Antibiotics MOA and Resistance Mechs. Flashcards

(49 cards)

1
Q

T or F: drugs that mess with the structure of bacteria are typically bacteriostatic

A

False

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2
Q

What are the most common drugs to form allergies?

A

-Penicillin

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3
Q

What is the preferred oral treatment for non-penicillinase producing streptococci?

A

-Penicillin V

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4
Q

Differentiate between

  • Penicillin
  • Monobactam
  • Carbapenem
  • Cephalosporins
  • Vancomycin
A

Penicillin – Thiazole Ring
Monobactam –sulfonic acid
- gets it inside the cell wall
Carbapenem
- Replaces thiazole sulfur with carbon giving it MORE RESITANCE to ß-lactamases, better penetration and affinity for more PBP
Cephalosporins
- 6 membered ring to make it more stable
Vanco – inhibits d-ala d-ala binding by transpeptidases

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5
Q

What drugs bind the 30S RSU? Which bind 50S?

A

Buy AT 30, CELL at 50
A = Aminoglycosides
T = Tetracyclines
30S

C = Chloramphenicol
E = Erthromycin (macrolides) 
L = Linezolid 
L = cLindomycin
50S
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6
Q

Why use muti-drug therapy?

A
  1. Treat polymicrobial infections
  2. Decrease emergence of resistance
  3. Descrease Dose-related toxicity
  4. Enhanced cell-kill
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7
Q

Why might tetracyclines and chloramphenicol antagonize bactericidal cell wall agents?

A

Cell wall agents require that the cell be dividing to be effective

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8
Q

Why might giving a ß-lactam antagonize an infection?

A

Some gram (-) bacilli possess inducible lactamases that will be induced by the presence of ß-lactams

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9
Q

Bactericidal Antibiotics

A
  1. Aminoglycosides*
  2. Fluroquinolones
  3. Nitrofurantion
  4. Sulfonamides with DHFR inhibitors
  5. Metronidazole
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10
Q

Bacteriostatic antibiotics

A

Protein synthesis inhibitors

Sulfonamides

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11
Q

What bacteria are often treated by combining Penicillins with aminoglycosides?

A
  1. Staphylococci
  2. Enterococci
  3. Streptococci
  4. P aeruginosa
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12
Q

4 methods by which antibiotic work

A
  1. Inhibition of Cell Wall Synthesis
  2. Inhibition of Protein Synthesis
  3. Inhibition of Folic acid biosynthetic paths
  4. Inhibition of DNA/RNA synth
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13
Q

MOA of ß-lactams

A

Bind Penicillin binding proteins (transpeptidase) which causes destruction of the bacterial cell wall gram (+) bacteria are really the only type of microbe affected by this

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14
Q

What are the protype penicillins?

A

Penicillin G and Penicillin V

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15
Q

What are the narrow spectrum penicillins?

A

Oxacillin and Nafcillin

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16
Q

What are the aminopenicillins?

A

Ampicllin and Amoxicillin

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17
Q

What are the broad spectrum penicillins?

A

Pipercillin

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18
Q

What are 2 examples of ß-lactamase inhibtors being combined with penicillins?

A
  • Clavulanic acid with Amoxicillin

- Tazobactam with Piperacillin

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19
Q

What is a common structural characteristic of Broad Spectrum Penicillin?

  • why are they called broad spectrum ?
  • What are they usually administered with?
A

Broad spectrum because AMINO group added increases ability to cross lipid layer in gram (-) bacteria
Usually administered with ß-lactamase inhibitors (clavulanic acid, or Tazobactam)

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20
Q

What are narrow spectrum penicillins?

A

Have larger molecules on their side chain that confers steric hinderance and ß-lactamase can’t twist molecule into different stereoisomers
- these are narrow spectrum because bulky side groups limit the amount of different bacterias that can be targeted

21
Q

What are the 3 major categories of ß-lactams?

A
  • Penicillins
  • Carbaenems
  • Cephalosporins
22
Q

General problem with aminoglycoside administration:

- affected organs?

A

Poorly absorbed in GI Tract so oral administration is not possible. In general intracellular concentrations are low except in proximal tubule of the kidney where they can accumulate and cause NEPHROTOXICITY

23
Q

Drugs ending in –mycin or –micin typically have what general function?

A
  • mycin = macrolides
  • micin = aminoglycosides
  • both inhibit protein synthesis
24
Q

T or F: most protein synthesis inhibitors are bactericidal

A

False, they are bacteriostatic with the exception of aminoglycosides, and Synpristin/dalfopristin (streptogramins) that are bactericidal

25
What is the general trend of cephalosporins across generations?
They get increasingly better at attacking gram (-) bacteria and worse at gram (+) bacteria
26
Fluroquinolones to know
CIPROFLOXACIN | Levofloxacin
27
Rifamycins to know
RIFAMPIN | Rifaximin
28
DHFR drugs to know
COTRIMOXAZOLE | Trimethroprim
29
Sulfonamides to know
COTRIMOXAZOLE | Sulfamethoxazole
30
MOA for Aminoglycosides
Initial site of Action: Outer bacterial membrane creating holes Low conc. Irreversibly bind the 30S ribosomal subunit at low concentrations causing misreading of mRNA. High conc. Halt protein synthesis by trapping AUG codon
31
Are aminoglycosides more effective against gram (+) or gram (-) bacteria? - aerobic bacteria or anaerobic bacteria? - Bacteriostatic or Bactricidal - Why?
Gram (-) because they deteriorate the outer membrane which is more protected in gram positive Aerobic because energy is needed for aminoglycoside uptake Typically bactericidal against aerobic gram (-) bacteria
32
MOA for Lincosamides
(protein synth targeting) Bind 50S ribosomal subunit (23S rRNA part) and inhibit Peptidyl Transferase, are phagocytosed by macrophages carrying them to the site of infection (ideally) **also slows toxin production by inhibiting bacterial growth
33
Lincosamides to know
CLINDAMYCIN
34
MOA of Tetracyclines
Bind 30S RSU (16S part) and inhibit protein synthesis by weaking ribosome-tRNA interaction
35
Tetracyclines to know:
DOXYCYCLINE TIGECYCLINE Minocycline Tetracycline
36
MOA for Macrolides
(protein synth targeting) Bind 50S ribosomal subunit (23S rRNA part) and inhibit Peptidyl Transferase, are phagocytosed by macrophages carrying them to the site of infection (ideally)
37
Macrolides: Bacteriostatic or Bactericidal
Bacteriostatic at most concentrations but become bactericidal at high enough concentrations
38
Why would you give penicillin with an aminoglycoside?
Penicillin can break the cell wall and the aminoglycoside can then be absorbed
39
Aminoglycosides to know
``` GENTIMICIN Amikacin Neomycin Stretomycin Tobramycin ```
40
Macrolides to know
AZITHROMYCIN CLARITHROMYCIN ETYHTROMYCIN
41
MOA for Streptogramins
Binds 50S ribosomal subunit (at the same site as macrolides)
42
Bacterial response to Aminoglycosides - Gram (+) - Gram (-) - Anaerobes - MRSA - VRE - Pseudomonas
- Gram (+) – Poor - Gram (-) – Great - Anaerobes – Resistant - MRSA – Resitant - VRE – Resistant - Pseudomonas - Good
43
Bacterial response to macrolides - Gram (+) - Gram (-) - Anaerobes - MRSA - VRE - Pseudomonas
- Gram (+) – Good - Gram (-) – Good - Anaerobes – Resistant - MRSA – Resistant - VRE – Resistant - Pseudomonas - Resistant
44
Bacterial response to Lincosamides - Gram (+) - Gram (-) - Anaerobes - MRSA - VRE - Pseudomonas
- Gram (+) – Good - Gram (-) – Resitant - Anaerobes – Very Good - MRSA – Pretty good - VRE – Resistant - Pseudomonas – Resistant
45
Bacterial response to Tetracyclines - Gram (+) - Gram (-) - Anaerobes - MRSA - VRE - Pseudomonas
- Gram (+)- Good - Gram (-) – Good - Anaerobes – Pretty good - MRSA – Resistant - VRE – Resistant - Pseudomonas – Resistant
46
What is Cilastin? | - how does it work?
- Cilastin is a reversible, competitive inhibitor of Renal Dehydropeptidase (DHP-1), an enzyme that breaks down Imipenem to inactive BUT NEPHROTOXIC metabolites
47
What group of bacteria is thought to be intrinsically resistant to aminoglycosides because of permability barriers?
Enterococci
48
Why are gram (-) bacteria less prone to lysis via ß-lactams?
They have a thinner peptidoglycan layer and LPS layer
49
When is a bacteria determined to be resistant to a drug?
When the MIC exceeds the breakpoint