Got it — you want the pharmacology notes reformatted to match the exact styling of the vascular pathology notes I just wrote (the ones from document 7) — meaning: Bold section headers with ### Bullet points with for narrative points Tables with --- formatting Bold key terms inline Practice questions at the end Summary table at the end Let me redo the full pharmacology notes in that exact style now. --- Summary This comprehensive document covers the pharmacotherapeutic management of infectious diseases, spanning antibiotic principles, antimicrobial resistance, drug classes targeting bacterial cell walls and ribosomes, antimycobacterials, antifungals, antivirals, antiparasitic agents, HIV management, and the pharmacotherapy of acne. Key Points Selective toxicity is the foundational principle of chemotherapy — drugs must harm the pathogen while sparing the host, exploiting differences between microbial and human biochemistry. Antimicrobial resistance (AMR) is driven by enzymatic inactivation, target site mutation, efflux pumps, and reduced permeability, and spreads most importantly via conjugation (plasmid transfer). Beta-lactams inhibit penicillin-binding proteins (PBPs) to block peptidoglycan cross-linking; resistance via beta-lactamases is countered by beta-lactamase inhibitor combinations. Vancomycin is the drug of choice for MRSA but carries risks of red man syndrome, nephrotoxicity, and ototoxicity; therapeutic drug monitoring is essential. Aminoglycosides are concentration-dependent bactericidal agents with irreversible ototoxicity and nephrotoxicity as dose-limiting toxicities. Fluoroquinolones inhibit DNA gyrase and topoisomerase IV and are contraindicated in children, pregnant women, and patients with myasthenia gravis due to tendinopathy and cartilage toxicity. First-line TB therapy (RIPE) targets multiple stages of mycobacterial metabolism; rifampicin is a potent CYP450 inducer with clinically critical drug interactions. HIV management relies on combination ART targeting multiple steps of the viral replication cycle; preferred first-line regimen is TDF + 3TC + DTG with a treatment goal of viral load <50 copies/mL. Isotretinoin is the most effective acne treatment but is highly teratogenic (Category X), mandating a strict pregnancy prevention programme. Detailed Notes --- SECTION 1 — INTRODUCTION TO CHEMOTHERAPY & THE IMMUNE SYSTEM Principles of Chemotherapy Chemotherapy = use of chemical agents to treat or control disease — includes all antimicrobials, not just oncology agents Paul Ehrlich — father of chemotherapy; coined the concept of the "magic bullet" — a drug that selectively destroys a pathogen without harming the host Selective toxicity = the ability of a drug to harm a microorganism while sparing host cells; this is possible because microorganisms possess unique biochemical targets absent in human cells (e.g. peptidoglycan cell walls, 70S ribosomes, ergosterol membranes) Key terminology: Term Definition --- --- Bactericidal Kills bacteria directly Bacteriostatic Inhibits bacterial growth; relies on host immunity to clear infection MIC Minimum Inhibitory Concentration — lowest drug concentration that inhibits visible growth MBC Minimum Bactericidal Concentration — lowest concentration killing 99.9% of bacteria Broad spectrum Active against both Gram-positive and Gram-negative organisms Narrow spectrum Active against a limited range of organisms Post-antibiotic effect Continued bacterial suppression after drug concentration falls below MIC The Immune System Innate immunity (non-specific, first line): Physical barriers — skin, mucous membranes, cilia, gastric acid, normal flora Cellular components — neutrophils (first responders), macrophages, NK cells, dendritic cells Soluble factors — complement system, interferons, acute phase proteins (CRP, fibrinogen, ferritin) Pattern recognition — Toll-like receptors (TLRs) on innate cells recognise PAMPs (pathogen-associated molecular patterns — LPS, flagellin, peptidoglycan) Response is rapid (minutes to hours) with NO immunological memory Adaptive immunity (specific, second line): Humoral immunity — B cells → plasma cells → antibodies (IgG, IgM, IgA, IgE, IgD); IgM = first responder; IgG = most abundant; IgA = mucosal secretions Cell-mediated immunity — T lymphocytes: CD4+ T helper cells — coordinate immune response; activate B cells and macrophages; subtypes: Th1, Th2, Th17, T-reg CD8+ cytotoxic T cells — directly kill virus-infected cells and tumour cells via perforin/granzyme Response is slower (days to weeks) but generates immunological memory (basis of vaccination) Key immunological concepts: Concept Detail --- --- Antigen Foreign molecule triggering an immune response Opsonisation Antibody/complement coating of pathogens → enhanced phagocytosis MHC class I Presents endogenous antigens to CD8+ T cells; expressed on all nucleated cells MHC class II Presents exogenous antigens to CD4+ T cells; expressed only on APCs Complement MAC Membrane attack