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For Test 3

Quiz yourself by thinking what should be in each of the black spaces below before clicking on it to display the answer.
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Question
Answer
Pathophysiological causes of anemia   Blood loss, decreased RBC production, increased RBC destruction  
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Signs and symptoms of anemia   Tired, loss of breath, pale in color, low BP, slight fever, some edema  
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Hemoglobin concentration, hematocrit, and RBC counts all decreased   Quantitative measures  
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Two types of Blood Loss Anemia   Acute and Chronic  
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Loss of 20% or more of blood due to traumatic condition   Acute Blood Loss Anemia causes  
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Shock and cardiovascular problems, does not produce immediate anemia   Results of Acute Blood Loss Anemia  
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Decrease of hematocrit, hemoglobin, RBC, platelet levels, and left shift of WBC   Acute Blood Loss Anemia clinical findings  
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Healthy people: normocytic normochromic cells, 3-5 days later macrocytosis will be seen   Acute Blood Loss Anemia microscope observations  
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Disorders of the GI tract, heavy menstruation, urinary tract abnormalities   Chronic Blood Loss Anemia causes  
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Continual loss of blood and usually leads to iron deficiency anemia   Chronic Blood Loss Anemia  
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Normal or slightly elevated retics, normal or slightly decreased WBC and platelets   Chronic Blood Loss clinical findings  
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Hypochromic microcytic cells   Chronic Blood Loss microscopic observations  
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Hypoproliferative disorder of pluripotential or erthroid committee stem cells   Aplastic Anemia  
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Failure to produce RBC, WBC, and megakaryocytes, CD34 cell population   Aplastic Anemia causes  
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Idiopathic, constitutional, iatrogenic, infection   Forms of Aplastic Anemia  
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Sudden appearance, immune process involving antibodies against stem cells and cellular immune mechanism   Aplastic Anemia pathophysiology  
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Phases of Aplastic Anemia   Onset, recovery, and late disease  
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Total bone marrow failure, high risk for malignant diseases or hemo disorders   Aplastic Anemia features  
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Pancytopenia, decreased granulocytes, platelets, and retics   Aplastic Anemia clinical findings  
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Deficient production of all blood types   Pancytopenia  
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Normocytic normochromic cells, few erythroid, myeloid, and megakaryocytes in bone marrow   Aplastic Anemia microscopic findings  
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Immunosuppressant therapy (transplant rejection drugs)   Aplastic Anemia treatment  
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Congenital form of Aplastic anemia   Fanconi's Anemia  
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Low birth weight, skin hyperpigmentation, skeletal disorders, may include mental retardation   Fanconi's Anemia symptoms  
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Progressive pancytopenia, low hemoglobin level   Fanconi's Anemia clinical findings  
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DNA test that determines abnormalities pre and post-natally with Fanconi's Anemia   HLA typing  
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Bone marrow transplant with steroids and androgens, recombinant granulocyte colony-stimulating factor   Fanconi's Anemia treatment  
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Subset of Fanconi's Anemia that's diagnosed 1-77 years old   Familial Aplastic Anemia  
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Pancytopenia, hypocellular bone marrow, no major development anomalies seen   Familial Aplastic Anemia clinical findings  
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Congenital, acquired chronic, acute   Pure Red Cell Aplasia causes  
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Selective failure of RBC production, WBC and platelets normal   Acquired Pure Red Cell Aplasia  
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Associated with drugs, collagen vascular and lympho-proliferative disorders   Chronic Pure Red Cell Aplasia  
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Congenital hypoplastic anemia, slow progressive and refractory anemia   Diamond-Blackfan Syndrome causes  
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Normal WBC and platelets   Diamond-Blackfan Syndrome clinical findings  
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Diamond-Blackfan Syndrome severe cases   RBC normochromic and slight macrocytic  
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Occurs in healthy children <8 years, previous viral infection common Transient   Erythroblastopenia of Childhood  
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Moderate to severe normocytic anemia, severe reticulocytopenia   Transient Erythroblastopenia clinical finding  
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Abnormality of erythropoiesis production, contains multinuclear erythroblasts   Congenital Dyseryhropoietic Anemia  
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Congenital Dyseryhropoietic Anemia most common type   Type 2  
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Decreased hemoglobin, hematocrit, and RBC, decreased WBC and platelets if all cell lines involved   Congenital Dyseryhropoietic Anemia clinical findings  
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Happens after body's iron stores depleted, most frequently occurring type of anemia   Iron Deficiency Anemia  
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Nutritional deficiency, fault/incomplete iron absorption, pregnancy, excessive blood loss   4 causes of Iron Deficiency Anemia  
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Average adult needs 3.5-5.0 g, more if pregnant or lactating   Iron requirements  
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Used for oxygen binding and biochemical reactions   Operational iron  
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2 types of dietary iron   Iron salts and heme iron  
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Non-heme iron, variable absorbtion   Iron salts  
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Mainly from hemoglobin and myoglobin in meat, readily absorbed   Heme iron  
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Fe2+ 5-10% absorbed of total dietary intake, absorbed iron attaches to transferrin   Iron absorption  
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Increased brain blood flow, reversible fontanels bulging in infants, craving things like wood, ice, chalk, or dirt   Iron Deficiency Anemia signs and symptoms  
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Hemoglobin, hematocrit, MCV, MCH, MCHC, retics, and ferritin levels all decreased, serum iron and transferrin saturation significantly decreased   Iron Deficiency Anemia clinical findings  
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Results from illness and not related to nutrition   Anemia of Inflammation or Chronic Disorders  
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Hemocrit fixed at 28-32% range, hemoglobin normal to decreased   Anemia of Inflammation or Chronic Disorders clinical findings  
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Normocytic normochromic mostly, hypochromic microcytic in 1/3-1/4 of cases   Anemia of Inflammation or Chronic Disorders microscopic findings  
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Also known as anemia of iron overload   Sideroblastic Anemia  
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Congenital and acquired defect, malignant marrow disorders, secondary to drugs, toxins   Sideroblastic Anemia causes  
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Sideroblastic Anemia clinical findings   Severe anemia  
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Hypochromic microcytic cells, target cells, basophilic stippling, dimorphic populations   Sideroblastic Anemia microscopic findings  
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May require blood transfusions   Sideroblastic Anemia treatment  
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2 categories of Megaloblastic Anemias   Vitamin B12 deficiencies and folic acid deficiencies  
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Megaloblastic Anemias types   Acquired (most common) and congenital  
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Measurement of Vitamin B12 or folic acid levels   Diagnosis for Megaloblastic Anemias  
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Parasitic infection, malabsorption syndrome, nutritional deficiencies of B12, Pernicious anemia   Vitamin B12 Deficiencies causes  
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Abnormal absorption, pregnancy, alcohol   Folic Acid Deficiencies causes  
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Most common megaloblastic anemia, can be asymptomatic 20-30 years before appearing   Pernicious Anemia  
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Lemon-yellow skin color, mouth corner cracking, painful tongue, tiredness, heart failure   Megaloblastic Anemia signs and symptoms  
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When one factor is missing and development of RBC is impacted   Megaloblastic dyspoiesis  
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Intrinsic factor, Transcobalamin II, R-proteins   Proteins that bind Vitamin B12  
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Binds to dietary Vitamin B12 and forms Vitamin B12-IF complex   Intrinsic factor  
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Receptor and principle carrier of B12 to liver and tissues   Transcobalamin II  
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Bind cobalamin with various cobalamin analogues   R-proteins  
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Reduced to methyl tetrahydrofolate and delivered to the tissues, methyl released to combine with homocyteine which coverts to an amino acid   Folic acid metabolism  
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Deficiencies in TCII   Can produce a vitamin deficiency  
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Hemoglobin and RBC levels very low, MCV and MCH increased, retics less than 1%, platelets decreased   Megaloblastic Anemia clinical findings  
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Significant anisocytosis and poiklocytosis, macrocytes and ovalocytes, cabot rings, Howell-Jolly bodies, basophilic stippling, neutropenia   Megaloblastic Anemia microscopic findings  
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Tests for evidence of impaired Vitamin B12 absorption   Shilling Test  
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Shilling Test indicates >10% Cbl excretion indicated lack of IF production   Pernicious Anemia after step 2  
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Shilling Test indicates low excreted amounts of Cbl at 2nd step   Abnormal intestinal absorption after step 2  
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Monthly injection of intramuscular B12 for deficiency   Treatment for Megaloblastic Anemia  
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Increased RCB destruction, bone marrow fails to increase RBC production   Hemolytic Anemia  
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Hemolytic Anemia where there is alteration in the RBC membrane   Inherited or acquired  
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Sites of hemolysis in Hemolytic Anemia   Intravascular or extravascular  
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Defects in basic membrane structure, hereditary spherocytosis, abnormality of membrane protein Ankyrin   Inherited Hemolytic Anemia  
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Assesses defects in the phospholipid bilayer of the RBC membrane   Osmotic Fragility Test  
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Heterogeneous group of inborn disorder where there is an overabundance of RBC   Hereditary Elliptocytosis  
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Rare autosomal recessive disorder seen mainly in Afro-Americans, severe anemia   Hereditary Pyropoikilocytosis  
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Genetic hemoglobin defects, Thalassemia, lead poisoning, and stem cells are seen   Hereditary Stomatocytosis  
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Permeability disorder which causes net loss of K+ with budding, fragments, and microspherocytes   Hereditary Xerocytosis  
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Rare hereditary disorder with mild chronic anemia and stomatocytes & spherocytes, hgb levels 11-13g/dL   Rh null Disease - Rh deficiency syndrome  
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Dense contracted or spherical RBC with spiny projections with causes mild anemia in adults   Acanthocytosis  
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Form of Acanthocytosis found in people with alcoholic cirrhosis, hgb 5-7g/dL, retics 10-20%   Spur Cell Hemolytic Anemia  
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Associated with Acanthocytosis in peripheral blood that is a neurodegenerative disorder   Neuroacanthocytosis  
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Deficiencies in G6PD-Glucose-Phosphate Dehydrogenase, Pyruvate Kinase, and Methemoglobin Reductase   Erythrocytic Enzyme Defects  
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Results in acute hemolysis of RBC and hemolytic anemia, may be caused by a severe burn or trauma   Acquired Hemolytic Anemia  
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Chemicals, drugs, venom, infectious microorganisms, and immune mechanisms   Causes intravascular hemolysis  
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Mediated by IgG warm antibodies, complement and IgM cold antibodies, patients may also have systemic lupus erythematosus   Warm & Cold - type Autoimmune Hemolytic Anemia  
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Following the administration of drugs   Drug Induced Immune Hemolytic Anemia  
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Optimally activated at 4C and can cause intravascular or extravascular hemolysis   Cold Autoimmune Hemolytic Anemia  
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Hallmark of hemolytic anemia seen in peripheral blood smear   Spherocytes  
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Clonal acquired hematopoietic stem cell disorder that causes intermittent, sleep associated blood in the urine   Paroxysmal Nocturnal Hemogloburia  
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Hemoglobin <6g/dL, hypochromic microcytic cells   Paroxysmal Nocturnal Hemogloburia clinical findings  
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Blood transfusion, antibiotics, and anticoagulants   Treatment for Paroxysmal Nocturnal Hemogloburia  
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Antibody attaches to RBC in cool temps, complement activates at warm temps which cause biphasic hemolysis   Paroxysmal Cold Hemogloburia  
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