Leukopenia And Leukemia Risk Factors Biology Essay
Disclaimer: This work has been submitted by a student. This is not an example of the work written by our professional academic writers. You can view samples of our professional work here.
Any opinions, findings, conclusions or recommendations expressed in this material are those of the authors and do not necessarily reflect the views of UK Essays.
Published: Mon, 5 Dec 2016
A clinical condition, known as leukopenia occasionally occurs in which the bone marrow produces very few white blood cells, leaving the body unprotected against many bacteria and other agents that might invade the tissues.
Normally, the human body lives in symbiosis with many bacteria, because all the mucous membranes of the body are constantly exposed to large numbers of bacteria. The mouth almost always contains various spirochetal, pneumococcal, and streptococcal bacteria, and these same bacteria are present to a lesser extent in the entire respiratory tract. The distal gastrointestinal tract is especially loaded with colon bacilli. Furthermore, one can always find bacteria on the surfaces of the eyes, urethra, and vagina. Any decrease in the number of white blood cells immediately allows invasion of adjacent tissues by bacteria that are already present.
Within 2 days after the bone marrow stops producing white blood cells, ulcers may appear in the mouth and colon, or the person might develop some form of severe respiratory infection. Bacteria from the ulcers rapidly invade surrounding tissues and the blood.
Without treatment, death often ensues in less than a week after acute total leukopenia begins. Irradiation of the body by x-rays or gamma rays, or exposure to drugs and chemicals that contain benzene or anthracene nuclei, is likely to cause aplasia of the bone marrow. Indeed, some common drugs, such as chloramphenicol (an antibiotic), thiouracil (used to treat thyrotoxicosis), and even various barbiturate hypnotics, on very rare occasions cause leukopenia, thus setting off the entire infectious sequence of this malady.
After moderate irradiation injury to the bone marrow, some stem cells, myeloblasts, and hemocytoblasts may remain undestroyed in the marrow and are capable of regenerating the bone marrow, provided sufficient time is available. A patient properly treated with transfusions, plus antibiotics and other drugs to ward off infection, usually develops enough new bone marrow within weeks to months for blood cell concentrations to return to normal.
Leukemia is a cancer of one class of white blood cells in the bone marrow, which results in the proliferation of that cell type to the exclusion of other types. Leukemia appears to be a clonal disorder, meaning one abnormal cancerous cell proliferates without control, producing an abnormal group of daughter cells. These cells prevent other blood cells in the bone marrow from developing normally, causing them to accumulate in the marrow. Because of these factors, leukemia is called an accumulation and a clonal disorder. Eventually, leukemic cells take over the bone marrow. This reduces blood levels of all nonleukemic cells, causing the many generalized symptoms of leukemia.
Types of Leukemia
Leukemia is described as acute or chronic, depending on the suddenness of appearance and how well differentiated the cancerous cells are. The cells of acute leukemia are poorly differentiated, whereas those of chronic leukemia are usually well differentiated.
Leukemia is also described based on the proliferating cell type. For instance, acute lymphoblastic leukemia, the most common childhood leukemia, describes a cancer of a primitive lymphocyte cell line. Granulocytic leukemias are leukemias of the eosinophils, neutrophils, or basophils. Leukemia in adults is usually chronic lymphocytic or acute myeloblastic. Long-term survival rates for leukemia depend on the involved cell type, but range to more than 75% for childhood acute lymphocytic leukemia, which is a remarkable statistic for what was once a nearly always fatal disease.
Risk Factors for Developing Leukemia
Risk factors for leukemia include a genetic predisposition coupled with a known or unknown initiator (mutating) event. Siblings of children with leukemia are 2 to 4 times more likely to develop the disease than other children. Certain abnormal chromosomes are seen in a high percentage of patients with leukemia. Likewise, individuals with certain chromosomal abnormalities, including Down syndrome, have an increased risk of developing leukemia. Exposures to radiation, some drugs that depress the bone marrow, and various chemotherapeutic agents have been suggested to increase the risk of leukemia. Environmental agents such as pesticides and certain viral infections also have been implicated.
Previous illness with a variety of diseases associated with hematopoiesis (blood cell production) has been shown to increase the risk of leukemia. These diseases include Hodgkin lymphoma, multiple myeloma, polycythemia vera, sideroblastic anemia, and myelodysplastic syndromes. Chronic leukemia may sometimes transform into acute leukemia.
Acute leukemia has marked clinical manifestations. Chronic leukemia progresses slowly and may have few symptoms until advanced.
Pallor and fatigue from anemia.
Frequent infections caused by a decrease in white blood cells.
Bleeding and bruising caused by thrombocytopenia and coagulation disorders.
Bone pain caused by accumulation of cells in the marrow, which leads to increased pressure and cell death. Unlike growing pains, bone pain related to leukemia is usually progressive.
Weight loss caused by poor appetite and increased caloric consumption by neoplastic cells.
Lymphadenopathy, splenomegaly, and hepatomegaly caused by leukemic cell infiltration of these lymphoid organs may develop.
Central nervous system symptoms may occur.
Laboratory findings include alterations in specific blood cell counts, with overall elevation or deficiency in white blood cell count variable, depending on the type of cell affected.
Bone marrow tests demonstrate clonal proliferation and blood cell accumulation.
Cerebral spinal fluid is examined to rule out central nervous system involvement.
Children who survive leukemia have an increased risk of developing a new malignancy later on in life when compared to children who have never had leukemia, most likely related to the aggressiveness of chemotherapeutic (or radiological) regimens.
Treatment regimens, including bone marrow transplant, are associated with temporary bone marrow depression, and increase the risk of developing a severe infection that could lead to death.
Even with successful treatment and remission, leukemic cells may still persist, suggesting residual disease. Implications for prognosis and cure are unclear.
Multiple drug chemotherapy.
Antibiotics to prevent infection.
Transfusions of red blood cells and platelets to reverse anemia and prevent bleeding.
Bone marrow transplant may successfully treat the disease. Blood products and broad spectrum antibiotics are provided during bone marrow transplant procedures to fight and prevent infection.
Immunotherapy, including interferons and other cytokines, is used to improve outcome.
Therapy may be more conservative for chronic leukemia.
The treatments described earlier may contribute to the symptoms by causing further bone marrow depression, nausea, and vomiting. Nausea and vomiting may be controlled or reduced by pharmacologic and behavioral intervention.
Anthocyanins (chemicals with known antioxidant and liver protecting properties) isolated from the plant Hibiscus sabdariffa are being studied as chemopreventive agents in that they cause cancer cell apoptosis (death) in human promyelocytic leukemia cells.
Anemia is a condition in which there is a reduced number of red blood cells or decreased concentration of hemoglobin in those cells or both. Anemia is often a manifestation of some disease process or abnormality within the body. Although there are many causes of anemia, the actual mechanism by which the anemia results is generally due to (1) excess loss or destruction of red blood cells and (2) reduced or defective production of red blood cells.
Anemias may be classified according to cause or effect on red cell morphology
RBC size is unchanged
Example: Blood loss anemia
RBC size is increased
Example: B12/folic acid deficiency anemia
RBC size is reduced
Example: Iron deficiency anemia
Color changes (due to altered hemoglobin content)
Normal hemoglobin concentration
Reduced hemoglobin concentration
Example: Iron deficiency anemia may be classified as a microcytic, hypochromic anemia as both red blood cell size and hemoglobin content are reduced
General manifestations of anemia
A major feature of anemia is a reduced capacity for the transport of oxygen to tissues. This reduced oxygen delivery can result in the following:
Breathlessness upon exertion
Increased susceptibility to infection
Types of anemia
Anemia that results from excess destruction of red blood cells (hemolysis). Factors that may cause hemolysis include the following:
Autoimmune destruction of red blood cells
Certain drugs (example: quinine) or toxins
Cancers such as lymphoma and leukemia
Certain viral infections (parvovirus)
Parasitic infections (malaria)
Blood loss anemia
Anemia that results from acute blood loss. With acute loss of large amounts of blood, shock is the major concern. With chronic loss of smaller amounts of blood, iron deficiency is a chief concern. Causes of acute and chronic blood loss may include the following:
Trauma and hemorrhage
Iron-deficiency anemia is a major cause of anemia worldwide. It can occur as a result of iron-deficient diets. Vegetarians are at particular risk for iron deficiency as are menstruating or pregnant women due to increased requirement for iron. Iron-deficiency anemia may also result from poor absorption of iron from the intestine or persistent blood loss (e.g., ulcers, neoplasia). Because iron is the functional component of hemoglobin, lack of available iron will result in a decreased hemoglobin synthesis and subsequent impairment of red blood cell oxygen-carrying capacity.
Cobalamin-deficiency or folate-deficiency anemia
Cobalamin (vitamin B 12) and folic acid are essential nutrients required for DNA synthesis and red cell maturation, respectively. Deficiency of these nutrients will lead to the formation of red blood cells that are of abnormal shape with shortened life spans due to weakened cell membranes. One important cause of vitamin B 12 deficiency is pernicious anemia that results from a lack of intrinsic factor production by the gastric mucosa. Intrinsic factor is required for normal absorption of vitamin B 12 from the intestine. Any intestinal abnormalities (e.g., neoplasia, inflammation) that interfere with the production of intrinsic factor can lead to vitamin B 12 deficiency. Folic acid deficiency most commonly results from poor diet, malnutrition or intestinal malabsorption.
Anemia may also result from genetic defects in red blood cell structure or function. Two common genetic disorders of erythrocytes are sickle cell anemia and thalassemia. Both of these disorders result from abnormal or absent genes for the production of hemoglobin.
Sickle cell disease
Sickle cell disease is a group of autosomal recessive disorders characterized by abnormal hemoglobin production. In the United States the highest prevalence of sickle cell disease is in blacks with a reported incidence of approximately 1 in 500 births. Sickle cell disease has several patterns of inheritance that determine the severity of the disease in afflicted individuals. In the homozygous form of the disease, most of the hemoglobin formed is defective and the clinical presentation is most severe. With the heterozygous form of the disease, less than half of the red cell hemoglobin is affected and the presentation is significantly milder. Individuals may also inherit the sickle cell trait and be carriers of the defective hemoglobin gene without significant clinical manifestations.
Manifestations of sickle cell disease: The abnormal hemoglobin formed in sickle cell disease results from a substitution mutation of a single amino acid. This mutation causes the deoxygenated hemoglobin to clump and become abnormally rigid. The rigidity of the defective hemoglobin deforms the pliable red blood cell membrane and causes erythrocytes to take on “sickled” or half-moon appearance. The degree of sickling that occurs is determined by the amount of abnormal hemoglobin within the red blood cell and only occurs when the abnormal hemoglobin is deoxygenated. As a result of their elongated shape and rigidity, affected blood cells do not pass easily through narrow blood vessels. Hemolysis of sickled red blood cells is also common. The spleen is a major site of red cell hemolysis since the blood vessels found within this organ are narrow and convoluted. As a result of the sluggish blood flow, many tissues and organs of the body are eventually affected by this disorder.
Specific manifestations may include the following:
Impaired oxygen-carrying capacity resulting in fatigue, pallor
Occlusion of blood vessels leading to ischemia, hypoxia, pain
Splenomegaly due to increased destruction of red blood cells in this organ
Jaundice as a result of increased amounts of hemoglobin released into circulation
Increased risk of infection and possible septicemia due to stagnation of blood
Thalassemia is a genetic disorder characterized by absent or defective production of hemoglobin Î± or Î² chains. As with sickle cell anemia, afflicted individuals may be heterozygous for the trait and have a milder presentation of the disease or homozygous and have a more severe form of the disorder.
The Î² form of thalassemia (defective formation of Î² hemoglobin chains) is most common in individuals from Mediterranean populations, whereas the Î± form of thalassemia (defective formation of Î± hemoglobin chains) occurs mostly in Asians. Both the Î± and Î² forms of thalassemia are common in blacks.
Manifestations of thalassemia
In heterozygous individuals enough normal hemoglobin is usually synthesized to prevent significant anemia. In these individuals symptoms of anemia may appear only with exercise or physiologic stress. Homozygous individuals are often dependent on frequent transfusions to treat the resulting severe anemia. Children affected with the homozygous form may suffer severe growth retardation. The widespread hypoxia that can result from impaired oxygen-carrying capacity leads to erythropoietin-induced increases in hematopoiesis that can eventually affect the structure of the long bones. Severe anemia may also lead to congestive heart failure and marked hepatosplenomegaly. Excessive hemolysis of red blood cells may occur in severe forms of the disease due to overproduction of the normal hemoglobin subunit. Iron deposits from increased absorption and frequent transfusions may injure the liver and heart as well.
Treatment of sickle cell anemia and thalassemia
Individuals with inherited anemia should avoid physiologic stresses that might exacerbate hypoxia. Infections should be avoided and promptly treated if they occur to prevent a possible hypoxic crisis. Proper immunizations and vaccinations should be administered to lessen the chance of infection. Frequent transfusions of normal erythrocytes are commonly used in individuals with severe forms of inherited anemia during periods of crisis. These individuals are at risk for iron accumulation as well as contracting blood-borne pathogens such as hepatitis and HIV from improperly screened blood. Bone marrow transplant may be utilized effectively to cure patients with genetic anemias; however, the procedure carries considerable risk of its own.
Aplastic anemia results from a lack of red blood cell production by the bone marrow. If erythrocyte stem cell precursors are lacking or destroyed, the process of erythropoiesis will be severely impaired. Aplastic anemia may result from a congenital defect in stem cell production or can be caused by exposure to agents that damage the bone marrow such as Chemicals (organic solvents, heavy metals), radiation, toxins, HIV infection, chemotherapeutic drugs and certain antibiotics (Chloramphenicol). Drug-induced aplastic anemia is usually a dose-dependent phenomenon.
The clinical manifestations of aplastic anemia will depend on the extent to which hematopoiesis is impaired. General symptoms of anemia such as pallor, fatigue and lethargy can occur initially. Bleeding in the skin and from the nose, mouth and body orifices may also occur from a lack of platelet production by the abnormal bone marrow. Increased susceptibility to infection is also seen as a result of diminished white blood cell production. The underlying cause of the aplastic anemia needs to be identified and further exposure prevented. Treatment should also include avoidance of physiologic stresses and infection. Transfusions are effective for temporarily improving oxygen-carrying capacity. In severe cases, bone marrow transplant may offer a cure.
Polycythemia is a disorder in which the number of red blood cells in circulation is greatly increased. There are two categories of polycythemia: relative and primary. Relative polycythemia results from an increase in the concentration of red blood cells due to a loss of plasma volume. In contrast, primary polycythemia (polycythemia vera) is caused by excessive proliferation of bone marrow stem cells. Polycythemia vera is a rare neoplastic disorder that occurs in men between the ages of 40 and 60. A secondary form of polycythemia may occur from excess erythropoietin production as a physiologic response to hypoxia. Secondary polycythemia may be seen in individuals living at high altitudes, in chronic smokers or in people with chronic obstructive pulmonary disease.
Increased blood volume and viscosity
Increased risk of thrombus
Occlusion of small blood vessels
Hepatosplenomegaly from pooling of blood
Impaired blood flow to tissues (ischemia)
Increasing fluid volume in relative polycythemia
Periodic removal of blood to reduce viscosity and volume in primary polycythemia
Chemotherapy or radiation to suppress activity of bone marrow stem cells in polycythemia vera
Thrombocytopenia represents a decrease in the number of circulating platelets (usually less than 100,000/mm3). It can result from decreased platelet production by the bone marrow, increased pooling of platelets in the spleen, or decreased platelet survival caused by immune or nonimmune mechanisms. Dilutional thrombocytopenia can result from massive transfusions because blood stored for more that 24 hours has virtually no platelets.
Decreased platelet production can result from suppression or failure of bone marrow function, such as occurs in aplastic anemia, or from replacement of bone marrow by malignant cells, such as occurs in leukemia. Infection with human immunodeficiency virus (HIV) suppresses the production of megakaryocytes. Radiation therapy and drugs such as those used in the treatment of cancer may suppress bone marrow function and reduce platelet production.
There may be normal production of platelets but excessive pooling of platelets in the spleen. The spleen normally sequesters approximately 30% to 40% of the platelets. However, as much as 80% of the platelets can be sequestered when the spleen is enlarged (splenomegaly). Splenomegaly occurs in cirrhosis with portal hypertension and in lymphomas.
Decreased platelet survival is an important cause of thrombocytopenia. In many cases, premature destruction of platelets is caused by antiplatelet antibodies or immune complexes. The antibodies can be directed against self-antigens (autoimmunity) or against nonself platelet antigens (from blood transfusions).
Autoimmune thrombocytopenias include idiopathic thrombocytopenic purpura and HIV-associated thrombocytopenias. Decreased platelet survival may also occur as the result of mechanical injury associated with prosthetic heart valves.
Some drugs, such as quinine, quinidine, and certain sulfa-containing antibiotics, may induce thrombocytopenia. These drugs act as a hapten and induce antigen-antibody response and formation of immune complexes that cause platelet destruction by complement-mediated lysis. In persons with drug-associated thrombocytopenia, there is a rapid fall in platelet count within 2 to 3 days of resuming use of a drug or 7 or more days (i.e., the time needed to mount an immune response) after starting use of a drug for the first time. The platelet count rises rapidly after the drug use is discontinued.
The anticoagulant drug heparin has been increasingly implicated in thrombocytopenia and, paradoxically, in thrombosis. The complications typically occur 5 days after the start of therapy and result from production of heparin-dependent antiplatelet antibodies that cause aggregation of platelets and their removal from the circulation. The antibodies often bind to vessel walls, causing injury and thrombosis. The newer, low-molecular-weight heparin has been shown to be effective in reducing the incidence of heparin-induced complications compared with the older, high-molecular-weight form of the drug.
Idiopathic Thrombocytopenic Purpura
Idiopathic thrombocytopenic purpura, an autoimmune disorder, results in platelet antibody formation and excess destruction of platelets. The IgG antibody binds to two identified membrane glycoproteins while in the circulation. The platelets, which are made more susceptible to phagocytosis because of the antibody, are destroyed in the spleen.
Acute idiopathic thrombocytopenic purpura is more common in children and usually follows a viral infection. It is characterized by sudden onset of petechiae and purpura and is a self-limited disorder with no treatment. In contrast, the chronic form is usually seen in adults and seldom follows an infection. It is a disease of young people, with a peak incidence between the ages of 20 and 50 years, and is seen twice as often in women as in men. It may be associated with other immune disorders such as acquired immunodeficiency syndrome (AIDS) or systemic lupus erythematosus. The condition occasionally presents precipitously with signs of bleeding, often into the skin (i.e., purpura and petechiae) or oral mucosa. There is commonly a history of bruising, bleeding from gums, epistaxis (i.e., nosebleeds), and abnormal menstrual bleeding. Because the spleen is the site of platelet destruction, splenic enlargement may occur.
Diagnosis usually is based on severe thrombocytopenia (platelet counts <20,000/mL), and exclusion of other causes.
Treatment includes the initial use of corticosteroid drugs, often followed by splenectomy and the use of immunosuppressive agents.
Thrombotic Thrombocytopenic Purpura
Thrombotic thrombocytopenic purpura (TPP) is a combination of thrombocytopenia, hemolytic anemia, signs of vascular occlusion, fever, and neurologic abnormalities. The onset is abrupt, and the outcome may be fatal. Widespread vascular occlusions consist of thrombi in arterioles and capillaries of many organs, including the heart, brain, and kidneys. Erythrocytes become fragmented as they circulate through the partly occluded vessels and cause the hemolytic anemia. The clinical manifestations include purpura and petechiae and neurologic symptoms ranging from headache to seizures and altered consciousness.
Although TTP may have diverse causes, the initiating event seems to be widespread endothelial damage and activation of intravascular thrombosis. Toxins produced by certain strains of Escherichia coli (e.g., E. coli O157:H7) are a trigger for endothelial damage and an associated condition called the hemolytic-uremic syndrome.
Treatment for TTP includes plasmapheresis, a procedure that involves removal of plasma from withdrawn blood and replacement with fresh-frozen plasma. The treatment is continued until remission occurs. With plasmapheresis treatment, there is a complete recovery in 80% to 90% of cases.
Factor I (or fibrinogen) deficiency is a very rare inherited disorder with complications that vary with the severity of the disorder. It is not well known, even among health professionals.
Factor I deficiency was described for the first time in 1920 by Fritz Rabe and Eugene Salomon. These two German physicians are credited with discovering the disorder. They studied the case of a 9-year-old boy who presented unexplained bleeding problems from birth. Blood tests finally demonstrated the absence of fibrinogen in the child’s blood. His parents were first cousins, but they showed no bleeding problems. The two researchers established that it was an inherited disorder often found in subjects whose parents were blood relatives. Since then, knowledge about the condition has advanced considerably.
What is Fibrinogen?
Fibrinogen, also called Factor I, is a blood plasma protein produced by the liver that plays an important role in blood coagulation. Blood coagulation is a process in which several components of the blood form a clot. When blood escapes from a rupture in a blood vessel, coagulation is triggered. Several proteins, called coagulation factors, go into action to produce thrombin. The thrombin then converts fibrinogen to fibrin. Fibrin produced from fibrinogen is the main protein in a blood clot. It surrounds the cells in the blood and plasma and helps form the clot. The resulting clot, which is stabilized by Factor XIII, remains intact from 10 to 14 days, the time required for healing to take place. When there is a problem with fibrinogen, i.e., either it is missing or it does not function properly, the clot has difficulty forming. This can result in hemorrhaging or thrombosis.
The normal volume of fibrinogen in the blood is from 2 to 4 g/l (grams/litre). The amount of fibrinogen in blood can be measured from a blood sample. The following diagram was devised by a Toronto laboratory technician. It shows the stages in clot formation in a way that makes it easier to understand the theoretical notions explained above.
Types of Fibrinogen Deficiency
There are three types of deficiency:
Afibrinogenemia: (absence of fibrinogen)
In this type of factor I deficiency, there is a complete absence of fibrinogen. The fibrinogen level is <0.2 g/L of plasma. About 5 people out of 10 million are affected by it. Of the three types, this one causes the most serious bleeding.
Hypofibrinogenemia (lower than normal level)
Dysfibrinogenemia (improper functioning)
Transmission of Fibrinogen Deficiency
Fibrinogen deficiency is a very rare inherited bleeding disorder. It is transmitted from parent to child at conception. The disorder is caused by an abnormal gene. It affects both men and women, as well as people of all races and ethnic origins.
Every cell of the body contains chromosomes. A chromosome is a long chain of a substance called DNA. DNA is organized in 30,000 units: these are called genes. The genes determine physical characteristics, such as eye colour. In the case of fibrinogen deficiency, one of the genes involved is defective.
The defective gene in fibrinogen deficiency is located on a chromosome that is not responsible for the child’s sex (autosomal). As a result, both girls and boys can be affected equally.
Afibrinogenemia (absence of fibrinogen)
This is a recessive disorder, which means that both parents must be carriers. In order for a person to inherit fibrinogen deficiency, he must receive two defective genes, one from the mother and the other from the father. A carrier is a person who has only one of the two defective genes,
but is not affected by the disorder: the second gene enables just enough fibrinogen to be made for good coagulation. The fibrinogen level will be lower than normal, but there will be no symptoms of the disorder.
Hypofibrinogenemia and dysfibrinogenemia
These are inherited disorders that can be either dominant or recessive. Dominant means that a single parent can transmit the disorder if he or she is a carrier.
Recessive means that both parents must be carriers of the disorder in order to transmit it.
Afibrinogenemia (absence of fibrinogen)
In congenital afibrinogenemia (fibrinogen level <0.2 g/L), bleeding can vary, from slight to severe. Many patients have very long intervals between bleeding episodes. A diagnosis of afibrinogenemia is generally made postnatally, usually because of bleeding from the umbilical cord and/or a hemorrhage following circumcision.
Other types of bleeding have been described:
bleeding from the gums
rupture of the spleen and hemorrhage in the spleen
About 20% of those suffering from afibrinogenemia present hemarthroses (bleeding in the joints). Because of this particular feature, the disorder may be confused with hemophilia A or B.
Hypofibrinogenemia (lower than normal level)
Bleeding in hypofibrinogenemia is much like what is seen in afibrinogenemia. It can be more or less serious, depending on fibrinogen levels, which can vary from 0.2 to 0.8 g/L of plasma. The higher the fibrinogen level, the less bleeding. The lower the fibrinogen level, the more bleeding.
Dysfibrinogenemia (improper functioning)
In dysfibrinogenemia, the quantity of fibrinogen is normal, which means between 2 and 4 g/L. Bleeding can vary depending on how the fibrinogen is functioning. Bleeding may:
be absent (no symptoms)
show a tendency toward hemorrhage (as described in afibrinogenemia)
show a tendency toward thrombosis
How to Recognize Bleeding
It is strongly recommended that people who suffer from afibrinogenemia or severe hypofibrinogenemia learn to recognize the signs and symptoms of bleeding that could threaten their lives or the integrity of a limb, so they can react adequately and in a reasonable time.
The information below describes the main types of bleeding that may occur in someone with a coagulation disorder.
Bleeding that affects the head, neck, thorax (chest) or abdomen can be life-threatening and may require immediate medical attention. Bear in mind that this kind of bleeding can occur either following an injury or spontaneously (without injury).
The brain, which is protected by the skull, controls all bodily functions that are essential to life. Bleeding in the brain is very serious.
Signs and symptoms:
Cite This Work
To export a reference to this article please select a referencing stye below: