Exam #4 - Microbials Flashcards Preview

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Flashcards in Exam #4 - Microbials Deck (32)
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1
Q

benefits of narrow spectrum ABX

A

o Most effective on susceptible organism

o Less disturbance of host flora

2
Q

benefits and consequences of broad spectrum ABX

A

greater scope of activity for initial empiric coverage

more likely to cause superinfections

3
Q

ABX with activity to MSSA

A
Dicloxacillin **
Amox/Clav-Augmentin **
PIP-TAZ **
Cephalosporins (all) **
Macrolides
Tetracyclines
Clindamycin
SMX/TMP (Bactrim)
4
Q

ABX with activity to MRSA

A

Vancomycin **
Tetracyclines **
Clindamycin **
SMX/TMP (Bactrim)

Note: possibly 5th Gen cephalosporins

5
Q

ABX that treat Gonorrhea (gram - cocci)

A

Ceftriaxone (3rd Gen) **
Macrolides
Tetracyclines

6
Q

ABX that treat pseudomonas (gram - rod with tough outer membrane)

A
PIP-TAZ **
Ceftazidime (3rd Gen) **
Aminoglycosides **
Cipro (uFQ) **
Levo (u+rFQ) **
7
Q

ABX that treat C. Diff (+ anaerobe)

A

Vancomycin ** (severe)

Metronidazole **

8
Q

ABX that treat B Fragilis (- anaerobe)

A

Amox/Clav (Augmentin)
PIP-TAZ **
Clindamycin **
Metronidazole **

9
Q

ABX that treat chlamydia (atypical)

A

Macrolides **
Tetracyclines **
FQs (all) **
SMX/TMP (Bactrim)

10
Q

ABX that treat mycoplasma (atypical)

A

Macrolides **
Tetracyclines **
FQs (all) **

11
Q

3 determinants of bactericidal vs. bacteriostatic

A

mechanism of action (target)
concentration in vivo
specific micro-organism

12
Q

targets for antimicrobials

A
  • Inhibition of synthesis/damage to cell wall
  • Inhibition of synthesis/damage to cell membrane
  • Inhibition/modification of protein synthesis
  • Modification of synthesis/metabolism of nucleic acids
  • Modification of intermediary metabolism (folate metabolism)
13
Q

bactericidal mechanisms (organisms killed)

A

o Inhibition of cell wall synthesis
o Disruption of cell membrane function
o Interference with DNA function or synthesis

14
Q

bacteriostatic mechanisms (organisms prevented from growing)

A

o Inhibition of protein synthesis (exception: aminoglycosides (AGs → -cidal)
o Inhibition of intermediary metabolic pathways (unless combo, TMP/SMX –> -cidal)

15
Q

advantages of bactericidal agents

A
  • Preferred in severe infections
  • Act more quickly and action is often irreversible
  • Compensate for pts with impaired host defense
  • Required for treatment of infections in locations that are not accessible to host immune system responses (e.g., endocarditic vegetations and cerebrospinal fluid / CNS)
16
Q

pharmacodynamics of antimicrobial therapy

A

ensures that the ABX has antimicrobial activity against the specific infectious organisms

17
Q

pharmacokinetics of antimicrobial therapy

A

ensures that a sufficient concentration gets to the site of infection and remains active for a sufficient duration
- absorption, distribution, and metabolism / elimination

18
Q

ABX that readily enter CNS

A

Cephalosporins (3rd/4th): best for use
TMP/SMX (Bactrim)
Metronidazole (DNA inhibitors)
Rifampin (anti-TB)

19
Q

ABX to avoid in pregnancy (cross placenta)

A

Tetracyclines –> bone/tooth development
Aminoglycosides –> 8th nerve/renal tox
Fluoroquinolones: black box for arthralgia / tendon rupture
Nitrofurantoin: no 3rd trimester (hemolytic anemia)
Metronidazole: no 1st trimester
TMP/SMX → kernicterus

20
Q

selective distribution: beneficial accumulations

A

Clindamycin into bone (osteomyelitis)

Macrolides into pulmonary cells (URI / pneumonia)

Tetracyclines into gingival crevicular fluid and sebum (periodontitis and acne)

Nitrofurantoin rapid excretion into urine (beneficial in UTIs)

21
Q

selective distribution: toxic accumulations

A

Amino glycoside: bind to cells of inner ear (ototoxicity) and renal brush border (nephrotoxicity)

Tetracyclines: bind to Ca++ in developing bone and teeth

22
Q

inducers of hepatic metabolism (CYP450) = hepatotoxicity

A
  • Rifampin: anti-tubercular agent

* Isoniazid: anti-tubercular agent

23
Q

inhibitors of hepatic metabolism (CYP450)

A

Fluoroquinolones (especially Ciprofloxacin)

Erythromycin and Clarithromycin (NOT Azithromycin)

Metronidazole → antabuse rx due to inhibition of liver metabolism of EtOH

Also, anti-fungal agents that inhibit CYP450 drug metabolism (not part of DQ-CRIMES)
• Itraconazole (Triazole)
• Ketaconazole (Imidazole)
• Terbinafine

24
Q

what anti-microbial agent can stain your contacts orange and make you have orange secretions (urine, sweat, tears)

A

rifampin (anti-TB)

25
Q

which ABX exhibit post-ABX effects (ABXs that continue to kill or inhibit growth of bacteria for several hours after the concentration of the drug falls below the MIC)

A

aminoglycosides

fluoroquinolones

26
Q

which ABX exhibits concentration-dependent killing

A

aminoglycosides

27
Q

why is multi-drug regime essential in treatment of TB

A

3 subpopulations exist and resistance to any one drug is very high
- no practical way to quantitate % in given patient
• Intracellular in caseating granulomas
• Extracellular and rapidly dividing
• Intracellular in macrophages

28
Q

candida - anti-fungal treatment

A

oropharyngeal/esophageal candidiasis and systemic vulvovaginal candidiasis: fluconazole (Diflucan)

oral and vaginal candidiasis: clotrimazole (Lotrimin) and Miconazole (Monistat): topical only

superficial: Nystatin (topical only)

29
Q

superficial dermatophytosis (athlete’s foot, jock itch, etc.) and onychomycosis (nail infection) - anti-fungal treatment

A

systemic therapy for either: itraconazole

once daily oral dose (nail infections): PO Terbinafine

topical for dermatophytosis: Terbinafine

30
Q

life-threatening systemic fungal infections - anti-fungal treatment

A

amphotericin B (IV or topical only)

  • very toxic: nephrotoxicity and anemia
  • pre-dose with Benadryl, Ibuprofen, Prednisone
31
Q

invasive aspergillosis

A

amphotericin B (1st choice)
itraconazole
caspofungin (if refractory to either of above)

32
Q

recommended premedication before Amphotericin B treatment (very toxic!)

A

diphenhydramine (Benadryl)
ibuprofen
prednisone