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  1. the major transport system of the body for essentials such as oxygen, glucose, and other nutrients, hormones, electrolytes, and cell wastes.
  2. how blood promotes homeostasis
    blood provides a mechanism for controlling body temp by distributing core heat throughout the peripheral tissues. It is the medium through which body fluid levels and BP are measures and adjusted by various controls, i.e. hormones.
  3. hemostasis
    blood clotting or controlling bleeding
  4. pH homeostasis levels
  5. What blood constitutes of
    • ● 55% plasma, mostly water
    • ● 45% formed elements: RBCs, WBCs, platelets 
  6. hematocrit
    • ● refers to the portion of cells (essentially the RBCs in blood) and indicates the viscosity of blood.
    • ● males avg. 42-52%
    • ● females avg 37-47%
  7. an elevated hematocrit could indicate
    • ● dehydration (due to loss of fluid)
    • ● excess RBCs
  8. plasma
    the clear yellowish fluid remaining after the cells have been removed
  9. serum
    the fluid and solutes remaining after the cells and fibrinogen have been removed
  10. plasma proteins inclue
    • ●albumin, which maintains osmotic pressure in the blood
    • ●globulins or antibodies
    • ●fibrinogen, essential for formation of blood clots
  11. erythropoietin
    hormone originating from the kidney that stimulates erythrocyte production in the red b.m. in response to tissue hypoxia
  12. b.m.
    bone marrow
  13. hypoxia
    insufficient O2 available to cells
  14. Raw materials that determine availability of RBC production
    • ● amino acids
    • ● iron
    • ● vitamin B12
    • ● vitamin B6
    • ● folic acid
  15. Hemoglobin
    • ● the oxygen-carrying pigment of RBCs that gives them their red color and serves to convey oxygen to the tissues: occurs in reduced form (deoxyhemoglobin) in venous blood and in combination with oxygen (oxyhemoglobin) in arterial blood.
    • ● Symbol:  Hb
  16. what Hb consists of
    • ● the globin portion
    • ● two pairs of amino acid chains
    • ● four heme groups, each containing a ferrous iron atom to which the oxygen molecule O2 can attach
    • ● a small portion of CO2 is carried on Hb attached to N in an amino acid group apart from the O2 group, mostly as a bicarbonate ion (in the buffer group)
  17. Common Pathway
    • Referring to the steps toward an "Insoluble fibrin clot"
    • 1. Factor X→Xa ("a" for "activated") →
    • 2. Factor V→
    • 3. Platelet phospholipid→
    • 4. Prothrombin Activator→
    • 5. Prothrombin→ Thrombin→
    • 6. Fibrinogen→ Fibrin
    • 7. XIII→
    • 8. Insoluble fibrin clot!
  18. Three steps toward Hemostasis
    • 1. Vasoconstriction or spasm: immediate response in order to decrease blood flow and create smaller clotting area
    • 2. Thrombocytes/platelets tend to adhere to underlying tissue at the site of injury, and if small enough, a platelet plug is formed
    • 3. Coagulation required for larger blood vessels.
  19. Fibrinolysis
    The breakdown of fibrin, usually by the enzymatic action of plasmin.
  20. agglutination
    the clumping of bacteria, red blood cells, or other cells, due to the introduction of an antibody.
  21. agglutinogen
    an antigen that causes the production of agglutinins.
  22. agglutigin
    an antibody that causes agglutination.
  23. antigens
  24. -penia
    a combining form used in the formation of compound words that have the general sense “lack, deficiency,” as specified by the initial element: leukopenia.
  25. -osis
    a suffix occurring in nouns that denote actions, conditions, or states (hypnosis; leukocytosis; osmosis), especially disorders or abnormal states (chlorosis; neurofibromatosis; tuberculosis).
  26. dyspnea
    difficult or labored breathing.
  27. tachycardia
    rapid heart beat
  28. stomatitis
    inflammation of the mouth caused by ulcers in the oral mucosa
  29. anemia
    a quantitative deficiency of the hemoglobin, often accompanied by a reduced number of red blood cells and causing pallor, weakness, dyspnea, and tachycardia.
  30. anemic compensatory mechanisms
    • include:
    • tachycardia
    • peripheral vasoconstriction→ pallor
  31. Signs of anemia
    • • fatigue, pallor, dyspnea, tachycardia
    • • stomatitis, inflamed and cracked lips, dysphagia, due to decreased regeneration of epithelial cells; glossitis
    • • angina, congestive heart failure, due to lack of oxygen to the heart
  32. causes of anemia
    • 1. deficiency of a required nutrient
    • 2. bone marrow function is impaired
    • 3. blood loss or excessive destruction of RBCs
  33. anemias may be classified by:
    morphology or etiology
  34. Iron Deficiency Anemia
    • • form of anemia where iron impedes the synthesis of Hb, thereby reducing the amount of oxygen trasnported in the blood
    • • results in microcytic and hypochromic RBCs
    • • very common in all age groups
    • • frequently a sign of an underlying problem
    • • reduction in stored iron, as indicated by decreased serum ferritin, hemosiderin, and decreased iron-containing histiocytes in bone marrow
  35. microcytic
    small cell
  36. hypochromic
    less color
  37. Etiology of iron-deficiency anemia
    • • low dietary intake of iron, esp. during adolescence's growth spurts, pregnancy and breast feeding.
    • • chronic blood loss from a bleeding ulcer, hemorrhoids, cancer, or menorrhagia
    • • impairment of duodenal absorption of iron, including malabsorption syndromes i.e. regional ileitis and achlorhydria
    • • severe liver disease
    • • infections and cancers
  38. why low iron-diet might cause iron-deficiency anema
    Normally only 5-10% of ingested iron is absorbed but during deficit of iron it could be 20%. Growth spurts require more iron for new tissue formation, pregnancy requires more iron for fetus, breast-feeding requires iron for milk.
  39. why chronic blood loss can cause i.d.anemia
    Continuous blood loss, even if small amounts, means that less iron is recycled to maintain an adequate production of Hb.
  40. menorrhagia
    Abnormally heavy or extended menstrual flow.
  41. ileitis
    Inflammation of the ileum
  42. achlorhydria
    • • an abnormal deficiency or absence of free hydrochloric acid in the gastric juice; often associated with severe anemias and cancer of the stomach
    • • interferes with the early digestion of protein in the stomach and with the absoption or iron; may lead to iron-deficiency anemia
  43. syncope
  44. glossitis
    Inflammation of the tongue
  45. diagnostic tests for i.d.anemia
    • • lab tests demonstrate low values for Hb, hematocrit, mean corpuscular volume (MCV) and mean corpuscular Hb, serum ferritin and serum iron, and transferrin saturation
    • • on microscope RBCs appear hypochromic and microcytic
  46. mean corpuscular volume
    • • AKA mean cell volume
    • • a measure of the average red blood cell size that is reported as part of a standard complete blood count
  47. mean corpuscular hemoglobin
    • • aka mean cell hemoglobin
    • • the average mass of hemoglobin per red blood cell in a sample of blood.
  48. treatment for i.d. anemia
    • • underlying cause must be identified and resolved
    • • iron-rich foods may be given
    • • iron supplements with food to reduce gastric irritation and nausea
  49. Megaloblastic Anemias
    • • include Pernicious Anemia, a Vitamin B12 Deficiency
    • • characterized by very large, immature, nucleated RBCs
    • • usually results from gradual development of deficit of folic acid (vit. B6) or vit. B12 (cyanocobalamin)
  50. Pathophysiology of pernicios anemia
    • • the common form of megaloblastic anemia
    • • caused by the malabsorption of vitamin B12 owing to a lack of intrinsic factor (IF) produced in the glands of the gastric mucosa
    • • additional problem occurs with the atrophy of the muscusa because the parietal cells can no longer produce HCl→ achlorhydria→iron-deficiency anemia
  51. effects of a deficit of vitamin b12
    • • deficit leads to impared maturation of RBCs owing to interference of DNA synthesis
    • • the RBCs are very large (megaloblasts or macrocytes) and still contain a nuclei
    • • macrocytes are destroyed prematurely, resulting in anemia
    • • often the maturation of granulocytes is affected, resulting in abnormally large hypersegmented neutrophils
    • • thrombocyte levels may be low
    • • demyelination of the peripheral nerves and eventually the spinal cord, which could be irreversible; sensory fibers first, followed by motor
    • • the hemoglobin of the RBCs is normal and still capable of transporting O2
  52. Etiology of pernicious anemia
    • • dietary insufficiency rarely a cause because small amounts of Vitamin B12 is required
    • • most common cause is malabsorption, which may result from an autoimmune reaction, esp. older ppl; from gastritis; or ileitis
    • • outcome of a surgery such as gastrectomy in which parietal cells are removed, or resection of the ileum, the site of absorption.
  53. gastritis
    • • Chronic or acute inflammation of the stomach, especially of the mucous membrane of the stomach
    • • causes atrophy of the gastric mucosa
  54. signs and symptoms of pernicious anemia
    • 1. tongue is typically enlarged, red, sore, and shiny
    • 2. the decrease in gastric acid leads to digestive discomfort, often with nausea and diarrhea
    • 3. neurologic effects include paresthesia in the extremities or loss of coordination and ataxia
  55. paresthesia
    A skin sensation, such as burning, prickling, itching, or tingling, with no apparent physical cause
  56. ataxia
    Loss of the ability to coordinate muscular movement.
  57. diagnostic tests for pernicious anemia
    • • erythrocytes appear macrocytic or megaloblastic
    • • bone marrow is hyperactive, with increased number of megaloblasts
    • • vitamin b12 serum levels are low
    • • Schilling's test, a radioactive vit. b12 is used to measure absoprtion
    • • presence of hypochlorhydria or achlorhydria confirms gastric atrophy
  58. treatment of pernicious anemia
    • • oral supplements
    • • vit. b12 injections
  59. Pathophysiology of Aplastic Anemia
    • • results from impairment or failure of bone marrow, leading to loss of stem cells and pancytopenia
    • • b.m. exhibits reduced cell components and increased fatty tissue
  60. etiology of aplastic anemia
    • • in aprox. half the cases, patients are middle-aged and the cause is idiopathic
    • • myelotoxins, such as radiation, industrial chemicals, and drugs (chloramphenicol, etc.) may damage bone marrow such as in cases of chemotherapy.
    • • viruses, particularly Hep. C
    • • autoimmune disease such as lupus erythromatosus (SLE)
    • • genetic abnormalities such as myelodysplastic syndrome
  61. signs and symptoms of aplastic anemia
    • Onset is insidious
    • 1. anemia (same signs, pallor, etc.)
    • 2. leukopenia resulting in recurrent or multiple infections
    • 3. thrombocytopenia (petechiae) and a tendency to bleed excessively esp in the mouth.
  62. thrombocytopenia
    An abnormal decrease in the number of platelets in circulatory blood
  63. diagnostic tests for aplastic anemia
    • • blood count indicates pancytopenia
    • • bone marrow biopsy to confirm
    • • RBCs appear normal
  64. treatment for aplastic anemia
    bone marrow transfusion
  65. hemolytic anemia
    • • result from excessive destruction of RBCs, leading to low erythrocyte and hemoglobin count.
    • • causes include genetic defects, immune reactions, infections, transfusion reactions, erythroblastosis fetalis.
    • • examples are Sickle Cell Anemia and Thalassemia
  66. pathophysiology of sickle cell anemia
    • • An abnormal, rigid, crescent-shaped red blood cell that results from a single change in the amino acid sequence of the cell's hemoglobin, which causes the cell to contort, especially under low-oxygen conditions.
    • • complications stem from the rigidity of the RBCs, resulting in thrombus formation and multiple infarctions throughout the body, affecting brain, bones, or organs.
    • • oxygen content is gradually reduced, leading to repeated instances of infarctions
    • • high rate of hemolyusis leads to hyperbilirubinemia, jaundice, and gallstones.
  67. etiology of sickle cell anemia
    • • gene for HbS is recessive and common in individuals from Africa and the Middle East
    • • homozygotes result in clinical signs of sickle cell anemia
    • • heterozygotes result in sick cell trait
    • 1 in 12 African Americans carry the trait; 1 in 600 have sickle cell anemia
  68. signs and symptoms of sickle cell anemia
    • • same as any anemia
    • • hyperbilirubinemia indicated by jaundice; may cause gallstones
    • • splenomegaly
    • • periodic painful crisis due to multiple infarctions
    • • growth and development are delayed, including late tooth eruption
    • • congestive heart failur
    • • frequent infections because of damaged spleen
  69. diagnostic tests for sickle cell anemia
    blood test can be performed because of it's genetic nature
  70. treatment of sickle cell anemia
    • • use of hydroxyurea has reduced the frequency of crisis but not effective for all patients
    • • dietary supplementation with folic acid
    • • avoidance of strenous activity and high altitudes
    • • bone marrow transplants
  71. Pathophysiology of Thalassemia
    • • results from a genetic defect in which one or more genes for Hb are missing or vaiant. When two genes are involved the condition is moderate to severe.
    • • This abnormality interferes with the production of the globin chains, and therefore the amount of Hb synthesized and number of RBCs is reduced.
    • • Normally there should be two alpha and two beta globin chains, but with this condition if one alpha chain is missing, a beta will take its place, causing hemolysis and anemia.
    • • in severe cases, increased hemolysis of RBCs causes splenomegaly, hepatomegaly, and hyperbilirubinemia + a hyperactive b.m. to compensate.
  72. signs and symptoms of thalessemia
    • • usual anemic signs and symptoms
    • • child growth impaired due to hypoxia and consequently fatigue and inactivity
  73. diagnostic tests for thalassemia
    • • RBCS are microcytic and hypochromic
    • • often there's an iron overload
  74. treatment for thalassemia
    • • blood transfusions and folate
    • • b.m. transplants helpful in children
  75. primary polycythemia
    • • aka polycythemia vera
    • • a condition in which there is an increased production of erythrocytes and other cells in the b.m.
    • • considered a neoplastic disorder
    • • serum erythropoietin levels are low
  76. secondary polycythemia
    • • aka erythrocytosis
    • • an increase in RBCs that occurs in response to prolonged hypoxia and increased erythropoitin secretion
    • • the increase in RBCs not as marked as in polycythemia vera
    • • more reticulocytes appear in the peripheral blood
  77. pathophysiology of polycythemia vera
    • • marked increase in erythrocytes and in granulocytes and thrombocytes, resulting in increased blood volume and viscosity
    • • BVs are distended and blood flow is sluggish→frequent thromboses and infarctions throughout the body, esp. when platelet counts are high
    • • BP is elevated and the heart hypertrophied
    • • hemorrhaging frequent in places where BVs are distended
    • • spleen and liver are congested and enlarged
    • • bone marrow is hypercellular and in some cases becomes fibrotic→ hematopoisis moves to spleen→ anemia.
    • • in some cases acute myeloblastic leukemia develops in later stages, esp. with use of chemotherapy
  78. etiology of polycythemia vera
    • • neoplastic disorder of unknown origin
    • • commonly develops between ages of 40-60 years of age
  79. etiology of secondary polycythemia
    • • may be a compensation mechanism intended to provide increased O2 transport bc of chronic lung disease, heart disease, or living at high altitudes
    • • some cases can result in erythropoitin secreting tumors
  80. signs and symptoms of polycythemia
    • • patient appears plethoric and cyanotic because of engorged BVs and sluggish blood flow
    • • hepatomegaly and splenomegaly
    • • pruritis
    • • BP goes up, pulse is full and bounding
    • • dyspnea, headache, or visual disturbances
    • • CHFbc of the increased work load
    • • high levels of uric acid→ joint pain
Card Set
Pathophysiology, Barbara E. Gould, Ruthana M. Dyer.
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