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Final Units 3-5 Heme
Hematology Final for El Amouri
| Question | Answer |
|---|---|
| What is the cause of Iron Deficiency Anemia (IDA)? | It is a deficiency of iron due to malnutrition, malabsorption, or blood loss |
| What is the cause of Anemia of Chronic Diseases (ACD)? | Iron is blocked from reaching the RBC precursors due to impaired release from stores |
| The stain used to view unused iron | Prussian blue |
| What is the cause of Sideroblastic Anemia (SA)? | Iron leaves the stores but cannot be inserted to protoporphyrin ring. It accumulates in the mitochondria and forms ringed sideroblasts. |
| What are the three progressions (stages) of IDA? | Stage 1: Iron store depletion Stage 2: Iron deficient erythropoiesis Stage 3: Iron deficiency anemia |
| What is the red cell morphology for stage 1 IDA? | Normocytic normochromic |
| What is the red cell morphology for stage 3 IDA? | Microcytic hypochromic |
| What are the iron studies for IDA? (ferritin, serum iron, TIBC, and % saturation) | Ferritin: decreased Serum iron: decreased TIBC: increased Transferrin saturation: decreased |
| What are the iron studies for ACD? (ferritin, serum iron, TIBC, and % saturation) | Ferritin: normal-increased Serum iron: decreased TIBC: normal-decreased Transferrin saturation: normal-decreased |
| What are the iron studies for SA? (ferritin, serum iron, TIBC, and % saturation) | Ferritin: normal-increased Serum iron: normal-increased TIBC: normal-decreased Transferrin saturation: increased |
| Primary megaloblastic anemia | Nutritional deficiency of B12 or folate that leads to impaired DNA synthesis. Causes impaired nuclear maturation and cell division. |
| Secondary megaloblastic anemia | Due to malabsorption condition such as pernicious anemia where there is a defect in HCl secretion and Intrinsic Factor (IF) |
| Cell types affected by megaloblastic anemia | All cell types (pancytopenia) |
| Nuclear cytoplasm asynchrony | Nuclear maturation defect characterized by high N:C ratio; immature nucleus with mature cytoplasm. Usually results in ineffective erythropoiesis. |
| Non-megaloblastic anemia | Unrelated to nutritional deficiency. Characterized by high liver enzymes from liver disease or alchoholism. |
| Peripheral blood findings in megaloblastic anemia | Pancytopenia Macrocytic normochromic cells Macro-ovalocytes Anisocytosis Hypersegmented neutrophils HJ bodies Ineffective erythropoiesis |
| BM findings in megaloblastic anemia | Marked N:C asynchrony |
| Chemistry findings in megaloblastic anemia | Decreased serum folate and/or B12 Increased MMA Increased homocysteine |
| Laboratory findings in non-megaloblastic anemia | Round macrocytes No hypersegmented neutrophils Normal WBC, and PLT Normal B12 and folate Normal MMA and homocysteine |
| Intravascular hemolytic anemia | Occurs within blood vessels Increased schistocyes Increased serum bilirubin Decreased haptoglobin Hemoglobinuria |
| Extravascular hemolytic anemia | Occurs mainly in spleen Increased spherocytes Increased serum bilirubin Hepatosplenomegaly |
| What is the job of haptoglobin in intravascular hemolysis? | To transport and elminate serum bilirubin |
| How is bilirubin eliminated in extravascular hemolysis? | By the spleen |
| DAT seperates hemolytic anemias into what two groups? | Immune-mediated (allo or auto immune) or non-immune (inherited) |
| Compensated hemolytic anemia | No anemia unless RBC destruction exceeds production |
| What are the three types of intrinsic RBC defects? | Membrane protein defects Enzyme defects Hgb (globin chain) defects |
| What are the intrinsic membrane protein defect HA's? | Hereditary spherocytosis (HS) Hereditary elliptocytosis (HE) Hereditary stomatocytosis PNH (CD55 and CD59) |
| What are the intrinsic enzyme defect HA's? | Glucose-6-phosphate dehydrogenase(G6PD Pyruvate kinase (PK) deficiency |
| What is hereditary spherocytosis (HS)? | Defect in vertical proteins. Shows elevated number of spherocytes and MCHC <36%. |
| What is the diagnostic test for HS? | Osmotic fragility test for spherocytes and negative DAT |
| What is hereditary elliptocytosis and it's severe form? | Horizontal protein defect. When fragmentation begins to occur it is called hereditary pyropoikilocytosis (HPP). |
| What is hereditary stomatocytosis? | Defect in membrane protein stomatin which helps regulate ions across the red cell channel |
| What two types of hereditary stomatocytosis are there? | Overhydrated: Excessive gain of Na+ and water rushes in causing uncompensated HA Dehydrated: Excessive loss of Na+ and water rushes out causing compensated HA |
| What is PNH? | Defect in GPI anchor for complement regulator proteins CD55 and CD59. C' reg. proteins missing = C' activated, cells destroyed |
| Tests for diagnosing PNH | Sucrose hemolysis (sugar water), Ham's (acid serum) and flow analysis |
| What is G6PD deficiency? | Causes impaired generation of glutathione in reduced state (GSH) that helps to prevent oxidative damage to Hgb. Causes denatured, oxidized Hgb forming Heinz bodies. |
| What type of stain is used to view Heinz bodies? | Supravital stain |
| What will the blood film of G6PD deficient patient look like? | Bite cells and blister cells |
| What is a source of error in testing for G6PD deficiency? | Reticulocytosis because retics have high G6PD activity causing false increase in levels |
| DAT tests for what antibodies associated with HA? | Autoimmune antibodies (Warm or cold) |
| IAT tests for what antibodies associated with HA? | Alloimmune antibodies (transfusion reaction or hemolytic disease of the newborn - HDN) |
| Warm and cold AIHA are associated with which HA? | Autoimmune hemolytic anemia |
| Amino acid substitution for Hgb S | B6(Glu) -> (Val) |
| Amino acid substitution for Hgb C | B6(Glu) -> (Lys) |
| Amino acid substitution for Hgb E | B26(Glu) -> (Lys) |
| Is Hgb SA sickle cell anemia or trait? | Trait; asymptomatic |
| Is Hgb SS sickle cell trait or anemia? | Anemia (also known as sickle cell disease) |
| Is Hgb S soluble in the deoxygentated state or the oxygenated state? | Oxygenated |
| Under what conditions does Hgb S turn into insoluble aggregates? | Under deoxygenated, deoxyhemoglobin state; Hgb S polymerizes |
| What clinical condition is the hallmark manifestation of sickle cell disease? | Vaso-occlusive crisis; causes very intense pain termed "body biting" |
| Deterioration of tissues from recurring vaso-occlusive episodes can cause what two things? | Autosplenectomy and overwhelming infections |
| Screening test for sickle cell and it's reagent | Solubility test - Sodium Dithionite (reducing agent that takes O2 from cells and causes sickling = turbidity) |
| Major difference in Thalassemia and Hemoglobinopathies? | Thalassemia is decreased or absent synthesis of structurally NORMAL globin chains. Hgbopathies are synthesis of structurally ABNORMAL globin chains. |
| Thalassemias are characterized by what RBC morphology and iron status | Microcytic hypochromic and NORMAL iron status |
| Types of alpha Thalassemia | Intermedia (Hgb H) [4 beta chains] Major (Hgb Barts/Hydrops Fetalis) [4 gamma chains] |
| Which alpha Thalassemia is incompatible with life? | Hydrops Fetalis |
| Type of beta Thalassemia | Major (Cooley's or Mediterranean anemia) [Little or no Beta chain synthesis; Majority are Hgb F] |
| Classification of anemia deals with stem cell defects | Aplastic anemia (Fanconi anemia) causing hypocellular BM and pancytopenia |
| Classification of anemia that deals with progenitor cell defects | Pure red cell aplasia (PRCA) where there is failure to produce erythroid progenitor cells but WBC's and PLT's are normal [Diamond Blackfan syndrome] |
| Classification of anemia dealing with bone marrow replacement | Myelophthisic anemia |
| Stages of neutrophil development | Myeloblast Promyelocyte Myelocyte Metamyelocyte Band Neutrophil |
| First stage of neutrophil development incapable of division | Metamyelocyte |
| Which pool are dividing cells located? | Mitotic pool |
| Which pool are non-dividing cells located? | Post-mitotic pool |
| Where do cells travel in the event of infection? | Directly from marginal pool to tissues |
| Formula for absolute count of WBC's | Absolute count = Relative count (in decimal)*WBC count |
| Is LAP higher in Leukemoid reaction or CML | Leukemoid reaction |
| Is Philidelphia chromosome associated with CLL or CML? | CML - Chronic Myeloid Leukemia |
| Causes malignancies and abnormal proliferation of cells after mutation | Proto-oncogene -> Oncogene |
| Causes inability to suppress malignant clones of cells | Loss of a tumor suppressor gene |
| Are Auer rods found in lymphoid or myeloid leukemias? | Myeloid leukemia |
| Organization classifies leukemia by someone having >30% blasts and relies on morphology | French-American-British (FAB) |
| Organization classifies leukemia by someone having >20% blasts and relies on immunophenotyping | The World Health Organization (WHO) |
| AML classified by t(8;21) | M2: Acute Myeloblastic Leukemia with maturation |
| AML classified by t(15;17) and multiple Auer rods | M3: Acute Promyelocytic (PG) Leukemia |
| AML classified by Inv (16) | M4: Acute Myelomonocytic leukemia |
| AML classified by t(9;11) | M5: Acute Monocytic leukemia |
| M6 also goes by what other name? | Acute Erythroblastic leukemia |
| AML classified by t(1;22) | Acute Megakaryoblastic leukemia |
| ALL classification with homogenous population of blasts and seen in children 2-10 years old | L1 |
| ALL with heterogeneous population of blasts seen in adolescents and adults | L2 |
| Burkitt's type leukemia with homogenous populations of LARGE blasts; seen in adults and children | L3 |
| Importance of immunophenotyping in ALL | To determine B or T cell origin; B cell has better prognosis and T cells more aggressive |
| Most important prognostic indicators of ALL | Age WBC count Cell type/Lineage |
| MPO, SBB, Specific esterase (SE) and NSE are all positive for which leukemia? | Acute Myeloid Leukemia (AML/ANLL) [SE pos for granuloblast; NSE pos for monoblast] |
| MPO, SBB, Specific esterase (SE) and NSE are all negative for which leukemia? | Acute Lymphoid Leukemia (ALL) |
| What is cytochemical in NSE? | a-naphthyl Butyrate/Acetate |
| TdT and PAS usually negative for what? | Acute Myeloid Leukemia (AML/ANLL) |
| TdT and PAS usually positive for what? | Acute Lymphoid Leukemia (ALL) |
| Chronic myelogenous/granulocytic leukemia is characterized by what? | Marked leukocytosis (>50,000/ul) and includes all three granulocytes maturation stages [immature granulocytes] (VS leukemoid with only neutrophils) |
| Philidephia (Ph') chromosome deals with which leukemia and is what translocation? | CGL and t(9;22) |
| What are other names for Ph' chromosome? | BCR-ABL fusion gene P210 protein Philidelphia chromosome Chronic granulocytic leukemia |
| Blast crisis | Where CGL progresses to produce 90% blasts and resembles AML. Must know of previous CML condition and patients usually die. |
| What mutation do Polycythemia Vera (PV) patients have? | JAK2 mutation |
| What is primary PV? | Polycythemia Vera; overproduction of all cells (no correlation with EPO) |
| Relative PV | Decreased plasma volume from vomitting, diarrhea, dehydration |
| Secondary PV | Appropriate and inappropriate increase in EPO; O2 elevated and EPO abnormal; associated with: Renal disease Tissue hypoxia Pulmonary disease High O2 affinity Hgb |
| What is Chronic Lympohocytic Leukemia (CLL)? | Overproduction of non-functional lymphs; immune system doesn't respond properly to infection |
| Hallmark blood film characteristic of absolute lymphocytosis patient | Smudge cells |
| Owl eyes are characteristic of what lymphoma? | Hodgkin Lymphoma (HL) |
| Difference between leukemia and lymphoma | Lymphoma is solid tumor involving lymphatic tissue Leukemia is liquid tumor where malignant cells circulate |
| Burkitt lymphoma with C-MYC gene rearrangement [t(8;14)] | Non-hodgkin Lymphoma (NHL) - Similar to L3 |
| Aggressive form of CLL | Prolymphocytic leukemia (PLL) |
| TRAP positive leukemia | Hairy Cell Leukemia (HCL) |
| What is TRAP? | Tartrate resistent acid phosphatase stain for HCL |
| Presence of Rouleaux Bence Jones Proteinuria M spike | Multiple Myeloma (plasma cell myeloma) |
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