Blood: Formed Elements Erythrocytes = red blood cells Leukocytes = white blood cells Platelets = cell fragments
Hematopoiesis In the adult, all blood cell formation (i.e., synthesis of RBCs, WBCs, and platelets) occurs in the red bone marrow Red bone marrow is primarily found in bones of the axial skeleton, pelvic and pectoral girdles, and in the proximal epiphyses of the humerus and femur. The formation of blood cell is referred to as hematopoiesis or hemopoiesis
Red bone marrow
Hematopoiesis Hematopoiesis begins with a stem cell known as the hemocytoblast the hemocytoblast goes through a series of morphological changes
Erythopoiesis The formation of erythrocytes is called erythropoiesis
Erythrocytes (Red Blood Cells) Anatomy of circulating erythrocytes Biconcave disks Essentially bags of hemoglobin Anucleate (no nucleus) Contain very few organelles Outnumber white blood cells 1000:1
Erythrocyte: Hemoglobin Hemoglobin is a protein that is essential to RBC function. Hemoglobin levels are reported in grams of Hb per 100mL of whole blood, i.e., grams per deciliter or g/dL. Typical values are: 14-18g/dL in adult males. 12-16g/dL in adult females. 14-20g/dL in infants.
Leukocytes (White Blood Cells) Crucial in the body’s defense against disease These are complete cells, with a nucleus and organelles Able to move into and out of blood vessels (diapedesis) Can respond to chemicals released by damaged tissues
Platelets Derived from ruptured multinucleate cells (megakaryocytes) Normal platelet count = 200,000-400,000/mm 3
Thrombopoiesis The formation of thrombocyte
Anemia Anemia is a common blood disorder that occurs when there are fewer red blood cells than normal, or there is a low concentration of hemoglobin in the blood.
Anemia Anemia is often a symptom of a disease rather than a disease itself. Anemia usually develops due to the presence of one of the following: excessive blood loss or hemorrhaging deficient production of red cells excessive red cell destruction both decreased production and excessive destruction of red blood cells
Anemia Generally, anemia may be caused by several problems, including the following: infections certain diseases certain medications poor nutrition blood loss
Anemia Symptoms: abnormal paleness or lack of color of the skin dizziness, or vertigo, especially when standing lack of energy, or tiring easily (fatigue) headache
Anemia Symptoms (cont.) irritability irregular menstruation cycles absent or delayed menstruation (amenorrhea) sore or swollen tongue (glossitis) jaundice, or yellowing of skin, eyes, and mouth enlarged spleen or liver (splenomegaly, hepatomegaly) impaired wound and tissue healing
Anemia: the types There are several different types of anemia, each with a specific cause and treatment, including the following: Deficiency: iron folic acid piridoksin (hipokrom) kobalamin Zinc (hipokrom)
Iron deficiency anaemia The RBC's are smaller than normal and have an increased zone of central pallor. This is indicative of a hypochromic (less hemoglobin in each RBC) microcytic (smaller size of each RBC) anemia.
Fe deficiency – microcytic hypochrome
Megaloblastic (perniciousa) anemia Due to folate or to B12 deficiency. Can be caused by inadequate intake or absorption of vitamin B 12. The stomach lining produces a chemical called intrinsic factor which is necessary for the absorption of ingested vitamin B 12. It is often a lack of intrinsic factor that causes pernicious anemia. Hypersegmented neutrophil that is present with megaloblastic anemias. There are 8 lobes instead of the usual 3 or 4. The size of the RBC's is also increased (macrocytosis).
Types of Anemia Hemolytic RBCs rupture (lyse) prematurely. Can be due to Hb abnormalities, mismatched blood transfusion, parasitic or bacterial infection, or as an autoimmune condition.
Types of Anemia Aplastic Results from destruction of red bone marrow by bacterial toxins, drugs or radiation. Impacts all blood cells, leading to clotting difficulties and immune problems.
Types of Anemia Sickle-Cell A mutation in the gene for the beta chain of Hb results in an abnormal hemoglobin called HbS. Under low-oxygen conditions, the beta chains link together and become stiff rods - this gives the RBC a sickle shape. Sickled RBCs can then block and clog small blood vessels.
Sickle cell anemia
Anaemia : treatment treatment of the causative disease vitamin and mineral supplements change in diet medication blood transfusion bone marrow transplant surgery (to remove the spleen, if related to hemolytic anemia) antibiotics (if an infection is the causative agent)
Micronutrition Deficiency Thiamine Riboflavin (B2) Pyridoxine (B6) Niacin Vitamin C Vitamin E Vitamin K Trace elements
Thiamine Deficiency Thiamine - as the majority of the B complex - is found in green vegetables, milk and liver. Thiamine is the co-factor for many enzymes in the glycolytic pathway. Lack of thiamine inadequate glucose metabolism accumulation of lactate and pyruvate peripheral vasodilatation oedema.
Thiamine Deficiency Thiamine deficiency (beri-beri) is found in persons consuming polished rice (classical beri-beri), in chronic alcoholics, and in marasmus Dry beri-beri is symmetrical polyneuropathy (ie, paresthesia, weakness, heaviness, and paresis of the legs). CNS involvement with ischaemic damage results in the Wernicke-Korsakoff syndrome (ie, ataxia, confusion and ophtalmoplegia). Wet beri-beri : oedemas of the legs, pleural effusions and ascites. - These disorders respond immediately to thiamine treatment.
Vitamin B2 (riboflavin) deficiency Riboflavin is widely distributed in animal and vegetable foods. In the human body riboflavin is converted into flavin mono- and di-nucleotides. These compounds are of crucial importance in the electron transport chain. Riboflavin deficiency is frequently only part of a combined vitamin B deficiency, but the classical manifestations are lesions around the natural openings: 1. interstitial keratitis of the cornea with vascularisation, 2. seborrhoic dermatitis (face, vulva, and scrotum), 3. angular stomatitis (ie, cheilosis or fissures at the angles of the mouth), and 4. glossitis. These lesions respond to riboflavin usually given parenterally as a vitamin B complex.
Vitamin B6 deficiency Vitamin B6 activity is found in three compounds found in both vegetable and animal foods: pyrodoxine, pyridoxal, and pyridoxamine. Pyridoxal phosphate is a co-enzyme for transaminases, carboxylases (formation of the neurotransmitter GABA) and other enzymes. Drugs like the antituberculosis drug, isoniazid, and the copper-chelating agent, penicillamine, are B6- antagonists. Certain types of polyneuropathy respond to vitamin B6 therapy.
Vitamin B7 deficiency Niacin deficiency or pellagra (ie, roughs skin) is recognized by the combination of the 3 diagnostic Ds: Dermatitis, diarrhoea, and dementia. Niacin is involved in the formation of nicotinamide adenine dinucleotide (NAD) and its phosphate (NADP). These molecules are important in many oxidation/reduction reactions of the intermediary metabolism. Niacin found in different types of grains (poor content in maize), and our endogenous synthesis is from tryptophan found in meat, eggs and milk.
Vitamin C deficiency (scurvy) Found in fresh fruit and vegetables. Humans cannot synthesise ascorbic acid from glucose as several animals. Ascorbic acid is necessary for the production of collagen in all tissues including the vessel walls. Vitamin C deficiency (scurvy or scorbutus) is found among food faddists and in developing countries, where infants are fed with excessively boiled milk.
Vitamin C deficiency (scurvy) Abnormal collagen without sufficient tensile strength bleedings : bruises of the skin, haemarthron, subperiosteal bleedings, bleeding anaemia. Infections are prolonged and the healing of wounds is poor. Gingivitis loose teeth, Lack of normal collagen in growing bones arrested bone growth. There is no advantage in the daily intake of large doses of vitamin C to prevent or improve common cold or cancer. In one controlled clinical trial there was an accumulation of cases with kidney stones. Rebound scurvy may occur following a sudden stop of the intake of large doses of vitamin C.
Vitamin E deficiency Vitamin E ( -tochoferol) is found in fish, fish oil and vegetable oil from Soya beans and corn. antioxidant, protects the phospholipids of the plasma membrane against peroxidation by free radicals produced by the cell metabolism. Prolonged vitamin E deficiency is rare, but leads to CNS lesions, haemolytic anaemia, and muscle disorders. Patients with fat malabsorption or patients receiving parenteral nutrition may develop vitamin E deficiency
Vitamin K deficiency Vitamin K occurs in two forms in nature. Vitamin K1 is produced in plants, and intestinal bacteria in animals synthesise vitamin K2. Insufficient dietary intake of vitamin K is infrequent, and occurs occasionally such as cases of anorexia nervosa. Fat malabsorption is accompanied by vitamin K deficiency.
Vitamin K deficiency Newborn babies sometimes suffer from vitamin K deficiency, because the molecule only crosses the placental barrier with difficulty, and because the sterile gut of the baby cannot produce vitamin K2. Destruction of the intestinal bacteria by long term antibiotic treatment may also lead to vitamin K deficiency.
Vitamin K deficiency Vitamin K deficiency can lead to terminal bleeding. This is because vitamin K normally activates four clotting factors: prothrombin, factor VII, factor IX, and factor X. These four proteins probably receive Ca2+ binding properties from vitamin K Therapy with intramuscularly administered vitamin K is rapid and effective.