PowerPoint Presentation

Anemia & Coagulation DisordersBy Tonie Metheny, MS, RN

Types of blood cellsErythrocytesLeukocytesPlatelets

Chapter 30 of Lewis (8th ed) has a good review of the hematologic system if you need it. 2

Erythropoiesis Erythrocyte= red blood cell (RBC)

Erythropoiesis NutrientFunction in erythropoiesis Cobalamin (B12)RBC maturationFolic AcidRBC maturationIronHemoglobin synthesis

Overview of AnemiaAnemia = Decreased RBC, decreased H/HRBC- erythrocyteMost abundant blood cell HemoglobinOxygen carrying proteinOxygen receptorsSp02%HematocritRBC/whole blood

Overview of AnemiaRBC production RBC destruction

http://www.youtube.com/watch?v=_ZV5140OykE

Overview of AnemiaCommon causesDietary intake, hemolysis, blood loss, cancerAnemia causes problems with O2 deliveryDecreased RBC= Decreased O2 carrying capacity\Lab findings vs. DiagnosticsCBCIronBilirubinErythropoetinBiopsyCT/MRI

Overview of AnemiaClinical manifestationsVagueSecondary to decreased O2 carrying capacityFatiguePallor or jaundiceIncreased HR and SVSHOBPalpitations

Overview of AnemiaNursing ManagementBlood transfusionEpoVitaminsIron supplementO2 therapyVolume replacementDietary teaching

Iron-Deficiency Anemia Look to your left and rightChronic conditionDecreased hemoglobin synthesisCausesInadequate intakeMalabsorptionBlood lossHemolysisAlcoholism Malnutrition

Iron-Deficiency Anemia Clinical ManifestationsLow RBCPallorSensitivity to coldHeadacheLow IronGlossitisCheilitis Parethesia

Iron-Deficiency Anemia DiagnosticsDetermine the cause of iron deficiencyGuaiac testhttp://www.youtube.com/watch?v=W4NCWt0hQJMEndoscopyColonoscopy

Iron-Deficiency Anemia Collaborative Care & Nursing ManagementTarget and treat causeIron rich foodsIron supplementEnteral vs. parenteral Monitor effectiveness of therapy

Thalassemia Decreased, malformed hemoglobin productionIncreased hemolysis of RBCsAutosomal, recessive geneThalassemia minor vs thalassemia major

Thalassemia Clinical Manifestations of thalassemia majorSymptoms of anemiaPhysical and mental retardationSplenomegaly and hepatomegalyJaundiceBone marrow expansion and hyperplasiaCranial & maxillary thickening

Thalassemia Clinical Manifestations of thalassemia minorTypically asymptomatic MicrocytosisHypochromia

ThalassemiaCollaborative Care and Nursing ManagementThalassemia majorNo drug or dietary treatment optionsManage anemia Transfusions to maintain Hb of 10g/dLChelation therapy Binds to excess serum ironReduces iron overloading secondary to transfusionsNo iron supplementsSplenectomyMonitor for complicationsHep C, cardiac issues, etc

Cobalamin (b12) DeficiencyDecreased intrinsic factor secretion by the parietal cells of the gastric mucosaFunctions in B12 uptakeDecreased intrinsic factor= decreased cobalamin uptakeDecreased RBC maturationDecreased erythropoiesis Anemia!Causes Pernicious anemiaAtrophy and autoimmune destruction of gastric mucosaGI surgery, gastritis, alcoholism

Pernicious AnemiaClinical Manifestations Secondary to tissue hypoxiaBeefy, red tonguen/v, abdominal pain, anorexiaWeakness, peripheral paresthesias, confusionDiagnositicsMacrocytic RBCLow serum cobalamin EndoscopyShilling test

Pernicious AnemiaCollaborative Care and Nursing Management Maintain good nutrition Lifelong B12 injections 1000mg IM QD x 2 weeksWeekly until H/H is normalizedMonthly for life

http://www.youtube.com/watch?v=VkgE6X_NErM

Aplastic AnemiaAKA pancytopeniaDecrease in RBC, WBC, and plateletsCausesCongential vs AcquiredClinical Manifestations Minor to severeSecondary to pathophysiologyAnemiaNeutropeniaThrombocytopenia

Aplastic AnemiaAKA pancytopeniaDecrease in RBC, WBC, and plateletsCausesCongential vs AcquiredClinical Manifestations Minor to severeSecondary to pathophysiologyAnemiaNeutropeniaThrombocytopenia

Aplastic AnemiaDiagnosticsBone marrow biopsy & aspirationHypocellular bone marrow with increased yellow marrow Collaborative Care and Nursing ManagementProtect patient from infection, bleeding, and complications of anemiaImmunosuppresive therapyStem cell transplantBlood and platelet transfusionshttp://www.youtube.com/watch?v=w8-jx1dtg0U

Sickle Cell AnemiaInherited, autosomal recessive disorderAbnormal hemoglobin that cause abnormal RBCsProne to sickling

Sickle Cell AnemiaSickle Cell crisisSudden onset, persists for days or weeksTriggered by low serum O2 and hypoxiaDehydration, infection, stress, exertionCells sickle and clump together in the small vascular pathways Occlusion occursSpleen destroys sickled cells causing anemia

Sickle Cell AnemiaSickle Cell crisis

Sickle Cell AnemiaSickle Cell crisisClinical ManifestationsExtremely painful FeverSwellingTendernessHypertensionn/v

Sickle Cell AnemiaCollaborative Care and Nursing ManagementPrevent complicationsAvoid triggersHigh altitudesStay hydratedTreat infection promptlyImmunizations

Coagulation Disorders Hemorrhagic disordersHemophiliaDeep Vein ThrombosisPulmonary EmbolismThrombocytopeniaDisseminated Intravascular Coagulation

Platelet

Blood ClotsFactors that affect normal coagulationHemostasis= blood clotting processFour componentsVascular response Vasoconstriction restricts blood flow and presses tissue together so blood cant escapePlatelet plugCongregate at site of damage to plug blood lossOriginate from stem cells in the bone marrowFibrin clotClot Lysis

Blood ClotsFactors that affect normal coagulationHemostasis= blood clotting processFour componentsVascular response Platelet plugFibrin clotClot forms over the platelet plugClot LysisNatural anticoagulantsHeparin, Protein S, Protein CKeeps blood in a fluid state

Your body produces clotting factors that work together to form the fibrin clot that develops over the platelet plugThere are 13 factors (pg 647 Lewis) Interference with any of these factors produces clotting issues

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Clotting StudiesACTActivated Clotting Time70-120 secondsPTTActivated Partial Thromboplastin Time25-35 secondsINRInternational Normalized RatioPTProthrombin Time11-16 seconds

Know this slide for exam 3.34

ThrombocytopeniaLow platelet countReduction of platelets below 150,000Causes abnormal hemostasisProlonged bleeding Inherited vs acquired thrombocytopenia

Immune Thrombocytopenic Purpura Most common type of thrombocytopeniaAutoimmune diseaseLysis of the platelets by the spleenClinical ManifestationsMucosal or cutaneous bleedingPetechiae, purpura, superficial ecchymosesProlonged bleeding after routine proceduresManifestations of internal hemorrhage

Immune Thrombocytopenic PurpuraDiagnostic StudiesCBCH/HPlatelet countPT/PTTAntigen assayBone Marrow AnalysisFlow CytometryAnalyzes antiplatelet antibodies

Immune Thrombocytopenic PurpuraCollaborative CareCorticosteroids suppress autoimmune response (phagocytosis)PrednisoneSolu-medrolSplenectomyIncreases number of circulating plateletsPlatelet transfusions

ThrombocytopeniaNursing ManagementTeach patients to avoid acquired thrombocytopeniaMedically prevent and control bleedingProceduresMenstruation Monitor for signs of internal bleedingTeach patient to prevent and control bleedingHow to avoid bleedingHow to manage bleeding

HemophiliaX-linked recessive genetic disorderDefective or deficient clotting factorsThree typesHemophilia A (Factor VIII) Hemophilia B (Factor IX)Von Willebrand disease (vWF, VIII, and platelets)

HemophiliaClinical Manifestations- Could lead to life threatening blood lossSlow, persistant, prolonged bleedingDelayed bleedingUncontrollable hemorrhageOccult blood, hematuria s/s of hematoma Nerve compression- pain, paralysisSubcutaneous hemotomaLimited ROM- Bleeding in the joints

HemophiliaDiagnostic studiesPlatelet countPT/PTTFactor assaysCollaborative carePrevent and treat bleedingReplace volume loss Replacement deficient clotting factorsAntifibrinolyticsEnhances clotting stabilityTreatment of complications

Hemophila Nursing ManagementStop bleeding quicklyCompression, ice, gelfoam, fibrin foam, hemostatic agentsJoint bleedsRest, ice, mobilization, treat painManage life-threats

Disseminated Intravascular CoagulationThrombotic disorderAbnormally initiated and accelerated clottingCauses a decrease in available clotting factorsLeads to uncontrollable hemorrhageOccurs in response to a disease/disorderExampleShockSepticemiaCardiac arrest Snakebites

DICClinical manifestationsBleeding with no history or obvious causeBleedinghematoma, petchiae, purpuraRespiratory tachypnea, hemoptysisCV-tachycardia, hyptotensionGI/GU-abdominal distension, bloody stoolsNeuro-headache, changes in neuro statusMS- bone and joint painThromboticPE, ARDS, ischemic tissue, paralytic ileus

DICDiagnostic studiesPT/PTT, Thrombin timeFibrinogen & platelet countsFactor assaysCollaborative CareStabilize patientO2Volume replacementTreat causeProvide supportive care of manifestations

DICNursing careEarly detection of bleedingAstute assessmentInternal vs. external bleedingIndications of microthrombiAdminister medications and blood products

http://www.npr.org/2011/06/28/137454415/the-child-cases-guilty-until-proven-innocent

To gauge how the blood is clotting, physicians typically begin with a pair of basic tests called the PT and PTT. In Isis, the "PT and PTT were markedly abnormal," Laposata said, adding that other tests also suggested a coagulation disorder. Where McClain had seen a "classic" case of blunt force trauma, Laposata saw something entirely different, a "classic picture" of Disseminated Intravascular Coagulation (DIC), a potentially lethal condition that can cause bleeding from sufferers' every orifice.Based on the baby's "dark, tarry stools," elevated white blood cell count, and abnormal liver function tests, Laposata concluded, "something had to be going on for days" long before the 40 minutes Lopez was alone with the baby.An infection could have led to DIC, and, eventually, to a fatal collapse, Laposata said. DIC could also explain Isis' bruises and the bumps on her head that Lopez and others believed were spider bites, he added."The reality is when your blood is so thin, when you're so unable to make a clot, you can just develop bruises and they can be spontaneous," he said.

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Deep Vein ThrombosisThrombus is a deep veinFemoralIliacsPoplitealVirchows triadVenous stasisEndothelial damageHypercoagulation

Deep vein ThrombosisPathophysiologyPlatelet aggregation creates entrapment of RBC, WBCs and more plateletsThrombus occurs usually at valve because of stasisThrombus can resolve or may eventually break offWhat is the difference in a thrombus and embolus?Where would an emboli caused by DVT travel to?

Deep Vein ThrombosisClinical ManifestationsUnilateral LE edemaPainSensation of fullness of the areaParethesiaWarmthErythema

Deep Vein ThrombosisDiagnostic studiesCBC, clotting studiesVenous compression ultrasoundDuplex ultrasoundMost commonly used

Deep Vein ThrombosisCollaborative careAnticoagulation therapy- DVT prophylaxis or treatmentCoumadin HeparinUnfractionated heparinHeparin SodiumLMWHLovenoxThrombolytic therapy- TPA (clot busting drug)Surgical interventionGreenfield filterthrombectomy

Deep Vein ThrombosisNursing interventions for anticoagulation therapyMinimize bleedingMonitor CBC and coagulation testUse electric razors- not straightSoft toothbrushesAdminister stool softenersAssess for mental status changes

Peripheral Blood flowVenous blood flow vs arterial blood flowIf a clot broke off where would it go?

Pulmonary EmbolismBlockage of the pulmonary arteries by thrombus, fat or air embolus, or tumor tissue.Embolus- plugEmboli- mobile plugs looking for a landing spotClinical manifestationsDyspneaChest painHemopytsisMay be sudden or develop slowly

Pulmonary embolismComplicationsPulmonary infarctionEmbolus cuts off collateral circulation of lungDecreased lung tissue=decreased oxygen perfusionPulmonary hypertensionEmboli lodged in pulmonary circulation causes blood flow to lungs to back upEventually the right ventricle is involved and we see right sided heart failureDx StudiesX-ray, CT scan, Pulmonary angiogram, D-Dimer, ABG analysis

Pulmonary EmbolismCollaborative CarePrevent DVT!Compression devices, ambulation, anticoagulants prophylacticallyEarly treatment of PEPrevent growth and spread, cardiopulmonary support as neededAdminister O2Intubation/mechanical ventilation if necessaryTreat symptomsFibrinolytic therapy (tPA or activase)Long term therapy with heparin and coumadinSurgical embolectomy for severe obstruction

Pulmonary embolismNursing interventionsSemi-fowlers positionAdminister 02, fluids and medications as orderedMonitor for complicationsEmotional supportEducation for long term anticoagulation therapy

CoumadinUsed to prevent thrombosisHas a delayed onsetInhibits Vitamin K Lots of clotting factors are dependent on vitamin K to be activeDecreased Vitamin K, decreased clottingVitamin K is the antidoteMonitor INR and PTVitamin K rich foodsGreen leafy veggiesDried herbsBroccoli, brussel sprouts

HeparinActivation of antithrombinInactivates clotting factorsImmediate effectsProtamine Sulfate is the antidoteMonitor PTT

Here are some extra memory slides!