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Pharm > Combined Test 3 > Flashcards

Combined Test 3 Flashcards

1
Q

*For what conditions is bactericidal antibiotic therapy required? (4 dz’s)

A
  • Meningitis - Endocarditis - Osteomyelitis - Febrile neutropenia
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2
Q

Bactericidal or bacteriostatic? Cell wall formation/synthesis inhibitors are in general _____________. Nucleic acid synthesis inhibitors are ___________. Protein synthesis inhibitors tend to be ____________. Metabolic inhibitors are usually ______________.

A

Cell wall formation/synthesis inhibitors are in general bacteriocidal. Nucleic acid synthesis inhibitors are bacteriocidal. (exception: aminoglycosides) Protein synthesis inhibitors tend to be bacteriostatic. Metabolic inhibitors are usually bacteriocidal.

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3
Q

What are the 3 key concepts to consider regarding infection when considering antibiotic tx?

A
  • Severity - Site - Organism
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4
Q

What are the 6 key concepts to consider regarding the host when considering antibiotic tx?

A
  • Allergies - Age - Pregnancy - Renal/hepatic function - Drug interactions (w/theirs) - Underlying disease
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5
Q

What are the 7 key concepts to consider regarding the drug when considering antibiotic tx?

A
  • Predicted activity/measured susceptibility - Clinical efficacy - “Drug of choice” - PK and tissue penetration - PD (need cidal?) - Side Effects - Cost
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6
Q

What are the 2 groups of natural PCNs?

A

PCN G and PCN VK (oral)

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7
Q

What are the 4 types of penicillinase-resistant penicillins?

A

Nafcillin, oxacillin, methacillin, dicloxacillin

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8
Q

What are the 2 aminopenecillins?

A

Ampicillin and amoxicillin

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9
Q

What is the name of the carboxypenicillin?

A

Ticarcillin (not avail.)

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10
Q

What is the name of the ureidopenicillin?

A

Piperacillin

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11
Q

Name 4 beta-lactamase inhibitor-combo treatments. (just the overall drug names)

A
  • Unasyn - Timentin - Zosyn - Augmentin
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12
Q

Are PCNs time- or conc-dependent killing?

A
  • Time-dependent
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13
Q

What group does PCNs have synergy w/?

A

Aminoglycosides (against Enterococcus spp., Staphylococcus spp., viridans strep, and gram-negative bacteria)

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14
Q

PCNs distribute throughout body tissues/fluids except for these 3 sites:

A

Eye, prostate, and uninflammed CSF.

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15
Q

*What 5 things are natural PCNs commonly used for treating, besides the organisms previously mentioned? (extra stuff that’s on slides but not blue)

A
  • Actinomyces - Bacillus anthracis (anthrax) - Endocarditis prophylaxis - Prevention of rheumatic fever
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16
Q

What type of infections (not organisms) are amino-PCNs used to treat?

A
  • Respiratory tract infections - Pharyngitis - Sinusitis - Otitis media - Bronchitis - UTIs
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17
Q

Although not clinically available, what types of conditions do ticarcillin and pipercillin typically treat?

A

Hospital-acquired infections

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18
Q

The beta-Lactamase Inhibitor Combination treatment Augmentin is typically used to treat what sx?

A

Sinusitis, otitis media, upper and lower respiratory tract infections, human or animal bite wounds (similar to amino-PCNs)

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19
Q

The beta-Lactamase Inhibitor Combination treatments Unasyn, Zosyn, Timentin are typically used to treat what major types of infections?

A
  • Polymicrobial infections - Empiric therapy for febrile neutropenia or hospital-acquired infections (Zosyn)
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20
Q

MoA of all beta-lactams? - Cidal or static?

A

Inhibit cell wall synthesis by binding and thus inhibiting PBPs. Inhibits final transpeptidation step of peptidoglycan synthesis. - Bactericidal

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21
Q

*Most beta-lactams are eliminated by the ___________. *What are the exceptions? (don’t forget cephalosporins)

A

Kidneys - Nafcillin, oxacillin, dicloxacillin (PRPs) - Ceftriaxone (cephalosporin) - Cefoperazone (cephalosporin)

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22
Q

What are the beta-lactam mechs of resistance? (Which is most important?)

A

Beta-lactamase enzymes (most important; cephalosporins are less susceptable), PBP alteration, decreased membrane penetration

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23
Q

2 eg’s of organisms that inhibit beta-lactams via beta-lactamase are:

A
  • PRSP - MRSA
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24
Q

What 2 drugs are contained in Unasyn?

A

Ampicillin-sulbactam

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25
Q

What 2 drugs are contained in Timentin?

A

Ticarcillin-clavulanate

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26
Q

What 2 drugs are contained in Zosyn?

A

Piperacillin-tazobactam

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27
Q

What 2 drugs are contained in Augmentin?

A

Amoxicillin-clavulanate

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28
Q

What is the route of administration of PCN G, aqueous form? Benzathine salt form? Procaine form?

A
  • Aqueous: IV - Benzathine: IM - Procaine: IM
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29
Q

What is the route of administration for PCN VK?

A

PO (acid stable)

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30
Q

Which of the 4 penicillinase-resistant penicillins can be given orally?

A

Dicloxacillin

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31
Q

Which of the amino-PCNs have better oral uptake?

A

Amoxicillin

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32
Q

Which of the 4 beta-lactamase inhibitor combo treatment drugs can be given orally?

A

Augmentin

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33
Q

How do drugs like sulbactam, clavulante, and tazobactam block bacteria from attacking PCNs, which are given together with these drugs?

A

Prevent beta-lactamase enzymes from working

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34
Q

With PCNs, do we want more time above MIC, or greater peak:MIC ratio?

A

More time above MIC (cuz time-dependent killing)

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35
Q

ALL penicillins have ________ elimination half-lives, and require (frequent/infrequent) dosing. - What are the 2 exceptions to this?

A

Short (

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36
Q

*Name the main target organisms of natural penicillins.

A
  • Penicillin-susceptible S. pneumoniae - infections due to other streptococci - Neisseria meningitidis - Syphilis - Clostridium perfringens + tetani
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37
Q

*Name the main target organism of penicillinase-resistant PCNs (PRPs).

A

Infections due to MSSA such as skin and soft tissue infections

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38
Q

*Name the main target organisms of aminopenicillins.

A
  • Enterococcal infections (often with an aminoglycoside) - Listeria monocytogenes
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39
Q

*Name the main target organisms of Carboxypenicillins and Ureidopenicillins.

A
  • Empiric therapy for HA-infections - Infections due to Pseudomonas aeruginosa (esp piperacillin)
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40
Q

Adverse effects of PCNs?

A
  • Hypersensitivity rxns (3-10%; cross-reactivity amongst all + some other beta-lactams) - Neurologic (seizures) (- Hematologic) (- GI) (- Interstitial nephritis)
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41
Q

What organisms do natural PCNs inhibit?

A

Gram +: PCN-susc. S. aureus (rare), *PCN-susc. S. pneumoniae, *group streptococci, viridans streptococci, enterococcus spp., bacillus spp. Gram -: *Neisseria spp., Pasteurella multocida. Anaerobes: above the diaphragm, *clostridium spp. Other: treponema pallidus (*syphilis; drug of choice)

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42
Q

What organisms do penicillinase-resistant penicillins inhibit?

A

Gram +: meth.-susc. S. aureus (*MSSA; target), group streptococci, viridans streptococci.

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43
Q

What organisms do aminopenicillins inhibit?

A

Gram +: pen. Susc. S. aureus (rare), pen. Susc. S. pneumoniae, group streptococci, viridans streptococci, *enterococcus spp., *listeria monocytogenes. *Gram -: Proteus mirabilis, some e coli, salmonella, shigella, beta-lactam h. influenzae.

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44
Q

What organisms do carboxypenicillins inhibit?

A

Gram +: “marginal” Gram -: Proteus mirabilis, some e coli, salmonella, shigella, beta-lactam h. influenzae, enterobacter spp., pseudomonas aeruginosa (target)

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45
Q

What organisms do ureidopenicillins inhibit? (Lots, maybe just name the 2 targets)

A

Gram +: Viridans strep, group strep, some enterococcus. Gram -: Proteus mirabilis, some e coli, salmonella, shigella, beta-lactam h. influenzae, enterobacter spp., *pseudomonas aeruginosa (target), serratia marcescens, some klebsiella spp. Anaerobes: faily good activity (target)

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46
Q

What organisms do beta-lactamase inhibitor-combos inhibit?

A

Gram +: S aureus (target; not MRSA). Gram -: H influenzae, e coli, proteus spp., klebsiella spp., Neisseria gonorrhea, moraella catarrhalis. Anaerobes (target): Bacterioids spp.

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47
Q

What is FQ’s MoA? - Bacteriocidal or bacteriostatic?

A

Inhibition of DNA gyrase and topoisomerase IV - Bacteriocidal

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48
Q

What is FQ’s primary mechanism of resistance? - What are some additional MoR’s it has?

A

Chromosomal mutations in DNA gyrase or topoisomerase IV - Also development of efflux pumps, plasmid-mediated resistance, altered cell wall permeability (porins)

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49
Q

Which of the FQ’s are active against gram-positive aerobes? (Which aren’t, then?)

A

Levofloxacin, moxifloxacin, gemifloxacin (Not ciprofloxacin!)

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50
Q

Describe the relative activity of FQs against gram-negative aerobes. What about for pseudomonas?

A

cipro = levo > moxi cipro > levo, NOT moxi or gemi

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51
Q

Which of the FQ’s are active against anaerobes?

A

Only moxifloxacin

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52
Q

Which of the FQ’s are active against atypical bacteria?

A

All FQs

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53
Q

Which FQ(s) are useful against CA-PNA (CAP)?

A

Levo, moxi, gemi

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54
Q

Which FQ(s) are useful against HA-PNA?

A

Cipro (+ something for gram-positive coverage), levo

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55
Q

Which FQ(s) are useful against sinusitis/bronchitis?

A

All

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56
Q

Which FQ(s) are useful against UTI/prostatitis?

A

Cipro, levo

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57
Q

Besides previously mentioned, what else are FQs useful for? (not sure how to ask this question)

A

Bone infections, STD’s, TB, intra-abdominal w/ added anaerobe coverage

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58
Q

What are the most common adverse affects of FQs? (2) What else can occur?

A

GI, CNS - Prolonged QTc interval - Tendonitis, tendon rupture - Hepatotoxicity, photosensitivity, hypersensitivity, rash, articular damage

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59
Q

What demo should not use FQs? (contraindicated)

A

Pregnant women and children

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60
Q

What drugs do FQs interact w/?

A
  • Divalent, trivalent cations: separate administration to avoid chelation and decreased absorption - Warfarin, cyclosporine, theophylline
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61
Q

Methicillin-susceptible Staphylococcus aureus, Streptococcus pneumoniae (including PRSP), Viridans streptococci, and Enterococcus spp. are eg’s of what class of bacteria?

A

Gram-positive aerobes

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62
Q

Enterobacteriaceae including Citrobacter spp. E. coli, Klebsiella spp, Enterobacter spp, Proteus spp, Salmonella, Shigella, Serratia marcescens, etc; H. influenzae, M. catarrhalis, Neisseria spp., and Pseudomonas aeruginosa are eg’s of what class of bacteria?

A

Gram-negative aerobes

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63
Q

Bacteroides spp such as b. fragilis are eg’s of what class of bacteria?

A

Anaerobes

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64
Q

Legionella pneumophila, Chlamydophila and Chlamydia spp., Mycoplasma spp. and Ureaplasma urealyticum are eg’s of what class of bacteria?

A

Atypical bacteria

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65
Q

All of the FQs are eliminated mostly through the __________ with the exception of __________, which is eliminated through the __________.

A
  • kidney - moxi - liver (therefore can’t treat UTI)
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66
Q

Metronidazole is mainly used against what class of microbe?

A

Anaerobes

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67
Q

What is the MoA of metronidazole? - What molecule is responsible for this and how? - Bacteriocidal or bacteriostatic?

A

Inhibits DNA synthesis - Ferredoxins (which nlly make ATP). Metronidazole binds them and creates an e- sink. Drives more drug into cell and reactive species are made. - Bacteriocidal

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68
Q

How common is the development of resistance w/metronidazole? What are 2 ways in which bugs acquire resistance to metronidazole?

A

*Uncommon - Altered growth requirements (e.g. higher local O2 conc.) - Altered ferredoxin levels (lower levels)

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69
Q

What 2 types of anaerobic bacteria is metronidazole most active against?

A
  • Bacteroides spp. (all) - Clostridium spp. (all)
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70
Q

Metronidazole: - IV/PO or both? - Does it penetrate the CSF? - How is it eliminated?

A
  • Both - Yes - Liver
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71
Q

What are the clinical uses of metronidazole? Metronidazole is the drug of choice for _____________.

A
  • Anaerobic Infections (including in the CNS): Intraabdominal, pelvic, (skin/soft tissue), diabetic foot and decubitus ulcer infections; brain abscess, trichomonas MILD to MODERATE c-dif dz
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72
Q

What are the most common side effects from metronidazole? What are the most serious side effects?

A
  • GI (stomatitis–metallic taste) - CNS (peripheral neuropathy) - Teratogenic (avoid during pregnancy)
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73
Q

What 2 important drugs does metronidazole interact with?

A
  • Warfarin (increased anticoagulant effect) - Alcohol (disulfiram rxn; don’t give to alcoholics)
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74
Q

FQs are the DOC for what atypical bacterium?

A

* Legionella

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75
Q

What is the target organism for cipro and levo when targeting gram-negative aerobes?

A

Pseudomonas aeruginosa (NOT moxi)

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76
Q

What are the target organisms for levo, moxi, and gemi when targeting gram-positive aerobes?

A
  • Methicillin-susceptible Staphylococcus aureus* - Streptococcus pneumoniae (including PRSP)*
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77
Q

Which FQ has good CSF penetration?

A

Moxifloxacin

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78
Q

Trichomonas vaginalis Entamoeba histolytica Giardia lamblia Gardnerella vaginalis are all examples of what class that metronidazole inhibits?

A

Anaerobic protozoa

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79
Q

Bacteroides spp. (ALL)* Fusobacterium Prevotella spp. Clostridium spp. (ALL)* Helicobacter pylori Are all examples of what class of organism that metronidazole inhibits?

A

Anaerobic bacteria

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80
Q

Name the 3 most important AGs. Which is a 4th that is less important?

A
  • Gentamycin (gent) - Tobramycin (tobr) - Amikacin (amik) Streptomycin
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81
Q

Which is the most important AG?

A

Gentamycin

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82
Q

What is the general class(es) of organism(s) that gentamycin targets? What are the 3 organisms in this class that it’s most effective against? (not sire if I need to be this specific)

A

Gram-negative *Can also target gram-pos if another drug allows it to get into the cell - E. coli, Klebsiella pneumoniae, Proteus

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83
Q

How does the activity of tobramycin differ from gentamycin?

A

Slightly weaker gram-neg activity but more effective against pseudomonas.

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84
Q

What type(s) of pathogen(s) is amikacin effective against?

A
  • Nosocomial gram-negatives (except not as good as tobr for pseudomonas) - Mycobacterial (M. tuberculosis and atypical) - Other: nocardia (rare)
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85
Q

What type(s) of pathogen(s) is streptomycin effective against?

A
  • Gram-pos: enterococcus (but gentamycin is preferable) - Mycobacterial (M. tuberculosis, but less effective against atypical vs. amikacin)
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86
Q

What type of drugs do AG’s have synergy w/?

A

Cell-wall inhibitors (likely due to enhanced AG uptake)

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87
Q

What is unique about the distribution of AGs?

A

1000-fold higher conc. in urine vs. plasma (good for treating UTIs)

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88
Q

Differentiate b/w “traditional” (MDD) and “extended interval” (ODA) dosing.

A
  • Traditional: multiple daily doses (q8-12 hrs) - Extended interval: once daily dosing (no less)
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89
Q

With conc-dependent killing, would you aim for higher or lower peak:MIC ratio?

A

Higher (make sure you understand why)

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90
Q

How is the post-antibiotic effect influenced by the peak:MIC ratio?

A

Bigger peak:MIC ratio = larger dose, and therefore larger PAE w/conc-dependent killing

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91
Q

Which is more likely to create resistance: infrequent large doses, or frequent smaller doses? (Why?) - Which leaves the bacterium more susceptible to killing?

A

Frequent smaller doses (bacteria more likely to survive) - 1 large dose more effective because bacteria more susceptible during drug-free time.

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92
Q

Which AGs are effective against gram-neg infections?

A
  • Gentamycin - Tobramycin - Amikacin
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93
Q

What type of dosing is preferred when using AGs to fight gram-neg infections?

A

Extended interval (once daily) dosing

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94
Q

Which AGs are effective against gram-pos infections?

A
  • Gentamycin - Strepamycin
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95
Q

What type of dosing is preferred when using AGs to fight gram-pos infections?

A

Traditional dosing * Counter to what has been said, but must be given in combo w/beta-lactam drug to get it into cell. Once in cell, there is synergy w/this other drug, and don’t need as high of a dose

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96
Q

Which AGs are effective against mycobacterial infections?

A
  • Amikacin - Streptomycin
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97
Q

What type of dosing is preferred when using AGs to fight mycobacterial infections?

A

Extended interval dosing (3 times weekly!) - Amikamycin preferable

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98
Q

Explain the reasons why extended-interval dosing is preferable to traditional dosing w/r/t AGs vs. gram-neg bacteria. (6)

A
  • Concentration-dependent bactericidal activity - Post-antibiotic effect (PAE) - Adaptive resistance - *Minimize toxicities - Cost savings - Efficacy
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99
Q

What are some factors that influence PAE? (4, not too important)

A
  • Organism - Drug concentration - Duration of drug exposure - Antimicrobial combinations
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100
Q

What are the 2 major toxicities related to AGs?

A
  • Nephrotoxicity - Ototoxicity
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101
Q

If gram-neg bacteria suspected, AGs can be used for the empiric treatment of __________, especially from a urinary source. What other conditions could they be used for?

A

Sepsis - Intraabdominal infections - Skin/soft tissue infections

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102
Q

If a pt has a h/o CF, which AG would you choose and why?

A

*Tobramycin (pt is more susceptible to pseudomonas)

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103
Q

If treating PNA with AGs, would you use a low, medium, or high dose?

A

High

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104
Q

Recall: when using gentamycin (or sometimes streptomycin) to treat gram positive infections, you would normally combine it with ___________, or sometimes even ___________ for severe infections (e.g. enterococcal or staphylococcal).

A
  • Beta-lactams (ampicillin, nafcillin) - Vancomycin (recall: lower, traditional dosing)
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105
Q

What part of the kidney is affected by AG nephrotoxicity?

A

Proximal tubule (AG uptake is saturable here)

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106
Q

How are AG’s administered? What are the exceptions?

A

They are all administered IV and IM (not PO)

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107
Q

What are AG’s mech of action? (Cidal or static?)

A

Irreversibly bind to 30S ribosomal subunit to inhibit ptn synth (bacteriocidal).

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108
Q

What are AG’s mech of resistance?

A

Synthesis of AG-modifying enzymes (often via plasmid), altered AG uptake (efflux pump of loss of porin channel), change in ribosomal binding site/target modification

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109
Q

What organ eliminates AGs?

A

Kidneys (dose must be adjusted in kidney failure)

110
Q

List the organisms that 1st gen cephalosporins are effective against. Which is target?

A

Gram-pos: - MSSA (*target) - PCN-susc. Strep pneumo - Group streptococci - Viridians streptococci Grem-neg: (PEK) = - Proteus mirabilis - E. coli - Klebsiella pneumoniae

111
Q

List the organisms that 2nd gen cephalosporins are effective against. *Which group is unique to this gen?

A

Gram-pos: (slightly less active than 1st gen) - MSSA (*target), PCN-susc. Strep pneumo, Group streptococci, Viridians streptococci. Gram-neg: (HENPEK) = - H. influenzae - Enterobacter spp. - Neisseria spp. - Proteus mirabilis - E. coli - Klebsiella pneumoniae (+ M. catarrhalis). Anaerobes: Bacteroides fragilis /group

112
Q

List the organisms that 3rd gen cephalosporins are effective against. *Which is target?

A

Gram-neg (HENPECKSSS P) = - H. influenzae - Enterobacter spp. - Neisseria gonorrhoeae - Proteus mirabalis - E. coli - Citrobacter spp. - Klebsiella pneumoniae - Serretia marcescens - Salmonella spp. - Shigella spp.; *Pseudomonas aeruginosa (target) (still have gram-pos activity but less active than earlier gens)

113
Q

Which 3rd gen. cephalosporin does NOT target pseudomonas, unlike the others? Which would you use instead?

A

Ceftriaxone - Ceftazidime

114
Q

How does the activity of 4th gen cephalosporins change compared to 3rd gen?

A

Gram-pos: similar to ceftriaxone. Gram-neg: Similar to ceftriaxone but also adds: - Pseudomonas aeruginosa - Beta-lactamse-producing enterobacter spp.

115
Q

List the categories/organisms that 5th gen cephalosporins are effective against. *Which is unique to this gen?

A

Resp pathogens - H. influenzae - strep. Pneumoniae - Moraxella - Staph aureus. Gram-pos + SSSI: - Strep pneumonia *MRSA*

116
Q

*What important organisms are cephalosporins NOT active against? (6)

A

SMACLE - Stenotrophomonas maltophilia - MRSA (*except for the 5th gen) - Atypical bacteria (eg Legionella; cuz no cell wall) - C-diff - Listeria - Enterococcus spp.

117
Q

All cephalosporins are eliminated via the ___________ except for ___________ and ___________ (how are each eliminated?)

A
  • Kidney - Ceftriaxone (bile) - Cefoperazone (liver)
118
Q

Which gens of cephalosporins are used for surgical prophylaxis?

A

1st and 2nd (2nd for more intense surgeries?)

119
Q

What are some of the uses of ceftriaxone? (4 orgs)

A
  • Uncomplicated gonorrhea (single IM dose) - CAP - PRSP - Viridans strep endocarditis
120
Q

What’s the most important organisms that 4th gen cephalosporins cover (that ceftriaxone doesn’t)?

A

Pseudomonas

121
Q

What are the major adverse effects of all gen cephalosporins? (2)

A
  1. Hypersensitivity 2. C-diff
122
Q
  • Are Carbapenems broad or narrow spectrum? - What major groups are they effective against? - What are their target organisms?
A
  • Most broad-spectrum available - Many gram-pos and gram-neg aerobes, as well as gram-pos/neg anaerobes. - Targets: MSSA, bacteroides.
123
Q

*What organisms are carbapenems NOT effective against? (7)

A

*NOT effective against: MRSA, PRSP, VRE, coag-neg staph, c-dif, atypical bacteria, S. maltophila

124
Q

-______________, a carbapenem, undergoes hydrolysis by a dihydropeptidase enzyme in the ________________ to a toxic metabolite. - Therefore, it’s comarketed with _________, a DHP inhibitor (to prevents this)

A
  • Imipenem - Renal brush border (hepatotoxic) - Cilastatin (not on test, but USMLE)
125
Q

What major drug category do cephalosporins fall under? Carbapenems?

A
  • Beta-lactams - Beta-lactams
126
Q

What are carbapenem’s mech of action? - Baciocidal or static? - Time or conc-dependent?

A

Inhibitors of cell wall synthesis by binding to and inhibiting PBPs; primary target is PBP-2 - Bacteriocidal - Time-dependent

127
Q

Name the major carbapenems. - Which 2 are the “best”?

A

DIME - Doripenem (best) - Imipenem (best) - Meropenem - Ertapenem

128
Q

What are the mechs of resistance for cephalosporins? (which is most important?)

A
  • Beta-lactamase enzymes (most important) - PBP alteration - Decreased membrane penetration
129
Q

Beta-lactams are all cross-allergenic except for which one?

A

Aztreonam

130
Q

Are cephalosporins bacteriocidal or bacteriostatic?

A

Bactericidal

131
Q

Which subset of the cephalosporins are the only ones that have activity against anaerobes? - Which generation is it in?

A

Cephamycins - 2nd gen

132
Q

*What gen. cephalosporin is used for the treatment of meningitis?

A

3rd gen

133
Q

When treating meningitis w/3rd gen cephalosporins, if pseudomonas is suspected or present, what specific drug would you use?

A

Ceftazidime

134
Q

What is the main thing that 5th gen cephalosporins are used for?

A

Drug-resistant organisms

135
Q

Why were cephalosporins developed?

A

Beta lactams that are less susceptable to beta-lactamase enzymes.

136
Q

Why were carbapenems developed?

A
  • Extended spectrum of activity - Further beta-lactamase stability
137
Q

What are the clinical uses of carbapenems?

A
  • Empiric therapy for HA-infections - Polymicrobial infections - Infections due to β-lactamase-producing organisms (SPICE, SPACE, others)
138
Q

*If pseudomonas is suspected, which carbapenem would you avoid?

A

*Avoid ertapenem if pseudomonas suspected

139
Q

What are the main adverse effects of carbapenems?

A
  • CNS (e.g. seizures) - GI - Hypersensitivity
140
Q

Do carbapenems have hypersensitivity/cross-reactivity w/PCNs like cephalosporins do?

A

Yes

141
Q

What category of drug is a monobactam? - How can it be administered?

A

Synthetic monocyclic beta-lactam - IV

142
Q

Monobactams are beta-lactams. What specific part of the cell wall do they target? - What is the main class of organisms they target?

A

PBP-3 - of gram-negative aerobes

143
Q

Recall: what class of organisms do monobactams inhibit? - What’s its main target?

A

Gram-neg aerobes * Pseduomonas

144
Q

Recall: what is the class of drugs that aztreonam is a member of? Since aztreonam is the only beta-lactam that does have cross-allergencitiy, what clinical implications does this have?

A
  • Monobactams - Can be used in PCN-allergic pts
145
Q

What are the major adverse effects of monobactams?

A

N/D

146
Q

What are the major adverse effects for 2nd gen cephalosporins, besides hypersensitivity and c-diff?

A
  • Hypoprothrombinemia - Ethanol intolerance due to disulfiram-like rxn
147
Q

Which gen’s of cephalosporins inhibit pseudomonas?

A
  • 3rd (except ceftriaxone) - 4th
148
Q

Which gen of cephalosporins are effective against anaerobes like bacteroides?

A

2nd gen only

149
Q

What are the 3 phenotypes of vancomycin resistance?

A

vanA, vanB, vanC

150
Q

What group of organisms is vancomycin capable of killing? (name the class and the 5 major targets)

A

Gram-pos ONLY - *MRSA, *MSSA, *coag-negative staph, *PRSP, *c-dif (clostridium spp.) - Also targets other strep pneumoniae, viridians strep, group strep, enterococcus, corynebacterium, bacillus, listeria, actinomyces, clostridium spp., peptococcus, peptostreptococcus.

151
Q

Since vanc is distributed widely in the tissues, you should use ________________ for dosing.

A

TBW (total body weight?)

152
Q

How long does it take for vanc to distribute into the tissues?

A

1 hour - Peak should be drawn 1 hr post-infusion

153
Q

For vancomycin, elimination T1/2 depends on _______ function.

A

renal function

154
Q

Can pts who are allergic to PCNs be given vancomycin?

A

Yes! (different structure)

155
Q

What’s an e.g. of a target of vancomycin that is a multi-drug-resistant bacterium?

A

PCN-resistant streptococcus pneumoniae (PRSP)

156
Q

Vanc treats ______-______ c-dif colitis.

A

moderate-severe

157
Q

Recall: what drug is used to treat mild-mod c-diff?

A

Metronidazole

158
Q

How does Red Man Syndrome occur? - Which drug is it a/w?

A

Infusion of vancomycin at too high a RATE - Also a/w other glycopeptides

159
Q

In what specific type of infection would you prefer the 2nd gen glycopeptide dalbavancin to vancomycin? - Which genes must be present?

A

VRE (must have vanB or vanC gene, not vanA.)

160
Q

What is the MoA of vancomycin?

A

Binds D-ala-D-ala to inhibit cell wall synthesis

161
Q

What is the MoA of linezolid? (is resistance common or uncommon?)

A

Binds 50S ribosomal binding site (resistance rare)

162
Q

What is the major class that linezolid can inhibit? List the main targets. - What is the other class?

A

Gram-pos: - *MSSA - *MRSA - *VRSA, - strep-pneumoniae (including *PRSP), - **enterococcus faecium and faecalis (including *VRE) Also: viridian streptococci, group streptococci, coag-neg staph, bacillis, listeria, clostridium spp (except c-diff), peptostreptococcus, c. acnes. Atypical bacteria: mycobacteria

163
Q

What is unique about the pharmacology of linezolid?

A

100% bioavailable

164
Q

What major category of pathogens is linezolid generally used for? What body area category is it NOT used for?

A

* Serious/complicated infections caused by resistant gram-positive bacteria: - Not used for UTIs

165
Q

What is linezolid contraindicated with and what condition does it cause?

A
  • SSRIs, MAOIs - Serotonin syndrome
166
Q

What are the major side effects a/w linezolid?

A

* Thrombocytopenia/anemia - SSRIs/MAOIs: serotonin syndrome. - Lactic acidosis - BM suppression - Neuropathy

167
Q

What category of drugs are linezolid and tedizolid?

A

Oxazolinidones

168
Q

What’s the advantage of tedizolid over linezolid? Why isn’t tedizolid prescribed more often?

A
  • Doesn’t cause serotonin syndrome - It’s even more expensive than linezolid
169
Q

What class of drugs does daptomycin belong in?

A

Lipopeptide

170
Q

What class of bacteria is daptomycin active against? Name the bacteria. (*or at least the targeted ones).

A

Gram-pos: *MRSA *MSSA *VRSA coag-neg staph strep pneumoniae (including *PRSP) viridians streptococi group streptococci *Enterococcus faecium and farcalis (including *VRE)

171
Q

*Daptomycin should NOT be used in the treatment of _____________.

A

*Pneumonia

172
Q

*What is the major adverse effect a/w daptomycin?

A

Myopathy and CPK elevation (must continually monitor them)

173
Q

Glycopeptides: mech of action (be specific)? - Time or conc-dependent? - Static or cidal?

A

Inhibits cell wall synth at a site different than beta-lactams, binding to D-alanyl-D-alanine portion of cell wall, preventing cross-linking. - Time-dependent - Bacteriocidal

174
Q

Vancomycin: mech of resistance? - In what 2 organisms, specifically, is this an issue?

A

Resistant in VRE/VRSA due to change in D-alanyl-D-alanine binding site of PG.

175
Q

Which glycopeptide is more potent than vanc?

A

Dalbavancin

176
Q

How can linezolid be administered?

A

PO or IV

177
Q

What class of drug is the quinupristin-dalfopristin combo? - MoA? - Static or cidal?

A

Synercid - Streptogramins - Protein synthesis inhibitor (50S ribosomal subunits; late stages) - Bacteriostatic, but syngeristic together to be bacteriocidal.

178
Q

What organism class are quinupristin-dalfopristin effective against? - What is the main target organism? What others are its targets?

A

Gram-positives, namely VRE. Gram-positive organisms (developed for VRE) - Enterococcus faecium (including VRE)* - MSSA, MRSA - Coagulase-negative staphylococci* - PRSP*, and many more. Also coverage vs. gram-neg aerobes and atypical bacteria (in vitro).

179
Q

How is quinupristin-dalfopristin cleared?

A

Hepatically/biliary

180
Q

What are the glycopeptides we need to know?

A

VDTO - Vancomycin - Dalbavancin - Telavancin - Oritavancin

181
Q

Name the 3 major side effects a/w vancomycin.

A
  • Red man syndrome - Nephrotoxicity - Ototoxicity
182
Q

Name the major side effects a/w dalbavancin.

A

GI s/s, skin rxns + flushing - Can also get red man syndrome

183
Q

Name drugs that are highly active/focused towards vs. resistant gram-pos organisms.

A

Vancomycin Dalbavancin Telavancin Oritavancin Linezolid Tedizolid Daptomycin Quinupristin-dalfopristin

184
Q

Quinupristin-dalfopristin: mech of resistance?

A
  • Alterations in ribosomal binding sites (erm) - Enzymatic inactivation - Active transport out of the cell
185
Q

Via what route is quinupristin-dalfopristin absorbed? - Does it penetrate CSF?

A

Parenterally - Minimally

186
Q

How is quinupristin-dalfopristin eliminated?

A

Both via hepatic and biliary

187
Q

What are the main clinical uses for Synercid (quinupristin-dalfopristin)? (2)

A
  • VRE bacteremia - Complicated skin and soft tissue infections due to MSSA or Streptococcus pyogenes
188
Q

Does quinupristin-dalfopristin affect CYP450?

A

P450 3A4 Inhibitor

189
Q

Adverse effects of quinupristin-dalfopristin?

A
  • Sever GI intolerance (N/V/D) - Venous irritation
190
Q

Although tetracyclines are cross-reactive, ____________ is resistant to this because it is in the tetracyclin derivative category known as ____________.

A

*Tigecycline - Glycylcylins

191
Q

What classes of microbials can tetracyclines be used against? (list some of the major targets) What 2 general conditions are they commonly used to treat?

A
  • Gram-pos aerobes (*MSSA) - Gram-neg aerobes - Anaerobes - bacteroides spp. - Misc. bacteria. - legionella, chlamydophila, chlamydia, mycoplasma, ureaplasma, rickettsia (sketchy) - Often used for STI infections and dz’s caused by tick bites!
192
Q

Does tigecyclin have a more or less broad spectrum of activity vs. tetracyclins? Which organism is tigecyline notably not active against?

A
  • Broader * Pseudomonas
193
Q

Although tetracyclines are cross-reactive, ____________ is resistant to this because it is in the tetracyclin derivative category known as ____________.

A

*Tigecycline - Glycylcylins

194
Q

What classes of microbials can tetracyclines be used against? (list some of the major targets) What 2 general conditions are they commonly used to treat?

A
  • Gram-pos aerobes (*MSSA) - Gram-neg aerobes - Anaerobes - bacteroides spp. - Misc. bacteria. - legionella, chlamydophila, chlamydia, mycoplasma, ureaplasma, rickettsia (sketchy) - Often used for STI infections and dz’s caused by tick bites!
195
Q

Although tetracyclines are cross-reactive, ____________ is resistant to this because it is in the tetracyclin derivative category known as ____________.

A

*Tigecycline - Glycylcylins

196
Q

What classes of microbials can tetracyclines be used against? (list some of the major targets) What 2 general conditions are they commonly used to treat?

A
  • Gram-pos aerobes (*MSSA) - Gram-neg aerobes - Anaerobes - bacteroides spp. - Misc. bacteria. - legionella, chlamydophila, chlamydia, mycoplasma, ureaplasma, rickettsia (sketchy) - Often used for STI infections and dz’s caused by tick bites!
197
Q

Does tigecyclin have a more or less broad spectrum of activity vs. tetracyclins? Which organism is tigecyline notably not active against?

A
  • Broader * Pseudomonas
198
Q

Besides being inactive vs. pseudomonas, what 2 other conditions does tigecycline NOT treat?

A

*UTIs and *bacteremia

199
Q

*What type of meds are tetracyclines and glycylcyclines contraindicated with?

A

Di and tri-valent cations (they should even avoid dairy due to Ca2+) - Must separate administration by a few hours

200
Q

What are the major serious side effects a/w tetracyclines/tigecycline?

A
  • Severe N/V - Photosensitivity (should avoid sun)
201
Q

What can occur if expired tetracyclines are prescribed?

A

Fanconi-like syndrome a/w renal failure

202
Q

What drug acts synergistically w/sulfas?

A

Trimethoprim (also inhibits folate/purine synth pw but at a different enzyme–dihydrofolate reductase)

203
Q

What is the precursor of purine synthesis? - How is it affected by purine synthesis pw inhibitors?

A

PABA - Builds up

204
Q

What drugs are in the combination Bactrim?

A

Trimethoprim-Sulfamethoxazole (TMP-SMX)

205
Q

Explain the target organisms (only) of the broad-spectrum antibiotic TMP-SMX (Bactrim).

A

gram-pos: *staph aureus (MRSA, CA-MRSA) Gram-neg: - Stenotrophomonas maltophilia. Other: - Pneumocystis carinii. Plus many more (broad spectrum)

206
Q

When giving Bactrim, what lab level should be monitored and why?

A

CrCl (kidney function; eliminated partially by kidney)

207
Q

*What are the (3) major clinical uses of TMP-SMX?

A
  1. Acute, chronic, or recurrent UTIs 2. Acute or chronic bacterial prostatitis 3. Skin infections due to CA-MRSA
208
Q

What are the major adverse effects a/w TMP-SMX/Bactrim?

A
  • Leukopenia - Thrombocytopenia - Rash/hypersensitvity - Renal impairment (crystaluria)
209
Q

Are dose adjustments required in renal failure when giving chloramphenicol?

A

No, metabolized by liver

210
Q

*What 2 major adverse effects are the reason that chloramphenicol isn’t available in the U.S.?

A
  • Gray Baby Syndrome (resp failure, death) - Aplastic anemia (no RBC production)
211
Q

What are the 2 urinary tract agents that we need to know?

A
  • Nitrofurantoin - Methenamine
212
Q

What is nitrofurantoin used for? What is methenamine used for?

A
  • Nitrofurantoin: used solely for UTIs - Methenamine: used solely as prophylaxis for UTIs if they’ve had recurrent UTIs
213
Q

Which of the enterobacteriacea are lactose fermenters and which are non-lactose fermenters? (All ferment glucose, oxidase negative, reduce nitrate, and use MacConkey)

A
  • Lactose fermenters: E. coli, klebsiella, Enterobacter, Citrobacter, Serratia - Non-lactose fermenters: Salmonella, Shigella, Proteus, Yersinia
214
Q

Distinguish the characteristics of the 5 types of E. coli.

A

o Enterotoxigenic E. coli (ETEC): Profuse watery diarrhea (Traveler’s diarrhea) o Enteropathogenic E. coli (EPEC): infants; diarrhea w/mucus but no gross blood o Enteroinvasive E. coli (EIEC): blood, mucus, and many leukocytes in stool o Enterohemorrhagic E. coli (EHEC): Bloody diarrhea w/o pyuria. May progress to HUS. ♣ Shiga-toxin producing E. coli (STEC) via E. coli O157:H7 o Enteroaggressive E. coli (EAggEC): Watery diarrhea w/blood and mucus

215
Q

MoA for tetracyclines/glycylcyclines? - Static or cidal?

A

Reversibly bind 30S ribosomal subunit to inhibit ptn synth. - Bacteriostatic.

216
Q

Mech of resistance for tetracyclines/glycylcyclines? (Which drug is more resistant to these mechs?)

A
  • Efflux pumps - Ribosomal protection proteins - Enzymatic inactivation (Tigecycline more resistant to these mechs)
217
Q

Where’s an important body areas that Tetracyclines/Glycylcyclines, distribute to? - What about Bactrim?

A

Prostate - Same for bactrim

218
Q

What 2 tetracyclines/glycylcyclines are excreted, unchanged, in the urine?

A

Demeclocycline/tetracycline

219
Q

Do tetra/glycylcyclines have to be modified w/renal disease?

A

No - Doxycycline, minocycline (metab) and tigecycline (biliary) - excreted mainly by non-renal routes

220
Q

What is tigecycline often used to treat?

A

Polymicrobial infections

221
Q

Which demo is tetra/tigecycline contraindicated in?

A

Pregnant (category D) - Affects their children (e.g. teet

222
Q

What’s the MoA of sulfonamides? - Static or cidal?

A

Inhibits dihydropterate reductase (folate/purine synthesis) - Bacteriostatic.

223
Q

What’s the MoA of trimethoprim? - Static or cidal, when combined w/sulfas?

A

Inhibits dihydrofolate reductase - Becomes cidal w/bacteriostatic sulfas

224
Q

What is another name for Trimethoprim-Sulfamethoxazole (TMP-SMX)? - How is the spectrum of activity/resistance affected when the drugs are combined?

A

Bactrim - Broader spectrum, decreased resistance

225
Q

What organism group does bactrim not have activity against?

A

Anaerobes

226
Q

What organisms are targeted by chloramphenicol?

A
  • Gram-pos - Gram-neg - Anaerobes (+ and -), etc. (3rd world use only)
227
Q

What is chloramphenicol’s MoA? (cidal or static)

A

Binds 50S ribosomal subunit (bacteriostatic)

228
Q

(MoA). In acidic pH, methenamine is converted to ammonia and ____________.

A

Formaldehyde

229
Q

What is the MoA for nitrofurantoin?

A

Not well understood

230
Q

Besides tetracyclines, what other drug class are di-tri-valent cations contraindicated in?

A

Fluoroquinolones (cipro, levo, moxi, gemi)

231
Q

Clindamycin: mech of resistance?

A
  • Altered target sites – encoded by the erm gene, which alters 50S ribosomal binding site; confers high level resistance to macrolides, clindamycin and Synercid (MLSb resistance) - Active efflux – mef gene encodes for an efflux pump that pumps antibiotic out of the cell - Drug inactivation
232
Q

Describe the spectrum of activity of clindamycin.

A

Gram positive aerobes: - *MSSA and some CA-MRSA - PSSP: PCN-susc. strep pneumo - Group + viridians strep Anaerobes: * Some bacteriodes spp. - Peptostreptococcus, actinomyces, prevotella spp, propionibacterium, fusobacterium, clostridium spp. (not C. difficile) Other bacteria: - Pneumocystis carinii, Toxoplasmosis gondii, Malaria

233
Q

How is clindamycin administrated? What is the % absorption?

A

IV, PO (90% absorption, can switch b/w IV and PO)

234
Q

Does clindamycin penetrate the CSF?

A

Not really

235
Q

Clindamycin primarily metabolized by the ___________. - Does it need adjustments during renal failure? - Is it removed during hemodialysis?

A
  • Liver - Doesn’t need adjustments during renal failure - No
236
Q

What are the clinical uses of clindamycin?

A
  • Anaerobic Infections OUTSIDE of the CNS: Pulmonary, intraabdominal, pelvic, diabetic foot and decubitus ulcer infections - Skin & Soft Tissue Infections: Good option for PCN-allergic patients and infections due to CA-MRSA - Alternative therapy: C. perfringens, PCP, Toxoplasmosis, malaria, bacterial vaginosis
237
Q

What are the 2 main side-effects for clindamycin?

A
  • GI - *C-diff colitis (one of the main inducers)
238
Q

What category of drug does clindamycin belong?

A

Lincosamide

239
Q

What are the 3 macrolides we should know?

A
  • Azithromycin - Clarithromycin - Erythromycin
240
Q

Which 2 macrolides are derivatives of the other?

A

Azithromycin and clarithromycin derivatives of erythromycin

241
Q

How do azithro and clarithromycin improve upon erythromycin?

A
  • Broader spectrum of activity - Improved PK properties: better bioavailability, better tissue penetration, prolonged half-lives - Improved tolerability
242
Q

Macrolides: MoA? - Cidal or static?

A
  • Reversibly binding to the 50S ribosomal subunit - Static (cidal at high conc)
243
Q

Which of the macrolides and time-dependent, and which are conc.-dependent?

A
  • Erythromycin and clarithromycin are time-dependent - Azithromycin is conc-dependent
244
Q

Macrolides: mech of resistance?

A
  • Active efflux pump (mef gene) - Altered target sites (erm gene)
245
Q

What is the spectrum of activity for macrolides? (groups are targets)

A
  • Gram-pos aerobes (*MSSA) - Gram-neg aerobes - Anaerobes (esp. upper airway) - Atypical bacteria (*Legionella, DOC) - Other bacteria
246
Q

What bacterium do macrolides importantly NOT have activity against?

A

Enterobacteriacea (gram-neg aerobe class)

247
Q

What are the relative levels of activity for the 3 macrolides against gram-positive aerobes?

A

CEA Clarithro > Erythro > Azithro (ACE for gram-neg)

248
Q

What are the relative levels of activity for the 3 macrolides against gram-negative aerobes?

A

ACE Azithro > Clarithro > Erythro (CEA for gram-pos)

249
Q

Discuss the bioavailabilities of each of the of the 3 macrolides. - Which are acid stable?

A
  • Erythromycin: variable absorption (15 to 45%) - Clarithromycin: well-absorbed (55%) - Azithromycin: 37% bioavail. regardless of food Acid stable: Clarithromycin and azithromycin
250
Q

Do macrolides penetrate the CSF?

A

Not really

251
Q

Describe the elimination routes of each of the 3 macrolides. * Which are metabolized by CYP450 enzymes?

A
  • Erythromycin: excreted in bile, metabolized by *CYP450 - Clarithromycin: also metabolized (*CYP450) and partially eliminated by the kidney - Azithromycin: liver, NO CYP450
252
Q

Name the clinical uses of macrolides.

A

Respiratory Tract Infections - Pharyngitis/ Tonsillitis: PCN-allergic pts - Sinusitis, COPD exacerbation, OM - CA-PNA: monotherapy in outpatients; with ceftriaxone for inpatients Uncomplicated Skin Infections STDs MAC Alternative for PCN-Allergic pts: - Group A Strep upper respiratory infections - Prophylaxis of bacterial endocarditis - Syphilis and gonorrhea - RF prophylaxis

253
Q

Which macrolide is best when H. influenzae is suspected?

A

Azithromycin

254
Q

Which macrolide is best for STDs?

A

Azithromycin

255
Q

How are macrolides used to treat MAC (mycobacterium avium complex)? I hope to god this doesn’t come up

A
  • Azithromycin for prophylaxis - Clarithromycin/ Azithromycin for tx
256
Q

What are the adverse effects of macrolides? (there is 1 common group and the others are rare)

A
  • GI (only ones that are common) - Cholestatic hepatitis (rare) - Thrombophlebitis - Prolonged QTc - Ototoxicity (tinnitus/deafness)
257
Q

*Erythromycin and clarithromycin– are inhibitors of cytochrome p450 system in the liver and may increase concentrations of: (just read)

A

Theophylline Digoxin, Disopyramide Carbamazepine Valproic acid Cyclosporine Terfenadine, Astemizole Phenytoin Cisapride Warfarin Ergot alkaloids

258
Q

Name all of the cell wall inhibitor drug classes we’ve learned andtheir specific protein targets.

A

PCN (PBP), cephalosporins (PBP), carbapenems (PBP-2), monobactams (PBP-3), glycopeptides (D-ala-D-ala)

259
Q

Name all of the 30S ribosome inhibitor drug classes we’ve learned.

A

AG’s, tetracyclins

260
Q

Name all of the 50S ribosome inhibitor drug classes that we’ve learned.

A

Oxazolidinones, quinupristin-dalfopristin, chloramphenicol, clindamycin, macrolides

261
Q

Name all of the folate pw inhibitor drug classes that we’ve learned.

A

Sulfas, trimethoprim

262
Q

Name all of the DNA gyrase/topoisomerase inhibitor drug classes that we’ve learned.

A

FQs

263
Q

Name all of the DNA synthesis inhibitor drug classes that we’ve learned.

A

Metronidazole (via ferrodoxins)

264
Q

Causes of meningitis in newborns?

6 months - 6 years?

Adolescents/young adults?

Older adults?

A

Newborns: Group B Streptococcus, Escherichia coli, Listeria monocytogenes, Elizibethkingia meningoseptica, Citrobacter

  • 6 months - 6 years: Streptococcus pneumoniae, Neisseria meningitidis, Haemophilus influenzae*
  • Adolescents/young adults: Neisseria meningitidis, Streptococcus pneumoniae*
  • Older adults: Listeria monocytogenes, gram-neg rods (?), *Streptococcus pneumoniae*, Neisseria meningitidis, Haemophilus influenzae* type b (Hib), Group B Streptococcus
  • ***Strep pneumo is highest overall (doesn’t occur in neonates; kids are the reservoir)*
265
Q

Define each bioterrorism category, and name the 3 diseases we need to know a/w bioterrorism categories A and B.

A
  • Category A: easy dissemination, high mortality, public panic, special response
    • Eg’s = Anthrax (bacillus anthraces), Plague (Yersinia pestis), Tularemia (Francisella tularemia)
  • Category B: Mod easy to disseminate, mod morbidity, low mortality, ^ CDC dx and surveillance
    • Eg’s = Brucellosis (Brucella spp.), Food safety threats (salmonella spp., E. coli 0157:H7, Shigella), Melioidosis (Burholderia pseudomallei)
  • Category C: emerging pathogens, could be modified for mass dissemination and fatalities; available
266
Q

What are the 5 organisms a/w neonatal meningitis?

  • Which was formerly a cause but eliminated via vaccine?
  • Which of the 5 is less common because we test mothers?
  • Overall most common cause amongst all age groups?
A

E coli, GBS, citrobacter, listeria, and elizibethkingia

  • Haemofluas influenzae
  • GBS (vaginal swag)
  • Strep pneumo
267
Q
A
268
Q

What specific organism do you not use ABX to treat?

A

STEC (specifically)

269
Q
A
270
Q

Do beta-lactams (PCNs, cephalosporins, carbapenems, monomactams) generally display time or conc-dependent killing?

A

*Time-dependent

271
Q

Name the abx eliminated by the kidney. (Good review) Liver?

A

Kidney: beta-lactams, vancomycin, the aminoglycosides, some FQs, Bactrim, daptomycin, tetracycline (Big, tearful dalmations teased Amy’s vag, some F’d).

Liver: Macrolides, Synercid, linezolid, clindamycin, metronidazole, some FQs, Bactrim, doxycycline, tigecycline.

272
Q

What is the DOC for Stenotrophomonoas maltophilia?

A

Bactrim

Pharm (32 decks)

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