Cd5 B Cells Autoimmune Diet RecipesNormocytic normochromic anemia . The World Health Organization has defined anemia as a hemoglobin concentration below 7. L (1. 2 g/d. L) in women and below 8. L (1. 3 g/d. L) in men. Peripheral blood smears from a patient with megaloblastic anemia (left) and from a normal subject (right), both at the same magnification. The smear from the patient shows variation in the size and shape of erythrocytes and the presence of macro- ovalocytes. From Goldman and Bennett, 2. Some types of anemia are named for the factors causing them: poor diet (nutritional anemia), excessive blood loss (hemorrhagic anemia), congenital defects of hemoglobin (hypochromic anemia), exposure to industrial poisons, diseases of the bone marrow (aplastic anemia and hypoplastic anemia), or any other disorder that upsets the balance between blood loss through bleeding or destruction of blood cells and production of blood cells. Anemias can also be classified according to the morphologic characteristics of the erythrocytes, such as size (microcytic, macrocytic, and normocytic anemias) and color or hemoglobin concentration (hypochromic anemia). A type called hypochromic microcytic anemia is characterized by very small erythrocytes that have low hemoglobin concentration and hence poor coloration. Data used to identify anemia types include the erythrocyte indices: (1) mean corpuscular volume (MCV), the average erythrocyte volume; (2) mean corpuscular hemoglobin (MCH), the average amount of hemoglobin per erythrocyte; and (3) mean corpuscular hemoglobin concentration (MCHC), the average concentration of hemoglobin in erythrocytes. Mild degrees of anemia often cause only slight and vague symptoms, perhaps nothing more than easy fatigue or a lack of energy. As the condition progresses, more severe symptoms may be experienced, such as shortness of breath, pounding of the heart, and a rapid pulse; these are caused by the inability of anemic blood to supply the body tissues with enough oxygen. Pallor, particularly in the palms of the hands, the fingernails, and the conjunctiva (the lining of the eyelids), may also indicate anemia. In very advanced cases, swelling of the ankles and other evidence of heart failure may appear. Common Causes of Anemia. Loss of Blood (Hemorrhagic Anemia): If there is massive bleeding from a wound or other lesion, the body may lose enough blood to cause severe and acute anemia, which is often accompanied by shock. Immediate transfusions are generally required to replace the lost blood. Chronic blood loss, such as excessive menstrual flow, or slow loss of blood from an ulcer or cancer of the gastrointestinal tract, may also lead to anemia. These anemias disappear when the cause has been found and corrected. To help the blood replenish itself, the health care provider may prescribe medicines containing iron, which is necessary to build hemoglobin, and foods with high iron content, such as kidney and navy beans, liver, spinach, and whole wheat bread. Dietary Deficiencies and Abnormalities of Red Blood Cell Production (Nutritional Anemia, Aplastic Anemia, and Hypoplastic Anemia): Anemia may develop if the diet does not provide enough iron, protein, vitamin B1. The combination of poor diet and chronic loss of blood makes for particular susceptibility to severe anemia. BY LEO GALLAND, M.D. From the perspective of function, the contents of the gut lumen lie outside the body and contain a toxic/antigenic load from which. INTRODUCTION: Exogenous lipoid pneumonia (ELP) is caused by the inhalation of animal fats, vegetable or mineral oil. It is commonly seen in patients at high risk for. Chest pain Chest pain may occur if the lymphoma affects the thymus Unexplained weight loss Sudden and unexpected weight loss of 10% or more of total body weight could. Chronic lymphocytic leukemia (CLL) Is a type of blood cancer that begins in the bone marrow; Can progress either slowly or quickly depending on the form it takes. However, no single test is sufficiently sensitive or. Chemotherapy forms the cornerstone of therapy. Micro description ===== Granulation tissue with scattered large, atypical mesenchymal cells resembling. The American Journal of Gastroenterology is published by Springer Nature on behalf of the American College of Gastroenterology (ACG). Ranked the #1 clinical journal. Anemias associated with folic acid deficiency are very common. Excessive Destruction of Red Blood Cells (hemolytic anemia): Anemia may also develop related to hemolysis due to trauma, chemical agents or medications (toxic hemolytic anemia), infectious disease, isoimmune hemolytic reactions, autoimmune disorders, and the paroxysmal hemoglobinurias. Patient Care. Assessment of patients with some form of anemia will depend to some extent on the specific type of blood dyscrasia presented. In general, these patients do share some common problems requiring special assessment skills and interventions. Anemia can affect many different body systems (see table). Although pallor of the skin is a sign of anemia, it is not the most reliable sign; many other factors can affect complexion and skin color. Jaundice of the skin and sclera can occur as a result of hemolysis and the release of bilirubin into the blood stream, where it eventually finds its way into the skin and mucous membranes. A bluish tint to the skin (cyanosis) can indicate hypoxia due to inadequate numbers of oxygen- bearing erythrocytes. Activity intolerance is a common problem for patients with anemia. Physical activity increases demand for oxygen, but if there are not enough circulating erythrocytes to provide sufficient oxygen, patients become physically weak and unable to engage in normal physical activity without experiencing profound fatigue. This can result in some degree of self- care deficit as the fatigue interferes with the patient's ability to carry on regular or enjoyable activities. AIHA) an acquired disorder characterized by hemolysis due to the production of autoantibodies against one's own red blood cell antigens. Immune complex problems: Ingestion of any of a large number of drugs is followed by immunization and the formation of a soluble drug–anti- drug complex that adsorbs nonspecifically to the erythrocyte surface. Drug absorption: Drugs bind firmly to erythrocyte membrane proteins, inducing the formation of specific antibodies; the drug most commonly associated with this mechanism is penicillin. Membrane modification: A nonimmunologic mechanism whereby the drug involved is able to modify erythrocytes so that plasma proteins can bind to the membrane. Autoantibody formation: Methyldopa (Aldomet) induces the production of autoantibodies that recognize erythrocyte antigens and are serologically indistinguishable from those seen in patients with warm autoimmune hemolytic anemia. Iron deficiency anemia is the most common nutritional disorder in the United States. It is unresponsive to hematinics or to withdrawal of toxic agents or drugs and may be preleukemic. West African descent, and less often in the Mediterranean basin and a few other areas; it is caused by hemoglobin S with abnormal erythrocytes (sickle cells) in the blood. Homozygous individuals have the full- blown syndrome with accelerated hemolysis, increased blood viscosity and vaso- occlusion, arthralgias, acute attacks of abdominal pain, and ulcerations of the lower limbs; some have periodic attacks of sickle cell crises. The heterozygous condition is called sickle cell trait and is usually asymptomatic. People are considered anemic when their hemoglobin levels are more than two standard deviations below the mean level in their hospital's laboratory. The diagnosis of anemia is influenced by variables such as the patient's age (neonates are anemic at levels of hemoglobin that would be considered polycythemic in some adults), gender (men have higher hemoglobin levels than women), pregnancy status (hemodilution in pregnancy lowers measured hemoglobin), residential altitude, and ethnic or racial background. If anemia develops slowly, however, there may be no functional impairment even though the hemoglobin is less than 7 g/1. L of blood. Anemia is not a disease but rather a symptom of other illnesses. It is classified on the basis of mean corpuscular volume as microcytic (8. Etiology. Anemia may be caused by bleeding, e. Signs of anemia may include a rapid pulse or rapid breathing if blood loss occurs rapidly. The chronically anemic may have pale skin, mucous membranes, or nail beds and fissures at the corners of the mouth. Treatment. Treatment of anemia must be specific for the cause. The prognosis for recovery from anemia is excellent if the underlying cause is treatable. Anemia due to excessive blood loss: For acute blood loss, immediate measures should be taken to stop the bleeding, to restore blood volume by transfusion, and to combat shock. Chronic blood loss usually produces iron- deficiency anemia. Anemia due to excessive blood cell destruction: The specific hemolytic disorder should be treated. Anemia due to decreased blood cell formation: For deficiency states, replacement therapy is used to combat the specific deficiency, e. B1. 2, folic acid, ascorbic acid. For bone marrow disorders, if anemia is due to a toxic state, removal of the toxic agent may result in spontaneous recovery. Anemia due to renal failure, cancer chemotherapy, HIV, and other chronic diseases: Erythropoietin injections are helpful. Patient care. The patient is evaluated for signs and symptoms, and the results of laboratory studies are reviewed for evidence of inadequate erythropoiesis or premature erythrocyte destruction. Prescribed diagnostic studies are scheduled and carried out. Rest: The patient is evaluated for fatigue; care and activities are planned and regular rest periods are scheduled. Mouth care: The patient's mouth is inspected daily for glossitis, mouth lesions, or ulcers. A sponge stick is recommended for oral care, and alkaline mouthwashes are suggested if mouth ulcers are present. A dental consultation may be required. Diet: The patient is encouraged to eat small portions at frequent intervals. Mouth care is provided before meals. The nurse or a nutritionist provides counseling based on type of anemia. Medications: Health care professionals teach the patient about medication actions, desired effects, adverse reactions, and correct dosing and administration. Patient education: The cause of the anemia and the rationale for prescribed treatment are explained to the patient and family. Teaching should cover the prescribed rest and activity regimen, diet, prevention of infection, including the need for frequent temperature checks, and the continuing need for periodic blood testing and medical evaluation. See: illustration. Treatment. Many patients can be treated effectively with bone marrow transplantation or immunosuppressive drugs. Patient care. The patient and family are educated about the cause and treatment of the illness. Measures to prevent infection are explained, and the importance of adequate rest is emphasized. Thyroid Regulation and Dysfunction in the Pregnant Patient. ABSTRACTThyroid disease in pregnancy is a common clinical problem. During the past 2 years significant clinical and scientific advances have occurred in the field. This chapter reviews the physiology of thyroid and pregnancy focusing on iodine requirements and advances in placental function. There follows discussion on thyroid function tests in pregnancy and their interpretation noting ethnic variation in pregnancy range. Sections on iodine nutrition, thyroid autoantibodies and pregnancy complications, thyroid considerations in infertile women, hypothyroidism in pregnancy, thyrotoxicosis in pregnancy, thyroid nodules and cancer in pregnant women, fetal and neonatal considerations, thyroid disease and lactation, screening for thyroid dysfunction in pregnancy will inform the reader of the current information on these areas. Postpartum thyroid disease is also discussed. Current topical fields of importance include the role of isolated hypothyroxinemia on obstetric outcomes and neurodevelopment, the influence of thyroid autoantibodies on the same parameters and the effect of recent data on malformations associated with antithyroid drug therapy on management guidelines for thyrotoxicosis in pregnancy. It also seems as if pregnancy may have a deleterious effect on the progression differentiated thyroid cancer in pregnancy; this requires more confirmation. The intense debate on whether to screen for thyroid function in all pregnant women continues. Although the few randomised trials which have been performed are negative several areas of the world and some clinics in USA recommend screening. In general recent guidelines from USA and Europe find no evidence to support routine screening. INTRODUCTIONDuring the past 3- 4 decades there has been a major expansion of our knowledge regarding thyroid disorders associated with pregnancy. The prevalence of hyperthyroidism is around 5 per 1. As the conditions are generally much more common in the female it is to be expected that they will appear during pregnancy. Developments in our understanding of thyroid physiology (1,2) and immunology (3) in pregnancy as well as improvements in thyroid function testing (4) have highlighted the importance of recognizing and providing appropriate therapy to women with gestational thyroid disorders (5). There has been much discussion and many publications on the optimal management of pregnant women who are hyper or hypothyroid(6,7). In addition. The field has advanced rapidly so that the evidence based guidelines on thyroid and pregnancy published in 2. The American Thyroid Association (1. The American Endocrine society (1. The European Thyroid Association(1. Pregnancy may affect the course of thyroid disorders and, conversely, thyroid diseases may affect the course of pregnancy. Moreover, thyroid disorders (and their management) may affect both the pregnant woman and the developing fetus. MATERNAL THYROID PHYSIOLOGYNumerous hormonal changes and metabolic demands occur during pregnancy, resulting in profound and complex effects on thyroid function Table 1. These changes are discussed below. Table 1. 4- 1. Factors affecting Thyroid Physiology during normal Pregnancy. Physiologic Change. Thyroid- related consequences. Increased renal I- clearance. Increased 2. 4- hr RAIUDecreased plasma I- and placental I- transport to the fetus. In I- deficient women, decreased T4, increased TSH, and goiter formation. Increased O2 consumption by fetoplacental unit, gravid uterus and mother. Increased BMRFirst- trimester increase in h. CGIncreased free T4 and T3. Decreased basal TSH (partial blunting of the pituitary- thyroid axis)Increased serum TBGIncreased total T4 and T3. Increased plasma volume. Increased T4 and T3 pool size. Inner- ring deiodination of T4 and T3 by placenta. Accelerated rates of T4 and T3 degradation and production. Iodine and Pregnancy. Physiologic adaptation of the thyroidal economy associated with normal pregnancy is replaced by pathologic changes when pregnancy takes place in conditions with iodine deficiency or even only mild iodine restriction. Globally, the changes in maternal thyroid function that occur during gestation can be viewed as a mathematical fraction, with hormone requirements in the numerator and the availability of iodine in the denominator. When availability of iodine becomes deficient during gestation, at a time when thyroid hormone requirements are increased, this situation presents an additional challenge to the maternal thyroid 1,2. Figure 1. 4- 1 illustrates the steps through which pregnancy induces a specific challenge for the thyroid gland and the profound difference between glandular adaptation in conditions with iodine sufficiency or deficiency. Figure 1. 4- 1 From physiological adaptation to pathological alterations of the thyroidal economy during pregnancy. The scheme illustrates the sequence of events occurring for the maternal thyroid gland, emphasizing the role of iodine deficiency to stimulate the thyroidal machinery (from Glinoer, Ref 1). Early in pregnancy there is an increase in renal blood flow and glomerular filtration which lead to an increase in iodide clearance from plasma (1,1. This results in a fall in plasma iodine concentrations and an increase in iodide requirements from the diet . In women with iodine sufficiency there is little thyroid impact of the obligatory increase in renal iodine losses, because the intrathyroidal iodine stores are plentiful at the time of conception and they remain unaltered throughout gestation. Pregnancy does not have a major influence on circulating iodine concentrations in iodine- sufficient regions. It should be noted, however, that the iodine excretion levels were unusually high in this study, ranging between 4. In addition, there is a further increment in iodine requirements, due to transplacental iodide transport necessary for iodothyronine synthesis by the fetal thyroid gland (1. When pregnancy takes place in conditions with borderline iodine availability, significant increments in both maternal and fetal thyroid volume occur, if no supplemental iodine is given during early pregnancy (2. Thus during pregnancy, the physiologic changes that take place in maternal thyroid economy lead to an increase in thyroid hormone production of ~5. In order to achieve the necessary increment in hormone production, the iodine intake needs to be increased during early pregnancy. Iodine deficiency present at critical stages during pregnancy and early childhood results in impaired development of the brain and consequently in impaired mental function (8,2. Iodine deficiency worldwide is a major cause of neurointellectual impairment and is discussed in detail in chapter 2. Although a variety of methods exists for the correction of iodine deficiency, the most commonly accepted and applied method is universal salt iodization (USI), i. A WHO committee recommended appropriate iodine intakes for pregnant and lactating women as well as for children (Table 1. Table. 14- 2. Recommended iodine intake during pregnancy and lactation and categorization of iodine nutrition adequacy based on urinary iodine excretion. Population Group. Median Urinary Iodine conc. Category of Iodine intake. Pregnant women. 25. Since breast milk provides approximately 1. Therefore iodine deficiency requires constant monitoring, even after the implementation of iodine supplementation in pregnant women. Recently, iodine deficiency has re emerged in Australia and the UK and even in USA there are groups of the population with suboptimal iodine levels (2. The importance of iodine deficiency in pregnancy on childhood IQ has been emphasized (2. In addition there is increasing evidence of the benficial effect of iodine supplementation before and during pregnancy in ameliorating this problem (2. After reduction to iodide, dietary iodine is rapidly absorbed from the gut. Then, iodide of dietary origin mixes rapidly with iodide resulting from the peripheral catabolism of thyroid hormones and iodothyronines by deiodination, and together they constitute the extra- thyroidal pool of inorganic iodide (PII). This pool is in a dynamic equilibrium with two main organs, the thyroid gland and the kidneys. Figure 1. 4- 2 schematically compares the kinetics of iodide in non- pregnant healthy adults with two different intake levels . A normal adult utilizes ~8. When the iodine intake is adequate (1. From the 8. 0 . In such conditions, the metabolic balance is in equilibrium, with 1. Thus, with an iodine intake level of 1. In contrast, when the iodine intake is restricted to only 7. The higher uptake allows to recover 3. To compensate for the missing amount (i. Over time, if the nutritional situation remains unchanged and despite some adaptation of urinary iodine losses, the metabolic balance becomes negative. The thyroid gland tries to adapt by an increased uptake, glandular hypertrophy, and a higher setting of the pituitary thyrostat. During pregnancy, two fundamental changes take place. There is a significant increase in the renal iodide clearance (by ~1. TH production requirements (by ~1. Since the renal iodide clearance already increases in the first weeks of gestation and persists thereafter, this constitutes a non- avoidable urinary iodine loss, which tends to lower circulating PII levels and, in turn, induce a compensatory increase in the thyroidal clearance of iodide. These mechanisms underline the increased physiologic thyroidal activity during pregnancy. Panel C in Figure 9 indicates that when the daily iodine intake is only 7. Thus in about one trimester after conception, the already low intra- thyroidal iodine stores become even more depleted and, when iodine deprivation prevails during the first half, it tends to become more severe with the progression of gestation to its final stages.
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