BLOOD  DISEASES

 

William  harvey 1578 – 1657

Is an English doctor, who discovered the circulation of the blood and the role of the heart in propelling it, thus refuting the theories of Galen and laying the foundation for modern physiology.

 

Born on April 1, 1578, at Folkestone, Kent, Harvey received his B.A. from Gonville and Caius College, University of Cambridge in 1597. He then went to Italy, where, at the University of Padua, he studied for five years under the celebrated anatomist Fabricius, who was already studying the valves of the veins. Having earned a medical degree Harvey returned to England and practiced medicine in the London area. He was elected a fellow of the College of Physicians and appointed physician to St Bartholomew's Hospital. Recognized eventually as one of the most distinguished doctors in England he became physician extraordinary to King James I, whom he attended in his last illness and physician in ordinary to his son Charles I.

From 1615 to 1656 Harvey served as Lumleian lecturer for the College of Physicians. As early as 1616 he discussed in his lectures the function of the heart and how it propelled the blood in a circular course. He arrived at his views not only by an elaborate series of dissections, but also by careful studies of the motion of the heart and blood in a wide range of living animals. These precise observations set a standard for future biological research.

Harvey formally presented his findings in 1628, when his Exercitatio Anatomica de Motu Cordis et Sanguinis in Animalibus (Anatomical Essay on the Motion of the Heart and Blood in Animals) was published. In this epoch-making work he explained the experimental method and gave an accurate account of the mechanism of the circulatory system. Because he had no microscope the only major part of the process he omitted was the role played by the capillaries. He did however propose their existence, which was affirmed not long afterwards by the Italian anatomist Marcello Malpighi.

 

Harvey's De Motu Cordis subjected him to severe criticism by some contemporaries, but this was more than compensated for by the later widespread recognition of his contribution. He also undertook research in embryology set forth in Exercitationes de Generatione Animalium (Essays on the Generation of Animals). The College of Physicians elected Harvey president in 1654 an honor he declined because of failing health. He died in London on June 3, 1657.

 

Karl Landsteiner 1868 – 1943

Born in Vienna he received his medical degree at the University of Vienna, where he taught pathology from 1909 to 1919. He was a member of the Rockefeller Institute for Medical Research (now Rockefeller University) in New York from 1922 to 1939. Landsteiner developed the modern classification of the four primary blood types, for which he was awarded the 1930 Nobel Prize for Physiology or Medicine.

 

Blood Type is classification of red blood cells by the presence of specific substances on their surface. Typing of red blood cells is a prerequisite for blood transfusion. In the early part of the 20^th century doctors discovered that blood transfusions often failed because the blood type of the recipient was not compatible with that of the donor. In 1901 the Austrian pathologist Karl Landsteiner classified blood types and discovered that they were transmitted by Mendelian heredity according to Mendel's Laws.

 

The four blood types are known as A, B, AB, and O. Blood type A contains red blood cells that have a substance A on their surface. This type of blood also contains an antibody directed against substance B, found on the red cells of individuals with blood type B. Type B blood contains the reverse combination. Serum of blood type AB contains neither antibody, but red cells in this type of blood contain both A and B substances. In type O blood, neither substance is present on the red cells, but the individual is capable of forming antibodies directed against red cells containing substance A or B. If blood type A is transfused into a person with B type blood, anti-A antibodies in the recipient will destroy the transfused A red cells. Because O type blood has neither substance on its red cells, it can be given successfully to almost any person. Individuals with blood type AB have no antibodies and can receive any of the four types of blood; thus blood types O and AB are called universal donors and universal recipients, respectively.

 

Other hereditary blood-group systems have subsequently been discovered. The hereditary blood constituent called Rh factor is of great importance in obstetrics and blood transfusions because it creates reactions that can threaten the life of newborn infants. Blood types M and N have importance in legal cases involving proof of paternity.

 

Disorders of the blood arise from abnormal changes in its composition. An abnormal reduction in the hemoglobin content or in the number of red blood cells is known as anemia, which is regarded as a symptom rather than a disease and has a number of causes. Probably the most common cause is blood loss or hemorrhage. Excessive destruction of the red blood cells a condition known as hemolytic anemia may be caused by a variety of toxins or by an antibody to the red blood cells. One type that occurs in the infant at or shortly before birth is erythroblastosis fetalis.

 

Anemia also results from decreased production of red cells, attributable to a loss of iron, to a deficiency of vitamin B12 or to a failure in the function of bone marrow. Finally one group of anemias is caused by inherited defects in the production of red cells (hemoglobin). These anemias include a number of hereditary disorders in which the red cells lack any one of several enzymes needed if the cell is to utilize glucose effectively.

 

Formation of abnormal hemoglobin is responsible for the hereditary defects called sickle-cell anemia and thalassemia major. Both are severe diseases that can be fatal in childhood.

 

An increase in the number of circulating red blood cells is called polycythemia, which can be a primary condition or one that follows decreased oxygenation of the blood or hypoxia. Extreme hypoxia occurs most commonly in advanced lung disease in certain types of congenital heart disease and at high altitudes.

 

Leukemia is accompanied by a disordered proliferation of white blood cells. Several types of leukemia exist each characterized by the cells involved.

A deficiency in any of the factors necessary for blood coagulation leads to excessive bleeding. A decrease in platelets is known as thrombocytopenia; a decrease in clotting factor VIII results in hemophilia A; a decrease in clotting factor IX results in hemophilia B commonly known as Christmas disease. Several of the hemorrhagic diseases such as hemophilia are hereditary. Preparations are available that contain some of the clotting factors in concentrated form for treating some of these disorders. In 1984 researchers developed a genetic engineering technique for making factor VIII a blood-clotting factor of vital importance for victims of the most common form of hemophilia.

 

Although clot formation is a normal process it sometimes occurs inappropriately and constitutes a threat to life. In patients hospitalized for a long time for example clots sometimes form in the large veins of the legs. If these clots or thrombi travel to the lungs they can cause death as a result of an embolism. Such venous thrombi are dissolved in many cases with a combination of drugs that prevent coagulation and break down clots. Anticoagulants include the natural compound heparin prepared from the lungs and livers of animals and the synthetic chemicals dicumarol and warfarin. Clot-dissolving drugs called thrombolytics include two enzymes urokinase and streptokinase approved for medical use in 1979 and tissue plasminogen activator (TPA) a product of genetic engineering.

 

Interaction of thrombocytes with the fatty deposits found in atherosclerotic heart disease is thought to contribute to heart attacks. Compounds such as aspirin and sulphinpyrazone, which inhibit platelet activity, may decrease heart attacks in persons with atherosclerotic disease.