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Amy Somerville > INF1 - F. CHROMOSOME AND RIBOSOME INHIBITORS-COVERED > Flashcards

INF1 - F. CHROMOSOME AND RIBOSOME INHIBITORS-COVERED Flashcards

1
Q

what are stages of DNA replication

A
  • origin: strand of DNA
  • helicase: splits 2 DNA strands
  • replication fork
  • DNA polymerase: joins 2 strands through covalent bonds
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2
Q

differences between genome of bacteria and humans

A
  • bacteria has single copies of one of more chromosomes (haploid)
    humans have 2 or more (diploid)
  • bacteria has plasmids
    humans don’t
  • bacteria have circular or linear dsDNA
    humans have linear dsDNA in nucleus and chloroplasts and circular dsDNA in mitochondria and plasmids
  • bacteria has DNA in nucleoid of cytoplasm and in plasmids
    humans have DNA in nucleus and mitochondria, chloroplasts and plasmids in cytosol
  • bacteria don’t have histones
    humans have histones in nuclear chromosomes
  • bacteria genome is is smaller than humans
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3
Q

what is transcription

A

mRNA synthesis

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4
Q

what steps are involved in transcription

A
  1. initiation
  2. elongation of RNA transcript
  3. termination
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5
Q

what do RNA polymerases do

A

synthesise RNA by binding to promoters locater near the beginning of a gene and initiate transcription

*target for antibiotics as structure is different to eukaryotic RNA polymerase

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6
Q

what do topoisomerases do

A

unravels coil of DNA
humans have 6
bacteria have 4

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7
Q

how do quinolones (ie - fluoroquinolones - only used in UK) work

A
  • selectively inhibit topoisomerases not found in mammalian cells
  • broad spectrum and bactericidal against gram-negative bacteria (E. coli) and gram-positive cocci (P. aeruginosa)
  • gram +ve exhibit higher rates of resistance than gram -ve

Ciprofloxacin
Moxifloxacin
Ofloxacin
Levofloxacin

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8
Q

what do quinolones treat

A
  • UTI, GI, genital, resp tract infections
  • Ciprofloxacin: only good oral anti-pseudomonal drug available
  • increased risk of C. difficile infection and MRSA colonisation
  • good for those that can’t take beta-lactams as similar activity
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9
Q

what is the mode of action of fluoroquinolones

A
  • selectively inhibit topoisomerases 2 and 4 in bacterial cells

gram -ve: DNA girase (2) is key target
uncoils the supercoils and recoils for packaging

gram +ve: topoisomerase 4 is key target
removes links and knots generated behind replication fork

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10
Q

structure of DNA gyrase and topoisomerase 4

A

enzyme tetramers - 2 A and B subunits
A subunits - cut both DNA strands on one chain, other chain passes through break and resealed
B subunits - derive energy for action of A subunits from hydrolysis of ATP

Fluoroquinolones bind to A subunit, trapping the broken DNA in a complex with DNA gyrase
DNA gyrase can’t reseal the DNA, chromosomes fragmented, cell death

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11
Q

what does rifampicin treat

A
  • bactericidal against Mycobacterium tuberculosis
  • treatment and prophylaxis
  • well absorbed orally
  • good penetration into bone, CNS, chest
  • used in combination as resistance emerges rapidly if used as mono therapy
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12
Q

what is the mode of action of rifampicin

A
  • acts upon B-subunit of bacterial RNA polymerase
  • inhibition of initiation stage of RNA transcription as prevents first nucleotide being incorporated into RNA chain
  • rifampicin resembles 2 adenosine nucleotides in RNA which form the basis of binding to B-subunit
  • doesn’t inhibit transcription once initiated
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13
Q

how do nitroimidazoles and nitrofurans work

A
  • causes strand breakage of DNA by a direct chemical method not through inhibiting an enzyme
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14
Q

what is the mode of action of metronidazole

A
  • nitroimidazole antibiotic
  • broad-sprectrum against aerobic protozoa, bacteria, helminths
  • pro-drug: active after reduction of nitro group
  • non-enzymatic reduction by reacting with reduced ferredoxin
  • metabolites are unstable and react with DNA causing irreversible damage
  • alternative to penicillin for mouth infections in combination (amoxicillin or clarithromycin plus omeprazole) with debridement
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15
Q

what is the mode of action of nitrofurantoin

A
  • nitrofuran antibiotic
  • active against range of gram+ve and gram-ve organisms (esp. E. coli)
  • forms reactive intermediates by reduction which react with DNA causing strand breakage
  • most active in acidic urine
  • first line for UTIs
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16
Q

differences in protein synthesis in bacteria and eukaryotes

A
  • 70S ribosome in bacteria, 80S in eukaryotes
  • active uptake of antibiotics into bacterial cell, limited penetration in mammalian cells
17
Q

why does resistance occur to these antibiotics which affect protein synthesis

A
  • alteration/protection of ribosome from antibiotic
  • active uptake and efflux of antibiotic issues
18
Q

where is the site of protein synthesis

A

ribosomes

19
Q

what is the structure of ribosomes

A

eukaryotes - 80S
prokaryotes - 70S

  • rRNA and ribosomal proteins
  • rRNAs fold an interact to give the ribosome 3D structure
  • proteins located more peripherally
  • translation works from 5’ to 3’ end
20
Q

what is the A site on ribosomes

A
  • binds incoming tRNA carrying its amino acid (aminoacyl tRNA site)
  • but the first tRNA binds directly to P site where codon AUG is and then the rest start at A site
21
Q

what is the P site on ribosomes

A
  • peptide bond is formed between the amino acid linked to the tRNA in P site and amino acid linked to tRNA in A site
  • catalysed by peptidyl transferase (ribozyme in large subunit)
22
Q

what is the E site on ribosomes

A
  • where the tRNA moves and is ejected from ribosome having delivered its amino acid and added it to growing polypeptide
23
Q

what are tetracyclines

A
  • 4 cyclic rings
  • broad-spectrum
  • bind to 30S ribosomal subunit and block tRNA binding at A site, protein synthesis stops
  • bacteriostatic
24
Q

what are tetracyclines used for

A
  • chlamydia
  • acne
  • resp infections
  • rickettsia
25
Q

why is there resistance to tetracyclines

A
  • failure of active uptake system
  • ribosomal protection/modification
    efflux mechanisms
26
Q

what are aminoglycoside-aminocyclitol antibiotics

A
  • bactericidal
  • take up by active transport under aerobic conditions
  • active against some gram+ve and many gram-ve
  • used in combo with beta-lactams
  • interfere with 30S subunits and block initiating factors and tRNA binding
  • causes mRNA codon to be misread
  • injection for sys infs as poorly absorbed from gut
27
Q

why does resistance to aminoglycosides occur

A
  • inactivation by amino glycoside-modifying enzymes
  • ribosomal alterations
  • loss of permeability
  • efflux pumps
28
Q

what is streptomycin used for

A

M. tuberculosis
*ototoxicity causing deafness is a side effect

29
Q

what is gentamicin used for

A

Septicaemia and endocarditis

30
Q

what are macrolides

A
  • similar to penicillins so used as an alternative
  • clarithromycin, azithromycin, clindamycin, telithromycin, erythromycin etc
  • GI side effects
31
Q

what are macrolides used for

A
  • resp, skin, soft tissue infections
  • Helicobacter pylori
32
Q

what is the mode of action of macrolides

A
  • inhibit protein synthesis by binding to 50S subunit, blocking translocation by preventing movement of peptide-tRNA from A to P site
33
Q

what bacteria does macrolides affect

A
  • gram +ve
  • gram -ve intrinsically resistant due to permeability of OM
34
Q

why is there resistance to macrolides

A
  • target modification - adenine methylation in 50s subunit
  • ATP-binding cassette efflux pump
  • ribosomal mutation
35
Q

what is chloramphenicol

A
  • broad-spectrum
  • gram -ve and gram +ve bacteria, mycoplasmas, rickettsia spp. and chlamydia spp.
  • inhibit protein synthesis by binding to 50S subunit at A site and inhibiting peptidyl transferase and inhibits peptide bond formation
  • mammalian subunit sensitive to chloramphenicol: inhibition can occur in rapidly growing cells (aplastic anaemia)
  • use is limited to serious infections
  • safe for ocular use - bacterial conjunctivitis
36
Q

why is there resistance to chloramphenicol

A
  • enzymatic modification
  • reduced uptake
  • target modification of 50S subunit
37
Q

what is used to treat conjunctivitis

A

chloramphenicol drops or ointment

38
Q

what is used to treat otitis media

A

macrolides

39
Q

what is used to treat sinusitis (inflam of nasal sinuses)

A

macrolides and tetracyclines

Amy Somerville (70 decks)

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