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Pharmacology > Part 2: Antimicrobials (Cell wall inhibitors) > Flashcards

Part 2: Antimicrobials (Cell wall inhibitors) Flashcards

1
Q

why is the peptidoglycan layer on bacteria cells a druggable target?

A

our cells dont have it

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2
Q

penicillins and cephalosporins are both ___ type antibiotics

A

beta-lactam

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3
Q

vancomycin is a ___ type antibiotic

A

glycopeptide

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4
Q

beta-lactam and glycopeptide antibiotics target pathways involved in ____

A

making the rigid cell wall

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5
Q

what happens to the bacteria when its cell wall is not properly formed?

A

get leaky, fill up with fluid and burst

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6
Q

what is the most common glycopeptide antibiotic?

A

vancomycin

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7
Q

which gram stain has the thick peptidogylcan layer?

A

+

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8
Q

the cell wall of gram neg contains _____ that selectively allow molecules to enter the cell

A

pores

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9
Q

t/f gram - still have a peptidoglycan layer, but it is thinner and surrounded by the outer envelope

A

t

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10
Q

within the inner membrane of a gram - bacteria there are ___ that assemble the cell wall

A

enzymes

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11
Q

the peptidogylcan layer of G- is between what other 2 layers?

A
  1. outer envelope

2. inner cytoplasmic layer

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12
Q

what is the role of bacterial transpeptidase?

A

one of the enzymes that crosslinks peptide subunits together to make the cell wall

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13
Q

Penicillin binds to and inactivates the ____ enzyme

A

transpeptidase

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14
Q

transpeptidase may also be called ___

A

penicillin binding protein (PBP)

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15
Q

in order for penicillins to be effective, they must get to the transpeptidases in the ___ layer

A

cytoplasmic

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16
Q

t/f to enter a gram - cell, penicillins must be transported in by ___

A

the membrane pores

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17
Q

why are many penicillins only useful for gram +?

A

many are unable to cross the membrane of G-

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18
Q

t/f some newer beta-lactam drugs facillitate the passage through G- pores

A

true

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19
Q

what is the function of transglycosylase?

A

links sugar groups together

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20
Q

what is the peptidoglycan wall made of?

A

cross-linked glycopeptides (sugars & aminoacids)

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21
Q

to make the peptidoglycan cell wall, the bacteria builds gylcopeptides in the ___ and shuttles them into the ____ space

A

cytoplasm; periplasmic space

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22
Q

what will happen to a G+ cell if we inhibit transpeptidase?

A

aminoacid cross-linking cannot occur and the wall will be weak

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23
Q

Beta-lactams bind to transpeptidase in what way?

A

covalently (irreversibly)

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24
Q

what part of the beta-lactam antibiotics binds to the transpeptidase?

A

beta-lactam 4 membered ring

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25
Q

what makes the beta-lactam ring reactive?

A

strain of small ring

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26
Q

what happens to the beta-lactam ring when it reacts with the transpeptidase?

A

it opens, relieving strain

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27
Q

what is the main difference between penicillins and cephalosporins?

A

the second ring; cephalosporins have a 6 C ring, penicillins have a 5 C ring

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28
Q

which are more stable, penicillins or cephalosproins? why?

A

cephalosporins bc the 6C ring is more stable than the 5C ring of penicillins

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29
Q

which is more reactive, penicillins or cephalosporins? why?

A

penicillins; 5C ring

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30
Q

bc penicillin is so reactive, what is it at risk of?

A

breakdown (ex: by reacting in the stomach with an H)

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31
Q

if the beta-lactam ring is opened before it reaches the transpeptidase, what happens to it?

A

its now inactive

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32
Q

t/f cephalosporins are less susceptible to inactivation at non-targets

A

t

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33
Q

what environment may cause a penicillin to inactivate

A

acidic stomach

34
Q

some bacteria exhibit ____ enzymes that are able to break the beta lactam ring to inactivate them

A

beta lactamases

35
Q

t/f cephalosporins are less susceptible to beta lactamases

A

true

36
Q

what structural part of beta-lactam antibiotics influences the liklihood of being inactivated by a beta-lactamase?

A

R groups

37
Q

t/f some changes to the R group of a penicillin can help the stability in the stomach

A

t

38
Q

t/f some of the changes to the R groups on penicillins can impact activity on different bacteria

A

t

39
Q

what are the 2 oldest penicilins used clinically?

A

G and V

40
Q

what is the function of the R group on Pen V?

A

makes it more stable in the acidic environment of the stomach

41
Q

Pen V is given as what doasge form?

A

oral

42
Q

Pen G is given as what dosage form?

A

IM or IV

43
Q

Pen G and Pen V have ___ spectrum and are active against ___

A

narrow; subset of G+

44
Q

t/f Pen V and Pen G are easily broken down by beta-lactamases

A

t

45
Q

ampicillin and amoxicillin have R groups that do what?

A
  1. make more stable in acidic environemnt

2. extend activity to some G-

46
Q

ampicillin and amoxicillin are ____ spectrum

A

extended

47
Q

how do the R groups of ampicillin and amoxicillin allow them to act against some G-?

A

facillitate crossing the pores

48
Q

t/f ampicillin and amoxicillin are still susceptible to beta-lactamases inside the bacteria

A

true

49
Q

what is the purpose of adding clavulanic acid with beta-lactam antibiotics?

A

beta-lactamase inhibitor

50
Q

how does clavulanic acid inactive beta-lactamases?

A

they also have a B-lactam ring, so B-lactamases target them rather than the antibiotic (and bind covalently, so enzyme cant be used again)

51
Q

does clavulanic acid have any antibiotic activity on its own?

A

no; bc it does not bind to transpeptidase

52
Q

cephalosporins are separated into “generations” based on what 2 factors?

A
  1. time of development

2. R group modifications that give different spectrums of activity

53
Q

cephalexin is a ___ gen cephalosporin

A

1st

54
Q

__ generation cephalosporins are similar to penicillins

A

1st

55
Q

1st generation ceph. are active primarily against Gram ___

A

+

56
Q

are 1st gen ceph. susceptible to beta-lactamses?

A

yes

57
Q

as the generations of ceph. get higher, the R groups have made these drugs ____ (more or less) active against G-

A

more

58
Q

how do the R groups of gen 2-4 ceph make them able to target some G-?

A

makes them able to cross the outer envelope

59
Q

are gen 2-4 ceph less susceptible to beta lactamases?

A

yes

60
Q

ceftazidime is a ___ generation ceph.

A

3rd

61
Q

3rd gen ceph are ____ spectrum

A

broad

62
Q

which gen of ceph are typically used empirically?

A

3rd

63
Q

cefuroxime is a ___ ge ceph and is mostly active against ___

A

2nd; G+, some G-

64
Q

cefepime is a ___ gen ceph. and active against__

A

4th; mostly G-, some G+

65
Q

what makes antibiotics generally very safe with low risk of ADRs?

A

they act on non-human targets

66
Q

penicillin allergy is mediated by IG__

A

E

67
Q

t/f there can be cross-allergies between penicillins and cephaolosporins

A

t

68
Q

if someone is allergic to penicillin, is it certain that they will be allergic to cephalosporins?

A

no

69
Q

t/f in some extraordinary circumstances, desensitization therapy can be given to reduce penicillin allergies

A

t

70
Q

vacomycin acts by preventing the ___ of peptidoglycan by binding to the ___

A

cross-linking; bacterial peptide chain

71
Q

vancomycin has a large structure, which part is most importnat?

A

peptide chain region in the middle

72
Q

the peptide backbone of vancomycin forms ___ bonds with the bacerial peptide chains of peptidoglycan subunitis

A

H

73
Q

which bacterial peptide does the peptide backbone of vancomycin bind to?

A

D-Ala-D-Ala

74
Q

how does vancomycin prevent transpeptidases from bringing bacterial peptide togther and linking them?

A

H bond to peptide back bone make the rest of the vancomycin molecule folds over the bacterial peptide

75
Q

how can bacteria make themselves resistant to vancomycin?

A

replace one of the 2 alanines that bind to vanco into a lactate, meaning only 4 H bonds rather than 5 can be made to vanco, so the interaction is much weaker, allowing transpeptidase to still be able to link the peptide into the wall

76
Q

the loss of 1 H bond due to vancomycin resistance makes the drug ____x weaker

A

1000

77
Q

is vancomycin resistance very common?

A

not really; but moreso in hospitals

78
Q

what is a disadvantage of the large size of vancomycin?

A

too large to fit through pores of G-

79
Q

how must vancomycin be given to treat systemic infections? why?

A

IV; it is too big to get absorbed from the GI tract

80
Q

in what situation would vancomycin be given orally?

A

to treat a GI infection, like C. dif (can give high dose to target, because it wont be absorbed systemically)

Pharmacology (49 decks)

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