Slide 1 - University of Virginia Health System

Document Sample
Slide 1 - University of Virginia Health System Powered By Docstoc
					DRAFT

Hematology - Week 1
Monday
Introduction
RBC, WBC & Plt structure & function hematopoiesis, stem cells, growth factors, hgb, metab,catab,

Tuesday
Lab venipuncture; Hct & indices, smear, normal morph Microcytic anemia Anemia Chr Dis Laboratory

Wednesday
Macrocytosis

Thursday
Hemolytic Anemia non-immune TTP, HS, G6PD, PK, etc.

Friday
Marrow Failure stem cells,aplastic anemia, PNH, Diamond-Blackfan, Fanconi, etc.

8:00

9:00

Hemolytic Anemia immune mediated intra/extra-vascular, DAT,

Hgb-opathies & Thalassemia

Patient Conclusion Rx of anemia

10:00

Define Anemia Lab & Clin Heme Microcytosis
Fe metabolism Fe def & related disorders - ACD, sideroblastic,

Lab Macrocyosis,hyper seg, ovals,etc. WAIHA spheres, Learning Studio

Lab schistocytes,etc. Sickle cell anemia, thalassemia, Learning Studio

Problem Set Approach to Anemia “15 Minute Heme Clinics” in the Learning Studio

11:00

Patient Presentation Anemia

-

Hemochromatosis

NOTES: Build treatment into the cases - Fe, B12, folate, diet, correct underlying problem,

DRAFT

Hematology - Week 2
Monday
Patient Presentation hemostasis

Tuesday
Transfusion Medicine I - ABO
antigens and antibodies, RhD, Screen & Cross

Wednesday
Transfusion Medicine II transfusion blood components, complications

Thursday
Thrombolytics, Anticoagulants

Friday

8:00

9:00

Intro to Hemostasis - Making a Blood Clot

The Bleeding Patient - defects of
hemostasis

The Thrombotic Patient - defects of
hemostasis

Patient Conclusion hemostasis

10:00

Thrombosis and Fibrinolysis - How Not to Make a Blood Clot

Lab
Learning Studio

Platelet disorders
- thrombocytopenia, thrombocytosis, abn plt function

Lab
Learning Studio

Problem Set Approach to Hemostasis “15 Minute Heme Clinics” in the Learning Studio

11:00

Lab
Learning Studio

Lab
Learning Studio

Lab
Learning Studio

NOTES: Pharmacology - thrombolytics, anticoagulants, drug eluting stents,

DRAFT

Hematology - Week 3
Monday
Benign/Malig WBC Disorders Blood borne parasites - malaria,
babesia, filariasis, etc.

Tuesday
Chronic Myeloprolifative Disorders - CML, ET,PV, MF

Wednesday
Non-Hodgkin Lymphoma

Thursday

Friday
Chemotherapy

8:00

9:00

Acute Leuk AML, ALL, Myelodysplasia

Chronic Lymphoproliferative Disorders - CLL, myeloma - amyloid, Waldenstroms

Hodgkin Lymphoma

Patient Conclusion Lymphadenopathy Splenomegaly
Lab - Lymphoma Learning Studio

10:00

Lab - Heme Learning Studio leukocytosis, leukopenia, leukemia, parasites, thrombocytosis

Lab - Heme Learning Studio leukocytosis, leukopenia, leukemia, parasites, thrombocytosis

Problem Set Leukemia and Lymphoma “15 Minute Heme Clinics” in the Learning Studio

11:00

Patient Presentation Leukemia or Lymphoma

NOTES: Pharmacology - chemotherapy for leukemia and lymphoma, (alkylating agents, antimetabolites, antitumor antibiotics,mitotic
ethics, cultural and professional issues

inhibitors, nitrosoureas, hormonal agents, biological agents, immunotherapy, immunologic cellular therapy, signal transduction inhibitors, radiopharmaceuticals, anticancer antibodies, anticancer vaccines, gene therapies ), administration and complications, genetics, biochem transcription factors,

Lecture

Hematopoiesis, stem cells, growth factors, kinetics & maturational sequence

DRAFT

1. Identify the different sites of hematopoiesis from fetal to adult life. 2. List the functional capabilities of hematopoietic growth factors by target cells. 3. Describe and recognize the maturation sequence in the development of erythroblasts to mature erythrocytes, including the temporal duration and the lifespan of these cells. 4. Describe the site of production for erythropoietin and the stimulus for its synthesis. 5. Describe the maturation sequence in the development of platelets, including the lifespan of these cells, and the key growth factor for megakaryopoiesis. 6. Describe the maturation sequence in the development of neutrophils, and the lifespan and function of these cells. -of eosinophils. -of basophils. 7. Describe the maturation sequence in the development of mature lymphocytes, including its temporal duration and the life span of these cells

Lecture

Hematopoiesis, stem cells, growth factors, kinetics & maturational sequence

DRAFT

1. Describe the pathway and rate-limiting steps by which heme is synthesized. 2. List the normal hemoglobins found in fetal and adult blood. 3. Draw a normal hemoglobin oxygen dissociation curve, identify P50 on the curve, and show the direction of shift of the curve elicited by increases or decreases of pH, 2,3-DPG concentration, C02 concentration, HbF, increased temperature, and HbS. 4. Apply knowledge of the RBC membrane and metabolism and to explain how defects in these structures and processes induce specific hematological disease states 5. Recognize the Embden-Meyerhof pathway and describe:
a. How the pathway helps regulate the reduction of methemoglobin back to hemoglobin. b. How the pathway relates to 2,3-DPG production.

6. Describe the function of the hexose monophosphate shunt and how this helps protect red cells from oxidant stress. 7. Identify the site of red blood cell destruction and the process by which this is accomplished.

Lecture

Hematopoiesis, stem cells, growth factors, kinetics & maturational sequence

DRAFT

1. Describe the pathophysiologic differences between absolute and pseudopolycythemia (erythrocytosis). List the functional capabilities of hematopoietic growth factors by target cells. 2. Given a patient with polycythemia list the major primary and secondary causes of polycythemia. 3. Describe the mechanisms for cellular oxygen sensing and to identify reasons for which increased oxygen delivery is necessary. 4. Describe the mechanisms, specific causes and consequences of an elevated erythropoietin level.

Lecture/Lab/Presentation

Define and classify anemia both laboratory and clinical

DRAFT

1. Identify the typical hemoglobin levels that define anemia in children/adolescents and post-pubertal men and women. 2. List the primary and secondary causes of polycythemia. 3. List the signs and symptoms of anemia and distinguish between the symptoms of acute anemia with volume depletion and chronic anemia in the euvolemic state. 4. Classify anemias according to the mean corpuscular volume. 5. Classify anemias according to the reticulocyte count. 6. List and describe the other laboratory examinations that can assist one in determining the etiology of the anemia. 7. List factors that impair the normal reticulocyte response to anemia.

8. Identify structural red cell abnormalities on a peripheral blood smear and to describe their clinical associations.

Lecture/Lab

Iron metabolism, iron deficiency, and the anemia of chronic inflammation, microcytic anemias

DRAFT

1. Describe the route by which iron from the diet becomes incorporated into hemoglobin (including the absorption, transport, delivery, storage and loss of iron in humans). 2. Describe the hematological changes associated with the development of iron deficiency and the timeline by which they occur. 3. Describe the symptoms, signs, and laboratory findings associated with iron deficiency anemia. 4. List the causes of iron deficiency and the appropriate investigational studies to evaluate for them. 5. Describe the role of hepcidin in the anemia of chronic inflammation and the resulting effects on serum iron, ferritin, and red cell size.
Differentiate between primary and secondary iron overload disorders. Recognize the signs and symptoms of hereditary hemochromatosis Understand management of HH, including identification of an initial management plan Describe the nature and origin of three clinical features noted in hereditary hemochromatosis. Relate the molecular basis of iron metabolism regulation to HH. Identify four genes and their products that are implicated in HH. Construct an algorithm of laboratory tests currently employed in the diagnosis of HH.

Lecture/Lab

Macrocytosis, macrocytic anemia, megaloblastic hematopoiesis

DRAFT

1. List common causes of macrocytosis and macrocytic anemia. 2. Describe the morphologic hallmarks of megaloblastic erythropoiesis and granulopoiesis in the blood and bone marrow. 3. Diagram the biochemical pathway which explains how folate and vitamin B12 deficiency ultimately impair thymidylate synthesis, and methionine and fatty acid metabolism. 4. Identify the dietary sources of vitamin B12 and folate and to describe their associated sites and mechanisms of absorption, means of transport, and duration and location of storage. 5. Describe the differences between vitamin B12 deficiency and folate deficiency with respect to: a. their most common causes b. time to development of the clinical deficiency state c. presence of neurologic and neuropsychiatric abnormalities 6. Describe the clinical, laboratory and autoimmune findings associated with pernicious anemia.

7. List the appropriate therapies for B12 deficiency and folate deficiency.

Lecture

Non-immune hemolytic anemia

DRAFT

Red Cell Degradation in the Normal State and Disease 1. Define the terms "intravascular hemolysis" and "extravascular hemolysis" and identify which mechanism predominates in normal red cell destruction. 2. Describe the fate of free hemoglobin following red blood cell destruction.

3. Explain why and in what direction the following laboratory measurements are altered from normal in hemolytic anemias: serum indirect bilirubin concentration, serum LDH level, reticulocyte count, serum haptoglobin concentration, and red blood cell survival.
Classification of Hemolytic Anemias 1. List hereditary and acquired non-immune causes of hemolytic anemia. For the hereditary conditions, be able to describe the mode of inheritance.

Lecture

Structural abnormalities of RBC membranes

DRAFT

Hereditary Spherocytosis (HS) 1. Determine whether a patient may have hereditary spherocytosis (HS), given the history, physical examination, hemogram, peripheral blood smear findings, reticulocyte count, and direct antiglobulin test (direct Coomb’s test) results. 2. Interpret the osmotic fragility test and distinguish between normal and HS red blood cells using this assay. 3. Define the molecular basis of hereditary spherocytosis and describe the resultant structural changes to red blood cells.

Lecture

Enzyme deficiencies, PNH, Fragmentation hemolysis

DRAFT

Enzyme Deficiency 1. Describe the pathway by which G6PD normally protects the red blood cell from oxidant stresses. 2. Describe the effects of pyruvate kinase deficiency on red blood cell survival. 3. Describe the inheritance patterns of G6PD and pyruvate kinase deficiencies. Paroxysmal Nocturnal Hemoglobinuria (PNH) 1. Discuss the molecular and pathophysiologic defects in paroxysmal nocturnal hemoglobinuria (PNH) and explain the tests used to diagnose this disorder. 2. List complications of PNH. Fragmentation Hemolysis 1. List the causes of fragmentation hemolysis.

Lecture

Immune hemolytic anemia

DRAFT

1. Describe the pathophysiology and site of red blood cell destruction of immunemediated hemolysis due to IgG, IgM, and complement. 2. Describe the procedures involved in performing a direct antiglobulin test (direct Coombs test) and an indirect antiglobulin test (indirect Coombs test). 3. List mechanisms by which drugs induce immune hemolytic anemia. 4. Distinguish warm antibody-induced autoimmune hemolytic anemia from cold antibody-induced autoimmune hemolytic anemia on the basis of: a. Immunoglobulin class of the antibody b. Presence of red blood cell agglutination c. Direct antiglobulin test results d. Clinical manifestations

Lecture

Hemoglobinopathies & Thalassemia

DRAFT

1. Identify the different chromosomes responsible for alpha-globin and beta-globin synthesis and to list the three types of hemoglobin found in normal adult blood. 2. Describe the precipitating factors and pathophysiologic process by which hemoglobin S causes sickling, as well as the symptoms and signs of the consequences of sickling. 3. List the rationale for the following sickle cell disease therapies: penicillin, folic acid, and hydroxyurea. 4. Describe the basic genetic differences between alpha-thalassemia and beta-thalassemia. 5. Describe the genetic, hematologic, and clinical differences between alpha-thalassemia trait, hemoglobin H disease, and hydrops fetalis. 6. Describe the hematologic findings and pathophysiological changes that are associated with beta-thalassemia major. 7. List the mechanisms and consequences of iron overload and infections associated with beta-thalassemia major. 8. Know the epidemiology and relative severity of the sickle cell genotypes. 9. Understand the organ system involvement by sickle cell disease as examples of the pathophysiology of the sickling process, specifically kidney and spleen. 10. Appreciate the significance of pain frequency as an indicator of disease severity 11. Describe the case definition, pathology and presentation of the major sickle cell complications of stroke, and acute chest syndrome 12. Understand the significance of abnormal cell adhesion and abnormal nitric oxide metabolism to sickle cell disease complications.

Lecture

Leukocyte function

DRAFT

1. Compare and contrast the morphology, cytoplasmic contents and functions of neutrophils, monocytes, eosinophils, and basophils. 2. Describe the normal function of neutrophils and monocytes/macrophages, including chemotaxis, phagocytosis, and killing and digestion of foreign materials. 3. Describe disorders of granulocytes, including congenital neutropenia and chronic granulomatous disease. 4. Describe the causes, clinical features, and treatment principles of neutropenia.

5. List the differential diagnosis for neutrophil leukocytosis and to define the phrase “left shift”.
6. Define the leukemoid reaction and list specific causes of this phenomenon. 7. List the differential diagnosis for eosinophilia. 8. Given a PBS be able to identify common blood borne parasites, e.g. malaria, babesia, trypanosomiasis, etc.

Lecture

Stem cell transplantation

DRAFT

1. List the indications for hematopoietic stem cell transplant and the rationale for this treatment choice. 2. Describe the different types and sources of hematopoietic stem cells. 3. Describe principles of pre-transplant conditioning and the role for post-transplant immunosuppression. 4. Describe graft versus host disease and graft versus tumor effect. 5. Describe the pathophysiologic basis for acute and chronic graft versus host disease. 6. Describe the changes in humoral and cellular immunity following stem cell transplant and how they relate to infectious complications. 7. Describe the mechanisms (production, destruction, and sequestration) and consequences of pancytopenia.

8. Identify the pathophysiologic mechanisms of bone marrow aplasia.

Lecture

Fibrin formation and regulation of hemostasis

DRAFT

1. Know the pathways for blood coagulation (the intrinsic, extrinsic, and common pathways) that lead to the formation of fibrin. 2. Know what events trigger coagulation. 3. Be able to identify which coagulation factors are dependent on vitamin K and how vitamin K modifies these coagulation factors. 4. State the crucial role of the cofactors V and VIII in coagulation. 5. Know how fibrinogen is converted into fibrin. 6. Know what Factor XIII does. 7. Be able to name key enzymes of fibrinolysis and inhibitors of fibrinolysis. 8. Be able to briefly discuss the mechanism of activation of the fibrinolytic system at the site of vascular injury with an overlying thrombus. 9. Be able to explain (or diagram) how activated protein C and antithrombin act as inhibitors of coagulation.

1

Lecture

Hemostasis and thrombosis

DRAFT

1. Given values for the PT/INR, PTT, TT (thrombin time), fibrinogen concentration, and platelet count, be able to construct an appropriate differential diagnosis of possible disorders giving rise to these abnormalities. 2. Given values for various clotting factor concentrations, be able to predict which screening tests of coagulation will be abnormal. 3. Be able to explain how a 1:1 mixing study can distinguish a clotting factor deficiency from an inhibitor of coagulation. 4. Be able to explain the utility and derivation of the INR.

5. Be able to compare and contrast three tests of platelet function - bleeding time, PFA-100, and platelet aggregation studies.
6. Be able to diagram the formation of the D-dimer and explain its utility in diagnosis venous thromboembolic disease.

2

Lecture

Platelets - numbers and function, disorders of platelet number or functio

DRAFT

1. Be able to diagram the structure of a mature platelet and show the location of: dense granules, alpha granules, glycoprotein Ib, glycoprotein IIb/IIIa, and phospholipids. 2. Be able to list three functions of platelets. 3. Be able to construct a simple diagram that depicts the process of platelet adhesion. Include in the drawing subendothelial collagen, von Willebrand factor, and glycoprotein Ib. Explain why platelet adhesion to blood vessels does not occur under normal circumstances. 4. Similarly, be able to construct a simple diagram that shows the process of platelet aggregation; include the release reaction (ADP), thromboxane synthesis, ADP and thromboxane receptors, glycoprotein IIb/IIIa, and fibrinogen. 5. List three mechanisms that could lead to thrombocytopenia. 6. Be able to identify three methods of treating ITP and the mechanism by which they increase the platelet counts.

3

Lecture

Hereditary and acquired thrombotic disorders

DRAFT

1. Identify the components of Virchow's triad and their pathophysiologic contribution to thrombosis. 2. Be able to describe at least three major clinical symptoms that occur when a patient suffers from an acute iliofemoral thrombosis of the leg, and indicate the pathophysiologic reason for each one (for example, dilated superficial veins of the calf due to obstruction of venous return in the occluded deep veins). 3. Be able to compare and contrast the cause and mechanism of a thrombus occurring in the arterial circulation (such as acute coronary artery thrombosis) from one that develops in a deep vein of the leg. Include the instigating factor(s) and composition of the clot. 4. Be able to list 3 clinical clues suggesting an inherited hypercoagulable disorder. 5. Be able to briefly describe (in one paragraph) at the molecular level the pathophysiologic reason that patients with deficiencies of antithrombin, protein C, or protein S, factor V Leiden or the prothrombin gene mutation are likely to have thrombosis. Explain what tests are used to identify these patients. 6. Be able to list at least three acquired disorders that are associated with recurrent venous or arterial thromboembolism. 7. Be able to describe the clinical features and criteria for diagnosis of antiphospholipid antibody syndrome. 8. What is the KEY factor in determining how long someone should be anticoagulated for a venous thrombosis?

4

Lecture

Antithrombotic therapy

DRAFT

1. Be able to name two oral antiplatelet agents and one intravenous one. 2. Be able to describe the mechanism of the antiplatelet effect of the following agents. a. Aspirin b. Clopidogrel c. Abciximab 3. Name the anticoagulant protein to which heparin binds. 4. Be able to list four key differences between standard heparin and low molecular weight heparin. 5. Be able to list four key differences between heparin and warfarin. 6. Be able to name a direct thrombin inhibitor and indicate one clinical use. 7. Be able to give the mechanism of how warfarin works and name at least four clotting factors it affects. 8. Name and know the pathophysiology of one unique side effect of both heparin and warfarin. 9. Name three disease states for which thrombolytic therapy is used. 10. Name one thrombolytic agent and describe how it works. 11. Given a brief patient scenario, be able to select from a list of agents the best anticoagulant for that patient

5

Lecture

Inherited bleeding disorders

DRAFT

1. Be able to describe five screening tests of hemostasis and list several causes of an abnormal result in each case. 2. Be able to distinguish between signs and symptoms of primary hemostasis defects and plasma coagulation defects. 3. Be able to explain why a marked deficiency of von Willebrand factor leads to excessive bleeding. 4. Recommend two potential forms of therapy for hemorrhage in a patient with type 1 von Willebrand disease and be able to explain a likely mechanism of its therapeutic effect in each case. 5. Be able to predict the results of hemostatic screening tests (PT/INR, PTT, fibrinogen, platelet count, bleeding time) in a patient with severe hemophilia A. 6. Explain why a patient with severe von Willebrand disease and a patient with hemophilia A may both have a prolonged PTT. 7. Using inheritance patterns, clinical history and the results of laboratory tests, be able to distinguish hemophilia A (factor VIII deficiency), hemophilia B (factor IX deficiency) and moderate to severe von Willebrand disease.

1

Lecture

Acquired bleeding disorders

DRAFT

1. Be able to briefly describe the pathogenesis, diagnostic tests, and therapeutic approach to patients with the following acquired disorders who are actively bleeding: a. end-stage liver disease b. acquired factor VIII inhibitor (auto-antibody against FVIII) c. severe DIC due to acute promyelocytic leukemia d. vitamin K deficiency

2

Lecture

Acquired Blood Groups And Compatibility Testing

DRAFT

1. Be able to name the two main “naturally occurring” antibodies to red cell antigens. 2. Be able to name the four major blood types (phenotypes) in the ABO system. 3. Be able to tell which of these two antibodies would be found in individuals of each ABO type, and briefly explain why ordinarily they would or would not be present. 4. Be able to explain why the ABO system is the most important red cell blood group system for transfusion therapy. 5. Given the Rh phenotype of a mother and her fetus, be able to state whether the baby may be at risk of developing hemolytic disease of the newborn (HDN) due to anti-Rh antibodies, and why (or why not). Be able to state the immunoglobulin class responsible for HDN, and give the reason that other classes of immunoglobulin do not cause HDN. 6. Be able to diagram the direct antiglobulin test (the Coombs test), indicating the main components and their source (patient vs. reagent). Be able to state what the direct antiglobulin test is capable of detecting. Be able to diagram the indirect antiglobulin test and state the major purpose for the indirect antiglobulin test. 7. Be able to list the three essential steps in blood compatibility testing, and the purpose of each step. 8. In an emergency situation, be able to indicate what kind of blood is given, if necessary, before typing is complete, and what kind of blood is given, if necessary, before cross-matching is complete.

1

Lecture

Cellular components

DRAFT

1. Be able to give three reasons why blood component therapy is preferable to whole blood therapy. 2. Be able to name the clinical indication for red cell transfusion. 3. Two methods of platelet product preparation are now commonly used. Be able to state what they are. 4. Approximately 30-40% of recipients of repeated platelet transfusions become alloimmunized. Be able to state what this means, how it can be prevented, and how it can be managed if it occurs. 5. Blood products are often ordered to be CMV negative, irradiated, and / or filtered. Be able to give one clinical indication for each.

2

Lecture

Plasma and Components

DRAFT

1. Be able to list two indications for transfusing fresh frozen plasma (FFP). 2. Be able to list the three major therapeutic constituents of cryoprecipitate, and name a clinical indication for its use. 3. Be able to name at least one common indication for each of the following blood derivatives: factor VIII concentrates, prothrombin complex concentrates, albumin, intravenous immune globulin. 4. List the main coagulation abnormalities that occur after massive transfusion, and outline the appropriate treatment for each.

3

Lecture

Non-infectious Transfusion Complications

DRAFT

1. Be able to list the major clinical effects of intravascular hemolytic transfusion reactions. 2. Be able to identify the most effective method known to prevent the majority of acute hemolytic transfusion reactions. 3. Be able to list the clinical symptoms and laboratory findings of delayed hemolytic transfusion reactions. 4. Be able to name three major clinical situations in which Rh Immune Globulin should be given to prevent HDN. 5. The most common reaction to transfused blood, particularly red cells and platelets, is fever. Be able to name two adverse consequences of transfusion that may first manifest themselves with fever. 6. Know the clinical presentation of Transfusion-Associated Acute Lung Injury (TRALI) and what causes it. 7. Be able to explain what transfusion-associated graft-versus-host disease is, who is at risk, and how to prevent it.

4

Lecture

Transfusion Transmitted Disease

DRAFT

1. Be able to name the blood component most likely to cause bacterial sepsis, and explain the reason why. 2. Be able to identify the two major causes of post-transfusion hepatitis, frequency of occurrence in the US population, and relative risk of transmission in blood transfusions. 3. Be able to give the approximate risk of HIV transmission per unit of blood. 4. Be able to explain the meaning of “window period” in the context of transmission of West Nile virus in blood or transplanted tissues. 5. Be able to explain why directed donation (blood given by relatives or friends) should not be regarded as safer than blood from a regular volunteer donor.

5

Lecture

Non-Hodgkin lymphoma

DRAFT

1. Describe the basic pathogenesis of NHL with respect to cytogenetic alterations involving the Bcl-2 and Myc oncogenes, and the t(14;18) translocation. 2. Describe the basic pathologic classification of NHL (the WHO classification). 3. Describe the predisposing factors to developing NHL, including infectious agents associated with development of specific lymphomas. 4. Compare and contrast the natural history and clinical features of follicular lymphoma and diffuse large B cell lymphoma. 5. Describe treatment approach and expected outcomes in patients with follicular lymphoma and in patients with diffuse large B cell lymphoma. 6. Name the common causes of generalized lymphadenopathy. 7. Identify the types of lymphoma and treatment approach in people with AIDS.

Lecture

Hodgkin lymphoma

DRAFT

1. Describe the background features of lymph nodes involved in Hodgkin lymphoma and the morphologic features and cell derivation of the ReedSternberg cell. 2. Describe the clinical features and hematologic findings associated with Hodgkin lymphoma, including the classic B symptoms. 3. Describe the staging work-up and apply the Ann Arbor staging classification to patients with Hodgkin lymphoma. 4. Describe short-term and long-term complications of radiation therapy, including cardiac, pulmonary, and endocrine complications, and risk of second malignancies. 5. Describe short and long-term toxicities of modern chemotherapy for Hodgkin lymphoma (ABVD).

Lecture

Chronic lymphocytic leukemia

DRAFT

1. Describe the presenting features of CLL, including the typical age at presentation, the most common symptoms, two major physical exam findings and typical blood counts. 2. Describe the predominant leukemic cell in the blood of patients with CLL, and distinguish this from the leukemic cells that can be seen in the blood of patients with ALL, AML, and CML. 3. Describe the staging of CLL, and features that correlate with a better or worse prognosis. 4. Describe complications of CLL that exemplify the immune dysfunction associated with this disease. 5. Name at least four symptoms and/or complications of CLL that are an indication for treatment. 6. Compare and contrast CLL and CML in terms of molecular mechanism, age at onset, symptoms, physical exam findings, typical blood counts, treatment, and outcome.

Lecture

Chronic myelogenous leukemia

DRAFT

1. Diagram the chromosomal translocation that generates the Philadelphia chromosome, identify the genes involved and the protein created by this translocation. 2. Describe how the bcr-abl fusion protein causes leukemia and provides a target for effective therapy in CML. 3. Describe the presenting features of CML, including age at presentation, the most common symptoms, one physical exam finding, and a typical CBC. 4. Describe the typical findings on the blood smear in patients with CML, emphasizing the number and types of leukocytes seen in the blood. 5. For a patient with chronic phase CML, compare and contrast treatment with imatinib and other tyrosine kinase inhibitors versus allogeneic stem cell transplantation in terms of goals of treatment, side effects, and long-term outcome.

Lecture

Acute Lymphoblastic leukemia

DRAFT

1. Identify the age and gender distribution of patients with ALL. 2. Name common symptoms/signs and common laboratory findings in a patient presenting with ALL. 3. Briefly describe two tests that can be used to distinguish leukemic blast cells of ALL from leukemic blast cells of AML. 4. Therapy of ALL commonly consists of an induction phase, post-remission therapy (consolidation and maintenance therapy), and central nervous system prophylaxis. Describe the goals of each of these three elements of therapy.

5. Describe one complication that leads to mortality in ALL.

Lecture

Acute Myelogenous Leukemia

DRAFT

1. Define “myeloblast” and describe the consequences of excess myeloblasts in the bone marrow and in the circulation. Name at least three disease features which result from replacement of marrow cells with myeloblasts or circulation of myeloblasts. 2. Describe the predominant cell types seen in the peripheral blood and/or bone marrow in each of the four major categories of leukemia (AML, ALL, CML, CLL).

3. Describe the unique features of acute promyelocytic leukemia (AML M3), including the morphologic appearance of the promyelocyte, hemorrhagic complications, chromosomal abnormality, and treatment with induction therapy and all trans retinoic acid.
4. Name two favorable and two adverse cytogenetic abnormalities in AML. 5. Therapy of AML commonly consists of an induction phase, followed by a consolidation phase. Be able to describe the principle goals of each phase of therapy. Be able to state the approximate success rate of chemotherapy for AML (rate of complete remission with induction chemotherapy and cure rate). 6. Be able to identify the complications of induction chemotherapy for AML. Name which complications contribute to mortality. 7. Compare and contrast AML and ALL in terms of age of patients, central nervous system involvement, treatment, and outcome.

Lecture

Multiple Myeloma And Other Plasma Cell Disorders

DRAFT

1. Identify the general structure of an immunoglobulin molecule, including the light chains and heavy chains, the constant and variable regions, the Fab and Fc fragments, and the differences between the various immunoglobulin classes. 2. Name the major criteria used to diagnose multiple myeloma. 3. Describe at least five complications that may occur in patients with multiple myeloma. 4. Describe the pathophysiology of renal failure in patients with multiple myeloma. 5. Describe the pathophysiology, x-ray appearance, complications, and treatment of bone abnormalities in multiple myeloma. 6. Describe indications for therapy, treatment, and prognostic indicators for patients with multiple myeloma. 7. Define the diagnostic criteria, incidence, and clinical course of patients with monoclonal gammopathy of unknown significance. 8. Define amyloid and indicate two proteins that can cause amyloid deposition in tissues. 9. Describe the clinical features and prognosis of patients with primary amyloidosis.

Lecture

Myelodysplastic Syndromes

DRAFT

1. Describe the typical age and classic peripheral blood findings of patients with myelodysplasia. 2. Describe the bone marrow findings and cytogenetics seen in patients with myelodysplasia. 3. Describe three laboratory determinants of prognosis in patients with myelodysplasia. 4. Name three treatments used in patients with myelodysplasia, the goals of such therapy, and the results of each treatment in terms of response rate, cure, and/or impact on survival.

Lecture

Myeloproliferative Disorders

DRAFT

1. Name the four major myeloproliferative disorders and describe the pathophysiologic features shared by these disorders. 2. Name four causes of reactive or secondary thrombocytosis. 3. Name the two major complications of essential thrombocythemia. 4. Describe the typical physical exam, and blood and bone marrow findings in patients with chronic idiopathic myelofibrosis. 5. Describe the common mutation associated with polycythemia vera and its biological consequences. 6. Describe the clinical features and complications of polycythemia vera. 7. Describe treatment approaches to polycythemia vera. 8. Name three causes of splenomegaly.

Lecture

Hematologic Disorders of Obstetrics & Pediatrics

DRAFT

1. Describe the changes which result in the physiologic anemia of pregnancy. 2. Describe nutritional causes and mechanisms of anemia that develops during pregnancy. 3. List a differential diagnosis for thrombocytopenia in pregnancy and recognize those which require urgent medical intervention. 4. Describe the impact pregnancy has on hemostasis and thrombosis. 5. Describe the normal development of the human immune system from birth to 12 months. 6. Describe the hematologic nutritional requirements of the newborn and the impact of breastfeeding on these requirements.

Lecture

Leukocyte function

DRAFT

1. Compare and contrast the morphology, cytoplasmic contents and functions of neutrophils, monocytes, eosinophils, and basophils. 2. Describe the normal function of neutrophils and monocytes/macrophages, including chemotaxis, phagocytosis, and killing and digestion of foreign materials. 3. Describe disorders of granulocytes, including congenital neutropenia and chronic granulomatous disease. 4. Describe the causes, clinical features, and treatment principles of neutropenia.

5. List the differential diagnosis for neutrophil leukocytosis and to define the phrase “left shift”.
6. Define the leukemoid reaction and list specific causes of this phenomenon. 7. List the differential diagnosis for eosinophilia. 8. Given a PBS be able to identify common blood borne parasites, e.g. malaria, babesia, trypanosomiasis, etc.


				
DOCUMENT INFO
Shared By:
Categories:
Tags:
Stats:
views:23
posted:11/15/2009
language:English
pages:39