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Anti-microbrial Drug
| Question | Answer |
|---|---|
| Goal of Antimicrobial Drugs | The primary goal of antimicrobial drugs is to interfere with the growth of microbes. This includes selectively finding and destroying pathogens to treat a diseas |
| Chemotherapy | The use of chemicals to treat a disease. |
| Antibiotics | A substance produced by a microbe that, in small amounts, inhibits another microbe. |
| Selective Toxicity | Selectively finding and destroying pathogens without damaging the host. |
| Narrow Spectrum | Drugs that affect only a narrow range of microbial types. Fungi treated by ketoconazole, G+ bacteria treated by Penicillin G |
| Broad Spectrum | Antibiotics that affect a broad range of gram-positive or gram-negative bacteria; these are often used for polymicrobic infections. Tetracycline, Streptomycin |
| Selective Toxicity | Selective toxicity refers to the ability of a drug to selectively kill or inhibit the growth of microbial targets while causing minimal or no harm to the host |
| Dosage | The amount of medication given during a specific time interval. It is carefully determined to ensure optimum therapeutic drug levels at the site of infection without causing significant side effects. |
| Route of administration | The method used to introduce a drug into the body. Oral: Convenient for home use, but some drugs are not easily absorbed by the GI tract. Parenteral (Intravenous or Intramuscular): Reaches high plasma concentrations quickly but is typically performed in healthcare settings. |
| Toxicity | The side effects caused by the drug itself. |
| Half-life | The rate at which 50% of a drug is eliminated from the plasma. It depends on metabolism and excretion functions (like renal health). shorter half - lifes need frequent dosage while longer half-life can be given SID or BID |
| Metabolic/Excretion efficiency | Issues like renal failure can lengthen a drug's half-life and the duration of adverse effects. |
| Synergism | Two antibacterial drugs may be administered together to improve efficacy |
| Antagonism | occurs between two antimicrobials or an antimicrobial and non-antimicrobial being used to treat other conditions. May cause loss of drug activity, decreased therapeutic levels due to increased metabolism and elimination, or increased potential for toxicity |
| Bactericidal | These drugs kill microbes directly. |
| Bacteriostatic | These drugs prevent microbes from growing rather than killing them immediately |
| Cell Wall Biosynthesis Inhibition | Drugs like natural penicillins contain a β-lactam ring that prevents the synthesis of peptidoglycan. (ex. penicillin's, ampicillin, amoxicllin, methicillin.) Semisynthetic penicillins contain chemically added side chains, making them resistant to penicillinases. |
| Protein Synthesis Inhibition | Drugs target different steps in bacterial translation (chloramphenicol, erythromycin,stretomycin, tetracyclines) For example, chloramphenicol inhibits peptide bond formation by binding to the 50S subunit of the ribosome. This makes 30S portion of mRNA to be read incorrectly and they interfere with attachment of tRNA like tetracyclines |
| Membrane Function Inhibition | Polypeptide antibiotics like Polymyxin B change membrane permeability. This mechanism is often not selectively toxic. |
| Nucleic Acid Synthesis Inhibition | Drugs interfere with DNA replication (by blocking DNA polymerase or helicase) or transcription (by inhibiting RNA polymerase). NOt as selectively toxic for DNA synthesis, but is for RNA synthesis |
| Metabolic Pathway Inhibition | Antimetabolites compete with normal substrates for an enzyme. For instance, sulfanilamide competes with para-aminobenzoic to stop folic acid synthesis. |
| Drug resistance | Antimicrobial resistance occurs when microbes evolve and develop the ability to defeat the drugs designed to kill them - bacteria, fungi, viruses, protozoa. This is often driven by selective pressures such as the overuse and misuse of antimicrobials. |
| Drug Modification or Inactivation: | Bacteria produce enzymes (like β-lactamase) that destroy the drug |
| Prevention of Uptake or Efflux: | Inhibiting drug accumulation or actively pumping the antibiotic out of the cell using transport proteins |
| Target Modification: | Spontaneous mutations change the structure of the drug's target, preventing the drug from binding. |
| Target Overproduction/Enzymatic Bypass: | Producing more of a target enzyme or finding alternative pathways to bypass the inhibited enzyme. |
| Target Mimicry: | Producing proteins that mimic the target and sequester the drug. |
| Kirby-Bauer Disk-Diffusion Test: | Paper disks with a chemotherapeutic agent are placed on agar; the resulting "zone of inhibition" determines sensitivity. |
| Dilution Test: | Determines the Minimum Inhibitory Concentration (MIC) and Minimal Bactericidal Concentration (MBC) by placing the organism in trays with varying drug dilutions. |
| E-Test | A gradient diffusion method used to estimate the MIC |
| consequences of not completing treatment | Patient noncompliance, such as stopping a prescribed antibiotic course early, provides selective pressure for the evolution of drug-resistant "superbugs". It allows more resistant mutants that arise spontaneously to be selected and survive. |
Created by:
agk236