Monday

1
Hematology - Week 1
Monday
Tuesday
Wednesday
Thursday
Friday
Macrocytosis
Introduction RBC, WBC Plt structure
function - hematopoiesis, stem cells, growth
factors, hgb, metab,catab,
Lab venipuncture Hct indices, smear, normal
morph Microcytic anemia Anemia Chr
Dis Laboratory
Hemolytic Anemia non-immune TTP, HS, G6PD, PK,
etc.
Marrow Failure - stem cells,aplastic anemia, PNH,
Diamond-Blackfan, Fanconi, etc.
800
Hgb-opathies Thalassemia
Hemolytic Anemia immune mediated intra/extra-vascu
lar, DAT,
900
Patient Conclusion Rx of anemia
1000
Define Anemia Lab Clin Heme
Problem Set Approach to Anemia 15 Minute Heme
Clinics in the Learning Studio
Lab Macrocyosis,hyperseg, ovals,etc. WAIHA
spheres, Learning Studio
Lab schistocytes,etc. Sickle cell anemia,
thalassemia, Learning Studio
Microcytosis Fe metabolism Fe def related
disorders - ACD, sideroblastic, Hemochromatosis
1100
Patient Presentation -Anemia
NOTES Build treatment into the cases - Fe,
B12, folate, diet, correct underlying problem,
2
Hematology - Week 2
Monday
Tuesday
Wednesday
Thursday
Friday
Patient Presentation - hemostasis
Transfusion Medicine I - ABO antigens and
antibodies, RhD, Screen Cross
Transfusion Medicine II - transfusion blood
components, complications
Thrombolytics, Anticoagulants
800
The Bleeding Patient - defects of hemostasis
Intro to Hemostasis - Making a Blood Clot
900
The Thrombotic Patient - defects of hemostasis
Patient Conclusion - hemostasis
1000
Thrombosis and Fibrinolysis - How Not to Make a
Blood Clot
Problem Set Approach to Hemostasis 15 Minute
Heme Clinics in the Learning Studio
Lab Learning Studio
Platelet disorders - thrombocytopenia,
thrombocytosis, abn plt function
Lab Learning Studio
1100
Lab Learning Studio
Lab Learning Studio
Lab Learning Studio
NOTES Pharmacology - thrombolytics,
anticoagulants, drug eluting stents,
3
Hematology - Week 3
Monday
Tuesday
Wednesday
Thursday
Friday
Chronic Myeloprolifative Disorders - CML, ET,PV,
MF
Benign/Malig WBC Disorders Blood borne parasites
- malaria, babesia, filariasis, etc.
Non-Hodgkin Lymphoma
800
Chemotherapy
Chronic Lymphoproliferative Disorders - CLL,
myeloma - amyloid, Waldenstroms
900
Hodgkin Lymphoma
Patient Conclusion Lymphadenopathy Splenomegaly
Acute Leuk AML, ALL, Myelodysplasia
1000
Lab - Lymphoma Learning Studio
Lab - Heme Learning Studio leukocytosis,
leukopenia, leukemia, parasites, thrombocytosis
Problem Set Leukemia and Lymphoma 15 Minute Heme
Clinics in the Learning Studio
Lab - Heme Learning Studio leukocytosis,
leukopenia, leukemia, parasites, thrombocytosis
1100
Patient Presentation Leukemia or Lymphoma
NOTES Pharmacology - chemotherapy for leukemia
and lymphoma, (alkylating agents,
antimetabolites, antitumor antibiotics,mitotic
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, ethics, cultural
and professional issues
4

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

5

• Describe the pathway and rate-limiting steps by
  which heme is synthesized.
• List the normal hemoglobins found in fetal and
  adult blood.
• 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.
• Apply knowledge of the RBC membrane and
  metabolism and to explain how defects in these
  structures and processes induce specific
  hematological disease states
• Recognize the Embden-Meyerhof pathway and
  describe
• a. How the pathway helps regulate the reduction
  of methemoglobin back to hemoglobin.
• How the pathway relates to 2,3-DPG production.
• Describe the function of the hexose monophosphate
  shunt and how this helps protect red cells from
  oxidant stress.
• Identify the site of red blood cell destruction
  and the process by which this is accomplished.

6

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

7

• Identify the typical hemoglobin levels that
  define anemia in children/adolescents and
  post-pubertal men and women.
• List the primary and secondary causes of
  polycythemia.
• 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.
• Classify anemias according to the mean
  corpuscular volume.
• Classify anemias according to the reticulocyte
  count.
• List and describe the other laboratory
  examinations that can assist one in determining
  the etiology of the anemia.
• List factors that impair the normal reticulocyte
  response to anemia.
• Identify structural red cell abnormalities on a
  peripheral blood smear and to describe their
  clinical associations.

8

• 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).
• Describe the hematological changes associated
  with the development of iron deficiency and the
  timeline by which they occur.
• Describe the symptoms, signs, and laboratory
  findings associated with iron deficiency anemia.
• List the causes of iron deficiency and the
  appropriate investigational studies to evaluate
  for them.
• 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.
9

• List common causes of macrocytosis and macrocytic
  anemia.
• Describe the morphologic hallmarks of
  megaloblastic erythropoiesis and granulopoiesis
  in the blood and bone marrow.
• Diagram the biochemical pathway which explains
  how folate and vitamin B12 deficiency ultimately
  impair thymidylate synthesis, and methionine and
  fatty acid metabolism.
• 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.
• 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
• Describe the clinical, laboratory and autoimmune
  findings associated with pernicious anemia.
• List the appropriate therapies for B12 deficiency
  and folate deficiency.

10

• 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.

11

• 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 Coombs 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.

12
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. Paroxys
mal 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.
13

• Describe the pathophysiology and site of red
  blood cell destruction of immune-mediated
  hemolysis due to IgG, IgM, and complement.
• Describe the procedures involved in performing a
  direct antiglobulin test (direct Coombs test) and
  an indirect antiglobulin test (indirect Coombs
  test).
• 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
• Immunoglobulin class of the antibody
• Presence of red blood cell agglutination
• Direct antiglobulin test results
• Clinical manifestations

14

• 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.
• Describe the hematologic findings and
  pathophysiological changes that are associated
  with beta-thalassemia major.
• List the mechanisms and consequences of iron
  overload and infections associated with
  beta-thalassemia major.
• Know the epidemiology and relative severity of
  the sickle cell genotypes.
• Understand the organ system involvement by sickle
  cell disease as examples of the pathophysiology
  of the sickling process, specifically kidney and
  spleen. 
• Appreciate the significance of pain frequency as
  an indicator of disease severity
• Describe the case definition, pathology and
  presentation of the major sickle cell
  complications of stroke, and acute chest syndrome
• Understand the significance of abnormal cell
  adhesion and abnormal nitric oxide metabolism to
  sickle cell disease complications. 

15

• 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.
• Define the leukemoid reaction and list specific
  causes of this phenomenon.
• List the differential diagnosis for eosinophilia.
• Given a PBS be able to identify common blood
  borne parasites, e.g. malaria, babesia,
  trypanosomiasis, etc.

16

• 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.
• Describe the pathophysiologic basis for acute and
  chronic graft versus host disease.
• Describe the changes in humoral and cellular
  immunity following stem cell transplant and how
  they relate to infectious complications.
• Describe the mechanisms (production, destruction,
  and sequestration) and consequences of
  pancytopenia.
• Identify the pathophysiologic mechanisms of bone
  marrow aplasia.

17

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

1
18

• 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 11 mixing study can
  distinguish a clotting factor deficiency from an
  inhibitor of coagulation.
• Be able to explain the utility and derivation of
  the INR.
• Be able to compare and contrast three tests of
  platelet function - bleeding time, PFA-100, and
  platelet aggregation studies.
• Be able to diagram the formation of the D-dimer
  and explain its utility in diagnosis venous
  thromboembolic disease.

2
19

• 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.
  
• List three mechanisms that could lead to
  thrombocytopenia.
• Be able to identify three methods of treating ITP
  and the mechanism by which they increase the
  platelet counts.

3
20

• Identify the components of Virchow's triad and
  their pathophysiologic contribution to
  thrombosis.
• 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).
• 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.
• Be able to list 3 clinical clues suggesting an
  inherited hypercoagulable disorder.
• 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.
• Be able to list at least three acquired disorders
  that are associated with recurrent venous or
  arterial thromboembolism.
• Be able to describe the clinical features and
  criteria for diagnosis of antiphospholipid
  antibody syndrome.
• What is the KEY factor in determining how long
  someone should be anticoagulated for a venous
  thrombosis?

4
21

• Be able to name two oral antiplatelet agents and
  one intravenous one.
• Be able to describe the mechanism of the
  antiplatelet effect of the following agents.
• Aspirin
• Clopidogrel
• Abciximab
• Name the anticoagulant protein to which heparin
  binds.
• 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.
• Be able to name a direct thrombin inhibitor and
  indicate one clinical use.
• Be able to give the mechanism of how warfarin
  works and name at least four clotting factors it
  affects.
• Name and know the pathophysiology of one unique
  side effect of both heparin and warfarin.
• Name three disease states for which thrombolytic
  therapy is used.
• Name one thrombolytic agent and describe how it
  works.
• Given a brief patient scenario, be able to select
  from a list of agents the best anticoagulant for
  that patient

5
22

• Be able to describe five screening tests of
  hemostasis and list several causes of an abnormal
  result in each case.
• Be able to distinguish between signs and symptoms
  of primary hemostasis defects and plasma
  coagulation defects.
• Be able to explain why a marked deficiency of von
  Willebrand factor leads to excessive bleeding.
• 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.
• 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.
• Explain why a patient with severe von Willebrand
  disease and a patient with hemophilia A may both
  have a prolonged PTT.
• 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
23

• 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
24

• Be able to name the two main naturally
  occurring antibodies to red cell antigens.
• Be able to name the four major blood types
  (phenotypes) in the ABO system.
• 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.
• Be able to explain why the ABO system is the most
  important red cell blood group system for
  transfusion therapy.
• 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.
  
• 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.
• Be able to list the three essential steps in
  blood compatibility testing, and the purpose of
  each step.
• 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
25

• Be able to give three reasons why blood component
  therapy is preferable to whole blood therapy.
• Be able to name the clinical indication for red
  cell transfusion.
• Two methods of platelet product preparation are
  now commonly used. Be able to state what they
  are.
• 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.
• Blood products are often ordered to be CMV
  negative, irradiated, and / or filtered. Be able
  to give one clinical indication for each.

2
26

• Be able to list two indications for transfusing
  fresh frozen plasma (FFP).
• Be able to list the three major therapeutic
  constituents of cryoprecipitate, and name a
  clinical indication for its use.
• 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.
• List the main coagulation abnormalities that
  occur after massive transfusion, and outline the
  appropriate treatment for each.

3
27

• Be able to list the major clinical effects of
  intravascular hemolytic transfusion reactions.
• Be able to identify the most effective method
  known to prevent the majority of acute hemolytic
  transfusion reactions.
• 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
28

• Be able to name the blood component most likely
  to cause bacterial sepsis, and explain the reason
  why.
• 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.
• Be able to give the approximate risk of HIV
  transmission per unit of blood.
• Be able to explain the meaning of window period
  in the context of transmission of West Nile virus
  in blood or transplanted tissues.
• 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
29

• Describe the basic pathogenesis of NHL with
  respect to cytogenetic alterations involving the
  Bcl-2 and Myc oncogenes, and the t(1418)
  translocation.
• Describe the basic pathologic classification of
  NHL (the WHO classification).
• Describe the predisposing factors to developing
  NHL, including infectious agents associated with
  development of specific lymphomas.
• Compare and contrast the natural history and
  clinical features of follicular lymphoma and
  diffuse large B cell lymphoma.
• Describe treatment approach and expected outcomes
  in patients with follicular lymphoma and in
  patients with diffuse large B cell lymphoma.
• Name the common causes of generalized
  lymphadenopathy.
• Identify the types of lymphoma and treatment
  approach in people with AIDS.

30

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

31

• 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.
• 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.
• Describe the staging of CLL, and features that
  correlate with a better or worse prognosis.
• Describe complications of CLL that exemplify the
  immune dysfunction associated with this disease.
• Name at least four symptoms and/or complications
  of CLL that are an indication for treatment.
• Compare and contrast CLL and CML in terms of
  molecular mechanism, age at onset, symptoms,
  physical exam findings, typical blood counts,
  treatment, and outcome.

32

• Diagram the chromosomal translocation that
  generates the Philadelphia chromosome, identify
  the genes involved and the protein created by
  this translocation.
• Describe how the bcr-abl fusion protein causes
  leukemia and provides a target for effective
  therapy in CML.
• Describe the presenting features of CML,
  including age at presentation, the most common
  symptoms, one physical exam finding, and a
  typical CBC.
• Describe the typical findings on the blood smear
  in patients with CML, emphasizing the number and
  types of leukocytes seen in the blood.
• 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.

33

• Identify the age and gender distribution of
  patients with ALL.
• Name common symptoms/signs and common laboratory
  findings in a patient presenting with ALL.
• Briefly describe two tests that can be used to
  distinguish leukemic blast cells of ALL from
  leukemic blast cells of AML.
• 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.
• Describe one complication that leads to mortality
  in ALL.

34

• 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.
• 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).
• 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.
• Name two favorable and two adverse cytogenetic
  abnormalities in AML.
• 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).
• Be able to identify the complications of
  induction chemotherapy for AML. Name which
  complications contribute to mortality.
• Compare and contrast AML and ALL in terms of age
  of patients, central nervous system involvement,
  treatment, and outcome.

35

• 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.
• Name the major criteria used to diagnose multiple
  myeloma.
• Describe at least five complications that may
  occur in patients with multiple myeloma.
• Describe the pathophysiology of renal failure in
  patients with multiple myeloma.
• Describe the pathophysiology, x-ray appearance,
  complications, and treatment of bone
  abnormalities in multiple myeloma.
• Describe indications for therapy, treatment, and
  prognostic indicators for patients with multiple
  myeloma.
• Define the diagnostic criteria, incidence, and
  clinical course of patients with monoclonal
  gammopathy of unknown significance.
• Define amyloid and indicate two proteins that can
  cause amyloid deposition in tissues.
• Describe the clinical features and prognosis of
  patients with primary amyloidosis.

36

• Describe the typical age and classic peripheral
  blood findings of patients with myelodysplasia.
• Describe the bone marrow findings and
  cytogenetics seen in patients with
  myelodysplasia.
• Describe three laboratory determinants of
  prognosis in patients with myelodysplasia.
• 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.

37

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

38

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

39

• 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.
• Define the leukemoid reaction and list specific
  causes of this phenomenon.
• List the differential diagnosis for eosinophilia.
• Given a PBS be able to identify common blood
  borne parasites, e.g. malaria, babesia,
  trypanosomiasis, etc.