para 1 The Non-Coding Genome: From "Junk" to Disease Reservoir

Dams and Reservoirs

ESS105 Study Guide: Chemical Reservoirs and Solid Earth Structure

Irregular -ir verbs (recevoir)

Reservoir Final

518 Song Repertoire Final America

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Antibodies in Host Defense: B Cell Repertoire, Classes, and Monoclonal Therapies

Regulation of Gene Expression Lecture Outline Overview: Differential Expression of Genes • Both prokaryotes and eukaryotes alter their patterns of gene expression in response to changes in environmental conditions. • Multicellular eukaryotes also develop and maintain multiple cell types. ○ Each cell type contains the same genome but expresses a different subset of genes. ○ During development, gene expression must be carefully regulated to ensure that the right genes are expressed only at the correct time and in the correct place. • Gene expression in eukaryotes and bacteria is often regulated at the transcription stage. ○ Control of other levels of gene expression is also important. • RNA molecules play many roles in regulating eukaryotic gene expressions. • Disruptions in gene regulation may lead to cancer. Concept 18.1 Bacteria often respond to environmental change by regulating transcription • Natural selection favors bacteria that express only those genes whose products are needed by the cell. ○ A bacterium in a tryptophan-rich environment that stops producing tryptophan conserves its resources. • Metabolic control occurs on two levels. • First, cells can adjust the activity of enzymes already present. ○ This may happen by feedback inhibition, in which the activity of the first enzyme in a pathway is inhibited by the pathway’s end product. ○ Feedback inhibition, typical of anabolic (biosynthetic) pathways, allows a cell to adapt to short-term fluctuations in the supply of a needed substance. • Second, cells can vary the number of specific enzyme molecules they make by regulating gene expression. ○ The control of enzyme production occurs at the level of transcription, the synthesis of messenger RNA coding for these enzymes. ○ Genes of the bacterial genome may be switched on or off by changes in the metabolic status of the cell. • The basic mechanism for the control of gene expression in bacteria, known as the operon model, was described by Francois Jacob and Jacques Monod in 1961. The operon model controls tryptophan synthesis. • Escherichia coli synthesizes tryptophan from a precursor molecule in a series of steps, with each reaction catalyzed by a specific enzyme. • The five genes coding for the subunits of these enzymes are clustered together on the bacterial chromosome as a transcription unit, served by a single promoter. • Transcription gives rise to one long mRNA molecule that codes for all five polypeptides in the tryptophan pathway. • The mRNA is punctuated with start and stop codons that signal where the coding sequence for each polypeptide begins and ends. • A key advantage of grouping genes with related functions into one transcription unit is that a single on-off switch can control a cluster of functionally related genes. ○ In other words, these genes are coordinately controlled. • When an E. coli cell must make tryptophan for itself, all the enzymes are synthesized at one time. • The switch is a segment of DNA called an operator. • The operator, located within the promoter or between the promoter and the enzyme-coding genes, controls the access of RNA polymerase to the genes. • The operator, the promoter, and the genes they control constitute an operon. ○ The trp operon (trp for tryptophan) is one of many operons in the E. coli genome. • By itself, an operon is turned on: RNA polymerase can bind to the promoter and transcribe the genes of the operon. • The operon can be switched off by a protein called the trp repressor. ○ The repressor binds to the operator, blocks attachment of RNA polymerase to the promoter, and prevents transcription of the operon’s genes. • Each repressor protein recognizes and binds only to the operator of a particular operon. • The trp repressor is the protein product of a regulatory gene called trpR, which is located at some distance from the operon it controls and has its own promoter. • Regulatory genes are transcribed continuously at slow rates, and a few trp repressor molecules are always present in an E. coli cell. • Why is the trp operon not switched off permanently? • First, binding by the repressor to the operator is reversible. ○ An operator vacillates between two states, with and without a repressor bound to it. ○ The relative duration of each state depends on the number of active repressor molecules around. • Second, repressors contain allosteric sites that change shape depending on the binding of other molecules. ○ The trp repressor has two shapes: active and inactive. ○ The trp repressor is synthesized in an inactive form with little affinity for the trp operator. ○ Only if tryptophan binds to the trp repressor at an allosteric site does the repressor protein change to the active form that can attach to the operator, turning the operon off. • Tryptophan functions in the trp operon as a corepressor, a small molecule that cooperates with a repressor protein to switch an operon off. • When concentrations of tryptophan in the cell are high, more tryptophan molecules bind with trp repressor molecules, activating them. ○ The active repressors bind to the trp operator and turn the operon off. • At low levels of tryptophan, most of the repressors are inactive, and transcription of the operon’s genes resumes. There are two types of operons: repressible and inducible. • The trp operon is an example of a repressible operon, one that is inhibited when a specific small molecule (tryptophan) binds allosterically to a regulatory protein. • In contrast, an inducible operon is stimulated (induced) when a specific small molecule interacts with a regulatory protein. • The classic example of an inducible operon is the lac operon (lac for lactose). • Lactose (milk sugar) is available to E. coli in the human colon if the host drinks milk. ○ Lactose metabolism begins with hydrolysis of lactose into its component monosaccharides, glucose and galactose. ○ This reaction is catalyzed by the enzyme ß-galactosidase. • Only a few molecules of b-galactosidase are present in an E. coli cell grown in the absence of lactose. ○ If lactose is added to the bacterium’s environment, the number of ß-galactosidase molecules increases by a thousandfold within 15 minutes. • The gene for ß-galactosidase is part of the lac operon, which includes two other genes coding for enzymes that function in lactose metabolism. • The regulatory gene, lacI, located outside the operon, codes for an allosteric repressor protein that can switch off the lac operon by binding to the operator. • Unlike the trp operon, the lac repressor is active all by itself, binding to the operator and switching the lac operon off. ○ An inducer inactivates the repressor. ○ When lactose is present in the cell, allolactose, an isomer of lactose, binds to the repressor. ○ This inactivates the repressor, and the lac operon can be transcribed. • Repressible enzymes generally function in anabolic pathways, synthesizing end products from raw materials. ○ When the end product is present in sufficient quantities, the cell can allocate its resources to other uses. • Inducible enzymes usually function in catabolic pathways, digesting nutrients to simpler molecules. ○ By producing the appropriate enzymes only when the nutrient is available, the cell avoids making proteins that are not needed. • Both repressible and inducible operons demonstrate negative control of genes because active repressors switch off the active form of the repressor protein. ○ It may be easier to see this for the trp operon, but it is also true for the lac operon. ○ Allolactose induces enzyme synthesis not by acting directly on the genome, but by freeing the lac operon from the negative effect of the repressor. Some gene regulation is positive. • Positive gene control occurs when a protein molecule interacts directly with the genome to switch transcription on. • The lac operon is an example of positive gene regulation. • When glucose and lactose are both present, E. coli preferentially uses glucose. ○ The enzymes for glucose breakdown in glycolysis are always present in the cell. • Only when lactose is present and glucose is in short supply does E. coli use lactose as an energy source and synthesize the enzymes for lactose breakdown. • When glucose levels are low, cyclic AMP (cAMP) accumulates in the cell. • The regulatory protein catabolite activator protein (CAP) is an activator of transcription. • When cAMP is abundant, it binds to CAP, and the regulatory protein assumes its active shape and can bind to a specific site at the upstream end of the lac promoter. ○ The attachment of CAP to the promoter increases the affinity of RNA polymerase for the promoter, directly increasing the rate of transcription. ○ Thus, this mechanism qualifies as positive regulation. • If glucose levels in the cell rise, cAMP levels fall. ○ Without cAMP, CAP detaches from the operon and lac operon is transcribed only at a low level. • The lac operon is under dual control: negative control by the lac repressor and positive control by CAP. ○ The state of the lac repressor (with or without bound allolactose) determines whether or not the lac operon’s genes are transcribed. ○ The state of CAP (with or without bound cAMP) controls the rate of transcription if the operon is repressor-free. ○ The operon has both an on-off switch and a volume control. • CAP works on several operons that encode enzymes used in catabolic pathways. It affects the expression of more than 100 E. coli genes. ○ If glucose is present and CAP is inactive, then the synthesis of enzymes that catabolize other compounds is slowed. ○ If glucose levels are low and CAP is active, then the genes that produce enzymes that catabolize whichever other fuel is present are transcribed at high levels. Concept 18.2 Eukaryotic gene expression is regulated at many stages • Like unicellular organisms, the tens of thousands of genes in the cells of multicellular eukaryotes turn on and off in response to signals from their internal and external environments. • Gene expression must be controlled on a long-term basis during cellular differentiation. Differential gene expression is the expression of different genes by cells with the same genome. • A typical human cell probably expresses about 20% of its genes at any given time. ○ Highly specialized cells, such as nerves or muscles, express a tiny fraction of their genes. ○ Although all the cells in an organism contain an identical genome, the subset of genes expressed in the cells of each type is unique. • The differences between cell types are due to differential gene expression, the expression of different genes by cells with the same genome. • The function of any cell, whether a single-celled eukaryote or a particular cell type in a multicellular organism, depends on the appropriate set of genes being expressed. ○ Problems with gene expression and control can lead to imbalance and disease, including cancer. • Our understanding of the mechanisms that control gene expression in eukaryotes has been enhanced by new research methods, including advances in DNA technology. • In all organisms, a common control point for gene expression is at transcription, often in response to signals coming from outside the cell. ○ For this reason, the term gene expression is often equated with transcription. • With their greater complexity, eukaryotes have opportunities for controlling gene expression at additional stages. Chromatin modifications affect the availability of genes for transcription. • The DNA of eukaryotic cells is packaged with proteins in a complex called chromatin. ○ The basic unit of chromatin is the nucleosome. • The location of a gene’s promoter relative to nucleosomes and to the sites where the DNA attaches to the chromosome scaffold or nuclear lamina affect whether the gene is transcribed. • Genes of densely condensed heterochromatin are usually not expressed. • Chemical modifications of the histone proteins and DNA of chromatin play a key role in chromatin structure and gene expression. • The N-terminus of each histone molecule in a nucleosome protrudes outward from the nucleosome. ○ These histone tails are accessible to various modifying enzymes, which catalyze the addition or removal of specific chemical groups. • Histone acetylation (addition of an acetyl group, —COCH3) and deacetylation of lysines in histone tails appear to play a direct role in the regulation of gene transcription. • Acetylation of lysines neutralizes their positive charges and reduces the binding of histone tails to neighboring nucleosomes, easing access for transcription proteins. ○ Some of the enzymes responsible for acetylation or deacetylation are associated with or are components of transcription factors that bind to promoters. • Thus, histone acetylation enzymes may promote the initiation of transcription not only by modifying chromatin structure but also by binding to and recruiting components of the transcription machinery. • Other chemical groups, such as methyl and phosphate groups, can be reversibly attached to amino acids in histone tails. ○ The attachment of methyl groups (—CH3) to histone tails leads to condensation of chromatin. ○ The addition of a phosphate group (phosphorylation) to an amino acid next to a methylated amino acid has the opposite effect. • The recent discovery that modifications to histone tails can affect chromatin structure and gene expression has led to the histone code hypothesis. ○ This hypothesis proposes that specific combinations of modifications, as well as the order in which they have occurred, determine chromatin configuration. ○ Chromatin configuration in turn influences transcription. DNA methylation reduces gene expression. • While some enzymes methylate the tails of histone proteins, other enzymes methylate certain bases in DNA itself, usually cytosine. ○ DNA methylation occurs in most plants, animals, and fungi. • Inactive DNA is generally more highly methylated than actively transcribed regions. ○ For example, the inactivated mammalian X chromosome is heavily methylated. ○ Individual genes are usually more heavily methylated in cells where they are not expressed. Removal of extra methyl groups can turn on some of these genes. • In some species, DNA methylation is responsible for the long-term inactivation of genes during cellular differentiation. ○ Deficient DNA methylation leads to abnormal embryonic development in organisms as different as mice and the plant Arabidopsis. • Once methylated, genes usually stay that way through successive cell divisions in a given individual. • Methylation enzymes recognize sites on one strand that are already methylated and correctly methylate the daughter strand after each round of DNA replication. • This methylation pattern accounts for genomic imprinting, in which methylation turns off either the maternal or paternal alleles of certain mammalian genes at the start of development. • The chromatin modifications just discussed do not alter the DNA sequence, and yet they may be passed along to future generations of cells. • Inheritance of traits by mechanisms not directly involving the nucleotide sequence is called epigenetic inheritance. • The molecular systems for chromatin modification may well interact with each other in a regulated way. ○ In Drosophila, experiments suggest that a particular histone-modifying enzyme recruits a DNA methylation enzyme to one region and that the two enzymes collaborate to silence a particular set of genes. ○ Working in the opposite order, proteins have also been found that bind to methylated DNA and then recruit histone deacetylation enzymes. ○ Thus, a dual mechanism, involving both DNA methylation and histone deacetylation, can repress transcription. • Researchers are amassing more and more evidence for the importance of epigenetic information in the regulation of gene expression. ○ Epigenetic variations may explain why one identical twin acquires a genetically based disease, such as schizophrenia, while another does not, despite their identical genomes. ○ Alterations in normal patterns of DNA methylation are seen in some cancers, where they are associated with inappropriate gene expression. • Enzymes that modify chromatin structure are integral parts of the cell’s machinery for regulating transcription. Transcription initiation is controlled by proteins that interact with DNA and with each other. • Chromatin-modifying enzymes provide initial control of gene expression by making a region of DNA more available or less available for transcription. • A cluster of proteins called a transcription initiation complex assembles on the promoter sequence at the upstream end of the gene. ○ One component, RNA polymerase II, transcribes the gene, synthesizing a primary RNA transcript or pre-mRNA. ○ RNA processing includes enzymatic addition of a 5¢ cap and a poly-A tail, as well as splicing out of introns to yield a mature mRNA. • Multiple control elements are associated with most eukaryotic genes. ○ Control elements are noncoding DNA segments that serve as binding sites for protein transcription factors. ○ Control elements and the transcription factors they bind are critical to the precise regulation of gene expression in different cell types. • To initiate transcription, eukaryotic RNA polymerase requires the assistance of proteins called transcription factors. • General transcription factors are essential for the transcription of all protein-coding genes. ○ Only a few general transcription factors independently bind a DNA sequence such as the TATA box within the promoter. ○ Others are involved in protein-protein interactions, binding each other and RNA polymerase II. • Only when the complete initiation complex has been assembled can the polymerase begin to move along the DNA template strand to produce a complementary strand of RNA. • The interaction of general transcription factors and RNA polymerase II with a promoter usually leads to only a slow rate of initiation and the production of few RNA transcripts. • In eukaryotes, high levels of transcription of particular genes depend on the interaction of control elements with specific transcription factors. • Some control elements, named proximal control elements, are located close to the promoter. • Distal control elements, grouped as enhancers, may be thousands of nucleotides away from the promoter or even downstream of the gene or within an intron. • A given gene may have multiple enhancers, each active at a different time or in a different cell type or location in the organism. ○ Eukaryotic gene expression can be altered by the binding of specific transcription factors, either activators or repressors, to the control elements of enhancers. • Two structural elements are common to many activator proteins: a DNA-binding domain and one or more activation domains. ○ Activation domains bind other regulatory proteins or components of the transcription machinery to facilitate transcription. • Protein-mediated bending of DNA brings bound activators in contact with a group of mediator proteins that interact with proteins at the promoter. ○ These interactions help assemble and position the initiation complex on the promoter. • Eukaryotic repressors can inhibit gene expression by blocking the binding of activators to their control elements or to components of the transcription machinery. ○ Other repressors bind directly to control-element DNA, turning off transcription even in the presence of activators. • Some activators and repressors act indirectly to influence chromatin structure. ○ Some activators recruit proteins that acetylate histones near the promoters of specific genes, promoting transcription. ○ Some repressors recruit proteins that deacetylate histones, reducing transcription or silencing the gene. • Recruitment of chromatin-modifying proteins seems to be the most common mechanism of repression in eukaryotes. The control of transcription in eukaryotes depends on the binding of activators to DNA control elements. • The number of different nucleotide sequences found in control elements is surprisingly small: about a dozen. • On average, each enhancer is composed of about ten control elements, each of which can bind to only one or two specific transcription factors. ○ The particular combination of control elements in an enhancer may be more important than the presence of a unique control element in regulating transcription of the gene. • Even with only a dozen control element sequences, a large number of combinations are possible. • A particular combination of control elements is able to activate transcription only when the appropriate activator proteins are present, at a precise time during development or in a particular cell type. • The use of different combinations of control elements allows fine regulation of transcription with a small set of control elements. • In prokaryotes, coordinately controlled genes are often clustered into an operon with a single promoter and other control elements upstream. ○ The genes of the operon are transcribed into a single mRNA and translated together. • In contrast, very few eukaryotic genes are organized this way. • More commonly, co-expressed genes coding for the enzymes of a metabolic pathway are scattered over different chromosomes. ○ Coordinate gene expression depends on the association of a specific control element or combination of control elements with every gene of a dispersed group. ○ A common group of transcription factors binds to all the genes in the group, promoting simultaneous gene transcription. • For example, a steroid hormone enters a cell and binds to a specific receptor protein in the cytoplasm or nucleus, forming a hormone–receptor complex that serves as a transcription activator. ○ Every gene whose transcription is stimulated by that steroid hormone has a control element recognized by that hormone–receptor complex. • Other signal molecules control gene expression indirectly by triggering signal-transduction pathways that lead to activation of transcription. ○ The principle of coordinate regulation is the same: Genes with the same control elements are activated by the same chemical signals. • Systems for coordinating gene regulation probably arose early in evolutionary history. • The nucleus has a defined architecture and regulated movements of chromatin. • Recent techniques allow researchers to cross-link and identify regions of chromosomes that associate with each other during interphase. • Loops of chromatin extend from individual chromosomal territories into specific sites in the nucleus. ○ Different loops from the same chromosome and loops from other chromosomes congregate in such sites, some of which are rich in RNA polymerases and other transcription-associated proteins. ○ These sites are likely areas specialized for a common function or transcription factories. Post-transcriptional mechanisms play supporting roles in the control of gene expression. • Regulatory mechanisms that operate after transcription allow a cell to rapidly fine-tune gene expression in response to environmental changes, without altering its transcriptional patterns. ○ RNA processing in the nucleus and the export of mRNA to the cytoplasm provide opportunities for gene regulation that are not available in prokaryotes. • In alternative RNA splicing, different mRNA molecules are produced from the same primary transcript, depending on which RNA segments are treated as exons and which as introns. ○ Regulatory proteins specific to a cell type control intron-exon choices by binding to regulatory sequences within the primary transcript. • Alternative RNA splicing significantly expands the repertoire of a set of genes. ○ It may explain the surprisingly low number of human genes: similar to those of a soil worm, a mustard plant, or a sea anemone. ○ Between 75% and 100% of human genes that have multiple exons probably undergo alternative splicing. ○ The extent of alternative splicing increases the number of possible human proteins, likely correlated with complexity of form. • The life span of an mRNA molecule is an important factor in determining the pattern of protein synthesis. ○ Prokaryotic mRNA molecules are typically degraded after only a few minutes, while eukaryotic mRNAs typically last for hours, days, or weeks. ○ In red blood cells, mRNAs for hemoglobin polypeptides are unusually stable and are translated repeatedly. • Nucleotide sequences in the untranslated trailer region (UTR) at the 3¢ end affect mRNA stability. ○ Transferring such a sequence from a short-lived mRNA to a normally stable mRNA results in quick mRNA degradation. Translation presents an opportunity for the regulation of gene expression. • The initiation of translation of an mRNA can be blocked by regulatory proteins that bind to specific sequences within the 5¢ or 3¢ UTR of the mRNA, preventing ribosome attachment. • The mRNAs present in the eggs of many organisms lack poly-A tails of sufficient length to allow initiation of translation. ○ During embryonic development, a cytoplasmic enzyme adds more adenine nucleotides so that translation can begin at the appropriate time. • Translation of all the mRNAs in a eukaryotic cell may be regulated simultaneously by the activation or inactivation of the protein factors required to initiate translation. ○ This mechanism starts the translation of mRNAs that are stored in eggs. ○ Just after fertilization, translation is triggered by the sudden activation of translation initiation factors, resulting in a burst of protein synthesis. • Some plants and algae store mRNAs during periods of darkness. Light triggers the reactivation of the translational apparatus. The final opportunities for controlling gene expression occur after translation. • Often, eukaryotic polypeptides are processed to yield functional proteins. ○ For example, cleavage of pro-insulin forms the active hormone. • Many proteins must undergo chemical modifications before they are functional. ○ Regulatory proteins may be activated or inactivated by the reversible addition of phosphate groups. ○ Proteins destined for the surface of animal cells acquire sugars. • Regulation may occur at any of the steps involved in modifying or transporting a protein. • The length of time a protein functions before it is degraded is strictly regulated. ○ Proteins such as the cyclins that regulate the cell cycle must be relatively short-lived. • To mark a protein for destruction, the cell attaches a small protein called ubiquitin to it. ○ Giant protein complexes called proteasomes recognize and degrade the tagged proteins. • Mutations making specific cell cycle proteins impervious to proteasome degradation can lead to cancer. • The scientists worked out the regulated process of protein degradation won the 2004 Nobel Prize in Chemistry. Concept 18.3 Noncoding RNAs play multiple roles in controlling gene expression • Only 1.5% of the human genome codes for proteins. Of the remainder, only a very small fraction consists of genes for ribosomal RNA and transfer RNA. • Until recently, it was assumed that most of the rest of the DNA was untranscribed. Recent data have challenged that assumption, however. ○ Study of a region comprising 1% of the human genome found that over 90% of the region was transcribed. ○ Introns accounted for only a fraction of this transcribed, nontranslated RNA. • A significant amount of the genome may be transcribed into non–protein-coding RNAs (or noncoding RNAs or ncRNAs), including a variety of small RNAs. • A large, diverse population of RNA molecules may play crucial roles in regulating gene expression in the cell. MicroRNAs can bind to complementary sequences in mRNA molecules. • In the past few years, researchers have found small, single-stranded RNA molecules called microRNAs (miRNAs) that bind to complementary sequences in mRNA molecules. • miRNAs are formed from longer RNA precursors that fold back on themselves to form one or more short, double-stranded hairpin structures stabilized by hydrogen bonding. • An enzyme called Dicer cuts each hairpin into a short, double-stranded fragment of about 22 nucleotide pairs. • One of the two strands is degraded. The other strand (miRNA) associates with a protein complex and directs the complex to any mRNA molecules that have a complementary sequence of 7-8 nucleotides. • The miRNA–protein complex either degrades the target mRNA or blocks its translation. • Expression of up to one-half of all human genes may be regulated by miRNAs. • The phenomenon of inhibition of gene expression by RNA molecules is called RNA interference (RNAi). • Injecting double-stranded RNA molecules into a cell somehow turns off expression of a gene with the same sequence as the RNA. ○ This RNA interference is due to small interfering RNAs (siRNAs), similar in size and function to miRNAs and are generated by similar mechanisms in eukaryotic cells. • Both miRNAs and siRNAs can associate with the same proteins, with similar results. ○ The distinction between these molecules is the nature of the precursor molecules from which they are formed. ○ Each miRNA forms from a single hairpin in the precursor RNA, while multiple siRNAs form from a longer, double-stranded RNA molecule. • Cellular RNAi pathways lead to the destruction of RNAs and may have originated as a natural defense against infection by double-stranded RNA viruses. ○ The fact that the RNAi pathway can also affect the expression of nonviral cellular genes may reflect a different evolutionary origin for the RNAi pathway. • Many species, including mammals, possess long, double-stranded precursors to small RNAs that interfere with various steps in gene expression. Small RNAs can remodel chromatin and silence transcription. • Small RNAs can cause remodeling of chromatin structure. ○ In yeast, siRNAs are necessary for the formation of heterochromatin at the centromeres of chromosomes. • An RNA transcript produced from DNA in the centromeric region of the chromosome is copied into double-stranded RNA by a yeast enzyme and then processed into siRNAs. ○ The siRNAs associate with a protein complex, targeting the complex back to the RNA sequences made from the centromeric sequences of DNA. ○ The proteins in the complex recruit enzymes to modify the chromatin, turning it into the highly condensed centromeric heterochromatin. • A newly discovered class of small ncRNAs, called piwi-associated RNAs (piRNAs) also induce formation of heterochromatin, blocking expression of parasitic DNA elements in the genome known as transposons. ○ piRNAs, 24–31 nucleotides in length, are processed from single-stranded RNA precursors. ○ In germ cells of many animal species, piRNAs help re-establish appropriate methylation patterns in the genome during gamete formation. • Chromatin remodeling not only blocks expression of large regions of the chromosome; RNA-based mechanisms may also block the transcription of specific genes. ○ Some plant miRNAs have sequences that bind to gene promoters and can repress transcription; piRNAs can also block expression of specific genes. ○ In some cases, miRNAs and piRNAs activate gene expression. • Small ncRNAs regulate gene expression at multiple steps and in many ways. ○ Extra levels of gene regulation may allow evolution of a higher degree of complexity of form. ○ An increase in the number of miRNAs encoded in the genomes of species may have allowed morphological complexity to increase over evolutionary time. • A survey of species suggests that siRNAs evolved first, followed by miRNAs and later piRNAs, which are found only in animals. ○ While there are hundreds of types of miRNA, there appear to be many thousands of types of piRNAs, allowing the potential for very sophisticated gene regulation by piRNAs. • Many ncRNAs play important roles in embryonic development, the ultimate example of an elaborate program of regulated gene expression. Concept 18.4 A program of differential gene expression leads to the different cell types in a multicellular organism • In the development of most multicellular organisms, a single-celled zygote gives rise to cells of many different types. ○ Each type has a different structure and corresponding function. ○ Cells of different types are organized into tissues, tissues into organs, organs into organ systems, and organ systems into the whole organism. • Thus, the process of embryonic development must give rise not only to cells of different types but also to higher-level structures arranged in a particular way in three dimensions. A genetic program is expressed during embryonic development. • As a zygote develops into an adult organism, its transformation results from three interrelated processes: cell division, cell differentiation, and morphogenesis. • Through a succession of mitotic cell divisions, the zygote gives rise to many cells. ○ Cell division alone would produce only a great ball of identical cells. • During development, cells become specialized in structure and function, undergoing cell differentiation. • Different kinds of cells are organized into tissues and organs. • The physical processes that give an organism its shape constitute morphogenesis, the “creation of form.” • Cell division, cell differentiation, and morphogenesis have their basis in cellular behavior. ○ Morphogenesis can be traced back to changes in the shape and motility of cells in the various embryonic regions. ○ The activities of a cell depend on the genes it expresses and the proteins it produces. ○ Because almost all cells in an organism have the same genome, differential gene expression results from differential gene regulation in different cell types. • Why are different sets of activators present in different cell types? • One important source of information early in development is the egg’s cytoplasm, which contains both RNA and proteins encoded by the mother’s DNA, distributed unevenly in the unfertilized egg. • Maternal substances that influence the course of early development are called cytoplasmic determinants. ○ These substances regulate the expression of genes that affect the developmental fate of the cell. ○ After fertilization, the cell nuclei resulting from mitotic division of the zygote are exposed to different cytoplasmic environments. ○ The set of cytoplasmic determinants a particular cell receives helps determine its developmental fate by regulating expression of the cell’s genes during cell differentiation. • The other important source of developmental information is the environment around the cell, especially signals impinging on an embryonic cell from nearby cells. ○ In animals, these signals include contact with cell-surface molecules on neighboring cells and the binding of growth factors secreted by neighboring cells. • These signals cause changes in the target cells, a process called induction. ○ The molecules conveying these signals within the target cells are cell-surface receptors and other proteins expressed by the embryo’s own genes. ○ The signal molecules send a cell down a specific developmental path by causing a change in its gene expression that eventually results in observable cellular changes. Cell differentiation is due to the sequential regulation of gene expression. • During embryonic development, cells become visibly different in structure and function as they differentiate. • The earliest changes that set a cell on a path to specialization show up only at the molecular level. ○ Molecular changes in the embryo drive the process, called determination, which leads to the observable differentiation of a cell. • Once it has undergone determination, an embryonic cell is irreversibly committed to its final fate. ○ If a determined cell is experimentally placed in another location in the embryo, it will differentiate as if it were in its original position. • The outcome of determination—observable cell differentiation—is caused by the expression of genes that encode tissue-specific proteins. ○ These proteins give a cell its characteristic structure and function. • Differentiation begins with the appearance of cell-specific mRNAs and is eventually observable in the microscope as changes in cellular structure. • In most cases, the pattern of gene expression in a differentiated cell is controlled at the level of transcription. • Cells produce the proteins that allow them to carry out their specialized roles in the organism. ○ For example, liver cells specialize in making albumin, while lens cells specialize in making crystalline. ○ Skeletal muscle cells have high concentrations of proteins specific to muscle tissues, such as a muscle-specific version of the contractile proteins myosin and actin, as well as membrane receptor proteins that detect signals from nerve cells. • Muscle cells develop from embryonic precursors that have the potential to develop into a number of alternative cell types. ○ Although the committed cells are unchanged, they are now myoblasts. ○ Eventually, myoblasts begin to synthesize muscle-specific proteins and fuse to form mature, elongated, multinucleate skeletal muscle cells. • Researchers have worked out the events at the molecular level that lead to muscle cell determination by growing myoblasts in culture and analyzing them with molecular biology techniques. ○ Researchers isolated different genes, caused each to be expressed in a separate embryonic precursor cell, and looked for differentiation into myoblasts and muscle cells. ○ They identified several “master regulatory genes” that, when transcribed and translated, commit the cells to become skeletal muscle. • One of these master regulatory genes is called myoD. ○ myoD encodes MyoD protein, a transcription factor that binds to specific control elements in the enhancers of various target genes and stimulates their expression. ○ Some target genes for MyoD encode for other muscle-specific transcription factors. ○ MyoD also stimulates expression of the myoD gene itself, helping to maintain the cell’s differentiated state. • All the genes activated by MyoD have enhancer control elements recognized by MyoD and are thus coordinately controlled. • The secondary transcription factors activate the genes for proteins such as myosin and actin to confer the unique properties of skeletal muscle cells. • The MyoD protein is capable of changing fully differentiated fat and liver cells into muscle cells. • Not all cells can be transformed by MyoD, however. ○ Nontransforming cells may lack a combination of regulatory proteins in addition to MyoD. Pattern formation sets up the embryo’s body plan. • Cytoplasmic determinants and inductive signals contribute to pattern formation, the development of spatial organization in which the tissues and organs of an organism are all in their characteristic places. • Pattern formation begins in the early embryo, when the major axes of an animal are established. • Before specialized tissues and organs form, the relative positions of a bilaterally symmetrical animal’s three major body axes (anterior-posterior, dorsal-ventral, right-left) are established. • The molecular cues that control pattern formation, positional information, are provided by cytoplasmic determinants and inductive signals. ○ These signals tell a cell its location relative to the body axes and to neighboring cells and determine how the cell and its progeny will respond to future molecular signals. • Studies of pattern formation in Drosophila melanogaster have established that genes control development and have identified the key roles of specific molecules in defining position and directing differentiation. • Combining anatomical, genetic, and biochemical approaches in the study of Drosophila development, researchers have discovered developmental principles common to many other species, including humans. • Fruit flies and other arthropods have a modular construction. ○ An ordered series of segments make up the three major body parts: the head, thorax (with wings and legs), and abdomen. • Cytoplasmic determinants in the unfertilized egg provide positional information for two developmental axes (anterior-posterior and dorsal-ventral axis) before fertilization. • The Drosophila egg develops in the female’s ovary, surrounded by ovarian cells called nurse cells and follicle cells that supply the egg cell with nutrients, mRNAs, and other substances. • During fruit fly development, the egg forms a segmented larva, which goes through three larval stages. ○ The fly larva forms a pupal cocoon within which it metamorphoses into an adult fly. • In the 1940s, Edward B. Lewis used mutants to investigate Drosophila development. ○ Bizarre developmental mutations were on the fly’s genetic map, providing the first concrete evidence that genes somehow direct the developmental process. ○ These homeotic genes control pattern formation in the late embryo, larva, and adult. • In the late 1970s, Christiane Nüsslein-Volhard and Eric Weischaus set out to identify all the genes that affect segmentation in Drosophila. They faced three problems. • First, because Drosophila has about 13,700 genes, there could be either only a few genes affecting segmentation or so many that the pattern would be impossible to discern. • Second, mutations that affect segmentation are likely to be embryonic lethals, leading to death at the embryonic or larval stage. ○ Flies with embryonic lethal mutations never reproduce, and cannot be bred for study. ○ Nüsslein-Volhard and Wieschaus focused on recessive mutations that could be propagated in heterozygous flies. • Third, because of maternal effects on axis formation in the egg, the researchers also needed to study maternal genes. • After exposing flies to mutagenic chemicals, Nüsslein-Volhard and Wieschaus looked for dead embryos and larvae with abnormal segmentation. ○ Through appropriate crosses, they found heterozygotes carrying embryonic lethal mutations. • Nüsslein-Volhard and Wieschaus identified 1,200 genes essential for embryonic development. ○ About 120 of these were essential for normal segmentation. • The researchers grouped the genes by general function, mapped them, and cloned many of them. • In 1995, Nüsslein-Volhard, Wieschaus, and Lewis were awarded a Nobel Prize. Gradients of maternal molecules in the early Drosophila embryo control axis formation. • Cytoplasmic determinants produced under the direction of maternal effect genes are deposited in the unfertilized egg. • A maternal effect gene is a gene that, when mutant in the mother, results in a mutant phenotype in the offspring, regardless of the offspring’s own genotype. ○ In fruit fly development, maternal effect genes encode proteins or mRNA that are placed in the egg while it is still in the ovary. ○ When the mother has a mutation in a maternal effect gene, she makes a defective gene product (or none at all) and her eggs will not develop properly when fertilized. • Maternal effect genes are also called egg-polarity genes because they control the orientation of the egg and consequently the fly. ○ One group of genes sets up the anterior-posterior axis, while a second group establishes the dorsal-ventral axis. • One gene called bicoid affects the front half of the body. • An embryo whose mother has a mutant bicoid gene lacks the front half of its body and has duplicate posterior structures at both ends. ○ This suggests that the product of the mother’s bicoid gene is essential for setting up the anterior end of the fly and might be concentrated at the future anterior end. • This is a specific version of the morphogen gradient hypothesis, in which gradients of morphogens establish an embryo’s axes and other features. • Using DNA technology and biochemical methods, researchers were able to clone the bicoid gene and use it as a probe for bicoid mRNA in the egg. ○ As predicted, the bicoid mRNA is concentrated at the extreme anterior end of the egg cell. • After the egg is fertilized, bicoid mRNA is transcribed into protein, which diffuses from the anterior end toward the posterior, resulting in a gradient of proteins in the early embryo. ○ Injections of pure bicoid mRNA into various regions of early embryos resulted in the formation of anterior structures at the injection sites. • The bicoid research is important for three reasons. 1. It identified a specific protein required for some of the earliest steps in pattern formation. 2. It increased our understanding of the mother’s role in the development of an embryo. 3. It demonstrated a key developmental principle: a gradient of molecules can determine polarity and position in the embryo. • Maternal mRNAs are crucial during development of many species. ○ In Drosophila, gradients of specific proteins encoded by maternal mRNAs determine the posterior and anterior ends and establish the dorsal-ventral axis. • Later, positional information encoded by the embryo’s genes establishes a specific number of correctly oriented segments and triggers the formation of each segment’s characteristic structures. Concept 18.5 Cancer results from genetic changes that affect cell cycle control • Cancer is a set of diseases in which cells escape the control mechanisms that normally regulate cell growth and division. ○ The gene regulation systems that go wrong during cancer are the systems that play important roles in embryonic development and immune response. • The genes that normally regulate cell growth and division during the cell cycle include genes for growth factors, their receptors, and the intracellular molecules of signaling pathways. ○ Mutations altering any of these genes in somatic cells can lead to cancer. ○ The agent of such changes can be random spontaneous mutations or environmental influences such as chemical carcinogens, X-rays, and some viruses. Proto-oncogenes can become oncogenes, contributing to the development of cancer. • Cancer-causing genes, oncogenes, were initially discovered in viruses. ○ Close counterparts have been found in the genomes of humans and other animals.å • Normal versions of cellular genes, called proto-oncogenes, code for proteins that stimulate normal cell growth and division. • A proto-oncogene becomes an oncogene following genetic changes that lead to an increase in the proto-oncogene’s protein production or in the intrinsic activity of each protein molecule. ○ These genetic changes include movement of DNA within the genome, amplification of the proto-oncogene, and point mutations in a control element or the proto-oncogene itself. • Cancer cells frequently have chromosomes that have been broken and rejoined incorrectly. ○ A fragment may be moved to a location near an active promoter or other control element. • Amplification increases the number of copies of the proto-oncogene in the cell. • A point mutation in the promoter or enhancer of a proto-oncogene may increase its expression. • A point mutation in the coding sequence may lead to translation of a protein that is more active or longer-lived. • All of these mechanisms can lead to abnormal stimulation of the cell cycle, putting the cell on the path to malignancy. Mutations to tumor-suppressor genes may contribute to cancer. • The normal products of tumor-suppressor genes inhibit cell division. • Some tumor-suppressor proteins normally repair damaged DNA, preventing the accumulation of cancer-causing mutations. • Other tumor-suppressor proteins control the adhesion of cells to each other or to an extracellular matrix, which is crucial for normal tissues and often absent in cancers. • Still others are components of cell-signaling pathways that inhibit the cell cycle. ○ Decreases in the normal activity of a tumor-suppressor protein may contribute to cancer. • The proteins encoded by many proto-oncogenes and tumor-suppressor genes are components of cell-signaling pathways. • Mutations in the products of two key genes, the ras proto-oncogene and the p53 tumor-suppressor gene, occur in 30% and over 50% of human cancers, respectively. • The Ras protein, the product of the ras gene, is a G protein that relays a growth signal from a growth factor receptor on the plasma membrane to a cascade of protein kinases. ○ At the end of the pathway is the synthesis of a protein that stimulates the cell cycle. • Many ras oncogenes have a point mutation that leads to a hyperactive version of the Ras protein that trigger the kinase cascade in the absence of growth factor, resulting in excessive cell division. • The p53 gene, named for its 53,000-dalton protein product, is a tumor-suppressor gene. ○ The p53 protein is a specific transcription factor for the synthesis of several cell cycle-inhibiting proteins. ○ The p53 gene has been called the “guardian angel of the genome.” • Once activated by DNA damage, the p53 protein functions as an activator for several genes. ○ The p53 protein can activate the p21 gene, whose product halts the cell cycle by binding to cyclin-dependent kinases, allowing time for DNA repair. ○ p53 also activates expression of a group of miRNAs, which inhibit the cell cycle. ○ The p53 protein can also turn on genes directly involved in DNA repair. ○ When DNA damage is irreparable, the p53 protein can activate “suicide genes” whose protein products cause cell death by apoptosis. • A mutation that knocks out the p53 gene can lead to excessive cell growth and cancer. Multiple mutations underlie the development of cancer. • More than one somatic mutation is generally needed to produce the changes characteristic of a full-fledged cancer cell. • If cancer results from an accumulation of mutations, and if mutations occur throughout life, then the longer we live, the more likely we are to develop cancer. • Colorectal cancer, with 140,000 new cases and 50,000 deaths in the United States each year, illustrates a multistep cancer path. ○ The first sign is often a polyp, a small benign growth in the colon lining. ○ The cells of the polyp look normal but divide unusually frequently. ○ Through gradual accumulation of mutations that activate oncogenes and knock out tumor-suppressor genes, the polyp can develop into a malignant tumor. ○ A ras oncogene and a mutated p53 tumor-suppressor gene are usually involved. • About a half dozen DNA changes must occur for a cell to become fully cancerous. • These changes usually include the appearance of at least one active oncogene and the mutation or loss of several tumor-suppressor genes. ○ Because mutant tumor-suppressor alleles are usually recessive, mutations must knock out both alleles. ○ Most oncogenes behave like dominant alleles and require only one mutation. Cancer can run in families. • The fact that multiple genetic changes are required to produce a cancer cell helps explain the predispositions to cancer that run in families. ○ An individual inheriting an oncogene or a mutant allele of a tumor-suppressor gene is one step closer to accumulating the necessary mutations for cancer to develop. • Geneticists are devoting much effort to finding inherited cancer alleles so that a predisposition to certain cancers can be detected early in life. • About 15% of colorectal cancers involve inherited mutations. • Many of these mutations affect the tumor-suppressor gene adenomatous polyposis coli or APC. ○ Normal functions of the APC gene include regulation of cell migration and adhesion. ○ Even in patients with no family history of the disease, APC is mutated in about 60% of colorectal cancers. • Between 5% and 10% of breast cancer cases show an inherited predisposition. ○ Breast cancer is the second most common type of cancer in the United States, annually striking more than 180,000 women and leading to 40,000 deaths. • Mutations in one gene, BRCA1, increase the risk of breast and ovarian cancer. ○ Mutations in BRCA1 and the related gene BRCA2 are found in at least half of inherited breast cancers. • A woman who inherits one mutant BRCA1 allele has a 60% probability of developing breast cancer before age 50 (versus a 2% probability in an individual with two normal alleles). ○ Both BRCA1 and BRCA2 are considered tumor-suppressor genes because their wild-type alleles protect against breast cancer and their mutant alleles are recessive. • BRCA1 and BRCA2 proteins function in the cell’s DNA damage repair pathway. ○ BRCA2, in association with another protein, helps repair breaks that occur in both strands of DNA. • Because DNA breakage can contribute to cancer, the risk of cancer can be lowered by minimizing exposure to DNA-damaging agents, such as ultraviolet radiation in sunlight and the chemicals found in cigarette smoke. • In addition to mutations and other genetic alterations, a number of tumor viruses can cause cancer in various animals, including humans. ○ In 1911, Peyton Rous, an American pathologist, discovered a virus that causes cancer in chickens. ○ The Epstein-Barr virus, which causes infectious mononucleosis, has been linked to several types of cancer in humans, notably Burkitt’s lymphoma. ○ Papillomaviruses are associated with cancer of the cervix, and a virus called HTLV-1 causes a type of adult leukemia. • Worldwide, viruses seem to play a role in about 15% of the cases of human cancer. • Viruses can interfere with gene regulation in several ways if they integrate their genetic material into a cell’s DNA. ○ Viral integration may donate an oncogene to the cell, disrupt a tumor-suppressor gene, or convert a proto-oncogene to an oncogene. ○ Some viruses produce proteins that inactivate p53 and other tumor-suppressor proteins, making the cell more likely to become cancerous. Lecture Outline for Reece et al., Campbell Biology, 10th Edition, Copyright © 2014 Pearson Education, Inc

Réservoirs

conjugating voir recevoir and apercivoir

History exam 3: 1920s america the Roaring twenties: Prosperity, culture, change, and contradiction (1920s-1929) Nicknamed: Roaring twenties/ jazz age Post ww1 boom after war and flu pandemic recovery Shift: Rural tradition to urban modern consumer society Key themes: optimism, excess, hidden cracks Republican dominance “Return to normalcy” President: Harding (1921-23, scandals) Coolidge (1923-29, pro- business) Hoover (1929, crash) Laissez fair: low taxes, limited regulation Isolationism: rejected league of nations “ Age of prosperity”: rising wages, low unemployment (for many) Mass production: Assembly line, electricity, consumer goods Key industries: Autos, radio, appliances Rise of credit and advertising - mass consumption Uneven: Farmers struggled Automobile explosion: Model T - suburbs, roads Aviation milestone: Lindbergh’s 1927 solo Atlantic flight Radio: national culture and entertainment Household tech: Refrigerators, vacuums 19th amendment (1920): women vote Flappers: Short hair/ skirts, smoking, dancing, independence More women working, challenge norms New freedom in dating and social life Jazz age: Born in New Orleans Louis armstrong, duke ellington Hollywood boom: silent films- talkies (1927) Sports heroes: Babe ruth, Jack dempsy Dances And fads: Charleston, dance marathons Great migration: Black to northern cities Harlem explosion: Art literature, music Key figures: WRiter and poet langston hughes, writer zora neale hurston, jazz duke ellington Celebration of black identity 18th amendment (1919-33) banned alcohol Results: Speakeasies, bootlegging, organized crime Gangster: AL Capone and rise of mafia Widespread hypocrisy and corruption Roaring twenties: KKK resurgence: anti- immigrants black catholic Nativism: 1924 immigration quotas- new law restricting immigrants - target eastern and southern europeans Radical violence: Tulsa massacre (1921) Scope trial (1925): evolution vs religion Stock market Bull market Stock prices steadily climbed throughout the 1920s Margin buying Middle class investing Economy roaring Frantic buying in 1920s Stock prices separate from the value of company Economy begins to weaken Before the stock crash when did the American economy begin to cool off? 1928 According to a top investor when a shoe shine boy is giving stock picks its time to do what? Sell out When do most stock market crashes occur? september/ october In the worst single day how much did the stock market lose in value? 14 billion Who was worse in the short run? Small investor Stock prices begin to fall in september1929 Crash in october 1929 Black tuesday october 29,1929 Great depression Unemployment skyrockets Thousands of banks collapsed Individual; saving gone Cause; Abundance ‘Great glut” too much production Overexpansion of credit High tariff- trade dried up Effects High employment Homes and farms lost to foreclosure Homelessness and hunger Bread and soup lines “Hoovervilles” Makeshift towns of homeless people Hoover and depression What happened to local government and local charities relief efforts? They were overwhelmed Hoover reluctant to use federal government Reconstruction Finance corporation Government loans to big business and some state governments Hoover In 1924 congress voted a bonus payment to world war 1 veterans To be paid in 1945 Bonus army In 1932 around 20,000 veterans converge on WAshington during the depression Camped out and demand full bonus immediately Vote failed in congress Hoover ordered removal of those who refused to leave Bloody confrontation- hoover hurt politically in election year Election of 1932 Herbert hoover (r.) Franklin roosevelt (d) Roosevelt offers new deal Roosevelt wins in landslide Lame duck period between election and inauguration economy worsened Banking catastrophe loomed Roosevelt and the new deal “ only thing we have to fear is fear itself’ First hundred days Intense burst of legislation New deal ‘ Three R- relief, recovery, reform Fireside chats Emergency banking act 1933 Aimed to restore public confidence Banks shut down for a weeklong bank holiday Only solvent bank reopen Firesides chats Regular radio broadcast by Roosevelt Roosevelt's way of going directly to the public Built support for new deal legislation New deal Banking crisis dealt with first Bank examiners determined bank health Glass steagall banking reform act 1933 Banks prohibited from using depositors funds for risky investments Federal deposit insurance corporation Created by glass steagall Independent agency of federal government Insures bank deposits Prevents bank panics Securities exchange act 1934 Securities and exchange commission created Stop fraudulent stock market practices Greater transparency in market Regulation and enforcement to determine stock manipulation Example: trading laws established The great depression Noble experiment ends 3.2% wine and beer legalized first 21st Amendment 1933 Proposed in feb. and ratified dec. 1933 Only constitutional amendment ratified by special state conventions Prohibition ended “Alphabet soup” new deal programs Three- or four lettered acronyms describe most new deal programs Civilian conservation corps FDR created by executive order For unemployed unmarried men between 17-28 years old Helped shaped modern national and state park system Federal emergency relief act 1933 Federally funded jobs for state and local government work Civilian works administration Emergency employment Provided temporary jobs and paycheck Tennessee valley authority Massive federal project Construction of dams and reservoirs on Tennessee river Flood control and navigation improvements Creation of cheap hydroelectric power Covers parts of seven states Over 2.5 million people living at the time Provided jobs and creation of long term project $13b Works progress administration Largest most ambitious new deal agency Nearly every community in united states impacted by building projects WPA included federal arts projects Strawberry stadium WPA project #3014 Dust bowl Drought and wind = dust storms Powdery topsoil in arid regions of the plains blown away Large areas of the plains became uninhabitable Caused by nature and manmechanized farming Tens of thousands forced out Steinbeck's grapes of wrath Huey Long Senator and former governor of Louisiana Built thousands of miles roads in louisiana Free textbooks and school lunches Charity hospital established National radio show “share our wealth” program reached millions “Every man a king” 5k for each family by taxing the rich Proposed free college Proposed old age pensions Long: FDR new deal was not bold enough Roosevelt worried long could be third party candidate Long assassinated at age 42 in state capital sept. 1935 Long help inspired social security Social security act 1935 One of the most far reaching laws ever Retirement pension regular payments Provided for federal- state unemployment insurance Disability payments Financed by payroll tax paid by employees and employers Over 70 million people receive social security payments today Wagner act 1935 National labor relations act 1935 Aimed to balance power between labor and management Workers rights Labor has right to organize and collective bargaining Strike without employer retaliation Government board established labor secretary Oversees workplace rights Election 1936 Franklin roosevelt vs alf landon Moderate republican who accepted some new deal reforms Republicans - franklin “Deficit “ roosevelt Republicans carried only two states Landslide win for roosevelt Democrats controlled both houses of congress Twentieth amendment Ratified in 1933 changed inauguration date to january 20 shorten lame duck period by 6 weeks Roosevelt sworn in on jan. 20 1937 Supreme court a road block for new deal Six of nine justices over the age of seventy Roosevelt second term Court packing plan Supreme court ruled some new deal laws unconstitutional Roosevelt implied justices were far behind on work Proposed to add six new justices to supreme court All new judges to be appointed by roosevelt Roosevelt hurt politically Court packing failed in congress However the supreme court began to be more sympathetic to new deal Fair labor standards act 1938 (wage and hours) Minimum wage established 40 hour work week Labor under 16 years old restricted “Roosevelt recession” sharp downtown in economy in 1937 Became a little more difficult to pass new deal legislation Mid-term election 1938 Republicans cut into large democratic majorities National attention turned to internal affairs Germany and japan New deal momentum slows Government soon transformed because of World war 2 World War 2 Neutrality Acts Passed by congress in 1935,1936,1937,1939 Because of the rise of fascism in Europe and possibility of another war Isolationist view still prevailed Four laws in all temporary at first, later made permanent Restricted trade with warning nations Embargo of arms Banned loans from U.S banks “Cash and carry” provision Causes of ww2 Problems with treaty of versallies Germany left out of treaty negotiations Everything on Germany War guilt cause Reparations payments Restriction on military Loss of territory Economic problems and general dissatisfaction allows for the rise of fascism Fascism Benito mussolini Gained power in italy 1922 Led the fascist party Rise of Fascist Nationalistic and Militaristic Dictators Difficult Life in post-world war 1 Radical extremism and the Nazi party Born out of post ww1 conditions Weimar republic German government after WW1 Weimar republic failed Nazi party slowly gained seats in German Parliament Adolph Hitler Leader of nazi party Gained power in Germany 1933 German problems blamed on Treaty of Versailles and Jewish population Mein kampf Published 1925 Autobiography antisemitic manifesto of hitler Wrote while in prison Plans for german future Labensraum Living space needed for the aaryn race Nuremberg laws 1935 Race laws against the german jews Restriction on jewish population citizenship denied intermarriage denied Hitler Hitler embarked on remilitarization of germany Remilitarization was violation of treaty of versailles Rhineland Area along french border Hilter placed troops 1936 German troops in Finland a violation of treaty of Versailles Austria German speaking Hitler born in austria Annexed 1938 making austria part of germany Sudetenland Area of czechoslovakia A few million german speaking residents Hitler demanded sudetenland Munich conference September 1938 Hilter invited british P.M neville chamberlain and french president Appeasement french and british give hitler what he wants Hitler takes all of Czechoslovakia within six months Nazi soviet nonaggressionpact Aug he

Basic Microbiology: Reservoirs and Epidemiology

Reservoirs & Transmission modes & Emerging Infectious Diseases

rservoir engineering exam 1

9g3 croire, voir, recevoir et les pronoms demonstratif

Reservoir Midterm

Week 5 Absolutely — here’s a condensed study guide that keeps the major concepts (the stuff most likely to be tested), without all the extra detail. Infection Control & Body Defenses — Condensed Study Guide (Major Concepts) Chain of Infection (6 Links + how to break them) 1. Infectious agent (bacteria, viruses, fungi, parasites, prions) ○ Break it: disinfect/sterilize/clean; antimicrobials as ordered 2. Reservoir (where it lives: people/animals/insects; soil, water, food, equipment, IV fluids, feces) ○ Break it: hand hygiene, pre-op skin prep, environmental cleaning 3. Portal of exit (blood/body fluids, respiratory/GI tract, mouth/nose/ears, skin) ○ Break it: contain drainage/secretions (dressings, drains) 4. Mode of transmission ○ Main: contact, droplet, airborne (also vehicle, vector) ○ Break it: hand hygiene + PPE + disinfect shared equipment 5. Portal of entry (orifices, mucous membranes, breaks in skin; invasive devices) ○ Break it: aseptic technique, protect skin, sterile technique when needed 6. Susceptible host (risk depends on immunity/health) ○ Break it: immunizations, nutrition, hygiene, blood sugar control Virulence: how efficient an organism is at making people ill. Modes of Transmission (what to recognize) Contact ● Direct: person-to-person (ex: blood to open abrasion) ● Indirect: contaminated objects/PPE/equipment (ex: bed rails, shared devices) Droplet ● From coughing/sneezing/singing/talking; some procedures (CPR, intubation) ● Examples: influenza, pertussis, RSV, adenovirus, rhinovirus ● Respiratory etiquette + masking when out of room Airborne ● Small particles remain suspended; travel farther ● Requires private room; negative pressure (AIIR) preferred ● Examples: TB, measles (rubeola), varicella Vehicle / Vector ● Vehicle: contaminated food/water (ex: E. coli produce) ● Vector: insects/rodents (mosquitoes, rats) Body Defenses (3 Types) 1. Physical & chemical barriers ○ Skin (primary defense), mucous membranes/mucus, tears/sweat, cilia + cough, stomach acid, normal flora 2. Nonspecific immunity ○ Neutrophils + macrophages (phagocytes “eat and destroy”) 3. Specific immunity ○ Antibodies (immunoglobulins) + lymphocytes Inflammatory Response (key steps + signs) Steps: ● Pattern receptors recognize harmful stimuli ● Inflammatory pathway activated ● Markers released (ex: CRP) ● Inflammatory cells recruited (leukocytes → monocytes/lymphocytes) Signs of inflammation (local tissue): ● heat, redness, swelling, pain, loss of function Triggers can be infectious (viruses/bacteria) or noninfectious (trauma, burns, irritants, toxins, radiation, etc.). Stages of Infection (in order) 1. Incubation (exposure → first symptom; may have lab changes) 2. Prodromal (vague symptoms: malaise, fever, aches) 3. Acute illness (most severe; specific symptoms) 4. Decline (symptoms decrease) 5. Convalescence (recover/return to baseline) Local vs Systemic Infection ● Local: confined to one area (often topical/oral treatment) ● Systemic: enters bloodstream, affects whole body (often IV antibiotics + monitoring) Diagnostic Tests (high-yield) ● UA for UTI symptoms → if WBCs present, culture & sensitivity ● CXR confirms pneumonia/atelectasis but doesn’t tell viral vs bacterial ● CBC + differential ○ Expected WBC: 5,000–10,000/mm³ ○ “Left shift” = increased bands (immature neutrophils) → infection ● Nonspecific markers: CRP, ESR, Procalcitonin Asepsis & Precautions Hand hygiene (most important) ● Soap/water when visibly soiled and for C. diff spores ● Alcohol sanitizer works unless hands visibly soiled Medical asepsis (clean technique) ● reduces microbes; includes isolation precautions Surgical asepsis (sterile technique) ● prevents introducing microbes during invasive procedures; uses sterile supplies/fields Isolation Precautions (major takeaways) Standard precautions ● For all clients ● Protect from blood/body fluids, secretions, excretions, nonintact skin, mucous membranes ● PPE based on expected exposure Contact precautions ● Gown + gloves ● Examples: C. diff, VRE, norovirus, RSV, large draining wounds ● Remove PPE inside room Droplet precautions ● Surgical mask ● Examples: influenza, pertussis, RSV Airborne precautions ● N95 or higher, private room; AIIR/negative pressure preferred ● Examples: TB, measles, varicella Protective isolation (protective environment) ● For severely immunocompromised (ex: post-allogenic HSCT) ● Positive airflow + HEPA (goal: protect the client) Health Care–Associated Infections (HAIs) — the “big 4” ● CLABSI ● CAUTI ● SSI ● VAP Devices/lines/wounds create portals of entry → strict asepsis reduces risk. MDROs (major concept) MDROs = resistant bacteria (hard to treat) Examples: MRSA, VRE, VRSA, VISA, ESBL, MDRSP Prevention: hand hygiene, contact precautions per policy. If you want, I can turn this condensed guide into a 20-question practice quiz (ATI/NCLEX-style) focusing on chain links, precautions, PPE, labs, and transmission. Week 6 Here is a more condensed study guide that keeps all main concepts from your content (no major topics removed), just simplified and streamlined for studying. Condensed Study Guide: Novice to Expert + Nursing Communication I. Novice to Expert Nursing (Benner Model) Lifelong Learning & Collaboration ● Learning occurs through study and working with others ● Nurses grow by: ○ observing experienced nurses ○ sharing knowledge and best practices ● Respect all experience levels (years ≠ only indicator of knowledge) ● Leaders promote: ○ collaboration ○ mutual respect ○ teamwork culture Benner’s 5 Stages of Competence 1. Novice – no experience; relies on rules; struggles to prioritize 2. Advanced Beginner – recognizes patterns; still rule-focused; needs help setting priorities 3. Competent – uses past experience to prioritize; more organized but slower than proficient 4. Proficient – sees the big picture; adapts to changing situations 5. Expert – intuitive, confident, and highly skilled with complex care II. Communication Foundations Definition Communication = transfer of information that is always occurring, even without speaking. Includes: verbal words, body language, emotions, and technology. Why Communication Matters ● Key to client safety (Joint Commission goal) ● Miscommunication → medical errors ● Nurses must detect when clients don’t understand III. Communication Models (Core Concepts) Shannon–Weaver Model (Linear) Sender → Encoder → Channel → Decoder → Receiver + Noise (distractions interfering with message) Schramm Model (Feedback) ● Sender and receiver exchange messages ● Feedback confirms understanding ● No feedback = communication incomplete Newcomb ABX Model (Social) ● A (sender), B (receiver), X (topic affecting interaction) ● Focus on relationships and shared topic Berlo S-M-C-R Model (One-way) ● Sender → Message → Channel → Receiver ● No feedback loop IV. Forms of Communication Verbal Spoken communication (face-to-face or phone) Nonverbal (Body Language) ● Eye contact, posture, facial expressions ● When verbal and nonverbal conflict → nonverbal dominates Auditory What the receiver hears (tone, speed, clarity) Emotional Speaker’s emotional state influences how message is received Energetic Speaker’s presence/empathy affects perception of message V. Modes of Communication (4 Types) 1. Verbal – spoken conversation 2. Nonverbal – gestures, posture, appearance 3. Electronic – email, text, video (must be secure/HIPAA compliant) 4. Written – letters, emails, documents (may lack tone/body language) HIPAA & Electronic Communication Must include: ● secure messaging ● unique logins ● auto logoff ● encrypted/indecipherable PHI VI. Communication Styles Most effective: Assertive ● Passive: avoids conflict; agrees despite concerns ● Assertive: clear, respectful, confident; uses “I” statements ● Aggressive: blaming, hostile, controlling ● Passive-aggressive: indirect expression (sarcasm, avoidance) VII. Therapeutic Communication Purpose Build trust and provide patient-centered, empathetic care Cornerstones ● Compassion ● Caring ● Empathy Peplau’s Nurse-Client Relationship Phases 1. Orientation – client seeks help 2. Identification – relationship forms 3. Exploitation – active teaching/working phase 4. Resolution – issue resolved; relationship ends Watson’s Theory of Human Caring ● Authentic presence ● Protect dignity ● Loving-kindness ● “Healing moment” interactions VIII. Therapeutic Communication Techniques (Must Know) ● Active listening – attend to verbal + nonverbal cues ● Open-ended questions – encourage discussion (“Tell me more…”) ● Silence – allows client to reflect and share more ● Restating / summarizing – repeat message to confirm understanding ● Reflection – mirror feelings (“What do you think you should do?”) ● Accepting – acknowledge message without judgment ● Giving recognition – note change without compliment ● Focusing – gently redirect to important topic ● Offering self – sit with client and be present IX. Nontherapeutic Communication (Avoid) ● Giving advice ● False reassurance (“You’ll be fine”) ● Criticizing or challenging ● Asking “Why” questions ● Rejecting or disagreeing ● Probing irrelevant topics ● Changing the subject Effects: ● increased stress ● damaged trust ● poor outcomes X. Interprofessional Communication Importance Effective teamwork improves: ● client outcomes ● safety ● efficiency ● reduces errors IPEC Core Competencies 1. Mutual respect among team members 2. Use shared knowledge collaboratively 3. Communicate effectively as a team 4. Support team values and client-centered care XI. Motivational Interviewing (MI) Purpose Encourage behavior change (diabetes, obesity, substance use) OARS Technique ● Open-ended questions ● Affirmations (positive encouragement) ● Reflective listening ● Summarizing XII. Group vs Individual Communication ● Individual: new diagnosis, personal teaching ● Group: ongoing education, support groups XIII. Communication Barriers (Major Categories) Cognitive/Developmental ● dementia, stroke, autism Physiological ● hearing loss, vision impairment Cultural & Language ● language differences, cultural beliefs, lack of cultural competence Environmental/Situational ● noise, lighting, temperature ● fear, anxiety, fatigue, stress Technological ● poor reception, distractions, electronic errors XIV. Strategies to Overcome Barriers Universal Strategies ● show empathy and respect ● avoid interrupting ● use simple, clear language ● confirm understanding (summarize/reflect) Language Barriers (CLAS Standards) ● Use qualified medical interpreter ● Do NOT use family members or translation apps ● Required for federally funded facilities Hearing Impairment Strategies ● face the client ● speak clearly/moderate pace ● reduce background noise ● use written info or visual aids ● ensure hearing aids in place ● speak to client (not interpreter) if interpreter present Vision Impairment Strategies ● introduce yourself ● give clear directions (“door at 10 o’clock”) ● allow client to hold your arm ● provide large print/audio/Braille materials Cognitive/Developmental Strategies ● use simple words ● avoid jargon/slang ● speak slowly and clearly ● reduce noise/bright distractions ● ensure glasses/hearing aids available Key Takeaways (Exam Focus) ● Benner’s stages: Novice → Advanced Beginner → Competent → Proficient → Expert ● Communication must include feedback to be effective ● Nonverbal cues often outweigh verbal messages ● Best communication style = Assertive ● Core therapeutic techniques = active listening, open-ended questions, silence, reflection, summarizing ● Use qualified interpreter for language barriers (CLAS standard) ● Barriers include cognitive, physical, cultural, environmental, and emotional factors ● Effective communication improves client safety and outcomes Here is a condensed but complete study guide that keeps all concepts from the Safety lesson while removing extra wording. SAFETY & PATIENT PROTECTION – CONDENSED STUDY GUIDE I. Joint Commission National Patient Safety Goals (NPSGs) Purpose Annual goals to improve: ● Client safety ● Safe, effective care ● Prevention of adverse outcomes 1. Identify Clients Correctly ● Use two identifiers (name, DOB, MRN, etc.) ● Confirm before meds, procedures, treatments ● Ask open-ended questions ● Verify ID band & EMR ● Use barcode scanning ● ❌ Never use room number 2. Improve Staff Communication ● Report critical results immediately ● Critical results = life-threatening abnormal labs/diagnostics ● Facility policies define: ○ critical result criteria ○ reporting timeframe ○ documentation requirements ● Communicate directly (in person/phone), not voicemail (HIPAA) 3. Use Medications Safely Label medications ● Label all syringes/containers with name, dose, date/time ● Discard unlabeled meds Anticoagulant safety ● Examples: warfarin, heparin, enoxaparin ● Monitor labs, weight, interactions, dosing ● Educate on risks, food interactions, follow-up labs Medication reconciliation ● Compare home meds with new prescriptions ● Done on admission, transfer, discharge ● Resolve discrepancies 4. Use Alarms Safely ● Clinical alarms warn of patient events or equipment malfunction ● Examples: IV pumps, ventilators, monitors, bed/chair alarms ● Risk: alarm fatigue ● Nurse role: ○ know alarm priorities ○ respond promptly ○ help develop alarm policies 5. Prevent Hospital-Acquired Infections (HAIs) Common HAIs: ● CLABSI ● CAUTI ● SSI ● VAP Concern: MDROs (MRSA, VRE, C. diff) ⭐ Hand hygiene = most important prevention Compliance required with monitoring and action plans. 6. Identify Safety Risks: Suicide Prevention ● Screen behavioral health clients ≥12 yrs ● Positive screen → detailed suicide assessment ● Implement: ○ constant observation ○ removal of harmful items ○ environmental safety checks ○ staff competency training 7. Universal Protocol (Surgery Safety) Prevent wrong-site/procedure/client: 1. Two identifiers 2. Mark surgical site (if applicable) 3. Time-out before procedure 4. Verify consent & procedure with client 8. Improve Health Care Equity (2024 Goal) Assess social determinants: ● literacy ● housing ● transportation ● food access Continue assessment throughout hospitalization and discharge planning. II. Standards of Compliance Former NPSGs now routine standards: ● Medical error prevention ● Staff competency verification ● Client rights & education ● Infection control ● Medication management ● Emergency preparedness III. Culture of Safety Promotes: ● open communication ● reporting of errors & near misses ● nonpunitive environment ● improved outcomes & staff satisfaction Nurses play key role due to frequent client contact. IV. Transforming Care at the Bedside Initiative 1. Spend 70% of time in direct bedside care 2. Leadership development 3. Rapid Response Team (RRT) 4. Standardized communication (ISBARR) Benefits: ● fewer falls, HAIs, med errors ● improved outcomes and satisfaction V. Rapid Response Team (RRT) Interdisciplinary team (ICU nurse, RT, provider) for sudden deterioration. Call RRT for: ● sudden vital sign changes ● low O₂ despite intervention ● chest pain after nitro ● seizure ● sudden mental status change ● serious clinical concern VI. ISBARR Communication Tool 1. Identity 2. Situation 3. Background 4. Assessment 5. Recommendation 6. Read-back VII. Types of Unexpected Events ● Near miss: error caught before harm ● Client safety event: event with potential harm ● Adverse event: unexpected harm occurred ● Sentinel event: severe harm/death (never event) Examples sentinel: ● wrong-site surgery ● suicide in facility ● serious fall injury VIII. Occurrence (Incident) Reporting Purpose: improve systems, prevent future errors (not punishment) Report: ● falls/injuries ● wrong meds ● adverse reactions ● blood/body fluid exposure ● property damage ● unsafe behaviors/events IX. Safety Assessment & Agencies Regulated by: ● TJC ● CMS ● OSHA ● State boards & local agencies Nursing safety focus: ● falls ● meds & allergies ● restraints ● pressure injury prevention ● infection control ● sharps & pathogen exposure ● body mechanics ● fire, chemical, radiation safety X. Electrical Safety Check: ● frayed cords ● grounded 3-prong plugs ● GFCI outlets ● no wet handling ● avoid extension cords ● tag/remove faulty equipment XI. Chemical Safety Exposure routes: ● inhalation ● skin/eyes ● ingestion ● injection (needlestick) Use: ● SDS sheets ● PPE (gloves, masks, gowns, goggles) ● ventilation systems ● emergency eye wash/showers XII. Radiation Safety Risk proportional to: ● exposure time ● distance from source Principles: 1. Reduce time 2. Increase distance 3. Shield (lead aprons, barriers) Types: ● Alpha (least risk, short travel) ● Beta (moderate risk, small distance) ● Gamma (highest risk, penetrates tissue) Initial symptoms: ● nausea, vomiting, diarrhea ● burns, alopecia ● immunocompromise ● psychological effects XIII. Age-Related Safety Risks Infants/Preschoolers ● burns, poisonings, choking, drowning ● car seat safety ● smoke detectors & safe storage of toxins School-Age ● sports injuries, firearm safety, internet risks Adolescents ● substance use, risky driving, violence, suicide risk Adults/Older Adults ● chronic illness, frailty, mobility decline ● ⭐ Major risk: falls ● frailty → poorer outcomes XIV. Hospital-Acquired Injuries Include: ● SSIs, CAUTIs, CLABSIs ● falls, trauma ● pressure injuries ● DVT ● insulin errors ● transfusion reactions ● burns/electrical shock High-risk clients: ● neurologic disorders (stroke, MS, Parkinson’s) ● cognitive impairment, dementia ● communication disabilities ● visual deficits ● behavioral disorders XV. Screening Tools Used to identify early risk: ● Morse Fall Scale (fall risk) ● Braden Scale (pressure injury risk) ● Tools must be valid/reliable Positive results → detailed assessment + individualized care plan. XVI. Home Hazard Safety Bathroom: ● grab bars, non-slip mats, raised toilet, step-free showers Bedroom: ● low bed, alarms, hospital bed if needed Kitchen: ● reachable items, automatic stove shut-off, secure chemicals General: ● good lighting, remove loose rugs, secure cords, install handrails ● cordless blinds for child safety ● emergency numbers accessible XVII. Fire Safety RACE ● Rescue ● Alarm ● Contain (close doors/windows) ● Extinguish PASS ● Pull pin ● Aim at base ● Squeeze ● Sweep Fire extinguisher types: ● A: paper/wood ● B: liquids/oils ● C: electrical ● D: metals ● K: kitchen grease ● ABC: multipurpose Evacuation: ● Lateral = same floor (preferred) ● Vertical = different floor XVIII. Workplace Safety Bullying ● Repeated harassment/belittlement ● Leads to burnout, errors, poor retention Workplace Violence Includes verbal abuse to homicide Risk factors: ● violent clients ● staff shortages ● long wait times ● lack of training/security Active Shooter Response 1. Run 2. Hide 3. Fight (last resort) XIX. Emergency Preparedness Facilities must have: ● disaster plans ● staff training & drills ● defined staff roles Types of mass exposure: ● Radiation ● Biological (anthrax, Ebola, COVID) ● Chemical toxins Response: ● PPE ● decontamination (remove clothing, shower) ● monitor vitals & mental status XX. Injury Prevention Strategies ● hourly rounding ● video monitoring ● bedside sitters ● individualized safety plans ● prompt call-light response XXI. Fall Prevention Risk factors: ● weakness, gait issues, vision problems ● confusion, dementia, impulsiveness ● clutter, poor lighting ● high-risk meds (antihypertensives, antidepressants) ● incontinence, age Universal precautions: ● nonskid footwear ● low bed & locked wheels ● clutter-free room ● call light within reach ● hourly rounding & quick response Movement alarms = warning device Siderails: ● 2 rails for safety ● 4 rails = restraint (intent matters) XXII. Restraints & Seclusion Types: ● Physical: manual holding ● Mechanical: mitts, wrist, vest, 4-point ● Chemical: sedatives/antipsychotics ● Barrier: enclosures, lapboards, 4 rails ● Seclusion: locked room Use ONLY as last resort when: ● danger to self/others ● removing life-saving devices ● severe aggression Care of restrained client: ● frequent circulation, skin, respiratory checks ● ROM, hygiene, fluids, elimination ● reevaluate every 24 hrs ● discontinue ASAP XXIII. Seizure Precautions Preseizure ● suction & oxygen ready ● padded rails ● IV access ● remove restrictive clothing/jewelry During seizure ● call for help ● side-lying position ● protect head ● do NOT restrain ● monitor duration & movements ● give benzodiazepine if ordered Postseizure ● assess gag reflex before oral intake ● reassure client ● labs, EEG, imaging as ordered XXIV. Musculoskeletal Injury Prevention (Nurse Safety) Use assistive devices: ● Hoyer lift (ground lift) ● ceiling lift ● slide sheets ● sit-to-stand lift Safe handling: ● clear area ● use correct sling size ● have 2 staff assist ● lock brakes ● never leave client unattended XXV. Patient-Centered Care Focus: ● client as center of care ● collaboration & shared decision-making ● respect cultural, spiritual, religious needs ● holistic & individualized care ● include pastoral care support FINAL MEMORY CHECK (High-Yield Core Concepts) ● Two identifiers before any care ● Hand hygiene prevents HAIs ● Time-out before surgery ● ISBARR improves communication ● RRT for sudden deterioration ● Fall prevention + restraints last resort ● RACE & PASS fire response ● Run–Hide–Fight for active shooter ● Time–distance–shielding for radiation safety ● Screening tools identify early risks Here is a fully condensed study guide that includes ALL major topics and concepts from your lesson (patient-centered care, caring theories, cultural care, spirituality, advocacy, sleep & rest) without leaving anything out. CONDENSED STUDY GUIDE: PATIENT-CENTERED CARE, CARING, CULTURE, ADVOCACY & SLEEP I. Patient-Centered Care Definition Patient-centered care = placing the client at the center of all care, focusing on preferences, culture, and holistic needs rather than just tasks or documentation. Key Concepts ● Improves client satisfaction and outcomes ● Involves caring, preferences, cultural respect, and shared decision-making ● Holistic care: physical, emotional, spiritual needs II. Caring in Nursing Definition Caring = nurturing another person with responsibility and commitment; core of professionalism. Holistic Caring Includes ● Healing environment ● Kindness, empathy, compassion ● Addressing physical, emotional, and spiritual needs III. Caring Theories A. Watson’s Theory of Human Caring Holistic model focusing on mind-body-spirit harmony through transpersonal (human-to-human) caring relationships. Core Ideas ● Caring moments foster healing and self-restoration ● Nurse must achieve inner balance and spirituality ● Establish trusting presence and relationships 10 Caritas Processes 1. Loving-kindness and compassion 2. Authentic presence and honoring beliefs 3. Sensitivity to self and others 4. Trusting caring relationships 5. Expression of feelings 6. Creative problem-solving through caring 7. Transpersonal teaching/learning 8. Healing environment (comfort, dignity, peace) 9. Reverent assistance with basic needs 10. Openness to spirituality and miracles B. Swanson’s Theory of Caring Caring improves well-being through empowerment, dignity, and respect. Five Caring Processes 1. Maintaining belief – instill hope and meaning 2. Knowing – understand client’s situation/perception 3. Being with – emotional and physical presence 4. Doing for – perform needed tasks for client 5. Enabling – guide and support through events/transitions IV. Caring Behaviors 1. Listening ● Active, empathetic listening ● Observe verbal and nonverbal cues ● Key for holistic assessment and trust 2. Touch ● Used for procedures and expressive caring ● Requires permission; consider culture, trauma, gender ● Can reduce anxiety and increase well-being 3. Being Present ● Physical and emotional availability ● Reduces loneliness and improves comfort ● Reflects “being with” (Swanson) 4. Providing Comfort ● Pharmacologic and nonpharmacologic comfort measures ● Examples: pillows, blankets, hygiene, music, temperature control ● Represents “doing for” 5. Showing Compassion ● Recognize suffering and act to relieve it ● View client as person, not diagnosis ● Requires self-awareness and adequate staffing V. Client Preferences in Care Clients are full members of the health care team and experts on their own experiences. Benefits ● Increased trust and satisfaction ● Improved healing and outcomes ● Greater sense of control Ways to Include Preferences 1. Endorsing participation – empower involvement 2. Promoting understanding – correct misinformation 3. Sharing information – two-way communication Barriers ● Power imbalance ● Medical jargon ● Weakness, fatigue, cognitive impairment ● Poor collaboration and language barriers VI. Cultural Competence Definition Evidence-based care aligned with client’s cultural values, beliefs, and practices. Influencing Factors ● Socioeconomic status ● Health literacy ● Racism experiences ● Sexual orientation ● Acculturation (adapting to another culture) Five Elements of Cultural Competence 1. Cultural awareness – self-examine biases 2. Cultural knowledge – learn client values/beliefs 3. Cultural skill – assess cultural needs accurately 4. Cultural encounters – interact with diverse cultures 5. Cultural desire – motivation to connect with cultures Cultural Assessment Includes ● Cultural/spiritual affiliation ● Health beliefs and practices ● Spiritual rituals ● Dietary preferences/prohibitions ● Care preferences to increase comfort VII. Age-Related (Generational) Care Preferences Generation Preferences Silent (1928–1945) Formal, face-to-face, written communication Baby Boomers Team-oriented, sincere, in-person communication Gen X Direct, independent, questions providers Millennials Tech-based communication, frequent feedback Gen Z Digital natives, prefer texting/email Gen Alpha Tech-savvy children; family-centered care VIII. Spiritual Nursing Care Spiritual Well-Being Feeling of meaning, purpose, and connection to higher power → improves quality of life. Spiritual Assessment Questions ● Source of spiritual strength? ● Meaning-of-life concerns? ● Relationship with higher power? ● Spiritual practices? ● Fear of dying? ● Relationship concerns? Assessment Tools FICA: ● Faith ● Importance ● Community ● Address in care HOPE: ● Hope sources ● Organized religion ● Personal spirituality/practices ● Effects on care/end-of-life issues IX. Spiritual Distress Definition Questioning life meaning or beliefs causing despair, anger, fear, uncertainty. Nursing Interventions ● Listen and be present ● Encourage spiritual expression ● Provide prayer, texts, pastoral referral ● Address emotional and spiritual needs X. Pastoral Care Provides: ● Ethical, religious, and spiritual support ● Counseling, prayer, rituals ● End-of-life and grief support ● Support for families and staff Chaplains assist all clients regardless of religion. XI. Access to Care Barriers ● Lack of insurance ● Transportation problems ● Limited providers/facilities (rural areas) ● Restricted clinic hours ● Medication cost barriers Solutions ● Telemedicine: remote diagnosis/testing ● Telehealth: broader remote clinical and nonclinical services ● Improves access, especially rural areas XII. Client Advocacy Definition Protect client autonomy, rights, and safety; act as client’s voice. Clients Needing Advocacy ● Unconscious ● Children ● Fearful/intimidated clients ● Uninformed about diagnosis/rights Advocacy Steps 1. Assess needs, values, cognition, resources 2. Verify client goals/preferences 3. Implement plan and communicate with team 4. Evaluate outcomes and self-determination Related Concepts ● Medically futile: treatment unlikely to cure or extend life ● Potentially inappropriate treatment: works but may not improve quality of life ● Palliative care: symptom relief + quality of life ● Quality of life: personal meaning, independence, relationships XIII. Sleep and Rest Importance of Sleep Supports: ● Memory, learning, concentration ● Immune system and tissue repair ● Hormone balance (ghrelin, leptin, cortisol) ● Mood, reaction time, coordination ● Prevention of obesity, diabetes, cardiovascular disease XIV. Physiology of Sleep Key Brain Structures ● Cerebral cortex: sensory processing & memory ● Brainstem: controls REM and muscle relaxation ● Hypothalamus: autonomic control, circadian rhythm (SCN) ● Thalamus: sensory filtering during sleep ● Pineal gland: produces melatonin XV. Sleep Regulation Mechanisms 1. Circadian rhythm – 24-hour internal sleep–wake cycle influenced by light and temperature 2. Sleep–wake homeostasis – pressure to sleep increases with sleep deprivation Factors affecting sleep: ● Light exposure ● Stress ● Medications ● Caffeine/food ● Environment XVI. Stages of Sleep NREM Sleep Stage 1: Light sleep; easily awakened (5%) Stage 2: Deeper sleep; decreased HR/temp; memory consolidation (50%) Stage 3: Deep sleep; delta waves; immune strengthening and tissue repair (15%) REM Sleep ● Dream stage ● Irregular breathing and increased HR ● Muscle atonia (prevents acting out dreams) ● Occurs ~90 minutes after sleep onset Sleep cycles repeat 4–6 times per night. XVII. Sleep Patterns by Age ● Newborns: multiple cycles, high REM ● Adults: 2–5% stage 1, 45–55% stage 2, 10–20% stage 3, 20–25% REM ● Older adults: less deep sleep, more awakenings XVIII. Sleep Deprivation Types ● Total: no sleep for extended period ● Partial: reduced sleep hours ● Chronic: ongoing insufficient sleep ● Selective: loss of specific sleep stage Effects ● Impaired judgment and memory ● Mood swings, depression ● Increased accidents and chronic illness risk ● Poor glucose control and obesity XIX. Promoting Sleep Nonpharmacologic Interventions ● Avoid caffeine, nicotine, alcohol before bed ● Keep room dark, quiet, cool ● Establish bedtime routine ● Consistent sleep schedule ● Exercise regularly (not right before bed) ● Limit naps (<30 minutes) ● Remove electronics/TV from bedroom XX. Sensory Overload in Hospital Definition: Excess stimuli beyond brain’s processing ability → sleep disruption. Nursing Interventions ● Lower noise and alarms ● Dim lights ● Provide earplugs/eye masks ● Cluster care tasks ● Control pain and medication effects XXI. Sleep Disorders Insomnia Difficulty falling/staying asleep → fatigue, poor concentration, mood changes Sleep Apnea ● Central: brain fails to signal breathing ● Obstructive: airway collapse; snoring; daytime sleepiness Treatment: CPAP, weight loss, avoid alcohol/smoking Narcolepsy Sudden sleep attacks; possible cataplexy (loss of muscle tone) Hypersomnia Excessive daytime sleepiness despite adequate sleep Restless Legs Syndrome (RLS) Urge to move legs; worsens at night; disrupts sleep Night Terrors Non-REM parasomnia causing panic and no recall; common in children XXII. Pharmacologic Sleep Therapies ● Benzodiazepines (GABA agonists): sedative but dependency risk ● Nonbenzodiazepine hypnotics (most common) ● Melatonin: low-risk first-line option ● Antihistamines: OTC but cause side effects XXIII. Nonpharmacologic Sleep Therapies ● Massage, acupuncture, thermotherapy ● Guided imagery, meditation, music therapy ● Yoga and relaxation techniques ● Sleep diaries to identify patterns and personalize care FINAL KEY POINT Patient-centered nursing integrates: ● Caring theories ● Cultural competence ● Spiritual support ● Client advocacy ● Sleep and comfort promotion Goal: provide holistic care that supports physical healing, emotional well-being, spiritual meaning, autonomy, and optimal quality of life. Week 7 Absolutely—here’s a more condensed study guide that still includes every concept you were given. CONDENSED STUDY GUIDE: ELIMINATION (ALL CONCEPTS) 1) Big Picture ● Elimination (urine + stool) is continuous and essential. Patterns vary, but changes require assessment + intervention to restore usual patterns or establish a new baseline. 2) Urinary System Basics Functions: excrete waste/fluid → urine, regulate electrolytes, support RBC production, help regulate BP, support bone health. Pathway: kidneys → ureters → bladder → urethra → urination. Control: internal sphincter + external sphincter + pelvic floor muscles prevent leakage. Urination: elimination of urine via urethra. 3) Urine Production & Assessment Normal: clear, light yellow, minimal odor. Typical daily amount: ~1–2 quarts/day (varies). Expected output by age: infant ~2 mL/kg/hr; toddler ~1.5; teen ~1; adult ~0.5. Color clues: ● Dark yellow/amber = need fluids ● Dark brown = dehydration/kidney/liver concern ● Red/pink = blood or foods (beets, blackberries, rhubarb) Diet/med effects: ● Fluids ↑ volume, lighter color ● Asparagus ↑ odor ● Dyes can turn blue/green ● Alcohol + caffeine ↑ urine output (can dehydrate if not balanced) Aging urinary changes: ↓ nephrons/kidney function, ↓ bladder tone → incontinence/retention risks. 4) GI System Basics Organs: mouth → esophagus → stomach → small intestine → large intestine → rectum → anus. Peristalsis: contractions that move contents through GI tract. Feces formation: digestion + absorption (small intestine), water absorption + stool formation (large intestine), bacteria help + make vitamin K, rectum stores stool until BM. Bristol Stool Chart: ● Types 1–2 = constipation ● Types 3–4 = expected ● Types 5–7 = diarrhea Aging GI changes: ↓ peristalsis/muscle tone → constipation; ↑ PUD risk (NSAIDs), ↓ elasticity/emptying changes, possible ↓ absorption/bacterial overgrowth, ↓ lactase → lactose intolerance; lifestyle factors (inactivity, low fiber/fluids, meds) contribute. 5) Expected Elimination ● Urine: clear, light yellow, varies with intake/activity/diuretics. ● Stool: frequency varies widely; should be soft/formed, easy to pass without straining. 6) Altered Urinary Elimination Urinary Incontinence (UI) Involuntary urine loss. Can cause skin breakdown + distress. Types: ● Stress: cough/sneeze/exertion ● Urge: sudden urge, leak before toilet ● Reflex: nerve damage, no warning ● Overflow: incomplete emptying → overfill/leak ● Functional: can’t reach toilet (mobility/dexterity issues) ● Nocturnal enuresis: nighttime (kids; adults w alcohol/caffeine/meds) Management: lifestyle changes (↓ caffeine/alcohol, smoking cessation, address constipation), pelvic floor exercises, bladder training, meds/devices/surgery; skin protection (pads/briefs, cleanser, barrier cream). Urinary Retention Incomplete bladder emptying (acute or chronic). Causes: BPH, cystocele/prolapse, obstruction (stones/lesions). Findings: hesitancy, weak stream, frequency, distention, pain, leakage. Risks: UTI, bladder/kidney damage. 7) Altered Bowel Elimination Constipation <3 BMs/week + hard/lumpy stools, difficult to pass. Risks: pregnancy/postpartum, older adults, low fiber/fluids, meds, GI disorders, immobility. Red flags: fever, GI bleeding, severe pain, vomiting, weight loss. Complication: fecal impaction/obstruction (liquid stool may leak around impaction). Tx: fiber + fluids + exercise + bowel training; meds; enema/manual removal; surgery if complete obstruction. Diarrhea Frequent loose/watery stools: acute (1–2d), persistent (>2w <4w), chronic (>4w). Risks: infection, meds, GI disorders, diet. Dangers: dehydration, malabsorption. Adult urgent follow-up: fever ≥102°F, >2 days, ≥6/day, severe pain, blood/black stool. Tx: rehydration; OTC (loperamide/bismuth) if appropriate; antibiotics/probiotics if infectious cause. Bowel Incontinence Urge (can’t reach toilet) most common; passive (unaware leakage). Leads to skin issues + reduced self-esteem. Children: encopresis. 8) Medications That Affect Elimination Constipation: antacids (Al/Ca), anticholinergics/antispasmodics, antiseizure meds, Ca-channel blockers, diuretics, iron, antiparkinsonian, opiates, antidepressants. Diarrhea: antibiotics, magnesium antacids; consider C. diff if severe/persistent after antibiotics. 9) Conditions Altering Urinary Patterns ● Dehydration: thirst, dry mouth, fatigue, dizziness, dark urine; severe needs IV fluids. ● UTI: dysuria, urgency/frequency; can progress to pyelonephritis (fever, flank pain, N/V, hematuria). Tx antibiotics + fluids. Higher risk: females, retention, obstruction, catheters, diabetes, menopause. ● Kidney stones: severe flank pain radiating to groin, hematuria, dysuria, fever/chills, N/V. Tx fluids, pain meds, strain urine, ESWL/surgery. ● Kidney failure: waste/fluid buildup → ↓ urine, HTN, anemia, itching; Tx dialysis or transplant. ● BPH: urethral constriction → retention, nocturia, weak stream; can cause UTIs/damage; Tx meds/surgery. 10) Conditions Altering Bowel Patterns ● Diverticulosis: pouches; Diverticulitis: inflamed/infected pouch → pain/bleeding; risk perforation → peritonitis. Prevent: fiber; nuts/seeds no longer restricted. Tx antibiotics + liquid/soft diet. ● IBS: pain + diarrhea/constipation (IBS-C, IBS-D, IBS-M); Tx diet (fiber/probiotics, avoid triggers), stress reduction, sleep/exercise, meds. ● Bowel obstruction: blockage → N/V, distention, severe constipation; NG decompression + surgical consult. ● Ileus: decreased/absent motility (often post-op/illness/meds) → absent bowel sounds, distention, N/V; Tx NPO, NG tube, IV fluids; consider TPN if prolonged. ● Ulcerative colitis: colon inflammation/ulcers → bloody diarrhea, fatigue, anemia; Tx meds; surgery if refractory/cancer risk. ● Crohn’s: inflammation anywhere (often small intestine) → diarrhea, weight loss, anemia; complications fistulas/abscess/obstruction; Tx meds + possible surgery. 11) Diversions & Ostomies Urinary Diversions ● Catheterization (temporary) ● Ureteral stent ● Ileal conduit/urostomy (stoma + pouch) ● Nephrostomy (kidney → external bag) ● Neobladder (internal reservoir, may need catheter) ● Continent cutaneous reservoir (internal pouch + valve; catheter to empty) ● Cystostomy (catheter directly into bladder) Complications: UTIs, kidney infection, skin breakdown; psychosocial concerns. Fecal Diversions ● Ileostomy ● Colostomy (+ irrigation option for some permanent colostomies) ● J-pouch (internal ileal reservoir connected to anus; often temporary ileostomy first) ● Kock pouch (continent ileostomy; catheter to empty) Complications: skin irritation, hernia/prolapse/stenosis, blockage, diarrhea, bleeding, electrolyte imbalance, infection, leakage. WOC nurse supports education + supplies + skin/stoma care. 12) Diagnostics & Specimen Collection Urinary ● Urodynamics: uroflowmetry, postvoid residual, cystometric test, leak point pressure, EMG, video urodynamics, pressure-flow study ● Scopes: cystoscopy, ureteroscopy ● Urinalysis: visual + dipstick + microscopic (WBC, RBC, bacteria, casts, crystals) ● Urine culture: clean catch midstream; grows organism + susceptibility testing (correct antibiotic; reduces resistance) ● 24-hour urine: collect all urine, refrigerate, avoid certain foods/meds Urine collection methods: clean catch vs catheter (sterile technique for intermittent/indwelling). GI ● Tests: celiac testing, colonoscopy, ERCP, sigmoidoscopy, upper/lower GI series, upper endoscopy ● FOBT: dietary/med restrictions to prevent false positives (ex: beets, red meat, some veggies; aspirin/ibuprofen/Vit C) ● Stool culture: for severe/persistent diarrhea (travel, contaminated food/water, antibiotics) 13) Nursing Interventions Promote Urinary Elimination ● Bedpan/urinal assistance + measure output + privacy + skin check ● Bladder irrigation (ordered; pain is NOT expected → report) ● Lifestyle: avoid bladder irritants; appropriate fluids; weight loss; stop smoking ● Bladder training + elimination journal ● Bladder scan to avoid unnecessary catheterization ● Catheters: intermittent, indwelling, external male condom, external female wick ● CAUTI prevention: sterile insertion for indwelling/intermittent; daily hygiene; handwashing; keep system clean Promote Bowel Elimination ● Fiber, hydration, activity, respond to urge, stress management ● Bowel training (may use laxatives) ● Enemas: cleansing vs retention; solutions hypotonic/isotonic/hypertonic (tap water can cause electrolyte shifts) ● Laxatives: ○ Bulk-forming ○ Surfactant (stool softener) ○ Stimulant ○ Osmotic ● Rectal tubes/fecal management systems for severe incontinence Skin Care for Incontinence ● Clean promptly, rinse, pat dry ● Moisturize (alcohol-free) ● Barrier ointments/pastes/sealants ● Assess for nonblanchable redness, blisters, wounds/ulcers NG Decompression (for obstruction/ileus) Measure nose → ear tragus → xiphoid, advance with swallowing, confirm placement (x-ray/capnography/pH per policy), secure + suction as ordered. If you want, I can also turn this into a 1-page “exam cram” sheet (still including every concept, just in ultra-compact bullets). Condensed Study Guide: Main Concepts (Elimination + Sensory Perception) 1) ELIMINATION (URINARY + BOWEL) Urinary system basics ● Organs: kidneys → ureters → bladder → urethra ● Kidneys: filter blood, remove waste/fluid, regulate electrolytes & BP hormones, support RBC production. ● Normal urine: clear, light yellow, minimal odor. ○ Dark yellow/amber: dehydration. ○ Red/pink: blood or foods (beets). ○ Brown: severe dehydration/liver/kidney issues or certain foods. Expected urine output (high-yield) ● Adults: ~0.5 mL/kg/hr ● Output generally decreases with age (↓ nephrons, ↓ renal blood flow). Urinary alterations Urinary incontinence = can’t control urination Types: ● Stress: cough/sneeze/exertion → leak ● Urge: sudden strong urge → can’t reach toilet ● Overflow: bladder overfills from incomplete emptying → dribbling/leak ● Reflex: nerve damage → unpredictable leakage ● Functional: can’t get to toilet in time (mobility/dexterity issues) ● Nocturnal enuresis: nighttime bedwetting Key nursing focus: skin protection (barrier creams, briefs/pads), reduce irritants, bladder training, pelvic floor exercises. Urinary retention = can’t empty bladder fully ● Causes: BPH, prolapse (cystocele), obstruction (stones), neuro issues. ● Findings: hesitancy, weak stream, frequency, distention, pain, leakage. ● Risks: UTI, bladder/kidney damage. ● Interventions: identify cause, drain bladder if needed, bladder scan, catheterization if ordered. Common urinary conditions ● Dehydration: thirst, dry mouth, dizziness, dark urine, low urine; severe → IV fluids. ● UTI: dysuria, urgency/frequency; untreated → pyelonephritis (fever, flank pain, N/V). Treat: antibiotics + fluids. ● Kidney stones: severe flank pain radiating to groin, hematuria, N/V; treat pain + fluids, strain urine, possible lithotripsy/surgery. ● Kidney failure: ↓ urine, HTN, anemia, itching; treat dialysis/transplant. ● BPH: frequency/nocturia, weak stream, retention/incontinence; treat meds/surgery. Bowel system basics ● GI tract: mouth → esophagus → stomach → small intestine → large intestine → rectum → anus ● Peristalsis moves contents forward. ● Stool: should be soft/formed, easy to pass (no straining). Bristol Stool Chart (quick) ● 1–2: constipation (hard/lumpy) ● 3–4: ideal/normal ● 5–7: diarrhea (loose/watery) Bowel alterations ● Constipation: <3 BMs/week + hard stool/straining ○ Risks: impaction/obstruction (esp immobile/neuro injury). ○ Tx: fiber, fluids, activity, bowel training, stool softeners/laxatives; impaction → enema/manual removal. ● Diarrhea: frequent loose watery stools ○ Danger: dehydration, electrolyte imbalance; red flags: blood/black stool, fever, severe pain, lasts >2 days. ○ Tx: rehydration, remove irritants; meds like loperamide (if appropriate); infection → meds/probiotics as ordered. ● Bowel incontinence: urge (can’t reach toilet) vs passive (leak without awareness). ○ Nursing: skin care, scheduled toileting, bowel training, protect dignity. Diversions (know names + purpose) Urinary diversions ● Catheterization: intermittent or indwelling ● Ureteral stent: keeps ureter open ● Urostomy/ileal conduit: urine exits through stoma into pouch ● Nephrostomy: kidney → external drainage ● Cystostomy (suprapubic): catheter directly into bladder ● Neobladder/continent reservoir: internal storage; may need catheter to empty Complications: infection, skin breakdown, psychosocial stress. Fecal diversions ● Ileostomy: ileum → stoma (often liquid stool) ● Colostomy: colon → stoma (more formed depending on location) ● J-pouch: internal ileal reservoir connected to anus ● Kock pouch: continent ileostomy; catheter to empty Complications: skin irritation, leaks, hernia/prolapse, blockage, diarrhea, electrolyte issues. Diagnostic tests/specimens (high-yield) Urinary ● Urinalysis: dipstick + microscopic ● Urine culture: clean catch; susceptibility testing picks the right antibiotic ● 24-hr urine: measures substances over time ● Urodynamics: bladder function (uroflowmetry, PVR, cystometrics, etc.) ● Cystoscopy/ureteroscopy: visualize urinary tract GI ● FOBT: check hidden blood (avoid foods/meds that cause false positives) ● Stool culture: severe/persistent diarrhea, travel, prolonged antibiotics ● Colonoscopy, sigmoidoscopy, upper GI endoscopy, ERCP, GI series as indicated Nursing priorities (elimination) ● Assess: amount, frequency, color/odor, pain, stool type. ● Prevent skin breakdown: cleanse, dry, barrier creams, frequent checks. ● Promote normal patterns: hydration, fiber, activity, timed toileting, privacy, proper equipment (bedpan/urinal). ● Reduce infection risk: sterile technique for invasive catheters; minimize indwelling catheter days (CAUTI prevention). 2) SENSORY PERCEPTION (ALL MAIN CONCEPTS) Big picture ● Stimulus → sensory organ → CNS/cranial nerves → brain interprets → response ● Problems can be in reception, perception, or response. Key terms ● Sensory deficit: reduced function (vision/hearing/touch/etc.) ● Sensory deprivation: too little stimulation ● Sensory overload: too much stimulation → anxiety/confusion ● SPD: detects stimuli but brain misprocesses → oversensitive/overwhelmed Cranial nerves (only what’s essential) ● I smell, II vision, III/IV/VI eye movement ● V facial sensation/jaw ● VII facial expression + taste (front tongue) ● VIII hearing/balance ● IX/X swallowing/gag/voice ● XI shoulder shrug/head turn ● XII tongue movement Vision: most tested disorders ● Refractive errors: myopia, hyperopia, astigmatism, presbyopia ● Cataracts: cloudy lens → blurry/hazy, ↓ color ● Diabetic retinopathy: retinal vessel damage → floaters/blur → blindness risk ● Glaucoma: ↑ intraocular pressure → loss of peripheral vision (irreversible) ● Macular degeneration: loss of central vision (older adults) Tests: Snellen/Tumbling E; slit lamp; fluorescein angiography; visual field test; intraocular pressure; Amsler grid. Hearing ● Anatomy: outer → middle (ossicles) → inner (cochlea) → CN VIII. ● Tinnitus: ringing/buzzing without sound. ● Types of loss: ○ Sensorineural: inner ear/nerve (aging = presbycusis, loud noise, ototoxic meds) ○ Conductive: sound can’t travel (wax, otitis media, perforation, otosclerosis) ○ Mixed: both Tests: Rinne, pure-tone audiometry; ABR/OAE (screening). Speech/Aphasia (stroke-related high yield) ● Broca/expressive: understands but can’t produce words well (“telegraphic” speech) ● Wernicke/fluent: lots of words, no meaning; poor comprehension ● Global: severe impairment of both Touch ● Hypersensitivity / defensiveness (painful to normal touch) vs hyposensitivity (reduced pain/temp). ● Major causes: peripheral neuropathy (diabetic), spinal cord injury. ● Testing: neuro exam, sensation checks, nerve conduction, EMG, MRI. Smell & taste (often linked) ● Taste disorders: hypogeusia (↓ taste), ageusia (no taste), dysgeusia (metallic/rancid), phantom taste ● Smell disorders: anosmia (no smell), hyposmia (reduced), parosmia (distorted), phantosmia (smell not real) ● Causes: URIs, sinus disease, head injury, smoking, meds, zinc deficiency, neuro disorders. Aging effects (must know) ● Vision & hearing decline most. ● Vision: smaller pupils, less lens flexibility, weaker extraocular muscles, ↓ tears/dry eyes. ● Hearing: high-frequency loss, cerumen impaction, tinnitus. ● Taste/smell: ↓ taste buds + ↓ saliva → ↓ appetite → malnutrition risk. ● Touch: ↓ circulation → ↓ temperature/pain sensitivity. Nursing priorities (sensory) ● Safety + independence + emotional support ● Vision: lighting, corrective lenses, remove clutter, orient to room, fall prevention. ● Hearing: face client, reduce background noise, check hearing aids, use written info/interpreter. ● Speech: allow time, don’t finish sentences, use boards/paper/tablet. ● Touch: injury prevention (diabetic foot care, protective footwear, daily inspection). ● Smell/taste: oral hygiene, season foods, smoke/CO detectors, avoid smoking. If you want, I can turn this into a one-page “test-ready” version (even shorter, like only definitions + red flags + key interventions). Condensed Study Guide: Complementary & Integrative Health (CIH) / CAM / Holistic Nursing 1) Key Terms (know the differences) ● Conventional (Western) medicine: Evidence-based diagnosis & treatment (meds, surgery, radiation). Also called mainstream, allopathic, biomedicine, orthodox. ● Complementary therapy: Used with conventional care (ex: aloe + NSAID for sunburn). ● Alternative therapy: Used instead of conventional care. ● Integrative health: Combines conventional + complementary + alternative in a coordinated plan (mind–body–spirit). ● Holistic nursing: Client-centered care treating the whole person (physical, emotional, spiritual, social, cultural, environment). Focus is healing + wellness, not just curing disease. 2) NCCIH Categories (how CIH is “delivered”) Nutritional approaches ● Herbs/botanicals, supplements, vitamins/minerals, probiotics, dietary therapies ● Usually OTC and labeled as dietary supplements Psychological (mind–body) approaches ● Relaxation, meditation, mindfulness/MBSR, guided imagery, biofeedback, hypnosis, prayer Physical approaches ● Hands-on body structures/systems: massage, chiropractic, osteopathy, spinal manipulation, heat/cold, reflexology Bioenergetic (energy) therapies ● Veritable energy = measurable EM fields/light/magnets ● Putative energy (biofields) = subtle energy concepts ● Examples: Healing Touch, Therapeutic Touch, Reiki, Tai Chi, qi gong, acupressure Whole medical systems ● Complete systems separate from Western medicine: ○ Ayurveda, Traditional Chinese Medicine (TCM), Unani, Kampo ○ Also: Homeopathy, Naturopathy, Functional medicine (root-cause focus) Combined approaches ● Blends multiple categories: yoga, mindfulness eating, dance/art/music therapy 3) Why it matters (nursing relevance) ● Many clients use CIH (often alongside prescriptions). Nurses must: ○ Assess what clients use ○ Prevent interactions/harms ○ Provide culturally congruent care ○ Support self-care + empowerment ● Holistic nursing priorities ○ Promote wellness, honor caring–healing relationship ○ Respect subjective experience of illness/healing ○ Encourage informed decisions + active participation ○ Incorporate cultural beliefs/folk practices safely 4) High-yield Mind–Body Therapies (what they do) ● Deep breathing: control rate/depth → ↓ anxiety/stress ● Meditation: quiet mind/focused attention → ↓ BP/HR, ↓ stress effects ● Mindfulness: present-moment awareness; can reduce stress and improve coping ● Guided imagery: mental visualization → relaxation, pain/anxiety reduction ● Prayer: spiritual coping/connection (client-defined) ● Progressive relaxation: systematically tense/relax muscle groups ● Yoga (meditative movement): poses + breathing ± meditation → stress, sleep, anxiety; also pain (back/neck) support ● Aromatherapy: essential oils (inhaled/topical) → relaxation, anxiety relief; some evidence for nausea (ex: ginger/lavender/peppermint blends) ● Acupuncture/acupressure: stimulates points/meridians → pain, nausea, fatigue, anxiety support ● Hypnotherapy: focused attention + suggestion → phobias, anxiety, pain, habits (smoking) ● Biofeedback: device-assisted control of body functions (HR, tension) → stress, headaches, rehab, pain 5) Manual Therapies (hands-on) ● Massage: manipulates soft tissues → pain/anxiety/insomnia support ○ Precautions: avoid over clots/tumors/prostheses; caution with anticoagulants/low platelets (bruising/bleeding); older adults risk (rare) fractures ● Reflexology: foot/hand zones thought to correspond to body functions ● Chiropractic: spinal manipulation + structural focus; no surgery/Rx meds ● Osteopathic medicine: structure-function relationship; osteopathic manipulation used by trained physicians 6) Bioenergetic / Movement Therapies ● Tai Chi / Qi gong: meditative movement; balance, function, stress reduction ● Alexander Technique: posture/neck-spine alignment awareness → chronic pain support ● Feldenkrais: mindful movement retraining → pain + mobility ● Rolfing/Structural integration: deep tissue/fascia work → posture/function ● Pilates: core/torso control, posture → balance, flexibility, pain relief ● Therapeutic Touch / Healing Touch / Reiki: energy-based touch; may support relaxation, pain reduction, agitation (ex: dementia) 7) Traditional / Indigenous Practices (cultural competence) ● Traditional medicine (WHO concept): culture-based knowledge/practices for prevention/diagnosis/treatment—often includes spirituality. ● Examples: Native healing practices (prayer, drumming, storytelling, sacred rituals), herbal use, cupping, etc. ● Nursing: respect beliefs, ask what practices are important, integrate safely. 8) Whole Medical Systems (quick ID) ● Ayurveda: balance mind–body–spirit; doshas; cleansing + diet + herbs + yoga/meditation ● TCM: acupuncture, Tai Chi/qi gong, herbs; balance yin/yang + qi flow ● Naturopathy: “body heals itself” supported by diet, lifestyle, herbs, supplements, homeopathy, etc. ● Homeopathy: “like cures like,” highly diluted remedies ● Functional medicine: root-cause, systems-based approach 9) Natural Products: BIG SAFETY POINTS (test favorites) FDA/supplements ● FDA regulates supplements, but manufacturers are responsible for quality/claims → variability exists. ● “Natural” ≠ safe. Must-do nursing action ● Always ask about herbs/supplements/vitamins OTC. ● Encourage a current med + supplement list shared with provider/pharmacist before starting anything new. Common interaction themes ● Bleeding risk (esp with anticoagulants like warfarin): ○ Garlic, ginger, ginkgo, cranberry (large amounts), evening primrose oil, etc. ● Serotonin syndrome risk when mixing certain herbs with antidepressants: ○ St. John’s wort + antidepressants (ex: duloxetine) ● CNS depression/sedation combos: ○ Valerian + sedatives/alcohol/antihistamines ● Vitamin K decreases warfarin effect: ○ Leafy greens (consistency matters) Specific high-yield herbal cautions ● Ephedra (ma huang): banned in U.S. supplements → serious CVA/MI risk (worse with caffeine) ● Kava: can cause liver damage ● Black cohosh: possible liver injury risk ● Tea tree oil: toxic if ingested ● Licorice root: ↑ BP, can lower K+ (esp with diuretics); avoid in pregnancy ● St. John’s wort: many interactions (reduces effectiveness of multiple meds) + photosensitivity Probiotics (basic) ● Support healthy gut flora; can help inhibit harmful bacteria (ex: Lactobacillus) 10) Vitamins & Minerals (core test facts) Vitamins ● Water-soluble: B-complex + C (not stored well → need regular intake) ● Fat-soluble: A, D, E, K (stored in fat/liver → toxicity risk if too much) Vitamin K newborn note: doesn’t cross placenta well; newborns get IM vitamin K to prevent bleeding. B-complex quick purpose (big picture) ● Mostly metabolism/energy, neuro function, RBC formation ● B12: neuro + RBCs (deficiency → anemia, fatigue, neuro changes) Minerals (core roles) ● Needed for: enzyme function, nerve/muscle contraction, fluid balance, bone/teeth ● Examples: ○ Calcium: bones + clotting + nerve impulses ○ Sodium: extracellular fluid, nerve/muscle ○ Potassium: nerve/muscle; high/low can cause arrhythmias ○ Magnesium: metabolic processes; low with alcohol use disorder/DM ○ Iron: oxygen transport; deficiency → anemia Food-drug/nutrient interactions (quick) ● Vitamin C ↑ non-heme iron absorption ● Coffee/tea/wine (polyphenols) + phytic acid (legumes/nuts) ↓ iron absorption Quick “Exam-Style” Reminders ● Complementary = with conventional; Alternative = instead; Integrative = coordinated blend. ● Nursing role: assess use, prevent interactions, educate, support self-care, respect culture. ● Biggest safety issue: herb/supplement interactions (bleeding, serotonin syndrome, sedation, warfarin/vit K). If you want, paste any practice questions from this lesson and I’ll answer them using only what’s in your notes

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Listening Quiz #1 Repertoire Overview