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Pharm Exam 4 > Anti-fungal > Flashcards

Anti-fungal Flashcards

1
Q

What are Dermatophytic inf?

A

Common in skin, hair, nails

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2
Q

What are Mucocutaneous inf?

A

Candidal infections involving moist skin or mucus membranes

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3
Q

Name the Anti-fungal drugs for subcutaneous and systemic drug infections.

A
  1. Amphotericin B (Fungizone)
  2. Flucytosine (Ancobon)
  3. Ketoconazole (Nizoral)
  4. Fluconazole (Diflucan)
  5. Itraconazole (Sporanox)
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4
Q

Name the drugs for Cutaneous Mycoses.

A
  1. Terbinafine (Lamisil)
  2. Griseofulvin (Fulvicin, Grifluvin)
  3. Nystatin (Mycostatin)
  4. Miconazole (Monistat)
  5. Clotrimazole (Lotrimin)
  6. Econazole (Spectazole)
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5
Q

What is Amphotericin B? What is its MOA?

A
  • -Large molecule produced by Streptomycin
  • -MOA: binds to sterol moiety (primarily ergosterol) present in membranes of sensitive fungi
  • -This interaction pore or channel formation  leakage of essential nutrients
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6
Q

Is Amphotericin B CIDAL or STATIC?

A

CIDAL

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7
Q

What is nice about Amphotericin B in reference to its spectrum?

A

Selective for fungi (no sterols in bacteria)

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8
Q

What is NOT nice about Amphotericin B in reference to its spectrum?

A

Some selective toxicity towards fungal membranes vs. mammalian cholesterol

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9
Q

What is Amphotercin B used for?

A

Drug of Choice for life-threatening systemic mycoses

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10
Q

T or F: Amp B is very important for immun compromised patients.

A

True

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11
Q

How is Amphotericin B administered?

A

IV or intrathecal if meningitis

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12
Q

Does Amphotericin B cross into the placenta?

A

Yes

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13
Q

Does Amphotericin B cross into the CSF?

A

No–little penetration

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14
Q

Do you have to adjust Amphotericin B dose in renal dysfunction?

A

Yes

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15
Q

What are some adv effects for Amphotericin B?

A
  1. Low therapeutic index – test for anaphylaxis/convulsions
  2. Infusion-related
    Fever/chills
    premedicate with antipyretic or steroid
    Phlebitis at IV site in 70% pts
3. Dose-related
Shock
Nephrotoxicity
Hypokalemia & Hypomagnesemia
Anemia
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16
Q

What is Flucytosine and what is its MOA?

A
  • -Fluorinated pyrimidine converted to fluorouracil

- -MOA – inhibits thymidylate synthetase, thus stops formation of thymidylic acid, an essential DNA component

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17
Q

Is Flucytosine CIDAL or STATIC?

A

STATIC

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18
Q

What is Flucytosine used for?

A

Used only in combination with amphotericin B for treatment of systemic mycoses & candidal or cryptococcal meningitis

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19
Q

T or F: Flucytosine has major issues with resistance, is rapidly orally absorbed and gets into the CSF.

A

True

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20
Q

What are the adv effects of Flucytosine?

A
  1. GI irritation
  2. Bone marrow suppression (WBC plt)
  3. Hepatic toxicity
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21
Q

What is the MOA of Ketoconazole? And when would you use it?

A
  • -MOA - Blocks demethylation of lanosterol to ergosterol

- -Additive with Flucytosine against Candida

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22
Q

What are the adverse effects of Ketoconazole?

A

–Suppresses testosterone & cortisol synthesis
–GI,Hepatic
–Decreases androgen = gynecomastia, impotence,
decreased libido,
menstrual irregularities

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23
Q

Where is Ketoconazole metabolized?

A

Extensively metabolized in liver

Blocks P450 = increases warfarin

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24
Q

How is Ketoconazole administered? What increases its absorption?

A

ORAL & Topical

Coca-Cola increases absorption = increased acidity

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25
Q

Does Ketoconazole enter the CSF?

A

No it does not

26
Q

What is Fluconazole used for ? What is its MOA?

A

–MOA: same as Ketoconazole: Blocks demethylation of lanosterol to ergosterol
–DOC for:
1. Cryptococcus neoformans
2. Candidemia
3. Histoplasmosis
–High rate of relapse
Chronic ambulatory Tx with fluconazole

27
Q

Can Fluconazole get into the CSF?

A

Yes

28
Q

Is Fluconazole STATIC or CIDAL?

A

Fungistatic

29
Q

What is nice about Fluconazole?

A

Lacks endocrine side effects

30
Q

What is Itraconazole? What is its MOA?

A
  • -Synthetic triazole

- -MOA: same as other azaleas; Blocks demethylation of lanosterol to ergosterol

31
Q

Is Itraconazole CIDAL or STATIC?

A

STATIC

32
Q

How is Itraconazole absorbed? What increases its bioavailability?

A
  • -Well-absorbed orally

- -Food!

33
Q

Does Itraconazole distribute into the CNS?

A

No

34
Q

Where is Itraconazole metabolized?

A

In the liver: Inhibits P 450

35
Q

A patient is experiencing N/V, rashes, hypokalemia, HTN, edema, HA. What is the causative agent?

A

Itraconazole

36
Q

What is Itraconazole used for?

A

Onychomycosis

37
Q

How is Itraconazole administered?

A

pulse-dosing”: 200 mg PO bid for 1st wk of month x 2 mo (fingernails) or 3-4 mo (toenails)

38
Q

What are the contraindications for Itraconazole?

A 
--Contraindicated with 
cisapride, 
dofetilide, 
lovastatin, 
PO midazolam, 
pimozide, 
quinidine, 
simvastatin, 
triazolam.

–Negative inotrope; do not use for onychomycosis if ventricular dysfunction

39
Q

What is Terbinafine’s MOA? And is it CIDAL or STATIC?

A

MOA: Inhibits synthesis of ergosterol

–CIDAL

40
Q

What is Terbinafine used for?

A

“Drug of Choice” for both dermatophytoses and onychomycoses

41
Q

When will you see the Optimal clinical effect of Terbinafine ?

A

Optimal clinical effect may not be apparent for several months following completion of therapy

42
Q

What drugs are the Echinocandins?

A
  1. Caspofungin (Cancidas)
  2. Micafungin (Mycamine)
  3. Anidulafungin (Eraxis)
43
Q

What is the MOA of the Echinocandins?

A

Inhibit synthesis of β (1,3)-D-glucan, essential fungal cell wall component

44
Q

What are the “Penicillins” of fungi world?

A

Echinocandins

45
Q

What are the contraindications of the Echinocandins?

A

Pregnancy

46
Q

What are the contraindications of the Echinocandins?

A

Pregnancy

47
Q

What is the MOA of Griseofulvin?

A

Interacts with microtubules to disrupt mitotic spindles and thus inhibit mitosis

48
Q

What is Griseofulvin used for?

A

Used for severe tinea infections unresponsive to other antifungal agents

49
Q

T or F: Griseofulvin ineffective topically.

A

True

Distributes chiefly to infected keratinized tissue

50
Q

T or F: Griseofulvin ineffective topically.

A

True

51
Q

Is Griseofulvin CIDAL or STATIC?

A

STATIC

Therapy MUST continue until infected tissue replaced

52
Q

What is the treatment of choice for “tinea” infections?
Skin – few days
Palm – few months
Nails – few months

A

Griseofulvin

53
Q

T or F: Griseofulvin does not induce hepatic cytochrome P-450 activity,

A

False; it does !

54
Q

What are the adverse effects of acute Griseofulvin?

A
  • -Allergy, HA, nausea
  • -May cause hepatotoxicity
  • -ETOH: POTENTIATES intoxicating effects of alcohol
  • -Pregnancy: TERATOGENIC
55
Q

What are the adverse effects of acute Griseofulvin?

A
  • -Allergy, HA, nausea
  • -May cause hepatotoxicity
  • -ETOH: POTENTIATES intoxicating effects of alcohol
  • -Pregnancy: TERATOGENIC
56
Q

What is the MOA of Nystatin? Is it CIDAL or STATIC?

A
  • -Structure, chemistry, MOA, resistance similar to amphotericin B
  • -CIDAL
57
Q

What is Nystatin used for?

A
  • -Thrush–Restricted to treatment of Candida infections because of its systemic toxicity
  • -Mycostatin
  • -Vulvovaginitis
  • -Candidiasis
58
Q

How is Nystatin administered?

A
  • -Thrush/Mycostatin: oral lozenges –Oral “swish & swallow”
  • -Never used parenterally
  • -Negligibly absorbed from GI tract
  • -Candidiasis (cream ointment)
  • -Vulvovaginitis (vaginal tablet)
59
Q

How is Nystatin excreted?

A

In the poo poo !!!

60
Q

What are the adverse effects of Nystatin?

A

Occasional N/V

61
Q

These OTHER topical agents are rarely administered parenterally because of severe toxicity–they are similar to ketoconazole in their MOA, antifungal spectrum, distribution, & metabolism–what are they?

A
  1. Clotrimazole (Lotrimin, Mycelex)
  2. Miconazole (Monistat, Micatin)
  3. Econazole (Spectazole)

Pharm Exam 4 (10 decks)

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