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
What is the minimum inhibitory concentration?
minimum concentration of antibiotic required to inhibit the bacteria
26
What is an example of an automated susceptibility testing system?
VITEK
27
What is a breakpoint?
chosen concentration (mg/L) of an antibiotic which defines whether a species of bacteria is susceptible or resistant to the antibiotic
28
What is clinical resistance?
when infection is highly unlikely to respond even to max does of antibiotic
29
What are the areas of confounding variables found in clinical that affect resistance?
co-morbidities pus collections foreign bodies biofilm site of infection
30
What is S in EUCAST defined as?
susceptible standard dosing regime when there is a high likelihood of therapeutic success using a standard dosing regimen of the agent
31
What is I in EUCAST defined as?
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
What is R in EUCAST defined as?
high likelihood of therapeutic failure even when there is increased exposure (not just numbers, pus mode of administration etc)
33
What are pharmacokinetics?
the absorption, distribution and elimination of drug affected by physiological factors (site of injection) drug factors (protein binding)
34
What are pharmacodynamics?
relationship between concentration of drug and the antimicrobial efffect
35
What is the killing effect of beta lactams dependent on?
time above the minimum inhibitory concentration (MIC)
36
Which is better, Pen V or amoxicillin and why?
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
What is angiosus streptococci sensitive to?
both pen v and amoxicillin
38
What do antimicrobial agents do to the ecological balance?
disturb the balance between the host and normal microflora
39
Why is amoxicillin not used anymore?
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