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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
AMPHOTERICIN B: Clinical Applications: What is almost exclusively used? DOC for? Use against:
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
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?
(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
ECHINOCANDINS: ``` MOA Pharmacokinetics: Spectrum of activity (2): DOC for: What is the 'Achilles-heel'? ```
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
ECHINOCANDINS Clinical use: DOC for: Side Effects:
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
Dealing with Yeast in the Blood (Algorithm): | 3 Steps:
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
FLUCYTOSINE (5-FC): MOA: Spectrum of Action (3):
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
FLUCYTOSINE (5-FC): Clinical Use:
Clinical Use: - Never as monotherapy** - Synergy with amphotericin B for severe infections: o Candida endocarditis o Cryptococcus neoformans CNS infections
32
FLUCYTOSINE (5-FC): Side effects (KNOW!)
• Side Effects: - Bone marrow suppression: dose-dependent; use therapeutic drug monitoring to avoid (levels <100) - Hepatotoxicity
33
Antifungals for Dermatophytes
Terbinafine | Griseofulvin
34
TERBINAFINE: MOA: Adverse Effects:
MOA: blocks ergosterol production by inhibiting squalene epoxidase production Adverse Effects: hepatotoxicity
35
GRISEOFULVIN: MOA: Adverse Effects:
MOA: prevents infections of new skin structures; eventually the infected ones die and get replaced Adverse Effects: allergic reactions and hepatotoxicity
36
``` Antifungal pharmacology goodies What causes hepatotoxicity? Nephrotoxicity? What penetrates the urine? What causes bone marrow suppression? ```
• 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
Common Viral Infections (4):
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
``` ACYCLOVIR: MOA: Modified by: Where? What does it act as in growing DNA? Competitively inhibits : ```
– 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
ACYCLOVIR | Pharmacokinetics:
Not well absorbed orally (requires higher dosing- not often used orally for this reason) Requires IV dosing for severe infections
40
ACYCLOVIR Spectrum of Activity: HSV: VZV: CMV: Influenza A and B:
- HSV: active against both 1 and 2 - VZV: active, but requires higher doses - CMV: no - Influenza A and B: no
41
``` ACYCLOVIR Adverse Effects (3): ```
Headaches Crystallization in urine: IV formulation in high doses (avoid by hydration) Neurotoxicity: IV formulation in high doses (rare)
42
VALCYCLOVIR (VALTREX): MOA Pharmacokinetics Everything else
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
What is the DOC for CMV?
Ganciclovir
44
GANCICLOVIR: MOA: Activated by:
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
GANCICLOVIR Spectrum of Activity (4): HSV 1 and 2 VZV: CMV: Influenza: Side Effects:
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
VALGANCICLOVIR | MOA:
MOA: oral produg of gangciclovir (allows for better absorption) *EQUIVALENT OF VALCYCLOVIR FOR ACYCLOVIR*
47
Ganciclovir and Valganciclovir Side effects
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
CIDOFOVIR: MOA: Spectrum of activity: Clinical use: Side Effects (2):
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
FOSCARNET: MOA: SE (3):
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
ANTIVIRALS FOR INFLUENZA: When does treatment need to be commenced? What is key?
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
ADAMANTANES MOA: Agents: Spectrum of Activity: Side Effects:
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
NEURAMINIDASE INHIBITORS: MOA: Agents: Spectrum of Action: Side Effects:
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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