Rickets
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Rickets
This document discusses rickets, a disease characterized by soft, weak, and deformed bones in children caused by vitamin D deficiency or disorders of vitamin D and phosphate metabolism. It defines rickets as occurring in growing children before bone growth plate closure, while osteomalacia occurs after closure in adults. The key roles and mechanisms of vitamin D in calcium and phosphate homeostasis are described. Causes, signs and symptoms, diagnosis using biochemical markers and radiology, treatment using large vitamin D doses, and prevention through diet and sunlight exposure are summarized. Other types of rickets including genetic and renal forms are also outlined.
Rickets a brief outlook
here there is a brief out look of rickets , mainly deals with the approach to different clinical types of rickets and its management
Rickets
This document summarizes rickets, a childhood bone disease caused by vitamin D deficiency or impaired vitamin D metabolism. It discusses the pathology of rickets, which involves abnormal cartilage cell maturation and failed bone mineralization. This leads to bone deformities and fractures. The document outlines various causes of rickets, including nutritional deficiencies, malabsorption, and genetic disorders affecting vitamin D and phosphate metabolism. Diagnosis involves x-rays showing characteristic bone changes. Treatment involves vitamin D, calcium, phosphate supplementation as needed, and sometimes surgery to correct deformities once the disease is resolved.
Rickets and osteomalacia
Rickets and osteomalacia are diseases characterized by impaired mineralization of bone and cartilage. Rickets occurs in children and affects growing bones and cartilage, while osteomalacia occurs in adults after growth is complete. Both are primarily caused by vitamin D deficiency or disturbances in its metabolism. The diseases result in softened, deformed bones and increased fracture risk. Diagnosis involves clinical features, elevated alkaline phosphatase levels, and radiographic signs of impaired mineralization. Treatment focuses on vitamin D supplementation, calcium, and addressing any underlying causes.
Rickets
INTRODUCTION — Normal bone growth and mineralization require adequate calcium and phosphate, the two major constituents of the crystalline component of bone. Deficient mineralization can result in rickets and/or osteomalacia. Rickets refers to deficient mineralization at the growth plate, as well as architectural disruption of this structure. Osteomalacia refers to impaired mineralization of the bone matrix. Rickets and osteomalacia usually occur together as long as the growth plates are open; only osteomalacia occurs after the growth plates have fused.
rickets is a nutritional deficiency disease that involves mainly calcium, vitamin d, or phosphate resulting in decreased bone stability and strength, Delayed closure of the fontanelles,Parietal and frontal bossing. Craniotabes (soft skull bones).
Enlargement of the costochondral junction visible as beading along the anterolateral aspects of the chest (the "rachitic rosary") . Formation of Harrison sulcus (or groove),Widening of the wrist and bowing of the distal radius and ulna, Progressive lateral bowing of the femur and tibia and causes defects in teeth.
there is two types of rickets: phosphopenic and calcipenic.
pathogenesis: Growth plate thickness is determined by two opposing processes: o chondrocyte proliferation and hypertrophy on the one hand. o vascular invasion of the growth plate followed by conversion into primary bone spongiosa on the other. • Vascular invasion requires mineralization of the growth plate cartilage and is delayed or prevented by deficiency of calcium or phosphorus growth plate cartilage accumulates and the growth plate thickens. • In addition, the chondrocytes of the growth plate become disorganized, losing their columnar orientation with characteristic expansion of the hypertrophic zone. • In the bone tissue below the growth plate (metaphysis), the mineralization defect leads to the accumulation of osteoid.
Rickets in children
Rickets is a disease characterized by softening and weakening of bones in children, caused by a vitamin D deficiency or impaired metabolism of calcium or phosphorus. It most commonly affects children between 6-24 months old and can lead to fractures and bone deformities. While historically more prevalent, rickets decreased in developed countries in the 20th century but remains common in developing nations and populations with dark skin where access to vitamin D-fortified foods is limited. Treatment involves increasing dietary intake of calcium, phosphorus and vitamin D through supplements, exposure to sunlight, or vitamin D-fortified foods and formula. Physical therapy can help reduce bone and muscle pain through stretching and strengthening exercises.
Rickets
This document discusses rickets, a disease characterized by weak and malformed bones in children due to a lack of vitamin D or calcium. It defines rickets and describes the various types, including nutritional rickets caused by vitamin D deficiency, vitamin D dependent rickets involving the kidneys or end organs, and genetic or malabsorption related forms. Symptoms, biochemical markers, x-ray findings and treatments are outlined. Management involves vitamin D or calcium supplementation depending on the type, with the goal of restoring normal bone growth and structure over 6 months to 2 years.
Rickets presentation
This document summarizes rickets, a disease characterized by softening and weakening of bones in children due to a lack of vitamin D or calcium and phosphate. It discusses calcium, phosphate, and vitamin D metabolism and how deficiencies can lead to inadequate mineralization of bone. Symptoms include bone pain, deformities like bowed legs, and fractures. Diagnosis involves biochemical testing showing low calcium, phosphate, and vitamin D levels as well as characteristic findings on x-rays of bones. Treatment is supplementation to correct nutritional deficiencies.
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Rickets
This document discusses rickets, a disease characterized by soft, weak, and deformed bones in children caused by vitamin D deficiency or disorders of vitamin D and phosphate metabolism. It defines rickets as occurring in growing children before bone growth plate closure, while osteomalacia occurs after closure in adults. The key roles and mechanisms of vitamin D in calcium and phosphate homeostasis are described. Causes, signs and symptoms, diagnosis using biochemical markers and radiology, treatment using large vitamin D doses, and prevention through diet and sunlight exposure are summarized. Other types of rickets including genetic and renal forms are also outlined.
Rickets a brief outlook
here there is a brief out look of rickets , mainly deals with the approach to different clinical types of rickets and its management
Rickets
This document summarizes rickets, a childhood bone disease caused by vitamin D deficiency or impaired vitamin D metabolism. It discusses the pathology of rickets, which involves abnormal cartilage cell maturation and failed bone mineralization. This leads to bone deformities and fractures. The document outlines various causes of rickets, including nutritional deficiencies, malabsorption, and genetic disorders affecting vitamin D and phosphate metabolism. Diagnosis involves x-rays showing characteristic bone changes. Treatment involves vitamin D, calcium, phosphate supplementation as needed, and sometimes surgery to correct deformities once the disease is resolved.
Rickets and osteomalacia
Rickets and osteomalacia are diseases characterized by impaired mineralization of bone and cartilage. Rickets occurs in children and affects growing bones and cartilage, while osteomalacia occurs in adults after growth is complete. Both are primarily caused by vitamin D deficiency or disturbances in its metabolism. The diseases result in softened, deformed bones and increased fracture risk. Diagnosis involves clinical features, elevated alkaline phosphatase levels, and radiographic signs of impaired mineralization. Treatment focuses on vitamin D supplementation, calcium, and addressing any underlying causes.
Rickets
INTRODUCTION — Normal bone growth and mineralization require adequate calcium and phosphate, the two major constituents of the crystalline component of bone. Deficient mineralization can result in rickets and/or osteomalacia. Rickets refers to deficient mineralization at the growth plate, as well as architectural disruption of this structure. Osteomalacia refers to impaired mineralization of the bone matrix. Rickets and osteomalacia usually occur together as long as the growth plates are open; only osteomalacia occurs after the growth plates have fused.
rickets is a nutritional deficiency disease that involves mainly calcium, vitamin d, or phosphate resulting in decreased bone stability and strength, Delayed closure of the fontanelles,Parietal and frontal bossing. Craniotabes (soft skull bones).
Enlargement of the costochondral junction visible as beading along the anterolateral aspects of the chest (the "rachitic rosary") . Formation of Harrison sulcus (or groove),Widening of the wrist and bowing of the distal radius and ulna, Progressive lateral bowing of the femur and tibia and causes defects in teeth.
there is two types of rickets: phosphopenic and calcipenic.
pathogenesis: Growth plate thickness is determined by two opposing processes: o chondrocyte proliferation and hypertrophy on the one hand. o vascular invasion of the growth plate followed by conversion into primary bone spongiosa on the other. • Vascular invasion requires mineralization of the growth plate cartilage and is delayed or prevented by deficiency of calcium or phosphorus growth plate cartilage accumulates and the growth plate thickens. • In addition, the chondrocytes of the growth plate become disorganized, losing their columnar orientation with characteristic expansion of the hypertrophic zone. • In the bone tissue below the growth plate (metaphysis), the mineralization defect leads to the accumulation of osteoid.
Rickets in children
Rickets is a disease characterized by softening and weakening of bones in children, caused by a vitamin D deficiency or impaired metabolism of calcium or phosphorus. It most commonly affects children between 6-24 months old and can lead to fractures and bone deformities. While historically more prevalent, rickets decreased in developed countries in the 20th century but remains common in developing nations and populations with dark skin where access to vitamin D-fortified foods is limited. Treatment involves increasing dietary intake of calcium, phosphorus and vitamin D through supplements, exposure to sunlight, or vitamin D-fortified foods and formula. Physical therapy can help reduce bone and muscle pain through stretching and strengthening exercises.
Rickets
This document discusses rickets, a disease characterized by weak and malformed bones in children due to a lack of vitamin D or calcium. It defines rickets and describes the various types, including nutritional rickets caused by vitamin D deficiency, vitamin D dependent rickets involving the kidneys or end organs, and genetic or malabsorption related forms. Symptoms, biochemical markers, x-ray findings and treatments are outlined. Management involves vitamin D or calcium supplementation depending on the type, with the goal of restoring normal bone growth and structure over 6 months to 2 years.
Rickets presentation
This document summarizes rickets, a disease characterized by softening and weakening of bones in children due to a lack of vitamin D or calcium and phosphate. It discusses calcium, phosphate, and vitamin D metabolism and how deficiencies can lead to inadequate mineralization of bone. Symptoms include bone pain, deformities like bowed legs, and fractures. Diagnosis involves biochemical testing showing low calcium, phosphate, and vitamin D levels as well as characteristic findings on x-rays of bones. Treatment is supplementation to correct nutritional deficiencies.
Rickets.. Dr.Padmesh
The document discusses the causes and presentation of rickets. The main causes are vitamin D disorders, calcium deficiency, phosphorus deficiency, renal losses, and distal renal tubular acidosis. Clinical features include bone deformities, softening of the skull, and leg pain. Diagnosis involves physical exam, x-rays showing bone changes, and lab tests showing abnormalities in calcium, phosphorus, vitamin D, and parathyroid hormone levels. Nutritional vitamin D deficiency is the most common cause globally. Treatment involves vitamin D, calcium, and phosphorus supplementation.
Rickets lecture
This document provides an overview of rickets presented by Lyudmyla Olexandrivna Rakovska from the Department of Pediatrics at V.N. Karazin Kharkiv National University. The 10-point plan discusses the definition, etiology, pathogenesis, classification, clinical manifestations, laboratory/radiological findings, differential diagnosis, treatment and prevention of rickets. Key points include that rickets is caused by vitamin D deficiency impairing bone mineralization, especially in children under 2 years old. Symptoms involve soft, deformed bones and skeletal abnormalities. Treatment focuses on vitamin D supplementation through either low daily doses or high single doses.
Rickets
This document provides information on rickets, a metabolic bone disease caused by vitamin D deficiency or impaired mineralization. It discusses the following key points:
- Rickets mainly affects children under 2 years old and causes soft, weak bones and skeletal deformities from imperfect bone mineralization.
- It is most commonly caused by nutritional deficiencies, especially of vitamin D, but can also be caused by genetic or other medical conditions.
- Symptoms include bone pain, softening of the skull and ribs, bowed legs, fractures, and delayed growth. Radiographs show widened growth plates and fraying of the metaphysis.
- Treatment involves high-dose vitamin D and calcium supplementation to promote bone mineralization and
Approach to a child with Rickets
This document discusses rickets, a disease caused by defective bone mineralization in children due to vitamin D or calcium/phosphate deficiencies. It defines rickets and describes the different types (nutritional, vitamin D dependent types 1 and 2, and vitamin D resistant). Nutritional rickets is most common, caused by inadequate sunlight exposure or vitamin D/calcium intake. The document outlines vitamin D metabolism and the pathogenesis of rickets. It then describes clinical features like bone deformities and laboratory abnormalities seen in a case of rickets. The recommended approach is to obtain a detailed history, perform a physical exam including skeletal assessment, order biochemical and radiological tests, and initiate vitamin D, calcium, and plastic surgery treatments as needed.
Lecture rickets
Rickets is a childhood bone disease caused by vitamin D deficiency and a lack of calcium and phosphate. It results in soft, weak bones that can lead to skeletal deformities. Symptoms include bowed legs, knock-knees, frontal bossing of the skull, and chest deformities like pigeon chest. Laboratory findings often include low calcium, phosphorus, and vitamin D levels as well as elevated alkaline phosphatase and parathyroid hormone levels. Radiographs show widened growth plates and fraying and cupping of the bone metaphysis. The condition is treated by supplementing with vitamin D and calcium.
Rickets lecture
This document discusses rickets, a disease characterized by defective bone mineralization due to vitamin D deficiency or abnormal metabolism. It covers the sources and types of vitamin D, how vitamin D is metabolized in the body, and its actions in increasing calcium and phosphate absorption and bone mineralization. Symptoms of rickets are described including bone deformities, craniotabes, and rosary beads. Diagnosis involves physical exam findings, elevated alkaline phosphatase levels, and x-rays showing metaphyseal changes. Treatment is aimed at correcting the vitamin D deficiency through sunlight exposure or vitamin D supplementation. Prognosis is generally good with treatment but deformities may require orthopedic correction.
Rickets
INTRODUCTION,ETIOLOGY, EPIDEMIOLOGY,CLINICAL MANIFESTATIONS,DIAGNOSIS,MANAGEMENT AND COMPLICATIONS OF RICKETS
Rickets
This document discusses rickets, a disease caused by vitamin D deficiency or impaired mineralization that affects growing bones in children. It defines rickets and outlines various types including nutritional, vitamin D dependent, and vitamin D resistant rickets. Clinical features like softening of bones and skeletal deformities are described. Laboratory findings of low calcium and phosphorus and high alkaline phosphatase are also summarized. The document outlines prevention through diet, supplementation, and sunlight exposure as well as treatment with high dose vitamin D or calcium therapy.
Rickets in children
Vitamin D deficiency is a common cause of rickets in children. It results from inadequate sunlight exposure, diet low in vitamin D, or malabsorption issues. Clinical features include bone pain, skeletal deformities, and hypocalcemia. Laboratory tests show low calcium and phosphorus levels and elevated alkaline phosphatase. Treatment involves high dose vitamin D supplementation and calcium. Rickets can also be caused by inherited disorders that impact calcium, phosphorus, or vitamin D metabolism.
Rickets
Rickets is a childhood bone disease caused by vitamin D deficiency and lack of calcium and phosphate. It results in soft and weak bones in children. Symptoms include bone pain, bowed legs, and skull deformities. Risk factors include lack of sunlight exposure, dark skin pigmentation, malnutrition, and liver or kidney diseases. Diagnosis involves blood tests showing low calcium, phosphate, and vitamin D levels and x-rays showing bone changes. Treatment consists of vitamin D and calcium supplementation to strengthen and repair bones. Prevention involves adequate sunlight exposure, vitamin D supplementation, and calcium-rich nutrition during childhood bone growth.
Nutritional rickets
Nutritional rickets is caused by defective bone growth and mineralization due to vitamin D deficiency or low calcium intake. It is diagnosed based on history, physical exam, biochemical testing and confirmed by radiographs. Serum 25-hydroxyvitamin D levels below 30 nmol/L indicate deficiency and levels below 50 nmol/L increase risk of rickets. Treatment involves high dose vitamin D supplementation of 2000 IU/day for at least 3 months along with calcium supplementation. Prevention involves adequate dietary vitamin D and calcium intake.
Rickets in children
This document provides information on rickets in children. It begins with an overview of vitamin D physiology and the sources of vitamin D. It then discusses the introduction, etiology, clinical features, radiology, diagnosis, and treatment of rickets. The main causes of rickets are outlined as vitamin D deficiencies, calcium deficiencies, phosphorus deficiencies, and renal losses. Symptoms and physical exam findings of rickets are explained. Laboratory tests useful in diagnosis are provided. Treatment involves high dose vitamin D supplementation either orally or via injection. Prognosis is typically excellent with treatment, though severe cases can cause permanent deformities.
Rickets
Rickets is a disease of growing bones caused by inadequate mineralization due to vitamin D deficiency or disorders of calcium and phosphorus. It occurs in children before bone growth plate fusion. Common causes include nutritional deficiencies of vitamin D, calcium, or phosphorus. Clinical features include bone softening and deformities, muscle weakness, and hypocalcemic symptoms. Diagnosis is confirmed by blood tests and radiographic findings of widened growth plates. Treatment involves high dose vitamin D supplementation along with adequate calcium and phosphorus intake.
Rickets and osteomalacia
Definition of Rickets &Osteomalacia.
Etiology of Rickets & Osteomalacia
Rickets :
is defective mineralization of bones before epiphyseal closure (at growth plate) due to deficiency or impaired metabolism of vitamin D, phosphorus or calcium ,potentially leading to fractures and deformity.
Osteomalacia :
is a similar condition occurring in adults, generally due to impaired mineralization of the bone matrix. Due to a deficiency of vitamin D.
Etiology:
Vit D deficiency :
low intake plus inadequate sunlight exposure
malabsorption
Abnormal Vit D metabolism:
Impaired 25 OH Vitamin D production (Liver diseases)
Impaired 1,25 OH2 Vitamin D production (chronic renal failure or vitamin D-resistant rickets type I ).
Vitamin D receptor defects (vitaminD-resistant rickets type II)
Low calcium intake
Hypophosphatemia :
Low intake.
Inherited or acquired defects in renal tubular phosphate reabsorption.
Tumors that secrete phosphaturic substance.
Rickets and Osteomalacia are impaired memorization of the bone.
Causes of Rickets and Osteomalacia :
Vit D deficiency
Low calcium intake
Abnormal Vit D metabolism
Hypophosphatemia
Rickets
Rickets is a disease caused by vitamin D deficiency or a lack of calcium or phosphorus in children, which results in soft, weakened bones. It occurs when osteoid, or bone matrix, fails to calcify during bone growth. Symptoms include bowed legs, bone pain, and fractures. Treatment involves high dose vitamin D supplementation orally or via injection to restore calcium and phosphorus levels.
rickets
Vitamin D is essential for calcium absorption and bone health. It is produced in the skin upon exposure to sunlight and is also obtained through dietary sources. Vitamin D must undergo hydroxylation in the liver and kidneys to become its active form. Deficiency can result in rickets in children or osteomalacia in adults due to impaired bone mineralization. Risk groups include those with inadequate sun exposure or dietary intake, as well as patients with liver or kidney disease.
Rickets
A brief presentation on Rickets with emphasis on nutritional rickets, the predominant form encountered in Nigeria.
Rickets
The document outlines the signs and symptoms of rickets, including abdominal protrusion, bone bowing, widened growth plates, delayed development, and joint deformities. It discusses the different types of rickets caused by calcium or phosphate deficiency. Blood tests typically show low calcium and phosphate levels and high alkaline phosphatase. Treatment involves high dose vitamin D3 to stimulate bone mineralization and healing, followed by maintenance doses of vitamin D3. Surgery is only performed once healing via vitamin D3 treatment begins.
Rickets & osteomalacia
Rickets, osteomalasia,vitamin-D metabolism, etiology, vit-D dependent Rickets, Clinical symptoms and signs, radiological features,investigations, management, vit-D resistent rickets type I & II, hypophostemeic rickets.
18 Rickets Of Vitamin D Deficiency,Tetany Of Vitamin D Deficiency
This document summarizes rickets of vitamin D deficiency, including its pathogenesis, clinical manifestations, diagnosis, prevention and treatment. Rickets results from failure of mineralization of growing bone due to vitamin D deficiency. Key symptoms include bone pain, softening of the skull, and bowed legs. Diagnosis is based on low vitamin D levels and x-ray findings. Treatment involves vitamin D supplementation to promote bone mineralization and prevent deformities.
Rickets
Rickets is a childhood bone disease caused by vitamin D deficiency and a lack of calcium and phosphate. It results in soft, weak bones that can lead to skeletal deformities. The disease develops when vitamin D levels are too low to absorb calcium and phosphate from the intestines, causing these minerals to be lost from the bones. Symptoms include bowed legs, soft skull, and bone pain. Diagnosis involves blood tests showing low calcium and vitamin D levels and high alkaline phosphatase. X-rays show widened growth plates and fraying and cupping of the bone. Treatment involves high dose vitamin D and calcium supplementation to strengthen the bones.
Vitamin D 1.ppt
Vitamin D is a fat-soluble vitamin obtained through exposure to sunlight, food sources like fatty fish and supplements. It plays an important role in calcium absorption and bone health. Deficiency can lead to rickets in children and osteomalacia in adults characterized by soft, weak bones and skeletal deformities. Recommended daily intake amounts vary from 200-600IU depending on age. Both deficiency and excess can impact multiple body systems.
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Rickets.. Dr.Padmesh
The document discusses the causes and presentation of rickets. The main causes are vitamin D disorders, calcium deficiency, phosphorus deficiency, renal losses, and distal renal tubular acidosis. Clinical features include bone deformities, softening of the skull, and leg pain. Diagnosis involves physical exam, x-rays showing bone changes, and lab tests showing abnormalities in calcium, phosphorus, vitamin D, and parathyroid hormone levels. Nutritional vitamin D deficiency is the most common cause globally. Treatment involves vitamin D, calcium, and phosphorus supplementation.
Rickets lecture
This document provides an overview of rickets presented by Lyudmyla Olexandrivna Rakovska from the Department of Pediatrics at V.N. Karazin Kharkiv National University. The 10-point plan discusses the definition, etiology, pathogenesis, classification, clinical manifestations, laboratory/radiological findings, differential diagnosis, treatment and prevention of rickets. Key points include that rickets is caused by vitamin D deficiency impairing bone mineralization, especially in children under 2 years old. Symptoms involve soft, deformed bones and skeletal abnormalities. Treatment focuses on vitamin D supplementation through either low daily doses or high single doses.
Rickets
This document provides information on rickets, a metabolic bone disease caused by vitamin D deficiency or impaired mineralization. It discusses the following key points:
- Rickets mainly affects children under 2 years old and causes soft, weak bones and skeletal deformities from imperfect bone mineralization.
- It is most commonly caused by nutritional deficiencies, especially of vitamin D, but can also be caused by genetic or other medical conditions.
- Symptoms include bone pain, softening of the skull and ribs, bowed legs, fractures, and delayed growth. Radiographs show widened growth plates and fraying of the metaphysis.
- Treatment involves high-dose vitamin D and calcium supplementation to promote bone mineralization and
Approach to a child with Rickets
This document discusses rickets, a disease caused by defective bone mineralization in children due to vitamin D or calcium/phosphate deficiencies. It defines rickets and describes the different types (nutritional, vitamin D dependent types 1 and 2, and vitamin D resistant). Nutritional rickets is most common, caused by inadequate sunlight exposure or vitamin D/calcium intake. The document outlines vitamin D metabolism and the pathogenesis of rickets. It then describes clinical features like bone deformities and laboratory abnormalities seen in a case of rickets. The recommended approach is to obtain a detailed history, perform a physical exam including skeletal assessment, order biochemical and radiological tests, and initiate vitamin D, calcium, and plastic surgery treatments as needed.
Lecture rickets
Rickets is a childhood bone disease caused by vitamin D deficiency and a lack of calcium and phosphate. It results in soft, weak bones that can lead to skeletal deformities. Symptoms include bowed legs, knock-knees, frontal bossing of the skull, and chest deformities like pigeon chest. Laboratory findings often include low calcium, phosphorus, and vitamin D levels as well as elevated alkaline phosphatase and parathyroid hormone levels. Radiographs show widened growth plates and fraying and cupping of the bone metaphysis. The condition is treated by supplementing with vitamin D and calcium.
Rickets lecture
This document discusses rickets, a disease characterized by defective bone mineralization due to vitamin D deficiency or abnormal metabolism. It covers the sources and types of vitamin D, how vitamin D is metabolized in the body, and its actions in increasing calcium and phosphate absorption and bone mineralization. Symptoms of rickets are described including bone deformities, craniotabes, and rosary beads. Diagnosis involves physical exam findings, elevated alkaline phosphatase levels, and x-rays showing metaphyseal changes. Treatment is aimed at correcting the vitamin D deficiency through sunlight exposure or vitamin D supplementation. Prognosis is generally good with treatment but deformities may require orthopedic correction.
Rickets
INTRODUCTION,ETIOLOGY, EPIDEMIOLOGY,CLINICAL MANIFESTATIONS,DIAGNOSIS,MANAGEMENT AND COMPLICATIONS OF RICKETS
Rickets
This document discusses rickets, a disease caused by vitamin D deficiency or impaired mineralization that affects growing bones in children. It defines rickets and outlines various types including nutritional, vitamin D dependent, and vitamin D resistant rickets. Clinical features like softening of bones and skeletal deformities are described. Laboratory findings of low calcium and phosphorus and high alkaline phosphatase are also summarized. The document outlines prevention through diet, supplementation, and sunlight exposure as well as treatment with high dose vitamin D or calcium therapy.
Rickets in children
Vitamin D deficiency is a common cause of rickets in children. It results from inadequate sunlight exposure, diet low in vitamin D, or malabsorption issues. Clinical features include bone pain, skeletal deformities, and hypocalcemia. Laboratory tests show low calcium and phosphorus levels and elevated alkaline phosphatase. Treatment involves high dose vitamin D supplementation and calcium. Rickets can also be caused by inherited disorders that impact calcium, phosphorus, or vitamin D metabolism.
Rickets
Rickets is a childhood bone disease caused by vitamin D deficiency and lack of calcium and phosphate. It results in soft and weak bones in children. Symptoms include bone pain, bowed legs, and skull deformities. Risk factors include lack of sunlight exposure, dark skin pigmentation, malnutrition, and liver or kidney diseases. Diagnosis involves blood tests showing low calcium, phosphate, and vitamin D levels and x-rays showing bone changes. Treatment consists of vitamin D and calcium supplementation to strengthen and repair bones. Prevention involves adequate sunlight exposure, vitamin D supplementation, and calcium-rich nutrition during childhood bone growth.
Nutritional rickets
Nutritional rickets is caused by defective bone growth and mineralization due to vitamin D deficiency or low calcium intake. It is diagnosed based on history, physical exam, biochemical testing and confirmed by radiographs. Serum 25-hydroxyvitamin D levels below 30 nmol/L indicate deficiency and levels below 50 nmol/L increase risk of rickets. Treatment involves high dose vitamin D supplementation of 2000 IU/day for at least 3 months along with calcium supplementation. Prevention involves adequate dietary vitamin D and calcium intake.
Rickets in children
This document provides information on rickets in children. It begins with an overview of vitamin D physiology and the sources of vitamin D. It then discusses the introduction, etiology, clinical features, radiology, diagnosis, and treatment of rickets. The main causes of rickets are outlined as vitamin D deficiencies, calcium deficiencies, phosphorus deficiencies, and renal losses. Symptoms and physical exam findings of rickets are explained. Laboratory tests useful in diagnosis are provided. Treatment involves high dose vitamin D supplementation either orally or via injection. Prognosis is typically excellent with treatment, though severe cases can cause permanent deformities.
Rickets
Rickets is a disease of growing bones caused by inadequate mineralization due to vitamin D deficiency or disorders of calcium and phosphorus. It occurs in children before bone growth plate fusion. Common causes include nutritional deficiencies of vitamin D, calcium, or phosphorus. Clinical features include bone softening and deformities, muscle weakness, and hypocalcemic symptoms. Diagnosis is confirmed by blood tests and radiographic findings of widened growth plates. Treatment involves high dose vitamin D supplementation along with adequate calcium and phosphorus intake.
Rickets and osteomalacia
Definition of Rickets &Osteomalacia.
Etiology of Rickets & Osteomalacia
Rickets :
is defective mineralization of bones before epiphyseal closure (at growth plate) due to deficiency or impaired metabolism of vitamin D, phosphorus or calcium ,potentially leading to fractures and deformity.
Osteomalacia :
is a similar condition occurring in adults, generally due to impaired mineralization of the bone matrix. Due to a deficiency of vitamin D.
Etiology:
Vit D deficiency :
low intake plus inadequate sunlight exposure
malabsorption
Abnormal Vit D metabolism:
Impaired 25 OH Vitamin D production (Liver diseases)
Impaired 1,25 OH2 Vitamin D production (chronic renal failure or vitamin D-resistant rickets type I ).
Vitamin D receptor defects (vitaminD-resistant rickets type II)
Low calcium intake
Hypophosphatemia :
Low intake.
Inherited or acquired defects in renal tubular phosphate reabsorption.
Tumors that secrete phosphaturic substance.
Rickets and Osteomalacia are impaired memorization of the bone.
Causes of Rickets and Osteomalacia :
Vit D deficiency
Low calcium intake
Abnormal Vit D metabolism
Hypophosphatemia
Rickets
Rickets is a disease caused by vitamin D deficiency or a lack of calcium or phosphorus in children, which results in soft, weakened bones. It occurs when osteoid, or bone matrix, fails to calcify during bone growth. Symptoms include bowed legs, bone pain, and fractures. Treatment involves high dose vitamin D supplementation orally or via injection to restore calcium and phosphorus levels.
rickets
Vitamin D is essential for calcium absorption and bone health. It is produced in the skin upon exposure to sunlight and is also obtained through dietary sources. Vitamin D must undergo hydroxylation in the liver and kidneys to become its active form. Deficiency can result in rickets in children or osteomalacia in adults due to impaired bone mineralization. Risk groups include those with inadequate sun exposure or dietary intake, as well as patients with liver or kidney disease.
Rickets
A brief presentation on Rickets with emphasis on nutritional rickets, the predominant form encountered in Nigeria.
Rickets
The document outlines the signs and symptoms of rickets, including abdominal protrusion, bone bowing, widened growth plates, delayed development, and joint deformities. It discusses the different types of rickets caused by calcium or phosphate deficiency. Blood tests typically show low calcium and phosphate levels and high alkaline phosphatase. Treatment involves high dose vitamin D3 to stimulate bone mineralization and healing, followed by maintenance doses of vitamin D3. Surgery is only performed once healing via vitamin D3 treatment begins.
Rickets & osteomalacia
Rickets, osteomalasia,vitamin-D metabolism, etiology, vit-D dependent Rickets, Clinical symptoms and signs, radiological features,investigations, management, vit-D resistent rickets type I & II, hypophostemeic rickets.
18 Rickets Of Vitamin D Deficiency,Tetany Of Vitamin D Deficiency
This document summarizes rickets of vitamin D deficiency, including its pathogenesis, clinical manifestations, diagnosis, prevention and treatment. Rickets results from failure of mineralization of growing bone due to vitamin D deficiency. Key symptoms include bone pain, softening of the skull, and bowed legs. Diagnosis is based on low vitamin D levels and x-ray findings. Treatment involves vitamin D supplementation to promote bone mineralization and prevent deformities.
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18 Rickets Of Vitamin D Deficiency,Tetany Of Vitamin D Deficiency
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Rickets
Rickets is a childhood bone disease caused by vitamin D deficiency and a lack of calcium and phosphate. It results in soft, weak bones that can lead to skeletal deformities. The disease develops when vitamin D levels are too low to absorb calcium and phosphate from the intestines, causing these minerals to be lost from the bones. Symptoms include bowed legs, soft skull, and bone pain. Diagnosis involves blood tests showing low calcium and vitamin D levels and high alkaline phosphatase. X-rays show widened growth plates and fraying and cupping of the bone. Treatment involves high dose vitamin D and calcium supplementation to strengthen the bones.
Vitamin D 1.ppt
Vitamin D is a fat-soluble vitamin obtained through exposure to sunlight, food sources like fatty fish and supplements. It plays an important role in calcium absorption and bone health. Deficiency can lead to rickets in children and osteomalacia in adults characterized by soft, weak bones and skeletal deformities. Recommended daily intake amounts vary from 200-600IU depending on age. Both deficiency and excess can impact multiple body systems.
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Rickets is caused by vitamin D deficiency which leads to low calcium and phosphate levels. This weakens the bones and causes skeletal deformities. Vitamin D is obtained from sunlight exposure and diet. Lack of sunlight, inadequate diet, dark skin pigmentation, liver or kidney problems can cause vitamin D deficiency and subsequent rickets. Symptoms include bowed legs, soft skull bones, spinal curvature and bone pain. Diagnosis involves blood tests showing low calcium, vitamin D and high alkaline phosphatase levels along with characteristic bone changes on x-ray. Treatment is vitamin D supplementation and ensuring adequate calcium and vitamin D in the diet.
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Rickets is a disease of growing bones in children caused by vitamin D deficiency or lack of calcium and phosphate. It results in soft, weak bones that can deform. Symptoms include bowed legs, fractures, and delayed growth. Diagnosis involves lab tests showing low calcium, vitamin D, and phosphate levels as well as characteristic bone changes on x-rays like widened growth plates. Treatment is vitamin D supplements and ensuring adequate calcium and phosphate intake. Prevention involves vitamin D supplementation, sunlight exposure, and a nutritious diet.
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Chemistry of Vitamin D, Biochemical functions of vitamin D, Recommended dietary Allowances of vitamin D, Dietary sources of Vitamin D, Deficiency symptoms of vitamin D, Hypervitaminosis of vitamin D, Toxicity of Vitamin D.
Rickets and osteomalacia
This document provides an overview of rickets and osteomalacia. It begins by defining rickets as a disease affecting the growth plates, causing deficient mineralization and impaired endochondral ossification due to failed apoptosis of hypertrophic chondrocytes. Osteomalacia is a similar disorder affecting mineralization of osteoid. Both result from insufficient calcium and phosphate levels. Vitamin D deficiency is a common cause and treatment involves vitamin D supplementation. Other causes discussed include hereditary disorders, prematurity, drugs, tumors, and renal osteodystrophy. Clinical features, radiographic findings, and management approaches are described for each condition.
VITAMIN D MUHAMMAD MUSTANSAR
Vitamin D is an essential nutrient that promotes calcium absorption in the intestines and maintains adequate serum calcium and phosphate concentrations to enable normal mineralization of bone. It exists in two main forms, D2 (ergocalciferol) and D3 (cholecalciferol), and is obtained through exposure to sunlight, dietary intake of oily fish, eggs, and vitamin D fortified foods. The liver converts vitamin D to calcidiol which is then converted by the kidneys to calcitriol, the biologically active form, which regulates calcium and phosphate levels. Deficiencies can lead to rickets in children and osteomalacia in adults, characterized by soft, deformed bones and muscle weakness.
Vitamin D
This document discusses vitamin D, including its sources, biochemical effects, and related diseases. It summarizes that vitamin D aids in calcium and phosphorus absorption in the intestine and bone mineralization. Deficiencies can cause rickets in children and osteomalacia in adults, resulting from insufficient mineralization of bones. Toxicity from oversupplementation can lead to excessive calcification.
Vitamin d3
This document discusses vitamin D, including its structure, biosynthesis from sunlight exposure, dietary sources, recommended daily allowance, metabolic functions in maintaining calcium and phosphate levels and bone mineralization, deficiency manifestations like rickets and osteomalacia, and potential non-skeletal roles. Vitamin D is fat-soluble and synthesized in the skin from sunlight exposure, with the biologically active form being calcitriol. Insufficient levels can lead to impaired bone mineralization and bone diseases while excess intake over prolonged periods can cause hypercalcemia.
Vit D
This document discusses vitamin D, including its forms, functions, metabolism, and deficiency/toxicity. Some key points:
- Vitamin D exists in two forms, D2 and D3. D3 is produced in the skin upon sun exposure and converted to its active form in the liver and kidneys.
- Its active form, calcitriol, regulates calcium and phosphorus levels by increasing their absorption in the intestine and reabsorption in kidneys. It also mobilizes calcium from bones.
- Deficiency causes rickets in children and osteomalacia in adults due to impaired bone mineralization. Toxicity leads to hypercalcemia which can damage soft tissues like kidneys.
Vitamin - D
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.
Metabolisme Vitamin D1 150207083340-conversion-gate01
1. Vitamin D is synthesized in the skin upon exposure to sunlight and is converted to its active form, calcitriol, in the kidneys.
2. Calcitriol increases intestinal absorption of calcium and phosphate and promotes their reabsorption in the kidneys to maintain mineral homeostasis.
3. It also supports bone mineralization by stimulating calcium and phosphate deposition from the blood into the bone.
VIT D ARUN A DR.pptx
1. Vitamin D is a fat-soluble vitamin that exists in two forms, D2 and D3, which are converted to calcitriol, the active form of vitamin D.
2. Calcitriol regulates calcium and phosphate levels by increasing their absorption in the intestine, reabsorption in the kidneys, and mobilization from bones.
3. Vitamin D deficiency can cause rickets in children and osteomalacia in adults, characterized by soft and deformed bones from mineralization problems.
VITAMIN D.pptx
Vitamin D chemistry synthesis, absorption, RDA, sources, Biochemical functions, deficiency, Rickets, osteomalacia, ricket rosary ,Hypervitaminosis D
CM & R.pptx
This document discusses calcium metabolism and rickets. It begins by introducing calcium's role in the body and dietary requirements. It then covers absorption, regulation by parathyroid hormone and calcitonin, and roles in bone mineralization. Rickets is defined as a childhood disease caused by calcium and vitamin D deficiencies, leading to softened, deformed bones. Causes, clinical features, investigations, management, and surgical options are described.
Vit d
This document discusses vitamin D in animals. It covers the chemical structure of vitamin D, how it is metabolized in the body through conversion in the liver and kidneys, its functions related to calcium and phosphorus homeostasis, and its roles in the intestines, bones and kidneys. The document also addresses requirements, natural sources, signs of deficiency such as rickets, and supplementation and toxicity concerns.
المحاضرة الاولى.pdf
Rickets is a metabolic bone disease caused by vitamin D deficiency or abnormalities in calcium and phosphate metabolism during bone development. It results in soft, weak bones in children that can lead to skeletal deformities. The key symptoms are bone pain, weak or soft bones, bowed legs, and skeletal deformities. Treatment involves high dose vitamin D supplementation combined with calcium and phosphate intake to mineralize the bones. Prevention focuses on adequate vitamin D from sunlight, diet, or supplements during pregnancy and childhood.
vitaminddeficiencyprats-pptx-121016120516-phpapp02 (1).pdf
Vitamin D is a group of fat-soluble prohormones that are mainly produced in the skin upon exposure to sunlight. It regulates calcium and phosphorus levels in the blood and promotes bone formation. Vitamin D deficiency can cause rickets in children, characterized by soft and weak bones and bone deformities, and osteomalacia in adults, which is the softening of bones. Risk factors include inadequate sunlight exposure, poor nutrition, and disorders inhibiting absorption. Treatment involves oral or injectable high-dose vitamin D to promote healing.
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Metabolisme Vitamin D1 150207083340-conversion-gate01
Metabolisme Vitamin D1 150207083340-conversion-gate01
vitaminddeficiencyprats-pptx-121016120516-phpapp02 (1).pdf
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Rickets
- 3. Rickets is defective mineralization or calcification of bones before epiphyseal closure in immature mammals due to deficiency or impaired metabolism of vitamin D, phosphorus or calcium potentially leading to fractures and deformity. Failureof osteoid to calcify in adults is called Osteomalacia. It is caused by failure of OSTEOID to calcify ingrowing person
- 5. Enamel hypoplasia is a defect of the teeth in which the enamel is hard but thin and deficient in amount. Harrison's groove, also known as Harrison's sulcus, is a horizontalgroove along the lower border of the thorax corresponding to the costal insertion of the diaphragm. Craniotabes is the finding of a softening or thinning of the skull. Pectus carinatum is a breastbone (sternum) and rib cartilage deformity that causes the chest to bow outward.
- 7. Some Other Features FTT (Failure To Thrive Or Flattering Weight) Listlessness (Showing No Interest In Anything) Protruding Abdomen, umbilical HERNIA Muscle Weakness (Specially Proximal) Fractures Craniosynostosis- Is A Condition In Which One Or More Of The Fibrous Sutures In An Infant Skull Prematurely Fuses By Turning Into Bone Thoracic Asymmetry, Widening Of Thoracic Bone Respiratory Infections, Atelectasis (Impairment Of Air Movement) Kyphosis, Lordosis Valgus Or Varus Deformities (Knock knee deformity) Windswept Deformity (combination Of Varus Deformity Of 1 Leg With Valgus Deformity Of Other Leg) Coxa Vara Leg Pain
- 9. Knock knee deformity (genu valgum) Bowleg deformity (genu varum) Wrist enlargement Rib beading (rachitic rosary)
- 11. HOW IT IS CAUSED
- 14. PATHOPHYSIOLOGY
- 15. Cholecalciferol (i.e., vitamin D-3) is formed in the skin from a derivative of cholesterol (5- dihydrotachysterol) under the stimulus of ultraviolet-B light.
- 16. Occurs at position 25 in the liver, producing calcidiol (25-hydroxycholecalciferol) The first hydroxylation This steroid undergoes hydroxylation in 2 steps. 16
- 17. Occurs in the kidney at the 1 position, where it undergoes hydroxylation to the active metabolite calcitriol (1,25-dihydroxycholecalciferol ) The second hydroxylation 17
- 18. Calcitriol Acts at 3 known sites to tightly regulate calcium metabolism: (1) It promotes absorption of calcium and phosphorus from the intestine (2) It increases reabsorption of phosphate in the kidney (3) It acts on bone to release calcium and phosphate.
- 20. Serum measurements in the workup for rickets may include the following: 1. Calcium 2. Phosphorus 3. Alkaline phosphatase 4. Parathyroidhormone 5. 25-hydroxy vitamin D 6. 1,25-dihydroxyvitamin D
- 21. Serum Chemistry Calcium (ionized fraction) is low Calcidiol (25-hydroxy vitamin D) is low Parathyroid hormone is elevated Phosphorus level is invariably low for age Alkaline phosphatase levels are uniformly elevated.
- 23. Anteroposterior and lateral radiographs of the WRIST of an 8-year-old boy with rickets demonstrates cupping and fraying of the metaphyseal region.
- 24. Radiograph in a 4-year-old girl with rickets depicts BOWING OF THE LEGS caused by loading.
- 25. Radiographs of the knee of a 3.6-year-old girl with hypophosphatemia depict severe fraying of the metaphysis.
- 27. Those at higher risk for developing rickets include: • Breast-fed infants whose mothers are not exposed to sunlight • Breast-fed infants who are not exposed to sunlight • Breast-fed babies who are exposed to little sunlight • Any child whose diet does not contain enough vitamin D or calcium
Editor's Notes
- Infants who are breastfed are at risk for rickets, especially those who: a. receive no oral supplementation b. have darkly pigmented skin
- http://www.slideshare.net/dangthanhtuan/vitamin-d-3591912