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Pharmacology > Antibiotics - notes > Flashcards

Antibiotics - notes Flashcards

1
Q

What are the different antibiotic classes that are cell wall inhibitors?

A
  • Beta-lactams
  • lipoglycoproteins
  • vancomycin
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2
Q

What are the different drugs included in beta-lactams?

A
  • penicillin
  • cephalosporins
  • monobactams
  • carbapenems
  • beta-lactamase inhibitor compounds
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3
Q
  • What are the drugs in the natural penicillin group?
  • What are their routes of administration?
  • What is their spectrum/coverage?
  • do they cover gram + or gram -?
A

penicillin G
- IV/IM
- narrow spectrum
- gram +
penicillin V
- oral (more stable)
- narrow spectrum
- gram +

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4
Q
  • What is the drug of choice for syphilis?
  • What is the drug of choice for GABHS rheumatic fever?
A
  • penicillin G
  • penicillin V
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5
Q

Are natural penicillins sensitive to beta-lactamase?

A

yes

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6
Q

What are some general uses of natural penicillins?

A
  • staph pharyngitis
  • soft tissue infections caused by strep A
  • some mouth/GI anaerobes (peptococcus/peptostreptococcus)
  • meningitis due to N. meningitides, S. pneumo, Listeria
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7
Q

What are the drugs in the antistaphylococcal penicillins?

A
  • dicloxacillin
  • methicillin
  • oxacillin
  • nafcillin
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8
Q
  • What is the spectrum of dicloxacillin?
  • Does it cover gram +/gram -?
  • What is its resistance to beta-lactamase?
  • Is there aerobic coverage?
  • What do you use dicloxacillin to treat?
A
  • narrow spectrum
  • gram +
  • beta-lactamase resistant
  • no aerobic coverage
  • MSSA
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9
Q
  • What antistaphylococcal penicillin won’t be used to treatment, only testing purposes?
  • What are the side effects of nafcillin?
A
  • methicillin
  • nephritis, neutropenia
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10
Q

What drugs are included in the aminopenicillins?

A
  • amoxicillin
  • ampicillin
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11
Q
  • What is the spectrum of aminopenicillins?
  • Do they cover gram+ or gram -?
  • What is their resistance to beta-lactamase?
  • What are they used to treat?
A
  • broader spectrum
  • good gram +, some gram -
  • beta-lactamase sensitive
  • H. flu, E. coli
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12
Q

What is the drug of choice for Listeria monocytogenes (meningitis)? How is this drug given for this treatment?

A

ampicillin - IV

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13
Q

What can you use amoxicillin to treat?

A
  • empirical treatment of sinusitis, otitis media (strep)
  • premed for endocarditis prophylaxis during dental/invasive procedures
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14
Q
  • What can you add to aminopenicillins to allow for treatment of MSSA?
  • What are inhibitor combinations for amoxicillin and ampicillin?
A
  • beta-lactamase inhibitors
    combinations:
  • ampicillin/sulbactam
  • amoxicillin/clavulanic acid
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15
Q

What are the drugs in the antipseudomonal penicillins?

A
  • piperacillin
  • carbenicillin
  • ticarcillin
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16
Q
  • What is the spectrum of piperacillin?
  • What does this drug cover, gram +/-?
  • What is its resistance to beta-lactamase?
  • What is its route of administration?
  • What is this drug used to treat?
A
  • broad spectrum
  • good gram +, improved gram -
  • beta-lactamase sensitive
  • IV only
  • Pseudomonas aeruginosa, polymicrobial, and nosocomial infections
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17
Q

What is piperacillin used to treat?

A
  • pseudomonas aeruginosa
  • polymicrobial infections
  • nosocomial infections
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18
Q
  • What are antipseudomonal penicillins effective in treating with the addition of beta-lactamase inhibitors?
  • Why would we not use this?
  • Which antipseudomonal penicillin is the most potent?
  • Antipseudomonal penicillins provide less coverage to what than ampicillin?
A
  • MSSA
  • there are other drugs that can treat MSSA; we don’t want to build resistance
  • piperacillin
  • less staph and strep coverage
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19
Q

What are the different types of side effects/reactions to penicillins?

A
  • type I: immediate response (anaphylactic shock)
  • type II: penicillin-associated hemolytic anemia (autoimmune)
  • type III: delayed response (skin rash, glomerular nephritis, polyarthritis, pericarditis/pleuritic, lymphadenopathy, angioedema)
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20
Q
  • What percentage of patients allergic to penicillins will be allergic to cephalosporins?
  • What is it okay to give cephalosporins in pts allergic to PCN?
A
  • 10%
  • okay to give to pts with type II or III reactions
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21
Q

What are other side effects of penicillins?

A
  • ampicillin-associated maculopapular rash
  • diarrhea (poor absorption)
  • nephritis
  • neurotoxicity w/ high doses given intrathecally; seizures
  • hematologic toxicity (piperacillin)
  • cation toxicity (hypokalemia/hyponatremia)
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22
Q

What side effect does piperacillin cause?

A

hematologic toxicity

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23
Q

What is the MOA of penicillins?

A
  • bactericidal
  • contain beta-lactam ring that interacts with PBP
  • inhibits transpeptidase (prevents cross-linking of peptidoglycan=weak cell wall)
  • binds autolysin inhibitors = increases autolysin activity = breakdown of cell wall
  • requires actively proliferating bacteria
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24
Q

What drugs treat MRSA?

A
  • sulfamethoxazole/TMP
  • clindamycin
  • fluoroquinolones
  • vancomycin
  • daptomycin
  • linezolid
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25
Q

What drugs are in the first generation of cephalosporins? What are their routes of administration?

A
  • cephalexin-po
  • cefadroxil-po
  • cefazolin-IV
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26
Q

What is the coverage of cephalexin?

A
  • good gram + (MSSA, staph, strep)
  • limited gram - (PEcK)
    **P. mirabilis, E. coli, K. pneumo
  • not good anaerobic coverage (no B. fragilis)
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27
Q

What is the resistance to beta-lactamase of cephalexin?

A

not sensitive to beta-lactamase

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28
Q

What are the general uses of first generation cephalosporins?

A
  • skin/soft tissue infections (not bites)
  • URI
  • cefazolin (surgical prophylaxis for orthoped surgeries d/t good bone penetration)
  • oral routes = not for serious infections
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29
Q

If a patient has type I reactions to PCN and is in need for treatment for MSSA, what antibiotic can you give them?

A

cephalexin

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30
Q
  • How is cephalexin excreted?
  • What is the cross-reactivity it has to PCN allergy?
A
  • renally eliminated
  • 10% cross-reactivity
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31
Q

What are the drugs in the second generation cephalosporins? What are their routes of administration?

A
  • cefuroxime-po/IV
  • cefprozil-po
  • cefaclor-po
  • cefoxitin-IV
  • cefotetan-IV
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32
Q

What is the coverage of second generation cephalosporins?

A
  • same as 1st generation coverage
  • more gram - (HENPEcK)
    ** H. flu
    ** Enterobacter
    ** Neisseria
    ** P. mirabilis
    ** E. coli
    ** K. pneumo
  • anaerobic coverage of B. fragilis w/ cefoxitin, cefotetan
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33
Q

What are some general uses of second generation cephalosporins?

A
  • CAP
  • otitis media
  • respiratory infections
  • sinusitis
  • skin/soft tissue infections
  • MSSA
  • cefuroxime not good with gut anaerobes
  • cefoxitin, cefotetan good gut/pelvic coverage
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34
Q

What are some of the drugs included in the third generation cephalosporins? What are their routes of administration?

A
  • cefdinir-po
  • ceftriaxone-IV/IM
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35
Q

What is the coverage of third generation cephalosporins?

A
  • vary in gram +
  • great gram -
    **Serratia marcescens, no enterobacter
    **ceftazidime covers. P. aeruginosa
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36
Q

What are the characteristics of ceftriaxone?

A
  • third generation cephalosporin
  • longest half-life of all cephalosporins
  • excreted in bile (good for pts w/renal failure)
  • good bone pentration
  • commonly used in gonorrhea treatment
  • effective in HACEK endocarditis
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37
Q

Which cephalosporin is commonly used in gonorrhea treatment?

A

ceftriaxone

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38
Q

What are the general uses of third generation cephalosporins?

A
  • bacterial meningitis
  • HAP
  • Lyme disease
  • ceftriaxone/cefotaxime: meningitis from pneumococci, H. flu, meningococci; no L. monocytogenes; empiric tx in serious infections, sepsis
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39
Q

Third generation cephalosporins have what type of resistance to beta-lactamase?

A

they are sensitive to beta-lactamases

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40
Q
  • What type of infections are you going to use third generation cephalosporins?
  • What type of spectrum does cefdinir have?
  • What can you use cefdinir to treat?
  • What can IV preps of third generation cephalosporins cross?
A
  • serious infections
  • broader spectrum
  • otitis media, CAP, sinusitis
  • BBB
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41
Q

What drug is a fourth generation cephalosporin? What is its route of administration?

A
  • cefepime-IV
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42
Q

What is the coverage of cefepime?

A
  • good gram + (MSSA)
  • good gram - (enterobacter, p. aeruginosa)
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43
Q

What can you use cefepime to treat?

A
  • p. aeruginosa infections
  • only ceph for enterobacter and serratia
  • meningitis
  • CAP
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44
Q

What is the sensitivity of cefepime to beta-lactamase?

A

used to be resistance but is now becoming more sensitive

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45
Q

What drug name is the fifth generation cephalosporin? What is its route of administration?

A
  • ceftarolene-IV
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46
Q

What is the coverage of ceftarolene?

A
  • enhanced gram + (MSSA, S. pneumo, E. faecilis)
  • gram -
  • no pseudomonas
  • poor anaerobic coverage
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47
Q

What can you use ceftarolene to treat?

A
  • MSSA
  • skin/soft tissue infections
  • CAP
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48
Q

What are the side effects of cephalosporins?

A
  • hypersensitivity
  • 10% cross-reactivity with PCN (occurs in 1st gen more often) = don’t use w/ pts who have had anaphylactic rxns to PCN
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49
Q

What is the MOA of cephalosporins?

A
  • binds to PBP and autolysin inhibitors
  • interrupts cell wall synthesis and activate autolysins
  • bactericidal
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50
Q
  • Where are cephalosporins distributed?
  • How are they excreted?
A
  • body fluids, CSF, bone
  • renally excreted except for ceftriaxone which is excreted in bile
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51
Q
  • What are the cephalosporin + inhibitor combinations?
  • What do they cover?
  • What are they FDA approved to treat?
A

inhibitor combo
- ceftolozone/tazobactam
- ceftazidime/avibactam
coverage
- excellent gram -
- P. aeruginosa
FDA approval
- complicated intra-abdominal infections along with anaerobic infections
- complicated UTI
- HAP and VAP

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52
Q
  • What drug is a monobactam?
  • What is its route of administration?
  • What is its coverage?
A
  • aztreonam
  • IV/IM
  • limited gram - (covers P. aeruginosa)
  • no gram + or anaerobic infections
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53
Q

What are the side effects of aztreonam?

A
  • no cross rxn with PCN
  • same allergies as PCN
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54
Q

What can you use aztreonam to treat?

A

pseudomonas treatment especially in cases where pt is allergic to PCN (type I rxn)

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55
Q

What are the drugs included in carbapenems? What are their routes of administration?

A
  • imipenem/cilastin-IV/IM
  • doripenem
  • ertopenem
  • meropenem
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56
Q

What is the coverage of carbapenems?

A
  • gram +
  • gram - (P. aeruginosa)
  • anaerobes
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57
Q

What can you use carbapenems to treat?

A
  • pseudomonas infections when organism is resistant to other drugs
  • mixed infections
  • very effective in enterobacter infections
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58
Q

What can you use to treat enterobacter infections due to them being very effective in treating these?

A

carbapenems (imipenem/cilastin)

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59
Q

What are the adverse reactions of carbapenems?

A
  • N/V/D
  • rash
  • 1% cross reactivity with PCN
  • imipenem: seizures, mental status changes
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60
Q

What are the adverse reactions of imipenem/cilastin?

A
  • seizures
  • mental status changes
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61
Q
  • How are carbapenems excreted?
  • Why do you need to give cilastin with imipenem?
  • When would you use carbapenems?
A
  • renally excreted
  • imipenem is inactivated in renal tubules; cilastin inhibits dehydropeptidase which stops imipenem from being broken down
  • would use them if pts culture came back pseudomonas resistant to other drugs (last resort due to severe side effects)
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62
Q

What drug is a glycopeptide antibiotic?

A

vancomycin

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63
Q

What is the MOA of vancomycin?

A
  • inhibits glycosylation of NAM-NAG units
  • doesn’t rely on transpeptidase
  • bactericidal
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64
Q

What is the coverage of vancomycin?

A

best for gram + (MRSA, MRSE, enterococci, clostridium)

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65
Q

What are the clinical uses of vancomycin?

A
  • MRSA sepsis, endocarditis
  • vanco + gentamicin = enterococcal endocarditis where pt is allergic to PCN
  • in combo with cephs = meningitis
  • C. diff via oral route
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66
Q

What type of vancomycin would you use to treat C. diff?

A

oral vancomycin

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67
Q

What are the adverse effects of vancomycin?

A
  • red man syndrome (given too rapidly)
  • phlebitis
  • ototoxicity/nephrotoxicity if given with other toxic drugs like aminoglycosides
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68
Q

What is the distribution of vancomycin?

A
  • CSF and adipose tissue
  • dose adjust in renal impairment:
    **normal half-life: 6-10 hours
    **renal disease half-life: 200 hours
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69
Q
  • What should you think of treating when using vancomycin?
  • What is vancomycin often given with?
  • What is the toxicity of this drug?
A
  • MRSA
  • gentamicin
  • very toxic
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70
Q

What drugs are protein synthesis inhibitors?

A
  • aminoglycosides
  • tetracyclines
  • macrolides
  • clindamycin
  • chloramphenicol
  • linezolid
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71
Q

What drug in included in aminoglycosides we need to know?

A

gentamicin

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72
Q

What is the coverage of aminoglycosides?

A
  • used w/ beta-lactams in serious gram - (vanco), gram + (endocarditis), and TB
  • no anaerobic coverage
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73
Q

What is the MOA of aminoglycosides?

A
  • passes through porin channels
  • uses oxygen dependent active transport
  • enhanced by other cell wall inhibitors
  • binds 30S subunit of ribosome irreversibly
  • bactericidal
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74
Q

What are the indications of aminoglycosides?

A
  • aerobic gram + (steph/strep with beta-lactams)
  • aerobic gram - (klebsiella, E. coli, proteus with beta-lactams; pseudomonas with antipseudomonals; brucella, taluremia, plague with tetracyclines)
  • severe gram - infections in combo
  • group B strep in neonates
  • intrathecal for gram - meningitis
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75
Q

What is treated when you combine aminoglycosides with tetracyclines?

A
  • brucella
  • taluremia
  • plague
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76
Q

What is the distribution of gentamicin?

A
  • poor oral absorption
  • not metabolized
  • distributes poorly to CSF/lungs (low Vd)
  • pregnancy category C/D = don’t use in lactation
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77
Q

What are the adverse affects of gentamicin?

A
  • nephrotoxicity
  • ototoxicity; can cause permanent deafness
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78
Q
  • What is the route of administration of aminoglycosides?
  • Will you use them by themselves in systemic infections?
  • What is an example of this?
A
  • IV, IM, intrathecally, intraventricular, topical
  • no
  • using vanco for gram +, gentamicin for gram -, so they can be used together in serious infections
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79
Q

What drugs are included in the tetracyclines?

A
  • tetracycline
  • doxycycline
  • minocycline
  • demecycline
80
Q

What is the MOA of tetracyclines?

A
  • bacteriostatic
  • enter bacteria through passive diffusion and active transport
  • binds reversibly to 30S subunit of bacterial ribosome; inhibits protein synthesis
81
Q

What is the coverage of tetracyclines?

A
  • broad spectrum
  • gram + and gram -
82
Q

What would you use tetracyclines for?

A
  • acne
  • peptic ulcers
  • infections from animals (Lyme disease, Rocky mountain spotted fever)
83
Q

What are the resistance mechanisms of tetracyclines?

A
  • efflux pump (doxy and mino poor substrates for pump)
  • production of proteins that prevent tetracyclines from binding to ribosomes
  • enzymatic destruction
84
Q

What impairs the absorption of tetracyclines?

A

food up to 50%
- food has less effect on doxy, mino
- binds to divalent cations (Ca, Mg, aluminum)

85
Q

What is the distribution of tetracyclines?

A
  • poor CSF penetration
  • crosses placental barrier and is excreted in breast milk (not recommended in pregnancy)
  • not metabolized
86
Q

How are tetracyclines excreted?

A

in bile and urine (enterohepatic reabsorptions = don’t have to dose as much because it is reabsorbed into the system)

87
Q

Which tetracycline is non-renal?

A

doxycycline

88
Q

What pregnancy category are tetracyclines?

A

category D

89
Q

What are the adverse affects of tetracyclines?

A
  • damage to growing bones/teeth = discoloration
  • sun sensitivity
  • one of the only drugs that is dangerous when expired = renal injury
90
Q
  • What should you not take with tetracyclines?
  • Because they’re excreted in bile, who can you use these drugs with?
A
  • Ca, Mg, Aluminum, cottage cheese, yogurt
  • pts with renal disease
91
Q

What drugs are included in macrolides?

A
  • erythromycin
  • azithromycin
  • clarithromycin
92
Q

What is the MOA of macrolides?

A
  • enters cell through passive/active diffusion
  • binds irreversibly to 50S subunit of ribosome
  • bacteriostatic
93
Q

What is the coverage of macrolides?

A
  • good gram +
  • descent gram -
  • gained atypical coverage (Legionella, Mycoplasma, Mycobacterium, Chlamydia)
94
Q

Because atypical bugs don’t have a peptidoglycan layer, what antibiotics can’t you use?

A

beta-lactams

95
Q

What is the drug of choice for chlamydia?

A

azithromycin

96
Q

What are uses of macrolides?

A
  • upper and lower respiratory infections including pneumonias
  • pertussis
  • peptic ulcer disease
  • gut infections
97
Q

What are resistance mechanisms of macrolides?

A

plasma encoded
- decreased permeability of cell membrane/efflux pump
- enterobacteriaceae esterase production = macrolide hydrolysis
- change in ribosomal binding site
cross-resistance among macrolides
- not first-line in pharyngitis, soft tissue infections, non-typical pneumo

98
Q
  • Which macrolide is poorly absorbed?
  • Which macrolide is best on an empty stomach?
  • Which macrolide diffuses into prostatic fluid?
  • Where do macrolides concentrate?
  • Tissue penetration is good for all macrolides except which one?
A
  • erythromycin
  • azithromycin
  • erythromycin
  • liver
  • erythromycin
99
Q
  • Which macrolide has the largest Vd?
  • Which macrolides are cytochrome inhibitors?
  • Which macrolide does not affect cytochromes?
  • How are macrolides excreted?
A
  • azithromycin
  • erythromycin, clarithromycin
  • azithromycin
  • in liver and renally
100
Q

What is the drug of choice for diptheria?

A

erythromycin

101
Q

What can be combined with neomycin for gut sterilization?

A

erythromycin

102
Q

What can erythromycin be used to treat but other drugs are better tolerated?

103
Q

Because erythromycin has similar coverage, what can this be an alternative for?

104
Q

What can you use azithromycin to treat?

A
  • prophylaxis of MAC
  • better H. flu
  • fantastic chlamydia treatment
  • CAP
105
Q

What are the adverse effects of macrolides?

A
  • N/V/D (most common)
  • QT prolongation and arrhythmias so don’t use w/ pts who have pre-existing arrhythmias
106
Q

What are adverse effects of erythromycin?

A
  • cholestatic hepatitis (hypersensitivity)
  • stimulate gut motility (hard on stomach)
  • inhibits cytochromes (drug interactions)
107
Q

What are adverse effects of azithromycin?

A

no concern of cytochrome issues seen with clarithromycin and erythromycin

108
Q
  • What should you always use for gut sterilization/gut surgery?
  • If CAP is suspected to be caused by an atypical bug, what should you use?
  • People with motility issues (such as from spinal cord injury), what might be good to use to help with gut motility?
A
  • erythromycin + neomycin
  • azithromycin
  • erythromycin
109
Q

What is the MOA of clindamycin?

A
  • same as erythomycin
  • penetrates tissues/abscesses well (no BBB penetration)
  • may be static or cidal
110
Q

What is most likely to cause a C. diff infection due it sitting in the gut and killing everything off?

A

clindamycin

111
Q

What is the coverage of clindamycin?

A
  • gram +
  • anaerobes
112
Q

What main things can you used clindamycin to treat?

A
  • skin/soft tissue infections
  • elimination of carrier state in strep
  • premed for endocarditis prophylaxis if can’t use PCN
  • topically for acne/vaginal infections
113
Q

What other things can you use clindamycin to treat?

A
  • intra-abdominal infections
  • pelvic infections
  • osteomyelitis
  • diabetic foot ulcers
  • aspiration pneumonia
  • dental infections
114
Q

What is the MOA of choramphenicol?

A
  • binds 50S ribosomal subunit reversibly
  • inhibits peptidyl transferase, preventing protein chain elongation
  • mostly static
115
Q

What is the coverage of chloramphenicol?

A
  • broad spectrum:
  • can be given IV or po
116
Q

What will you use chloramphenicol to treat?

A
  • primarily in rickettsial infections or bacterial meningitis where there’s no other option
  • meningitis
  • plague
  • cholera
  • typhoid fever
117
Q

What are the primary illnesses treated with chloramphenicol?

A
  • meningitis
  • plague
  • typhoid fever
  • cholera
118
Q

What are the adverse side effects of chloramphenicol?

A
  • highly toxic (limited to life-threatening illnesses)
  • fatal blood dyscrasias (aplastic anemia, thrombocytopenia)
  • liver toxicity
  • gray baby syndrome (neonates can’t glucuronidate well; vomiting, limp, gray skin, cyanosis, hypotension, cardiovascular collapse)
119
Q

What symptoms are associated with gray baby syndrome?

A
  • vomiting
  • limp
  • gray skin
  • cyanosis
  • hypotension
  • cardiovascular collapse
120
Q
  • Chloramphenicol is toxic to humans because (…)
  • If this is on a culture and sensitivity and there are other options, what should you use?
A
  • it interrupts the 50S subunit in humans as well
  • use other options; reserve this for very sick patients
121
Q

What is the MOA of linezolid?

A
  • binds to 50S subunit at unique site
  • no cross-resistance w/ other drugs
  • inhibits bacterial initiation of mRNA translation
  • mostly bacteriostatic
  • 100% bioavailable in both IV and oral
122
Q

What percent is linezolid bioavailable and in which routes of administration?

A
  • 100%
  • IV and orally
123
Q

What is the coverage of linezolid?

A
  • mostly gram +
    **Corynebacterium, Listeria, Bacillis, Micrococcus
124
Q

What is the distribution of linezolid?

A
  • distributes well in perfused tissues
  • no cytochrome interactions
125
Q

What do you use linezolid in treating?

A
  • MDR gram + infections
  • HAP due to MRSA
  • CAP due to S. pneumo and MSSA
  • VRE infections
  • skin/soft tissue infections
126
Q

What are the adverse affects of linezolid?

A
  • thrombocytopenia
  • peripheral neuropathy
  • optic neuropathy
  • inhibits MAO (serotonin syndrome)
127
Q
  • What should you reserve linezolid for?
  • Should you use this empirically?
A
  • MDR, MRSA, and VRE infections where bugs are resistant to everything else
  • no, don’t use empirically
128
Q
  • What was the original formulation of quinolones?
  • What was their coverage?
  • How was their absorption and distribution?
  • Were they cidal or static?
A
  • nalidixic acid
  • too narrow; some gram negative, no gram positive and no atypicals
  • good oral absorption, poor distribution (stayed in the blood)
  • bactericidal
129
Q
  • What is the formulation of fluoroquinolones?
  • What were their improvements from quinolones?
A
  • fluorinated analogs of nalidixic acid
  • retains good oral bioavailability
  • good distribution with deep tissue penetration
  • affects intracellular organisms
  • broad spectrum
130
Q
  • What type of potency do fluoroquinolones have?
  • Are they cidal or static?
  • How safe are they?
A
  • very potent = very effective
  • bactericidal
  • very safe
131
Q
  • Fluoroquinolones gained coverage for what type of organisms that quinolones did not cover?
  • What are the names of these organisms?
A
  • atypical bacteria
  • chlamydia, TB, legionella
132
Q
  • What is the MOA of 1st and 2nd fluoroquinolone generations?
  • Describe the MOA
  • What type of coverage do these have?
A
  • inhibits topoisomerase II (DNA gyrase)
  • DNA gyrase typically eases tenses on bacteria DNA coil to aide in replication by cutting/gluing parts of the chain; when it is inhibited, the cutting continues, but the gluing stops
  • more active in gram negative
133
Q

What is the MOA of 3rd and 4th fluoroquinolone generations?
- Describe the MOA
- What type of coverage do these have?

A
  • inhibits topoisomerase IV
  • topoisomerase IV usually takes progeny DNA, cuts it, glues it together, and then passes it along for replication; when inhibited, progeny DNA is destroyed and cannot be passed on to replicate (no more gluing)
  • improved gram + activity
134
Q

What are the resistance mechanisms to fluoroquinolones?

A
  • efflux pump
  • alteration of drug target
  • porin alteration
  • enzymatic deactivation of drug
    resistance to one means resistance to all
135
Q
  • What is the drug name in the 1st generation fluoroquinolones?
  • What is its coverage?
  • When do you use these?
A
  • nalidixic acid
  • gram negative (narrow)
  • uncomplicated UTIs
136
Q
  • What are the drug names in the 2nd generation fluoroquinolones?
  • What is their coverage?
A
  • ciprofloxacin, ofloxacin
  • gram negative, some gram positive
  • gained atypical coverage
137
Q

What can 2nd generation fluoroquinolones be used to treat?

A
  • Enterobacteriaceae
  • P. aeruginosa
  • anthrax
138
Q
  • What are the drug names in the 3rd generation fluoroquinolones?
  • What is their coverage?
A
  • levofloxacin
  • gram negative, gram positive, and atypicals (S. pneumo, P. aeruginosa)
139
Q

What can 3rd generation fluoroquinolones be used to treat?

A
  • acute exacerbation of chronic pneumonia
  • STD (not syphilis)
  • prostatitis
  • skin infections
  • acute sinusitis
  • CAP and HAP
140
Q
  • What are the drug names in the 4th generation fluoroquinolones?
  • What is their coverage?
A
  • moxifloxacin
  • gram negative, gram positive, atypicals (S. pneumo, anaerobes)
141
Q

What can 4th generation fluoroquinolones be used to treat?

A
  • mixed infections
  • NO p. aeruginosa
142
Q

Out of all of the fluoroquinolones we need to know, which one cannot treat pseudomonas infections?

A

moxifloxacin

143
Q
  • How are fluoroquinolones absorbed?
  • What do they bind to?
  • How is their distribution?
  • How are they eliminated?
A
  • well absorbed orally
  • divalent, trivalent cations and is bound by sucralfate and others
  • good tissue penetration
  • eliminated renally except for moxifloxacin which is excreted in bile
144
Q

Fluoroquinolones can enter (…) cells to kill (…) bacteria

A
  • host cells
  • intracellular bacteria
145
Q

Which fluoroquinolones have a long half-life so you only need to do daily dosing with these drugs?

A
  • levofloxacin
  • moxifloxacin
146
Q

Which fluoroquinolone is excreted through bile?

A

moxifloxacin

147
Q
  • Which fluoroquinolone is most likely to cause QT prolongation? Which is least likely?
  • What are 3rd and 4th generation fluoroquinolones used mostly for?
  • Which one have the most gram negative treatment and can be used for travelers diarrhea?
A
  • (most likely) moxi>levo>cipro (least likely)
  • used mostly for respiratory infections
  • ciprofloxacin
148
Q
  • What sulfonamide drug do we need to know?
  • What is its route of administration?
A
  • sulfamethoxazole/trimethoprim (SMX/TMP)
  • oral/po
149
Q

What is the MOA of sulfonamides?

A
  • bacteriostatic/synergism
  • inhibits production of folic acid; bacteria must make their own folic acid
150
Q
  • Sulfa antibiotics are structural analogs of PABA, so they inhibit what?
  • They are combined with trimethoprim, which does what?
A
  • dihydropterate synthetase/synthase
  • dihydrofolate reductase inhibitor; stops additional step in folate production
151
Q

What is the coverage of sulfonamides?

A
  • some gram positive (good staph/strep)
  • some gram negative (good H. flu)
    no anaerobes or atypicals
152
Q

Do sulfonamides cover anaerobes or atypical bacteria?

153
Q
  • How are sulfonamides absorbed?
  • What is their distribution?
  • How are they eliminated?
  • What happens to them in the liver?
A
  • orally absorbed; topically for burns
  • good tissue penetration
  • renally eliminated
  • glucuronidated pr acetylated in the liver (need good liver function)
154
Q

There is a resistance issue with sulfonamides, so (…) is rare

A

single agent use

155
Q

What can sulfonamides be used to treat?

A
  • MRSA
  • PCP prophylaxis and treatment (good for HIV)
  • E. coli and proteus predominant UTI
  • gut infections due to enterobacteriacae
  • bacterial respiratory infections
  • acute otitis media
156
Q

What are the adverse effects of sulfonamides?

A
  • crystalluria (adequate hydration)
  • hemolytic anemia (if G6PD deficient)
  • kernicterus of newborn (bilirubin is displaced by sulfas)
157
Q

What is safe in pregnancy but not at term and is not given to newborns?

A

sulfonamides

158
Q

What does sulfonamide displace? What does this mean?

A
  • warfarin
  • methotrexate
  • sulfonylureas
  • phenytoin
    highly protein bound
159
Q

What cytochrome does sulfonamide inhibit?

160
Q

What do you have to keep in mind about sulfonamides (sensitivity)?

A

many strains are sensitive in vitro but not in vivo, limiting the utility of many sulfas

161
Q
  • Is nitrofurantoin cidal or static?
  • What is its coverage?
  • How is it metabolized?
  • How is it excreted?
  • What do you use nitrofurantoin for?
  • What are the adverse effects?
A
  • bactericidal
  • gram positive, gram negative
  • quickly metabolized (not good for systemic use)
  • renally excreted
  • only use for UTIs
  • anorexia, hemolytic anemia (G6PD deficient), neuropathies, N/V common
162
Q
  • Because nitrofurantoin is renally excreted, it is contraindicated in which individuals?
  • What organisms are not sensitive to nitrofurantoin?
A
  • pts with CrCl < 60 mL/min
  • P. aeruginosa and Proteus
163
Q

What is the MOA of amphotericin B?

A
  • only IV
  • binds ergosterol fairly sensitive
  • inserts itself in cell membrane forming pores that allow cellular contents to leak out
  • fungistatic or fungicidal
164
Q

Amphotericin B is not water soluble, so how is it given? Describe the structure of this antifungal?

A
  • given in a suspension
  • has a lipid and water loving side
165
Q
  • How many formulations of amphotericin B are there?
  • Describe the newer formulations
  • How does ampho B distribute?
  • Is it highly protein bound or no?
A
  • 4 available formulations
  • newer formulations are less toxic, concentrate better in the liver, lung and spleen
  • distributes and binds to tissues; but not good CSF penetration, vitreous humor, and amniotic fluid
  • highly protein bound
166
Q
  • What does ampho B cross?
  • What pregnancy category is this antifungal?
A
  • crosses placenta
  • category B
167
Q
  • What is the toxicity of ampho B?
  • What are the types of toxicity side effects associated with this?
  • What occurs in the first few weeks so you have to monitor electrolytes?
A
  • very toxic, low TI
  • infusion related toxicity; cumulative toxicity
  • hypomagnesemia and hypokalemia
168
Q
  • Describe the side effects of infusion related toxicity with ampho B?
  • How can you lessen these reactions?
A
  • fever, chills, muscle spasms, vomiting, HA, hypotension
  • test dosing, premedication, slow IV infusion, or decrease daily dosing
169
Q

Describe the side effects of cumulative toxicity with ampho B?

A
  • renal damage is nearly all pts (leading to dialysis)
  • permanent renal damage due to cumulative dosing
170
Q

What is the MOA of azole antifungals?

A
  • inhibits fungal CYP450 enzyme needed to make ergosterol
  • fungistatic
171
Q

What drugs are azole antifungals?

A
  • fluconazole
  • itraconazole
  • voriconazole
  • ketoconazole
  • posaconazole
172
Q
  • What is the bioavailability of fluconazole?
  • How is this drug available?
  • What is its distribution?
  • What is its metabolism?
  • How is it excreted?
  • What is its TI? What does this mean?
A
  • good oral bioavailability (nearly 100%)
  • oral and IV (GI acidity not a concern)
  • penetrates CSF (cryptococcal meningitis)
  • poor metabolism
  • renally excreted
  • large TI = very safe
173
Q

What is fluconazole used for?

A

reserve for candida infections

174
Q

What are the side effects of fluconazole?

A
  • highly sensitive for fungal CYP450 (no endocrine side effects)
  • lots of drug interactions than others, but not as severe
  • not safe in pregnancy
175
Q

What cytochromes does fluconazole inhibit?

A
  • CYP2C19
  • CYP2C9
  • CYP3A4
176
Q
  • What does itraconazole require for absorption?
  • What is its distribution?
  • How is this bound to proteins?
  • How is this antifungal metabolized?
A
  • requires high acidity = drink a coke
  • distributes well into bones but not CSF
  • highly protein bound
  • hepatically metabolized
177
Q

Because itraconazole is hepatically metabolized, what should you do?

A

use cautiously in severe renal/hepatic insufficiency

178
Q

What is itraconazole used for?

A
  • candida
  • aspergillus
  • histoplasma
  • onychomycosis (male fungal infections)
179
Q

What are the less severe side effects associated with itraconazole?

A
  • GI (most common)
  • HA
  • rash
  • increases LFTs
180
Q

What are the black box warnings associated with itraconazole?

A
  • don’t give with drugs that increase QT intervals or pts with arrhythmias
  • negative inotropic effects so don’t give to CHF pts
181
Q

Itraconazole is a substate and potent inhibitor of what cytochrome? What does this mean?

A
  • CYP3A4
  • will have significant drug interactions
182
Q
  • What is the distribution of voriconazole?
  • What versions are there?
  • What is this a safer alternative for?
A
  • penetrates tissues and CSF
  • oral version (and IV) so it is safe to send pts home on this
  • safer alternative for amphotericin B
183
Q

What is voriconazole metabolized and and inhibits?

A
  • CYP2C6
  • CYP3A4
  • CYP2C19
184
Q

What is voriconazole used to treat?

A
  • candida, aspergillus, fusarium, molds
  • replaces ampho B in tx of invasive aspergillus
185
Q

What are the side effects associated with voriconazole?

A
  • visual/auditory disturbances
  • hypertension/cardiac
  • GI
  • increased LFTs
  • HA
  • not safe in pregnancy
186
Q

What are other antifungals that are not azole antifungals?

A
  • terbinafine
  • griseofulvin
187
Q

What is the MOA of terbinafine?

A
  • non-azole, allylamine antifungal
  • inhibits fungal squalene epoxidase (interrupts cell wall synthesis)
  • toxic amounts of squalene accumulate in fungi causing death
188
Q

How is terbinafine available?

A

orally and topically

189
Q

What can terbinafine be used for?

A
  • dermatophytoses, especially onychomycoses due to lipophilicity
  • nail infections (choose this, less toxic)
190
Q

If a pt have a fungal nail infection, what drug should you choose and why?

A
  • terbinafine
  • less toxic
191
Q

What are the side effects of terbinafine?

A
  • GI complaints, not well absorbed
  • rare hepatotoxicity and neutropenia (monitor LFTs)
192
Q

What pregnancy category is terbinafine?

A
  • category B
  • wait until no longer pregnant - non-life-threatening illnesses are treated with this
193
Q

What is the MOA of griseofulvin?

A
  • allylamine
  • inhibits fungal mitosis
  • fungistatic
194
Q
  • Where does griseofulvin deposit? What does this allow for?
  • Because this antifungal is fungistatic, it requires how long of therapy?
  • How is this antifungal available?
A
  • deposits in skin, protecting from further infection
  • requires 2-6 months of therapy depending on infection
  • oral suspension or tablets
195
Q
  • What can griseofulvin be used for?
  • How must this be given?
A
  • skin dermatophytoses and ring worm
  • must be given with high fat mean
196
Q

What are the side effects of griseofulvin?

A
  • cytochrome interactions common
  • contraindicated in pregnancy
  • men should wait 6 months after therapy to have kids

Pharmacology (13 decks)

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