Overview of Antimicrobial Agents Flashcards

1
Q

Natural Penicillins

A

Penicillin G(IV, IM)

Penicillin V (PO)

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2
Q

Anti-staphylococcal Penicillins

A

Oxacillin(IV, IM)
Dicloxacillin(PO)
Nafcillin (IV, IM)

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3
Q

Aminopenicillins*

A

Ampicillin(PO, IV, IM)

Amoxicillin(PO)

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4
Q

Anti-pseudomonalPenicillins

A

Piperacillin (IV)

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5
Q

First Generation Cephalosporins

A

Cefazolin(IV, IM)

Cephalexin [Keflex] (PO)

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6
Q

Second Generation Cephalosporins

A

Cefoxitin(IV)

Cefuroxime (PO, IV, IM)

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7
Q

Third Generation Cephalosporins*

A

Ceftriaxone[Rocephin] (IV, IM)

Ceftazidime(IV, IM)

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8
Q

Fourth Generation Cephalosporins*

A

Cefepime(IV, IM)

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9
Q

Carbapenems

A

Imipenem/cilastatin (IV)
Meropenem(IV)*
Ertapenem(IV, IM)*

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10
Q

Monobactams

A

Aztreonam (IV, IM, INH)

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11
Q

B-lactamase Inhibitors*

A

Ampicillin-sulbactam(IV)
Amoxicillin-clavulanic acid [Augmentin] (PO)
Piperacillin-tazobactam(IV)

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12
Q

Glycopeptides*

A

Vancomycin(PO, IV)

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13
Q

Lipopeptides

A

Daptomycin(IV)

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14
Q

Fluoroquinolones

A

Ciprofloxacin [Cipro] (PO, IV, topical)
Levofloxacin(PO, IV, topical)*
Moxifloxacin (PO, IV, topical)

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15
Q

Aminoglycosides

A

Tobramycin (IV, IM, INH, topical)

Gentamicin(IV, IM, topical)*

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16
Q

Tetracyclines/Glycylcyclines

A

Minocycline (PO, IV)

Doxycycline(PO, IV)*

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17
Q

Macrolides/Ketolides

A

Clarithromycin (PO)

Azithromycin[Zithromax, Z-pak] (PO, IV, topical)*

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18
Q

Lincosamides*

A

Clindamycin[Cleocin] (PO, IV, IM, topical)

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19
Q

Metronidazole

A
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20
Q

Sulfonamides/Trimethoprim

A

Sulfamethoxazole/trimethoprim (PO, IV)

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21
Q

Most common categories

A

penicillins and macrolides

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22
Q

Top 5 drugs:

A
Azithromycin
Amoxicillin
Amoxicillin-clavulanate
Ciprofloxacin
Cephalexin
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23
Q

Ask yourself whether an antimicrobial agent is warranted:

A

Is an antimicrobial indicated based on clinical findings?
Have appropriate cultures been obtained?
What is the most likely causative organism?
What must be done to prevent secondary exposure?
Is there clinical evidence or established guidelinesthat have determined antimicrobial therapy provides a clinical benefit?

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24
Q

prophylaxis

A

no infection

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25
Q

pre-emptive

A

infection

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26
Q

empiric

A

symptoms

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27
Q

definitive

A

pathogen isolated

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28
Q

suppression

A

resolution

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29
Q

A 37 yofemale with a history of end-stage renal disease, on dialysis, is admitted to the hospital with healthcare-associated pneumonia. Antibiotics are initiated to cover the most likely pathogen(s).

A

empiric

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30
Q

A 68 yomale presents for a total hip replacement. Prior to surgery, he is given one dose of cefazolin to prevent development of a surgical wound infection

A

prophylaxis

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31
Q

A 37 yofemale with a history of end-stage renal disease, on dialysis, is admitted to the hospital with healthcare-associated pneumonia. Cultures result with sensitive Pseudomonas, vancomycin is discontinued

A

definitive

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32
Q

An 8 yomale presents to the ED with a perforated appendix. Antibiotics are initiated pre-operatively to reduce risk of intra-abdominal abscess & wound infection

A

pre-emptive

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33
Q

A 75 yomale presents to his PCP for follow-up of prosthetic hip joint infection. He receives continued low dose antimicrobial therapy. Hip prosthesis was unable to be removed and replaced during hospitalization.

A

suppressive

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34
Q

Gram Positive cocci anaerobic

A

peptococcus

peptostreptococcus

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35
Q

Gram Positive cocci aerobic clusters coagulase positie

A

staph aureas

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36
Q

Gram Positive coccie aerobic clusters coagulase negative

A
staph epi
staph
saprophyticus
staph hominis
staph hemolyticus
staph warneri
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37
Q

Gram Positive cocci aerobic diplococci

A

streptococcus pneumonia

entrococcus

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38
Q

Gram Positive cocci aerobic chains b hemolytic

A

strep pyogenes group a
strep agalectiae group b
strep groups cfg

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39
Q

Gram Positive cocci aerobic chains a hemolytic

A

viridans strep

strep pneumonia

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40
Q

Gram Positive bacilli anaerobic

A
c diff
clostridium
perfringens
actinomyces
lactobacillus
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41
Q

Gram Positive bacilli aerobic

A

bacillus anthracis
nocardia
listeria
acynebacterium jelkelium

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42
Q

Gram Negative bacilli anaerobic

A

prevotella
fusobacterium
bacteroides

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43
Q

Gram Negative bacilli aerobic lactose fermenting oxidase positive

A

aeromonas
pasteurella
vibrio

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44
Q

Gram Negative bacilli aerobic lactose fermenting oxidase negative

A

ecoli
klebsiella
enterobacter
citrobacter

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45
Q

Gram Negative bacilli aerobic non lactose fermenting oxidase postiive

A
pseudomonas
flavobacterium
aitaligenes
achromobacter
moraxella
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46
Q

Gram Negative bacilli aerobic non lactose fermenting oxidase negative

A
proteus
proficendia
serrates
morganella
slamonella
shigella
strenotrophomonas
acinetobacter
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47
Q

Gram Negative bacilli aerobic misc

A
brucella
bordetella
campylobacter
pasteurella
vibrio
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48
Q

Gram Negative cocci

A

Neisseria meningitides
neisseriia gonohorrhoaea
vellionella

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49
Q

Gram Negative coccbacilli

A

h influenza

Moraxella catarrhalis

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50
Q

Susceptible:

A

Likely to inhibit pathogenic microorganism

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51
Q

Intermediate:

A

May be effective at higher dosage, more frequent administration, or in specific body site

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52
Q

Resistant:

A

Not effective at inhibiting growth of microorganism

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53
Q

Minimum inhibitory concentration (MIC):

A

lowest concentration of drug required to inhibit growth

Breakpoints established by Clinical and Laboratory Standards Institute (CLSI)

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54
Q

Clinical and Laboratory Standards Institute (CLSI) Breakpoints

MIC (μg/mL

A

Susceptible ≤ 4

Intermediate 8-16

Resistant ≥ 32

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55
Q

Clinical and Laboratory Standards Institute (CLSI) Breakpoints

Zone Diameter (mm)

A

Susceptible ≥ 20

Intermediate 15-19

Resistant ≤ 14

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56
Q

Zone Diameter (mm)

A

Act on a single or a limited group of microorganisms

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57
Q

Extended-spectrum

A

Active against gram-positive bacteria but also against significant number of gram-negative bacteria

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58
Q

Broad-spectrum

A

Act on a wide variety of bacterial species, including both gram-positive and gram-negative

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59
Q

Bacteriostatic:

A

arrests growth and replication of bacteria (limits spread of infection)

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60
Q

Bactericidal:

A

kills bacterial

Concentration-dependent killing: rate and extent of killing increase with increasing drug concentrations

Time-dependent killing: activity continues as long as serum concentration above minimum bactericidal concentration

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61
Q

Bacteriostatic vs. Bactericidal

This concept is relative

A

Certain drugs are –cidalagainst specific bacteria while –static against others

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62
Q

Drug-drug enhancement or synergism

A

Gentamicin –ineffective against enterococci in the absence of a cell-wall inhibitor
Combining penicillin with gentamicin leads to bactericidal activity

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63
Q

Antimicrobials classified based on

A

Class and spectrum of microorganisms it kills
Biochemical pathway it interferes with
Chemical structure

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64
Q

Site of Antibacterial Action

cell wall synthesis

A
cycloserine
vancomycin
bacitracin
fosfomycin
penicillins
cephalosporins
monbactams
carbapenems
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65
Q

Site of Antibacterial Action folic aid metabolism

A

Bactrim both

paba

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66
Q

Site of Antibacterial Action

cell membrane

A

polymyxins

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67
Q

Site of Antibacterial Action

dna replication (dna gyrase)

A

nalidixic acid

quinolones

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68
Q

Site of Antibacterial Action

dna dependent rna polymerase

A

rifampin

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69
Q

Site of Antibacterial Action

protein synthesis (50 S)

A

erythromycin
chloramphenicol
clindamycin

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70
Q

Site of Antibacterial Action

protein synthesis (30S)

A
tetracyclin
spectinomycin
streptomycin
gentamicin
tobramycin
amikacin
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71
Q

Site of Antibacterial Action

A
Cell wall synthesis
Cell membrane synthesis
Protein synthesis
Nucleic acid metabolism
Function of topoisomerases
Folate synthesis
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72
Q

cell wall inihbitors

blactams

A

penicillins

cephalosporins
1-4th gnereations

carbapenems

monobactams

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73
Q

cell wall inihbitors

other antibiotics

A

bacitracin

vancomycin

daptomycin

74
Q

cell wall inihbitors

blactamase inhibitors

A

clavulanic acid
sulbactam
tazobactam

75
Q

β-Lactam Mechanism of Action

A

Time-dependent; structural analogs of D-Ala-D-Ala; covalently bind penicillin-binding proteins (PBPs), inhibit the last transpeptidation step in cell wall synthesis

76
Q

β-Lactamase Inhibitors

A

Amoxicillin + clavulanic acid, ticarcillin + clavulanic acid, ampicillin + sulbactam, piperacillin + tazobactam

MOA: prevent destruction of B-lactam antibiotics

77
Q

Fluoroquinolone Mechanism of Action

A

Concentration-dependent, targets bacterial DNA gyrase& topoisomerase IV. Prevents relaxation of positive supercoils

78
Q

Inhibitors of Protein Synthesis

A

Formation of initiation complex
Amino-acid incorporation
Formation of peptide bond
Translocation

79
Q

Aminoglycosides moa

A

blocks initiation of protein synthesis

blocks further translation and elicits premature termination

incorporation of incorrect amino acid

80
Q

Tetracyclines moa

A

binds 30 s and block the a site

81
Q

Macrolides moa

A

bind 50s they inhibit translocation

82
Q

Sulfonamides and Trimethoprim moa

A

Inhibit folic acid synthesis; block sequential steps in pathway.

pcp pneumonia

block sequential steps in folic acid production

83
Q

Β-Lactams

MOA

A

structural analogs of D-Ala-D-Ala; covalently bind penicillin-binding proteins (PBPs), inhibit transpeptidation

84
Q

Β-Lactams

resistance

A

Structural difference in PBPs
Decreased PBP affinity
Inability for drug to reach site of action (i.e. gram-negative organisms)
Active efflux pumps
Drug destruction/inactivation by B-lactamases

85
Q

Natural Penicillins

drugs

A

Penicillin G (IV, IM), penicillin V (PO)

86
Q

Natural Penicillins spectrum

A

highly effective against gram-positive cocci (GPC) but easily hydrolyzed by penicillinase

87
Q

Natural Penicillins

therapeutic use

A

narrow-spectrum, Streptococcus pneumoniaepneumonia and meningitis. Penicillin V for Streptococcus pyogenespharyngitis, toxic shock, viridians streptococci endocarditis if susceptible, syphilis

88
Q

Anti-Staphylococcal Penicillins

drugs

A

Oxacillin (IV, IM), dicloxacillin (PO), nafcillin (IV, IM)

89
Q

Anti-Staphylococcal Penicillins

spectrum

A

penicillinase resistant; agents of first choice for Staphylococcus aureus(MSSA) and Staphylococcus epidermidis(MSSE) that are not methicillin resistant

90
Q

Anti-Staphylococcal Penicillins

therapeutic use

A

estricted to infections with known Staphylococcussensitivity

91
Q

Aminopenicillins

drugs*

A

Ampicillin(PO, IV, IM), amoxicillin(PO)

92
Q

Aminopenicillins

spectrum*

A

extended-spectrum; extends beyond gram-positive to gram-negative (Haemophilus influenzae, Escherichia coli, Proteus mirabilis), Listeria monocytogenes, susceptible meningococci, enterococci

93
Q

Aminopenicillins

therapeutic use*

A

upper respiratory tract infections (S. pyogenes, S. pneumoniae, H. influenzae), sinusitis, otitis media, enterococcalinfections

94
Q

Anti-PseudomonalPenicillins

drugs

A

Ticarcillin(IV), piperacillin(IV)*

95
Q

Anti-PseudomonalPenicillins

spectrum*

A

Spectrum: extends spectrum to Pseudomonas aeruginosa, Enterobacter, and Proteusspp.

96
Q

Anti-PseudomonalPenicillins

therapeutic use*

A

serious gram-negative infections, hospital acquired pneumonia (HAP), immunocompromised patients, bacteremia, burn infections, UTI

97
Q

Penicillins

Adverse effects:

A

Allergic reactions (0.7-10%)
Anaphylaxis (0.004-0.04%)
Nausea, vomiting, mild to severe diarrhea
Pseudomembranous colitis

98
Q

1st-Generation Cephalosporins

drugs

A

Cefazolin(IV, IM), cephalexin (PO)

99
Q

1st-Generation Cephalosporins

spectum

A

good gram-positive coverage, modest gram-negative (covers Moraxella, E. coli, Klebsiellapneumoniae, P. mirabilis), orally active anaerobes

100
Q

1st-Generation Cephalosporins

therapeutic use

A

skin and soft tissue infections (SSTIs), surgical prophylaxis

101
Q

2nd-Generation Cephalosporins

drugs

A

Cefoxitin (IV), cefuroxime (PO, IV, IM)

102
Q

2nd-Generation Cephalosporins

spectrum

A

somewhat increased activity against gram-negative, but less active than 3rd-generation. Subset active against Bacteroidesfragilis

103
Q

2nd-Generation Cephalosporins

therapeutic use

A

used in gram-negative mixed anaerobic (intra-abdominal infections, pelvic inflammatory disease, diabetic foot infections)

104
Q

3rd-Generation Cephalosporins

drugs*

A

Ceftriaxone(IV, IM), ceftazidime(IV, IM)

105
Q

3rd-Generation Cephalosporins

spectrum*

A

less active against gram-positive, more active against Enterobacteriaceae(although resistance increasing due to B-lactamase producing strains)

106
Q

3rd-Generation Cephalosporins

therapeutic use*

A

serious gram-negative infections (Klebsiella, Proteus, Providencia, Serratia, Haemophilus), ceftriaxone DOC for all forms of gonorrhea & severe Lyme’s disease; meningitis. Ceftazidimecovers Pseudomonas

107
Q

4th-Generation Cephalosporin

drugs*

A

Cefepime(IV, IM)

108
Q

4th-Generation Cephalosporin

spectrum*

A

extends beyond 3rd-generation, useful in serious infections in hospitalized patients. Effective against Pseudomonas

109
Q

4th-Generation Cephalosporin

therapeutic use*

A

empirical treatment of nosocomial infections

110
Q

Cephalosporins

Adverse effects:

A

1% risk of cross-reactivity to penicillins

Diarrhea

111
Q

Carbapenems

drugs*

A

Imipenem/cilastatin (IV), meropenem(IV), ertapenem(IV, IM)

112
Q

Carbapenems

spectrum*

A

aerobes & anaerobes; gram-positive, Enterobacteriaceae, Pseudomonas, Acinetobacter.Stenotrophomonasmaltophiliais resistant.

113
Q

Carbapenems

therapeutic use

A

UTI, lower respiratory tract infection (LRTI), intra-abdominal, gynecological, SSTI, bone and joint infections

114
Q

Carbapenems

adverse effects*

A

Nausea/vomiting (1-20%), seizures (1.5%), hypersensitivity

115
Q

Monobactam

drugs

A

Aztreonam (IV, IM, INH)

116
Q

Monobactam

spectrum

A

activity against gram-negative (Enterobacteriaceae, Pseudomonas, H. influenzae, gonococci), no activity against GPC or anaerobes

117
Q

Monobactam

therapeutic use

A

patients who are allergic to B-lactams appear not to react to aztreonam > effective for gram-negative infections which would usually be treated with B-lactam

118
Q

Glycopeptides

drugs

A

Vancomycin (PO, IV)

119
Q

Glycopeptides

moa

A

inhibits cell wall synthesis binding with high affinity to D-Ala-D-Ala terminal of cell wall precursor units.

120
Q

Glycopeptides

resistance

A

alteration of D-Ala-D-Ala target to D-alanyl-D-lactate or D-alanyl-D-serine which binds glycopeptides poorly. Intermediate resistance may also occur

121
Q

Glycopeptides

spectrum

A

broad gram-positive coverage –S. aureus(including MRSA), S. epidermidis(including MRSE), Streptococci, Bacillus, Corynebacterium spp., Actinomyces, Clostridium

122
Q

Glycopeptides

therapeutic use

A

osteomyelitis, endocarditis, MRSA, Streptococcus, enterococci, CNS infections, bacteremia, orallyfor C. difficile

123
Q

Glycopeptides

adverse effects

A

Macular skin rash, chills, fever, rash
Red-man syndrome (histamine release): extreme flushing, tachycardia, hypotension
Ototoxicity, nephrotoxicity (33% with initial trough > 20 mcg/mL)

124
Q

Fluoroquinolones

moa

A

concentration-dependent; targets bacterial DNA gyrase & topoisomerase IV.

125
Q

Fluoroquinolones

spectrum

A

E. coli, Salmonella, Shigella, Enterobacter, Campylobacter, Neisseria, Pseudomonas aeruginosa, S. aureus(not MRSA), limited coverage of Streptococcusspp.

*Levofloxacin, moxifloxacin, “respiratory fluoroquinolones” cover Streptococcusspp.

126
Q

Fluoroquinolones

therapeutic use

A

UTI, prostatitis, STI (chlamydia, Neisseria gonorrhoeae), traveler’s diarrhea, shigellosis, bone, joint, SSTI infections, diabetic foot infections

127
Q

Fluoroquinolones

Adverse effects:

A

GI 3-17% (mild nausea, vomiting, abdominal discomfort)
CNS 0.9-11% (mild headache, dizziness, delirium, rare hallucinations)
Rash, photosensitivity, Achilles tendon rupture (CI in children)

128
Q

Aminoglycosides

drugs*

A

Tobramycin (IV, IM, INH, topical), gentamicin(IV, IM, topical)*

129
Q

Aminoglycosides

moa*

A

concentration-dependent; binds 30S ribosomal subunit, disrupts normal cycle of ribosomal function

130
Q

Aminoglycosides

spectrum*

A

aerobic gram-negative bacteria, limited action against gram-positive, synergistic bactericidal effects in gram-positive with cell wall active agent

131
Q

Aminoglycosides

therapeutic use*

A

UTI (not uncomplicated), used if resistance to other agents, seriously ill patients, pneumonia (infective against S. pneumoniaeand anaerobes), HAP, peritonitis, synergy in bacterial endocarditis, tobramycin inhalation in CF

132
Q

Aminoglycosides

adverse effects*

A

Ototoxicity (may be as high as 25%)
Nephrotoxicity (8-26%)
Neuromuscular block and apnea

133
Q

Tetracyclines/Glycylcyclines

drugs*

A

Minocycline (PO, IV), doxycycline(PO, IV)*, tigecycline(IV)

134
Q

Tetracyclines/Glycylcyclines

moa*

A

bacteriostatic; binds 30S bacterial ribosome. Prevents access of aminoacyl tRNAto acceptor (A) site on mRNA ribosome complex

135
Q

Tetracyclines/Glycylcyclines

spectrum*

A

wide range of aerobic/anaerobic gram-positive and -negative activity; effective for: Rickettsia, Coxiellaburnetii, Mycoplasma pneumoniae, Chlamydiaspp, Legionella, atypical mycobacterium, Plasmodium, Borreliaburgdorferi(Lyme’s disease), Treponema pallidum(syphilis)

136
Q

Tetracyclines/Glycylcyclines

therapeutic use*

A

CAP, atypical CAP coverage, community acquired SSTIs, community acquired MRSA, acne, Rickettsialinfections (Rocky Mountain Spotted Fever), Q fever, anthrax

137
Q

Tetracyclines/Glycylcyclines

adverse effects*

A
GI (epigastric burning, nausea, vomiting, diarrhea)
Superinfections of C. difficile
Photosensitivity
Teeth discoloration
Thrombophlebitis
138
Q

Macrolides/Ketolides

drugs*

A

Clarithromycin (PO), azithromycin(PO, IV, topical)*

139
Q

Macrolides/Ketolides

moa*

A

bacteriostatic; binds reversibly to 50S ribosomal subunit, inhibits translocation

140
Q

Macrolides/Ketolides therapeutic use*

A

respiratory tract infections (spectrum S. pneumoniae, H. influenzae, and atypicals: Mycoplasma, Chalmydophilia, Legionella), alternative for otitis media, sinusitis, bronchitis, and SSTIs. Pertussis, gastroenteritis, H. pylori, Mycobacterial infections

141
Q

Macrolides/Ketolides

adverse effects*

A

GI (epigastric distress)
Hepatotoxicity
Arrhythmia
QT prolongation

142
Q

Macrolides/Ketolides

drug interaction*

A

CYP3A4 inhibition –prolongs effects of digoxin, warfarin….

143
Q

Lincosamides

drugs*

A

Clindamycin(PO, IV, IM, topical)

144
Q

Lincosamides

moa*

A

binds 50S subunit of bacterial ribosome, suppresses protein synthesis

145
Q

Lincosamides

spectrum*

A

pneumococci, S. pyogenes, viridansStreptococci, MSSA, anaerobes (B. fragilis)

146
Q

Lincosamides

therapeutic use*

A

SSTIs, necrotizing SSTIs, lung abscesses, anaerobic lung and pleural space infections, topically for acne vulgaris

147
Q

Lincosamides

adverse effects*

A
GI diarrhea (2-20%)
Pseudomembranous colitis (0.01-10%)
      Due to C. difficile
Skin rashes (10%)
Reversible increase in aminotransferase activity
May potentiate neuromuscular blockade
148
Q

Oxazolidinones

drug*

A

Linezolid(PO, IV)

149
Q

Oxazolidinones

moa*

A

inhibits protein synthesis binding P site of 50S ribosomal subunit, prevents formation of initiation complexes

150
Q

Oxazolidinones

spectum

A

gram-positive Staphylococcus(MSSA, MRSA, VRSA), Streptococcus(penicillin resistant S. pneumoniae), enterococci (VRE), gram-positive anaerobic cocci, gram-positive rods (Corynebacterium, L. monocytogenes)

151
Q

Oxazolidinones

therapeutic use*

A

VRE faecium(SSTI, UTI, bacteremia), nosocomial pneumonia caused by MSSA and MRSA, CAP, complicated/uncomplicated SSTI infections

152
Q

Oxazolidinones

adverse effects*

A

Myelosuppression [thrombocytopenia (2.4%),anemia, leukopenia]
Headache
Rash

153
Q

Oxazolidinones

drug interactions*

A

weak, nonspecific inhibitor of monoamine oxidase

154
Q

no novel antimocrobial moa since

A

1987

155
Q

azithromycin used mostly for

A

cap

156
Q

amoxicillin used mostly for

A

upper resp tract

otitis media

157
Q

teichoic acid

A

stabilized peptidoglycin

158
Q

lps

A

it is hydrophobic and is toxic called endotoxin when released can cause shock

159
Q

concentration dependant killing drugs

A

aminoglycosides and fluoroquinolones

160
Q

time dependent killing drugs

A

b lactams and vancomycins

cell wall inhibitors

161
Q

bacteriostatic are usually

A

protein synthesis inhibitors

162
Q

cd dependant dosing

A

qd

163
Q

time dependant dosing

A

require frequent dosing to make sure we have enough over a certain amount of time

164
Q

enterococci are

A

gram pos

165
Q

fq extra

A

normal gyrase prevents this so they inhibit this and it is not allowed to reform the dna strands that have been cleaved already and it is released and damaged

166
Q

Aminoglycosides

A

bacterialcidial bind 30s

167
Q

Tetracyclines

A

binds 30 s and block the a site

168
Q

Macrolides

A

bind 50s they inhibit translocation

169
Q

bind 50s they inhibit translocation extra

A

pcp pneumonia

block sequential steps in folic acid production

170
Q

2nd-Generation Cephalosporins used for

A

aspiration related mbc of mixed anaerobic

171
Q

Ceftriaxone has no

A

pseudomonal coverage

172
Q

ceftazidimehas good

A

psuedomonal coverage

173
Q

Carbapenems save for

A

save for last line more serious infections if there is another drug that would work

serious resistant infecction

174
Q

carbapenams must be stopped with

A

renal problems

175
Q

use linezolid if resistant to

A

vancomycin

176
Q

Red-man syndrome (histamine release): extreme flushing, tachycardia, hypotension

A

direct toxic effect on mass cells, not an allergy

177
Q

fq spectrum

A

broad gram neg

178
Q

Fluoroquinolones ci

A

chondorocyte damage

pregnancy breast feeding and children it is ci

179
Q

ag don’t target

A

anaerobes bc they require o2 to get into the cell

180
Q

tetracyclines cover

A

atypicals

181
Q

lincosamide coverage

A

good gram positive and anaerobes

aspiration pneumonia

182
Q

Oxazolidinones di

A

serotonin syndrome

cant give with ssri