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What does anisocytosis mean?
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Varying sizes of cells
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What does poikilocytosis mean?
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Varying shapes of cells
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Name two drugs that inhibit ADP-induced GpIIb/IIIa expression.
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Clopidogrel and Ticlopidine. They irreversibly block ADP receptors, thus inhibiting expression of GpIIb/IIIa, resulting in inhibition of fibrinogen binding.
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Which enzyme activates vitamin K? Which drug inhibits this enzyme?
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Epoxide reductase activates vitamin K, and is inhibited by vitamin K. This prevents the synthesis of factors II, VII, IX, X, C and S.
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Where is antithrombin synthesized? Which factors are inhibited by antithrombin? What is it activated by?
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Synthesized in the liver, antithrombin inactivates factors II, VII, IX, X and XI. It is activated by heparin. In ATIII deficiency you would see a reduced increase in PTT after administration of heparin.
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What is protein C? How is it actiaved? What is its function?
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Protein C is an endogenous anticoagulant, activated by thrombomodulin on the endothelial cell walls, it cleaves and inactivates factors V and VIII. It also inactivates the tPA inhibitor, thus allowing tPA to convert plasminogen to plasmin. Plasmin in turn cleaves the fibrin mesh.
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What is Factor V Leiden disease?
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Mutation in factor V that makes it resistant to protein C degradation. This is the most common cause of inherited hypercoagulability.
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What is tPA? How is it activated?
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TPA (tissue plasminogen activator) is an enzyme synthesized by endothelial cells that catalyzes the conversion of plasminogen to plasmin. Plasmin is responsible for cleavage of the fibrin mesh. tPA is activated indirectly by protein C, which inactivates tPA inhibitor.
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What is acanthocytosis? Name two diseases that produce acanthocytosis.
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Acanthocytosis is the presence of acanthocytic red blood cells (spur cells). Acanthocytes are seen in abetalipoproteinemia and liver disease.
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What is Plummer-Vinson syndrome? What is it caused by? What type of cancer is it associated with?
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Triad of esophageal web, atrophic glossitis and anemia, all caused by iron deficiency. Associated with squamous cell carcinoma of the esophagus.
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What are the 5 diseases that present as microcytic, hypochromic anemia?
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Iron deficiency, α-thalassemia, β-thalassemia, lead poisoning and sideroblastic anemia.
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What is sideroblastic anemia? What type of anemia does it produce? What do the RBCs look like? How is it Rx'ed?
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X-linked defect in heme synthesis, caused by a defect in the δ-aminolevulinic acid synthase gene (rate limiting enzyme in heme synthesis). See ringed sideroblasts (with iron-laden mitochondria). Can also be caused by alcohol and lead. R: pyridoxine (vitamin B6).
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What is the rate limiting enzyme in heme synthesis? Which cofactor is required? What disease is caused by a defect in this enzyme? What is the inheritence of this disease?
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δ-aminolevulinic acid synthase, converts glycine and succinyl coA to δ-aminolevulinic acid. Requires vitamin B6 (pyridoxine). Sideroblastic anemia is caused by deficiency in this enzyme. X linked.
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What are the 3 diseases that present as macrocytic anemia?
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Megaloblastic anemia caused by folate deficiency, megaloblastic anemia caused by vitabim B12 deficiency, and nonmegaloblastic macrocytic anemias (liver disease, alcoholism, reticulocytosis, metabolic disorders like congenital deficiencies in purine/pyrimidine sunthesis, and drugs like 5-FU, AZT and hydroxyurea).
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What are bite cell RBCs seen in?
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G6PD deficiency
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