Chapter 9 Flashcards
blood function
carry oxygen, bring WBC to injury, nutrient carrier, platelets for clotting, waste products
blood components
- cells/cell fragments
- plasma
how much plasma is in the blood
55%
how much RBC in the blood?
45%
how much WBC and platelets in the blood?
<1%
hematocrit
% of blood thats RBC
hematopoiesis
normal blood production
where does blood production take place?
bone marrow
what are the two main lineages of blood production?
- lymphoid: lymphocytes
- myeloid: everything else (RBC, platelets)
erythrocytes
RBC
RBC functions
carries oxygen and carbon dioxide to cells
hemoglobin
- normal = HbA
- structure: alpha globin chain, beta globin chain, heme mineral (in the middle, contains iron)
erythropoiesis
formation and development of RBC (don’t divide)
substances needed for erythropoiesis
- protein
- vitamin B12
- folic acid (B vitamin)
- iron
what is red cell production regulated by?
osygen content of arterial blood
erythropoietin (EPO)
- released by kidneys - regulate blood volume
- abused by endurance athletes
how long to RBC live?
120 days
how are RBC removed?
spleen/liver
leukocytes
WBC
types of leukocytes
- granulocytes
- monocytes
- lymphocytes
platelets
- cytoplasmic fragments of megakaryocyte (bio cell in bone marrow)
- not cells (no nucleus and only limited metabolic machinery)
- contain granules of chemical mediators of clotting and inflammation
- participate in hemostasis
- must be replaced continuously
- only live 10 days
symptoms of anemia
- headache and easy fatiguability
- loss of appetite and heartburn
- shortness of breath
- numbness and tingling sensations
- pica (craving of nonfood substance)
how does palpation detect anemia?
detects enlargement of lymph nodes, spleen and liver
lab tests for hematopoietic disease
- complete blood count (analysis of blood cells (RBC, WBC, hematocrit, hemoglobin)
- blood smear (look at cells under microscope)
- biopsy of lymph nodes or bone marrow (look for changes)
disorders of RBCs
- anemia (too little)
- polycythemia (too many)
disorders of WBC
- too many
- too little
- cancer
anemia
abnormally low hemoglobin
- low Hgb in RBC
- low RBC
diagnosis of anemia
- CBC (RBC indices, number of RBCs/hematocrit, size of RBC)
- visual inspection (reticulocyte - immature RBCs, kicked out of bone marrow too early)
- Hb < 12 g/dl blood
RBC indices
- MCV = mean corpuscle volume (size of RBC)
- MCHC = mean corpuscle hemoglobin content (measure of hemoglobin per RBC)
anemia: morphologic classification
classification based on red cell appearance suggests the etiology of the anemia
normocytic anemia
normal size and appearance
macrocytic anemia
cells larger than normal (folic acid/B12 deficiency)
microcytic anemia
cells smaller than normal
hypochromic anemia
reduced hemoglobin content
hypochromic microcytic anemia
smaller than normal and reduced hemoglobin content
anemia symptoms
- lightheadedness/fainting
- pica
- cold more easily
- fatigue all the time
most common types of anemia
- nutrient deficiencies (starting materials in bone factory)
- hemolytic anemia (finished products in bone factory, finished too early)
- disorder of bone marrow (factory)
anemia associated with nutrient deficiencies
- iron deficient anemia (most common type)
- RBC (hypochromic microcytic anemia)
- pathogenesis = inadequate iron intake in diet, chronic blood loss
- treatment = administer supplementary iron
macrocytic anemia
- deficiency of vitamin B12 (animal products) or folic acid (green leafy)
- both required for normal hematopoiesis, DNA replication
- mature red cells formed are larger than normal or macrocytes
pernicious anemia
- lack of intrinsic factor results in macrocytic anemia
- vitamin B12 in food combines with intrinsic factor in stomach
- vitamin B12 intrinsic factor complex absorbed in ileum
- receptor in ileum for intrinsic factors = absorbed into blood
causes of pernicious anemia
- gastric resection and bypass (vitamin B12 not absorbed)
- distal bowel resection or disease (impaired absorption of vitamin B12 intrinsic factor complex)
- may develop among elderly (reduced amount of HCl, cannot free B12 from protein)
- autoimmune (associated with autoantibodies against gastric mucosal cells and intrinsic factor)
conditions that depress bone marrow function
- anemia of chronic disease
- aplastic anemia
- myelopthisic anemia
anemia of chronic disease
mild suppression of bone marrow function
aplastic anemia
atrophy of bone marrow (injured by chemicals or autoantibodies)
myelopthisic anemia
bone marrow infiltrated by tumor or replaced by fibrous tissue/cancer cells
hemolytic anemia
premature destruction of RBC
characteristics of hemolytic anemia
- active bone marrow
- increased EPO
- increase reticulocytes
causes of hemolytic anemia
- genetic defects (sickle cell/thalassemia)
- non genetic (acquired hemolytic anemia)
sickle cell disease (HbS)
- pathogenesis: mutation
- autosomal recessive
- missense mutation in beta globin chain
- RBC sickle
- microinfarcts
thalassemia
- genetic disease affecting synthesis of normal adult hemoglobin (hemoglobin A)
- autosomal recessive
- severe complications include overloading the heart
acquired hemolytic anemia
- autoimmune (attacked and destroyed by antibodies)
- destruction of red cells by mechanical trauma (artificial heart valve)
- passing through enlarged spleen (splenomegaly)
diagnostic evaluation of anemia
- history and physical exam
- CBC to assess degree of anemia, leukopenia, and thrombocytopenia
- blood smear to determine if normocytic, macrocytic, or hypochromic microcytic
- reticulocyte count to assess rate of production of new red cells
- lab tests to determine iron, B12, folic acid levels
- bone marrow study to see characteristic abnormalities in marrow cells
- evaluation of blood loss from gastrointestinal tract to localize site of bleeding
polycythemia
too many RBC
types of polycythemia
- primary
- secondary
primary polycythemia
- bone marrow malignancy
- overproduction of red cells, white cells, and platelets
secondary polycythemia
- outside of bone marrow
- reduced arterial oxygen saturation leads to compensatory increase in RBC (lung cancer, life at altitude, increase in EPO)
polycythemia complications
- thick blood (viscous)
- heart works harder
- blood clots
- thrombus
- increase risk of stroke
polycythemia treatment
- primary: drugs that suppress marrow function
- secondary: periodic removal of excess blood
leukopenia
deficiencies in the quality and quantity of leukocytes
- always abnormal
- low WBC count predisposes to infections more often
leukocytosis
increased numbers of leukocytes
- normal protective physiologic response to stressors
- benign or malignant
infection of lymphocytes
- infectious mononucleosis
- acute, self-limiting infection of B lymphocytes transmitted by saliva through personal contact (characterized by enlarged, tender lymph nodes)
- caused by the epstein-barr virus (EBV)
treatment of mononucleosis
rest 5-6 weeks
leukemias
malignant diease involving WBC precursors in bone marrow (myeloid = everything else, lymphoid = T/B cell)
lymphomas
malignant diseases involving lymphocytes (non/hodgkins lymphoma)
myeloma
malignant disease of plasma cells (plasma cells in bone marrow making antibodies = bone affected)
most common types of leukemias
- granulocytic
- lymphocytic
- monocytic
- uncontrolled proliferations of malignant leukocytes
classification of leukemias
- maturity
- cell types
clinical features of leukemia
- manifestations caused by impairment of bone marrow function
- leukemic cells crowd out normal cells causing -
- anemia
- thrombocytopenia: causes bleeding/clots
- infections from inadequate number of normal white cells
- usually produce high WBC counts in peripheral blood = blasts (immature WBC)
signs and symptoms of leukemia
- recurrent infections
- generalized weakness
- anemia
- bleeding
- bruising
treatment for leukemia
chemotherapy (targets rapidly dividing cells)
diagnosis of leukemia made by..
- biopsy of bone marrow
- blood smear (look for blasts)
types of leukemia
- acute lymphocytic leukemia (most common iin children, ALL)
- acute myelogenous leukemia (AML)
- chronic myelogenous leukemia (CML)
- chronic lymphocytic leukemia (CLL)
lymphomas normally have..
B cell phenotype, usually malignant cells not present in blood
how does lymphoma present?
solid tumor of lymphoid cells
does lymphoma affect any age group?
yes, all
malignant cells often..
infiltrate lymph nodes, spleen, thymus, or bone marrow, but may also involve other organs
non-hodgkins lymphomas
- risk increases with age
- 6th most common cancer in U.S
- cancer cells can spill over into blood; present as leukemia
- involve lymph nodes, bone marrow, spleen, thymus, cut can be extranodal origin
hodgkins lymphoma
- most common malignant neoplasm of Americans 10-30 yrs of age
- characterized by reed-sternberg cells (B cell gone awry, epstein barr virus)
treatment of leukemia/lymphoma
- depends on age, severity, and type
- chemo and radiation (cancer may become resistant)
- HSC stem cell transplantation (from bone marrow, need to match HLA, DNA between the two)
myeloma
B cell that becomes plasma cell
myeloma is a malignant disease that only affects..
plasma cells
myeloma tumors can be..
solitary or multifocal, proliferate in bone marrow
how old are most myeloma patients?
over 45 yrs
pathophysiology of myeloma
- functionally useless antibodies (breakdown antibodies and toxic to kidneys)
- impaired humoral immunity (sick more often, hypogammaglobulinemia)
- anemia
what is the most common cause of death for myeloma patients?
infection/renal failure due to kidney toxins
thrombocytosis
too many platelets
thrombocytopenia
too little platelets
primary thrombocytopenia
- idiopathic thrombocytopenia purpura (ITP)
- associated with platelet antibodies
- bone marrow produces platelets, but they are rapidly destroyed
secondary thrombocytopenia
- damage to bone marrow from drugs or chemicals (chemo)
- bone marrow infiltrated by leukemic cells or metastatic carcinoma
