This document discusses microcytic anemia and iron deficiency anemia. It defines anemia according to the World Health Organization and American Society of Hematology. It describes the causes, symptoms, and evaluation of microcytic anemia including complete blood count measures. Iron deficiency is the most common cause of microcytic anemia, which can result from blood loss, poor diet, or malabsorption. Treatment involves oral or intravenous iron replacement depending on the severity and cause of the anemia.
Iron deficiency anemia is caused by a lack of iron in the body. Common symptoms include fatigue, palpitations, tinnitus, and headaches. Diagnosis involves blood tests showing low iron levels and microcytic, hypochromic red blood cells. Treatment depends on the severity, and involves oral or intravenous iron supplements to replenish iron stores over 6-12 months. Parenteral iron is used for severe cases or those unable to tolerate oral iron.
The document discusses newer aspects of iron supplementation. It summarizes that iron amino acid chelate, or ferrous bis glycinate, has advantages over other forms of iron supplementation, including being non-buffered in the stomach, non-precipitated in the intestine, not antagonized by phytates, and having superior and dependable bioavailability due to its unique chelate design, which potentially allows for smaller doses with fewer side effects. The document examines what is known, unknown, and needs to be known about different forms of iron supplementation and their absorption parameters.
This document discusses iron deficiency anemia, including its causes, symptoms, signs, and laboratory investigations used to confirm and determine the cause of the condition. Iron deficiency anemia is the most common form of anemia and is caused by inadequate iron intake, blood loss, or malabsorption. Key lab tests to confirm include low hemoglobin, MCV, serum ferritin and transferrin saturation. Tests to determine the underlying cause include stool samples, endoscopy, and imaging of the gastrointestinal tract.
Zinc plays an important role in immunity and diarrhea. Zinc deficiency is common in acute and chronic diarrhea and leads to impaired immune function. Studies show that zinc supplementation in children with diarrhea reduces duration and severity of diarrhea episodes. It does so by accelerating regeneration of the intestinal mucosa and enhancing cellular immunity. As zinc deficiency is prevalent in developing countries, zinc supplements can be useful as both a preventive and therapeutic intervention for diarrhea.
Anemia is one of the most commonly seen condition predominantly in women due to various causes such as some chronic infection conditions and all. There are different types of anemias are there here we discuss mainly about Iron deficiency and sickle cell anemia.
This document discusses sideroblastic anemia, a type of anemia where the bone marrow produces abnormal red blood cells called ringed sideroblasts that cannot incorporate iron efficiently. Ringed sideroblasts have iron granules accumulated in mitochondria around the nucleus. Sideroblastic anemia can be hereditary or acquired through toxins, drugs, nutritional deficiencies, or other conditions. Symptoms include paleness, dizziness, fatigue, and organ enlargement. Diagnosis involves blood tests showing low hemoglobin and iron studies. Bone marrow biopsies reveal excess ringed sideroblasts. Treatment depends on the severity and cause but may include blood transfusions, iron chelation therapy, vitamins, or
This document summarizes key haematological changes during pregnancy. Physiological changes include anaemia due to plasma volume expansion, increased white blood cell counts dominated by neutrophils, and lower platelet counts. Common causes of anaemia are iron deficiency and folate deficiency. Thrombocytopenia is usually due to gestational thrombocytopenia, but may also result from preeclampsia or immune thrombocytopenic purpura. Pregnancy induces a hypercoagulable state through increased clotting factors and reduced inhibitors. Low molecular weight heparin is the anticoagulant of choice for treating thromboembolic disorders during pregnancy.
Iron deficiency anemia is caused by a lack of iron in the body. Common symptoms include fatigue, palpitations, tinnitus, and headaches. Diagnosis involves blood tests showing low iron levels and microcytic, hypochromic red blood cells. Treatment depends on the severity, and involves oral or intravenous iron supplements to replenish iron stores over 6-12 months. Parenteral iron is used for severe cases or those unable to tolerate oral iron.
The document discusses newer aspects of iron supplementation. It summarizes that iron amino acid chelate, or ferrous bis glycinate, has advantages over other forms of iron supplementation, including being non-buffered in the stomach, non-precipitated in the intestine, not antagonized by phytates, and having superior and dependable bioavailability due to its unique chelate design, which potentially allows for smaller doses with fewer side effects. The document examines what is known, unknown, and needs to be known about different forms of iron supplementation and their absorption parameters.
This document discusses iron deficiency anemia, including its causes, symptoms, signs, and laboratory investigations used to confirm and determine the cause of the condition. Iron deficiency anemia is the most common form of anemia and is caused by inadequate iron intake, blood loss, or malabsorption. Key lab tests to confirm include low hemoglobin, MCV, serum ferritin and transferrin saturation. Tests to determine the underlying cause include stool samples, endoscopy, and imaging of the gastrointestinal tract.
Zinc plays an important role in immunity and diarrhea. Zinc deficiency is common in acute and chronic diarrhea and leads to impaired immune function. Studies show that zinc supplementation in children with diarrhea reduces duration and severity of diarrhea episodes. It does so by accelerating regeneration of the intestinal mucosa and enhancing cellular immunity. As zinc deficiency is prevalent in developing countries, zinc supplements can be useful as both a preventive and therapeutic intervention for diarrhea.
Anemia is one of the most commonly seen condition predominantly in women due to various causes such as some chronic infection conditions and all. There are different types of anemias are there here we discuss mainly about Iron deficiency and sickle cell anemia.
This document discusses sideroblastic anemia, a type of anemia where the bone marrow produces abnormal red blood cells called ringed sideroblasts that cannot incorporate iron efficiently. Ringed sideroblasts have iron granules accumulated in mitochondria around the nucleus. Sideroblastic anemia can be hereditary or acquired through toxins, drugs, nutritional deficiencies, or other conditions. Symptoms include paleness, dizziness, fatigue, and organ enlargement. Diagnosis involves blood tests showing low hemoglobin and iron studies. Bone marrow biopsies reveal excess ringed sideroblasts. Treatment depends on the severity and cause but may include blood transfusions, iron chelation therapy, vitamins, or
This document summarizes key haematological changes during pregnancy. Physiological changes include anaemia due to plasma volume expansion, increased white blood cell counts dominated by neutrophils, and lower platelet counts. Common causes of anaemia are iron deficiency and folate deficiency. Thrombocytopenia is usually due to gestational thrombocytopenia, but may also result from preeclampsia or immune thrombocytopenic purpura. Pregnancy induces a hypercoagulable state through increased clotting factors and reduced inhibitors. Low molecular weight heparin is the anticoagulant of choice for treating thromboembolic disorders during pregnancy.
This document discusses anaemia in pregnancy, including its definition, causes, types, diagnosis, and management. It defines anaemia in pregnancy as a hemoglobin level below 11 g/dL in the first trimester and below 10.5 g/dL in the second and third trimesters. The most common cause is iron deficiency anaemia, which can be diagnosed based on microcytic, hypochromic blood and a low serum ferritin level below 15 ng/mL. Treatment involves oral iron supplementation, with increased doses for deficiency and continued supplementation postpartum. Parenteral iron or blood transfusion may be considered for non-response or severe cases. Regular screening and treatment of anaemia can help improve health outcomes for
1) Microcytic hypochromic anemia is characterized by small, pale red blood cells and can be caused by iron deficiency, thalassemia, sideroblastic anemia, or other conditions.
2) Iron deficiency anemia is the most common cause and results from inadequate iron intake or absorption. It disrupts hemoglobin synthesis and cellular proliferation.
3) Thalassemia is an inherited disorder of hemoglobin production that can range from mild to severe. Thalassemia major requires regular blood transfusions and causes severe anemia from ineffective erythropoiesis and hemolysis.
IDA is the most common form of anemia worldwide, affecting approximately 50% of anemia cases. It results from prolonged negative iron balance in the body due to factors like inadequate iron intake, decreased absorption, increased demand, or blood loss. Diagnosis involves a complete history, physical exam, and lab tests showing low indicators of iron stores like serum ferritin and iron, along with an elevated TIBC. Treatment aims to replenish iron stores and typically consists of oral iron supplementation of 200mg elemental iron per day for 3-6 months.
Iron deficiency anemia (IDA) is caused by not having enough iron available to make hemoglobin, limiting red blood cell and hemoglobin production and resulting in less oxygen delivery to tissues. IDA is common where meat intake is low and intestinal parasites are present. Symptoms include pallor, fatigue, and weakness. Studies in Saudi Arabia found IDA prevalence of 8.5-55.4% among children and 31.9-32% among pregnant women. Treatment involves iron supplementation and addressing underlying causes, while prevention focuses on iron-rich foods and supplements during pregnancy and breastfeeding.
Megaloblastic anemia is caused by a defect in DNA synthesis due to deficiencies in vitamin B12 or folate. It is characterized by abnormal bone marrow erythroblasts with delayed nuclear development. Causes include dietary deficiencies, malabsorption, increased cell turnover, and drugs. Treatment involves transfusion, vitamin B12 injections or oral folic acid supplementation depending on the underlying deficiency.
Biotine and folic acid role in pregnancystatushigh5
Biotin and folic acid play important roles in pregnancy by preventing birth defects when taken as supplements. Biotin is a B vitamin coenzyme involved in lipid metabolism, and biotin deficiency can cause fetal defects like cleft palate or abnormal limb growth. Studies show biotin supplements reduce biomarkers indicating deficiency. Folic acid also reduces neural tube defects when taken before and during early pregnancy. Both biotin and folic acid are involved in cell growth and development and prevent deficiencies that could harm fetal development.
1. Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common enzyme deficiency in humans, affecting over 200 million people worldwide.
2. G6PD deficiency results from mutations in the G6PD gene and causes decreased production of NADPH, leading to hemolytic anemia in response to oxidative stress.
3. Diagnosis is made through tests that measure G6PD enzyme activity levels in red blood cells, with deficiency diagnosed if levels are significantly decreased. Management focuses on avoiding triggers that cause hemolysis and blood transfusions in acute cases.
Ferrous ascorbate current clinical place in management of idaNARENDRA C MALHOTRA
Ferrous ascorbate is an effective oral iron supplement for treating iron deficiency anemia. It has a higher bioavailability than other iron preparations, with absorption rates as high as 67%. Ferrous ascorbate is stable in the gastrointestinal tract and does not dissociate. It prevents iron from oxidizing to the ferric state, allowing for greater absorption. Clinical studies show ferrous ascorbate effectively raises hemoglobin levels and is well tolerated with minimal side effects. Therefore, ferrous ascorbate plays an important role in managing iron deficiency anemia.
Iron deficiency anemia is a common type of microcytic anemia caused by low levels of iron available to produce hemoglobin. It affects people with high iron demands like pregnant women, young children, and menstruating women. Symptoms include fatigue, weakness, and shortness of breath. Treatment involves oral iron supplementation and dietary changes to restore iron stores. Prevention focuses on adequate iron intake through diet or supplements in at-risk groups.
Iron Chelation Therapy
Ashutosh Lal, MD.
January 18, 2014
Thalassemia Patient and Family Conference
Northern California Comprehensive Thalassemia Center
Children's Hospital Oakland
Megaloblastic Anaemia - Vit B12 deficiencyShahin Hameed
This document discusses megaloblastic anemia caused by vitamin B12 deficiency. It covers the normal metabolism and absorption of vitamin B12, the causes of deficiency including pernicious anemia, clinical features such as macrocytic anemia and neurological changes, diagnostic tests, and management with parenteral B12 injections. Deficiency results in defective DNA synthesis and affects all proliferating cells.
G6PD deficiency is a defect in the G6PD enzyme, which provides protection against oxidative stress in red blood cells. It is an X-linked inherited condition, though female heterozygotes have some protection against malaria. Those with G6PD deficiency experience hemolytic anemia during times of oxidative stress caused by factors like infections, medications, or foods like fava beans. The deficiency results in inadequate levels of NADPH and glutathione, leaving red blood cells vulnerable to damage and hemolysis. Symptoms of the acute hemolytic anemia appear 24-48 hours after exposure to the triggering agent. Laboratory tests show signs of hemolysis and low G6PD enzyme activity. There is no cure or treatment other than
- Iron is an essential trace element that is mainly present in blood, liver, bone marrow and muscles. It is required for hemoglobin, myoglobin and other protein synthesis.
- Iron deficiency anemia results from inadequate iron intake, absorption or increased losses and can be diagnosed based on low serum iron, ferritin and transferrin saturation along with microcytic hypochromic anemia.
- Treatment involves oral iron supplementation long-term or intravenous iron for severe cases. Blood transfusions are needed for acute blood loss.
Hemolytic anemias are a group of disorders characterized by premature destruction of red blood cells exceeding the bone marrow's ability to produce new cells. They can be classified as hereditary or acquired, and involve intracorpuscular or extracorpuscular hemolysis. Common causes include abnormalities of red blood cell enzymes or membrane, autoimmune reactions, infections, and extrinsic factors like hypersplenism. Clinical manifestations vary but often include anemia, jaundice, and splenomegaly. Laboratory findings provide evidence of increased red blood cell destruction and bone marrow compensation. Membrane disorders like hereditary spherocytosis and elliptocytosis are caused by genetic defects affecting membrane proteins.
This document provides information on G6PD deficiency and favism. It describes a case of a 3-year old boy presenting with pallor, red urine, and abdominal pain, which are signs of hemolytic anemia. It then discusses the characteristics of hemolytic anemia and explains that G6PD deficiency is a genetic disorder where individuals are at risk of hemolytic anemia when consuming fava beans or certain drugs due to inadequate NADPH production and antioxidant effects in red blood cells. The document concludes with treatment recommendations of blood transfusions and avoiding triggers like fava beans, certain medications, infections, and chemicals for people with G6PD deficiency.
This document provides definitions and information about anemia and iron deficiency anemia. It begins by defining anemia based on hemoglobin and hematocrit levels below certain thresholds. It then classifies anemias based on pathophysiology and morphology. Iron deficiency anemia is discussed in depth, including iron metabolism, sources of iron, clinical manifestations, investigations, and management with oral or parenteral iron supplementation or blood transfusions. Megaloblastic anemia is then introduced, focusing on vitamin B12 and folate, causes of B12 deficiency including pernicious anemia and effects of aging, and symptoms of B12 deficiency including neurological effects.
Iron deficiency anemia is the most common type of anemia globally. It results from inadequate iron intake or absorption to meet physiological needs. Common symptoms include pallor, weakness, and fatigue. Diagnosis involves blood tests showing microcytic hypochromic anemia, low serum iron and ferritin levels, and high total iron binding capacity. Treatment consists of oral iron supplementation in the form of ferrous salts to replenish iron stores.
Dr. S. Ismat Bukhari's document discusses G6PD deficiency, the most common enzyme deficiency worldwide. It affects over 200 million individuals, predominantly in areas like the Middle East, Africa, and Asia. G6PD deficiency is caused by mutations in the G6PD gene and results in inadequate protection of red blood cells from oxidative stress. This can lead to hemolysis, jaundice, and anemia, especially after exposure to oxidizing drugs or foods. The document outlines the inheritance, clinical manifestations, treatment, and screening of G6PD deficiency.
This document defines anemia as a deficiency in red blood cells or hemoglobin that reduces oxygen-carrying capacity in the blood. It notes normal red blood cell counts differ between males and females and lists several risk factors for anemia including poor diet, menstrual periods, pregnancy, and chronic illnesses. The document classifies anemias and discusses symptoms, diagnostic tests, and treatments which include iron supplements, vitamins, medications, and blood transfusions depending on the underlying cause of the anemia.
This document discusses anaemia in pregnancy, including its definition, causes, types, diagnosis, and management. It defines anaemia in pregnancy as a hemoglobin level below 11 g/dL in the first trimester and below 10.5 g/dL in the second and third trimesters. The most common cause is iron deficiency anaemia, which can be diagnosed based on microcytic, hypochromic blood and a low serum ferritin level below 15 ng/mL. Treatment involves oral iron supplementation, with increased doses for deficiency and continued supplementation postpartum. Parenteral iron or blood transfusion may be considered for non-response or severe cases. Regular screening and treatment of anaemia can help improve health outcomes for
1) Microcytic hypochromic anemia is characterized by small, pale red blood cells and can be caused by iron deficiency, thalassemia, sideroblastic anemia, or other conditions.
2) Iron deficiency anemia is the most common cause and results from inadequate iron intake or absorption. It disrupts hemoglobin synthesis and cellular proliferation.
3) Thalassemia is an inherited disorder of hemoglobin production that can range from mild to severe. Thalassemia major requires regular blood transfusions and causes severe anemia from ineffective erythropoiesis and hemolysis.
IDA is the most common form of anemia worldwide, affecting approximately 50% of anemia cases. It results from prolonged negative iron balance in the body due to factors like inadequate iron intake, decreased absorption, increased demand, or blood loss. Diagnosis involves a complete history, physical exam, and lab tests showing low indicators of iron stores like serum ferritin and iron, along with an elevated TIBC. Treatment aims to replenish iron stores and typically consists of oral iron supplementation of 200mg elemental iron per day for 3-6 months.
Iron deficiency anemia (IDA) is caused by not having enough iron available to make hemoglobin, limiting red blood cell and hemoglobin production and resulting in less oxygen delivery to tissues. IDA is common where meat intake is low and intestinal parasites are present. Symptoms include pallor, fatigue, and weakness. Studies in Saudi Arabia found IDA prevalence of 8.5-55.4% among children and 31.9-32% among pregnant women. Treatment involves iron supplementation and addressing underlying causes, while prevention focuses on iron-rich foods and supplements during pregnancy and breastfeeding.
Megaloblastic anemia is caused by a defect in DNA synthesis due to deficiencies in vitamin B12 or folate. It is characterized by abnormal bone marrow erythroblasts with delayed nuclear development. Causes include dietary deficiencies, malabsorption, increased cell turnover, and drugs. Treatment involves transfusion, vitamin B12 injections or oral folic acid supplementation depending on the underlying deficiency.
Biotine and folic acid role in pregnancystatushigh5
Biotin and folic acid play important roles in pregnancy by preventing birth defects when taken as supplements. Biotin is a B vitamin coenzyme involved in lipid metabolism, and biotin deficiency can cause fetal defects like cleft palate or abnormal limb growth. Studies show biotin supplements reduce biomarkers indicating deficiency. Folic acid also reduces neural tube defects when taken before and during early pregnancy. Both biotin and folic acid are involved in cell growth and development and prevent deficiencies that could harm fetal development.
1. Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common enzyme deficiency in humans, affecting over 200 million people worldwide.
2. G6PD deficiency results from mutations in the G6PD gene and causes decreased production of NADPH, leading to hemolytic anemia in response to oxidative stress.
3. Diagnosis is made through tests that measure G6PD enzyme activity levels in red blood cells, with deficiency diagnosed if levels are significantly decreased. Management focuses on avoiding triggers that cause hemolysis and blood transfusions in acute cases.
Ferrous ascorbate current clinical place in management of idaNARENDRA C MALHOTRA
Ferrous ascorbate is an effective oral iron supplement for treating iron deficiency anemia. It has a higher bioavailability than other iron preparations, with absorption rates as high as 67%. Ferrous ascorbate is stable in the gastrointestinal tract and does not dissociate. It prevents iron from oxidizing to the ferric state, allowing for greater absorption. Clinical studies show ferrous ascorbate effectively raises hemoglobin levels and is well tolerated with minimal side effects. Therefore, ferrous ascorbate plays an important role in managing iron deficiency anemia.
Iron deficiency anemia is a common type of microcytic anemia caused by low levels of iron available to produce hemoglobin. It affects people with high iron demands like pregnant women, young children, and menstruating women. Symptoms include fatigue, weakness, and shortness of breath. Treatment involves oral iron supplementation and dietary changes to restore iron stores. Prevention focuses on adequate iron intake through diet or supplements in at-risk groups.
Iron Chelation Therapy
Ashutosh Lal, MD.
January 18, 2014
Thalassemia Patient and Family Conference
Northern California Comprehensive Thalassemia Center
Children's Hospital Oakland
Megaloblastic Anaemia - Vit B12 deficiencyShahin Hameed
This document discusses megaloblastic anemia caused by vitamin B12 deficiency. It covers the normal metabolism and absorption of vitamin B12, the causes of deficiency including pernicious anemia, clinical features such as macrocytic anemia and neurological changes, diagnostic tests, and management with parenteral B12 injections. Deficiency results in defective DNA synthesis and affects all proliferating cells.
G6PD deficiency is a defect in the G6PD enzyme, which provides protection against oxidative stress in red blood cells. It is an X-linked inherited condition, though female heterozygotes have some protection against malaria. Those with G6PD deficiency experience hemolytic anemia during times of oxidative stress caused by factors like infections, medications, or foods like fava beans. The deficiency results in inadequate levels of NADPH and glutathione, leaving red blood cells vulnerable to damage and hemolysis. Symptoms of the acute hemolytic anemia appear 24-48 hours after exposure to the triggering agent. Laboratory tests show signs of hemolysis and low G6PD enzyme activity. There is no cure or treatment other than
- Iron is an essential trace element that is mainly present in blood, liver, bone marrow and muscles. It is required for hemoglobin, myoglobin and other protein synthesis.
- Iron deficiency anemia results from inadequate iron intake, absorption or increased losses and can be diagnosed based on low serum iron, ferritin and transferrin saturation along with microcytic hypochromic anemia.
- Treatment involves oral iron supplementation long-term or intravenous iron for severe cases. Blood transfusions are needed for acute blood loss.
Hemolytic anemias are a group of disorders characterized by premature destruction of red blood cells exceeding the bone marrow's ability to produce new cells. They can be classified as hereditary or acquired, and involve intracorpuscular or extracorpuscular hemolysis. Common causes include abnormalities of red blood cell enzymes or membrane, autoimmune reactions, infections, and extrinsic factors like hypersplenism. Clinical manifestations vary but often include anemia, jaundice, and splenomegaly. Laboratory findings provide evidence of increased red blood cell destruction and bone marrow compensation. Membrane disorders like hereditary spherocytosis and elliptocytosis are caused by genetic defects affecting membrane proteins.
This document provides information on G6PD deficiency and favism. It describes a case of a 3-year old boy presenting with pallor, red urine, and abdominal pain, which are signs of hemolytic anemia. It then discusses the characteristics of hemolytic anemia and explains that G6PD deficiency is a genetic disorder where individuals are at risk of hemolytic anemia when consuming fava beans or certain drugs due to inadequate NADPH production and antioxidant effects in red blood cells. The document concludes with treatment recommendations of blood transfusions and avoiding triggers like fava beans, certain medications, infections, and chemicals for people with G6PD deficiency.
This document provides definitions and information about anemia and iron deficiency anemia. It begins by defining anemia based on hemoglobin and hematocrit levels below certain thresholds. It then classifies anemias based on pathophysiology and morphology. Iron deficiency anemia is discussed in depth, including iron metabolism, sources of iron, clinical manifestations, investigations, and management with oral or parenteral iron supplementation or blood transfusions. Megaloblastic anemia is then introduced, focusing on vitamin B12 and folate, causes of B12 deficiency including pernicious anemia and effects of aging, and symptoms of B12 deficiency including neurological effects.
Iron deficiency anemia is the most common type of anemia globally. It results from inadequate iron intake or absorption to meet physiological needs. Common symptoms include pallor, weakness, and fatigue. Diagnosis involves blood tests showing microcytic hypochromic anemia, low serum iron and ferritin levels, and high total iron binding capacity. Treatment consists of oral iron supplementation in the form of ferrous salts to replenish iron stores.
Dr. S. Ismat Bukhari's document discusses G6PD deficiency, the most common enzyme deficiency worldwide. It affects over 200 million individuals, predominantly in areas like the Middle East, Africa, and Asia. G6PD deficiency is caused by mutations in the G6PD gene and results in inadequate protection of red blood cells from oxidative stress. This can lead to hemolysis, jaundice, and anemia, especially after exposure to oxidizing drugs or foods. The document outlines the inheritance, clinical manifestations, treatment, and screening of G6PD deficiency.
This document defines anemia as a deficiency in red blood cells or hemoglobin that reduces oxygen-carrying capacity in the blood. It notes normal red blood cell counts differ between males and females and lists several risk factors for anemia including poor diet, menstrual periods, pregnancy, and chronic illnesses. The document classifies anemias and discusses symptoms, diagnostic tests, and treatments which include iron supplements, vitamins, medications, and blood transfusions depending on the underlying cause of the anemia.
This document discusses hematological disorders in pregnancy, focusing on anemia. It notes that anemia is the most common hematological disorder seen in pregnancy. The majority of cases are due to iron, folate or vitamin B12 deficiency, though other conditions like thalassemia can also cause anemia. Anemia is a major public health concern in developing countries, where incidence ranges from 40-80% compared to developed countries. Treatment involves oral iron supplementation, with intravenous iron used for severe or late-presenting cases. Untreated anemia can increase risks for the mother and baby.
This document provides information on iron deficiency anemia (IDA), including its global burden, pathophysiology, causes, clinical features, investigations, and management. Some key points:
- IDA is the most common cause of anemia globally, with over 50% of anemias due to iron deficiency. It accounts for 8.4 lakh deaths annually, most in Africa and Asia.
- IDA occurs when iron stores are decreased and total body iron is reduced. It develops in stages from initial iron deficiency without anemia to latent IDA to overt IDA.
- Causes of IDA include blood loss, inadequate dietary iron intake, malabsorption, increased demands in pregnancy/growth. Daily iron requirements vary from
The document discusses iron deficiency anemia (IDA), including its definition, causes, signs and symptoms, classifications, treatment, nursing care, and complications. IDA is defined as anemia with biochemical evidence of iron deficiency, characterized by a low hemoglobin level and caused by blood loss, insufficient dietary iron intake, or impaired iron absorption. Common causes include heavy menstruation, ulcers, cancers, and dietary deficiencies. Treatment involves iron supplementation, vitamins, blood transfusions, and addressing the underlying cause. Nursing care focuses on managing fatigue, nutritional intake, and complications which can impact multiple organs if left untreated.
The document discusses different types of anemia including iron deficiency, vitamin B12 and folate deficiency, chronic disease, and hemolytic anemias. It provides definitions, causes, signs and symptoms, diagnostic evaluations, and medical and nursing management approaches for various forms of anemia. The nursing management focuses on assessing and addressing fatigue, maintaining adequate nutrition and tissue perfusion, and monitoring for complications related to anemia.
Iron-deficiency anemia is a common form of anemia caused by insufficient dietary iron intake and absorption or iron loss from bleeding. It affects about half of all anemia cases worldwide and women more often than men, with over one billion people affected globally. Causes include a lack of iron in the diet, inability to absorb iron, insufficient red blood cell production, and bleeding from various sources like parasites, ulcers, cancers, or hemolytic conditions. Symptoms are non-specific but may include pallor, fatigue, weakness, and breathlessness. Treatment involves dietary changes to increase iron intake or iron supplements, while intravenous iron is used when oral intake is not possible or effective.
This document discusses the approach to diagnosing and classifying anemia. It defines anemia and notes that normal hemoglobin levels vary by age, gender, and race. A thorough history and physical exam can reveal potential causes like diet, blood loss, infections, or medications. Laboratory tests including a CBC, smear, and reticulocyte count help classify anemias as microcytic, normocytic, or macrocytic based on red blood cell size. Iron deficiency is a common cause of anemia in children. Hemolytic disorders cause shortened red blood cell survival.
Anemia - Types, Pathophysiology, Clinical Manifestations, Etiology, TreatmentMd Altamash Ahmad
Anaemia can be defined as a reduction from normal of the quantity of haemoglobin in the blood.
It is not one disease, but a condition that results from a number of different pathologies.
The World Health Organisation defines anaemia in adults as haemoglobin levels less than 13g/dL for males and less than 12g/dL for females.
The low haemoglobin level results in a corresponding decrease in the oxygen-carrying capacity of the blood.
Anaemia is possibly one of the most common conditions in the world and results in significant morbidity and mortality, particularly in the developing world.
Anemia occurs when there are not enough healthy red blood cells to carry oxygen to the body's organs. The most common type is iron-deficiency anemia, which can be caused by blood loss or not getting enough iron in the diet. Anemia is diagnosed through a blood test called a complete blood count. Treatment depends on the underlying cause but may include iron supplements, changing diet, or blood transfusions. Maintaining a healthy diet with iron and vitamins can help prevent some forms of anemia.
Anemia occurs when there are not enough healthy red blood cells to carry oxygen to the body's organs. The most common type is iron-deficiency anemia, which can be caused by blood loss or not getting enough iron in the diet. Anemia is diagnosed through a blood test called a complete blood count. Treatment depends on the underlying cause but may include iron supplements, changing diet, or blood transfusions. Maintaining a healthy diet with iron and vitamins can help prevent some forms of anemia.
1. Hematologic disorders are those that produce quantitative or qualitative defects in blood cells or elements related to hemostasis.
2. Hematopoiesis begins in the yolk sac and liver in early gestation, then shifts to the bone marrow by mid-gestation, where it remains the primary site of blood cell production after birth.
3. Anemia is defined as a hemoglobin level below the reference level for age and sex, and can be caused by decreased production, increased destruction, or blood loss.
Iron deficiency anemia is a common global health problem affecting 30% of the population. It causes decreased work productivity and increases maternal, child, and infant mortality. Good dietary sources of iron include liver, oats, legumes, and cashew nuts. Iron deficiency can be treated with oral iron supplements taken for 8 weeks, while severe cases may require intravenous iron or blood transfusions. Prevention strategies include iron fortification of infant formula and treating iron deficiency in at-risk groups like adolescent females.
This document discusses anaemia, including its definition, causes, symptoms, classifications, and treatment. Anaemia is a blood disorder where there are low red blood cell counts or haemoglobin levels. It can be caused by blood loss, insufficient red blood cell production, or increased red blood cell destruction. Common types include iron deficiency, vitamin B12/folate deficiency, and chronic disease-related anaemia. Symptoms vary based on severity but can include fatigue, weakness, and shortness of breath. Treatment involves addressing the underlying cause, such as taking iron or B12 supplements. Anaemia is a widespread problem globally and in India, where nearly 50% of pregnant women are estimated to be anaemic.
Thalassemia Unveiled: Insights into Diagnosis, Treatment, and Care.pptxNoorulainMehmood1
Thalassemia, a group of inherited blood disorders, presents a complex interplay of genetic mutations and clinical manifestations. This presentation delves into the intricacies of thalassemia, exploring its genetic underpinnings, clinical spectrum, diagnostic modalities, and therapeutic approaches. Through comprehensive analysis and case studies, attendees will gain a deeper understanding of thalassemia's impact on patients' lives and the latest advancements in management strategies.
Keywords:
Thalassemia
Genetic Disorders
Hemoglobinopathies
Blood Disorders
Anemia
Genetic Mutations
Clinical Spectrum
Diagnosis
Treatment Modalities
Transfusion Therapy
Iron Chelation Therapy
Genetic Counseling
Patient Care
Hematological Disorders
Research Advancements
This document discusses anemia in pregnancy. It defines anemia as having insufficient red blood cells or hemoglobin. Anemia is common in pregnancy, affecting 18-75% of pregnant women globally. Anemia is classified as mild, moderate or severe based on hemoglobin levels. Common causes of anemia in pregnancy include iron deficiency, folic acid deficiency, vitamin B12 deficiency, and genetic disorders like sickle cell anemia. Left untreated, anemia can negatively impact both mother and baby by increasing risks of infection, hemorrhage, low birth weight, and other complications. Routine screening and treatment with iron, folic acid and other supplements can help prevent and manage anemia during pregnancy.
This document discusses anemia in pregnancy. It defines anemia as having insufficient red blood cells or hemoglobin. Anemia is common in pregnancy, affecting 18-75% of pregnant women globally. Anemia is classified as mild, moderate or severe based on hemoglobin levels. Common causes of anemia in pregnancy include iron deficiency, folic acid deficiency, vitamin B12 deficiency, and genetic disorders like sickle cell anemia. Left untreated, anemia can negatively impact both mother and baby by increasing risks of infection, hemorrhage, low birth weight, and other complications. Routine screening and treatment with iron, folic acid and other supplements can help prevent and manage anemia during pregnancy.
Anemia should not be accepted as an inevitable consequence of aging. A cause is found in approximately 80 percent of elderly patients. The most common causes of anemia in the elderly are chronic disease and iron deficiency. Vitamin B12 deficiency, folate deficiency, gastrointestinal bleeding and myelodysplastic syndrome are among other causes of anemia in the elderly. Serum ferritin is the most useful test to differentiate iron deficiency anemia from anemia of chronic disease. Not all cases of vitamin B12 deficiency can be identified by low serum levels. The serum methylmalonic acid level may be useful for diagnosis of vitamin B12 deficiency. Vitamin B12 deficiency is effectively treated with oral vitamin B12 supplementation. Folate deficiency is treated with 1 mg of folic acid daily.
Clinical Presentation
Even though the high prevalence of anemia in the elderly makes it a condition that clinicians might expect to find frequently, several features of anemia make it easy to overlook. The onset of symptoms and signs is usually insidious, and many elderly patients adjust their activities as their bodies make physiologic adaptations for the condition. Typical symptoms of anemia, such as fatigue, weakness and dyspnea, are not specific and in elderly patients tend to be attributed to advancing age. Pallor can be a helpful diagnostic clue, but pallor can be hard to detect in the elderly. Conjunctival pallor is a reliable sign, and its presence should prompt the clinician to order blood tests for anemia.6
Aside from conjunctival pallor, few other signs are attributable specifically to anemia. Frequently, patients have signs of a disorder that is made worse by the anemia, such as worsening congestive heart failure, cognitive impairment, dizziness and apathy. Unless clinicians consider anemia as a possibility in the elderly, it can be easily overlooked. Anemia in older persons poses a clinical challenge in daily practice as the population ages. In many cases, 1 or more etiologies are detected, and a thorough investigation immediately leads to the correct diagnosis. In these patients, management is largely dependent on the underlying etiology, and in many cases, anemia can be corrected by interventional therapy independent of age. Good examples are iron, vitamin B12, or folate deficiency. EPO deficiency with or without overt exocrine kidney insufficiency can be detected quite often in older persons. A large number of patients turn out to have an underlying (chronic) inflammatory disease. The concept of a subclinical proinflammatory state called inflammaging may be a good explanation for the development of anemia in senior persons. In other cases, a clonal myeloid or other neoplasm is detected. In a relevant proportion of patients, no underlying cause of anemia is found after a first examination, resulting in the provisional diagnosis of UA. However, in many cases no underlying etiology is found even after a thorough diagnostic workup that includes an ex…
Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
Does Over-Masturbation Contribute to Chronic Prostatitis.pptxwalterHu5
In some case, your chronic prostatitis may be related to over-masturbation. Generally, natural medicine Diuretic and Anti-inflammatory Pill can help mee get a cure.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...Donc Test
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by Stamler, Verified Chapters 1 - 33, Complete Newest Version Community Health Nursing A Canadian Perspective, 5th Edition by Stamler, Verified Chapters 1 - 33, Complete Newest Version Community Health Nursing A Canadian Perspective, 5th Edition by Stamler Community Health Nursing A Canadian Perspective, 5th Edition TEST BANK by Stamler Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Pdf Chapters Download Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Pdf Download Stuvia Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Study Guide Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Ebook Download Stuvia Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Questions and Answers Quizlet Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Studocu Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Quizlet Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Pdf Chapters Download Community Health Nursing A Canadian Perspective, 5th Edition Pdf Download Course Hero Community Health Nursing A Canadian Perspective, 5th Edition Answers Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Ebook Download Course hero Community Health Nursing A Canadian Perspective, 5th Edition Questions and Answers Community Health Nursing A Canadian Perspective, 5th Edition Studocu Community Health Nursing A Canadian Perspective, 5th Edition Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Pdf Chapters Download Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Pdf Download Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Study Guide Questions and Answers Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Ebook Download Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Questions Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Studocu Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Stuvia
Promoting Wellbeing - Applied Social Psychology - Psychology SuperNotesPsychoTech Services
A proprietary approach developed by bringing together the best of learning theories from Psychology, design principles from the world of visualization, and pedagogical methods from over a decade of training experience, that enables you to: Learn better, faster!
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
2. • The World Health Organization defines Anemia as:[1]
• Hb <11 g/dL in children under 5 years and in pregnant women
• Hb <11.5 g/dL in children aged 5 to 11 years
• Hb <12 g/dL in children aged 12 to 14 years and in women (aged over 15 years)
• Hb <13 g/dL in men (aged over 15 years)
• HB <12 g/dL in women.
3. • The American Society of Hematology defined anemia as Hb<13.6 g/dl for men and <12g/dl
for women.
• Anemia is the most common hematological disorder seen in general medical practice.
• Risk factors include extremes of age, female sex, lactation, and pregnancy.
• severity scale for Anemia :-
• Life-threatening Anemia: Hb <65 g/L (<6.5 g/dL)
• Severe Anemia: Hb <80 g/L (<8 g/dL)
• Mild to moderate Anemia: Hb 80 to 110 g/L (8-11.0 g/dL)
4.
5. • MCV – Mean corpuscular volume (MCV) is the average volume (size) of the RBCs.
• (MCV in femtoliters [fL] = 10 x HCT [in percent] ÷ RBC [in millions/microL])
• MCH – Mean corpuscular hemoglobin (MCH) is the average hemoglobin content in a RBC.
• (MCH in picograms [pg]/cell = hemoglobin [in g/dL] x 10 ÷ RBC [in millions/microL])
• MCHC – Mean corpuscular hemoglobin concentration (MCHC) is the average hemoglobin
concentration per RBC.
• (MCHC in grams [g]/dL = hemoglobin [in g/dL] x 100 ÷ HCT [in percent]).
• RDW – Red cell distribution width (RDW) is a measure of the variation in RBC size RDW =
[standard deviation/MCV] x 100).
7. General clinical information
• Family history of a specific type of anemia such as sickle cell disease or thalassemia
• Causes of acquired anemia
• Dietary practices (eg, vegan diet lacks vitamin B12)
• Travel (eg, acquired parasitic infections)
• Infections
• Bleeding (heavy menses, melena)
• Chronicity of the anemia
• Symptoms or conditions that would suggest hemolysis
• Dark urine
• Jaundice
• History of gallstones
• Anemia with certain food or drug exposures (fava beans, oxidant drugs)
• Symptoms or findings that suggest kidney or liver disease or hypersplenism
10. Iron deficiency
• Iron deficiency and iron deficiency anemia (IDA) may be seen in individuals of any age but
are especially common in children and menstruating females.
• Iron deficiency is more frequently due to blood loss that exceeds iron intake.
• In females with heavy menstrual periods or pregnancy, the cause is obvious. In others, the
source of blood loss may not be immediately apparent.
• A search for the source of blood loss is almost always indicated, especially in individuals over
50 years of age with new onset iron deficiency, for whom colorectal cancer is not an
uncommon underlying cause of blood loss. Another cause is reduced iron absorption as in H.
Pylori and celiac disease.
11. Epidemiology
• The global prevalence of Anemia is reported to be approximately 33%, and iron deficiency is
the most common cause.
• The prevalence of IDA varies widely across different regions of the world, with the lowest
prevalence in higher income regions (e.g., North America and western Europe) and highest
prevalence in lower income regions (e.g., southern Asia and Caribbean).
12. Aetiology
• IDA has many causes and is not an end diagnosis in and of itself.
• Diagnosis of IDA should prompt further investigation to determine the cause, and to correct if possible.
• inadequate dietary iron intake
• Impaired iron absorption (e.g., due to achlorhydria, gastric surgery, or coeliac disease)
• Increased iron loss because of bleeding, usually in the gastrointestinal tract (e.g. haemorrhoids, salicylate
ingestion, peptic ulcer disease, hiatal hernia, diverticulosis, neoplasm, ulcerative colitis, hookworm, milk
allergy in infants, Meckel's diverticulum).
• Other causes of iron loss include menorrhagia, blood loss from hemodialysis, runner's Anemia,
schistosomiasis, trichuriasis, blood donation, hemoglobinuria, self-induced bleeding, idiopathic pulmonary
hemosiderosis, Goodpasture's syndrome, hereditary hemorrhagic telangiectasia, angiodysplasia, and
disorders of haemostasias
• Increased iron requirements of young children (e.g., due to growth, and inadequate dietary iron intake),
pregnancy, or lactation PPIs
• Unknown cause.
13. Pathophysiology
• Iron is required for the formation of hemoglobin, myoglobin, and haem enzymes
• essential for red blood cell (RBC) production and cellular processes (e.g., cell metabolism,
DNA replication/repair, and cell cycle regulation)
• The body does not have a regulatory pathway for iron excretion. Physiological iron loss
occurs through menstrual bleeding, sweating, skin desquamation, and urinary/faecal
excretion.
• Men and post-menopausal women lose approximately 1 mg of iron daily, and menstruating
women lose approximately 2 mg of iron daily.
• Pregnancy results in a net loss of approximately 580 mg of iron during the gestation period
due to expansion of maternal RBC mass and growth of the fetus and placenta, with the
highest loss occurring in the third trimeste
14. History and exam
• Fatigue does not appear to be increased in patients with mild-to-moderate anemia
(hemoglobin from 8 to 12 g/dL) and treatment of this range of anemia does not necessarily
lead to improvements in fatigue.
• Dyspnoea
• Pica in up to 55%
• Restless legs syndrome
• Headache
• Exercise intolerance
• Exertional dyspnea
• Weakness
15. Findings on examination
• Esophageal web, which may be accompanied by dysphagia (eg, Plummer-Vinson or
Patterson-Kelly syndrome; rare)
• Alopecia (rare) in especially severe cases
• Chlorosis pale, faintly green complexion; extremely rare)
• Patients with more severe anemia may have tachycardia, a cardiac murmur, or (rarely)
hemodynamic instability
16. Iron studies
• Serum iron the test measures circulating iron, most of which is bound to the transport protein
transferrin
• Serum transferrin Transferrin is a circulating transport protein for iron
• Transferrin saturation ransferrin saturation (TSAT) is the ratio of serum iron to TIBC: (serum
iron ÷ TIBC x 100)
• Serum ferritin is a circulating iron storage protein that is increased in proportion to body iron
stores.
17.
18.
19. screnning
• The CDC recommends periodic screening for Anemia with haemoglobin checks among high-risk populations of infants, preschool
children, pregnant women, and women of childbearing age.
• The American Academy of Family Physicians (AAFP) concludes that there is insufficient evidence to recommend routine
screening for IDA in pregnant women and in children aged 6 to 24 months.
• Start with a CBC including review of MCV. Obtain iron studies only if anemia or microcytosis is found. This may be most
reasonable for individuals with a lower risk of iron deficiency and those for whom returning for a second test would not be
overly burdensome.
• The frequency of screening is individualized:
• Annual screening may be reasonable for those at the highest risk, such as menstruating females with heavy periods.
• Less frequent, or even one-time screening, may be reasonable for other individuals, especially males and postmenopausal
females.
• Screening of adolescent and adult females of childbearing age every 5 years with a hemoglobin or hematocrit, with more
frequent screening (yearly) if there is extensive menstrual blood loss, low iron intake, or a history of iron deficiency
20. INITIAL CONSIDERATIONS
• all patients with iron deficiency anemia and most with iron deficiency without anemia should
be treated
• Routine iron administration to individuals without iron deficiency is not advised.
• Treatment of iron deficiency and iron deficiency anemia involves more than simply replacing
iron
21.
22. Oral versus IV iron
• Settings in which one route or the other may be preferable include the following:
• ●Oral
• Oral supplements are the only form of iron available to many patients
• For many patients, oral iron may be more cost effective due to the lack of need for monitored infusion.
• Use of oral iron avoids the need for IV access and monitored infusion.
• Use of oral iron eliminates the potential for infusion reactions and/or anaphylaxis.
• Oral supplements are generally used for infants, children, and adolescents.
• ●IV
• IV iron is appropriate for patients who are unable to tolerate gastrointestinal side effects of oral iron.
• individuals with abnormal uterine bleeding in which oral iron cannot keep up with losses, individuals who are pregnant in the second or third
trimester.
• IV iron may be needed for those with severe/ongoing blood loss .
• Gastric surgery (bypass, resection) that reduces gastric acid may severely impair intestinal absorption of oral iron.
• Inflammatory bowel disease.
• Malabsorption syndromes (celiac disease, Whipple's disease, bacterial overgrowth) may limit absorption of oral iron.
• In the second trimester of pregnancy, if the Hb is less than 10.5 g/dL, or at any time in the third trimester, at which oral iron is unlikely to supply
adequate iron to the developing fetus
23. Change from oral to IV
• Patients not responding to oral iron or who are intolerant of oral iron can be considered for
intravenous iron replacement.
• if haemoglobin response with oral iron is (<1.0 g/dL) at day 14
• Intravenous iron should be considered as a first-line treatment for selected patients with
inflammatory bowel disease, including those with active disease or previous intolerance of oral
iron.
• Intravenous iron may be considered before or after surgery for patients with IDA who: are unable
to tolerate, absorb, or adhere to oral iron
• Intravenous iron increases the response to erythropoiesis stimulating agents in patients with
cancer and chemotherapy-related Anemia
• In women with postnatal Anemia, use of ferric carboxymaltose may restore haemoglobin and
ferritin levels faster than other intravenous iron preparations
24. Oral
• ferrous sulfate (20 to 30% elemental iron per mg ferrous sulfate salt but can vary by
manufacturer): adults: 50-100 mg orally three times daily
• ferrous fumarate (33% elemental iron per mg ferrous fumarate salt ): adults: 50-100 mg orally
three times daily
• ferrous gluconate (approximately 10 to 14% elemental iron per mg ferrous gluconate salt)
: adults: 50-100 mg orally three times daily
• ferric maltol: adults: 30 mg orally twice daily
25. IV
• Iron dextran is only available as a low-molecular-weight preparation. dverse effects include
anaphylaxis, arthralgias, and myalgias.
• Iron sucrose has a similar safety profile to low-molecular-weight iron dextran
• Sodium ferric gluconate complex has a superior safety profile compared with iron dextran
• Ferric carboxymaltose has superior safety and efficacy compared with oral iron
• Ferumoxytol has a more convenient dosing schedule than iron dextran and iron sucrose s
safe to use in patients with chronic kidney disease, but if haemodialysis is required, it should
be given >1 hour after haemodialysis when blood pressure has stabilized
• Ferric derisomaltose can also be given as a single infusion; therefore, dosing is more
convenient than other preparations. It has superior efficacy and is faster acting than iron
sucrose
26. Side effects (oral iron)
• These include metallic taste , nausea, flatulence, constipation, diarrhea, epigastric distress,
and/or vomiting.
• Patients may also be bothered by itching and by black/green or tarry stools that stain
clothing or cause anxiety about bleeding.
• As a result, compliance with oral iron administration may be low.
27. Monitoring
• The British Society of Gastroenterology recommends regular laboratory follow-up after
replacement of iron.
• Haemoglobin concentration and red cell indices should be measured every 3 months for a year,
again after one further year, and thereafter when symptomatic.
• This depends upon the underlying cause of the IDA. Uncomplicated IDA secondary to multiple
pregnancies has a very good prognosis with relatively simple treatment.
• However, if the IDA is secondary to a gastrointestinal cancer, prognosis is dependent upon tumor
staging.
• Once the haemoglobin is corrected, it takes an additional 6 months or so of iron replacement
therapy to replenish iron stores.
For patients receiving oral iron, we often re-evaluate the patient two weeks after starting.
we generally see patients four to eight weeks after the iron has been administered.
29. Aetiology
• is principally caused by inflammation.
• Various processes (e.g., infection, neoplasm, autoimmune reactions, and injury to tissue from
trauma and major surgery) trigger release of pro-inflammatory cytokines.
• Systemic changes in iron metabolism, regulated by the inflammatory cytokine cascade and
hepcidin (an iron-regulatory peptide hormone produced by the liver), decrease red blood cell
(RBC) production and reduce RBC survival
• A range of underlying conditions can result in release of pro-inflammatory cytokines, often
with activation of the reticuloendothelial system.These cytokines trigger changes in
intracellular iron metabolism (notably up-regulation of hepcidin synthesis and ferritin
transcription).
• Interleukin (IL)-6 and IL-1 play a role in some inflammatory states and they have been shown
to directly up-regulate hepcidin synthesis
30. • Hepcidin and erythroferrone are the major regulators of iron metabolism.
• Hepcidin negatively regulates free iron by increased expression of divalent metal transporter
1 and down-regulation of ferroportin.
• Hepcidin also causes iron-trapping in macrophages, decreased iron absorption in the
gastrointestinal tract, splenic sequestration of iron, and impaired bone marrow
responsiveness to erythropoietin. Erythroferrone, a protein hormone produced by erythroid
progenitor cells in response to erythropoietin, makes iron available for erythropoiesis by
inhibiting the production of hepcidin.
32. Symptoms and signs
• Pallor, fatigue, weakness, decreased exercise tolerance, and shortness of breath with
exercise are non-specific symptoms of Anemia.
• There may be a history of an underlying autoimmune, malignant, or infectious disorder;
recent major surgery, major trauma, or a critical illness; or of chronic kidney disease,
congestive heart failure, or chronic pulmonary disease
• fever, anorexia, night sweats, arthralgia, myalgia, weight loss, the presence of a mass,
adenopathy, hepatomegaly, splenomegaly, decreased breath sounds with rales, stiff neck,
rash, abdominal tenderness, and tenderness of joints, shoulder girdle, or bones.
33. investigations
• Full blood count, peripheral blood smear, reticulocyte count, serum iron and ferritin, total iron-
binding capacity (TIBC), transferrin saturation, and creatinine are part of the initial workup.
• The ACD syndrome is defined by the following constellation of laboratory test results:
• Mild to moderate Anemia that is either normocytic normochromic or microcytic hypochromic
• Otherwise normal red blood cell (RBC) morphology
• Normal or elevated serum ferritin
• Transferrin saturation <15%.
34. • ACD/AI is most likely when all (or most) of the following are present :
• Normochromic, normocytic anemia (HB between 10 and 12 g/dL)
• Low reticulocyte count (or inappropriately low for the degree of anemia)
• Low serum iron (generally <60 mcg/dL)
• Normal to low serum transferrin (generally <300 mcg/dL)
• Low transferrin saturation (TSAT; generally <20 percent)
• Normal to increased serum ferritin (>100 mcg/L)
• Elevated CRP (generally >5 mg/L)
• ESR
35. Management
• Initial treatment in patients with mild to moderate Anemia (Hb [8 to 11 g/dL])
• if the underlying disorder can be ameliorated or cured, the Anemia usually improves or
dissipates.
• Patients with mild to moderate ACD can usually be managed with simple observation.
• Treatment of Anemia in cancer and chronic renal disease do not recommend routine, ongoing
RBC transfusion principally because of the risks of iron overload
36. • Iron deficiency should be ruled out prior to initiating therapy. Because ESAs often produce
functional iron deficiency in iron-replete subjects, supplementary iron therapy may be
required to achieve an adequate therapeutic response
• a ferritin <100 mcg/L and a transferrin saturation (TSAT) <20 percent are typical indicators of
iron deficiency in individuals with ACD/AI
• People without iron deficiency – We generally do not give iron to individuals with ACD/AI
who are iron replete.
37. erythropoiesis-stimulating agents (ESAs)
• do not use ESAs in individuals with ACD/AI, with the following exceptions in which an ESA
may be appropriate:
• Individuals with CKD who may have a deficiency of erythropoietin
• Selected individuals with cancer who are receiving chemotherapy.
• Selected patients with low-risk myelodysplastic syndromes
• Certain individuals with inflammatory bowel disease or rheumatologic disorders who do not
have an adequate improvement in hemoglobin with iron supplementation
• Selected individuals scheduled for elective surgery
• are strongly recommended for Anemia in CKD due to low erythropoietin
• Red blood cell transfusion may be required until benefits from ESA therapy become manifest
38. severe (Hb [<8 g/dL]) OR life-threatening (Hb [<6.5 g/dL])
• RBC transfusion
• treatment should begin with the number of RBC units needed to raise Hb to 90 to 100 g/L
39. Emerging therapies
• epcidin and ferroportin – Studies are underway using agents capable of altering/inhibiting
the function of hepcidin (eg, hepcidin antagonists) and increasing the iron export activity of
the hepcidin receptor (ferroportin) to alleviate the various disorders of iron metabolism
associated with increased levels of hepcidin, including ACD/.However, this approach has yet
to demonstrate conclusive efficacy in clinical trials.
• Prolyl hydroxylase inhibitors – Prolyl hydroxylase inhibitors (PHI) stabilize hypoxia-inducible
factor (HIF), promote production of endogenous EPO, and increase intestinal iron absorption.
Their efficacy has been explored especially in anemia associated with CKD. Positive results
have been demonstrated in randomized trials in individuals undergoing dialysis or those with
predialysis CKD [128,129]. Treatment with these compounds for anemia of CKD is approved in
China, Japan, and Europe but not in United States. Their role in ACD/AI has yet to be
demonstrated [130].
40.
41. Beta-thalassaemia
• The underlying pathophysiology of beta-thalassaemia syndromes is ineffective
erythropoiesis.
• When the production of beta-globin chains is deficient or absent, the imbalance between
alpha and beta chains leads to precipitation of the excess alpha chains in erythroid
precursors and maturing red cells, resulting in membrane damage and cell destruction.
• The inability of these cells to survive is the cause of ineffective erythropoiesis, resulting in
Anemia and a compensatory erythroid hyperplasia.
42. Bone marrow features of iron deficncy anemia
• Cellularity – increased
• Erythroid hyperplasia
• Micronormoblastic reaction
• Normoblast are smaller
• Late micronormoblast demonstrates
persistent basophilia and fraying of
cytoplasmic borders indicating lack of
complete hemoglobinization
• Myelopoiesis – Normal
• Megakaryopoiesis – Normal
• Depleted bone marrow iron
43.
44. Bone marrow features of anemia chronic
disease
• Bone marrow aspirate demonstrating increased
iron staining in a fragment representing increased
marrow iron stores. . This finding is present in a
patiet with anemia of chronic disease.
• Normal iron staining in
• histiocytes is shown for Comparison
45. Genotypic classification
• Silent carrier: completely asymptomatic with normal haematological parameters.
• Beta-thalassaemia minor (trait): usually asymptomatic; diagnosis is made based on
screening when there is a positive family history, or during a work-up for mild Anemia; the
mild microcytic Anemia is often misdiagnosed as iron deficiency Anemia.
• Beta-thalassaemia intermedia: usually a similar presentation to beta-thalassaemia major
but as a toddler or older child; symptoms are usually less pronounced, and the course is
usually more insidious.
• Beta-thalassaemia major (also called Cooley's Anemia): complete absence of haemoglobin
A; often presents at a few months of age with progressive pallor and abdominal distension;
perinatal history is most often uneventful, and the infant may be pale, possibly with poor
feeding and decreased activity; hepatosplenomegaly and bony abnormalities are often
present at presentation, most often of the skull (frontal and parietal bossing, and chipmunk
facies).
46.
47. Bone marrow features of thalassemia
• Hypercellular
• Erythroid hyperplasia
• M:E ratio 1:5
• Dyserythropoisis
• Myelopoisis and megakaryopoisis are normal
• Bone marrow iron increased
• Dr. Monika Nema
48. Bone marrow features of thalassemia
• Top and bottom panels show bone
• marrow aspirate and
• biopsy, respectively, from a case of
• thalassemia trait.
• The bone marrow has increased
• numbers of erythroid precursors (a
• low myeloid to erythroid ratio)
• related to the increased peripheral
• RBC destruction in this disease.
49.
50. sideroblastic anemia:
• a heterogeneous group of disorders associated with
• various defects in the porphyrin biosynthetic
• pathway:
• -porphyrn biosynthesis defects
• -diminished heme synthesis
• -increased cellular iron uptake
• characterized by the association of anemia with
• presence of ringed sideroblast (a normoblast containing
• excessive deposits of iron within mitochondria) in bone
• marrow
51. • Sub-types:
• 1-Hereditary Sideroblastic Anemias:
• -hereditary sex-linked -inheritance undetermined
• 2-Acquired Sideroblastic Anemias
• 1-primary (idiopathic) sideroblastic anemia
• 2-secondary (drug- or toxin-induced) sideroblastic anemia
• -anti TB drugs (isoniazid, cycloserine, pyrazinamide)
• lead poisoning chloramphenicol thanol
• clinical: characterized by hypochromic, often microcytic, red cells in the blood usually mixed with normochromic cells
• hypochromic anemia ,hyperferremia ,increased transferrin saturation
• Lab: serum iron: increased
• TIBC: decreased
• % saturation: greatly elevated
• bone marrow: - markedly increased iron storage
• - erythroid hyperplasia
• - increased sideroblasts
52. • Treatment:Treatment of sideroblastic anemia may include
• 1- removal of toxic agents;
• 2- administration of pyridoxine, thiamine, or folic acid;
• 3-transfusion (along with antidotes if iron overload develops from
• transfusion);
• 4- other medical measures; or bone marrow or liver transplantation.