This document discusses megaloblastic anemia, specifically focusing on vitamin B12 and folate deficiencies. It defines megaloblastic anemia and describes the mechanisms, causes, metabolism, functions, and pathophysiology of vitamin B12 and folate. It also discusses pernicious anemia, masked megaloblastic anemia, and provides diagrams of vitamin B12 absorption, transport, and biochemical functions. The key points covered are the roles of vitamin B12 and folate in DNA synthesis, the resulting impaired cell proliferation and megaloblast formation in bone marrow, and the clinical effects of ineffective hematopoiesis.
This document discusses megaloblastic anemias caused by deficiencies in vitamin B12 or folate. These deficiencies impair DNA synthesis, causing abnormal nuclear maturation in bone marrow precursors called megaloblasts. This leads to large, dysfunctional red blood cells and macrocytic anemia. Vitamin B12 and folate are essential cofactors in reactions involved in DNA synthesis. Deficiencies can result in neurological complications due to trapping of folate or impaired methylation reactions. Clinical features include macrocytic anemia, glossitis, neuropathy, and other symptoms.
Vitamin B12 deficiency is a potentially serious condition that can affect multiple body systems. It presents as macrocytic anemia but can also cause neurological abnormalities and gastrointestinal issues. Vitamin B12 is essential for DNA synthesis and hematopoiesis. It is absorbed in the ileum with the help of intrinsic factor. Causes of deficiency include pernicious anemia, gastrointestinal disorders, vegetarian diets, and certain medications. Deficiency is diagnosed based on low B12 levels and hematological and neurological examination findings.
This document discusses anemias caused by diminished red blood cell production. It covers various inherited and acquired causes, including nutritional deficiencies, bone marrow failure disorders, infiltrative bone marrow disorders, and decreased erythropoietin production. It focuses in depth on megaloblastic anemias caused by vitamin B12 and folate deficiencies, providing details on the mechanisms, morphology, and clinical features of pernicious anemia specifically.
Hematinics-maturation factors and ErythropoetinDr. Advaitha MV
This document discusses hematinics and maturation factors required for red blood cell formation. It focuses on vitamin B12 and folic acid, explaining their roles, dietary sources, daily requirements, pharmacokinetics, metabolic functions, deficiencies, and therapeutic uses. Erythropoietin, which stimulates red blood cell production, is also covered briefly. The key relationship discussed is how vitamin B12 and folic acid work together in methylation reactions important for DNA synthesis and preventing megaloblastic anemia.
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.
Megaloblastic anemias are caused by an impairment of DNA synthesis leading to large, abnormally shaped red blood cells and their precursors. Pernicious anemia is a specific megaloblastic anemia caused by an autoimmune destruction of gastric parietal cells, resulting in impaired absorption of vitamin B12 and deficient DNA synthesis. It is characterized by megaloblastic changes in the bone marrow and gastrointestinal tract, and the presence of autoantibodies against intrinsic factor and gastric proton pumps. Left untreated, the impaired hematopoiesis leads to pancytopenia and anemia.
This document provides an overview of megaloblastic anemias, specifically focusing on vitamin B12 and folic acid deficiencies. It covers the introduction and pathophysiology of megaloblastic anemias. It then discusses the causes, clinical features, laboratory investigations, diagnosis, and pathophysiology of vitamin B12 and folic acid deficiencies. Key points include the roles of these vitamins in DNA synthesis and their malabsorption due to various gastric and intestinal conditions.
This document discusses megaloblastic anemias caused by deficiencies in vitamin B12 or folate. These deficiencies impair DNA synthesis, causing abnormal nuclear maturation in bone marrow precursors called megaloblasts. This leads to large, dysfunctional red blood cells and macrocytic anemia. Vitamin B12 and folate are essential cofactors in reactions involved in DNA synthesis. Deficiencies can result in neurological complications due to trapping of folate or impaired methylation reactions. Clinical features include macrocytic anemia, glossitis, neuropathy, and other symptoms.
Vitamin B12 deficiency is a potentially serious condition that can affect multiple body systems. It presents as macrocytic anemia but can also cause neurological abnormalities and gastrointestinal issues. Vitamin B12 is essential for DNA synthesis and hematopoiesis. It is absorbed in the ileum with the help of intrinsic factor. Causes of deficiency include pernicious anemia, gastrointestinal disorders, vegetarian diets, and certain medications. Deficiency is diagnosed based on low B12 levels and hematological and neurological examination findings.
This document discusses anemias caused by diminished red blood cell production. It covers various inherited and acquired causes, including nutritional deficiencies, bone marrow failure disorders, infiltrative bone marrow disorders, and decreased erythropoietin production. It focuses in depth on megaloblastic anemias caused by vitamin B12 and folate deficiencies, providing details on the mechanisms, morphology, and clinical features of pernicious anemia specifically.
Hematinics-maturation factors and ErythropoetinDr. Advaitha MV
This document discusses hematinics and maturation factors required for red blood cell formation. It focuses on vitamin B12 and folic acid, explaining their roles, dietary sources, daily requirements, pharmacokinetics, metabolic functions, deficiencies, and therapeutic uses. Erythropoietin, which stimulates red blood cell production, is also covered briefly. The key relationship discussed is how vitamin B12 and folic acid work together in methylation reactions important for DNA synthesis and preventing megaloblastic anemia.
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.
Megaloblastic anemias are caused by an impairment of DNA synthesis leading to large, abnormally shaped red blood cells and their precursors. Pernicious anemia is a specific megaloblastic anemia caused by an autoimmune destruction of gastric parietal cells, resulting in impaired absorption of vitamin B12 and deficient DNA synthesis. It is characterized by megaloblastic changes in the bone marrow and gastrointestinal tract, and the presence of autoantibodies against intrinsic factor and gastric proton pumps. Left untreated, the impaired hematopoiesis leads to pancytopenia and anemia.
This document provides an overview of megaloblastic anemias, specifically focusing on vitamin B12 and folic acid deficiencies. It covers the introduction and pathophysiology of megaloblastic anemias. It then discusses the causes, clinical features, laboratory investigations, diagnosis, and pathophysiology of vitamin B12 and folic acid deficiencies. Key points include the roles of these vitamins in DNA synthesis and their malabsorption due to various gastric and intestinal conditions.
This document provides definitions and classifications for anemia. It begins by defining anemia based on hemoglobin concentration ranges for males, females, and pregnant females. It then discusses classifying anemia based on morphology, etiology/mechanism, impaired red blood cell production, hemolytic anemias, and blood loss. Specific types of anemia are then discussed in more detail, including iron deficiency anemia, vitamin B12 deficiency, folate deficiency, and anemia of chronic disease. Causes, clinical features, investigations, and treatment are outlined for each type.
Vitamin B12 deficiency can result in megaloblastic anemia characterized by large, immature red blood cells. It is most commonly caused by pernicious anemia where autoimmune destruction of gastric parietal cells leads to lack of intrinsic factor needed for vitamin B12 absorption. Clinical features include anemia, jaundice, and neurological problems. Diagnosis is based on morphological changes in blood and bone marrow showing megaloblasts, low vitamin B12 levels, and a positive Schilling test demonstrating impaired absorption. Treatment involves lifelong vitamin B12 injections or high dose oral supplementation.
Vitamin B12 and folate deficiencies can cause megaloblastic anemia due to impaired DNA synthesis. Vitamin B12 deficiency specifically can also cause neurological manifestations like peripheral neuropathy. Diagnosis involves blood tests showing macrocytic anemia and low vitamin levels. Treatment is with high dose vitamin B12 injections initially then maintenance doses to correct the deficiency. Folate deficiency has similar blood features but no neurological involvement, and is treated with oral folic acid supplementation.
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.
Vitamin B12 deficiency is common in India, especially among vegetarians and the elderly. It causes hematological, neurological, gastrointestinal and vascular issues. The document discusses causes of B12 deficiency including pernicious anemia and intestinal malabsorption. Clinical manifestations and investigations for diagnosis are explained. Treatment involves lifelong B12 supplementation through injections or high dose oral supplements. Preventive measures for high risk groups like vegetarians and post-gastric surgery patients are also covered.
Cobalamin is also called vitamin b12.
Group of compounds called corrinoids (a group of cobalamin)- Coenzyme form: methylcobalamin and 5-deoxyadenosylcobalamin are forms of vitamin B12 in the human body- Humans can convert most of the other cobalamins into an active coenzyme form.
Once absorbed, cobalamin travels in the portal blood to the liver, and then to the rest ofthe body, bound to the transport protein, transcobalamin
Methionine synthase- converts homocysteine to methionine. Reduces blood homocysteine concentrations (reduces CVD).
Megaloblastic anemias are disorders characterized by defective nuclear maturation caused by impaired DNA synthesis, usually due to vitamin B12 or folate deficiencies. Vitamin B12 is produced by microorganisms and fungi and is present in animal foods. It plays an important role in DNA synthesis and the Krebs cycle. Pernicious anemia is a type of megaloblastic anemia characterized by gastric parietal cell atrophy leading to decreased intrinsic factor and gastric juices, resulting in vitamin B12 malabsorption.
This document discusses vitamin B12 deficiency. It covers the roles of vitamin B12, absorption, causes of deficiency, clinical presentation, laboratory findings, diagnosis, and treatment. The key points are:
- Vitamin B12 is a water-soluble vitamin involved in DNA synthesis and hematopoiesis. Deficiency can cause megaloblastic anemia and neurological issues.
- Absorption requires intrinsic factor in the ileum. Causes include pernicious anemia, gastric issues, malabsorption, vegetarian diets.
- Symptoms include anemia, neurological changes, gastrointestinal issues. Diagnosis involves low B12 levels and response to parenteral B12 treatment. Lifelong B12 replacement
Megaloblastic anemias are a group of disorders characterized by large, immature red blood cells in the bone marrow. They are caused by vitamin B12 or folate deficiency which prevents DNA synthesis. Common causes include pernicious anemia, malabsorption, medication use, and dietary deficiencies. Patients present with anemia, gastrointestinal symptoms, and neurological findings. Diagnosis involves blood tests showing low B12/folate and high MCV with hypersegmented neutrophils and megaloblasts on smear. Treatment is with lifelong B12 injections or high dose oral supplementation for B12 deficiency and oral folate for folate deficiency.
This document provides information on megaloblastic anemia, including its causes, signs and symptoms, and treatment. Megaloblastic anemia is a macrocytic anemia caused by vitamin B12 or folic acid deficiency, which impairs DNA synthesis and cell proliferation in red blood cell precursors. Common symptoms include paleness, fatigue, numbness, and neurological issues. Treatment involves administration of vitamin B12 and folic acid supplements to correct the deficiencies. Vitamin B12 exists in several forms used in treatment, with different regimens depending on the underlying cause of the megaloblastic anemia.
This document summarizes megaloblastic anemias caused by vitamin B12 deficiency. It describes the normal metabolism and absorption of vitamin B12, the causes of deficiency including pernicious anemia and diseases interfering with absorption. The morphological features in blood and bone marrow include macrocytic anemia and megaloblasts. Diagnosis involves low B12 levels, elevated methylmalonic acid and homocysteine, and an abnormal Schilling test. Treatment is lifelong intramuscular B12 injections.
There are two main types of macrocytic anemia - megaloblastic anemia and non-megaloblastic anemia. Megaloblastic anemia is caused by vitamin B12 or folate deficiency and is characterized by megaloblastic changes in the bone marrow and presence of oval macrocytes and hypersegmented neutrophils. Causes of vitamin B12 and folate deficiency include inadequate intake, malabsorption, increased requirements, impaired absorption or utilization. Deficiencies can cause neurological symptoms in addition to anemia. Diagnosis involves blood tests showing macrocytic anemia and markers of vitamin deficiency.
Vit b12 deficiency causes and managementrajeetam123
This document discusses vitamin B12 deficiency, including its structure, dietary sources, absorption, transport, storage, and metabolic roles. It also covers the causes, manifestations, and laboratory findings of B12 deficiency. The key points are:
1. Vitamin B12 is essential for DNA synthesis and fatty acid/amino acid metabolism. Deficiency can cause megaloblastic anemia and neurological issues.
2. Dietary sources are animal products. Absorption requires intrinsic factor in the ileum. Deficiency can be caused by pernicious anemia or other issues impairing absorption.
3. Manifestations include megaloblastic anemia, neurological changes, and other issues. Laboratory findings show macro
Megaloblastic anaemia (lecture for v year mbbs)mona aziz
Megaloblastic anemia results from vitamin B12 or folic acid deficiency. It causes impaired DNA synthesis and nucleocytoplasmic asynchrony in proliferating cells. Deficiencies in vitamin B12 or folic acid lead to elevated homocysteine and impaired conversion of uracil to thymidine, arresting cell development. This causes megaloblastic changes notably in the bone marrow and gastrointestinal tract. Neurological changes in B12 deficiency are due to demyelination. Investigations show macrocytic anemia and megaloblastic bone marrow changes. Treatment involves vitamin B12 injections and oral folic acid supplementation.
Information about megaloblastic anemia and it's etiology and its classification.
Vitmain b12 deficiencies
Folic acid deficiencies
Signs and symptoms of megaloblastic anemia
Neural tube defects
This document discusses vitamin B12 and folic acid deficiency, which can cause megaloblastic anemia. It provides details on the pathophysiology, sources, absorption, functions, and treatment of vitamin B12 and folic acid deficiency. Specifically, it explains that vitamin B12 and folic acid are essential for DNA synthesis and red blood cell formation. A deficiency impairs this process leading to large immature red blood cells (megaloblasts) and anemia. Pernicious anemia is an important cause of vitamin B12 deficiency due to autoimmune destruction of intrinsic factor. Treatment involves vitamin B12 and folic acid supplementation.
Megaloblastic anemia is caused by impaired DNA synthesis leading to ineffective red blood cell production. It results from vitamin B12 or folate deficiencies. Vitamin B12 is only produced by microorganisms and is obtained through animal products in the diet, while folate is found in many plant foods. Both are required as cofactors in important metabolic reactions. Deficiencies can be due to inadequate intake, impaired absorption, or genetic disorders affecting metabolism. Symptoms include megaloblastic changes in blood cells and pancytopenia.
This document discusses megaloblastic anemias, which result from deficiencies in vitamin B12 or folate. It causes ineffective hematopoiesis affecting all blood cell lines, particularly red blood cells (RBCs). Diagnosis is based on a complete blood count and peripheral smear showing a macrocytic anemia with large, oval RBCs and other abnormalities. Treatment involves treating the underlying deficiency of vitamin B12 or folate. The document also discusses nonmegaloblastic macrocytosis, which can occur due to other clinical factors unrelated to B12/folate deficiencies.
🔥🔥🔥🔥🔥🔥🔥🔥🔥
إضغ بين إيديكم من أقوى الملازم التي صممتها
ملزمة تشريح الجهاز الهيكلي (نظري 3)
💀💀💀💀💀💀💀💀💀💀
تتميز هذهِ الملزمة بعِدة مُميزات :
1- مُترجمة ترجمة تُناسب جميع المستويات
2- تحتوي على 78 رسم توضيحي لكل كلمة موجودة بالملزمة (لكل كلمة !!!!)
#فهم_ماكو_درخ
3- دقة الكتابة والصور عالية جداً جداً جداً
4- هُنالك بعض المعلومات تم توضيحها بشكل تفصيلي جداً (تُعتبر لدى الطالب أو الطالبة بإنها معلومات مُبهمة ومع ذلك تم توضيح هذهِ المعلومات المُبهمة بشكل تفصيلي جداً
5- الملزمة تشرح نفسها ب نفسها بس تكلك تعال اقراني
6- تحتوي الملزمة في اول سلايد على خارطة تتضمن جميع تفرُعات معلومات الجهاز الهيكلي المذكورة في هذهِ الملزمة
واخيراً هذهِ الملزمة حلالٌ عليكم وإتمنى منكم إن تدعولي بالخير والصحة والعافية فقط
كل التوفيق زملائي وزميلاتي ، زميلكم محمد الذهبي 💊💊
🔥🔥🔥🔥🔥🔥🔥🔥🔥
This document provides definitions and classifications for anemia. It begins by defining anemia based on hemoglobin concentration ranges for males, females, and pregnant females. It then discusses classifying anemia based on morphology, etiology/mechanism, impaired red blood cell production, hemolytic anemias, and blood loss. Specific types of anemia are then discussed in more detail, including iron deficiency anemia, vitamin B12 deficiency, folate deficiency, and anemia of chronic disease. Causes, clinical features, investigations, and treatment are outlined for each type.
Vitamin B12 deficiency can result in megaloblastic anemia characterized by large, immature red blood cells. It is most commonly caused by pernicious anemia where autoimmune destruction of gastric parietal cells leads to lack of intrinsic factor needed for vitamin B12 absorption. Clinical features include anemia, jaundice, and neurological problems. Diagnosis is based on morphological changes in blood and bone marrow showing megaloblasts, low vitamin B12 levels, and a positive Schilling test demonstrating impaired absorption. Treatment involves lifelong vitamin B12 injections or high dose oral supplementation.
Vitamin B12 and folate deficiencies can cause megaloblastic anemia due to impaired DNA synthesis. Vitamin B12 deficiency specifically can also cause neurological manifestations like peripheral neuropathy. Diagnosis involves blood tests showing macrocytic anemia and low vitamin levels. Treatment is with high dose vitamin B12 injections initially then maintenance doses to correct the deficiency. Folate deficiency has similar blood features but no neurological involvement, and is treated with oral folic acid supplementation.
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.
Vitamin B12 deficiency is common in India, especially among vegetarians and the elderly. It causes hematological, neurological, gastrointestinal and vascular issues. The document discusses causes of B12 deficiency including pernicious anemia and intestinal malabsorption. Clinical manifestations and investigations for diagnosis are explained. Treatment involves lifelong B12 supplementation through injections or high dose oral supplements. Preventive measures for high risk groups like vegetarians and post-gastric surgery patients are also covered.
Cobalamin is also called vitamin b12.
Group of compounds called corrinoids (a group of cobalamin)- Coenzyme form: methylcobalamin and 5-deoxyadenosylcobalamin are forms of vitamin B12 in the human body- Humans can convert most of the other cobalamins into an active coenzyme form.
Once absorbed, cobalamin travels in the portal blood to the liver, and then to the rest ofthe body, bound to the transport protein, transcobalamin
Methionine synthase- converts homocysteine to methionine. Reduces blood homocysteine concentrations (reduces CVD).
Megaloblastic anemias are disorders characterized by defective nuclear maturation caused by impaired DNA synthesis, usually due to vitamin B12 or folate deficiencies. Vitamin B12 is produced by microorganisms and fungi and is present in animal foods. It plays an important role in DNA synthesis and the Krebs cycle. Pernicious anemia is a type of megaloblastic anemia characterized by gastric parietal cell atrophy leading to decreased intrinsic factor and gastric juices, resulting in vitamin B12 malabsorption.
This document discusses vitamin B12 deficiency. It covers the roles of vitamin B12, absorption, causes of deficiency, clinical presentation, laboratory findings, diagnosis, and treatment. The key points are:
- Vitamin B12 is a water-soluble vitamin involved in DNA synthesis and hematopoiesis. Deficiency can cause megaloblastic anemia and neurological issues.
- Absorption requires intrinsic factor in the ileum. Causes include pernicious anemia, gastric issues, malabsorption, vegetarian diets.
- Symptoms include anemia, neurological changes, gastrointestinal issues. Diagnosis involves low B12 levels and response to parenteral B12 treatment. Lifelong B12 replacement
Megaloblastic anemias are a group of disorders characterized by large, immature red blood cells in the bone marrow. They are caused by vitamin B12 or folate deficiency which prevents DNA synthesis. Common causes include pernicious anemia, malabsorption, medication use, and dietary deficiencies. Patients present with anemia, gastrointestinal symptoms, and neurological findings. Diagnosis involves blood tests showing low B12/folate and high MCV with hypersegmented neutrophils and megaloblasts on smear. Treatment is with lifelong B12 injections or high dose oral supplementation for B12 deficiency and oral folate for folate deficiency.
This document provides information on megaloblastic anemia, including its causes, signs and symptoms, and treatment. Megaloblastic anemia is a macrocytic anemia caused by vitamin B12 or folic acid deficiency, which impairs DNA synthesis and cell proliferation in red blood cell precursors. Common symptoms include paleness, fatigue, numbness, and neurological issues. Treatment involves administration of vitamin B12 and folic acid supplements to correct the deficiencies. Vitamin B12 exists in several forms used in treatment, with different regimens depending on the underlying cause of the megaloblastic anemia.
This document summarizes megaloblastic anemias caused by vitamin B12 deficiency. It describes the normal metabolism and absorption of vitamin B12, the causes of deficiency including pernicious anemia and diseases interfering with absorption. The morphological features in blood and bone marrow include macrocytic anemia and megaloblasts. Diagnosis involves low B12 levels, elevated methylmalonic acid and homocysteine, and an abnormal Schilling test. Treatment is lifelong intramuscular B12 injections.
There are two main types of macrocytic anemia - megaloblastic anemia and non-megaloblastic anemia. Megaloblastic anemia is caused by vitamin B12 or folate deficiency and is characterized by megaloblastic changes in the bone marrow and presence of oval macrocytes and hypersegmented neutrophils. Causes of vitamin B12 and folate deficiency include inadequate intake, malabsorption, increased requirements, impaired absorption or utilization. Deficiencies can cause neurological symptoms in addition to anemia. Diagnosis involves blood tests showing macrocytic anemia and markers of vitamin deficiency.
Vit b12 deficiency causes and managementrajeetam123
This document discusses vitamin B12 deficiency, including its structure, dietary sources, absorption, transport, storage, and metabolic roles. It also covers the causes, manifestations, and laboratory findings of B12 deficiency. The key points are:
1. Vitamin B12 is essential for DNA synthesis and fatty acid/amino acid metabolism. Deficiency can cause megaloblastic anemia and neurological issues.
2. Dietary sources are animal products. Absorption requires intrinsic factor in the ileum. Deficiency can be caused by pernicious anemia or other issues impairing absorption.
3. Manifestations include megaloblastic anemia, neurological changes, and other issues. Laboratory findings show macro
Megaloblastic anaemia (lecture for v year mbbs)mona aziz
Megaloblastic anemia results from vitamin B12 or folic acid deficiency. It causes impaired DNA synthesis and nucleocytoplasmic asynchrony in proliferating cells. Deficiencies in vitamin B12 or folic acid lead to elevated homocysteine and impaired conversion of uracil to thymidine, arresting cell development. This causes megaloblastic changes notably in the bone marrow and gastrointestinal tract. Neurological changes in B12 deficiency are due to demyelination. Investigations show macrocytic anemia and megaloblastic bone marrow changes. Treatment involves vitamin B12 injections and oral folic acid supplementation.
Information about megaloblastic anemia and it's etiology and its classification.
Vitmain b12 deficiencies
Folic acid deficiencies
Signs and symptoms of megaloblastic anemia
Neural tube defects
This document discusses vitamin B12 and folic acid deficiency, which can cause megaloblastic anemia. It provides details on the pathophysiology, sources, absorption, functions, and treatment of vitamin B12 and folic acid deficiency. Specifically, it explains that vitamin B12 and folic acid are essential for DNA synthesis and red blood cell formation. A deficiency impairs this process leading to large immature red blood cells (megaloblasts) and anemia. Pernicious anemia is an important cause of vitamin B12 deficiency due to autoimmune destruction of intrinsic factor. Treatment involves vitamin B12 and folic acid supplementation.
Megaloblastic anemia is caused by impaired DNA synthesis leading to ineffective red blood cell production. It results from vitamin B12 or folate deficiencies. Vitamin B12 is only produced by microorganisms and is obtained through animal products in the diet, while folate is found in many plant foods. Both are required as cofactors in important metabolic reactions. Deficiencies can be due to inadequate intake, impaired absorption, or genetic disorders affecting metabolism. Symptoms include megaloblastic changes in blood cells and pancytopenia.
This document discusses megaloblastic anemias, which result from deficiencies in vitamin B12 or folate. It causes ineffective hematopoiesis affecting all blood cell lines, particularly red blood cells (RBCs). Diagnosis is based on a complete blood count and peripheral smear showing a macrocytic anemia with large, oval RBCs and other abnormalities. Treatment involves treating the underlying deficiency of vitamin B12 or folate. The document also discusses nonmegaloblastic macrocytosis, which can occur due to other clinical factors unrelated to B12/folate deficiencies.
🔥🔥🔥🔥🔥🔥🔥🔥🔥
إضغ بين إيديكم من أقوى الملازم التي صممتها
ملزمة تشريح الجهاز الهيكلي (نظري 3)
💀💀💀💀💀💀💀💀💀💀
تتميز هذهِ الملزمة بعِدة مُميزات :
1- مُترجمة ترجمة تُناسب جميع المستويات
2- تحتوي على 78 رسم توضيحي لكل كلمة موجودة بالملزمة (لكل كلمة !!!!)
#فهم_ماكو_درخ
3- دقة الكتابة والصور عالية جداً جداً جداً
4- هُنالك بعض المعلومات تم توضيحها بشكل تفصيلي جداً (تُعتبر لدى الطالب أو الطالبة بإنها معلومات مُبهمة ومع ذلك تم توضيح هذهِ المعلومات المُبهمة بشكل تفصيلي جداً
5- الملزمة تشرح نفسها ب نفسها بس تكلك تعال اقراني
6- تحتوي الملزمة في اول سلايد على خارطة تتضمن جميع تفرُعات معلومات الجهاز الهيكلي المذكورة في هذهِ الملزمة
واخيراً هذهِ الملزمة حلالٌ عليكم وإتمنى منكم إن تدعولي بالخير والصحة والعافية فقط
كل التوفيق زملائي وزميلاتي ، زميلكم محمد الذهبي 💊💊
🔥🔥🔥🔥🔥🔥🔥🔥🔥
A Free 200-Page eBook ~ Brain and Mind Exercise.pptxOH TEIK BIN
(A Free eBook comprising 3 Sets of Presentation of a selection of Puzzles, Brain Teasers and Thinking Problems to exercise both the mind and the Right and Left Brain. To help keep the mind and brain fit and healthy. Good for both the young and old alike.
Answers are given for all the puzzles and problems.)
With Metta,
Bro. Oh Teik Bin 🙏🤓🤔🥰
How Barcodes Can Be Leveraged Within Odoo 17Celine George
In this presentation, we will explore how barcodes can be leveraged within Odoo 17 to streamline our manufacturing processes. We will cover the configuration steps, how to utilize barcodes in different manufacturing scenarios, and the overall benefits of implementing this technology.
Philippine Edukasyong Pantahanan at Pangkabuhayan (EPP) CurriculumMJDuyan
(𝐓𝐋𝐄 𝟏𝟎𝟎) (𝐋𝐞𝐬𝐬𝐨𝐧 𝟏)-𝐏𝐫𝐞𝐥𝐢𝐦𝐬
𝐃𝐢𝐬𝐜𝐮𝐬𝐬 𝐭𝐡𝐞 𝐄𝐏𝐏 𝐂𝐮𝐫𝐫𝐢𝐜𝐮𝐥𝐮𝐦 𝐢𝐧 𝐭𝐡𝐞 𝐏𝐡𝐢𝐥𝐢𝐩𝐩𝐢𝐧𝐞𝐬:
- Understand the goals and objectives of the Edukasyong Pantahanan at Pangkabuhayan (EPP) curriculum, recognizing its importance in fostering practical life skills and values among students. Students will also be able to identify the key components and subjects covered, such as agriculture, home economics, industrial arts, and information and communication technology.
𝐄𝐱𝐩𝐥𝐚𝐢𝐧 𝐭𝐡𝐞 𝐍𝐚𝐭𝐮𝐫𝐞 𝐚𝐧𝐝 𝐒𝐜𝐨𝐩𝐞 𝐨𝐟 𝐚𝐧 𝐄𝐧𝐭𝐫𝐞𝐩𝐫𝐞𝐧𝐞𝐮𝐫:
-Define entrepreneurship, distinguishing it from general business activities by emphasizing its focus on innovation, risk-taking, and value creation. Students will describe the characteristics and traits of successful entrepreneurs, including their roles and responsibilities, and discuss the broader economic and social impacts of entrepreneurial activities on both local and global scales.
This document provides an overview of wound healing, its functions, stages, mechanisms, factors affecting it, and complications.
A wound is a break in the integrity of the skin or tissues, which may be associated with disruption of the structure and function.
Healing is the body’s response to injury in an attempt to restore normal structure and functions.
Healing can occur in two ways: Regeneration and Repair
There are 4 phases of wound healing: hemostasis, inflammation, proliferation, and remodeling. This document also describes the mechanism of wound healing. Factors that affect healing include infection, uncontrolled diabetes, poor nutrition, age, anemia, the presence of foreign bodies, etc.
Complications of wound healing like infection, hyperpigmentation of scar, contractures, and keloid formation.
THE SACRIFICE HOW PRO-PALESTINE PROTESTS STUDENTS ARE SACRIFICING TO CHANGE T...indexPub
The recent surge in pro-Palestine student activism has prompted significant responses from universities, ranging from negotiations and divestment commitments to increased transparency about investments in companies supporting the war on Gaza. This activism has led to the cessation of student encampments but also highlighted the substantial sacrifices made by students, including academic disruptions and personal risks. The primary drivers of these protests are poor university administration, lack of transparency, and inadequate communication between officials and students. This study examines the profound emotional, psychological, and professional impacts on students engaged in pro-Palestine protests, focusing on Generation Z's (Gen-Z) activism dynamics. This paper explores the significant sacrifices made by these students and even the professors supporting the pro-Palestine movement, with a focus on recent global movements. Through an in-depth analysis of printed and electronic media, the study examines the impacts of these sacrifices on the academic and personal lives of those involved. The paper highlights examples from various universities, demonstrating student activism's long-term and short-term effects, including disciplinary actions, social backlash, and career implications. The researchers also explore the broader implications of student sacrifices. The findings reveal that these sacrifices are driven by a profound commitment to justice and human rights, and are influenced by the increasing availability of information, peer interactions, and personal convictions. The study also discusses the broader implications of this activism, comparing it to historical precedents and assessing its potential to influence policy and public opinion. The emotional and psychological toll on student activists is significant, but their sense of purpose and community support mitigates some of these challenges. However, the researchers call for acknowledging the broader Impact of these sacrifices on the future global movement of FreePalestine.
3. Macrocytic Anemias
• In macrocytic anaemia the red cells are abnormally large
(mean corpuscular volume, MCV > 98 fL)
• There are several causes but they can be broadly subdivided
into megaloblastic and non-megaloblastic, based on the
appearance of developing erythroblasts in the bone marrow.
Megaloblastic :
• Vitamin B12 or folate deficiency
Non Megaloblastic:
• Alcohol, liver disease, myelodysplasia, aplastic anaemia, etc.
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4. MEGALOBLASTIC ANAEMIA
The megaloblastic anaemias are a group of disorders characterized
by
o Presence Megaloblast in Bone marrow,
o Oval macrocytic cells and Hyper segmented Neutrophils, giant
platelets
o Pancytopenia.
The cause is usually deficiency of either cobalamin (vitamin B 12 ) or
folate, but megaloblastic anaemia may arise because of inherited or
acquired abnormalities affecting the metabolism of these vitamins
or because of defects in DNA synthesis not related to
cobalamin or folate.
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5. Megaloblast
• Megaloblast describes a bone marrow cell that is part of the
factory making red cells that has become abnormally large
and has an abnormal appearance.
• Usually large oval shaped cells with large nucleus, open
chromatin, and due to nuclear cytoplasmic asynchronisim .
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6. CAUSES
• Cobalamin deficiency or abnormalities of cobalamin
metabolism.
• Folate deficiency or abnormalities of folate metabolism.
• Therapy with antifolate drugs. (e.g. methotrexate)
• Independent of either cobalamin or folate deficiency and
refractory to cobalamin and folate therapy.
• Therapy with drugs interfering with synthesis of DNA. (e.g.
cytosine arabinoside)
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8. Vitamin B12 Metabolism
Sources:
• This vitamin is synthesized in nature by microorganisms;
animals acquire it by eating other animal foods, by internal
production from intestinal bacteria (not in humans) or by
eating bacterially contaminated foods.
•
The vitamin consists of a small group of compounds, the
cobalamins, which have the same basic structure, with a
cobalt atom at the centre of a corrin ring which is attached
to a nucleotide portion
• The vitamin is found in foods of animal origin such as liver,
meat, fish and dairy products but does not occur in fruit,
cereals or vegetables.
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10. Vitamin B12 Absorption
• A normal diet contains a large excess of B 12 compared with
daily needs.
• B12 is released from protein - binding in food and is
combined with the glycoprotein intrinsic factor (IF) which is
synthesized by the gastric parietal cells.
• The IF – B12 complex can then bind to a specific surface
receptor for IF, cubilin, which then binds to a second protein,
amnionless, which directs endocytosis of the cubilin IF – B12
complex in the distal ileum where B12 is absorbed and IF
destroyed
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13. TRANSPORT:
• Vitamin B 12 is absorbed into portal blood where it becomes
attached to the plasma - binding protein transcobalamin.
TC 1: it is an α1 globulin synthesized by macrophages and
granulocyte, which carries from 70-90% of
circulating vitamin B12. Also called Haptocorrin.
• It is primarily a storage protein and its absence doesn’t
lead to clinical signs of B12 deficiency.
• Functionally dead
TC 2: It is a β-globulin and it is essential for transport of
vitamin B12 from one organ to the other and in and out
of cells. (Bone marrow and other tissues).
• Congenital deficiency of TC2 leads to severe
megaloblastic anaemia.
TC 3: Similar to TC1, binds only a small quantity of circulating
B12.
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14. Storage sites of Vitamin B12
• The total amount of vitamin B12 in the body is 2 to 5 mg
(adequate for 2 to 4 years).
• The major site of storage is the liver.
• Vitamin B12 is excreted through the bile and shedding of
intestinal epithelial cells.
• Most of the excreted vitamin B12 is again absorbed in the
intestine (enterohepatic circulation).
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15. FUNCTIONS
Vitamin B12 acting as co-enzyme for two important
biochemical reactions in humans:
The conversion of methylmalonyl-CoA to succinyl-CoA.
Synthesis of methionine from homocystine.
Vitamin B12 is required for maintenance of the
integrity of nervous system.
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16. Biochemical Function
• Vitamin B 12 is a coenzyme for two biochemical reactions in
the body:
• First, as methyl B 12 it is a cofactor for methionine synthase,
the enzyme responsible for methylation of homocysteine to
methionine using methyl tetrahydrofolate (methyl THF) as
methyl donor and,
• Secondly, as deoxyadenosyl B 12 (ado B 12 ) it assists in
conversion of methylmalonyl coenzyme A (CoA) to succinyl
CoA.
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18. MEGALOBLASTIC ANAEMIA DUE
TO VITAMIN B12 DEFICIENCY
MECHANISM DISORDER
Decreased intake Nutritional deficiency
Impaired absorption
i). Gastric causes Pernicious anaemia
Gastrectomy (total or partial)
ii). Intestinal causes Lesions of small intestine
Coeliac disease
Tropical Sprue
Tapeworm Infestation
Zollinger -Ellison Syndrome
Abnormalities of cobalamin metabolism
i). Transport protein defects Inherited TC 2 deficiency
ii). Congenital intrinsic factor Present before the age of two
deficiency years
iii). Congenital methylmalonic acidaemia Infants are ill from birth
and aciduria
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19. METABOLISM OF FOLATE
• Folic acid (Pteroylglutamic) was synthesized as a yellow crystalline
powder.
• Folic acid doesn’t exist as such in nature, but is a parent compound
of a large number of derivatives referred to as folates which plays an
important role as co-enzymes in cellular metabolism.
• Reduction to dihydro - and tetrahydrofolate derivatives is necessary
to participate in metabolic reactions.
Sources:
Contents in food Green Vegetables: rich
Meat: moderate
Effect of cooking 60-90% loss
Adult daily requirements 200 micro gram
Adult daily intake 100-150 micro gram
Site of absorption Duodenum & jejunum
Body stores 10-12 mg
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20. ABSORPTION:
• Normally absorbed from duodenum and upper jejunum and to a
lesser extent from lower jejunum and ileum.
• Absorption of folate is a rapid active process 80% is absorbed
unchanged.
• Synthetic polyglutamates are absorbed as well as
monoglutamates.
• Polyglutamates are cleaved to monoglutamates by the enzyme
pteroylpolyglutamate conjugase.
• Monoglutamates than undergo reduction and enters in
circulation as methyltetrahydrofolate.
TRANSPORT:
• Folate circulates in plasma as methyltetrahydrofolate
monoglutamate, either in a free form or weekly bound to a
variety of proteins.
STORAGE:
• Liver is the main site of storage where it is stored mainly as
methyl tetrahydrofolate polyglutamate.
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21. FUNCTION
Folate co-enzymes are required for several bio-chemical
reactions in the body involving transfer of one-carbon units
from one compound to another.
Two reactions that are important in the context of clinical
folate deficiency are:
Methylation of homocysteine to methionine.
Synthesis of pyrimidine nucleotide, thymidylate
monophosphate from deoxyuridylate monophosphate
in the DNA synthesis pathway.
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24. Pathophysiology
• In megaloblastic anaemia, the anaemia results from failure
of the megaloblastic bone marrow to compensate for a
moderate reduction in red cell life span.
• Red cell survival studies have shown the presence of mild
haemolysis.
• Lack of vitamin B12 or folate causing slowing of DNA
synthesis in developing erythroblasts with an accumulation
of cells in premitotic phase of cell cycle.
• Some of these cells die within the marrow.
• The neutropenia and thrombocytopenia also appear to
result from ineffective production by abnormal precursor
cells in the marrow.
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26. PATHOGENESIS
• Both vitamin B12 and folic acid are required for ordered
DNA synthesis.
• But due to deficiency of vitmain B12 & folic acid in
megaloblastic anaemia DNA synthesis is impaired or
blocked in rapidly dividing cells.
• As a result the cells proliferates abnormally and increases
in size and become megaloblasts which are fully
heamoglobinized cells and abnormal in appearance and
function.
• Because of their increased size they occupy much of the
space in marrow and they disturb other cell lines too.
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27. MASKED MEGALOBLASTIC
ANAEMIA
• In certain megaloblastic anaemias , iron deficiency is
sometimes present at the same time as folate or B12
deficiency.
• Associated iron deficiency may partly mask the typical
haematological features of megaloblastic anaemia.
• PF showes double population (dimorphic blood picture) some
red cells being oval and well haemoglobinized, and others
small and poorly haemoglobinized.
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28. MASKED MEGALOBLASTIC
ANAEMIA
• In other cases masking takes the form of a lesser degree of
macrocytosis, so that most cells are of normal size and MCV is
normal or even mildly reduced.
• However, careful scrutiny of blood film shows a small no. of
oval macrocytes and hypersegmented neutrophils.
Other disorders:
• Thalassaemia, Infection, chronic renal disease, rheumatoid
arthritis.
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29. Pernicious Anemia
• This is caused by autoimmune attack on the gastric mucosa
leading to atrophy of the stomach. The wall of the stomach
becomes thin.
• There is achlorhydria and secretion of IF is absent or almost
absent. Serum gastrin levels are raised.
• Helicobater pylori infection may initiate an autoimmune
gastritis which presents in younger subjects as iron deficiency
and in the elderly as pernicious anaemia.
• More females than males are aff ected (1.6 : 1), with a peak
occurrence at 60 years, and there may be associated
autoimmune disease including the autoimmune
polyendocrine syndrome
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30. CLINICAL MANIFESTATIONS
Features of anaemia: Pallor, anorexia, weight loss,
diarrhoea.
i). Macrocytic megaloblastic anaemia.
ii). Glossitis.
iii). Subacute combined degeneration
(demyelination) of spinal cord due to vit B12
deficiency
iv). Perephral neuropathy and Neural tube defects
due to Vit B12 or Folate deficiency
NOTE: Deficiency of folate doesn’t produce sub-acute
combined degeneration of spinal cord, but peripheral
neuropathy is occasionally seen.
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43. Thrombopoiesis
• Megakaryocytes may
be decreased, normal,
or increased.
• Maturation, however, is distinctly
abnormal.
• Some larger than normal forms can
be found with separation
of nuclear lobes and
fregments
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44. Grannulopoiesis
• Is abnormal large as
typical granulocytes giant
metamyelocytes(30µm)
and bands with loose,
open chromatin in the
nuclei are diagnostic.
• Myelocytes show poor
granulation more mature
stages
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47. SPECIAL TESTS
Serum vitamin B12 assay:
It is performed by two ways:
• Microbiological assay.
• Radio-isotope assay.
Radioactive vitamin B12 absorption test:
The ability of body to
absorb vitamin B12 can be assessed by measuring the
absorption of a small dose of Co- labelled vitamin B12.
The test is called Schilling test.
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48. SCHILLING TEST
• An oral dose of 1 micro gram radioactive vitamin B12 is
administered to the fasting subject followed two hours later
by a large parenteral injection of unlabelled B12(1000 micro
gm).
• The injection flushes out about one-third of absorbed
radioactive B12 into the urine in the next 24 hours.
• Normal subject excretes 10% of 1 micro gm dose. Patients
with pernicious anaemia excrete less than 5%. If the patient
absorbs normal amounts of vitamin B12 no further testing is
required.
UNSATURATED B12 BINDING CAPACITY
• Measurement of unsaturated B12 binding capacity which in
the normal subject reflects the amount of TC2 and to a lesser
extent TC1 & TC3, may be diagnostically useful. Normal range
is 500-1200 ng/l.
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49. Deoxyuridine Suppression Test
• In normal bone marrow, dU considerably suppresses the
uptake of radioactive thymidine into DNA.
• This is thought to be due to conversion of dU to thymidine
triphosphate via dUMP, which inhibits thymidine kinase, on
which thymidine uptake depends.
• Deoxyuridine suppresses radioactive thymidine incorporation
less effectively in meg. Anaemia due to folate or cobalamin
deficiency because of the block in dUMP methylation to
dTMP.
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50. Tests for the cause of cobalamin
deficiency
Clinical History :diet, drugs,operation etc.
Cobalamin absorption using radioactive cobalamin: Alone,
with food, with intrinsic factor.
Tests for tissue specific antibodies in serum (e.g. IF, parietal
cells etc)
Endoscopy with gastric biopsy.
Measurement of intrinsic factor in gastric juice after maximal
stimulation. (rarely performed)
Small intestinal studies.
Stool for fish tapeworm ova.
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51. SERUM FOLATE ASSAY
• Microbiological Assay.
• Radio-isotope Assay.
(Levels below 3micro gm/l suggest clinically significant folate
deficiency).
RED CELL FOLATE ASSAY
• Red cells contain 20-50 times as much folate as serum.
• It is usually a more reliable indicator of tissue folate stores
than the serum folate.
• It reflects mean folate that existed in plasma during
maturation of precursors.
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52. Parietal cell antibodies:
• Serum antibodies to surface membrane
and cytoplasmic antigens of gastric parietal cells are found in at
least 85% of patients with pernicious anaemia.
Intrinsic factor antibodies:
Two types of antibodies are found:
Blocking antibodies.
Binding antibodies.
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