vitamins : hyper and hypovitaminosis.pptx

Study vitamins

1. VITAMINS HYPO AND HYPER VITAMINOSIS Submitted By: Dr. N. Sujatha Submitted By: Atul Saini

2. INTRODUCTION Vitamins are a group organic essential substance, needed in tiny amounts to facilitate normal metabolism. Vitamins serve diverse functions such as cofactors and coenzymes in enzyme systems (e.g., vitamin B complex), hormones ( eg , vitamin D), and antioxidants (e.g., vitamin E). Their action as cofactors in many enzyme systems makes them essential for various body functions, such as energy production, hematopoiesis , neurological functions

3. Vitamin deficiencies may be caused by: (1) Deficient intake (ignorance and faulty cooking method (2) Faulty absorption ( malabsorption and chronic diarrhea) (3) Poor utilization (chronic liver disease); (4) Greater demand. The requirement of vitamins increases in preterm babes.

4. VITAMIN A : Vitamin A is a subgroup of retinoids exhibiting the biological activity of retinol. Vitamin A from the diet is ingested as carotene (from plant sources) and retinal (from animal sources). Breast milk fulfills the needs of vitamin A entirely for first 6 months of life and continues to be an important source up to 2 years) . V itamin A (retinol) is abundant in fish liver oils, liver, dairy products, and egg yolk. Vegetarian sources of vitamin A are green leafy vegetables, and yellow fruits and vegetables, where it is present as carotenoids .

5. Vitamin A is necessary for the integrity of epithelial tissues and functioning of retina and vision. Retinol is necessary for spermatogenesis and integrity of testicular and vaginal epithelium Vitamin A as retinoic acid is involved in growth especially skeletal growth, fertility, and immune response. It is also termed as an anti-infective vitamin. This is attributed to its role in maintaining integrity of epithelial tissue for resisting invasion by pathogens and for functional immune response)

6. VITAMIN A DEFICIENCY Causes : Insufficient intake of vitamin A (not consuming vitamin A rich fruit, vegetables, etc.) is the most common cause of vitamin A deficiency. Severe malnutrition is another important cause. The requirement of vitamin A is increased in preterm neonates and during infections ( eg , measles and respiratory Infections) making children prone to its deficiency during these states. Chronic diarrhea, malabsorptive states, and chronic liver disease cause significant vitamin A deficiency

7. Indicators of Vitamin A Deficiency: Clinically, presence of night blindness is used as the best indicator for vitamin A deficiency (VAD). Serum retinol of <0.70 µmol/L is used to identify those at risk for biochemical VAD.

8. Xerophthalmia Prolonged deficiency of vitamin A in the diet results in a syndrome of xerophthalmia , especially prevalent in 6-36 months old. Xerosis (dryness) of the conjunctiva is usually the first clinical sign. Palpebral conjunctiva loses its sheen and wetness. Wrinkling appears in the conjunctiva which can be appreciated as conjunctival folds when the child moves the eyeball toward the opposite side. Bitot spots are the most characteristic feature of xerophthalmia . These appear as triangular areas on the temporal aspects of junction of cornea with sclera. The spots are made up of heaped up dry masses of conjunctival epithelium. The spots are whitish gray, look dry, non- reflective, and may have embedded wrinkles. Cornea dries up as the next step: A dry cornea is susceptible to exposure injury and can get ulcerated easily

9. Acute Hypervitaminosis A It causes pseudotumor cerebri manifesting as bulging fontanel, vomiting, and irritability in young infants. Older children may c omplain of diplopia and headache. Chronic Hypervitaminosis A I t results in skin desquamation, hepatosplenomegaly , bone swellings, and increased intracranial tension. The shaft of long bones may show hyperostosis. Chronic toxicity usually do results from intake of medicinal vitamin A over a period of in; several weeks. Excessive intake of vitamin A is teratogenic during first trimester of pregnancy.

10. Vitamin D Vitamin D3 is synthesized In the skin on exposure of 7-dehydrocholesterol (present under normal skin) to ultraviolet rays in the sunlight. (The metabolically active form of vitamin D is 1,25(OH)2D 3 which is obtained by Conversion of cholecalciferol to 25-hydroxy-cholecalciferol 25(OH)D3 in the liver followed by another hydroxylation in the kidney. 1,25(OH)2D 3 is a hormone which helps in absorption calcium and phosphorus in the gut, thereby increasing the serum calcium. Daily requirement: 400IU/ day for breastfeeding infants. SOURCES Fish oils, liver, egg yolk, and fortified foods are main sources of vitamin D besides exposure to sunlight. Milk, including breast milk, provides very less amounts of vitamin D.

11. ROLE IN HEALTH : Main functions of vitamin D are (1) To enhance intestinal calcium and phosphate absorption. (2) To inhibit parathormone production. (3) To ensure formation and mineralization of bone. (4) protection against a number of autoimmune diseases including multiple sclerosis and inflammatory bowel disease.

12. Vitamin D deficiency (VDD) VDD is common in infants who are dark-skinned and exclusively breastfed beyond 3-6 months of age. Use anticonvulsant or antiretroviral medication. Additional risk factors include residence at higher latitudes, winter season, and other causes of low-sun exposure. Clinical Features: Most clinical manifestations of rickets are due to bone changes related to deposition of unmineralized osteoid and softening. Craniotabes , the earliest manifestation of rickets, is the ping pong ball feeling of skull in infants on giving pressure over the occipital or parietal bones.

13. Anterior fontanel is large and its closure is delayed beyond 18 months. There is clinically apparent widening of the wrists. Long bones of legs get deformed when the child starts bearing weight (after 1 year). Anterior bowing of legs, knock knee. Scoliosis, kyphosis , or lordosis may occur in severe cases.

14. US Endocrine Society classification based on serum levels of 25(OH)D3 vitamin D status is classified as: Severe deficiency. <5 ng/mL; Deficient: <12 ng/mL; Insufficient 12-20 ng/mL; Sufficient: >20 ng/mL; and Toxic: >150 ng/mL. HYPERVITAMINOSIS D Causes Administration of vitamin D in therapeutic doses for long periods results in toxicity. The upper limit of daily intake of vitamin D is 1,000 IU for infants and 2,000 IU for older children and adults. Clinical Features Renal manifestations are secondary to hypercalcemia and hypercalciuria ; and include polyuria , nephrolithiasis , and renal failure. Gastrointestinal manifestations are anorexia, abdominal pain, and constipation Child may have disorientation, convulsions, and coma.

15. VITAMIN E ROLE IN HEALTH Vitamin E is an antioxidant that protects membrane phospholipids from free radical induced peroxidase damage. It has anti-inflammatory effect and may raise the concentration of high-density lipoprotein cholesterol. SOURCES Nuts such as almond and peanut, and polyunsaturated vegetable oils such as canola and olive, are rich sources Seeds, whole wheat grain, egg yolk, milk fat, butter, green leafy vegetable, liver and fortified cereals, are good sources. Intake of 4-5 mg/day is considered adequate for infants.

16. VITAMIN E DEFICIENCY Causes Vitamin E deficiency might be observed in low-birth-weight infants. Majority of children with vitamin E deficiency have cholestatic disease with coexistent fat malabsorption . premature infants are associated with hemolytic anemia, hyperbilirubinemia , and intraventricular hemorrhage. VITAMIN E TOXICITY Vitamin E toxicity occurs due to excessive vitamin supplementation, not due to dietary intake. Vitamin E may inhibit platelet aggregation and also vitamin K-dependent clotting cascade resulting in enhanced risk of bleeding, specifically in patients on anticoagulation or ant platelet therapy.

17. VITAMIN K ROLE IN HEALTH It is an essential cofactor of the enzyme vitamin K-dependent carboxylase that catalyzes formation of prothrombin . It is also needed for the generation of several proteins involved in hemostasis (blood clotting) and bone metabolism, and other physiological functions. SOURCES Phylloquinone is the main dietary form of vitamin K, present primarily in green leafy vegetables (spinach, cabbage, and lettuce). Cheese, egg yolk, and liver contain the vitamin in fair amounts .

18. VITAMIN K DEFICIENCY Less placental transfer of phylloquinone , low clotting factor levels, and low vitamin K content of breastmilk lead to deficiency in newborns, resulting in hemorrhagic disease of the newborn. Idiopathic vitamin K deficiency of infants or acquired pro thrombin complex deficiency is a bleeding disorder of infants between 2 weeks and 2 months old. Diagnosis Serum level of phylloquinone (K1) <0.15 µg/L are indicative of deficiency and is most commonly used marker.

19. VITAMIN C ROLE IN HEALTH AND DISEASE Vitamin C (ascorbic acid) is essential for formation of collagen and intercellular matrix in teeth, bones, and capillaries. It is also involved in adrenal cortical functioning, and electron transport. Being a strong reducing agent, it provides protection to eyes and lungs against oxidizing agents and reduces oxidation of low-density lipoproteins and prevents deposition of atheromatous plaques. DIETARY SOURCES Leafy vegetables, citrus fruits, Indian gooseberry ( amla ), and tomatoes are rich sources of the vitamin E. Even roots and tubers such as potatoes, cabbage, leafy greens, and germinating pulses contain considerable amounts of it, as do guavas. Large quantities occur in liver and kidney but not in lean meat. Eggs, meat, and poultry are poor in vitamin C. Vitamin C is destroyed in cooking and storage.

20. SCURVY Severe vitamin C deficiency causes scurvy. The usual age of onset is 6-18 months. Severely malnourished children, and children dependent on boiled animal milk for their nutritional needs are at significant risk of scurvy. Breastfed children are protected as at significant contains enough vitamin C to meet most of the requirements in the first 2 years of life. Clinical Features Irritability, anorexia, low grade fever and crying on handling are early features of scurvy. This is followed by swelling of limbs with the child assuming a frog-like position (abduction of thighs and slight flexion of knees). Child may be so reluctant to move his limbs that he appears paralyzed (pseudo paralysis). Gums are swollen and purplish which start bleeding easily during the period of dentition. TOXICITY: Safe in higher doses.

21. VITAMIN B COMPLEX Vitamin B complex includes thiamine (B1), riboflavin (B2), niacin (B3), pyridoxine (B6), folic acid, cyanocobalamin (B12). Being water-soluble, excess amounts are excreted in the urine, rarely posing a threat of toxicity. THIAMINE (B1): ROLE IN HEALTH: Synthesis of nucleic acid, and fatty acid synthesis. It maintains good appetite, normal digestion, the muscle tone, and a healthy mental attitude. Its deficiency causes mental and neurological disturbances. It is also required for the synthesis of acetylcholine and gamma- aminobutyric acid (GABA)

22. Sources Liver, organ meat, egg yolk, fish, dry beans and peas, soybean, peanuts, whole grains, enriched bread, cereals, and dried yeast are rich sources. Daily Requirement Normal requirements depend on age, physiological status, level of physical activity, and range between 0.5 and 1.7 mg per day. Thiamine Deficiency Thiamine is readily lost from rice during the process of milling. Being a water-soluble vitamin, further losses take place during cooking due to leaching of the vitamin into the cooking water. Clinical Features Thiamine deficiency mainfests as beriberi.

23. Initial symptoms are nonspecific such as nausea, and abdominal pain. Fatigue. Dry beriberi: Neuritic form manifests as irritability, ataxia, tenderness of calf muscles, hypotonia , and diminished deep tendon reflexes. These children present with altered sensorium , signs of raised intracranial pressure, meningeal irritation, and neurologic deficit. This presentation is known as Wernicke encephalopathy. Wet beriberi: This manifests in apparently healthy infants between the ages of 2-4 months with cardiovascular involvement, is characterized by cardiomegaly , edema, and congestive heart failure.

24. RIBOFLAVIN (VITAMIN B₂) Riboflavin enzymes are involved in many oxidative enzyme systems in energy metabolism, synthesis of glycogen and erythropoiesis . Riboflavin is cardinal to cellular growth and tissue respiration. Retina also contains free riboflavin. Sources Eggs, green leafy vegetables, organ meats liver, milk and its pr ducts (cheese, whey, curds, and butter milk) are some source. Daily Requirement The requirement of B2 is related to energy intake, being 0.9 per 1,000 kcal for men and 1.1 mg/1,000 for women per day.

25. Riboflavin Deficiency Clinical Features Malnutrition, malabsorption , and prolonged diarrhea are the main causes of riboflavin deficiency. Characterized by lesions in oral cavity, eye, and skin. Oral lesions: fissuring and cracking at the angles of mouth and fissuring, redness, or paleness of tongue; seen in riboflavin deficiency. Eye manifestations include photophobia, lacrimation , itching.

26. NIACIN (PELLAGRA PREVENTING FACTOR) (B3) Niacin is essential for functioning of skin, intestinal tract, and nervous system. It plays an important role in DNA synthesis and repair. Niacinamide is part of coenzymes connected with glycolysis , tissue respiration, and synthesis of macromolecules. Sources Cereals, pulses, groundnut, and green leafy vegetables are main sources in vegetarian diet whereas fish, meat and poultry form are for non-vegetarians. Pellagra Pellagra is the classical syndrome resulting from niacin deficiency. The classical triad of three D's-diarrhea, dermatitis, and dementia summarizes the clinical presentation of pellagra.

27. PYRIDOXINE (B6) Pyridoxine is essential for normal brain metabolism and growth of infants. Through its active coenzyme form ( pyridoxal phosphate), vitamin B6 is needed for important pathways - like gluconeogenesis , synthesis of neurotransmitters such as serotonin, dopamine, taurine , GABA, norepinephrine , and histamine. Sources Liver, meat, fish, yeast, cereals, pulses, and peas potatoes, and bananas are rich sources. Pyridoxine Deficiency Clinical Features Clinical features include failure to thrive, hyperirritability, microcytic hypochromic anemia, nausea and vomiting. TOXICITY- Very high dosage of B6 may cause neuropathy.

28. COBALAMIN (VITAMIN B12) Vitamin B12, plays an important role in lipid and carbohydrate metabolism, nucleic acid synthesis, protein synthesis, and affects myelin formation. Sources Vitamin B12, is present only in foods of animal origin such as liver, meat, eggs, and milk. Fortified cereals main sources for vegetarian populations. Vitamin B12 Deficiency Causes Vegans have low serum B levels which can pose a serious risk of deficiency. Lack of intrinsic factor in the stomach results in failure of absorption of vitamin B12, and causes pernicious anemia.

29. Clinical Features Anemia: In the bone marrow, erythropoiesis is arrested in the later stages. The failure of maturation does not prevent hemoglobinization , resulting in macrocytic normochromic anemia. Neuropathy : Demyelination of large nerve fibers of the spinal cord, Early signs are numbness and tingling sensation in the fingers and toes. Newborn : Vitamin B12 deficiency occurs in >50% women. Maternal vitamin B12 deficiency has been linked to offspring insulin resistance.

30. FOLIC ACID Along with vitamin B12, folic acid has a role in the synthesis of nucleic acids. Sources Green leafy vegetables especially spinach and broccoli, asparagus, cereals, beans, nuts, fruits, liver, and yeast, are good sources of folate . Folic Acid Deficiency Risk of folate deficiency is increased during periods of rapid growth as in infancy. It can also result from poor-nutritional intake, malabsorption (celiac disease and inflammatory bowel disease). Clinical Features Impaired synthesis of DNA in the cells results in abnormal cell division. Growth retardation, and impaired immunity. Neural tube defects: Maternal folic acid deficiency during the first trimester (phase of embryogenesis) is associated with neural tube defects in the fetus.

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