Hematology Questions

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<p>Hematology</p> <p>Introduction to anemia &amp; data interpretation</p> <p>What is the definition of anemia? Anemia is a clinical state where the hemoglobin, total RBC count or hematocrit is below the normal limit for sex and age Consequence of another underlying disease Decrease in O2 delivery capacity</p> <p>What factors regulate erythropoiesis? Erythropoiesis= RBC formation Hypoxia= lox O2 more brc neede kidney secrete erythropoietin Inc. erythropoiesis Altitude= high altitude inc erythropoietin Androgen= inc erythropoietin ERYTHROPOIETIN controls ERYTHROPOIESIS!!!</p> <p>What is the difference between true &amp; relative anemia?True Anemia Decrease in red cell mass Due to Decreased RBC production Increased RBC destruction Both simultaneously</p> <p>Relative Anemia Increase in plasma volume Dilution Seen in pregnancy Due to introduction of iv fluids</p> <p>What do each of the following measure? Which type of anemia show the results below?MCV raised Macrocytic Megaloblastic anemia B12 deficiency Folic acid deficiency</p> <p>MCH &amp; MCHC decreased Microcytic hypochromic </p> <p>Iron deciriency Thalassaemia Chronic renal failure Sideroblastic anemia</p> <p>Give 2 examples of normocytic and normochromic anaemia Normocytic= rbc normal size Normochromic= normal rbc color Normocytic normochromic anemia= anemia with normal rbc size and color MCH &amp; MCV normal</p> <p> Hemolysis, Acute blood loss, Marrow infiltration</p> <p>Nutritional deficiency anemia</p> <p>What is needed for the transport of iron in the blood? What is needed for the absorption of vit. B12? Iron Transferrion for transport</p> <p> B12 Intrinsic factor + transcobalamin II</p> <p>What are the causes of iron deficiency anemia? Name two. Chronic blood loss GI bleeding: most common anemia cause worldwide Poor diet intake Malabsorption Gastric resection Pancreatic insuffiency GIT infection Crohon s disease Short bowel syndrome</p> <p>Menstruation Childbirth Pulmonary: haemoptysis Urinary: renal disease Rapid growth with insuffiecient Fe: premature infants, children, teenagers Pregnancy Lactation</p> <p>What is the aetiology of megaloblastic anaemia? Megaloblastic anemia Deficiency of cobalamin (vit B12) and/or Folate (folic acid)</p> <p>What is pernicious anaemia? What is the main morphological change seen?</p> <p>What complication is seen in vit. B12 deficiency and not in folate deficiency?</p> <p>Blood, blood products &amp; transfusion service</p> <p>What are the major blood groups</p> <p>Match the following RBC antigens with the appropriate added sugars</p> <p>Antigen O A B AB</p> <p>Sugar Added</p> <p>What does Fresh Frozen Plasma contain? Give 3 conditions where FFP is used</p> <p>Match the following to their appropriate uses.Blood Product A. Whole Blood B. Packed Cells C. Cryoprecipitate D. Cryosupernatant Uses Liver failure, vit. K deficiency, warfarin overdose Chronic anemia, thalassemia Von Willebrand disease Blood volume replacement, exchange transfusion</p> <p>What are donated blood tested for?</p> <p>How is ABO cell grouping done?</p> <p>How is ABO serum grouping done?</p> <p>List 3 possible agents of transmission of infection by transfused blood.</p> <p>Hemostasis and bleeding disorders</p> <p>Name the steps in hemostasis</p> <p>What are the 2 main functions of thrombin?</p> <p>Name the Coagulation factorsCoagulation factor I II III IV V VII VIII IX X XI XII XIII Name</p> <p>What is hemophilia A &amp; ? Give a characteristic sign of hemophilia.</p> <p>What is von Willebrand disease?</p> <p>List 3 causes of thrombocytopenia</p> <p>Give 2 causes of Disseminated Intravascular Coagulation? What are the effects of IDC?</p> <p>List 2 screening tests for vascular and platelet disorders</p> <p>List 3 screening tests for coagulation disorders</p> <p>What is Prothrombin time? What deficiencies can it detect?</p> <p>What is partial thromboplastin time? What deficiencies can it detect?</p> <p>What is thrombin time?</p> <p>Hematinics</p> <p>Name 4 substances that chelate with iron</p> <p>State 4 ways iron can be lost from the body</p> <p>How is iron poisoning treated?</p> <p>Fill in the blanks about vit. B12Absorbed complexed with Location of absorption Bound in plasma with Deficiency in</p> <p>Thalassemia</p> <p>B-thalassemia is cause by mutations in the genes of the affected individuals. Name one type of gene mutation that can lead to b-thalassemia.</p> <p>Regarding b-thalassemia: explain why the red blood cells are hypochromatic</p> <p>Explain why the rbc have a chortened life span</p> <p>State 3 clinical features b-thalassemia. Explain why iron overlaod may occur in b-thalassemia patients.</p> <p>Gice 2 investigations and their expected findings for patients with bthalassemia.</p> <p>State 2 common forms of treatment for b-thalassemia</p> <p>Deletions of the a-globin gene loci result in a-thalassemia. State the number of a-globin genes deleted in the following conditions:Silent carrier state A-thalassemia trait HbH HbBart</p> <p>Explain how fetal death due to hydrops fetalis occurs</p> <p>Chronic fatigue syndrome</p> <p>True/ false Patients with CFS suffer severe fatigue that can be reduced with sufficient rest Disturbed sleep, muscle pain, &amp; impaired memory are among the diagnostic criteria for CFS Anti-depressant &amp; anxiolytic agents are among the medication treatment for CFS Cognitive behavioural therapy can be used to cure patients with CFS A doctor can facilitate the treatment outcome of CFS by being empathetic to the patient and educate them about this condition</p> <p>Aplastic anemia</p> <p>Describe the morphology of the bone marrow in a patient with aplastic anemia</p> <p>Give 3 possible causes of aplastic anemia</p> <p>Give 2 medical treatment for aplastic anemia</p> <p>What occurs during myelodysplastic syndromes &amp; what medical condition can it predispose to?</p> <p>Hemoglobinopathies</p> <p>State the pathogenesis of sickle cell anemia. Include the changes that happen to the haemoglobin and blood flow in response to low oxygen</p> <p>State 3 factors that affect RBC sickling</p> <p>What are the main consequences of HbS</p> <p>What are the 3 main characteristics of Sickle cell anemia?</p> <p>Is x-ray important for the diagnosis of sickle cell anemia?</p> <p>State the 3 morphologies of organs found in sickle cell anemia</p> <p>State 5 clinical signs and symptoms in sickle cell anemia</p> <p>Explain why is there autosplenectomy</p> <p>What are the complications in Sickle cell anemia? Name 4</p> <p>State 6 investigations that can be carried out other than RBC smear. Include positive and negative findinds</p> <p>Why homozygous sickle cell trait is more ganderous that the heterozygous cell trait?</p> <p>Apart from the patient experiencing tiredness and breathlessness due to anemia, what other clinically important signs and symptoms that can be picked up?</p> <p>Why does the sickle cell trait protect against malaria?</p> <p>Name ove virus that can cause aplastic crisis in sickle cell anemia</p> <p>Haemopoiesis II</p> <p>Name 3 chemicals that influence platelet production and elaborate on how each chemical affects platelet production</p> <p>Explain the development steps of granulocyte cells</p> <p>What are the differences between granulocytes and agranulocytes?</p> <p>Name 2 chemmicals that control the development of granulocytes</p> <p>In which from do monocytes appear in bone marrow and in the periphery</p> <p>In which form are neutrophil granulocytes seen in the bone marrow and in peripheral blood</p> <p>Platelet biology and Hemostasis</p> <p>Name the 3 major steps in hemostasis</p> <p>Name the 3 functions of platelets</p> <p>Name 2 substances that is released from the surface endothelium</p> <p>Name 1 stimulatory substance for each of the following processesVasoconstriction Platelet aggregation Blood coagulation</p> <p>Describe the roles of thromboxane A2 and Prostacyclin in the process of platelet aggregation</p> <p>Name 2 clotting factors for each of the following 3 categoriesContact factors Vik. K dependant factors Fibrinogen factors</p> <p>What are the factors that will trigger the following pathway?Intrinsic pathway Extrinsic pathway</p> <p>Give an example of a prothrombin activator</p> <p>Name an anti-clotting system and briefly describe its process</p> <p>Name a fibrinolytic system and briefly describe its process</p> <p>Abnormalities of haemostasis</p> <p>Write down the effects of Hemophilia A and von Willebrand Factor deficiencyHemophilia A Bleeding time Platelet count Clotting time APTT Prothrombin time Von Willebrand Factor deficiency</p> <p>What are the 2 functions of the von Willebrand factor?</p> <p>Define the following temrBleeding time Clotting time Plateled count Prothrombin time Thrombin time Activated Partial</p> <p>Hemolytic Anemia</p> <p>A young boy, aged 6, was admitted into the hospital for lethargy. The doctor who examined him found the patient to be slightly jaundiced and pale. Splenomegaly was also present. The following are a few of the test results: Peripheral blood smear: microcytic, hyperchromic RBCs. Presence of spherocytes Reticulocyte count: increased Plasma bilirubin: increased Mean cell hemoglobin concentration: inceased</p> <p>On further questioning, the doctor discovered that the boy s uncle and two other cousings also had the same condition. The doctor later concluded that the boy has hereditary spherocytosisName another important test which is used to diagnose the pathology. What would the results be if the person has such condition, and what would you say?</p> <p>The following statements make up the pathogenesis of hereditary spherocytosis. Arrange them in the proper chronological order.The cells assume the smallest possible diameter for a given volume. They become spheres Mutations in the ankyrin molecule cause a secondary deficiency of spectrin, which results in reduced membrane stability of the red blood cells The affected cells consequently lose membrane fragments as they are exposed to the sheer stresses in the blood circulation The spherocytes are later sequestered in the sleen and phagocytosed by splenic macrophages. Haemolytic anaemia occurs</p> <p>Splenomegaly was also present how did this happen?</p> <p>In terms of treatment for hereditary spherocytosis, splenectomy is done when there is a markedly enlarged spleen, severe anemia or complications such as gall stone formation. Then why is such treatment usually delayed in patients below 5 years old?</p> <p>Give 2 features seen on peripheral blood smears in hereditary spherocytosis</p> <p>Match the answers given to the following statements. The answers can be used more than once or none at allA: G6PD def. B: Extravascular hemolysis C: Hereditary spherocytosis D: Paroxysmal nocturnal hemoglobinuria E: Intravascular hemolysis F: hemolytic anemia No. I Statement Only form of haemolytic anemia that results from an acquired membrane defect secondary to mutation involving the phosphatidyl inositol glycan A (PIG-A) gene which affects myeloid stem cells Asymptomatic unless RBCs are subjected to oxidant injury by exposure to certain drugs, toxins or infections Schistocytes (made up of Burr cells, Helmet cells, triangle cells, microspherocytes) seen on peripheral blood smears Heinz bodies and bite cells Only disease associated with increased mean cell hemoglobin concentration (MCHC) Desttruction of RBCs within cells of mononuclear phagocyte system (MPS) Ans.</p> <p>Ii Iii Iv v vi</p> <p>Both intravascular and extravascular hemolysis occur in G6PD dieficiency. List 2 differences between intravascular and extravascular hemolysisIntravascular hemolysis Extravascular hemolysis</p> <p>Why are the serum haploglobin level characteristically low in hemolytic anemia?</p> <p>Why would G6PD def. lead to hemolytic anemia?</p> <p>Plasma cell Dyscriasis</p> <p>A 45 year old man went to a hospital yesterday after he fell down in the park while taking his dog out for a walk. When examined, his right leg was a little swollen and quite tender. The patients also noted that he gets tires easily in the last 3 months. He can no longer play badminton continuously with his friends, not swin 40 laps like he used to. He also tends to bruise easily, and suffers from excruciating bond pains. A number of investigations were carried out:X-ray of the right leg: numerous bone lesions noted Urine test: presence of Bence-jones proteins Serum electrophoresis: M spike absent Calcium levels in serum: elevated Peripheral blood smear: Normocytic, normochromic anemia. There is rouleaux formation Bone marrow aspiration: increased numbers of plasma cells</p> <p> What is your probably diagnosis? What is bence-jones proteins? Why is the M spike not present in this case?</p> <p>Give 3 complications of this medical condition</p> <p>Match the following with the most appropriate answersA: Cryiglobulinaemia B: Durie-Salmon staging system C: Monoclonal gammopathy of uncertain significance D: Multiple myeloma E: Extramedullary plasmacytoma F: Rai s Staging System G: Waldestorm Macoglobulinaemia No. Statements i ii iii iv v vi This is used to stage multiple myeloma and determine prognosis Presence of M proteins in serum of asymptomatic, healthy people Precipitation of macroglobulins at low temperaturm, producing Reynaud s phenomenon and cold urticaria X-rays show characteristic soap-bubble/ pepper-pot appearance Found in the upper respiratory tract in 80% cases Mott cells and Russell bodies present Ans.</p> <p>Leukocyte abnormalities and their benign disorders</p> <p>Where is the highest concentration of bone marrow found?</p> <p>What is the peripheral leukocyte count influenced by?</p> <p>What is the contrasting feature of a leukaemoid reaction compared with chronic myeloid leukaemia?</p> <p>Name 5 drugs that induce neutropenia</p> <p>What are 2 mechanisms that lead to neutropenia?</p> <p>Acute &amp; Chronic Leukemia</p> <p>Regarding chronic leukemia The indolent and low grade quality of most chronic leukemias allow time to achieve cures with appropriate therapy Many cases exhibit specific chromosome abnormalities Chronic myelogenous leukemia almost always progresses to an acute leukemia Chronic lymphocytic leukemia is generally a neoplasm of B lymphocytes Chronic leukemias are proliferations or accumulations of mature or differentiated cells</p> <p>Regarding leukemias The Philadelphia chromosome can be onserved in CML and ALL The poorest prognosis for patients with CLL is associated with anemia and thrombocytopenia In hairy cell leukemia, there will be pancytopenia, splenomegaly, and clonal proliferation of b lymphoid cells There will be positive tartrate resistnace and phosphate test in AML Serum vitamin b12 level measurement can be used to differentiate AML &amp; ALL</p> <p>Lymphoma</p> <p>State 2 macroscopic appearances of the affected lymph nodes in Hodgkin s disease</p> <p>What is specific name for the true neoplastic cell seen in Hidgkin disease? Describe how it looks like</p> <p>Name the 2 types of Burkitt Lymphoma and give 2 differences between them</p> <p>How does non-hidgkins lymphoma spread?</p> <p>Give 2 clinical features of Nonhodgkins lymphoma</p> <p>Between hidgkins and non-hidgkins lymphoma, in which is staging a useful guide to therapy?</p> <p>State two viruses that can be etiological agent in lymphoma</p> <p>Myeloproliferative Disorders</p> <p>Define myeloproliferative disorders</p> <p>What characterizes the spent phase?</p> <p>characteristic of its progenitor cells may be a possible explaintation for the increased pro...</p>