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[blank_start]Chemotherapeutics[blank_end] prepared synthetically in the lab
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Antibiotics are [blank_start]by-products[blank_end] of [blank_start]metabolic activity[blank_end] of bacteria and fungi
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by-products
-
metabolic activity
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Classification of antibacterial agents
A- According to spectrum:
1- [blank_start]Narrow[blank_end] spectrum
2- [blank_start]Broad[blank_end] spectrum
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Classification of antibacterial agents
B- According to the antibacterial effect
1- [blank_start]Bacteriostatic[blank_end]
2- [blank_start]Bactericidal[blank_end]
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Bacteriostatic
-
Bactericidal
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Classification of antibacterial agents
C- According to mechanism of action:
1- Inhibition of [blank_start]cell wall synthesis[blank_end]
2- Inhibition of [blank_start]cell membrane function[blank_end]
3- Inhibition of [blank_start]protein synthesis[blank_end]
4- Inhibition of [blank_start]nucleic acid synthesis[blank_end]
5- Inhibition of [blank_start]bacterial metabolism[blank_end]
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cell wall synthesis
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cell membrane function
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protein synthesis
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nucleic acid synthesis
-
bacterial metabolism
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Target receptor for Inhibition of cell wall synthesis
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2 groups for Inhibition of cell wall synthesis
1. [blank_start]B lactam[blank_end] drugs
2. [blank_start]Vancomycin[blank_end] & [blank_start]bacitracin[blank_end]
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B lactam
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Vancomycin
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bacitracin
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Antworten
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Penicillin
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cephalosporin
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polymyxin
-
polyene
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Penicillins & cephalosporins inhibit early precursors in transpeptidation
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[blank_start]Vancomycin[blank_end] & [blank_start]bacitracin[blank_end] inhibit early precursors in transpeptidation
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advantage of β Lactam drugs
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bacitracin act only on growing cells
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Inhibition of cell membrane function drugs
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polymyxins
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polyenes
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Amikacin
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Tetracyclines
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Advantages of polymyxins & polyenes
1. [blank_start]Bactericidal[blank_end]
2. [blank_start]can act on non growing cells[blank_end]
Disadvantage of polymyxins & polyenes
1. [blank_start]Toxic effects on kidney & CNS[blank_end]
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Bactericidal
-
Selective toxicity
-
can act on non growing cells
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bacteriostatic
-
Toxic effects on kidney & CNS
-
Act only on growing cells
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Drugs acting on the 30S ribosomal subunit
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Amikacin
-
Gentamicin
-
Tetracyclines
-
Lincomycin
-
Erythromycin
-
oleandomycin
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Aminoglycosides
1.[blank_start]Amikacin[blank_end]
2. [blank_start]Gentamicin[blank_end]
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Tetracyclines effective in treatment of Chlamydophila
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oleandomycin is effective in treatment of intracellular bacteria
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Tetracyclines: Effective in treatment of intracellular bacteria e.g. [blank_start]Chlamydophila[blank_end] & [blank_start]Brucella[blank_end]
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Aminoglycosides are [blank_start]Bactericidal[blank_end]
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Bactericidal
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Bacteriostatic
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Tetracyclines are [blank_start]Bacteriostatic[blank_end]
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Bacteriostatic
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Bactericidal
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Drugs acting on the 50S ribosomal subunit except
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Chloramphenicol
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Lincomycin
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Macrolides
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polymyxins
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Drugs acting on the 50S ribosomal subunit are [blank_start]Bacteriostatic[blank_end]
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Bacteriostatic
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Bactericidal
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Macrolides
1. [blank_start]Erythromycin[blank_end]
2. [blank_start]oleandomycin[blank_end]
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Erythromycin
-
oleandomycin
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Inhibition of nucleic acid synthesis
1. [blank_start]Rifampin[blank_end]
2. [blank_start]Quinolones[blank_end]
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Rifampin: inhibit [blank_start]DNA dependent RNA polymerase[blank_end]
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Quinolones: inhibit [blank_start]DNA gyrase[blank_end]
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[blank_start]Rifampin[blank_end]: inhibit DNA dependent RNA polymerase
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Rifampin
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Quinolones
-
oleandomycin
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Inhibition of bacterial metabolism
1. [blank_start]Sulphonamides[blank_end]
2. [blank_start]Trimethoprim[blank_end]
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-
Sulphonamides
-
Trimethoprim
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Sulphonamides: inhibit [blank_start]DHFA synthetase[blank_end]
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Trimethoprim: inhibits [blank_start]DHFA reductase[blank_end]
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Trimethoprim: inhibits DHFA synthetase
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Bacterial Resistance to chemotherapeutic agents
1. [blank_start]Non genetic origin[blank_end]
(natural/inherent)
2. [blank_start]Genetic origin[blank_end]
(acquired)
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Non genetic origin
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Genetic origin
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Genetic origin ([blank_start]acquired[blank_end]) is [blank_start]Unpredictable[blank_end]
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acquired
-
inherent
-
Unpredictable
-
predictable
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Genetic origin
([blank_start]acquired[blank_end])
[blank_start]Unpredictable[blank_end]
1- [blank_start]Chromosomal[blank_end]
([blank_start]Mutation[blank_end]=change in [blank_start]receptor[blank_end])
2- [blank_start]Extrachromosomal[blank_end]
([blank_start]R factor[blank_end] carrying destroying enzymes
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acquired
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Unpredictable
-
receptor
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Chromosomal
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R factor
-
Mutation
-
Extrachromosomal
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Non genetic origin
([blank_start]natural[blank_end]/inherent)
[blank_start]Innate[blank_end], [blank_start]predictable[blank_end]
1- Absence of cell wall ([blank_start]Mycoplasma[blank_end])
2- Permeability barrier in cell envelope ([blank_start]Pseudomonas[blank_end])
3- Non multiplying ([blank_start]TB[blank_end])
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natural
-
Innate
-
predictable
-
Mycoplasma
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Pseudomonas
-
TB
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Mechanisms of Resistance
1. [blank_start]Drug Inactivation[blank_end]
2. [blank_start]Change of Permeability[blank_end]
3. [blank_start]Alter Target Structure[blank_end] e.g.[blank_start]PBP[blank_end]s, [blank_start]30S[blank_end], [blank_start]50S[blank_end]
4. [blank_start]Alter Metabolic Pathway[blank_end] ([blank_start]utilize preformed FA[blank_end])
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Drug Inactivation
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Change of Permeability
-
Alter Target Structure
-
PBP
-
30S
-
50S
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Alter Metabolic Pathway
-
utilize preformed FA
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[blank_start]Cross Resistance[blank_end]
Bacteria resistant to a drug may be resistant to a [blank_start]chemically related[blank_end] one.
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Cross Resistance
-
chemically related
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Antibacterial Drug Combinations
1- [blank_start]Indifference[blank_end] ( 1 + 1= 1 )
2- [blank_start]Addition[blank_end] (1 + 1 = 2 )
3- [blank_start]Synergism[blank_end] ( 1 + 1= 3 )
4- [blank_start]Antagonism[blank_end] ( 1 + 1= 0 )
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Indifference
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Addition
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Synergism
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Antagonism
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reciprocal
-
commensal
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Synergism
[blank_start]Penicillin[blank_end] + [blank_start]aminoglycoside[blank_end]
[blank_start]Carbenicillin[blank_end] + aminoglycoside
[blank_start]Ampicillin[blank_end] + [blank_start]Metronidazole[blank_end]
Antworten
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Penicillin
-
Erythromycin
-
aminoglycoside
-
Rifampin
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Carbenicillin
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Chloramphenicol
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Ampicillin
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Tetracycline
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Metronidazole
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Macrolides
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Control of Drug Resistance
1- Give only when [blank_start]indicated[blank_end]
2- Proper choice (according to [blank_start]susceptibility[blank_end])
3- Give in the proper [blank_start]dose[blank_end] for proper [blank_start]time[blank_end]
(To prevent [blank_start]selection pressure[blank_end])
4- Use drug [blank_start]combinations[blank_end]
(simultaneous use of 2 drugs)
5- Avoid [blank_start]abuse[blank_end] of [blank_start]valuable[blank_end] drugs
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indicated
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susceptibility
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dose
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time
-
selection pressure
-
combinations
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abuse
-
valuable