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Micro Exam 1 > Pogue: Antimicrobials III > Flashcards

Pogue: Antimicrobials III Flashcards

1
Q

Which of the following drugs would not be
expected to have activity versus e.faecalis.
– A) piperacillin
– B) ampicillin
– C) ceftazadime
– D) ampicillin/sulbactam

A

C.

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2
Q

A patient has pneumonia with P.aeruginosa.
Which antibiotic would never be appropriate
– A) Ertapenem
– B) Doripenem
– C) Piperacillin
– D) Cefepime

A

A.

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3
Q 
Which cephalosporin would you expect to
have the best Gram‐negative activity
– A) Cefuroxime
– B) Cephalexin
– C) Ceftriaxone
A

C.

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4
Q 
Which of the following MRSA agents also has
broad spectrum Gram (‐) activity?
– Vancomycin
– Tigecycline
– Daptomycin
– Linezolid
A

Tigecycline

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5
Q 
If a patient was placed on tigecycline, which of
the following would be the major adverse
event of concern?
– Hepatotoxicity
– Rhabdomyolysis
– Thrombocytopenia
– Nausea/vomiting
A

Nausea/Vomiting

Hepatotoxicity = Rifampin
Rhabdomyolysis = Daptomycin
Thrombocytopenia = Linezolid
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6
Q

If you had a patient on linezolid, which of the
following agents would you be concerned for
a potential drug interaction with?
– A) rifampin
– B) multivitamins
– C) paroxetine
– D) triamterene

A

C. SSRI, Linezolid is an MAOI

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7
Q

Fungi to know (of clinical

relevance/importance)

A 
• Dermatophytes
• Candida spp.
– C.albicans vs. C.glabrata vs. others
• “Endemic fungi”
– Histoplasmosis, Blastomycosis, Coccidiomycoses
• Aspergillus spp.
• Mucormycoses
• Cryptococcus neoformans
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8
Q

General classes of antifungals (4)

A

Azoles
Polyene
Echinocandins (newest)
Misc.

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9
Q

Antifungals

Azoles (4)

A

– Fluconazole
– Itraconazole
– Voriconazole
– Posaconazole

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10
Q

Antifungals

Polyene (2)

A

– Amphotericin B

– Nystatin

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11
Q

Antifungals

Echinocandins (3)

A

– Caspofungin
– Micafungin
– Anidulafungin

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12
Q

Antifungals

Miscellaneous (3)

A

– Flucytosine
– Griseofulvin
– Terbinafine

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13
Q

What is first line against C.Albicans, C.Tropicalis, C.parapsilosis?

A

Fluconazole

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14
Q

What is first line against C.krusei, C.glabrata?

A

Echinocandins

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15
Q

What is first line against Endemic mycoses?

A

Itraconazole, Amphtericin B

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16
Q

What is first line against aspergillus?

A

Voriconazole

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17
Q

What is first line against mucor?

A

Amphotericin B

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18
Q

AZOLES:

MOA:

What is inhibited?
What enzyme inhibits?

A

Inhibit production of ergosterol, which is a key component of the fungal cell membrane

Enzyme that inhibits is a fungal CYP450 enzyme (making it more specific for fungus, but can also inhibit your P450 enzymes)

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19
Q

AZOLES

Pharmacokinetics:

Absorption:
Bioavailability
What needs a high fatty meal for absorption?

Metabolism
Excretion

A

Absorption:
o Highly bioavailable (IV dose=PO dose), but variable among patients
o Therapeutic drug monitoring (dose adjustment)
o Posaconazole needs a high fatty meal for absorption

Metabolism: by CYP450 system (drug interactions)

Excretion: only fluconazole needs to be renally dosed

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20
Q

AZOLES

Spectrum of activity (6):

All have excellent coverage of:
All endemic fungi except:
Some:
What is voriconazole first line against?
Which drugs can be used against mucomycoses?
A
  1. Candida spp: all have excellent coverage for albicans; variable coverage for glabrata
  2. Cryptococcus neoformans
  3. Endemic fungi: all except fluconazole
  4. Some dermatophytes: but not mainstay of therapy
  5. Aspergillus: voriconazole is first line; itraconazole and posaconazole can also be used
  6. Mucormycoses: posaconazole only
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21
Q

AZOLES

Clinical uses

Fluconazole:
Itraconazole:
Voriconazole:
Posaconazole:

A

Fluconazole: empiric antifungal treatment; candida infections

Itraconazole: DOC for non-life threatening cases of endemic mycoses

Voriconazole: DOC for aspergillus

Posaconazole: mucormycoses and in some prophylaxis regimens

22
Q

AZOLES

Side effects:
Main issue for the class:

DDI: (KNOW!)
Worst with:
Notable interactions (4):

A

Side Effects:

  • Hepatotoxicity: main issue for this class; must monitor LFTs*
  • Nephrotoxiticy: IV voriconazole only
  • Visual Disturbances: voriconazole only (related to concentration)

Drug Interactions: LOTS

  • Worst with voriconazole and itraconazole
  • Keep MOA in mind
  • Always check concomitant drugs
Notable Interactions:
o	HIV medications
o	Calcineurin inhibitors (cyclosporine, tacroliumus)
o	Anticonvulsants
o	Rifampin
23
Q

AMPHOTERICIN B:

MOA:

A

Binds to ergosterol in fungal cell membrane, and forms pores that allow molecules to leak in/out of the cell, resulting in cell death

24
Q

AMPHOTERICIN B:
Spectrum of Activity (5)

For Candida:
First line against:

A

Candida spp: broad spectrum, including glabrata (but not lusitaniae- does not cause a lot of infections)

Cryptococcus neoformans: first line

Endemic fungi: first line for life-threatening illnesses

Aspergillus: second line

Mucormycoses

25
Q

AMPHOTERICIN B:
Clinical Applications:

What is almost exclusively used?
DOC for?
Use against:

A

Lipid formulation almost exclusively used now: higher doses and somewhat decreased toxicity

Broadest spectrum antifungal: DOC for cryptococcus and endemic mycoses (life-threatening)

Use against “oddball” fungi

26
Q

AMPHOTERICIN B (3):

Side Effects:
What occurs in over 20% of pts?
Results in:
What is thought to be less toxic? Why

Premedicate with what to decrease symptoms?

A

(Ampho-terrible)
Nephrotoxicity: can also “punch holes” into renal cell walls; occurs in over 20% of patients
o Dose dependent and usually reversible
o Results in electrolyte abnormalities (K, Mg); consider sodium loading
o Renal tubular acidosis
o Lipid base formulations thought to be less toxic: no deoxycholate (may be the cause); but still high rates

Infusion Reactions: fevers, chills, rigors, hypotension; can premedicate to decrease symptoms (antipyretics, antihistamines, corticosteroids)

Hepatotoxicity

27
Q

ECHINOCANDINS:

MOA
Pharmacokinetics:
Spectrum of activity (2):
DOC for:
What is the 'Achilles-heel'?
A

MOA: inhibit production of 1-3-B-D-glucan (key component of SOME fungal cell walls) by inhibiting 1-3-B-D glucan synthase enzyme

Pharmacokinetics:

  • IV formulations only
  • Not renally eliminated: avoid for UTIs!

Spectrum of Activity:

  • Candida spp: albicans and DOC for glabrata (does not cover C.parapsilosis)
  • C.parapsilosis is the ‘Achilles-heel’
  • Aspergillus: generally not first line, but can be used in combination therapy
28
Q

ECHINOCANDINS
Clinical use:
DOC for:

Side Effects:

A

Clinical Use:
DOC for C.glabrata: used as both definitive and empiric treatment
- Aspergillus: rarely as monotherapy (unless patient cannot tolerate voriconazole or amphotericin); can be used as prophylaxis in some patients

Side Effects: VERY WELL TOLERATED
- Hepatotoxicity: rare

29
Q

Dealing with Yeast in the Blood (Algorithm):

3 Steps:

A
  1. Make sure patient not at risk for Cryptococcus (HIV, immunosuppressed) –> if it is Cryptococcus, treat with amphotericin B
  2. If not Cryptococcus, most likely a candida spp. (albicans or glabrata)
  3. Decide if the patient is at risk for a fluconazole-resistant organism (recent azole exposure or known colonizer with glabrata?)
    o If yes –> treat with echinocandin
    o If no –> treat with fluconazole

.

30
Q

FLUCYTOSINE (5-FC):

MOA:

Spectrum of Action (3):

A

MOA: converted by fungal cells to 5-FU (chemotherapeutic agent) and then to other products to inhibit DNA/RNA synthesis

Spectrum of Action:

  • Candida
  • Aspergillus
  • Cryptococcus
  • Not used as monotherapy (equate to aminoglycosides)
31
Q

FLUCYTOSINE (5-FC):

Clinical Use:

A

Clinical Use:

  • Never as monotherapy**
  • Synergy with amphotericin B for severe infections:
    o Candida endocarditis
    o Cryptococcus neoformans CNS infections
32
Q

FLUCYTOSINE (5-FC):

Side effects (KNOW!)

A

• Side Effects:

  • Bone marrow suppression: dose-dependent; use therapeutic drug monitoring to avoid (levels <100)
  • Hepatotoxicity
33
Q

Antifungals for Dermatophytes

A

Terbinafine

Griseofulvin

34
Q

TERBINAFINE:
MOA:
Adverse Effects:

A

MOA: blocks ergosterol production by inhibiting squalene epoxidase production

Adverse Effects: hepatotoxicity

35
Q

GRISEOFULVIN:
MOA:
Adverse Effects:

A

MOA: prevents infections of new skin structures; eventually the infected ones die and get replaced

Adverse Effects: allergic reactions and hepatotoxicity

36
Q 
Antifungal pharmacology goodies
What causes hepatotoxicity?
Nephrotoxicity?
What penetrates the urine?
What causes bone marrow suppression?
A

• All cause hepatotoxicity
– Most associated with azoles

• Nephrotoxicity and amphotericin

• Penetrating the urine
– Fluconazole, amphotericin

• Azoles and drug interactions

• Flucytosine synergy and bone marrow
suppression

37
Q

Common Viral Infections (4):

A

Herpes simplex virus (HSV) 1 and 2

Varicella-Zoster virus (VZV)
o Varicella: chicken pox
o Zoster: shingles

Cytomegalovirus (CMV)

Influenza A and B

38
Q 
ACYCLOVIR:
MOA:
Modified by: 
Where?
What does it act as in growing DNA?
Competitively inhibits :
A

– Inactive entity
– Modified by viral enzyme (thymidine kinase)
intracellularly into a monophosphate derivative
– Then host enzymes convert it into a tri‐phosphate
– This active moiety acts as a chain terminator in
growing DNA
• Also competitively inhibits viral DNA polymerase

39
Q

ACYCLOVIR

Pharmacokinetics:

A

Not well absorbed orally (requires higher dosing- not often used orally for this reason)

Requires IV dosing for severe infections

40
Q

ACYCLOVIR
Spectrum of Activity:

HSV:
VZV:
CMV:
Influenza A and B:

A
  • HSV: active against both 1 and 2
  • VZV: active, but requires higher doses
  • CMV: no
  • Influenza A and B: no
41
Q 
ACYCLOVIR
Adverse Effects (3):
A

Headaches

Crystallization in urine: IV formulation in high doses (avoid by hydration)

Neurotoxicity: IV formulation in high doses (rare)

42
Q

VALCYCLOVIR (VALTREX):

MOA
Pharmacokinetics
Everything else

A

MOA: oral prodrug of acyclovir (same MOA)

Pharmacokinetics:

  • Well absorbed, and then converted to acyclovir
  • Still need to use IV acyclovir for severe infections

Everything Else: same as acyclovir

43
Q

What is the DOC for CMV?

A

Ganciclovir

44
Q

GANCICLOVIR:
MOA:
Activated by:

A

HSV and VZV: similar to acyclovir (thymidine kinase activation)

CMV: inactive drug that is activated by kinase phosphotransferase that is present in CMV; then follows the same host mediated phosphorylations as acyclovir
o Note: does not act as a true host terminator, but forms smaller, ineffective DNA fragments

45
Q

GANCICLOVIR

Spectrum of Activity (4):

HSV 1 and 2
VZV:
CMV:
Influenza:

Side Effects:

A

Spectrum of Action:

  • HSV 1 and 2: less than acyclovir
  • VZV: less than acyclovir
  • CMV: DOC*
  • Influenza: no

Side Effects:

  • Bone Marrow Suppression: happens A LOT; especially when used with other suppressing agents (CMV common in immunosuppressed patients)
  • CNS Side Effects: headache –> coma (5-15%)
46
Q

VALGANCICLOVIR

MOA:

A

MOA: oral produg of gangciclovir (allows for better absorption)

EQUIVALENT OF VALCYCLOVIR FOR ACYCLOVIR

47
Q

Ganciclovir and Valganciclovir

Side effects

A

BONE MARROW SUPPRESSION
• Happens a lot!
• Especially with other suppressing agents
– Extremely common in the patient population that needs these
drugs (immunosuppressants)

CNS side effects
• Range from headache to coma (5‐15%)

48
Q

CIDOFOVIR:

MOA:
Spectrum of activity:
Clinical use:
Side Effects (2):

A

MOA: cytosine nucleotide (like the others above), but does NOT require viral activation

Spectrum of Activity:

  • HSV, VZV and CMZ
  • Some oddball viruses

Clinical Use:
- CMV resistant to others (ganciclovir/foscarnet) or if patients cannot tolerate these agents

Side Effects:

  • Nephrotoxicity: 20-30%
  • Neutropenia: ~25%
49
Q

FOSCARNET:

MOA:
SE (3):

A

MOA: inorganic pyrophosphate compound that inhibits DNA polymerase, RNA polymerase and HIV reverse transcriptase

Spectrum of Acitivity:

  • HSV, VZV, CMV (major)
  • Some oddball viruses
  • HIV (in vitro- not clinically used)

Side Effects:

  • Nephrotoxicity: 33%
  • Headache and Seizures
  • Chelator of divalent cations in the blood: hypokalemia, hypocalcemia, hypomagnesmia
50
Q

ANTIVIRALS FOR INFLUENZA:

When does treatment need to be commenced?
What is key?

A

Only have a modest effect in the treatment of influenza

Treatment needs to be commenced within 48 hours of symptom onset

VACCINATION IS KEY

51
Q

ADAMANTANES

MOA:
Agents:
Spectrum of Activity:
Side Effects:

A

MOA: prevents viral uncoding of influenza A only (blocks penetration into the host)

Agents:

  • Amantadine
  • Rimantadine

Spectrum of Action:

  • Influenza A (more recently, high levels of resistance)
  • Also used in Parkinson’s Disease (DA reuptake)

Side Effects:
- CNS Effects: nervousness, lightheadedness, inability to concentration (due to DA reuptake)

52
Q

NEURAMINIDASE INHIBITORS:

MOA:
Agents:
Spectrum of Action:
Side Effects:

A

MOA: inhibits viral neuraminidase, which is necessary for viral replication and release from host

Agents:

  • Zanamivir
  • Oseltamivir

Spectrum of Action:
- Influenza A and B (effective against H1N1)

Side Effects:
- Zanamivir (Inhalation): can exacerbate COPD

Micro Exam 1 (18 decks)

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