Antibiotics Flashcards

(29 cards)

1
Q

selective toxicity

A

antibiotics must be more toxic to the pathogen than to the pathogen’s host

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2
Q

bacteriostatic

A

inhibits the growth of bacteria but doesn’t otherwise kill them

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3
Q

bacteriocidal

A

level of antibiotic that kills the bacteriu

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4
Q

quantitative determination of antibiotic activity

A

E test

  • use a piece of paper with antibiotic concentartions in a gradient
  • look for lowest necessary to inhibit growth
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5
Q

qualitiative determination of antibiotic activity

A
  • kirby bauer disc diffusion test

- measures the size of zone of inhibition

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6
Q

4 mechanisms of bacterial resistance to antibiotics

A
  1. naturally lack the drug target
  2. outer membrane of gram-negative block many meds
  3. spontaneous mutations
  4. Horizontal gene transfer
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7
Q

therapeutic index

A

lowest dose toxic to patient/therapeutic dose

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8
Q

clinical situations where antibiotic prophylaxais may be warranated

A
  • bite
  • meningitis
  • heart valve
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9
Q

Beta lactam antibodies

A
  • cell wall synthesis inhibitors
  • penicillins, cephalosporins, and carbapanems
  • inhibits cross linking of peptidoglycans
  • Most effective against GRAM POSITIVE bacteria (they have a thick peptidoglycan layer)
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10
Q

Penicillins

A
  • 5 types with varying side chains

- varying resistance to beta lactamases

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11
Q

cephalosporins

A
  • resistant to some beta lactamases

- 4 generations

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12
Q

carbapenems

A
  • resist most beta lactamases
  • last resort antibiotics
  • NDM1 are resistant
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13
Q

non beta lactam cell wall inhibitor

A
  • Vancomycin
  • binds to D-Ala-D-Ala subunit to prevent cross linking
  • cause cell lysis
  • treat Gram positve and C. Diff
  • also last resort

Tx: poorly absorbed so administer IV

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14
Q

Cell membrane inhibitors

A
  • Polymyxin B
  • toxicity –> only apply topically
  • insert into the membrane –> lysis

Gram NEGATIVE bacteria

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15
Q

Nucleic Acid Synthesis inhibitors

A
  • Fluoroquinolones
  • inhibit prokaryotic topoisomerase (DNA Gyrase)
  • may have some toxicity, still oral
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16
Q

Protein synthesis inhibitors

A
  • Clindomycin, Streptomycin, Erythromycin

- Macrolides, Aminoglycosides, Lincosamides, Tetracyclines

17
Q

Macrolides

A
  • prevent continuation of protein synthesis
  • bind to 50S subunit
  • Erythromycin
18
Q

Lincosamides

A
  • bind to 50S subunit
  • block initiation of translation
  • Clindamycin
19
Q

Aminoglycosides

A
  • bind to 30S subunit
  • mRNA is misread and causes truncated proteins
  • Streptomycin
20
Q

Tetracyclines

A
  • block attachment of tRNA to ribosome

- binds to 50S

21
Q

Metabolic inhibitors

A
  • Sulfonamides
  • Analogs of essential metabolites used in FOLIC ACID synthesis
  • mimics PABA, comp. inhibition
  • can not outcompete PABA
22
Q

ways of determing MIC

A
  1. Kirby bauer diffusion test

2. E test

23
Q

side effects of clindamycin

A
  • protein synthesis inhibitor
  • disrupts normal gut microbiota
  • proliferation of C. diff
  • can lead to enterocolitis
24
Q

side effects of tetracyclin

A
  • broad spectrum antibiotic
  • blocks binding of tRNA to ribosome
  • inhibits lactobacillus in vagina, changing the pH, allowing C. albicans to grow into yeast infection

-also causes tooth staining, dont prescribe to children or pregnant women

25
side effects of chloramphenicol
-aplastic anemia
26
side effects of streptomycin
auditory damage | *don't give to young
27
How does drug resistance develop?
- most common plasmid transfer via conjugation - HGT in same generation of bacteria - antibiotic SELECTS For mutations
28
Mechanisms of drug resistance
1. Efflux pump 2. Drug inactivating enzyme 3. Alteration in target molecule (can't bind) 4. Decreased uptale (entry prevention) - Use of alternative metabolic pathway
29
enterobacteriaeceae
- intrinsically resistant to many Abs | - Klebsiella resistant to beta lactams and carbapenem