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Class introduction to chemoTHERAPY

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Dr. RAGHU PRASADA M S
MBBS,MD
ASSISTANT PROFESSOR
DEPT. OF PHARMACOLOGY
SSIMS & RC.

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Cause of disease
Means
Invasiveness
Toxigenesis
Stages
Colonization
Adherence
Nonspecific (dock)
Specific (anchor)
Invasio...

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Natural Source-Fungal molds-Actinomycetes , Bacteria Bacillus,
Chemotherapeutic- Chemical
Semi-synthetic-Hybrid

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Class introduction to chemoTHERAPY

  1. 1. Dr. RAGHU PRASADA M S MBBS,MD ASSISTANT PROFESSOR DEPT. OF PHARMACOLOGY SSIMS & RC.
  2. 2. Cause of disease Means Invasiveness Toxigenesis Stages Colonization Adherence Nonspecific (dock) Specific (anchor) Invasion Enzymes and Toxins
  3. 3. Natural Source-Fungal molds-Actinomycetes , Bacteria Bacillus, Chemotherapeutic- Chemical Semi-synthetic-Hybrid
  4. 4. Those that inhibit cell wall synthesis: Isoniazid; pyrizinamide: Mycolic acid synthesis inhibitors Ethambutol: Inhibits MA incorporation to cell wall Those that affect nucleic acid metabolism: Rifampin; rifabutin: DNA dependent RNA polymerase inhibitors Clofazimine: Binds to DNA and inhibits the template function of DNA Those that inhibits intermediary metabolism: Dapsone; sulfoxone: The same as that of sulfonamides.
  5. 5. Aminoglycosides β-lactams -Penicillins -Cephalosporins -Carbapenams -Monobactams -Fluoroquinolones -Glycopeptides Ketolides Lincosamides Macrolides Oxazolidinones Streptogramins Sulphonamides Tetracyclines
  6. 6. Considerations Identification of microbe Drug sensitivity of microbe Host factors Site of infection Immune status Empirical therapy
  7. 7. Ability of an antibiotic to destroy target cells without damaging host cells Differences between microbes and host Prokaryotic vs Eukaryotic Cell wall Inhibition of microbial enzymes Disruption of bacterial protein synthesis
  8. 8. Host defense (immune system, skin) Site of infection BBB, vascularity, heart valves, abscess Age Pregnancy & Lactation Previous Allergic Reaction Genetic Host defense mechanism: A chemotherapeutic regimen that is perfectly adequate for immuno-competent patient may be totally ineffective for immuno-incompetent patient. Immuno-incompetence may be due to deficiencies in Immunoglobulin, phagocytic cells and cellular immune system.
  9. 9. Hepatic function: Erythromycin, clindamycin, rifampin, Chloramphenicol depend on liver metabolisms for the inactivation of antimicrobial mechanisms. Patients with impaired liver function may accumulate in the body active form of the drugs to a toxic level if the dosage adjustment is not made. Kidney function: Normal kidney function is essential for disposal of -lactams, aminoglycosides, vancomycin, Active form of these drugs may accumulate in the patient with renal diseases.
  10. 10. Surgery Bacterial endocarditis Neutropenia Other
  11. 11. MIC: Minimum inhibitory concentration if drug does not get the concentration, then drug is ineffective Mechanisms Drug inactivating enzymes Cease uptake of drug Change in bacterial receptors Synthesize drug antagonists Acquisition Spontaneous mutation – single resistance Conjugation –multiple drug resistance
  12. 12. Natural (Inherent) Lack target or transport Acquired Mutation Horizontal transfer Vertical Horizontal Transformation Transduction Conjugation
  13. 13. Prevent cross linking Binds to transpeptidases Add new monomers Reseal wall Osmotic Lysis Bacterial Resistance Penicillinase, MRSA VRSA Beta Lactamases Cephalosporinases
  14. 14. Use of antibiotics to treat viral infections Inadequate pathogen coverage Excessive use of broad spectrum agents Sub-optimal dosing Retaining unfinished antibiotic for later use
  15. 15. Increased rate of treatment failure Poor patient compliance Increased mortality Need for combination therapy Increased cost of treatment
  16. 16. THANKYOU Download slides from Authorstream-raghuprasada Slideshare-raghuprasada Youtube-raghuprasada

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