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Acute Care II - Summer 2017 > Weeks 1 & 2: Antibiotics > Flashcards

Weeks 1 & 2: Antibiotics Flashcards

1
Q

do positive cultures indicate an infection?

A

no, not sole criteria for diagnosing an infection. could be contamination (improper site prep). colonization (bacteria/fungus present but not causing active disease)

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2
Q

what other things should you think about regarding an infection?

A

-related symptoms. Vital Signs: fever, hypotension. Labs: leukocytosis, leukopenia. Imagine: CXR, CT

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3
Q

what do you often see colonized, but no infection?

A

candida

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4
Q

what color corresponds to what type of bacteria on Gram stain?

A

purple: Gram Positive. pink: Gram negative

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5
Q

what does aerobic mean?

A

requires O2 for growth

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6
Q

what does cocci mean?

A

sphere

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7
Q

example of aerobic gram + cocci clusters, coagulase +

A

S. aureus (MRSA, MSSA)

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8
Q

example of aerobic gram + cocci clusters, coagulase -

A

S. epidermidis, S. haemolyticus, S. lugdunensis

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9
Q

what is coagulase?

A

it’s an enzyme

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10
Q

example of aerobic gram positive diplococcus quellung +

A

S. pneumoniae

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11
Q

example of aerobic gram positive cocci chains, PNA FISH +

A

E. faecium, E. faecalis

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12
Q

example of aerobic gram positive cocci chains, PNA FISH -

A

Streptoccus app.

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13
Q

what is PNA FISH

A

molecular assay

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14
Q

aerobic gram positive large bacilli

A

Bacillus spp

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15
Q

aerobic gram positive cocco bacillus

A

listeria monocytogenes, Lactobacillus spp.

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16
Q

aerobic gram positive bacilli, small pleomorphic

A

Corynebacterium spp.

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17
Q

aerobic gram positive bacilli branching filaments

A

Nocardia spp. Streptomyces spp.

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18
Q

anaerobic gram positive bacilli, large

A

Clostridium spp.

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19
Q

anaerobic gram positive bacilli, small, pleomorphic

A

P. acnes, Actinomyces spp.

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20
Q

anaerobic gram positive cocci

A

Peptostreptococcus spp.

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21
Q

where is coliform bacteria found?

A

in the gut/colon

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22
Q

Aerobic gram negative bacillus lactose fermenter

A

Escherichia coli, Klebsiella spp, Enterobacter spp., Serratia spp., Citrobacter spp., Proteus spp.,

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23
Q

aerobic gram negative bacillus non lactose fermenter, oxidase +

A

Pseudomonas spp. Aeromonas spp. Vibrio spp.

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24
Q

aerobic gram negative bacillus non lactose fermenter oxidase -

A

Acinetobacter spp. Stenotrophomonas spp. Burkholderia spp. Shigella spp. Salmonella spp.

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25
Q

aerobic gram negative diplococci

A

N. meningitis, N. gonorrhoeae, Moraxella catarrhalis

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26
Q

aerobic gram negative cocci-bacillus

A

Haemophilus influenzae, Acinetobacter spp., Eikenella, Kingella, Aggregatibacter, Cardiobacterium

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27
Q

anaerobic gram negative bacilli

A

Bacteroides spp., Fusobacterium spp., Prevotella spp.

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28
Q

anaerobic gram negative cocci

A

veillonella spp.

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29
Q

what is the qualitative way for sensitivity testing?

A

disk diffusion. it does not provide MIC, it only labels sample as susceptible or resistant

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30
Q

what is the quantitative way for sensitivity testing

A

minimum inhibitory concentration (MIC) method. performed by utilizing an automated system (BD Phoenix)

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31
Q

what is MIC?

A

the lowest concentration of antibiotic which inhibits the growth of the bacterium

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32
Q

how does JHH determine susceptibilities?

A

microbiology lab uses standard reference methods for determining susceptibilities (CLSI)

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33
Q

what does resistant mean?

A

growth not inhibited by usually achievable concentrations at normal doses

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34
Q

what does intermediate mean re: antibiotics

A

antibiotic level can usually be obtained in the tissue or blood, but response may be diminished

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35
Q

what does susceptible mean?

A

strain can be treated with antibiotic at recommended doses and schedules. useful to know when treating an organism in an area that is difficult to penetrate (CSF, osteomyelitis)

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36
Q

what is time dependent killing

A

how long you have to maintain level above MIC. (TIME > MIC).

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37
Q

what antibiotics work via time dependent killing

A

b-lactams, macrolides, clindamycin, glycopeptides, tetracyclines, oxazolidones

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38
Q

what is concentration dependent killing

A

Cmax/MIC or AUC/MIC. the max concentration you can achieve in the blood.

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39
Q

what antibiotics work via concentration dependent killing

A

aminoglycosides, fluoroquinolones, daptomycin, colistin

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40
Q

what is synergy

A

marked increased killing

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41
Q

example of synergy?

A

beta lactam + aminoglycoside

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42
Q

what is additive

A

increased killing

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43
Q

example of additive?

A

beta lactam + fluoroquinolone

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44
Q

what is antagonism

A

decreased killing

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45
Q

example of antagonism

A

double beta lactam

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46
Q

what is indifference

A

no difference in killing

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47
Q

example of indifferences

A

pip/tazo+metronidazole. both kill the same bacteria.

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48
Q

what are beta lactams

A

penicillins (IV/PO), cephalosporins (IV/PO), carbapenems (IV), monobactam (IV)

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49
Q

what is the mechanism of action for beta lactams

A

interferes w/ cell wall synthesis by preventing cross linking of peptidoglycan

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50
Q

spectrum of activity for natural PCN

A

non-PCNase producing gram positives (streptococci, staphylococcus aureus, Coagulase negative staph, enterococcus). Oral anaerobes (some clostridium) actinomycetes. T. palladum (syphilis)

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51
Q

spectrum of activity for PCNase resistant PCN

A

enhanced activity against staph aureus (MRSA). decreased activity against streptococcus. lacks activity against enterococcus

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52
Q

spectrum of activity for amino PCNs

A

same as natural PCN. enhance activity against listeria and enterococcus. Enhanced activity against listeria and enterococcus. enhanced activity against gram-negatives ( E. coli, proteus, haemophilus)

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53
Q

ureidopenicillin, spectrum of activity

A

enhanced gram negative activity ( E. coli, Pseudomonas, Enterobacter, Proteus, Providencia) decreased activity against enterococcus)

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54
Q

spectrum of activity for PCN + beta lactamase inhibitor

A

enhanced activity against staph aureus. Activity against Haemophilus, Moraxella, E. Coli. Klebisella and enterobacteriacae. Piperacillin-tazobactam is only one w/ activity against pseudomonas

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55
Q

which PCN + beta lactase has activity against Pseudomonas?

A

piperacillin-tazobactam.

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56
Q

reaction to PCN

A

hypersensitivity reactions, interstitial nephritis, gastrointestinal (n/v/d, pseudomembranous colitis) hematologic (anemia, neutropenia, thrombocytopenia)

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57
Q

which PCN has hepatotoxicity?

A

oxacillin, increase LFTs. less w/ nafcililin

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58
Q

what PCN causes electrolyte abnormalities?

A

PCN G since it has to be bound to a salt (Na or K)

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59
Q

do PCN need to be renal dosed?

A

yes, they are all renal cleared and need to be adjusted for renal insufficiency

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60
Q

which PCN doesn’t need to be renally dosed

A

dicloxacillin, oxacillin

61
Q

how many generations of cephalosporins?

A

5!

62
Q

spectrum of activity of 1st generation cephlasporin, cefazolin

A

MSSA, streptococci, limited gram negative.

63
Q

spectrum of activity for 2nd generation cephalosporins, cefoxitin/cefuroxime, cefotetan?

A

MSSA, streptococci, Haemophilus, Moraxella, Neisseria spp.

64
Q

spectrum of activity for 3rd generation cephalosporin, ceftriaxone?

A

decreased activity against MSSA, streptococci, enhanced gram negative activity (E.coli, Klbsiella, Proteus, Citrobacter, Serratia)

65
Q

what does ceftazidime work against?

A

pseudomonas

66
Q

spectrum of activity for 4th generation cephalosporins, cefepime

A

MSSA, streptococci, pseudomonas

67
Q

what is 5th generation cephalosporin good against?

A

skin/soft tissue infections, CAP

68
Q

spectrum of activity of 5th generation cephalosporin, ceftaroline.

A

streptococci. MRSA/MSSA

69
Q

clinical use of 1st generation cephalosporins?

A

surgical prophylaxis, skin/soft tissue infections, UTIs

70
Q

clinical use of 2nd generation cephalosporins

A

surgical prophylaxis

71
Q

clinical use of 3rd generation cephalosporins

A

CAP, meningitis, endocarditis, STDs

72
Q

clinical use of 4th generation cephalosporins

A

neutropenic fever, UTIs HAP, VAP, Meningitis, broad spectrum

73
Q

clinical use of 5th generation cephalosporins

A

skin & soft tissue infections, CAP

74
Q

how are cephalosporins elminated?

A

renally

75
Q

do you need to dose adjust cephalosporins for renal insufficiency

A

yes! except ceftriaxone

76
Q

how does food change bioavailability of cephalosporins

A

bioavailability usually enhanced w/ food d/t the acid production

77
Q

are first generation cephalosporins good for meningitis?

A

no b/c they don’t cross the blood brain barrier.

78
Q

safety concerns for cephalosporins

A

generally well tolerated, common: hypersensitivity, GI upset, Rare: neutropenia, thrombocytopenia, interstitial nephritis.

79
Q

examples of carbapenems

A

meropenem, ertapenem, imipenem/cilastatin, doripenem.

80
Q

spectrum of activity for carbapenems

A

MSSA, strep pneumoniae, many gram-negative rods (including multi-drug resistant gram negatives). anaerobes (B. fragilis). does not cover MRSA, VRE

81
Q

ertapenem does not cover….

A

pseudomonas spp. or acinetobacter spp.

82
Q

characteristics of imipenem

A

hydrolyzed by renal dihydropeptiase to a toxic metabolite. that’s why cilastatian is included b/c it inhibits dihydropeptiase. need to dose adjust for renal insufficiency.

83
Q

safety of carbapenems

A

generally well tolerated. Rare: seizures, neutropenia, thrombocytopenia, interstitial nephritis.

84
Q

spectrum of activity for monobactams (ex: aztreonam)

A

gram negative aeroobes, fair coverage for Pseudomonas, NO COVERAGE for gram positive or anaerobic.

85
Q

what’s good about aztreonam (a monobactam, part of the beta lactam family)

A

weakly immunogenic so can be used in patients w/ a true PCN allergy

86
Q

clinical use of aztreonam?

A

alternative empiric therapy for gram negative coverage.

87
Q

what family is colistin part of

A

polymixin E antibiotic

88
Q

how many forms is colistin available in?

A

2 forms: colistin sulfate (topical) & Colistimethate sodium (IV)

89
Q

mechanism of action of Colistin?

A

disrupts gram negative bacteria outer membrane by displacing divalent cations (Mg, Ca) from membrane lipids

90
Q

spectrum of activity for Colistin?

A

only gram negative bacilli: MDR Pseudomonas, Acinetobacter, E Coli, Klebsiella, Enterobacter

91
Q

what does Colistin not protect against?

A

Gram positive and gram negative cocci are naturally resistant

92
Q

what are resistance issues for Colistin?

A

-has been reported worldwide to P. aeruginosa, A baumanni, K pneumonia w & w/o previous exposure to Colistin -heteroresistance reported as well -resistence has been linked to inadequate dosing -has been suggested to be relative to environment, low Mg concentrations, low pH, high iron concentrations

93
Q

mechanism of action for colistin?

A

reduced binding affinity - not fully understood.

94
Q

clinical use for colistin

A

Salvage therapy for MDR gram negative organisms.

95
Q

safety issues of colistin

A

neuro: dizziness, paresthesia, vertigo, confusion, visual disturbances, ataxia renal: ATN reported in 20-25% w/ older formulation, but lower in recent reports

96
Q

how can you tell if colistin is dosed high enough?

A

ataxia. neuropathy can develop that is not reversable

97
Q

mechanism of action of oxazolidinones

A

inhibits protein synthesis by inhibiting initiation complex 50s rRNA and 30S

98
Q

what family does linezolid belong?

A

oxazolidinones

99
Q

what is the spectrum for oxazolidinones

A

E. faecalis, E. faecium (including VRE), S. aureus (including MRSA), coagulase-negative staphylococci (MRSE), S. pneumoniae, Nocardia, Mycobacteria (TB and other Non TB microbacterimum) not active against gram negative organisms

100
Q

clinical use of linezolid

A

VRE infections, MRSA pneumonia in patients failing vancomycin

101
Q

safety of linezolid

A

reversible bone marrow suppression; thrombocytopenia & leukopenia - resolves w/ discontinuation reversible optic neuritis & irreversible sensory motor polyneuropathy (with prolonged therapy > 28 days) Serotonin syndrome when administered w/ serotonergic agents (controversial)

102
Q

which is better, vancomycin or linezolid

A

in the long term it doesn’t matter

103
Q

dosing guidelines for vancomycin

A

slowly bactericidal (compared to beta lactams

104
Q

when do you get a trough for vancomycin?

A

prior to 4th dose.

105
Q

what should trough levels of vancomycin be?

A

15-20 mg/L (assuming MIC < 1 mg/L)

106
Q

loading dose of vancomycin

A

25-30 mg/kg

107
Q

when do you see nephrotoxicity with vancomyocin?

A

when co-administered w/ aminoglycosied

108
Q

when is vancomycin resistane?

A

when trough levels are < 10

109
Q

mechanism of action for clindamycin

A

inhibiting bacterial protein synthesis by binding to 50s ribosomal subunit

110
Q

absorption & CSF penetration for clindamycin

A

good oral absorption (90%) but poor CSF penetration

111
Q

spectrum of clindamycin

A

gram positive aerobes & anaerobes including community acquired MRSA, MSSA w exception of Enterococcus

many gram negative anaerobes

112
Q

clinical use of clindamycin

A

provides anaerobic coverage for intra abdominal or pulmonary infections

skin & soft tissue community acquired MRSA, MSSA strep

necrotizing fascitis group A strep

alternative PCP, toxoplasmosis, malaria

used for dental prophylaxis

113
Q

safety concerns for clindamycin

A

c. difficile pseudomembranous colitis / GI issues: N/V

incidence of C difficile is greater with PO vs IV

114
Q

mechanism of action for fluoroquinolones

A

inhibit bacterial topoisomerases IV and DNA gyrase to inhibit DNA replecation & bacterial growth

115
Q

examples of fluoroquinolones

A

norfloxacin, ciprofloxacin, moxifloxacin, ofloxacin, levofloxacin, gemifloxacin

116
Q

what causes the difference in the fluoroquinolones?

A

substituions at positions on the core quinolong structure affects type and thus specrtum of activity

117
Q

spectrum of activity for fluoroquinolones

A
  • gram negatives including Enterbactericeae spp.
    • pseudomonas - use ciprofloxacin & levoflxacin only
  • gram positives (Streptococcus - S. pneumo & S. viridans) Staphylococcal spp.
    • moxifloxacin, levofloxacin, gemifloxacin
    • ciprofloxacin limited activity f/t resistance
  • atypical organism
  • anaerobes, tb, mycobacteria
118
Q

clinical use of fluoroquinolones

A
  • second line agent in patients with peicillin allergies
  • CAP & URI - avoid ciprofloxacin d/t unreliable activity against gram positive organisms except VAP/HAP when used in combo w/ gram positive agent
  • UTIs/prostatitis
    • avoid moxifloxacin d/t poor renal penetration and inadequat urinary concentration
  • intra abdominal infections
  • infectious diarrhea
  • second line agent for treatment of pulmonary TB
119
Q

safety concerns for fluoroquinolones

A
  • GI upset
  • CNS: HA, insomnia, dizzines
  • photosensitivity
  • prolonged QT interval
  • glucose dysregulation
  • pseudomembranous colitis (C difficile)
  • ******connetive tissue damage
    • black box warning for tendon injury
    • teratogen/impaired cartilage development - have to stop if have cartilage injury while one it & cant receive it again
  • interstitial nephritis - rare
120
Q

mechanism of action for macrolides

A

inhibit RNA dependent protein synthesis by reversibly binding to 50S ribosomal subunit

121
Q

examples of macrolides

A

azithromycin, clarithrmycin, erythromycin

122
Q

spectrum of activity for macrolides

A

gram postive MSSA, S. pneumoniae, S. pyogenes

gram negatives: H. influenzae, M. catarrhalis, N gonorrhoeae

atypicals - mycoplasma

non TB mycobacteria

H. pyloria

emergence of resistance limits macroline use

possesses anti-inflammatory properties - good for CF patients, lung transplant recipients

123
Q

clinical use of macrolides - clarithromycin & azithromycin

A

community aquired pneumonia

COPD exacerbations

pharyngitis, tonsillitis, acute otitis media, acute sinusitis

myobacterium avium complex - first line

lyme disease (early)

124
Q

clinical use of macrolides - erythromycin & azithromycin

A

chlamydia trachomatis infections (cervicitis, urethritis)

infectious diarrhea (salmonella typhi, shigella)

campylobacter jejuni assocaited diarrhea - first line

125
Q

what to use for helicobacter pylori infection?

A

clarithromycin

126
Q

what antibiotic can you use as a motility agent (hint it’s a macrolide)

A

erythromycin

127
Q

name a tetracycline?

A
128
Q

tigecycline

A
129
Q

what is tigecycline?

A

a derivative of minocycline

130
Q

what is good/bad about tigecycline?

A

low concentrations in the blood - so don’t use for bactermia

it goes into the tissues

131
Q
A
132
Q

spectrum for tigecycline?

A

gram positive organisms (MRSA, MSSA, VRE)

gram negative organisms (Citrobacter freundii, E. coli, Klebsiella spp, acinetobacter baumanii)

anaerobes

DOES NOT COVER: pseudomonas spp., proteus spp., providentia spp. (the three P’s)

133
Q

clinical use of tigecycline

A

intra-abdominal infections in patients with contraindications to both beta-lactams and fluoroquinolones

infections d/t MDR gram negative organisms including acinetobacter spp. (MDR aAb) & Stenotrophomonas maltophilia, non-TB mycobacteria

134
Q

safety issues w/ tigecycline

A

nausea, vomiting, diarrhea, pacreatitis

135
Q

what are considerations for antibiotics?

A

host factors:

age, body weight, volume of distribution, renal function (CVVHD, HD), allergy history

infection factors:

location of infection, organisms (gram positive vs gram negative vs fungal vs other), resistance profile, mechanisms of action

antibiotic factors:

frequency of administration, time dependent killing, concentration dependent killing, tissue penetration, renally cleared vs hepatic, drug/drug interactions

136
Q

information on host factors for antibiotics

A

use the Cockcroft-Gault equation

weight

volume of distribution: higher volume of distribution in critically ill patient

Allergy history: IgE mediated vs non-IgE vs ‘intolerance’

use skin testing for IgE mediated PCN allergy & possibly desentizie

137
Q

infection factors for antibiotics

A

location of infection

organism: gram positive vs. gram negative vs. fungal vs viral

resistance profile: MRSA (VISA, VRSA). VRE (liver failure/transplant), MDR GNR (Acinetobacter, Klebsiella, Pseudomonas)

Mechanism of resistance: Gene vs plasmid (transmissibility) & ESBL, NDM-1 (carbapenamase producer)

138
Q

CNS ICU infections

A

meningitis/encephalitis

shunt infections

post op infections

139
Q

respiratory icu infections

A

pneumona (CAP, VAP, HCAP), viral, fungal

transplant

140
Q

cardiovascular icu infections

A

endocarditis, vascular graft infections, device infections (ICD, LVAD)

transplant

141
Q

GI ICU infections

A

spontaneous (perforation, rupture, peritonitis)

post op

c. difficile colitis

transplant

142
Q

genitourinary ICU infections

A

urosepsis

pyelonephritis

transplant

143
Q

musculoskeletal ICU infections

A

necrotizing fascitis

144
Q

time dependent antibiotics

A

beta lactams

carbapenems

linezolid

erythromycin

clarithromycin

lincosamides

145
Q

concentration dependent antibiotics

A

aminoglycosides

metronidazole

fluroquinolones

telithromycin

daptomycin

quinupristin/dalfopristin

146
Q

concentration dependent with time dependence

A

fluroquinolones

aminoglycoside

azithromycin

tetracyclines

glycopeptides

tigecycline

quinupristin/dalfopristin

linezolid

147
Q

antibiotics with good tissue penetration

A

CNS infection: PCN, 3rd generation cephalosporin, linezolid, flagyl

Pulmonary infections: beta lactams, fluoroquinolones, linezolid

GU infections: kidney: fluoroquinolones, 3rd generation cephalosporins; bladder: fluroquinolones, cephalosporins (IV), aminoglycosides

148
Q

antibiotics with poor tissue penetration

A

CNS infection: vancomycin, PCN+Beta lactamase inhibitor, 1st generations cephalosporin, aminoglycosides

pulmonary infections: aminoglycosides

GU infection: moxifloxacin (not adequate urine levels)

Acute Care II - Summer 2017 (10 decks)

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