ANTIMICROBIAL CHEMOTHERAPY REGIMENS
DOSE AND DURATION OF THERAPY
This varies depending on the nature, severity, and response to therapy. The long-term treatment (up to 6 weeks) is required for some varieties of infective endocarditis when pulmnary tuberculosis were treated for at least 6 months. Treat many common infections, improvement occurs within 2-3 days, when the patient is afebrile or leukocytosis have been resolved, the mouth should be considered in these parenteral therapy.Five started seven days of therapy is sufficient for most infections. A short course of therapy (3 days or less) should these symptoms of uncomplicated bacteria (cystitis), minimizing the duration of treatment reduces the risk of side effects and super-infection of Candida spp or Clostridium difficile, as well as the cost of care. Breasts that concentrates in the cell, such as erythromycin, quinolones and tetracyclines are used in the treatment of mycoplasma, brucellosis, and Legionella infections.
RENAL AND HEPATIC INSUFFICIENCY
Many drugs require dose reduction of renal failure to prevent toxic buildup. This is particularly true beta lactums and aminoglycosides. Nalidixic acid and tetracycline, other doxycyclines, should be avoided. This hepatic impairment, caution and the dose should be reduced by agents such as isoniazid, ketoconazole, rifampin, and interferon.
THERAPEUTIC DRUG MONITORING
In order to ensure more non-toxic concentrations of therapeutic drugs, drugs such as aminoglycosides and vancomycin serum monitored, especially those with impared renal or change function.Peak (after 1 hour - the dose) and through the (pre-dose) on serum samples be tested. However, the increasing use of once daily doses of aminoglycosides, but the time randm serum analysis are being adopted.
MECHANISMS OF ACTION AND RESISTANCE TO ANTIMICROBIAL AGENTS
Antibiotic works in different places for bacteria. Penecillin, cephalosporins and vancomycin, erythromycin cell wall and protein synthesis aminoglycosides, rifampicin effect on RNA synthesis and effect of metronidazole, quinolones and DNA synthesis. Sulfonamides and trimethoprim are folic acid antagonists and amphotericin B to prevent the synthesis of fungal sterols. Antibiotic resistance may be due to:
- Failure to reach the target site, for example, because the causes of deterioration of permeability does not reach the outer membrane of bacteria (eg, penicillin and Gram-negative).
- Enzyme inactivation (eg, enzymes beta-lactamase).
- Change the target site (eg, a point mutation in E. coli penicillin binding protien Strep.pneumoniae lead to resistance.
The development or acquisition of resistance to an antibiotic that the bacteria always involves either a mutation in a single point in a gene or transfer of genetic material from another organism. large fragments of DNA can be introduced into bacteria either by transfer of " naked " DNA or by a bacteriophage (a virus) DNA vector.Both the past (processing), and one (transduction) depend integration of new DNA into the chromosomal DNA recipient. This requires a high degree of homology between donor and recipient of the chromosomal DNA. Finally, resistance to antibiotics can be transferred from one bacterium to another by conjugation, where DNA extrachromosomal (plasmid) that contains resistance factor (R factor) is transferred from one cell to another by contact Direct. Transfer of these plasmids R factors can occur between unrelated bacterial strains and involve large amounts of DNA and often code for multiple resistance antbiotic.
The transformation is probably the least clinically relevant mechanism, while the transduction and transfer of R factors are generally responsible for the immediate emergence of antibiotic resistance in bacteria, increasing resistance to many antibiotics has developed...... read more
ANTIMICROBIAL CHEMOTHERAPY REGIMENS
DOSE AND DURATION OF THERAPY
RENAL AND HEPATIC INSUFFICIENCY
THERAPEUTIC DRUG MONITORING
Antibiotic works in different places for bacteria. Penecillin, cephalosporins and vancomycin, erythromycin cell wall and protein synthesis aminoglycosides, rifampicin effect on RNA synthesis and effect of metronidazole, quinolones and DNA synthesis. Sulfonamides and trimethoprim are folic acid antagonists and amphotericin B to prevent the synthesis of fungal sterols. Antibiotic resistance may be due to:
The transformation is probably the least clinically relevant mechanism, while the transduction and transfer of R factors are generally responsible for the immediate emergence of antibiotic resistance in bacteria, increasing resistance to many antibiotics has developed...... read more
This varies depending on the nature, severity, and response to therapy. The long-term treatment (up to 6 weeks) is required for some varieties of infective endocarditis when pulmnary tuberculosis were treated for at least 6 months. Treat many common infections, improvement occurs within 2-3 days, when the patient is afebrile or leukocytosis have been resolved, the mouth should be considered in these parenteral therapy.Five started seven days of therapy is sufficient for most infections. A short course of therapy (3 days or less) should these symptoms of uncomplicated bacteria (cystitis), minimizing the duration of treatment reduces the risk of side effects and super-infection of Candida spp or Clostridium difficile, as well as the cost of care. Breasts that concentrates in the cell, such as erythromycin, quinolones and tetracyclines are used in the treatment of mycoplasma, brucellosis, and Legionella infections.
RENAL AND HEPATIC INSUFFICIENCY
Many drugs require dose reduction of renal failure to prevent toxic buildup. This is particularly true beta lactums and aminoglycosides. Nalidixic acid and tetracycline, other doxycyclines, should be avoided. This hepatic impairment, caution and the dose should be reduced by agents such as isoniazid, ketoconazole, rifampin, and interferon.
THERAPEUTIC DRUG MONITORING
In order to ensure more non-toxic concentrations of therapeutic drugs, drugs such as aminoglycosides and vancomycin serum monitored, especially those with impared renal or change function.Peak (after 1 hour - the dose) and through the (pre-dose) on serum samples be tested. However, the increasing use of once daily doses of aminoglycosides, but the time randm serum analysis are being adopted.
MECHANISMS OF ACTION AND RESISTANCE TO ANTIMICROBIAL AGENTS
Antibiotic works in different places for bacteria. Penecillin, cephalosporins and vancomycin, erythromycin cell wall and protein synthesis aminoglycosides, rifampicin effect on RNA synthesis and effect of metronidazole, quinolones and DNA synthesis. Sulfonamides and trimethoprim are folic acid antagonists and amphotericin B to prevent the synthesis of fungal sterols. Antibiotic resistance may be due to:
- Failure to reach the target site, for example, because the causes of deterioration of permeability does not reach the outer membrane of bacteria (eg, penicillin and Gram-negative).
- Enzyme inactivation (eg, enzymes beta-lactamase).
- Change the target site (eg, a point mutation in E. coli penicillin binding protien Strep.pneumoniae lead to resistance.
The development or acquisition of resistance to an antibiotic that the bacteria always involves either a mutation in a single point in a gene or transfer of genetic material from another organism. large fragments of DNA can be introduced into bacteria either by transfer of " naked " DNA or by a bacteriophage (a virus) DNA vector.Both the past (processing), and one (transduction) depend integration of new DNA into the chromosomal DNA recipient. This requires a high degree of homology between donor and recipient of the chromosomal DNA. Finally, resistance to antibiotics can be transferred from one bacterium to another by conjugation, where DNA extrachromosomal (plasmid) that contains resistance factor (R factor) is transferred from one cell to another by contact Direct. Transfer of these plasmids R factors can occur between unrelated bacterial strains and involve large amounts of DNA and often code for multiple resistance antbiotic.
The transformation is probably the least clinically relevant mechanism, while the transduction and transfer of R factors are generally responsible for the immediate emergence of antibiotic resistance in bacteria, increasing resistance to many antibiotics has developed...... read more
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