15: antibiotics Flashcards

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1
Q

how penicilin is discovered?

A

alexander fleming worked on staphlycoccus & noticed the lack of bacteria surround the colony (Penicilium)
=> failed to isolate subst from the mold
=> called in Penicilin

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2
Q

broad spectrum vs narrow spectrum antiobiotic

A

if drug target pathogen from many taxonimic group, even beneficial series = broad spectrum
if few groups tartgeted = narrow spectrum

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3
Q

how sulfonamides cause bacterial death?

A

By cell wall synthesis!

Since folic acid needed for DNA synthesis, folic acid needs PABA

In structure, SMZ is similar to PABA : fit into the active site of enzyme & compete w/ PABA

=> block folic acid synthesis => no nucleotide synthesis => bacterial death

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4
Q

how beta lactam antiobiotics cause cell death?
examples?

A

BY cell wall synthesis!

When cells growing & dividing, h=ave to add NAG-NAM subunits
Transpeptidase cross link the new subunit
Penicilin e.g block it

=> Cell wall is weak, lyse due to osmotic P

Penicilin, Cephalosporin, meropenum

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5
Q

how have bacteria resist penicilin?

A

Beta-lactamase enzyme cut out the beta-lactam ring
Convert it to penicilloic acid, which is not hamrsul to bacteria

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6
Q

2 ways to determine bacterial subsceptibility to antiobiotic

A

1/ put = amnt of 2 bacterium onto plastic plate
diff concentra of antiobiotic
=? find min. concentra to kill the bacteria
2/ diff concentra of antibiotic onto agar plate
Zone of inhibition used to find min. concentra

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7
Q

why the rise in antibiotic resistance?

A

Overall misuse of antibiotics and innovation gap
Most major drug groups created btw 1930-1930
Lack of new classes since then

  1. Prescription abuse: from drug companies & doctors
  2. Prescription misuse from personal: self-diagnosis & eating leftoevers
  3. …from health organization: overdosing it in hospital
  4. abuse on lifestock: in feed
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8
Q

strategies to develop antibiotic resistance

think 3 modifications

A
  1. antibiotic hydrolysis: split apart the antibiotic
  2. …modification: change/ add chemical molec
  3. membrane modification / efflux: inhibit drug entry into cytoplasm & project it back
  4. target modification: alter cell structure targeted by antibiotics
  5. alter metabolic pathways: some drugs are competitive inhibitor
    => create alternate patjways to make = product
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9
Q

antibiotic to fight ____ disease bt not ____ ____ because it’s diffcult to find drugs to harm ____ without being toxic to ____ ____

remind of theurapic window

A

bacterial / microbial pathogens / pathogens / host tissue

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10
Q

developing antibiotic resistence via…, (redacted) change to DNA

A

mutation = rare, spontaneous change to DNA; often from DNA replication
may transfer horizontally from other bacteria

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11
Q

new approach to antimicorbial therapy

A

careful use of antibiotics: preseve ones that are still effective via prudent use and educated medical corp
find new ones!

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