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POM Exam 2 > Antimicrobials > Flashcards

Antimicrobials Flashcards

1
Q

minimum inhibitory concentration

A
  • lowest concentration of drug that can inhibit growth of a particular bacterial species
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2
Q

minimum bactericidal concentration

A
  • smallest concentration of a drug to kill 50% of the bacterial population
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3
Q

if you have bacteriostatic

A
  • MBC&raquo_space;> MIC
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4
Q

If you have bactericidal

A
  • MBC = MIC
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5
Q

culture based methods to determine microbial susceptibly/resistance

A
  • disk diffusion

- E-test

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6
Q

molecular detection of resistance mutations

A
  • PCR

- sequencing

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7
Q

antibiograms

A
  • summaries of antibiotic susceptibilities of local isolates
  • sent to clinical micro lab
  • aid in selecting empiric therapy
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8
Q

efficacy of antimicrobial drugs limited by

A
  • mechanism of action
  • susceptibility of the target organism
  • side effects on the host
  • pharmacodynamics
  • cost
  • patient compliance
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9
Q

efficacy of antimicrobial drugs mechanism of action

A
  • has to be able to get to the site of infection
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10
Q

efficacy of antimicrobial drugs cost

A
  • if the prescription is more than your patient can afford
  • they won’t take it
  • won’t be efficacious
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11
Q

efficacy of antimicrobial drugs patient compliance

A
  • will the patient actually take it
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12
Q

Cmax

A
  • max concentration you can get from a dose
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13
Q

area under curve

A
  • total concentration of drug that has accumulated in the patient during that dosing interval
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14
Q

time dependent killing

A
  • maximize time above MIC
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15
Q

drugs that use TDK

A 
Wall inhibitors
- penicillins
- cephalosporins
Protein inhibitors
- macrolides
- clindamycin
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16
Q

concentration dependent killing

A
  • maximize Cmax and therefore AUC
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17
Q

drugs that use CDK

A

DNA inhibitors
- fluoroquinolones
Protein inhibitors
- Aminoglycosides

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18
Q

post antibiotic effect

A
  • the time it takes bacteria to return to log-phase growth following removal of antibiotic
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19
Q

post antibiotic effect TDK

A
  • minimal because we have extended amount of time where the drug is above MIC
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20
Q

post antibiotic effect CDK

A
  • quite long to extend amount of time before next drug needs to be administered
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21
Q

importance of long PAEs

A
  • reduce required frequency of dosing

- reduce toxicities and cost

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22
Q

cefriaxone

A
  • subclass: cephalosporin

- class: beta lactam

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23
Q

bacterial cell envelope includes

A
  • cell membrane
  • peptidoglycan layer
  • outer membrane
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24
Q

bacterial cell envelope doesn’t include

A
  • intracellular structures
  • extracellular polysaccharide capsules
  • secreted molecules
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25
Q

classes of agents that interfere with bacterial cell envelope

A
  • beta lactamase
  • glycopeptides
  • isoniazid
  • ethambutol
  • bacitracin
  • phosphomycin
  • cycloserine
  • lipopeptides
  • polymyxins
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26
Q

beta lactam examples

A
  • penicillins
  • cephalosporins
  • carbapenems
  • monobactams
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27
Q

gram negative cell envelope

A
  • small peptidoglycan layer
  • lipopolysaccharide layer (important for gram negatives)
  • Lipid A
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28
Q

LPS layer

A
  • outer membrane of gram negative cell envelope
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29
Q

lipid A

A
  • endotoxin

- toxic molecule of LPS

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30
Q

gram positive cell envelope

A
  • lots of peptidoglycan

- lipotechoic acid unique to gram positives

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31
Q

peptidoglycan

A
  • alternating units of NAG and NAM
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32
Q

what do beta lactams inhibit?

A
  • transpeptidation
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33
Q

peptidoglycan amino acids

A
  • D-Ala-D-Ala

- this what penicillin targets

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34
Q

penicillin binding proteins

A
  • have the transpeptidase activity

- may also have the transglycosylation activity to put sugar backbone together

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35
Q

structural basis of beta lactams

A
  • they look a lot like D-Ala-D-Ala
  • drug named for beta lactam ring
  • inhibits activity of enzyme that looks for D-Ala-D-Ala
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36
Q

Classes of B lactams

A
  • penicillin

- cephalosporins

37
Q

antibiotic resistance mechanisms

A
  • enzymatically inactivate drug
  • alter drug target
  • alter drug exposure
38
Q

enzymatically inactivate drug

A
  • beta lactamases

- often on mobile genetic elements

39
Q

alter drug target

A
  • mutation

- can occur via horizontal exchange

40
Q

alter drug exposure

A
  • decreased uptake (gram negatives)

- increased efflux

41
Q

how do gram negatives have decreased uptake?

A
  • they can change the size of their pores to allow nutrients to get in
  • exclude drugs because they are bigger
42
Q

beta lactamases

A
  • break bond in beta lactam ring of penicillin

- disables molecule

43
Q

types of beta lactamases

A
  • ESBL

- metal dependent (NDM-1)

44
Q

ESBL

A
  • mostly derived from active site mutations in TEM/SHV

- results in activity against extended spectrum cephalosporins

45
Q

clavulanic acid

A
  • resistance to cleavage by beta lactamases

- will deactivate beta lactamase

46
Q

alternative penicillin resistant PBP

A
  • have low affinity for B-lactams but retain transpeptidase activity
  • can arise through mutation (gonorrhea)
  • can be acquired horizontally (MRSA)
47
Q

fitness cost of antibiotic resistance

A
  • it costs the bacteria something to become resistance to antibiotic
  • won’t grow as well as the susceptible drug
48
Q

rationale for understanding mechanisms of resistance

A
  • choose antibiotics with higher fitness cost for resistance
49
Q

altered penicillin transport

A
  • decreased membrane permeability

- increased efflux

50
Q

altered penicillin transport decreased membrane permeability

A
  • only relevant for gram negatives

- can arise via spontaneous mutations in porin genes

51
Q

altered penicillin transport increased efflux

A
  • horizontal acquisition of new pump

- mutation that alters specificity or expression

52
Q

multiple mechanisms of resistance

A
  • higher levels of resistance
53
Q

multiple mechanisms of resistance examples

A
  • alterations in porin (gram -)
  • alternations in PBPs
  • production of beta lactamases
  • over expression of efflux pump
54
Q

glycopeptide example

A
  • vancomycin

- for gram positives

55
Q

what do glycopeptides do?

A
  • inhibit transglycosylation of peptidoglycan

- binds to D-ala-D-ala and blocks incorporation

56
Q

vancomycin resistance mechanisms

A
  • synthesis of D-ala-D-lac precursors that cannot bind vancomycin
57
Q

bacitracin

A
  • inhibits regeneration of PG lipid carrier
58
Q

phosphomycin

A
  • prevents attachment of NAG to NAM
59
Q

cycloserine

A
  • prevents attachment of peptide to NAM
60
Q

mycobacterium species

A
  • have mycolic acid
  • and arabinogalactan
  • acid fast stain
61
Q

agents that work on mycobacterial species

A
  • isoniazid

- ethambutol

62
Q

isoniazid

A
  • inhibits mycolic acid synthesis
63
Q

ethambutol

A
  • inhibits arabinotransferases
64
Q

lipopeptides MOA

A
  • form pores in cytoplasmic membrane of gram positive cell
  • bind to phosphatidylglycerol which is abundant in bacterial cell membranes
  • rare in eukaryotic cell membranes
65
Q

lipopeptides example

A
  • daptomycin
66
Q

why don’t we use lipopeptides to treat pneumonia

A
  • surfactant is coated in phosphatidylglycerol

- not good because lipopeptides break holes in this

67
Q

bacterial folate synthesis inhibitors

A
  • sulfonamides
  • trimethoprim
  • humans don’t synthesize their own folate.
  • bacteria do
68
Q

sulfonamides

A
  • bacteriostatic on their own
  • generally included trimethoprim
  • sulfamethoxazole
69
Q

resistance to sulfonamides altered drug target

A
  • spontaneous mutation of dhps

- horizontal acquisition of alternate DHPS

70
Q

resistance to sulfonamides swamp the system

A
  • increased production of folate precursor PABA
71
Q

resistance to sulfonamides altered drug exposure

A
  • decreased uptake
72
Q

combinatorial synergy

A
  • lower amount of each drug we need to use and get same outcome
  • each drug works better in presence of the other drug
73
Q

trimethoprim

A
  • bactericidal

- inhibits dihydrofolate reductase

74
Q

Tmp/Smx

A
  • synergistic combination

- smx becomes bactericidal with combined with tmp

75
Q

quinolones/fluoroquinolones

A
  • inhibit DNA gyrase (topo II and topo IV)
  • bactericidal
  • work best against gram negatives
76
Q

quinolones/fluoroquinolones example

A
  • ciprofloxacin
77
Q

role of topoisomerase IV

A
  • separates newly replicated chromosomes into daughter cells
78
Q

problem with cipro

A
  • may rupture tendons
79
Q

resistance of quinolones altered drug target

A
  • chromosomal mutation in gyrase and topoisomerase genes
80
Q

resistance of quinolones altered drug exposure

A
  • decreased uptake via mutations in gram negative porin proteins
  • increased efflux due to mutations in efflux pump activity
  • cross-resistance leading to multi drug resistance
81
Q

rifamycins

A
  • inhibit DNA synthesis

- can be bactericidal or static dependent on concentration

82
Q

rifamycins MOA

A
  • bind to bacterial DdRp with higher affinity than for human enzyme
83
Q

rifamycins example

A
  • rifampin

- mostly used for mycobacterium or meningococcal

84
Q

resistance to monotherapy

A
  • spontaneous mutations in RNA pol gene

- rarely used as mono therapy

85
Q

nitroimidazole use

A
  • bactericidal

- anaerobic microbes

86
Q

nitroimidazole type of drug

A
  • pro-drug - must be converted by microbial enzyme to active form
87
Q

nitroimidazole MOA

A
  • active drug forms toxic free radicals that damage DNA
88
Q

nitroimidazole example

A
  • metronidazole
89
Q

resistance to nitroimidazole

A
  • failture to enzymatically activate drug

- mutations in enzymes that convert the prodrug to the active compound.

POM Exam 2 (21 decks)

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