1. MR OGUNDELE
CVS blood disorders

2. VESSELS
The three major types of blood vessels are arteries, capillaries, and veins
The walls of all blood vessels, except the very smallest, have three distinct layers, or tunics that surround a central blood-containing space, the vessel LUMEN
 The innermost tunic is the Tunica Intima: It is the only part of a vessel that is in contact with blood. It is made of simple squamous epithelium called endothelium

3. VESSELS
The Tunica Media, or middle layer, is made of smooth muscle and elastic connective tissue. Both of these tissues are involved in the maintenance of normal blood pressure, especially diastolic blood pressure when the heart is relaxed.
Fibrous connective tissue forms the outer layer, the Tunica Externa. This tissue is very strong, which is important to prevent the rupture or bursting of the larger arteries that carry blood under high pressure

5. VESSELS
The same three tissue layers are present in veins as in the walls of arteries, but there are some differences when compared to the arterial layers.
The inner layer of veins is smooth endothelium, but at intervals this lining is folded to form valves. Valves prevent backflow of blood and are most numerous in veins of the legs.

6. VESSELS
The middle layer of veins is a thin layer of smooth muscle. It is thin because veins do not regulate blood pressure and blood flow into capillaries as arteries do.
Capillaries carry blood from arterioles to venules. Their walls are only one cell in thickness; capillaries are actually the extension of the endothelium, the simple squamous lining, of arteries and veins

7. RAYNAUD'S DISEASE
Raynaud's disease occurs as a result of exaggerated response to cold leading to vasospasm.
Raynaud’s disease is characterized by spasms of small arteries in the digits. These spasms prevent arterial blood from perfusing the fingertips and sometimes the toes

8. RAYNAUD'S DISEASE
Blood flow to the extremities decreases as peripheral arteries narrow from vasospasm when exposed to cold or emotional stress. 
This results in the fingers, toes, nose, and ears changing to a pale shade and/or turning blue and red as blood flow decreases.
In about 10% of those affected, it can progress to the a point where ischemia from arterial spasm is so severe that gangrene occurs and amputation is necessary.

9. S/S Fingers and toes may display colour changes
Numbness or prickly sensation in the extremities
Decrease sensory perception in the extremities
Edema may be present

10. MGT Conservative treatment is attempted first
Avoidance of aggravating factors
Stress control
Cessation of smoking
Administer calcium channel blockers to ameliorate symptoms:(dilate capillaries) nifedipine
Administer vasodilators to aid in blood flow.
Surgical removal of a part of a sympathetic nerve (sympathectomy).

11. NURSING MANAGEMENT
Education is the primary goal for patients with Raynaud’s disease.
Teaching the patient to use of gloves in cold climates, reducing vasoconstrictive activity, and decreasing stress levels
Teach the patient to Stop smoking, Avoid cold , use Moisturizers.

12. VARICOSE VEIN
Varicose veins are enlarged and tortuous veins that are distended in shape by accumulation of pooled blood.
Veins that develop varicosities have incompetent valves that allows reflux of blood from the deep to the superficial vein
The increased blood flow and resultant pressure on the vein walls cause the vessel to dilate and become tortuous.

13. PATHO
Venous blood is accomplished by the pumping action of the calf muscle against the venous wall
Valves within the vein protects against backflow of blood in the venous system. When the valvular system fails, venous return is compromised leading to enlargement of superficial and deep veins.
As pressure increases in the vein, fluid leaks into interstitial space.

14. S/S Dilated, twisted appearance of superficial vessels
Swelling of foot and ankle
Pain and itching along the varicose vein
Increased pigment of skin, scaling, dryness

15. MGT Elastic support hose Elevating the leg and exercising the leg
Nsaid can be given for pain
Thrombolytics or anticoagulants may be prescribed if thrombus occours
Surgical intervention (thrombectomy)

16. NURSING MGT Encourage weight reduction
Avoid Prolong standing , sitting or crossing of leg
Stop smoking
Stop alcohol intake
Avoid constricting cloth
Frequent change in position

17. THROMBOPHLEBITIS
This is inflammation of the superficial vein caused by blood clot. It occurs from inactivity, trauma, infection from an IV line etc
Trauma to venous wall leads to inflammation and aggregation of blood components at the site of the inflammation. Clot forms at this site leading to obstruction of blood flow

18. S/S
Swelling
Redness
Edema, tenderness, and warmth in the affected area as part of an inflammatory Response
Cramping because blood flow to the area is impaired due to the presence of the clot

19. MGT
Administer anti-inflammatory medication to decrease the inflammation within the vessel (aspirin)
Administer anticoagulant medication to prevent the clot from becoming larger: ( heparin, warfarin)

20. NURSING CARE
Monitor breathing because changes in respiratory status can signal that a clot has dislodged and moved to the lung.
Apply warm moist compresses over affected area because it enhances blood flow to area.
Patient should be allowed to move about frequently—discourages chances of developing another clot.
Educate patient not to cross legs—avoid constriction of lower extremity vessels. Elevate affected area.

21. BLOOD
There are three kinds of blood cells: red blood cells, white blood cells, and platelets. Blood cells are produced from stem cells in hemopoietic tissue.
After birth this is primarily the red bone marrow, found in flat and irregular bones such as the sternum, hip bone, and vertebrae.
Lymphocytes mature and divide in lymphatic tissue, found in the spleen, lymph nodes, and thymus gland. 

22. BLOOD
Blood is a sticky, opaque fluid with a characteristic metallic taste. The color of blood varies from scarlet (oxygen rich) to dark red (oxygen poor).
Blood is slightly alkaline, with a pH between 7.35 and 7.45, and its temperature (38°C) is always slightly higher than body temperature.
Blood accounts for approximately 8% of body weight. Its average volume in healthy adult males is 5–6 L while 4–5 L in healthy adult female.

23. BLOOD
Blood plasma is a straw-colored, sticky fluid, it is mostly water (about 90%), but also contains nutrients, gases, hormones, wastes and products of cell activity, ions, and proteins(Albumin accounts for some 60% of plasma protein)

24. BLOOD

25. PRODUCTION OF RBC
Blood cell formation is referred to as hematopoiesis. This process occurs in the red bone marrow, which is composed largely of a soft network of reticular connective tissue bordering on wide blood capillaries called blood sinusoids. Within this network are immature blood cells, macrophages, fat cells, and reticular cells (which secrete the fibers).

26. PRODUCTION OF RBC
In adults, red marrow is found chiefly in the bones of the axial skeleton and girdles, and in the proximal epiphyses of the humerus and femur. Each type of blood cell is produced in different numbers in response to changing body needs and different regulatory factors.
All blood cell arise from the same type of stem cell, the pleuripotent hematopoietic stem cell, or hemocytoblast, which resides in the red bone marrow. However, their maturation pathways differ; and once a cell is committed to a specific blood cell pathway, it cannot change

28. PRODUCTION OF RBC
 Erythrocyte production, or erythropoiesis begins when a hemocytoblast descendant called a myeloid stem cell is transformed into a proerythroblast
Proerythroblasts, in turn, give rise to the early (basophilic) erythroblasts that produce huge numbers of ribosomes. During these first two phases, the cells divide many times.
Hemoglobin synthesis and iron accumulation occur as the early erythroblast is transformed into a late erythroblast and then a normoblast.

29. PRODUCTION OF RBC
When a normoblast has accumulated almost all of its hemoglobin, it ejects most of its organelles. Additionally, its nuclear functions end and its nucleus degenerates and is pinched off, allowing the cell to collapse inward and assume the biconcave shape.
The result is the reticulocyte (essentially a young erythrocyte). The entire process from hemocytoblast to reticulocyte takes about 15 days. The reticulocytes, filled almost to bursting with hemoglobin, enter the bloodstream to begin their task of oxygen transport.

30. PRODUCTION OF RBC
Usually they become fully mature erythrocytes within two days of release as their ribosomes are degraded by intracellular enzymes
The direct stimulus for erythrocyte formation is provided by erythropoietin (EPO), a glycoprotein hormone. The drop in normal blood oxygen levels that triggers EPO formation can result from
1.Reduced numbers of red blood cells due to hemorrhage or excessive RBC destruction
2.Insufficient hemoglobin per RBC (as in iron deficiency)
3.Reduced availability of oxygen, as might occur at high altitudes or during pneumonia 

31. PRODUCTION OF WBC

34. WBC PRODUCTION
An early branching of the pathway divides the lymphoid stem cells, which produce lymphocytes, from the myeloid stem cells, which give rise to all other formed elements.
In each granulocyte line, the committed cells, called myeloblasts accumulate lysosomes, becoming promyelocytes.
The distinctive granules of each granulocyte type appear next in the myelocyte stage and then cell division stops.

35. WBC PRODUCTION
The bone marrow stores mature granulocytes and usually contains about ten times more granulocytes than are found in the blood. The normal ratio of granulocytes to erythrocytes produced is about 3:1, which reflects the much shorter life span (0.5 to 9.0 days) of the granulocytes, most of which die combating invading microorganisms.

36. Granulocytes
The granulocytes are all phagocytic cells and are identifiable because of their cytoplasmic granules.
These white blood cells are spherical and have distinctive multilobar nuclei. The granulocytes are divided into three types (neutrophils, eosinophils, and basophils) according to the staining properties of the granules

37. WBC

38. Granulocytes
Neutrophils. The neutrophils, which constitute 55% to 65% of the total number of white blood cells, have granules that are neutral and thus do not stain with an acidic or a basic dye. primarily responsible for maintaining normal host defenses against invading bacteria, fungi, products of cell destruction, and a variety of foreign substances

39. Granulocytes
Eosinophils. The cytoplasmic granules of the eosinophils stain red with the acidic dye eosin. These leukocytes constitute 1% to 3% of the total number of white blood cells and increase in number during allergic reactions.
Eosinophils are also involved in parasitic infections.

40. Granulocytes
Basophils. The granules of the basophils stain blue with a basic dye. These cells constitute only about 0.3% to 0.5% of the white blood cells.
The basophils in the circulating blood are similar to the large mast cells located immediately outside the capillaries in body tissues. Both the basophils and mast cells release heparin, an anticoagulant, into the blood. The mast cells and basophils also release histamine, a vasodilator, and other inflammatory mediators.

41. Lymphocytes
The lymphocytes have their origin in the lymphoid stem cells that are found in the bone marrow. The lymphocytes constitute 20% to 30% of the white blood cell count.
They have no identifiable granules in the cytoplasm and are sometimes referred to as agranulocytes. They move between blood and lymphoid tissues, where they may be stored for hours or years 

42. lymphocytes
There are two types of lymphocytes: B lymphocytes and T lymphocytes
The B lymphocytes differentiate to form antibody producing plasma cells and are involved in humoral-mediated immunity.
The T lymphocytes are responsible for orchestrating the immune response (CD4+ T cells) and effecting cell mediated immunity (CD8+ T cells).

43. Monocytes and Macrophages
Monocytes are the largest of the white blood cells and constitute about 3% to 8% of the total leukocyte count. They have abundant cytoplasm and a darkly stained nucleus, which has a distinctive U or kidney shape
The monocytes, which are phagocytic cells, are often referred to as macrophages when they enter the tissues

44. Glucose-6-phosphate dehydrogenase (G6PD) deficiency
It is an X-linked genetic enzyme deficiency resulting in abnormal metabolism within red cells and haemolysis
Congenital,
Males affected, females have 50% of cells affected

45. Pathophysiology
The gene for G6PD is carried on the X chromosome. Gene produces an enzyme within the RBC that is essential for membrane stability
Normally red cells are protected from the action of free radicals by glutathione. The pentose-phosphate pathway is used to keep glutathione in its reduced form.
G6PD is one of the enzymes involved in the pentose phosphate pathway

46. Path0 G6PDdeficiency is a cause of prolonged neonatal jaundice.
G6PD deficiency leads to haemolysis in times of high oxidative stress and results in membrane oxidation and, which decreases flexibility and increases permeability of the red cell membrane.
 There is oxidation of haemoglobin to methaemoglobin; the globin chains then precipitate as Heinz bodies, which are removed from the red cells in the spleen.

47. Diagnosis
The diagnosis is made by a screening test or by a quantitative assay of G-6-PD
Signs and symptoms
Patients are usually asymptomatic
May develop pallor, jaundice, and hemoglobinuria (hemoglobin in the urine).
Reticulocyte count rises, and symptoms of hemolysis develop 

48. Management Avoid causative drugs and foods, treat infections
Transfusion is necessary only in the severe hemolytic state,

49. Polycythemia
Polycythemia refers to an increased volume of RBCs. It is a term used when the hematocrit is elevated

50. Polycythaemia vera
Polycythaemia vera (PV) is an overproduction of mature red blood cells due to a clonal proliferation in the bone marrow.
Most commonly presents over the age of 50 years.
Idiopathic disorder, although genetic and environmental factors have been suggested.

51. Patho
There is clonal expansion of a pluripotent stem cell capable of differentiating into red blood cells, granulocytes and platelets.
It is a proliferative disorder in which the myeloid stem cells seem to have escaped normal control mechanisms

52. Patho
The bone marrow is hypercellular, and the RBC, WBC, and platelet counts in the peripheral blood are elevated. However, the RBC elevation is predominant; the hematocrit can exceed 60%.
Polycythemia results in increased blood viscosity increasing the risk of arterial or venous thrombosis. Platelet function is often disrupted risking bleeding. 

53. S/S
Increased blood volume can cause headache, dizziness, tinnitus, fatigue, paresthesias, and blurred vision
Increased blood viscosity can lead to angina, claudication, dyspnea, and thrombophlebitis
Patients may complain of pruritus especially after a hot bath or shower
Investigations
Full blood count shows an increased red blood cell count,
haemoglobin and packed cell volume.

54. Complication
Risk for thromboses resulting in a CVA (brain attack, stroke) or heart attack
(MI); thrombotic complications are the most frequent cause of death.
Bleeding is also a complication,

55. Management
Treatment is aimed at maintaining a normal blood count (PCV below45%) and prevention of the associated complications.
Venesection may be of benefit in treating symptoms but has not been shown to reduce complications(This is achieved by removing enough blood (initially 500 mL once or twice weekly) to deplete the patient’s iron stores, thereby rendering the patient iron deficient and consequently unable to continue to manufacture RBCs excessively)

56. Management
Radioactive phosphorus or chemotherapeutic agents (eg, hydroxyurea [Hydrea]) can be used to suppress marrow function, but they may increase the risk for leukemia.
Newer therapies under evaluation include α interferon, venesection with low doses of aspirin and anagrelide (inhibits platelet aggregation).

57. NSG MGT Monitor for bleeding. Monitor for signs of infections.
Keep the patient mobilized to decrease chance of clot formation.
Increase fluid intake.
Teach patient to use soft toothbrush, and avoid flossing to decrease chances of bleeding.
Teach patient to avoid activities that could cause injury.

58. Von Willebrand’s disease
It is the most common hereditary bleeding disorder., is usually inherited as a dominant trait.
The disease is caused by a deficiency of von Willebrand factor (vWF), which is necessary for factor VIII activity.

59. Patho
von Willebrand factor (vWF) is a glycoprotein that has two functions in haemostasis.
vWF acts as a bridging molecule between allowing platelet aggregation and adhesion to damaged endothelium.
vWF acts as a carrier protein for circulating factor VIII increasing the half-life of factor VIII.
vWF carries factor VIII, its deficiency may also be accompanied by reduced levels of factor VIII and results in defective clot formation

60. s/s
Symptoms include bruising, excessive menstrual flow, and bleeding from the nose, mouth, and gastrointestinal tract

61. MGT
In severe cases, factor VIII products that contain vWF are infused to replace the deficient clotting factors.
The disorder also responds to desmopressin acetate (DDAVP), a synthetic analog of the hormone vasopressin, which stimulates the endothelial cells to release vWF and plasminogen activator.

62. Disseminated Intravascular Coagulation
Disseminated intravascular coagulation is a paradox in the hemostatic sequence and is characterized by widespread intravascular coagulation and bleeding. It is not a primary disease but occurs as a complication of a wide variety of conditions
DIC begins with massive activation of the coagulation sequence as a result of unregulated generation of thrombin, resulting in systemic formation of fibrin. In addition, levels of all the major anticoagulants are reduced

63. DIC
The generation of microthrombi results in vessel occlusion and tissue ischemia. Multiple organ failure may ensue. Clot formation consumes all available coagulation proteins and platelets, and severe hemorrhage results.
The disorder can be initiated by activation of the intrinsic or extrinsic pathways, both of which involve the formation of thrombin .

64. DIC
Initiation of DIC through the extrinsic pathway, as occurs with trauma and cancer, begins with the liberation of tissue factor.
The intrinsic pathway may be activated through extensive endothelial damage caused by viruses, infections, or immune mechanisms, or stasis of blood.

65. DIC
Although coagulation and formation of microemboli initiate the events that characterize DIC, its acute manifestations usually are more directly related to the bleeding problems that occur.
The bleeding may be present as petechiae, purpura, oozing from puncture sites, or severe hemorrhage.

66. DIC
Cardiovascular shock is a common complication. Uncontrolled postpartum bleeding may indicate DIC.
Microemboli may obstruct blood vessels and cause tissue hypoxia and necrotic damage to organ structures, such as the kidneys, heart, lungs, and brain.

67. TREATMENT
The treatment of DIC is directed toward managing the primary disease, replacing clotting components, and preventing further activation of clotting mechanisms.
Heparin may be given to decrease blood coagulation, thereby interrupting the clotting process

68. TREATMENT Transfusions
Packed RBC to replace what has been lost due to bleeding.
Fresh frozen plasma—replaces coagulation factor deficiency.
Platelets—replaces needed cells.
Cryoprecipitate—replaces fibrinogen.

69. NSG MGT
Monitor for bleeding from obvious sites (wounds, suture lines, venipuncture, etc.)
Avoid cleaning clots from exposed areas
Avoid situations that might cause bleeding— soft toothbrush, don’t floss between teeth.

70. LYMPHOMA
The lymphomas,( Hodgkin’s disease and non-Hodgkin’s lymphoma) represent solid tumors derived from neoplastic lymphoid tissue cells (i.e., lymphocytes) and their precursors or derivatives.

71. LYMPHOMA

72. Staging of Lymphoma

73. Hodgkin’s Disease
Hodgkin’s disease is a specialized form of lymphoma that features the presence of an abnormal cell called a Reed-Sternberg cell.

74. ETIOLOGY
The cause of Hodgkin’s disease is unknown. Although exposure to carcinogens or viruses as well as genetic and immune mechanisms have been proposed as causes, Infectious agents particularly Epstein Barr virus have been implicated

75. Hodgkin’s Disease
Hodgkin’s disease is characterized by painless and progressive enlargement of a single node or group of nodes.
 It is believed to originate in one area of the lymphatic system, and if unchecked, it spreads throughout the lymphatic network. The initial lymph node involvement typically is above the level of the diaphragm.

76. Staging of Lymphoma

77. Hodgkin’s Disease
Involvement of the retroperitoneal lymph nodes, liver, spleen, and bone marrow occurs after the disease becomes generalized.
A distinctive tumor cell (the Reed-Sternberg cell) is considered to be the true neoplastic element in Hodgkin’s disease
These malignant proliferating cells may invade almost any area of the body and may produce a wide variety of signs and symptoms. The spleen is involved in one third of the cases at the time of diagnosis.

78. Clinical Manifestations
A common finding in Hodgkin’s disease is the presence of painless lymph node enlargement, involving a single lymph node or groups of lymph nodes
Persons with Hodgkin’s disease are commonly designated as stage A if they lack constitutional symptoms and stage B if significant weight loss, fever, or night sweats are present.
Other symptoms such as fatigue, pruritus, and anemia are indicative of disease spread.

80. Diagnosis and Treatment.
A definitive diagnosis of Hodgkin’s disease requires that the Reed-Sternberg cell be present in a biopsy specimen of lymph node tissue.
Computed tomographic (CT) scans of the abdomen commonly are used in screening for involvement of abdominal and pelvic lymph nodes.
The staging of Hodgkin’s disease is of great clinical importance because the choice of treatment and the prognosis ultimately are related to the distribution of the disease.

81. TREATMENT
Irradiation and chemotherapy are used in treating the disease. Most people with localized disease are treated with radiation therapy.  

82. Non-Hodgkin’s Lymphomas
The non-Hodgkin’s lymphomas are a heterogeneous group of solid tumors composed of neoplastic lymphoid cells.
The heterogeneity reflects the potential for malignant transformation at any stage of B- and T-lymphocyte differentiation. The non- Hodgkin’s lymphomas occur three times more frequently than does Hodgkin’s disease

83. Non-Hodgkin’s Lymphomas
The etiology of most of the non-Hodgkin’s lymphomas is unknown. A viral cause is suspected in at least some of the lymphomas

84. Non-Hodgkin’s Lymphomas
Non Hodgkin’s lymphomas commonly are divided into three groups, depending on the grade of the tumor:
Low-grade lymphomas, which are predominantly B-cell tumors;
Intermediate-grade lymphomas, which include B-cell and some T-cell lymphomas; and
High-grade lymphomas, which are largely immunoblastic (B-cell), lymphoblastic (T-cell), Burkitt’s, and non-Burkitt’s lymphomas

85. Aetiology Most NHLs are of B-cell origin.
Multiple chromosomal translocations have been identified.
Other factors include viruses (Epstein-Barr virus particularly associated with Burkitt lymphoma), enviromental factors, congenital and acquired immunodeficiency and some autoimmune conditions. Helicobacter pylori is associated with primary gastrointestinal lymphomas.

87. Clinical features Indolent:
Most patients present with painless slowly progressive lymphadenopathy.
Other symptoms are fever >38◦C, night sweats, weight loss of more than 10% within 6 months
Bone marrow failure leads to anaemia, recurrent infections and bleeding. On examination there is lymphadenopathy and hepatosplenomegaly.

88. Aggressive lymphomas
Most patients present with lymphadenopathy, extranodal involvement (gastrointestinal tract, skin, genitourinary tract, thyroid and central nervous system) and B symptoms.
On examination there is bulky lymphadenopathy and hepatosplenomegaly.

89. Diagnosis
As with Hodgkin’s disease, a lymph node biopsy is used to confirm the diagnosis of non-Hodgkin’s lymphoma. Bone marrow biopsy, blood studies,
computed tomographic scans, and nuclear medicine studies often are used to determine the stage of the disease.

90. Treatment
For early-stage disease, radiation therapy is used as a single treatment. However, because most people present with late stage disease, combination chemotherapy, combined adjuvant radiation therapy, or both are recommended.
For rapidly progressive intermediate- or high-grade lymphomas, CNS prophylaxis is achieved with high doses of chemotherapeutic agents that can cross the blood-brain barrier or cranial irradiation.

91. Doxorubicin (Adriamycin)
CHEMOTHERAPY
Alkylating agents 
Cyclophosphamide
Chlorambucil
Corticosteroids
Prednisone 
Dexamethasone
Platinum drugs
Cisplatin
Carboplatin
Purine analogs 
Fludarabine
Pentostatin
Anti-metabolites 
Cytarabine (ara-C)
Gemcitabine
Methotrexate
Others
Vincristine
Doxorubicin (Adriamycin)
Bleomycin
Etoposide (VP-16)

92. Side Effect Nausea/vomiting Hair loss Diarrhea Mouth sores Weight loss
Depression
Fertility problems
Shortness of breath
Cardiotoxicity (heart damage

93. Hodgkin’s Disease Stanford V
ABVD
doxorubicin (adriamycin), bleomycin, vinblastine, dacarbazine
BEACOPP
Bleomycin, Etoposide (VP-16), Adriamycin (doxorubicin), Cyclophosphamide (Cytoxan®), Oncovin® (vincristine), Procarbazine, Prednisone
Stanford V
mechlorethamine, doxorubicin, vinblastine, vincristine, bleomycin, etoposide, prednisone

94. NON Hodgkin’s Disease
The most common chemotherapy combination for the initial treatment of aggressive NHL is called CHOP and contains
CHOP
cyclophosphamide, doxorubicin (hydroxydaunorubicin), vincristine (Oncovin) and prednison
R-CVP
cyclophosphamide, prednisone, rituximab, and vincristine

95. Leukemia
Leukemia is a malignant disease of the WBCs that affects all age groups.
The immature WBCs (blast cells) generate in an explosive fashion in the bone marrow, lymph tissue, and spleen.
The cells are abnormal and unable to effectively fight infection. There are so many abnormal cells developed and dumped into the peripheral circulation that they tend to collect in the body tissues and organs, especially where circulation is sluggish.

96. Leukemia
Areas especially prone to infiltration with immature WBCs are the oral mucosa, anus, sinuses, and lungs. At the time of diagnosis, these areas are often inflamed, painful, and infected.
As the disease progresses, the bone marrow continues to produce large numbers of the useless cells, the peripheral circulation is filled with them, and the bone marrow is packed with blast cells.

97. Leukemia
Because so many of the blood stem cells are being used to make defective white cells, production of most other normal cells is impossible.
The patient becomes anemic because of the lack of RBC production, and bleeding becomes a problem as fewer and fewer platelets are manufactured.

98. Leukemia

99. Leukemia
The patient often begins to have raging infections that do not respond to antibiotics. Without treatment, leukemia leaves the patient unable to fight infection, unable to control bleeding.

100. Classifications
Leukemias are classified as either acute or chronic and either lymphoid or myeloid.
Lymphoid leukemias affect the lymphocytes. Myeloid leukemias originate in the stem cells of the bone marrow that develop into monocytes, granulocytes, erythrocytes, and platelets.

102. ACUTE LEUKEMIAS.
Acute lymphocytic leukemia (ALL) commonly affects children younger than age 15
It involves abnormal growth of the lymphocyte precursors (lymphoblasts).it results from an uncontrolled proliferation of immature cells (lymphoblasts) derived from the lymphoid stem cell.

103. Acute myelogenous (myeloblastic) leukemia
Acute myelogenous (myeloblastic) leukemia (AML) results from a defect in the hematopoietic stem cell that differentiates into all myeloid cells: monocytes, granulocytes (neutrophils, basophils, eosinophils), erythrocytes, and platelets.
It usually affects persons older than age 20 and has a poor prognosis.

104. CHRONIC LEUKEMIAS.
Chronic lymphocytic leukemia (CLL) predominantly affects the B and T lymphocytes and usually occurs in adults older than age 40.
CLL typically derives from a malignant clone of B lymphocytes. In CLL, cell escapes apoptosis (programmed cell death), with the result being an excessive accumulation of the cells in the marrow and circulation.

105. Chronic myelogenous leukemia (CML)
In CML, a section of DNA is found to be missing from chromosome 22 (the Philadelphia chromosome).
CML arises from a mutation in the myeloid stem cell. There is uncontrolled proliferation of cells, the marrow expands into the cavities of long bones (eg, the femur), and cells are also formed in the liver and spleen (extramedullary hematopoiesis), resulting in enlargement of these organs that is sometimes painful enlargement of these organs that is sometimes painful

106. Signs and Symptoms
Symptoms are similar for all types of leukemia and include low-grade fever caused by infection and pallor, weakness, shortness of breath, and malaise caused by anemia
The patient may also have fatigue, tachycardia, palpitations, and abdominal pain.
Sternal pain and rib tenderness may result from crowding of bone marrow.

107. Diagnostic Tests
Although a simple CBC often points toward the diagnosis, only bone marrow aspiration can show the degree of proliferation of the malignant WBCs and confirm the diagnosis of leukemia.
A lumbar puncture helps determine if the central nervous system is involved.

108. TREATMENT
CHEMOTHERAPY. Systemic chemotherapy aims to eradicate the leukemic cells and induce a remission.
Chemotherapy types vary with the types of leukemia and the level of involvement.
Radiation therapy is also sometimes used for initial treatment of leukemia.
Bone marrow transplant and immunosuppression.

109. TREATMENT
There are four phases to the treatment of leukemia: induction, intensification, consolidation, and maintenance.
Induction is the period in which an attempt to get the patient into remission is made. This first phase is difficult because chemotherapy is given in extremely high doses and on an aggressive timetable.

110. TREATMENT
Intensification is similar to the initial induction phase, using the same drugs at even higher doses.
The next phase, consolidation, is used to ensure that all leukemic cells have been eradicated from the body
Finally, the patient graduates to maintenance therapy in which the patient is kept free of leukemic cells (and in remission) for a period of years (and hopefully a lifetime). This requires years of continued chemotherapy treatments, often on a monthly basis.

111. TREATMENT
BONE MARROW TRANSPLANT. Bone marrow transplant (BMT) is sometimes used to treat leukemia. Preparation for BMT includes high-dose chemotherapy and/or total body irradiation. The goal is to destroy all the patient’s malignant bone marrow and then, at the last possible moment, replace it with a donor’s clean and healthy bone marrow (allogenic transplant).

112. Assignment
Read up
Anemia
Thalassemia
Haemophilia