Chapter 4- blood PDF

Dr. Lina Al Kury Chapter 4 The blood Main learning points Describe the chemical composition of plasma Discuss the structure, function, and formation of red blood cells Discuss the functions and formation of the different types of white blood cells Outline the role of pl...

Dr. Lina Al Kury Chapter 4 The blood Main learning points Describe the chemical composition of plasma Discuss the structure, function, and formation of red blood cells Discuss the functions and formation of the different types of white blood cells Outline the role of platelets in blood clotting Erythrocyte disorders Lymphocyte disorders  Blood is a connective tissue Key role in communication ¤ Oxygen ¤ Nutrients ¤ Waste products ¤ Hormones ¤ Heat transport ¤ Protective substances (WBC, antibodies|) to areas of infection ¤ Clotting factors Plasma ¤ Water (90-92%) ¤ Plasma proteins ¤ Inorganic salts ¤ Nutrients (mainly digested food) ¤ Waste materials (Urea, uric acid, etc) ¤ Hormones ¤ Gases (oxygen, CO2, Nitrogen)  Plasma Proteins: 7% of plasma Responsible for osmotic pressure of blood. Will not leave blood vessels. 1. Albumin: Produced by liver. Main function is to maintain normal plasma osmotic pressure. Transports fatty acids and hormones. Most abundant. 2. Globulin: Antibodies (immunoglobulins), produced by lymphocytes. 3. Fibrinogen: essential for blood clotting (clotting factor). Cellular componenet ˜ Erythrocytes (RBC) ˜ Leukocytes (WBC) ˜ Platelets (thrombocytes) All blood cells arise from Pluripotent stem cells by a process of heamopoiesis  1. RBC (Erythrocytes) Main function transport Oxygen and some CO2 Biconcave discs: no nucleus ¤ Produced in red bone marrow (ends of long bones) ¤ Life span 120 days ¤ Erythropoiesis: formation of RBCs from stem cells. Immature cells are released into bloodstream as reticulocytes and mature within two days in the circulation  Oxygen Transport ¤ Haemoglobin (globin + haem) ¤ 1 molecule of HB carries 4 molecules of Oxygen ¤ Average RBC carries about 280 million haemoglobin (HB) molecules ¤ HB + O2 HBO (oxyhemoglobin) ¤ Oxygen rich blood has a bright red color. The haemoglobin molecule HB + O2 HBO (oxyhemoglobin)….reversible 1. Low pH: Metabolically active tissue (eg exercise) pH decreases, HBO breaks down. 2. Low oxygen levels (hypoxia): HBO breaks down releasing oxygen and vice versa. 3. Temperature: High temperature (high during increased metabolic activity shift the equation to the left). Control of haemopoiesis: Number of RBCs should be maintained. Primary stimulus hypoxia Blood groups: ABO system  2. WBC (Leukocytes) Granulocytes Granulocytes: Polymorphonuclear leukocytes Agranulocytes  Main functions A. Granulocytes ˜ Neutrophoils: protect body from invading microbes (bacterial infection), remove cell debris and are attracted by chemotaxins (released by damaged cells). They carry out phagocytosis. ˜ Eosinophils: Elimination of parasites (such as worms). Found at allergic sites (eg asthma). They carry out phagocytosis. ˜ Basophils: Involved in allergic reactions and contain inflammatory agents such as histamine. Activated by allergens (antigens that cause allergy). © 2006 Elsevier Ltd. B. Agranulocytes Large nucleus and no granules ¤ Monocytes: Mononuclear cells that originate in bone marrow. In the blood they are phagocytic. In tissues, they differentiate into macrophages (also phagocytic). Imp functions in inflammation and immunity. Macrophage interacting with bacteria ¤ Lymphocytes: Great numbers in lymphatic tissue. After production in bone marrow and in lymphoid tissue, they travel in blood to lymphoid tissue elsewhere in the body where they become activated. Lymphocytes are of two types: B and T- lymphocytes. (discussed later).  3. Platelets (thrombocytes) ¤ Small non-nucleated cells (2-4 microns) ¤ They contain substances that cause haemostasis (the cessation of blood loss). ¤ Blood count: 200000-350000/ml ¤ Thrombopoietin from the kidneys stimulate platelet synthesis ¤ Life span 8-11 days and then if not involved in haemostasis, destroyed by macrophages in the spleen  Haemostasis 1. Vasoconstriction: Platelets stick to damaged blood vessel surface and release serotonin. Damaged vessel releases thromboxanes. Both result in vasoconstriction. 2. Platelet plug formation: platelets clump together and amplify the effect by release of ADP, which attracts more platelets. 3. Coagulation: A complex process. There are several factors involved (see table 4.3 in the book) Stages of blood clotting © 2006 Elsevier Ltd. Fibrinolysis ¤ After a clot is formed, it has to be removed (after healing has occurred) Activators (from damaged endothelial cells) Fibrin Plasminogen (enzyme activator)) Plasmin (active enzyme) Breakdown products (Soluble) Erythrocyte disorders Anaemias ¤ No enough Hb to carry oxygen ¤ Rate of production of mature blood cell ≠ rate of haemolysis. ¤ Classification (based on cause): 1- Impaired RBC production: Iron deficiency anaemia, megaloblastic anaemia (Deficiency in Vit B12 and/or Folic acid), hypoplastic anaemia (bone marrow failure) could be due to certain drugs. 2- Increased RBC loss: haemolytic anaemia, normocytic anaemia. Signs and symptoms ¤ Tachycardia: increased heart rate ¤ Palpitations: being aware of heartbeat ¤ Breathlessness: oxygen requirements increase, in effort to meet demand 1- Impaired RBC production: 1.a Iron deficiency anaemia ˜ Most common (normal iron intake 1 to 2 mg/day). Meat and coloured vegetables ˜ Woman 3 mg/day. ˜ Causes -Deficient intake/Iron malabsorption (due to abnormalities in GI tract). - Increased demand for iron (Ex during pregnancy) increases chance of anemia - Chronic blood loss (ulcers etc) 1.b Megaloblastic anaemia ¤ Maturation of RBC in impaired due to Vitamin B12 and/or folic acid deficiency (both are required for RBC development). ¤ Large RBC are found in the blood, which are immature and nucleated. ¤ Cells are fragile and die early by lysis and result in anemia.  1.c Hypoplastic and aplastic anaemia ˜ Due to varying degrees of bone marrow failure. ˜ Hypoplastic (low number of blood cells) or Aplastic (empty). ˜ This will affect also the number of WBC (leukopenia) and platelets (thrombocytopenia). ˜ Pancytopenia: all cells are reduced in number (anemia, immunosuppression and bleeding). ˜ Condition is often idiopathic. ˜ Due to certain drugs (cytotoxic drugs, anti-inflammatory, some antibiotics), radiation, some chemicals (benzene and its derivatives), malignant diseases and viral diseases. 2- Increased RBC loss: 2.a Haemolytic anaemias When RBC are destroyed while in circulation, or removed prematurely. § Congenital haemolytic anemia (genetic condition abnormal HB is produced). Most common types: 1- Sickle cell anemia (abnormal Hb synthesis) 2- Thalassaemia (reduced globin synthesis), severe cases might cause death in infants and children. Most common in the Mediterranean countries. 3- Haemolytic disease of the newborn. § Acquired haemolytic anemia: drugs, infection, radiation. © 2006 Elsevier Ltd. The mothers immune system makes antibodies against the baby’s RBCs If Rh- mother is given anti-Rh abs within 72 hr of delivery of Rh+ baby then protection is obtained 2.b Normocytic anaemia Cells are normal but the numbers are reduced (ex., after severe haemorrhage). 35  Polycythaemia ˜ Abnormally large numbers of erythrocytes in the blood. Increase in blood viscosity increased risk of blood clotting and infarction. ˜ Relative: RBC are normal but blood volume is reduced (burns etc) ˜ Physiological: true increase in RBC. Prolonged hypoxia due to many factors (high altitude, smoking etc.) Leukocyte disorders Leukopenia (low WBC count) ¤ Granulocytopenia (reduced circulating granulocytes), also known as neutropenia. ¤ Due to certain drugs (antibiotics, cytotoxic drugs etc), irradiation, diseases of bone marrow, severe microbial infections. Leukemia ¤ Malignant proliferation of white blood cell precursors in the bone marrow. ¤ Uncontrolled production of leukocytes, which are immature. ¤ Depressed immunity ¤ Can be caused by ionizing radiation, chemicals, genetic factors, viruses Types of leukaemias ¤ Acute leukaemias: sudden onset affect the poorly differentiated blast cells. Aggressive, bone marrow invasion. ¤ Chronic leukaemias: Less aggressive and leukocytes more differentiated (at the ‘cyte’ stage).