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BDS2 BAMS > antimicrobials > Flashcards

antimicrobials Flashcards

1
Q

which antibiotics’s mechanism of action is inhibiting cell wall synthesis or function?

A

beta lactams

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2
Q

common antibiotics prescribed in dentistry

A

beta lactams group
- penicillin v
- amoxicillin

macrolide group
- clarithromycin

  • metronidazole
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3
Q

is beta lactams penicillin related

A

yes

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4
Q

members of the beta lactam housing tree

A
  1. penicillins
  2. penicillinases resistant
  3. cephalosporins
  4. carbapenems
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5
Q

how do beta lactams work?

A

they work against the peptidoglycan layer in gram positive bacteria

they interfere with penicillin binding proteins which are needed for making the peptidoglycan layer

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6
Q

PBP

A

penicillin binding proteins

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7
Q

what is the name of the enzyme that breaks down beta lactams?

A

beta lactamases (antibiotic resistance)

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8
Q

what micrograms produces beta lactamases

A

prevotella
fusobacteria
mostly gram negative

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9
Q

what is the function of clavulanic acid?

A

beta lactamase inhibitor,

thus protecting the beta lactams from getting broken down before it gets the chance to work

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10
Q

augmentin contains what

A

amoxicillin and clavulanic acid

the clavulanic acid protects amxocillin

little use in dentistry tho

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11
Q

what is ABR?

A

when microorganisms change in ways that render medications used to cure the infections they cause ineffective

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12
Q

basically

antibiotic => penicillin, beta lactams

ABR from bacteria => penicillinases and beta lactamases

A
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13
Q

relevance of klebsiella pneumoniae in dentistry

A

this bacteria is present in ESBL infections

this bacteria is resistant to MANY antibiotics, hard to treat

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14
Q

ESBL full name

A

Extended-spectrum beta-lactamases

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15
Q

how to treat ESBL infections?

A

carbapenems

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16
Q

carbapenems function

A

ultimate beta lactam

they are able to fight against extended spectrum beta lactamases

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17
Q

Enterobacteriaceae structure

A

intestinal bacteria of the small rod family

plasmid encoded

thick capsule

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18
Q

other names of Enterobacteriaceae

A

coliforms
enteric rods

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19
Q

why is it so hard to get rid of Enterobacteriaceae with antibiotics?

A

surrounded by thick capsule that antibiotics have trouble penetrating

they are resistant to very many antibiotics

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20
Q

what enzyme does Enterobacteriaceae produce

A

carbapenemase

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21
Q

CPE

A

carbapenemase producing enterobactericeae

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22
Q

why do we need to worry about CPE?

A
  • carbapenem antibiotics are seen as the last therapeutic option to treat complex infections, and yet CPE can fight these antibiotics, no “higher” antibiotic available
  • transmitted easily in healthcare facilities
  • plasmids can transfer resistance to other strains and species
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23
Q

can we find Enterobacteriaceae in the oral cavity? where else

A

yes, can be carried in the oral cavity

dental relevance also in maxillofacial surgery

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24
Q

how to screen for CPE?

A

rectal swab

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25
Q

what are the CPE protocols for a positive patient in dental hospital?

A

SIPCEPs

26
Q

mode of transmission of CPE

A

pets
travels
household members
food

27
Q

what is the mechanism of action of macrolides and clindamycin?

A

inhibits protein synthesis and inhibits 50S subunit

28
Q

what family does erythromycin and clarithromycin come under

A

macrolide

29
Q

what is the mechanism of action of tetracyclines?

A

inhibit 30S subunit
inhibit protein synthesis

30
Q

what is the mechanism of action of metronidazole?

A

inhibits nucleic acid synthesis or function

creates free radicals which interfere with the structure and function of bacteria dna

PFOR enzyme in anaerobes adds an electron, making metronidazole a reactive anion species that can destroy dna

31
Q

drugs that interferes with 30s subunit on bacteria ribosome?

A

tetracyclines

32
Q

drugs that interferes with 50s subunit on bacteria ribosome?

A

macrolides and clindamycin

33
Q

what is metronidazole effective against?

A

strictly anaerobes

34
Q

which pathogens are strict anaerobes?

A

anerobic streptococci
prevotella species

(can be found in acute dental abscess and perio disease)

35
Q

key system in anaerobes that metronidazole acts on?

A

PFOR system = pyruvate ferredoxin oxido reductase

36
Q

NIM genes

A

nitro imidazole reductases

37
Q

what happens when bacteria gets the NIM genes

A

they add two electrons and hydrogen to metronidazole

so it bypass the PFOR system to render metronidazole inactive

38
Q

why has there been a 17% increase in dental amoxicillin since 2019?

A

penicillin v is now recommended as a first line antibiotics for acute dentoalveolar infections

39
Q

how is resistance defined from a biological perspective?

A

minimum inhibitory concentration MIC

disc diffusion testing

automated susceptibility testing system - vitek

40
Q

disc diffusion testing measures?

A

measures zone of inhibition

41
Q

breakpoint

A

chosen conc of an antibiotic which defines whether a species of bacteria is susceptible or resistant to the antibiotic

42
Q

clinical resistance (EUCAST def)

A

when infection is highly unlikely to respond even to maximum doses of antibiotics

43
Q

MIC

A

minimum inhibitory concentration

44
Q

what are some confounding variables, ie variables that affect how an antibiotics performs?

A
  • co morbidities (can affect metabolism of antibiotics)
  • pus collection (antibiotic cannot penetrate to the center of a pus)
  • foreign bodies
  • site of infection (some AB has poor penetration of bone)`
  • biofilms
45
Q

susceptible vs resistant

A

susceptible = high likelihood of therapeutic success using a standard dosing regimen

resistant = high likelihood of therapeutic failure even when there is increased exposure

46
Q

what does it mean to increase exposure to antibiotics

A

increase dosage

dosing intervals shorter

mode of administration

distribution of antibiotic

interactions with bacteria at site of infection

47
Q

why is pen v recommended over amoxicillin

A

because amxoxicillin is a broader spectrum antibiotics than can disrupt the commensal flora and cause more harm, example c.diff infection or candidasis

48
Q

does pen v or amxoxicillin have better oral absorption

A

amox has a higher peak, better oral absorption

49
Q

why do you need to dose more frequently for pen v?

A

lower peak conc
less time above MIC

50
Q

how to determine the killing effect of beta lactams?

A

killing effect dependent on time ABOVE MIC

51
Q

is beta lactam activity concentration dependent?

A

no

52
Q

is anginosus streptococci sensitive to pen v and amoxicillin?

A

yes!

53
Q

is the choice of antibiotics important in treating dental abscess?

A

all equally as effective once drained,

local surgical interventions more important

54
Q

colonization resistance def

A

Protection against growth of opportunistic microorganism like c diff and candida

55
Q

antimicrobial stewardship

A

limiting unintended consequences of antimicrobial use

56
Q

does antibiotics cure toothache

A

no

57
Q

first line therapy in treating dental abscess

A

pen v

58
Q

recommended dosage for pen v

A

500mg
6h
5 days

59
Q

does giving a larger dose improve success

A

larger doses less frequently improves success

60
Q

effect of antibiotic is dependent on what for success

A

concentration and time

**but rmb that pen v and amoxicillin is not dependent on concentration, only time above the MIC

61
Q

does increasing dose increase efficacy ?

A

increasing dose to achieve higher concentration does NOT increase efficacy once above MIC

62
Q

peak conc of amox and pen v

A

peak conc amox is 7.5ug/ml

peak conc pen v is 4ug/ml

BDS2 BAMS (27 decks)

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