Lecture No.

6
Vitamins ADEK

• At the end of this lecture, student will be able to

–Explain vitamin deficiency disorders

–Describe the preventive measures

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 VITAMIN DEFECIENCY

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 VITAMIN –A
 Also called as RETINOL
 It is fat soluble alcohol
FUNCTIONS OF VIT-A
 Maintenance of normal vision
• Rhodopsin (rods) →light sensitive pigment
→ Important in reduced light.
• 3 Iodopsins(cone )→specific colours in bright light.
 Maintenance of structure & function of specialized
epithelium
 Maintenance of normal cartilaginous & bone growth.
 Anti-proliferative effect.
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 Vitamin-A Deficiency
OCULAR LESIONS
 Lesions in the eyes
 Night blindness is the first sign
 Xerophthalmia-Replacement metaplasia of mucus-
secreting cells by squamous cells, there is dry & scaly
scleral conjunctiva.
 Hyperkeratosis in lachrymal duct.
 Corneal ulcers may occur which may get infected & causes
Keratomalacia.
 Bitot’s spots may appear which are focal triangular areas
of opacities due to accumulation of keratinized epithelium.

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 Cutaneous Lesions
 XERODERMA- The skin develops popular lesions giving toad-
like appearance.
 This is due to follicular hyperkeratosis & keratin plugging in
sebaceous glands.
OTHER LESIONS
 Squamous metaplasia of respiratory epithelium of bronchus &
trachea → predispose respiratory infections.
 Squamous metaplasia of pancreatic ductal epithelium
→obstruction & cystic dilatation.
 Squamous metaplasia of urothelium of the pelvis of kidney
→predispose to pyelonephritis & perhaps to renal calculi.

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 Vitamin E
 Also known as α-Tocopherol.
 Absorbed from intestine & transported in blood in the form of
chylomicrons.
 Stored in fat depots, liver & muscle.

VITAMIN E FUNCTION
 Antioxidant activity.

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 Vitamin E Deficiency
 Vitamin E deficiency ─ Disorders affecting its absorption &
transport
 Eg. Betalipoproteinaemia.
 Intra & extra hepatic biliary cholestasis.
 Cystic fibrosis of pancreas.
 Malabsorption syndrome.
 Infant low birth weight with immature liver & GIT tract.
 Neurons with long axons develop degeneration in the
posterior columns of spinal cord.
 Peripheral nerves develop myelin degeneration in the
axons.

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  Skeletal muscles develop denervation.
 Retinal pigmentary degeneration occur.
 RBCs deficient in vitamin E have reduced life span
(Eg. Premature infants).

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 Vitamin -D
 Also known as calcitrol.
 This vitamin exists in 2 activated sterol form,
 Vitamin D2 (or) calciferol.
 Vitamin D3 (or) cholecaciferol.
VITAMIN-D FUNCTION
1. Maintenance of normal plasma levels of calcium &
phosphorus.
 To promote mineralization of bone by
 Intestinal absorption of calcium & phosphorous.
 On bones ─ In hypocalcaemia Vit-D collaborates with
parathyroid hormone & cause osteoclastic resorption of
calcium & phosphorus from bone.

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 Vitamin-D Deficiency
 On kidneys  Stimulate reabsorption of calcium at distal
tubular level→ this also parathyroid hormone dependent
2. IMMUNE REGULATION
Presence of receptors for metabolite of vit-D on activated
lymphocytes & macrophages.
Lesions In Vitamin-d Deficiency
 Reduced endogenous synthesis.
 Dietary deficiency.
 Pancreatic insufficiency & Malabsorption syndrome.
 Derangements of vit-D metabolism ─ kidney disorders, liver
disorders, genetic disorders.
 Resistance of end-organ to vit-D.

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 Vitamin-D Deficiency
1. Rickets in growing children
2. Osteomalacia in adults.
3. Hypocalcaemic tetany due to neuromuscular dysfunction.
RICKETS
 Proliferation of cartilage cells at the epiphyses followed by
inadequate provisional mineralization.
 Persistence & overgrowth of epiphyseal cartilage.
 Deformation of bones due to lack of structural rigidity.
 Irregular over growth of small blood vessels in disorganised &
weak bone.

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 Vitamin-D Deficiency
• Rickets has following lesions & clinical characteristics
1. Biochemical changes.
2. Skeletal changes.
BIOCHEMICAL CHANGES
• Active metabolites (1,25-dihyroxy vitamin-D)-low
level.
• Plasma calcium level-slightly low.
• Plasma phosphate levels-low.
• Plasma alkaline phosphate-raise (due to osteoblastic
activity).

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 Vitamin-D Deficiency
SKELETAL CHANGES
CRANIOTABES
Small round unossified area in the membranous bones of the
skull & Skull looks square & box-like.
HARRISON’S SULCS
Due to indrawing of soft ribs on inspiration.
RACHITIC ROSARY
Deformation of chest due to cartilaginous overgrowth at
costochondral junction.
PIGEON-CHEST DEFORMITY
Anterior prostrusion of sternum due to action of respiratory
muscle.

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 BOW LEGS Vitamin-D Deficiency
In children due to weak bones of lower legs.
KNOCK KNEES
Due to enlarged ends of the femur, tibia & fibula.
LUMBAR LORDOSIS
Due to involvement of the spine & pelvis.
OSTEOMALACIA
• occur in adult.
• Failure of mineralization of the osteoid matrix.
• Dietary deficiency.

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 Clinical Feature
• Muscular weakness
• Vague bony pains
• Fracture following trivial trauma
• Incomplete (or) green-stick fractures
• Looser’s zones (or) pseudo fractures at weak places in
bones
BIOCHEMICAL CHANGES
• Serum calcium levels ─ normal or low
• Plasma phosphate levels ─ low
• Serum alkaline phosphates ─ raise (↑sed osteoblastic
activity)

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 Vitamin-c
• Also known as ASCORBIC ACID
PHYSIOLOGICAL FUNCTIONS
Ability to carry out oxidation-reduction reaction.
AS OXIDANT
• Hydroxylation of proline to hydroxyproline – Essential
component of collagen.
• Ground substance of other mesenchymal structures.
Eg. Osteoid, chondroitin, Sulfate, dentin & cement
substances of vascular endothelium.
AS REDUCTANT
• Hydroxylation of dopamine to nor epinephrine.

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 Vitamin- C Deficiency
• Maintenance of folic acid level by preventing oxidation of
tetrahydrofolate
• Role in iron metabolism in its absorption & keeping it in
reduced state
• Play a role in synthesis of neurotransmitters, neuropeptide
hormone synthesis & Immune response
VITAMIN-C DEFICIENCY: SCURVY
1. HAEMORRHAGIC DIATHESIS
2. SKELETAL LESIONS
3. DELAYED WOUND HEALING
4. ANAEMIA
5. LESIONS IN TEETH & GUMS
6. SKIN RASHS

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 Vitamin-C Deficiency

1. HAEMORRHAGIC DIATHESIS
• A marked tendency to bleeding
• Due to deficiency of intercellular cement-hold cells
together
• Hemorrhages ─ skin, mucous membrane, gums,
muscles, joints & underneath the periosteum
2. SKELETAL LESIONS
• More in growing children
• Deranged formation of osteoid matrix not
deranged mineralization
• Growing tubular bones & flat bones get affected
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 Vitamin-C Deficiency
• Hemorrhage haematomas under the periosteum & bleeding
into the joint spaces.
3. DELAYED WOUND HEALING
• Deranged collagen synthesis
• Poor preservation & maturation of fibroblasts
• Localisation of infection in the wounds
4. ANAEMIA
• Common in scurvy
• Due to
Haemorrhage
Interference with formation of folic acid
Deranged iron metabolism

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 Vitamin-C Deficiency
5. LESIONS IN TEETH & GUMS
• Scurvy interfere with development of dentin
– The gum are soft, swollen
– Bleed readily
– Get infected
6. SKIN RASH
• Hyperkeratotic & follicular rash

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 Recommended Dietary Allowances (RDA) and
Adequate Intakes (AI) for Vitamins

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 Summary

• Vitamin deficiency disorders

• Sources of different vitamins
• Symptoms of vitamin disorders

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