Chapter 3 Hematopoietic Function. Hematopoiesis Process of forming blood Plasma - liquid protein...
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Transcript of Chapter 3 Hematopoietic Function. Hematopoiesis Process of forming blood Plasma - liquid protein...
![Page 1: Chapter 3 Hematopoietic Function. Hematopoiesis Process of forming blood Plasma - liquid protein Leukocytes - white blood cells Erythrocytes - red blood.](https://reader034.fdocuments.net/reader034/viewer/2022042501/56649e0b5503460f94af27af/html5/thumbnails/1.jpg)
Chapter 3Hematopoietic Function
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Hematopoiesis
• Process of forming blood
• Plasma - liquid protein
• Leukocytes - white blood cells
• Erythrocytes - red blood cells– Hemoglobin – oxygen carrying component– Hematocrit - amount of blood volume
occupied by erythrocytes
• Thrombocytes - platelets
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Hemostasis
• Stoppage of blood flow
• Normal when it seals a blood vessel to prevent blood loss and hemorrhage
• Abnormal when it causes inappropriate clotting or when clotting is insufficient to stop blood flow.
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Stages of Hemostasis
1. Vessel spasm
2. Formation of platelet plug
3. Blood coagulation
4. Clot retraction
5. Clot dissolution
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Disorders of the WBCs
• Leukocytes key players in the inflammatory response and fighting infections
• Normal range = 5,000 to 10,000 mm3
• Leukopenia-decreased levels
• Leukocytosis-increased levels
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Neutrophils
• One type of leukocytes
• Usually the first to arrive at the site of infection
• Normal range is 2,000–7,500 cells/µL
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Neutropenia
• Neutrophils < 1500
• Causes– Increased usage– Drug suppression– Radiation therapy– Congenital conditions– Bone marrow cancers– Spleen destruction– Vitamin deficiency
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Neutropenia
• Manifestations– Depends on severity and cause– Infections and ulcerations especially of the
respiratory tract, skin, vagina, and gastrointestinal tract
– Signs and symptoms of infection (e.g., fever, malaise, and chills)
• Diagnosis: neutrophil levels and bone marrow biopsy
• Treatment: Antibiotic therapy and hematopoietic growth factors
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Infectious Mononucleosis• “Kissing Disease”-oral transmission• Self-limiting• Most prevalent in adolescents and young adults • Caused by Epstein-Barr virus in the herpes family• EBV infects the B cells by killing the cell or being
incorporated into its genome• Those B cells incorporated with EBV produce
heterophile antibodies• Once the disease is eliminated, a few B cells
remain altered, giving the individual an asymptomatic infection for life and occasional spreading the EBV to others
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Infectious Mononucleosis• Manifestations
– Insidious onset
– Incubation = 4 to 8 weeks
– Initially see anorexia, malaise, and chills
– Manifestations intensify to include leukocytosis, fever, chills, sore throat, and lymphopathy
– Acute illness usually last 2-3 weeks; may not fully recover for 2-3 months
• Treatment: symptomatic and supportive
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Lymphomas
• Cancers affect lymphatic system
• Most common hematologic cancer in the US
• Two main types– Hodgkin’s – Non-Hodgkin’s
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Hodgkin’s Lymphoma• Lest common of the two• Solid tumors with the presence of Reed-
Strenberg cells• Typically originate in the lymph nodes of the
upper body• Several subtypes• Very curable with treatment• Manifestations: painless enlarge nodes, weight
loss, fever, night sweats, pruritis, coughing, difficulty breathing, chest pain, recurrent infections, and splenomegaly
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Hodgkin’s Lymphoma Staging• Stage I: The lymphoma cells are in one lymph node group or one
part of a tissue or an organ.
• Stage II: The lymphoma cells are in at least two lymph node groups on the same side of the diaphragm, or the lymphoma cells are in one part of a tissue or an organ and the lymph nodes near that organ.
• Stage III: The lymphoma cells are in lymph nodes above and below the diaphragm. Lymphoma cells may be found in one part of a tissue or an organ near these lymph node groups. Cells may also be found in the spleen.
• Stage IV: Lymphoma cells are found in several parts of one or more organs or tissues, or the lymphoma cells are in an organ and in distant lymph nodes.
• Recurrent: The disease returns after treatment.
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Hodgkin’s Lymphoma• Diagnosis: physical examination,
presence of Reed-Sternberg cells in a lymph node biopsy, complete blood count, chest X-rays, computed tomography scan, magnetic resonance imaging, positron emission tomography scan, and bone marrow biopsy
• Treatment: chemotherapy, radiation, and surgery
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Non-Hodgkin’s Lymphoma
• More common
• Poor prognosis
• Many different types
• Similar to Hodgkin’s manifestations, staging, and treatment
• Different in the spread and diagnosis
• Can originate in the T or B cells
• No Reed-Sternberg cells
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Leukemia• Cancer of the leukocytes• Leukemia cells abnormally proliferate,
crowding normal blood cells
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Types of Leukemia
• Acute lymphoblastic leukemia– Affects primarily children
– Responds well to therapy
– Good prognosis
• Acute myeloid leukemia– Affects primarily adults
– Responds fairly well to treatment
– Prognosis somewhat worse than that of acute lymphoblastic leukemia
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Types of Leukemia
• Chronic lymphoid leukemia– Affects primarily adults
– Responds poorly to therapy, yet most patients live many years after diagnosis
• Chronic myeloid leukemia– Affects primarily adults
– Responds poorly to chemotherapy, but the prognosis is improved with allogenic bone marrow transplant
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Leukemia
• Manifestations: leukopenia, anemia, thrombocytopenia, lymphadenopathy, joint swelling, bone pain, weight loss, anorexiam hepatomegaly, splenomegaly, and central nervous system dysfunction
• Diagnosis: a history, physical examination, peripheral blood smears, complete blood count, and bone marrow biopsy
• Treatment: chemotherapy and bone marrow transplant
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Multiple Myeloma• Plasma cell cancer
• Excessive numbers of abnormal plasma cells in the bone marrow crowd the blood-forming cells and cause Bence Jones proteins to be excreted in the urine
• Bone destruction leads to hypercalcemia and pathologic fractures
• Often well advanced upon diagnosis
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Multiple Myeloma• Manifestations
– Insidious onset– Include: anemia, thrombocytopenia,
leukopenia, decreased bone density, bone pain, hypercalcemia, and renal impairment
• Diagnosis: serum and urine protein, calcium, renal function tests, complete blood count, biopsy, X-rays, computed tomography, and magnetic resonance imaging
• Treatment: chemotherapy and complication management
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Disorders of the RBCs
• Erythropoiesis
–Production of erythrocytes
–Regulated by erythropoietin
–Occurs in bone marrow
• Disorders typically result from a deficit or defect in the erythrocytes
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Anemia• Results from decreased number of erythrocytes,
reduction of hemoglobin, or abnormal hemoglobin • Decreases O2 carrying capacity, leading to tissue
hypoxia• Several types with varying etiology• General manifestations: weakness, fatigue, pallor,
syncope, dyspnea, and tachycardia
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Iron-Deficiency Anemia• Very common
• Iron is necessary for hemoglobin production
• Causes: decreased iron consumption, decreased iron
absorption, and increased bleeding
• Additional manifestations: cyanosis to sclera, brittle
nails, decreased appetite, headache, irritability,
stomatitis, pica, and delayed healing
• Diagnosis: complete blood count (low hemoglobin,
hematocrit, MCV, and MCHC), serum ferritin, serum
iron, and transferring saturation
• Treatment: identify and treat cause, increase dietary
intake, and iron supplements
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Pernicious Anemia• Vit B12 deficiency usually caused by a lack of intrinsic factor
• Causes: autoimmune
• Vit B12 is required for DNA synthesis
• Leads to decreased maturation & cell division• May see myelin breakdown & neurological complications• Manifestations: bleeding gums, diarrhea, impaired smell,
loss of deep tendon reflexes, anorexia, personality or memory changes, positive Babinski’s sign, stomatitis, paresthesia, and unsteady gait
• Diagnosis: serum B12 levels, Schilling’s test, complete blood count, gastric analysis, and bone marrow biopsy
• Treatment: injectable B12
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Aplastic Anemia• Bone marrow depression of all blood cells (pancytopenia)• Causes: insidious, autoimmune, medications, medical
treatments, viruses, and genetic • Onset may be insidious sudden & severe • Manifestations:
– Anemia (e.g., weakness, pallor, dyspnea)– Leukocytopenia (e.g., recurrent infections)– Thrombocytopenia (e.g., bleeding)
• Diagnosis: complete blood count and bone marrow biopsy• Treatment: identify and manage underlying cause, oxygen
therapy, infection control, infection treatment, bleeding precautions, blood transfusions, and bone marrow transplants
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Hemolytic Anemia• Excessive erythrocyte destruction
• Causes: idiopathic, autoimmune, genetics, infections, blood transfusion reactions, and blood incompatibility in the neonate
• Several types including sickle cell anemia, thalassemia, and erythroblastosis fetalis
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Sickle Cell Anemia• Neither recessive nor dominant but co-dominant
• Hemoglobin S causes erythrocytes to be
abnormally shaped
• Abnormal erythrocytes carry less oxygen and clog
vessels, causing hypoxia and tissue ischemia
• More common in people of African and
Mediterranean descent
– Also seen in people from South and Central America,
the Caribbean, and the Middle East
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Forms of Sickle Cell Anemia
1. Sickle cell trait
• Heterozygous
• Less than half of erythrocytes are sickled
2. Sickle cell disease
• Homozygous
• Most severe
• Almost all erythrocytes are sickled
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Sickle Cell Anemia• Manifestations
– Typically appear around 4 months of age– Sickle cell crisis
• Painful episodes that can last for hours to days• Pain is caused by tissue ischemia and necrosis• Triggered by dehydration, stress, high altitudes, and fever
– Include: abdominal pain, bone pain, dyspnea, delayed growth and development, fatigue, fever, jaundice, pallor, tachycardia, skin ulcers, angina, excessive thirst, frequent urination, priapism, and vision impairment
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Sickle Cell Anemia• Diagnosis: hemoglobin electrophoresis, complete
blood count, and bilirubin test • Life expectancy improving with better management• Treatment:
– No cure, palliative– Stem cell research showing promise – Medications (e.g., Hydrea [hydroxyurea])– Avoid triggers– Other strategies: oxygen therapy, hydration, pain
management, infection control, vaccinations, blood transfusions, bone marrow transplants, genetic counseling
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Thalassemia• Autosomal dominant inheritance
• Abnormal hemoglobin from a lack of one of two proteins that makes up hemoglobin (alpha and beta globin)
• Most common in people of Mediterranean descent– Also seen in those of Asian, Indian, and African descent
• Manifestations: abortion, delayed growth and development, fatigue, dyspnea, heart failure, hepatomegaly, splenomegaly, bone deformities, jaundice
• Severe cases can lead to death in childhood
• Life expectancy can improve with effective management
• Diagnosis: complete blood count (low MCV, MCHC) and iron levels
• Treatment: blood transfusion, chelation therapy, and splenectomy
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Polycythemia
• Abnormally high erythrocytes
• Rare
• Considered a neoplastic disease
• Increased blood volume and viscosity, leading to tissue ischemia and necrosis
• Complications: thrombosis, hypertension, heart failure, hemorrhage, splenomegaly, hepatomegaly, and acute myeloblastic leukemia
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Polycythemia
• Manifestations: cyanotic or plethoric skin, high blood pressure, tachycardia, dyspnea, headaches, visual abnormalities
• Diagnosis: complete blood counts, bone marrow biopsy, and uric acid levels
• Treatment: chemotherapy, radiation, phlebotomy and managing clotting disorders
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Disorder of Platelets
• Normal platelet levels range from 150,000 to 350,000 mm3
• Include issues in quantity and quality of platelets
• Thrombocytosis – increased levels
• Thrombocytopenia – decreased levels
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Hemophilia A• X-linked recessive bleeding disorder• Deficiency or abnormality of clotting factor VIII • Varies in severity• Manifestations: bleeding or indications of bleeding
(e.g. bruising, petechia, etc)• Diagnosis: clotting studies and serum factor VIII
levels• Treatment: clotting factor transfusions, recombinant
clotting factors, desmopressin (DDAVP), and bleed precautions
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Von Willebrand’s Disease• Most common hereditary bleeding
disorder• Decreased platelet adhesion and
aggregation• Manifestations: bleeding or indications
of bleeding (e.g. bruising, petechia, etc)
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Forms of Von Willebrand’s Disease• Type 1
– Most common and mildest form
– Autosomal dominant
– Reduced von Willebrand’s factor levels
– Can cause significant bleeding with trauma or surgery
• Type 2
– Either autosomal dominant or recessive
– Five subtypes
– von Willebrand’s factor building blocks are smaller than usual or break down easily
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Forms of Von Willebrand’s Disease
• Type 3 – Autosomal recessive – no measurable von Willebrand’s factor or
factor VIII – Causes severe bleeding problems
• Aquired type – Occurs with Wilms’ tumor, congenital heart
disease, systemic lupus erythematosus, and hypothyroidism
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Von Willebrand’s Disease
• Diagnosis: bleeding studies and factor VIII levels
• Treatment: – Mild cases usually do not require treatment
– Cryoprecipitate infusions
– Desmopressin (DDAVP)
– Bleeding precautions
– Measures to control bleeding
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Disseminated Intravascular Coagulation
• Life-threatening complications of many conditions• Results from an inappropriate immune response• Widespread coagulation followed by massive
bleeding because of the depletion of clotting factors• Manifestations: tissue ischemia and bleeding• Complications: shock and multisystem organ failure• Diagnosis: complete blood count and bleeding
studies• Treatment: identify and treat underlying cause,
replace clotting components, and preventing activation of clotting mechanisms
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Idiopathic Thrombocytopenia Purpura
• Hypocoagulation resulting from an autoimmune destruction of platelets
• Acute form– More common in children
– Sudden onset
– Self-limiting
• Chronic form– More common in adults age 20-50
– More common in women
• Causes: idiopathic, autoimmune diseases, immunizations with a live vaccine, immunodeficiency disorders, and viral infections
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Idiopathic Thrombocytopenia Purpura
• Manifestations: bleeding or indications of bleeding (e.g. bruising, petechia, etc)
• Diagnosis: complete blood count (platelet levels < 20,000) and bleeding studies
• Treatment– Acute ITP: glucocorticoid steroids, immunoglobulins,
plasmapheresis, and platelet pheresis
– Chronic ITP:glucocorticoid steroids, immunoglobulins, splenectomy, blood transfusions, and immunosuppressant therapy
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Thrombotic Thrombocytopenic Purpura
• Deficiency of enzyme necessary for cleaving von
Willebrand’s factor, leading to hypercoagulation
• Hypercoagulation depletes platelet levels
• Characterized by thromboses, thrombocytopenia,
and bleeding
• Causes: idiopathic causes, heredity, bone marrow
transplants, cancer, medications, pregnancy, and
HIV
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Thrombotic Thrombocytopenic Purpura
• Manifestations: purpura, changes in consciousness, confusion, fatigue, fever, headache, tachycardia, pallor, dyspnea on exertion, speech changes, weakness, and jaundice
• Diagnosis: complete blood counts, blood smears, and lactate dehydrogenase levels
• Treatment: plasmapheresis, splenectomy,
and glucocorticoid steriods