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Pharmacology > Intro to Antimicrobials > Flashcards

Intro to Antimicrobials Flashcards

1
Q

Antimicrobial Hx

A
  1. Antibiotic: cmpd produces by living microorganism w/ antimicrobial activity
  2. Synthetic cmpds
    A. Not true antibiotics
    B. Rational drug design, cmpd screening, serendipity
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2
Q

Factors influencing MIC/MBC

A
  1. MIC/MBC not best indicator of clinical efficiency
  2. Antimicrobials must reach MIC/MBC at site to cause infection
  3. Challenge
    A. Absorption and distribution
    B. Bone, CNS, adipose
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3
Q

Effective dose must balance toxicity

A
  1. Mechanism targeted has similar mammalian counterpart
    A. Mitochondria, protein synthesis
  2. Off-target effects
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4
Q

Non-dose dependent toxicity

A
  1. Allergic rxns

2. Idiosyncratic - pharmacogenomic

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5
Q

Bacteriocidal

A

Kills microbe

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6
Q

Basteriostatic

A

Stops growth

1. Can -> resistance in immunocompromised pts.

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7
Q

Chemotherapeutic spectrum

A

Range of organisms antimicrobial can fight

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8
Q

Broad spectrum

A

Wide range

1. Gram (+) and (-) and some parasites

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9
Q

Narrow spectrum

A

Few organisms

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10
Q

Extended spectrum

A

Intermediate range

1. Usually narrow modified to include more

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11
Q

Protein synthesis inhibitors

A 
1. 30S subunit
  A. Tetracycline
  B. Aminoglycosides
2. 50S subunit
  A. Macrolides
  B. Clindamycin
  C. Linezolid
  D. Chloramphenicol
  E. Streptogramins
3. Bacteriostatic
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12
Q

Resistance mech to protein synthesis inhibitors

A 
1. Dec. porins 
  A. Gram (-)
2. Inc. export of drug by efflux pumps
3. Microbial enzymes alter/destroy drug
4. Alter target proteins
5. Alter targeted pathways
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13
Q

Ways translation is inhibited by antimicrobials

A
  1. Drugs bind ribosomes
    A. Prevent translocation (erythromycin)
    B. Disrupt tRNA interaction (tetracycline)
  2. Prevent peptide chain formation
    A. Chloramphenicol
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14
Q

Cell wall synthesis inhibitors

A 
1. Mech: prevent peptidoglycan formation
  A. Prevent cross-linking 
    1. Transpeptidase links D-alanine on Muriel monomers
2. Destabilization = bactericidal
  A. H2O in -> cell bursts
  B. Most effective in growing pop
3. Beta lactams
4. Glycopeptides
5. Lipopeptides
6. Bacitracin
7. Polymyxins
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15
Q

Beta lactams

A

Largest class

  1. Penicillins
  2. Cephalosporins (biggest subclass)
  3. Carbapenems
  4. Monobactams
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16
Q

Penicillins

A 
Beta lactam
1. Natural: gram (+) and syphilis
2. Extended: gram (+) and (-)
  A. Aminopenicillins
  B. Amoxicillin
  C. Ampicillin
17
Q

Cephalosporins

A

Beta lactam, biggest subclass

  1. 5 generations: altered spectra and resistance to degradation by some bacteria
  2. Ceph or cef in name
18
Q

Carbapenems

A

Beta lactam

  1. Combo therapy common
  2. Potent
  3. Broad spectrum
19
Q

Monobactams

A
  1. Not true beta lactams (missing a ring)

2. Narrow spectrum: gram (-)

20
Q

Allergic response to beta lactams

A
  1. Beta lactams + human protein -> allergic response
    A. Anaphylaxis
    B. Cytolytic anemia
  2. Allergy = contradiction for using any beta lactam
    A. Exception: monobactams usually safe
21
Q

Bacterial resistance to beta lactams

A
  1. Open ring -> inactive
  2. Strategies to combat lactamases
    A. Combo therapy: stronger given w/ weaker one
    1. Weak competitively inhibits lactamases
    2. Strong allowed to work
    3. Ex: amoxicillin/clavulanate
      B. Chem mod of antibiotic to change enzyme affinity to access to ring
    4. Steric hinderance
    5. Ex: methicillin
22
Q

Glycopeptides

A
  1. Bind D-alanine needed for peptidoglycan crossing
  2. One of last effective drugs against MRSA infections
  3. Vancomycin
    A. Only gram (+)
    B. Resistant organisms don’t use D-alanine
23
Q

Lipopeptides

A 
Daptomycin
1. Insert into plasma membrane -> disrupt wall
  A. Gram (+)
  B. Vancomycin-resistant strains
  C. Bactericidal
24
Q

Bacitracin

A
  1. Prevents peptidoglycan subunits transfer to cell surface

2. Bactericidal

25
Q

Polymyxins

A

Small, (+) peptides

  1. Disrupt membrane structures
  2. Bactericidal
  3. Gram (-)
26
Q

DNA/RNA stability and synthesis inhibitors

A
  1. Direct= bactericidal
    A. Target polymerase
    B. Target stability/structure of DNA
    C. Resistance
    1. Antibiotic modification
    2. Altered protein targets
    3. Protective proteins
  2. Indirect = bacteriostatic
    A. Competitive folate synthesis inhibitors
    B. Act syngergistically
    1. Sulfonamide: inhibit dihydropteroate synthesis
    2. Trimethoprim: inhibit dihydrofolate reductase
      C. Resistance: inc. bioavailability of precursors
  3. Broad spectrum
27
Q

Reasons to use combo therapy

A
  1. Broad spectrum therapy in seriously ill pts
  2. Treat polymicrobial infection
  3. Dec. emergence of resistant and multi-drug resistant strains
  4. Dec dose-related toxicity
  5. Inc inhibition/killing
28
Q

Additive effects

A
  1. Beta-lactamase inhibitors + beta-lactam drugs

A. Amoxicillin/clavulanate

29
Q

Antagonistic effects

A
  1. Bacteriostatic + cell way synth inhibitors

A. Tetracycline dec efficiency of penicillins

Pharmacology (4 decks)

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