"of Vitamin K may also contribute to bleeding disorders because clotting factor maturation depends on Vitamin K. Thrombosis is the pathological development of blood clots. These clots may break free and become mobile, forming an embolus or grow to such a size that occludes the vessel in which it developed. An embolism is said to occur when the thrombus (blood clot) becomes a mobile embolus and migrates to another part of the body, interfering with blood circulation and hence impairing organ function downstream of the occlusion. This causes ischemia and often leads to ischemic necrosis of tissue. Most cases of"
"be prescribed depending on the type of disease. Vitamins (K, P and C) are essential in case of obstruction to walls of blood vessels. Also, vitamin K is required for the production of blood clotting factors, hence the injection of vitamin K (phytomenadione) is recommended to boost blood clotting. Herbal treatment is an alternative form of treatment which make use of plants to stimulate body's metabolism, stimulate blood coagulation and enhance tissue healing. Bleeding diathesis In medicine (hematology), bleeding diathesis (h(a)emorrhagic diathesis) is an unusual susceptibility to bleed (hemorrhage) mostly due to hypocoagulability (a condition of irregular and slow blood"
"resulting lack of fat soluble vitamins, including vitamin K, can result in hemorrhagic diathesis — bleeding from the gut and from under the skin. Children suffering with this condition were typically given blood transfusions, but with little improvement. In 1959, Dr. Fakhri, Tajeldin and Nouri at the Children’s Welfare Hospital in Baghdad discovered that these patients suffered from low prothrombin, which is essential for blood clotting. This could be remedied simply with vitamin K, a precursor of prothrombin. With this treatment the condition could be rapidly reversed, saving the lives of hundreds of patients threatened by this disease. Until the"
"blood should be immediately corrected if possible. Platelets should be maintained above 50,000/mL and clotting abnormalities should be corrected with vitamin K or fresh frozen plasma. Vitamin K should be taken orally unless the patient has cirrhosis or biliary obstruction, in which case it should be administered subcutaneously. The full effect of vitamin K is not obtained for 12–24 hours, unlike fresh frozen plasma which immediately reverses clotting abnormalities. The intravenous formulation of vitamin K reverses coagulopathy more quickly and may be used in cases of severe bleeding, however, patients should be monitored for anaphylaxis. The effects of fresh frozen"
"In severe vitamin A deficiency, lack of glycoproteins may lead to corneal ulcers or liquefaction. Vitamin A is essential to maintain intact epithelial tissues as a physical barrier to infection; it is also involved in maintaining a number of immune cell types from both the innate and acquired immune systems. These include the lymphocytes (B-cells, T-cells, and natural killer cells), as well as many myelocytes (neutrophils, macrophages, and myeloid dendritic cells). Vitamin A may be needed for normal red blood cell formation; deficiency causes abnormalities in iron metabolism. Vitamin A is needed to produce the red blood cells from stem"
"normal vitamin A levels in blood plasma. It also helps vitamin A become metabolized by the liver. However evidence suggests that when someone is deficient in both vitamin A and zinc, memory is more improved when just vitamin A is increased than when just zinc is increased. Of course memory has the largest improvement when both are increased. When one of these nutrients is not balanced, the other is most likely to be affected because they rely on each other for proper functioning in learning. Vitamin B, also known as thiamine, is a coenzyme essential for the metabolism of carbohydrates."
"being essential for blood to clot. Citrate is very effective in preventing blood from clotting; however, its use can lead to life-threateningly low calcium levels. This can be detected using the Chvostek's sign or Trousseau's sign. To prevent this complication, calcium is infused intravenously while the patient is undergoing the plasmapheresis; in addition, calcium supplementation by mouth may also be given. Other complications include: Donating plasma is similar in many ways to whole blood donation, though the end product is used for different purposes. Most plasmapheresis is for fractionation into other products; other blood donations are transfused with relatively minor"
"beta-thromboglobulin, which promote blood clotting. Other than nephrotic syndrome, there are many other factors that can promote hypercoagulability. Hypercoagulability can be promoted by increased platelet count, enhanced platelet aggregation, increased protein S count, and a decrease in coagulation inhibiters like antithrombin. Hypercoagulability can be inherited and/or acquired. Hyperhomocysteinemia, a condition known to promote clots, can be caused by a combination of genetic factors and vitamin B6, vitamin B12 and folic acid deficiency. Factor V Leidan and mutations of the prothrombin gene are the two most common genetic causes of hypercoagulability. About 5% of the general population have these heterozygous mutations"
"clotting factors II, VII, IX and X, as well as the regulatory factors protein C, protein S, and protein Z. Other proteins not involved in blood clotting, such as osteocalcin, or matrix Gla protein, may also be affected. The precursors of these factors require gamma carboxylation of their glutamic acid residues to allow the coagulation factors to bind to phospholipid surfaces inside blood vessels, on the vascular endothelium. The enzyme that carries out the carboxylation of glutamic acid is gamma-glutamyl carboxylase. The carboxylation reaction will proceed only if the carboxylase enzyme is able to convert a reduced form of vitamin"
"the body, sustaining good bone health as well as muscle function. When calcium in the body becomes under provided for normal bodily functions, calcitriol, an active form of Vitamin D, pairs with parathyroid hormone. Together they act to assemble cells in order to increase the calcium stores taken from bone. The popular term Sunshine vitamin, as it’s often called, is one of the one main sources of achieving sufficient Vitamin D through sunlight on the skin known as D3. The second form is commonly known as D2, which is found in foods such as fatty fish and fortified products like"
"A and vitamin C. Beta-Carotene is required to synthesize vitamin A and vitamin A is needed to synthesize retinol. A lack of retinol-binding protein is due to a lack of retinol which is required to trigger its production. The damaging effects of porphyrins interacting with iron, absorbing photons to then emit reactive oxygen species is the mechanism of action that results in the itchy, painful blisters that are common with PCT. The reactive oxygen species that are formed interact with and exhaust the antioxidants in the skin, primarily those of beta-Carotene, vitamin E, and vitamin C. Supplementation of these three"
"least five lobes). These hypersegmented neutrophils can be detected in the peripheral blood (using a diagnostic smear of a blood sample). The blood film can point towards vitamin deficiency: Blood chemistries will also show: Normal levels of both methylmalonic acid and total homocysteine rule out clinically significant cobalamin deficiency with virtual certainty. Bone marrow (not normally checked in a patient suspected of megaloblastic anemia) shows megaloblastic hyperplasia. The gold standard for the diagnosis of Vitamin B deficiency is a low blood level of Vitamin B. A low level of blood Vitamin B is a finding that normally can and should"
"and inhibit the aggregation of blood platelets. Through their role in vasodilation, prostacyclins are also involved in inflammation. They are synthesized in the walls of blood vessels and serve the physiological function of preventing needless clot formation, as well as regulating the contraction of smooth muscle tissue. Conversely, thromboxanes (produced by platelet cells) are vasoconstrictors and facilitate platelet aggregation. Their name comes from their role in clot formation (thrombosis). A significant proportion of the fatty acids in the body are obtained from the diet, in the form of triglycerides of either animal or plant origin. The fatty acids in the"
"vitamin K epoxide to vitamin K, which is the rate-limiting step in the physiological process of vitamin K recycling. The availability of reduced vitamin K is of importance for activation vitamin K 2,3-epoxide. The reduction of vitamin K epoxide is then responsible for the carboxylation of glutamic acid residues in some blood-clotting proteins, including factor VII, factor IX, and factor X. VKORC1 is of therapeutic interest both for its role in contributing to high interpatient variability in coumarin anticoagulant dose requirements and as a potential player in vitamin K deficiency disorders. Warfarin is a commonly prescribed oral anticoagulant, or blood"
"is commonly used to refer to B-deficient anemia as a whole, regardless of cause. Vitamin B refers to a group of compounds called cobalamins that are available in the human body in a variety of mostly interconvertible forms. Together with folate, cobalamins are essential cofactors required for DNA synthesis in cells where chromosomal replication and division are occurring—most notably the bone marrow and myeloid cells. As a cofactor, cobalamins are essential for two cellular reactions: Cobalamins are characterized by a porphyrin-like corrin nucleus that contains a single cobalt atom bound to a benzimidazolyl nucleotide and a variable residue (R) group."
"that lead to the synthesis of serotonin and catecholamine neurotransmitters. Concentrations of blood plasma folate and homocysteine concentrations are inversely related, such that an increase in dietary folate decreases homocysteine concentration. Thus, dietary intake of folate is a major determinant of homocysteine levels within the body. The relationship between folate and B is so interdependent that deficiency in either vitamin can result in megaloblastic anemia, characterized by organic mental change. The link between levels of folate and altered mental function is not large, but is sufficient enough to suggest a causal association. Deficiency in folate can cause an elevation of"
"large amount of blood or bleeding occurs over a long period of time. Anemia is also commonly associated with an iron deficiency, due to the importance of iron in the formation of red blood cells (RBCs). When anemia is diagnosed as a result of blood in the stool, vitamins that are important for RBC formation (folate, vitamin B12, and vitamin C) are frequently prescribed in order to ensure that all the materials are available for those cells that are made. Diagnostic measures can be used as interventions to help stop bleeding in some cases. Bleeding that occurs due to a"
"Gla-residues are inadequately formed and the Gla-proteins are insufficiently active. Menaquinone (vitamin K), but not phylloquinone (vitamin K), intake is associated with reduced risk of CHD mortality, all-cause mortality and severe aortic calcification. The prevalence of vitamin K deficiency varies by geographic region. For infants in the United States, vitamin K deficiency without bleeding may occur in as many as 50% of infants younger than 5 days old, with the classic hemorrhagic disease occurring in 0.25-1.7% of infants. Therefore, the Committee on Nutrition of the American Academy of Pediatrics recommends that 0.5 to 1.0 mg Vitamin K be administered to"
"The gut bacteria make vitamin K and are killed by antibiotics. This decreases vitamin K levels and therefore the production of these clotting factors. Deficiencies of platelet function may require platelet transfusion while deficiencies of clotting factors may require transfusion of either fresh frozen plasma or specific clotting factors, such as Factor VIII for patients with hemophilia. Dioxaborolane chemistry enables radioactive fluoride (F) labeling of red blood cells, which allows for positron emission tomography (PET) imaging of intracerebral hemorrhages. The word ""Haemorrhage"" (or ""hæmorrhage""; using the æ ligature) comes from Latin haemorrhagia, from Ancient Greek αἱμορραγία (haimorrhagía, “a violent bleeding”),"
"and permanent bone damage. Vitamin D, also coined as the sunshine vitamin, is necessary within a child’s diet as it allows body tissues and in particular bone to be properly nourished and mineralized. Vitamin D3, which is gained from dietary nutrients, is also essential for calcium absorption and homeostasis, which ensures standard muscle contraction and the transport of blood throughout the body. Without adequate consumption of vitamin D, children can become predisposed to conditions such as rickets, which is the ""softening or weakening of bones"". which can only be treated with vitamin D supplements, sunlight and surgery. Vitamin D is"
"indicators of Vitamin deficiency. Vitamin adenosylcobalamin is needed as cofactor in methylmalonyl-CoA mutase—MUT enzyme. Processing of cholesterol and protein gives propionyl-CoA that is converted to methylmalonyl-CoA, which is used by MUT enzyme to make succinyl-CoA. Vitamin is needed to prevent anemia, since making porphyrin and heme in mitochondria for producing hemoglobin in red blood cells depends on succinyl-CoA made by vitamin . Poor absorption of vitamin may be related to coeliac disease. Intestinal absorption of vitamin requires successively three different protein molecules: haptocorrin, Intrinsic Factor and Transcobalamin II. Cyanocobalamin Cyanocobalamin is a synthetic form of vitamin. Vitamin is the ""generic"
"an organic chelator, such as citrate ion, causes their dysfunction, and prevents blood from coagulating. Thus, citrate addition to blood is the most common method of storing it in a liquid state between harvest and transfusion. Carboxyglutamic acid Carboxyglutamic acid (or the conjugate base, carboxyglutamate), is an uncommon amino acid introduced into proteins by a post-translational carboxylation of glutamic acid residues. This modification is found, for example, in clotting factors and other proteins of the coagulation cascade. This modification introduces an affinity for calcium ions. In the blood coagulation cascade, vitamin K is required to introduce gamma-carboxylation of clotting factors"
"life-threatening. People should seek immediate medical care for serious symptoms, including heavy external bleeding, blood in the urine or stool, double vision, severe head or neck pain, repeated vomiting, difficulty walking, convulsions, or seizures. They should seek prompt medical care if they experience mild but unstoppable external bleeding or joint swelling and stiffness. The normal clotting process depends on the interplay of various proteins in the blood. Coagulopathy may be caused by reduced levels or absence of blood-clotting proteins, known as clotting factors or coagulation factors. Genetic disorders, such as hemophilia and Von Willebrand's disease, can cause a reduction in"
"and rats, because the amount and effectiveness of the VKORC enzyme has not changed, but the ability of warfarin to exert its effect (antagonize the enzyme) has changed. These isoform mutations are rare except in Ethiopian and certain Jewish populations. VKORC1 The human gene ""VKORC1"" encodes for the enzyme, Vitamin K epOxide Reductase Complex (VKORC) subunit 1. This enzymatic protein complex is responsible for reducing vitamin K 2,3-epoxide to its active form, which is important for effective clotting. In humans, mutations in this gene can be associated with deficiencies in vitamin-K-dependent clotting factors. The VKORC1 protein is a key enzyme"
"propensity to develop thrombosis in a disorder causing a decrease in a critical protein for blood clotting may be due to the function of fibrin (the split product of fibrinogen that is the basis for forming blood clots) to promote the lysis or desolution of blood clots. Lower levels of fibrin may reduce the lysis of early fibrin strand depositions and thereby allow these depositions to develop into clots. Congenital hypofibrinogenemia must be distinguished from: a) congenital afibrinogenemia, a rare disorder in which blood fibrinogen levels are either exceedingly low or undetectable due to mutations in both fibrinogen genes; b)"
"has been known to cause bleeding diathesis, especially in undiagnosed infants, due to malabsorption of fat soluble vitamins like vitamin K. There are autoimmune causes of coagulation disorders. They include acquired antibodies to coagulation factors, termed inhibitors of coagulation. The main inhibitor is directed against clotting factor VIII. Another example is antiphospholipid syndrome, an autoimmune, hypercoagulable state. Bleeding diathesis may also be caused by impaired wound healing (as in scurvy), or by thinning of the skin, such as in Cushing's syndrome. Some people lack genes that typically produce the protein coagulation factors that allow normal clotting. Various types of hemophilia"
"depend on adequate levels of folate within blood plasma. Concentrations of blood plasma folate and homocysteine concentrations are inversely related, such that an increase in dietary folate decreases homocysteine concentration. Thus, dietary intake of folate is a major determinant of homocysteine levels within the body. Autoantibodies against folate receptor alpha have been found in up to 75% of children with autism. Folate deficiency most commonly arises from insufficient folate intake from the diet, but may also stem from inefficient absorption or metabolic utilization of folate, usually a result of genetic variation. The relationship between folate and B is so interdependent"
"and genetic or disease-related deficiencies in the blood's clotting abilities. Platelet activation can occur through different mechanisms such as a vessel wall breach that exposes collagen, or tissue factor encryption. The platelet activation causes a cascade of further platelet activation, eventually causing the formation of the thrombus. This process is regulated through thromboregulation. Blood clot prevention and treatment reduce the risk of stroke, heart attack and pulmonary embolism. Heparin and warfarin are used to inhibit the formation and growth of existing thrombi, with the former used for acute anticoagulation while the latter is used for long-term anticoagulation. The mechanism of"
"on a daily basis, with some 5–10 microgram of the vitamin B involved in enterohepatic circulation. This is in general a principal characteristic of water-soluble vitamins, in that no matter the oral intake, there is a certain threshold for intestinal absorption hence, low or non-existent chance of intoxication, as opposed to fat-soluble vitamins. Vitamin B has a major function in the nuclear replication of the DNA. It is therefore logical that its deficiency causes decrease bone marrow production, one of the most common manifestations of which is decreased red blood cell production or as it is referred to medically, anemia."
"formation of anticoagulant factors protein C and S. It is commonly used to treat warfarin toxicity, and as an antidote for coumatetralyl. Vitamin K is required for bone protein formation. Phytomenadione Phytomenadione, also known as vitamin K or phylloquinone, is a vitamin found in food and used as a dietary supplement. As a supplement it is used to treat certain bleeding disorders. This includes in warfarin overdose, vitamin K deficiency, and obstructive jaundice. It is also recommended to prevent and treat hemorrhagic disease of the newborn. Use is typically recommended by mouth or injection under the skin. Use by injection"
"prothrombin time and thus can result in coagulopathy, a bleeding disorder. Symptoms of K deficiency include anemia, bruising, nosebleeds and bleeding of the gums in both sexes, and heavy menstrual bleeding in women. Osteoporosis and coronary heart disease are strongly associated with lower levels of K (menaquinone). Vitamin K (as menaquinones MK-4 through MK-10) intake level is inversely related to severe aortic calcification and all-cause mortality. The function of vitamin K in the animal cell is to add a carboxylic acid functional group to a glutamate (Glu) amino acid residue in a protein, to form a gamma-carboxyglutamate (Gla) residue. This"
"biochemical point of view, two essential enzymatic reactions require vitamin B (cobalamin). Intracellular vitamin B is maintained in two active coenzymes, methylcobalamin and 5-deoxyadenosylcobalamin. In the face of vitamin B deficiency, conversion of methylmalonyl-CoA to succinyl-CoA cannot take place, which results in accumulation of methylmalonyl-CoA and aberrant fatty acid synthesis. In the other enzymatic reaction, methylcobalamin supports the methionine synthase reaction, which is essential for normal metabolism of folate. The folate-cobalamin interaction is pivotal for normal synthesis of purines and pyrimidines and the transfer of the methyl group to cobalamin is essential for the adequate supply of tetrahydrofolate, the substrate"
"the body, and thus need to be obtained from food. B-complex vitamins are water-soluble vitamins, which means that they are not stored within the body. In consequence, the B vitamins need ongoing replenishment. It is possible to identify broad cognitive effects of certain B vitamins, as they are involved in many significant metabolic processes within the brain. This vitamin is important for the facilitation of glucose use, thus ensuring the production of energy for the brain, and normal functioning of the nervous system, muscles and heart. Thiamine is found throughout mammalian nervous tissue, including the brain and spinal cord. Metabolism"