Avitaminosis is any disease caused by chronic or long-term vitamin deficiency or a disease caused by a defect in metabolic conversion, such as that of tryptophan to niacin.
Fat-soluble vitamins are K, A, D, and E. Precisely because they are fat-soluble, they can accumulate in the body, and avitaminosis occurs when fat absorption is impaired. Their lack is noticed only after a few months since they are stored. Diseases of the pancreas, liver, bile, and bile ducts and prolonged and fatty diarrhea can cause a deficiency of these vitamins.
Vitamin A avitaminosis
Vitamin A (retinol, carotene) is important for maintaining normal differentiation of epithelium, skeletal muscle, and cell membrane components. It is essential for photosensitive retinal epithelium. Because vitamin A deficiency (ICD-10: E50) causes xerophthalmia and night blindness. In nature, vitamin A appears as retinol (a more important form in which it is stored, transmitted, and actively involved in the function of sight) or as beta-carotene (provitamin A in yellow and leafy vegetables).
In the absence of vitamin A, the epithelium irregularly keratinizes and shows signs of the cylindrical epithelium’s squamous metaplasia. We see such changes in the trachea, bronchi, renal droplets, uterus, pancreatic ducts, and salivary gland ducts. You cannot regenerate rhodopsin so that vision disorders will occur. In short, in vitamin A deficiency, we have:
- eye changes – night blindness due to retinol deficiency, xerophthalmia (dry eyes), increased frequency of infections, Bitot spots, softening of the cornea with consequent susceptibility to infections (keratomalacia).
- skin changes – follicular hyperkeratosis due to impaired keratinization of the epithelium in hair follicles,
- respiratory epithelial metaplasia with favoring infections and bronchopneumonias
Vitamin D deficiency
Vitamin D’s function is to maintain normal plasma calcium and phosphorus levels. Calcium deficiency disrupts neural excitation and muscle relaxation, leading to hypocalcemic tetany. You should remember the sign of hypocalcemia – Chvostek’s sign (tapping on the facial muscle causes facial muscle spasms) and Trousseau’s sign (arm muscle spasms when a cuff like a pressure gauge is put on).
Vitamin D deficiency in children causes rickets, and in adults, osteomalacia. The underlying disorder in both diseases is reduced mineralization of the newly formed bone matrix. In children, growth is not yet complete, so the pineal glands are open, there is insufficient mineralization of the newly formed bone and cartilaginous matrix in the growth zone. Epiphyseal cartilage overgrows without adequate calcification and normal cartilage cell maturation. The growth zone is wide and irregular. The cartilaginous cells are large, irregularly distributed, only in rows. The thickened ossification border is macroscopically observed as a spherical spindle thickening called a rickets crown.
Due to the abundance of osteoids, the bone is soft, flexible, and suitable for distortion and deformation. The softened occipital bone that dies when touched is called the craniotabes. The head takes on a square shape due to many osteoids created in frontal and parietal protuberances (square head – square head ). And the spine is softened, causing kyphoscoliosis. The sternum protrudes or dents (pectus carinatum or pectus excavatum). The bones of the limbs are thick and stocky and shorter. The softer bones in the legs bend and form deformed O or X-shaped legs. In women, the pelvis becomes narrowed due to the sacrum’s impression and the suppression of the acetabulum ( pelvis angusta ) or flat ( pelvis plan ).
Vitamin K comes in two forms: K 1 in plants and K 2, synthesized by the bacterial intestinal flora. Vitamin K serves as a cofactor in glutamic acid’s carboxylation to gamma-carboxyglutamic acid (in the liver). It is necessary for the functioning of the three clotting factors (VII, IX, and X) and proteins C and S. The natural deficiency of vitamin K occurs in newborns because they have sterile intestines. The most important complication is hemorrhagic diathesis (bleeding tendency), with the most dangerous manifestation being intracranial hemorrhage. Therefore, vitamin K is given to newborns prophylactically to avoid vitamin K avitaminosis.
Vitamin B 1 (thiamine)
Vitamin B avitaminosis 1 (thiamine) is known as beriberi. It most commonly occurs in alcoholics. Thiamine deficiency is manifested by changes in peripheral nerves, the brain, and the heart. Peripheral nonspecific neuropathy or dry beriberi is asymmetrical neuropathy that first appears on the legs, followed by weakened reflexes, atrophy, and muscle weakness. It is characterized by myelin degeneration and axon fragmentation. Changes in the cardiovascular system or wet beriberi are characterized by peripheral vasodilation leading to AV shunts and consequent dilatation of the heart.
The heart is dilated, thinned walls, heavier and reduced stroke volume, leading to peripheral edema. As mentioned earlier, alcoholics develop Wernicke-Korsakoff syndrome due to thiamine deficiency, two syndromes, Wernicke’s encephalopathy and Korsakoff’s psychosis, which often occurs together for the same cause. Encephalopathy is characterized by ophthalmoplegia (weakening of extraocular muscles), ataxia (incoordination of voluntary movements), and confusion.
Korsakoff’s syndrome is also called an amnesia-confabulatory syndrome due to retrograde amnesia, inability to remember new information, and confabulation.
Vitamin B 2 (riboflavin)
Vitamin B 2 (riboflavin) coenzyme is in various oxidation and reduction reactions. Today, its deficiency is a rarity. The morphological changes it causes are changes in the scalp, lips, tongue, cornea, and erythroid lineage. Ketosis is a characteristic change. Some fissures radiate and sometimes become secondarily infected in the corner of the lips. Glossitis is also present.
Vitamin B 3 (niacin)
Niacin avitaminosis causes a disease called pellagra. It is most commonly found in alcoholics and chronic patients and in people whose diet is poor in tryptophan and rich in leucine (leucine inhibits the conversion of tryptophan to niacin). Pellagra is clinically manifested by dermatitis, diarrhea, and dementia. Long-term untreated pellagra is fatal.
Vitamin B 6 (pyridoxine)
Vitamin B 6 (pyridoxine) is a cofactor in a number of enzymes involved in the metabolism of lipids and amino acids, and its deficiency is rare
Vitamin B 12 and folic acid
Vitamin B 12 or cyanocobalamin occurs in two active forms – coenzyme B 12 and methylcobalamin. It is essential to synthesize methionine, nucleic acids, and folic acid metabolism. It is found exclusively in food of animal origin. Plants cannot produce it (that is why people who eliminate animal origin products from their diet sometimes cannot compensate for B 12, and they should be suspected of B after 12 deficiency). For the absorption of vitamin B. 12, gastric cells’ intrinsic factor is necessary.
Vitamin B 9 or folic acid (pteroylmonoglutamic acid) is an oxidized folate form. It has a similar role as cobalamin.
Both vitamins are absorbed in the small intestine. Avitaminosis of both vitamins causes megaloblastic anemia. Since DNA synthesis is disrupted, changes are first observed in the fastest-dividing hematopoietic cells. Glossitis is present. The mucosa of the digestive tract is atrophied. The bone marrow is hyperplastic and, as in the blood, megalocytes and megakaryoblasts predominate.
Anemia leads to tissue hypoxia, so there will be a fatty change in the parenchymal organs. The posterior and lateral columns of the spinal cord are demyelinated. A diet low in folic acid in the first trimester of pregnancy increases the risk of neural tube rupture.
Vitamin C ( ascorbic acid ) has the property of reversible oxidation and reduction, on which its action is based. In the body, there is a balance of reduced (L-ascorbic acid) and oxidized (L-dehydroascorbic acid) form:
L-ascorbic acid ↔ dehydro-L-ascorbic acid + 2H + + 2e – .
Vitamin C as a cofactor of proline hydroxylase
This system is associated with other reducing and oxidizing agents. Vitamin C acts in the synthesis of collagen as a coenzyme hydroxylase that hydroxylates the amino acid residues (prolyl and lysyl) of procollagen, a condition for the stabilization of collagen. It also participates in the synthesis of norepinephrine from 3,4-dihydroxy phenyl-ethylamine, carnitine from butyrobetaine 5-hydroxy-tryptophan from tryptamine. The absorption of iron from the intestine is better with ascorbic acid because it reduces the ferric form of iron to the ferrous form. Before the ferritin release, iron is converted to ferric form with ascorbic acid. Ascorbic acid protects tetrahydrofolate from the action of oxidizing substances.
In addition to collagen synthesis, vitamin C is important in synthesizing intercellular substances such as ostemucine, chondromucine, and dentin.
Humans, monkeys, and guinea pigs cannot synthesize ascorbic acid due to a mutation in the gene for the enzyme L-gluconolactone oxidase, which catalyzes the transition L-gluconogamalactone to L-ascorbic acid. The daily requirement for vitamin C in quiet conditions is 60 mg, but this need increases two to three times in stress, infection, after surgery, in pregnancy, breastfeeding, and hyperthyroidism. The reserve is small, so it wears out quickly. The kidneys excrete it as oxalate or sulfate.
Vitamin C avitaminosis is rare and causes scurvy, a disease characterized by bone disorders, bleeding, and inability to heal wounds. The cause of this is the formation of abnormal collagen, where the bleeding that accompanies scurvy is the result of a defect in collagen as an integral part of the capillary wall and venules. Therefore, we often see spotting (ecchymoses and purpura) on the mucous membranes.
Often bleeding gums, teeth can fall out due to alveolar bone resorption. Poor connection between the periosteum and bone can lead to subperiosteal bleeding. Due to insufficient production of the osteoid matrix and excessive cartilage growth, wide pineal glands are formed. Anemia is common due to frequent bleeding and reduced release of iron from ferritin reduced absorption of iron from the intestine, and reduced amount of effective folate due to the irreversible oxidation of N 10 formyl-tetrahydrofolate into ineffective metabolites.
Susceptibility to infections is a logical outcome.