antibiotics

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  • Created by: hadar
  • Created on: 23-11-15 17:15
Benzyl Penicillin- mechanism of action
inhibition of cell wall synthesis through penicillin G binding to penicillin binding proteins (PBPs). inhibiting the protein that is involoved in cross linking peptidoglycan --> cell lysis
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Benzyl Penicillin- therapeutic affect
Cell lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins- inhibition of cell wall synthesis Bacteriocidal to growing bacteria and bacteriostatic to colony
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Ceftriaxone (b lactam)- mechanism of action
binding to penicillin binding proteins (PBPs).inhibiting the mucopeptide synthesis in the bacterial cell wall.
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Ceftriaxone (b lactam)- therapeutic affect
inhibiting the mucopeptide synthesis in the bacterial cell wall. that catalyze the cross-linking of the peptidoglycan polymers forming the bacterial cell wall.
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Metronidazole (nitroimizole)- mechanism of action
to intracellularly reduce metronidazole to its active form. covalently binds to DNA, disrupt its helical structure, inhibiting bacterial nucleic acid synthesis and resulting in bacterial cell death.
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Metronidazole (nitroimizole)- therapeutic affect
inhibiting bacterial nucleic acid synthesis and resulting in bacterial cell death.
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Macrolide- mechanism of action
binding reversibly to the P site on the subunit 50S of the bacterial ribosome.
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Macrolide- therapeutic affect
inhibition of bacterial protein biosynthesis- bactriostayic →stop dissociation of tRNA from ribodsome →inhibits elongation of chain by inhibiting the transfer to growing chain →Inhibit ribisome synthesis
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Clarythromycine (macrolide)- mechanism of action
→ inhibits bacterial protein synthesis by binding to the bacterial 50S ribosomal subunit.inhibits peptidyl transferase activity and interferes with amino acid translocation during the translation and protein assembly process.
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Clarythromycine (macrolide)- therapeutic affect
inhibition of bacterial protein biosynthesis- bactriostayic →stop dissociation of tRNA from ribodsome →inhibits elongation of chain by inhibiting the transfer to growing chain →Inhibit ribisome synthesis
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Rifampicin (macrocyclic)- mechanism of action
inhibits DNA-dependent RNA polymerase activity by forming a stable complex with the enzyme.
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Rifampicin (macrocyclic)- therapeutic affect
by physically blocking the formation of the phosphodiester bond in the RNA backbone, preventing extension of RNA products. . inhibits bacterial DNA-dependent RNA synthesis. suppression of RNA synthesis and cell death.
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Ethambutol- mechanism of action
inhibits the transfer of mycolic acids into the cell wall. inhibits arabinosyl transferases which is involved in cell wall biosynthesis.
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Ethambutol- therapeutic affect
bacteriostatic- bacterial cell wall complex production is inhibited→ increased cell wall permiability
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Pyrazinamide- mechanism of action
enzyme pyrazinamidase converts pyrazinamide to the active form pyrazinoic acid. Under acidic conditions, the pyrazinoic acid that slowly leaks out converts to the protonated conjugate acid- diffuses back and accumulates (acid pH)
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Pyrazinamide- therapeutic affect
bacteriostatic, but can be bacteriocidal pyrazinoic acid disrupts membrane potential and interferes with energy production, necessary for survival of M. tuberculosis at an acidic site of infection.
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Isoniazide- mechanism of action
inhibits the synthesis of mycoloic acids, an essential component of the bacterial cell wall. → fas2/ inhibits InhA, the enoyl reductase
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Isoniazide- therapeutic affect
blocking of the formation of mycolic acid, which is an essential part of the mycobacterial cell wall. Disruption of the cell wall results in cell death and isoniazid can fight colonization at both the intracellular and extracellular level.
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Card 2

Front

Cell lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins- inhibition of cell wall synthesis Bacteriocidal to growing bacteria and bacteriostatic to colony

Back

Benzyl Penicillin- therapeutic affect

Card 3

Front

binding to penicillin binding proteins (PBPs).inhibiting the mucopeptide synthesis in the bacterial cell wall.

Back

Preview of the back of card 3

Card 4

Front

inhibiting the mucopeptide synthesis in the bacterial cell wall. that catalyze the cross-linking of the peptidoglycan polymers forming the bacterial cell wall.

Back

Preview of the back of card 4

Card 5

Front

to intracellularly reduce metronidazole to its active form. covalently binds to DNA, disrupt its helical structure, inhibiting bacterial nucleic acid synthesis and resulting in bacterial cell death.

Back

Preview of the back of card 5
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