POM Exam 2 > Antimicrobials > Flashcards

Antimicrobials Flashcards

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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»_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
classes of agents that interfere with bacterial cell envelope
- beta lactamase - glycopeptides - isoniazid - ethambutol - bacitracin - phosphomycin - cycloserine - lipopeptides - polymyxins
26
beta lactam examples
- penicillins - cephalosporins - carbapenems - monobactams
27
gram negative cell envelope
- small peptidoglycan layer - lipopolysaccharide layer (important for gram negatives) - Lipid A
28
LPS layer
- outer membrane of gram negative cell envelope
29
lipid A
- endotoxin | - toxic molecule of LPS
30
gram positive cell envelope
- lots of peptidoglycan | - lipotechoic acid unique to gram positives
31
peptidoglycan
- alternating units of NAG and NAM
32
what do beta lactams inhibit?
- transpeptidation
33
peptidoglycan amino acids
- D-Ala-D-Ala | - this what penicillin targets
34
penicillin binding proteins
- have the transpeptidase activity | - may also have the transglycosylation activity to put sugar backbone together
35
structural basis of beta lactams
- 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
36
Classes of B lactams
- penicillin | - cephalosporins
37
antibiotic resistance mechanisms
- enzymatically inactivate drug - alter drug target - alter drug exposure
38
enzymatically inactivate drug
- beta lactamases | - often on mobile genetic elements
39
alter drug target
- mutation | - can occur via horizontal exchange
40
alter drug exposure
- decreased uptake (gram negatives) | - increased efflux
41
how do gram negatives have decreased uptake?
- they can change the size of their pores to allow nutrients to get in - exclude drugs because they are bigger
42
beta lactamases
- break bond in beta lactam ring of penicillin | - disables molecule
43
types of beta lactamases
- ESBL | - metal dependent (NDM-1)
44
ESBL
- mostly derived from active site mutations in TEM/SHV | - results in activity against extended spectrum cephalosporins
45
clavulanic acid
- resistance to cleavage by beta lactamases | - will deactivate beta lactamase
46
alternative penicillin resistant PBP
- have low affinity for B-lactams but retain transpeptidase activity - can arise through mutation (gonorrhea) - can be acquired horizontally (MRSA)
47
fitness cost of antibiotic resistance
- it costs the bacteria something to become resistance to antibiotic - won't grow as well as the susceptible drug
48
rationale for understanding mechanisms of resistance
- choose antibiotics with higher fitness cost for resistance
49
altered penicillin transport
- decreased membrane permeability | - increased efflux
50
altered penicillin transport decreased membrane permeability
- only relevant for gram negatives | - can arise via spontaneous mutations in porin genes
51
altered penicillin transport increased efflux
- horizontal acquisition of new pump | - mutation that alters specificity or expression
52
multiple mechanisms of resistance
- higher levels of resistance
53
multiple mechanisms of resistance examples
- alterations in porin (gram -) - alternations in PBPs - production of beta lactamases - over expression of efflux pump
54
glycopeptide example
- vancomycin | - for gram positives
55
what do glycopeptides do?
- inhibit transglycosylation of peptidoglycan | - binds to D-ala-D-ala and blocks incorporation
56
vancomycin resistance mechanisms
- synthesis of D-ala-D-lac precursors that cannot bind vancomycin
57
bacitracin
- inhibits regeneration of PG lipid carrier
58
phosphomycin
- prevents attachment of NAG to NAM
59
cycloserine
- prevents attachment of peptide to NAM
60
mycobacterium species
- have mycolic acid - and arabinogalactan - acid fast stain
61
agents that work on mycobacterial species
- isoniazid | - ethambutol
62
isoniazid
- inhibits mycolic acid synthesis
63
ethambutol
- inhibits arabinotransferases
64
lipopeptides MOA
- 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
lipopeptides example
- daptomycin
66
why don't we use lipopeptides to treat pneumonia
- surfactant is coated in phosphatidylglycerol | - not good because lipopeptides break holes in this
67
bacterial folate synthesis inhibitors
- sulfonamides - trimethoprim - humans don't synthesize their own folate. - bacteria do
68
sulfonamides
- bacteriostatic on their own - generally included trimethoprim - sulfamethoxazole
69
resistance to sulfonamides altered drug target
- spontaneous mutation of dhps | - horizontal acquisition of alternate DHPS
70
resistance to sulfonamides swamp the system
- increased production of folate precursor PABA
71
resistance to sulfonamides altered drug exposure
- decreased uptake
72
combinatorial synergy
- lower amount of each drug we need to use and get same outcome - each drug works better in presence of the other drug
73
trimethoprim
- bactericidal | - inhibits dihydrofolate reductase
74
Tmp/Smx
- synergistic combination | - smx becomes bactericidal with combined with tmp
75
quinolones/fluoroquinolones
- inhibit DNA gyrase (topo II and topo IV) - bactericidal - work best against gram negatives
76
quinolones/fluoroquinolones example
- ciprofloxacin
77
role of topoisomerase IV
- separates newly replicated chromosomes into daughter cells
78
problem with cipro
- may rupture tendons
79
resistance of quinolones altered drug target
- chromosomal mutation in gyrase and topoisomerase genes
80
resistance of quinolones altered drug exposure
- 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
rifamycins
- inhibit DNA synthesis | - can be bactericidal or static dependent on concentration
82
rifamycins MOA
- bind to bacterial DdRp with higher affinity than for human enzyme
83
rifamycins example
- rifampin | - mostly used for mycobacterium or meningococcal
84
resistance to monotherapy
- spontaneous mutations in RNA pol gene | - rarely used as mono therapy
85
nitroimidazole use
- bactericidal | - anaerobic microbes
86
nitroimidazole type of drug
- pro-drug - must be converted by microbial enzyme to active form
87
nitroimidazole MOA
- active drug forms toxic free radicals that damage DNA
88
nitroimidazole example
- metronidazole
89
resistance to nitroimidazole
- failture to enzymatically activate drug | - mutations in enzymes that convert the prodrug to the active compound.
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