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For Test 3

Pathophysiological causes of anemia Blood loss, decreased RBC production, increased RBC destruction
Signs and symptoms of anemia Tired, loss of breath, pale in color, low BP, slight fever, some edema
Hemoglobin concentration, hematocrit, and RBC counts all decreased Quantitative measures
Two types of Blood Loss Anemia Acute and Chronic
Loss of 20% or more of blood due to traumatic condition Acute Blood Loss Anemia causes
Shock and cardiovascular problems, does not produce immediate anemia Results of Acute Blood Loss Anemia
Decrease of hematocrit, hemoglobin, RBC, platelet levels, and left shift of WBC Acute Blood Loss Anemia clinical findings
Healthy people: normocytic normochromic cells, 3-5 days later macrocytosis will be seen Acute Blood Loss Anemia microscope observations
Disorders of the GI tract, heavy menstruation, urinary tract abnormalities Chronic Blood Loss Anemia causes
Continual loss of blood and usually leads to iron deficiency anemia Chronic Blood Loss Anemia
Normal or slightly elevated retics, normal or slightly decreased WBC and platelets Chronic Blood Loss clinical findings
Hypochromic microcytic cells Chronic Blood Loss microscopic observations
Hypoproliferative disorder of pluripotential or erthroid committee stem cells Aplastic Anemia
Failure to produce RBC, WBC, and megakaryocytes, CD34 cell population Aplastic Anemia causes
Idiopathic, constitutional, iatrogenic, infection Forms of Aplastic Anemia
Sudden appearance, immune process involving antibodies against stem cells and cellular immune mechanism Aplastic Anemia pathophysiology
Phases of Aplastic Anemia Onset, recovery, and late disease
Total bone marrow failure, high risk for malignant diseases or hemo disorders Aplastic Anemia features
Pancytopenia, decreased granulocytes, platelets, and retics Aplastic Anemia clinical findings
Deficient production of all blood types Pancytopenia
Normocytic normochromic cells, few erythroid, myeloid, and megakaryocytes in bone marrow Aplastic Anemia microscopic findings
Immunosuppressant therapy (transplant rejection drugs) Aplastic Anemia treatment
Congenital form of Aplastic anemia Fanconi's Anemia
Low birth weight, skin hyperpigmentation, skeletal disorders, may include mental retardation Fanconi's Anemia symptoms
Progressive pancytopenia, low hemoglobin level Fanconi's Anemia clinical findings
DNA test that determines abnormalities pre and post-natally with Fanconi's Anemia HLA typing
Bone marrow transplant with steroids and androgens, recombinant granulocyte colony-stimulating factor Fanconi's Anemia treatment
Subset of Fanconi's Anemia that's diagnosed 1-77 years old Familial Aplastic Anemia
Pancytopenia, hypocellular bone marrow, no major development anomalies seen Familial Aplastic Anemia clinical findings
Congenital, acquired chronic, acute Pure Red Cell Aplasia causes
Selective failure of RBC production, WBC and platelets normal Acquired Pure Red Cell Aplasia
Associated with drugs, collagen vascular and lympho-proliferative disorders Chronic Pure Red Cell Aplasia
Congenital hypoplastic anemia, slow progressive and refractory anemia Diamond-Blackfan Syndrome causes
Normal WBC and platelets Diamond-Blackfan Syndrome clinical findings
Diamond-Blackfan Syndrome severe cases RBC normochromic and slight macrocytic
Occurs in healthy children <8 years, previous viral infection common Transient Erythroblastopenia of Childhood
Moderate to severe normocytic anemia, severe reticulocytopenia Transient Erythroblastopenia clinical finding
Abnormality of erythropoiesis production, contains multinuclear erythroblasts Congenital Dyseryhropoietic Anemia
Congenital Dyseryhropoietic Anemia most common type Type 2
Decreased hemoglobin, hematocrit, and RBC, decreased WBC and platelets if all cell lines involved Congenital Dyseryhropoietic Anemia clinical findings
Happens after body's iron stores depleted, most frequently occurring type of anemia Iron Deficiency Anemia
Nutritional deficiency, fault/incomplete iron absorption, pregnancy, excessive blood loss 4 causes of Iron Deficiency Anemia
Average adult needs 3.5-5.0 g, more if pregnant or lactating Iron requirements
Used for oxygen binding and biochemical reactions Operational iron
2 types of dietary iron Iron salts and heme iron
Non-heme iron, variable absorbtion Iron salts
Mainly from hemoglobin and myoglobin in meat, readily absorbed Heme iron
Fe2+ 5-10% absorbed of total dietary intake, absorbed iron attaches to transferrin Iron absorption
Increased brain blood flow, reversible fontanels bulging in infants, craving things like wood, ice, chalk, or dirt Iron Deficiency Anemia signs and symptoms
Hemoglobin, hematocrit, MCV, MCH, MCHC, retics, and ferritin levels all decreased, serum iron and transferrin saturation significantly decreased Iron Deficiency Anemia clinical findings
Results from illness and not related to nutrition Anemia of Inflammation or Chronic Disorders
Hemocrit fixed at 28-32% range, hemoglobin normal to decreased Anemia of Inflammation or Chronic Disorders clinical findings
Normocytic normochromic mostly, hypochromic microcytic in 1/3-1/4 of cases Anemia of Inflammation or Chronic Disorders microscopic findings
Also known as anemia of iron overload Sideroblastic Anemia
Congenital and acquired defect, malignant marrow disorders, secondary to drugs, toxins Sideroblastic Anemia causes
Sideroblastic Anemia clinical findings Severe anemia
Hypochromic microcytic cells, target cells, basophilic stippling, dimorphic populations Sideroblastic Anemia microscopic findings
May require blood transfusions Sideroblastic Anemia treatment
2 categories of Megaloblastic Anemias Vitamin B12 deficiencies and folic acid deficiencies
Megaloblastic Anemias types Acquired (most common) and congenital
Measurement of Vitamin B12 or folic acid levels Diagnosis for Megaloblastic Anemias
Parasitic infection, malabsorption syndrome, nutritional deficiencies of B12, Pernicious anemia Vitamin B12 Deficiencies causes
Abnormal absorption, pregnancy, alcohol Folic Acid Deficiencies causes
Most common megaloblastic anemia, can be asymptomatic 20-30 years before appearing Pernicious Anemia
Lemon-yellow skin color, mouth corner cracking, painful tongue, tiredness, heart failure Megaloblastic Anemia signs and symptoms
When one factor is missing and development of RBC is impacted Megaloblastic dyspoiesis
Intrinsic factor, Transcobalamin II, R-proteins Proteins that bind Vitamin B12
Binds to dietary Vitamin B12 and forms Vitamin B12-IF complex Intrinsic factor
Receptor and principle carrier of B12 to liver and tissues Transcobalamin II
Bind cobalamin with various cobalamin analogues R-proteins
Reduced to methyl tetrahydrofolate and delivered to the tissues, methyl released to combine with homocyteine which coverts to an amino acid Folic acid metabolism
Deficiencies in TCII Can produce a vitamin deficiency
Hemoglobin and RBC levels very low, MCV and MCH increased, retics less than 1%, platelets decreased Megaloblastic Anemia clinical findings
Significant anisocytosis and poiklocytosis, macrocytes and ovalocytes, cabot rings, Howell-Jolly bodies, basophilic stippling, neutropenia Megaloblastic Anemia microscopic findings
Tests for evidence of impaired Vitamin B12 absorption Shilling Test
Shilling Test indicates >10% Cbl excretion indicated lack of IF production Pernicious Anemia after step 2
Shilling Test indicates low excreted amounts of Cbl at 2nd step Abnormal intestinal absorption after step 2
Monthly injection of intramuscular B12 for deficiency Treatment for Megaloblastic Anemia
Increased RCB destruction, bone marrow fails to increase RBC production Hemolytic Anemia
Hemolytic Anemia where there is alteration in the RBC membrane Inherited or acquired
Sites of hemolysis in Hemolytic Anemia Intravascular or extravascular
Defects in basic membrane structure, hereditary spherocytosis, abnormality of membrane protein Ankyrin Inherited Hemolytic Anemia
Assesses defects in the phospholipid bilayer of the RBC membrane Osmotic Fragility Test
Heterogeneous group of inborn disorder where there is an overabundance of RBC Hereditary Elliptocytosis
Rare autosomal recessive disorder seen mainly in Afro-Americans, severe anemia Hereditary Pyropoikilocytosis
Genetic hemoglobin defects, Thalassemia, lead poisoning, and stem cells are seen Hereditary Stomatocytosis
Permeability disorder which causes net loss of K+ with budding, fragments, and microspherocytes Hereditary Xerocytosis
Rare hereditary disorder with mild chronic anemia and stomatocytes & spherocytes, hgb levels 11-13g/dL Rh null Disease - Rh deficiency syndrome
Dense contracted or spherical RBC with spiny projections with causes mild anemia in adults Acanthocytosis
Form of Acanthocytosis found in people with alcoholic cirrhosis, hgb 5-7g/dL, retics 10-20% Spur Cell Hemolytic Anemia
Associated with Acanthocytosis in peripheral blood that is a neurodegenerative disorder Neuroacanthocytosis
Deficiencies in G6PD-Glucose-Phosphate Dehydrogenase, Pyruvate Kinase, and Methemoglobin Reductase Erythrocytic Enzyme Defects
Results in acute hemolysis of RBC and hemolytic anemia, may be caused by a severe burn or trauma Acquired Hemolytic Anemia
Chemicals, drugs, venom, infectious microorganisms, and immune mechanisms Causes intravascular hemolysis
Mediated by IgG warm antibodies, complement and IgM cold antibodies, patients may also have systemic lupus erythematosus Warm & Cold - type Autoimmune Hemolytic Anemia
Following the administration of drugs Drug Induced Immune Hemolytic Anemia
Optimally activated at 4C and can cause intravascular or extravascular hemolysis Cold Autoimmune Hemolytic Anemia
Hallmark of hemolytic anemia seen in peripheral blood smear Spherocytes
Clonal acquired hematopoietic stem cell disorder that causes intermittent, sleep associated blood in the urine Paroxysmal Nocturnal Hemogloburia
Hemoglobin <6g/dL, hypochromic microcytic cells Paroxysmal Nocturnal Hemogloburia clinical findings
Blood transfusion, antibiotics, and anticoagulants Treatment for Paroxysmal Nocturnal Hemogloburia
Antibody attaches to RBC in cool temps, complement activates at warm temps which cause biphasic hemolysis Paroxysmal Cold Hemogloburia
Created by: DChalue413
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