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Introduction and overview of lecture
2
Overview of similarities between Clindamycin, Macrolide and chloramphenicol
3
Clindamycin, macrolide and chloramphenicol work as protein synthesis inhibitors
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MOA of clindamycin, macrolide and chloramphenicol on Bacterial Ribosomes
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MOA of clindamycin, macrolide and chloramphenicol on larger 50s ribosomal subunit
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Action of clindamycin , macrolide and Chloramphenicol on 23s Ribosomal RNA
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Summary of above 4 similarities in the MOA of Clindamycin , Macrolide and Chloramphenicol
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MOA of Clindamycin, Macrolide and Chloramphenicol on Ribozyme
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What is Peptidyl Transferase?
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Summary of all above similarities between Clindamycin, Macrolide and Chloramphenicol
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Detailed explanation on the functions of Peptidyl Transferase
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Transpeptidation and Ribosomal Translocation
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Peptide chain elongation
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How Clindamycin, Macrolide and chloramphenicol inhibit the protein synthesis by inhibiting the chain elongation process?
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Summary of similarities between Clindamycin, Macrolide and Chloramphenicol
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MOA; Clindamycin
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MOA; Clindamycin as bacteriostatic and bactericidal
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Summary of MOA of Clindamycin
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MOA; Macrolides
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MOA; Chloramphenicol binding site.
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MOA; Comparison of binding site of clindamycin vs macrolide vs chloramphenicol.
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MOA; Chloramphenicol.
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Chloramphenicol; Adverse effects.
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Why clindamycin and macrolide don’t produce gray baby syndrome?
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Clinical co-relation; Competitive Inhibition; Why clindamycin and erythromycin are not used together for a treatment of any infection?
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Summary of role of clindamycin in TSS.
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Clinical co-relation; Cross resistance.
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Mechanism of resistance involving the changes at binding site, 23s rRNA.
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Mechanism#1; Mutant ribosomal protein.
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Mechanism#2; Mutation of adenine group at target site, 23s rRNA.
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Mechanism#3; Methylation of adenine group at target site, 23s rRNA.
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Clinical co-relation; Cross resistance because of erm genes.
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Clinical co-relation; post-antibiotic effect in relation to clindamycin, erythromycin
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Secondary effect#1; Reduced quantity of proteins
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Secondary effect#2; Distorted proteins.
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Bacteriostatic action/ Bactericidal action
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Surface bacterial proteins altered; Decrease adherence of bacteria.
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Surface bacterial proteins altered; Increased opsonization and phagocytosis.
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Summary of effects on membrane produced by clindamycin.
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Increased active uptake of clindamycin by neutrophils and macrophages leading to increased intra-cellular killing.
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Excellent choice for abscesses produced by the susceptible bacteria.
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Penetration of drug; Bones.
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Penetration of drug; Can’t cross BBB.
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Summary of all effects produced by clindamycin.
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Black box warning for Clindamycin.
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Pathogenesis of Pseudomembranous colitis.
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Risk factors for Pseudomembranous colitis.
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Directions to be given to the patient while prescribing clindamycin.
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Treatment for C. diff colitis.
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Summary of Black box warning for Clindamycin.
Description:
Save Big on Coursera Plus. 7,000+ courses at $160 off. Limited Time Only! Grab it Dive into a comprehensive video lecture exploring the mechanisms of action and clinical correlations of Clindamycin, Erythromycin, and Chloramphenicol. Learn about their roles as protein synthesis inhibitors, their effects on bacterial ribosomes, and the similarities in their modes of action. Understand the functions of peptidyl transferase, the process of peptide chain elongation, and how these antibiotics inhibit protein synthesis. Explore the specific mechanisms of each drug, including their bacteriostatic and bactericidal properties. Discover clinical correlations, including competitive inhibition, cross-resistance, and post-antibiotic effects. Examine secondary effects, drug penetration, and important considerations like the black box warning for Clindamycin. Gain insights into pseudomembranous colitis, its risk factors, and treatment options.

Clindamycin, Erythromycin, and Chloramphenicol - Mechanisms of Action and Clinical Correlations

Dr. Najeeb Lectures
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#Health & Medicine #Health Care #Pharmacology #Science #Biology #Microbiology #Antibiotics #Drug Resistance
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Introduction and overview of lecture