1. Cytogenetic abnormalities c

Cytogenetic abnormalities can either be structural or numerical alteration of the number of chromosomes that an individual has. The chromosomes are in alleles for a genetically normal individual with a specific structure.

I). Philadelphia chromosome

There is overproduction of Philadelphia chromosome in 85% of the patients, 25% of which there is a translocation of Philadelphia chromosome throughout the disease process of Chronic Myeloid Lymphoma (CML). As CML disease continues to progress, there are alteration of the Philadelphia chromosomes. It may occur two to six months before the hematological progression or at times can occur at blast crisis. Common numerical changes that occur are trisomy 8, trisomy 19, trisomy 21 and loss of one sex chromosome. Studies also show that deletions occur in the chromosome 9 which leads to a shorter chronic phase and hence the overall survival time of the patient (Bain, 2010).

I). Hyperdiploidy

More than 90% of the patients with Acute Lymphoblastic Leukemia (ALL) have karyotypic abnormalities, whereby there are clonal chromosomal aberrations. The children and the adults with numerical aberration of 50 or more chromosomes usually have a favorable prognosis during their disease process. Although hyperdiploidy is most favorable to the adults with ALL, the rate of treatment failure is much higher than that of the pediatrics with ALL. If translocations occur, it is clear that the prognosis will end up being poor (Bain, 2010).

Q2. Morphological features of infectious mononucleosis.

There are four main characteristic features of infectious mononucleosis. These are:

I). Apoptotic Lymphocytes that have lost the cell volume

II). Condensation of the chromatic along the nuclear membrane

III). Intense basophilic staining

IV). The nucleus is fragmented into spherical shape

The biochemistry test of interest to the morphologist includes testing the body fluid samples including blood, serum, urine, cerebrospinal fluid and synovial fluids. These tests are used to analyze liver functions, electrolyte balance, renal functions and diabetic status. The mono test is also important in identifying if a person who presents with these symptoms is suffering from infectious mononucleosis (Bain, 2010).

3. Assessment of adequacy of the peripheral blood collected in the laboratory.

Flow cytometric count of CD34 cells is used to evaluate the adequacy of the peripheral blood collected. In addition, it is used to plan the apheresis sessions needed to obtain the grafts. The CD34 is identified due to their characteristics in light scatter feature by utilizing the fluorescent counting beads. The cells that bear CD34 antigen are responsible for the engraftment. The assessment by flow cytometry provides a reliable and fast assay for determining the adequacy of peripheral blood in the autographs (Bain, 2010).

4. Differences between chronic myeloid leukemia and leukamoid reaction

Chronic myeloid leukemia is a malignant disorder that involves clonal proliferations of the multipotent stem cell that leads to accumulation of the granulocytes, which predominates in the bone marrow, and in blood. This disorder is associated with Philadelphia chromosome translocation, where there is the juxtaposition of the genes trisomy of chromosome 8 is also common with this disorder. The white blood cells are increased above 100 x10^9/L. Leukaemoid reaction, on the other hand, is an exaggerated response by the body to stress or to infection by microorganisms. It leads to the elevation of the leukocytes in the blood, and it is a benign condition that resolves once the stressor agent gets out of the body (Bain, 2010). There is no cytogenetic association in leaikamoid reaction as opposed to chronic myeloid leukemia.

5. Features of Myelodysplastic syndrome.

The patient presents with symptoms of bone marrow failure, which include anemia symptoms, bacterial infection, bleeding, and easy-bruising. More than 10% of the patients present with splenomegaly. Morphological features of blood cells in patients with myelodysplastic syndrome include macrocytes which are oval in shape, basophilic stippling, neutrophils that are hypo-granulated, neutrophils nucleus that is hyperlobated and agranular thrombocytes. In addition, the features in the marrow include nucleus with abnormal shape and chromatin pattern, ring sideroblast and megakaryocytes with separated nuclei (Bain, 2010).

6. Dysplastic morphological changes in the three lineages of blood cells.

a) Granulocytic series (white blood cells)

The morphological changes that occur in the white blood cells include hyper-segmented or hypo-segmented neutrophils, hypo-granular neutrophils, presence of dimorphic granules. Within the eosinophils. This is common in the chronic myelomonocyte leukemia.

b) Erythroid series (red blood cells)

The morphological changes that occur in the binucleated erythroid precursors and erythroid nuclear budding include erythroid nuclear strings, loss of E-cadherin in the normoblast, and Ringed sideroblasts which is seen especially in refractory anemia with ring sideroblast (Bain, 2010).

c) Megakaryocytic series

Hyposegmented nuclear features in platelets producing megakaryocytes. It is common in MDS associated with isolated Del (5q) chromosome abnormality. The morphological changes include: hyper-segmented megakaryocytes and ballooning of the platelets.

Long Answer Questions:

1. Prothrombin time and activated thromboplastin time

Determination of the time taken by the blood to clot can assist in identifying the coagulation disorder of the blood. Prothrombin time and also the activated partial thromboplastin time are among the tests done to determine the coagulation disorders. Prothrombin time (PT) measures the coagulation in the extrinsic pathway of blood coagulation. Prothrombin is the factor II, which is made in the liver. Vitamin K is required for this process. Factors I, II, V, VII, and X are measured using prothrombin time. It is sometimes referred to as the international normalized ration (INR), as a way of standardizing the prothrombin time, regardless of the method used to do the test. It is normally in the range of12-13 seconds. Abnormal prothrombin time may result due to liver disease or injury or treatment with blood thinners. It can be prolonged in cases of blood thinning medicines, low levels of clotting factors, the absence of the clotting factors, inactivity of the clotting factors, an increase in the use of the clotting factors and inhibitors of the clotting factors. Prothrombin time is used to test the availability of the clotting factors, to check if blood thinners are working, to check for availability of vitamin K and to check how well the liver is working (Bain, 2010).

Activated partial thromboplastin time (aPTT), on the other hand, measures the efficiency of blood clotting in the intrinsic and common pathway of blood coagulation. It can be used to monitor the heparin effect in the treatment. The plasma sample is mixed with an activator such as silica and calcium to start off intrinsic pathway. The time is calculated until the clot is formed. The normal range is between 30 and 50 seconds. A shorter time has little clinical significance. Factors I, II, V, VIII, IX, X, and XII must be present for normal aPTT. Inadequacy of factors VII and XII are not detected by this test. This time may be prolonged in heparin usage, coagulation factor deficiency like in hemophilia, sepsis and in the presence of factor inhibitors (Bain, 2010).

2. Morphological difference between normal promyelocyte and abnormal one

Promyelocytes are immature white blood cells that have a tendency of accumulating in the bone marrow of a person who is suffering from acute promyelocytic leukemia. The hypogranular subtype of the acute myeloid leukemia is the one that has the abnormal promyelicytes. The abnormal promyelocytes present with an irregularly-shaped nucleus. The normal promyelocyte present with an almost regularly shaped nucleus. In addition, the nucleus of the abnormal promyelocyte appears bilobed and with infrequent contours in its morphology. Further, the cytoplasm of the abnormal promyelocytes contains some rod-shaped auer rods and many large azurophillic granules. In some instances, the azurophilic granules and the auer rods are so abundant that they obscure the nucleus of the abnormal promyelocyte. The numeracy of the auer cells and the azurophilic granules makes the cell appear as a bundle of straw, thus referred to as faggot cells (Bain, 2010).

The abnormal promyelocytes are likely to be found in acute promyelocytic leukemia, a disease condition (cancer) of the bone-marrow. Apart from the irregular nucleus, the features discussed above are likely to be found in a film of this condition. The criticality of such a finding is that a cell may be a blast, which may predispose the patient to megaloblastic anemia (Bain, 2010).

3. Megalobalastic anemia

This is a type of anemia in which the red blood cells formed are bigger than normal. This means that the mean cell volume of the cells is above the normal range, which is 80-95 FL. The nuclei becomes immature than the cell’s cytoplasm. The underlying cause of this is a defective DNA synthesis. It can be caused by vitamin b 12 deficiency and folate deficiency. This may be due to malabsorption of the nutrients. Folate deficiency may be due to pregnancy, chronic hemolytic anemia, or prematurity. Vitamin B 12 is usually not absorbed in the absence of intrinsic factor, a condition referred to as pernicious anemia. Some drugs like anticonvulsants may cause folate deficiency (Bain, 2010).

The clinical features include pallor and severe jaundice. The patient may present with congestive cardiac failure. Neuropathy develops in vitamin B12 deficiency. Neural tube defects develop in cases of folate deficiency.

The most important assays are the vitamin B 12 and folate levels in the blood. Their deficiency serves as the causative factors of megaloblastic anemia. Assays on the level of the serum homocysteine and methyl-malonic acid can also help diagnose megaloblastic anemia. These are raised in vitamin B12 and folate deficiency. Endoscopy for vit B12 to determine if there is pernicious anemia. Serum test for antigliadin and anti –endomysal antibodies that are autoantibodies. Liver and thyroid gland function test are also important in diagnosing megaloblastic anemia (Bain, 2010).

4. Error in blood collection, storage and interpretation

The total testing process of the blood is divided into three sections: pre-analytical, analytical and post analytical. Each stage has associated errors that can lead to inaccurate results of the tests. The sources of pre-analytical errors include: inappropriate test requested or the test is appropriate, but has not been requested at all. It can occur when there is a patient identification error, and also inadequate patient preparation. It can also bring up an error in cases of inadequate information from the patient (Bain, 2010).

Errors during the analytical phase can result from the inadequate specimen collection, inappropriate tube mixing of blood that leads to clotting, and inappropriate tube for the specimen. The error can also occur due to contamination of the infusion route and also the incorrect order of drawing the specimen.

The errors in post analytical phase may be due to inappropriate labeling of the tubes. Improper specimen transport and storage may also contribute to the error. Additionally, improper centrifugation time or speed may lead to the error as well. The laboratory scientist should therefore remain alert for these errors so as to provide as accurate results as possible (Bain, 2010).

5. Error in blood collection, storage and interpretation

The total testing process of the blood is divided into three sections: pre-analytical, analytical and post analytical. Each stage has associated errors that can lead to inaccurate results of the tests. The sources of pre-analytical errors include: inappropriate test requested or the test is appropriate, but has not been requested at all. It can occur when there is a patient identification error, and also inadequate patient preparation. It can also bring up an error in cases of inadequate information from the patient (Bain, 2010).

Errors during the analytical phase can result from the inadequate specimen collection, inappropriate tube mixing of blood that leads to clotting, and inappropriate tube for the specimen. The error can also occur due to contamination of the infusion route and also the incorrect order of drawing the specimen.

The errors in post analytical phase may be due to inappropriate labeling of the tubes. Improper specimen transport and storage may also contribute to the error. Additionally, improper centrifugation time or speed may lead to the error as well. The laboratory scientist should therefore remain alert for these errors so as to provide as accurate results as possible (Bain, 2010).

6. Blood films with thrombocytopenia and red cell fragments

A blood film that has fragmented red blood cells and thrombocytopenia shows serious hemolysis that is taking place in the blood vessels of the patients. It is, therefore, important to refer the patient to a higher level of health care, where blood for transfusion may be available, and resuscitation can be done easily. This is a sign of micro-angiopathic hemolytic anemia. In this condition, the coagulation factors are increased, which leads to the formation of fibrin mesh in the blood vessels. The red blood cells are curtailed by this network of proteins and the fragments are identical as schistocytes on microscopy (Bain, 2010). The red blood cells are also targeted to be destroyed by the reticuloendothelial system of the spleen as they cannot pass through the narrowed vessels. This condition is common in disseminated intravascular coagulation, hemolytic uremic syndrome, and also malignant hypertension among others.

7. Morphological features of blood film in HUS and TTP

Hemolytic uremic syndrome and thrombotic thrombocytopenic purpura are disorders that are characterized by microangiopathic thrombosis and hemolysis. In blood film, there is presence of schistocytes, that result from the curtailing of the red blood cells by the fibrin mesh. Signs of anemia in the blood film, including microcytosis, and hypochromic red blood cells are also indicative of HUS and TTP. The schistocytes may have different morphological features including keratocytes, helmet cells and spherocytes.

As a medical scientist, it is important to call or to refer the patient immediately to receive intensive care. Apart from the fact that professional practice and ethics demand so, the disorder causes destruction of the blood vessels in the kidney and can lead to acute renal failure. Cross matching of the blood can be done promptly to ease in blood transfusion. Moreover, as a medical scientist, one should prevent injury to the patient as it may cause excess loss of blood due to the interrupted clotting of blood. In this case, the medical scientist goes with the option of transferring or calls for reinforcement, for the sake of protecting the health of the patient (Bain, 2010).

8. Causes of artefactual thrombocytopenia

Artefactual thrombocytopenia can also be referred to as false thrombocytopenia. It is a sampling error which has been found to lead to the misdiagnosis of a severe condition referred to as thrombocytopenia. The error may result when an anticoagulant used during the collection of the blood sample causes the platelets to clump together. This imitates low levels of platelets in the blood. The use of EDTA during the collection of the blood samples is commonly associated with the pseudo thrombocytopenia. In addition, the use of automated machines and gadgets may also lead to false results. To prove that the results are valid, one needs to examine the sample of the blood under a microscope, and count the number of the platelets (Bain, 2010). The process helps rule out pseudothrombocytopenia.

9 Disseminated intravascular coagulation

This is a clotting abnormality where there is activation of the clotting factors in the body without the necessary presence of injury. It leads to the formation of thrombi in the blood vessels, which can cause their damage. The thrombi may impair blood circulation to the vital organs like the kidneys, brain and the heart. In addition, in case an injury occurs, massive hemorrhage may occur due lack of clotting factors, which have already initiated coagulation within the blood vessels. Disseminated Intravascular Coagulation can be caused by hematologic malignancies, obstetric complications (amniotic fluid embolism), massive tissue injury, and transfusion reactions, among others. The onset of Disseminated Intravascular Coagulation can be insidious. It can lead to multiple organ failures. Massive hemorrhage from various sites is the most common clinical feature of DIC (Bain, 2010).

An investigation carried out in the diagnosis include: getting the clinical history of the patient. Prothrombin time and activated thromboplastin time are prolonged in Disseminated Intravascular Coagulation. This reflects the continuous consumption of the clotting factors in the blood. The platelet count will rapidly decline. The levels of fibrin degradation factors will increase in the bolos including d-dimers. Peripheral blood smear shows schistiocytes which are the fragments of red blood cells (Bain, 2010).

10. Malaria

This is a mosquito-borne disease, which is transmitted by an infected female anopheles mosquito. It is caused by a parasite belonging to the genus Plasmodium. The mosquito introduces the parasite into the blood circulation during its feeding, where the parasite moves to the liver. In the liver, the parasite matures and starts reproducing. The parasites exist in two phases; one in the liver, and the other the in red blood cells. In the liver, the sporozoites multiply asexually and asymptomatically, after which they differentiate to merozoites. The merozoites escapes and infects the red blood cells where again they continue to reproduce asexually, thus causing fever and chills to the host. The parasite is always hidden from the immunologic cells, since it resides in the red blood cells and the liver cells. The red cells with merozoites can pass through the blood-brain barrier thereby causing cerebral malaria. As they avoid moving to the spleen for destruction, they cause the sequestration of the red blood cells within the vasculature, which can cause symptoms like placental malaria (Bain, 2010).

The clinical symptoms of malaria include headaches, shivering, joint pain, vomiting, jaundice, hemolytic anemia, retinal damage and neurological symptoms. Diagnosis is done by taking the history of recent travel. The findings include low platelet level in the blood, high levels of bilirubin in the blood, splenomegaly (enlargement of the spleen), and higher than normal level of white blood cells in the blood. Microscopy is the most widely used test done for malaria, where the merozoites are seen in the red blood cells in a curved shape. History of fever and recent travel are enough indication of commencing treatment if laboratory work is not available. Polymerase chain reactions have been developed, but rarely are they used for diagnosis of malaria.

11. This question is already answered in question one above.

Prothrombin time and activated thromboplastin time

Determination of the time taken by the blood to clot can assist in identifying the coagulation disorder of the blood. Prothrombin time and also the activated partial thromboplastin time are among the tests done to determine the coagulation disorders. Prothrombin time (PT) measures the coagulation in the extrinsic pathway of blood coagulation. Prothrombin is the factor II, which is made in the liver. Vitamin K is required for this process. Factors I, II, V, VII, and X are measured using prothrombin time. It is sometimes referred to as the international normalized ration (INR), as a way of standardizing the prothrombin time, regardless of the method used to do the test. It is normally in the range of12-13 seconds. Abnormal prothrombin time may result due to liver disease or injury or treatment with blood thinners. It can be prolonged in cases of blood thinning medicines, low levels of clotting factors, the absence of the clotting factors, inactivity of the clotting factors, an increase in the use of the clotting factors and inhibitors of the clotting factors. Prothrombin time is used to test the availability of the clotting factors, to check if blood thinners are working, to check for availability of vitamin K and to check how well the liver is working (Bain, 2010).

Activated partial thromboplastin time (aPTT), on the other hand, measures the efficiency of blood clotting in the intrinsic and common pathway of blood coagulation. It can be used to monitor the heparin effect in the treatment. The plasma sample is mixed with an activator such as silica and calcium to start off intrinsic pathway. The time is calculated until the clot is formed. The normal range is between 30 and 50 seconds. A shorter time has little clinical significance. Factors I, II, V, VIII, IX, X, and XII must be present for normal aPTT. Inadequacy of factors VII and XII are not detected by this test. This time may be prolonged in heparin usage, coagulation factor deficiency like in hemophilia, sepsis and in the presence of factor inhibitors (Bain, 2010).

Reference

Bain, J. B. (2010). Hematology: a core curriculum. Hackensack, NJ: World Scientific.

1. Cytogenetic abnormalities c

Cytogenetic abnormalities can either be structural or numerical alteration of the number of chromosomes that an individual has. The chromosomes are in alleles for a genetically normal individual with a specific structure.

I). Philadelphia chromosome

There is overproduction of Philadelphia chromosome in 85% of the patients, 25% of which there is a translocation of Philadelphia chromosome throughout the disease process of Chronic Myeloid Lymphoma (CML). As CML disease continues to progress, there are alteration of the Philadelphia chromosomes. It may occur two to six months before the hematological progression or at times can occur at blast crisis. Common numerical changes that occur are trisomy 8, trisomy 19, trisomy 21 and loss of one sex chromosome. Studies also show that deletions occur in the chromosome 9 which leads to a shorter chronic phase and hence the overall survival time of the patient (Bain, 2010).

I). Hyperdiploidy

More than 90% of the patients with Acute Lymphoblastic Leukemia (ALL) have karyotypic abnormalities, whereby there are clonal chromosomal aberrations. The children and the adults with numerical aberration of 50 or more chromosomes usually have a favorable prognosis during their disease process. Although hyperdiploidy is most favorable to the adults with ALL, the rate of treatment failure is much higher than that of the pediatrics with ALL. If translocations occur, it is clear that the prognosis will end up being poor (Bain, 2010).

Q2. Morphological features of infectious mononucleosis.

There are four main characteristic features of infectious mononucleosis. These are:

I). Apoptotic Lymphocytes that have lost the cell volume

II). Condensation of the chromatic along the nuclear membrane

III). Intense basophilic staining

IV). The nucleus is fragmented into spherical shape

The biochemistry test of interest to the morphologist includes testing the body fluid samples including blood, serum, urine, cerebrospinal fluid and synovial fluids. These tests are used to analyze liver functions, electrolyte balance, renal functions and diabetic status. The mono test is also important in identifying if a person who presents with these symptoms is suffering from infectious mononucleosis (Bain, 2010).

3. Assessment of adequacy of the peripheral blood collected in the laboratory.

Flow cytometric count of CD34 cells is used to evaluate the adequacy of the peripheral blood collected. In addition, it is used to plan the apheresis sessions needed to obtain the grafts. The CD34 is identified due to their characteristics in light scatter feature by utilizing the fluorescent counting beads. The cells that bear CD34 antigen are responsible for the engraftment. The assessment by flow cytometry provides a reliable and fast assay for determining the adequacy of peripheral blood in the autographs (Bain, 2010).

4. Differences between chronic myeloid leukemia and leukamoid reaction

Chronic myeloid leukemia is a malignant disorder that involves clonal proliferations of the multipotent stem cell that leads to accumulation of the granulocytes, which predominates in the bone marrow, and in blood. This disorder is associated with Philadelphia chromosome translocation, where there is the juxtaposition of the genes trisomy of chromosome 8 is also common with this disorder. The white blood cells are increased above 100 x10^9/L. Leukaemoid reaction, on the other hand, is an exaggerated response by the body to stress or to infection by microorganisms. It leads to the elevation of the leukocytes in the blood, and it is a benign condition that resolves once the stressor agent gets out of the body (Bain, 2010). There is no cytogenetic association in leaikamoid reaction as opposed to chronic myeloid leukemia.

5. Features of Myelodysplastic syndrome.

The patient presents with symptoms of bone marrow failure, which include anemia symptoms, bacterial infection, bleeding, and easy-bruising. More than 10% of the patients present with splenomegaly. Morphological features of blood cells in patients with myelodysplastic syndrome include macrocytes which are oval in shape, basophilic stippling, neutrophils that are hypo-granulated, neutrophils nucleus that is hyperlobated and agranular thrombocytes. In addition, the features in the marrow include nucleus with abnormal shape and chromatin pattern, ring sideroblast and megakaryocytes with separated nuclei (Bain, 2010).

6. Dysplastic morphological changes in the three lineages of blood cells.

a) Granulocytic series (white blood cells)

The morphological changes that occur in the white blood cells include hyper-segmented or hypo-segmented neutrophils, hypo-granular neutrophils, presence of dimorphic granules. Within the eosinophils. This is common in the chronic myelomonocyte leukemia.

b) Erythroid series (red blood cells)

The morphological changes that occur in the binucleated erythroid precursors and erythroid nuclear budding include erythroid nuclear strings, loss of E-cadherin in the normoblast, and Ringed sideroblasts which is seen especially in refractory anemia with ring sideroblast (Bain, 2010).

c) Megakaryocytic series

Hyposegmented nuclear features in platelets producing megakaryocytes. It is common in MDS associated with isolated Del (5q) chromosome abnormality. The morphological changes include: hyper-segmented megakaryocytes and ballooning of the platelets.

Long Answer Questions:

1. Prothrombin time and activated thromboplastin time

Determination of the time taken by the blood to clot can assist in identifying the coagulation disorder of the blood. Prothrombin time and also the activated partial thromboplastin time are among the tests done to determine the coagulation disorders. Prothrombin time (PT) measures the coagulation in the extrinsic pathway of blood coagulation. Prothrombin is the factor II, which is made in the liver. Vitamin K is required for this process. Factors I, II, V, VII, and X are measured using prothrombin time. It is sometimes referred to as the international normalized ration (INR), as a way of standardizing the prothrombin time, regardless of the method used to do the test. It is normally in the range of12-13 seconds. Abnormal prothrombin time may result due to liver disease or injury or treatment with blood thinners. It can be prolonged in cases of blood thinning medicines, low levels of clotting factors, the absence of the clotting factors, inactivity of the clotting factors, an increase in the use of the clotting factors and inhibitors of the clotting factors. Prothrombin time is used to test the availability of the clotting factors, to check if blood thinners are working, to check for availability of vitamin K and to check how well the liver is working (Bain, 2010).

Activated partial thromboplastin time (aPTT), on the other hand, measures the efficiency of blood clotting in the intrinsic and common pathway of blood coagulation. It can be used to monitor the heparin effect in the treatment. The plasma sample is mixed with an activator such as silica and calcium to start off intrinsic pathway. The time is calculated until the clot is formed. The normal range is between 30 and 50 seconds. A shorter time has little clinical significance. Factors I, II, V, VIII, IX, X, and XII must be present for normal aPTT. Inadequacy of factors VII and XII are not detected by this test. This time may be prolonged in heparin usage, coagulation factor deficiency like in hemophilia, sepsis and in the presence of factor inhibitors (Bain, 2010).

2. Morphological difference between normal promyelocyte and abnormal one

Promyelocytes are immature white blood cells that have a tendency of accumulating in the bone marrow of a person who is suffering from acute promyelocytic leukemia. The hypogranular subtype of the acute myeloid leukemia is the one that has the abnormal promyelicytes. The abnormal promyelocytes present with an irregularly-shaped nucleus. The normal promyelocyte present with an almost regularly shaped nucleus. In addition, the nucleus of the abnormal promyelocyte appears bilobed and with infrequent contours in its morphology. Further, the cytoplasm of the abnormal promyelocytes contains some rod-shaped auer rods and many large azurophillic granules. In some instances, the azurophilic granules and the auer rods are so abundant that they obscure the nucleus of the abnormal promyelocyte. The numeracy of the auer cells and the azurophilic granules makes the cell appear as a bundle of straw, thus referred to as faggot cells (Bain, 2010).

The abnormal promyelocytes are likely to be found in acute promyelocytic leukemia, a disease condition (cancer) of the bone-marrow. Apart from the irregular nucleus, the features discussed above are likely to be found in a film of this condition. The criticality of such a finding is that a cell may be a blast, which may predispose the patient to megaloblastic anemia (Bain, 2010).

3. Megalobalastic anemia

This is a type of anemia in which the red blood cells formed are bigger than normal. This means that the mean cell volume of the cells is above the normal range, which is 80-95 FL. The nuclei becomes immature than the cell’s cytoplasm. The underlying cause of this is a defective DNA synthesis. It can be caused by vitamin b 12 deficiency and folate deficiency. This may be due to malabsorption of the nutrients. Folate deficiency may be due to pregnancy, chronic hemolytic anemia, or prematurity. Vitamin B 12 is usually not absorbed in the absence of intrinsic factor, a condition referred to as pernicious anemia. Some drugs like anticonvulsants may cause folate deficiency (Bain, 2010).

The clinical features include pallor and severe jaundice. The patient may present with congestive cardiac failure. Neuropathy develops in vitamin B12 deficiency. Neural tube defects develop in cases of folate deficiency.