Exam 2 (ch. 13 & 15) Flashcards
What is the function of the blood?
- Transport (CO2, O2, nutrients, hormones)
- Immune system response
- Plasma proteins needed to help maintain BP, temp. -regulation, coagulants and the complement system
Plasma vs. serum
Plasma is all the liquid portion of the blood. Serum is all the liquid portion of the blood, but without coagulation proteins
Cells and cell fragments are within what part of the blood?
plasma
Why do we say “cellular ELEMENTS of human blood”?
Because some are cells, some are parts of cells
Erythrocytes
RBC
- primary job is to transport O2
- most numerous cells
Erythroblasts
Precursor cell of erythrocytes in bone marrow
Hemoglobin
Oxygen-carrying protein formed by the developing red cell.
Cellular elements of human blood
Erythrocytes (RBC)
Leukocytes (WBC)
Thrombocytes (platelets/fragments)
What are the components of erythrocytes
erythroblasts
hemoglobin
Hematopoesis
the normal making of cells in the blood
Bone marrow is what type of stem cell?
Multipotent stem cell
What are the 2 main lineages of hematopoiesis?
- Myeloid Lineage
- makes thrombocytes, PMNS, mast cells, macrophages, RBC - Lymphoid Lineage
- makes all lymphocytes
What is normal/healthy hemoglobin called?
HbA –> hemoglobin A (adult)
What is the structure of hemoglobin?
- alpha globin chain (x2)
- beta globin chain (x2)
Where does synthesis of hemoglobin take place?
mitochondria and cytosol of RBC
Heme
Structural chemical group in the middle of each heme is iron, which is where the O2 binds
Erythropoiesis
The formation and development of RBC
Substances needed for erythropoiesis
- protein
- vitamin B12
- folic acid (one of the vitamin B groups)
- iron
Where is iron in the body stored?
75% of iron is found in RBC, the rest is stored in the liver, bone marrow, and spleen
Where does iron uptake take place?
Iron uptake is controlled in the gut
What is Hepcidin?
It is a protein in the gut that is made by the liver; it affects the GIs uptake of iron
What is RBC production regulated by?
RBC production is regulated by oxygen content of the arterial blood
Erythropoietin (EPO)
Made by the kidneys; EPO is released by the kidneys and it affects the bone marrow stimulating the production of RBC
Where are RBC removed at?
spleen and liver
*when destroyed, we recycle iron and beta-globin as amino acids; heme is eliminated at bilirubin
Anemia
Abnormally low hemoglobin
Causes of anemia
- Low HgB in RBC
2. Low RBC count
How might you diagnose anemia
- Complete blood count (CBC)
- RBC indices (color, count, size, volume) - Visual inspection
- Reticulocyte - Hb< 12 g/dl blood
Reticulocyte
An immature RBC characterized by still having organelles
- body kicks RBC out of bone marrow to soon in order to increase O2
- RBc do not have organelles; right before a RBC is kicked out of the bone marrow, it loses it’s nucleus/organelles
Anemia: morphologic classification
classification is based on red cell appearance which can suggest the etiology of anemia
Normocytic anemia
RBC with normal size and appearance
Macrocytic anemia
RBC that are larger than normal
- folic acid deficiency (green leafy)
- vitamin B12 deficiency (animal products)
Microcytic anemia
RBC smaller than normal
Hypochromic anemia
reduced hemoglobin content
Hypochromic microcytic anemia
RBC smaller than normal and reduced hemoglobin content
Symptoms of anemia
fatigue
cyanosis (blue tint)
increased pica (appetite for non-food)
headache
Causes of anemia
- Iron-deficiency Hemorrhage
- Insufficient RBC production
- Hemolytic anemia
- Chronic disease
- Aplastic anemia
Most common type of anemia
Iron-deficiency anemia
When you see Iron-deficiency anemia, what morphologic classification should you think of
Hypochromic microcytic anemia
Iron-deficiency anemia: pathogenesis
- Inadequate iron in diet
- Infants during periods of rapid growth
- Adolescents with bad diet
- Inadequate reutilization of iron present in red cells due to chronic blood loss (periods, ulcer/cancer in GI tract) `
Iron-deficiency anemia: treatment
Primary focus: learn cause of it
- direct treatment towards cause than symptoms
- administer supplementary iron
Macrocytic anemia is a of what what?
megaloblastic anemia
Why are the deficiencies of vitamin B12 and folic acid an issue in Macrocytic anemia?
They are both required for normal hematopoesis, DNA replication, and the deficiencies may affect other cells as well such as WBC/platelets
What morphological classification of anemia does this statement describe: Mature RBC formed are larger than normal or macrocytes
Macrocytic anemia
Pernicious Anemia
Lack of intrinsic factors in the stomach which results in Macrocytic anemia
- vitamin B12 combines with intrinsic factors in stomach and is absorbed in ileum
Pernicious Anemia: Causes
- Gastric resection and bypass: vitamin B12 is not absorbed
- Distal bowel resection or disease: impaired absorption of vitamin B12 intrinsic factor complex
- May develop among elderly because they produce less hydrochloric acid in stomach
- Autoimmune: associated with autoantibodies against gastric mucosal cells and intrinsic factor
Conditions that depress bone marrow function
- Anemia of chronic disease
a. mild suppression of bone marrow function
b. cannot find cause - Aplastic Anemia
a. marrow injured by radiation, anti-cancer drugs, chemicals or autoantibodies - Cancer
a. Bone marrow infiltrated by tumor or replaced by fibrous tissue
Hemolytic Anemia
Premature destruction of RBC
Characteristics of Hemolytic Anemia
- Active bone marrow trying to increase RBC count
- Increased EPO
- Increased reticulocytes
Causes of Hemolytic Anemia
genetic and non-genetic defects
Genetic Hemolytic Anemia: Sickle cell disease
Pathophysiology = HbS
- autosomal RECESSIVE (2 copies)
- missense (misbase) mutation on Beta globin chain
- RBC sickle
- Microinfarcts
due to mutation
Non-genetic Hemolytic Anemia: Acquired Hemolytic Anemia
- Normal red cells but are unable to survive due to “hostile environment”
- attacked and destroyed by antibodies
- destruction of red cells by mechanical trauma
- passing through enlarged spleen (splenomegaly)
- in contract with some part of artificial heart valve
Polycythemia
Too many RBC
Polycythemia: types
- Primary
a. in bone marrow
b. bone marrow malignancy
c. overproduction of RBC, WBC, platelets - Secondary
a. outside of bone marrow
b. reduced arterial O2 saturation leads to compensatory increase in RBC
- lung cancer
- life at altitude
- increase in EPO
Polycythemia complications
Increase in clots, blood is more viscous which causes heart to work harder leading to heart failure
Polycythemia treatments for each type
Primary = drugs that suppress marrow function Secondary = periodic removal of excess blood
Hemorrhagic Anemia
Loss of iron –> loss of O2 carrying capacity
Hemorrhagic Anemia types
- Acute
- due to trauma or wounds - Chronic
- periods
- intestinal bleeding
- presents as iron-deficiency anemia
What is the main threat to acute Hemorrhagic Anemia
low BP and low blood volume –> could go into shock
Primary Thrombocytopenia
- associated with platelet antibodies
- bone marrow produces platelets, but they are rapidly destroyed
- encountered in children and subsides after short time
- tends to be chronic in adults
Secondary Thrombocytopenia
- Damage to bone marrow from drugs or chemicals
- Bone marrow infiltrated by leukemic cells or metastatic carcinoma
Thrombocytopenia
a low blood platelet count.
Primary function of lymphatic system
Provide immunologic defenses against foreign material
lymph nodes
Bean-shaped structures consisting of a mass of lymphocytes
Explain how lymph works
As lymph flows though the nodes, phagocytic cells filter out and destroy microorganisms and foreign matter