The document defines anaemia and describes its classification and types. It is classified into morphological anaemia, based on changes seen in red blood cells, and etiological anaemia, based on the underlying cause. The key types of morphological anaemia are normocytic normochromic, microcytic hypochromic, and macrocytic normochromic. Etiological anaemia includes anaemia due to blood loss, nutritional deficiencies, bone marrow failure, and haemolytic anaemia. Common causes, clinical features, laboratory findings, and treatments are discussed for different types of anaemia.
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.
This document summarizes various blood disorders that affect red blood cells. It begins by describing anemia of blood loss from acute hemorrhage or chronic blood loss. It then discusses hemolytic anemias, where red blood cells are destroyed faster than normal, including hereditary spherocytosis, sickle cell anemia, and thalassemia. Hereditary spherocytosis is caused by inherited defects in the red blood cell membrane. Sickle cell anemia results from a genetic mutation that causes hemoglobin to polymerize and distort the red blood cells into a sickle shape. Thalassemias are caused by mutations that decrease alpha or beta globin synthesis. The document also reviews impaired red cell production and other acquired
Polycythemia Vera is a chronic myeloproliferative disorder characterized by an overproduction of red blood cells from bone marrow due to a mutation in the JAK2 gene. This leads to thickening of the blood and complications like blood clots and spleen enlargement. It is diagnosed through blood tests showing increased red blood cells. While there is no cure, treatment focuses on reducing blood cell counts through regular blood removal and medications to suppress bone marrow production and stimulate the immune system.
Sickle cell disease is a genetic disorder that causes red blood cells to take on a sickle shape during periods of low oxygen. It is most common among those of African descent and is caused by a mutation in the beta-globin gene. The sickling of red blood cells leads to hemolytic anemia, damage to blood vessels, and painful vaso-occlusive crises in the bones, lungs, and other organs. Treatments include blood transfusions, hydroxyurea to increase fetal hemoglobin levels, antibiotics to prevent infection, and pain management. Future treatments may involve stem cell transplants or gene therapy.
This document discusses diabetic nephropathy, which is kidney damage caused by diabetes. It begins with an introduction on the increasing prevalence of diabetes in India and how about 25-40% of diabetics develop end stage renal disease or chronic kidney disease. The natural history of kidney disease progression through 5 stages is described from early increased filtration to end stage requiring dialysis or transplant. Risk factors, screening methods, management including controlling blood glucose and blood pressure, and treatment options like dialysis and transplant are covered.
This document summarizes a seminar on aplastic anemia in children. It defines aplastic anemia as a rare condition where the bone marrow fails to produce sufficient blood cells. Causes can include inherited conditions, infections, medications, radiation, and environmental toxins. Symptoms include fatigue, pale skin, easy bruising, and bleeding. Diagnosis involves blood tests and bone marrow examination. Treatment may include blood transfusions, bone marrow transplant, immunosuppressive drugs, and antibiotics. Nursing care focuses on monitoring for complications, providing support, and educating patients and their families.
Haemolytic anaemias are a group of anemias caused by the premature breakdown of red blood cells in the bloodstream or spleen. There are two main types - intrinsic defects that cause red blood cell damage from within, such as hereditary spherocytosis, and extrinsic defects that cause damage from outside factors like immune mediated hemolysis. Symptoms include anemia, jaundice, splenomegaly and gallstones. Laboratory tests show signs of increased red blood cell breakdown like elevated bilirubin and LDH, as well as signs of the bone marrow attempting to compensate with reticulocytosis and nucleated red blood cells. Intravascular hemolysis specifically causes hemoglobinemia,
1. Aplastic anemia is a condition characterized by pancytopenia (low red blood cells, white blood cells, and platelets) due to bone marrow failure.
2. It can be caused by exposure to toxins, radiation, viruses, or immune system attacks on the bone marrow. The bone marrow is hypocellular with fatty replacement of hematopoietic tissue.
3. Symptoms include anemia, increased risk of infection, bruising/bleeding due to low blood cell counts. Diagnosis involves blood tests showing pancytopenia and a bone marrow biopsy revealing a hypocellular marrow. Treatment options include supportive care, immunosuppressants, bone marrow transplant, or androgens
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.
This document summarizes various blood disorders that affect red blood cells. It begins by describing anemia of blood loss from acute hemorrhage or chronic blood loss. It then discusses hemolytic anemias, where red blood cells are destroyed faster than normal, including hereditary spherocytosis, sickle cell anemia, and thalassemia. Hereditary spherocytosis is caused by inherited defects in the red blood cell membrane. Sickle cell anemia results from a genetic mutation that causes hemoglobin to polymerize and distort the red blood cells into a sickle shape. Thalassemias are caused by mutations that decrease alpha or beta globin synthesis. The document also reviews impaired red cell production and other acquired
Polycythemia Vera is a chronic myeloproliferative disorder characterized by an overproduction of red blood cells from bone marrow due to a mutation in the JAK2 gene. This leads to thickening of the blood and complications like blood clots and spleen enlargement. It is diagnosed through blood tests showing increased red blood cells. While there is no cure, treatment focuses on reducing blood cell counts through regular blood removal and medications to suppress bone marrow production and stimulate the immune system.
Sickle cell disease is a genetic disorder that causes red blood cells to take on a sickle shape during periods of low oxygen. It is most common among those of African descent and is caused by a mutation in the beta-globin gene. The sickling of red blood cells leads to hemolytic anemia, damage to blood vessels, and painful vaso-occlusive crises in the bones, lungs, and other organs. Treatments include blood transfusions, hydroxyurea to increase fetal hemoglobin levels, antibiotics to prevent infection, and pain management. Future treatments may involve stem cell transplants or gene therapy.
This document discusses diabetic nephropathy, which is kidney damage caused by diabetes. It begins with an introduction on the increasing prevalence of diabetes in India and how about 25-40% of diabetics develop end stage renal disease or chronic kidney disease. The natural history of kidney disease progression through 5 stages is described from early increased filtration to end stage requiring dialysis or transplant. Risk factors, screening methods, management including controlling blood glucose and blood pressure, and treatment options like dialysis and transplant are covered.
This document summarizes a seminar on aplastic anemia in children. It defines aplastic anemia as a rare condition where the bone marrow fails to produce sufficient blood cells. Causes can include inherited conditions, infections, medications, radiation, and environmental toxins. Symptoms include fatigue, pale skin, easy bruising, and bleeding. Diagnosis involves blood tests and bone marrow examination. Treatment may include blood transfusions, bone marrow transplant, immunosuppressive drugs, and antibiotics. Nursing care focuses on monitoring for complications, providing support, and educating patients and their families.
Haemolytic anaemias are a group of anemias caused by the premature breakdown of red blood cells in the bloodstream or spleen. There are two main types - intrinsic defects that cause red blood cell damage from within, such as hereditary spherocytosis, and extrinsic defects that cause damage from outside factors like immune mediated hemolysis. Symptoms include anemia, jaundice, splenomegaly and gallstones. Laboratory tests show signs of increased red blood cell breakdown like elevated bilirubin and LDH, as well as signs of the bone marrow attempting to compensate with reticulocytosis and nucleated red blood cells. Intravascular hemolysis specifically causes hemoglobinemia,
1. Aplastic anemia is a condition characterized by pancytopenia (low red blood cells, white blood cells, and platelets) due to bone marrow failure.
2. It can be caused by exposure to toxins, radiation, viruses, or immune system attacks on the bone marrow. The bone marrow is hypocellular with fatty replacement of hematopoietic tissue.
3. Symptoms include anemia, increased risk of infection, bruising/bleeding due to low blood cell counts. Diagnosis involves blood tests showing pancytopenia and a bone marrow biopsy revealing a hypocellular marrow. Treatment options include supportive care, immunosuppressants, bone marrow transplant, or androgens
Usman Ghani, a 7-year-old boy, presented with pallor, easy fatigability, and bruising. Investigations revealed very low blood counts and a bone marrow biopsy showed hypoplastic/aplastic bone marrow. He was diagnosed with aplastic anemia. Aplastic anemia is a condition where the bone marrow fails to produce sufficient new blood cells, leading to pancytopenia. Treatment involves blood transfusions, antibiotics, growth factors, immunosuppressive drugs, and stem cell transplantation depending on the severity of the condition.
Iron deficiency anemia is a hypoproliferative anemia resulting from insufficient iron intake or absorption to support normal red blood cell production. Globally, iron deficiency affects over 2 billion people and is most prevalent in children, pregnant women, and those from Africa and Asia. Iron is essential for oxygen transport and cellular enzyme functions. Causes of iron deficiency anemia include inadequate dietary iron, malabsorption, blood loss, and increased demands from growth or pregnancy. The condition progresses from depleted iron stores to iron deficient erythropoiesis and finally anemia, with associated clinical features like pallor, fatigue, and glossitis. Diagnosis involves blood tests showing microcytic hypochromic anemia and low iron indicators.
Pancytopenia is a condition defined by low levels of red blood cells, white blood cells, and platelets. It can be caused by bone marrow failure, bone marrow infiltration, ineffective hematopoiesis, or peripheral destruction/pooling of blood cells. Evaluating the history, examination, blood counts, blood film, bone marrow aspiration/biopsy, and other tests can help determine the underlying cause, such as aplastic anemia, leukemia, lymphoma, or myelodysplastic syndrome. The bone marrow may appear hypocellular, normocellular, or hypercellular, providing clues to diagnoses like aplastic anemia or hematologic malignancies.
Anemia of chronic disease (ACD), also known as anemia of inflammation, is a common type of anemia associated with chronic infections, inflammatory disorders, and some cancers. It is characterized by inadequate red blood cell production, low serum iron levels, and low iron binding capacity. The anemia is usually mild to moderate in severity. Treatment involves addressing the underlying chronic condition causing the inflammation.
Sickle cell anemia is a hereditary blood disorder caused by a genetic mutation that results in abnormal hemoglobin and sickle-shaped red blood cells. It affects approximately 90,000-100,000 people in the United States, primarily those of African descent. Symptoms include episodes of severe pain, organ damage, infections, and stroke due to sickled cells blocking blood flow. While there is no cure, treatment focuses on managing pain, preventing infections, receiving blood transfusions, and in some cases, stem cell transplants or gene therapy.
Esophageal varices are enlarged veins in the esophagus that usually occur in people with liver disease. They develop when blood flow to the liver is blocked, forcing blood to flow through smaller veins not meant to carry large volumes. This can cause the veins to rupture and bleed. Symptoms of bleeding include vomiting blood or black stools. Treatment focuses on preventing further bleeding through medications, procedures to tie off veins, and potentially a liver transplant. Managing liver disease risk factors can help prevent esophageal varices.
Kidney disorders, Laboratory Investigation and Renal Function TestsMadhukar Vedantham
The document discusses kidney disorders, including their presentation, common diseases, and laboratory tests used in evaluation and diagnosis. It covers the functions of the kidneys, risk factors and symptoms of kidney failure, treatment options like dialysis and transplantation. Common kidney diseases described include polycystic kidney disease, hypertensive nephrosclerosis, glomerulonephritis, urinary tract infections, kidney stones, and diabetic kidney disease. Laboratory tests for kidney function include urine analysis, renal function tests of glomerular and renal blood flow, and renal biopsy.
This document discusses hemolytic anemia and focuses on sickle cell disease. It defines hemolytic anemia as increased destruction of red blood cells outside the bone marrow. Key diagnostic findings include increased reticulocyte count, hyperbilirubinemia, decreased haptoglobin, and increased lactate dehydrogenase. Hemolytic anemias are classified as hereditary defects within red blood cells or acquired external causes. Sickle cell disease results from a hereditary hemoglobinopathy and causes chronic hemolytic anemia. Complications include infections, acute chest syndrome, stroke, leg ulcers, splenic sequestration, and retinopathy. Diagnosis is made by finding sickle cells on peripheral smear and abnormal hem
Hemolytic anemia is characterized by accelerated red blood cell destruction and vigorous blood regeneration. It can be classified as intrinsic or extrinsic, congenital or acquired. The site of red blood cell destruction can be intravascular or extravascular. Common causes of hemolytic anemia include hereditary spherocytosis, thalassemias, sickle cell anemia, glucose-6-phosphate dehydrogenase deficiency, paroxysmal nocturnal hemoglobinuria, and immune-mediated hemolytic anemia. Evaluation of hemolytic anemia involves determining whether the anemia is hemolytic, the site of red blood cell destruction, the etiology, and severity through blood smears, reticulocyte counts, LDH and
This document defines and compares nephrotic syndrome and nephritic syndrome. It provides details on various causes of glomerular disease including minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy, IgA nephropathy, lupus nephritis, anti-GBM disease, and rapidly progressive glomerulonephritis. Evaluation of glomerular disease involves history, exam, urinalysis, and complement levels with renal biopsy used to confirm specific diagnoses.
Portal hypertension occurs when there is increased resistance to blood flow through the portal vein, causing elevated pressure. It is defined as a hepatic venous pressure gradient over 5 mmHg. Measurement involves catheterization of the hepatic vein. Causes include cirrhosis and other liver diseases. Complications include variceal bleeding, ascites, and encephalopathy. Treatment of acute bleeding involves vasoactive drugs, endoscopic therapy, and TIPS. Secondary prevention uses beta-blockers to reduce portal pressure and risk of rebleeding.
Megaloblastic anemias are caused by impaired DNA synthesis due to vitamin B12 or folate deficiency. The summary examines megaloblastic anemias, including causes such as vitamin B12 or folate metabolism defects, clinical features like pallor and neurological symptoms, investigation findings in peripheral blood and bone marrow showing megaloblasts and macroovalocytes, and treatment involving vitamin B12 or folate supplementation.
This document discusses anemia, specifically iron deficiency anemia and megaloblastic anemia. It defines anemia and provides classifications. It then describes iron metabolism, daily iron requirements, sources of iron, and factors affecting iron absorption. It discusses the causes, clinical features, laboratory findings, and management of iron deficiency anemia and megaloblastic anemia. Key points covered include the role of vitamin B12 and folic acid in megaloblastic anemia, and morphological and etiological classifications of anemia.
Pernicious anemia is a type of vitamin B12 deficiency caused by a lack of intrinsic factor, a substance produced by stomach lining that aids B12 absorption. It results in reduced red blood cells and nerve damage if untreated. The most common cause is an autoimmune destruction of stomach cells that produce intrinsic factor. Pernicious anemia is diagnosed through tests and treated through lifelong vitamin B12 injections or pills.
This document discusses proteinuria, or increased protein in the urine. It defines proteinuria and outlines its causes, which can include primary kidney diseases, overflow of abnormal proteins, or secondary causes from non-kidney diseases. The document describes different types of proteinuria including glomerular, tubular, and overflow, and explains how to detect, evaluate, and differentiate between the types using urine tests like dipstick, sulfosalicylic acid, protein electrophoresis, and immunoassay. It provides guidance on classifying and further investigating persistent proteinuria to determine its underlying cause and renal pathology.
The document discusses different types and causes of anemia. It classifies anemia into etiologic categories including impaired red blood cell production, excessive destruction of RBCs, and blood loss. It further describes morphologic classifications such as macrocytic, microcytic hypochromic, and normocytic normochromic anemia. Specific causes are provided for each category including deficiencies, diseases, and genetic disorders. Hemolytic anemia is discussed in more detail including hereditary and acquired causes. Laboratory findings associated with different types of anemia are also summarized.
Aplastic anemia is a condition where the bone marrow fails to produce sufficient new blood cells, leading to low blood cell counts and fatigue. It can be classified as idiopathic, secondary to drug reactions or infections, or constitutional/congenital forms like Fanconi anemia. Fanconi anemia is a genetic disorder characterized by bone marrow failure, physical abnormalities, and cancer predisposition. Diagnosis involves blood tests showing low cell counts and a bone marrow biopsy displaying a hypocellular marrow. Treatment options include blood transfusions, immunosuppressive drugs, and bone marrow transplantation.
Anemia is a decrease in red blood cells (RBCs), hemoglobin (Hgb), or hematocrit (HCT) levels compared to normal levels for age and sex. Anemias can be classified based on RBC size and hemoglobin content as normocytic normochromic, microcytic hypochromic, or macrocytic normocytic. Common causes of anemia include iron deficiency, anemia of chronic disease, thalassemia, vitamin B12 or folate deficiency, blood loss, and aplastic anemia.
This document discusses megaloblastic anemias, which are caused by a deficiency in vitamin B12 or folic acid. These deficiencies impair DNA synthesis during erythropoiesis, leading to large, abnormally developed red blood cells. Key findings include macrocytic anemia, hypersegmented neutrophils, and megaloblasts visible in bone marrow samples showing nuclear-cytoplasmic asynchrony. Pernicious anemia, an autoimmune disorder causing vitamin B12 deficiency, is described. Treatment involves vitamin B12 or folate supplementation.
Usman Ghani, a 7-year-old boy, presented with pallor, easy fatigability, and bruising. Investigations revealed very low blood counts and a bone marrow biopsy showed hypoplastic/aplastic bone marrow. He was diagnosed with aplastic anemia. Aplastic anemia is a condition where the bone marrow fails to produce sufficient new blood cells, leading to pancytopenia. Treatment involves blood transfusions, antibiotics, growth factors, immunosuppressive drugs, and stem cell transplantation depending on the severity of the condition.
Iron deficiency anemia is a hypoproliferative anemia resulting from insufficient iron intake or absorption to support normal red blood cell production. Globally, iron deficiency affects over 2 billion people and is most prevalent in children, pregnant women, and those from Africa and Asia. Iron is essential for oxygen transport and cellular enzyme functions. Causes of iron deficiency anemia include inadequate dietary iron, malabsorption, blood loss, and increased demands from growth or pregnancy. The condition progresses from depleted iron stores to iron deficient erythropoiesis and finally anemia, with associated clinical features like pallor, fatigue, and glossitis. Diagnosis involves blood tests showing microcytic hypochromic anemia and low iron indicators.
Pancytopenia is a condition defined by low levels of red blood cells, white blood cells, and platelets. It can be caused by bone marrow failure, bone marrow infiltration, ineffective hematopoiesis, or peripheral destruction/pooling of blood cells. Evaluating the history, examination, blood counts, blood film, bone marrow aspiration/biopsy, and other tests can help determine the underlying cause, such as aplastic anemia, leukemia, lymphoma, or myelodysplastic syndrome. The bone marrow may appear hypocellular, normocellular, or hypercellular, providing clues to diagnoses like aplastic anemia or hematologic malignancies.
Anemia of chronic disease (ACD), also known as anemia of inflammation, is a common type of anemia associated with chronic infections, inflammatory disorders, and some cancers. It is characterized by inadequate red blood cell production, low serum iron levels, and low iron binding capacity. The anemia is usually mild to moderate in severity. Treatment involves addressing the underlying chronic condition causing the inflammation.
Sickle cell anemia is a hereditary blood disorder caused by a genetic mutation that results in abnormal hemoglobin and sickle-shaped red blood cells. It affects approximately 90,000-100,000 people in the United States, primarily those of African descent. Symptoms include episodes of severe pain, organ damage, infections, and stroke due to sickled cells blocking blood flow. While there is no cure, treatment focuses on managing pain, preventing infections, receiving blood transfusions, and in some cases, stem cell transplants or gene therapy.
Esophageal varices are enlarged veins in the esophagus that usually occur in people with liver disease. They develop when blood flow to the liver is blocked, forcing blood to flow through smaller veins not meant to carry large volumes. This can cause the veins to rupture and bleed. Symptoms of bleeding include vomiting blood or black stools. Treatment focuses on preventing further bleeding through medications, procedures to tie off veins, and potentially a liver transplant. Managing liver disease risk factors can help prevent esophageal varices.
Kidney disorders, Laboratory Investigation and Renal Function TestsMadhukar Vedantham
The document discusses kidney disorders, including their presentation, common diseases, and laboratory tests used in evaluation and diagnosis. It covers the functions of the kidneys, risk factors and symptoms of kidney failure, treatment options like dialysis and transplantation. Common kidney diseases described include polycystic kidney disease, hypertensive nephrosclerosis, glomerulonephritis, urinary tract infections, kidney stones, and diabetic kidney disease. Laboratory tests for kidney function include urine analysis, renal function tests of glomerular and renal blood flow, and renal biopsy.
This document discusses hemolytic anemia and focuses on sickle cell disease. It defines hemolytic anemia as increased destruction of red blood cells outside the bone marrow. Key diagnostic findings include increased reticulocyte count, hyperbilirubinemia, decreased haptoglobin, and increased lactate dehydrogenase. Hemolytic anemias are classified as hereditary defects within red blood cells or acquired external causes. Sickle cell disease results from a hereditary hemoglobinopathy and causes chronic hemolytic anemia. Complications include infections, acute chest syndrome, stroke, leg ulcers, splenic sequestration, and retinopathy. Diagnosis is made by finding sickle cells on peripheral smear and abnormal hem
Hemolytic anemia is characterized by accelerated red blood cell destruction and vigorous blood regeneration. It can be classified as intrinsic or extrinsic, congenital or acquired. The site of red blood cell destruction can be intravascular or extravascular. Common causes of hemolytic anemia include hereditary spherocytosis, thalassemias, sickle cell anemia, glucose-6-phosphate dehydrogenase deficiency, paroxysmal nocturnal hemoglobinuria, and immune-mediated hemolytic anemia. Evaluation of hemolytic anemia involves determining whether the anemia is hemolytic, the site of red blood cell destruction, the etiology, and severity through blood smears, reticulocyte counts, LDH and
This document defines and compares nephrotic syndrome and nephritic syndrome. It provides details on various causes of glomerular disease including minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy, IgA nephropathy, lupus nephritis, anti-GBM disease, and rapidly progressive glomerulonephritis. Evaluation of glomerular disease involves history, exam, urinalysis, and complement levels with renal biopsy used to confirm specific diagnoses.
Portal hypertension occurs when there is increased resistance to blood flow through the portal vein, causing elevated pressure. It is defined as a hepatic venous pressure gradient over 5 mmHg. Measurement involves catheterization of the hepatic vein. Causes include cirrhosis and other liver diseases. Complications include variceal bleeding, ascites, and encephalopathy. Treatment of acute bleeding involves vasoactive drugs, endoscopic therapy, and TIPS. Secondary prevention uses beta-blockers to reduce portal pressure and risk of rebleeding.
Megaloblastic anemias are caused by impaired DNA synthesis due to vitamin B12 or folate deficiency. The summary examines megaloblastic anemias, including causes such as vitamin B12 or folate metabolism defects, clinical features like pallor and neurological symptoms, investigation findings in peripheral blood and bone marrow showing megaloblasts and macroovalocytes, and treatment involving vitamin B12 or folate supplementation.
This document discusses anemia, specifically iron deficiency anemia and megaloblastic anemia. It defines anemia and provides classifications. It then describes iron metabolism, daily iron requirements, sources of iron, and factors affecting iron absorption. It discusses the causes, clinical features, laboratory findings, and management of iron deficiency anemia and megaloblastic anemia. Key points covered include the role of vitamin B12 and folic acid in megaloblastic anemia, and morphological and etiological classifications of anemia.
Pernicious anemia is a type of vitamin B12 deficiency caused by a lack of intrinsic factor, a substance produced by stomach lining that aids B12 absorption. It results in reduced red blood cells and nerve damage if untreated. The most common cause is an autoimmune destruction of stomach cells that produce intrinsic factor. Pernicious anemia is diagnosed through tests and treated through lifelong vitamin B12 injections or pills.
This document discusses proteinuria, or increased protein in the urine. It defines proteinuria and outlines its causes, which can include primary kidney diseases, overflow of abnormal proteins, or secondary causes from non-kidney diseases. The document describes different types of proteinuria including glomerular, tubular, and overflow, and explains how to detect, evaluate, and differentiate between the types using urine tests like dipstick, sulfosalicylic acid, protein electrophoresis, and immunoassay. It provides guidance on classifying and further investigating persistent proteinuria to determine its underlying cause and renal pathology.
The document discusses different types and causes of anemia. It classifies anemia into etiologic categories including impaired red blood cell production, excessive destruction of RBCs, and blood loss. It further describes morphologic classifications such as macrocytic, microcytic hypochromic, and normocytic normochromic anemia. Specific causes are provided for each category including deficiencies, diseases, and genetic disorders. Hemolytic anemia is discussed in more detail including hereditary and acquired causes. Laboratory findings associated with different types of anemia are also summarized.
Aplastic anemia is a condition where the bone marrow fails to produce sufficient new blood cells, leading to low blood cell counts and fatigue. It can be classified as idiopathic, secondary to drug reactions or infections, or constitutional/congenital forms like Fanconi anemia. Fanconi anemia is a genetic disorder characterized by bone marrow failure, physical abnormalities, and cancer predisposition. Diagnosis involves blood tests showing low cell counts and a bone marrow biopsy displaying a hypocellular marrow. Treatment options include blood transfusions, immunosuppressive drugs, and bone marrow transplantation.
Anemia is a decrease in red blood cells (RBCs), hemoglobin (Hgb), or hematocrit (HCT) levels compared to normal levels for age and sex. Anemias can be classified based on RBC size and hemoglobin content as normocytic normochromic, microcytic hypochromic, or macrocytic normocytic. Common causes of anemia include iron deficiency, anemia of chronic disease, thalassemia, vitamin B12 or folate deficiency, blood loss, and aplastic anemia.
This document discusses megaloblastic anemias, which are caused by a deficiency in vitamin B12 or folic acid. These deficiencies impair DNA synthesis during erythropoiesis, leading to large, abnormally developed red blood cells. Key findings include macrocytic anemia, hypersegmented neutrophils, and megaloblasts visible in bone marrow samples showing nuclear-cytoplasmic asynchrony. Pernicious anemia, an autoimmune disorder causing vitamin B12 deficiency, is described. Treatment involves vitamin B12 or folate supplementation.
1. The document discusses hematologic disorders including hematopoiesis, anemia, polycythemia, and hematologic malignancy.
2. It provides details on the pathophysiology of hematopoiesis, the definition and classification of anemia, the general approach to evaluating anemic patients, and discussions of common anemia types and their treatments.
3. Key anemia types covered include iron deficiency anemia, megaloblastic anemia due to vitamin B12 and folate deficiencies, and the morphological features seen in peripheral blood and bone marrow in these conditions.
This document provides an overview of anemia, including its definition, cut-off levels used to diagnose it, common causes, classification approaches, and key details about specific types like iron deficiency anemia, megaloblastic anemias, sickle cell disease, and thalassemias. It covers diagnostic testing and clinical manifestations, emphasizing the importance of considering a patient's red blood cell morphology, erythropoiesis, and underlying pathophysiology when evaluating the cause of an anemia.
This document provides an outline for a course on blood disorders. It covers topics like anatomy and physiology of blood, hematologic studies, conditions like anemia, sickle cell anemia and leukemia. Specific types of anemia discussed in detail include iron deficiency anemia, megaloblastic anemias (pernicious anemia and folic acid deficiency), and aplastic anemia. Hemolytic anemia and sickle cell anemia are also summarized.
This document summarizes key information about red blood cells (RBCs), including their general features, composition, lifespan, counts in adults and newborns, functions in transporting gases, and regulation of erythropoiesis. It also covers RBC indices, the stages of erythropoiesis, factors that regulate RBC production, common anemias like iron deficiency and sickle cell anemia, jaundice, and physiological neonatal jaundice.
This document provides information about megaloblastic anemia in children through a seminar presentation. It begins with an overview of hematology and the components of blood. It then discusses the causes of megaloblastic anemia as deficiencies in vitamins B12 and folic acid. The pathophysiology is described as impaired cell division leading to enlarged red blood cells called megaloblasts. Clinical manifestations include weakness, pale skin, and neurological issues. Diagnostic tests include blood counts and smears to examine red blood cells. Management involves vitamin B12 or folic acid supplementation through oral or injectable routes. Nursing care focuses on risks of ineffective tissue perfusion and activity intolerance due to anemia.
This document discusses various types of anemia. It defines anemia as a reduction in hemoglobin levels and describes the most common causes as iron deficiency and nutritional deficiencies. Specific types discussed in detail include iron deficiency anemia, megaloblastic anemia caused by vitamin B12 and folate deficiencies, sickle cell anemia caused by an abnormal hemoglobin gene, thalassemias caused by genetic defects in hemoglobin production, and G6PD deficiency which affects the ability to prevent oxidative damage to red blood cells. The document covers epidemiology, pathophysiology, clinical manifestations, investigations, and treatments for each type.
This document discusses different types of anemia. It begins by introducing the three main blood cell groups - red blood cells, white blood cells, and platelets. It then focuses on red blood cells and hemoglobin, the oxygen-carrying molecule. The document defines anemia and provides reference levels for hemoglobin. It describes different types of anemia classified by mean corpuscular volume (MCV), including microcytic (low MCV), normocytic (normal MCV), and macrocytic (high MCV) anemias. Microcytic anemias discussed in more detail include iron deficiency anemia, thalassemia, and sideroblastic anemia. Macrocytic anemias are
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1-Differentiate between the different causes of anemia
2. Discuss the investigations that may clarify the diagnosis
3. Recognize the predisposing factors and consequences of iron deficiency anemia and discuss how to manage it
4. Discuss the hereditary basis and clinical features of sickle cell anemia and thalassemia .
prepared by med_students0
Anemia is caused by a decrease in hemoglobin levels or red blood cell count. There are several types of anemia classified by etiology or morphology. Iron deficiency anemia, the most common type worldwide, is caused by inadequate iron intake or increased iron loss. Megaloblastic anemias like pernicious anemia result from vitamin B12 or folate deficiencies and are characterized by abnormally large red blood cells. Pernicious anemia specifically involves failure of intrinsic factor secretion due to gastric atrophy. Treatment involves vitamin B12 injections to correct the deficiency.
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.
This document provides information on hematological disorders including anemias, polycythemias, and bleeding disorders. It begins by defining hematological disorders as diseases affecting blood and blood forming tissues. It then discusses different types of anemias classified by cause or cell morphology. Common anemias described include iron deficiency anemia, anemia of chronic disease, and thalassemia. Symptoms, diagnostic tests, and treatment options for anemias are also outlined. The document also introduces polycythemias including definitions and types like primary and secondary polycythemia. Primary polycythemia vera is described in more detail regarding its cause, risk factors, signs and symptoms, and diagnostic evaluation. Finally, bleeding disorders
This document provides an overview of hematopathology, focusing on red blood cell disorders including anemia and polycythemia. It defines anemia and classifies it based on underlying mechanisms such as blood loss, diminished erythropoiesis, and hemolytic anemias. Megaloblastic anemias caused by vitamin B12 and folate deficiencies are described in detail. Pernicious anemia, a specific form of vitamin B12 deficiency, is also summarized, covering its pathogenesis, morphology, clinical features and diagnosis.
The document discusses various types of anemia including their causes, symptoms, diagnostic tests, and treatment. It covers iron deficiency anemia, thalassemia, sickle cell anemia, hereditary spherocytosis, megaloblastic anemia, and aplastic anemia. The key signs and findings for each type are outlined along with recommended treatment approaches.
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.
This document discusses anemia in children. It defines anemia and provides WHO cut-off values used to define anemia in children of different ages. It describes the different types of anemia - microcytic, macrocytic, and normocytic anemia - based on red blood cell indices. The causes, clinical features, investigations, management, and prevention of iron deficiency anemia are explained in detail. Other types of anemia like thalassemia, sickle cell anemia, and anemia of chronic disease are also briefly mentioned. Ayurvedic correlations between anemia and pandu are discussed through references from classical texts.
Iron-deficiency anemia is the most common nutritional disorder worldwide. It occurs when iron levels in the body are low and there is not enough iron to produce normal red blood cells. Symptoms can include pallor, fatigue, and irritability. Diagnosis involves blood tests showing low iron levels, smaller and fewer red blood cells. Treatment is oral iron supplementation which leads to improved hemoglobin levels within weeks. Prevention focuses on breastfeeding, iron-fortified formula for infants, and limiting milk intake after age 1.
This document provides an overview of hematopoiesis, erythropoiesis, and anemia. It discusses where blood cell formation occurs, the lifespan and production rate of red blood cells, and how hypoxia stimulates erythropoietin production. It defines anemia, lists global and country prevalence data, and compensatory mechanisms. It describes classifications of anemia including morphological and etiological, and covers causes such as blood loss, bone marrow disorders, nutritional deficiencies, and hemolytic anemias. Laboratory evaluation of anemia and peripheral blood smear findings are also summarized.
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Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
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2. • Definition
1) It is a pathological condition in which the
haemoglobin level of the blood goes down below the
lower limit of the normal range of the age and sex of
the individual.
OR
2) It is a pathological condition in which the RBC
charring capacity of blood is decrease.
OR
3) It is a pathological condition in which the RBC count
or haemoglobin concentration or both goes down.
3. CLASSIFICATION
Mainly two types :
1. Morphological anaemia :-
based on absolute indices of morphological changes
seen in RBC in peripheral blood smeared .
Which is follow by pathologist.
2. Etiological anaemia:-
based on cause of anaemia . Which is follow by
clinician to know the cause so that can be treated.
4. Morphological Anaemia
• Based on the value of absolute indices of
morphological changes in RBC. like change in size ,
shape and concentration of Hb.
• On the base of change in RBC ; three subtypes of
morphological anaemia is there:-
1. Normocytic normochromic
2. Microcytic hypochromic
3. Macrocytic normocromic
• Absolute indices are three:
1. M.C.V = Mean corpuscular volume.
2. M.C.H =Mean corpuscular haemoglobin.
3. M.C.H.C=Mean corpuscular haemoglobin
concentration.
5.
6. ATEOLOGICAL ANAEMIA
This classification is based on the etiology (cause) of anaemia.
1. Due to blood loss(post haemorrhagic)
• acute blood loss :
Like in accident, surgery ,APH ,PPH , etc…
• Chronic blood loss:
Eg. Piles ,peptic ulcer , hook-warm infection, etc….
2. Due to deficiency of haemopoatic factor OR Nutritional anaemia
eg: Fe –deficiency anaemia
Vit-B12 or folic acid deficiency anaemai.
3. APLASTIC ANAEMIA
caused by bone marrow failure
7. 4. Haemolytic anaemia:
It is divided in to two subtypes
A) Intracorpuscular : thalassaemias ,
haemoglobinopthis
B)Extracorpuscular: malaria, haemolytic disease of
new born, incompatible blood
8. Clinical feature of Anaemia
Lassitude
Fatigue
Palpitation
Breathlessness on exertion
Dimness of vision
Insomnia
Angina
Tingling sensation
Pallorness of skin , mucous membrane, conjunctiva
Trechycardia
9.
10. Systolic murmur
oedema
Amenorrhea
Menorrhagia
Attacks of giddiness
Headache
Drowsiness
Flatulence of abdomen after eating
( In mild anaemia there may not be any symptoms)
11. Anisocytosis : Increase variation in size of RBC.
normal size of RBC= 6.7-7.7 μ (normocyte)
o average -7.2 μ
• Larger than 8μ is
called- Macrocyte.
• Smaller than 6μ is
Called- Microcyte.
13. Hypochromasia :central pallor area of RBC is
increased more than 1/3rd . seen in Fe
deficiency anaemia, thalassaemias ,
sideroblastic anaemia.
14. Most common type of anaemia.
More common in vegetarian people than non-veg
people.
because non-vegetarian food is rich in iron.
• Contain heam-Fe which is ferrous form of iron does not need
HCL of gastric juice and vitamin for absorption.
• Easily absorbed.
• Absorbed in duodenum and upper jejunum.
In vegetarian Fe is in ferric form.
Need HCL of gastric juice and vitamin to convert into ferrous
form.
15
15. Source of iron :-
Non –vegetarian food rich in iron :
liver , kidney , egg-yolk, meat , fish fat.
Vegetarian food rich in iron:
cereal pulse base diet is rich in iron.
dark green vegetable like spinach , leafy vegetables , dry
fruits , whole pulses like channa, rajma , bajra etc… ,
jiggery , dates , banana , apple etc..
Daily requirement= 18 mgm/day ( in adult)
Daily loss = 0.5 to 1.0 mgm/day
16
16. Body iron store in hair , nails , sweat etc..
Absorption :-
-> depend upon need of body.
-> controlled by mucosal block.
-> in anaemic person more absorption.
-> increased by vit-C , gastric juice,
-> decreased by milk , antacids , phylates , tannin
etc..
17. AETIOLOGY
1. Blood loss.
Acute chronic
-accident - piles
-APH - hook warm infection
-PPH - bleeding from peptic ulcer
-menorrhagia - intestinal malignancy
- apistexis
In India malaria and hook worm infection are most
common cause for chronic blood loss
18. 2. Increase requirement of iron:
eg. Growing age , pregnancy , lactation etc..
3. Inadequate dietary intake:
eg. Due to poverty , anorexia(in TB, cancer) , vegetarian diet
4. Decrease absorption of iron:
eg. Partial or total gastectomy, achlohydria ,
intestinal malabsorbtion in coeliac disease
19. Lab Diagnosis
1) Hb – decreased
2) RBC count – decreased
3) PCV – decreased
4) Absolute indices-
M.C. V
M.C.H ALL are decreased
M.C.H.C
5) P.s – anisocytosis and Poikilocytosis.
microcytic hypochromic RBC
6) Reticulocyte count – may be normal , decreased or
slightly increased(normal in adult->0.2-2% , in
infants 2-6%, total 24000-48000/cumm)
20. 7) WBC count - normal
8)Differential count – normal
9)Platelet count – normal or slightly increased
in case of bleeding.
10)Bone marrow biopsy – hyper cellular due to
erytheiod hyperplasia
11)Parssian blue stain – Negative.(shows
absence of iron store in REcell of bone
marrow)
12)Biochemical findings –
A. Serum iron level -> decreased(normal 18-
180μgm/day)
21.
22. Difference
Heam iron
It is in ferrous form
Can be easily absorbed
Soluble
Vit-C and HCL is not
needed.
High bio availability
Found in non-veg food i.e
red meat
NON HEAM IRON
It is in ferric form.
Has to be converted in to
ferrous form and then
absorbed
Insoluble
Gastric HCL make is soluble
& vit-C convert it in ferrous
form.
Low bio availability
Found in vegetarian food.
23. Etiology & Pathogenesis:-
Deficiency of vit-B12(cobalamine) & / or folic acid
Impaired DNA synthesis
Delayed maturity of nucleus of RBC precursor
Slow division of cell.
(the cytoplasmic development progress normally)
24. • It leads to formation of large nucleated RBC precursor
: Megalobasts.
• Megaloblastas are morphologically & functionally
abnormal so that RBCs are formed from them released
into the peripheral blood is also abnormal in
size(macrocyte ).
25. Cause
B-12 deficiency.
due to:
1. inadequate dietary intake- more common in
vegetarian and breast feed baby.
2. Malabsorption – due to lack of intrinsic factor ,
gastractomy , disease of small intestine like
Clohn’s disease.
3. Increase demand – eg.pregnancy , lactation ,
infancy etc…
26. source
• Non-veg food like kidney, liver, heart , muscle meat
etc are rich in B12.
• Fish , egg , cheese & milk also rich in B12.
• Vegetable are poor in source(B12)
Daily requirement : 2-4μg
Absorption : in distal Ilium.
Storage :
Mainly in liver -> 2mgm
Kidney
Heart 2mgm
Brain
27. function
• DNA synthesis.
• Myelination of peripheral nerves , spinal
cord and cerebrum.
28. Folic acid deficiency
(same as B-12 deficiency)
due to:
1. inadequate dietary intake- more common in
vegetarian and breast feed baby.
2. Malabsorption – due to lack of intrinsic factor ,
gastractomy , disease of small intestine like Clohn’s
disease.
3. Increase demand – eg.pregnancy , lactation , infancy
etc…
29. Diet : Non-veg food is rich in folic acid than
vegetarian food .
Daily requirement :100 – 200 mg/ day
Absorption :whole of small intestine
Nervous manifestation : numbness ,
weakness , ataxia , diminished reflexes
Atrophic gastritis in stomach is seen.
31. e
• Tear drop cells may be seen.
• Basophilic stipping of RBC.
WBC count : TLC ( total leukocyte count)
slightly decrease
D.C ( differential count)
• Neutrophils → hyper segmented nucleus )
(lobes more than 5)
Platelet : slight thrombocytopenia with
Megathrombocytes.
Pancytopaenia is characteristic feature.
32. Biochemical findings :
• Serum B-12 level are decreased : >100 ng/litter
(normal 200-900 ng/litter )
• Serum iodate : >4 μg/litter
(normal 6-12 μg/litter)
• Megaloblastic erythroid hyperplasia.
• This abnormality of RBC , destroy in bone marrow and
seen in 2 forms
a) Abnormal mitosis
b) Degenerated giant mitocyte(wbc)
33. Bone marrow finding
• Bone marrow is hypercellular due to
megaloblastic erythroid hyperplasia.
• They may shows abnormal mitosis.
• Giant metamylocytes are also seen
34. • Also known as Addison’s megaloblastic
anaemia.
• Uncommon in India
• Age incidence :- middle and old age people
• When occur in children called - juvenile
pernicious anaemia.
• Both sex are similarly affected.
35. aetiology
• Deficiency of intrinitsic factor.
• Atrophy of gastric mucosa due to
prodenetion of autoimmune antibodies
against parietal cell and intrinsic fator
• Antibodies are found in serum and gastric
juice of the patient
Pathological changes in gastric mucos :
Certain mucosal atrophy affecting acid and
pepsin secreting cells of stomach.
Result : deficiency of intrinsic factors leads to
megaloblastic anaemia and subsent
combined degeneration of spinal cord and
peripheral neuropathy.
36. Classification ( according to cause)
Haemolytic anaemia
Intracorpuscular Extracorpuscul
- thalassaemia - Infection
- enzymatic deficiency - drugs & chemical
in RBC -miscellaneou
-Defect in cell mambrane
37. Aetiology – pathogenesis
Increase haemolysis of RBCs
Decrease life span of RBC
Increased destruction of RBC
Increased release of haem
Increased formation of bilirubin
(uncongugated)
goes to liver
Congugated bilirubin
Goes to intestine
38. CAUSES :
1. Intracorpuscular cause
Mainly three intacorpuscular causes
A. Thalassaemia and haemoglobinopathy
B. Enzymatic deficiency in RBCs . Eg -> G-6PD deficiency &
P.K deficiency & haemoglobinopthisis
C. Defect in cell-membrane
eg. Hereditory sperocytosis & hereditory
eliptocytosis.
It is a qualitative disorder of HB . Decreased of HB
synthesis leads to abnormal HB.
39. • Defect in the popypeptide chain of HB.
• over 100 abnormal Hbs are known. Hb-S, Hb-C Hb-D,
Hb-E etc..
• Out of all this Hb-s is most common. Which cause
sickle cell anaemia.
THALASSAEMIA
Quontative defect of haemoglobin.
Hereditary disorder.
Defect : reduced ret of synthesis of one or more of
globin peptide chains.
Two types: α & β
40. Lab diagnosis
• Hb : decreased
• RBC :decreased
• PCV : decreased
• MCV
• MCH normal
• MCHC
• Peripheral blood smear :
• normocytic normochromic.
• Polychorm cell is may seen.
• RBC lies much apart from each other
WBC : normal
Platelets : normal
41. • Reticulocyte : increased up to 20-30 %
• Bone marrow : hyper cellular of erythroid
hyparplasia
• Electrophoresis : separation of Hbs.
Abnormal Hbs may be detected (Hb-s)
• Osmotic fragility of RBC – increased
• Sickle cell for Hb-S may be positive.
• G-6PD deficiency may be seen.
• Blood bilirubin level : increased.
• Urobilinogen in urine : increased
• Sterkobilirogen in stool : increased.
42. Characterised by pancytopaenia
Anaemia
Leucopaenia
Thrombocytopaenia
Cause atrophy of bone marrow
46. • Platelet : increased (thrombocytopaenia)
• Bone marrow : dry tap
• Tryphling biopsy : hypocellular
Bone marrow is aplastic . Replaced by fat with
patchy areas of cell
Sever decreased f myeloid cells
Megakareyocyte and erythroid cells.
Pancytopaenia : marrow consist chiefly of
lymphocytes and plasma cells….