Antimicrobial Pharm Flashcards

1
Q

Cell wall synthesis inhibitors

A

Beta-lactam

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2
Q

Folate synthesis inhibitors

A

Sulfonamides

Trimethroprim

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3
Q

DNA gyrase inhibitors

A

Fluoroquionlones

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4
Q

RNA polymerase inhibitors

A

Rifampin

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5
Q

Protein synthesis inhibitors

A

Tetracyclines
Aminoglycosides
Macrolides

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6
Q

Bacteriostatic

A

Inhibit/stop growth and reproduction of bacteria - works with your own immune system to remove microorganisms from the body

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7
Q

Bactericidal

A

Kill bacteria by interfering with a process essential for life (concentration-dependent or time-dependent)

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8
Q

Time-dependent

A

Killing effect is directly proportional to the amount of TIME the drug concentration at the site of infection is ABOVE the MIC of the organism

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9
Q

MIC

A

Lowest concentration of a drug that inhibits bacterial growth

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10
Q

Concentration-dependent

A

Bacterial kill increases with increasing levels of drug; have to avoid toxicity

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11
Q

Which type (static vs. cidal) should be used in patients with impaired immune defense mechanisms?

A

Bactericidal (required for endocarditis, meningitis, and neutropenic cancer pt)

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12
Q

Five principle MOAs in antimicrobial classification

A
  1. ) Inhibition of cell wall synthesis
  2. ) Disruption of cell membrane function
  3. ) Inhibition of protein synthesis
  4. ) Inhibition of nucleic acid synthesis
  5. ) Action as antimetabolites
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13
Q

Common target for agents that inhibit cell wall synthesis

A

Peptidoglycan synthesis and incorporation into bacterial cell wall

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14
Q

How do beta-lactam antibiotics work?

A
  • They bind to PBPs (transpeptidase enzymes)
  • PBP is unable to crosslink peptidoglycan chains
  • Bacteria unable to synthesize a stable cell wall
  • Weakened cell wall leads to lysis of bacteria from osmotic pressure
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15
Q

What is the key chemical structure found in every beta-lactam antibiotic?

A

Beta-lactam ring with beta-lactam bond (N-C=O)

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16
Q

Beta-lactamases

A

Bacteria can encode this enzyme that can cleave the beta-lactam bond; drug resistance

17
Q

MRSA

A

Beta-lactam antibiotics WON’T WORK!!

-PBP is mutated in MRSA so no beta-lactam antibiotics can bind since the target site is altered

18
Q

Beta-lactam antibiotics groups and characteristics

A
  • Natural penicillins, Cephalosporins, Carbapenems, and Monobactams
  • Beta-lactams are bactericidal and time-dependent killers
19
Q

Penicillin groups and drugs

A
  • Natural penicillins (penicillin G)
  • Penicillinase-resistant penicillins or Antistaphylococcal penicillins (nafcillin)
  • Extended-spectrum penicillins (amoxicillin)
  • Antipseudomonal penicillins (ticarcillin)
20
Q

Penicillin G active against…

A

Gram+ bac

21
Q

Cephalosporins groups and drugs

A
First gen (cephalexin)
Second gen (cefoxitin)
Third gen (ceftriaxone)
Fourth gen (Cefepime)
22
Q

First gen mainly active against…

A

Gram+ cocci

23
Q

With each generation of cephalosporins there is increasing…

A
  • Activity against g- bac and less activity against g+
  • Resistance to beta-lactamases
  • Ability to cross BBB
24
Q

Carbapenem drug

A

Imipenem

25
Q

Monobactam drug

A

Aztreonam

26
Q

Vancomycin action and characteristics

A
  • Inhibits transglycosylase (prevents building block bound to phospholipid carrier from binding to growing peptidylglycan chain)
  • Does not cross lipid membrane of g-
  • Acquired resistance most often due to amino-acid alterations in side chain peptidoglycan building blocks (mutates binding site so Vanco can’t bind)
27
Q

Bacitracin action and characteristics

A
  • Interferes with transport of peptidoglycan precursors across cytoplasmic membrane (cell wall synthesis inhibited)
  • Toxicity limits use to topical apps
  • Common ingredient in non-prescription in first-aid ointments (Neosporin)
28
Q

Agents that act directly on the cell membrane…

A
  • Disrupt the integrity of the cell membrane (increase permeability leading to leakage of intracellular components)
  • polymyxin and daptomycin
  • Bactericidal and concentration-dependent killers
29
Q

Colistin (polymyxin E)

A
  • Binds to LPSs and phospholipids on outer cell membrane of gram-
  • competitvely displaces Ca and Mg from PO4 groups of membrane lipid
  • Leads to disruption of outer cell membrane, leakage of intracellular contents, bacterial death
30
Q

MOA of daptomycin

A
  • daptomycin binds to the membrane
  • Ca allows many daptomycin to recruit and “poke a hole” in the membrane
  • Leakage of K»depolarization»arrest of cell processes»cell death
31
Q

Agents that inhibit bacterial protein synthesis….

A
  • Translation inhibitors that target either 30S or 50S bacterial ribosome subunits
  • Typically reversible inhibitors
  • Generally bacteriostatic
32
Q

Classes of antibiotics that inhibit bacterial protein synthesis and their drugs

A
  • Tetracyclines (doxycycline)
  • Macrolides (erythromycin)
  • Aminoglycosides (gentamycin - exception to rule: AGs irreversibly inhibit protein synthesis and are generally bactericidal)
33
Q

Inhibition of DNA gyrase (affect nucleic acid metabolism)

A
  • Bacterial DNA is negatively supercoiled
  • Supercoiling maintained by gyrase (topoisomerase)
  • Inhibition of gyrase and type IV topoisomerase interferes with DNA replication, causes cell death
  • Eukaryotic topoisomerases differ in structure
34
Q

Drug that inhibits RNA polymerase

A

Rifampin

35
Q

Drug class and drug that inhibits DNA replication

A

Fluoroquinolones; ciprofloxacin

36
Q

Classes that target folic acid synthesis and their drugs

A

Sulfonamides (sulfamethoxazole) and drug: trimethoprim

37
Q

Inhibition of folate synthesis

A

Folic acid is a cofactor needed for synthesizing the building blocks of DNA; metabolic inhibitors that target folic acid synthesis are selectively toxic to bacteria because bacteria have to synthesize a large proportion of cofactors (2-step process so you need to have both drugs to stop the pathway)