Pharm Test 2 Antifungals

Front 1

1)What are mycoses?
2)Fungi are pro or eukaryotic?
3)Does there cell membrane have cholesterol?

Back 1

1)Infection by fungus (are chronic)
2)Eukaryotic
3)No,Ergosterol

Front 2

1)The 3 types of drugs that alter cell membrane permeability are?

2)The type of drug that blocks nucleic acid synthesis is?

3)The drug that disrupts microtubule function is?

4)The drug that disrupts the fungal cell wall is?

Back 2

1)Polyenes, Azoles, Allylamines

2)Flucytosine

3)Griseofulvin

4)Echinocandins (equiv to penicillin)

Front 3

1)Can classify drugs in terms of use as

Back 3

1)Systemic drugs for subcutaneous and systemic mycoses

or

Drugs for superficial mycoses (give systemic or topical)

Front 4

1)Systemic drugs given for subcutaneous and systemic mycoses are (most severe type):

Back 4

1)Amphotericin B,
Flucytosine
Azoles
Echinocandins

Front 5

Amphotericin B

1)What is it for?
2)MOA
3)CU
4)How to give?
5)What do you give after induction regimen for maintenance?

Back 5

1)Most severe, life threatening fungal infections(MOST BROAD SPECTRUM)

2)binds to ERGOSTEROL, forming pores in cell membrane->ions and molecules leak in and cause death

3)Kills everything (even yeasts and endemics) (good initial induction regimen = kills everything quick)

4)Not orally absorbed, must give IV

5)Azoles, because much less AE

Front 6

Amphotericin B

6)The DOC for systemic fungal infection during Pregnancy is?

7)What are the Infusion Related Toxicities of it (happens immediately?

8)How can you decrease the infusion related toxicity?

Back 6

6)Amphotericin B

7)Fever Chills, Spasms, Hypotension (HAPPENS IN EVERYONE

8)slow infusion rase
decrease daily dose
give with antihistamines, steroids, antipyretics, meperidine

Front 7

Amphotericin B

9)What are the related Slower Toxicities?

10)How to decrease to Slower toxicities?

11)The 3 lipid formulations are:

Back 7

9)amphotericin B binds to cholesterol in also mammal membranes (not purely selective) -> effects kidney -> RENAL TOXICITY (almost all patients)
Anemia (d/t dec EPO)
Seizures

10)come up with lipid forumulations of amphotericin B (dec exposure to nephron)

11)Amphotec, Abelcet, and AmBisome

Front 8

Flucytosine

1)structure
2)MOA
3)combo of flucytosine and amphotericin B is

Back 8

1)pyrimidine Antimetabolite

2)SELECTIVELY taken up by fungal cells via the enzyme CYTOSINE PERMEASE (mammal cells dont have this) -> converted to 5-FU-> 5-FdUMP -> inhibits Thymidylate Synthetase and blocking synthesis of dTMP ->inhibits DNA snythesis

3)Synergistic (amphotericin B makes pores, flucytosine gets in easier and inhibits DNA and protein synthesis)

The 5-FU also becomes 5-FUTP which also inhibits Protein Synthesis

Front 9

Flucytosine

4)Static or Cidal? Broad or Narrow Spectrum? Can you use alone?

5)CU
6)How to treat Systemic infection?

Back 9

4)Fungistatic, Narrow; NEVER, because not good enough to prevent resistance

5)Serious Infections by Candida or Cryptococcus

6)Use in combo with amphotericin B to treat systemic candida or cryptococcus

7)metabolized to 5-fluorouracil by intestinal flora -> Bone Marrow Toxicity (flucytosine by itself not toxic)

Front 10

Azoles

1)How do you give?, why are they good?

2)Where are imidazoles found? What are the 3 of them?

3)What are Triazoles for? What are the 4 of them?

Back 10

1)Oral, relatively nontoxic

2)Creams; Ketoconazole, Miconazole, Clotrimazole

3)More systemic infections; Itraconazole, Fluconazole, Voriconazole, Posaconazole

Front 11

Azoles

4)MOA
5)Which are more specific, imidazole or triazole?

6)AE

Back 11

4)all inhibit cyp p450 enzyme 14 alpha demethylase (which normally converts lanosterol to ergosterol) -> causes leaky membrane

5)Triazoles are more specific
6)Relatively nontoxic

Front 12

Ketoconazole

1)AE
2)AE caused by high dose?
3)Effect on CYP3A4?

4)Absorbed best at what gastric pH? Thus absorption blockd by?
5)CU

Back 12

1)dec testosterone levels -> gynecomastia, dec libido, menstrual irregularities

2)inhibits adrenal steroid synthesis -> dec plasma cortisol conc

3)Inhibitor

4)Low pH; H2 Blockers or proton pump inhibitors

5)superficial mycoses

Front 13

Flucanazole

1)Kinetics?
2)Effect on CYP3A4 and CYP2C9

3)DOC for
4)DOC for invasive what?
5)What do you use when infection fluconazole resistant, or patient immunocompramised?

Back 13

1)Penetrates CSF -> good for fungal meningitis

2)Inhibitor (inc plasma level of warfairn, phenytoin)

3)esophageal, oropharyngeal vaginal, or urinary Candida

4)Disseminated or Invasive Candida
5)when invasive candida is resistant, use Amphotericin B

Front 14

Flucanazole

6)DOC after induction therapy with amphotericin B for maintenance therapy of

7)Alternative to amphotericin B for patients whose what disease is not severe?

8)DOC for prophylaxis of what disease?

9)is ineffective against what fungi?

10)give to dec incidence of what in patients who are undergoing bone marrow tranplantation d/t radiation

Back 14

6)Cryptococcal meningitis

7)Cryptococcal meningitis

8)Cryptococcal meningitis

9)Aspergillus

10)Candida

Front 15

Itraconazole

1)metabolized and inhibited by what?

2)what dec its absorption?

3)

Back 15

1)CYP 3A4 -> fatally arrhythmia when give with quinidine

2)antacids, h2 blockers, proton pump inhibitors

3)dimorphic fungi: Blastomyces, Sporothrix, and Histoplasma
Also aspergillus (not DOC)
Dermatophytoses and Onychomycosis

Front 16

Voriconazole

1)DOC for
2)AE
3)metabolized AND inhibited by

Back 16

1)Invasive Aspergillosis

2)transient visual disturbances

3)CYP2C19, CYP2C9, CYP3A$

Front 17

Posaconazole

1)used for

2)action on CYP3A4

Back 17

1)zygomyetes such as Mucor

2)inhibition

Front 18

1)Which azole's penetrates CSF well?

2)Which is the only Azole metabolized by Kidney (rest liver)

Back 18

1)Fluconazole and Voriconazole (thus good for crypto meningitis) (Fluconazole is Best)

2) Fluconazole

Front 19

Echinocandin: Caspofungin

1)only available in:

2)CU
3)Not effective on
4)MOA

Back 19

1)IV
2)Candida and Aspergillus
3)Cryptococcus

4)inhibits synthesis of D-glucans-> disrupts cell wall and cell dies

Front 20

1)What are the systemic drugs given for superficial mycoses?

Back 20

1)Griseofulvin, Terbinafine, Ketoconazole, Fluconazole, Itraconazole

Front 21

Griseofulvin

1)CU
2)Absorption improved when given with what?
3)MOA
4)effect of Cyp P450

Back 21

1)Dermatophytosis of skin, hair, nails
2)Fatty Foods
3)disrupts mitotic spindle and inhibits mitosis
4)Inducer

Front 22

Terbinafine

1)Given how?
2)MOA
3)CU
4)Affect on P450

Back 22

1)Orally
2)inhibits Squalene Epoxidase (cant make squalene 2 3 oxide from squalene) -> cant form ergosterol (SQUALENE is also toxic to fungal cell)

3)Onychomycosis (infection under nail)

4)Does not Affect it (thus no drug interactions)

Front 23

1)which azoles can used to treat dermatophytoses?

Back 23

1)Ketoconazole, Fluconazole, Itraconazole

Front 24

What are the topical drugs for superficial mycoses?

Back 24

Nystatin, Amphotericin B, Clotrimazole, Miconazole, Ketoconazole, Terbinafine

Front 25

Nystatin

1)MOA
2)diff from amphotericin B
3)CU

Back 25

1)binds to ergosterol -> leaky membrane (same as amphotericin

2)cant be used systemically, too toxic (as long as used topically, not much toxicity)

3)Candida

Front 26

1)The 2 most commonly used topical Azoles are?

2)Does amphotericin B come in a topical form? Used for?

3)Topical Terbinafine used for?

Back 26

1)Clotrimazole, Miconazole (both over the counter)

2)YES; Cutaneous Candida

3)Tinea Cruris and Tinea Corporis

Front 27

Pneumocystis Jirovecii Pneumonia (PCP)

1)respond to antifungals?
2)DOC to treat
2)DOC for prophylaxis in immunocompromizeed

3)Alternative

Back 27

1)NO, but is a fungus (p carinii affects animals, not humans)

2)Co-Trimoxazole (trimethroprim plus sulfamethoxazole

3)Cotrimoxazole

Front 28

P. jirovecci

3)Alternative therapies
4)Patient with moderate to sever disease should also be given?

Back 28

3) Clindamycine and Primaquine
Dapsone and trimethoprim
Atovaquone
Pentamidine

4)Prednisone (actually life saving even though immunocompromised patient)