shin splints

anterior compartment syndrome of the lower extremity

Glasgow coma scale

check tms in head injury

the vitamins

Vitamin B1               Thiamin                beriberi

Vitamin B2               Riboflavin             riboflavin deficiency

Niacin                   Niacin                 pellagra

Vitamin B6               Pyridoxine             pyridoxine deficiency

Vitamin B12              Cobalamin              cobalamin deficiency

Vitamin C                Ascorbic Acid          scurvy

Vitamin A                Retinol                retinol deficiency

Vitamin D                ergocalciferol         rickets, osteomalacia

Vitamin E                tocopherol             tocopherol deficiency

Vitamin K                phylloquinone          phylloquinone deficiency 

 


vitamin related syndromes

 ____  ____  ___  _  _  ____  ____  ___ 
(  _ \(_  _)/ __)( )/ )( ___)(_  _)/ __)
 )   / _)(_( (__  )  (  )__)   )(  \__ \
(_)\_)(____)\___)(_)\_)(____) (__) (___/

from medconnect pediatric archives RICKETS Rickets is a disorder of calcification at the epiphyseal plate of long bones while osteomalacia is a defect of calcification in bone remodeling. In adults, only osteomalacia can be seen because the epiphyses have closed. Vitamin D deficiency is uncommon because of public health measures aimed at prevention but there are still numerous ways for children to get this disorder today. Vitamin D stores are usually adequate for the first 2 months of life. At different ages, the clinical presentation varies. In children less than 6 months, craniotabes (soft cranial bones) may be seen. Other signs of early rickets include increased sweating, rachitic rosary (enlarged costochondral junction) and enlargement of the wrists and ankles. As the child becomes older, frontal bossing and an enlarged anterior fontanelle which may not close till the second year of life can be seen. Eruption of teeth is frequently delayed and defects in enamel can occur. Other bony deformities include spinal lordosis, kyphosis, and scoliosis. Bending of the shafts of the tibia, fibula and femur may result in knock knees, bowlegs and other changes in the legs. In the child presented, a rachitic rosary could be palpated, and bowlegs could be observed once his tetany was treated and he once again was ambulatory. Tetany is a rare complication and occurs most frequently between 4 months and 2 years. It may be precipitated by short exposures to sunlight or Vitamin D in children who already have rickets. In the case presented, the child’s exposure to sunlight in the spring season after a long winter probably precipated calcium from serum into bone. When serum calcium falls below 7.5 mg/dl, muscular irritability is seen. Signs of tetany may be identified by a positive Chvostek’s, Trousseau’s or Erb’s sign. This may be followed by carpopedal spasm, seizures, and laryngospasm. Fatalities are associated with the latter. The diagnosis is made by the history and clinical exam and confirmed by results of serum chemistries and radiographs. The calcium and phosphorous are usually low but may be normal and the alkaline phosphatase and parathyroid hormone are usually elevated. Measurements of low levels of 25OHD can confirm the diagnosis. Radiographic changes in the radius and ulna include loss of definition of the distal metaphysis, splying and cupping of the metaphysis and an apparent increase between the ends of the shaft and the epiphyseal ossification center. Causes of rickets include calcium deficiency (inadequate intake) which can be seen in exclusively (non supplemented) breast fed infants and premature babies. Rickets can also be called by malabsorption. Examples include children with inadequate exposure to sunlight or stores of Vitamin D. Diseases associated with malabsorption include renal and hepatic insufficiency. Drug such as phenytoin have a direct effect on the intestinal mucosa thereby decreasing calcium absorption. Antacids may bind phosphate in the intestine and prevent absorption. Increased renal losses (excretion) of phosphate and/or calcium is a third mechanism which may be cause rickets and is seen with diseases that cause renal tubular dysfunction such as Fanconi syndrome and renal tubular acidosis. Suggested Readings 1.Bergtrom WH: Twenty ways to get rickets in the 1990’s. Contemporary Pediatrics 1991;8:88 2.Barness LA: Vitamins in nutition. In Practice of Pediatrics - Harper and Row Volume 6 1987 (7) 25-34



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