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pcol350 final > Sawicki- Antimicrobials > Flashcards

Sawicki- Antimicrobials Flashcards

1
Q

greatest cause of morbidity and mortality worldwide

A

infections from parasitic organisms

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2
Q

therapeutic index (ratio)

A

amount that causes therapeutic effect vs toxic.. LD50/ED50

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3
Q

empirical therapy

A

used when not possible to obtain specimen (broader than therapy based on susceptibility testing or directed at a certain pathogen)

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4
Q

antibiogram

A

result of lab testing for the sensitivity of an isolated bacterial strain to different antibiotics (in vitro sensitivity)- directed therapy

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5
Q

bacteriocidal

A

killed

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6
Q

bacteriostatic

A

prevented from growing

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7
Q

sulfonamides (static or cidal?)

A

static

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8
Q

trimetoprim (static or cidal?)

A

s

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9
Q

chloramphenicol (static or cidal?)

A

s

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10
Q

tetracycline (static or cidal?)

A

s

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11
Q

erythromycin (static or cidal?)

A

s

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12
Q

quinolones (static or cidal?)

A

c

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13
Q

penicillins (static or cidal?)

A

c

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14
Q

cephalosporins (static or cidal?)

A

c

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15
Q

aminoglycosides (static or cidal?)

A

most c

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16
Q

aminoglycosides (static or cidal?)

A

most c

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17
Q

MIC

A

minimum inhibitory concentration: lowest concentration of antimicrobial agent that prevents visible growth after 18-24 hr incubation

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18
Q

MBC

A

minimal bactericidal concentration= minimal concentration of antimicrobial agent that kills 99.9% cells

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19
Q

treatment for areas protected from host immune response, or neutropenic individuals

A

cidal

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20
Q

treatment for uncomplicated infections

A

static

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21
Q

drugs exhibiting concentration dependent kiling

A

kills bacteria faster at higher concentrations: fluoroquinolones and aminoglycosides. Also have a post antibiotic effect (inhibit for several hours after drug concentration falls below MIC in serum. 2 properties= administered less frequently than predicted by half life. Most beta lactams DO NOT have either of these

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22
Q

site of infection influences

A

dose, route, duration and type of antibiotic. Peak concentration at infection site should be at least 4x MIC

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23
Q

route required to treat pleural and pericardial infections

A

parenteral

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24
Q

nephro and otto toxicity

A

aminoglycosides (beta lactams and fluroquinolones are better choice)

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25
Q

allergies common with

A

beta lactams (penicilins) and sulfonamides

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26
Q

tetracyclines and children

A

no- bind to developing teeth and bone

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27
Q

sulfonamides in newborns

A

displace bilirubin from albumin and cause nervous system disorders

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28
Q

age dependent infection

A

bacterial meninjitis

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29
Q

antimicrobial combination: indifferent effect

A

combined effect equals sum of seperate

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30
Q

antimicrobial combination: synergism

A

combined effect is greater than sum of independent activities

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31
Q

antimicrobial combination: antagonistic

A

combination effect is less than could be achieved by using seperately

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32
Q

3 combinations with synergistic effects

A

1) penicillin/ampicillin (inh cell wall synthesis)-allow gent to enter- and gentamycin (aminogycoside that inh protein synthesis) *enterococcal endocarditis
2) act on sequential steps in metabolic pathway (trimethoprim and sulfamethoxazole)
3) claculanate (beta lactamase inh) inh the enzyme that inactivates amoxicillin

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33
Q

intrinsic antibiotic resistance vs acquired

A

acquired: mutation of existing genetic info, acquisition of new genes, exchange of genetic material among bacteria

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34
Q

mechanisms of genetic exchange

A

1) conjugation (physically attach and exhange plasmid DNA)
2) transduction: happens with a virus (bacteriophage) carrying resistance to target bacteria
3) transformation: certain bacteria pick up free DNA from environment

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35
Q

mechanisms of genetic exchange

A

1) conjugation (physically attach and exhange plasmid DNA)
2) transduction: happens with a virus (bacteriophage) carrying resistance to target bacteria
3) transformation: certain bacteria pick up free DNA from environment

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36
Q

4 mechanisms of resistance

A

1) develop altered receptors or targets so drug can’t bind
2) decrease rate of entry or rate of removal (reduce concentration of drug that reaches receptors)
3) enhance destruction or inactivation of drug
4) create resistant metabolic pathways

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37
Q

act by inhibiting cell wall

A

-beta lactams
includes penicillins, beta lactamase inhibitors, cephalosporins,carbapenams, monobactams
-glycopeptides
includes bacitracin and vancomycin

-maximal activity against rapidly dividing bacteria

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38
Q

beta lactams (static or cidal)

A

c

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39
Q

penicillans

A
  • gram positive

- distribute to eye, brain, CSF and prostate low

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40
Q

penicillans

A
  • gram positive

- distribute to eye, brain, CSF and prostate low

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41
Q

cephalosporins

A
  • few enter CSF in sufficient concentration
  • Generations:
    1) don’t enter CSF
    2) better gram neg, retain some gram pos. more resistant to beta lactamase
    3) further increased gram neg, broad spectrum. Decreased gram pos. Enter CSF
    4) extended spectrum, similar gram positive as 1st gen, greater resistance to beta lactamase than 3rd. Many cross BBB and effective in meningitis
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42
Q

cephalosporins

A
  • few enter CSF in sufficient concentration
  • Generations:
    1) don’t enter CSF
    2) better gram neg, retain some gram pos. more resistant to beta lactamase
    3) further increased gram neg, broad spectrum. Decreased gram pos. Enter CSF
    4) extended spectrum, similar gram positive as 1st gen, greater resistance to beta lactamase than 3rd. Many cross BBB and effective in meningitis
43
Q

carbapenams

A

-highly resistant to beta lactamase

44
Q

impenem is given with

A

cilastatin; b/c im is hydrolyzed in mammalian kidney by a dehydropeptidase enzyme, so give dehydropeptidase inh. Im is a carbapenam

45
Q

beta lactam where ring is alone and not fused

A

monobactam (only one available is aztreonam)

46
Q

beta lactam where ring is alone and not fused

A

monobactam (only one available is aztreonam-activity against gram negative, synergistic with aminoglycosides)

47
Q

vancomycin

A

glycopeptide antibiotic

  • IV or oral
  • cell wall inh that doesn’t contain beta lactam nucleus
  • gram positive
  • high resistance therefore *last resort
48
Q

bacitracin

A

glycopeptide antibiotic

  • topical (due to SEs)
  • cell wall inh that doesn’t contain beta lactam nucleus
  • gram positive and some gram neg
49
Q

3 mechanisms of resistance to beta lactams

A

1) destruction by beta lactamase enzymes
2) failure to reach target penicillin binding proteins
3) failure to bind target penicillin binding proteins

50
Q

Ma’s special ox clint-tetra chloroformed a muppet with strep

A

Bind to bacterial ribosomes and interfere with protein synthesis

  • Macrolides
  • spectinomycin
  • oxazolidinones
  • clindamycin
  • tetracyclines
  • chloramphenicol
  • mupirocin
  • streptogramins
51
Q

Ma’s special ox clint-tetra chloroformed a muppet with strep

A

Bind to bacterial ribosomes and interfere with protein synthesis

  • Macrolides
  • spectinomycin
  • oxazolidinones
  • clindamycin
  • aminoglycosides (cidal)
  • tetracyclines
  • chloramphenicol
  • mupirocin (cidal)
  • streptogramins
52
Q

tetracyclines entering cytoplasm

A
  • gram positive (energy dependent)

- gram negative (diffusion through porins)

53
Q

tetracyclines entering cytoplasm

A
  • gram positive (energy dependent)

- gram negative (diffusion through porins)

54
Q

macrolides and statins

A

myopathy

55
Q

aminoglycosides ineffective against

A

anaerobic

56
Q

aminoglycosides administered

A

IV and IM

57
Q

chloramphenicol

A
  • static

- low income countries, rare serious side effect aplastic anemia

58
Q

chloramphenicol

A
  • static

- low income countries, rare serious side effect aplastic anemia

59
Q

3 resistance mechanism to aminoglycosides

A

1) altered ribosomes, relatively uncommon, but in enterococci sometimes
2) inadequate transport across cytoplasmic membrane seen in strict anaerobes, but uncommon in aerobic or facultative
3) enzymatic modification of drug is most common, through phosphorylation/adenylation/acetylation

60
Q

3 resistance mechanisms to tetracyclines

A

1) drug efflux (from a new protein)
2) alteration of outer membrane proteins (mutation in chromosomal genes)
3) ribosomal binding site protected (by plasmid generated protein)

61
Q

3 resistance mechanisms to tetracyclines

A

1) drug efflux (from a new protein)
2) alteration of outer membrane proteins (mutation in chromosomal genes)
3) ribosomal binding site protected (by plasmid generated protein)

62
Q

tetrahydrofolic acid

A

form of folic acid fully reduced, carries 1 C groups

-bacteria synthesize folic acid, humans get from diet

63
Q

sulfonamids and trimethoprim

A

folate antagonists

64
Q

sulfonamides MOA

A

stucutral analogues of PABA and competitively inhibit dihydropteroate s*ynthase and block folate synthesis
-mainly for UTIs (AEs= GI

65
Q

trimethoprim MOA

A

blocks tetrahydrofolate from dihydrofolate by reversible inh of dihydrofolate reductase
-mainly for UTIs (AEs=GI, allergic skin

66
Q

trimethoprim and sulfamethoxazole combo

A

synergistic and gives bactericidal activity (static on own)

67
Q

resistance to sulfonamides

A
  • inhibition by sulfonamides can be reversed by addition of purines, thymidine, methionine and serine
  • widespread
    1) reduced cellular uptake
    2) altered dihydropteroate synthase
    3) production of increased PABA
    4) altered enzyme (can develop during therapy)
68
Q

inhibit or damage bacterial DNA

A

fluoroquinolones (floxacins)

nitrofurans (nitrofurantoine)

69
Q

nitrofurans were widely used but now

A

are banned in canada (mutagenicity and carcinogenicity concern) for treatment of animal from food chain

  • UTIs
  • reduced form highly reactive so resistance based on inhibition of its reductase
70
Q

nitrofurans (static or cidal)

A

cidal

71
Q

do not use in patients with creatinine clearance of 60ml/min or less

A

nitrofurantoin (nitrofuran)

72
Q

fluoroquinolones MOA

A

-bind to enzyme DNA complex and trap DNA synthesis, eventually lethal (possibly by releasing lethal double stand DNA breaks from complex)

73
Q

fluroquinolones resistance

A

1) mutations in DNA topoisomerase (most of them this*)
2) decreased permeability
3) active efflux
4) plasmid mediated resistance

74
Q

fluroquinolones resistance

A

1) mutations in DNA topoisomerase (most of them this*)
2) decreased permeability
3) active efflux
4) plasmid mediated resistance

75
Q

2 drugs used to inhibit synthesis or damage cytoplasmic membrane

A

-polymixin E (colistin) and B

76
Q

polymixins indication

A

IM for pseudomonas aeruginosa and acinetobacter baumannii

  • not well absorbed from GI therefore occasionally for diarrhea
  • use abandoned except in cystic fibrosis because of toxicity (affect human cell membranes too= kidney and neuro tox)
  • cyclic decapeptides
77
Q

polymixins (static or cidal)

A

cidal

78
Q

resistance to polymixins

A

1) cell walls restrict transport

2) elevated concentrations of Ca or Mg reduce activity

79
Q

resistance to polymixins

A

1) cell walls restrict transport

2) elevated concentrations of Ca or Mg reduce activity

80
Q

cause of TB and leprosy

A

actinobacteria (mycobacterium)

-gram pos, aerobic

81
Q

second leading cause of death worldwide

A

TB

  • more than 8 million new cases and 2 million deaths per year
  • can be latent or active pulmonary or extrapulmonary disease
  • long term treatment needed
  • resistance= concern therefore need drug combo
82
Q

therapy for TB

A

direct observed, combo drugs

83
Q

caused by mycobacterium leprae

A
  • leprosy (hansen’s disease)
  • aerobic
  • grows 2-4 years (slow)
  • clinical manifestations depend on immune response
84
Q

therapy for leprosy

A

long term multi drug therapy

85
Q

therapy for TB

A

direct observed, combo/multi drugs (never single due to resistance)

86
Q

therapy for leprosy

A

long term multi drug therapy

  • can give thalidominde–> birth defects
  • WHO gives free treatment for ppl worldwide
87
Q

TB drugs MOA

A
  • classified 1st or 2nd line
    1) inhibit DNA dependent RNA polymerase
    2) inh protein synthesis
    3) inhibit mycolic acid synthesis
    4) affect THF synthesis
    5) disrupt plasma membrane
88
Q

TB drugs MOA

A
  • classified 1st or 2nd line
    1) inhibit DNA dependent RNA polymerase
    2) inh protein synthesis
    3) inhibit mycolic acid synthesis
    4) affect THF synthesis
    5) disrupt plasma membrane
89
Q

isoniazid MOA

A
  • anti TB first line
  • enters by passive diffusion, activated by catalase, attacks multiple targets
  • unique susceptibility of m tuberculosis to it can be from deficient efflux and insufficient metabolism of isoniazid derived radicals (active form)
90
Q

pyrazinamide MOA

A
  • first line anti TB
  • fatty acid synthase and mycobacterial membranes are targets
  • selective defect in POA efflux in M TB gives selectivity to kill M TB not other mycobacteria
91
Q

anti leprosy drugs

A

1) rifampin
2) dapsone
3) clofazimine

92
Q

anti leprosy MOA

A

rifampin- inhibit DNA dependent RNA polumerase

dapsone- inhibit dihydropteroate synthase (like sulfonamides)

93
Q

fungi unique properties

A

different ribosomes, cell wall different components, discrete nuclear membrane

94
Q

capsofungin

A

antifungal

targets cell wall 1-3 beta d glucan

95
Q

target ergosterol (antifungals) (cell membranes)

A

ketoconazole, amphotericin (polyenes), triazoles, terbinafine

96
Q

capsofungin

A

antifungal
targets cell wall 1-3 beta d glucan
IV

97
Q

target ergosterol (antifungals) (cell membranes)

A

ketoconazole, amphotericin (polyenes), triazoles, terbinafine (allylamines)

98
Q

target nuclear division (antifungal)

A

griseofulvin- inhibit mitosis by binding tubulin

99
Q

target nucleic acid synthesis (antifungal)

A

flucytosine- inh DNA synthase

100
Q

antifungal that may intensify or induce subacute cutaneous lupus erythematosus

A

terbinafine

101
Q

most widely used antifungal

A

amphotericin B

  • binds to sterols (ergosterol-which has a higher affinity for polyenes than cholesterol), form channels in membrane, K and Mg leak out
  • polyenes show greater activity against fungal cells than mammalian
102
Q

fungi without ergosterol are not susceptible to

A

amphotericin B or polyenes

103
Q

amphotericin B SEs

A
  • fever as high as 40=initial reaction

- anemia with hematocrit of 22-35% develops with normal use

104
Q

nystatin

A

polyene, minimal SEs, not allergic on skin

pcol350 final (3 decks)

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