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I YEAR PG
CONTENTS
INTRODUCTION
CLASSIFICATION
DIFFERENCES BETWEEN FAT AND WATER SOULBLE VITAMINS
VITAMIN A
VITAMIN D
VITAMIN E
VITAMIN K
VITAMIN C
VITAMIN B COMPLEX
HYPERVITAMINOSES
VITAMIN LIKE COMPOUNDS
ANTI-VITAMINS
CONCLUSION
INTRODUCTION
Christiaan E
Pancreatic
hydrolases
in the
Intestinal
intestine cells
2 TYPES
Rods Cones
Dim Bright
light light
Rhodopsin Iodopsin
Reproduction
Sources
Vitamin A Deficiency
Causes
MANIFESTATIONS:
• Inadequate intake Night blindness (earliest symptom)
Keratomalacia
Infections
Growth retardation
XEROPHTHALMIA BITOT’S SPOTS
In young rats, whose mothers have been fed on a deficiency diet for five
months preceding the birth of the off spring, there is distortion in the shape
of the incisors and molars.
ACTIVE FORMS
(Hormones) :
1,25(OH)2dihydroxycholecalciferol or calcitriol
BIOCHEMICAL ACTIONS
Calcitriol is biologically active form and regulates the plasma levels
of calcium and phosphate. It acts as 3 different levels ( intestine,
kidney and bone) to maintain plasma calcium (normal- 9-11mg/dl)
SITES OF ACTION :
Intestinal mucosal cells:
Calcitriol promotes the absorption of calcium from the intestine. It
increases the synthesis of Calbindin (calcium binding protein)
Osteoblasts of bone:
Calcitriol increases the activity of osteoblasts to secrete alkaline
phosphatase. Due to this the local concentration of Ca and P is
increased leading to mineralization of bone.
In renal tubules
It increases the reabsorption of calcium and phosphorous in the
tubules.
Pregnancy : 10 μg/day
Postmenopausal women: 15 µg until age 70, and 20 µg in > 71 yrs
SOURCES
VITAMIN D DEFICIENCY
DEFICIENCY: CAUSES
Vitamin D deficiency Impaired 25-hydroxylation
• Impaired cutaneous production Liver disease, isoniazid
• Dietary absence
• Malabsorption
Impaired 1 alpha
hydroxylation
Accelerated loss
• Increased metabolism (barbiturates, Hypoparathyroidism
phenytoin, rifampin) Renal failure
• Impaired enterohepatic circulation Ketoconazole
• Nephrotic syndrome
1 alpha-hydroxylase
mutation
• Bone deformities
• Bow legs
• Knock knee
• Rachitic rosary
• Pigeon chest
Crowns of permanent central incisors and first molars and occasionally the
lateral incisors and cuspids are involved.
The bones of the jaw may be deformed because of the tension of the
attached muscles on the markedly weakened (hypocalcified) structures.
In severe chronic deficiency the dentine matrix does not mineralize so that the
predentine is wider.
In very severe deficiency there may be pulp inclusions and the rate of formation
is retarded.
Function:
Protects red blood cells from hemolysis by oxidizing agents such as 𝑯𝟐 𝑶𝟐
This enzyme neutralizes free radicals that would otherwise damage cell
membranes.
Pregnancy : 10 mg/day
Manifestations of deficiency
Human deficiency has not been reported. But in animals, have been shown to
produce
Muscular dystrophy
Hemolytic anemia
Hepatic necrosis
Sterility
Hypervitaminosis E
CHEMISTRY:
Vitamin K1( Phylloquinone) : Green leafy vegetables
SOURCES
DEFICIENCY OF VITAMIN K
In normal adults, dietary deficiency rarely occurs since the intestinal
bacteria synthesize sufficient.
Liver disease
Obstructive jaundice
Malabsorption syndrome
Lack of this vitamin may cause excessive gingival bleeding after tooth-
brushing or spontaneously.
In severe case, a slow constant, mild hemorrhage occurs from the gums.
VITAMIN C
In 1933, vit. C was named ascorbic acid owning its anti-scorbutic
properties.
ABSORBED in small intestine and excreted in urine.
CHEMISTRY:
Reversible reaction
BIOCHEMICAL FUNCTIONS
COLLAGEN FORMATION- VIT c plays role of coenzyme in hydroxylation of
proline and lysine while procollagen is converted to collagen.
Hydroxylation reaction is catalysed by lysyl hydroxylase and prolyl
hydroxylase and this reaction is dependent on vit c.
Proline and lysine are essential for collagen cross linking.
“Cork screw” hair pattern with tiny bleeding points around the orifice of a
hair follicle.
First named Aneurin for the detrimental neurological effects if not present in
the diet.
SOURCES
DEFICIENCY MANIFESTATIONS
Chronic alcoholism
DRY BERI-BERI
Bilateral and symmetric,
predominantly involving the
lower extremities
Continued deficiency causes loss of knee jerk, loss of vibratory and position
sensation in the toes, atrophy of the calf and thigh muscles, and finally foot
drop and toe drop.
That the arms can be affected after leg signs are well established.
WET BERI-BERI
Thiamine deficiency when myocardial disease is prominent.
A more rapid form of wet beriberi has been termed acute fulminant
cardiovascular beriberi or Shoshin beriberi, in which vasodilation continues,
resulting in shock in a patient with heart failure.
WERNICKE-KORSAKOFF SYNDROME
Also called Wernicke encephalopathy.
Hypersensitive dentin.
SOURCES
DEFICIENCY MANIFESATIONS
Its termed ariboflavinosis.
In Italian vernacular, pellagra means "skin that is rough" and refers to the
thickened, rough skin of persons with pellagra.
The disease pellagra involves skin, gastrointestinal tract and central nervous
system.
DIARRHEA
DEMENTIA
As the condition progresses the papilla (fungiform and filiform) atrophy, and
there is desquamation of the superficial epithelial layers, leaving a smooth
glistening, red dorsal surface.
Staggering gait
Sleep disturbances
VITAMIN –B6 (PYRIDOXINE)
Vitamin B6 is used to collectively represent the three compounds :
Pyridoxine
Pyridoxal
Pyridoxamine
The active form is Pyridoxal Phosphate (PLP).
FUNCTIONS
PLP is a cofactor for the synthesis of important neurotransmitters:
• Serotonin
• Dopamine
• Epinephrine
• Norepinephrine
• GABA
RECOMMENDED DIETARY ALLOWANCE
Adult : 1-1.2 mg/day
Pregnancy: 1.9 mg/day
Lactation: 2.0 mg/day.
Children : 0.5 to 1.0 mg/day.
DEFICIENCY MANIFESTATIONS
Formerly known as
vitamin H
Coenzyme R
Anti-egg white injury factor
Adults : 30 μg/day
Pregnancy : 30 μg/day
Lactation : 35 μg/day
Children : 8 to 25 μg/day.
DEFECIENCY MANIFESTATIONS
Biotin deficiency is not common, since it is well distributed in foods and also
supplied by the intestinal bacteria
VITAMIN-B9 (FOLIC ACID)
Also called :
Folacin (Latin for leaf)
It is important for one carbon metabolism and is required for the synthesis
of certain amino acids, purines and the pyrimidine-thymine.
Degradation of histidine
Histidine ->->->formiminoglutamate(FIGLU)
Methionine Synthesis
Homocysteine + 5-Me-THF -> Methionine + THF
"Beefy tongue"
SOURCES
DEFICIENCY MANIFESTATIONS
Pernicious anemia
Megaloblastic anemia
Homocystinuria
Glossopyrosis
HYPERVITAMINOSIS OF B COMPLEX
Thiamine (B1):
Causes paralysis. Blocks nerve transmission. Restlessness, convulsions,
labored respiration, death (respiratory paralysis and cardiac failure).
Riboflavin (B2):
Bright yellow urine, fatigue, vomiting, itching, numbness, burning or
prickling sensation, sensitivity to light and hypotension occurs.
Niacin (B3):
Hyperemia of skin, Pruritus, GIT disturbances and acanthosis nigricans.
Low blood pressure, light headedness, insomnia, liver damage, peptic
ulcer, skin rash, altered liver function tests may occur.
Pantothenic acid (B 5):
Overdose produce diarrhea, GIT problems, water retention may
occur.
Pyridoxine (B6):
Progressive ataxia, impaired vision and vibration senses, and loss of
deep tendon reflexes are seen. Perioral numbness and clumsy limbs
are present. Loss of appetite, stomach upset and skin lesions also
occurs.
Biotin (B 7):
Hyperkeratosis of superficial follicular epithelium of skin
Choline:
More than 3.5 gm/day in take causes skin rash and increased blood
sugar.
VITAMIN LIKE COMPOUNDS
Besides the vitamins that are described, there are many other
compounds present in food as accessory factors.
• Choline
• Inositol
• Lipoic Acid
• Para-amino Benzoic Acid
ANTIVITAMINS
• For the most part vitamins are obtained from food but few are
obtained by other means like Vitamin K from gut flora.