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Antibiotics Flashcards

(45 cards)

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1
Q

therapeutic index

A

toxic dose- 50/effective dose-50

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2
Q

What determines the efficacy of an antibiotic against a specific bacterium.

A
  1. reach target
  2. bind target & inhibit function
  3. resist inactivity
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3
Q

When and how antibiotic susceptibility is performed

A
  • presence of selected resistance mechanisms
  • performed if antibiotic has therapeutic potential for org at infected body site
  • performed if can’t be predicted from species of org
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4
Q

minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC)

A
  • [ABx] which inhibits visible growth of bacteria

- [ABx] which kills 99.9% of bacteria

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5
Q

4 mechanisms ABx can by synergistic

A
  1. reach greater conc at site of activity
  2. enhances binding of another to target
  3. blocks destruction of other
  4. partially inhibit separate steps in synthetic pathway
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6
Q

The advantages and disadvantages of the different routes of antibiotic administration.

A
  • oral: convenient, some drugs not absorbed; systemic levels variable, some drugs not absorbed, pt compliance
  • IV: bypasses absorption; inconvenient
  • IM: bypasses absorption; inconvenient, pnful
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7
Q

What determines the concentration of penicillin in the CSF, and the role of inflammation in this

A
  • normally low bc pumped out by choroid plexus

- choroid plexus inflamed & can’t pump pcn out

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8
Q

The role of folate in synthetic reactions

A

Folate –> Dihydrofolate –> Tetrahydrofolate
Tetrahydrofolate is used to transfer single carbons in synthetic pathways for
amino acids and nucleotides for DNA and RNA synthesis

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9
Q

The mechanism of activity of sulfonamides

A

inhibit Dihydropteroate Synthase
blocks folate synthesis in bacteria
–> inhibits nucleotide synthesis for DNA/RNA

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10
Q

The adverse effects of trimethoprim and sulfonamides

A
  • trimethoprim: rare suppressive effect on bone marrow cells, reducing production of RBC, WBC and platelets
  • sulfonamides: Hypersensitivity reactions
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11
Q

Why sulfonamides and trimethoprim are selective for bacterial cells

A

Sulfonamides: because only bacteria make folate
Trimethoprim:

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12
Q

Why trimethoprim and sulfonamides are synergistic

A

because they each inhibit a separate step in a single synthetic pathway (the
production of tetrahydrofolate).

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13
Q

trimethoprim-sulfamethoxazole combination therapy spectrum

A

broad spectrum effect against both gram positive and negative

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14
Q

The mechanism of fluoroquinolone activity

A

Quinolones block the activity of gyrase and topoisomerase IV at the step where the DNA has a double stranded break.
–> DSBs accumulate and kill bacteria

(gyrase and topoisomerase IV normally allow DNA supercoiling relief and can unlink DNA loops)

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15
Q

Fluoroquinolones spectrum

A

have broad spectra of activity, including Gram positive and Gram negative bacteria. Some have activity against anaerobes and mycobacteria. o Good activity against common urinary and respiratory pathogens, so can be used as empiric therapy for these

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16
Q

Why rifamycins are used in combination therapy for a few serious infections.

A

resistance quickly develops due to small changes in the bacterial RNA polymerase

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17
Q

The adverse effects of rifamycins

A
  • discoloration of secretions - orange
  • (rarely) injure the liver in the presence of other sources of hepatic injury
  • increase metabolism of other drugs
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18
Q

The adverse effects of fluoroquinolones

A
  • animal models, weaken cartilage formation in young
  • cause a rare tendinitis and tendon rupture in adults
  • cardiac arrythmias (potential predisposition)
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19
Q

The mechanism of activity of rifamycins

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A

block RNA synthesis by binding to the -subunit of the RNA polymerase

(stops the nucleic acids from progressing through the channel)

20
Q

The mechanism of activity of trimethoprim

Study These Flashcards
A

inhibit dihydrofolate reductase (DHFR)
blocks tetrahydrofolate synthesis in bacteria
–> inhibits nucleotide synthesis for DNA/RNA

21
Q

Usually Bactericidal Drugs (shortlist 5)

Study These Flashcards
A 
Aminoglycosides
Rifamycins
Cell-wall synthesis inhibitors
Daptomycin
Fluoroquinolones
22
Q

Usually bacteriostatic Drugs (3)

Study These Flashcards
A

most Protein-Synthesis Inhibitors
Trimethoprim
Sulfonamides

23
Q

Fidaxomicin - Bonus one…
too expensive/new for real use but:
disease of interest
mechanism

Study These Flashcards
A

narrow spectrum of activity that includes C. difficile

binds the RNA polymerase-DNA complex before the DNA strands are separated to initiate RNA synthesis

24
Q

The steps in synthesis of peptidoglycan

Study These Flashcards
A
  1. assembly of peptidoglycan monomers (in bacteria cytosol: glucose –> NAG –> NEM (via PEP) –> diamino AA added; L-alanine –> D-alanine via racemase –> ligase add these 2 together & add to growing chain to make 5 AA chain
  2. transport of peptidoglycan monomers (peptidoflycan bind to bactoprenol embedded in plasma membrane, NAG added & then flips orientation in membrane)
  3. polymerization of peptidoglycan (transglycosylase remove peptidoglycan from bactoprenol to add it to growing chain)
  4. cross linking of peptidoglycan polymers
25
That cell wall synthesis inhibitors are bacteriostatic or bactericidal drugs?
bactericidal
26
How cycloserine, fosfomycin and bacitracin inhibit peptidoglycan synthesis
- fosfomycin - PEP analogue to prevent NAG --> NAM - cycloserine: D-ala analogue, so inhibit racemase (no L-ala to D-ala) & ligase (linking 2 D-ala together to add to AA chain) - bacitracin: bind to bactoprenol to prevent txp of peptidoglycan from inside to outside
27
How vancomycin inhibits peptidoglycan synthesis
inhibit peptidoglycan polymerization: binds to D-ala, D-ala, inhibits transglycosylase to prevent adding peptidoglycan monomer to growing chain
28
vancomycin is effective against....
most Gram positive bacteria
29
Why vancomycin is not active against Gram negative bacteria
too large to get through porins to get to site of activity; peptidoglycan sits btwn outer membrane & inner membrane; porins in outer membrane
30
adverse effects of vancomycin
- red man syndrome: release of histamines from mast cells, not mediated by Ab, causing erythema, pruritis & hypotension - less common: neutropenia, nephrotoxicity
31
How β-lactam antibiotics inhibit peptidoglycan cross-linking
inhibit transpeptidases = penicillin-binding proteins to prevent cross-linking of peptidoglycans; B-lactam resembles D-ala/D-ala & binds to transpeptidase
32
The categories of β-lactams and their general spectrums of activity and, if discussed, the mechanisms by which the spectrum is determined
1. penicillin (natural: Strep A & B, S penumo, N. mening, some enterococci, syphillis; penicillinase-resistant pn: methicillin for staph; aminopenicillins: pass through porrins, strep A&B, S. pneumo, enterococci, listeria, some enteric, some haemophilus) 2. cephalosporin 3. monobactam 4. carbapenems
33
3 things which determine the spectrum of activity of a β-lactam antibiotic
1. ability to reach transpeptidase (ie. go through porin) 2. affinity for essential transpeptidases (diff kinds) 3. whether B-lactam cleaved by B-lactamase
34
adverse effects of penicillin drugs
- allergic response (IgE) --> pruritis, flushing,wheezing, hypotension, shock = anaphylaxis - less common: hemolytic anemia, thrombocytopenia, nephritis
35
most protein-synthesis inhibitors are bacteriostatic or bactericiadal
bacteriostatic
36
tetracyline
- mech of axn: block aminoacyl-tRNA into A site - common uses: atypical orgs: mycoplasma pneumoniae, borrelia burgdorferi, chlamydia, ricketsia, erhlichia chaffeenis, A. phagocytophilum - adverse effects: teeth discoloration <8 or pregnant (bind to calcium)
37
aminoglycosides are unique among the protein synthesis inhibitors because
o they are bactericidal and | o they alter decoding of mRNA
38
bacteria can become resistant to antibiotics in 3 ways
o They can change the antibiotic o They can change the target of the antibiotic o They can keep the antibiotic away from their target
39
enzymes which inactivate antibiotics can work by
o Cleaving the antibiotic (example: β-lactamase produced by S. aureus --> add bulky groups to prevent B-lactamase binding - add small groups to antimicrobial
40
bacteria can change the antibiotic target by:
o Making an alternative target which doesn’t bind the antibiotic (MRSA: PBP2a, which methicillin can't bind, rather than normal PBP 1-4; vancomycin resistance in enterococci and staphylococci)
41
bacteria can keep antibiotics away from their target by...
o Pumping the antibiotic out of the cell (gaining a pump) (example: pumps for tetracycline and macrolides) o Losing the channel through which the antibiotic enters the cell (loss of a porin can lead to resistance to multiple antibiotics of multiple classes)
42
aminoglycosides
- mech of axn: constitutive signal to large subunit that right codon to tRNA match, so incorporate wrong AA - common uses: synergistic w/B-lactams & vancomycin (Staph, Strep A&B, enterococci, listeria); enteric GNR, P aerug - adverse effects: nephrotoxicity reversible, ototoxicity irrecersible (why don't use much), neuromuscular blockade very rare
43
chloramphenicol
- mech of axn: blocks A site & prevents transpeptidation (peptide bond formation) - common uses: S. typhi & meningitis (Hiv, S pneumo, N menig) - adverse effects: uncommon permanent aplastic anemia, common transient suppression of RBC, WBC, platelets; gray baby syndrome
44
lincosamides (clindamycin)
- mech of axn: bind A & P site to prevent peptide bond formation - common uses: anaerobic enterics; combo therapy for severe staph & strep (TSS) - adverse effects: diarrhea; pseudomembranous colitis (C diff)
45
macrolide
- mech of axn: bind exit tunnel to prevent translocation - common uses: resp infections (legionella, pertussis) & chlamydia - adverse effects: generally safe & well tolerated; GI upset; cholestatic hepatitis

Microbiology (8 decks)

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