Rahistismul If not treated during the growing child, skeletaldeformity and short stature may be permanent. However, iftreatment is done on time, bone deformity is reduced and disappears with time.
Symptoms disappear by the intake of calcium, phosphorus and / or vitamin D.
Food sources of vitamin D are fish, liver and milk.
Systematic preventive treatment consists of prescribing vitamin Dfor infants:
-800 = 400 IU (international units) / day if the baby is exposed toenough sunlight
= 800 IU / day if sun exposure is poor
= 1200 IU / day in children with pigmented skin
Baby milk manufacturers are required to supplement vitamin D inmilk 400-500 IU / liter. However, we recommend continuing vitamin D supplementation in infants -800 400 IU / day to avoid rahistismulDeficiency.
Should not be neglected but the risk of overdose. Doses of vitamins should be prescribed by the physician ashypervitaminosis D is serious. Parents need to recognize thewarning signs:
- Anorexia (loss of appetite), constipation, pallor
- Thirst, polyuria
- Nausea, vomiting, abdominal pain
- Behavioral
Friday, June 24, 2011
Rickets - Signs and symptoms
Clinical signs appear between 3 months and 2 years and include:
- Pain in bones and legs, spine and pelvis
- Deformation of the skeleton: abnormal curvature of the legs(genu varum or valgum), prominent sternum ("pigeon breast") or blind (pectus excavatum)
- Extremities protruding ribs ("rosary cost"), "bracelets rickety" thewrists or ankles (thickening of the radius and tibia extremities,spine deformity: scoliosis or kyphosis, pelvic distortion.
- Craniotabes rickety: softening of skull bones, which appear to touch a ball of celluloid
- Fontanelle (membranous space between the skull bones of anewborn) is higher than normal
- Increased tendency to fracture bones
- Delay the appearance of teeth
- Defects in tooth structure
- Increasing the number of cavities
- Progressive weakening
- Decrease muscle tone
- Muscle cramps
- Stopping growth
- Fever (especially at night)
- Flatulence
- Umbilical hernia
- Ptosis liver
- Hiperlaxitate ligamentous
- Delay to maintain head and went
- Pain in bones and legs, spine and pelvis
- Deformation of the skeleton: abnormal curvature of the legs(genu varum or valgum), prominent sternum ("pigeon breast") or blind (pectus excavatum)
- Extremities protruding ribs ("rosary cost"), "bracelets rickety" thewrists or ankles (thickening of the radius and tibia extremities,spine deformity: scoliosis or kyphosis, pelvic distortion.
- Craniotabes rickety: softening of skull bones, which appear to touch a ball of celluloid
- Fontanelle (membranous space between the skull bones of anewborn) is higher than normal
- Increased tendency to fracture bones
- Delay the appearance of teeth
- Defects in tooth structure
- Increasing the number of cavities
- Progressive weakening
- Decrease muscle tone
- Muscle cramps
- Stopping growth
- Fever (especially at night)
- Flatulence
- Umbilical hernia
- Ptosis liver
- Hiperlaxitate ligamentous
- Delay to maintain head and went
Rickets - Diagnosis
Blood tests are performed to measure the quantity of minerals(calcium and phosphorus). Abnormalities characteristic of ricketsbone radiographs reveals.
Other tests that can be performed to diagnose rickets aims:
1.Hormonul parathyroid (PTH)
2.Calciuria (amount of calcium in urine)
3.Calciul ionic
4.Fosfataza alkaline
Other tests that can be performed to diagnose rickets aims:
1.Hormonul parathyroid (PTH)
2.Calciuria (amount of calcium in urine)
3.Calciul ionic
4.Fosfataza alkaline
Rickets
Rickets is a disease of childhood and adolescence, which is characterized by incomplete mineralization of bone under the deficiency of vitamin D. This is due to calcium loss from bones, which are flexible and deforms.
Rickets occurs mainly in children between 3 months and 2 years, during which the child grows quickly and its body requires a high level of calcium and phosphorus. The condition is rare in newborns.Vitamin D allows calcium intestinal absorption, bone mineralization acting on, and on urine calcium excretion. Most vitamin D is synthesized in the epidermis, where inactive sterols are activated by ultraviolet rays.
Causes of rickets:
The main cause of rickets is vitamin D deficiency during childhood.Vitamin D is a fat-soluble vitamins (fat soluble), which can be absorbed from the intestines or the skin may be produced when skin is exposed to sunlight (UV rays contribute to vitamin D synthesis by the body). Vitamin D is converted assimilated into its active form, functioning as a hormone that regulates calcium absorption from the intestines and that regulates the calcium and phosphorus in bones. When these minerals in the blood level is too low to destroy bone matrix protein.
In rickets, another mechanism comes into operation to increase blood calcium level. Parathyroid glands (four glands located behind the thyroid hormone) increase its functioning to compensate for low levels of calcium in the blood. To increase the level of blood calcium, bone calcium destroys the hormone, resulting in further loss of calcium and phosphorus in bones. In severe cases, cysts may develop in the bones.
Vitamin D deficiency can have several causes:
environmental factors: limited exposure to the sun, winter, temperate, etc..vitamin D in dietintestinal malabsorption (steatorrhea) - the body can not absorb fats, which went directly into the feces. Thus, vitamin D, which is usually absorbed with fat and calcium are poorly absorbed.Renal tubular acidosis - increase the amount of acid in body fluids due to a congenital or acquired kidneylack of calcium and phosphorus in the diet favors the appearance of ricketsa dietary deficiency of vitamin D may occasionally occur and vegetarians who do not consume dairy products, or people with lactose intolerance.
Rickets occurs mainly in children between 3 months and 2 years, during which the child grows quickly and its body requires a high level of calcium and phosphorus. The condition is rare in newborns.Vitamin D allows calcium intestinal absorption, bone mineralization acting on, and on urine calcium excretion. Most vitamin D is synthesized in the epidermis, where inactive sterols are activated by ultraviolet rays.
Causes of rickets:
The main cause of rickets is vitamin D deficiency during childhood.Vitamin D is a fat-soluble vitamins (fat soluble), which can be absorbed from the intestines or the skin may be produced when skin is exposed to sunlight (UV rays contribute to vitamin D synthesis by the body). Vitamin D is converted assimilated into its active form, functioning as a hormone that regulates calcium absorption from the intestines and that regulates the calcium and phosphorus in bones. When these minerals in the blood level is too low to destroy bone matrix protein.
In rickets, another mechanism comes into operation to increase blood calcium level. Parathyroid glands (four glands located behind the thyroid hormone) increase its functioning to compensate for low levels of calcium in the blood. To increase the level of blood calcium, bone calcium destroys the hormone, resulting in further loss of calcium and phosphorus in bones. In severe cases, cysts may develop in the bones.
Vitamin D deficiency can have several causes:
environmental factors: limited exposure to the sun, winter, temperate, etc..vitamin D in dietintestinal malabsorption (steatorrhea) - the body can not absorb fats, which went directly into the feces. Thus, vitamin D, which is usually absorbed with fat and calcium are poorly absorbed.Renal tubular acidosis - increase the amount of acid in body fluids due to a congenital or acquired kidneylack of calcium and phosphorus in the diet favors the appearance of ricketsa dietary deficiency of vitamin D may occasionally occur and vegetarians who do not consume dairy products, or people with lactose intolerance.
Thursday, June 23, 2011
Prematurity - evolution premature baby
An increased degree of prematurity will result in severe respiratory distress, which will cause the death of infants shortly after birth.
Another category of preamturi be recorded in their stationaryweight evolution, remains fragile.
A third group of premature infants presents initially at a rate of growth slowed, then weight is the net upward curve equaling other children during infancy.
Premature presents a very accelerated pace of growth compared to the weight of the newborn at term. He doubled their weight after 2-3 months of life, one triple to reach age 6 months and 1 year to have 6 times more weight at birth.
Perimeter of the head of it equals that of the premature babynewborn to 3 months. Physiologic jaundice is installed earlier,being more intense and more prolonged risk of hyperbilirubinemiaencephalopathy.
Missing or genital crisis occurs later. Neuro-psychologicaldevelopment and mental impairment may have deficiencies,idiocy, epilepsy, paralysis, disease Little.
The prognosis depends on prematurity, hypoxia at birth, causes that triggered preterm birth, care and subsequent morbidity.
Another category of preamturi be recorded in their stationaryweight evolution, remains fragile.
A third group of premature infants presents initially at a rate of growth slowed, then weight is the net upward curve equaling other children during infancy.
Premature presents a very accelerated pace of growth compared to the weight of the newborn at term. He doubled their weight after 2-3 months of life, one triple to reach age 6 months and 1 year to have 6 times more weight at birth.
Perimeter of the head of it equals that of the premature babynewborn to 3 months. Physiologic jaundice is installed earlier,being more intense and more prolonged risk of hyperbilirubinemiaencephalopathy.
Missing or genital crisis occurs later. Neuro-psychologicaldevelopment and mental impairment may have deficiencies,idiocy, epilepsy, paralysis, disease Little.
The prognosis depends on prematurity, hypoxia at birth, causes that triggered preterm birth, care and subsequent morbidity.
Subscribe to:
Posts (Atom)