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Blood and Lymphatic Diseases
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Overview Blood Lymphatic Disorders The leukemias Diagnostic Test
Blood Therapies Blood Dyscrasias The anemias Iron deficiency anemia Hemolytic anemia Sickle cell anemia Blood clotting disorders The leukemias Lymphatic Disorders Lymphomas Hodgkin’s lymphoma Non-Hodgkin lymphoma
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Blood Diagnostic Tests
CBC (Complete blood count) Characterization of blood cells important Hematocrit Hb measured Bone marrow function Blood clotting disorders differentiated by test
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Blood Therapies Administration of whole blood, packed RBC/platelets
Plasma or colloidal volume-expanding solutions Artificial blood products
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Blood Dyscrasias—The Anemias
Cause decrease in oxygen transport Oxygen deficit results in: Decreased energy produced by cells Tachycardia (irregular heartbeat) Decreased regeneration of epithelial cells Severe anemia
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Iron Deficiency Anemia—Pathophysiology
Common among all ages Typically there is an underlying problem Decreased iron impedes synthesis of Hemoglobin (Hb)
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Anemic RBCs vs Normal
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Iron Deficiency Anemia
Low dietary intake of iron (Fe) Chronic blood loss Impaired absorption in duodenum Severe liver disease Infection, cancer
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Iron Deficiency Anemia—Signs and Symptoms
Pallor of skin and mucous membranes Fatigue, lethargy, cold intolerance Irritability Menstrual irregularities Delayed healing Severe Tachycardia, heart palpitations, dyspnea, syncope
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Iron Deficiency Anemia--Treatment
Underlying cause determined and treated Depends on cause Fe rich foods and supplements
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Hemolytic Anemias—Sickle Cell Anemia—Pathophysiology
Abnormal Hb (called HbS) Due to amino acid switch HbS deoxygenated results in crystallization Changes shape to crescent shape Cell membrane damaged Hemolysis, shorter life span Transports oxygen normally But low erythrocyte count Therefore low Hb level Sickeling is major problem Shape obstructs small vessels Thrombus formation, tissue necrosis, infarctions
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Sickle Cell vs. Normal RBC
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Sickle Cell Anemia—Etiology
Inherited; recessive gene Homozygotes Mostly HbS Clinical signs Heterozygotes Half HbS Only possess trait Common in the black population Africans w/ SCA resistant to malaria
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Sickle Cell Anemia—Treatment
Search continues for more effective drugs Avoid strenuous activity, high altitude, infection Most do not survive past 20 years old
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Blood Clotting Disorders
Indicated by spontaneous bleeding or excessive bleeding after minor injury Warning signs Persistent bleeding in gums, nose bleeds Petechiae Purpura and ecchymoses Hemarthroses Hemophysis Hematemesis Blood in feces Anemia Feeling faint, anxious, low bp, rapid pulse
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Petechiae
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Ecchymoses
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Blood Clotting Disorders—Causes of Excessive Bleeding
Defective platelet function Vitamin K deficiency Liver disease Inherited defects Hemorrhagic fever viruses (Ebola) Long-term anticoagulant drug treatment
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The Leukemias—Pathophysiology
Neoplastic disorders involving WBC 1 or more leukocyte types present as: Undifferentiated, immature, nonfunctional cells Multiply uncontrollably Lg quantities released into general circulation
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Acute Lymphocytic Leukemia
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Acute vs. Chronic Leukemia
High proportion of very immature, nonfunctional cells in bone marrow and periph circ Abrupt onset Marked signs, complications Higher proportion of mature cells Insidious onset Mild signs Better prognosis
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Types of Leukemia Type Malignant Cells
Acute lymphocytic leukemia (ALL) Lymphocytes Acute myelocytic leukemia (AML) Granulocytes (neutrophils, eosinophils, basophils) Chronic lymphocytic leukemia (CLL) B lymphocytes Chronic myelocytic leukemia (CML) Granulocytes
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The Leukemias—Pathophysiology
Cell growth in bone marrow suppresses production of normal cells Leads to: Anemia, lack of normal functioning leukocytes Bone marrow presses on nerves = pain As disease progresses, increase # leukemic cells cause: Congestion and enlargement of lymphoid tissue
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The Leukemias—Etiology
Chronic More common in older people Acute Primarily in kids, young adults ALL 2-6 years old Cause unknown Leukemias in adults associated with exposure to chemicals, radiation, viruses Some causes related to chromosomal abnormalities
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The Leukemias—Signs and Symptoms: Acute
Onset marked by infection that is unresponsive to treatment or excessive bleeding Multiple infections (b/c nonfunc. WBC) Severe hemorrhage Anemia Severe and steady bone pain Weight loss and fatigue Fever Enlarged lymph nodes, spleen, liver Chronic: onset milder, insidious
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The Leukemias— Diagnostic Tests
Peripheral blood smears Show immature leukocytes Altered # WBCs # RBC, platelets low
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The Leukemias—Treatment
Prognosis related to: WBC count Proportion of immature cells at time of count Individuals with chronic may live 10 yrs. with treatment Chemo Less effective in adults with AML May have to be discontinued if blood cell count drops too low Thrombocytopenia, neutropenia Transfusion of platelets might be req Bone marrow transplant If chemo ineffective Must find suitable donor Drugs Only some respond ALL does well
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Lymphatic Disorders—Lymphoma
Malignant neoplasms involving lymphocyte proliferation in lymph nodes Hodgkin’s and non-Hodgkin’s differentiated by lymph node biopsy
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Hodgkin’s Lymphoma—Pathophysiology
Occurs primarily in adults yrs. old Initially involves one lymph node Spreads to adjacent nodes then organs Via lymph vessels T lymphocytes appear defective, low lymphocyte count
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Hodgkin’s Lymphoma— Signs and Symptoms
1st indicator is large, painless, nontender lymph node Later enlarged lymph nodes Pressure effects General signs of cancer Recurrent infection
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Hodgkin’s Lymphoma—Treatment
Radiation, chemo, surgery Prognosis in early stages excellent Most effective drug combo is ABVD Remission common in advanced stages
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Non-Hodgkin’s Lymphoma
Increase in incidence Similarities to Hodgkin’s: Initial manifestation Clinical signs, staging, treatment Differences: Multiple node involvement scattered throughout body Pattern of widespread metastasis, often at diagnosis Much more difficult to treat
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