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MANAGEMENTOFPATIENTS
https://t.me/medicina_free
WITHLIVERDISEASESAND
HEMATOLOGICALDISEASES
CHAPTER 18
Roman G. Meyliker, Helen Giannakopoulos, Osama Soliman
MANAGEMENT OF PATIENTS WITH LIVER DISEASES*
1. What functions does the liver perform?
• Storesglycogen
• Gluconeogenesis
• Maintainsbloodglucoselevels
• Deaminationofaminoacids
• Beta-oxidationoffattyacids
• Excretesbilesalts
• Synthesizesplasmaproteins
• Metabolizesendogenousandexogenouscompounds
• Phagocytizesbacteria
• Excretesbilirubin
2. What are the common risk factors for developing liver disease?
• Intravenousdrugabuse
• Multiplesexualcontacts
• Cocaineuse
• Diabetes
• Contactwithblood
• Familyhistoryofliverdisease
• Bloodtransfusionbefore1989
• Intakeofcertainmedicationsandfoodsupplements
• Alcoholabuse
3. What are the signs and symptoms of hepatocellular disease?
Dependingonthecause,severity,andchronicityofliverdysfunction,thefollowingmaybepresent:
• Malaise
• Anorexia
• Pruritus
• Low-gradefever
• Rightupperquadrant(RUQ)discomfort
• Darkurine
• Jaundice
• Amenorrhea
• Tender,enlargedliverorhepatomegaly
• Splenomegaly
• Spidertelangiectasias
• Palmarerythema
• Ascites
• Gynecomastia
• Testicularatrophy
• Asterixis
*WrittenbyHelenGiannakopoulosandOsamaSoliman.
192
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4. What are the signs and symptoms of biliary obstruction?
• ColickyRUQpain
• Weightloss(suggestingcarcinoma)
• Jaundice
• Darkurine
• Light-coloredstools
5. What are the orofacial features of patients with chronic alcoholism?
• Poororalhygiene
• Impairedhealing
• Jaundiceoftheoralmucosa
• Candidiasis
• Glossitis
• Bruxism
• Parotidglandenlargement
• Petechiae
• Angularcheilosis
• Xerostomia
6. Which laboratory studies make up the liver function tests (LFTs), and how are they
used to evaluate liver disease?
LFTsareacollectivegroupofbloodteststhatindicatetheoverallhealthoftheliverintermsofenzy-
maticactivity,syntheticcapability,anddetoxifyingcapacity.
Elevatedserumaminotransferases(AST,ALT)resultfromdirectinjurytothelivermanifestingas
hepatocellularnecrosisorinammation.ALTismorespecicfortheliverthanAST.ASTisalsofound
intheheart,skeletalmuscle,pancreas,kidney,andredbloodcells.
Elevatedalkalinephosphataselevelssuggestcholestasis,obstructiveorinltrativeliverdisease
(i.e.,tumor,abscess,granuloma).Alkalinephosphataseelevationduespecicallytoliverdiseasewill
resultinconcomitantelevationofgamma-glutamyltranspeptidase(GGT).
Elevatedbilirubin(conjugatedandunconjugated)ispresentinthecholestaticpatternof
disease.
7. What is a MELD score, and how should it influence the surgical plan?
MELDisanacronymformodelforend-stageliverdiseaseandwasoriginallycreatedtopredictthe
3-monthmortalityrateofpatients.Ithasbecomeastandardinevaluatingpatientsforlivertransplant.
Itutilizesapatient’screatinine,bilirubin,andinternationalnormalizedratio(INR)withthenalnumber
rangingfrom6to40.Ahigherscoreisindicativeofmoreadvanceddisease.
• <10=Patientsaresuitableforalltypesofsurgery.
• 10to15=Thesurgeonistoutilizecautionandonlyperformnecessarysurgeries.
• >15=Noelectivesurgeriesshouldbeperformed.
8. What class of drugs can cause spasm of the choledochoduodenal sphincter
Opioids.Onlyapproximately3%ofpatientsreceivingopioidsexperiencesphincterspasmandintra-
9. Which inhaled anesthetic is best for maintaining hepatic blood flow and hepato-
Isourane.
10. What is the effect of inhaled anesthetics on hepatic blood flow?
A20%to30%decreaseinhepaticbloodowresultsfromdecreasedperfusionpressure.The
11. What is the effect of positive pressure ventilation on hepatic blood flow?
Decreasedhepaticbloodowsecondarytoincreasedcentralvenouspressuredecreaseshepatic
TheMELDscorehasbeenusedtodetermineapatient’ssuitabilityforsurgeryasfollows:
(sphincter of Oddi)?
biliarypressure.
cyte oxygenation?
metabolitesofinhalationalanestheticscancauseinammationordeathofhepatocytesbydirect
toxicityandresultinanasymptomatictransientelevationofASTandALT.
perfusionpressure.
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12. Which muscle relaxants are the best choices to use in a patient with liver
dysfunction?
Cisatracurium,atacurium,andmivacurium,becausetheyaremetabolizedviaaprocessknownas
Hofmanneliminationandthereforeareindependentofliverfunction.
13. How does liver dysfunction affect metabolism of procaine?
Theliverisresponsiblefortheproductionofpseudocholinesterase,whichmetabolizesprocaine
(andotheresteranesthetics).Decreasedproductioncanresultinprolongedhalf-lifeofthese
drugs.
14. What mechanism is responsible for metabolism of amide anesthetics?
Hepaticmicrosomalenzymeshavethemajorroleinmetabolismofamidelocalanesthetics.A
decreaseinliverfunctioncanthereforeprolongtheplasmahalf-lifeofamideanesthetics.
15. How is drug protein binding affected by liver disease?
Decreasedalbuminproductionbytheliverresultsinadecreasednumberofprotein-bindingsites.The
amountofunbound,pharmacologicallyactivedrugis,inturn,increased.
16. What are the most common drugs used in the dental office that are metabolized
primarily by the liver?
Localanesthetics,includingarticaine(Septocaine),lidocaine(Xylocaine),mepivacaine(Carbocaine),
prilocaine(Citanest),andbupivacaine(Marcaine)aremetabolizedbytheliver.Analgesicsthatare
metabolizedintheliverincludeaspirin,acetaminophen(Tylenol),codeine,meperidine(Demerol),and
ibuprofen(Motrin).Commonlyusedsedationdrugsthataremetabolizedintheliverincludediazepam
(Valium)andmidazolam(Versed).Valiumismetabolizedintotheactivemetabolitesdesmethyldiazepamandoxazepam,therebyprolongingitseffectsonthecentralnervoussystem.Antibioticsthat
aremetabolizedintheliverincludeampicillin,penicillin,clindamycin,erythromycin,andtetracycline.
ErythromycininhibitssubstratesCYP1A2and3A4,therebyincreasingplasmaconcentrationsofmany
otherdrugs.Becauseofthis,closescrutinyofothermedicinesapersonmaybetakingisrequired
whenprescribingerythromycin.
17. What are the signs of acetaminophen toxicity, and how should it be
treated?
Themaximumrecommendeddoseofacetaminophenis80mg/kginchildrenand4gramsover
24hoursinadults.Typicallypatientswillremainasymptomaticuntillevelsof250mg/kgor12grams
over24hoursareseen.Intherst24hours(stage1)afteringestion,signsandsymptomscanbe
vagueandoftenconsistofnausea,vomiting,diaphoresis,pallor,lethargy,andmalaise.Overthefollowing48hours(stage2),patientswilloftenshowclinicalimprovementwhiletheirLFTsrise,andRUQ
painwithhepatomegalyisseen,indicatingtrueliverdamage.Overthenext24hours(stage3),the
patientwilltypicallyexperiencejaundice,hepaticencephalopathy,hyperammonemia,andbleeding
diathesis.Ifthepatientsurvivesstage3,thenheorsheentersstage4,whichisroughly2weeksof
healinginwhichtheliveractuallyreturnstonormalfunction.
Ifapatientpresentswithin4hoursofingestion,itmaybebenecialtoundergoGIdecontaminationwithactivatedcharcoal(maximumof50g).Accordingtothe20-hourIVprotocol,administering
N-acetylcysteine150mg/kgover60minutesfollowedbya4-hourinfusionat12.5mg/kgperhourand
thennallya16-hourinfusionat6.25mg/kgperhourisrecommended.
18. How is drug metabolism affected by liver cirrhosis?
Fibrosisleadstodecreasesinbloodowfromthehepaticarterytothemostdistalareasoftheliver.
TheseareasareconcentratedwiththecytochromeP450system,whichisimportantinmetabolizing
manydrugs.Prolongedplasmahalf-lifeofthesedrugsisaconsequenceofcirrhosis.
19. Which are the Vitamin K–dependent clotting factors?
FactorsII,VII,IX,andX,andproteinsSandC.
20. How can liver disease affect the bleeding time?
Thebleedingtimemaybeincreasedinpatientswithportalhypertensionbysplenicsequestrationof
plateletsleadingtothrombocytopenia.
21. What lab values will be affected by a deficiency in the factors produced by the
liver?
Prothrombintime(PT)andpartialthromboplastintime(PTT).
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22. What is the treatment for bleeding diathesis from liver disease?
Freshfrozenplasma(FFP).Ifthepatientisthrombocytopenic,heorshemayneedplatelettransfusion
aswell.VitaminK–dependentclottingfactorsalonearenotsufcientbecausetheydonotinclude
factorV,whichisalsoproducedintheliver.
23. How are each of the hepatitis viruses transmitted?
• HepatitisAvirus(HAV):fecal-oralrouteresultingfromcontaminatedfoodorwater
• HepatitisBvirus(HBV):inoculationofinfectedbloodorbloodproductsorbysexualcontact
• Deltaagent:causeshepatitisonlyinassociationwithhepatitisBinfection
• HepatitisCvirus(HCV):parenteralrouteasseenwithIVdrugabuse
• HepatitisEvirus:enteralroute
24. What are the differences among the various viral hepatitides?
HAVisa28-nmRNAviruswhosemodeoftransmissionisprimarilyfecal-oralfromcontaminatedfood
orwater.ThediagnosticmarkerforhepatitisAisanti-HAV.HepatitisAisanacutediseaseanddoes
notexistinachronicstate.AntivirusIgMmarksactiveinfection,whiletheantivirusIgGisprotective,
anditspresenceindicatespriorinfectionorimmunization.AvaccineisavailableforHAV.
HBVisa42-nmDNAviruswhosemodeoftransmissionispredominatelyparenteral(bloodor
bloodproducts)orthroughsexualcontact.DiagnosticmarkersforHBVincludeimmunoglobulinM
(IgM)anti-HBc(acute),HBsAg(acute/chronic/infective),HBeAg(infectious),anti-HBs(recovery/immunity),andanti-HBcIg(ongoingorpastinfection).Infectionsresultinchronicdiseaseapproximately
20%ofthetime.InfectedpatientsaretreatedwithhepatitisBimmunoglobulinandwilldevelop
lifetimeimmunity.AvaccineisavailableforHBV.
HCVisa38-to50-nmRNAviruswhosemodeoftransmissionispredominantlyparenteral.
Diagnosticmarkersincludeanti-HCV(recovery/immunity)andHCVRNA(infectivity).Infectionsare
mainlychronicinnature.PatientswithchronichepatitisC,whodevelopcirrhosis,haveatwentyfold
greaterriskofdevelopinghepatocellularcarcinoma.Immunityfollowinginfectionisweakandineffective,andnovaccinecurrentlyexists.Therehavebeennewtreatmentmethods,includinginterferon
therapyandmostrecentlyaclassofdrugscalleddirect-actingantivirals(DAAs),whichinterferewith
theenzymestheHCVneedstomultiply.Genotype1HCVisthemostcommoninfection,accountingfor
approximately70%to75%ofallhepatitisCinfections.
Hepatitis D virus (HDV)isaviralinfectionthatoccursonlyinpatientswithpreexistingHBV.This
co-infectionoftencausesmarkeddeclineinhepaticfunctionandmaycausefulminatehepaticfailure.
HDVisusuallytransmittedbyneedlesindrugusers.
Hepatitis E virus (HEV)isa32-nmRNAviruswhosemodeoftransmissionispredominatelyfecaloral.Thediagnosticmarkerusedisanti-HEV(recovery).Notreatmentiscurrentlyusedforinfectedpatients.
Infectedpatientswilldeveloplifetimeimmunity,butnovaccineiscurrentlyavailableforHEV.HEVinfection
inpregnantwomenisassociatedwithfulminanthepatitis(liverfailurewithmassivelivernecrosis).
25. What causes jaundice?
Jaundiceresultsfromtheaccumulationofbilirubin,aproductofhememetabolism,inthebodytissue.
Itistypicallyrstnotedinthesclera.
26. What is the difference between unconjugated and conjugated bilirubin?
• Unconjugated(indirect):Thisisabreakdownproductofhemolysisthatisgeneratedbyreticu-
loendothelialcellsofthespleen.Thisformofbilirubinisveryinsolubleandutilizesalbuminfor
transportationthroughtheblood.Unconjugatedhyperbilirubinemiamayresultfromoverproduction
ofbilirubinbecauseofhemolysis,impairedhepaticuptakeofbilirubinduetocertaindrugs,hyperthyroidism,orimpairedglucoronidationofbilirubinasseeninGilbert’ssyndrome.
• Conjugated(direct):Whenunconjugatedbilirubinisdeliveredtotheliver,itdissociatesfromalbu-
minandisconjugatedwithglucoronide.Itisthenwatersoluble.Conjugatedhyperbilirubinemiais
seenwithhepatocellulardisease,drugs,sepsis,orextrahepaticbiliaryobstruction.
27. What is Gilbert’s syndrome?
Gilbert’ssyndrome,themostcommoncauseofidiopathichyperbilirubinemia,isanautosomaldomi-
nanttraitwithvariablepenetrance.Decreasedbilirubinuptakebyhepatocytesresultsinincreased
plasmaconcentrationofunconjugatedbilirubin.
28. What is the definitive study that determines the cause and severity of the
hepatocellular dysfunction or infiltrative liver disease?
PercutaneousliverbiopsyisperformedwithultrasoundorCTguidance.
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29. What is hepatic encephalopathy, and how is it treated?
Hepaticencephalopathyisalteredmentalstatus(rangingfromsubtletosevere)duetotheaccumulation
ofneurotoxicsubstancestraditionallyclearedbyahealthyliver.Themostcommonlyassociatedtoxinis
ammoniathatbypassesthehepatocytesandendsupintheastrocytesofthebrain.Here,theammonia
increasesGABAanddecreasesglutamateforanoverallinhibitoryactionontheCNS.Thelaxativelactuloseistypicallyusedforeliminationofby-productsuntiltheprecipitatingfactorisbroughtundercontrol.
30. How is cardiovascular function affected in a patient with liver disease?
Cardiovascularfunctionischaracterizedbyahyperdynamiccirculatorystate.
• Increasedcardiacoutput
• Decreasedsystemicvascularresistance
• Increasedbloodvolume
• Unchangedbloodpressureandheartrate
• Decreasedportalveinbloodow
• Maintainedordecreasedhepaticarterybloodow
• Maintainedordecreasedrenalbloodow
• Presenceofarteriovenousstulasinmanysites
• Possiblecardiomyopathy
31. What is hepatorenal syndrome?
Hepatorenalsyndromeisaprogressiverenalfailurethatoccursinpatientswithsevereliverdisease.
Itisconsideredafunctionalrenalfailuresincethekidneysaremorphologicallynormalandresume
normalfunctionwhentransplantedintorecipientswhodon’thaveahistoryofliverdysfunction.
32. What are contraindications to surgery in the patient with liver disease?
• Acuteliverfailure
• Acuterenalfailure
• Acuteviralhepatitis
• Alcoholichepatitis
• Cardiomyopathy
• Hypoxemia
• Severecoagulopathy(despitetreatment)
• MELDscore>15
33. What precautions should be taken before oral and maxillofacial surgery in a
patient with viral hepatitis?
Thepatient’sliverfunctionstatusshouldbedeterminedbymeansofliverfunctionenzymes(AST,ALT,
andALP).Drugchoiceanddosageshouldbedeterminedwiththeselabvaluesinmind.Thepatient’s
bleedingtendencyshouldalsobeassessedbyPT,PTT,INR,andbleedingtime.Forpatientsundergoingmajorsurgicalprocedures,ifthePTorPTTismorethan1.5times>controlvaluesoriftheINR
is≥3.0,transfusionofFFPshouldbeconsidered.ThissuppliesthepatientwithfactorsII,VII,IX,X,XI,
XII,andXIIIandheat-labilefactorsVandVII.Inpatientswithaplateletcountof<50,000/mm3,platelet
administrationtoalevelabove50,000mm3isindicated.Universalprecautionsshouldalsobetakento
preventhepatitisexposuretothesurgeonandassistants.
34. What is the preoperative therapy for patients with liver disease?
Preoperativemaximizationofliverfunctioninpatientswithliverdiseaseshouldincludeevaluatingand
optimizingthenutritionalstatusandcorrectingelectrolyteandcoagulationabnormalities.Thepatient
shouldstopalcoholintakeandincreaseproteinintake.Ifthepatienthasactivehepatitis,allelective
surgeriesshouldbepostponeduntilthehepatitishasresolvedcompletely.Defectsincoagulationshould
becorrectedwithFFP.Ifthepatientistakingsteroids,intravenouscorticosteroidsshouldbegiven.Finally,
preoperativeoroperativesedationshouldbedonetoadegreethatiscompatiblewiththepatient’s
decreasedabilitytometabolizedrugsbytheliver,especiallybenzodiazepines,barbiturates,andother
sedatives.
35. How can bleeding diathesis due to liver disease be corrected?
IncreasedPT/INR.
• VitaminKandFFP(vitaminKalonedoesnotincreasefactorVlevelsandrequires12to48hoursto
synthesize)
Decreasedplatelets/increasedbleedingtime.
• Transfusionofplatelets±DDAVPifimpairedvonWillebrandfactor
CHAPTER 18 MANAGEMENTOFPATIENTSWITHLIVERDISEASESANDHEMATOLOGICALDISEASES 197
INR
(
)
ISI
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36. What are the intraoperative considerations in patients with liver disease?
Itisimportanttomaintainadequateliverperfusionduringsurgerybymaintainingadequateblood
pressure.Thiscanbedonebyinfusingsaline,FFP,andplateletsifthereisthrombocytopenia.Ifthe
patientswallowedblood,thestomachshouldbeevacuatedtopreventproteinloadingandfalse-positive
bloodinthestool.Ifthepatientistakingcorticosteroids,supplementalsteroidsshouldbegiven.
37. What are the surgical considerations in post-liver transplant patients?
Duringtherst3monthsofthepostoperativeperiod,andinpatientswithchronicrejectionofthe
graft,onlyemergencyoralsurgicalproceduresshouldberendered.Suchproceduresshouldbe
performedonlyafterconsultationwiththepatient’stransplantservice,andwheneverpossible,
antibioticprophylaxisshouldbegiventopreventbacterialendarteritis.Aftertherst3months,the
patientisusuallyonimmunosuppressants.Ifthepatienthasastablefunctionalgraft,goodliver
functionisestablished.However,thereisstilltheriskofacquiredinfectionincludinginuenza,fungal
infections,andpost-transplantviralinfections.Inthesepatients,preventionandtreatmentofany
possibleinfectionisimportant,andconsiderationmustbegiventothepatient’simmunosuppressant
doses,supplementationofsteroids(ifnecessary),anduseofeffectiveinfectioncontrolmeasures.
MANAGEMENT OF PATIENTS WITH
HEMATOLOGICAL DISEASES
†
38. Which blood clotting factors are dependent on vitamin K for their synthesis?
FactorsII,VII,IX,andX.
39. Which blood test is used to monitor the effect of warfarin?
Prothrombintime(PT)test.
40. What is the international normalized ratio (INR)?
TheINRisacalculatedvaluedevelopedtonormalizethereportingofPT.
=
patient protime
mean of the normal range
TheISIistheInternationalSensitivityIndexvalueassignedbythemanufacturertoeachlotof
thromboplastincalibratedtotheWorldHealthOrganizationreferencematerial.TheINRstandardizes
reportingofanticoagulationactivityandmonitorspatientsonstabilizedoralanticoagulanttherapy
only.ThetherapeuticINRrangeis2.0to3.0formostclinicalsituations.Patientswithmechanical
prostheticheartvalvesaremaintainedat2.5to3.5.
41. What are the three phases of hemostasis?
Vascular,platelet,andcoagulationphases.
42. What effect can long-term antibiotic therapy have on hemostasis?
Long-termantibiotictherapycansuppressthenormalorainthegastrointestinaltractthatareneces-
saryforthesynthesisofvitaminK.ClottingfactorsII,VII,IX,andXrequirevitaminKfortheirsynthesis.
43. What is the mechanism of action of warfarin?
WarfarinisavitaminKantagonistthatleadstoadecreaseinfactorsII,VII,IX,andXproteinsCandS.
Warfarinisusedforlong-termanticoagulationandismonitoredbyfrequentINRandPT.
44. If warfarin (Coumadin) is to be discontinued before oral surgery, how soon should
this occur before the planned procedure?
Althoughdosedependent,ingeneral,thedurationofactionforwarfarinis3to5dayswithanonsetin
12to24hours.Thehalf-lifeis1.5to2.5days.Warfarinshouldbediscontinuedatleast3daysbefore
theprocedure,andaPTtestshouldbedonewithin24hoursofthesurgery.
45. How does administering vitamin K affect warfarin?
VitaminKreversestheactionofwarfarin;however,theprocesstakesabout6to14hours.Intheevent
ofsevereandacutebloodloss,transfusions(e.g.,FFP)maybenecessarytoreplenishmissingfactors.
†
WrittenbyRomanG.Meyliker.
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OncevitaminKisadministered,thepatientmayberesistanttofurtheranticoagulationwith
warfarinforafewdays.Inaddition,certainpatientsmayhaveanunderlyingthrombotictendencythat
putsthematriskforthrombosisandemboliccomplicationsshouldtheeffectsoftheanticoagulantbe
stoppedabruptly.ThereforeadministeringvitaminKorabruptlystoppingwarfarinmedicationcanbe
harmfultosomepatients.
46. How does heparin affect blood clotting?
HeparinpotentiatesantithrombinIII,and,asaresult,clottingfactorsIIa,IXa,Xa,Xia,andXIIaare
inhibited.FactorsIIaandXaaremoresensitivetotheheparinandantithrombinIIIcomplexandare
consideredtobemoreclinicallyrelevantthantheremainingfactorslistedabove.
47. Why are PT and PTT not used to monitor low molecular weight heparin (LMWH)?
LMWHbindstoantithrombinIIIandpotentiatesitsinhibitionoffactorXa;unlikeinheparin,theeffect
onfactorIIaissignicantlyless.ThereforePTandPTTareunreliableformonitoringLMWH.
48. How can the effects of heparin be reversed?
Protaminesulfateisusedtoreversetheeffectsofheparin.Protamine,whichitselfisananticoagulant,
mustbeadministeredwithcaution.Whenprotamineisgivenwithheparin,theanticoagulanteffectof
bothdrugsislost.Carefulcontroloftheprotaminedosingisnecessarytopreventbleedingfroman
overdose.Toorapidadministrationofprotaminecanresultinhypertensiveandanaphylactoidreactions.
49. What is the pathophysiology of heparin-induced thrombocytopenia (HIT)?
Heparinboundtoplateletbindingprotein4onplateletscanformantigeniccomplexesthatinduce
theformationofIgGantibodies.Theseantibodiescausetheformationofcross-bridgesthatresultin
plateletaggregation,whichcausesadecreaseinplateletcount.
50. What is a major complication of heparin-induced thrombocytopenia (HIT)?
Thrombosisoccursinupto75%ofcasesofHIT.
51. How does aspirin affect blood coagulation?
Aspirin(acetylsalicylicacid[ASA])andothernonsteroidalantiinammatorydrugs(NSAIDs)affectthe
plateletphaseofcoagulation.Thesedrugsaltercyclooxygenaseactivitywithinplatelets.Cyclooxygenasecontrolsthereleaseoftheadhesiveproteinsfromplateletsthatarenecessaryforthemtoaggregateandsticktogetherinresponsetotrauma.Inhibitionofcyclooxygenaseactivitybyeitheraspirin
oranotherNSAIDwillcausethedevelopmentofanineffectiveplateletplug,resultinginprolonged
bleeding.ThissideeffectofASAhasledtoitsacceptedcontrolleduseasaprophylacticmeasure
againstcoronaryandcerebralvesselthrombosis.
52. What are the components of the extrinsic, intrinsic, and common pathways of the
coagulation cascade?
ThecomponentsoftheintrinsicpathwayarefactorsVIII,IX,XI,andXII.Thecomponentsoftheextrin-
sicpathwaysincludetissuefactorsandfactorVII.ThecommonpathwayinvolvesfactorsXandXIII,
prothrombin,thrombin,brinogen,andbrin.
53. Which factors are measured by PT, and which ones are measured by PTT?
PTmeasuresfactorsII,VII,IX,andX,andbrinogen.PTTmeasurestheintegrityoftheintrinsicpathways
beforetheactivationoffactorXandtheactivityoffactorsI,II,V,VIII,IX,X,XI,andXII,andbrinogen.
54. What is anemia?
Adecreaseintheoxygen-carryingcapacityoftheblood.Generalsymptomsincludeweakness,
fatigue,palpitations,tingling,andnumbnessofthengersandtoes,aburningtongue,bonepain,and
shortnessofbreath.Clinicalsignsofanemiaincludepallor,spooningandbrittlenails,andasmooth,
redtonguecausedbylossofliformpapillae.
55. What causes iron deficiency anemia?
Irondeciencyanemiaismostcommonlycausedbylowdietaryironintakeorbloodloss.Whenblood
lossissuspectedinmenornon-menstruatingfemales,themostlikelysourceisthegastrointestinal
tractandfurtherinvestigationforasourceisnecessary.Inpatientswithdietarydeciency,oraliron
replacementwithferroussulfateisaneffectivetreatment.
56. What is pernicious anemia?
Normally,vitaminB12bindstointrinsicfactor,whichisnecessaryforitsabsorptionintheileum.
Theintrinsicfactorisaglycoproteinthatissecretedbytheparietalcellsinthestomach.Inpatients
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withperniciousanemia,thereisautoimmunedestructionofparietalcellsleadingtomalabsorptionof
vitaminB12andsubsequentformationoffragilemegaloblasticerythrocytes.
57. What causes sickle cell anemia?
Theinherentdefectcausingsicklecellanemiaisthesubstitutionofvalineforglutamineonthebeta
chainofthehemoglobinmolecule.Thisdefectivehemoglobin,nowcalledhemoglobinS,ultimately
causestheRBCstobecomesickleshapedwhenexposedtolowoxygentension.
58. What is the perioperative management of a patient with sickle cell disease?
Perioperativemanagementofasicklecellanemiapatientinvolvesavoidingallpossibleprecipitating
factors,whichincludehypoxia,dehydration,stress,andinfection.Thiscanbedonewithintravenous
(IV)uids,sedation,oxygensupplementation,andallmeasuresthatpreventinfection,including
antibioticcoverage.Inpatientswithseveresicklecelldiseasewhoareundergoingmajorsurgical
procedures,exchangetransfusionsmaybeusedtodilutethedefectiveRBCsby50%,keepingthe
hematocritunder35%.Treatmentofsicklecellcrisisinvolvesmaintenanceofhydration,administrationofoxygen,andanalgesics.
59. What is the result of a deficiency of glucose-6 phosphate dehydrogenase (G6PD)?
Theenzymeglucose-6phosphatedehydrogenaseislargelyresponsibleformaintainingintracellular
levelsofNADPHandconsequentlyprotectingtheerythrocytefromoxidativedamage.Instatesof
oxidativestress,thesepatientsareathighriskforhemolyticanemia.
Someoftheknownsubstancesthatcanprecipitateanexacerbationareaspirin,favabeans,
sulfonamides,nitrofurantoin,anddimercaprol.Infectionshavealsobeenlinkedwithinducing
hemolysis.
60. Which variant of G6PD is potentially fatal?
TherearetwotypesofG6PDdeciency.TheMediterraneantypecanbeacuteandfatal;theAformis
mildandself-limiting.
61. What is the normal WBC count?
Between4500and11,000/mm3.AnincreaseinWBCsistermedleukocytosis,andadecreaseis
leukopenia.
62. Which form of leukemia is most often associated with the Philadelphia
chromosome?
Chronicmyelogenousleukemia.Thismarkercanbefoundinthemetaphaseandisassociatedwitha
poorprognosis.
63. Can you list risk factors associated with non-Hodgkin lymphoma?
• HIV/AIDS
• Sjogren’ssyndrome
• Hashimotothyroiditis
• Helicobacter pylorigastritis
• Epstein-Barrvirus(EBV)
• HumanT-celllymphotropicvirustype1(HTLV-1)
• Organtransplant
• Immunosuppression
64. Reed-Sternberg cells are found in which disease?
HodgkinDisease.
65. Bence Jones proteins are found in which diseases?
MultiplemyelomaandWaldenströmmacroglobulinemia.
66. What is von Willebrand disease?
VonWillebranddiseaseisaninheriteddisorderinwhichvonWillebrandfactor,requiredforplatelet
adhesion,iseitherdecientordefective.
67. What are the known functions of von Willebrand factor (vWF)?
1. Enhancesplateletaggregation
2. StabilizesfactorVIII
3. Contributestotheabilityofplateletstoattachtoinjuredvascularendothelium
200 PART IV MANAGEMENTCONSIDERATIONS
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68. What are the four hereditary types of von Willebrand disease (vWD)?
• Type 1 vWD:quantitativedefectthatisheterozygousforthedefectivegene.Theproductionofvon
Willebrandfactor(vWF)isdecreased.
• Type 2 vWD:aqualitativedefect;foursubtypesexist(2A,2B,2M,and2N):
• 2A:ThisisaqualitativedefectinthevWFresultinginadecreasedabilitytobindtoplatelet
• 2B:ThisisaqualitativedefectinthevWFresultinginabnormallyenhancedbindingtothe
• 2M:ThisisaqualitativedefectofvWFcharacterizedbyitsdecreasedabilitytobindtotheGP1
• 2N:ThisischaracterizedbyanormalquantityofvWFbutadeciencyofthebindingofvWFto
• Type 3 vWD:completeabsenceofproductionofvWF,resultinginlowfactorVIIIlevelsfromlack
• Platelet-type vWD:vWFisqualitativelynormal,andthevWFproteinlacksanymutationalaltera-
69. How can hemophilia A and B be differentiated?
HemophiliaAisanX-linkedrecessivedisorderinwhichfactorVIIIisdecient,whereastheaffected
70. Which hemostatic agents can be used to manage hemophilia patients prior to
PatientswithhemophiliaAaremanagedaccordingtotheseverityoftheirdisorderandanticipated
71. What is the replacement therapy for hemophilia B?
PuriedfactorIX.
72. What is DIC?
Disseminatedintravascularcoagulation(DIC)istheconsequenceofintravascularactivationofboth
73. What is Plummer-Vinson syndrome?
Plummer-Vinsonsyndromeoccurswithirondeciencyanemiaandisapredisposingfactortooral
74. What is tranexamic acid, and how is it used?
Tranexamicacidisanantibrinolyticagentthatisusedtopromotestabilityofaformedbloodclot.
75. Can you list adverse events associated with erythrocyte transfusions?
• Acutehemolyticreaction
• Acutelunginjury
glycoprotein1(GP1)aswellasadecreasedcapabilityatmultimerization.
GP1receptorontheplateletmembrane,leadingtoitsspontaneousbindingtoplateletsand
subsequentrapidclearanceoftheboundplateletsandofthelargevWFmultimers.DDAVPis
contraindicatedforthistype.
receptorontheplateletmembrane,anditretainsanormalcapabilityatmultimerization.
coagulationfactorVIII.ThisresultsinlowlevelsoffactorVIIIduetolackofvWFstabilizationfrom
proteolyticdegradation.
ofvWFtopreventproteolyticdegradation.ThisisthemostseveretypeofvWDandcanbelife
threatening.
tion.ThedefectliesinthealteredGP1receptorontheplateletmembrane,whichincreasesits
afnitytobindtovWF.
serineproteaseintypeBisfactorIX.
surgery?
bloodloss.PatientswithseverehemophiliashouldreceivereplacementoffactorVIIIwithfactor
VIIIconcentrate.Formildhemophiliacs,desmopressin(DDAVP)canboostplasmalevelsoffactor
VIII,andvWFandcanbeusedsafelyinthesepatients.FFPandcryoprecipitateisnotrecommendedduetopotentialadverseeffectsandshouldonlybereservedwhennoothermodalitiesare
available.
thecoagulationandbrinolyticsystems.DICischaracterizedbywidespreadmicrovascularthrombosisandseverecoagulopathyduetodeletionofplateletsandcoagulationfactors.
carcinoma.Itisfoundprimarilyinwomeninthefourthandfthdecadesoflife.Clinicalsignsinclude
crackingatthelipcommissure;lemon-tintedpallor;smooth,red,painfultonguewithatrophyofthe
liform;and,later,fungiformpapillae.Acharacteristicesophagealwebbingorstrictureisalsoidentied.Irondeciencyanemiarespondswelltoironreplacementtherapy.
Thenalphaseinthecommonpathwaytobloodclotformationistheactivationofbrinogentobrin
inthepresenceofthrombin.Fibrinformsthebasisforthebloodclot.Fibrinolysisorclotbreakdown
beginsinthepresenceofplasminthatisformedfromactivatedplasminogen.Tranexamicacidinhibits
theactivationofplasminogen,therebypromotingstabilityofthebloodclot.
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• Urticaria
• Anaphylaxisandanaphylacticshock
• Non-hemolyticfever
• Bacterialandviralinfections
• Transfusionerrorssuchasincompatibletransfusionorwrongperson
76. What is the mechanism of action of dabigatran etexilate?
Dabigatranetexilateisalowmolecularweightprodrugthatexhibitsnopharmacologicalactivity.After
oraladministration,dabigatranetexilateisconvertedtoitsactiveform,dabigatran,apotent,competitive,andreversibledirectinhibitoroftheactivesiteofthrombin.
77. What is the mechanism of action of Rivaroxaban?
Rivaroxabanisanorallyactive,direct-actingfactorXainhibitor.
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