8. Antibiotics Flashcards

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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

A

UTIs

24
Q

what is a side effect of aminoglycosides

A

hearing loss

25
Q

how are aminoglycosides administered

A

in IV drip

26
Q

how does resistance emerge in aminoglycosides , give an example

A

mutations to ribosome binding site, e.g. streptomycin = no longer fits in the binding site

27
Q

how do tetracyclines work

A

bacteriostatic
bind to 30S subunit to prevent rRNA binding to the A site =
prevents bacterial protein synthesis

28
Q

what can tetracyclines be used to treat

A

Gram-positive bacteria

diseases such as lymes disease

29
Q

how are tetracyclines administered, what can inhibit their absorption

A

administered orally

- absorption inhibited by dairy (bind to calcium forming an insoluble complex)

30
Q

what is a side effect of tetracyclines

A

photosensitivity to sunlight

31
Q

how have bacteria cells become resistant to tetracycline

A

efflux resistance genes:

pump tetracycline out of the cell faster than its uptake

32
Q

what are ribosomal protection proteins

A

tet (M), tet (O) ….

bind to ribosome changing its conformation - prevents tetracycline from binding without stopping synthesis

33
Q

what is the effect of the tet (X) gene

A

produces a cytoplasmic protein that chemically modified tetracycline in the presence of oxygen and NADPH

34
Q

describe MRSA in england

A

significant decrease in resistant strain, this is due to better cleaning regimes, screening and hand washing practises