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Altered Hematologic Function: Erythrocytes

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Title: Altered Hematologic Function: Erythrocytes


1
Altered Hematologic FunctionErythrocytes
2
Physical Characteristics of Blood
  • Heavier, thicker, and 3-4 X more viscous than
    water
  • 38o C (100.4oF)
  • pH 7.35 7.45
  • 4-6 liters in an adult
  • Varies with electrolyte concentration and amount
    of adipose tissue

3
Blood Volume
  • Blood volume is about 8 of body weight.
  • 1 kg of blood 1 L of blood
  • 70 kg X 0.08 5.6 Kg 5.6 L
  • 45 is formed elements
  • 55 plasma

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Plasma
  • 92 Water
  • 8 Solutes organic and inorganic
  • Plasma proteins largest proportion of solutes
  • Albumins 58 of the proteins maintain
    osmotic (oncotic) pressure hold water in the
    blood
  • Globulins 38 - antibodies synthesized by
    plasma cells
  • Clotting factors fibrinogen 4 (Serum
    without)

6
Other components of plasma
  • Nutrients
  • Hormones
  • Electrolytes
  • Waste products
  • Dissolved gases

7
Formed elements
  • Three types
  • Erythrocytes red blood cells- RBCs
  • Leukocytes white blood cells WBCs
  • Thrombocytes platelets cell fragments

8
Hemopoiesis (Hematopoiesis)
  • All blood cells common from a common stem cell
    Hemocytoblast
  • These are in the bone marrow (red) and develop
    into blood cells as needed by the body
  • Mitosis is signaled by biochemicals released from
    the body ?
  • Stem cell is signaled to differentiate into the
    needed type of blood cell
  • Hematopoiesis / cell breakdown continue through
    life.

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Erythrocytes (RBCs)
  • Most abundant blood cell type
  • Transport gases
  • Shape is important
  • Large surface to volume ratio
  • Reversible deformability can change shape
  • Development is called erythopoiesis
  • Erythropoietin is a hormone produced by the
    kidneys in response to low blood oxygen levels
    signals bone marrow to increase RBC production

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  • Cytoplasm is mostly hemoglobin (lacks organelles,
    no nucleus)
  • Made up of 4 peptide chains that form the globin
    portion and four molecules of the pigment heme
    which contains an atom of iron
  • Oxygen binds to iron in heme (also CO)
  • 23 of CO2 is bound to globin portion
  • If there is a problem with any part of the
    molecule it may not be functional.

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RBC breakdown
  • Healthy RBCs live about 120 days we break down
    about 174 million per minute
  • RBCs are removed from circulation by the liver
    and spleen
  • Broken down into heme and globin portions
  • Globin is broken down into amino acids
  • Iron is removed from heme and stored or recycled
  • Heme is broken down into biliverdin and then into
    bilirubin

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  • Usually eliminated in bile.
  • If liver insufficiency, bilirubin accumulates in
    blood ? Jaundice ? too much ? kernicterus
  • To produce more RBCs, the body needs sufficient
    iron and amino acids as well as the vitamins
    folate (folic acid) and vitamin B12

17
Abnormalities Anemias
  • Anemia is the inability of the blood to carry
    sufficient oxygen to the body.
  • low s of RBCs
  • lack of hemoglobin

18
Clinical Manifestations
  • Pallor
  • Fatigue
  • Weakness exercise intolerance
  • Dyspnea
  • Syncope (fainting) and dizziness
  • Angina
  • Tachycardia (increased heart rate)
  • Organ dysfunctions

19
Classification of Anemias
  • Identified by their causes or by the changes that
    affect the size, shape or substance of the
    erythrocyte
  • Terms that end with cytic refer to cell size,
    and those that end in chromic refer to
    hemoglobin content.

20
Macrocytic / Megaloblastic Anemia
  • Characterized by abnormally large stem cells
    (megaloblasts) in the marrow that mature into
    erythrocytes that are unusually large in size,
    thickness and volume. The hemoglobin content is
    normal, so these are normochromic anemias.

21
  • These anemias are the result of
  • Ineffective DNA synthesis
  • Commonly due to folate and B12 (cobalamin)
    deficiencies mal-absorption or malnutrition
  • These cells die prematurely, decreasing the
    numbers of RBCs in circulation

22
Pernicious Anemia
  • Common megaloblastic anemia
  • Caused by a Vitamin B12 deficiency
  • Pernicious means highly injurious or destructive
    this condition was once fatal

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  • Can be congenital baby born with a deficiency
    in a protein , intrinsic factor, necessary to
    absorb B12 from the stomach
  • Adult onset one example is an autoimmune
    dysfunction - type A chronic atrophic gastritis
    where there is destruction of the gastric
    mucosa
  • Most commonly affects people over 30
  • Females are more prone to pernicious anemia , and
    black females have an earlier onset.

25
  • Pernicious Anemia is also associated with
  • Heavy alcohol consumption
  • Hot tea
  • Cigarette smoking
  • Other autoimmune conditions
  • Complete or partial removal of the stomach can
    cause intrinsic factor deficiency

26
  • Develops slowly over 20 - 30 years
  • Usually severe by the time individual seeks
    treatment
  • Early symptoms ignored because they are
    nonspecific and vague- infections, mood swings,
    and gastrointestinal, cardiac or kidney ailments.
  • Usually a degree of neuropathy occurs
  • Untreated, it is fatal, due to heart failure

27
Folate deficiency anemia
  • Folic acid also needed for DNA synthesis
  • Demands are increased in pregnant and lactating
    females
  • Absorbed from small intestine and does not
    require any other elements for absorption.
  • Folate deficiency is more common than B12
    deficiency

28
  • Folate deficiency is more common than B12
    deficiency , esp. in alcoholics and those who are
    malnourished because of fat diets or diets low in
    vegetables.
  • Estimated that 10 of North Americans are folate
    deficient.
  • Specific manifestations include cheilosis,
    (scales and fissures of the mouth), inflammation
    of the mouth, and ulceration of the buccal mucosa
    and tongue.

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Microcytic Hypochromic Anemias
  • Characterized by abnormally small RBCs that
    contain reduced amounts of hemoglobin.
  • Possible causes
  • Disorders of iron metabolism
  • Disorders of porphyrin and heme synthesis
  • Disorders of globin synthesis

32
Iron Deficiency Anemia
  • Most common type of anemia throughout the world.
  • High risk
  • Individuals living in poverty
  • Females of childbearing age
  • Children
  • Common causes
  • Insufficient iron intake
  • Chronic blood loss even 2- 4 ml/ day
  • In men gastrointestinal bleeding
  • In women profuse menstruation, pregnancy

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  • Other causes
  • Use of medications that cause GI bleeding
  • Surgical procedures that decrease stomach
    acidity, intestinal transit time, and absorption
  • Eating disorders such as pica

35
Clinical manifestations
  • Early symptoms are nonspecific
  • Later - changes in epithelial tissue
  • Fingernails become brittle and concave
    (koilonychia)
  • Tongue papillae atrophy and cause soreness,
    redness and burning
  • Corners of mouth become dry and sore
  • Difficulty in swallowing due to web of mucus and
    inflammatory cells at opening of esophagus

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Treatment
  • Stop blood loss
  • Iron replacement therapy

39
Normocytic Normochromic Anemias
  • RBCs are normal in size and hemoglobin content,
    but are too few in number.
  • Less common than the macrocytic and microcytic
    anemias

40
  • Several types that do not have anything else in
    common
  • Aplastic
  • Posthemorrhagic
  • Hemolytic
  • Sickle cell
  • Anemia of chronic inflammation

41
Aplastic anemia
  • Fortunately, this condition is rare it means the
    RBCs are not being produced. Bone marrow stem
    cells are not functioning.
  • Can result from disorders of the bone marrow,
    such as cancer autoimmune diseases renal
    failure due to lack of erythropoietin B12 or
    folate deficiency congenital problems or it may
    be induced by radiation, toxins or the use of
    some drugs, such as chloramphenicol.
  • Treatment treat the underlying disorder, blood
    transfusions, and possibly bone marrow transplant

42
Posthemorrhagic
  • Caused by sudden loss of blood.
  • Can be fatal if loss exceeds 40- 50 of plasma
    volume.
  • Treatment is to restore blood volume by
    intravenous administration of saline, dextran,
    albumin, plasma or whole blood.

43
Hemolytic Anemia
  • Red blood cells are formed, but are broken down.
  • May be acquired or hereditary.
  • Acquired hemolytic anemia is extrinsic, due to
    factors outside the red blood cell, such as an
    abnormal autoimmune response that targets red
    cells, or by improper matches during
    transfusions or due to infection, systemic
    diseases, or drugs or toxins.

44
Hereditary or intrinsic hemolytic anemias
  • Sickle cell anemia due to a change in one amino
    acid in each of the beta-chains in the globin,
    under conditions of low oxygen the hemoglobin
    forms insoluble threads that change the shape of
    the erythrocyte into a crescent. This shape is
    not as flexible and tend to be trapped in the
    capillaries, where they obstruct blood flow and
    cause ischemic injury.

45
  • The life span of a sickled cell is only 20 days
    rather than 120, and is removed from circulation
    by the spleen.
  • Either mechanism causes a chronic anemia.
  • Sickle crisis episodes of acute sickling that
    block blood flow, posing the threat of widespread
    and possibly life-threatening ischemic organ
    damage.

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  • This is an inheritable condition.
  • If a person has only one defective gene, it is
    called sickle cell trait, and the person is
    essentially normal. This condition tends to
    persist because it protects against malaria. When
    a cell becomes infected by the parasite, the cell
    sickles and is removed from circulation,
    preventing reproduction of the parasite.
  • Only when a person inherits two defective genes
    does sickle cell anemia occur.

48
  • Thalassemia is another hemolytic disorder where
    the alpha or beta chains of the globin are
    defective, or the beta chain is not produced.
    When the beta protein is lacking, the alpha
    protein accumulates and causes destructive
    membrane effects, causing these cells to be
    rapidly removed from the circulation.
  • Highest incidence in populations around the
    Mediterranean and Southeast Asia.
  • Problem occurs when two defective genes are
    inherited heterozygotes are essentially normal.

49
  • Thalassemia major is an inherited form of
    hemolytic anemia, characterized by red blood cell
    (hemoglobin) production abnormalities. This is
    the most severe form of anemia, and the oxygen
    depletion in the body becomes apparent within the
    first 6 months of life. If left untreated, death
    usually results within a few years. Note the
    small, pale (hypochromic), abnormally-shaped red
    blood cells associated with thalassemia major.

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Myeloproliferative Disorders
  • The opposite of anemias here we have too many
    RBCs.
  • Polycythemia excessive production of RBCs
  • Primary polycythemia cause is unknown, but is
    in effect, a benign tumor of the marrow, leading
    to increased numbers of stem cells and therefore
    RBCs, and splenomegally.
  • Polycythemia vera rare, mostly Northern
    European Jewish males between 60 80 yrs.

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Secondary Polycythemia
  • Due to the overproduction of erythropoietin
    caused by hypoxia. This is more common.
  • Seen in
  • Persons living at high altitudes
  • Smokers
  • COPD patients
  • Congestive heart failure patients

54
  • Polcythemia leads to
  • Increased blood volume and viscosity
  • Congestion of liver and spleen
  • Clotting
  • Thrombus formation
  • (last two may be due increased numbers of
    platelets along with the increase in RBCs due to
    bone marrow dysfunction.)

55
Clinical manifestation of Polycythemia
  • Headache
  • Dizziness
  • Weakness
  • Increased blood pressure
  • Itching / sweating

56
Treatment of polycythemia
  • Reduce blood volume by phlebotomy 300-500 ml.
  • Treat underlying condition - Stop smoking
  • Radioactive phosphorus injections
  • Prevent thrombosis
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