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AP Biology Chapter 12: Cell Cycle Flashcards

cell division

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528848682cell divisionthe process in reproduction and growth by which a cell divides to form daughter cells
528848683genomethe ordering of genes in a haploid set of chromosomes of a particular organism
528848684binary fissiona form of asexual reproduction in single-celled organisms by which one cell divides into two cells of the same size
528848685somatic cellany of the cells of a plant or animal except the reproductive cells
528848686chromosomesthreadlike structures made of DNA molecules that contain the genes
528848687chromatinthe readily stainable substance of a cell nucleus consisting of DNA and RNA and various proteins
528848688sister chromatidsidentical copies of a chromosome; full sets of these are created during the S(DNA replication) subphase of interphase
528848689centromerethe region of the chromosome that holds the two sister chromatids together during mitosis
528848690centriolein animal cells, a cytoplasmic organelle that organizes the mitotic spindle fibers during cell reproductions
528848691cell cycleseries of events that cells go through as they grow and divide
528848692mitosiscell division in which the nucleus divides into nuclei containing the same number of chromosomes
528848693M phasemitosis and cytokinesis
528848694cytokinesisThe final stage of the cell cycle, in which the cell's cytoplasm divides, distributing the organelles into each of the two new cells.
528848695interphasecell grows, performs its normal functions, and prepares for division; consists of G1, S, and G2 phases
528848696S phaseThe synthesis phase of the cell cycle; the portion of interphase during which DNA is replicated.
528848697g1 phasethe first gap phase of interphase where the cells do most of their growing, cells increase in size and make new proteins and organelles
528848698G2 phasePeriod of time during interphase--usually the shortest--during which many of the organelles and molecules required for cell division are produced (p. 245).
528848699prophasefirst and longest phase of mitosis, during which the chromosomes become visible and the centrioles separate and take up positions on the opposite sides of the nucleus
528848700prometaphaseThe second stage of mitosis, in which discrete chromosomes consisting of identical sister chromatids appear, the nuclear envelope fragments, and the spindle microtubules attach to the kinetochores of the chromosomes.
528848701metaphasethe stage in mitosis in which the duplicated chromosomes line up along the equatorial plate of the spindle
528848702anaphasethe third phase of mitosis, during which the chromosome pairs separate and move toward opposite poles
528848703telophasethe final stage of mitosis before cytokinesis in which the separated chromosomes reach the opposite poles of the dividing cell and the nuclei of the daughter cells form around the two sets of chromosomes
528848704mitotic spindleAn assemblage of microtubules and associated proteins that is involved in the movements of chromosomes during mitosis.
528848705centrosomeStructure present in the cytoplasm of animal cells, important during cell division; functions as a microtubule-organizing center. A centrosome has two centrioles.
528848706kinetochore microtubulesConnects the centrosome with the kinetochore in the centromere region of the chromosome
528848707kinetochorea specialized condensed region of each chromosome that appears during mitosis surrounding centromere where the chromatids are held together to form an X shape
528848708nonkinetochore microtubulesProduces elongation of the cell as they slide past each other away from the middle of the cell (anaphase)
528848709dyneinA large contractile protein forming the side-arms of microtubule doublets
528848710astersmicrotubules and fibers that radiate out from the centrioles
528848711metaphase plateAn imaginary plane during metaphase in which the centromeres of all the duplicated chromosomes are located midway between the two poles
528848712cleavage furrowThe first sign of cleavage in an animal cell; a shallow groove in the cell surface near the old metaphase plate.
528848713cell plateA double membrane across the midline of a dividing plant cell, between which the new cell wall forms during cytokinesis.
528848714Density dependent inhibitionThe phenomenon observed in normal animal cells that causes them to stop dividing when they come into contact with one another.
528848715growth factorsregulatory proteins that ensure that the events of cell division occur in the proper sequence and at the correct rate
528848716restriction pointThe point in the G1 stage where the cell is committed to continue through the rest of the cell cycle and divide. (Some never reach this point, entering a nondividing phase G0)
528848717kinaseGeneric term for an enzyme that phosphorylates proteins.
528848718cyclinA cellular protein that occurs in a cyclically fluctuating concentration and that plays an important role in regulating the cell cycle.
528848719CdkCyclin-dependent kinases. A protein kinase that is active only when attached to a particular cyclin. Activity rises and falls depending on the concentration of the cyclin partner.
528848720MPFA cyclin-Cdk complex that causes the cell to move from interphase into mitosis
528848721cancerany malignant growth or tumor caused by abnormal and uncontrolled cell division
528848722transformationprocess that converts a normal cell to a cancer cell
528848723cleavageThe process of cytokinesis in animal cells, characterized by pinching of the plasma membrane; specifically

AP Biology Prefixes Flashcards

Prefixes A-B for AP Bio.

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437488234anot, without
437488235abyssdeep, bottomless
437488236acrotip
437488237adenogland
437488238agglutinatglued together
437488239agona contest
437488240aktina ray
437488241-alexito ward off
437488242allo-different
437488243alvelola cavity
437488244amatogether
437488245amphidual
437488246anwithout, not
437488247anaup
437488248analogproportion
437488249andromale
437488250aneuwithout
437488251-angiovessel
437488252annus, ennisyear
437488253anthflower
437488254anthropman
437488255antiagainst
437488256-aphysuck
437488257apictip
437488258apo-off, away
437488259-apsisjuncture
437488260aquawater
437488261arachnspider
437488262archancient, beginning
437488263arthrojointed
437488264astroa star
437488265atrioa vestibule
437488266auto-self
437488267auxgrow, enlarge
437488268bacula rod
437488269benthothe depths of the sea
437488270bitwo
437488271bintwo at a time
437488272bio-,biot-life
437488273-bioslife
437488274-blastbud, sprout
437488275blastoproduce
437488276brachioan arm
437488277bryomoss

AP Biology Chapter 9 Key Terms Flashcards

Doc Voc AP Bio

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225625886Hereditythe transmission of traits from one generation to the next
225625887Geneticsthe scientific study of heredity
225625888Charactera heritable feature that varies among individuals, such as flower color
225625889Traiteach varient for a character, such as purple or white flowers, brown or blond hair
225625890Self-fertilizesperm-carrying pollen grains released from the stamens land on the egg-containing carpel of the same flower
225625891Cross-fertilizationfertilization of one plant from the pollen of another plant
225625892True-breeding varietiesvarieties for which self-fertilization produced offspring all identical to the parent
225625893Hybridthe offspring of two different varieties
225625894Genetic crosscross fertilization is simply referred to as this
225625895P generationthe true-breeding parental plants
225625896F1 generationthe parental plants hybrid offspring
225625897F2 generationthe self or cross fertilized offspring of the F1 generation
225625898Dihybrid crossa mating of parental varieties differing in two characters
225625899Law of Independent Assortmentthe inheritance of one character has no effect on the inheritance of another
225625900Testcrossa mating between and individual of unknown genotype (a BB or Bb black lab, you dont know) and a homozygous recessive (bb, chocolate lab) individual.
227682766Monohybrid Crossa cross in which the parents differ in only one characteristic
227682767Allelethe alternative version of a gene
227682768Homozygousan organism that has two identical alleles for a gene is said to be this
227682769Heterozygousan organism that has two different alleles for a gene is said to be this
227682770dominant allelethe allele that if present will always show, PP or Pp
227682771recessive allelethe allele that will only show if two of the same, pp
227682772law of segregationa sperm or egg carries only one allele for each inherited character because allele pairs separate from each other during the production of gametes
227682773Punnett Squarea chart that shows all the possible combinations of alleles that can result from a genetic cross
227682774Phenotypean organisms physical trates (purple or white flowers)
227682775Genotypean organisms genetic makeup (PP,Pp,pp)
227682776Locusa specific location of a gene along the chromosome
227682777Rule of multiplicationthe probability of such a compound event is the product of the probabilities of each independent event
227682778Rule of additionthe probability that an event can occur in two or more alternative ways is the sum of the separate probabilities of the different ways
227682779Wild-type traitstraits prevailing in nature
227682780Pedigreea family tree that contains all the information of who in the family had or didnt have a specific trait
227682781Carriersomeone who has a recessive allele but also has a dominant one
227682782Cystic Fibrosis (CF)the most common life threatening genetic disease in the US, caused by a recessive allele, excess mucus in the lungs, increased susceptibility to infections, death in early childhood if not treated
227682783Inbreedingmatings between close blood relatives
227682784Achondroplasiaa form of dwarfism in which the head and torso of the body develop normally but the arms and legs are short
227682785Huntington's Diseasea degenerative disorder of the nervous system that usually does not appear until middle age, fatal
227682786Amniocentesisthe collections of fetal cells, from the amniotic fluid that bathes the fetus, for genetic testing
227682787Chorionic villus sampling (CVS)a physician extracts a tiny sample of chorionic villus tissue from the placenta, the organ that carries nourishment and wastes between the fetus and the mother, and uses them to make a karyotype
227682788Ultrasound imaginguses sound waves to produce a picture of the fetus directly
228597719Complete Dominancethe dominant allele has the same phenotypic effect whether present in one or two copies
228597720Incomplete Dominancethe appearance of the F1 hybrids falls between the phenotypes of the two parents varieties
228597721ABO Blood Groupgenetically determined classes of human blood that are based on the presence or absence of carbohydrates A and B on the surface of red blood cells; the phenotypes, also called blood types, are A, B, AB, and O
228597722Codominantthe expression of both alleles in a heterozygous individual
228597723PleiotropyA single gene having multiple effects on an individuals phenotype
228597724Sickle-cell diseasemakes red blood cells produce abnormal hemoglobin proteins
228597725Polygenic inheritancethe additive effects of two or more genes on a single phenotypic character, the converse of pleiotropy
228597726The Chromosome Theory of Inheritancegenes occupy specific loci on chromosomes, and it is the chromosomes that undergo segregation and independent assortment during meiosis. Thus, it is the behavior of chromosomes during meiosis and fertilization that accounts for inheritance patterns
228597727Linked Genesgenes located close together on the same chromosome
228597728Recombinant Frequencythe percentage of recombinants
228828169Linkage Mapa diagram of relative gene location
228828170Sex chromosomesthe pair of chromosomes, designated x and y, that determine and individuals sex
228828171Sex-linked genea gene located on either sex chromosome
228828172Hemophiliaan x-linked recessive trait with a long, well-documented history. Hemophiliacs bleed excessivley when injured because they lack one of more of the proteins required for blood clotting.
228828173Red-green colorblindnessa sex-linked recessive disorder in humans that causes a malfunction of light-sensitive cells in the eyes
228828174Duchenne muscular dystrophya condition characterized by a progressive weakening of the muscles and a loss of coordination, is another human x-linked recessive disorder

Immigration, Urbanization, and Industrialization Flashcards

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523851612Andrew Carnegieinvested well and became rich in steel industry - started as a "bobbin boy" - donated a lot of $ and built libraries, etc. "captain of industry" 1865 Keystone Bridge Company. wealthiest man in history - worth about 670 trillion dollars today. "The Gospel of Wealth"
523851613Montgomery WardFirst catalogue sales business - 1872 - shipped via RR - good for farmers - cheaper than buying items in a store - more variety
523851614Sears, Roebuck, & Co."the great wishbook" - another catalogue company
523851615C.J. Walkersold hair products by mail and door to door. first AOAD millionaire
523851616Granville T. Woodsinvented the railroad telegraph system - prevented collisions
523851617Gustavus Swift & Philip Armourinvented refrigerated rail cars - helped with the transport of meat by railroad
523851618George Pullmaninvented sleeping railroad cars (helped for long trips)
523851619rebatesrefunds - part of shipping costs with large shippers - often secret deals - illegal kickbacks/payment made to RR customers
523851620consolidationcurbing competition - combination of companies to form a big business together
523851621Cornelieus Vanderbuiltmaster of RR consolidation - more efficient and cheap - could charge a lot - no competition
523851622Collis Huntington & Lyman Huntingtonfather and son team of great eastern RR developers
523851623The Great Northern RailroadVanderbuilt's RR - NY to Chicago
523851624The Canadian Shieldforest region of rocks, swamps, and marshes - accessible only by foot or canoe - where most of the iron ore came from for making steel
523851625Leonidas Merrittfound iron ore in Canadian Shield in Mesabi Range in 1890. Rockefeller financed the operation
523851626regulatemake rules for (RR & other big companies) in 1866 the Supreme Court ruled that states couldn't regulate the rates of RRs that crossed state lines
523851627free enterpriseeconomic system in which businesses are free to compete without government rules
523851628Interstate Commerce Actpassed by Congress in 1887 which declared that all RR rates must be "reasonable and just" and the Interstate Commerce Commission investigated
523851629Henry BessemerBritish inventor who created the "Bessemer Process" - a process that reduced the cost of making steel
523851630J.P. Morganmost powerful investment banker. took over Carnegie's RR - formed U.S. Steel Corp. - largest in the world
523851631John D. Rockefellerfrom Cleveland. in 1862 made Oil Refinery business. 1870 - Standard Oil Company, by 1880 it was a monopoly
523851632trustbusiness combination - a board of trustees (managers) control member corporations. stockholders get dividends (money) from their investment in the company
523851633monopolysingle business with the power to control the prices in the market
523851634Sherman Antitrust Actcreated in 1890 and said that the combinations of companies were illegal, but it didn't define a trust or monopoly, so it was a hard act to enforce. broke up Standard Oil Trust in the early 1900s
523851635Triangle Shirtwaist Fire1911. 146 workers died.
523851636Mary Harris Jones"the most dangerous woman in America" - "Mother Jones" - between 1870s and 1920s she traveled and urged workers to join Unions
523851637Knights of Laborfounded in 1869. Union that accepted women and children. 700,000 members by 1886
523851638Terrance Powderlymayor of Scranton, PA, leader of Knights of Labor in 1879. wanted an 8 hour work day and end child labor and have equal pay for all workers. Unions gained strength at this time. He liked arbitration
523851639Great Railroad Strike1877 - Baltimore and Ohio RR workers went on strike and then it went nationwide. unsuccessful strike. 100 workers killed
523851640Haymarket BombingMay 3, 1886 - Chicago strikers and police clash, May 4 - meeting to protest killings, bomb exploded, police fired on the crowd. 16 killed, 100 wounded. Knights of Labor membership declined after this
523851641Samuel Gompersliked strikes. president of AFL, which had many members. wanted collective bargaining, increased wages, fewer hours, better working conditions
523851642AFLAmerican Federation of Labor - skilled laborers. No women, AOAD, or immigrants
523851643Homestead StrikeJuly 6, 1892. workers in Carnegie's Steel Plant in PA went on strike - people were hired to replace them. guards arrived. fight broke out. Union broke up.
523851644Henry Clay Frickmajor lieutenant of Carnegie, leader of the resistance to the Homestead strike. Believed in the use of force or scab labor to keep factories running
523851645Pullman StrikePullman Palace Car Company. cut wages, didn't lower rent. May 1894 was the strike. There was a federal injunction in July 1894 and federal troops were sent to Chicago. Riots broke out
523851646ARUAmerican Railway Union. Supported Pullman Strike. derailed railcars and blocked tracks
523851647Eugene Debsfounded ARU - sent to jail. leader of the Socialist Party of America (1901)
523857402Westinghouseinvented RR airbrakes
523857403Robber BaronsCarnegie, JP Morgan, Rockefeller
523877761Where was the nation's first oil well?Pennsylvania
523877762Injunctioncourt order to stop an action by a business or individual
523877763Emperor Meijiannounced a plan in 1867 to make Japan a major industrial nation
523989488scabUnion member who crosses the picket like to work for the company instead of continuing to strike with the rest of the union members. (Not a popular thing to do)
523989489Thomas Anshutzmajor American painter of the day to day life of the time
523989490standard gaugedevelopment was a great RR breakthrough
523989491Brooklyn Bridgelongest steel suspension bridge in the world
523989492socialismthe belief that government should own a nation's industries
523992988CIOCongress/Committee of Industrial Organizations - proposed by John L. Lewis in 1938, was a federation of unions that organized workers in industrial unions.The CIO merged with the AFL to form the AFL-CIO in 1955.

AP The Earth and its People Chap 12 Flashcards

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535615044Ashikaga ShogunateThe second of Japan's military governments headed by a a military ruler
535615046BeijingChina's northern capital, first used as an imperial capital in 906 and now the capital of the People's Republic of China
535621523Bubonic PlagueA bacterial disease of fleas that can be transmitted by flea bites to rodents and humans; humans in late stages of the illness can spread the bacteria by coughing. Because of its very high mortality rate and the difficulty of preventing its spread, major outbreaks have created crises in many parts of the world.
535615048Genghis KhanThe title of Temüjin when he ruled the Mongols (1206-1227). It means the "oceanic" or "universal" leader. He was the founder of the Mongol Empire.
535615050Golden HordeMongol khanate founded by Genghis Khan's grandson Batu. It was based in southern Russia and quickly adopted both the Turkic language and Islam.
535615052Il-khanA "secondary" or "peripheral" khan based in Persia. Was founded by Hülegü, a grandson, and was based at Tabriz in modern Azerbaijan. It controlled much of Iran and Iraq.
535615054kamikazeThe "divine wind," which the Japanese credited with blowing Mongol invaders away from their shores in 1281.
535630319Khubilai KhanLast of the Mongol Great __________. Founder of the Yuan Empire.
535615056lamaIn Tibetan Buddhism, a teacher.
535615058MongolsA people of this name is mentioned as early as the records of the Tang Empire, living as nomads in northern Eurasia. After 1206 they established an enormous empire under Genghis Khan, linking western and eastern Eurasia.
535615060Nasir al-DinPersian mathematician and cosmologist whose academy near Tabriz provided the model for the movement of the planets that helped to inspire the Copernican model of the solar system.
535615061Alexander NevskiiPrince of Novgorod. He submitted to the invading Mongols in 1240 and received recognition as the leader of the Russian princes under the Golden Horde.
535615063nomadismA way of life, forced by a scarcity of resources, in which groups of people continually migrate to find pastures and water.
535615065Ottoman EmpireIslamic state founded by Osman in northwestern Anatolia ca. 1300. After the fall of the Byzantine Empire, this empire was based at Istanbul (formerly Constantinople) from 1453 to 1922. It encompassed lands in the Middle East, North Africa, the Caucasus, and eastern Europe.
535615066Rashid al-DinAdviser to the Il-khan ruler Ghazan, who converted to Islam.
535615067TimurMember of a prominent family of the Mongols' Jagadai Khanate. Through conquest gained control over much of Central Asia and Iran. He consolidated the status of Sunni Islam as orthodox, and his descendants maintained his empire for nearly a century and founded the Mughal Empire in India
535615068tsarFrom Latin caesar, this Russian title for a monarch was first used in reference to a Russian ruler by Ivan III
535615069YiThis dynasty ruled Korea from the fall of the Koryo kingdom to the colonization of Korea by Japan.
535615070YongleReign period of Zhu Di (1360-1424), the third emperor of the Ming Empire (r. 1403-1424). He sponsored the building of the Forbidden City, a huge encyclopedia project, the expeditions of Zheng He, and the reopening of China's borders to trade and travel.
535615071Yuan EmpireEmpire created in China and Siberia by Khubilai Khan.
535615072Zheng HeAn imperial eunuch and Muslim, entrusted by the Ming emperor Yongle with a series of state voyages that took his gigantic ships through the Indian Ocean, from Southeast Asia to Africa.
535630320Ming EmpireEmpire based in China that Zhu Yuanzhang established after the overthrow of the Yuan Empire. The Ming emperor Yongle sponsored the building of the Forbidden City and the voyages ofthe Zheng He. The later years of the Ming saw a slowdown in technological development and economic decline.

Chapter 16 Campbell Vocab Flashcards

Anderson AP Bio

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494713844BacteriaOne of two prokaryotic domains, the other being Archaea.
494713845BacteriophageA virus that infects bacteria; also called a phage.
494713846BacteriumMember of the prokaryotic domain Bacteria.
494713847ChromatinThe complex of DNA and proteins that makes up a eukaryotic chromosome. When the cell is not dividing, chromatin exists in its dispersed form, as a mass of very long, thin fibers that are not visible with a light microscope.
494713848deoxyriboseThe sugar component of DNA nucleotides, having one fewer hydroxyl group than ribose, the sugar component of RNA nucleotides.
494713849DNA ligaseA linking enzyme essential for DNA replication; catalyzes the covalent bonding of the 3' end of one DNA fragment (such as an Okazaki fragment) to the 5' end of another DNA fragment (such as a growing DNA chain).
494713850DNA polymeraseAn enzyme that catalyzes the elongation of new DNA (for example, at a replication fork) by the addition of nucleotides to the 3' end of an existing chain. There are several different DNA polymerases; DNA polymerase III and DNA polymerase I play major roles in DNA replication in prokaryotes.
494713851Double helixThe form of native DNA, referring to its two adjacent antiparallel polynucleotide strands wound around an imaginary axis into a spiral shape.
494713852EuchromatinThe less condensed form of eukaryotic chromatin that is available for transcription.
494713853HelicaseAn enzyme that untwists the double helix of DNA at the replication forks, separating the two strands and making them available as template strands.
494713854HeterochromatinEukaryotic chromatin that remains highly compacted during interphase and is generally not transcribed.
494713855HistoneA small protein with a high proportion of positively charged amino acids that binds to the negatively charged DNA and plays a key role in chromatin structure.
494713856Lagging strandA discontinuously synthesized DNA strand that elongates by means of Okazaki fragments, each synthesized in a 5'3' direction away from the replication fork.
494713857Leading strandThe new complementary DNA strand synthesized continuously along the template strand toward the replication fork in the mandatory 5'?3' direction.
494713858Mismatch repairThe cellular process that uses specific enzymes to remove and replace incorrectly paired nucleotides.
494713859NucleaseAn enzyme that cuts DNA or RNA, either removing one or a few bases or hydrolyzing the DNA or RNA completely into its component nucleotides.
494713860NucleoidA dense region of DNA in a prokaryotic cell.
494713861Nucleoid regionA dense region of DNA in a prokaryotic cell.
494713862NucleosomeThe basic, bead-like unit of DNA packing in eukaryotes, consisting of a segment of DNA wound around a protein core composed of two copies of each of four types of histone.
494713863Nucleotide excision repairA repair system that removes and then correctly replaces a damaged segment of DNA using the undamaged strand as a guide.
494713864Okazaki fragmentA short segment of DNA synthesized away from the replication fork on a template strand during DNA replication, many of which are joined together to make up the lagging strand of newly synthesized DNA.
494713865Origin of ReplicationSite where the replication of a DNA molecule begins, consisting of a specific sequence of nucleotides.
494713866PhageA virus that infects bacteria; also called a bacteriophage.
494713867PrimaseAn enzyme that joins RNA nucleotides to make the primer using the parental DNA strand as a template.
494713868PrimerA short stretch of RNA with a free 3' end, bound by complementary base pairing to the template strand, that is elongated with DNA nucleotides during DNA replication.
494713869PyrimidineOne of two types of nitrogenous bases found in nucleotides, characterized by a six-membered ring. Cytosine (C), thymine (T), and uracil (U) are pyrimidines.
494713870Radioactive isotopeAn isotope (an atomic form of a chemical element) that is unstable; the nucleus decays spontaneously, giving off detectable particles and energy.
494713871Repetitive DNANucleotide sequences, usually noncoding, that are present in many copies in a eukaryotic genome. The repeated units may be short and arranged tandemly (in series) or long and dispersed in the genome.
494713872Replication forkA Y-shaped region on a replicating DNA molecule where the parental strands are being unwound and new strands are growing.
494713873Semiconservative modelType of DNA replication in which the replicated double helix consists of one old strand, derived from the old molecule, and one newly made strand.
494713874Single-strand DNA-binding protein (SSBPs)A protein that binds to the unpaired DNA strands during DNA replication, stabilizing them and holding them apart while they serve as templates for the synthesis of complementary strands of DNA.
494713875TelomeraseAn enzyme that catalyzes the lengthening of telomeres in eukaryotic germ cells.
494713876TelomereThe tandemly repetitive DNA at the end of a eukaryotic chromosome's DNA molecule that protects the organism's genes from being eroded during successive rounds of replication. See also repetitive DNA.
494713877Template strandThe DNA strand that provides the pattern, or template, for ordering the sequence of nucleotides in an RNA transcript.
494713878TopoisomeraseA protein that breaks, swivels, and rejoins DNA strands. During DNA replication, topoisomerase helps to relieve strain in the double helix ahead of the replication fork.
494713879Transformation(1) The conversion of a normal animal cell to a cancerous cell. (2) A change in genotype and phenotype due to the assimilation of external DNA by a cell.
494713880X-ray crystallographyA technique that depends on the diffraction of an X-ray beam by the individual atoms of a crystallized molecule to study the three-dimensional structure of the molecule.

ACE PT Exam Chapter 1 Exercise Physiology Flashcards

Study aid to prepare for the ACE personal trainer certification exam: Chapter 1 Exercise Physiology

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439652927Vena cava, right atrium, right ventricle, pulmonary valve, pulmonary arteries, lungs, pulmonary veins, left atrium, mitral valve, left ventricle, aortasequence of blood flow through the heart
439652928Oxygen extractionhas the greatest influence on exercise performance
439652929diastolephase in which the heart refills
439652930Frequency, time, type, and intensity (FITT)basis of exercise program development
439652931have a higher aerobic capacity than fast-twitch fiberscharacteristic of slow-twitch muscle fibers
439652932Isotonicmuscle action in which the tension created by the muscle is variable throughout the range of motion
439652933Contractile forceGolgi tendon organs serve as a protective mechanism against excessive
439652934A nervous impulse from the central nervous systemAccording to the sliding filament theory of muscle contraction, which of the following is the FIRST step in the sequence of events
439652935isometricsame length; high intensity/maximal contraction; ex: pushing against an immovable object
439652936isotonicsame tone or tension: given resistance challenged through entire range of motion; ex: biceps curl with dumbbell
439652937isokineticsame speed; muscles generate maximum force through the entire range of motion while keeping the speed constant
439652938ATPadenosine triphosphate; the body's energy source produce from fat, carbs (glucose) and some protein
439652939ways to replenish ATPaerobic system and anaerobic systems: anaerobic glycolysis and creatine phosphate
439652940glycogenchain of glucose stored in muscles & liver; primary source of anaerobic ATP production
439652941optimum exercise intensity for fitness improvement50-80% VO2 max (maximum oxygen consumption) which corresponds to 60-90% maximum heart rate
4396529423,500calories that must be burned to lose 1 pound
439652943VO2 maxmaximum oxygen consumption OR maximum aerobic capacity; total capacity of the body to consume oxygen at the cellular level
439652944formula to calculate VO2 maxVO2 max (ml/kg/min OR L O2/min) = cardiac output max X O2 extraction max
439652945cardiac outputheart rate (beats per minute) X stroke volume (amount of blood pumped from each ventricle with each heart beat)
439652946typical cardiac output at rest60 bpm X 70 ml = 4,200 ml/min or 1 gallon of blood per minute
439652947aerobicwith oxygen; the first system to produce ATP; dominant system when adequate oxygen is delivered to the cell to meet energy production needs; ex: when muscle is at rest; uses fatty acids and glucose to produce ATP; produces more than anaerobic because fat = 9 calories of energy per gram
439652948anaerobicwithout oxygen; when inadequate oxygen supply is available, anaerobic glycolysis and creatine phosphate systems produce ATP; carbs/glucose 4 calories of energy per grams
439652949mitochondriasite of ATP production in cells; the more mitochondria - the more aerobic energy production capability of the cell
439652950ischemiadecreased blood flow to the heart leading to insufficient oxygen to the heart and chest pain or angina
439652951anaerobic thresholdpoint during high intensity exercise when the body can no longer meet its oxygen needs and switches to anaerobic metabolism; 50-80% maximum effort
439652952slow twitch muscle fiberslow speed of contraction & high capacity for aerobic glycolysis (e.g., marathon runner)
439652953fast twitch muscle fiberfast speed of contraction & high capacity for anaerobic glycolysis (e.g., sprinter, power lifter)
439652954golgi tendon organtendon organ/part of nervous system protecting the muscle from too much contractile force; causes muscle to relax
439652955Inability to extract O2 and use it at the muscle efficientlyprimary limiting factor to no longer be able to aerobically produce ATP
439652956Muscle stores little CP and ATPprimary limitation of producing ATP in the phosphagen system
439652957creatine phosphate systemsecondary source anaerobic ATP (to glycogen); high energy phosphate molecule store in cells; can be used to resynthesize ATP immediately; system of energy transfer for resynthesis of ATP without oxygen via breakdown of the CP molecule
439652958glucose and fatty acidprimary energy source for runner 45-60 min @ 65% VO2 max
43965295985%upper limit max HRR for submax bike ergonometer test
439652960family history heart disease, 200+ cholesterol, cigarette smokingACSM positve coronary risk factors
439652961isometric trainingstrength increases specific to joint angle where contraction occurs
439652962max HR/resting HR too highKarvonen formula error for client with overexertion during aerobics w/max HR within range
439652963caffeinediuretic, increases HR & may enhance endurance performance
439652964increased cardiac output at restphysiological effects of high altitude
439652965regular exercise, modify intensity & avoid prolonged supine positionACOG guidelines for pregnant women 2 & 3 trimesters
439652966optimum fitnesscardio endurance, muscular strength, flexibility & maintain ideal body weight
43965296721 - 24%fit woman body fat %age
43965296814 - 17%fit man body fat %age
439652969hemoglobinprotein that carries oxygen in red blood cells
439652970benefit of cv fitnessheart spends more time in relaxation phase/diastole -- at rest or during exercise
439652971ejection fraction% total blood volume remaining in ventricles @ the end of diastole that is subsequently ejected during contraction
439652972lactic acidbyproduct of anaerobic ATP production
439652973METmetabolic equivalent; resting VO2 max of 3.5 mL/kg/min
439652974changes in cardiac output due to aerobic conditioningventricles hold more blood/resting HR decreases; stroke volume @ rest increases; same cardiac output can be maintained at lower HR; and increased mitichondrial density
439652975changes in O2 extraction due to aerobic conditioningmore capillaries; more mitochondria & more activity of mitochondrial enzymes
439652976muscle pumprhythmic squeezing of large muscles leg/butt against veins; increases blood supply/flow to/from heart
43965297750-80%max O2 consumption for general fitness improvement
43965297860-90%max HR for general fitness improvement
43965297920 minutes 3-4X per weekminimum duration and frequency of exercise sessions
439652980benefits aerobic exerciseimproved body comp; decreased appetite; burn calories; strengthen skeletal system; & increase insulin sensitivity
439652981cardiac, smooth & skeletaltypes of muscle cells
439652982myofibrilsprotein strands running the length of each muscle fiber
439652983actin and myosincontractile proteins in the myofibrils
439652984sarcomeresrepeating units running the length of each muscle fiber
439652985sliding filament theory1. CNS sends nerve impulse; 2. sufficient ATP near actin and myosin protein; 3. myosin heads/filamints attach to actin to form crossbridge; 4. myosin pulls actin to the center; 5. sacromere shortens/contraction occurs
439652986size of fibers contracting & # of fibers contracting simultaneouslytwo factors that determine amount of force generated during contaction in the whole muscle
439652987all-or-nothing principlewhen a skeletal muscle is stimulated to contract it does so with maximum force; can't grade contractile force like caridiac muscle cells can
439652988muscle spindlesfibers in the muscle tissue protecting against too much stretching; causes to muscle to contract
439652989factors limiting flexibility1. elastic limits ligaments & tendons; 2. muscle tissue elasticity; 3. bone & joint structure; 4. the skin
439652990immediate muscle sorenesslactic acid build up
439652991delayed onset muscle sorenesssmall tears in the muscle
439652992CV effects of single exercise session1. systolic bp increases; 2. diastolic bp no change or decreases; 3. blood flow to abdomen decreases (goes to the limbs); 4. peripheral resistance in vascular system decreases; 5. ATP production increases
439652993causes of muscular fatigue1. power event 1-30 seconds: depleted ATP; 2. 30 minutes heavy exercise: build up of lactic acid; 3. 3 hour marathon: depletion of glycogen stores
439652994ejection fraction50% @ rest and 100% during exercise
439652995reach anaerobic thresholdat 50-80% of maximal effort
439652996responses to aerobic training1. resting HR: decreases; 2. stroke volume at rest: increases; 3. VO2 max: increases; 4. max HR: no change (based on your age); 5.mitochondrial density in muscle: increases; 6. anaerobic threshold: increases; 7. HR at submax intensity: decreases
439652997training rules for cv fitness1. appropriate activity: rhythmic large muscle movements; 2. freq: 3X weekly; 3. duration: 10-20 min per session; 4. intensity: 50-80% VO2 max
439652998phosphagenscreatine phosphate & ATP; muscles store only enough to provide 10 seconds of max effort; in even well trained athletes

Adrenal Physiology Flashcards

ACTH + Adrenal Physiology

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407365299HPA AxisThis is the hypothalamic-Pituitary Adrenal axis and control
407365300CRHCorticotropin Releasing Hormone
407365301ACTHAdreno-CorticoTropin Hormone
407365302ADH=AVPAnti-Diuretic Hormone
407365303GC'sGlucocorticoids
407365304Primary DeficiencyThis is an issue with the target hormone
407365305SecondaryThis is a pituitary issue
407365306TertiaryThis is an issue with the hypothalamus
407365307SecretagogueThis is something that increases the secretion of substance [X]
407365308Key feedback pointsCortisol production normally turns off ACTH and CRH synthesis -Cortisol also turns off ADH synthesis meaning you retain more H2O -The lack of ADH synthesis leads to hyponatremia "hyperwateremia"
407365309GFRThis is the acronym that helps you to remember the three layers of the adrenal cortex G-Glomerulosa (makes Aldoseterone) -RAS acts here F-Fasciculata (Makes Cortisol) -ACTH acts here and does its thing R-Reticularis (Makes sex steroids) The Adrenal Cortex is completely under the control of the sympathetic nervous system
407365310ACTH Secretagogues to watch for-CRH (BIG ONE), ADH, cholycystokin plays a role to Another critical thing to watch out for is for tanned skin in these individuals
407365311Glucocorticoid Function-All cells have receptors!! -Monitor many of the critical functions within the cell! -Also manage the metabolism of various biologic compounds -Important in immunity and wounds -Maintains CVS integrity and contractility Type of shock with a lack of glucocorticoids: -Distributive (lack of vasoconstriction) and Hypovolemic (lack of aldosterone + contractility)!!
407365312Clinical Features of Primary AI-Tanned Skin -Vitilgo (other autoimmune conditions) -Decreased body hair -Hyperkalemia -Salt craving
407365313Clinical Features of Secondary AIDouble Vision, Decreased Acuity, Headaches, Nausea, Vomiting and other pituitary related symptoms
407365314Normal Cortisol SecretionIt is PULSATILE -Circadian Rhythm similar directly opposite to GH secretion -Highest between 4 am to 8 am -Lowest between 11 pm and 4 am -Negative feedback inhibition by glucocorticoids
407365315Severe Stress leading to cortisol release•Severe Trauma •Burns •Illness •Major surgery •Hypoglycemia •Fever •Hypotension •Exercise •Cold exposure Activation? -It activates the HPA stimulating the release of CRH and AVP -When you get this sort of activation
407365316The "Steroid Fork"SEE THE CHART THA YOU MADE -Only biochemical pathway to memorize before the exam
407365317Congenital Adrenal Hyperplasia21 Hydroxylase deficiency!! -This is the most common enzyme deficiency -Autosomal Recessive condition that you are dealing with Because you aren't making any aldosterone or cortisol you end up with a ton of ACTH -this makes your skin very tanned No ALDO -hypo Na, Hyper K, acidosis, hypotension, circulatory collapse No Cortisol -Failure to thrive, lethargy, hypoglycemia Androgen effect on females -Ambiguous Genitalia (fusion of labial folds, clitoromegaly, penile urethra, urogenital sinus) -most common cause of ambiguous genetalia in XX females Androgen Effect on males: -Normal male anatomy -Precocious puberty (Excess growth, acne, pubic hair) -Easily missed if not presenting with adrenal insufficiency Diagnosis: You want to try and stimulate with ACTH -you won't get an adequate response in these people -You will also get a buildup of side products as you try to stimulate it -Consider making it in females with ambiguous genitalia, cryptochid males, an infant with shock, hypoglycemia, hyper K Treatment: -Acute fluid resuscitation (Isotonic saline) -Acute glucocorticoid/mineralocorticoid replacement (aldosterone and cortisol) -Surgical Therapy (Clitoris reconstruction, vafinoplasty/correction of urogenital sinus)
407365318Primary Adrenal InsufficiencyDisease of the cortex in both glands: Destruction or surgical removal Infiltration Hypoplasia Infarction -Potentially life-threatening deficiency of both glucocorticoids and mineralocorticoids Common Causes: -Autoimmune or addisons disease (Developed world) -Developing world #1 cause is TB (5% of all cases) Rare Causes: Congenital, Infectious, Drugs, Hemorrhage/thrombosis Epidemiology: 1/10000 people -5 cases per 1 million per year -50% of these people present in life threatening crisis even though they have had symptoms up to a year before! Diagnosis: -You can do anti-adrenal antibodies to help you figure out what you are deficient in -Often have low aldosterone and hyponatremia -Also can be hyperkalemia -Mildly elevated TSH
407365319Secondary Adrenal Insufficiency1. Suppression of normal hypothalamic-pituitary-adrenal axis with exogenous glucocorticoids -Eg: Prednisone 30 mg daily x 2 years for Crohn's disease 2. Diseases of the hypothalamus/pituitary leading to deficiency of adrenocorticotrophic hormone ACTH -Eg: Pituitary tumour infiltrating the normal gland 3. Adrenal suppression following successful therapy of endogenous Cushing's syndrome -Eg: Post-op day #1 from laparoscopic adrenalectomy Diagnosis: -Steroid History (any type) -Headaches (pituitary issues) -Polyuria, polydypsia, nocturia -Head trauma or other CNS disease -Pituitary surgery/radiation -Pale alabaster skin -No salt craving -Post Partum bleed -Mildly elevated TSH
407365320Tests of Adrenal FunctionRandom Cortisol -this is a test that is rarely useful -ACTH can only help you to interpret these tests not give you the actual diagnosis Insulin Tolerance test -This is the gold standard and should induce the production of a TON of Cortisol -Contraindicated in seizure disorders/heart disease -Can only be done in major centres ACTH stimulation -this is clinical clerk proof -If you don't get the desired response than you have shown to have cortisol deficiency
407365321Treating of acute deficient patientsABC's IV access + bolus normal saline IV hydrocortisone 100 mg q8h Look for infectious, cardiac, or metabolic precipitants Close monitoring; may need ICU
407365322Treatment of Chronic PatientsYou need to give a physiologic dose that matches what you would expect in a normal person -Too little would give you weight loss and hypotension -Too much gives you cushing, diabetes, htn and osteoporosis In primary cases you need to give salt because you are going to waste a ton of it!! You shouldnt give sex steroids in primary adrenal insufficiency because you can't get compounds containing the correct amount of hormone in it
407365323Hypercortisolemia presentationsNon-Cushings syndromes: 1. Rapid onset of disease -Ex. new high dose of exogenous corticosteroids 2.High serum cortisol does not reflect the action of free cortisol on the receptor -could be just high cortisol binding globulin (birth control pill) -could also be due to resistance syndrome (rare)
407365324Road map to follow1. Make a clinical diagnosis 2. Confirm unequivocal hypercortisolism 3. ACTH dependent or independent ? 4. More tests to elicit and image the source 5. Treatment
407365325Epidemiology of HyperCEndogenous 2-10 cases per million -2-3% = DM -HTN 0.5-1% of all cases -Incidental Adrenal mass 6-9% Exogenous: unknown but much higher -Untreated: mortality 4-5 times increased -Average disease duration before diagnosis
407365326Incidence of causes of CushingsCushing disease ->70% Ectopic ACTH ->10% Ectopic CRH <1% Adrenal Adenoma -> 10% Adrenal Carcinoma -> 5% Adrenal (other) -> 4%
407365327Clinical Diagnosis-Emotional Disturbance -Enlarged Sella turcica -Moon Facies (wide face) -Osteoporosis (fragility fractures) -Cardiac hypertrophy (HTN related) -Buffalo Hump (dorsocervical) -Obesity (Central!!!) -Adrenal turmor or hyperplasia -Think wrinkled skin (bruises easily to) -Abdominal Striae -Amenorrhea (Hirsutism) -Muscle Weakness (proximal) -Purpura -Skin Ulcers Difficulties: -You may have a huge overlap with other conditions -Type II diabetes -Obesity -Polycystic ovarian syndrome Helping ->Take pictures and seek old photos
407365328Unequivocal Hypercortisolism3 tests to use in combination 1) 24 hr urine free cortisol -gold standard but patient compliance kind of sucks 2) Late night salivary cortisol -chew, soak at 11pm and then collect -new kid on the block 3) Overnight low dose dexamethasone suppression test -should be suppressed however in people with cushings it will still be elevated
407365329ACTH dependent of Independent??Basal plasma ACTH level Suppressed <1.1 pmol/L ACTH-independent cause High or inappropriately normal >3.3 pmol/L ACTH-dependent cause Indeterminate: 1.1-3.3 pmol/L Repeat ACTH; consider CRH stimulation test
407365330Tests to elicit the sourceACTH-Independent -You want to do a CT scan to look for an adrenal tumor -small is an adenoma -large can be an adrenal carcinoma!!! ACTH dependent -Tell between pituitary or ectopic sources -Pituitary: these can often be seen on CT or MRI (6mm or larger is cushings disease) -Ectopic is the ACTH sampling (Central:Peripheral ACTH > 2:1 is cushing's disease)
407365331Ectopic causesCarcinoid tumors producing ACTH -Bronchial, lung, pancreas -Small cell lung cancer Pheochromocytoma Gastrinoma
407365332TreatmentCushing's Disease (most common) Trans-sphenoidal pituitary surgery to resect adenoma Cure: post-op hypocortisolemia- steroids until recovers but need lifelong surveillance Post-op persistence or recurrence: -Repeat surgery may need total hypophysectomy -Pituitary radiation -Medical treatment: ketoconazole & others -Bilateral adrenalectomy +/- pituitary radiation -Permanent Adrenal Insuffciency!
408402322Primary AldosteronismThis was previously believed to be an uncommon condition!! -The sheer number of hypertensive patients out there call into question how much primary aldosteronism there really is -First described as Conn's syndrome Pathogenic Findings: -You have a marked increase in sodium and water and sometimes hypokalemia Symptoms -The only one of real note is Hypertension -Very oligo-symptomatic -Edema is very UNCOMMON (adaptation) Causes: Common (aldosterone secreting adenoma or bilateral adrenal hyperplasia) Uncommon: (Unilateral adrenal hyperplasia, adrenal carcinoma, familial hyperaldosteronism type 1 or 2) When to consider: 1. Hypertension with hypokalemia 2. Resistant HTN: needing 3 or more meds 3. Hypertension onset age 20 or younger or 80 and older 4. Severe Hypertension: > 160/100 5. Incidental Adrenal Mass & hypertension Workup: SCREENING Aldosterone: Renin ratio: -If it is greater than 555 you need to do further testing -Test is very sensitive but not specific!!! CONFIRMATORY Salt Load: -You give them a ton of salt for a couple days and see if their aldosterone goes down at all Fludrocorticone Load: -Adds mineralocorticoid to suppress aldosterone -look to see if you can turn it off Treatment: -Depends on the issue and the individual -You need to image in order to decide CT: -Looking for the associated masses Adrenal Vein Sampling: -Looking to see if you have abnormal secretion on both sides -Very good tests as long as you get the catheters in the right location Surgery -Well tolerated because it is laproscopic!! -HTN gets better in all and about half become normotensive!!! Medical -Spironolactone can mask the effect and make things significantly better ($) -Eplerenon is a much more selective antagonist but you have to pay ($$$$)
408402323PheochromocytomaThese are life threatening conditions that need to be found!!! -Adrenal 80-85% -Extra-renal 15-20% (paragangliomas) Prevalence -Relatively rare however it can KILL YOU!! Pre-Disposing Genetic conditions: Multiple Endocrine Neoplasia Type 2A & 2B Von Hippel Lindau Syndrome Neurofibromatosis Type 1 Familial Paragangliomas (SDHB/SDHD mostly) New emerging genetic mutations All can be screened for and family members identified pre-clinically as most are Autosomal Dominant mutations Signs and Symptoms: -Headache, Palpitations, Sweating in an episodic manner is the classic one -A ton of symptoms can be there to but are less likely to be related to pheochromocytoma Who to Screen: Paroxysmal spells Resistant Hypertension Hypertensive emergencies Adrenal Incidentalomas Unusual BP response under anesthesia Biochemical testing: 1) 24 hour urine collection of metanephrines and normetanephrines 2) Plasma Free Metanephrines fasting and supine -Both are very good tests although it is important to know that some places won't offer certain tests -> You do have to be careful with false positives (DRUGS ->anti-depressants, anti-hypertensives, beta blockers, CCB's, decongestants, cocaine, amphetamines) Imaging -CT / MRI / Nuclear MIBG Treatment: -You need to take these suckers out -Need to prep the patients by putting the tumor into submission -> catecholamine blockade using alpha adrenergic antagonists then salt intake with beta-blockers Post op: -Watch out for hypotension and hypoglycemia -The recurrence rate is 15-20% so you need to be careful that it isn't going to occur (following up with biochemical tests
408402324What is a metanephrine??It is the breakdown product of epinephrine and the associated products
408402325Pheo dynamicsThe tumor cells are continually making new materials and storing them -You get really weird stimulation signals that force it out and circulating through the body
408402326Incidental Adrenal Mass DefinitionAdrenal Mass >1 cm discovered incidentally during imaging for a "non-adrenal" indication Vast majority >80-90%: Benign & Non-functioning  About 5% are pheochromocytomas and 5% are Adrenocortical carcinoma Incidence from autopsy & CT series: 4-6% of all adults Incidence increasing with more & better scans!
408402327Approach to Investigation1. Functioning or Non-Functioning -Do a history and physical looking for signs of hormonal secretion irregularities -Everyone gets screened for pheochromocytoma because it can kill you -Do further study of those who have positive results 2. Benign or Malignant -Suspect malignant with (Age, Mass effects, Constitutional Symptoms, History of a known non-adrenal malignancy) -Lung, breast, colon, kidney, melanoma, lymphoma are the most common historical points Other keys of when to treat: 1. Size: -Surgery for all > 6 cm, some suggest > 4 cm -> 4 cm: 90% sensitivity for adrenal Ca but only 24% specificity. Close observation if no surgery 2. Imaging phenotype: -Uses techniques to take advantage of the fact that 70% of adenomas have a high lipid content. -Attenuation or Hounsfield Units (HU) < 10. -HU <10 ~98% sensitivity for benign adenoma -PET scan high sensitivity but non-specific 3. Rapid growth of the tumor Biopsy?? -Don't go there because the histology isn't overly useful and you can spread the malignancy
408402328HUHounsfield Units -This is a measure of how many lipids are within a mass -lower than 10 = lipids mostly -Higher than 10 (or 25) is a good chance of malignancy

Excercise Physiology - Chapter 1-9 Life University Flashcards

Undergrad Exercise Physiology course @ Life University. Chapters 1-9

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438645565What are Carbohydrates?Long, repeating chains of sugar, that serve as the bodys most efficient source of energy.
438645566What sugars make up carbohydrates?Glucose, Frutose, Galactose
438645567What is the base Chemical Formula for these Sugars?C6H12O6
438645568What are the three types of Carbohydrates?Monosaccaride (glucose, fructose, galatose) Disaccaride (Sucrose, Lactose, Maltose) Polusaccharide (Starch, Fiber)
438645569How are disaccharides formed?Condensation (H2O to combine 2 monosaccharides)
438645570What is Sucrose made up of?Glucose + Glucose (Cane sugar, Maple Syrup)
438645571What is Lactose made up of?Glucose + Galatose (Milk Sugar)
438645572What is Maltose made up of?Glucose + Glucose
438645573What is HydrolysisBreaking down the chains of sugar using water
438645574What is starch?A chain of 10 or more glucose units that the body can digest
438645575What is Fiber?A polysaccharide that the human body CANT digest. 2 types Insoluble and Soluable
438645576Health Benefits of FiberLower Cholestral Lower blood sugar levels Reduce risk of colon cancer
438645577What is GlycogenThe storage from of Carbohydrates. Glycongen is stored in the liver and muscle tissue and is made up of a chain of a few hundred to 30,000 glucose units.
438645578Where do Carbohydrates come from in the Human Diet?Mostly from plants, with the exception coming from Lactose (milk) and trace amounts of Glycogen in Animal Products
438645579Where is Glycogen stored. How much is stored?Glycogen is stored in the Muscle tissue primarly (4/5s of total Glycogen), then in the Liver (highest concentration of Glycogen), and trace amounts in the blood.
438645580How many kcals does 1g of glycogen provide?4 kcals
438645581How long can the body's glycogen stores lastNot long. A person on a low-carb diet can nearly deplete the bodies reserves in 24 hours.
438645582What provides the major source of energy during exercise?Muscle Glycogen, as well as the liver reconverting the glycogen to glucose for blood transport to the muscles to help with exercise.
438645583What percent of calories should carbohydrates make up in a typical diet?In an average person, 40 - 50% of calories should be carbs, in an active person 60% should be from carbs.
438645584How many grams of fiber should be consumed daily?25-35grams
438645585How do carbohydrates spare protein?Carbs are the bodies preferred source of glucose. The body uses these first so muscle tissue isnt broken down to get to glycogen reserves (prevents amino acids from being used in glyconeogenis)
438645586What is glucose?The simplest form of carbohydrates (can't be broken down more), often called blood sugar
438645587Where do we get glucose from?From carbohydrates in our diet and from the process of gluconeogenis in the liver
438645588How does the body use glucose?After absorption by the small intestine, 1) becomes available for energy for cellular metabolism, 2) gets stored in the liver or muscles as glycogen, 3) gets converted to fat for later use.
438645589How does depletion of carbs affect A) short term exercise, B) Prolonged endurance exercise?A) less then 10secs, no affect. Body is using anaerobic energy systems and ATP stores. anything great then 10secs, negative affect. B) When glycogen depletes during long endurance exercises (marathons) muscles will no longer work. You will "hit the wall"
438645590What is the current % of carbs and lipids in the American diet? What is recommended?Too little Carbs (too many from simple sugars), too much fat (primarily saturated) Recommended levels are 50 - 60% carbs, and 30% or less of lipids.
438645591How and Why are proteins used for catabolic processes?When the body doesn't have enough carbs for energy, proteins are broken down to Amino Acids, then they go through Deamination.
438645592Why is it good to reduce protein in pre-event meals?Because A) proteins take longer and more energy to digest (will fill full and sluggish) and B) Your body has to use extra H2O to digest protein.
438645593What is the caloric content of 1gram of Protein?4 kcals
438645594What is the caloric content of 1gram of Fat?9 kcals
438645595What is the Chemical Formula for the Cellular Respiration process?C6H2O6 + 6O2 ---> 6CO2 = H2O & (heat + ATP)
438645596What is Oxidative Phosphorylation?The making of ATP using oxygen
438645597What are 3 prereqs for the continual aerobic resynthesis of ATP?1. Oxygen Supply 2. Macronutriants 3. Carrier Molecules
438645598What are macronutrients?Carbohydrates, Lipids, and Proteins
438645599What are lipids?Fat
438645600What are triglycerides?Glycerol + 3 fatty acids
4386456012 natural types of lipidsSaturated (no double bonds) and Unsaturated (at least 1 C=C double bond.
438645602What is hydrogenation?Adding hydrogen to break the C=C double bond (to extend shelf life) These are bad for you (lard, margarine)
438645603Where is Cholesterol found?Only in animal products.
438645604What are Phospholipids?Molecule made up of Phosphorus and Lipids, membrane allows both Fat and Water to pass
438645605What are Lipoproteins?Molecule made up of a Lipid and a Protein. Major function is to carry fats in the blood stream.
438662875What are Trans-Fats?Derived from partialyl hydrogenated corn, soybean, or sunflower oils, These fats behave like saturated fats and can raise LDL levels and unlike saturated fats, can also decrease HDL levels.
438662876What are functions of Cholesterol?Cholesterol plays a crucial role in forming tissues, organs and body structures during fetal development, and also help build plasma membranes, synthesizing Vitamin D, Adrenal glands hormones, sex hormones, and bile.
438662877What is HDLHigh Density Lipoprotein. Helps carry fat away from the arteries. Exercise and Estrogen help increase HDL levels. HDL is "good" Cholesterol
438662878What is LDLLow Density Lipoprotein. Carry fat to the arteries, upon oxidation the remaining plaque builds up on Artery walls. LDL is"bad" Cholesterol
438662879What is Lipolysis?The breakdown of fat, Exercise/Fasting main cataylst.
438662880What is LipogenesisThe creation of fat, Eating (over) is the major cataylst
438662881AdiposeFat Tissue
438662882AdipocyteFat Cell
438662883What are some functions of Lipids?Energy storage, mobilization, and utilization (helps spare protein) Protection of organs Thermal Insulation Provides transport/storage for Fat Soluble Vitamins (A,D,E,K)
438662884What is the fat content of a typical young adult15% in males, 25% in females
438662885What is a negative of a high fat diet in terms of training?not able to perform at high levels for sustained amounts of time due to the length of time the body takes to convert fat into usable energy, when compared to a high carb diet.
438662886What are proteins made up ofSimilar to Carbs and Lipids with Carbons, Oxygens, and Hydrogen structures, they also contain nitrogen (NH2 Amine group).
438662887How many Amino Acids are there?20
438662888How many "Essential" Amino Acids are there?8
438662889What are Complete proteinsProteins containing all 8 Essential Amino Acids
438662890What is Transamination?The transfer of an Amine group, usually from an Amino Acid to a Alpha Keto Acid
438662891What is an Alpha Keto Acid?Amino Acid lacking the NH2 group
438662892What is Deamination?The process of removing NH2 from the body. NH2 --> NH3 --> Amonia --> Urea --> Urine
438662893Functions of ProteinsMake Muscle Produce Enzymes / Hormones Make Antibodies
438662894Anabolism vs CatabolismAnabolism is building up, Catabolism is breaking down (epinephrine)
438662895Nitrogen Balance+ balance intake is > then output (growth, building muscle, recovery from surgery) - balance output is > then Input (fasting, low card diet, disease)
438662896Alanine-Glucose CycleAmine Group + Pyruvate = Alanine. Alanine --> Blood --> Liver --> pyruvate --> glucose --> back to muscle
438829115What are 3 body sources of lipids catabolized for energy?Adipose Tissue, Muscle, Lipoproteins
4388291163 hormones that augment the activation of lipase, lipolysis, and mobilization of FFA from adipose tissue1) Epinephrine 2) Glucagon 3) Cortesol
438829117Function of the Cori CycleThe Cori Cycle removes lactate buildup and uses it to replenish glycogen reserves depleted from exercise
438829118Process of the Cori CycleLactate (H+) builds up in muscle --> Lactate goes through blood --> Liver converts Lactate into Pyruvate then Glucose --> Glucose travels through the blood to the muscle --> Muscle uses glucose, Lactate builds up
438829119How many ATPs does 1 glucose molecule yield in the Kerbs Cycle?32 ATP
438829120What do Fatty Acids transform into during Beta-Oxidation?Acetyl-CoA
438829121How does low carbs impede fat burning?Low pyruvate levels (formed from glucose metabolism) reduce levels of citric acid cycle intermediates, which slows the citric acid cycle activity to breakdown fat, resulting in less fat molecules being broken down into Acetyl-CoA
438829122What can cause Glycogen depletion?1) Marathon Running 2) Consecutive days in intense training 3) Inadequate energy intake 4) Dietary elimination of carbohydrates 5) Diabetes
438829123What is Acetyl-CoAIts is a molecule/enzyme that serves as the entrant to the kerbs (citric acid) cycle. Acetyl-CoA is produced during the second step of aerobic cellular respiration, before it then enters the Kerbs cycle for ATP synthesis.
438829124Where does Acetyl-CoA come fromActeyl-CoA can be formed from Carbohydates, Fats (lipids) and Protein. Carbs --> Pyruvate --> Actetyl-CoA Fats --> undergo Beta-Oxidation --> Actetyl-CoA Proteins --> DeAmination --> Pyruvate --> Actetyl-CoA (some deaminatied proteins can go directly to Actetyl-CoA
438829125Slow Twitch Muscle Fibersused for light work/exercise and endurance. Aerobic energy system
438829126Fast Twitch Muscle Fibersused for heavy exercise/strength. Anarobic energy system

Physiology II: Block II Flashcards

Sayeski Review of Pulmonary Physiology

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414204730What are the properties that affect gas diffusion?Surface area of the membrane Thickness of the membrane Pressure gradient - delta P Solubility of the gas The molecular weight of the gas (square root of the MW)
414204731How do you calculate gas diffusion of the lung?DL= V/ΔP The diffusion of a gas through a membrane (V) α (A/T) x (solubility/√MW) x ΔP (V) = DL x ΔP or DL= V/ΔP
414204732Define and explain perfusion limited and diffusion limited.Perfusion limited: The amount of gas that can be taken up is entirely limited by the blood in the pulmonary capillaries, not by the diffusion of the gas. The gas will come into diffusion equilibrium (ΔP = 0) and the only way change the pressure gradient is to increase perfusion (blood flow). Diffusion limited: The gas is limited by the properties of the blood-gas barrier and the gas itself, not the blood flow. When the blood leaves the pulmonary capillary, the gas has not reached diffusion equilibrium.
414204733Explain perfusion vs. diffusion limited in disease.Disease and exercise will cause O₂ to change toward diffusion limited. (Rightward shift on the curve). The more severe the disease, the more severe the rightward shift.
414204734What is the role of Hb in O₂ diffusion?The total amount of O₂ transferred from the alveolar capillary blood is dependant on how much Hb there is to remove O₂ from the dissolved state. Changes in [Hb] in blood can affect the measured value of DL. The amount of O₂ transferred before equilibrium is reached will be less if the [Hb] is decreased. Mathematically, DL = (V)/ ΔP. With less O₂ in the blood, the ΔP will increase, thus lowering DL.
414204735Explain dissolved O₂ qualitative and quantitative properties.Qualitative: ~ 1% Quantitative: solubility x PaO₂
414204736Explain oxyhemoglobin qualitative and quantitive properties.Qualitative: ~ 99% Quantitative: HbO₂ = [Hb] x carrying capacity x % saturation
414204737Calculate total oxygen content. ***This will be a test question***Total oxygen content is the sum of dissolved O₂ and HbO2. [Hb] x carrying capacity x % saturation + 0.0031 x PaO₂ mm Hg
414204738Briefly explain the relationship of PaO₂ and Hb saturation as the relate to the HbO₂ curve.The extent to which we saturate will be driven by our PaO₂. Normally with 98% saturation, we are at ~100 mm Hg. PaO2 = 100 mm Hg, Hb = 98% sat., O2 content = 20 mL O2/dL blood PaO2 = 60 mm Hg, Hb = 90% sat., O2 content = 18 mL O2/dL blood PaO2 = 40 mm Hg, Hb = 75% sat., O2 content = 15 mL O2/dL blood PaO2 = 27 mm Hg, Hb = 50% sat., O2 content = 10 mL O2/dL blood
414204739What is the 60/90 rule?When Hb saturation = 90%, PaO2 = 60 mm Hg. This is clinical hypoxia.
414204740Explain the significance of a rightward shift on the HbO₂ curve.Rightward shift means less O2 will bind to Hb at any given PO2. Ex.: exercise, 2,3-DPG, increased temperature, increased PaCO2, and decreased pH. This tells the Hb to give up O2.
414204741Explain the significance of a leftward shift on the HbO₂ curve.Leftward shift means more O2 will bind to Hb at any given PO2. This tells the Hb to hang onto the O2. CO shifts the curve leftward.
414204742Explain how CO poisoning affects the shape of the HbO₂ curve.CO shifts the curve leftward. Decreases our saturation 2° competitive binding.
414204743Calculate oxygen delivery.Cardiac output x (arterial content - venous content) Cardiac Output x ((Arterial) [Hb] x carrying capacity x % saturation + 0.0031 x PaO2 mm Hg) - (Venous) [Hb] x carrying capacity x % saturation + 0.0031 x PaO2 mm Hg)
414204744Explain the changes in O₂ content during polycythemia, anemia, CO poisoning and hyperbaric therapy.Polycythemia: [Hb] increases Anemia: [Hb] decreases CO poisoning: % saturation Hyperbaric: dissolved O₂ increases
414204745What are the 3 forms by which CO₂ is transported?Dissolved gas ~5% Carbamino ~5% (CO2 binds to terminal amine groups in blood proteins, Hb) Bicarbonate (HCO3-) ~90% rxn catalyzed via carbonic anhydrase
414204746Explain the Bohr effect.Increased CO2 and H+ binding to Hb decreases the affinity of Hb for O2. This occurs in metabolic tissues. This causes a Rightward shift (offloads O2) of the PO2 / Hb saturation curve
414204747Explain the Haldane effect.Deoxygenation of Hb in the tissues increases the affinity of Hb for CO2. This shifts the CO2 blood equilibrium curve up and to the left. Results in a higher content of CO2 in the venous blood.
414204748What is pulse oximetry measuring, what can we deduce from it and what are it's limitations?Ratio of R/IR of pulsatile portion of arterial signal. SpO2 is an approximation of the saturation of Hb. Can deduce PaO₂. Can't tell what is bound to Hb. COHb & metHb will give saturation reading, however, this means a false report of high SpO2. The device may give false readings if the battery is low. Acrylic nails wont transmit the signal.
414204749What is capnography measuring, what can we deduce from it and what are it's limitations?Measures CO2 in a sample of air Approximate the quality of ventilation. Main-stream requires intubation. Side-stream is susceptible to dilution error (under estimates carbon dioxide because of mixing with the room air which contains virtually no carbon dioxide).
414204750Explain the principles of fluid movementFluid movement is determined by the balance between hydrostatic (pushes out) and oncotic pressures (pulled back in) of the capillaries and interstitial fluid.
414204751Explain the impact pulmonary edema has on gas diffusionDiffusion capacity is decreased when fluid in the alveoli increase the thickness of the diffusion path.
414204752Explain the impact pulmonary edema has on shunt.Shunt: V/Q = 0. Decreased ventilation results in vasoconstriction and diversion of blood. Pulmonary edema results in diffusion limitation and shunting
414204753Explain the impact pulmonary edema has on surfactant.Washes away surfactant.
414204754Explain the impact pulmonary edema has on compliance.Decreases compliance. Compliance is ΔV/ΔP
414204755Explain the impact pulmonary edema has on recoil.Increases recoil.
414204756Explain the impact pulmonary edema has on the work of breathing.Increases work
414204757Why is pulmonary edema a restrictive lung disorder?Decreased ability to inflate the lungs, resulting in decreased TLC. "Ceiling comes down." Obstructive, the "floor comes up."
414204758What is the Henderson-Hasselbalch equation?pH=6.1 + log [HCO3-]/(0.03)[pCO2]
414204759Why is ventilation is α 1/PaCO2The respiratory drive (CNS) is controlled by the [PaCO2], NOT [PaO2]. When PaCO2 is high, the respiratory rate increases to remove/decrease [PaCO2]. The definition of ventilation is the removal of CO2. Mathematically: if ventilation increases (the removal of CO2, PaCO2 goes down, thus the inverse relationship.
414204760Explain how CO2 and HCO3- levels change in the four principle acid/base disordersRespiratory acidosis with renal compensation: PCO2 increases due to hypoventilation & HCO3- increases due to kidney reabsorption. Respiratory alkalosis with renal compensation: PCO2 decreases due to hyperventilation & HCO3- decreases due to kidney elimination. Metabolic acidosis with respiratory compensation: Blood pH decreases 2° to a metabolic issue that the kidneys can't keep up with, so the lungs respond by increasing ventilation, which decreases PCO2. HCO3- is decreased due to the response to pH. Metabolic alkalosis with respiratory compensation: Loss of acids results in an increase in pH - (HCO3- is high), so the lungs compensation by decreasing ventilation, which retains CO2.
414204761What is anion gap? How do you calculate it? What is it used for?The anion gap is the difference in the measured cations and the measured anions. The normal anion gap is 8-12 mEq per liter. Anion Gap = ([Na+]+[K+])-([Cl-]+[HCO3-])=(137+5)-(108+24)=10 mEq per liter The gap is used for determining metabolic acidosis.
414204762Explain the role of DRG.Dorsal Respiratory Group (DRG), located in the medulla and is responsible for inspiration.
414204763Explain the role of VRG.Ventral Respiratory Group (VRG) are also located in the medulla and mediate expiration under non-rest conditions, such as exercise. Otherwise, they are quiet.
414204764Describe the central chemoreceptors.Located in the medulla and are connected to the inspiratory neurons of the DRG. They are directly activated by H+. They do not respond to PaO2 or PaCO2. However, CO2 crosses the BBB and is converted into H+. So, Central Chemoreceptors respond indirectly to PCO2.
414204765Describe the peripheral chemoreceptors.Respond to H+, PaCO2 and PaO2. There are two different peripheral receptors, Aortic Bodies and Carotid Bodies. The Aortic Bodies are located in the aortic arch and extend nerves into the inspiratory control neurons of the medulla (DRG). Carotid bodies are located in the bifurcation of the common carotid artery and extend nerves into the inspiratory control neurons of the medulla (DRG).
414204766What happens when a patient becomes desensitized to chronically increased levels of CO2 as in the case of COPD?In COPD PaCO2 levels are chronically evelated. Over time, the central chemoreceptors become desensitized to the high PaCO2. Eventually, patients will rely in the low PaO2 acting via the peripheral chemoreceptors for their "drive to breathe" Supplemental O2 will increase PaO2, which the peripheral chemoreceptor responds to by decreasing the ventilation/breathing rate.
414204767When do we ventilate the best?We ventilate the greatest when PCO2 is high and PO2 is low
414204768Reduction in PaO₂ does what to the sensitivity of PaCO₂?Increases.
414204769Reduction in PaCO₂ does what to the sensitivity of PaO₂?Decreases.
414204770What is the role of the Apneustic center?The Apneustic center alters the respiratory rhythm by electrical stimulation that excites the medullary inspiratory center (DRG) to produce a sustained contraction of the diaphragm.
414204771What is the role of the Pneumotaxic center?Electrical stimulation late in inspiration facilitates termination of inspiration. The Pneumotaxic center can inhibit the Apneustic center.
414204772What is the role or PSRs?located in the smooth muscle of airways. Neural discharge is dependent on lung inflation. Discharge increases with inflation and decreases with deflation.
414204773What is the role of J-receptors?accessible through pulmonary circulation. They respond strongly to histamine, prostaglandins, pulmonary congestion and pulmonary embolism. They promote rapid shallow breathing (tachypnea) or sometimes apnea.
414204774What is the role of RARs?are located in airway epithelium and smooth muscle and are activated by mechanical and chemical irritants. They can discharge during both inflation and deflation. The consequence of discharge is cough and/or sneeze
414204775How does compliance change in exercise?Overall we see a decrease in lung compliance with exercise because it is harder to inflate any more air to a full lung.
414204776What is the main factor that regulates breathing during exercise?Increased CO2 acting on the central chemoreceptors is the main driving force to increase respiratory rates during exercise and after exercise.
414204777What factor contributes to hypoxemia at high altitude?High altitude hypoxemia is due to decreased barometric pressure and not decreased FIO2.
414204778Describe high altitude induced pulmonary edema.Decreased barometric pressure results in low PAO2 in ALL alveoli. The resulting hypoxic vasoconstriction increases pulmonary vascular resistance throughout both lungs and results in a marked increase in hydrostatic pressure within the pulmonary vasculature, which pushes fluid out of the blood and into the alveoli. This pulmonary edema is a rapid onset (within hours) and results in a painful death.

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