Antibiotics 1 Flashcards

1
Q

Cell wall of bacteria is made up of…

A

Peptidoglycan

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2
Q

Macromolecule composed of peptides and sugars that provide a rigid support structure only found in bacteria

A

Peptidoglycan

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3
Q

Lipopolysaccharide (LPS)
Makes up which membrane?
Which kind of bacteria?
Consists of (2)?

A

Makes up the outer membrane of gram (-) bacteria cell wall and consists of phospholipids and polysaccharides

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4
Q

4 features of gram (-) bacteria that influence antibiotics

A

LPS
Lipid Bilayer
Hydrophilic pores
Nutrient receptors

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5
Q

How does LPS inhibit antibiotics?

A

Retards or prevents penetration of bulky, high MW antibiotics such as erythromycin

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6
Q

How does the lipid bilayer inhibit antibiotic action?

A

Penetration of water-soluble drugs is severely hindered

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7
Q

How do hydrophilic pores influence antibiotic action?

A

The pores actually allow penetration of water-soluble molecules up to 650 Daltons (like sulfonamides) but that’s it…nothing bigger

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8
Q

3 factors of gram + bacteria that influence antibiotic action

A

Teichoic and teichuronic acid
Lipid bilayer of cytoplasmic membrane
Nutrient transporters

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9
Q

How do teichoic and teichuronic acid influence antibiotics on gram + bacteria?

A

The strong anionic action affects rate of penetrations. They literally repel drugs with negative charge

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10
Q

How does the bilayer affect antibiotics on gram + bacteria?

A

Same thing…Penetration of water-soluble drugs is inhibited

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11
Q

How does the nutrient transporter work on either bacteria?

A

If a drug is similar to the nutrient normally transported, then it will go through. Otherwise, not so much

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12
Q

Bactericidal

A

Agent that will kill the bacteria. Once the organism is exposed to the drug…it dies…like real quick

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13
Q

Bacteriostatic

A

Agent will inhibit bacterial growth but will not kill it. Therapeutic success is dependent on host defense
If the drug is removed, the bacteria will grow again

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14
Q

Pre-emptive therapy

A

Treatment of high-risk patients that are infected but asymptomatic

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15
Q

Empirical therapy

A

Treatment of symptomatic patient without further testing or confirmation of the organism

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16
Q

Definitive therapy

A

Organism is identifed

17
Q

Suppressive therapy

A

Low does therapy used as secondary prophylaxis

18
Q

6 ways resistance develops

A
  1. Reduced drug entry into organism
  2. Increased drug export from organism
  3. Expression of enzymes by organism that destroy drug
  4. Changes in expression of enzymes that activate the drug (pro-drug)
  5. Impaired drug binding to the original target
  6. Development of new/different pathways what are not inhibited by the drug
19
Q

ESKAPE bacteria

A
Enterococcus facecium
Staph aureus
Klebsiella pneumonia
Acinetobacter baumannii
Psuedomonas aeruginosa
Enterobacter species
20
Q

Daptomycin resistance mechanism

A

Gene mutation of mprF that results in overall increase in net positive charge of inner and outer membranes that repel antibiotics with cationic charge

21
Q

Tetracycline resistance mechanism

A

Overexpression of an efflux pump

22
Q

Metronidazole resistance mechanism

A

Metronidazole needs to be reduced to generate ROS. Mutation in the rdxA gene alters or decreases activation of the drug

23
Q

Streptomycin resistance mechanism

A

Aminoglycoside-modifying enzymes chemically modify the antibiotic and alter the binding of the drug to its target

24
Q

Amoxicillin resistance mechanism

A

Expression of beta-lactamases

25
Q

TMP-SMX resistance mechanism

A

Expression of the drug INSENSITIVE enzymes dihydropteroate synthase and dihydrofolate reductase

26
Q

Vancomycin resistance mechanism

A

Substitution on the peptidoglycan stem so that the agent can no longer bind to its target