Vitamins hemorrhagic disease

Parenteral Anticoagulant-induced prothrombin deficiency hypoprothrombinemia secondary to conditions limiting absorption or synthesis of vitamin K (eg, obstructive jaundice, biliary fistula, sprue, ulcerative colitis, celiac disease, intestinal resection, cystic fibrosis of the pancreas, regional enteritis) drug-induced hypoprothrombinemias due to interference with vitamin K metabolism (eg, antibiotics, salicylates) prophylaxis and therapy of hemorrhagic disease of the newborn. 

Hypoprothrombinemia may occur in malabsorption syndromes and also the use of broad-spectrum antibiotics may produce a hypoprothrombinemia that responds readily to small doses of vitamin K. In premature infants and in infants with hemorrhagic disease of the newborn the use of vitamin K may be indicated. However, the main indication for the use of vitamin K is to antagonize the anticoagulant activity of coumarins. Oral absorption of phytonadione and the menaquinones is by the lymph while menadione and its water-soluble derivatives are absorbed directly. The absorption of phytonadione is energy-dependent and saturable. Intravenous administration of phytonadione has produced flushing, dyspnea, chest pains, and cardiovascular collapse. 

Deficiency of vitamin K in the newborn Newborns have sterile intestines and cannot initially synthesize vitamin K. Because human milk provides only about one fifth of the daily requirement for vitamin K, it is recommended that all newborns receive a single intramuscular dose of vitamin K as prophylaxis against hemorrhagic disease. 

Vitamin K A. plays an essential role in preventing thrombosis. B. increases the coagulation time in newborn infants with hemorrhagic disease. C. is present in high concentration in cow or breast milk. D. is synthesized by intestinal bacteria. E. is a water-soluble vitamin. Correct answer = D. Vitamin K is essential for clot formation, decreases coagulation time, and is present in low concentrations in milk. 

Vitamin K was discovered in 1935 as a result of studies of a hemorrhagic disease of chickens fed on solvent-extracted fat-free diets and cattie fed on silage made from spoiled sweet clover. The problem in the chickens was a lack of the vitamin in the diet, whereas in the catde it was from the presence of di-coumarol, an antimetabolite of the vitamin. It soon became apparent that vitamin K was required for the synthesis of several of the proteins required for blood clotting, but it was not until 1974 that Stenflo and coworkers (1974) elucidated the mechanism of action of the vitamin. A new amino acid, y-carboxyglutamate (Gla) was found to be present in the vitamin K-dependent proteins, but absent from the abnormal precursors that circulate in deficiency. y-Carboxyglutamate is chemically unstable and undergoes spontaneous decarboxylation to glutamate when proteins are hydrolyzed in acid for amino acid analysis. 

Over the first 6 weeks of postnatal life, the plasma concentrations of clotting factors gradually rise to the adult level in the meantime, they are at risk of potentially fatal hemorrhage that was formerly called hemorrhagic disease of the newborn and is now known as vitamin K deficiency bleeding in infancy. It is usual to give all newborn infants prophylactic vitamin K, either orally or by intramuscular injection (Sutor et al., 1999). At one time, menadione was used, but, because of the association between menadione and childhood leukemia (Section 5.6.1), phylloquinone is preferred. 

Vitamin K is routinely administered in many countries to newborn babies in varying doses and by various routes, most commonly either orally or by intramuscular injection, to prevent hemorrhagic disease of the newborn (see Table 1). 

Hemorrhagic disease of the newborn can develop readily because of (1) poor placental transfer of vitamin K, (2) hepatic immaturity leading to inadequate synthesis of coagulation proteins, and (3) the low vitamin K content of early breast milk. Prothrombin levels during this period are only about 25% of the adult levels. Severe diarrhea and antibiotics used to suppress diarrhea readily exacerbate the situation, so prothrombin levels can drop below 5% of the adult level and bleeding can occur. This condition is routinely prevented by the prophylactic administration of 0.5 to 1.0 mg of phylloquinone intramuscularly, or 2.0 mg given orally immediately after birth. 

Rarely is a vitamin K deficiency caused by insufficient diet. It more likely is attributable to a medical condition. At one time, multivita-itdn supplements rarely contained vitamin K. It is now routinely found in these products. Causes of vitamin K deficiency include obstructive jaundice (now uncommon), loss of intestinal flora in preparation for intestinal surgery, and hemorrhagic disease of the newborn. 

The third cause is hemorrhagic disease of the newborn. Infants are born with a sterile intestinal tract. Until the flora are established, the infant will have to get along with the vitamin K they received from the mother. In the past an infant might die from hemorrhaging. Most states require that each newborn receive an injection of phytonadione. Menadione injection is not given because it can cause a hemolytic anemia in the newborn. 

Vitamin K antagonists were first identified by K. R Link while he was investigating a hemorrhagic disease in... 

The answer is c. (Murray, pp 627-661. Scriver, pp 3897—3964. Sack, pp 121-138. Wilson, pp 287-320.) Hemorrhagic disease of the newborn is caused by poor transfer of maternal vitamin K through the placenta and by lack of intestinal bacteria in the infant for synthesis of vitamin K. The intestine is sterile at birth and becomes colonized over the first few weeks. Because of these factors, vitamin K is routinely administered to newborns. Deficiencies of the fat-soluble vitamins A, E, D, and K can occur with intestinal malabsorption, but avid fetal uptake during pregnancy usually prevents infantile symptoms. Hypervltaminosis A can cause liver toxicity but not bleeding, and deficiencies of E (neonatal anemia) or C (extremely rare in neonates) have other symptoms besides bleeding. 

Healthy newborn infants show decreased plasma concentrations of vitamin K-dependent clotting factors for a few days after birth, the time required to obtain an adequate dietary intake of the vitamin and to establish a normal intestinal flora. In premature infants and in infants with hemorrhagic disease of the newborn, the concentrations of clotting factors are particularly depressed, possibly reflecting vitamin K deficiency. Measurements of non-y-carboxylated prothrombin suggest that true vitamin K deficiency occurs in - 3% of live births. 

Hemorrhagic disease of the newborn has been associated with breast-feeding human milk has low concentrations of vitamin K. In addition, the intestinal flora of breast-fed infants may lack microorganisms that synthesize the vitamin. Commercial infant formulas are supplemented with vitamin K. 

In the neonate with hemorrhagic disease of the newborn, the administration of vitamin K raises the concentration of these clotting factors to the level normal for the newborn infant and controls the bleeding tendency within -6 hours. The routine administration of 1 mg phylloquinone intramuscularly at birth is required by law in the U.S.. This dose may have to be increased or repeated if the mother has received anticoagulant or anticonvulsant drug therapy or if the infant develops bleeding tendencies. Alternatively, some clinicians treat mothers who are receiving anticonvulsants with oral vitamin K prior to delivery (10-20 mg/day for 2 weeks). 

---