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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
Does Ketoconazole enter the CSF?
No it does not
26
What is Fluconazole used for ? What is its MOA?
--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
Can Fluconazole get into the CSF?
Yes
28
Is Fluconazole STATIC or CIDAL?
Fungistatic
29
What is nice about Fluconazole?
Lacks endocrine side effects
30
What is Itraconazole? What is its MOA?
- -Synthetic triazole | - -MOA: same as other azaleas; Blocks demethylation of lanosterol to ergosterol
31
Is Itraconazole CIDAL or STATIC?
STATIC
32
How is Itraconazole absorbed? What increases its bioavailability?
- -Well-absorbed orally | - -Food!
33
Does Itraconazole distribute into the CNS?
No
34
Where is Itraconazole metabolized?
In the liver: Inhibits P 450
35
A patient is experiencing N/V, rashes, hypokalemia, HTN, edema, HA. What is the causative agent?
Itraconazole
36
What is Itraconazole used for?
Onychomycosis
37
How is Itraconazole administered?
pulse-dosing”: 200 mg PO bid for 1st wk of month x 2 mo (fingernails) or 3-4 mo (toenails)
38
What are the contraindications for Itraconazole?
``` --Contraindicated with cisapride, dofetilide, lovastatin, PO midazolam, pimozide, quinidine, simvastatin, triazolam. ``` --Negative inotrope; do not use for onychomycosis if ventricular dysfunction
39
What is Terbinafine's MOA? And is it CIDAL or STATIC?
MOA: Inhibits synthesis of ergosterol | --CIDAL
40
What is Terbinafine used for?
“Drug of Choice” for both dermatophytoses and onychomycoses
41
When will you see the Optimal clinical effect of Terbinafine ?
Optimal clinical effect may not be apparent for several months following completion of therapy
42
What drugs are the Echinocandins?
1. Caspofungin (Cancidas) 2. Micafungin (Mycamine) 3. Anidulafungin (Eraxis)
43
What is the MOA of the Echinocandins?
Inhibit synthesis of β (1,3)-D-glucan, essential fungal cell wall component
44
What are the “Penicillins” of fungi world?
Echinocandins
45
What are the contraindications of the Echinocandins?
Pregnancy
46
What are the contraindications of the Echinocandins?
Pregnancy
47
What is the MOA of Griseofulvin?
Interacts with microtubules to disrupt mitotic spindles and thus inhibit mitosis
48
What is Griseofulvin used for?
Used for severe tinea infections unresponsive to other antifungal agents
49
T or F: Griseofulvin ineffective topically.
True | Distributes chiefly to infected keratinized tissue
50
T or F: Griseofulvin ineffective topically.
True
51
Is Griseofulvin CIDAL or STATIC?
STATIC | Therapy MUST continue until infected tissue replaced
52
What is the treatment of choice for “tinea” infections? Skin – few days Palm – few months Nails – few months
Griseofulvin
53
T or F: Griseofulvin does not induce hepatic cytochrome P-450 activity,
False; it does !
54
What are the adverse effects of acute Griseofulvin?
- -Allergy, HA, nausea - -May cause hepatotoxicity - -ETOH: POTENTIATES intoxicating effects of alcohol - -Pregnancy: TERATOGENIC
55
What are the adverse effects of acute Griseofulvin?
- -Allergy, HA, nausea - -May cause hepatotoxicity - -ETOH: POTENTIATES intoxicating effects of alcohol - -Pregnancy: TERATOGENIC
56
What is the MOA of Nystatin? Is it CIDAL or STATIC?
- -Structure, chemistry, MOA, resistance similar to amphotericin B - -CIDAL
57
What is Nystatin used for?
- -Thrush--Restricted to treatment of Candida infections because of its systemic toxicity - -Mycostatin - -Vulvovaginitis - -Candidiasis
58
How is Nystatin administered?
- -Thrush/Mycostatin: oral lozenges --Oral “swish & swallow” - -Never used parenterally - -Negligibly absorbed from GI tract - -Candidiasis (cream ointment) - -Vulvovaginitis (vaginal tablet)
59
How is Nystatin excreted?
In the poo poo !!!
60
What are the adverse effects of Nystatin?
Occasional N/V
61
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?
1. Clotrimazole (Lotrimin, Mycelex) 2. Miconazole (Monistat, Micatin) 3. Econazole (Spectazole)

Pharm Exam 4 (10 decks)

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