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63 Cards in this Set
- Front
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Blood Vessels
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Arteries—arterioles Transport blood away from heart Veins—venules Return blood back to the heart Capillaries Microcirculation within tissues Systemic circulation Exchange of gases, nutrients, and wastes intissues Pulmonary circulation Gas exchange in lungs |
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Histology of Arteries and Veins
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Tunica intima—endothelium (simplesquamous epithelium) Tunica media—middle layer, mostly smoothmuscle Tunica adventitia (externa)—connectivetissue with fibrocytes, collagen (type I), andelastic fibers |
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Composition of Blood
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Plasma Plasma proteins Cellular component Erythrocytes Leukocytes Thrombocytes (platelets) deffence system! avrg human has 4-5L of blood pg 186* |
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Erythrocytes
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(Red Blood Cells) Biconcave flexible discs No nucleus in mature state Contains hemoglobin Globin portion Heme group Life span—120 days Erythropoietin produced in the kidney stimulates erythrocyte production. |
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Hematopoiesis |
the process of making blood cells Hematopoiesisstem cell; can become any kind of blood cell |
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Blood Clotting—Hemostasis
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Three steps: Vasoconstriction or vascular spasm after injury Platelet clot Coagulation mechanism *Plasmin will eventually break down the bloodclot. |
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Blood Typing
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Blood typing is based on antigens in the plasmamembrane of the erythrocytes. ABO system Based on the presence or absence of specificantigens Antibodies in the blood plasma |
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Rh system
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Antigen D in plasma membrane: Rh+ Absence of antigen D: Rh
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Diagnostic Tests
< Complete blood count (CBC) Differential count for WBCs > |
-Includes total red blood cells (RBCs), white bloodcells (WBCs), and platelets -Leukocytosis (increased WBCs) • Associated with inflammation or infection Leukopenia (decreased WBCs) • Associated with some viral infections, radiation,chemotherapy Increased eosinophils • Common in allergic responses -Increased eosinophils • Common in allergic responses -Differential count for WBCs |
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Diagnostic Tests :Morphology |
Observed with blood smears Shows size, shape, uniformity, maturity of cells• Different types of anemia can be distinguished. |
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Diagnostic Tests :Hematocrit |
Percent by volume of cellular elements in blood |
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Diagnostic Tests:Hemoglobin |
-Amount of hemoglobin per unit volume of blood -Mean corpuscular volume (MCV) • Indicates the oxygen-carrying capacity of blood |
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Diagnostic Tests : Reticulocyte count |
Assessment of bone marrow function |
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Diagnostic Tests :Chemical analysis |
Determines serum levels of components, such as iron,vitamin B12, folic acid, cholesterol, urea, glucose |
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Diagnostic Tests : Bleeding time |
Measures platelet function |
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Diagnostic Tests < Prothrombin time (PT) and partial thromboplastin time (PTT) > |
-Measure function of various factors in coagulation process -International normalized ratio (INR) is a standardizedversion. |
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blood therapies Whole blood, packed red blood cells, packed platelets |
For severe anemia or thrombocytopenia |
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blood therapies Plasma or colloid volume-expanding solutions |
To maintain blood volume (will increase ossmois) |
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blood therapies Artificial blood products |
Compatible with all blood types None of them can perform all the complex functions of normal whole blood. |
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Epoetin alfa |
-Artificial form of erythropoietin • Before certain surgical procedures • Anemia related to cancer • Chronic renal failure |
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Bone marrow or stem cell transplantation |
-Close tissue match necessary • Treatment of some cancers • Severe immunodeficiency • Severe blood cell diseases |
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Drug treatment Aids |
in the clotting process |
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Anemia
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causes a reduction in oxygen transport. Basic problem is hemoglobin deficit |
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Oxygen deficit leads to:
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Less energy production in all cells • Cell metabolism and reproduction diminished Compensation mechanisms • Tachycardia and peripheral vasoconstriction General signs of anemia • Fatigue, pallor (pale face), dyspnea, tachycardia |
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Oxygen deficit leads to CONT! |
Decreased regeneration of epithelial cells • Digestive tract becomes inflamed and ulcerated, leading to stomatitis • Inflamed and cracked lips • Dysphasia • Hair and skin may show degenerative changes. Severe anemia may lead to angina or congestive heart failure (CHF) |
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Iron Deficiency Anemia
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-Insufficient iron impairs hemoglobin synthesis. Microcytic, hypochromic RBCs • Result of low hemoglobin concentration in cells -Very common •Ranges from mild to severe •Occurs in all age groups, but more common in women of childbearing age (d/t menstration) -Estimated that one in five women is affected • Proportion increases for pregnant women Frequently sign of an underlying problem |
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Iron Deficiency Anemia: Causes
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-Dietary intake of iron below minimum requirement -Chronic blood loss: As from bleeding, ulcer, hemorrhoids, cancer Impaired duodenal absorption of iron In many disorders, malabsorption syndromes -Severe liver disease May affect iron absorption as well as storage |
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Iron Deficiency Anemia: Signs and Symptoms
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-Pallor of skin and mucous membranes -Fatigue, lethargy, cold intolerance -Irritability - (CNC response * ASK) -Degenerative changes -Stomatitis and glossitis -Menstrual irregularities -Delayed healing -Tachycardia, heart palpitations, dyspnea, syncope |
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Pernicious Anemia: Vitamin B12 Deficiency
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Basic problem is lack of absorption of vitamin B12 because of lack of intrinsic factor ~ Intrinsic factor secreted by gastric mucosa ~ Required for intestinal absorption of vitamin B12 Characterized by very large, immature, nucleated erythrocytes Carry less hemoglobin Shorter life span ( reg is 120 days) |
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Pernicious Anemia: Vitamin B12 Deficiency (Cont.)
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Dietary insufficiency is very rarely a cause. Genetic factors have been implicated. ~More common in light-skinned women of northern European ancestry Often accompanies chronic gastritis May also be an outcome of gastric surgery |
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Vitamin B12 and Nerve Cells
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-Vitamin B12 is needed for the function and maintenance of neurons. -Significant deficit of the vitamin will cause symptoms in the peripheral nerves. -These may be reversible. |
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Pernicious Anemia: Vitamin B12 Deficiency (Cont.) Manifestations in addition to those typical for anemias + plus
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Tongue is typically enlarged, red, sore, and shiny. Digestive discomfort, often with nausea and diarrhea Feeling of pins and needles, tingling in limbs |
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Diagnostic tests for pernicious anemia
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-Microscopic examination (erythrocytes) -Bone marrow examination (hyperactive) -Vitamin B12 serum levels below normal -Presence of hypochlorhydria or achlorhydria •Presence of gastric atrophy |
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Aplastic Anemia
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Impairment or failure of bone marrow -May be temporary or permanent -Often idiopathic but possible causes include: Myelotoxins • Radiation, industrial chemicals, drugs Viruses • Particularly hepatitis C Genetic abnormalities • Myelodysplastic syndrome • Fanconi’s anemia Blood counts indicate pancytopenia. Anemia, leukopenia, thrombocytopenia Bone marrow biopsy may be required. Erythrocytes often appear normal. Identification of cause and prompt treatment needed for bone marrow recovery Removal of any bone marrow suppressants Failure to identify cause and treat effectively is life-threatening! |
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Hemolytic Anemia |
Results from excessive destruction of RBCs
Causes Genetic defects Immune reactions Changes in blood chemistry Infections such as malaria Toxins in the blood Antigen-antibody reactions • Incompatible blood trans *CBC's, hematocrit, hemoglobin: would be lower. |
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Sickle Cell Anemia
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Genetic condition Autosomal Incomplete dominance Anemia occurs in homozygous recessive. Diagnostic testing is available. More common in individuals of African ancestry• Heterozygous condition is somewhat protective againstmalaria.• One in ten African Americans is heterozygous for thetrait. |
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Sickle Cell Anemia (Cont.)
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Abnormal hemoglobin (HbS) Sickle cell crisis occurs whenever oxygenlevels are lowered. Altered hemoglobin is unstable and changesshape in hypoxemia. Sickle-shaped cells are too large to passthrough the microcirculation. Obstruction leads to multiple infarctions andareas of necrosis. |
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Sickle Cell Anemia (Cont.)
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Multiple infarctions affect brain, bones,organs In addition to basic anemia: Hyperbilirubinemia, jaundice, gallstones• Caused by high rate of hemolysis Clinical signs Do not usually appear until the child is about 12months old |
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Sickle Cell Anemia: Signs and Symptoms
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Severe pain because of ischemia of tissues andinfarction Pallor, weakness, tachycardia, dyspnea Hyperbilirubinemia—jaundice Splenomegaly Vascular occlusions and infarctions In lungs• Acute chest syndrome Smaller blood vessels• Hand-foot syndrome Delay of growth and development Congestive heart failure |
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Sickle Cell Anemia - Diagnostic tests
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Blood test• Hemoglobin electrophoresis Prenatal DNA analysis |
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Sickle Cell Anemia - Treatment |
Hydroxyurea has reduced the frequency of this crisis. Dietary supplementation with folic acid Bone marrow transplantation Immunization in children • Against pneumonia, influenza, meningitis
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Polycythemia
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Primary polycythemia—polycythemia vera - Increased production of erythrocytes and othercells in the bone marrow - Neoplastic disorder - Serum erythropoietin levels are low. Secondary polycythemia—erythrocytosis - Increase in RBCs in response to prolongedhypoxia - Increased erythropoietin secretion - Compensation mechanism to provide increasedoxygen transport |
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Polycythemia: Signs and Symptoms
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Distended blood vessels, sluggish blood flow Increased blood pressure Hypertrophied heart (inlarged) Hepatomegaly Splenomegaly Dyspnea Headaches Visual disturbances Thromboses and infarctions |
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Polycythemia - Diagnostic tests
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Increased cell counts Increased hemoglobin and hematocrit values Hypercellular bone marrow Hyperuricemia (higher acid in urine) |
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Polycythemia - Treatment |
Identify cause
Drugs or radiation • Suppression of bone marrow activity Periodic phlebotomy (taking lots of blood) |
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Indications of Blood-Clotting Disorders
***measuments** |
Persistent bleeding from gums Repeated epistaxis Petechiae - Pinpoint, flat, red spots on skin and mucousmembrane Frequent purpura and ecchymosis More than normal bleeding in trauma Bleeding into joint—hemarthroses Swollen, red, painful Hemoptysis |
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Blood-Clotting Disorders
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Hematemesis - Coarse brown particles (coffee ground emesis) Blood in feces - Black or occult Anemia Feeling faint and anxious Low blood pressure Rapid pulse |
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Hemophilia A
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Classic hemophilia - Deficit or abnormality of factor VIII Most common inherited clotting disorder - X-linked recessive trait - Manifested in men, carried by women Varying degrees of severity Prolonged bleeding after minor tissue trauma Spontaneous bleeding into joints Possible hematuria or blood in feces |
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Hemophilia A - Diagnostic tests |
Bleeding time and PT normal PTT, activated PTT (aPTT), coagulation timeprolonged Serum levels of factor VIII are low. |
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Hemophilia A - Treatment |
Desmopressin (DDAVP) Replacement therapy for factor VIII |
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Von Willebrand’s Disease
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Most common hereditary clotting disorder Three major types |
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Von Willebrands Disease - Signs and symptoms include:
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Skin rashes Frequent nosebleeds Easy bruising Bleeding of gums Abnormal menstrual bleeding
Treatment based on type and severity |
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Disseminated Intravascular Coagulation
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Involves both excessive bleeding and clotting Excessive clotting in circulation Thrombi and infarcts occur. Clotting factors are reduced to a dangerous level. Widespread, uncontrollable hemorrhage results. Very poor prognosis, with high fatality rate Complication of many primary problems Obstetrical complications, such as abruptio placentae Infections Carcinomas Major trauma |
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Thrombophilia
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Group of inherited or acquired disorders Risk of abnormal clots in veins or arteries Blood testing for clotting factor levels andabnormal antibody levels Causative condition should be treated. |
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Myelodysplastic Syndromes
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Diseases that involve inadequate productionof cells by the bone marrow Signs and symptoms include anemia;dependent on type of deficiencies that occur May be idiopathic or occur afterchemotherapy or radiation treatment Treatment measures depend on deficiencytype. - Transfusion replacement - Chelation therapy to reduce iron overload - Bone marrow transplantation |
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The Leukemias
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Group of neoplastic disorders involving white bloodcells Uncontrolled WBC production in bone or lymphnodes Other hemopoietic tissues are reduced. One or more types of leukocytes are undifferentiated,immature, and nonfunctional. Large numbers released into general circulation Infiltrate lymph nodes, spleen, liver, brain, otherorgans |
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Acute leukemias (ALL and AML)
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- High proportion of immature nonfunctional cells inbone marrow and peripheral circulatio - Onset usually abrupt , marked signs ofcomplications• Occurs primarily in children and younger adults |
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Chronic leukemias (CLL and CML)
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Higher proportion of mature cells
Insidious onset Mild signs and better prognosis • Common in older adults |
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Signs and Symptoms of Acute Leukemia
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Usual signs at onset -Frequent or uncontrolled infections -Petechiae and purpura -Signs of anemia ~Severe and steady bone pain ~Weight loss, fatigue, possible fever ~Enlarged lymph nodes, spleen, liver ~Headache, visual disturbances, drowsiness,vomiting |
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The Leukemias - Diagnostic tests
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Peripheral blood smears• Immature leukocytes and altered numbers of WBCs• Numbers of RBCs and platelets decreased• Bone marrow biopsy for confirmation |
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The Leukemias - Treatment
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Chemotherapy ALL in young children responds well to drugs Biological therapy (interferon)• May be used to stimulate the immune system |
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Complications of Leukemia
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-Opportunistic infections, including pneumonia -Sepsis -Congestive heart failure -Hemorrhage -Liver failure -Renal failure -CNS depression and coma |
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Multiple Myeloma
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-Neoplastic disease that involves increasedproduction of plasma cells in bone marrow -Unknown cause -Occurs in older adults -Production of other blood cells is impaired -Multiple tumors in bone -Loss of bone -Severe bone pain -Prognosis poor, with short life expectancy |