Blood and Lymphatic Diseases

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

Blood Diagnostic Tests CBC (Complete blood count) Characterization of blood cells important Hematocrit Hb measured Bone marrow function Blood clotting disorders differentiated by test

Blood Therapies Administration of whole blood, packed RBC/platelets Plasma or colloidal volume-expanding solutions Artificial blood products

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

Iron Deficiency Anemia—Pathophysiology Common among all ages Typically there is an underlying problem Decreased iron impedes synthesis of Hemoglobin (Hb)

Anemic RBCs vs Normal

Iron Deficiency Anemia Low dietary intake of iron (Fe) Chronic blood loss Impaired absorption in duodenum Severe liver disease Infection, cancer

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

Iron Deficiency Anemia--Treatment Underlying cause determined and treated Depends on cause Fe rich foods and supplements

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

Sickle Cell vs. Normal RBC

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

Sickle Cell Anemia—Treatment Search continues for more effective drugs Avoid strenuous activity, high altitude, infection Most do not survive past 20 years old

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

Petechiae

Ecchymoses

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

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

Acute Lymphocytic Leukemia

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

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

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

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

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

The Leukemias— Diagnostic Tests Peripheral blood smears Show immature leukocytes Altered # WBCs # RBC, platelets low

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

Lymphatic Disorders—Lymphoma Malignant neoplasms involving lymphocyte proliferation in lymph nodes Hodgkin’s and non-Hodgkin’s differentiated by lymph node biopsy

Hodgkin’s Lymphoma—Pathophysiology Occurs primarily in adults 20-40 yrs. old Initially involves one lymph node Spreads to adjacent nodes then organs Via lymph vessels T lymphocytes appear defective, low lymphocyte count

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

Hodgkin’s Lymphoma—Treatment Radiation, chemo, surgery Prognosis in early stages excellent Most effective drug combo is ABVD Remission common in advanced stages

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