DNA Function Inhibitors Flashcards Preview

Disease & Defense - Unit 2 > DNA Function Inhibitors > Flashcards

Flashcards in DNA Function Inhibitors Deck (22)
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1
Q

Fluoroquinolones: examples

A
  • ciprofloxacin
  • levofloxacin
  • gemifloxacin
  • moxifloxacin
2
Q

Fluoroquinolones: mechanism of action

A
  • DNA transcription inhibitor
  • targets bacterial DNA gyrase and topoisomerase IV
  • rapidly bactericidal
3
Q

Fluoroquinolones: pharmacokinetics

A
  • good oral, parenteral also available
  • good penetration into most tissues
  • primarily kidney excretion
4
Q

Fluoroquinolones: spectrum/clinical uses

A
  • gram+ cocci (strep. pneumoniae, MSSA)
  • gram- cocci (moraxella catarrhalis)
  • gram+ bacilli (bacillus anthracis)<–cipro
  • gram- bacilli (pseudomonas aeruginosa, E. coli)
  • anaerobes
  • atypical organisms (chlamydia, mycoplasma pneuemoniae, richettsia)
5
Q

Fluoroquinolones: adverse reactions

A
  • well tolerated
  • increased risk of tendon rupture
  • GI disturbances
  • drug-drug: reduced absorption w/anacids
6
Q

Fluoroquinolones: “1st generation” + spectrum

A

Naldixic acid: gram- anaerobes (++)

7
Q

Fluoroquinolones: “2nd generation” + spectrum

A

Cipro & Levo: gram- anaerobes (++), pseudomonas (+), gram+ (+/++)

8
Q

Fluoroquinolones: “3rd generation” + spectrum

A

Gemi & Moxi: gram- anaerobes (+), pseudomonas (+/-), gram+ (++), atypical (+), anaerobes (++)

9
Q

Nitrofurantoin: mechanism of action

A
  • DNA damage-inducer

- concentration-dependent bacteriostatic/bactericidal effect

10
Q

Nitrofurantoin: pharmacokinetics

A
  • good oral

- short half-life –> urine (renal excretion)

11
Q

Nitrofurantoin: spectrum/clinical uses

A
  • 2nd line urinary tract antiseptic (cannot safely reach plasma levels, but concentrated in renal tubules)
  • E. coli & enterocci
12
Q

Nitrofurantoin: adverse reactions

A
  • GI disturbances

- possible link to birth defects

13
Q

Metronidazole: mechanism of action

A
  • DNA damage inducer
  • prodrug–>reactive nitro radical anion
  • radical anion damages DNA
  • bactericidal
14
Q

Metronidazole: pharmacokinetics

A
  • good oral
  • good distribution (including bone/CSF)
  • liver metabolism
  • excreted in breast milk
15
Q

Metronidazole: spectrum/clinical uses

A
  • anaerobes (C. difficile, Bacteriodes fragilis)

- protozoa

16
Q

Metronidazole: adverse reactions

A
  • some GI disturbance
  • headaches, dry mouth
  • candidal superinfection
17
Q

Sulfonamides: mechanism of action

A
  • DNA synthesis inhibitor
  • inhibits folic acid synthesis (PABA analog) which is required for DNA synthesis
  • bacteriostatic
18
Q

Sulfonamides: pharmacokinetics

A
  • good oral (best on empty stomach)
  • widely distributed
  • some protein binding
  • n-acetylation metabolism (can be toxic)
  • excreted by kidney
19
Q

Sulfonamides: spectrum/clinical uses

A
  • broad spectrum; most common use in TMP/SMX form
  • gram+ cocci (MRSA)
  • gram- cocci (Moraxella catarrhalis)
  • gram- bacilli (enetrobacter, shigella, pseudomonas aeruginosa)
  • atypical (chlamydia)
20
Q

Sulfonamides: adverse reactions

A
  • generally safe
  • sensitization reactions
  • drug-drug: displace from proteins –> bilirubin, anticoagulants
21
Q

Sulfonamides: bacterial resistance

A
  • widespread in vivo
  • acquired: increase PABA production or DHPS altered to decrease binding to sulfonamides
  • escape: obtain end products of metabolic pathway from pus (why we must drain some purulent infections)
  • natural: organisms w/no folic acid requirement
22
Q

Sulfonamides: common drug combination

A
  • synergy w/trimethoprim (TMP)

- sulfamethoxazole + TMP (aka TMP/SMX or “Bactrim”= bactericidal