Antibiotic Mechanism of Action Flashcards
1
Q
Nitroimidazole (targets)
A
- kills both gram POS and gram NEG bacteria
- protozoa
- parasitic infections
- treats meningitis
2
Q
Nitroimidazole (where and how)
A
- disrupted DNA synthesis of bacteria
- cause loss of HELIX strands = strand break
- inhibits protein synthesis of cell wall = cell death
3
Q
Polymyxins (targets)
A
- gram NEG bacteria (l infections)
- treats systemic infections caused by susceptible strains of multidrug-resistant organisms (ex.: pseudomonas aeruginosa)
4
Q
Polymyxins (where)
A
- phospholipid bilayer (outer membrane of bacteria)
- target any cells with membrane (so can kill human cells)
5
Q
Polymyxins (how)
A
- bonds to the hydrophilic phosphate head (insert into cell membrane)
- pulls apart the cell membrane
- dissolves cell and the cytoplasmic contents leak out (lysis)
6
Q
Sulfonamids (targets)
A
- primarily gram POS
- effective against certain gram NEG
7
Q
Sulfonamids (where)
A
- inhibits dihydropteroate synthase
8
Q
Sulfonamids (how)
A
- competitive inhibitor of DHPS
- resembles and competes with PADA (p-aminobenzoic acid) for binding site of dihydropteroate synthase
- blocks folate synthesis which bacteria need to survive (can’t obtain folate from food like animals)
- prevents bacterial reproduction (repair of DNA; cell growth, division, replication)
9
Q
Macrolides (targets)
A
- affect all gram POS (except enterococci)
- some gram NEG
10
Q
Macrolides (where)
A
- bacterial ribosome (specifically the nascent peptide exit tunnel)
11
Q
Macrolides (how)
A
- inhibit protein synthesis by binding to nascent peptide exit tunnel of the 50s unit (plugs it) of the 80s ribosomes
- prevents translation of mRNA
- w/o protein synthesis, bacteria cannot perform necessary functions = cell death
12
Q
Penicillin (targets)
A
- gram POS (rods)
- cocci gram NEG
- bacilli
- branching filaments
13
Q
Penicillin (where)
A
- peptidoglycan cell wall
14
Q
Penicillin (how)
A
- inhibits TRANSPEPTIDASE
- transpeptidase makes peptidoglycan (cell wall)
- so w/o it, gram POS cells burst
15
Q
Fluroquinolones (target)
A
- active against wide range of gram POS and gram NEG
16
Q
Fluroquinolones (where)
A
- bacterial enzymes: DNA gyrase and topoisomerase IV (crucial for DNA replication & maintenance)
17
Q
Fluroquinolones (how)
A
- inhibits DNA gyrase and topoisomerase IV
- prevents it from introducing suppercoils into the DNA and disrupts the separation of replicated chromosomes
18
Q
Tetracyclines (targets)
A
- gram POS
- gram NEG
19
Q
Tetracyclines (where)
A
- (competitive inhibitor) binds to 30S ribosomal subunit and prevents the amino-acyl tRNA from binding to this site
20
Q
Tetracyclines (how)
A
- inhibits protein synthesis
- inhibits bacteria growth by inhibiting translation (tRNA)
21
Q
Aminoglycosides (targets)
A
- gram NEG
22
Q
Aminoglycosides (where)
A
- ribosomes
23
Q
Aminoglycosides (how)
A
- creates fissures in cell membrane
- binds to 30s subunit ribosome inside bacteria cell
- binds to aminocyl site of 16s ribosomal RNA
- makes the bacteria misread genetic code
- leads to wrong amino acid chain
- any proteins made are ineffective or harmful
- leads to decline of bacteria production
24
Q
Cephalosporins (target)
A
- mostly gram POS
- gram NEG
25
Q
Cephalosporins (where)
A
- bacteria cell wall
26
Q
Cephalosporins (how)
A
- beta-lactam ring structure allows penetration of cell wall in gram POS and gram NEG
- binds to one or more of the penicillin binding proteins in the cytoplasmic membrane
- PBP are enzymes that cross link peptidoglycan units for bacteria to build cell wall
- in cell division, the daughter cells are unable to close cell wall due to cephalosporin
- cell wall can’t close = cell death
