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BIOL 101 Complete Study Guide Unit 1: DNA, RNA, and Genetics 1. DNA structure What is DNA? DNA stands for deoxyribonucleic acid. It stores the genetic information that tells cells how to function, grow, and reproduce. What is the shape of DNA? DNA has a double-helix shape, which looks like a twisted ladder. What are the building blocks of DNA? Nucleotides. What are the three parts of a DNA nucleotide? * A phosphate group * A five-carbon sugar called deoxyribose * A nitrogenous base What are the four nitrogenous bases in DNA? * Adenine (A) * Thymine (T) * Cytosine (C) * Guanine (G) What are the DNA base-pairing rules? * Adenine pairs with Thymine (A–T). * Cytosine pairs with Guanine (C–G). What does complementary base pairing mean? Each DNA base has a specific partner. Knowing one DNA strand allows you to determine the matching strand. Example: * Original: A T C G * Complement: T A G C What holds the two DNA strands together? Hydrogen bonds between the nitrogenous bases. 2. DNA vs. RNA What is RNA? RNA stands for ribonucleic acid. It helps use the genetic instructions stored in DNA to make proteins. What are the main differences between DNA and RNA? DNA RNA Usually double-stranded Usually single-stranded Contains deoxyribose sugar Contains ribose sugar Uses thymine (T) Uses uracil (U) Stores genetic information Helps make proteins What are the four bases in RNA? * Adenine (A) * Uracil (U) * Cytosine (C) * Guanine (G) What replaces thymine in RNA? Uracil. What are the three main types of RNA? * mRNA (messenger RNA): Carries genetic instructions from DNA to the ribosome. * tRNA (transfer RNA): Brings amino acids to the ribosome. * rRNA (ribosomal RNA): Makes up part of the ribosome and helps build proteins. 3. DNA replication What is DNA replication? DNA replication is the process of making an identical copy of DNA before a cell divides. Why is DNA replication important? It ensures that each new cell receives a copy of the genetic information. What does semiconservative replication mean? Each new DNA molecule contains one original strand and one newly made strand. What enzyme unzips DNA? Helicase. What enzyme adds new DNA nucleotides? DNA polymerase. What enzyme connects DNA fragments on the lagging strand? DNA ligase. What is the leading strand? The strand that is copied continuously in the direction of the replication fork. What is the lagging strand? The strand that is copied in short sections called Okazaki fragments. What are Okazaki fragments? Short pieces of newly made DNA that form on the lagging strand. What is the job of DNA ligase? It joins the Okazaki fragments together. What are telomeres? Protective sections of DNA found at the ends of chromosomes. What is the purpose of telomeres? They help protect important genetic information from being lost when DNA is copied. What is DNA repair? The process cells use to identify and correct mistakes or damage in DNA. 4. Transcription What is transcription? Transcription is the process of copying genetic information from DNA into mRNA. Where does transcription happen in eukaryotic cells? In the nucleus. What enzyme helps make RNA during transcription? RNA polymerase. What is the purpose of transcription? To create an mRNA copy of a gene that can be used to make a protein. What are the RNA base-pairing rules? * DNA A pairs with RNA U. * DNA T pairs with RNA A. * DNA C pairs with RNA G. * DNA G pairs with RNA C. Example: DNA: A T C G RNA: U A G C What happens to mRNA before it leaves the nucleus in eukaryotic cells? It undergoes RNA processing. What are introns? Sections of RNA that are removed during RNA processing. What are exons? Sections that remain and are joined together to form mature mRNA. What is RNA splicing? The removal of introns and joining of exons. 5. Translation What is translation? Translation is the process of using mRNA instructions to build a protein. Where does translation happen? At the ribosomes in the cytoplasm or on the rough endoplasmic reticulum. What is a codon? A group of three mRNA bases that codes for an amino acid or a stop signal. What is an anticodon? A group of three bases on tRNA that pairs with a matching mRNA codon. What is the role of tRNA? It carries amino acids to the ribosome. What is the role of the ribosome? It reads mRNA and connects amino acids to build a protein. What is the start codon? AUG. What amino acid does AUG code for? Methionine. What are the three stop codons? * UAA * UAG * UGA What happens when a stop codon is reached? Translation ends, and the completed protein is released. 6. Gene expression and regulation What is gene expression? Gene expression is the process of using information from a gene to make a functional product, such as a protein. What is gene regulation? Gene regulation controls when, where, and how much a gene is expressed. Why is gene regulation important? It allows cells to perform different functions even though many cells contain the same DNA. What is an operon? A group of genes controlled together, commonly found in bacteria. What is the lac operon? A group of bacterial genes involved in breaking down lactose. What happens when lactose is present? Lactose helps remove the repressor’s blockage, allowing the genes to be expressed. What happens when lactose is absent? The repressor binds to the operator and prevents the genes from being expressed. Unit 2: Evolution and Natural Selection 1. Understanding evolution What is evolution? Evolution is the change in inherited characteristics of a population over generations. Does an individual organism evolve during its lifetime? No. Populations evolve over generations. What is a population? A group of individuals of the same species living in the same area. What is a species? A group of organisms that can reproduce with one another and produce fertile offspring, under the biological species concept. What is natural selection? Natural selection is the process in which organisms with inherited traits that improve survival or reproduction tend to leave more offspring. Who is associated with the theory of evolution by natural selection? Charles Darwin. What is adaptation? An inherited characteristic that helps an organism survive or reproduce in its environment. What is biological fitness? An organism’s ability to survive and reproduce, measured by its contribution of offspring to the next generation. Does the strongest organism always have the highest fitness? No. Fitness depends on how well an organism’s inherited traits help it reproduce in its particular environment. 2. Natural selection What are the main requirements for natural selection? * Individuals in a population have variation. * Some variation is inherited. * Organisms produce more offspring than can survive. * Individuals with certain inherited traits reproduce more successfully. What happens to helpful inherited traits over generations? They may become more common in the population. Can natural selection create traits because organisms need them? No. Natural selection acts on existing inherited variation. It does not create a needed trait simply because an organism needs it. What is an example of natural selection? If insects vary in color and birds more easily spot one color, insects with the less visible color may survive and reproduce more often. Over generations, that color may become more common. 3. Population genetics What is an allele? An alternative version of a gene. What is a gene pool? All the alleles present in a population. What is allele frequency? The proportion of a particular allele in a population. What does it mean when allele frequencies change? The population is evolving. What is genetic variation? Differences in genetic information among individuals in a population. Why is genetic variation important? It provides the differences that natural selection can act on. 4. Mechanisms of evolution What are the five major mechanisms that can change allele frequencies? * Mutation * Gene flow * Genetic drift * Natural selection * Nonrandom mating can change genotype frequencies and, in some circumstances, influence allele frequencies indirectly through selection. What is mutation? A change in DNA sequence. How can mutations affect evolution? They can introduce new genetic variations and sometimes create new alleles. What is gene flow? The movement of alleles between populations when individuals or their reproductive cells move between them. What is genetic drift? A random change in allele frequencies, especially noticeable in small populations. What is the bottleneck effect? A type of genetic drift that happens when a population becomes much smaller due to a random event. What is the founder effect? A type of genetic drift that occurs when a small group separates from a larger population and starts a new population. What is the difference between natural selection and genetic drift? Natural selection is based on differences in reproductive success associated with inherited traits. Genetic drift changes allele frequencies randomly. 5. Hardy-Weinberg equilibrium What is Hardy-Weinberg equilibrium? A model that describes a population that is not evolving with respect to the gene being studied. What are the five Hardy-Weinberg conditions? * No mutations * Random mating * No natural selection * Very large population * No gene flow What is the Hardy-Weinberg equation? p+q=1 What does p represent? The frequency of one allele. What does q represent? The frequency of the other allele. What is the genotype frequency equation? p^2+2pq+q^2=1 What does each part represent? * : Homozygous dominant * : Heterozygous * : Homozygous recessive What does homozygous mean? Having two identical alleles for a gene. What does heterozygous mean? Having two different alleles for a gene. Practice question: If q = 0.4, what is p? Answer: p=1-0.4=0.6 Practice question: If p = 0.6 and q = 0.4, what is the frequency of homozygous dominant individuals? Answer: p^2=0.6^2=0.36 Practice question: If p = 0.6 and q = 0.4, what is the frequency of heterozygous individuals? Answer: 2pq=2(0.6)(0.4)=0.48 Practice question: If p = 0.6 and q = 0.4, what is the frequency of homozygous recessive individuals? Answer: q^2=0.4^2=0.16 6. Evidence for evolution What are some forms of evidence for evolution? * Fossil records * Comparative anatomy * Molecular similarities * Embryology * Biogeography What are fossils? Preserved remains or traces of organisms that lived in the past. What is homologous anatomy? Similar body structures inherited from a common ancestor, even if they serve different functions. What is an example of homologous structures? The forelimbs of humans, whales, bats, and cats. What is analogous anatomy? Structures that perform similar functions but evolved independently and do not come from the same ancestral structure. What is an example of analogous structures? The wings of birds and insects. What is biogeography? The study of where organisms live and how their geographic distribution relates to evolution. How can DNA provide evidence for evolution? Organisms with more similar DNA sequences often share a more recent common ancestor. 7. Speciation What is speciation? The formation of new species. What is reproductive isolation? When populations can no longer successfully reproduce with one another. What is geographic isolation? When physical barriers separate populations, such as mountains, rivers, or oceans. What is allopatric speciation? Speciation that occurs when populations are geographically separated. What is sympatric speciation? Speciation that occurs without geographic separation. Unit 3: Classification, Taxonomy, and Phylogeny 1. Classification What is taxonomy? The science of naming and classifying organisms. What is systematics? The study of biological diversity and evolutionary relationships. What is binomial nomenclature? The two-part scientific naming system for organisms. What are the two parts of a scientific name? Genus and species. How should scientific names be written? The genus is capitalized, the species name is lowercase, and both are italicized. Example: Homo sapiens. What are the main taxonomic levels from broadest to most specific? * Domain * Kingdom * Phylum * Class * Order * Family * Genus * Species What are the three domains of life? * Bacteria * Archaea * Eukarya 2. Phylogenetic trees What is a phylogenetic tree? A diagram showing evolutionary relationships among organisms. What does a branch point represent? A common ancestor where evolutionary lineages split. What is a common ancestor? An ancestral organism or population from which two or more groups evolved. What are sister taxa? Two groups that share an immediate common ancestor. What does a node represent on a phylogenetic tree? A branching point representing a common ancestor. Does being next to another organism on a tree always mean they are closely related? No. Relationships are determined by shared branch points, not simply by how close the names appear. What is a clade? An ancestor and all of its descendants. What is a derived trait? A trait that evolved in a particular lineage and can help identify relationships among organisms. Unit 4: Prokaryotes, Eukaryotes, Bacteria, and Archaea 1. Cell types What are prokaryotic cells? Cells that do not have a nucleus or membrane-bound organelles. What are eukaryotic cells? Cells that have a nucleus and membrane-bound organelles. What organisms are prokaryotes? Bacteria and Archaea. What organisms are eukaryotes? Animals, plants, fungi, and protists. What is the main difference between prokaryotic and eukaryotic cells? Eukaryotic cells have a nucleus and membrane-bound organelles. Prokaryotic cells do not. Where is DNA located in a prokaryotic cell? In a region called the nucleoid. What is the function of the cell membrane? It controls what enters and leaves the cell. What is the function of ribosomes? They make proteins. 2. Bacteria and Archaea What are bacteria? Single-celled prokaryotic organisms found in many environments. What are Archaea? Single-celled prokaryotic organisms that are genetically and chemically distinct from bacteria. What is binary fission? A form of asexual reproduction in which one cell divides into two cells. Do bacteria and archaea have a nucleus? No. What is a bacterial cell wall commonly made of? Peptidoglycan. What is peptidoglycan? A material that provides structure and support to bacterial cell walls. 3. Gram-positive and Gram-negative bacteria What are Gram-positive bacteria? Bacteria with a thick peptidoglycan cell wall that usually stain purple during Gram staining. What are Gram-negative bacteria? Bacteria with a thinner peptidoglycan layer and an outer membrane that usually stain pink or red during Gram staining. What is the major difference between Gram-positive and Gram-negative bacteria? Gram-positive bacteria have thick peptidoglycan walls, while Gram-negative bacteria have thin peptidoglycan walls and an outer membrane. 4. Endosymbiotic theory What is the endosymbiotic theory? The theory that mitochondria and chloroplasts originated from free-living bacteria that were taken into ancestral eukaryotic cells. What organelles are explained by endosymbiotic theory? Mitochondria and chloroplasts. What evidence supports endosymbiotic theory? * They contain their own DNA. * They have their own ribosomes. * They divide in a way similar to bacteria. * They have double membranes. What is the function of mitochondria? They produce most of the cell’s ATP through cellular respiration. What is the function of chloroplasts? They carry out photosynthesis in plants and some other organisms. 5. Protists and fungi What are protists? A diverse group of eukaryotic organisms that do not fit into the traditional plant, animal, or fungi kingdoms. Are all protists single-celled? No. Many are single-celled, but some are multicellular. What are fungi? Eukaryotic organisms that absorb nutrients from their surroundings. What is the cell wall of fungi made of? Chitin. What are examples of fungi? * Mushrooms * Molds * Yeasts How do fungi obtain nutrients? They release digestive enzymes into their surroundings and absorb the broken-down nutrients. What is the role of decomposers? They break down dead organisms and recycle nutrients into the environment. Unit 5: Plants 1. Plant characteristics What are the major characteristics of plants? Plants are multicellular eukaryotes that generally have chloroplasts, cellulose cell walls, and carry out photosynthesis. What is photosynthesis? The process of using light energy to convert carbon dioxide and water into sugars and oxygen. What is the function of chlorophyll? It absorbs light energy for photosynthesis. What is the function of roots? They absorb water and minerals and help anchor the plant. What is the function of stems? They support the plant and transport materials. What is the function of leaves? They are the main organs where photosynthesis occurs in most plants. 2. Alternation of generations What is alternation of generations? A plant life cycle that alternates between two multicellular stages: the haploid gametophyte and the diploid sporophyte. What is a gametophyte? The haploid stage that produces gametes. What is a sporophyte? The diploid stage that produces spores through meiosis. What does haploid mean? Having one set of chromosomes, represented by . What does diploid mean? Having two sets of chromosomes, represented by . What is fertilization? The joining of two gametes to form a diploid zygote. What is meiosis? A type of cell division that reduces the chromosome number by half and produces haploid cells. What is the difference between spores and gametes? Spores can develop into a new organism without fusing with another cell. Gametes must fuse during fertilization to form a zygote. 3. Major plant groups What are the major groups of plants? * Nonvascular plants * Seedless vascular plants * Gymnosperms * Angiosperms What are nonvascular plants? Plants that lack specialized vascular tissues for transporting water and nutrients. What are examples of nonvascular plants? Mosses and liverworts. What are vascular plants? Plants that have specialized tissues to transport water, minerals, and sugars. What are the two major vascular tissues? * Xylem * Phloem What is the function of xylem? It transports water and minerals from the roots toward the rest of the plant. What is the function of phloem? It transports sugars and other organic nutrients throughout the plant. What are seedless vascular plants? Vascular plants that reproduce using spores instead of seeds. What is an example of a seedless vascular plant? Ferns. What are gymnosperms? Seed-producing plants with seeds that are not enclosed within fruits. What is an example of a gymnosperm? Pine trees. What are angiosperms? Flowering plants that produce seeds enclosed within fruits. What is the main difference between gymnosperms and angiosperms? Gymnosperms have exposed seeds, while angiosperms produce seeds enclosed in fruits. 4. Plant reproduction What is pollination? The transfer of pollen from the male reproductive structure to the female reproductive structure of a plant. What is pollen? A structure that carries the male gametophyte in seed plants. What is the purpose of flowers? Flowers are reproductive structures of angiosperms. What develops into a fruit? The ovary of a flower. What develops into a seed? The ovule after fertilization. What is the purpose of seeds? They protect and provide resources for the developing plant embryo. Unit 6: Animals 1. Animal characteristics What are the major characteristics of animals? Animals are multicellular eukaryotes that obtain nutrients by consuming other organisms or organic material. They do not have cell walls. Are animals prokaryotic or eukaryotic? Eukaryotic. Are animals unicellular or multicellular? Multicellular. Are animals autotrophs or heterotrophs? Heterotrophs. What is a heterotroph? An organism that obtains energy and nutrients by consuming other organisms or organic material. 2. Animal body plans What is symmetry? The arrangement of body parts around an axis or center. What is asymmetry? A body shape that cannot be divided into matching halves. What is radial symmetry? A body arrangement in which body parts are organized around a central axis. What is an example of an animal with radial symmetry? A jellyfish. What is bilateral symmetry? A body arrangement that can be divided into approximately equal left and right halves. What is an example of an animal with bilateral symmetry? A human. What is cephalization? The concentration of sensory organs and nervous tissue toward the front or head region of an animal. What is a body cavity? A fluid-filled space within an animal’s body that can contain and protect internal organs. 3. Major animal groups What are sponges? Simple aquatic animals that lack true tissues and organs. What is the scientific phylum for sponges? Porifera. How do sponges obtain food? They filter small food particles from water flowing through their bodies. What are cnidarians? Aquatic animals with specialized stinging cells. What is the scientific phylum for cnidarians? Cnidaria. What are examples of cnidarians? * Jellyfish * Corals * Sea anemones What are cnidocytes? Specialized stinging cells used for capturing prey and defense. What are arthropods? Animals with segmented bodies, jointed appendages, and an external skeleton. What is an exoskeleton? A hard external structure that supports and protects an animal’s body. What are examples of arthropods? * Insects * Spiders * Crabs * Lobsters What is molting? The process of shedding an old exoskeleton so an arthropod can grow. What are the major animal groups covered in this section? * Porifera: Sponges * Cnidaria: Jellyfish, corals, and sea anemones * Arthropoda: Insects, spiders, and crustaceans Note: Your lecture material did not provide a complete list of characteristics for every animal phylum, so I have not added unsupported details to those sections. Unit 7: Biotechnology 1. Biotechnology basics What is biotechnology? The use of living organisms, cells, or biological processes to develop useful products and technologies. What is genetic engineering? The process of directly changing an organism’s DNA. What is recombinant DNA? DNA made by combining genetic material from different sources. What is a plasmid? A small circular DNA molecule commonly found in bacteria. Why are plasmids useful in biotechnology? They can be used to carry selected genes into cells. 2. PCR What does PCR stand for? Polymerase chain reaction. What is PCR used for? To make many copies of a specific DNA segment. What are the three main stages of PCR? * Denaturation * Annealing * Extension What happens during denaturation? The DNA strands separate. What happens during annealing? Primers attach to complementary DNA sequences. What happens during extension? DNA polymerase adds nucleotides to build new DNA strands. 3. Gel electrophoresis What is gel electrophoresis? A laboratory technique used to separate DNA fragments based on size. How does gel electrophoresis separate DNA? An electric current moves DNA fragments through a gel. Smaller fragments generally travel farther than larger fragments. Why does DNA move toward the positive end of the gel? DNA has a negatively charged phosphate backbone. What can gel electrophoresis help scientists do? Compare DNA fragments and examine DNA samples. 4. Restriction enzymes and cloning What are restriction enzymes? Enzymes that cut DNA at specific sequences. What is DNA cloning? The process of making copies of a DNA segment or gene. What is a GMO? A genetically modified organism whose genetic material has been altered using genetic engineering or other genetic modification methods. What is a transgenic organism? An organism that contains genetic material introduced from another species. What is CRISPR? A gene-editing technology that allows scientists to make targeted changes to DNA. What is gene therapy? A medical approach that aims to treat or prevent disease by changing genetic material in a person’s cells. What is genomics? The study of an organism’s entire genome. What is proteomics? The study of the proteins produced by a cell, tissue, or organism. Practice Questions: Multiple Choice The answer is immediately underneath each question. Try answering before reading it. 1. What is the basic building block of DNA? A. Amino acid B. Nucleotide C. Protein D. Lipid Answer: B. Nucleotide 2. Which base pairs with adenine in DNA? A. Guanine B. Cytosine C. Thymine D. Uracil Answer: C. Thymine 3. Which enzyme separates DNA strands during replication? A. Ligase B. Helicase C. RNA polymerase D. Ribosome Answer: B. Helicase 4. What is the purpose of DNA replication? A. To create proteins B. To make RNA C. To copy DNA before cell division D. To destroy old DNA Answer: C. To copy DNA before cell division 5. What is the process of making mRNA from DNA called? A. Translation B. Transcription C. Replication D. Mutation Answer: B. Transcription 6. Where does translation occur? A. Nucleus B. Ribosome C. Cell membrane D. Golgi apparatus Answer: B. Ribosome 7. What does tRNA carry? A. DNA B. Glucose C. Amino acids D. Lipids Answer: C. Amino acids 8. What is the start codon? A. UAA B. AUG C. UGA D. UAG Answer: B. AUG 9. What is evolution? A. An individual changing during its lifetime B. A population changing genetically over generations C. An organism growing larger D. A cell dividing Answer: B. A population changing genetically over generations 10. Who is associated with evolution by natural selection? A. Gregor Mendel B. Charles Darwin C. Louis Pasteur D. Robert Hooke Answer: B. Charles Darwin 11. What is genetic drift? A. A random change in allele frequencies B. The movement of water C. The creation of proteins D. The copying of DNA Answer: A. A random change in allele frequencies 12. What is gene flow? A. DNA replication B. Movement of alleles between populations C. Protein synthesis D. Natural death Answer: B. Movement of alleles between populations 13. Which equation represents Hardy-Weinberg allele frequencies? A. B. C. D. Answer: B. 14. What are the three domains of life? A. Plants, animals, fungi B. Bacteria, Archaea, Eukarya C. Mammals, reptiles, birds D. Protists, fungi, plants Answer: B. Bacteria, Archaea, Eukarya 15. Which cells do not have a nucleus? A. Eukaryotic B. Prokaryotic C. Animal D. Plant Answer: B. Prokaryotic 16. What is the function of mitochondria? A. Protein storage B. ATP production C. DNA protection D. Photosynthesis Answer: B. ATP production 17. What is the cell wall of fungi made of? A. Cellulose B. Peptidoglycan C. Chitin D. Starch Answer: C. Chitin 18. What tissue transports water in plants? A. Phloem B. Xylem C. Epidermis D. Pollen Answer: B. Xylem 19. What is the function of phloem? A. Transport sugars B. Absorb sunlight C. Produce pollen D. Protect seeds Answer: A. Transport sugars 20. Which plants produce flowers? A. Mosses B. Ferns C. Gymnosperms D. Angiosperms Answer: D. Angiosperms 21. What is the scientific phylum for sponges? A. Cnidaria B. Porifera C. Arthropoda D. Chordata Answer: B. Porifera 22. What do arthropods have? A. Jointed appendages and an exoskeleton B. No body structure C. Only soft bodies D. Chloroplasts Answer: A. Jointed appendages and an exoskeleton 23. What is PCR used for? A. Separating proteins B. Copying DNA C. Producing ATP D. Growing plants Answer: B. Copying DNA 24. What does gel electrophoresis separate DNA by? A. Color B. Shape only C. Fragment size D. Temperature Answer: C. Fragment size 25. What is CRISPR used for? A. Editing DNA B. Separating cells C. Making ATP D. Producing pollen Answer: A. Editing DNA Fill-in-the-Blank Practice 1. DNA stands for __________. Answer: Deoxyribonucleic acid. 2. RNA uses __________ instead of thymine. Answer: Uracil. 3. The enzyme that unzips DNA is __________. Answer: Helicase. 4. The enzyme that connects Okazaki fragments is __________. Answer: DNA ligase. 5. The process of making RNA from DNA is called __________. Answer: Transcription. 6. The process of making proteins from mRNA is called __________. Answer: Translation. 7. A group of three mRNA bases is called a __________. Answer: Codon. 8. The movement of alleles between populations is called __________. Answer: Gene flow. 9. Random changes in allele frequencies are called __________. Answer: Genetic drift. 10. The formation of new species is called __________. Answer: Speciation. 11. The three domains are Bacteria, Archaea, and __________. Answer: Eukarya. 12. The cell wall of fungi contains __________. Answer: Chitin. 13. The plant tissue that transports water is __________. Answer: Xylem. 14. The plant tissue that transports sugars is __________. Answer: Phloem. 15. Flowering plants are called __________. Answer: Angiosperms. 16. The haploid plant stage is called the __________. Answer: Gametophyte. 17. The diploid plant stage is called the __________. Answer: Sporophyte. 18. Sponges belong to the phylum __________. Answer: Porifera. 19. Jellyfish belong to the phylum __________. Answer: Cnidaria. 20. The process used to make many copies of DNA is called __________. Answer: PCR. Important Terms to Memorize Term Meaning DNA Stores genetic information RNA Helps make proteins Nucleotide Building block of DNA and RNA Helicase Separates DNA strands DNA polymerase Builds new DNA DNA ligase Connects DNA fragments Transcription DNA to RNA Translation RNA to protein Codon Three mRNA bases Mutation Change in DNA Evolution Change in inherited traits in a population over generations Natural selection Differences in reproductive success based on inherited traits Genetic drift Random allele frequency change Gene flow Movement of alleles between populations Speciation Formation of new species Taxonomy Naming and classifying organisms Phylogeny Evolutionary relationships Prokaryote Cell without a nucleus Eukaryote Cell with a nucleus Mitochondria ATP production Chloroplast Photosynthesis Xylem Transports water Phloem Transports sugars Gametophyte Haploid plant generation Sporophyte Diploid plant generation Angiosperm Flowering plant Gymnosperm Plant with exposed seeds PCR Makes copies of DNA Gel electrophoresis Separates DNA fragments by size CRISPR Gene-editing technology Final Cram Sheet: What You Should Know Before Your Exam DNA and genetics * DNA: A–T and C–G * RNA: A–U and C–G * Helicase: unzips DNA * DNA polymerase: builds DNA * Ligase: joins DNA fragments * Transcription: DNA → RNA * Translation: RNA → protein * AUG: start codon * UAA, UAG, UGA: stop codons Evolution * Darwin: natural selection * Mutation: changes DNA * Genetic drift: random change * Gene flow: movement between populations * Bottleneck: population becomes much smaller * Founder effect: small group starts a population * Speciation: new species form * Hardy-Weinberg: , Classification and cells * Three domains: Bacteria, Archaea, Eukarya * Prokaryotes: no nucleus * Eukaryotes: have a nucleus * Mitochondria: ATP * Chloroplasts: photosynthesis * Fungi: chitin cell walls * Bacteria: peptidoglycan cell walls Plants * Xylem: water * Phloem: sugar * Gametophyte: haploid * Sporophyte: diploid * Gymnosperms: exposed seeds * Angiosperms: flowers and enclosed seeds * Mosses: nonvascular * Ferns: seedless vascular Animals and biotechnology * Porifera: sponges * Cnidaria: jellyfish, corals, sea anemones * Arthropoda: jointed appendages and exoskeleton * PCR: copies DNA * Gel electrophoresis: separates DNA by size * Restriction enzymes: cut DNA * CRISPR: edits DNA Study tip: Cover the answers with a piece of paper and try to answer every question from memory. Then uncover the answer and check yourself. Focus especially on DNA replication, transcription versus translation, Hardy-Weinberg equations, evolution mechanisms, plant life cycles, and the differences between prokaryotic and eukaryotic cells.
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# Neuro Exam Essentials Only what your instructor said to know: lectures, live class, slides, and the assigned book pages (with the "do not read" parts left out). Read in book = a part your instructor told you to read in the textbook. How to use this ## One tab. One chunk. Then flip cards. - Read the colored **60-second box** first. That's the big idea. - Open **one** chunk at a time. Close it when done (it'll say ✓ seen). - Do the **tap-to-flip cards**, then the **quiz**. - Hit **Mark done** at the bottom. Take a break between tabs. **Your instructor's study advice:** the nursing care **overlaps** across all these diseases. Eye problem → protect the eye. Can't swallow → nutrition support (weights, calorie counts, prealbumin). Weak or stiff → mobility and fall prevention. **Don't memorize slide by slide. Understand the idea.** But do notice how brain, spinal cord, and peripheral nerve problems look different. The nervous system map Think of a house. The brain is the electrical panel. The spinal cord is the main cable running down the wall. Peripheral nerves are the wires going out to every room. | Central (CNS) | Peripheral (PNS) | | --- | --- | | Brain + spinal cord | Spinal nerves (from the spine) · **12 cranial nerves** (from the brain) · autonomic system | **Autonomic system** = automatic, not under your control: - **Sympathetic** = "fight or flight." Speeds things up (heart rate, breathing). - **Parasympathetic** = "rest and digest." Slows things down. Word bank (terms that show up everywhere) | Word | Plain meaning | | --- | --- | | **intracranial pressure (ICP)** | Intracranial pressure: pressure inside the skull | | **level of consciousness (LOC)** | Level of consciousness: how awake and aware | | **Glasgow Coma Scale (GCS)** | Glasgow Coma Scale: scores LOC from 3 (no response) to 15 (normal) | | **Aura** | A warning sign right before a migraine or seizure | | **Dysphagia** | Trouble swallowing → aspiration risk | | **Dysarthria** | Trouble speaking clearly (slurred) | | **Diplopia** | Double vision | | **Nystagmus** | Eyes jerk side to side on their own | | **Ptosis** | Drooping eyelid | | **Photophobia** / **phonophobia** | Light hurts / sound hurts | | **Paresthesia** | Numbness or tingling | | **Acetylcholine (ACh)** | The "go" chemical that makes muscles move | | **Dopamine** | The "brake" chemical that smooths movement (also pleasure) | Your instructor's 15 neuro terms have their own tab: **Terms**. Review class: exam breakdown + how to study Review class From the in-class exam review (Joline case study + NCLEX questions). | Exam section | Points | | --- | --- | | Peripheral nervous system (PNS) | 28 | | Trauma: stroke, head injury, intracranial pressure (ICP) | 32 | | Renal: acute and chronic kidney disease (lecture recordings) | 18 | | Michelle's content (use her posted study guide) | 10 | | **Total** | **90** · about 1 hr 35 min. Don't rush. | - You only need what she **did not cross off** in the book + what's in the **lecture recordings** and **PowerPoint**. Some lecture content isn't in the book. That's okay, it still counts. - Use the **outline in the syllabus** as quiz questions. - Studying alone? **Record yourself answering out loud** on your phone, then play it back next to your notes. Saying it out loud moves it to long-term memory. - On her big day-one med chart, write **only the "exception to the rule"** facts. Those are what get tested. - Stuck? **Email her** instead of going down a YouTube rabbit hole. Quick recall · tap to flip The 60-second version ## 15 words. Break them into pieces and they explain themselves. - **a-** = without · **dys-** = hard or bad · **hemi-** = half (one side) - **-plegia** = paralyzed (can't move) · **-paresis** = weak (can move a little) - **-phasia** = speech/language · **-lexia** = reading · **-graphia** = writing - **-opia / -opsia** = vision · **gnosia** = knowing/recognizing · **praxia** = doing From your instructor's "Neurology – Medical Terminology" list Talking, reading & writing (4) ### 1. Aphasia **Word parts:** a- (without) + phasia (speech) **Means:** trouble with **language**. The brain can't make or understand words. The brain's dictionary is broken. The mouth works fine; the words don't come out right, or what you hear makes no sense. **Example:** a stroke patient wants water but says "chair," or can't understand "squeeze my hand." **3 types:** **Expressive (Broca)** = understands, can't speak · **Receptive (Wernicke)** = can't understand · **Global (mixed)** = both. ### 2. Dysarthria **Word parts:** dys- (hard) + arthr (joint/articulate) **Means:** **slurred speech** because the mouth, tongue, or face muscles are weak. The words are right, but the mouth is clumsy, like talking after a dentist numbs you. **Example:** the patient knows exactly what to say, but it sounds mumbled. **Don't mix up:** **Aphasia = a word problem** (brain's language center). **Dysarthria = a muscle problem** (words are right, just slurred). ### 3. Alexia **Word parts:** a- (without) + lexia (reading) **Means:** **can't read**, even though they could before and their eyes work. **Example:** the patient looks at a menu but the letters mean nothing. ### 5. Agraphia **Word parts:** a- (without) + graphia (writing) **Means:** **can't write**, even though the hand can hold the pen. **Example:** asked to sign a consent form, they can't form the letters of their name. Eyes & vision (4) ### 4. Papilledema (choked disc) **Word parts:** papilla (optic disc) + edema (swelling) **Means:** the **optic disc** (where the eye nerve connects, at the back of the eye) is **swollen**. The provider sees it with an ophthalmoscope. Pressure in the skull pushes on the eye nerve and "chokes" it, like a garden hose swelling when the water can't get out. **Key point:** papilledema = **always a sign of ↑intracranial pressure (ICP)**. ### 9. Nystagmus **Means:** the eyes **jerk or bounce side to side** (or up and down) on their own. Like the eyes are watching a fast tennis match that isn't there. **Seen in:** multiple sclerosis (MS), meningitis, stroke, brainstem problems. ### 12. Ptosis **Means:** a **drooping upper eyelid**. Ptosis sounds like "toe-sis": the lid falls down toward your toes. **Seen in:** myasthenia gravis, uncal herniation (CN III), stroke. ### 13. Diplopia **Word parts:** dipl (double) + opia (vision) **Means:** **double vision**. Sees two of everything. **Nursing:** eye patch, switched between eyes every few hours. ### 14. Homonymous hemianopsia **Word parts:** homonymous (same) + hemi (half) + an (without) + opsia (vision) **Means:** blind in the **same half** of the vision field **in both eyes**. For example, they can't see anything to their left. Like someone put tape over the left half of both lenses of their glasses. **Nursing:** teach to **turn the head side to side (scan)**. Put food and items on the side they can see. They may eat only half the plate. Movement & coordination (5) ### 7. Hemiparesis **Word parts:** hemi (half/one side) + paresis (weakness) **Means:** **weakness** on one side of the body. They can still move it, just not strongly. **Example:** weak right hand grip and right leg after a left-brain stroke. ### 15. Hemiplegia **Word parts:** hemi (one side) + plegia (paralysis) **Means:** **paralysis** on one side of the body. Can't move it at all. **Memory trick:** **Paresis = Partial** (weak). **Plegia = Paralyzed** (can't move). Both are on the side **opposite** the brain injury. ### 8. Apraxia **Word parts:** a- (without) + praxia (doing/action) **Means:** can't do **learned, planned movements**, even though the muscles are strong and they understand the request. The muscles work, but the brain lost the "instructions" for the task. **Example:** handed a toothbrush, they don't know the steps to brush their teeth. **Nursing:** simple, short, one-step directions; be patient. ### 10. Ataxia **Word parts:** a- (without) + taxia (order/coordination) **Means:** **poor coordination and balance**. Wobbly, unsteady walking; clumsy movements. Walking like you're on a moving boat. **Nursing:** **fall precautions**. ### 6. Proprioception **Means:** your body's sense of **where its parts are** without looking (body position sense). It's how you can touch your nose with your eyes closed. **If lost:** the patient doesn't know where their arm or foot is → falls, injuries. Watch the affected limb. Recognizing things (1) ### 11. Agnosia **Word parts:** a- (without) + gnosia (knowing) **Means:** can't **recognize** familiar objects, people, or sounds, even though their senses work. The eyes see a fork, but the brain can't name it or tell what it's for. **Nursing:** safety. They might misuse objects. **The "A" trio:** **Apraxia** = can't **do** (action) · **Agnosia** = can't **know** (recognize) · **Ataxia** = can't **coordinate** (wobbly). All 15 at a glance | # | Term | Simple meaning | | --- | --- | --- | | 1 | **Aphasia** | Trouble with language (words) | | 2 | **Dysarthria** | Slurred speech (weak mouth muscles) | | 3 | **Alexia** | Can't read | | 4 | **Papilledema** | Swollen optic disc = ↑intracranial pressure (ICP) | | 5 | **Agraphia** | Can't write | | 6 | **Proprioception** | Sense of where your body is | | 7 | **Hemiparesis** | One-sided weakness | | 8 | **Apraxia** | Can't do learned movements | | 9 | **Nystagmus** | Jerky, bouncing eyes | | 10 | **Ataxia** | Poor coordination/balance | | 11 | **Agnosia** | Can't recognize things | | 12 | **Ptosis** | Droopy eyelid | | 13 | **Diplopia** | Double vision | | 14 | **Homonymous hemianopsia** | Blind in the same half of both eyes | | 15 | **Hemiplegia** | One-sided paralysis | Flashcards · tap to flip Practice A client clearly says "I want my glasses," but the words are mumbled and hard to understand. This is: The right words, but slurred = a muscle problem = dysarthria. Practice A client eats only the food on the right side of the plate. The nurse suspects: They can't see the left half of their field. Teach head scanning; turn the plate. Practice A client holds a comb but can't figure out how to use it, even though the arm is strong. This is: Strong muscles, lost "how-to" for a learned task = apraxia. Practice The provider documents papilledema. The nurse knows this means: A swollen optic disc is always a sign of ↑ICP. Practice A client after a stroke can lift the right arm a little but it's weak. Correct term? Paresis = partial (weak). Plegia = paralyzed. Practice A client walks with a wide, wobbly gait and loses balance. Priority nursing action? Ataxia = poor coordination → fall risk. The 60-second version ## Stroke = a "brain attack." Time is brain. - **transient ischemic attack (TIA)** = mini warning stroke; symptoms gone in 30–60 min. Prevent the real one. - **\~90% are ischemic** (clot). The rest are **hemorrhagic** (bleed). - **computed tomography (CT) head WITHOUT contrast first**, to rule out a bleed. - **tissue plasminogen activator (tPA) (alteplase)** within **3 to 4.5 hrs** of when symptoms started, only for ischemic. - First sign of trouble (↑intracranial pressure (ICP)) = **change in mental status**. A stroke is a heart attack of the brain. Ischemic = a clogged pipe (no blood gets through). Hemorrhagic = a burst pipe (blood leaks where it shouldn't). The treatment for one is dangerous for the other, which is why the computed tomography (CT) comes first. transient ischemic attack (TIA): the warning sign - Brief drop in blood flow to the brain → **temporary** stroke-like symptoms. - Usually gone in **30–60 minutes**, often before reaching the emergency room (ER). Many people never go. - Symptoms are **one-sided**: numbness or weakness of face/arm, blurred or double vision, slurred speech, trouble swallowing. - It's a **red flag**: high risk of an ischemic stroke soon. **Prevention is the key intervention:** - #1 risk factor = **hypertension**. Control blood pressure (BP). - **Diabetes**: keep glucose in range. Exercise, healthy food. - **Antiplatelets**: **aspirin** and **clopidogrel**. Both together = **dual antiplatelet therapy** (same as after a myocardial infarction (MI)). **Don't mix up the classes:** **Antiplatelets** = aspirin, clopidogrel (stop platelets sticking). **Anticoagulants** = heparin, warfarin, direct oral anticoagulants (DOACs) like apixaban, rivaroxaban, dabigatran. Ischemic vs. hemorrhagic Blood flow cut off for more than a few minutes → brain cells starve of oxygen → **brain infarction** (like a myocardial infarction (MI), but in the brain). | Type | Cause | Onset | | --- | --- | --- | | **Thrombotic** (ischemic) | Clot builds slowly from **atherosclerosis**, often where arteries split (carotids, circle of Willis) | **Slow/gradual**: symptoms come and go, or slowly worsen. Body grows **collateral circulation**. | | **Embolic** (ischemic) | Clot travels, usually from the **left side of the heart**. Big risk: **A-fib**, valve disease | **Sudden**; often improves quickly too | | **Hemorrhagic** | Vessel breaks: **severe hypertension (HTN)** (incl. **cocaine**), ruptured **aneurysm**, or an ischemic stroke that turned into a bleed | Sudden or slow (depends on the bleed) | Right-heart clot → lungs (PE). Left-heart clot → brain (stroke). Left vs. right brain stroke The brain controls the **opposite** side of the body. Left brain stroke → **right** side weak. Right brain stroke → **left** side weak. | Left hemisphere (dominant) | Right hemisphere | | --- | --- | | Language, math, analytical thinking | Visual and spatial awareness | | Trouble **understanding and using language** (aphasia) | **Unilateral neglect**: ignores the left side of the body | | **Slow, cautious**; anxious with new tasks | **Impulsive**, poor judgment, unaware of deficits, denial | | Depressed, guilty, quickly angry and frustrated (they know something's wrong) | Memory loss, disoriented | | Right-side weakness | Left-side weakness · top priority: **risk for injury** | Brain-area map slide: your instructor said **do not memorize it**. BE FAST: teach the public B**Balance**: loss of balance or coordination, dizzy E**Eyes**: blurred or double vision F**Face**: smile. One side drooping? A**Arms**: raise both. One weak or drifting down? S**Speech**: repeat "You can't teach an old dog new tricks." Slurred? Garbled? T**Time**: call **911** right away. Note the **exact time symptoms started**. **Why call 911 instead of driving?** The ambulance **calls ahead**: computed tomography (CT) room ready, stroke scale started, tissue plasminogen activator (tPA) prepared, oxygen and glucose checked. In the emergency room (ER): assessment & computed tomography (CT) - Priority = get them to a **stroke center**. Not the time for a full head-to-toe. - **airway, breathing, circulation (ABCs) first**, then a rapid neuro (stroke) assessment. - **National Institutes of Health (NIH) Stroke Scale**: trained, certified staff; checks level of consciousness (LOC), movement, feeling, speech, understanding. Broader than BE FAST. **Don't memorize its parts**; just know it's a valid, reliable, evidence-based tool for consistent tracking. **CT of the head WITHOUT contrast** (or magnetic resonance imaging (MRI)) is one of the first tests. Why no contrast? Contrast would look like a bleed. CT shows a **hemorrhage**, sets a **baseline**, rules out tumors. An ischemic stroke often **doesn't show for 24 hrs**, so a negative CT doesn't rule it out. tissue plasminogen activator (tPA) (alteplase): clot buster - For **ischemic only**. **Never** for hemorrhagic. - Must start within **3 hours** of symptom onset (often extended to **4.5 hrs**). Counted from when symptoms **started at home**, not emergency room (ER) arrival. You don't need the extension criteria. - Not everyone qualifies: check bleeding risk. **Before you hang tPA:** make sure the **head computed tomography (CT) is done** and shows no bleed. Not ordered? Get it ordered. - Big risk = **bleeding** → bleeding precautions. - Keep blood pressure (BP) controlled so ischemic doesn't turn hemorrhagic. - **Repeat CT** after the infusion to check for a new bleed. **Other procedures (know the name and idea only):** - **Intra-arterial thrombolysis**: tPA put directly into the clot; up to **6 hrs**. - **Endovascular thrombectomy**: catheter pulls the clot out. - **Prevent future strokes:** angioplasty with **stent** (filter catches pieces) or **carotid endarterectomy** (neck incision to remove plaque). **After any of these:** check the site for bleeding, vital signs, **neuro checks** (new stroke from loose clots?), **hoarseness and trouble swallowing** (nerves in the neck, like the vagus), and **cerebral hyperperfusion** (a rush of blood into an area used to low flow → can bleed). Signs to assess - **Cognition**: restless, confused, memory, focus. level of consciousness (LOC) drop = late. - **Motor**: hand grips, push/pull feet. Equal both sides? - **Flaccid** paralysis = limp, can't beat gravity (e.g., **foot drop**). **Spastic** = constant contraction → **contractures**. - **Sensory**: touch, pain, numbness, neglect. - **Eyes**: pupils equal, round, reactive to light and accommodation (PERRLA) *plus* the whole visual field (lost side vision?). - **Heart**: usually hypertensive; **murmur** (clot on a valve?); **rhythm** (A-fib). - Psychosocial: personality and emotion changes. Nursing priorities (acute stroke) 1. **Oxygen first.** oxygen saturation (SpO₂) under 94%? Think: **partial airway obstruction** (tongue), **hypoventilation**, **aspiration** (most common). 2. **intravenous (IV)** (emergency meds; they may not swallow). 3. **Cardiac monitor** (A-fib). 4. **nothing by mouth (NPO) until a swallow screen.** The registered nurse (RN) does the bedside screen. Coughing, pocketing food, slurred speech → **speech therapy** consult. 5. **Glucose under 140** (high sugar blocks reperfusion). 6. **blood pressure (BP) slightly high** to push blood to the brain. Book guideline **≤150 systolic**, but follow the patient's own orders and baseline. 7. Watch for **↑intracranial pressure (ICP)**. Neuro checks **every 15–30 min** acutely; BP at least every 15 min. **Never skip pupils.** **Patient declining 24 hrs after a stroke** (more lethargic, vitals changed, sluggish pupils)? **Call Rapid Response** and the provider. Expect a computed tomography (CT). - Most likely complication = **↑ICP** (→ seizures, respiratory failure, ↓level of consciousness (LOC)). - Don't take BP on the **affected arm**: inaccurate (less vascular tone). Aspirin & stroke core measures **Why no aspirin right away (unlike a myocardial infarction (MI))?** Could be a **bleed**, may be getting **tissue plasminogen activator (tPA)**, may have **dysphagia**. Giving it early doesn't improve stroke outcomes. - Give aspirin **325 mg within 24–48 hrs** after onset. - **No aspirin within 24 hrs of tPA.** **Core measures** (hospital must do + document to get paid): 1. **tPA** if they qualify (3–4.5 hrs). 2. **venous thromboembolism (VTE) prevention**: sequential compression devices (SCDs), enoxaparin/heparin, walking. 3. By end of **day 2**: **antiplatelet** or **anticoagulant** (A-fib/flutter → anticoagulant). Discharged on it. 4. Discharged on a **statin** (cholesterol med). 5. **Stroke education** documented (signs, 911, meds). 6. **physical therapy (PT)/occupational therapy (OT) rehab** assessment. Tests & swallow nerves (Mr. Stokes case) | Test | Why | | --- | --- | | Non-contrast computed tomography (CT) head | Rule out bleed, baseline, rule out tumor | | Cardiac monitor | A-fib (with rapid ventricular response (RVR)) | | **Echocardiogram** | Shows **heart valves** (clots?) and ejection fraction | | **Carotid ultrasound** | **% of plaque** blocking the carotids | | Swallow study | Diet texture (thickened liquids, pudding, no water) | **The 2 cranial nerves you MUST know:** **cranial nerve (CN) IX (glossopharyngeal)** and **CN X (vagus)**, the swallowing nerves. They must be intact before the patient eats or drinks. "If you don't know, pick vagus." **Delegation tip** from class: licensed practical nurse (LPN) can give **routine injections** (like insulin). Hygiene → **unlicensed assistive personnel (UAP)**. NCLEX wants you to use each person's role wisely. Hemorrhagic stroke treatment Goal: **stop the bleeding** and **lower pressure on the brain**. - Stop any meds that cause bleeding; may need blood products. - Anti-seizure meds (a seizure raises intracranial pressure (ICP)). - **Bed rest** and supportive care so the body can absorb the blood. Don't push them up to the chair. **Surgery:** - **Aneurysm** → **coiling** (coils fill the bulge) or **clipping** (clip at its base). - **arteriovenous malformation (AVM)** (arteriovenous malformation: tangled weak vessels, often in kids) → surgically removed. Read in book Iggy Ch. 38, pp. 941–955 · skipped per your list: National Institutes of Health Stroke Scale (NIHSS) table, Box 38.3, alteplase dosing, calcium channel blocker paragraph transient ischemic attack (TIA) workup (book)Read in book - Symptoms usually resolve in **30–60 min** but can last up to **24 hrs**. - Box 38.2 signs: blurred/double vision, tunnel vision, one-eye blindness; arm/leg weakness, **ataxia**; numbness, **vertigo**; aphasia, dysarthria. - Workup: National Institutes of Health Stroke Scale (NIHSS), labs (**prothrombin time (PT), international normalized ratio (INR), activated partial thromboplastin time (aPTT)**, lipids), electrocardiogram (ECG), **head computed tomography (CT)** then magnetic resonance imaging (MRI), computed tomography angiography (CTA)/magnetic resonance angiography (MRA) of brain and neck. - Common causes: **carotid stenosis** (narrowed artery from plaque) and **A-fib**. - **ABCD2 score** predicts stroke risk: **A**ge ≥60 · **B**P ≥140/90 · **C**linical signs (one-sided weakness, speech) · **D**uration · **D**iabetes. - Treatment: carotid endarterectomy or stent, **aspirin/clopidogrel**, lower blood pressure (BP). Stroke types & risk (book)Read in book Brain can't store oxygen or glucose. Blood flow cut for **a few minutes** → infarction. "Brain attack" = treat like a myocardial infarction (MI). | | Thrombotic | Embolic | Hemorrhagic | | --- | --- | --- | --- | | Onset | Gradual; steps/worsening | Sudden | Sudden (gradual if from hypertension (HTN)) | | level of consciousness (LOC) | Awake | Awake | Deepening lethargy → coma | | Linked to | HTN, atherosclerosis; transient ischemic attack (TIA) first | Heart disease (A-fib) | HTN, vessel problems, genetics | | Headache | Slight | — | **Severe**; seizures common | | Recovery | Weeks–months | Usually rapid | Variable; often permanent deficits | - **Intracerebral hemorrhage (ICH)**: bleeding into brain tissue, usually from **severe HTN**; cocaine can trigger it. - **Subarachnoid hemorrhage (SAH)**: bleeding between pia and arachnoid, usually a ruptured **aneurysm** or **arteriovenous malformation (AVM)**. **Vasospasm** (artery clamps down) afterward → more ischemia. - Leading causes: **smoking, obesity, HTN, diabetes, high cholesterol**. Also cocaine, heavy alcohol, birth control pills in at-risk women, family history. - 5th leading cause of death; #1 cause of long-term disability. "Stroke belt" = 8 southeastern states. - Prevent with the **ABCS**: **A**spirin when appropriate, **B**lood pressure, **C**holesterol, **S**moking cessation. Assessment (book)Read in book - First priority: get to a **stroke center**. Assess within **10 minutes** of arrival (ABCs, neuro). - History: **exact time symptoms started**, did they get better or worse, meds (anticoagulants), drug use. - Sudden drop in level of consciousness (LOC)? Rule out **low blood sugar or low oxygen** first. They look like a stroke but are easy to fix. - **subarachnoid hemorrhage (SAH)**: "worst headache of my life," nausea/vomiting, photophobia, stiff neck. - Most important ongoing check = **LOC** (GCS or National Institutes of Health Stroke Scale (NIHSS)). - **Impaired airway defense**: weak cough + dysphagia → aspiration pneumonia. Screen swallowing. - Heart: murmur, A-fib, heart failure, endocarditis. - **blood pressure (BP)**: often 180–200/110–120 on arrival. A somewhat high BP (about **150/100**) keeps the brain perfused; higher can extend the stroke. - **Psychosocial**: body image, coping, money worries; screen for **depression**. **Emotional lability** = sudden laughing or crying for no reason (frontal lobe or right brain). Tell the family it's the stroke, not them. - Labs: no test confirms stroke. High **Hgb/Hct** = severe stroke; high white blood cell count (WBC) = infection or stress; glucose and **hemoglobin A1C (A1C)** check diabetes. NIHSS (Table 38.2): your instructor said don't memorize it, just be familiar. It scores 0 (normal) to 42 (worst) and helps decide who gets tissue plasminogen activator (tPA). tissue plasminogen activator (tPA) (alteplase) rules (book)Read in book - Explain to patient/family and get **informed consent**. - Door-to-needle goal: **45 minutes** from emergency department (ED) arrival. - If blood pressure (BP) is too high, give a fast antihypertensive first. BP must be **below 185/110** to start, and kept there. **Box 38.4: care during and after alteplase** - Admit to critical care or a stroke unit. **Double-check** the drug. - Give with a **programmable pump** over 60 min (10% as a 1-minute bolus). **Never push it by hand.** - Neuro checks + vitals: **every 10–15 min during the infusion**, then **every 30 min for at least 6 hrs**, then **hourly for 24 hrs**. - Use the **same BP device** each time (manual vs. automatic vs. arterial line readings differ). - BP **≥185/110 before** tPA, or **>180/105 after** (first 24 hrs) → give antihypertensive as ordered, e.g., **intravenous (IV) labetalol**. - **No invasive tubes** (NG tube, Foley) until stable, usually **24 hrs** (bleeding). - **Stop the infusion** and call for severe headache, sudden high BP, nausea/vomiting. - Follow-up computed tomography (CT)/magnetic resonance imaging (MRI) **before** starting anticoagulants or antiplatelets. **Drug Alert:** watch closely for bleeding: brain bleed (headache, level of consciousness (LOC) change) and any other site. Procedures & intracranial pressure (ICP) after stroke (book)Read in book - **Endovascular**: intraarterial tissue plasminogen activator (tPA) (within **6 hrs**), mechanical embolectomy (pull clot out), carotid stent. - After a **carotid stent**, teach to report: severe headache, level of consciousness (LOC) change (drowsy), muscle weakness, severe neck pain, **neck swelling**, **hoarseness or trouble swallowing** (nerve damage). - Hemorrhagic from arteriovenous malformation (AVM)/aneurysm: procedure to stop bleeding. - **↑ICP risk is highest the first 72 hrs**. Reassess every 1–4 hrs. **Critical Rescue:** the **first sign of ↑ICP is a declining LOC**. Report any decline to the provider or Rapid Response right away. **Prevent ↑ICP:** - **head of bed (HOB) up** per protocol. **Head midline**, neutral. - O₂ if oxygen saturation (SpO₂) **under 95%**. - No sharp hip or neck bending. - **Don't cluster care** (bath right after linen change spikes ICP). - **Hyperoxygenate** before and after suctioning; avoid unneeded suctioning and coughing. - Quiet room, **dim lights**. - Watch blood pressure (BP), rhythm, SpO₂, glucose, temperature. **Box 38.5 signs of ↑ICP:** ↓LOC (earliest), restless/irritable/confused, headache, vomiting (may be projectile), speech changes, pupil changes (dilated nonreactive = "blown"), seizures, Cushing's triad and posturing (very late). Meds, blood pressure (BP) & swallowing (book)Read in book **BP Critical Rescue:** no tissue plasminogen activator (tPA) or embolectomy → BP may be allowed up to **220** systolic. After tPA/embolectomy → report systolic **above 180**. Avoid a sudden BP drop: it can cause brain ischemia. - **Aspirin and clopidogrel** = standard for ischemic stroke and preventing the next one. - **Anticoagulants** (heparin, warfarin, direct oral anticoagulants (DOACs)) for **A-fib**. High-alert: bleeding risk. - Low-dose **aspirin within 24–48 hrs**; **not within 24 hrs of tPA**. Teach to report bruising or bleeding. - Stool softeners (no straining = no intracranial pressure (ICP) spike), pain and anxiety meds. - **nothing by mouth (NPO) until a swallow screen**. Positive screen → speech-language pathologist. - Weigh daily; check prealbumin; dietitian. - **Flaccid arm**: support it on a pillow so the shoulder doesn't dislocate (subluxation). Don't pull on it. - Early mobility; prevent deep vein thrombosis (DVT) with **compression devices**. Aphasia & communication (book)Read in book | Expressive (Broca) | Receptive (Wernicke) | Global (mixed) | | --- | --- | --- | | **Frontal** lobe. Understands but **can't speak** (or write). Knows it → frustrated, angry. | **Temporoparietal**. **Can't understand**. Can talk, but words are often meaningless. | **Both**: can't speak **and** can't understand. Reading and writing are affected the same way. Usually a large stroke involving the **left** (dominant) side. | "Broca = broken speech. Wernicke = words wacky. Global = gone both ways." - One idea at a time. Simple one-step commands. - Speak **slowly, not loudly**. Use gestures. - Yes/no questions for expressive aphasia. - **Global aphasia**: rely on **gestures, pictures, touch, and facial expression**. Keep a calm tone; watch body language for needs. - Picture boards, tablets, flash cards. **Don't rush**. - Work with the speech-language pathologist. Vision, neglect & left vs. right (book)Read in book **Right-brain stroke** (trouble with space and distance, right vs. left): - Use frequent verbal and touch cues; break tasks into small steps. - **Approach from the unaffected side.** Patient faces the door. **Unilateral neglect** (usually right-brain stroke): ignores one side. - Teach to **touch and use both sides**. Dress the **affected side first**. - **Homonymous hemianopsia**: teach to **turn the head side to side (scan)** while eating and walking. Put objects in the field of vision. - **Diplopia**: patch the affected eye; switch every 2–4 hrs. **Left-brain stroke** (memory problems): - Reorient to day and time; **structured routine** with repetition. - **Apraxia**: give simple, short directions; be patient. Core measures & going home (book)Read in book **Core measures (ischemic stroke):** venous thromboembolism (VTE) prevention · discharged on antithrombotic · anticoagulant for A-fib/flutter · tissue plasminogen activator (tPA) when eligible · antithrombotic by end of day 2 · discharged on statin · stroke education · rehab assessed. **Box 38.6 discharge teaching:** - Drugs: name, purpose, dose, timing, side effects. - Climbing stairs, getting in and out of bed, chair, and car safely; using mobility aids. - Who to call with questions; what to do in an emergency. - They're **at risk for another stroke**. Teach **FAST** (face drooping, arm weakness, speech difficulty, time to call 911). - Watch for **depression or dementia within 3 months** (poststroke depression). - Caregivers get overwhelmed → **respite**, social services, American Stroke Association. - Return demonstrations to check family skills. Book · NCLEX Challenge 38.1 · Select all A client has a **left middle cerebral artery** embolic stroke. Which findings does the nurse expect? Left brain → right side of the body. The left side controls speech, so dysarthria fits. Ataxia and vertigo point to the back of the brain (vertebrobasilar). Book · NCLEX Challenge 38.2 A client was just admitted to the emergency department (ED) with new-onset ischemic stroke. Which drug does the nurse anticipate? New ischemic stroke in the time window = tPA (after the CT shows no bleed). Aspirin waits 24–48 hrs. Book · Mastery Q1 A client with an acute ischemic stroke is receiving alteplase. Priority nursing action? Bleeding (especially into the brain) is the biggest danger with tPA. Book · NGN Challenge 38.1 **Case:** 74-year-old with diabetes in the ED. Right arm felt weak and tingly; now feels "more normal." **Bilateral carotid bruits.** blood pressure (BP) 168/92, heart rate (HR) 88, oxygen saturation (SpO₂) 96%. History: type 2 diabetes, hypertension (HTN), alcohol, **69 pack-year smoking**. Glucose 231. Quick recall · tap to flip NCLEX The nurse has an order to start alteplase for a client with stroke symptoms. What must the nurse confirm first? tPA in a hemorrhagic stroke could be fatal. CT first, every time. NCLEX A client just admitted with an ischemic stroke asks for water. What does the nurse do? Aspiration is the most common cause of hypoxia in stroke. Screen first; refer to speech if any concern. NCLEX A client with a right-hemisphere stroke keeps trying to get out of bed alone. Priority problem? Right-brain strokes cause impulsivity and poor judgment. Safety first. NCLEX A client's wife says his face drooped "about 2 hours ago, then got better, now it's back." Most important info for the nurse? tPA eligibility is timed from first symptom onset. The 60-second version ## The skull is a closed box. Swelling has nowhere to go. - Normal **intracranial pressure (ICP) 10–15**. Over **20** = brain cells die. - **cerebral perfusion pressure (CPP) = mean arterial pressure (MAP) − ICP**. Keep it **above 70**. - First sign of ↑ICP = **mental status change**. Late = **Cushing's triad**, posturing. - **Glasgow Coma Scale (GCS) 8 or less → intubate.** A **2-point drop** = call. - Head injury → **assume neck injury** too (jaw thrust). The skull holds 3 things: brain, blood, and cerebrospinal fluid (CSF). It's a full suitcase that can't stretch. If one thing gets bigger (swelling, a bleed, extra fluid), something gets crushed, starting with the blood vessels. Types of brain injury **Primary injury** = direct damage from the hit. Most common causes: **car crashes** and **falls** (teach seat belts, helmets, fall prevention). | Term | Meaning | | --- | --- | | **Open** head injury | Skull broken/pierced (e.g., gunshot) → **infection risk** | | **Closed** head injury | Blunt hit, skull intact. **More dangerous**: swelling has no escape → ↑intracranial pressure (ICP) | | Contusion | Bruised brain | | Laceration | Torn vessels (inside of skull is bumpy and sharp) | | Diffuse axonal injury | Widespread damage from high-speed crash (speed up, sudden stop) | | Severity | Glasgow Coma Scale (GCS) | Unconscious for | | --- | --- | --- | | **Mild** (= concussion) | — | Usually sent home | | **Moderate** | **9–12** | 30 min – 6 hrs | | **Severe** | **8 or less** | Over 6 hrs → intensive care unit (ICU) | Concussion discharge teaching Your instructor: "Don't memorize the list, but know it. You'll get yes/no examples." - **Acetaminophen** for pain is OK. **No nonsteroidal anti-inflammatory drugs (NSAIDs)** (Motrin, Advil): bleeding risk. - Return to the emergency room (ER) for signs of **↑intracranial pressure (ICP)** (swelling or bleed): worse headache, vomiting, confusion, hard to wake, weakness, seizures, vision changes. - **Clear fluid from the nose or ears** → return. Could be a **cerebrospinal fluid (CSF) leak** or **skull fracture**. The full book list (Box 38.8) is in the "Mild traumatic brain injury (TBI) teaching" chunk below. Secondary injury: hypoxia & ↑intracranial pressure (ICP) Happens **after** the first hit and makes it worse. End result: brain tissue damaged, blood flow interrupted. - **Post-concussion syndrome** (mild injury): headaches, dizziness, foggy thinking for weeks to months. - **Cerebral hypoxia**: from clots, respiratory failure, **low blood pressure (BP)**. Risk for **neurogenic shock**. Brain perfusion drops when **mean arterial pressure (MAP) is under 65–70**. **↑ICP numbers:** - Normal ICP = **10–15 mmHg**. Coughing, sneezing, straining (Valsalva) raise it briefly. OK. - **Over 20** for long = **neurons die**. - **cerebral perfusion pressure (CPP)** (blood flow to the brain) = **MAP − ICP**. Goal **above 70**. Example: MAP 85, ICP 25 → CPP = 60. Too low! The brain isn't getting enough blood. **ICP monitors** (just recognize the names): **ventriculostomy** (intraventricular catheter, can also drain cerebrospinal fluid (CSF)) and **subarachnoid screw / ICP bolt** (placed through a **burr hole**). Signs of ↑intracranial pressure (ICP) - **First: mental status change** (restless, confused). level of consciousness (LOC) drop comes later. - Pupil changes: unequal, dilated, **non-reactive**. **Cushing's triad** (late sign; near death). Really 4 parts:\ 1\. **Severe hypertension**\ 2\. **Bradycardia**\ 3\. **Widened pulse pressure**\ 4\. **Irregular breathing** (Cheyne-Stokes) | Decorticate | Decerebrate | | --- | --- | | Abnormal **flexion**: arms bent in toward the "core" | Abnormal **extension**: arms straight out. **Worse** | Both are late signs. Brain bleeds (hematomas) No room in the skull → life-threatening. Your instructor: "kind of something you just have to memorize." | Type | Where | Key sign | | --- | --- | --- | | **Epidural** | **Above** the dura ("epi" = above) | **Lucid interval**: knocked out → wakes up and talks (seems better) → **rapidly declines**. Emergency surgery. Neuro checks every 5–10 min. | | **Subdural** | **Below** the dura ("sub" = below) | **Slow**: weeks to months. Easy to miss. | | **Subarachnoid** | Subarachnoid space | **"Worst headache of my life,"** sudden | | **Intracerebral** | Deep in brain tissue | — | Hydrocephalus & herniation **Hydrocephalus** = too much cerebrospinal fluid (CSF) (not absorbed, or blocked) → big ventricles → ↑intracranial pressure (ICP). **Herniation** = brain shifts to make room: - **Uncal**: sideways (temporal lobe). - **Central**: downward onto the **brainstem**. Don't memorize which pupil means which. Know: pupils change (unequal, dilated), **always non-reactive** → call **Rapid Response** and the provider. level of consciousness (LOC) drops, Cheyne-Stokes breathing. Assessment after head injury - **airway, breathing, circulation (ABCs) first.** Assume a **cervical spine injury** → spinal precautions; open airway with **jaw thrust**. - **Autoregulation is lost**: blood pressure (BP) and heart rate (HR) can swing **either way**. Get a baseline; may seem stable then crash. - Do the **neuro exam BEFORE sedatives** or paralytics. - **Pupils**: any change → call right away. - **Motor**: deficit on the **opposite side** of the lesion. **Skull fracture signs:** - cerebrospinal fluid (CSF) leak: clear fluid from nose/ears; **positive glucose** on dipstick; **halo sign**. - **Battle sign**: bruising behind the ear (mastoid). - **Raccoon eyes**: bruising around the eyes. Glasgow Coma Scale practice Your instructor: **don't memorize the scale**. You'll be given it; know how to **apply** it. - Highest = **15**. Lowest = **3**. - **7 or less** = coma. "**Less than 8, intubate.**" - A **2-point drop** = clinically significant → Rapid Response / provider. Eyes open Verbal Motor Preloaded with the class example: opens eyes to pain (2) + withdraws (4) + moans (2) = **8**. Interventions to lower intracranial pressure (ICP) **Respiratory:** prevent low oxygen, and keep **carbon dioxide (CO₂) 35–45**. **"High CO₂ dilates, low CO₂ constricts."** High → brain vessels swell → ↑ICP. Low → vessels clamp → poor blood flow. Both bad. - **Cardiovascular:** know the patient's blood pressure (BP) range; call if above or below. **Cardiac monitor** (lost autoregulation → dysrhythmias). - **Therapeutic hypothermia:** cooling lowers the brain's oxygen demand. **Mannitol** (osmotic diuretic): - Pulls water **out of brain tissue into the blood** → kidneys pee it out → less swelling, lower ICP. - Dosed by **serum osmolality**; goal **310–320** (normal \~300), slightly "salty" blood. - Watch: **dehydration**, electrolyte imbalance, **acute kidney injury**. **Foley + hourly I&O** (an exception to avoiding Foleys). - Often given with **furosemide**: mannitol pulls fluid from the brain, furosemide removes it from the body. **Hypertonic saline (3% or 5%)** works like mannitol. intensive care unit (ICU) only, and it shows why it's dangerous for regular patients. Your instructor said a case study (due next week, from the book) covers ICP prevention in detail, plus post-op craniotomy care. Brain tumors & craniotomy - **Primary** = starts in the brain. **Secondary** = spread from elsewhere (lung, breast). - Any tumor → **↑intracranial pressure (ICP)** and squeezes brain tissue and vessels. - **Meningioma** (benign, common) → usually removed with a good outcome. Malignant → surgery + radiation/chemo. - Common signs: **headache, seizures**, dizziness, memory loss. | Craniotomy | Decompressive craniectomy | | --- | --- | | Skull opened, fixed, closed right away | Piece of skull **removed** and frozen; put back weeks/months later. Leaves room to swell. Patient wears a **helmet**. | Read in book Iggy Ch. 38, pp. 956–973 · skipped per your list: chronic traumatic encephalopathy (CTE) paragraph, pinpoint/ovoid pupil sentences, supra/infratentorial paragraph, chemo & direct drug delivery traumatic brain injury (TBI) basics (book)Read in book - **TBI** = brain damage from an outside force. Affects cognition, movement, senses, and emotions. - **Acceleration** injury = something hits the still head. **Deceleration** = moving head hits something still. Shearing → diffuse axonal injury. - **Open** = skull or dura broken (infection risk). **Closed** = skull intact. - Top causes: **falls**, self-harm, car crashes, assaults. Alcohol/drugs contribute. Young men most; **falls** most in older adults and kids. | Mild (concussion) | Moderate | Severe | | --- | --- | --- | | Blow to the head + brief confusion or feeling dazed, plus one or more: out **up to 30 min**, memory loss right before/after, focal neuro deficit. **Doesn't need** loss of consciousness. **computed tomography (CT)/magnetic resonance imaging (MRI) normal.** Symptoms usually gone in **72 hrs**. | Out **30 min–6 hrs**; Glasgow Coma Scale (GCS) **9–12**. CT/MRI often shows injury. Memory loss up to **24 hrs**. Short acute/critical care stay to watch for swelling, bleeding. | GCS **3–8**; out **over 6 hrs**. Critical care: hemodynamic, neuro, possibly **intracranial pressure (ICP) monitoring**. High risk for secondary injury. | - **Postconcussion syndrome** (most common secondary injury after mild TBI): headache, foggy thinking, dizziness for **4+ weeks**. Also posttraumatic headaches or vertigo; irritability, depression, anxiety, mood swings; insomnia; trouble concentrating or memory loss; **lower alcohol tolerance**. - **Second-impact syndrome**: a second hit before the brain heals → rapid brain swelling, can be catastrophic. Mostly athletes. Teach return-to-play rules. Secondary injury numbers (book)Read in book - **Hypotension** = mean arterial pressure (MAP) **under 70**. **Hypoxemia** = partial pressure of arterial oxygen (PaO₂) **under 80**. Both starve the brain → swelling → worse perfusion (vicious cycle). - intracranial pressure (ICP) normal **10–15**; coughing or straining spikes are OK. Sustained **over 20** → neurons die. - Body compensates: shifts cerebrospinal fluid (CSF), absorbs more CSF, moves venous blood out. When it can't, ICP rises → herniation. - **↑ICP is the leading cause of death** in head-trauma patients who reach the hospital alive. Bleeds & herniation (book)Read in book | Bleed | Book detail | | --- | --- | | **Epidural** | **Arterial** (middle meningeal artery), often a temporal skull fracture. Brief unconsciousness → **lucid interval** (awake, talking for minutes) → rapid decline. **Critical Rescue:** neuro checks **every 5–10 min**; loss of consciousness = **neurosurgical emergency** → provider/Rapid Response now. Document trends. | | **Subdural (SDH)** | **Venous**, slower. Acute (within 48 hrs), subacute (48 hrs–2 wks), chronic (weeks–months). Common in **older adults** and people on **anticoagulants/antiplatelets**. Signs: worsening headache, confusion, ↓level of consciousness (LOC). | | **Intracerebral (ICH)** | Bleeding into brain tissue; may appear up to 10 days later. | - **Uncal herniation**: pushes on **cranial nerve (CN) III** → dilated nonreactive pupil, **ptosis**, fast LOC decline. - **Central herniation**: downward onto the brainstem → **Cheyne-Stokes** breathing, then nonreactive pupils, unstable vitals. - All herniations are life-threatening → **Rapid Response / provider immediately**. - **Hydrocephalus**: **communicating** = cerebrospinal fluid (CSF) not absorbed (after subarachnoid hemorrhage (SAH) or meningitis); **noncommunicating** = outflow blocked (swelling, tumor, debris). traumatic brain injury (TBI) assessment (book)Read in book - History: **when, where, how**; lost consciousness, and how long? Get it from witnesses if needed. Amnesia is common. Older adults: screen for abuse/neglect. - **carbon dioxide (CO₂)**: high (over 45) → vasodilation → ↑intracranial pressure (ICP). Low (under 35, from hyperventilating) → vasoconstriction → ischemia. Track with **end-tidal carbon dioxide (ETCO₂)**. - Treat as a **cervical spine injury** until x-rays prove otherwise. **Rigid collar**; spine precautions: bed rest, no neck or back bending or twisting, **log roll**, check skin under the collar. Spine "clearance" is the provider's call. - Brainstem injury → Cheyne-Stokes or apnea; may need a ventilator. - **Cushing's triad** = severe hypertension (HTN), widened pulse pressure, bradycardia → **death is near**. - **Glasgow Coma Scale (GCS) change of 2 points** = report. **level of consciousness (LOC) is the most important thing to assess**; a change is the **first sign** of worsening. - Pupils: unequal, sluggish, or dilated = herniation until proven otherwise. **Fixed and dilated ("blown") = poor prognosis**. - Check vision (read your name tag, count fingers). - Late ↑ICP signs: severe headache, vomiting (often projectile), seizures. **Papilledema = always ↑ICP**. - Highest ICP risk: first hours, up to **3–4 days** after injury. - Motor loss is on the **opposite** side. - **cerebrospinal fluid (CSF) leak**: clear fluid from nose/ear, **positive glucose**, **halo sign** on white gauze. **Raccoon eyes**, **Battle sign** = basilar skull fracture. - **computed tomography (CT) first**. magnetic resonance imaging (MRI) shows diffuse axonal injury but **not with ICP monitors**. **Critical Rescue:** check pupils (size, shape, reaction) often, especially if they can't follow directions. Report any change to Rapid Response; it may mean ↑ICP. traumatic brain injury (TBI) interventions (book)Read in book - Vitals every **1–2 hrs** or more. Report dysrhythmias, high or low blood pressure (BP); get target ranges from the provider. - **Fever** = worse outcomes. Goal is **normal temperature** (targeted temperature monitoring). - Keep partial pressure of arterial carbon dioxide (PaCO₂) normal; avoid over-hyperventilating. **Positioning Action Alert:** head **midline**, no extreme neck flexion/extension. **Log roll**. head of bed (HOB) **at least 30°** (or as ordered). Avoid sudden HOB changes; a big BP drop when sitting up can hurt the brain. **Mannitol** (book adds): - Pulls water out of swollen brain tissue. Works best as **boluses**, not a continuous drip. - Give through a **filter** in the intravenous (IV) tubing, or draw up with a **filtered needle** for IV push (removes tiny crystals). - Serum **electrolytes and osmolarity every 6 hrs**; goal osmolarity **310–320**. Serum and urine osmolarity and sodium checked **at least daily**. - **Strict hourly urine output**, I&O. Watch for **severe dehydration**, **acute kidney failure**, weakness, edema, urine output changes. - **Furosemide** (loop diuretic) is often added: prevents mannitol "rebound," boosts its effect, lowers edema and blood volume, and **reduces cerebrospinal fluid (CSF) production**. **Hypertonic saline (HTS)**: draws fluid out like mannitol. Usually **3%** sodium chloride (NaCl) (can be up to 23%). Nursing: constant neuro checks, **serial sodium levels**, fluid status, watch for **pulmonary edema** (especially heart or kidney disease). Some hospitals require **intensive care unit (ICU) + central line**. Evidence box: HTS is at least as effective as mannitol for lowering intracranial pressure (ICP); some studies say better. Choice depends on the patient. **Opioids** (fentanyl, morphine) and sedation (propofol, dexmedetomidine) may help ventilated patients; check neuro first. **Brain death** requires: coma of known cause, temp **above 96.8°F (36°C)**, systolic **≥100**, at least 1 neuro exam. Before it's declared, call the **organ procurement** agency (the nurse doesn't bring up donation alone). Support grieving families; ethics, chaplain, social work. Cognition, seizures & trauma-informed care (book)Read in book - **Memory and thinking**: cognitive rehab; reorient; hazard-free room. - **Sensory stimulation** for comatose patients: one stimulus at a time (show a family photo and say who it is). Audio no longer than **10–15 min** or it becomes "white noise." - Seizure precautions and antiepileptic drugs (AEDs) as ordered. - **Trauma-informed care** (6 principles): **safety**, **trust and transparency** (plain language), **peer support**, **collaboration**, **empowerment** (patient has a voice), **cultural and historical sensitivity**. Mild traumatic brain injury (TBI) teaching: Box 38.8Read in book - Headache → **acetaminophen every 4 hrs** as needed (no nonsteroidal anti-inflammatory drugs (NSAIDs)). - **No sedatives, sleeping pills, or alcohol** for at least **24 hrs** (unless the provider says otherwise). - **No strenuous activity** for at least **48 hrs**. - Caregiver: balance problems can cause falls; plan safe movement. - **Call 911 / return** for: seizure, severe or worsening headache, persistent vomiting, blurred vision, **clear drainage from ear or nose**, increasing weakness, slurred speech, **progressive sleepiness**, **unequal pupils**. - Keep follow-up appointments. Home care after traumatic brain injury (TBI) (book)Read in book - Rehab goal: **highest possible function** (OT, physical therapy (PT), speech). - Home safety: working **smoke and fire alarms**; brain injury often takes away the **sense of smell**. - Dietitian: many gain weight within a year (inactivity, stress eating). - Personality and behavior changes: **structured, consistent routine** with repetition. Reinforce **positive** behavior. - Expect fatigue, irritability, temper outbursts, depression, memory problems. Some need constant supervision. - Families feel isolated → regular **respite**, support groups (Brain Injury Association of America). Brain tumors (book)Read in book - **Primary** tumors start in the central nervous system (CNS) and rarely spread out of it. **Secondary** tumors spread from lung, breast, kidney, skin, gastrointestinal (GI). - Any tumor → swelling, ↑intracranial pressure (ICP), possible herniation. Pituitary tumors can cause **syndrome of inappropriate antidiuretic hormone (SIADH)** or **diabetes insipidus** (fluid and sodium problems). - **Meningiomas** (benign) can usually be removed with a good outcome. - Malignant tumors mostly at ages **40–70**. **Signs:** **headache worse on waking**, nausea/vomiting, seizures, numbness or vision changes, dizziness, one-sided weakness, trouble speaking, personality changes. **Diagnosis:** computed tomography (CT) first, then magnetic resonance imaging (MRI) for detail. **Symptom meds:** - Codeine/acetaminophen for headache. - **Dexamethasone** (steroid) for brain swelling. - **Levetiracetam** or other antiepileptic drugs (AEDs) to prevent seizures. - proton pump inhibitors (PPIs) to prevent **stress ulcers**. **Gamma Knife / CyberKnife** (stereotactic radiosurgery): focused radiation, no incision, for hard-to-reach tumors or arteriovenous malformations (AVMs). **Tumor Treating Fields**: electric fields through skin pads. **Glioblastoma** = most aggressive; few survive 5 years. Craniotomy care (book)Read in book **Before surgery:** very anxious (head opened, hair shaved, fear of new deficits). Reassure; teach what to expect after. **Action Alert:** neuro checks + vitals **every 15–30 min for 4–6 hrs**, then **hourly**. Stable 24 hrs → every 2–4 hrs. Report: ↓level of consciousness (LOC), new weakness or paralysis, aphasia, less feeling, **sluggish pupils**, agitation, personality change. | Supratentorial (top of brain) | Infratentorial (brainstem/back) | | --- | --- | | **head of bed (HOB) 30°** (venous drainage). Head midline; no extreme hip or neck bending. Turn side to side or supine. | Keep **flat or 10°**. **Side-lying**, alternating every 2 hrs, for 24–48 hrs. **nothing by mouth (NPO) until fully awake** (swelling near medulla → vomiting, aspiration). | - Check the head **dressing every 1–2 hrs**; mark drainage once a shift. - Drain (Hemovac/Jackson-Pratt (JP)): measure every 8 hrs; usually **30–50 mL / 8 hrs**. **Critical Rescue:** report a **saturated dressing** or drainage **over 50 mL in 8 hrs** right away. Watch for ↑intracranial pressure (ICP). - Swollen, bruised eyes are normal → **cool compresses**; rinse with warm saline or artificial tears. - Cardiac monitor (dysrhythmias). Strict **I&O for 24 hrs**; fluid limit \~**1500 mL/day** if the pituitary is involved. - Labs: complete blood count (CBC), electrolytes, osmolality, clotting. Watch for **low sodium** (SIADH, steroids) → confusion, weakness. **High sodium** (DI, dehydration) → thirst, restlessness. - venous thromboembolism (VTE): compression devices until walking. Deep breathing every 2 hrs. **Box 38.9 complications:** - **Early:** ↑ICP, hematomas, subarachnoid hemorrhage (SAH), hypovolemic shock, hydrocephalus, breathing problems (atelectasis, pneumonia, neurogenic pulmonary edema). - **Late:** wound infection, meningitis, fluid/electrolyte problems, seizures, **cerebrospinal fluid (CSF) leak**, cerebral edema. Book · NCLEX Challenge 38.4 A client just returned from an open craniotomy for a frontal lobe tumor. Which finding needs immediate report to the surgeon or Rapid Response? ↓level of consciousness (LOC) = possible ↑intracranial pressure (ICP) or bleeding. Headache and eye swelling are expected; 25 mL is under the 50 mL limit. Book · NCLEX Challenge 38.3 A client with a mild traumatic brain injury (TBI) is learning about home care. Which statement shows a need for **more teaching**? Box 38.8: no strenuous activity for at least 48 hrs, and balance problems make construction work unsafe. The others are correct teaching. Book · Mastery Q3 Which finding is an **early** change in LOC in a client with a mild TBI? Behavior changes (irritable, restless) come first. Posturing and lost reflexes are late. Book · Mastery Q2 · Select all The nurse is giving mannitol to a client with a severe TBI. Which actions are appropriate? Only A is wrong: urine output is measured **every hour**, not every 4–8. Filtered needle, electrolytes, osmolarity, and dehydration watch all match p. 964. (My answer; check your book's key.) Book · NGN Challenge 38.2 **Case:** 79-year-old fell at home 2 days ago and broke her right arm. Over 2 days: Glasgow Coma Scale (GCS) **15 → 14**, headache **4 → 5 → 8/10**, blood pressure (BP) and pulse creeping up. Review class: Joline head-injury case (what she stressed) Review class From the in-class exam review (Joline case study + NCLEX questions). Joline fell from a third-story balcony. Think: head injury **and** spine injury until proven otherwise. 1. **Most important thing to monitor: level of consciousness (LOC).** First sign of trouble = changes in behavior. 2. **Cushing's triad** (the "triad" that has **4** parts): severe hypertension, widened pulse pressure, **bradycardia**, irregular breathing. Normally high blood pressure makes the heart speed up, so slow heart rate + high blood pressure is the weird exception. It is a **late** sign of increased intracranial pressure. **Be able to apply it:** "blood pressure 200/80, heart rate 40" = Cushing's. 3. **Neuro assessment, know what's wrong AND how you check it:** pupils equal, round, reactive to light and accommodation (PERRLA), LOC, Glasgow Coma Scale (GCS), motor (squeeze my hands, push/pull feet, raise arms), sensory, reflexes, cranial nerves, vital signs (which part is off and why), breathing pattern. 4. **Orogastric (OG) tube, not nasogastric (NG)**, with severe facial trauma or skull fracture (like basal skull fracture). A tube through the nose could go up through the fracture into the brain. Going through the mouth avoids that. 5. **Blood alcohol** makes the neuro assessment **unreliable**. 6. **When she wakes up:** first tell her where she is and what happened ("You're in the hospital. You were in an accident."). This lowers fear. **Then** check orientation. (Students often pick "ask where she is." That's second.) 7. **Epidural hematoma:** knocked out right away → **lucid interval** (seems better, "it's a trick") → then crashes. 8. **Bruising and swelling around the eyes** (periorbital edema and ecchymosis) is expected with this injury. Apply **cold compresses** (decrease swelling) and **artificial tears** (comfort). Assess, and notify the provider as needed. 9. **3 reasons for a fever:** infection, inflammation (body's response to brain injury), and damage to the **hypothalamus** (the body's thermostat). **Glasgow Coma Scale:** don't memorize the scale. The test will give it to you. Just know how to apply it. The tricky part is motor: **withdraws / pulls in = 4**. **Pushes the stimulus away = 5** (localizes pain). Her examples: eyes to pain 2 + verbal none 1 + withdraws 4 = **7**. Eyes to sound 3 + incomprehensible sounds 2 + localizes 5 = **10**. Review class: spinal precautions + preventing ↑intracranial pressure (ICP) Review class From the in-class exam review (Joline case study + NCLEX questions). **Backboard and cervical collar:** used because spinal cord injury and head injury go together. They stay until spinal cord injury is ruled out. - **Spinal precautions:** supine (bed rest), spine in **neutral** position. No twisting, no neck flexion forward or back, **no pillow**. - **Remove the long backboard as soon as possible**: go back to basics: a hard board causes **skin breakdown**. - **Repositioning = log roll** as a unit, with help. - **Every time the patient is moved** (turns every 2 hrs, trip to head computed tomography (CT) scan), do **another neuro assessment**. - **Head of bed position depends on cerebral perfusion pressure (CPP).** Up can pull blood away from the brain; flat can send too much and raise ICP. It's individualized. **Don't memorize** the book's exact rules; just know CPP guides the choice. **Nursing care to avoid increasing ICP:** 1. **Quiet, calm room.** Noise, bright light, anxiety, agitation all raise ICP. Limit upsetting visitors (a screaming parent may need to step out). 2. **No Valsalva** (bearing down): give **stool softeners**; manage coughing. 3. **Suction only if you must** (airway, breathing, circulation (ABCs) come first). Try repositioning and other measures first. If you suction, **hyperoxygenate first**. 4. **Keep the whole body straight:** no head flexion, **no pillow under the knees** (bent knees block blood flow back from the head). 5. **Frequent vital signs + neuro checks.** 6. **Arterial blood gas (ABG): watch carbon dioxide (CO₂)** closely. CO₂ is a **potent vasodilator** → more blood in the brain → ↑ICP. 7. **Do NOT cluster care.** Exception to the rule! Repositioning + bath + linen change + suppository all at once = ICP spike. **Space activities out.** 8. **Control fever.** Fever → shivering → more oxygen demand → more CO₂ → vasodilation → ↑ICP. 9. **Mannitol** (see below). | Mannitol: know it cold | | | --- | --- | | Class | Osmotic diuretic | | How it works | Treats brain swelling. Pulls water out of the brain tissue into the blood vessels → kidneys excrete it. Sometimes given with **furosemide** (loop diuretic) to work together. | | Dosing guide | **Serum osmolality.** Normal ≈ 300 (just remember 300). Goal = slightly hypertonic, **310–320**. Pump rate is adjusted to stay there. | | Filter needle | **Always.** It has microscopic crystals. Any time you read "use a filter needle," remember it. | | Monitor | Intake and output (I&O); urinary catheter is often used here (an exception, we usually avoid catheters); dehydration; blood pressure; labs: **sodium, potassium, serum osmolality** | **Legal/ethical (organ donation):** Joline is an adult whose **driver's license** says organ donor. In **Michigan, Ohio, and Kentucky** that is **legally binding**, so the hospital follows it even if family disagrees (it varies by state). Help the grandmother: let her express feelings; involve the **chaplain, social services, organ donation team**, and possibly the **ethics committee**. Quick recall · tap to flip NCLEX A client hit his head, was knocked out, then woke up talking normally. An hour later he's hard to wake. The nurse suspects: Lucid interval then rapid decline = epidural. Emergency surgery. NCLEX MAP 80, ICP 22. What is the CPP, and what does the nurse do? 80 − 22 = 58. Under 70 means poor brain perfusion, and ICP over 20 is dangerous. NCLEX A client's GCS dropped from 13 to 11. Best action? A 2-point drop is clinically significant. NCLEX Which finding in a client on mannitol needs follow-up first? Mannitol should cause big diuresis. Very low output suggests acute kidney injury. NCLEX Clear fluid is draining from a head-injury client's nose. Best assessment? CSF contains glucose and forms a halo on gauze. Possible skull fracture. The 60-second version ## Migraine = overexcited nerves + swollen, widened brain blood vessels - One-sided, **throbbing** pain. Nausea. Light and sound hurt. Some get an **aura** first. - **Pain management is the priority.** First step: avoid triggers. - Most migraine meds work by **narrowing the blood vessels**. - **Triptans:** NO for heart disease, high blood pressure (BP), peripheral vascular disease (PVD), or with selective serotonin reuptake inhibitors (SSRIs). The vessels are like a garden hose that's swollen too wide and throbbing. The fixes squeeze the hose back down: caffeine, triptans, even a cool cloth. Signs & finding the cause - Usually **one-sided**, throbbing. - Nausea, **photophobia**, **phonophobia**. - **Aura** = warning before it hits (vision changes). **Nurse's job:** detailed interview. How often? How long? What sets it off? **Headache diary** → finds patterns and triggers. Common triggers: **caffeine, red wine, monosodium glutamate (MSG)** (a food flavor additive). Treatment step 1 & 2: triggers + comfort 1. **Avoid triggers.** 2. **Comfort measures:** lie down in a **dark room**, **cool cloth** on the forehead, relaxation, yoga, massage, acupuncture. 3. **Medications** if still needed. Abortive meds (stop it now) Take **as soon as symptoms start**, ideally during the aura. - **First:** acetaminophen, nonsteroidal anti-inflammatory drugs (NSAIDs) (ibuprofen, naproxen), or over-the-counter (OTC) combos with **caffeine** (like Excedrin). Caffeine narrows blood vessels. - **Next: triptans**, like **sumatriptan (Imitrex)** and **rizatriptan (Maxalt)**. They activate serotonin → narrow brain arteries → less pain. **Triptan safety:** they narrow vessels *everywhere*, not just the brain.\ • Think twice with **high blood pressure (BP)** or **heart disease**.\ • **Peripheral vascular disease: absolutely not.**\ • Teach: report **chest pain** right away (heart not getting enough blood).\ • Don't mix with **selective serotonin reuptake inhibitors (SSRIs)** (sertraline, fluoxetine) or **St. John's wort** → **serotonin syndrome**. **Lasmiditan:** newer, doesn't narrow vessels outside the brain, so safer. Side effects: **sleepiness, dizziness**. **Rebound headache:** a new headache after the first one goes away. Caused by taking the medicine **too often or too much**. Preventive meds (stop it from coming) For migraines that are **frequent** or **severe**: - nonsteroidal anti-inflammatory drugs (NSAIDs) - **Beta blockers** - **Topiramate** (an anti-seizure drug) Read in book Iggy Ch. 36, pp. 899–902 · crossed-out parts skipped Migraine basics (book)Read in book - Recurrent attacks of head pain that serve **no protective purpose**. - Throbbing, unilateral. Nausea + sensitivity to **light, sound, or head movement**. - Lasts **4 to 72 hours**. Runs in families. **Women** more than men. - Linked to **major depression**, and higher risk of **stroke** and **epilepsy**. **How the pain happens:** cerebral arteries dilate → **prostaglandins** released → inflammation, swelling, leaking → throbbing pain. Full trigger listRead in book - **Caffeine**, **red wine**, **monosodium glutamate (MSG)** - High-intensity light, stress, excessive fatigue, change in weather - **Tyramine**: pickled foods, aged cheese, smoked sausage, beer - Preservatives, artificial sweeteners Triggers set off **hyperexcitable neurons**. Each patient's triggers are different. Types & phases (Box 36.8)Read in book | With aura ("classic") | Without aura ("common") | | --- | --- | | Aura right before the headache | **Most migraines** are this type | **Chronic** = 15+ days a month. **Episodic** = less often. 1. **Prodrome** (1–2 days before): yawning a lot, constipation, mood changes, food cravings. 2. **Aura** (5–60 min, usually one-sided): flashing lights, spots, zigzag lights; numb or tingling lips/tongue, confusion, aphasia, vertigo, one-sided weakness, drowsiness. 3. **Migraine phase**: nausea/vomiting; one-sided throbbing pain, often worse **behind one eye or ear**; photophobia, phonophobia. Without aura: pain gets worse with routine activity; often early morning, with stress, or premenstrual. **Diagnosis:** history + physical, neuro, and psych assessment. Patients tend to have the same symptoms each time. **Women over 50 with migraines:** teach cardiovascular risk factors. **Call 911** for facial drooping, arm weakness, or trouble speaking (stroke). Abortive drugs: the full lineupRead in book **Priority of care = pain management.** | Severity | Drugs | | --- | --- | | Mild | Acetaminophen; nonsteroidal anti-inflammatory drugs (NSAIDs) (ibuprofen, naproxen); over-the-counter (OTC) nonsteroidal anti-inflammatory drug (NSAID) + caffeine | | Nausea | Antiemetics; **metoclopramide** with NSAIDs (speeds stomach emptying) | | Severe | Triptans, ditans | **Caffeine** narrows vessels by blocking **adenosine** (which widens vessels and adds inflammation). **Triptans** (sumatriptan, eletriptan, naratriptan, almotriptan) activate **5-HT (serotonin)** receptors → vasoconstriction. Sumatriptan comes as a pill, injection, or nasal spray. **Contraindicated:** ischemic heart disease, cerebrovascular ischemia, hypertension (HTN), peripheral vascular disease (PVD), **Prinzmetal angina** (coronary vasospasm risk). **Triptan teaching (Drug Alert):** take as soon as symptoms start · report chest pain right away · **use birth control** (not safe in pregnancy) · expect **flushing, tingling, hot feeling** that fades · no selective serotonin reuptake inhibitors (SSRIs) or St. John's wort. **Ditans (lasmiditan):** block one serotonin receptor **without** constricting vessels → safer and more effective than triptans. When to start preventive drugsRead in book Start prevention when **any** of these is true: - More than **2 migraines a month** - Headache lasts more than **24 hours** - Interferes with activities of daily living (ADLs) for **3+ days** - Abortive meds used more than **twice a week** - Not relieved by acute treatment | Drug | Key point | | --- | --- | | **Beta blockers** (propranolol, timolol) | Calm hyperexcitable neurons, block vasodilation. **Lower blood pressure (BP) and heart rate (HR).** | | **Calcium channel blocker** (verapamil) | | | **Topiramate** (AED) | Use in **low doses** | | **Nortriptyline** (TCA) | Dry mouth, urinary retention, constipation. **Not for older adults** (delirium). | **beta blocker (BB) / calcium channel blocker (CCB) teaching:** take your **pulse** · report **bradycardia**, fatigue, shortness of breath · change position slowly (orthostatic hypotension). Diary, comfort & complementary careRead in book - **Headache diary**: type of headache + response to meds. - Report if the headache **changes** in quality or intensity, has **new visual changes**, or the drug stops working. - At onset: lie down, dark room, **both eyes covered**, cool cloth, undisturbed. - **Cannabis:** cannabidiol (CBD) eases pain better; tetrahydrocannabinol (THC) is the mind-altering part. Tolerance can develop. - Yoga, meditation, massage, exercise, **biofeedback**, acupuncture/acupressure. - Riboflavin and **magnesium** supplements may help prevent migraines. - All herbs must be **approved by the provider** first (drug interactions). Heads-up: the book prints "vitamin B12 (riboflavin)," but riboflavin is actually **vitamin B2**. Book · NCLEX Challenge 36.4 · Select all Client prescribed propranolol (prevention) and sumatriptan (acute). Which teaching statements should the nurse include? Beta blockers cause **bradycardia** (report a LOW pulse, not >100) and orthostatic hypotension. Triptans go in early, and chest pain = possible ischemia. Vitamin D isn't part of this plan. Review class: migraine meds (prevent vs. abortive) Review class From the in-class exam review (Joline case study + NCLEX questions). | Goal | Drug | Key point | | --- | --- | --- | | **Prevent** migraines | **Propranolol** (beta blocker) | Taken regularly to prevent attacks | | **Abortive** (once headache starts) | **Triptans** (sumatriptan): "triptan" is in the name | Activates serotonin → **vasoconstriction** of the dilated brain vessels | Triptans squeeze blood vessels. They don't only squeeze the brain's vessels, they squeeze them **everywhere**. **Do NOT give triptans with:** - **Hypertension**, **peripheral vascular disease** (vessels already narrowed) - **Angina / heart disease**: chest pain after a triptan = coronary vasoconstriction - **Selective serotonin reuptake inhibitors (SSRIs)** like fluoxetine (Prozac), paroxetine → too much serotonin = **serotonin syndrome** - **St. John's wort** (and grapefruit) interact with lots of meds. If it shows up as an answer choice, don't pick it. Quick recall · tap to flip NCLEX A client is prescribed sumatriptan. Which history should the nurse report first? Triptans narrow blood vessels, which makes PVD worse. NCLEX After taking a triptan, the client says "my chest feels tight." What does the nurse do? Narrowed vessels can starve the heart of oxygen. Chest pain is a red flag. NCLEX Which statement shows the client understands migraine self-care? The diary finds triggers. Meds go early, daily use causes rebound headaches, and red wine is a trigger. The 60-second version ## A seizure is an electrical storm in the brain - Seizure with a clear cause (fever, electrolytes, alcohol withdrawal, brain injury) = **NOT epilepsy**. Treat the cause. - **Epilepsy** = seizures that keep coming back on their own. - During a seizure: **turn to side, move objects, never restrain, nothing in the mouth**. - **Status epilepticus** (>5 min) = emergency → **airway** first, then **lorazepam intravenous (IV)**. Think of a power surge in a house. Anti-seizure meds are surge protectors: they keep surges from happening, but they don't rewire the house (no cure). **Caption alert:** the video captions say "fentanyl," but your instructor means **phenytoin** (Dilantin). "Phosphantinoin" = **fosphenytoin**. Seizure vs. epilepsy **Seizure** = sudden, uncontrolled burst of electrical activity in brain cells. **Secondary causes** (fix these first): **high fever, electrolyte imbalance, alcohol withdrawal, brain injury**. These are NOT epilepsy. **Epilepsy** = chronic, **recurrent, unprovoked** seizures. Cause: abnormal brain cells or a chemical imbalance (like **gamma-aminobutyric acid (GABA)**, the brain's calming chemical). Diagnosis starts with a detailed **history and physical**. Seizure types (slides)Slides Your instructor said these are **review from Peds**. You won't be tested on each type directly, but the words may show up in a question. **Generalized** = **both** sides of the brain: - **Tonic-clonic** (2–5 min): stiffening + level of consciousness (LOC) (tonic), then rhythmic jerking (clonic). Tongue biting, incontinence. - **Myoclonic:** quick jerks of arms or legs. - **Atonic:** suddenly goes limp → falls → injury. - **Absence:** brief blank stare; lip smacking or picking (automatisms). **Partial (focal)** = **one** side: **complex** (blacks out 1–3 min, no memory after) or **simple** (stays awake, has an aura). electroencephalogram (EEG) test prep EEG records the brain's electrical activity. Electrodes are glued to the scalp. - **Clean hair**: no conditioner, gel, or spray (electrodes won't stick). - **Eat before the test.** Low blood sugar changes the reading. - **No sedatives, stimulants, or caffeine.** - Quiet room, sign on the door. We want a picture of the brain's normal self. Anything that speeds it up, slows it down, or starves it ruins the picture. Anti-seizure meds **Slide drugs:** phenytoin (Dilantin), carbamazepine (Tegretol), valproic acid (Depakote), topiramate (Topamax). You don't need to know which drug is for which seizure type. Know these rules: - They slow the brain → **drowsiness**. - Can cause **depression and suicidal thoughts**. Screen mood. - **Liver damage** → check liver enzymes. **Low white blood cells (WBCs)** → infection risk. - **Narrow safe range** → regular **blood levels**. - **Phenytoin** → **gums overgrow** (gingival hyperplasia). Teach: soft toothbrush, regular dentist visits. **Never stop suddenly.** Seizures come back and can turn into status epilepticus. - **Pregnancy category D**: can cause birth defects, but uncontrolled seizures hurt the baby too. Tough decision with the provider. - **Birth control pills** work less well → use a **second method**. - **Warfarin** needs close monitoring. **No grapefruit** (toxicity). Vagal nerve stimulator (VNS) For seizures meds can't control. A device in the **left chest** (like a pacemaker) sends pulses up the **vagus nerve** to the brain. - Feels an **aura**? **Swipe the magnet** over the device to stop the seizure. - Like a pacemaker: **magnetic resonance imaging (MRI) can be dangerous**, sets off airport metal detectors, wear a **medical alert bracelet**, carry a wallet card. Before: seizure precautions - **Suction + oxygen** at the bedside. - **intravenous (IV) access** (saline lock). They can't swallow pills during a seizure. - **Padded side rails?** Debated (could count as a restraint). **Follow hospital policy.** Some use a mattress on the floor. - Keep them **active and independent**. Don't keep them stuck in bed. **NO padded tongue blades.** A chipped tooth can be breathed in, or the blade can block the airway. During a seizure **Patient safety is the priority.** 1. Turn to the **side** so spit drains out → no aspiration. 2. **Move objects** away so they don't get hurt. 3. **Never restrain.** Nothing in the mouth. 4. **Watch and document** what happens, in order. It tells the provider the seizure type → which drug. Status epilepticus: emergency Seizure lasting **longer than 5 minutes**, or seizures back-to-back over 30 minutes. Over 10 minutes can be deadly. **Call the Rapid Response Team.** 1. **Airway** (may need intubation) + **oxygen**. 2. **intravenous (IV) with normal saline**. Draw blood: **arterial blood gases (ABGs), electrolytes, drug levels**. 3. **Stop it:** **lorazepam (Ativan)** or diazepam (Valium) IV push. 4. **Prevent the next one:** **fosphenytoin** (preferred, safer) or phenytoin. Firefighter first (lorazepam puts out the fire). Then the sprinkler system (fosphenytoin stops the next fire). Patient & family teaching - Meds: take every dose, know interactions, keep blood level appointments. - Family knows what to do during and after a seizure, and when to call 911. - **Seizure diary.** Medical alert bracelet or card. - **Driving laws** by state: **Michigan = 6 months** seizure-free · Wisconsin = 3 months · Ohio = no waiting period. - Employment concerns → refer to **social services / case manager**. - Support groups: Epilepsy Foundation. Read in book Iggy Ch. 36, pp. 902–907 · crossed-out parts skipped (seizure types, Table 36.2) Definitions & secondary causesRead in book **Seizure** = sudden, excessive, uncontrolled electrical discharge of neurons → changes in level of consciousness (LOC), motor/sensory ability, or behavior. **Epilepsy** = chronic, **repeated, unprovoked** seizures. Cause: abnormal electrical activity and/or neurotransmitter imbalance, especially **gamma-aminobutyric acid (GABA)**. **Primary (idiopathic)**: no clear cause, likely genetic. **Secondary**: from a brain lesion (tumor, trauma) or: - Metabolic disorders, **electrolyte problems** (hyperkalemia, water intoxication, hypoglycemia) - Acute alcohol withdrawal, substance abuse - High fever, stroke, head injury, heart disease **Triggers:** more physical activity, stress, fatigue, alcohol or caffeine, certain foods or chemicals. Assessment & diagnosisRead in book - How many seizures, how long, any **pattern**? Have family describe them. - Any **aura** before (the **preictal phase**)? - Meds, herbs, head trauma, high fever, alcohol or drug use, past stroke or hypertension (HTN). - New seizures: ask about any past **loss of consciousness or brain injury**, even in childhood. **Tests:** electroencephalogram (EEG), computed tomography (CT), magnetic resonance imaging (MRI), single-photon emission computed tomography (SPECT)/positron emission tomography (PET). antiepileptic drug (AED) teaching (book adds)Read in book - Provider adds **one AED at a time**. - Keep lab appointments: **complete blood count (CBC) + liver enzymes** (most antiepileptic drugs (AEDs) cause **leukopenia** and liver dysfunction) + drug levels. - Take on time. Sensitivity can build with age ("drug decline and sensitivity") → frequent levels. - **Phenytoin + warfarin** = don't combine. - **Grapefruit juice** raises drug levels → toxicity. **Women with epilepsy:** hormones and birth control pills change AED effects → monitor more often. AEDs can add to **osteoporosis** after menopause. During a seizure: Box 36.9Read in book - Protect from injury; **nothing forced in the mouth**. - Turn to the **side** (prevents aspiration, keeps airway clear). - Remove objects; **suction gently** if possible; **loosen clothing**. - **Don't restrain**; guide movements if needed. - **Record start and end time.** **After:** vital signs, neuro checks, keep on side, let them rest. **Document:** pupils and eye deviation, level of consciousness (LOC), apnea/cyanosis/salivation, incontinence, eye fluttering, how motor activity spread, lip smacking, tongue biting, length, aura, behavior after, time to return to baseline. **Cyanosis** during tonic-clonic seizures is common and usually self-limiting. High-risk patients may get O₂ postictally. Status epilepticus: book detailsRead in book **Acute seizures** (more intense, more often, or in clusters) → lorazepam or diazepam to **prevent** status. **Common causes of status:** **suddenly stopping antiepileptic drugs (AEDs)**, infection, alcohol/drug withdrawal, traumatic brain injury (TBI), cerebral edema, metabolic problems. **Critical Rescue:** **airway is the priority** → call provider / Rapid Response → O₂ → **large-bore intravenous (IV)** with 0.9% sodium chloride (NaCl) → usually intensive care unit (ICU). **Untreated:** hypoxia, hypotension, hypoglycemia, dysrhythmias, lactic acidosis. Muscle breakdown → **myoglobin → acute kidney injury** (especially older adults). - **Lorazepam IV push over 2 minutes** (may repeat). Diazepam rectal gel is an option. - **Phenytoin IV:** infusion pump · **normal saline only** (precipitates in other fluids) · flush normal saline (NS) before and after · then oral doses. - **Fosphenytoin:** water-soluble, works with most IV fluids **including dextrose**, fewer heart complications. vagal nerve stimulator (VNS): book detailsRead in book - Device in the **left chest wall**, lead on the **left vagus nerve**. \~2 hrs under general anesthesia. - Turned on in the operating room (OR) or, more often, **2 weeks after surgery**. Runs continuously. - **Voice change** = the nerve is being stimulated (expected). - Complications: **hoarseness (most common)**, cough, dyspnea, neck pain, dysphagia. - Avoid **magnetic resonance imaging scans (MRIs), microwaves, shortwave radios, ultrasound diathermy**. Patient & family teaching: Box 36.10Read in book - Know drug name, dose, timing, side effects, what to do if a dose is missed. - **Never stop antiepileptic drugs (AEDs)**, even if seizures stop. - Keep blood-level appointments. No over-the-counter (OTC) drugs without asking. - Wear a **medical alert** bracelet or carry an ID card. - Family knows how to help during a seizure and **when to call emergency medical services (EMS)**. - Follow **state driving and machinery laws**. - Avoid **alcohol and excessive fatigue**. Balanced diet, rest, stress reduction. **Seizure diary.** - Can't afford meds? Refer to **social services** / case manager. - Discrimination is illegal, but risky jobs (construction, heavy equipment, pilots) may need to change. Book · Mastery Q3 · Select all A hospitalized client has a tonic-clonic seizure. Which actions are most appropriate *during* the seizure? During: suction gently, remove hazards. Nothing goes in the mouth. Vitals come **after**. Benzos are for status or clusters, not every single seizure. Book · NGN Challenge 36.1 **Case:** 54-year-old had **3 tonic-clonic seizures** (2–3 min each) in the past hour. Got intravenous (IV) lorazepam; fosphenytoin infusing; O₂ 2 L. Now back to baseline, A&O ×4, vitals normal. Review class: seizure priorities + meds Review class From the in-class exam review (Joline case study + NCLEX questions). - **Tonic-clonic seizure, loses consciousness → priority: turn to the side** (aspiration risk). If there's no trauma/fall in the story, you're not worried about spinal injury. - **Status epilepticus** = seizure that keeps going. **Stop it** with a benzodiazepine ending in **-pam**: **diazepam** or lorazepam. - **Phenytoin / fosphenytoin** (fosphenytoin more common) **do NOT stop** a seizure in progress. They **prevent future** seizures. Quick recall · tap to flip NCLEX A client is having a tonic-clonic seizure in bed. What should the nurse do first? Side-lying protects the airway. Never restrain, never put anything in the mouth, never leave. NCLEX A client has been seizing for 6 minutes. Priority action? Over 5 minutes = status epilepticus. Airway first. Nothing by mouth. NCLEX A client on an anti-seizure drug takes birth control pills. Best teaching? These drugs make the pill less effective. Never stop them suddenly, and no grapefruit. NCLEX Which finding in a client on long-term anti-seizure meds needs follow-up first? These drugs can cause depression and suicidal thoughts. Safety first. The 60-second version ## Infected brain covering = pressure + sepsis danger - **Meningitis** = inflamed **meninges** (the wrapping around brain and spinal cord). - **Viral** = more common, gets better in 7–10 days. **Bacterial** = emergency, can kill in 24 hrs. - **Meningococcal** (bacterial) → **droplet precautions**. - Diagnose with a **lumbar puncture**, but **computed tomography (CT) first** if signs of ↑intracranial pressure (ICP). - Top 3 checks: **neuro, vital signs, circulation**. The brain sits in a sealed jar. Swelling raises the pressure inside. Opening the bottom of the jar (lumbar puncture) can make the brain shift down. Check the pressure with a computed tomography (CT) before you open it. How it gets in A germ gets into the blood and **crosses the blood-brain barrier**. - Sources: **brain or spine surgery**, **ear or sinus infection**, **flu or pneumonia**. - Prevention = **vaccines**: flu, pneumonia, meningococcal. - **Meningococcal vaccine: age 11–12, booster at 16.** Viral vs. bacterial | | Viral | Bacterial (meningococcal) | | --- | --- | --- | | How common | **More common** | Less common | | How bad | Most recover in **7–10 days** | **Emergency.** Can kill within **24 hrs** | | Spread | — | Highly contagious; outbreaks in **dorms**, group homes | | Isolation | **Standard** | **Droplet** | **Encephalitis** = inflamed **brain tissue** itself. Same signs, but more **long-term brain damage**. Signs & symptoms - **Nuchal rigidity**: stiff, sore neck. - **Severe headache**, **photophobia**, **nystagmus**, pupil changes. - Altered mental status, **seizures**, **↑intracranial pressure (ICP)**, **positive Babinski**, **sepsis**. **Fever may be missing. Why?**\ 1\. **Older adults** run cooler, so 98.6°F might already be a fever for them.\ 2\. They're **already on antibiotics** for the first infection (like sinusitis). The drug didn't kill the germ, and it reached the brain. Babinski reflex **How:** stroke the bottom of the foot from the **heel up to the toes**. | Toes do… | Name | Adult meaning | | --- | --- | --- | | **Curl down** | Absent Babinski | **Normal** (what we want) | | Big toe **up**, others **fan out** | Positive Babinski | **Problem in the brain or spinal cord** | **Exception:** positive Babinski is **normal under age 2**. Their nervous system isn't mature yet. Lumbar puncture (spinal tap) Meningitis is diagnosed by testing **cerebrospinal fluid (CSF)**. - Position: **side-lying, knees to chest** (fetal position). - Patient must stay **very still** (may need help holding or sedation). **Danger:** if there are signs of ↑intracranial pressure (ICP), letting CSF out fast can make pressure worse. **computed tomography (CT) scan first.** Cultures & antibiotics: the exception **Normal rule:** get cultures first, then antibiotics. **Exception** (signs of ↑intracranial pressure (ICP), no time for computed tomography (CT) + lumbar puncture (LP)): 1. Draw **blood cultures** immediately. 2. Start a **broad-spectrum antibiotic right away**. 3. Skip the cerebrospinal fluid (CSF) culture (LP too risky). 4. Germ identified → switch to a **narrow-spectrum** antibiotic. Top 3 nursing priorities 1. **Neuro status.** **First sign of ↑intracranial pressure (ICP) = change in behavior** (restless, irritable, "something's off"). Seizure precautions. 2. **Vital signs**: clues to rising ICP. 3. **Circulation check**: color, temperature, cap refill, pulses in hands and feet. Watch for **bleeding** (gums, urine, intravenous (IV) site). **Why bleeding?** Sepsis makes tons of tiny clots. They use up all the platelets and clotting factors, so none are left for normal clotting → bleeding. This is **disseminated intravascular coagulation (DIC)** (disseminated intravascular coagulation). Read in book Iggy Ch. 36, pp. 907–909 · crossed-out parts skipped What & how it enters (book)Read in book Infection of the **pia mater and arachnoid mater**. Usually bacterial or viral; also fungal or protozoal. **Sterile meningitis** can come from cancer, nonsteroidal anti-inflammatory drugs (NSAIDs), antibiotics, intravenous (IV) immunoglobulin. **Ways in:** bloodstream, or directly through penetrating trauma, brain/spine surgery, ruptured brain abscess. **Basilar skull fracture:** clear "runny nose" (**rhinorrhea**) or ear drainage (**otorrhea**) may actually be **cerebrospinal fluid (CSF)** → path for infection. **Higher risk:** head/neck infections (otitis media, sinusitis, tooth abscess, even tongue piercing); immunocompromised (no spleen, immunosuppressants, transplant, cancer); older adults. Can cause permanent cranial/spinal nerve damage and **↑intracranial pressure (ICP)**. Organisms & vaccinesRead in book **Viral = "aseptic" meningitis** (no organism grows in cerebrospinal fluid (CSF) culture): enterovirus, herpes simplex virus (HSV)-2, varicella zoster, mumps, human immunodeficiency virus (HIV). **Bacterial:** *Streptococcus pneumoniae* and *Neisseria meningitidis* (= meningococcal). Outbreaks: dorms, **military barracks**, crowded housing. **Vaccine schedule (CDC):** highest risk = **ages 16–21**. First meningococcal dose at **11–12**, booster at **16**. Adults: shared housing, travel, or no spleen. Booster OK as early as 8 weeks after first dose. Other vaccines that prevent meningitis: **Hib**, pneumococcal, mumps, varicella, meningococcal. Key features: Box 36.11Read in book - **↓level of consciousness (LOC)**, disorientation - **Photophobia**, **nystagmus** (jerky repetitive eye movements) - Motor normal early → later hemiparesis/hemiplegia - Cranial nerve problems: **cranial nerve (CN) III, intravenous (IV), VI, VII, VIII** - Short attention span, personality changes - Severe, unrelenting headache; myalgia; N/V; fever, chills; tachycardia - **Red macular rash** = meningococcal Nuchal rigidity, **Kernig** and **Brudzinski** signs show up in only a **small percentage**. Diagnostics (book)Read in book **computed tomography (CT) before lumbar puncture (LP)** for: age **over 60**, immunocompromised, or signs of ↑intracranial pressure (ICP). - LP delayed? Draw **blood cultures** (C&S) first. - Broad-spectrum antibiotic **right after the LP** (or right away if LP is delayed). - cerebrospinal fluid (CSF) tested for cell count, differential, protein, glucose, culture, Gram stain. - **complete blood count (CBC):** white blood cell count (WBC) well above normal. Electrolytes checked. - X-rays of chest, sinuses, mastoids (find the infection source). - CT/magnetic resonance imaging (MRI): ↑ICP, hydrocephalus, abscess. Treatment & isolationRead in book - Broad-spectrum antibiotic until culture and Gram stain return. - Bacterial: usually a **2-week intravenous (IV) antibiotic course**. Start within **1–2 hours** of the order. - **Mannitol** for ↑intracranial pressure (ICP); antiepileptic drugs (AEDs) for seizures. **Droplet Precautions** (in addition to Standard) for *N. meningitidis* and *H. influenzae*: private room · stay **3 feet** away without a mask · patient wears a mask outside the room · teach visitors. All other meningitis: **Standard Precautions**. Nursing care: Box 36.12Read in book **Most important nursing action:** accurately monitor and document **neuro status**. Neuro checks + vital signs (VS) **every 2–4 hours**. - airway, breathing, circulation (ABCs) first. Cranial nerve checks. - **Vascular check every 4 hrs**, especially the **hands**: temp, color, pulses, nail cap refill. Missed compromise → gangrene → loss of the arm. - Strict I&O, prevent fluid overload; **daily weight**. - Quiet room, **dim lights** (photophobia). - Bed rest, **head of bed (HOB) 30°**. Reposition (pressure injuries); range of motion (ROM) every 4 hrs. - Watch for: ↑intracranial pressure (ICP), vascular problems, fluid/electrolyte imbalance, seizures, shock. Also septic shock, clotting disorders, acute respiratory distress syndrome (ARDS), septic arthritis. Book · NGN Challenge 36.2 **Case:** 21-year-old with suspected bacterial meningitis. Temp 101.6 → **102.4°F** → 100.8°F. white blood cell count (WBC) **18,000**. At 0600: A&O ×4, headache 8/10. At 0700: **drowsy, oriented ×2**, unsure of day and time, "very sleepy," headache 5/10. Review class: bacterial meningitis: order of actions Review class From the in-class exam review (Joline case study + NCLEX questions). 1. **Isolation first** (protect yourself and the team). **Droplet** precautions: regular **surgical mask**, private room. No negative-pressure room needed. 2. **Insert an intravenous (IV) line** (circulation; emergency meds). 3. **Computed tomography (CT) of the head before the lumbar puncture**: rule out ↑intracranial pressure (ICP). A lumbar puncture with high ICP pushes it even higher. 4. **Broad-spectrum antibiotic** right away while waiting on the culture and sensitivity (C&S). 5. Once the organism is identified → switch to a **narrow-spectrum** antibiotic. **NCLEX mindset:** even if the patient is blue, you don't skip your own protection. Quick recall · tap to flip NCLEX A client with suspected bacterial meningitis becomes newly restless and irritable. Priority? Behavior change is the earliest sign of ↑ICP. Sedation would hide the neuro exam. NCLEX A college student has meningococcal meningitis. Which precautions? Meningococcal spreads by droplets. Viral meningitis uses standard precautions. NCLEX Stroking an adult's sole makes the big toe go up and the toes fan out. This means: In adults, toes should curl down. Fanning up signals a brain or spinal cord problem. The 60-second version ## Not enough dopamine → movement gets shaky, stiff, and slow - Progressive brain disease that affects **movement**. - Signs = **TRAP** + low blood pressure (BP) when standing, drooling, peeing at night. - Main drug: **carbidopa-levodopa (Sinemet)**. Take with carbs, **not protein**. - Biggest nursing job: **fall prevention** and nutrition. Acetylcholine is the gas pedal. Dopamine is the brake. In Parkinson's the brake wears out but the gas stays the same → shaky, jerky, hard-to-control movement. Signs: TRAP T**Tremor**: "pill rolling" (thumb rubs finger) at rest. Handwriting gets tiny and squiggly. R**Rigidity**: muscles can't relax → **mask-like face**, less blinking/smiling, trouble speaking, **trouble swallowing**, drooling. A**Akinesia/bradykinesia**: slow movement. Eating, writing, shaving get hard. P**Postural instability**: stooped, shuffling, **freezing gait** ("feet stuck to the floor") → **falls**. Automatic-body problems Dopamine also helps run the "fight or flight" system. Less dopamine → it underperforms: - **Orthostatic hypotension**: blood pressure (BP) drops on standing → dizzy → falls. - **Drooling**: less automatic swallowing. - **Nocturia**: peeing at night. Meds: carbidopa-levodopa (Sinemet) Your instructor said these are the most common Parkinson's meds and **the only ones you need to know**. Replaces the missing dopamine (the brake). - **Nausea** is common → take with food, but **carbs, not protein** (protein blocks absorption). - Long-term: **dyskinesia** (uncontrolled movements). - **"On-off"**: symptoms controlled (on), then back (off), several times a day. Meds: dopamine agonists Copy dopamine. Side effects are less common but **more serious** → often **not safe for older adults**. - **Impulse control problems**: gambling, hypersexuality (dopamine = pleasure). - Mood changes. Tolerance, toxicity & drug holiday | Tolerance | Toxicity | | --- | --- | | Med just isn't working as well | **Delirium** (sudden confusion) | **Delirium = sudden. Dementia = slow and long-term.** **Fix for both:** lower the dose or frequency, change meds, or a **drug holiday** (off the med 1 week up to 10 days, then restart). Deep brain stimulation (DBS) When meds aren't enough. Approved for **severe tremors**. - Electrodes go into the brain; wires run under the skin to a device in the **left chest** (like a pacemaker). - Sends pulses that **decrease involuntary movements** and block tremors. - **Not a cure.** Disease still progresses. - Same precautions as a pacemaker: avoid **electromagnetic fields and magnetic resonance imaging scans (MRIs)**. Nursing management (slides)Slides - **Injury prevention (falls)**: muscle strengthening, stretching, flexibility, balance and coordination. - Exercise, range of motion (ROM), walking; self-care; sleep problems. - Communication and speech help; emotional support; support groups. - **Nutrition:** **high protein, high calorie** (unless liver or kidney disease) · soft diet, thickened liquids · **weigh weekly** · swallow evaluation. Watch the trap: high-protein diet for weight, but keep protein away from the Sinemet dose. Captions mishear: `Echinacea` = bradykinesia · `pastoral` = postural · `cinnamon` = Sinemet · `bacteria` = nocturia Read in book Iggy Ch. 36, pp. 894–899 · crossed-out parts skipped (stages box, monoamine oxidase (MAO)-B/catechol-O-methyltransferase (COMT) drugs, imaging, other surgeries) Patho & early signs (book)Read in book **Primary (idiopathic)** is most common. **Secondary** parkinsonism: brain tumors, some **antipsychotics**. Substantia nigra degenerates → less dopamine. Protein **alpha-synuclein** is thought to drive it. Symptoms appear only after a big dopamine drop (book: 70–80%). **Non-motor signs can appear YEARS before TRAP:** constipation, soft voice, **micrographia** (tiny handwriting), **loss of smell**, sexual dysfunction, sleep problems. - **traumatic brain injury (TBI)** raises Parkinson's disease (PD) risk → teach contact-sport athletes to wear **helmets**. - Veterans: TBI, **Agent Orange** exposure. - **Lewy bodies** (abnormal proteins) → some get Lewy body dementia. - About **50% more men** than women. Assessment (book)Read in book - **Rigidity** = resistance to **passive** movement; present early. - Stage 4: needs a **walker** and help with activities of daily living (ADLs). Stage 5: trouble chewing and swallowing. - Late: dementia, psychosis (delusions, paranoia, hallucinations), depression, anxiety, apathy. - Autonomic: **excessive sweating**, orthostatic hypotension. - Speech: soft, slurred, monotone, halting, or rapid. - Bladder: incontinence **or** trouble urinating. Bowel: **constipation**. **No specific test.** Diagnosis is clinical, after ruling out other neuro diseases. **Priority problems:** 1) ↓mobility (self-care deficit) · 2) impaired cognition. **Priority of care: keep mobility and activities of daily living (ADL) independence as long as possible.** Box 36.7: best-practice careRead in book - Give patients **extra time** to answer and to do activities of daily living (ADLs); help only as needed. - Give meds **on time, on their individual schedule** (steady drug levels). - Fall Precautions; physical therapy (PT)/occupational therapy (OT). - Prevent immobility complications: constipation, pressure injuries, contractures. - Schedule activities **late morning** or at their best time of day. - Teach to speak slowly and clearly; communication board; refer to **speech-language pathologist (SLP)**. - Monitor swallowing and intake; **high-protein, high-calorie** foods. - Focus on strengths (self-esteem). Assess depression, anxiety, cognition, insomnia. Drug details (book)Read in book **Dopamine agonists** (apomorphine, pramipexole, ropinirole; **rotigotine patch**): best in the first **3–5 years**; fewer dyskinesias and less "wearing off." **Agonist Drug Alert:** orthostatic hypotension, hallucinations, **sleepiness** → no driving or heavy machinery · rise slowly · shouldn't be prescribed to older adults. **Carbidopa/levodopa:** nearly everyone takes it eventually. Cheaper and better for motor function than agonists. Comes as immediate-release (IR), controlled-release (CR), enteral infusion, and an **inhaled form for "off" periods**. **Safinamide** is an add-on. **Book says:** give levodopa **before meals** for better absorption. **Lecture says:** if it causes nausea, take with carbs, not protein. Both point the same way: **keep protein away from the dose**. **Toxicity** = delirium, hallucinations, less effect. Compare to the pre-drug baseline. **Tolerance** = effects wear off sooner. Drug holiday lasts up to 10 days; monitor and document Parkinson's disease (PD) symptoms during it. **Symptom helpers:** baclofen (spasms), **sublingual atropine** (drooling), zolpidem (insomnia). Medical cannabis: stay **nonjudgmental**. Freezing gait, sleep, eating & speechRead in book **Freezing gait tricks:** step **sideways, then forward** · shift weight side to side, then step · picture an object on the floor to **step over**. Yoga and tai chi help early. range of motion (ROM), stretching, out of bed. **Sleep:** poor nights + short naps they may not notice → risk of **falling asleep while driving**. - speech-language pathologist (SLP) swallowing evaluation. **Soft diet, thick cold fluids** (milkshakes), small frequent meals, thickener (Thick-It). - **Elevate the head** to prevent aspiration. Weigh **weekly**. - Speech: slow, deep breaths, exaggerate words; reduce background noise; listener watches lips. Cognition, home care & deep brain stimulation (DBS) (book)Read in book - About **50%** develop cognitive problems. Depression is common (venlafaxine may be used). - Don't force social events; emphasize strengths. - Teach to report **dizziness, falls, delirium, hallucinations**. - Constipation: fluids, high fiber, bowel program. Sleep hygiene: no alcohol or caffeine, dark room. - Impulse control problems: remind family the patient **can't control** them. Watch for caregiver strain. - Late disease → palliative or hospice care. - **DBS**: reduces the need for levodopa; usually **not offered while meds still work**. Book · Mastery Q2 An ambulatory client was recently diagnosed with **early** Parkinson's. What finding does the nurse expect? Resting tremor is an early sign. Dementia and swallowing problems come late. Book · NCLEX Challenge 36.3 · Select all Client prescribed **ropinirole**. Which teaching statements should the nurse include? Ropinirole is a dopamine agonist: orthostatic hypotension, sleepiness, possible dyskinesias. The patch is rotigotine, and the food rule is for monoamine oxidase inhibitors (MAOIs). Review class: Parkinson's meds + earliest sign Review class From the in-class exam review (Joline case study + NCLEX questions). - **Earliest (initial) sign: tremor.** All the classic signs are Parkinson's, but tremor usually comes first. - **Ropinirole = dopamine agonist** (mimics dopamine). **Caution in older adults:** orthostatic hypotension and drowsiness → falls. - **Carbidopa-levodopa** (Sinemet): levodopa is turned into dopamine. Causes **nausea** → take **with food, but NOT protein** (protein blocks absorption: no peanut butter, eggs). Quick recall · tap to flip NCLEX Which breakfast is best with the morning carbidopa-levodopa dose? Protein blocks levodopa. Carbs help nausea without blocking it. NCLEX Top safety concern for a client with Parkinson's? Low BP on standing + poor balance = high fall risk. NCLEX A family says their dad on a dopamine agonist is suddenly gambling a lot. The nurse knows: Dopamine drives pleasure and reward, so agonists can cause impulse control problems. The 60-second version ## Inherited disease: dementia + "dancing" movements - **Hereditary.** Symptoms start at **age 30–50**. - Brain cells die → **progressive dementia** + **chorea**. - Child of a parent with it: **50/50 chance**. - **No cure.** Control symptoms, prevent complications. "Chorea" is Greek for dance (like "choreography"). Picture fast, jerky dance moves the person can't stop. Chorea & treatment **Chorea** = rapid, jerky movements of the **arms, legs, and face**. The term is used only for Huntington's. - The movements have **no purpose**. - The patient **can't stop or control them**. Care is the same as for anyone with a movement or memory disorder (Parkinson's, Alzheimer's): - Assistive devices; physical therapy (PT), occupational therapy (OT), speech therapy. - **Keep familiar routines.** Break tasks into **small steps**. - **Avoid open-ended questions** (ask yes/no or simple choices). - To-do lists and calendars. Genetics & testing - Parent has it → each child has a **50% chance**. - Child **doesn't carry the gene** → won't get it and **can't pass it on**. - A test can show the gene. Hard question: is it better to know? - **Not done under age 18**: they may feel pressured and aren't mature enough for the results. - **Genetic counseling** is very important for the children (ethical dilemma). Quick recall · tap to flip NCLEX A 16-year-old whose father has Huntington's asks to be tested. Best response? No testing under 18. Risk is 50%, and it doesn't skip generations. NCLEX Which communication works best for a client with Huntington's? Avoid open-ended questions. Simple yes/no choices work better with cognitive decline. The 60-second version ## multiple sclerosis (MS): the immune system strips the wire coating - **Autoimmune.** Damages **myelin** in the brain and spinal cord → signals weak or blocked. - Comes in waves: **flare-ups** and **remissions**. - Top symptoms: **fatigue, mobility problems, vision changes**. - Avoid **heat, stress, fatigue**. No hot showers, no hard exercise. - amyotrophic lateral sclerosis (ALS): **movement only**. Mind and senses stay intact. Myelin is the plastic coating on a phone charger cord. Strip patches off and the signal flickers or cuts out. What multiple sclerosis (MS) is - Myelin **cushions and protects** nerves and helps signals travel between brain, cord, and body. - Demyelination → signals are **weaker**, or don't get through. - Progresses at **different speeds** in different people. **Why diagnosis takes so long** (frustrating for patient and family): - No single test confirms it. - Symptoms look like other neuro problems, which must be ruled out. - Symptoms go away for a while, so people don't seek care. Signs & symptoms - **Overwhelming fatigue.** - **Weak, stiff legs**: hard to move them, hesitant → **fall risk**. - **Vision** (optic nerve): **nystagmus**, **double vision**, blurry vision. - **Dysarthria**: slurred or **scanning speech** (long pauses between words; can sound like stuttering). - Spasticity, numbness/tingling, **intention tremor** (shakes when reaching), poor coordination, positive Babinski. - Trouble swallowing; bowel, bladder, and sexual problems; memory and focus problems. **Don't mix up tremors:** Parkinson's = shakes **at rest**. multiple sclerosis (MS) = shakes **when moving** (intention). Nursing care **Prevent flare-ups:** avoid **fatigue, stress, temperature extremes** (hot showers). **Keep them independent:** - Stay organized; keep often-used items **within reach** (saves energy). - Speech therapy for swallowing trouble. **Eye patch** for double vision. - **Strength and stretching** exercises (PT/occupational therapy (OT)) for balance and coordination. - **No rigorous exercise**: raises body temp → more fatigue, less movement. **Main goal = symptom control.** multiple sclerosis (MS) meds (only 2 to know) No cure. **Immunomodulators** slow the disease and make attacks fewer and milder. Your instructor said know only these: | Drug | Key points | | --- | --- | | **Interferon beta** | Shot under the skin (every other day or weekly). **Infection risk**, bone marrow suppression, **flu-like symptoms**. | | **Glatiramer** | Shot under the skin. **Fewer side effects.** | amyotrophic lateral sclerosis (ALS) (Lou Gehrig's disease) - **Motor neurons** die → weakness, muscle wasting, stiffness → **paralysis**. Cause unknown. - **Only movement is affected.** They can still see, hear, and feel, and **thinking stays intact**. - Starts in one area, then spreads. Lose the ability to talk, swallow, and breathe. - Signs: tired while talking, **tongue shrinking**, slurred speech, trouble swallowing, **face twitching** (fasciculations). - Death usually within **3 years**, from **respiratory failure**. - No cure. Meds treat pain, spasms, **extra secretions**, sleep problems. Communication aids. - May need a feeding tube and ventilator. Get **advance directives** early. **Hospice** supports the family. Read in book Iggy Ch. 37, pp. 913–920 · crossed-out parts left out (MS types except relapsing-remitting multiple sclerosis (RRMS), cerebrospinal fluid (CSF)/evoked potentials, other MS drugs) What happens in multiple sclerosis (MS)Read in book - Cause: **immune, genetic, and/or infectious** factors. - **Demyelination** slows or stops nerve signals → patchy **plaques** in white matter. - Early on, myelin repairs itself and symptoms fade. Over time, damage builds and **muscle atrophy** sets in. - Often hits the **optic nerves**, spinal tracts, brainstem, and the area around the ventricles. - A leading cause of neuro disability in **young and middle-age adults**. Types of multiple sclerosis (MS)Read in book | Type | Pattern | | --- | --- | | **relapsing-remitting multiple sclerosis (RRMS)** (relapsing-remitting) | **Most common.** Flares over weeks to months, then back to baseline. | RRMS is a roller coaster that returns to the station. Who gets itRead in book - **Women 2–3×** more than men (some studies say up to 4×). - Ages **20–50**. About 1 million people in the US. - More common in **colder climates** (Great Lakes, Pacific Northwest). - A **first-degree relative** with multiple sclerosis (MS) raises risk. multiple sclerosis (MS) vs. amyotrophic lateral sclerosis (ALS) (Table 37.1)Read in book | | MS | ALS | | --- | --- | --- | | Cause | Immune attack on myelin; remissions + flares | Unknown (genetic + environmental); progressive muscle wasting → **respiratory paralysis** | | Who | Common; women 2× men; ages 20–50 | Uncommon; **men** more; ages 40–60 | | Signs | Fatigue, spasticity, **diplopia**, scotomas, nystagmus, paresthesias, bladder problems, intention tremor | Fatigue, muscle atrophy (incl. tongue), twitching of face and tongue, dysarthria, dysphagia | | Outlook | Many disease-modifying drugs | **100% fatal**; no cure. Supportive + palliative care | Signs & symptoms (Box 37.1)Read in book **History:** early symptoms are **vague** and come and go, so diagnosis often takes years. Ask about vision, motor, and sensory changes. Ask what makes it worse: **fatigue, stress, temperature extremes, hot showers or baths**. **Common:** - Muscle **weakness and spasticity**; flexor spasms - **Fatigue**, worse with heat - **Paresthesia** (numbness, tingling) - Vision: **diplopia** (double vision), **nystagmus**, ↓acuity, **scotomas** (blind spots) - Bowel and bladder problems (flaccid or spastic); sexual dysfunction - Cognitive changes: memory, judgment, problem solving - Depression, emotional changes - **"MS hug"** (dysesthesia): squeezing feeling around the torso. Often an early sign. - Trouble walking, **dysmetria** (can't control movement range), vertigo, pain, itching **Less common:** **intention tremor** (shaking when reaching for something), hypalgesia, dysarthria, dysphagia, hearing loss, tinnitus, loss of taste, seizures. **Don't mix up the tremors:** Parkinson's = **resting** tremor (pill-rolling at rest). multiple sclerosis (MS) = **intention** tremor (during movement). PsychosocialRead in book - Long road to diagnosis → **anger and frustration**. Let them vent. - After diagnosis: anxiety. Later: apathy, emotional lability. - **Secondary depression** is the most common mental health problem in multiple sclerosis (MS). - Some are **euphoric** (from the disease or the drugs). - Cognition changes are usually **late**: memory, concentration, calculation, judgment. - Fatigue affects sexuality. Women: less sensation and orgasm. Men: erection and ejaculation problems. DiagnosisRead in book **No single test.** Results are put together. - **magnetic resonance imaging (MRI)** of brain and spinal cord showing plaques in **at least 2 areas** = diagnostic. Drug therapyRead in book Goal: slow the disease and reduce flares. Most drugs **suppress immunity** → infection risk. Teach: **avoid crowds and sick people**, wash hands. | Drug | Key nursing point | | --- | --- | | **Interferon beta**; **glatiramer** | Subcutaneous self-injections. **Rotate sites**. Flulike symptoms → acetaminophen/ibuprofen. Bone marrow suppression → report infection. | **Symptom drugs:** **baclofen** or tizanidine (spasticity; severe → intrathecal baclofen pump) · carbamazepine or tricyclic antidepressants (TCAs) (paresthesia) · propranolol, clonazepam (ataxia). Medical cannabis may ease pain and stiffness. Stem cell therapy is being studied. multiple sclerosis (MS) drugs are **very expensive** (health equity issue). Nursing care: mobility, vision, cognitionRead in book - physical therapy (PT)/occupational therapy (OT): **range of motion (ROM)**, stretching, strengthening. - **Avoid things that raise body temp** (worsen fatigue and vision). - Home safety: remove rugs and clutter; adapt for a wheelchair. Plan rest periods. - **Dysarthria / dysphagia** → speech-language pathologist (SLP); thickened liquids if needed; watch for aspiration. - **Diplopia:** **eye patch, switched eye to eye every few hours**. - Peripheral vision loss: teach **scanning** (turn the head side to side). - Cognition: single-date calendar, written lists, keep items in familiar places, phone reminders. Going homeRead in book **Teach to avoid triggers:** overexertion, stress, **temperature extremes** (fever, hot baths, saunas, hot tubs, overheating, getting chilled), humidity, people with infections. - Energy conservation: balance rest and activity. - Know every med: dose, time, route, side effects. - Personality changes: family can agree on a signal for inappropriate behavior. - Sexual dysfunction: phosphodiesterase (PDE)-5 inhibitors (sildenafil) for men; refer to counseling or urology. - Refer to the National multiple sclerosis (MS) Society. Book · NCLEX Challenge · Select all A client was recently diagnosed with MS. Which common findings does the nurse expect? Weakness, vision changes, spasticity, and fatigue are common early. Cognitive changes come later; hallucinations aren't typical. Book · Mastery Q2 · Select all A client will start **interferon beta-1a**. What should the nurse teach? Interferon = immune suppression, subcutaneous injections, flulike aches. The pulse and confusion options belong to other MS drugs that are crossed out of your reading. Quick recall · tap to flip NCLEX Which MS client statement needs more teaching? Heat worsens MS symptoms. NCLEX A client starting interferon beta asks what to watch for. Best answer? Interferon suppresses immunity and often causes flu-like symptoms. NCLEX The family of a client with late ALS asks if he still understands them. Best response? ALS spares thinking and senses. The 60-second version ## Spinal cord injury: protect the neck, watch the blood pressure (BP), find the trigger - Trauma = **safety first**, then **airway, breathing, circulation, disability, exposure (ABCDE)**, then head-to-toe. - Open the airway with a **jaw thrust** (protects the neck). - **Neurogenic shock** = low BP + **LOW heart rate**. - **Autonomic dysreflexia** = sudden **HIGH BP** → **sit up**, check the bladder. The spinal cord is the phone line between brain and body. Cut it, and messages can't get through either way. Below the cut, the body can panic, and the brain's "calm down" message never arrives. Basics - Top causes: **car crashes** and **falls**. About **80% are men**. - **Complete** = no messages below the injury. **Incomplete** = some movement or feeling left. - **Primary injury** = the trauma: bending forward too far (hyperflexion), back too far (hyperextension), crushed downward (axial loading), twisted, or stabbed/shot. - **Secondary injury** = makes it worse: bruising, **swelling** presses on the cord → low blood flow; bleeding; neurogenic shock. Trauma steps: safety, A & B 1. **Safety first**: scene and team. **personal protective equipment (PPE) on** (gloves, gown, eye protection, mask, cap, shoe covers). 2. **Primary survey (ABCDE)**: find and fix life threats. 3. **Secondary survey**: head-to-toe exam. **A = Airway.** Suction; check for face injuries blocking it. **Protect the neck:** **jaw thrust**, not head tilt. Keep the neck straight and in line. **"C3, 4, 5 keeps the diaphragm alive."** These nerves run the breathing muscle. A high neck injury can stop breathing. **Glasgow Coma Scale (GCS) under 8 → intubate.** **B = Breathing.** Breathing isn't enough; it must be **effective**. - Weak effort (gasping, respiratory rate (RR) about 6) → **bag-valve mask**. Oxygen alone won't help. - Breathing well on their own → **non-rebreather mask**. - Check **both sides of the chest rise equally** (collapsed lung?). C, D & E **C = Circulation.** - Outside bleeding: **direct pressure**, pack the wound, **tourniquet above** it. Log roll to check the back. - Inside bleeding shows as **shock**: low blood pressure (BP), fast heart rate (HR), weak pulse. Check the belly and **pelvis**. - **Two big intravenous lines (IVs) (16-gauge)** in the inner elbows. - **No BP cuff? Feel for pulses.** Systolic is at least: **radial 80 · femoral 70 · carotid 60**. **Exception:** **massive uncontrolled bleeding** → order becomes **C-A-B**. Stop the bleeding first. **D = Disability** (quick neuro): Glasgow Coma Scale (GCS), pupils, can they feel and move all 4 limbs? **E = Exposure.** Remove clothing to see everything. - Burns: clothing can melt into skin. - **Save evidence** (weapons, rape kits) for court. - Prevent **hypothermia**: blankets, warm room, warm intravenous (IV) fluids. Cover for dignity. **Secondary survey:** head-to-toe exam, splints, dressings, **nasogastric (NG) or orogastric (OG) tube** (empties stomach), **urinary catheter** (monitors kidneys). Neurogenic shock vs. spinal shock | | Neurogenic shock | Spinal shock | | --- | --- | --- | | What | Lost "fight or flight" tone → vessels go slack | Cord's reaction to injury and **swelling** (not a true shock) | | Signs | **Low blood pressure (BP)** (SBP \<90 or mean arterial pressure (MAP) \<65) + **LOW heart rate**, low temp, abnormal rhythms | Temporary loss of movement, feeling, reflexes, and automatic functions below the injury; **limp paralysis**; bowel stops (**paralytic ileus**) | | Care | **Emergency!** Fluids, vasopressors | Usually gone within **48 hrs** as swelling goes down | **The trick:** every other shock has a **fast** heart rate. Neurogenic shock has a **slow** one. Positioning, collars & halo - **Constant, detailed** movement and feeling checks catch problems early. - Keep the body **aligned**: log roll, turning sheet, slider board. - Thoracic or lumbar injury: may wear a **brace** out of bed. - Possible neck injury: **hard cervical collar** stays on until a **specific provider order** says remove. - Cord being squeezed → **surgery**: remove blood clot, bone pieces, or object; **spinal fusion**. **Halo device** (pins in skull, ring, vest), worn **8–12 weeks**: - **Never** tighten or loosen the screws. **Never** pull on it to move them. - **Wrench taped to the vest** for emergencies (CPR). - **Pin care**: watch for redness, drainage; clean them. Prevents skull bone infection. - Check skin under the vest. Itchy? **Nothing goes inside** (like a cast). - Drinks through a **straw**. Autonomic dysreflexia: emergency A huge, uncontrolled "fight or flight" surge. Usually after the acute phase (often first seen **3–6 months** after injury). **Cause:** something irritating below the injury. Most often a **full bladder** or **constipation**. Also pressure sores, pain, a wrinkled sheet. | Sign | Why | | --- | --- | | **Sudden severe high blood pressure (BP)** | Vessels below clamp down → risk of **stroke** | | **Slow heart rate** | Body tries to lower BP | | Severe **headache**, vision changes | High BP | | **Sweating + flushing ABOVE** injury | Vessels above open up | | **Cool, pale skin BELOW** injury | Vessels below stay tight | 1. **Sit them up** (High Fowler's) right away. 2. **Find and fix the cause.** Kinked Foley? Feel for a full bladder. No catheter → insert one. Check for constipation. 3. **Call the provider.** **Nifedipine** or a nitrate as ordered. 4. Check BP every **2–5 minutes**. Body systems after spinal cord injury (SCI) | System | Watch for / do | | --- | --- | | Lungs | Secretions build up → assisted coughing, incentive spirometer | | Heart | Low blood pressure (BP), low heart rate (HR), low temp, abnormal rhythms, **dizzy when sitting up**, autonomic dysreflexia, **blood clots** (compression devices, low molecular weight heparin) | | Gut | Belly bleeding, paralytic ileus, nutrition | | Bowel/bladder | Retention or incontinence; constipation (fluids, fiber, stool softeners); may learn self-cath | | Muscles/bones | Muscle wasting, spasticity → contractures; **osteoporosis** → fractures | | Skin | Turn **every 1–2 hrs** in bed. In a wheelchair, shift weight **more than every hour** (**wheelchair push-ups**, chair pad) | | Feelings | **Anger** (don't want to depend on others), depression. Check the home for safety and equipment. | Read in book Iggy Ch. 10 (trauma), pp. 208–210 Mechanism of injury (MOI)Read in book | Type | Examples | | --- | --- | | **Blunt** | Car crash, fall, assault (fists, kicks, bat), **blast effect** from a bomb | | **Acceleration-deceleration** (a blunt type) | High-speed crash, fall from a height → tearing, shearing, compression of tissues | | **Penetrating** | Knives, ice picks, gunshot wounds (GSW), shrapnel, falling onto a sharp object | A **GSW to the chest or abdomen** or a **stab wound to the neck** automatically calls the trauma team. Safety & primary survey (book)Read in book - **Scene safety** first, in the field and the emergency department (ED). Standard Precautions every time. - personal protective equipment (PPE): impervious gown, gloves, eye protection, facemask, surgical cap; shoe covers if heavy blood loss is expected. - Resuscitation happens **at the same time** as the survey. Fix airway, breathing, circulation, disability, exposure (ABCDE) problems before lower priorities like splints and dressings. **Airway Critical Rescue:** minutes without oxygen → anoxic brain injury. Clear the airway (suction or by hand), keep the neck **neutral and in line**, use a **jaw thrust**, give O₂. - Breathing on own → **non-rebreather**. Needs help → **bag-valve mask (BVM) with 100% O₂**. - **Glasgow Coma Scale (GCS) 3–8** → endotracheal tube + ventilator. - Breathing check: breath sounds, effort, chest expansion, chest trauma. **Circulation:** - Firm **direct pressure** with thick dry dressing first. Tourniquet if pressure fails. Wound packing, hemostatic dressings. - Suspect **internal bleeding** in any shock state. - **Hypotension is a late sign**: the body's compensation is already used up. - intravenous lines (IVs): two **16-gauge antecubital**; central line or **intraosseous** if veins can't be reached. - Fluids: **lactated Ringer's or 0.9% normal saline (NS)**; hypertonic saline for head trauma. **Warm** all fluids and blood. - Blood: packed red blood cells (PRBCs), fresh frozen plasma (FFP), platelets, or whole blood. But the priority is always to **stop the bleeding**. **Disability:** **AVPU** = Alert, responds to Voice, responds to Pain, Unresponsive. **GCS** 3 (totally unresponsive) to 15 (normal). Low blood sugar, hypoxia, drugs, or alcohol can lower level of consciousness (LOC). Reassess often. **Exposure:** **cut clothing off with scissors** (fast access, avoid moving injured limbs, burned fabric stuck to skin). Preserve **evidence** (clothing, weapons, bullets, drugs) for rape, abuse, assault, homicide, overdose. Nurses may testify in court. **Hypothermia** = 96.8°F (36°C) or lower. Secondary survey & after (book)Read in book - Gastric tube (prevent vomiting and aspiration), urinary catheter (urine output), diagnostic tests, head-to-toe exam, splints, temporary dressings. - **Disposition:** straight to operating room (OR) or interventional radiology, admit, or **transfer to a trauma center**. - Then assess **psychosocial needs**: social services, rehab, pastoral care, mental health, substance use counseling. Include the family. Book · NCLEX Challenge 10.3 Which mechanism of injury does the nurse document for a client with one gunshot entry point and two stab wounds? Bullets and knives both pierce the body = penetrating trauma. Read in book Iggy Ch. 37, pp. 920–929 · crossed-out parts left out (neuro level/dermatomes, clonidine) Types & mechanisms of injuryRead in book **Complete** spinal cord injury (SCI) = no function below the injury. **Incomplete** = some function left (more common). | Mechanism | Example | | --- | --- | | **Hyperflexion** | Head snaps forward: head-on crash, diving | | **Hyperextension** | Head snaps back: rear-end crash, fall hitting the chin | | **Axial loading** | Vertical compression: diving, landing on buttocks or feet | | **Excessive rotation** | Head turned past normal range | | **Penetrating** | Knife (low speed) or gunshot (high speed) | **Secondary injury** (worsens the first): hemorrhage, ischemia, hypovolemia, low perfusion from neurogenic shock, swelling. **Top causes of death:** **pneumonia** and **septicemia**. **Leading cause:** trauma (more than 1/3 vehicle crashes); falls in older adults; violence; sports. **Prevention:** helmets and padding, seat belts, no impaired driving, water at least **9 feet deep** before diving. Assessment termsRead in book | Term | Meaning | Injury level | | --- | --- | --- | | **Tetraplegia** (quadriplegia) | Paralysis of all 4 limbs | Cervical / upper thoracic | | **Quadriparesis** | Weakness of all 4 limbs | | | **Paraplegia** | Paralysis of legs only | Lower thoracic / lumbosacral | | **Paraparesis** | Weakness of legs only | | - Reflexes: biceps **C5**, triceps **C7**, patella **L3**, ankle **S1**. Absent during spinal shock. Autonomic dysreflexia: book detailsRead in book **Box 37.2 key features:** - Sudden big rise in blood pressure (BP) **+ bradycardia** - Profuse **sweating above** the injury (face, neck, shoulders) - **Flushing above** the injury; goose bumps - **Blurred vision, spots** in the visual field - **Nasal congestion** - Severe **throbbing headache** - Feeling of apprehension **Triggers:** bladder distention, urinary tract infection (UTI), scrotal compression, constipation/impaction, hemorrhoids, pain, **tight clothing**, hard or sharp objects, temperature changes. **Box 37.3: what to do** 1. **Sit them up** (first priority). 2. Check the bladder: retention, catheter **kinks**. No catheter → check for distention and catheterize (anesthetic ointment on the tip). 3. Check for UTI or bladder stones. 4. Check for **fecal impaction** using anesthetic ointment. 5. Check skin for pressure injuries. 6. BP every **10–15 minutes**. 7. **Nifedipine** or a nitrate as ordered. Lecture said BP every 2–5 min; the book says 10–15 min. Go with your instructor on exams, but know both. Airway & breathing (book)Read in book **Airway is the priority** for cervical spinal cord injury (SCI). Injuries at or above **T6**: risk of respiratory distress and **pulmonary embolism (PE) in the first 5 days**. - Breath sounds every **2–4 hrs** the first few days. Act if **oxygen saturation (SpO₂) drops below 95%**. - Incentive spirometer; suction as needed. - **Cough assist** ("quad cough"): hands on the upper abdomen below the ribs; push **inward and upward** as the patient coughs. Neurogenic shock: book detailsRead in book Usually within **24 hrs**, in injuries **above T6**. **Critical Rescue (check at least hourly):** warm, flushed skin (temp dysregulation) · symptomatic bradycardia · ↓level of consciousness (LOC) · ↓urine output · systolic blood pressure (SBP) \<90 or mean arterial pressure (MAP) \<65 → Rapid Response. - intravenous (IV) and oral fluids. **Dextran** (plasma expander). - **Atropine** if heart rate (HR) drops below 50–60. - Severe hypotension: IV vasopressors (phenylephrine, dopamine). Collar, surgery & halo (book)Read in book - Hard collar (**Miami J, Philadelphia**) until an order says remove. Pad pressure points, especially the **back of the head**. - Keep alignment; **log roll**. - After spinal fusion: neuro checks + vital signs (VS) **every hour for 4–6 hrs**, then every 4 hrs. - Thoracic/lumbar fusion: Harrington rods, molded plastic brace. **Halo:** 4 pins into the skull, worn **6–12 weeks** (lecture said 8–12). **Halo Action Alert:** never move the patient by the halo · never adjust screws · **one finger** should fit between the jacket and skin · **wrench taped to the vest** · nothing sharp under the vest · pin care per policy. Report fever or pus from pins. Serious complications: **osteomyelitis of the skull**, subdural abscess. Meds for spinal cord injury (SCI)Read in book | Drug | Why | | --- | --- | | **Pantoprazole** (PPI) | Prevent **stress ulcers** | | Anticoagulant (LMWH) | Prevent venous thromboembolism (VTE) | | Bulk laxatives, stool softeners | Prevent constipation | | Celecoxib | Prevent heterotopic ossification (↑myocardial infarction (MI) and stroke risk) | | Calcium, bisphosphonates | Prevent osteoporosis | | **Intrathecal baclofen (ITB)** | Spasticity. Sedation, fatigue, headache, hypotension. **Never stop suddenly** → seizures, hallucinations. | Long-term complicationsRead in book - **Paralytic ileus** within **72 hrs**; check bowel sounds. Stress ulcers. - **Heterotopic ossification (HO)**: bony overgrowth into muscle. Not visible on x-ray for several weeks. - Pressure injuries, venous thromboembolism (VTE), osteoporosis → fractures, contractures (splints, range of motion (ROM)). - **Orthostatic hypotension**: change position slowly. - Transfers: paraplegic patients often transfer alone; tetraplegic may use a **sliding board**. | Lesion | Bowel/bladder | Care | | --- | --- | --- | | **Upper motor neuron** (cervical, high thoracic) | **Spastic**; reflex emptying still works | Bladder/bowel training; rectal suppositories | | **Lower motor neuron** (lower thoracic, lumbosacral) | **Flaccid**; no reflex | Intermittent catheterization; manual disimpaction | All: **1.5–2 L fluid a day** + stool softeners. Psychosocial, sexuality & rehabRead in book - Often **young men**; may feel guilt (diving, racing). Many veterans (blast injuries). - Be realistic but offer hope. - Men with injuries **above T6** may have reflex erections. A vasodilator before sex can prevent autonomic dysreflexia (AD). - Women can still become pregnant. - Rehab goal: **live independently**. Functional electrical stimulation (FES), exoskeletons. - Older adults with spinal cord injury (SCI): vaccines (respiratory infections are the top cause of death), osteoporosis prevention, skin care. Book · NCLEX Challenge A client with a recent **T1** spinal cord injury (SCI) is flushed and sweating on the face and neck and reports "seeing spots." Which action first? Autonomic dysreflexia. Sitting up lowers blood pressure (BP) immediately. Then find the cause. Book · NCLEX Challenge 37.3 A client with SCI is in a halo fixator with vest. Which action is **most important** for safety? The wrench lets staff remove the vest fast for cardiopulmonary resuscitation (CPR). That's life-saving; the others are routine care. Book · Mastery Q1 A client with a **C6** fracture just got a halo device. Which statement needs **immediate** follow-up? A **new** change in sensation moving upward = possible worsening cord injury. Numb feet were already there. Book · NGN Challenge 37.1 (C7 SCI, halo + vest) **Case:** 21-year-old, C7 SCI. At 1435: new throbbing frontal headache, blurred vision, very sleepy, face and neck flushed with sweating. T 99°F, **heart rate (HR) 58**, **BP 184/95**, oxygen saturation (SpO₂) 95%. Foley draining. At 1450: BP 192/98, headache 8/10. Review class: spinal shock, autonomic dysreflexia, trauma priority Review class From the in-class exam review (Joline case study + NCLEX questions). - **Spinal shock:** swelling right after the injury knocks out movement, feeling, and reflexes. It does **not** mean permanent paralysis. The injury **can't be classified until spinal shock resolves** (about **48 hours**). - **Spinal shock is over when** things come back: they can urinate, reflexes return, they feel an itch or pain, they can move. - **Autonomic dysreflexia:** blood pressure shoots up + pounding headache. Caused by any irritating stimulus. Even a **fan's cool breeze** can trigger it. Find and remove the cause. - **Trauma (Ch. 10 pages):** normally airway, breathing, circulation, disability, exposure (ABCDE), but **massive uncontrolled external bleeding comes first**. No airway will help if they bleed out. Exception to the rule. Quick recall · tap to flip NCLEX A client with a T4 injury suddenly has BP 210/110, HR 48, a pounding headache, and a flushed face. First action? Autonomic dysreflexia. Sitting up lowers BP right away. Then check the bladder. NCLEX Which vital signs suggest neurogenic shock? Low BP with a LOW heart rate. Low BP + fast HR points to bleeding (hypovolemic shock). NCLEX A trauma client is gasping with a respiratory rate of 6. Priority? Weak breathing needs breaths given. Oxygen alone won't help. NCLEX A client in a halo vest says the skin under it itches. Best response? Nothing inside the vest. Never touch the screws or pull on the frame. The 60-second version ## Back pain: mostly a squished disc pressing a nerve - **Neck** and **low back** get hurt most (most flexible parts). - #1 cause of **workplace injury**. Protect your own back! - Comfort: **Williams position**, heat or ice, nonsteroidal anti-inflammatory drugs (NSAIDs). - After back surgery: **cerebrospinal fluid (CSF) leak** = lower head of bed (HOB), call. Must **void** before going home. - After neck surgery: **airway first**. A disc is a jelly donut between two bones. Squeeze it wrong and the jelly (nucleus pulposus) leaks out and presses on the nerve next to it. Protect your own back - **Bend at the knees**, not the back. - **Raise the bed** when repositioning a patient or giving a 2–3 minute intravenous (IV) push. - Good posture, proper shoes, weight control, ergonomics. - Use **ceiling lifts** and get help. No equipment? **Advocate** for it. Disc problems & nerve pain - Disc's jelly center = **shock absorber**. - **Bulging** disc = pushes out. **Herniated** disc = **much worse**, the wall breaks open. - Pressure on a nerve → **burning or stabbing** pain, spasms, numbness, tingling. - Low back → pain down the **leg** (sciatic nerve). Neck → pain down the **arm**. - Big herniation can press on the **spinal cord** → leg/arm weakness, bladder or bowel problems. - **Spinal stenosis** = narrowed spinal canal (from a disc, arthritis, infection, trauma, swelling). Tests | Test | Shows | | --- | --- | | **magnetic resonance imaging (MRI)** | Cord, bones, discs, and **nerve root compression** | | **electromyography (EMG)** | Needle in the muscle checks its electrical activity → nerve damage | | **Nerve conduction study** | **How fast** nerves send signals | Comfort & meds - **Williams position**: semi-Fowler's with a **pillow under the knees**. A recliner works too. - **Firm mattress.** Change positions often. - **Moist heat or ice: 20–30 min, 4 times a day** (whichever works for them). - physical therapy (PT), weight control, massage, chiropractor, acupuncture, **transcutaneous electrical nerve stimulation (TENS) unit**. | Med | Know this | | --- | --- | | **nonsteroidal anti-inflammatory drugs (NSAIDs)** (first choice) | Block prostaglandins (inflammation). Side effect: **gastrointestinal (GI) upset**. Adverse: **bleeding**. | | **Muscle relaxants** (baclofen, cyclobenzaprine) | **Drowsiness, fatigue** | | **Gabapentin** | Anti-seizure drug used for nerve pain | | **Tramadol (Ultram)** | If an opioid is needed: least potent, low dependency | | **Epidural injection** | Steroid + numbing med | Surgery | Minimally invasive | Open | | --- | --- | | Scope removes the piece pressing the nerve. Less pain and blood loss. **Home same or next day**. Walk daily. | Bigger incision. Used when the **spinal cord is compressed**. | - **Discectomy** = remove disc. **Laminectomy** = remove part of a vertebra. - Spine unstable → **spinal fusion**, often with bone from the **hip** → 2 painful sites that can get infected. After open back surgery - Vitals + neuro checks **every hour for 4–6 hrs**, then every 4 hrs. - Watch for fever, low blood pressure (BP), fast heart rate (HR). **cerebrospinal fluid (CSF) leak:** clear drainage, a **"halo"** ring on the dressing, bulging at the incision, or a sudden headache → **lower the head of the bed** and **call the provider**. - Check for a **hematoma**. Check the hip donor site. - Patient **must void before discharge**. - Turn **as a unit** (log roll). **No twisting. No overhead trapeze.** Neck (cervical) surgery - **Front of the neck** (anterior) is most common. Back (posterior) = more pain. **Priority = airway.** Swelling can press on the windpipe. Check **swallowing** and **hoarseness**. Read in book Iggy Ch. 37, pp. 929–937 · crossed-out parts left out (muscle relaxant list, ziconotide, failed back surgery syndrome) Nonsurgical care (book pp. 932–933)Read in book - **Non-drug measures come first.** A short period of bed rest with **heat** may help; heat gives short-term relief. - Start stretching and **resume normal activity as soon as possible**. Aerobic exercise has good evidence. - **Change position often**: long standing, sitting, or lying increases pain. Shoe insoles or floor pads can help. - **Williams position** for acute low back pain from a bulging or herniated disc. - Reassure patients: many fear the pain won't go away. Most won't have another episode with good care. - Chronic pain: stress reduction, mindfulness, progressive muscle relaxation, yoga. **cognitive behavioral therapy (CBT) + physical therapy (PT)** helps pain lasting over 12 months. - **McKenzie exercises** (extension and flexion) move pain toward the center of the back. Start only **after acute pain eases**. Water therapy builds muscle without strain. - **Weight loss** if more than 10% over ideal weight. Meds & muscle relaxant alert (book)Read in book - **nonsteroidal anti-inflammatory drugs (NSAIDs)** (aspirin, ibuprofen, naproxen) help. - Antidepressants and gabapentin are often prescribed, but national guidelines **don't recommend them** for low back pain (antidepressants OK if the patient is also depressed). - Opioids: very limited role, used sparingly and short-term for acute pain. - Topical **capsaicin**: short-term relief. Lidocaine patches: no real benefit. - **Ziconotide**: strong analgesic for severe persistent pain. **Drug Alert:** centrally acting muscle relaxants cause **sedation, dizziness, lightheadedness** and anticholinergic effects (dry mouth, urinary retention, blurred vision, constipation, tachycardia). **Avoid in older adults** (falls). No driving, alcohol, or other central nervous system (CNS) depressants. **Metaxalone** can damage the liver. Surgery details (book)Read in book Done when conservative care fails or **neuro deficits keep getting worse**. minimally invasive surgery (MIS) isn't used if the disc presses on the spinal cord. **Pre-op teaching:** getting in and out of bed, turning, **report new numbness, tingling, or weakness** in the legs, home restrictions. | Minimally invasive | Open | | --- | --- | | **Microdiskectomy** (1-inch incision, endoscope) · **PED** (percutaneous endoscopic diskectomy, may add laser) · **Laser-assisted laparoscopic** (belly-button incision; bulging discs only; risks: infection, nerve root injury) · robot-assisted. Home same day or in 23–48 hrs. | **Diskectomy** (remove disc) · **laminectomy** (remove part of the lamina) · **spinal fusion** (bone graft, metal rods/screws) · interbody cage fusion (titanium mesh) · artificial disc. Pain control may use intrathecal or epidural patient-controlled analgesia (PCA). | **Open-surgery complications:** nerve injury, **diskitis** (disc inflammation), **dural tears**. - Book: vital signs (VS) **at least every 4 hrs for 24 hrs** (fever, hypotension, severe pain); neuro checks every 4 hrs (movement, strength, sensation in legs). - Check ability to **void after catheter removal**. Pain and lying flat make voiding hard, **especially for men**. Lecture said VS every hour for the first 4–6 hrs, then every 4 hrs. The book only says "at least every 4 hrs." Use your instructor's version for exams. Causes & risk factorsRead in book - Muscle strain or spasm, ligament sprain, disk degeneration, **herniated nucleus pulposus (HNP)**. - **Spinal stenosis**: narrowing of the spinal canal, usually over age 50. - Most common in ages 30–60; women a bit more than men. - Risks: heavy lifting, falls, crashes, repetitive bending and twisting, **obesity**, **smoking** (less blood flow to disks), scoliosis. - Older adults: osteoporosis, vertebral fractures, arthritis. Prevention (Box 37.5)Read in book - Safe lifting; ask for help with heavy chores. - Regular exercise: swimming, walking, back strengthening. - No high heels; good posture; footstool and ergonomic chairs. - Avoid prolonged sitting or standing. - Weight within **10% of ideal**. Enough calcium and vitamin D. - **Stop smoking.** **Nurses:** avoid lifting patients by hand. Use the lift equipment. AssessmentRead in book - Main complaint: **continuous pain**. Stiff, flexed posture; limp; can't bend. - **Sciatic pain:** sharp, burning down the back of the thigh or calf, maybe to the ankle or toes. Worse with **sneezing, coughing, straining**. - Raising the straight leg causes severe pain (nerve compression). - Check both legs for sensation (cotton ball, paper clip) and strength. - Ask about **bladder or bowel changes** (new incontinence or retention). - Ask about sadness and suicidal thoughts with persistent pain. - Tests: imaging only if severe; **electromyography (EMG)** and nerve conduction studies. Treatment & meds (slides)Slides **Diagnosis:** magnetic resonance imaging (MRI), electromyography (EMG), nerve conduction study. **Interventions:** positioning · moist heat or cold · physical therapy · weight control · complementary therapies · meds (NSAIDs, muscle relaxants, gabapentin, tramadol, epidural injection). | Class | Examples | | --- | --- | | **NSAIDs** (block prostaglandins → less inflammation and nerve sensitivity) | over-the-counter (OTC): aspirin, ibuprofen (Advil, Motrin), naproxen (Aleve). Rx: **celecoxib** (Celebrex), **meloxicam** (Mobic) | | **Muscle relaxants** | Baclofen, **cyclobenzaprine** (Flexeril), tizanidine (Zanaflex), methocarbamol (Robaxin) | **Surgery:** minimally invasive (microscopic or endoscopic discectomy: shorter stay, less blood loss and pain) or open (**discectomy, laminectomy, spinal fusion**). **Post-op (slide):** vital signs (VS) **hourly for 4–6 hrs**, then every 4 hrs (fever, ↓blood pressure (BP), tachycardia) · neuro checks (movement, strength, sensation) · cerebrospinal fluid (CSF) leak signs → **head of bed (HOB) flat** and call the provider · ability to void · log roll · pain control. After lumbar surgery (Table 37.2)Read in book | Complication | Watch for / do | | --- | --- | | **cerebrospinal fluid (CSF) leak** | Clear fluid on dressing; "halo" ring. **Lay flat**, report to surgeon now. | | Fluid deficit | I&O, hypotension, tachycardia | | **Urinary retention** | Get them to the bathroom early; men may stand to void | | Paralytic ileus | Flatus or stool, distention, N/V | | Fat embolism | Chest pain, dyspnea, anxiety, confusion; **petechiae** on neck, chest, mouth | | Nerve root pain | Pain not relieved by meds | | Infection | Temp spike after **day 2** post-op | **Critical Rescue:** a sudden headache + clear drainage = possible CSF leak. Keep on bed rest, lower the head of the bed, report right away. Bulging at the incision = CSF leak or hematoma. - **Log roll every 2 hrs**. **No overhead trapeze** (strains the back). - Sit in a straight-back chair, feet flat. - venous thromboembolism (VTE) prevention: early mobility, compression devices, anticoagulant. **Home (first 4–6 weeks):** limit stairs and driving · lift nothing over **5 lb** · no bending or twisting · walk daily. Clear drainage from incision → call the surgeon. **Spinal cord stimulation** may help persistent pain: check neuro status below the device and make sure they can void. Cervical neck painRead in book - Usually a herniated disk at **C5–C6** or **C6–C7**. - Pain radiates to the shoulder and arm with numbness or tingling; may disrupt sleep. - Conservative care: exercises (shoulder shrugs, squeezes); soft collar at night, **no longer than \~10 days**. - Surgery: anterior cervical discectomy and fusion (ACDF) (fusion with bone graft) or newer anterior interbody cervical fusion (AICF)/lateral interbody cervical fusion (LICF) (titanium device; shorter recovery). Collar for 2–3 weeks after ACDF. **After ACDF, priority = airway.** Neck swelling can narrow the trachea; the surgery can affect swallowing. Check **swallowing** and breathing; keep suction ready; sit upright; report changes now. **Box 37.6 discharge:** someone stays with them the first few days · no lifting · no driving until cleared · walk daily · call if pain, numbness, or swallowing get worse. Book · Mastery Q3 · Select all A nurse teaches a community group about preventing back injury. Which recommendations are correct? Log rolling is post-op care, not prevention. Everything else is in Box 37.5. Review class: after disc surgery Review class From the in-class exam review (Joline case study + NCLEX questions). - **Distended bladder = urinary retention** → possible spinal nerve damage. Priority finding. - **Reposition every 2 hours** (not every 4). - **Nothing by mouth (NPO) is based on sedation / gag reflex return**, not on whether they've voided or have nausea. - An indwelling catheter, echo, or dietary assessment isn't needed unless the story gives a reason. Quick recall · tap to flip NCLEX Best position for a client with low back pain? Bent knees take pressure off the nerve and relax back muscles. NCLEX After lumbar fusion, a client wants to use the overhead trapeze. Best response? No twisting after back surgery. NCLEX After a laminectomy, the dressing has a clear ring around blood and the client has a sudden headache. First action? Halo sign + headache = possible CSF leak. The 60-second version ## Problems in the wires outside the brain and cord - **Myasthenia gravis**: muscles get weak with use. Keep meds with them always. - **Peripheral nerve injury**: protect the numb area. - **Trigeminal neuralgia (CN V)**: lightning-bolt face pain. - **Bell's palsy (CN VII)**: one side of the face droops. Protect the eye. **Cranial nerves:** your instructor said **don't memorize all 12**. Know V (trigeminal) and VII (facial), plus the swallowing nerves **IX (glossopharyngeal) and X (vagus)** from the stroke lecture. Myasthenia gravis: what it is Acetylcholine is a key. The muscle has locks. In myasthenia gravis (MG), the immune system jams the locks, so the key can't make the muscle move. - **Autoimmune.** Attacks **acetylcholine receptors** where nerve meets muscle. - **Extreme fatigue**; muscles weaken very easily. - First: **eyes** (droopy eyelid = ptosis, double vision). Then **face**: hard to smile, chew, swallow, shave, brush teeth. - Advanced: all muscles, including bowel, bladder, and **breathing**. Edrophonium test & pyridostigmine **Edrophonium (Tensilon) test:** gives more acetylcholine. myasthenia gravis (MG) → muscles improve **within 1 minute**, lasting 4–5 min. **Can cause serious bradycardia.** **Atropine** (the antidote) must be at the bedside. **Pyridostigmine:** keeps more acetylcholine around. Controls symptoms; **doesn't cure**. - Dose can change day to day (weaker days = higher dose). - **Eat 45–60 min after** the dose: muscles strongest → **no aspiration**. Myasthenic vs. cholinergic crisis | | Myasthenic crisis | Cholinergic crisis | | --- | --- | --- | | Cause | **Not enough** medicine | **Too much** medicine | | Edrophonium test | Muscles **improve** | No improvement; may get **weaker** | | Clue | Worsening weakness, **breathing trouble** (may need ventilator) | **Extra secretions**: drooling, sweating, lung secretions | | Treat | More medicine | **Atropine** | Memory trick: **cholinergic = "too much choline" = too much fluid pouring out** (spit, sweat, secretions). Other myasthenia gravis (MG) treatments - **Steroids** (calm the immune system). - **Plasmapheresis & intravenous immunoglobulin (IVIG)**: **short-term only**, for emergencies like breathing distress. Work fast; last weeks to a couple of months. - **Plasmapheresis** = filters out the plasma carrying the bad antibodies; returns the blood cells. Watch for: **low blood pressure (BP)** (fluid loss), **electrolyte imbalance**, **hypothermia**, **access-site infection**. - **IVIG** = donor antibodies that block the bad antibodies. - **Thymectomy** = remove the thymus. MG is linked to a thymus tumor, and the bad antibodies are made there. myasthenia gravis (MG) nursing care - **Breathing support** first. - Plan activities around **peak medicine times**. - Keep pyridostigmine **with them always**: nightstand, car, work. - **Rest is essential.** Repetitive movement can trigger a myasthenic crisis. - Help with communication and nutrition (weak face muscles). - **Eye protection** at night (eyes may not close); **artificial tears** during the day. Peripheral nerve injury From a cut, burn, crush, stretch, and more. The nerve past the injury dies back → weakness, limp paralysis, burning, numbness. - Both nerve ends try to grow back together. **Lined up** → normal function. **Not lined up** → weakness, spasms, less feeling. - **Infection** or **older age** slows healing. - Some function can return early through **backup (collateral) nerves**. - Treatment: **splint or cast** to rest it; surgery to realign the ends. **Teach:** they can't feel the area well → **protect it**. Cover it in cold and heat. Keep skin moisturized. Trigeminal neuralgia (CN V) Irritated **cranial nerve 5** (one on each side of the face) → **one-sided**, excruciating, sharp, shooting bursts of pain. - Triggers: touch, chewing, **brushing teeth**, even **smiling**. Patients start avoiding these things. **Priority = pain management.** 1. **Antiepileptics**: carbamazepine (Tegretol), gabapentin, pregabalin. 2. **Nerve block.** 3. **Surgery** (see below). - **Rhizotomy**: heated needle destroys nerve fibers → that side is **permanently numb**. Teach to **look for injuries** (poked eye, cavity) they can't feel. - **Microvascular decompression**: moves an artery pressing on the nerve. More serious: needs a **craniotomy**. Bell's palsy (CN VII) Sudden paralysis of the **facial nerve (CN 7)**, triggered by the **herpes simplex virus** waking up (infection, cold exposure). - **One side** of the face: can't close the eye, smile, or wrinkle the forehead. Taste is affected. - Can hurt **body image**. - **Antivirals**: acyclovir, valacyclovir. - **Protect the eye** (can't blink or close it). - Nutrition, massage, warm moist heat, facial exercises, emotional support. - Most recover fully in **weeks to months**; a few keep some weakness. Review class: myasthenia gravis + trigeminal neuralgia Review class From the in-class exam review (Joline case study + NCLEX questions). **Pyridostigmine**: **cholinesterase inhibitor** for **myasthenia gravis**. Keeps more acetylcholine around so nerve signals reach the muscles. - **Never miss a dose.** - **Take it so it peaks before activities that need energy**, like **eating**. Eating at a low level → weak swallow → **aspiration**. - **Dose changes daily** based on symptoms and energy (like sliding-scale insulin). Exception to the rule! | Myasthenic crisis | Cholinergic crisis | | --- | --- | | **Not enough** pyridostigmine → weakness, poor oxygenation | **Too much** pyridostigmine ("cholin-" is in the name) | - **Plasmapheresis** (myasthenia gravis treatment) risks: fluid and electrolyte loss, blood pressure changes, site infection. - **Trigeminal neuralgia:** brushing teeth or shaving triggers intense pain, so patients may stop doing them. Address hygiene. Quick recall · tap to flip NCLEX A client with myasthenia gravis (MG) has severe weakness, drooling, sweating, and heavy lung secretions after extra pyridostigmine. The nurse suspects: Too much medicine → too much acetylcholine → secretions. Atropine reverses it. NCLEX Most important teaching for an MG client going home on pyridostigmine? Weakness can hit anytime. Eat 45–60 min after the dose, and rest often. NCLEX Priority teaching for a client with Bell's palsy? The eye can't close, so it can dry out and get hurt. NCLEX A client with a nerve injury to the hand is going outside in winter. Best teaching? Decreased sensation means they can't sense cold or heat injury. Cover it and keep skin hydrated. The 60-second version ## Every med from your lectures & slides, in one place - Only meds your instructor mentioned (no book-only drugs). - **★** = your instructor stressed it most. - Learn the **one big safety point** for each, not every detail. Think of each drug as having one "headline." Sinemet: no protein. Phenytoin: gums. Pyridostigmine: eat 45–60 min later. Mannitol: hourly urine. Migraine | Drug | Know this | | --- | --- | | Acetaminophen, nonsteroidal anti-inflammatory drugs (NSAIDs) (ibuprofen, naproxen), over-the-counter (OTC) + **caffeine** (Excedrin) | First try. Caffeine narrows vessels. Take at first sign/aura. | | **★ Triptans**: sumatriptan (Imitrex), rizatriptan (Maxalt) | Activate serotonin → narrow vessels. **NO** with heart disease, hypertension (HTN), **peripheral vascular disease (PVD)**. Report **chest pain**. No selective serotonin reuptake inhibitors (SSRIs) or St. John's wort (serotonin syndrome). | | Lasmiditan | Doesn't narrow body vessels. Causes sedation, dizziness. | | Prevention: NSAIDs, **beta blockers**, **topiramate** | For frequent or severe migraines | **Rebound headache** = taking meds too often or too much. Seizures | Drug | Know this | | --- | --- | | **★ Phenytoin (Dilantin)** | **Gingival hyperplasia** → soft toothbrush, dentist | | Carbamazepine (Tegretol), valproic acid (Depakote), topiramate (Topamax) | Same class rules below | **All anti-seizure meds:** drowsiness · depression/**suicidal thoughts** · liver damage · low white blood cells (WBCs) · **blood levels** (narrow range) · **never stop suddenly** (status epilepticus) · pregnancy category D · birth control less effective (use 2nd method) · watch **warfarin** · no **grapefruit**. **Status epilepticus:** 1. **★ Lorazepam (Ativan)** or diazepam (Valium) intravenous (IV) → **stops** the seizure 2. **Fosphenytoin** (preferred, safer) or phenytoin → **prevents** the next one Meningitis - **Broad-spectrum antibiotic** right away (after blood cultures) if ↑intracranial pressure (ICP) signs. Switch to **narrow-spectrum** once the germ is known. - **Vaccines**: meningococcal (age 11–12, booster 16), flu, pneumonia. Parkinson's | Drug | Know this | | --- | --- | | **★ Carbidopa-levodopa (Sinemet)** | Replaces dopamine. Nausea → take with **carbs, NOT protein**. Long-term: dyskinesia, "on-off." | | Dopamine agonists | **Impulse control** problems (gambling). Not for older adults. | **Tolerance** (stops working) or **toxicity** (delirium) → lower dose, change meds, or **drug holiday** (1 week–10 days). multiple sclerosis (MS) (only 2 to know) | Drug | Know this | | --- | --- | | **★ Interferon beta** | Shot under the skin. **Infection risk**, bone marrow suppression, **flu-like symptoms** | | **★ Glatiramer** | Shot under the skin. Fewer side effects | Both slow the disease and make attacks fewer and milder. **No cure.** Spinal cord injury - **Nifedipine** or a nitrate → autonomic dysreflexia (after sitting up and fixing the cause). - **Fluids, vasopressors** → neurogenic shock. - **Low molecular weight heparin** → prevent blood clots. - **Stool softeners** → constipation. Back & neck pain | Drug | Know this | | --- | --- | | **nonsteroidal anti-inflammatory drugs (NSAIDs)** (first choice): aspirin, ibuprofen (Advil, Motrin), naproxen (Aleve), celecoxib (Celebrex), meloxicam (Mobic) | Block prostaglandins. Side effect: **gastrointestinal (GI) upset**. Adverse: **bleeding** | | **Muscle relaxants**: baclofen, cyclobenzaprine (Flexeril), tizanidine (Zanaflex), methocarbamol (Robaxin) | **Drowsiness**, fatigue (act on central nervous system (CNS)) | | Gabapentin | Anti-seizure drug for **nerve pain** | | **★ Tramadol (Ultram)** | If an opioid is needed: least potent, low dependency | | Epidural injection | Steroid + numbing med | Myasthenia gravis | Drug | Know this | | --- | --- | | **★ Pyridostigmine** | Keeps more acetylcholine (ACh) around. **Eat 45–60 min after** (no aspiration). **Carry it always.** Dose changes daily. | | Edrophonium (Tensilon) | **Test** drug. myasthenia gravis (MG) improves within 1 min. Can cause **bradycardia**. | | **★ Atropine** | Antidote for edrophonium; treats **cholinergic crisis**. Keep at bedside. | | Corticosteroids, intravenous immunoglobulin (IVIG) | Calm the immune system; IVIG is short-term for crises | **Too little med** = myasthenic crisis. **Too much** = cholinergic crisis (secretions). Trigeminal neuralgia & Bell's palsy - **Trigeminal**: carbamazepine (Tegretol), gabapentin (Neurontin), pregabalin (Lyrica); nerve block. - **Bell's palsy**: antivirals **acyclovir**, **valacyclovir** (HSV-1). Stroke & transient ischemic attack (TIA) | Drug | Know this | | --- | --- | | **★ tissue plasminogen activator (tPA) (alteplase)** | Ischemic only. Within **3 (up to 4.5) hrs** of symptom onset. **computed tomography (CT) first.** Bleeding risk. Repeat CT after. | | **Antiplatelets**: aspirin, clopidogrel | Prevent clots. Both together = dual antiplatelet therapy | | **Anticoagulants**: heparin, warfarin, direct oral anticoagulants (DOACs) | For **A-fib** | | Aspirin 325 mg | 24–48 hrs after stroke. **Not within 24 hrs of tPA** | | Statin | Must be discharged on one (core measure) | | Enoxaparin / heparin | Prevent blood clots | | Anti-seizure meds | Hemorrhagic stroke (seizure ↑intracranial pressure (ICP)) | Head injury & intracranial pressure (ICP) | Drug | Know this | | --- | --- | | **★ Mannitol** | Pulls water out of the brain. Osmolality goal **310–320**. **Hourly urine** (Foley). Watch dehydration, electrolytes, kidney injury. | | Furosemide | Given with mannitol; removes fluid from the body | | Hypertonic saline (3% or 5%) | Works like mannitol. intensive care unit (ICU) only | | Acetaminophen | Concussion pain. **No nonsteroidal anti-inflammatory drugs (NSAIDs)** (bleeding) | Dialysis (kidney lecture) - **Hold** antihypertensives and antidysrhythmics until after (low blood pressure (BP)). - **Give after**: antibiotics, anticonvulsants, vitamins (dialyzed out). - **Heparin** during dialysis lasts **4–6 hrs**. Antidote: **protamine sulfate**. Review class: med "exceptions" she stressed Review class From the in-class exam review (Joline case study + NCLEX questions). - **Mannitol:** filter needle; dose by serum osmolality (goal 310–320); intake and output (I&O); sodium, potassium. - **Propranolol** prevents migraine; **triptans** abort it (avoid with hypertension, peripheral vascular disease, angina, selective serotonin reuptake inhibitors (SSRIs)). - **Diazepam/lorazepam** stop status epilepticus; **phenytoin/fosphenytoin** only prevent future seizures. - **Ropinirole**: careful in older adults (orthostatic hypotension). **Carbidopa-levodopa**: with food, not protein. - **Pyridostigmine**: don't miss doses, take before eating, dose changes daily. Quick recall · tap to flip NCLEX Which med should the nurse hold before a client's dialysis? Antihypertensives wait until after dialysis (low blood pressure (BP) risk). NCLEX A client on phenytoin says, "I feel fine, so I stopped my pills." Priority concern? Stopping anti-seizure meds suddenly can trigger status epilepticus. NCLEX Which client should NOT get sumatriptan? Triptans narrow vessels everywhere. NCLEX A client on a dopamine agonist starts gambling heavily. The nurse: Impulse control problems are a known adverse effect. The 60-second version ## Dialysis = an artificial kidney - Started based on **symptoms**, not lab numbers. - **Fistula/graft arm:** feel the **thrill**, hear the **bruit**. No blood pressure (BP), intravenous lines (IVs), or sticks in that arm. - **Hold** antihypertensives and dialyzable meds until **after** dialysis. - After: watch for **low BP** and **bleeding** (heparin lasts 4–6 hrs). - Peritoneal dialysis: biggest risk = **peritonitis**. The dialyzer is a coffee filter. Blood flows on one side, a clean solution (dialysate) on the other. Waste and extra fluid pass through the filter and get thrown away. **Note:** this is renal (kidney) content from a different lecture. It's here because you asked to add it. What dialysis is - **Kidney replacement therapy** = umbrella term for **dialysis or transplant**. Those are the only 2 options. - Used when kidneys fail (acute or chronic) to remove extra **fluid and waste**. - Blood passes through an artificial **semipermeable membrane** in the **dialyzer** (artificial kidney). - **Dialysate** = solution that looks like plasma. Fixes electrolytes and acid-base balance. Pause activity: added vs. removed during dialysis. The answer slide wasn't in your transcript; standard answer: **removed** = urea (BUN), creatinine, potassium, uric acid, extra fluid; **added** = bicarbonate (fixes acidosis). Check against your slide. When to start dialysis - Based on **signs and symptoms**, NOT labs (BUN, creatinine, glomerular filtration rate (GFR)). - chronic kidney disease (CKD): started when **uremic** symptoms appear. **Emergency dialysis:** - **Pulmonary edema** - Severe electrolyte or acid-base imbalance, e.g., **hyperkalemia with electrocardiogram (EKG) changes** - **Pericarditis** Pause question: why does pericarditis need emergency dialysis? Standard answer: it's caused by **uremic toxins** irritating the heart sac. Fluid can build up around the heart → **cardiac tamponade**. Dialysis removes the toxins. Check against your slide. Intermittent vs. continuous | | Intermittent hemodialysis | Continuous (CRRT) | | --- | --- | --- | | Schedule | **3×/week, 4 hrs** each | Over **24 hrs** | | Flow | \~300–500 mL/min → **big fluid shifts**, blood pressure (BP) changes | Only 10–80 mL/min (gentler) | | Who | Stable patients | **Unstable** (heart problems) · **intensive care unit (ICU) only** | | Also called | — | Hemofiltration, ultrafiltration | Access: dialysis catheter Regular veins can't handle the high flow, so special access is needed. - **Short-term** (a few sessions or weeks). - Tip in the **superior vena cava** (just above the right atrium); 2 ports: one out to the machine, one back. - Watch for **infection and bleeding** at the site. - **Sterile** dressing changes by the **dialysis nurse only**, not floor nurses. **Dialysis only.** Nothing else goes through it: no intravenous (IV) fluids, no meds. Access: arteriovenous (AV) fistula or graft - **Long-term** dialysis. - **Fistula** = artery and vein sewn together in the arm. **Graft** = synthetic tube connects them. - Needs time to **mature** (fistula \~**12 weeks**). Meanwhile, a catheter is used, so a patient may have **both**. **"Feel the thrill, hear the bruit."** **Thrill** = palpate (buzzing). **Bruit** = auscultate (whooshing, like a loud murmur). Check and document **every 4 hrs**. Also check circulation below the site to the fingertips. **Protect the arm (keep it from clotting):** - **No intravenous lines (IVs), no blood pressure (BP), no compression** on that arm. - No carrying heavy things with it. - Don't sleep on it. Caring for patients after hemodialysis **Meds:** - Most meds are **dialyzable** (removed by dialysis). Give **antibiotics, anticonvulsants, vitamins AFTER**. - **Hold antihypertensives and antidysrhythmics** until after (dialysis already drops blood pressure (BP)). - **Heparin** is used during dialysis and stays active **4–6 hrs** → **no invasive procedures**, watch for bleeding. Antidote = **protamine sulfate**. **Vital signs** for several hours: - **Hypotension** is the big risk. - Slightly **warm** temp is normal (dialysate is warmed: prevents hypothermia, vasodilation speeds toxin removal). **Ongoing fever** → infection or **sepsis**. **Weights** before and after. After = **dry weight**. **1 kg = 1 L** of fluid. Peritoneal dialysis (PD) The **peritoneum** (belly lining) is the filter. Done at home; more freedom (even on vacation). **Won't work** with belly scarring or adhesions from past surgery. 1. **Infuse**: 1–2 L dialysate flows in by gravity. 2. **Dwell**: stays 4–8 hrs. Patient disconnects and walks around. Extra weight can cause **back pain**. 3. **Drain**: fluid flows out by gravity into a bag. Outflow = **effluent**. Types: continuous ambulatory (CAPD), small machines, or overnight while sleeping. Depends on needs and insurance. peritoneal dialysis (PD) complications | Problem | Fix | | --- | --- | | **Peritonitis** (#1) | From contamination at the connection. **Sterile technique**: hand hygiene, sterile gloves, clean and assess site, **mask** when connecting/disconnecting. | | Pain with infusion | Common the first 1–2 weeks. **Warm** the dialysate (warmer or heating pad). **Never the microwave.** | | Poor flow | Kinks or clots. Top causes: **position** (turn to other side, supine or low Fowler's, align body) and **constipation** (high fiber, stool softeners). | | Leakage | Clear fluid around catheter, from too much volume at first. Builds up to a full \~**2 L** over a couple weeks. | Non-compliance (Carlos) - Dialysis for life, 3–4 hrs, 3 days a week. Many feel **denial**: "I feel better, I'll skip today." - Find the **reason** first: money, work, **no ride** to the clinic. - Don't just tell them what to do. Ask what they're **thinking and feeling**. Class prep: how will you bring up non-compliance with Carlos? Try an open question, like "Tell me what makes getting to dialysis hard." Quick recall · tap to flip NCLEX A client returns from hemodialysis. Which order should the nurse question? Never use the access arm for IVs, BP, or compression. NCLEX A client is scheduled for dialysis at 0900. Which 0800 med should the nurse hold? Dialysis already lowers BP. Antihypertensives wait until after. NCLEX A client on peritoneal dialysis has cloudy effluent and belly pain. The nurse suspects: Peritonitis is the major PD complication, from contamination at the connection. NCLEX A client weighed 82 kg before dialysis and 79.5 kg after. How much fluid was removed? 82 − 79.5 = 2.5 kg = 2.5 L.
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Updated 22d ago
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Adjunto Adnominal
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Updated 44d ago
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# Glandular Tissue & Lymphatic System ## Chapter 7: Glandular Tissue ### Summary This chapter details the endocrine and exocrine glands of the head and neck, their locations, secretions, functions, innervations, lymphatic drainage, and blood supply. Understanding these glands is crucial for dental professionals to identify disease processes. ### Key Information #### Gland Types - **Exocrine Gland:** Has a duct to empty secretions directly to the site of use (e.g., salivary glands). - **Endocrine Gland:** Ductless, secretes directly into the vascular system (e.g., thyroid gland). - Motor nerves regulate secretion flow; sensory nerves are also present. #### Lacrimal Glands - **Type:** Paired almond-shaped exocrine glands. - **Secretions:** Lacrimal fluid (tears) for lubricating the conjunctiva and eyeball. - **Location:** Lacrimal fossa of the frontal bone, just inside the lateral part of the supraorbital rim. - **Ducts:** Lacrimal ducts collect tears, which then pass to the lacrimal punctum, lacrimal sac, nasolacrimal duct, and finally drain into the inferior nasal meatus. - **Innervation:** Parasympathetic fibers from the greater petrosal nerve (branch of facial nerve), synapsing at the pterygopalatine ganglion. Postganglionic fibers reach the gland via maxillary branches of the trigeminal nerve and lacrimal nerve. - **Lymphatic Drainage:** Superficial parotid lymph nodes. - **Blood Supply:** Lacrimal artery (branch of ophthalmic artery); venous return via superior ophthalmic vein. - **Pathology:** Dry eye syndrome (DES) or keratoconjunctivitis sicca (KCS) due to reduced lacrimal fluid production. #### Salivary Glands - **Function:** Produce saliva to lubricate and cleanse the oral cavity, aid digestion, and contribute to immune defense. - **Control:** Autonomic nervous system. - **Types:** Major (large, encapsulated, named ducts) and Minor (smaller, more numerous, unencapsulated, shorter unnamed ducts). Both are exocrine. ##### Major Salivary Glands 1. **Parotid Salivary Gland** - **Type:** Largest encapsulated major salivary gland. - **Secretions:** Serous type only (25% of total salivary volume). - **Location:** Parotid space, posterior to mandibular ramus, anterior and inferior to each ear, overlying the masseter muscle. - **Duct:** Parotid duct (Stensen duct) opens into the oral cavity opposite the maxillary second molar. - **Innervation:** Efferent (parasympathetic) fibers from the otic ganglion of the glossopharyngeal nerve (ninth cranial nerve) via the lesser petrosal nerve. Postganglionic fibers carried by the auriculotemporal nerve (mandibular division of trigeminal nerve). Facial nerve passes through but does not innervate. - **Lymphatic Drainage:** Deep parotid lymph nodes. - **Blood Supply:** Transverse facial artery (branch of external carotid artery); venous return via retromandibular vein. - **Pathology:** Enlargement and tenderness with mumps (parotitis), most salivary gland cancers involve the parotid. 2. **Submandibular Salivary Gland** - **Type:** Second largest encapsulated major salivary gland. - **Secretions:** Mixed serous and mucous (60-65% of total salivary volume). - **Location:** Submandibular fossa in the submandibular space, inferior and posterior to the body of the mandible. - **Duct:** Submandibular duct (Wharton duct) opens at the sublingual caruncle in the floor of the mouth. - **Innervation:** Efferent (parasympathetic) fibers of the chorda tympani nerve (facial nerve) synapsing in the submandibular ganglion. Postganglionic fibers delivered by the lingual nerve (mandibular division of trigeminal nerve). - **Lymphatic Drainage:** Submandibular lymph nodes. - **Blood Supply:** Glandular branches of the facial artery; venous return mainly by the facial vein. - **Pathology:** Most common site for salivary stones (sialoliths). 3. **Sublingual Salivary Gland** - **Type:** Smallest, most diffuse, and only unencapsulated major salivary gland. - **Secretions:** Mixed, predominately mucous (10% of total salivary volume). - **Location:** Sublingual fossa in the sublingual space at the floor of the mouth, deep to the sublingual fold, anterior to the submandibular gland. - **Ducts:** Ducts of Rivinus (8-20 small ducts) open along the sublingual fold; sometimes form a larger Bartholin duct opening at the sublingual caruncle. - **Innervation:** Same as submandibular gland: efferent (parasympathetic) fibers of the chorda tympani nerve (facial nerve) and submandibular ganglion. Postganglionic fibers delivered by the lingual nerve (mandibular division of trigeminal nerve). - **Lymphatic Drainage:** Submandibular lymph nodes. - **Blood Supply:** Sublingual artery (off lingual artery); parallel venous return. ##### Minor Salivary Glands - **Type:** More numerous than major glands, unencapsulated. - **Secretions:** Mainly mucous, except von Ebner glands (serous only). - **Location:** Scattered throughout oral mucosa (buccal, labial, lingual, soft palate, posterior hard palate, floor of mouth). Von Ebner glands associated with circumvallate lingual papillae. - **Ducts:** Single, short ducts directly into the oral cavity. - **Innervation:** Preganglionic from facial nerve, postganglionic from various branches of the trigeminal nerve. - **Lymphatic Drainage & Blood Supply:** Various nodes and arteries depending on location. - **Pathology:** Mucocele (blockage of duct from trauma). #### Thyroid Gland - **Type:** Largest endocrine gland (ductless). - **Secretions:** Thyroxine (hormone) directly into the vascular system to stimulate metabolic rate. - **Location:** Anterolateral regions of the neck, inferior to the thyroid cartilage, at the junction of the larynx and trachea. - **Innervation:** Sympathetic nerves through cervical ganglia (do not control secretion; pituitary gland regulates hormone release). - **Lymphatic Drainage:** Superior deep cervical lymph nodes. - **Blood Supply:** Superior and inferior thyroid arteries (possibly thyroid ima artery); venous return via superior, middle, and inferior thyroid veins. - **Pathology:** Goiter (enlarged thyroid gland), loss of mobility indicating neoplastic growth. #### Parathyroid Glands - **Type:** Usually four small endocrine glands (ductless). - **Secretions:** Parathyroid hormone directly into the vascular system to regulate calcium and phosphorus levels. - **Location:** Adjacent to or within the thyroid gland on its posterior surface (not visible or palpable). - **Innervation:** Same as thyroid gland: sympathetic nerves through cervical ganglia. - **Lymphatic Drainage:** Superior deep cervical lymph nodes. - **Blood Supply:** Primarily inferior thyroid arteries (possibly anastomotic branch between inferior and superior thyroid arteries); venous return via superior, middle, and inferior thyroid veins. #### Thymus Gland - **Type:** Endocrine gland (ductless) and part of the immune system. - **Function:** T-cell lymphocytes mature here. Grows until puberty, then shrinks (involution). - **Location:** Thorax and anterior region of the base of the neck, inferior to the thyroid gland, superficial and lateral to the trachea, deep to the sternum. - **Innervation:** Branches of the vagus nerve (tenth cranial nerve) and cervical spinal nerves. - **Lymphatic Drainage:** Lymphatic system begins within the gland and terminates in the internal jugular vein (no afferent vessels). - **Blood Supply:** Inferior thyroid and internal thoracic arteries; venous return via veins in the posterior surface directly into brachiocephalic veins. - **Pathology:** Thymic rests (ectopic accessory thymic tissue). ## Chapter 10: Lymphatic System ### Summary This chapter covers the lymphatic system, its components (vessels, nodes, ducts, tonsils), and its role in fighting disease. It details the location, drainage patterns, and clinical significance of lymph nodes and tonsils in the head and neck. ### Key Information #### Lymphatic System Overview - **Components:** Vessels, nodes, ducts, tonsils. - **Function:** Part of the immune system, fights infection and cancer, drains tissue fluid (lymph). - **Lymphatic Vessels:** Parallel venous blood vessels, have one-way valves, drain lymph. - **Lymph Nodes:** Bean-shaped bodies in clusters, filter toxic products from lymph, contain lymphocytes (white blood cells), involved in lymphocyte production. - **Afferent vessels:** Lymph flows into the node. - **Efferent vessel:** Lymph flows out of the node at the hilus. - **Primary node (regional/master node):** First node lymph drains into from a particular region. - **Secondary node (central node):** Node that primary nodes drain into. - **Lymphatic Ducts:** Larger vessels formed by converging lymphatic vessels. - **Right lymphatic duct:** Drains right side of head and neck, right arm, and thorax into the junction of the right subclavian and right internal jugular veins. - **Thoracic duct:** Drains left side of head and neck, left arm, thorax, and entire lower half of the body into the junction of the left subclavian and left internal jugular veins. - **Tonsils:** Masses of lymphoid tissue near airway and food passages, contain lymphocytes, drain into superior deep cervical lymph nodes. #### Lymph Nodes of the Head ##### Superficial Lymph Nodes of the Head - **Occipital Lymph Nodes:** - **Location:** Posterior base of the head (occipital region). - **Drainage:** Scalp in the occipital region. - **Empties into:** Deep cervical nodes. - **Posterior Auricular, Anterior Auricular, and Superficial Parotid Lymph Nodes:** - **Posterior Auricular:** Posterior to each auricle and external acoustic meatus. - **Anterior Auricular:** Immediately anterior to each tragus. - **Superficial Parotid:** Superficial to each parotid salivary gland. - **Drainage:** External ear, lacrimal gland, adjacent scalp and face. - **Empties into:** Deep cervical nodes. - **Facial Lymph Nodes:** - **Location:** Along the facial vein. - **Subgroups:** Malar (infraorbital), Nasolabial (along nasolabial sulcus), Buccal (around labial commissure), Mandibular (superior to mandible, anterior to masseter). - **Drainage:** Skin and mucous membranes where located, drain superior to inferior. - **Empties into:** Deep cervical nodes via submandibular nodes. ##### Deep Lymph Nodes of the Head - Cannot be palpated extraorally. - **Deep Parotid Lymph Nodes:** - **Location:** Deep within the parotid salivary gland. - **Drainage:** Middle ear, auditory tube, parotid salivary gland. - **Empties into:** Deep cervical nodes. - **Retropharyngeal Lymph Nodes:** - **Location:** Near deep parotid nodes, at the level of the atlas. - **Drainage:** Posterior palate, pharynx, paranasal sinuses, nasal cavity. - **Empties into:** Deep cervical nodes. #### Cervical Lymph Nodes - Paired, unilaterally drain tissues (except submental nodes, which drain bilaterally). - Categorized into superficial and deep. - Medical community uses a 7-level classification (Node Levels I-VII). ##### Superficial Cervical Lymph Nodes - **Submental Lymph Nodes (Node Level I, Sublevel a):** - **Location:** Inferior to the chin, within the submental fascial space and submental triangle. - **Drainage:** Lower lip, chin, floor of mouth, apex of tongue, mandibular incisors with periodontium and gingiva. - **Empties into:** Submandibular nodes or directly into deep cervical nodes. - **Clinical Significance:** Risk for spread of cancers from floor of mouth, apex of tongue, mandibular anterior alveolar process, lower lip. - **Submandibular Lymph Nodes (Node Level I, Sublevel b):** - **Location:** Inferior border of the mandibular ramus, superficial to the submandibular salivary gland. - **Drainage:** Cheeks, upper lip, body of tongue, anterior hard palate, most teeth (except mandibular incisors and maxillary third molars), sublingual and submandibular salivary glands. Secondary nodes for submental and facial regions. - **Empties into:** Deep cervical nodes. - **Clinical Significance:** Risk for spread of cancers from oral cavity, anterior nasal cavity, midface structures, submandibular salivary gland. - **External Jugular Lymph Nodes (Superficial Cervical Nodes):** - **Location:** Along the external jugular vein, superficial to the SCM muscle. - **Drainage:** Secondary nodes for occipital, posterior auricular, anterior auricular, and superficial parotid nodes. - **Empties into:** Deep cervical nodes. - **Anterior Jugular Lymph Nodes (Anterior Cervical Nodes):** - **Location:** Along the anterior jugular vein, anterior to larynx, trachea, superficial to SCM muscle. - **Drainage:** Infrahyoid region of the neck. - **Empties into:** Deep cervical nodes. ##### Deep Cervical Lymph Nodes - **Location:** Along the internal jugular vein, deep to the SCM muscle, from skull base to root of neck. - Divided into superior and inferior based on omohyoid muscle crossing internal jugular vein. - **Node Level II (Superior one-third):** - **Location:** From digastric muscle superiorly to hyoid bone/carotid bifurcation inferiorly. - **Drainage:** Oral cavity, nasal cavity, nasopharynx, oropharynx, laryngopharynx, larynx, parotid salivary gland. - **Jugulodigastric lymph node (tonsillar node):** Prominent node in this group, drains palatine tonsils. - **Node Level III (Middle one-third):** - **Location:** From hyoid bone/carotid bifurcation superiorly to cricothyroid notch/cricoid cartilage/omohyoid muscle inferiorly. - **Drainage:** Oral cavity, nasopharynx, oropharynx, laryngopharynx, larynx. - **Node Level IV (Inferior one-third):** - **Location:** From omohyoid muscle superiorly to clavicle inferiorly. - **Drainage:** Laryngopharynx, esophagus, larynx. - **Node Level V (Posterior cervical triangle):** - **Location:** From skull base at posterior SCM border to clavicle. - **Drainage:** Nasopharynx, oropharynx (Sublevel a), thyroid gland (Sublevel b). - **Node Level VI (Anterior compartment):** - **Location:** Inferior to hyoid bone, between medial margins of common carotid arteries. - **Drainage:** Thyroid gland, specific parts of larynx, esophagus. - **Superior Deep Cervical Lymph Nodes:** - **Location:** Deep to SCM muscle, superior to omohyoid muscle crossing internal jugular vein. - **Drainage:** Posterior nasal cavity, posterior hard palate, soft palate, base of tongue (bilateral drainage), maxillary third molars, TMJ, esophagus, trachea, thyroid gland. Secondary nodes for most other head and neck nodes. - **Empties into:** Inferior deep cervical nodes or directly into jugular trunk. - **Inferior Deep Cervical Lymph Nodes:** - **Location:** Deep to SCM muscle, inferior to omohyoid muscle crossing internal jugular vein, extending into supraclavicular fossa. - **Drainage:** Posterior scalp and neck, superficial pectoral region, part of arm. Secondary nodes for superficial head nodes and superior deep cervical nodes. - **Jugulo-omohyoid lymph node:** Drains tongue and submental triangle; enlarged node can indicate tongue carcinoma. - **Empties into:** Jugular trunk (right) or thoracic duct (left). - **Clinical Significance:** Communicates with axillary lymph nodes, high risk for spread of breast cancer. - **Accessory Lymph Nodes:** - **Location:** Along the eleventh cranial (accessory) nerve. - **Drainage:** Scalp and neck regions. - **Empties into:** Supraclavicular nodes. - **Supraclavicular Lymph Nodes:** - **Location:** Superiorly along the clavicle. - **Drainage:** Lateral cervical triangles. - **Empties into:** Jugular trunks or directly into right lymphatic duct/thoracic duct. - **Clinical Significance:** Final endpoint of lymphatic drainage from entire body, high risk for spread of cancers from lungs, esophagus, stomach. #### Tonsils - **Palatine Tonsils:** - **Location:** Oral cavity, between anterior and posterior faucial pillars. - **Lingual Tonsil:** - **Location:** Dorsal surface of the base of the tongue. - **Pharyngeal Tonsil (Adenoids):** - **Location:** Midline of the posterior wall/roof of the nasopharynx. - **Tubal Tonsil:** - **Location:** Nasopharynx, posterior to openings of the auditory tube. - **Drainage:** All tonsils drain into the superior deep cervical lymph nodes, particularly affecting the jugulodigastric lymph node if infected. #### Clinical Considerations with Lymphatic System Pathology - **Lymphadenopathy:** Dramatic increase in size and change in consistency of lymphoid tissue due to infection or cancer. - **Infection:** Nodes are slightly firmer, extremely mobile, and tender. - **Cancer:** Nodes can become bony hard, fixed to surrounding tissue, usually not tender initially (pain is a late finding). - **Lymphadenitis:** Inflammation of a lymph node, common with microbial infections. - **Metastasis:** Spread of cancer from a primary site to a secondary site via lymph. - Involvement of primary nodes offers a better prognosis than secondary nodes or lymphatic ducts. - Head and neck cancers frequently spread to cervical lymph nodes (80% of cases). - Node metastasis is a significant prognostic factor for squamous cell carcinoma survival. ### Learning Objectives Tasks: - Define and pronounce key and anatomic terms. - Locate and identify glands and associated structures on diagrams, skulls, and patients. - Discuss glandular pathology. - Integrate understanding into clinical dental practice. - List and discuss lymphatic system components. - Locate and identify lymph nodes and tonsils on diagrams and patients. - Identify lymphatic drainage patterns for the head and neck. - Describe and discuss pathology of lymphoid tissue. - Compare the relationship of the lymphatic system to the overall function of the immune system.
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bio Genetics is the study of heredity and how traits are passed from parents to offspring. Gregor Mendel is known as the “Father of Genetics.” Why did Mendel use pea plants? * Easy to grow * Short generation time * Many visible traits * Can self-pollinate or cross-pollinate * Produce many offspring Examples of traits studied: * Flower colour * Seed shape * Plant height ⸻ VOCABULARY Gene * A segment of DNA that controls a trait. Allele * Different forms of the same gene. Example: P = purple flowers p = white flowers Dominant Allele * Expressed whenever it is present. * Represented by a capital letter. Example: P = purple Recessive Allele * Only expressed when two copies are present. * Represented by a lowercase letter. Example: p = white Genotype * Genetic makeup of an organism. Examples: PP Pp pp Phenotype * Physical appearance of an organism. Examples: Purple flower White flower Homozygous * Two identical alleles. Examples: PP pp Heterozygous * Two different alleles. Example: Pp Pure Breeding * Homozygous for a trait. Gamete * Sex cell (sperm or egg). ⸻ MENDEL’S LAWS Law of Dominance * A dominant allele masks a recessive allele. Example: Pp = Purple flower Law of Segregation * Alleles separate during gamete formation. * Each gamete receives only one allele. Example: Parent = Pp Gametes: P p Law of Independent Assortment * Different genes assort independently during meiosis. ⸻ MONOHYBRID CROSSES A monohybrid cross studies one trait. Example: P = Purple p = White Cross: Pp × Pp Punnett Square INCOMPLETE DOMINANCE Neither allele completely dominates. Example: Snapdragons RR = Red WW = White RW = Pink Cross: RW × RW Genotype Ratio: 1 RR : 2 RW : 1 WW Phenotype Ratio: 1 Red : 2 Pink : 1 White CODOMINANCE Both alleles are expressed equally. Example: AB Blood Type Genotype: IAIB Phenotype: AB MULTIPLE ALLELES More than two alleles exist in a population. Example: ABO Blood Group Alleles: IA IB i BLOOD TYPES Type A Genotypes: IAIA or IAi Type B Genotypes: IBIB or IBi Type AB Genotype: IAIB Type O Genotype: ii Can Type A and Type B Parents Have a Type O Child? Yes. If: Father = IAi Mother = IBi Possible Blood Types: AB A B O CELL CYCLE Purpose: * Growth * Repair * Replacement of cells Stages: G1 S G2 Mitosis Cytokinesis INTERPHASE G1 Phase Cell grows and carries out normal functions. S Phase DNA replication occurs. G2 Phase Cell prepares for division. MITOSIS Purpose: Growth and repair. Produces: 2 genetically identical diploid cells. PROPHASE Events: * Chromosomes condense * Nuclear membrane disappears * Nucleolus disappears * Spindle fibres form METAPHASE Events: * Chromosomes line up at the equator ANAPHASE Events: * Sister chromatids separate TELOPHASE Events: * Nuclear membranes reform * Chromosomes uncoil CYTOKINESIS Division of the cytoplasm. Animal Cells: Cleavage furrow forms. Plant Cells: Cell plate forms. CHROMOSOME STRUCTURE Chromosome consists of: * Two sister chromatids * One centromere DIPLOID VS HAPLOID Diploid (2n) * Two sets of chromosomes * Human body cells * 46 chromosomes Haploid (n) * One set of chromosomes * Human gametes * 23 chromosomes HOMOLOGOUS CHROMOSOMES Chromosome pairs that: * Carry the same genes * One comes from the mother * One comes from the father Humans have 23 homologous pairs. MEIOSIS Purpose: Produce gametes. Produces: 4 genetically unique haploid cells. MEIOSIS I Separates homologous chromosomes. CROSSING OVER Occurs during Prophase I. Definition: Exchange of DNA between homologous chromosomes. Importance: Creates genetic variation. RANDOM ASSORTMENT Occurs during Metaphase I. Definition: Homologous pairs line up randomly. Importance: Creates unique chromosome combinations. MEIOSIS II Separates sister chromatids. MITOSIS VS MEIOSIS Mitosis * 2 cells produced * Diploid * Genetically identical * Growth and repair Meiosis * 4 cells produced * Haploid * Genetically different * Produces gametes NONDISJUNCTION Failure of chromosomes to separate properly during meiosis. Can result in extra or missing chromosomes. DOWN SYNDROME Cause: Extra chromosome 21. Chromosome Number: 47 Usually caused by nondisjunction during meiosis. DNA DNA = Deoxyribonucleic Acid Shape: Double Helix Function: Stores genetic information. NUCLEOTIDE Three Components: * Phosphate Group * Deoxyribose Sugar * Nitrogenous Base NITROGENOUS BASES Adenine (A) Thymine (T) Cytosine (C) Guanine (G) COMPLEMENTARY BASE PAIRING A pairs with T C pairs with G DNA REPLICATION Purpose: Make identical copies of DNA. Location: Nucleus Result: Two identical DNA molecules. TRANSCRIPTION Purpose: Create mRNA from DNA. Location: Nucleus DNA → mRNA Remember: RNA uses Uracil (U) instead of Thymine (T). TRANSLATION Purpose: Make proteins. Location: Ribosome mRNA is read and amino acids are joined together to form a protein. MUTATIONS A mutation is a change in DNA sequence. Types: * Deletion * Duplication * Inversion * Translocation DELETION DNA segment removed. DUPLICATION DNA segment repeated. INVERSION DNA segment reversed. TRANSLOCATION DNA segment moves to another chromosome. SEX-LINKED TRAITS Traits located on sex chromosomes. Most are located on the X chromosome. RED-GREEN COLOUR BLINDNESS Inheritance: X-linked recessive. XC = Normal Vision Xc = Colour Blind Male: XcY Colour blind boys inherit the allele from their mother because fathers pass a Y chromosome to their sons. TAY-SACHS DISEASE Cause: Missing enzyme that breaks down lipids in nerve cells. Inheritance: Autosomal recessive. Treatment: No cure currently available. SICKLE CELL ANEMIA Cause: Mutation in hemoglobin gene. Effects: * Sickle-shaped red blood cells * Reduced oxygen transport * Blocked blood vessels Inheritance: Autosomal recessive. HUNTINGTON’S DISEASE Cause: Dominant mutation. Effects: * Nervous system degeneration * Loss of motor control * Cognitive decline Inheritance: Autosomal dominant. KARYOTYPE A photograph of chromosomes arranged in pairs. Used to: * Determine sex * Detect chromosome abnormalities * Diagnose genetic disorders PEDIGREE A family tree used to track inheritance patterns. Symbols: Square = Male Circle = Female Shaded = Has trait CLONING Producing genetically identical organisms. Uses: * Research * Agriculture * Medicine * Conservation GENETIC COUNSELLING Provides information about: * Inherited disorders * Family risk * Testing options AMNIOCENTESIS Prenatal test in which amniotic fluid is sampled and fetal cells are analyzed. Can detect: * Genetic disorders * Chromosomal disorders GMOs Genetically Modified Organisms. Definition: Organisms whose DNA has been altered through biotechnology. Advantages: * Increased crop yield * Disease resistance * Pest resistance Disadvantages: * Ethical concerns * Environmental concerns DNA REPLICATION → TRANSCRIPTION → TRANSLATION DNA (Nucleus) ↓ Replication DNA Copy DNA ↓ Transcription mRNA mRNA ↓ Translation Protein Final Product: Protein RESPIRATORY SYSTEM Function: * Brings oxygen into the body * Removes carbon dioxide * Works with the circulatory system to supply cells with oxygen Why do organisms require oxygen and produce carbon dioxide? Oxygen is required for cellular respiration. Cellular Respiration: Glucose + Oxygen → Energy (ATP) + Carbon Dioxide + Water Cells use oxygen to release energy from food. Carbon dioxide is produced as a waste product and must be removed. ⸻ PATHWAY OF AIR Nasal Cavity ↓ Pharynx ↓ Larynx ↓ Trachea ↓ Bronchi ↓ Bronchioles ↓ Alveoli ⸻ NASAL CAVITY Functions: * Warms air * Moistens air * Filters air Nasal Hairs: * Trap large particles Mucus: * Traps dust and microorganisms Blood Capillaries: * Warm incoming air ⸻ PHARYNX Common passageway for: * Air * Food Also called the throat. ⸻ UVULA Functions: * Prevents food from entering nasal cavity * Helps with speech ⸻ EPIGLOTTIS Functions: * Covers trachea during swallowing * Prevents choking ⸻ LARYNX Also called the voice box. Contains vocal cords. ⸻ TRACHEA Also called the windpipe. Contains cartilage rings that prevent collapse. Lined with: * Cilia * Mucus ⸻ CILIA Tiny hair-like structures. Function: * Sweep mucus upward toward throat ⸻ BRONCHI Two branches of the trachea leading to lungs. Right Bronchus → Right Lung Left Bronchus → Left Lung ⸻ BRONCHIOLES Smaller branches inside lungs. Lead to alveoli. ⸻ ALVEOLI Tiny air sacs. Site of gas exchange. Adaptations: * Thin walls * Moist surface * Large surface area * Rich blood supply Gas Exchange: Oxygen moves: Alveoli → Blood Carbon Dioxide moves: Blood → Alveoli By diffusion. ⸻ BREATHING MECHANICS Two main muscles: 1. Diaphragm 2. Intercostal Muscles ⸻ INHALATION (INSPIRATION) Diaphragm: * Contracts * Moves downward Intercostal Muscles: * Contract * Lift ribs upward Result: * Chest cavity volume increases * Pressure decreases * Air enters lungs ⸻ EXHALATION (EXPIRATION) Diaphragm: * Relaxes * Moves upward Intercostal Muscles: * Relax Result: * Chest cavity volume decreases * Pressure increases * Air leaves lungs ⸻ MEDULLA OBLONGATA Located in the brainstem. Function: * Controls breathing rate Responds to: * Carbon dioxide levels More CO₂: * Faster breathing Less CO₂: * Slower breathing ⸻ LUNG VOLUMES Tidal Volume * Normal amount of air breathed in and out Inspiratory Reserve Volume * Extra air inhaled after normal breath Expiratory Reserve Volume * Extra air exhaled after normal breath Residual Volume * Air remaining in lungs after maximum exhalation Vital Capacity * Maximum amount of air exhaled after deepest breath Total Lung Capacity * Total amount of air lungs can hold ⸻ CIRCULATORY SYSTEM Functions: * Transport oxygen * Transport nutrients * Remove wastes * Maintain homeostasis * Transport hormones Humans have a CLOSED circulatory system. Blood remains inside vessels. ⸻ BLOOD VESSELS ARTERIES Function: * Carry blood away from heart Characteristics: * Thick walls * High pressure * Small lumen * No valves Usually oxygen-rich Exception: Pulmonary artery ⸻ VEINS Function: * Carry blood toward heart Characteristics: * Thin walls * Low pressure * Large lumen * Valves present Usually oxygen-poor Exception: Pulmonary vein ⸻ CAPILLARIES Smallest blood vessels. Functions: * Gas exchange * Nutrient exchange * Waste exchange Walls are one cell thick. ⸻ HEART STRUCTURE Blood Flow: Body ↓ Vena Cava ↓ Right Atrium ↓ Right Ventricle ↓ Pulmonary Artery ↓ Lungs ↓ Pulmonary Vein ↓ Left Atrium ↓ Left Ventricle ↓ Aorta ↓ Body ⸻ HEART CHAMBERS Right Atrium * Receives deoxygenated blood Right Ventricle * Pumps blood to lungs Left Atrium * Receives oxygenated blood Left Ventricle * Pumps blood to body ⸻ SEPTUM Wall separating left and right sides of heart. Prevents mixing of blood. ⸻ HEART VALVES Function: * Prevent backflow of blood Types: Atrioventricular (AV) Valves Pulmonary Semilunar Valve Aortic Semilunar Valve ⸻ SA NODE Sinoatrial Node Known as: * Natural pacemaker Initiates heartbeat. ⸻ AV NODE Atrioventricular Node Receives signal from SA node. Delays impulse slightly. Allows ventricles to fill before contraction. ⸻ BLOOD Components: 1. Plasma 2. Red Blood Cells 3. White Blood Cells 4. Platelets ⸻ PLASMA Liquid component of blood. Functions: * Transport nutrients * Transport hormones * Transport wastes ⸻ RED BLOOD CELLS (ERYTHROCYTES) Function: * Carry oxygen Contain: * Hemoglobin ⸻ HEMOGLOBIN Protein in red blood cells. Function: * Binds oxygen Allows oxygen transport. ⸻ WHITE BLOOD CELLS (LEUKOCYTES) Function: * Fight infection * Defend body Part of immune system. ⸻ PLATELETS Function: * Blood clotting Prevent blood loss. ⸻ BLOOD PRESSURE Force of blood against artery walls. Measured using: Sphygmomanometer Example: 120/80 120 = Systolic Pressure 80 = Diastolic Pressure ⸻ SYSTOLIC PRESSURE Pressure when heart contracts. ⸻ DIASTOLIC PRESSURE Pressure when heart relaxes. ⸻ HYPERTENSION High blood pressure. Can increase risk of: * Stroke * Heart attack * Kidney disease ⸻ STROKE VOLUME Amount of blood pumped per heartbeat. ⸻ CARDIAC OUTPUT Amount of blood pumped per minute. Formula: Cardiac Output = Heart Rate × Stroke Volume ⸻ ECG Electrocardiogram Measures electrical activity of heart. Used to detect: * Irregular heartbeat * Heart damage ⸻ PULMONARY CIRCULATION Heart → Lungs → Heart Purpose: * Oxygenate blood ⸻ SYSTEMIC CIRCULATION Heart → Body → Heart Purpose: * Deliver oxygen to tissues ⸻ HOMEOSTASIS DURING EXERCISE Body responds by: * Increasing heart rate * Increasing breathing rate * Increasing cardiac output * Redirecting blood to muscles * Sweating to cool body Purpose: Maintain stable internal conditions. ⸻ DIGESTIVE SYSTEM Functions: * Break down food * Absorb nutrients * Eliminate waste ⸻ DIGESTIVE TRACT Mouth ↓ Pharynx ↓ Esophagus ↓ Stomach ↓ Small Intestine ↓ Large Intestine ↓ Rectum ↓ Anus ⸻ MECHANICAL DIGESTION Physical breakdown of food. Examples: * Chewing * Churning ⸻ CHEMICAL DIGESTION Chemical breakdown of food using enzymes. Examples: * Amylase * Pepsin ⸻ SALIVA Functions: 1. Moistens food 2. Contains amylase Amylase begins carbohydrate digestion. ⸻ TONGUE Functions: 1. Forms bolus 2. Pushes food for swallowing ⸻ ESOPHAGUS Moves food to stomach. Uses: Peristalsis ⸻ PERISTALSIS Wave-like muscular contractions. Move food through digestive tract. ⸻ STOMACH Functions: * Stores food * Mixes food * Begins protein digestion Produces: * HCl * Pepsin * Mucus ⸻ HCl Hydrochloric Acid Functions: * Kills bacteria * Activates pepsin ⸻ PEPSIN Function: * Digests proteins ⸻ MUCUS Function: * Protects stomach lining ⸻ CHYME Semi-liquid food mixture leaving stomach. ⸻ HEARTBURN Cause: Stomach acid enters esophagus. Usually caused by weakened cardiac sphincter. ⸻ SMALL INTESTINE Main site of: * Digestion * Absorption Adaptations: * Long length * Folds * Villi * Microvilli Large surface area increases absorption. ⸻ DUODENUM First section. Functions: * Receives bile * Receives pancreatic enzymes * Most chemical digestion ⸻ JEJUNUM Main nutrient absorption. ⸻ ILEUM Final nutrient absorption. ⸻ VILLI Finger-like projections. Function: Increase surface area. ⸻ LIVER Functions: * Produces bile * Processes nutrients * Detoxifies blood ⸻ GALL BLADDER Functions: * Stores bile * Releases bile into small intestine ⸻ PANCREAS Functions: * Produces digestive enzymes * Produces bicarbonate ⸻ BILE Function: Emulsifies fats. Breaks large fat droplets into smaller droplets. Makes fat digestion easier. ⸻ DIGESTION OF CARBOHYDRATES Mouth: * Amylase begins digestion Small Intestine: * Pancreatic amylase continues digestion End Product: Glucose ⸻ DIGESTION OF PROTEINS Stomach: * Pepsin begins digestion Small Intestine: * Trypsin continues digestion End Product: Amino Acids ⸻ DIGESTION OF LIPIDS Small Intestine: * Bile emulsifies fats * Lipase digests fats End Product: Fatty Acids + Glycerol ⸻ EVOLUTION Evolution: Change in populations over time. Individuals do NOT evolve. Populations evolve. ⸻ DARWIN Proposed: Natural Selection Book: On the Origin of Species ⸻ WALLACE Independently developed theory of natural selection. ⸻ LAMARCK Proposed: Inheritance of acquired characteristics Example: Giraffes stretch necks and pass longer necks to offspring. This theory is incorrect. ⸻ NATURAL SELECTION Requirements: 1. Variation 2. Overproduction 3. Competition 4. Differential Survival 5. Reproduction Result: Adaptation ⸻ ADAPTATION Inherited characteristic that increases survival and reproduction. ⸻ SELECTIVE ADVANTAGE A characteristic that improves survival or reproduction. Example: Antibiotic resistance ⸻ SELECTIVE PRESSURE Environmental factor that influences survival. Examples: * Predators * Disease * Climate * Competition ⸻ VARIATION Differences among individuals in a population. Sources: * Mutation * Crossing Over * Random Assortment ⸻ MUTATION Ultimate source of new alleles. Creates genetic variation. ⸻ FOSSIL Preserved remains or traces of organisms. ⸻ FOSSIL RECORD Collection of fossils showing evolutionary history. Provides evidence for evolution. ⸻ RADIOACTIVE DATING Uses radioactive isotopes to determine fossil age. ⸻ UNIFORMITARIANISM Proposed by Lyell. Earth changes gradually over long periods of time. ⸻ CATASTROPHISM Proposed by Cuvier. Earth shaped by sudden catastrophic events. ⸻ BIOGEOGRAPHY Study of species distribution around Earth. Provides evidence for evolution. ⸻ EMBRYOLOGY Study of embryos. Similar embryos suggest common ancestry. ⸻ HOMOLOGOUS STRUCTURES Same evolutionary origin. Different functions. Example: Human arm Whale flipper Bat wing Evidence of common ancestry. ⸻ ANALOGOUS STRUCTURES Different origins. Same function. Example: Bird wing Insect wing Not evidence of close ancestry. ⸻ VESTIGIAL STRUCTURES Structures with little or no function. Examples: * Human appendix * Whale pelvis Evidence of evolution. ⸻ MIMICRY One species resembles another. Example: Syrphid fly resembles wasp. Provides protection. ⸻ ARTIFICIAL SELECTION Humans select traits. Examples: * Dog breeding * Crop breeding ⸻ DIRECTIONAL SELECTION One extreme phenotype favored. Graph shifts in one direction. ⸻ STABILIZING SELECTION Average phenotype favored. Extremes selected against. ⸻ DISRUPTIVE SELECTION Both extremes favored. Middle selected against. ⸻ GENETIC DRIFT Random change in allele frequencies. Most significant in small populations. ⸻ FOUNDER EFFECT Small group starts new population. Different allele frequencies from original population. ⸻ BOTTLENECK EFFECT Population drastically reduced. Loss of genetic variation. ⸻ GENE FLOW Movement of alleles between populations. Occurs through migration. ⸻ NON-RANDOM MATING Individuals choose specific mates. Can reduce variation. ⸻ SPECIES A group of organisms that can interbreed in nature and produce fertile offspring. ⸻ SPECIATION Formation of new species. ⸻ ALLOPATRIC SPECIATION Requires: Geographic isolation Example: Mountain separates populations. ⸻ SYMPATRIC SPECIATION Occurs without geographic isolation. ⸻ PRE-ZYGOTIC ISOLATION Prevents fertilization. Examples: * Different mating seasons * Different mating songs * Different habitats ⸻ POST-ZYGOTIC ISOLATION Occurs after fertilization. Example: Sterile hybrids Example: Mule DIVERSITY Prokaryotes vs Eukaryotes PROKARYOTES * No nucleus * No membrane-bound organelles * Circular DNA * Smaller * Examples: Eubacteria, Archaebacteria EUKARYOTES * Nucleus present * Membrane-bound organelles * Linear chromosomes * Larger * Examples: Protists, Fungi, Plants, Animals Three Differences: 1. Nucleus vs no nucleus 2. Organelles vs no organelles 3. Larger vs smaller ⸻ Taxonomy Kingdom Phylum Class Order Family Genus Species Mnemonic: King Philip Came Over For Good Soup ⸻ Binomial Nomenclature Genus + Species Example: Homo sapiens Rules: * Genus capitalized * Species lowercase * Italicized Purpose: * Universal naming system * Avoids confusion * Shows relationships ⸻ Dichotomous Key Used to identify organisms using paired choices. Example: 1a Has wings → Step 2 1b No wings → Step 3 ⸻ Six Kingdoms 1. Archaebacteria 2. Eubacteria 3. Protista 4. Fungi 5. Plantae 6. Animalia ⸻ VIRUSES Virus Structure: * DNA or RNA * Capsid * Attachment proteins * Sometimes envelope Why Viruses Are Not Living: * Not made of cells * Cannot reproduce independently * No metabolism * Need host cell ⸻ DNA Virus vs RNA Virus DNA Virus: * Contains DNA * More stable RNA Virus: * Contains RNA * Mutates faster ⸻ Lytic Cycle Attachment ↓ Penetration ↓ Replication ↓ Assembly ↓ Lysis Host cell bursts. ⸻ Lysogenic Cycle Attachment ↓ Penetration ↓ Integration into host DNA ↓ Host reproduces ↓ Virus DNA copied Cell survives initially. ⸻ ARCHAEBACTERIA Characteristics: * Prokaryotic * Unicellular * Extreme environments Three Groups: Methanogens * Produce methane Halophiles * Salt-loving Thermoacidophiles * Hot acidic environments ⸻ EUBACTERIA Characteristics: * Prokaryotic * Peptidoglycan cell wall * Binary fission Examples: * E. coli * Streptococcus ⸻ Binary Fission DNA Replication ↓ Cell Growth ↓ Cell Division ↓ Two Identical Cells ⸻ Conjugation DNA transfer through pilus. Importance: * Genetic variation * Antibiotic resistance ⸻ Antibiotic Resistance Mutation ↓ Antibiotic kills susceptible bacteria ↓ Resistant bacteria survive ↓ Resistant bacteria reproduce Natural Selection ⸻ PROTISTS Characteristics: * Eukaryotic * Mostly unicellular * Aquatic Three Groups: Animal-like * Amoeba * Paramecium Plant-like * Algae * Euglena Fungus-like * Slime molds ⸻ Amoeba * Uses pseudopods * Phagocytosis ⸻ Algae * Photosynthetic * Oxygen producer ⸻ Euglena * Chloroplasts * Flagellum * Photosynthesis * Can also feed heterotrophically ⸻ Malaria Cause: Plasmodium Kingdom: Protista ⸻ FUNGI Characteristics: * Eukaryotic * Heterotrophic * Chitin cell walls * Reproduce with spores Examples: * Mushrooms * Mold * Yeast ⸻ External Digestion Release enzymes ↓ Digest food outside body ↓ Absorb nutrients ⸻ Fungi vs Plants FUNGI * Heterotrophic * Chitin * No chloroplasts PLANTS * Autotrophic * Cellulose * Chloroplasts ⸻ PLANTS Biodiversity vs Monoculture BIODIVERSITY * Many species * Stable ecosystem * Disease resistance MONOCULTURE * One crop species * Low diversity * Disease risk ⸻ Bryophytes Definition: Nonvascular plants Examples: * Mosses * Liverworts Characteristics: * No xylem * No phloem * Need water for reproduction ⸻ Vascular Plants Contain: * Xylem * Phloem ⸻ Xylem Function: Water and minerals Direction: Roots → Leaves ⸻ Phloem Function: Sugars Direction: Throughout plant ⸻ Alternation of Generations Sporophyte (2n) ↓ meiosis Spores (n) ↓ Gametophyte (n) ↓ Gametes ↓ fertilization Zygote (2n) ↓ Sporophyte ⸻ Moss Life Cycle Spores ↓ Gametophyte ↓ Egg + Sperm ↓ Zygote ↓ Sporophyte ↓ Capsule ↓ Spores Know: * Capsule * Sporophyte * Gametophyte * Spores ⸻ Fern Life Cycle Fern ↓ Sori ↓ Spores ↓ Prothallus ↓ Gametes ↓ Fertilization ↓ Young Fern Know: * Frond * Sori * Sporangia * Prothallus ⸻ Gymnosperms Characteristics: * Naked seeds * Cones * Wind pollination * Evergreen Examples: * Pine * Spruce * Fir ⸻ Angiosperms Characteristics: * Flowers * Fruit * Seeds enclosed Examples: * Apple tree * Rose * Maple ⸻ Flower Structure Anther * Produces pollen Pollen Grain * Male gamete Stigma * Receives pollen Style * Connects stigma and ovary Ovary * Contains ovules Ovule * Female gamete Petals * Attract pollinators ⸻ Plant Tissues Meristematic * Growth Dermal * Protection Ground * Photosynthesis * Storage Vascular * Transport ⸻ Leaf Structure Blade * Main leaf surface Petiole * Connects leaf to stem Cuticle * Reduces water loss Palisade Mesophyll * Photosynthesis Spongy Mesophyll * Gas exchange Veins * Xylem + Phloem ⸻ Stomata Openings in leaves. Functions: * Gas exchange * Water loss ⸻ Guard Cells Control opening and closing of stomata. ⸻ Transpiration Water loss from leaves. Functions: * Pulls water upward * Cools plant * Moves minerals ⸻ Simple vs Compound Leaves Simple: * One blade Compound: * Multiple leaflets ⸻ Monocots vs Dicots MONOCOTS * 1 cotyledon * Parallel veins * Fibrous roots * Flower parts in 3s Examples: Corn Grass DICOTS * 2 cotyledons * Net veins * Taproot * Flower parts in 4s or 5s Examples: Bean Maple ⸻ Seeds Contain: * Embryo * Stored food * Seed coat Functions: * Protection * Survival * Dispersal ⸻ Seed Dispersal Wind * Dandelion Water * Coconut Animals * Burrs Explosive * Touch-me-not ⸻ Fruit vs Vegetable Fruit: * Comes from ovary * Contains seeds Examples: Tomato Apple Pepper Vegetable: * Root, stem, leaf, or flower Examples: Carrot Celery Broccoli ⸻ Factors Affecting Plant Growth 1. Light 2. Water 3. Carbon dioxide 4. Temperature 5. Soil nutrients 6. Oxygen 7. Soil pH 8. Space 9. Pollinators 10. Disease and pests
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Updated 148d ago
flashcards
1. 90 kg ağırlığında sağlıklı bir erkek hastanın plazma volümü yaklaşık olarak kaç litredir? C) 4.5 L ✅ 2. 70 kg ağırlığındaki sağlıklı yetişkin bir erkekte, interstisyel (dokular arası) sıvı hacmi yaklaşık olarak kaç litredir? A) 10.5 L ✅ 3. Damar sıvısı ile dokular arasındaki sıvı geçişlerinde, aşağıdaki basınç türlerinden hangisi sıvıyı damar dışına (interstisyel alana) doğru iter? C) Kanın hidrostatik basıncı ✅ 4. Sıvı geçişlerinde, suyun düşük yoğunluktaki ortamdan yüksek yoğunluktaki ortama doğru yarı geçirgen bir zardan geçmesine ne ad verilir? A) Ozmoz ✅ 5. Sağlıklı bir insanda normal plazma ozmolaritesi (osmolalite) değer aralığı aşağıdakilerden hangisidir? B) 275-295 mOsm/kg ✅ 6. Plazma proteinlerinin (özellikle Albümin) normal değer aralığı kaç g/dL'dir? C) 6-8 g/dL ✅ 7. Plazma onkotik basıncını damar içinde tutarak ödem oluşumunu engelleyen temel plazma proteini hangisidir? C) Albümin ✅ 8. Aşağıdakilerden hangisi ödem klinik ayırıcı tanısında yer alan fizyopatolojik mekanizmalardan biri değildir? A) Hidrostatik basınç artışı B) Venöz dönüş bozukluğu C) Onkotik basınç artışı ✅ D) Kapiller permeabilite (geçirgenlik) artışı E) Lenfatik drenaj bozukluğu 9. Aşağıdakilerden hangisi hidrostatik basınç artışına bağlı gelişen ödemin klinik özelliklerinden biri değildir? A) Kısa süreli gode (çukur) bırakması B) Özellikle göz kapaklarında belirgin olması ✅ C) Soluk görünümlü olması D) Anazarka tarzında yaygın olması 10. Aşağıdaki venöz dönüş bozukluklarından hangisi fizyopatolojik tutulum yeri bakımından diğerlerinden klinik olarak farklıdır? A) Travma B) Varis C) Dışarıdan bası (tümör vb.) D) Perikardit ✅ E) Tromboflebit 11. Ödem şikayeti ile kliniğe başvuran bir bireyde, etiyolojiyi belirlemek amacıyla aşağıdaki laboratuvar incelemelerinden hangilerine bakılmalıdır? (1. Kan protein düzeyleri, 2. Tam idrar analizi, 3. 24 saatlik gaitada protein kaybı) B) Hepsi ✅ 12. Aşağıdakilerden hangisi vücut sıvılarındaki ana katyonlardan (pozitif yüklü iyon) biri değildir? A) Sodyum (Na^+) B) Potasyum (K^+) C) Klor (Cl^-) ✅ (Anyondur) D) Kalsiyum (Ca^{2+}) E) Magnezyum (Mg^{2+}) 13. Hücre içi (intrasellüler) ve hücre dışı (ekstrasellüler) alanların ana katyonları sırasıyla hangi şıkta doğru verilmiştir? B) Potasyum (K^+) / Sodyum (Na^+) ✅ 14. HCO_3^- (Bikarbonat) iyonunun normal intravasküler (plazma) değeri kaç mEq/L'dir? C) 24 ✅ 15. Sıvı-elektrolit dengesinde hayati öneme sahip olan Na^+/K^+ ATPaz pompasının bir döngüdeki çalışma mekanizması nasıldır? A) 3 Na^+ dışarı pompalanırken, 2 K^+ hücre içine alınır ✅ 16. Vücutta suyun geri emilimini (reabsorbsiyonunu) tübüllerden doğrudan arttırarak su dengesini sağlayan temel hormon hangisidir? D) Antidiüretik Hormon (Vazopresin) ✅ 17. Kadın ve erkek bireyler arasında total vücut suyu oranının farklı olmasının en temel nedeni aşağıdakilerden hangisidir? C) Vücut yağ dokusu oranı farklılığı ✅ (Kadınlarda yağ oranı yüksek olduğunun göstergesidir) 18. Aşağıdakilerden hangisi hücreler arası potasyum (K^+) geçişini (şift) tetikleyerek "hipokalemiye" yol açan durumlardan biri değildir? D) Aşırı laksatif kullanımı ✅ (Hücre içi şift yapmaz; GİS yoluyla K net uzaklaştırır) 19. Hipertonik dehidratasyon tablosunda serum sodyum (Na^+) düzeyinin klinik olarak hangi seviyede olması beklenir? D) > 150 mEq/L ✅ 20. Hipotonik dehidratasyon klinik tablosunda serum sodyum (Na^+) miktarının ne kadar olması tanı kriteridir? C) 130 mEq/L altı ✅ 21. Aşağıdakilerden hangisi total vücut suyu fazlalığı (hipervolemi) sonucunda dilüsyonel hiponatremiye yol açan klinik durumlardan biridir? A) Glukokortikoid eksikliği ✅ 22. Laktatlı Ringer solüsyonu infüzyonu, aşağıdaki klinik tabloların hangisinde laktik asidoz riskinden dolayı kesinlikle kontrendikedir? C) Karaciğer yetmezliği ✅ (Karaciğer laktatı bikarbonata metabolize edemez) 23. Endotelden salgılanan ve "Endothelium Derived Relaxing Factor" (EDRF) olarak , düz kasları gevşeten en güçlü lokal vazodilatatör molekül hangisidir? B) Nitrik Oksit (NO) ✅ 24. Aşağıda B-Tipi Natriüretik Peptidlerin (BNP) etki mekanizmasına yönelik bilgiler yer almaktadır. Yanlış seçeneği işaretleyiniz. A) BNP, miyokardiyal ve atriyal duvar gerilimine bağlı olarak salınan diüretik etkili bir hormondur. B) Böbreklerde ve periferik dolaşımda sodyum (Na^+) atılımını azaltırlar. ✅ (Doğrusu: Sodyum atılımını arttırır) C) Renin salınımını ve kaskadını baskılarlar. D) Aldosteron salınımını azaltarak tuz tutulmasının önüne geçerler. E) Damar düz kaslarında vazodilatasyona neden olurlar. 25. Aşağıdakilerden hangisi endotel hücrelerinden salgılanan veya endotel bağımlı çalışan lokal "vazodilatatör" (damar genişletici) maddelerden biri değildir? A) Nitrik Oksit B) Adenozin C) Anjiyotensin II ✅ (En güçlü vazokonstriktörlerdendir) D) Prostasiklin (PGI_2) 26. Aşağıdakilerden hangisi Nitrik Oksit (NO) salınımını endotelden doğrudan "uyaran" (tetikleyen) durumlardan biri değildir? D) Katekolaminler ✅ (Damarı kasmaya meyillidir, NO salınımını doğrudan uyarmaz) 27. Aşağıdakilerden hangisi endotel dokusunun vücutta üstlendiği fizyolojik görevlerden veya kontrol mekanizmalarından biri değildir? A) Vasküler tonusun ve damar çapının kontrolünün düzenlenmesi B) Kan basıncının sistemik homeostazının ayarlanması C) İnflamatuar hücre göçünün ve lokal inflamasyonun düzenlenmesi D) Hücre içi kohezyonun (bağlılığın) endotel bariyeri dışından düzenlenmesi ✅ E) Koagülasyon (pıhtılaşma) ve antikoagülan dengenin kontrolü 28. Renin-Anjiyotensin-Aldosteron Sisteminde (RAAS) karaciğer kökenli Anjiyotensinojen'den oluşan Anjiyotensin I'i, biyolojik olarak aktif olan Anjiyotensin II'ye dönüştüren ACE enzimi en yoğun olarak hangi organda sentezlenir? C) Akciğer kılcal damar endoteli ✅ 29. Kalp yetmezliği sürecinde devreye giren nöroendokrin (nörohumoral) kompanzasyon mekanizmalarının uzun dönemdeki kronik "olumsuz" sonuçlarından biri değildir? A) Aşırı sıvı, su ve sodyum birikimine bağlı ödem B) Miyokardiyal patolojik hipertrofi ve ventriküler dilatasyon C) Ölümcül aritmiler ve ani kardiyak ölüm sıklığında artış D) Refleks taşikardi ile birlikte ön ve ard yükte net azalma ✅ (Kompanzasyon ard yükü azaltmaz, vazokonstriksiyon ile arttırır) E) Kalp yetersizliği klinik tablosunun progresyonu (kötüleşmesi) 30. Klinik pratik ve acil tıp departmanlarında, sol kalp yetmezliği / konjestif kalp yetmezliği tanısında ve progresyon takibinde serumda düzeyi en güvenilir artış gösteren biyobelirteç hormon hangisidir? B) BNP ✅ 31. Aşağıdakilerden hangisi endotel bağımlı dilatasyon (gevşeme) fonksiyonlarında bozulmaya (endotel disfonksiyonuna) neden olan klinik tablolardan biri değildir? E) Triptofan yüklenmesi ✅ (Doğrusu modellemede Metiyonin yüklenmesidir) 32. Aşağıdakilerden hangisi şok patofizyolojisinin "Kompanse (Erken)" evresinde vücudun gösterdiği sistemik yanıtlardan biridir? D) Vital organ kan akımını korumak için sistemik vazokonstriksiyon gerçekleşmesi ✅ 33. Aşağıdakilerden hangisi hipovolemik şok tablosundaki bir hastadan alınan kan örneğinin laboratuvar analizinde "görülmesi beklenmeyen" (gözlenmeyen) bir bulgudur? B) Serum bikarbonat (HCO3^-) düzeyinde artış ✅ (Bikarbonat tüketilir, düzeyi azalır) 34. Klinik sıvı/şok tedavisine ve agresif resüsitasyona hiçbir şekilde yanıt vermeyen "refrakter şok" hastalarında, arka planda yatan ve gözden kaçabilecek olası nedenlerden biri değildir? E) Anksiyeteye bağlı çocuksu davranış sergileme ✅ 35. Sistemik vazodilatasyon ve ani kapiller geçirgenlik artışı ile, alerjik bir reaksiyon tetiklediği mediyatörlerle ortaya çıkan anafilaktik şokun etiyolojisinde yer almayan durum hangisidir? E) Kardiyak aritmiler ✅ (Kardiyojenik şok nedenidir) 36. Bradikardi (kalp hızında yavaşlama) ve hipotansiyon birlikteliği ile seyreden, sempatik tonus kaybına bağlı gelişen özel şok tipi hangisidir? B) Nörojenik şok ✅ 37. Aterosklerozun patogenezinde, subendotelyal alana geçen makrofajların modifiye/okside LDL'yi kontrolsüz ve sınırsız bir şekilde yutarak "köpük hücresine" (Foam Cell) dönüşmesini sağlayan temel mekanizma hangisidir? A) Makrofaj yüzeyindeki Çöpçü (Scavenger) reseptörlerinde "down-regülasyon" mekanizmasının olmaması ✅ 38. Ateroskleroz sürecinde, monosit ve T lenfositlerin hasarlı damar duvarına tutunmasını ve içeri sızmasını sağlayan endotel kökenli "ilk önemli yapışkan adezyon molekülleri" hangileridir? B) VCAM-1 ve Selektinler (E-Selektin, P-Selektin) ✅ 39. Rüptür (yırtılma) ve akut tromboz riski taşıyan "Hassas (Unstabil) Plak" ile "Kararlı (Stabil) Plak" karşılaştırmasında hangisi hassas plağın özelliklerinden biri değildir? D) Düz kas hücresi ve kollajen içeriğinin çok zengin olması ✅ (Stabil plağın özelliğidir) 40. Sigara kullanımının ateroskleroz ve koroner arter hastalığı patofizyolojisindeki etkilerine yönelik verilen bilgilerden hangisi biyolojik olarak yanlıştır? A) Geri dönüştürülemez (değiştirilemez) majör bir risk faktörüdür. ✅ (Doğrusu: Değiştirilebilir en önemli faktördür) 41. Aşağıdakilerden hangisi hücre zedelenmesinde "Geri Dönüşümsüz (İrreversibl)" aşamaya geçildiğinin kesin bir morfolojik/biyokimyasal göstergesidir? C) Lizozomların parçalanması ve otolitik enzimlerin serbest kalması ✅ 42. Aşağıdakilerden hangisi hücreyi serbest radikallerin hasarından koruyan "Enzimatik Antioksidan" sınıfında yer alan bir moleküldür? C) Katalaz ✅ 43. Aşağıdakilerden hangisi endojen veya eksojen kaynaklı bir "Serbest Radikal" (Reaktif Oksijen Ürünü) moleküldür? C) Çevre kirleticiler (Ozon, NO_2 vb.) ✅ 44. Aşağıdakilerden hangisi hücresel düzeyde "oksidan/hasar yapıcı" ajanlardan biri değildir? A) Süperoksit Dismutaz (SOD) ✅ (Koruyucu antioksidan enzimdir) 45. Aşağıdakilerden hangisi enzimatik antioksidanlar (SOD, Katalaz, Glutatyon Peroksidaz) arasında "yer almayan" koruyucu yapılardan biridir? E) Koenzim Q10 ✅ (Non-enzimatik antioksidandır) 46. Akut inflamasyonun vasküler (damarsal) fazında gerçekleşen olayların doğru mikroskobik sırası hangisidir? B) Geçici vazokonstriksiyon \ Vazodilatasyon \ Kapiller geçirgenlik artışı ✅ 47. Aşağıdakilerden hangisi akut inflamasyonun vasküler fazından ziyade "Hücresel Fazında" yer alan lökositik olaylardan biri değildir? E) Prostaglandin salınımı ✅ (Kimyasal mediyatördür, hücresel eylem değildir) 48. Doku zedelenmesi oluştuktan sonra, inflamasyon alanına ve hasarlı bölgeye kemotaktik uyaranlarla "ilk giden/akut fazı domine eden" fagositer hücre hangisidir? C) Nötrofil ✅ 49. Paraziter enfeksiyonlarda, alerjik cevap mekanizmalarında ve stresle baş etme süreçlerinde rol oynayan hücre savunma elemanı hangisidir? B) Eozinofil ✅ 50. Aşağıdakilerden hangisi inflamatuar süreçlerin lokal veya sistemik nihai sonucunu etkileyen mikrobiyal/konakçı faktörlerden biri değildir? D) Hücrelerin Pinositoza karşı direnç mekanizması ✅ 51. Aşağıdakilerden hangisi inflamasyon sürecinde lökositlerin yaptığı eylemlerden biri "değildir"? A) Ekzositoz ✅ 52. Aşağıdakilerden hangisi inflamasyon sürecinde görev alan ve ilk salınan "vazoaktif amin" grubu mediyatörlerden biridir? D) Histamin ✅ 53. Akut inflamasyon ile Kronik inflamasyon tablolarını birbirinden ayıran patofizyolojik kriterler arasında yer almayan hangisidir? C) Hastada oluşan psikolojik değişiklikler seviyesi ✅ 54. Asit-Fast (ARB) boyanan, damlacık yoluyla bulaşan ve akciğerlerde kazeifikasyon nekrozu içeren granülomlar (Ghon odakları) oluşturan Tüberküloz (Verem) hastalığının en yaygın etkeni hangisidir? E) Mycobacterium tuberculosis ✅ 55. Diabetes Mellitus (Diyabet) klinik tanısının standardizasyonunda altın standart olarak kabul edilen ve 75 gram susuz glukoz yüklemesiyle yapılan laboratuvar testinin adı nedir? C) Oral Glukoz Tolerans Testi (OGTT) ✅ 56. Bir bireye standart 75 gram OGTT yapıldığında, "Bozulmuş Glukoz Toleransı" (IGT / Prediyabet) tanısı koyabilmek için 2. saat plazma glukoz değeri hangi aralıkta saptanmalıdır? B) 140 - 200 mg/dL arası ✅ 57. Kas ve yağ dokusu hücrelerinde, insülin reseptörüne bağından sonra glukozun hücre içine kolaylaştırılmış difüzyonla taşınmasını sağlayan "insüline duyarlı ana taşıyıcı protein" hangisidir? GLUT-4 ✅ 58. Geriye dönük yaklaşık 3 aylık (120 günlük) ortalama eritrosit ömrü boyunca maruz kalınan kan şekeri düzeyini yansıtan laboratuvar tetkiki hangisidir? C) HbA1c (Glikozillenmiş Hemoglobin) ✅ 59. Pankreasın endokrin fonksiyonunda insülin salınım kaskadını "baskılayan/inhibe eden" hormonal veya fizyolojik durum hangisidir? B) Somatostatin ve Ghrelin hormonları ✅ 60. Tarihte diyabet klinik tedavisinde karbonhidratlardan fakir, proteinden zengin diyet modelini ilk öneren bilim insanı kimdir? John Rollo ✅ 61. Mide mukozasında yer alan Antrumdaki G hücrelerinden sentezlenen, paryetal hücreleri doğrudan uyararak Hidrojen iyonu (H^+ / Asit) salgılanmasını tetikleyen majör hormon hangisidir? Gastrin ✅ 62. Kompleman sisteminin "Klasik Yolunun" (Classical Pathway) aktive olabilmesi için ortamda mutlaka bulunması gereken başlatıcı temel faktör hangisidir? B) Antijen-Antikor Kompleksi (IgG veya IgM yapısında) ✅ 63. Kompleman kaskadının hedef patojen hücre zarında silindirik bir delik açarak ozmotik lize (öldürmeye) neden olan "Membran Atak Kompleksi" (MAK) hangi protein diziliminden oluşur? C) C5b - C9 arası kompleman serisi ✅ 64. Kompleman kaskad sisteminde, her üç aktivasyon yolunun (Klasik, Alternatif, Lektin) da birleştiği, eksikliğinde en ağır ve tekrarlayan bakteriyel enfeksiyon tablolarının görüldüğü merkez protein hangisidir? B) Kompleman C3 ✅ 65. Anne sütüyle bebeğe pasif bağışıklık sağlayan, mukoza yüzeylerinde (gözyaşı, tükürük, havayolu sekresyonları) dimerik yapıda bulunarak ilk savunma bariyerini oluşturan antikor (immünglobülin) tipi hangisidir? A) İmmünglobülin A (IgA) ✅ 66. Kemik iliğinde lökosit serisinin aşırı uyarılması sonucu, periferik yaymada lökosit sayısının lösemiyi taklit edecek şekilde 40.000 - 100.000 / mm^3 sınırına fırlamasına ne ad verilir? B) Lökomoid Reaksiyon ✅ 67. Aşağıdakilerden hangisi insan vücudunda gelişen "Otoimmün" patolojilere (bağışıklık sisteminin kendi dokusuna saldırması) örnek bir hastalık değildir? A) Tip 1 Diabetes Mellitus B) Sistemik Lupus Eritematozus (SLE) C) Romatoid Artrit (RA) D) Tip 2 Diabetes Mellitus ✅ (İnsülin direnci ve reseptör defektlidir, otoimmün değildir) 68. Renin, Anjiyotensin, Aldosteron ve Vazopressin (ADH) salgılanma mekanizmalarıyla ilgili verilen RAAS öncüllerinin Doğru (D) / Yanlış (Y) seçeneği hangisidir? ⁠(D)⁠ Renin jukstaglomerüler hücrelerden salgılanır. ⁠(D)⁠ Anjiyotensin I, akciğerde ACE ile Anjiyotensin II'ye dönüşür. ⁠(Y)⁠ Vazopressin (ADH) ön hipofizden salgılanır. (Doğrusu: Arka hipofizden salgılanır) ⁠(Y)⁠ Aldosteron potasyumu tübüllerden geri emer. (Doğrusu: Potasyumu idrarla atar) Doğru Sıralama Seçeneği: D - D - Y - Y ✅ 69. Dehidratasyon durumunda vücudun verdiği hormonal ve homeostatik yanıt öncüllerinin Doğru (D) / Yanlış (Y) analizi hangisidir? ⁠(D)⁠ ADH (Vazopresin) salınımı artar. ⁠(Y)⁠ Aldosteron salınımı baskılanır. (Doğrusu: Tuz ve su tutmak için artar) ⁠(D)⁠ Susama merkezi uyarılır. ⁠(Y)⁠ Tübüllerden Na ve H_2O reabsorbsiyonu engellenir. (Doğrusu: Geri emilim artar) 70. Mide mukozasının korunmasına yönelik verilen öncüllerin Doğru (D Yanlış (Y) ⁠(D)⁠ Prostaglandinler mukus ve bikarbonat salgısını uyararak mideyi korur. ⁠(D)⁠ NSAİİ (Aspirin vb.) ilaçlar prostaglandin sentezini baskılayarak hasarı artırır. ⁠(Y)⁠ Glukokortikoidler (kortizon) mide mukozasını korur. (Doğrusu: Mideyi korumaz, ülser riskini artırır) 71. Natriüretik Peptitlerin (ANP ve BNP) fizyolojisine yönelik verilen Doğru (D) / Yanlış (Y) klinik sıralaması aşağıdakilerden hangisidir? ⁠(D)⁠ Hem ANP hem de BNP kalp duvar gerilimi (volüm yükü) artınca miyosilerden salınır. ⁠(Y)⁠ ANP, kronik ventriküler basınç artışına bağlı transkripsiyonel regülasyonla salınır. (Doğrusu: Akut gerilmeye yanıt verir) ⁠(D)⁠ RAAS aktivasyonu sırasında ANP ve BNP, bu sisteme ters (zıt) düzenleyici görev yaparak sodyum/su dengesini korur. ⁠(Y)⁠ BNP, atriyal basınçtaki akut mikroskobik değişikliklere bağlı kısa patlamalar halinde salınır. (Doğrusu: Kronik süreçlerde ventrikülden salgılanır) 72. KOAH gelişim mekanizmalarına ve hücresel rollere yönelik verilen klinik? ⁠(D)⁠ Oluşan progressif alveol duvar hasarı amfizem tablosuna neden olur. ⁠(D)⁠ Makrofaj ve nötrofillerden salgılanan proteazlar mukus hipersekresyonuna (kronik bronşit) yol açar. ⁠(D)⁠ CD8^+ T lenfositleri fibroblast aktivasyonu ve havayolu fibrozisinde etkilidir. 73. Aşağıdakilerden hangisi ateroskleroz /evrelerinden biri değildir? Cevap: "Endotel hasarı olmadan doğrudan plak vaskülarizasyonu başlaması" ifadesi yanlıştır. Ateroskleroz endotel hasarı ile başlar. 74. Aşağıdakilerden hangisi endotelin antikoagülan (pıhtılaşma engelleyici) görevlerinden biri değildir? Cevap: Tromboksan A2 (TXA2). Çünkü TXA2 pıhtılaşmayı engellemez; aksine trombositleri kümeleştirir ve damarı kasar. 75. Aşağıdaki moleküllerden hangisi lökositlerin endotele yapışmasını sağlayan moleküllerden değildir? Cevap: Kadherin. Kadherinler hücre içi yapısal bağlantılardır, selektin veya integrinler gibi lökosit adezyon görevi üstlenmezler. 76. Endotel hasarı sonucu aşağıdaki lipitlerden hangisi, endotel hasar bölgesine yapışmaz (Aterosklerozdan sorumlu değildir)? Cevap: HDL. Çünkü HDL yüksek yoğunluklu "iyi" kolesteroldür, damar duvarında plak oluşturmaz, tam tersine temizler. 77. Peptik ülser patofizyolojisinde mukoza hasarında / savunmasında rol oynayan faktörlerden hangisi yanlıştır (agresif/koruyucu)? Cevap: Artmış prostaglandin seviyesi yanlıştır. Prostaglandinlerin artması hasar yapmaz, aksine mukozayı korur. 78. Aşağıdakilerden hangisi kalp yetmezliğinin progresyonu (ilerlemesi) süreçlerini gösteren klinik değişimlerden biridir? Cevap: Miyokardiyal hipertrofi ve dilatasyon, arteriyel ve venöz kan akımında değişiklikler, kapiller hidrostatik basınç artışı. 79. Kalp duvar gerilimi artınca salgılanan Natriüretik Peptitlere (ANP ve BNP) yönelik verilen bilgilerden hangisi doğrudur? Cevap: ANP ve BNP'nin her ikisi de kalp duvar gerilimi artınca salgılanır ve RAAS aktivasyonu sırasında antagonist görev yaparak sodyum ve su homeostazisini sağlarlar. 80. Aşağıda Anjiyotensin II'nin etkileri yer almaktadır. Yanlış olanı işaretleyiniz. Cevap: "ADH salınımını baskılar" ifadesi yanlıştır. Anjiyotensin II su tutmak için ADH'ı baskılamaz, aksine salınmasını uyarır. 81. Aşağıdakilerden hangisi endotel bağımlı vazodilatasyonda (gevşemede) bozulmaya (endotel disfonksiyonuna) neden olan durumlardan biri değildir? Cevap: Kısa süreli fizyolojik egzersiz reaksiyonu. Egzersiz damar fonksiyonlarını bozmaz, iyileştirir. 82. Aşağıdakilerden hangisi ödem klinik ayırıcı tanı fizyolojik mekanizmaları için yanlıştır? Cevap: Onkotik basınç artışı ödem yapar ifadesi yanlıştır. Onkotik basıncın artması sıvıyı damarda tutarak ödemi engeller. 83. Aşağıdakilerden hangisi inflamasyon (iltihap) sürecinde yer alan kimyasal tepkilerden/mediatörlerden biri değildir? Cevap: "Sedimantasyon" veya "Kan Rengi" gibi ifadeler doğrudan kimyasal mediatör değildir (laboratuvar/fiziksel bulgudur). Histamin, Serotonin, Prostaglandin ve Komplemen ise gerçek kimyasal mediatörlerdir. 84. Aşağıdaki vitamin yetersizliklerinden hangisi yara iyileşmesini olumsuz etkileyen genel faktörler arasında en kritiktir (kollajen sentezi kofaktörüdür)? Cevap: Vitamin C ✅ 85. Hücre içine glukoz alımını sağlayan insülden bağımsız, karaciğer hepatositleri ve pankreas beta hücrelerinde glukoz sensörü (algılayıcı) olarak çalışan taşıyıcı protein hangisidir? Cevap: GLUT-2 ✅ 86. Tip 1 Diyabet etiyopatogenezinde majör rol oynayan, genetik yatkınlıktan sorumlu tutulan insan lökosit antijeni (HLA) gen lokusları hangileridir? Cevap: HLA-DR3 ve HLA-DR4 ✅ 87. Diyabet hastalarında insülin direnci gelişimini tetikleyen patolojik süreçler arasında yer almayan durum hangisidir? Cevap: Başarılı bariatrik obezite cerrahisi. (Çünkü obezite cerrahisi insülin direncini tetiklemez, aksine düzeltir). 88. Pnömoni patofizyolojisinde alveolar lümenin nötrofil, fibrin ve eritrositlerle tamamen dolduğu, akciğerin makroskobik olarak karaciğer kıvamını aldığı evre hangisidir? Cevap: Kırmızı Hepatizasyon evresi ✅ 89. Sol kalp yetmezliğinde sol ventrikül pompalama gücü azalınca kanın geriye doğru göllenmesi sonucu ilk olarak hangi klinik tablo gelişir? Cevap: Pulmoner ödem (Akciğer ödemi) ve dispne ✅ 90. Akut faz reaktanı olan ve aterosklerotik plak rüptür riskini, damar sertliği derecesini öngörmede klinik olarak yaygın kullanılan karaciğer kaynaklı protein hangisidir? Cevap: C-Reaktif Protein (CRP) ✅ 91. Aşağıdakilerden hangisi hücrelerin patolojik dış etkenler (iskemi, toksin vb.) sonucu kontrollü olmaksızın şişerek patlaması ile karakterize ölüm şeklidir? Cevap: Nekroz ✅ 92. Hücrenin büyüme sinyallerini kendi kendine üretmesi, apoptotik sinyallerden kaçması ve sınırsız çoğalma potansiyeline sahip olması durumuna ne ad verilir? Cevap: Kanseröz Hücre Dönüşümü ✅ 93. Stresör bir ajanla karşılaşıldığında vücutta nöroendokrin olarak ilk uyarılan ana kontrol merkezi neresidir? Cevap: Hipotalamus ✅ 94. Hipotansiyonu olan bir hastada afferent arteriyollerden salgılanarak RAAS kaskadını başlatan böbrek kökenli enzim hangisidir? Cevap: Renin ✅ 95. İltihaplı bölgede lokal olarak kızarıklık (Rubor) ve sıcaklık (Calor) artışına neden olan temel vasküler olay hangisidir? Cevap: Vazodilatasyon ✅ 96. Aşağıdakilerden hangisi yaralanma sonrası dokunun eski orijinal anatomik yapısını ve hücre tipini tamamen kazanması işlemine verilen addır? Cevap: Rejenerasyon ✅ 97. Kronik havayolu inflamasyonu ve parankim hasarı ile giden KOAH klinik tablosunun patogenezinde elastik lifleri parçalayan ana enzim grubu hangisidir? Cevap: Proteazlar (Elastazlar) ✅ 98. Mide parietal hücrelerinden asit salgılanmasını bloke ederek peptik ülser tedavisinde kullanılan mide koruyucu ajanların fizyolojik hedefi hangisidir? Cevap: H^+/K^+ ATPaz Pompası (Proton Pompası) ✅ 99. Aşağıdakilerden hangisi diyabetin üç klasik kardinal klinik semptomundan (3P) biri değildir? Cevap: Polidaktili (Çok parmaklılık anlamına gelir, diyabetle ilgisi yoktur) 100. Hücreler arası potasyumun hücre dışına net çıkışı sonucu plazmada potasyum yükselmesi (Hiperkalemi) durumuna yol açan metabolik dengesizlik hangisidir? Cevap: Asidoz ✅ (Alkaloz hipokalemi yaparken, asidoz hidrojen-potasyum değişimi ile hiperkalemiye yol açar) 101. Bir doku ya da organın kronik uyaranlar veya kan akımı azalması sonucu hücre hacminin ve boyutunun küçülmesine ne ad verilir? Cevap: Atrofi ✅ 102.Hipotonik bir dehidratasyon (serum\ Na^+ < 130\ mEq/L) tablosunda, osmotik basınç dengesindeki değişim nedeniyle sıvı geçişi hangi yöne doğru gerçekleşir? Cevap: Hücre dışından (ekstrasellüler) hücre içine doğru. ✅ (Gerekçe: Hücre dışı sıvı hipotonik hale geldiğinde, su osmotik olarak daha yoğun olan hücre içine girer ve hücreler şişer). 103. [Kardiyovasküler Slaytı / Ses Kaydı Vurgusu] Sol kalp yetmezliğinde pulmoner kapiller hidrostatik basınç artışı sonucu alveollere sızan eritrositleri yutan hemosiderin yüklü makrofajlara ne ad verilir? Cevap: Kalp hatası/yetmezliği hücresi (Heart failure cell) ✅ 104. [Ateroskleroz Slaytı] Aterosklerotik plağın stabilitesini sağlayan, düz kas hücreleri tarafından sentezlenen ve rüptürü engelleyen en önemli fibröz matriks elemanı hangisidir? Cevap: Kollajen ✅ (Gerekçe: Fibröz kepi kalınlaştırarak plağı kararlı hale getirir). 105. [İnflamasyon Slaytı] Akut inflamasyon alanında lökositlerin endotele tutunması sırasında, lökositlerin yüzeyindeki İntegrinler ile endotel yüzeyindeki hangi molekül "sıkı yapışma" (firm adhesion) fazını gerçekleştirir? Cevap: ICAM-1 / VCAM-1 ✅ (Gerekçe: Selektinler yuvarlanmadan, integrin-ICAM/VCAM etkileşimi ise sıkı yapışmadan sorumludur). 106. [Solunum Slaytı] Kronik Bronşit tanısı olan bir hastada, havayollarında mukus hipersekresyonuna neden olan patolojik anatomik değişiklik aşağıdakilerden hangisidir? Cevap: Submukozal bezlerin hiperplazisi ve kadeh (Goblet) hücre sayısının artması ✅ 107. [İmmünoloji PDF'i] Aşağıdakilerden hangisi Tip II hipersensitivite (Sitotoksik tip) mekanizmasıyla gelişen klinik tablolara bir örnektir? Cevap: Kan transfüzyon reaksiyonları ve Rh uyuşmazlığı ✅ (Eritrosit yüzeyindeki antijenlere karşı gelişen antikor bağımlı sitotoksik reaksiyondur). 108. [İmmünoloji PDF'i / Ses Kaydı] Antijen-antikor komplekslerinin dokularda çökmesi ve kompleman aktivasyonuyla karakterize "Tip III Hipersensitivite" reaksiyonuna en tipik klinik örnek hangisidir? Cevap: Sistemik Lupus Eritematozus (SLE) ve Akut Glomerulonefrit ✅ (SLE, sistemik immün kompleks hastalığıdır). 109. [Diyabet Slaytı] İnsülin reseptör sinyal yolağında, IRS fosforilasyonunu bozarak obezite kaynaklı "insülin direncine" neden olan, yağ dokusundan salgılanan proinflamatuar sitokin/adipokin ikilisi hangisidir? Cevap: TNF-Alfa ve İnterlökin-6 (IL-6) ✅ 110. [IBS-EBH Slaytı] Sadece kolonu ve rektumu tutan, mukozada psödopolip (yalancı polip) oluşumu ve kript abseleri ile karakterize İnflamatuar Bağırsak Hastalığı hangisidir? Cevap: Ülseratif Kolit ✅ 111. [Mide/Siroz Slaytı] Siroz patofizyolojisinde, karaciğer disfonksiyonuna bağlı olarak "Amonyak (NH_3)" gazının üreye dönüştürülemeyip beyne geçmesi ve astreksis ile karakterize nörolojik tabloya ne ad verilir? Cevap: Hepatik Ensefalopati ✅ 112. Vaka 1 (Glukoz Metabolizması Analizi): Rutin tetkik sonucunda açlık plazma glukozu 117 mg/dL ve 75 gr glukozla yapılan Oral Glukoz Tolerans Testi'nde (OGTT) 2. saat kan glukozu 120 mg/dL saptanan hastanın tanısıyla ilgili hangisi doğrudur? Çözüm ve Teşhis: Hastanın açlık kan şekeri 100-125 mg/dL sınırında olduğu için bozuktur; ancak 2. saat şekeri 140 mg/dL'nin altında olduğundan glukoz toleransı normaldir. Bu nedenle hastanın tanısı Bozulmuş Açlık Glukozu (BAG / İzole IFG) şeklindedir. 113. Vaka 2 (Ülseratif Kolit Şiddet Analizi): Ülseratif Kolit teşhisi alan hastada lökosit sayısı normal, günde dörtten az dışkılama, dışkıda kan miktarı az/orta, ateş normal, taşikardi yok, anemi hafif ve sedimantasyon hızı 20 mm/saat altında ise Truelove-Witts tablosuna göre hangi seviyededir? Teşhis: Hafif (Mild) Derece Ülseratif Kolit ✅ Sağlıklı yetişkin bir erkekte vücut ağırlığının %60'ı sudur. Kadınlarda yağ oranının daha yüksek, kas oranının düşük olması nedeniyle bu oran %50 civarına düşer. Hücre İçi Sıvı (İCS): Total suyun 2/3'ünü (%40) oluşturur. Ana katyonu Potasyum (K^+), ana anyonları ise fosfat ve proteinlerdir. Hücre Dışı Sıvı (ECS): Total suyun 1/3'ünü (%20) oluşturur. Kendi içinde İnterstisyel Sıvı (%15) ve İntravasküler Sıvı (Plazma) (%5) olarak ikiye ayrılır. Hücre dışı sıvının ana katyonu Sodyum (Na^+), ana anyonları ise Klor (Cl^-) ve Bikarbonat (HCO_3^-)'tır. Plazmada normal HCO_3^- değeri 24 mEq/L'dir. Sıvı Hareketini Düzenleyen Starling Güçleri Kapiller Hidrostatik Basınç: Kanın damar duvarına yaptığı basınçtır. Sıvıyı damar dışına (interstisyel alana) itmeye çalışır. Plazma Onkotik (Kolloid Osmotik) Basıncı: Plazma proteinlerinin (özellikle Albümin) suyu damar içinde tutma gücüdür. Sıvıyı damar içine çekmeye çalışır. Ödem Oluşum Mekanizmaları 1 Kapiller Hidrostatik Basınç Artışı: Venöz dönüş bozukluklarında (kalp yetmezliği, varis, tromboflebit) kan damarda göllenir ve dokuya sızar. Kalp yetmezliğine bağlı ödemler genelde sistemik, simetriktir ve gode bırakır. 2 Plazma Onkotik Basıncının Azalması: Karaciğer sirozunda (albümin sentezi azaldığında) veya nefrotik sendromda (idrarla protein kaybedildiğinde) damarın suyu tutma gücü azalır ve sıvı dokuya kaçar. Albümin 3.5 g/dL altına düşerse ödem başlar. 3 Kapiller Geçirgenlik (Permeabilite) Artışı: İnflamasyon, yanık veya alerjik reaksiyonlarda (histamin etkisiyle) endotel aralıkları açılır; proteinler ve sıvı dokuya sızar (Eksüda karakterinde ödem). 4 Lenfatik Obstrüksiyon (Tıkanıklık): Tümör basısı veya lenf nodu cerrahisi nedeniyle lenfatik drenaj bozulursa dokular arası sıvı drene edilemez ve lokal ödem (lenfödem) gelişir. ÜNİTE 2: Kardiyovasküler Sistem, RAAS Kaskadı, Natriüretik Peptitler ve Şok Sıvı Azaldığında Devreye Giren Sistem: RAAS Vücutta kan hacmi veya kan basıncı düştüğünde böbrekteki jukstaglomerüler hücrelerden Renin salgılanır. 1 Renin, karaciğerde üretilen Anjiyotensinojen'i Anjiyotensin I'e çevirir. 2 Anjiyotensin I, akciğer endotelinde bulunan ACE (Anjiyotensin Dönüştürücü Enzim) ile Anjiyotensin II'ye dönüşür. 3 Anjiyotensin II'nin Etkileri: * Vücudun en güçlü vazokonstriktör (damar daraltıcı) maddelerindendir. Adrenal korteksten Aldosteron salınımını uyarır (tübüllerden sodyum ve su tutulumu ) Hipofiz arka lobundan ADH (Vazopresin) salınımını uyarır (sadece suyun geri emilimini sağlar) Beyindeki susama merkezini uyarır. Sıvı Artığında Devreye Giren Sistem: Natriüretik Peptitler Kalbe gelen sıvı yükü (volüm yükü) arttığında, kalp duvarı gerilir ve buna yanıt olarak natriüretik peptitler salgılanır: ANP (Atriyal Natriüretik Peptid): Atriyumlardan, basınçtaki akut değişikliklere bağlı olarak salınman bir hormondur. BNP (B-Tipi Natriüretik Peptid): Ventriküllerden, kronik basınç ve volüm yüküne bağlı olarak salınır. Kalp yetmezliğinde serumda düzeyi en çok artan biyobelirteç hormondur. Etkileri: RAAS'ı baskılarlar. Böbrekten sodyum ve su atılımını arttırarak (natriürez ve diürez) kan hacmini ve tansiyonu düşürmeye çalışırlar. Şok Patofizyolojisi ve Evreleri Kompanse (Erken) Evre: Kan basıncını korumak için sempatik sistem ve RAAS aktive olur. Hayati olmayan organ yataklarında (cilt, böbrek, GİS) vazokonstriksiyon gerçekleşir; nabız hızlanır (taşikardi). Progresif (İlerleyen) Evre: Kompanzasyon yetersiz kalır. Hücre metabolizması aerobikten anaerobiğe döner. Laktik asit birikir, metabolik asidoz gelişir. Na^+/K^+ pompası bozulur, hücreler şişer. İrreversibl (Geri Dönüşümsüz) Evre: Lizozomlar parçalanır, hücre içi otolitik enzimler salınır ve yaygın hücre/organ ölümü gerçekleşir. Şok İndeksi: Nabız} / \ Sistolik Kan Basıncı} formülüyle hesaplanır. Normal değeri 0.5-0.7 arasındadır. 1.0 ve üzerinde olması masif kan kaybına (%40 üstü) işaret eder. ÜNİTE 3: Akut İnflamasyon Kaskadı, Eksüda-Transüda Farkı ve Yara İyileşmesi Akut İnflamasyon Fazları Vasküler Faz Sıralaması: Hasar anında ilk olarak saniyeler süren geçici vazokonstriksiyon olur. Ardından lokal kan akımını arttırmak için vazodilatasyon gelişir (kızarıklık ve sıcaklık artışı). Son olarak kapiller geçirgenlik artar ve dokuya protein zengin sıvı (Eksüda) sızar (şişlik/ödem). Hücresel Faz Sıralaması: Lökositlerin hasar bölgesine gitme sürecidir. Sıralama: Marginasyon (Döşenme) \ Rolling (Yuvarlanma) \ Sıkı Yapışma \ Diyapedez (Göç) Kemotaksis \ Fagositoz. Bölgeye ilk giden akut hücre Nötrofil'dir. 1. Derece Yara: Sadece epidermisin yüzeyel kaybı ve güneş yanığı benzeri hafif doku hasarı ile karakterizedir. 2. Derece Yara: Epidermisin tamamen elden çıktığı, bül (su toplanması) oluşumuyla karakterize yüzeyel dermal yanıklardır. Keloid: Granülasyon fazında aşırı ve kontrolsüz kollajen birikimi (hipertrofik skar) sonucu oluşan kabarık tümöral doku yapısıdır. ÜNİTE 4: Solunum Sistemi Fizyopatolojisi (Pnömoni, KOAH ve Tüberküloz) Pnömoninin Patofizyolojik Evreleri 1 Konjesyon Evresi: Mikroorganizmaların alveollere ulaşmasıyla başlar, damarlarda genişleme ve bakteri yüklü sıvı birikimi ile karakterizedir. 2 Kırmızı Hepatizasyon Evresi: Alveollerin fibrin, nötrofil ve bol miktarda eritrosit ile dolarak akciğerin makroskobik olarak karaciğer kıvamını aldığı evre. 3 Gri Hepatizasyon Evresi: Eritrositlerin parçalandığı, fibrinli eksüdanın alveolleri doldurmaya devam ettiği evre. 4 Rezolüsyon Evresi: İyileşme fazıdır. Alveollerdeki debrilerin makrofajlar tarafından temizlendiği dönemdir. Klinik Skorlama: Pnömoni hastalarının hayati riskini belirlemede CURB-65 (Confusion, Urea, Respiratory rate, Blood pressure, Age \ge 65) kriterleri kullanılır. KOAH (Kronik Obstrüktif Akciğer Hastalığı) Kaskadı Patofizyoloji: Sigara kullanımı, koruyucu bir anti-proteaz olan Alfa-1 Antitiripsin aktivitesini inhibe eder (azaltır). Buna bağlı olarak makrofaj ve nötrofillerden salgılanan proteaz (elastaz) aktivitesi artar, alveollerdeki elastik lifler yok olur (elastolizis). Amfizem: Terminal bronşiyollerin arkasındaki hava yollarının kalıcı ve anormal genişlemesi/yıkımıdır. Hava hapsi sonucu hastada Fıçı Göğüs görünümü ve Pembe Üfleyen (Pink Puffer) kliniği oluşur. Kronik Bronşit: En az iki yıl üst üste ve bu yılların en az 3 ayı boyunca balgamlı öksürük ile karakterizedir. Histopatolojisinde submukozal bezlerin hiperplazisi ve Goblet hücre artışı izlenir. ÜNİTE 5: Diabetes Mellitus (Diyabet) Patofizyolojisi ve Tanı Kriterleri Hücresel Düzeyde İnsülin Etki Mekanizması ve Direnç İnsülin, tirozin kinaz aktivitesine sahip spesifik İnsülin Reseptörü'ne bağlanır, hücre içinde IRS (İnsülin Reseptör Substratı) proteinleri aktive olur. Bu kaskad, veziküllerde bekleyen GLUT-4 kapılarının membran yüzeyine göç etmesini tetikler. Kas ve yağ dokusu glukoz almak için insüline (GLUT-4'e) bağımlıdır. Karaciğer ve pankreas beta hücreleri ise insülinden bağımsız çalışan GLUT-2 taşıyıcısını bir glukoz sensörü olarak kullanır. Obezitede İnsülin Direnci: Genişleyen yağ dokusundan salgılanan proinflamatuar sitokinler (TNF-Alfa ve IL-6), IRS proteinlerini tirozin yerine serin rezidülerinden fosforilleyerek insülin sinyal yolağını tamamen bloke eder. Tip 1 vs Tip 2 Diabetes Mellitus Ayrımı Tip 1 Diyabet: Otoimmün kökenlidir. Pankreas beta hücreleri tamamen tahrip olmuştur, insülin üretimi yoktur. Ketozise (DKA) yatkınlık çok yüksektir. HLA-DR3 ve HLA-DR4 gen lokusları ile güçlü ilişkisi vardır. Tip 2 Diyabet: İnsülin üretimi vardır ancak insülin direnci ve reseptör defekti baskındır. Genetik yatkınlık (aile öyküsü) Tip 2'de çok daha güçlüdür. Böbrek Şeker Eşiği ve Semptomlar Kan glukoz düzeyi biyolojik böbrek eşiği olan 180 mg/dL sınırını aştığında, tübüllerden geri emilim yetersiz kalır ve idrarda şeker görülür (Glukozüri). Bu durum renal lümende osmotik basınç yaratarak osmotik diüreze, yani diyabetin 3P semptomuna (Poliüri, Polidipsi, Polifaji) yol açar. ÜNİTE 6: İnflamatuar Bağırsak Hastalıkları (EBH) ve İBS Patolojisi Crohn Hastalığı ve Ülseratif Kolit Makroskobik Ayrımı İrritabl Bağırsak Sendromu (İBS) Yapısal veya biyokimyasal bir bozukluk olmaksızın seyreden, visseral hipersensitivite (bağırsakların uyarılara aşırı hassasiyeti) ile karakterize fonksiyonel bir hastalıktır. Tanısında Roma Kriterleri kullanılır. Beslenme tedavisinde gaz ve şişkinliği azaltmak amacıyla Düşük FODMAP diyeti uygulanır. ÜNİTE 7: Karaciğer Sirozu, Portal Hipertansiyon ve Sistemik Sonuçları Karaciğer parankim dokusunun kronik hasar sonucu fibrozis (kollajenleşme) ve rejenere nodüllerle kaplanarak vasküler mimarisinin bozulmasıdır. Organın fonksiyon kaybına bağlı olarak iki ağır sistemik tablo gelişir: 1. Portal Hipertansiyon ve Asit Mekanizması Karaciğer içindeki sinüzoidlerde vasküler direnç arttıkça, portal ven basıncı yükselir (Portal Hipertansiyon). Karın boşluğunda patolojik sıvı birikmesi (Asit) iki ayağın birleşmesiyle tavan yapar: Hidrostatik Ayak: Portal hipertansiyon nedeniyle periton kılcallarındaki hidrostatik basınç artar ve sıvı karın boşluğuna itilir. Onkotik Ayak: Sirozlu karaciğer plazma proteini olan Albümin'i sentezleyemez. Plazma onkotik basıncı düşer ve damar suyu tutamaz. 2. Hepatik Ensefalopati ve Astreksis Mekanizması [Image showing ammonia metabolism pathway from intestine to liver and brain] Normal şartlarda proteinlerin bağırsakta bakterilerce yıkılmasıyla ortaya çıkan toksik Amonyak (NH_3) gazı, portal venle karaciğere gelerek üre döngüsünde zararsız üreye dönüştürülür. Sirozda parankim çalışmadığı için amonyak temizlenemez, kanda birikir ve kan-beyin bariyerini geçerek beyindeki astrositlerde glutamin birikimine ve Serebral Ödeme yol açar. Klinik Yansıması: Hastada bilinç bulanıklığı, kişilik değişiklikleri ve en tipik motor bulgu olan Astreksis (Kuş kanadı sallama titremesi / Flapping Tremor) tablosu ortaya çıkar.
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Updated 165d ago
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Adenosine
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Updated 182d ago
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NURS 348 — EXAM 4 STUDY GUIDE Hypertension Definition & Overview • Persistent elevation of BP ≥130/80 mmHg (systolic at/greater than 130 OR diastolic at/greater than 80) on at least 2 separate visits, 2+ weeks apart. • Primary (Essential): No identifiable cause, most common (90–95% of cases). • Secondary: Caused by another condition or adverse effects of medications. Etiology/Pathophysiology • ↑ Peripheral resistance and/or ↑ cardiac output → ↑ blood pressure → When blood vessels get narrower (increased resistance) or the heart pumps more forcefully (increased output), pressure inside the vessels rises “like squeezing a hose while water is running” → Over time, this high pressure damages the vessel walls and heart muscle, increasing the risk for atherosclerosis, heart attack (myocardial infarction), and stroke. • ↑ Increased peripheral resistance (arteriolar constriction) → ↑ afterload → left ventricular hypertrophy → heart failure → The heart pushes against more resistance (afterload), making the heart muscle thicker (hypertrophy). Over time, it becomes weaker and can lead to heart failure. • Kidneys retain sodium and water → ↑ circulating volume → The kidneys hold onto extra salt and water, adding more fluid to the blood. More fluid means higher pressure—like overfilling a water balloon. • Activation of renin–angiotensin–aldosterone system (RAAS) = vasoconstriction + fluid retention. RAAS is like the “blood pressure booster” → When this system turns on, blood vessels tighten and the kidneys save even more salt and water, both of which raise blood pressure. Risk Factors: • Primary: family history, ↑ sodium intake, Obesity (BMI >25), African-American ethnicity, smoking, hyperlipidemia, diabetes mellitus, and stress. • Secondary: kidney disease, Cushing’s, pregnancy, pheochromocytoma, medic (steroids, OCPs). Clinical Manifestations (S/S) • Often asymptomatic (“silent killer”)!!! • Headache, dizziness, fainting, vision changes • Retinal damage on exam (cotton wool spots, papilledema). • Note: if blood pressure reading is elevated then take in both arms; pt legs uncrossed, and arms above heart; correct cuff Diagnostics (Dx)/Labs • Multiple BP readings (both arms, sitting and standing) • ECG → Left-Ventricular hypertrophy. evaluates cardiac function. • Labs → ↑ BUN/creatinine (kidney disease), lipids, glucose, cortisol (Cushing’s) Nursing Care / Nursing Interventions • Monitor pt BP regularly and accurately, check both arms/correct cuff • Put on DASH diet (Dietary Approach to Stop Hypertension) Medications • ⭐️Diuretics (first-line): excess fluids, they need to remove; increase urine • Thiazides (hydrochlorothiazide) inhibits water & sodium reabsorption and increases potassium excretion • Side effects/SE: hypokalemia; monitor potassium(K⁺) levels • Loop (furosemide) decreases sodium reabsorption & increase potassium excretion– SE: hypokalemia; monitor potassium(K⁺) levels • Potassium-sparing (spironolactone) – SE: hyperkalemia; monitor potassium levels. EKG: peaked T waves • Also watch out for muscle weakness, irregular, pulse, and dehydration. • ⭐️Calcium channel blockers (verapamil, amlodipine, and diltiazem) Calcium channel blockers relax and widen blood vessels by preventing calcium from entering muscle cells, leading to lower blood pressure (vasodilation) • SE: constipation; take fiber for verapamil, and all can ↓HR • Avoid grapefruit juice ➡️ toxicity, hypotensive effects Calcium= contract • ⭐️ACE inhibitors (lisinopril, enalapril): prevents angiotensin II → vasodilation • SE: - hypotension; monitor BP and pulse HR -hyperkalemia; monitor potassium levels -erectile dysfunction -⭐️cough linked to angioedema (swollen tissue under the skin around lips, tongue, and glottis); report swelling & discontinue med • ⭐️ARBs (valsartan, losartan): for ACE-intolerant pts from cough/hyperkalemia. ARBs lower blood pressure by blocking angiotensin II from binding to its receptors, preventing vasoconstriction, and reducing fluid retention. • SE: angioedema, heart failure, hyperkalemia • Change position, slowly, report, angioedema, edema, and avoid foods that are high in potassium (bananas, potatoes, apricots, spinach, beans); monitor potassium levels • Aldosterone-receptor antagonists (eplerenone, spironolactone): blocks aldosterone action. • SE: kidney damage, hypertriglyceridemia, hyponatremia, and hyperkalemia; monitor kidney function, triglycerides, sodium, and potassium levels • Avoid Grapefruit juice and St. John’s wort, salt substitutes, and potassium rich foods • ⭐️Beta blockers (metoprolol, atenolol): blocks beta receptors (adrenaline/epinephrine) ➡️reduces heart rate, cardiac output, and blood pressure ↓HR, ↓CO; use cautiously in diabetics • SE: -⭐️erectile dysfunction, -Fatigue, weakness, depression -hypoglycemia • Monitor heart rate (hold if HR is less than 60) and do not suddenly stop taking med (cause rebound hypertension); and don’t give to pts with asthma, airway disease (cause bronchospasms) • Central Alpha-2 agonists (clonidine): calm the nerves that raise blood pressure, letting blood vessels, relax, and BP go down, ↓SNS tone • SE: sedation, orthostatic, hypotension, and sexual dysfunction/impotence • Monitor BP and pulse • Alpha-adrenergic blockers (prazosin, doxazosin): vasodilator= relaxed BP; give at night to avoid first-dose hypotension. Start with low dose. • SE: postural hypotension; make sure patient rises slowly and caution. • Monitor BP 2 hrs after initiation Complications • Hypertensive Crisis: usually when patients do not follow the medication regimen • BP >180/120 → organ damage (encephalopathy, renal failure) • S/S: severe headache, dizziness, blurred vision, confusion, epistaxis • Treat: IV antihypertensives (nitroprusside, nicardipine, labetalol); the goal is to lower BP gradually by 20-25% in first hour. Not less than 140/90. Monitor BP every 5-15 mins Patient Education • Adhere to medication regimen, don’t abruptly stop even when you feel better • Change positions slowly • Encourage DASH diet (low sodium, high fruits/veggies, low-fat dairy) ex: grilled salmon, brown rice, steamed broccoli, and low-fat milk • Avoid high-sodium foods. Consume less than 2.3 g/day • Monitor BP at home • Report signs or symptoms of electrolyte imbalances • Encourage Weight loss, exercise 3x weekly • Encourage Smoking cessation • Encourage Limit alcohol (≤2/day men, ≤1/day women) • Manage stress • Report persistent cough or swelling (ACE inhibitor red flag) Peripheral Venous Disorders(PVD) Patho: problems with veins where Deoxygenated blood can't get back to the heart Oxygenated blood pools in the extremities. The valves are preventing backflow. • Venous Thromboembolism (VTE): blood clot that starts in a vein. -Two types: deep vein thrombosis (DVT) and pulmonary embolism (PE) • Venous insufficiency: Improper functioning of the veins. Veins aren’t able to push back blood to the heart which results in swelling, venous stasis ulcers, or cellulitis. Blood can go down into the veins just fine but cannot come back up. a. VTE ex: Deep Vein Thrombosis (DVT) Pathophysiology • Thrombus (Blood clot) forms in deep veins (usually in legs) → can embolize (travel and block vessel) its way to lungs (PE). • Caused by Virchow’s triad: venous/blood flow stasis, endothelial injury, hypercoagulability. Risk Factors • Surgery (hip, knee, prostate) • Immobility • Heart failure • Pregnancy • Family hx • Oral contraceptives or hormone therapy • Cancer • COVID-19 (elevated D-dimer) • Central venous catheters Clinical Manifestations • Note that clients can be asymptomatic • Calf/groin pain (dull/achy), tenderness, warmth, edema • Unilateral swelling • Shallow, irregular shaped wounds • Too much blood, brown/yellow discoloration • Sudden SOB and sharp chest pain → suspect PE • Positioning: “Elevate Veins”, position up in “V” shape, above heart. Worsens: if dangling, sitting/dangling for long periods of time. Diagnostics • ⭐️Venous duplex ultrasonography = gold standard; it’s an ultrasound of Leg to see blood clot/blood flow through the vessel. • ⭐️D-dimer ↑ = clot breakdown evidence • Venogram/MRI if ultrasound inconclusive Nursing Interventions • Bed rest until anticoagulation started • Elevate leg slightly above heart (no knee gatch). Positioning: “EleVate Veins”, think V as veins are up, to keep the veins open. • Warm compresses • DO NOT massage leg • Compression stockings (after swelling ↓) • Encourage early ambulation when safe • SCDS Medications/Procedures (Anticoagulants) stops blood from clotting, another nurse must be with you • Unfractionated heparin (given IV): prevents clots and growth of existing clot; monitor platelets, and aPTT (how long it takes blood to clot) (1.5–2× normal). Must be given in facility. MUST MONITOR CLOSELY • Antidote: protamine sulfate • Low-molecular-weight heparin (Lovenox/enoxaparin): given SubQ, weight-based, prevention and treatment of DVT, given twice daily, can be used in home setting. Don’t need labs. Monitor for bleeding, and take bleeding precautions (Electric razor, soft toothbrush, environment safety) • Warfarin (Coumadin): oral, inhibits vitamin K clotting factors overlaps; combined with heparin 3–4 days until INR 2–3 (takes awhile to kick in; therapeutic affect) • Antidote: vitamin K • Avoid high vitamin K foods (green leafy veggies) • Monitor PT (range: 11-13.5 secs), INR (must know range: 2–3) • Factor Xa inhibitors (fondaparinux; SubQ) (rivaroxaban, apixaban; oral): Prevents development of Thromboses; transitional medication; initial labs are PT and PTT; not routinely • Direct thrombin inhibitors (dabigatran): directly prevents growth of thrombus Formation, given sub Q ; initiate initial lab values only for PT and APTT. • Antidote: idarucizumab • Thrombolytics (tPA): for massive DVT/PE, directly infused into clot, start within 24hrs- 5 days of clot formation; monitor for bleeding, neuro status, dizziness, headache. Take bleeding precautions, pt must use electric razor and, brush teeth with a soft toothbrush. • Inferior vena cava filter: prevents embolus from reaching lungs (PE), inserted in femoral vein; catches blood clot. Used when pt is unresponsive to other treatments. Monitor: bleeding, hematoma, infection, PE (dyspnea, chest pain, tachycardia). Nursing actions: assess circulation and encourage leg exercises/ambulation early, have patient not sit for too long Anticoagulant Therapy Nurse’s Role • Verify labs,;Double-check with another RN for IV heparin, Assess for bleeding (bruises, gums, stools) and Monitor vitals, mental status (signs of intracranial bleed) Reversal Agents • Heparin → protamine sulfate • Warfarin → vitamin K • Dabigatran → idarucizumab Patient Education • Avoid contact sports • Soft toothbrush, electric razor • Avoid sudden diet changes (vitamin K) Complications (anticoagulants) • ⭐️Pulmonary embolism: sudden dyspnea, chest pain, SOB, anxiety, tachypnea → emergency; sit, patient in high Fowlers, and administer oxygen and anticoagulants • ⭐️Ulcer formation(venous): often formed over the medial malleolus, chronic, hard to heal, can reoccur. Can lead to amputation/death. Neuropathic patients might not feel this. Nursing care: Dressing is left 3–7 days; wound vacuums, diet: high in zinc, protein, iron, and vitamins A and C, debride necrotic tissue so wound can heel. Patient Education(Anticoagulants) • Bleeding precautions (soft toothbrush, electric razor) • Report bruising or black stools • Avoid prolonged sitting/crossing legs • Wear compression stockings b. Venous insufficiency Pathophysiology • Valves and legs are damaged due to prolong venous HTN Our previous blood clot Risk factors: • Sitting/standing in one position for a long period of time • Obesity • Pregnancy • Thrombophlebitis Clinical manifestations: • Status dermatitis(brown discoloration along ankles) • Edema • Stasis ulcers around ankles Labs/DX • D-dimer ↑ = clot breakdown evidence, detects clot Nursing interventions: Elevate legs to increase venous return (20 mins, 4-5/day), position: legs above heart, “Elevate Veins”, Apply stockings, and monitor for cellulitis Patient education: avoid sitting/standing still for too long, change positions often, avoid crossing legs, tight clothing. Apply stockings before getting out of bed in the morning Peripheral Arterial Disease (PAD) : affects blood vessels that carry blood away from the heart; artery carries blood away from heart but has difficulty going down to extremities. Pathophysiology • Atherosclerosis in lower extremities → decreased blood flow to tissues. Risk Factors • Smoking, DM, hypertension, hyperlipidemia, obesity, age, sedentary lifestyle. Clinical Manifestations • Intermittent claudication: leg pain with exercise, relieved by rest; not enough oxygen makes the tissue suffer = pain; ischemia • Pain(sharp) that is only relieved when resting in dependent position • Cool, pale, cyanotic skin • Loss of hair on legs, thick toenails • Weak/absent pedal pulses; dorsalis pedis; Doppler(verify), +1 • Numbness, burning at night • No blood and no edema due to an adequate blood flow • Note: think “A” in PAD as Antarctica, where it’s cold! For cold, pale skin! Diagnostics • ⭐️ABI < 0.9 = PAD; ankle pressure compared to break your pressure; expected finding is 0.9–1.3; less than is PAD • ⭐️Arteriography for visualization of occlusion/decreased arterial flow with contrast injection on a x-ray. Monitor for bleeding, hemorrhage, marked, pedal pulses • Doppler studies → decreased flow in DM patients • ⭐️Exercise tolerance testing → decreased pressure in lower limbs, read the workload of the heart/circulation, and clarification during exercise. May use treadmill or meds (dipyridamole, adenosine). Finding of a BP/pulse waveform = arterial disease. Monitor vitals before, during, and after. Stop test if chest pain or symptoms are severe. Nursing Interventions • Encourage graded exercise until pain, rest, repeat • Avoid elevating legs above heart (impairs flow) • Avoid cold, caffeine, nicotine, tight clothing • Keep extremities warm (no heating pad), they can’t feel • Foot care: inspect daily, no bare feet, toenails straight Medications • Antiplatelets: (aspirin, clopidogrel) reduces blood viscosity and increases blood flow and extremities. Monitor: bleeding, abdominal pain, black, tarry stools. • Statins: (atorvastatin, simvastatin). Relieved manifestations like intermittent claudication. • Pentoxifylline: improves RBC flexibility (claudication). Monitor for bleeding, abdominal pain, black tarry stools. Procedures • Angioplasty (balloon/stent). Opens and helps, maintain the patency of the vessel, however, laser vaporizes atherosclerosis plaque. Monitor for bleeding, vital signs, pulses, cap Refill. As patients rest limbs are straight for 2-6 hrs before ambulation. Anticoagulant/Antiplatelet therapy given 1-3 months after. • Atherectomy rotation, device removes, arterial plaque. Monitor for bleeding and distal pulses. rest limbs are straight for 2-6 hrs. Anticoagulant/Antiplatelet therapy given 1-3 months after. • Arterial revascularization bypass surgery • Used for clients at risk for losing a limb, severe claudication, or limb pain at rest. It reroutes the circulation around the arterial occlusion. • Post-op: ⭐️ maintain adequate circulation in repaired artery, mark pedal/dorsalis pulses(compare both), monitor color/temp, pain, cap refill, blood pressure (HTN= risk for bleeding; Hypotension=clot risk). • Complications: for these notify provider first -graft occlusion: acute blockage of bypass graft within 24 hr(absent pulse, cold foot, increased pain) -compartment syndrome: tissue pressure restricting blood flow; causing ischemia (numbness, tingling, edema, worsening/passive pain) -infection: infection of site (warm, tenderness, elevated, WBC, purulent drainage, use sterile technique) Patient Education • Walk until pain → rest → walk more • Stop smoking • Avoid crossing legs • Diet low in cholesterol and fat Postoperative Care – Peripheral Bypass/Revascularization Priorities • Assess extremity: color, temperature, cap refill, sensation, pulses q15min ×1hr • Mark pedal pulses before surgery • Maintain adequate BP (avoid hypo or hypertension) • Do not flex hip/knee excessively • Encourage ambulation when ordered • Report sudden pain, loss of pulse, pale/cool extremity = graft occlusion Complications • Graft occlusion, Compartment syndrome, Wound infection Arterial vs. Venous Ulcers Feature Arterial Ulcer Venous Ulcer Location Toes, feet, lateral ankle Medial ankle Appearance Pale, dry, round “punched out”, no drainage Irregular, leaky/moist, brown discoloration Pain Severe, worse with elevation Achy, relieved with elevation Skin Cool, shiny Warm, thickened Treatment Improve arterial flow Compression therapy, elevate legs Valvular Heart Disease OVERVIEW Overview • Stenosis = narrowed opening/thickening and hardening • Regurgitation = backflow of blood • Causes: rheumatic fever, degenerative calcification, endocarditis Diagnostics • Chest X-ray → chamber enlargement • ⭐️ECG → hypertrophy • Echo → valve dysfunction • TEE → direct view of valves ⭐️ Medications overview • Diuretics [furosemide, hydrochlorothiazide, spironolactone]: reduce pulmonary congestion, by removing excessive extracellular fluid. Monitor: hypokalemia, eats foods high in potassium, and administer furosemide IV slowly over 1 – 2 minutes. • Afterload–reducing agents [Beta-blockers (-lol); calcium channel blockers (-dipine); ACE inhibitors (-pril); angiotensin–receptor blockers (-artan); vasodilators (hydralazine]): control heart rate, by lessening resistance to contraction. Monitor: hypotension. • Inotropic agents (digoxin): increases contractility, improves cardiac output. Hold medication if pulse rate (abnormal) is less than 60/min or greater than 100/min. Take medication same time every day, avoid combining with antacids (2hrs). Monitor: toxicity such as weakness, confusion, visual changes, low appetite. • Anticoagulants: reduces risk of thrombus. Monitor: stroke, PT, INR, bleeding/bruising. Procedures • Valvuloplasty (balloon dilation) • Valve replacement • Mechanical = lifelong anticoagulants • Tissue = replace every 7–10 years Patient Education • Prophylactic antibiotics before dental procedures • Good oral hygiene • Daily weights • Sodium restriction • Avoid caffeine/alcohol • Report HF signs (weight gain, edema, SOB) • Avoid alcohol, epinephrine, and ephedrine= can cause dysrhythmias THE 4 VALVULAR DISORDERS Mitral Stenosis Etiology/Pathophysiology: Narrowed mitral valve obstructs blood flow from left atrium (LA) → left ventricle (LV), increasing LA pressure and pulmonary congestion → right-sided heart failure. Often caused by rheumatic fever. Clinical Manifestations: Dyspnea on exertion, orthopnea, pitting edema, fatigue, palpitations, hemoptysis, apical diastolic murmur. Risk Factors: Rheumatic heart disease, aging, congenital malformations. Labs/Diagnostics: Echocardiogram (valve narrowing, pressure gradient), ECG (A-fib), chest X-ray (LA enlargement). Medications/Management: • Diuretics [furosemide, hydrochlorothiazide, spironolactone]: reduce pulmonary congestion, by removing excessive extracellular fluid. Monitor: hypokalemia, eats foods high in potassium, and administer furosemide IV slowly over 1 – 2 minutes. • Afterload–reducing agents [Beta-blockers (-lol); calcium channel blockers (-dipine): control heart rate, by lessening resistance to contraction. Monitor: hypotension. • Anticoagulants: reduces risk of thrombus; prevent emboli from A-fib. Monitor: stroke, PT, INR, bleeding/bruising. • Surgical: Balloon valvuloplasty or valve replacement. NCLEX Tip: Rheumatic fever is the most common cause. Mitral Insufficiency Etiology/Pathophysiology: Incomplete closure of mitral valve causes blood to leak back into LA during systole → LV dilation and hypertrophy. Clinical Manifestations: Fatigue, dyspnea, orthopnea, palpitations, holosystolic murmur at apex, pitting edema, S3 sounds Risk Factors: Mitral valve prolapse, rheumatic disease, MI, endocarditis. Labs/Diagnostics: Echocardiogram (regurgitant volume), ECG (A-fib), BNP (HF indicator). Medications/Management: • Beta-blockers (-lol); ACE inhibitors (-pril); ARBS/angiotensin–receptor blockers (-artan): reduce afterload /control heart rate, by lessening resistance to contraction. Monitor: hypotension. • Diuretics [furosemide, hydrochlorothiazide, spironolactone]: manage fluid overload. Monitor: hypokalemia, eats foods high in potassium, and administer furosemide IV slowly over 1 – 2 minutes. • Anticoagulants if A-fib present; reduces risk of thrombus; prevent emboli from A-fib. Monitor: stroke, PT, INR, bleeding/bruising. • Surgery for severe cases. NCLEX Tip: Afterload reduction decreases regurgitant flow. Aortic Stenosis Etiology/Pathophysiology: Narrowed aortic valve → obstructed LV outflow → ↑ LV pressure → hypertrophy → ↓ cardiac output. Clinical Manifestations: Triad: angina, syncope, dyspnea (heart failure); systolic murmur radiating to carotids. Risk Factors: Aging (calcification), congenital bicuspid valve, rheumatic fever. Labs/Diagnostics: Echocardiogram (valve area), ECG (LV hypertrophy), cardiac cath (pressure gradient). Medications/Management: • Avoid nitrates/vasodilators (can cause hypotension). • Use beta-blockers (-lol) cautiously. reduce afterload /control heart rate, by lessening resistance to contraction. Monitor: hypotension. • Surgical aortic valve replacement (definitive). NCLEX Tip: Do not aggressively lower preload; maintain perfusion. Aortic Insufficiency Etiology/Pathophysiology: Incomplete closure of aortic valve → backflow of blood into LV → volume overload → dilation and LV hypertrophy. Clinical Manifestations: Dyspnea, palpitations, fatigue, bounding (“water hammer”) pulse, wide pulse pressure, diastolic murmur. Risk Factors: Rheumatic fever, endocarditis, Marfan syndrome, trauma. Labs/Diagnostics: Echocardiogram (backflow volume), ECG (LV enlargement), chest X-ray (cardiomegaly). Medications/Management: • Calcium channel blockers (-dipine); ACE inhibitors (-pril); vasodilators (hydralazine]): reduce afterload /control heart rate, by lessening resistance to contraction. Monitor: hypotension. • Diuretics for volume management. • Surgical valve replacement when severe. NCLEX Tip: Bounding pulse and wide pulse pressure are hallmark findings. General Nursing & Exam Focus • Best diagnostic test: Echocardiogram (for all). • Monitor for A-fib in mitral disorders. • Valve replacement (mechanical): Lifelong anticoagulation. • Daily weights & fluid balance: Detect early HF. • Positioning: High-Fowler’s for dyspnea, low-sodium diet. Inflammatory Heart Disorders (Endocarditis, Pericarditis, Myocarditis, Rheumatic Carditis) Risk Factors • IV drug use, valve replacement, streptococcal infection, immunosuppression, lower socioeconomic status Pericarditis: inflammation of the pericardium (sac around heart) -RF: heart attack, lupus, rheumatoid arthriti -Clinical manifestations: Chest pain (relieved when leaning forward), coughing, Pericardial friction rub, fever, dysrhythmias, and SOB -Labs/DX: • High WBCs, EKG showing ST or T spiking, echocardiogram (inflamed heart) -Nursing care/Intervention: address pain/inflammation, and monitor for cardiac tamponade, position, patient upright, leaning forward, and monitor ECG - Medications: NSAIDs, corticosteroids, anti antibiotics for bacterial • Ibuprofen/NSAIDs for inflammation (pericarditis). Avoid if patient has peptic ulcer, monitor for G.I. bleeding, platelets, liver/kidney function. Must be taken with food, avoid alcohol. • Corticosteroids (prednisone) for autoimmune causes (pericarditis/myocarditis). Low-dose first, take with food, and patient must not stop abruptly. Monitor BP, glucose, electrolytes, wounds, infection, sudden weight gain. -Complication: cardiac tamponade → muffled heart sounds, paradoxical pulse, JVD, hypotension (Beck’s triad) Myocarditis: inflammation of the myocardium (heart muscle itself) -RF: viral (covid, Coxsackie), fungal, or bacterial infection; autoimmune disorder -Clinical Manifestations: Tachycardia, chest pain, murmur, friction rub, dysrhythmias, peripheral swelling, cardiomegaly. -Labs/Dx: ECG, echocardiogram, high troponin, CK – MB, ESR in CRP for inflammation/injury -Nursing Care/interventions: monitor for heart failure, and dysrhythmia’s, provide rest and activity restriction -Medication: • Amphotericin B for fungal infection (myocarditis/endocarditis). Monitor liver/kidney function for a G.I. upset. • Corticosteroids (prednisone) for autoimmune causes (pericarditis/myocarditis). Low-dose first, take with food, and patient must not stop abruptly. Monitor BP, glucose, electrolytes, wounds, infection, sudden weight gain. Endocarditis: bacterial infection that leaves inflammation of the endocardium (inner layer of the heart); bacterial or fungal Infection of endocardial tissues that leads to necrosis and embolization of growth -RF: congenital/valvular heart disease, prosthetic valve, IV drug use -Clinical Manifestations: janeway lesions, Fever, murmur, petechiae, splinter hemorrhages (red streaks under nail beds), Osler’s nodes -labs/dx: positive blood culture, echocardiogram -nursing interventions/care: administer IV antibiotics, antipyretics for fever, and anticoagulants, patient should use soft toothbrush, and prophylactic antibiotics before dental/invasive procedures -medication: • Penicillin for infection (rheumatic fever/endocarditis). Monitor for allergic reaction, kidney function/electrolytes. • Amphotericin B for fungal infection (myocarditis/endocarditis). Monitor liver/kidney function for a G.I. upset. Rheumatic Carditis/heart disease: infection of endocardium due to complication of rheumatic fever; GABHS triggers, rheumatic fever leading to inflammatory lesions in the heart -RF: children, Follows untreated strep infection -Clinical Manifestations: tachycardia, Fever, rash(trunk/extremities), joint pain, murmur, chest pain, muscle spasms, friction rub -Labs/Dx: throat culture (strep infection), positive ASO titer, echocardiogram -Nursing care/Interventions: administering antibiotics to stop strep infection, and promote rest, monitor for heart failure, and encourage life on prophylactic antibiotics. -Medications: antibiotics, valve replacement/repair • Penicillin for infection (rheumatic fever/endocarditis). Monitor for allergic reaction, kidney function/electrolytes. Nursing Interventions (Overview for Inflammatory disorders) • Monitor for tamponade & HF • Administer antibiotics (penicillin) • Pain relief (NSAIDs for pericarditis) • Bed rest • Emotional support • Auscultate heart sounds; murmur or friction rub • Collab with cardiologist and physical therapists Procedures (Overview for Inflammatory disorders) • Pericardiocentesis for fluid removal, then sent to laboratory; monitor for recurrence of cardiac tamponade. ( pericarditis.) • Valve surgery if damaged Complications (Overview for Inflammatory disorders) • Cardiac tamponade: medical emergency resulted from fluid accumulation in pericardial sac. S/S: dyspnea, dizziness, tightness in chest, restlessness. Administer IV fluids, notify the provider, obtain chest, x-ray or ECG Cardiac Diagnostics & Vascular Access (Ch. 28) Transesophageal Echocardiography (TEE) Provides clear heart images via probe in the esophagus to detect valve disease, thrombi, or heart failure. NPO 4–6 hr, monitor VS, ECG, and sedation; check gag reflex before eating post-procedure; keep HOB 45°. Stress Testing (Exercise or Pharmacologic) Assesses heart’s response to stress for angina, HF, MI, or dysrhythmia. NPO 2–4 hr, avoid caffeine/tobacco, wear comfortable clothes; stop test for chest pain, SOB, dizziness. Post: monitor ECG & BP until stable. Coronary Angiography (Cardiac Catheterization) Identifies coronary artery blockages using contrast dye via femoral, radial, or brachial artery. NPO 4–6 hr, assess renal function, allergies (iodine/shellfish), and hold metformin 48 hr before/after. Post: monitor VS and site for bleeding, hematoma, or thrombosis, keep limb straight, maintain bedrest. Complications: cardiac tamponade (↓BP, JVD, muffled heart sounds), embolism, hematoma, AKI—notify provider. Teach: report chest pain, bleeding, SOB, avoid lifting >10 lb, and take antiplatelets as prescribed if stent placed. Vascular Access Devices (VADs) Provide reliable central access for fluids, meds, TPN, or blood. Verify tip placement via x-ray before use. PICC: up to 12 mo use, insert in basilic/cephalic vein → SVC; no BP/venipuncture in that arm, keep dressing dry. Tunneled Catheter: long-term use, subcutaneous tunnel prevents infection; no dressing once healed. Implanted Port: long-term chemo access; access with Huber needle, flush with heparin after use. Complications: • Phlebitis: redness, pain, warmth—maintain sterile technique. • Occlusion: flush gently with 10 mL syringe; never force. • Mechanical issues: swelling or pain at port site = dislodgement → notify provider
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Updated 213d ago
flashcards
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
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