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.Pharmacology > Part 3: Antimicrobial Inhibitors of Bacterial Protein Synthesis > Flashcards

Part 3: Antimicrobial Inhibitors of Bacterial Protein Synthesis Flashcards

1
Q

bacteria have ____ ribosomal subunits and humans have ____ ribosomal subunits

A

30S & 50s; 40S & 60S

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2
Q

what are the 3 main classes of protein synthesis inhibitors?

A

tetracyclines, aminoglycosides, macrolides

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3
Q

t/f protein synthesis inhibitors can be bacteriostatic or bactericidal

A

true

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4
Q

besides the 3 main classes, what are 2 other drugs that act by protein synthesis inhibition?

A

clindamycin and chloramphenicol

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5
Q

doxycycline is from the ____ family of antibiotics

A

tetracycline

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6
Q

tetracyclines are ___ spectrum

A

broad

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7
Q

describe the structure of tetracyclines

A

4 fused rings

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8
Q

what part of a tetracycline structure cannot be altered, or activity will be lost?

A

the O2 groups at the top

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9
Q

what part of a tetracycline can be changed without loss of activity

A

R groups along the bottom

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10
Q

altering the R groups of a tetracyline alters the ____ properties

A

pharmacokinetic

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11
Q

tetracyclines bind to the ___ subunit near the ___ site

A

30s ; A

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12
Q

the binding of a tetracyline to a bacterial ribosome prevents ___ from binding, which prevents the elongation of the ___

A

tRNA; bacterial peptide chain

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13
Q

what are 3 mutations that make bacteria more resistant to tetracyclines?

A

mutation in the 30s that reduce drug binding ; efflux pumps; enzymes that break down drug structure

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14
Q

t/f tetracylines are typically inly used to target a specific infection due to the prevalenace of mutations and resistance

A

t

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15
Q

the O2 containing groups along the top of the tetracyline structure bind strongly to ____

A

cations (mg, ca, Fe, Zn)

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16
Q

when tetracylines bind to a cation it is called ___

A

chelation

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17
Q

why is the binding of tetracylines to cations problematic?

A

can bind to calcium in developing teeth and discolour them; if taken with dairy they cant be absorbed very well (too big) so they are less effective

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18
Q

why are tetracylines less of an issue for people with developed teeth?

A

bc as adults the bone matrix os constantly changing, so tetracyline will eventually be replaced

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19
Q

tetracylines can cause an increase sensitivity to ___

A

sunlight

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20
Q

why do tetracylines cause skin rashes and sunburns when patients are exposed to sun?

A

tetracyline accumulates in the skin

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21
Q

gentamicin is an example of a ___ antibiotic

A

aminoglycoside

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22
Q

aminoglycosides bind to the ____subunit

A

30s

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23
Q

how do the aminoglycosides bind to the 30s subunit?

A

covalently (irreversibly)

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24
Q

what is the reason for the long post-antibiotic effect of aminoglycosides?

A

their covalent binding to the 30s subunit

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25
Q

aminoglycosides cause a disruption in the ___ of the ribosome subunit

A

shape

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26
Q

when aminoglycosides cause a shape change in the 30s, what i sthe result?

A

mRNA reading frame becomes distorted, leading to the wrong AA being added to the peptide chain

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27
Q

aminoglycosides also impair the translocation of the peptide, meaning ___

A

the growing chain is not able to move as easily from the A site to the P site b/c of obstruction caused by drug

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28
Q

aminoglycosides cause newly formed bacterial proteins to be ___

A

dysfunctional; or not even made

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29
Q

aminoglycosides binding to the 30s can also impair proper formation of the ribosome complex, which prevents ____

A

initiation of protein synthesis

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30
Q

aminoglycosides are _____ (cidal or static_

A

cidal

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31
Q

aminoglycosides are ____ spectrum

A

broad

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32
Q

aminoglycosides have particularly good activity against Gram ____

A

negative

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33
Q

why do aminoglycosides have good activity against G-?

A

their structure (several linked sugars and amino groups) are substrates for the G- pores

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34
Q

t/f increasing the concentrations of aminoglycosides inside bacterial cells increases the bactericidal effecst

A

true

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35
Q

adding what type of antibiotic with an aminoglycoside would result in significant synergistic effect?

A

cell wall inhibitor like a beta lactam

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36
Q

why would a beta lactam and an aminoglycoside have a synergistic effect?

A

beta lactam breaks down the wall, letting more aminoglycoside in

37
Q

aminoglycosides are not suitable for ____(route) dosing

A

oral

38
Q

why are aminoglycosides given by IV?

A

they have poor oral bioavailability

39
Q

aminoglycosides have ____ dependent bactericidal effects

A

concentratio

40
Q

what are some ADRs of high dose aminoglycosides

A

irreversible hearing loss, damage to the kidneys

41
Q

why are blood levels carefully monitored for patients on IV aminoglycoside?

A

dont want too high dose that would cause aADRs

42
Q

bacterial resistance to aminoglycosides typically occurs by ____

A

bacteria reducing entry or inactivating it in the cytoplasm

43
Q

aminoglycosides can be inactivated by beta lactams if ___

A

they are direltly mixed togther

44
Q

t/f the binding of a beta lactam ring to an aminoglycoside results in the inactivation of both drug

A

t

45
Q

what is the key difference between tetracylines and aminoglycosides?

A

aminoglycosides bind irreversibly

46
Q

macrolides bind to the ____ subunit

A

50s

47
Q

what is the MOA of macrolides?

A

binding to the 50s prevents translocation of growing peptide from A site to P site and it also blocks the peptidlu transferase rxn which links new AA to the growing chain

48
Q

give 3 examples of macrolide antibiotics

A

erythromycin, azithromycin, clairithromycin

49
Q

what was the 1st macrolide used clinically?

A

erythromycin

50
Q

which macrolides are more typically used today? why?

A

clairithromycin and azithromycin bc they have fewer drug interactions

51
Q

what is the characteristic structure of macrolides?

A

the large open ring (macrolide ring)

52
Q

t/f macrolides have several R groups that can be varied to give the diffrent drugs in the family

A

t

53
Q

what is the role of the large macrolide ring?

A

significant interference with the ribosomal complex structure, leading to many dysfunctions

54
Q

binding of macrolides is _____

A

reversible

55
Q

what happens is macrolide concentrations are too low?

A

some protein synthesis can still occur (growth only slowed)

56
Q

at high concentrations of macrolides, the effect can be ___

A

bactericidal

57
Q

macrolides have ____ spectrum

A

broad

58
Q

macrolides are commonly used if a pateint has an allergy to ___

A

beta lactams

59
Q

how does resistance to macrolides typically occur? (3)

A

mutations of the 50s at the binding site; increased efflux; ezymatic breakdown of the ring

60
Q

resistance to macrolides is less common than resistance to ___

A

tetracylines

61
Q

resistance to macrolides is most common in ____ infections

A

oral

62
Q

erythromycin and clairithromycin are known to inhibit host ___ enzymes

A

CYP450; particularly CYP 3A4

63
Q

why is it an issue that erythromycin and clairithromycin inhibit CYP 3A4 enzymes?

A

many drugs are metabolized by this enzyme, so it can lead to toxic build up of other drugs (or too low levels of prodrugs)

64
Q

what is unique about azithromycin?

A

does not impact CYP and has a very long half life, so it can be given as one large daily dose

65
Q

what is the half life of azithromycin?

A

12 hours

66
Q

is azithromycin renally excreted>

A

no

67
Q

clindamycin binds to the ___ subunit

A

50 s

68
Q

clindamycin has some of the same properties as ___ antibiotics

A

macrolide

69
Q

why is clindamycin not a member of the macrolide family?

A

does not have the macrolide ring

70
Q

MOA of clindamycin

A

binds to 50s and prevents bacterial peptide translocation from A to P

71
Q

at doses used clinically, clindamycin is ____ (cidal or static?

A

static

72
Q

the spectrum of activity of clindamycin makes it particularly useful for treating ____ infections

A

oral

73
Q

clindamyin is effective against G____ and. some G____

A

+ and some -

74
Q

t/f clindamycin is effective against some anaerobes

A

true

75
Q

clindamyin may be a drug of choice for those with a ____ allergy

A

penicillin

76
Q

resistance patterns to clindamycin? (3)

A

change binding site, efflux, enzymatic inactivation

77
Q

t/f chloremphenicol is not used much in North America, but still used in other places

A

t

78
Q

chloremphenicol binds to the ___ subunit

A

50s

79
Q

the MOA of chloremphenicol is similar to that of ___

A

macrolides

80
Q

MOA of chloremphenicol

A

bind 50s and prevent bacterial peptide elongation and peptidyl transferase rxn

81
Q

chloremphenicol is a ___ spectrum

A

broad

82
Q

bacterial resistance to chlorempheicol

A

not as commonly, but by enzymes that break down the drug

83
Q

chloramphenicol distributes ___ to the tissues in the body, especially the CNS

A

extensively

84
Q

what is a unique ADR to chloramphenicol?

A

aplastic anemia

85
Q

what is the big deal if chloramphenicol casues aplastic anemia?

A

low levels of WBC can reduce host immune response (counter-productive to the treatment)

86
Q

t/f chloramphenicol has a high rate of metabolism into ___

A

inactive metabolites

87
Q

chloramphenicol inhibits _____, which results in many ___

A

CYP450; drug interactions

88
Q

when might chloramphenicol be used?

A

for very specific cases (meningitis) or if nothing else is available

.Pharmacology (55 decks)

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