Vitamins

 Vitamins are non-energy yielding, essential for normal

human metabolism.
 Required in small quantities (diet).
 Precursors of a vitamin can be called as Vitamers.
 Trace minerals, a.a’s & F.A’s are required in larger
quantities.
 Vitamin deficiencies- due to inadequate intake,
malabsorption, tissue needs & excretion, genetic
abnormalities & drug- vitamin interactions.
 Vitamins- prevention & treatment of deficiency diseases.
 Vitamins are traditionally divided into two groups:
(a) Fat-soluble (A, D, E, K)
(b) Water-soluble (B complex, C)
 VITAMIN A-
 Vit.A occurs in nature in several forms- Retinol (Vit. A1),
Dehydro-retinol (Vit A2) & Carotenoids.
 Physiological role & actions- (a) Visual cycle (b) Epithelial
tissue (c) Reproduction (d) Immunity.
Deficiency symptoms-
 Xerosis, keratomalacia, corneal opacities, blindness,
hyperkeratinization, keratinization of epithelium, susceptibility
to infection. tendency to urinary stone formation, sterility,
abortions, foetal malformations, growth retardation.
 Vit.A Therapeutic uses
1.Prophylaxis of vit A deficiency- infants, pregnancy, lactation,
hepatobiliary diseases, steatorrhoea: 3000–5000 IU/day.
2. Treatment of established vit A deficiency:
50,000–100,000 IU i.m or orally for 1–3 days followed by
intermittent supplemental doses.
3. Skin diseases- like acne, psoriasis, ichthyosis.
 Interactions
(i) Vit E promotes storage & utilization of retinol & its toxicity.
(ii) Liquid paraffin + vit. A can result in deficiency.
(iii)Neomycin induces steatorrhoea & interferes with vit A
absorption
 Hypervitaminosis A- Excess retinol consumption (100,000 IU
daily for months) produces toxicity—N,V, dermatitis,
exfoliation, hair loss, bone & joint pains, loss of appetite,
bleeding, increased ICT & chronic liver disease.
 Excess retinol is also teratogenic.
 A/c poisoning- consumption of polar bear liver (30,000 IU/g vit
A).
Treatment-
 Vit E which promotes storage of retinol in tissues & speeds
recovery.
 Excess intake of carotenoids doesn’t produce hypervitaminosis
A, because conversion to retinol has a ceiling.
 VITAMIN E:
 α tocopherol is the most abundant & potent Vit. E.
 d-isomer is more potent than l-isomer.
 Daily requirement- 10 mg & is increased by high intake of
polyunsaturated fats.
 Physiological role & actions-

 Vit E acts as antioxidant, protecting unsaturated lipids in cell

membranes, coenzyme Q, etc. from free radical oxidation
damage & X generation of toxic peroxidation products.
 Vit E deficiency symptoms-
 In animals- abortion, spinal cord degeneration, sk. muscles and
heart & haemolytic anaemia.
 In humans- neuromuscular diseases in children, neurological
defects & haemolytic anaemia.
 Therapeutic uses-
1. Primary vit E deficiency- Supplemental doses (10–30 mg/ day)
may be given to pt’s at risk.
2. G-6-PD deficiency- 100 mg/day increases survival time of
erythrocytes.
3.Acanthocytosis- 100 mg /week i.m: normalizes oxidative fragility
of RBC’s.
4. The risk of retrolental fibroplasia in premature infants exposed
to high oxygen concentrations can be reduced by 100 mg/kg/day.
5. Along with vit A- enhance its absorption & storage, and in
hypervitaminosis A to reduce its toxicity.
6. Large doses (400–600 mg/day) - Symptomatic improvement in
intermittent claudication, fibrocystic breast disease & nocturnal
muscle cramps.
7. Antioxidant property- recurrent abortion, sterility, menopausal
syndrome, toxaemia of pregnancy, prevention of CVD, cancer,
skin diseases, neurodegenerative disorders, post-herpetic
neuralgia, scleroderma.
 Interactions-
 Vit E can interfere with iron therapy.
Antioxidant vitamins-
 Antioxidants are believed to quench free radicals (highly
reactive).
 Oxidative free radicals causes lipid peroxidation, DNA
damage, etc. which can cause atherosclerosis, cancers,
neurodegenerative diseases & inflammatory bowel diseases.
 Many endogenous & dietary compounds like SOD, ferritin,
transferrin, ceruloplasmin, α tocopherol, β carotene &
ascorbic acid have antioxidant & free radical scavenging
properties.
 Several observational studies & meta analysis have failed to
demonstrate benefit of antioxidants in prevention of CVD &
cancer etc.,
 α tocopherol (>400 mg/day)- may increase CHF risk.
 High dose of vit A - increase risk of hip fracture among
postmenopausal women.
 Its advised to adopt a healthy lifestyle (eating fruits, vegetables, regular,
exercise, avoiding overweight & smoking), rather than consuming
antioxidant medications.
 Antioxidant preparations containing widely variable amounts of
β-carotene, vit A, E & C, Se, Zn, CU, Mn, carnitine are highly
promoted & consumed, but with no credible evidence of benefit,
and may be some potential harm.
WATER-SOLUBLE VITAMINS-

Thiamine (Vit B1)-

 Physiological role- converts into thiamine pyrophosphate,
coenzyme in CHO metabolism (decarboxylation of ketoacids &
HMP shunt), NMT.

 Pyrithiamine & oxythiamine are synthetic thiamine antagonists.

Tea also contains a thiamine antagonist.

 Deficiency symptoms- Dry (neurological symptoms are

prominent) & Wet beriberi (CVS is primarily affected).
Thiamine uses-

1. Prophylactic- (2–10 mg daily) in infants, pregnancy, diarrhoeas.

2.Beriberi- 100 mg/day i.m. or i.v. till symptoms regress & then
maintenance doses orally.

3.A/c alcoholic intoxication:100 mg. Most neurological symptoms

in chr. alcoholics are due to thiamine deficiency.

4.In neurological, CVD, hyperemesis gravidarum, chronic anorexia

& obstinate constipation- symptoms are improve dramatically if
thiamine deficiency has been causative.
 Riboflavin (Vit B2)
Actions & physiological role- Flavin adenine dinucleotide (FAD)
and flavin mononucleotide (FMN) are coenzymes for
flavoproteins involved in many oxidation-reduction reactions.
Riboflavin deficiency symptoms- angular stomatitis, sore tongue,
mouth ulcers, vascularization of cornea, dry skin, hair loss,
anaemia & neuropathy.
Therapeutic uses-
1.To prevent and treat ariboflavinosis (2–20 mg/day oral or
parenteral), generally along with other B complex members.
 Niacin (Vit B3) -Tryptophan (a.a’s) is precursor.
Physiological role & actions-
 Nicotinic acid (NA) is converted to amide which is a component
of the coenzyme Nicotinamide adenine-dinucleotide (NAD) and
its phosphate (NADP) involved in oxidation-reduction reactions.
 Large doses of N.A cutaneous vasodilation & also lowers plasma
lipids.
Niacin deficiency- ‘Pellagra’, cardinal manifestations of
Dermatitis, Diarrhoea, Dementia).
 Chronic alcoholics are particularly at risk of developing pellagra.
N.A therapeutic uses-
1. Prophylactic (20–50 mg/day oral) in people at risk of developing
pellagra.
2. Treatment of pellagra—200 to 500 mg/day in divided doses
orally or parenteral. Improvement occurs in 1–2 days, but skin
lesions take weeks to months. Nicotinamide is preferred over the
N.A.
3. Hartnup’s disease: in which tryptophan transport is impaired, &
in carcinoid tumours which converts tryptophan to 5-HT, need
niacin supplementation.
4. PVD & hypolipidemic agent- N.A is used.
 Pyridoxine (Vit B6)
Physiological role & actions-
 Pyridoxal dependent enzymes include transaminases &
decarboxylases involved in synthesis of nonessential a.a’s,
metabolism of tryptophan & sulfur containing a.a metabolism,
formation of 5-HT, DA , H, GABA & aminolevulinic acid.
 High ptn diet increases pyridoxine requirement.
Deficiency of vit B6 symptoms-
 Dermatitis, glossitis, growth & mental retardation, convulsions,
neuritis & anaemia.
Therapeutic uses-
1. Prophylactic (2–5 mg daily) in alcoholics, infants & pt’s with
Vit B deficiency.
2.To prevent & treat (10–50 mg/day) INH, hydralazine &
cycloserine induced neurological disturbances.
3.To treat mental symptoms in women on oral contraceptives (50
mg daily).
4.Pyridoxine responsive anaemia (due to defective haeme
synthesis) & homocystinuria. (50–200 mg/day).
5. Convulsions in infants & children.
Drug interactions
1. INH reacts with pyridoxal to form a hydrazone, & X generation
of pyridoxal phosphate. INH combine & interferes with it
coenzyme function. Thus, INH therapy produces a pyridoxine
deficiency state.
2. Hydralazine, cycloserine & D-penicillamine also interfere with
pyridoxine utilization & action.

3.Oral contraceptives reduce pyridoxal phosphate levels in women.

4. Pyridoxine promotes DA formation from L-dopa in peripheral

tissues, reduces its availability in the brain, reduces anti-
parkinsonism effect, but not when a peripheral decarboxylase
inhibitor is combined with it.

5. 4-deoxypyridoxine is a Vit B6 antagonist

 VITAMIN C
 Physiological role & actions- Vit C plays a role in many
oxidative, hydroxylation, conversion of F.A folinic acid,
synthesis of adrenal steroids, CA, oxytocin & vasopressin, P.G’s
metabolism .
 It directly stimulates collagen synthesis & important for
maintenance of intercellular connective tissues.
Therapeutic uses
1. Prevention of Vit.C deficiency- 50–100 mg/ day. Vit C or orange
juice can be routinely included in infant diet.
2. Treatment of scurvy - 0.5–1.5 g/day.
3. Postoperatively (500 mg daily): accelerates healing of bedsores
and chronic leg ulcers.

4.Anaemia: It enhances iron absorption & is frequently combined

with ferrous salts (maintains them in reduced state).

Anaemia of scurvy is corrected by ascorbic Acid.

5. To acidify urine (1 g TDS–QID) in urinary tract infections.

6. Large doses (2–6 g/day)- tried from common cold to cancer but
results are inconsistent.
Thank u