Antimicrobials Flashcards

1
Q

beta lactam drugs include

A

include the penicillin and cephalosporin

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2
Q

beta lactam drugs all have a

A

beta lactumn ring

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3
Q

how does the b-lactam drugs worrk.

A

bacteria cell wall is made up peptide bridge that is synthesis by the enzyme penicillin binding proteins. beta latam drugs inhibit this enzyme, therefore the cell wall of the bacteria becomes weak and the cell dies.

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4
Q

in order for the b lactam drugs to work the bacteria must be

A

growing

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5
Q

penicilin binding proteins are responsible for

A

peptidoglycan synthesis

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6
Q

bacteria becomes resistant to b-lactam drugs by release which enzyme

A

beta lactamase

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7
Q

cephalosporin are

A

new penicillin

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8
Q

pencillin are made from these fungi

A

penicillium chrysogenium

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9
Q

penicillin V is more stable then penicillin G because

A

it is more stable in acid

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10
Q

penicillin G

A

natural pencillin, narrow spectum

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11
Q

pencillin G and V are good in treating

A

gram positive bacteria

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12
Q

oxacillin or dicloxicillin

A

narrow range, good absorption, resistant to penicillase.

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13
Q

disadvantage of oxacillin, dicloxacillin

A

expensive

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14
Q

methicillin or nafcillicin

A

not susceptible to penicillase,

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15
Q

disadvantage of methicillin or nafcillin

A

allergies, poor absorption

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16
Q

would you choose methicillin over oxacillin

A

no, methicillin has poor absorption compare to oxacillin

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17
Q

is ampillicin and amoxicillin naroow or broad range?

A

broad range

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18
Q

ampillicin

A

hydrolysis by pencillinase and can cause allergies. they can also work on negative bacteria. and have a fair absorption rate.

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19
Q

examples of extended spectrum penicillins

A

ticarcillin, piperacillin

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20
Q

ticarcillum and pipercillin are

A

good for pseudomas spp but less on the gram positive organisms

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21
Q

Augmentin is an example of a

A

pencillin with a beta lactamase inhibitor.

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22
Q

augmentin is a combination of

A

amoxicillin and clavulanic acid

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23
Q

cephalosporins are derived from

A

acremonium cephalosprium.

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24
Q

what drug canbe given to patients who are allergic to penicillin

A

aztreonam

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25
Q

carbapenems are bata lactams that are resistant to

A

b-lactamse, treat both gm negative and gram positive bacteria

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26
Q

two types of ccarbapenems

A

imipenem and meropenem

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27
Q

imipenem

A

is a member of the carbapenems and is destroy by kidney enzymes and most be administered with a combination that inhibits the enzyme.

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28
Q

monobactam are used

A

aztreonam is an example and is used against enterobacteriaceae.

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29
Q

how does vancomycin work?

A

binds to the terminal amino acids (D- alanine and D-alanyl) of the peptide side chain of NAM molecules that are being assembled to form glycan chains. it therefore blockssynthesis of peptioglycan resulting in weakening of the cell wall.

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30
Q

can vancomycin be used to treat gram negative bacteria

A

no, it does not pass the outer membrane of gram negative bacteria.

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31
Q

how is vancomycin given

A

intravenously

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32
Q

resistanceto vancomycin is due to

A

changes in the peptide side chain of NAM THAT PREVENTS VANCOMYYCIN from binding

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33
Q

vancomycin is produced by

A

nocardia orientalis

34
Q

vancomycin is bactericial or bacterostatic

A

bacteriostatic

35
Q

what are the 4 phenotypes of vancomycin

A

van A, B,C,D

36
Q

which vancomycin phenotypes have the highest resistance?

A

Van A,B,D

37
Q

the fluoroquinolones work by

A

attacking enzymes (topoisomerase) that maintain the supercoiling of closed circular DNA within the bacterial cell.

38
Q

what are the name if the enzymes that the fluoroquinolines attack

A

DNA gyrase and topoisomerase II and IV.[

39
Q

Fluoroquinones are used to treat

A

gram negative and atypical bacteria. mycobacterium tuberculosis and bacillus anthracisfi88h888

40
Q

resistance to FQ

A

altered cell wall, altered sites of DNA gyrase and topoisomerase IV and II, altered cell wall permeablity, expression of active efflux, cross resistance

41
Q

examples of rifamycins

A

rifapentine, rifabutin

42
Q

how does rifamycin work?

A

by binding to RNA polymerase, that initiates transcription.

43
Q

rifamycins are bactericidal or bacteriostatic

A

bactericidal

44
Q

rifamycin are used to treat

A

tuberculosis and Hansen’s disease (leprosy) , gram positive or gram positive

45
Q

the structure of 70s ribosomes are

A

30s ribosomes and 50s ribosomes

46
Q

what type of ribosomes are found in humans?

A

80s ribosomes

47
Q

/the mitochronis has what type of ribsosome

A

70s

48
Q

Aminoglycosides

A

are bactericidal drug that are irreversibly bound to the 30s ribosomal subunit, causing it to distort and malfunction.this blocks the the translation and cause misreading of mRNA by ribosomes that have already pass the initiation step.

49
Q

aminoglycosides are used with and for

A

used with a b LACTAM DRUG and lung infections in cystic fibrosis caused by Pseudomas aeruginosa.

50
Q

which aminoglycoside is too toxic for systemic use?

A

nneomycin

51
Q

is aminoglycosides bactercidal or bacterostatic?

A

bacteriostatic

52
Q

disadvantgae of tetracycline?

A

teeth discoloration in children

53
Q

tetracyclines work how?

A

binds reversibly to the 30 subunit, blocking the attachment of tRNA to the ribosome and preventing the continuation of protein synthesis.

54
Q

tetracyclines are used to treat?

A

gram pos, gram neg, atypical, anerobes

55
Q

macrolides work by?

A

by binding reversibly to the 50s ribosome.

56
Q

macrolide are bactericidal or bacteriostatic

A

bacteriostatic

57
Q

macrolide are used to treat

A

atypical pneumonia and gram positive

58
Q

macrolides are used as alternative when a patient is allergic to

A

pencillicin

59
Q

which species of bacteria does the marcolide not work on?

A

enterobacteriacae

60
Q

examples of marcolides

A

erythromycin, clarithromycin, azithromycin

61
Q

chloramphenicol works?

A

by binding to 50s ribosomes, preventing peptide bonds from being formied and consequently blocking protein synthesis.

62
Q

chloramphenicol is only used when and why

A

life threatening conditions and it causes aplastic anaemia.

63
Q

lincosamides work by

A

binding to the 50s ribosomal subunit and prevent the continuation of protein synthesis. and inhibts gram positve and negative organisms.

64
Q

lincosamides are primarily used to treat

A

bacteriodes flora

65
Q

oxazolidinones

A

they bind to 50s ribosomes, and interfere with the initation of protein synthesis.

66
Q

what is the first drug in the oxazolidinones

A

linezoid

67
Q

streptogramins

A

quinupristin and dalfopristin are administered together in a new medication called synercid.

68
Q

when are stretogramins used?

A

in the cases when beta lactams and vancomycin are resistat.

69
Q

drugs that bind to the 50 ribsome

A

macrolides
chloramphenicol
lincosamide
oxazolidinones

70
Q

30s ribsomes

A

aminoglycosides
tetracyclines
streptogramins

71
Q

Sulfonamides work by

A

Sulfa drugs are structurally similar to. To paraaminobenzoic acid (PABA) , a substate in the pathway for folic acid biosynthesis, because of these similarities the the enzyme that normally binds to PABA binds to sulfa drugs resulting in competitive binding

72
Q

Sulfadrugs inhibit

A

Gram neg, gram pos , protozoan

73
Q

Resistance to sulfa drugs

A

Acquisition of a plasmid encoded enzyme that has a Lower affinity for the drug.

74
Q

Trimethoprim

A

Inhibits the bacterial enzyme that catalyses a metabolic step following the one inhibited by sulfonamide a.

75
Q

The synergistic effect of trimethoprim and sulfanomide treat

A

Uti

76
Q

Action of polymyxin B

A

Seen in first aid kits, it binds to the membrane of gram negative and alters the permeablity leading to leakage of the cellular components.

77
Q

Disadvantage of polymyxin b

A

Also industal eukaryote cells

78
Q

Daptomycin

A

Inds to the bacterial cytoplasmic membrane resulting in death of the cell by mechanism.

79
Q

Why is it so hard to treat tb?

A

Slow growth, chronic growth, waxy cell

80
Q

Isoniazids work?

A

Inhibits the synthesis of mycolic acids

81
Q

Ethambutol

A

Inhibits the enzyme that are required for synthesis of other mycobacterial cell wall components.