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105 Cards in this Set
- Front
- Back
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What are the structures of the Hematologic system
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1. Bone marrow
2. Blood 3. spleen 4. lymph system 5. Liver |
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Functions of Bone Marrow
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1. Blood cell production (hematopoiesis) by red marrow
2. All cells develop from stem cells - which is a nondifferentiated immature blood cell 3. uses negative feedback to meet the bodies need for blood cells |
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functions of blood ( a type of connective tissue)
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1. Transportation of O2, nutrients,hormones,and waste products
2. regulation of fluid, electrolyte, and acid base balance 3. protection via clotting and fighting infections |
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Plasma functions
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1. Water, proteins, elytes, gases, nutrients and waste
2. Serum refers to plasma minus clotting factors |
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what are plasma proteins
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Albumin, globulin, and clotting factors
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Erythrocytes (RBC) main functions
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Transport of gasses, (o2 and co2) and assistance in maintaining acid - base balances
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Erythropoieses is stimulate by A.______________________
and controled by B._______________ which is synthesized and released by the C. ____________ |
A. Hypoxia
B. Erythropoietin C. Kidney |
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A. Erythropoiesis is affected by:
B. This is why ____________is associated with some disorders like ______________________ |
A. Nurtients, endocrine hormones.
B. anemia , hypothyroidism |
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What are reticulocytes?
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Immature Erythrocytes
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A. What is Hemolysis
B. Where does it occur |
A. Destruction of RBC's by monocytes and macrophages
and removal of abnormal RBC's B. in the bone marrow, liver, and spleen |
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What is Bilirubin?
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A byproduct that is produced by hemolysis and is metabolized by the liver
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Leukocytes (WBC) are produced by?
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Stem cells in the bone marrow
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What are the 3 types of granulocytes?
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Neutrophil - Eosinophil - Basophil
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Neutrophils do what?
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Phagocytosis, especially during the early phase of
inflammation |
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Eosinophils do what?
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Phagocytosis (not as effective as
neurtophil ) allergic response, protection from parasitic infections |
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Basophils do what?
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inflammatory response and allergic response, release
of bradykinin, heparin, histamine, serotonin, limited phagocytosis. |
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What are the two types of Agranulocytes
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Lymphocytes and Monocytes
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What do Lymphocytes do?
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Form the basis of cellular and humoral immune responses
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Thrombocytes are ______________ and do what?
What are they regulated by |
Platelets, initiate clotting by producing a platelet plug.
Thrombopoietin |
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Thrombocytopenia is platelets below?
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150,000/ul
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What are causes of thrombocytopenia?
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some are inherited, most are acquired, induced by drugs, myelosuppressive agents, herbs, and foods,
So a H&P is very important to diagnosis |
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Immune (idiopathic) Thrombocytopenic purpura (ITP)
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Most common acquired, autoimmune, platelets are coated w/antibiodies and work fine until they hit the spleen and are recognized as intruders and destroyed by macrophages.
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Thromotic Thrombocytopenic Purpura (TTP)
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Uncommon, but cause is usually a deficiency in the enzyme that breaks down the vWF clotting factor
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Heparin - induced Thrombocytopenia
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8-17% of pt on heparin therapy develop this. Main problem is venous thrombosis and PE. Platelet destruction and vascular endothelial injury are the two major responses to an immune mediated response to heparin.
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Common Manifestations of Thrombocytopenia
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Bleeding, cutaneous or mucosal, epistaxis, and gigival bleeding with large bullous hemorrhages on buccal mucosa, Etichiae, purpura.
Prolonged bleeding after procedures. Major complication is CEREBRAL HEMORRHAGE. |
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How is Thrombocytopenia Diagnosed?
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Lab tests
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What is used to treat ITP?
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Corticosteroids, Splenectomy, IVIG, Anti-Rho(D), Romiplostim (Nplate), Eltrombopag (Promacta), Danazol, Immunosupressives, High Dose Cyclohosphamideor Chemotherapy, Platelet transfusions
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What is used to treat TTP?
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Identify and treat underlying cause is first plan of treatment.
Plasmapheresis, high - dose prednisone Dextran Chemotherapy: vincristine (oncovin,), vinblastine (velban) |
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What is used to treat Heparin - Induced Thrombocytopenia
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Direct thrombin inhibitor: Lepirudin (refludan), agatroban (acoval)
Indirect thrombin inhibitor: fondaparinux (arixtral) Warfarin (coumadin), PlasmapheresisProtamine sulfate, Thrombolytic agents |
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Decreased platelet production is treated how?
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Identify and treat cause, corticosteroids, platelet transfusions, Oprelvekin (neumega), romiplostim (nplate), eltrombopag (promacta)
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Clinical manifestations and Complications of Hemophilia
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1. slow, persistent,prolonged bleeding from minor trauma and cuts.
2. delayed bleeding from minor injuries(delay may be several hours or days) 3. Uncontrollable hemorrhage after dental extractions,etc 4. epistaxis 5.GI bleeding from ulcers and gastritis 6. hematuria from gu trauma and splenic rupture from falls or abdominal trauma 7. ecchymoses and sub q hematomas 8. neurologic signs from nerve compression caused by hematoma formations 9. hemarthrosis (bleeding in joints) |
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What is goal of theraphy for hemophilia
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prevent and treat bleeding, replacement of clotting factors
Acute intervention treatment of joint pain, manage life threatening complications |
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What is DDAVP? and what does it do?
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DDAVP (vasopressin) stimulates increase in VIII and vWF
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What is DIC?
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Disseminated intravascular coagulation is a serious bleeding and thrombotic disorder. Tissue factor triggers release of thrombin and subsuquent conversion of fibrinogen to fibrin. platelets and fibrin deposit in capillaries and arterioles causing multiorgan failure. The firbinolytic system is activated and clotting factors and platelets are depleted causing hemorrhage.
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What are clinical manifestations of DIC
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there is no well-defined sequence of events in acute DIC, however, bleeding in a preson with no previous hx may be one of the first manifestations of acute DIC.
Other non specific manifestations can include weakness, malaise, and fever |
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What is the treatment for DIC?
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Heparin although controversial, is used if pt shows manifestations of thrombosis
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Nursing implementation for DIC includes:
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Assess for s/s of bleeding, oozing, neuro signs. Replace blood loss with blood products.
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What is Neutropenia?
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Reduction in neurtrophis, <500 severe: <1000 moderate
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What is neurtopenia caused by?
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Drug induced , hematologic disorders, autoimmune disorders, infections.Severe sepsis, bonemarrow infiltration, hypersplenism diseases, transfusion reaction, hemodialysis
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Clinical manifestations of neutropenia
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Fever is very important. s/s of infections, minor complaints must be taken seriously
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Treatment of Neutropenia includes:
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Determining the cause, instituting prophylactic or therapeutic antiobiotic therapy, hematopoietic growth factofs, and instituting safety measures.
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Leukemia is?
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General term used to describe a group of malignant disorders affecting the blood and blood forming tissues of the bone marrow, lymph system and spleen
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What is leukemia caused by?
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A combination of factors, including genetic and environmental factors.
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Acute Leukemia is characterized by ?
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Clonal proliferation of IMMATURE hematopoietic cells, it develops following malignant transformation of a single type of immature hematopoietic cell, followed by cellular replication and expansion of that malignant clone.
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Chronic Leukemia is characterized by?
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involve more MATURE forms of WBC and the disease onset is more gradual.
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What are the 4 main types of Leukemia?
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ALL, AML, CML and CLL
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AML represents only 1/4 of all leukemias, but, it makes up _____ of the acute leukemias in adults with peak incidence at ages____ to ____
What are the clinical manifestations of AML |
85% 60-70yrs
Fatigue and wkns, h/a, mouth sores,anemia, bleeding, fever,infection, sternal tenderness, gingival hyperplasia, minimal hepatosplenomegaly, and lymphadenopathy |
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ALL is the _____ _______ type of leukemia in children and accounts for ___% of adult leukemia.
What is the process of ALL |
Most common, usually manifests before 14 yr of age with 2-9 being peak incidence ages. 15%.
Immature lymphocytes proliferate in the Bone marrow, most of which are B-cell in origin. |
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What are clinical manifestations of ALL
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Fever,pallor,bleeding,anorexia,fatigue,weakness,bone, joint, and abd pain, generalized lymphadenopathy, infections, wt loss, hepatosplenomegaly, h/a, mouth sores, neurologic manifestations, including CNS involvement, increased ICP, secondary to meningeal infiltration.
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CML is caused by?
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Excessive development of MATURE neoplastic granulocytes in the bone marrow. The excessive neopl.granulo. move into the peripheral blood in massive numbers and ultimately infiltrate the liver and spleen. They contain a distinctive cytogenetic abnormality called the Philadelphia chromosome
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CML age of onset and peak is?
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20-60 yr of age, peak is 45yr of age
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CML Clinical manifestations are:
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No symptoms early in disease. fatigue, weakness, fever, sternal tenderness,wt loss, joint pain, bone pain, MASSIVE splenomegaly, increased sweating.
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CLL
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Is the most common leukemia in adults. its characterized by production and accumulation of functionally inactive ,but, long lived SMALL, MATURE appearing lymphocytes. Usually its the B-cell lymphocyte that's involved. they infiltrate the bone marros, spleen, and liver.
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Clinical Manifestations of CLL:
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No symptoms frequently, detection of the dz often during exam for unrelated condition..chronic fatigue, anorexia, splenomegaly and lymphadenopathy, hepatomegaly. May progress to fever, night sweats, wt loss, fatigue and freq infections.
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Age of Onset of typical CLL
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50-70 is rare below age 30 and is shows predominance in men.
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What tests are used to detect Leukemias?
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Labs, Bone marrow biopsies, CT, and LP
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What is the goal of treatment in Leukemias?
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Attaining remission. Age and chromosome analysis help form the basis of treatment decisions. Drugs, radiation, hsct (hematopoietic stem cell transplant) are treatments
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Nursing goals for treatment of Leukemias
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Understand and cooperate with treatment plan, experience minimal side effects and complications, and feel hopeful
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Lymphomas are?
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Malignant neoplasms originating in the bone marrow and lymphatic structures resulting in the proliferation of lymphocytes. They are the 5th most common type of cancer in the U.S.
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Hodgkins Lymphoma
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Makes up 11% of all lymphomas, it is a malignant condition characterized by proliferation of abnormal GIANT, multinucleated cells. Called REED-STERNBERG cells, which are located in lymph nodes. B-lymphocytes. Localized to region, but can be widespread
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Clinical Manifestations of Hodgkins Lymphoma are:
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Onset is usually insidious, initial development is most often enlargement of cervical, axillary, or inguinal lymph nodes. A mediastinal mass is the second most common location. the nodes remain moveable and non tender unless they are pressing on a nerve. WT loss, fatigue/weakness,fever, chills, tachycardia, nt sweats
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Non-Hodgkins Lymphoma
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Heterogenous group of malignant neoplasms of primarily B or T Cells. B-cell lymphomas constitue about 90% of all NHL's. Disseminated, may mimic leukemia
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Clinical manifestation of Non hodgkins lymphoma
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Primary clinical manifestation is painless lymph node enlargement.
testing is similar to Hodgkins lymphoma. however NHL is classified based on morphologic, genetic ,immunophenotypic and cinical features. |
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Treatment for NHL
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chemotherapy, and sometimes radiation therapy.
the more aggressive lymphomas are more responsive to treatment and more likely to be cured than the indolent lymphomas. |
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Multiple Myeloma:
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Aka plasma cell myeloma is a condition in which neoplastic plasma cells infiltrate the bone marrow and destroy bone. Accounts for 1% of all annual malignancies and 10% of all hematologic malignancies. Is twice as common in men as women and usually develops after age 40, with avg age of 65. occurs in african americans more than whites.
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Multiple myeloma clinical manifestation
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Develops slowly and insidiously. Often symptoms are not displayed until disease is advanced. Skeletal pain is the major manifestation.
Hypercalcemia due to bone destruction, which can cause renal,gi, or neurologic manifestations, such as polyuria, anorexia, confusion, seizures,coma & cardiac problems. High protein levels as well. |
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Diagnostic studies for Multiple Myeloma include:
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Labs, radiologic exam, and bone marrow exams.
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Treatment for Multiple Myeloma includes:
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managing the dz and symp. Corticosteroids, chemotherapy, biologic therapy, HSTC. MM is seldom cured but, treatment can relieve symptoms.
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Normal Iron Metabolism:
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5-10% of ingested iron is absorbed, the heme in hemoglobin accounts for 2/3 of the body's iron. The other 1/3 is stored as feretin and hemosiderin in the bone marrow, spleen, liver and macrophages.
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Transferrin is?
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synthesized in the liver and serves as a carrier plasma protein for iron.
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Homeostasis
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Is the term used to describe the blood clotting process.
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Describe the Vascular response in homeostasis
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Vascular response - immediate vasoconstriction, 20-30 min. allowing time for the platelet and clotting responses to be activated.
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Platelet plug formation involves:
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Platelets are activated when exposed to interstitial collagen from an injured blood vessel. Platelets stick to one another to form clumps (aggregation or agglutination) Exposure to the collagen causes release of platelet factor 3 and serotonin, adenosine diphosphate which increase adhesiveness.
von Willebrans's factor (vWF)helps form a an adhesive bridge btwn platelets and vascular subendothelial structures. It is synthesized and acts as a carrier for factor VII |
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Plasma clotting factors include intrinsic and extrinsic pathways, explain:
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Intrinsic pathways activated by collagen exposure from blood vessel injury
Extrinsic pathways initiated when tissue factor or tissue thromboplastin is released from injured tissues. |
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Lysis of a Clot involves:
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Anticoagulation, Antighrombins like endogenous heparin, protein C, and protein S. Fibrinolysis is iniated when plasminogen activated to plasmin which breaks down fibrin/fibrinogen into fibrin split products.
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What are the functions of the Spleen:
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1.Hematopoietic - production of RBC's during fetal dev.
2.Filtration - removed defective RBC's via mononuclear phagocytosis. also, returns iron from cells that are broken down to the bone marrow for reuse. Filters Bacteria. 3.Immunologic: Lymphocytes, monocytes, and stored immunoglobulins. 4.Storage: RBC's and platelets. |
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What is the Lymph system composed of?
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Lymph fluid, lymphatic capillaries, ducts and lymph nodes
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What are the functions of the lymph system
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1. carries fluid from interstitial space to blood.
2. carries fats & proteins from GI tract and certain hormones to the circulatory syst. Returns excess IF to the blood (prevents edema) 3.Lymph nodes - 200+ mostly in abd. around GI tract, primary function is filtration of pathogens and foreign particles . |
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What are the functions of the Liver?
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1. Filter
2. produces procoagulants 3. stores iron and produces hepcidin with is a regulator of iron |
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What are Gerontologic Considerations:
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Decrease in red marrow and stem cells
Problems with clotting, O2 transport and fighting inf due to low reserves Decreased Hgl Decreased reticulocyte prod. in response to hemorrhage Iron intake often lower |
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Subjective Assessment should include:
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Health information
functional health patterns |
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Objective assessment should include:
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Physical exam
Diagnostic studies Blood typing and Rh factor |
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Anemia is ?
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Deficiency in the number of RBC's , the quantity of HGL and/or the volume of HCT. this leads to hypoxia which accounts for the s/s of anemia.
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Causes of Anemia are:
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Blood loss, Decreased production of RBC's and increased destruction of RBC's
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Anemia is diagnosed by:
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Health hx and lab tests
Primary changes - morphologic :cellular characteristics secondary - etiologic :underlying cause |
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Clinical manifestations of Anemia;
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Integumentary changes - pallor, jaundice, and pruitis
Eyes and mucous membranes - may show jaundice Mouth - glossitis, smooth tongue Cardiovascular - palppatations, tachycardia, inc pulse pressures, systolic murmurs, intermittent claudication, angina, HF, MI Pulmonary - excertional dyspnea or dyspnea GI - anorexia hepatomegaly splenomegaly,difficulty swallowing and sore mouth Muscoskeletal - bone pain General - fatigue, sens to cold, wt loss lethargy |
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Nursing Diagnosis for Anemia?
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Altered nurtition : less than body requirements r/t inadequate nutritional intake and anorexia AEB wt loss, low werum albumin, decreased iron levels, vitamin def.
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Nutrients needed for Erythropoiesis, function of each and sources of each
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Cobalamin (B12) - RBC maturation - red meats especially liver, eggs, enriched grain products
Folic acid - RBC maturation - green leafy veg, liver, meat, fish, legumes, whole grain Iron - hemoglobin synthesis - liver and muscle meats, eggs, dried fruits, legumes, dk green leafy veg. whole grain and enriched bread and cereals and potatoes. Pyridoxine (Vit B6) - Hemoglobin synthesis - meats, wheat germ, legumes, potatoes, cornmeal, bananas. Amino acids - synthesis of nucleoproteins - eggs, meat, milk and milk products, poultry, fish, legumes, nuts Ascorbic Acid (vit C) - Conversion of folac acid to its active forms, aids in iron absorption - Citrus, green leafy veg, strawberries, canteloupe. |
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Gerontoligical considerations
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Decrease in RBC, 1/3 is nutritional and vitamin def.
s/s pallor, confusion, ataxia, fatigue, worsening angina, hf can be missed. |
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Anemia caused by decreased erythrocyte production
(Erythropoiesis) |
Decreased hemoglobin synthesis which may lead to iron def anemia, thalassemia, and sideorblastic anemia.
Defective DNS synthesis in RBC's may lead to megaloblastic anemias Diminished availability or erythrocyte precursors may result in aplastic anemia |
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Iron deficiency anemia
Whos at highest risk? |
One of the most common types found in up to 30% of world population
Very young, poor diets, and women in reproductive years. |
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Clinical manifestations of Iron Def Anemia:
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General integumentary plus glossitis (inflam of tongue) and chelitis( inflam of lips)
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Treatment involves underlying cause identification and various methods of iron administration such as
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Oral or parental iron supplements
Oral should be taken on an empty stomach and since its best absorbed from the duodenum to the jejunum it should be enteric coated. Taking with Vit C helps absorption. Liquid iron can stain teeth, so it should be taken through a straw. Parental use of iron is indicated for malabsorption, intolerance or oral iron, and a need for beyond oral limits. |
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Parental Iron is administered how?
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IV or IM
IM can stain the skin so seperate needles must be used to draw up and administed the iron. Use the Z-track method. |
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Thalassemia
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Genetic insufficient production of normal hb, mediterreanean, treatment transufsion therapy, splenectomy, iron chelation. Growth and dev delays s/s develop by 2 years of age.
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Megaloblastic anemias
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Impaired DNA synthesis and characterized by LARGE RBC's
Cobalamin (B12) involves IF which is necessarry for B12 absorption (distal ileum), commonly caused by pernicious anemia. (low secretion of IF from mucosa) GI Surgery. |
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Clinical Manifestations of Megaloblastic anemia
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Hypoxia, neuromuscular, sore, beefy, shiny tongue, anorexia, n&V, abd pain, parathesiasis of feet and hands. Diet does not correct.
Folic acid def can also cause - which is treated by folic acid replacement therapy |
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Nursing treatment r/t megaloblastic anemia is
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Safety r/t diminished sensitivity to cold and heat due to neuro impairment
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Anemia of Chronic disease
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Occurs secondary to chronic illness, is primaryily immune driven. Underproduction of RBC's
Findings: increased serum ferritin and iron stores distinguish it from iron def anemia. Treatment is Erythropoietin |
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Aplastic anemia
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Pancytopeniaand hypocellular bone marrow
Thought to be autoimmune (70%) Can be chronic, managed with erythropoietin or acute, critical condition with hemorrhage and sepsis. Very high risk of infection r/t neuropenia |
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Congenital Aplastic Anemias:
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Fanconi syndrome, Congenital dyskeratosis, amegakaryocytic thrombocytopenia, Schwachman - Diamond syndrome
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Treatment of Aplastic Anemia
Prognosis: |
Treatment of underlying cause, Immunosuppressive therapy, cyclophosphamide, stem cell transfusion.
Poor 70% if severe and untreated |
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Anemia caused by blood loss
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Acute: result of sudden hemorrhage causes Hypovolemic shock. If gradual acute loss - increased production of plasma results
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Clinical Manifestations based on blood lost:
10% 20% 30% 40% 50% ***May take 2 - 3 days to see drop in Hgl or Hct. *** |
10- none
20- no detect. s/s at rest, tachy w/ exercise, and slight postural hypotension 30 - normal supine b/p and pulse at rest, postural hypotension and tachy w/ exercise 40- BP , central venous pressure, and cardiac output below normal at rest, rapid, thready pulse and cold clammy skin 50- Shock and potential death |
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Treatments
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Replace blood and fix cause, IV's dextran albumin, crystalloid elecctrolyte solutions, (RL) May need iron. Takes 2-5 days to make RBC's
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