Hematology Question Set 1

by Lecturio USMLE

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    About the Lecture

    The lecture Hematology Question Set 1 by Lecturio USMLE is from the course Hematology - High Yield Questions.

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    1. It can be treated with proper diet and iron supplementation.
    2. It can be treated with proper diet only.
    3. It can be treated with lead supplementation.
    4. It can be treated with iron supplementation only.
    5. It can be treated with multivitamins.
    1. Immune thrombocytopenic purpura (ITP)
    2. Von Willebrand disease
    3. Acute lymphoblastic leukemia (ALL)
    4. Hemophilia A
    5. Hemophilia B
    1. Complete resolution is expected
    2. Lifelong thrombocytopenia is expected
    3. Survival rate is up to 70% depending on risk stratification
    4. Lifelong disease dependent on factor VIII substitution
    5. Lifelong disease dependent on factor IX substitution
    1. Coumadin is antagonizing vitamin K reductase necessary for production of factors II, VII, IX and X
    2. Local irritation of bowels because of the ingestion of rodenticide
    3. Coumadin is antagonizing vitamin K reductase necessary for production of factors VIII and IX
    4. Coumadin caused thrombocytopenia
    5. Coumadin caused disseminated intravascular coagulation (DIK)
    1. Bone marrow examination
    2. Watch and wait strategy with repeated CBCs for several weeks to see if blood count parameters will improve
    3. Symptomatic treatment of pain and fever and transfusion for blood count parameters disturbance
    4. Antibiotics administration
    5. Corticosteroids administration
    1. Hemolytic anemia caused by glucose-6-phosphate dehydrogenase deficiency
    2. Microcytic anemia caused by iron deficiency
    3. Anemia caused by renal failure
    4. Autoimmune hemolytic anemia
    5. Aplastic anemia
    1. Watch and wait strategy
    2. Transfusion to repair neutropenia
    3. Antibiotics administration to prevent infection
    4. Multivitamins administration
    5. Corticosteroids administration
    1. Total hemolytic complement activity (CH50) is usually reduced.
    2. It is transmitted as autosomal recessive codominant trait.
    3. Serum C3 levels are normal.
    4. Disseminated gonococcal infection could be a clinical presentation.
    5. Congenital deficiency of factor D is more common than congenital deficiency of factor B.
    1. As hemoglobin level rises, the amount of iron absorbed is reduced.
    2. Delayed-release oral iron preparations are significantly more effective as compared to simple oral iron preparations in treatment of iron deficiency.
    3. An asymptomatic patient with established iron deficiency anemia does not require oral iron therapy and can be managed with dietary changes.
    4. Oral iron preparations are best taken after food for better absorption as micronutrients in food aids absorption of iron.
    5. Reticulocyte count begins to increase after 1st week of oral iron therapy.
    1. Screen for celiac disease
    2. Hemoglobin electrophoresis to identify β-thalassemia trait
    3. Endoscopy and/or barium studies of lower gastrointestinal tract to identify source of occult blood loss or malignancy
    4. A 3 months trial of oral iron therapy followed by repeat laboratory evaluation
    5. Evaluate as anemia of inflammation
    1. Spherocytes
    2. Polychromasia
    3. Bite cells
    4. Blister cells
    5. Heinz bodies
    1. Most possible diagnosis consistent with clinical history and laboratory evaluation is type 1 von Willebrand disease.
    2. As bleeding time and aPTT are normal, diagnosis of von Willebrand disease is ruled out.
    3. As she is a female, diagnosis of hemophilia A or B cannot be suspected.
    4. As there is history of mucocutaneous bleeding, prothrombin (factor II) deficiency is the most likely diagnosis, and serum factor II assay should be ordered.
    5. Most possible diagnosis consistent with clinical history and laboratory evaluation is type 3 von Willebrand disease.
    1. Pigmentary skin changes & cafe-au-lait spots
    2. Short stature
    3. Absent radii and anomalies of thumbs
    4. Anomalies of lower limbs
    5. Microcephaly
    1. Warfarin is secreted in breast milk and is hence contraindicated to lactating mothers.
    2. Bleeding is the major side effect of warfarin.
    3. Warfarin crosses placenta and if given during first trimester of pregnancy, it can lead to embryopathy characterized by nasal hypoplasia and stippled epiphyses.
    4. Factor X levels can be used to monitor warfarin therapy in patients with antiphospholipid antibody syndrome.
    5. Warfarin-induced skin necrosis is more common in patients with deficiencies of protein C or protein S.
    1. Administration of intravenous immunoglobulin (IVIG) is the treatment of choice.
    2. Selective IgA deficiency may evolve into common variable immunodeficiency in some patients
    3. B cells in isolated IgA deficiency are phenotypically normal.
    4. Patients with selective IgA deficiency are at increased risk of autoimmune diseases and malignancy.
    5. Selective IgA deficiency is the most common primary antibody deficiency.
    1. Lifelong salicylates are indicated for prevention of thrombosis.
    2. Periodic phlebotomies are mainstay of the treatment.
    3. Asymptomatic hyperuricemia does not require treatment.
    4. Acquired von Willebrand disease is a known complication of the disease.
    5. Incidence of Helicobacter pylori infection is increased in this condition.

    Author of lecture Hematology Question Set 1

     Lecturio USMLE

    Lecturio USMLE

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