Vitamin B12- Chemical structure, Forms of B12, Sources, absorption, storage, transportation, metabolic role, deficiency, megaloblastic anemia and neurological changes, laboratory diagnosis and treatment
Folic acid is a water-soluble B vitamin that acts as a coenzyme in single-carbon transfers in amino acid and nucleotide metabolism. It is required for DNA synthesis and cell division. A deficiency can lead to megaloblastic anemia due to impaired DNA synthesis. Rich dietary sources include green leafy vegetables. Folic acid supplementation is important during pregnancy to prevent neural tube defects in newborns.
Vitamin B12- definition, functions, absorption, storage, transportation, deficiency, pernicious anemia, relationship between vitamin B12 and folate deficiency, sign & symptoms, deficiency in case of maternal & child health care, RDA, sources, prevention and treatment.
Vitamin B12, also called cobalamin, is a water-soluble vitamin that plays a key role in the functioning of the brain and nervous system. It is involved in DNA synthesis, fatty acid and amino acid metabolism. Vitamin B12 is produced by bacteria and archaea and is found naturally in animal products like meat, eggs and dairy. Deficiency can cause fatigue, neurological problems, and psychosis. It is used to treat deficiency, cyanide poisoning, and hereditary conditions.
Vitamin B12, also known as cobalamin, is an essential water-soluble vitamin that contains cobalt. It plays critical roles in DNA synthesis, neurological function, and energy production. A deficiency can result in megaloblastic anemia and neurological disorders due to its roles in methylation reactions and DNA synthesis. Rich dietary sources include meat, eggs, dairy products, and fish. Absorption requires intrinsic factor produced by stomach parietal cells. Storage occurs mainly in the liver bound to transport proteins.
VITAMIN B3
GUL MUNEER
Niacin
Niacinamide 0R Nicotinamide
Vitamin P OR PP (pellagra preventive)
Pellagra preventive factor
Anti black tongue factor
Nicotinic acid
Vitamin G (after Goldberger’s death, vitamin B3 was some times called in his honor)
Structure of Vitamin B3
Function of Vitamin B3
DISCOVERY of Vitamin B3
PROPERTIES of Vitamin B3
Nicotinic Acid (Plant form)
CHEMISTRY of Vitamin B3
Sources of Vitamin B3
RECOMMENDED DAILY ALLOWANCE (RDA) of Vitamin B3
BIOCHEMICAL FUNCTIONS of Vitamin B3
Digestion and Absorption of Dietary Niacin
Metabolism of B-3
Deficiency of B3
Selenium is an essential mineral that plays an important antioxidant role in the body. It is present in tissues like the liver at around 10 mg total. Sources of selenium include meats, seafood, grains and organs like liver and kidney. Selenium is absorbed in the duodenum and transported bound to proteins in the bloodstream. It is mainly excreted through urine and has a recommended daily intake of 50-200 μg. Selenium is an important component of the antioxidant enzyme glutathione peroxidase, which helps convert harmful oxygen free radicals into less toxic forms. It also aids in thyroid hormone conversion and protects against heavy metal toxicity. Selenium deficiency can result in conditions like cardiomyopathy, muscular dystrophy and Keshan disease.
Folic acid is essential for one carbon metabolism and the synthesis of DNA, RNA, and proteins. Rich sources include green leafy vegetables and yeast. Deficiency can cause megaloblastic anemia and fetal neural tube defects. It is caused by inadequate intake, increased need during pregnancy, malabsorption, medications, and B12 deficiency trapping folate. Symptoms include fatigue, sore tongue, and neurological issues. Diagnosis involves blood tests of folate, B12, and homocysteine levels. Treatment is oral folic acid supplementation.
Folic acid is a water-soluble B vitamin that acts as a coenzyme in single-carbon transfers in amino acid and nucleotide metabolism. It is required for DNA synthesis and cell division. A deficiency can lead to megaloblastic anemia due to impaired DNA synthesis. Rich dietary sources include green leafy vegetables. Folic acid supplementation is important during pregnancy to prevent neural tube defects in newborns.
Vitamin B12- definition, functions, absorption, storage, transportation, deficiency, pernicious anemia, relationship between vitamin B12 and folate deficiency, sign & symptoms, deficiency in case of maternal & child health care, RDA, sources, prevention and treatment.
Vitamin B12, also called cobalamin, is a water-soluble vitamin that plays a key role in the functioning of the brain and nervous system. It is involved in DNA synthesis, fatty acid and amino acid metabolism. Vitamin B12 is produced by bacteria and archaea and is found naturally in animal products like meat, eggs and dairy. Deficiency can cause fatigue, neurological problems, and psychosis. It is used to treat deficiency, cyanide poisoning, and hereditary conditions.
Vitamin B12, also known as cobalamin, is an essential water-soluble vitamin that contains cobalt. It plays critical roles in DNA synthesis, neurological function, and energy production. A deficiency can result in megaloblastic anemia and neurological disorders due to its roles in methylation reactions and DNA synthesis. Rich dietary sources include meat, eggs, dairy products, and fish. Absorption requires intrinsic factor produced by stomach parietal cells. Storage occurs mainly in the liver bound to transport proteins.
VITAMIN B3
GUL MUNEER
Niacin
Niacinamide 0R Nicotinamide
Vitamin P OR PP (pellagra preventive)
Pellagra preventive factor
Anti black tongue factor
Nicotinic acid
Vitamin G (after Goldberger’s death, vitamin B3 was some times called in his honor)
Structure of Vitamin B3
Function of Vitamin B3
DISCOVERY of Vitamin B3
PROPERTIES of Vitamin B3
Nicotinic Acid (Plant form)
CHEMISTRY of Vitamin B3
Sources of Vitamin B3
RECOMMENDED DAILY ALLOWANCE (RDA) of Vitamin B3
BIOCHEMICAL FUNCTIONS of Vitamin B3
Digestion and Absorption of Dietary Niacin
Metabolism of B-3
Deficiency of B3
Selenium is an essential mineral that plays an important antioxidant role in the body. It is present in tissues like the liver at around 10 mg total. Sources of selenium include meats, seafood, grains and organs like liver and kidney. Selenium is absorbed in the duodenum and transported bound to proteins in the bloodstream. It is mainly excreted through urine and has a recommended daily intake of 50-200 μg. Selenium is an important component of the antioxidant enzyme glutathione peroxidase, which helps convert harmful oxygen free radicals into less toxic forms. It also aids in thyroid hormone conversion and protects against heavy metal toxicity. Selenium deficiency can result in conditions like cardiomyopathy, muscular dystrophy and Keshan disease.
Folic acid is essential for one carbon metabolism and the synthesis of DNA, RNA, and proteins. Rich sources include green leafy vegetables and yeast. Deficiency can cause megaloblastic anemia and fetal neural tube defects. It is caused by inadequate intake, increased need during pregnancy, malabsorption, medications, and B12 deficiency trapping folate. Symptoms include fatigue, sore tongue, and neurological issues. Diagnosis involves blood tests of folate, B12, and homocysteine levels. Treatment is oral folic acid supplementation.
Biotin is a water-soluble B vitamin and coenzyme that is essential for carboxylation reactions in metabolism. It is required by the enzymes pyruvate carboxylase, acetyl-CoA carboxylase, propionyl-CoA carboxylase, and β-methylcrotonyl-CoA carboxylase, which are involved in glucose metabolism, fatty acid synthesis, and amino acid catabolism. Biotin deficiency is rare in humans due to its presence in many foods and synthesis by gut bacteria, but can cause dermatitis, weakness, and nausea. Avidin in raw egg whites binds strongly to biotin and prevents its absorption.
1) The Schilling test evaluates a patient's ability to absorb vitamin B12 by measuring the amount of radioactive B12 excreted in urine after oral administration.
2) If a patient can absorb B12 normally, the radioactive B12 will enter the bloodstream and be excreted in urine. If absorption is impaired, it will pass through the digestive tract and be excreted in feces.
3) Giving intrinsic factor along with radioactive B12 can determine if a patient's B12 absorption issue is due to intrinsic factor deficiency, as is the case with pernicious anemia.
Niacin, or vitamin B3, is an essential vitamin that acts as a coenzyme in many metabolic reactions related to energy production. It is synthesized from the amino acid tryptophan. Niacin deficiency causes the disease pellagra, with symptoms of dermatitis, diarrhea, and dementia. Treatment of pellagra involves niacin supplementation. Therapeutically, niacin is used to treat hypercholesterolemia and hypertriglyceridemia by lowering LDL and VLDL cholesterol levels and raising HDL levels.
Pantothenic acid, also known as vitamin B5, is essential for the synthesis of coenzyme A (CoA) which plays a key role in numerous metabolic pathways. It is absorbed in the small intestine and transported to tissues where it is phosphorylated and linked to cysteine to form 4'-phosphopantetheine, which is then converted to dephospho-CoA and CoA. CoA is involved in the synthesis of fatty acids, cholesterol, amino acids, and ketone bodies as well as the oxidation of pyruvate and fatty acids through acetyl-CoA in the citric acid cycle. Deficiency of pantothenic acid is rare but can cause burning feet syndrome in experimental
1. Vitamin D3 is synthesized in the skin by exposure to sunlight and is converted to calcitriol, the biologically active form, in the kidney.
2. Calcitriol acts on the intestine, bone, and kidney to regulate calcium levels by increasing calcium absorption from the intestine, mobilizing calcium from bone, and enhancing calcium reabsorption in the kidney.
3. Vitamin D deficiency causes rickets in children, characterized by bone deformities and softening, and osteomalacia in adults, characterized by demineralization of bones.
Thiamine (vitamin B1) is a water-soluble vitamin that acts as a coenzyme in carbohydrate metabolism. It contains pyrimidine and thiazole rings connected by a methylene bridge. Thiamine is converted to its active coenzyme form, thiamine pyrophosphate (TPP), which is involved in several metabolic reactions like pyruvate dehydrogenase complex and transketolase. Deficiency of thiamine causes beriberi disease characterized by peripheral neuropathy or heart failure.
Vitamin B12, also known as cobalamin, is a water-soluble vitamin that plays a key role in normal brain and nervous system function and blood formation. It was first discovered in the late 1920s as the substance that cured pernicious anemia. Vitamin B12 exists in several forms including cyanocobalamin, methylcobalamin, and hydroxocobalamin. It is produced through fermentation by microorganisms but not by plants or animals. Good dietary sources include meat, fish, eggs, and dairy products. Vitamin B12 deficiency can cause megaloblastic anemia and neurological problems if left untreated.
- Iron is an essential trace element that is present in many proteins and enzymes in the body. It is required to transport oxygen via hemoglobin and is involved in many redox reactions in the body.
- Iron is absorbed in the small intestine and transported through the blood bound to transferrin. It is stored in the liver, spleen and bone marrow bound to ferritin.
- Disorders of iron metabolism include iron deficiency anemia due to low intake or absorption of iron and iron overload disorders like hemochromatosis where iron accumulates in tissues and can damage organs like the liver, pancreas and heart.
Vitamin D has two main forms, D2 and D3. It is a steroid compound that plays an essential role in regulating calcium and phosphorus metabolism. The active form, calcitriol, maintains normal plasma calcium and phosphorus levels by acting on the intestine, bone, and kidneys. A vitamin D deficiency can lead to rickets in children, characterized by soft bones and skeletal deformities.
This document discusses folic acid and vitamin B12. It describes:
1) Folic acid is present in vegetables and consists of three parts. It is involved in DNA synthesis and preventing cancer and heart disease.
2) Deficiencies can result from pregnancy, malabsorption, drugs that inhibit enzyme activity, and lack of vegetables in the diet. This leads to megaloblastic anemia.
3) Vitamin B12 contains cobalt and is only found in animal products. Deficiencies can result from gastric issues or lack of intrinsic factor leading to neurological problems like subacute combined degeneration of the spinal cord.
B vitamins are a class of water-soluble vitamins that play important roles in cell metabolism. Though these vitamins share similar names, research shows that they are chemically distinct vitamins that often coexist in the same foods. In general, supplements containing all eight are referred to as a vitamin B complex. Individual B vitamin supplements are referred to by the specific name of each vitamin (e.g., B1, B2, B3 etc.).
Riboflavin, also known as vitamin B2, is a yellow pigment that contains a 6,7-dimethylisoalloxazine ring. It functions as an important cofactor in redox reactions as FMN and FAD. Riboflavin is absorbed in the small intestine and transported to tissues like the liver, where it is converted to its coenzyme forms. Deficiency can cause cheilosis, glossitis and corneal vascularization. Rich dietary sources include milk, meat, eggs and liver.
The document discusses the urea cycle, which involves a cyclic set of chemical reactions that occur in the liver to convert ammonia into urea for excretion. It details the 5 enzyme-catalyzed reactions, participating amino acids and cofactors. One molecule of urea requires 3 ATP and utilizes ammonia, bicarbonate, and aspartate. The cycle is regulated by N-acetyl glutamate and compartmentalized between mitochondria and cytosol. Disorders cause hyperammonemia due to deficient enzymes, with earlier blocks causing more severe symptoms like vomiting and lethargy.
This document discusses creatine, creatinine, and creatine kinase (CK). It explains that creatine is synthesized in the liver and kidneys and stored in muscles, where it is converted to phosphocreatine to provide energy. Creatinine is a breakdown product of creatine and phosphocreatine. Serum creatinine levels indicate kidney function, while CK levels indicate damage to heart and skeletal muscles. The document outlines creatine synthesis and breakdown, the roles and clinical importance of creatinine and CK, and how they are used as biomarkers.
Vitamin A is a fat-soluble vitamin that exists in multiple forms including retinol, retinal, and retinoic acid. It plays an essential role in vision, cell growth and differentiation. Vitamin A is absorbed in the small intestine and transported to the liver where it is stored. A deficiency can impair vision and cause dry eyes and corneal ulceration or blindness in severe cases. The recommended daily intake is 400-1000 μg depending on age, sex and life stage.
Pyridoxine (vitamin B6) is a water-soluble vitamin that exists as three closely related compounds - pyridoxine, pyridoxal, and pyridoxamine. All three can be converted to the active coenzyme form, pyridoxal phosphate (PLP), which is involved in many important metabolic processes like amino acid metabolism, synthesis of neurotransmitters and heme. Deficiency of vitamin B6 can cause neurological, dermatological and hematological issues due to impairment of these metabolic pathways. While essential for many functions, excess intake of vitamin B6 beyond recommended limits may cause sensory neuropathy.
B12 metabolism..................................... and role of various proteins in b12 metabolism..... necessity of supplementation..........................................
This document discusses vitamin C, including its functions, dietary sources, and the clinical features of scurvy resulting from vitamin C deficiency. Key points include:
- Vitamin C is a water-soluble vitamin that functions as an antioxidant and is necessary for collagen synthesis. It supports iron absorption and plays roles in neurotransmitter and steroid synthesis.
- Good dietary sources include amla, guava, citrus fruits, and green leafy vegetables.
- Scurvy results from vitamin C deficiency and causes bleeding gums, tooth loss, bruising and bleeding into joints and skin. Bone growth is impaired in children with scurvy.
Vitamin B3, also known as niacin, is a water-soluble vitamin that exists in two forms - nicotinamide and nicotinic acid. It is the precursor to the important coenzymes NAD+ and NADP+, which participate in many oxidation-reduction reactions during carbohydrate, lipid, and protein metabolism. As a result, niacin plays a key role in generating energy through the electron transport chain.
This document discusses vitamin B12, including its structure, functions, deficiency, production, and uses. It provides details on the microbial production of cyanocobalamin (vitamin B12) through fermentation using Propionibacterium shermanii. The process involves anaerobic fermentation to produce precursors, aerobic fermentation, cell harvesting, acid treatment to release precursors, addition of cyanide to produce cyanocobalamin, and downstream purification using chromatography and crystallization. Vitamin B12 is important for normal functioning of the brain/nervous system, blood formation, and cellular metabolism. Deficiency can cause anemia and fatigue.
Vitamin B12 is essential for normal cell metabolism and DNA synthesis. Deficiency can result from inadequate dietary intake or impaired absorption. Initial signs include fatigue and pallor, while long-term deficiency leads to megaloblastic anemia and peripheral neuropathy. Diagnosis involves measuring serum B12 levels along with metabolites like methylmalonic acid and homocysteine, which increase with deficiency. The Schilling test evaluates absorption by measuring urinary excretion of radioactive B12.
Biotin is a water-soluble B vitamin and coenzyme that is essential for carboxylation reactions in metabolism. It is required by the enzymes pyruvate carboxylase, acetyl-CoA carboxylase, propionyl-CoA carboxylase, and β-methylcrotonyl-CoA carboxylase, which are involved in glucose metabolism, fatty acid synthesis, and amino acid catabolism. Biotin deficiency is rare in humans due to its presence in many foods and synthesis by gut bacteria, but can cause dermatitis, weakness, and nausea. Avidin in raw egg whites binds strongly to biotin and prevents its absorption.
1) The Schilling test evaluates a patient's ability to absorb vitamin B12 by measuring the amount of radioactive B12 excreted in urine after oral administration.
2) If a patient can absorb B12 normally, the radioactive B12 will enter the bloodstream and be excreted in urine. If absorption is impaired, it will pass through the digestive tract and be excreted in feces.
3) Giving intrinsic factor along with radioactive B12 can determine if a patient's B12 absorption issue is due to intrinsic factor deficiency, as is the case with pernicious anemia.
Niacin, or vitamin B3, is an essential vitamin that acts as a coenzyme in many metabolic reactions related to energy production. It is synthesized from the amino acid tryptophan. Niacin deficiency causes the disease pellagra, with symptoms of dermatitis, diarrhea, and dementia. Treatment of pellagra involves niacin supplementation. Therapeutically, niacin is used to treat hypercholesterolemia and hypertriglyceridemia by lowering LDL and VLDL cholesterol levels and raising HDL levels.
Pantothenic acid, also known as vitamin B5, is essential for the synthesis of coenzyme A (CoA) which plays a key role in numerous metabolic pathways. It is absorbed in the small intestine and transported to tissues where it is phosphorylated and linked to cysteine to form 4'-phosphopantetheine, which is then converted to dephospho-CoA and CoA. CoA is involved in the synthesis of fatty acids, cholesterol, amino acids, and ketone bodies as well as the oxidation of pyruvate and fatty acids through acetyl-CoA in the citric acid cycle. Deficiency of pantothenic acid is rare but can cause burning feet syndrome in experimental
1. Vitamin D3 is synthesized in the skin by exposure to sunlight and is converted to calcitriol, the biologically active form, in the kidney.
2. Calcitriol acts on the intestine, bone, and kidney to regulate calcium levels by increasing calcium absorption from the intestine, mobilizing calcium from bone, and enhancing calcium reabsorption in the kidney.
3. Vitamin D deficiency causes rickets in children, characterized by bone deformities and softening, and osteomalacia in adults, characterized by demineralization of bones.
Thiamine (vitamin B1) is a water-soluble vitamin that acts as a coenzyme in carbohydrate metabolism. It contains pyrimidine and thiazole rings connected by a methylene bridge. Thiamine is converted to its active coenzyme form, thiamine pyrophosphate (TPP), which is involved in several metabolic reactions like pyruvate dehydrogenase complex and transketolase. Deficiency of thiamine causes beriberi disease characterized by peripheral neuropathy or heart failure.
Vitamin B12, also known as cobalamin, is a water-soluble vitamin that plays a key role in normal brain and nervous system function and blood formation. It was first discovered in the late 1920s as the substance that cured pernicious anemia. Vitamin B12 exists in several forms including cyanocobalamin, methylcobalamin, and hydroxocobalamin. It is produced through fermentation by microorganisms but not by plants or animals. Good dietary sources include meat, fish, eggs, and dairy products. Vitamin B12 deficiency can cause megaloblastic anemia and neurological problems if left untreated.
- Iron is an essential trace element that is present in many proteins and enzymes in the body. It is required to transport oxygen via hemoglobin and is involved in many redox reactions in the body.
- Iron is absorbed in the small intestine and transported through the blood bound to transferrin. It is stored in the liver, spleen and bone marrow bound to ferritin.
- Disorders of iron metabolism include iron deficiency anemia due to low intake or absorption of iron and iron overload disorders like hemochromatosis where iron accumulates in tissues and can damage organs like the liver, pancreas and heart.
Vitamin D has two main forms, D2 and D3. It is a steroid compound that plays an essential role in regulating calcium and phosphorus metabolism. The active form, calcitriol, maintains normal plasma calcium and phosphorus levels by acting on the intestine, bone, and kidneys. A vitamin D deficiency can lead to rickets in children, characterized by soft bones and skeletal deformities.
This document discusses folic acid and vitamin B12. It describes:
1) Folic acid is present in vegetables and consists of three parts. It is involved in DNA synthesis and preventing cancer and heart disease.
2) Deficiencies can result from pregnancy, malabsorption, drugs that inhibit enzyme activity, and lack of vegetables in the diet. This leads to megaloblastic anemia.
3) Vitamin B12 contains cobalt and is only found in animal products. Deficiencies can result from gastric issues or lack of intrinsic factor leading to neurological problems like subacute combined degeneration of the spinal cord.
B vitamins are a class of water-soluble vitamins that play important roles in cell metabolism. Though these vitamins share similar names, research shows that they are chemically distinct vitamins that often coexist in the same foods. In general, supplements containing all eight are referred to as a vitamin B complex. Individual B vitamin supplements are referred to by the specific name of each vitamin (e.g., B1, B2, B3 etc.).
Riboflavin, also known as vitamin B2, is a yellow pigment that contains a 6,7-dimethylisoalloxazine ring. It functions as an important cofactor in redox reactions as FMN and FAD. Riboflavin is absorbed in the small intestine and transported to tissues like the liver, where it is converted to its coenzyme forms. Deficiency can cause cheilosis, glossitis and corneal vascularization. Rich dietary sources include milk, meat, eggs and liver.
The document discusses the urea cycle, which involves a cyclic set of chemical reactions that occur in the liver to convert ammonia into urea for excretion. It details the 5 enzyme-catalyzed reactions, participating amino acids and cofactors. One molecule of urea requires 3 ATP and utilizes ammonia, bicarbonate, and aspartate. The cycle is regulated by N-acetyl glutamate and compartmentalized between mitochondria and cytosol. Disorders cause hyperammonemia due to deficient enzymes, with earlier blocks causing more severe symptoms like vomiting and lethargy.
This document discusses creatine, creatinine, and creatine kinase (CK). It explains that creatine is synthesized in the liver and kidneys and stored in muscles, where it is converted to phosphocreatine to provide energy. Creatinine is a breakdown product of creatine and phosphocreatine. Serum creatinine levels indicate kidney function, while CK levels indicate damage to heart and skeletal muscles. The document outlines creatine synthesis and breakdown, the roles and clinical importance of creatinine and CK, and how they are used as biomarkers.
Vitamin A is a fat-soluble vitamin that exists in multiple forms including retinol, retinal, and retinoic acid. It plays an essential role in vision, cell growth and differentiation. Vitamin A is absorbed in the small intestine and transported to the liver where it is stored. A deficiency can impair vision and cause dry eyes and corneal ulceration or blindness in severe cases. The recommended daily intake is 400-1000 μg depending on age, sex and life stage.
Pyridoxine (vitamin B6) is a water-soluble vitamin that exists as three closely related compounds - pyridoxine, pyridoxal, and pyridoxamine. All three can be converted to the active coenzyme form, pyridoxal phosphate (PLP), which is involved in many important metabolic processes like amino acid metabolism, synthesis of neurotransmitters and heme. Deficiency of vitamin B6 can cause neurological, dermatological and hematological issues due to impairment of these metabolic pathways. While essential for many functions, excess intake of vitamin B6 beyond recommended limits may cause sensory neuropathy.
B12 metabolism..................................... and role of various proteins in b12 metabolism..... necessity of supplementation..........................................
This document discusses vitamin C, including its functions, dietary sources, and the clinical features of scurvy resulting from vitamin C deficiency. Key points include:
- Vitamin C is a water-soluble vitamin that functions as an antioxidant and is necessary for collagen synthesis. It supports iron absorption and plays roles in neurotransmitter and steroid synthesis.
- Good dietary sources include amla, guava, citrus fruits, and green leafy vegetables.
- Scurvy results from vitamin C deficiency and causes bleeding gums, tooth loss, bruising and bleeding into joints and skin. Bone growth is impaired in children with scurvy.
Vitamin B3, also known as niacin, is a water-soluble vitamin that exists in two forms - nicotinamide and nicotinic acid. It is the precursor to the important coenzymes NAD+ and NADP+, which participate in many oxidation-reduction reactions during carbohydrate, lipid, and protein metabolism. As a result, niacin plays a key role in generating energy through the electron transport chain.
This document discusses vitamin B12, including its structure, functions, deficiency, production, and uses. It provides details on the microbial production of cyanocobalamin (vitamin B12) through fermentation using Propionibacterium shermanii. The process involves anaerobic fermentation to produce precursors, aerobic fermentation, cell harvesting, acid treatment to release precursors, addition of cyanide to produce cyanocobalamin, and downstream purification using chromatography and crystallization. Vitamin B12 is important for normal functioning of the brain/nervous system, blood formation, and cellular metabolism. Deficiency can cause anemia and fatigue.
Vitamin B12 is essential for normal cell metabolism and DNA synthesis. Deficiency can result from inadequate dietary intake or impaired absorption. Initial signs include fatigue and pallor, while long-term deficiency leads to megaloblastic anemia and peripheral neuropathy. Diagnosis involves measuring serum B12 levels along with metabolites like methylmalonic acid and homocysteine, which increase with deficiency. The Schilling test evaluates absorption by measuring urinary excretion of radioactive B12.
This document discusses electrolyte imbalances, including causes, signs and symptoms, and treatment approaches. It covers the major electrolytes: sodium, potassium, calcium, magnesium, and their roles in the body. Key points include how electrolytes are involved in neuromuscular function, acid-base balance, and fluid distribution. Electrolyte imbalances like hyponatremia, hyperkalemia, hypocalcemia and hypomagnesemia are described in terms of their definitions, causes, and clinical manifestations that clinicians should look for as well as treatment goals.
The following presentation is only for quick reference. I would advise you to read the theoretical aspects of the respective topic and then use this presentation for your last minute revision. I hope it helps you..!!
Mayur D. Chauhan
Fluid and electrolyte balances and imbalanceskatherina Rajan
This document discusses fluid and electrolyte balance and disturbances. It covers the mechanisms of fluid and electrolyte movement including osmosis, diffusion, and filtration. It then discusses sodium, potassium, calcium, magnesium, chloride, bicarbonate, and phosphate levels and imbalances including causes, clinical manifestations, and nursing interventions for conditions like hyponatremia, hypernatremia, hypokalemia, hyperkalcemia, hypocalcemia, hypercalcemia, hypomagnesemia, and hypermagnesemia. Food sources of important electrolytes are also provided.
This document discusses enzymes, their structures, properties, sources, and uses. It provides details on several specific enzymes including papain, pepsin, rennin, lactase, catalase, and lipases. It describes how these enzymes are used in various food applications and industries like dairy, meat processing, baking, and more. The key roles of enzymes in food include tenderizing meat, curdling milk to make cheese, aiding in digestion, and preventing spoilage through microbial control.
Vitamins are organic substances essential for health, growth, and reproduction. They are classified as either fat-soluble or water-soluble vitamins. Vitamins must be obtained through diet as the human body cannot synthesize most of them. The document then provides details on the specific vitamins, their chemical composition, sources, and production methods.
1. Serine proteases use a catalytic triad of serine, histidine, and aspartate residues to hydrolyze peptide bonds through a nucleophilic attack by the serine residue.
2. Site-directed mutagenesis experiments have demonstrated the importance of these catalytic residues and the oxyanion hole for stabilizing the reaction intermediate. Mutating these residues reduces catalytic activity by several orders of magnitude.
3. Recent evidence suggests additional mechanisms such as low barrier hydrogen bonds and substrate assisted catalysis may contribute to the efficiency of serine protease catalysis.
Dokumen tersebut membahas tentang enzim protease. Secara singkat, protease adalah enzim yang memecah ikatan peptida pada protein, ditemukan pada berbagai makhluk hidup. Enzim protease diklasifikasi menjadi empat golongan berdasarkan mekanisme kerjanya, yaitu protease serin, sistein, aspartat, dan logam. Salah satu contoh protease tumbuhan adalah enzim papain yang berasal dari pepaya.
This document discusses fermentative production of vitamins, including key vitamins like B12, B2, C, H, E, and K. It covers the industrial production and market scenario of vitamins globally and in India. It provides details on the microbial production processes and downstream processing for various water-soluble and fat-soluble vitamins. Overall, the document presents an overview of fermentative vitamin production as compared to chemical synthesis.
The document discusses the use of enzymes in bioremediation. It outlines that enzymatic bioremediation uses isolated enzymes to transform contaminants into less toxic compounds. Extracellular enzymes from white rot fungi have been shown to effectively degrade pollutants like PAHs, PCBs, and dyes. Major enzymes used include lignin peroxidase, manganese peroxidase, and laccase. Case studies demonstrate how these enzymes can decolorize over 90% of textile dyes. While enzymatic bioremediation provides advantages over chemical and microbial methods, further research is needed to reduce costs and improve enzyme stability and activity under various conditions.
Enzymes can be used in agriculture to improve farming yields and reduce waste. Applying enzymes to animal feed and surrounding areas decreases odors and flies. Manure treated with enzymes becomes a natural, non-toxic fertilizer that allows plants to grow in places they couldn't before like ponds. Crops watered or sprayed with enzyme solutions require less time to grow larger and are healthier with stronger roots, stems, and higher flowering rates. Soils treated with enzymes become softer and richer, allowing for improved plant growth where nothing grew before.
This document discusses the development of inoculum for industrial fermentation processes. It defines inoculum as a mixture of cultured microbes and the media they are growing in. The key steps in inoculum development are preparing a suitable growth media, maintaining optimal pH and nutrient levels, and conducting growth in stepwise increasing volumes. Examples of common inoculum media compositions are provided for vitamin and bacterial insecticide production processes. Developing high quality inoculum is important for efficiently adapting cultures to fermentation conditions.
This document discusses the nature and properties of enzymes. It defines enzymes as proteins that function as biological catalysts and notes that they speed up specific metabolic reactions. Enzymes have molecular weights ranging from 10,000 to 2,000,000 and are composed of amino acids. They require cofactors like coenzymes, prosthetic groups, or metal ions to be catalytically active. Enzymes exhibit specificity for certain reactions, substrates, or stereoisomers. Their active sites complement the shapes of substrates and undergo induced fit for catalysis. The document outlines industrial uses of enzymes like glucose isomerase in food processing.
Enzymes have many uses in daily life such as cleaning dishes, carpets, curtains, and other household items in a way that is more effective, cleaner, and environmentally friendly compared to traditional chemicals. Enzymes can also be used to reduce pests like flies and cockroaches, control bacteria, care for pets, reduce toilet odors, and remove stains from kitchen walls. Enzymes added to soaps and shampoos can enhance their cleaning power while reducing chemical side effects. When applied topically, enzymes have been shown to improve skin conditions like pimples and wounds.
This document discusses bioremediation and the enzymes used in the process. It begins with background information on bioremediation and enzymes. Major enzymes that aid in bioremediation are then outlined, including peroxidases, oxygenases, and dioxygenases. An example is given of lignin peroxidase and its effectiveness in bioremediating pollutants. The advantages of bioremediation include it being relatively inexpensive and allowing toxic waste to naturally break down. Limitations include difficulty controlling bacteria and potential to spread illness. In conclusion, bioremediation offers a safer, more cost-effective cleaning method for contaminated sites.
The document discusses the use of enzymes in various industries. It begins with an introduction to enzymes and biotechnology. Enzymes are proteins that act as biological catalysts and are used in pharmaceuticals to produce medicines like insulin through genetic engineering. They are also used in biofuels to break down cellulose into sugars for fermentation. In paper and pulp, enzymes degrade starch and lignin. In brewing, enzymes from barley are released to degrade starch and proteins during beer production. Overall, the document explains how enzymes are vital components in biotechnology and are used across many industries.
This document discusses bioremediation and biodegradation strategies for cleaning the environment. It defines bioremediation as using microorganisms like Pseudomonas, Flavobacterium, and Azotobacter to remove toxic pollutants. Biodegradation is the breakdown of substances by microbes through biochemical reactions. Examples of microbes that aid biodegradation in different environments are provided. Recent approaches discussed include using earthworms, deep sea bacteria, and genetically modified organisms to remediate contamination.
This document discusses the industrial production of several vitamins including vitamin B12, riboflavin, vitamin C, and provitamin A. It describes the microorganisms used such as Streptomyces olivaceus for vitamin B12 production and Eremothecium ashbyii and Ashbya gossypii for riboflavin production. The document outlines the fermentation processes including medium composition, fermentation conditions, and recovery methods. It provides details on the multi-step chemical process using D-glucose to synthesize vitamin C via the Reichstein process and fermentation with Acetobacter suboxydans.
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
Vitamin B12, also known as cobalamin, is essential for normal cell metabolism and blood cell formation. It contains a cobalt ion at its core and different attachments to the cobalt determine the type of B12. The main sources are animal products. B12 requires intrinsic factor for absorption in the ileum. A deficiency can cause megaloblastic anemia and neurological problems due to impaired DNA synthesis and methylation reactions. Pernicious anemia is a type of B12 deficiency caused by a lack of intrinsic factor.
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.
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).
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.
Vitamin B12, also called cobalamin, is a water-soluble vitamin that contains cobalt. It is involved in two critical reactions in the body: the conversion of methylmalonyl CoA to succinyl CoA, and the conversion of homocysteine to methionine. Vitamin B12 must be bound to intrinsic factor in order to be absorbed in the ileum, then transported to tissues bound to transcobalamin. Deficiencies can result from failures in transport or metabolism, leading to megaloblastic anemia or neurological damage.
This document discusses megaloblastic anemia, which is caused by vitamin B12 or folate deficiency and results in abnormal red blood cell maturation in the bone marrow. The primary defect is in DNA synthesis, leading to large immature red blood cells called megaloblasts. This causes hypercellular bone marrow with megaloblasts and giant neutrophils. Peripheral blood smears show macrocytic anemia, hypersegmented neutrophils, and poikilocytosis. Diagnosis involves blood tests of vitamin B12, methylmalonic acid, and homocysteine. Pernicious anemia, the most common cause of B12 deficiency, is an autoimmune condition that lacks intrinsic factor. Non-me
Folate and vitamin B12 (cobalamin) play key roles in cell metabolism and the production of DNA. A deficiency of either can lead to megaloblastic anemia, where red blood cells are abnormally large with impaired DNA synthesis. Cobalamin deficiency specifically results in an intracellular folate deficiency through a "folate trap" mechanism. Pernicious anemia, caused by autoimmune destruction of gastric parietal cells and a lack of intrinsic factor, is the most common cause of cobalamin deficiency. Symptoms of megaloblastic anemia include fatigue, palpitations, and shortness of breath.
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.
This document discusses megaloblastic anemias caused by cobalamin and folate deficiencies. It covers the absorption, transport, biochemical functions and deficiencies of cobalamin and folate. The key clinical features of megaloblastic anemia are described, including neurological manifestations. Causes, hematological and bone marrow findings, ineffective hematopoiesis, and treatment approaches are summarized. Lifelong cobalamin injections are usually needed to treat deficiency, while folate deficiency responds to oral supplementation.
Cobalamin (vitamin b12) – Lippincott’s Illustrated Reviews World Wide Web Maryam Fida
Vitamin B12 is synthesized only by microorganisms and it is not present in plants
Animals obtain the vitamin preformed from their natural bacterial flora or by eating foods derived from other animals
Present in appreciable amounts in liver, red meat, fish, eggs , dairy products , and fortified cereals
Required in humans for two essential enzymatic reactions
Remethylation of homocysteine (Hcy) to methionine
Isomerization of methylmalonyl coenzyme A (CoA), which is produced during the degradation of some amino acids (isoleucine, valine, threonine and methionine ) and fatty acids (FAs ) with odd numbers of carbon atoms
DEFICIENCY
When cobalamin is deficient, Fatty Acids accumulate and become incorporated into cell membranes , including those of the central nervous system (CNS) resulting in neurologic symptoms
The physiologic coenzyme forms of cobalamin are 5'- deoxyadenosylcobalamin and methylcobalamin
Folic acid (as N5-methyl THF) is also required in the remethylation of Hcy. Therefore , deficiency of B12 or folate results in elevated Hcy levels.
Folate and cobalamin are essential vitamins that play important roles in metabolism. Folate must be reduced to tetrahydrofolate to be functional, and a single enzyme catalyzes both steps of this reduction. Cobalamin is required for two key metabolic reactions involving methyltetrahydrofolate-homocysteine methyltransferase and methylmalonyl CoA mutase. Cobalamin deficiency can cause a "folate trap" by impairing methionine synthase and blocking folate metabolism. Tests for folate and cobalamin deficiencies include serum and RBC levels as well as metabolites like methylmalonic acid and homocysteine. The Schilling test evaluates cobalamin absorption by measuring ex
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.
Vitamin B12 deficiency is the most likely diagnosis for this patient based on her history, examination findings, and laboratory results. The underlying problem is likely inadequate dietary intake of vitamin B12 as a result of her vegan diet. The two most common causes of megaloblastic anemia are vitamin B12 deficiency and folate deficiency. However, her history of fatigue, numbness, diarrhea, weight loss, and beefy red tongue point more specifically to vitamin B12 deficiency, as folate deficiency would be less likely given her dietary habits.
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.
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Recombinant DNA technology allows for the creation of novel gene combinations not found in nature. Genes can be inserted into host cells and replicated. This technology is used in research, medicine, agriculture, and industry. In medicine, it enables production of insulin, growth factors, vaccines, and gene therapy. It is also used for genetic mapping, disease diagnosis, forensics, and prenatal testing. In agriculture, it improves crop yields and develops pest/drought resistance. Industry utilizes it to produce enzymes, additives, sugars, and chemicals.
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إضغ بين إيديكم من أقوى الملازم التي صممتها
ملزمة تشريح الجهاز الهيكلي (نظري 3)
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تتميز هذهِ الملزمة بعِدة مُميزات :
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2- تحتوي على 78 رسم توضيحي لكل كلمة موجودة بالملزمة (لكل كلمة !!!!)
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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
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3. Structure
• Cobalamin is analogous to heme in its
structure having as its base a tetrapyrrole ring.
• Instead of iron as a metal cofactor for heme,
cobalamin has cobalt in a coordination state
of six with
o a benzimidazole group nitrogen coordinated
to one axial position,
o the four equatorial positions coordinated by
the nitrogens of the four pyrrole groups and
3Namrata Chhabra
4. Structure of Vitamin B12
oThe sixth position occupied by either a deoxyadenosine group, a methyl group or a
CN– group in the commercially available form in vitamin tablets.
4Namrata Chhabra
5. Forms of Cobalamin
• Cobalamin (vitamin B12) exists in a number of different
chemical forms.
• All have a cobalt atom at the center of a corrin ring.
• In nature, the vitamin is mainly in the 2-deoxyadenosyl
(ado) form, which is located in mitochondria
• The other major natural cobalamin is
methylcobalamin, the form in human plasma and in
cell cytoplasm.
• There are also minor amounts of hydroxocobalamin to
which methyl- and adenosyl cobalamin are rapidly
converted by exposure to light.
5Namrata Chhabra
6. Dietary Sources
• Cobalamin is synthesized solely by
microorganisms.
• Ruminants obtain cobalamin from the foregut,
but the only source for humans is food of animal
origin, e.g. meat, fish, and dairy products.
• Vegetables, fruits, and other foods of non-animal
origin are free from cobalamin unless they are
contaminated by bacteria.
• Strict vegetarians are at risk of developing B12
deficiency.
6Namrata Chhabra
8. Requirements of vitamin B12
• A normal Western diet contains between
5 and 30 μg of cobalamin daily.
• Adult daily losses (mainly in the urine
and feces) are between 1 and 3 μg
(~0.1% of body stores) and, as the body
does not have the ability to degrade
cobalamin, daily requirements are also
about 1 to 3 μg.
• Body stores are of the order of 2 to 3
mg, sufficient for 3 to 4 years if supplies
are completely cut off.
8Namrata Chhabra
9. Absorption
• Two mechanisms exist for cobalamin absorption.
• Passive absorption-occurring equally through
buccal, duodenal and ileal mucosa; it is rapid but
extremely inefficient, <1 percent of an oral dose
being absorbed by this process.
• Active absorption-The normal physiologic
mechanism is active; it occurs through the ileum
and is efficient for small (a few micrograms) oral
doses of cobalamin and is mediated by gastric
intrinsic factor (IF).
9Namrata Chhabra
10. Absorption
• Dietary cobalamin is released from protein
complexes by enzymes in the stomach,
duodenum, and jejunum
• It combines rapidly with a salivary glycoprotein
that belongs to the family of cobalamin-binding
proteins known as haptocorrins (HCs).
• In the intestine, the haptocorrins are digested by
pancreatic trypsin and the cobalamin transferred
to intrinsic factor(IF).
10Namrata Chhabra
12. Absorption and the role of Intrinsic
factor
• Intrinsic factor (IF) is produced in the gastric
parietal cells of the fundus and body of the
stomach, its secretion parallels that of
hydrochloric acid.
• The IF-cobalamin complex passes to the ileum,
where IF attaches to a specific receptor (Cubulin)
on the microvillus membrane of the enterocytes.
• Cubulin with its ligand IF-cobalamin complex is
endocytosed.
• The cobalamin-IF complex enters the ileal cell
where IF is destroyed.
12Namrata Chhabra
13. Intrinsic factor deficiency
• In the absence of the intrinsic factor
inadequate amounts of cobalamin are
absorbed (the dietary requirement is
approximately 200 ng/day) resulting in
Megaloblastic anemia.
• When the root cause of the resultant
Megaloblastic anemia is absence of or
inadequate amounts of intrinsic factor the
condition is called pernicious anemia.
13Namrata Chhabra
14. Transportation of Cobalamin
• Three plasma transport proteins have been
identified.
• Transcobalamine I and III (differing only in
carbohydrate structure) are secreted by white
blood cells.
• Although approximately 90 percent of plasma
vitamin B12 circulates bind to these proteins,
only transcobalamine II is capable of
transporting vitamin B12 into cells.
14Namrata Chhabra
15. Storage of Cobalamin
• The liver contains 2000 to 5000 mcg of stored
vitamin B12.
• Since daily losses are 1 to 3 mcg/day, the body
usually has sufficient stores of vitamin B12 so
that vitamin B12 deficiency develops more
than 3 years after vitamin B12 absorption
ceases.
15Namrata Chhabra
16. Metabolic Role of Cobalamin
1)Cobalamin plays a vital role in the
catabolism of odd-chain fatty acids,
threonine, methionine, and the branched-
chain amino acids (leucine, isoleucine, and
valine).
• The degradation of each of these compounds
produces the same metabolite, Propionyl-
CoA.
16Namrata Chhabra
18. Fate of Propionyl CoA in B12
deficiency
• In cases of cobalamin deficiency these reactions
of utilization of propionyl co A are compromised
leading to an accumulation of methylmalonyl-
CoA in serum, which has been suggested as a
possible source of neurologic defects seen in
cobalamin deficiency by decreasing lipid
synthesis.
• Excess methylmalonyl-CoA in B12 deficiency gets
excreted in urine causing methylmalonic aciduria
18Namrata Chhabra
19. 2.Role of cobalamin in DNA synthesis and the
biochemical basis of Megaloblastic anemia
• The cause of megaloblastic anemia seen in
strict vegetarians is attributed to the effects of
cobalamin deficiency on DNA synthesis,
specifically the thymidylate synthesize
reaction which converts dUMP→ dTMP.
19Namrata Chhabra
21. Implications of Inadequate
Thymidylate synthesis
• Inadequate dTMP restricts DNA but not RNA
synthesis leading to the appearance of large
erythroid cells with small nuclei containing a
high ratio of RNA to DNA.
• These cells are removed from the circulation,
thus stimulating erythrogenesis and giving rise
to anemia with an elevated presence of
megaloblasts.
21Namrata Chhabra
22. 3. Role of cobalamin in methionine
metabolism
• Cobalamin is required for the conversion of
homocysteine into methionine.
• Cobalamin must first undergo methyl transfer
to form methyl cobalamin.
• It receives the methyl group from N5-
methyltetrahydrofolate thus regenerating
tetrahydrofolate to participate in other one-
carbon transfers in purine metabolism or
pyrimidine remodeling.
22Namrata Chhabra
23. Folate trap
• In cobalamin deficiency, the methionine synthase reaction
cannot occur, N5-methyltetrahydrofolate accumulates and
the other C-1 donor forms of tetrahydrofolate cannot be
formed.
• The methionine synthesis from homocysteine ceases
allowing the “trapping” of the folate pool as N5-
methyltetrahydrofolate, diminishing levels of N5, N10-
methylenetetrahydrofolate
• N5,N10-methylenetetrahydrofolate, is required for the
methylation of dUMP to dTMP, thus in it’s deficiency ,the
thymidylate synthase reaction is slowed and dTMP levels
drops and hence DNA synthesis is also slowed down due to
non availability of deoxy ribonucleotides
23Namrata Chhabra
24. Roles of cobalamin and folic acid in
methionine metabolism
24Namrata Chhabra
25. Vitamin B12 deficiency
Causes of Vitamin B12 Deficiency
• Dietary deficiency (rare)
• Decreased production of intrinsic factor
• Pernicious anemia
• Gastrectomy
• Pancreatic insufficiency
• Fish tapeworm (rare)
• Helicobacter pylori infection
25Namrata Chhabra
26. Vitamin B12 deficiency
• Crohn’s disease
• Surgical resection
• Decreased ileal absorption of vitamin B12
• Transcobalamine II deficiency (rare)
• Competition for vitamin B12 in gut Blind loop
syndrome
• The most common cause of vitamin B12
deficiency is associated with pernicious anemia
26Namrata Chhabra
28. Megaloblastic anemia
Clinical Findings
• The hallmark of symptomatic vitamin B12 deficiency is
megaloblastic anemia.
• However, subclinical cobalamin deficiency is an increasingly
recognized condition, especially in those with predisposing
conditions such as ileal disease or gastric surgery.
• In advanced cases, the anemia may be severe, with hematocrit as
low as 10 to 15 percent, and may be accompanied by leucopenia
and thrombocytopenia.
• The megaloblastic state also produces changes in mucosal cells,
leading to glossitis, as well as other vague gastrointestinal
disturbances such as anorexia and diarrhea.
• Patients are usually pale and may be mildly icteric
28Namrata Chhabra
29. Peripheral blood smear in
Megaloblastic anemia
Blood film in vitamin B12deficiency showing macrocytic red
cells and a hyper segmented neutrophil.
29Namrata Chhabra
30. Neurological changes in B12
deficiency
• Vitamin B12 deficiency also leads to a complex
neurologic syndrome.
• Peripheral nerves are usually affected first,
and patients complain initially of paresthesias.
• The posterior columns next become impaired,
and patients complain of difficulty with
balance.
30Namrata Chhabra
31. Neurological changes in B12
deficiency
• In more advanced cases, cerebral function
may be altered as well, and on occasion
dementia and other neuropsychiatric changes
may precede hematologic changes.
• Neurologic examination may reveal decreased
vibration and position sense but is more
commonly normal in early stages of the
disease.
31Namrata Chhabra
33. Laboratory Findings
• The MCV is usually strikingly elevated, between 110
and 140 fL.
• The peripheral blood smear is usually strikingly
abnormal, with anisocytosis and poikilocytosis. A
characteristic finding is the macro-ovalocyte, but
numerous other abnormal shapes are usually seen. The
neutrophils are hyper segmented.
• The reticulocyte count is reduced.
• Because vitamin B12 deficiency affects all
hematopoietic cell lines, in severe cases the white
blood cell count and the platelet count are reduced,
and pancytopenia is present.
33Namrata Chhabra
34. Laboratory Findings
• Bone marrow morphology is characteristically
abnormal.
• Marked erythroid hyperplasia is present as a response
to defective red blood cell production (ineffective
erythropoiesis).
• Megaloblastic changes in the erythroid series include
abnormally large cell size and asynchronous
maturation of the nucleus and cytoplasm—i.e.
cytoplasmic maturation continues while impaired DNA
synthesis causes retarded nuclear development.
• In the myeloid series, giant metamyelocytes are
characteristically seen.
34Namrata Chhabra
35. Laboratory Findings
• Other laboratory abnormalities include
elevated serum lactate dehydrogenase (LDH)
and a modest increase in indirect bilirubin.
• These two findings are a reflection of
intramedullary destruction of developing
abnormal erythroid cells and are similar to
those observed in peripheral hemolytic
anemias
35Namrata Chhabra
36. Laboratory Findings
• Serum cobalamin level: The diagnosis of vitamin
B12 deficiency is made by finding an abnormally
low vitamin B12 (cobalamin) serum level.
• The normal vitamin B12 level is > 240 pg/ml,
• Most patients with overt vitamin B12 deficiency
can have serum levels < 170 pg/ml, with
symptomatic patients usually having levels < 100
pg/ml.
• A level of 170 to 240 pg/ml is borderline.
36Namrata Chhabra
37. Laboratory Findings
Estimation of serum methylmalonic acid levels
• When the serum level of vitamin B12 is
borderline, the diagnosis is best confirmed by
finding an elevated level of serum methylmalonic
acid (> 1000 nmol/L
• However, elevated levels of serum methylmalonic
acid can also be due to renal insufficiency.
• The Schilling test is now rarely used.
37Namrata Chhabra
38. Essentials of diagnosis
• Essentials of diagnosis are macrocytic anemia.
• Macro-ovalocytes and hyper segmented
neutrophils on peripheral blood smear, and
• serum vitamin B12 level less than 100 pg/ml.
38Namrata Chhabra
39. Differential Diagnosis
• Vitamin B12 deficiency should be differentiated
from folic acid deficiency, the other common
cause of megaloblastic anemia, in which red
blood cell folate is low while vitamin B12 levels
are normal.
• The distinction between vitamin B12 deficiency
and myelodysplasia (the other common cause of
macrocytic anemia with abnormal morphology) is
based on the characteristic morphology and the
low vitamin B12 level
39Namrata Chhabra
40. Pernicious Anemia
• Pernicious anemia is a chronic illness caused
by impaired absorption of vitamin B12
because of a lack of intrinsic factor (IF) in
gastric secretions.
• The disease was named pernicious anemia
because it was fatal before treatment became
available
• The term pernicious is no longer appropriate,
but it is retained for historical reasons.
40Namrata Chhabra
41. Pernicious Anemia
• Pernicious anemia occurs as a relatively
common adult form of anemia that is
associated with gastric atrophy and a loss of IF
production and
• as a rare congenital autosomal recessive form
in which IF production is lacking without
gastric atrophy.
41Namrata Chhabra
42. Clinical manifestations in Pernicious
anemia
• General findings: Weight loss of 10 to 15
pounds occurs in about 50 percent of
patients and probably is due to anorexia,
which is observed in most patients.
• Anemia: The anemia often is well tolerated in
pernicious anemia, and many patients are
ambulatory with hematocrit levels in the mid
teens.
42Namrata Chhabra
43. Clinical manifestations in Pernicious
anemia
Gastrointestinal findings:
• Approximately 50 percent of patients have a smooth tongue with
loss of papillae. The tongue may be painful and beefy red. These
symptoms may be associated with changes in taste and loss of
appetite.
• Patients may report either constipation or having several semisolid
bowel movements daily. This has been attributed to megaloblastic
changes of the cells of the intestinal mucosa.
• Nonspecific gastrointestinal symptoms include anorexia, nausea,
vomiting, heartburn, flatulence, and a sense of fullness.
• Rarely, patients present with severe abdominal pain associated with
abdominal rigidity; this has been attributed to spinal cord
pathology.
43Namrata Chhabra
44. Clinical manifestations in Pernicious
anemia
Nervous system:
• Neurological symptoms can be elicited in most
patients with pernicious anemia, and the most
common symptoms are paresthesias, weakness,
clumsiness, and an unsteady gait.
• These neurological symptoms are due to myelin
degeneration and loss of nerve fibers in the
dorsal and lateral columns of the spinal cord and
cerebral cortex.
44Namrata Chhabra
45. Clinical manifestations in Pernicious
anemia
Genitourinary system:
• Urinary retention and
• Impaired micturition may occur because of
spinal cord damage.
• This can predispose patients to urinary tract
infections.
45Namrata Chhabra
46. Laboratory Studies
• The peripheral smear shows oval macrocytes,
hyper segmented granulocytes, and
anisopoikilocytosis.
• In severe anemia, red blood cell inclusions
may include Howell-Jolly bodies, Cabot rings,
and punctate basophilia.
46Namrata Chhabra
47. Laboratory Studies
• Gastric secretions: Total gastric secretions are
decreased to about 10 percent of the
reference range.
• Most patients with pernicious anemia are
achlorhydric, even with histamine stimulation.
• IF is either absent or markedly decreased.
47Namrata Chhabra
48. Laboratory Studies
• Serum Cbl levels: The serum Cbl is low in
patients with pernicious anemia; however, it
may be within the reference range in certain
patients with other forms of Cbl deficiency.
48Namrata Chhabra
49. Laboratory Studies
• Schilling test: The Schilling test measures Cbl
absorption by increasing urine radioactivity after
an oral dose of radioactive Cbl.
• The test is useful in demonstrating that the
anemia is caused by an absence of IF and is not
secondary to other causes of Cbl deficiency.
• It is used to identify patients with classic
pernicious anemia, even after they have been
treated with vitamin B12
49Namrata Chhabra
50. Laboratory Studies
• Serum: The indirect bilirubin may be elevated
because pernicious anemia is a hemolytic
disorder associated with increased turnover
of bilirubin.
• The serum lactic dehydrogenase usually is
markedly increased
50Namrata Chhabra
51. Histological Findings
• The bone marrow biopsy and aspirate usually
are hyper cellular and show trilineage
differentiation.
• Erythroid precursors are large and often oval.
51Namrata Chhabra
52. Complications
• If patients are not treated early in the disease,
neurological complications can become
permanent.
• Severe anemia can cause congestive heart
failure or precipitate coronary insufficiency.
• The incidence of gastric adenocarcinoma is 2-
to 3-fold greater in patients with pernicious
anemia than in the general population of the
same age.
52Namrata Chhabra
53. Prognosis
• Early recognition and treatment of pernicious
anemia provides a normal, and usually
uncomplicated, lifespan.
• Delayed treatment permits progression of the
anemia and neurological complications. The
mental and
• neurological damage can become irreversible
without therapy.
53Namrata Chhabra
54. Treatment of vitamin B12 deficiency
• The indications for starting cobalamin therapy
are :
• A well-documented Megaloblastic anemia
• or other hematological abnormalities
• or neuropathy due to the deficiency.
54Namrata Chhabra
55. Treatment of vitamin B12 deficiency
• Patients with pernicious anemia have historically been
treated with parenteral therapy.
• Intramuscular injections of 100 mcg of vitamin B12 are
adequate for each dose.
• Replacement is usually given daily for the first week,
weekly for the first month, and then monthly for life.
• It is a lifelong disorder, and if patients discontinue their
monthly therapy the vitamin deficiency will recur.
• Oral cobalamin may be used instead of parenteral
therapy and can provide equivalent results. The dose is
1000 mcg/day and must be continued indefinitely.
55Namrata Chhabra
56. Further reading
• A case oriented approach towards
Biochemistry- By Namrata Chhabra
http://www.jaypeedigital.com/(X(1)S(vclizd4r0zr
y5eoz45exstdx))/Book/BookDetail?isbn=9789
350901885
56Namrata Chhabra