antibiotic lecture Flashcards

1
Q

big names in penecillin

A

alex fleming, ernst chain and howard flory

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2
Q

traits of an ideal antibiotic

A

broad spectrum of activity
wouldn’t induce resistance
high therapeutic index (want a dose that’s effective against pathogen w/out being too toxic to you; 1=you need a toxic dose to kill path)
selective toxicity

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3
Q

targets for antibiotics

A
inhibit cell wall synth
disrupt cell membrane fcn
inhibit prot synth
inhibit nucleic acid synth
act as antimetabolite
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4
Q

places where cell wall synth can be inhibited

A
linking NAG and NAM
linking NAM and peptide
stoping NAM-NAGs from transporting into periplasmic space
inhibit polymerization
inhibit peptide side chain bonds
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5
Q

how does penecillin work?

A

prevents peptide bond (btwn lys-ala on gram + or DAP or ala on gram -) by not letting the bact cleave off the terminal d-ala (the subterminal d-ala binds) penicillin out competes and is cleaved instead (cleaves into even more toxic form)

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6
Q

base structure of penecillin

A

B-lactin ring

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7
Q

how does polymyxin work?

A

displaces LPS molecule in gram - bact causing instability

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8
Q

how does inhibition of prot synth work?

A

can target in many places such as:
formation of ribosome subunits
inhib. of tRNAs from bringing in AA’s
can change configuration of ribosome (changes tunnel or binding groove)
inhibits start site recognition (trunkated cycle)
prevents peptide elongation

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9
Q

prob w/ drugs that inhibit nuc. acid synth and what’s the exception?

A

too toxic

metronidazole

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10
Q

how does metronidazole work?

A

inert in aerobic environment but activated by anaerobic microbes

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11
Q

how do sulfanilamides work?

A

work as antimetabolites and sub in for things bact need with similar structure
ex. stop PAB from turning into folic acid b/c looks v. similar

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12
Q

steps of action of antibiotics

A

penetration into the envelope
transport into the cell
bind target

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13
Q

ways antibiotic resistance spreads

A

chromosome associated resistance,
plasmid mediated resistance
rapid spread of natural resistance thru selective pressures

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14
Q

how do drugs affect ea other?

A

synergism (kill everything well together)
antagonism (stop ea. other from working)
indifference (target diff things)

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15
Q

probs w/ giving lots of antibiotics

A

makes super resistant if doesn’t kill everything, or causes synergistic toxicity in host

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