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Mechanism of Drug Action > Chemotherapy (Antibiotics) > Flashcards

Chemotherapy (Antibiotics) Flashcards

1
Q

What are the pharmacological benefits of synthetically modifying natural antibiotics?

A
  1. Increased oral bioavailability
  2. Increased stability
  3. Increased specificity
  4. Increased efficacy
  5. Extended spectum of activity
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2
Q

What are the groups of antibiotics based on range of bacteria affected?

A
  1. Limited spectrum: Effective against one particular species of organisms only.
  2. Narrow spectrum: Effective against Gram +ve or Gram –ve bacteria only.
  3. Broad spectrum: Effective against both Gram +ve and Gram –ve bacteria.
  4. Extended spectrum: Chemically altered variants of common antibiotics that are effective against increased number of bacteria compared to original molecule.
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3
Q

What are the types of antibiotics based on their effects on bacterial growth?

A
  1. Bacteriostatic
  2. Bactericidal
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4
Q

What are the effects of bacteriostatic antibiotics?

A

Inhibits bacterial growth, but does not kill existing bacteria in body. This process is dependent on host immune system. All the agents do is give immune system more time to clear infection.

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5
Q

What are the effects of bacteriocidal antibiotics?

A

Kills existing bacteria in the body, decreasing the infection burden.

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6
Q

Why is selectivity often unrelated to therapeutic index?

A

Antibiotics with high selectivity can still have low therapeutic index if high concentrations cause toxicity unrelated to its mechanism of antibiotic action

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7
Q

What are the types of multi-antibiotic interactions?

A
  1. Synergism: When A and B are given at specific concentrations, their combined effect is greater than the sum of their individual effects at the given concentrations.
  2. Antagonism: When A and B are given at specific concentrations, their combined effect is less than the sum of their individual effects.
  3. No interactions: When 2 antibiotics don’t interact with each other.
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8
Q

What causes synergism?

A

If 2 antibiotics inhibit different components parts of the same pathway.

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9
Q

What causes antagonism?

A

This can occur if 2 antibiotics oppose each other’s actions. For example, when penicillin is given with bacteriostatic, action of penicillin is reduced as cell division needed for its action, which is inhibited by bacteriostatic.

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10
Q

What are the classes of purely synthetic antibiotics?

A
  1. Sulfa drugs
  2. Fluoroquinolones
  3. Oxazolidinones
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11
Q

What are the pathways in bacterial lifecycle acted on by antibiotics?

A
  1. Cell wall biosynthesis
  2. Protein biosynthesis
  3. Membrane stability
  4. DNA replication, repair and expression
  5. Folic acid synthesis
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12
Q

What is the process of bacterial cell wall synthesis?

A
  1. UTP bound to NAG to form UDP-NAG
  2. PEP and 3 amino acids are added to form UDP-NAM-tripeptide (NAG converted to NAM via addition of PEP)
  3. D-Ala-D-Ala is added to UDP-NAM-tripeptide to form UDP-NAM-pentapeptide
  4. NAG added to UDP-NAM-pentapeptide
  5. The complex is linked to a bactoprenol phosphate (BP) in membrane via phosphate bridge
  6. The BP chaperones cell wall precursor complex to the outer surface of the membrane
  7. The complex is transferred from BP to growing PG chain by peptidoglycan transglycosylase
  8. BP is freed
  9. BP is recycled back across the membrane to the inner surface where it is able to carry further precursor complexes across the membrane
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13
Q

What is the mechanism of fosfomycin?

A

Inhibits pyruvyl transferase, which catalyses the addition of PEP to UDP-NAM. Inhibits formation of UDP-NAM-tripeptide.

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14
Q

What is the mechanism of D-cycloserine?

A

Strucutual analogue of D-Ala, thus inhibits activity of:

  1. L-Ala racemase
  2. D-Ala-D-Ala synthetase
  3. D-Ala-D-Ala/muramyl tripeptide ligase
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15
Q

What is the mechanism of bacitracin?

A

Forms tight complex with Mg2+ and BP, preventing it from being recycled to inner surface of membrane.

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16
Q

What is the process of PG cross-linking?

A
  1. Nucleophilic attack of D-Ala4-D-Ala5 so that D-Ala5 is released and D-Ala4 (and PG strand) is covalently joined to Ser to form acyl-O-Ser intermediate.
  2. The acyl moiety is transferred to neighbouring diaminopimelic acid on neighbouring GP strand.
17
Q

What is the mechanism of β-lactam antibiotics (penicillin)?

A
  1. The Ser group reacts with the 4-carbon lactam carbonyl, opening the lactam ring and forming the penicilloyl-O-TPase intermediate.
  2. The bond between the lactam group and Ser is very slow to hydrolyse (t1/2 = ~90 minutes) compared to D-Ala and Ser (t1/2 = ~4 ms).
  3. This effectively inactivates the transpeptidase enzyme.
  4. During cell growth, autolysins breakdown the PG to allow for re-shaping of the bacterial cell.
  5. Absence of transpeptidase means that no PG is produced to replace those broken down, thus the cell eventually bursts under osmotic pressure.
18
Q

What is the mechanism of vancomycin?

A

Inhibits cell wall synthesis by binding to the D-Ala-D-Ala group on PG and preventing its access to the active site of transpeptidase, thus inhibiting the crosslinking process.

19
Q

What are the classes of antibiotics that inhibit protein synthesis?

A
  1. Chloramphenicol
  2. Tetracyclines
  3. Macrolides
  4. Aminoglycosides
  5. Fusidic acid
20
Q

What effect do protein synthesis inhibitors have on bacterial growth?

A
  • Bacteriostatic
  • Most bacteria are adapted to surviving long periods of low nutrients so can survive in absemce of protein synthesis
21
Q

Why are the aminoglycosides bacteriocidal?

A

Because they cause erroneous proteins to be made, these proteins may damage the bacteria and cause death (e.g. erroneous membrane protein may increase permeability of membrane to ions, thus causing ionic leakage and disruption of ion gradient, causing cell death).

22
Q

What is the post-administration effect (PAE)?

A

Some antibiotics (e.g. aminoglycosides) show activity even when administration is ceased.

23
Q

What are the mechanisms by which antibiotics can disrupt DNA?

A
  1. Inhibition of DNA topoisomerase
  2. Inhibition of RNA synthesis
  3. Disruption of structure of dsDNA
24
Q

What are the benefits of combining sulfamethoxazole and trimethoprim?

A
  1. Synergism
  2. Prevents antibiotic resistance
  3. Increases rate of drug action beyond inhibidual drugs (Sulfamethoxazole depletes folic acid stores, which may take several generations to have an effect. Trimethoprim inhibits folic acid metabolism, so is much quicker acting.)

Mechanism of Drug Action (28 decks)

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