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138 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(not Folate), folate deficiency much easily reached through bad diet.
Shows marked reticulocytosis
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)
What is 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 and labs)?
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.
Blood Dyscrasias-Sickle Cell Anemia: 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.
Blood Dyscrasias-Sickle Cell Anemia: What can precipitate sickling?
Low O2, dehydration.
Blood Dyscrasias-Sickle Cell Anemia: 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.
Blood Dyscrasias-Sickle Cell Anemia: What is the HbC defect?
Different Beta-chain mutation, the patients with HbC or HbSC have milder dz than HbSS patients.
Blood Dyscrasias-Sickle Cell Anemia: 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.
Blood Dyscrasias-Beta-Thalassemia: Patient Presentation of Beta-Thalassemia major?
severe anemia requiring blood transfusion. Cardiac failure is often due to secondary hemochromatosis.
Blood Dyscrasias-Beta-Thalassemia: Etiology of Beta-Thalassemia major?
Beta chain is absent, fetal Hgb production is compensatorily increased but is inadequate.
Blood Dyscrasias-Beta-Thalassemia: 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.
DIC: What is the definition of DIC?
Activation of the coagulation cascade leading to microthrombi and global consumption of platelets, fibrin, and coagulation factors.
DIC: What causes DIC?
Obstetric complications (most common cause), gram-negative sepsis, transfusion, trauma, malignancy, acute pancreatitis, nephrotic syndrome.
DIC: What are the lab findings in DIC?
Increased PT, increased PTT, incrased fibrin split products (D-dimers), decreased platelet count.
Bleeding Disorders: 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).
Bleeding Disorders: 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)
Bleeding Disorders: What is the deficiency in Hemophilia A?
Factor VIII
Bleeding Disorders: What is the deficiency in Hemophilia B?
Factor IX
Bleeding Disorders: What is the deficiency in vW dz?
Deficiency of von Willebrand's antigen.
Bleeding Disorders: Which factors does the PT measure?
Extrinsic: Factors II, V, VII, and X.
Bleeding Disorders: Which factors does the PTT measure?
Intrinsic: All factors except VII and XIII.
Hemorrhagic disorders: What presents with increased bleeding time, normal platelet count, 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.
Hemorrhagic disorders: What presents with decreased platelet count, increased bleeding time, and normal PT/PTT?
Thrombocytopenia
Hemorrhagic disorders: Which diseases present with increased PTT and normal PT, platelet count, and bleeding time?
Hemophilia A and B
Hemorrhagic disorders: What presents with a high PTT, normal PT, normal platelets, and increased bleeding time?
vW disease
Hemorrhagic disorders: What presents with increased Bleeding time/Pt/PTT and decreased platelet count?
DIC
Lymphomas: Hodgkin's Versus NHL: Which one presents with Reed-Sternberg cells?
Hodgkin's
Lymphomas: Hodgkin's Versus NHL: Which one is associated with HIV and immunosuppression?
NHL
Lymphomas: Hodgkin's Versus NHL: Which one involves multiple, peripheral nodes, with common extranodal involvement?
NHL
Lymphomas: Hodgkin's Versus NHL: Which one is localized to a single group of nodes, with contiguous spread and rare extranodal involvement?
HL
Lymphomas: Hodgkin's Versus NHL: Which one presents with constitutional signs/symptoms: low-grade fever, night sweats, weight loss?
HL (NHL has few signs/symptoms)
Lymphomas: Hodgkin's Versus NHL: Which one presents with mediastinal lymphadenopathy?
HL
Lymphomas: Hodgkin's Versus NHL: Which one involves mostly the B cells (except lymphoblastic origin)?
NHL
Lymphomas: Hodgkin's Versus NHL: Which one has hypergammaglobulinemia?
neither. Multiple Myeloma has hypergammaglobulinemia, where the excess B cells are in the resting state.
Lymphomas: Hodgkin's Versus NHL: Which one has a 50% association with EBV?
HL
Lymphomas: Hodgkin's Versus NHL: Which one has bimodal age distribution?
HL (NHL has peak incidence at 20-40 years old)
Lymphomas: Hodgkin's Versus NHL: Which one has more common male presentation?
HL
Hodgkin's: What factors denote a good prognosis?
Increased lymphocytes, decreased RS cells.
Hodgkin's: Which HL type has the best prognosis?
Nodular sclerosing (65-75%), which has least RS cells and lots of lymphocytes. Lymphocyte-predominant LH also has excellent prognosis.
Hodgkin's: Which HL type is the most common?
Nodular sclerosing, affecting women more than men and primarily young adults.
Hodgkin's: What is the prognosis of mixed cellular HL?
Intermediate. There are lots of lymphocytes but also lots of RS cells.
Hodgkin's: Which HL type has the worst prognosis?
Lymphocyte-depleted, which affects older males with disseminated disease.
Hodgkin's: Which HL type has the most RS cells?
Mixed cellular.
NHL: Which NHL type has only B cells?
Small Lymphocytic lymphoma, follicular lymphoma, Burkitt's
NHL: Which NHL type has a mix of B cells and T cells?
Diffuse large cell , occurring mostly in elderly but sometimes in children.
NHL: Which NHL type has only T cells?
Lymphoblastic Lymphoma, which has immature T cells. It is a very aggressive T-cell lymphoma.
NHL: Which type is associated with a t(8;14) c-myc gene mutation?
Burkitt's Lymphoma, occurring mostly in children. Has a high-grade "starry sky" apearance.
NHL: Which type is associated with a t(14;18) mutation and overexpression of bcl-2?
Follicular lymphoma, which is difficult to cure but has an indolent course.
NHL: Which type is associated with EBV infection and is endemic in africa?
Burkitt's
NHL: Which is the most common childhood NHL?
Lymphoblastic Lymphoma, which also presents with ALL and a mediastinal mass.
NHL: Which is the most common adult version of NHL?
Follicular lymphoma.
NHL: Which types occur in adults?
Small lymphocytic lymphoma, follicular lymphoma.
NHL: Which types occur in children?
Lymphoblastic lymphoma, Burkitt's lymphoma.
NHL: Which one has a distribution of 80% adults and 20% children?
Diffuse large cell lymphoma, which ALSO has an 80% B cells 20% T cell distribution.
NHL: Which low-grade NHL type presents like CLL?
Small Lymphocytic lymphoma.
NHL: AUTHOR
John Peoples
Leukemias: Peripheral and bone marrow characteristics
Increased circulating leukocytes, bone marrow infiltrates of leukemic cells
Leukemias: Consequences of marrrow failure
Anemia (dec. RBC's), infections (dec. WBC's), hemorrhage (dec. platelets)
Leukemias: Common organs of infiltration
Liver, spleen, lymph nodes
Leukemias: Characteristics of acute leukemias
Blasts predominate, children or elderly, short or drastic course
Leukemias: ALL characteristics (4)
Lympholasts (pre-B or pre-T), children, most responsive to therapy, associated with Down's Syndrome
Leukemias: AML characteristics
Myeloblasts, adults, auer rods
Leukemias: Characteristics of chronic leukemias
More mature cells, midlife age range, longer, less devastating course
Leukemias: CLL characteristics - cells
Lymphocytes, non-Ab producing B cells, increased smudge cells on peripheral blood smear
Leukemias: CLL - population
older adults
Leukemias: CLL - presentation and course
lymphadenopathy, hepatosplenomegaly, few sx., indolent course
Leukemias: CLL is similar to?
very similar to SLL (small lymphocytic lymphoma)
Leukemias: CLL is associated with what type of anemia?
warm antibody autoimmune hemolytic anemia
Leukemias: CML cell characteristics
Myeloid stem cells, increased neutrophils and metamyelocytes
Leukemias: CML translocation?
Ph Chromosome, t(9;22), bcr-abl
Leukemias: CML acute complications?
blast crisis (AML)
Chromosomal translocations - the following disorder is associated with what translocation?: CML
Ph chromosome, t(9;22), bcr-abl
Chromosomal translocations - the following disorder is associated with what translocation?: Burkitt's lymphoma
t(8;14), c-myc activation
Chromosomal translocations - the following disorder is associated with what translocation?: Follicular lymphomas
t(14;18), bcl-2 activation
Chromosomal translocations - the following disorder is associated with what translocation?: AML- M3 type
t(15;17), responsive to all-trans retinoic acid (ATRA)
Chromosomal translocations - the following disorder is associated with what translocation?: Ewing's sarcoma
t(11;22)
Chromosomal translocations - the following disorder is associated with what translocation?: Mantle cell lymphoma
t(11;14)
Lymphomas and Leukemias: What are the chronic leukemias associated with T-lymphoblasts?
Sezary Syndrome, CLL-T (both L2)
Lymphomas and Leukemias: What are the acute leukemias associated with T-lymphoblasts?
ALL-T (L2), ALL-null (L1), ALL-common(L1)
Lymphomas and Leukemias: What are the chronic leukemias associated with B-lymphoblasts?
CLL-B (L3)
Lymphomas and Leukemias: What are the acute leukemias associated with B-lymphoblasts?
ALL-B (L3)
Lymphomas and Leukemias: What are the chronic leukemias associated with monoblasts?
Chonic monocytic (M5), chronic myelomonocytic (M4)
Lymphomas and Leukemias: What are the acute leukemias associated with monoblasts?
Acute monocytic (M5), acute myelomonocytic (M5)
Lymphomas and Leukemias: What are the chronic leukemias associated with myeloblasts?
CML (M1, 2 and 3), Polycythemia rubra vera (M1), myelofibrosis (M1)
Lymphomas and Leukemias: What are the acute leukemias associated with myeloblasts?
AML (M2 and M1), Promyelocytic (M1)
Lymphomas and Leukemias: What are the chronic leukemias associated with eos-myeloblasts?
Eosinophilic (rare)
Lymphomas and Leukemias: What are the chronic leukemias associated with normoblasts?
Chronic erythroid (M6, rare)
Lymphomas and Leukemias: What are the acute leukemias associated with normoblasts?
acute erythroleukemia (M6)
Lymphomas and Leukemias: What are the chronic leukemias associated with megakaryoblasts?
Idiopathic thrombocytopenia (M7)
Lymphomas and Leukemias: What are the acute leukemias associated wwith megakaryoblasts?
acute megakaryocytic leukemias (M7)
Multiple Myeloma: What type of cell proliferates in MM, and what is its histologic appearance
Monoclonal plasma cell, fried egg apearance
Multiple Myeloma: Where does MM arise?
bone marrow
Multiple Myeloma: The 2 most common ab's, in order, are:
IgG (55%), IgA (25%)
Multiple Myeloma: Common symptoms are:
lytic bone lesions and hypercalcemia, renal insifficiency, increased suscpetibility to infection, anemia
Multiple Myeloma: This disease is associated with:
primary amyloidosis
Multiple Myeloma: Ig light chains are also called:
Bence Jones proteins
Multiple Myeloma: 3 key diagnostic features:
lytic bone lesions on x-ray, M-spike on serum protein electrophoresis, Bence-Jones proteins in urine
Multiple Myeloma: Red blood cell appearance on peripheral smear:
Rouleaux formation (poker chips)
Multiple Myeloma: What 2 differences are seen in Waldenstrom's macroglobulinemia?
M-spike is IgM, no lytic lesions
Blood composition: Plasma-clotting factors = what?
serum
Blood composition: Blood is ___% of body weight
0.08
Blood composition: Blood is ___% plasma.
55% The rest is formed elements (hematocrit)
Blood composition: Plasma is ____% proteins.
0.07
Blood composition: Plasma proteins are ___% albumin.
0.55
Blood composition: Plasma proteins are ___% globulins
0.38
Blood composition: Leukocytes are normally ____% PMNs, ___% lymphocytes, ___% monocytes, ___% eosinophils, ___basophils.
40-70% PMNs, 20-40% lymphos, 2-10% monos, 1-6% eos, <1% basophils
Blood composition: AUTHOR
Chris Leander
Coagulation Cascade: Factor initiating intrinsic pathway?
XII
Coagulation Cascade: Factor(s) initiating extrinsic pathway?
VII and tissue factor
Coagulation Cascade: Function of factor XIII?
Forms cross-linked fibrin
Coagulation Cascade: Factors examined with prothrombin time (PT)?
VII, X, V, prothrombin, fibrinogen (Hoffbrand. Haematology. 247)
Coagulation Cascade: Factors examined with partial thromboplastin time (PTT)?
VIII, IX, XI, XII, X, V, prothrombin, fibrinogen (Hoffbrand. Haematology. 247)
Coagulation Cascade: Vitamin K dependent factors?
II, VII, IX, X, protein C, protein S (243)
Coagulation Cascade: Factors requiring phospholipid surface for activation?
IX and X
Coagulation Cascade: Factor I also known as?
Fibrinogen
Coagulation Cascade: Factor II also know as?
Prothrombin
Convergence of coagulation, complement, and kinin pathways: Two substrates of Factor XIIa?
Factor XI and Prekallikrein
Convergence of coagulation, complement, and kinin pathways: Components involved in the activation of factor XII?
Collagen, basement membrane, activated platelets, HMWK (cofactor [high molecular weight kallikrein])
Convergence of coagulation, complement, and kinin pathways: Two substrates of kallikrein?
HMWK and Plasminogen
Convergence of coagulation, complement, and kinin pathways: Complement protein on which plasminogen acts?
C3
Convergence of coagulation, complement, and kinin pathways: Three functions of bradykinin?
Increase vasodilation, increase permeability, increase pain
Convergence of coagulation, complement, and kinin pathways: What converts HMWK to bradykinin?
kallikrein
Convergence of coagulation, complement, and kinin pathways: What does plasmin's action on fibrin produce?
fibrin split products