Antimicrobials Flashcards

1
Q

What is the structure of beta lactam?

A

beta-lactam ring
looks like a house with a garage

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2
Q

What is a common antibiotic used that has the beta-lactam structure?

A

phenoxymethyl penicillin (pen v)

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3
Q

What are families of antimicrobials that have a beta-lactam ring?

A

penicilins
cephaloporins
carbapenems
monobactams

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4
Q

What are types of penicillins and what are examples of each?

A

natural - pen V

aminopenicilin - amoxicilin

penicilinase resistant - flucloxacilin (meticilin)

extended spectrum - piperacilin

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5
Q

How do the beta-lactams work?

A

by interfering with penicilin binding proteins (PBP) on bacteria which are responsible for cross-linked structure of peptidoglycan cell wall

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6
Q

What did bacteria evolve to develop against beta-lactams?

A

enzymes called beta-lactamases

very common in gram negative bacteria (provotella and fusobacterium)

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7
Q

What is a example of beta-lactamase inhibitor and how does is work?

A

block active site of bacteria beta-lactmase

clavulanic acid

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8
Q

How do bacteria overcome beta-lactmase inhibitors?

A

produce lots and lots of beta-lactmase to overwhelm the inhibiors

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9
Q

What is an esbl infection and how did it arise?

A

extended spectrum beta lactamase infection

from extended spectrum antibiotics that created a resistant extended spectrum beta lactamase

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10
Q

How is a ESBL infection treated?

A

carbapenems

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11
Q

What is the new class of beta-lactam antibiotics?

A

carbapenems

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12
Q

What bacteria developed after carbapenems?

A

carbapenmase producing bacteria

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13
Q

What is an example of a bacteria that produces carbapenemase?

A

carbapenemase producing enterobactericeae ( CPE)

rectal swab for screening

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14
Q

What types of infection do CPE/CRE cause?

A

Pneumonia
UTI
Wound infections
Bacteraemia

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15
Q

Why are CPE’s important to control?

A
  1. They can be efficiently transmitted in healthcare facilities
  2. Plasmids can transfer Resistance to other strains and species
  3. Often the last resort for treating multidrug-resistant (MDR) infections.
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16
Q

What do macrolides (erythromycin, clarithromycin) and lincosamides (clindmycin) inhibit?

A

inhibit 50S subunit of protein synthesis

17
Q

What do tetracyclines inhibit?

A

inhibit 30S sub unit of protein sythesis

18
Q

Wha does metronidazole inhibit and create?

A

inhibit nucleic acid synthesis or function

creates free radicals

19
Q

What kind of bacteria does metronidazole kill?

what are examples?

A

strict anaerobes
(anerobic streptococci, prevotella)

20
Q

What enzyme does metronidazole use?

A

pyruvate ferredoxin oxido reductase (PFOR)

21
Q

What type of ring is the chemical structure of metronidazole?

A

imidazole with nitro group

22
Q

What gene helps bateria bypass metronidazole and how does it work?

A

nim gene
adds two electrons and hydrogen metronidazole making it inactive

23
Q

What antibiotic is used most in dentistry?

A

metronidazole

24
Q

What did the governement change as first line antibiotic for dentoalveolar infections?

A

from amoxicillin to pen V

25
Q

What is the minimum inhibitory concentration?

A

minimum concentration of antibiotic required to inhibit the bacteria

26
Q

What is an example of an automated susceptibility testing system?

A

VITEK

27
Q

What is a breakpoint?

A

chosen concentration (mg/L) of an antibiotic which defines whether a species of bacteria is susceptible or resistant to the antibiotic

28
Q

What is clinical resistance?

A

when infection is highly unlikely to respond even to max does of antibiotic

29
Q

What are the areas of confounding variables found in clinical that affect resistance?

A

co-morbidities
pus collections
foreign bodies
biofilm
site of infection

30
Q

What is S in EUCAST defined as?

A

susceptible standard dosing regime
when there is a high likelihood of therapeutic success using a standard dosing regimen of the agent

31
Q

What is I in EUCAST defined as?

A

susceptible increased exposure
when there is a high likelihood of therapeutic success because exposure to the agent is increased by adjusting the dosing regimen or by it’s concentration at the site of infection

32
Q

What is R in EUCAST defined as?

A

high likelihood of therapeutic failure even when there is increased exposure (not just numbers, pus mode of administration etc)

33
Q

What are pharmacokinetics?

A

the absorption, distribution and elimination of drug
affected by physiological factors (site of injection)
drug factors (protein binding)

34
Q

What are pharmacodynamics?

A

relationship between concentration of drug and the antimicrobial efffect

35
Q

What is the killing effect of beta lactams dependent on?

A

time above the minimum inhibitory concentration (MIC)

36
Q

Which is better, Pen V or amoxicillin and why?

A

amoxicillin possesses the same spectrum as Pen V (against oral strep, anaerobes, and selected gram negative cocci)

plus

more active against gram negative cocci and members of the family enterobacteriaceae

37
Q

What is angiosus streptococci sensitive to?

A

both pen v and amoxicillin

38
Q

What do antimicrobial agents do to the ecological balance?

A

disturb the balance between the host and normal microflora

39
Q

Why is amoxicillin not used anymore?

A

amoxicillin has a broader spectrum of activity than peniciliin V, it has a greater impaact on selection of resistance in the host microflora

not needed