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Hematology ineemia) · CLymphoma · Topic I · Topic Coagulation Disseminated Intravascular 2 (DIC) Thrombocytopenic> ·...

Hematology ineemia) · CLymphoma · Topic I · Topic Coagulation Disseminated Intravascular 2 (DIC) Thrombocytopenic> · Topic 3 · Polycythemic  Leukemia Cancers of the blood and · blood-forming tissue(bone marrow) characterized by overproduction of abnormal/dysfunctional · white blood cells 4 types 1 acute. lymphocytic 2 Chronic. lymphocytic 3acute myelogenous. Chronic myelogenous 4 +2 p Leukemia A - excessive production of immature cells decreases ability healthy cells to create - can not make healthy 1 Red Blood Cells-leading to anemic. (Fatigue , Malaise, Impaired gas exchange).Platelets 2 Thrombocytopenia (Increase bleeding risk) -. 3 White blood cells-LeukopeniaIncreasedris D  3 p + Leukemia-Risk Factors /Presentation Risk Factors · Genetic predisposition labnormal genes Oncogenisis - · Environment Conizing radiation viral infection chanical) , , drugs Presentation (Refer back to previous slide) Ecchymosis (bleeding) petechiae, open/infected lesions · , , delayed wound healing bleeding gums, , nematuria , fatigue Done pain joint , fever , dyspnea on exertion, , swelling/pain , anorexia, weight loss, enlarged liver/spleen  Acute Myelogenous Leukemia (AML) o Accounts for one third of all leukemias 20% adults · seen in are often dramatic and abrupt symptoms · ofatigue,weakesternaltendernessgigil a a · Low RBC, hemoglobin , hematocrit) - anania Low Platlet thrombocytopenia - · Hypercellular bone manor w/ myeloblasts · Acute Lymphocytic Leukemia (a) · most common leulimia in childhood CNS involvement is causelethargy,cran · common ol fever Usually with fatigue : present bone orjoint , pain , bleeding tendencies  Chronic Myelogenous Leukemia (CML) Increases we advancing age median age 67y10 · , crave in children) · excessive neoplastic granulocytes in the bone marrow no symptoms early,then acutely aggressive (blastic phase) · once in blastic · phase,treatment should be more aggressive massive splenomegalyjoint pain, weight loss sternal · , · tenderness Labs - same as otherstpresence of philadelphia chromosome Inew combination 9000 of pts Chronic Lymphocytic Leukemia (CLL) · Most common leukemia in adults in Western countries and accumulation of · production functionally inactive, long lived ,small , mature appearing lymphocytes Lymphadenopathy is present throughout · the swollen lymph nodes body  Leukemia Complications - Acute plast crisis (CML) pneumatic tube pseudo-hyperkalemia (walk blooda - - lenkostasis (AML) > decresed tissue perfusion > no - oxygento - neutropenia /low WBC) - cens thomocytopenia - releasingunicaddosphate) - Tumor lysis syndromeHumor cells Leukostasis-vascular occlusion - life threatening - WBC CountT10 1 00 fluids lungi kidney damage good - -  Lymphoma cancers · originating in the blood marrow Hymphatic structure o characterized by abnormal proliferation of the white blood cells found normally in lymphoid tissue can occur anywhere · there is lymph tissue · 2main types - Hodgkins Lymphoma (-worst Non-Hodgkins -  Hodgkins Lymphomas %0% of all lymphomas · A cancer that affect any age can group , however it appears to peak in two age groups.Teens and young adults 1 o Adults 2 in their 50's and 60 Begin in node · a single lymph or chain of lymph nodes contain a specific cell · type, the · reed-strembling spread is predictable  +2 p Hodgkins-Clinical Mechanisms - Initial Presentation Cervical , axillary fatiguinguilnymphadenopag - also may notice-weight loss - , -Morevere B-symptoms-fevendrenchingnightsweatens - Bsymptomsmore severe , serious , aggressive presentation Diagnostic Tests - CTIMRI ,PET Scan node - Lymph biopsy Bone Marrow Biopsy - CBC ; microcytic hypo chromic anemia leukopenia, - , thrombocytopenia,hypercalcemiafrom bone involvement Staging Involvementofsinglymph noda on one side of diaphragm 11 Lymph node involvement about below diaphragm In Involvement outside of diaphragm (LiverBone Marroco)  Non-Hodgkins Lymphoma % B cell lymphomas constitute 85 of NHL's - cause is unknown ,but possible geneticenvironment - predisposition - Viruses/bacteria , nepB CH Pylori campylobacter. , - pesticides/insecticides Chlamydophilia - can mimic leukemia burkitt's lymphoma - is most aggressive case Diagnostic - peripheral blood smear fine needle aspiration/biopsy - CBC, CMP - - CTScan , CTIMRI DET Scan , ptz Treatment Chemotherapy post : Given in stages ; induction, induction/post remission, maintenance rememberdoenotdiscriminate a betwe HematopoieticStemcel transplantationsso to neutralize the existing dysfunctional marrow and new healthy transplanted normal and stem cells take over and hopefully make only healthy cells Radiation Therapy ?Particles attack cells disrupting their genetic material , and preventing them from reproducing remember ; does not discriminatebetweenheals)  Lecture II IDIC)  Disseminated Intravascular Coagulation - Definition ( International - anacquired His different causes that can and if severe enough can damage produce the microvasculature organ damage Simplified Definition - - an exaggerated response by the body to begin clotting which results in small clots forming the all over that decreases the body's ability to clot later body means /BecauseMusesupall the things necessary to I So then the patient can bleed to a point where it not be easy to control may Summary A and issue initiated from an clotting bleeding outside stimulus (infection ,trauma  Disseminated Intravascular Coagulation (DIC) · a serious bleeding and clotting (thrombotic disorder · (Abnormal clot inition) (Clot->Bleed > Clot - (clotting factors deplete, uncontrolled hemorrhage ensues) There is usually an underlying · condition involved Cancer OB conditions CHELLD)-Shock - - TissuelDamage - Transfusion Reaction - Burns/Trauma - - Cardiac Arrest - Autoimmune Disease => Sepsis/Infection - Liver Its disease its · not a an abnormal response to an underlying disease process of disorder Endotoxicins · in bacteria -activates cascade-> intravascular coagulation thrombinkcoagulaneconverts brinogentonotenhancesplatelet aggegration she -results in multi organ failure(blood can't get to organs) Dat 1st clotting (thrombotic manifestations) - * (skin-cyanosis ,Tissue necrosis, peachypnaa , Bleeding Manifestation tachycardia , hypotension, - - bleeding from IV site , GiBleed I Stool, hemoptysis) Homaturia My Role as the Nurse symptoms of · Recognized DIC · Bleeding precautions Anticipate transfusions clottingfactors) · as needed (platelets , If Hemorrhagic - - - Anticipate low molecular weight heparin(enoxaparin) if thrombotic - administration  Lecture Part11I Thrombocytopenia 3 Polycythemia - a Thrombocytopenia decrease in platelets (150 000 , per microliter) caused by - 1 under production /Bone Marrow not working). 2 over destruction (ontoimmune disease drug inducedHIT. ,. Splenic Sequestration 3 Phypersplenism , gestational,PE liver disease C Immune Thrombocytopenia There different broad are types: - Immune thrombocytopenia - abnormal destruction antiplatelet antibodies - datelets gettaggedbyantibodieswhenis macrophages (Destroyed)  Thrombotic Thrombocytopenic Purpura Unknown syndrome characterized by 1 Hemolytic Anemia 2 Thrombocytopenia 3 neurological abnormalities 4 Fever and renal abnormalities These do not all occur at Study Tip once or Fever (10 infection) together AnemiaHemota Renal Abnormalities Meurologic Abnormalities - caused by a deficiency in ADAMTS13 - ADAMTS12 normally cleaves Von Willebrand Factor la protein that helps platelets stick together LW/ ADAMTSI3, NWF would not be cleared and microthrombi can occur in the body Lat risk for and thrombosis bleeding  Heparin Induced Thrombocytopenia L not 0% incidence looking a PTT specific · to the use of this anticoagulant Typically occurs 5t0 days after the onset heparin of therapy · Criteria - a decrease in 50 % of platelet leven if value is normal Ex : 400 , 000 to 200,000 Platelets · begin to aggregate or clump together usedup -The hard concept to here is that a grasp decrease in platelets (thrombocytopenia) causing - clotting problems ; prothrombotic problems , stroke, mesentric Ischemia , myocardial infarction Platelets don't drop far for enough breeding - - pt2 Interventions Because these · are often found incidentially inquire about , bleeding tendencies History · of Heparin use 2 Imanifest 5-10 days after heparin admin) - - - Alconol use o Pregnant patients volvisual changes abnormal pain, headaches , Monitor CSC · especially platelet count 1150, 000 but also , hemoglobin is as a drop in hemoglobin means the pt bleeding elsewhere · monitor, prevent, anticipate bleeding "bleeding precautions Treatment ↓electric razors no get typing screen , foley) Hp corticostenoids are given (immune - driven) steroids suppress the immune response - HIT byinkcoubluemlymphonin I stop heparin) s 210, 000 giveargatranmantananticoagupt heparin ac a LNO platelets may worsen thrombotic effects of Hit -  Polycythemia The production and - presence of increased number of RBC - can Impair blood circulation due to two important 1 Hyperviscosity. Mechanisms Hypervolemia. 2 There are tw types 10PrimaryPolycythemia We are Vera Polycythemia ochronic myeloproliferative disorderlactual increase inRic involves RBPWBC, platelets Congest · organs (splenomegaly , hepatomegaly ( Predisposed to clotting · Associated wh of JAKZ Gene · genetic mutation pt2 Secondary Polycythemia - unlike vera is , hypoxia driven Chypoxia-EPO->RBC production or cancer - secreting epo Splenomegaly does not occur - Polycythemia-CM/Labs/Treatment Generalized itching especially wh hot stimulus - - - a ruddy complexion Chistamine a -vertigo, dizziness ,tinnitus Labs thrombophlebitis,strokedut/ , F CBC High hemoglobin +REC Count Low EPOlvera High or Treatment = po(secondary( Phlebotomy-blood drawing Hydroxyurea - inhibits dra synthesis kills , cells (cancausedestructioninnormace leading to