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42 Cards in this Set

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Anemia presenting with increased TIBC, decreased ferritin, decreased serum iron.
Mycrocytic, Hypochromic, usually secondary to iron deficiency. Also seen with Thalassemia, lead poisoning
Anemia in patients with B12/Folate deficiency
Macrocytic (MCV>100), presents with PMN hypersegmentation on blood smear. B12 deficiency presents with neuro effects, folate deficiency much easily reached through bad diet. Also seen in patients taking drugs blocking DNA synthesis (sulfa drugs, AZT)
Anemia in patients with normocytic, normochromic smears?
Hemorrhagic, autoimmune hemolytic, enzyme defects (G6PD), bone marrow dz, anemia of chronic dz. Decreased serum haptoglobin and increased LDH indicate RBC hemolysis. Direct Coomb's test can show an immune-mediated process.
Anemia in patients with a decreased TIBC, decreased serum iron, and decreased iron saturation?
Anemia of chronic disease
Anemia in patients with an increased TIBC, decreased serum iron, and normal iron saturation?
Iron-deficiency anemia.
Patient with normal TIBC, increased serum iron, and 100% iron saturation (normal is 20-50%)
Iron overload (hemosiderosis)
Aplastic Anemia: Who presents with aplastic anemia?
Patients with pancytopenia characterized by severe anemia, neutropenia, and thrombocytopenia caused by failure or destruction of multipotent myeloid stem cells.
Aplastic Anemia: What causes aplastic anemia?
Radiation, benzene, chloramphenicol, alkylating agents, antimetabolites, viral agents, Fanconi's anemia, idiopathic causes.
Aplastic Anemia: Common Sx?
Fatigue, malaise, pallor, purpura, mucosal bleeding, petechiae, infection.
Aplastic Anemia: How do the blood smear and bone marrow aspirate appear?
Blood smear: pancytopenia with normal cell morphology. Aspirate:hypocellular marrow with fatty infiltration.
Aplastic Anemia: What's the treatment of aplastic anemia?
Withdraw offending agent, BMT, RBC/platelet transfusion, G-CSF or GM-CSF.
Hereditary Spherocytosis How do patients with hereditary psherocytosis present?
Smear shows microcytic RBCs that are small and round with no central pallor. The patients will have normal Hgb and MCV.
Hereditary Spherocytosis What's the cause of hereditary spherocytosis?
Intravascular hemolysis due to spectrin defect.
Hereditary Spherocytosis How is it confirmed and tested?
Will be Coombs' negative (unlike warm antibody hemolysis), can perform osmotic fragility test.
Hereditary Spherocytosis What are some associated diseases?
Gallstones, splenomegaly, anemia, and jaundice.
What is the HbS mutation?
Glutamate-->Valine in a Beta chain. Heterozygotes are usually malaria-resistant. *% of Af-Ams carry the HbS trait, 0.2% have the disease.
What can precipitate sickling?
Low O2, dehydration.
What are the common complications of HbS homozygotes?
aplastic crises from parvovirus infection, autosplenectomy, risk of encapsulated organism infection, salmonella osteomyelitis, vaso-occlusive pain crises, and splenic sequestration crises.
What is the HbC defect?
Different Beta-chain mutation, the patients with HbC or HbSC have milder dz than HbSS patients.
What are the treatment options?
Hydroxyurea (increased HbF) and bone marrow transplantation.
Blood Dyscrasias-Alpha-Thalassemia What populations have the most prevalence?
Mediterranean populations. (thalaSEAmia)
Blood Dyscrasias-Alpha-Thalassemia What is the etiology?
Underproduction of the alpha-globin chain, with no compensatory increase of any other chains. HbH has Beta-4 tetramers and lacks 3 alpha-globin genes.
Blood Dyscrasias-Alpha-Thalassemia What is the presentation of a patient lacking all four alpha-globin genes?
hydrops fetalis and intrauterine fetal death.
Patient Presentation of Beta-Thalassemia major?
severe anemia requiring blood transfusion. Cardiac failure is often due to secondary hemochromatosis.
Etiology of Beta-Thalassemia major?
Beta chain is absent, fetal Hgb production is compensatorily increased but is inadequate.
Etiology of Beta-thalassemia minor?
The Beta chain is underproduced, again see fetal HgB compensatory increase. HbS/Beta-thalassemia heterozygote has mild to moderate disease.
What is the definition of DIC?
Activation of the coagulation cascade leading to microthrombi and global consumption of platelets, fibrin, and coagulation factors.
What causes DIC?
Obstetric complications (most common cause), gram-negative sepsis, transfusion, trauma, malignancy, acute pancreatitis, nephrotic syndrome.
What are the lab findings in DIC?
Increased PT, increased PTT, incrased fibrin split products (D-dimers), decreased platelet count.
What disorder type presents with mucous membrane bleeding, petechiae, purpura, and prolonged bleeding time?
Platelet abnormalities (microhemorrhages), which can be caused by ITP (antiplatelet antibodies and increased megakaryocytes), TTP (schistocytes), drugs, and DIC (increased fibrin split products).
What disorder type presents with hemarthroses (bleeding into joints), easy brusing, prolonged PT and/or PTT?
Coagulopathies (macrohemorrhages), which can be caused by Hemophilia A/B and von Willebrand's disease (most common)
What is the deficiency in Hemophilia A?
Factor VIII
What is the deficiency in Hemophilia B?
Factor IX
What is the deficiency in vW dz?
Deficiency of von Willebrand's antigen.
Which factors does the PT measure?
Extrinsic: Factors II, V, VII, and X.
Which factors does the PTT measure?
Intrinsic: All factors except VII and XIII.
What presents with increased bleeding time and normal PT/PTT and platelet count?
Qualitative platelet defects, can be Bernard Soulier disease (defect in adhesion) or Glanzmann's thrombasthenia (defect in aggregation). Can also see these labs in vascular bleeding.
What presents with decreased platelet count, increased bleeding time, and normal PT/PTT?
Which diseases present with increased PTT and normal PT, platelet count, and bleeding time?
Hemophilia A and B
What presents with a high PTT, normal PT, normal platelets, and increased bleeding time?
vW disease
What presents with increased Bleeding time/Pt/PTT and decreased platelet count?
Which one presents with Reed-Sternberg cells?