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PHRM 865 > Exam Two > Flashcards

Exam Two Flashcards

1
Q

Mechanism of action of beta lactam antibiotics

A

inhibitors of cell wall synthesis

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2
Q

mechanism of resistance of beta lactam antibiotics

A
  • destruction by beta lactamase enzymes
  • alteration in PBPs (not aztreonam)
  • decrease permeability of the outer cell membrane in gram negative bacteria
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3
Q

what are the pharmacodynamic properties of beta lactams

A

time dependent bactericidal activity (except against enterococcus)

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4
Q

What is the elimination half life of most beta lactams

A

< 2 hours

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5
Q

How are most beta lactams eliminated

A

renally

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6
Q

Which beta lactams are not eliminated renally?

A
  • nafcillin
  • oxacillin
  • ceftriaxone
  • cefoperazone
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7
Q

Are all beta lactams cross allergenic?

A

all except aztreonam

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8
Q

Natural Penicillins SOA

A
  • Most non beta lactamase producing gram positive cocci and bacilli
  • very little staphylococcus
  • gram negative cocci
  • anaerobes
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9
Q

Penicillinase-Resistant Penicillins (nafcillin, methicillin, oxacillin, dicloxacillin) SOA

A

MSSA

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10
Q

Aminopenicillins (ampicillin and amoxacillin) SOA

A
  • ineffective against staphylococcus aureus
  • better against enterococcus
  • excellent against listeria monocytogenes
  • Gram Negatives
  • anaerobes
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11
Q

What is ampicillin the drug of choice for

A

listeria monocytogenes and enterococcus

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12
Q

Carboxypenicillins (ticarcillin) SOA

A
  • weak gram positive activity (no activity against staphylococcus)
  • gram negative (including pseudomonas)
  • not active against klebsiella or serratia
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13
Q

Ureidopenicillins (piperacillin) SOA

A
  • good gram positive
  • no activity against staphylococcus
  • improved activity of gram negatives (including pseudomonas aeruginosa)
  • anaerobes similar to Pen G with some activity against B fragilis
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14
Q

Which penicillin has the most activity against pseudomonas

A

piperacillin

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15
Q

Beta lactamase inhibitor combination penicilllins SOA

A
  • staphylococcus aureus (MSSA)
  • enahnced activity of some gram negative
  • Anaerobes (B. fragilis and DOT organisms)
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16
Q

Are penicillins bactericidal or bacteriostatic against enterococcus

A

bacteriostatic

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17
Q

Does food delay the rate and/extent of absorption of penicillins?

A

Yes

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18
Q

Penicillin distribution to the CSF

A

only in the presence of inflamed meninges when high, maximal doses of parenteral penicillins are used

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19
Q

Where are nafcillin and oxacillin eliminated?

A

liver

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20
Q

Where is piperacillin eliminated

A

dual elimination

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21
Q

Which agents cause sodium load and must be considered in patients with CHF or renal dysfunction?

A
  • aqueous penicillin G
  • nafcillin
  • ticarcillin
  • piperacillin
  • carbenicillin
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22
Q

Natural penicillin use

A
  • streptococcus pneumonia (PSSP or PISP)
  • treponema pallidum (syphilis)
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23
Q

Penicillinase Resistant Penicillins (nafcillin, oxacillin)

A
  • MSSA
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24
Q

Aminopenicillin use

A

Enterococcal infections and listeria monocytogenes

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25
Q

Ureidopenicillins (piperacillin) use

A

pseudomonas aeruginosa

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26
Q

beta lactamase inhibitor combination product use

A
  • Augmentin useful for above the diaphragm infections
  • Unasyn and Zosyn for polymicrobial infections such as intraabdominal, gynecological, and adiabetic foot
  • Zosyn covers pseudomonas aeruginosa like HAP
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27
Q

Adverse Effects of penicillins

A
  • hypersensitivity
  • direct neurologic toxic effect (seizures)
  • leukopenia, neutropenia, thrombocytopenia
  • C diff
  • interstitial nephritis
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28
Q

What are the characteristics of interstitial nephritis in penicillin use?

A
  • fever
  • eosinophiluria and eosinophilia
  • an abrupt increase in serum creatinine
  • associated with methicillin and nafcillin
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29
Q

Nafcillin specific advere effect

A
  • phlebitis
  • interstitial nephritis
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30
Q

ticarcillin specific adverse effect

A
  • hypokalemia
  • sodium overload and fluid retention
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31
Q

piperacillin specific adverse effect

A
  • sodium overload and fluid retention
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32
Q

MOA of cefiderocol

A

binds to extracellular free ferric iron and actively transported across the outer cell membrane of bacteria into periplasmic space using a siderophore iron uptake mechanism

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33
Q

First generation cephalosporins SOA

A
  • best activity against gram positive aerobes (PSSP, MSSA)
  • Gram negative aerobes (PEK)
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34
Q

PEK

A
  • proteus mirabilis
  • escherichia coli
  • klebsiella pneumoniae
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35
Q

Second generation cephalosporins SOA

A
  • gram positive aerobes
  • gram negative aerobes (HENPEK)
  • anaerobes (bacteroides fragilis) only with cefoxitin, cefotetan, cefmetazole
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36
Q

HENPEK

A
  • haemophilus influenzae
  • moraxella catarrhalis
  • neisseria
  • enterobacter
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37
Q

Which second generation cephalosporins cover anaerobes like bacteroides fragilis

A
  • cefoxitin
  • cefotetan
  • cefmetazole
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38
Q

What are the most commonly used first generation cephalosporins

A
  • cefazolin
  • cephalexin (oral)
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39
Q

What are the most commonly used second gen cephalosporins

A
  • cefuroxime
  • cefprozil
  • cefoxitin
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40
Q

Third Generation cephalosporin SOA

A
  • Gram positive aerobes like PRSP (ceftriaxone and cefotaxime)
  • gram negative aerobes (HENPECKSSS with Pseudomonas)
  • limited anaerobes
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41
Q

Which cephalosporin is a strong inducer of ESBLs in gram negative bacteria

A

ceftazidime

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42
Q

HENPECKSSS

A
  • haemophilus influenzae
  • moraxella catarrhalis
  • neisseria
  • enterobacter
  • citrobacter
  • morganella
  • providencia
  • Serratia
  • Salmonella
  • Shigella
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43
Q

What are the most commonly used third generation cephalosporin agents

A
  • ceftriazone
  • ceftazidime
  • cefpodoxime
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44
Q

Fourth generation cephalosporin SOA

A
  • gram positive aerobes
  • gram negative aerobes including pseudomonas and b-lactamase producing enterobacter
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45
Q

which cephalosporin is a poor inducer of ESBLs in gram negative aerobic bacteria

A

cefepime

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46
Q

Ceftaroline SOA

A
  • coverage against staphylococci and streptococci including PRSP and MRSA (ceftriaxone w/ MRSA activity)
  • gram negative aerobes (HENPEK)
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47
Q

Does ceftaroline cover pseudomonas?

A

No

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48
Q

Cefiderocol SOA

A
  • no gram positive
  • gram negative aerobes (HENPECKSSS w/ pseudomonas and MDR carbapenamase strains)
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49
Q

Ceftolazane-tazobactam SOA

A
  • gram positive streptococci
  • gram negative coverage like cefepime including ESBL and some AmpC pseudomonas
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50
Q

Ceftazidime-avibactam SOA

A
  • gram positive streptococci
  • gram negative coverage like cefepime incljuding ESBLs, some AmpC enterobacterales and pseudomonas
  • some KPC producing and OXA producing enterobacterales
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51
Q

What are cephalosporins mostly unactive against

A
  • MRSA (except ceftaroline)
  • enterococcus
  • Legionella
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52
Q

Which cephalosporins achieve concentrations in the CSF

A
  • cefuroxime (2nd gen)
  • IV third gen
  • IV fourth gen
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53
Q

Which cephalosprins are not eliminated in the kidneys

A
  • ceftriaxone (biliary)
  • cefoperazone (liver)
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54
Q

Which cephalosporin has a long half life

A

ceftriaxone

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55
Q

What is cefazolin the drug of choice for?

A

surgical prophylaxis

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56
Q

first gen cephalosporin use

A
  • MSSA
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57
Q

Should first gen cephalosporins be used for meningitis?

A

no

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58
Q

Second gen cephalosporin use

A
  • polymicrobial infections of anaerobes and aerobes (intraabdominal, cefazolin not great, use second gen)
  • B fragilis
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59
Q

Third generation use

A
  • pseudomonas (ceftazidime or cefoperazone)
  • ceftriaxone for uncomplicated gonorrhea
  • PRSP with cefotaxime and ceftriaxone
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60
Q

Fourth generation cephalosporin use

A
  • CAP and HAP
  • pseudomonas
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61
Q

Ceftaroline use

A

MRSA

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62
Q

Cefiderocol

A

MDR gram negative bacteria who have limited or no therapeutic options

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63
Q

Clinical signficance of 5-NMTT side chain

A
  • hypoprothrombinemia
  • disulfiram reaction
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64
Q

Which agents have 5-NMTT side chain

A
  • cefamandole
  • cefotetan
  • cefmetazole
  • cefoperazone
  • moxalactam
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65
Q

Which cephalosporins have a reaction with alcohol?

A
  • cephamycins and 5-NMTT side chains
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66
Q

Adverse effects of cephalosporins

A
  • hypersensitvity
  • leukopenia, neutropenia, thrombocytopenia
  • biliary sludging (ceftriaxone)
  • C-diff
  • nonconvulsive status epilepticus
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67
Q

Which cephalosporins cause nonconvulsive status epilepticus in renal insufficiency

A
  • cefepime
  • ceftazidime
  • cefiderocol
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68
Q

Which cephalosporin precipitates with calcium

A

ceftriaxone

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69
Q

Carbapenems SOA

A
  • gram positive aerobes including MSSA and enterococcus faecalis (imipenem)
  • gram negative aerobes HENPECKSSS w/ pseudomonas (not ertapenem)
  • gram negative aerobes
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70
Q

What are carbapenems the drug of choice for

A

ESBL and AmpC producing bacteria

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71
Q

Which carbapenems are best for gram positive aerobes

A

imipenem and doripenem

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72
Q

which carbapenems are the best for gram negative aerobes

A

doripenem and meropenem

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73
Q

Which carbapenem does not cover pseudomonas

A

ertapenem

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74
Q

Carbapenems do not cover what

A
  • MRSA
  • C diff
  • Stenotrophomonas
  • Atypicals
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75
Q

CSF penetration of carbapenems

A

meropenem penetrates into the CSF better

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76
Q

Elimination of carbapenems

A

renal

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77
Q

Which carbapenems require dose adjustments

A

all of them

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78
Q

purpose of cilastatin

A

prevent renal metabolism and protect against potential nephrotoxicity due to DHP

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79
Q

Clinical uses of carbapenems

A
  • polymicrobial infections including pseudomonas
  • infections due to ESBLs/AmpCs
  • KPC producing enterobacterales (combination drugs)
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80
Q

Major side effect of carbapenems

A

CNS toxicity (seizures) in patients that have CNS disorders, high doses, and presence of renal dysfunction

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81
Q

Aztreonam SOA

A

gram negative aerobes (HENPECKSSS + pseudomonas)

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82
Q

Does aztreonam penetrate in into the CSF

A

yes

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83
Q

Elimination of aztreonam

A

renal (dose adjsutment needed)

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84
Q

Use of aztreonam

A
  • gram negative aerobes including pseudomonas
  • penicillin allergy infections
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85
Q

Use of aztreonam in pen allergic patients

A
  • low to negligible cross reactivity
  • can be used in patients
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86
Q

Carbapenem and Monobactam general adverse effects

A
  • neutropenia/thrombocytopenia
  • transient LFT increases
  • drug fever
  • phlebitis
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87
Q

FQ MOA

A

inhibition of DNA synthesis by binding to and inhibiting bacterial topoisomerases

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88
Q

FQ resistance mechanisms

A
  • mutation in the genes that code for DNA gyrase or topoisomerase IV (change in binding site)
  • efflux
  • alteration in cell wall permeability
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89
Q

FQ Activity

A

concentration dependent bactericidal activity

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90
Q

FQ SOA

A
  • new FQs have enhanced activity including PRSP (not cipro) and MSSA
  • delafloxacin against MRSA
  • HENPECKSSS + against gram negative aerobes + pseudomonas
  • Legionella
  • Mycobacterium
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91
Q

Which FQ is least active against gram negatives

A

moxifloxacin)

92
Q

Which FQs cover pseudomonas

A

cipro, levo, dela

93
Q

PK advantages of FQs

A
  • penetration into prostate
  • display PAE against both gram positive and negative aerobes
  • well absorbed after oral administration
94
Q

How are FQs eliminated

A
  • levo cipro and dela renally, need dose adjustments
  • moxifloxacin is hepatic
95
Q

Which FQ does not have to be dose adjusted renally

96
Q

FQ clinical uses

A
  • prostatitis
  • pseudomonas
  • respiratory infections
97
Q

FQ adverse effects

A
  • peripheral neuropathy
  • hepatotoxicity (trova)
  • QTc prolongation
  • articular damage (contraindicated in pregnancy)
  • tendonitis
98
Q

Which class of antibiotics cause QTc prolongation

99
Q

Should FQs be taken during pregnancy

100
Q

Drug interactions of FQs

A
  • warfarin
  • divalent and trivalent
101
Q

Macrolide MOA

A
  • reversibly bind to 50s ribosomal subunit to induce dissociation of peptidyl transferase RNA from the ribosome
102
Q

Macrolide activity

A

bacteriostatic (reversibly binds)

103
Q

Macrolide MOR

A
  • active efflux by mef gene confers low level resistance
  • alteration in the binding site by erm confers high level resistance
104
Q

Macrolide SOA

A
  • gram positive aerobes (C>E>A) including PSSP and MSSA
  • Gram Negative aerobes (A>C>E)
  • Legionella and mycobacterium avium complex (azithro and clarithro)
105
Q

do macrolides distribute into the CSF

106
Q

Which macrolides reqiuire renal dosage adjustment

A

clarithromycin in patients with CrCl < 30 mL/min

107
Q

Which macrolide is inhibited by CYP3A4 and 2C9

A
  • clarithromycin and erythromycin
108
Q

Clinical uses of macrolides

A
  • CAP especially for atypical coverage
  • chlamydia (azithromycin)
  • MAC (clarihtyromycin)
109
Q

Major adverse effects of macrolides

A
  • GI distress
  • thrombophelbitis and infusion site irritaiton
  • QTc prolongation
110
Q

Drug interactions with macrolides

A
  • warfarin
  • theophylline
  • carbamazepine
  • valproate
  • cyclosporine
  • digoxin
  • phenytoin
111
Q

Vancomycin MOA

A
  • inhibits the synthesis of the bacterial cell wall during the second stage (D-Ala D-Ala)
112
Q

Mechanism of Resistance of Vancomycin

A
  • modification of D-Ala D-Ala binding site into D-Lactate by VanA
  • thickening of peptidoglycan wall in VISA
113
Q

Vancomycin SOA

A
  • gram positve aerobic and anaerobic
  • MRSA
  • PRSP
  • C diff
114
Q

Vancomycin activity

A

slowly bactericidal in a time dependent manner

115
Q

Vancomycin penetration into CSF?

116
Q

What is the drug of choice for MRSA

A

vancomycin

117
Q

What dosage form of vancomycin is used for C diff

118
Q

How is vancomycin eliminated

A

renaly, need dose adjustment

119
Q

Clinical uses of Vancomycin

A
  • MRSA (the drug of choice)
  • PRSP
  • Cdiff
120
Q

Adverse effects of vancomycin

A
  • red man syndrome related to the rate of infusion
  • reversible nephrotoxicity
  • irreversible ototoxicity
121
Q

Synercid MOA

A

inhibit protein synthesis by binding to 50S ribosomal subunit

122
Q

Synercid MOR

A

alteration of ribosomal binding site by erm gene

123
Q

Synercid activity

A

time dependent bacteristatic

124
Q

Synercid SOA

A
  • VRE (faecium)
  • PRSP
  • MSSA and MRSA
125
Q

When to consider Synercid for VRE

A

Enterococcus faecium VRE

126
Q

Elimination of synercid

A

hepatic clerance

127
Q

Renally adjust synercid?

128
Q

Drug interactions Synercid

A
  • HMG-CoA reductase
  • immunosuppressive agents
  • carbamazepine
129
Q

Synercid adverse effects

A
  • myalgias, arthralgia
  • venus irritation
130
Q

Linezolid MOA

A

inhibits protein synthesis by binding to 50s near 30S interface, producing inhibition of the 70S initiation complex

131
Q

Linezolid activity

A

bacteriostatic

132
Q

linezolid MOR

A

alteration of the ribosomal subunit (rare)

133
Q

Linezolid SOA

A
  • VRE faecium AND faecalis
  • MSSA, MRSA
  • VISA, VRSA
  • inactive against gram negatives and atypicals
134
Q

PK characteristics of linezolid

A
  • PAE
  • rapidly and orally abosrbed 100%
135
Q

Linezolid distribution into CSF

A

limited data

136
Q

Elimination of linezolid

A
  • both renal and nonrenal
  • does not require renal dosage adjustment
137
Q

When is linezolid used?

A
  • Both Faecalis and faecium VRE
  • MRSA, VISA, VRSA
138
Q

Drug interactions Linezolid

A
  • MOAi
  • serotonergic agents
139
Q

Adverse Effects linezolid

A
  • peripheral neuropathy
  • thrombocytopenia and anemia
140
Q

Daptomycin MOA

A

binds to bacterial membranes and inserts lipophilic tail into cell wall to cause leakage

141
Q

Daptomycin activity

A

concentration dependent bactericidal activity

142
Q

Daptomycin MOR

A
  • rarely reported
  • altered cell membrane
143
Q

Daptomycin SOA

A
  • gram positive aerobes - PRSP
  • VRE (both)
  • MSSA
  • MRSA
  • VISA
    -VRSA
  • LRSA
144
Q

When to use daptomycin

A
  • When vancomycin or linezolid cannot be used
  • enterococcus faecium and faecalis including VRE
  • MSSA, MRSA
  • VISA, VRSA
  • linezolid resistant staphylococcus aureus
145
Q

Elimination of daptomycin

A

renal dose adjustment needed

146
Q

When should daptomycin not be used

A

treatment of pneumonia

147
Q

clinical uses for daptomycin

A

Staphylococcus aureus bacteremia and endocardidits

148
Q

Drug interactions daptomycin

149
Q

adverse effects daptomycin

A
  • myopathy and CPK elevation
  • acute eosinophllic pneumonia
150
Q

Lipoglycopeptides MOA

A
  • inhibit second stage of protein synthesis
  • oritavancin and telavancin bind to bacterial cell membranes and insert lipophilic tails
151
Q

lipoglycopeptides MOR

A
  • alteration of D-ala D-ala binding site
152
Q

lipoglycopeptides activity

A

concentration dependent bactericidal

153
Q

lipoglycopeptides SOA

A
  • gram positive aerobes including both VRE (oritavancin) and MRSA, VISA, VRSA (oritavancin)
154
Q

CSF penetration lipoglycopeptides

155
Q

Which lipoglycopeptide requires renal adjustment

A
  • telavancin and dalbavancin
156
Q

lipoglycopeptides adverse effects

A
  • infusion syndrome
  • nephrotoxicity
  • QTc prolongation
  • taste disturbances
157
Q

Which lipoglycopeptide should not be used in pregnancy

A

telavancin

158
Q

aminoglycosides MOA

A

irreversibly bind to the 30s ribosomal subunit

159
Q

aminoglycoside activity

A

concentration dependent bactericidal

160
Q

aminoglycoside MOR

A
  • alteration in aminoglycoside uptake
  • synthesis of aminoglycoside modifying enzymes
  • alteration in ribosomal binding site (strepto)
161
Q

aminoglycosides SOA gram positives

A
  • never use alone
  • always use with low doses with cell wall agents
  • most strains of staphy aureus (never use alone for MSSA and MRSA)
162
Q

aminoglycosides SOA gram negatives

A
  • often use with cell wall active agents to provide synergy
  • higher doses uses
  • PPPEEACKSSS
  • Pseudomonas!
163
Q

Which aminoglycoside is used in gram positives

A

gentamicin, low dose with other agents

164
Q

Which aminoglycoside is active against atypicals

A

streptomycin - mycobacteria

165
Q

PK of aminoglycosides

A
  • interpatient variability exists in the PK parameters of Vd and clearance
  • influences dosing for each individual patient
166
Q

distribution of aminoglycosides

A
  • poorly in the CSF
  • ideal body weight should be used
  • volume differences must be taken into account because they are concentration dependent agents
167
Q

When is it important to achieve therapeutic concentrations in aminoglycoside

A

within 24 hours for gram negative sepsis

168
Q

Standard dosing principles

A
  • smaller doses (1-2.5 mg/kg/dose)
  • for gram negative and gram positive synergy
169
Q

Gram negative moderate infections PK paramenters aminoglycosides

A
  • Peak 4-6
  • Trough 0.5-1.5
170
Q

Gram negative moderate to severe infections PK paramenters aminoglycosides

A
  • Peak 6-8
  • trough 1.0-1.5
  • soft tissue, bacteremia
171
Q

Gram negative severe infections PK paramenters aminoglycosides

A
  • Peak 8-10
  • trough <2
  • pneumonia, life threatening, burn
172
Q

Gram positive moderate PK aminoglycosides

A
  • gent only
  • peak 3-5
  • trough 1
173
Q

Aminoglycoside extended dosing

A

5-7 mg/kg as single daily dose (use IBW or ADW)

174
Q

When should extended dosing be considered

A
  • urospesis
  • intraabdominal
  • skin and soft tissue
175
Q

Extended dosing used in caution with aminoglycosides

A
  • immunocompromised patients
  • patient with large or small Vd
  • patients with high clearance (young,burn)
176
Q

When should serum concentrations be taken in extended dosing

A
  • 2 and 10 hours after the end of infusion
  • 8-12 hours after the first dose
177
Q

Extending dosing PK paramenters

A
  • gram negatives only
  • peak 13-20
  • trough < 0.5
178
Q

use of aminoglycosides

A
  • serious infections due to gram negative aerobic bacteria includihng pseudomonas
179
Q

Adverse effects aminoglycosides

A
  • neprotoxicity for prolonged high trough concentrations
  • ototoxocity irreversible
180
Q

tetracycline MOA

A

reversibly bind to the 30s blocking the A site

181
Q

tetracycline activity

A

bacteriostatic time dependent

182
Q

tetracycline MOR

A
  • decreased accumulation due to tetracycline specific efflux pumps
  • decreased access due to robosomal protection proteins
  • enzymatic inactivation
183
Q

tetracycline analogs MOR

A

multidrug efflux pump

184
Q

Tetracycllines SOA

A
  • gram positive aerobes (mino and doxy) including PSSP and MSSA
  • gram negative aerobes , not enterobacteraales
185
Q

tetracycline analogs SOAA

A
  • MSSA and MRSA
  • garam negative aerobes EEACKSS
  • anaerobes bacteroides
  • atypicals mycobacterium
186
Q

drug interctions tetracyclines

A
  • divalent or trivalent cations
187
Q

distribution of tetracyclines

A
  • prostataic
  • small amounts in CSF
188
Q

Which tetracyclines required renal dose adjustments

A

demecycline and tetracycline

189
Q

Which tetracyclines require hepatic adjustments

A

tigecycline eraavacycline

190
Q

Uses of doxycyline

A
  • CAP
  • chlamydial infectiosn and nongonococcal urethritis
191
Q

adverse effects tetracyclines

A
  • GI
  • photosensitivity
  • pregnancy contraindication
192
Q

TMP SMX MOA

A
  • block microbial folic acid synthesis
  • SMX block dihydropteroate synthetase
  • TMP blocks DHFR
193
Q

activity of TMP SMX

A
  • bactericidal time dependent
194
Q

MOR TMP SMX

A
  • point mutations in dihydropteroatre synthase or altered production of DHFR
195
Q

TMP SMX SOA

A
  • gram positive aerobes (MRSA, CA-MRSA)
  • gram negative aerobes (most including stenotrophomoas and HENPEACKSSS)
196
Q

What is TMP SMX the drug of choice for

A

pneumocystis carinii/jirovecci

197
Q

Does TMP SMX cover anaerobes

198
Q

distribution of TMP SMX

A

urine, prostatic tissue

199
Q

Dose adjustment of TMP SMX

200
Q

Clinical uses TMP SMX

A
  • UTI
  • pneumocystis carinii jirovecci pneumonia
  • CA MRSA
  • stenotrophomonas
201
Q

TMP SMX Adverse effects

A
  • leukopenia
  • rash
  • crystalluria
  • renal insufficiency
  • pregancy (kernicterus in newborns)
202
Q

Drug interactions TMP SMX

203
Q

Polymyxins MOA

A

displacement of calcium and magnesium causing leakage of cellular contents

204
Q

polymyxins activity

A

concentration-dependent bactericidal

205
Q

CMS vs Colisitin

A
  • less toxicic and is a prodrug
206
Q

polymyxin MOR

A
  • alteration of the outer cell membrane
  • decreased lipopolysaccharide content and calciium and magnesium
207
Q

polymyxins SOA

A

Gram negative AEROBES
- acintobacter
- pseudomonas

208
Q

Dose adjustments for polymyxins

A

CMS renal adjustment when CrCl is < 80 mL /min

209
Q

clinical uses of polymyxins

A

gram negative aerobic infections including pseudomonas

210
Q

adverse effects of polymyxins

A
  • nephrotoxicity
  • neurotoxicity
211
Q

clindamycin MOA

A

binds reversibly to 50S subunit

212
Q

activity clindamycin

A

primarily bacteriostatic time dependent

213
Q

Clindamycin MOR

A

alteration in ribosomal binding site

214
Q

clindamycin SOA

A

Gram positives aerobes (MSSA and CA-MRSA)
- gram negative above the diaphragm anaerobes (bacteroides)

215
Q

Does clindamycin penetrate the CSF

216
Q

clinical uses clindamycin

A
  • infections due to anaerobes outside the CNS
  • CA MRSA
217
Q

adverse efffects of clindamycin

A

C diff
hepatotoxicity

218
Q

metronidazole MOA

A

inhibit nucleic acid synthesis

219
Q

metronidazole activity

A

bactericidal in concentration dependent manner

220
Q

Metronidazole MOR

A
  • altered growth requirements (higher oxygen)
  • altered levels of ferredoxin gene, decreasing electron donating
221
Q

metronidazole SOA

A
  • gram negative anaerobes
  • b frag and bdot organisms
  • gram positive anerobes including cdiff
222
Q

Does metronidazole penetrate into the CSf

223
Q

Metronidazole uses

A
  • infections due to anaerobes (need additional coverage for aerobes)
  • c diff
  • trichomoas vaginalis
224
Q

Metronidazole adverse effects

A
  • metallic taste
  • CNS disorders (seizures/peripheral neuropathy)

PHRM 865 (13 decks)

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