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Hematology/Oncology
Pathology: Hematology & Oncology
| Question | Answer |
|---|---|
| Which molecules does t-PA act on? | t-PA converts plasminogen into plasmin which in turn degrades fibrin clots |
| 1. Platelets link to each other through fibrinogen. Which is the fibrinogen receptor on the platelet? 2. Which molecule causes receptor activation? | 1. GPIIb-IIIa 2. ADP |
| What role does Clopidogrel (plavix) play in coagulation homeostasis? | - clopidogrel blocks the ADP receptor on platelets preventing GpIIb-IIIa expression - prevents clotting |
| 1. The intrinsic and extrinsic coagulation pathways converge at the activation of which factor? 2. What does the activated factor do? | 1. factor X 2. converts prothrombin to thrombin |
| What is the main purpose of thrombin? | to turn fibrinogen into fibrin monomers |
| 1. How does Warfarin (coumadin) inhibit clotting? 2. How does Heparin inhibit clotting? | 1. inhibits the epoxide reductase that activates Vitamin K 2. heparin activates antithrombin which inactivates clotting factors |
| 1. Determining __ time can monitor heparin therapy. 2. Which coagulation pathway is this? | HEP, PTT, INT 1. partial thromboplastin 2. intrinsic |
| 1. Determining __ time can monitor Warfarin therapy. 2. Which coagulation pathway is measured? | 1. Prothrombin 2. extrinsic |
| 1. disorder with hypersegmented neutrophils 2. Rh- mother exposed to Rh+ blood; next Rh+ pregnancy may have what disorder? What is the treatment | 1. megaloblastic macrocytic anemia caused by B12 deficiency 2. hemolytic disease of the newborn; Rh antigen immunoglobulin (Rhogam) |
| Clotting factor deficiency in: 1. Hemophilia A 2. Hemophilia B 3. Is prothrombin time or activated partial thromboplastin time changed? | 1. factor 8 2. factor 9 3. factor 8 & 9 are in the intrinsic pathway so only PTT pathway is elevated not PT |
| What protein forms interaction between platelets and collagen? | von Willebrand factor |
| 1. Where is fibrinogen made? 2. What happens to it after it enters the blood stream? 3. When is it released again? | 1. liver 2. endocytized by platelets and stored in alpha granules 3. released upon platelet activation |
| 1. Which cells are in the lymphoid stem cell line? 2. How does aspirin effects clotting? | 1. B cells, T cells and NK cells 2. inhibits COX to prevent TXA2 synthesis by platelets |
| What is the overall cause of the microcytic anemias? | decreased production of hemoglobin |
| 1. What is the MCV of microcytic anemia? 2. What is the MCV of macrocytic anemia? | 1. < 80 2. > 100 |
| 1. What is the pathophysiologic cause of megaloblastic macrocytic anemia? 2. What are the biological causes? | 1. impaired DNA synthesis → cells don't progress from G2 to M phase → continue growth without cell division 2. Folate or vitamin B12 deficiency |
| What are the nonhemolytic, normocytic anemias? | 1. Anemia of chronic disease 2. Aplastic anemia 3. kidney disease (↓erythropoieten) |
| What is porphyria? | defective enzymes involved in heme synthesis |
| 1. genetic GpIb deficiency 2. genetic GpIIb/IIIa deficiency 3. antibodies against GpIIb/IIIa 4. ↓ ADAMTS13 involved in vWF degradation | 1. Bernard-Soulier disease 2. Glanzmann's thromboasthenia 3. Immune thrombocytopenic purpura 4. Thrombotic Thrombocytopenic purpura |
| What would PT and PTT in Vitamin K deficiency be? | ↑ PT and ↑ PTT |
| Associated RBC pathology 1. acanthocyte (spur cell) 2. Basophilic stippling 3. Bite cell | 1. liver disease, abetalipoproteinemia 2. thalassemias, anemia of chronic disease, iron deficiency, lead poisoning 3. G6PD deficiency |
| Associated RBC pathology 1. iron-laden mitochondria forming ring around nucleus 2. Schistocyte, helmet cell 3. Spherocyte | 1. sideroblastic anemia 2. DIC, TTP/HUS 3. hereditary spherocytosis, autoimmune hemolysis |
| Associated RBC pathology 1. Teardrop cell 2. Target cell 3. Heinz body 4. Howell-Jolly bodies | 1. bone marrow infiltration (myelofibrosis) 2. Thalassemia 3. G6PD deficiency 4. asplenia |
| How do homocysteine and methylmalonic acid levels change in: 1. folate deficiency 2. B12 deficiency | 1. ↑ homocysteine, normal methylmalonic 2. ↑ homocysteine, ↑ methylmalonic |
| Hodgkins or Non-Hodgkins? 1. Reed Sternberg cells 2. low grade fever, night sweats, weight loss 3. associated with immunosuppression (HIV) 4. extranodal presentation 5. Bimodal distribution | 1. Hodgkins 2. Both have "B" symptoms 3. NHL 4. NHL 5. Hodgkins |
| 1. Which finding indicates the best prognosis in Hodgkin lymphoma? 2. Which Hodgkin lymphoma has the best prognosis? | 1. ↑ lymphocytes 2. nodular sclerosis |
| What are Bence Jones protein and in which condition is it found? | Ig light chains (κ or λ) in urine found in Multiple Myeloma |
| Patient with dizziness, blurred vision, anemia and M spike on protein electrophoresis. | Waldenstrom's macroglobulinemia |
| Patient with back pain, anemia and M spike on protein electrophoresis. | Multiple myeloma |
| 1. Which Non-Hodgkins Lymphoma is associated with Epstein-Bar Virus? 2. A high reticulocyte count is usually indicative of ____. | 1. Burkitt's Lymphoma 2. RBC hemolysis |
| Most like leukemia by age: 1. 0 - 14 2. 15 - 39 3. 40 - 59 4. 60+ | 1. ALL 2. AML 3. AML, CML 4. CLL |
| Hemolytic Uremic Syndrome is characterized by (3): | 1. anemia 2. thrombocytopenia 3. acute renal failure |
| How is chronic myeloid leukemia differentiated from a leukemoid reaction? | CML has: 1. negative leukocyte alkaline phosphatase 2. increased basophils |
| Cancer commonly occuring in AIDS patients | Kaposi's sarcoma and Non Hodgkin's Lymphoma |
| What is the difference between intravascular and extravascular hemolysis? | 1. intravascular is RBC hemolysis within vascular system 2. extravascular is RBC hemolysis by macrophages of the spleen |
| Positive osmotic fragility test | hereditary spherocytosis or thalassemia |
| Why does Glucose-6-phosphate dehydrogenase deficiency lead to anemia? | 1. G6PD is involved in the Pentose Phosphate pathway leading to the production of Glutathione 2. without glutathione, RBCs can't break down reactive oxygen species and cannot handle oxidant stress as well |
| 1. What is the likely cause of anemia if there is reticulocytosis? 2. What bacterial agent causes aplastic crisis in patients with preexisting marrow stress? 3. What bacterial agent causes osteomyelitis in patients with sickle cell disease? | 1. one of the hemolytic anemias → ↑ erythropoeisis 2. parvovirus B19 → aplastic crisis 3. Salmonella → osteomyelitis |
| What is the cause of Paroxysmal nocturnal hemoglobinuria (PNH)? | 1. Decay-accelerating factor (DAF) inhibits complement on RBC membrane 2. In PNH, the GPI anchor that attaches DAF to the membrane is absent |
| 1. Mutation involved in sickle cell. 2. Mutation involved in HbC defect. | 1. valine for glutamic acid at position 6 of β chain 2. lysine for glutamic acid at position 6 of β chain |
| 1. Positive Coombs test 2. Schistocytes (helmet cells) seen in... | 1. autoimmune hemolytic anemia 2. mechanical destruction of RBCs in a microangiopathic anemia (DIC, TTP-HUS) |
| 1. Mechanism of action of abciximab 2. How does von Willebrand's disease effect PT and PTT tests? 3. Why is this result seen? | 1. platelet aggregation inhibitor that blocks GpIIb/IIIa 2. ↑ PTT 3. von Willebrand's factor carries factor 8 so without it there is an intrinsic pathway coagulopathy |
| What mutation is involved in Polycythemia vera? | JAK2 mutation (growth factor signaling) |
| Mechanism of Action: 1. Heparin 2. Warfarin 3. Aspirin 4. tPA 5. Clopidogrel 6. Amciximab | 1. activates antithrombin III 2. inhibits vitamin K 3. inhibits COX; prevents TXA2 synthesis 4. converts plasminogen to plasmin 5. block ADP receptor on platelet → inhibit fibrinogen binding 6. antibody binds IIb/IIIa reeptor on platelets |
| 1. Which coagulation factors are tested by prothrombin time? 2. Which coagulation factors are tested by partial thromboplastin time? 3. Which coagulation factors are carboxylated by vitamin K? | 1. 1, 2, 5, 7, and 10 2. all factors except 7 and 13 3. 2, 7, 9, 10, C and S |
| 1. Deletion of 1 α-gobulin genes 2. Deletion of 3 α-gobulin genes 3. Deletion of 2 α-gobulin genes 4. Deletion of 4 α-gobulin genes | 1. asymptomatic 2. β chains form tetramers (β2β2) 3. α-thalassemia minor 4. lethal in utera (hydrops fetalis); γ chains form tetramers (γ2γ2) |
| 1. Heterozygate with under-produced β hemoglobin chain. 2. Homozygote with absent β hemoglobin chain. | 1. β-thalassemia minor 2. β-thalassemia major |
| What is the difference between a direct and indirect Coombs test? | 1. Direct: anti-Ig antibody added to patients blood. Agglutination occurs in there Ig on the patients RBCs 2. Indirect: Normal RBCs are added to patient's serum. Agglutination occurs if patient has Ig in serum against RBCs |
| Iron Lab values in anemia: 1. ↓ serum iron; ↑ TIBC; ↓ ferritin 2. ↓ serum iron; ↓ TIBC; ↑ ferritin 3. ↑ serum iron; ↓ TIBC; normal ferritin | 1. Iron deficiency 2. Anemia of chronic disease 3. Lead poisoning |
| Where is von Willebrand's factor produced? | only clotting component not produced in the liver; made by endothelial cells and megakaryocytes |
| Patient with CLL 1. now with lymph node involvement and generalized lymphadenopathy 2. transformation into diffuse large B-cell lymphoma | 1. small lymphocytic lymphoma 2. Richter syndrome |
| 1. What is essential thrombocytosis? 2. What is myelofibrosis? 3. What is the mutation involved in both? | 1. increased megakaryocyte sensitivity to growth factors 2. proliferation of abnormal bone marrow stem cells results in replacement with collagenous connective tissue 3. JAK2 mutation |
| 1. What two structures release vWF 2. What does vWF bind? | 1. Weibel-Palade bodies of endothelial cells and α-granules of platelets 2. subendothelial collagen and GpIb on platelets |
| Where are autoantibodies against GPIIb/IIIa produced? | spleen (Immune thrombocytopenic purpura) |
| How does TTP lead to a hemolytic anemia? | vWF multimers form that cannot be cleaved leading to microthrombi |
| Function of ristocetin in diagnosing a coagulopathy | ristocetin induces platelet aggregtion by causing vWF to bind platelet GPIb; von Willebrand disease has abnormal test |
| Treatment for von Willebrand disease | desmopessin (ADH analog), increases vWF release from Weibel-Palade bodies of endothelial cells |
| Treatment for tissue plasminogen activator toxicity | aminocaproic acid |
| What are the following values in tPA toxicity: 1. PT 2. PTT 3. bleeding time | tPA cleaves fibrin, destroys coagulation factors and blocks platelet aggregation so all are increased |
| What are lines of Zahn seen in a DVT? | alternating layers of platelets/fibrin and RBCs |
| Which deficiency increases risk for warfarin skin necrosis? | protein C deficiency (proteins C and S have shorter half-life so are deficient before the other coagulation factors) |
| Most common inherited hypercoagulable state | Factor V Leiden (lacks cleavage site for protein C and S) |
| How do oral contraceptive produce a hypercoagulable state? | estrogen increases production of coagulation factors in liver |
| Which coagulation pathway do the following activate? 1. tissue thromboplastin 2. subendothelial collagen | 1. extrinsic 2. intrinsic |
| Anemia, glossitis and dysphagia. | Plummer-Vinson syndrome |
| How does chronic disease lead to anemia? | chronic disease results in production of acute phase reactants from liver, including hepcidin which sequesters iron in storage sites |
| What is the defect in sideroblastic anemia? | defective protoporphyrin synthesis, the protein that combines with iron to form heme. Usually deficiency in the enzyme ALA Synthase or B6 metabolism. |
| What is the relationship between ferritin and TIBC? | 1. when ferritin is high, TIBC will be low 2. when ferritin is low, TIBC will be high |
| Why are the thalassemias microcytic anemias while other hemobloginopathies are normocytic? | thalassemias have decreased globin production while the others have defective production |
| 1. HB Barts 2. HbH | 1. tetramers of γ Hb chains that form in utero in 4 gene α thalassemia 2. tetramers of β hemoglobin chains that form in 3 gene α thalassemia |
| How do target cells form in thalassemia? | ↑membrane to Hb ratio leads to membrane bleb in center of cell. This bleb is and the outer ring f the cell are then filled with Hb. |
| Why may vitamin B12 deficiency be seen in pancreatic insufficiency? | pancreatic proteases detach B12 from R-binder so that it can bind intrinsic factor |
| 1. What is haptoglobin? 2. Does haptoglobin levels change with intra or extravascular hemolysis? | 1. protein in the blood that binds free floating heme 2. ↓ haptoglobin levels with intravascular |
| What do Howell-Jolly bodies form? | Occassionally the RBC nucleus is not extruded from the cell and the spleen must remove it. With asplenia, these cells persist and are referred to as Howell-Jolly bodies. |
| Patient with dark urine in the morning. | paroxysmal nocturnal hemoglobinuria |
| Which microbes are associated with cold agglutinin? | high IgM against RBCs associated with Mycoplasma pneumoniae and EBV |
| The Hematopoietic stem cell contains which cluster of differentiation marking? | CD34 |
| What condition is known to have basophilia? | chronic myeloid leukemia |
| 1. What are Auer rods? 2. Which condition are they found in? | 1. crystal aggregates of myeloperoxidase 2. Acute Myeloid Leukemia (AML) |
| Mature B cells that are positive for tartrate-resistant acid phosphatase | Hairy Cell Leukemia |
| Neoplastic proliferation of mature CD4+ T cells that infiltrate skin, producing skin rash and nodules. | Mycosis Fungoides |
| What is the defect in follicular lymphoma? | 1. bcl2 on chromosome 18 translocates to Ig heavy chain locus on chromosome 14 2. overexpression of bcl2, which inhibits apoptosis of B cells that usually die after somatic hypermutation |
| What causes bone pain and hypercalcemia in multiple myeloma? | neoplastic plasma cells secrete IL-1 and IL-6 which activates osteoclasts |
| 1. Universal blood donor 2. Universal acceptor | 1. Group O - do not have any antigens with which an immune response might be made 2. Group AB - no Ab’s to attack foreign blood antigens |
| Released by eosinophils in the defence against helminths. | Major basic protein |
| 1. Coagulation factor carried by vWF 2. Which coagulation pathway is it found in? | 1. factor 8 2. intrinsic (prothrombin time) |
| Hemolytic anemia with an increased MCHC | hereditary spherocytosis (less membrane to Hb ration causes an increased MCHC) |
| How does hydroxyurea help treat sickle cell patients? | increases synthesis of HbF |
| Which enzymes are inhibited by lead poisoning? | Ferrochelatase and ALA dehydratase |
| Enzyme defective in sideroblastic anemia | ALA synthase |
| painful abdomen, red wine-colored urine, polyneuropathy. | 1. acute intermittent prophyria 2. deficient porphobilinogen deaminase |
| Blistering cutaneous photosensitivity. | 1. porphyria cutanea tarda 2. deficient uroporphyrinogen decarboxylase |
| How is hemolytic uremia syndrome distinguished from DIC using coagulation tests and bleeding time? | 1. both disorders have increased bleeding time from platelet usage 2. only DIC has ↑PT and PTT from coagulation factor consumption |
| Patient with increased WBC and smudge cells on blood smear. | CLL |
| 1. Why is hepatosplenomegaly seen in sickle cell disease? 2. What leads to asplenia? | 1. overwork hypertrophy b/c of extramedulalry erythropoiesis 2. multiple splenic infarcts |
| 1. alcoholic with microcytic anemia 2. alcoholic with macrocytic anemia | 1. sideroblastic anemia 2. folate deficiency |
| Which type of anemia is caused by lead poisoning? | sideroplastic anemia from decreased heme synthesis |
| What is the most likely cause of iron deficiency anemia: 1. women under 50 2. men under 50 3. men and women over 50 | 1. menorrhagia 2. peptic ulcer disease 3. colorectal cancer |
| What is the cause of pernicious anemia? | autoantibodies directed against gastric parietal cells leading to ↓ intrinsic factor and achlorhydria |
| Deficiency of CD55 and CD59 proteins leading to anemia and thrombocytopenia? | Paroxysmal Nocturnal Hemoglobinuria; CD55 is Decay Accelerating Factor |
| Which factor converts prothrombin to thrombin? | Factor V (factor V leiden is mutated form that cannot be inactivated by protein C) |
| Elevated WBC count with immature myeloid stem cells and elevated neutrophil alkaline phosphatase. | Leukamoid Reaction (not CML) |
| Treatment for uremia induced platelet dysfunction. | desmopressin |
| Treatment for CML. | Imatinib |
| Patient with immunoglobulin spike on protein electrophoresis without systemic manifestations. | Monoclonal Gammopathy of Uncertain Significance (MGUS) |
Created by:
amichael87
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