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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 the cell, such as hereditary spherocytosis, and extrinsic defects that cause damage from outside the cell, such as immune-mediated hemolytic anemia. Symptoms include anemia, jaundice, splenomegaly, and gallstones. Laboratory tests show signs of increased red blood cell destruction like elevated bilirubin and LDH, as well as signs of increased red blood cell production like reticulocytosis and nucleated red blood cells on blood smear. Intra
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Haemolytic anemia pratyasha paripurna
Hemolytic anemia occurs when the destruction of red blood cells outpaces their production. It can develop intrinsically due to abnormalities in red blood cells, such as in sickle cell anemia or thalassemia. Or it can occur extrinsically due to infection, autoimmune disorders, medications or splenic sequestration of normal red blood cells. Symptoms include pallor, fatigue, jaundice and dark urine. Treatment depends on the underlying cause but may include blood transfusions, medications to suppress the immune system, splenectomy or stem cell transplant.
Haemolytic anaemias lecture for v yr mbbs
Haemolytic anaemia refers to the pathological breakdown of red blood cells (RBCs). There are many potential causes, both inherited and acquired. Inherited causes include defects in the RBC membrane proteins or enzymes, leading to chronic haemolysis. Acquired causes include autoimmune haemolysis where antibodies destroy RBCs, and alloimmune haemolysis following blood transfusions. Investigation involves blood film examination for abnormal RBCs and the Coombs test to detect antibodies. Management depends on the underlying cause but may include transfusions, steroids, splenectomy or immunosuppression.
Hemolytic anemia and post hemorrhagic syndrome
Hemolytic anemia is a condition where red blood cells are destroyed faster than the body can replace them, leading to anemia. It can be caused by intrinsic issues with red blood cells themselves or extrinsic factors like infections, medications, autoimmune disorders, or enlarged organs destroying healthy cells. Symptoms include paleness, fatigue, fever, and abdominal pain. Diagnosis involves blood tests measuring red blood cell counts and liver function. Treatment options depend on the underlying cause but may include blood transfusions, immunosuppressants, corticosteroids, or spleen removal. Posthemorrhagic anemia develops after acute blood loss and is treated by addressing the cause of bleeding with fluids, transfusions, or surgery along
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This document discusses various types of anemia. It defines anemia and describes how it is classified based on red blood cell size, hemoglobin content, and underlying pathophysiological mechanism. Several specific types of anemia are then discussed in more detail, including iron deficiency anemia, aplastic anemia, pure red cell aplasia, anemia of chronic disease, hereditary spherocytosis, and glucose-6-phosphate dehydrogenase deficiency. For each type, the document outlines causes, pathophysiology, clinical manifestations, laboratory/blood smear findings, and treatment.
Hemolytic anemia
Haemolysis indicates that there is shortening of the normal red cell lifespan of 120 days. There are many causes.
To compensate, the bone marrow may increase its output of red cells six- to eightfold by increasing the proportion of red cells produced, expanding the volume of active marrow, and releasing reticulocytes prematurely. Anaemia occurs only if the rate of destruction exceeds this increased production rate.
Anemia Presentation
Normocytic anaemia can be caused by a variety of inherited and acquired conditions. Inherited causes include red blood cell membrane defects like hereditary spherocytosis and elliptocytosis. Metabolic defects such as G6PD deficiency and pyruvate kinase deficiency can also cause haemolytic anaemia. Acquired causes include immune haemolytic anaemias such as autoimmune haemolytic anaemia and alloimmune haemolytic anaemia seen in haemolytic disease of newborn. Non-immune causes include paroxysmal nocturnal haemoglobinuria and mechanical destruction of red blood cells. Investigation and management depends on the underlying cause but may include corticosteroids, splenectomy or blood transfusions.
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Blood functions include transportation of oxygen, carbon dioxide, nutrients, waste, and hormones. It also helps regulate pH, temperature, and water content of cells. Blood protects the body from blood loss via clotting and from foreign microbes via white blood cells. The components of blood include formed elements like red blood cells, white blood cells, and platelets. Plasma is the fluid portion that contains water, proteins, nutrients, gases, electrolytes, waste, enzymes, and hormones. Hematopoiesis is the process where blood cells are formed from stem cells in the bone marrow. Erythropoiesis involves the formation of red blood cells from stem cells in the bone marrow under the influence of the hormone ery
Hemolytic anemia
Hereditary spherocytosis is a hereditary hemolytic anemia caused by a red blood cell membrane defect that results in spherocytosis. The misshapen red blood cells, called spherocytes, are destroyed by the spleen, leading to hemolysis and a shortage of red blood cells. Clinical features include jaundice, splenomegaly, and gallstones. Laboratory findings show microspherocytes on peripheral blood film and increased reticulocytes, with normal red blood cell size.
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Haemolytic anemia pratyasha paripurna
Hemolytic anemia occurs when the destruction of red blood cells outpaces their production. It can develop intrinsically due to abnormalities in red blood cells, such as in sickle cell anemia or thalassemia. Or it can occur extrinsically due to infection, autoimmune disorders, medications or splenic sequestration of normal red blood cells. Symptoms include pallor, fatigue, jaundice and dark urine. Treatment depends on the underlying cause but may include blood transfusions, medications to suppress the immune system, splenectomy or stem cell transplant.
Haemolytic anaemias lecture for v yr mbbs
Haemolytic anaemia refers to the pathological breakdown of red blood cells (RBCs). There are many potential causes, both inherited and acquired. Inherited causes include defects in the RBC membrane proteins or enzymes, leading to chronic haemolysis. Acquired causes include autoimmune haemolysis where antibodies destroy RBCs, and alloimmune haemolysis following blood transfusions. Investigation involves blood film examination for abnormal RBCs and the Coombs test to detect antibodies. Management depends on the underlying cause but may include transfusions, steroids, splenectomy or immunosuppression.
Hemolytic anemia and post hemorrhagic syndrome
Hemolytic anemia is a condition where red blood cells are destroyed faster than the body can replace them, leading to anemia. It can be caused by intrinsic issues with red blood cells themselves or extrinsic factors like infections, medications, autoimmune disorders, or enlarged organs destroying healthy cells. Symptoms include paleness, fatigue, fever, and abdominal pain. Diagnosis involves blood tests measuring red blood cell counts and liver function. Treatment options depend on the underlying cause but may include blood transfusions, immunosuppressants, corticosteroids, or spleen removal. Posthemorrhagic anemia develops after acute blood loss and is treated by addressing the cause of bleeding with fluids, transfusions, or surgery along
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This document discusses various types of anemia. It defines anemia and describes how it is classified based on red blood cell size, hemoglobin content, and underlying pathophysiological mechanism. Several specific types of anemia are then discussed in more detail, including iron deficiency anemia, aplastic anemia, pure red cell aplasia, anemia of chronic disease, hereditary spherocytosis, and glucose-6-phosphate dehydrogenase deficiency. For each type, the document outlines causes, pathophysiology, clinical manifestations, laboratory/blood smear findings, and treatment.
Hemolytic anemia
Haemolysis indicates that there is shortening of the normal red cell lifespan of 120 days. There are many causes.
To compensate, the bone marrow may increase its output of red cells six- to eightfold by increasing the proportion of red cells produced, expanding the volume of active marrow, and releasing reticulocytes prematurely. Anaemia occurs only if the rate of destruction exceeds this increased production rate.
Anemia Presentation
Normocytic anaemia can be caused by a variety of inherited and acquired conditions. Inherited causes include red blood cell membrane defects like hereditary spherocytosis and elliptocytosis. Metabolic defects such as G6PD deficiency and pyruvate kinase deficiency can also cause haemolytic anaemia. Acquired causes include immune haemolytic anaemias such as autoimmune haemolytic anaemia and alloimmune haemolytic anaemia seen in haemolytic disease of newborn. Non-immune causes include paroxysmal nocturnal haemoglobinuria and mechanical destruction of red blood cells. Investigation and management depends on the underlying cause but may include corticosteroids, splenectomy or blood transfusions.
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Blood functions include transportation of oxygen, carbon dioxide, nutrients, waste, and hormones. It also helps regulate pH, temperature, and water content of cells. Blood protects the body from blood loss via clotting and from foreign microbes via white blood cells. The components of blood include formed elements like red blood cells, white blood cells, and platelets. Plasma is the fluid portion that contains water, proteins, nutrients, gases, electrolytes, waste, enzymes, and hormones. Hematopoiesis is the process where blood cells are formed from stem cells in the bone marrow. Erythropoiesis involves the formation of red blood cells from stem cells in the bone marrow under the influence of the hormone ery
Hemolytic anemia
Hereditary spherocytosis is a hereditary hemolytic anemia caused by a red blood cell membrane defect that results in spherocytosis. The misshapen red blood cells, called spherocytes, are destroyed by the spleen, leading to hemolysis and a shortage of red blood cells. Clinical features include jaundice, splenomegaly, and gallstones. Laboratory findings show microspherocytes on peripheral blood film and increased reticulocytes, with normal red blood cell size.
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This document discusses hemolytic anemia, which is a condition characterized by the premature destruction of red blood cells in the circulation. It defines hemolytic anemia as a reduced red blood cell lifespan. Some key points covered include:
- Causes of hemolytic anemia include genetic disorders like sickle cell anemia and thalassemia as well as acquired conditions like autoimmune hemolytic anemia.
- Signs and symptoms include fatigue, jaundice, and dark urine due to the breakdown of hemoglobin. Laboratory findings provide diagnostic clues like elevated bilirubin, reticulocytes, and lactate dehydrogenase.
- Different types of anemia are classified based on whether hemolysis
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This document provides an overview of blood disorders and their classification. It discusses red blood cell disorders such as polycythemia vera, iron deficiency anemia, sickle cell anemia, and thalassemia. It also covers white blood cell disorders, platelet disorders, coagulation disorders, and disease-related coagulopathies. The document defines each disorder, describes their signs and symptoms, laboratory findings, treatment considerations, and oral health implications.
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This document provides an overview of blood disorders, focusing on disorders of red blood cells, white blood cells, platelets, and coagulation. It begins with an introduction to blood and then covers specific disorders such as polycythemia vera, iron deficiency anemia, sickle cell anemia, and coagulation disorders. For each disorder, it discusses causes, clinical manifestations, oral manifestations, laboratory findings, and treatment considerations. The document aims to give healthcare practitioners a comprehensive review of various blood disorders and their impacts.
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This document provides an overview of blood disorders and summarizes key information about red blood cells and related disorders. It discusses the structure and function of red blood cells, variations in red blood cell count, and disorders involving too many or too few red blood cells such as polycythemia, anemia, sickle cell anemia, thalassemia, and erythroblastosis fetalis. Specific conditions are defined and their signs, symptoms, causes, and treatments are outlined.
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1. Acute variceal hemorrhage refers to bleeding from enlarged veins (varices) in the esophagus or stomach that is caused by portal hypertension from liver cirrhosis. Variceal bleeding is a severe complication and is the cause of bleeding in 70% of upper GI bleeds in cirrhotic patients.
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Hypertension emergencies require rapid reduction of blood pressure to prevent end organ damage. Hypertensive urgency can be managed as an outpatient but emergencies require hospitalization. Initial evaluation assesses for signs of damage to heart, kidneys, brain, or vasculature. Parenteral drugs like nicardipine, labetalol, and esmolol are used to lower blood pressure 10-15% within 1 hour and further to 160/100 mmHg in 2-6 hours, with goals tailored to specific conditions like stroke, heart failure, or aortic dissection. Oral agents like clonidine or nifedipine may be used after initial parenteral treatment to control blood pressure before discharge
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Hypertension emergencies require rapid reduction of blood pressure to prevent end organ damage. Hypertensive urgency can be managed as an outpatient with oral medications, while emergencies require hospitalization and intravenous drugs. Initial evaluation assesses for signs of heart, brain, kidney and vascular damage. Parenteral drugs like nicardipine, labetalol and esmolol are used but sodium nitroprusside is no longer first-line due to risks. Treatment goals depend on the specific organ involved and reduce pressure by 10-25% within 1-2 hours.
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Denis is a dynamic and results-driven Chief Information Officer (CIO) with a distinguished career spanning information systems analysis and technical project management. With a proven track record of spearheading the design and delivery of cutting-edge Information Management solutions, he has consistently elevated business operations, streamlined reporting functions, and maximized process efficiency.
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Date: May 29, 2024
Tags: Information Security, ISO/IEC 27001, ISO/IEC 42001, Artificial Intelligence, GDPR
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LAND USE LAND COVER AND NDVI OF MIRZAPUR DISTRICT, UP
This Dissertation explores the particular circumstances of Mirzapur, a region located in the
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cover support policymakers and scientists in making well-informed decisions, as alterations in
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Syllabus
Chapter-1
Introduction to objective, scope and outcome the subject
Chapter 2
Introduction: Scope and Specialization of Civil Engineering, Role of civil Engineer in Society, Impact of infrastructural development on economy of country.
Chapter 3
Surveying: Object Principles & Types of Surveying; Site Plans, Plans & Maps; Scales & Unit of different Measurements.
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- 2. Haemolytic Anaemia • Definition: –Anaemias which result from an increase in the rate of red cell destruction.
- 3. Normal red cell destruction • A red blood cell survives for 120 days in the circulation; about 1% of human red blood cells break down each day. • The spleen is the main organ which removes old and damaged RBCs from the circulation
- 5. Red cell destruction haemoglobin Globin Haem Amino acids Co Protoporphyrin Reutilization Respiration Biliverdin Bilirubin Stercobilin urobilinogen
- 6. Definitions Hemolysis: • is the destruction or removal of red blood cells from the circulation before their normal life span of 120 days. Haemolytic anaemias: • Are a group of anaemias in which red- cell lifespan is shortened.
- 7. • As RBCs have no nucleus, enzymes are degraded and not replaced, red cell metabolism gradually deteriorates and the cell become non-viable. Normal red cell destruction
- 8. RBCs breakdown • When the rate of breakdown increases, the body compensates by producing more RBCs • The normal adult marrow, after full expansion, able to increase erythropoietic activity 6-8 times normal • This may occur before the patient get anemic (compensated hemolytic disease)
- 9. Mechanisms of hemolysis • Extravascular red cells destruction occurs in reticuloendothelial system • Intravascular red cells destruction occurs in vascular space .
- 14. Intrinsic Defects Hereditary • Membrane defect • Haemoglobin defect • Enzyme defect Acquired Paroxysmal nocturnal haemoglobinuria .
- 15. Intrinsic Haemolytic anaemias 1. Membrane defect: • Hereditary spherocytosis. • Hereditary elliptocytosis.
- 16. Intrinsic Haemolytic anaemias Haemoglobin defect • Sickle cell disease. • Thalassaemia • Hb-C, Hb-D, Hb-E….etc
- 17. Intrinsic Haemolytic anaemias Enzyme defect: • G6PD deficiency. • Pyruvate kinase (PK) deficiency.
- 19. Extrinsic haemolytic anaemias Hereditary 1.LCAT deficiency. 2.Abetalipoproteinemia.
- 20. Acquired 1. Immune mediated H.A 2. Non-immune mediated HA: • Mechanical • Infectious agent • Hypersplenism • Thermal Extrinsic haemolytic anaemias
- 21. Immune mediated H.A • Autoimmune H.A. • Alloimmune H.A. • Drug induced mediated I.H.A (hapten mechanism).
- 22. Intravascular Haemolysis • Hb binds to haptoglobin and the complexes are rapidly taken up by hepatocytes. • Haptoglobin also play a role in extravascular haemolysis due to the escape of some Hb from macrophages when they phagocytosed damaged red cells.
- 23. • Haem is released from the Hb and rapidly oxidized to ‘haematin’. • Haematin binds to haemopexin and the complexes are removed by hepatocytes. • When haemopexin saturated, the haematin bind to albumin to form methaemalbumin. Intravascular Haemolysis
- 24. • When haemoglobinaemia is present, some of the free Hb dissociate to dimers and the dimers pass through the glomerulus causing haemoglobinuria. • Some of the dimers are taken up by renal tubular cells and converted to haemosiderin which can be detected in urine (haemosiderinuria). Intravascular Haemolysis
- 25. Red cell destruction Extravascular Intravascular RES Haem Globin Plasma iron pool Plasma protein pool Protoporphyrin Expired CO Unconjugated bilirubin Liver Conjugated bilirubin GI tract Urobilinogen Faeces Urine Free plasma Hb Hb- Hpt complex Liver Hpt and Hpx Haemopexin-methem Excess Hb methaemalbumin Kidney Hb Haemosiderin Haem+globin Hb methem metHb
- 26. Clinical Manifestations in Summary • Symptoms and signs of anemia • Jaundice • Splenomegaly • Cholelithiasis (gall stones) • Leg ulcers (sickle cell) • Skeletal abnormalities (thalassemia)
- 28. Evidence of haemolysis • The lab. Findings are divided into 2 groups: 1- Features of increased red cell breakdown. 2- Features of increased red cell production.
- 29. Features of increased red cell destruction • Serum bilirubin: high • Serum LDH: high • Urine urobilinogen: high • Serum haptoglobins: absent
- 30. Features of increased red cell production • P.B: Reticulocytosis and Circulating nucleated red cells • B.M: Erythroid hyperplasia.
- 31. • Morphology: microsphercytes, fragments,…etc • Shortened red cell survival. • Special tests: osmotic fragility, Damaged red cells
- 33. Main features of Intravascular Haemolysis • Haemoglobinaemia • Haemoglobinuria • Haemosiderinuria • Methaemalbuminaemia
- 34. Thanks