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Why clindamycin and macrolide don’t produce gray baby syndrome?
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Classroom Contents
Clindamycin, Erythromycin, and Chloramphenicol - Mechanisms of Action and Clinical Correlations
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- 1 Introduction and overview of lecture
- 2 Overview of similarities between Clindamycin, Macrolide and chloramphenicol
- 3 Clindamycin, macrolide and chloramphenicol work as protein synthesis inhibitors
- 4 MOA of clindamycin, macrolide and chloramphenicol on Bacterial Ribosomes
- 5 MOA of clindamycin, macrolide and chloramphenicol on larger 50s ribosomal subunit
- 6 Action of clindamycin , macrolide and Chloramphenicol on 23s Ribosomal RNA
- 7 Summary of above 4 similarities in the MOA of Clindamycin , Macrolide and Chloramphenicol
- 8 MOA of Clindamycin, Macrolide and Chloramphenicol on Ribozyme
- 9 What is Peptidyl Transferase?
- 10 Summary of all above similarities between Clindamycin, Macrolide and Chloramphenicol
- 11 Detailed explanation on the functions of Peptidyl Transferase
- 12 Transpeptidation and Ribosomal Translocation
- 13 Peptide chain elongation
- 14 How Clindamycin, Macrolide and chloramphenicol inhibit the protein synthesis by inhibiting the chain elongation process?
- 15 Summary of similarities between Clindamycin, Macrolide and Chloramphenicol
- 16 MOA; Clindamycin
- 17 MOA; Clindamycin as bacteriostatic and bactericidal
- 18 Summary of MOA of Clindamycin
- 19 MOA; Macrolides
- 20 MOA; Chloramphenicol binding site.
- 21 MOA; Comparison of binding site of clindamycin vs macrolide vs chloramphenicol.
- 22 MOA; Chloramphenicol.
- 23 Chloramphenicol; Adverse effects.
- 24 Why clindamycin and macrolide don’t produce gray baby syndrome?
- 25 Clinical co-relation; Competitive Inhibition; Why clindamycin and erythromycin are not used together for a treatment of any infection?
- 26 Summary of role of clindamycin in TSS.
- 27 Clinical co-relation; Cross resistance.
- 28 Mechanism of resistance involving the changes at binding site, 23s rRNA.
- 29 Mechanism#1; Mutant ribosomal protein.
- 30 Mechanism#2; Mutation of adenine group at target site, 23s rRNA.
- 31 Mechanism#3; Methylation of adenine group at target site, 23s rRNA.
- 32 Clinical co-relation; Cross resistance because of erm genes.
- 33 Clinical co-relation; post-antibiotic effect in relation to clindamycin, erythromycin
- 34 Secondary effect#1; Reduced quantity of proteins
- 35 Secondary effect#2; Distorted proteins.
- 36 Bacteriostatic action/ Bactericidal action
- 37 Surface bacterial proteins altered; Decrease adherence of bacteria.
- 38 Surface bacterial proteins altered; Increased opsonization and phagocytosis.
- 39 Summary of effects on membrane produced by clindamycin.
- 40 Increased active uptake of clindamycin by neutrophils and macrophages leading to increased intra-cellular killing.
- 41 Excellent choice for abscesses produced by the susceptible bacteria.
- 42 Penetration of drug; Bones.
- 43 Penetration of drug; Can’t cross BBB.
- 44 Summary of all effects produced by clindamycin.
- 45 Black box warning for Clindamycin.
- 46 Pathogenesis of Pseudomembranous colitis.
- 47 Risk factors for Pseudomembranous colitis.
- 48 Directions to be given to the patient while prescribing clindamycin.
- 49 Treatment for C. diff colitis.
- 50 Summary of Black box warning for Clindamycin.
