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Fat Soluble Vitamin Deficiencies

Vitamin A (Retinol, Retinal or Retinoic Acid) functions as a component of light reception pigment in the retina. Therefore, deficiencies affect vision and cause Night Blindness. Vitamin A also acts as a growth factor that causes the differentiation of cells. Therefore, vitamin A can be used to treat certain types of AML as it causes differentiation of immature leukemic cells. This effect of differentiation of Vitamin A also means deficiencies can affect the immune response. Vitamin A supplements for deficient patients can be an effective treatment for disease like Measles. Deficiencies can result from fat malabsorption or inadequate intake of foods high in vitamin A (Liver, fruits, & vegetables).

Vitamin A is also a teratogen that can cause numerous problems for an unborn fetus. This makes sense as prenatal development is a period where cell differentiate needs to be highly orchestrated. Too much vitamin A could interrupt this delicate process due to its effects on cell differentiation. Vitamin A should not be used as a treatment for women who may be pregnant.

Vitamin A toxicity can result in a wide array of non-specific symptoms like nausea, irritability, headaches, visual problems, and changes to skin or hair. Most other vitamin deficiencies or toxicities have a more specific classic presentation. Therefore, I usually just rule out the other answer choices and select Vitamin A toxicity if nothing else fits.

Vitamin D [1,25-(OH)2D3] is synthesized in the body as a result of sun exposure or ingested as part of cow’s milk (breast milk is actually low in vitamin D). The inactive precursor to Vitamin D undergoes enzymatic processing in the liver and the kidney to become 1,25-(OH)2D3. This active form of Vitamin D primarily increases the absorption of calcium and phosphate from the diet. Therefore, deficiencies of Vitamin D lead to decreased bone mineralization. Vitamin D deficiency in children leads to Rickets and in adults it leads to Osteomalacia.

Vitamin K is responsible for the modification of numerous proteins required for coagulation. Therefore, deficiencies of Vitamin K lead to deficiencies of Coagulation Factors II, VII, IX & X as well as deficiencies in Protein C & S. This can lead to an increased PT, increased PTT, bruising (purpura, ecchymosis, perifollicular hemorrhages) and other problems related to clotting.

Vitamin K is taken in through the diet & synthesized by normal gut flora. Both of these routes lead to an inactive form of Vitamin K that must be activated by liver Epoxide Reductase. Coumadin (AKA Warfarin) inhibits Epoxide Reductase to intentionally create a Vitamin K deficiency and inhibit clotting. Patients with liver failure may have difficulty activating their vitamin K also. Patients who are on wide spectrum antibiotics may have a deficiency if Vitamin K because antibiotics can kill off the normal gut flora which produce Vitamin K. Newborns also often have Vitamin K deficiency because they have not yet been colonized with the normal flora that create Vitamin K and breast milk is low in Vitamin K. This is referred to as Hemorrhagic disease of the Newborn and is why newborns are usually given a shot of Vitamin K soon after birth.

Now that you are done with this video you should check out the next video in the Vitamins section which covers Folate & B12 Deficiency (http://www.stomponstep1.com/folate-b12-deficiency-megaloblastic-anemia-hypersegmented/)