
Q

Amphotericin B Mechanism

A

Interaction with membrane sterols to form a pore and/or alter the membrane fluidity
Binding to ergosterol of fungal cell membrane causes a loss of K, altering Na/K-ATPase activity, permeability, and amino acid uptake

21
Q

Amphotericin B fungicidal or static?

A

Fungicidal

22
Q

Amphotericin B selectivity

A

Binds to fungal ergosterol much more readily than human cholesterol

23
Q

Amphotericin B Clinical uses

A

Best choice for treating systemic fungal infections

  • Candidiasis
  • Histoplasmosis
  • Coccidiomucosis
  • Blastomycosis
  • Aperigillus
  • Cryptococcoses
24
Q

Amphotericin B Toxicities

A

A whole bunch

-Nephrotoxicity the main one?

25
Q

Amphotericin B Resistance mechanisms

A

Rare - may occur due to alteration of sterol content or composition

26
Q

Amphotericin B Drug interacitons

A

Can increase the cytotoxicit of Rifampicin
5-FC plus Amphotericin B can used to treat Cryptococcal meningitis
Syntergism or additivity with Amph B + Triazoles

27
Q

Nyastatin Mechanism

A

Interaction with membrane sterols to form a pore and/or alter the membrane fluidity
Binding to ergosterol of fungal cell membrane causes a loss of K, altering Na/K-ATPase activity, permeability, and amino acid uptake

28
Q

Nyastatin Clinical use

A

Topical treatment for candidiasis, thrush, esophaginitis, vaginitis

29
Q

Nyastatin toxicities

A

Minimal

30
Q

Azoles Mechanism

A

Bind through ring nitrogen to heme of cytochrome p450 and inhibit the lanosterol C-dimethylase system

31
Q

Are Azoles fungistatic or fungicidal?

A

Fungistatic at low concentrations

Fungicidal at high concentrations

32
Q

Azoles selectivity

A

100-fold greater binding affinity to fungal cell lanosterol C14-demethylase compared to mammalian enzyme

33
Q

Azoles resistance

A

Overproduction/mutation in C14-demethylase

Dug efflux

34
Q

Azoles drug interactions

A

Inhibitors/substrates of liver p450 enzumes change PK effects and have cardiovascular effects

35
Q

What are the different Allylamines?

A

Naftifine

Terbinafine (Lamisil)

36
Q

What are the different Azoles

A

Imidiazoles

Triazoles

37
Q

Allylamines Mechanism

A

Inhibits Sqalene Epoxidase - leading to acucmulation of sqalene

38
Q

Are Allylamines fungicidal or static?

A

Fungicidal

39
Q

Allylamines selectivity

A

Hose squalene epoxidase is much less effected

40
Q

Allylamine clinical uses

A

treatment of skin and nail infections

Topical use for dermatophytes

41
Q

Allylamine Toxicities

A

Potential liver toxicity

42
Q

Echinocandins Mechanism

A

Osmotic lysis due to loss of cell wall integrity - due to the inhibition of B-glucan synthase

43
Q

Echinocandins Clinical uses

A

Systemic candidiases, asperfillosis, antifungal prophylaxis in bone marrow transplant patients

44
Q

Echinocandinds toxicities

A

Well tolerated but some fears of allergic histamine release

45
Q

Travaborole Mechanism

A

Inhibits the ability of Leucyl-tRNA to be attached to leucine - protein synthesis is inhibited since amino=acyl tRNA for leucine is not formed

46
Q

Travaborole selectivity

A

Mammalian enzyme has a different structure than fungal enzume at critical aa recognition site

47
Q

Travaborole clinical use

A

Topical for onychomycosis of nail in 10% of formulation along with ciclopirox

AU 15 - Pharm Final (7 decks)

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