Patho Ch 13

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Patho Ch 13
2014-10-23 16:42:28
Exam #4 Red Blood Cells
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  1. Erythrocytes
    • Most abundant cell in the body
    • Responsible for tissue oxygenation
    • Biconcavity and reversible deformity (flexible)
    • 120-day life cycle
    • No nucleus

    Erythrocytes are derived from erythroblasts (normoblasts)

    Maturation is stimulated by erythropoietin

    • blasts⇢give rise to other cells
    • blood cells⇢from bone marrow

    erythropoietinmade by the kidney that tells the blood cells to grow up! erythroblasts⇀erythrocytes

    If kidneys are messed up, not going to have happy healthy red blood cells to carry oxygen = anemia
  2. Adult Hemoglobin
    • Two alpha chains
    • Two beta chains
    • Each protein chain holds one iron-containing heme group
    • oxygen binds to the heme groups

    Each heme group (4 chains=4 heme groups) is capable of carrying 1 molecule of oxygen

    Read the book to understand!!
  3. Hemoglobin synthesis
    Nutritional requirements:

    Protein: amino acids

    Vitamins: Vitamin B12 Cobalomin), B6 (pyridoxine), B2 (riboflavin), E (tocopherol) and C (ascorbic acid); folic acid (B9); pantothenic acid (B5); and niacin (B3)

    Minerals: iron and copper


    All important in the building/needed for blood
  4. Regulation of Erythropoiesis
    Numbers of circulating red cells in healthy individuals remain constant

    The peritubular cells of the kidney produce erythropoietin

    Hypoxia stimulates the production and release of erythropoietin

    • Erythropoietin causes an increase in red cell production and release from bone marrow
    • _______________

    more red blood cells⇢thicker. ei- dehydration

    Hypoxia⇢too little oxygen⇢stimulates erthropoietin⇢increase in red blood cell production⇢blood becomes thicker
  5. Normal Destruction of Old RBCs
    Aged red cells are sequestered and destroyed  by macrophages of the MPS (mononuclear phagocyte system), primarily in the spleen

    The liver takes over if the spleen is absent

    Globin chains are broken down into amino acids

    Porphyrin is reduced to bilirubin, transported to the liver, and secreted in the bile

    Iron is "recycled" in the body
  6. Tests of Bone Marrow Function
    • bone marrow aspiration (break into bone and test bone marrow)
    • bone marrow biopsy
    • measurement of bone marrow iron stores
    • differential cell count
  7. Red Blood Cells and Aging
    Erythrocyte life span is normal but erythrocytes are replaced more slowly

    possible causes:

    • iron depletion
    • decreased total serum iron, iron-binding capacity, and intestinal iron absorption


    as you get older RBC not replaced as quickly. Kidney function decreases
  8. Lab Tests

    Normal Ranges
    • RBC Count: number of cells in the blood
    • Men: 4.2-5.4
    • Women: 3.6-5.0

    • Hemoglobin: hemoglobin content of blood
    • Men: 14-16.5
    • Women: 12-15

    • Hematocrit: volume of cells in 100 ml blood (number of cells)
    • Men: 40-50%
    • Women: 37-47%
  9. Hemoglobin

    Elevated and Low
    Elevated: dehydration (look at BUN and sodium) or polycythemia (COPD, high elevations, cancer)

    Low: anemia, hemorrhage, bone marrow suppression

    Critical: <5

    (BUN: The liver produces urea in the urea cycle as a waste product of the digestion of protein. Normal human adult blood should contain between 6 to 20 mg of urea nitrogen per 100 ml of blood.)
  10. Hematocrit

    Elevated and Low
    Elevated: dehydration (look at BUN and sodium); or polycythemia

    Low: over hydration; hemorrhage; anemia

    Critical: <15% or >60%
  11. Process of erythropoiesis
    Decreased blood oxygen⇢kidneys secrete erythropoietin⇢bone marrow stimulated⇢creates new red blood cells
  12. Different stages of RBC
    Immature RBCs (nucleated)

    Reticulocytes (RBCs that still have their endoplasmic reticulum)

    Mature RBCs


    They last about 120 days

    • -Their membranes become weakened
    • -Because they have no nuclei, RBCs cannot make new membrane components
    • -Eventually, RBCs break as they squeeze through the capillaries
  13. Most RBCs break in the spleen
    break in capillaries in the spleen⇢eaten by white blood cells in the spleen, liver, bone marrow, or lymph nodes⇢hemoglobin processed into unconjugated bilirubin
  14. Unconjugated Bilirubin
    unconjugated bilirubin is toxic


    Unconjugated bilirubin in blood⇢bilirubinemia⇢jaundice

    Unconjugated bilirubin in blood⇢liver links to gluconuride⇢conjugated bilirubin⇢bile

    bile gives poop brown color and urine yellow color.

    too much built in the body and not released in waste-bilirubinemia
  15. RBCs destroyed outside the spleen
    Hemoglobinemia makes the plasma turn red

    Hemoglobinuria makes the urine cola-colored


    Malaria called "blackwater fever" because red blood cells are bursting in the plasma and the urine looks dark red/brown because of the RBC

    RBC break in capillaries outside the spleen⇢hemoglobin released into the blood⇢hemoglobinemia-hemoglobinuria
  16. Anemia and causes
    Reduction in the total number of erythrocytes in the circulating blood or in the quality or quantity of hemoglobin

    • impaired erythrocyte production
    • acute or chronic blood loss
    • increased erythrocyte destruction
    • combination of the above


    • blood loss
    • hemolysis
    • impaired RBC production
  17. Types of Anemia

    • identified by terms that end in "-cytic"
    • macrocytic, microcytic, normocytic

    Hemoglobin content

    • indentfied by terms that end in "-chromic"
    • normochromic and hypochromic


    Anisocytosis: red cells are present in various sizes

    Poilkilocytosis: red cells are present in various shapes

    physiologic manifestation: reduced oxygen-carrying capacity

    variable symptoms based on severity and the ability for the body to compensate

    Classic anemia symptoms: fatigue, weakness (reduced oxygen), dyspnea (difficulty breathing), and pallor (pale)
  18. Macrocytic-Normochromic Anemias (2)
    Big fat cells that still look normal and red

    Also termed megaloblastic anemias

    Characterized by defective DNA synthesis⇢caused by deficiencies in vitamin B12 or folatecoenzymes for nuclear maturation and the DNA synthesis pathway

    • Large red blood cells (High MCV). Cell looses the dimple in the middle
    • Causes: folate or Vitamin B12 deficiency
  19. Pernicious Anemia
    A macrocytic-normochromic anemia

    Lack of intrinsic factor from the gastric parietal cells:

    • required for vitamin B12 absorption
    • results in vitamin B12 deficiency
    • typical anemia symptoms

    • neurologic manifestations: nerve demyelinatin; absence of intrinsic factor
    • other: <appetite, abdominal pain, beefy red tongue (atrophic glossititis), iceterus (jaundice), spleen enlarged
    • treatment: parenteral or high oral doses of vitamin B12 (need an outside source of B12)


    No intrinsic factor from gastric parietal cells of the stomach⇢cannot absorb B12
  20. Folic acid deficiency 


    B12 deficiency
    Megaloblastic anemias
  21. Folate Deficiency Anemia
    A macrocytic-normochromic anemia

    • Absorption of folate occurs in the upper small intestine
    • Not dependent on any other factor
    • Similar symptoms to pernicious anemia except neurologic manifestations generally not seen
    • Treatment requires daily oral administration of folate
  22. Microcytic-Hypochromic Anemias (3)
    Characterized by red cells that are abnormally small and contain reduced amounts of hemoglobin

    Related to:

    • disorders of iron metabolism (iron deficiency
    • pale=less hemoglobin)
    • disorders of porphyrin and heme synthesis
    • disorders of globin synthesis (Thalassemias)
    • lead poisoning

    Small cell size (microcytic: low MCV) and low amount hemoglobin makes the cell appear pale (hypochromic: low MCH)
  23. Iron Deficiency Anemia
    A microcytic-hypochromic anemia

    Most common type of anemia worldwide

    • Nutritional iron deficiency
    • Metabolic or functional deficiency

    Progression of iron deficiency causes:

    • brittle, thin, coarsely ridged, and spoon-shaped nails
    • a red, sore, and painful tongue
    • Low MCV; Low MCH


    Do not have enough iron

    Vitamin C⇢help to absorb iron


    • Hypochromic and microcytic erythrocytes
    • Poikilocytosis (irregular shape)
    • Anisocytosis (irregular size)
  24. Sideroblastic Anemias
    A microcytic-hypochromic anemia

    • group of disorders characterized by anemia
    • altered mitochondrial metabolism causing ineffective iron uptake and resulting in dysfuntional hemoglobin synthesis

    Ringed sideroblasts within the bone marrow are diagnostic

    sideroblasts are erythroblasts that contain iron granules that have not been synthesized into hemoglobin


    Problems with mitochondrial metabolism⇢not able to take up the iron or use it in the hemoglobin
  25. Normocytic-Normochromic Anemias (2)
    Cells right size and right color but bone marrow is not making enough

    Characterized by red cells that are relatively normal in size and hemoglobin content but insufficient in number

    Aplastic anemia (bone marrow does not make enough new blood cells); acute blood loss; prosthetic heart valves; sepsis (severe response to bacterial or germs); tumor

    Sickle cell anemia

    Anemia of chronic inflammation:

    Mild to moderate anemia seen in- AIDS, rheumatoid arthritis, lupus erythematosus, hepatitis, renal failure, and malignancies
  26. Hemolytic Anemia

    types of hemolytic anemias (2)

    • Accelerated destruction of red blood cells
    • Autoimmune hemolytic anemias
    • Immunohemolytic anemia
    • Warm antibody immunohemolytic anemia
    • Drug-induced hemolytic anemia
    • Cold agglutinin (causes coagulation)  immunohemolytic anemia
    • Cold hemolysin hemolytic anemia


    Hemolytic-being destroyed. Red blood cells bust

    Membrane disorders: -hereditary spherocytosis; -acquired hemolytic anemias and hemolytic disease of the newborn

    Hemoglobinopathies: -Sickle cell disease; -Thalassemia (alpha, beta)

    G6PD deficiency
  27. Vitamin B12 Deficiency
    (Pernicious Anemia)

    • Megaloblastic anemia
    • erythrocytes are large, often with oval shape
    • poikilocytosis and teardrop shaped
    • neutrophils are hypersegmented (6-10 lobes as opposed to 3-4)
  28. Microcytic/Normochromic
    Small cell size (microcytic), but normal amount of hemoglobin in the cell (normochromic)

    Causes: erythropoietin deficiency from chronic renal failure (CRF)
  29. Sickle Cell Disease
    Mutations in beta chains of hemoglobin

    When hemoglobin is deoxygenated, beta chains link togetherforming long protein rods that make the cell "sickle"

    Recessive inheritance

    Hypoxia, more likely to occur in lung/pulmonary disease, is an exacerbating factor for increased sickling and vessel occlusion


    because of its shape, it can get caught on each other and cause a log jam which would hinder the tissue on the other side from getting the blood and oxygen.

    • cold, stress, infection, physical exertion=more necessity of oxygen use
    • ________________

    Heterozygous: sickle cell trait; may not have symptoms enough to know they have it.

    Homozygous: sickle cell disease

    • Factors associated with sickling: cold, stress, physical exertion, infection, sleep, illnesses that cause hypoxia, dehydration, or acidosis
  30. Problems caused by Sickle Cell
    Sickled cells block capillaries:

    • Acute pain (the pain is horrible)
    • Infarctions cause chronic damage to liver, spleen, heart, kidneys, eyes, bones
    • Pulmonary infarction⇢acute chest syndrome
    • Cerebral infarction⇢stroke

    Sickled cells more likely to be destroyed: Jaundice


    The blood on the other side is not going where it needs to be.
  31. Fetal Hemoglobin Has No Beta Chains
    It has alpha chains and gamma chains

    This means it cannot sickle (because sickle is related to beta chains)

    Person with some fetal hemoglobin are partially protected from sickle cell disease
  32. Thalassemias
    Heterogenous group of inherited disorders caused by mutations that decrease the rate of alpha or beta-globin chains.

    Inherited as a Mendalian trait. May be heterozygous and have mild case or homozygous and have severe form. (Not sex-linked; inherited)

    Beta-thalassemia sometimes called Cooley anemia or Mediterranean anemia.

    Beta in Italians and Greeks; Alpha in Asians; both in Africans and African Americans


    Both have deficiency in hemoglobin due to decreased synthesis of the affected chain, with excess production of unaffected chain

    Results in hypochromic, microcytic anemia

    Accumulation of unaffected chain leads to problems with RBC maturation, lead to hemolysis and anemia
  33. Thalassemias

    Alpha and Beta

    Defective gene for alpha-chain synthesis

    May have 1-4 defective genes

    Affects both fetal and adult Hb

    In fetus, gamma4 Hb may form; in adult, beta4 Hb may form



    Defective gene for beta-chain synthesis

    May have 1-2 defective genes

    Affects only adult Hb

    Alpha4 Hb may form
  34. Polycythemia
    Lots (abnormal amount) of cells in blood

    Abnormally high total RBC count with hematocrit >50% (number of RBC in blood)

    Categorized as relative or absolute

    Relative (relative to amount of fluid): hematocrit rises because of loss of plasma volume without a decrease in RBCs. Causes: water deprivation; excess diuretics (promote increase of flow of water out of body), GI losses.

    Absolute (more RBC to be created): rise in hematocrit due to increase in total red cell mass; classified as primary or secondary


    • loss of plasma volume w/o decrease in RBC.
    • Everything is more concentrated⇢dehydrated
  35. Polycythemia Vera
    Primary polycythemia (polycythemia vera)

    Neoplastic disease of pluripotent cells (problem with top level in bone marrow so increase in all types of blood cells) of bone marrow.

    Absolute increase in RBC massincrease WBC; increase platelets

    Manifestations are variable

    Viscosity interferes with cardiac output and blood flow.

    Hypertension, headache, dizziness, problems with concentration, difficulty with hearing/vision

    Venous stasis (vein blood just sitting there; no movement) =dusky redness

    May have cyanosis of lips, fingernails, mucus membranes

    May have itching, pain (bc blood flow not efficient) in fingers, toes; night sweats, weight loss

    Thromboembolism (clots occur) and bleeding are problems

    Treatment: therapeutic phlebotomy (making an incision in a vein with a needle-need them to be well hydrated and pull out some of the cells) to decrease hematocrit to <42%; low-dose aspirin (prevents platelet aggregation); chemotherapy.
  36. Secondary Polycythemia
    Secondary: results from physiologic increase in level of erythropoietin

    Commonly as compensation for hypoxia

    Causes: high altitudes, chronic heart/lung disease, smoking, anabolic steroids

    May be caused by neoplasm secreting erythropoietin

    Treatment focuses on relieving hypoxia
  37. Hyperbilirubinemia in the Neonate

    Look on pg 295!!
    Increased level of serum bilirubin

    Common cause of jaundice in newborn

    Usually benign; self-limited; rarely pathological

    If remains elevated may cause kernicterus

    • Kernicterus = accumulation of unconjugated bilirubin in brain cells; serious brain injury
    • Factors that contribute to elevated bilirubin: breast-feeding, hemolytic disease in newborn, hypoxia, infections, acidosis

    Risk factors: prematurity, Asian, maternal diabetes, breast-feeding

    Treated with phototherapy or exchange transfusion (when s/sx kernicterus)

    Exposure to fluorescent light in the blue range converts bilirubin to isomer that is easily exceted in stool and urine
  38. Hemolytic Disease of the Newborn
    = Erythroblastosis fetalis

    Occurs in Rh-positve infants of Rh-negative mothers who have been sensitized

    First Rh-positive infant usually not affected

    Infants with Rh-negative blood have no antigens to react with maternal antibodies and are not affected


    After being sensitized, Rh antibodies from mother's blood are transferred to subsequent fetuses through placental circulation

    Antibodies react with red cell antigens of the Rh-postive fetus causing agglutination and hemolysis

    Results in severe anemia with compensatory hyperplasia (increased cell production) and enlargement of spleen and liver

    Liver function is impaired, decreased production of albumin causing massive edema called hydrops fetalis

    Injection of Rh immune globulin prevents sensitization in Rh-negative mothers who have given birth to Rh-positive infants if given at 28 weeks gestation and within 72 hours of birth or maternal-fetal bleeding

    After sensitization has developed immune globulin is of no value

    Hemolysis in fetuses can be treated with intrauterine transfusions; after birth with exchange transfusions
  39. Red Cell Changes in Elderly
    Anemia is common problem of elderly

    Highest prevalence in men >= 85 years old. 

    If undiagnosed/untreated, associated with > risk mortality, cardiovascular disease, self-care deficits, cognitive disorders, increased risk of fractures (<bone density)

    RBCs not replaced as quickly in elderly

    Diagnosis: exam, CBC (including reticulocyte count and index), rule out comorbidities (simultaneous presence of two chronic diseases) and problems (bleeds)

    Correct underlying cause; orally administered iron is poorly used in the elderly; may require administration of erythropoietin