STUDY - Technical - New Dacian's Medicine
Anemia
(1)
Translation Draft
My wonderful vacation this year has passed, so it's time to get to work. Posts will follow that will no longer have a daily "graphic" (I think the correct expression would be "periodic") because my efforts are already oriented towards the development of the "new" www.dorinm.ro and the "resettlement" and the development of all the elements already presented at The New Medicine (the time has come for serious and structured approaches to this part of the activity of my life). Anyway, I'll keep you updated as best I can. But let's get to work!
Oxygen required for normal tissue metabolism is supplied by circulating red blood cells (erythrocytes). Erythrocite is ideally structured for oxygen distribution. Essentially, it is a "container" with hemoglobin, the protein responsible for transporting oxygen. Being devoid of a nucleus, the erythrocytes exhibit deformability, which allows it countless passages through microcirculation. At the same time it has only those metabolic structures necessary to maintain cellular integrity for just over 100 days. For this reason, constant regeneration of red blood cells is necessary in a regular process of production of new cells called erythropoiesis.
Interstitial kidney cells are responsible for regulating the production of erythropoietin according to changes in oxygen intake. Low levels of erythropoietin are secreted daily to maintain basal erythropoiesis. When haemoglobin levels drop below 100 to 10 g/l new cells are "recruited" and erythropoietin levels increase logarithmically, consistent with the severity of anaemia. This stimulates the proliferation of erythrocytic precursors in the marrow and increases red blood cell production several times. This functional capacity of erythropoiesis requires normal renal function, a healthy marrow and an adequate supply of nutrients, especially iron. Altering one or more essential steps in erythropoiesis leads to the development of anaemia.
By definition, a patient has anemia if the level of hemoglobin or the number of circulating erythrocytes is significantly reduced. From a biological point of view, the presence and severity of anaemia are easily determined on the basis of the deviation of the patient's haemoglobin/haematocrit from a standard level of values considered normal. However, the diagnosis of anaemia is much more clinically complex. If the most sensitive indicator of anaemia could be achieved, it would be the direct measurement of the oxygen level delivered to peripheral tissues.
This is not possible, clinically significant anaemia is best detected and defined by observation of changes occurring in the normal erythropoiesis process. Measurement of the production, maturation, morphology and iron reserves of red blood cells is done to identify and classify the anaemia as a defect either in the medullary production and maturation of erythrocyte precursors or in the lifetime of erythrocytes. Functional classification of anaemia is useful in selecting a number of clinical and laboratory studies necessary to complete the differential diagnosis of the disease.
From the point of view of the clinical picture, the presence of anaemia can be suspected based on the nature of the patient's disease. Severe bleeding will cause anaemia through an acute loss of blood, while chronic bleeding will lead to an iron deficiency. On the other hand, a patient with a vascular collagen disease will present with autoimmune hemolytic anaemia. The clinical signs and symptoms of anaemia depend on the rapidity of installation, its severity and the age of the patient. Mild anaemia is rapidly compensated by the innate ability of the hemoglobin-oxygen dissociation curve to maintain the oxygen supply to tissues, even if the hemoglobin level decreases.
However, changing the curve will progressively reduce the ability of erythrocytes to respond to situations where demand increases. Patients will experience loss of fatigue resistance, increased heart rate and dyspnea to exercise. When haemoglobin drops below 70 to 80 g/l, the exercise capacity is reduced marked, any physical exertion being associated with dyspnoea, palpitations, pulsating headache and rapid exhaustion. Elderly people with cardiovascular disease may experience aggravated angina, claudication and heart failure.
The compensation capacity also depends on the cause of the anaemia and how it is installed. Acute blood loss involves a sudden reduction in both blood volume and erythrocytic mass. While adjusting the hemoglobin-oxygen dissociation curve to release more oxygen into tissues can cope with a reduction in the number of circulating erythrocytes, even a modest decrease in total blood volume interferes with cardiovascular response. A patient with severe bleeding will show signs and symptoms of tissue hypoxia and vascular collapse. This is not the case in patients who develop chronic anaemia, whose total blood volume remains normal, and changes in heart rate and regional blood flow help to compensate for loss of oxygen transport capacity.
From the point of view of the patient's approach, anamnesis and detailed physical examination are essential for the diagnosis and therapeutic approach of anaemia. Indices of etiology can occur in any segment of the history, following present diseases, those of history, family history or after examination of all systems. Symptoms of acute or chronic diseases, information on transfusions or haemograms, nutritional skills, alcohol or drug intake and family history of anaemia may be useful. It is important the breed to which the patient belongs, because many of the metabolic defects erythrocytes follow an ethnic line. Certain charges provide clues to the specific types of anaemia. For example, patients with sickle cell disease will describe severe bone and joint pain that has been occurring periodically for a very long time. Patients with severe iron deficiency frequently experience pain in the oral cavity and dysphagia or craving to eat ice or earth (pica or picaphagy).
Physical examination of the patient with anaemia should assess, in particular, the degree of oxygenation of the tissues. After acute bleeding, signs of hypovolemia and tissue hypoxia indicate the severity of anaemia most accurately. When more than 30% of blood volume is rapidly lost, patients can no longer compensate by the usual mechanisms represented by venous spasm and changes in the regional blood flow. These patients remain in clinostatism and have persistent hypotension and tachycardia if mobilized. If the loss of blood volume exceeds 40% (i.e. more than 2l in an adult of average weight), signs of hypovolemic shock with thirst for air, confusion, diaphoresis, hypotension and tachycardia appear. These patients have significant deficits in the infusion of vital organs and require immediate vascular refilling.
When anemia develops gradually, hypovolemia does not occur. In fact, a small expansion in blood volume and an increase in heart rate are signs of effective compensation. Patients experience a strong apex shock, ample peripheral pulse with increased pressure and a meso or holosystolic breath secondary to increased blood flow and turbulence. Another sign of severe anaemia (with haemoglobin levels below 80 - 100 g/l) is the pallor of the skin and mucous membranes. This sign is inconclusive in patients with subcutaneous edema, marked decrease in skin blood flow or intensely pigmented skin. Therefore, the areas where the vessels are close to the surface should be carefully examined, for example, in the mucous membranes, nail bed and palm grooves of the hand. When the latter are paler than the surrounding skin, the level of hemoglobin is usually less than 80 g/l.
Very mild anemias do not cause obvious clinical signs and symptoms. This is due to the own compensation mechanism of erythrocytes (the ability of the hemoglobin-oxygen dissociation curve to adjust the oxygen supply of tissues). Normally, only the peak portion of the curve is used, causing a considerable increase in oxygen delivery capacity when oxygen needs are high. In the case of acute anaemia, slight changes in pH and CO2 concentration in the periphery will instantly displace the right (Bohr effect), which increases the release of oxygen at the tissue level. In chronic anaemia, each erythrocyte maintains this displacement by increasing intracellular production by 2.3 diphosphoglycerate. This compensation mechanism is sufficient by itself to maintain a normal supply of oxygen to the tissues, despite the decrease in hemoglobin of 0 to 30 g/l. Because of this, mild anaemia is detected by routine testing of hemoglobin or hematocrit, rather than by anamnesis or physical examination.
I will complete this post by listing the laboratory tests useful in diagnosing anemia... These are represented by: I. Hemoleucogram (A. Number of erythrocytes with 1. hemoglobin and 2. hematocrit; B. Erythrocytic indices with 1. average erythrocytic volume - VEM, 2. medium erythrocytic haemoglobin - HEM, 3. average erythrocytic haemoglobin concentration - CMHE and 4. volume of distribution of erythrocytes - VDE; C. Number of leukocytes with 1. distinct cells and 2. nuclear segmentation of neutrophils; D. Number of platelets; E. Erythrocytic morphology with 1. cell size, 2. haemoglobin content, 3. anisocytosis, 4. poikiloocytosis and 5. polychromia), II. Number of reticulocytes, III. Iron deposits (with 1. serum iron, 2. total iron binding capacity and 3. serum ferritin, medullary smear), IV. Examination of bone marrow (with A. aspirated medullary with 1. e/G ratio - the ratio between erythrocytic precursors and granulocytes, 2. cell morphology and 3. smear and B. medullary biopsy with 1. cellularity and 2. morphology).
I will continue in the following post with the presentation of the "detailed" elements related to laboratory tests useful in diagnosing anaemia (I will seek to keep the "volume of posts" within the limit of 1,500 words of each post - the more words, the better)...
My wonderful vacation this year has passed, so it's time to get to work. Posts will follow that will no longer have a daily "graphic" (I think the correct expression would be "periodic") because my efforts are already oriented towards the development of the "new" www.dorinm.ro and the "resettlement" and the development of all the elements already presented at The New Medicine (the time has come for serious and structured approaches to this part of the activity of my life). Anyway, I'll keep you updated as best I can. But let's get to work!
Oxygen required for normal tissue metabolism is supplied by circulating red blood cells (erythrocytes). Erythrocite is ideally structured for oxygen distribution. Essentially, it is a "container" with hemoglobin, the protein responsible for transporting oxygen. Being devoid of a nucleus, the erythrocytes exhibit deformability, which allows it countless passages through microcirculation. At the same time it has only those metabolic structures necessary to maintain cellular integrity for just over 100 days. For this reason, constant regeneration of red blood cells is necessary in a regular process of production of new cells called erythropoiesis.
Interstitial kidney cells are responsible for regulating the production of erythropoietin according to changes in oxygen intake. Low levels of erythropoietin are secreted daily to maintain basal erythropoiesis. When haemoglobin levels drop below 100 to 10 g/l new cells are "recruited" and erythropoietin levels increase logarithmically, consistent with the severity of anaemia. This stimulates the proliferation of erythrocytic precursors in the marrow and increases red blood cell production several times. This functional capacity of erythropoiesis requires normal renal function, a healthy marrow and an adequate supply of nutrients, especially iron. Altering one or more essential steps in erythropoiesis leads to the development of anaemia.
By definition, a patient has anemia if the level of hemoglobin or the number of circulating erythrocytes is significantly reduced. From a biological point of view, the presence and severity of anaemia are easily determined on the basis of the deviation of the patient's haemoglobin/haematocrit from a standard level of values considered normal. However, the diagnosis of anaemia is much more clinically complex. If the most sensitive indicator of anaemia could be achieved, it would be the direct measurement of the oxygen level delivered to peripheral tissues.
This is not possible, clinically significant anaemia is best detected and defined by observation of changes occurring in the normal erythropoiesis process. Measurement of the production, maturation, morphology and iron reserves of red blood cells is done to identify and classify the anaemia as a defect either in the medullary production and maturation of erythrocyte precursors or in the lifetime of erythrocytes. Functional classification of anaemia is useful in selecting a number of clinical and laboratory studies necessary to complete the differential diagnosis of the disease.
From the point of view of the clinical picture, the presence of anaemia can be suspected based on the nature of the patient's disease. Severe bleeding will cause anaemia through an acute loss of blood, while chronic bleeding will lead to an iron deficiency. On the other hand, a patient with a vascular collagen disease will present with autoimmune hemolytic anaemia. The clinical signs and symptoms of anaemia depend on the rapidity of installation, its severity and the age of the patient. Mild anaemia is rapidly compensated by the innate ability of the hemoglobin-oxygen dissociation curve to maintain the oxygen supply to tissues, even if the hemoglobin level decreases.
However, changing the curve will progressively reduce the ability of erythrocytes to respond to situations where demand increases. Patients will experience loss of fatigue resistance, increased heart rate and dyspnea to exercise. When haemoglobin drops below 70 to 80 g/l, the exercise capacity is reduced marked, any physical exertion being associated with dyspnoea, palpitations, pulsating headache and rapid exhaustion. Elderly people with cardiovascular disease may experience aggravated angina, claudication and heart failure.
The compensation capacity also depends on the cause of the anaemia and how it is installed. Acute blood loss involves a sudden reduction in both blood volume and erythrocytic mass. While adjusting the hemoglobin-oxygen dissociation curve to release more oxygen into tissues can cope with a reduction in the number of circulating erythrocytes, even a modest decrease in total blood volume interferes with cardiovascular response. A patient with severe bleeding will show signs and symptoms of tissue hypoxia and vascular collapse. This is not the case in patients who develop chronic anaemia, whose total blood volume remains normal, and changes in heart rate and regional blood flow help to compensate for loss of oxygen transport capacity.
From the point of view of the patient's approach, anamnesis and detailed physical examination are essential for the diagnosis and therapeutic approach of anaemia. Indices of etiology can occur in any segment of the history, following present diseases, those of history, family history or after examination of all systems. Symptoms of acute or chronic diseases, information on transfusions or haemograms, nutritional skills, alcohol or drug intake and family history of anaemia may be useful. It is important the breed to which the patient belongs, because many of the metabolic defects erythrocytes follow an ethnic line. Certain charges provide clues to the specific types of anaemia. For example, patients with sickle cell disease will describe severe bone and joint pain that has been occurring periodically for a very long time. Patients with severe iron deficiency frequently experience pain in the oral cavity and dysphagia or craving to eat ice or earth (pica or picaphagy).
Physical examination of the patient with anaemia should assess, in particular, the degree of oxygenation of the tissues. After acute bleeding, signs of hypovolemia and tissue hypoxia indicate the severity of anaemia most accurately. When more than 30% of blood volume is rapidly lost, patients can no longer compensate by the usual mechanisms represented by venous spasm and changes in the regional blood flow. These patients remain in clinostatism and have persistent hypotension and tachycardia if mobilized. If the loss of blood volume exceeds 40% (i.e. more than 2l in an adult of average weight), signs of hypovolemic shock with thirst for air, confusion, diaphoresis, hypotension and tachycardia appear. These patients have significant deficits in the infusion of vital organs and require immediate vascular refilling.
When anemia develops gradually, hypovolemia does not occur. In fact, a small expansion in blood volume and an increase in heart rate are signs of effective compensation. Patients experience a strong apex shock, ample peripheral pulse with increased pressure and a meso or holosystolic breath secondary to increased blood flow and turbulence. Another sign of severe anaemia (with haemoglobin levels below 80 - 100 g/l) is the pallor of the skin and mucous membranes. This sign is inconclusive in patients with subcutaneous edema, marked decrease in skin blood flow or intensely pigmented skin. Therefore, the areas where the vessels are close to the surface should be carefully examined, for example, in the mucous membranes, nail bed and palm grooves of the hand. When the latter are paler than the surrounding skin, the level of hemoglobin is usually less than 80 g/l.
Very mild anemias do not cause obvious clinical signs and symptoms. This is due to the own compensation mechanism of erythrocytes (the ability of the hemoglobin-oxygen dissociation curve to adjust the oxygen supply of tissues). Normally, only the peak portion of the curve is used, causing a considerable increase in oxygen delivery capacity when oxygen needs are high. In the case of acute anaemia, slight changes in pH and CO2 concentration in the periphery will instantly displace the right (Bohr effect), which increases the release of oxygen at the tissue level. In chronic anaemia, each erythrocyte maintains this displacement by increasing intracellular production by 2.3 diphosphoglycerate. This compensation mechanism is sufficient by itself to maintain a normal supply of oxygen to the tissues, despite the decrease in hemoglobin of 0 to 30 g/l. Because of this, mild anaemia is detected by routine testing of hemoglobin or hematocrit, rather than by anamnesis or physical examination.
I will complete this post by listing the laboratory tests useful in diagnosing anemia... These are represented by: I. Hemoleucogram (A. Number of erythrocytes with 1. hemoglobin and 2. hematocrit; B. Erythrocytic indices with 1. average erythrocytic volume - VEM, 2. medium erythrocytic haemoglobin - HEM, 3. average erythrocytic haemoglobin concentration - CMHE and 4. volume of distribution of erythrocytes - VDE; C. Number of leukocytes with 1. distinct cells and 2. nuclear segmentation of neutrophils; D. Number of platelets; E. Erythrocytic morphology with 1. cell size, 2. haemoglobin content, 3. anisocytosis, 4. poikiloocytosis and 5. polychromia), II. Number of reticulocytes, III. Iron deposits (with 1. serum iron, 2. total iron binding capacity and 3. serum ferritin, medullary smear), IV. Examination of bone marrow (with A. aspirated medullary with 1. e/G ratio - the ratio between erythrocytic precursors and granulocytes, 2. cell morphology and 3. smear and B. medullary biopsy with 1. cellularity and 2. morphology).
I will continue in the following post with the presentation of the "detailed" elements related to laboratory tests useful in diagnosing anaemia (I will seek to keep the "volume of posts" within the limit of 1,500 words of each post - the more words, the better)...
Have understanding, love
and gratitude!
Dorin, Merticaru