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Antimicrobials Flashcards

1
Q

various ways antimicrobials work (6)

A
  1. disrupt folic acid synthesis
  2. disrupt DNA topoisomeras
  3. damage DNA
  4. disrupt mRNA synthesis
  5. disrupt protein synthesis
  6. disrupt cell wall synthesis
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2
Q

classes that disrupt folic acid synthesis (2)

A
  1. sulfonamides

2. trimethoprim

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3
Q

classes that disrupt DNA topoisomerase (2)

A
  1. fluoroquinolone

2. quinolone

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4
Q

classes that damage DNA (1)

A
  1. metronidazole
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5
Q

classes that disrupt mRNA synthesis (1)

A

rifampin

via RNA polymerase

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6
Q

classes that disrupt protein synthesis @ 50S subunit

A
  1. macrolides
  2. streptogramins
  3. chloramphenicol
  4. clindamycin
  5. linezolid
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7
Q

classes that disrupt protein synthesis @ 30S subunit (2)

A
  1. aminoglycosides

2. tetracyclines

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8
Q

classes that disrupt cell wall synthesis via PDG synthesis disruption (1)

A
  1. glycopeptides
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9
Q

classes that disrupt cell wall synthesis via PDG cross-linking mess up (6)

A
  1. PCNase-sensitive PCN
  2. PCNase-resistant PCN
  3. Antipseudomonal PCN
  4. Cephalosporin (I-V)
  5. Carbapenem
  6. Monobactam
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10
Q

examples of sulfonamides (3)

A
  1. sulfamethoxazole
  2. sulfisoxazole
  3. sulfadiazine
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11
Q

examples of fluoroquinolones (2)

A
  1. ciprofloxacin

2. levofloxacin

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12
Q

examples of quinolone (1)

A

nalidixic acid

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13
Q

example of macolides (3)

A
  1. azithromycin
  2. clarithromycin
  3. erythromycin
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14
Q

example of streptogramin (2)

A
  1. quinupristin

2. dalfopristin

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15
Q

example of aminoglycoside (5)

A
  1. gentamicin
  2. neomycin
  3. amikacin
  4. tobramycin
  5. streptomycin
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16
Q

example of tetracycline (3)

A
  1. tetracycline
  2. doxycycline
  3. minocyclien
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17
Q

example of glycopeptide (2)

A
  1. vancomycin

2. bacitracin

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18
Q

example of PCNase-sensitive PCN (3)

A
  1. PCN G
  2. ampicillin
  3. amoxicillin
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19
Q

example of PCNase-resistant PCN (3)

A
  1. oxacillin
  2. nafcillin
  3. dicloxacillin
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20
Q

example of antipseudomonal PCN (2)

A
  1. piperacillin

2. ticarcillin

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21
Q

examples of 1st gen ceph

A

cephazolin

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22
Q

example of 2nd gen ceph

A

cefoxitin

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23
Q

ex of 3rd gen ceph

A

ctx

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24
Q

ex of 4th gen ceph

A

cefipime

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25
Q

ex of 5th gen ceph

A

ceftraroline

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26
Q

ex of carbapenem (4)

A
  1. imipenem
  2. meropenem
  3. ertapenem
  4. doripenem
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27
Q

ex of monobactam (1)

A
  1. aztreonam
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28
Q

PCN G vs PCN V difference

A

G is IV and IM

V is PO

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29
Q

mechanism of PCN G and V

A

bind PCN-binding protein (transpeptidase) and block cross-linking of PDGN

also activates autolytic enzymes

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30
Q

PCN G, V used against: (5)

bactericidal or lytic?

A

GP:

  1. strep pneumo
  2. strep pyogenes
  3. actinomyces
  4. meningococcus
  5. treponem pallidum

bactericidal

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31
Q

toxicity of PCN G, V (2)

A

hypersentivity reactions

hemolytic anemia

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32
Q

how do bacteria get resistance to PCN G,V

A

penicillinase (beta-lactamase) that cleaves the beta-lactam ring of PCN

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33
Q

Ampicillin vs. amoxicillin

A

they’re both wider spectrum PCN but amoxicillin has greater oral bioavailability

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34
Q

use of ampicillin and amoxicillin vs PCN G, V

A

they also cover:

  1. H flu
  2. E coli
  3. Listeria monocytogenes
  4. Proteus mirabilis
  5. Salmonella
  6. Shigella

amp and amox HELPSS kill enterococci

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35
Q

mechanism of penicillinase-resistant PCN’s:

oxacillin, nafcillin, dicloxacillin

A

disrupt cross-linking of PDGN but they also have bulky R group that blacks beta-lactam ring from beta-lactamase

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36
Q

use of penicillinase-resistant PCN

A

simple staph aureus

not for MRSA

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37
Q

toxicity of penicillinase-resistant PCN (2)

A
  1. hypersensitivity reactions

2. interstitial nephritis

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38
Q

toxicity of amipcillin/amoxicillin (3)

A
  1. hypersensitivity reactions
  2. rash
  3. pseudomembranous colitis
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39
Q

beta-lactamase inhibitors (3)

A
  1. clavulanic acid
  2. sulbactam
  3. tazobactam

CAST

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40
Q

organisms not covered by cephalosporins? (5)

A

LAME

  1. Listeria
  2. Atypical: mycoplasma
  3. Atypical: chlamydia
  4. MRSA (except 5th gen ceph Ceftaroline)
  5. Enterococci
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41
Q

1st gen ceph

  • examples (2)
  • covers what (3)
  • what’s used before surgery; why?
A
  • cefazolin and cephalexin
  1. proteus mirabilis
  2. e. coli
  3. klebsiella

“PEcK”

  • cefazolin used to prevent staph aureus infection
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42
Q

2nd gen ceph

  • examples (3)
  • covers what (7)
A
  • cefoxitin; cefaclor; cefuroxime
  1. H Flu
  2. Enterobacter
  3. Neisseria spp
  4. Proteus
  5. E Coli
  6. Klebsiella
  7. Serratia

HEN PEcKS

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43
Q

3rd gen ceph
- examples (3)

what infections

A
  • ceftriaxone; cefotaxime; ceftazidime (cef-T’s)
    1. GN infections resistant to other beta-lactams

CTX for meningitis and gonorrhea
Ceftazidime for pseudomonas

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44
Q

4th gen ceph

  • examples (1)
  • what infection
A
  • cefepime

used for pseudomonas and GP’s

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45
Q

5th gen ceph

  • example (1)-
  • covers what
A

ceftaroline

broad spectrum GP and GN including MRSA

BUT does not cover pseudmonas

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46
Q

toxicity of cephalosporins (3)

A
  1. hypersensitivity reactions
  2. vitamin K def
  3. increased nephrotoxicity of aminoglycoside
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47
Q

monobactam

  • example
  • toxicity
A
  • aztreonam

- usually nontoxic; just some GI upset

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48
Q

aztreonam

- mechanism

A

beta-lactamase resistant abx

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49
Q

aztreonam synergistic with what

A

aminoglycoside

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50
Q

aztreonam used against

  • what situations
A

GN rods only

no activity against GP or anaerobes

used in pts with PCN-allergy and pts with renal insufficiency who cannot tolerate aminoglycoside

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51
Q

carbapenem mechanism

A

beta-lactamase resistant abx

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52
Q

carbapenem always given with what? why?

A

cilastatin

inhibits renal dehydropeptidase I to prevent it from becoming inactivated in renal tubules

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53
Q

carbapenem use (3 general classes)

A

GP cocci
GN rods
anaerobes

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54
Q

toxicity of carbapenem (3)

A
  1. GI distress
  2. skin rash
  3. CNS: seizure
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55
Q

vanco mechanism

A

binds D-ala D-ala of cell wall precursoors

bactericidal

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56
Q

vanco use

A

GP only

  • MRSA
  • enterococci
  • c. dif
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57
Q

vanco toxicity (3)

A
  1. nephro
  2. oto
  3. thrombophlebitis
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58
Q

how do bacteria become resistant against vanco?

A

D-ala D-ala —> D-ala D-lac

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59
Q

30S inhibitors

A

aminoglycosides (bactericidal)
tetracycline (bacteristatic)

buy AT 30

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60
Q

50S inhibitors

A

chloramphenicol
clindamycin
macrolides (erythromycin)
linezolid

CCEL at 50

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61
Q

what abx prevents ribosomes from even finding mRNA

A

linezolid

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62
Q

which abx prevents initiation complex formation

A

aminoglycosides

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63
Q

what abx prevents peptidyl transferase

A

chloamphenicol

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64
Q

what abx prevents translocation of ribosome in translation? (2)

A

Macrolides

Clindamycin

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65
Q

what abx prevents A-site tRNA binding

A

Tetracycline

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66
Q

what abx are bateristatic

A

all protein synthesis inhibitors except for aminoglycosides, which are bactericidal

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67
Q

which abx needs O2 for uptake?

A

aminOglycOsides 2Os, O2

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68
Q

What bugs covered by aminoglycoside?

A

severe GN rod infections

synergistic with beta-lactams

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69
Q

which aminoglycoside is used for bowel surgery?

A

neomycin

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70
Q

toxicity of aminoglycoside (4)

A
  1. nephrotoxicity (esp if with cephalosporin)
  2. ototoxicity (esp if with loop diuretics)
  3. NMJ blockade
  4. teratogen
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71
Q

how bacteria become resistant to aminoglycosides

A

bacterial transferase enzyme inactivates drug by transferring acetyl, phosphate, adenyl group

72
Q

aminoglycoside mechanism

A

prevents initiation factor for translation

73
Q

tetracyclin mechanism

A

prevents attachment of amino-acyl tRNA

74
Q

what should you avoid when on tetracycline?

A

dairy or antacaids b/c Ca and Mr inhibit absorption in gut

75
Q

use of tetracyclines (4)

A
  1. borrelia burgdorferi (doxycycline)
  2. m. pneumoniae
  3. rickettsia
  4. chlamydia
76
Q

why can we use tetracyclines for rickettsiae and chlamydia even though they’re intracellular bugs

A

it accumulates intracellularly

77
Q

tetracyclin toxicity (4)

A
  1. GI distress
  2. teeth and bone bad
  3. photosensitivity
  4. teratogen
78
Q

how bacteria become resistant to tetracycline

A

decrease uptake and increase efflux using plasmid-encoded transport pumps

79
Q

mechanism of macrolide

A

blocks translocation during sliding of ribosome

“macroSLIDES”

80
Q

use of macrolides (3)

A
  1. atypical PNA (mycoplasma, chlamydia, legionella)
  2. STD (chlamydia)
  3. GP cocci (strep infections in pts w/PCN allergies)
81
Q

macrolide toxicity (6)

A

MACRO

  1. motility issues
  2. arryhthmias (QT prolongation)
  3. cholestatic hepatitis
  4. rash
  5. eOsinophilia
  6. increases concentration of tehophylline and warfarin
82
Q

how bacteria become resistant to macrolides

A

they methylate 23S rRNA -binding site to prevent drug from binding to it

83
Q

mechanism of chloramphenicol

A

blocks peptidyltransferase at 50S

84
Q

use of chloramphenicol 2)

A
  1. meningitis (h flu, neisseria, strep)

2. rocky mountain spotted fever (ricketsseiae rickettsii)

85
Q

chloramphenicol toxicity (3)

A
  1. anemia
  2. aplastic anemia
  3. gray baby syndrome (in premies b/c they lack UDP-glucoronyl transferase)
86
Q

how bacteria become resistant to chloramphenicol

A

plasmid-encoded acetyltransferase inactivates it

87
Q

mechanism of clindamycin

A

blocks translocation at 50S

88
Q

Clinda uses (4)

A
  1. anaerobic infections (bacteroides, c perfringens) in aspiration PNA
  2. lung abscess
  3. oral infections
  4. GAS
89
Q

what treats anaerobes above the diaphragm

what treats anaerobes below the diaphragm

A

above: clinda
below: metro

90
Q

clinda toxicitiy (3)

A

psuedomembranous colitis (c difficile)
fever
diarrhea

91
Q

sulfonamide mechanism

A

inhibits folate synthesis

92
Q

use of sulfonamides (5)

A
  1. GP
  2. GN
  3. nocardia
  4. chlamydia
  5. UTI
93
Q

sulfonamide toxicity (6)

A
  1. hypersensitivity reaction
  2. hemolysis if G6PD def
  3. nephrotoxicity (tubulointerstitial nephritis)
  4. photosenstiive
  5. kernicterus in infants
  6. displace warfarin from albumin
94
Q

how bacteria become resistant to sulfonamides

A

decresae uptake
increase PABA synthesis
alter enzyme needed to make DHF

95
Q

trimethoprim mechanism

A

inhibits bacterial DHF reductase

96
Q

trimethoprim use

A

ppx in pneumocystis PNA, toxo

also in UTI, shigella, salmonella

97
Q

trimethoprim toxicity (3)

A
  1. megaloblastic anemia
  2. leukopenia
  3. granulocytopenia
98
Q

fluoroquinolone mechanism

A

inhibit DNA gyrase (topo II) and topo IV

99
Q

fluoroquinolone use

A

GN rods of GU and GI

pseudomonas, neisseria

some GPs

100
Q

fluoroquinolone toxicity

A
  1. Gi upset
  2. rash, h/a dizzy
  3. tendonitis w/ tendon rupture
  4. leg cramps and myalgias
  5. teratogen
  6. arrhyhtmia

TERRIBLE

101
Q

how bacteria become resistant to fluoroquinolone (2)

A

chromosome encoded mutation in DNA gyrase

plasmid can also code for efflux pumps

102
Q

metronidazole mechanism

A

free radical metabolites damage DNA

103
Q

use of metronidazole (6)

A

GET GAP

  1. giardia
  2. entamoeba
  3. trichomonas
  4. gardnerella vaginalis
  5. anaerobes (bacteroides, c diff)
  6. pylori (H pylori) triple therapy
104
Q

metronidazole toxicity (3)

A
  1. disulfiram-like reaction (flushing, tachy, hypotension) with alcohol
  2. h/a
  3. metallic taste
105
Q

anti mycobacterium tuberculosis drug

  • ppx
  • tx
A

ppx: INH
tx: RIPE - rifampin, INH, pyrazinamide, ethambutol

106
Q

anti mycobacterium avium-intracellulare drug

  • ppx
  • tx
A

ppx: azithromycin and firabutin
tx: azithro/clarithro + ethambutol … can add rifabutin or cipro too

107
Q

anti mycobacterium leprae

  • ppx
  • tx
A

ppx: none
tx: long-term dapsone and rifampin for tuberculoid form

add clofazimine for lepromatous form

108
Q

INH mechanism

A

decrease synthesis of mycolic acid

109
Q

what does bacteria need to have for INH to become activated

A

bacterial catalase-peroxidase

110
Q

INH toxicity (2)

A
  1. nephro

2. hepato

111
Q

what can be given with INH to prevent neurotoxitity and possible drug-induced lupus

A

vitamin B6 (pyridoxine)

112
Q

examples of rifamycin (2)

A
  1. rifampin

2. rifabutin

113
Q

rifamycin mechanism

A

inhibits DNA-dep RNA polymerase

114
Q

use of rifamycin (4)

A
  1. mycoTB
  2. delays resistance to dapsone when used for leprosy
  3. ppx for meningogoccus
  4. ppx for h flu
115
Q

tifamycin toxicity (3)

A
  1. minor hepatotoxicitiy
  2. increase cyt p450
  3. orange body fluids (nonhazardous)
116
Q

rifampin or rifabutin has less cyt p-450 stimulation … therefore, which one used more for HIV infection

117
Q

pyrazinamide mechanism

A

uncertain… effective in acidic environment of phagolysosome where TB resides in macrophages

118
Q

pyrazinamide toxicity (2)

A
  1. hyperuricemia

2. hepato

119
Q

ethambutol mechanism

A

decrease carb polymerization of myco cell wall by blocking arabinosyltransferase

120
Q

ethambutol toxicity (1)

A

optic neuropathy (red-green color blindness)

121
Q

abx for endocarditis w/surgical or dental procedures

122
Q

abx for gonorrhea

123
Q

abx for h/o recurrent UTIs

124
Q

abx for meningococcal infetion

A

ciprofloxacin in adults

rifampin in chidlren

125
Q

abx for pregnant woman with GBS

A

ampicillin

126
Q

abx for prevention of gonorrheal or chlamydial conjunctivitis in newborn

A

erythromycin

127
Q

abx to prevent post surg infection with staph aureus

128
Q

abx for ppx of strep pharyngitis in child with prior rheumatic fever

129
Q

abx for syphilis

A

benzathine PCN G

130
Q

in HIV w/ < 200 CD4, what infection risk?

- what abx for ppx?

A

pneumocystis PNA

TMP-SMX

131
Q

in HIV w/ <100 CD4, what infection risk?

what abx for ppx

A

pnuemocystis PNA
Toxo

TMP-SMX

132
Q

in HIV w/<50 CD4, what infection risk

what abx for ppx

A

mycobacterium avium

azithromycin

133
Q

abx for MRSA (5)

A
  1. vanco
  2. linezolid
  3. tigecycline
  4. ceftaroline
  5. daptomycin
134
Q

abx for VRE(2)

A
  1. linezolid

2. streptogramin

135
Q

abx for pseudomonas (6 classes:12 abxs)

A
  1. PCN: piperacillin; ticarcillin
  2. cephalosporin: ceftazidime (3); cefepime (4)
  3. aminogylcoside: amikacin, gentamicin, tobramycin
  4. fluoroquinolones: ciprofloxacin, levofloxacin
  5. monobactam: aztreonam
  6. carbapenem: imipenem, meropenem
136
Q

various ways anti-fungals work (5)

A
  1. inhibit cell wall synthesis
  2. forms membrane pores
  3. inhibit nucleic acid synthesis
  4. inhibit lanosterol synthesis
  5. inhibits ergosterol synthesis
137
Q

ex of fungal cell wall synthesis inhibitors class and (3)

A

Echinocandins:

  1. caspo.fungin
  2. mica.fungin
  3. anidula.fungin
138
Q

ex of fungal membrane pore formers class and (2)

A

Polyenes

  1. amphotericin B
  2. nystatin
139
Q

ex of fungal nucleic acid synthesis inhibitors (1)

A

5-Flucytosine

140
Q

ex of lanosterol synthesis inhibitors (1)

A

Terbinafine

141
Q

ex of ergosterol synthesis inhibitors class and (6)

A

Azoles

  1. fluconazole
  2. ketoconazole
  3. clotrimazole
  4. miconazole
  5. itraconazole
  6. voriconazole
142
Q

Amphotericin B mechanism

A

binds to ergosterol (fungal MB lipid) and makes a pore to leak electrolytes

143
Q

use of amphotericin B (7)

A
  1. serious systemic mycoses
  2. cryptococcus
  3. blastomyces
  4. coccidiodes
  5. histoplasma
  6. candida
  7. mucor

intrathecal for fungal meningitis

144
Q

what do you need to give also when giving amphotericin B? why?

A

K and Mg

altered renal tubule permeability

145
Q

amphotericin B toxicity (6)

A
  1. f/c
  2. hypotension
  3. nephro
  4. arrhythmias
  5. anemia
  6. IV phlebitis
146
Q

nystatin mechanism

A

makes a pore in fungal MB

147
Q

nystatin difference from amphotericin B

A

it’s the topical version

148
Q

nystatin use (3)

A
  1. oral candida
  2. diaper rash
  3. vaginal candidiasis
149
Q

mechanism of Azoles

A

inhibit fungal ergosterol synthesis by inhibiting cyt p450 enzyme that converts lanosterol to ergosterol

150
Q

use of Azoles

A
  1. local and less serious systemic mycoses
  2. fluconazole for suppression of cryptococcal meningitis in AIDS and all candida
  3. itraconazole for Blastomyces, coccidiodes, histoplasma
  4. clotrimazole and miconazole for topical fungal infections
151
Q

itraconazole for what? (3)

A

blastomyces
cocciciodes
histoplasma

152
Q

Azole toxicity (2)

A
  1. gynecomastia (2/2 testosterone synthesis inhibition)

2. liver dysfunction (2/2 inhibit cyt-p450)

153
Q

5-Flucytosine mechanism

A

inhibtis DNA and RNA biosynthesis by conversion to 5-fuorouracil by cytosine deaminase

154
Q

5-flucytosine use (1)

A
  1. systemic fungal infection (esp cryptococcus meningitis) in combo with amphotericin B
155
Q

cryptococcus meningitis antifungals

A

5-flucytosine with amphotericin B

156
Q

5-Flucytosine toxicity

A

BM suppression

157
Q

Echinocandin mechanism

A

inhibit cell wall syntehsis by inhibiting syntehsis of beta-glucan

158
Q

Echinocandin use (2)

A
  1. invasive aspergiloosis

2. candida

159
Q

Echinocandin toxicity (2)

A
  1. GI upset

2. flushing (2/2 histamine release)

160
Q

Terbinafine mechanism

A

inhibits fungal enzyme squalene epoxidase –> prevents formation lanosterol and ultimately ergosterol

161
Q

Terbinafine use

A
  1. dermatophytoses (esp onychomycosis - fungal infection of toenails or finger nails)
162
Q

what is onychomycosis

A

fungal infection of toenails and finger nails

163
Q

Terbinafine toxicity (4)

A
  1. GI upset
  2. taste disturbance
  3. hepatotoxitiy
  4. h/a
164
Q

Griseofulvin mechanism

A

interferes with microtubule function - disrupts mitosis

165
Q

Griseofulvin deposits where?

A

keratin-containing tissues (nails)

166
Q

Griseofulvin use (2)

A
  1. oral Tx of superficial infections

2. inhibits growth of dermatophytes (tinea, ringworm)

167
Q

Griseofulvin toxicity (5)

A
  1. teratogen
  2. carginogen
  3. confusion
  4. h/a
  5. increase p-450 and warfarin metabolism
168
Q

Antiprotozoan therapy ex (5)

A
  1. Pyrimethamine
  2. suramin
  3. melarsoprol
  4. nifurtinmox
  5. sodium stibogluconate
169
Q

tx for toxo

A

pyrimethamine

170
Q

tx for trypanosoma brucei

A

suramin and melarsoprol

171
Q

tx for trypanosoma cruzi

A

nifurtimox

172
Q

tx for leishmaniasis

A

sodium stibogluconate

173
Q

chloroquine mechanism

A

blocks detoxification of heme into hemozin –> heme accumulates and is toxic to plasmodia

174
Q

antihelminth therapy ex (5)

A
  1. mebendazole
  2. pyrantel pamoate
  3. ivermectin
  4. diethylcarbamazine
  5. praziquantel
175
Q

what to use against flukes (trematodes)like Schistosoma

A

praziquantel

Microbiology (11 decks)

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