Preclinical Pathology Review 2023: For USMLE Step 1 and COMLEX-USA Level 1 (2023)

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PRECLINICALPATHOLOGYREVIEW2023FORUSMLEUSMLE®®STEP1ANDCOMLEXUSALEVEL1®andUnitedStatesMedicalLicensingExamination®isajointprogramoftheNationalBoardofMedicalExaminers(NBME)andtheFederationofStateMedicalBoards(FSMB),whicharenotaffiliatedwithKaplanandwerenotinvolvedintheproductionof,anddonotendorse,thisproduct.COMLEXUSA®(NBOME),whichisnotaffiliatedwithKaplanandwasnotinvolvedintheproductionof,anddoesnotendorse,thisproduct.isaregisteredtrademarkoftheNationalBoardofOsteopathicMedicalExaminers,Inc

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PRECLINICALPATHOLOGYREVIEW2023FORUSMLE®COMLEXUSA®STEP1ANDLEVEL1USMLE®andUnitedStatesMedicalLicensingExamination®isajointprogramoftheNationalBoardofMedicalExaminers(NBME)andtheFederationofStateMedicalBoards(FSMB),whicharenotaffiliatedwithKaplanandwerenotinvolvedintheproductionof,anddonotendorse,thisproduct.COMLEXUSA®wasnotinvolvedintheproductionof,anddoesnotendorse,thisproduct.isaregisteredtrademarkoftheNationalBoardofOsteopathicMedicalExaminers,Inc.(NBOME),whichisnotaffiliatedwithKaplanandKP00710.indb113/10/221:51P

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USMLE®andUnitedStatesMedicalLicensingExamination®isajointprogramoftheNationalBoardofMedicalExaminers(NBME)andtheFederationofStateMedicalBoards(FSMB),whicharenotaffiliatedwithKaplanandwerenotinvolvedintheproductionof,anddonotendorse,thisproduct.COMLEXUSA®isaregisteredtrademarkoftheNationalBoardofOsteopathicMedicalExaminers,Inc.(NBOME),whichisnotaffiliatedwithKaplanandwasnotinvolvedintheproductionof,anddoesnotendorse,thisproduct.Thispublicationisdesignedtoprovideaccurateinformationinregardtothesubjectmattercoveredasofitspublicationdate,withtheunderstandingthatknowledgeandbestpracticeconstantlyevolve.Thepublisherisnotengagedinrenderingmedical,legal,accounting,orotherprofessionalservice.Ifmedicalorlegaladviceorotherexpertassistanceisrequired,theservicesofacompetentprofessionalshouldbesought.Thispublicationisnotintendedforuseinclinicalpracticeorthedeliveryofmedicalcare.Tothefullestextentofthelaw,neitherthePublishernortheEditorsassumeanyliabilityforanyinjuryand/ordamagetopersonsorpropertyarisingoutoforrelatedtoanyuseofthematerialcontainedinthisbook.©2023byKaplanNorthAmerica,LLCPublishedbyKaplanMedical,adivisionofKaplanNorthAmerica,LLC.1515WCypressCreekRoadFortLauderdale,FL33309Allrightsreserved.Thetextofthispublication,oranypartthereof,maynotbereproducedinanymannerwhatsoeverwithoutwrittenpermissionfromthepublisher.109876 54321CourseISBN:9781506284545AllrightsreservedunderInternationalandPanAmericanCopyrightConventions.Bypaymentoftherequiredfees,youhavebeengrantedthenonexclusive,nontransferablerighttoaccessandreadthetextofthiseBookonscreen.Nopartofthistextmaybereproduced,transmitted,downloaded,decompiled,reverseengineered,orstoredinorintroducedintoanyinformationstorageandretrievalsystem,inanyformorbyanymeans,whetherelectronicormechanical,nowknownorhereinafterinvented,withouttheexpresswrittenpermissionofthepublisher.KP00710.indb213/10/221:51P

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EditorsJohnBarone,MDAnatomicandClinicalPathologistBeverlyHills,CAManuelA.Castro,MD,AAHIVSDiplomateoftheAmericanBoardofInternalMedicineCertifiedbytheAmericanAcademyofHIVMedicineWiltonManors,FLTheeditorswouldliketoacknowledgeHenrySanchez,MD(UCSF,SanFrancisco),AlexisPeedin,MD,andMonaWood,MDfortheirinvaluablecontributions.KP00710.indb313/10/221:51P

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Wewanttohearwhatyouthink.WhatdoyoulikeornotlikeabouttheNotes?Pleaseemailusatmedfeedback@kaplan.com.KP00710.indb413/10/221:51P

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TableofContentsCHAPTER1:FundamentalsofPathology.....................1CHAPTER2:CellularInjuryandAdaptation.. .. . . . . . . . . .. .. . ..5CHAPTER3:Inflammation. . . . . . . . .. .. . . . . . . . ..... . .15CHAPTER4:TissueRepair. . . . . . . . .. .. . . . . . . . ..... . .23CHAPTER5:CirculatoryPathology. . . . .. .. . . . . . . . ..... . .27CHAPTER6:GeneticDisordersandDisordersofSexualDevelopment. ... . .39CHAPTER7:Immunopathology.CHAPTER8:Amyloidosis.................................................53.63CHAPTER9:PrinciplesofNeoplasia. . . .. .. . . . . . . . . .. .. . .65CHAPTER10:SkinPathology.........................75CHAPTER11:RedBloodCellPathology:Anemias. . . . . . . . . .. .. . .87CHAPTER12:VascularPathology.......................97CHAPTER13:CardiacPathology. . . . . .. .. . . . . . . . ......105CHAPTER14:PulmonaryPathology.....................119CHAPTER15:RenalPathology. . . . . . .. .. . . . . . . . ......137CHAPTER16:GastrointestinalTractPathology... . . . . . . . . .. ...155CHAPTER17:PancreaticPathology.........CHAPTER18:GallbladderandBiliaryTractPathology........................167.171CHAPTER19:LiverPathology. . . . . . .. .. . . . . . . . ......175CHAPTER20:CentralNervousSystemPathology...............185vKP00710.indb513/10/221:51P

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CHAPTER21:HematopoieticPathology:WhiteBloodCellDisorders&LymphoidandMyeloidNeoplasms. . . . . ....205CHAPTER22:FemaleGenitalPathology.CHAPTER23:BreastPathology........................................219.231CHAPTER24:MalePathology. . . . . . ... . . . . . . . . ... . ..237CHAPTER25:EndocrinePathology. . . . ... . . . . . . . . ... . ..243CHAPTER26:BonePathology. . . . . . ... . . . . . . . . ... . ..253CHAPTER27:JointPathology. . . . . . ... . . . . . . . . ... . ..263CHAPTER28:SoftTissueandPeripheralNervePathology..INDEX.........................................269.277viKP00710.indb613/10/221:51P

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FundamentalsofPathologyLEARNINGOBJECTIVES❏Definetheetiology,pathogenesis,morphology,andclinicalsignificanceofdisease❏Listtechniquesforstainingpathologicspecimens❏UnderstandthestainsusedtoidentifyspecificstructuresPathologyisthestudyofallaspectsofdisease,i.e.symptoms/signs,pathogenesis,complications,andmorphologicconsequences(includingstructural,functionalandmolecularalterationsincells,tissues,andorgans).Morphologicchangesofthediseaseprocessincludebothgrosschangesandmicroscopicchanges.DIAGNOSTICTECHNIQUESGrossexaminationoforgans(onexamquestions)isdonein2steps:identifytheorganandthenidentifythepathologicabnormality(e.g.,nodulesinacirrhoticliver,necrotictumorinalung).Grossfeaturesthatmaycontributetomakingadiagnosisincludesize,shape,consistency,andcolorofthetissue/organ.Tissuesectionsfromtheorganaresubmittedformicroscopicexaminationtomaketheultimatediagnosis.Thefollowingtechniquesareusedtohelpexaminemicroscopicsectionsoftissue.Asinglespecimenmayrequiremultipleslidessothatvariousstains/techniquescanbeappliedandhelptoconfirmthediagnosis.•Histochemicalstains,whichusechemicalreactionstohighlightvariousstructuresorpathogens•Hematoxylin&eosin(H&E)stain(goldstandardforhistologicalevaluation),inwhichhematoxylinbindsnucleicacidsandcalciumsalts,whileeosinstainsbothextracellularandintracellularproteins)•Immunohistochemical(antibody)stains(usuallydarkbrown=positive)–Cytokeratin(stainsepithelialcells)–Vimentin(stainscellsofmesenchymaloriginexceptthe3muscletypes;stainsmanysarcomas)–Desmin(stainssmooth,cardiac,andskeletalmyosin),prostatespecificantigen,andmanyothersNOTEReticulinandtrichromehelptoidentifynodulesoffibrosisinthecirrhoticliver.NOTETheetiology(cause)ofadiseasemaybegeneticorenvironmental.Thepathogenesisofadisease definesthetemporalsequenceandpatternsofcellularinjuryleadtodisease.Theclinicalsignificanceofadiseaserelatestoitssignsandsymptoms,diseasecourseincludingcomplications,andprognosis.NOTETheterm“eosinophilic”isoftenusedinpathologytorefertocellsthatareverypink.1#1KP00710.indb113/10/221:51P

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PhysiologyMedicalGeneticsPATHOLOGYPathologyBehavioralScience/SocialSciences•Ancillarystudiesusedontissuesections–Microbiology–Immunofluorescencemicroscopy(IFM),usedforrenalandautoimmunediseaseTransmissionelectronmicroscopy(EM),usedforrenaldisease,neoplasms,infections,andgeneticdisorders•Moleculartechniquesusedonfreshandformalinfixedtissue–Proteinelectrophoresis–SouthernandWesternblots–Polymerasechainreaction(PCR)–Nextgenerationsequencing(NGS)–HISTOCHEMICALSTAINSTable11.StructuresStainedbyH&EHematoxylinStainsbluetopurple•Nuclei•Nucleoli•Bacteria•CalciumCytogeneticanalysis(karyotyping,insituhybridizationstudies)EosinStainspinktored•Cytoplasm•Collagen•Fibrin•RBCs•Thyroidcolloid2KP00710.indb213/10/221:51P

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CHAPTER1|FUNDAMENTALSOFPATHOLOGYTable12.HistochemicalStainsandSelectDiseasesinwhichtheymightbePositiveStainPrussianBlueCongoRedAcidfast(ZiehlNeelsen,Fite)PeriodicacidSchiff(PAS)TargetIronAmyloidAcidfastbacilliMoleculeswithhighcarbohydratecontentTrichromeReticulinConnectivetissue,typeIVcollagenTypeIIIcollagenSelectAssociatedDiseaseStatesHemochromatosis,hemosiderosisAmyloidosisM.tuberculosis,MACinfectionsCandida,a1antitrypsindeficiency(hepatocytes),glycogenstoragediseases,diabeticnephropathy(KimmelstielWilsonnodules)Cirrhosis,crescenticglomerulonephritisCirrhosis,myelofibrosisFigure11.PrussianBlueStainShowsHemosiderinCausedbyRBCBreakdownwithinMacrophages3KP00710.indb313/10/221:51P

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CellularInjuryandAdaptationLEARNINGOBJECTIVES❏Explaincausesofcellularinjury❏Demonstrateunderstandingofcellularchangesduringinjuryandcelldeath❏Answerquestionsaboutcellularadaptiveresponsestoinjury❏Describecellularalterationsduringinjury2CELLULARINJURYCausesofCellularInjury•Hypoxia(mostcommon)occurswhenlackofoxygenpreventsthecellfromsynthesizingsufficientATPbyaerobicoxidation.Majormechanismsofhypoxiaareischemia,cardiopulmonaryfailure,anddecreasedO2carryingcapacityoftheblood(e.g.,anemia).Ischemia,duetoalossofbloodsupply,isthemostcommoncauseofhypoxiaandistypicallyrelatedtoadecreaseinarterialfloworvenousoutflow(e.g.,atherosclerosis,thrombus,thromboembolus).•Pathogens(viruses,bacteria,parasites,fungi,andprions)caninjurethebodybydirectinfectionofcells,productionoftoxins,orhostinflammatoryresponse.•Immunologicdysfunctionincludeshypersensitivityreactionsandautoimmunediseases.•Geneticabnormalitiescausecongenitaldisorders,e.g.,lysosomalstoragedisorders,whichcauseintracellularaccumulationsofproteins,triggeringcelldeath.•Chemicalinjurycanoccurwithdrugs,poisons(cyanide,arsenic,mercury,etc.),pollution,occupationalexposure(CCl4,asbestos,carbonmonoxide,etc.),andsocial/lifestylechoices(alcohol,smoking,IVdrugabuse,etc.).•Physicalinjuryincludestrauma(blunt/penetrating/crushinjuries,gunshotwounds,etc.),burns,frostbite,radiation,andpressurechanges.•Nutritionalorvitaminimbalance–Inadequatecalorie/proteinintakecancausemarasmus(decreaseintotalcaloricintakecausesadiposestorestobedepletedsoskeletalmusclesisused,leadingtomusclewastingi.e.cachexia)andkwashiorkor(decreaseintotalproteinintake,leadingtoedemaandabdominaldistension).5#KP00710.indb513/10/221:51P

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PhysiologyMedicalGeneticsPATHOLOGYPathologyBehavioralScience/SocialSciences–Excesscaloricintakecancauseobesity(secondleadingcauseofprematurepreventabledeathintheUnitedStates)andatherosclerosis.Microbiology–VitamindeficienciescanbeseenwithvitaminA(nightblindness,squamousmetaplasia,immunedeficiency),vitaminC(scurvy),vitaminD(ricketsandosteomalacia),vitaminK(bleedingdiathesis),vitaminB12(megaloblasticanemia,neuropathy,andspinalcorddegeneration),folate(megaloblasticanemiaandneuraltubedefects),andniacin(pellagra[diarrhea,dermatitis,anddementia]).–Hypervitaminosis(uncommon)canresultintissuespecificabnormalities.NOTERiskfactorsforvitaminKdeficiencyincludeprematurity(neonates)andfatmalabsorptionsyndromes(cysticfibrosis,celiacdisease)Figure21.RadiographofaChildwithRicketsShowsBowedLegsCellularChangesDuringInjuryCellularresponsestoinjuryincludeadaptation(hypertrophyoratrophy;hyperplasiaormetaplasia),reversibleinjury,andirreversibleinjuryandeventualcelldeath(necrosis,apoptosis,ornecroptosis).Thecellularresponsetoinjurydependsonseveralimportantfactors,includingtypeofcellinjuredandthecell’sabilitytoadapt.6KP00710.indb613/10/221:51P

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CHAPTER2|CELLULARINJURYANDADAPTATIONHomeostaticcellMetabolicchangesIschemiaToxins,etc.AdaptationInjuryReversiblechangespointofnoreturnIrreversiblechangesApoptosisNecrosisFigure22.CellularResponsetoStressandInjuriousStimuliImportantintracellulartargetsandtheirmechanismsofcellinjuryareasfollows:•DamagetoDNA,proteins,lipidmembranes,andcirculatinglipids(LDL)canbecausedbyoxygenderivedfreeradicals,includingsuperoxideanion(O2•−),hydroxylradical(•OH),andhydrogenperoxide(H2O2).•SeveralkeybiochemicalpathwaysaredependentonATP.DisruptionofNa+/K+orCa++pumpscauseimbalancesinsoluteconcentrations.Additionally,ATPdepletionincreasesanaerobicglycolysisthatleadstoadecreaseincellularpH.ChronicATPdepletioncausesmorphologicalandfunctionalchangestotheERandribosomes.•Severaldefectscanleadtomovementoffluidsintothecell,includingformationofthemembraneattackcomplexviacomplement,breakdownofNa+/K+gradients(i.e.,causingsodiumtoenterorpotassiumtoleavethecell),etc.•Influxofcalciumcancauseproblemsbecausecalciumisasecondmessenger,whichcanactivateawidespectrumofenzymes.Theseenzymesincludeproteases(proteinbreakdown),ATPases(contributestoATPdepletion),phospholipases(cellmembraneinjury),andendonucleases(DNAdamage).•MitochondrialdysfunctioncausesdecreasedoxidativephosphorylationandATPproduction,formationofmitochondrialpermeabilitytransition(MPT)channels,andreleaseofcytochromec(atriggerforapoptosis).NOTEProtectivefactorsagainstfreeradicalsinclude:•Antioxidants(vitaminsA,E,C)•Superoxidedismutase(convertssuperoxide→hydrogenperoxide)•Glutathioneperoxidase(convertshydroxylionsorhydrogenperoxide→water)•Catalase(convertshydrogenperoxide→oxygenandwater)7KP00710.indb713/10/221:51P

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PhysiologyMedicalGeneticsPATHOLOGYPathologyBehavioralScience/SocialSciencesMyocardialIschemiaMicrobiologyDecreasedOxidativePhosphorylation(DecreasedATP)Na+K+ATPasepumpGlycolysisRibosomaldetachmentInfluxofNa+EffluxofK+CellswellingEndoplasmicreticulumswellingLossofmicrovilliMembraneblebspHFigure23.ClassicExampleofCellularInjuryCausedbyHypoxiaNormalNormalcellSwellingofendoplasmicreticulum,mitochondriaInjuryDeathLysosomeruptureHealingMembraneblebsNecrosisReversibleCellInjuryIrreversibleInjuryMorphologicalchangesinnucleusMyelinfiguresSwellingofendoplasmicreticulumandlossofribosomesSwollenmitochondriawithamorphousdensitiesGlycogenLacticacidProteinsynthesisSeveremembranedamageInfluxofCa2+Cytoplasmicenzymeleakoutofcell(i.e.,TroponinI)BreakdownofcellmembraneandnucleusInflammatoryresponseNecrosisFigure24.CellInjury8KP00710.indb813/10/221:51P

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