HIGHLIGHTS of 18th Edition Ebook
- Build your knowledge with widely cross-medicated drugs.
- Stay up to date with drug news from the FDA.
- Audio pronunciations for nearly 890 generic drugs
- Over 700 built-in drug dosage calculation tools. Simply review a medication, calculate the dosage and administer all in one step
- without the need to switch to a separate medication dosing program
Comprehensive coverage of over 1,400 drug monographs, including over:
- 5,000 commercial and generic drugs, as well as greater coverage of herbal products
- 150 drug classifications, both therapeutic and pharmacological (if available)
- 500 commonly used combination drugs, including the dosage amount of the active generic ingredient
- More Comprehensive Lifetime Drug Dosing Considerations for Adult, Pediatric, and Geriatric Patients
Davis’s Drug Guide for nurses 18th edition PDF
The human genome is made up of approximately 3 billion nucleotide base pair sequences that encode molecular DNA, and each individual has their own unique human genomic sequence (except in the case of identical twins). Four nucleotide bases (adenine, guanine, cytosine, and thymine) for the sequence of each single strand of DNA. Variations in nucleotide sequences can occur and contribute to alterations in the expression and activities of certain genes as well as their protein products. The location of these variations within a DNA sequence on a particular chromosome can have a profound impact on the biological activity of that gene; however, it should also be understood that some genetic variants may lead to little or no detectable changes in biological activity. As new genetic variants are discovered, the process of understanding the degree of impact becomes the focus of researchers. Proteins participate in most of the enzymatic, structural, and biological functions associated with the disposition and effects of drugs. The processes involved in DNA replication, RNA transcription, and translation into synthesized proteins are complex. Each of these processes is potentially susceptible to the consequences of DNA sequence variations. Genetic variations can take many forms, but most fall into three general categories:
- Single nucleotide base substitutions (eg, a cytosine substituted for an adenine)
- Insertions or deletions of a nucleotide base within a sequence
- Deletions or extra copies of complete DNA sequences (eg, trisomy 21, in which an extra copy of all genes is present on chromosome 21)
Variations in DNA that occur with a frequency greater than 1% in the population are called polymorphisms. The most common genetic variants in humans are single nucleotide polymorphisms (SNPs), pronounced like the word “snips” in dialogue). SNPs result from the substitution of one nucleotide base for another. The location of a SNP within a gene is important, as the location may or may not cause a downstream effect on a protein made from the gene. It is helpful to remember the importance of introns and exons to mRNA manufacturing when considering how SNPs can affect protein function. An important point to keep in mind is that any genetic variant can have a spectrum-like impact on protein production ranging from zero clinical consequences (no discernible effect on proteins) to a complete lack of functional proteins associated with significant alterations in protein production. the response to the drug. Furthermore, clinical pharmacogenomic effects must always be considered within the broader sphere of environmental influences on and responses to drugs. Finally, due to the similarity of the polymorphisms, multiple genetic variants can be present in the same patient, which makes the prediction of drug response particularly challenging.
SNPs and other genetic variations influence drug response at different levels through alterations in the activities of enzymes or proteins involved in absorption, transport, metabolism, elimination, or at the drug’s target receptor (binding site). drug action). Clinically relevant polymorphisms have been identified for genes encoding most of the common enzymes involved in drug metabolism. Most enzymes are located intracellularly in a wide variety of body tissues, including the enterocytes lining the intestine and within hepatocytes. Variants that cause decreased or absent enzyme activity decrease drug metabolism processes. In this case, if the drug is metabolized to an inactive product, prolonged persistence of the parent drug in the body could lead to excessive pharmacological effects and potential toxicities. If the drug requires enzymatic conversion to a pharmacologically active metabolite, the response to the drug may be reduced or absent. Conversely, if the variation is due to additional copies of a gene resulting in increased enzyme activity, opposite effects on drug metabolism and response may occur. Similar results can be associated with polymorphisms in genes encoding membrane transport proteins that are responsible for transporting drugs into cells (influx), as well as proteins that participate in energy-dependent processes that export drugs out of cells (efflux transporters).
Davis’s Drug Guide for nurses 18th edition PDF free 2022 has the following chapters
- How to Use Davis’s Drug Guide for Nurses
- Evidence-Based Practice and Pharmacotherapeutics: Implications for Nurses
- Medication Errors: Improving Practices and Patient Safety
- Detecting and Managing Adverse Drug Reactions
- Overview of Risk Evaluation and Mitigation Systems (REMS)
- Special Dosing Considerations
- The Cytochrome P450 System: What Is It and Why Should I Care?
- Educating Patients About Safe Medication Use
- Drug Monographs in Alphabetical Order by Generic Name
- Drugs Approved in Canada
- Natural/Herbal Products
- Medication Safety Tools