Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharm II > Antifungals > Flashcards

Antifungals Flashcards

1
Q

when you think Fungus you generally think of?

Candida spp. is a ?

Cryptococcus spp. is a ?

Aspergillus spp. is a ?

A

yeast and mold

Candida spp. is a yeast

Cryptococcus spp. is a yeast

Aspergillus spp. is a mold

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What type of patients are at risk for fungal infections?

A

-Increasing number of immunocompromised and immnocompetent

-Can occur in immunocompetent patients as well
→ patients that have chronic catheters or chronic antibiotic use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the different routes of transmission for fungal infections?

A
  • Respiratory→ pores inhalation (aspergillus is present in the soil)
  • Traumatic implantation
  • Direct contact (dermatoid infections)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the different categories of anti fungal agents available ?

A
  • Allylamines (topical agents)
  • Polyenes
  • Azoles
  • Echinocandins
  • Miscellaneous→ Flucytosine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Allylamines:

  1. ) Forumulations available?
  2. ) Indications?
  3. )MOA?
A

1.) Topical agents

  1. ) Indications:
    - Tinea cosporis (ring worm)
    - Tinea pedis (athlete’s foot)
    - Tinea cruris (jock itch)
    - Onychomycosis (terbinafine) → nail fungus
  2. )MOA:
    - inhibition of squalene epoxidase → reducing fungal cell membrane ergosterol synthesis (allylamines-ES stands for squalene epoxidase)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Terbinafine:

  1. ) Excretion?
  2. )Monitoring?
  3. ) Great for treating fungal infections of the?
A

1.) Excretion: Renally eliminated, caution in hepatic impairment

2.) Monitoring:
-SCr
-LFTs
*at baseline and throughout the treatment)
-CBC
→ only if > then 6 weeks of tx in immunodeficient patients

  1. ) great for treating fungal infections of the
    - fingernails → esp nail fungus
    - toenails→ esp nail fungus
    - tinea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the mechanism of action for azoles?

A
  • Inhibition of 14 alpha-demethylase which converts lanosterol to ergosterol → disruption in cell membrane synthesis
  • also blocks steroid synthesis in humans
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the indications for use of Imidazoles?

A 
Indications:
􏰀 Tinea cotporis
􏰀 Tinea pedis
􏰀 Tinea cruris
􏰀 Oropharyngeal candidiasis 
􏰀 Vulvovaginal candidiasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What Imidazole agents do we have available?

A

􏰀 Ketoconazole
􏰀 Clotrimazole
􏰀 Miconazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Ketoconazole:

  1. ) Imidazole or Triazole?
  2. ) Effective against? High failure rate in?
  3. ) Excretion?
A

1.) Imidazole

  1. )Effective against:
    - Candida spp.
    - Blastomycosis,
    - Histoplasmosis(high failure rates)

3.) Excreted in feces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Ketoconazole:

  1. ) CYP interactions?
  2. ) Considerations
A
  1. ) -CYP450 3A4 substrate→ CYP inhibition = drug interactions!!!
  2. ) Needs acidic gastric pH for absorption-think interactions with tums and omperazole (will make t & o not work)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Ketoconazole:

  1. ) Side Effects?
  2. ) C/I’s?
A
  1. ) Can cause QTc prolongation → black box warning

2. ) C/I in patients with hepatic impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q
  1. )What Triazole agents do we have available?

2. ) What do we commonly associate Triazole agents with?

A 
1.)
􏰀 Fluconazole
􏰀 Itraconazole 
􏰀 Voriconazole 
􏰀 Posaconazole 
􏰀 Isavuconazole

2.) Systemic invasive fungal infections (REALLY BAD INFECTIONS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Triazoles:

  1. ) MOA?
  2. ) Fungicidal or fungal static?
A
  1. ) MOA: inhibition of CYP450-34A and sterol C-14alpha-demethylation
  2. ) Primarily fungistatic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How are the newer triazoles different from the older triazoles?

A 
The newer triazoles have....
 less hormonal inhibition, 
broader spectrum,
 less toxic, 
better tissue distribution
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Fluconazole: (Diflucan)

1.) Indication?

A
  1. ) Indication:
    - Candidiasis: invasive →(oroesophageal/urogenital/vulvovaginal)
  • ProphylaxisinBMTrecipients/txtpatients
  • Cryptococcosis: consolidation phase (used after initial treatment)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Fluconazole:

  1. ) DDI’s?
  2. ) This drug is beneficial also for _____ b/c it can ……?
  3. ) Side effects and dose adjustments?
A
  1. ) CYP interactions:
    - Minor inhibition of CYP 3A4
    - Moderate inhibitor of CYP 2C9

2.)Fungal meningitis because it can cross the BBB
→ Can penetrate the CNS

  1. )Side effects and dose adjustments:
    - Needs to be adjusted in renal failure
    - Check QTc
    - Pt’s may experience Alopecia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Itraconazole:

  1. ) Indication?
  2. ) What DDI’s do you have to be aware of and why?
A

1.)Indication:
-Candidiasis: oropharengeal and esophageal
→ Maybe a step down therapy in Aspergillosis ( NOT 1st line!)

2.) warfarin b/c this drug is ***99% protein bound

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Itraconazole:

1.) Formulations available? What do you have to considerations when giving the dose?

A
  1. )
    - Available in capsules in solution BUT, CANNOT interchange
    - Capsules need to be given w/ meal
    - Solution should be given on an empty stomach and is preferred formulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Itraconazole:
1.) Side effects?

2.) C/I’s?

A
  1. )
    - HTN
    - Edema
    - Hypokalemia
    - QTc-prolongation

2.) Cardiac Patients- QTc prolongation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Voriconazole:

1.) Indication?

A
  1. )Indication: (you “vori” because they must be really sick)
    - Resistant Candida infections
    - Aspergillosis
22
Q

Voriconazole:

  1. ) Bioavailabilty?
  2. )Additional Info?
  3. ) DDI’s?
A

1.)
-95% oral bioavailability, BUT:
→ Can be unpredictable
→ Reduced wT/ high fat meal
→ Administer 1 hour before or one hour after a meal

  1. ) Large Vd and good CNS penetration
  2. ) Substrate and inhibitor of CYP3A4, CYP2C9, and CYP2C19→ DRUG INTERACTIONS!!!
23
Q

Voriconazole:

  1. ) Monitoring?
  2. ) Side effects?
A

1.)Monitoring: Cmin → for severe infections
→ If Level id > 5mg/L = CNS toxicity

  • SCr, electrolytes, LFTs, ophthalmic exam if therapy >4weeks
  • QTc so EKG
  1. ) Side Effects: Not Lying Very Hot Hot S**
    - N/V/D
    - Liver dysfunction
    - Visual and auditory abnormalities
    - HA
    - Hepatotoxicity
    - Steven Johnson syndrome
24
Q

Posaconazole:

1.) Indication?

A
  1. )Indication:
    - Resistant Candida infections
    - Aspergillosis
    - Mucorales and other mold infections → *only azole indicated for this *
25
Q

Posaconazole:

1.) Oral bioavailability

A

1.) Oral bioavailability: >90% w/ high fat meal
meat
→ so pt should be taking this med with a high Fat meal

26
Q

Posaconazole:

  1. ) Where does this drug extensively distribute?
  2. ) DDI’s?
A

1.) Extensive distribution and penetration into tissues/ potentially therapeutic CSF levels

  1. )
    - Potent inhibitor of CYP3A4
  • Inhibitor and substrate of P-glycoprotein → ex: apixaban
  • ↓ absorption w/ PPIs, H2RA
27
Q

Posaconazole:

  1. ) Which formulation should you administer and why?
  2. )Monitoring
A
  1. )
    - Start with IV formulation because oral has slow onset (No PO -POsaconazole cause slOW) so use IV to get it quickly → loling

2.) Monitoring
-SCr, electrolytes, and LFTs
→ No renal adjustment

28
Q

Posaconazole:

Side effects?

A
  • GI
  • HA
  • rare hepatotoxicity***
  • QTc prolongation**
  • hemolytic uremic syndrome***
29
Q

Isavuconazole:

  1. ) Indication?
  2. ) Excretion?
  3. ) Half life?
A
  1. ) Indication:
    - Invasive Aspergillosis
    - Mucormycosis
  2. ) Excretion:
    - Cleared primarily via fecal excretion

3.)Half-life: 130HRS!!!!

30
Q

Isavuconazole:

  1. )How is the drug administered?
  2. ) C/I’s?
A

1.)Administered as a pro-drug: isavuconazonium***

3.)
→ Contraindicated with potent 3A4 inhibitors and inducers
→ Contraindicated in familial short QT syndrome

31
Q

Isavuconazole:

  1. ) DDI’s?
  2. ) Side Effects?
A
  1. )DDI’s:
    - inhibits CYP3A4, P-glycoprotein, and OCT-2
  2. )Side Effects:
    - GI
    - Hypokalemia
    - Elevated LFTs
    - HA
32
Q

Polyenes:

  1. ) MOA?
  2. ) Agents available?
A

1.) MOA: bind w/ sterols in the fungal cell membrane ( principally ergosterol), leads to the cell contents to leak out and ultimately cell death

  1. )
    - Nystatin
    - Amphotericin B
33
Q

Nystatin:

  1. ) Indication?
  2. ) Formulations available?
A
  1. ) Indication:
    - Candida spp. only!→ used for thrush

2.) Comes as liquid formulation and topical
→ No IV b/c too toxic for systemic administration

34
Q

Amphotercin B:

  1. )What type of agent is it?/What does it cover?
  2. ) How many formulations available? how do they travel through the blood stream?
A
  1. ) Broad spectrum agent:
    - Most Candida spp. and Aspergiluss spp.
    - Most fungi except Fusarium spp. and A. terreus

2.) 3 diff. formulations available-99% protein bound

35
Q

Amphotercin B:

1.) What does Amphoteric mean in regards to this drug?

A

1.) Amphoteric
→ Soluble in both basic and acidic environments
→ Insoluble in water

36
Q

AmB-d:

1.) Side Effects? (8 side effects) how do you prevent 2 out of the 8 side effects

A

1.) Side Effects:
-Neprotoxic! (d in AmB-d for damages kidneys)
→ ARF in 50% of patients

-Infusion- related rxn’s
→ Pre-medicate w/ APAP or IBU, diphenhydramine +/- steroids develop
→ Rigors: meperidine

  • Thrombophlebitis,
  • cardiac arrhythmias,
  • rash
  • decrease in GFR ( vasoconstrictive effect on renal arterioles)
  • Decreases erythropoietin production
  • Electrolyte derangement
37
Q

AmB-d:

1.) Monitoring?

A 
Monitor:
SCr,
BUN,
electrolytes,
CBC,
LFTs
38
Q

L-AmB:

  1. ) Differences from AmB-d: (4 things)
  2. ) Side effects?
A

1.)
􏰀 Less nephrotoxic-(L in L-AmB stands for Less Nephrotoxic)
􏰀 Reduced frequency and severity of infusion related reactions
􏰀 Higher Cmax and larger AUC
􏰀 Higher tissue concentrations vs other AmB formulations

  1. ) Side effects:
    - Hepatotoxicity
39
Q

Echinocandins:

  1. ) Indication?
  2. ) MOA?
A 
1.) Indication:
􏰀 Invasive candidiasis
􏰀 Empiric coverage in neutropenic fever
  → Fungicidal against most Candida spp 
  → Fungistatic against Aspergillus

2.) MOA: inhibit the synthesis of glucan in the cell wall

40
Q

Echinocandins:

Agents available?

A

􏰀 Caspofungin
􏰀 Micafungin
􏰀 Anidulafungin

41
Q

Echinocandins:

  1. ) Formulations available?
  2. ) Additional information? ( 3 things)
A

1.) IV formulations only for all 3 agents

2.)
-Extensive distribution into tissues
-Minimal CSF penetration
→ not for pts with CNS infections
-97-99% protein bound

42
Q

Echinocandins:

  1. ) Half life?
  2. ) Side effects/Monitoring?
A

1.) Extensive half life: → once daily dosing

  1. )
    - Well tolerated-low adverse event rate
    - No renal adjustments required
43
Q

Caspofungin:

Facts? ( 3 things)

A

-CYP inducers reduce dose→ so you need to increase dose ( 70mg/day)
-Cyclosporine may increase AUC by 35%
-Reduces tacrolimus levels by 20%
→ Tacrolimus is an immunosuppressant used in patients post transplant

44
Q

Micafungin:

Facts? (2 things)

A
  • Increases concentration of sirolimus
    → Sirolimus=prevent organ transplant rejection and to treat a rare lung disease called lymphangioleiomyomatosis.
  • Increases AUC and Cmax of nifedipine
    → nifedipine= DHP: Calcium channel blocker- used for Hypertension b/c it has a stronger reduction on systemic vascular resistance
45
Q

Flucytosine:
1.) Indication?

2.)MOA:?

A

1.) Indication:
􏰀 Candida spp. ( except C. krusei)
􏰀 Cryptococcus neoformans
􏰀 Aspergillus spp.

2.) MOA: Converted to 5-florouracil by susceptible fungi

46
Q

Flucytosine:

  1. ) How do you administer this drug?
  2. ) Is this drug given as monotherapy or in combination with something else?
A

1.) Administer over 15min and w/ food to limit n/v

2.)Usually not administered as a single agent! → bc of resistance
→ Has demonstrated synergy w/ AmB

47
Q

Flucytosine:

  1. ) Bioavailability?
  2. ) CNS penetration?
A
  1. ) Bio- availability:
    - 80-90% orally bioavailable

2.) 74% CNS penetration

48
Q

Flucytosine:

1.) DDI’s?

A
  1. ) DDI’s:

- Avoid with other nephrotoxic and bone marrow suppressive drugs

49
Q

Flucytosine:

What side effects can this drug cause?

A

􏰀 N/V/D
􏰀 Bone marrow suppression ( dose dependent)
􏰀 Enterocolitis
􏰀 Hepatotoxicity

50
Q

Flucytosine:

Monitoring?

A

-CBC, SCr, LFTs
-Serum levels ( especially in pts w/ rapidly changing renal function)
→ Needs to be renally adjusted

51
Q

What allylamine agents are available?

A 
*Always Touch Naked Butt*
Amorolfine 
Terbinafine
Naftifine
Butenafine

Pharm II (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions