For Test 3
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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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