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Test Bank for Understanding Pathophysiology, 6th Edition by Huether & McCance | 2026 Updated Comprehensive Exam Questions (Chapters 1–42)

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This document contains a comprehensive test bank for Understanding Pathophysiology (6th Edition) by Huether and McCance, covering all chapters 1–42. It includes multiple-choice questions designed to support nursing and health science students in mastering disease processes and pathophysiological mechanisms. Topics include cellular injury, inflammation, immune response, genetic and congenital disorders, fluid and electrolyte imbalance, and system-specific diseases across major body systems. The material is structured to strengthen clinical reasoning and exam performance. It is suitable for revision, quizzes, and full-course pathophysiology exam preparation. TABLE OF CONTENT Introduction to Pathophysiology PART ONE: BASIC CONCEPTS OF PATHOPHYSIOLOGY Unit 1: The Cell 1. Cellular Biology 2. Genes and Genetic Diseases 3. Epigenetics and Disease (NEW) 4. Altered Cellular and Tissue Biology 5. Fluids and Electrolytes, Acids and Bases Unit 2: Mechanisms of Self-Defense 6. Innate Immunity: Inflammation and Wound Healing 7. Adaptive Immunity 8. Infection and Defects in Mechanisms of Defense 9. Stress and Disease Unit 3: Cellular Proliferation: Cancer 10. Biology of Cancer 11. Cancer Epidemiology 12. Cancer in Children and Adolescents PART TWO: BODY SYSTEMS AND DISEASES Unit 4: The Neurologic System 13. Structure and Function of the Neurologic System 14. Pain, Temperature, Sleep, and Sensory Function 15. Alterations in Cognitive Systems, Cerebral Hemodynamics and Motor Function 16. Disorders of the Central and Peripheral Nervous Systems and Neuromuscular Junction 17. Alterations of Neurologic Function in Children Unit 5: The Endocrine System 18. Mechanisms of Hormonal Regulation 19. Alterations of Hormonal Regulation Unit 6: The Hematologic System 20. Structure and Function of the Hematologic System 21. Alterations in Hematologic Function 22. Alterations of Hematologic Function in Children Unit 7: The Cardiovascular and Lymphatic Systems 23. Structure and Function of the Cardiovascular and Lymphatic Systems 24. Alterations of Cardiovascular Function 25. Alterations of Cardiovascular Function in Children Unit 8: The Pulmonary System 26. Structure and Function of the Pulmonary System 27. Alterations of Pulmonary Function 28. Alterations of Pulmonary Function in Children Unit 9: The Renal and Urologic Systems 29. Structure and Function of the Renal and Urologic Systems 30. Alterations of Renal and Urinary Tract Function 31. Alterations of Renal and Urinary Tract Function in Children Unit 10: The Reproductive Systems 32. Structure and Function of the Reproductive Systems 33. Alterations of the Female Reproductive System 34. Alterations of the Male Reproductive System Unit 11: The Digestive System 35. Structure and Function of the Digestive System 36. Alterations of Digestive Function 37. Alterations in Digestive Function in Children Unit 12: The Musculoskeletal and Integumentary Systems 38. Structure and Function of the Musculoskeletal System 39. Alterations of Musculoskeletal Function 40. Alterations of Musculoskeletal Function in Children 41. Structure, Function, and Disorders of the Integument 42. Alterations of the Integument in Children Chapter 01: Cellular Biology MULTIPLE CHOICE 1. A student is observing a cell under the microscope. It is observed to have supercoiled DNA with histones. Which of the following would also be observed by the student? a. A single circular chromosome b. A nucleus c. Free-floating nuclear material d. No organelles Answer:: B The cell described is a eukaryotic cell, so it has histones and a supercoiled DNA within its nucleus; thus, the nucleus should be observed. A single circular chromosome called a prokaryote contains free-floating nuclear material but has no organelles. REF: p. 2 2. A nurse is instructing the staff about cellular functions. Which cellular function is the nurse describing when an isolated cell absorbs oxygen and uses it to tr Answer:form nutrients to energy? a. Metabolic absorption b. Communication c. Secretion d. Respiration Answer:: D The cell’s ability to absorb oxygen is referred to as respiration while its communication ability involves maintenance of a steady dynamic state, metabolic absorption provides nutrition, and secretion allows for the synthesizing of new substances. REF: p. 2 3. A eukaryotic cell is undergoing DNA replication. In which region of the cell would most of the genetic information be contained? a. Mitochondria b. Ribosome c. Nucleolus d. Nucleus Cytoplasm Answer:: C The region of the cell that contains genetic material, including a large amount of ribonucleic acid, most of the DNA, and DNA-binding proteins, is the nucleolus, which is located within the cell’s nucleus. Mitochondria is associated with cellular respiration, while ribosomes are involved with protein manufacturing. Cytoplasm is a fluid filling that is a component of the cell. REF: p. 2 4. Whichtofthefollowingtcantremovetproteins attachedtothecell’s bilayerbydissolvingtthe layer itself? a. Peripheralmembraneproteins b. Integralmembraneproteins c. Glycoproteins d. Celladhesionmolecules Answer:: B Proteinstdirectlyattached to themembranebilayer can betremovedtbythetaction ofintegral me mbraneproteinsthattdissolvethebilayer. Peripheralmembranetproteinsreside at the surfacetw hiletcell adhesionmoleculesaretontheoutsideofthetmembrane. Glycoprotein markscellsand doestnot float. REF: p. 7 5. Whichtofthefollowingtcan bindtoplasmamembranereceptors? a. Oxygen b. Ribosomes c. Amphipathiclipids d. Ligands Answer:: D Ligandsaretheonlyspecificmoleculestthatcanbindtwithreceptorsontthetcellmembrane. REF: p. 9 6. Anursetisreviewingareportfromapatienttwithtmetastaticcancer. Whattalternationintthet extr acellularmatrix wouldtsuNpUpoRrtSthIeNdGiaTgnBCs oOfMmetastatictcancer? a. Decreasedfibronectin b. Increasedcollagen c. Decreasedelastin d. Increasedglycoproteins Answer:: A Onlyareducedamountoftfibronectin istfound insometypesofcancerouscells, allowingt themt to travelormetastasize. REF: p. 10 7. Whichformofcell communicationisusedtotrelate to othercellsindirectphysical contact? a. Celljunction b. Gaptjunction c. Desmosome d. Tightjunction Answer:: A Celljunctionsholdtcellsttogetherandtpermitmoleculestotpassfromcelltocell. Gaptjunctionsallowforcellularcommunicationbetweencells. Neitherdesmosomesnortight jun ctionsareassociated with cellular communication. REF: p. 11 8. Pancreaticbetacellssecreteinsulin, whichinhibitssecretiontofglucagontfrom neighboringt alp hacells. Thistaction istan exampleofwhichofthefollowingtsignalingttypes? a. Paracrine b. Autocrine c. Neurohormonal d. Hormonal Answer:: A Paracrinetsignalinginvolvesthereleasetoflocalchemicalmediatorsthatarequicklytakenup, des troyed, orimmobilized, astin thetcaseofinsulin andttheinhibitiontofthesecretionof glucagon. No neoftheotheroptions involvesignalingtthattis associatedwithatlocalchemical mediatorliketinsu lin. REF: p. 12 9. In cellularmetabolism, eachenzymehastahightaffinityfor a: a. solute. b. substrate. c. receptor. d. ribosome. Answer:: B Eachtenzymehas ahightaffinityforasubstrate,taspecificsubstancetconvertedtoatproductof ther eaction. Cellularmetabolismisnotdependenton an attraction between an enzymeand anyofther emainingoptions. REF: p. 16 10. An athlete runsamarathon, afterwhichhistmusclestfeelfatiguedandtunabletocontract. Thet athlet easkstthetnursewhythishappened. Thenurse’s responseisbasedonthetknowledgethat theproble misresultofadeficiencyof: a. GTP b. AMP c. ATP d. GMP Answer:: C When ATPistdeficient, impairedmuscletcontractionresults. Noneoftheotheroptionsaret invo lvedinmusclecontraction. REF: p. 16 11. Whichtphaseofcatabolism producestthetmost ATP? a. Digestion b. Glycolysis c. Oxidation d. Citricacidcycle Answer:: D WhilesometATPisproducedduringttheoxidation andglycolysis phases, mostofthe ATPis TEST BANK FOR UNDERSTANDING PATHOPHYSIOLOGY Huether & McCance: Understanding Pathophysiology, 6th Edition Chapter01:Cellular Biology generatedduringtthecitricacidcycle. DigestiondoestnotproduceanyATP. TEST BANK FOR UNDERSTANDING PATHOPHYSIOLOGY Huether & McCance: Understanding Pathophysiology, 6th Edition Chapter01:Cellular Biology REF: p. 16 12. Anursetisteachingtthetstaffaboutthetphasesofcellularcatabolism. Whichphasesshouldtthet nurs einclude? a. Digestion, glycolysis, oxidation,tandthecitricacidcycle b. Diffusion, osmosis, andmediatedtr Answer:port c. Sphase, Gphase, and Mphase d. Metabolicabsorption, respiration, andtexcretion Answer:: A Onlydigestion,tglycolysis, oxidation, andtthetcitricacidtcycle aretthetphases ofcellular catabolis m. REF: p. 16 13. Arunnerhasdepletedtalltheoxygenavailabletformuscleenergy. Whichofthetfollowingwill facil itate hiscontinuedtmuscleperformance? a. Electron-tr Answer:portchain b. Aerobicglycolysis c. Anaerobicglycolysis d. Oxidativephosphorylation Answer:: C Whennotoxygentisavailable, anaerobictglycolysis occurs. Thetelectron-tr Answer:portchain ispart ofthecitricacidcycle. Aerobicglycolysis involvesthepresenceofoxyg en. Oxidativet phosphorylationisthemechanismbywhichtheenergyproducedfromcarbohydrat es, fats, andtproteinsisttr Answer:ferredtto ATP. Ittis nottparttofmuscleperformance. REF: p. 16 14. Afacultymemberasksastudenttoidentifytheappropriatettermforthemovementofasolute from an areaofgreatertolesserconcentration. Which Answer:werindicatesthenursingstudent understoodthetteaching? a. Osmosis b. Diffusion c. Hydrostaticpressure d. Activettr Answer:port Answer:: B Diffusionistthetmovementofasolutemoleculefrom an areatofgreatersoluteconcentrationto an a reaoflessersoluteconcentrationthroughapermeablemembrane. Osmosisisthet movementof wa teracrosstasemipermeabletmembranetfromaregionofhigherwater concentrationto oneoflower concentration. Hydrostatictpressureis thetforce oftfluid against acellmembrane. Intactivettr Answer:port, moleculestmovetupatconcentrationtgradient. REF: p. 19 15. Whichtdescriptiontaccuratelydescribestelectrolytes? a. Smalltlipid-solublemolecules b. Largeproteinmolecules TEST BANK FOR UNDERSTANDING PATHOPHYSIOLOGY Huether & McCance: Understanding Pathophysiology, 6th Edition Chapter01:Cellular Biology c. Micronutrientsusedtoproduce ATP TEST BANK FOR UNDERSTANDING PATHOPHYSIOLOGY Huether & McCance: Understanding Pathophysiology, 6th Edition Chapter01:Cellular Biology d. Electricallycharged molecules Answer:: D Electrolytesareelectricallychargedmolecules. Theyarenotlipidsoluble, theyarenotmade uptof protein, andtheydonotplayaroletin ATP production. REF: p. 18 16. Anurseisreadingachartandseesthetermoncoticpressure. Thenurserecalls thatoncotic pres suret(colloidosmotictpressure)tisdetermined by: a. theconcentrationofsodium. b. plasmatproteins. c. hydrostatictpressure. d. theavailabilityofmembranettr Answer:porterproteins. Answer:: B Oncoticpressuretis determined bythe effect ofcolloidstorplasmaproteins. Thetconcentration ofs odiumplaystatroletin tonicity. Hydrostaticpressure is theforcewithinavessel. Membrane tr Answer:porterproteinsareinvolvedinactivettr Answer:portwithinaconcentrationgradient. REF: p. 20 17. Apatienthasabodyfluidof 300 mOsm/kg. Thislabresultismeasuring: a. osmolality. b. osmolarity. c. osmotictpressure. d. oncotictpressure. Osmolalitymeasures thetnumberofmilliosmolestperkilogramtofwater, ortheconcentration oftm oleculestper weight ofwater,twhileosmolaritymeasuresthenumberofmilliosmoles per liter ofso lution, ortheconcentrationofmoleculesper volume ofsolution. Osmoticpressuretis theamountof hydrostaticpressuretrequiredttoopposettheosmoticmovementofwater. Oncoticpressuretistfrom plasmatproteins, notbodyfluids. REF: p. 19 18. Anursetisdiscussingthetmovementoffluidacrossthearterialendofcapillarymembranest into thetinterstitial fluid surroundingthetcapillary. Whichprocessoffluidtmovementistthet nursed escribing? a. Hydrostaticpressure b. Osmosis c. Diffusion d. Activettr Answer:port Answer:: A Bloodreachingthecapillarybedhas ahydrostaticpressureof 25– 30tmm Hg,twhichist sufficient forcettopushtwateracrossthethincapillarymembranesintothetint erstitial space. Osmosistinvolvestthetmovementoffluidfrom an areaofhigherconcentrationto an areaof lowerconcentration. Ittdoestnottinvolvetpressuretor force. Diffusiontisthepassivemoveme nt ofasolutefrom an areaofhighersolutetconcentrationtto an areaoflowersolute TEST BANK FOR UNDERSTANDING PATHOPHYSIOLOGY Huether & McCance: Understanding Pathophysiology, 6th Edition Chapter01:Cellular Biology concentration. Active tr Answer:portinvolvesmovementtupatconcentrationtgradient. TEST BANK FOR UNDERSTANDING PATHOPHYSIOLOGY Huether & McCance: Understanding Pathophysiology, 6th Edition Chapter01:Cellular Biology REF: p. 19 19. Howaretpotassiumtandsodium tr Answer:portedacrossplasmamembranes? a. Bypassivetelectrolytechannels b. Bycoupledtchannels c. Byadenosinettriphosphateenzyme(ATPase) d. Bydiffusion Answer:: C Thetr Answer:porterprotein ATPasetisdirectlyrelatedtosodiumandpotassiumtr Answer:portvia activetr Answer:port. Electrolytemovements requireenergyanddotnottmovetpassively, norare theytr Answer:portedbydiffusion. Enzymes, notelectrolytes, arepassedviacoupledchannels. REF: p. 21 20. Theiontr Answer:porterthatmoves Na+ and Ca2+ simultaneouslyinthetsamedirectionis an exampl eofwhichtofthefollowingtypesoftr Answer:port? a. Biport b. Uniport c. Antiport d. Symport Answer:: D Whenionsarettr Answer:portedinonedirection, it is termedsymport. Theretisnosuchterm as biport. Uniportrefe rs tothemovementtofatsingle molecule. Antiportrefersttothemovement ofmoleculestintheoppo sitedirection. REF: p. 19, Figure 1-22 21. Duringwhichtprocessarebacteriatengulfedtforingestion? a. Endocytosis b. Pinocytosis c. Phagocytosis d. Exocytosis Answer:: C Phagocytosis(cell eating) involvestheingestionoflargeparticles, such astbacteria, through thetf ormationtoflargevesicles. Endocytosisinvolvestheformationtofvesicles to facilitate movement intothecell. Pinocytosisisatypeofendocytosisintwhichfluidstandsolutet moleculesareingested throughtheformationtofsmallvesicles. Exocytosisoccurswhent coatedpitstinvaginatetandinter nalizeligand-receptorcomplexesincoatedtvesicles. REF: p. 22 22. Somecancerdrugsworkduringtthetcell cycletphasewherenuclearand cytoplasmicdivisions occ ur. Whatisthiscell cyclephasetcalled? a. G1 b. S c. M TEST BANK FOR UNDERSTANDING PATHOPHYSIOLOGY Huether & McCance: Understanding Pathophysiology, 6th Edition Chapter01:Cellular Biology d. G2 Answer:: C The Mphaseincludestbothtnuclearandtcytoplasmicdivisions. The G1 phasetincludestthet periodtb etweentthe Mphaseandtthetstarttof DNA synthesis. The Sphasetincludestsynthesistof DNA intthe c ellnucleus. The G2 phaseincludes RNAandproteinsynthesis. REF: pp. 25-26 23. Whichtcausestherapid changeintherestingtmembranepotentialthatinitiates antaction pot ential? a. Potassium gatesopen, andpotassiumrushesintotthetcell, changingthemembranet pot ential fromnegativettopositive. b. Sodium gatesopen, andsodiumtrushesintothecell,tchangingtthetmembranet pot ential fromnegativettopositive. c. Sodium gatesclose, allowingtpotassiumintotthetcelltotchangetthemembrane pot ential frompositivetonegative. d. Potassium gatesclose, allowingtsodiumintothecellttochangetthemembrane pot ential frompositivetonegative. Answer:: B Whenthethreshold is reached,tthetcell willcontinuetto depolarizewithtnofurtherstimulation. The sodiumgatesopen, andsodiumrushesintothecell, causingthemembranetpotentialto reducettoz eroandthentbecomepositive(depolarization). Sodium istinvolved intcreatingthe actionpotential, nottpotassium. Thesodiumtgateandtchannelmusttbe open, nottclosed. Thet actiontpotentialis nota ffectedtbyatchangeinthepotassium gate. REF: pp. 24-25 24. Acellisisolated, andelectroNphUyRsioSlIogNyGstTuBCreOvMealtthat therestingtmembranepotentialis 70 mV. Thetpredominantintracellularionis Na+, andthetpredominantextracellularionis K+. Withtvoltagechange, whichofthetfollowingtwouldresultintan actiontpotential? a. K+ rushingintothecell b. Na+ rushingtintothecell c. Na+ rushingtout ofthetcell d. K+ rushingout ofthecell Answer:: A Withtvoltagechange, potassium rushesinto, notoutof, thetcell. Sodiumtmovement isnot related t otthisprocess. REF: pp. 24-25 25. Anursetteachingthestaff aboutplatelet- derivedgrowthtfactorincludesinformationtthat platelet- derivedgrowthtfactor(PDGF) stimulatestheproductionof: a. platelets. b. epidermalcells. c. connectivetissuetcells. d. fibroblastcells. Answer:: C Differenttypestofcells requiretdifferenttgrowth factors; forexample, PDGFstimulatesthe productionofconnectivetissuecells, butnotplatelets, epidermalcells, orfibroblastcells. REF: p. 27 26. Thephasetofthe cell cycle duringtwhichthecentromeressplitandtthetsisterchromatidsare pull ed apartisreferredto as: a. anaphase. b. telophase. c. prophase. d. metaphase. Answer:: A Anaphasetbeginswhenthecentromeressplittandthesisterchromatidsarepulledapart. During tel ophase,tanewnuclearmembraneisformedaroundeach groupoft46 chromosomes, the spindlefib erstdisappear, andthetchromosomesbegintotuncoil. Duringprophase, thefirst appearanceof chro mosomes occurs. Metaphasetoccurs whenttwo centrioleslocated at oppositetpolesofthetcell pull t hechromosomesttooppositesidesofthecell. REF: p. 26 27. Whattistheroleofcytokines intcell reproduction? a. Providegrowthfactorfortissuegrowthanddevelopment. b. Blockprogresstofcellreproductiontthroughthecell cycle. c. Restraincelltgrowthandtdevelopment. d. Providenutrientstforcell growthanddevelopment. Answer:: A Cytokinesplayamajorroleinthetregulationoftissuegrowthanddevelopmentbutdonot restra in it. CytokinesthelptovNercoRmeiIntrGaceBllul.aCrtbrMakingtmechanisms thatrestrain cell growthand promotecell growth, butttheydotnottprovidetnutrients. REF: p. 26 28. Abiopsyofthetlungbronchirevealedciliatedepithelialcellsthataretcapableofsecretionand abs orption. Thesecells arecalled columnarepithelium. a. simple b. ciliatedsimple c. stratified d. pseudostratifiedciliated Answer:: B Ciliated simpletcolumnarepitheliumistfoundinthetlungs. Simplecolumnarepitheliumis foundf romthestomachtotheanus. Stratifiedtcolumnarepitheliumistfoundintheliningof theepiglottis, parttofthepharynx, theanus, andthemaleturethra. Pseudostratifiedtciliate columnarepitheliumi sfoundinttheliningofthelargeductstofsomeglands(parotid, salivary), maleurethra, respiratory passages, and Eustachiantubesofthetears. REF: p. 30, Table 1-6 29. Astudentistreviewingtfunctionsofthecell. Thestudentwouldtbecorrecttintidentifyinga chie ffunctiontofthenervecellas: a. sensoryinterpretation. b. conductivity. c. maintenanceofhomeostasis. d. communication. Answer:: B Conductivity, notsensoryinterpretation, homeostasis, orcommunication, is oneoftheeight chie ffunctionsofnervecells. REF: p. 2 MULTIPLE RESPONSE 1. Anursetrecallsthatthebasictypesoftissuesare:(selectalltthatapply) a. nerve. b. epithelial. c. mucosal. d. connective. e. skeletal. f. muscle. Answer:: A,tB, D, F Thebasictissuettypes includetnerve, epithelial, connective, andmuscle. Mucosal ista typeof epit helialcell, whiletskeletal is atypeofconnectivetissue. REF: p. 27 2. Characteristicsoftprokaryotesincludewhichofthefollowing? (select all that apply) a. Theycontaintnoorganelles. b. Theirnuclear materialistNnoUttRenScIasNedGbTyBCcOleMar membrane. c. Theycontaintadistinctnucleus. d. Theycontainthistones. e. Theycontaintacellularmembrane. Answer:: A, B Theprokaryotestlack atcellularmembranetthattencasesnuclearmaterial, thus theyhaveno distin ct nucleus; organellestandhistonesaretalsomissing. REF: p. 1 Chapter02: Genes and Genetic Diseases Huether&McCance:UnderstandingPathophysiology,6thEdition MULTIPLE CHOICE 1. Anursetrecallsthebasiccomponentstof DNA are: a. pentosesugarstandfourphosphatebases. b. aphosphatemolecule, deoxyribose, andfournitrogenousbases. c. adenine,tguanine,tandpurine. d. codons, oxygen, andcytosine. Answer:: B Thethreebasiccomponentsof DNA aredeoxyribose; aphosphatetmolecule; andfourtypesof nitr ogenous, notphosphate, bases. DNA doesnottcontaincondone. REF: p. 38 2. Whichtofthefollowingtmutationshavetthetmostsignificanteffectontproteinsynthesis? a. Basepairsubstitutions b. Silentmutations c. Introntmutations d. Frameshiftmutations Answer:: D Theframeshifttmutationtinvolvestthetinsertiontordeletiontofoneormorebasepairsofthet DNAmo lecule. Thistgreatlyalterstheaminoacidsequence, whichaffectsproteinsynthesis. Thebasetpairsubstitutionis NattUypReSofItNmGutTatBio.nCinOwMhich onetbasepair replacestanother. Silent m utationsdotnotchangeaminoacidsorproteintsynthesis. Intronmutations aretpart of RNA sequencing. REF: p. 39 3. Thebasetcomponentsof DNAtare: a. A, G, C,tand U. b. P, G, C, and T. c. A, G, C,tand T. d. X, XX, XY, and YY. Answer:: C Thefourbasecomponentsof DNA arecytosine, thymine, adenine,tandguanine, andare common lyrepresentedbytheirfirsttletters (A, C, T, andtG)tand nottcomponentstidentifiedtas Por U. X, XX , XY, and YY aretcomponentsofthumanchromosomes. REF: p. 38 4. A DNA strandhasaregiontwiththetsequence ATCGGAT. Whichofthefollowingwouldbea com plementarystrand? a. CGATACGT b. TAGCCTAG c. TUGCCTUG d. UAGCCUAG Answer:: B Theconsistentpairingtofadeninewithtthymineandtof guaninewithtcytosineisknown as comple mentarybasepairing; thus, Acomplementsto Tand Cto Gandtviceversathroughout thetstrand. Acomplementsto T; thus, the first lettermust beatT. Udoestnotrepresent a complementintheseq uence. REF: p. 39 5. Abiologististexplaininghow RNAdirectstthesynthesis ofprotein. Whichtprocessisthe biol ogistdescribing? a. Termination b. Tr Answer:cription c. Tr Answer:location d. Tr Answer:lation Answer:: D In tr Answer:lation, RNAdirectsthesynthesisofapolypeptide, interactingtwithtr Answer:fer RNA (tRNA), acloverleaf- shapedstrandofabout 80tnucleotides. Terminationdoesnotinvolvet synthesistofprotein. Tr Answer:criptionistheprocessbywhich DNA specifiesta sequenceof messenger RNA(mRNA). Tr Answer:locationistthetinterchangetofgenetictmaterial between nonhomologouschromosomes. REF: p. 41 6. Whatistheresultofhomologouschromosomesfailingttoseparatetduringmeiosis? a. Neurofibromatosis b. Nondisjunction c. Polyploidy d. Conjoinedtwins Answer:: B Nondisjunctionis an errorinwhichthomologouschromosomesorsisterchromatids fail tot separat enormallyduringmeiosis ormitosis. Neurofibromatosisistnotduetochromosomet failureduring meiosis. Polyploidyoccurstwhenateuploidtcellhastmorethantthetdiploid numberofchromosome s. Conjoinedtwins aretnotduetotchromosometfailureduringmeiosis. REF: p. 45 7. Acellthatdoesnot containtamultipletof 23 chromosomestis calledta cell. a. diploid b. euploid c. polyploid d. haploid Answer:: C Apolyploidcellisoneintwhichaeuploidcell hasmoretthant23 pairstof chromosomes. A diploid cell iswhenthesomatictcellnucleusthas 46 chromosomesin 23 pairs. Aeuploidcell is acellwith multiplesofthenormalnumberofchromosomes. Ahaploidtcellhastonlyone TEST BANK FOR UNDERSTANDING PATHOPHYSIOLOGY Huether & McCance: Understanding Pathophysiology, 6th Edition Chapter01:Cellular Biology memberof each chromosomepair, for attotal of 23 chromosomes. REF: p. 42 8. A 20-year- oldpregnantfemalegivesbirthtoastillbornchild. Autopsyrevealsthattthetfetus has 92 chromo somes. Whatttermmaybeontthetautopsyreporttodescribethistcondition? a. Biploidy b. Triploidy c. Tetraploidy d. Aneuploidy Answer:: C Tetraploidyistacondition inwhicheuploidcellshave 92 chromosomes. Biploidyisaeuploid cell withtwotimestmoretchromosomes, or 46. Triploidyistatzygotethatthas threecopiesof each chro mosome, ratherthantheusualttwo. Aneuploidyiswhen an aneuploidcelldoesnot containtamulti pleof 23 chromosomes. REF: p. 42 9. Theconditioninwhich antextra portiontofatchromosometispresentinteachtcell is called: a. reciprocaltr Answer:location. b. partialtrisomy. c. inversion. d. Downsyndrome. Answer:: B Partialtrisomyistacondition inwhichonlyan extraportionofachromosometispresenttint eachtcel l. Areciprocaltr Answer:locationoccurswhenbreakstakeplacetinttwodifferent chromosomesandthetmaterialtis exchanged. An inversionoccurswhentwobreakstakeplace ontachromosome, followed bNyUthReSrIeinNsGerTtioBn.oCftthMetmissing fragmenttattitsoriginalsite, butin invertedorder. Downsyndrometis antaneuploidyof thetwenty-firstchromosome. REF: p. 46 10. Afterageneticisttalkstoapatienttabouttbeingtachromosomalmosaic, thepatienttaskstthe nurs ewhatthattme Answer:. Howshouldthenurserespond? Youmay geneticdisease(s). a. onlybeacarrierofthe b. haveatmildformtofthe c. havetwo d. besterile as aresult ofthe Answer:: B Achromosomalmosaic me Answer: thebodyhastwoormoretdifferenttcelllines, each ofwhich hastatdifferenttkaryotype; t hus, thepersonthastamildformofthedisease. Mosaicstaretnot onlycarriers; theyhavethediseas e; theyhavetwo different linesbuttnottwotdifferent diseases; andttheyaretnot necessarilysterile . REF: p. 46 11. Whattisthemosttcommoncausetof Downsyndrome? a. Paternalnondisjunction b. Maternalttr Answer:locations c. Maternaltnondisjunction d. Paternaltr Answer:locations Answer:: C Themost commoncause of Downsyndromeismaternal, notpaternal,tnondisjunction. Tr Answer:locationistnotacauseofthissyndrome. REF: p. 46, Table 2-1 12. ApatientwantstotknowthetriskfactorsforDownsyndrome. Whatisthenurse’s best resp onse? a. Fetalexposuretotmutagenstinttheuterus. b. Increasedpaternal age. c. Familyhistoryof Downtsyndrome. d. Pregnancytinwomenoverage 35. Answer:: D Theprimaryrisktfor Downtsyndromeispregnancyintwomenover 35. Downtsyndrome is a trisom yandnotduetofetalexposuretorpaternalage. Downsyndromeistachromosomal abnormalityan dtisnot relatedtto familyhistory. REF: pp. 46-47 13. A 13-year- old girl hastatkaryotypetthat revealstantabsentthomologous Xtchromosome with onlyasingle X chromosometpresent. Whattmedicaldiagnosiswill thenursetobserveonthe chart? a. Downsyndrome b. Criduchatsyndrome c. Turnersyndrome d. FragileXsyndrome Answer:: C Aconditiontwiththetpresenceoftasingle XchromosomeandnohomologoustXtor Y chromosome , sotthetindividual hastatotal of 45 chromosomes, is known as Turnersyndrome. Downtsyndrome ista changetinonearm ofachromosome. Criduchattsyndromeisduetota chromosomedeletion. F ragiletXsyndromeisduettoabreakoragapin achromosome. REF: p. 47 14. Whatgeneticdisorderistheresultif an individualpossesses an XXY chromosome co nfiguration? a. Turner b. Klinefelter c. Down d. Fragile X Answer:: B Individualswith at least twotXchromosomesand onetYchromosometin each cell(47 XXY karyot ype)thavetadisorderknown as Klinefeltersyndrome. Aconditiontwiththetpresenceofa single Xc hromosome andtnohomologoustXor Y chromosome, so thetindividualhasatotal of 45 chromoso mes, isknown astTurner syndrome. Downtsyndrometisattrisomy. FragiletX TEST BANK FOR UNDERSTANDING PATHOPHYSIOLOGY Huether & McCance: Understanding Pathophysiology, 6th Edition Chapter01:Cellular Biology syndrometisduettoabreakoragapin achromosome, not antextra chromosome. REF: p. 47 15. Apatientdemonstratesseverementalretardation causedtbyadeletionofparttof chromosome 5. Whatgenetictdisorderwillthenursetseedocumentedinthechart? a. Prader-Willisyndrome b. Downsyndrome c. Criduchattsyndrome d. TrisomyX Answer:: C Criduchatsyndromeme Answer:“cryofthetcat” anddescribesthetcharacteristiccryofthe affectedchild. Anothersympt omofthedisorderismentalretardation. Thediseasetiscausedt byatdeletion ofpartofthetshort ar mofchromosomet5. Prader- Willisyndromeis characterizedbyshortstature, obesity, andhypogonadism. Downsyndromed oestcauset mentalretardationbutisduettochromosome 21, notchromosome 5. TrisomyX can re sultin mentalretardationbutisduetto an extra Xchromosome. REF: p. 48 16. An aidetasks thenursetwhypeopletwhothavetneurofibromatosiswillshowvaryingtdegreesof thet disease. Whichgeneticprincipletshouldthenurseexplainttotthetaide? a. Penetrance b. Expressivity c. Dominance d. Recessiveness Answer:: B Expressivityistthetextent of vNaUriRatiSoIntiNnGphTeBnot.CypeMassociatedtwith aparticular genotype. Forn eurofibromatosis, avarietyofmanifestationsoccuramongindividuals. Thetpenetrancetofta trait is thepercentageofindividuals withaspecifictgenotypetwhotalsoexhibit theexpectedt pheno type. Dominancetreferstotobservablettraitsandrisktof tr Answer:mission. Recessiveness referstosilentstrainstwithreducedtriskofoccurrence. REF: p. 51 17. Cysticfibrosisiscausedbywhat genetabnormality? a. X-linkeddominant b. X-linkedrecessive c. Autosomaldominant d. Autosomalrecessive Answer:: D Cysticfibrosisis an autosomalrecessivedisorder. It is notaresultof Xlinksordominant pathol ogy. REF: p. 52 18. A 15-year-oldfemaleisdiagnosedwith Prader-Willi syndrome. Thisconditionis an example of: a. genomictimprinting. b. an autosomalrecessivetrait. c. an autosomaldominant trait. d. asex-linkedttrait. Answer:: A Prader-Willi, antexampletof geneimprinting, isnotassociatedtwithanyautosomaltsex- linked abnormality. REF: p. 52 19. Apatient, age 9, is admittedtoapediatricunitwith Duchennetmusculardystrophy. When pla nningcarethenurserecallstthepatienttinheritedthisconditionthroughtatraittthat is: a. X-linkeddominant. b. X-influenced. c. X-limited. d. X-linkedrecessive. Answer:: D Duchennemusculardystrophyistarelativelycommon X- linkedrecessive, not dominant, disorder. While it istsex linked,tit is not X-limitedor X- influenced. REF: p. 55 20. Achildistdiagnosedtwithcysticfibrosis. Historyrevealsthatthechild’stparents aresiblings. Cy sticfibrosiswasmosttlikelytheresultof: a. X-inactivation. b. genomictimprinting. c. consanguinity. d. obligatecarriers. Answer:: C Consanguinityreferstothematingtoftworelatedindividuals, andthetoffspringtofsuch mating saresaidtobe inbred. Consanguineousmatingsproducetasignificantincrease in recessivedis orders andareseenmostofteninpedigreesforrarerecessivetdisorders. X- inactivationoccurswhentonetXchromosomeinthesomaticcellstoffemalesistpermanently inacti vated. Genomicimprintingistrelatedttomethylationandotherchanges. Obligatecarriers arethos ewhohave antaffected parentandaffectedchildrenand, therefore, must themselves carrythemut ation. REF: p. 54 21. A 12-year- oldmaletisdiagnosedtwith Klinefeltersyndrome. Hiskaryotypewouldreveal whichofthetf ollowing? a. XY b. XX c. XYY d. XXY Answer:: D Apersontwith Klinefeltersyndromehas an XXYkaryotype. An XY isanormalmale. An XX is an ormalfemale. An XYY is antaneuploid karyotype. TEST BANK FOR UNDERSTANDING PATHOPHYSIOLOGY Huether & McCance: Understanding Pathophysiology, 6th Edition Chapter01:Cellular Biology REF: p. 47 22. To expressatpolygenictrait: a. genestmustinteractwiththeenvironment. b. severalgenesmust act together. c. multipletmutationsmusttoccurinthesametfamily. d. penetrancemusttoccur. Answer:: B Polygenictraitsarethosethatresultfromtseveralgenesactingtogether. Whenenvironmental fact orsinfluencetheexpressiontofthetrait, the termmultifactorialinheritanceisused. When multiple mutationsoccurinthetsametfamily,tthe mechanismmost likelyresponsibleistermed germlinetmo saicism. Penetranceofatraittisthepercentagetofindividualswithatspecific genotypetwhoalso ex hibittthetexpectedphenotype. REF: pp. 57-58 23. Whattisthediagnosisofat13-year- oldfemalewhohasakaryotypethatreveals an absentt homologous Xtchromosomewithonlyasin gle Xchromosomepresent? Herfeaturesincludea shortstature, widelyspaced nipples, andaredu ced carryingangletat thetelbow. a. Downsyndrome b. Criduchatsyndrome c. Turnersyndrome d. Klinefeltersyndrome Answer:: C Turnersyndromeischaracterizedbyshortstature, femalegenitalia, webbedneck, shield- like chestwithunderdevelopedbreaststandwidelyspacednipples,tandimperfectlydeveloped o varies. Downsyndromeis cNhaUraRcSteIrizNeGdtTbyBdi.sCtiOncMtivetcharacteristics: lownasalbridge, epicanthalfolds, protrudingtongue, andlow-setears. Criduchatsyndromeistcharacterized bylowbirth weight, severetmentalretardation, microcephaly(smallerthannormalheadsize), and heartdefects. Klinefelter syndrome is characterizedbysmalltestes, somedevelopmentof thetbre asts, sparsetbodyhair,tandlonglimbs. REF: p. 46, Table 2-1 24. Thegradualincreaseintheighttamongtthethumantpopulationoverthetpast 100tyearsistan exa mpletof: a. apolygenictrait. b. amultifactorialtrait. c. crossing over. d. recombination. Answer:: B Thegradualincreaseinheightistan exampleofmultifactorialtraitstinfluencedbygenesand alsob yenvironment. Polygenictraitsresult fromseveral genesactingtogether. Crossingover is an abn ormalchromosomestructure. Recombinationresultsfromtnewarrangementsof alleles. REF: p. 58 25. WhendiscussingtDNA replication, whichtenzymetismostimportant? a. RNApolymerase b. Tr Answer:fer RNA c. Messenger RNA d. DNA polymerase Answer:: D DNA polymerase, not RNApolymerase, istthetprimaryenzymeinvolvedinreplication. It addsba sestotthetnew DNA strandtandperforms“proofreading” functions. Neithermessenger RNAnortr Answer:fer RNAis astimportant to DNAreplication. REF: p. 39 26. Theregionsoftheheterogeneousnuclear RNAthatmust betsplicedouttoformtfunctional RN Aarecalled: a. promotersites. b. introns. c. exons. d. anticodon. Answer:: B WhenthemRNAisfirstttr Answer:cribed from the DNA template, it reflects exactlythebaset sequencetofthe DNA. In eukar yotes,tmanyRNAsequencesareremovedbynuclearenzymes,t andthetremainingsequencesares plicedtogethertoformthefunctionalmRNAthatmigratest tothecytoplasm. Thetexcisedsequenc estaretcalledtintrons (interveningsequences), andthet sequencesthattaretleftttotcodetforproteinstar ecalledexons. Inttr Answer:lation, RNAdirectsthe synthesisoftapolypeptide, acloverleaf- shapedstrandoftabout 80 nucleotides. ThettRNA moleculehasasitewheretan aminoacidattache s. Thethree-nucleotidesequence at the oppositesideofthecloverleaNftUisRcaSllIedNtGheTaBCoOdoMn. REF: p. 41 27. A 50-year-oldmalewasrecentlydiagnosedwith Huntingtontdisease. Tr Answer:missiontofthis diseaseisassociated with: a. penetranceofatrait. b. recurrencerisk. c. expressivity. d. delayed ageofonset. Answer:: D Akeyfeatureof Huntingtontdiseasetisits delayed ageofonsetsuchthatsymptomstaretnot seenu ntil 40 yearsofagetorlater. Thepenetranceofatraitisthepercentagetofindividuals withaspecif icgenotypewhoalsoexhibittthetexpectedtphenotype. Recurrencerisktisthe percentagetoffamil ymemberstwhotwillinheritthedisease. Expressivityis thetextent of variationtin phenotypeasso ciatedwithtaparticulargenotype. REF: p. 51 28. Whatttypeofmutationtdoesnottchangetthetamino acidsequenceandtthusthasnotobservablet cons equence? a. Frameshift b. Spontaneous c. Silent d. Missense Answer:: C Silentmutationsdotnotchangetheaminotacidsequenceandthereforethavetnoconsequences. Fra meshiftmutationstinvolvetheinsertionordeletionofoneormorebasepairsofthe DNA molecule . Theyaltertheaminoacidsequence. Spontaneousmutationsoccurinthetabsenceof exposurettoa mutagentandtproducechangestintthetaminotacidsequence. Missensemutations, aformtoftbasetpai rsubstitution, alteraminoacids, whichproduceachange(i.e., thet“sense”) intasingleaminoacid. REF: p. 39 29. Anursetisreviewingthepedigreetchart. Whentcheckingforaproband, what is thenurse look ingfor? a. Thepersonwhoistfirstdiagnosedwithtageneticdisease. b. Theindividualwhohasadiseasetgenetbutistphenotypicallynormal. c. Thephenotypeofgeneticmaterial. d. Thecodominance. Answer:: A Thepedigreetcharttsummarizes familyrelationshipsandshowstwhich memberstofafamily aretaff ectedtbyatgenetic disease. Thepedigreetbeginswiththetproband. Thepersontwhohasta disease ge nebuttisphenotypicallynormalisacarrier. Thetphenotypetistheresultofboth genotypetandenvir onment; it is notaproband. Codominancetisnotrepresentedbyaproband, but ittoccurs whenttheth eterozygoteisdistinguishablefrombothhomozygotes. REF: p. 50 30. Whichtofthefollowingdisorderstismanifestedtprimarilyinmales? a. Cysticfibrosis b. Neurofibromatosis c. Musculardystrophy d. Klinefeltersyndrome Answer:: C Musculardystrophyismanifestedprimarilyinmales. Cysticfibrosis, neurofibromatosis, and Kl inefeltersyndrometaretmanifestedinbothmalesandfemales. REF: p. 55 MULTIPLE RESPONSE 1. Whenthenursetisteachingthestaffabout X- linkedtrecessivedisorders, whichinformationt shouldthenursetinclude? (select alltthat apply) a. Thetraittisseentmuchtmoretofteninfemalesthantinmales. b. Thetraittisnevertr Answer:mittedfromfathertotson. c. Thegene can bettr Answer:mitted throughaseriesofcarrierfemales. d. Thegeneispassedfrom antaffected fathertoallhistdaughters. TEST BANK FOR UNDERSTANDING PATHOPHYSIOLOGY Huether & McCance: Understanding Pathophysiology, 6th Edition Chapter01:Cellular Biology e. Thetraitneverskipsgenerations. Answer:: B, C, D Theprinciplesof X- linkedtrecessivetinheritanceinclude: the trait isseentmuchtmoretoftentin malesthanintfemales; thet trait isnevertr Answer:mittedfrom fathertoson; thegene can be tr Answer:mittedthroughaseriestofcarrierfemales; thegeneispassedfrom an affectedfathertoall histdaughters, who, as phenotypicallynormalcarriers, tr Answer:mitittotapproximatelyhalftheir sons, whoaretaffected. X- linkedrecessivetdisorders can skipgenerationstsincetit istaonein fourchance. REF: p. 55 Chapter03: EpigeneticsandDisease Huether&McCance:UnderstandingPathophysiology,6thEdition MULTIPLE CHOICE 1. Whenconsideringabnormalepigeneticmodifications, whatfactoriscurrentlybeingtviewedt ast stronglyassociatedwithtthetdevelopmenttofsometcancers? a. Familygenetics b. Lifestyletchoices c. Environmentalstressors d. Emotionalcopingskills Answer:: C Environmentalstressorstcantmarkedlyincreasettheriskofaberrantepigeneticmodification andtar estronglyassociatedtwithsomecancers. Whilegenetics, lifestyletchoices, andcoping skills can af fectthetdevelopment andmanagementofcancer,ttheyaretnotcurrentlyconsidered astbeingtthe pri maryfactorsintheepigeneticmodificationthatoccurs. REF: p. 62 2. Housekeepingtgenesarevitaltothefunctiontandtmaintenanceofallthebody’stcells. What cha racteristicisassociatedtwith thesegenes? a. Theylackencodingthistones. b. Theyaretr Answer:criptionallyactive. c. RibosomaltRNAgenesaretabsent. d. Epigeneticsilencinghas occurred. GB.CM USNT O Answer:: B Asmallpercentageofgenes, termedhousekeepinggenes,taretnecessaryforthefunctionand main tenanceofallcells. Thesetgenesescapeepigeneticsilencingandtremaintr Answer:criptionally activeinall ornearlyall cells. Housekeepingtgenesincludeencodinghiston es, DNA and RNApolymerases, and ribosomal RNAgenes. REF: p. 64 3. Whattcharacteristicof Prader-Willisyndrome is nottacharacteristicof Angelmansyndrome? a. It is inherited fromthefather. b. Mentalretardationisobservable. c. Imprintingtof an abnormaltchromosomet15. d. Seizuretdisorderispresent. Answer:: A Awell- knowndiseaseexampleofimprintingisassociatedwithadeletiontofabout 4 million baset(Mb)tpai rs ofthetlongtarmofchromosome 15. Whenthisdeletionisinheritedfromthe father,tthe childmani feststPrader- Willisyndrome, whosetfeatures includeshorttstature, hypotonia,tsmallhandsandfeet, obesity, mil dtomoderatemental retardation, and hypogonadism. Thetsamet4 Mbdeletion,twheninherited fro mthemother, causes Angelman syndrome, which is characterizedbyseverementalretardation, se izures, and an ataxicgait. TEST BANK FOR UNDERSTANDING PATHOPHYSIOLOGY Huether & McCance: Understanding Pathophysiology, 6th Edition Chapter01:Cellular Biology REF: p. 65 4. Researchhastdemonstratedthatneuralstemcellshavetan impairedabilitytodifferentiatetinto fun ctionalneuronswhen subjectedtto: a. ethanol. b. marijuana. c. insufficienttnutrients. d. pooroxygenation. Answer:: A Itthas beenfoundthattreatingtculturedtneuralstemcellswithtethanolimpairstheirabilityto differ entiatetofunctional neurons; thistimpairmentseemstobetcorrelated withaberrant, densemethyl ation at loci thatareactiveinnormalneuronaltissue. Theresearchdoesnot supporttheteffectsof marijuana, insufficient nutrition, orpooroxygenation onthestemcell’s abilitytodifferentiatetap propriately. REF: p. 67 5. Whattistheroleofinactive MLH1 intthetdevelopmenttofsomeformsofinheritedcolon canc er? a. DeletiontofatnucleotiderepeattinthetDUX4 gene. b. DNA damageisleftunrepaired. c. Exp Answer:iontinthenumberofcytosine-guanine(CG) dinucleotide. d. Abnormalitiestofchromosome 11p15.5 thatleadtodownregulationof IGF2. Answer:: B Amajorcauseofoneformofinheritedcoloncancer(hereditarynonpolyposis colorectal cancer[ HNPCC])tisthemethylation ofthepromoterregionofagene, MLH1, whoseproteint productrepa irsdamaged DNNAU. WRhSeInNMGLTHBCcoOmMes inactive, DNAdamageaccumulates, eventuallyresultingtincolontumors. Facioscapulohumeralmusculardystrophy(FSHMD) is associatedtwiththe DUX4 gene. FragiletXtis associatedwiththecytosine- guaninet(CG) dinucleotide. Downregulationof IGF2tisassociatedwith Russell- Silversyndrome. REF: p. 69 6. Mutationsintheencodingofhistone- modifyingproteinshavetbeenshowntoinfluencetthe developmentofwhat congenialtconditio n? a. Cleftpalate b. Acephalous c. Heartdisease d. Webbedtdigits Answer:: C Mutationsingenestthatencodehistone- modifyingproteinshavetbeentimplicatedincongenital heartdisease. Researchhastyettto provideta relationship between abnormal histone- modifying proteinsandtcleftpalate, acephalous, andwebbedtdigits. REF: p. 64 7. Whichtembryonicstem cell characteristicistreferredtto asttotipotent? a. Abilitytodifferentiatetinto anytypeofsomaticcell. b. Abilitytorepairitsowndamaged DNA. c. Abilitytodeterminewhichparentalchromosomecopyitwillimprint. d. Abilitytominimizetheimpacttofpoor inuterotnutrition. Answer:: A Eachtofthecellsinttheveryearlyembryohasthetpotentialtotgivetrisetoatsomaticcelltofany type. Theseembryonicstemcellsarethereforesaidtobetotipotent(“possessing allpowers”). Theterm totipotentdoesnotinferthetabilitytorepairdamaged DNA, select specific chromosomecopies, or adjust forpoor inutero nutrition. REF: p. 64 8. 5-Azacytidinehasdemonstratedpromiseinthetreatmentofwhichformoftcancer? a. Liver b. Colon c. Gallbladder d. Pancreatic Answer:: D Thoughtassociatedwithtvarioussideeffects,tincludingdigestivetdisturbance,t5- azacytidine hastshownpromisetinthetreatment ofpancreaticcancer. Theretisnosupportforitsus eintthe treatmenttofliver, colon, orgallbladder cancers. REF: p. 70 9. Duringwhichtstagetofhumandevelopmentdoestheroleofepigeneticshavethegreatestt im pacttonthedevelopmenttof epigeneticabnormalities? a. Infancy b. Puberty c. In utero d. Middleage Answer:: C Conditions encountered in utero, duringtchildhood, andevenduringtadolescenceorlater cant hav elong-termimpacts onepigenetictstates, whichsometimes can bettr Answer:mittedacross generations. Theimpact istnot supportedforthetperiodsofinfancy, pubert y, andmiddleage. REF: p. 66 10. Whattcomorbidtconditiontdoestan individualdiagnosedwithtBeckwith- Wiedemannsyndrome have antincreased riskof developing? a. Cancer b. Diabetes c. Depression d. Foodallergies Answer:: A Beckwith- Wiedemannsyndrometisaccompaniedbyan increasedpredispositiontotcancer. Thereisnocurr entcorrelationbetween Beckwith- Wiedemanntsyndromeandtdiabetes, depression,torfoodtallergies. REF: p. 65 MULTIPLE RESPONSE 1. Screeningtoolstthatareepigeneticallybasedhaveshownpromisetindiagnosingtwhichtypest ofc ancer? (select all thatapply) a. Colon b. Breast c. Skin d. Bladder e. Prostate Answer:: A,tB, D, E Monitoringformisregulation ofmiRNAshasshownpromisetas attooltfor earlydiagnosisof canc ersofthecolon,tbreast, andprostate. Otherepigenetics- basedtscreeningapproacheshave showntpromisefordetectionofcancerstofthebladder, lung, an dprostate. Suchscreenings havetnot yetbeendevelopedforskincancers. REF: p. 69 2. Researchhastprovidedsupporttforthetheorythatepigeneticmodifications can resulttfrom def icient inutero nutritioncausingwhichchronictdisease? (select all thatapply) a. Obesity b. Asthma c. Cardiovasculardisease d. Diabetes e. Crohn’s disease Answer:: A, C, D Whenresearcherssought to investigatehowexposurettofamine inutero hadimpacted individual sborntintahistoricallyprosperoustcountrywhosetnutritionalintaketwas dramaticallyimpactedby WWII,ttheyfoundthattindividuals whosufferedtnutritional deprivation inutero weremorelikely tosufferfromobesityanddiabetes as adultsthan individuals whothadnotexperiencednutritional deprivationtduringtgestation. Otherdatasets revealelevatedriskofcardiovascularandmetabolic diseaseforoffspringtofindividuals exposedduringtearlydevelopmenttofluctuationsinagricultu ral yields. Theresearchdoes supportthedevelopment oftasthmator Crohn’s disease. REF: p. 66 Chapter04: Altered Cellularand TissueBiology Huether&McCance:UnderstandingPathophysiology,6thEdition MULTIPLE CHOICE 1. A report comestbacktindicatingtthatmuscularatrophyhastoccurred. Anurserecallsthat mu scularatrophyinvolvestadecreasetintmuscletcell: a. number. b. size. c. vacuoles. d. lipofuscin. Answer:: B Atrophyistadecreasetorshrinkagetincellularsize. Hyperplasia is an increasetintthetnumberof cells . Vacuolesaremembrane- boundvesicleswithinthecellthatcontaincellulardebrisand hydrolytictenzymes. Lipofuscintis th e yellow-brownagepigment. REF: p. 74 2. Duringtchildhood, thethymusdecreasesinsize, andthisisreferredto as whattypeof atro phy? a. Physiologic b. Pathologic c. Disuse d. Neurogenic Answer:: A Anormaldecreasetincell size is physiologicatrophy. Atrophycan result fromdisease (pathologic), disuse,tornerveinjury(neurogenic). REF: p. 74 3. Whenplanningtcareforacardiactpatient, thenurseknowsthatinresponsetotan increased wor kload, cardiactmyocardialcellstwill experiencehypertrophywhichisan: a. increasetinsize. b. decreasetinlength. c. increasetinexcitability. d. decreasetinnumber. Answer:: A Hypertrophyisacompensatoryincreaseinthesize of cellsin responsetomechanical stimuli (also calledmechanicalloadorstress, suchtas fromtstretching,trepetitive,tchronic,tpressure, or volumeo verload) andconsequentlyincreasesthesizetoftheaffectedorgan. Thecellsofthet heartandkidney s aretparticularlypronetoenlargement. Adecrease in length is notassociated withhypertrophy. A deficiencyofelectrolytesormineralscouldleadto antincrease int excitability; it isnotduettoincrea sedtworkloadorrelatedtothypertrophy. Adecreasetin cell numbersistreferredtto asthypoplasia. REF: p. 75 4. A 55-year-oldmalewithta 30- yearhistoryoftsmokingtistexaminedforrespiratorydisturbance. Examinationtofhisairway(bronc hial) revealsthatstratifiedsquamousepithelialcellshave replacedthenormalcolumnarciliatedc ells. Thistypetofcellularadaptation iscalled: a. anaplasia. b. hyperplasia. c. metaplasia. d. dysplasia. Answer:: C Metaplasia is thetreversible replacementtof one maturetcell type byanother, sometimes a lesst diff erentiatedcelltype. Anaplasiaislossoftcellulardifferentiation. Hyperplasiais an increaset in thetn umberofcellsresultingfrom an increasedrateofcellulardivision. Dysplasiareferstto abnormalc hangestintthetsize, shape, andtorganizationofmaturecells. REF: p. 77 5. Whenplanningtcareforthepregnanttpatient, thetnursewill recall thatthemammaryglandst enla rgetas aconsequence of: a. compensatoryhyperplasia. b. hormonalhyperplasia. c. hormonalanaplasia. d. compensatoryanaplasia. Answer:: B An increasetin themammaryglandstduringpregnancyisaresult ofhormonalchanges. The numb er ofmammarycells increasestin responsetoincreasedhormonelevels, not asta compensatoryme chanism. Anaplasiatisatreversal to lessmaturecells. REF: p. 76 6. A 24-year- old female presentstwithtexcessivetmenstrual bleeding. The physiciantidentified endometrialc hangestthatareduettohormonalimbalances. Thesecellularchangeswouldbe referredto as: a. dysplasia. b. pathologicdysplasia. c. hyperplasia. d. pathologichyperplasia. Answer:: D Becausethechangesareduetto an imbalance, theywouldtbetconsideredtpathologic hyperplasia,tat termtmoretdescriptivethansimplehyperplasia. Theendometrialchangestwere nottabnormalintsi zeandshape; thus, it isnotdysplasiatregardlessofcause. REF: pp. 76-77 7. A 55-year- oldmaletisdiagnosedtwithhepatocellularcancersecondarytothepatitistC. If the cancerousregi ontoftheliver is removed, thetremainingtcellstwouldundergo: a. pathologichyperplasia. b. pathologicmetaplasia. c. compensatoryhyperplasia. d. compensatoryaplasia. Answer:: C Compensatoryhyperplasiais antadaptive, notpathologic, mechanismtthatenablescertain org Answer: totregenerate. Metaplasiaisthetreversiblereplacementtofonematuretcelltypeby anothe r, sometimeslesstdifferentiated, cell type. Aplasiaisnotatcompensatorymechanism. REF: p. 76 8. A 40-year-oldfemale’s Papsmearindicatestabnormalchangesintthetshapeandorganization ofcervicaltcells. Whichtermwouldbetusedtoidentifythistypeofchange? a. Metaplasia b. Atrophy c. Hypertrophy d. Dysplasia Answer:: D Whencervical cellstundergodysplasia, thereisachangetintheirsize,tshape, andtorganization. Me taplasiais thereversiblereplacementofonetmaturecellttype. Thetcellshavenotdecreased insize; therefore, atrophyistincorrect. Thecellshavetnotincreasedinsizeinresponse tot stimuli; therefore , theyhavetnothypertrophied. REF: p. 77 9. A 75-year- oldmaletpresentswith chesttpaintonexertion. The chestpainismost likelyduetot hypoxicinjurys econdaryto: a. malnutrition. b. freeradicals. c. ischemia. d. chemicalttoxicity. Answer:: C Thecardiaccellsaredeprivedofoxygen, leadingtto ischemia, areductioninbloodsupplyto tissue s. The cells aredeprivedoftoxygen; theyarenotmalnourished. Freetradicals are electricallyuncha rgedatomsorgroupsofatomsthathavetan unpairedelectron. Chemical toxicityis notatfactorintth echestpain. REF: pp. 78-79 10. Apatienthasaheartattackthatleadstoprogressivecellinjurythatcausescelldeathwith sever ecell swellingandtbreakdownoforganelles. Whattermwouldtthetnursetusetodefinet this proce ss? a. Adaptation b. Calcification c. Apoptosis d. Necrosis Answer:: D Necrosisistthetsumofcellular changes afterlocal cell death. Cellularadaptation is a reversible, str uctural, orfunctional responsettobothnormalorphysiologicconditionsand adversetorpathologi cconditions. Calcificationis an accumulationofcalciumsalts. Apoptosis istan active processofc ellularself-destruction. TEST BANK FOR UNDERSTANDING PATHOPHYSIOLOGY Huether & McCance: Understanding Pathophysiology, 6th Edition Chapter01:Cellular Biology REF: p. 78, Table 4-1 11. Sodium andwateraccumulationtintan injuredcell areta directtresult of: a. decreased ATPproduction. b. karyorrhexis. c. ribosomedetachment. d. dehydration. Answer:: A Areductiontin ATPlevelscausestheplasmatmembrane’s sodium-potassium(Na+- K+)tpump andsodium-calciumtexchangetotfail. Sodium andwater cantthententer thecellfreely. Karyorrhexisme Answer: fragmentationofthetnucleustintotsmallerparticles or“nucleardust.” Ribosomedet achmentreducesprotein synthesis. Dehydrationtleadsttolossofsodiumtand water. REF: p. 80 12. Theearlydilationt(swelling) ofthetcell’stendoplasmic reticulumresultstin: a. increasedtaerobicmetabolism. b. failuretoftDNA. c. reducedtprotein synthesis. d. increased Na+-K+ pumpfunction. Answer:: C Earlydilationofthetendoplasmicreticulumcausesttheribosomestodetachfrom therough endopl asmicreticulum, reducingtproteintsynthesis. Aerobictmetabolism ista normal processt andwould notleadtoswelling. Cellularswellingwillnotaltercellular DNA. Areductionin the Na+- K+tpumpleadstotan intracellularaccumulation ofsodiumandtcalcium andtdiffusion ofpotassiumouttofthecell. SNoUdRiuSmIaNndGwTaBte.r cCaOntMthen enterthecellfreely, and cellular swel lingresults. REF: p. 80 13. A 52-year- oldmaletsufferedamyocardialinfarctionsecondarytotatherosclerosisand ischemia. Oncetbl oodflowisreturnedtothedamagedheart,treperfusion injuryoccurs as a result of: a. oxidation stress. b. vacuolation. c. decreasedtintracellular calcium. d. lipidtacceptorproteins. Answer:: A Reperfusioninjurycan resulttfromoxidativestress, increasedintracellularcalcium, inflammatio n, orcomplementactivation. Oxidativetstresscausesthetformationofradicalsthatt causetfurtherm embranetdamageandmitochondrialtcalciumoverload. Vacuolationleadstot cellularswellingbut istnot associatedwithreperfusion. An increaseofintracellularcalciumis acauseofreperfusionin jury. Lipidacceptorproteinsbindwithttriglycerides to createfatty liver, andtheydonottaffectthe myocardium. REF: p. 81 14. Afamilypresentstottheirprimarycareproviderreportingtheadache, nausea, weakness, tinnitus, andvomiting. Whichofthefollowingtwouldbethemost likelyexplanationfortheset symptoms? a. Leadexposure b. Carbontmonoxidepoisoning c. Ethanolexposure d. Mercurypoisoning Answer:: B Symptomstrelatedttocarbonmonoxidepoisoningtincludeheadache,tgiddiness, tinnitus (ringingi ntthetears), nausea, weakness, andvomiting. Althoughnauseaandtvomitingcan occurwithleadte xposure, leadtoxicityisprimarilymanifestedbyconvulsionsanddelirium and,twithperipheraln erveinvolvement, wrist, finger, andsometimesfootparalysis. Ethanol exposurethas CNSeffectst and would notaffectthewholefamily. Mercurypoisoningtis manifestedbyCNSeffectsandwoul dtnottleadttonauseaandtvomiting. REF: p. 90 15. Acommonpathwayofirreversibletcell injuryinvolves increasedtintracellular: a. sodium. b. potassium. c. magnesium. d. calcium. Answer:: D Increasedintracellularcalciumlevelsactivatetcell enzymes(caspases) that promotetcelldeath by apoptosis. Persistentischemiatisassociatedtwithtirreversibleinjuryand necrosis. IrreversibleinjuryisassociatNedUsRtruSctIuNraGllTyBCsOevMeretswellingoftthetmitochondria,severe d amagettoplasmatmembranes, andswellingtoftlysosomes. Cellularinjuryisnot associated withsodium, potassium, or magnesiumlevels. REF: p. 81 16. A 50-year- oldmaletsustainedtaclosedheadtinjuryas atresult oftamotorvehicletaccident. CT scanrevealedatc ollectionofbloodtbetweentheinnersurfaceoftheduratmaterandtthetsurface oftthetbrain. Whichtt ypetofinjurywillthenursetbecaringtfor? a. Subduralthematoma b. Epiduralhematoma c. Contusion d. Abrasion Answer:: A Asubduralthematomatoccurswhentbloodistbetweentheinnersurfacetoftheduratmater and thesur facetofthebrain; it canresultfromblows, falls, orsuddenacceleration/decelerationof thehead. A ntepiduralhematomaisacollectiontofbloodbetweentthetinnersurfaceoftheskull andthetdura; it i smostoftenassociatedwithtaskullfracture. Acontusionisbleedingtintotthet skinorunderlyingttis sues. An abrasion(scrape) results fromremovalofthetsuperficiallayers oftheskincausedbyfricti ontbetweentthetskinandtinjuringobject. REF: p. 94, Table 4-8 17. A 20-year-oldmalepresentstotheemergencydepartmentwithtajaggedsharp- forceinjury that istlongerthan it isdeep. Whichtypeofwound willtthenursebetcaringtfor? a. Stabwound b. Incisedwound c. Puncturewound d. Choppingwound Answer:: B An incisedwoundtisatcutthattislongerthantittisdeep. Astabtwoundtisatpenetrating sharp- forceinjurythatis deeperthantittislong. Apuncturetwoundiswithoutsharpedges and istmadetwit htan instrumentlikeatnail. Heavy, edgedinstruments(axes, hatchets, propeller blades) producetw oundswithacombinationofsharpandbluntforcetcharacteristics. REF: p. 94, Table 4-8 18. A 30-year- oldfemaletpresentswithtagunshotwoundtothehead. Thetwoundthassearedtedges andatdeeptpen etration oftsmoketandgunpowder fragments. Thiswound wouldbe documented as a(n): a. exit. b. intermediaterangeentrance. c. contactrangetentrance. d. indeterminaterangetentrance. Answer:: C Acontactrangetentrancetwoundisadistinctivetypeofwoundthathappenswhenagunis heldsott hemuzzlerestsontorpressestintotthetskinsurface; inadditionttothethole, theretis searingoftheedg es ofthewoundfromtflameandtsootorsmokeontthetedgesofthetwound. It isunlikelyitisanexitwoundNsUinRceStIheNreGiTsBonl.yCoOnMetwound andithassearededgesandgunpow derfragments. Antintermediatetrange entrancewoundissurroundedbygunpowder tattooingorstippling. An indeterminatetrangeentrancewoundoccurswhen flame,tsoot, or gunpo wderdoestnotreachthetskinsurfacebutthetbullet does. REF: p. 95, Table 4-8 19. A 15-year- oldfemaletpresentstotthetERtfollowing atphysical assault. Shethastinternaldamaget totthenecktwit htdeeptbruising. X- raytreveals fractures ofthehyoidboneandtrachealand cricoidcartilage. Whichofthefollowing most likelycausedtherinjuries? a. Chemicalasphyxiation b. Chokingasphyxiation c. Ligaturestrangulation d. Manualstrangulation Answer:: D Squeezingofthetnecktas withtstrangulationwould fractionthehyoidbone. Chemical asphyxiatio ntwouldlead tobreathingtproblemsbutwouldnotresultintfracture. Chokingt asphyxiationwould leadttoswellingoftissuesbut wouldnottresultinfracture. In ligature strangulation, themarkontth eneckishorizontalwithoutthetinverted Vpatternseentint hangings. It wouldnotleadttotfracture. REF: p. 96 20. A 55-year- oldmalethastswellingtofthetfeet. Whichofthetfollowingtaidedinthedevelopment ofswelling? a. Increased ATP b. Chloridetmovement outofthecell c. Na+ movementintothecell d. Decreasedoncoticpressure Answer:: C Whensodiumandtwaterenterthecellfreely, cellularswelling, as well as earlydilationofthet endo plasmictreticulum, results. Decreased ATPwouldtleadttotswelling. Chloridetmovement outtof th ecellwouldaffectmusclecontractionbutdoesnotleadtoswelling. Increased oncoticpressuretw ouldnotaffectswelling. REF: p. 97 21. A 35-year- oldfemaletisdiagnosedtwithmultipletmyeloma. Biopsyofthetumorreveals Russellbodies, andla boratorytestingreveals kidneydysfunction. Whichsubstancetshouldthe nursemonitor as ittis acc umulatingintthetpatient’s body? a. Glycogen b. Protein c. Pigment d. Melanin Answer:: B Russellbodiestoccurdue totexcess aggregatesofprotein. Excessglycogen wouldaffectblood gluc ose. Increasedtpigmentwouldtnottleadttokidneydysfunction. Melanintaccumulatesint epithelial c ells (keratinocytes) oftheskintandretina. REF: p. 99 22. Anewbornmaleisdiagnosedtwithalbinismbasedonskin, eye, andthairappearance. Which find ingwillsupportthisdiagnosis? a. Increasedmelanin b. Increasedhemoproteins c. Inabilitytotconvert tyrosinetto DOPA(3,4-dihydroxyphenylalanine) d. Inabilitytotconvert biletobilirubin Answer:: C Thepersonwithalbinism is unablettoconverttyrosineto DOPA, an intermediateinmelanin biosy nthesis. Antincrease intmelanintwouldcausetskinto be darker. Hemoprotein accumulationsincell sarecausedbyexcessivestorageofiron,twhich is tr Answer:ferredtothecells fromthebloodstream. An inabilityto convertbiletto bilirubinwouldno t leadtoalbinism. REF: p. 100 23. A 23-year- oldmaletdevelopsablackeyetfollowingatfight. Whentheaidetaskstthetnursewhy thisoccurred, th enurse’s besttresponsetis that thebruisingisduetotan accumulationof: a. tr Answer:ferrin. b. bilirubin. c. albumin. d. hemosiderin. Answer:: D Hemosiderinistresponsibletforthecolorchangesinatblackeye. Tr Answer:ferrinisatr Answer:port proteinresponsibleforiron tr Answer:port. Bilirubinisthetnormal, yellow-to- greenpigmentofbile derivedfromthetporphyrinstructureofhemoglobin. Albuministthetprotei ntintheserum,t responsibletforcellularintegrity. REF: p. 100 24. Liquefactivetnecrosisoccursinthetbrainbecause: a. debristis notdigestedbyhydrolases. b. ofproteintdenaturation. c. it istrichtin hydrolyticenzymestandlipids. d. ischemiaresultsinchemicalinjury. Answer:: C Liquefactivetnecrosis is duettoenzymatictactionandbecausecellsofthe brain aretrichin enzymes. Proteindenaturationoccursprimarilyintthetkidneys. Liquefactivetnecrosisisdueto enzymatic re actiontandtnottothypoxia or hydrolases. REF: p. 103 25. A 2-year- oldswallowedwatchbatteries. Followingingestion,tkidneyfunctiontwasimpaired, andthehear tbegantofail. Whichofthetfollowingtwasthetmostlikelycause? a. Karyorrhexis b. Coagulativenecrosis c. Ammoniataccumulation d. Caseoustnecrosis Answer :: B Coagulativenecrosisoccursprimarilyinthekidneys, heart, andadrenaltglandsandcommonly res ults fromhypoxia. Karyorrhexisme Answer: fragmentationofthenucleusintosmallerparticles or“nucleardust.” Ammoniaaccumul ationtis nottassociatedwiththisttoxicity. Caseous necrosisresultsfromtuberculosistpulmonaryinf ection. REF: pp. 102-103 26. Agrouptofprisoninmatesdevelopedtuberculosisfollowingexposuretto an infectedtinmate. Onte xamination, tissuesweretsofttandgranular(liketclumpedcheese). Whichofthetfollowingt is them osttlikelycause? a. Coagulativenecrosis b. Liquefactivetnecrosis c. Caseousnecrosis d. Autonecrosis Answer:: C Caseousnecrosisresultsfromtuberculosispulmonaryinfection. Coagulativenecrosistoccurs pri marilyinthetkidneys, heart, andtadrenal glands, andcommonlyresultsfromhypoxia. Liquefactivetnecrosis resultstfromischemicinjurytoneuronsandglialcellsinthebrain. Autonec rosisistaprocess ofcellularself-digestion andistnotduetoinfectionsuch as tuberculosis. TEST BANK FOR UNDERSTANDING PATHOPHYSIOLOGY Huether & McCance: Understanding Pathophysiology, 6th Edition Chapter01:Cellular Biology REF: p. 103 27. A 50-year- oldfemaletbecameinfectedwithtClostridium bacteriaanddiedatweeklater. Examination ofherr ed bloodtcellstrevealedtlysis ofmembranes. Whichtof thetfollowingtwast thetmost likelycausetof herdeath? a. Fatnecrosis b. Wettgangrene c. Gangrenousnecrosis d. Gasgangrene Answer:: D Gas gangreneistaspecial typeof gangrenetcausedbyinfectiontofinjuredtissuetbyonetof manyspe ciesof Clostridium. Fatnecrosistiscellulardissolutioncausedbypowerfulenzymes, calledlipase s, thattoccur intthetbreast, pancreas, andotherabdominaltstructures. Wett gangrenedevelopswhen neutrophilsinvadethesite, causingtliquefactivenecrosis. Gangrenousnecrosisisduetotdeathoftissueand results fromtseverehypoxicinjury. REF: p. 104 28. Whilereadingatextbook, astudentreadsthetermapoptosis. Thetstudentrecalls that apo ptosisisaconditioninwhichcellsprogramthemselvesto: a. atrophy. b. die. c. regenerate. d. age. Answer:: B In apoptosis, cells areprogrammedtotdie. Apoptosisistnotassociatedwithcellatrophy, regeneration, oraging. REF: p. 104 29. A 50-year- oldmaletintravenousdrugtuserisdiagnosedwiththepatitis C. Examinationofthet liverrevealstce ll deathsecondaryto: a. fatnecrosis. b. physiologicapoptosis. c. infection-inducedapoptosis. d. pyknosis. Answer:: C Withthepatitis C,tthetliverwill demonstrateapoptosisthatisaresultoftheviralinfection. Fat necr osisoccurswithenzymatictactionduetotlipases. Apoptosistisnotanormalphysiological process. Pyknosisoccurswhenthenucleustshrinkstandbecomesasmall, densemassof geneticmaterial. REF: p. 104 30. Whatprincipleshouldthetnursetrememberwhentryingtodistinguishagingtfromdiseases? a. Ittis difficult tottell thedifferencetbecausetbothprocessesarebelievedttoresult fro mcellinjury. b. Ittis easytotellnormalprocessesfromabnormalprocesses. c. Disease,tunlike aging, hasagenetictcomponent. d. Agingtistdefinedtas exceedingtlifeexpectancy, butnotmaximallifetspan. Answer:: A Ittis difficult totdifferentiatetbetweentagingtanddiseasebecausebothoccursecondaryto cellular ag ing. It istnotteasytotdifferentiatetnormal processesfromtabnormalbecauseaging appears as anorm al process. Diseaseand agingthaveapossiblegeneticcomponent. Agingisa time- dependentlosstofstructureandfunctionthatproceedsslowlyandinsuchsmall incrementsthat it a ppearstotbetthetresultofthetaccumulationofsmall, imperceptibletinjuries. It is notatimetperiodto utsideoftlifeexpectancy. REF: p. 107 31. Whenanurseobservesmuscletstiffeningtoccurringtwithin 6– 14thourstafterdeath, thetnurse shoulddocumentthistfindingtastthetpresence of: a. livormortis. b. gangrene. c. algormortis. d. rigormortis. Answer:: D Rigormortisoccurswithin 6 hoursafterdeathtandistevidencedbymusclestiffening. Livor morti s is apurplediscoloration. Gangrenetreferstodeath of tissueandresultsfrom severe hypoxicinju ryanddoes notleadtostiffening. Algormortistis postmortemreductiontofbody temperature. REF: pp. 109-110 32. Whenanurseischecking a uNrinaRlysisI, thGe fiBndi.Cng tMhat wouldalerttthenursetotcellularinjuryisth epresenceof: a. slightglucose. b. excessiveprotein. c. blood. d. urea. Answer:: B Thepresencetofproteinintheurinein significant amountsindicatescellularinjuryand altered cell ularfunction. Neitherglucosenorbloodisnormallypresenttintheurin

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Instelling
Biology And Health Sciences
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Biology and Health Sciences

Voorbeeld van de inhoud

TEST BANK Understanding Pathophysiology 6th Edition By
Huether & McCance All Chapters 1 to 42

,TABLE OF CONTENT

Frontmatter

Introduction to Pathophysiology

PART ONE: BASIC CONCEPTS OF PATHOPHYSIOLOGY

Unit 1: The Cell

1. Cellular Biology

2. Genes and Genetic Diseases

3. Epigenetics and Disease (NEW)

4. Altered Cellular and Tissue Biology

5. Fluids and Electrolytes, Acids and Bases

Unit 2: Mechanisms of Self-Defense

6. Innate Immunity: Inflammation and Wound Healing

7. Adaptive Immunity

8. Infection and Defects in Mechanisms of Defense

9. Stress and Disease

Unit 3: Cellular Proliferation: Cancer

10. Biology of Cancer

11. Cancer Epidemiology

12. Cancer in Children and Adolescents

PART TWO: BODY SYSTEMS AND DISEASES

Unit 4: The Neurologic System

13. Structure and Function of the Neurologic System

14. Pain, Temperature, Sleep, and Sensory Function

,15. Alterations in Cognitive Systems, Cerebral Hemodynamics and Motor Function

16. Disorders of the Central and Peripheral Nervous Systems and Neuromuscular Junction

17. Alterations of Neurologic Function in Children

Unit 5: The Endocrine System

18. Mechanisms of Hormonal Regulation

19. Alterations of Hormonal Regulation

Unit 6: The Hematologic System

20. Structure and Function of the Hematologic System

21. Alterations in Hematologic Function

22. Alterations of Hematologic Function in Children

Unit 7: The Cardiovascular and Lymphatic Systems

23. Structure and Function of the Cardiovascular and Lymphatic Systems

24. Alterations of Cardiovascular Function

25. Alterations of Cardiovascular Function in Children

Unit 8: The Pulmonary System

26. Structure and Function of the Pulmonary System

27. Alterations of Pulmonary Function

28. Alterations of Pulmonary Function in Children

Unit 9: The Renal and Urologic Systems

29. Structure and Function of the Renal and Urologic Systems

30. Alterations of Renal and Urinary Tract Function

31. Alterations of Renal and Urinary Tract Function in Children

Unit 10: The Reproductive Systems

32. Structure and Function of the Reproductive Systems

33. Alterations of the Female Reproductive System

34. Alterations of the Male Reproductive System

, Unit 11: The Digestive System

35. Structure and Function of the Digestive System

36. Alterations of Digestive Function

37. Alterations in Digestive Function in Children

Unit 12: The Musculoskeletal and Integumentary Systems

38. Structure and Function of the Musculoskeletal System

39. Alterations of Musculoskeletal Function

40. Alterations of Musculoskeletal Function in Children

41. Structure, Function, and Disorders of the Integument

42. Alterations of the Integument in Children

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