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Antibiotics > Basics and Mechanisms of Action > Flashcards

Basics and Mechanisms of Action Flashcards

1
Q

Chemotherapy

A

Treatment of disease w/ antibiotics or other chemical agents

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2
Q

Antibiotics Characteristics

A
  1. Microbial origins (fungi) classically, some synthetic now
  2. Low molecular weight
  3. Spectrum of Activity
    a. broad: wide variety of unrelated
    b. narrow: few related
  4. Mechanism of action
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3
Q

Basis of Selective Toxicity

A
  1. Absence of target from host (inhibit bacteria w/o hurting host
  2. Permeability differences: antibiotics must be effective at concentrations that don’t hurt the host
  3. Structural differences in target: ex. different ribosomal subunits
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4
Q

Bacteriostatic agents

A

Reversibly inhibit bacterial growth; resemble metabolite analogs and act as competitive inhibitors

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5
Q

Bactericidal agents

A

lethal; may/may not cause cell lysis; generally only effective against growing cells
Often irreversible competitive inhibitors

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6
Q

Minimal Inhibitory Concentration (MIC)

A

lowest concentration of drug that inhibits more than 99% of bacterial population

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7
Q

Minimal Lethal Dose (MLD)

A

Lowest concentration of drug that kills more than 99.9% of bacterial population

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8
Q

Drug interactions: Indifference

A

Combined action of drug A and B is not greater than the more effective drug alone, nor is it less effective

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9
Q

Drug interactions: additive

A

The effects of A and B sum together

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10
Q

Drug interactions: synergism

A

Effects of A and B are greater than the sum of A and B. Often occurs with 2 bactericidal drugs

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11
Q

Drug interactions: Antagonism

A

The effects of A and B together are less than the most effective drug. Often occurs when a bactericidal drug is used with a bacteriostatic drug

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12
Q

Intrinsic antibiotic resistance

A

The target of the antibiotic is missing

Ex. Vancomycin not effective against mycoplasm b/c no peptidoglycan

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13
Q

Acquired antibiotic resistance: Horizontal gene transfer

A

Antibiotic target is present but the bacteria acquired a mutation by exchanging genetic material via plasmids or transposable elements

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14
Q

Acquired antibiotic resistance: Spontaneous mutation

A

Mutations arise spontaneously & randomly in absence of selection

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15
Q

3 Antibiotic Mechanisms of Action

A
  1. Target essential metabolic pathway
  2. Target nucleic acid synthesis
    a. Transcription
    b. DNA replication
  3. Disrupt bacterial membranes
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16
Q

Sulfonamides/Sulfa drugs

A

-Broad spectrum bacteriostatic
-Inhibit Folic acid biosynthesis (bacteria must produce via tetrahydrofolic acid), but host can acquire (Selective toxicity)
-Inhibit dihydropteroate synthase
-Structural analog of PABA
Often used w/ trimethoprim that inhibits dihydrofolate reductase (analog of DHFA)

17
Q

Sulfa drugs w/ Trimethoprim

A
  • Synergism
  • Sulfas only block new THFA but old stores can be utilized by bacteria
  • Trimethoprim blocks usage of preexisting DHAF
  • Together these drugs block both branches
18
Q

p-aminosalicylic Acid (PAS)

A
  • MOA similar to sulfonamides

- Effective against mycobacterium tuberculosis (sulfas are NOT)

19
Q

Rifampin ad Rifabutin

A
  • Affecting nucleic acid synth: Inhibition of Transcriptional Initiation
  • Bactericidal
  • Narrow spectrum: gram positive, Neisseria, mycobacteria
  • MOA: binds beta subunit of RNA polymerase, inhibits transcription initiation, but not transcription in progress
  • Selective toxicity: Host RNA polymerase not sensitive, mito impermeable
20
Q

Quinolones

A
  • Affecting nucleic acid synth: Inhibition of DNA replication
  • Bactericidal
  • Nalidixic acid: narrow for G- UTI
  • Ciprofloxacin: broad spectrum against pseudomonas
  • MOA: Inhibits DNA gyrase
  • Selective toxicity: Humans have no DNA gyrase or topoisiomerase IV
  • Resistance: decreased uptake, target mutation
21
Q

Metronidazole

A
  • Affecting nucleic acid synth: damage DNA structure
  • Bactericidal
  • MOA: disrupts DNA structure, inhibits DNA replication, DNA breaks and mutations
  • Selective toxicity: given as prodrug, and only bacteria have the enzyme to convert to active form
  • Uses: narrow spectrum against anaerobic H. pylori giardia lamblia
  • Resistance: mutations to oxidoreductases that affect conversion of pro-drug
22
Q

Polymixins

A
  • Affecting cell membranes
  • bactericidal narrow spectrum for pseudomonas
  • MOA: hydrophobic tail inserts into cell membrane and hydrophilic head binds polar phosphatidylethanolamine (PE) and lipopolysaccharide (LPS) and disrupts cytoplasmic membrane
  • Selective toxicity: host cells have no PE or LPS
  • Resistance: G- have lipid A in LPS that makes outer membrane impermeable

Antibiotics (9 decks)

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