Hematology Continued Class Slides PDF

Disseminated Intravascular Coagulation (DIC)  Review ‘Predisposing conditions to DIC’ in textbook Disseminated Intravascular Coagulation (DIC)  a serious bleeding and thrombotic disorder  results from the abnormally initiated and accelerated clotting and anticlot...

Disseminated Intravascular Coagulation (DIC)  Review ‘Predisposing conditions to DIC’ in textbook Disseminated Intravascular Coagulation (DIC)  a serious bleeding and thrombotic disorder  results from the abnormally initiated and accelerated clotting and anticlotting processes that occur in response to disease or injury  it is characterized by the profuse bleeding resulting from the depletion of platelets and clotting factors  An underlying disease or condition always causes DIC  The underlying disease must be treated for the DIC to resolve. Bleeding Manifestations  Integumentary manifestations Pallor Petechiae Purpura oozing blood Hematomas  Respiratory manifestations -> Hemoptysis  Cardiovascular manifestations -> Hypotension  GI manifestations -> upper and lower GI bleeding abdominal distension Bleeding Manifestations  Bloody stools  Urinary manifestations -> Hematuria  Neurological manifestations -> changes in mental status  Musculo-skeletal complaints -> bone and joint pain. Thrombotic Manifestations  Fibrin or platelet deposition in the microvasculature  Integumentary changes Cyanosis ischemic tissue necrosis (e.g., gangrene), and hemorrhagic necrosis  Respiratory changes tachypnea, dyspnea pulmonary emboli acute respiratory distress syndrome (ARDS) Thrombotic Manifestations  Cardiovascular changes electrocardiogram (ECG) changes venous distension  GI changes -> abdominal pain and paralytic ileus  Urinary changes -> oliguria, leading to renal failure.  Acute Chronic DIC DIC  Acute develops  Chronic DIC (reflects a suddenly compensated state)  Severe consumptive  More frequently observed coagulopathy leading in solid tumors and in large to hemorrhage. aortic aneurysms  Organ failure  Clinical manifestations may frequently occurs with only be easy bruising to acute DIC hemorrhage and from hypercoagulability to thrombosis Diagnostic Tests  Prolonged  PT, PTT, aPTT  Reduced platelets, fibrinogen  Special Tests  Fibrin split products (FSPs)  Factor assays (for factors V, VIII, X, XIII)  D-dimers (cross-linked fibrin fragments)  Antithrombin III (AT III)  Protein C and S -> anti-thrombotic proteins  Plasminogen, tissue activator  Peripheral blood smear  Management  Stabilize the patient (e.g., oxygenation, volume replacement)  Treat the underlying causative disease or problem  Provide supportive care for the manifestations  If chronic DIC is diagnosed in a patient who is not bleeding, no therapy for DIC is necessary.  Treatment of the underlying disease may be sufficient to reverse the DIC (e.g., chemotherapy when DIC is caused by malignancy)  When the patient with DIC is bleeding, therapy is directed toward providing support with necessary blood products while treating the primary disorder.  Classification  Acute Myelogenous Leukemia  Clinical Manifestations  Acute Lymphocytic Leukemia  Diagnostic Studies  Chronic Myelogenous Leukemia  Collaborative Care  Chronic Lymphocytic Leukemia  Chemotherapy Regimens  Hairy Cell Leukemia  Bone Marrow and Stem  Unclassified Leukemias Cell Transplantation Malignancy involving the abnormal overproduction of leukocytes (Immature) in the bone marrow. 110 96  A group of malignant disorders affecting the blood and blood-forming tissues of  Bone marrow  Lymph system  Spleen  Often thought of as a childhood disease  The number of adults affected is 10 times that of children  Characterized by diffuse replacement of bone marrow with proliferating leukocyte precursors -> dysfunctional cells  Leukemia -> progressive -> fatal if untreated 98  Clinical Manifestations  Related to problems caused by  Leukemic cells infiltrate client’s organs (including bone marrow) ○ Fatigue and weakness, ○ Headache, mouth sores, anemia, bleeding, fever, infection, sternal tenderness, gingival hyperplasia ○ Hepatomegaly ○ Lymphadenopathy ○ Bone pain, meningeal irritation, oral lesions (chloromas) ○ Marrow-suppression  Diagnostics  Low RBC count, Hb, Hct; low platelet count; low to high WBC count with myeloblasts; high LDH; greatly hypercellular bone marrow with myeloblasts  Peripheral blood evaluation  Bone marrow examination  Morphological, histochemical, immunological, and cytogenetic methods are all used to identify cell subtypes and the stage of development of leukemic cell populations.  lumbar puncture and CT scan can determine the presence of leukemic cells outside of the blood and the bone marrow.  Specific cytogenetic abnormalities:  Care/Management physical and psychosocial needs treatment and prognosis of the patient family also needs help adjusting to the stress Comorbid conditions that affect treatment decisions maximizing the patient's physical functioning teaching patients that acute adverse effects of treatment are usually temporary encouraging patients to discuss their quality-of-life issues nurse must be knowledgeable about all medications being administered nurse must know how to assess laboratory data   Wk 1 -> Chemo cycle 1 Chemotherapy  Wk 2 -> CBC check  Wk 3 -> CBC check  Combination chemotherapy  Mainstay treatment  Wk 4 -> Chemo cycle 2  3 purposes  Wk 5 -> CBC check ○ ↓ drug resistance  Wk 6 -> CBC check ○ ↓ drug toxicity to the client by using  Wk 7 -> Chemo cycle 3 multiple drugs with  Wk 8 -> CBC check varying toxicities  Wk 9 -> CBC check ○ Interrupt cell growth at multiple points in  Wk 10 -> Chemo cycle 4 the cell cycle  Wk 11 -> CBC check  Wk 12 -> CBC check  Bone Marrow & Stem Cell Transplantation  Goal  Totally eliminate leukemic cells from the  Eradicates client’s body using combinations of chemotherapy hematopoietic stem cells with or without total body irradiation  Replaced with those of an HLA-matched ○ Sibling ○ Volunteer ○ Identical twin ○ Client’s own stem cells removed before autologous vs allogeneic 117 102 117 102 Side and adverse effects result from the effects of antineoplastic medication on normal cells  Antineoplastic medication  causes the rapid destruction of cells  Resulting in increased uric acid. Adverse Reactions  Mucositis  Alopecia  Anorexia, nausea, and vomiting  Diarrhea  Anemia  Neutropenia  Thrombocytopenia  Neuropathy Neutropenia  Decreased neutrophils  Risk for infection  Gradual  Sudden  Consequence of other conditions / diseases  Drug therapy  Hematological disorders  Autoimmune disorders  Infections  Hemodialysis Neutropenia – Clinical Manifestations  Clinical manifestation signs of inflammation—redness, heat, and swelling—may not occur pus formation is also absent  Presence of a low-grade fever in neutropenic patients may indicate infection and quickly lead to septic shock and death.  A fever greater than 38°C and a neutrophil count less than 0.5 × 109/L is a medical emergency. Hodgkin’s disease Non-Hodgkin’s Lymphoma (NHL) 125 110  Hodgkin’s disease is characterized by  Proliferation of abnormal giant, multinucleated cells - Reed-Sternberg cells  Located in the lymph nodes 126 111 Clinical Manifestation ✤ Insidious ✤ lymphadenopathy -> nodes remain movable and nontender. ✤ B- symptoms noted ✤ Fever ✤ Night sweats ✤ Weight loss ✤ Advanced: Hepatomegaly & splenomegaly ✤ Anemia Clinical Manifestation ✤ Depending on site: ✤ intrathoracic ->superior vena cava syndrome ✤ retroperitoneal -> abdominal masses or interfere with renal function ✤ jaundice -> may liver involvement ✤ spinal cord compression -> paraplegia ✤ Bone involvement -> bone pain  Stage One – One group of lymph nodes, same side of diaphragm Stage Two - Two or more groups on the same side of the diaphragm Stage Three – On both sides of the diaphragm occasionally with involvement of another organ (spleen is stage III) Stage Four – Liver, lung, bone marrow involvement 129 114   Wk 1 -> Chemo cycle 1  Wk 2 -> CBC check  Wk 3 -> CBC check Treatment  Wk 4 -> Chemo cycle 2 Radiation therapy  Wk 5 -> CBC check  Wk 6 -> CBC check –95% of stage I or stage II clients cured with 4 to  Wk 7 -> Chemo cycle 3 6 weeks of radiation  Wk 8 -> CBC check therapy  Wk 9 -> CBC check Combination chemotherapy  Wk 10 -> Chemo cycle 4 –Resistant disease or  Wk 11 -> CBC check high risk of relapse  Wk 12 -> CBC check –MOPP and ABVD 130 115  Varies from  Types of NHLs  Burkitt’s lymphoma slowly developing  Diffuse large B cell to rapidly lymphoma progressive  Follicular lymphoma disease  …and many more! Type of NHLs –90% B cells  No hallmark feature, but…  All NHLs involve –10% T cells lymphocytes arrested in various stages of development 131 116   Chemotherapy Collaborative Care regimen  CHOP  CVP  Treatment consists  COPP of chemotherapy +/- radiation  More aggressive  Biological therapy lymphomas are  Alpha interferon (Intron) more responsive to  Rituximab (Rituxan) treatment  Ibritumomab tiuxetan (Zevalin) 121  Collaborative Care (cont’d) Complete remissions are uncommon  Most respond with improvement in adenopathy and symptoms  Radiation alone may be treatment enough for localized stage I or stage II disease  Asymptomatic clients with advanced disease followed with “watchful waiting” to assess the disease progress 122  Myeloma is  Bone pain/fracture malignant tumor of plasma cells (B cell  Kidney damage subtype) arising from a Byproduct of plasma single clone cells causing damage to nephron  Multiple myeloma accounts for > 40% of  M protein primary malignant immunoglobulin made by tumors of bone. abnormal plasma cells 139 124  Myeloma is malignant  Bone pain/fracture tumor of plasma cells within the bone (B cell  Kidney damage subtype) arising from a Byproduct of plasma cells causing single clone damage to nephron  Multiple myeloma  M protein accounts for > 40% of immunoglobulin primary malignant tumors made by abnormal of plasma cells 139bone. 124  Bone pain especially ribs, spine & pelvis Weakness & fatigue Recurrent infections Urinalysis shows Bence Jones proteinuria Osteoporosis Elevated calcium and uric acid levels Kidney failure Spinal cord compression 139 124  Disorders of the Spleen Three things to know about the spleen: Enlargement causes sequestration of blood products Removal predisposes to infection potential Rupture may cause radiating pain... 143 129 Hemochromatosis Hemophilia & Thrombocytopenia please review in your text  Hereditary- Genetic Condition where excessive Iron is deposited in organs  No evidence of disease until middle age  Men have more issues than Women  Treatment phlebotomy  Can have an acquired form- mainly in alcoholics Hemophilia  Two inherited disorders A & B  A has lack of factor VIII  B (aka Christmas disease) lack of factor IX  Men get this disease Women are gene carriers  Bleeding is the major issue  Bleeding into the joints major symptom is swelling and pain 147Can bleed even without trauma  von willebrand’s disease  Common bleeding disorder but effects males and females equally  vWF is needed for factor VIII activity  Bleeding especially nose bleeds, excessive bleeding from cuts, heavy menses, postoperative bleeding  Prolonged bleeding times  Treatment for both (Similar to Hemophilia) DDAVP (increases Factor VIII Cryoprecipitate needed prior to major surgeries Platelets adhere to damaged endothelium What Should You Do?  A patient with hemophilia has experienced recent trauma  What should the nurse monitor with this patient? Thrombocytopenia  Reduction of platelets below 150 x 109/L  Immune thrombocytopenic purpura  Heparin-induced thrombocytopenia  Apheresis  AKA Plasmapheresis  Sends a patients blood through a centrifuge and the components are removed  Can get extra platelets  WBC  Harvest stem cells for stem cell transplant