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D&D Infectious Disease Midterm > Pharm - Glycopeptides & MISC > Flashcards

Pharm - Glycopeptides & MISC Flashcards

1
Q

name 3 glycopeptide antibiotics

A

vancomycin
telavancin
dalbavancin

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2
Q

just from looking at the structure of glycopeptides, what can you say about their activity

A

they are very bulky - cannot cross the membrane and not given orally - given by IV.
also, so many peptide bonds - will be very susceptible to rapid hydrolysis if given orally.

also, active for GRAM POSITIVE bacteria bc for gram negative they must cross a membrane to get to the cell wall, but not for +

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3
Q

explain the MOA of vancomycin

A

binds D-ala D-ala to prevent transglycosylation and transpeptidation

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4
Q

true or false

unlike B lactams, vancomycin does NOT structurally mimic D-ala D-ala

A

true

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5
Q

through which bonds does vancomycin bond D-ala D-ala

A

FIVE HYDROGEN BONDS

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6
Q

name and explain 2 methods of vancomycin resistance

A

Van-A: vancomycin resistant staph aureus. happens when D-Ala-D-Ala is converted to D-Ala-D-LACTATE. This decreases the number of hydrogen bonds formed from 5->4 which reducess binding by more than 100 fold

Van B: The cell wall is thickened with INCREASED NUMBERS of D-Ala-D-Ala residues - serve as dead end binding sites for vanco. Vancomycin-intermediate resistance strains of staph aureus

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7
Q

differentiate and explain the significance of the MIC of Van-A resistance vs Van-B resistance

A

Van-A: MIC is greater than 16mcg/mL

Van-B: MIC is between 4-8mcg/mL

therefore, Van-A resistance is much more significant

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8
Q

intermediate vancomycin resistance is due to……

A

too many D-Ala-D-Ala on thickened cell wall – serves as dead end targets for vanco

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9
Q

vanco is a _______ dependent _____ agent

A

time dependent bactericidal

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10
Q

explain the antimicrobial spectrum of vancomycin

A

GRAM POSITIVE BACTERIA, staph producing b lactamases, and for many gram positive anaerobes like C DIFF

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11
Q

vancomycin is synergistic in vivo with…..

A

gentamicin and streptomycin (aminoglycosides)

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12
Q

name some clinical uses for vanco

A

pneumonia treatment for MRSA

C diff

osteomyelitis, endocarditis, SSTI, bone/joint infections

CNS inf like community aquired meningitis

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13
Q

when is the only time vanco is given orally?
explain why

A

for C difficile

bc the bacteria is in the intestines. while most of the drug will be destroyed, whatever is left can kill the c diff in the intestines

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14
Q

vanco is administered by ______ for serious infections

A

IV infusion

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15
Q

true or false

vanco is widely distributed

A

TRUE

gets to CSF - can treat meningitis

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16
Q

how is vanco mainly excreted

A

through KIDNEYS - watch renal function

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17
Q

vanco has clinically relevant __________

A

PAE (post antibiotic effect)
can be 2-6.5 hrs

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18
Q

important consideration when giving vanco

A

serum concentrations should be monitored

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19
Q

name some AE of vanco

A

ototoxicity (ear) and nephrotoxicity (kidney)

also infusion reactions like flushing (redness) bc of histamine

GIVE SLOWLY, AND GIVE ANTIHISTAMINES

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20
Q

differentiate between the structures of vancomycin and telavancin and what this means about telavancin’s activity

A

telavancin is a LIPOglycopeptide - not just a glycopeptide

therefore, it has the same MOA as vanco (D-Ala-D-ala binding) + an additional mechanism of disrupting the bacterial cell membrane potential by increasing its permeability

its lipophilic portion allows it to interact with the membrane

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21
Q

disadvantage of telavancin vs vancomycin

A

telavancin is teratogenic and not used in pregnant women

(not a concern for vanco)

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22
Q

dalbavancin and oritavancin MOA

A

also a lipoglycopeptide

has THREE MOAs

  1. bind D-Ala-D-Ala
  2. Bind membrane to affect potential and permeability
  3. INHIBIT RNA SYNTHESIS!!!
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23
Q

ADVANTAGE of dalbivancin and oritavancin over vanco

A

does NOT require dose adjustment based on renal or hepatic impairment

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24
Q

spectrum of telavancin

A

gram positive bacteria

active against many strains with reduced susceptibility to vanco

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25
Q

telavancin is a ____ derivative of vancomycin

A

semisynthetic

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26
Q

dalbavancin and oritavancin are NOT used for ________ infections

A

VRE

(vanco resistant enterococci)

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27
Q

briefly explain structure of daptomycin

A

cyclic lipopeptide

does NOT contain sugar

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28
Q

why is daptomycin clinically important

A

can be used for vanco resistant strains

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29
Q

daptomycin has _________- dependent ________- activity

A

concentration dependent bactericidal

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30
Q

explain the MOA of daptomycin

A

it’s a surfactant - has hydrophilic head and hydrophobic tail

CALCIUM DEPENDENT - binds to membrane of bacteria and forms a PORE - which causes removal of electrolytes and ultimate death of the bacteria

31
Q

explain how daptomycin resistance can happen

A

by mutations in the mprF gene that regulates the cell membrane charge

32
Q

what kind of bacteria is dapto used for

A

ALL GRAM POSITIVE

cant get thru membrane of negative

33
Q

explain the spectrum of vanco vs dapto

A

similar, but dapto is active against vanco-resistant dtrains of staph aureus and enterococci

34
Q

name something daptomycin CANNOT be used for and why

A

CAP (community acquired pneumonia)

bc the alveoli make their own surfactant which neutralizes dapto (a surfactant)

35
Q

how is daptomycin administered

A

IV route

36
Q

name some AE of daptomycin

A

damage to MUSCULOSKELETAL SYSTEM – rhabdomyolysis, esp when combined with statins or aminoglycosides

also risk of nephro and hepatic toxicity

37
Q

just by the name “fosfomycin” what can you say about the structure

A

contains a phosphate group

38
Q

what structure does fosfomycin mimic

A

phosphoenol pyruvate (PEP)

39
Q

explain the mechanism of fosfomycin

A

acts on sugar polymerization of the bacterial cell wall

NORMALLY:

PEP + NAG, through enolpyruvate transferase, will form UDP-NAM which forms NAM

NAM is essential sugar for the bacterial cell wall. not enough sugars = not good cell wall

fosfomycin inhibits enolpyruvate transferase (by mimicing PEP), the enzyme that produces NAM

40
Q

what is the spectrum of fosfomycin and how is it able to do this

A

both gram (+) and (-)!!!!

because unlike vanco and its derivatives - it’s a very small molecule - able to get through the membrane of gram (-) into where the sugars are being synthesized for the cell wall

41
Q

how can resistance to fosfomycin happen

A

normally, the drug is transported in by glycerophosphate or glucose-6-phosphate transport system.

if mutation in these transporters, not enough of the drug will get into the cell

42
Q

fosfomycin has narrow or broad spectrum

A

broas - both gram pos and neg

43
Q

is fosfomycin cidal or static

A

cidal

44
Q

2 main uses fosfomycin

A

-uncomplicated UTI in women

-abdominal infections

45
Q

main AE of fosfomycin and why

A

c diff diarrhea

bc it’s broad spectrum - kills lot of good bacteria and c diff can take over

46
Q

fosfomycin has synergy with what 3 other antibiotics

A

beta lactams
aminoglycosides
fluoroquinolones

47
Q

explain the MOA of bacitracin

A

interferes with the lipid carrier system of bacteria

normally, the lipid carrier carries peptidoglycan subunits from within the bacteria and goes up to the membrane to deliver the units

in order for the carrier to go ack down and get more “building blocks”, it must be dephosphorylated. however, bacitracin prevents this dephosphorylation by binding.

therefore, the carrier can’t get back in to get more subunits for the cell wall and the bacteria can’t survive

48
Q

why is bacitracin not used systemically

A

not well absorbed and also highly nephrotoxic

49
Q

only time bacitracin is used orally

A

for c diff diarrhea

50
Q

what is bacitracin used for

A

used topically for surface lesions of the skin - on wounds or on mucous membranes

51
Q

preparations of bacitracin

A

can have neomycin and polymyxin as topical OTC product

52
Q

polymyxin MOA

A

interacts with phospholipids - disrupts the structure of bacterial cell membrane.
binds lipid A portion of LPS (endotoxin) on the outer layer of gram (-) bacteria and inactivates it

53
Q

resistance to polymyxin

A

some bacteria way prevent access to their cell wall

54
Q

spectrum of polymyxin

A

gram (-) bacteria (binds LPS!)

lot of nosocomial infection coverage like pseudomonas

55
Q

name 3 things in polymyxin group of antibiotics

A

polymyxin B (parenteral)
colistin (topical and oral)
colistimethate (oral)

56
Q

chemically, what do the polymyxins look like and what does this say about their activity

A

cationic detergents - like surfactants - have head and tail = therefore, must interact with membrane

57
Q

true or false

polymyxin is NOT well absorbed orally

A

TRUE

given parenterally

only given oral for c diff diarrhea

58
Q

AE polymyxin

A

nephrotixicity (renally excreted also - need adjustment)

neuromuscular blockade - muscular weakness

59
Q

systemic uses of the polymyxins

A

for multi-drug resistant gram negative organisms

used systemically as like a last resort

60
Q

name of the polymyxin used topically otic and ophthalmic

A

polymyxin B sulfate

61
Q

chemically, what is fidaxomicin

A

a macrolide

62
Q

true or false

fidaxomide is NOT a cell wall synthesis inhibitor

A

TRUE

63
Q

uses of fidaxomicin

A

bactericidal against c diff

64
Q

MOA fidaxomicin

A

bactericidal

inhibits RNA synthesis by RNA polymerases

65
Q

true or false

fidaxomicin is bacteriostatic

A

false - bactericidal

66
Q

fidaxomicin has broad or narrow spectrum

A

narrow

67
Q

how does resistance to fidaxomicin happen

A

mutations in bacterial RNA polymerase

68
Q

only treatment fidaxomicin

A

clostridium difficile associated diarrhea

69
Q

MOA bezlotoxumab and clinical use

how can you remember

A

bezloTOXumab

binds to the toxin B or c. diff — NOT C DIFF ITSELF

by binding toxin, reduces the recurrence of C diff infection. NOT USED TO TREAT C DIFF AND NOT AN ANTIBIOTIC

only used in conjunction with AB to treat c diff infection

70
Q

how is bezlotoxumab administered

A

IV infusion over 60 mins (SLOWLY)

71
Q

AE of bezlotoxumab

A

incidence of heart failure in CHF patients and potential for immunogenecity

72
Q

bacterial target of vanco*****

A

a dipeptide

D-ala-D-ala

73
Q
A

D&D Infectious Disease Midterm (26 decks)

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