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pharmocology > antimicrobials > Flashcards

antimicrobials Flashcards

1
Q

Deep sternal wound infections:
~Significantly worse long-term survival
*Costs between

A

$200 and $250k to treat!!!

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2
Q

MIC =

A

Minimum INHIBITORY

Concentration”

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3
Q

MBC =

A

Minimum BACTERIOCIDAL

Concentration”

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4
Q

problem with VAD besides thrombosis

A

Infection/sepsis

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5
Q

cidal

A

min. conc. at which you are killing bacteria

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6
Q

static

A

min conc at which you stop bacteria growth

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7
Q

1) Gram Positive Bacteria

A

thick cell wall take up blue dye

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8
Q

gram negative bacteria

A

thin cell wall no blue dye . peptidoglycan is protected

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9
Q

fungi

A

valley fever depressed immune system

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10
Q

Penicillins & Cephalosporins

A

β-Lactam antibiotics
• *Prevent bacterial cell wall peptidoglycan cross-linking so newly produced bacterial cell walls are “weak” and the bacteria “fall apart” (think bacterial Marfan’s Disease)
• Theseantibioticsare“cidal”

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11
Q

Penicillins & Cephalosporins

*Classified by their

A

pectrum of activity” and resistance to β-lactamases (as well as potency, methods of administration, toxicities, expense, and pharmacokinetics and –dynamics)
• “R group” attachment differentiates the penicillins

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12
Q

penicilli derived from

A

Penicillium mold

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13
Q

First Generation” Penicillins

are effective against

A

gram-positive organisms (particularly Strep), gram negative cocci (what’s that?) and a few others, but resistance levels are high and growing!

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14
Q

Penicillin-G

A

(benzylpenicillin) 1st gen

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15
Q

Anti-staphylococcal Penicillins

• Developedinresponse

A

to
growing resistance among Staph. *These antibiotics have a much
narrower “spectrum” and are used specifically for Methicillin resistant Staphylococcus aureus…
…AND SHOULD BE USED SPARINGLY (why?)

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16
Q

Dicloxacillin

A

(Dynapen) Anti-staphylococcal Penicillins

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17
Q

Nafcillin

A

(Nallpe) Anti-staphylococcal Penicillins

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18
Q

-Oxacillin

A

Anti-staphylococcal Penicillins

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19
Q

Broad-Spectrum Penicillins

• Spectrum similar to Pen-G against

A 
ram negatives (such as?)
• Resistance to broad-spectrum pens has increased dramatically (especially MRSA)
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20
Q

-Ampicillin

A

Broad-Spectrum Penicillins

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21
Q

-Amoxicillin

A

Broad-Spectrum Penicillins DRUG OF CHOICE

for pre-cardiac surgery dental prophyllaxis

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22
Q

Antipseudomonal Penicillins

A

Pseudomonas aeruginosa is a very problematic, very pathogenic gram negative that readily develops resistance to antibiotics. Also effective against other gram-negative bacilli.

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23
Q

-Pseudomonas aeruginosa is notorious for causing

A

blue/green pus!

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24
Q

Carbenicillin

A

(Geocillin) Antipseudomonal Penicillins

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25
Q

Piperacillin

A

(Piperacil) Antipseudomonal Penicillins

26
Q

Ticarcillin

A

(Ticar) Antipseudomonal Penicillins

27
Q

Clavulanic acid (CA) also has

A

β-lactam ring like the penicillins but no antimicrobial activity.

28
Q

Clavulanic acid (CA) is a

A

suicide inhibitor of bacterial β-lactamase that

attaches to and permanently deactivates the enzyme.

29
Q

Clavulanic acid (CA)

A

with amoxicillin (Augmentin) and ticarcillin (Timentin) (why?

30
Q

penicillins are not excreted or metabolized by the kidneys so…

A

x

31
Q

penicillins Don’t cross the blood/brain barrier except.

A

when meninges are inflamed

32
Q

β-lactams essentially just like penicillins

*Classified as

A

1st, 2nd, 3rd, & 4th generation based on their resistance to β-lactamases and their antimicrobial spectrums
*Very commonly used in open heart surgery and as part of the “prime”

33
Q

1st Generation Cephalosporins

A

The “Pen-G’s” of Cephs. • Less expensive then 2nd, 3rd, 4th generations. • Since the main open-heart infection culprits
are Staph. (mostly) and Strep. sp., no advantage found using more expensive later-generation cephalosporins for ECC prophyllaxis!

34
Q

Cefazolin

A

Kefzol) -The only parenteral 1st generation -Typically dosed at a fixed
amount (1 gram/circuit, e.g.) or by weight (50mg/kg, e.g.)
*Cleared by the kidneys
*Cross sensitivity with penicillins is high (so check the charts!!!)

35
Q

2nd Generation Cephalosporins

A

Again, no proven advantage over 1st gens when used in the pump prime!
• May provide the theoretical advantage of a greater V.O.D. and slightly broader spectrum of activity.

36
Q

-Cefoxitin

A

2nd Generation Cephalosporins(Mefoxin)

37
Q

Cefotetan

A

2nd Generation Cephalosporins Cefotan)

38
Q

Cefuroxime

A

2nd Generation Cephalosporins (Ceftin)

39
Q

Vancomycin

A

A glycopeptide • Similar action to pens/cephs

  • Prevents peptidoglycan polymerization in the bacterial cell wall so they “fall apart.”
  • Spectrum of activity limited to gram positives
40
Q

vancomycin *Reserved for use in

A

MRSA, Methicillin Resistant Staph epidermidis (MRSE) and enterococcal infections.

41
Q

Vancomycin

• Excreted

A

renally (like pens and cephs)

• Side effects much more common than pens and cephs:

42
Q

sides of vancomycin

A

fever chills flushing phlebitis

43
Q

Aminoglycosides

• Derived

A

from fungi (like penicillins)

44
Q

-If they end in “…mycin

A

they’re from

Streptomyces sp.

45
Q

If they end in “…micin

A

they’re from Micromonospora sp.`

46
Q

Aminoglycosides

• Interfere with bacterial

A

protein synthesis by binding to bacterial ribosomal 30S subunit..*This action is “cidal

47
Q

Aminoglycosides

• Spectrum of activity

A

limited to gram negative bacteria, such as E. coli, Proteus mirabilis, and Pseudomonas aeruginosa

48
Q

Aminoglycosides Exhibit a synergistic effect when used with

A

pens, cephs, and vancomycin (why?) for resistant bacteria.

49
Q

Aminoglycosides

• Exhibit

A

oncentration-dependentkilling:

  • Increasing concentrations of aminoglycosides kill increasing proportions of bacteria at increasing rates.
  • **All aminoglycosides are given parenterally or used topically!
50
Q

Aminoglycosides

• Unlike other drugs discussed,

A

aminoglycosides exhibit poor CNS penetration even in the presence of meningitis.

51
Q

Resistance to aminoglycosides is complicated.

A

Multiple methods of resistance, but cross- resistance doesn’t necessarily occur (bugs can be resistant to gentamycin and not amikacin)
-Streptomycin (little used, lots of resistance)

52
Q

Tobramycin

A

(Nebcin) Streptomyces sp.

53
Q

gentamicin

A

Micromonospora sp.`

54
Q

Amikacin

A

Micromonospora sp.`(Amikin) = LEAST bacterial resistance

55
Q

Aminoglycosides

• All are excreted

A

renally and readily become “more toxic” in the presence of renal failure (a self-fulfilling prophecy since one of their major side-effects is renal toxicity!)

56
Q

Aminoglycosides

• Adequate hydration/urine output

A

minimizes side effects (what’s that mean for us?)

57
Q

All aminoglycosides cross the

A

blood/placenta barrier and concentrate in fetal tissue!

58
Q

Aminoglycoside Toxicity

*This reflects a “classic triad” of

A 
#1) Ototoxicity: vestibular &/or cochlear
#2) Neuromuscular Paralysis
PARTICULARLY with myasthenia gravis patients.
#3) Nephrotoxocity ranging from mild to total renal destruction
59
Q

Neomycin:

A

used only topically (too nephrotoxic)

60
Q

Streptomycin

A

first produced. LOTS of microbial resistance has developed

61
Q

Gentamicin and Tobramycin

A

mid-level microbial resistance

62
Q

Amikacin

A

least microbial resistance (also most expensive!)

pharmocology (20 decks)

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