Exam #1 Blueprint Pharm.xlsx - 1.Pharmacodynamics and Pharmacokinetics a.Drug interactions the desired therapeutic effect of the drug Pharmacokinetics

Exam #1 Blueprint Pharm.xlsx - 1.Pharmacodynamics and...

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1. Pharmacodynamics and Pharmacokinetics a. Drug interactions * Pharmacotherapeutics: the desired therapeutic effect of the drug * Pharmacokinetics: the changes that occur to the drug while it is inside the body - Absorption: movement of drug from site of administration to bloodstream - Distribution: movement of drug through bloodstream, into tissues, and eventually to cells - Metabolism: conversion of drug into substance or substances - Excretion: removal of drug, or what drug became after metabolism, from the body - Drugs cross cell membranes between spaces or channels if small, or need transport system which m - Other: chemistry of drug, half-life (time to remove half of blood concentration of drug), steady stat * Pharmacodynamics: the effects of the drug on the body i. Additive effect: When two or more “like” drugs are combined, and the result is the sum of the drugs’ ii. Antagonistic effect: The opposite of a synergistic effect. It results in a therapeutic effect that is less than t second drug either diminishes or cancels the effect of the first drug (i.e. 1 + 1 = 0) 2. Principles of anti-microbial therapy a. Goal of antibiotic therapy * Antimicrobial classified by mechanism of action: o Inhibition of bacterial cell wall synthesis: drugs can weaken cell wall by absorbing water, bind to pr inhibit cell wall synthesis, or activate autolytic enzymes that destroy wall; w/o the rigid cell well, the absorb water, swell, and lyse o Inhibition of protein synthesis: drugs can differentiate human ribosomes from bacterial; will bind o subunits of the process of protein synthesis necessary for bacteria w/o harming human protein synt o Inhibition of nucleic acid synthesis: inhibit enzymes needed for replication o Inhibition of metabolic pathways (antimetabolites): inhibits bacterial synthesis of folate (acts as co biosynthetic rxns) by acting as an antimetabolite of folate precursor PABA o Disruption of cell wall permeability: causes cell to leak components vital for survival o Inhibition of viral enzymes: interrupt important enzymes required for viral replication * Bacteriostatic = inhibit bacteria but effect is reversible if drug is removed so needs immune system (unless host defense mechanisms are gone) vs. bacteriocidal = kill bacteria; postantibiotic effect = or growing for several hours after exposure *Peak and trough- Peak is when drug levels are highest in the blood, and trough is when levels are d before. *Selective toxicity - Ability to suppress or kill and infecting microbe without injury to the host. *Cross sensitivity reaction- one antibiotic renders sensitivity to other antibiotic of similar chemical s b. Spectrums of antibiotic activity (broad versus narrow) * narrow–spectrum (effective against few) * broad-spectrum (effective against many)
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c. Principles of Antibiotic Resistance - Antimicrobial classified by mechanism of action: o Inhibition of bacterial cell wall synthesis: drugs can weaken cell wall by absorbing water, bind to pr inhibit cell wall synthesis, or activate autolytic enzymes that destroy wall; w/o the rigid cell well, the
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