This presentation consists of detailed information about vitamins A,D,E,K, B complex, C. In depth information about function, signs in deficiency, management and toxicity.

1. VITAMINS
Dr SANGAM H B

2. Introduction
• Definition – organic compounds present in small amounts in various
food substances needed for growth and maintenance of the body
• Classification –
✓ Fat soluble vitamins – A,D,E,K
✓ Water soluble vitamins – B complex vitamins + vitamin C
ENERGY RELEASING HEAMATOPOIETIC OTHER
B1 – Thiamine B9 – Folic acid B6 – Pyridoxine
B2 – Riboflavin B12 – Cobalamin
B3 - Niacin
B6 – Pantothenic acid
Biotin

3. VITAMIN A
• Function –
✓Vision – 11 cis retinal
✓Skin of mucosa – maintenance of epithelium
✓Reproduction – retinol
✓Regulation of gene expression – retinoic acid
✓Growth and development
✓Tissue differentiation
✓Antioxidant vitamin – beta carotene (photoprotective)

4. • Deficiency -
✓Loss of vision to green light is the earliest sign
✓Earliest symptom – Nyctalopia (night blindness)
✓Dryness in conjunctiva and cornea (dry eyes – xerophthalmia)
✓Keratitis
✓Bitot’s spots
✓Keratomalacia
✓Phrynoderma
✓Squamous metaplasia in mucus secreting epithelium- urinary tract,
respiratory tract

5. Factors contributing to deficiency –
• Fat malabsorption,
• infection,
• measles,
• alcoholism,
• protein-energy malnutrition

7. Treatment –
• For children at high risk of vitamin A deficiency, such as those with
measles, diarrhea, respiratory disease, or severe malnutrition,
WHO recommended vitamin A supplementation is,
✓Infants < 6 months of age: 50,000 international units orally
✓Infants 6 to 12 months of age: 100,000 international units orally
✓Children >12 months: 200,000 international units orally

8. • For treatment of xerophthalmia,
✓vitamin A is given in three doses at the age-specific doses listed
above.
✓The dose for adolescent and adults is 200,000 international units
orally
✓The first dose is given immediately on diagnosis,
✓the second on the following day,
✓and the third dose at least two weeks later

9. Toxicity –
✓Acute toxicity - is manifested by,
• increased intracranial pressure,
• vertigo,
• diplopia,
• bulging fontanels (in children),
• seizures,
• exfoliative dermatitis.

10. ✓Chronic toxicity - concern in industrialized countries and has been seen in
otherwise healthy adults who ingest 15 mg/d and children who ingest 6 mg/d
over a period of several months. Manifestations include ,
• dry skin, cheilosis, glossitis,
• vomiting,
• alopecia,
• bone demineralization and pain, hypercalcemia,
• lymph node enlargement,
• hyperlipidemia,
• amenorrhea,
• features of pseudotumor cerebri with increased intracranial pressure and
papilledema
• Liver fibrosis with portal hypertension

11. VITAMIN D
Functions -
• Regulation of calcium and phosphate
• Bone development
• Immunomodulatory
• Anti-proliferative

12. Vitamin d sufficiency
• Most specific screening test for vitamin D deficiency is a serum
25(OH)vitamin D level
• Categorization of vitamin D status in adults
✓Vitamin D sufficiency:- > 20 ng/ml
✓Vitamin D insufficiency :- 12 to 20 ng/ml
✓Vitamin D deficiency:- <12 ng/ml
✓Risk of vitamin D toxicity:- > or = 100ng/ml

14. Osteomalacia
• Osteomalacia refers to impaired mineralization of bone matrix
• Clinical features-
✓Bone pain and muscle weakness
✓Bone tenderness
✓Fracture
✓Difficulty walking and waddling gait in four
✓Muscle spasms, cramps
• Most accurate way to diagnose – tetracycline labelling and
histomorphometric assessment

15. Rickets
• Rickets refers to deficient mineralization at the growth plate, as well as
architectural disruption of this structure
• Skeletal findings include-
✓Delayed closure of the fontanelles
✓Parietal and frontal bossing
✓Craniotabes (soft skull bones)
✓Rachitic rosary – beading of costochondral junction
✓Formation of Harrison sulcus at the lower margin of thorax by inward
pull of diaphragmatic attachments

18. Treatment of vitamin D deficiency
• Vitamin D should always be repleted in conjunction with calcium
supplementation
• In patients in whom D 1-α hydroxylase is impaired, metabolites that
don’t require activation step are the treatment of choice. They include
calcitriol and doxercalciferol
• If the pathway required for activation of vitamin D is intact, severe
vitamin D deficiency can be treated with pharmacologic repletion
initially (50000 IU weekly for 3-12 weeks, maintenance therapy (800
IU)
• Calcium supplementation should include 1.5-2 gm/day of elemental
calcium

19. Vitamin D intoxication
• Occurs generally after inappropriate use of vitamin D supplements
• May occur in dieters who consume megadoses of supplements or in
patients who take vitamin D replacement for malabsorption, renal
osteodystrophy, osteoporosis, or psoriasis
• Prolonged exposure of the skin to sunlight does not produce toxic
amounts of vitamin D3

20. • Symptoms
✓ Acute intoxication - hypercalcemia and include confusion, polyuria,
polydipsia, anorexia, vomiting and muscle weakness
✓Chronic intoxication – nephrocalcinosis, bone demineralization and
pain

21. VITAMIN E
Function –
• Naturally occurring most potent antioxidant vitamin (chain breaking
antioxidant)
• Lipid phase antioxidant – in biomembranes, prevents oxidation of
PUFA
• Prevents oxidation of LDL

22. Deficiency –
• Axonal degeneration – posterior column affected, decreased position
and vibration sense
• Spinocerebellar symptoms – ataxia
• Peripheral neuropathy
• Skeletal myopathy
• Pigmented retinopathy and opthalmoplegia
• RBC – increased free radical injury and decreased antioxidant can lead
to haemolytic anemia

23. Factors contributing to deficiency –
• Occurs only with fat malabsorption or genetic abnormalities of
vitamin E metabolism/transport

24. Treatment –
• Symptomatic vitamin E deficiency should be treated with 800– 1200
mg of α-tocopherol per day.
• Patients with abetalipoproteinemia may need as much as 5000–7000
mg/d.
• Children with symptomatic vitamin E deficiency should be treated
orally with water-miscible esters (400 mg/d); alternatively, 2 mg/kg/d
may be administered intramuscularly

25. Therapeutic uses of high dose vitamin E –
• Retrolental fibroplasia
• Bronchopulmonary dysplacia
• Intraventricular hemorrhage of prematurity
• Treatment of intermitt claudication
Toxicity - rare as long as liver function is normal.
• High doses of vitamin E (>800 mg/d) may reduce platelet aggregation
and interfere with vitamin K metabolism
• Nausea, flatulence, and diarrhea have been reported at doses >1 g/d.

26. Vitamin K
Function –
It is required for the posttranslational carboxylation of glutamic acid,
which is necessary for calcium binding to γ-carboxylated proteins such
as,
• factors II, VII, IX, and X; protein C; protein S [thus helps in coagulation]
• In bone (osteocalcin)
• In vascular smooth muscle (e.g., matrix Gla protein)

27. Deficiency –
• The symptoms of vitamin K deficiency are due to hemorrhage;
• newborns are particularly susceptible because of
✓low fat stores,
✓low breast milk levels of vitamin K,
✓relative sterility of the infantile intestinal tract, liver immaturity, and
poor placental transport.
Intracranial bleeding as well as gastrointestinal and skin bleeding can
occur in vitamin K–deficient infants 1–7 days after birth. Thus, vitamin K
(0.5–1 mg IM) is given prophylactically at delivery.

28. Vitamin K deficiency in adults may be seen in patients with,
• chronic small-intestinal disease (e.g., celiac disease, Crohn’s disease),
• obstructed biliary tracts, or after small-bowel resection.
• Broad-spectrum antibiotic treatment can precipitate vitamin K
deficiency by reducing numbers of gut bacteria,

29. Treatment –
• Vitamin K deficiency is treated with a parenteral dose of 10 mg.
• If clinical evidence of coagulopathy persists despite the administration
of a single dose of vitamin K, repeat the dose in 48 to 72 hours.
• Single 10 mg dose is generally more than necessary to correct the
deficiency,
• For patients with chronic malabsorption, 1–2 mg/d should be given
orally or 1–2 mg per week can be taken parenterally.

30. VITAMIN B1 - Thiamine
Function –
• Decarboxylation of α-ketoacids (e.g., pyruvate α-ketoglutarate) and
branched-chain amino acids and thus is essential for energy
generation.
• Thiamine pyrophosphate acts as a coenzyme for a transketolase
reaction that mediates the conversion of hexose and pentose
phosphates. ( HMP pathway )
• Plays role in peripheral nerve conduction.

31. Factors contributing to deficiency –
• Alcoholism,
• chronic diuretic use,
• hyperemesis,
• thiaminases in food

32. Deficiency – clinical manifestations
• In early stage induces anorexia and nonspecific symptoms (e.g.,
irritability, decrease in short-term memory).
• Prolonged thiamine deficiency causes beriberi, which is classically
categorized as wet or dry although there is considerable overlap.
• In either form of beriberi, patients may complain of pain and
paresthesia.

33. Wet beriberi presents primarily with cardiovascular symptoms that
are due to impaired myocardial energy metabolism and dysautonomia
• It can occur after 3 months of a thiamine-deficient diet.
• Patients present with,
✓enlarged heart (cardiomegaly),
✓tachycardia,
✓high-output congestive heart failure,
✓peripheral edema, and
✓peripheral neuritis.

35. Dry beriberi patients present with
• a symmetric peripheral neuropathy of the motor and sensory systems,
with diminished reflexes.
• The neuropathy affects the legs most markedly, and patients have
difficulty rising from a squatting position.

37. Alcoholic patients with chronic thiamine deficiency also may have
central nervous system (CNS) manifestations known as Wernicke’s
encephalopathy, which consists of,
• horizontal nystagmus,
• ophthalmoplegia (due to weakness of one or more extraocular
muscles),
• cerebellar ataxia, and
• mental impairment.
• When there is an additional loss of memory and a confabulatory
psychosis, the syndrome is known as Wernicke-Korsakoff syndrome.

38. Treatment –
• In acute thiamine deficiency with either cardiovascular or neurologic
signs, 200 mg of thiamine three times daily should be given
intravenously until there is no further improvement in acute
symptoms
• oral thiamine (10 mg/d) should subsequently be given until recovery is
complete

39. VITAMIN B2 – Riboflavin
Function –
• Riboflavin is an essential component of coenzymes involved in multiple
cellular metabolic pathways, including the energy-producing respiratory
pathways.
• This includes a reaction in the tricarboxylic acid (TCA) cycle and beta-
oxidation of fatty acids for energy.
• Flavoproteins are catalysts in a number of mitochondrial oxidative and
reductive reactions and function as electron transporters
Factors contributing to deficiency – Alcoholism, individuals with poor diets
and low intake of milk products

40. Deficiency -
Clinical manifestations include,
• sore throat,
• hyperemia of pharyngeal mucous membranes,
• edema of mucous membranes,
• cheilitis, stomatitis, glossitis – magenta coloured tongue, loss of
papillae
• normocytic-normochromic anemia, and
• seborrheic dermatitis
• Conjunctivitis, keratitis, corneal vascularisation

42. Treatment –
• 6 - 30 mg per oral divided daily for replacement, until deficiency is
corrected
• Co – existing B complex deficiency has to be looked for too.

43. Vitamin B3 – Niacin
Functions –
• Many enzymatic redox reactions depend upon NAD and NADP as a
cofactor.
• Needed for reductive biosynthesis of fatty acid, cholesterol, steroid
hormone
• Needed for free radical scavenging
Factors contributing to deficiency –
Alcoholism, vitamin B6 deficiency, riboflavin deficiency, tryptophan
deficiency

44. Deficiency – clinical manifestations
Pellagra (meaning "raw skin") is characterized by 4 D’s
• Dermatitis (typically located in sun-exposed areas) - Casal’s necklace
• Diarrhea,
• Dementia,
• Death.

46. Treatment –
• oral supplementation with 100–200 mg of nicotinamide or nicotinic acid
three times daily for 5 days.
Toxicity –
• Prostaglandin-mediated flushing - premedication with aspirin may
alleviate these symptoms
• Hepatic toxicity - presents as jaundice with elevated AST, ALT levels. A
few cases of fulminant hepatitis are also reported
• Glucose intolerance
• Hyperuricemia,
• Macular edema, and macular cysts.

47. VITAMIN B6 – Pyridoxine
Functions -
• Vitamin B6 refers to a family of compounds that includes
pyridoxine,pyridoxal, pyridoxamine, and their 5′-phosphate
derivatives.
• 5′-Pyridoxal phosphate (PLP) is a cofactor for enzymes involved in
amino acid metabolism.
• It is also involved in heme and neurotransmitter synthesis and
• In the metabolism of glycogen, lipids, steroids, sphingoid bases, and
several vitamins, including the conversion of tryptophan to niacin.

48. Factors contributing to deficiency - Alcoholism, isoniazid
Deficiency – clinical manifestations
• Peripheral neuropathy,
• Nutritional melalgia – Gopalan’s burning foot syndrome
• Abnormal electroencephalograms, and
• Personality changes that include depression and confusion.
Treatment –
• Vitamin B6 supplement 50 mg/d;
• higher doses of 100–200 mg/d are given if the deficiency is related to
medication use.

49. VITAMIN B12
Functions -
• It is a co-factor in folate co-enzyme recycling
• Methylcobalamin is a cofactor in the synthesis of methionine from
homocysteine.
• Needed for nerve myelination
• Important in DNA synthesis in RBC

50. Deficiency – causes
• Gastric abnormalities
✓Autoantibodies to Intrinsic factor or parietal cells (pernicious anemia)
✓Gastrectomy, bariatric surgery, gastritis
• Small bowel disease
✓Malabsorption syndrome
✓Ileal resection or bypass
✓Inflammatory bowel disease
✓Celiac disease
✓Bacterial overgrowth
✓Diphyllobothrium latum

51. • Pancreatitis
• Strict vegan diet
• Agents that block or impair vitamin b12 absorption- eg, neomycin,
metformin etc
• Inherited transcobalamin II deficiency

52. FOLIC ACID
Function -
• It works as a methyl donor for cellular methylation and protein
synthesis
• It is directly involved in DNA and RNA synthesis
• It is also a coenzyme for methionine synthesis

53. Deficiency – causes
• Nutritional deficiency -
✓Substance abuse, alcoholism
✓Poor dietary intake
• Malabsorption-
✓Celiac disease (sprue)
✓Inflammatory bowel disease
✓Short bowel syndrome
• Drugs – methotrexate, trimethoprim, phenytoin
• Increased requirement – pregnancy, lactation

54. Clinical features of vitamin b12 and folate
deficiency
• Megaloblastic anemia, anorexia, weight loss
• Glossitis, angular cheilosis, constipation or diarrhoea
• Jaundice (unconjugated),
• Hyperpigmentation may occur with a deficiency of either folate or
cobalamin.
• Symmetric paresthesias or numbness and gait problems –with vitamin
b12 deficiency
• The classic neurologic finding in vitamin B12 deficiency is subacute
combined degeneration of the dorsal (posterior) and lateral columns
(white matter) of the spinal cord due to demyelination.

56. Treatment
• Vitamin B12 deficiency - The dose for adults is 1000 mcg parenterally
once per week until the deficiency is corrected and then once per month
(cyanocobalamin) or once every other month (hydroxocobalamin).
• Folic acid deficiency – is treated with oral folic acid (1 to 5 mg daily. For
those with a reversible cause of deficiency, therapy is generally given for
one to four months or until there is laboratory evidence of hematologic
recovery.
✓For those with a chronic cause of folate deficiency, therapy may be
given indefinitely.

57. VITAMIN C – Ascorbic acid
Function –
• antioxidant activity,
• promotion of nonheme iron absorption,
• carnitine biosynthesis,
• conversion of dopamine to norepinephrine,
• synthesis of many peptide hormones.
• It is also important for connective tissue metabolism and cross-linking
(proline hydroxylation),
• and it is a component of many drug-metabolizing enzyme systems,
particularly the mixed-function oxidase systems.

58. Factors contributing to deficiency - Smoking, alcoholism
Deficiency - The clinical deficiency syndrome known as scurvy is largely
due to impaired collagen synthesis and disordered connective tissue. The
most specific symptoms
• follicular hyperkeratosis
• perifollicular hemorrhage, with petechiae and coiled hairs
• ecchymoses, gingivitis,
• arthralgias,
• edema,
• anemia, and
• impaired wound healing

60. Treatment -
• For children, recommended doses are 100 mg ascorbic acid given
three times daily (orally, intramuscularly or intravenously) for one
week, then once daily for several weeks until the patient is fully
recovered
• Adults are usually treated with 300 to 1000 mg daily for one month

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