8. Antibiotics Flashcards

1
Q

define antibiotic

A

a substance that is selectively toxic to microorganisms

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2
Q

by what 3 ways can antibiotics be delivered

A

prescription, injection, IV drip

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3
Q

what does penicillin target

A

the peptidoglycan layer found in Gram-positive bacteria, making the cells leaky and fragile

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4
Q

how does gentamicin work, what is a limitation of this

A

inhibits pathways found in human cells

limitation: causes side effects

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5
Q

by what 3 factors can we classify antibiotics

A

chemical structure
spectrum of activity
mode of action

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6
Q

name a beta-lactam antibiotic

A

penicillin

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7
Q

what does bacteriostatic mean

A

agents that prevent the growth of bacteria

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8
Q

what does bactericidal mean

A

agents that kill bacteria

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9
Q

name two differences between bactericidal and bacteriostatic agents

A

bactericidal agents are irreversible, bacteriostatic are reversible

bactericidal agents do not involve the immune system , bacteriostatic agents work with the immune system to prevent growth

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10
Q

name 3 modes of action for antibiotics

A
  • inhibit protein synthesis
  • inhibit cell wall synthesis (penicillin)
  • inhibit pathogen adhesion to host cells
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11
Q

who discovered penicillin

A

Alexander Fleming

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12
Q

what is penicillin’s mode of action

A

bactericidal

- bind to and destroy cell walls by inhibiting cross-link formation = lysis

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13
Q

what can penicillin be used to treat

A

wide spectrum of infections, e.g. chest infections

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14
Q

what can be a side effect of penicillin use

A

allergic reactions

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15
Q

describe resistance to penicillin

A

relatively common:
beta-lactamase in restraint bacteria destroy pencillin’s beta-lactam ring = no effect on bacteria and cell wall formation

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16
Q

why is ampicillin a better beta-lactam antibiotic

A

contains beta lactamase inhibitor = destroy reisstant bacteria, so applicable to a variety of infections

17
Q

what group of antibiotics does gentamicin belong to

A

aminoglycosides

18
Q

how do aminoglycosides work?

A

bactericidal:

- bind to ribosomes preventing protein synthesis

19
Q

name 3 Gram negative bacteria

A

e.coli, pseudomonas, klebsiella

20
Q

name 2 Gram positive bacteria

A

streptococci

staphylococci

21
Q

what do aminoglycosides target

A

mainly Gram-negative bacteria

22
Q

how can aminoglycosides be used to treat Gram positives

A

used in combination with Beta-lactam antibiotics

23
Q

what infection are aminoglycosides commonly used to treat

24
Q

what is a side effect of aminoglycosides

A

hearing loss

25
how are aminoglycosides administered
in IV drip
26
how does resistance emerge in aminoglycosides , give an example
mutations to ribosome binding site, e.g. streptomycin = no longer fits in the binding site
27
how do tetracyclines work
bacteriostatic bind to 30S subunit to prevent rRNA binding to the A site = prevents bacterial protein synthesis
28
what can tetracyclines be used to treat
Gram-positive bacteria | diseases such as lymes disease
29
how are tetracyclines administered, what can inhibit their absorption
administered orally | - absorption inhibited by dairy (bind to calcium forming an insoluble complex)
30
what is a side effect of tetracyclines
photosensitivity to sunlight
31
how have bacteria cells become resistant to tetracycline
efflux resistance genes: | pump tetracycline out of the cell faster than its uptake
32
what are ribosomal protection proteins
tet (M), tet (O) .... bind to ribosome changing its conformation - prevents tetracycline from binding without stopping synthesis
33
what is the effect of the tet (X) gene
produces a cytoplasmic protein that chemically modified tetracycline in the presence of oxygen and NADPH
34
describe MRSA in england
significant decrease in resistant strain, this is due to better cleaning regimes, screening and hand washing practises