Mechanism of action : All drugs in pharmacology - Part 6

Mechanism of action : All drugs in pharmacology - Part 6

Chemotherapy

• Penicillins :

  It interfers with the last step in bacterial cell wall synthesis that have peptidoglycan and in rapidly growing bacteria , resulting in exposure of the osmotically less stable membrane. It inactivates numerous proteins on cell wall involved in cell wall synthesis.
  It also inhibits transpeptidase required for cell wall integrity.
  It also destruct existing cell wall by autolysins.
  
  
  

• Vancomycin :

  It inhibits synthesis of bacterial cell wall phospholipids as well as peptidoglycan polymerization. This leads to weakening of the cell wall and damaging the underlying cell membrane.
  
  

• Daptomycin :

  It induces rapid depolarization of the bacterial cytoplasmic membrane , thus disrupting multiple aspects of membrane functions and inhibiting intracellular synthesis of DNA , RNA and protein.
  
  

• Tetracyclines :

  It enters the bacteria by passive diffusion or by energy-dependent transport system. Then it is concentrated intracellularly. it binds reversibly to the 30s subunit of the bacterial ribosome ,thereby blocking access of the amino acyl-tRNA to the mRNA-ribosome complex at the receptor site. This causes inhibition of bacterial protein synthesis.
  
  

• Aminoglycosides :

  It diffuses through porin channels in bacteria's outer membrane. Then it binds to 30s subunit of bacterial ribosome and causes it to misread the genetic code. Polysomes become depleted because their disaggregation and assembly is interrupted.
  
  
  

• Macrolides :

  It binds irreversibly to a site on 50s subunit of bacterial ribosome , thus inhibiting the translocation steps of protein synthesis.
  
  

• Chloramphenicol :

  It binds to the 50s subunit of bacterial ribosome and inhibits protein synthesis at the peptidyl transferase reaction.
  
  
  

• Linezolid :

  It binds to a site on the 50s subunit near the interface with 30s subunit , thus , inhibiting the formation of 70s initiation complex and inhibits bacterial protein synthesis.
  
  

• Fluoroquinolones :

  It enters the bacterium by passive diffusion through porins in the outer membrane. Then it inhibits the replication of bacterial DNA by interfering with the action of DNA gyrase and topio isomerase IV required for cell division.
  
  

• Sulfonamides :

  It competes with PABA for the bacterial enzyme dihydropteroate synthetase , thus inhibiting the synthesis of bacterial dihydrofolic acid and ,thereby, the formation of its essential cofactor forms.
  
  
  

• Cotrimoxazole :

  It inhibits two sequential steps in synthesis of tetrahydrofolic acid :

        1- Sulfamethoxazole inhibits the incorporation of PABA into dihydrofolic acid
             precursors.
        2- Trimethoprim prevents the reduction of dihydrofolic acid to tetrahydrofolic acid. 

• Amphotericin B:

  Several amphotericin B molecules bind to ergosterol in the plasma membrane of sensitive fungal cells . Then , they form pores which disrupt membrane functions allowing electrolytes and small molecules to leak from the cell resulting in cell death.
  
  
  

• Metronidazole :

  The nitro group of metronidazole serve as electron acceptor, forming reduced cytotoxic compounds that bind to proteins and DNA resulting in cell death.
  
  
  

• Praziquantel :

  It increases the permeability of cell membrane to calcium causing contracture and paralysis of the parasite.
  .
  
  
  

• Aspirin ( as NSAID ):

  It irreversibly acetylates and inactivates cyclo-oxygenase leads to blockade of prostaglandin synthesis. This results in anti-inflammatory , analgesic and anti-pyretic effects.
  
  

• Piroxicam and Meloxicam:

  It irreversibly inhibits both COX-1 and COX-2 .
  
  

• Dimenhydrinate :

  It is a histamine H1 receptor blocker > by blocking the receptor-mediated response of target tissues.